The Theory of Evolution is a mathematically irrational belief system

[Alan Kleinman MD PhD]

Google has again splintered this thread so I am restarting this thread
again as round three and reposting responses from posts 851 through
875 as a single post. Please continue your posts on this thread and
not on the splinter threads as I will not follow the splinter threads.
I will post the rest of my responses to posts from round 2 in bulk on
this thread. Sorry for any inconvenience.

hersheyh Aug 10, 6:06 pm
On Wednesday, August 10, 2011 4:35:46 PM UTC-4, Alan Kleinman MD PhD
wrote:

>> On Jul 13, 9:35 am, hersheyh <hers...@yahoo.com> wrote:
>> > On Jul 12, 8:37 pm, Alan Kleinman MD PhD <klei...@sti.net> wrote:
>> > > On Jun 6, 9:16 pm, hersheyh <hers...@yahoo.com> wrote:
>> > > > On Jun 6, 12:45 pm, Alan Kleinman MD PhD <klei...@sti.net> wrote:
>> > > > > On May 24, 4:25 pm, "Frank F. Smith" <f....@cornell.edu> wrote:
>> > > > > Simultaneous mutations mean that both mutations must occur
in a single
>> > > > > individual in a single generation.

>I only require that both mutations be present in a single individual at the time the trial (individual) is tested for >the binary question (double-mutant or not-double-mutant). The mutations can occur at any time prior to the >time of testing.
It’s already clear to you how the multiplication rule of probabilities
makes it very unlikely that a “double mutant” will occur. What you are
still having difficulty understanding is that even when the mutations
accumulate from the first mutation occurring on a progenitor to the
second mutation occurring on a descendent of that progenitor, the
multiplication rule of probabilities still governs the probabilities
that these events will occur. The descendents of the progenitor have
two ways of improving the probabilities that the second mutation will
occur on one of its members of that subpopulation. The members of the
population can reproduce (amplify) the first mutation and the
population can survive to reproduce additional generations. Both these
factors increase the number of trials for the next mutation in the
sequence. If the subpopulation is unable to amplify the first mutation
in the sequence, the small number of members in the subpopulation will
have very low probability of the next mutation in the sequence of
occurring at the proper locus. Amplification is the central principle
that a population uses to overcome the effects of the multiplication
rule. Without amplification, mutation and selection is brought to a
standstill because of the multiplication rule of probabilities.

>> > > > > Not simultaneously means that the
>> > > > > beneficial mutation only has to accumulate in a descendent of an
>> > > > > ancestor who had the first beneficial mutation.

>The crucial time-point is the time of testing for the alternative traits. Not simultaneously means sequential >selection for first one trait and then for the other.
And what subpopulations are not able to do in parallel is to
successfully test for alternative traits simultaneously. This is why
combination therapy works. Subpopulations must do sufficient number of
tests (trials) for there to be a reasonable probability that that a
test will successfully find a beneficial alternative trait. And the
number of tests is governed by the number of members doing the test
and the number of generations which the members are able to reproduce.

>> > > > Simultaneous actually refers to the selection conditions. That is,
>> > > > you are selecting for resistance to both A and B simultaneously. You
>> > > > are presenting the cells with selection conditions that require both
>> > > > mutations to be in the same individual. Serial selection refers to
>> > > > selection conditions where first one trait is selected for (regardless
>> > > > of the state of the other gene) and, after recovery, selection
>> > > > conditions are changed.

>> > > Amazing, the light actually may be shining through, Combination
>> > > selection pressures, ie selection pressures which target more than a
>> > > single gene require that the mutations occur simultaneously in a
>> > > single individual in order to improve fitness for that individual.

>Combination selection pressures means that more than one selective pressure is applied. That does not require >that the mutations occur in any particular order or be present at the time of selection. You are referring to >strong combination selective pressure that drastically reduces population size by suddenly changing and >affecting the survival or growth of the w.t. organism. If you have two selective pressures, one of which is a >toxin and the other being a resource that cannot be used, the situation is quite different. In the absence of >ability to use the resource, the organism grows just as well as it always did. Adding the resource to the media >doesn't change the ability of the w.t. organism to grow and survive (making it the only resource available >would). Now add both the toxin and the resource. The toxin immediately reduces the survival of any organism >that is not resistant and we have a population collapse of the large sensitive supopulation. This dramatically >increases the frequency,

but not initially, the number, of cells resistant to the toxin. The added resource has no >effect on population numbers. The population will recover back to its original level, but will be almost >entirely composed of a toxin-resistant strain. Now sometime after this there is a mutation that allows a subset >of the organism to use the previously unavailable resource. When this mutation occurs, there will be a rapid >rise in the frequency of that variant and an increase in the size of the population. Whether the new variant will >increase to fixation will depend on any detrimental effects of the mutation wrt growing in the absence of the >resource and the amount of resource. IOW, there is combination selection added simultaneously, but, under >these conditions, you have an initial change in population due to the toxin, but the two mutations found (one >for toxin resistant and one for being able to use the resource) can certainly occur simultaneously with only a >short period of growth. If neither sele

ctive pressure reduced population *numbers*, then there is nothing to >prevent serial selection or parallel selection (if there is recombination or horizontal transfer).

You are wrong here hersheyh. The order of events is always important
in the mutation and selection phenomenon. If a mutation does not
improve fitness to reproduce, the members of that subpopulation can
not amplify that mutation. Unless the sequence of mutations gives ever
increasing fitness to reproduce, the subpopulation can not follow that
trajectory on the fitness landscape. As soon as a neutral mutation
occurs in the sequence, the subpopulation can not amplify that neutral
mutation and the probabilities for the next mutation in the sequence
are very small because of the multiplication rule of probabilities.
HIV can easily evolve resistance against single drug therapy but when
combination therapy is used, a mutation which would be beneficial for
single drug therapy is not beneficial in the combination therapy
environment. That mutation which we know would be beneficial for the
virus if single drug therapy was used does not improve fitness for
that member with that mutation because the selection pressure
targeting the other gene prevents the subpopulation from amplifying
that mutation.

If you know of a real, measurable and repeatable example of parallel
selection, post it, otherwise you are just making a mathematically
irrational speculation. And we are still waiting for you to derive the
correct probability function for random recombination. Of course you
still haven’t derived the correct probability function for two
mutations occurring but you still haven’t run out of mathematically
irrational speculations and extrapolations.
>All of your examples involve not just combination selection, but combination selection where each selective >factor must dramatically reduce the population *numbers*. Absent the reduction in *numbers* there is no >need for the mutations to already be present at the time of selection.
You’ve been so intensely indoctrinated into evolutionist folklore that
you imagine selection pressures which don’t kill or inhibit the
reproduction of some or all members of a population. For mutation and
selection to work effectively, subpopulations must amplify their
beneficial mutations. This doesn’t happen when selection targets more
than a single gene at a time. Give us a thrill and post a real example
of your mathematically irrational claims but alas, I’m afraid we will
be bored with your same old blah, blah, blah over and over again.
>> > Under the conditions of lethal or extremely strong selection (which
>> > all of your examples involve), combination selection pressures require
>> > that the mutations *be* (not *occur*) present in the same individual
>> > *before* the combination selective conditions are applied. Because
>> > the mutations are independent of each other, that means that the
>> > probability of a pre-existing double mutant (the only survivors of
>> > your selective conditions) is the correct probability for selection
>> > for *both* traits. Again, the *selection* step of the mutation
>> > followed by selection process does not cause the mutations. It only
>> > selects for mutations that actually pre-exist the selection step if
>> > that selection step is lethal or strong.
>> The example of the evolution of HIV to combination selection pressures
>> is not lethal.

>A dramatic reduction in *number* of infectious particles is the equivalent of lethality in bacteria. The very >purpose of each toxic agent is to reduce the *number* of infectious particles. And, of course, fewer infectious >particles *means* that the number of trials is drastically reduced. And that, in turn, *means* that the expected >mean number of "successful events" (which is the product of events/trial * number of trials) is reduced. And >since the probability of one or more "successes" in a population of trials is determined by the mean expected >number and the mutation rate/trial doesn't change, the drastic reduction in the number of trials is the reason >why the probability of one or more double mutants is drastically decreased.

Why don’t you quantify what you mean by a “dramatic reduction in
number” because in successfully treated patients with HIV, they can
still have millions of viral particles in their system. And just how
large was the population of humans and chimpanzees when this
population diverged? You are squirming around like a worm on a hook.

But let’s abandon your mathematically irrational world of speculation
and extrapolation and design the experiment that would demonstrate
what you claim. Start with Lenski’s E coli starvation experiment but
instead of running his experiment at ideal incubation temperature; run
his experiment several degrees off of ideal incubation temperature. So
now, instead of evolving more efficient glucose metabolizers (and in
one case a citrate metabolizer) you now have populations which must
adapt to both thermal and starvation stress simultaneously. No “toxic”
agents lethal to the bacteria involved. One bacterium gets a mutation
which is beneficial for the starvation conditions. Another different
bacterium gets a beneficial mutation for the thermal stress
conditions. But now you have two different progenitors starting
subpopulations taking different trajectories on the fitness landscape.
Each subpopulation now has its own particular set of beneficial
mutations it must acquire each giving improved fitness and a
beneficial mutation for one subpopulation will not necessarily be a
beneficial mutation for a different subpopulation. And even when a
subpopulation gets a beneficial mutation for the starvation
conditions, the thermal stress will be impairing the reproduction of
that subpopulation slowing the mutation and selection process. And
visa versa, a beneficial mutation for the thermal stress in a
different subpopulation would still be impaired from reproduction by
the starvation selection pressure.

So you are left with the argument that recombination will overcome
this mathematical difficulty but you don’t derive the probability
function for random recombination. All you have is blah, blah, blah to
support your mathematically irrational belief system.

>> If you want to call these selection pressures extremely
>> strong, ie high intensity, then the evolutionary process should
>> proceed more quickly but it doesn’t.

>Both toxins independently reduce population size (if the toxins are not independent, the situation is more >complex -- think cross-resistance against beta-lactams). Absent that greater reduction in the number of trials, >as indicated by the case of a toxin and previously unusable resource, we see no reduction in the number of >trials and no prohibition of serial or parallel evolution or mathematical irrationality.

The reason why you see no reduction in the number of trials is because
in your evolutionist mathematically irrational mind you imagine
selection pressures that don’t kill or impair the reproduction of
members of a population. Why don’t you tell us what these imaginary
selection pressures are? Why don’t you present us with real,
measurable and repeatable empirical data for your claims? You don’t
present these examples because they don’t exist. All that exists in
your mathematically irrational evolutionist mind is a collection of
folklore and speculations. And this folklore and speculation has
harmed millions of people suffering from diseases subject to the
mutation and selection phenomenon by not properly describing the basic
science and mathematics of the mutation and selection phenomenon
properly.

>> When you are talking about
>> selection targeting multiple genes simultaneously, it is highly
>> unlikely that the double or multiple mutants are pre-existing in the
>> population. That’s why it takes hundreds of generations of
>> amplification before there is a reasonable probability that the next
>> beneficial mutation will occur on a member with a previous beneficial
>> mutation when only a single selection pressure is targeting a single
>> gene.

>More important is the absence of recombination or horizontal transfer. The reason sequential evolution (which >is quite possible and seen in many of the examples you give, which are largely viral or bacterial under >conditions that prevent recombination) is so effective is that it works mathematically. Evolution does not >involve assembling random nucleotides nor does it involve conditions similar to human attempts to radically >change environments so that they are doubly toxic.
Your own citation states that HIV does recombination yet that virus
can not evolve efficiently against selection pressures targeting two
genes simultaneously. The only reason many of the examples I give
involve the evolution of viral or bacterial populations is that the
rapid generation times gives results that can be seen in a human life
span. If you want to consider higher life forms with longer generation
times such as humans and chimpanzees, you have to work with the
sequences of the genomes that we have today and try to do the
accounting based on evolutionist claims of when the divergence of the
two life forms occurred. And the mathematically irrational
evolutionist claims do not add up whether you consider selective or
neutral evolution.

Whenever you are ready, you can derive the probability function for
random recombination and show us how this phenomenon works. I think
we’ll have a really long wait for that one, but no shortage of blah,
blah, blah.

>> As soon as selection targets multiple genes, the amplification
>> process is stifled and that’s if only two genes are targeted.

>That is true only if the two w.t. alleles targeted by both toxic agents independently produce a drastic reduction >in population numbers or reproductive success for the w.t. alleles. Absent that, we have no problem with >serial or parallel evolution.

So you have no problem with a population evolving to both thermal
stress and starvation stress simultaneously? Perhaps you think the
sorting and optimization process goes more quickly when you have
multiple selection pressures acting simultaneously? Why don’t you tell
this to Lenski so his experiments can run in shorter times?

>> If three
>> or more genes are targeted, your probabilities only get worse for
>> those events to occur.

>Again only when all three independently produce a dramatic decrease in population size.

It still doesn’t register with you that the entire population does not
contribute to the mutation and selection process. A beneficial
mutation for a member with a particular genome sequence may not be
beneficial for another member with a different genome sequence. Each
subpopulation has its own trajectory on the fitness landscape with its
own set of beneficial mutations. Members of other subpopulations only
represent competition for the resources available in the environment.
This is why amplification of beneficial mutations is essential for a
subpopulation to overcome the multiplication rule of probabilities.

But any time you want to present real, measurable and repeatable
empirical evidence of your mathematically irrational claims, go for
it. But it seems that the best you can do is post citations which
shows the HIV does recombination yet this virus still can not evolve
efficiently against selection pressures targeting two genes.

Hersheyh, why don’t you give us three selection pressures which don’t
produce a dramatic decrease in population size?

>> The multiplication rule of probabilities which
>> you so erroneously claim does not apply to biological evolution kills
>> your theory of evolution.

>I have never claimed that the multiplication rule of probabilities does not apply to biological evolution. I have >only encouraged the correct use of it. It does not apply to the idea that proteins or DNA is assembled by >random linkage of subunits because the premise that proteins or DNA are assembled by random linkage is >false. It does not apply to most biological evolution, which does not involve a rapid change in the >environment to include two independent high level toxins lethal (or otherwise causing great population >reduction) to the w.t. alleles. You incorrectly apply it in cases of serial evolution where it does not apply. > And you incorrectly deny even the possibility of parallel evolution of traits.

You don’t know how to use the multiplication rule of probability
correctly. Your three step process consists of starting with the wrong
probability distribution (Poisson), second step assumes population
sizes of 10^9 and your third blunder is multiplying three numbers with
values close to 1 when there are only two mutational events. You don’t
understand how the mathematics of mutation and selection works and
your evolutionist blunders have given us multidrug resistant microbes,
multiherbicide resistant weeds, multipesticide resistant insects and
less than durable cancer treatments. You are a mathematically
incompetent evolutionist crank.

>> You know this and that’s why you claim that
>> every selection event occurs on a population size of 10^9, but it
>> doesn’t.

>Sometimes it is larger. Sometimes it is smaller. But those numbers are quite reasonable for bacteria. For >eucaryotes, you need to talk about recombination.

When a beneficial mutation occurs on a progenitor the subpopulation
size is really small. Of course you wouldn’t understand this because
you are too busy using the wrong probability distribution for your
erroneous calculations. And we all know that you know how to blah,
blah, blah about recombination. Why don’t you derive for us the
correct probability function for random recombination? Am I asking too
much of a mathematically irrational evolutionist?

>> The particular mutation has to occur on a member of the
>> subpopulation who would benefit from that mutation and that’s not just
>> any member of a 10^9 population.

>Again, you are *assuming* that only the double-mutant has any increase in fitness (that is what your claim >that a mutation only has utility when it occurs in a subpopulation that would benefit, presumably because it >already has a second variant).

You are wrong again hersheyh. You see this 10^9 population size as a
homogenous collection of members but they are not. And even if they
were a homogeneous collection, when the first beneficial mutation
occurs, you now have a subpopulation size of 1 which must amplify in
order for the next beneficial mutation to accumulate on the descendent
of that progenitor. The other 10^9 - 1 members are not on that
trajectory of the fitness landscape, they are only competing for the
resources of the environment with that 1 member with the beneficial
mutation. It’s amazing how your evolutionist indoctrination causes you
to make so many fundamental blunders in the basic science and
mathematics of the mutation and selection phenomenon.

hersheyh Aug 10, 6:36 pm
Newsgroups: talk.origins
From: hersheyh <hershe...@yahoo.com>
Date: Wed, 10 Aug 2011 18:36:18 -0700 (PDT)
Local: Wed, Aug 10 2011 6:36 pm
Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

On Wednesday, August 10, 2011 4:37:33 PM UTC-4, Alan Kleinman MD PhD
wrote:
> > John, you only know A->A when you know what that A was the base at
>> that locus a priori. You don’t know that so from the probabilistic
>> viewpoint there are four possible outcomes from a point mutation at a
>> particular locus.

>No. There are four possible n.t. at any nt site. The question is what does that have to do with determining the >rate of mutation from A-sensitive to A-resistant or from brown eyes to blue or from HbA to HbS? If you don't >know what the n.t. at a particular site is, either before or after the mutation, how can you tell you have had a >mutation? There is an answer to that one, because geneticists have been determining that mutations have >occurred well before they knew DNA was the genetic material. In fact, they have been determining mutations >since just about the time the Mendel's work was rediscovered. About the turn of the last century. More than >100 years ago. They have been determining mutation rates since at least the 1930s.

When there is a point mutation (error) in the replication of a genome,
the only thing that you can say with surety is that you will have one
of the four bases. The mutation can be detrimental, neutral or
beneficial. This can only be determined by the response of the
subpopulation with that mutation over generations.

>Hint: They have been doing what I have described. They distinguish between a mutant and a non-mutant by >the phenotype the genes produce. They determine mutation rates by the probability of finding mutants in a >population grown from non-mutants. But if you cannot distinguish a mutant from a non-mutant, and when >you say you can't do that because you have no idea what the nt is at some site, then you cannot talk about >mutation and you cannot use your ignorance about the difference between mutant and non-mutant to >arbitrarily divide a rate you can determine by a number.
Your outdated definition for a mutation has been supplanted with a
mathematically much more precise definition. Now that genomes can be
sequenced, a more accurate definition for a point mutation is
required, not your hundred year old definition before DNA was actually
identified.
>> There are certainly not 16 possible outcomes from a
>> point mutation. When are you going to start learning something about
>> probability theory?

>This isn't about "probability theory". It is about what the word "mutation" means and how it and the rate of >mutation is determined. It is how you empirically distinguish between mutant and non-mutant and use that >distinction to determine the probability of a mutant per trial/organism. There is no theory here. It is an >empirical determination.

Certainly it is about probability theory. It’s all about computing the
number of trials a population can make in a given number of
generations. The correct definition of the mutation rate is required
for computing the number of trials. If you depend on the ability of
identifying the mutant state phenotypically, you ignore neutral
mutations and underestimate the mutation rate. But to an evolutionist
this doesn’t matter because evolutionism is a doctrine which doesn’t
require scientific accuracy in identifying variables.

>> After all, it is probability theory which provides
>> the mathematical tools to describe the random mutation and natural
>> selection process.

>Yadda. Yadda. Yadda. I do wish you would try to understand these pat phrases you puck out.

We are still waiting for you to post the correct probability function
for the mutation and selection phenomenon let alone the correct
probability function for the random recombination phenomenon. The best
you can do with the probability function I derived for you is question
the correct definition for the mutation rate. You would rather use a
hundred year old definition before DNA was even recognized. Point
mutations can be detrimental, neutral or beneficial. The definition I
used in the derivation of the probability function for the mutation
and selection phenomenon takes that mathematical effect into account.

>> You need to start recognizing what variables affect
>> the number of trials for an event

>The number of trials is the total number of individual tests of the binary question asked. The question asked >requires that one know the distinction between the 'event' and the 'not-event'. In our case, the total number of >individuals tested is the number of trials, be that determined by the total number of individuals in a test tube or >the total number of individuals tested taken from repeated samplings over many generations. The total >number tested is the value we need.

And you are asking the wrong question based on hundred year old
limited understand of what a point mutation is. The probability
function I’ve derived for you give the total number of tests (trials)
for a particular set of two mutations as a function of population size
and number of generations doing the sampling. The way you determine if
the first mutation is beneficial is by the way the subpopulation size
responds over generations. If the mutation is beneficial, the
subpopulation increases over generations. If the mutation is neutral
the subpopulation size remains constant over generations. And if the
mutation is detrimental, the subpopulation sizes with this mutation
decreases over time.

>The event is "mutation" or "double-mutation" and the not-event is "not mutation" or "not double-mutation" >depending on the specifics of the conditions being examined.
Hersheyh, you are stuck with the idea that the mutation is analogous
to a coin tossing process with only a head or tail possible outcome.
Your analogy is wrong; the mutation and selection phenomenon is more
analogous to dice rolling where you have multiple possible outcomes
for a point mutation. You may be able to convince your evolutionist
ideologue cohort of this mathematical blunder but anyone with an ounce
of common sense will recognize that there are more than two possible
outcomes for a point mutation. You stick with your 20th century
definitions because that where the theory of evolution started to fall
apart. Now in the 21st century we have both the empirical and
mathematical evidence that shows that the theory of evolution is a
mathematically irrational belief system.
>> and how these trials affect the
>> probabilities of an event happening. Once you understand these
>> principles, you will understand how to prevent drug resistance and
>> develop more durable cancer treatments.

>No one is arguing that multidrug treatment, where and when possible (and it isn't always), isn't useful. Only >you seem to think that evolutionary biologists didn't understand that.

That’s a load of crap and you know it. Evolutionary biologist have not
understood or taught this fact. It was only with the advent of the
combination therapy treatment of HIV that this understanding of
mutation and selection became immediately crucial. This concept was
understood by Edward Tatum more than 50 years ago in his Noble
Laureate lecture but is never taught because the multiplication rule
of probabilities shows how mathematically irrational the theory of
evolution is.

>> You will also understand how
>> to prevent herbicide resistant weeds and pesticide resistant insects.

>Well, at least slow their appearance.

Orders of magnitude slower, single drug therapy of HIV gives resistant
viruses in a week; combination therapy gives you Magic Johnson
advertising Rent-A-Center after two decades of HIV.

>> If all this mathematics is too difficult for your mathematically
>> incompetent evolutionist mind, just remember it’s harder to win two
>> lotteries than one.

>And it is harder to find double-mutants directly from double-sensitive populations. No one is arguing that. It >is just the claim that somehow this makes evolution irrational that there is no logical connection to.

The reason you can not make the logical connection is that you don’t
understand the basic science and mathematics of the mutation and
selection phenomenon. You understand the need for large populations
for there to be a reasonable probability for a single mutation to
occur. This is why amplification is required before there is a
reasonable probability for the second mutation to occur. If
amplification does not occur then you are left with probabilities of
the order of double-mutants occurring, ie very low probability events.
And the way you get this circumstance is for the population to be
forced to evolve to selection pressures targeting two or more genes
simultaneously. This is pure mathematical and empirical logic, a thing
which is lacking in the theory of evolution.

>> That’s what the multiplication rule of
>> probabilities does to the probabilities of multiple independent events
>> occurring. Of course this is also why the theory of evolution is a
>> mathematically irrational belief system.

>What do you think the "theory of evolution" actually has to say?

Reptiles are transformed into birds by the mutation and selection
process, humans and chimpanzees evolved from a common progenitor… and
any of numerous other mathematically irrational claims.

Mark Isaak Aug 10, 7:36 pm
Newsgroups: talk.origins
From: Mark Isaak <eci...@curioustaxonomyNOSPAM.net>
Date: Wed, 10 Aug 2011 19:36:10 -0700
Local: Wed, Aug 10 2011 7:36 pm
Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

On 8/10/11 1:46 PM, Alan Kleinman MD PhD wrote:

>> On Jul 13, 6:05 pm, Mark Isaak<eci...@earthlink.net> wrote:
>>> On Tue, 12 Jul 2011 17:54:43 -0700, Alan Kleinman MD PhD wrote:
>>>> On Jun 7, 9:41 am, Mark Isaak<eci...@earthlink.net> wrote:
>>>>> On Mon, 06 Jun 2011 17:39:41 -0700, Alan Kleinman MD PhD wrote:
>> Mark, I’m really impressed with all zero examples of how engineers use
>> the theory of evolution in designing.

>Doc, I'm really impressed with your zero effort to look anything up.
>But since you have to be hand-led, here are a couple references:

>Mitsuo Gen & Runwei Cheng, _Genetic Algorithms and Engineering
>Optimization_ (Wiley, 2000).
>J.M. Johnson & V. Rahmat-Samii, "Genetic Algorithms in Engineering
>Electomagnetics", _Antennas and Propagation Magazine, IEEE_, 39 (1997),
>7-21.
>You may also want to read
>Agoston E. Eiben & J.E. Smith, _Introduction to Evolutionary Computing_,
>(Springer, 2008).
>Don't come back until you have read at least one of them, or any of
>hundreds of other books and professional articles on the subject.
Post one single quote from any of your references which justifies your
claim that the more complex the sorting conditions, the easier it is
to do the sorting process. Do you think that a google search on the
words “genetic algorithm engineering” is going to make me go away? It
is much more important to properly describe the basic science and
mathematics of mutation and selection properly. I’m here to educate
your evolutionist indoctrinated mathematically irrational mind. You
can choose to be educated about how mutation and selection actually
works or you can let your mind dwell on mathematically irrational
evolutionist folklore.
>> Now I have applied engineering
>> principles to the mutation and selection process and this mathematical
>> analysis show how to design selection pressures to prevent drug
>> resistant microbes, herbicide resistant weed, pesticide resistant
>> insects and produce more durable cancer treatments.

>You have applied nothing. You have made up fantasies about those
>things, and the only place anything has been done with your ideas is
>inside your own head.

It may be in my head but it is also in the infections my patients
suffer from. Infections which obey the basic science and mathematics
of the mutation and selection phenomenon, something which
evolutionists have failed to teach or understand.

>>>> If you understand how mutation and selection works, you understand how
>>>> to interfere with the formation of multidrug resistant microbes,
>>>> multiherbicide resistant weeds, multipesticide resistant insects and
>>>> produce more durable cancer treatments. This analysis also shows why
>>>> mutation and selection can not make rapid transformation and why the
>>>> theory of evolution is a mathematically irrational belief system. This
>>>> is what happens when you correctly apply engineering principles to
>>>> understanding a physical phenomenon.

>>> Don't tell me, tell reality. That is who your argument is with.
>> I’ve given you a mathematical analysis of reality.

>The fact that your analysis directly contradicts reality should tell you
>something. The fact that it does not tell you something makes me
>question your sanity.

If you think I’m insane, file a complaint with the California Medical
Board where I hold my medical license or the California Department of
Consumer Affairs where I hold my engineering license. And then see if
you can get any of my patients who suffered from infections which I
have treated based on my engineering analysis of mutation and
selection to support your complaint.

>Seriously. Get your brain checked.
I did get my brain checked and was found to have a very low level of
evolutionist indoctrination. The mathematical center of my brain
rejected evolutionism as mathematically irrational nonsense.
Mark Isaak Aug 10, 7:42 pm
Newsgroups: talk.origins
From: Mark Isaak <eci...@curioustaxonomyNOSPAM.net>
Date: Wed, 10 Aug 2011 19:42:51 -0700
Local: Wed, Aug 10 2011 7:42 pm
Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

On 8/10/11 2:21 PM, Alan Kleinman MD PhD wrote:

>> On Jul 14, 8:58 am, Mark Isaak<eci...@earthlink.net> wrote:
>>> On Tue, 12 Jul 2011 18:18:51 -0700, Alan Kleinman MD PhD wrote:
>>>> On Jun 7, 2:45 pm, Mark Isaak<eci...@earthlink.net> wrote:
>>>>> On Mon, 06 Jun 2011 17:47:21 -0700, Alan Kleinman MD PhD wrote:
> >> Fine. But then you need to put a notice with your work saying,
>>> "These calculations apply ONLY to the treatment of HIV."

>[Snipped repetitious justifications, which include not a word about the
>salient difference between the HIV and populations in general. I doubt
>the good doctor doctor even knows the difference, despite the dozens of
>attempts of people here telling it to him.]

Why would I want to accept the mathematically irrational arguments of
evolutionists about how their folklore tells them mutation and
selection works? I’m interested in an accurate engineering
mathematical analysis of how this phenomenon works and the empirical
evidence which supports this analysis, not the mathematically
irrational evolutionist claims. These principles are too important to
my patients to be left to the mathematically irrational speculations
and extrapolations of evolutionists.

Mark Isaak Aug 10, 7:45 pm
Newsgroups: talk.origins
From: Mark Isaak <eci...@curioustaxonomyNOSPAM.net>
Date: Wed, 10 Aug 2011 19:45:10 -0700
Local: Wed, Aug 10 2011 7:45 pm
Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

On 8/10/11 2:21 PM, Alan Kleinman MD PhD wrote:
>> On Jul 14, 8:58 am, Mark Isaak<eci...@earthlink.net> wrote:

>> Not at all Mark, the only thing I m saying is event B must occur on a
>> member which already has had event A occur.
>In other words, "I'm not saying B is dependent on A, I'm saying B is
>dependent on A."

Event B does not have to happen on a member with event A, it can
happen on any member of the population. It’s only when event B happens
to occur on a member with event A that it happens to be a beneficial
event. Event B is independent of event A. You only have to have enough
trials on members with event A for event B to have a reasonable
probability of happening. Mark, do you really have a degree in
engineering? It’s not like social engineering is it?


John Harshman Aug 11, 7:16 am
Newsgroups: talk.origins
From: John Harshman <jharsh...@pacbell.net>
Date: Thu, 11 Aug 2011 07:16:37 -0700
Local: Thurs, Aug 11 2011 7:16 am
Subject: Re: Trying to salvage something from this Re: The Theory of
Evolution
Alan Kleinman MD PhD wrote:
>> On Jul 13, 1:56 pm, John Harshman <jharsh...@pacbell.net> wrote:
>>> g...@risky-biz.com wrote:


>> You couldn’t be more wrong John, over 70% of the genes in humans and
>> chimpanzees don’t code identical proteins.

>While true, that has nothing to do with anything we've been discussing.
>Do you understand that a single base change can produce non-identical
>proteins? If there are 30,000 genes, that's 21,000 mutations. Out of 40
>million. And even many of those are neutral.

It has everything to do with what we are discussing. There are huge
stretches of the two genomes which can not be matched up for homology.
This data is presented for those areas which can be matched and the
match is not close at all. Evolutionists claim that humans and
chimpanzees come from a common progenitor. Now you are claiming that
many of these differences are neutral which is typical evolutionist
speculation. Tell us which are neutral differences and which are
selective differences. And then compute the joint probability of two
neutral mutations being fixed in a population.

>>>> How many with other known functions? How much "junk"?
>>> Almost all is junk, just as almost all the genome is junk. Non-coding,
>>> functional regions are just another few percent of the genome.
>> This is the type of stupidity that evolutionist perpetuate. If they
>> don’t know what a portion of the genome does, it is junk.

>No, that's not how it works. We recognize junk by the fact that it
>evolves at the rate of mutation.

Take a look at this URL: http://www.sciencemag.org/content/295/5552/131.abstract
In this URL, they studied chromosome 21. They report “We detected
candidate positions, including two clusters on human chromosome 21
that suggest large, nonrandom regions of difference between the two
genomes.” Nonrandom means these are selective differences and we all
should know by now that selective differences take hundreds of
generations per base substitution. But you claim that neutral
mutations fix at the rate of a couple of hundred per generation,
thousands of times faster than selection can fix a beneficial
mutation.

>> If they
>> don’t understand how to do a mathematical computation it is junk.
>> John, just because you are ignorant what a non-coding region of a
>> genome does, don’t impose your ignorance on us by claiming this is
>> junk. If a region of DNA has no coding function for proteins but
>> remains non-random, it does so because it has stabilizing selection
>> acting on those sequences.

>True. Which has nothing to do with what I'm talking about. Stabilizing
>selection makes loci evolve at less than the neutral rate. Such loci are
>only a few percent of the genome. By the way, evolution isn't so fast as
>to randomize sequences in 5 million years.

Just what are you talking about? I guess you missed the study I posted
above about the large non-random differences on chromosome 21 between
humans and chimpanzees. 70% of genes code for different proteins,
large stretches of non-random differences between human and chimpanzee
genomes yet neutral evolution will fix all these differences a rate of
a couple of hundred per generation, thousands of times faster than a
single beneficial mutation can be fixed in a population. What you are
talking about is mathematical irrationality.

>> And the reason it has stabilizing selection
>> pressures acting on those sequences is that it has some type of
>> important function on maintaining the life and reproductive capability
>> of that member. The only junk in this discussion is the evolutionist
>> junk science which fails to properly explain how mutation and
>> selection works.

>You mistake evolution at the rate of mutation for stabilizing selection,
>presumably because you have a false understanding of the mutation rate.
>Neutral evolution produces only a bit more than 1% difference over 5
>million years, not a randomization of sequences.

You will only get randomization of sequences if there is no selection
acting on that sequence. Your mathematics is faulty because 5 million
years only represents about 500,000 generations and you can not fix
40,000,000 differences in two divergent populations in such a short
period of time. It is mathematical irrationality to believe this.

>>>> Of the ones that are in coding areas, how many are thought to make
>>>> significant "interesting" morphological differences rather than minor,
>>>> possibly non-function-altering changes to a protein?
>>> Again, very few. The vast majority of differences in coding regions are
>>> silent, i.e. making no difference in the protein being coded for.
>> Really John? Is that why over 70% of the genes in humans and
>> chimpanzees code for different proteins? I can’t tell what you are
>> worse at, mathematics or the interpretation of data.

>This is silly. "Over 70% of the genes code for different proteins" is a
>reasonable expectation for neutral evolution. Few of these differences
>mean anythng.

We all know about evolutionist expectations, they are mathematically
irrational. But if you want to show your work and compute the joint
probability of two neutral mutations being fixed in a population, that
would be some interesting evolutionist folklore to hear.

>>>> I assume this is ongoing research; perhaps the answers are not yet
>>>> clear.
>>> Oh, no. They're quite clear. What isn't clear is the exact number and
>>> identities of the comparatively few functional differences.
>> John, your irrational speculations don’t form a scientific basis for
>> any of your claims. You don’t know how mutation and selection works
>> and you can’t explain why over 70% of the genes code for different
>> proteins in humans and chimpanzees.

>By "different" you merely mean -- though you probably don't know it --
>that there is at least one amino acid difference, i.e. one point
>mutation. Trivial.

Tens of thousands of different proteins between humans and chimpanzees
fixed in 500,000 generations, that’s what a mathematically irrational
evolutionist would call “trivial”. Maybe these proteins diverged
during the pre-split period, you know, the banana split period.

>[mantra snipped]
Repeat after me, reptiles transform into birds, reptiles transform
into birds, reptiles transform into birds…

John Harshman Aug 11, 7:22 am
Newsgroups: talk.origins
From: John Harshman <jharsh...@pacbell.net>
Date: Thu, 11 Aug 2011 07:22:49 -0700
Local: Thurs, Aug 11 2011 7:22 am
Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

Alan Kleinman MD PhD wrote:
>> On Jul 19, 9:20 am, John Harshman <jharsh...@pacbell.net> wrote:
>>> Alan Kleinman MD PhD wrote:
>>>> On Jun 8, 1:49 pm, John Harshman <jharsh...@pacbell.net> wrote:
>>>>> William Hughes wrote:
>>>>>> On Jun 8, 12:35 pm, Alan Kleinman MD PhD <klein...@sti.net> wrote:
>>>>>>> On Jun 1, 8:39 am, William Hughes <wpihug...@gmail.com> wrote:
>>>>>>>> On Jun 1, 11:52 am, Alan Kleinman MD PhD <klein...@sti.net> wrote:
>> You mean to say that A and B must amplify? But I thought you
>> evolutionists said that recombination would solve all of your
>> mathematical problems for your mathematically irrational theory. Now
>> why don�t you derive the probability function for two beneficial
>> alleles (or for that matter any two alleles) to randomly recombine?
>Depends on the frequencies of the alleles, doesn't it? If they "amplify"
>individually, the probability is eventually going to be 1.

Are you sure about that? Have you derived the probability function
which would describe this stochastic process? For example do A and B
both have to amplify? What happens to the probabilities of the random
recombination of A and B if only one of the two all alleles amplify?
I’ll give you a hint; don’t use the Poisson distribution to do this
computation.

>>>> That is unless you think that mutations for one or
>>>> another drug are not occurring in the HIV population when subjected to
>>>> combination therapy.
>>> As usual, you misunderstand the necessary conditions.
>> I�ve already derived the probability function for the two alleles to
>> randomly recombine.
>No you haven't. You haven't taken into account that they are
>individually advantageous.

Oh really, I haven’t take that into account? Obviously your
evolutionist telepathy is leading you astray once again. We should
really call your thinking evolutionist telepathetic.

>> I�m not confused, the reason why selection pressures targeting
>> multiple genes simultaneously interfere with the mutation and
>> selection process is that even if a member gets a single mutation that
>> would be beneficial for one or another selection pressure, the fitness
>> of that member is not improved because of the other selection
>> pressures acting on another of its genes.
>See? You don't know what "beneficial" means. Under the conditions you
>propose, neither allele is beneficial.

More evolutionist telepathetic. Let me repeat a previous hint for you
to show you how to derive the correct probability function for two
alleles to randomly recombine. This random process obeys the same
mathematical principles as random card drawing. With that hint and
google, you should be able to solve this probabilities problem by this
evening.

>> The point is that you have failed to properly describe the basic
>> science and mathematics of mutation and selection and now you are
>> failing to describe the basic science and mathematics of
>> recombination. There are mathematical reasons why recombination works
>> when it does work just as there are mathematical reasons why mutation
>> and selection works when it does work. You don�t understand either of
>> these mathematical principles.
>Out of curiosity, do you agree that 0.999... = 1?

I can understand you wanting to change the subject to anything other
than how mutation and selection works and why recombination does not
rescue your mathematically irrational belief system. Learn to stay on
topic. And now that I’ve all but given you the equations to describe
random recombination, let’s see if you can derive that probability
function.

hersheyh Aug 11, 9:01 pm
Newsgroups: talk.origins
From: hersheyh <hershe...@yahoo.com>
Date: Thu, 11 Aug 2011 21:01:46 -0700 (PDT)
Local: Thurs, Aug 11 2011 9:01 pm
Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

On Wednesday, August 10, 2011 5:45:33 PM UTC-4, Alan Kleinman MD PhD
wrote:
>> On Jul 19, 4:59 pm, hersheyh <hers...@yahoo.com> wrote:
>> > On Jul 19, 10:55 am, Alan Kleinman MD PhD <klei...@sti.net> wrote:
>> > > On Jun 8, 1:07 pm, hersheyh <hers...@yahoo.com> wrote:> On Jun 8, 11:33 am, Alan Kleinman MD PhD <klei...@sti.net> wrote:
>> > > > > On May 26, 4:54 pm, "Frank F. Smith" <f....@cornell.edu> wrote:
>> > > > > > On 5/25/2011 8:40 AM, Alan Kleinman MD PhD wrote:
>> > > > > > > On May 16, 7:20 pm, "Frank F. Smith"<f....@cornell.edu> wrote:
>> > > > > > >> On 5/16/2011 8:20 PM, Alan Kleinman MD PhD wrote:
>> > > > > > >>> On May 9, 4:38 pm, "Frank F. Smith"<f....@cornell.edu> wrote:
>> > > > > > >>>> On 5/4/2011 12:35 AM, hersheyh wrote:> On May 3, 6:50 pm, Alan Kleinman MD PhD<klei...@sti.net> wrote:
>> > > > > > >>>>>> On Apr 20, 10:29 am, hersheyh<hers...@yahoo.com> wrote:
>> I don’t think that the antibiotic induces the mutation either.
>You certainly do not make that clear.

You have no idea what clear is.

>> But I
>> do know that when a point mutation occurs that there are four possible
>> outcomes not two as you claim.
>For *any* kind of mutation, there are only two outcomes: mutant and not-mutant. There most certainly are not four >possible outcomes. Mutation *means* change from one defined genetic state to a different genetic state. Typically this >change in state is defined by a change in phenotype rather than genotype. In all the cases we have been discussing >with HIV, bacteria, pesticide resistance, etc., the change in genetic state has been defined phenotypically, usually by >distinguishing between a toxin-sensitive and a toxin-resistant state. In other bacterial cases, the distinction is between >ability to use a resource or inability to use a resource (e.g. citrate), the amount of resistance to an antibiotic, or the ability >to grow efficiently in defined conditions as measured by population produced per unit time. In some cases, the genetic >changes are directly known (e.g., a change from a C to a T), but in other cases they are not known.

You have used phenotypic change as the definition of mutation, I have
not. It is not my fault that this is not clear to you. I made my
definitions of variables explicitly clear. And your definition is the
wrong mathematical definition for mutation. With your sloppy
definition, there is no such thing as a neutral mutation because there
is no phenotypic change. I’ll stick with the correct definitions and
probability function to describe the mutation and selection phenomenon
and you can stick with your sloppy incorrect definition of a mutation
and the wrong probability distribution (Poisson).
>>And the reason why there is four, not
>> three possible outcomes is that a priori you do not know what the base
>> was at that locus before the mutation occurred.
>If you don't know the initial genetic state or the final genetic state, you cannot even say whether or not there has been a >mutation or change in that state. And four would still not be the correct number since, obviously, at least one of the nts >represents no change. Basically, unless I am specifically calling a change from C (which I have to know is the w.t. nt at >that position) to A, G, or T or only one or only two other nt's the mutation of interest, the genetic nature of the change >(which need not be at a single site or be a point mutation) is irrelevant. Mutation has *always* been defined as a change >in genetic state from one state (often the w.t. state) to a different state as evidenced by a change in phenotype. When I >measure mutation rate, I have to be able to distinguish the mutant state from the non-mutant state in some way. That >means I need to be able to empirically determine a change. I can do that with resistant to A or sensitive to A.

You don’t need to know what a particular coin flip gives to write a
probability function which describes coin tossing. You don’t need to
know what a particular roll of the dice gives to write a probability
function to describe dice rolling. What a probability function gives
you is a mathematical representation of the frequency of events if you
were to do the experiment many times. I have used the most general
mathematical definition of a point mutation at a locus. Your
definition ignores other possible outcomes.

>> This has nothing to do with distinguishing a mutant state from a non-
>> mutant state.
>You don't seem to understand what "mutation" means. Being able to distinguish between the mutant state and the non->mutant state has everything to do with determination of the mutation rate. Namely, you cannot determine mutation rate if >you cannot identify and distinguish between the mutant and non-mutant states. You can determine mutation rates >without knowing anything about the nts involved in the mutation. Or you can use the "phenotype" of what nt actually is >present at a site as the defining feature of the difference between non-mutant and mutant (although sequencing is more >often done later to find out what change(s) are responsible for the phenotypic differences). You do not, however, flip-flop >and conflate the phenotypic description of a mutation with some nebulous bullshit about there being 4 possible nt's that >we know nothing about. There is simply no logical reason to divide the *actual* measured mutation rate by 4, even if we >knew which nt was the original one and which was the chang

ed one in the mutant.

You are simply are unable to derive the correct mathematical equations
to describe the mutation and selection phenomenon. You don’t
understand what a probability function is. You have used the wrong
probability function to describe the mutation and selection phenomenon
your entire career and can’t comprehend the fact that when a point
mutation occurs at a particular locus, the only thing that you can say
with certainty is that you have one of four possible outcomes. I am
not going to use your definition because you limit your ability to
measure whether a mutation occurs based on a phenotypic change. Yours
is a wrong definition for mutation and it has led you to draw a series
of mathematically irrational conclusions.
>For example, the spontaneous rate of mutation to achondroplastic dwarfism to normal parents is known because >achondroplastic dwarfism is a dominant mutation that is fully penetrant.
>http://www.google.com/url?sa=D&q=http://omim.org/entry/100800
>The mutation rate from the normal, non-achondroplastic allele to the achondroplasia allele can thus be calculated by >counting the number of children born to 'normal' parents (normal in this context means that the parents are not >achondroplastic dwarfs) who are achondroplastic dwarfs and dividing this by 2 times the total number of children born to >'normal' parents in the same area and time. That is: u = Na/2Nt where Na is the number of children with achondroplasia >born to 'normal' parents and Nt is the total number of children born to 'normal' parents. The factor 2 here has *nothing* >to do with nucleotides. It is due to the fact that every human child is diploid and the mutation rate is the rate of mutation >from the 'nonachondroplasia' allele to the 'achondroplasia' allele, so we have to count the number of new mutant alleles >and divide it by the total number of alleles examined. Each achondroplastic child has only one dominant >'achondroplasia' allele (the new mutant allele, since the parents we

re 'normal') yet every child has two alleles.
>Now, to me it makes sense that we call Na/2Nt the mutation rate for the conversion of the normal allele to the >achondroplasia (ACH) allele. BTW, this rate is in the order of 10^-5. There have been several studies and the rates >differ in the different studies. Some of this difference may be due to diagnostic confusions by the doctor involved. >There are some other traits that have similar diagnostic features. After all this is data that has to be collected from a >large number of births attended to by many doctors, some of whom may have the competence shown here by our Dr. Dr. > [There would now be a DNA diagnostic test that could, with 99% accuracy, confirm diagnoses, but most of these studies >only involved phenotypic diagnosis by the attending physician.] The mutation rates from normal allele to ACH allele >range from around 0.5 to 1.5 X 10^-5/per allele. BTW, because, in this measurement (unlike the bacterial cases) all the >starting alleles are w.t., there is no Luria-Delbruck skew because it

is the case that every event has the same probability >of occurring. [There might be a minor effect due if the same normal parents give rise to ACH siblings, since this is more >likely due to a parent's gametic mosaicism than to independent mutation.
>Such siblings (and monozygotic twins) should probably only be counted once.)
>But that rate is not one Dr. Dr. would agree to. In his mind, the true mutation rate is not the actual rate at which the >normal allele mutates to an allele that causes ACH. His 'true mutation rate' is that rate divided by 4. Because there are >four possible nucleotides at any nucleotide site. Exactly why the fact that any nt site can have one of 4 possible nt's >means one has to divide that actual rate at which
>ACH alleles arise by mutation from w.t. alleles I have not been able to discern. Certainly no logical reason has been >given, aside from some mumbling about loci and randomness.
You are correct here, I do not agree with your definition of mutation
rate. If you want to measure the mutation rate correctly, you would
need to sequence numerous parent and child genomes and compare the
sequences for differences in the replication process. That’s the
mathematically correct way to measure the frequency of mutation. This
is no different than flipping a coin to determine the frequencies of
heads and tails. If you depend on phenotype changes as your measure,
you will miss all the neutral mutations that are occurring and you
will have a mathematically incorrect value for the mutation rate.
>But, perhaps the problem is that the above determination of mutation rate was done by deducing the mutation rate from >the phenotypic difference produced by the mutant allele relative ...
hersheyh Aug 13, 4:59 pm
Newsgroups: talk.origins
From: hersheyh <hershe...@yahoo.com>
Date: Sat, 13 Aug 2011 16:59:27 -0700 (PDT)
Local: Sat, Aug 13 2011 4:59 pm
Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2
On Wednesday, August 10, 2011 5:33:41 PM UTC-4, Alan Kleinman MD PhD
wrote:
>> On Jul 14, 5:39 pm, hersheyh <hers...@yahoo.com> wrote:
>> > On Jul 12, 9:22 pm, Alan Kleinman MD PhD <klei...@sti.net> wrote:
>> > > On Jun 7, 5:18 pm, hersheyh <hers...@yahoo.com> wrote:
>> > > > On Jun 7, 5:45 pm, Mark Isaak <eci...@earthlink.net> wrote:
>> > > > > On Mon, 06 Jun 2011 17:47:21 -0700, Alan Kleinman MD PhD wrote:
>> > > > > > On May 25, 12:08 pm, Mark Isaak <eci...@earthlink.net> wrote:
>> > > > > >> On Wed, 25 May 2011 05:08:58 -0700, Alan Kleinman MD PhD wrote:
>> > > > > >> > On May 12, 1:40 pm, Mark Isaak <eci...@earthlink.net> wrote:
>> > > > > >> >> On Wed, 11 May 2011 14:18:56 -0700, Alan Kleinman MD PhD wrote: [...]
>> That’s why the probability function I derived is a more general
>> equation than the Luria-Delbruck equation.
>No it isn't. The probability function you attempted to derive, but mucked up by your division by 4, is the joint probability >of one or more individuals with both mutation A and mutation B. It isn't even a probability "distribution", as there are only >two values you can calculate with this method -- the probability of zero individuals with the event or joint events and the >reciprocal probability of one or more individuals with the event or joint events. For you to generate a probability >"distribution" you would need to be able to calculate the probability of 0, 1, 2, 3,...n individuals with the event(s). And >Luria-Delbruck is not an equation. It also is a distribution of probabilities that occurs under some specified conditions, >namely conditions in which the binomial probability assumption (which is built into the probability function you derived, >ignoring your stupid division by 4) of each event having the same probability (rate) of occurrence is the same is violated.
Sure it is. The equation I derived makes no assumption about the
relationship between population size and number of generations as the
Haldane’s solution for the Luria-Delbruck equation does. And I also
considered two events (A and B) in my derivation where the Luria-
Delbruck equation only considers a single mutation (event). I also
make no assumption about the how the sizes of populations can change
each generation. What this equation gives you is the frequency at
which these events would occur if you were to perform this experiment
many times and I assure that in the replication process of
populations, this experiment is performed many times. You don’t need
to generate the probability distribution for the probability function
I derived. You are the one obsessed with computing the mean value for
the number of mutations which would occur in a particular generation.
You don’t need that value since the effects of selection will swamp
that value once a beneficial mutation has occurred. And your inability
to measure if a neutral mutation has occurred should not be the
limiting factor for the definition of a mutation.

Ultimately, what my equation shows you (if you understood the
mathematics which you don’t) is that without amplification, the joint
probability of event B occurring after event A has occurred is
extremely small due to the multiplication rule of probabilities. This
is why the theory of evolution is a mathematically irrational belief
system.

hersheyh Aug 13, 8:29 pm
Newsgroups: talk.origins
From: hersheyh <hershe...@yahoo.com>
Date: Sat, 13 Aug 2011 20:29:28 -0700 (PDT)
Local: Sat, Aug 13 2011 8:29 pm
Subject: Re: Trying to salvage something from this Re: The Theory of
Evolution
On Thursday, August 11, 2011 10:16:37 AM UTC-4, John Harshman wrote:
>> Alan Kleinman MD PhD wrote:
>> > On Jul 13, 1:56 pm, John Harshman <jhar...@pacbell.net> wrote:
>> >> g....@risky-biz.com wrote:

>> By "different" you merely mean -- though you probably don't know it --
>> that there is at least one amino acid difference, i.e. one point
>> mutation. Trivial.
>In general, and not surprisingly, there is greater sequence conservation (fewer differences in aa sequence) in protein >coding sequences than would be predicted if all aa sequences were equally fit and thus selectively neutral. It is not, >however, so great a sequence conservation as someone who regards proteins to be as fragile as words. That is >because a significant fraction of nt changes in protein coding sequences does not change the aa sequence (there are >only 20 aa coded by 61 different codons; the other 3 are stop codons). Synonymous substitutions at the aa level tend to >be neutral. And, in fact, synonymous substitutions (those that do not change the aa) are significantly more likely than >non-synonymous ones (those that change an aa).

The nt changes in humans and chimpanzees have caused more than 70% of
genes to produce different proteins. You have about 500,000 thousand
generations to do this transformation and this does not include the
tens of millions of other differences which occur in non-protein
coding regions. There is no rational mathematical way to account for
these differences in this short number of generations. This is why the
theory of evolution is a mathematically irrational belief system.
>Specifically, at sites which are non-degenerate (all nt changes change the aa) the rate of substitution is about >0.5/nt/10^9 yrs. For two-fold degenerate (one of 3 possible changes changes the aa), the rate is about 2/nt/10^9 yrs. > For four-fold degenerate (any nt change produces the same aa), the rate is close to 4/nt/10^9 yrs and that is also near >the rate for introns, 3' flanking regions, or pseudogenes.
>Even then many changes in aa sequence have little or no effect on protein form or function (there are many different >sequences that can encode, say, cytochrome c form and function as can be seen by looking at sequence differences in >that protein in different organisms). But proteins are under strong *conservative* selection. Non-coding sequences are >even less constrained. Most non-coding sequences are only slightly less constrained than pseudogenes.

This is evolutionist junk science at its best. You can claim that
changes in aa sequences have little effect on protein form or function
but it’s a simple fact of life that when there is a difference in aa
sequence, it takes generations, lots of generations for the difference
to be spread through a population. And now you have the hard empirical
evidence that more than 70% of genes in humans and chimpanzee produced
different proteins. Even if those different proteins differ due to a
single base substitution, the populations must fix tens of thousands
of different mutations in about 500,000 generations. And you still
haven’t addressed the tens of millions of other differences between
the two genomes that would have to occur in so short a period of time.
Evolutionists are mathematically incompetent bunglers who have no idea
how mutation and selection works.
>We are talking about, on average, one aa difference per 300 aa sequence length (the average protein is about 300 aa >long). Different proteins or peptide sequences within protein have radically different levels of conservation and >evolutionary constraint. The amount of aa difference seen between human and chimp are not out of line with >expectations. Other than a few cases of deletion, most of these aa differences are selectively irrelevant. In fact, the >differences that we *know* were selected for in the human lineage tend to be in regulatory and not protein coding >regions.
And without selection the spread of a mutation is slowed profoundly.
This mathematical fact of life simply can’t penetrate the evolutionist
indoctrinated mind.
>A significant exception might be the human FOXP2 gene, a strongly conserved protein, which differs from chimp, gorilla, >and rhesus gene in two aa (out of 715). This is surprising because the other great ape proteins are not only identical to >each other but differ by only 1 aa from mouse (and that is probably a neutral site).
>See
>http://www.google.com/url?sa=D&q=http://en.wikipedia.org/wiki/FOXP2
>for a quick review.
>It is certainly true that most of the aa differences between human and chimp that do exist have no effect on the protein's >form or function and are selectively neutral.
>The only changes in coding sequences that we can be reasonably certain are neutral are those that don't change the >amino acid. Surprisingly, there are actually more neutral (no change in aa) point mutation differences between human >and chimp in exons (coding sequences) than there are in pseudogenes, introns, or intergenic regions! And not by a >small amount, but 30-60% higher. This is almost entirely a consequence of the higher level of CpG dinucleotides in >exons. CpG mutates to CpA or TpG at rates that are 7X higher than the rate of mutation of CpA or TpG to CpG. This >may be related to changes in regulation of methylation of these dinucleotides. Surprising results are always interesting.
On one hand hersheyh claims that you can not measure a mutation
without a phenotypic change and now he claims that most of these
mutations are neutral. This is the kind of garbage evolutionists come
up with when their initial assumption is that humans and chimpanzees
have diverged from a common progenitor 500,000 generations ago.
Evolutionists have to make a mathematically irrational song and dance
to try to explain away these huge numbers of differences in so small
number of generations. This is what happens when the mathematically
incompetent plug population sizes of 10^9 into the Poisson
distribution, the wrong distribution function to describe the mutation
and selection phenomenon.
>http://www.google.com/url?sa=D&q=http://genome.cshlp.org/content/13/5/838.full
>Showing the variance in mutation rates...
>http://www.google.com/url?sa=D&q=http://genome.cshlp.org/content/12/9/1350.full
>The problem seems not to be that the rate of substitution between human and chimp is too much or too fast but that it is >slow...
>http://www.google.com/url?sa=D&q=http://mbe.oxfordjournals.org/content/19/12/2191.full
>The authors have also provided you with a list of articles that direct you to how mutation rates are determined in >human/chimp comparisons.
Why would I want to immerse myself into evolutionist junk science? I
would much rather understand how mutation and selection actually works
rather than take up with the mathematically irrational belief that
more than 70% protein differences between humans and chimpanzee can be
fixed in less than 500,000 generations. Evolutionists have developed
an extensive body of junk science and mathematics to support their
mathematically irrational phenomenon but have failed to properly
describe the basic science and mathematics of the mutation and
selection phenomenon. The end result of this evolutionist blunder is
multidrug resistant microbes, multiherbicide resistant weeds,
multipesticide resistant insects and less than durable cancer
treatments.
Greg Guarino Aug 14, 9:41 am
Newsgroups: talk.origins
From: Greg Guarino <gdguar...@gmail.com>
Date: Sun, 14 Aug 2011 12:41:32 -0400
Local: Sun, Aug 14 2011 9:41 am
Subject: Re: Trying to salvage something from this Re: The Theory of
Evolution
On 8/10/2011 4:42 PM, Alan Kleinman MD PhD wrote:
>> On Jul 13, 1:56 pm, John Harshman<jharsh...@pacbell.net> wrote:
>>> g...@risky-biz.com wrote:
>Others have now responded more substantively than I would be able to,
>but I still have a few questions.

Hersheyh has presented a plethora of words without any mathematical or
empirical evidence for his claims. He is confused by the correct
probability function which describes the mutations and selection
phenomenon and dismisses all the real, measurable and repeatable
examples of mutation and selection. John Harshman as well has shown
that he doesn’t understand the simplest principles of a stochastic
process. Any of the other posters on this forum who have the slightest
understanding of how to analyze a stochastic process have left this
discussion. Do you think they want to try to defend Schneider’s claim
that the multiplication rule of probabilities does not apply to
biological evolution? Why would they want to look as mathematically
incompetent as hersheyh is? Defending the theory of evolution from a
mathematical approach is going to leave you looking mathematically
incompetent.

>>>> It's clear by now that Kleinman has no intention of answering the
>>>> questions posed to him. But I've learned some interesting biology from
>>>> this group, even from unpromising threads.
>>>> "Harshman's" count of genetic differences between humans and chimps
>>>> has been bandied about in this thread. I've been wondering, could you
>>>> characterize those differences a bit? How many of them are in coding
>>>> areas?
>>> Very few. Coding regions are only around 3% of the genome, and
>>> accumulate about a third the number of differences per base as neutrally
>>> evolving regions.
>> You couldn’t be more wrong John, over 70% of the genes in humans and
>> chimpanzees don’t code identical proteins.
>What made you think that answer was germane to the question asked? I was
>trying to get at how many of the 40 million differences make significant
>changes in the species. How many do YOU think it is?

It doesn’t matter what you or I think which mutations are significant.
What is significant is that these tens of millions of differences must
spread through populations in less than a million generations. Whether
they are significant or not, the differences exist between the two
life forms and you don’t have nearly enough generations to do the
accounting for these differences.

>>>> How many with other known functions? How much "junk"?
>>> Almost all is junk, just as almost all the genome is junk. Non-coding,
>>> functional regions are just another few percent of the genome.
>> This is the type of stupidity that evolutionist perpetuate. If they
>> don’t know what a portion of the genome does, it is junk.
>I have not come across a biologist who would make that claim. But more
>importantly...
>If they
>> don’t understand how to do a mathematical computation it is junk.
>> John, just because you are ignorant what a non-coding region of a
>> genome does, don’t impose your ignorance on us by claiming this is
>> junk. If a region of DNA has no coding function for proteins but
>> remains non-random, it does so because it has stabilizing selection
>> acting on those sequences. And the reason it has stabilizing selection
>> pressures acting on those sequences is that it has some type of
>> important function on maintaining the life and reproductive capability
>> of that member. The only junk in this discussion is the evolutionist
>> junk science which fails to properly explain how mutation and
>> selection works.
>... amid the gratuitous insults, you seem to tacitly agree that some of
>the genome is junk. How much?

I don’t agree with anything of the kind. What I am doing is properly
describing how mutation and selection works and then using
evolutionist supplied numbers (40,000,000 differences and 500,000
generations) to try and do the accounting for these differences. What
you come up with is a mathematically irrational belief system called
evolutionism. And at the same time we find that evolutionists have
bungled the basic science and mathematics of the mutation and
selection phenomenon causing multidrug resistant microbes,
multiherbicide resistant weeds, multipesticide resistant insects and
less than durable cancer treatments.

>> John, your irrational speculations don’t form a scientific basis for
>> any of your claims. You don’t know how mutation and selection works
>> and you can’t explain why over 70% of the genes code for different
>> proteins in humans and chimpanzees.
>On the contrary, it seems that several people here have offered the
>standard mechanisms. You have as yet not chosen to engage on any
>scenario that does not include massive reduction of a population, and
>thus have made no case about evolution in general.

In the twisted evolutionist mind there exist selection pressures which
don’t kill or impair the reproduction of some or all the members of a
population. Where and what are these selection pressures? We have the
Lenski E coli model where he puts his population under starvation
conditions but still allows populations in the tens of millions. It
still takes his populations hundreds of generations to amplify a
single beneficial mutation. What do you think would happen if Lenski
put his populations under thermal stress or some other selection
pressure? Do you think this would accelerate the mutation and
selection process or do you think that a member with a beneficial
mutation which improves glucose metabolism would still be able to
amplify that mutation efficiently while being stress by thermal
pressure? Evolutionists simply refuse to learn the lessons given by
the real, measurable and repeatable empirical examples presented here.
Evolutionists have an obsession with the theory of evolution which is
psychotic. Evolutionists have lost contact with reality.

One of the many lessons evolutionists must learn about the mathematics
of the mutation and selection phenomenon is that the entire population
does not contribute to the trials for the next beneficial mutation,
only members of the population which would benefit from that next
beneficial mutation. Having large numbers of members of a population
that are not on the particular trajectory of the fitness landscape
does not help that subpopulation that needs the next beneficial
mutation to improve fitness. Those other members of the population are
competing for the resources of the environment taking away the
necessary resources from that subpopulation which needs this to
reproduce efficiently. It is much more efficient in the mutation and
selection process to remove all those members who are not on the best
trajectory of the fitness landscape and leave the niche wide open for
those members who are on the best trajectory. All the resources of the
environment are now available to those members for reproduction. The
mathematics of the mutation and selection phenomenon is all about
improving the probability for the next beneficial mutation to occur
and the way that happens is by the particular subpopulation amplify
(multiplying) its members so more trials will be done for the next
beneficial mutation. Other members of the population who are not on
this trajectory only slow the process for those members who are on the
best fitness trajectory.

>> You’ve bungled the mathematics of
>> mutation and selection and given us multidrug resistant microbes,
>> multiherbicide resistant weeds, multipesticide resistant insects and
>> less than durable cancer treatments because of your scientific and
>> mathematical failures and now you want to claim that there are only a
>> few functional differences between humans and chimpanzees. The theory
>> of evolution is supported by irrational speculations, gross over-
>> extrapolations, and sloppy misinterpretation of data.
>Another piece of friendly advice: You shoehorn the bit above in at every
>opportunity, over and over and over and over and over. Intelligent
>people tend to recognize that sort of thing for what it is: a
>smokescreen, designed to cover the lack of a good argument. If you wish
>to be taken seriously, don't repeat stuff so much, especially the parts
>that don't add up to an argument.

Drug resistant microbes, herbicide resistant weeds, pesticide
resistant insects and less than durable cancer treatments are a fact
of life. If you don’t want to understand how mutation and selection
works and want to dwell in the mathematically irrational world of
evolutionism then you should find another discussion thread to post
on. Here we are talking about how the physical phenomenon mutation and
selection works and the consequences of what happens when you don’t
understand this phenomenon.

>>>> I ask this because I have the impression that Kleinman thinks
>>>> every one of those differences would have to have been a separate
>>>> response to a "selective pressure" (were evolution true, of course).
>>> Putting the words "Kleinman" and "thinks" in juxtaposition is always a risk.
>> John, do you want to put some probability theory to that risk? You’ve
>> already proven you don’t understand how to do a probability
>> calculation and that you are a mathematically incompetent bungler.
>> I’ve already had to correct you on two basic principles of probability
>> theory. Now I have to correct you on your gross misinterpretation of
>> the data.
>And then, you don't.

I have, you just don’t want to accept it. You’ve claimed that the
real, measurable and repeatable examples of mutation and selection
presented here do not represent how mutation and selection works
because these selection conditions drive populations down (which of
course selection pressures do). But then you choose to ignore the most
studied example of mutation and selection available, the evolution of
HIV to combination therapy. Even in a properly treated person, the
viral populations can be large yet the mutation and selection process
does not work efficiently. The virus does recombination, can not be
driven to extinction and yet can not evolve efficiently to combination
therapy. There is a mathematical explanation why this happens and it
also happens to be the same explanation why the theory of evolution is
a mathematically irrational belief system.
>I offered (above) my interpretation of part of your argument. It seems
>to boil down to the following:
>Evolutionary theory has to account for at least 20 million changes in
>each line (chimps and humans) from an alleged common ancestor. Each one
>of those changes would have to be a response to a separate "selection
>pressure". Each selection pressure and genetic response would have to
>happen serially, with many generations in between for the population to
>rebound, as selection pressures always greatly reduce the population.
>There has not been (nearly) enough time for this process to occur 20
>million times.
>Firstly, is that approximately correct?
Pretty good, let’s see you present the evidence that amplification of
a beneficial allele can occur in parallel.
>If not , tell us how. If so, several question have been asked that you
>have as yet not responded to in any clear fashion.
>1. Do you assert that all of the 40 million differences are required to
>explain the phenotypic differences between the species? Or are some of
>the differences without significant (or any) effect. How many of the
>genetic differences do you estimate are important?

It doesn’t matter whether the differences are important or not, the
differences are there and it takes time, lots of time to spread those
differences through a population. Evolutionists want to try to
categorize whether some differences are important or not. From a
mathematical point of view, this categorization is irrelevant.
Obviously if the theory of evolution were true, these differences were
important enough to be spread through the respective populations. Now
how do you properly do the accounting for these differences? Do you do
what John Harshman does and claim that a couple hundred neutral
mutations are fixed every generation, generation after generation for
hundreds of thousands of generations?

>2. You seem (above) to agree that absent stabilizing selection, some
>genetic change will occur. If so, what is your argument against neutral
>evolution?

My argument against the evolutionist gross over-extrapolation of a
mathematical model of the substitution of a single neutral allele to
the substitution of millions of neutral alleles is that it completely
ignores the multiplication rule for joint random independent events.
Why don’t you try to do the mathematics to extend that model to the
fixation of just two neutral alleles in a population? Just as with
mutation and selection, the multiplication rule comes into play when
you are talking about more than a single beneficial mutation, so will
this rule come into play when you are talking about neutral mutations.
But in the case of neutral evolution, you won’t have the benefit of
selection to help improve your probabilities.

>3. Why can't "less-intense" selection amplify more than one mutation in
>parallel?
>You have so far offered two responses to number 3. The first is to
>assert that such selection is "not efficient". But absent a severe
>reduction in the population, it is not clear why "efficiency", by which
>you actually mean "rapidity", is necessary. As it would allow parallel
>amplification of several beneficial alleles, it would seem more
>"efficient" in the aggregate, even if it takes longer for each one to
>spread.
If you want to get a better understanding of how intensity of
selection affects the evolutionary process, you should study the
mathematics developed by Haldane in his “Cost of Natural Selection”.
Evolutionists have discarded Haldane’s model because it doesn’t fit
with their belief system, however his estimates for the number of
generations for the substitution of a more beneficial allele for a
less beneficial allele are right in line with the results from the
Lenski experiment. Today if Haldane was alive, other evolutionists
would try to ruin his career. The only thing which I would question
about Haldane’s model is that he was only considering the substitution
of a more beneficial allele for a less beneficial allele when
actually, I believe that it is the ability of a subpopulation to
amplify the beneficial allele which is important in order to improve
the probability of the next beneficial mutation occurring at the
proper locus. Substitution of a beneficial allele in a small
population does little to improve the probabilities of the next
beneficial mutation occurring at the proper locus. You need large
subpopulations as hersheyh well understands, that why he is always
using 10^9 population sizes.

Now don’t get me wrong. Numerous alleles are being amplified
simultaneously when a subpopulation is able to amplify a beneficial
allele. All the other alleles in the genomes of those members are
being amplified simultaneously. But unless those alleles are involved
in the particular evolutionary process, the amplification of those
alleles does not accelerate the mutation and selection process. In
order for the mutation and selection process to be accelerated when
selection targets more than a single gene, two beneficial alleles for
two genes which are subject to selection must be amplified
simultaneously. Any member of the population which has only a single
beneficial allele for one or the other gene will still be inhibited
from reproducing efficiently by the selection pressure targeting the
gene for which it doesn’t have the beneficial allele. So the
requirement becomes that the members of this subpopulation must have
simultaneous or near simultaneous beneficial mutations, a very low
probability event. Or as evolutionists are now arguing that
recombination will recombine these two beneficial alleles to give a
better replicator. This doesn’t happen in reality as demonstrated by
the evolution of HIV to combination therapy despite the fact that HIV
does recombination. There is a mathematical reason why this doesn’t
happen and this reason is given by the probability function which
describes random recombination. None of the evolutionists posting on
this forum have the mathematical training or skills to do this type of
computation.

Greg, the bottom line is that evolutionists need to recognize that
only certain segments of a population are on a particular trajectory
of a fitness landscape. You can’t as hersheyh does willy-nilly is
assign population size of 10^9. The population size is often much
smaller in the mutation and selection process, especially if the
subpopulation can not amplify its mutations. This is the point
evolutionists should learn from the Lenski and Weinreich experiments.
Only those members of the populations which are able to take a
particular trajectory on a fitness landscape, amplifying their
beneficial mutations one by one are able to pass their genetic
information on to the next generation. The other members of the
population who are not on the trajectory ultimately go extinct,
sometimes in a single generation as with the intense selection
pressure of an antibiotic or more slowly as with the starvation
pressure which Lenski uses. Huge populations do not rescue your
mathematically irrational belief system.

>Your second claim actually undercuts your original premise; that the
>Theory of Evolution is *mathematically* irrational. You claim that none
>of the "real repeatable examples" studied exhibit such a process. I
>don't know if that is accurate, but it represents a decidedly
>non-mathematical argument. You have demonstrated yourself to be quite
>overfond of "educating" your opponents on the basics of probability, yet
>you shy away from it when responding to questions about more gentle
>selection. That you pass up the opportunity to play the pedagogue is a
>tacit admission that you do not have a mathematical argument to make in
>that scenario.

I know of two ways of analyzing the effects of intensity of selection,
one is empirical and one is mathematical. One could devise an
empirical experiment with let’s say antibiotics used in combination at
less than minimal inhibitory concentrations and measure that rate at
which the bacterial population can evolve resistance to both drugs
simultaneously. Since I don’t have a microbiology laboratory and no
evolutionist who has such a lab seems willing to do such an
experiment, we have a paucity of data on this. Lenski did some work
with combination pressures by changing the environment slightly but
has not published his data that I am aware of. So we are left with the
mathematical argument. And one of the best ways of approaching this
argument mathematically is with a mathematical model like Schneider’s
ev model of evolution of biological information. This model is not
trivial and takes some time to learn and understand but it does show
what happens when selection does not wipe out populations. His model
always allows the most fit half of the population to reproduce yet his
model can not sort and optimize beneficial mutations on anything other
than trivially small genomes. There’s much more to be said about why
his model behaves like this and why it is an accurate simulation of
real examples of mutation and selection but for now, this is enough.

>I'll ask again: Suppose two mutations exist in a population in a
>particular environment. One confers a 10% advantage in reproduction, the
>other 7%. Why - mathematically - can't they both spread through the
>population simultaneously?

If both mutations exist on members of the same subpopulation, they
will amplify but if they don’t exist initially when the selection
pressures are applied, you have very low probabilities that both
mutations will occur on the same member of the subpopulation or will
accumulate one after another on descendents of the subpopulation
because the beneficial mutation for one selection pressure will be
inhibited from amplifying by the selection pressure targeting the
other gene. This is why combination therapy works against HIV and any
other population for which combination pressures are applied. The
multiplication rule of probabilities is a killer of populations and
the theory of evolution.

>If you would like to argue that we have not observed such a process, or
>that it is "speculation", please do so AFTER either showing us why it is
>mathematically "irrational", or admitting that it is not in fact so.

No one has observed the process which you are arguing for either
mathematically or empirically. The reason why no one has observed this
process of parallel evolution is the multiplication rule of
probabilities. This is why the correct analysis of the mutation and
selection process and random recombination require a proper
application of the rules of probability theory in order to give a
predictable model of these phenomenons. Using the Poisson distribution
for a stochastic process where a mutation is not a Poisson random
variable is not a proper application of probability theory. This is
why evolutionists have such a confused understanding of how mutation
and selection works. And it doesn’t help when evolutionists claim that
the multiplication rule of probabilities does not apply to biological
evolution. This kind of mathematical and scientific blunder only
confuses the matter worse.
>Greg Guarino

[Charles Brenner]

On Sep 16, 6:09 am, Alan Kleinman MD PhD <klein...@sti.net> wrote:
> Google has again splintered this thread so I am restarting this thread
> again as round three and reposting responses from posts 851 through
> 875 as a single post. Please continue your posts on this thread and
> not on the splinter threads as I will not follow the splinter threads.
> I will post the rest of my responses to posts from round 2 in bulk on
> this thread. Sorry for any inconvenience.

[snip many pages randomly running one topic after another, leaving it
to the less important readers who have scads more time than the self-
important and pompous author to sort out what is what]

I wonder how an intelligent person would have handled the problem?

But then, if the problem is to get people to stop paying attention,
this might work.

[Bob Casanova]

On Fri, 16 Sep 2011 07:46:01 -0700 (PDT), the following
appeared in talk.origins, posted by Charles Brenner
<cbre...@berkeley.edu>:

It worked for me quite a while back; the Good MD is immune
to logic, and highly resistant to appropriate snippage.
--

Bob C.

"Evidence confirming an observation is
evidence that the observation is wrong."
- McNameless

[Alan Kleinman MD PhD]

pnyikos Sep 15, 7:37 am
>There may be unintended irony in the title: the thread has fragmented
>into many pieces in Google, and we may have a big salvage job on our
>hands just on that account.
>I've been told that once an ongoing thread passes 1000 posts, it
>fragments in Google. This is apparently exactly what has happened. I
>wonder whether it has also fragmented in e.g. Giganews.

Welcome to the discussion pnyikos. This is now the second time this
thread has exceeded 1000 posts. Last time I had to consolidate the
splinter threads for a few weeks to get the discussion back in order.
At the rate at which evolutionists are learning the correct
mathematics to describe mutation and selection, this thread will be
going on for a lot longer than 2000 posts.
>On Sep 14, 1:01 pm, Alan Kleinman MD PhD <klein...@sti.net> wrote:
>I've heard a bit about you, Dr. Dr. Kleinman. Now that we are in a
>thread a mere 2 posts deep (before I post this) maybe we can get
>acquainted without a lot of confusion about who said what when.

So you don’t get confused about what I’ve said, let me repeat the
first few paragraphs what I said initially from the first post (more
than 2000 posts ago).

The Theory of Evolution is a mathematically irrational belief system
which has harmed and continues to harm millions of people. This theory
is mathematically irrational because of the way the mutation and
selection phenomenon works mathematically (and empirically) and it is
harmful because the failure to understand how the mutation and
selection phenomenon works leads to drug resistant microbes, herbicide
resistant weeds, pesticide resistant insects, reduced durability of
cancer treatments and so on.

Biologists and other adherents to the doctrines of evolution have
utterly failed to properly describe how the mutation and selection
phenomenon works. This is equivalent to an engineer not understanding
how Newton’s laws work or how the Laws of Thermodynamics work. Here
are two examples of how evolutionists bungle the basic science and
mathematics of mutation and selection.

Edward Max from the Food and Drug Administrations says the following
on http://www.talkorigins.org/faqs/fitness/ . In particular, he said
the following statement: “The theory of evolution includes a number of
ideas that some people find difficult to accept intuitively. One of
the most difficult seems to be the notion that the intricate and
interdependent structures we observe in modern plants and animals
arose through random genetic mutations selected over time.”

What Edward Max and other evolutionists do not understand is that the
mutation and selection phenomenon is nothing more than a sorting and
optimization process. What are being sorted are beneficial and
detrimental mutations and what is being optimized is/are the fitness
to reproduce to the sorting (selection) condition(s). The ability of
this process to sort and optimize is dominated by the complexity of
the sorting conditions. The failure to understand this leads to
recommendations of the single drug therapy for the treatment of
antimicrobial diseases. This is the fastest way to get multidrug
resistant microbes.

The complexity of the selection conditions is dependent on the number
of genes targeted and the number of beneficial mutations required in
each gene in order to carry out the evolutionary process to increased
fitness. The governing mathematical principle for the chance that
multiple beneficial mutations will occur is the multiplication rule of
probabilities. Thomas Schneider from the National Cancer Institute is
incorrect when he makes the following claim on his web site
http://www-lmmb.ncifcrf.gov/~toms/paper/ev/AND-multiplication-error.html
, “The multiplication rule does not apply to biological evolution.”
The multiplication rule is in fact the central and governing
mathematical principle for understanding how the mutation and
selection phenomenon works and his failure to understand this harms
the people he is paid to help, that is people who suffer from cancer
(a mutating and selecting disease).

Evolutionist dogma and speculation is no replacement for hard
mathematical science and accurate measurement of empirical evidence.
Both the mathematical and empirical evidence show that the theory of
evolution by mutation and selection is mathematically irrational and
illogical. The failure to properly understand how the mutation and
selection phenomenon works has caused and continues to cause harm to
millions of people.

>> On Aug 11, 7:16 am, John Harshman <jharsh...@pacbell.net> wrote:
>> > Alan Kleinman MD PhD wrote:
>> > > On Jul 13, 1:56 pm, John Harshman <jharsh...@pacbell.net> wrote:
>> > >> g...@risky-biz.com wrote:

>> > >>> <snip all>

>> > >>> It's clear by now that Kleinman has no intention of answering the
>> > >>> questions posed to him.

>I've seen many claims like the above turn out to be false due to the
>person making them having "answering the questions posed to him" mean,
>in addition "to my satisfaction." I wonder whether that is the case
>here.
>[ditto "addressing" statt "answering"]
>[the German "statt" is so much easier to type than the English
>"instead of", nicht wahr?]

Why don’t you work with the mathematics statt grammatically?

>> > >>> "Harshman's" count of genetic differences between humans and chimps
>> > >>> has been bandied about in this thread. I've been wondering, could you
>> > >>> characterize those differences a bit? How many of them are in coding
>> > >>> areas?
>> > >> Very few. Coding regions are only around 3% of the genome, and
>> > >> accumulate about a third the number of differences per base as neutrally
>> > >> evolving regions.
>> > > You couldn t be more wrong John,

>The following doesn't seem to support the "couldn't be more wrong"
>assertion:

Evolutionists try to draw a distinction between selective differences
and neutral differences. In order for any difference (whether they are
selective or neutral) to be fixed in a genome, it takes time
(generations). We have John Harshman’s claim that there are 40,000,000
differences between human and chimpanzee genomes and we have the
evolutionist claim that the two species diverged about 5,000,000 years
ago. Do the math statt blah, blah, blah.

>> > > over 70% of the genes in humans and
>> > > chimpanzees don t code identical proteins.

>This shows how the claim that humans share 98% or more of their
>"genetic material" with chimps needs to be clarified. Way back in
>1995 or 1996 I asked whether this referred to loci, alleles, or base
>pairs.
>You've just now confirmed that it is NOT "alleles". Harshman seems to
>opt for "base pairs":

I’ve let evolutionists define what they mean by differences and then
say to them, do the math. Spread 40,000,000 differences through two
populations in 500,000 generations, how do you do the mathematics?

>> > While true, that has nothing to do with anything we've been discussing.
>> > Do you understand that a single base change can produce non-identical
>> > proteins?

>And thus, 98% of the base pairs might be identical yet
>physiologically, the two organisms might be very dissimilar.

I’ve accepted evolutionist numbers only for the sake of discussion.
Even with these very conservative estimates of the number of
differences between the two genomes, you are not anywhere near the
ballpark for mutation and selection to do the accounting for these
differences. Not only are evolutionists not anywhere near the
ballpark, they are not even on the same planet.

>> > If there are 30,000 genes, that's 21,000 mutations. Out of 40
>> > million. And even many of those are neutral.
>> It has everything to do with what we are discussing. There are huge
>> stretches of the two genomes which can not be matched up for homology.

>Apparently you mean "matched up BASE FOR BASE". But loci can be
>matched up in most cases even if the bases differ, no?

I missed that part. Are you saying that humans and chimpanzees have
identical number of chromosomes and you can line up each chromosome
and the genes match up on a loci by loci basis?

>> This data is presented for those areas which can be matched and the
>> match is not close at all. Evolutionists claim that humans and
>> chimpanzees come from a common progenitor. Now you are claiming that
>> many of these differences are neutral which is typical evolutionist
>> speculation.

>It may be based on solid data, as even you seem to allow for here:

Here is the crux of the argument pnyikos, can you do the accounting
for the number of differences between the two genomes in the given
number of generations. To do this accounting requires that you
understand mathematically how mutation and selection works and if you
want to add into the calculation, how neutral evolution works. In the
process of understanding how mutation and selection works, you also
will understand how to logically deal with multidrug resistant

microbes, multiherbicide resistant weeds, multipesticide resistant

insects and produce more durable cancer treatments because all these
are subject to the mutation and selection phenomenon.

>> Tell us which are neutral differences and which are
>> selective differences. And then compute the joint probability of two
>> neutral mutations being fixed in a population.

>The non-neutral mutations (especially the beneficial ones) would seem
>to be also relevant to your skepticism about humans and chimps being
>related.

It’s more than skepticism; it is mathematically irrational to believe
that humans and chimpanzees came from a common progenitor. You have
far too many genetic differences and far too few generations to make
the transformation.

>By the way, does "neutral" mean "coding for the same protein, only
>differering in the mRNA"? Does it include that? It's been a while
>since I've looked at this part of genetics.

The probability function I derived to compute the probability of two
mutations occurring is applicable to detrimental, neutral or
beneficial mutations. What distinguishes whether the mutation is
detrimental, neutral or beneficial is how the subpopulation with the
particular mutation responds over generations. If the mutation is
beneficial, the subpopulation will increase in number, if the mutation
is neutral, the subpopulation size will remain relatively constant
over generations and if the mutation is detrimental, the subpopulation
size will decrease over time. The mathematical significance of this
relates to the probability of the next beneficial mutation occurring
at the proper locus (position on the genome).

>> > >>> How many with other known functions? How much "junk"?
>> > >> Almost all is junk, just as almost all the genome is junk. Non-coding,
>> > >> functional regions are just another few percent of the genome.
>> > > This is the type of stupidity that evolutionist perpetuate. If they
>> > > don t know what a portion of the genome does, it is junk.
>> > No, that's not how it works. We recognize junk by the fact that it
>> > evolves at the rate of mutation.

>No direct testing to see whether it is ever translated into
>polypeptides? I'm disappointed.

I believe you are making and error here pnyikos. Coding of
polypeptides is not necessarily the only function of DNA. If coding
polypeptides was the only function of DNA, then all the non-coding
regions would have no selective benefit and would be random sequences
of bases.

>> Take a look at this >URL:http://www.google.com/url?sa=D&q=http://www.sciencemag.org/content/295/5552/131.abstract&usg=AFQjCNF6LJ>DM3GHffyRjXPABtkVjwnfm9w

>> In this URL, they studied chromosome 21. They report We detected
>> candidate positions, including two clusters on human chromosome 21
>> that suggest large, nonrandom regions of difference between the two
>> genomes. Nonrandom means these are selective differences and we all
>> should know by now that selective differences take hundreds of
>> generations per base substitution.

>I don't know it, being new to this thread and not having studied
>population genetics in sufficient depth.

You won’t get the mathematics of mutation and selection in a
population genetics course. You may get the Hardy-Weinberg Law but you
won’t get the correct probability functions to describe either the
mutation and selection phenomenon or the random recombination
phenomenon.

>> But you claim that neutral
>> mutations fix at the rate of a couple of hundred per generation,
>> thousands of times faster than selection can fix a beneficial
>> mutation.

>It all depends on how "large" those nonrandom regions are.

The rate of fixation of a single mutation is relatively constant and
measures in the hundreds of generations per mutation.

>> > True. Which has nothing to do with what I'm talking about. Stabilizing
>> > selection makes loci evolve at less than the neutral rate. Such loci are
>> > only a few percent of the genome. By the way, evolution isn't so fast as
>> > to randomize sequences in 5 million years.
>> Just what are you talking about? I guess you missed the study I posted
>> above about the large non-random differences on chromosome 21 between
>> humans and chimpanzees. 70% of genes code for different proteins,
>> large stretches of non-random differences between human and chimpanzee
>> genomes yet neutral evolution will fix all these differences a rate of
>> a couple of hundred per generation, thousands of times faster than a
>> single beneficial mutation can be fixed in a population. What you are
>> talking about is mathematical irrationality.

>There seems to be a real problem here with distinguishing "beneficial"
>and "non-harmful".

Real populations have no trouble making that distinction. If the
mutation is “beneficial”, the subpopulation with that mutation is able
to amplify (increase the number of members over generations) that
mutation because they are now more fit replicators. The importance of
this fact is that by increasing the subpopulation size with that
mutation increases the number of members doing trials for the next
beneficial mutation in the evolutionary sequence.

>The genomes are huge. Lots of non-harmful mutations could be fixed
>simultaneously, no?

The answer to this question is yes and no. The neutral mutations which
happen to reside on the most fit replicators will increase in
frequency over time just because these neutral mutations happen to be
hitchhiking along with the beneficial alleles. However, in the
mutation and selection phenomenon, when selection conditions target
more than a single gene, it requires amplification of two genes
simultaneously subject to selection pressures. All the empirical data
of mutation and selection show that this does not happen. This is why
combination therapy works for the treatment of HIV. Combination
selection pressures force the virus to amplify mutations at two genes
simultaneously. Even if the virus gets a beneficial mutation in one
gene, selection pressure acting on the other gene interferes with the
ability of that virus to amplify that mutation. And visa versa for
mutations occurring on the other gene, selection pressure acting at
the other gene prevents amplification of any mutation which would be
beneficial to drugs acting at that gene. What selection acting at two
or more genes does is force a member of the population to get two or
more beneficial mutations simultaneously, a very low probability
event.
>I think this will do for a start. With the thread having shattered
>the way it has, it may take you quite some time to get around to this
>fragment.
Professor Nyikos, if you found this post you realize that I’ve
consolidated these splintered threads.

pnyikos Sep 15, 8:04 am
Newsgroups: talk.origins
From: pnyikos <nyik...@bellsouth.net>
Date: Thu, 15 Sep 2011 08:04:08 -0700 (PDT)
Local: Thurs, Sep 15 2011 8:04 am

Subject: Re: Trying to salvage something from this Re: The Theory of
Evolution

On Sep 14, 5:24 pm, John Harshman <jharsh...@pacbell.net> wrote:
>> Alan Kleinman MD PhD wrote:

>I've snipped a great deal, a lot of it addressed in my own reply to
>Kleinman. John, feel free to comment on some of what I wrote to him,
>especially if you get to this thread before he does,

>> > large stretches of non-random differences between human and chimpanzee
>> > genomes yet neutral evolution will fix all these differences a rate of
>> > a couple of hundred per generation, thousands of times faster than a
>> > single beneficial mutation can be fixed in a population. What you are
>> > talking about is mathematical irrationality.

>> I've become convinced that you know almost nothing about mathematics
>> beyond the scraps rote learning you have displayed here.
>That may be, but since I tuned in very, very late (after 1000 posts
>went by, apparently) I wonder if you could give me a short synopsis of
>what this "mathematical irrationality" is all about.

Peter, John is not the one to give you a synopsis and this thread is
not 1000 posts but is now over 2000 posts. The short description of
this discussion is about the proper mathematical description of two
stochastic processes, the first is the random mutation and natural
selection phenomenon and the second is the random recombination
phenomenon.

Evolutionists for decades have used the Poisson distribution function
in an attempt to describe the mutation and selection phenomenon. I
believe this is not the correct probability distribution to use
because the random mutation is not a Poisson random variable. In
addition, the Poisson distribution does not properly relate population
size, number of generations and mutation rate for computing the number
of trials for a particular mutation. I have derived what I believe is
the correct probability function for computing the probability of two
mutations A and B to occur. I’ll repeat the derivation here for you.

Probability of two beneficial mutations occurring (not simultaneously)
at two loci as a function of population size and number of
generations.

The following are the definition of the variables used.
n -- is the total population size
nA -- is the fraction of the total population size with mutation A
nGA – is the number of generations for beneficial mutation A to occur
nGB – is the number of generations for beneficial mutation B to occur
mA -- the probability that in one organism in one generation, a
mutation A will affect a specific locus in the genome
mB -- the probability that in one organism in one generation, a
mutation B will affect a specific locus in the genome
P(A) is the probability that beneficial mutation A will occur at a
particular locus
P(Ac) is the probability that beneficial mutation A will NOT occur at
a particular locus
P(B) is the probability that beneficial mutation B will occur at a
particular locus
P(Bc) is the probability that beneficial mutation B will NOT occur at
a particular locus

First, compute the probability the beneficial mutation A will NOT
occur at a particular locus

divide mA by four

mA/4 -- the probability that in one organism in one generation, a
mutation A will turn a specific locus into a specific nucleotide other
than the one it already is -- for instance, turn G, C, or T into A.

subtract that result from 1

1-(mA/4) -- the probability that in one organism in one generation,
the specific mutation in question will NOT occur
raise that result to the power of n

(1-(mA/4))^n -- the probability that in the entire population in one
generation, the specific mutation will NOT occur in ANY individual.
raise that result to the power of nGA
((1-(mA/4))^n)^nGA = (1-(mA/4))^(n*nGA) -- the probability that in the
entire population in nGA generations, the specific mutation will NOT
occur in ANY individual

Then by the complementation rule of probabilities P(A) = 1 – P(Ac)
where P(A) is the probability that the specific mutation will occur at
a particular locus in nGA generations in the population size n and
P(Ac) is the probability that a specific mutation will NOT occur at a
particular locus in nGA generations in the population size n. Gives:
P(A) = 1 - (1-(mA/4))^(n*nGA)
is the probability that a specific mutation will occur at a particular
locus in nGA generations in a population size n.

Now, compute the probability the beneficial mutation B will NOT occur
at a particular locus

divide mB by four

mB/4 -- the probability that in one organism in one generation, a
mutation B will turn a specific locus into a specific nucleotide other
than the one it already is -- for instance, turn G, C, or T into A.

subtract that result from 1

1-(mB/4) -- the probability that in one organism in one generation,
the specific mutation B in question will NOT occur
raise that result to the power of nA

(1-(mB/4))^nA -- the probability that in the subset of the population
with mutation A in one generation, the specific mutation B will NOT
occur in ANY individual.
raise that result to the power of nGB
((1-(mB/4))^nA)^nGB = ((1-(mB/4))^(nA*nGB) -- the probability that in
the entire population in nGB generations, the specific mutation will
NOT occur in ANY individuals of the nA subgroup.
Then by the complementation rule of probabilities P(B) = 1 – P(Bc)
where P(B) is the probability that the specific mutation will occur at
a particular locus in nGB generations in the subpopulation size nA and
P(Bc) is the probability that a specific mutation will NOT occur at a
particular locus in nGB generations in the subpopulation size nA.
Gives:
P(B) = 1 – ((1-(mB/4))^(nA*nGB)
is the probability that a specific mutation B will occur at a
particular locus after mutation A has occurred as a function of
subpopulation size nA and the number of generations nGB after mutation
A has occurred.

And finally, the probability that mutation B will fall on a member of
the subpopulation with mutation A by the multiplication rule of
probabilities is:

P(A)*P(B) = {1 - (1-(mA/4))^(n*nGA)} * {1 – ((1-(mB/4))^(nA*nGB)}

This is the correct probability function for two point mutations A
then mutation B occurring not simultaneously as a function of
population and subpopulation size and the number of generations for
each event for given mutation rates. This is a significantly different
probability function than you would see for the Poisson distribution
function.

>> >>> And the reason it has stabilizing selection
>> >>> pressures acting on those sequences is that it has some type of
>> >>> important function on maintaining the life and reproductive capability
>> >>> of that member. The only junk in this discussion is the evolutionist
>> >>> junk science which fails to properly explain how mutation and
>> >>> selection works.
>> >> You mistake evolution at the rate of mutation for stabilizing selection,
>> >> presumably because you have a false understanding of the mutation rate.
>> >> Neutral evolution produces only a bit more than 1% difference over 5
>> >> million years, not a randomization of sequences.

>What is meant by "neutral evolution"?

This is an evolutionist concept of neutral alleles randomly fixing in
a population that is without selection. Evolutionists have a bad habit
of neglecting the multiplication rule of probabilities for joint
probabilities of multiple random events.

>> > You will only get randomization of sequences if there is no selection
>> > acting on that sequence. Your mathematics is faulty because 5 million
>> > years only represents about 500,000 generations and you can not fix
>> > 40,000,000 differences in two divergent populations in such a short
>> > period of time. It is mathematical irrationality to believe this.

>> You seem to have stopped even pretending to have an argument and are
>> just repeating your mantra regardless of what you are supposedly
>> responding to.
>Has the flaw in this mantra been laid bare?

Peter, you need to understand something about John and other
evolutionists debating this topic here. I see this problem as a simple
accounting calculation. What you need to do is properly define the
rules and apply the correct mathematical principles to do the
accounting calculation. John doesn’t understand the basic accounting
rules of probability theory and he refuses to understand the empirical
data available which substantiates the proper mathematical formulation

of the mutation and selection phenomenon.

>> >>>>> Of the ones that are in coding areas, how many are thought to make
>> >>>>> significant "interesting" morphological differences rather than minor,
>> >>>>> possibly non-function-altering changes to a protein?
>> >>>> Again, very few. The vast majority of differences in coding regions are
>> >>>> silent, i.e. making no difference in the protein being coded for.

>Has anyone tried to compare the ones that DO make a difference? See
>below.

From a mathematical point of view it doesn’t make a difference. If you
start from a common progenitor with essential similar genomes and then
have a species split, how many genetic differences can spread through
a population in a given number of generations? That’s the important
mathematical question. The first part of this analysis is to determine
how quickly (how many generations) it takes to spread a single
mutation through a population.

>> >>> Really John? Is that why over 70% of the genes in humans and
>> >>> chimpanzees code for different proteins? I can’t tell what you are
>> >>> worse at, mathematics or the interpretation of data.
>> >> This is silly.

>You have yet to show it is silly. To do that, you'd have to show that
>there are also a lot of differences that make no difference in the
>protein being coded for. The vast majority, in fact.

Peter, it takes time to spread a genetic change through a population.
How quickly can that change spread through a population whether it has
some phenotypic affect or not?

>> >> "Over 70% of the genes code for different proteins" is a
>> >> reasonable expectation for neutral evolution. Few of these differences
>> >> mean anythng.

>What do you mean by "mean anything"? Are you suggesting that a
>substitution is only significant if it changes an amino acid of one of
>the four kinds (polar, etc.--I forget their names) into one of another
>kind?

This is John’s claim, not mine. Again, whether these differences mean
anything or not is a distraction from the correct question which is
how many generations does it take to spread a single genetic change
through a population and how do populations do that substitution
process. It should be obvious that a beneficial genetic difference
should spread through a population more quickly than a neutral or
detrimental difference.

>> > We all know about evolutionist expectations, they are mathematically
>> > irrational. But if you want to show your work and compute the joint
>> > probability of two neutral mutations being fixed in a population, that
>> > would be some interesting evolutionist folklore to hear.

>> Mantra. At least your mantra does evolve over time, though it seems to
>> be randomly so.
>Hmmm...I wonder how many mantras I could pick out from you if I tried,
>John? [keywords: ivory tower]

Peter, we all have our mantras and biases, it just happens that John’s
are mathematically irrational mantras. Whose mantras can stand up to
hard mathematical and empirical scientific scrutiny? I’ve given you a
mathematical representation for the probability function for two
random mutational events to occur. This gives very precise targets to
question my logic. I think you will find that the empirical evidence
substantiates this equation.

>> >>>>> I assume this is ongoing research; perhaps the answers are not yet
>> >>>>> clear.
>> >>>> Oh, no. They're quite clear. What isn't clear is the exact number and
>> >>>> identities of the comparatively few functional differences.
>> >>> John, your irrational speculations don’t form a scientific basis for
>> >>> any of your claims.

>That's what several people keep telling me over and over again wrt
>intellligent design and directed panspermia, although they often
>soften it by leaving out words on the order of "irrational."

I’m not here to defend intelligent design or directed panspermia. I’m
here to properly describe the basic science and mathematics of
mutation and selection, something which you won’t get in a course on
evolutionism. It is important to have a correct understanding of the
mutation and selection phenomenon because it gives a rational basis
for dealing with multidrug resistant microbes, multiherbicide
resistant weeds, multipesticide resistant insects and development of
more durable cancer treatments.

>> >>>You don’t know how mutation and selection works
>> >>> and you can’t explain why over 70% of the genes code for different
>> >>> proteins in humans and chimpanzees.
>> >> By "different" you merely mean -- though you probably don't know it --
>> >> that there is at least one amino acid difference, i.e. one point
>> >> mutation. Trivial.

>Really? There are genetic "diseases" that hinge on only one point
>mutation. Would you like for me to look one up for you?

You don’t need to look them up for me Peter. That again is John’s
claim. What you are seeing is a stubborn resistance on the part of
evolutionists to accept mathematical and empirical facts of life. What
evolutionists are failing to do is to properly train young people in

the basic science and mathematics of the mutation and selection
phenomenon.

>> > Tens of thousands of different proteins between humans and chimpanzees
>> > fixed in 500,000 generations, that’s what a mathematically irrational
>> > evolutionist would call “trivial”. Maybe these proteins diverged
>> > during the pre-split period, you know, the banana split period.
>> >> [mantra snipped]
>> > Repeat after me, reptiles transform into birds, reptiles transform
>> > into birds, reptiles transform into birds…

>> That is indeed what the data show. Care to discuss it?
>Repeat after me: dinosaurs transform into birds... :-)
>Can't say it, can you? All you can say is "birds are
>dinosaurs". :-) :-)

Peter, didn’t you know that blizzard turn lizards into buzzards with
gizzards.

[Inez]

<snip rat king of replies>

So I have a question for you. I'm studying a certain sort of fungus,
and have discovered that it has 100 neutral fixations per generation
and only 10 selected mutations. How fast did each of these types of
mutations spread throughout the population? Can you show me how to
calculate that using only those numbers? John Harshman tells me that
you need other information, but you seem to be able to just look at
the final numbers and tell the speed that the genes spread at, so I
turn to you for illumination.

[Rolf]

Alan Kleinman MD PhD wrote:

[deleted]

Another creationist on a spree I see.

Fascinating how anybody can stand up and disprove 150 years of science,
thousands of scientists hard at work in almost all fields of science
gathering evidence
and putting together one of the beste researched and documented scientific,
scientific!
theories of all time, with more empirical evidence than anyone could cover
in a lifetime.

The MD PhD doesn't impress me, my son in law is a MD and when he isn't a PhD
it certainly is not for lack of potential! But that is another story. My
lack of a PhD is
because of no education but that doesn't bother me. Faraday didn't have much
of an
education either, but when offered a job as a bookbinder I ran as fast as I
could.

We have had many interesting evilutionist atheist discussions.

Why should I listen to Kleinman? If the subject is of such importance to him
he better
gets himself a lab coat and say goodbye to his patients, he's got a world to
save, millions
of souls to rescue from sinister evilutionism.

I didn't read much, but I got it right, didn't I?

Fair enough?

Yawn.

Rolf,

[r norman]

On Fri, 16 Sep 2011 23:55:14 +0200, "Rolf" <rolf.a...@tele2.no>
wrote:

Kleinman has two things going -- bugs up his ass is the best metaphor
I can think of.

1) He says that single drug treatment of many diseases, especially
HIV-AIDS, is the sole responsiblilty of ignormant evolutionary
biologists who forced a mathematically invalid theory of evolution
down the throats of medical students so they do not know any better.
He has been told that evolutionary biologists do not teach in medical
school, that medical genetiics is not the same as evolution, that
medical doctors are responsible for the education of medical students,
that medical doctors are responsible for choosing treatments, and
that evoloutionary biologists have long known and taught that
organisms can develop resistance to single drugs. None of this
matters. Evolutionary biologists are responsible for killing and
suffering of millions because they (we) don't understand mathematics.

2) He has a background in engineering and therefore is master of
anything and everything mathematical. Of course he has already
demonstrated a total lack of understanding of biological evolution, he
has beend reminded repeatedly of the many extremely sophisticated
mathematical analyses of evolution by population geneticists, he
utterly fails to understand what is meant by genetic drift, his own
so-called mathematical anaysis of the probability that two beneficial
mutations become fixed in a population is completely independent of
any fitness advantage offered by the mutations, he has already made
some monumental mathematical blunders and egregious biological
blunders. None of this matters. He has mastered mathematics and
understands the law of multiplication of probabilities. No
evolutionary biologist understands probability theory. And, besides,
because of this total lack of understanding we have of mathematics, we
are responsible for the death and suffering of millions of people
because of how we lie to medical students and mistrain them.

I think this covers it, except for the point that he makes these same
two points over and over and over and over again.

[Bob Casanova]

On Fri, 16 Sep 2011 19:09:41 -0400, the following appeared
in talk.origins, posted by r norman
<r_s_n...@comcast.net>:

A third point...

After his second (and third, and fourth, etc) iteration of
his errors, people kept responding. And very few did any
relevant snippage of the resulting 500-1000 line posts; it's
certain that he did none at all.

[hersheyh]

On Friday, September 16, 2011 4:34:53 PM UTC-4, Alan Kleinman MD PhD wrote:

[snip]

Wherein I reduce the Dear Dr.Dr.'s garbage to its crucial elements.

>
> The probability function I derived to compute the probability of two
> mutations occurring is applicable to detrimental, neutral or
> beneficial mutations.

It is appropriate only when and if the Dear Dr. Dr. could actually understand the conditions where it is correct. And the division by 4 part of his "derivation" of the binomial probability distribution (for that *is* what he derived although he apparently is unaware of that fact) is wrong under any conditions.

> What distinguishes whether the mutation is
> detrimental, neutral or beneficial is how the subpopulation with the
> particular mutation responds over generations.

Agreed. One uses the terms "beneficial" or "detrimental" to describe statistically significant changes in the fraction of the population with a particular genetic state from generation to generation relative to its alternative genetic state under specific environmental conditions. Such changes only occur when the two genetic states produce a *phenotypic difference* that matters wrt relative reproductive success. One uses the term "neutral" to describe the state when either the different genetic states produce no phenotypic difference that the environment can use to discriminate between the genetic states on the metric of relative reproductive success or when the phenotypic difference produced is irrelevant on the metric of relative reproductive success. Empirically, this is identified by the fact that the generation to generation changes in fraction of the population having a particular state varies by no more than the expected amount of variance due to chance alone. The percentage amount of expected

chance variance is a function of population size. Typically the 95% confidence level is used to distinguish chance differences generation to generation from statistically significant differences generation to generation.

> If the mutation is
> beneficial, the subpopulation will increase in number,

More important than number is the change in fractional distribution. Take antibiotic resistance. Upon selection (the addition of the antibiotic), the population size drastically decreases because of the deaths of the sensitive cells. What matters is that the fraction of the population with the genetic state of antibiotic resistance increases from 10^-8 to 1.0. Whether or not one continues with the selective condition, subsequent growth (and growth is all that is required to increase numbers at this point) will not change the fraction of the population that has the 'genetic resistant state' significantly until there is mutation to a different genetic state that has a significant reproductive advantage over the resistant state under the environmental conditions at these post-selection times.

> if the mutation
> is neutral, the subpopulation size will remain relatively constant
> over generations

Again, it is the fraction of the population that is important, not the number. Under neutral conditions (conditions where the two genetic states have no reproductive advantage relative to each other, either because they don't produce a phenotypic difference or because the phenotypic difference does not affect reproductive success), the generation to generation differences in the frequency of the two genetic states will be due to chance alone. *Because chance has no memory* (a point you forget), this means that the frequencies of the two genetic states will undergo neutral drift (a drunkard's walk) that will only end by fixation of one trait or the other. The percentage effect of such chance variation is higher in small populations. Random walks will happen because one of the assumptions of the Hardy-Weinberg rule is that the population is of infinite size and real populations are not of infinite size.

So, assuming a large enough population, the generation to generation effect of chance variation in the fraction of the population with a particular allele will be close to whatever the original fraction was. If that fraction is 10^-8, one would expect the next generation to have a fraction close to that. New mutation will not have a significant effect on this fraction because new mutations will have only a [1-(1/2N)] chance of not going to extinction by chance. If, by chance, one new neutral mutation has increased in frequency to a significant level, new mutations of the same particular type will be an insignificant fraction of the frequency of that mutation type in the population.

> and if the mutation is detrimental, the subpopulation
> size will decrease over time.

No. In this case, the frequency of the mutant genotype will essentially equal the rate of new mutation to that genotype. Any particular new mutant genotype that is deleterious will be driven to extinction, but new mutations of that genotype will occur every generation. Eventually, you will have an equilibrium level where the loss of m deleterious mutant alleles each generation equals the gain of m deleterious mutant allleles each generation. Thus the *fraction* of the population having a deleterious allele will remain constant. [This is slightly different in the case of diploid organisms, where a 'recessive' allele can be selectively neutral in the heterozygous state and only harmful in the homozygous state. But the rule that an equilibrium between gain and loss of the allele each generation still holds.]

> The mathematical significance of this
> relates to the probability of the next beneficial mutation occurring
> at the proper locus (position on the genome).

The probability of any subsequent or second mutation occurring is a function of the rate of mutation to that state and the number of individuals in a population that have the needed previous genetic state. The number of individuals in a population that have the requisite genetic state is a function of both selection for that state and the number of generations of growth under selective conditions for that state.

Thus, the precise order of selective events matters. If the genetic state of antibiotic resistance is selectively neutral or detrimental under conditions where there is no antibiotic, then the steady-state fraction of the population having that state is essentially equal to the mutation rate assuming that there has not been sufficient time for a drunkard's walk to, by chance, having increased the frequency. And in the examples we have been using, where the initial population was grown from a double-sensitive organism, there hasn't been sufficient time for a significant amount of drift. Thus the *number* of individuals with resistance to the antibiotic is equal to the mutation rate to that genetic state times the population size examined for that genetic state. At generation one of selection for the genetic state of antibiotic resistance, the *number* of individuals with the resistant genetic state has not changed. But the *fraction* of the population with the resistant state has changed dramatically und

er these conditions, from 10^-8 to 1.0. After 30 generations of population doubling, almost regardless of whether or not one continues to use the selective conditions of antibiotic present, the *fraction* of the population resistant to the antibiotic remains essentially unchanged (1.0, with only back mutation providing the sensitive genetic state), but the *number* has increased.

I certainly agree that the probability of finding a double-mutant is importantly a function of the number of individuals with the first mutation selected for. The odds of finding a double-mutant for a second mutation in the cells selected for resistance to the first antibiotic is low if you do that selection in the first few generations after selection. But it becomes increasingly possible in larger cells precisely because the size of the population with the first genetic resistant state is now large. It is large precisely because of the earlier selection changing the fraction of cells with the first resistant state and subsequent selective growth of that subfraction.
>
[snip]

>
> Evolutionists for decades have used the Poisson distribution function
> in an attempt to describe the mutation and selection phenomenon. I
> believe this is not the correct probability distribution to use
> because the random mutation is not a Poisson random variable.

The Poisson is only used as an estimate of the binomial probability distribution when certain conditions apply. They apply in the cases I used it in. So your real problem is that you disagree with the use of the binomial probability distribution. You do so even though, with the exception of the division of 4, the equation you "derived" is nothing but the binomial probability distribution and is based on its assumptions.

> In
> addition, the Poisson distribution does not properly relate population
> size, number of generations and mutation rate for computing the number
> of trials for a particular mutation. I have derived what I believe is
> the correct probability function for computing the probability of two

> mutations A and B to occur. I�ll repeat the derivation here for you.

>
> Probability of two beneficial mutations occurring (not simultaneously)
> at two loci as a function of population size and number of
> generations.
>
> The following are the definition of the variables used.
> n -- is the total population size
> nA -- is the fraction of the total population size with mutation A

> nGA � is the number of generations for beneficial mutation A to occur
> nGB � is the number of generations for beneficial mutation B to occur

> mA -- the probability that in one organism in one generation, a
> mutation A will affect a specific locus in the genome

Ordinarily this would be considered the "mutation rate." But the Dr. Dr. does not use mA as the mutation rate. He uses mA/4 as the mutation rate. That is the only difference between the Dr. Dr.'s derived probability function and the binomial derived probability function.

Interestingly enough, the Dr. Dr. doesn't ever tells us how he is able to identify that a *mutation A* has (or will) "affect[ed] a specific locus in the genome". That is, he doesn't tell us what change occurred at this site so that he can identify it as a mutation. Moreover, he doesn't tell us how he identifies the "specific locus in the genome". Later it appears that what means by "specific locus" is "specific nucleotide site". And that *after* he identifies somehow that there "will be" (his wording) a mutation in this nucleotide site, he then tosses a 4-sided dice to determine what that mutation is. Which means that even the original nt at that site can be considered a "mutational change".

This, of course, makes no sense at all. The only way it makes sense is if the Dr. Dr. is under some delusion that a nt site remains empty of any nt until there is some event (a mutation event) that, apparently, is determined by ESP and then the nt for that empty site is randomly chosen from equimolar pools of the 4 possible nts.

> mB -- the probability that in one organism in one generation, a
> mutation B will affect a specific locus in the genome
> P(A) is the probability that beneficial mutation A will occur at a
> particular locus
> P(Ac) is the probability that beneficial mutation A will NOT occur at
> a particular locus
> P(B) is the probability that beneficial mutation B will occur at a
> particular locus
> P(Bc) is the probability that beneficial mutation B will NOT occur at
> a particular locus
>
> First, compute the probability the beneficial mutation A will NOT
> occur at a particular locus
>
> divide mA by four
>
> mA/4 -- the probability that in one organism in one generation, a
> mutation A will turn a specific locus into a specific nucleotide other
> than the one it already is -- for instance, turn G, C, or T into A.

Yet, by dividing by 4, he is assuming that all 4 nts (*including* the original one at that site) are all equally likely to fill this apparently empty nt site, but *only* when you already know that a "mutation" has occurred at that site. After all mA is "the probability that in one organism in one generation, a mutation A will affect a specific locus in the genome". And apparently this event can be determined without any knowledge of the phenotypic difference produced or even what genotypic event occurred, not even that it occurs at a specific nt.

My guess is that he really does believe the creationist nonsense that genes are made by assembling nts by pure chance one nt at a time. That, after all, is the assumption behind the creationist nonsense about the probability of assembling a 747 in a tornado. That is what underlies the creationist idea of the chance of evolution of a gene being one in 4^n where n is the number of nucleotides. That is, he does not believe in reproduction, where genes are assembled by an imperfect copy mechanism. Otherwise, I cannot think of a single reason for dividing the mutation rate by 4.

If one is talking about mutation that produces a *selectively relevant* change, one can talk about change in phenotype due to change in genotype, since what nature works on during selection -- beneficial or detrimental -- is phenotypic difference. In the case of selectively neutral mutation, one must still know the initial starting point and end point, be that a phenotypic difference that has no selective effect or a change in a gene that can only be identified by knowing that a *change* in sequence has occurred.

> subtract that result from 1
>
> 1-(mA/4) -- the probability that in one organism in one generation,
> the specific mutation in question will NOT occur
> raise that result to the power of n
>
> (1-(mA/4))^n -- the probability that in the entire population in one
> generation, the specific mutation will NOT occur in ANY individual.

That is (again, except for the divided by 4 bit) essentially the binomial probability under the assumption that n = number of trials/generation and the number of generations actually tested = 1. n is not necessarily the *entire* population of organisms; it is only the number of individuals tested for the "event", be that 'event' mutation to A-resistance or both A-and B-resistance.

Again, remove the divided by 4 bit, and this is the assumption of binomial probability.

> raise that result to the power of nGA

nGA, as I recall, is = number of generations in which n (or a mean of n) individuals/generation are tested.

Or, mathematically equivalently, multiply n, the number tested/generation by nGA, the number of generations in which n individuals are tested. The result of that multiplication is more easily identifiable as "the total number of trials performed" that is in the binomial probability distribution. Using an exponent is not wrong, but it is obfusticating the terms to hide the fact that you have a binomial probability distribution (except for the division of the probability of the "event" -- aka, the mutation event -- by 4).

> ((1-(mA/4))^n)^nGA = (1-(mA/4))^(n*nGA) -- the probability that in the
> entire population in nGA generations, the specific mutation will NOT
> occur in ANY individual

Again, remove the divided by 4 and use the mathematically identical multiplication form instead of the exponential, and the equation is not different from the expectations of one or more mutants in the binomial probability distribution, which, under conditions we are using, can be estimated to more than 6 significant figures by use of the Poisson.
>
> Then by the complementation rule of probabilities P(A) = 1 � P(Ac)

> where P(A) is the probability that the specific mutation will occur at
> a particular locus in nGA generations in the population size n and
> P(Ac) is the probability that a specific mutation will NOT occur at a
> particular locus in nGA generations in the population size n. Gives:
> P(A) = 1 - (1-(mA/4))^(n*nGA)
> is the probability that a specific mutation will occur at a particular
> locus in nGA generations in a population size n.
>
> Now, compute the probability the beneficial mutation B will NOT occur
> at a particular locus
>
> divide mB by four
>
> mB/4 -- the probability that in one organism in one generation, a
> mutation B will turn a specific locus into a specific nucleotide other
> than the one it already is -- for instance, turn G, C, or T into A.
>
> subtract that result from 1
>
> 1-(mB/4) -- the probability that in one organism in one generation,
> the specific mutation B in question will NOT occur
> raise that result to the power of nA
>
> (1-(mB/4))^nA -- the probability that in the subset of the population
> with mutation A in one generation, the specific mutation B will NOT
> occur in ANY individual.
> raise that result to the power of nGB
> ((1-(mB/4))^nA)^nGB = ((1-(mB/4))^(nA*nGB) -- the probability that in
> the entire population in nGB generations, the specific mutation will
> NOT occur in ANY individuals of the nA subgroup.

> Then by the complementation rule of probabilities P(B) = 1 � P(Bc)

> where P(B) is the probability that the specific mutation will occur at
> a particular locus in nGB generations in the subpopulation size nA and
> P(Bc) is the probability that a specific mutation will NOT occur at a
> particular locus in nGB generations in the subpopulation size nA.
> Gives:

> P(B) = 1 � ((1-(mB/4))^(nA*nGB)

> is the probability that a specific mutation B will occur at a
> particular locus after mutation A has occurred as a function of
> subpopulation size nA and the number of generations nGB after mutation
> A has occurred.
>
> And finally, the probability that mutation B will fall on a member of
> the subpopulation with mutation A by the multiplication rule of
> probabilities is:
>

> P(A)*P(B) = {1 - (1-(mA/4))^(n*nGA)} * {1 � ((1-(mB/4))^(nA*nGB)}
>
> This is the correct probability function for two point mutations. A

> then mutation B occurring not simultaneously as a function of
> population and subpopulation size and the number of generations for
> each event for given mutation rates. This is a significantly different
> probability function than you would see for the Poisson distribution
> function.

Again, except for the division by 4, I recognize this as a binomial probability distribution. And if the event is tested for when P(A) approximately equals 10^-8 (that is, when the frequency of the mutant in a population is 10^-8) rather than 1 (after both selection and growth for A resistance) and P(B) approximately equals 10^-8 the result will be quite different for the same n.
>
[snip]

[Alan Kleinman MD PhD]

The following replies are from a splinter threads
Virgil Sep 14, 1:35 pm
Newsgroups: talk.origins
From: Virgil <vir...@ligriv.com>
Date: Wed, 14 Sep 2011 14:35:43 -0600
Local: Wed, Sep 14 2011 1:35 pm

Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

In article
<7f7ca969-1404-4f7e-9147-bc7b95ada...@x11g2000prb.googlegroups.com>,

Alan Kleinman MD PhD <klein...@sti.net> wrote:

>> On Aug 10, 7:42 pm, Mark Isaak <eci...@curioustaxonomyNOSPAM.net>

>> wrote:
>> > On 8/10/11 2:21 PM, Alan Kleinman MD PhD wrote:
>> > > On Jul 14, 8:58 am, Mark Isaak<eci...@earthlink.net> wrote:
>> > >> On Tue, 12 Jul 2011 18:18:51 -0700, Alan Kleinman MD PhD wrote:
>> > >>> On Jun 7, 2:45 pm, Mark Isaak<eci...@earthlink.net> wrote:

>> > >>>> On Mon, 06 Jun 2011 17:47:21 -0700, Alan Kleinman MD PhD wrote:
>> Why would I want to accept the mathematically irrational arguments of
>> evolutionists about how their folklore tells them mutation and
>> selection works? I m interested in an accurate engineering
>> mathematical analysis of how this phenomenon works and the empirical
>> evidence which supports this analysis, not the mathematically
>> irrational evolutionist claims. These principles are too important to
>> my patients to be left to the mathematically irrational speculations
>> and extrapolations of evolutionists.

>Evolutionists are quite as rational about how Evolution works as anyone
>else.
>Probably a good deal more so!
>So whom do you trust to be MORE rational about Evolution than those who
>have dedicated themselves to figuring out just how nature does it?
Welcome to the discussion Virgil. What makes you think that I am not
dedicated to figuring out how mutation and selection works? I have to
deal with the consequences of this phenomenon on a daily basis in my
medical practice and it is of great importance that I understand how
this phenomenon works especially since I am advocating a non-standard
of care treatment for infections. In fact I directly oppose the
recommendation to primary care physicians to reduce the usage of
antibiotics to prevent the evolution of resistant strains. I advocate
the usage of combination therapy to suppress the appearance of
resistant microbes. You see Virgil, I put my professional licenses and
career on the line when I make these arguments. Evolutionists on the
other hand walk away without paying a price for their failure to
properly describe the basic science and mathematics of the mutation
and selection phenomenon.

John Harshman Sep 14, 11:39 am

Newsgroups: talk.origins
From: John Harshman <jharsh...@pacbell.net>

Date: Wed, 14 Sep 2011 11:39:30 -0700
Local: Wed, Sep 14 2011 11:39 am

Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

>> On Aug 11, 7:22 am, John Harshman <jharsh...@pacbell.net> wrote:
>>> Alan Kleinman MD PhD wrote:

>>>> On Jul 19, 9:20 am, John Harshman <jharsh...@pacbell.net> wrote:
>>>>> Alan Kleinman MD PhD wrote:

>>>>>> On Jun 8, 1:49 pm, John Harshman <jharsh...@pacbell.net> wrote:
>>>>>>> William Hughes wrote:
>>>>>>>> On Jun 8, 12:35 pm, Alan Kleinman MD PhD <klein...@sti.net> wrote:
>>>>>>>>> On Jun 1, 8:39 am, William Hughes <wpihug...@gmail.com> wrote:

>>>>>>>>>> On Jun 1, 11:52 am, Alan Kleinman MD PhD <klein...@sti.net> wrote:
>>> Depends on the frequencies of the alleles, doesn't it? If they "amplify"
>>> individually, the probability is eventually going to be 1.
>> Are you sure about that?

>Yes.
Are you sure that both alleles have to have a frequency of 1?

>> Have you derived the probability function
>> which would describe this stochastic process? For example do A and B
>> both have to amplify?

>No, but we have already assumed that they both amplify independently.
>Remember?
I haven’t made that assumption, you have. The correct probability
function for random recombination does not require that you consider
selection. The affects of selection on random recombination only
affects the probabilities implicitly by altering the number of members
with each of the particular alleles.

>> What happens to the probabilities of the random
>> recombination of A and B if only one of the two all alleles amplify?

>Not relevant.
John, you shouldn’t be making this argument until you derive the
probability function for random recombination. I’m not going to give
the derivation of that probability function now but consider this.
What if in your population every member has allele A except the member
which has allele B, that is A has a frequency close to 1 in the
population? That member with allele B that is B has a frequency very
close to 0. What is the chance that a member with allele A will meet
and recombine with the member with allele B?

>> I�ll give you a hint; don�t use the Poisson distribution to do this
>> computation.
>It's really quite simple. Given various simple assumptions, such as
>independent assortment, panmixis, a constant population, and frequencies
>p and q for the two alleles, the expected frequency of AB individuals is
>just pq. As p and q increase, pq increases. We have already specified
>that p and q are increasing. If AB phenotypes are favored over A, B, and
>"wild type" phenotypes, p and q will increase faster than they would in
>the absence of that advantage.
John, the only thing that the Hardy-Weinberg law gives you is that the
frequency of alleles remains constant when the population is in
equilibrium (selection is not acting). If you want to estimate the
probability of two alleles randomly recombining, you need to write the
probability function for that stochastic process. Once you do that,
you can consider how selection will change the probabilities over
generations as the frequencies and population sizes of the alleles
change.

>>>>>> That is unless you think that mutations for one or
>>>>>> another drug are not occurring in the HIV population when subjected to
>>>>>> combination therapy.
>>>>> As usual, you misunderstand the necessary conditions.
>>>> I�ve already derived the probability function for the two alleles to
>>>> randomly recombine.
>>> No you haven't. You haven't taken into account that they are
>>> individually advantageous.

>> Oh really, I haven�t take that into account? Obviously your

>> evolutionist telepathy is leading you astray once again. We should
>> really call your thinking evolutionist telepathetic.

>I missed the part where you did that, then. Could you repeat your math?
Since I haven’t posted the derivation of the probability function for
random recombination yet, I can’t repeat the math. I’m trying to get
you to think about this phenomenon first.

>>> See? You don't know what "beneficial" means. Under the conditions you
>>> propose, neither allele is beneficial.
>> More evolutionist telepathetic. Let me repeat a previous hint for you
>> to show you how to derive the correct probability function for two
>> alleles to randomly recombine. This random process obeys the same
>> mathematical principles as random card drawing. With that hint and
>> google, you should be able to solve this probabilities problem by this
>> evening.

>I'm not reading your mind. I'm reading your words. Admittedly, your
>words are only loosely connected to your mind, and that connection is
>perhaps looser than for a rational person. But the words themselves are
>fairly clear.
When you derive the correct probability function for random
recombination, “beneficial” doesn’t come into play in a particular
generation. Only when you extend the probability function for random
recombination over generations does beneficial come into play and that
only implicitly. The way selection enters into the mathematics of
random recombination over generations is manifest by changes in the
frequency of alleles and population size changes over the generations.

>> I can understand you wanting to change the subject to anything other
>> than how mutation and selection works and why recombination does not
>> rescue your mathematically irrational belief system. Learn to stay on

>> topic. And now that I�ve all but given you the equations to describe
>> random recombination, let�s see if you can derive that probability
>> function.
>Would you agree that if the frequencies of A and B are both 1, then the
>probability of recombination is also 1?
What would happen to the probabilities of random recombination of A
and B if either A or B had a frequency of 1?

John Harshman Sep 14, 2:24 pm

Newsgroups: talk.origins
From: John Harshman <jharsh...@pacbell.net>

Date: Wed, 14 Sep 2011 14:24:24 -0700
Local: Wed, Sep 14 2011 2:24 pm

Subject: Re: Trying to salvage something from this Re: The Theory of
Evolution

> On Aug 11, 7:16 am, John Harshman <jharsh...@pacbell.net> wrote:
>> Alan Kleinman MD PhD wrote:
>>>> On Jul 13, 1:56 pm, John Harshman <jharsh...@pacbell.net> wrote:
>>>>> g...@risky-biz.com wrote:
>> It has everything to do with what we are discussing. There are huge
>> stretches of the two genomes which can not be matched up for homology.

>True. Do you know how they got there? Most of them are retrotransposons,
>yet another class of neutral mutations.
John, chromosome 21 has large stretches if non-random sequences which
are not on the chimpanzee genome. So where are these stretches of
bases on the chimpanzee genome? You are going to paint yourself in a
corner with these types of arguments because human genomes and
chimpanzee genomes must remain homologous to themselves for
consistently successful reproduction. Transposons may occur commonly
in immunologic cells but in germ cell line this phenomenon would
disrupt homology.

>> This data is presented for those areas which can be matched and the
>> match is not close at all.

>It isn't? 98.7% identity isn't close? What would constitute close, then?
When you are talking about mutation and selection, you are not close
at all. Mutation and selection working under ideal conditions may be
able to substitute 10-20,000 bases in 500,000 generations. Using your
numbers, you have to account for 20,000,000 bases in each of the human
and chimpanzee populations. And remember, you don’t have a population
size of 10^9 until about the last century. Human population size never
really grew rapidly until the advent of mechanized farming about
5-10,000 years ago. Chimpanzee mechanized farming is limited to a
chimp putting a stick down a hole to harvest ants. What do you think
the maximum size of the chimpanzee population has ever been?

>> Evolutionists claim that humans and
>> chimpanzees come from a common progenitor. Now you are claiming that
>> many of these differences are neutral which is typical evolutionist
>> speculation.

>Simple observation of how proteins work.
More like simple minded observation. I suppose if you look out toward
the horizon and say, “sure looks flat to me”, that’s enough to
convince you that the earth is flat. I suggest you take a look at
Google Earth.

>> Tell us which are neutral differences and which are
>> selective differences.

>Well, it seldom matters whether a protein has leucine, isoleucine, or
>phenylalanine in a particular spot.
Well then you have some explaining to do. How do all these neutral
variants get fixed in a population because greater than 70% of
proteins differ between humans and chimpanzees and you only have
500,000 generations to explain the differences?

>> And then compute the joint probability of two
>> neutral mutations being fixed in a population.

>Are you still on about that? Your joint probability is irrelevant. We
>don't care about the joint probability of some particular set of
>mutations being fixed, only about the probability that any set of
>mutations will be fixed. Different, no?
Now John, when you make a claim like that you are proving that you
accept as true a mathematical irrational belief system. Whenever you
are considering a stochastic process, the joint probability of events
is governed by the product of the individual probabilities. The
multiplication rule of probabilities is the monkey wrench in the works
of your irrational belief system. You will never have a good
understanding how this phenomenon work without a good understanding of
probability theory.

>>>>>> How many with other known functions? How much "junk"?
>>>>> Almost all is junk, just as almost all the genome is junk. Non-coding,
>>>>> functional regions are just another few percent of the genome.
>>>> This is the type of stupidity that evolutionist perpetuate. If they
>>>> don’t know what a portion of the genome does, it is junk.
>>> No, that's not how it works. We recognize junk by the fact that it
>>> evolves at the rate of mutation.

>> Take a look at this URL: >http://www.google.com/url?sa=D&q=http://www.sciencemag.org/content/295/5552/131.abstract&usg=AFQjCNF6LJDM3>GHffyRjXPABtkVjwnfm9w

>> In this URL, they studied chromosome 21. They report “We detected
>> candidate positions, including two clusters on human chromosome 21
>> that suggest large, nonrandom regions of difference between the two
>> genomes.” Nonrandom means these are selective differences

>No it doesn't.
Or really John? So how do we get non-random sequences of bases without
selection? How did these bases become arranged without selection?

>> and we all
>> should know by now that selective differences take hundreds of

>> generations per base substitution. But you claim that neutral

>> mutations fix at the rate of a couple of hundred per generation,
>> thousands of times faster than selection can fix a beneficial
>> mutation.

>Once again you confuse numbers with rates.
I don’t think so John. I think you’ve made contradictory claim. On one
hand you are claiming that neutral evolution is slower than selective
evolution and then on the other hand you claim that a couple hundred
neutral mutations are fixed every generation. I think you are the one
how is more than a little bit confused.

>>>> If they
>>>> don’t understand how to do a mathematical computation it is junk.
>>>> John, just because you are ignorant what a non-coding region of a
>>>> genome does, don’t impose your ignorance on us by claiming this is
>>>> junk. If a region of DNA has no coding function for proteins but
>>>> remains non-random, it does so because it has stabilizing selection
>>>> acting on those sequences.

>>> True. Which has nothing to do with what I'm talking about. Stabilizing
>>> selection makes loci evolve at less than the neutral rate. Such loci are
>>> only a few percent of the genome. By the way, evolution isn't so fast as
>>> to randomize sequences in 5 million years.
>> Just what are you talking about? I guess you missed the study I posted
>> above about the large non-random differences on chromosome 21 between
>> humans and chimpanzees.

>So? How is that relevant? Do you have access to the whole article? I don't.
Yes I do have the whole article. I was able to subscribe to Science
Magazine online without charge. Go to their web page and ask for an
account. And the reason why this is relevant is that there are more
differences between the human and chimpanzee genomes than your simple
minded analysis accounts for.

>> 70% of genes code for different proteins,

>....if by "different" you mean having at least one different amino acid.
Do you have a different definition for the word “different” because if
so you need to tell us how our definitions for the word “different”
are different. And then perhaps we can work out our differences unless
you want to differ on our differences.

>> large stretches of non-random differences between human and chimpanzee
>> genomes yet neutral evolution will fix all these differences a rate of
>> a couple of hundred per generation, thousands of times faster than a
>> single beneficial mutation can be fixed in a population. What you are
>> talking about is mathematical irrationality.
>I've become convinced that you know almost nothing about mathematics
>beyond the scraps rote learning you have displayed here.

Now what have you against rote learning? If it wasn’t for rote
learning, evolutionists would have no way of indoctrinating naïve
school children. You certainly don’t have any mathematical logic to

support your mathematically irrational belief system.

>>> You mistake evolution at the rate of mutation for stabilizing selection,
>>> presumably because you have a false understanding of the mutation rate.
>>> Neutral evolution produces only a bit more than 1% difference over 5
>>> million years, not a randomization of sequences.

>> You will only get randomization of sequences if there is no selection
>> acting on that sequence. Your mathematics is faulty because 5 million
>> years only represents about 500,000 generations and you can not fix
>> 40,000,000 differences in two divergent populations in such a short
>> period of time. It is mathematical irrationality to believe this.
>You seem to have stopped even pretending to have an argument and are
>just repeating your mantra regardless of what you are supposedly
>responding to.

You are the one closing your eyes to the argument. You have said there
are 40,000,000 differences between human and chimpanzee genomes and by
your numbers the two species diverged 5,000,000 years ago. How do you
account for those differences in such a small number of generations
(other than your mathematically irrational claim that a couple of
hundred neutral mutations fix every generation). Do you want some more
generations from the pre-split split period?

>> We all know about evolutionist expectations, they are mathematically
>> irrational. But if you want to show your work and compute the joint
>> probability of two neutral mutations being fixed in a population, that
>> would be some interesting evolutionist folklore to hear.
>Mantra. At least your mantra does evolve over time, though it seems to
>be randomly so.

My new mantra for you is “multiplication rule of probabilities, theory
of evolution irrational”. This mantra is to be sung to the theme from
the Beatles song, Shake it up baby, twist and shout.

>> Repeat after me, reptiles transform into birds, reptiles transform
>> into birds, reptiles transform into birds…
>That is indeed what the data show. Care to discuss it?

When I decide to take a course in fictional writing that will be our
first topic.

The following are responses from posts 876-900 round 2

John Harshman 17, 7:58 am
>> Of course these neutral mutations don’t show up all at once, sweeping
>> through the population like a tsunami. They also don’t show up dozens
>> per generation, generation after generation for hundreds of thousands
>> of generations. This is part of the evolutionist mathematically
>> irrational speculations. My arguments are made from hard mathematical
>> and empirical evidence. If you didn’t have your mathematically
>> irrational speculations and gross over-extrapolations, you
>> evolutionists would have no argument at all for your mathematically
>> irrational belief system.
>So far, just a content-free rant.
That’s how an evolutionist responds to mathematical and empirical
evidence. Is it any wonder that we have multidrug resistant microbes,
multiherbicide resistant weed, multipesticide resistant insects and
less than durable cancer treatments. It is the failure of
evolutionists to properly explain the mutation and selection
phenomenon that has caused these problems.

>> Now I have shown you mathematically why neutral mutations do not
>> spread through populations rapidly if at all.
>Nobody claims that neutral mutations spread rapidly.
You have, you have claimed that a couple hundred of them are fixed
every generation. Can you make the theory of evolution any more
mathematically irrational? I expect so.

>> The probability function
>> I derived for you of two mutations accumulating is not only applicable
>> for the accumulations of beneficial mutations;
>In fact, it isn't applicable to beneficial mutations at all.
Not only is that probability function applicable to beneficial
mutations, it is applicable to any two mutations whether they are
detrimental, neutral or beneficial. What distinguishes what type of
first mutation that has occurred is what happens with the
subpopulation size in the ensuing generations. If the mutation is
beneficial, the subpopulation size for the first mutation will
increase over time improving the probability that the next mutation
will occur on one of its members. If the mutation is neutral or
detrimental, the subpopulation size will remain constant or decrease
of time respectively.

>> it is also applicable
>> for computing the probability of neutral or detrimental mutations
>> accumulating in a population. Of course neutral and detrimental
>> mutations do not amplify because they don’t give increased fitness to
>> reproduce for those members with those mutations. Because of this,
>> there is a very low probability that neutral or detrimental mutations
>> will accumulate in a population.
>True. In fact the probability of a neutral mutation ever becoming fixed
>is 1/2N. In a population of 1 billion, that's one in 2 billion. However,
>in that population, there are in the neighborhood of 100 billion
>mutations in every generation. Can you do the math to calculate how many
>of those mutations will eventually become fixed? (Just calculate the
>mean of the distribution if you like.) Now repeat for every generation
>and see what you get.
Sure I can do the math John; you use the multiplication rule of
probabilities for random independent events. The joint probability of
two neutral mutations being fixed in the population is (1/(2*10^9))*(1/
(2*10^9)). Do you want me to do the math for the probability of three
neutral mutations being fixed in the population?

>>>> This is the kind of irrational
>>>> nonsense that evolutionists are now enamored with rather than properly
>>>> describing the basic science and mathematics of mutation and
>>>> selection.
>>> Selection is by definition irrelevant to neutral evolution.
>> And without selection, amplification of mutations does not occur.
>True, if indeed you define amplification as increase in frequency due to
>selection. But surely even you can realize that increases in frequency
>due to pure chance are also possible.
I don’t agree that you define amplification as an increase in
frequency due to selection. I define amplification as an increase in
number of a subpopulation due to that subpopulation’s improved
fitness. You also happen to have amplification of neutral alleles for
those that happen to be on the more fit members. For the theory of
evolution to have mathematical rationality though, subpopulations must
be able to amplify multiple beneficial alleles for multiple selection
conditions acting on multiple genes. The reason why this doesn’t
happen is the multiplication rule for probabilities. Selection
targeting multiple genes simultaneously requires that multiple
beneficial mutations occur simultaneously on individual members. The
multiplication rule of probabilities makes this a very low probability
event. There is absolutely no empirical evidence that this happens.
That is why your theory of evolution is a mathematically irrational
belief system.

>> And
>> without amplification, you have very low probabilities of accumulating
>> mutations.
>True. In the above example, it's 1 in 2 billion. How does that prevent
>some fraction of the billions of mutations in every generation from
>becoming fixed eventually? Doesn't it, in fact, pretty much mandate that
>some of them will?
You do understand that the joint probability of multiple independent
events occurring is governed by the multiplication rule of
probabilities? It is more likely that you don’t understand this.

>> Why evolutionists would think that the mathematics of
>> abiogenesis
>Beg pardon? Abiogenesis?
When you remove selection from the equation, you have the same
mathematics which governs the probabilities of abiogenesis. You know
that fantasy where untold number of random chemical reactions over
billions of years and out pops life from the primordial alphabet soup.
This is where evolutionist mathematical training shows up on
mathematical testing scales just slightly below that of a chimpanzee.
Is that why you think evolutionists and chimpanzees came from a common
precursor because you have mathematical skills very similar to a
chimpanzee?

>> will somehow cause the spread of neutral mutations through
>> a population faster than the mathematics of selection can only be
>> explained by the fact that evolutionists are mathematically
>> incompetent.
>Or perhaps evolutionists can read while you can't. Nobody thinks drift
>is faster than selection. You've been told this dozens of times already,
>and still you repeat the same absurd claim. Any given neutral mutation
>is much, much less likely to be fixed than any given beneficial
>mutation. But there are astronomically more neutral mutations than
>beneficial ones. Can you tell that the number of fixations depends both
>on the individual probability and upon the number of mutations? Do the math.
The problem you have John is that you’ve been reading evolutionist
folklore for so long that you now believe that these fairytales are
true. John, I’ve done the math and you theory of evolution is a
mathematically irrational belief system. Mutation and selection
doesn’t work the way you claim.

Mark Isaak Aug 17, 8:04 am
Newsgroups: talk.origins
From: Mark Isaak <eci...@curioustaxonomyNOSPAM.net>
Date: Wed, 17 Aug 2011 08:04:09 -0700
Local: Wed, Aug 17 2011 8:04 am

Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

>On 8/17/11 7:28 AM, Alan Kleinman MD PhD wrote:
>> On Jul 22, 7:37 pm, Mark Isaak<eci...@curioustaxonomyNOSPAM.net>
>>> [snip, about neutral genetic drift]
>>> First, let me ask you: How many mutations do you have that were not in
>>> either your father or mother? Go ahead, sequence the three genomes and
>>> count the differences. I'll wait.
>> You mean we actually have an evolutionist who wants to do some actual
>> measurements?
>We do. You, I note, do not.
Mark, first you have to recognize what a measurement is and we note
you do not.

>So let me ask again. How many mutations do you have that were not in
>either your father or mother?
It doesn’t matter for correctly describing the mathematics of mutation
and selection.

>>> Second, learn how to read.
>> I d rather do the mathematics, ...
>Too bad you suck at mathematics, too. I suspect your reading disability
>is part of the issue there, too, because it is the word problems where
>you have the real problem.
Mark, you are the one who claims that the more complex the
optimization conditions are the easier it is to do the optimization.
You obviously were trained as a social engineer.

John Harshman Aug 17, 8:03 am
Newsgroups: talk.origins
From: John Harshman <jharsh...@pacbell.net>
Date: Wed, 17 Aug 2011 08:03:52 -0700
Local: Wed, Aug 17 2011 8:03 am

Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

>>> You are completely failing to understand Greg's example. Let's think of
>>> it this way. The mutations that are becoming fixed in this generation
>>> were nearly fixed in the previous generation. Consider this example. We
>>> have alleles A and B for some gene. Allele A was originally fixed in the
>>> population. But a million years ago, allele B arose by mutation. Purely
>>> by chance, the person with allele B had a lot of kids, and passed on
>>> allele B to some of them. The relative frequencies of alleles A and B
>>> changed randomly over time, depending on just what individuals
>>> reproduced to what degree, and the chance of allelic assortment into
>>> gametes. But eventually, again by chance, Allele B found itself in the
>>> majority. Just last generation, again by chance, there were only three
>>> people left with allele A, all of them heterozygotes. Two of these
>>> people had no children, while the third had three kids but passed on
>>> allele B to each of them (a 1/8 probability). So now allele A is extinct
>>> and allele B is fixed. Notice that no big change happened in any
>>> generation, and allele B didn't suddenly appear throughout the
>>> population. Now do you understand?
>> Of course I understand your example.
>Sadly, what follows demonstrates that you understand nothing.
>> Without selection you have
>> millions of members of populations having lots of kids sweeping all
>> their neutral mutations through the entire population without the
>> benefit of selection. This happens dozens of times every generation
>> and it happens over and over again for hundreds of thousands of
>> generations. And it happens far more rapidly for neutral mutations
>> than it does for beneficial mutations despite the fact that beneficial
>> mutations have selection working to increase the size of the
>> population for the more fit members.
>None of the above bears the slightest resemblance to anything Greg or I
>said.
That’s right; you said it happens a couple hundred times per
generation. Did you ever hear of the multiplication rule of
probabilities for computing the joint probabilities of multiple
independent random events? Oh, now I remember, you evolutionists claim
that the multiplication rule of probabilities does not apply to
biological evolution.

>> So now you claim that members
>> with neutral mutations have more descendents than members with
>> beneficial mutations.
>Nor does that.
Well then explain to us all how neutral mutations get fixed in a
population without increasing in number.

>> And now your claim is no longer survival of the
>> fittest, it is survival of the neutralist.
>Nor does that.
Nor does your mathematically and empirically baseless claims make your
theory of evolution mathematically rational.

>> You are doing a lovely job
>> displaying how mathematically irrational your belief system is. Every
>> parent should want their naïve child to grow up to be a mathematically
>> incompetent evolutionist. They will be lucky to have sufficient
>> mathematical skills to balance their checkbook.
>Reading comprehension is also an important skill. Try again. Read the
>examples and attempt to understand them. Selection is much faster than
>neutral evolution. It's just that there are astronomically more neutral
>alleles than beneficial ones. If there are 5 beneficial mutations, each
>one with a 50% chance of becoming fixed, and 1 billion neutral
>mutations, each one with a one-millionth chance of becoming fixed, which
> contributes more to fixation? Do some math for me here.
John, try doing your math computing the joint probabilities with the
multiplication rule of probabilities. Then you might start figuring
out why your theory of evolution is a mathematically irrational belief
system.

John Harshman Aug 17, 8:12 am

Newsgroups: talk.origins
From: John Harshman <jharsh...@pacbell.net>

Date: Wed, 17 Aug 2011 08:12:09 -0700
Local: Wed, Aug 17 2011 8:12 am

Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

>>>> It’s you evolutionists who have bungled the basic science and
>>>> mathematics mutation and selection and have given us multidrug
>>>> resistant microbes, multiherbicide resistant weed, multipesticide
>>>> resistant weeds and less than durable cancer treatments.
>>> When in doubt, fall back on an irrelevant mantra.
>> Now are you going to tell us John that multidrug resistant microbes,

>> multiherbicide resistant weeds, multipesticide resistant insects and

>> less than durable cancer treatments don’t exist?
>No. But I'm also not going to tell you that walnuts don't exist, and
>that has just as much to do with the matter at hand.
John, it does matter because all these situations have come about by
mutation and selection and the failure of evolutionists to properly
describe the basic science and mathematics of this phenomenon.

>> This is the legacy of
>> evolutionism from the failure of evolutionists to properly describe

>> the mutation and selection phenomenon.

>Says the guy who thinks mutation and selection are a single phenomenon.
Says the guy who used to think that the probability of a beneficial
mutation occurring was proportional to population size. John, you were
able to correct your error for that claim. Why are you having such
difficulty understanding the correct probability function for two
mutations occurring? Is it so hard to accept how mutation and
selection actually works? The correct understanding of this phenomenon
gives a way to look for rational solutions for multidrug resistant

microbes, multiherbicide resistant weeds, multipesticide resistant

insects and producing more durable cancer treatments.

>>>> So now you claim that drift is what gives accounts for the 40,000,000
>>>> differences between humans and chimpanzees in less than a million
>>>> generations.
>>> That's what I've always claimed. Are you on drugs?
>> Of course I understand this is what you have claimed and it is you who
>> have lost contact with reality. By definition that is a psychotic
>> state and you should be on drugs.
>So when you said "now" it was a meaningless addition.
John, I’ve presented to you the mathematical and empirical evidence of
how mutation and selection actually works. You can go into denial. You
can stamp your feet. You can say na, na, na. This will not change the
mathematical and empirical reality of how mutation and selection
actually works.

>>>> So just tell us what neutral mutations have drifted up in
>>>> your genome and the genomes of every member of the population of the
>>>> earth in your generation. Some of them must have reached the end of
>>>> the pipeline, ie the evolutionist sewer pipeline.
>>> The only way to know that would be to sequence the genomes of everyone
>>> in this generation and the preceding one. Why do you ask?
>> There are only three ways that a particular mutation can show up in a
>> descendent. The descendent can receive the mutation from its
>> progenitor, the descendent can get the mutation during the replication
>> process of the genome or the descendent can get the mutation by
>> lateral transfer (recombination).
>Even this is highly confused. Germ-line mutations happen during
>gametogenesis, and so are inherited by the individuals who display them.
>The sole, very rare exception would be mutations during the first few
>rounds of the zygote's cell division. Somatic mutations are irrelevant
>here. Recombination happens during meiosis, again during gametogenesis,
>and so is inherited by the individual. Your three cases appear to be
>one. Do doctors even learn anything about human reproduction?
Somatic mutations are totally relevant if you are talking about
cancers. John, do you care to write the probability function for
random recombination?

>> I’ve already derived the probability
>> functions for a particular mutation occurring and for two mutations
>> accumulating in a population.
>....under the assumption that both are neutral. Now consider how many
>neutral mutations happen in the human population in one generation.
>What's the probability that at least one of them will accumulate? What's
>the mean number that will accumulate per generation?
Are you still having difficulty understanding the correct probability
function which I have derived for you giving the probability of two
mutations accumulating on an individual in a population?

>> Now it only remains to write the
>> probability function for random recombination. That’s what I’m asking
>> you to derive, the probability function for random recombination. Then
>> perhaps you will understand how mathematically irrational your
>> arguments are.
>This has nothing to do with the matter at hand, which is neutral
>evolution, about which you understand, apparently, nothing.
What I do understand is that you claim that a couple of hundred
neutral mutations are randomly fixed each generation and that you
totally ignore the multiplication rule of probabilities for computing
the joint probabilities of multiple random independent events. This is
what happens when evolutionists take dumbbell math courses. They end
up claiming that mutation and selection turns reptiles into birds.


John Harshman Aug 17, 8:15 am

Newsgroups: talk.origins
From: John Harshman <jharsh...@pacbell.net>

Date: Wed, 17 Aug 2011 08:15:33 -0700
Local: Wed, Aug 17 2011 8:15 am

Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

>>>>> All mutations start out in a single individual. It is just that every
>>>>> human has 50-200 new mutations that his/her parents don't have. Some
>>>>> fraction of these, over many generations will have drifted to
>>>>> fixation. Fixation of neutral mutations does not occur in only two
>>>>> years. It occurs at a rate of one or two per year. Fixation is the
>>>>> end of a process, not an instantaneous event.
>>>> Now you are correct,
>>> He's always been correct.
>> Hersheyh doesn’t even know that (a^x)^y = a^(x*y).
>Doubtful. I have learned not to believe any naked assertions you make.
Ask hersheyh if he didn’t make this one of many mathematical blunders.
If he won’t admit it, I’ll go back and find his posts where he does
admit it.

>> Hersheyh has spent
>> so much time bungling the mathematics of mutation and selection with
>> the incorrect probability distribution that when he finally sees the
>> correct probability function for two mutations occurring that he is
>> totally confused. And John, we don’t need to go into how confused you
>> have been about how to apply the principles of probability theory. You
>> evolutionists really have some homework to do if you want to have a
>> meaningful discussion on this topic.
>Empty and irrelevant rhetoric, which misses all the prior discussion.
John, if you want to have a meaningful discuss on stochastic processes
such as random mutation and natural selection, random recombination or
neutral evolution, you had better do some homework at learn how
probability theory works. Until then, your arguments will be a mangled
collection of garbage. However, once you do learn how probability
theory works, you will realize that the theory of evolution is a
mathematically irrational belief system.

>> John, this is such a load of mathematically irrational evolutionist
>> crap. So now you are claiming that the frequency of a particular
>> mutation is also the probability that the mutation will be fixed in a
>> population.
>Yes. Elementary random walk math.
>> Let’s apply some principles of probability theory to your
>> mathematically irrational claims. First, tell us whether those neutral
>> mutations are random independent events or not.
>Yes, they are. Go on.
Are you sure you want to go here? Well you said “go on”. Now tell us
whether the fixation of these neutral mutations is random process?

Vincent Maycock Aug 17, 8:36 am
Newsgroups: talk.origins
From: "Vincent Maycock" <vam...@aol.com>
Date: Wed, 17 Aug 2011 11:36:30 -0400
Local: Wed, Aug 17 2011 8:36 am

Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

>> Perhaps the greatest impetus for the theory of evolution was the
>> evolution of drug resistant microbes. Now that it is clear that this
>> evolutionary process is stifled if combination therapy is used, where
>> are your empirical examples that show that the theory of evolution is
>> mathematically rational? Let’s see if your fertile but mathematically
>> irrational mind can come up with selection conditions that behave
>> otherwise, and please don’t forget to give us the measured
>> experimental examples of your mathematically irrational claims. I
>> might as well find a comfortable chair because we are going to have a
>> long wait for that example.
>Pseudogenes disprove creationism.
Vincent, I’m not advocating any other theory. I’m here to give you the
correct basic science and mathematics of the mutation and selection
phenomenon and show that the theory of evolution is a mathematically
irrational belief system.


Inez Aug 17, 9:57 am
Newsgroups: talk.origins
From: Inez <savagemouse...@hotmail.com>
Date: Wed, 17 Aug 2011 09:57:56 -0700 (PDT)
Local: Wed, Aug 17 2011 9:57 am

Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

>> > They don't show up all at once. Most people have had them in their
>> > family tree for a long time. It's just that dozens get fixed every
>> > generation. Your argument from incredulity is ignorant and boring.
>> > If you don't think that neutral mutations can spread through a
>> > population, why don't you show why not?
>> Of course these neutral mutations don’t show up all at once, sweeping
>> through the population like a tsunami. They also don’t show up dozens
>> per generation, generation after generation for hundreds of thousands
>> of generations. This is part of the evolutionist mathematically
>> irrational speculations. My arguments are made from hard mathematical
>> and empirical evidence. If you didn’t have your mathematically
>> irrational speculations and gross over-extrapolations, you
>> evolutionists would have no argument at all for your mathematically
>> irrational belief system.
>A lot of fist shaking, but not a real argument. Why couldn't a
>neutral mutation spread through the population by chance?
Inez, it’s very difficult to use a key board and mouse with a shaking
fist. All I’m doing is a little finger tapping. So you want to know if
a neutral mutation could spread through a population by chance? Your
own evolutionist computations show that there is a very small chance
that this will happen equal to the frequency of that allele. And that
model only applies when you only have two neutral alleles for a single
gene. Now what’s the probability of two neutral mutations being fixed
by chance? Shouldn’t that joint probability of that event be governed
by the multiplication rule of probabilities?

>> Now I have shown you mathematically why neutral mutations do not
>> spread through populations rapidly if at all.
>No one claims they spread rapidly.
They better if you want to do the accounting to explain the 40,000,000
differences between human and chimpanzee genomes in 500,000
generations.

>> The probability function
>> I derived for you of two mutations accumulating is not only applicable
>> for the accumulations of beneficial mutations; it is also applicable
>> for computing the probability of neutral or detrimental mutations
>> accumulating in a population. Of course neutral and detrimental
>> mutations do not amplify because they don’t give increased fitness to
>> reproduce for those members with those mutations. Because of this,
>> there is a very low probability that neutral or detrimental mutations
>> will accumulate in a population.
>Yes...and if there are a whole lot of neutral mutations, a few will
>beat the odds.
You need far, far, far more than a few to beat the odds to do the
accounting for the 40,000,000 differences between human and chimpanzee
genomes in 500,000 generations.
>> > > This is the kind of irrational
>> > > nonsense that evolutionists are now enamored with rather than properly
>> > > describing the basic science and mathematics of mutation and
>> > > selection.
>> > Selection is by definition irrelevant to neutral evolution.
>> And without selection, amplification of mutations does not occur.
>> And without amplification, you have very low probabilities of accumulating
>> mutations.
>Right...and if there are a ton of neutral mutations, a few will make
>it.
The multiplication rule of probabilities for computing the joint
probability of random independent events shows that your claim is
mathematically irrational. You evolutionists have clearly missed the
probability part of the probability and statistics course.

>> Why evolutionists would think that the mathematics of
>> abiogenesis will somehow cause the spread of neutral mutations through
>> a population faster than the mathematics of selection can only be
>> explained by the fact that evolutionists are mathematically
>> incompetent.
>This is a odd strawman that you have made up and insist on repeating
>for no apparent reason. Who said that neutral mutations spread more
>quickly than beneficial ones? Can you provide a link?
The only thing that separates the mathematics of abiogenesis from the
mathematics of mutation and selection is replication and selection. Do
you really need a link for that?

Greg Guarino Aug 17, 12:21 pm

Newsgroups: talk.origins
From: Greg Guarino <gdguar...@gmail.com>

Date: Wed, 17 Aug 2011 15:21:16 -0400
Local: Wed, Aug 17 2011 12:21 pm

Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

On 8/17/2011 10:21 AM, Alan Kleinman MD PhD wrote:
>> On Jul 22, 1:32 pm, "g...@risky-biz.com"<gdguar...@gmail.com> wrote:
>>> Same old, same old.
>>> Despite repeated attempts to get you to engage on certain topics, you
>>> simply refuse to address:
>>> -How many of the genetic changes between humans and chimps have any
>>> function at all. (certainly a small fraction of 40 million)
>> Greater than 70% of genes in humans and chimpanzees produce different
>> proteins.
>A non-answer. Let's read the question again. "How many of the genetic
>changes between humans and chimps have any function at all? (certainly a
>small fraction of 40 million)"
Greg, from a mathematical point of view it doesn’t matter whether the
changes have function or not. They are changes which have spread
through the populations. And in order to spread through the population
they had to be either selective changes or neutral changes. And we
already have numerous evolutionists saying that neutral changes spread
through a population more slowly than selective changes (which still
take hundreds of generations per change. So you are asking the wrong
question in an attempt to understand how evolution works and why
humans and chimpanzees could not have come from a common progenitor in
only 500,000 generations. It is mathematically irrational to make such
a claim.

>It certainly seems that any *mathematical* argument against evolution
>would require the number of *functional* changes that are necessary.
>Let's start with how many differences there are in your 70% of proteins.
>Then maybe you can estimate for us how many of those make functional
>differences.
It does not require the distinction you are trying to make. Changes
whether functional or non-functional will take time to spread through
any population and the non-functional changes will take much more time
than the functionally beneficial changes to spread through a
population.

>> So are you now going to argue that all these different
>> proteins perform the same functions?
>Now you'll have to address the biologists here, but they do indeed seem
>to be saying that many of the changes in the proteins make little
>functional difference.
And this argument ignores the fact that any genetic mutation (neutral
or beneficial) that spreads through a population will take time and
the time for a neutral change to spread through a population will be
much greater than for a beneficial change which takes hundreds of
generations per beneficial mutation. This type of argument that
evolutionists are making demonstrates that evolutionists do not
understand that any genetic transformation of a population is a very
time consuming process, much too time consuming for the theory of
evolution to be mathematically rational.
>> There are no differences at all?
>Upon reading something like this, some people are content to conclude
>that the person who wrote it is either dishonest or an idiot. In your
>case I think it is that you have such a desperate need to see your
>opponents as irrational that you are too frightened to try to actually
>comprehend their arguments. One of the manifestations of that is your
>inability to distinguish any gradations between "none" and "all".
Stop being an ignoramus Greg. If you are going to snip my responses do
it in an honest manner. My original quote was “Greater than 70% of
genes in humans and chimpanzees produce different proteins. So are you
now going to argue that all these different proteins perform the same
functions? There are no differences at all?” And understand that
whether a change has beneficial function or is neutral, either change
requires time to spread through a population.

>Humans and chimps are not identical. Their genomes are not identical.
>Some of the differences in the genome are without doubt quite important.
>I am asking you how many you think fall into that category.
And I’m telling you that you are asking the wrong mathematical
question. Any change whether beneficial or neutral takes time to
spread through a population. If the change is neutral, it takes much
greater time than if the change is beneficial it will take less time
to fix in the population but it will still be hundreds of generations
per fixation.

>>> -Why the changes must be stepwise. (they don't, if each mutation
>>> confers it's own advantage)
>> Beneficial mutations must accumulate in populations somehow, if it is
>> not stepwise, how does it occur and give us empirical examples of your
>> claims. All the real, measurable and repeatable examples of mutation
>> and selection show that the mutations must be accumulated stepwise and
>> if the selection conditions interfere with the population’s ability to
>> accumulate these mutations stepwise, the mutation and selection
>> process is stifled.
>Here I will again remind you that the above is not a mathematical
>argument. You are now asserting that such examples are not *observed*.
>Let's please dispense with your original argument first.
Good scientific analysis (which evolutionists don’t do) requires the
use of both mathematical and empirical studies. That’s how scientific
advancements are made. When I worked on the space shuttle, we had our
mathematical models to describe the physical phenomenon but we also
had numerous sensors on the shuttle measuring the physical data and
this data was correlated with the mathematical models. If the
mathematical predictions didn’t fit the measured data, the models were
studied to try to figure out why the anomaly existed.

So I’ve presented you with the mathematical model of the probability
function for two mutations occurring and it becomes quite apparent
that the change in subpopulation size with the first mutation is the
driving factor whether there will be a reasonable probability for the
next mutation to occur at the proper locus. I’ve presented to you two
measured empirical models of mutation and selection which demonstrate
that fact (the Lenski and Weinreich models). Now if you want to
understand why the mutation and selection process must occur stepwise
by a beneficial mutation/amplification of beneficial mutation cycle it
is because of the multiplication rule of probabilities. It is actually
an easy matter to write the probability function for two sets of
mutation and selection processes to occur simultaneously for mutations
A and B for one process and mutations C and D for the second process
and to write the joint probability function for all four mutations to
occur. Why don’t you try to derive that equation and see why the
subpopulation for mutation A must amplify simultaneously with
subpopulation for mutation C before mutations B and D have reasonable
probabilities of occurring and try to find an empirical example where
this happens. Then try to give us a logical reason why these empirical
examples don’t exist.

>>> -Why the changes must be "efficient", when stepwise progress is not
>>> required. (if each confers an advantage and the population is not
>>> greatly diminished, they may "amplify" in parallel)
>> The mutation and selection process is not efficient unless the
>> mutations can be accumulated stepwise. If you force the population to
>> get its beneficial mutations simultaneously, the multiplication rule
>> of probabilities shows that this is an extremely low probability
>> event. This is why combination therapy works.
>The only person "forcing" them to be simultaneous is you, by your
>insistence that multiple antibiotics represent a good model for all
>selection.
Lenski didn’t use antibiotics for his selection condition, he used
starvation and all of his populations demonstrate stepwise changes.
This is a consequence of common descent. And his empirical model still
exhibited the same mathematical behavior as antimicrobial selection
pressure. You have yet to learn of the mathematical consequences of
selection pressures.

>>> -Why many generations of "recovery" are needed when the population is
>>> not greatly diminished, or diminished at all. (It isn't)
>> Selection by its very nature kills or impairs the reproduction of some
>> or all of the members of a population.
>Impairs? A mathematical argument would tell us "how much" they are
>impaired.
Selection pressures and intensity of selection are empirically
determined variables. The values of these variables are dependent on
the populations which are subjected to the selection pressures. When
you are talking about cause and effect phenomenon, you can write a
mathematical relationship for this cause and effect phenomenon but
there will always be some experimentally determined proportionality
component to this relationship. That “how much” is dependent on the
selection conditions, the population be subjected to the selection
conditions and the intensity of the selection conditions. These
principles are ABCs for those trained in the hard mathematical
sciences but are clearly neglected in the mushy indoctrination of
evolutionists.

>> Weak selection conditions only
>> slow the mutation and selection process. And reducing the intensity of
>> selection is the way you increase the diversity of populations but
>> this does not improve the genetic transformation properties of
>> selection. Genetic transformation requires amplification of members
>> with the beneficial mutation to improve the probability that the next
>> beneficial mutation will occur on a member with the previous
>> beneficial mutation.
>And you fail yet again to tell us why the second mutation has to occur
>in a member with the first, assuming most of the population survives and
>they reproduce sexually.
The mutation and selection process is all about the accumulation of
beneficial mutations on the members of the population which give
resistance to the selection pressures the population is subjected to.
If one member gets a mutation beneficial for one selection pressure
and another member get a beneficial mutation for a different selection
condition, these members will still be suppressed from reproducing
because of the other selection conditions. If this were not the case,
combination therapy would never work. No member of the population will
be an efficient replicator until it has adapted to all the selection
it is subjected to. And replication is how beneficial mutations are
amplified to overcome the multiplication rule of probabilities. Now
you again bring up recombination. How can random recombination
recombine two beneficial alleles with a reasonable probability? To
answer that question requires that you write the probability function
for that stochastic process. So far, no one on this forum has derived
this calculation.

>> Low intensity selection conditions do not
>> accelerate the amplification process.
>So? Think about that for a second.
>Shall we visit the Toyota factory again?
>It probably takes them months to make a car from stem to stern,
>including casting and machining the engine, shaping the individual parts
>etc. If they were to devote the entire resources of the company to
>producing one car in the shortest possible time, it might only take a
>day. Quicker? Sure. But they'd only produce a few hundred a year. By
>having thousands in the pipeline at different levels of completion, they
>take longer to complete each, but manage to produce 1500 a day.
>Low intensity selection would indeed slow the spread of a beneficial
>mutation (partly by allowing so much of the non-mutant population to
>survive and reproduce). But many slower processes that occur in parallel
>can be more "efficient" in the aggregate.
Greg, last I heard, automobiles are not replicators. They may be
replications but they do not replicate each other. Of course it would
be cute to see a Toyota Corolla grow up to be a Tundra and the Tundra
marries a Prius and they have a family of Camrys. What would the
selection pressures this population would be subject to? Well rust
certainly shortens the life of the members of this population so we
have these Toyotas evolving undercoating. And crashes clearly are a
selection pressure for these populations so they evolve ABS and
airbags. Isn’t mutation and selection marvelous?

>>> -Why your cherished multiplication rule applies in cases in which each
>>> mutation confers it's own advantage and the selection is less
>>> intense.
>> Its not my cherished multiplication rule, it is a theorem of
>> probability theory which governs the joint probabilities of
>> independent random events which random mutations are.
>Show us how it works for less intense selection in a
>sexually-reproducing population in which each mutation confers an
>advantage.
I’ve already given you the derivation of the probability function for
two beneficial mutations to occur and it should be clear to you of the
importance of the amplification of the first mutation in order to give
a reasonable probability for the second mutation to occur. Now when
you factor in random recombination, you have a slightly different
probability problem and a different probability function to describe
the behavior of this stochastic process. Why don’t you try to derive
that equation? The multiplication rule shows up in that derivation as
well.

>Do you really doubt that this happens, by the way? How do you imagine
>that the various (physical) ethnic differences between human beings came
>about?
A flat fitness landscape will allow for many variants but it is
directional selection pressures which transform populations. And
directional selection pressures don’t give a flat fitness landscape.

>>Selection has
>> the property of altering the probabilities of these events by
>> amplifying the previous beneficial event.
>>> -Neutral evolution. (so far you have not even bothered to understand
>>> your opponents' claims here)
>> How do you understand an irrational and incoherent argument?
>You start be restating it as best you can, and asking the other party if
>you have done so fairly. You may note that I have done that with several
>of your arguments. Failing that, you can ask for details first and then
>give it a try.
I have. You are starting with a model of a single gene with two
neutral alleles and computing the probability of one or the other
allele being fixed in the population. Evolutionists then make the
irrational extrapolation of this model to the fixation of a couple
hundred neutral alleles being fixed every generation. This is why the
arguments of evolutionists are irrational and incoherent.

>> I’ve
>> given you a mathematical explanation of the probabilities of two
>> mutations occurring.
>You don't seem to have addressed the probability of mutations
>*occurring* at all. That would seem to be an empirical question.
Don’t be silly.

>>That’s a mathematically rational and coherent
>> argument. And that argument fits the empirical data. If you want to
>> believe that neutral mutations spread through a population more
>> quickly than beneficial mutations
>You are testing my resolve again.
No Greg, I’m testing your mathematical and scientific skills.

>Right here, right now, drop everything and find me a single person on
>this group or anywhere in the biological profession that would make that
>assertion. There aren't any. What, other than your utter addiction to
>the idea that everyone else is an idiot, could cause you to repeat this
>over and over?
I have no idea what John Harshman’s background is but he has claimed
that a couple hundred neutral mutations fix every generation. That’s
how he is trying to account for his claim of 40,000,000 differences
between human and chimpanzee genomes in 500,000 generations. You are
stuck with this type of mathematical irrationality if you are going to
try to defend the theory of evolution.

>To understand someone else's argument, the very least you have to to is
>read it.
I’ve been reading evolutionist folklore for decades. You can’t avoid
it if you want to go to medical school. What is clear is that
evolutionists have bungled the basic science and mathematics of the
mutation and selection phenomenon. This blunder could not be ignored
when HIV came along. This virus’ ability to mutate and select and
lethality was so rapid that nothing other than combination therapy
could control this virus and the basic science and mathematics of the
mutation and selection phenomenon had to be properly understood and
applied. Other microbes demonstrate the same behavior but on a longer
time scale because of their longer generation times so the use
combination therapy is ignored. So Greg, stop this crap that I don’t
try to understand evolutionist arguments. I do understand evolutionist
arguments and they are mathematically irrational and have harmed
millions of people suffering from diseases subject to the mutation and
selection phenomenon.

>> despite the fact that beneficial
>> mutations have selection assisting the spread of the mutation, that’s
>> your right. However I find that to be mathematically irrational and
>> incoherent without any mathematical or empirical basis,
>And that should be your first clue that perhaps that is not what anyone
>thinks.
Then if that’s not what you think, you have opened the door in your
thinking to understanding why the theory of evolution is
mathematically irrational.

>Greg Guarino

hersheyh Aug 17, 12:19 pm

Newsgroups: talk.origins
From: hersheyh <hershe...@yahoo.com>

Date: Wed, 17 Aug 2011 12:19:37 -0700 (PDT)
Local: Wed, Aug 17 2011 12:19 pm

Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

>> > > Do this calculation: Consider 3 possible alleles which can be randomly
>> > > recombined, alleles A, B, and C where C is any non-A or non-B allele
>> > > member.
>> > I will do you better, by actually *correctly* using the terms 'allele'
>> > and 'gene' (yet another fail on your part). Let us take a population
>> > that contains two unlinked *genes*, one affecting the layering of body
>> > fat under the skin rather than inside the abdomen, the F gene, and the
>> > other affecting hair density, the H gene. Each gene has two alleles
>> > that have a co-dominant effects on phenotype. For the F gene, these
>> > are the F (w.t.) allele that deposits fat abdominally and the F'
>> > allele (mutant) that deposits the fat under the skin where it can act
>> > as insulation. Heterozygotes have an intermediate phenotype. For the
>> > H gene, the alleles are H (w.t.) that has low hair density and
>> > H' (mutant) that has high hair density providing more warmth in the
>> > winter. The heterozygote has an intermediate phenotype. [I choose
>> > that because most evolution actually does not deal with single genes
>> > and single mutants, but involves pre-existing variation in
>> > quantitative traits. Using single genes with co-dominance most
>> > accurately reflects this while still talking about single genes.] Our
>> > diploid organism used to live primarily in the deep South, but lately
>> > has been migrating to the north, where there is modestly strong
>> > selective pressure during the winter which kills a substantial
>> > fraction of the population each year. Migration of largely w.t. (that
>> > is F/F;H/H) individuals each year during the spring helps to replenish
>> > the Northern population, keeping breeding population level constant.
>> > Obviously, individuals that are F'/F';H'/H' would survive the winter
>> > kill-off better than the w.t. individuals can (the more of these
>> > mutants and the fewer total organisms that die during the winter
>> > results in subsequent less in-migration from the South) and thus can
>> > outcompete the w.t. in the Northern environment, as can any organism
>> > with either mutant allele. Let's assume that F' and H' are very
>> > slightly deleterious or neutral in the warmer environment, but is
>> > strongly adaptive in the cold environment.
>> > Let's say that individuals with H' or F' mutant either appears de novo
>> > among the Northern population or migrates into that area at least once
>> > every 10 generations. *When* that happens, we will have, in the
>> > Northern environment individuals that are heterozygous for *either*
>> > (but let's assume not both) F/F' or H/H' with the w.t. alleles at the
>> > other gene locus. I will let you tell me the size of the Northern
>> > population (reasonable numbers like 10,000 to 100,000 during the
>> > summer would be nice), and the fraction that are killed each winter.
>> > In either the case of the F/F';H/H individual or the F/F;H/H'
>> > individual, the frequency of the mutant allele will increase in the
>> > Northern population simultaneously at the expense of their respective
>> > w.t. alleles. When there is a sufficiently high % of F/F';H/H
>> > individuals we will start to get F'/F';H/H individuals.
>> > Simultaneously, there will be an increase in F/F;H/H' individuals and,
>> > eventually, some F/F;H'/H' individuals. The homozygotes for the
>> > mutant alleles are favored over the respective w.t. alleles. Let's
>> > say that the selective advantage of the mutants are the same for both
>> > genes (this can vary). Thus we need to look at individual relative
>> > fitnesses, W, for all the possible combinations *before* we consider
>> > the recombination that occurs via sex each generation are: W(F'/F';H/
>> > H) = W(F/F;H'/H') > W(F/F';H/H) = W(F/F;H/H') > W(F/F;H/H). When
>> > fitnesses are equal there is no selection relative to the two types of
>> > individuals and, in general, no rapid increase or decrease relative to
>> > the other in the environment. Obviously, fitness relationships can
>> > deviate from the one I describe here, but you haven't specified a
>> > different one.
>> > Now, we do know how to calculate (approximately) the probability of
>> > generating individuals with different genotypes in a population if we
>> > assume random mating. And that is dependent solely on the frequency
>> > of the alleles for a gene in that population. It is described by the
>> > Hardy-Weinberg equation. That is, if the frequency of F in the
>> > population is p and the frequency of F' is q, then *regardless of what
>> > the case is for the alleles at any other unlinked gene locus*, there
>> > will be p^2 F/F, pq F/F', and q^2 F'/F' individuals in the next
>> > generation. And if the frequency of H in the population is x and the
>> > frequency of H' is y, then there will be x^2 H/H, xy H/H', and y^2 H'/
>> > H' in the next generation. It is then simple algebra to note that,
>> > because the genes are unlinked, that the probability of F/F;H/H is
>> > p^2*x^2, the probability of F/F;H/H' is p^2*xy; F/F;H/H' is p^2*y^2,
>> > etc. The important point is that the probability of F/F';H/
>> > H' (heterozygous at both loci) is pq*xy; F'/F';H/H' is q^2*xy; F/F';H'/
>> > H' is pq*y^2; and F'/F';H'/H' is q^2*y^2. All of these are
>> > individuals that have at least one mutant allele at each gene locus.
>> > How high the actual probability in any given generation would be would
>> > be determined, then, by the frequency of the alleles in the
>> > population.
>> Blah, blah, blah. Why don’t you just admit you don’t know how to
>> derive the probability function for the recombination of two
>> beneficial alleles?
>Why don't you just admit that you do not even understand the difference between the term "allele" and the term "gene" >or "gene locus". Alleles are different forms (sequences) of a gene at a specific gene locus. Recombination typically >occurs between *genes*, not alleles of the same gene. Intragenic (intra means 'within') recombination can produce new >variants when one is dealing with more than two alternative alleles, but that is much rarer than recombination between >genetically unlinked genes. Even in bacteria, but with a vengence in eucaryotes.
What I will admit to you is that you are a mathematically incompetent
ignoranus who doesn’t know how to derive the correct probability
function for the mutation and selection phenomenon and does not know
how to derive the probability function for random recombination.

> You didn’t and still don’t understand the correct
> probability function for the accumulation of two beneficial mutations.
I have correctly calculated the probability function for the
accumulation of two mutant phenotypes, both when one selects for both
in one step and also when one selects for them serially. All you have
presented is the first and *asserted* that it applied in all cases. I
have asked you repeatedly where my calculation of probability in the
three-step serial process was wrong, where you would insert your joint
probability. You have repeatedly ignored it and again simply asserted
that it must be present.
Hell you have. You have used the Poisson distribution for a stochastic
process where the random mutation is not a Poisson random variable. Go
find a lower division mathematics text which has the derivation of the
Poisson distribution and find out why you are wrong. If you can’t find
the text, I’ll give you the name of a text with the derivation that
was used at the high school I attended that has the derivation of the
Poisson probability function.

>> And now you are showing that you don’t understand how to derive the
>> probability function for the recombination of two beneficial alleles.
>I have stated again that you do not know the difference between the words "allele" and "gene". To me that is a clear "tell" >that the person speaking doesn't know much about genetics. That recombination between unlinked *genes* is high, but >(with rare exception) recombination within a gene (that is, between the difference between two mutant alleles of a w.t. >gene -- recombination between a mutant allele and the w.t. allele produces no detectable change unless you have gene >conversion) is rare. Why don't you get a clue by looking up the words "allele" and "gene".
> http://www.google.com/url?sa=D&q=http://en.wikipedia.org/wiki/Homologous_recombination
> http://www.google.com/url?sa=D&q=http://encyclopedia2.thefreedictionary.com/intragenic%2Brecombination
>Intragenic recombination was the reason why Seymour Benzer, from some ag school up the road, got his Nobel prize, >for work done in the 1950s, more than a half-century ago, yet you apparently know nothing about it.
> http://www.google.com/url?sa=D&q=http://www.plantsciences.ucdavis.edu/ggg291/ppt08/Nuradilla- >Intragenic%2520Recom.pdf
>Hint: they use the words muton and cistron, so you might need to look those up.
> http://www.google.com/url?sa=D&q=http://www.pnas.org/content/102/15/5380.full.pdf%2Bhtml
> http://www.google.com/url?sa=D&q=http://en.wikipedia.org/wiki/Gene_conversion
Hersheyh, you are a mathematically incompetent nitwit who has no idea
how the mathematics of mutation and selection phenomenon works and has
even less of an understanding how the mathematics of recombination
works. You attempt to cover your ignorance with a plethora of blah,
blah, blah but it’s clear that you don’t understand how either
phenomenon works mathematically. Why don’t you be honest with John
Harshman and tell him that you didn’t know that (a^x)^y = a^(x*y)?

hersheyh Aug 17, 12:42 pm
Newsgroups: talk.origins
From: hersheyh <hershe...@yahoo.com>
Date: Wed, 17 Aug 2011 12:42:58 -0700 (PDT)
Local: Wed, Aug 17 2011 12:42 pm

Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

On Wednesday, August 17, 2011 10:28:23 AM UTC-4, Alan Kleinman MD PhD
wrote:
> On Jul 22, 7:37 pm, Mark Isaak <eci...@curioustaxonomyNOSPAM.net>
> wrote:
>[snip]
>> > Second, learn how to read.
>> I’d rather do the mathematics, wading through evolutionist
>> speculations is not the way to learn how mutation and selection
>> actually works. Doing the mathematics is the way to learn how mutation
>> and selection works. Of course, evolutionists like you don’t know how
>> to do the mathematics.
>So rather than actually try to *learn* what scientists say, Dr. Dr. Kleinman prefers to reiterate his bogus numerology >without reading or trying to understand why it is limited to special cases again, and again, and again, and again..... >Mindless repetition like that is primarily found in autistics and obsessive compulsives.
I’ve been reading mathematically irrational evolution crap for
decades; you can’t avoid it when you go to medical school. If you
don’t want to learn how mutation and selection actually works, read
and study evolutionist folklore. Based on this mathematically
incompetent evolutionist folklore you can learn how to produce

multidrug resistant microbes, multiherbicide resistant weeds,

multipesticide resistant insects and produce less than durable cancer
treatments. That’s the reward for the studies of mathematically
irrational evolutionist folklore.

>[snip]
Let’s snip mathematically irrational evolutionist folklore out of
school science curriculums and actually train naïve school children in
the correct basic science and mathematics of the mutation and
selection phenomenon. Put the theory of evolution into a fictional
writing course where it belongs.

Mark Isaak More options Aug 17, 1:32 pm

Newsgroups: talk.origins
From: Mark Isaak <eci...@curioustaxonomyNOSPAM.net>

Date: Wed, 17 Aug 2011 13:32:46 -0700
Local: Wed, Aug 17 2011 1:32 pm

Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

>On 8/17/11 7:05 AM, Alan Kleinman MD PhD wrote:
>> On Jul 22, 12:51 pm, Inez<savagemouse...@hotmail.com> wrote:
>>> On Jul 22, 12:35 pm, Alan Kleinman MD PhD<klein...@sti.net> wrote:
>>> [...]
>>>> This is the kind of irrational
>>>> nonsense that evolutionists are now enamored with rather than properly
>>>> describing the basic science and mathematics of mutation and
>>>> selection.
>>> Selection is by definition irrelevant to neutral evolution.
>> And without selection, amplification of mutations does not occur.
>Yes it does. Not always, but often enough. You can see for yourself by
>programming a simulation of a small population with mutations and no
>selection, and then watching it run a bunch of times.
Really now Mark, you’ve done that simulation? Why don’t you tell us
which simulation you used? Because I have done the same simulation
with a peer reviewed and published model of mutation and selection.
And when you turn off selection in that model, the genetic sequences
revert to random sequences.

hersheyh Aug 17, 2:15 pm

Newsgroups: talk.origins
From: hersheyh <hershe...@yahoo.com>

Date: Wed, 17 Aug 2011 14:15:26 -0700 (PDT)
Local: Wed, Aug 17 2011 2:15 pm

Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

>> > Again, all your examples are of human designed challenges in which a
>> > double mutation is required for survival. Everyone here has been
>> > telling you that this is not typical of natural selection. Apparently
>> > your skull is made of Bozonium and this idea cannot penetrate.
>> I understand that most indoctrinated evolutionist dogmatists like you
>> have no mathematical training or experience to derive a probability
>> function or analyze stochastic problems like the mutation and
>> selection or random recombination processes. Let’s see if from your
>> fertile but mathematically irrational mind you can describe “natural”
>> selection conditions that behave differently from the “human designed
>> challenges” and give us measured examples of these so called “natural”
>> selection conditions. Let’s see what your skull is made of.
>> Perhaps the greatest impetus for the theory of evolution was the
>> evolution of drug resistant microbes.
>When Darwin proposed the basic idea of evolution via natural selection, the germ theory of disease was not yet in >existence [Pasteur's discovery that microbes can cause infection was in 1865. Lister's discovery that disinfectants could >reduce infection was in 1867. Koch's discovery that *specific* microbes caused specific diseases was 1867. And it >wasn't until 1890 that Halsted showed the benefit of using gloves during surgery.] Much less the idea of evolution of >drug-resistant microbes. There were only folk antibiotics until the 1880s (Paul Erlich). The first commercially available >antibacterial antibiotic was Prontosil (in 1932).
When I was in elementary school and first introduced to the theory of
evolution, the evolution of drug resistance was the empirical example
given to us. DNA had been discovered and the physical sequence of
events was starting to be elucidated how mutation and selection
actually works. My fifth grade science teacher had the wisdom to
introduce us to Edward Tatum’s 1958 Nobel Laureate speech and his
explanation of why combination therapy works. I’ve never saw Tatum’s
findings again in any evolutionist folklore course because it shows
why the theory of evolution is mathematically irrational.

>The impetus for the theory of evolution had to do with the patterns of species in nature. In addition to the incompetence >of dividing mutation rate by 4, thus demonstrating that you do not understand the numbers you manipulate, you also >have a poor grasp of history.
You are the mathematically incompetent evolutionist who can’t derive
the probability function for a stochastic process. You don’t know how
to do it for the mutation and selection process which is the reason
you use the Poisson distribution for your calculations (where the
random mutation is not a Poisson random variable) and you don’t know
how to derive the probability function for random recombination. Do
you think your ignorance of the field of mathematics qualifies you to
make your mathematically irrational judgments?

>> Now that it is clear that this
>> evolutionary process is stifled if combination therapy is used, where
>> are your empirical examples that show that the theory of evolution is
>> mathematically rational? Let’s see if your fertile but mathematically
>> irrational mind can come up with selection conditions that behave
>> otherwise, and please don’t forget to give us the measured
>> experimental examples of your mathematically irrational claims. I
>> might as well find a comfortable chair because we are going to have a
>> long wait for that example.
>> > > The mathematics of random
>> > > recombination shows why this is so. Why don’t you try doing the
>> > > following computation: Consider 3 possible alleles which can be
>> > > randomly recombined, alleles A, B, and C where C is any non-A or non-B
>> > > allele member. The alleles can recombine two at a time. If alleles A
>> > > and B recombine, that descendent has improved fitness, however if
>> > > alleles A and A or A and C or B and B or B and C and C and C recombine
>> > > those members have no improved fitness to reproduce.
>> > Instead, why don't you try this one? A and B both confer reproductive
>> > benefits, but those members of the population who don't have them
>> > aren't instantly slain, they just don't have as many babies. Do the
>> > math on that.
>> I have already done the calculation and it is perfectly applicable to
>> the evolution of HIV which does recombination and isn’t instantly
>> slain. Let’s see if you can do the calculation. But of course you
>> don’t have the mathematical training to do such a calculation because
>> you are an evolutionist.
>And any mathematician who, as you do, creates and uses terms without understanding them, is engaged in numerology, >not useful math. For example, you repeatedly confuse *frequency* with *number* and seem to think that evolution only >can occur concomitant with a population crash.
Hersheyh, you are full of crap and you know it. You understand that
you need large populations in order to have sufficient trials for a
particular mutation to have a reasonable probability of occurring at a
particular locus but then you go out of your way to ignore that once a
population is on a trajectory of a fitness landscape that the
subpopulation size diminishes to tiny numbers unless the subpopulation
can amplify that beneficial mutation. Even if the total population
doesn’t crash, the subpopulation size becomes very small for those
members on a particular trajectory on the fitness landscape unless
amplification can occur on each and every step of the trajectory. And
stop being a stupid jerk. Just because you don’t know how to derive a
probability function for the mutation and selection phenomenon and the
random recombination phenomenon does not mean that I don’t know the
difference between frequency and number or gene and allele. You are
acting like an ignoranus when you level these accusations.

>That is not true. Take the following tables:
>Assumption: Selection is lethal to allele A. Mutant allele A' survives the selection. The frequency of A and A' when a >population with 10^9 A individuals and 10 A' individuals are exposed to the selective conditions. Generation 0 is the >generation before selection. Generation 1 is the first exposed to the new selective conditions.
>Generation: 0 1 2 3 30 200
>Number of A': 10 10 20 40 10^9 10^9
>Frequency of A': 10^-8 100% 100% 100% ~100% ~100%
>Number of A: 10^9 0 0 0 10 10
>Frequency of A: ~100% 0% 0% 0% 10^-8 10^-8
>Note that the change in frequency is immediate and more or less permanent, changing only by new back mutation.
Why do you waste our time with this? You know that I have said many
times that frequency of an allele is not the important number when
computing the probability of a particular mutation occurring at a
particular locus, it is the absolute number of members which is used
in computing the number of trials. If you understood the correct
probability function that I derived for you for the mutation and
selection phenomenon, you would recognize this mathematical fact but
you don’t understand the mathematics.
>Assumption: Selection favors A' so that the frequency increases about 20% per generation and the frequency of A >decreases concomitantly. IOW, population size remains constant.
>Generation: 0 1 2 3 30 200
>Number of A': 10 10 12 15 5X10^3 10^9
>Frequency of A': 10^-8 10^-8 1.2X10^-8 1.5 X 10^-8 5X10^-5 ~100%
>Number of A: 10^9 10^9 10^9 ~10^9 ~10^9 10 (mutation freq.)
>Frequency of A: ~100% ~100% ~100% ~100% 10^-8 10^-8
What a surprise, you reduce the intensity of selection and it takes
about seven times more generations to amplify your beneficial allele.
So even your hypothetical substantiates what I have said to you from
the very beginning. And recognize that the A members are on a
different trajectory of the fitness landscape from the A’ members. The
presence of the A members with the A’ members in the population do not
help the A’ members mathematically for getting the next beneficial
mutation in the sequence. The A members are competitors for the
resources in the environment with the A’ members.

>Assumption: Population size doubles because of a mutation allowing use of previously unavailable resource. Selection >favors A' so that its frequency increases by doubling so as to use the new resource. Initially the number of non-mutants >remains unchanged. Then the new mutant starts displacing the non-mutants.
>Generation: 0 1 2 3 30 200
>Number of A': 10 20 40 80 ~10^9 2X10^9
>Frequency of A': 10^-8 2X10^-8 4X10^-8 8X10^-8 50% ~100%
>Number of A: 10^9 10^9 10^9 ~10^9 ~10^9 20 (mutation freq.)
>Frequency of A: ~100% ~100% ~100% ~100% 50% 10^-8
>There are other possibilities.
None of which show that the theory of evolution is anything other than
a mathematically irrational belief system, all you have shown here is
that when selection is intense, if the remaining population can
survive and reproduce it still take large number of generations to
amplify a single beneficial allele. Hersheyh, I do like it when your
hypothetical examples substantiate the probability function I derived
for you. Occasionally your hypothetical examples correlate with
reality.

This is the end of responses to post number 876 through 900. Again I
apologize that I don’t respond to the post individually but this would
give dozens of more splinter threads. Once I finish responding to
posts 901 though 1000 and any of the splinter posts, I will again
respond individually to posts.

[Alan Kleinman MD PhD]

The following replies are from a splinter threads
Virgil Sep 14, 1:35 pm
Newsgroups: talk.origins
From: Virgil <vir...@ligriv.com>
Date: Wed, 14 Sep 2011 14:35:43 -0600
Local: Wed, Sep 14 2011 1:35 pm

Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

In article
<7f7ca969-1404-4f7e-9147-bc7b95ada...@x11g2000prb.googlegroups.com>,

Alan Kleinman MD PhD <klein...@sti.net> wrote:

>> On Aug 10, 7:42 pm, Mark Isaak <eci...@curioustaxonomyNOSPAM.net>
>> wrote:

>> > On 8/10/11 2:21 PM, Alan Kleinman MD PhD wrote:
>> > > On Jul 14, 8:58 am, Mark Isaak<eci...@earthlink.net> wrote:
>> > >> On Tue, 12 Jul 2011 18:18:51 -0700, Alan Kleinman MD PhD wrote:
>> > >>> On Jun 7, 2:45 pm, Mark Isaak<eci...@earthlink.net> wrote:

>> > >>>> On Mon, 06 Jun 2011 17:47:21 -0700, Alan Kleinman MD PhD wrote:
>> Why would I want to accept the mathematically irrational arguments of
>> evolutionists about how their folklore tells them mutation and
>> selection works? I m interested in an accurate engineering
>> mathematical analysis of how this phenomenon works and the empirical
>> evidence which supports this analysis, not the mathematically
>> irrational evolutionist claims. These principles are too important to
>> my patients to be left to the mathematically irrational speculations
>> and extrapolations of evolutionists.

>Evolutionists are quite as rational about how Evolution works as anyone
>else.
>Probably a good deal more so!
>So whom do you trust to be MORE rational about Evolution than those who
>have dedicated themselves to figuring out just how nature does it?
Welcome to the discussion Virgil. What makes you think that I am not
dedicated to figuring out how mutation and selection works? I have to
deal with the consequences of this phenomenon on a daily basis in my
medical practice and it is of great importance that I understand how
this phenomenon works especially since I am advocating a non-standard
of care treatment for infections. In fact I directly oppose the
recommendation to primary care physicians to reduce the usage of
antibiotics to prevent the evolution of resistant strains. I advocate
the usage of combination therapy to suppress the appearance of
resistant microbes. You see Virgil, I put my professional licenses and
career on the line when I make these arguments. Evolutionists on the

other hand walk away without paying a price for their failure to
properly describe the basic science and mathematics of the mutation
and selection phenomenon.

John Harshman Sep 14, 11:39 am

Newsgroups: talk.origins
From: John Harshman <jharsh...@pacbell.net>

Date: Wed, 14 Sep 2011 11:39:30 -0700
Local: Wed, Sep 14 2011 11:39 am

Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

>> On Aug 11, 7:22 am, John Harshman <jharsh...@pacbell.net> wrote:
>>> Alan Kleinman MD PhD wrote:

>>>> On Jul 19, 9:20 am, John Harshman <jharsh...@pacbell.net> wrote:
>>>>> Alan Kleinman MD PhD wrote:

>>>>>> On Jun 8, 1:49 pm, John Harshman <jharsh...@pacbell.net> wrote:
>>>>>>> William Hughes wrote:
>>>>>>>> On Jun 8, 12:35 pm, Alan Kleinman MD PhD <klein...@sti.net> wrote:
>>>>>>>>> On Jun 1, 8:39 am, William Hughes <wpihug...@gmail.com> wrote:

>>>>>>>>>> On Jun 1, 11:52 am, Alan Kleinman MD PhD <klein...@sti.net> wrote:
>>> Depends on the frequencies of the alleles, doesn't it? If they "amplify"
>>> individually, the probability is eventually going to be 1.
>> Are you sure about that?

>Yes.
Are you sure that both alleles have to have a frequency of 1?

>> Have you derived the probability function
>> which would describe this stochastic process? For example do A and B
>> both have to amplify?

>No, but we have already assumed that they both amplify independently.
>Remember?
I haven’t made that assumption, you have. The correct probability
function for random recombination does not require that you consider
selection. The affects of selection on random recombination only
affects the probabilities implicitly by altering the number of members
with each of the particular alleles.

>> What happens to the probabilities of the random
>> recombination of A and B if only one of the two all alleles amplify?

>Not relevant.
John, you shouldn’t be making this argument until you derive the
probability function for random recombination. I’m not going to give
the derivation of that probability function now but consider this.
What if in your population every member has allele A except the member
which has allele B, that is A has a frequency close to 1 in the
population? That member with allele B that is B has a frequency very

close to 0. What is the chance that a member with allele A will meet
and recombine with the member with allele B?

>> I�ll give you a hint; don�t use the Poisson distribution to do this
>> computation.

>It's really quite simple. Given various simple assumptions, such as
>independent assortment, panmixis, a constant population, and frequencies
>p and q for the two alleles, the expected frequency of AB individuals is
>just pq. As p and q increase, pq increases. We have already specified
>that p and q are increasing. If AB phenotypes are favored over A, B, and
>"wild type" phenotypes, p and q will increase faster than they would in
>the absence of that advantage.
John, the only thing that the Hardy-Weinberg law gives you is that the
frequency of alleles remains constant when the population is in
equilibrium (selection is not acting). If you want to estimate the
probability of two alleles randomly recombining, you need to write the
probability function for that stochastic process. Once you do that,
you can consider how selection will change the probabilities over
generations as the frequencies and population sizes of the alleles
change.

>>>>>> That is unless you think that mutations for one or
>>>>>> another drug are not occurring in the HIV population when subjected to
>>>>>> combination therapy.
>>>>> As usual, you misunderstand the necessary conditions.
>>>> I�ve already derived the probability function for the two alleles to
>>>> randomly recombine.
>>> No you haven't. You haven't taken into account that they are
>>> individually advantageous.

>> Oh really, I haven�t take that into account? Obviously your

>> evolutionist telepathy is leading you astray once again. We should
>> really call your thinking evolutionist telepathetic.

>I missed the part where you did that, then. Could you repeat your math?
Since I haven’t posted the derivation of the probability function for
random recombination yet, I can’t repeat the math. I’m trying to get
you to think about this phenomenon first.

>>> See? You don't know what "beneficial" means. Under the conditions you
>>> propose, neither allele is beneficial.
>> More evolutionist telepathetic. Let me repeat a previous hint for you
>> to show you how to derive the correct probability function for two
>> alleles to randomly recombine. This random process obeys the same
>> mathematical principles as random card drawing. With that hint and
>> google, you should be able to solve this probabilities problem by this
>> evening.

>I'm not reading your mind. I'm reading your words. Admittedly, your
>words are only loosely connected to your mind, and that connection is
>perhaps looser than for a rational person. But the words themselves are
>fairly clear.
When you derive the correct probability function for random
recombination, “beneficial” doesn’t come into play in a particular
generation. Only when you extend the probability function for random
recombination over generations does beneficial come into play and that
only implicitly. The way selection enters into the mathematics of
random recombination over generations is manifest by changes in the
frequency of alleles and population size changes over the generations.

>> I can understand you wanting to change the subject to anything other
>> than how mutation and selection works and why recombination does not
>> rescue your mathematically irrational belief system. Learn to stay on

>> topic. And now that I�ve all but given you the equations to describe
>> random recombination, let�s see if you can derive that probability
>> function.

>Would you agree that if the frequencies of A and B are both 1, then the
>probability of recombination is also 1?
What would happen to the probabilities of random recombination of A
and B if either A or B had a frequency of 1?

John Harshman Sep 14, 2:24 pm

Newsgroups: talk.origins
From: John Harshman <jharsh...@pacbell.net>

Date: Wed, 14 Sep 2011 14:24:24 -0700
Local: Wed, Sep 14 2011 2:24 pm

Subject: Re: Trying to salvage something from this Re: The Theory of
Evolution

> On Aug 11, 7:16 am, John Harshman <jharsh...@pacbell.net> wrote:
>> Alan Kleinman MD PhD wrote:
>>>> On Jul 13, 1:56 pm, John Harshman <jharsh...@pacbell.net> wrote:
>>>>> g...@risky-biz.com wrote:
>> It has everything to do with what we are discussing. There are huge
>> stretches of the two genomes which can not be matched up for homology.

>True. Do you know how they got there? Most of them are retrotransposons,
>yet another class of neutral mutations.
John, chromosome 21 has large stretches if non-random sequences which
are not on the chimpanzee genome. So where are these stretches of
bases on the chimpanzee genome? You are going to paint yourself in a
corner with these types of arguments because human genomes and
chimpanzee genomes must remain homologous to themselves for
consistently successful reproduction. Transposons may occur commonly
in immunologic cells but in germ cell line this phenomenon would
disrupt homology.

>> This data is presented for those areas which can be matched and the
>> match is not close at all.

>It isn't? 98.7% identity isn't close? What would constitute close, then?
When you are talking about mutation and selection, you are not close
at all. Mutation and selection working under ideal conditions may be
able to substitute 10-20,000 bases in 500,000 generations. Using your
numbers, you have to account for 20,000,000 bases in each of the human
and chimpanzee populations. And remember, you don’t have a population
size of 10^9 until about the last century. Human population size never
really grew rapidly until the advent of mechanized farming about
5-10,000 years ago. Chimpanzee mechanized farming is limited to a
chimp putting a stick down a hole to harvest ants. What do you think
the maximum size of the chimpanzee population has ever been?

>> Evolutionists claim that humans and
>> chimpanzees come from a common progenitor. Now you are claiming that
>> many of these differences are neutral which is typical evolutionist
>> speculation.

>Simple observation of how proteins work.
More like simple minded observation. I suppose if you look out toward
the horizon and say, “sure looks flat to me”, that’s enough to
convince you that the earth is flat. I suggest you take a look at
Google Earth.

>> Tell us which are neutral differences and which are
>> selective differences.

>Well, it seldom matters whether a protein has leucine, isoleucine, or
>phenylalanine in a particular spot.
Well then you have some explaining to do. How do all these neutral
variants get fixed in a population because greater than 70% of
proteins differ between humans and chimpanzees and you only have
500,000 generations to explain the differences?

>> And then compute the joint probability of two
>> neutral mutations being fixed in a population.

>Are you still on about that? Your joint probability is irrelevant. We
>don't care about the joint probability of some particular set of
>mutations being fixed, only about the probability that any set of
>mutations will be fixed. Different, no?
Now John, when you make a claim like that you are proving that you
accept as true a mathematical irrational belief system. Whenever you
are considering a stochastic process, the joint probability of events
is governed by the product of the individual probabilities. The
multiplication rule of probabilities is the monkey wrench in the works
of your irrational belief system. You will never have a good
understanding how this phenomenon work without a good understanding of
probability theory.

>>>>>> How many with other known functions? How much "junk"?
>>>>> Almost all is junk, just as almost all the genome is junk. Non-coding,
>>>>> functional regions are just another few percent of the genome.
>>>> This is the type of stupidity that evolutionist perpetuate. If they
>>>> don’t know what a portion of the genome does, it is junk.
>>> No, that's not how it works. We recognize junk by the fact that it
>>> evolves at the rate of mutation.

>> Take a look at this URL: >http://www.google.com/url?sa=D&q=http://www.sciencemag.org/content/295/5552/131.abstract&usg=AFQjCNF6LJDM3>GHffyRjXPABtkVjwnfm9w

>> In this URL, they studied chromosome 21. They report “We detected
>> candidate positions, including two clusters on human chromosome 21
>> that suggest large, nonrandom regions of difference between the two
>> genomes.” Nonrandom means these are selective differences

>No it doesn't.
Or really John? So how do we get non-random sequences of bases without
selection? How did these bases become arranged without selection?

>> and we all
>> should know by now that selective differences take hundreds of

>> generations per base substitution. But you claim that neutral

>> mutations fix at the rate of a couple of hundred per generation,
>> thousands of times faster than selection can fix a beneficial
>> mutation.

>Once again you confuse numbers with rates.
I don’t think so John. I think you’ve made contradictory claim. On one
hand you are claiming that neutral evolution is slower than selective
evolution and then on the other hand you claim that a couple hundred
neutral mutations are fixed every generation. I think you are the one
how is more than a little bit confused.

>>>> If they
>>>> don’t understand how to do a mathematical computation it is junk.
>>>> John, just because you are ignorant what a non-coding region of a
>>>> genome does, don’t impose your ignorance on us by claiming this is
>>>> junk. If a region of DNA has no coding function for proteins but
>>>> remains non-random, it does so because it has stabilizing selection
>>>> acting on those sequences.

>>> True. Which has nothing to do with what I'm talking about. Stabilizing
>>> selection makes loci evolve at less than the neutral rate. Such loci are
>>> only a few percent of the genome. By the way, evolution isn't so fast as
>>> to randomize sequences in 5 million years.
>> Just what are you talking about? I guess you missed the study I posted
>> above about the large non-random differences on chromosome 21 between
>> humans and chimpanzees.

>So? How is that relevant? Do you have access to the whole article? I don't.
Yes I do have the whole article. I was able to subscribe to Science
Magazine online without charge. Go to their web page and ask for an
account. And the reason why this is relevant is that there are more
differences between the human and chimpanzee genomes than your simple
minded analysis accounts for.

>> 70% of genes code for different proteins,

>....if by "different" you mean having at least one different amino acid.
Do you have a different definition for the word “different” because if
so you need to tell us how our definitions for the word “different”
are different. And then perhaps we can work out our differences unless
you want to differ on our differences.

>> large stretches of non-random differences between human and chimpanzee
>> genomes yet neutral evolution will fix all these differences a rate of
>> a couple of hundred per generation, thousands of times faster than a
>> single beneficial mutation can be fixed in a population. What you are
>> talking about is mathematical irrationality.
>I've become convinced that you know almost nothing about mathematics
>beyond the scraps rote learning you have displayed here.

Now what have you against rote learning? If it wasn’t for rote
learning, evolutionists would have no way of indoctrinating naïve

school children. You certainly don’t have any mathematical logic to

support your mathematically irrational belief system.

>>> You mistake evolution at the rate of mutation for stabilizing selection,
>>> presumably because you have a false understanding of the mutation rate.
>>> Neutral evolution produces only a bit more than 1% difference over 5
>>> million years, not a randomization of sequences.

>> You will only get randomization of sequences if there is no selection
>> acting on that sequence. Your mathematics is faulty because 5 million
>> years only represents about 500,000 generations and you can not fix
>> 40,000,000 differences in two divergent populations in such a short
>> period of time. It is mathematical irrationality to believe this.
>You seem to have stopped even pretending to have an argument and are
>just repeating your mantra regardless of what you are supposedly
>responding to.

You are the one closing your eyes to the argument. You have said there
are 40,000,000 differences between human and chimpanzee genomes and by
your numbers the two species diverged 5,000,000 years ago. How do you
account for those differences in such a small number of generations
(other than your mathematically irrational claim that a couple of

hundred neutral mutations fix every generation). Do you want some more
generations from the pre-split split period?

>> We all know about evolutionist expectations, they are mathematically
>> irrational. But if you want to show your work and compute the joint
>> probability of two neutral mutations being fixed in a population, that
>> would be some interesting evolutionist folklore to hear.
>Mantra. At least your mantra does evolve over time, though it seems to
>be randomly so.

My new mantra for you is “multiplication rule of probabilities, theory
of evolution irrational”. This mantra is to be sung to the theme from
the Beatles song, Shake it up baby, twist and shout.

>> Repeat after me, reptiles transform into birds, reptiles transform
>> into birds, reptiles transform into birds…
>That is indeed what the data show. Care to discuss it?

When I decide to take a course in fictional writing that will be our
first topic.

The following are responses from posts 876-900 round 2

John Harshman 17, 7:58 am
>> Of course these neutral mutations don’t show up all at once, sweeping
>> through the population like a tsunami. They also don’t show up dozens
>> per generation, generation after generation for hundreds of thousands
>> of generations. This is part of the evolutionist mathematically
>> irrational speculations. My arguments are made from hard mathematical
>> and empirical evidence. If you didn’t have your mathematically
>> irrational speculations and gross over-extrapolations, you

>> evolutionists would have no argument at all for your mathematically
>> irrational belief system.

>So far, just a content-free rant.
That’s how an evolutionist responds to mathematical and empirical
evidence. Is it any wonder that we have multidrug resistant microbes,
multiherbicide resistant weed, multipesticide resistant insects and
less than durable cancer treatments. It is the failure of
evolutionists to properly explain the mutation and selection
phenomenon that has caused these problems.

>> Now I have shown you mathematically why neutral mutations do not
>> spread through populations rapidly if at all.
>Nobody claims that neutral mutations spread rapidly.
You have, you have claimed that a couple hundred of them are fixed
every generation. Can you make the theory of evolution any more
mathematically irrational? I expect so.

>> The probability function

>>>> describing the basic science and mathematics of mutation and
>>>> selection.

Mark Isaak Aug 17, 8:04 am
Newsgroups: talk.origins
From: Mark Isaak <eci...@curioustaxonomyNOSPAM.net>

Date: Wed, 17 Aug 2011 08:04:09 -0700

Local: Wed, Aug 17 2011 8:04 am

Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

>On 8/17/11 7:28 AM, Alan Kleinman MD PhD wrote:
>> On Jul 22, 7:37 pm, Mark Isaak<eci...@curioustaxonomyNOSPAM.net>
>>> [snip, about neutral genetic drift]
>>> First, let me ask you: How many mutations do you have that were not in
>>> either your father or mother? Go ahead, sequence the three genomes and
>>> count the differences. I'll wait.
>> You mean we actually have an evolutionist who wants to do some actual
>> measurements?
>We do. You, I note, do not.
Mark, first you have to recognize what a measurement is and we note
you do not.

>So let me ask again. How many mutations do you have that were not in
>either your father or mother?
It doesn’t matter for correctly describing the mathematics of mutation
and selection.

>>> Second, learn how to read.
>> I d rather do the mathematics, ...
>Too bad you suck at mathematics, too. I suspect your reading disability
>is part of the issue there, too, because it is the word problems where
>you have the real problem.
Mark, you are the one who claims that the more complex the
optimization conditions are the easier it is to do the optimization.
You obviously were trained as a social engineer.

John Harshman Aug 17, 8:03 am
Newsgroups: talk.origins
From: John Harshman <jharsh...@pacbell.net>

Date: Wed, 17 Aug 2011 08:03:52 -0700

Local: Wed, Aug 17 2011 8:03 am

Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

that the multiplication rule of probabilities does not apply to
biological evolution.

John Harshman Aug 17, 8:12 am

Newsgroups: talk.origins
From: John Harshman <jharsh...@pacbell.net>

Date: Wed, 17 Aug 2011 08:12:09 -0700
Local: Wed, Aug 17 2011 8:12 am

Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

>>>> It’s you evolutionists who have bungled the basic science and
>>>> mathematics mutation and selection and have given us multidrug
>>>> resistant microbes, multiherbicide resistant weed, multipesticide
>>>> resistant weeds and less than durable cancer treatments.
>>> When in doubt, fall back on an irrelevant mantra.

>> Now are you going to tell us John that multidrug resistant microbes,

>> multiherbicide resistant weeds, multipesticide resistant insects and

>> less than durable cancer treatments don’t exist?
>No. But I'm also not going to tell you that walnuts don't exist, and
>that has just as much to do with the matter at hand.
John, it does matter because all these situations have come about by
mutation and selection and the failure of evolutionists to properly
describe the basic science and mathematics of this phenomenon.

>> This is the legacy of

>> evolutionism from the failure of evolutionists to properly describe

>> the mutation and selection phenomenon.

>Says the guy who thinks mutation and selection are a single phenomenon.
Says the guy who used to think that the probability of a beneficial
mutation occurring was proportional to population size. John, you were
able to correct your error for that claim. Why are you having such
difficulty understanding the correct probability function for two
mutations occurring? Is it so hard to accept how mutation and
selection actually works? The correct understanding of this phenomenon

gives a way to look for rational solutions for multidrug resistant

microbes, multiherbicide resistant weeds, multipesticide resistant

insects and producing more durable cancer treatments.

>>>> So now you claim that drift is what gives accounts for the 40,000,000

>>>> differences between humans and chimpanzees in less than a million
>>>> generations.

John Harshman Aug 17, 8:15 am

Newsgroups: talk.origins
From: John Harshman <jharsh...@pacbell.net>

Date: Wed, 17 Aug 2011 08:15:33 -0700
Local: Wed, Aug 17 2011 8:15 am

Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

>> mutation is also the probability that the mutation will be fixed in a
>> population.

>Yes. Elementary random walk math.
>> Let’s apply some principles of probability theory to your
>> mathematically irrational claims. First, tell us whether those neutral
>> mutations are random independent events or not.
>Yes, they are. Go on.
Are you sure you want to go here? Well you said “go on”. Now tell us
whether the fixation of these neutral mutations is random process?

Vincent Maycock Aug 17, 8:36 am
Newsgroups: talk.origins
From: "Vincent Maycock" <vam...@aol.com>
Date: Wed, 17 Aug 2011 11:36:30 -0400
Local: Wed, Aug 17 2011 8:36 am

Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

>> Perhaps the greatest impetus for the theory of evolution was the
>> evolution of drug resistant microbes. Now that it is clear that this
>> evolutionary process is stifled if combination therapy is used, where
>> are your empirical examples that show that the theory of evolution is
>> mathematically rational? Let’s see if your fertile but mathematically
>> irrational mind can come up with selection conditions that behave
>> otherwise, and please don’t forget to give us the measured
>> experimental examples of your mathematically irrational claims. I
>> might as well find a comfortable chair because we are going to have a
>> long wait for that example.
>Pseudogenes disprove creationism.
Vincent, I’m not advocating any other theory. I’m here to give you the
correct basic science and mathematics of the mutation and selection
phenomenon and show that the theory of evolution is a mathematically
irrational belief system.


Inez Aug 17, 9:57 am
Newsgroups: talk.origins
From: Inez <savagemouse...@hotmail.com>
Date: Wed, 17 Aug 2011 09:57:56 -0700 (PDT)
Local: Wed, Aug 17 2011 9:57 am

Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

>> > They don't show up all at once. Most people have had them in their
>> > family tree for a long time. It's just that dozens get fixed every
>> > generation. Your argument from incredulity is ignorant and boring.
>> > If you don't think that neutral mutations can spread through a
>> > population, why don't you show why not?
>> Of course these neutral mutations don’t show up all at once, sweeping
>> through the population like a tsunami. They also don’t show up dozens

>> per generation, generation after generation for hundreds of thousands
>> of generations. This is part of the evolutionist mathematically
>> irrational speculations. My arguments are made from hard mathematical
>> and empirical evidence. If you didn’t have your mathematically
>> irrational speculations and gross over-extrapolations, you

>> evolutionists would have no argument at all for your mathematically
>> irrational belief system.

>A lot of fist shaking, but not a real argument. Why couldn't a
>neutral mutation spread through the population by chance?
Inez, it’s very difficult to use a key board and mouse with a shaking
fist. All I’m doing is a little finger tapping. So you want to know if
a neutral mutation could spread through a population by chance? Your
own evolutionist computations show that there is a very small chance
that this will happen equal to the frequency of that allele. And that
model only applies when you only have two neutral alleles for a single
gene. Now what’s the probability of two neutral mutations being fixed
by chance? Shouldn’t that joint probability of that event be governed
by the multiplication rule of probabilities?

>> Now I have shown you mathematically why neutral mutations do not
>> spread through populations rapidly if at all.
>No one claims they spread rapidly.

They better if you want to do the accounting to explain the 40,000,000
differences between human and chimpanzee genomes in 500,000
generations.

>> The probability function

>> I derived for you of two mutations accumulating is not only applicable
>> for the accumulations of beneficial mutations; it is also applicable
>> for computing the probability of neutral or detrimental mutations
>> accumulating in a population. Of course neutral and detrimental
>> mutations do not amplify because they don’t give increased fitness to
>> reproduce for those members with those mutations. Because of this,
>> there is a very low probability that neutral or detrimental mutations
>> will accumulate in a population.
>Yes...and if there are a whole lot of neutral mutations, a few will
>beat the odds.

You need far, far, far more than a few to beat the odds to do the
accounting for the 40,000,000 differences between human and chimpanzee
genomes in 500,000 generations.

>> > > This is the kind of irrational
>> > > nonsense that evolutionists are now enamored with rather than properly

>> > > describing the basic science and mathematics of mutation and
>> > > selection.

>> > Selection is by definition irrelevant to neutral evolution.
>> And without selection, amplification of mutations does not occur.
>> And without amplification, you have very low probabilities of accumulating
>> mutations.
>Right...and if there are a ton of neutral mutations, a few will make
>it.
The multiplication rule of probabilities for computing the joint
probability of random independent events shows that your claim is
mathematically irrational. You evolutionists have clearly missed the
probability part of the probability and statistics course.

>> Why evolutionists would think that the mathematics of
>> abiogenesis will somehow cause the spread of neutral mutations through
>> a population faster than the mathematics of selection can only be
>> explained by the fact that evolutionists are mathematically
>> incompetent.
>This is a odd strawman that you have made up and insist on repeating
>for no apparent reason. Who said that neutral mutations spread more
>quickly than beneficial ones? Can you provide a link?
The only thing that separates the mathematics of abiogenesis from the
mathematics of mutation and selection is replication and selection. Do
you really need a link for that?

Greg Guarino Aug 17, 12:21 pm

Newsgroups: talk.origins
From: Greg Guarino <gdguar...@gmail.com>

Date: Wed, 17 Aug 2011 15:21:16 -0400
Local: Wed, Aug 17 2011 12:21 pm

Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

>> I’ve

arguments and they are mathematically irrational and have harmed
millions of people suffering from diseases subject to the mutation and
selection phenomenon.

>> despite the fact that beneficial
>> mutations have selection assisting the spread of the mutation, that’s
>> your right. However I find that to be mathematically irrational and
>> incoherent without any mathematical or empirical basis,
>And that should be your first clue that perhaps that is not what anyone
>thinks.
Then if that’s not what you think, you have opened the door in your
thinking to understanding why the theory of evolution is
mathematically irrational.

>Greg Guarino

hersheyh Aug 17, 12:19 pm

Newsgroups: talk.origins
From: hersheyh <hershe...@yahoo.com>

Date: Wed, 17 Aug 2011 12:19:37 -0700 (PDT)
Local: Wed, Aug 17 2011 12:19 pm

Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

hersheyh Aug 17, 12:42 pm
Newsgroups: talk.origins

From: hersheyh <hershe...@yahoo.com>
Date: Wed, 17 Aug 2011 12:42:58 -0700 (PDT)
Local: Wed, Aug 17 2011 12:42 pm

Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

On Wednesday, August 17, 2011 10:28:23 AM UTC-4, Alan Kleinman MD PhD
wrote:

> On Jul 22, 7:37 pm, Mark Isaak <eci...@curioustaxonomyNOSPAM.net>
> wrote:
>[snip]
>> > Second, learn how to read.
>> I’d rather do the mathematics, wading through evolutionist
>> speculations is not the way to learn how mutation and selection
>> actually works. Doing the mathematics is the way to learn how mutation
>> and selection works. Of course, evolutionists like you don’t know how
>> to do the mathematics.
>So rather than actually try to *learn* what scientists say, Dr. Dr. Kleinman prefers to reiterate his bogus numerology >without reading or trying to understand why it is limited to special cases again, and again, and again, and again..... >Mindless repetition like that is primarily found in autistics and obsessive compulsives.
I’ve been reading mathematically irrational evolution crap for
decades; you can’t avoid it when you go to medical school. If you
don’t want to learn how mutation and selection actually works, read
and study evolutionist folklore. Based on this mathematically
incompetent evolutionist folklore you can learn how to produce

multidrug resistant microbes, multiherbicide resistant weeds,

multipesticide resistant insects and produce less than durable cancer
treatments. That’s the reward for the studies of mathematically
irrational evolutionist folklore.

>[snip]
Let’s snip mathematically irrational evolutionist folklore out of
school science curriculums and actually train naïve school children in
the correct basic science and mathematics of the mutation and
selection phenomenon. Put the theory of evolution into a fictional
writing course where it belongs.

Mark Isaak More options Aug 17, 1:32 pm

Newsgroups: talk.origins
From: Mark Isaak <eci...@curioustaxonomyNOSPAM.net>

Date: Wed, 17 Aug 2011 13:32:46 -0700
Local: Wed, Aug 17 2011 1:32 pm

Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

>On 8/17/11 7:05 AM, Alan Kleinman MD PhD wrote:
>> On Jul 22, 12:51 pm, Inez<savagemouse...@hotmail.com> wrote:

>>> On Jul 22, 12:35 pm, Alan Kleinman MD PhD<klein...@sti.net> wrote:
>>> [...]

>>>> This is the kind of irrational
>>>> nonsense that evolutionists are now enamored with rather than properly

>>>> describing the basic science and mathematics of mutation and
>>>> selection.

>>> Selection is by definition irrelevant to neutral evolution.
>> And without selection, amplification of mutations does not occur.
>Yes it does. Not always, but often enough. You can see for yourself by
>programming a simulation of a small population with mutations and no
>selection, and then watching it run a bunch of times.
Really now Mark, you’ve done that simulation? Why don’t you tell us
which simulation you used? Because I have done the same simulation
with a peer reviewed and published model of mutation and selection.
And when you turn off selection in that model, the genetic sequences
revert to random sequences.

hersheyh Aug 17, 2:15 pm

Newsgroups: talk.origins
From: hersheyh <hershe...@yahoo.com>

Date: Wed, 17 Aug 2011 14:15:26 -0700 (PDT)
Local: Wed, Aug 17 2011 2:15 pm

Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

>> are your empirical examples that show that the theory of evolution is
>> mathematically rational? Let’s see if your fertile but mathematically
>> irrational mind can come up with selection conditions that behave
>> otherwise, and please don’t forget to give us the measured
>> experimental examples of your mathematically irrational claims. I

[Alan Kleinman MD PhD]

The following replies are from a splinter threads
Virgil Sep 14, 1:35 pm
Newsgroups: talk.origins
From: Virgil <vir...@ligriv.com>
Date: Wed, 14 Sep 2011 14:35:43 -0600
Local: Wed, Sep 14 2011 1:35 pm

Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

In article
<7f7ca969-1404-4f7e-9147-bc7b95ada...@x11g2000prb.googlegroups.com>,

Alan Kleinman MD PhD <klein...@sti.net> wrote:

>> On Aug 10, 7:42 pm, Mark Isaak <eci...@curioustaxonomyNOSPAM.net>
>> wrote:

>> > On 8/10/11 2:21 PM, Alan Kleinman MD PhD wrote:
>> > > On Jul 14, 8:58 am, Mark Isaak<eci...@earthlink.net> wrote:
>> > >> On Tue, 12 Jul 2011 18:18:51 -0700, Alan Kleinman MD PhD wrote:
>> > >>> On Jun 7, 2:45 pm, Mark Isaak<eci...@earthlink.net> wrote:

>> > >>>> On Mon, 06 Jun 2011 17:47:21 -0700, Alan Kleinman MD PhD wrote:
>> Why would I want to accept the mathematically irrational arguments of
>> evolutionists about how their folklore tells them mutation and
>> selection works? I m interested in an accurate engineering
>> mathematical analysis of how this phenomenon works and the empirical
>> evidence which supports this analysis, not the mathematically
>> irrational evolutionist claims. These principles are too important to
>> my patients to be left to the mathematically irrational speculations
>> and extrapolations of evolutionists.

>Evolutionists are quite as rational about how Evolution works as anyone
>else.
>Probably a good deal more so!
>So whom do you trust to be MORE rational about Evolution than those who
>have dedicated themselves to figuring out just how nature does it?
Welcome to the discussion Virgil. What makes you think that I am not
dedicated to figuring out how mutation and selection works? I have to
deal with the consequences of this phenomenon on a daily basis in my
medical practice and it is of great importance that I understand how
this phenomenon works especially since I am advocating a non-standard
of care treatment for infections. In fact I directly oppose the
recommendation to primary care physicians to reduce the usage of
antibiotics to prevent the evolution of resistant strains. I advocate
the usage of combination therapy to suppress the appearance of
resistant microbes. You see Virgil, I put my professional licenses and
career on the line when I make these arguments. Evolutionists on the

other hand walk away without paying a price for their failure to
properly describe the basic science and mathematics of the mutation
and selection phenomenon.

John Harshman Sep 14, 11:39 am

Newsgroups: talk.origins
From: John Harshman <jharsh...@pacbell.net>

Date: Wed, 14 Sep 2011 11:39:30 -0700
Local: Wed, Sep 14 2011 11:39 am

Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

>> On Aug 11, 7:22 am, John Harshman <jharsh...@pacbell.net> wrote:
>>> Alan Kleinman MD PhD wrote:

>>>> On Jul 19, 9:20 am, John Harshman <jharsh...@pacbell.net> wrote:
>>>>> Alan Kleinman MD PhD wrote:

>>>>>> On Jun 8, 1:49 pm, John Harshman <jharsh...@pacbell.net> wrote:
>>>>>>> William Hughes wrote:
>>>>>>>> On Jun 8, 12:35 pm, Alan Kleinman MD PhD <klein...@sti.net> wrote:
>>>>>>>>> On Jun 1, 8:39 am, William Hughes <wpihug...@gmail.com> wrote:

>>>>>>>>>> On Jun 1, 11:52 am, Alan Kleinman MD PhD <klein...@sti.net> wrote:
>>> Depends on the frequencies of the alleles, doesn't it? If they "amplify"
>>> individually, the probability is eventually going to be 1.
>> Are you sure about that?

>Yes.
Are you sure that both alleles have to have a frequency of 1?

>> Have you derived the probability function
>> which would describe this stochastic process? For example do A and B
>> both have to amplify?

>No, but we have already assumed that they both amplify independently.
>Remember?
I haven’t made that assumption, you have. The correct probability
function for random recombination does not require that you consider
selection. The affects of selection on random recombination only
affects the probabilities implicitly by altering the number of members
with each of the particular alleles.

>> What happens to the probabilities of the random
>> recombination of A and B if only one of the two all alleles amplify?

>Not relevant.
John, you shouldn’t be making this argument until you derive the
probability function for random recombination. I’m not going to give
the derivation of that probability function now but consider this.
What if in your population every member has allele A except the member
which has allele B, that is A has a frequency close to 1 in the
population? That member with allele B that is B has a frequency very

close to 0. What is the chance that a member with allele A will meet
and recombine with the member with allele B?

>> I�ll give you a hint; don�t use the Poisson distribution to do this
>> computation.

>It's really quite simple. Given various simple assumptions, such as
>independent assortment, panmixis, a constant population, and frequencies
>p and q for the two alleles, the expected frequency of AB individuals is
>just pq. As p and q increase, pq increases. We have already specified
>that p and q are increasing. If AB phenotypes are favored over A, B, and
>"wild type" phenotypes, p and q will increase faster than they would in
>the absence of that advantage.
John, the only thing that the Hardy-Weinberg law gives you is that the
frequency of alleles remains constant when the population is in
equilibrium (selection is not acting). If you want to estimate the
probability of two alleles randomly recombining, you need to write the
probability function for that stochastic process. Once you do that,
you can consider how selection will change the probabilities over
generations as the frequencies and population sizes of the alleles
change.

>>>>>> That is unless you think that mutations for one or
>>>>>> another drug are not occurring in the HIV population when subjected to
>>>>>> combination therapy.
>>>>> As usual, you misunderstand the necessary conditions.
>>>> I�ve already derived the probability function for the two alleles to
>>>> randomly recombine.
>>> No you haven't. You haven't taken into account that they are
>>> individually advantageous.

>> Oh really, I haven�t take that into account? Obviously your

>> evolutionist telepathy is leading you astray once again. We should
>> really call your thinking evolutionist telepathetic.

>I missed the part where you did that, then. Could you repeat your math?
Since I haven’t posted the derivation of the probability function for
random recombination yet, I can’t repeat the math. I’m trying to get
you to think about this phenomenon first.

>>> See? You don't know what "beneficial" means. Under the conditions you
>>> propose, neither allele is beneficial.
>> More evolutionist telepathetic. Let me repeat a previous hint for you
>> to show you how to derive the correct probability function for two
>> alleles to randomly recombine. This random process obeys the same
>> mathematical principles as random card drawing. With that hint and
>> google, you should be able to solve this probabilities problem by this
>> evening.

>I'm not reading your mind. I'm reading your words. Admittedly, your
>words are only loosely connected to your mind, and that connection is
>perhaps looser than for a rational person. But the words themselves are
>fairly clear.
When you derive the correct probability function for random
recombination, “beneficial” doesn’t come into play in a particular
generation. Only when you extend the probability function for random
recombination over generations does beneficial come into play and that
only implicitly. The way selection enters into the mathematics of
random recombination over generations is manifest by changes in the
frequency of alleles and population size changes over the generations.

>> I can understand you wanting to change the subject to anything other
>> than how mutation and selection works and why recombination does not
>> rescue your mathematically irrational belief system. Learn to stay on

>> topic. And now that I�ve all but given you the equations to describe
>> random recombination, let�s see if you can derive that probability
>> function.

>Would you agree that if the frequencies of A and B are both 1, then the
>probability of recombination is also 1?
What would happen to the probabilities of random recombination of A
and B if either A or B had a frequency of 1?

John Harshman Sep 14, 2:24 pm

Newsgroups: talk.origins
From: John Harshman <jharsh...@pacbell.net>

Date: Wed, 14 Sep 2011 14:24:24 -0700
Local: Wed, Sep 14 2011 2:24 pm

Subject: Re: Trying to salvage something from this Re: The Theory of
Evolution

> On Aug 11, 7:16 am, John Harshman <jharsh...@pacbell.net> wrote:
>> Alan Kleinman MD PhD wrote:
>>>> On Jul 13, 1:56 pm, John Harshman <jharsh...@pacbell.net> wrote:
>>>>> g...@risky-biz.com wrote:
>> It has everything to do with what we are discussing. There are huge
>> stretches of the two genomes which can not be matched up for homology.

>True. Do you know how they got there? Most of them are retrotransposons,
>yet another class of neutral mutations.
John, chromosome 21 has large stretches if non-random sequences which
are not on the chimpanzee genome. So where are these stretches of
bases on the chimpanzee genome? You are going to paint yourself in a
corner with these types of arguments because human genomes and
chimpanzee genomes must remain homologous to themselves for
consistently successful reproduction. Transposons may occur commonly
in immunologic cells but in germ cell line this phenomenon would
disrupt homology.

>> This data is presented for those areas which can be matched and the
>> match is not close at all.

>It isn't? 98.7% identity isn't close? What would constitute close, then?
When you are talking about mutation and selection, you are not close
at all. Mutation and selection working under ideal conditions may be
able to substitute 10-20,000 bases in 500,000 generations. Using your
numbers, you have to account for 20,000,000 bases in each of the human
and chimpanzee populations. And remember, you don’t have a population
size of 10^9 until about the last century. Human population size never
really grew rapidly until the advent of mechanized farming about
5-10,000 years ago. Chimpanzee mechanized farming is limited to a
chimp putting a stick down a hole to harvest ants. What do you think
the maximum size of the chimpanzee population has ever been?

>> Evolutionists claim that humans and
>> chimpanzees come from a common progenitor. Now you are claiming that
>> many of these differences are neutral which is typical evolutionist
>> speculation.

>Simple observation of how proteins work.
More like simple minded observation. I suppose if you look out toward
the horizon and say, “sure looks flat to me”, that’s enough to
convince you that the earth is flat. I suggest you take a look at
Google Earth.

>> Tell us which are neutral differences and which are
>> selective differences.

>Well, it seldom matters whether a protein has leucine, isoleucine, or
>phenylalanine in a particular spot.
Well then you have some explaining to do. How do all these neutral
variants get fixed in a population because greater than 70% of
proteins differ between humans and chimpanzees and you only have
500,000 generations to explain the differences?

>> And then compute the joint probability of two
>> neutral mutations being fixed in a population.

>Are you still on about that? Your joint probability is irrelevant. We
>don't care about the joint probability of some particular set of
>mutations being fixed, only about the probability that any set of
>mutations will be fixed. Different, no?
Now John, when you make a claim like that you are proving that you
accept as true a mathematical irrational belief system. Whenever you
are considering a stochastic process, the joint probability of events
is governed by the product of the individual probabilities. The
multiplication rule of probabilities is the monkey wrench in the works
of your irrational belief system. You will never have a good
understanding how this phenomenon work without a good understanding of
probability theory.

>>>>>> How many with other known functions? How much "junk"?
>>>>> Almost all is junk, just as almost all the genome is junk. Non-coding,
>>>>> functional regions are just another few percent of the genome.
>>>> This is the type of stupidity that evolutionist perpetuate. If they
>>>> don’t know what a portion of the genome does, it is junk.
>>> No, that's not how it works. We recognize junk by the fact that it
>>> evolves at the rate of mutation.

>> Take a look at this URL: >http://www.google.com/url?sa=D&q=http://www.sciencemag.org/content/295/5552/131.abstract&usg=AFQjCNF6LJDM3>GHffyRjXPABtkVjwnfm9w

>> In this URL, they studied chromosome 21. They report “We detected
>> candidate positions, including two clusters on human chromosome 21
>> that suggest large, nonrandom regions of difference between the two
>> genomes.” Nonrandom means these are selective differences

>No it doesn't.
Or really John? So how do we get non-random sequences of bases without
selection? How did these bases become arranged without selection?

>> and we all
>> should know by now that selective differences take hundreds of

>> generations per base substitution. But you claim that neutral

>> mutations fix at the rate of a couple of hundred per generation,
>> thousands of times faster than selection can fix a beneficial
>> mutation.

>Once again you confuse numbers with rates.
I don’t think so John. I think you’ve made contradictory claim. On one
hand you are claiming that neutral evolution is slower than selective
evolution and then on the other hand you claim that a couple hundred
neutral mutations are fixed every generation. I think you are the one
how is more than a little bit confused.

>>>> If they
>>>> don’t understand how to do a mathematical computation it is junk.
>>>> John, just because you are ignorant what a non-coding region of a
>>>> genome does, don’t impose your ignorance on us by claiming this is
>>>> junk. If a region of DNA has no coding function for proteins but
>>>> remains non-random, it does so because it has stabilizing selection
>>>> acting on those sequences.

>>> True. Which has nothing to do with what I'm talking about. Stabilizing
>>> selection makes loci evolve at less than the neutral rate. Such loci are
>>> only a few percent of the genome. By the way, evolution isn't so fast as
>>> to randomize sequences in 5 million years.
>> Just what are you talking about? I guess you missed the study I posted
>> above about the large non-random differences on chromosome 21 between
>> humans and chimpanzees.

>So? How is that relevant? Do you have access to the whole article? I don't.
Yes I do have the whole article. I was able to subscribe to Science
Magazine online without charge. Go to their web page and ask for an
account. And the reason why this is relevant is that there are more
differences between the human and chimpanzee genomes than your simple
minded analysis accounts for.

>> 70% of genes code for different proteins,

>....if by "different" you mean having at least one different amino acid.
Do you have a different definition for the word “different” because if
so you need to tell us how our definitions for the word “different”
are different. And then perhaps we can work out our differences unless
you want to differ on our differences.

>> large stretches of non-random differences between human and chimpanzee
>> genomes yet neutral evolution will fix all these differences a rate of
>> a couple of hundred per generation, thousands of times faster than a
>> single beneficial mutation can be fixed in a population. What you are
>> talking about is mathematical irrationality.
>I've become convinced that you know almost nothing about mathematics
>beyond the scraps rote learning you have displayed here.

Now what have you against rote learning? If it wasn’t for rote
learning, evolutionists would have no way of indoctrinating naïve

school children. You certainly don’t have any mathematical logic to

support your mathematically irrational belief system.

>>> You mistake evolution at the rate of mutation for stabilizing selection,
>>> presumably because you have a false understanding of the mutation rate.
>>> Neutral evolution produces only a bit more than 1% difference over 5
>>> million years, not a randomization of sequences.

>> You will only get randomization of sequences if there is no selection
>> acting on that sequence. Your mathematics is faulty because 5 million
>> years only represents about 500,000 generations and you can not fix
>> 40,000,000 differences in two divergent populations in such a short
>> period of time. It is mathematical irrationality to believe this.
>You seem to have stopped even pretending to have an argument and are
>just repeating your mantra regardless of what you are supposedly
>responding to.

You are the one closing your eyes to the argument. You have said there
are 40,000,000 differences between human and chimpanzee genomes and by
your numbers the two species diverged 5,000,000 years ago. How do you
account for those differences in such a small number of generations
(other than your mathematically irrational claim that a couple of

hundred neutral mutations fix every generation). Do you want some more
generations from the pre-split split period?

>> We all know about evolutionist expectations, they are mathematically
>> irrational. But if you want to show your work and compute the joint
>> probability of two neutral mutations being fixed in a population, that
>> would be some interesting evolutionist folklore to hear.
>Mantra. At least your mantra does evolve over time, though it seems to
>be randomly so.

My new mantra for you is “multiplication rule of probabilities, theory
of evolution irrational”. This mantra is to be sung to the theme from
the Beatles song, Shake it up baby, twist and shout.

>> Repeat after me, reptiles transform into birds, reptiles transform
>> into birds, reptiles transform into birds…
>That is indeed what the data show. Care to discuss it?

[Alan Kleinman MD PhD]

The following are responses from posts 876-900 round 2 presented in
this format to prevent more splinter threads.

John Harshman 17, 7:58 am
>> Of course these neutral mutations don’t show up all at once, sweeping
>> through the population like a tsunami. They also don’t show up dozens
>> per generation, generation after generation for hundreds of thousands
>> of generations. This is part of the evolutionist mathematically
>> irrational speculations. My arguments are made from hard mathematical
>> and empirical evidence. If you didn’t have your mathematically
>> irrational speculations and gross over-extrapolations, you

>> evolutionists would have no argument at all for your mathematically
>> irrational belief system.

>So far, just a content-free rant.
That’s how an evolutionist responds to mathematical and empirical
evidence. Is it any wonder that we have multidrug resistant microbes,
multiherbicide resistant weed, multipesticide resistant insects and
less than durable cancer treatments. It is the failure of
evolutionists to properly explain the mutation and selection
phenomenon that has caused these problems.

>> Now I have shown you mathematically why neutral mutations do not
>> spread through populations rapidly if at all.
>Nobody claims that neutral mutations spread rapidly.
You have, you have claimed that a couple hundred of them are fixed
every generation. Can you make the theory of evolution any more
mathematically irrational? I expect so.

>> The probability function

>>>> describing the basic science and mathematics of mutation and
>>>> selection.

Mark Isaak Aug 17, 8:04 am
Newsgroups: talk.origins
From: Mark Isaak <eci...@curioustaxonomyNOSPAM.net>

Date: Wed, 17 Aug 2011 08:04:09 -0700

Local: Wed, Aug 17 2011 8:04 am

Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

>On 8/17/11 7:28 AM, Alan Kleinman MD PhD wrote:
>> On Jul 22, 7:37 pm, Mark Isaak<eci...@curioustaxonomyNOSPAM.net>
>>> [snip, about neutral genetic drift]
>>> First, let me ask you: How many mutations do you have that were not in
>>> either your father or mother? Go ahead, sequence the three genomes and
>>> count the differences. I'll wait.
>> You mean we actually have an evolutionist who wants to do some actual
>> measurements?
>We do. You, I note, do not.
Mark, first you have to recognize what a measurement is and we note
you do not.

>So let me ask again. How many mutations do you have that were not in
>either your father or mother?
It doesn’t matter for correctly describing the mathematics of mutation
and selection.

>>> Second, learn how to read.
>> I d rather do the mathematics, ...
>Too bad you suck at mathematics, too. I suspect your reading disability
>is part of the issue there, too, because it is the word problems where
>you have the real problem.
Mark, you are the one who claims that the more complex the
optimization conditions are the easier it is to do the optimization.
You obviously were trained as a social engineer.

John Harshman Aug 17, 8:03 am
Newsgroups: talk.origins
From: John Harshman <jharsh...@pacbell.net>

Date: Wed, 17 Aug 2011 08:03:52 -0700

Local: Wed, Aug 17 2011 8:03 am

Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

that the multiplication rule of probabilities does not apply to
biological evolution.

John Harshman Aug 17, 8:12 am

Newsgroups: talk.origins
From: John Harshman <jharsh...@pacbell.net>

Date: Wed, 17 Aug 2011 08:12:09 -0700
Local: Wed, Aug 17 2011 8:12 am

Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

>>>> It’s you evolutionists who have bungled the basic science and
>>>> mathematics mutation and selection and have given us multidrug
>>>> resistant microbes, multiherbicide resistant weed, multipesticide
>>>> resistant weeds and less than durable cancer treatments.
>>> When in doubt, fall back on an irrelevant mantra.

>> Now are you going to tell us John that multidrug resistant microbes,

>> multiherbicide resistant weeds, multipesticide resistant insects and

>> less than durable cancer treatments don’t exist?
>No. But I'm also not going to tell you that walnuts don't exist, and
>that has just as much to do with the matter at hand.
John, it does matter because all these situations have come about by
mutation and selection and the failure of evolutionists to properly
describe the basic science and mathematics of this phenomenon.

>> This is the legacy of

>> evolutionism from the failure of evolutionists to properly describe

>> the mutation and selection phenomenon.

>Says the guy who thinks mutation and selection are a single phenomenon.
Says the guy who used to think that the probability of a beneficial
mutation occurring was proportional to population size. John, you were
able to correct your error for that claim. Why are you having such
difficulty understanding the correct probability function for two
mutations occurring? Is it so hard to accept how mutation and
selection actually works? The correct understanding of this phenomenon

gives a way to look for rational solutions for multidrug resistant

microbes, multiherbicide resistant weeds, multipesticide resistant

insects and producing more durable cancer treatments.

>>>> So now you claim that drift is what gives accounts for the 40,000,000

>>>> differences between humans and chimpanzees in less than a million
>>>> generations.

John Harshman Aug 17, 8:15 am

Newsgroups: talk.origins
From: John Harshman <jharsh...@pacbell.net>

Date: Wed, 17 Aug 2011 08:15:33 -0700
Local: Wed, Aug 17 2011 8:15 am

Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

>> mutation is also the probability that the mutation will be fixed in a
>> population.

>Yes. Elementary random walk math.
>> Let’s apply some principles of probability theory to your
>> mathematically irrational claims. First, tell us whether those neutral
>> mutations are random independent events or not.
>Yes, they are. Go on.
Are you sure you want to go here? Well you said “go on”. Now tell us
whether the fixation of these neutral mutations is random process?

Vincent Maycock Aug 17, 8:36 am
Newsgroups: talk.origins
From: "Vincent Maycock" <vam...@aol.com>
Date: Wed, 17 Aug 2011 11:36:30 -0400
Local: Wed, Aug 17 2011 8:36 am

Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

>> Perhaps the greatest impetus for the theory of evolution was the
>> evolution of drug resistant microbes. Now that it is clear that this
>> evolutionary process is stifled if combination therapy is used, where
>> are your empirical examples that show that the theory of evolution is
>> mathematically rational? Let’s see if your fertile but mathematically
>> irrational mind can come up with selection conditions that behave
>> otherwise, and please don’t forget to give us the measured
>> experimental examples of your mathematically irrational claims. I
>> might as well find a comfortable chair because we are going to have a
>> long wait for that example.
>Pseudogenes disprove creationism.
Vincent, I’m not advocating any other theory. I’m here to give you the
correct basic science and mathematics of the mutation and selection
phenomenon and show that the theory of evolution is a mathematically
irrational belief system.


Inez Aug 17, 9:57 am
Newsgroups: talk.origins
From: Inez <savagemouse...@hotmail.com>
Date: Wed, 17 Aug 2011 09:57:56 -0700 (PDT)
Local: Wed, Aug 17 2011 9:57 am

Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

>> > They don't show up all at once. Most people have had them in their
>> > family tree for a long time. It's just that dozens get fixed every
>> > generation. Your argument from incredulity is ignorant and boring.
>> > If you don't think that neutral mutations can spread through a
>> > population, why don't you show why not?
>> Of course these neutral mutations don’t show up all at once, sweeping
>> through the population like a tsunami. They also don’t show up dozens

>> per generation, generation after generation for hundreds of thousands
>> of generations. This is part of the evolutionist mathematically
>> irrational speculations. My arguments are made from hard mathematical
>> and empirical evidence. If you didn’t have your mathematically
>> irrational speculations and gross over-extrapolations, you

>> evolutionists would have no argument at all for your mathematically
>> irrational belief system.

>A lot of fist shaking, but not a real argument. Why couldn't a
>neutral mutation spread through the population by chance?
Inez, it’s very difficult to use a key board and mouse with a shaking
fist. All I’m doing is a little finger tapping. So you want to know if
a neutral mutation could spread through a population by chance? Your
own evolutionist computations show that there is a very small chance
that this will happen equal to the frequency of that allele. And that
model only applies when you only have two neutral alleles for a single
gene. Now what’s the probability of two neutral mutations being fixed
by chance? Shouldn’t that joint probability of that event be governed
by the multiplication rule of probabilities?

>> Now I have shown you mathematically why neutral mutations do not
>> spread through populations rapidly if at all.
>No one claims they spread rapidly.

They better if you want to do the accounting to explain the 40,000,000
differences between human and chimpanzee genomes in 500,000
generations.

>> The probability function

>> I derived for you of two mutations accumulating is not only applicable
>> for the accumulations of beneficial mutations; it is also applicable
>> for computing the probability of neutral or detrimental mutations
>> accumulating in a population. Of course neutral and detrimental
>> mutations do not amplify because they don’t give increased fitness to
>> reproduce for those members with those mutations. Because of this,
>> there is a very low probability that neutral or detrimental mutations
>> will accumulate in a population.
>Yes...and if there are a whole lot of neutral mutations, a few will
>beat the odds.

You need far, far, far more than a few to beat the odds to do the
accounting for the 40,000,000 differences between human and chimpanzee
genomes in 500,000 generations.

>> > > This is the kind of irrational
>> > > nonsense that evolutionists are now enamored with rather than properly

>> > > describing the basic science and mathematics of mutation and
>> > > selection.

>> > Selection is by definition irrelevant to neutral evolution.
>> And without selection, amplification of mutations does not occur.
>> And without amplification, you have very low probabilities of accumulating
>> mutations.
>Right...and if there are a ton of neutral mutations, a few will make
>it.
The multiplication rule of probabilities for computing the joint
probability of random independent events shows that your claim is
mathematically irrational. You evolutionists have clearly missed the
probability part of the probability and statistics course.

>> Why evolutionists would think that the mathematics of
>> abiogenesis will somehow cause the spread of neutral mutations through
>> a population faster than the mathematics of selection can only be
>> explained by the fact that evolutionists are mathematically
>> incompetent.
>This is a odd strawman that you have made up and insist on repeating
>for no apparent reason. Who said that neutral mutations spread more
>quickly than beneficial ones? Can you provide a link?
The only thing that separates the mathematics of abiogenesis from the
mathematics of mutation and selection is replication and selection. Do
you really need a link for that?

Greg Guarino Aug 17, 12:21 pm

Newsgroups: talk.origins
From: Greg Guarino <gdguar...@gmail.com>

Date: Wed, 17 Aug 2011 15:21:16 -0400
Local: Wed, Aug 17 2011 12:21 pm

Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

>> I’ve

arguments and they are mathematically irrational and have harmed
millions of people suffering from diseases subject to the mutation and
selection phenomenon.

>> despite the fact that beneficial
>> mutations have selection assisting the spread of the mutation, that’s
>> your right. However I find that to be mathematically irrational and
>> incoherent without any mathematical or empirical basis,
>And that should be your first clue that perhaps that is not what anyone
>thinks.
Then if that’s not what you think, you have opened the door in your
thinking to understanding why the theory of evolution is
mathematically irrational.

>Greg Guarino

hersheyh Aug 17, 12:19 pm

Newsgroups: talk.origins
From: hersheyh <hershe...@yahoo.com>

Date: Wed, 17 Aug 2011 12:19:37 -0700 (PDT)
Local: Wed, Aug 17 2011 12:19 pm

Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

hersheyh Aug 17, 12:42 pm
Newsgroups: talk.origins

From: hersheyh <hershe...@yahoo.com>
Date: Wed, 17 Aug 2011 12:42:58 -0700 (PDT)
Local: Wed, Aug 17 2011 12:42 pm

Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

On Wednesday, August 17, 2011 10:28:23 AM UTC-4, Alan Kleinman MD PhD
wrote:
> On Jul 22, 7:37 pm, Mark Isaak <eci...@curioustaxonomyNOSPAM.net>

> wrote:
>[snip]
>> > Second, learn how to read.
>> I’d rather do the mathematics, wading through evolutionist
>> speculations is not the way to learn how mutation and selection
>> actually works. Doing the mathematics is the way to learn how mutation
>> and selection works. Of course, evolutionists like you don’t know how
>> to do the mathematics.
>So rather than actually try to *learn* what scientists say, Dr. Dr. Kleinman prefers to reiterate his bogus numerology >without reading or trying to understand why it is limited to special cases again, and again, and again, and again..... >Mindless repetition like that is primarily found in autistics and obsessive compulsives.
I’ve been reading mathematically irrational evolution crap for
decades; you can’t avoid it when you go to medical school. If you
don’t want to learn how mutation and selection actually works, read
and study evolutionist folklore. Based on this mathematically
incompetent evolutionist folklore you can learn how to produce

multidrug resistant microbes, multiherbicide resistant weeds,

multipesticide resistant insects and produce less than durable cancer
treatments. That’s the reward for the studies of mathematically
irrational evolutionist folklore.

>[snip]
Let’s snip mathematically irrational evolutionist folklore out of
school science curriculums and actually train naïve school children in
the correct basic science and mathematics of the mutation and
selection phenomenon. Put the theory of evolution into a fictional
writing course where it belongs.

Mark Isaak More options Aug 17, 1:32 pm

Newsgroups: talk.origins
From: Mark Isaak <eci...@curioustaxonomyNOSPAM.net>

Date: Wed, 17 Aug 2011 13:32:46 -0700
Local: Wed, Aug 17 2011 1:32 pm

Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

>On 8/17/11 7:05 AM, Alan Kleinman MD PhD wrote:
>> On Jul 22, 12:51 pm, Inez<savagemouse...@hotmail.com> wrote:

>>> On Jul 22, 12:35 pm, Alan Kleinman MD PhD<klein...@sti.net> wrote:
>>> [...]

>>>> This is the kind of irrational
>>>> nonsense that evolutionists are now enamored with rather than properly

>>>> describing the basic science and mathematics of mutation and
>>>> selection.

>>> Selection is by definition irrelevant to neutral evolution.
>> And without selection, amplification of mutations does not occur.
>Yes it does. Not always, but often enough. You can see for yourself by
>programming a simulation of a small population with mutations and no
>selection, and then watching it run a bunch of times.
Really now Mark, you’ve done that simulation? Why don’t you tell us
which simulation you used? Because I have done the same simulation
with a peer reviewed and published model of mutation and selection.
And when you turn off selection in that model, the genetic sequences
revert to random sequences.

hersheyh Aug 17, 2:15 pm

Newsgroups: talk.origins
From: hersheyh <hershe...@yahoo.com>

Date: Wed, 17 Aug 2011 14:15:26 -0700 (PDT)
Local: Wed, Aug 17 2011 2:15 pm

Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

>> are your empirical examples that show that the theory of evolution is
>> mathematically rational? Let’s see if your fertile but mathematically
>> irrational mind can come up with selection conditions that behave
>> otherwise, and please don’t forget to give us the measured
>> experimental examples of your mathematically irrational claims. I

[johnetho...@yahoo.com]

On Sep 16, 4:09 pm, r norman <r_s_nor...@comcast.net> wrote:
> On Fri, 16 Sep 2011 23:55:14 +0200, "Rolf" <rolf.aalb...@tele2.no>

I decided a while back that he is psychotic with respect to this issue.

[John Harshman]

Just to let you know: I'm never going to reply to anything you post in
this format. Then again, I probably won't reply to anything you post in
any format; it's futile either way.

[chris thompson]

On Sep 16, 7:09�pm, r norman <r_s_nor...@comcast.net> wrote:
> On Fri, 16 Sep 2011 23:55:14 +0200, "Rolf" <rolf.aalb...@tele2.no>

Quite a roundabout way of conceding defeat, Richard!

Chris

[r norman]

I clearly yield to his bull-headed staying power. Even the
indefatigable Harshman seems to be throwing in the towel.

[Bob Casanova]

On Tue, 20 Sep 2011 11:42:19 -0700 (PDT), the following
appeared in talk.origins, posted by Alan Kleinman MD PhD
<klei...@sti.net>:

>The following replies are from a splinter threads

Thanks, but no thanks. Welcome to my bit bucket.

<snip remainder of error-filled 1465-line post>

[Inez]

The splintering effect of your thread only happens in Google Groups
when the thread hits 1000 posts. People with real newsreaders are not
patient with working around the vagueries of Googles Groups, and it is
unlikely that many people will respond to your massive cut-and-paste
threads.

What you migh try is reading people's posts for comprehension and
responding to what they actually say, which might get the thread
wrapped up on under 1,000 (or in this case 2,000) posts.

> Inez Aug 17, 9:57 am
> Newsgroups: talk.origins
> From: Inez <savagemouse...@hotmail.com>
> Date: Wed, 17 Aug 2011 09:57:56 -0700 (PDT)
> Local: Wed, Aug 17 2011 9:57 am
> Subject: Re: The Theory of Evolution is Mathematically Irrational
> Round 2>> > They don't show up all at once. Most people have had them in their
> >> > family tree for a long time. It's just that dozens get fixed every
> >> > generation. Your argument from incredulity is ignorant and boring.
> >> > If you don't think that neutral mutations can spread through a
> >> > population, why don't you show why not?
> >> Of course these neutral mutations don’t show up all at once, sweeping
> >> through the population like a tsunami. They also don’t show up dozens
> >> per generation, generation after generation for hundreds of thousands
> >> of generations. This is part of the evolutionist mathematically
> >> irrational speculations. My arguments are made from hard mathematical
> >> and empirical evidence. If you didn’t have your mathematically
> >> irrational speculations and gross over-extrapolations, you
> >> evolutionists would have no argument at all for your mathematically
> >> irrational belief system.
> >A lot of fist shaking, but not a real argument. Why couldn't a
> >neutral mutation spread through the population by chance?
>
> Inez, it’s very difficult to use a key board and mouse with a shaking
> fist. All I’m doing is a little finger tapping.

But none of that resulted in a real argument.

> So you want to know if
> a neutral mutation could spread through a population by chance? Your
> own evolutionist computations show that there is a very small chance
> that this will happen equal to the frequency of that allele. And that
> model only applies when you only have two neutral alleles for a single
> gene. Now what’s the probability of two neutral mutations being fixed
> by chance? Shouldn’t that joint probability of that event be governed
> by the multiplication rule of probabilities?

No. The question isn't what the odds are of two *specific* mutations
being fixed is, the question is what the odds are of *any* two (or
more) mutations being fixed.

> >> Now I have shown you mathematically why neutral mutations do not
> >> spread through populations rapidly if at all.
> >No one claims they spread rapidly.
>
> They better if you want to do the accounting to explain the 40,000,000
> differences between human and chimpanzee genomes in 500,000
> generations.

Why does it have to be 500,000 generations?

>
> >> The probability function
> >> I derived for you of two mutations accumulating is not only applicable
> >> for the accumulations of beneficial mutations; it is also applicable
> >> for computing the probability of neutral or detrimental mutations
> >> accumulating in a population. Of course neutral and detrimental
> >> mutations do not amplify because they don’t give increased fitness to
> >> reproduce for those members with those mutations. Because of this,
> >> there is a very low probability that neutral or detrimental mutations
> >> will accumulate in a population.
> >Yes...and if there are a whole lot of neutral mutations, a few will
> >beat the odds.
>
> You need far, far, far more than a few to beat the odds to do the
> accounting for the 40,000,000 differences between human and chimpanzee
> genomes in 500,000 generations.

The math has been presented to you numerous times.

>> > > This is the kind of irrational
> >> > > nonsense that evolutionists are now enamored with rather than properly
> >> > > describing the basic science and mathematics of mutation and
> >> > > selection.
> >> > Selection is by definition irrelevant to neutral evolution.
> >> And without selection, amplification of mutations does not occur.
> >> And without amplification, you have very low probabilities of accumulating
> >> mutations.
> >Right...and if there are a ton of neutral mutations, a few will make
> >it.
>
> The multiplication rule of probabilities for computing the joint
> probability of random independent events shows that your claim is
> mathematically irrational.

But that isn't the right way to compute the probability. The question
isn't what the chances are of a specific set of mutations getting
fixed is, the question is what the chances of any set of mutations
being fixed. As John Harshman pointed out earlier, the chances of any
specific bridge hand being dealt is vanishingly small, but the chances
of some bridge hand being dealt is a certainty.

> You evolutionists have clearly missed the
> probability part of the probability and statistics course.
>
> >> Why evolutionists would think that the mathematics of
> >> abiogenesis will somehow cause the spread of neutral mutations through
> >> a population faster than the mathematics of selection can only be
> >> explained by the fact that evolutionists are mathematically
> >> incompetent.
> >This is a odd strawman that you have made up and insist on repeating
> >for no apparent reason. Who said that neutral mutations spread more
> >quickly than beneficial ones? Can you provide a link?
>
> The only thing that separates the mathematics of abiogenesis from the
> mathematics of mutation and selection is replication and selection. Do
> you really need a link for that?
>

No idea why you suddenly started talking about abiogenesis here. I
asked for a link to someone claiming neutral mutations spread faster
than selected ones. Who claimed that?

[Mike Lyle]

On Tue, 20 Sep 2011 16:18:31 -0400, r norman <r_s_n...@comcast.net>
wrote:

I wonder if there may be a clue in the records of malpractice
hearings: I believe he mentioned that he'd had one. I, of course,
apologise if my memory is at fault in this matter.

--
Mike.

[r norman]

For all his faults I still wouldn't look into that. Far too many
capable and competent practicioners get hit with malpractice claims.

Note: I wouldn't want to cut off all such claims -- there is more
than enough medical incompetence going around that the medical
profession itself seems unwilling or unable to control internally.
Still, a little common sense in throwing out really frivolous claims
would be in order. People do get worse and die for mysterious reasons
and, often enough, for no known reason. Doctors can't stop it, merely
stem the tide.

[Alan Kleinman MD PhD]

The following are responses to posts 901-925 done in this format to
prevent the formation of more splinter threads.

Mark Isaak Aug 23, 7:52 pm

Newsgroups: talk.origins
From: Mark Isaak <eci...@curioustaxonomyNOSPAM.net>

Date: Tue, 23 Aug 2011 19:52:58 -0700
Local: Tues, Aug 23 2011 7:52 pm

Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

>> Since you are incapable of doing a mathematical computation and insist
>> on doing your speculations grammatically, we need to parse your claims
>You are unable to do that. Learn to read first.
Sorry, I can’t read, what are you saying?

>> and try do determine exactly what you are saying. Let’s start with
>> your speculation that fifty generations before your neutral allele is
>> fixed (substituted) for some other neutral allele, the frequency of
>> your particular allele is 0.5. Fifty generations later, your neutral
>> allele is now fixed in the population. So what happened to the other
>> half of the population and all its descendents that did not have your
>> particular neutral allele? And remember, its not just two neutral
>> alleles which have to be fixed every generation, it’s dozens of
>> neutral alleles which must be fixed every generation, generation after
>> generation for hundreds of thousands of generations. What happened to
>> all the members of the population and their descendents which did not
>> have your particular neutral mutations? Did they stop replicating? If
>> they did stop replicating, why would the lack of a neutral mutation
>> prevent them from replicating? Come on Mark, tell us a bedtime story.
>>> Please, please, please learn how to read.
>> Sory, i twarn’t a inglish mager in kolije.
>It's time you learn, then.
What if I can’t? Would you tell me an evolutionist bedtime story? I
just love hearing fairytales.

>Seriously, have you had your mental health checked yet?
Yes, and I have been found to have a severe deficiency of evolutionist
mathematical irrationality. I also suffer from
aevolutionistfolkloremania but fortunately I don’t suffer from
evolutionistspeculationitis or evolutionistoverextrapolation obsession
syndrome. But Mark, I do thank you for thinking of my well being.

hersheyh Aug 24, 12:59 pm
>> On Jul 22, 9:18 pm, hersheyh <hers...@yahoo.com> wrote:
>> > The figure here
>> > http://www.google.com/url?sa=D&q=http://en.wikipedia.org/wiki/File:Random_genetic_drift_chart.png
>> > which can be found in this article
>> > http://www.google.com/url?sa=D&q=http://en.wikipedia.org/wiki/Genetic_drift
>> > shows the relationship between fixation of one of two alleles at a
>> > single gene locus that started out at 50% in a population and the size
>> > of the population. For populations of size 20, it is very clear that
>> > completely random variation from generation to generation can lead to
>> > fixation of one or the other allele rather quickly. For larger
>> > populations, the neutral drift away from the starting point is slower,
>> > but is still significant after a mere 50 generations. What this graph
>> > does not show is that the probability of mutation per generation also
>> > increases with population size. We have gone thru that math several
>> > times, and each time you have ignored it because you don't understand
>> > it. Why would it be any different this time?
>> I ve read this page previously. Your gross over-extrapolation of this
>> mathematics demonstrates your evolutionist bias.
>So, exactly what is wrong with the math, mathematically? Is it the statement that the probability of a neutral mutation >that has just occurred at a nt site becoming fixed in a population = 1/(2Ne), where Ne is the effective population size? Is >it the statement that the probability of a mutation at that nt site occurring being 2Ne*u, where u is the mutation rate for >that site (again, assuming selective neutrality or near neutrality)? Are you claiming that there are not 3 X 10^9 nt sites in >the haploid human genome? Are you claiming that the vast majority of those sites are selectively crucial (a statement >that is contrary to evidence since the mean mutation rate for point mutation is around 10^-8), or do you agree that most >mutation is selectively neutral?
There is nothing wrong with the mathematics. What is wrong is your
extrapolation of this mathematics to multiple neutral mutations
simultaneously being fixed in the population. You have this enormous
mathematical blind spot in your thinking. You somehow throw out the

multiplication rule of probabilities for computing the joint

probability of multiple independent events for every stochastic
process you see fit. This is not mathematically based science you are
practicing. This is evolutionist mathematical irrationality.

What I am saying is that whether the genetic differences are selective
or neutral makes no real difference in the mathematics of evolution.
Let all the genetic differences between humans and chimpanzees be
selective which gives the most rapid fixation of mutations. You are
still no where close to being able to do the mathematical accounting
for these differences in 500,000 generations. You can be as derisive
as possible but that will not give you any scientific or mathematical
evidence to support your mathematically irrational belief system and
in the meantime you have bungled the basic science and mathematics of
the mutation and selection phenomenon and harmed millions of people in
the process.

>> You try to take this
>> model and impose the results derived on John Harshman s 40,000,000
>> differences between human and chimpanzee genomes.
>Quite successfully.
If you want to call it a mathematically irrational extrapolation that
throws out the multiplication rule of probabilities for the joint
probabilities of multiple independent events for a stochastic process,
it’s a perfect fit for your mathematically irrational belief system.

>> On average, to
>> account for these differences requires the fixation of dozens of
>> neutral mutations generation after generation for hundreds of
>> thousands of generations.
>Yes. But fixation is actually a fuzzy boundary when you have a population of 6 billion people because that size almost >guarantees new point mutation at every site. Basically, all that is required for fixation is that the last step from Ne-1 (or >several) individuals having an originally new mutant allele that was first acquired long ago become Ne - 0 by loss of the >few individuals having the original w.t. allele. When you look at the chimp compared to human genome and the time >available since last divergence, the amount of difference seen is that expected if most of the genome is selectively >neutral. That is, the mathematics appears to work in the real world under the assumption that most of the nt's in the >human and chimp genome are selectively neutral (any of the 4 possibilities will have the same functional effect). We >*know* that not all the sequence differences are due to drift (the slowest mechanism for producing a difference). Some >(small) fraction of difference is of selective importanc

e.
Hersheyh, you play fast and loose with population sizes. Do you think
that five million years ago there was a population of 6 billion
progenitors? This is why your analysis is a crock of hot steaming bs.
Why don’t you try doing the analysis of the fixation of two neutral
mutations in a similar manner as the fixation of a single neutral
mutation and present the algebra to us? Oh, I forgot, all you know how
to do is blah, blah, blah and plug in numbers in the wrong probability
distribution.
>> This drift model only takes into account the
>> fixation of one of two alleles as you describe above, not the fixation
>> of dozens of neutral alleles every generation and when in reality, you
>> have more than two possible alleles at a single locus.
>We are talking about point mutational changes in nt's, not alleles or alternate forms of genes. Learn the meaning of >genetic terminology, why don't you -- at least before you say more ignorant things? In most genes (say, a coding >sequence for a 300 aa protein, thus 900 nt), neutral drift is 1) less likely since the protein must function and there is more >constraint on nt sequences, 2) when it occurs, is more likely to be a point mutation that does not change the aa >sequence encoded, 3) when an aa is changed by neutral fixation, it will tend to be similar in characteristics (e.g., >hydrophobicity) or in an unnecessary part of the protein, 4) will, given the time of divergence between chimps and >humans, produce an average of somewhat less than one aa change per average size protein (in a Poisson distribution, >btw), 4) nt changes will be somewhat less frequent than in non-coding regions.
Your sloppy analysis by blah, blah, blah doesn’t cut it. And the
Poisson distribution is not the correct probability distribution for
the mutation and selection phenomenon. A random mutation is not a
Poisson random variable. Are you too ignorant to look up the
derivation of that probability distribution to understand why this is
not the correct way to do the mathematics of this phenomenon? You need
to rise above this mathematically irrational dogmatism that you’ve
been indoctrinated with and learn how to do the mathematics of
mutation and selection properly.

>> I don t ignore this model; I ignore your inappropriate over-
>> extrapolation of this model. You have failed to understand the basic
>> science and mathematics of the mutation and selection phenomenon, you
>> are now failing to understand the mathematics of random recombination
>> and now you take a model based on the random substitution of a single
>> allele for another allele and claim that this entire process occurs in
>> parallel allowing the random substitution of dozens of neutral alleles
>> to occur simultaneously.
>I know that you deny even the possibility of parallel changes in sexually reproducing organisms, be those changes >neutral or even somewhat beneficial, yet the only type of parallel changes you have ruled out are when the selection is >lethal or highly population-size deleterious to the w.t. alleles in organisms where ...

And the reason I deny this possibility is based on two facts. The
first fact is there is no empirical evidence that mutation and
selection can work in parallel, all the data contradicts this belief.
And the second fact is the multiplication rule of probabilities which
governs the joint probabilities of multiple independent events
occurring. You know that mathematical rule from probability theory,
the one that Schneider claims does not apply to biological evolution
and you are now claiming does not apply to neutral evolution. Now why
don’t you try to derive the probability function which would describe
random recombination? I don’t think we are going to see that one from
you; you are too busy doing blah, blah, blah trying to defend your
mathematically irrational belief system.


hersheyh Aug 24, 3:02 pm

Newsgroups: talk.origins
From: hersheyh <hershe...@yahoo.com>

Date: Wed, 24 Aug 2011 15:02:36 -0700 (PDT)
Local: Wed, Aug 24 2011 3:02 pm

Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

>> On Jul 24, 10:42 am, hersheyh <[email address]> wrote:
>> > 1) Cranks overestimate their own knowledge and ability, and
>> > underestimate that of acknowledged experts.
>> Here’s one of my favorite quotes from hersheyh “I have *forgotten*
>> more about mutation and selection than you are
>> capable of learning.”
>That is a statement of fact as demonstrated by your discussion here. It actually says nothing about my competence >other than relative to yours. I am not overestimating my own knowledge and ability relative to yours. And I certainly do >not underestimate the greater knowledge of acknowledged experts from which I learned about mutation and selection >(including Hermann Joseph Muller, Tracey Sonneborn, Howard Temin, Gobind Khorana, J. Herbert Taylor, James F. >Crow directly and many others through their writings) and from teaching genetics for over 20 years.

Oh really hersheyh, well why don’t you see what James F. Crow wrote as
recently as two years ago in the Journal of Biology, http://jbiol.com/content/8/2/13
“Mayr, mathematics and the study of evolution” where Professor Crow
said the following: “In 1959 Ernst Mayr challenged the relevance of
mathematical models to evolutionary studies and was answered by JBS
Haldane in a witty and convincing essay. Fifty years on, I conclude
that the importance of mathematics has in fact increased and will
continue to do so.” I contacted Professor Crow and made the following
argument to him:

“Any attempt to describe the mutation and selection sorting/
optimization process solely using empirical evidence will encounter a
massive data acquisition barrier. How does one gather the data
necessary to describe the mutation and selection process empirically?
How do population sizes, mutation rates, complexity of selection
conditions and other variable affect this process?” Professor Crow’s
response to me was “It is increasingly clear that there are some
problems that are too difficult to sort through verbally and which
require mathematics for deeper understanding.”

Professor Crow recognizes the importance of mathematics to describe
the mutation and selection phenomenon and the correct mathematical
derivations of the behavior of this stochastic process is obtained by
the proper application of the principles of probability theory.
Likewise the correct mathematical behavior of random recombination is
also obtained using the correct application of probability theory. You
hersheyh do not know how to apply the principles of probability theory
correctly. All you know how to do is plug in numbers into the wrong
probability distribution.

>Again, I make no claim to be a giant, merely someone who is able to understand what actual giants in the field say.

James F. Crow says it requires mathematics for a deeper understanding
of this problem and you don’t have the mathematical skills and are too
stubborn to learn them. Evolutionists are derisive, stubborn and
ignorant; no wonder we have multidrug resistant microbes,

multiherbicide resistant weeds, multipesticide resistant insects and

less than durable cancer treatments. All of this because of the crappy
pseudo-science practiced by mathematically irrational evolutionists
who are the teachers of the incorrect basic science and mathematics of

the mutation and selection phenomenon.

>> That claim alone certainly qualifies hersheyh as
>> a crank. Hersheyh claims that the joint probability of random events
>> is not governed by the multiplication rule of probabilities,
>When have I ever made that claim? This alone tells me that you are not capable of understanding what you read. Other >than your stupid division of the mutation rate by 4, we come up with the exact same joint probability for the situation you >describe where you select simultaneously for double-mutants under conditions where single mutation has no selective >advantage. I then describe a different selective scenario with quite different results and do so mathematically. You fail >to even attempt to calculate the probability of that scenario, essentially mumbling garbage that implies that somehow the >same numbers apply in that situation.

How many posts have you made defending Schneider’s claim that the
multiplication rule does not apply to biological evolution? And now
you are tossing out this rule with the random fixation of neutral
alleles. Hersheyh, your mathematical skills are limited to plugging in
numbers in someone else’s derived equation and invariably you use the
wrong equation to describe the particular phenomenon. Why don’t you
study the derivation of the Poisson distribution and find out why you
are wrong to use this equation, especially in the manner which you are
using it here.

>> hersheyh
>> uses the wrong probability distribution for his calculations,
>No I don't. Show me where you think I did so that you do not do so.
Go look up the derivation of the Poisson equation and look at the
stochastic process it is used to describe and find out why you are
wrong. If you don’t do it, you will remain a stubborn ignoramus. I’ve
derived the correct probability function for the mutation and
selection phenomenon and the best you can do is claim that a point
mutation is a binary process. You are wrong there as well.

>> hersheyh
>> thinks that the mathematical model that describes the fixation of a
>> single neutral mutation should describe the fixation of dozens of
>> neutral mutations simultaneously,
>No. It describes the final step of fixation of dozens of neutral mutations in the same generation. It is highly unlikely that >those fixations occur in the same organisms. Just in the population of that generation. I also recognize that, in large >populations, the very concept of fixation is fuzzy.

You are a squirming fabricator of evolutionist folklore. You remove
selection from the mathematics of mutation and somehow think that this
phenomenon can work in parallel when mutation with selection does not
work in parallel. This is the kind of mathematically irrational crap
that forms the foundation for your mathematically irrational belief
system.

>> hersheyh thinks that there are only
>> two possible outcomes from a point mutation
>I have never said that. I said that mutation is a binary event where an organism goes from one defined genetic state to a >different defined genetic state or states, even if the different genetic state is "any nucleotide different from the w.t. >original nt". But, in our case, we (and by that I include you) are NOT talking about point mutations. We are talking >about genetic mutations that produce a different phenotypic state. From antibiotic sensitive to antibiotic resistant. That >is how we identify something as a mutation different from the original state. You call that phenotypic difference >"beneficial" because you define survival in the presence of antibiotic as "beneficial" (although it is not likely to be >'beneficial' in the absence of the antibiotic).

You are wrong hersheyh. The probability function I derived was made
without making any assumption about a phenotypic change. I only
assumed that there would be a point change at a particular locus. Your
thinking is so sloppy and mushy, who knows what you believe.

>> and now hersheyh is going
>> to fumble around trying to cover up his ignorance of the probability
>> function which governs random recombination.
>Your description (aside from your stupid division of the defined mutation rate by four; apparently for no logical reason >related to how the mutation is identified, but solely because there are four possible nts in DNA) is nothing but simple >binomial probability distribution that can also be adequately described by other existing mathematical descriptions. As >pointed out, in many of the specific examples and scenarios used, the actual probability distribution is a Luria-Delbruck >distribution, which differs somewhat from the binomial distribution you write about (except for your stupid division by 4).

For those of you reading this post, the correct description of a
binomial process is one where you have only two choices such as 0 or
1, yes or no, positive or negative and so on. A point mutation has
more than two possible outcomes, detrimental, neutral or beneficial,
something for which hersheyh has yet to come to understand. And note
that hersheyh does not derive for us the probability function which
describes random recombination. I guess that’s one of the many things
that he doesn’t teach in his genetics courses.
>> > 2) Cranks insist that their alleged discoveries are urgently
>> > important.
>> Hersheyh obviously doesn’t think MRSA and other multidrug resistant
>> microbes are a problem. Since hersheyh has never practiced medicine, I
>> can see how he could make such an ignorant claim.
>You are the one who thinks you have 'discovered' the mathematics of multi-toxin selection. You aren't.
It certainly wasn’t taught to me by a mathematically incompetent
geneticist. Why don’t you look up in your mathematically baseless
lecture notes the derivation of the probability function for random
recombination? Or why don’t you look it up in your library of genetics
texts? Or why don’t google “random recombination probability function”
and see if you can find that derivation. It wasn’t any mathematically
incompetent evolutionists who derived the probability function for the
mutation and selection phenomenon. Mathematically incompetent
evolutionists plug in numbers in the wrong probability function and
think how bright they are.

>> > 3) Cranks rarely if ever acknowledge any error, no matter how trivial.
>> Hersheyh’s blunders are not trivial, they are major scientific
>> blunders such as his claim that the multiplication rule of

>> probabilities does not apply to biological evolution.

>If that were true rather than a lie, you might have a point. But a lie is a lie. What I said, and will repeat, is that proteins >and DNA did not evolve by simultaneous random assembly of genes from their constituent parts. That model of >evolution is a common creationist canard.

Hersheyh, you are a mathematically incompetent nitwit who lacks the
mathematical skills of a C grade high school student. You are a jerk
that thinks that removing selection from the mutation equation gives
more rapid evolution than does mutation and selection. You believe
things for which there is no empirical evidence such as parallel
evolution and you make claims for random recombination when you have
no idea how this phenomenon works. The only thing you are an expert on
is mathematically irrational evolutionist mush and we have multidrug

resistant microbes, multiherbicide resistant weeds, multipesticide

resistant insects and less than durable cancer treatments to thank you
for.

>At least I am not so stupid as to misunderstand how mutation rates are determined by stupidly dividing the determined >mutation rate by 4.
You are more than stupid; you are an ignoranus who can’t tell when a
process is binary or not.

>> It’s this type
>> of blunder which gives us MRSA.
>> > 4) Cranks love to talk about their own beliefs, often in inappropriate
>> > social situations, but they tend to be bad listeners, and often appear
>> > to be uninterested in anyone else's experience or opinions.
>> That’s a perfect definition for evolutionists. You indoctrinate naïve
>> school children with the mathematically irrational belief that
>> reptiles can be transformed into birds but neglect the correct
>> teaching of the basic science and mathematics of mutation and
>> selection.
>You are the one who is repeatedly presenting mathematical nonsense time every time you divide the determined >mutation rate by 4.
Go learn what a binary process is.

>> > http://www.google.com/url?sa=D&q=http://en.wikipedia.org/wiki/Crank_%2528person%2529
>> > It goes on:
>> > Many cranks
>> > 1) seriously misunderstand the mainstream opinion to which they
>> > believe that they are objecting,
>> I only disagree with evolutionists’ mathematically irrational beliefs.
>Only by misunderstanding the mainstream opinion.
We see what the evolutionist mainstream opinion has given us. The
mainstream evolutionist opinion has given us multidrug resistant

microbes, multiherbicide resistant weeds, multipesticide resistant

insects and less than durable cancer treatments. This has occurred by
the bungled mainstream evolutionist teaching of how mutation and
selection works. Mutation and selection does not work the way
evolutionist mainstream opinion claims.

>> The day that evolutionists hypothesizing and speculation disagree with
>> the mathematical and empirical evidence is the day that I disagree
>> with evolutionist indoctrination.
>And I agree with your mathematics of selection for double-mutation in selective conditions where single mutation is not >beneficial and total population size is greatly reduced (except, of course, for your stupid division by 4 and your apparent >failure to recognize that you are only testing individuals in one generation).
Well hersheyh, you almost understand how mutation and selection works
mathematically and the equation I derived for you is written as a
function of population sizes. And perhaps one day you will understand
the mathematical properties for a binomial process. And you just have
to learn that the population sizes used in this probability function I
derived for you are the subpopulations which would benefit from the
particular mutation. And that additional generations are one of the
ways that populations increase the number of trials for a particular
mutation. You are coming along heels dug in the entire way
demonstrating your stubbornness.

>> > 2) stress that they have been working out their ideas for many
>> > decades, and claim that this fact alone entails that their belief
>> > cannot be dismissed as resting upon some simple error,
>> Now I haven’t been studying mutation and selection for decades.
>It shows.
It doesn’t take very long to learn how to derive the probability
function which describes the mutation and selection process. All you
have to do is have some skill with the mathematics of dice rolling. It
also doesn’t take very long to learn the mathematics of random
recombination. All you need to understand to derive that probability
function is to have some understanding of random card drawing. What
shows hersheyh is that you have no skill in either of those areas. I
could give you every hint in the book and you still couldn’t derive

the correct probability function for random recombination.

>> I only
>> seriously started studying the phenomenon when I analyzed Schneider’s
>> ev simulation of evolution. Once I saw the behavior of his model and
>> how this behavior correlates with the empirical data, it became
>> obvious how mutation and selection works. And evolutionists have made
>> a simple but major error when analyzing the stochastic process of
>> mutation and selection and that error was and is to believe that the
>> multiplication rule of probabilities does not apply to this process.
>Does that mean that you think that genes are produced in organisms by random assembly of the entire sequence from a >pool of nucleotides?
You are such a mathematically incompetent jerk hersheyh. Abiogenesis
is the dumber of the two dumb concepts that form the foundation of the
mathematically irrational evolutionist belief system.

>> Evolutionists have demonstrated a stubborn intransigence to
>> acknowledge this major scientific blunder.
>It is not error to claim that evolution does not involve (and no biologist thinks it does) the random assembly of genes from >constituent nucleotides.
So is it the evolutionist irrational belief that when the era of
abiogenesis ended that every gene known was already available in the
gene pool of the early life forms? That’s a load of mathematically
irrational evolutionist crap.

> > 3) compare themselves with Galileo or Copernicus (or in a religious
> > context, Noah), implying that the mere unpopularity of some belief is
> > in itself evidence of plausibility,
> So hersheyh, who do you compare yourself to,
Anyone with a reasonably good understanding of genetics, mutation, and
selection.
So if you have a reasonably good understanding of genetics, derive for
us the probability function which describes random recombination. I’ve
given you hints which should enable you to easily derive this
equation. We already know that you think that the Poisson distribution
is a good approximation of the mutation and selection phenomenon. That
blunder definitely disqualifies you as someone with a reasonably good
understanding of mutation and selection phenomenon. Now if you want to
understand why you are wrong, look up the derivation of the Poisson
equation and find out why the random mutation does not qualify as a
Poisson random variable.

hersheyh Aug 24, 4:32 pm

Newsgroups: talk.origins
From: hersheyh <hershe...@yahoo.com>

Date: Wed, 24 Aug 2011 16:32:36 -0700 (PDT)
Local: Wed, Aug 24 2011 4:32 pm

Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

>> > Replacement of allele does not require lethality or toxicity.
>> If you were correct then no microbes would ever evolve resistance to
>> any antibiotics
>Totally irrelevant to what I said. I said that replacement of an allele in a population does not require either lethality or >toxicity. It does require *differential reproductive success*. Differential reproductive success is inherently relative rather >than absolute. Organisms with allele A can outcompete organisms with allele A' with either no change in population size >or increase in population size as well as your cases, which involve a massive decline in population size.

Hersheyh, why don’t you tell us what you think a selection pressure
does to a population? Tell us what thermal stress does, tell us what
starvation stress does and tell us how this differs mathematically
from chemical selection pressures. What happens if a population is
under both thermal stress and starvation stress?

>> but obviously you are not correct. All selection
>> conditions have lethality or reduce fecundity to some or all members
>> of a population.
>Only relative to individuals with the alternate allele.
That is not correct at all. Do you think that some members of a
population are only sensitive to a selection pressure if other members
are not? Where do you get these off the wall ideas? Oh, I forgot, you
are an evolutionist.

>Take the following example where the population size remains constant and the % of population with A' changes >dramatically from 1% (I chose a total population of 100 so even you could calculate the percentages) to 100% as the >number of A' individuals doubles each generation. It isn't that individuals with A were *worse* at growing at the end than >they were at the beginning. Just that those with A' were, relative to A, better. If there were no individuals with the A' >allele at the beginning (as in the first two generations), the population would not have decreased at all.
>Generation: 1 2 3 4 5 6 7 8 9 10
>Allele A #: 100 100 99 98 96 92 84 68 36 0
>Allele A' #: 0 0 1 2 4 8 16 32 64 100
>Total #: 100 100 100 100 100 100 100 100 100 100
>Are you saying that the above is impossible?

Hersheyh, you are so low on the learning curve, it’s incredible. And
you say you’ve been teaching genetics for 20 years? No wonder we have

multidrug resistant microbes, multiherbicide resistant weeds,
multipesticide resistant insects and less than durable cancer
treatments.

>> You continually ignore the results of the evolution
>> of HIV to combination therapy where none of these drugs are lethal to
>> the virus
>Both intentionally greatly reduce virus production for the w.t. virus. So, yes, they meet the criteria of being toxic agents >that kill or greatly reduce reproduction of the genetically sensitive organisms.
You still haven’t done the following computation. If the viral load is
reduced to 40 viruses/ml of blood, how many viruses in a patient with
a controlled HIV infection. And note, that does not include viruses in
tissue.

>> and therefore the virus is not driven to extinction.
>Since the *number* of resistant viruses is the product of the rate of generation of resistant virus times the population >size, the consequence of using the toxic agent (and the purpose for using it) is to reduce the population size to one >which does not cause problems at least for the length of the host's life. That is why one uses agents that are toxic to HIV >reproduction.
That’s a crap equation you have come up with since you have ignored
the number of generations for which the population can reproduce which
increases the number of trials for the beneficial mutations. The
reason why the population can not come up with resistant viruses is
that any mutations beneficial to one drug or another can not be
amplified due to the competing selection pressures. In your
mathematically irrational evolutionist mind, you think that
“combination natural selection pressures” like thermal stress and
starvation will not inhibit amplification of beneficial mutations to
one stress or another.

>> Yet HIV
>> can not evolve efficiently to selection conditions targeting two genes
>> simultaneously. This is all due to the multiplication rule of
>> probabilities; the rule which you and Schneider so erroneously claim
>> does not apply to biological evolution.
>Liar. Liar. Pants on fire. I have *never* claimed that and neither did Schneider. We both claim that genes are not >poofed into existence by random assembly from pools of precursor nts. I specifically (and unlike you, correctly, since I >don't divide by 4) used the multiplication rule in my description of selection conditions that select only for double-mutants. > Is it possible that you did not recognize that I used the multiplication rule in all my probability descriptions? If so, that is >your problem, not mine.

Hersheyh, there is no ambiguity to Schneider’s claim and you now know
that the multiplication rule applies whenever more than a single
beneficial mutation is required for an evolutionary process. Schneider
understands what a binary process is even though you don’t. I’ve
derived for you the correct probability function for two mutations to
occur and these equation form the basic science to explain why
Schneider’s ev model behaves the way it does. The multiplication rule
of probabilities is the central governing mathematical principle for
the mutation and selection phenomenon. And Schneider has made a half
hearted retraction of his claim on his blog but believes that
recombination will somehow come to the rescue of his mathematically
irrational theory of evolution. The correct derivation of the
probability function for random recombination shows that he is wrong
and explains why random recombination does not have a significant
effect on the mutation and selection of HIV to combination therapy.

hersheyh Aug 25, 8:50 am

Newsgroups: talk.origins
From: hersheyh <hershe...@yahoo.com>

Date: Thu, 25 Aug 2011 08:50:58 -0700 (PDT)
Local: Thurs, Aug 25 2011 8:50 am

Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

On Tuesday, August 23, 2011 8:52:29 PM UTC-4, Alan Kleinman MD PhD
wrote:
>> > > > > > > > > I understand that but you are making a variety of assumptions such as
>> > > > > > > > > assuming such that the Poisson distribution is the appropriate
>> > > > > > > > > distribution function to describe these probabilities. I m not making
>> > > > > > > > > this assumption. I m starting from the fundamental axioms of
>> > > > > > > > Do you even know what a Poisson distribution means? Can you explain
>> > > > > > > > it? Can you please explain why you think a Poisson distribution is not
>> > > > > > > > appropriate here?
>> > > > > > > The Poisson distribution is a distribution function which has
>> > > > > > > importance in statistics. This function has some application in
>> > > > > > > physical problems and is sometimes used when the exact distribution
>> > > > > > > function is not known.
>> > > > Nice. Which statistics text are you parroting here, without
>> > > > attribution.
>> > > That’s a basic concept from any introductory text on probability
>> > > theory.
>> > You seem to have taken a segment of that introductory text that
>> > doesn't tell you shit about what the 'importance' of the Poisson is.
>> > There is no way to tell from your squawking parroting whether or not
>> > my use of the Poisson is appropriate in the context I used it. It is.
>> Being a foul mouthed evolutionist crank, I doubt you have ever gone
>> through the derivation of the Poisson probability or distribution
>> function.
>Nope. Never have. But I bet you haven't either. I, OTOH, am capable of reading and understanding what I read. It is >not like the Poisson has been unexplored until now. Mathematicians do set the parameters under which these equations >are useful and when they are less useful. I am using the Poisson under conditions where it is an excellent >approximation of the binomial probability distribution.
Well now, we have a mathematically incompetent evolutionist who wants
to make a wager and I do enjoy making wagers where there are no
probabilities involved. So you wager that I have never gone through
the derivation of the Poisson probability function. Let’s make this
wager for an interesting amount. I would estimate that an over-paid
mathematically incompetent geneticist should be able to come up with
$10,000. Let’s make the wager to the charity of the winner’s choice
and don’t forget to get your pen and checkbook ready.

So here it is, we have a mathematically incompetent evolutionist who
uses the wrong probability function, makes the wrong assumptions about
population sizes and has never taken the time out to go through the
derivation of the equation that he uses improperly. Could you ever be
less thorough in the analysis of a physical phenomenon? No wonder you
have no idea how mutation and selection actually works.

>> If you had, you would immediately see that it is the wrong

>> probability function to describe the mutation and selection

>> phenomenon.
>Where exactly is the error. Sorry if I do not accept your word for it, since you have demonstrated gross incompetence >here in understanding terms like "mutation rate", "event", "trial", "gene", "allele", etc. Show me *exactly* why the Poisson >does not work (accurate within about 10 significant figures) under the conditions described. Is it because you think your >division by 4 has some meaning other than "Take the mutation rate and arbitrarily divide it by 4 because there are 4 >possible nts"?
I’ve accepted your wager and if you think you are so smart, do your
wager for $10,000 to the charity of the winner’s choice. I think its
time for you to start doing your own homework. Your first assignment
is to go through the derivation of the Poisson probability function.
Your second assignment is to go through the analysis of when the
Poisson distribution is a limiting case of the binomial distribution
(which is not the distribution function for the mutation and selection
phenomenon). Under what circumstances does the Poisson distribution
give a reasonable approximation of the binomial distribution? When you
do these assignments you will know where your error is. Let’s see if
you are actually ready to learn some mathematics.

>> If you had ever taken a decent lower division mathematics
>> course, you might have seen that derivation. You would find that
>> derivation in a different chapter from the one which teaches (a^x)^y =
>> a^(x*y) but they are both lower division mathematical concepts. But
>> you are a crank evolutionist and won’t admit this
>I prefer the form a^(x*y) in our case because it clarifies rather than muddies what we are looking at in terms of events (a) >and trials (x*y). That the two forms are mathematical identities is irrelevant to that reasoning. But perhaps you have >good reason for trying to muddy up and complexify the equation you present. It fools the rubes you see as your main >audience.
You are the rube hersheyh and a mathematically incompetent one at
that. What I wrote can be found in any lower division algebra text, a
course which you obviously couldn’t pass. Your mind is muddied up with
evolutionist dogma and you are easily confused when the correct
probability function is derived for the mutation and selection
phenomenon. I am so sorry I confused you with a basic algebraic
principle. This is why you are an evolutionist crank who believes in a
mathematically irrational belief system. You simply don’t have the
skills or training to do this type of computation.

>> > > I may have parroted that from that text
>> > Mindlessly, as parrots seem to do.
>> > > but at least I don’t
>> > > parrot the evolutionist bird brained concept that birds were
>> > > transformed from reptiles.
>There is ample evidence (from fossil evidence to DNA evidence) that modern birds have been transformed from >ancestral birds which were, in turn, transformed from reptile-like birds which were transformed from bird-like reptiles. > Which particular step in that process do you regard as "bird-brained"?
The evolutionist bird brained claim that mutation and selection can
make such transformations. It is mathematically irrational and the
only thing dumber than that evolutionist claim is that randomly
reacting chemicals can spontaneously give rise to living replicators.
This kind of mathematically irrational crap has no place in any
science course. It only obscures the basic science and mathematics of
the mutation and selection phenomenon, the teaching of which does have
a place in a science course but which is not taught by evolutionists.

>> > Again, birds didn't evolve from modern reptiles but from theropod
>> > dinosaurs that were hard to distinguish from the oldest birds.
>> Written from the hand of hersheyh, an evolutionist crank that neither
>> understands the basic science and mathematics of the mutation and
>> selection phenomenon nor understands the mathematics of random
>> recombination.
>Repeating falsehoods without supporting evidence won't harm me. If you can actually point out where I do not >understand the basic science and mathematics of the mutation *or* selection phenomenon or the mathematics of >random recombination in eucaryotes I will happily acknowledge that. So far, all you have demonstrated is the it is you >who doesn't understand much about either mutation or selection and the mathematics concerned with it.

You have already admitted that you use a probability distribution
which you have never gone through the derivation of. You use
population sizes in your calculation which have no real correlation to
the mutation and selection phenomenon. You claim that mutation and
selection can occur in parallel but have yet to post a single
empirical example of your claim. You grossly over-extrapolate a simple
model of neutral evolution and we have John Harshman making the claim

that a couple hundred neutral mutations are fixed every generation

when at the same time you claim that neutral evolution is slower than
the fixation of a mutation with selection and that process takes
hundreds of generations per mutation. You have no idea how to derive
the probability function that describes random recombination. You are
confused by a basic algebraic identity and accuse me of trying to
confuse you when you were confused before this discussion ever
started. And you are stupid enough to bet me that I have never gone
through the derivation of the Poisson probability function. I’m going
to enjoy choosing the charity to send your $10,000 check.

>Again, I have *repeatedly* said that your derivation of the binomial probability distribution equation where you divide the >rate by 4 is stupid. If you can point me to a single scientific article in either an math or science journal or a textbook >where they present the mutation rate and divide it by 4, I will seriously consider that you might be right. But it is clear >that you have done that division for no good reason, most likely because, in your pea brain you thought that somehow >the number of possible nt forms should be included.
You have a problem with anything that is presented to you that you are
not familiar with. You are comfortable with your mathematically
irrational theory of evolution. You have never put much thought into
how the stochastic process of mutation and selection actually works.
You still don’t understand when the Poisson distribution is a good
approximation of the binomial distribution and that’s because you
never did a good analysis of the equations involved. And you still
don’t understand that the correct probability function for the
mutation and selection phenomenon is not the binomial probability
function.

>I again point out that mutation rates have been measured well before there was even the knowledge that DNA was the >genetic material, so clearly it is not measured by division by 4. Mutation is defined as a change in genetic state from an >initial condition (typically identified by its phenotypic effect in some environment) to a different genetic

Hersheyh, that is a load of crap and you should know it. The
techniques used to estimate the mutation rate can and often are off by
several orders of magnitude. If you are depending on a phenotypic
change, you will not be able to detect neutral mutations at all. But
the greatest blunder you are making is not understanding how mutation
rate affects the mutation and selection phenomenon when compared to
the other variables involved. And you don’t understand this because
you have never done the analysis. You don’t study and test the
validity of the equations you use and the end results is that you have
a sloppy and confused understanding of how mutation and selection
actually works. What you need to learn about is ill-conditioned
equations because the probability function for mutation and selection
is ill-conditioned with respects to the mutation rate.

hersheyh Aug 25, 11:27 am

Newsgroups: talk.origins
From: hersheyh <hershe...@yahoo.com>

Date: Thu, 25 Aug 2011 11:27:16 -0700 (PDT)
Local: Thurs, Aug 25 2011 11:27 am

Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

> [snip]
>> > (1-p)^(n*g) is the probability of k = exactly zero mutants in a tested
>> > population of size n*g. 1 - that probability (the probability of
>> > finding zero mutants in a population of size n*g -- now do you see why
>> > I prefer to use the non-exponential form?) is the probability that
>> > there will be one or more mutants in a tested population of size n*g.
>> This must fall into the category of what you have forgotten from your
>> meager mathematical training. (a^x)^y = a^(x*y) and you didn’t know
>> this and you won’t admit this. This is why you are an evolutionist
>> crank.
>I didn't say that the two are unequal. I said I *prefer* a^(x*y) in this case because it more clearly conveys what is actually >going on, which is the binomial probability distribution. That is because x*y, or N (number of individuals per >generation)*g (number of generations) in our case, is clearly the total number of tested individuals or, in terms of the >equation, the total number of trials tested for the presence of the event. Using the exponential form, although equivalent, >hides that relationship between the actual measurements made and the general form of the binomial probability >distribution.

Why don’t you just admit that you don’t remember this from your
dumbbell evolutionist math course (if they ever got that far)? And you
are still bungling the math anyway. N*g does not give the total number
of trials. The total number of trials is also dependent on the
mutation rate. By far, most of the population replicates at a give
locus without error when you have a mutation rate of 10^-8 and thus no
trials are being performed. The only time a trial occurs is when a
mutation happens at a particular locus. You can think of it this way,
if the mutation rate were zero and the population could reproduce
perfectly, there would be no trials at all. A trial only occurs when
there is an error in reproduction. The actual numbers of trials
performed is very small, this is why you need your population sizes of
10^9 to get a reasonable number of trials (3 or 4) when the mutation
rate is 10^-8. This is the main reason why you can’t use the Poisson
distribution to approximate this stochastic process. The number of
trials needs to be going to infinity in order for the Poisson
distribution to be used to approximate a binomial distribution and in
the mutation and selection phenomenon, the number of trials is
actually very small. When the trial (mutation) does occur, you have a
1 in 4 probability that you will get the beneficial mutation.


>> > > Then the complement rule is used
>> > > to compute the probability that the particular mutation WILL occur at
>> > > a particular locus in population size n in g generations.
>> > I agree. 1 - (1-p)^n*g is the probability of finding at least one
>> > mutant in a tested population of size n*g.
>> Other than your failure to understand that a random point mutation has
>> 4 possible outcomes,
>I don't give a flying fig whether the mutant in question (which is a cell that is resistant to a toxin) has an A, G, C, or T >present. All I need to calculate the mutation rate from the original genetic state (observed by the empirical feature that >the original cell population was toxin-sensitive) to the mutant genetic state (observed and counted by the empirical >feature that the cell is toxin-resistant). The *event* is not some nebulous 4 outcomes. It is the presence of the mutant >phenotype which is contrasted to the absence of that phenotype in the original population.

Hersheyh, you still don’t understand the mathematical behavior of this
probability function. The probability function for mutation and
selection is an ill-condition equation. Since it is highly unlikely
you ever studied the principles of ill conditioned equations, I’ll try
to explain this in layman terms. Errors in the estimates for mutation
rate will only have a small affect on the computed probability for the
event to occur. However, if you turn the situation around and try to
estimate the mutation rate from a known population size and number of
generations can give you very large errors in your estimates of the
mutation rates. You have to have extremely high accuracy in the
measurement of your variables to give an accurate estimate of the
mutation rate. If you want to get accurate estimates of mutation
rates, you need to sequence the parent and child genomes and actually
measure the differences. You really need to go back and study
mathematics if you want to understand how to analyze these types of
equations.


>> it has taken only dozens, perhaps hundreds of
>> your crank evolutionist posts to finally admit this. But you still
>> don’t quite get it.
>The rate of mutation to achondroplastic dwarfism is determined by counting the number of achondroplastic dwarfs born >to normal parents and dividing by the number of all children in the population examined that are born to normal parents. > It is not determined by dividing that number by 4. I cannot think of a single reason to divide by 4 *even* if one were >examining the change from the original nt to any other nt. Such a division is stupid, stupid, stupid. You probably think >that doing so is brilliant. You are wrong. Even if you were looking at the mutation rate from the genetic state of having a >C at position 1093 to having any other nt, you would not simply divide by 4 (or even 3). You would empircally determine >*by measurement*, the number of individuals with some nt other than C, which would be the "event", and divide by the >number of individuals tested, which would be the number of "trials". It is highly likely (because transition is favored over >transversion) that most of the mutants wo

uld have a T at this position.

This is the conundrum of arguing mathematics with a mathematically
incompetent nitwit. Doing a computation the way you describe can give
an estimate of mutation rate that can be orders of magnitude
inaccurate. But it has no bearing on the way the mutation and
selection phenomenon actually works. If it makes you happy to compute
mutation rates this way, go for it. But you can’t expect to use that
value to understand how mutation and selection actually works.

>> It is not a population size of n*g, it is a
>> population size which is a function of generations times the number of
>> generations which is proportional to the total number of trials.
>I thought your claim was that the two equations ((1-(m/4))^n)^g = (1-(m/4))^(n*g) were mathematically equivalent? Are >you now claiming that they are different? Of course, I would not divide the mutation rate, m, by 4, but would use the >actual measured mutation rate. If that were mutation from a state of toxin-sensitivity to a state of toxin-resistance, the >number of resistant individuals would be the numerator and the number of tested cells would be the denominator. If that >were mutation from C to not-C at a nt site, the number of individuals with not-C would be the numerator and the number >of cells examined would be the denominator.

The two equations are equivalent. A trial only occurs when a mutation
occurs. The value of n*g does not give the number of trials performed.
This is the mistake you make in substituting the Poisson distribution
for the binomial distribution. In order to make that approximation,
your number of trials needs to be large, going to infinity. The number
of trials in the mutation and selection phenomenon is actually quite
small but when they do occur, you have a 1 in 4 probability that you
will get a particular mutation. There is another reason why the
Poisson distribution is not the correct probability distribution for
the mutation and selection phenomenon. Go through the derivation of
the Poisson distribution and find out why.

>> For
>> example in generation 1, you have population size n1 which is
>> proportional to the number of possible trials. In generation 2 you
>> have population n2 giving you n2 which is proportional to the number
>> of possible trials and so on.
>You do not have any trials until you examine the cells for the presence of event. What you must mean, if you have any >brains at all, is that *if* one were to examine the cells in generation 2, when the total population is n*2^g (n is the starting >population size, 2 is the growth factor and g is the number of generations of doubling), the total number of trials would be >n*4. When you do not examine until generation 30, the correct number is n*2^30. I have used 10^9 as a rough estimate >for the number of individuals tested after 30 generations. But a 'trial' only exists when an individual is tested, and once >tested, it must not be tested again in the next generation.

Mutations occur whether there are selection pressures or not. The
population does not need to be examined to determine if it will
respond or not. And the way the population will respond is that less
fit members will reproduce less and more fit members will reproduce
more. What this will do is change the subpopulation sizes on a
generation by generation basis. And if the subpopulation size can
increase enough and has enough generations of reproduction, the
subpopulation will have a reasonable probability that one of its
members will do the trial (mutation) and it has a 1 in 4 probability
that the next beneficial mutation occurs at the proper locus and it
will be the progenitor of the new subpopulation for the next
beneficial mutation.

>> And those trials must occur on members
>> of the population who would benefit from that particular mutation.
>If by this you mean that the *event or events* (not 'trials') must be detectable in each *trial* examined for an event, sure. > If your selective conditions are such that only double-mutants can be detected, then single mutants do not exist for you. > They would be lumped into the category of not-a-double-mutant.

What I mean is that not only to the beneficial mutations have to occur
at particular loci, they have to occur in a subpopulation which would
benefit from those mutations. Go back and read the Weinreich paper. A
beneficial mutation for one subpopulation (variant) may not be
beneficial for a different subpopulation (variant). Any time an
evolutionary process requires more than a single beneficial mutation
you will have a double mutant or in the case of the Weinreich
experiment, a quintuple mutant. It is very unlikely that these
mutations would accumulate without amplification between each
mutational step.

>> How
>> many more of your crank evolutionist posts will it take before you
>> admit that I derived the correct joint probability of two mutations
>> occurring?
>Except for your stupid division by 4 and some confusion on your part about what a trial means, your equation is the >same as the one I would use in examining a set of trials (individuals) for the presence or absence of double-mutants >under conditions where the single-mutants have no independent utility and are ignored.

Well, we’ll still have to conclude that you are a mathematically
incompetent nitwit who has yet to learn that when a trial (point
mutation) does occur at a particular locus that there are 4 possible
outcomes from that trial. The trial is the mutation and if a member of
a population reproduces without error at the particular locus, that
member is not performing a trial. You seem to think that any
reproduction of a member constitutes a trial but it doesn’t. Only when
there is an error in reproduction is a trial being performed.

>If the single-mutants do have selective utility and increase in frequency because of their independent utility and >assuming the absence of recombination, then the frequency of both single-mutants will change from generation to >generation. That secular increase in the frequency of the single mutants would change the probability of finding one or >more double-mutants each generation.

An increase in frequency is not what improves the probability for the
next beneficial mutation to occur at the proper locus. It is an
absolute increase in number of the subpopulation that would benefit
from the next mutation. If the subpopulation size is 1 as would occur
with the progenitor of a new subpopulation on the next step of the
fitness landscape; that beneficial allele would have a frequency of 1
but until that progenitor and its descendents amplify that beneficial
mutation, the probability is extremely small that the next beneficial
mutation will occur at the proper locus. The subpopulation must grow
and until there is a reasonable probability that one of its members
will perform the trial for the next beneficial mutation.
>> A computation which requires the invocation of the
>> multiplication rule of probabilities, a principle which both you and
>> Schneider claim does not apply to biological evolution. Hersheyh, you
>> and Schneider are both crank evolutionists who will not admit when you
>> are wrong despite the fact that your mathematical and scientific
>> blunder harms millions of people.
>I certainly will not admit that the assumption that genes are generated by random assembly of subunits from scratch in >evolution is true. But that has nothing to do with the use of the multiplication rule. Under the false assumption that >genes are made by random assembly from scratch, the creationists use of the multiplication rule is just fine. But it is >GIGO nonsense that has no relevance to how evolution actually works.

Good for you. It’s good to see that you discard the concept of
abiogenesis except when you apply these principles to your neutral
evolutionary theory. I suppose you don’t admit to the shooting of John
Kennedy or the disappearance of Jimmy Hoffa but you really should
admit to the multiplication rule of probabilities being the central
governing mathematical principle for the mutation and selection
phenomenon.

>> > > The
>> > > population size n does not need to remain constant over the
>> > > generations g. Changing the population size in any given generation
>> > > simply changes the number of trials done for the particular mutation
>> > > in that generation.
>> > Sure. All that matters is the total number of trials (individuals
>> > tested for the described event).
>> And what you fail to understand is that the trials must occur on
>> individuals who would benefit from the particular mutation, not just
>> any member of the population. But you won’t admit this because you are
>> an evolutionist crank.
>Oh. I know it quite well. Which is why I contrasted the probability of finding one or more double-mutants in the one-step >procedure you describe and, using the same numbers, for the 3-step mechanism I describe. You know the one you >keep implying has as low a probability of success as your 1-step process but never actually analyze mathematically.

Here’s another load of your mathematically irrational evolutionist
crap coming at us. You do keep a regular delivery schedule on this bs.
You always use a population size of 10^9 in your incorrect
computations. And you already owe me $10,000 for your wager whether I
went through the derivation of the Poisson equation. Care to make
another wager whether I analyzed the probability function I have
derived for you? And mutation and selection is a beneficial mutation/
amplification of beneficial mutation cycle when it works, not any of
your silly 1 or 3 step mechanisms.


>> > > > p is (pick whatever value you'd like, I don't care)
>> > > > g is 5
>> > > > What's n?
>> > > n is the population size
>> > No. n, as you define it, is the population size tested per
>> > generation. That is why I define n as the total population tested and
>> > use N for the population tested per generation. If N varies from
>> > generation to generation, you can either use a mean value for N or you
>> > can use the equation 1 - (1-p)^(sumN for N1, N2, N3...) where you
>> > basically add together the N value of generations 1, 2, 3... for as
>> > many generations as you test for the event.
>> Reread my post above. n is the population size tested in the
>> particular generation and n also has the requirement that members of
>> that group will benefit from the particular mutation. You can’t willy
>> nilly use a population size of 10^9 like you so sloppily do.
>I used that to show that you can have a high probability of double-mutants in that small a population if you look at the 3->step mechanism rather than the 1-step mechanism, which used the same sized population at its one step, AIR. ...

And if amplification is suppressed as what occurs when you have
selection targeting two or more genes, the probability of obtaining a
double-mutant becomes vanishingly small. This is why combination
therapy works wherever it is tried and why the theory of evolution is

a mathematically irrational belief system.

hersheyh Aug 25, 8:37 pm

Newsgroups: talk.origins
From: hersheyh <hershe...@yahoo.com>

Date: Thu, 25 Aug 2011 20:37:59 -0700 (PDT)
Local: Thurs, Aug 25 2011 8:37 pm

Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

>> > And doing a botch of it. Your equation, as you wrote it, is wrong
>> > because you take mutation rate and divide it by 4 for reasons that
>> > make no sense whatsoever. Once you correct for that bit of idiocy,
>> > you do calculate the probability of finding one or more double-mutants
>> > in a population correctly. Of course, for some reason you think that
>> > you are dealing with multiple generations when, in actuality, I have
>> > been discussing testing 10^9 bacteria in a single generation for the
>> > presence or absence of the mutant or double-mutant individuals. You
>> > seem to have a very weak understanding of the probability formula you
>> > are using, not even understanding that it is *exactly* the same
>> > argument as a binomial probability mass distribution argument.
>> Hersheyh, you can remain a mathematically incompetent nit wit for as
>> long as you wish. A point mutation can have more outcomes than
>> beneficial mutation or not beneficial mutation.
>How do you identify a mutation if the only thing you know about it is that it is "beneficial"? In fact, if you cannot identify >the mutation, how do you know it is "beneficial"? Can you tell me how to identify "beneficial"? I know how to identify >"toxin-resistance" and "toxin-sensitive". I know how to identify red eyes and white eyes in Drosophila. I know how to >identify a C at a specific nt site and when some other nt is present. I may even know the conditions under which one of >these detectable traits is "beneficial" relative to the other. But I cannot identify some nebulous concept like "beneficial".

It’s not important whether you identify the mutation as beneficial or
not. The population will do that for you. And the way the population
will do that for you is by amplifying the mutation. If the mutation is
neutral or detrimental, you will have a much more difficult time
identifying its presence because the number in the population will
remain constant or drop over time.

>> And I understand that
>> in your limited evolutionist indoctrinated mind you can not comprehend
>> trials for events in more than a single generation.
>Sure I can. No problem at all. I've already described

I’ve derived the mathematical relationship for you, none of your blah,
blah, blah descriptions.

Greg Guarino Aug 26, 7:35 am

Newsgroups: talk.origins
From: Greg Guarino <gdguar...@gmail.com>

Date: Fri, 26 Aug 2011 10:35:40 -0400
Local: Fri, Aug 26 2011 7:35 am

Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

On 8/26/2011 9:35 AM, Alan Kleinman MD PhD wrote:

>> On Aug 1, 6:34 pm, John Harshman<jharsh...@pacbell.net> wrote:
>>> Alan Kleinman MD PhD wrote:

>> John, if you are going to claim that the probability of fixation of a
>> neutral allele is equal to its frequency, then the probability of
>> fixation of two neutral mutations is the product of the individual
>> frequencies, an extremely low probability event.
>My knowledge of probability is limited, and yet I can spot your error
>immediately. You have computed the probability of two *particular*
>mutations proceeding to fixation, not the probability that *any two*
>mutations will.
>Can you grasp the difference between the probability that *any* two
>people will win the lottery as opposed to the probability that Mr.
>Arthur Feinberg and Ms. Anna Giannelli will win simultaneously?
>Incidentally, I am not claiming that this example uses the same math.
Greg, imagine our political leaders decide that the way to solve our
societal economic problems is to run lotteries, lots of lotteries in
fact millions of lotteries. So our wise leaders institute this program
and now millions of people start buying lottery tickets randomly in
several lotteries. What do you think the probabilities will be that
anyone will win two lotteries, “any two” lotteries?

>>>> Differences in genomes only accumulate by common descent
>>>> whether these differences are beneficial, neutral or detrimental.
>>> When has anyone claimed otherwise?
>> And selection is the only efficient way to transform genomes. The
>> claim that drift does it more quickly is mathematically irrational.
>>>> So tell us John, if the neutral differences appeared millions of years
>>>> ago and are only being fixed now, when did these 40,000,000
>>>> differences between the human and chimpanzee genomes occur?
>>> What do you mean by "occur"? If you refer to fixations, a few of them
>>> have happened each generation for the past 5 million years or so. If you
>>> refer to the original mutations (the ones that eventually became fixed),
>>> a few of them happened each generation starting many millions of years
>>> before that.
>> It’s much more than a few which have to be fixed each generation, its
>> dozens of neutral mutations which must sweep through the entire
>> population each generation. This is in contrast to the rate at which a
>> beneficial mutation can sweep through a population. In that case it
>> takes hundreds of generations for a single beneficial mutation to
>> substitute into a population.
>>> I remain amazed at your inability to understand the simplest features of
>>> neutral evolution. How is this possible?
>> I admit I have a problem understanding the incoherent and
>> mathematically irrational evolutionist arguments.
>No, you have a deep seated need to believe that all of your opponents
>are not just mistaken, but idiots. This allows you to dismiss their
>arguments without bothering to actually comprehend them. It makes you
>look silly though, tilting mightily against arguments no one has made.

Greg, I don’t think evolutionists are idiots; I think they are
mathematically incompetent and failed to properly describe the basic
science and mathematics of the mutation and selection phenomenon and
in the process have harmed millions of people. Evolutionists start
acting like idiots when they are presented with the mathematical and
empirical evidence of how mutation and selection actually works but I
attribute this to someone challenging their indoctrination. You
recognize that there is an accounting problem with the fixation of
millions of substitutions in a population in only 500,000 generations.
Evolutionists do not have a mathematically rational argument to
explain how these genetic transformations can occur so quickly in such
a small number of generations.


>Once again, John claims that each neutral fixation takes a very long
>time, much longer than a mutation that has been selected for, but many
>many of them are in flux at once, as are the much, much greater number
>that are disappearing.

I know, you have Toyota Tundras and Priuses giving birth to little
Corollas, some of them evolving undercoating, others evolving ABS and
airbags, all being done in parallel until they recombine and we have a
Lexus.

>>Now if you could
>> ever make a rational and coherent argument and support it with more
>> than “conceptual examples”
>Your argument is about "mathematical irrationality", which makes
>conceptual examples appropriate. If you would like to concede that such
>examples are not "mathematically" irrational, we could then discuss
>whether they are representative of real-world processes.
>Greg Guarino
Go for it Greg. Hersheyh and others are arguing that the mathematical
and empirical evidence does not preclude the possibility that mutation
and selection can occur in parallel. It’s easy to say in a
hypothetical example that two beneficial mutations can amplify
simultaneously therefore allowing mutation and selection to work in
parallel but present a real world example of this. The reason why I
discount this argument is that there is not empirical evidence which
supports this concept and in fact all the empirical evidence
contradicts this notion. And there is a good explanation for why there
is no empirical evidence for your hypothetical parallel evolution
process and that is selection pressures acting on multiple genes do
not form a cooperative process. Both selection pressures are
inhibiting growth of those populations. So even if a beneficial
mutation occurs for one of the genes, selection pressure acting at the
other gene will inhibit reproduction of that member impairing the
amplification process.

You can develop a similar type of argument for random recombination.
In an evolutionist hypothetical argument, an allele A for one
selection condition can recombine with a beneficial allele B in
another member of the population to give a descendent with both
beneficial alleles A and B. But why doesn’t this happen with HIV which
does recombination. The answer is found by deriving the correct
probability function which describes random recombination.


John Harshman Aug 26, 8:14 am

Newsgroups: talk.origins
From: John Harshman <jharsh...@pacbell.net>

Date: Fri, 26 Aug 2011 08:14:43 -0700
Local: Fri, Aug 26 2011 8:14 am

Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

>>>> Millions of years ago,
>>>> millions of neutral mutations are now being fixed in everyone s
>>>> genomes today.
>>> No. Only a couple of hundred per generation.
>> So the joint probability of that mathematically irrational claim is
>> the product of the initial frequencies of those neutral alleles. And
>> if we use your assumption of an initial frequency of 1/(5*10^9) and
>> raise that to the 200 power and that happens every generation,
>> generation after generation for hundreds of thousands of generations,
>> I would say you flunked Sesame Street.
>That's a stupid calculation. You are calculating the probability that
>200 particular mutations will be fixed, when in fact it's just a random
>200 from many billions. This is like calculating the probability of a
>particular bridge hand (1 in 52 factorial) and using that as evidence
>that no bridge hand is possible.
I see, your particular neutral mutations being fixed are not subject
to the multiplication rule of probabilities. I think the tried and
true rules of probability theory and the multiplication rule of
probabilities for the joint probability of events trumps your
mathematically irrational claims.

>>>> This is the kind of irrational crap that evolutionists
>>>> have to dredge up to try to explain why mutation and selection didn t
>>>> do it.
>>> What exactly is irrational about these claims? Be very specific.
>> (1/(5*10^9))^200
>Or to take another analogy, if the probability that you will win the
>lottery is 1 in 200 million, what's the probability that someone will
>win the lottery? A bit larger, I would think, not smaller.
John, you are claiming that millions of lotteries are being won by the
same population. This is mathematically irrational nonsense on your
part.
>>>> Evolutionists have bungled the basic science and mathematics of
>>>> mutation and selection and then compensate for it by creating a new
>>>> junk science.
>>> If so, you will be able to explain what's wrong with neutral evolution.
>>> Make an attempt.
>> (1/(5*10^9))^200, generation after generation for hundreds of
>> thousands of generations.
>You are calculating a meaningless probability. To put it in terms you
>might understand, let's suppose again that for any given mutation the
>probability of eventual fixation is 1/(5*10^9). And suppose there are
>200 mutations per individual, or 1*10^12 per generation. What is the
>probability that at least one of these mutations will become fixed?
>Pretty good, huh? Now go for the full binomial: determine the mean
>number that will be fixed per generation (or the modal number, which is
>the same thing here). What do you come up with?
What I come up with is you are a crappy mathematician. Millions of
people can but lottery tickets in numerous lotteries but the
probability that any one individual will win multiple lotteries is
extremely low because of the multiplication rule of probabilities. Now
you want to claim that a single population can win millions of
lotteries without ever considering the joint probability of these
events. No wonder evolutionists have bungled the basic science of
mutation and selection; evolutionists throw out the governing
mathematics of probability theory and then claim how bright they are.

>>> Nobody claims that drift is faster than selection. Quite the reverse.
>>> Again, this shows that you completely misunderstand neutral evolution.
>> Quoting John Harshman from a long ago and far away place, No. Only a
>> couple of hundred per generation.
>How is that relevant? How does the number fixed per generation say
>anything about the speed of fixation? Consider an analogy. I have a
>pipeline filled with water. If I tell you 200 gallons come out the far
>end ever minute, can you tell me how fast the water is moving?
The number of fixed neutral mutations per generation says volumes
about the speed of the process. What you are claiming is that hundreds
of neutral mutations are spreading through the population every

generation, generation after generation for hundreds of thousands of

generations. This is mathematical irrationality at its finest. And I
certainly can tell you how fast the water is moving when you specify
the cross-sectional area of the pipe. Did you ever hear of the law of
continuity?

>>>> This is evolutionist mathematical
>>>> irrationality on full display.
>>> This is your indomitable ignorance on display for anyone to see.
>> John, do you still believe that the probability of a beneficial
>> mutation occurring is proportional to population size?
>Never did. In fact you once claimed you were going to stop bringing that
>up. Do you remember that claim? Attempts to deflect attention aren't
>very useful to you.
When you make claims of how smart you are and present this kind of
mathematical garbage and claim that I am ignorant for pointing out
your mathematical irrationality, I will remind you of your blunders.
If you want to have a serious discussion about the mathematics which
describes how populations transform genetically then I’ll stop
reminding you of a fundamental error you made in describing the
mathematics of the stochastic process of mutation and selection. If
you want to continue to claim that you have a stochastic process where
the joint probability of events is not computed using the
multiplication rule of probabilities, I’ll keep reminding you of this
and your previous blunders.

John Harshman Aug 26, 8:20 am

Newsgroups: talk.origins
From: John Harshman <jharsh...@pacbell.net>

Date: Fri, 26 Aug 2011 08:20:16 -0700
Local: Fri, Aug 26 2011 8:20 am

Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

>>>> This is why it is nonsense to believe that on average
>>>> dozens of neutral mutations spread throughout the population every
>>>> generation for hundreds of thousands of generations to do the
>>>> accounting of the 40,000,000 differences between humans and
>>>> chimpanzees.
>>> Non sequitur. Again, you are assuming that this spread is rapid, when I
>>> have told you many times that it's very slow. In every generation there
>>> are billions of mutations. Only a couple hundred of these will ever
>>> become fixed, and it will take millions of years for the average
>>> mutation, of those that do become fixed, to increase to a frequency of
>>> 1. Only small changes in allele frequency happen in a single generation
>>> in large populations.
>> John, if you are going to claim that the probability of fixation of a
>> neutral allele is equal to its frequency, then the probability of
>> fixation of two neutral mutations is the product of the individual
>> frequencies, an extremely low probability event.
>True. But irrelevant. We aren't talking about two particular mutations,
>but about two mutations selected only a posteriori. Just as any given
>bridge hand is vanishingly unlikely, or any particular complex set of
>random events. Still, some bridge hand will happen, as will some set of
>random events.
John, the multiplication rule of probabilities applies to the joint
probabilities of all random independent events occurring. Do you think
that if you found someone after they happened to win two lotteries
that the probability of winning those two lotteries was not governed
by the multiplication rule because you found him after he won the two
lotteries? Think about the weird claim that you are making. You are
claiming that millions of neutral mutations are spreading through the
entire population based strictly on a random process. The
multiplication rule of probabilities shows that you are making a
mathematically irrational claim.

>>>> Differences in genomes only accumulate by common descent
>>>> whether these differences are beneficial, neutral or detrimental.
>>> When has anyone claimed otherwise?
>> And selection is the only efficient way to transform genomes. The
>> claim that drift does it more quickly is mathematically irrational.
>Are you reading at all? Nobody says drift does it more quickly. It's
>just that drift tries more often.
The only thing being done more often here is your discarding of the
multiplication rule of probabilities.

>>>> So tell us John, if the neutral differences appeared millions of years
>>>> ago and are only being fixed now, when did these 40,000,000
>>>> differences between the human and chimpanzee genomes occur?
>>> What do you mean by "occur"? If you refer to fixations, a few of them
>>> have happened each generation for the past 5 million years or so. If you
>>> refer to the original mutations (the ones that eventually became fixed),
>>> a few of them happened each generation starting many millions of years
>>> before that.
>> It’s much more than a few which have to be fixed each generation, its
>> dozens of neutral mutations which must sweep through the entire
>> population each generation.
>Not true. No sweeping in a single generation. Why can't you understand
>this simple fact?
Because I can understand the multiplication rule of probabilities and
you don’t understand probability theory. You are claiming that
hundreds of rare stochastic events are occurring every generation in a
population and this is happening generation after generation for
hundreds of thousands of generations. You evolutionists love to ignore

the multiplication rule of probabilities.

>> This is in contrast to the rate at which a
>> beneficial mutation can sweep through a population. In that case it
>> takes hundreds of generations for a single beneficial mutation to
>> substitute into a population.
>Haven't you been paying attention at all? It takes thousands of
>generations for a single neutral mutation to substitute. It's just that
>there are many billions of those neutral mutations.
And the probability of a single neutral allele being fixed is equal to
its frequency. And you are claiming millions of the neutral alleles
are being fixed in 500,000 generations when only about 10-20,000
beneficial mutations could be fixed at the same time. John, you are a
master of mathematical irrationality and you have done this by
throwing out the multiplication rule of probabilities for the joint
probability of random independent events.

>>> I remain amazed at your inability to understand the simplest features of
>>> neutral evolution. How is this possible?
>> I admit I have a problem understanding the incoherent and
>> mathematically irrational evolutionist arguments. Now if you could
>> ever make a rational and coherent argument and support it with more
>> than “conceptual examples” then perhaps I could believe that the
>> theory of evolution is more than a mathematically irrational belief
>> system.
>How can you tell if an argument is coherent if you have no idea what
>that argument is? You persist in the simplest errors, like your claim
>that I think drift is faster than selection.
Because I do understand your argument and it is based on the
elimination of the multiplication rule of probabilities for the joint
probability of random independent events.

John Harshman Aug 26, 8:38 am

Newsgroups: talk.origins
From: John Harshman <jharsh...@pacbell.net>

Date: Fri, 26 Aug 2011 08:38:34 -0700
Local: Fri, Aug 26 2011 8:38 am

Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

>>>> All the real, measurable and repeatable examples of mutation and
>>>> selection show that there are no cases of selection at two loci
>>>> (genes) for which amplification of beneficial alleles can occur at
>>>> both loci simultaneously. If you know of any real, measurable and
>>>> repeatable examples, post them.
>>> That would require me to look something up, and I'm just too lazy. So
>>> let me ask why such a thing would be a priori impossible.
>> There you go; the key attributes of an evolutionist, ignorance and
>> apathy. So you want to know why amplification can not occur
>> efficiently at two genetic loci simultaneously. Just ask yourself why
>> it doesn’t occur in all the real, measurable and repeatable examples
>> of mutation and selection. When you answer that question correctly
>> then you will understand why there are no examples which behave
>> otherwise.
>Once again you fail to answer a simple question.
I’m trying to motivate you so that you are not so lazy.

>>>> I’ve said repeatedly that selection pressures can either kill or
>>>> impair the replication of members of the population.
>>> Not required. There just have to be differences in amount of
>>> replication. In a growing population, a new mutation may just increase
>>> the reproduction of individuals that have it without the reproduction of
>>> other individuals being reduced at all.
>> The Weinreich example somewhat represents what you are hypothesizing.
>> His experimental model has a variety of different subpopulations each
>> taking different trajectories to fitness optima on the fitness
>> landscape but only one gene is being selected for at a time. The
>> problem for the theory of evolution is not that different
>> subpopulations can take different trajectories on a fitness landscape;
>> it is for a particular subpopulation to be able to amplify more than a
>> single beneficial mutation at a time. Because mutation and selection
>> can not work in parallel efficiently, the theory of evolution is a
>> mathematically irrational belief system.
>You just responded to that one with another repetition of your mantra.
>You don't read at all.
You are the lazy bones here. I’ve read your arguments and they are
based on the concept that the multiplication rule of probabilities for
the joint probability of events does not apply to your random
processes. Just how do you imagine that you get differential
reproduction without taking into account fitness to reproduce? You
continue to paint yourself further and further into a corner.

>>>> In the case of
>>>> combination therapy for HIV, these selection pressures are not lethal
>>>> for all members of the population; the population still has members
>>>> which can replicate, just not efficiently. RNAases and other enzymes
>>>> prevent these populations from becoming huge.
>>> Which is close enough to lethal for our purposes. So why is this a
>>> universal situation, not one dependent on the special requirement of
>>> each gene not having an individually advantageous allele.?
>> And your purpose here is to twist reality to try to make it fit your
>> mathematically irrational belief system. The virus is either dead and
>> can no longer reproduce or it is still alive and able to reproduce. I
>> don’t think you would suggest to someone with HIV that since is
>> infection is close enough to dead; he no longer needs to take his
>> combination therapy.
>Indeed I wouldn't. Under that combination, the virus is alive yet unable
>to reproduce. Hey, look: there's a third possible condition you haven't
>considered.
How wrong you are John. The virus is still replicating when subject to
combination therapy.

>>>>>> As far as your junk mathematics and science goes, you now claim that
>>>>>> 30 neutral mutations are fixed in the human and chimpanzee populations
>>>>>> every generation. Would you tell us what 30 mutations were fixed in
>>>>>> your genome?
>>>>> Do you know what "fixed" means? It has nothing to do with individual
>>>>> genomes, but with populations. Nothing is fixed "in your genome".
>>>> So how do all the members of the population get identical neutral
>>>> mutations in each of their genomes?
>>> By inheriting them from their parents. Why is this difficult to understand?
>> It’s not difficult to understand at all. It’s easy to see how
>> beneficial mutations amplify in a population. The descendents with
>> these beneficial mutations are better replicators and over
>> generations, their alleles become predominant in the population. When
>> you claim that dozens of neutral mutations sweep through populations
>> every generation without the benefit of amplification by improved
>> fitness; your claims are coming from La, La land.
>That's because I make no such claim. Nothing is sweeping through
>populations in a single generation. Please look up random walks. It's a
>fairly simple proof to see that there are only two possible results of a
>random walk in allele frequency: loss or fixation. One of these must
>happen eventually, and the probability of each end result is at any
>given moment equal to 1 minus the distance from that end point. Thus is
>an allele has a frequency of 30%, its probability of loss is 70% and of
>fixation is 30%. None of that, however, tells you how long the end
>result will take. Then again, if the frequency is currently 99.999%,
>eventual fixation is highly likely, and will probably happen fairly soon.
So you are claiming that millions of neutral mutations are sweeping
through a population in 500,000 generations. It is still a
mathematically irrational claim.

>The only reason there are many neutral fixations happening in every
>generation is that there are astronomical numbers of polymorphisms in
>the pipeline.
I got it now John, you have millions of neutral mutations sweeping
through a population in 500,000 generations. Just what are you smoking
in that pipeline?

>>> No. When did I say anything that could possibly cause you to think I
>>> meant that? Do you even read what I write with any attempt to understand?
>> Certainly I read and attempt to understand your claims.
>Then you are very very bad at it.
I’ve never been very good at understanding evolutionist illogic, gross
over-extrapolation and mathematically irrational speculation.


John Harshman Aug 26, 8:50 am

Newsgroups: talk.origins
From: John Harshman <jharsh...@pacbell.net>

Date: Fri, 26 Aug 2011 08:50:48 -0700
Local: Fri, Aug 26 2011 8:50 am

Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

>>> As I have explained previously at length, Lenski's results don't mean
>>> what you think they do. I know that, and so do Lenski and all his
>>> co-authors.
>> Both Lenski’s and Weinreich’s models demonstrate that selection
>> conditions predetermine the trajectories on fitness landscapes. As
>> Weinreich and his co-authors wrote “…we conclude that much protein
>> evolution will be similarly constrained. This implies that the protein
>> tape of life may be largely reproducible and even predictable.” It is
>> this principle which allows clinicians to sequence HIV and look for
>> particular mutations as indicators of drug resistance patterns. This
>> empirical data may not agree with your “conceptual examples” but good
>> scientific practice requires correlation of “conceptual examples” with
>> empirical data. Lenski has published a very similar statement as what
>> Weinreich and his co-authors have written.
>Yes? What was that very similar statement?

John you are so lazy!!! I’ve already posted in for you and you use the
only argument you have left and that is to ignore it.

>>>>>> Why do you think the bacteria in the Weinreich
>>>>>> paper have to get their mutations in a specific sequence?
>>>>> That's the known case, apparently.
>>>> Then we have the examples of HIV where the same mutations increase in
>>>> frequency in the populations when subjected to particular selection
>>>> pressures. This behavior is so predictable; it is used to determine if
>>>> an individual is infected with drug resistant strains of HIV.
>>> Which has what to do with anything?
>> It has everything to do with understanding how mutation and selection
>> works.
>So nothing to do with the question, then.
I’m finally able to boil down your argument to one simple principle;
the underlying principle for the theory of evolution is that the
multiplication rule of probabilities does not exist.

>>> Note: these are phenotypes, not genotypes. The same expression changes,
>>> yes, but no clue that the same mutations in each case caused those
>>> expression changes. See why I don't trust your reading skills?
>> Read the entire paper John. The Lenski paper is demonstrating the same
>> principle that the Weinreich paper demonstrates which is once a
>> population starts a particular trajectory on the fitness landscape
>> that subpopulations path is predetermined.
>This is just a repetition of your claim, not a response to me.
You just don’t like these responses; they don’t fit your
mathematically irrational belief system.

>> Here’s another paper for
>> you not to read published by Lenski this year “Evolution in Action: a
>> 50,000-Generation Salute to Charles Darwin”
>> “To my surprise, evolution was pretty repeatable. All 12 populations
>> improved quickly early on, then more slowly as the generations ticked
>> by. Despite substantial fitness gains compared to the common ancestor,
>> the performance of the evolved lines relative to each other hardly
>> diverged. As we looked for other changes—and the “we” grew as
>> outstanding students and collaborators put their brains and hands to
>> work on this experiment—the generations flew by. We observed changes
>> in the size and shape of the bacterial cells, in their food
>> preferences, and in their genes. Although the lineages certainly
>> diverged in many details, I was struck by the parallel trajectories of
>> their evolution, with similar changes in so many phenotypic traits and
>> even gene sequences that we examined.”
>Note again: phenotypes, not genotypes; "even gene sequences" means that
>parallel mutations were rarer than parallel phenotypic changes.
Oh really, post the data from his paper that supports your claim.

>> If that’s not enough for you John, pull this Lenski paper; “Genome
>> evolution and adaptation in a long-term experiment with Escherichia
>> coli” and since you are too lazy to read the paper I’ll pull the
>> appropriate quote for you.
>> “Fourteen genes in which mutations were found in our study population
>> have been sequenced in all the other populations after 20,000
>> generations. There is substantial parallelism, mutations in the same
>> gene, nine additional genes with mutations in other lines, and only
>> two cases where no other line has a mutation in the same gene (Table
>> 1).”
>Note: mutations in the same gene, not the same mutation.
You are on the hook for this one John, tell us which genes and
mutations Lenski is talking about. And remember, the Weinreich
experiments had different variants which adapted to his selection
pressure but each subpopulation had their own particular trajectory
and took their trajectories by a beneficial mutation/amplification of
beneficial mutation cycle.


>> And if you read that the entire paper you will find that:
>> “Figure 1 shows all mutations identified in the evolved clones through
>> 20,000 generations. The 45 mutations in the 20K clone include 29
>> single-nucleotide polymorphisms (SNPs) and 16 deletions, insertions
>> and other polymorphisms (DIPs). Figure 2 shows that the number of
>> mutational differences between the ancestral and evolved genomes
>> accumulated in a near-linear fashion over this period. Any deviation
>> from linearity was not statistically significant based on
>> randomization tests.
>> The near-linearity of the trajectory for genomic evolution is rather
>> surprising, given that such constancy is widely taken as a signature
>> of neutral evolution12, whereas the fitness trajectory for this
>> population 23 shows profound adaptation that is strongly nonlinear. In
>> particular, the rate of fitness improvement decelerates over time
>> (Fig. 2), which indicates that the rate of appearance of new
>> beneficial mutations is declining, their average benefit is becoming
>> smaller, or both. These effects, in turn, should cause the rate of
>> genomic evolution to decelerate.”
>> How do we know what your reading skills are John when you are too lazy
>> and apathetic to read?
>I read it. You apparently didn't, as none of that quote had anything to
>do with your attempted point.
You are so silly John, you had better stick with your mathematically
irrational claim that millions of neutral mutations sweep through a
population in 500,000 generations. And limit your arguments to those
with naïve school children.

This ends responses to post 901-925

[Steven L.]

"r norman" <r_s_n...@comcast.net> wrote in message
news:46l777pqufop933rv...@4ax.com:

Maybe Dr. Kleinman, M.D., can't deal with the fact that it's *doctors*
(and patients), not evolutionists, who bear such responsibility for the
rise of antibiotic-resistant bacteria. By overusing and misusing
antibiotics.

When I was a kid, doctors would prescribe penicillin just for simple
colds. And today just as back then, doctors still hand out antibiotics
for minor pus pimples and skin abscesses rather than lancing and
draining them.

The answer was not to use multiple antibiotics according to some
evolutionary theory. The answer was to avoid prescribing antibiotics
for colds and boils *at all*, unless a systemic bacterial infection had
gotten underway.

And any doctor with even a rudimentary understanding of the ToE would
understand why.



-- Steven L.

[r norman]

You know that and I know that and just about everybody else here and
everywhere knows that. Somehow Kleinman, MD, PhD, fails to get it.

[hersheyh]

On Tuesday, September 20, 2011 2:42:19 PM UTC-4, Alan Kleinman MD PhD wrote:
> The following replies are from a splinter threads
> Virgil Sep 14, 1:35 pm
> Newsgroups: talk.origins
> From: Virgil <vir...@ligriv.com>
> Date: Wed, 14 Sep 2011 14:35:43 -0600
> Local: Wed, Sep 14 2011 1:35 pm
> Subject: Re: The Theory of Evolution is Mathematically Irrational
> Round 2
> In article

> <7f7ca969-1404-4f7e...@x11g2000prb.googlegroups.com>,

> Alan Kleinman MD PhD <klei...@sti.net> wrote:
> >> On Aug 10, 7:42 pm, Mark Isaak <eci...@curioustaxonomyNOSPAM.net>
> >> wrote:
> >> > On 8/10/11 2:21 PM, Alan Kleinman MD PhD wrote:
> >> > > On Jul 14, 8:58 am, Mark Isaak<eci...@earthlink.net> wrote:
> >> > >> On Tue, 12 Jul 2011 18:18:51 -0700, Alan Kleinman MD PhD wrote:
> >> > >>> On Jun 7, 2:45 pm, Mark Isaak<eci...@earthlink.net> wrote:
> >> > >>>> On Mon, 06 Jun 2011 17:47:21 -0700, Alan Kleinman MD PhD wrote:

[snip]

> What makes you think that I am not
> dedicated to figuring out how mutation and selection works?

Everything you have posted on the subject and your complete refusal to do any research into the math, try to actually discuss your bogus assumptions, or even try to listen. You come across as both profoundly arrogant and ignorant. And I don't think that is just my opinion.

> The correct probability
> function for random recombination does not require that you consider
> selection. The affects of selection on random recombination only
> affects the probabilities implicitly by altering the number of members
> with each of the particular alleles.

The probability of *recombination*, in random sexually reproducing eucaryotes (organisms that go through a meiotic cycle), is determined by the *frequencies* of the alleles in the parent generation and is described by the logic of the Punnet Square, which makes it about as old as modern genetics. Note that I said frequencies in the parent generation and not the *frequency of mutation* from w.t. to mutant allele. The *frequency* of alleles in any particular generation is a function of its history, specifically the selective pressures that have historically acted upon different phenotypes produced by the genotypes and/or the chance history of neutral drift. Again, it is the *relative frequency* of different alleles in a randomly sexually reproducing population that determines the probability of recombination, NOT the absolute number of members NOR the mutation probability.

In procaryotes and viruses, recombination is a rarer event, as these organisms generally reproduce clonally, and one has to define what mechanism of genetic exchange one is talking about: exchange resulting from double infection of different viruses, transmission via plasmids and other extra-chromosomal agents, transformation, or by viral transduction.

> >> What happens to the probabilities of the random
> >> recombination of A and B if only one of the two all alleles amplify?

So, are A and B different alleles of the same gene or are they different genes? Do you know the difference? And why it makes a difference?

> >Not relevant.

> John, you shouldn�t be making this argument until you derive the
> probability function for random recombination. I�m not going to give

> the derivation of that probability function now but consider this.
> What if in your population every member has allele A except the member
> which has allele B, that is A has a frequency close to 1 in the
> population? That member with allele B that is B has a frequency very
> close to 0. What is the chance that a member with allele A will meet
> and recombine with the member with allele B?

This again shows your confusion about the difference between the term 'allele' and the term 'gene' or your confusion between the 'probability of mutation' and the 'probability of recombination'. You treat A and B here as if they were alternate alleles of the same gene. And given your confusion between a 'gene locus' and a 'nt site', you are probably treating the two, A and B, as different nts at the same nt site. If that is what you mean, then recombination will not produce anything but the same two alleles (unless the two alleles contain *different* mutations at *different* nt sites from each other rather, in which case a rare recombination between those two independent mutations will produce a double-mutant and a non-mutant).

Ordinarily, recombination refers to recombination between *gene loci*, not recombination within a gene, and recombination between alleles that differ by having different nt's at a single nt site is impossible because a nt site is the limit for recombination.

So tell us what you mean when you talk about *recombination*. Are you concerned with eucaryotic recombination, which occurs each and every generation? Or are you concerned with some type of gene exchange that goes on in procaryotes or viruses? When you use the term 'allele' in your discussion above, are you talking about different forms of a specific gene locus (the actual definition) or are you talking about differences in nt's at a single nt site or are you talking about two *different* unlinked genetic loci, each of which has alternate alleles? Or do you not understand what I am talking about?

[snip stupidity about the Poisson, which is irrelevant]

> >It's really quite simple. Given various simple assumptions, such as
> >independent assortment, panmixis, a constant population, and frequencies
> >p and q for the two alleles, the expected frequency of AB individuals is
> >just pq. As p and q increase, pq increases. We have already specified
> >that p and q are increasing. If AB phenotypes are favored over A, B, and
> >"wild type" phenotypes, p and q will increase faster than they would in
> >the absence of that advantage.

John is possibly falsely thinking that you were talking about eucaryotic recombination involving organisms with a meiotic cycle and also are thinking of A and B as alternate alleles of the same gene. I think you are probably thinking of A and B as different *genes* rather than alleles of the same gene. But it is hard to tell what you mean since you have *repeatedly* refused to clarify what you mean. Probably because you don't understand the criticisms, in this case don't know the difference between "allele" and "gene locus" and "nt site".

> John, the only thing that the Hardy-Weinberg law gives you is that the
> frequency of alleles remains constant when the population is in
> equilibrium (selection is not acting).

And the H-W equilibrium only really exists when the population is of infinite size.

But if you consider A and B to be two different unlinked *genes*, each with certain *frequency* of alternate alleles in the population, say p for A and q for A's alternate allele, a, and r for B and s for b, then you can use the expansion to determine the frequencies of any kind of diploid offspring assuming randomness. The frequency, in the population, of gametes with the *haploid genotype* A;B would be pr. The frequency of A;b would be ps. Of a;B would be qr. [As an exercise to show that the frequencies of the gametes add up to 1, which is the whole population of possibilities: pr+ps+qr+qs = p(r+s)+q(r+s) = (p+q)(r+s) = (1)(1) = 1] And of a;b would be qs.

Using a Punnet Square and crossing the gametes to each other along with the appropriate frequency of the gametes in the population will generate the frequencies of different genotypes in the progeny population.

But that is assuming that A and B are two different unlinked genes in a eucaryotic population.

> If you want to estimate the
> probability of two alleles randomly recombining, you need to write the
> probability function for that stochastic process. Once you do that,
> you can consider how selection will change the probabilities over
> generations as the frequencies and population sizes of the alleles
> change.

Selection increases the relative frequency of the allele of a gene which has the selectively advantageous phenotype. It will do so each generation relative to the alternative allele. That is the very definition of selection. So the relevant question is "What is the *frequency* of the alleles in reproducing individuals is there at the generation I am looking at?" Not, for recombination in sexually reproducing eucaryotes, "How many, numbers, of allele a are present in reproducing members of the population?"

Of course, you could be talking about recombination in procaryotes or viruses, which are mostly growing in a clonal fashion. Until you choose to actually respond intelligently, it is hard to parse out what you are talking about here.

[snip major material which I will try to cover in smaller chunks and re-label the subject heading]

[John Harshman]

hersheyh wrote:
> On Tuesday, September 20, 2011 2:42:19 PM UTC-4, Alan Kleinman MD PhD wrote:

>>> It's really quite simple. Given various simple assumptions, such as
>>> independent assortment, panmixis, a constant population, and frequencies
>>> p and q for the two alleles, the expected frequency of AB individuals is
>>> just pq. As p and q increase, pq increases. We have already specified
>>> that p and q are increasing. If AB phenotypes are favored over A, B, and
>>> "wild type" phenotypes, p and q will increase faster than they would in
>>> the absence of that advantage.
>
> John is possibly falsely thinking that you were talking about
> eucaryotic recombination involving organisms with a meiotic cycle and
> also are thinking of A and B as alternate alleles of the same gene.
> I think you are probably thinking of A and B as different *genes*
> rather than alleles of the same gene. But it is hard to tell what
> you mean since you have *repeatedly* refused to clarify what you
> mean. Probably because you don't understand the criticisms, in this
> case don't know the difference between "allele" and "gene locus" and
> "nt site".

No, John is possibly falsely thinking that he was talking about
eukaryotic recombination with A and B as alleles at two unlinked loci.

[Alan Kleinman MD PhD]

The following are a compilation of responses to posts 926-950
presented in this manner to prevent splinter threads.

hersheyh Aug 26, 8:53 am

Newsgroups: talk.origins
From: hersheyh <hershe...@yahoo.com>

Date: Fri, 26 Aug 2011 08:53:04 -0700 (PDT)
Local: Fri, Aug 26 2011 8:53 am

Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

On Friday, August 26, 2011 9:29:16 AM UTC-4, Alan Kleinman MD PhD
wrote:
> On Jul 26, 12:06 pm, hersheyh <hers...@yahoo.com> wrote:
> > On Jul 25, 8:56 pm, Alan Kleinman MD PhD <klei...@sti.net> wrote:
> > > On Jun 19, 3:28 pm, hersheyh <hers...@yahoo.com> wrote:> On Jun 13, 8:57 am, Alan Kleinman MD PhD <klei...@sti.net> wrote:
> > > > > On Jun 1, 12:57 pm, hersheyh <hers...@yahoo.com> wrote:> On Jun 1, 10:33 am, Alan Kleinman MD PhD <klei...@sti.net> wrote:
[snip]
>> > They can also be generated even if the selection pressures are used
>> > simultaneously. It just takes longer to generate enough trials
>> > (infectious viral particles that sneak through the selection
>> > pressures). That is because most antivirals are not virucidal but
>> > merely virustatic. Compared to bacteria, HIV has a significantly
>> > higher mutation rate because RNA polymerases lack editing functions.
>> > The mutation rate of HIV is about 3X10^-5/base/replication cycle (in a
>> > genome of about 10^4 bases). The rate of reproduction of the virus in
>> > an infected person in the absence of selective drugs is about 10^10
>> > viruses/day, leading to anywhere between 10^2 and 10^7 virus copies/ml
>> > of blood in an untreated person. Obviously, in the absence of any
>> > treatment, you would have about one mutation in every n.t. per day
>> > (with some viruses having two or more mutations). Not all the viruses
>> > will, of course, find a cell to infect. Of course you have always
>> > been lying when you claim that evolutionary biology has misunderstood
>> > the problems of viral therapy. The following analysis of treatment of
>> > HIV demonstrates exactly the problem I have stated. The first anti-
>> > HIV drug, AZT, quickly led to resistant strains and thus was found not
>> > to lead to a significant lengthening of life. Often it was only given
>> > late in infection because it was known to quickly generate resistant
>> > strains. This was because even in the presence of the drug, the level
>> > of HIV in the blood was only reduced and not to negligible levels.
>> > http://www.google.com/url?sa=D&q=http://pathmicro.med.sc.edu/lecture/hiv14a.htm
>> What a surprising piece of wisdom an evolutionist crank is coming
>> forth with. Single drug therapy for HIV leads to rapid selection of
>> drug resistance. Who would have guessed this?
>Every single virologist and evolutionary biologist would have guessed this. I certainly would have. Based on my >understanding of mutation and selection and my understanding of how toxic agents work (by interacting with and >interfering with some normal biologic function).

This was not mainstream thinking before the 1990s when HIV hit. Read
the literature from the 1990s about the treatment of HIV and the use
of combination therapy. There was a lot of debate for and against.
However, if virologists and evolutionary biologists had read Edward
Tatum’s 1958 Nobel Laureate lecture, and understood what he was saying
about using combination therapy, the debate would have been much
shorter.

>> I suppose the next thing
>> you are going to tell us is that combination therapy suppresses the
>> mutation and selection process.
>Of course it does, as any biologist would have told you. But in the early days of antivirals directed against HIV -- when >only AZT was available, there was no choice but to use single-gene therapy. The other option was to intentionally not >treat patients. When other antivirals came on-line, they were used. The initial 'other antivirals' were also anti-reverse >transcriptases, so there was a possibility of cross-interaction (non-independence) of action, which would render >combination therapy much less useful.

That’s a line of crap and you know it. Combination therapy has never
been a mainline approach to treating diseases and still is not. The
reason is that evolutionists do not teach the basic science and
mathematics of the mutation and selection phenomenon. And the reason
they don’t teach it is that they don’t understand it. You are the
perfect example of this deficiency in understanding. You’ve been
teaching genetics for 20 years and how many lectures have you given on
the basic science and mathematics of mutation and selection? All you
know is that you apply the Poisson distribution which is the wrong
distribution function and then you mislead a generation of students.


>> And then I suppose you are going to
>> tell us these are unnatural selection pressures
>They are. Population-wide (in this case, the infected individual) instantaneous appearance of large amount of toxic >compounds are novel selection pressures that typically are artificially introduced by humans for their purposes.

Oh, I see, no populations ever went extinct until humans came along.
There was just single targeted selection pressures in nature targeting
one gene at a time and “poof” reptiles transformed into birds. This is
the mathematically and empirically irrational crap that forms the
basis of evolutionism.

>> and nature never
>> targets more than a single gene at a time with starvation,
>> dehydration, disease, thermal stress, predation…
>It is not like populations never are exposed to those conditions. The result is a large population decline with the >survivors (if any -- local extinction happens) including the organisms *better* fitted to at least one of those conditions. All >that matters is that the organism be *better fit* for those conditions relative to the w.t., not that they be optimally resistant >to all those conditions. The result would be a population genetically enriched in individuals *more* resistant to >dehydration, individuals *more* resistant to starvation, *more* resistant to thermal stress, etc. There is nothing that says >that those genetic traits must all be in the same individual, only that the individual traits selected for have independent >selective value relative to the w.t. individuals that lack that specific trait. Of course, if the conditions are so harsh that no >individuals survive in the most stressed area, then only those individuals in the surrounding less stressed area will >survive to try to repopu

late the central. Since those individuals, regardless of how few they are, are genetically enriched >to survive the stress relative to organisms that have not been exposed (again, not necessarily at the same gene loci; all >that is required is survival better than the w.t. individual, not complete optimality at all loci that enhance survival) their >progeny will also be enriched in all those traits. Moreover, because of random recombination in these sexually >reproducing organisms, there will be new genetic combinations of those enriched-to-survive alleles. IOW, parallel >increases of benefical alleles at *any* locus that increases survival relative to the w.t. followed by random recombination >of the higher frequency of those alleles producing new combinations, some of which will have even greater survival >value. A step-wise ratcheting of beneficial alleles at *all* loci where such alleles exist, are expressed, and produce >organisms better fit in that environment than the w.t. individual.

This is the evolutionist mantra but try putting some mathematics to
your blah, blah, blah. And try to find an empirical example where
mutation and selection occurs in parallel. All the empirical examples
which exist contradict your blah, blah, blah so you call these
empirical examples “unnatural”. The ratcheting affect requires
amplification because of the multiplication rule of probabilities, a
rule which you discard whenever it doesn’t fit your belief system.

>> We understand the
>> evolutionist philosophy, which is blizzards turn lizards into buzzards
>> with gizzards.
>Lizards (specifically and relevantly, alligators and crocodiles, the closest living relatives to dinosaurs) have gizzards. As, >likely, did a number of plant-eating dinosaurs (based on gizzard stones found near their fossils; meat-eating birds, and >probably dinosaurs, also have gizzards, but don't often swallow stones and gizzards themselves don't fossilize). So >buzzards certainly inherited their gizzards from their lizard ancestors. Blizzards have nothing to do with gizzards. They >may have something to do with the selective pressures for *feathers*, which initially (and still today) are often functionally >relevant as air- and heat-trapping insulation.

Well my, my, are you going to tell us that cold-blooded alligators and
crocodiles without feathers, wings or beaks are closely related to
birds because they have gizzards. I guess the weather just hasn’t been
cold enough for these reptiles to grow feathers, wings and beaks.
[snip]
Mark Isaak Aug 26, 11:04 am

Newsgroups: talk.origins
From: Mark Isaak <eci...@curioustaxonomyNOSPAM.net>

Date: Fri, 26 Aug 2011 11:04:22 -0700
Local: Fri, Aug 26 2011 11:04 am

Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

On 8/26/11 6:33 AM, Alan Kleinman MD PhD wrote:

> On Aug 1, 4:28 pm, Mark Isaak<eci...@curioustaxonomyNOSPAM.net>
> wrote:
>> On 8/1/11 2:14 PM, Alan Kleinman MD PhD wrote:
>>> On Jul 5, 4:05 pm, Mark Isaak<eci...@earthlink.net> wrote:
>>>> On Tue, 05 Jul 2011 05:08:29 -0700, Alan Kleinman MD PhD wrote:
>>>>> On Jun 3, 12:16 pm, Mark Isaak<eci...@earthlink.net> wrote:
>>>>>> On Thu, 02 Jun 2011 17:33:33 -0700, Alan Kleinman MD PhD wrote:
>>>>>>>> [lots of snip]
>>>>>>>> The ToE is utterly useless as a scientific framework. Those
>>>>>>>> indoctrinated into this belief system have great difficulty
>>>>>>>> understanding how mutation and selection actually works and can not
>>>>>>>> recognize their biases when the empirical data is presented which
>>>>>>>> shows how mutation and selection actually works.
>>>>>>> Out of curiosity, how do you explain the fact that *engineers* are
>>>>>>> successfully using the theory of evolution, relying especially on the
>>>>>>> understanding of how mutation, recombination, and selection, to solve
>>>>>>> problems that they could not solve without it? Is that not the very
>>>>>>> definition of a successful scientific framework?
>>>>>> Which *engineers* are you talking about?
>>>>> Check out the subject of genetic algorithms. There are entire books
>>>>> written on the subject. You might also look at:
>>>>> Joyce, G. F., 2004. Directed evolution of nucleic acid enzymes. _Annual
>>>>> Review of Biochemistry_ 73: 791-836.
>>>> Mark, any engineer would understand that the more complex the
>>>> optimization (selection) conditions are, the more difficult it is to
>>>> do the optimization process.
>>> As it happens, I am an engineer, and I understand that the more complex
>>> the conditions are, the easier it is to do some optimization.
>> You must be a graduate of the Rube Goldberg School of Design. Now that
>> you are claiming that the more complex the optimization conditions,
>> the easier the optimization, you need to present your examples.
>When things are more complex, there are more ways to change it, and
>proportionally more ways to make it better. Plus, things that are
>complex typically get that way because the designer was not interested
>in optimization in the first place.

Mark, your arguments get weirder and weirder. We are talking about
random mutations which occasionally improve fitness to reproduce.
Clearly the mathematics which describes this phenomenon is over your
head showing that you are not an engineer. The simplest optimization
problem to solve for both engineers and replicating populations is a
single optimization condition. The mathematics gets much more complex
with more than a single optimization condition. That’s why combination
therapy works for HIV and every other disease subject to mutation and
selection phenomenon.


>>>> This is why the complexity of the
>>>> selection conditions dominates the mutation and selection process.
>>> That does not even mean anything.
>> In the mutation and selection process, it means everything. Without
>> amplification of a beneficial mutation, the probability that the next
>> beneficial mutation in the sequence occurring at the proper locus is a
>> very low probability event.
>Oh, you are pretending again that sex does not exist.
Mark, you don’t understand the mathematics of mutation and selection
so why would I imagine that you understand the mathematics of
recombination. Let’s pretend that you do understand the empirical
evidence of mutation and selection when recombination is also
occurring and that HIV which does recombination does not help this
virus to mutate and select beneficial mutations when two genes are
targeted simultaneously.

>>>> Now if your citation shows otherwise, post the quotes and the gives
>>>> us real examples which demonstrates the phenomenon.
>>> Go read.
>> Obviously your citation does not have any real examples which
>> demonstrate your claims, otherwise you would have posted them and
>> ended this discussion.
>Don't be silly. You know perfectly well that no amount of factual
>information will ever change your mind. The people who are interested
>in truth can go back to find the citations, look them up, and read.
I missed that part Mark, when have you ever presented factual
information. All I’ve seen you do is present evolutionist doctrine and
make mathematically irrational claims about optimization.


>>>>>> And exactly how is the ToE
>>>>>> useful for understanding how mutation and selection works?
>>>>> The theory of evolution shows that mutation and selection together are an
>>>>> extremely creative force, which one may profitably duplicate in other,
>>>>> non-biological, environments.
>>>> I disagree with your use of the word "creative" with respects to the
>>>> mutation and selection process.
>>> Disagree all you want, but the mutation and selection process has
>>> created. The process has created, for example, a custom antenna, an
>>> efficient detergent, and a checker-playing program.
>> I just saw an antenna mutate and select into a fishing pole. It caught
>> an evolutionist hook, line and sinker.
>See what I mean? When facts are presented to you, you escape into fantasy.
How can you avoid going into fantasyland when discussing mathematical
and scientific principles with an evolutionist? Invariably you end up
going down Alice’s rabbit hole when trying to understand evolutionist
logic.

>>> There's something very basic you do not understand about math. If a
>>> mathematical model says, with rock-solid certainty, that bumblebees
>>> cannot fly, and yet bumblebees fly, then the problem is with the
>>> mathematical model, not with the bumblebees. Your mathematical model
>>> says evolution cannot work efficiently via mutation and selection. And
>>> yet evolution works efficiently via mutation and selection -- more
>>> efficiently even than design in some cases. Ergo your mathematical
>>> model is wrong. The sane thing to do now is to toss out that model.
>> Mark, you obviously are not an engineer because the aerospace
>> engineers I worked with had a saying, “Put a big enough engine on
>> anything and you can make it fly”. The problem you have is you don’t
>> have a big enough engine for the theory of evolution to make it fly;
>> you just can’t get it off the ground.
>Then how do you explain the fact that things evolve adaptively? Oh,
>that's right. You escape into fantasy.
This is another reason I know you are not an engineer. What you do is
observe a phenomenon and then wildly extrapolate the behavior way
beyond the limits of what the phenomenon actually does. If you
actually understood how mutation and selection works, you could
develop strategies to prevent drug resistant microbes, herbicide
resistant weeds, pesticide resistant insects and develop more durable
cancer treatments. However, you don’t understand how mutation and
selection works. Instead you wildly extrapolate this phenomenon and
claim that reptiles turn into birds.

>> Mark, don’t you have any interest in preventing drug resistant
>> microbes, herbicide resistant weeds, pesticide resistant insects and
>> producing more durable cancer treatments? If you do, you need to
>> understand how mutation and selection actually works and it doesn’t
>> work the way evolutionists claim. Why would I want to toss out the
>> correct probability function which describes how mutation and
>> selection works actually works?
>"Works"? You have said repeatedly that it does not work. How does your
>probability function explain the many genetic differences between human
>and chimp? It can't. The mathematics of neutral drift, however,
Mark, do you realize how much of your life has been wasted being
indoctrinated into this mathematically irrational evolutionist crap?

hersheyh Aug 26, 12:53 pm

Newsgroups: talk.origins
From: hersheyh <hershe...@yahoo.com>

Date: Fri, 26 Aug 2011 12:53:47 -0700 (PDT)
Local: Fri, Aug 26 2011 12:53 pm

Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

On Friday, August 26, 2011 9:33:02 AM UTC-4, Alan Kleinman MD PhD
wrote:

>> On Aug 1, 4:28 pm, Mark Isaak <eci...@curioustaxonomyNOSPAM.net>
>> wrote:
>> > On 8/1/11 2:14 PM, Alan Kleinman MD PhD wrote:
>> > > On Jul 5, 4:05 pm, Mark Isaak<eci...@earthlink.net> wrote:
>> > >> On Tue, 05 Jul 2011 05:08:29 -0700, Alan Kleinman MD PhD wrote:
>> > >>> On Jun 3, 12:16 pm, Mark Isaak<eci...@earthlink.net> wrote:
>> > >>>> On Thu, 02 Jun 2011 17:33:33 -0700, Alan Kleinman MD PhD wrote:
>> > >>>>> [lots of snip]
>> > >>>>> The ToE is utterly useless as a scientific framework. Those
>> > >>>>> indoctrinated into this belief system have great difficulty
>> > >>>>> understanding how mutation and selection actually works and can not
>> > >>>>> recognize their biases when the empirical data is presented which
>> > >>>>> shows how mutation and selection actually works.
>> > >>>> Out of curiosity, how do you explain the fact that *engineers* are
>> > >>>> successfully using the theory of evolution, relying especially on the
>> > >>>> understanding of how mutation, recombination, and selection, to solve
>> > >>>> problems that they could not solve without it? Is that not the very
>> > >>>> definition of a successful scientific framework?
>> > >>> Which *engineers* are you talking about?
>> > >> Check out the subject of genetic algorithms. There are entire books
>> > >> written on the subject. You might also look at:
>> > >> Joyce, G. F., 2004. Directed evolution of nucleic acid enzymes. _Annual
>> > >> Review of Biochemistry_ 73: 791-836.
>> > > Mark, any engineer would understand that the more complex the
>> > > optimization (selection) conditions are, the more difficult it is to
>> > > do the optimization process.
>> > As it happens, I am an engineer, and I understand that the more complex
>> > the conditions are, the easier it is to do some optimization.
>> You must be a graduate of the Rube Goldberg School of Design.
>Evolution certainly is a graduate of the Rube Goldberg School of Design. Any engineer worth his degree would have >completely, rather than partially, separate entries for air and food and a completely separate exit for waste and entry/exit >for reproduction. And none would reuse the musculature for quadripeds in bipeds. A really sharp engineer would have >both an entry and exit for the uptake of oxygen and the exit of carbon dioxide rather than use a blind sac with its >necessary "dead" zone. And where is the eye in the back of the head of prey animals? That is not to even mention the >molecular redundancies of the blood-clotting system.
>Such stupid engineering literally cries out for an explanation. Hint: Historical constraint (as opposed to new design for >each case) provides one.

Hersheyh, you certainly don’t have the engineering skills to provide
that explanation. You are still back using the wrong probability

function for the mutation and selection phenomenon.

>> Now that
>> you are claiming that the more complex the optimization conditions,
>> the easier the optimization, you need to present your examples. You
>> are like John Harshman, he only presents conceptual examples, no real
>> examples.
>If you want evidence for parallel evolution in organisms that do engage in regular and frequent recombination (aka >eucaryotes), pick any multigenic trait in a eucaryote (height, weight, fruit size, egg production, bristle number in >Drosophila) where we use heritability to describe the results and follow selection in those cases. There will be change in >the trait until one hits the point where there is no more variation in the population or until there is a minimax optimum due >to deleterious pleiotropic effects on fitness.
>http://www.google.com/url?sa=D&q=http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1206456/pdf/ge13931273.pdf
>http://www.google.com/url?sa=D&q=http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1460816/pdf/10545462.pdf
>http://www.google.com/url?sa=D&q=http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1207261/pdf/ge1431277.pdf
If you are trying to convince me that Chihuahuas and Great Danes can
be created by recombination, don’t waste my time because that’s all
you’ve demonstrated with these examples. Here’s a quote from your
first citation.

“Lines divergent for high and low abdominal bristle number were
created by 25 generations of artificial selection from a large base
population, with an intensity of 25 individuals of each sex selected
from 100 individuals of each sex scored per generation.”

Now if you can demonstrate the creation of a bird by recombination of
alligators and crocodiles, then you will impress me. You already have
a running start; after all they both have gizzards.

> > > This is why the complexity of the
> > > selection conditions dominates the mutation and selection process.
> > That does not even mean anything.
> In the mutation and selection process, it means everything. Without
> amplification of a beneficial mutation,
>By which, of course, you mean that the survivors of selection must be able to reproduce, since selection itself changes >the *frequency* of the alleles present. Assume that there is sexual reproduction and the survivors of selection are >enriched in both individuals that have alleles Aa or AA rather than aa and *also* enriched in survivors with alleles Bb or >BB rather than bb (both genes being unlinked) even though, prior to selection, let's assume that there were no >individuals with both an A allele in the A gene locus and a B allele in the B gene locus simultaneously because those >alleles were quite rare relative to the a and b alleles prior to selection. But selection now has greatly increased the >*frequency* of *both* the A and of the B allele in the population (the real losers were the aa, bb individuals) Let's say >that all aa, bb individuals have died during selection, to be extreme about it. Moreover, in the previous population, let's >say that A and B were so rare that the only individuals

with those alleles were heterozygous Aa or Bb. That means that >after selection, the population only has Aa, bb individuals and aa, Bb individuals. Let's put frequencies on them. Say >that 70% of the survivors were Aa, bb and 30% were aa, Bb. That ratio could be due to a difference in the reproductive >success of individuals with the A allele relative to those with the B or it could be due to chance (the population had more >A individuals by chance). That means that the frequency of the A *allele* in the population is 0.35, a is 0.65, b is 0.85, >and 0.15 B. [There are twice as many alleles as individuals and the survivors with the capital letter only have one such >allele per individual.] Please note that the a and b alleles survive by being hidden in a heterozygote.

You write so much and say so little. Amplification is the requirement
for a population to overcome the multiplication rule of probabilities.
If the population can not amplify the allele, there is a very low
probability that the next beneficial mutation will occur at the proper
locus.

>With the assumption of random mating, we would expect 0.35 for the frequency of Aa, 0.0 for the frequency of AA, and >0.65 for aa in the next generation (because we are crossing Aa X aa). Similarly, we would expect 0.15 Bb and 0.85 bb >individuals. Since the genes are assumed to be unlinked and *using* the multiplication rule of probabilities (correctly), >then I would expect the progeny of this mating to be (0.65)*(0.85) = 0.55 aa, bb; (0.65)*(0.15) = 0.10 aa, Bb; >(0.35)*(0..85) = 0.30 Aa, bb; and (0.35)*(0.15) = 0.05 Aa, Bb individuals. That adds up to 1.0.

You still haven’t figured out how to write the probability function
for random recombination. This is reasonable since it has taken months
for you to get any understanding of the probability function for
mutation and selection.

>Now, assuming that the same selective conditions still exist, all the aa, bb individuals produced will die before >reproducing. Let us assume that individuals that are Aa, Bb are twice as fit as individuals that are Aa, bb or aa, Bb. > That would give us, when these individuals reach reproduction, out of every surviving 100 alleles (remembering to >multiply the 5% Aa, Bb individuals by 2 because of its selective advantage) 10 aa,Bb individuals, 30 Aa, bb individuals, >and 10 Aa, Bb individuals. These individuals should, assuming random meiosis, produce gametes in the ratio of 0.15 >a,B; 0.45 a,b; 0.35 A,b; and 0.05 A,B.

Hersheyh, I really find your hypothetical examples quite boring. You
have yet to figure out why the Poisson distribution is the wrong
probability distribution for the mutation and selection phenomenon and
you don’t have a clue of how to derive the correct probability
function for random recombination.

>Assuming random mating (use a Punnet square to make the computation easy -- you do know how to do that, don't >you?), that would mean progeny in the ratio of (0.45)*(0.45) = 0.20 aa,bb; 2*(0.15)*(0.45) = 0.135 aa,Bb; 2*(0.35)*(0.45) >= 0.315 Aa,bb; 2*(0.45)*(0.05) + 2*(0.15)*(0.35) = (0.045)+(0.105) = 0.15 Aa,Bb ;(0.15)*(0.05) = 0.0075 Aa,BB; >2*(0.35)*(0.05) = 0.035 AA,Bb; (0.0.15)*(0.15) = 0.0225 aa,BB, (0.35)*(0.35) = 0.1225 AA,bb and (0.05)*(0.05) = 0.0025 >AA,BB.
>Again, the aa,bb individuals will die and individuals with Aa,Bb; AA,Bb; AA,BB; Aa,Bb, or Aa,BB (having both an A and a >B allele) all are twice as likely to reach adulthood as the individuals who are AA,bb; Aa,bb; aa,BB; or aa,Bb (being aa or >bb). If you have some problems with continuing, I would be happy to continue this for a few more generations.
>Suffice it to say that both the A and B alleles will increase in frequency in parallel by the repeated loss of the aa, bb >individuals until the population contains only small frequencies of a and b. Equilibirum will only be reached when the >loss each generation of the a and b alleles due to aa and/or bb individuals equals the rate of new mutation from A to a >or B to b. At that point, most of the population will be AA, BB. The increase will be in parallel rather than sequential.
>All of this has been worked out long, long ago.

Ok hersheyh, take your hypothetical example and tell us why HIV
doesn’t do this. The Punnet square won’t explain this. You need to
derive the probability function for random recombination to understand
why HIV can’t use recombination to accelerate the mutation and
selection process.

>[snip]
>> > There's something very basic you do not understand about math. If a
>> > mathematical model says, with rock-solid certainty, that bumblebees
>> > cannot fly, and yet bumblebees fly, then the problem is with the
>> > mathematical model, not with the bumblebees. Your mathematical model
>> > says evolution cannot work efficiently via mutation and selection. And
>> > yet evolution works efficiently via mutation and selection -- more
>> > efficiently even than design in some cases. Ergo your mathematical
>> > model is wrong. The sane thing to do now is to toss out that model.
>> Mark, you obviously are not an engineer because the aerospace
>> engineers I worked with had a saying, “Put a big enough engine on
>> anything and you can make it fly”. The problem you have is you don’t
>> have a big enough engine for the theory of evolution to make it fly;
>> you just can’t get it off the ground.
>Again, you yourself have repeatedly pointed out examples where even sequential evolution produces significant results >requiring 5 or more sequential steps in less than a human lifetime. Why doesn't that give you pause wrt your claim that >evolution is mathematically impossible? Then if you add in the parallelism possible in eucaryotic genetics, you do have >to recognize that your mathematical model is restricted to a narrow set of examples, mostly involving multiple >simultaneous resistance to toxins.

Time in the mutation and selection process is not measured in years,
days, minutes or seconds, it is measured by generations (one of the
reasons why the Poisson distribution is not the correct probability
function for the mutation and selection phenomenon). There is
absolutely no evidence that parallelism occurs with the mutation and
selection phenomenon. You present breeding programs which your own
citation calls “unnatural selection”, and claim there is parallelism.
It takes hundreds of generations to amplify a beneficial mutation and
this process does not occur in parallel. This is why the theory of
evolution is mathematically irrational. It takes to many generations
to amplify a single beneficial mutation and the process does not occur
in parallel.
>[snip]
Greg Guarino Aug 26, 12:59 pm

Newsgroups: talk.origins
From: Greg Guarino <gdguar...@gmail.com>

Date: Fri, 26 Aug 2011 15:59:58 -0400
Local: Fri, Aug 26 2011 12:59 pm

Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

>On 8/17/2011 10:07 AM, Alan Kleinman MD PhD wrote:
>
>> On Jul 22, 1:07 pm, "g...@risky-biz.com"<gdguar...@gmail.com> wrote:
>>> On Jul 22, 3:35 pm, Alan Kleinman MD PhD<klein...@sti.net> wrote:
>>>> Each and every generation dozens
>>>> of neutral mutations must show up in the genomes of every person on
>>>> earth per evolutionist claims. This happens regardless where they live
>>>> and who they are descended from. Now why don’t you tell us which 50
>>>> neutral mutations have shown up in your genome and every other member
>>>> of the population of the earth?
>>> Really? You honestly believe that is the claim? That the same mutation
>>> occurs in every person on Earth at the same time? You believe that
>>> "evolutionists", which is to say, biologists, believe that?
>> You have John Harshman’s claim that the human and chimpanzee genomes
>> differ by 40,000,000. You have less than a million generations to
>> accumulate for those differences.
>Why can't you seem to answer the most basic questions? Do you or do you
>not think that the "evolutionist" argument includes neutral mutations
>spreading quickly through a population? (as opposed to slowly, but in
>massively parallel fashion)
Greg, the reason why you and other evolutionists are wrong about this
is that you are taking a very low probability process and claim that
millions of these processes are happening simultaneously. This is
incorrect mathematically because of the multiplication rule of
probabilities which governs the joint probabilities of random
independent events and this is wrong conceptually. This is wrong
conceptually because of common descent. What you are claiming is that
neutral mutations are appearing all throughout the population and that
they are spreading through to every member of the population
simultaneously. It just doesn’t make sense that neutral mutations in
one family line will show up in a different family line now or ever.
You have to have 20,000,000 neutral mutations show up in a single
family line. That is mathematically irrational thinking.

>>And you have every weird
>> mathematically irrational hypothesis coming from the fertile but
>> mathematically irrational minds of evolutionists to try to explain
>> away this accounting problem. In the process of bungling the basic
>> science and mathematics of mutation and selection with these
>> mathematically irrational hypotheses, evolutionists have managed to
>> harm millions of people suffering from diseases subject to the
>> mutation and selection phenomenon.
>We tend to ignore this little fugue of yours, but that doesn't mean it
>isn't complete nonsense. Evolutionary theory predicts antibiotic
>resistance, and indeed predicts that combinations of deadly agents will
>be difficult to evolve your way out of. If medical and agricultural
>people have made choices that ignore this, it is certainly not because
>evolutionary theory does not describe it accurately.
Greg, that’s a line of crap you are putting out. If evolutionists have
understood this, why haven’t they stepped into the debate and taught
medical students the correct basic science and mathematics of the
mutation and selection phenomenon. It hasn’t been taught correctly in
the past and it still is not taught correctly now. You have hersheyh
using the Poisson distribution to try to describe the mutation and
selection phenomenon yet he doesn’t understand why it is the wrong
distribution function. Evolutionist doctrine has so permeated the
thinking of biologists that you have Schneider at the National Cancer
Institute claiming on his government sponsored web site that the
multiplication rule does not apply to biological evolution when in
fact that is the reason combination therapy works. That is the
mathematical irrationality which is being taught by evolutionists.


>>> [ Breathe in. Breathe out. ]
>>> I made myself a promise some time ago not to use insulting language in
>>> my arguments. I think it's counterproductive, for one thing, giving my
>>> "opponent" an easy out.
>>> So I won't.
>> Good for you Greg. However without mathematically irrational
>> hypotheses and insults, evolutionists don’t have much of an argument
>> to support their mathematically irrational belief system.
>You've use the magic words twice in one sentence (again) and still
>managed not to say anything that approaches an argument.
You want it in a nutshell? The reason why the theory of evolution is
mathematically irrational is the multiplication rule of probabilities.
It doesn’t matter whether the process occurs with selection or not.
The random mutation can not make massive genetic transformations. And
if you understand that the multiplication rule of probabilities is the
central governing rule for the evolutionary process, it becomes an
easy matter to understand how to suppress the mutation and selection
process. Simply force the population to evolve against two selection
pressures simultaneously and then your problems with multidrug

resistant microbes, multiherbicide resistant weeds, multipesticide

resistant insects and less than durable cancer treatments have a
logical solution. Of course you will not transform reptiles into birds
or humans and chimpanzees from a common progenitor by this process.

>>On the other
>> hand, if you properly apply the theorems of probability theory to the
>> mutation and selection phenomenon, you can easily derive the
>> probability function that gives the probability of two mutations
>> accumulating in a population and you will find that this mathematics
>> fits the real behavior of mutating and selecting populations. In
>> addition, if you properly apply the theorems if probability theory to
>> the random recombination process, you will also understand why HIV
>> does not recombine mutations to accelerate the mutation and selection
>> process. This mathematics is above the skill level of most
>> evolutionists.
>The math you present isn't even above *my* skill level. And yet you
>think it is some sort of revelation. Mathematics must be applied
>properly to the question at hand. That's where your disagreement with
>standard biology is.

That’s my point Greg. This mathematics is not that difficult. The
mathematics of mutation and selection is very similar to the
mathematics of dice rolling yet we have geneticists like hersheyh
using the Poisson distribution to describe the phenomenon. Lenski’s
team is still using the Poisson distribution because this is what is
being taught and it is wrong. And the mathematics of recombination is
also quite straightforward. But you don’t see hersheyh posting the
derivation of that probability function. What are you evolutionists
going to do after I post the correct derivation for the probability
function for random recombination? Are you going to claim that that’s
what you’ve been doing all along? If that’s the case, post the
derivation now before I post it. What is being taught in biology
courses now is a collection of mathematically irrational evolutionist
crap. And we have multidrug resistant microbes, multiherbicide

resistant weeds, multipesticide resistant insects and less than

durable cancer treatments to show for this bungled evolutionist
teaching. And lest you think that physicians, farmers and
exterminators are too stupid to understand what I am saying here,
combination selection pressures are being used more and more in all of
these fields and not because evolutionists are teaching this but
because the necessities of reality are requiring it in order to deal
with these problems.

>>If they did have these mathematical skills, they would
>> understand why the theory of evolution is a mathematically irrational
>> belief system. With a correct understanding of basic science and
>> mathematics of mutation and selection and random recombination, you
>> can rationally and logically develop strategies for how to use
>> selection pressures to prevent multidrug resistant microbes,

>> multiherbicide resistant weeds, multipesticide resistant insects and

>> develop more durable cancer treatments. Evolutionists do not
>> understand or teach this basic science and mathematics of mutation and
>> selection and random recombination because it shows that the theory of
>> evolution is mathematically irrational.
>What are your goals, I wonder? If they are limited to convincing
>yourself that evolution is false, or perhaps preaching to the choir,
>continue as you have. But if you expect knowledgeable (or even merely
>intelligent) people to take you seriously, you'll need to spend less
>time repeating the talking points and more time addressing real
>questions in a substantive way.
>You choose.
>Greg Guarino
No Greg, you choose. You choose to understand that in any stochastic
process, the joint probability of random independent occurring is
governed by the multiplication rule of probabilities. That’s what all
the empirical evidence for the random mutation and natural selection
phenomenon shows. If you choose otherwise, you are choosing to believe

in a mathematically irrational belief system.

hersheyh Aug 26, 3:05 pm

Newsgroups: talk.origins
From: hersheyh <hershe...@yahoo.com>

Date: Fri, 26 Aug 2011 15:05:15 -0700 (PDT)
Local: Fri, Aug 26 2011 3:05 pm

Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

>> > > > All mutations start out in a single individual. It is just that every
>> > > > human has 50-200 new mutations that his/her parents don't have. Some
>> > > > fraction of these, over many generations will have drifted to
>> > > > fixation. Fixation of neutral mutations does not occur in only two
>> > > > years. It occurs at a rate of one or two per year. Fixation is the
>> > > > end of a process, not an instantaneous event.

>> > > Now you are correct, all mutations start out in a single individual.
>> > > But give us the step by step sequence how this neutral mutation for
>> > > this single individual ultimately ends up in the entire population of
>> > > the earth.

>> > The figure here
>> > http://www.google.com/url?sa=D&q=http://en.wikipedia.org/wiki/File:Random_genetic_drift_chart.png
>> > which can be found in this article
>> > http://www.google.com/url?sa=D&q=http://en.wikipedia.org/wiki/Genetic_drift
>> > shows the relationship between fixation of one of two alleles at a
>> > single gene locus that started out at 50% in a population and the size
>> > of the population. For populations of size 20, it is very clear that
>> > completely random variation from generation to generation can lead to
>> > fixation of one or the other allele rather quickly. For larger
>> > populations, the neutral drift away from the starting point is slower,
>> > but is still significant after a mere 50 generations. What this graph
>> > does not show is that the probability of mutation per generation also
>> > increases with population size. We have gone thru that math several
>> > times, and each time you have ignored it because you don't understand
>> > it. Why would it be any different this time?
>> I’ve read this page previously.

>Not, obviously, with any understanding.

Sure I understand what you are doing with this model. You are taking a
model for the fixation of a single neutral allele of two possible
alleles and grossly over-extrapolating the model to the fixation of
millions of alleles simultaneously. This is the mathematically
irrational crap that evolutionists are prone to do.

>> Your gross over-extrapolation of this

>> mathematics demonstrates your evolutionist bias. You try to take this

>> model and impose the results derived on John Harshman’s 40,000,000
>> differences between human and chimpanzee genomes.

>No. All I intended was that you understand why neutral drift happens. The end result of neutral drift can only be one of >two possibilities for a new mutational change in nt. Either that specific mutation will become fixed or it will go to >extinction. The probability that it will eventually become fixed is 1/2Ne, which is the initial frequency of that *specific* >historical mutant in the population. The probability that it will eventually become lost is 1-(1/2Ne). In the graph, instead >of the initial frequency of the alternate allele being 1/2Ne, it is set at 0.5 in the population. The Hardy-Weinberg equation >(you have heard of it, haven't you?) would imply that the next generation and all subsequent generation would also have >the two alleles in the same ratio. But that equation assumes an infinite population. In *real* populations, there is >generation to generation variance due to chance. The smaller the population of alleles, the larger the variance as a %. > And as many a gambler has learn

ed to his chagrin "Chance has no memory."

What exactly are you trying to say with all this blah, blah, blah? Are
you trying to say that John Harshman is making a mathematically
irrational extrapolation of this model to millions of neutral
mutations being fixed in 500,000 generations? Or are you trying to say
that the Hardy-Weinberg equations only tell you that the frequencies
of alleles remain constant when the system is in equilibrium? That
equation tells you nothing about the probability of two alleles to
randomly recombine. In order to do that, you need to derive the
probability function for random recombination. You haven’t done that
yet. Isn’t that equation in one of your genetics texts? Or are they
filled with the use of the Poisson distribution incorrectly?

>> On average, to
>> account for these differences requires the fixation of dozens of
>> neutral mutations generation after generation for hundreds of

>> thousands of generations. This drift model only takes into account the

>> fixation of one of two alleles as you describe above,

>In this case, the 'allele' is a single nucleotide pair and demonstrates that rather than the frequency being a constant, it >changes from generation to generation by chance for any specific *selectively neutral* alleles.

So now an allele is a single nucleotide pair. And you claim that I
don’t know what an allele is and now your claiming an allele is a
nucleotide pair. This must be one of your many classic brain farts.

>> not the fixation
>> of dozens of neutral alleles every generation

>That would be about 30/generation out of 3X10^9 possible sites or about 0.000001% of all sites having reached the state >of fixation.

You’ve never heard of the multiplication rule of probabilities for
computing the joint probability of random independent events, have
you? This is the rule which makes the theory of evolution
mathematically irrational and what you’ve made a career out of
teaching.

>> and when in reality, you
>> have more than two possible alleles at a single locus.

>Actually, any natural population has a degree of heterozygosity at any locus or site, which is measured by F-statistics >(fixation indices).
>http://www.google.com/url?sa=D&q=http://www.library.auckland.ac.nz/subject-guides/bio/pdfs/733Pop-g-stats2.pdf
>Basically, what you might expect at neutral sites is that a fraction of them will have heterozygosity at detectable levels >between 1 and 99% (typically divided between two alternatives rather than 3 or 4, although there can be a small >scattering of the other possible nts). Most neutral sites will be almost completely one nt or another, with a small >scattering of other nt's. That is effective fixation. That is what is seen. The amount of heterozygosity in a population's >neutral changes is affected by the amount of inbreeding. Populations that have undergone constrictions recently, either >because of a population crash or because of the founder effect, will show less heterozygosity. Old, large, stable, >randomly reproducing populations will tend to show more heterozygosity.

Do you want to try rewriting your model for drift using multiple
neutral alleles? Do you think that will make the gross over-
extrapolation of this model to fit your belief system any less
mathematically irrational?

> I don’t ignore this model; I ignore your inappropriate over-
> extrapolation of this model. You have failed to understand the basic
> science and mathematics of the mutation and selection phenomenon, you
> are now failing to understand the mathematics of random recombination

I wasn't even mentioning recombination here. Do you spout these words
just because you can?

Not only can I spout the words, I can back it up with the mathematics.
I’ve already presented the derivation of the correct probability
function for the mutation and selection phenomenon and you almost
understand it. We still need to work on your inappropriate use of the
Poisson distribution. Have you done your homework yet and gone through
the derivation of the equation that you blindly use without
understanding? And have you gone through the conditions when the
Poisson distribution is an appropriate approximation for a binomial
distribution (which mutation and selection is not). Once you have done
this, I’ll show you how to derive the probability function for random
recombination so you can actually get beyond the Punnett square and
the Hardy-Weinberg equation.

>> and now you take a model based on the random substitution of a single
>> allele for another allele and claim that this entire process occurs in
>> parallel allowing the random substitution of dozens of neutral alleles
>> to occur simultaneously.

>That is exactly correct, although simultaneous is wrong for fixation, as the *individuals* in which the final step of fixation >occurs each generation are almost certainly not going to be a single individual, but different individuals in the population. > If you have problems understanding that, let me know and I will patiently try to teach you, cricket.

I’m really not interested in being indoctrinated by you. If you have
some mathematics to show us, present it but in the meantime, we have
to wade through your blah, blah, blah in hopes of finding something
beyond your brain farts.

>> I suppose you are now going to claim that the
>> multiplication rule of probabilities
>The multiplication rule of ...
Always applies for computing the joint probabilities of multiple
random independent events whether selection is involved or without
selection as with neutral evolution.


hersheyh Aug 26, 10:12 pm

Newsgroups: talk.origins
From: hersheyh <hershe...@yahoo.com>

Date: Fri, 26 Aug 2011 22:12:08 -0700 (PDT)
Local: Fri, Aug 26 2011 10:12 pm

Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

On Friday, August 26, 2011 9:21:46 AM UTC-4, Alan Kleinman MD PhD
wrote:

>> On Jul 25, 9:49 pm, John Harshman <jhar...@pacbell.net> wrote:
>> > Alan Kleinman MD PhD wrote:

>> > > On Jul 5, 7:55 am, John Harshman <jhar...@pacbell.net> wrote:
>> > >> Alan Kleinman MD PhD wrote:

>> > >>> On Jun 6, 8:40 am, John Harshman <jhar...@pacbell.net> wrote:
>> > >>>> Alan Kleinman MD PhD wrote:

>> > >>>>> On May 16, 9:55 pm, John Harshman <jhar...@pacbell.net> wrote:
>> > >>>>>> Alan Kleinman MD PhD wrote:

>> > >>>>>>> On May 9, 9:51 am, John Harshman <jhar...@pacbell.net> wrote:
>> > >>>>>>>> Alan Kleinman MD PhD wrote:

>[snip]
>> > >> I don't have to show you an example in order to show that it's possible
>> > >> for something to happen. Can you explain why it's not possible? What
>> > >> would prevent part of allele A from recombining with part of allele B to
>> > >> produce allele C, different from both?
>> > > A chimera is an error in recombination.
>> > What do you mean by that? It doesn't appear to make any sense, or to
>> > have any relevance.
>> Sexual recombination is not an error in replication but a shuffling of
>> existing alleles.
>It is the generation of different combinations of genes wrt their parentage. That is, if the allele marked m is of maternal >origin, regardless of whether or not is identical or different from the allele marked p, which of paternal origin, and two >genes, A and B, are unlinked -- written as Am/Ap; Bm/Bp -- then you expect the following haploid gametes in the >following ratio: 1 Am;Bm: 1Am;Bp: 1Ap;Bm: 1Ap;Bp.

Really hersheyh, why would you expect that ratio? How many members in
your population? How many have each allele?

>If mating of such individuals is random, you expect the following progeny (arranged in Punnet Square):
> 1 Am;Bm 1Am;Bp 1Ap;Bm 1Ap;Bp
>1 Am;Bm Am/Am; Bm/Bm Am/Am; Bm/Bp Am/Ap; Bm/Bm Am/Ap; Bm/Bp
>1Am;Bp Am/Am; Bm/Bp Am/Am; Bp/Bp Am/Ap; Bm/Bp Am/Ap; Bp/Bp
>1Ap;Bm Ap/Am; Bm/Bm Ap/Am; Bm/Bp Ap/Ap; Bm/Bm Ap/Ap; Bm/Bp
>1Ap;Bp Ap/Am; Bp/Bm Ap/Am; Bp/Bp Ap/Ap; Bp/Bm Ap/Ap; Bp/Bp
>I am of course guessing, but I do hope that the Dr.Dr. is reasonably familiar with this very basic sort of Mendelian >genetics. If the m and p alleles were related by phenotypic dominance and recessiveness, this would be a familiar >1:3:3:9 phenotypic ratio.

I am and the Punnett square is used to predict the outcome of a
breeding program, not random recombination. If you think this is the
mathematics which describes the random recombination HIV is doing, why
not tell us why recombination does not accelerate the evolutionary
process for HIV when selection pressures are targeting two genes
simultaneously. In order to understand this you can’t use the Punnett
square, you have to derive the probability function for random
recombination and you don’t know how to do this despite the fact that
you are a teacher of genetics for the past 20 years. Perhaps your
indoctrination as an evolutionist neglected some aspect of your
training as a scientist.

>> New genetic information in the gene pool is not
>> created by recombination
>New combinations certainly can produce new phenotypically variant individuals. Assuming that the capital letter is the >dominant allele, the individual with the genotypes A/A;b/b has a different genotype (and hence different phenotypes) >from the individual with the genotype a/a;B/B. And both can exhibit different phenotypes than their progeny with the >genotype A/a;B/b. For example, if A is dominant for brown eyes, B is dominant for brown hair, and a and b are recessive >with the phenotypes blue eyes and blond hair, the individual with the genotype A/A;b/b is brown-eyed and blond, the >individual with a/a;B/B is a blue-eyed brunette and the A/a;B/b individual is a brown-eyed brunette. I can tell them apart, >even if our good Dr. Dr. cannot. Moreover if I crossed individuals which were A/a;B/b to each other I would even get >blue-eyed blonds by recombination. That is four different phenotypes by my count that one can get by recombination.

Of course recombination can change the expression of existing alleles.
Are you going to tell us that a breeding program of alligators and
crocodiles will give us birds? Are you going to tell us that
recombination explains the 40,000,000 differences between human and
chimpanzee genomes? When are you going to derive for us the
probability function that describes random recombination? Why don’t
you admit that with all your expertise as an evolutionist and
geneticist that you don’t know how to do this calculation and have
never been taught how?

>> as can be done by mutation and selection
>> unless there happens to be an error in the recombination process.
>> Directional selection pressures require the creation of new alleles.
>No. As even the good Dr. Dr. might guess from the word "selection", all selection does is differentially affect the >reproductive success of different phenotypes (and indirectly genotypes to the extent that such phenotypes are due to >different genotypes). Selection can only work on alleles that *either* pre-exist in the population or that spontaneously >and randomly occur later (which, of course, means that for the variant to appear later, the selection cannot be lethal to >the w.t. and even substantial toxicity, by reducing population size, affects the probability of mutations actually occurring). > Selection requires that the selected variant actually exist in the population.

You don’t tell the whole story, you don’t even tell most of the story.
Certainly when a population is subjected to a new selection condition,
some members must be able to tolerate the selection condition or the
population will go extinct. But then the mutation and selection
process put the variants of the population on particular trajectories
of the fitness landscape if those variants are able to become better
replicators by beneficial mutations. What you don’t tell in your blah,
blah, blah is how the selection conditions affect the shape of the
fitness landscape and what happens when selection targets more than a
single gene at a time. That’s why you have to use the correct
probability function to describe the phenomenon and the Poisson
distribution is not the correct equation. And I expect you still
haven’t studied the derivation of the Poisson distribution yet. You
use the equation blindly without understanding what is being
calculated.

>> How do populations do this and under what circumstances and how
>> quickly does this creation of information occur? If the creation of
>> information by mutation and selection is not quick enough, the theory
>> of evolution is a mathematically irrational belief system and the
>> creation of information by mutation and selection is not quick enough
>Except, of course, in the many examples the Dr. Dr. has presented here where it is quick enough to actually be observed >in bacteria which must evolve by sequential processes rather than in parallel processes.

So is your story now changing? Are you now claiming that mutation and
selection does work in parallel but much more slowly? Once you figure
out that the rate of an evolutionary process is measured using
generations, not years, days, hours, minutes or seconds then perhaps
you will understand HIV which can evolve resistance to a single drug
in days but with three drug therapy, people can and do live for
decades with the virus. How many tens of thousands of generations will
it take HIV to evolve resistance to directional selection pressures
targeting just two genes in parallel?

> > >> > And do you believe that inbreeding doesn�t cause the loss of
> > >> > alleles in a population?
> > >> It certainly can. How is that relevant to your previous claim? What does
> > >> inbreeding have to do with recombination?
> > > Selection always causes the loss of alleles in a population whether it
> > > is mutation and selection or recombination and selection. Selection
> > > always causes the loss of genetic information from the population. The
> > > only way you can increase the diversity of populations is through
> > > mutations.
>> > Not true. Selection causes a change in frequency of alleles. It may not
>> > cause a loss of alleles. Balancing selection, for example, maintains
>> > alleles in a population, i.e. it prevents loss of alleles.
>> Of course it’s true. If selection pressures are intense enough it
>> drives the population to extinction and all the alleles of that
>> population are history. If white moths are much more susceptible to
>> predation, members with that coloration will be selected out until
>> that variant becomes extinct. New white moths will only appear because
>> of mutation.
>Or because the allele for white is recessive with the allele decreasing to the point where p^2 is really small and most of >the white alleles are hidden in heterozygotes, with homozygotes only seen in small inbreeding populations that, by >chance, have such a hidden allele.

But that possibility does not make the theory of evolution
mathematically rational. It takes a lot more than a recessive trait to
make the theory of evolution mathematically rational.

> > But anyway, how is this relevant either to showing how your previous
> > statement is relevant or to the question at hand?
> Selection always causes the reduction in diversity of a population.
No it doesn't. Again, we have mentioned frequency dependent selection
before and you seem to have had that information go into the black
hole of your memory along with the idea that neutral evolution is
slow. Perhaps late onset Alzheimers? I say late because you already
stated that your last academic work, in some kind of algebra, was in
the dinosaur age.

You’re the one who claims that you’ve forgotten more about mutation
and selection than I could ever learn. You’ve forgotten how to derive
the correct probability function for mutation and selection, you’ve
forgotten how to derive the correct probability function for random
recombination and now you use one of the few evolutionist tools of
argument, the slogan. Why don’t you give us an example of frequency
dependent selection and show us how it increases the diversity of the
population?

>> Selection does this because it always kills or impairs reproduction of
>> some or all member of a population. Selection pressures are not your
>> friendly transform reptiles into birds force; selection pressures are
>> killing or impairing the weaker members of a population from
>> reproducing.
>Selection involves *differential* reproductive success for sure. Killing only sometime. Again, you can easily have a >change in the frequency of two alleles from 0 to 100% and from 100% to 0% with little or no effect on total population. > Selection does not require a population crash or reduction. It can even occur with an increase in population, as the >Lenski experiment demonstrated both early and after the mutation that allowed citrate metabolism. At no time did that >population decrease in size or even slow down in doubling. It only increased in rate and numbers.

Again, sloganeering, no empirical examples. Lenski’s populations only
increased after they improved fitness. They only reason that his
populations didn’t decrease in size or slow down in doubling is that
they replenished glucose on a regular basis. You wouldn’t want his
entire population to starve to death?
>[snip]
>> On the other hand, I’ve derived the correct probability function for
>> two beneficial mutations to occur and correlated that with the
>> empirical evidence.
>Where have you presented a "correct" probability function? You have repeatedly presented an amateurish derivation of >the binomial probability distribution mucked up by somehow thinking that mutation rates need to be divided by four. And >you cannot even do that correctly.

Only a mathematically incompetent evolutionist nitwit would think that
the Poisson distribution is the correct probability function for the
mutation and selection phenomenon. And what kind of nitwit would use a
distribution function for decades without going through the derivation
of the function? Someone who doesn’t know that (a^x)^y = a^(x*y) would
do that. And what is becoming clearer and clearer is that you will
never figure this out yourself. I am going to have to hold your hand
and go step by step through the calculation to show you why you are
wrong. You don’t know when the Poisson distribution is an accurate
approximation of the binomial distribution and you can’t tell the
difference between the mutation and selection probability distribution
and the binomial distribution. I’m going to let you stew in your
mathematically irrational primordial soup for a while and then I’ll
walk you through the mathematics so you can finally start teaching
genetics properly. How pathetic that you’ve wasted yours and students
time and money with your bungled mathematics.
>> I’ve demonstrated both mathematically and
>> empirically how crucial amplification of beneficial mutations are for
>> the mutation and selection process to work.
>Amazing. It took the good Dr. Dr. to remind us that reproductive growth is a rather important function of life and that >dead organisms generally leave no progeny. Amazing what a creationist considers profound!

And it’s the bungled stupidity of evolutionists who fail to recognize
that if this doesn’t occur that the multiplication rule of
probabilities makes the probability of the next beneficial mutation
occurring a very low probability event. How could you evolutionists
miss such a simple finding? Perhaps it started with claims like
Schneider’s that the multiplication rule of probabilities does not
apply to biological evolution. That is the fundamental blunder of
evolutionism. This is why the theory of evolution is mathematically
irrational.

> Once hersheyh demonstrates
> his inability to derive the correct probability function for the
> random recombination of two alleles,
As I have pointed out, different alleles of the same gene can and do
recombine, but are typically tightly linked and so do not do so
"randomly". Until you actually state a reasonable problem using
correct definitions, I have no idea what you are talking about when
you talk about recombination of two alleles.

You are so slow and confused hersheyh. Let’s put this calculation in
terms of a real physical case. Start with a population of HIV in a
patient treated with combination therapy. In that population are some
viruses with a protease allele that would give resistance to the
protease drug (call this the A allele) and other viruses with a
reverse transcriptase allele that would give resistance to the reverse
transcriptase drugs (call this the B allele). Let C be all the other
alleles. Let N be the total population of viruses, nA be the number in
the subpopulation with the A allele, nB be the number in the
subpopulation with the B allele and nC be the rest of the population
without either the A or B allele. What is the probability that an A
and B member will meet and recombine to produce a member that has both
the A and B alleles? None of your blah, blah, blah, we want an
amateurish derivation of the algebraic probability function that would
describe the probabilities of this event. I don’t want you to worry
about this calculation, it doesn’t require recognizing that (a^x)^y =
a^(x*y). And I’ll give you a big hint; it is not the Poisson
distribution, the only distribution function you ever use because it
is easy, not because it’s correct.

>> I will present that probability
>> function to you with the derivation of that mathematics as well. It
>> will give the mathematical explanation why HIV (and other mutating and
>> selecting populations) can not evolve efficiently to two selection
>> conditions simultaneously despite the fact this population can do
>> recombination.
>Rarely and sporadically. Why don't you show what you mean with some eucaryotic sexually reproducing organism >rather than almost always clonal organisms like HIV or bacteria (especially since most experimental evolutionary work >with bacterial genomes -- as opposed to plasmid genomes -- is done under conditions designed to prevent bacterial >recombination)?

As usual, you forget what your own citation show which is that HIV
does recombination. But I assure you if you do the calculation
properly, it will apply to eukaryotic organisms as well.


John Harshman Aug 29, 4:33 pm

Newsgroups: talk.origins
From: John Harshman <jharsh...@pacbell.net>

Date: Mon, 29 Aug 2011 16:33:19 -0700
Local: Mon, Aug 29 2011 4:33 pm

Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

>>>> John, you need to do a little better job explaining your junk science
>>>> and mathematics. So now the 40,000,000 differences between the human
>>>> and chimpanzee genomes occurred millions of years ago?
>>> If by "occurred" you mean the mutations themselves, that's always been
>>> the case. Don't blame me for your inability to read and understand.
>> So now you are claiming that millions of mutations occurred millions
>> of years ago and they are all being fixed today?
>No. If only you could read, this would be an easier conversation.
>> Or are you saying a
>> few mutations occurred millions of years ago and they are now being
>> fixed today?
>No.
>> Or are you saying that millions of mutations occur today
>> and they were fixed millions of years ago?
>No.
>So, what I really am saying: Billions of mutations occur in every
>generation. Of these billions, a couple of hundred will eventually
>become fixed, but the mean time until fixation is very long, a number of
>generations equal to 4 times the effective population size. The rest
>will be eliminated, most within a few generations. In any given
>generation, there are many, many alleles at intermediate frequencies,
>some of which will eventually become fixed.

I get your mathematically irrational argument now. You are claiming
that a very low probability event will happen 20,000,000 times in
500,000 generations and that the multiplication rule of probabilities
for computing the joint probability of events does not apply because
this is a hand of bridge. You obviously are playing dummy in this
hand.
>Standard neutral theory. Read up on it.
>>>> I thought
>>>> evolutionists claim that humans and chimpanzees diverged only 5-10
>>>> million years ago.
>>> Yes. But do you understand that the populations that diverged already
>>> had genetic polymorphisms? Many of the 40 million differences were
>>> already present in the pre-split population, as polymorphisms.
>> Oh, now I get you.
>Experience shows that you never do. A look below shows that experience
>is right.

Sure I do, you are playing dummy.

>> Human and chimpanzee populations actually pre-split
>> millions of years earlier than when they actually split. These
>> populations were still interbreeding but their pre-split differences
>> didn’t recombine in this pre-split period. When these two populations
>> finally did make their final split after their pre-split period, how
>> did they split the community property? Maybe they just had a pre-split
>> personality. Or am I just splitting hairs here. I do find your
>> conceptual examples a banana split.
>Nothing you say above is true.

Oh John, I’m so disappointed in you. I thought you were telling the
truth when you said that humans and chimpanzees had a pre-split
period.

>>>> So now you are claiming that the 40,000,000
>>>> differences occurred millions of years ago. Your claims are not
>>>> measurable and your mathematics is irrational and incoherent.
>>> Only because you have no idea what I'm saying, for some reason I can't
>>> figure out.
>> Of course I understand what you are saying. Before humans and
>> chimpanzees made their split, they had a pre-split period where they
>> were still interbreeding but they did not recombine their pre-split
>> differences before the final split was made. John, how long was the
>> pre-pre-split period when humans and chimpanzees still recombined?
>There is no such period.
Then why did you mislead us John. Oh John, oh John.

>>> [snip mantra]
>>> I see you still refuse to answer simple questions.
>Still. Or maybe it's just that you can't.
Sorry, I don’t have time now, I have to split, or is that pre-split.


John Harshman Aug 29, 4:39 pm

Newsgroups: talk.origins
From: John Harshman <jharsh...@pacbell.net>

Date: Mon, 29 Aug 2011 16:39:24 -0700
Local: Mon, Aug 29 2011 4:39 pm

Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

Alan Kleinman MD PhD wrote:

> On Aug 1, 6:42 pm, John Harshman <jharsh...@pacbell.net> wrote:
>> Alan Kleinman MD PhD wrote:

>>>> You need to explain that to Mark Isaak because he thinks that
>>>> mutationandselectiondiddoit.
>>> Based on prior experience, I am unwilling to take your word for anyone
>>> else's opinion, since you show so little ability to read for
>>> comprehension. And I'm pretty shure that Mark accepts the standard
>>> theory of neutral evolution. Can you back up this claim? Based on prior
>>> experience, I think not.
>And it turns out I was right. You don't even try.

Now John, you are the lazy one here, you had a burst of honesty and
admitted it.
>> Mark’s mathematically irrational claims are all over the place, not
>> just literally but also figuratively. Just because Mark might accept a
>> mathematically irrational concept does not make it true or correct.
>> Even you make irrational conflicting claims about neutral evolution.
>> In one sentence you are claiming about neutral evolution “No. Only a
>> couple of hundred per generation.”, and then just a few sentences
>> later you make the following claim “Nobody claims that drift is faster
>> than selection. Quite the reverse.”
>Part of your amazing incomprehension is your belief that these are
>somehow contradictory claims.

Maybe you have a split personality or perhaps it’s a pre-split
personality.

>> So are you now claiming that
>> selection fixes more than hundreds of mutations per generation? This
>> is what you get from evolutionists, mathematically irrational mumbo
>> jumbo and one conflicting claim after another.
>You have confused quantity with speed. Which delivers more water over a
>given time: a one-inch diameter pipe flowing at 10ft/sec or a
>hundred-inch diameter pipe flowing at 1ft/sec?

I think you are right. We are getting a large quantity of
mathematically irrational evolutionist crap at an ever increasing
rate. I wonder if there is a physical limit to this like the speed of
light? We can call it the speed of croc. It is measured by the amount
of raw evolutionist sewage that flows through a hundred-inch diameter
pipe at 1ft/sec.

>>>>>> And
>>>>>> driftdidn�tdoiteither.
>>>>> How do you know that?
>>>> Hersheyh said �A rare few will become relatively more frequent.� I
>>>> would think that 40,000,000 neutral mutations being fixed is more than
>>>> a �rare few�.
>>> That's one of your most basic misunderstandings. Remember that this
>>> requires only a couple of hundred out of the billions of mutations that
>>> happen in the population to ever become fixed. That's what "a rare few"
>>> means. I would call 40 million out of untold billions "rare". What about
>>> you?
>> I think your mathematical skills are rare. When will you evolutionists
>> ever come to grips with the mathematical reality that in any
>> stochastic process, the joint probability of random independent events
>> occurring is governed by the multiplication rule of probabilities?
>> This is true whether selection is acting or not. Once you understand
>> this, the behavior of empirical examples of mutation and selection and
>> neutral evolution will become more clear to you. But then you will
>> realize that the theory of evolution is a mathematically irrational
>> belief system.
>As I've told you so many times, your fallacy here lies in computing the
>joint probability of two particular events, rather than the probability
>of any two of many events.

John, I think you should apply your mathematical logic with the
purchase of many lottery tickets. And then you can tell us how many of
the two of many events you won. And remember, the more tickets you
buy, the better your chances of winning two of many events.

>>>>>> Of course you could tell us how 25 neutral
>>>>>> mutations from the population of the world got into your genome. You
>>>>>> must have a lot of people drifting by your place.
>>>>> I have no idea what you think that means, but your idea of neutral
>>>>> evolution is clearly wrong.
>>>> So the 40,000,000 differences between the human and chimpanzee genomes
>>>> weren�t neutral differences?
>>>>> So how do you suppose those 35 million differences got there? Why won't
>>>>> you answer?
>>>> John, what I can tell you that it is a mathematical impossibility to
>>>> get those 35 or 40 million genetic differences fixed into the genomes

>>>> in less than a million generations.

>>> Why won't you answer the question, no matter how many times it's asked?
>> What I can tell you from hard mathematical science that neither
>> mutation and selection nor neutral evolution can do the accounting
>> required for the transformation. That’s why the theory of evolution is
>> a mathematically irrational belief system. You just won’t accept that
>> mathematical and empirical reality of how mutation and selection
>> actually works. It must be against your evolutionist religion.
>Why won't you answer the question, no matter how many times it's asked?

Asked and answered. How many lottery tickets have you bought so far?
Have you won two lotteries yet?

>>> And could you back up your claim of impossibility with some kind of
>>> calculation? Based on prior experience, I'm sure you can't.
>[snip mantra again]
Reptiles turn into birds, no multiplication rule of probabilities,
reptiles turn into birds, no multiplication rule of probabilities…


John Harshman Aug 29, 4:42 pm

Newsgroups: talk.origins
From: John Harshman <jharsh...@pacbell.net>

Date: Mon, 29 Aug 2011 16:42:16 -0700
Local: Mon, Aug 29 2011 4:42 pm

Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

>>>> Don�t you know that a beneficial mutation at the particular locus can
>>>> mutate back to a detrimental or neutral mutation? Unless you know a
>>>> priori what the base at the particular locus is, a point mutation can
>>>> give any of the four possible bases.
>>> That's just as nonsensical as it was the first time you made the claim.
>>> The ability of back mutations to happen is irrelevant to the mutation
>>> rate. Regardless of the original base, one of your four possibilities is
>>> not a mutation. A->A is not a mutation. C->C is not a mutation. G->G is
>>> not a mutation. T->T is not a mutation. Your inability acknowledge the
>>> error of a prior claim, regardless of how stupid it is, makes you look
>>> seriously insane.
>> What it makes you look is mathematically incompetent which you are.
>> You have hersheyh claiming there are only two possible outcomes for a
>> point mutation.
>No he doesn't.

Sure he does John, the two outcomes are either beneficial or not
beneficial. What do you thing the probability is on a single trial for
the probability of either beneficial or not beneficial? What do you
think the probabilities for the outcome are for single trial for one
of the four bases? This is a simple mathematical question. This is a
question you have to answer if you are assuming a binomial
distribution or the distribution I derived for you. It also addresses
the conditions whether the Poisson distribution can be used to
approximate this stochastic process.

>> The day that you can tell us where a random point
>> mutation will occur before it occurs and the base that was at that
>> locus before the mutation occurred is the day that I’ll change the 4
>> in the correct probability function for a 3 but that day will never
>> come.
>The day you learn anything new will never come. I can tell you that,
>whatever and wherever a point mutation occurs, it will change the base
>that was there to a different base. Tell me, for any given prior base,
>how many possible different bases are there?
If you know what the prior base is three, if you don’t know what the
prior base is, you can only say with certainty that it is one of the
four possible bases.

Bill Aug 29, 5:26 pm
Newsgroups: talk.origins
From: Bill <brogers31...@gmail.com>
Date: Mon, 29 Aug 2011 17:26:09 -0700 (PDT)
Local: Mon, Aug 29 2011 5:26 pm

Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

On Aug 30, 7:09 am, Alan Kleinman MD PhD <klein...@sti.net> wrote:
>> > > And who has 6 billion bases in their genome?
>> > Pretty much ever single human being. How many do you think? (Remember
>> > that you are presumably diploid.)
>> Now John, we have about 3 billion base pairs in our genome so I guess
>> you could claim there are six billion bases in our genome. Are you
>> trying to claim there are 6 billion possible point mutations that
>> could occur?
>Well, you seem not to be sure about what diploid means. But apart from
>that, you also seem to have forgotten your favorite factor of four.

Sure I remember what diploid means. Like you have a mathematically
irrational twin who is a match for you, are you both still using the
linear term of the Taylor Series expansion inappropriately?

This ends responses to post 926-950

[hersheyh]

On Wednesday, September 21, 2011 7:27:54 PM UTC-4, Alan Kleinman MD PhD wrote:
[snip]

> hersheyh Aug 24, 12:59 pm

> >> On Jul 22, 9:18 pm, hersheyh <her...@yahoo.com> wrote:
> >> > The figure here
> >> > http://www.google.com/url?sa=D&q=http://en.wikipedia.org/wiki/File:Random_genetic_drift_chart.png
> >> > which can be found in this article
> >> > http://www.google.com/url?sa=D&q=http://en.wikipedia.org/wiki/Genetic_drift
> >> > shows the relationship between fixation of one of two alleles at a
> >> > single gene locus that started out at 50% in a population and the size
> >> > of the population. For populations of size 20, it is very clear that
> >> > completely random variation from generation to generation can lead to
> >> > fixation of one or the other allele rather quickly. For larger
> >> > populations, the neutral drift away from the starting point is slower,
> >> > but is still significant after a mere 50 generations. What this graph
> >> > does not show is that the probability of mutation per generation also
> >> > increases with population size. We have gone thru that math several
> >> > times, and each time you have ignored it because you don't understand
> >> > it. Why would it be any different this time?

> >> I ve read this page previously. Your gross over-extrapolation of this
> >> mathematics demonstrates your evolutionist bias.

So tell us why the math is a "gross over-extrapolation" due to "evolutionist bias".

> >So, exactly what is wrong with the math, mathematically? Is it the statement that the probability of
> > a neutral mutation that has just occurred at a nt site becoming fixed in a population = 1/(2Ne),
> > where Ne is the effective population size? Is it the statement that the probability of a mutation at
> > that nt site occurring being 2Ne*u, where u is the mutation rate for that site (again, assuming
> > selective neutrality or near neutrality)? Are you claiming that there are not 3 X 10^9 nt sites in
> >the haploid human genome? Are you claiming that the vast majority of those sites are selectively
> > crucial (a statement that is contrary to evidence since the mean mutation rate for point mutation is
> > around 10^-8), or do you agree that most mutation is selectively neutral?

> There is nothing wrong with the mathematics. What is wrong is your
> extrapolation of this mathematics to multiple neutral mutations
> simultaneously being fixed in the population.

So, are you saying, then, that there is nothing wrong with the calculation that the probability of fixation per nt site is u, the mutation rate? That your problem then comes from the multiplication of the probability of fixation per nt site by the total number of nt sites per haploid genome to get the rate of fixation per generation per haploid genome? Exactly how is that mathematically wrong or an extrapolation? The terms do come out to give the rate of fixation per generation per haploid genome, don't they? It is no different from saying that if the probability of a 6 per roll is 1/6, in 600 independent rolls I would expect to see 100 6's. Or saying, if I line up 100 coins and the odds of heads is 1/2 per coin flip, that I would expect, over all 100 coins flipped to see 50 heads. Are those irrational mathematical extrapolations?

> You have this enormous
> mathematical blind spot in your thinking. You somehow throw out the
> multiplication rule of probabilities for computing the joint
> probability of multiple independent events for every stochastic
> process you see fit. This is not mathematically based science you are
> practicing. This is evolutionist mathematical irrationality.

Exactly where, in the above, did I "throw out the multiplication rule of probabilities" or use it incorrectly? Are you claiming that, if the probability of heads per coin flip is 1/2, that if I flip a hundred coins I should multiply the probability of heads in each coin flip together to get (1/2)^100? Is that what you think the *correct* use of the multiplication rule implies? It sure seems like you are claiming that the *correct* use of the multiplication rule in the above equations would involve u^3000000000, that is, multiplying the probability of fixation per nt by itself 3 billion times. Again, that would be like claiming that the probability of getting heads in flips in 100 coins is (1/2)^100.

> What I am saying is that whether the genetic differences are selective
> or neutral makes no real difference in the mathematics of evolution.
> Let all the genetic differences between humans and chimpanzees be
> selective which gives the most rapid fixation of mutations. You are
> still no where close to being able to do the mathematical accounting
> for these differences in 500,000 generations.

Show your math here: Ooops. All we get is your WAG.

> You can be as derisive
> as possible but that will not give you any scientific or mathematical
> evidence to support your mathematically irrational belief system and
> in the meantime you have bungled the basic science and mathematics of
> the mutation and selection phenomenon and harmed millions of people in
> the process.
>
> >> You try to take this
> >> model and impose the results derived on John Harshman s 40,000,000
> >> differences between human and chimpanzee genomes.
> >Quite successfully.
> If you want to call it a mathematically irrational extrapolation that
> throws out the multiplication rule of probabilities for the joint
> probabilities of multiple independent events for a stochastic process,

> it�s a perfect fit for your mathematically irrational belief system.

>
> >> On average, to
> >> account for these differences requires the fixation of dozens of
> >> neutral mutations generation after generation for hundreds of
> >> thousands of generations.
> >Yes. But fixation is actually a fuzzy boundary when you have a population of 6 billion people because that size almost >guarantees new point mutation at every site. Basically, all that is required for fixation is that the last step from Ne-1 (or >several) individuals having an originally new mutant allele that was first acquired long ago become Ne - 0 by loss of the >few individuals having the original w.t. allele. When you look at the chimp compared to human genome and the time >available since last divergence, the amount of difference seen is that expected if most of the genome is selectively >neutral. That is, the mathematics appears to work in the real world under the assumption that most of the nt's in the >human and chimp genome are selectively neutral (any of the 4 possibilities will have the same functional effect). We >*know* that not all the sequence differences are due to drift (the slowest mechanism for producing a difference). Some >(small) fraction of difference is of selective importa

nc
>
> e.
> Hersheyh, you play fast and loose with population sizes. Do you think
> that five million years ago there was a population of 6 billion
> progenitors?

Not at all. In fact, the best estimate is that during most of its existence, human populations were closer to 10,000 individuals. But I was just commenting on the difficulty of defining "fixation" in a large population. I wasn't using the number 6 billion anywhere in any equation. Can you possibly try to read for comprehension?

> This is why your analysis is a crock of hot steaming bs.

> Why don�t you try doing the analysis of the fixation of two neutral

> mutations in a similar manner as the fixation of a single neutral
> mutation and present the algebra to us? Oh, I forgot, all you know how
> to do is blah, blah, blah and plug in numbers in the wrong probability
> distribution.

No probability distribution. But if I correctly calculated the probability of fixation for a single nt site, the probability for fixation in one of two nt sites would be twice the probability of fixation for a single nt site. I am not interested in the probability that both of the two nts have a fixation. I am interested in how many fixation events there will be if I look at N nts. That is equivalent to asking the probability of getting a six in six flips of the dice. That answer is one, and that is an answer to a different question than asking the probability of getting a six in all six flips of the dice, which is the question you are asking. The mathematical answer to the first is (1/6)(probability of a six per flip)*6(number of flips) = 1 six per six flips. The mathematical answer to the second is (1/6)^6 = 0.0000214 the probability that 6 flips will give a 6 every time.

> >> This drift model only takes into account the
> >> fixation of one of two alleles as you describe above, not the fixation
> >> of dozens of neutral alleles every generation and when in reality, you
> >> have more than two possible alleles at a single locus.

It is just correctly multiplying the probability of an event per trial times the number of trials to get the expected mean number per that many trials. Like multiplying the probability of a 6 per dice throw by the number of dice throws to get the expected mean number of 6's in that larger number of throws.

> >We are talking about point mutational changes in nt's, not alleles or alternate forms of genes. Learn
> > the meaning of genetic terminology, why don't you -- at least before you say more ignorant things?
> > In most genes (say, a coding sequence for a 300 aa protein, thus 900 nt), neutral drift is 1) less
> > likely since the protein must function and there is more constraint on nt sequences, 2) when it
> > occurs, is more likely to be a point mutation that does not change the aa sequence encoded, 3)
> > when an aa is changed by neutral fixation, it will tend to be similar in characteristics (e.g.,
> >hydrophobicity) or in an unnecessary part of the protein, 4) will, given the time of divergence
> > between chimps and humans, produce an average of somewhat less than one aa change per
> > average size protein (in a Poisson distribution, btw), 4) nt changes will be somewhat less frequent
> >than in non-coding regions.

> Your sloppy analysis by blah, blah, blah doesn�t cut it. And the

> Poisson distribution is not the correct probability distribution for
> the mutation and selection phenomenon.

A Poisson distribution of aa changes in protein (per 350 aa lengths) is what an intelligent person with mathematical knowledge would predict if most aa changes in proteins were selectively neutral. However, it is a fact that larger proteins tend to differ more than smaller proteins in which more of the sequence is functionally relevant so the observed data may not be exactly in a Poisson distribution, but I would expect the distribution of aa differences to be close to one.

http://genome.cshlp.org/content/15/12/1746.long

> A random mutation is not a Poisson random variable.

Where did I ever claim that random mutation is a Poisson distribution? I do claim that, to the extent that mutation is a random binomial event (with not mutant being the alternative state), it also meets the criteria for being able to use a Poisson to estimate the values of the distribution. That is, under these conditions, there is little difference between a value calculated by the Poisson and the binomial distributions. Of course, you don't use a binomial distribution in which one determines the mutation rate and uses that. You somehow (it remains unexplained) determine the mutation rate and then divide it by 4. Other than that, you are using a binomial distribution in your equations. But you still have to determine the mutation rate somehow. How do you determine the rate you then divide by 4. ESP?

> Are you too ignorant to look up the
> derivation of that probability distribution to understand why this is
> not the correct way to do the mathematics of this phenomenon?

I most certainly have looked up both the binomial probability distribution and the Poisson approximation and when it can be used. I have pointed the web sites out to you. I even pointed out to you that in some cases the actual probability distribution differs from both the binomial and Poisson because it violates the assumption that every trial has the same probability of generating an event (and that is the reason why we have a Luria-Delbruck probability distribution). But the probability distribution you "derived" from false assumptions about what mutation means and how one determines a mutation rate led you to divide the *real* mutation rate by 4.

> You need
> to rise above this mathematically irrational dogmatism that you�ve

> been indoctrinated with and learn how to do the mathematics of
> mutation and selection properly.

I *am* doing it properly. You have derived a probability distribution based on false assumptions and never tell us how you would determine the mutation rate you divide by 4. If you can't measure the *actual* mutation rate or mutation probability, you can't divide it by 4. But if you have the actual mutation rate, why do you need to divide it by 4?
>
[snip rest to make this readable]

[Robert Carnegie: Fnord: cc talk-origins@moderators.isc.org]

On Sep 23, 4:13 pm, "Steven L." <sdlit...@earthlink.net> wrote:
> "r norman" <r_s_nor...@comcast.net> wrote in message
>
> news:46l777pqufop933rv...@4ax.com:
>

And farmers. Feeding antibiotics labelled as "growth promoters" to
meat animals and thereby depriving human beings of their use as
effective cures is extremely wicked, in my opinion.

I gather that the very first patient treated with penicillin got an
inadequate dose - as much as they could manufacture of it - and he
ended up with a thriving and fatal infection of resistant microbes,
and died. So then it's not a big secret.

The modern problem arises from drug companies that want doctors to
prescribe one product, theirs. Not a combination. Somewhat
corrective to this is seeing House, M.D., on television prescribing
several pills at once for diseases that the semi-diagnosed patient may
be dying of, possibly simultaneously, but the episodes I've seen (till
about series four) still tend to be one treatment for one disease.

[Robert Carnegie: Fnord: cc talk-origins@moderators.isc.org]

On Sep 23, 4:13 pm, "Steven L." <sdlit...@earthlink.net> wrote:

> "r norman" <r_s_nor...@comcast.net> wrote in message
>
> news:46l777pqufop933rv...@4ax.com:
>

And farmers. Feeding antibiotics labelled as "growth promoters" to

[hersheyh]

On Friday, September 23, 2011 3:45:07 PM UTC-4, Alan Kleinman MD PhD wrote:
> The following are a compilation of responses to posts 926-950
> presented in this manner to prevent splinter threads.
>
> hersheyh Aug 26, 8:53 am
> Newsgroups: talk.origins

> From: hersheyh <hers...@yahoo.com>

> Date: Fri, 26 Aug 2011 08:53:04 -0700 (PDT)
> Local: Fri, Aug 26 2011 8:53 am
> Subject: Re: The Theory of Evolution is Mathematically Irrational
> Round 2
>

[snip]

> >> What a surprising piece of wisdom an evolutionist crank is coming
> >> forth with. Single drug therapy for HIV leads to rapid selection of
> >> drug resistance. Who would have guessed this?

> >Every single virologist and evolutionary biologist would have guessed this. I certainly would have.
> > Based on my understanding of mutation and selection and my understanding of how toxic agents
> > work (by interacting with and interfering with some normal biologic function).
>
> This was not mainstream thinking before the 1990s when HIV hit. Read
> the literature from the 1990s about the treatment of HIV and the use
> of combination therapy. There was a lot of debate for and against.

As, of course, there should have been. Not every type of combination therapy will work without too much toxicity to the patients. Sometimes the cure can indeed be worse than the disease. Note that there was *debate for and against*, not uniform claims from the scientific community that "combination therapy cannot work".

> However, if virologists and evolutionary biologists had read Edward
> Tatum’s 1958 Nobel Laureate lecture, and understood what he was saying
> about using combination therapy, the debate would have been much
> shorter.

Tatum was a biologist and a geneticist. He was also, as any competent biologist is, fully accepting of evolution.

>
> >> I suppose the next thing
> >> you are going to tell us is that combination therapy suppresses the
> >> mutation and selection process.

> >Of course it does, as any biologist would have told you. But in the early days of antivirals directed
> >against HIV -- when only AZT was available, there was no choice but to use single-gene therapy.
> > The other option was to intentionally not treat patients. When other antivirals came on-line, they
> > were used. The initial 'other antivirals' were also anti-reverse transcriptases, so there was a
> > possibility of cross-interaction (non-independence) of action, which would render combination
> > therapy much less useful.

> That’s a line of crap and you know it.

No. It is the truth. It is your interpretation of HIV/AIDS treatment history that is crap. The full recognition that AIDS was due to a virus didn't occur until after 1984. But as the virus was a retrovirus and there was no good way to screen for it on a commercial scale early on, it wasn't clear that the virus was replicating between infection and the onset of immune deficiency syndrome. AZT clinical trials did not start until 1986.

The results of ACTG019, a trial, using AZT, still the only drug available and an extremely expensive drug at that, about *when* to start treating patients, before or only after they exhibit symptoms of AIDS were announced in 1989. It showed that using AZT early slowed progression to AIDS. But cost was still a factor. It is only in 1999 that a second drug, ddI, also a reverse transcriptase inhibitor, became available.

At this point, in the early 1990s, it was still unclear what the best way to treat patients was. Do you wait until they show symptoms of disease? Do you treat with AZT early and hope for some other drug that will be useful latter? In 1991, we see the introduction of a third reverse transcriptase inhibitor, ddC. Now, *because* all three available drugs attack the same enzyme, it is not at all clear that they would have additive effects. That is, if you treat with AZT *and* ddI, you may not get much additional inhibitory effect from the ddI. In that case, it might indeed be better to use one of the reverse transcriptase inhibitors until resistance to that builds up and then switch to the second. That is because the two drugs may not have *independent* effects and combining them might have no positive effect and could have negative effects.

In 1992, the FDA approved the use of ddC *and* AZT for advanced patients with advanced HIV who were continuing to show signs of clinical or immunological deterioration. So, the idea of using drugs in combination was not something biologists did not think of. In fact, given that ddC was just introduced in 1991, trials using the drugs as *possible* combination therapy started almost immediately. As in most trials, the initial population tested were those in which current therapy was ineffective.

The *real* argument about therapy (I am ignoring the idiotic claims of HIV/AIDS denialists and religious extremists who prevented good public health ideas like teaching condom use and having needle exchanges) in the early 1990s was not so much about combination therapy as it was about *when* to start treating with these then very expensive drugs (although cost was certainly a factor). Do you only start treatment when you start to see clinical effects or do you start treatment when a person is classified as HIV+, but is otherwise healthy?

The initial discovery of the *spread* of AZT-resistant HIV was in early 1993. Also, in 1993, preliminary results from a clinical trial of AZT indicated that it was NOT useful therapy for patients without clinical symptoms. Again, the real argument in the early 1990s was about *when* to start treating, not whether combination therapy (again all the drugs available, most introduced less than 1-2 years ago, were reverse transcriptase inhibitors and, without trials, one could not predict that combination therapy would be better, worse, or of the same effectiveness).

In 1993, a number of *trials* were underway comparing the effectiveness of AZT alone or in combination with ddI and ddC. Again, because these drugs act on the same enzyme, it is not necessarily the case that combination therapy would be significantly more effective than serial use of the drugs. Hence trials to actually test whether combination therapy works.

The first protease inhibitor. saquinavir, was approved in 1995. This would be the first drug that could reasonably be used in combination therapy and which we would *know* would likely be acting independently to the reverse transcriptase inhibitors. But you still need to run *trials* to see if there would be any unforeseen interactions.

In 1996, the first drug that was a non-nucleoside reverse transcriptase inhibitor was approved (Viramune -- nevirapine). And it is only now that we see the introduction of the viral load test, which is used to provide information about the risk of disease progression. And it is only now that you start seeing real optimism about treatment, especially in people taking combination therapy. That was THE excitement in 1996. But such combination therapies, again combination therapy was being used almost as soon as one had two drugs to combine in such therapy, still needed to be fully vetted by future work. What combinations worked best? Had the least side effects? Were less expensive so that these treatments might be used in communities with high rates of infection -- Africa, Asia, IV drug users, sex workers -- that don't have the resources of the wealthy? Again, should treatment start early in HIV infection or should one wait for symptoms? At that time, these questions still had no answers.

By spring 1997, the use of combination therapy was having its expected (by evolutionary biologists) effects and we were seeing declines in deaths, declines in children born with HIV, but were also seeing some of the early detrimental consequences of combination therapy: unpleasant and sometimes serious side effects and resistance, even when 3 antivirals were being taken (mostly because of complex schedules with many pills needed each day leading to less than stellar adherence by patients. Note to the Dr. Dr.: this failure of adherence would lead to viruses resistant not just to one antiviral, but to three, despite your claims that this would be "mathematically irrational".

But, still, there was argument about *when* to start treatment (with the U.S. doctors being more likely to start treatment upon HIV identification and U.K. doctors only when symptoms start). The hope of the U.S. strategy of "hit early, hit hard" was that HIV could be totally eradicated. They found that it could not be eradicated, but the strategy had important public health effects by reducing the probability of spread of the virus to others. But that determination was still for the future.

In 1998, patients taking combination therapy (now the standard treatment) were showing signs of long term effects like lipodystrophy (fat redistribution) that might be indicators of long-term safety issues. By this time it was clear that *single drug therapy* with AZT (administered to the mother before birth), combined with Cesarian birth, could drastically reduce mother to child transmission to less than 1%. AZT was becoming significantly cheaper at this time.

In 1999, we start to trace the *evolutionary history* of the HIV-1 virus from its origin in chimpanzees to humans. Nevirapine, in a single dose, is also found to be an affordable and effective block to mother-child transmission.

In 2003, a new class of drugs that prevent fusion of the virus with cell membranes (Fuzeon, enfuvirtide, T-20) became available. Unfortunately it can only be administered by injection and thus is given primarily in combination therapy to patients who have become resistant to other drugs.

Since that time, the main changes in treatment has been finding out which kinds of combination therapy work best and have the best compliance rates. And a reduction in cost as patents expire for many of the drugs. But the real pool of new HIV drug-resistant variants lies outside the borders of the U.S. Especially in countries where there is an epidemic of bogus drugs being sold alongside real ones. Remember that even three-drug combination therapy can be overcome by poor compliance. The first one-a-day pill (Atripla), which required unprecedented co-operation between two drug makers (cynic that I am, this was probably because patents were running out on the single drugs), was introduced in the U.S. in 2006.

In 2006, we start seeing extreme drug-resistant tuberculosis (XDR-TB) arise in HIV co-infected individuals. [TB is typically treated by combination therapy.] The worry is a new epidemic, this time of virtually untreatable TB.

In 2008, four studies show that people with HIV who take effective antiviral therapy cannot (to the extent determinable) pass on the virus via unprotected sex (so long as they adhere to protocol, have undetectable viral load for 6 months, and no other sexually transmitted diseases).

http://www.avert.org/hiv-aids-history.htm

> Combination therapy has never
> been a mainline approach to treating diseases and still is not.

Judging by your fake history of HIV when the real history of HIV shows that combination therapy was tested almost as soon as a second antiretroviral was available, even though the two drugs acted on the same enzyme and there was a real possibility that there would be no independent effect on disease progression or that resistance to one drug also led to resistance to the other.

The *real* question at that time (and continuing from that time) was the question of *when* to treat, not whether it was useful to try combination therapy.

> The
> reason is that evolutionists do not teach the basic science and
> mathematics of the mutation and selection phenomenon. And the reason
> they don’t teach it is that they don’t understand it. You are the
> perfect example of this deficiency in understanding. You’ve been
> teaching genetics for 20 years and how many lectures have you given on
> the basic science and mathematics of mutation and selection? All you
> know is that you apply the Poisson distribution which is the wrong
> distribution function and then you mislead a generation of students.

I use the correct distribution function because I know what the terms "mutant" and "not mutant" mean and you clearly don't understand how those terms link up to the terms "event" in already well-developed probability distribution equations. It is like you never took (or at least never understood) any statistics or probability courses.

As I have *repeatedly* pointed out, your so-called derivation only differs from the binomial probability distribution (for the probability of one or more events in a trial of a given size) by the fact that you divide the "probability of mutation per trial" by the arbitrary number 4, claiming that somehow the number 4 is magically relevant by virtue of the fact that there are four possible nt's at a single nt site. Yet you have not defined how you can operationally identify the term you call "probability of mutation" that you then divide by the number 4. Your analogy of a 4-sided die is nonsense, since such a device assumes that the site where you somehow identify that a "mutation" has occurred or will occur then has an equal probability of getting one of the 4 nts as if it had no nt originally. My only guess is that such stupidity is derivative of the idiotic creationist arguments that claim that proteins are assembled by random chance and the probability of any particular site having a specific aa is 1/2

0, as if drawn from equimolar pools of aa's.

[snip remainder to keep each argument focused]

[hersheyh]

On Friday, September 23, 2011 3:45:07 PM UTC-4, Alan Kleinman MD PhD wrote:
> The following are a compilation of responses to posts 926-950
> presented in this manner to prevent splinter threads.
>
> hersheyh Aug 26, 8:53 am
> Newsgroups: talk.origins

> From: hersheyh <hers...@yahoo.com>

> Date: Fri, 26 Aug 2011 08:53:04 -0700 (PDT)
> Local: Fri, Aug 26 2011 8:53 am
> Subject: Re: The Theory of Evolution is Mathematically Irrational
> Round 2
>
> On Friday, August 26, 2011 9:29:16 AM UTC-4, Alan Kleinman MD PhD
> wrote:

> > On Jul 26, 12:06 pm, hersheyh <her...@yahoo.com> wrote:

[snip]

> >> And then I suppose you are going to
> >> tell us these are unnatural selection pressures

> >They are. Population-wide (in this case, the infected individual) instantaneous appearance of large
> > amount of toxic compounds are novel selection pressures that typically are artificially introduced
> > by humans for their purposes.
>
> Oh, I see, no populations ever went extinct until humans came along.

Irrelevant since I did not say that.

> There was just single targeted selection pressures in nature targeting
> one gene at a time and “poof” reptiles transformed into birds.

It is your myth that selection can only target one gene at a time. Selection in procaryotes and viruses, because those organisms are most often clonal in nature, does require either serial selection for changes to accumulate in a single organism or that there either be a gene exchange event of the type seen occasionally in procaryotes and viruses. Selection in eucaryotes is greatly speeded up by the fact that these organisms engage in recombination every generation. But in both cases, there is nothing preventing the selection at more than one locus at a time. It is just that in the procaryotic and viral cases, there is not a regular mechanism for introducing the two genes into the same organism.

> > This is
> the mathematically and empirically irrational crap that forms the
> basis of evolutionism.
>

You keep claiming that evolution is mathematically irrational, yet you are the one presenting mathematical garbage and calling it a "derivation" of the "correct probability distribution".

> >> and nature never
> >> targets more than a single gene at a time with starvation,
> >> dehydration, disease, thermal stress, predation…

So, let me correct my math in my previous example and see what happens when you select, in a procaryotic organism, for non-lethal variants, but still absent recombination. Let's talk about two independent traits, resistance to higher salt and resistance to a temperature increase in an organism that has been grown for generations in lower salt and temperature and, hence, is optimally adapted to those conditions.

Let's assume that what happens when you look at either selective condition independently is that, under the new selective conditions, growth rates slow down. Under the original selective conditions, the bacteria grow with a doubling time of 20 min. When grown under the higher salt conditions, growth slows to a 30 min. doubling time. When grown under the higher temperature conditions, growth slows to a 25 min growing time. When grown in both higher salt and higher temperature, growth slows to a 40 min doubling time.

In the environments with higher salt *or* higher temperature, mutation at a single gene locus, mutation from A to alternate allele a in the case of higher salt, from B to b in the case of higher temperature, causes growth to increase to near, but slightly slower, than the original 20 min *because* the mutant genotype produces a mutant phenotype that grows better under the new conditions. But when cells with the genotype A;B are grown in the double selective conditions, mutation at only one of the loci does not bring the growth rate back up to 20 min, but only to level that would be expected for cells resistant to only one of the conditions (either 30 min if the genotype is A;b or 25 min if the genotype is a;B). Cells that have *both* mutations (genotype a;b) grow at a doubling rate of 21 min under the new environmental conditions.

Important and relevant numbers to remember:
Genotype Doubling time in higher salt, higher temperature environment
A;B 40 min
A;b 30 min
a:B 25 min
a;b 21 min

Doubling time is a measure of differential reproductive success. Bacteria with faster rates of growth in an environment are *selected for*.

Now, let's start with a population of bacteria that are A;B that have been grown in the lower salt, lower temperature environment in which it has a slight selective advantage over any of the other genotypes. Because you don't like my use of populations of bacteria that are 10^9, I will grow the bacteria in a 10 ml chemostat at a constant concentration of 10^7 bacteria/ml. That gives me a population of 10^8 bacteria. Because the environmental conditions I am looking at does not *kill* cells, but merely slows their growth, I can maintain the same population size by keeping the optical density (OD) of the bacteria in the chemostat constant. As the bacteria increase in number and increases the OD, bacteria are pumped out and an equivalent amount of media replaces them. The time taken for the volume removed to equal the volume in the chemostat is the mean doubling time of the population in the chemostat.

At time zero, nearly all the cells in the chemostat are genetically A;B. But if the mutation rate is 10^-8 for A to a and 10^-8 for B to b, I would expect, a mean value of 1 A;b cell and 1 a:B cell in the chemostat containing 10^8 cells. I would expect no a;b cells at this point (because the probability of a double-mutant at this point in a single individual is the product of their individual probabilities at this time which = 10^-16). [In reality, this would be a Poisson probability distribution, with a 36.8% chance of no mutant, a 36.8% chance of one mutant, and a 100-2(36.8)% = 26.4% chance of 2 or more mutants in each gene. But for purposes of this argument, I will assume 1 mutant of each type of single mutation in a population of 10^8 cells in a chemostat containing the new selective conditions.]

Now, since selection involves *differential reproductive success*, we need to know the relative fitness of the three genotypes we have in the chemostat. The doubling times can be used for this. The *relative fitness of the genotype A;B, the overwhelming number and frequency of individuals initially present, is set at 1, or 40/40, if you will. The genotype A:b has a doubling time of 30 min. The genotype a:B has a doubling time of 25 min. That means that, relative to A;B, A;b grows 40/30 times as fast = 1.33 times as fast. IOW, for every time that A;B doubles, A;b increases 2^1.33 times as much. Similarly, a;B has a doubling time of 40/25 = 1.6 times as fast as A;B. Specifically the higher rate of growth of A;b will produce 1X(1.33)^g individuals in the chemostat. [The 1 is the mean number of A;b individuals expected initially, 1.33 is the relatively higher exponential growth rate of A;b relative to A;B, and g is the number of doubling generations. I will let you do the equation for the genotype a:B.



Initially, of course, the two mutants are primarily competing against the A;B genotype, since both are but a tiny fraction of the population. At some point that will not be the case. After 30 generations, the frequency of the two mutants will have greatly increased at the expense of genotype A;B *because* of selection while the population size has not changed. However, because of the increase in the two mutants as a fraction of the population, the doubling time of the population will have increased. Specifically, we would expect to see 5,600 A;b individuals (fractionally, this is 5.6X10^-5) and 1.3X10^6 a:B individuals (fractionally, this is 1.3 X 10^-2). So, at 30 generations, we still are 98+% A;B and the selective competition is still almost entirely between each mutant and the still larger number of A;B individuals. But by 35 generations, the frequency of a;B individuals is 0.14 (14% of the population). The fractional population of A;b is 2.3X10^-4. And the fraction of the 10^8 cells that are A;

B has declined to 0.86. Within a few generations, the A;B fraction will have decreased to the point where it is negligible and almost the entire population will be composed of either A;b or a:B individuals, with a;B being the more common genotype because of its higher rate of growth relative to A;B. At this point or near it, competition between the two mutant genotypes will occur.

But more importantly, when nearly the entire population of 10^8 cells in the chemostat are either a;B or A;b, the probability of mutation in these cells of the *other* gene to produce the double mutant a;b is merely the probability of a cell being (most likely in this scenario) a:B, which would be close to 1, times the probability of a mutation of B to b times the number of a;B cells in the chemostat (close to 10^8). Such a double mutation is, in fact, quite likely. Although less probable, the mutation of A to a in the only other type of cell present in the chemostat (A;b) would also produce a double mutant. Now, with a double mutant, we have a new selective phenotype. One which is more fit in this environment (grows faster) than the a;B individuals that are most of the environment. The a;B individuals grow with a doubling time of 25 min (which, BTW, will be the doubling rate seen now in the chemostat). The a;b individuals grow with a doubling time of 21 min. Thus, the double mutants have a selective

advantage of 25/21 = 1.19 relative to the single mutant individuals (a;B). Another 40-50 generations of selection and the population will be essentially all a;b.

As an example of this actually happening, look at the early parts of the Lenski experiment, although in that case it is not known exactly what environmental differences are optimized by the different mutations. That, and instead of a change in the doubling time, they took out a certain amount of bacteria in a set amount of time (adding that back in new media), so the observed change would be an increase in the OD in the chemostat.

[snip]

[Charles Brenner]

On Sep 24, 11:12 am, hersheyh <hershe...@yahoo.com> wrote:

> > > But in the early days of antivirals directed

> > >against HIV...
>
> At this point, in the early 1990s, it was still unclear ...

Thanks, very good lecture. I enjoyed it.

[hersheyh]

[snip]

>
> On Friday, August 26, 2011 9:29:16 AM UTC-4, Alan Kleinman MD PhD
> wrote:

> > On Jul 26, 12:06 pm, hersheyh <her...@yahoo.com> wrote:
> > > On Jul 25, 8:56 pm, Alan Kleinman MD PhD <kle...@sti.net> wrote:
> > > > On Jun 19, 3:28 pm, hersheyh <her...@yahoo.com> wrote:> On Jun 13, 8:57 am, Alan Kleinman MD PhD <kle...@sti.net> wrote:
> > > > > > On Jun 1, 12:57 pm, hersheyh <her...@yahoo.com> wrote:> On Jun 1, 10:33 am, Alan Kleinman MD PhD <kle...@sti.net> wrote:
> [snip]

>
> >> We understand the
> >> evolutionist philosophy, which is blizzards turn lizards into buzzards
> >> with gizzards.
> >Lizards (specifically and relevantly, alligators and crocodiles, the closest living relatives to
> > dinosaurs) have gizzards. As, likely, did a number of plant-eating dinosaurs (based on gizzard
> > stones found near their fossils; meat-eating birds, and >probably dinosaurs, also have gizzards,
> > but don't often swallow stones and gizzards themselves don't fossilize). So buzzards certainly
> > inherited their gizzards from their lizard ancestors. Blizzards have nothing to do with gizzards.
> >They may have something to do with the selective pressures for *feathers*, which initially (and still
> > today) are often functionally >relevant as air- and heat-trapping insulation.
>
> Well my, my, are you going to tell us that cold-blooded alligators and
> crocodiles without feathers, wings or beaks are closely related to
> birds because they have gizzards.

Obviously taxonomy and anatomy are also not your strong points.

No. Cold-blooded crocodilians and birds are the sole surving groups in the Division Archosauria, the group of diapsid amniotes (within the class Reptilia, which is where Aves should also be) that also included the now extinct dinosaurs and pterosaurs.

The evolutionary relationship is that the first split was between Crurotarsi (modern crocodilians and its now extinct relatives) and the group Avemetatarsalia (dinosaurs, pterosaurs). Birds arose within the dinosaur lineage, from feathered theropods. Again, only birds and crocodilians survived to the present.

The distinguishing common characteristics of all archosaurs (their synapomorphies or shared characteristics) does NOT, unsurprisingly, include "gizzards". That is because one must determine relationships from features that fossilize (bones and teeth).

"The simplest and most widely-agreed synapomorphies of archosaurs include teeth set in sockets, antorbital and mandibular fenestrae (openings in front of the eyes and in the jaw, respectively), and a fourth trochanter (a prominent ridge on the femur). Being set in sockets, the teeth were less likely to be torn loose during feeding. This feature is responsible for the name "thecodont" (meaning "socket teeth"), which paleontologists used to apply to many Triassic archosaurs. Some archosaurs, such as birds, are secondarily toothless. Antorbital fenestrae reduced the weight of the skull, which was relatively large in early archosaurs, rather like that of modern crocodilians. These fenestrae are often larger than the orbits, or eye sockets. Mandibular fenestrae may also have reduced the weight of the jaw in some forms. The fourth trochanter provides a large site for the attachment of muscles on the femur. Stronger muscles allowed for erect gaits in early archosaurs, and may also be connected with the ability of t

he archosaurs or their immediate ancestors to survive the catastrophic Permian-Triassic extinction event."

> I guess the weather just hasn’t been
> cold enough for these reptiles to grow feathers, wings and beaks.

Lizard, of course, is kindergarten taxonomy. Most modern living lizards, though distantly related to archosaurs, are not archosaurs. The only living archosaurs in the reptile class are crocodilians and birds. For historical reasons related to the fact that only modern organisms were available, crocodilians are classified, in many taxonomies, within the reptile class and birds are classified as a class of their own. But birds, nonetheless, did evolve from feathered, toothed, theropods.

Feathers are useful for distinguishing modern birds from other modern groups of organisms. But they would not have been useful in distinguishing ancient birds from theropod dinosaurs, since those dinosaurs also had feathers.

Beaks, again, are useful in distinguishing modern birds from other modern groups of organisms. But many primitive (now extinct) birds had teeth. Even modern birds (chickens for example) have the capacity to induce the development of teeth. Dinosaurs also had beaks, for example, Ornithomimids. Notably, many beaks were also found in theropod dinosaurs (the group from which birds likely arose).

Wings, of course, also existed in the pterosaurs (and in bats). Moreover, many modern (as well as extinct) birds do not use their wings for flying (ratites, penguins, kiwi, dodo) or only rarely for flying (turkeys). Perhaps you mean that bird forelimbs are modified for flight in a *specific* way that also is seen in birds that do not fly and in most extinct birds (the moa was an exception -- it had lost its wings entirely). Early birds, however, often had wings that had claws and also had bony tails instead of the pygostyle of modern birds.

The main point is that none of the features you mention that are easy to use to identify and distinguish modern birds from other modern organisms were really always useful in distinguishing early birds from the closely related theropod dinosaurs, which also had feathers (often in the young), beaks in some species, bony tails, and teeth.

So every single bit of your mockery is bogus and based on a typical creationist kindergarten understanding of taxonomy. Birds are even less closely related to modern lizards than they are to modern crocodilians. Gizzards are not unique to modern birds even among modern organisms and were never used as identifying features of the group. And, although blizzards may make *feathers* selectively useful, the theropod dinosaurs from whence birds evolved already had feathers.

[snip]

[hersheyh]

hersheyh Aug 26, 12:53 pm
Newsgroups: talk.origins

From: hersheyh <hers...@yahoo.com>

Date: Fri, 26 Aug 2011 12:53:47 -0700 (PDT)
Local: Fri, Aug 26 2011 12:53 pm
Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

On Friday, August 26, 2011 9:33:02 AM UTC-4, Alan Kleinman MD PhD
wrote:

[snip]

> >If you want evidence for parallel evolution in organisms that do engage in regular and frequent
> > recombination (aka eucaryotes), pick any multigenic trait in a eucaryote (height, weight, fruit size,
> > egg production, bristle number in Drosophila) where we use heritability to describe the results and > > follow selection in those cases. There will be change in the trait until one hits the point where

[snip]

> >http://www.google.com/url?sa=D&q=http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1206456/pdf/ge13931273.pdf
> >http://www.google.com/url?sa=D&q=http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1460816/pdf/10545462.pdf
> >http://www.google.com/url?sa=D&q=http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1207261/pdf/ge1431277.pdf

> If you are trying to convince me that Chihuahuas and Great Danes can
> be created by recombination, don’t waste my time because that’s all
> you’ve demonstrated with these examples. Here’s a quote from your
> first citation.

Yet producing differences as large as that between Chihuahuas and Great Danes from *existing* variation in a population is exactly what can be accomplished by *recombination and selection* alone. According to your so-called "mathematical" argument, the *only* way I should be able to generate the two breeds is by serial mutation and selection of one trait at a time. I am well aware of the fact that all genetic variation starts as mutation.

Speciation, of course doesn't require large phenotypic differences. Many species in nature differ by less than the difference between Chihuahuas and Great Danes (who were 'breed' into existence in but a few hundred years at maximum). Speciation requires reproductive isolation in nature (by the most common operational definition).

> “Lines divergent for high and low abdominal bristle number were
> created by 25 generations of artificial selection from a large base
> population, with an intensity of 25 individuals of each sex selected
> from 100 individuals of each sex scored per generation.”
>
> Now if you can demonstrate the creation of a bird by recombination of
> alligators and crocodiles, then you will impress me. You already have
> a running start; after all they both have gizzards.

This is the very definition of "moving the goalposts". The process of producing the difference between crocodilians and aves was a process that took many serial speciation events and more years than humans have existed on the earth. In particular, the last common ancestor of modern crocodilians (the crurotarsi) and avemetatarsalia was an archosaur that probably lived near the Permian/Triassic boundary. [As you might guess from the names, ankle bone structure was an important identifier.] Now, you may not believe in the age of the earth that *scientists* have produced (probably favoring 6000 years or so), but the early Triassic (250 mybp) was quite some time earlier than when birds first evolved from the theropod dinosaurs (during the Jurrassic, 160 mybp). A 100 million years is a looooong time, involving many, many, many evolutionary changes and serial as well as parallel speciation events.

To go from fairly substantial changes that can be *demonstrated* to occur over a couple of hundred years (different dog breeds; speciation events in insects, etc) or even shorter times and then declare that you now need demonstrations of things that took 100 million years (but only if it can be done in a year) is talking about thousands of orders of magnitude. I can show you how far I can walk in a minute, but I can't show you how far I can walk in 100 million minutes (that is about 190 years; I don't have that much time left alive).

> > > > This is why the complexity of the
> > > > selection conditions dominates the mutation and selection process.
> > > That does not even mean anything.


> > In the mutation and selection process, it means everything. Without
> > amplification of a beneficial mutation,

> >By which, of course, you mean that the survivors of selection must be able to reproduce, since
> > selection itself changes the *frequency* of the alleles present. Assume that there is sexual
> > reproduction and the survivors of selection are enriched in both individuals that have alleles Aa or
> > AA rather than aa and *also* enriched in survivors with alleles Bb or BB rather than bb (both genes
> > being unlinked) even though, prior to selection, let's assume that there were no individuals with
> > both an A allele in the A gene locus and a B allele in the B gene locus simultaneously because those
> >alleles were quite rare relative to the a and b alleles prior to selection. But selection now has greatly
> > increased the *frequency* of *both* the A and of the B allele in the population (the real losers were > > the aa, bb individuals) Let's say that all aa, bb individuals have died during selection, to be
> > extreme about it. Moreover, in the previous population, let's say that A and B were so rare that the
> > only individuals with those alleles were heterozygous Aa or Bb. That means that after selection, the population only has Aa, bb individuals and aa, Bb individuals. Let's put frequencies on them. Say >that 70% of the survivors were Aa, bb and 30% were aa, Bb. That ratio could be due to a difference in the reproductive >success of individuals with the A allele relative to those with the B or it could be due to chance (the population had more >A individuals by chance). That means that the frequency of the A *allele* in the population is 0.35, a is 0.65, b is 0.85, >and 0.15 B. [There are twice as many alleles as individuals and the survivors with the capital letter only have one such >allele per individual.] Please note that the a and b alleles survive by being hidden in a heterozygote.
>
> You write so much and say so little. Amplification is the requirement
> for a population to overcome the multiplication rule of probabilities.
> If the population can not amplify the allele, there is a very low
> probability that the next beneficial mutation will occur at the proper
> locus.

If by "amplification" you mean that the *frequency* of particular alleles in the population changes, sure. That is the definition of what happens during selection.

>
> >With the assumption of random mating, we would expect 0.35 for the frequency of Aa, 0.0 for the frequency of AA, and >0.65 for aa in the next generation (because we are crossing Aa X aa). Similarly, we would expect 0.15 Bb and 0.85 bb >individuals. Since the genes are assumed to be unlinked and *using* the multiplication rule of probabilities (correctly), >then I would expect the progeny of this mating to be (0.65)*(0.85) = 0.55 aa, bb; (0.65)*(0.15) = 0.10 aa, Bb; >(0.35)*(0..85) = 0.30 Aa, bb; and (0.35)*(0.15) = 0.05 Aa, Bb individuals. That adds up to 1.0.
>
> You still haven’t figured out how to write the probability function
> for random recombination. This is reasonable since it has taken months
> for you to get any understanding of the probability function for
> mutation and selection.

No. I have understood what mutation does, what selection does, and what recombination does. You, OTOH, have repeatedly and stupidly presented your messed up derivation of the binomial probability, where you divide the mutation rate by 4, all the while claiming that that stupidity is a work of genius.

>
> >Now, assuming that the same selective conditions still exist, all the aa, bb individuals produced will die before >reproducing. Let us assume that individuals that are Aa, Bb are twice as fit as individuals that are Aa, bb or aa, Bb. > That would give us, when these individuals reach reproduction, out of every surviving 100 alleles (remembering to >multiply the 5% Aa, Bb individuals by 2 because of its selective advantage) 10 aa,Bb individuals, 30 Aa, bb individuals, >and 10 Aa, Bb individuals. These individuals should, assuming random meiosis, produce gametes in the ratio of 0.15 >a,B; 0.45 a,b; 0.35 A,b; and 0.05 A,B.
>
> Hersheyh, I really find your hypothetical examples quite boring. You
> have yet to figure out why the Poisson distribution is the wrong
> probability distribution for the mutation and selection phenomenon and
> you don’t have a clue of how to derive the correct probability
> function for random recombination.

So you keep stupidly repeating. Despite your inability to actually present a coherent argument as to why you need to divide the mutation rate (which you can't calculate) by 4.

>
> >Assuming random mating (use a Punnet square to make the computation easy -- you do know how to do that, don't >you?), that would mean progeny in the ratio of (0.45)*(0.45) = 0.20 aa,bb; 2*(0.15)*(0.45) = 0.135 aa,Bb; 2*(0.35)*(0.45) >= 0.315 Aa,bb; 2*(0.45)*(0.05) + 2*(0.15)*(0.35) = (0.045)+(0.105) = 0.15 Aa,Bb ;(0.15)*(0.05) = 0.0075 Aa,BB; >2*(0.35)*(0.05) = 0.035 AA,Bb; (0.0.15)*(0.15) = 0.0225 aa,BB, (0.35)*(0.35) = 0.1225 AA,bb and (0.05)*(0.05) = 0.0025 >AA,BB.
> >Again, the aa,bb individuals will die and individuals with Aa,Bb; AA,Bb; AA,BB; Aa,Bb, or Aa,BB (having both an A and a >B allele) all are twice as likely to reach adulthood as the individuals who are AA,bb; Aa,bb; aa,BB; or aa,Bb (being aa or >bb). If you have some problems with continuing, I would be happy to continue this for a few more generations.
> >Suffice it to say that both the A and B alleles will increase in frequency in parallel by the repeated loss of the aa, bb >individuals until the population contains only small frequencies of a and b. Equilibirum will only be reached when the >loss each generation of the a and b alleles due to aa and/or bb individuals equals the rate of new mutation from A to a >or B to b. At that point, most of the population will be AA, BB. The increase will be in parallel rather than sequential.
> >All of this has been worked out long, long ago.
>
> Ok hersheyh, take your hypothetical example and tell us why HIV
> doesn’t do this.

Because, as even a cursory examination of reality would show you, recombination is not something that happens every generation in either viruses or procaryotes. In HIV, in particular, it only occurs in double-infected cells and that has only been really observed in the laboratory on petri dishes.

In the bacterial experiments, the conditions in the labs running the experiments are designed specifically to prevent the known mechanisms of gene exchange in procaryotes.

Neither bacteria nor viruses automatically undergo the sexual cycle of eucaryotes.

Didn't you learn that in your basic introductory genetics course? Even in the dinosaur age when I took it, they knew that only eucaryotes underwent "Mendelian" genetics and that bacteria and viruses underwent "Nonmendelian" genetics.

> The Punnet square won’t explain this. You need to
> derive the probability function for random recombination to understand
> why HIV can’t use recombination to accelerate the mutation and
> selection process.

Given that HIV only undergoes recombination *when* a cell is double-infected, one would need to know the probability that a cell will be double-infected with two viruses *and* that those two viruses will be genetically different from each other. That is rare enough that one can, in general, ignore the role of recombination in HIV and treat it as a clonal organism with no recombination. Which is what I have been doing.

Same goes for bacteria in lab settings. Which is why I ignore recombination in bacterial experiments. In nature, plasmid exchange (a common form of gene exchange in bacteria) is frequent enough that it is responsible for the spread of multiple resistances involving traits that require more than one gene to appear. Typically, this involves taking genes from a naturally resistant organism and transferring it to a different species which was sensitive. Other gene exchange mechanisms involve transformation and transduction. Like plasmid transfer, these mechanisms are both sporadic and rare. No "probability function" for recombination has any universal meaning in these nonmendelian organisms.

You cannot say the same about eucaryotes. There, population values for a randomly reproducing population is, in fact, adequately described by the use of a Punnet Square using population frequency values. Is that clear enough?
>
[snip]

> >Again, you yourself have repeatedly pointed out examples where even sequential evolution
> > produces significant results requiring 5 or more sequential steps in less than a human lifetime.
> > Why doesn't that give you pause wrt your claim that evolution is mathematically impossible? Then
> > if you add in the parallelism possible in eucaryotic genetics, you do have to recognize that your
> > mathematical model is restricted to a narrow set of examples, mostly involving multiple
> > simultaneous resistance to toxins.
>
> Time in the mutation and selection process is not measured in years,
> days, minutes or seconds, it is measured by generations

And generation time is measured in years, days, minutes, or seconds.

> (one of the
> reasons why the Poisson distribution is not the correct probability
> function for the mutation and selection phenomenon).

Since you have not demonstrated any understanding of when and where the Poisson is, in fact, used appropriately, this is like listening to a crazy person talking to the space aliens in his head.

> There is
> absolutely no evidence that parallelism occurs with the mutation and
> selection phenomenon. You present breeding programs which your own
> citation calls “unnatural selection”, and claim there is parallelism.

> It takes hundreds of generations to amplify a beneficial mutation and
> this process does not occur in parallel.

30 generations of doubling to reach >10^9 individuals is not "hundreds of generations." The number of generations it takes for the *frequency* of a new mutation to take over from the old allele is a function of their relative reproductive rates, not on whether the population will increase, decrease, or remain the same. If the *organism* is clonal in nature, selection will occur in parallel, but the only way for a double-mutant to occur is serially (or, more rarely, simultaneously). If the organism is sexually reproducing, selection will occur in parallel, but now recombination is the more likely mechanism for generating a double-mutant. Selection is always a competition between two alleles, measured as relative fitness in a particular environment. If, at gene locus A, the A allele is more fit than the a allele, then the frequency of the a allele will increase. If, at gene locus B, the B allele is more fit than the b allele, the b allele will increase in frequency. If both A and B allele are present in

a population, both will increase relative to their respective alternative alleles a and b. Whether A increases faster than B is a function of their relative fitness. If A is 1.2 relative to a's 1.0 and B is 1.3 relative to b's 1.0, the B allele will increase in frequency faster than A. But in a sexually reproducing organism, recombination will produce an A ;B individual faster than the same genotype of individual would be produced by mutation to A in a B individual or mutation to B in an A individual.

> This is why the theory of
> evolution is mathematically irrational. It takes to many generations
> to amplify a single beneficial mutation and the process does not occur
> in parallel.

So you keep asserting without showing any evidence to support that view except for cases of lethal toxicity where single mutation has no benefit.

[snip]

[pnyikos]

NOTE TO THE GENERAL READERSHIP of talk.origins: I need to cut back on
my posting time for the rest of 2011. If you really want me to see
something, post it in direct reply to one of my posts.

On Sep 16, 5:35 pm, Inez <savagemouse...@hotmail.com> wrote:
> <snip rat king of replies>
>
> So I have a question for you.  I'm studying a certain sort of fungus,
> and have discovered that it has 100 neutral fixations per generation
> and only 10 selected mutations.  How fast did each of these types of
> mutations spread throughout the population?

To answer that question, it is necessary to know how large the
population is. Obviously, it takes much longer to fix something in a
large population [in the Wikipedia sense of the WHOLE population
having the same mutation] than it does for a small one.

> Can you show me how to
> calculate that using only those numbers?  John Harshman tells me that
> you need other information, but you seem to be able to just look at
> the final numbers and tell the speed that the genes spread at, so I
> turn to you for illumination.

I suspect you already know what I told you in the last paragraph, so I
wish you had left in some of the post to which you are replying, to
see what elicited this particular comment.

Peter Nyikos

[pnyikos]

On Sep 16, 4:34 pm, Alan Kleinman MD PhD <klein...@sti.net> wrote:
> pnyikos  Sep 15, 7:37 am

> >On Sep 14, 1:01 pm, Alan Kleinman MD PhD <klein...@sti.net> wrote:
> >I've heard a bit about you, Dr. Dr. Kleinman.  Now that we are in a
> >thread a mere 2 posts deep (before I post this) maybe we can get
> >acquainted without a lot of confusion about who said what when.
>
> So you don’t get confused about what I’ve said, let me repeat the
> first few paragraphs what I said initially from the first post (more
> than 2000 posts ago).

I've deleted an introductory paragraph here.

> Biologists and other adherents to the doctrines of evolution have
> utterly failed to properly describe how the mutation and selection
> phenomenon works. This is equivalent to an engineer not understanding
> how Newton’s laws work or how the Laws of Thermodynamics work. Here
> are two examples of how evolutionists bungle the basic science and
> mathematics of mutation and selection.
>
> Edward Max from the Food and Drug Administrations says the following
> onhttp://www.talkorigins.org/faqs/fitness/. In particular, he said
> the following statement: “The theory of evolution includes a number of
> ideas that some people find difficult to accept intuitively. One of
> the most difficult seems to be the notion that the intricate and
> interdependent structures we observe in modern plants and animals
> arose through random genetic mutations selected over time.”
>
> What Edward Max and other evolutionists do not understand is that the
> mutation and selection phenomenon is nothing more than a sorting and
> optimization process.

A very imperfect optimization process, this being a very imperfect
world. A single asteroid can wipe out millions of years of
optimization.

> The complexity of the selection conditions is dependent on the number
> of genes targeted and the number of beneficial mutations required in
> each gene in order to carry out the evolutionary process to increased
> fitness.

The size of the population also enters crucially into it. See my
reply to Inez less than an hour ago. See also below [keywords:
hominids, hundred].

Also "to increased fitness" is somewhat misleading because a lot of
changes can be accounted for by genetic drift, without fitness being
brought into the picture.

> The governing mathematical principle for the chance that
> multiple beneficial mutations will occur is the multiplication rule of
> probabilities.

True. However, If two mutations are beneficial, the combination would
probably be more selected for than either in isolation, and so the
probability of an organism surviving to breed would be more than just
the percentage of such organisms in the population.

> Thomas Schneider from the National Cancer Institute is
> incorrect when he makes the following claim on his web site
>http://www-lmmb.ncifcrf.gov/~toms/paper/ev/AND-multiplication-error.html
> , “The multiplication rule does not apply to biological evolution.”

See above. Schneider also makes survival to breed the issue and goes
on to give illustrative examples.

[snip something that didn't address Schneider's argument]

> >> On Aug 11, 7:16 am, John Harshman <jharsh...@pacbell.net> wrote:

> >> > Alan Kleinman MD PhD wrote:

> >> > > On Jul 13, 1:56 pm, John Harshman <jharsh...@pacbell.net> wrote:
> >> > >> g...@risky-biz.com wrote:
> >> > >>> <snip all>
> >> > >>> It's clear by now that Kleinman has no intention of answering the
> >> > >>> questions posed to him.
> >I've seen many claims like the above turn out to be false due to the
> >person making them having "answering the questions posed to him" mean,
> >in addition "to my satisfaction."  I wonder whether that is the case
> >here.
> >[ditto "addressing" statt "answering"]
> >[the German "statt" is so much easier to type than the English
> >"instead of", nicht wahr?]
>
> Why don’t you work with the mathematics statt grammatically?

I'll do it when I get the right kind of data.

> >> > >>> "Harshman's" count of genetic differences between humans and chimps
> >> > >>> has been bandied about in this thread. I've been wondering, could you
> >> > >>> characterize those differences a bit? How many of them are in coding
> >> > >>> areas?
> >> > >> Very few. Coding regions are only around 3% of the genome, and
> >> > >> accumulate about a third the number of differences per base as neutrally
> >> > >> evolving regions.
> >> > > You couldn t be more wrong John,
> >The following doesn't seem to support the "couldn't be more wrong"
> >assertion:
>
> Evolutionists try to draw a distinction between selective differences
> and neutral differences. In order for any difference (whether they are
> selective or neutral) to be fixed in a genome, it takes time
> (generations). We have John Harshman’s claim that there are 40,000,000
> differences between human and chimpanzee genomes and we have the
> evolutionist claim that the two species diverged about 5,000,000 years
> ago. Do the math statt blah, blah, blah.

I need to know more about how that 40 million figure was arrived at.
Otherwise we might just be doing a GIGO (Garbage In, Garbage Out)
exercise.

For instance, if it turned out that the comparison was based on the
genome of ONE chimp individual and ONE human individual, that number
would be worthless. There are big differences in the DNA of human
beings; otherwise, Bill Clinton could not have been impeached for
perjury [NOT sexual hanky-panky, as knee-jerk Democrats love to
pretend].

Other pitfalls mentioned below.

> >> > > over 70% of the genes in humans and
> >> > > chimpanzees don t code identical proteins.
> >This shows how the claim that humans share 98% or more of their
> >"genetic material" with chimps needs to be clarified.  Way back in
> >1995 or 1996 I asked whether this referred to loci, alleles, or base
> >pairs.
> >You've just now confirmed that it is NOT "alleles".  Harshman seems to
> >opt for "base pairs":
>
> I’ve let evolutionists define what they mean by differences and then
> say to them, do the math. Spread 40,000,000 differences through two
> populations in 500,000 generations, how do you do the mathematics?

Missing is from that 40 million figure is the word "fixed". See
above for why that is important.

[...]
[Harshman, about "non-junk" mutations:]
> >> > If there are 30,000 genes, that's 21,000 mutations. Out of 40
> >> > million. And even many of those are neutral.

> >> It has everything to do with what we are discussing. There are huge
> >> stretches of the two genomes which can not be matched up for homology.

> >Apparently you mean "matched up BASE FOR BASE".  But loci can be
> >matched up in most cases even if the bases differ, no?
>
> I missed that part. Are you saying that humans and chimpanzees have
> identical number of chromosomes and you can line up each chromosome
> and the genes match up on a loci by loci basis?

No, of course not. What I *am* saying is that presumably they've been
able to account for most of the mutations that are not of the point
kind (such as migration of loci from one chromosome pair to another,
fusion of chromosomes, etc.) and thus match up a hefty fraction of
loci even if they are located in different chromosomes or different
places on the same chromosome.

Unless that is true, the 40 million figure is utterly worthless
because you could be matching up the wrong genes and getting far more
"mutations" than you would if the genes were properly matched up. And
even if it is true, we'd need to know just how large that "hefty
fraction" is, and what was done about the genes that they couldn't
match up.

You say that they discarded the genes for which they could not find a
match:

> >> This data is presented for those areas which can be matched and the
> >> match is not close at all.

Can you give me a reference? Does it say how hefty that fraction was?

> >> Evolutionists claim that humans and
> >> chimpanzees come from a common progenitor. Now you are claiming that
> >> many of these differences are neutral which is typical evolutionist
> >> speculation.

"Neutral" apparently includes "silent," meaning they still code for
the same amino acid. There is no speculatioin there: you can see the
changes.

> >It may be based on solid data, as even you seem to allow for here:
>
> Here is the crux of the argument pnyikos, can you do the accounting
> for the number of differences between the two genomes in the given
> number of generations.

Not yet. And even if I get the data I'm asking about above, we'll
still have to speculate on how many times our ancestors were down to
less than a total population of a hundred hominids during those 5
million years. That makes a huge difference in what the calculations
come out to be.
[...]

> >> Tell us which are neutral differences and which are

> >> selective differences. And then compute the joint probability of two
> >> neutral mutations being fixed in a population.
> >The non-neutral mutations (especially the beneficial ones) would seem
> >to be also relevant to your skepticism about humans and chimps being
> >related.
>
> It’s more than skepticism; it is mathematically irrational to believe
> that humans and chimpanzees came from a common progenitor. You have
> far too many genetic differences and far too few generations to make
> the transformation.

We'll see about that if I get good enough data.

> >By the way, does "neutral" mean "coding for the same protein, only
> >differering in the mRNA"?  

The right word for what I described is "silent". "Neutral" does not
mean that, it has to do with "negligible effect on the survival
rate". So it includes "silent" AFAIK.

> Does it include that?  It's been a while
> >since I've looked at this part of genetics.
>
> The probability function I derived to compute the probability of two
> mutations occurring is applicable to detrimental, neutral or
> beneficial mutations. What distinguishes whether the mutation is
> detrimental, neutral or beneficial is how the subpopulation with the
> particular mutation responds over generations. If the mutation is
> beneficial, the subpopulation will increase in number, if the mutation
> is neutral, the subpopulation size will remain relatively constant
> over generations and if the mutation is detrimental, the subpopulation
> size will decrease over time. The mathematical significance of this
> relates to the probability of the next beneficial mutation occurring
> at the proper locus (position on the genome).

It relates to a whole lot more than that. See what I wrote way up
there after "True."

> >> > >>> How many with other known functions? How much "junk"?
> >> > >> Almost all is junk, just as almost all the genome is junk. Non-coding,
> >> > >> functional regions are just another few percent of the genome.
> >> > > This is the type of stupidity that evolutionist perpetuate. If they
> >> > > don t know what a portion of the genome does, it is junk.
> >> > No, that's not how it works. We recognize junk by the fact that it
> >> > evolves at the rate of mutation.

> >No direct testing to see whether it is ever translated into
> >polypeptides?  I'm disappointed.
>
> I believe you are making and error here pnyikos. Coding of
> polypeptides is not necessarily the only function of DNA.

But it IS one of the functions, and that is what I was getting at.

Remainder deleted, to be replied to when I have more time. See my
comment at the beginning of my reply to Inez.

Peter Nyikos
Professor, Dept. of Mathematics -- standard disclaimer--
University of South Carolina
http://www.math.sc.edu/~nyikos/
nyikos @ math.sc.edu

[Inez]

On Sep 28, 8:25 am, pnyikos <nyik...@bellsouth.net> wrote:
> NOTE TO THE GENERAL READERSHIP of talk.origins: I need to cut back on
> my posting time for the rest of 2011. If you really want me to see
> something, post it in direct reply to one of my posts.
>
> On Sep 16, 5:35 pm, Inez <savagemouse...@hotmail.com> wrote:
>
> > <snip rat king of replies>
>
> > So I have a question for you. I'm studying a certain sort of fungus,
> > and have discovered that it has 100 neutral fixations per generation
> > and only 10 selected mutations. How fast did each of these types of
> > mutations spread throughout the population?
>
> To answer that question, it is necessary to know how large the
> population is.  Obviously, it takes much longer to fix something in a
> large population [in the Wikipedia sense of the WHOLE population
> having the same mutation] than it does for a small one.
>

I suspect that you also need to know how many neutral mutations and
selectable mutations occur per generation.

> > Can you show me how to
> > calculate that using only those numbers? John Harshman tells me that
> > you need other information, but you seem to be able to just look at
> > the final numbers and tell the speed that the genes spread at, so I
> > turn to you for illumination.
>
> I suspect you already know what I told you in the last paragraph, so I
> wish you had left in some of the post to which you are replying, to
> see what elicited this particular comment.
>
> Peter Nyikos

Dr. Kleinman believes that the claim that there are more neutral
mutations fixed per generation than selected ones is equivilent to the
claim that neutral mutations spread more quickly through the
population than selected ones. Efforts to get him to see this is not
true have proven fruitless, so I thought I would try and get him to
think about the math himself.

[hersheyh]

[snip]

>
> >On 8/17/2011 10:07 AM, Alan Kleinman MD PhD wrote:
> >

> >> On Jul 22, 1:07 pm, "g....@risky-biz.com"<gdgu...@gmail.com> wrote:

> >>> On Jul 22, 3:35 pm, Alan Kleinman MD PhD<klei...@sti.net> wrote:
> >>>> Each and every generation dozens
> >>>> of neutral mutations must show up in the genomes of every person on
> >>>> earth per evolutionist claims. This happens regardless where they live
> >>>> and who they are descended from. Now why don’t you tell us which 50
> >>>> neutral mutations have shown up in your genome and every other member
> >>>> of the population of the earth?

> >>> Really? You honestly believe that is the claim? That the same mutation
> >>> occurs in every person on Earth at the same time? You believe that
> >>> "evolutionists", which is to say, biologists, believe that?

> >> You have John Harshman’s claim that the human and chimpanzee genomes
> >> differ by 40,000,000. You have less than a million generations to
> >> accumulate for those differences.

> >Why can't you seem to answer the most basic questions? Do you or do you
> >not think that the "evolutionist" argument includes neutral mutations
> >spreading quickly through a population? (as opposed to slowly, but in
> >massively parallel fashion)

> Greg, the reason why you and other evolutionists are wrong about this
> is that you are taking a very low probability process and claim that
> millions of these processes are happening simultaneously.

We are correctly calculating the probability of neutral fixation *per nucleotide* in a given generation as u, the mutation rate. You have agreed that that is the correct probability of neutral fixation *per nucleotide* per generation. That is indeed a low probability for any given nucleotide in the human genome. If the human genome only contained a single nucleotide, then the probability of neutral fixation *per genome* would be the same value. But each nucleotide is an independent trial. Thus the probability of neutral fixation is the probability of neutral fixation *per nucleotide* times the number of nucleotides per genome. If this comes out to be greater than one, then it is appropriate to talk about the mean number of fixations per genome per generation.

This is no different than having a row of 100 coins. The probability that any one of these coins will, when flipped, show heads is 1/2. That is the probability of heads *per coin.* But if you flip 100 coins, the probability of heads *per 100 coins* is (1/2)*100 = 50. [That is the expected *mean* value. The probability of getting exactly 50 heads is smaller because you will have a normal curve of distributions of k.] That is, one expects to see a mean value of 50 heads if all 100 honest coins are flipped. One does not calculate the probability of heads per 100 coins by taking the probability of heads per coin flip and multiplying it by itself 100 times, (1/2)^100 = a very small probability, which is how *you* apparently think it should be done. That would be the probability that *every* coin comes up heads.

> This is
> incorrect mathematically because of the multiplication rule of
> probabilities which governs the joint probabilities of random
> independent events and this is wrong conceptually. This is wrong
> conceptually because of common descent. What you are claiming is that
> neutral mutations are appearing all throughout the population

And are you claiming that neutral mutations do not appear throughout the population? Given that there are 40+ mutations per genome in any given individual.

> and that
> they are spreading through to every member of the population
> simultaneously.

No. Most of them will disappear. For any *given* nt, the probabilty that there will be neutral fixation is u. The probability that a given new mutation (and there are 40+ new mutations per generation per individual) will go to fixation is 1/2Ne. It is merely that the sheer number of trials (nucleotides) is so large that even rare events per nucleotide have a high probability of occurring. Think of it like this. You have a die that has 10^8 faces, one and only one of which is labelled "neutral fixation change". The probability that you will have that face show up in a single flip is 10^-8, a very low probability. But if you flip the die 3X10^9 times (or more accurately, have a row of such die that contains 3X10^9 identical dice), the probability of getting more than one of the die showing the "neutral fixation change" face is actually pretty high.

> It just doesn’t make sense that neutral mutations in
> one family line will show up in a different family line now or ever.

Are you actually claiming that humans don't have sex but are clonal organisms? If humans do have sex, mutations will cross family lines via recombination.

> You have to have 20,000,000 neutral mutations show up in a single
> family line. That is mathematically irrational thinking.

Rather the above sentence is completely irrational gibberish unrelated to any kind of mathematical thinking.

>
> >>And you have every weird
> >> mathematically irrational hypothesis coming from the fertile but
> >> mathematically irrational minds of evolutionists to try to explain
> >> away this accounting problem. In the process of bungling the basic
> >> science and mathematics of mutation and selection with these
> >> mathematically irrational hypotheses, evolutionists have managed to
> >> harm millions of people suffering from diseases subject to the
> >> mutation and selection phenomenon.

> >We tend to ignore this little fugue of yours, but that doesn't mean it
> >isn't complete nonsense. Evolutionary theory predicts antibiotic
> >resistance, and indeed predicts that combinations of deadly agents will
> >be difficult to evolve your way out of. If medical and agricultural
> >people have made choices that ignore this, it is certainly not because
> >evolutionary theory does not describe it accurately.

> Greg, that’s a line of crap you are putting out.

No. It is the truth. You have built your whole edifice solely on the sands of a phrase used as a caption to a paragraph that clearly is not about multitoxin therapies but about the creationist idiotic claims that proteins and genes are somehow assembled from scratch by completely random processes.

As I have pointed out, the problem with that particular creationist idiocy is with the underlying assumption that evolution involves assembly of any particular gene by random assembly from equimolar pools of subunits, not in their use of the multiplication rule. Indeed, *if* evolution involved random assembly of genes or proteins from equimolar pools of subunits, the math would be quite correct. But that assumption is not just wrong; it is intentionally idiotic and an insult to one's intelligence. Just like your apparent use of these idiotic ideas in your division of the *actual* mutation rate by 4, which seems to be related to the fact that you believe that genes are assembled by chance from equimolar pools.

> If evolutionists have
> understood this, why haven’t they stepped into the debate and taught
> medical students the correct basic science and mathematics of the
> mutation and selection phenomenon.

Why would they teach med students that functional genes are assembled at random from equimolar pools of nucleotides? Why would they falsely teach med students that mutation rates are determined by ESP (since one has no way to determine a mutation other than by sequencing) and then are divided by 4 because there are 4 possible nucleotides to get a value that means nothing but the mutation probability divided by 4? Why wouldn't they teach students what the word mutation actually means? Why wouldn't they teach students that selection is environmentally contingent and correctly describe the mathematics of selective neutrality? The answer is that they do. If you actually had something to add to that mathematics, you or someone else would have already published it. Clearly what you have come up with is nothing but a binomial probability distribution (if you ignore your division of the actual event probability by 4). And that is neither novel nor correct. That you, despite being pointed out to the math inv

olved and the underlying assumptions, do not recognize that the Poisson is a quite accurate substitute for the binomial probability distribution under the conditions I used it tells me that your grasp on the underlying meaning of the terms and the relationships is weak.

> It hasn’t been taught correctly in
> the past and it still is not taught correctly now. You have hersheyh
> using the Poisson distribution to try to describe the mutation and
> selection phenomenon yet he doesn’t understand why it is the wrong
> distribution function.

Again, I use the Poisson as a mathematically easier substitute for the binomial probability distribution calculation. I agree that if your equation, which differs from the binomial probability distribution by the division of the event probability by 4, were correct, the Poisson would not come close to that number. But, as I keep pointing out, the division by 4 is stupidity based on ignorance of what event you are measuring -- the mutation probability, not the mutation probability divided by 4.

> Evolutionist doctrine has so permeated the
> thinking of biologists that you have Schneider at the National Cancer
> Institute claiming on his government sponsored web site that the
> multiplication rule does not apply to biological evolution when in
> fact that is the reason combination therapy works. That is the
> mathematical irrationality which is being taught by evolutionists.

This is a distortion of what Schneider actually talks about. The multiplication rule of probability and *how* it is properly used in biology depends on the assumptions you make. The use of the multiplication rule by ignorant creationists who claim that evolution of a gene involves the random assembly of long specific sequences by random drawing from equimolar pools is a stupid assumption that no evolutionary biologist would make, but creationists regularly do. The math using the multiplication rule under these assumptions would be better termed GIGO. It is not mathematically wrong, but it is garbage-in and garbage-out that is based on stupid irrelevant assumptions.

Schneider, specifically is NOT talking about combination therapy, where, sometimes, the assumption of the need for two independent events being present simultaneously in a single individual is correct.
>
[snip]

> You want it in a nutshell? The reason why the theory of evolution is
> mathematically irrational is the multiplication rule of probabilities.

That is not an argument. In the case of the stupid creationist idea that evolution requires the building of a 747 in a tornado, they correctly use the math of the multiplication rule to produce GIGO nonsense because they use it under false assumptions. The mere existence of the rule does not mean it is being correctly used in any particular case. I have pointed out, in the three step process involving lethal antibiotics, as opposed to the one-step process you describe, how different processes can produce the same result with radically different probabilities. You, yourself, have presented example after example of cases where multiple serial mutation in a number of genes can work in relatively short time frames. Examples that *never* would have worked if all the mutations had to be present simultaneously in a single individual before selection. I have also pointed out the way in which *sometimes* the probability distribution for mutation can differ from the binomial probability distribution (which is yo

ur probability distribution, or would be if you recognized that your division of the event probability by 4 makes no sense) and produce the skewed distribution that is called the Luria-Delbruck distribution.

I have never argued that the multiplication of probabilities rule does not hold. In fact, I often have used it. I just point out that the probability of a particular genetic state can change depending on prior historical events (either because of selection for or against that state or because of neutral drift). The probabiilty of a particular genetic state is not *always* the probability of mutation to that state.

> It doesn’t matter whether the process occurs with selection or not.
> The random mutation can not make massive genetic transformations. And
> if you understand that the multiplication rule of probabilities is the
> central governing rule for the evolutionary process, it becomes an
> easy matter to understand how to suppress the mutation and selection
> process.

By arranging conditions that require that two independent low-probability events occur in the same trial. Yes. That will certainly work. But, as I have pointed out, the same two events can occur in the same trial if one of them is first converted into a high probability event and the number of trials is also o.k. In that case, one cannot use the multiplication of the two low-probability events, because one of the events is no longer low-probability.

> Simply force the population to evolve against two selection
> pressures simultaneously and then your problems with multidrug
> resistant microbes, multiherbicide resistant weeds, multipesticide
> resistant insects and less than durable cancer treatments have a
> logical solution.

Empirically, however, even that can be overcome by, say, patients that do not take a full course of antibiotics by stopping too early or that don't use them correctly, thus reducing the toxicity of some of the agents (if, for example, one agent requires taking on a full stomach and the other requires an empty stomach). Or (and this is a serious problem with some drugs) getting fake drugs.

> Of course you will not transform reptiles into birds
> or humans and chimpanzees from a common progenitor by this process.

That would only be a problem if you think that evolution works by a modern lizard laying an egg out of which pops a chicken. Or that a chimpanzee must give birth to a modern human. Otherwise, the transformations need not occur simultaneously. And, in fact, the fossil evidence shows that it didn't occur simultaneously.

>
> >>On the other
> >> hand, if you properly apply the theorems of probability theory to the
> >> mutation and selection phenomenon, you can easily derive the
> >> probability function that gives the probability of two mutations
> >> accumulating in a population and you will find that this mathematics
> >> fits the real behavior of mutating and selecting populations. In
> >> addition, if you properly apply the theorems if probability theory to
> >> the random recombination process, you will also understand why HIV
> >> does not recombine mutations to accelerate the mutation and selection
> >> process. This mathematics is above the skill level of most
> >> evolutionists.

> >The math you present isn't even above *my* skill level. And yet you
> >think it is some sort of revelation. Mathematics must be applied
> >properly to the question at hand. That's where your disagreement with
> >standard biology is.
>
> That’s my point Greg. This mathematics is not that difficult. The
> mathematics of mutation and selection is very similar to the
> mathematics of dice rolling yet we have geneticists like hersheyh
> using the Poisson distribution to describe the phenomenon.

Depends on how many sides the die has and the number of trials. The mathematics of dice rolling is basically that of a binomial probability distribution. If the mean probability of an event is low and the number of trials is high, then the Poisson is essentially the same distribution as the binomial probability distribution. The Poisson can be used instead of the binomial probability distribution when n>20 and p <0.05 or, alternatively, when n>100 and np< 10. And the *fact* is that your equation is nothing but the binomial probability distribution except for your erroneous division of the probability of the event by 4.

> Lenski’s
> team is still using the Poisson distribution because this is what is
> being taught and it is wrong. And the mathematics of recombination is
> also quite straightforward. But you don’t see hersheyh posting the
> derivation of that probability function.

And you apparently don't know the difference between recombination in eucaryotes and in procaryotes.

> What are you evolutionists
> going to do after I post the correct derivation for the probability
> function for random recombination?

Depends. If you screw it up as bad as your derivation for the probability of *mutation and selection*, we will point out where it differs from reality. It is highly unlikely that a mind that cannot tell the difference between "mutation probability" and "mutation probability divided by 4" is going to come up with something useful.

> Are you going to claim that that’s
> what you’ve been doing all along? If that’s the case, post the
> derivation now before I post it. What is being taught in biology
> courses now is a collection of mathematically irrational evolutionist
> crap.

Like the use of the Punnet Square for randomly mating populations of sexually-reproducing eucaryotes and the frequencies of different genotypes that would produce?

Sure. But the probability of different genetic states in a population is not a constant and is not always equal to the probability of mutation.

> That’s what all
> the empirical evidence for the random mutation and natural selection
> phenomenon shows. If you choose otherwise, you are choosing to believe
> in a mathematically irrational belief system.

If you could only show us that it *always* is irrational, that would help.
[snip]

[Greg Guarino]

On 9/23/2011 3:45 PM, Alan Kleinman MD PhD wrote:
> It just doesn’t make sense that neutral mutations in
> one family line will show up in a different family line now or ever.
> You have to have 20,000,000 neutral mutations show up in a single
> family line. That is mathematically irrational thinking.

This further convinces me that you have no feel for numbers at all.

I have two parents, four grandparents, etc. Forty generations back, a
mere 800 years or so, that works out to over a trillion ancestors.
That's already more human beings than have ever lived, so there must be
quite a lot of overlap. If you were to pick any one of those ancestors,
I'd likely be descended from him or her by thousands of paths ("family
lines")

Now imagine hundreds of thousands of generations. What does "in a single
family line" mean in that context? Moreover, what would it mean in any
context? My own daughter's great grandparents were born on three
continents, plus an island for good measure.

[Greg Guarino]

On 9/23/2011 3:45 PM, Alan Kleinman MD PhD wrote:

First I will note that you still, STILL haven't answered the question.
See, there it is, right below:

>> Why can't you seem to answer the most basic questions? Do you or do you
>> >not think that the "evolutionist" argument includes neutral mutations
>> >spreading quickly through a population? (as opposed to slowly, but in
>> >massively parallel fashion)

> Greg, the reason why you and other evolutionists are wrong about this
> is that you are taking a very low probability process and claim that
> millions of these processes are happening simultaneously. This is
> incorrect mathematically because of the multiplication rule of
> probabilities which governs the joint probabilities of random

> independent events.

Even if we don't care which ones "win"? What makes the events "joint"
exactly?

This is why it *does* matter how many of the genetic changes are
"important". The neutral ones, especially the neutral ones that have no
phenotypic effect, form a vast pool of "entries" into your low
probability lottery. If we don't care which ones "win", and if there are
large enough numbers of "entries" to overwhelm the "low" probability, we
can expect multiple "winners".

"Joint" probability only comes into play if we need a specific set of
entries to "win". We don't.

[Greg Guarino]

On 9/23/2011 3:45 PM, Alan Kleinman MD PhD wrote:
>> You've use the magic words twice in one sentence (again) and still
>> >managed not to say anything that approaches an argument.
> You want it in a nutshell? The reason why the theory of evolution is
> mathematically irrational is the multiplication rule of probabilities.
> It doesn’t matter whether the process occurs with selection or not.

And, in a nutshell, your application of the multiplication rule without
any consideration for how it fits the question at hand is why you are
wrong.

That it applies well in the case of multiple simultaneous lethal agents
in an asexual population comes as no surprise to anyone, as that is
exactly what standard evolutionary theory would predict. It is
bewildering that you use the word "derived" for such a simple
calculation, and equally strange that you think you have "taught"
something so obvious to anyone here.

[hersheyh]

[snip]

>
>
> hersheyh Aug 26, 3:05 pm
> Newsgroups: talk.origins

> From: hersheyh <hers...@yahoo.com>

No, I am determining the rate or probability of neutral fixation per nucleotide per generation. Then I am multiplying that rate by the number of nucleotides in a genome to get the rate of neutral fixation per generation per *genome*. This is standard probability theory. If you have six thousand dice in a "genome" and the probability of getting a two-face per die is 1/6, then the probability (mean expectation) of getting two-faces in a "genome" (a 'genome', remember is 6 thousand dice) is 1/6*6000 or 1000, not (1/6)^1000.

>
> >> Your gross over-extrapolation of this
> >> mathematics demonstrates your evolutionist bias. You try to take this
> >> model and impose the results derived on John Harshman’s 40,000,000
> >> differences between human and chimpanzee genomes.

> >No. All I intended was that you understand why neutral drift happens. The end result of neutral
> > drift can only be one of two possibilities for a new mutational change in nt. Either that specific
> > mutation will become fixed or it will go to extinction. The probability that it will eventually become
> > fixed is 1/2Ne, which is the initial frequency of that *specific* historical mutant in the population.
> > The probability that it will eventually become lost is 1-(1/2Ne). In the graph, instead of the initial
> > frequency of the alternate allele being 1/2Ne, it is set at 0.5 in the population. The Hardy-
> > Weinberg equation (you have heard of it, haven't you?) would imply that the next generation and all
> > subsequent generation would also have the two alleles in the same ratio. But that equation
> > assumes an infinite population. In *real* populations, there is generation to generation variance
> > due to chance. The smaller the population of alleles, the larger the variance as a %. And as many a

> > gambler has learned to his chagrin "Chance has no memory."

>
> What exactly are you trying to say with all this blah, blah, blah? Are
> you trying to say that John Harshman is making a mathematically
> irrational extrapolation of this model to millions of neutral
> mutations being fixed in 500,000 generations? Or are you trying to say
> that the Hardy-Weinberg equations only tell you that the frequencies
> of alleles remain constant when the system is in equilibrium?

Neither. Obviously you haven't read (or more likely haven't understood) what I actually wrote. I said that the H-W law only produces the exact same frequency every time if the population is infinite in size. Real populations are not infinite in size. Thus there is chance variation from generation to generation, and, because chance has no memory of what the original frequency was, the next generation according to the H-W will have whatever the current frequencies are as the mean to which it will approximately reach in the next generation. That is, if the initial generation had the ratio of 500 to 500, the next generation will likely only give something close to that ratio, say 490 to 510, because of chance variations alone. But the generation after that has a H-W expectation of 490 to 510, not the original 500 to 500. *Because chance has no memory.*

> That
> equation tells you nothing about the probability of two alleles to
> randomly recombine.

What does "random recombination" have to do with the H-W expectations? Ans: Absolutely nothing. Perhaps you do because you don't know what the term allele frequency means.

> In order to do that, you need to derive the
> probability function for random recombination. You haven’t done that
> yet. Isn’t that equation in one of your genetics texts? Or are they
> filled with the use of the Poisson distribution incorrectly?

I used the Poisson to estimate the binomial probabiity distribution for one or more mutants correctly, given that I refuse to stupidly divide the mutation probability by 4 like you do.

> >> On average, to
> >> account for these differences requires the fixation of dozens of
> >> neutral mutations generation after generation for hundreds of
> >> thousands of generations. This drift model only takes into account the
> >> fixation of one of two alleles as you describe above,

> >In this case, the 'allele' is a single nucleotide pair and demonstrates that rather than the frequency
> > being a constant, it changes from generation to generation by chance for any specific *selectively
> > neutral* alleles.

> So now an allele is a single nucleotide pair.

Are you so stupid that you did not understand the meaning of the "In this case" clause? An allele is a specific form of a gene. In *some* cases, the difference is nothing but a difference in a nucleotide pair that makes no phenotypic difference. Those types of changes are typically selectively neutral, since selection depends on there being an environmentally detectable phenotypic difference.

> And you claim that I
> don’t know what an allele is and now your claiming an allele is a
> nucleotide pair. This must be one of your many classic brain farts.

Not when I precede that with "In this case". This is more an example of your inability to understand clear language.

>
> >> not the fixation
> >> of dozens of neutral alleles every generation

> >That would be about 30/generation out of 3X10^9 possible sites or about 0.000001% of all sites
> > having reached the state of fixation.
>
> You’ve never heard of the multiplication rule of probabilities for
> computing the joint probability of random independent events, have
> you? This is the rule which makes the theory of evolution
> mathematically irrational and what you’ve made a career out of
> teaching.

And I have no problem with the multiplication rule when it is used correctly. You use it indiscriminantely and without any understanding of the assumptions you are making. Thus you are misusing it.

>
> >> and when in reality, you
> >> have more than two possible alleles at a single locus.

> >Actually, any natural population has a degree of heterozygosity at any locus or site, which is measured by F-statistics (fixation indices).
> >http://www.google.com/url?sa=D&q=http://www.library.auckland.ac.nz/subject-guides/bio/pdfs/733Pop-g-stats2.pdf
> >Basically, what you might expect at neutral sites is that a fraction of them will have heterozygosity at detectable levels >between 1 and 99% (typically divided between two alternatives rather than 3 or 4, although there can be a small >scattering of the other possible nts). Most neutral sites will be almost completely one nt or another, with a small >scattering of other nt's. That is effective fixation. That is what is seen. The amount of heterozygosity in a population's >neutral changes is affected by the amount of inbreeding. Populations that have undergone constrictions recently, either >because of a population crash or because of the founder effect, will show less heterozygosity. Old, large, stable, >randomly reproducing populations will tend to show more heterozygosity.
>
> Do you want to try rewriting your model for drift using multiple
> neutral alleles? Do you think that will make the gross over-
> extrapolation of this model to fit your belief system any less
> mathematically irrational?

The human genome is almost entirely composed of selectively neutral nucleotides. After all, protein coding sequences account for only about 3% of the genome and many of the nucleotides within a coding sequence can be changed (at least to *some* other nts) without having any selective consequence.

>
> > I don’t ignore this model; I ignore your inappropriate over-
> > extrapolation of this model. You have failed to understand the basic
> > science and mathematics of the mutation and selection phenomenon, you
> > are now failing to understand the mathematics of random recombination
> I wasn't even mentioning recombination here. Do you spout these words
> just because you can?
>
> Not only can I spout the words, I can back it up with the mathematics.
> I’ve already presented the derivation of the correct probability
> function for the mutation and selection phenomenon and you almost
> understand it. We still need to work on your inappropriate use of the
> Poisson distribution.

In what way have I used the Poisson distribution inappropriately? I used it as an approximation of the binomial probability distribution, which, except for your dividing the event probability by 4, is what you generated in your 'derivation'. After all,

"The binomial distribution converges towards the Poisson distribution as the number of trials goes to infinity while the product np remains fixed. Therefore the Poisson distribution with parameter λ = np can be used as an approximation to B(n, p) of the binomial distribution if n is sufficiently large and p is sufficiently small. According to two rules of thumb, this approximation is good if n ≥ 20 and p ≤ 0.05, or if n ≥ 100 and np ≤ 10.[8]

http://en.wikipedia.org/wiki/Binomial_distribution#Poisson_binomial_distribution

So are you claiming that your 'derivation' has no relationship to the binomial probability distribution (again, with the exception of the division of the event probability by 4, I can demonstrate that your 'derivation' is nothing but the binomial probability distribution) or are you claiming that I am using the Poisson when n <20 and p> 0.05? Or when n<100 and np>10? The "event probability" I have been using is 10^-8 (the mutation rate). [You have been using the mutation rate divided by 4 and calling that the mutation rate.] But in either case, that is p, which, seems to meet the criteria. n was 10^9. And, in fact, your np is even smaller than mine, and is certainly less than 10 (although n is way larger than 100 in either case).

> Have you done your homework yet and gone through
> the derivation of the equation that you blindly use without
> understanding? And have you gone through the conditions when the
> Poisson distribution is an appropriate approximation for a binomial
> distribution (which mutation and selection is not).

I don't need to derive an already existing equation to know when it is useful. And, yes, I have *again* pointed out that the conditions in which I used the Poisson were indeed appropriate just above. So stop your stupidity about the Poisson. If you think you have derived something other than a binomial distribution, then you need to show that that is the case rather than talk about the Poisson. [I do know that the binomial actually is not really the case in many examples; that the Luria-Delbruck is better because of the faulty assumption that every trial has the same probability to generate a mutant the next generation when we know that the probability that an already mutant cell will produce a mutant the next generation is much higher than the probability that a non-mutant will produce a mutant. But that doesn't matter if the equation you generated was nothing but the binomial probability distribution.]

> Once you have done
> this, I’ll show you how to derive the probability function for random
> recombination so you can actually get beyond the Punnett square and
> the Hardy-Weinberg equation.

That should be interesting. Given that you haven't even recognized that there is a difference in the way recombination works in procaryotes and viruses and eucaryotes and that we were not talking about unlinked genes but different alleles of the same gene in the above discussion. I wonder how you will screw up that math?

> >> and now you take a model based on the random substitution of a single
> >> allele for another allele and claim that this entire process occurs in
> >> parallel allowing the random substitution of dozens of neutral alleles
> >> to occur simultaneously.

> >That is exactly correct, although simultaneous is wrong for fixation, as the *individuals* in which
> > the final step of fixation occurs each generation are almost certainly not going to be a single
> > individual, but different individuals in the population. If you have problems understanding that, let > > me know and I will patiently try to teach you, cricket.

> I’m really not interested in being indoctrinated by you.

Well, if you really do prefer ignorance, keep on keeping on.

> If you have
> some mathematics to show us, present it but in the meantime, we have
> to wade through your blah, blah, blah in hopes of finding something
> beyond your brain farts.

> >> I suppose you are now going to claim that the
> >> multiplication rule of probabilities
> >The multiplication rule of ...

> Always applies for computing the joint probabilities of multiple
> random independent events whether selection is involved or without
> selection as with neutral evolution.

Which, I presume is why you determine the expected number of sixes you would get from rolling 100 dice by taking the probability of a six per roll (1/6) and multiplying it by itself 100 times [(1/6)^100 = very small probability] rather than by multiplying 1/6 by 100 = 16.7. [In my math, the first equation tells me the probability of getting only sixes in 100 rolls of an honest die and the second tells me the expectation for sixes in 100 rolls of an honest die. Your math, however, seems to differ from mine on this point.]

[snip]

[hersheyh]

[snip]

>
> John Harshman Aug 29, 4:42 pm
> Newsgroups: talk.origins

> From: John Harshman <jhar...@pacbell.net>

> Date: Mon, 29 Aug 2011 16:42:16 -0700
> Local: Mon, Aug 29 2011 4:42 pm
> Subject: Re: The Theory of Evolution is Mathematically Irrational
> Round 2
>
> >>>> Don�t you know that a beneficial mutation at the particular locus can
> >>>> mutate back to a detrimental or neutral mutation?

Since a mutation is described as beneficial by comparing it on a metric of reproductive success relative to either an organism with the original genomic state or a different mutant, that means you cannot even determine whether a mutation is beneficial unless you can identify the two genetic states (usually by their phenotypes). And, of course, terms like beneficial are conditional to a specific environment.

> > >>> Unless you know a
> >>>> priori what the base at the particular locus is, a point mutation can
> >>>> give any of the four possible bases.

Mutation (a change in genetic state) of course, is not the same as point mutation. If you know you have a point mutation, that means you must know the original nt present at that site and that there has been a change in that nt. Otherwise you don't even know that you have a point mutation.

> >>> That's just as nonsensical as it was the first time you made the claim.
> >>> The ability of back mutations to happen is irrelevant to the mutation
> >>> rate. Regardless of the original base, one of your four possibilities is
> >>> not a mutation. A->A is not a mutation. C->C is not a mutation. G->G is
> >>> not a mutation. T->T is not a mutation. Your inability acknowledge the
> >>> error of a prior claim, regardless of how stupid it is, makes you look
> >>> seriously insane.

> >> What it makes you look is mathematically incompetent which you are.
> >> You have hersheyh claiming there are only two possible outcomes for a
> >> point mutation.

> >No he doesn't.

Actually I do claim two possible outcomes for purposes of the math. The two possible outcomes are 'changed' and 'not-changed'. That is, of course, is in perfect congruity with what the word 'mutant' really means: change. In order to operationally *identify* a mutation, aka, a change event, you have to know what the original genetic state was and also be able to operationally identify the end state.

In real genetics, of course, this is always done by looking at some sort of "phenotype" related to "genotype". In some rare cases, the "phenotype" examined is a specific band on a DNA sequencing gel or the tightness of binding of a genetic probe or the loss/gain of a restriction site. But most of the time, and certainly when it comes to changes that have a selective effect, one determines "change" in some functional or morphological phenotype that can be traced to a "change" (aka, mutation) in a specific gene. Such as "achondroplasia". Or "cystic fibrosis". Or "hemophilia A" Or "resistant to antibiotic A". Or "white eyes". That is because, when one is looking at real consequences to real organisms and real selection, it is the phenotype produced by the change that is important. Not whether the mutation is a point mutation at a particular site.

>
> Sure he does John, the two outcomes are either beneficial or not
> beneficial.

No. The two outcomes are "unchanged" and "changed". Which is the same as saying "not mutant" and "mutant". In fact, I have *specifically* and *repeatedly* said that "beneficial" and "not beneficial" are conditional terms that can only be used in particular environments because the same "mutation" (that is, "change in genetic state" can be beneficial in one environment and neutral or detrimental in another. The genetic state (and phenotypic state) is unchanged, but the selective value is changed.

> What do you thing the probability is on a single trial for
> the probability of either beneficial or not beneficial?

That cannot be determined unless there is a phenotypic difference that you can identify as the "mutant state" from the "nonmutant state". But being able to distinguish between the mutant and nonmutant phenotypes is a necessary, but not sufficient, condition for distinguishing between "beneficial" and "not beneficial". For that you need to be able to *both* identify the mutant and nonmutant phenotypic state, but also identify how those two states perform on a metric of reproductive success in a specific environment relative to the other. *When* you are using a particular selective environment to identify genetic mutants with a specific mutant phenotype, such as an environment with an antibiotic toxic to organisms with the initial genetic state (aka, antibiotic sensitive cells), you are identifying a genetic change based on a phenotypic difference produced by that mutational change. Or you could screen for mutants on the basis of a phenotypic difference (e.g. white-eyed flies instead of the original red).

> What do you
> think the probabilities for the outcome are for single trial for one
> of the four bases? This is a simple mathematical question.

No. It is an utter irrelevancy to whether or not there has or has not been a change in genetic state from a known initial state, aka, mutation. Again, you cannot have or even identify a mutation if you cannot identify both the starting and end genetic states.

> This is a
> question you have to answer if you are assuming a binomial
> distribution or the distribution I derived for you. It also addresses
> the conditions whether the Poisson distribution can be used to
> approximate this stochastic process.
>
> >> The day that you can tell us where a random point
> >> mutation will occur before it occurs

If we cannot determine where or when a random point mutation will occur before it occurs, exactly what are you detecting and measuring when you talk about the mutation rate that you then divide by 4? You have provided us with the following description of m.

m -- the probability that in one organism in one generation, a
mutation will affect a specific locus in the genome
divide by four

How do you determine m for a specific site? Wild-assed guess? More importantly, how is the organism with this mutation in a specific nucleotide site (the word 'locus' is used to describe a 'gene locus', not a nucleotide site within that locus) identified? If you can't measure m, then m/4 is also nothing but a meaningless hypothetical.

m/4 -- the probability that in one organism in one generation, a
mutation will turn a specific locus into a specific nucleotide other
than the one it already is -- for instance, turn G, C, or T into A.
subtract that result from 1

This means you have already identified the organism that has a "mutated" nucleotide site, apparently. How did you do this if you don't use phenotype? And if you know that that nucleotide site that has no phenotypic effect has mutated (changed), how can you not know what the original nt at that site was?

> >> and the base that was at that
> >> locus before the mutation occurred is the day that I’ll change the 4
> >> in the correct probability function for a 3 but that day will never
> >> come.

Three would also be stupid. Slightly less stupid, perhaps. But you are the one claiming to be able to identify that a site has had a mutational change without knowing what the original state was. How does one with your mindset empirically determine m or identify organisms that have had a mutation?

> >The day you learn anything new will never come. I can tell you that,
> >whatever and wherever a point mutation occurs, it will change the base
> >that was there to a different base. Tell me, for any given prior base,
> >how many possible different bases are there?

> If you know what the prior base is three, if you don’t know what the
> prior base is, you can only say with certainty that it is one of the
> four possible bases.
>

[snip]

[G]

hersheyh <hers...@yahoo.com> wrote:
[big snip]

>You have provided us with the following description of m.
>
> m -- the probability that in one organism in one generation, a mutation will
> affect a specific locus in the genome divide by four
>
> How do you determine m for a specific site? Wild-assed guess? More
> importantly, how is the organism with this mutation in a specific nucleotide
> site (the word 'locus' is used to describe a 'gene locus', not a nucleotide
> site within that locus) identified? If you can't measure m, then m/4 is
> also nothing but a meaningless hypothetical.
>

[big snip]
>

It's not that hard to determine m. You take the bacteria, subject them to a
lethal dose of Antibiotics and determine what percentage survive, then , as
this is only one possible nt mutation you multiply the result by 4.

And I am sure the Good Good Dr. Dr. will take this seriously too.

G

[Alan Kleinman MD PhD]

The following are a compilation of responses to posts 951-975 to
prevent splinter threads. Sorry for any inconvenience.

Greg Guarino Aug 29, 7:06 pm

Newsgroups: talk.origins
From: Greg Guarino <gdguar...@gmail.com>

Date: Mon, 29 Aug 2011 22:06:17 -0400
Local: Mon, Aug 29 2011 7:06 pm

Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

On 8/29/2011 8:01 PM, Alan Kleinman MD PhD wrote:

>> On Aug 2, 8:40 pm, "g...@risky-biz.com"<gdguar...@gmail.com> wrote:

>>> On Monday, August 1, 2011 9:50:40 PM UTC-4, John Harshman wrote:
>>>> Alan Kleinman MD PhD wrote:

>>>>> Unless you know a
>>>>> priori what the base at the particular locus is, a point mutation can
>>>>> give any of the four possible bases.

>>>> That's just as nonsensical as it was the first time you made the claim.
>>>> The ability of back mutations to happen is irrelevant to the mutation
>>>> rate. Regardless of the original base, one of your four possibilities is
>>>> not a mutation. A->A is not a mutation. C->C is not a mutation. G->G is
>>>> not a mutation. T->T is not a mutation. Your inability acknowledge the
>>>> error of a prior claim, regardless of how stupid it is, makes you look
>>>> seriously insane.

>>> Worse yet, one of the bases *was* original whether or not we know which one it is. Thus one of the four >>>possibilities has a massively greater probability than the others, rendering any "division by four" >>>mathematically nonsensical.
>> Mathematics is always nonsensical to the mathematically incompetent.
>Do you disagree that one possibility is greatly more likely than the
>other three?
What I agree is that when a point mutation occurs that there are only
four possible outcomes and unless you know what the base was before
the mutation occurred then any of the four possible outcomes are
equally likely and that’s how you must express this mathematically.

John Harshman Aug 29, 9:51 pm
Newsgroups: talk.origins
From: John Harshman <jharsh...@pacbell.net>
Date: Mon, 29 Aug 2011 21:51:53 -0700
Local: Mon, Aug 29 2011 9:51 pm

Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

>> On Aug 4, 12:41 pm, John Harshman <jharsh...@pacbell.net> wrote:
>>> Alan Kleinman MD PhD wrote:

>>>> On Jul 8, 8:07 am, John Harshman <jharsh...@pacbell.net> wrote:
>>>>> Alan Kleinman MD PhD wrote:

>>>>>> Hersheyh is using a value of 30 generations to amplify the beneficial
>>>>>> allele, that s a catastrophic event where the entire population is
>>>>>> decimated and only a single tiny subpopulation remains. Even using his
>>>>>> value of 30 generations per beneficial mutation amplification (or what
>>>>>> hersheyh calls recovery), you can not do the accounting for John
>>>>>> Harshman s claim that there are 40,000,000 differences between humans
>>>>>> and chimpanzees in less than a million generations.
>>>>> That's because one involves selection and the other involves neutral
>>>>> evolution. And one involves a single allele while the other involves the
>>>>> entire genome of 6 billion bases.
>>>> I comprehend your mathematically irrational claims.
>>> Doubtful.
>>>> Millions of random
>>>> neutral mutations accumulate in every member of the population in just
>>>> a few generations.
>>> As I suspected. You comprehend nothing.
>> Sure I comprehend your mathematically irrational claims. You claim
>> that dozens of very low probability events occur every generation,

>> generation after generation for hundreds of thousands of generations.

>> John, would you compute the joint probabilities of you mathematically
>> irrational claims for us?
>The question is nonsensical. I've tried in other posts to explain why.
>Let's see if you respond to any of them.
I have responded to them and your willful ignorance of the

multiplication rule of probabilities for computing the joint

probability of events demonstrates what is required to believe in the

mathematically irrational theory of evolution.

>>>> Five million years from now, your 30 or so neutral
>>>> mutations will spread through every member of the population of the
>>>> earth.
>>> Ditto. Nothing.

>>>> And who has 6 billion bases in their genome?
>>> Pretty much ever single human being. How many do you think? (Remember
>>> that you are presumably diploid.)
>> Now John, we have about 3 billion base pairs in our genome so I guess
>> you could claim there are six billion bases in our genome.

>No, that's not what I'm talking about. A haploid human genome has about
>3 billion base pairs. A diploid human genome (again, I assume that you
>are diploid; I am) has twice that many, or 6 billion. I would have
>assumed that a doctor would know this.
John, I’ve really never paid attention to the exact number of bases in
the human genome. If you look at the web sites for the human genome
project http://www.ornl.gov/sci/techresources/Human_Genome/project/info.shtml
and http://www.genome.gov/11006943 for example give human genome size
of 3 billion base pairs. Of course we are diploid. The exact number of
bases in the human genome has no importance in the practice of
medicine however understanding the basic science and mathematics of
mutation and selection has critical importance in the field of
infectious diseases and oncology. You would assume that evolutionists
would understand this but they don’t. Perhaps you would explain to us
what knowing the exact number of bases in the human genome is
important in the practice of medicine?

>> Are you
>> trying to claim there are 6 billion possible point mutations that
>> could occur?

>No. But there are 6 billion sites at which point mutations could occur.
>There are of course 3 times that number of possible point mutations.
The number of possible point mutations in a genome is equal to the
number of bases. There are four possible outcomes to any point
mutations. And are there 3^(6*10e9) possible combinations of bases or
4^(6*10e9) possible combinations of bases?

>>>>>> This is why these
>>>>>> evolutionist turn to the junk science of the concept of drift to
>>>>>> account for all these differences.
>>>>> What exactly is wrong with the concept of drift. Do you deny that it
>>>>> happens? If so, what prevents it?
>>>>>> Do you want to tell us what 30
>>>>>> neutral mutations have shown up in your genome as well as the rest of
>>>>>> the world s population in this generation?
>>>>> Nobody makes that claim. All you do here is reveal your gross
>>>>> misunderstanding of neutral evolution.
>>>> I understand your claims now; your 30 neutral mutations will show up
>>>> in the entire population of the earth in 5 million years.
>>> It really shouldn't be difficult to understand, yet you seem incapable
>>> of comprehending the least little bit. But no, you have nothing right so
>>> far. Try again.
>> It’s not at all difficult to understand your mathematically irrational
>> claims. You claim that dozens of low probability events occur every
>> generation, generation after generation for hundreds of thousands of
>> generations.
>Not exactly. If you refer to fixation, at the time it actually happens
>it has become a high probability event. But of course dozens of low
>probability events can happen. It all depends on how many "attempts"
>there are, doesn't it?
The difference between your argument and my argument is that I have
derived the probability function that correctly describes how many
attempts are required to give that reasonable probability and how
selection (amplification) is necessary. You on the other hand don’t
provide any mathematics or empirical evidence to substantiate your
argument. And the central blunder you are making with your semantic
argument is ignoring the multiplication rule of probabilities. So
instead of doing the gross over-extrapolation of a model of a single
gene with two neutral alleles, why don’t you try to formulate the
problem of thousands or millions of neutral alleles being fixed
simultaneously and explain to us how this happens mathematically? I’ll
even make the challenge simpler, formulate the problem for two genes
each with two neutral alleles for each gene and compute for us the
time to fixation for two genes simultaneously by neutral evolution.

And the rational semantic argument to your mathematically irrational
semantic argument is that you claim that because there are untold
billions of neutral mutations that it is possible for 20,000,000
neutral mutations to be fixed in 500,000 generations. You are claiming
that tens of millions of neutral mutations scattered all throughout
the population are somehow showing up in the entire population of the
earth today. You are saying that neutral mutations in one family line
are somehow showing up in a different unrelated family lines, not just
now and then but over and over millions of times. Just how do these
neutral mutations move from one unrelated family line to another?

>> Would you compute the joint probability of those
>> individual events for us?
>A meaningless number. Please compute the probability of dealing a bridge
>deal in which one player gets all spades, a second all hearts, etc. Got
>it? Now compute the probability of each player getting some deal, any
>deal. Which one is more appropriate here?
It’s a meaningless number to you because you are ignoring the

multiplication rule of probabilities for computing the joint

probability of events. This is the fundamental evolutionist blunder
which is ignoring the multiplication rule of probabilities. When you
properly include this mathematical principle, the behavior of mutation
and selection or mutation without selection becomes easily
predictable.

hersheyh Aug 30, 7:18 am
Newsgroups: talk.origins
From: hersheyh <hershe...@yahoo.com>
Date: Tue, 30 Aug 2011 07:18:06 -0700 (PDT)
Local: Tues, Aug 30 2011 7:18 am

Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

>> On Aug 1, 6:43 pm, John Harshman <jhar...@pacbell.net> wrote:
>> > Mark Isaak wrote:
>> > > On 8/1/11 2:19 PM, Alan Kleinman MD PhD wrote:

>> > >> On Jul 6, 7:31 am, John Harshman<jhar...@pacbell.net> wrote:
>> > >>> Alan Kleinman MD PhD wrote:

>> > >>> [...]
>> > >>>> Well at least you and I agree that mutationandselectiondidn tdoit.
>> > >>> Everyone agrees on that.

>> > >> You need to explain that to Mark Isaak because he thinks that
>> > >> mutationandselectiondiddoit.

>> > > Yup. That explains why I repeatedly said just the opposite.
>> > Obviously, Kleinman understands your opinions much better than you do,
>> > because you're causing millions of people to die through lack of proper
>> > medical treatment.
>> And now Mark is making the claim, “I am an engineer, and I understand

>> that the more complex the conditions are, the easier it is to do some

>> optimization.” I wonder which mathematically irrational conceptual
>> claim will take longer to have a real empirical example given, your
>> claim that two beneficial alleles can be amplified simultaneously or
>> Mark’s claim that the more complex the conditions are, the easier it
>> is to do some optimization. At least you are not as ridiculous as
>> hersheyh’s and Schneider’s claim that the multiplication rule of
>> probabilities does not apply to biological evolution.
>A lie. A claim I have NEVER made. I certainly have claimed that the creationist *misuse* of the >multiplication rule that Schneider points out is an egregiously ignorant claim. That misuse rests on the >obviously false assumption that evolution works to produce any and every extant gene by random assembly of >that gene from its constituent parts. Evolution makes no such claim. Biology makes no such claim. Only >creationists make that claim.

So now you are claiming that Thomas Schneider of the National Cancer
Institute is a creationist???? Because Schneider has made this very
claim and he is incorrect when he makes the claim on his web site
http://www-lmmb.ncifcrf.gov/~toms/paper/ev/AND-multiplication-error.html
, “The multiplication rule does not apply to biological evolution.”
The multiplication rule is in fact the central and governing
mathematical principle for understanding how the mutation and
selection phenomenon works and his failure to understand this harms
the people he is paid to help, that is people who suffer from cancer
(a mutating and selecting disease).

And now hersheyh, perhaps you would explain to us why you have spent
so much time defending Schneider’s blunder? The behavior of mutation
and selection and mutation without selection are both governed by the
multiplication rule of probabilities because both phenomena are
stochastic processes. And this is why abiogenesis and the theory of
evolution are both mathematically irrational belief systems. And these
are the two pillars of evolutionism.


John Harshman Aug 30, 7:33 am
Newsgroups: talk.origins
From: John Harshman <jharsh...@pacbell.net>
Date: Tue, 30 Aug 2011 07:33:44 -0700
Local: Tues, Aug 30 2011 7:33 am

Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

>>>>>>>> Well at least you and I agree that mutationandselectiondidn tdoit.
>>>>>>> Everyone agrees on that.

>>>>>> You need to explain that to Mark Isaak because he thinks that
>>>>>> mutationandselectiondiddoit.

>>>>> Yup. That explains why I repeatedly said just the opposite.
>>>> Obviously, Kleinman understands your opinions much better than you do,
>>>> because you're causing millions of people to die through lack of proper
>>>> medical treatment.
>>> And now Mark is making the claim, “I am an engineer, and I understand

>>> that the more complex the conditions are, the easier it is to do some

>>> optimization.” I wonder which mathematically irrational conceptual
>>> claim will take longer to have a real empirical example given, your
>>> claim that two beneficial alleles can be amplified simultaneously or
>>> Mark’s claim that the more complex the conditions are, the easier it
>>> is to do some optimization. At least you are not as ridiculous as
>>> hersheyh’s and Schneider’s claim that the multiplication rule of
>>> probabilities does not apply to biological evolution.
>> A lie.
>Why suppose a lie when he simpler explanation is that Kleinman can't
>read for comprehension? You know he can't. You know he makes up his own
>story in his head to fit what he already thinks and can't be bothered
>with any contradictions. And once he makes up a story, he sticks with it
>forever.

John, I can’t tell for sure whether you are more ignorant than
Schneider or more deceptive. You are probably both since Schneider
does have some mathematical skill. You on the other hand covertly
throw out the multiplication rule of probabilities and Schneider does
this overtly. So in this case you are both more ignorant and more
deceptive.

Mark Isaak Aug 30, 8:30 am

Newsgroups: talk.origins
From: Mark Isaak <eci...@curioustaxonomyNOSPAM.net>

Date: Tue, 30 Aug 2011 08:30:27 -0700
Local: Tues, Aug 30 2011 8:30 am

Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

>>>>>> John, would you tell us what 25 base substitutions you ve gotten this
>>>>>> generation? And which of your neutral mutations have you spread
>>>>>> through the entire human population of the earth.
>>>>> Color me perplexed.
>>>>> Unlike you, I do not easily conclude that the person I am arguing with
>>>>> is irrational or impenetrably dense. But how else to explain your
>>>>> continued repetition of the statement above? Perhaps you simply don't
>>>>> read the arguments addressed to you?
>>>> You see Greg, John is now claiming that the neutral mutations fixed in
>>>> his genome occurred millions of years ago.
>>> It has been obvious to me that such was his position from the
>>> first time he presented it. What explains that, I wonder? I, who
>>> am not at all well-versed in the concept of neutral evolution,
>>> immediately understood that John could not be claiming that it
>>> happens quickly. You, on the other hand, not only assume he might
>>> be asserting such a preposterous notion, but persist in that
>>> belief despite having it explained multiple times.
>> Let’s see if I can put some verse in your not so well versed
>> understanding of what John is claiming. John has already said that the
>> fixation of a neutral mutation is a very low probability event. Then
>> John turns around and claims that it happens a couple hundred times
>> per generation for hundreds of thousands of generations. Greg, you had
>> better watch your step before you find yourself neck deep in
>> mathematically irrational evolutionist horse pucky.
>In other words, Mr. Kleinman, John's claim is perfectly reasonable,
>whereas you are admitting utter incompetence at mathematical reasoning.

Mark, social engineer, we are still waiting for you to give us an
example of an optimization problem where the more complex the
optimization conditions the easier it is to optimize.
>Consider: There are roughly 25 million neutral mutations added to the
>human population *every day*. That is roughly 9 billion per year. Now
>John turns around and claims that four or so get fixed per year. Hmm.
>Four out of nine billion. Who would *not* consider .0000000004 to be a
>very low probability? Only someone who is mathematically irrational.

I understand this hard for a social engineer to understand but the
multiplication rule of probabilities applies to computation of the
joint probability of events occurring. If you can’t understand this,
perhaps you might understand that it is irrational to believe that
neutral mutations in one family line of a population will somehow show
up in another unrelated family line.

Jack Dominey Aug 30, 9:02 am
Newsgroups: talk.origins
From: Jack Dominey <jack_domi...@email.com>
Date: Tue, 30 Aug 2011 16:02:22 +0000 (UTC)
Local: Tues, Aug 30 2011 9:02 am

Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

>> you can say that if you have a point mutation at a particular locus that
>> the result of that point mutation will be a Ade, Gua, Cyt, or Thy with a
>> probability given by Pr{Ade} + Pr{Gua} + Pr{Cyt} + Pr{Thy} = 1 where
>> each of the individual probabilities is 1/4.
>Except one of those four isn't a mutation. Replacing one base with the
>same base would be "staying the same".

Welcome to the discussion Jack. When you are talking about a random
process such as a point mutation, the only thing you can say with
certainty is that after a point mutation has occurred, you have only
one of four possible outcomes. If you know what the base was before
the point mutation has occurred then you can say with certainty that
the outcome will be one of three possible remaining bases. However you
do not know what the base was before a random mutation has occurred so
the only thing you can say with certainty is that after a point
mutation has occurred, the base will be one of the four possible
bases.

johnethompson2001@yahoo.c¬om Aug 30, 1:02 pm
Newsgroups: talk.origins
From: "johnethompson2...@yahoo.com" <johnethompson2...@yahoo.com>
Date: Tue, 30 Aug 2011 13:02:09 -0700 (PDT)
Local: Tues, Aug 30 2011 1:02 pm

Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

>> > you can say that if you have a point mutation at a particular locus that
>> > the result of that point mutation will be a Ade, Gua, Cyt, or Thy with a
>> > probability given by Pr{Ade} + Pr{Gua} + Pr{Cyt} + Pr{Thy} = 1 where
>> > each of the individual probabilities is 1/4.
>> Except one of those four isn't a mutation. Replacing one base with the
>> same base would be "staying the same".
>This has been pointed out to him numerous times. His response has
>always that everyone but him is an idiot at math.
I don’t call evolutionists idiots, I call them mathematically
incompetent. Look how much difficulty evolutionists are having
recognizing the fact when a point mutation occurs, the only thing you
can say with certainty is that after the mutation has occurred that it
will be one of four possible outcomes. You can only say with certainty
that the base will be one of three possible outcomes when you know
what the base was before the mutation occurred but you don’t know
that.

Greg Guarino Aug 30, 8:58 pm

Newsgroups: talk.origins
From: Greg Guarino <gdguar...@gmail.com>

Date: Tue, 30 Aug 2011 23:58:35 -0400
Local: Tues, Aug 30 2011 8:58 pm

Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

>>>>>> John, would you tell us what 25 base substitutions you ve gotten this
>>>>>> generation? And which of your neutral mutations have you spread
>>>>>> through the entire human population of the earth.
>>>>> Color me perplexed.
>>>>> Unlike you, I do not easily conclude that the person I am arguing with
>>>>> is irrational or impenetrably dense. But how else to explain your
>>>>> continued repetition of the statement above? Perhaps you simply don't
>>>>> read the arguments addressed to you?
>>>> You see Greg, John is now claiming that the neutral mutations fixed in
>>>> his genome occurred millions of years ago.
>>> It has been obvious to me that such was his position from the first time he presented it. What explains that, >>>I wonder? I, who am not at all well-versed in the concept of neutral evolution, immediately understood that >>>John could not be claiming that it happens quickly. You, on the other hand, not only assume he might be >>>asserting such a preposterous notion, but persist in that belief despite having it explained multiple times.
>> Let s see if I can put some verse in your not so well versed
>> understanding of what John is claiming.
>Experience suggests otherwise.

What experience are you talking about? Are you now claiming you were
there millions of generations ago?

>> John has already said that the
>> fixation of a neutral mutation is a very low probability event.
>Yes.

And the way an evolutionist gets from the claim that a low probability
event occurs once in a great while to a low probability event happens
over and over is by ignoring the multiplication rule of probabilities.
And this is why the theory of evolution is a mathematically irrational
belief system.

>> Then
>> John turns around and claims that it happens a couple hundred times
>> per generation for hundreds of thousands of generations.
>I don't buy lottery tickets, so I may be wrong about how the game works.
>But I just looked it up. It seems you pick 5 numbers between 1 and 56,
>plus another number between 1 and 46. If so, I make the odds of winning
>to be about one in 21 billion. A very low probability event, no? Yet
>people win, many times a year, surely hundreds in a generation.
>What do you think explains that?

It’s very easy to explain Greg. If you have lots of people buying lots
of lottery tickets, a small number of those will win a single lottery.
A much, much smaller number of those winners will win two lotteries
and a vanishingly small number will win three lotteries. What you have
John arguing is that a single population will win millions of
lotteries. That’s like claiming there is some lottery winner out there
who has won millions of lotteries. That is mathematically irrational,
but that’s John for you.

>>Greg, you had
>> better watch your step before you find yourself neck deep in
>> mathematically irrational evolutionist horse pucky.
>It is very odd how often you use the same phrase.

I think that’s the first time I used the phrase “horse pucky”.

>>> Your willingness to believe an entire branch of science hopelessly irrational cripples your ability to do any >serious analysis, in my opinion. It's like a shield you use to fend off dangerous ideas.
>> I wouldn t call evolutionism a branch of science;
>I was referring to biology. Do you doubt that biologists, nearly all of
>them, accept basic evolutionary theory?

Evolutionists have transformed the field of biology into folklore.
Evolutionists have long ago abandoned hard mathematical science. If
evolutionists did attempt to do hard mathematical science, they would
run head-on to the multiplication rule of probabilities and find out
that their theory is mathematically irrational.

>> it is a
>> mathematically irrational belief system. Even the mathematically
>> incompetent hersheyh agrees that I have derived the correct
>> probability function for a single mutation occurring. He s still
>> arguing that there shouldn t be a factor of 4 in the denominator of
>> the mutation rate but that s why hersheyh is still mathematically
>> incompetent. Hersheyh still hasn t come to grips with the joint
>> probability function for two mutations occurring but that requires he
>> abandon the notion that the multiplication rule of probabilities does
>> not apply to biological evolution.
>I really can't fathom how you can keep repeating this. He certainly does
>not say that the multiplication rule does not apply to *some* biological
>evolution.

Hersheyh has finally come to grips with the fact that I have derived
the correct probability function for a single mutation except he is
still confused by the fact that when a point mutation occurs that you
have more than a single alternative outcome. As hersheyh works a
little more on understanding the computation for the joint probability
of two mutations occurring, he will see how the multiplication rule
comes into play. You have to understand, hersheyh’s mathematical
skills are limited to plugging numbers into a canned equation like the
Poisson distribution. Hersheyh has used this equation his entire
career without ever going through the derivation of the equation. If
hersheyh actually did his homework and went through the derivation of
the Poisson equation, he would understand that this is the wrong
distribution function to describe the mutation and selection
phenomenon. The Poisson distribution is not even a good approximation
for the binomial distribution is this case of mutation and selection
but hersheyh does not know why because he only knows what he is
indoctrinated with. Deprogramming an indoctrinated evolutionist is a
long and arduous process.

>>And I will post the correct
>> probability function for random recombination but I m waiting for
>> hersheyh to try to blah, blah, blah his way through the computation. I
>> love watching hersheyh squirm. He s not a very good squirmer but he
>> does so much of it.

>>>> Millions of years ago,
>>>> millions of neutral mutations are now being fixed in everyone s
>>>> genomes today.

>>> And still you do not have it right. A few are fixed in each generation. The ones that have just become fixed >>>didn't just "get into my genome" in my generation. In all likelihood I and nearly every other human on the >>>planet have had them in our lineages for many, many generations. But a few people still had a variant until >>>very recently.
>> So these randomly fixed neutral mutations had a probability of being
>> fixed. What was the probability of each of these neutral mutations
>> being fixed and then what was the joint probability of each of these
>> neutral mutations being fixed each generation?
>After all the braying about mathematics, is it really possible that you
>think the multiplication rule applies to this situation?

If I wanted to be a mathematically incompetent evolutionist I would
say no but if you want to practice hard mathematical science you have
to give the correct answer which is yes.
>Suppose we have two lotteries, each with a probability of winning of one
>in a billion. Further suppose that by some incredible coincidence, only
>ticket is sold for each game, both to a man named Buonafortuna. What are
>his chances of winning both lotteries? One in 10^18, right?
>Multiplication rule.
>Now is that the same math that would be required to predict the
>possibility of *any* two people winning those two lotteries in a more
>typical week, in which many millions of tickets are sold?

If you want to make the claim that millions of different populations
have a small probability of fixing a neutral mutation in a couple of
different populations, I’d say fine, you have a small probability of
that happening. But if you want to claim that millions of neutral
mutations are fixed in a single population, I’d say that is
mathematical irrationality. How do all these neutral mutations show up
in totally unrelated family lines?

>>>> This is the kind of irrational crap that evolutionists
>>>> have to dredge up to try to explain why mutation and selection didn t

>>>> do it. Evolutionists have bungled the basic science and mathematics of

>>>> mutation and selection and then compensate for it by creating a new
>>>> junk science.

>>> The paragraph above is what people present when they don't have an actual argument. I, for one, would >>>welcome a serious discussion of the salient points of neutral evolution. I might learn something. Calling it >>>"irrational crap" is a cop out.
>> If I didn t present the correct mathematics for the mutation and
>> selection phenomenon and the empirical evidence which substantiates
>> this mathematics, I would agree it is a cop out. But when John claims
>> that rare events happening hundreds of times every generation,

>> generation after generation for hundreds of thousands of generations

>What's wrong with that exactly? Think carefully. How many "attempts"
>will have been made in the same period of time?

Greg, what is wrong with that is that you and the other evolutionists
are claiming that a single population is now your sample space and in
that sample space you are now having millions of low probability
events occurring, many simultaneously. Your own model for neutral
evolution of a single gene with two neutral alleles shows how low the
probabilities are. But somehow in the mathematically irrational
evolutionist mind, the multiplication rule of probabilities does not
apply to this situation.

>> I call this mathematically irrational evolutionist crap. You see how
>> John is now trying to squirm out of his mathematically irrational
>> claim by now claiming there were pre-split neutral alleles that were
>> being fixed before humans and chimpanzees actually split. John better
>> start thinking about pre^1000. You might find this type of
>> evolutionist confabulation convincing but try doing the math.
>You seem to be suggesting that the math involves raising the probability
>that any particular mutation will become fixed to the 20 millionth
>power. I find that astounding.

That’s what happens when you are requiring millions of random events
to occur in a single population. Each random event has their own
associated probability and the joint probability of all these events
occurring is the product of the individual probabilities. That is
millions of numbers with values much, much less than one is being
multiplied together. That is the mathematical requirement you are
asking for when you claim that 20,000,000 neutral mutations are being
fixed in a single population. Somehow these random events have to
occur in totally unrelated family lines. Selection demonstrates
exactly how this occurs by common descent but now you are claiming
that this process doesn’t require selection and it occurs in parallel.
How do these millions of neutral mutations show up in the entire
population, especially in totally unrelated family lines?

>>>>> In the first place, I don't know how you could judge your opponents
>>>>> stupid enough to believe a mutation could spread through a population
>>>>> in one generation. But by now it has been clarified for you any number
>>>>> of times. Still you continue, with attempted sarcasm thrown in for
>>>>> good measure. I'll advise you again; when you understand someone to
>>>>> assert something preposterous, consider that perhaps you have
>>>>> misunderstood them. Ask for clarification.
>>>>> I'm hardly knowledgeable enough to explain this concept to you, but
>>>>> I'll try, again. No one claims that Harshman has traveled the world
>>>>> tirelessly spreading his precious personal mutations. The claim is
>>>>> that of the countless mutations that have occurred in the human
>>>>> lineage over the last several million years, a small fraction have
>>>>> become fixed through neutral evolution. Those alleles that became
>>>>> fixed in the latest generation likely arose millions of years ago and
>>>>> were nearly fixed (i.e. were possessed by nearly every person on
>>>>> earth) in the previous generation. Thus the last step in the
>>>>> "fixation" process involved a small group; those born of a parent who
>>>>> was among the small number who remained with a variant allele.
>>>> Greg, in case you haven t noticed, selection takes hundreds of
>>>> generations to fix a single beneficial mutation in a population
>>> To clarify what I have (already) noticed, selection takes many generations to fix "each" beneficial >>>mutation, but many may be in progress simultaneously, in cases in which the selection is not severe.
>> Post a single empirical example of your claim. They don t exist. This
>> is the stuff of evolutionist pseudo-science, present a conceptual
>> concept but don t present any evidence that it happens. On the other
>> hand, I ve presented dozens of empirical examples which show that it
>> doesn t happen and evolutionists try to squirm out of this by saying
>> these are cases of unnatural selection as if they understood what
>> selection is.
>>>> and
>>>> now you want to buy this garbage that drift fixes millions of neutral
>>>> mutations much more rapidly? This is evolutionist mathematical
>>>> irrationality on full display.
>>> Again, what I "notice" is no actual argument from you, with a generous helping of "still not getting it" >>>thrown in for good measure. No one says Neutral Evolution works more rapidly. No one. Several people >>>have in fact said the exact opposite. But as it does not involve selection, especially not "intense" selection, it >>>can operate on many many changes in parallel. That each one requires a vast stretch of time is thus no >>>impediment.
>> How true, no actual argument from me, except the correct probability
>> function which describes the probability of one and two mutations
>> occurring and empirical evidence which substantiates this mathematics.
>> And you are wrong, John Harshman has claimed that neutral evolution
>> will fix a couple hundred neutral mutations per generation when
>> mutation and selection takes hundreds of generations to fix a single
>> beneficial mutation.
>You really have no feel for numbers at all, do you? Selection is quicker
>for each "attempt", but neutral evolution fixes more changes ...

Is that what the evolutionist indoctrinators are telling you?
Evolutionists can’t explain to you how mutation and selection works
correctly. Why would you think that the can explain how mutation
without selection works? What do you think would happen if you had 3
neutral alleles for a gene instead of the model for two neutral
alleles? Do you think that one of the three alleles will be fixed more
quickly than in the model for two neutral alleles?

hersheyh Aug 30, 9:11 pm
Newsgroups: talk.origins
From: hersheyh <hershe...@yahoo.com>
Date: Tue, 30 Aug 2011 21:11:40 -0700 (PDT)
Local: Tues, Aug 30 2011 9:11 pm

Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

>> On Aug 2, 4:56 pm, "Frank F. Smith" <f....@cornell.edu> wrote:
>> > On 7/19/2011 11:15 AM, Alan Kleinman MD PhD wrote:
>
>> > > On Jun 8, 5:44 pm, "Frank F. Smith"<f....@cornell.edu> wrote:
>> > >> On 6/8/2011 11:33 AM, Alan Kleinman MD PhD wrote:
>> > >>> On May 26, 4:54 pm, "Frank F. Smith"<f....@cornell.edu> wrote:
>> > >>>>>> In the futile hope that it might sink in:
>> > >>>>>> (1) The number of possible point mutations at a specific site is not 4.
>> > >>>>>> So 4 is the wrong number.
>> > >>>>>> (2) The possible point mutations are not equally likely. So division by
>> > >>>>>> the number of possible point mutations is not justified.
>> > >>>>>> (3) Mutation rates are determined empirically. If one is interested in
>> > >>>>>> the rate of occurrence of a _particular specified mutation_, one would
>> > >>>>>> determine the rate _of that mutation_.
>> > >>>>>> (4) 10^-8 has been used in much of the discussions because it is
>> > >>>>>> convenient and within a reasonable range for actual mutation rates. For
>> > >>>>>> a particular mutation, the actual value might be 2.5E-9, or
>> > >>>>>> 3.46078293E-8. For these hypothetical cases, the choice of mutation rate
>> > >>>>>> and population size is arbitrary. As long as they are within a
>> > >>>>>> reasonable range of actual values, they serve to give answers within a
>> > >>>>>> reasonable range. So why _not_ pick numbers that are easy to work with?
>> > >>>> <snip non-response>
>> > >>>>> The factor of 4 in the denominator has
>> > >>>>> little impact in the overall scheme of things but demonstrates the
>> > >>>>> similarity of the mutation and selection process with the
>> > >>>>> probabilities of dice rolling.
>
>No. Fr example, the rolling of a "6" in a die is a detectable 'event' in the language of probability.

What bizarre non-sense you are coming up with. So you are now saying
unless you hear the tree fall, trees never fall in the forest. Some
mutations (beneficial and detrimental) are easily measurable by a
change in phenotype; others (neutral) require genetic sequencing to
detect.

>The rolling of any other number is a 'not-event'.

And there are 5 possible “not-events” for a single trial of the roll
of the die. So if you are looking for a particular event its
probability for a single roll is going to be one out of six and the
probability of the “not-event” is going to be five out of six. If you
are going to try to analyze the probabilities for a single trial for a
mutation then the probability for the event will be one out of four
and the probability for the “not-event” will be three out of four.
This should be your first clue that the Poisson distribution is not a
good approximation for this computation. Hersheyh, why isn’t the
Poisson distribution a good approximation for the binomial
distribution based on the above mathematical facts?

>The number of sides that represent the event divided by the total number of sides is the *probability* of the >'event'. Assuming that each trial has an equal probability of rolling the 'event' (a conditions which is >sometimes violated in biological analysis), the *probability* of an event can be determined by rolling a die a >number of times and seeing often it comes up with a '6-face'. Each roll of the die represents a 'trial' in the >language of probability. And the probability of a '6-face' is the number of times one sees a '6-face' in n trials >divided by n trials. That is how we get the *probabiilty* empirically. In the case of a 6-sided die, assuming >honest die, we can *also* simply count the number of sides and see how many of them have a 6. That is, one >can, by making certain assumptions, come up with a theoretical reason for the 1 in 6 probability. However, >with mutation, there is no way to calculate a mutation probability *theoretically*. It can only be calculated >*empirically* by div

iding the number of 'mutants' seen by the number of independent times one looks for >them.

And that’s correct that the number of trials for rolling a dice is
going to be equal to the number of dice times the number of rolls of
the dice. And the number of times that a particular number on a die
will appear such as the 6 in your example will be the number of trials
times 1/6 and as you do more and more empirical trials, that value
will get closer and closer to 1/6 of the number of trials and the
number of times the “not-event” occurs will be 5/6 of the trials.

Where the dice rolling metaphor diverges from the mutation and
selection phenomenon is that a particular die is not rolled every
replication. It is only rolled occasionally given by the mutation
rate. So if you have a mutation rate of 10^-8, very few members of the
population are going to perform a trial in a given generation even if
the population size is 10^9. If your probability of the particular
beneficial event is 1/4 and the probability of the “not-beneficial
event” is 3/4 then you don’t need very many trials for the probability
is reasonable for the particular beneficial event to occur. But the
mutation rate doesn’t allow for many trials, even when the population
size is huge. This should be your second clue why the Poisson
distribution is not a good approximation for the mutation and
selection phenomenon. Hersheyh, why is this the case?

>In mutation, the 'event' is a mutation, a *detectable* change in a genetic state. A mutation is typically >*detectable* by virtue of having a phenotype different from the original genetic state.

You are wrong here hersheyh when you claim that a mutation has to be
“detectable” by a phenotypic change. A neutral mutation is not
detectable by a phenotypic change and you have claimed that most
mutations are neutral (which is one of many unsubstantiated claims
which you have made). So if you are going to claim that most mutations
are neutral and you are going to define a mutation as a change which
is detectable by a phenotypic change then you will grossly under-
measure the mutation rate.

>For example, if the original genetic state was "antibiotic-sensitive" and the *detectable* change in that state >was "antibiotic-resistant", the probability of mutation, comparing it to a die, would be *empirically* >determined by dividing the number of *detectable* mutants seen by the number of independent trials >examined. And trials represents the total population size examined (again assuming that the probability of >mutation per trial is the same for all trials (which, as discussed with Luria-Delbruck, is not always the case, but >we can ignore that for the present, since we are instead discussing why one would take the mutation rate (the >number of 'events' divided by the number of 'trials') and then divide it *again* by 4.

The mutation rate gives the frequency at which a trial is performed in
a given member, in a given generation at a particular locus. When a
trial (mutation) does occur then the probability of a particular event
is 1/4 because there are 4 possible outcomes (events) for a mutation.
That is why you divide the mutation rate by 4.

>If you wish to look at the point mutation rate at a particular nt site, you *must* be able to detect mutation, a >change in genetic state.

Are you sure you want to make this claim? Because if you are, you are
claiming that mutation and selection did not start occurring until
humans were able to detect mutations.

>Mutation rates can only be determined empirically.

This may be true but it doesn’t mean that you can’t study the behavior
of mutation and selection without first accurately measuring mutation
rates. If you develop good mathematical models which are reasonable
representations of the physical phenomenon then you can study the
effects of different mutation rates on the behavior of the
mathematical model. I’m pretty sure you have never done this because
of your claims of how mutation and selection works. On the other hand,
I have done this with a peer reviewed and published mathematical model
of mutation and selection. And it shows that the mutation rate is a
minor variable in the mutation and selection phenomenon.

>You cannot do that if you don't know and can't tell what the original genetic state was at that nt site. The >general rate of point mutation at a particular nt site is the rate of conversion from the w.t nt to *any* other nt. > This must be determined empirically by examining that site in each trial for which nt is present. This rate is >different than the rate of change from the w.t. nt to a *specific* other nt. In that case, changes to any other nt >other than the specified one are simply ignored as irrelevant since the 'event' has been described as, say C to T. > And, as has been pointed out to you, the rate of transition (Pu to Pu or Py to Py) is typically much higher than >the rate of transversion (Pu to Py or Py to Pu). And there is likely to be a different rate even in the two >possible transversion possibilities. Thus the mutation rate of an original C to T will be different than the >mutation rate of C to G which will also differ from C to A. The sum of those three will be the mutation rate o

f >C to any other n.t., the general rate of point mutation at that site when C is the w.t. allele.

So what values do you want to use instead of 1/4 for the probability
of a particular base change? Do you really think this will have a
significant effect on the mathematics of mutation and selection? You
are still so far down on the learning curve for the basic science and
mathematics of mutation and selection; you don’t realize that the
multiplication rule of probabilities is the dominant mathematical
factor governing the behavior of the phenomenon. At least you are
starting to get some understanding of why the factor of 4 appears in
the denominator of the mutation rate in the correct probability
function describing the mutation and selection phenomenon.

>You seem to be assuming that you can actually measure the rate of mutation on some theoretical grounds and >be able to do so without having any knowledge about what the original nt was nor what the mutant changes >were. You simply cannot do that. Whatever mutation rate you are measuring, you have to know and be able >to identify both the original genetic state and the changed state.

I’m not making that assumption at all. What I am saying to you is that
you don’t need to have accurate empirical measurements of the mutation
rate to study the effects of different mutation rates on the mutation
and selection phenomenon. To study the effects of mutation rate on the
mutation and selection phenomenon you first need to correctly model
the phenomenon mathematically. You have not done this with your use of
the Poisson equation. I have derived the correct probability function
for you and it includes a factor of 4 in the denominator of the
mutation rate. If you want to examine a brute force mathematical model
of mutation and selection, study Schneider’s ev model of mutation and
selection. It demonstrates all the behavior that is described by the
probability function I derived for you. Then you can look at the
empirical data and you will see it demonstrates behavior analogous to
the mathematical models.

>If you wish to determine the rate of mutation to a "beneficial state", you must be able to distinguish such a >state from the "not-beneficial state". That means you cannot determine the rate of mutation to a "benficial" >state unless you define what differentiates it from a state of not-beneficial.

That’s not so and I think you need to reconsider your argument. The
probability function I derived for you is applicable to beneficial,
neutral or detrimental mutations. The nature of the mutation will be
manifested by the change in subpopulation size from that progenitor
with that first mutation. If the mutation is beneficial, the
subpopulation size will increase over generations, if neutral the
subpopulation size will remain constant over generations and if
detrimental the subpopulation size will decrease over generations.

>Again, mutation was defined well before one knew that DNA was the genetic material. And mutation rates are >determined by being able to identify a mutation 'event' as different from the original state in each trial.

That was the only way to identify when a mutation occurred until DNA
could be sequenced but now there is a precise way to determine when a
mutation has occurred and your definition is mathematically and
scientifically inaccurate and outdated. And this precise way of
determining whether a mutation has occurred or not is used in the
treatment of HIV to identify drug resistant strains.

>So, the real comparison between die and mutation if the *empirically* determined rate of mutation from w.t. C >nt at position 1432 in a specific gene (again assuming you are willing to sequence all the trials) to any other nt >(all not-C), would be the ratio of the number of mutational events (in this case, any and all the not-C sightings >at that nt are an *event*) divided by the number of trials. Let's say that that empirically determined ratio is >10^-8. That would mean that in every 10^8 rolls of the die, we would expect to see one non-C at that position. > Thus the die would, in direct comparison to the 6-sided die, have 10^8 sides with one of the sides labelled >"not-C" and all the other sides labelled "C".

Hersheyh, you still do not understand the mathematics of the mutation
and selection phenomenon. You only need a very small number of rolls
of the die to get your particular mutation. The probability for any
particular roll (mutation) is 1/4. And the mutation rate only gives
the frequency when the four sided die will be rolled. The vast
majority of the time when a population replicates, they don’t roll the
die at a particular locus. That’s why you need such huge populations
so that you will know that you will have sufficient members who will
roll the die at that locus and that number of members who roll the die
is nowhere near 10^8. If one member rolls the die you will have a 1 in
4 probability that you will get your beneficial mutation. Do you want
to try and compute the probabilities of getting your beneficial
mutation if two members roll the die? How about if 3 members roll the
die at that locus?

>But, of course, we are not actually looking at nt sequences to identify our mutation. Nor are we looking at >"beneficial" to identify our mutants. We are looking at the phenotype "resistance-to-A" or or and "resistance >to B" to identify our mutants (events) in the number of trials (total population examined for those traits).

You are not looking at the nt sequences because you teach genetics out
of the 1930’s understanding. I’m trying to get you into the 21st
century understanding of genetics including the mathematics but you
are very slow to learn.

>Division of the actual observed rate of change from the non-mutant to mutant state *is* the mutation rate. It >makes no sense to divide the mutation rate by 4. Period.

It would make sense if you understood that there can be mutations
occurring at the locus which have no phenotypic affect but for your
own evolutionist motivations you won’t accept this physical reality.
Exclamation point.

>> > >>>> Except the "die" doesn't have four sides, and it is known to be loaded.
>> > >>>> But that's been explained numerous times already, so I doubt you'll
>> > >>>> learn anything this time, either.
>> > >>> When we are talking about point mutations which are by far the most
>> > >>> common and important form of mutation, the die has only four sides.
>> > >>> But don t stop there Frank, tell us how the die has more than four
>> > >>> sides and how it is loaded. Then tell us what the correct probability
>> > >>> function is.
>> > >> I have never written anything suggesting that "the die" has more than
>> > >> four sides.
>Which means that you seem to be suggesting that you are *making* a gene by random assembly by tossing a >four-sided die (equivalent to assuming that all four nts are present in equal amounts). That certainly is a >common creationist idea, but it has nothing to do with *mutation*. Mutation is not the process of assembling >a gene by complete random chance and has nothing to do with that particular stupid creationist idea.

Don’t get my correct application of mathematical principles confused
with your mathematically irrational speculations and extrapolations of
how neutral evolution works. You are the one who claims that millions
of neutral mutations are amplified and fixed in 500,000 generations
without selection. You are the one who defends Schneider’s claim that
the multiplication rule does not apply to biological evolution. And
that is the fundamental blunder of evolutionism which is the denial
that the multiplication rule for the probability of joint events
occurring does not apply to biological evolution. You can see where
this evolutionist blunder has led us to, multidrug resistant microbes,

multiherbicide resistant weeds, multipesticide resistant insects and

less than durable cancer treatments. But every cloud has a silver
lining; your evolutionist blunder has given me a lucrative medical
practice treating MRSA.

>> Each of these stochastic processes has their own particular features.
>> It just so happens that dice rolling has features in common with the
>> mutation and selection process. Now it so happens that random
>> recombination has features in common with card drawing.
>Actually more in common with card shuffling.

Really hersheyh? Are you ready to present us with the mathematics of
how random recombination works. You still haven’t learned how mutation
and selection works. You are using the wrong probability function (the
Poisson distribution) which you have never gone through the derivation
of despite the fact that you’ve been teaching this for 20 years and
you still haven’t figured out that mutations can occur which don’t
give a phenotypic change. I pity the poor students who were confused
by your poorly considered and poorly prepared lectures.

>> > As for the binomial distribution -- you have assiduously avoided
>> > presenting anything other than one term (the probability of 0 successes
>> > in n trials), so it is difficult to judge. Nothing you have presented
>> > for probabilities of mutations is inconsistent with a binomial
>> > distribution, and a binomial distribution is certainly applicable (at
>> > least over a short time period, and I think the actual distribution is
>> > likely to be indistinguishable over longer periods). But I will accept
>> > that you do not recognize whether or not you are applying a binomial
>> > distribution.
>> I am not using a binomial distribution because the derivation of that
>> probability function does not consider the order of events.
>Then why, except for the stupid division by 4, is your equation exactly that derived from binomial probability? > Really. Remove the 4 from your "equation" and it is simply binomial probability. And that *includes* the >cases where you look at simultaneous selection for two mutants.

It is not exactly the same as the binomial distribution because you
have failed to do the same thing you failed to do with the Poisson
distribution, you have failed to go through the derivation of the
equations. In the derivation of the binomial distribution, the order
of events was assumed to not matter so a combinatorial term is
included in the derivation. The correct derivation of the probability
function does not include the combinatorial term because the order of
events does matter in the mutation and selection phenomenon. And
anyone with an ounce of common sense would understand that your
definition of a mutation based on a phenotypic change will ignore all
mutations which do not cause a phenotypic change. You are sloppy in
your mathematics and sloppy in your science. What a pity of your
students.

hersheyh Sep 7, 12:54 pm
Newsgroups: talk.origins
From: hersheyh <hershe...@yahoo.com>
Date: Wed, 7 Sep 2011 12:54:51 -0700 (PDT)
Local: Wed, Sep 7 2011 12:54 pm

Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

>> Sexual recombination is not an error in replication but a shuffling of

>> existing alleles. New genetic information in the gene pool is not
>> created by recombination as can be done by mutation and selection

>> unless there happens to be an error in the recombination process.

>New combinations of alleles from different genes, however, can produce new phenotypes from those existing >alleles that otherwise would have to be produced by serial mutation in a clonal organism. Evolution by natural >selection, of course, actually works at the level of phenotype, which is all that the natural environment can >differentially affect. It matters not to nature whether the deer has no limbs due to a genetic condition, an >accident, a birth defect, or drugs during development. For natural selection to have an *evolutionary* effect, >however, the phenotype must have a heritable component. Note that I did not say that it must be determined >by a gene. Only that genes have an effect.

You still haven’t presented us with the probability function that
would describe random recombination. But that’s not surprise; you
still don’t understand the probability function for mutation and
selection despite the fact that I’ve presented to you a step by step
derivation of the equation. So is your new claim that a bird is
nothing more than a changed phenotypic expression of a reptile? Let’s
see your breeding program where you get a bird from a crocodile. You
already have a running start, the crocodile has a gizzard.

>> Directional selection pressures require the creation of new alleles.

>No they don't. Directional selection pressure will change the frequency of existing alleles. The selection >process doesn't give a fig if the allele was already present well before the environmental change in selection >pressures or is a new one that just popped up this generation. Selection pressure can only affect alleles that >actually exist.

So are you now claiming that multidrug resistant microbes,
multiherbicide resistant weeds and multipesticide resistant insects
pre-existed the use of antibiotics, herbicides and pesticides? Are you
claiming that all 4^G possible variants are in a population? I pity
the poor students who have to take your genetics class.

>Of course, what you are *trying* to claim here is that *all* evolution must proceed serially, one gene and one >change at a time. That is false. Certainly so for sexually reproducing organisms. For organisms with less >regularized gene exchange, the process is more often serial since even when selective conditions allow both >traits to increase, new mutation is typically required to introduce the other trait in the same organism.

We are all impress with all zero of your empirical examples where you
demonstrate how mutation and selection occurs in parallel. And then
you deny all the empirical and mathematical evidence that mutation and
selection does not occur in parallel which proves that you are an
evolutionist crank and pseudo-scientist. And we are still waiting for
you to derive the probability function for random recombination.
That’s going to be a long wait.

>> How do populations do this and under what circumstances and how
>> quickly does this creation of information occur? If the creation of
>> information by mutation and selection is not quick enough, the theory
>> of evolution is a mathematically irrational belief system and the
>> creation of information by mutation and selection is not quick enough

>The point mutation rate, interestingly enough, is rather similar in both bacteria and eukaryotes, but can vary, >with some bacteria being particularly resistant to the mutagenic effects of ionizing radiation.

Did you ever think this is the case because the DNA replicase system
has error checking proteins? Hersheyh, do you care to tell us what the
purpose of helicase and gyrase were before DNA could be replicated? We
always like to hear a good fairytale.
>http://www.ncbi.nlm.nih.gov/pubmed/16677295
>http://www.biochem.wisc.edu/faculty/cox/lab/publications/pdfs/119.pdf
>This is thought to be a consequence of a minimax solution to the problems that arise from either too high a >mutation rate or too low a mutation rate (which typically requires much energy in repair systems and slower >growth). This can be evidenced by the fact that increased resistance can evolve in even sensitive bacteria (E. >coli). This occurs (given that E. coli grows as a clone) by a stepwise process. Read the second paper and you >will see that, despite your claim that multiple mutations should be impossible, that reality tells us yet again that >selection can produce organisms that differ at multiple sites in much less time than a human life-time.

Hersheyh, I know it is your bad habit to not go through the
derivations of the equations you are using. When you don’t do that, it
is even less likely that you will study the behavior of the equations
you use. You have no idea how mutation rate affects the behavior of
these equations because you have never done the study. That’s never
stopped you from making mathematically irrational claims.

>> > >> > And do you believe that inbreeding doesn�t cause the loss of
>> > >> > alleles in a population?
>> > >> It certainly can. How is that relevant to your previous claim? What does
>> > >> inbreeding have to do with recombination?
>> > > Selection always causes the loss of alleles in a population whether it
>> > > is mutation and selection or recombination and selection. Selection
>> > > always causes the loss of genetic information from the population. The
>> > > only way you can increase the diversity of populations is through
>> > > mutations.
>> > Not true. Selection causes a change in frequency of alleles. It may not
>> > cause a loss of alleles. Balancing selection, for example, maintains
>> > alleles in a population, i.e. it prevents loss of alleles.
>> Of course it’s true. If selection pressures are intense enough it
>> drives the population to extinction and all the alleles of that
>> population are history. If white moths are much more susceptible to
>> predation, members with that coloration will be selected out until
>> that variant becomes extinct. New white moths will only appear because
>> of mutation.

>You are missing the point. Look up "balancing selection" for sickle cell allele to see how selection (especially >in diploid organisms) can lead to maintenance of allele frequencies. An even more dramatic form of balancing >selection is "negative frequency dependent selection" for traits like self-sterility alleles in plants or alleles at >histocompatability loci.

If you think that balance selection or negative frequency dependent
selection makes your theory of evolution mathematically rational,
forget it. That’s the point of this discussion and you have missed
this point by a country mile. You stick with indoctrinating your poor
students with the notion that a mutation only occurs when there is a
phenotypic change and you will successfully train these poor students
to be mathematically incompetent nitwits. And do you think that self-
sterility alleles increase the diversity of the population?

>> > But anyway, how is this relevant either to showing how your previous
>> > statement is relevant or to the question at hand?
>> Selection always causes the reduction in diversity of a population.

>Again. Look up negative frequency-dependent selection.

Give us an empirical example of your claim and show us how the
diversity of the population is greater after the selection pressure
has been applied. But you never give us empirical examples; you only
give us your hypothetical examples.

>> Selection does this because it always kills or impairs reproduction of
>> some or all member of a population. Selection pressures are not your
>> friendly transform reptiles into birds force; selection pressures are
>> killing or impairing the weaker members of a population from
>> reproducing.

>Selection is differential (relative) reproductive success of different phenotypes (and their causal genotypes). > Period.

That’s right, and the members which don’t have sufficient fitness to
reproduce in the face of the selection pressures do not pass their
genes on to the next generation reducing the diversity of the
population. Exclamation Point.
>[snip]
>> > > When selection targets two or more genes, you don’t get individually
>> > > advantageous mutations, that’s why they can’t be amplified
>> > > simultaneously.
>> > But that isn't true. You have been given many conceptual examples of
>> > multiple mutations, each individually advantageous. Consider, for
>> > example, a quantitative case in which two genes influence height. Each
>> > has a tall and a short allele. You could then have genotypes (haploid
>> > for this example) of TT, ss, Ts, or sT. And say the effects on height
>> > are additive, so TT > Ts or sT > ss. Further suppose that tall
>> > phenotypes are advantageous, so that TT is better than Ts or sT, either
>> > of which is better than ss. Do you deny that the two tall alleles will
>> > both be amplified under those conditions? If so, show your work.
>> The key phrase in your paragraph is “conceptual examples”. You don’t
>> have empirical examples of your claims because they don’t exist.

>Essentially every example of artificial selection for a quantitative trait involves parallel selection akin to that >described above. The only difference between such artificial selection and natural selection is the rate of >change. And need I point out that most evolution involves such quantitative traits.

You conflate artificial selection (breeding) and mutation and
selection. If recombination could do what you claim when directional
selection pressures are acting then HIV would be more easily able to
evolve resistance to selection pressures targeting two genes. This is
why your conceptual examples do not carry the weight of evidence as do
real measurable and repeatable empirical examples of mutation and
selection (except with mathematically irrational indoctrinated
evolutionists).

>> It
>> seems in your mind you’ve convinced yourself with your hypothetical
>> examples that the theory of evolution is true. What you have left out
>> of the scientific method is producing the empirical evidence of your
>> hypothetical examples.

>> On the other hand, I’ve derived the correct probability function for
>> two beneficial mutations to occur and correlated that with the
>> empirical evidence.

>With the exception of your perpetually stupid division of the mutation rate by 4, you have 'derived' the >binomial probability for the presence of one or more of a particular event (in your case, the 'event' is the >simultaneous existence in the same individual of two rare independent mutational events) in a given number of >'trials'. Big whoopee doo. Anyone with a cursor can find the equation for that by looking up "binomial >probability distribution". Been done well before you were born. Identical in principal (again, except for the >stupid division by 4) to the probability of your rolling two dice (one red; one blue) and having snake-eyes. > The trial is each roll of the two dice. The event is snake-eyes.

Once again you demonstrate your mathematical incompetence by failing
to understand that neutral mutations do not cause phenotypic changes.
How did you manage to become a teacher of genetics with this bungled
understanding of the mutation and selection phenomenon? Oh yes, you
were trained by evolutionists who also did not understand the basic
science and mathematics of mutation and selection. That also explain
why we have multidrug resistant microbes, multiherbicide resistant

weeds, multipesticide resistant insects and less than durable cancer

treatments thanks to mathematically incompetent evolutionists. Have
you gone through the derivation of the Poisson distribution yet? Or
are you going to continue to bungle this mathematics?

>> I’ve demonstrated both mathematically and

>> empirically how crucial amplification of beneficial mutations are for
>> the mutation and selection process to work. Once hersheyh demonstrates

>> his inability to derive the correct probability function for the
>> random recombination of two alleles,

>In general, it is genes that recombine. Intragenic recombination between two alleles is quite rare. Please learn >to use the right words rather than make up your own language.

It doesn’t matter how I phrase it, you can’t do the derivation of the
probability function for random recombination. You couldn’t derive the
correct probability function which describes the mutation and
selection phenomenon and instead use the wrong probability function
and you don’t have the mathematical training or skills to derive the
correct probability function for random recombination. So what exactly
do you indoctrinate your pitiful genetics student with, reptiles turn
into birds, reptiles turn into birds?

hersheyh Sep 7, 1:25 pm
Newsgroups: talk.origins
From: hersheyh <hershe...@yahoo.com>
Date: Wed, 7 Sep 2011 13:25:22 -0700 (PDT)
Local: Wed, Sep 7 2011 1:25 pm

Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

> [snip]

>> > This is your indomitable ignorance on display for anyone to see.
>> John, do you still believe that the probability of a beneficial
>> mutation occurring is proportional to population size?

>Like John, I know that the probability of a mutational event is not related to population size.

Neither John nor you understood this until I showed you mathematically
that you were both wrong. Do you want me to post your quotes? And
neither you nor John understands probability theory or even basic
algebra. You think I am trying to trick you when I use the algebraic
identity (a^x)^y = a^(x*y). And you still don’t understand how
mutation rate relates to the number of trials performed. You think
every replication of a member of the population represents a trial for
the particular mutation but it doesn’t

>It can be affected by the presence or absence of mutagens, however. But the probability of there being one or >more mutations in a specific population is a function of the population size.

One of the many problems you have with this calculation is that when a
trial (mutation) occurs at a particular locus, you don’t understand
that you don’t necessarily get the beneficial mutation. Your mistake
leads to a mathematically and empirically incorrect value for the
mutation rate.

>It is the latter probability that we (including you) are interested in. We are arbitrarily (but using a reasonable >value) assuming that the mutation rate (probabiilty per trial of our mutational event) is 10^-8. We actually >would have to empirically determine that value for the specific example, but, for simplicity, are just using a >reasonable value for point mutation (that is, the rate of change from the original nt to any other nt). You seem >to have no problems with that value. If you do, please say so.

The reason I don’t argue with you about the 10^-8 mutation rate you
like to use is not whether it was appropriately measured or not, it’s
whether that value has a significant effect on the mutation and
selection phenomenon. The mutation rate is not the dominant variable
in the mutation and selection phenomenon but you would not know that
since you never study the equations you use. You simply plug the
numbers into the wrong probability distribution and imagine how bright
you are.

>Similarly, we are also assuming that the size of the population we are examining for the mutational event (or >the simultaneous events) is 10^9 because that value is reasonable. You seem to sometimes have problems >with that value and sometimes don't. Explain why.

Your usage of the value of 10^9 arbitrarily for the population size is
not generally correct. When you use this population size, you are
implicitly assuming that this entire population would benefit from a
particular mutation. Only those variants on a particular trajectory of
the fitness landscape will benefit from the particular mutation. You
failed to see the point of the Weinreich studies where there were
several different variants, each with their own set of beneficial
mutations. You don’t use the entire population size to compute the
probabilities that the next beneficial mutation will occur on any one
of the members of the entire population because the next beneficial
mutation depends on which subpopulation the mutation must occur on.

>When we use those values, we are trying to determine the probability of finding one or more such mutant(s) in >a population of a given size. That is the probability we are interested in.

Not every member of the population is playing the same lottery. Each
subpopulation has their own particular lottery it must win and the
probabilities must be computed with the correct subpopulation size.
You won’t get the correct probabilities by arbitrarily using a
population size of 10^9 and you won’t get the correct basic science
and mathematics of the mutation and selection phenomenon by
arbitrarily using a particular population size.


Greg Guarino Sep 7, 2:44 pm

Newsgroups: talk.origins
From: Greg Guarino <gdguar...@gmail.com>

Date: Wed, 07 Sep 2011 17:44:16 -0400
Local: Wed, Sep 7 2011 2:44 pm

Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

>>>>> On Jul 6, 2:01 pm, hersheyh<hers...@yahoo.com> wrote:
>>>>> Going on, the probability of not-6s in two flips is 5/6*5/6 =
>>>>> 25/36. Thus the probability distribution of *at least one 6* in two
>>>>> flips (trials) is 1-(25/36) = 11/36, which is not equal to 1/6. For
>>>>> 1200 tosses of the die, the probability of all not-6s is (5/6)^1200.
>>>>> Thus the probability of at least one 6 is 1-(5/6)^1200. I haven't
>>>>> bothered to calculate that, but it is undoubtedly very close to 1.
>>>> Considering I presented this mathematics hundreds of posts ago, you
>>>> are doing a nice job repeating it here.
>>> Your continued assertion that the disagreement is about this (simple) mathematics is astounding. Everyone >understands it.
>> When you mean everyone, you mean all the evolutionists who couldn’t
>> derive the correct probability function for a particular mutation
>> occurring at a particular locus. I wouldn’t expect the mathematically
>> incompetent to make sense out of a mathematical equation.
>>>> Perhaps this is a good time
>>>> for me to go over the fact that dice rolling is a very good metaphor
>>>> for the mutation and selection process.
>>> Only if the die has a few billion faces, almost all of which have the original allele on them. (the rest >>>wouldn't be equally distributed either, would they?)
>> Greg, the die has only four faces for a point mutation, A, C, G and T.
>> If you think the die has billions of faces why don’t you tell us what
>> a few of them are?
>Nearly all would be the original base, wouldn't they? The rest (a
>handful) would be labeled with the other bases, in numerical proportion
>to their empirically-determined probability. Surely you don't imagine
>that a four-sided die, with a 25% chance of landing on any letter, is a
>good model.

Once again Greg, you are demonstrating that you don’t understand this
probability problem. The mutation is the trial. Since the mutation
rate is a low frequency value, most bases in the genome do not undergo
the trial. When a subpopulation is doing the search for the beneficial
mutation, the mutation must occur at a specific locus and the
particular mutation must be for the base that would improve fitness,
not just any base of the four bases. And yes, the four-side die for
each locus in the genome is the correct model for the point mutation
and selection model of the mutation and selection phenomenon.

>>> <snip>
>>>> The final step you need to learn hersheyh is that the population that
>>>> would benefit from the next beneficial mutation in an evolutionary
>>>> sequence is not the entire population but only a fraction of that
>>>> population, the subpopulation with the previous beneficial mutation in
>>>> that sequence.
>>> If we need to learn that, we'll have to do it on our own, because you simply refuse to tell us why this would >>>be so, outside of the limited case of an asexual population in the presence of lethal selection, with only one >>>mutational avenue for survival.
>> Mutations don’t magically fly through space landing anywhere willy
>> nilly. They have to accumulate through common descent. It is possible
>> that a mutation in one member of the population can recombine with a
>> different mutation at a different locus in another member. Do you care
>> to derive the probability function for that event? And when you do
>> write that probability function for recombination, you will see why it
>> doesn’t help HIV evolve resistance to combination therapy.
>>> So for what must be the 100th time, suppose a population of animals migrates to a colder climate. Or the >>>climate simply gets colder where they are. Suppose the climate change is enough to affect the survival >>>chances of some individuals, but does not kill off most of the population. Does that seem an unrealistic >>>scenario to you?
>> It’s a totally realistic scenario.
>>> Suppose further that several different genetic changes can *each* confer some advantage in the changed >>>climate. Does that seem unrealistic?
>> The first thing that will happen is that members of the populations
>> which do not have sufficient fitness to reproduce will fail to pass
>> their genetic information on to the next generation. The members of
>> the population which have sufficient fitness to reproduce will pass on
>> their genetic information to the next generation and their will be
>> mutations in these replicators. Some mutations will be detrimental,
>> some mutations will be neutral and some mutations will be beneficial
>> for the particular environment.
>>> Now tell us why several of those genetic changes could not spread simultaneously. And once they have >>>spread, tell us why they could not be combined in the progeny of individuals who have only one of the >>>beneficial alleles.
>> Mutations must accumulate through lines of common descent. It should
>> be clear to you that when recombination is not involved;
>Surely you understand that in animals (like chimps and humans)
>recombination IS involved.

Greg, do you want to tell us how recombination accelerates the
mutation and selection process because clearly it has no significant
effect when combination selection pressures are used with HIV. The
mathematical answer for this question is obtained by deriving the
correct probability function for random recombination.

>>the only way
>> you can get a sequence of beneficial mutations is for them to all
>> happen simultaneously on a single individual or to accumulate one by
>> one starting on a progenitor and accumulating on descendents over
>> generations.
>You continually belabor the obvious as if there is someone who doesn't
>understand it.

So how is it that you believe that tens of millions of neutral
mutations will spread through a population in 500,000 generations?
Greg, tell us how a neutral mutation is transferred from one totally
unrelated family line to another? It would seem obvious that you would
understand that this can’t happen.

>> With recombination, you add the possibility of lateral
>> transfer of a beneficial mutation but that event has probabilities
>> associated with this occurrence. So let’s say your population of
>> animals starts accumulating beneficial mutations for your cold
>> environment. One member gets a mutation which gives thicker fur.
>> Another member gets a mutation which allows for fat storage, another
>> member gets a mutation that gives beneficial effects on metabolism,
>> another member gets a beneficial mutation which affects size giving a
>> better surface to volume ratio for the environment. There are any
>> number of mutations that are occurring throughout the population.
>Firstly, do you have any doubt that scenarios like this exist?

Certainly scenarios like this exist. But to extrapolate this scenario
to the evolution of birds from reptiles or humans and chimpanzees from
a common progenitor is mathematically irrational because of the huge
genetic differences. Neither mutation and selection nor recombination
can make this transformation in the small number of generations
available. It is mathematically irrational to believe that these
genetic transformations can occur in so few generations. And 500,000
generations is not very many generations for the mutation and
selection process.

>>How
>> do you recombine all these traits into one descendent? Do the math.
>Do the math...WHEN? When each of the "cold weather beneficial" mutations
>is limited to a single individual, or later on, when some of them have
>spread to a greater percentage of the population? If each confers an
>advantage (and some survive the first few generations without "bad
>luck"), eventually the chances are going to be pretty good.

Greg, the chances are only pretty good when only a single gene is
targeted at a time with the a selection pressure. As soon as the
selection conditions target more than a single gene, amplification is
impaired and the chances are no longer pretty good that the mutation
and selection process will work.
>Let's see if I can apply my rather basic probability skills to this.
>Suppose two of our cold alleles have spread to 20% of the population
>(meaning 20% of the alleles at that locus are of the new variant type,
>each individual having two, which may not match), but without any
>doubly-enhanced members yet.
>Assuming random mating (which we can't assume, since our "enhanced"
>members have an advantage), each offspring would have a 4% chance of
>being doubly-enhanced, which is to say, a 96% chance of not getting both
>enhancements.

Why do your “enhanced” members have an advantage?
>So if only one female and one male mate (and have one offspring), there
>is a 96% possibility of failure. But if two pairs mate, then the
>probability of failure becomes 1 - .96^2 = .92, already a bit better.
>Now what if 50 pairs mate at random? I make that out to be a 4% chance
>of failure, meaning, a 96% chance that at least one doubly-enhanced
>offspring will result.
>Hey, these numbers are fun. Let's assume 2 mutations at 5% of the
>population.
>Chance of "success" with one pairing? .0025
>Chance of at least one success with 100 pairings? We're already up to
>22%. We only need 300 pairings (offspring, really) to be at better than
>50-50.
>Most importantly, our "attempts" need not all come in the same
>generation. Our singly-enhanced critters increase in proportion with
>each generation, which means the odds will only improve. And our "thick
>fur and added fat" members will have an even greater advantage. If we
>could imagine a situation in which the weather changed so quickly, and
>so radically, that only a double-mutant could survive, then your math
>could come into play.
>But that seems much more "conceptual" than the scenario we have been
>discussing.
>Someone can now scold me if all of this has been incorrect. I do realize
>some of the ways in which this is oversimplified. It leaves out sexual
>selection, for one, and as I mentioned before, makes no allowance for
>the greater number of offspring that our enhanced members would be
>expected to produce.

You are actually much closer than the genetics teacher with 20 years
of indoctrination experience. Why don’t you try to express your
example algebraically? Why don’t you try to write the probability
function for random recombination and include generations in the
calculation?
Greg Guarino
Frank F. Smith Sep 7, 7:16 pm
Newsgroups: talk.origins
From: "Frank F. Smith" <f...@cornell.edu>
Date: Wed, 07 Sep 2011 22:16:40 -0400
Local: Wed, Sep 7 2011 7:16 pm

Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

>>>>>>> <snip bunches>
>>>>>>> but keeping this bit, it's so precious
>>>>>>>>>>> [Kleinman] nA -- is the fraction of the total population size with mutation A
>>>>>>>>> [Kleinman, clarifying] nA is the number of members in the population which has mutation A.
>>> <snip>
>>>>>>> (1) The first and most critical is the assumption (explicit or implicit)
>>>>>>> that population size is constant over however many generations are
>>>>>>> involved. Using a product over multiple generations rather than
>>>>>>> exponentiating could eliminate that assumption (though perhaps at the
>>>>>>> cost of any pretense at prediction).
>>>>>> Not so Frank, I am not assuming population sizes are constant, the
>>>>>> population size can vary as a function of generation and in fact the
>>>>>> populations will vary with generation.
>>>>> I recall seeing a post from you in which you explicitly made the
>>>>> constant population assumption, but it's not worth my time to hunt that
>>>>> post down. No matter.
>>>> I have done calculations by assuming constant population size but in
>>>> the derivation of the probability function for two beneficial
>>>> mutations occurring, I have not made that assumption. An accurate
>>>> mathematical simulation of the mutation and selection process requires
>>>> the understanding that population and subpopulation sizes are dynamic
>>>> changing every generation. These population and subpopulation size
>>>> changes affect the probabilities of the beneficial mutations occurring
>>>> at the proper locus.
>>>>> This would be a good place for a worked example.
>>>>> Here's a simple case, only 5 generations with populations and only one
>>>>> gene, one mutation.
>>>>> 1E5, 5E5, 1E6, 4E6, 6E6
>>>>> Given p: the probability that the mutation of interest occurs in an
>>>>> individual, g: the number of generations, and n: the population size.
>>>>> Your formula for the probability that the mutation of interest occurs at
>>>>> least one time during those five generations is
>>>>> (1 - ((1-p)^n)^g)
>>>> Recall that (1-p)^n is the probability that the particular mutation
>>>> WILL NOT occur at a particular locus in a population size n in a given
>>>> generation. ((1-p)^n)^g = (1-p)^(n*g) is the probability that the
>>>> particular mutation WILL NOT occur at a particular locus in a
>>>> population size n in g generations. Then the complement rule is used

>>>> to compute the probability that the particular mutation WILL occur at

>>>> a particular locus in population size n in g generations. The

>>>> population size n does not need to remain constant over the
>>>> generations g. Changing the population size in any given generation
>>>> simply changes the number of trials done for the particular mutation
>>>> in that generation.

>>>>> p is (pick whatever value you'd like, I don't care)
>>>>> g is 5
>>>>> What's n?

>>>> n is the population size and this value can change from generation to
>>>> generation. Changing the population size simply changes the number of
>>>> trials for your beneficial mutation.
>>>>> I know _my_ answer. (It's actually implied by my prior post.) I'd rather
>>>>> not guess yours. Can you, for a change, give a simple and direct answer
>>>>> to a simple and direct question?
>>>> n is the population size which can vary as a function of time
>>>> (generations).
>>> That's a non-answer. Let's try again.
>> n is the number of members in the population in a given generation. If
>> you like, in generation 1, the population size is n1, in generation 2,
>> population size is n2 and so on. When you are talking about
>> amplification of a beneficial mutation, this notion is important to
>> improve the probability of the next beneficial mutation to occur on a
>> member with the previous beneficial mutation.
>... and you repeat your previous non-answer.

Let me try to be as explicit and complete as possible. The population
size n in the probability function that I derived for you is the
population size that would benefit from a particular trial and the
beneficial mutation that possibly could occur. Not every mutation that
is beneficial for one subpopulation will be necessarily beneficial for
a different subpopulation. It depends on the trajectory that the
particular subpopulation is on. If the subpopulation is able to
reproduce despite the selection pressure it must endure, the trial and
beneficial mutation does not have to occur in any particular
generation. If the subpopulation size is large then it will take fewer
generations for the trial to finally occur which gives the beneficial
mutation. If the subpopulation is small, it will take more generations
of replication before one of the members finally does the trial for
the beneficial mutation.

>I realize it's only been two and a half months since I asked you to
>provide a worked example to support your claim. Some people might wonder
>why it is apparently so hard for you to use your own formula when you
>have been given all of the necessary parameters.

I have presented worked examples of this formula. You just haven’t
seen them in the midst of the plethora of evolutionist verbiage. In
fact a presented a table of values for different mutation rates and
population sizes. If you want, I’ll repost the examples.
>>> Right now, I am looking exclusively at the probability that the mutation
>>> of interest does not occur in the population -- not especially
>>> controversial.
>>> You have given that as ((1-p)^n)^g or equivalently (1-p)^(n*g).
>>> You have previously defined n as the "total population size".
>> More precisely one should consider n as the effective population size
>> that would benefit from a particular mutation.
>AFAIK, this is the first mention of effective population size in this
>context. Your original presentation defined n as "total population
>size", so you appear to be modifying your claim on the fly.

You are not reading this thread very carefully. I’ve presented a
published empirical example of mutation and selection where several
different variants exist. Each of the different variants has their own
subpopulation and takes their own particular trajectory on the fitness
landscape. We’ll leave it at that you weren’t able to see this
clarification because you have to wade through an ocean of
mathematically irrational evolutionist crap in this thread. I’ve made
the definition for population size more precise around 1400 posts ago
and have re-enforced the concept many times since.

>I suspect you have your own private definition of "effective population
>size" that differs from that introduced by Sewall Wright back in the
>1930s. I could be convinced of the contrary, but I also suspect you
>won't try.

The definition for effective population size in the mutation and
selection phenomenon that I use is not the definition given by Wright.
The effective population size in the mutation and selection phenomenon
is the size of the subpopulation that would benefit from a particular
mutation. Not only is the sequence of mutations important for the
mutation and selection process, the subpopulation on which the
mutation occur determine whether they are beneficial or not for the
given selection conditions.


>> Consider the Weinreich
>> example for the highly efficient beta lactamase where he gives a
>> number of variants of 5 mutations which would give resistance to the
>> beta lactam drug. If the mutations for one variant are A1, B1, C1, D1
>> and E1 and for a second variant A2, B2, C2, D2 and E2, a B2 mutation
>> on the one series variant would not give benefit because these
>> variants are on different trajectories of the fitness landscape. You
>> must distinguish which subpopulation would benefit from a particular
>> mutation.

>(1) As I wrote previously, I am considering ONLY the simple case of a
>single mutation in a single gene from wild-type to a single alternative
>allele. The case covered by the (1 - ((1-p)^n)^g) portion of your
>formula. The relevance of Weinreich's research here is unclear.

The Weinreich experiment includes the simple case of a single gene
from wild-type to an alternative allele. It just so happens that there
is multiple alternative alleles for his experiment. Each member with
its particular allele becomes the progenitor of the subpopulation
which will take its own particular trajectory on the fitness
landscape. The first mutation in the sequence represents the case
which you want to discuss. The ensuing second through fifth mutations
is represented by the joint probability of multiple mutations
occurring as can be computed by generalizing the probability function
for two mutations occurring.

>(2) We are considering the probability that the mutation of interest
>_occurs_ in a population. It is a well known result in biology that
>mutations occur independently of need (going back to the seminal work of
>Luria and Delbrueck and frequently verified thereafter). That is,
>whether or not this particular mutation occurs does not depend on
>whether or not the resulting phenotype provides a reproductive advantage
>over the prior phenotype.

And the model I derived is consistent with what you say.

>You have yourself claimed that the formula you provided works regardless
>of whether the resulting change is beneficial, neutral, or detrimental
>under the prevailing conditions.
>So this paragraph appears to be irrelevant. It certainly does not
>provide any progress toward a _worked example_ of your formula.

Here’s the worked example that I posted during the first round of this
thread well over a thousand posts ago.
Let’s take hersheyh’s example and try some computations. In his case,
mA = mB = m = 10^-8 and N = 10^7 and P(A) = 1 - ((1-((10^-8)/4))^10^7)
= 0.02469, not his value of 0.1
The following is a table of values for different population values of
nA
nA P(B) P(A)*P(B)
1 2.5E-09 6.17252E-11
10 2.5E-08 6.17252E-10
100 2.5E-07 6.17252E-09
100,000 0.000249969 6.17175E-06
10^7 0.024690088 0.0006096
Note, if we do the same series except instead of a population of 10^7,
we use a population of 10^12, P(A)=~1 and P(A)*P(B)=>P(B). However,
the multiplication rule of probabilities still enters into the
calculation through the probability that a beneficial mutation will
NOT occur at a particular locus.
>>> Pick any reasonable value for p.
>>> I have given you values for population varying in size over several
>>> generations. For the values I supplied (above), g = 5.
>>> What _VALUE_ for n do you think we should use to evaluate the function
>>> in this case?
>>> I want the actual NUMBER, not a restatement of the definition.
>>> (And a justification for that number might be nice...)
>> Before I do the arithmetic for you,
>I have only been asking for two and a half months! What more are you
>waiting for?

Would you stop whining Frank!!! Show some patience, I’m discussing
this topic with many others.

>> you need to recognize where the
>> dice rolling metaphor diverges from the mutation and selection
>> phenomenon.
>Gosh -- wasn't I the one who told you that dice rolling was not a good
>metaphor?

Well golly gee whiz Frank. You are still trying to understand the
probabilities for the first mutation to occur and you have already
come to the conclusion that dice rolling is the wrong metaphor for
mutation and selection. Wait until you see the derivation for the
probability function for random recombination because it is exactly
analogous to the probabilities of random card drawing. You had better
learn to like the probabilities involved with parlor games if you want
to understand how mutation and selection and random recombination
works.

>> In the dice rolling metaphor, a trial is done every time a
>> die is rolled whether you roll the same die over and over or whether
>> you have multiple dice. With the mutation and selection phenomenon,
>> one only rolls a particular die with a frequency given by the mutation
>> rate. Not every member rolls the die in a given generation; in fact
>> the die is only rolled very rarely given by the mutation rate. So in
>> the case of mutation and selection, the number of trials is only
>> proportional to the population size and number of generations, not
>> equal to that number as in the case of the number of dice and the
>> number of times the dice are rolled.
>I am refraining from commenting here until you *show your work*.

I’ve done a step by step derivation of the probability functions of a
particular mutation occurring in a population and then for two
mutations occurring in a population. I know I confused you with my
definition of population size but I hope I have clarified that for
you. You do understand that when a point mutation occurs, the only
thing that you can say with certainty is that the change will be to
one of the four bases and unless you know what the base was before the
random point mutation has occurred, you can not say with certainty
that the change will be to one of the three remaining bases. And you
should be able to recognize that a trial only occurs when a mutation
occurs, not every time a member of the population replicates.

>> That said, for your example of 5
>> generations with populations 1E5, 5E5, 1E6, 4E6, 6E6 respectively, the
>> total number of trials done would be proportional to 1E5 + 5E5 + 1E6 +
>> 4E6 + 6E6, the actual number of trials would be dependent on the
>> mutation rate.
>OK, that looks like a step toward providing a worked example of your
>formula for a single mutation occurring in a multi-generational
>population. Now all you need to do is finish it.

No problem Frank, take the sum of the subpopulations for each
generation and multiply that number by the mutation rate. That gives
you the number of trials performed over the generations. If we use
hersheyh’s favorite mutation rate of 10^-8, that’s not going to give
you very many trials for a population this size and so few
generations. Do you want me to slide the beads on my abacus and
compute the actual value? We could now use the dice rolling analogy
directly and based on four possible outcomes instead of six, compute
the probability of a particular mutation occurring from the number of
trials performed.

>Shouldn't take you more than another three to six months...

The wheels of hard mathematical science grind slowly especially when
discussing the issues with evolutionists.


Frank F. Smith Sep 7, 7:17 pm
Newsgroups: talk.origins
From: "Frank F. Smith" <f...@cornell.edu>
Date: Wed, 07 Sep 2011 22:17:18 -0400
Local: Wed, Sep 7 2011 7:17 pm

Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

>>>>>>> Let's see -- the question he posed was usually something (close enough
>>>>>>> to be copied and pasted, as I recall) like:
>>>>>>> "Compute the probability of two beneficial mutations occurring
>>>>>>> (not simultaneously) in a population as a function of population size."
>>>>>>> There's the ambiguity in "not simultaneously". What would it mean for
>>>>>>> two mutations to occur "simultaneously"? Would the sites need to be
>>>>>>> equidistant from origin of replication fork?
>>>>>> Simultaneous mutations mean that both mutations must occur in a single
>>>>>> individual in a single generation.
>>>>> Fine. That's what I thought you meant. It is a peculiar and
>>>>> idiosyncratic use of "simultaneous", but no matter.
>>>>> I've also presumed that you meant (but did not write) "not _necessarily_
>>>>> simultaneously".
>>>> The probability function I derived is applicable whether the mutations
>>>> occur simultaneously or not. You simply adjust the number of
>>>> generations and population sizes appropriately.
>>>>>> Not simultaneously means that the
>>>>>> beneficial mutation only has to accumulate in a descendent of an
>>>>>> ancestor who had the first beneficial mutation.
>>>>> Here there's a problem.
>>>>> You see, in my world, "simultaneously" and "not simultaneously" are
>>>>> complements. If "two mutations occur simultaneously in a population"
>>>>> means that both mutations occur within a single individual, then "two
>>>>> mutations occur _not simultaneously_ in a population" means the two
>>>>> mutations occur in different individuals.
>>>> Ok, let me clarify this. We are in agreement that “simultaneous” means
>>>> both mutations have to occur in a single individual.
>>> We agree that _you_ mean by "simultaneous" that both mutations occur in
>>> a single individual.
>>> That happens not to be what _I_ mean by "simultaneous", which would be
>>> closer to "existing or occurring at the same time"
>>> (<http://www.merriam-webster.com/dictionary/simultaneous?show=0&t=13123...>)
>> The probability function I’ve derived for two mutations occurring is
>> valid whether the mutations occur at the same time on the same
>> individual or the mutations accumulate sequentially over some number
>> of generations, the first mutation on a progenitor and the second on a
>> descendent of the progenitor.
>>>> When I use the
>>>> term “not simultaneously” what I mean is that both beneficial
>>>> mutations accumulate in a single individual but the first mutation
>>>> occurs in a progenitor. After some numbers of generations, descendents
>>>> of that progenitor have amplified that first beneficial mutation and
>>>> some generations later, the subpopulation with that first beneficial
>>>> mutation is large enough for there to be a reasonable probability that
>>>> the second beneficial mutation occurs on a descendent of the
>>>> progenitor with the first beneficial mutation. The mutations are
>>>> occurring in different individuals but the second beneficial mutation
>>>> is occurring on a descendent of the progenitor who had the first
>>>> beneficial mutation. The probability function I’ve derived is for this
>>>> situation and I believe this is the correct way to model the mutation
>>>> and selection phenomenon.
>>> So in your usage, "simultaneously" and "not simultaneously" are not
>>> complementary sets. The two mutations could occur simultaneously, not
>>> simultaneously, and in a variety of other configurations.
>> No, simultaneously and not simultaneously includes all possibilities
>> for the events to occur.
>Not as you define them above.

So tell us Frank, what are this variety of other configurations beside
simultaneously and not simultaneously?

>> The probability function I’ve derived will
>> give the correct probability values if the two mutations occur on a
>> single individual at the same time (simultaneously) or the first
>> mutation occurs on a progenitor and then some generations later, the
>> second mutation occurs on one of the descendents of that progenitor.
>>> I must therefore conclude that you not only have a private definition
>>> for "simultaneous" but also a private definition for "not". Probably for
>>> "occur" as well.
>> If they don’t occur simultaneously or not simultaneously when do they
>> occur or not occur?
>Remember that the original question -- which _you_ posed -- was to
>calculate the probability that two [beneficial] mutations *occur in* a
>population.

And the probability function I derived for you does that for two
beneficial mutations. It just so happens that this probability
function also is applicable to neutral and detrimental mutations as
well.

>Thus, we are considering two general, unspecified mutations. One
>produces the A allele (of some gene), the other produces the B allele
>(of some gene -- there is no reason to presume as the general case that
>A and B are alternative alleles of a single gene).

The mutations can be anywhere, either in two different genes or in a
single gene. If the two mutations must be in the same gene then we are
talking about the mathematical representation of what is happening in
the Weinreich experimental model for the first two mutations for a
particular subpopulation where a single selection pressure targets a
single gene. When the mutation A must occur in one gene and mutation B
must occur in a second different gene, we are mathematically modeling
what happens with combination therapy such as the treatment of HIV.

>There are several ways that the A-producing mutation and the B-producing
>mutation can occur in a population.
>(1) Both mutations occur in a single individual. You choose to call this
>occurrence "simultaneously".

More precisely, “simultaneously” means that both mutations occur in a
single individual in a single generation.

>(2) The A-producing mutation occurs in an individual. The B-producing
>mutation occurs in a descendant of that individual. You choose to call
>this occurrence "not simultaneously".

Correct.
>It should be obvious to anyone who actually thinks about the situation
>for more than a few seconds that (1) and (2) do not exhaust the logical
>possibilities for the occurrence of both mutations in a population.
>Other possibilities include:
>(3) The B-producing mutation occurs in an individual and the A-producing
>individual occurs in a descendant of that individual.

And if the mutation and selection phenomenon was a purely binomial
process where the sequence of events didn’t matter you would be
correct. In order for a mutation to be beneficial, it must improve
fitness for this member to become the progenitor for the subpopulation
on which the next beneficial mutation to occur. If the sequence of
mutations does not give a trajectory of ever increasing improved
fitness then amplification of the particular mutation in the sequence
which does not give improved fitness will not occur and the
subpopulation size will not grow. With a small un-amplified
subpopulation and the low frequency of trials given by the mutation
rate you will have very low probabilities that the next mutation in
the sequence will occur at the proper locus. This is demonstrated by
the data gathered in the Weinreich experiment where his population are
able to amplify each mutation sequentially improving the probabilities
for the next mutations to occur at the proper locus. You can label
your mutations any way you want but however you label the mutations
whether A is first and B is second or visa versa, each ensuing
mutation must give improved fitness over the previous mutation
otherwise amplification of the mutation will not occur.

>(4) The A-producing mutation occurs in one individual and the
>B-producing mutation occurs in a different individual, with neither
>individual a descendant of the other.

That does occur with the use of combination therapy for the treatment
of HIV. Mutations are very likely occurring which would be beneficial
for one drug or another but because selection is occurring on two
genes simultaneously, mutations which would be beneficial for one drug
are not being amplified because of the selection pressure on those
members by the other drug(s).

>Perhaps you will claim that (3) and (4) always have negligible
>probability (though you actually need probability 0). I won't be
>surprised if you make that claim. I also won't be surprised when you
>fail to provide any support for that claim.

I’m not making that claim at all. What I am showing you with the
probability function for two mutations to occur on a single member
requires amplification of the first mutation in order to improve the
probability of the second mutation occurring on a member with the
first mutation. If the first mutation is beneficial for that member,
that member will become the progenitor for the subpopulation to get
the next beneficial mutation in the sequence because improved fitness
allows that progenitor and its descendents to amplify its beneficial
mutation. If you uses hersheyh’s estimate, it takes 30 generations to
do the amplification process. If you use Haldane’s numbers, it takes
about 300 generations. With Lenski’s E coli experiment, it takes about
500 generations to do the amplification process.

>In the unlikely event that you _attempt_ to support that claim, keep in
>mind that below you agreed
>">>>> (2) A particular mutation occurs with the same probability for all
>>>>> individuals in the population.
>>>> Yes"

Yes^2. But if you choose to study the mathematics in more detail, you
will find that this assumption need not be made. The mutation rate is
not a dominant variable in the mutation and selection phenomenon. You
will also find from the empirical data that the mutation can be of any
form not just a point mutation but the population will still be
governed by the same mathematical behavior.

>Thar means that in general the B-producing mutation occurs with the same
>probability in individuals with the A allele as in those with the wt
>variant.

In the probability function I derived for you, I did not make that
assumption. I allowed for different mutation rates for the A and B
mutations but again, this will not give a significant change in the
mathematical behavior of this phenomenon. For mutation and selection
to work, amplification is the key requirement. The reason
amplification is the key requirement for the mutation and selection
process to work is that this is how a subpopulation improves the
probability that the next beneficial mutation will occur. If the
subpopulation can not amplify a mutation, the only other way this
subpopulation can try to do more trials is by replicating for more
generations and that in one of those generations, a member finally
does the trial for the beneficial mutation.

>>>>> <snip>
>>>>>>>> Somehow, your "beneficial" mutations fail to be beneficial except
>>>>>>>> under specific circumstances; circumstances nowhere specified in the
>>>>>>>> description of the problem but added on post-hoc.
>>>>>>> And because he introduces other unwarranted assumptions as well, he ends
>>>>>>> up produces an incorrect "answer" to a different question.
>>>>>> Mutations are only beneficial under specific circumstances and those
>>>>>> circumstances are determined by the selection conditions. I am not
>>>>>> making any assumptions here Frank, what I am doing is describing how
>>>>>> mutation and selection occurs.
>>>>> If you are referring to the probability formula you posted elsethread,
>>>>> then _of course_ you are making assumptions.
>>>>> (Generally, it is helpful to recognize the assumptions one makes. It
>>>>> facilitates identifying the conditions under which a solution applies.)
>>>>> Some of the assumptions allow reasonable simplifications of the
>>>>> calculations, probably without _drastically_ affecting the results. Some
>>>>> are quite reasonable reflections of the underlying biology. Some are
>>>>> reasonable, but only for some organisms or under some conditions --
>>>>> which means that your solution only applies to those organisms or under
>>>>> those conditions. Some are incompatible with the question you posed.
>>>>> I'm going from memory here, so I am likely to miss a few.
>>>>> (1) Mutations are independent across individuals. Whether or not a
>>>>> particular mutation occurs in one individual is independent of whether
>>>>> or not it occurs in another individual in the population.
>>>> Yes
>>>>> (2) A particular mutation occurs with the same probability for all
>>>>> individuals in the population.
>>>> Yes
>>> Given that in a single individual (strictly, a single copy of the wt
>>> allele) the particular mutation either _happens_ or _does not happen_,
>>> the number of mutations in the population will have a binomial
>>> distribution. (1) and (2) are the necessary and sufficient conditions.
>> The binomial distribution does not consider the order of events
>> important. In the mutation and selection phenomenon, the order of
>> events is crucial.
>Why does it matter in which individual(s) the A-producing mutation occurs?

It matters because in order for the mutation to be amplified, it must
be a beneficial mutation to the selection conditions the subpopulation
is subjected to. And the particular mutation which may be beneficial
for one subpopulation will not necessarily be beneficial in a
different subpopulation. This is what the Weinreich experiment is
demonstrating.

>> Each mutation must give improved fitness so that
>> amplification of that new allele can occur. In addition, there are
>> more than two possible outcomes from a point mutation.
>Irrelevant to the calculation you claim to be performing.

It may be irrelevant to the general mathematical behavior of the
mutation and selection phenomenon but from the point of view when a
trial is performed (a mutation) there is more than one possible
outcome from that trial. The outcomes can beneficial, neutral or
detrimental. And that is determined by which of the four bases
possible bases occurs.

Frank F. Smith Sep 8, 4:48 am
Newsgroups: talk.origins
From: "Frank F. Smith" <f...@cornell.edu>
Date: Thu, 08 Sep 2011 07:48:22 -0400
Local: Thurs, Sep 8 2011 4:48 am

Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

>>>> If you're interested in waiting times, a gamma distribution might be
>>>> helpful.
>Correction: that should be geometric (for failures to first success in a
>sequence of Bernoulli trials). Gamma distribution is conceptually
>similar, but continuous rather than discrete.
>> No,
> OK, so you're not interested in the number of trials (DNA replications)
> before "success" (the mutation of interest) occurs. Fine.

DNA replication doesn’t represent a trial. The mutation is the trial.
And when the trial is performed, you have four possible outcomes for
the trial. Think of it this way. If DNA replicated without error
(mutation rate equals zero) no trials are performed at all.

--
Frank F. Smith

Klaus Hellnick Sep 8, 6:59 am
Newsgroups: talk.origins
From: Klaus Hellnick <khelln...@sbcglobal.net>
Date: Thu, 08 Sep 2011 08:59:54 -0500
Local: Thurs, Sep 8 2011 6:59 am

Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

On 8/23/2011 7:31 PM, Alan Kleinman MD PhD wrote:

>> This is what an evolutionist crank would say. He would claim that the
>> evolution of a reptile into a bird is like a journey of 1000 miles by
>> foot. I’ve already shown you what one step of the evolutionary process
>> requires and you can’t take multiple steps simultaneously. It would be
>> more appropriate to say that the evolution of a reptile into a bird is
>> more like a journey of 100,000,000 miles by foot. It is a
>> mathematically irrational belief of evolutionist cranks. Your sloppy
>> use of metaphors demonstrates that you are an evolutionist crank.
>Just what is so hard to believe about small, warmblooded, feathered
>theropods evolving long arms and sickle claws to better climb trees, and
>exploit a new habitat and food sources? How about some of these arboreal
>dinosaurs then gradually developing longer feathers on their arms and
>legs to extend leaps by gliding? How about some of these gliding
>dinosaurs then extending their flights by flapping their arms, leading
>to selection of those with stronger breast muscles and bigger sternums?
>Just which step is impossible to select for?
>Klaus

Welcome to the discussion Klaus. It’s hard to believe that you can
transform the (at least) eight genes to turn a reptile scale into a
feather and the genes which control skeletal formation to transform
arms into wings and produce flight muscles. And what are the selection
pressures which would do this? How can mutation and selection
transform all these genes simultaneously and if not simultaneously,
what are the selection conditions which would transform all these
genes one by one?

hersheyh Sep 8, 3:55 pm
Newsgroups: talk.origins
From: hersheyh <hershe...@yahoo.com>
Date: Thu, 8 Sep 2011 15:55:37 -0700 (PDT)
Local: Thurs, Sep 8 2011 3:55 pm

Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

>> On Aug 2, 5:01�pm, hersheyh <hers...@yahoo.com> wrote:
>> > On Aug 1, 5:27 pm, Alan Kleinman MD PhD <klei...@sti.net> wrote:
>> > > On Jul 6, 1:10 pm, hersheyh <hers...@yahoo.com> wrote:> On Jul 6, 8:42 am, Alan Kleinman MD PhD ><klei...@sti.net> wrote:
>> > > > > On Jun 6, 9:24 am, Inez <savagem...@hotmail.com> wrote:
>> > > > > > On Jun 6, 7:01 am, Alan Kleinman MD PhD <klei...@sti.net> wrote:
>> > > > > > > On May 24, 9:34 am, Inez <savagem...@hotmail.com> wrote:
>> > > > > > > > On May 24, 6:50 am, Alan Kleinman MD PhD <klei...@sti.net> wrote:
>> > > > > > > > > On May 12, 6:39 am, Inez <savagem...@hotmail.com> wrote:
>[snip]
>> > The above discussion has to do with how one defines "mutation", not in
>> > the derivation of the correct probability (which you do not get right
>> > because you do not understand what the terms "mutation" and
>> > "beneficial mutation" actually mean. �You repeatedly wrongly define
>> > "mutation" by claiming that a change of an unspecified n.t. to the
>> > *same* n.t. is a "mutation." Because mutation requires a *change* from
>> > one specified state to another specified state, you are in error both
>> > because you cannot determine whether a mutation has occurred in the
>> > absence of defined initial state and also because you claim that a
>> > mutation can occur in the absence of change.
>> No, I�m pointing out to you that there are 4 possible bases at a
>> locus.

>I am fully aware that there are 4 possible bases. But that has nothing to do with determining the rate of >mutation (mean number of mutation events per trial) unless you *know* the original genetic state and can >determine the change in genetic state from that original state. Determining mutation rates does not require >knowing that there are 4 possible bases. It requires knowing that there has been a genetic change.

Hersheyh, the mutation is the trial and when the trial is performed,
you have 4 possible outcomes. Exact replication of DNA does not
perform trials. Only when there is a mutation is there a trial.

>And there is nothing in probability theory that requires division by 4 possible bases. Let's give a more realistic >dice example. I will use two die and empirically determine the rate of snake eyes. I realize that if I were to >use cubic 6-sided dice which is equally weighted on all sides, that I could *theoretically* determine that the >probability of snake eyes (the rate of snake eyes) should be 1/6*1/6 = 1/36. I should get somewhere close to >this ratio if I empirically roll the two die 3600 times. That is I should get reasonably close to 100 snake eyes >in my 3600 rolls of an honest pair of dice (one red, one blue).

The mutation rate gives the frequency for which there is a mutation in
a given member at a particular locus in a given generation. A trial is
not done every replication of DNA at every locus, only when a mutation
occurs is there a trial for a beneficial (or neutral or detrimental
mutation). When you have a mutation rate of 10^-8 and a population
size of 10^9, you are only doing about 10 trials (mutations) at a
particular locus in a given generation. If you want to do the dice
analogy correctly, you have 10 four sided dice (for your 10 trials)
being rolled in a given generation with that population and mutation
rate. You can then compute the probabilities of how many of those
trials will give you A’s, C’s, G’s and T’s. You can also compute the
probability that you will get your beneficial mutation.

>But mutation rates cannot be determined theoretically, but can only be determined empirically. This would be >like rolling a pair of dice where the size of the individual sides is not identical (the shape of each die is not a >cube and not identical to each other). Moreover, the die are each independently "loaded" or weighted. Except >we do not *know* _a priori_ what the different face areas and weights are when we roll the dice pairs. That >means that the only way we can determine the probability of snake eyes is by *empirically* running n trials >(in this case, rolling the two die n times) and counting the number of snake eyes (the event) seen in those n >times rolling. Let's say that we see 50 snake eyes in 3600 trials. That is significantly different from what one >would expect from a "perfectly balanced and cubic" 6-sided die (not surprising, given that these die are not >"perfectly balanced and cubic", but 50/3600 = 0.0139 is the *empirically* determined rate of snake eyes. > *That* is the rate

of snake eyes for these die, not 100/3600 = 0.0278.

What you continue to miss is that when rolling dice, every roll of
every die gives a trial. In the mutation and selection phenomenon, a
trial (roll of a die) only occurs with a frequency given by the
mutation rate. And of course I know that the mutation rate is an
empirically determined value. But you don’t have to know the mutation
rate explicitly in order to study the mutation and selection
phenomenon. If you write your mathematical model correctly, you can
study the behavior of the phenomenon mathematically. I’ve done this
with Schneider’s ev model and with the probability function I’ve
derived for you describing the probabilities associated with mutation
and selection. When you do this, you will find out how the mutation
rate affects the mathematical behavior of the mutation and selection
phenomenon. And it doesn’t affect the phenomenon in the way you say.

>Moreover, it would be stupid to divide the *empirically determined" rate (probability) of snake eyes by 6 >because there are 6 sides to each die (although the sides are not equal in either weight or area). Yet that is >pretty much what you do. You take the *empirically determined* rate (probability) of an event (in our case, >the number of mutants observed per n trials) and divide it by the arbitrary number of 4 for some unstated and >not clearly understood "theoretical" reason.

You still don’t comprehend that when a point mutation occurs, you can
only say with certainty that you will have one of the four bases as
the outcome. And as long as you continue to claim that the mutation
rate can only be determine by a phenotypic change, you will miscount
the mutation rate by all the neutral mutations occurring.

>> > And you are further wrong when you repeatedly imply that "beneficial"
>> > is an inherent property rather than a conditional property of a
>> > *change* in a gene sequence. �The *ONLY* correct way to correctly
>> > describe a mutation is to specify the beginning and end states. �For
>> > example, mutation from antibiotic-sensitive to antibiotic-resistant or
>> > mutation from unable to metabolize citrate to being able to metabolize
>> > citrate. �Those descriptions tell us not only what the mutation is,
>> > but how one can distinguish mutant from non-mutant. �Calling a
>> > mutation "beneficial" does not tell us the beginning or end states,
>> > tells us nothing about when the mutation is beneficial, and is an
>> > inadequate description for specifying the mutational event. � It is
>> > like calling a person "happy" as opposed to calling the person "6 foot
>> > tall". �One of those is a conditional state that can depend upon the
>> > local environment and the other is inherent and measurable to a
>> > reasonable degree of accuracy.
>> In the probability function that I derived for you for two mutations
>> occurring, there is no explicit condition that the two mutations have
>> to beneficial. What will determine if the first mutation is beneficial
>> or not is seen in the subpopulation size for mutation A. If mutation A
>> is detrimental, the subpopulation size with that mutation will decline
>> over generations.
>No. There will be continual input of the "mutant" state by mutation. Eventually there will be a rough >equilibrium level between input of new mutation and loss of old mutations.

Are you now going to claim that the transformation of reptiles into
birds occurred in an equilibrium state? Directional selection is a non-
equilibrium state and the ability of the population to reach a new
equilibrium state is strongly dependent on the complexity of the
selection conditions. Unless the selection conditions are simple that
is only targeting a single gene at a time, the population is going to
have extreme difficulty getting to a new equilibrium by mutation and
selection.

>> If the mutation A is neutral, the subpopulation size
>> will remain relatively constant

>Only over the short run. That is the ideal expectation of the Hardy-Weinberg math. However, in real >populations rather than infinite ones where the H-W rules hold, there will be generation to generation >fluctuation in the frequency of the mutants. The relative size of these generation to generation fluctuations >will be larger in small populations than in larger ones, but, because *chance has no memory*, and each >generations H-W expectation will not "remember" what the original frequency of alleles was, there will be a >random walk until one of the alleles becomes (nearly) extinct.

But fluctuations of frequency of mutants is not what drives the
mutation and selection phenomenon, amplification of the allele is what
is required to improve the probabilities of the next beneficial
mutation occurring at the proper locus.

> and if the mutation A is beneficial,
> the subpopulation with that mutation will amplify over the generations
> improving the probabilities that mutation B will occur on one of the
> members which already has mutation A.

>Since selection doesn't know or care that it is selecting only for mutation A, it will select for *any* variant that >has greater fitness relative to the w.t. for *any* selective pressure that exists in the population. That is, if >mutation B has independent selective value relative to the alternate allele in its gene, it will also tend to >increase in the population at the same time that organisms with A are increasing.

Present the empirical evidence for your argument because all the
empirical evidence available when selection pressures target more than
a single gene show that even if you have a beneficial mutation for one
gene, it will not be amplified due to selection pressure targeting the
other gene. This is why combination therapy works, especially for HIV.

>If the organisms are clonal in nature (like bacteria and, generally, viruses, as well as some eucarotes) then this >parallel increase is only relevant in that it increases the likelihood of getting the second mutational event (A in >a B-containing cell or B in an A-containing cell). If recombination, as in eucaryotes, occurs every generation, >the parallel increase in frequencies of both A and B increases the chances of generating offspring with new >combinations of the alleles in gene loci A and B.

Are you going to write the probability function for random
recombination or are you going to just give us blah, blah, blah?

>> > > I ve
>> > > presented a step by step derivation of the correct probability
>> > > function which describes the probability of two beneficial mutations
>> > > occurring.
>> > And if the binary feature is the "probability of an individual having
>> > both mutations at the time of selection for both" as opposed to the
>> > "probability of an individual not having both mutations at the time of
>> > selection for both" when there has been no selection for either prior
>> > to the time of selection for both", your "probability" values (except,
>> > of course, for the stupid and ignorant division of the mutation rate
>> > by 4) would be correct and the subsequent calculation of the
>> > "probability of having at least one such double-mutant" in a total
>> > tested population of given size would also be correct. �But, as I
>> > point out, serial selection by the three step process gives much
>> > higher probabilities for these events because one is never selecting
>> > for individuals that must be simultaneous double-mutants without prior
>> > selection for one of the mutants.
>> The same probability function I derived for you for two mutations
>> occurring applies whether the mutations occur simultaneously on a
>> single individual or sequentially where mutation A occurs on a
>> progenitor and mutation be occurs on one of the descendents of the
>> progenitor which already has mutation A.
>
>Except that the *frequency* of the A mutation (and/or B mutation), if they are *independently* beneficial will >have consistently increased during those selective conditions. That means that you need to determine the >*frequency* of the different mutations at the time you run the "trial" (examine individuals for the presence of >both in the same individual). That *frequency* will NOT be the same as the mutation rate. It will be higher. > How much higher depends on the independent selective advantage of the variant.

The problem you have is that when selection pressures target more than
a single gene, you don’t get “independently” beneficial mutations A
and B. If you know of an empirical example which substantiates your
claim, present it. All the examples of mutation and selection which I
have found where selection pressures target more than a single gene do
not give cases where mutations A and B are independently beneficial.
The selection pressure targeting the other genes always inhibits the
amplification of any beneficial mutation for the gene. This is why
your theory of evolution is mathematically irrational.

This is the end of the compilation of responses for posts 951-975.

[Inez]

On Sep 30, 2:27 am, G <g...@nowhere.invalid> wrote:

How do you know it's a mutation at a single nucleotide site? How do
you know a mutation to each of the different nucleotide is equally
likely? Why would you multiply by 4, given that one of the
nucleotides wouldn't be a mutation? And even assuming you can
determine what the odds of a site changing randomly, why do you care
about that number? The goal of this math is to determine what the
odds of antibiotic resistance occuring, which in your calculation is
the starting number.

[Charles Brenner]

On Sep 30, 8:56 am, Alan Kleinman wrote:

> >>> On Monday, August 1, 2011 9:50:40 PM UTC-4, John Harshman wrote:
> >>>> Alan Kleinman MD PhD wrote:
> >>>>> Unless you know a
> >>>>> priori what the base at the particular locus is, a point mutation can
> >>>>> give any of the four possible bases.
> >>>> That's just as nonsensical as it was the first time you made the claim.
> >>>> The ability of back mutations to happen is irrelevant to the mutation
> >>>> rate. Regardless of the original base, one of your four possibilities is
> >>>> not a mutation. A->A is not a mutation. C->C is not a mutation. G->G is
> >>>> not a mutation. T->T is not a mutation. Your inability acknowledge the
> >>>> error of a prior claim, regardless of how stupid it is, makes you look
> >>>> seriously insane.
> >>> Worse yet, one of the bases *was* original whether or not we know which one it is. Thus one of the four >>>possibilities has a massively greater probability than the others, rendering any "division by four" >>>mathematically nonsensical.
> >> Mathematics is always nonsensical to the mathematically incompetent.
> >Do you disagree that one possibility is greatly more likely than the
> >other three?
>
> What I agree is that when a point mutation occurs that there are only
> four possible outcomes and unless you know what the base was before
> the mutation occurred then any of the four possible outcomes are
> equally likely and that s how you must express this mathematically.

I understand Alan's point - to the problem: "Given mutation rate mu at
some unknown genome position, what is the probability that the site
will mutate and end an a G?" the answer (near enough) is mu/4.

The context seems a bit lost at this point. But as best I recall it
wasn't equivalent to the above; the relevant probability question was
quite different. For resolution, calling one another names is a
pretty good approach especially for the Internet. Another is to spell
out explicitly what the problem is and to remember that the language
of mathematics includes declarative sentences. (However I think Howard
Hershey did try that.)

I believe that the traditional wail of schoolchildren complaining
about a forthcoming math test: "It won't have *word* problems on it
will it?" is telling. The most important obstacle most people have
with math is understanding how to move from words to mathematics. I am
not surprised that someone might be able to solve differential
equations but stumble at application of simple probability ideas.

[hersheyh]

[snip]

>
> hersheyh Aug 26, 10:12 pm
> Newsgroups: talk.origins

> From: hersheyh <hers...@yahoo.com>

> Date: Fri, 26 Aug 2011 22:12:08 -0700 (PDT)
> Local: Fri, Aug 26 2011 10:12 pm
> Subject: Re: The Theory of Evolution is Mathematically Irrational
> Round 2
>
> On Friday, August 26, 2011 9:21:46 AM UTC-4, Alan Kleinman MD PhD
> wrote:
>

> >> On Jul 25, 9:49 pm, John Harshman <jha...@pacbell.net> wrote:
> >> > Alan Kleinman MD PhD wrote:

> >> > > On Jul 5, 7:55 am, John Harshman <jha...@pacbell.net> wrote:
> >> > >> Alan Kleinman MD PhD wrote:

> >> > >>> On Jun 6, 8:40 am, John Harshman <jha...@pacbell.net> wrote:
> >> > >>>> Alan Kleinman MD PhD wrote:

> >> > >>>>> On May 16, 9:55 pm, John Harshman <jha...@pacbell.net> wrote:
> >> > >>>>>> Alan Kleinman MD PhD wrote:

> >> > >>>>>>> On May 9, 9:51 am, John Harshman <jha...@pacbell.net> wrote:
> >> > >>>>>>>> Alan Kleinman MD PhD wrote:
> >[snip]
> >> > >> I don't have to show you an example in order to show that it's possible
> >> > >> for something to happen. Can you explain why it's not possible? What
> >> > >> would prevent part of allele A from recombining with part of allele B to
> >> > >> produce allele C, different from both?
> >> > > A chimera is an error in recombination.
> >> > What do you mean by that? It doesn't appear to make any sense, or to
> >> > have any relevance.
> >> Sexual recombination is not an error in replication but a shuffling of
> >> existing alleles.

> >It is the generation of different combinations of genes wrt their parentage. That is, if the allele
> > marked m is of maternal origin, regardless of whether or not is identical or different from the allele
> > marked p, which of paternal origin, and two genes, A and B, are unlinked -- written as Am/Ap;
> > Bm/Bp -- then you expect the following haploid gametes in the following ratio: 1 Am;Bm: 1Am;Bp: > > 1Ap;Bm: 1Ap;Bp.
>
> Really hersheyh, why would you expect that ratio? How many members in
> your population? How many have each allele?

In a *population* that is randomly mating (and eucaryotic in its sexual cycle), if the frequency of the
alleles A and a are p and q, respectively and the frequency of the alleles B and b are r and s,
respectively. Then the frequency of the gametes will be in the following ratios: pr A;B, ps A;b, qr a:B,
and qs a;b. The frequencies of the different genotypes produced will follow from that. Again, the
Punnet square is a handy way to calculate the frequencies of the different genotypes.

> >If mating of such individuals is random, you expect the following progeny (arranged in Punnet Square):
> > 1 Am;Bm 1Am;Bp 1Ap;Bm 1Ap;Bp
> >1 Am;Bm Am/Am; Bm/Bm Am/Am; Bm/Bp Am/Ap; Bm/Bm Am/Ap; Bm/Bp
> >1Am;Bp Am/Am; Bm/Bp Am/Am; Bp/Bp Am/Ap; Bm/Bp Am/Ap; Bp/Bp
> >1Ap;Bm Ap/Am; Bm/Bm Ap/Am; Bm/Bp Ap/Ap; Bm/Bm Ap/Ap; Bm/Bp
> >1Ap;Bp Ap/Am; Bp/Bm Ap/Am; Bp/Bp Ap/Ap; Bp/Bm Ap/Ap; Bp/Bp
> >I am of course guessing, but I do hope that the Dr.Dr. is reasonably familiar with this very basic sort of Mendelian >genetics. If the m and p alleles were related by phenotypic dominance and recessiveness, this would be a familiar >1:3:3:9 phenotypic ratio.

> I am and the Punnett square is used to predict the outcome of a
> breeding program, not random recombination.

It also can be used to predict the outcome of random mating in a population which has two alternative
alleles at two different gene loci. That is a simple extrapolation of the H-W equilibrium.

> If you think this is the
> mathematics which describes the random recombination HIV is doing, why
> not tell us why recombination does not accelerate the evolutionary
> process for HIV when selection pressures are targeting two genes
> simultaneously.

It's obvious. HIV is a virus, not a eucaryotic organism. Recombination between different viruses is not a
regular component of its reproduction. Not that it cannot happen. But it is a relatively rare and unusual
event.

> In order to understand this you can’t use the Punnett
> square, you have to derive the probability function for random
> recombination and you don’t know how to do this despite the fact that
> you are a teacher of genetics for the past 20 years.

For HIV, I would have to know the frequency of double infection of cells with different strains of HIV in
any given individual. No one knows that. It is rare, which is why recombination is not considered
important in HIV reproduction. Recombination, however, is not rare in the sexual cycle of multicellular
eucaryotic organisms. It happens once per generation during meiosis.

> Perhaps your
> indoctrination as an evolutionist neglected some aspect of your
> training as a scientist.
>
> >> New genetic information in the gene pool is not
> >> created by recombination

> >New combinations certainly can produce new phenotypically variant individuals. Assuming that the
> > capital letter is the dominant allele, the individual with the genotypes A/A;b/b has a different
> > genotype (and hence different phenotypes) from the individual with the genotype a/a;B/B. And
> > both can exhibit different phenotypes than their progeny with the genotype A/a;B/b. For example,
> > if A is dominant for brown eyes, B is dominant for brown hair, and a and b are recessive with the
> > phenotypes blue eyes and blond hair, the individual with the genotype A/A;b/b is brown-eyed and
> > blond, the individual with a/a;B/B is a blue-eyed brunette and the A/a;B/b individual is a brown-
> > eyed brunette. I can tell them apart, even if our good Dr. Dr. cannot. Moreover if I crossed
> > individuals which were A/a;B/b to each other I would even get blue-eyed blonds by recombination.
> > That is four different phenotypes by my count that one can get by recombination.
>
> Of course recombination can change the expression of existing alleles.

No. Recombination can change the phenotype of *organisms* because the alleles are in different
combinations. Recombination usually does not change the expression of existing alleles. Again,
evolution only works with existing alleles, not imaginary ones.

> Are you going to tell us that a breeding program of alligators and
> crocodiles will give us birds?

No. But a breeding program of nature did change a feathered, toothed, tailed, theropod dinosaur into a
feathered, toothed, tailed bird.

> Are you going to tell us that
> recombination explains the 40,000,000 differences between human and
> chimpanzee genomes?

No. But recombination facilitates the spread of these differences in a population. Unlike with clonal
organisms, sexually reproducing organisms have recombination as an alternate way of obtaining new
allele combinations.

> When are you going to derive for us the
> probability function that describes random recombination? Why don’t
> you admit that with all your expertise as an evolutionist and
> geneticist that you don’t know how to do this calculation and have
> never been taught how?

I did it several times. But you, oh genius with a deep understanding of biology, apparently thinks that
HIV and E. coli undergo meiotic recombination each generation. It is a rather profound level of
ignorance when someone doesn't understand the difference between humans and a retrovirus.

>
> >> as can be done by mutation and selection
> >> unless there happens to be an error in the recombination process.
> >> Directional selection pressures require the creation of new alleles.


> >No. As even the good Dr. Dr. might guess from the word "selection", all selection does is
> > differentially affect the reproductive success of different phenotypes (and indirectly genotypes to
> > the extent that such phenotypes are due to different genotypes). Selection can only work on alleles
> > that *either* pre-exist in the population or that spontaneously and randomly occur later (which, of
> > course, means that for the variant to appear later, the selection cannot be lethal to the w.t. and
> > even substantial toxicity, by reducing population size, affects the probability of mutations actually
> > occurring). Selection requires that the selected variant actually exist in the population.
>
> You don’t tell the whole story, you don’t even tell most of the story.
> Certainly when a population is subjected to a new selection condition,
> some members must be able to tolerate the selection condition or the
> population will go extinct.

In many cases *most* of the population members can tolerate the new conditions. The new conditions
just slow their growth or reproduction.

> But then the mutation and selection
> process put the variants of the population on particular trajectories
> of the fitness landscape if those variants are able to become better
> replicators by beneficial mutations. What you don’t tell in your blah,
> blah, blah is how the selection conditions affect the shape of the
> fitness landscape and what happens when selection targets more than a
> single gene at a time.

Elsewhere, I have given a mathematical treatment of the type of parallelism that *will* occur in a clonally
reproducing bacterial population subjected to higher salt and higher temperature, conditions which, for
the w.t., slows its rate of doubling without affecting the maximum population density it can achieve (the
limiting condition is glucose).

> That’s why you have to use the correct
> probability function to describe the phenomenon and the Poisson
> distribution is not the correct equation. And I expect you still
> haven’t studied the derivation of the Poisson distribution yet. You
> use the equation blindly without understanding what is being
> calculated.

I understand when it can be used as a good estimate of the binomial probability distribution. And the
binomial probability distribution is what you have "derived", despite your division of the actual mutation
probability by 4.
Your equation that calculates the probability that one or more individuals with mutation A will be
present in a population of total size, n, is:

P(A) = 1 - (1-(mA/4))^(n*nGA)



Now I am going to simplify the symbols of that equation to demonstrate that it is nothing more than the
binomial probability distribution solved to answer the question "What is the probability that there will be
one or more A mutants in a total examined population of n*nGA?" where n = number of trials per
generation and nGA = number of generations or times in which n trials are conducted or examined?

First, I will change the meaning of n to the meaning it has in most binomial probability equations. n, in
standard terminology is "the total number of trials". Thus it actually is a replacement for your n*nGA,
which means that your n is NOT "the total number of trials" but only the "number of trials per
generation". It has to be that or the generations term does not cancel out. It would be better if you had
used the term N and specifically said it was the number of trials per generation, but, hey, you weren't
doing real math here anyway and so sloppy terminology is O.K. But to avoid confusion, I will call the
term n'. n' is the total number of trials. It equals your n*nGA.

That makes your equation now:

P(A) = 1 - (1-(mA/4))^(n*nGA)
 = 1 - (1-(mA/4))^n')

Now I claim that the "real" mutation probability is mA per trial and you think the "real" mutation
probability per trial is mA/4 per trial. [The per trial clause is needed for the equation to actually work
out as an equation. Any *frequency* or *probability* is always a division of something by something.
And I am calling mA the mutation probability or frequency rather than the mutation *rate*, because the
term mutation rate assumes that we are looking at the rate of change from not-A to A rather than the
frequency of a particular state in all cases. That is not true. We are interested in the probability of the
state of the trial looked at being A. The mutation rate from not-A to A is the *minimum* frequency of A
in any population. The *maximum* probability of A in a population is 1.0.]

The discussion of mA versus (mA/4) is merely a quantitative disagreement and not a qualitative one. So
I will coin a term I will call pA, which symbolizes the "real" mutation probability per trial for A. I would
plug in mA for pA. You would plug in a number that is 1/4 that. But pA can still stand for the "real"
probability of the 'event' (real presence of mutation A) per trial. That makes your equation now

P(A) = 1 - (1-(mA/4))^(n*nGA)
 = 1 - (1-(mA/4))^n' = 
 1 - (1-pA)^n'

or

P(A) = 1 - (1-pA)^n

where P(A) is the probability of one or more A events (in this case the 'event' is the 'real' presence of A
rather than not-A) in a total number of n trials (in this case, the total number of trials is the total
number of individuals examined for A or not-A whether that involves examination of a number of
individuals per generation over a number of generations or a number of individuals in a single
generation). More generally, then, the probability of one or more 'events' in n 'trials' is:

P(E) = 1 - (1-pE)^n

Are you following this math so far?

Now, what exactly does the term (1-pE)^n mean? (1-pE) is the probability of not-E per trial. And that
makes (1-pE)^n the probability that *every* trial of the n trials done will come up as not-E. IOW, (1-
pE)^n is the probability of seeing exactly zero 'events' in n 'trials'. Thus, 1 - (1-pE)^n = 1 - the
probability of seeing exactly zero events in n trials = the probability of seeing one or more events in n
trials, P(E).

Now, if we had a way of directly determining the probability of exactly zero events in n trials, we could
use that instead of (1-pE)^n, right? Well, *if* the above equation (your equation) is the same as the
equation for one or more events from a binomial probability distribution, I should be able to show it.
The mass probability function for a binomial distribution with the parameters n (total number of trials)
and p (probability of the event per trial) is [n!/k!(n-k)!]*p^k((1-p)^(n-k)). k = the exact number of
events being examined.

http://en.wikipedia.org/wiki/Binomial_distribution

Since we have shown above that your equation = 1 - the probability of seeing exactly zero events in n
trials, that means that P(E) should = 1 - [n!/k!(n-k)!]*pE^k(1-pE)^n-k when k = 0 if we are looking at a
binomial probability distribution. And, if I am correct that your 'derivation' is nothing but a binomial
probability distribution, then when k = 0,

1 - [n!/k!(n-k)!]*pE^k(1-pE)^n-k = 1 - (1-pE)^n

Now, since k! = 0! = 1, the [n!/k!(n-k)!] part above reduces to [n!/0!(n-0)!] = n!/n! = 1. Moreover p^0
= 1 too.

That reduces the left side of the equal sign to 1 - [1*1*(1-pE)^(n-0)] = 1 - (1-pE)^n
That is:

1 - (1-pE)^n = 1 - (1-pE)^n

The above sure looks like an equality to me. This demonstrates that what you derived in calculating the
probability of there being one or more mutants in a population of size n is (drumroll please) nothing but
the binomial probability distribution.

Moreover, because "the binomial distribution converges towards the Poisson distribution as the number of trials goes to infinity while the product np remains fixed. Therefore the Poisson distribution with parameter λ = np can be used as an approximation to B(n, p) of the binomial distribution if n is sufficiently large and p is sufficiently small. According to two rules of thumb, this approximation is good if n ≥ 20 and p ≤ 0.05, or if n ≥ 100 and np ≤ 10."

That means that, assuming the above conditions are met, 1 - (1-pE)^n should also approximately equal 1 - the Poisson probability when k = 0.

That is:

http://en.wikipedia.org/wiki/Poisson_distribution

1 - (1-pE)^n should roughly equal [((p*n)^k)(e^(-p*n))]/k! when k = 0. I have switched the lambda in the equation (expected mean number of occurrences of E in n trials with p*n, which is the same thing).

Because k! = 1 and (p*n)^k = 1 when k = 0, the Poisson in this case simplifies to e^-(p*n). Which
means (again assuming that n ≥ 20 and p ≤ 0.05, or if n ≥ 100 and np ≤ 10, which it is in all the cases
we have looked at) that

1-e^(np) =~ 1 - (1-pE)^n

So, unless you can find something wrong with my math, stop pretending that your probability
distribution is something different from the binomial probability distribution. It isn't. That you are not
aware of that fact is your problem, not mine.

At this point, let's talk about the equation you claim gives the joint probability or something. Your
language is so muddled, it is hard to tell what you think you are saying.

"And finally, the probability that mutation B will fall on a member of
the subpopulation with mutation A by the multiplication rule of
probabilities is:
P(A)*P(B) = {1 - (1-(mA/4))^(n*nGA)} * {1 – ((1-(mB/4))^(nA*nGB)}
This is the correct probability function for two point mutations A
then mutation B occurring not simultaneously as a function of
population and subpopulation size and the number of generations for
each event for given mutation rates."

In actuality, the above is the multiplication of the binomial probability that there will be one or more A
mutants in a population of total size n' (which, if you remember = n*nGA) times the binomial probability
there there will one or more B mutants in a population of total size nA', where nA is the number of
individuals that have mutation A. Note that nowhere in that latter equation is there any requirement
that the B mutations must actually occur in an organism that has an A mutation. Only that it occur in
population of the same size as the population containing A. I strongly suspect that is not the equation
you thought you were writing. I suspect you wanted to calculate the joint probability of one or more
trials with *both* A and B occurring in a single trial (that is, jointly). That equation would be written
(using the simplified terminology of binomial probability distributions:

P(A,B) = 1 - (1-pA*pB)^n

Note that this is just the general binomial probability distribution calculating the probability of one or
more 'events' in n 'trials', P(E) = 1 - (1-pE)^n. The difference is that the 'event' is now the *joint*
probability of both A and B being present per trial. The probability of that 'event' (the joint event) is
pA*pB per trial, assuming that the A and B events are independent events.

At this point, it is worth reminding you that pA and pB are not constants and are not always equal to the
mutation probability to A or B from the non-mutant state. Again, the mutation probability is the
*minimum* probability that a trial will have that mutant. *When* we directly select for cells that have
both mutant state A and mutant state B *from* cells that were initially neither A nor B, the mutation
probability is, in fact, a reasonable estimate of the probability that any given trial will have that mutant.

However, if I first select for A mutants and grow up a population that is 100% A mutant, the mutation
probability of A from not-A no longer holds. Instead the probability of A in that population is 1.0 per
trial or close to it. That is, pA and pB are not constants but depend crucially on the past history of the
organism.

I would be interested in seeing how you deal with the above that shows that all you have derived is the binomial probability distribution. Please go through it step by step. The math isn't all that hard.

[snip]

[Inez]

On Sep 30, 8:56 am, Alan Kleinman MD PhD <klein...@sti.net> wrote:
> The following are a compilation of responses to posts 951-975 to
> prevent splinter threads. Sorry for any inconvenience.
>
> Greg Guarino  Aug 29, 7:06 pm
> Newsgroups: talk.origins
> From: Greg Guarino <gdguar...@gmail.com>
> Date: Mon, 29 Aug 2011 22:06:17 -0400
> Local: Mon, Aug 29 2011 7:06 pm
> Subject: Re: The Theory of Evolution is Mathematically Irrational
> Round 2
>
> On 8/29/2011 8:01 PM, Alan Kleinman MD PhD wrote:

Snip

>
> The number of possible point mutations in a genome is equal to the
> number of bases. There are four possible outcomes to any point
> mutations. And are there 3^(6*10e9) possible combinations of bases or
> 4^(6*10e9) possible combinations of bases?
>

When are you going to address the point that one of the 4 nucleotides
is not a mutation? Can you not see that this is true? Given that a
site must start with one or another nucleotide, the maximum number of
changes possible is 3, not 4.

[Greg Guarino]

On 9/30/2011 11:56 AM, Alan Kleinman MD PhD wrote:
>> A meaningless number. Please compute the probability of dealing a bridge
>> >deal in which one player gets all spades, a second all hearts, etc. Got
>> >it? Now compute the probability of each player getting some deal, any
>> >deal. Which one is more appropriate here?

> It’s a meaningless number to you because you are ignoring the
> multiplication rule of probabilities for computing the joint
> probability of events.

It's pointless at this stage, but, hey, I'll give it another shot. Your
reflexive insistence that events are "joint" renders just about any
combination of events impossible.

As part of my attempt to get back into reasonable shape, I walk 2 miles
each way to and from my train station every day. To fend off boredom,
and to try to find the approximate mid-point of my daily walk, I counted
my steps one day. It was about 4500, if I remember correctly.

What is the combined probability that each of my footfalls would land
exactly where it did along my route? Preposterously low, I would think.
By your logic, it must not have happened.

How about another?

I shuffle a deck of cards. The resulting order, whatever it is, had a
chance of 1 in 52 factorial, right? 1 in 8 × 10^67. Holy crap. A miracle
then?

Wait, it get's better. I shuffle the deck again and produce another
combination of equal improbability. Heck I could even repeatedly shuffle
the deck while walking from the train. There might not be as many atoms
in the galaxy as there are potential combinations of those "joint"
playing card and footstep events.

If you make out everything as "joint" then just about anything is
impossible. And if we require a very specific outcome, then the
probabilities are indeed very low. I'm sure I couldn't make the same
footstep locations every day even if they were painted for me to see.
But the probability of me reaching the train station is quite close to
one. Likewise the probability that I will end up with 13 spades, 13
clubs, etc. when I shuffle the deck.

The same logic applies to the vast majority of genetic changes, the
"neutral" ones. It is indeed preposterously improbable that our
particular result came about, but barring extinction, it was guaranteed
that SOME combination would occur.

[John Harshman]

Pretty sure it isn't. Practically speaking, mutation rates are
considerably different depending on what we start with and what we end
with. And the number of mutations depends not only on rates given
particular starting and ending bases but also upon the frequencies of
those starting bases in the genome. Further, if we start at G and end at
G, is that a mutation at all?

What exactly do you mean by "the mutation rate"?

[Charles Brenner]

True, but for the probability that I defined that doesn't matter. My
statement is only inaccurate to the extent that G isn't 1/4 of all
nucleotides genome-wide or if some transitions are slightly different
in probability to occur than other transitions (or same for
transversions).

> And the number of mutations depends not only on rates given
> particular starting and ending bases but also upon the frequencies of
> those starting bases in the genome.

I agree with that, per my preceding remark.

> Further, if we start at G and end at
> G, is that a mutation at all?

No, it's not.

> What exactly do you mean by "the mutation rate"?

*exactly" is going to depend on the context of the discussion. For
example, if the discussion is about neutral fixation we may be
interested only in mutations among junk DNA, which distinguish child
from parent, and which are only counted when and if the child reaches
maturity. In another context we may simply look at DNA duplication
during mitosis. I don't think there's much difference between the two
though.

That said, I define "mutation rate" by the following "probability
experiment":

Pick a genomic location at random. Watch a duplication event. If the
copy differs from the original, that's a mutation. Repeat many times
and observe the long-run rate of mutations.

To a reasonable approximation, the mutation product will be G whenever
the pre-mutation type was A (because transitions predominate) and
that's about 1/4. Slightly more accurately we could take also
transversions into account which would probably make the answer even
closer (slightly) to 1/4.

[hersheyh]

On Friday, September 30, 2011 4:32:46 PM UTC-4, Charles Brenner wrote:

The key requirement for there to be a "mutation" is for there to be a "change". In genetics, it is most common to limit the discussion to a single gene locus and to use a "change" in function to identify and distinguish a "mutant" from a "non-mutant". This is particularly the case when "selection" is used to distinguish a "mutant" from a "non-mutant". Selection must, of course, involve a difference that the environment can distinguish between; that is, it must involve a phenotypic difference caused, at least in part, by the underlying genetic difference.

In the case of selective neutrality, you can *sometimes* use phenotypic difference (not all phenotypic difference results in a selective difference by the environment). But often the only way to actually observe a change is to look at changes in sequence (either at the protein or DNA level) that have no effect on phenotype. This can be done either by looking at a *change* in sequence (which means you know the original sequence), a *change* in a restriction enzyme or protease site, or a *change* in the intensity of binding of a probe. But in all cases, mutation involves being able to observe and detect a *change* from the original genetic state to a different genetic state or several different, yet equivalent, genetic states, depending on what sort of *change* you consider important.

Most mutational states of interest do not depend on knowing the sequence. For example, if I want to examine mutation from the genetic state of normal blood clotting to a genetic state of seriously defective blood clotting involving the hemophilia A gene locus and how frequently there is new mutation to the hemophilia A state, it would not matter to me, at least initially and not at all for detecting new mutations, if the new mutation involves a deletion or nonsense codon or a missense mutation. I may subsequently be interested in where in the hemophilia A gene there are missense mutations that cause near complete loss-of-function effects. That would tell me where functionally important aa'a are. I might be interested in finding mutations in the gene that have little or no effect because that would tell me where functionally less-important regions are.

But, in terms of *selective effect*, that is, the evolutionary effect, it doesn't matter if the mutation that leads to loss-of-function of the hemophilia A gene is in aa 23 or in aa 223. What matters is that loss-of-function often leads to the early death of males having a loss-of-function mutation. It is the rate of change from functional gene to non-functional that matters in evolution by selection.

[John Harshman]

If only Dr. Dr. understood that little bit.

> For
> example, if the discussion is about neutral fixation we may be
> interested only in mutations among junk DNA, which distinguish child
> from parent, and which are only counted when and if the child reaches
> maturity. In another context we may simply look at DNA duplication
> during mitosis. I don't think there's much difference between the two
> though.
>
> That said, I define "mutation rate" by the following "probability
> experiment":
>
> Pick a genomic location at random. Watch a duplication event. If the
> copy differs from the original, that's a mutation. Repeat many times
> and observe the long-run rate of mutations.
>
> To a reasonable approximation, the mutation product will be G whenever
> the pre-mutation type was A (because transitions predominate) and
> that's about 1/4. Slightly more accurately we could take also
> transversions into account which would probably make the answer even
> closer (slightly) to 1/4.

Nice. But I believe Dr. Dr. is actually referring to the mutation rate
at some particular site, and claiming that there are four possible
mutations at any single site.

[Charles Brenner]

We agree.

Since your reply is to my post, I might infer that in some way you
meant to disagree, and acting on that hunch I could then rebut
(obliquely) by picking up on "rate" (the other word in the phrase
"mutation rate") and discussing the definition of it's attendant,
"probability." But that would be really dumb if my hunch is wrong, and
would lead to one of those mysterious hidden-agenda discussions even
if it is right.

And the hidden argument would be pointless as well - in your
discussion with Alan, I think you are right because I think I had the
same reaction to some of his nonsense some months ago (plus external
reasons). However, my problem - which I was in a way hoping to goad
you to helping me with via my post quasi-sympathetic to Alan - is that
I can't pick up your discussion with him and follow it. I am
interested and would be grateful if one of you would briefly but
explicitly lay out the population genetic problem under discussion for
me as if I just walked into the room: Simply, what is being
calculated? I suspect Alan is incapable of giving a clear, simple and
unambiguous explanation. But possibly he does mean something, possibly
you have figured out what it is, in which case you might be prevailed
upon to set down a short orientation paragraph or sentence for those
like me who have a sense of occasionally visiting a long ongoing but
not quite clear argument.

[hersheyh]

On Friday, September 30, 2011 12:44:25 PM UTC-4, Inez wrote:

> On Sep 30, 8:56�am, Alan Kleinman MD PhD <klei...@sti.net> wrote:
> > The following are a compilation of responses to posts 951-975 to
> > prevent splinter threads. Sorry for any inconvenience.
> >
> > Greg Guarino �Aug 29, 7:06 pm
> > Newsgroups: talk.origins

> > From: Greg Guarino <gdgu...@gmail.com>

> > Date: Mon, 29 Aug 2011 22:06:17 -0400
> > Local: Mon, Aug 29 2011 7:06 pm
> > Subject: Re: The Theory of Evolution is Mathematically Irrational
> > Round 2
> >
> > On 8/29/2011 8:01 PM, Alan Kleinman MD PhD wrote:
>
> Snip
> >
> > The number of possible point mutations in a genome is equal to the
> > number of bases. There are four possible outcomes to any point
> > mutations. And are there 3^(6*10e9) possible combinations of bases or
> > 4^(6*10e9) possible combinations of bases?

Which would only matter if genomes were constructed by random assembly and only the one perfect genome were allowed to live. What does that number have to do with evolution?

> >
> When are you going to address the point that one of the 4 nucleotides
> is not a mutation? Can you not see that this is true? Given that a
> site must start with one or another nucleotide, the maximum number of
> changes possible is 3, not 4.

Not, of course, that dividing a *mutation rate* determined by other means by the arbitrary number 3 is any better than dividing a *mutation rate* determined by other means by 4 and claiming that one has pulled out a plum (idea) and exclaiming "What a good boy am I" makes it so.

[Just an amusing historical note, the original poem was a satire on Ambrose Philips, who wrote infantile poems for the young children of his aristocratic patrons. Writing infantile math and proclaiming it genius doesn't make it so.]

[hersheyh]

On Saturday, October 1, 2011 11:45:51 AM UTC-4, Charles Brenner wrote:

> On Sep 30, 3:32 pm, hersheyh <hers...@yahoo.com> wrote:
> > On Friday, September 30, 2011 4:32:46 PM UTC-4, Charles Brenner wrote:

A key feature, then, in observing an actual 'mutation' or 'change', is that you need to know what the starting state is and how the end state differs from that starting state. If you know neither or only one, then you cannot detect whether or not a mutation or change has occurred. This rather simple idea seems to elude the good Dr. Dr. He seems to think one can determine that a mutation has occurred without knowing anything about either the original or end state.

>
> Since your reply is to my post, I might infer that in some way you
> meant to disagree, and acting on that hunch I could then rebut
> (obliquely) by picking up on "rate" (the other word in the phrase
> "mutation rate") and discussing the definition of it's attendant,
> "probability." But that would be really dumb if my hunch is wrong, and
> would lead to one of those mysterious hidden-agenda discussions even
> if it is right.

Let me make a distinction, then, between "mutation rate" and "mutation probability". The two terms are, in important ways, not identical. If you have a state that you have determined to be the "mutant" state and you want to know the *rate* at which the original "non-mutant" state gets converted by random spontaneous (or induced) mutation to the "mutant" state, you do that by generating a population of non-mutant individuals (typically by growth from a non-mutant individual, in the case of clonal organisms, or non-mutant individuals in the case of sexually reproducing organisms) and determine the frequency of "mutant" states that occur in that population. If the mutant state is either neutral or deleterious, that frequency is often close to the rate of mutation when you sample from a large enough populations.

Because the binomial probability assumption that every trial has the same probability of producing a "mutant" is not exactly true because early "mutants" tend to cause "jackpots", we actually have a Luria-Delbruck distribution which skews right relative to a binomial probability distribution. That is, the mean, median, and mode are not identical and the mode is often a better measure of "mutation rate" rather than "mutation frequency", aka "mutation probability" in a population. We (meaning both the Dr. Dr. and myself, although I know it and the Dr. Dr. doesn't) are ignoring that complication and using binomial probability theory to determine the "mutation rate".

The "mutation rate" is the lowest possible mean *frequency* or *probability* of mutants in any population. It is the frequency one sees when replenishing lost mutants requires new mutation events.

However, *after* mutation occurs and depending on the environment, the frequency or *probability* of a mutant can dramatically change in one, a few dozen, or hundreds of generations if the "mutant" is beneficial. If the environment has changed, say by the addition of a toxin, the entire population of the original "non-mutant" individuals can cease to exist and only the few "mutants" survive and grow. In that case, in a single generation, one has gone from a mutant probability of the smallest possible frequency or probability that a living individual in the population is "mutant" to a state where *every* individual in the (now much smaller) population is a "mutant". In our example, that is going from a probability of a living cell being a mutant going from 10^-8 to 1.00 in a single generation.

When you do the multiplication of probabilities rule, it is important to realize the difference between the "mutation rate" and the "probability that a cell is mutant". In many cases, like my three step double-resistant cells, the third step involves a "probability of cell being mutant" of 1.00 for one of the mutants. Mindlessly using the "mutation rate" when you should be using the "probability that a cell is a mutant" can be extremely misleading. The probability that a cell is a mutant can depend on its past history of selection and/or chance and can be any value between the mutation probability and one.

[Alan Kleinman MD PhD]

The following are a compilation or responses to posts 976-1001 and
splinter posts. Sorry for any inconvenience.

John Harshman Sep 8, 4:15 pm

Newsgroups: talk.origins
From: John Harshman <jharsh...@pacbell.net>

Date: Thu, 08 Sep 2011 16:15:55 -0700
Local: Thurs, Sep 8 2011 4:15 pm

Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

> On Aug 4, 5:41 pm, "Vincent Maycock" <vam...@aol.com> wrote:
>> "Alan Kleinman MD PhD" <klein...@sti.net> wrote in messagehttp://groups.google.com/groups?as_umsgid=c26c3472-eef4-471d...@m6g2000prh.googlegroups.com...
>>>> On Jul 11, 9:19 am, John Harshman <jharsh...@pacbell.net> wrote:
>>>>> hersheyh wrote:

>>>>>> On Jul 8, 11:07 am, John Harshman <jharsh...@pacbell.net> wrote:
>>>>>>> Alan Kleinman MD PhD wrote:

>>>>>>>> Hersheyh is using a value of 30 generations to amplify the beneficial
>>>>>>>> allele, that s a catastrophic event where the entire population is
>>>>>>>> decimated and only a single tiny subpopulation remains.

>>>>>> That would be 30 population doublings to go from a population of 1 to
>>>>>> a population of more than 10^9 in an extreme case of selection
>>>>>> involving lethality for most of the population except the tiny
>>>>>> subpopulation. That, of course, is *selection* and even *extreme
>>>>>> selection*. But *you* were the one who always chose such extreme
>>>>>> selection, typically using some model of *artificial* selection using
>>>>>> toxins applied at high dosage by humans with the intent of wiping out
>>>>>> or drastically reducing the size of a population of organisms from a
>>>>>> particular organism in order to have your math work out properly.

>>>>>>>> Even using his
>>>>>>>> value of 30 generations per beneficial mutation amplification (or
>>>>>>>> what
>>>>>>>> hersheyh calls recovery), you can not do the accounting for John
>>>>>>>> Harshman s claim that there are 40,000,000 differences between humans
>>>>>>>> and chimpanzees in less than a million generations.

>>> snip
>>> Which in relative terms, is not that much. Does it bother you that chimps
>>> and humans are so similar, Alan?
>> Vincent, 70% of the genes in humans and chimpanzees produce different
>> proteins.
>....for a definition of "different protein" equalling "at least one
>different amino acid". To most people, cytochrome c is the same protein
>in humans, flies, and yeast, even though its sequence differs.

I wonder if your immune system would agree.

>> What makes you think that humans and chimpanzees came from a
>> common progenitor when so many genes differ and you have less than a
>> million generations to make this transformation of tens of thousands
>> of genes?
>Because a) we have strong evidence that it actually did happen and b)
>almost all of it could be accomplished by neutral evolution, and is in
>fact within the neutral expectation.

Repeating the same folklore over and over does not constitute strong
evidence. It is already clear that mutationandselectiondidn’tdoit. And
your argument about neutral evolution ignores the multiplication rule
of probabilities. John, why don’t you tell us how neutral mutations in
one family line are transferred over to an unrelated family line.

>> Do you realize how long it takes mutation and selection to
>> transform a single gene?
>That's your main problem: you won't let go of the idea that there is a
>single "mutation-and-selection-process", when we're talking about
>mutation but not selection.

It’s not my problem; in fact I use this principle in treating
infections by forcing the population to evolve to two selection
pressures simultaneously. Of course this mathematical and empirical
facts of life shows that your theory of evolution is mathematically
irrational. Tell us again how neutral mutations in one family line
find there way into an unrelated family line.

>> It is mathematically irrational to believe

>> that humans and chimpanzees came from a common progenitor less than a
>> million generations ago when you would have to transform tens of
>> thousands of genes in such few generations.
>Unless they are transformed by drift, eh?

The only thing you get from drift is flotsam and jetsam.

John Harshman Sep 8, 4:19 pm

Newsgroups: talk.origins
From: John Harshman <jharsh...@pacbell.net>

Date: Thu, 08 Sep 2011 16:19:28 -0700
Local: Thurs, Sep 8 2011 4:19 pm

Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

>>>> On Jul 13, 1:29 am, G<g...@nowhere.invalid> wrote:
>>>>> Alan Kleinman MD PhD <klein...@sti.net> wrote:
>>>>> [snip other stuff..]
>>>>>> You continue to be confused why I divide the mutation rate by 4. If
>>>>>> you use a mutation rate which give the frequency for which any
>>>>>> mutation occurs then you must divide that value by 4 to give the rate
>>>>>> at which a beneficial mutation would occur. If you use a mutation rate
>>>>>> which gives the frequency at which a beneficial mutation would occur,
>>>>>> you would not divide by 4. In my derivation of the probability
>>>>>> function, I use the mutation rate for which any change at the locus
>>>>>> would occur, not the rate at which a beneficial mutation would occur.
>>>>> In that case as the possible mutations are:
>>>>> A->C, A->G, A->T,
>>>>> C->A, C->G, C->T
>>>>> G->A, G->C, G->T,
>>>>> T->A, T->G, T->C
>>>>> You should divide by 12!
>>>> You evolutionists are more predictable than a broken clock, you are
>>>> wrong all the time. G, there are only 4 possible outcomes for a point
>>>> mutation at a particular locus, those 4 outcomes are A, C, G or T.
>>>> There are not 12 possible outcomes.
>>> Still clinging to that, eh? One of those four outcomes isn't a mutation.
>>> Which one isn't a mutation depends on the original base. If you don't
>>> know the original base, how do you know there's been a mutation at all?
>>> If A->A is a mutation, then the mutation rate is 1/site/generation, i.e.
>>> 100%.
>> It’s a fact of life that you don’t know what the original base was
>> before a random point mutation occurs, you only know that the outcome
>> from that mutation will be one of four possible bases.
>Don't you know that the outcome will be a base that's different from the
>one that's there now?

Can you tell us what the base was before the mutation occurred?

>> You don’t need
>> to know what the original base was to compute the probability of a
>> particular mutation occurring.
>Of course you do, even at the molecular level. For one thing,
>transitions are much more common than transversions. It's much more
>likely that C will change to T than that G will change to T.

Can you tell us how this was measured and why this happens? In fact,
give us a table of frequencies of mutations of one base to another.

>>>> That would be insane and thus fit perfectly with the rest of your
>>>> "math". G, 2 + 2 = 4, not 12. Now your bit of mathematical illogic
>>>> may impress a mathematically incompetent evolutionist like John
>>>> Harshman who has no idea how to apply the principles of probability
>>>> theory but it will impress few others.
>>> Do you understand that he was making fun of you? Probably not.
>> John, I find you evolutionists amusing when you make your serious
>> claims like reptiles can be transformed into birds by the mutation and
>> selection phenomenon. I find it particularly amusing when you claim
>> that selective evolution occurs more rapidly than neutral evolution
>> and then you claim that a couple hundred neutral mutations are fixed

>> every generation, generation after generation for hundreds of

>> thousands of generations when the selective evolution of a single
>> beneficial mutation takes hundreds of generations.
>You may find it amusing, but it's amusement occasioned by your own
>ignorance. I've explained all this many times before.

Then would you explain to us how hundreds of neutral mutations can be
transferred from one family line to an unrelated family line?

>> It’s weird
>> discussing hard mathematical science with mathematically irrational
>> evolutionist dogmatists. It’s like talking with someone with a drug
>> addictive personality.
>We all think that way of you. The difference is that we're right.
>Where's your hard math here, by the way?

I’ve already given you the hard mathematical science of mutation and
selection and substantiated this mathematics with empirical evidence.
On the other hand you give us rank and gross over extrapolation of a
model which describes fixation of one of two neutral allele and claim
that it happens a couple hundred times per generation, generation
after generation for hundreds of thousands of generations. The hard
math that argues against your mathematically irrational claim is the
multiplication rule of probabilities. Of course if you can explain how
hundreds of neutral mutations can be transferred from one family line
to an unrelated family line, we would be amused by your folklore.

John Harshman Sep 8, 4:25 pm
Newsgroups: talk.origins
From: John Harshman <jharsh...@pacbell.net>
Date: Thu, 08 Sep 2011 16:25:14 -0700
Local: Thurs, Sep 8 2011 4:25 pm

Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

>> On Aug 4, 4:37 pm, John Harshman <jharsh...@pacbell.net> wrote:
>>> Alan Kleinman MD PhD wrote:

>>>> On Jul 11, 9:19 am, John Harshman <jharsh...@pacbell.net> wrote:
>>>>> hersheyh wrote:

>>>>>> On Jul 8, 11:07 am, John Harshman <jharsh...@pacbell.net> wrote:
>>>>>>> Alan Kleinman MD PhD wrote:

>>>>>>>> Hersheyh is using a value of 30 generations to amplify the beneficial
>>>>>>>> allele, that s a catastrophic event where the entire population is
>>>>>>>> decimated and only a single tiny subpopulation remains.

>>>>>> That would be 30 population doublings to go from a population of 1 to
>>>>>> a population of more than 10^9 in an extreme case of selection
>>>>>> involving lethality for most of the population except the tiny
>>>>>> subpopulation. That, of course, is *selection* and even *extreme
>>>>>> selection*. But *you* were the one who always chose such extreme
>>>>>> selection, typically using some model of *artificial* selection using
>>>>>> toxins applied at high dosage by humans with the intent of wiping out
>>>>>> or drastically reducing the size of a population of organisms from a
>>>>>> particular organism in order to have your math work out properly.

>>>>>>>> Even using his
>>>>>>>> value of 30 generations per beneficial mutation amplification (or what
>>>>>>>> hersheyh calls recovery), you can not do the accounting for John
>>>>>>>> Harshman s claim that there are 40,000,000 differences between humans
>>>>>>>> and chimpanzees in less than a million generations.

>>>>>> The 40,000 differences are not all at the same nucleotide site.
>>>>>> Indeed, the average human sperm or egg (sperm more than eggs) have
>>>>>> 30-200 mutations relative to the sperm or egg maker.

>>>>>>> That's because one involves selection and the other involves neutral
>>>>>>> evolution.

>>>>>> Well, duh. Then why do you insist on applying math that requires
>>>>>> simultaneous or sequential mutation and strong selection?
>>>>> Because that was me and you seem to be arguing with Kleinman.
>>>> John, the probability function I derived for the computing the
>>>> probability of two beneficial mutations (or as r norman pointed out
>>>> any two mutations, detrimental, neutral or beneficial) can be used to
>>>> compute the probabilities whether these mutations occur sequentially
>>>> or simultaneously.
>>> Don't care.
>> Of course you don’t care. Why would an evolutionist actually want to
>> understand how mutation and selection works? If an evolutionist
>> actually understood how mutation and selection works, he would
>> understand that he believes in a mathematically irrational belief
>> system.
>No, the reason I don't care is that it's irrelevant to the questions
>under consideration.

The only thing you care about is ignoring the multiplication rule of
probabilities because as soon as you stop ignoring that mathematical
principle governing the joint probabilities of events, it becomes
obvious that your theory of evolution is a mathematically irrational
belief system.

>>>> I don t recall you applying any mathematical
>>>> principles to the mutation and selection phenomenon. What I do recall
>>>> you claiming is that there are 40,000,000 differences between human
>>>> and chimpanzee genomes. Do you care to tell us how many of these
>>>> differences are neutral or selective?
>>> I have, many times. You don't pay attention. Approximately 40,000,000 of
>>> them are neutral. The selective fixations are a tiny percentage of the
>>> total.
>> And you have also said “Nobody claims that drift is faster than
>> selection. Quite the reverse.” And in your mathematically irrational
>> beliefs when it takes hundreds of generations to fix a single mutation
>> by selection you then claim that a couple hundred neutral mutations
>> fix every generation, generation after generation for hundreds of
>> thousands of generations. I certainly do pay attention to your
>> mathematically irrational claims.
>You seem to ignore this every time I try it, but let's see if this time
>works. Which delivers more water: a 3-inch diameter pipe with water
>traveling at 10 feet per second or a 3-foot diameter pipe with water
>traveling at 1 foot per second? In which pipe is the water moving
>faster? Does the speed of the water tell you everything you have to know?

John, tell us how you deliver neutral mutations from one family line
to a totally unrelated family line? What kind of pipe do you have that
does this delivery of neutral mutations throughout the population?

>>>>>> The
>>>>>> assumptions of neutral mutation do not involve the assumptions of
>>>>>> selection nor does change in genomes in humans or their ancestors
>>>>>> *require* that mutations accumulate sequentially one at a time.

>>>>>>> And one involves a single allele while the other involves the
>>>>>>> entire genome of 6 billion bases.

>>>>>> Yes. And yet you apply mathematics that only makes sense if one
>>>>>> assumes that the 40 million differences (20 million per lineage)
>>>>>> involved sites that were prespecified, changes that were strongly
>>>>>> selected for, and organisms that did not engage in genetic exchange
>>>>>> and recombination. None of those assumptions are true.
>>>>> Again, that was me. Watch your attributions.
>>>> What I would like to hear from either of you evolutionists is a
>>>> reasonable explanation how neutral mutations can spread through a
>>>> population faster than beneficial mutations which have selection
>>>> assisting in the spread of these beneficial mutations.
>>> They can't. The don't. After all this time, you still have no idea how
>>> neutral evolution works. Sad.
>> Then why do you claim that a couple of hundred neutral mutations fix
>> every generation? You evolutionists always contradict yourself but
>> that’s what happens when you make mathematically irrational claims.
>> It’s sad for those suffering from diseases subject to the mutation and
>> selection phenomenon, a phenomenon that evolutionists have failed to
>> understand or teach the basic science and mathematics which describes
>> its behavior.
>It never ceases to amaze me that you can't understand this very simple
>point. Please try again with the two pipes just above.

John, just what are you smoking in those pipes? Could you tell us how
your pipes deliver neutral mutations from one family line to a
different unrelated family line?

>>>> And it is
>>>> already clear that it takes hundreds of generations to spread a single
>>>> beneficial mutation through a population and yet you want us non-
>>>> believers in your mathematically irrational theory of evolution to
>>>> accept that neutral mutations spread through a population at a rate
>>>> that s not just a little faster than what selection can do to spread a
>>>> beneficial mutation through the population but that on average dozens
>>>> of neutral mutations have spread through populations generation after
>>>> generations for hundreds of thousands of generations.
>>> No such thing has happened. I despair of getting you to understand the
>>> least little thing about neutral evolution. Random changes in allele
>>> frequency in any one generation will be slight. The mutation that
>>> becomes fixed in this generation was a tiny bit short of fixation in the
>>> previous generation, and has probably fluctuated in frequency for
>>> millions of years until that point. The mutation that becomes fixed in
>>> this generation is one of billions of mutations that occurred in the
>>> same generation, millions of years ago. Only a few of those mutations
>>> ever became fixed and the rest were eliminated, with the highest single
>>> probability of loss being in a single generation. You won't read or
>>> understand this, apparently.
>> Don’t despair, watching you trying to blah, blah, blah your way
>> through your mathematically irrational claims is actually an
>> interesting experience. It’s like watching people who believe that the
>> earth is flat seeing a picture of the earth from space. They go into a
>> denial and self deception mode. On one hand, you claim that neutral
>> evolution is slower than selective evolution but on the other hand you
>> claim that hundreds of neutral mutations are fixed every generation
>> when the mathematical and empirical evidence show that selectively
>> beneficial mutations take hundreds of generations to spread through a
>> population. It’s weird to watch you go through your gyrations, it’s
>> like you are addicted to evolutionism. Perhaps you should join
>> Evolutionists Anonymous.
>So you have no response?

Sure I do, you are claiming that these neutral mutations are sweeping
through the population. How do they sweep from one family line to
another unrelated family line? Or are you going to claim that this
question is irrelevant?

>>>> You can t
>>>> properly explain how mutation and selection works but you can
>>>> speculate that drift causes the spread of neutral mutations through
>>>> entire populations at rates thousands of times faster than selection
>>>> can spread a beneficial mutation.
>>> Nobody makes any such claim. You know and understand nothing.
>> You see what I mean. On one hand you claim that neutral evolution is
>> slower than selective evolution yet you can claim that hundreds of
>> neutral mutations are fixed every generation when it takes hundreds of
>> generations to fix a single selectively beneficial mutation.
>> Evolutionism is a psychotic state.
>Or perhaps you just don't understand the water-pipe analogy?

There is a little more than water in your pipes.

>>>>>>>> This is why these
>>>>>>>> evolutionist turn to the junk science of the concept of drift to
>>>>>>>> account for all these differences.
>>>>>>> What exactly is wrong with the concept of drift. Do you deny that it
>>>>>>> happens? If so, what prevents it?
>>>>>>>> Do you want to tell us what 30
>>>>>>>> neutral mutations have shown up in your genome as well as the rest of
>>>>>>>> the world s population in this generation?
>>>>>>> Nobody makes that claim. All you do here is reveal your gross
>>>>>>> misunderstanding of neutral evolution.

>>> Hey, look. Here we are, five posts on, and you're still making the same
>>> absurd misrepresentation. Is it any wonder nobody has any respect for you?
>> John, what you don’t have respect for is hard mathematical logic and
>> empirical evidence. Both these elements of scientific analysis are
>> enemies to your mathematically irrational belief system.
>I will devote my life to getting you to understand one simple feature of
>neutral evolution: that if there are lots of mutations that spread
>slowly and have a low probability of fixation, it's still possible that
>more of them may be fixed per generation than a very few mutations that
>spread quickly and have a high probability of fixation.

I’ve never seen such devotion to a mathematically irrational belief
system. How do neutral mutations spread slowly or otherwise from one
family line which has the neutral mutation to another unrelated family
line which doesn’t have the neutral mutation?

hersheyh Sep 8, 8:53 pm
Newsgroups: talk.origins
From: hersheyh <hershe...@yahoo.com>
Date: Thu, 8 Sep 2011 20:53:01 -0700 (PDT)
Local: Thurs, Sep 8 2011 8:53 pm

Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

> [snip]

>> >>> Perhaps this is a good time
>> >>> for me to go over the fact that dice rolling is a very good metaphor
>> >>> for the mutation and selection process.
>> >> Only if the die has a few billion faces, almost all of which have the original allele on them. (the rest wouldn't be >equally distributed either, would they?)
>> > Greg, the die has only four faces for a point mutation, A, C, G and T.
>> > If you think the die has billions of faces why don t you tell us what
>> > a few of them are?

>The die, to properly produce the ratio of the 'event' to 'trials', which is what your dice analogy does, has to have as many >faces as the minimum number of 'trials' needed to produce one 'event'. In dice, that would be six faces with only one of >those faces being the 'event'; that is what will give you the 1 to 6 ratio. [The assumption is that the die are fair.] The >'event' in our case is a *mutation*, which is any change from an identifiable non-mutant genetic state to an identifiable >different mutant state. That does mean, given a ratio of mutant (the 'event') to trials of 10^-8 that the "die" have 10^8 >faces, all but one of which is labelled not-mutant and the other face being labelled "mutant". When you roll such a die, >the probability that it will come up "mutant" is 10^-8, isn't it?

Hersheyh, how did you get so confused on this topic? Here is a quote
from “Advanced Engineering Mathematics” by Kreyszig. “The statement “E
has the probability P(E) then means that if we perform the experiment
very often, it is practically certain that the relative frequency f(E)
is approximately equal to P(E)” If we are flipping a coin and do it a
large number of times, half the time we will get heads and half the
time we will get tails. If we are rolling a die many times, 1/6 the
time we will get a 1, 1/6 the time we will get a 2 and so on.

In the mutation and selection phenomenon, the trial is the mutation.
Consider if the mutation rate was 0 and the DNA replicated perfectly
each time. No mutations gives no trials. The mutation rate is simply
the frequency which the die is rolled at a particular locus and with a
mutation rate of 10^-8, the die is not rolled at that locus very
often. That’s why you need such large populations with this tiny
mutation rate. You need a large population like 10^9 so that at least
a few members will roll the die at that locus. But when those members
do roll the die, there are four possible outcomes, A, C, T or G. I
know this sticks in the craw of evolutionists because you can’t have a
mutation from the original base to the original base but you don’t
know what the original base is before the point random mutation
occurs. You can only say with certainty after the mutation occurs it
will be one of the four bases. There are not 10^8 faces on the die,
there are four faces on the die and the die is only rolled once in
10^8 replications when the mutation rate is 10^-8.

>> Nearly all would be the original base, wouldn't they? The rest (a
>> handful) would be labeled with the other bases, in numerical proportion
>> to their empirically-determined probability. Surely you don't imagine
>> that a four-sided die, with a 25% chance of landing on any letter, is a
>> good model.

>Actually, as a creationist, he probably does think that because he thinks that genes are assembled by scratch by >randomly choosing each nt from equimolar pools of the four nt's. Yeah, I know that is a ridiculous description of >evolution, but the "747 formed by a tornado" scenario seems to be stuck in the creationist brain. It is what allows them to >say that a 900 nt gene has the probability of forming "randomly" of 1 in 4^900. Pure GIGO.

Don’t be silly hersheyh, I don’t believe in abiogenesis. The concept
of abiogenesis is more mathematically irrational than the theory of
evolution and the theory of evolution is really mathematically
irrational.

>[snip]

> >> So for what must be the 100th time, suppose a population of animals migrates to a colder climate. Or the climate simply gets colder where they are. Suppose the climate change is enough to affect the survival chances of some individuals, but does not kill off most of the population. Does that seem an unrealistic scenario to you?
> > It s a totally realistic scenario.
>> >> Suppose further that several different genetic changes can *each* confer some advantage in the changed climate. >Does that seem unrealistic?
>> > The first thing that will happen is that members of the populations
>> > which do not have sufficient fitness to reproduce will fail to pass
>> > their genetic information on to the next generation.

>What would happen is that the frequency of *all* such beneficial traits would increase at the expense of the original w.t. >alleles. *All* of them. If that is five unlinked genes that can change so as to be more fit than the individuals with no >changes, any organism with *any* of the altered alleles in *any* of the five genes have a selective advantage over >individuals with no change. Eventually, you will have new combinations of these altered genes.

All the empirical evidence shows that doesn’t happen. Of course if you
can find an example where it does happen, post your evidence, I might
as well get in a comfortable chair for this wait because it’s going to
be a long one.

>> > The members of
>> > the population which have sufficient fitness to reproduce will pass on
>> > their genetic information to the next generation and their will be
>> > mutations in these replicators. Some mutations will be detrimental,
>> > some mutations will be neutral and some mutations will be beneficial
>> > for the particular environment.

>And this is relevant how?

>> >> Now tell us why several of those genetic changes could not spread simultaneously. And once they have spread, tell >us why they could not be combined in the progeny of individuals who have only one of the beneficial alleles.
>> > Mutations must accumulate through lines of common descent. It should
>> > be clear to you that when recombination is not involved;
>> Surely you understand that in animals (like chimps and humans)
>> recombination IS involved.

>Apparently not. He has never even tried to present a scenario with eucaryotic organisms.

You really don’t pay attention. Besides posting examples of
combination selection pressures with HIV, I’ve also posted examples of
combination selection pressures with malaria, mosquitoes, rodenticides
and herbicides. All these life forms do recombination and all are
stifled in the mutation and selection process when combination
selection pressures are applied to these populations. Or aren’t you
aware that malaria, mosquitoes, rats and weeds are eukaryotic? All
these examples including HIV do recombination. Hersheyh, would you
write the probability function for random recombination?

>> > the only way
>> > you can get a sequence of beneficial mutations is for them to all
>> > happen simultaneously on a single individual or to accumulate one by
>> > one starting on a progenitor and accumulating on descendents over
>> > generations.

>That is more or less true if you are talking about changes in genetically linked sequences. Or in clonal organisms like >bacteria (most of the time), most viruses, and a few eucaryotes. It is false if you are talking about changes occurring in >different unlinked genes in eucaryotic organisms.

Would you please give an empirical example of your claim?

>> You continually belabor the obvious as if there is someone who doesn't
>> understand it.

>> > With recombination, you add the possibility of lateral
>> > transfer of a beneficial mutation but that event has probabilities
>> > associated with this occurrence. So let s say your population of
>> > animals starts accumulating beneficial mutations for your cold
>> > environment. One member gets a mutation which gives thicker fur.
>> > Another member gets a mutation which allows for fat storage, another
>> > member gets a mutation that gives beneficial effects on metabolism,
>> > another member gets a beneficial mutation which affects size giving a
>> > better surface to volume ratio for the environment. There are any
>> > number of mutations that are occurring throughout the population.
>> Firstly, do you have any doubt that scenarios like this exist?

>> How
>> do you recombine all these traits into one descendent? Do the math.

>Any organism which has *any* of those traits is selectively favored. *All* of those traits can increase in parallel in >frequency in the population relative to the w.t. organism with none. Eventually some of them will be frequent enough to, >after recombination, produce organisms with more than one trait. That organism will now have two such traits and have >a selective advantage over organisms with only one.
>Again, the frequency of such organisms can easily be determined by using a Punnet square.

The Punnett square is used to compute the outcome from a breeding
program not random recombination. And you keep making the claim that
“traits” can increase in parallel. Give us a real, measurable and
repeatable example where that happens with the mutation and selection
process, not your ever present hypothetical examples.


Greg Guarino Sep 9, 8:44 am
Newsgroups: talk.origins
From: Greg Guarino <gdguar...@gmail.com>
Date: Fri, 09 Sep 2011 11:44:03 -0400
Local: Fri, Sep 9 2011 8:44 am

Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

On 9/8/2011 6:34 PM, Alan Kleinman MD PhD wrote:
>>> > Because there are a lot more of them. Today, approximately 25 million
>>> > *new* neutral mutations entered the human population, in newborn
>>> > infants. In somewhat less than 18 years, some of those neutral
>>> > mutations will start to spread to other people, along with some of the
>>> > 25 million mutations that entered the human population yesterday, and
>>> > the 25 million from the day before that, etc. Meanwhile, mutations from
>>> > past ages are spreading as we speak. One of the infants born today with
>>> > his share (50 or so) of new neutral mutations was also bequeathed
>>> > several hundred thousand other prior neutral mutations which are still
>>> > drifting to fixation or extinction. I have no idea how many different
>>> > neutral mutations there currently are in humanity, but there are
>>> > estimated to be between 10 and 30 million that have spread to at least
>>> > 1% of the population.
>> Mark, you claim to be an engineer. Compute for us the joint
>> probability of two neutral mutations being fixed in a population.
>I've become convinced that you don't actually know how to do this
>calculation. You reflexively use the multiplication rule, whatever
>question is at issue.

Greg, I have derived the formula for this calculation. It’s the same
probability function used for computing the probability of two
beneficial mutations occurring. The only difference is that with
neutral mutations you won’t have selection amplifying the
subpopulation for the first mutation and so the probability of the
second mutation occurring on a member with the first mutation is very
low. And of course I use the multiplication rule, that’s how you
compute the joint probability of two random events occurring.
>Suppose two cities run separate lotteries, but with the same rules. You
>pick some combination of numbers for each "ticket". Let's say the odds
>of any particular ticket winning are 10^-6.
>Suppose you buy one ticket for each lottery. What are your chances of
>winning both? 10^-12, right? But what is the probability of there being
>at least one winning ticket in each lottery, assuming 500,000 tickets
>are sold for each? Do you recognize that that is a different
>mathematical question?

Sure I recognize the difference. In one case you computing the
probability an individual winning both lotteries and the second case
you are looking at the probability of any two people each winning one
of the lotteries. For the mutation and selection phenomenon to work,
the mutations can’t occur on just any member of the population, they
have to occur on members who would benefit from the particular
mutation. And if more than a single mutation is required for
adaptation, then a progenitor gets the first mutation which improves
fitness and his descendents amplify over generations until there are
sufficient number of descendents so that there is a reasonable
probability that the next beneficial mutation will occur on one of the
descendents with the first beneficial mutation. The mutations can’t
just occur anywhere in the population, the mutations must occur on
members who would benefit from the mutations. Mutation and selection
requires that you keep the lottery winnings in the family.

>Without the constraint that it must be YOUR two tickets, the odds are a
>great deal better, aren't they? We don't use the multiplication rule,
>because, among other things, there is no linkage between the two lotteries.

No Greg, winning of both lotteries still are random independent events
but in your second case you have hundreds of thousands of trial
takers, many more tickets are bought.

>Let's go further. Suppose there are 100 such lotteries. Do you think the
>appropriate math to predict how many of the lotteries will produce
>winners involves raising an individual ticket's winning probability to
>the hundredth power? Considering that there *are* in fact hundreds of
>lotteries and hundreds of winners, you might want to rethink that.

Greg, it’s you who needs to rethink that. If you want to compute the
probabilities correctly, you need to consider how many trials are done
(tickets bought) and the probabilities of each individual lottery.
Like I said above, mutation and selection is like a lottery but you
have to keep the winners in the family. Not anyone can win the
mutation and selection lottery, the winners have to those who get
increased fitness and not every mutation gives increased fitness.

>>Then
>> when you do that calculation, compute the joint probability of dozens
>> of neutral mutations being fixed in a population every generation,
>Each one is in effect a separate "lottery" with a low probability, but
>with an enormous number of entry "tickets". Why would the number of
>lotteries affect the chances of a some of them having winners? (here we
>need to depart from actual lotteries, which presumably compete for
>limited contestant dollars)

There are many lotteries going on all the time with large numbers of
people buying tickets. Only a small number are winners of a single
lottery and a much, much smaller number of ticket buyers are winners
of two lotteries. The mutation and selection process has its own
particular method of improving the probabilities of a lottery winner
(or descendent of a lottery winner) winning another lottery. If you
understand what populations must do to win two lotteries, it is very
easy to disrupt this process.

When the mutation and selection phenomenon is working correctly, only
certain members are even valid players in the lottery. First these
members need sufficient fitness to reproduce despite the selection
pressure. Then these members must be candidates for a beneficial
mutation or multiple beneficial mutations. If they are candidates for
the mutation and selection process, these members and their
descendents must find a sequence of beneficial mutation and
amplification of beneficial mutations cycles in order to accomplish
the evolutionary cycle. Anything which disrupts the amplification
process stifles the mutation and selection process. This is why
combination therapy works for the treatment of HIV.


hersheyh Sep 9, 11:59 am
Newsgroups: talk.origins
From: hersheyh <hershe...@yahoo.com>
Date: Fri, 9 Sep 2011 11:59:21 -0700 (PDT)
Local: Fri, Sep 9 2011 11:59 am

Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

>> On Aug 10, 11:29 am, hersheyh <hers...@yahoo.com> wrote:
>> > On Thursday, August 4, 2011 2:24:23 PM UTC-4, Alan Kleinman MD PhD wrote:
>> > > On Jul 7, 1:31 pm, hersheyh <her...@yahoo.com> wrote:
>> > > > On Jul 5, 8:10 am, Alan Kleinman MD PhD <kle...@sti.net> wrote:
>> > > > > On Jun 3, 12:52 pm, hersheyh <her...@yahoo.com> wrote:
>> > > > > > On Jun 2, 8:42 pm, Alan Kleinman MD PhD <kle...@sti.net> wrote:
>> > > > > > > On May 19, 12:31 pm, Nashton <n....@no.ca> wrote:
>> > > > [snip]
>> > > > > > I wish you would stop using the term "beneficial mutation" to refer to
>> > > > > > antibiotic resistance alleles. Those are better referred to as
>> > > > > > "resistant to A" rather than "beneficial" because they are only
>> > > > > > beneficial in a particular selective environment (ones with A). In
>> > > > > > other environments the same variant may be either "neutral" or
>> > > > > > "detrimental" relative to the w.t. individual.
>> > > > > This issue is only confusing for those who don t understand that a
>> > > > > mutation is beneficial only in the context of the selection conditions
>> > > > > imposed on the population. You are the one introducing confusion when
>> > > > > you claim in your calculations that mutations are either beneficial or
>> > > > > not beneficial by using a binomial probability function.
>> > > > We are talking about a binomial factoring. Specifically the rate of
>> > > > mutation from sensitive to A to resistant to A. There are two
>> > > > possibilities: 'resistant to A' and 'not-resistant to A' (aka,
>> > > > sensitive to A). That is a "binomial" statement. And it doesn't
>> > > > pretend or imply that resistant to A is always "beneficial". It
>> > > > simply specifies what the mutation is and what it is not. As in a
>> > > > binomial factoring. You know, 'event' and 'not-event', 'heads' and
>> > > > 'not-heads', '6-pips' and 'not-6-pips'.
>> > > Mutation A is the event, not the selection condition.
> > > The event is a mutation for which one can distinguish the new genetic state from the old one. The way we can > > > distinguish 'resistant to A' from 'sensitive to A', which are two genetic states is by the phenotype that the genotypes > > > produce *when* they are tested. Are you claiming that the mutation to A-resistance is NOT fundamentally a genetic > > > change from the genetic state of A-sensitive? The mutation(s) that produces A-resistance from the A-sensitive state need > > > not be at a specific nucleotide site (several different mutations at different sites can produce the result). Even if the > > > mutation(s) that produces A-resistance is at a single nucleotide site, we cannot know whether the A-resistance can > > > arise only when a specific n.t. change occurs or whether all three produce the effect or only 2 of the 3 produce A-> > > resistance. We know none of that since we are not observing where the mutations occur (1 site or many) and which > > > mutations produce the effect. But we

*do* describe what we *are* using to test the *genetic change* that is behind the *phenotypic* change we can see.


>> You can’t necessarily distinguish the new genetic state from the old
>> genetic state phenotypically, you can only distinguish the change by
>> sequencing.
>Being able to empirically identify the nt present at a site is a "phenotype". It is "observed" by some form of sequencing. > But *we* (meaning anyone that has ever taken and understood an undergrad genetics class) are not using sequence to >identify a mutant genetic state. *We* are using 'mutation' to describe a genetic change that produces a specific >phenotype (antibiotic resistance) from a different original specific phenotype (antibiotic sensitive). By *your* argument, >geneticists cannot determine that a phenotypic change is due to a change at the genotype level unless we sequence. > That would be a surprise to the generations of geneticists that existed before the 1980s. Biologists have been able to >identify genetic variants since before Mendel, although they did not call these variants "mutants" until Hugo DeVries >coined it to describe heritable (non-point mutation; the changes were actually chromosomal mutations) changes in the >Evening Primrose in 1901, when he published _Die Mutationstheorie

_. And,
>of course, they were able to follow the Mendelian pattern of simple identifiable allelic changes after Mendel's >rediscovery.
>You essentially are telling us that all this previous history of what genes and mutation are should be tossed out the >window.

The gold standard for identifying a nucleotide at a particular locus
is genetic sequencing. Before DNA could be sequenced, people studying
genetics were limited to observing phenotype changes to determine when
a mutation occurred but the science has advanced and you refuse to do
the advancement. What I am telling you is that the Poisson
distribution is the wrong mathematics to describe the mutation and
selection phenomenon and you are failing to recognize how the
multiplication rule of probabilities dominates the joint probability
of events in the mutation and selection phenomenon.

>> What I am stating is that when a point mutation occurs at
>> a locus, you have four possible bases which can occur at that locus.
>As has been pointed out many times to you, but you appear to be too dense to understand it, a point mutation occurs >when, and only when, there is a *change* of the original nt at that site to one of the three others. Mutation requires >*change*, not the same thing. You do not have *change*when a C at a particular site produces a C in that site in its >progeny. C to C is a non-mutant event and one that happens almost all the time (in our example, non-mutation happens >with a frequency of (1 - 10^-8)). Moreover, the probability of *change* is not equal even for the three possible *changes* >(mutation means "change", not existence of a site). That alone means that division by 4 is GIGO nonsense. Moreover, >it is always possible that some of the possible nt changes, even at a site, do not produce any change in phenotype.

If you are so smart hersheyh, tell us what the base was before the
mutation occurred. But you are not so smart because you can’t. That’s
why when you formulate the mathematics, you must allow for all four
bases as possible outcomes when a point mutation occurs because that’s
the only thing you know with certainty is that after a point mutation
occurs, you only know for sure that it will be one of the four bases.
Someday you might learn how to actually do a calculation using
probability theory rather than plugging numbers into the wrong
probability distribution.

>> The change from one base to another does not imply that the change
>> will be beneficial.
>Well, duh. That is because the terms "beneficial", "neutral", and "detrimental" are conditional and are descriptions of the >effects of particular genetically caused phenotypes. That is why I use the correct description of "antibiotic-resistant" or >"antibiotic-sensitive" to describe the different genetic states. Those are the genetic states of the cell described whether >that cell is in media with an antibiotic where being resistant is "strongly beneficial" or is in an environment without the >antibiotic where it is likely that the same genetic state is "neutral" or "weakly detrimental". Unless you are claiming that >most of the time antibiotic resistance is an environmentally induced or non-genetic state.

And this is why you can not properly formulate the mutation and
selection phenomenon as a strictly binomial process. The mutation and
selection process is more than a beneficial or not beneficial mutation
process. You are failing to make this distinction. It is you that is
claiming that antibiotic resistance is already present in the
population before the toxin is ever introduced.

>>> The change can be neutral or detrimental as well.
>>>The simple observable fact of *change* is insufficient to determine whether that *change* is beneficial, neutral, or >>>detrimental. You also need to know the environmental conditions. Again, applying these terms can only be done >>>empirically by examining the differential reproductive success of the identifiable traits in pairwise comparisons in a >>>specified environment.
>> The effect of selection on that change will only be identifiable based
>> on the reproductive capabilities of that member for the given
>> environmental conditions. If the change is beneficial, this will be
>> seen in the increase in subpopulation size with this beneficial
>> mutation, that is the change will be amplified.
>Again, the *change* is not inherently 'beneficial'. It is only beneficial when you describe the specified environment. > Using the word "beneficial" without describing the environment it is beneficial in is intentionally misleading. Antibiotic->resistance is not a "beneficial mutation" unless you add the phrase "in environments with antibiotic" each and every time. > If antibiotic resistance is *also* "beneficial" in the absence of antibiotic (likely not the case), you can use the phrase "in >environments with or without antibiotic".

You are only misled by your confusion of how the mutation and
selection phenomenon works. Populations have no trouble identifying
whether a particular mutation is beneficial, neutral or detrimental.
Populations also don’t need to be instructed on the selection
conditions they are forced to respond to. You are having trouble
understanding the mathematical behavior of populations when they are
responding to selection conditions.

>> On the other hand, if

>> the change is neutral or detrimental, that will be reflected in the
>> subpopulation size as staying relatively constant or decreasing over
>> generations respectively.
>Only if you *specify* the environment. When I use "antibiotic-resistant" to refer to a genetic and phenotypic state, you >automatically know the condition in which that variant is "beneficial".

I’m the only one posting on this thread who gives empirical examples
which “specify” the environment and the populations’ response to the
environment. On the other hand, you claim that mutation and selection
occurs in parallel without ever specifying the environment or
providing any measurements. Instead, evolutionists claim that reptiles
turn into birds and humans and chimpanzees come from a common
progenitor without ever specifying the environment which would cause
such a massive genetic transformation. This is why evolutionists have
to come up with the junk science of neutral evolution. Hersheyh, you
are in dire need of training in the hard mathematical sciences, your
indoctrination into evolutionism just doesn’t cut it.

>> > Mutation A is defined as the change from a genetic state which produces a cell resistant to antibiotic A from a cell > >> which was sensitive to antibiotic A. Again, mutation means change. In order to identify change, you have to be able to >> > identify both the start point (state before change) and the changed state. In our case, A-sensitive is the starting genetic >> > point and A-resistance is the changed genetic state.
>> Not necessarily so. Mutation A can be beneficial and give improve
>> fitness to reproduce for that member but mutation A can also be
>> neutral or detrimental. You measure that effect by changes in
>> subpopulation size with the particular mutation.
>You identify antibiotic-resistant cells by virtue of their resistant to (certain specified levels of) the antibiotic as opposed to >the sensitivity of the original cells to that level. You do not identify antibiotic resistance by sequencing the entire genome >and looking for changes in nt sequence. How do you plan to identify cells with a genetic mutation that causes the cell to >be antibiotic resistant in your world? Would you identify a mutant white-eyed fruit fly (red-eye is the w.t.) by asking a >blind man to do it visually? Or would you sequence the entire genome to identify sequence differences first? Me. I >would, like Thomas Hunt Morgan, look for white eyes to identify the white-eye mutants (this was the first sex-linked >mutation found in Drosophila, in 1910).

Apparently you are blind to genetic sequencing because that is the
most accurate way of identifying an error in genetic replication.

>In this case, like in the case of cystic fibrosis and unlike achondroplastic dwarfism, there are a number of different alleles >of the gene that can produce the same mutant phenotype. Some are deletions or frameshifts. Others are point >mutations at different sites in that gene. I may, after identifying the gene, sequence it and all the various mutations in >that gene that produce an

And Weinreich’s experiment identified several different variants of
the highly resistant beta-lactamase bacteria and these variants were
identified by genetic sequencing. And not only were the variants
identified, the sequence in which the mutations had to occur was
identified as well. You don’t do this type of measurement by simply
identifying a phenotype change, you must sequence the DNA. You are
teaching genetics from the 19th century. Hersheyh, you need to bring
your teaching up to the 21st century.


Inez Sep 9, 12:42 pm
Newsgroups: talk.origins
From: Inez <savagemouse...@hotmail.com>
Date: Fri, 9 Sep 2011 12:42:33 -0700 (PDT)
Local: Fri, Sep 9 2011 12:42 pm

Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

On Sep 9, 7:59 am, Alan Kleinman MD PhD <klein...@sti.net> wrote:
>> On Aug 10, 1:45 pm, Inez <savagemouse...@hotmail.com> wrote:> On Aug 4, 4:05 pm, Alan Kleinman MD PhD <klein...@sti.net> wrote:
>> > <snippers>
>> > > What I would like to hear from either of you evolutionists is a
>> > > reasonable explanation how neutral mutations can spread through a
>> > > population faster than beneficial mutations which have selection
>> > > assisting in the spread of these beneficial mutations.
>> > You are tediously thick headed. No one made that claim.
>> You had better tell that to John Harshman because he has claimed that
>> a couple hundred neutral mutations are fixed every generation,

>> generation after generation for hundreds of thousands of generations.

>That is not a claim that neutral mutations spread quickly. A very few
>neutral mutations happened a very long time ago, and very slowly they
>spread through the population. Many many many years later they become
>fixed. Every generation some become fixed, but the original mutations
>were long ago.

Inez, John Harshman didn’t say a “very few”, he said a “couple
hundred” and this was every generation. This is the kind of
evolutionist nonsense required to explain the tens of millions of
genetic differences between humans and chimpanzees when you only have
500,000 generations to do the transformation.

>Do you not realize how stupid you look by being unable to understand
>this? It's been explained to you time and time again. Can you really
>not get it? A neutral mutation that is fixed in this generation was
>99.99999999% fixed in the previous one, 99.999999998% fixed in the one
>before that, and so on back for millions of years. It's not that
>complicated. If you disagree, at least disagree with what people are
>saying.

Inez, don’t you realize how stupid evolutionists look with all the

multidrug resistant microbes, multiherbicide resistant weeds,
multipesticide resistant insects and less than durable cancer

treatments due to the evolutionist failure to properly describe
mutation and selection? So if you are going to claim that neutral
mutations spread through a population, tell us how a neutral mutation
in one family line shows up in the genomes of an unrelated family
line? And of course I disagree with the mathematically irrational
nonsense which evolutionists broadcast.

>> Would you care to compute the joint probability of all those neutral
>> mutations being fixed?
>Already been done, many times.

Come on Inez, do it for me one more time. Tell me how tens of millions
of neutral mutations sweep through a population in 500,000
generations.

>> Or are you one of those mathematically
>> incompetent evolutionists who think that the multiplication rule of
>> probabilities does not apply to biological evolution?
>> > > And it is
>> > > already clear that it takes hundreds of generations to spread a single
>> > > beneficial mutation through a population and yet you want us non-
>> > > believers in your mathematically irrational theory of evolution to
>> > > accept that neutral mutations spread through a population at a rate
>> > > that s not just a little faster than what selection can do to spread a
>> > > beneficial mutation through the population but that on average dozens
>> > > of neutral mutations have spread through populations generation after
>> > > generations for hundreds of thousands of generations.
>> > Read slowly, and perhaps it will aid your comprehension.
>> > Each...of...these...mutations...takes...a...very...very...long...time...to.¬¬¬..be...fixed.
>> > They...do...not...spread...faster...than...selected...mutations.
>> > There...are...many...more...of...them...than...there...are...selected...mut¬¬¬>>>ations...but...the...individual...mutations...spread...slowly.
>> So let’s see you do the mathematics which explains 40,000,000

>> differences between humans and chimpanzees in less than a million

>> generations. I always like to hear a good fairytale.
>That question has already been answered.

And a mathematically irrational answer it is. And of course, that’s
what the theory of evolution is, a mathematically irrational belief
system.

> > >You can t
> > > properly explain how mutation and selection works but you can
> > > speculate that drift causes the spread of neutral mutations through
> > > entire populations at rates thousands of times faster than selection
> > > can spread a beneficial mutation.
> > Dr.Kleinman finds a barn with 500 arrow holes and 1 bullet hole, and
> > determines that arrows move 500 times as fast.
> Inez, your analogy is not quite correct. I haven’t found a barn full
> of holes;
It's an analogy, the barn is not literal.

Your analogy is Swiss cheese. It’s full of holes.

>> I have found a theory of evolution with 500 arrow holes and
>> 1 bullet hole. The 500 arrow holes are all the empirical examples
>> which demonstrates your theory is incorrect and the 1 bullet hole is
>> the multiplication rule of probabilities which shows your theory of
>> evolution to be mathematically irrational belief system. It’s time to
>> find a new barn for your mathematically irrational belief system.
>I see that you prefer to make a ponderous non-witty insult rather than
>actually try to understand my point. How's that defense mechanism
>working out for you? And more importantly, why are you here if not to
>have a discussion?

I know, I’m so mean to evolutionists by pointing out that the
multiplication rule of probabilities applies to the joint probability
of events in a stochastic process. How could I be so rude to question
your mathematically irrational theory and explain correctly how
mutation and selection actually works so that people can take a
rational and logical approach to dealing with multidrug resistant

microbes, multiherbicide resistant weeds, multipesticide resistant

insects and less than durable cancer treatments? Am I really
ponderous? Do you think I need a course in evolutionist fluff?


Mark Isaak Sep 9, 1:36 pm

Newsgroups: talk.origins
From: Mark Isaak <eci...@curioustaxonomyNOSPAM.net>

Date: Fri, 09 Sep 2011 13:36:08 -0700
Local: Fri, Sep 9 2011 1:36 pm

Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

>> On Aug 10, 1:45 pm, Inez<savagemouse...@hotmail.com> wrote:
>>> On Aug 4, 4:05 pm, Alan Kleinman MD PhD<klein...@sti.net> wrote:
>>> <snippers>
>>>> What I would like to hear from either of you evolutionists is a
>>>> reasonable explanation how neutral mutations can spread through a
>>>> population faster than beneficial mutations which have selection
>>>> assisting in the spread of these beneficial mutations.
>>> You are tediously thick headed. No one made that claim.
>> You had better tell that to John Harshman because he has claimed that
>> a couple hundred neutral mutations are fixed every generation,

>> generation after generation for hundreds of thousands of generations.

>> Would you care to compute the joint probability of all those neutral
>> mutations being fixed?
>The chance of any one new neutral mutation being fixed is 1/2N. The
>number of new neutral mutations per person is about 50. The number of
>people is N. You can do the math from there. Don't forget to multiply.

Social engineer Mark Isaak wants to do mathematics. So the probability
of a single neutral mutation being fixed in the population is 1/2N.
Using the multiplication rule of probabilities to compute the joint
probability that 50 neutral mutations will be fixed is (1/2N)^50 . If
you are having trouble with exponents like hersheyh does that’s
(1/2N)*(1/2N)… 50 times. Do you want to do that for the entire
population N? ((1/2N)^50)^N, now I’m really trying to trick you
because ((1/2N)^50)^N = (1/2N)^(50*N).

hersheyh Sep 9, 4:32 pm
Newsgroups: talk.origins
From: hersheyh <hershe...@yahoo.com>
Date: Fri, 9 Sep 2011 16:32:28 -0700 (PDT)
Local: Fri, Sep 9 2011 4:32 pm

Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

>http://www.google.com/url?sa=D&q=http://www.sciencedirect.com/science%3F_ob%3DMImg%26_imagekey%3DB6VR>T-4D1TYHJ-V->1%26_cdi%3D6243%26_user%3D10%26_pii%3DS0960982296007002%26_origin%3Dgateway%26_coverDate%3D10>%252F31%252F1996%26_sk%3D%2523TOC%25236243%25231996%2523999939989%2523573004%2523FLA%252>3display%2523Volume_6,_Issue_10,_Pages_1203->1354_(October_1996)%2523tagged%2523Volume%2523first%253D6%2523Issue%2523first%253D10%2523Pages%2>523first%253D1203%2523last%253D1354%2523date%2523(October_1996)%2523%26view%3Dc%26_gw%3Dy%26w>chp%3DdGLzVzb->zSkzk%26md5%3D1912d4d2995dbe59c31f818943b74ee4%26ie%3D/sdarticle.pdf&usg=AFQjCNFiTgddWx1MIvRwOU>e9xdC4hkhBVQ
>I think the following site, which allows you to go to the pdf will be simpler.
>I was thinking of the work of Schrag and Perrot (see references in this review), but I misremembered the conditions. The >secondary mutation that increased the growth rate of the strep-resistant mutants to match that of the w.t. was under >conditions of no selection, when the mutants had to compete with the w.t.
>http://www.google.com/url?sa=D&q=http://www.cell.com/current->biology/retrieve/pii/S0960982296007002&usg=AFQjCNH-9r4DwVqUthDIC9DXDuHcNoLAvw
>> This is something which you never do.
>I have cited reference after reference to support what I say. I have *repeatedly* asked you to show me a single >researcher that has *ever* used your division by 4 of the mutation rate. You either are refusing (or more likely are >unable) to do so. I would be amazed if you were the only supergenius to recognize the need to divide by 4.

You never quote from your references and invariably your references
support my argument. For example your reference on HIV, they argued
that HIV does recombination and you continually refuse to acknowledge
this. And we’ll have to leave it that you don’t know how to apply
probability theory. You only know how to plug numbers into canned
equations even though the equation doesn’t apply to the situation.

>> Lenski’s bacteria took thousands of generations to
>> become more efficient glucose metabolizers.
>It took thousands of generations to produce, by *serial* evolution since bacteria are clonal organisms, changes in at >least 10 different genes. It was about 200 generations for each evolutionary step, AIR. And not all the changes were for >the bacteria to become more efficient glucose metabolizers. Selection was only for growth rate increases in the >conditions of the experiment.

I thought you claimed that it only takes 30 generations to amplify the
beneficial mutation. Now you are claiming that the Lenski experiment
takes 200 generations to amplify the beneficial mutation. Explain to
us why clonal replicators can not perform mutation and selection in
parallel while non-clonal replicators can. This is going to be another
good evolutionist fairytale.

>> What do you think his
>> populations would do if subjected to antibiotics simultaneously, or a
>> shift in osmotic pressures or a less than optimal incubation
>> temperature or any other selection pressure you could imagine.
>If the changes were lethal, extinction of the local population. It's not that hard to generate conditions that kill a small >local population in a controlled uniform environment. If the conditions were non-lethal, I would expect stepwise >increases in rates of growth as the clonal population accumulates changes that allow adaptation to the new conditions. > The time it takes in generations would depend on the population size; as population size increases, the rate of selective >change will increase.

So let’s consider the case when the temperature of culture is not the
optimal temperature. The combination of thermal stress and starvation
stress are not sufficient to drive the population to extinction. Do
you think the evolutionary process for both selection conditions will
be more rapid or less rapid than with the starvation stress alone?

>> Mutation and selection does not work efficiently when more than a
>> single gene is targeted by selection conditions simultaneously.
>Organisms are adapted to environments. If too many features of the environment change simultaneously or too rapidly, >evolution cannot keep pace. In some cases, the population size will permanently collapse. Extinction happens.

That’s correct, mutation and selection can only work at a particular
pace. When a beneficial mutation occurs, the subpopulation with that
beneficial mutation must amplify that mutation before there is a
reasonable probability that the next beneficial mutation in the
sequence occurs. Haldane addressed this issue with his “Cost of
Natural Selection” paper which you evolutionists have tossed out. You
recognized this with your 30 generations to get a billion bacteria
calculation and now you recognize this from the Lenski study which you
claim takes 200 generations per mutation. And now you claim that
clonal populations can not evolve by mutation and selection in
parallel but non-clonal populations can. Explain to us how this
happens.

>> > But, frankly, I think you are either lying or you misheard/mis-
>> > understood what this un-named "professor of evolutionary biology"
>> > said. I will assume the latter, given your level of understanding
>> > shown here. Perhaps you can give me a better citation to follow up on
>> > than "some un-named professor of evolutionary biology said something
>> > like this about some unspecified resistance mutation, as I heard
>> > him". Such a citation makes it hard to tell what you heard.
>> Hersheyh, numerous times you have called me a liar.
>No. I said your division by 4 was stupid. I said that the above claim was *either* a lie or mishearing/misunderstanding. I >would be perfectly happy for it to be the latter, since you have given us ample evidence that you are quite capable of >misunderstanding even the simplest things.

It is you mathematically incompetent evolutionist nitwits who have
given us multidrug resistant microbes, multiherbicide resistant weeds,

multipesticide resistant insects and less than durable cancer

treatments by bungling the basic science and mathematics of the
mutation and selection phenomenon. You have used the Poisson
distribution inappropriately without ever going through the derivation
of the equation that you have used for more than two decades. You
don’t understand basic algebra of exponents and you think I am trying
to trick you when I use a basic algebraic identity. I pity the poor
students who wasted their time in a genetics class taught by you.
Let’s just hope they forget the mathematically irrational garbage you
spread about.

>> You are a stupid
>> jack ass who thinks that the multiplication rule of probabilities does
>> not apply to biological evolution,
>I have never said that. I have said that the multiplication rule is often misapplied by creationists to produce GIGO >nonsense. But that is generally a consequence of making false and ignorant assumptions about how genes or proteins >evolve. In fact, if you look at my equations and math, you will see that I use the multiplication rule of probabilities quite >regularly.

The multiplication rule of probabilities applies to abiogenesis as
well as mutation and selection and you have yet to apply the
multiplication rule of probabilities correctly to the mutation and
selection phenomenon. Schneider has made a mathematical blunder with
his claim that the multiplication rule of probabilities does not apply
to biological evolution and your defense of his claim has been a waste
of time. Schneider knows his claim is wrong but is now clinging to the
hope that recombination will somehow revive the mathematically
irrational theory of evolution. Aside from you evolutionists not
understanding how mutation and selection works, you don’t understand
how random recombination works either.


>> you think that mutations are not random independent events,
>In fact, I do think mutations at different sites are random independent events and use that assumption in the simplified >calculations involving the binomial probability distribution. However the binomial *assumption* that the probability of >generating a mutant state is the same for all trials is violated because once a cell has a mutant state, all that cell's >progeny have a much, much higher probability of having a mutant state than do cells that still have the orginal genetic >state. That is the reason for the skew of the probability distribution of the Luria-Delbruk analysis.

If you do understand that random mutations are random independent
events, you should understand that the joint probability of these
events occurring is governed by the multiplication rule of
probabilities. And the binomial “assumption” you make is not the
correct probability function for the mutation and selection
phenomenon, however it is more accurate than your assumption that the
Poisson distribution is a good approximation.

>> you think that the Poisson distribution is
>> a good approximation of the mutation and selection phenomenon,
>Under the conditions stated, the Poisson is indeed a good approximation of a binomial probability distribution and >(except for the aforementioned complications of Luria-Delbruck) a binomial probability is a good approximation for >determining the probability of there being one or more mutations in the population examined.

What conditions have you stated for the use of the Poisson
distribution? You’ve never gone through the derivation of the Poisson
distribution. How would you know if it is a valid approximation for
the mutation and selection phenomenon? You don’t even know when the
Poisson distribution is a reasonable approximation of the binomial
distribution. The only thing you have done is screwed up this
mathematics royally. But what can you expect; you were indoctrinated
by mathematically incompetent evolutionists and now have become one.

>> you are
>> unable to derive the correct probability functions for either the
>> mutation and selection phenomenon
>You have never demonstrated that I have not used the correct probability function. I presume that your definition of >"correct" means the probability function, such as it is, that you bastardized from binomial probability by dividing the >mutation rate by 4. I beg to differ with your egocentric definition of what is "correct". I have clearly stated the reasons >why your function makes no sense.

You are so brilliant hersheyh, you know what the base was before the
random point mutation occurs and because of this you know that when
the mutation occurs there are only three possible alternatives instead
of four. You are telepathetic. You still don’t recognize when a trial
is done in the mutation and selection process.

>> or random recombination,
>I have no problem with that either. Simple Mendelian genetics. You, OTOH, cannot seem to understand the difference >between alleles of unlinked genes and alleles of the same gene.

You have yet to get beyond the simple breeding process described by
Mendelian genetics. You don’t know how to derive the probability
function for random recombination. You really need to get beyond 19th
century genetics.

>> you don’t
>> know that (a^x)^y=a^(x*y).
>Both work. The first is an obfustication meant to hide the fact that your so-called derivation is nothing but the binomial >probability distribution mucked up by dividing the mutation rate by 4 and pretending that the number of generations >matter even if all the tested individuals (trials) all came from a single generation.

Stop trying to hide your mathematical incompetence by my use of a
simple algebraic identity. Do you want me to give you the name of my
lower division mathematics text which has a chapter on exponents? This
book also has the derivation of the Poisson probability function in
it. Study and learn some mathematics and then perhaps you can give an
intelligent discussion of the mathematics of the mutation and
selection phenomenon instead of complaining when I use a basic
algebraic identity and claim that I am obfuscating the discussion.
Your arguments are so pathetic.

>> You are simply a mathematically incompetent
>> evolutionist nit wit. You don’t have the intelligence to tell the
>> truth from a lie.
>Funny. I feel the same way about your understanding of the math you are using. The first clue is that you fail to define >your terms and the question you are asking.

You are the one using the Poisson distribution without ever studying
the derivation of the equation. That’s incredible. I can not imagine
an engineer using an equation to describe a physical phenomenon
without understanding the derivation of the equation. But for
evolutionists, this is the standard operating procedure. No wonder we

have multidrug resistant microbes, multiherbicide resistant weeds,
multipesticide resistant insects and less than durable cancer

treatments. We have mathematically incompetent evolutionist nitwits
using equations that they never bother studying the derivation of.

>> > > My question to this professor of evolution is then why don t
>> > > these drug resistant strains increase in frequency even when the
>> > > selection pressures don t exist?
>> > It would. Which is why I question your understanding of what was
>> > said.
>Let me clarify that. In many cases, where the drug-resistant cells have to compete with w.t., they do indeed tend to lose >out in conditions without the drug. However, as the article I pointed you to earlier points out, that is not always the case. > Secondary

And if it is not the case, the drug should not be required for these
strains to appear because they are more efficient replicators even in
the drug free environment.


Charles Brenner Sep 9, 5:34 pm
Newsgroups: talk.origins
From: Charles Brenner <cbren...@berkeley.edu>
Date: Fri, 9 Sep 2011 17:34:10 -0700 (PDT)
Local: Fri, Sep 9 2011 5:34 pm

Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

>> On 9/9/11 7:59 AM, Alan Kleinman MD PhD wrote:
>> > On Aug 10, 1:45 pm, Inez<savagemouse...@hotmail.com> wrote:
>> >> On Aug 4, 4:05 pm, Alan Kleinman MD PhD<klein...@sti.net> wrote:
>> >> <snippers>
>> >>> What I would like to hear from either of you evolutionists is a
>> >>> reasonable explanation how neutral mutations can spread through a
>> >>> population faster than beneficial mutations which have selection
>> >>> assisting in the spread of these beneficial mutations.
>> >> You are tediously thick headed. No one made that claim.
>> > You had better tell that to John Harshman because he has claimed that
>> > a couple hundred neutral mutations are fixed every generation,

>> > generation after generation for hundreds of thousands of generations.

>> > Would you care to compute the joint probability of all those neutral
>> > mutations being fixed?
>> The chance of any one new neutral mutation being fixed is 1/2N. The
>> number of new neutral mutations per person is about 50. The number of
>> people is N. You can do the math from there. Don't forget to multiply.
>This simplistic argument is driving me nuts.

Of course Mark Isaak’s argument is nuts.

>What have you in mind for N? If you are thinking billions, then you
>are thinking modern humans and Dr. Dr.'s confused picture of mutations
>propagating among living people like a plague is what you have.

I’m just putting John Harshman’s confused picture into words. If he
thinks that a couple of hundred neutral mutations are spreading
through the population every generation, generation after generation
for hundreds of thousands of generations than a plague is the correct
word to describe this spread of neutral mutations. That’s why John’s
claim is mathematically irrational garbage.

>So what should our model be?
>What does the bottleneck at which human and monkey separated look
>like?
>Note that fixation isn't really the issue - fortunately as absolute
>fixation of neutral single nucleotide mutations rarely happens. 10^8
>human births per year times 10^-8 mutation rate means that just when
>you think the last surviving rare type is about to die, a backmutation
>in a newborn somewhere extends the the persistence of the type.
>So what is the data that the supposed 35 million SNP differences
>between man an monkey comes from, and what does it really mean? I
>don't know. Even if it's a matter of comparing sequences (rather than
>e.g. extrapolating based on assumptions about population histories) I
>think it's more statistical that just counting -- humans too have many
>neutral differences from one another. Lots of definitional
>complications.
>Not easy questions.

Of course there are a lot of definitional complications if you want to
claim that humans and chimpanzees come from a common progenitor now
that we have genetic sequences for both. This now becomes an
accounting problem for evolutionists. Somehow you have to explain how
tens of millions of differences between the two genomes can be spread
through the populations for each population in only 500,000
generations. Clearly, mutation and selection can not do this
transformation is so few generations. And the failure on the part of
evolutionists to properly describe mutation and selection has cause
great societal harm.

hersheyh Sep 9, 9:11 pm
Newsgroups: talk.origins
From: hersheyh <hershe...@yahoo.com>
Date: Fri, 9 Sep 2011 21:11:59 -0700 (PDT)
Local: Fri, Sep 9 2011 9:11 pm

Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

On Friday, September 9, 2011 10:52:29 AM UTC-4, Alan Kleinman MD PhD
wrote:
> On Aug 10, 12:28 pm, hersheyh <hers...@yahoo.com> wrote:
> > On Thursday, August 4, 2011 3:55:49 PM UTC-4, Greg Guarino wrote:
> > > On 8/4/2011 2:44 PM, Alan Kleinman MD PhD wrote:
> > > > On Jul 8, 8:22 am, "g....@risky-biz.com"<gdg...@gmail.com> wrote:
> > > >> On Jul 8, 9:08 am, Alan Kleinman MD PhD<kle...@sti.net> wrote:
>[snip]
>> > > > One of the basic theorems of probabilities is the Multiplication Rule.
>> > > > If A and B are independent events in a sample space S and the
>> > > > probability of event A is P(A) ≠ 0 and the probability of event B is
>> > > > P(B) ≠ 0 then the combined probability of both events occurring is the
>> > > > product of the individual probabilities P(A)*P(B).
>>> > You forgot to understand the important qualifier "in a sample space S". In our case, this is the same as "in a single >>>trial" or "in a single organism". In that case, the combined probability of both events occurring "in a sample space S"/"in >>>a single trial"/"in a single organism" is indeed the product of the individual probabilities. That is true for the single step >>>process you are fixated upon where the two probabilities are both the probability of mutation/per trial generating a >>>resistant cell from a sensitive cell. It is also true for the third step of my three step process where the probability of A->>>resistance is essentially 1 because of the previous first step (where I did selection for A-resistance) and subsequent >>>growth for 30 doublings, and the probability of B-resistance from B-sensitivity.
>> You are wrong again hersheyh, the number of trials in the sample space
>"In a sample space" *is* a single trial. That is what the term means. So talking about "the number of trials in the sample >space" is nonsense by someone who doesn't understand what these terms mean and is just making wild-assed >guesses. Again, a trial is the individual cell in this case that is examined for the presence or absence of the event (the >*presence* of a mutation for A-resistance, say), or events (the *presence* of mutations for both A- and B-resistance, say) >in this case. Note that *presence* of two events does not tell us anything about *when* these mutations occurred or in >what order they occurred, only that they be *present* in the same sample space, in this case, a single examined >individual.

What are you babbling about hersheyh? The sample space for the
mutation and selection phenomenon is the population. The trial is the
mutation and the mutation rate is the frequency at which a trial
occurs.

> are governed by the population size,number of generations which the
> population is able to reproduce and the mutation rate. Events A and B
> do not have to occur simultaneously, if they did, that would be your
> “double mutation” case.
All that matters is that the two events be *present* in a single cell
(trial) at the time that the trial is examined for the presence or
absence of the two events. In dice rolling, using a blue and red die
(analogous to different genes) to determine the probabiilty of snake
eyes, a single trial is a rolling of *both* the red and blue die, and
snake-eyes still counts as snake eyes event in a trial whether you
roll both die simultaneously, the blue die first, or the red die
first. In our case, a trial is an individual examined for the
presence of both A- and B-resistance.

Random mutations don’t recognize whether they occur in one or two
genes. And where did this idea of a cell come into this discussion?
Does HIV have a cell? Hersheyh, your thinking is becoming more and
more confused and weird.

>> If the events A and B occur one after another
>> as they do when mutation and selection is working efficiently, the
>> subpopulation with mutation A has generations for which it can amplify
>> its beneficial mutation by increasing its subpopulation size. The
>> subpopulation with mutation A is increasing its number of trials using
>> both population size and generations for mutation B to occur. The
>> joint probability of those two events A and B occurring are still
>> governed by the same probability function I derived for you.
>Prove it. I gave a simple example of just this in the three step process. I gave numbers. i gave equations. You give >nothing but meaningless verbiage.

I’ve presented two empirical examples which demonstrate how the
mutation and selection phenomenon works. The first is the Weinreich
example of the evolution of the highly resistant beta-lactamase allele
and the Lenski experiment which you now agree is an example of serial
evolution. I have also presented dozens of empirical examples where
mutation and selection does not work when combination selection
pressures are applied to the population. And I have presented the
correct probability function for mutation and selection which you
agree is correct except for your confused understanding that when a
mutation occur the only thing certain is that after the mutation
occurs you have one of four possible bases as the outcome. What is now
clear is that you don’t understand what the sample space is for the
mutation and selection phenomenon, you don’t understand what the trial
is for the mutation and selection phenomenon and you don’t understand
what the possible outcomes are for a point mutation. You are confused
by the mathematics, empirical examples and the verbiage.

>> > > This rule extends
>> > > > to any number of independent events. This mathematical principle
>> > > > applies to all situations where you have random independent events
>> > > > such as random mutations.
>> > "In a sample space S." And if you use the correct individual probabilities. Again, in the three step process the >correct probability of A-resistance in the third step is >1.0. In the first step, it was 10^-8.
>> Why don’t you write out you equations algebraically? Don’t use
>> constants, use variables and define what your variables are.
>How many times have I f**king done this! Unlike you, I do actually define what my variables are both in the terminology >of the specific genetics and also in the terminology of probability and statistical analysis. I also have included the metrics >so that you can see that they also multiply out. Like saying that n = the total number of trials/individuals examined for an >event. And that in some cases n = N*g, where N = number of trials examined per generation and g = the number of >generations. Don't you f**king read what I write! Or are you too stupid to know what the math means?

Sure I read what a foul mouth evolutionist writes and this foul mouth
evolutionist uses populations of 10^9 and mutation rates of 10^-8
because doesn’t know how to write the equation algebraically. That’s
because this evolutionist was trained to use the Poisson distribution
and never questioned the validity of the equation. In fact this foul
mouth evolutionist never went through the derivation of the equations
he uses. He thinks that if someone uses the algebraic identity (a^x)^y
= a^(x*y) is obfuscating the mathematics. Hersheyh, you are the one to
fails to understand what the math means.

>There have been many times in this thread where you have defined things several different mutually incompatible ways >and demonstrated that you don't know the meaning of really fundamental concepts in both genetics and math, like >"mutation" and "mutation rate" and "event" and "trial".

Feel free to post a quote where I do any of what you claim. It is you
mathematically incompetent evolutionists who have given us multidrug

resistant microbes, multiherbicide resistant weeds, multipesticide

resistant insects and less than durable cancer treatments because of
your bungled teaching and understanding of how mutation and selection
actually works.

>> Show us
>> how your step one using the Poisson distribution is wrong,
>I have *shown* you that the use of the Poisson distribution is recognized to be a useful (because mathematically >simpler) estimate that is very close to the binomial probability distribution under certain conditions and that those >conditions are met. But because you seem to be too stupid to recognize that, I have gone on to using the binomial >probability distribution that you seem to think you derived independently and improved upon by dividing the probability of >the event by an arbitrary number.

Who recognizes that the Poisson distribution is useful for the
mutation and selection phenomenon, those of you who have been
indoctrinated into evolutionism and who have never gone through the
derivation of the Poisson distribution? The only thing the Poisson
distribution is good for is giving a highly inaccurate estimate of the
mutation rate. Hersheyh, why don’t you actually go through the
derivation of the Poisson distribution and learn why this is not the
correct probability distribution for the mutation and selection
phenomenon? Since is clear that you won’t study the derivation of the
Poisson distribution and why it is not the correct approximation for
the mutation and selection phenomenon, I’ll have to post the reason
why it is the wrong distribution function. I’ll start with why the
Poisson distribution is not the correct distribution function to
approximate the binomial distribution in the case of mutation and
selection. The Poisson distribution can be obtained as the limiting
case of the binomial distribution if you let the probability of the
event p -> 0 and the number of trials -> infinity. The probability of
the event p (the beneficial mutation) from a single trial will never
get close to 0, it will always have a value of 1/4 because there are
four possible outcomes. Now if you are telepathetic like hersheyh and
know what the base was before the mutation occurs, you could claim
that the probability of the beneficial mutation occurring is 1/3.
Either way, the probability for the occurrence of the event from a
single trial will be well above 0. With respects to the number of
trials for mutation and selection even with hersheyh’s favorite
population size of 10^9 and mutation rate of 10^-8, the number of
trials will only be about 10. Maybe in the evolutionist mathematically
irrational mind 1/4 or 1/3 is close enough to 0 and 10 is close enough
to infinity to use the Poisson distribution but what can you say to
these bunglers who would cause multidrug resistant microbes,

multiherbicide resistant weeds, multipesticide resistant insects and

less than durable cancer treatments to occur.

>> step two
>> assuming population sizes of 10^9 is wrong
>I don't *assume* population sizes of 10^9. I *assume* that the surviving A-resistant population from the first step is >viable and will, therefore, have a high probability of being able to grow to the size of 10^9 individuals. And I pointed out >that this should occur in about 30 generations. The equation for such doubling growth is x*2^30, where n = the >population size after the first selection step. Given the values of that selection step (a probability per trial of 10^-8 for >mutation to A-resistance and hence survival and a population of 10^9 bacteria), the mean expected value for n would be >10. But 30 generations of doubling will be sufficient to produce a population of 10^9 even if there was only one survivor.

Why does the Lenski experiment take your claimed 200 generations? And
here you claim 30 generations. What is clear is this mathematics is
why out of your league.

>> and step three, multiplying
>> three numbers for two events is your wrong concept of using the
>> multiplication rule.
>Don't make assertions without explaining why you think it is wrong. That you don't tells me only that you cannot do so. I >have given you numbers and equations. Deal with those.

So tell us what the three numbers you are multiplying together. If you
are computing the probability of two mutations occurring, why are you
multiplying three numbers together and what are these three numbers?

>> > > If you think that hersheyh is knowledgeable
>> > > > on this topic, my suggestion is that you don’t take his advice when
>> > > > you go to Las Vegas.
>> > > Everyone, including my pet cats, gets this bit of math, which applies
>> > > when only a double mutant has an advantage. What if several mutations
>> > > each confer an advantage and the population is not severely reduced?
>> > > My cats died years ago, by the way.
>> > So you are saying that the dear Dr. Dr. isn't any better at math than brain-dead cats?
>> I don’t have to do math better than brain-dead cats, I only have to do
>> math better than mathematically incompetent evolutionists who make
>> brain-dead cats look like Einsteins.
>It is funny to see insults from people who clearly cannot back them up with intelligent argument.

Mathematical and empirical evidence never constitutes and intelligent
argument to an evolutionist. Evolutionists are satisfied with

multidrug resistant microbes, multiherbicide resistant weeds,
multipesticide resistant insects and less than durable cancer

treatments are the consequence of the evolutionist arguments.

>[snip]
>> > > > What hersheyh does not understand or won’t to admit to is that
>> > > > when a population has to accumulate multiple beneficial mutations such
>> > > > as demonstrated by the Weinreich example of the high efficiency beta
>> > > > lactamase producer, these sequences of beneficial mutations can not
>> > > > occur anywhere in the population, they must accumulate on members of
>> > > > subpopulations who would benefit from these mutations.
>What makes you think I don't understand that? Especially in clonal organisms, haven't I explicitly pointed out that >mutation must occur sequentially. In the Weinreich cases, he demonstrates the different pathways by which such >stepwise evolution between a highly sensitve and a highly resistant genetic strain not only can occur but *did* occur, in >nature. Or did you fail to note that he did not evolve the resistant strain, he only artificially generated all combinations of >intermediates and tested them for resistance.
>[snip]

And the Lenski experiment demonstrates the exact same mathematical
behavior as the Weinreich experiment and the mathematics is not
described by the Poisson distribution, the favorite but wrong
distribution function used by evolutionists. And the mathematics works
the same for populations which do recombination and for clonal
populations. That’s why combination therapy works for HIV. And that’s

why the theory of evolution is a mathematically irrational belief
system.

John Harshman Sep 9, 11:01 pm

Newsgroups: talk.origins
From: John Harshman <jharsh...@pacbell.net>

Date: Fri, 09 Sep 2011 23:01:11 -0700
Local: Fri, Sep 9 2011 11:01 pm

Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

>Charles Brenner wrote:
>> On Sep 9, 1:36 pm, Mark Isaak <eci...@curioustaxonomyNOSPAM.net>
>> wrote:
>>> On 9/9/11 7:59 AM, Alan Kleinman MD PhD wrote:
>>>> On Aug 10, 1:45 pm, Inez<savagemouse...@hotmail.com> wrote:
>>>>> On Aug 4, 4:05 pm, Alan Kleinman MD PhD<klein...@sti.net> wrote:
>>>>> <snippers>
>>>>>> What I would like to hear from either of you evolutionists is a
>>>>>> reasonable explanation how neutral mutations can spread through a
>>>>>> population faster than beneficial mutations which have selection
>>>>>> assisting in the spread of these beneficial mutations.
>>>>> You are tediously thick headed. No one made that claim.
>>>> You had better tell that to John Harshman because he has claimed that
>>>> a couple hundred neutral mutations are fixed every generation,

>>>> generation after generation for hundreds of thousands of generations.

>>>> Would you care to compute the joint probability of all those neutral
>>>> mutations being fixed?
>>> The chance of any one new neutral mutation being fixed is 1/2N. The
>>> number of new neutral mutations per person is about 50. The number of
>>> people is N. You can do the math from there. Don't forget to multiply.
>> This simplistic argument is driving me nuts.
>> What have you in mind for N? If you are thinking billions, then you
>> are thinking modern humans and Dr. Dr.'s confused picture of mutations
>> propagating among living people like a plague is what you have.
>No it isn't. Why would you think so?

Charles Brenner uses the word “plague” to describe what you are
claiming about a couple hundred neutral mutations spreading through a
population, generation after generation for hundreds of thousands of
generations and I use the term “sweep”. I think I like Charles term
better.

>> So what should our model be?
>> What does the bottleneck at which human and monkey separated look
>> like?
>Who says there is a bottleneck?

I think that evolutionists have been tipping the bottle a bit too
much.

>> Note that fixation isn't really the issue - fortunately as absolute
>> fixation of neutral single nucleotide mutations rarely happens. 10^8
>> human births per year times 10^-8 mutation rate means that just when
>> you think the last surviving rare type is about to die, a backmutation
>> in a newborn somewhere extends the the persistence of the type.
>Yes, we have no absolute fixation, just frequencies too low to be
>noticed in a reasonable sample. But the difference isn't important.

No fixation, no amplification just evolutionist mathematical
irrationality.

> So what is the data that the supposed 35 million SNP differences
> between man an monkey comes from, and what does it really mean? I
> don't know.
I do. It's a comparison of the complete genomes of human and chimp,
base
by base.

Does that include chromosome 21?

>> Even if it's a matter of comparing sequences (rather than
>> e.g. extrapolating based on assumptions about population histories) I
>> think it's more statistical that just counting -- humans too have many
>> neutral differences from one another. Lots of definitional
>> complications.
>> Not easy questions.
>Easier than you may imagine. Now the human genome is a composite
>sequence of pieces from more than on individual, but any human should be
>good enough to compare with a chimp, since humans are 99.9% similar as
>opposed to 98.7% similarity between chimps and humans.

Let’s see, 70% of genes produce different proteins between humans and
chimpanzees and there are large stretches of chromosome 21 with non-
random differences between humans and chimpanzees. Who knows what you
are comparing to get your 98.7% number? You still can not do the
accounting in 500,000 generations to account for the genetic
differences between humans and chimpanzees without neutral mutations
spreading through the population like a plague.

Charles Brenner Sep 10, 8:44 am
Newsgroups: talk.origins
From: Charles Brenner <cbren...@berkeley.edu>
Date: Sat, 10 Sep 2011 08:44:07 -0700 (PDT)
Local: Sat, Sep 10 2011 8:44 am

Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

On Sep 9, 11:01 pm, John Harshman <jharsh...@pacbell.net> wrote:
>> Charles Brenner wrote:

>> > On Sep 9, 1:36 pm, Mark Isaak <eci...@curioustaxonomyNOSPAM.net>
>> > wrote:
>> >> On 9/9/11 7:59 AM, Alan Kleinman MD PhD wrote:
>> >>> On Aug 10, 1:45 pm, Inez<savagemouse...@hotmail.com> wrote:
>> >>>> On Aug 4, 4:05 pm, Alan Kleinman MD PhD<klein...@sti.net> wrote:
>> >>>> <snippers>
>> >>>>> What I would like to hear from either of you evolutionists is a
>> >>>>> reasonable explanation how neutral mutations can spread through a
>> >>>>> population faster than beneficial mutations which have selection
>> >>>>> assisting in the spread of these beneficial mutations.
>> >>>> You are tediously thick headed. No one made that claim.
>> >>> You had better tell that to John Harshman because he has claimed that
>> >>> a couple hundred neutral mutations are fixed every generation,

>> >>> generation after generation for hundreds of thousands of generations.

>> >>> Would you care to compute the joint probability of all those neutral
>> >>> mutations being fixed?
>> >> The chance of any one new neutral mutation being fixed is 1/2N. The
>> >> number of new neutral mutations per person is about 50. The number of
>> >> people is N. You can do the math from there. Don't forget to multiply.
>> > This simplistic argument is driving me nuts.
>> > What have you in mind for N? If you are thinking billions, then you
>> > are thinking modern humans and Dr. Dr.'s confused picture of mutations
>> > propagating among living people like a plague is what you have.
>> No it isn't. Why would you think so?
>Because I think that N in the billions means recent history, far too
>recent for any new mutations to proliferate around the globe.
>Therefore I suppose that any (near) fixation of man-monkey difference
>occurred when N was small. That means the argument that billions of
>people provide billions of candidates for mutation is irrelevant. The
>real analysis must be more subtle and take into account the
>approximate population sizes over time.

Now don’t start using logic Charles, it just confuses evolutionists.

>In particular, note that we will NOT find a back-of-the-envelope
>calculation that shows that 35 million differences is easy to achieve,
>a conservative estimate. It's a barely possible estimate given the
>actual historical facts, since it is the number of difference that
>have barely been achieved.

The calculations get only more difficult as you reduce the number of
generations. How do you get neutral mutations into unrelated family
lines of a population? Selection enables the accumulation of mutation
by eliminating family lines which do not have the fitness to
reproduce.

>> > So what should our model be?
>See below.
>> > What does the bottleneck at which human and monkey separated look
>> > like?
>> Who says there is a bottleneck?
>I had in mind the path back in time tracing the human population to
>the schism then forward via the monkeys. Perhaps it is incorrect to
>use the word "bottleneck" in this way. Anyway, what I wonder is what
>is the right way to visualize the population genetic picture of
>separation; how mutations propagate in one branch or the other to
>distinguish them.

Humans and chimpanzees have different chromosome number, they are not
homologous, 70% of the genes produce different proteins, bottleneck is
a very generous expression for describing the problem evolutionists
have when they say humans and chimpanzees came from a common
progenitor.

>> > Note that fixation isn't really the issue - fortunately as absolute
>> > fixation of neutral single nucleotide mutations rarely happens. 10^8
>> > human births per year times 10^-8 mutation rate means that just when
>> > you think the last surviving rare type is about to die, a backmutation
>> > in a newborn somewhere extends the the persistence of the type.
>> Yes, we have no absolute fixation, just frequencies too low to be
>> noticed in a reasonable sample. But the difference isn't important.
>Maybe not. What is our "reasonable sample" size? 1? 6?

Nothing is important to John except his mathematically irrational
belief system. John can take one sequenced human genome and one
sequenced chimpanzee genome and claim that they are 98.7% similar when
they don’t have the same chromosome number, are not homologous and 70%
of the genes produce different proteins.

>> > So what is the data that the supposed 35 million SNP differences
>> > between man an monkey comes from, and what does it really mean? I
>> > don't know.
>> I do. It's a comparison of the complete genomes of human and chimp, base
>> by base.

Hey John, how close are chromosomes 47 and 48 in the chimpanzee genome
with chromosomes 47 and 48 in the human genome? Are they 98.7%
similar?
>> > Even if it's a matter of comparing sequences (rather than
>> > e.g. extrapolating based on assumptions about population histories) I
>> > think it's more statistical that just counting -- humans too have many
>> > neutral differences from one another. Lots of definitional
>> > complications.
>> > Not easy questions.
>> Easier than you may imagine. Now the human genome is a composite
>> sequence of pieces from more than on individual, but any human should be
>> good enough to compare with a chimp, since humans are 99.9% similar as
>> opposed to 98.7% similarity between chimps and humans.
>Ok, that's a helpful point (though not an answer - any two humans
>already differ by 35 million SNPs, so a sample of 1 isn't enough. With
>small samples there remains, I think, an issue of ascertainment). But
>you did skip over my question about "what model?"

John will tell you that’s irrelevant.

hersheyh Sep 10, 12:48 pm
Newsgroups: talk.origins
From: hersheyh <hershe...@yahoo.com>
Date: Sat, 10 Sep 2011 12:48:38 -0700 (PDT)
Local: Sat, Sep 10 2011 12:48 pm

Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

>> On Aug 6, 10:01 am, hersheyh <hers...@yahoo.com> wrote:
>> > On Aug 1, 6:14 pm, Alan Kleinman MD PhD <klei...@sti.net> wrote:
>> > > On Jul 7, 11:59 am, Prof Weird
>> wrote:
>> > > > On Jul 7, 1:22 pm, hersheyh <hers...@yahoo.com> wrote:
>> > > > Dr Dr Kleinman doth asserted :
>> > > > > > This is not
>> > > > > > always the case and probably not usually the case. Reread the
>> > > > > > Weinreich paper about the high efficiency beta-lactamase bacteria. Do
>> > > > > > you think all these variants existed in the population de novo?
>> > > > Do you mean the paper "Darwinian evolution can follow only a very few
>> > > > mutational paths to fitter proteins", Weinreich DM, Delaney NF,
>> > > > DePristo MA, Hartl DL, Science 312, 111-114, 7 April 2006 ?
>> > > > There is no reason WHY particular single mutants would NOT already be
>> > > > in a population. But, with no cefotaxime around, they would be
>> > > > neutral mutations. And, by their model, the probability of fixation
>> > > > for deleterious and neutral mutations was set to zero.
>> > > Now you are making an assumption here my dear Prof Weird. Your
>> > > assumption is that these mutations which would give resistance to
>> > > cefotaxime are neutral when cefotaxime is not present in the
>> > > environment. This is not necessarily the case. I have not seen the
>> > > data on these particular drug resistant strains but there is a large
>> > > volume of data on HIV which show that these drug resistant strains are
>> > > not as efficient replicators as their wild strain relatives. I ve even
>> > > heard a professor of evolutionary biology claim that drug resistant
>> > > strains of microbes are better replicators than the non-drug resistant
>> > > strains.
>It doesn't matter. Single point mutations in bacteria, on average, occur at a rate of 10^-8. Thus, in a population of size >10^9 or greater (easily reached by bacteria infecting a person), one would expect to have at least one individual with >each of the 5 possible single point changes (especially if they represent transitions; perhaps less so if the change >represents a transversion) in the population. Since each of the single point changes have a selective advantage at >certain levels of antibiotic, it all depends on the patient spreading his bacteria after selection at a level of antibiotic that >these single point mutants can survive and increase their frequency in. Initially, lower levels of antibiotic are used >because that reduces toxicity or side-effects like diarrhea while still killing the bacteria. A patient that doesn't continue >using the antibiotic (perhaps because it causes diarrhea) after s/he feels better but before his/her immune system has >completely eliminated the infection provid

es a perfect vehicle for the amplification and spread to new patients of bacteria >enriched in those resistant to *low* levels of the antibiotic. But the same thing can occur if the level of antibiotic >fluctuates frequently or where the antibiotic has problems reaching. The result is, in nature, the step-wise evolution of >increasingly resistant bacteria.

You certainly did not do a very good job reading the Weinreich paper.
The five point mutations have to occur in a particular sequence so it
doesn’t help for the five mutations to be scattered through the
population. They have to accumulate one by one where each mutation
improves the fitness to reproduce allowing amplification of the
alleles sequentially for the mutations to accumulate. And how would
you know what side effects are produced by antibiotics? Have you ever
prescribed antibiotics and observed the consequences of their usage?
You have no idea of the mathematics of mutation and selection and you
have no experience in the empirical usage of antibiotics but because
you are an evolutionist, you are an expert (in evolutionist folklore).

>> > Which, of course, means that under conditions that lack the
>> > antibiotic, the resistant strains can be slightly less fit than the
>> > w.t. and their *frequency* in the population will tend to decrease by
>> > a certain amount each generation. [This is in contrast to the case
>> > where the antibiotic is present, in which only the resistant strains
>> > survive. Recovery of w.t. alleles will need to await the growth of
>> > the mutants until they reach a sufficient n to produce revertants and
>> > then, if the antibiotic is no longer present, there will be a *slow*
>> > decrease in the frequency of mutants and a *slow* increase in the
>> > frequency of revertants.]
>> Drug resistant strains are often less efficient replicators than the
>> wild strains. This principle would point to a logical strategy for
>> regaining the use of antimicrobials but evolutionists have so bungled
>> the basic science and mathematic of mutation and selection that the
>> basis for the use of selection pressures is an incoherent mess.
>Except for the minor problem that secondary mutations can sometimes eliminate the typically small relative fitness >differential between the w.t. and resistant strains. As pointed out in a reference I sent you.

Give us an empirical example of your claims. But you never give us
empirical examples; you only give your hypothetical examples which are
empirically wrong.

>> Thank
>> you evolutionists for making the basic science and mathematics of
>> mutation and selection an unintelligible collection of garbage.
>> Evolutionists like you claim that the multiplication rule of
>> probabilities does not apply to biological evolution and now you are
>> claiming that random mutations are not independent events.
>Again, I do not claim that the multiplication rule does not apply. I have, correctly, used in both the single step selection >for double-mutation from double-non-mutants and in the three-step selection for double-mutation from an original >double-non-mutant. I do point out that its use in the "747 in a tornado" creationist argument is GIGO because no >biologist thinks that biological evolution works by randomly assembling genes from scratch. That is, false assumptions >lead to a GIGO use of the multiplication rule. But perhaps that distinction is too subtle for you, given that you clearly do >not understand the terms of either biology or probability.

You evolutionists have so fouled up the field of biology that

multidrug resistant microbes, multiherbicide resistant weeds,
multipesticide resistant insects and less than durable cancer

treatments are a consequence. Go look up the derivation of the Poisson
distribution and find out one of the many reasons you are wrong.

>> > In the absence of the antibiotic, an equilibrium level will be reached
>> > when the loss of the mutant allele each generation of the mutant is
>> > balanced by the input of that allele by new mutation from the w.t.
>> > allele. This steady state level of mutant will fluctuate randomly
>> > around a value, but there will always be mutants at a certain,
>> > typically very low, level even in populations that never get exposed
>> > to the antibiotic. Under conditions with the presence of the
>> > antibiotic, these pre-existing variants are the ones selected for.
>> So are you claiming that all 4^17000 possible combination of bases for
>> the HIV virus exist in equilibrium in the environment?
>That is a different question. The probability that there will be at least one mutant allele in the entire population at any >given nt site in a population of size 10^9 and a mutation rate of 10^-8 would be roughly 0.99995 per site. Most likely that >mutant would be a transition rather than a transversion. That is only one of the 4 possible changes. But the only thing >you have learned from your calculation is the number of possible combinations.

Just how crappy can you get at your mathematics? Just because you may
have a particular mutation at a particular locus in a population
doesn’t mean that every possible variant exists in a population of
10^9.

>What you are *interested* in, however, is calculated differently. First, you need to know the probability of mutation rate >per genome, not per site. Since the mutation rate per site is, on average, about 10^-8 and there are 1.7 x 10^4 sites, the >mean rate of mutation per genome is (10^-8 mutations events per site) * (1.7 x 10^4 sites per genome) = 1.7 x 10^-4 >mutations per genome. That is a sufficiently small value that we can say, without it being off by much, that every >genome that has a mutation is likely to only have one mutation in its genome. [The probability of a cell having two >independent mutations would be roughly 1.7 X 10^-4 * 1.7 x 10^-4 (the product of the two independent mutational events >occurring in the same sample space or trial).]

Now what are you babbling about? Are you now going to claim the drug
resistant viruses already pre-exist in an HIV population? And that
combination therapy for the treatment of HIV doesn’t work? Are you now
going to claim that there are 1.7 x 10^-4 mutations in each HIV
genome? Just what do you think the mutation rate is for HIV?

>In a population of 10^9 cells, we would predict that about 1.7 x 10^5 cells (again assuming only one mutation per >genome) would have a mutation. That is, for each site in the virus, we would expect to see, on average, 10 mutations. > That doesn't mean that there will be any specific mutation. After all the probability that a given site will have a mutation >is not 100%. It is only 99.995%.
>The probability that any specific site in the genome would not have a mutant in a population of 10^9 individuals is >0.005%. The probability that there will be *some* site among the 1.7 x 10^4 sites that lacks a mutation under these >assumptions would be (1-0.00005)^17000 = 0.9185.
>http://www.google.com/url?sa=D&q=http://stattrek.com/tables/binomial.aspx&usg=AFQjCNFD6jhcrRqTto04yeg5U72fu->B9Fw
>I am assuming a binomial distribution and calculating for k = 0, in which case many of the terms cancel out of the >probability mass function; see:
> http://www.google.com/url?sa=D&q=http://en.wikipedia.org/wiki/Binomial_distribution&usg=AFQjCNEtuJmLDMfl_gR551>KO9FX_GDoTIw
>The probability of the event (no mutation) is the probability of no mutant per site and the number of trials is the number of >sites.
>That means that there is about a 92% probability that at least one nt site in the genome will not exhibit a mutant event >somewhere in a population of 10^9 viruses. Of course, if the population is larger, this probability will decrease.

Hersheyh, perhaps an intracranial injection of simethicone would help.

Now that we know some of the more relevant probabilities, what is the
precise question that you were trying to ask? Assuming it wasn't the
uninteresting and irrelevant question of how many combinations are
possible.

I have no further questions. However I would ask the moderators of the
google talkorigin discussion site to issue protective suits when
hersheyh has a brain flatulence attack which occur on a regular basis
and are often for prolonged periods.
>> > > My question to this professor of evolution is then why don t
>> > > these drug resistant strains increase in frequency even when the
>> > > selection pressures don t exist?
>> > See above. Because they are either neutral or detrimental in an
>> > environment without the selection pressures. That does not mean that
>> > a given population won't have any resistance mutants. Again, there
>> > will be an equilibrium between loss of the mutant allele and gain of
>> > new mutants of that type (at least for mutations due to point
>> > mutations).
>> Of course they are but beneficial or detrimental are a function of the
>> environment. But somehow you evolutionists conjured up a belief that
>> an environment exists which would transform reptiles into birds. Do
>> you think the environment remains constant for millions of years?
>In fact, if environments did remain constant, evolution would slow down because the population would already be >optimized. Not stop. But slow down.

It frightens me to ask this question but if I get on my hersheyh anti-
brain flatulence protective suit first I can safely read the response,
is the Lenski environment constant?

John Harshman Sep 10, 2:10 pm

Newsgroups: talk.origins
From: John Harshman <jharsh...@pacbell.net>

Date: Sat, 10 Sep 2011 14:10:59 -0700
Local: Sat, Sep 10 2011 2:10 pm

Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

>Charles Brenner wrote:

>> On Sep 9, 11:01 pm, John Harshman <jharsh...@pacbell.net> wrote:
>>> Charles Brenner wrote:

>>>> On Sep 9, 1:36 pm, Mark Isaak <eci...@curioustaxonomyNOSPAM.net>
>>>> wrote:
>>>>> On 9/9/11 7:59 AM, Alan Kleinman MD PhD wrote:
>>>>>> On Aug 10, 1:45 pm, Inez<savagemouse...@hotmail.com> wrote:
>>>>>>> On Aug 4, 4:05 pm, Alan Kleinman MD PhD<klein...@sti.net> wrote:
>>>>>>> <snippers>
>>>>>>>> What I would like to hear from either of you evolutionists is a
>>>>>>>> reasonable explanation how neutral mutations can spread through a
>>>>>>>> population faster than beneficial mutations which have selection
>>>>>>>> assisting in the spread of these beneficial mutations.
>>>>>>> You are tediously thick headed. No one made that claim.
>>>>>> You had better tell that to John Harshman because he has claimed that
>>>>>> a couple hundred neutral mutations are fixed every generation,

>>>>>> generation after generation for hundreds of thousands of generations.

>>>>>> Would you care to compute the joint probability of all those neutral
>>>>>> mutations being fixed?
>>>>> The chance of any one new neutral mutation being fixed is 1/2N. The
>>>>> number of new neutral mutations per person is about 50. The number of
>>>>> people is N. You can do the math from there. Don't forget to multiply.
>>>> This simplistic argument is driving me nuts.
>>>> What have you in mind for N? If you are thinking billions, then you
>>>> are thinking modern humans and Dr. Dr.'s confused picture of mutations
>>>> propagating among living people like a plague is what you have.
>>> No it isn't. Why would you think so?
>> Because I think that N in the billions means recent history, far too
>> recent for any new mutations to proliferate around the globe.
>> Therefore I suppose that any (near) fixation of man-monkey difference
>> occurred when N was small.
>Certainly smaller than today. But that isn't a bottleneck. A bottleneck
>is a sharp, temporary decrease in population size.

Charles, you are going to catch yourself in a mathematical trap.
Mutation and selection requires large (sub)populations to achieve the
probabilities necessary for the beneficial mutation to occur at the
proper locus. Selection gives these bottlenecks and improved
replicators to go through these bottle necks to increase the
population size after going through the bottleneck. On the other hand,
neutral evolution requires smaller populations in order to have
reasonable probabilities that all the members will get these neutral
mutations by common descent. The human and chimpanzee genomes have
some major differences such as being non-homologous and having
different chromosome number. Either humans and/or chimpanzees had to
have simultaneous equivalent massive mutational changes giving
identical chromosomal rearrangement and renumbering of chromosomes in
both male and female members of the population and the male and female
members with those chromosomal rearrangements would have to find each
other and mate with these newly generated massively mutated but
freshly minted homologous chromosomes. Either way, your mathematics
collapses either on the weight of the population size or the lack of
population size.

>> That means the argument that billions of
>> people provide billions of candidates for mutation is irrelevant. The
>> real analysis must be more subtle and take into account the
>> approximate population sizes over time.
>Yes, it's irrelevant. Fortunately, it's easy to show that population
>size doesn't actually affect the number of neutral substitutions. It
>completely cancels out of the equations. (Though it does effect the
>speed of individual fixations, it doesn't affect their numbers.)

Charles, why don’t you present your model of neutral fixation? So far
the model is based on a single gene with two neutral alleles. What
happens if there are three neutral alleles? What happens if there are
two unlinked genes each with two neutral alleles each and so on? John
is doing the typical evolutionist gross over-extrapolation of a simple
model of the fixation of a single neutral allele and claiming that
hundreds of neutral alleles are being fixed every generation,

generation after generation for hundreds of thousands of generations.

You use the word plague and I use the word sweep to describe what John
is claiming.

>> In particular, note that we will NOT find a back-of-the-envelope
>> calculation that shows that 35 million differences is easy to achieve,
>> a conservative estimate. It's a barely possible estimate given the
>> actual historical facts, since it is the number of difference that
>> have barely been achieved.
>That makes no sense at all. Are you saying that anything that actually
>happens is therefore unlikely?

Mathematical expressions of likely or unlikely require the correct
formulation of the probability calculations. It is clear that
evolutionists have not formulated the probability calculations for
mutation and selection correctly and now evolutionists are trying to
take a simple model of a single gene with two alleles and the fixation
of one or the other allele and then claim that hundreds of neutral
alleles are spreading through a population like a plague or sweeping
through the population. What evolutionists always leave out of the
discussion is the multiplication rule of probabilities for the
computation of the joint probabilities of multiple random events
occurring. This is why if you try to extend your neutral model to the
fixation of two or more neutral alleles, you are going to hit a
massive mathematical barrier. And this is why the theory of evolution

is a mathematically irrational belief system.

>>>> So what should our model be?
>> See below.
>>>> What does the bottleneck at which human and monkey separated look
>>>> like?
>>> Who says there is a bottleneck?
>> I had in mind the path back in time tracing the human population to
>> the schism then forward via the monkeys. Perhaps it is incorrect to
>> use the word "bottleneck" in this way.
>It is indeed.

How would you know John? You don’t understand the simplest principles
of probability theory and your claims justify Charles’ use of the word
“plague” to describe how you think that neutral mutations spread
through a population.

>> Anyway, what I wonder is what
>> is the right way to visualize the population genetic picture of
>> separation; how mutations propagate in one branch or the other to
>> distinguish them.
>Consider, hypothetically, an originally unpartitioned population filled
>with genetic polymorphisms. Now suppose that for some reason that
>population splits into two (hypothetically, instantly). They start out
>with identical polymorphisms. But gradually, in each population, some
>become fixed and others become extinct. Viola: divergence.

And now all you have to do John is explain how the populations
diverged by tens of millions of neutral mutations, massive chromosomal
rearrangements and homology changes in 500,000 generations. So far
your explanation has been mathematically irrational.

>>>> Note that fixation isn't really the issue - fortunately as absolute
>>>> fixation of neutral single nucleotide mutations rarely happens. 10^8
>>>> human births per year times 10^-8 mutation rate means that just when
>>>> you think the last surviving rare type is about to die, a backmutation
>>>> in a newborn somewhere extends the the persistence of the type.
>>> Yes, we have no absolute fixation, just frequencies too low to be
>>> noticed in a reasonable sample. But the difference isn't important.
>> Maybe not. What is our "reasonable sample" size? 1? 6?
>Depends on the frequency you want to find. Why?

John, perhaps you don’t care what the sample space size is for a
probability problem but others who are interested in do the
mathematics correctly are. When are you going to learn the basics of
probability theory? Or don’t you think that probability theory is
applicable to this stochastic process?

>>>> So what is the data that the supposed 35 million SNP differences
>>>> between man an monkey comes from, and what does it really mean? I
>>>> don't know.
>>> I do. It's a comparison of the complete genomes of human and chimp, base
>>> by base.
>>>> Even if it's a matter of comparing sequences (rather than
>>>> e.g. extrapolating based on assumptions about population histories) I
>>>> think it's more statistical that just counting -- humans too have many
>>>> neutral differences from one another. Lots of definitional
>>>> complications.
>>>> Not easy questions.
>>> Easier than you may imagine. Now the human genome is a composite
>>> sequence of pieces from more than on individual, but any human should be
>>> good enough to compare with a chimp, since humans are 99.9% similar as
>>> opposed to 98.7% similarity between chimps and humans.
>> Ok, that's a helpful point (though not an answer - any two humans
>> already differ by 35 million SNPs, so a sample of 1 isn't enough.
>No they don't. They differ by a few million at most, depending on
>closeness of relationship.
>> With
>> small samples there remains, I think, an issue of ascertainment). But
>> you did skip over my question about "what model?"
>It seemed obvious. The standard neutral model works pretty well, and
>when estimating the number of expected fixations does not require any
>information about population sizes.

John, show your work.

A continuation or responses to posts 976-1001 will be done in the next
msg.

[Alan Kleinman MD PhD]

The following are the remainder of responses to posts 976-1001 and
splinter threads.
Mark Isaak Sep 10, 5:12 pm

Newsgroups: talk.origins
From: Mark Isaak <eci...@curioustaxonomyNOSPAM.net>

Date: Sat, 10 Sep 2011 17:12:16 -0700
Local: Sat, Sep 10 2011 5:12 pm

Subject: Re: The Theory of Evolution is Mathematically Irrational
Round 2

>On 9/9/11 5:34 PM, Charles Brenner wrote:
>> On Sep 9, 1:36 pm, Mark Isaak<eci...@curioustaxonomyNOSPAM.net>
>> wrote:
>>> On 9/9/11 7:59 AM, Alan Kleinman MD PhD wrote:
>>>> On Aug 10, 1:45 pm, Inez<savagemouse...@hotmail.com> wrote:
>>>>> On Aug 4, 4:05 pm, Alan Kleinman MD PhD<klein...@sti.net> wrote:
>>>>> <snippers>
>>>>>> What I would like to hear from either of you evolutionists is a
>>>>>> reasonable explanation how neutral mutations can spread through a
>>>>>> population faster than beneficial mutations which have selection
>>>>>> assisting in the spread of these beneficial mutations.
>>>>> You are tediously thick headed. No one made that claim.
>>>> You had better tell that to John Harshman because he has claimed that
>>>> a couple hundred neutral mutations are fixed every generation,
>>>> generation after generation for hundreds of thousands of generations.
>>>> Would you care to compute the joint probability of all those neutral
>>>> mutations being fixed?
>>> The chance of any one new neutral mutation being fixed is 1/2N. The
>>> number of new neutral mutations per person is about 50. The number of
>>> people is N. You can do the math from there. Don't forget to multiply.
>> This simplistic argument is driving me nuts.
>> What have you in mind for N?

>Doesn't matter. Notice that the Ns cancel. The result is the same
>whether the population is in the hundreds, as may have been the case
>shortly after the human-chimp split, or in the billions, as today. The
>equation does *not* handle quickly growing or shrinking populations, but
>those are probably relatively few generations out of millions.

I see, so our social engineer thinks that mutation and selection works
efficiently with populations of hundreds. Mark, I like hearing a good
evolutionist fairytale, tell us how humans got a different number of
chromosomes from chimpanzees and tell us how both a male and female
both got the same chromosome number when the change occurred and the
lucky bride and groom met each other?

>> If you are thinking billions, then you
>> are thinking modern humans and Dr. Dr.'s confused picture of mutations
>> propagating among living people like a plague is what you have.

>Neutral mutations, by definition, cannot be plague-like, unless you are
>counting invisible, inconsequential plagues.

So Mark, tell us how these neutral mutations in one family line find
there way into unrelated family lines?

>> So what should our model be?
>> What does the bottleneck at which human and monkey separated look
>> like?
>> Note that fixation isn't really the issue - fortunately as absolute
>> fixation of neutral single nucleotide mutations rarely happens. 10^8
>> human births per year times 10^-8 mutation rate means that just when
>> you think the last surviving rare type is about to die, a backmutation
>> in a newborn somewhere extends the the persistence of the type.
>> So what is the data that the supposed 35 million SNP differences
>> between man an monkey comes from, and what does it really mean? I
>> don't know. Even if it's a matter of comparing sequences (rather than
>> e.g. extrapolating based on assumptions about population histories) I
>> think it's more statistical that just counting -- humans too have many
>> neutral differences from one another. Lots of definitional
>> complications.

>I'm not sure, but I'm pretty sure the number of differences does come
>from comparing the sequences and counting. After all, both genomes have
>been sequenced, and the comparing and counting is pretty easy to do by
>computer.
>As to what they all mean, that is why there are still geneticists working.

Mark, you actually hit the nail on the head here. One of the main
reasons evolutionists are fighting so hard here is job security. How
many people would want to hear hersheyh’s babble once they understand
he knows nothing about how mutation and selection actually works?

John Harshman Sep 14, 2:24 pm

Newsgroups: talk.origins
From: John Harshman <jharsh...@pacbell.net>

Date: Wed, 14 Sep 2011 14:24:24 -0700
Local: Wed, Sep 14 2011 2:24 pm
Subject: Re: Trying to salvage something from this Re: The Theory of
Evolution

>Alan Kleinman MD PhD wrote:

>> On Aug 11, 7:16 am, John Harshman <jharsh...@pacbell.net> wrote:
>>> Alan Kleinman MD PhD wrote:

>>>> On Jul 13, 1:56 pm, John Harshman <jharsh...@pacbell.net> wrote:
>>>>> g...@risky-biz.com wrote:
>>>>>> <snip all>
>>>>>> It's clear by now that Kleinman has no intention of answering the

>>>>>> questions posed to him. But I've learned some interesting biology from
>>>>>> this group, even from unpromising threads.

>>>>>> "Harshman's" count of genetic differences between humans and chimps
>>>>>> has been bandied about in this thread. I've been wondering, could you
>>>>>> characterize those differences a bit? How many of them are in coding
>>>>>> areas?
>>>>> Very few. Coding regions are only around 3% of the genome, and
>>>>> accumulate about a third the number of differences per base as neutrally
>>>>> evolving regions.

>>>> You couldn’t be more wrong John, over 70% of the genes in humans and

>>>> chimpanzees don’t code identical proteins.

>>> While true, that has nothing to do with anything we've been discussing.
>>> Do you understand that a single base change can produce non-identical
>>> proteins? If there are 30,000 genes, that's 21,000 mutations. Out of 40

>>> million. And even many of those are neutral.
>> It has everything to do with what we are discussing. There are huge
>> stretches of the two genomes which can not be matched up for homology.

>True. Do you know how they got there? Most of them are retrotransposons,
>yet another class of neutral mutations.

So how did either human or chimpanzee males and females get identical
retrotransposons and get them simultaneously to maintain homology
within their own breeding group? And how many times must this happen
to account for the differences in the two genomes. And are you going
to tell us that the chimpanzee 47 and 48 chromosomes are nothing more
than neutral mutations? You are not doing a base by base comparison of
the two genomes. Evolutionists look for stretches in the two genomes
that have some similarity and line these stretches up. Your 98.7%
similarity is a load of evolutionist crap. Why don’t you line up
chromosome 21 and tell us how similar these chromosomes are?

>> This data is presented for those areas which can be matched and the
>> match is not close at all.

>It isn't? 98.7% identity isn't close? What would constitute close, then?

You evolutionists are cherry picking data out of the two chromosomes.
Your claim is an evolutionist fabrication and is a totally
untrustworthy estimate. Have you gotten your subscription to “Science”
yet? Read the full article
http://www.sciencemag.org/content/295/5552/131.abstract&usg=AFQjCNF6LJDM3GHffyRjXPABtkVjwnfm9w
and tell us how similar chromosome 21 is for humans and chimpanzees.

In this URL, they studied chromosome 21. They report “We detected
candidate positions, including two clusters on human chromosome 21
that suggest large, nonrandom regions of difference between the two
genomes.” Nonrandom means these are selective differences. Perhaps you
want to claim these differences are due to a retrotransposon, from
where?

>> Evolutionists claim that humans and
>> chimpanzees come from a common progenitor. Now you are claiming that
>> many of these differences are neutral which is typical evolutionist
>> speculation.

>Simple observation of how proteins work.

More like simple minded evolutionist speculation. Why don’t you
explain to us why humans and chimpanzees produce identical insulin
molecules but do not produce identical preproinsulin molecules?

> Tell us which are neutral differences and which are
> selective differences.

Well, it seldom matters whether a protein has leucine, isoleucine, or
phenylalanine in a particular spot.

You are not answering. The authors of the study of chromosome 21 said
there are long non-random stretches of bases. You have claimed that
you don’t need selection to get non-random sequences. Tell us how you
distinguish neutral differences from selective differences in a
genome.

> And then compute the joint probability of two

> neutral mutations being fixed in a population.

Are you still on about that? Your joint probability is irrelevant. We
don't care about the joint probability of some particular set of
mutations being fixed, only about the probability that any set of
mutations will be fixed. Different, no?

John, we all know that you don’t know how to analyze a stochastic
process and both mutation and selection and mutation without selection
are stochastic processes. The joint probability of events occurring in
a stochastic process has been and always will be governed by the
multiplication rule of probabilities. The accumulation of mutations
must always occur by common descent unless you have some lateral form
of transfer of mutations. The probability of these mutations
accumulating will always be governed by the multiplication rule of
probabilities.

>>>>>> How many with other known functions? How much "junk"?
>>>>> Almost all is junk, just as almost all the genome is junk. Non-coding,
>>>>> functional regions are just another few percent of the genome.
>>>> This is the type of stupidity that evolutionist perpetuate. If they
>>>> don’t know what a portion of the genome does, it is junk.
>>> No, that's not how it works. We recognize junk by the fact that it
>>> evolves at the rate of mutation.

>> Take a look at this URL: http://www.google.com/url?sa=D&q=http://www.sciencemag.org/content/295/5552/131.abstract&usg=AFQjCNF6LJDM3GHffyRjXPABtkVjwnfm9w
>> In this URL, they studied chromosome 21. They report “We detected
>> candidate positions, including two clusters on human chromosome 21
>> that suggest large, nonrandom regions of difference between the two
>> genomes.” Nonrandom means these are selective differences
>No it doesn't.

This is the second time you have made this claim. So tell us how you
distinguish selective genetic differences from non-selective. You go
around claiming that most of the differences between human and
chimpanzee genomes are neutral. Tell us how you have come to this
conclusion. Or don’t you think that explaining how you come to your
conclusions is relevant? You have claimed that 98.7% of the human and
chimpanzee genomes are identical yet these authors studied chromosome
21 and found large non-random differences between the two chromosomes.

>> and we all
>> should know by now that selective differences take hundreds of
>> generations per base substitution. But you claim that neutral
>> mutations fix at the rate of a couple of hundred per generation,
>> thousands of times faster than selection can fix a beneficial
>> mutation.
>Once again you confuse numbers with rates.

No I haven’t John. Even Charles Brenner is using the word “plague” to
describe what you are claiming.

>>>> If they
>>>> don’t understand how to do a mathematical computation it is junk.
>>>> John, just because you are ignorant what a non-coding region of a
>>>> genome does, don’t impose your ignorance on us by claiming this is
>>>> junk. If a region of DNA has no coding function for proteins but
>>>> remains non-random, it does so because it has stabilizing selection
>>>> acting on those sequences.
>>> True. Which has nothing to do with what I'm talking about. Stabilizing
>>> selection makes loci evolve at less than the neutral rate. Such loci are
>>> only a few percent of the genome. By the way, evolution isn't so fast as
>>> to randomize sequences in 5 million years.
>> Just what are you talking about? I guess you missed the study I posted
>> above about the large non-random differences on chromosome 21 between
>> humans and chimpanzees.
>So? How is that relevant? Do you have access to the whole article? I don't.

It is relevant because you have claimed that the human and chimpanzee
genomes are 98.7% similar and here is data from chromosome 21 which
shows you are wrong. Yes I have access to the whole article and I told
you how you could get access to the article without cost. Don’t use
ignorance as a defense to your irrational claims.

> 70% of genes code for different proteins,
....if by "different" you mean having at least one different amino
acid.

At least one amino acid different.

>> large stretches of non-random differences between human and chimpanzee
>> genomes yet neutral evolution will fix all these differences a rate of
>> a couple of hundred per generation, thousands of times faster than a
>> single beneficial mutation can be fixed in a population. What you are
>> talking about is mathematical irrationality.
>I've become convinced that you know almost nothing about mathematics
>beyond the scraps rote learning you have displayed here.

John, I am not the one who has thrown out the multiplication rule of
probabilities. This is the governing rule of the joint probability of
events for a stochastic process. And every time you claim that I know
almost nothing about mathematics, I’m going to remind you about how
population size affects the probabilities of events. If you continue
in this discussion, I’m going to teach you something about the
practice of hard mathematical science and show you why your theory of

evolution is a mathematically irrational belief system.

>>>> And the reason it has stabilizing selection
>>>> pressures acting on those sequences is that it has some type of
>>>> important function on maintaining the life and reproductive capability
>>>> of that member. The only junk in this discussion is the evolutionist
>>>> junk science which fails to properly explain how mutation and
>>>> selection works.
>>> You mistake evolution at the rate of mutation for stabilizing selection,
>>> presumably because you have a false understanding of the mutation rate.
>>> Neutral evolution produces only a bit more than 1% difference over 5
>>> million years, not a randomization of sequences.
>> You will only get randomization of sequences if there is no selection
>> acting on that sequence. Your mathematics is faulty because 5 million
>> years only represents about 500,000 generations and you can not fix
>> 40,000,000 differences in two divergent populations in such a short
>> period of time. It is mathematical irrationality to believe this.
>You seem to have stopped even pretending to have an argument and are
>just repeating your mantra regardless of what you are supposedly
>responding to.

Here’s your big opportunity to show us how my mantra is wrong. Show us
how 40,000,000 neutral or selective mutations sweep through or spread
like a plague through the two populations.

>>>>>> Of the ones that are in coding areas, how many are thought to make
>>>>>> significant "interesting" morphological differences rather than minor,
>>>>>> possibly non-function-altering changes to a protein?
>>>>> Again, very few. The vast majority of differences in coding regions are
>>>>> silent, i.e. making no difference in the protein being coded for.
>>>> Really John? Is that why over 70% of the genes in humans and
>>>> chimpanzees code for different proteins? I can’t tell what you are
>>>> worse at, mathematics or the interpretation of data.
>>> This is silly. "Over 70% of the genes code for different proteins" is a
>>> reasonable expectation for neutral evolution. Few of these differences
>>> mean anythng.
>> We all know about evolutionist expectations, they are mathematically
>> irrational. But if you want to show your work and compute the joint
>> probability of two neutral mutations being fixed in a population, that
>> would be some interesting evolutionist folklore to hear.
>Mantra. At least your mantra does evolve over time, though it seems to
>be randomly so.

My mantras are selective John. They are based on hard mathematical and
empirical evidence. Even hersheyh now agrees that I’ve derived the

correct probability function for the mutation and selection phenomenon

except he is whining about the 4 in the denominator of the mutation
rate. Hersheyh still hasn’t figured out that there is more than a
single possible outcome from a mutation. So I guess you are not going
to derive for us the probability of two neutral mutations being fixed
in a population.

>>>>>> I assume this is ongoing research; perhaps the answers are not yet
>>>>>> clear.
>>>>> Oh, no. They're quite clear. What isn't clear is the exact number and
>>>>> identities of the comparatively few functional differences.
>>>> John, your irrational speculations don’t form a scientific basis for
>>>> any of your claims. You don’t know how mutation and selection works
>>>> and you can’t explain why over 70% of the genes code for different
>>>> proteins in humans and chimpanzees.
>>> By "different" you merely mean -- though you probably don't know it --
>>> that there is at least one amino acid difference, i.e. one point
>>> mutation. Trivial.
>> Tens of thousands of different proteins between humans and chimpanzees
>> fixed in 500,000 generations, that’s what a mathematically irrational
>> evolutionist would call “trivial”. Maybe these proteins diverged
>> during the pre-split period, you know, the banana split period.
>>> [mantra snipped]
>> Repeat after me, reptiles transform into birds, reptiles transform
>> into birds, reptiles transform into birds…
>That is indeed what the data show. Care to discuss it?

So John, are you now going to claim that 98.7% of the data shows that
reptiles transform into birds?

pnyikos Sep 15, 7:37 am

Newsgroups: talk.origins
From: pnyikos <nyik...@bellsouth.net>
Date: Thu, 15 Sep 2011 07:37:25 -0700 (PDT)
Local: Thurs, Sep 15 2011 7:37 am
Subject: Re: Trying to salvage something from this Re: The Theory of
Evolution

>There may be unintended irony in the title: the thread has fragmented
>into many pieces in Google, and we may have a big salvage job on our
>hands just on that account.
>I've been told that once an ongoing thread passes 1000 posts, it
>fragments in Google. This is apparently exactly what has happened. I
>wonder whether it has also fragmented in e.g. Giganews.

>On Sep 14, 1:01 pm, Alan Kleinman MD PhD <klein...@sti.net> wrote:
>I've heard a bit about you, Dr. Dr. Kleinman. Now that we are in a
>thread a mere 2 posts deep (before I post this) maybe we can get
>acquainted without a lot of confusion about who said what when.

What do you want to know about me?

>> On Aug 11, 7:16 am, John Harshman <jharsh...@pacbell.net> wrote:
>> > Alan Kleinman MD PhD wrote:

>> > > On Jul 13, 1:56 pm, John Harshman <jharsh...@pacbell.net> wrote:
>> > >> g...@risky-biz.com wrote:
>> > >>> <snip all>
>> > >>> It's clear by now that Kleinman has no intention of answering the
>> > >>> questions posed to him.
>I've seen many claims like the above turn out to be false due to the
>person making them having "answering the questions posed to him" mean,
>in addition "to my satisfaction." I wonder whether that is the case
>here.
>[ditto "addressing" statt "answering"]
>[the German "statt" is so much easier to type than the English
>"instead of", nicht wahr?]

Evolutionists get very uncomfortable when you actually do the
mathematical accounting which describes mutation and selection.
Presenting the correct mathematical formulation of the mutation and
selection phenomenon pertains more than just to showing that the
theory of evolution is mathematically irrational, it gives the proper
understanding of how to deal with drug resistant microbes, herbicide
resistant weeds, pesticide resistant insects and giving the proper
logic for developing more durable cancer treatments. Evolutionists are
either unable to understand the basic science and mathematics of
mutation and selection or unwilling to teach the basic science and
mathematics correctly.

>> > >>> "Harshman's" count of genetic differences between humans and chimps
>> > >>> has been bandied about in this thread. I've been wondering, could you
>> > >>> characterize those differences a bit? How many of them are in coding
>> > >>> areas?
>> > >> Very few. Coding regions are only around 3% of the genome, and
>> > >> accumulate about a third the number of differences per base as neutrally
>> > >> evolving regions.
>> > > You couldn t be more wrong John,
>The following doesn't seem to support the "couldn't be more wrong"
>assertion:

>> > > over 70% of the genes in humans and
>> > > chimpanzees don t code identical proteins.
>This shows how the claim that humans share 98% or more of their
>"genetic material" with chimps needs to be clarified. Way back in
>1995 or 1996 I asked whether this referred to loci, alleles, or base
>pairs.

You need to understand something about John’s claims. He never
describes how he comes up with his numbers. John is now claiming that
the vast majority of genetic differences between humans and
chimpanzees are not selective and that neutral evolution will allow
him to do the accounting for these tens of millions of differences
between the two genomes in about 500,000 generations. It is already
clear that mutation and selection can not make these types of massive
transformations in such a small number of generations. So now John
claims that mutation without selection will allow neutral mutations to
spread through a population like a “plague”.

>You've just now confirmed that it is NOT "alleles". Harshman seems to
>opt for "base pairs":

The creation of new alleles requires mutation. If the adaptation
process requires more than a single mutation to create the new adapted
allele the process has a particular mathematical behavior for the
accumulation of those beneficial mutations. Earlier in the thread I
presented the probability function which describes the mathematics of
this stochastic process.

>> > While true, that has nothing to do with anything we've been discussing.
>> > Do you understand that a single base change can produce non-identical
>> > proteins?
>And thus, 98% of the base pairs might be identical yet
>physiologically, the two organisms might be very dissimilar.

No one is arguing here that a breeding program can give you Chihuahuas
and Great Danes from the canine family. What the question is here is
how do you do the accounting for the tens of millions of genetic
differences between humans and chimpanzees in 500,000 generations. Any
attempt to do this mathematically will show that this type of
transformation in so few numbers of generations is mathematically
irrational.

>> > If there are 30,000 genes, that's 21,000 mutations. Out of 40
>> > million. And even many of those are neutral.
>> It has everything to do with what we are discussing. There are huge
>> stretches of the two genomes which can not be matched up for homology.
>Apparently you mean "matched up BASE FOR BASE". But loci can be
>matched up in most cases even if the bases differ, no?

No! If you look at the genomes in more detail, there are large
stretches of the two genomes for which there are not base for base
matches. And these stretches are not random sequences. And you have
only 500,000 generations to do the accounting for any of these
mismatches.

>> This data is presented for those areas which can be matched and the

>> match is not close at all. Evolutionists claim that humans and

>> chimpanzees come from a common progenitor. Now you are claiming that
>> many of these differences are neutral which is typical evolutionist
>> speculation.

>It may be based on solid data, as even you seem to allow for here:

What solid data? John Harshman won’t get a free subscription to
“Science” and read the full citation I gave him which shows the large
non-random differences between human and chimpanzee chromosome 21.
Evolutionists are cherry picking their data to try to support their

mathematically irrational theory of evolution.

>> Tell us which are neutral differences and which are

>> selective differences. And then compute the joint probability of two

>> neutral mutations being fixed in a population.

>The non-neutral mutations (especially the beneficial ones) would seem
>to be also relevant to your skepticism about humans and chimps being
>related.

A genetic difference is a genetic difference is a genetic difference.
Somehow all these differences must spread through the populations. It
takes time (generations) for this process to happen. 500,000
generations is not nearly enough generations for mutation and
selection to do this process. This is why evolutionists have
fabricated neutral evolution to attempt to do the accounting. It’s
bizarre that evolutionists would think that mutation without selection
would be more efficient at spreading a mutation through a population.

>By the way, does "neutral" mean "coding for the same protein, only

>differering in the mRNA"? Does it include that? It's been a while

>since I've looked at this part of genetics.

There are really two parts to the “neutral” claim. The first part is
due to the redundancy of the genetic code. More than one codon can
code for a single amino acid. The second part is that some amino acid
substitutions do not affect protein conformation much. Regardless, if
you are going to claim that humans and chimpanzees come from a common
progenitor then diverged for 500,000 generations, you have to account
for the genetic differences spreading through the two populations.
That process takes generations, lots of generations to do and you
don’t have sufficient number of generations to make this
transformation.

>> > >>> How many with other known functions? How much "junk"?
>> > >> Almost all is junk, just as almost all the genome is junk. Non-coding,
>> > >> functional regions are just another few percent of the genome.
>> > > This is the type of stupidity that evolutionist perpetuate. If they
>> > > don t know what a portion of the genome does, it is junk.
>> > No, that's not how it works. We recognize junk by the fact that it
>> > evolves at the rate of mutation.
>No direct testing to see whether it is ever translated into
>polypeptides? I'm disappointed.

DNA has more functions than simply producing polypeptides. Some points
on DNA are binding sites for proteins. If those binding sites are
transformed by mutation, the binding protein may not find that site.
Also the DNA molecule must also have the correct conformation to
expose those binding sites at the correct time for the control of
protein synthesis and replication. Cells operate under very tight
control. The non-protein portions of the DNA molecule gives that
control system. It would not be very efficient for cells to have to
replicate large portions of unnecessary DNA.

>> Take a look at this >URL:http://www.google.com/url?sa=D&q=http://www.sciencemag.org/content/295/5552/131.abstract&usg=AFQjCNF6LJDM3GHffyRjXPABtkVjwnfm9w
>> In this URL, they studied chromosome 21. They report We detected
>> candidate positions, including two clusters on human chromosome 21
>> that suggest large, nonrandom regions of difference between the two
>> genomes. Nonrandom means these are selective differences and we all
>> should know by now that selective differences take hundreds of
>> generations per base substitution.
>I don't know it, being new to this thread and not having studied
>population genetics in sufficient depth.

This citation has nothing to do with population genetics. These
scientists simply compared human chromosome 21 with chimpanzee
chromosome 21 and found large stretches of non-random differences
between the two chromosomes. I wonder if John Harshman has ever tried
to do a base by base comparison of chromosomes 47 and 48 from
chimpanzees with chromosomes 47 and 48 from humans?

>> But you claim that neutral
>> mutations fix at the rate of a couple of hundred per generation,
>> thousands of times faster than selection can fix a beneficial
>> mutation.
>It all depends on how "large" those nonrandom regions are.

The authors in the article do not specifically say how large the
regions are. But mutation and selection only works efficiently one
base at a time. And it takes hundreds of generations to amplify a
single mutation sufficiently so that there is a reasonable probability
for the next beneficial mutation to occur. 500,000 generations only
gives enough generations to mutate and select about 20,000 bases.

>> > > If they
>> > > don t understand how to do a mathematical computation it is junk.
>> > > John, just because you are ignorant what a non-coding region of a
>> > > genome does, don t impose your ignorance on us by claiming this is
>> > > junk. If a region of DNA has no coding function for proteins but
>> > > remains non-random, it does so because it has stabilizing selection
>> > > acting on those sequences.
>> > True. Which has nothing to do with what I'm talking about. Stabilizing
>> > selection makes loci evolve at less than the neutral rate. Such loci are
>> > only a few percent of the genome. By the way, evolution isn't so fast as
>> > to randomize sequences in 5 million years.
>> Just what are you talking about? I guess you missed the study I posted
>> above about the large non-random differences on chromosome 21 between
>> humans and chimpanzees. 70% of genes code for different proteins,
>> large stretches of non-random differences between human and chimpanzee
>> genomes yet neutral evolution will fix all these differences a rate of
>> a couple of hundred per generation, thousands of times faster than a
>> single beneficial mutation can be fixed in a population. What you are
>> talking about is mathematical irrationality.
>There seems to be a real problem here with distinguishing "beneficial"
>and "non-harmful".

Populations have no difficulty making that distinction. And if the
mutation is beneficial, it will be amplified because it gives a member
with improved fitness over other members. That beneficial mutation
will become the dominant variant in the population. On the other hand,
if the mutation is “non-harmful”, the only way it will amplify is if
it happens to have occurred on a member with a beneficial mutation.

>The genomes are huge. Lots of non-harmful mutations could be fixed
>simultaneously, no?

Tell us how all these non-harmful mutations spread through the
population. How does a neutral mutation in one family line show up in

a totally unrelated family line?

>I think this will do for a start. With the thread having shattered
>the way it has, it may take you quite some time to get around to this
>fragment.

Peter, I hope you find this post. I don’t have time to deal with
splintered threads and so I’m consolidating the threads. We need more
people with mathematical skills to address this mathematical
irrationality that evolutionists are spreading around. Naïve school
children are being trained to be mathematically incompetent nitwits
and evolutionists are bungling the basic science and mathematics of

the mutation and selection phenomenon.

pnyikos Sep 15, 8:04 am
Newsgroups: talk.origins
From: pnyikos <nyik...@bellsouth.net>
Date: Thu, 15 Sep 2011 08:04:08 -0700 (PDT)
Local: Thurs, Sep 15 2011 8:04 am
Subject: Re: Trying to salvage something from this Re: The Theory of
Evolution

>On Sep 14, 5:24 pm, John Harshman <jharsh...@pacbell.net> wrote:
>> Alan Kleinman MD PhD wrote:

>I've snipped a great deal, a lot of it addressed in my own reply to
>Kleinman. John, feel free to comment on some of what I wrote to him,
>especially if you get to this thread before he does,
>> > large stretches of non-random differences between human and chimpanzee
>> > genomes yet neutral evolution will fix all these differences a rate of
>> > a couple of hundred per generation, thousands of times faster than a
>> > single beneficial mutation can be fixed in a population. What you are
>> > talking about is mathematical irrationality.
>> I've become convinced that you know almost nothing about mathematics
>> beyond the scraps rote learning you have displayed here.
>That may be, but since I tuned in very, very late (after 1000 posts
>went by, apparently) I wonder if you could give me a short synopsis of
>what this "mathematical irrationality" is all about.

Peter, you are not going to get a good synopsis of evolutionist
“mathematical irrationality” from John Harshman. In one sentence,
evolutionist mathematical irrationality is based on discarding the

multiplication rule of probabilities for computing the joint

probability of random independent events for a stochastic process.

>> >>> And the reason it has stabilizing selection
>> >>> pressures acting on those sequences is that it has some type of
>> >>> important function on maintaining the life and reproductive capability
>> >>> of that member. The only junk in this discussion is the evolutionist
>> >>> junk science which fails to properly explain how mutation and
>> >>> selection works.
>> >> You mistake evolution at the rate of mutation for stabilizing selection,
>> >> presumably because you have a false understanding of the mutation rate.
>> >> Neutral evolution produces only a bit more than 1% difference over 5
>> >> million years, not a randomization of sequences.
>What is meant by "neutral evolution"?

Yes John, tell us how neutral mutations can spread through a
population like a plague without selection.

>> > You will only get randomization of sequences if there is no selection
>> > acting on that sequence. Your mathematics is faulty because 5 million
>> > years only represents about 500,000 generations and you can not fix
>> > 40,000,000 differences in two divergent populations in such a short
>> > period of time. It is mathematical irrationality to believe this.
>> You seem to have stopped even pretending to have an argument and are
>> just repeating your mantra regardless of what you are supposedly
>> responding to.
>Has the flaw in this mantra been laid bare?

Peter, this is what John does. If I had left off the sentence “It is
mathematical irrationality to believe this”, John would just say my
argument is irrelevant. John knows that he’s put himself in a logical
box and rather than admit he’s wrong, he uses words like mantra and
irrelevant to avoid the mathematical facts of life.

>> >>>>> Of the ones that are in coding areas, how many are thought to make
>> >>>>> significant "interesting" morphological differences rather than minor,
>> >>>>> possibly non-function-altering changes to a protein?
>> >>>> Again, very few. The vast majority of differences in coding regions are
>> >>>> silent, i.e. making no difference in the protein being coded for.
>Has anyone tried to compare the ones that DO make a difference? See
>below.

The point is you don’t have to do the comparison. You only have to
explain how these differences managed to spread through the population
in 500,000 generations. When you try to do that then it becomes
apparent why the theory of evolution is mathematically irrational.

>> >>> Really John? Is that why over 70% of the genes in humans and
>> >>> chimpanzees code for different proteins? I can’t tell what you are
>> >>> worse at, mathematics or the interpretation of data.
>> >> This is silly.
>You have yet to show it is silly. To do that, you'd have to show that
>there are also a lot of differences that make no difference in the
>protein being coded for. The vast majority, in fact.

How do you get mutations which make no difference spread through a
population?

>> >> "Over 70% of the genes code for different proteins" is a
>> >> reasonable expectation for neutral evolution. Few of these differences
>> >> mean anythng.
>What do you mean by "mean anything"? Are you suggesting that a
>substitution is only significant if it changes an amino acid of one of
>the four kinds (polar, etc.--I forget their names) into one of another
>kind?

If you want to get a mutation to spread through a population as
quickly as possible, it requires selection. John is now taking a
position that mutation without selection causes the mutations to
spread more quickly and for the process to work in parallel. John has
a fertile but mathematically irrational imagination.

>> > We all know about evolutionist expectations, they are mathematically
>> > irrational. But if you want to show your work and compute the joint
>> > probability of two neutral mutations being fixed in a population, that
>> > would be some interesting evolutionist folklore to hear.
>> Mantra. At least your mantra does evolve over time, though it seems to
>> be randomly so.
>Hmmm...I wonder how many mantras I could pick out from you if I tried,
>John? [keywords: ivory tower]

John has his mantras like reptiles transform into bird. It just so
happens his mantras are mathematically irrational.

>> >>>>> I assume this is ongoing research; perhaps the answers are not yet
>> >>>>> clear.
>> >>>> Oh, no. They're quite clear. What isn't clear is the exact number and
>> >>>> identities of the comparatively few functional differences.
>> >>> John, your irrational speculations don’t form a scientific basis for
>> >>> any of your claims.
>That's what several people keep telling me over and over again wrt
>intellligent design and directed panspermia, although they often
>soften it by leaving out words on the order of "irrational."

I’m not here to defend one world view or another; I’m here to present
the correct basic science and mathematics which describes how mutation
and selection works. Once you do understand how mutation and selection
works, you will realize that the theory of evolution is a
mathematically irrational belief system but you also will realize how
to address logically multidrug resistant microbes, multiherbicide
resistant weeds, multipesticide resistant insects and develop more
durable cancer treatments. You certainly won’t get this in a lecture
from an evolutionist.

>> >>>You don’t know how mutation and selection works
>> >>> and you can’t explain why over 70% of the genes code for different
>> >>> proteins in humans and chimpanzees.
>> >> By "different" you merely mean -- though you probably don't know it --
>> >> that there is at least one amino acid difference, i.e. one point
>> >> mutation. Trivial.
>Really? There are genetic "diseases" that hinge on only one point
>mutation. Would you like for me to look one up for you?
>> > Tens of thousands of different proteins between humans and chimpanzees
>> > fixed in 500,000 generations, that’s what a mathematically irrational
>> > evolutionist would call “trivial”. Maybe these proteins diverged
>> > during the pre-split period, you know, the banana split period.
>> >> [mantra snipped]
>> > Repeat after me, reptiles transform into birds, reptiles transform
>> > into birds, reptiles transform into birds…
>> That is indeed what the data show. Care to discuss it?
>Repeat after me: dinosaurs transform into birds... :-)
>Can't say it, can you? All you can say is "birds are
>dinosaurs". :-) :-)

Blizzards turn lizards into buzzards with gizzards. :-)

John Harshman Sep 15, 8:55 am

Newsgroups: talk.origins
From: John Harshman <jharsh...@pacbell.net>

Date: Thu, 15 Sep 2011 08:55:59 -0700
Local: Thurs, Sep 15 2011 8:55 am
Subject: Re: Trying to salvage something from this Re: The Theory of
Evolution
>pnyikos wrote:

>> On Sep 14, 5:24 pm, John Harshman <jharsh...@pacbell.net> wrote:
>>> Alan Kleinman MD PhD wrote:

>> I've snipped a great deal, a lot of it addressed in my own reply to
>> Kleinman. John, feel free to comment on some of what I wrote to him,
>> especially if you get to this thread before he does,
>>>> large stretches of non-random differences between human and chimpanzee
>>>> genomes yet neutral evolution will fix all these differences a rate of
>>>> a couple of hundred per generation, thousands of times faster than a
>>>> single beneficial mutation can be fixed in a population. What you are
>>>> talking about is mathematical irrationality.
>>> I've become convinced that you know almost nothing about mathematics
>>> beyond the scraps rote learning you have displayed here.
>> That may be, but since I tuned in very, very late (after 1000 posts
>> went by, apparently) I wonder if you could give me a short synopsis of
>> what this "mathematical irrationality" is all about.
>Simply put, Kleinman thinks that it's impossible for two loci to be
>under selection at the same time. His only model of evolution is
>combination drug therapy for HIV, because resistance to one drug is not
>advantageous in the presence of other drugs to which the virus is not
>resistant.

And I have presented dozens of empirical examples besides HIV
including examples of combination antiviral agents, antibiotics and
anti-parasitic agents for the prevention of resistance in the
treatment of infectious diseases, combination anti-cancer agents for
giving more durable cancer treatments, combination herbicide usage for
the prevention of herbicide resistant weeds in agriculture,
combination pesticides for the prevention of insecticide resistant
insects, all which show that when selection is targeting two genes
simultaneously, the mutation and selection process is stifled. And
John you have given us zero, zilch, nada empirical examples which show
that selection can occur at two loci simultaneously. In addition, I
have given you the correct derivation of the probability function for
two mutations to occur and it is clear that unless amplification of
the first mutation occurs, the probability of the second mutation
occurring is very low. This is the mathematical explanation why
selection can not occur at two loci simultaneously and why your theory

of evolution is a mathematically irrational belief system.

>>>>>> And the reason it has stabilizing selection
>>>>>> pressures acting on those sequences is that it has some type of
>>>>>> important function on maintaining the life and reproductive capability
>>>>>> of that member. The only junk in this discussion is the evolutionist
>>>>>> junk science which fails to properly explain how mutation and
>>>>>> selection works.
>>>>> You mistake evolution at the rate of mutation for stabilizing selection,
>>>>> presumably because you have a false understanding of the mutation rate.
>>>>> Neutral evolution produces only a bit more than 1% difference over 5
>>>>> million years, not a randomization of sequences.
>> What is meant by "neutral evolution"?
>Google is your friend. Look up "neutral theory", "Motoo Kimura", and
>such. Briefly, it's stochastic variation in allele frequency in the
>absence of selection, which will inevitably result in either loss or
>fixation, eventually.

Remember this Peter, John is lazy and apathetic. John would rather
refer you to the plethora of junk science that has developed around
his mathematically irrational belief system than try to explain this
junk science himself.

>>>> You will only get randomization of sequences if there is no selection
>>>> acting on that sequence. Your mathematics is faulty because 5 million
>>>> years only represents about 500,000 generations and you can not fix
>>>> 40,000,000 differences in two divergent populations in such a short
>>>> period of time. It is mathematical irrationality to believe this.
>>> You seem to have stopped even pretending to have an argument and are
>>> just repeating your mantra regardless of what you are supposedly
>>> responding to.
>> Has the flaw in this mantra been laid bare?
>Many, many times.

The only thing that John has laid bare is his inability to do a
probability calculation correctly. And if you want to model a
stochastic process like the mutation and selection phenomenon, you had
better learn how to apply the principles of probability theory. John
doesn’t like me reminding him that I had to show him how population
size affects the probabilities of a beneficial mutation occurring but
I will keep reminding him as long as he refuses to learn the
principles of probability theory. In particular, he needs to learn how
the multiplication rule of probabilities governs the joint probability
of multiple independent events occurring and he’s not the only
evolutionist who needs to learn this lesson. We have Schneider over at
the National Cancer Institute making the claim that the multiplication
rule does not apply to biological evolution. This mathematical and
scientific blunder only harm the people he is paid to help, that is
those people suffering from cancer.

>>>>>>>> Of the ones that are in coding areas, how many are thought to make
>>>>>>>> significant "interesting" morphological differences rather than minor,
>>>>>>>> possibly non-function-altering changes to a protein?
>>>>>>> Again, very few. The vast majority of differences in coding regions are
>>>>>>> silent, i.e. making no difference in the protein being coded for.
>> Has anyone tried to compare the ones that DO make a difference? See
>> below.
>Frequently.

Whether the mutations are neutral or beneficial, somehow they get into
all the genomes of every member of the population. John, if you don’t
like the word “sweep” then perhaps you are more comfortable with
Charles Brenner’s description that they spread like a “plague” through
a population.

>>>>>> Really John? Is that why over 70% of the genes in humans and
>>>>>> chimpanzees code for different proteins? I can’t tell what you are
>>>>>> worse at, mathematics or the interpretation of data.
>>>>> This is silly.
>> You have yet to show it is silly. To do that, you'd have to show that
>> there are also a lot of differences that make no difference in the
>> protein being coded for. The vast majority, in fact.
>What exactly are you asking for here?

You don’t have to show me which differences are neutral and which are
selective John, you simply need to show us how these mutations spread
like a plague through the population.

>>>>> "Over 70% of the genes code for different proteins" is a
>>>>> reasonable expectation for neutral evolution. Few of these differences
>>>>> mean anythng.
>> What do you mean by "mean anything"? Are you suggesting that a
>> substitution is only significant if it changes an amino acid of one of
>> the four kinds (polar, etc.--I forget their names) into one of another
>> kind?
>No, but you're close. There are many sites in the average protein that
>have a wide tolerance for different amino acids without any noticeable
>effect on activity.

So tell us John, why do tens of millions of variants show up in one
population in 500,000 generations and not in the other when it makes
no difference in the function of the proteins?

>>>> We all know about evolutionist expectations, they are mathematically
>>>> irrational. But if you want to show your work and compute the joint
>>>> probability of two neutral mutations being fixed in a population, that
>>>> would be some interesting evolutionist folklore to hear.
>>> Mantra. At least your mantra does evolve over time, though it seems to
>>> be randomly so.
>> Hmmm...I wonder how many mantras I could pick out from you if I tried,
>> John? [keywords: ivory tower]
>Feel free to try.

Reptiles turn into birds, reptiles turn into birds…

>>>>>>>> I assume this is ongoing research; perhaps the answers are not yet
>>>>>>>> clear.
>>>>>>> Oh, no. They're quite clear. What isn't clear is the exact number and
>>>>>>> identities of the comparatively few functional differences.
>>>>>> John, your irrational speculations don’t form a scientific basis for
>>>>>> any of your claims.
>> That's what several people keep telling me over and over again wrt
>> intellligent design and directed panspermia, although they often
>> soften it by leaving out words on the order of "irrational."
>Why is that relevant?

I’m shocked; I’m actually going to agree with John here. This
discussion is about how mutation and selection actually works and it
doesn’t work the way John thinks and why the theory of evolution is a
mathematically irrational belief system.

>>>>>> You don’t know how mutation and selection works
>>>>>> and you can’t explain why over 70% of the genes code for different
>>>>>> proteins in humans and chimpanzees.
>>>>> By "different" you merely mean -- though you probably don't know it --
>>>>> that there is at least one amino acid difference, i.e. one point
>>>>> mutation. Trivial.
>> Really? There are genetic "diseases" that hinge on only one point
>> mutation. Would you like for me to look one up for you?
>No. How is that relevant? If I say that most crows are black, can you
>refute me by showing me a white crow?

Once again John, you missed the point. A single detrimental mutation
can be lethal.

>>>> Tens of thousands of different proteins between humans and chimpanzees
>>>> fixed in 500,000 generations, that’s what a mathematically irrational
>>>> evolutionist would call “trivial”. Maybe these proteins diverged
>>>> during the pre-split period, you know, the banana split period.
>>>>> [mantra snipped]
>>>> Repeat after me, reptiles transform into birds, reptiles transform
>>>> into birds, reptiles transform into birds…
>>> That is indeed what the data show. Care to discuss it?
>> Repeat after me: dinosaurs transform into birds... :-)
>> Can't say it, can you? All you can say is "birds are
>> dinosaurs". :-) :-)
>Thank you for your contribution, such as it was.

What’s the matter John, don’t you appreciate your mantra?

John Harshman Sep 15, 9:03 am

Newsgroups: talk.origins
From: John Harshman <jharsh...@pacbell.net>

Date: Thu, 15 Sep 2011 09:03:26 -0700
Local: Thurs, Sep 15 2011 9:03 am
Subject: Re: Trying to salvage something from this Re: The Theory of
Evolution
>pnyikos wrote:
>> There may be unintended irony in the title: the thread has fragmented
>> into many pieces in Google, and we may have a big salvage job on our
>> hands just on that account.
>> I've been told that once an ongoing thread passes 1000 posts, it
>> fragments in Google. This is apparently exactly what has happened. I
>> wonder whether it has also fragmented in e.g. Giganews.

>> On Sep 14, 1:01 pm, Alan Kleinman MD PhD <klein...@sti.net> wrote:
>> I've heard a bit about you, Dr. Dr. Kleinman. Now that we are in a
>> thread a mere 2 posts deep (before I post this) maybe we can get
>> acquainted without a lot of confusion about who said what when.

>>> On Aug 11, 7:16 am, John Harshman <jharsh...@pacbell.net> wrote:
>>>> Alan Kleinman MD PhD wrote:

>>>>> On Jul 13, 1:56 pm, John Harshman <jharsh...@pacbell.net> wrote:
>>>>>> g...@risky-biz.com wrote:
>>>>>>> <snip all>
>>>>>>> It's clear by now that Kleinman has no intention of answering the
>>>>>>> questions posed to him.
>> I've seen many claims like the above turn out to be false due to the
>> person making them having "answering the questions posed to him" mean,
>> in addition "to my satisfaction." I wonder whether that is the case
>> here.
>> [ditto "addressing" statt "answering"]
>> [the German "statt" is so much easier to type than the English
>> "instead of", nicht wahr?]

>>>>>>> "Harshman's" count of genetic differences between humans and chimps
>>>>>>> has been bandied about in this thread. I've been wondering, could you
>>>>>>> characterize those differences a bit? How many of them are in coding
>>>>>>> areas?
>>>>>> Very few. Coding regions are only around 3% of the genome, and
>>>>>> accumulate about a third the number of differences per base as neutrally
>>>>>> evolving regions.
>>>>> You couldn t be more wrong John,
>> The following doesn't seem to support the "couldn't be more wrong"
>> assertion:

>>>>> over 70% of the genes in humans and
>>>>> chimpanzees don t code identical proteins.
>> This shows how the claim that humans share 98% or more of their
>> "genetic material" with chimps needs to be clarified. Way back in
>> 1995 or 1996 I asked whether this referred to loci, alleles, or base
>> pairs.

>To repeat a general theme: nobody cares how long ago you first asked a
>question.

John, do you have to rude as well as a mathematically incompetent
nitwit? It is your evolutionist stupidity which has given us multidrug

resistant microbes, multiherbicide resistant weeds, multipesticide

resistant insects and less than durable cancer treatments.

>> You've just now confirmed that it is NOT "alleles". Harshman seems to
>> opt for "base pairs":

>That is indeed the basis for that number. See, for example, The
>Chimpanzee Sequencing and Analysis Consortium. 2005. Initial sequence of
>the chimpanzee genome and comparison with the human genome. Nature
>437:69-87.

Perhaps those authors didn’t have a subscription to “Science” either.
Let’s just forget about chromosome 21 and make up what ever numbers
that make evolutionists happy. On the other hand, let’s toss out this
mathematically irrational evolutionist crap and actually describe how
mutation and selection works correctly.

>>>> While true, that has nothing to do with anything we've been discussing.
>>>> Do you understand that a single base change can produce non-identical
>>>> proteins?
>> And thus, 98% of the base pairs might be identical yet
>> physiologically, the two organisms might be very dissimilar.
>Might, if indeed all those single changes were important to function.

So tell us John, how do these tens of millions unimportant single
changes sweep like a plague through a population in 500,000
generations? There is nothing like evolutionists throwing out the
multiplication rule of probabilities to try and substantiate their
mathematically irrational belief system.

>>>> If there are 30,000 genes, that's 21,000 mutations. Out of 40
>>>> million. And even many of those are neutral.
>>> It has everything to do with what we are discussing. There are huge
>>> stretches of the two genomes which can not be matched up for homology.
>> Apparently you mean "matched up BASE FOR BASE". But loci can be
>> matched up in most cases even if the bases differ, no?

>Yes. We're talking here about sequences that have no homologs (or,
>really, orthologs) between genomes.

I am so disappointed in you John. I thought you were lining up
chromosome 1 in humans and chimpanzees and then chromosome 2 and 3…47
and 48 and they were 98.7% identical.

>>> This data is presented for those areas which can be matched and the

>>> match is not close at all. Evolutionists claim that humans and

>>> chimpanzees come from a common progenitor. Now you are claiming that
>>> many of these differences are neutral which is typical evolutionist
>>> speculation.

>> It may be based on solid data, as even you seem to allow for here:

>>> Tell us which are neutral differences and which are

>>> selective differences. And then compute the joint probability of two

>>> neutral mutations being fixed in a population.

>> The non-neutral mutations (especially the beneficial ones) would seem
>> to be also relevant to your skepticism about humans and chimps being
>> related.

>> By the way, does "neutral" mean "coding for the same protein, only

>> differering in the mRNA"? Does it include that? It's been a while

>> since I've looked at this part of genetics.

>Neutral simply means "not subject to selection", i.e. a difference in
>sequence that does not produce any difference in fitness.

Which John means will fix at a rate of a couple of hundred per

generation, generation after generation for hundreds of thousands of

generations to account for the tens of millions of differences between
human and chimpanzee genomes. These neutral mutations sweep like a
plague through populations.

>>>>>>> How many with other known functions? How much "junk"?
>>>>>> Almost all is junk, just as almost all the genome is junk. Non-coding,
>>>>>> functional regions are just another few percent of the genome.
>>>>> This is the type of stupidity that evolutionist perpetuate. If they
>>>>> don t know what a portion of the genome does, it is junk.
>>>> No, that's not how it works. We recognize junk by the fact that it
>>>> evolves at the rate of mutation.
>> No direct testing to see whether it is ever translated into
>> polypeptides? I'm disappointed.

>That would be a fine test if indeed all neutrally evolving sequences
>were not translated into peptides and all sequences not translated into
>peptides were evolving neutrally. But neither is the case.

Tell us John, what makes huge stretches of DNA junk DNA? How do you
know when DNA is junk?

>>> Take a look at this >URL:http://www.google.com/url?sa=D&q=http://www.sciencemag.org/content/295/5552/131.abstract&usg=AFQjCNF6LJDM3GHffyRjXPABtkVjwnfm9w
>>> In this URL, they studied chromosome 21. They report We detected
>>> candidate positions, including two clusters on human chromosome 21
>>> that suggest large, nonrandom regions of difference between the two
>>> genomes. Nonrandom means these are selective differences and we all
>>> should know by now that selective differences take hundreds of
>>> generations per base substitution.
>> I don't know it, being new to this thread and not having studied
>> population genetics in sufficient depth.
>Clearly.

Clearly, neither do you John, neither does hersheyh or any other
evolutionist population geneticist. But we have a measurement of
chromosome 21 in humans and chimpanzees that shows long stretches of
non-random bases which clearly means subject to selection, more
empirical evidence that your theory of evolution is a mathematically
irrational belief system.

>>> But you claim that neutral
>>> mutations fix at the rate of a couple of hundred per generation,
>>> thousands of times faster than selection can fix a beneficial
>>> mutation.
>> It all depends on how "large" those nonrandom regions are.
>No, it depends on what the abstract meant by "nonrandom".

Tell us what “nonrandom” means to you John. And tell us how all these
differences have shown up in chromosome 21. I thought you claimed that
that human and chimpanzee genomes were 98.7% identical.

pnyikos Sep 15, 5:24 pm
Newsgroups: talk.origins
From: pnyikos <nyik...@bellsouth.net>
Date: Thu, 15 Sep 2011 17:24:42 -0700 (PDT)
Local: Thurs, Sep 15 2011 5:24 pm
Subject: Re: Trying to salvage something from this Re: The Theory of
Evolution

>On Sep 15, 12:03 pm, John Harshman <jharsh...@pacbell.net> wrote:
>> pnyikos wrote:
>> > On Sep 14, 1:01 pm, Alan Kleinman MD PhD <klein...@sti.net> wrote:

>> >> On Aug 11, 7:16 am, John Harshman <jharsh...@pacbell.net> wrote:
>> >>> Alan Kleinman MD PhD wrote:

>> >>>> On Jul 13, 1:56 pm, John Harshman <jharsh...@pacbell.net> wrote:

>> >>>>> g...@risky-biz.com wrote:
>> >>>>>> "Harshman's" count of genetic differences between humans and chimps
>> >>>>>> has been bandied about in this thread.

>I've never seen any reason to suspect that "Harshman" is not his real
>name. I knew a father-son pair in high school named "Harshman". The
>father ran an ice cream parlor, the son helped out from time to time.

>> >>>>>> I've been wondering, could you
>> >>>>>> characterize those differences a bit? How many of them are in coding
>> >>>>>> areas?
>> >>>>> Very few. Coding regions are only around 3% of the genome, and
>> >>>>> accumulate about a third the number of differences per base as neutrally
>> >>>>> evolving regions.
>> >>>> You couldn t be more wrong John,
>> > The following doesn't seem to support the "couldn't be more wrong"
>> > assertion:

>> >>>> over 70% of the genes in humans and
>> >>>> chimpanzees don t code identical proteins.
>> > This shows how the claim that humans share 98% or more of their
>> > "genetic material" with chimps needs to be clarified. Way back in
>> > 1995 or 1996 I asked whether this referred to loci, alleles, or base
>> > pairs.

>> To repeat a general theme: nobody cares how long ago you first asked a
>> question.
>Oh, dear, I shouldn't have written how long ago I knew the
>Harshmans. :-)
>But seriously, someone might be curious as to how that question was
>answered, and this give them some idea.

Peter, this is really a side bar discussion. John admits to 40,000,000
differences between human and chimpanzee genomes and you have the
evolutionist claim that the divergence occurred 5 million years ago.
At 10 years per generations, you have 500,000 generations to do this
transformation. John’s numbers are ridiculously low but even his
ridiculously low numbers show how mathematically irrational his
argument is.

>> > You've just now confirmed that it is NOT "alleles". Harshman seems to
>> > opt for "base pairs":

>> That is indeed the basis for that number. See, for example, The
>> Chimpanzee Sequencing and Analysis Consortium. 2005. Initial sequence of
>> the chimpanzee genome and comparison with the human genome. Nature
>> 437:69-87.
>> >>> While true, that has nothing to do with anything we've been discussing.
>> >>> Do you understand that a single base change can produce non-identical
>> >>> proteins?
>> > And thus, 98% of the base pairs might be identical yet
>> > physiologically, the two organisms might be very dissimilar.
>> Might, if indeed all those single changes were important to function.

>> >>> If there are 30,000 genes, that's 21,000 mutations. Out of 40
>> >>> million. And even many of those are neutral.
>> >> It has everything to do with what we are discussing. There are huge
>> >> stretches of the two genomes which can not be matched up for homology.
>> > Apparently you mean "matched up BASE FOR BASE". But loci can be
>> > matched up in most cases even if the bases differ, no?

>> Yes. We're talking here about sequences that have no homologs (or,
>> really, orthologs) between genomes.
>Has anyone estimated what percentage those are?

Again, those percentages will not alter the mathematical reality that
you can’t get tens of millions of genetic differences spread through a
population in 500,000 generations. Any more accurate measure of the
differences between human and chimpanzee genomes will only make John’s
argument look more ridiculous.

>> >> This data is presented for those areas which can be matched and the

>> >> match is not close at all. Evolutionists claim that humans and

>> >> chimpanzees come from a common progenitor. Now you are claiming that
>> >> many of these differences are neutral which is typical evolutionist
>> >> speculation.

>> > It may be based on solid data, as even you seem to allow for here:

>> >> Tell us which are neutral differences and which are

>> >> selective differences. And then compute the joint probability of two

>> >> neutral mutations being fixed in a population.

>> > The non-neutral mutations (especially the beneficial ones) would seem
>> > to be also relevant to your skepticism about humans and chimps being
>> > related.

>> > By the way, does "neutral" mean "coding for the same protein, only
>> > differering in the mRNA"?

>Ah, the exact word for that is "silent", isn't it?
>> > Does it include that?
>Well, does it? I would guess your word "sequence" refers to amino
>acids, and if so the answer would be negative.

>> > It's been a while
>> > since I've looked at this part of genetics.

>> Neutral simply means "not subject to selection", i.e. a difference in
>> sequence that does not produce any difference in fitness.

>> >>>>>> How many with other known functions? How much "junk"?
>> >>>>> Almost all is junk, just as almost all the genome is junk. Non-coding,
>> >>>>> functional regions are just another few percent of the genome.
>> >>>> This is the type of stupidity that evolutionist perpetuate. If they
>> >>>> don t know what a portion of the genome does, it is junk.
>> >>> No, that's not how it works. We recognize junk by the fact that it
>> >>> evolves at the rate of mutation.
>> > No direct testing to see whether it is ever translated into
>> > polypeptides? I'm disappointed.

>> That would be a fine test if indeed all neutrally evolving sequences
>> were not translated into peptides and all sequences not translated into
>> peptides were evolving neutrally. But neither is the case.
>It would at least narrow things down. Calling something "junk" just
>on the basis of its mutation rate sounds almost as bad as Plato
>defining a human being as a "featherless biped". [Later amended,
>according to one book, to "a featherless biped with flat nails" after
>some wag plucked a chicken and announced, "This is Plato's human."]

Anything which evolutionists don’t agree with they call junk.
Evolutionists have discarded Haldane’s classic work on the “Cost of
Natural Selection” because he estimated that it would take 300
generations for a beneficial allele to be substituted in a population.
We now have hersheyh admitting that the empirical evidence from the
Lenski experiment is showing that it takes 200 generations per
mutation. Hersheyh doesn’t show how he got his number of 200
generations per mutation when if he does his mathematics correctly it
is actually more generations per mutation.

>> >> Take a look at this >URL:http://www.google.com/url?sa=D&q=http://www.sciencemag.org/content/295/5552/131.abstract&usg=AFQjCNF6LJDM3GHffyRjXPABtkVjwnfm9w
>> >> In this URL, they studied chromosome 21. They report We detected
>> >> candidate positions, including two clusters on human chromosome 21
>> >> that suggest large, nonrandom regions of difference between the two
>> >> genomes. Nonrandom means these are selective differences and we all
>> >> should know by now that selective differences take hundreds of
>> >> generations per base substitution.
>> > I don't know it, being new to this thread and not having studied
>> > population genetics in sufficient depth.
>> Clearly.
>Also, Kleinman's last sentence is ambiguous since "fixed" means it is
>now 100% all through the population, according to the Wikipedia entry
>on Kimura's theory [thanks for the tip] of neutral evolution. But the
>sentence does not contain that word.

Peter, there are a lot of words being used in this discussion such as
“fixed”, “substituted” or what I believe is the correct mathematical
term, “amplified”. For mutation and selection to work properly, simply
fixing or substituting one allele for another is not sufficient to
improve the probabilities of the next beneficial mutation occurring in
an evolutionary sequence. What is required is that the beneficial
allele be “amplified”. There are two ways a subpopulation can improve
the probability that the next beneficial mutation will occur on one of
the members of its subpopulation. The subpopulation can increase the
number of trials for the beneficial mutation by increasing its number
of members by replication and the subpopulation can increase the
number of trials for the beneficial mutation by surviving to replicate
another generation. Amplification of the beneficial mutation is the
correct term when talking about the mathematics of mutation and
selection. It doesn’t matter whether the mutation is fixed or
substituted in a population if the population has small numbers. It’s
the amplification of the beneficial mutation which improves the
probabilities of the next beneficial mutation occurring in an
evolutionary sequence.

>And it would be a grotesque understatement if it contained it, given
>the size of the human race today. But if it refers to the hominids of
>the Pliocene, then we may be down to very small size populations going
>their separate ways, and selective differences (and even genetic
>drift) taking only a few generations per base substitution, especially
>if the substitution produces a dominant allele with significantly
>enhanced survival value.

Mutation and selection requires large subpopulation sizes if the
evolutionary process requires more than a single beneficial mutation.
This is why the terminology of base substitution or fixation is
misleading terminology. If a member of the population happens to get a
beneficial mutation, unless that member becomes the progenitor of a
huge subpopulation with that beneficial mutation, the probabilities
are very low that the next beneficial mutation in an evolutionary
sequence will occur on a member of that subpopulation with the
previous beneficial mutation. And the empirical evidence clearly shows
that amplification can only occur efficiently when a single gene is
targeted by a single selection pressure. Target two genes
simultaneously with selection pressures and the mutation and selection
process is stifled. Populations can not efficiently amplify two
alleles for two genes subject to selection simultaneously. That’s why
combination therapy works for the treatment of HIV.

>> >> But you claim that neutral
>> >> mutations fix at the rate of a couple of hundred per generation,
>That could be because thousands of them are in the process of being
>"fixed" by genetic drift, no? See my last comment below.

That’s the evolutionist claim which is thousands of neutral mutations
are being fixed or substituted simultaneously. How do these thousands
of neutral mutations find their way into unrelated family lines?
Mutation and selection does the substitution process by the selection
pressure killing off the unrelated family lines. With neutral
evolution, you don’t have selection killing off the unrelated family
lines but somehow mysteriously these neutral mutations find there way
into the genomes of unrelated families, not just one or two mutations,
tens of millions of neutral mutations. This is a weird fantasy trip
evolutionists have gone on.


>> >> thousands of times faster than selection can fix a beneficial
>> >> mutation.
>> > It all depends on how "large" those nonrandom regions are.
>> No, it depends on what the abstract meant by "nonrandom".
>That too. But if the regions are small, it could be a statistical
>fluke, no?
>[...]

John has chosen a number of 98.7% similarity based on a biased
sampling. I present the citation on chromosome 21 to demonstrate
John’s bias. I’m willing to try to do this computation based on his
biased numbers and it still is not close mathematically to showing how
such a massive genetic transformation can be made in so few numbers of
generations.

>> >> 70% of genes code for different proteins,
>> >> large stretches of non-random differences between human and chimpanzee
>> >> genomes yet neutral evolution will fix all these differences a rate of
>> >> a couple of hundred per generation, thousands of times faster than a
>> >> single beneficial mutation can be fixed in a population. What you are
>> >> talking about is mathematical irrationality.
>> > There seems to be a real problem here with distinguishing "beneficial"
>> > and "non-harmful".
>Apparently the right word for the latter, "neutral," has been staring
>me in the face all the time. [Well, I did say I was very rusty on this
>stuff.]

Peter, if you think you are rusty on this topic, wait until you get a
good look at the corrosion of evolutionist mathematics or should I say
mathematical irrationality.

>> > The genomes are huge. Lots of non-harmful mutations could be fixed
>> > simultaneously, no?

John Harshman Sep 15, 10:18 pm

Newsgroups: talk.origins
From: John Harshman <jharsh...@pacbell.net>

Date: Thu, 15 Sep 2011 22:18:30 -0700
Local: Thurs, Sep 15 2011 10:18 pm
Subject: Re: Trying to salvage something from this Re: The Theory of
Evolution

>pnyikos wrote:
>> On Sep 15, 12:03 pm, John Harshman <jharsh...@pacbell.net> wrote:
>>> pnyikos wrote:
>>>> On Sep 14, 1:01 pm, Alan Kleinman MD PhD <klein...@sti.net> wrote:

>>>>> On Aug 11, 7:16 am, John Harshman <jharsh...@pacbell.net> wrote:
>>>>>> Alan Kleinman MD PhD wrote:

>>>>>>> On Jul 13, 1:56 pm, John Harshman <jharsh...@pacbell.net> wrote:

>>>>>>>> g...@risky-biz.com wrote:
>>>>>>>>> "Harshman's" count of genetic differences between humans and chimps
>>>>>>>>> has been bandied about in this thread.

>> I've never seen any reason to suspect that "Harshman" is not his real
>> name. I knew a father-son pair in high school named "Harshman". The
>> father ran an ice cream parlor, the son helped out from time to time.
>Yes, the fact that Peter knew someone with the same surname as I do,
>especially one who ran an ice cream parlor, is wonderful evidence that
>I'm who I say I am. Alternatively, one could look up the publication
>record I keep citing at random moments.

>>>>>>>>> I've been wondering, could you
>>>>>>>>> characterize those differences a bit? How many of them are in coding
>>>>>>>>> areas?
>>>>>>>> Very few. Coding regions are only around 3% of the genome, and
>>>>>>>> accumulate about a third the number of differences per base as neutrally
>>>>>>>> evolving regions.
>>>>>>> You couldn t be more wrong John,
>>>> The following doesn't seem to support the "couldn't be more wrong"
>>>> assertion:

>>>>>>> over 70% of the genes in humans and
>>>>>>> chimpanzees don t code identical proteins.
>>>> This shows how the claim that humans share 98% or more of their
>>>> "genetic material" with chimps needs to be clarified. Way back in
>>>> 1995 or 1996 I asked whether this referred to loci, alleles, or base
>>>> pairs.

>>> To repeat a general theme: nobody cares how long ago you first asked a
>>> question.
>> Oh, dear, I shouldn't have written how long ago I knew the
>> Harshmans. :-)
>It certainly isn't relevant to anything.
>> But seriously, someone might be curious as to how that question was
>> answered, and this give them some idea.
>No it wouldn't.

Of course you wouldn’t John because if you did, you would reveal your
evolutionist bias. That’s why you won’t get a subscription to
“Science” or at least go to you library and read that chromosome 21
has long stretches of nonrandom sequences which differ from human and
chimpanzee genomes. But we don’t need this to show that your claims
are mathematically irrational. We can use your claim of 40,000,000
differences between human and chimpanzee genomes and your gross over-
extrapolation of a model of a single gene with two neutral alleles,
one being randomly fixed in the population to you idea of hundreds of
neutral alleles being fixed simultaneously. This is the kind of silly
mathematical irrationality that evolutionism is based on.

>>>> You've just now confirmed that it is NOT "alleles". Harshman seems to
>>>> opt for "base pairs":

>>> That is indeed the basis for that number. See, for example, The
>>> Chimpanzee Sequencing and Analysis Consortium. 2005. Initial sequence of
>>> the chimpanzee genome and comparison with the human genome. Nature
>>> 437:69-87.
>>>>>> While true, that has nothing to do with anything we've been discussing.
>>>>>> Do you understand that a single base change can produce non-identical
>>>>>> proteins?
>>>> And thus, 98% of the base pairs might be identical yet
>>>> physiologically, the two organisms might be very dissimilar.
>>> Might, if indeed all those single changes were important to function.

>>>>>> If there are 30,000 genes, that's 21,000 mutations. Out of 40
>>>>>> million. And even many of those are neutral.
>>>>> It has everything to do with what we are discussing. There are huge
>>>>> stretches of the two genomes which can not be matched up for homology.
>>>> Apparently you mean "matched up BASE FOR BASE". But loci can be
>>>> matched up in most cases even if the bases differ, no?

>>> Yes. We're talking here about sequences that have no homologs (or,
>>> really, orthologs) between genomes.
>> Has anyone estimated what percentage those are?
>Percentage of what? Non-homologous indels are about 5% of the
>comparison, or around 2.5% of the length of each genome. Then again,
>they can be accounted for by 5 million mutations, vs. 35 million point
>mutations.

This is more than enough differences to show that your theory of
evolution is a mathematically irrational belief system. You believe
that neutral mutations sweep like a plague through a population.

>>>>> This data is presented for those areas which can be matched and the

>>>>> match is not close at all. Evolutionists claim that humans and

>>>>> chimpanzees come from a common progenitor. Now you are claiming that
>>>>> many of these differences are neutral which is typical evolutionist
>>>>> speculation.

>>>> It may be based on solid data, as even you seem to allow for here:

>>>>> Tell us which are neutral differences and which are

>>>>> selective differences. And then compute the joint probability of two

>>>>> neutral mutations being fixed in a population.

>>>> The non-neutral mutations (especially the beneficial ones) would seem
>>>> to be also relevant to your skepticism about humans and chimps being
>>>> related.

>>>> By the way, does "neutral" mean "coding for the same protein, only
>>>> differering in the mRNA"?

>> Ah, the exact word for that is "silent", isn't it?
>Yes.
>>>> Does it include that?
>> Well, does it? I would guess your word "sequence" refers to amino
>> acids, and if so the answer would be negative.
>Your guess is wrong. Sequence, here, is DNA. All silent differences are
>either neutral or nearly so; some non-silent differences are neutral or
>nearly so.

John, how do all these tens of millions of silent differences sweep
like a plague through the population in 500,000 generations? And
remember, show your work?

>>>> It's been a while
>>>> since I've looked at this part of genetics.

>>> Neutral simply means "not subject to selection", i.e. a difference in
>>> sequence that does not produce any difference in fitness.

>>>>>>>>> How many with other known functions? How much "junk"?
>>>>>>>> Almost all is junk, just as almost all the genome is junk. Non-coding,
>>>>>>>> functional regions are just another few percent of the genome.
>>>>>>> This is the type of stupidity that evolutionist perpetuate. If they
>>>>>>> don t know what a portion of the genome does, it is junk.
>>>>>> No, that's not how it works. We recognize junk by the fact that it
>>>>>> evolves at the rate of mutation.
>>>> No direct testing to see whether it is ever translated into
>>>> polypeptides? I'm disappointed.

>>> That would be a fine test if indeed all neutrally evolving sequences
>>> were not translated into peptides and all sequences not translated into
>>> peptides were evolving neutrally. But neither is the case.
>> It would at least narrow things down. Calling something "junk" just
>> on the basis of its mutation rate sounds almost as bad as Plato
>> defining a human being as a "featherless biped". [Later amended,
>> according to one book, to "a featherless biped with flat nails" after
>> some wag plucked a chicken and announced, "This is Plato's human."]
>It may sound that way to you, but I think that's because you don't know
>much about the subject. People who do know think it's a pretty good
>criterion. Note: it isn't the mutation rate, it's the fixation rate.

You don’t know much about the subject either John. That’s why you
would claim that tens of millions of neutral mutations are sweeping
like a plague through a population in 500,000 generations. How do all
these neutral mutations end up in unrelated family lines? This is such
a weird evolutionist concept.

>>>>> Take a look at this >URL:http://www.google.com/url?sa=D&q=http://www.sciencemag.org/content/295/5552/131.abstract&usg=AFQjCNF6LJDM3GHffyRjXPABtkVjwnfm9w
>>>>> In this URL, they studied chromosome 21. They report We detected
>>>>> candidate positions, including two clusters on human chromosome 21
>>>>> that suggest large, nonrandom regions of difference between the two
>>>>> genomes. Nonrandom means these are selective differences and we all
>>>>> should know by now that selective differences take hundreds of
>>>>> generations per base substitution.
>>>> I don't know it, being new to this thread and not having studied
>>>> population genetics in sufficient depth.
>>> Clearly.
>> Also, Kleinman's last sentence is ambiguous since "fixed" means it is
>> now 100% all through the population, according to the Wikipedia entry
>> on Kimura's theory [thanks for the tip] of neutral evolution. But the
>> sentence does not contain that word.
>I don't think that's important. It's assumed that most differences
>between a human and chimp genome are fixed, or close enough for gov't work.

Get a copy of the above citation and show us how these long stretches
of nonrandom bases were fixed in the human genome chromosome 21. And I
wouldn’t use gov’t work as a comparison with the massive deficits and
debt being accumulated.

>> And it would be a grotesque understatement if it contained it, given
>> the size of the human race today.
>You need to cut down on the ambiguously reference pronouns. But what
>about the size of the human race?

You do understand that population size affects the probability of
events don’t you John?

>> But if it refers to the hominids of
>> the Pliocene, then we may be down to very small size populations going
>> their separate ways, and selective differences (and even genetic
>> drift) taking only a few generations per base substitution, especially
>> if the substitution produces a dominant allele with significantly
>> enhanced survival value.
>I am not sure what you're trying to say. Is this an argument against
>something Kleinman said?
>>>>> But you claim that neutral
>>>>> mutations fix at the rate of a couple of hundred per generation,
>> That could be because thousands of them are in the process of being
>> "fixed" by genetic drift, no? See my last comment below.
>Yes.

Why yes, thousands of neutral mutations are sweeping though a
population like the plague. In fact tens of millions of neutral
mutations are randomly being fixed like a tsunami washing over the
population. Hey John, would you compute the probability of the
fixation of a single neutral allele of three neutral alleles for one
gene instead of two neutral alleles?

>>>>> thousands of times faster than selection can fix a beneficial
>>>>> mutation.
>>>> It all depends on how "large" those nonrandom regions are.
>>> No, it depends on what the abstract meant by "nonrandom".
>> That too. But if the regions are small, it could be a statistical
>> fluke, no?
>The size of the region doesn't necessarily matter. But without knowing
>what the paper actually said, it's hard to tell what they meant.

Go to the library John.

Greg Guarino Sep 14, 7:24 pm

Newsgroups: talk.origins
From: Greg Guarino <gdguar...@gmail.com>

Date: Wed, 14 Sep 2011 22:24:40 -0400
Local: Wed, Sep 14 2011 7:24 pm
Subject: Re: Trying to salvage something from this Re: The Theory of
Evolution

On 9/14/2011 2:06 PM, Alan Kleinman MD PhD wrote:
>> On Aug 14, 9:41 am, Greg Guarino<gdguar...@gmail.com> wrote:
>>> On 8/10/2011 4:42 PM, Alan Kleinman MD PhD wrote:
>>>> On Jul 13, 1:56 pm, John Harshman<jharsh...@pacbell.net> wrote:
>>>>> g...@risky-biz.com wrote:
>>>>>> <snip all>
>>> Others have now responded more substantively than I would be able to,
>>> but I still have a few questions.
>> Hersheyh has presented a plethora of words without any mathematical or
>> empirical evidence for his claims. He is confused by the correct
>> probability function which describes the mutations and selection
>> phenomenon and dismisses all the real, measurable and repeatable
>> examples of mutation and selection. John Harshman as well has shown
>> that he doesn’t understand the simplest principles of a stochastic
>> process. Any of the other posters on this forum who have the slightest
>> understanding of how to analyze a stochastic process have left this
>> discussion. Do you think they want to try to defend Schneider’s claim

>> that the multiplication rule of probabilities does not apply to

>> biological evolution? Why would they want to look as mathematically
>> incompetent as hersheyh is? Defending the theory of evolution from a
>> mathematical approach is going to leave you looking mathematically
>> incompetent.
>137 words without any argument at all. A plethora by any standard.
>Worse, some of it is simply, flatly false. I don't know Schneider, but
>you repeatedly claim that people on T.O. deny a role for the
>multiplication rule. They don't. Not any of them as far as I can see.
>They just don't use it where it doesn't work.

Just what do you mean where it (the multiplication rule) doesn’t work?
The multiplication rule always applies when computing the joint
probability of multiple random events. Thomas Schneider from the
National Cancer Institute is incorrect when he makes the following

claim on his web site http://www-lmmb.ncifcrf.gov/~toms/paper/ev/AND-multiplication-error.html
, “The multiplication rule does not apply to biological evolution.”
The multiplication rule is in fact the central and governing
mathematical principle for understanding how the mutation and
selection phenomenon works and his failure to understand this harms
the people he is paid to help, that is people who suffer from cancer

(a mutating and selecting disease). And when I pointed out his
blunder, here is his response to his error: Schneider made a half
hearted retraction of his claim when he made the following post on
another page of his site http://www.ccrnp.ncifcrf.gov/~toms/paper/ev/blog-ev.html
where he made the following concession, “Note: I agree with his point
that combinatoric drug application is useful.” I have asked him why he
thinks combination therapy is useful, he hasn’t replied. Edward Tatum
answered that question in his 1958 Nobel Laureate lecture. Dr
Schneider really needs to withdraw his scientifically incorrect claim
about biological evolution. There are too many naïve school children
and evolutionists who believe this.

Then we have hersheyh who has spent numerous posts trying to defend
Schneider’s mathematically irrational claim. It is mathematically
incompetent evolutionist bunglers like hersheyh who have given us

multidrug resistant microbes, multiherbicide resistant weeds,
multipesticide resistant insects and less than durable cancer

treatments. And how did hersheyh do this, he did this by failing to
properly understand and teach the basic science and mathematics of the
mutation and selection phenomenon. The fact that hersheyh is still
trying to defend the Poisson distribution as a model for mutation and
selection is a testament that he doesn’t understand the phenomenon.
Hersheyh hasn’t even gone through the derivation of the equation has
used for more than 20 years. This is the kind of sloppy thinking that
evolutionist practice.

>Speaking of which, I have never claimed any special mathematical
>competence in this area, but I can only conclude that as regards simple
>probability, it is superior to yours.

Good for you Greg. Why don’t you demonstrate your superiority by
deriving the probability function that describes random recombination?
When you do that, you will understand why recombination doesn’t have a
significant effect on the mutation and selection phenomenon as
demonstrated when combination therapy is used to treat HIV. I look
forward to your demonstration of superiority.

>>>>>> It's clear by now that Kleinman has no intention of answering the

>>>>>> questions posed to him. But I've learned some interesting biology from
>>>>>> this group, even from unpromising threads.

>>>>>> "Harshman's" count of genetic differences between humans and chimps
>>>>>> has been bandied about in this thread. I've been wondering, could you
>>>>>> characterize those differences a bit? How many of them are in coding
>>>>>> areas?
>>>>> Very few. Coding regions are only around 3% of the genome, and
>>>>> accumulate about a third the number of differences per base as neutrally
>>>>> evolving regions.

>>>> You couldn’t be more wrong John, over 70% of the genes in humans and

>>>> chimpanzees don’t code identical proteins.

>>> What made you think that answer was germane to the question asked? I was
>>> trying to get at how many of the 40 million differences make significant
>>> changes in the species. How many do YOU think it is?
>> It doesn’t matter what you or I think which mutations are significant.
>Humor me. Give me your sense of the number.

If you are talking about humans and chimpanzees coming from a common
progenitor, none of the mutations are selective or neutral because
humans and chimpanzees could not have come from a common progenitor.
You don’t have enough generations to make the genetic transformation
so it is silly to try to determine which differences are neutral or
selective. Only mathematically irrational evolutionists think that
this type of massive genetic transformation can occur in 500,000
generations. And we all know what mathematically irrational
evolutionists have given us; multidrug resistant microbes,
multiherbicide resistant weed, multipesticide resistant insects and

less than durable cancer treatments.

>> What is significant is that these tens of millions of differences must
>> spread through populations in less than a million generations. Whether
>> they are significant or not, the differences exist between the two
>> life forms and you don’t have nearly enough generations to do the
>> accounting for these differences.
>Why? You've done nothing to support the idea that they need to be
>serial, and have yet to make any substantive (and especially not
>mathematical) response to the suggestion that most of the changes are
>neutral.

I’ve presented numerous real, measurable and repeatable examples of
mutation and selection which show that mutation and selection must
proceed serially in order to work efficiently. You and the other
evolutionists on the other hand have yet to produce a single empirical
example where mutation and selection can occur in parallel. If you
want to believe that neutral mutations can sweep through populations
like a plague, that’s alright by me but don’t teach this to naïve
school children. And would you care to explain to use how neutral
mutations in one family line appear in a totally unrelated family
line? In fact, tell us how tens of millions of neutral mutations
appear throughout a population of many different unrelated family
lines?

>>>>>> How many with other known functions? How much "junk"?
>>>>> Almost all is junk, just as almost all the genome is junk. Non-coding,
>>>>> functional regions are just another few percent of the genome.
>>>> This is the type of stupidity that evolutionist perpetuate. If they
>>>> don’t know what a portion of the genome does, it is junk.

>>> I have not come across a biologist who would make that claim. But more
>>> importantly...
>>> If they
>>>> don’t understand how to do a mathematical computation it is junk.
>>>> John, just because you are ignorant what a non-coding region of a
>>>> genome does, don’t impose your ignorance on us by claiming this is
>>>> junk. If a region of DNA has no coding function for proteins but
>>>> remains non-random, it does so because it has stabilizing selection
>>>> acting on those sequences. And the reason it has stabilizing selection
>>>> pressures acting on those sequences is that it has some type of
>>>> important function on maintaining the life and reproductive capability
>>>> of that member. The only junk in this discussion is the evolutionist
>>>> junk science which fails to properly explain how mutation and
>>>> selection works.
>>> ... amid the gratuitous insults, you seem to tacitly agree that some of
>>> the genome is junk. How much?
>> I don’t agree with anything of the kind.
>I parse that to mean you think none of it is junk. But why am I still
>guessing about such a simple point? What DO you think?

What I am saying is that biological systems are extremely efficient
and the idea that large amounts of DNA serve no purpose other than
forcing the cell to expend energy to replicate that useless DNA makes
no biological sense. The most efficient replicators are the ones who
are most fit. Expending energy unnecessarily will put that replicator
at a reproductive disadvantage. The biologic function of DNA is just
starting to be understood. Ask Schneider about binding sites on DNA.
Proteins aren’t produced by these binding sites but they serve a
crucial function in cell activity. What I think is that most of the
DNA serves as the control system for cell activity, not for protein
synthesis. Because turning on and off proteins is as important as
manufacturing the protein.

>>> What I am doing is properly
>>> describing how mutation and selection works and then using
>>> evolutionist supplied numbers (40,000,000 differences and 500,000
>>> generations) to try and do the accounting for these differences. What
>>> you come up with is a mathematically irrational belief system called
>>> evolutionism. And at the same time we find that evolutionists have
>>> bungled the basic science and mathematics of the mutation and
>>> selection phenomenon causing multidrug resistant microbes,

>>> multiherbicide resistant weeds, multipesticide resistant insects and
>>> less than durable cancer treatments.

>I have to ask, when you are involved in a debate with someone and they
>trot out the same pet phrases, especially in lieu of answering a simple
>direct question, what does that make you think?

It makes me think they are evolutionists.

>So, is NONE of the genome junk? What makes you think so?

Survival of the fittest is all about which members of a population can
use the resources of the environment most efficiently to reproduce.
Any replicator which expends energy unnecessarily will thereby be at a
disadvantage.

>>>>>> Of the ones that are in coding areas, how many are thought to make
>>>>>> significant "interesting" morphological differences rather than minor,
>>>>>> possibly non-function-altering changes to a protein?
>>>>> Again, very few. The vast majority of differences in coding regions are
>>>>> silent, i.e. making no difference in the protein being coded for.
>>>> Really John? Is that why over 70% of the genes in humans and
>>>> chimpanzees code for different proteins? I can’t tell what you are
>>>> worse at, mathematics or the interpretation of data.
>>>>>> I assume this is ongoing research; perhaps the answers are not yet
>>>>>> clear.
>>>>> Oh, no. They're quite clear. What isn't clear is the exact number and
>>>>> identities of the comparatively few functional differences.
>>>> John, your irrational speculations don’t form a scientific basis for
>>>> any of your claims. You don’t know how mutation and selection works
>>>> and you can’t explain why over 70% of the genes code for different
>>>> proteins in humans and chimpanzees.
>>> On the contrary, it seems that several people here have offered the
>>> standard mechanisms. You have as yet not chosen to engage on any
>>> scenario that does not include massive reduction of a population, and
>>> thus have made no case about evolution in general.
>> In the twisted evolutionist mind there exist selection pressures which
>> don’t kill or impair the reproduction of some or all the members of a
>> population.
>Kill OR impair some OR all? I don't hear any math in there. How much do
>they impair? Must they "impair" at all? Or could some genetic change
>give an advantage to the mutant without "impairing" the wild type? Or
>could the environment have the capacity to support a certain population
>such that only the relative numbers of the different types would change?
>Or...

The mathematics is in the intensity of selection which was very well
modeled by Haldane in his “Cost of Natural Selection” paper. Here’s an
example of how selection pressures can impair or reduce the fecundity
of a population. Let’s say you are raising herd animals on a limited
size pasture. The females can give birth to singles, twins, triplets
and even quads and quints but in order for the mother to provide
sufficient milk to raise her offspring, she must have enough feed to
produce the milk. But drought or cold weather stress the population
and only the strongest mothers can raise twins and the weaker mothers
can raise only singles if any offspring at all. The population is not
driven to extinction but the limitations of food and water and thermal
stress only allow the strongest (most efficient users of resources) to
replicate. You can reduce the selection pressure by providing
supplemental food and water and provide a barn to control the
temperature the animals are exposed to but by doing this you are
allowing the weaker replicators to pass the genes to the next
generation.

>>Where and what are these selection pressures? We have the
>> Lenski E coli model where he puts his population under starvation
>> conditions but still allows populations in the tens of millions. It
>> still takes his populations hundreds of generations to amplify a
>> single beneficial mutation. What do you think would happen if Lenski
>> put his populations under thermal stress or some other selection
>> pressure? Do you think this would accelerate the mutation and
>> selection process or do you think that a member with a beneficial
>> mutation which improves glucose metabolism would still be able to
>> amplify that mutation efficiently while being stress by thermal
>> pressure? Evolutionists simply refuse to learn the lessons given by
>> the real, measurable and repeatable empirical examples presented here.
>> Evolutionists have an obsession with the theory of evolution which is
>> psychotic. Evolutionists have lost contact with reality.
>Hmmm. Where to start. Biologists (nearly all, no?) are evolutionists.
>Now they are not merely mathematically irrational, they are psychotic
>and have lost contact with reality. Shouldn't that sort of hyperbolic
>language clue us in that your position may not be entirely based on ,
>what's the word, rational grounds? Psychotic? Really?

If you are going to say seriously that you believe that mutation and
selection can transform reptiles into birds or humans and chimpanzees
from a common progenitor then you had better be able to describe
exactly how the mutation and selection phenomenon works. This has not
been done by evolutionists. In fact, evolutionists have failed to
properly describe the mutation and selection phenomenon. This is why

we have multidrug resistant microbes, multiherbicide resistant weeds,
multipesticide resistant insects and less than durable cancer

treatments. You have people like hersheyh defending Schneider’s
mathematically irrational claim that the multiplication rule does not
apply to biological evolution and you have John Harshman’s claim that
tens of millions of neutral mutations are sweeping like a plague
through a population in 500,000 generations, another mathematically
irrational claim. Evolutionists stubbornly cling to their beliefs
despite all the empirical and mathematical evidence. If you think that
mutation and selection can occur in parallel, present your evidence,
otherwise join the evolutionist Thorazine for lunch bunch.

>Next, your argument is illogical. You claim, in effect, that research
>that describes how one kind of evolution ("mutation and selection" to
>you) works precludes any other kind. This is especially illogical when
>every single example you cite involves drastic human intervention.

Did you ever notice that evolutionists never present an empirical
example of mutation and selection behaving any other way than I’ve
described? Greg, if you have any empirical evidence that mutation and
selection behaves differently than the empirical examples I’ve
presented, we would all enjoy your contribution to the discussion. Oh
yes, and don’t forget to present the derivation of the probability
function which describes random recombination as a demonstration of
your mathematical superiority.

Will in New Haven Sep 15, 8:21 am
Newsgroups: talk.origins
From: Will in New Haven <bill.re...@taylorandfrancis.com>
Date: Thu, 15 Sep 2011 08:21:54 -0700 (PDT)
Local: Thurs, Sep 15 2011 8:21 am
Subject: Re: Trying to salvage something from this Re: The Theory of
Evolution

>On Sep 14, 2:06 pm, Alan Kleinman MD PhD <klein...@sti.net> wrote:
>> On Aug 14, 9:41 am, Greg Guarino <gdguar...@gmail.com> wrote:
>OK, Kleinman, you have proved beyond a reasonable doubt that a person
>can have multiple degrees and still be a fucking moron. Meanwhile,
>this thread has fragmented to the point where none of the _other_
>loons who come to this newsgroup can get their fair share of abuse.
>Start a new thread or STFU
>Courteously as always

Now Will, don’t put temptation in front of me. I do enjoy annoying
mathematically incompetent evolutionists and a post like yours makes
me want to cause hundreds of splinter threads just to irritate you.
But alas, your post is worth nothing more than the PgDn button.

Annoyingly as always to evolutionists

This is the end of compilation of responses to posts 976-1001 TOEMIR
round 2 and splinter threads. I will again respond to individual posts
until we reach 3000 posts when I will again do compilations.

[Alan Kleinman MD PhD]

On Sep 16, 11:36 am, Bob Casanova <nos...@buzz.off> wrote:
> On Fri, 16 Sep 2011 07:46:01 -0700 (PDT), the following
> appeared in talk.origins, posted by Charles Brenner
> <cbren...@berkeley.edu>:
>
> >On Sep 16, 6:09 am, Alan Kleinman MD PhD <klein...@sti.net> wrote:
> >> Google has again splintered this thread so I am restarting this thread
> >> again as round three and reposting responses from posts 851 through
> >> 875 as a single post. Please continue your posts on this thread and
> >> not on the splinter threads as I will not follow the splinter threads.
> >> I will post the rest of my responses to posts from round 2 in bulk on
> >> this thread. Sorry for any inconvenience.
> >[snip many pages randomly running one topic after another, leaving it
> >to the less important readers who have scads more time than the self-
> >important and pompous author to sort out what is what]
>
> >I wonder how an intelligent person would have handled the problem?
>
> >But then, if the problem is to get people to stop paying attention,
> >this might work.
>
> It worked for me quite a while back; the Good MD is immune
> to logic, and highly resistant to appropriate snippage.
Should I snippage this post?
> --
>
> Bob C.
>
> "Evidence confirming an observation is
> evidence that the observation is wrong."
>                           - McNameless

[Alan Kleinman MD PhD]

On Sep 16, 2:35 pm, Inez <savagemouse...@hotmail.com> wrote:
> <snip rat king of replies>
>
> So I have a question for you.  I'm studying a certain sort of fungus,
> and have discovered that it has 100 neutral fixations per generation
> and only 10 selected mutations.  How fast did each of these types of

> mutations spread throughout the population?  Can you show me how to

> calculate that using only those numbers?  John Harshman tells me that
> you need other information, but you seem to be able to just look at
> the final numbers and tell the speed that the genes spread at, so I
> turn to you for illumination.

Well mouse queen of mathematical incompetence. What I can tell you is
that as Haldane’s calculations of more than 50 years ago showed, it
takes about 300 generations to do the substitution of a more
beneficial allele than a less beneficial allele. So if an evolutionary
process requires 10 selected mutations, you can figure that the
beneficial mutation/amplification of beneficial mutation cycle will
take about 3000 generations. And that’s if you have a subpopulation
size sufficient to give the necessary trials for the beneficial
mutation. That’s why hersheyh uses population sizes of 10^9 when the
mutation rate is 10^-8. If the population is small like 10^4 or 10^5,
you can forget it. The mutation and selection process will die on the
vine due to the lack of trials for the beneficial mutation. Now for
your hypothetical claim that you have 100 neutral fixations per
generation, that’s a crocrich of evolutionist mathematical
irrationality.

[Alan Kleinman MD PhD]

On Sep 16, 2:55 pm, "Rolf" <rolf.aalb...@tele2.no> wrote:
> Alan Kleinman MD PhD wrote:
>

> [deleted]
>
> Another creationist on a spree I see.
>
> Fascinating how anybody can stand up and disprove 150 years of science,
> thousands of scientists hard at work in almost all fields of science
> gathering evidence
> and putting together one of the beste researched and documented scientific,
> scientific!
> theories of all time, with more empirical evidence than anyone could cover
> in a lifetime.
Look at hersheyh. He has been a teacher of genetics for 20 years and
he has never bothered to go through the derivation for the equation
which he uses to describe mutation and selection. Is it any surprise
that we have multidrug resistant microbes, multiherbicide resistant

weeds, multipesticide resistant insects and less than durable cancer

treatments when we have evolutionists bungling the basic science and
mathematics of the mutation and selection phenomenon?
>
> The MD PhD doesn't impress me, my son in law is a MD and when he isn't a PhD
> it certainly is not for lack of potential! But that is another story. My
> lack of a PhD is
> because of no education but that doesn't bother me. Faraday didn't have much
> of an
> education either, but when offered a job as a bookbinder I ran as fast as I
> could.
Why don’t you ask your son in law if he ever received a lecture on how
mutation and selection works other than the evolutionist claim that
reptiles turn into birds by mutation and selection? And why don’t you
ask your son in law why combination therapy works for HIV and why it
took so long to figure this out despite the fact that Edward Tatum
described how to do this more than 50 years ago in his Nobel Laureate
lecture?
>
> We have had many interesting evilutionist atheist discussions.
>
> Why should I listen to Kleinman? If the subject is of such importance to him
> he better
> gets himself a lab coat and say goodbye to his patients, he's got a world to
> save, millions
> of souls to rescue from sinister evilutionism.
>
> I didn't read much, but I got it right, didn't I?
>
> Fair enough?
>
> Yawn.
>
> Rolf,

You got it right Rolf; you are asleep at the wheel.

[Alan Kleinman MD PhD]

On Sep 16, 7:46 am, Charles Brenner <cbren...@berkeley.edu> wrote:
> On Sep 16, 6:09 am, Alan Kleinman MD PhD <klein...@sti.net> wrote:
>
> > Google has again splintered this thread so I am restarting this thread
> > again as round three and reposting responses from posts 851 through
> > 875 as a single post. Please continue your posts on this thread and
> > not on the splinter threads as I will not follow the splinter threads.
> > I will post the rest of my responses to posts from round 2 in bulk on
> > this thread. Sorry for any inconvenience.
>
> [snip many pages randomly running one topic after another, leaving it
> to the less important readers who have scads more time than the self-
> important and pompous author to sort out what is what]

The responses are not random, they were done sequentially and the
majority of the responses were to John Harshman and hersheyh. Stop
whining Charles, if you want to read the responses to your posts and
not read what anyone else has to say, just search for your name. You
do have a search feature in your software?

>
> I wonder how an intelligent person would have handled the problem?

Instead of whining, offer a different solution. It seems your solution
is to only respond to your posts. That’s a rude way to treat people.

And you actually made an intelligent comment when you used the term
bottleneck but you let John Harshman bully you out of the term. If you
are going to argue that chimpanzees and humans came from a common
progenitor, when a population goes through a selective bottleneck, not
only will the beneficial alleles which allowed the population to
survive the selection pressure be amplified after the population
recovers, so will all the neutral alleles be amplified that these
members are carrying at all their gene loci. This idea that tens of
millions of neutral mutations will amplify and fix in a population
without the aid of selection is mathematically irrational evolutionist
crap.

>
> But then, if the problem is to get people to stop paying attention,
> this might work.

My solution worked after the first thousand posts. Let’s see what
happens after the second thousand posts as we start the third thousand
of posts.

[Alan Kleinman MD PhD]

On Sep 16, 4:09 pm, r norman <r_s_nor...@comcast.net> wrote:
> On Fri, 16 Sep 2011 23:55:14 +0200, "Rolf" <rolf.aalb...@tele2.no>

> wrote:
>
>
>
>
>
> >Alan Kleinman MD PhD wrote:
>
> >[deleted]
>
> >Another creationist on a spree I see.
>
> >Fascinating how anybody can stand up and disprove 150 years of science,
> >thousands of scientists hard at work in almost all fields of science
> >gathering evidence
> >and putting together one of the beste researched and documented scientific,
> >scientific!
> >theories of all time, with more empirical evidence than anyone could cover
> >in a lifetime.
>

> >The MD PhD doesn't impress me, my son in law is a MD and when he isn't a PhD
> >it certainly is not for lack of potential! But that is another story. My
> >lack of a PhD is
> >because of no education but that doesn't bother me. Faraday didn't have much
> >of an
> >education either, but when offered a job as a bookbinder I ran as fast as I
> >could.
>

> >We have had many interesting evilutionist atheist discussions.
>
> >Why should I listen to Kleinman? If the subject is of such importance to him
> >he better
> >gets himself a lab coat and say goodbye to his patients, he's got a world to
> >save, millions
> >of souls to rescue from sinister evilutionism.
>
> >I didn't read much, but I got it right, didn't I?
>
> >Fair enough?
>

> Kleinman has two things going -- bugs up his ass is the best metaphor
> I can think of.
If I do, it’s multipesticide resistant bugs thanks to you
mathematically incompetent evolutionists. Now tell us r norman,
graduate student in probability theory, why don’t you derive for us
the probability function for random recombination. I’ve already
derived the correct probability function for two mutations occurring;
let’s see if your graduate classes in probability did anything for
you.
>
> 1)  He says that single drug treatment of many diseases, especially
> HIV-AIDS, is the sole responsiblilty of ignormant evolutionary
> biologists who forced a mathematically invalid theory of evolution
> down the throats of medical students so they do not know any better.
> He has been told that evolutionary biologists do not teach in medical
> school, that medical genetiics is not the same as evolution, that
> medical doctors are responsible for the education of medical students,
> that medical doctors are responsible for choosing treatments,  and
> that evoloutionary biologists have long known and taught that
> organisms can develop resistance to single drugs.  None of this
> matters.  Evolutionary biologists are responsible for killing and
> suffering of millions because they (we) don't understand mathematics.
Of course evolutionists are responsible for bungling the basic science
and mathematics of the mutation and selection phenomenon and this has
caused great societal and personal harm. Who teaches this to naïve
school children if not evolutionists? Now you have no excuse since you
have taken graduate courses in probability theory yet you never
correct hersheyh’s blunder when he uses the Poisson distribution to
describe mutation and selection. And you should know why because you
have taken graduate courses in probability theory.
>
> 2)  He has a background in engineering and therefore is master of
> anything and everything mathematical.  Of course he has already
> demonstrated a total lack of understanding of biological evolution, he
> has beend reminded repeatedly of the many extremely sophisticated
> mathematical analyses of evolution by population geneticists, he
> utterly fails to understand what is meant by genetic drift,  his own
> so-called mathematical anaysis of the probability that two beneficial
> mutations become fixed in a population is completely independent of
> any fitness advantage offered by the mutations, he has already made
> some monumental mathematical blunders and egregious biological
> blunders.  None of this matters.  He has mastered mathematics and
> understands the law of multiplication of probabilities.  No
> evolutionary biologist understands probability theory.  And, besides,
> because of this total lack of understanding we have of mathematics, we
> are responsible for the death and suffering of millions of people
> because of how we lie to medical students and mistrain them.
You don’t have to master all of probability theory to understand how
mutation and selection works, you only have to understand the
probabilities of dice rolling since mutation and selection is simply a
variation of that stochastic process. You do know what a stochastic
process is, don’t you? Now if you want to derive the probability
function for random recombination, master the probabilities of card
drawing. Let’s see if you can do that graduate student of probability
theory.
>
> I think this covers it, except for the point that he makes these same
> two points over and over and over and over again.
Evolutionists are slow learners.
- Hide quoted text -
>
> - Show quoted text -

[Alan Kleinman MD PhD]

On Sep 18, 12:00 pm, hersheyh <hershe...@yahoo.com> wrote:
> On Friday, September 16, 2011 4:34:53 PM UTC-4, Alan Kleinman MD PhD wrote:
>
> [snip]
>
> Wherein I reduce the Dear Dr.Dr.'s garbage to its crucial elements.
>
>
>
> > The probability function I derived to compute the probability of two
> > mutations occurring is applicable to detrimental, neutral or
> > beneficial mutations.
>
> It is appropriate only when and if the Dear Dr. Dr. could actually understand the conditions where it is correct.  And the division by 4 part of his "derivation" of the binomial probability distribution (for that *is* what he derived although he apparently is unaware of that fact) is wrong under any conditions.

As I said in my previous post, evolutionists are slow learners. There
is more than one possible outcome from a point mutation and unless you
know what the base was before the mutation occurred, you can only be
certain that it is one of four possible outcomes.

>
> > What distinguishes whether the mutation is
> > detrimental, neutral or beneficial is how the subpopulation with the
> > particular mutation responds over generations.
>
> Agreed.  One uses the terms "beneficial" or "detrimental" to describe statistically significant changes in the fraction of the population with a particular genetic state from generation to generation relative to its alternative genetic state under specific environmental conditions.  Such changes only occur when the two genetic states produce a *phenotypic difference* that matters wrt relative reproductive success.  One uses the term "neutral" to describe the state when either the different genetic states produce no phenotypic difference that the environment can use to discriminate between the genetic states on the metric of relative reproductive success or when the phenotypic difference produced is irrelevant on the metric of relative reproductive success.    Empirically, this is identified by the fact that the generation to generation changes in fraction of the population having a particular state varies by no more than the expected amount of variance due to chance alone.  The percentage amount of expecte

d
>
> chance variance is a function of population size.  Typically the 95% confidence level is used to distinguish chance differences generation to generation from statistically significant differences generation to generation.

The point you are missing hersheyh is that the same probability
function for two mutations accumulating in a population applies
whether the mutations are beneficial, neutral or detrimental. When
mutations are neutral, you don’t have the benefit of amplification to
improve the probability that the next mutation will occur on a member
with the previous mutation. This is why when John Harshman argues that
hundreds of neutral mutations are being fixed in the population
simultaneously every generation; you are requiring that hundreds of
neutral mutations are accumulating simultaneously. The multiplication
rule of probabilities makes John’s claim mathematically irrational
nonsense.

>
> > If the mutation is
> > beneficial, the subpopulation will increase in number,
>
> More important than number is the change in fractional distribution.  Take antibiotic resistance.  Upon selection (the addition of the antibiotic), the population size drastically decreases because of the deaths of the sensitive cells.  What matters is that the fraction of the population with the genetic state of antibiotic resistance increases from 10^-8 to 1.0.  Whether or not one continues with the selective condition, subsequent growth (and growth is all that is required to increase numbers at this point) will not change the fraction of the population that has the 'genetic resistant state' significantly until there is mutation to a different genetic state that has a significant reproductive advantage over the resistant state under the environmental conditions at these post-selection times.

That’s not correct hersheyh. It is not the frequency of a beneficial
allele which determines the number of trials for the beneficial
mutation; it’s the number of members in the subpopulation who are able
to reproduce which determine the number of trials for the next
beneficial mutation. And as the Weinreich experiment demonstrates, you
can have multiple variants, each with their own subpopulations which
have to amplify their own particular beneficial mutations.

>
> > if the mutation

> > is neutral, the subpopulation size will remain relatively constant

> > over generations
>
> Again, it is the fraction of the population that is important, not the number.  Under neutral conditions (conditions where the two genetic states have no reproductive advantage relative to each other, either because they don't produce a phenotypic difference or because the phenotypic difference does not affect reproductive success), the generation to generation differences in the frequency of the two genetic states will be due to chance alone.  *Because chance has no memory* (a point you forget), this means that the frequencies of the two genetic states will undergo neutral drift (a drunkard's walk) that will only end by fixation of one trait or the other.  The percentage effect of such chance variation is higher in small populations.  Random walks will happen because one of the assumptions of the Hardy-Weinberg rule is that the population is of infinite size and real populations are not of infinite size.

What makes you think that it is the fraction of the population which
determines the probability of events rather than the absolute number
of members in a particular subpopulation? If it was the fraction of
the population which drives the mutation and selection phenomenon,
then it would only take a few generations to accumulate the mutations
necessary to give drug resistance in the Weinreich experiment. Even
you recognize that under ideal conditions it requires 30 generations
to rebuild (amplify) the population in order for there to be a
reasonable probability that the next beneficial mutation will occur.
Chance has no memory but it does obey mathematical rules. If you are
going to require that lots of low probability events are going to
happen over and over, you are going to be making claims that run
counter to the rules of probability theory. And the Hardy-Weinberg law
does not give you the probabilities associated with random
recombination. This law only tells you that when the system is in
equilibrium that the frequency of alleles remains constant over
generations. If you want to describe the probabilities of two alleles
recombining in a random recombination event, you need to apply the
rules of probability to predict the probability of that random
recombination event occurring.

>
> So, assuming a large enough population, the generation to generation effect of chance variation in the fraction of the population with a particular allele will be close to whatever the original fraction was.   If that fraction is 10^-8, one would expect the next generation to have a fraction close to that.  New mutation will not have a significant effect on this fraction because new mutations will have only a [1-(1/2N)] chance of not going to extinction by chance.  If,  by chance, one new neutral mutation has increased in frequency to a significant level, new mutations of the same particular type will be an insignificant fraction of the frequency of that mutation type in the population.

You do know that John Harshman is arguing that population size does
not affect neutral evolution. And you are trying to apply a model of
neutral evolution of one of two alleles for a particular gene. What do
you think would happen to the model if you had three neutral alleles
for that one gene, or four? Do you think that the probabilities of the
fixation of one of the neutral alleles increases compared with the two
allele model? The reason why I don’t think your model of neutral
fixation is very good is that it doesn’t simulate reality very well.
If I were going to look at a model of neutral fixation, I would link
the neutral alleles that are being fixed with the most fit
replicators. To completely disconnect neutral fixation from selection
is to ask that a neutral allele amplify without selective benefit.
This may happen on rare occasions just as someone winning a lottery
happens rarely. But to extend the model beyond its scope is running
smack into the multiplication rule of probabilities. A population may
win one neutral mutation but winning hundreds or tens of millions is
mathematically irrational.

>
> > and if the mutation is detrimental, the subpopulation
> > size will decrease over time.
>
> No.  In this case, the frequency of the mutant genotype will essentially equal the rate of new mutation to that genotype.  Any particular new mutant genotype that is deleterious will be driven to extinction, but new mutations of that genotype will occur every generation.  Eventually, you will have an equilibrium level where the loss of m deleterious mutant alleles each generation equals the gain of m deleterious mutant allleles each generation.  Thus the *fraction* of the population having a deleterious allele will remain constant.  [This is slightly different in the case of diploid organisms, where a 'recessive' allele can be selectively neutral in the heterozygous state and only harmful in the homozygous state.  But the rule that an equilibrium between gain and loss of the allele each generation still holds.]

The members who get that detrimental mutation will not be good
replicators. In order for the mutation and selection phenomenon to
function, it requires good replicators. Of course as generations go
on, more of these detrimental mutations can appear but the number of
descendents with these detrimental mutations will not increase. But it
is not detrimental mutations which drives the mutation and selection
process, it is beneficial mutations. And as I have shown you with the
empirical evidence, the process only works efficiently when a single
beneficial allele has to be amplified at a time. And that
amplification process has to be sufficient to give a subpopulation
size large enough to do a reasonable number of trials for the next
beneficial mutation in the sequence.

>
> > The mathematical significance of this
> > relates to the probability of the next beneficial mutation occurring
> > at the proper locus (position on the genome).
>
> The probability of any subsequent or second mutation occurring is a function of the rate of mutation to that state and the number of individuals in a population that have the needed previous genetic state.  The number of individuals in a population that have the requisite genetic state is a function of both selection for that state and the number of generations of growth under selective conditions for that state.

You still don’t understand how little the mutation rate contributes to
the behavior of the mutation and selection phenomenon. HIV has a
mutation rate 3 or 4 orders of magnitude larger than the rate you like
to use yet this virus still can not evolve efficiently to selection
pressures which target two genes simultaneously. The mutation rate
only determines the frequency at which trials are done for a
particular mutation. When selection pressures target more than a
single gene, you need exponentially more trials for the two beneficial
mutations and larger mutation rates only increase the number of trials
additively and improve the probability of the events less than
additively.

>
> Thus, the precise order of selective events matters.  

And now you should understand why the canned binomial distribution is
not the correct mathematical formulation for the mutation and
selection process because in the derivation of that function, the
order of events was not important and because of that a combinatorial
term appears in the equation.

> If the genetic state of antibiotic resistance is selectively neutral or detrimental under conditions where there is no antibiotic, then the steady-state fraction of the population having that state is essentially equal to the mutation rate assuming that there has not been sufficient time for a drunkard's walk to, by chance, having increased the frequency.  And in the examples we have been using, where the initial population was grown from a double-sensitive organism, there hasn't been sufficient time for a significant amount of drift.  Thus the *number* of individuals with resistance to the antibiotic is equal to the mutation rate to that genetic state times the population size examined for that genetic state.  At generation one of selection for the genetic state of antibiotic resistance, the *number* of individuals with the resistant genetic state has not changed.  But the *fraction* of the population with the resistant state has changed dramatically und
>
> er these conditions, from 10^-8 to 1.0.  After 30 generations of population doubling, almost regardless of whether or not one continues to use the selective conditions of antibiotic present, the *fraction* of the population resistant to the antibiotic remains essentially unchanged (1.0, with only back mutation providing the sensitive genetic state), but the *number* has increased.

Hersheyh, you are conflating your ideas before you even properly
understand mutation and selection. You first need to understand that
it is not the fraction of population which determines the number of
trials for a particular mutation; it is the absolute size of the
subpopulation. This is why recovery of the subpopulation size must
occur first before there is a reasonable probability that the next
beneficial mutation in an evolutionary sequence will occur. Even if
the fraction of the population with the first beneficial mutation is
1, the population size still must be large enough to do sufficient
trials that the next beneficial mutation will occur at the proper
locus.

>
> I certainly agree that the probability of finding a double-mutant is importantly a function of the number of individuals with the first mutation selected for.  The odds of finding a double-mutant for a second mutation in the cells selected for resistance to the first antibiotic is low if you do that selection in the first few generations after selection.  But it becomes increasingly possible in larger cells precisely because the size of the population with the first genetic resistant state is now large.  It is large precisely because of the earlier selection changing the fraction of cells with the first resistant state and subsequent selective growth of that subfraction.

Why does the “size” of the cell have anything to do with this? It is
the size of the subpopulation with the first beneficial mutation which
drives the probabilities of the second beneficial mutation occurring.
Any of the remaining population that is not on the same fitness
trajectory only represents competitors for the resources of the
environment and slows the growth of the subpopulation that is trying
to amplify its first beneficial mutation. This is why in the Lenski
experiment it takes hundreds of generations to amplify a beneficial
mutation, not your estimate of 30 generations of clonal doubling.
Lenski’s diverse populations are competing for the limiting resource,
glucose.

>
>
>
> [snip]
>
> > Evolutionists for decades have used the Poisson distribution function
> > in an attempt to describe the mutation and selection phenomenon. I
> > believe this is not the correct probability distribution to use
> > because the random mutation is not a Poisson random variable.
>
> The Poisson is only used as an estimate of the binomial probability distribution when certain conditions apply.  They apply in the cases I used it in.  So your real problem is that you disagree with the use of the binomial probability distribution.  You do so even though, with the exception of the division of 4, the equation you "derived" is nothing but the binomial probability distribution and is based on its assumptions.

And for the conditions of the mutation and selection phenomenon, the
Poisson distribution is not a good approximation for the binomial
distribution. I pointed this out to explicitly why the Poisson
distribution is not correct here. In the mutation and selection
process, the number of trials is actually quite small (only 10 per
generation using your numbers) and the probability of the beneficial
event is much larger than zero. If you use my numbers the probability
of the beneficial event is 1/4 when the trial occurs. If you want to
claim that there are only three possible outcomes from a point
mutation then the probability of the beneficial event is 1/3 from a
single trial. Either way, the probability is much larger than zero and
the Poisson distribution is not the correct approximation for either
the binomial distribution or the correct probability function which
describes the mutation and selection phenomenon in this case. And you
should recall that I never said that the binomial distribution was a
bad approximation for the mutation and selection phenomenon, I said
the Poisson distribution was a bad approximation for the process and I
have provided the mathematical justification for this reasoning. But
there are also two significant differences between the binomial
probability function and the correct probability function for mutation
and selection. The first is there are four possible outcomes from a
point mutation, not two. The second is the binomial distribution was
derived without consideration of the order of events. The order of
events is crucial in the mutation and selection process as you have
now finally acknowledged above.

>
>
>
>
>
> > In
> > addition, the Poisson distribution does not properly relate population
> > size, number of generations and mutation rate for computing the number
> > of trials for a particular mutation. I have derived what I believe is
> > the correct probability function for computing the probability of two
> > mutations A and B to occur. I�ll repeat the derivation here for you.
>
> > Probability of two beneficial mutations occurring (not simultaneously)
> > at two loci as a function of population size and number of
> > generations.
>
> > The following are the definition of the variables used.
> > n -- is the total population size

> > nA -- is the fraction of the total population size with mutation A

> > nGA � is the number of generations for beneficial mutation A to occur
> > nGB � is the number of generations for beneficial mutation B to occur
> > mA -- the probability that in one organism in one generation, a
> > mutation A will affect a specific locus in the genome
>
> Ordinarily this would be considered the "mutation rate."  But the Dr. Dr. does not
> ...
>
> read more »- Hide quoted text -

[Alan Kleinman MD PhD]

On Sep 20, 12:53 pm, John Harshman <jharsh...@pacbell.net> wrote:
> Just to let you know: I'm never going to reply to anything you post in
> this format. Then again, I probably won't reply to anything you post in
> any format; it's futile either way.

John, how disappointing, just when I though you were going to spend
your life trying to convince me of your mathematically irrationality.
But I recognize something about your evolutionist addictive
personality. You are obsessed with the theory of evolution no matter
how mathematically irrational this concept is. I suspect you will be
with us for a while longer.

[Alan Kleinman MD PhD]

On Sep 20, 1:18 pm, r norman <r_s_nor...@comcast.net> wrote:
> On Tue, 20 Sep 2011 13:01:58 -0700 (PDT), chris thompson
>
>
>
>
>
> <chris.linthomp...@gmail.com> wrote:

> >On Sep 16, 7:09 pm, r norman <r_s_nor...@comcast.net> wrote:
> >> On Fri, 16 Sep 2011 23:55:14 +0200, "Rolf" <rolf.aalb...@tele2.no>
> >> wrote:>
>

> >> >Alan Kleinman MD PhD wrote:
>

> >> 1)  He says that single drug treatment of many diseases, especially
> >> HIV-AIDS, is the sole responsiblilty of ignormant evolutionary
> >> biologists who forced a mathematically invalid theory of evolution
> >> down the throats of medical students so they do not know any better.
> >> He has been told that evolutionary biologists do not teach in medical
> >> school, that medical genetiics is not the same as evolution, that
> >> medical doctors are responsible for the education of medical students,
> >> that medical doctors are responsible for choosing treatments,  and
> >> that evoloutionary biologists have long known and taught that
> >> organisms can develop resistance to single drugs.  None of this
> >> matters.  Evolutionary biologists are responsible for killing and
> >> suffering of millions because they (we) don't understand mathematics.
>

> >> 2)  He has a background in engineering and therefore is master of
> >> anything and everything mathematical.  Of course he has already
> >> demonstrated a total lack of understanding of biological evolution, he
> >> has beend reminded repeatedly of the many extremely sophisticated
> >> mathematical analyses of evolution by population geneticists, he
> >> utterly fails to understand what is meant by genetic drift,  his own
> >> so-called mathematical anaysis of the probability that two beneficial
> >> mutations become fixed in a population is completely independent of
> >> any fitness advantage offered by the mutations, he has already made
> >> some monumental mathematical blunders and egregious biological
> >> blunders.  None of this matters.  He has mastered mathematics and
> >> understands the law of multiplication of probabilities.  No
> >> evolutionary biologist understands probability theory.  And, besides,
> >> because of this total lack of understanding we have of mathematics, we
> >> are responsible for the death and suffering of millions of people
> >> because of how we lie to medical students and mistrain them.
>

> >> I think this covers it, except for the point that he makes these same
> >> two points over and over and over and over again.
>

> >Quite a roundabout way of conceding defeat, Richard!
>
> I clearly yield to his bull-headed staying power.  Even the
> indefatigable Harshman seems to be throwing in the towel.

Sure r norman, graduate student of probability theory. It has nothing
to do with the fact that evolutionists have bungled the basic science
and mathematics of the mutation and selection phenomenon and harmed
millions of people while they were at it. Even the mathematically
incompetent hersheyh now recognizes that I have derived the correct
probability function for two mutations occurring except he has yet to
figure out that when a point mutation occurs that you only know with
certainty that there will be one of four possible outcomes. If
Harshman drops out it will be because I have taken away his best
argument strategy, derision. Any time he wants to tell me I don’t know
how to do mathematics, I simply remind him how he didn’t understand
the basic concept of how population size affects the probability of
events. Evolutionists whine so much when you show them that they have
made mathematical and scientific blunders. But they never admit they
are wrong, even when they harm millions of people with their
mathematical irrationality.

[Alan Kleinman MD PhD]

On Sep 21, 10:36 am, Inez <savagemouse...@hotmail.com> wrote:
> The splintering effect of your thread only happens in Google Groups
> when the thread hits 1000 posts.  People with real newsreaders are not
> patient with working around the vagueries of Googles Groups, and it is
> unlikely that many people will respond to your massive cut-and-paste
> threads.
That’s not my problem. I’m here to properly describe the basic science
and mathematics of the mutation and selection phenomenon and I am
willing to work within the limitations of the forum.
>
> What you migh try is reading people's posts for comprehension and
> responding to what they actually say, which might get the thread
> wrapped up on under 1,000  (or in this case 2,000) posts.
We are already well into our first hundred of the third round and I am
only now responding to individual posts again. You are dreaming if you
think this discussion will end in 3000 posts. You evolutionists are
just very slow learners.
>
>
>
>
>
> > Inez   Aug 17, 9:57 am

> > Newsgroups: talk.origins
> > From: Inez <savagemouse...@hotmail.com>

> > Date: Wed, 17 Aug 2011 09:57:56 -0700 (PDT)
> > Local: Wed, Aug 17 2011 9:57 am

> > Subject: Re: The Theory of Evolution is Mathematically Irrational

> > Round 2>> > They don't show up all at once.  Most people have had them in their
> > >> > family tree for a long time.  It's just that dozens get fixed every
> > >> > generation.  Your argument from incredulity is ignorant and boring.
> > >> > If you don't think that neutral mutations can spread through a
> > >> > population, why don't you show why not?
> > >> Of course these neutral mutations don’t show up all at once, sweeping
> > >> through the population like a tsunami. They also don’t show up dozens

> > >> per generation, generation after generation for hundreds of thousands

> > >> of generations. This is part of the evolutionist mathematically
> > >> irrational speculations. My arguments are made from hard mathematical
> > >> and empirical evidence. If you didn’t have your mathematically
> > >> irrational speculations and gross over-extrapolations, you
> > >> evolutionists would have no argument at all for your mathematically
> > >> irrational belief system.
> > >A lot of fist shaking, but not a real argument.  Why couldn't a
> > >neutral mutation spread through the population by chance?
>
> > Inez, it’s very difficult to use a key board and mouse with a shaking
> > fist. All I’m doing is a little finger tapping.
>
> But none of that resulted in a real argument.
Evolutionists never see empirical and mathematical evidence as a real
argument. If you think that mutation and selection can occur in
parallel present an empirical example or show us mathematically how
this can occur because I have given you both empirical evidence that
it doesn’t occur and a mathematical explanation as well. So get your
fingers tapping and present a counter argument (if you have one which
I don’t believe you have).
>
> > So you want to know if
> > a neutral mutation could spread through a population by chance? Your
> > own evolutionist computations show that there is a very small chance
> > that this will happen equal to the frequency of that allele. And that
> > model only applies when you only have two neutral alleles for a single
> > gene. Now what’s the probability of two neutral mutations being fixed
> > by chance? Shouldn’t that joint probability of that event be governed
> > by the multiplication rule of probabilities?
>
> No.  The question isn't what the odds are of two *specific* mutations
> being fixed is, the question is what the odds are of *any* two (or
> more) mutations being fixed.
So present your mathematical model which demonstrates your claim. You
are using the model for the fixation of a single neutral allele from a
gene that has only two neutral alleles. What makes you think that you
can extrapolate that model to the fixation of any two (or more)
mutations being fixed simultaneously? Are you one of those
evolutionists who don’t think that the multiplication rule applies to
the joint probability of two or more events occurring in a random
process? You must be if you are making the above claim.
>
> > >> Now I have shown you mathematically why neutral mutations do not
> > >> spread through populations rapidly if at all.
> > >No one claims they spread rapidly.
>
> > They better if you want to do the accounting to explain the 40,000,000
> > differences between human and chimpanzee genomes in 500,000
> > generations.
>
> Why does it have to be 500,000 generations?
This should be clear to you, I’m using evolutionist numbers.
>
>
>
>
>
>
>
> > >> The probability function
> > >> I derived for you of two mutations accumulating is not only applicable
> > >> for the accumulations of beneficial mutations; it is also applicable
> > >> for computing the probability of neutral or detrimental mutations
> > >> accumulating in a population. Of course neutral and detrimental
> > >> mutations do not amplify because they don’t give increased fitness to
> > >> reproduce for those members with those mutations. Because of this,
> > >> there is a very low probability that neutral or detrimental mutations
> > >> will accumulate in a population.
> > >Yes...and if there are a whole lot of neutral mutations, a few will
> > >beat the odds.
>
> > You need far, far, far more than a few to beat the odds to do the
> > accounting for the 40,000,000 differences between human and chimpanzee
> > genomes in 500,000 generations.
>
> The math has been presented to you numerous times.
>
> >> > > This is the kind of irrational
> > >> > > nonsense that evolutionists are now enamored with rather than properly
> > >> > > describing the basic science and mathematics of mutation and
> > >> > > selection.
> > >> > Selection is by definition irrelevant to neutral evolution.
> > >> And without selection, amplification of mutations does not occur.
> > >> And without amplification, you have very low probabilities of accumulating
> > >> mutations.
> > >Right...and if there are a ton of neutral mutations, a few will make
> > >it.
>
> > The multiplication rule of probabilities for computing the joint
> > probability of random independent events shows that your claim is
> > mathematically irrational.
>
> But that isn't the right way to compute the probability.  The question
> isn't what the chances are of a specific set of mutations getting
> fixed is, the question is what the chances of any set of mutations
> being fixed.  As John Harshman pointed out earlier, the chances of any
> specific bridge hand being dealt is vanishingly small, but the chances
> of some bridge hand being dealt is a certainty.

John likes to throw out sloppy analogies. You are not dealing out
bridge hands here. You are claiming that a neutral mutation will show
up in every member of a population without selection or in John’s
argument, tens of millions of neutral mutations are showing up in
every member of a population without the benefit of selection. Tell us
Inez, how do neutral mutations in one family line show up in a totally
unrelated different family line? How do tens of millions of neutral
mutations show up in every different unrelated family line? Let’s see
how you deal out grand slams with every deal of the cards.
>
>
>
>
>
> > You evolutionists have clearly missed the
> > probability part of the probability and statistics course.
>
> > >> Why evolutionists would think that the mathematics of
> > >> abiogenesis will somehow cause the spread of neutral mutations through
> > >> a population faster than the mathematics of selection can only be
> > >> explained by the fact that evolutionists are mathematically
> > >> incompetent.
> > >This is a odd strawman that you have made up and insist on repeating
> > >for no apparent reason.  Who said that neutral mutations spread more
> > >quickly than beneficial ones?  Can you provide a link?
>
> > The only thing that separates the mathematics of abiogenesis from the
> > mathematics of mutation and selection is replication and selection. Do
> > you really need a link for that?
>
> No idea why you suddenly started talking about abiogenesis here.  I
> asked for a link to someone claiming neutral mutations spread faster
> than selected ones.  Who claimed that?
The mathematics of abiogenesis involves probabilities without
selection. Now you are trying to remove selection from the mutation
and selection process and claim that tens of millions of neutral
mutations can be fixed in 500,000 generations.

- Hide quoted text -
>

> - Show quoted text -- Hide quoted text -
>
> - Show quoted text -- Hide quoted text -

[Alan Kleinman MD PhD]

On Sep 21, 12:52 pm, r norman <r_s_nor...@comcast.net> wrote:
> On Wed, 21 Sep 2011 20:39:31 +0100, Mike Lyle
>
>
>
>
>
> <mike_lyle...@yahoo.co.uk> wrote:
> >On Tue, 20 Sep 2011 16:18:31 -0400, r norman <r_s_nor...@comcast.net>

> >I wonder if there may be a clue in the records of malpractice
> >hearings: I believe he mentioned that he'd had one. I, of course,
> >apologise if my memory is at fault in this matter.
>
> For all his faults I still wouldn't look into that.  Far too many
> capable and competent practicioners get hit with malpractice claims.
Go ahead, look into it r norman. And if you want to learn a lesson
about me from my single malpractice case is that I will not give up if
I believe I am correct, even if the fight goes on for years. And the
courts found that I was correct and I believe I am correct here with
mathematical and empirical certainty.
>
> Note:  I wouldn't want to cut off all such claims -- there is more
> than enough medical incompetence going around that the medical
> profession itself seems unwilling or unable to control internally.
> Still, a little common sense in throwing out really frivolous claims
> would be in order.  People do get worse and die for mysterious reasons
> and, often enough, for no known reason. Doctors can't stop it, merely
> stem the tide.
And if you want to stem the tide of drug resistant microbes, learn the
empirical lesson taught by the use of combination therapy for HIV and
the mathematical lesson I am giving you evolutionists now. And you
evolutionists need to start teaching the basic science and mathematics
of the mutation and selection phenomenon correctly despite the
questions it will raise in the minds of naďve school children about
the theory of evolution. Or is that what you fear? Do you fear anyone
who would question your mathematically irrational beliefs?

[r norman]

I'd given up reading your nonsense so I didn't realize even that you
had finally abandoned the notion of calculating the probability of two
_beneficial_ mutations in favor of merely two mutations. Perhaps you
finally learned a tiny bit of evolutionary biology to understand what
"beneficial" means. No, I doubt it.

It is, in fact, my graduate level courses in stochastic processes that
allow me to understand that the Poisson distribution can be an
excellent mathematical tool to describe many such processes, just as
the binomial distribution or the Gaussian are used to describe other
processes. My elementary undergraduate courses in probability theory
taught me that you cannot do probability with using a distribution
function. So what is wrong with Hershey's work?

Everybody has known about microbial resistance to antibiotics from the
very beginning. Sulfonamide resistant bacteria were known in the
30's, soon after the introduction of these first antibiotics.
Penicillinase in bacteria was discovered even before penicillin was
first used therapeutically and penicillin and streptomycin resistant
strains of bacteria were identified in the 40's.

You should know that the development and application of antibiotics,
the discovery of drug resistance, and the continued treatment of
patients with single drug treatment after resistance was well known
was all done by medical doctors long before the so-called "modern
synthesis" of evolution had fully taken root. You are simply ignorant
both of medicine and evolution.

You are also ignorant of the "millions and millions" of people whose
lives have been saved by the proper application ffin medicine of
biological, bacteriological, and immunological ideas, all with firm
evolutionary biology foundations.

[Alan Kleinman MD PhD]

On Sep 23, 8:13 am, "Steven L." <sdlit...@earthlink.net> wrote:
> "r norman" <r_s_nor...@comcast.net> wrote in message
>
> news:46l777pqufop933rv...@4ax.com:

> > 1)  He says that single drug treatment of many diseases, especially
> > HIV-AIDS, is the sole responsiblilty of ignormant evolutionary
> > biologists who forced a mathematically invalid theory of evolution
> > down the throats of medical students so they do not know any better.
> > He has been told that evolutionary biologists do not teach in medical
> > school, that medical genetiics is not the same as evolution, that
> > medical doctors are responsible for the education of medical students,
> > that medical doctors are responsible for choosing treatments,  and
> > that evoloutionary biologists have long known and taught that
> > organisms can develop resistance to single drugs.  None of this
> > matters.  Evolutionary biologists are responsible for killing and
> > suffering of millions because they (we) don't understand mathematics.
>

> > 2)  He has a background in engineering and therefore is master of
> > anything and everything mathematical.  Of course he has already
> > demonstrated a total lack of understanding of biological evolution, he
> > has beend reminded repeatedly of the many extremely sophisticated
> > mathematical analyses of evolution by population geneticists, he
> > utterly fails to understand what is meant by genetic drift,  his own
> > so-called mathematical anaysis of the probability that two beneficial
> > mutations become fixed in a population is completely independent of
> > any fitness advantage offered by the mutations, he has already made
> > some monumental mathematical blunders and egregious biological
> > blunders.  None of this matters.  He has mastered mathematics and
> > understands the law of multiplication of probabilities.  No
> > evolutionary biologist understands probability theory.  And, besides,
> > because of this total lack of understanding we have of mathematics, we
> > are responsible for the death and suffering of millions of people
> > because of how we lie to medical students and mistrain them.
>

> > I think this covers it, except for the point that he makes these same
> > two points over and over and over and over again.
>

> Maybe Dr. Kleinman, M.D., can't deal with the fact that it's *doctors*
> (and patients), not evolutionists, who bear such responsibility for the
> rise of antibiotic-resistant bacteria.  By overusing and misusing
> antibiotics.
Steven, if you ever show up in my clinic with a fever and sore throat,
simply tell me you are an evolutionist and you don’t want to
contribute to the rise of antibiotic resistance. I will withhold your
antibiotics as long as you wish. And you can check my records, I have
never had a patient die because an infection was left untreated but I
have seen patients of other doctors who have taken your ill-conceived
advice and died from untreated infections. Of course you not being an
MD and never have treated an infection makes you an expert in the
field.
>
> When I was a kid, doctors would prescribe penicillin just for simple
> colds.  And today just as back then, doctors still hand out antibiotics
> for minor pus pimples and skin abscesses rather than lancing and
> draining them.
How do you know they were simple colds? And can you recognize the
difference between cellulitis and an abscess? Steven, would you
explain to us why community acquired MRSA is still sensitive to
several oral antibiotics while hospital acquired MRSA is resistant to
virtually all oral antibiotics (except for perhaps one)? Steven, it’s
your sloppy understanding of mutation and selection which has caused
multidrug resistant bacteria to proliferate.
>
> The answer was not to use multiple antibiotics according to some
> evolutionary theory.  The answer was to avoid prescribing antibiotics
> for colds and boils *at all*, unless a systemic bacterial infection had
> gotten underway.
Why don’t you go to medical school and start practicing medicine and
find out why you are wrong? Hopefully it will only require a single
death to change your mind but you being an evolutionist, I suspect you
are a slow learner.
>
> And any doctor with even a rudimentary understanding of the ToE would
> understand why.
That’s the problem Steven; physicians only have a rudimentary
understanding of the mutation and selection phenomenon. This is all
that evolutionists are able to teach because this is all they know.
That’s why we have multidrug resistant microbes proliferating today as
well as multiherbicide resistant weeds, multipesticide resistant
insects and less than durable cancer treatments. Steven, I suppose you
are going to argue that physicians should not treat cancer because it
might lead to drug resistant cancers. Or farmers should not be using
herbicides or pesticides because it might lead to herbicide resistant
weeds and pesticide resistant insects. Your narrow minded evolutionist
understanding of the mutation and selection phenomenon transcends your
ignorance of the practice of medicine.
>
> -- Steven L.- Hide quoted text -

[Alan Kleinman MD PhD]

On Sep 20, 1:01 pm, chris thompson <chris.linthomp...@gmail.com>
wrote:

> Quite a roundabout way of conceding defeat, Richard!

Evolutionists will never admit they have bungled the basic science and
mathematics of the mutation and selection phenomenon. It would reveal
that they have developed a mathematically irrational belief system
around a physical phenomenon that doesn’t work the way they claim.
>
> Chris- Hide quoted text -

[Alan Kleinman MD PhD]

On Sep 21, 12:39 pm, Mike Lyle <mike_lyle...@yahoo.co.uk> wrote:
> On Tue, 20 Sep 2011 16:18:31 -0400, r norman <r_s_nor...@comcast.net>
> wrote:
>
>
>
>
>
> >On Tue, 20 Sep 2011 13:01:58 -0700 (PDT), chris thompson

> >I clearly yield to his bull-headed staying power.  Even the
> >indefatigable Harshman seems to be throwing in the towel.
>
> I wonder if there may be a clue in the records of malpractice
> hearings: I believe he mentioned that he'd had one. I, of course,
> apologise if my memory is at fault in this matter.

So that’s what comes out when you squeeze the carbuncle between an
evolutionist’s ears. Let me help you with your memory deficit Mike. In
my more than 20 years of practicing medicine and doing close to
100,000 patient visits, I have had one malpractice case which lasted
more than seven years before I finally won the case on summary
judgment. I have no complaints against me with the Medical Board of
California. I only have a very busy medical practice treating MRSA
caused by the evolutionist failure to properly understand and teach

the basic science and mathematics of the mutation and selection

phenomenon. So feel free to investigate me Mike and you will find that
the only thing you have in your evolutionist brain is the evolutionist
doctrine that has turn your grey matter into pus.
>
> --
> Mike.- Hide quoted text -

[Alan Kleinman MD PhD]

On Sep 23, 12:19 pm, hersheyh <hershe...@yahoo.com> wrote:
> On Tuesday, September 20, 2011 2:42:19 PM UTC-4, Alan Kleinman MD PhD wrote:
>
>
>
>
>
> > The following replies are from a splinter threads
> > Virgil   Sep 14, 1:35 pm
> > Newsgroups: talk.origins
> > From: Virgil <vir...@ligriv.com>
> > Date: Wed, 14 Sep 2011 14:35:43 -0600
> > Local: Wed, Sep 14 2011 1:35 pm

> > Subject: Re: The Theory of Evolution is Mathematically Irrational
> > Round 2

> > In article
> > <7f7ca969-1404-4f7e...@x11g2000prb.googlegroups.com>,

> >  Alan Kleinman MD PhD <klei...@sti.net> wrote:

> > >> On Aug 10, 7:42 pm, Mark Isaak <eci...@curioustaxonomyNOSPAM.net>
> > >> wrote:
> > >> > On 8/10/11 2:21 PM, Alan Kleinman MD PhD wrote:
> > >> > > On Jul 14, 8:58 am, Mark Isaak<eci...@earthlink.net> wrote:
> > >> > >> On Tue, 12 Jul 2011 18:18:51 -0700, Alan Kleinman MD PhD wrote:
> > >> > >>> On Jun 7, 2:45 pm, Mark Isaak<eci...@earthlink.net> wrote:
> > >> > >>>> On Mon, 06 Jun 2011 17:47:21 -0700, Alan Kleinman MD PhD wrote:
>
> [snip]
>
> > What makes you think that I am not
> > dedicated to figuring out how mutation and selection works?
>
> Everything you have posted on the subject and your complete refusal to do any research into the math, try to actually discuss your bogus assumptions, or even try to listen.  You come across as both profoundly arrogant and ignorant.  And I don't think that is just my opinion.

Hersheyh, you are the one who doesn’t do research into the equations
you use. You have used the Poisson equation incorrectly for the
mutation and selection phenomenon without ever studying the derivation
of the equation and knowing the limitations of the use of the
equation. Evolutionists always think that anyone who claims they are
wrong are arrogant and ignorant but it is not my teaching which has
led to the occurrence of multidrug resistant microbes, multiherbicide

resistant weeds, multipesticide resistant insects and less than
durable cancer treatments.

>

> > The correct probability
> > function for random recombination does not require that you consider
> > selection. The affects of selection on random recombination only
> > affects the probabilities implicitly by altering the number of members
> > with each of the particular alleles.
>
> The probability of *recombination*, in random sexually reproducing eucaryotes (organisms that go through a meiotic cycle), is determined by the *frequencies* of the alleles in the parent generation and is described by the logic of the Punnet Square, which makes it about as old as modern genetics.  Note that I said frequencies in the parent generation and not the *frequency of mutation* from w.t. to mutant allele.  The *frequency* of alleles in any particular generation is a function of its history, specifically the selective pressures that have historically acted upon different phenotypes produced by the genotypes and/or the chance history of neutral drift.  Again, it is the *relative frequency* of different alleles in a randomly sexually reproducing population that determines the probability of recombination, NOT the absolute number of members NOR the mutation probability.

The Punnett square is only useful for predicting the results of a
breeding experiment. It is not useful for predicting the results of
random recombination. To do that prediction, you have to apply the
principles of probability theory correctly and you have already shown
that you can’t do that. You do have some idea of what the variables
are including the frequencies of the alleles. Since no evolutionist
has derived the correct probability function that would describe
random recombination here, I’ll do the derivation for you in a week or
two. Then you can say how amateurish the derivation is and whine about
some feature of the calculation before you finally admit it’s correct.

>
> In procaryotes and viruses, recombination is a rarer event, as these organisms generally reproduce clonally, and one has to define what mechanism of genetic exchange one is talking about: exchange resulting from double infection of different viruses, transmission via plasmids and other extra-chromosomal agents, transformation, or by viral transduction.

Do you think it is the rarity of recombination for HIV that prevents
the lateral transmission of beneficial alleles? Why don’t you present
the mathematics to substantiate your claim?

>
> > >> What happens to the probabilities of the random
> > >> recombination of A and B if only one of the two all alleles amplify?
>
> So, are A and B different alleles of the same gene or are they different genes?  Do you know the difference?  And why it makes a difference?

Let A be a resistance allele to a protease inhibitor and B be a
resistance allele to a reverse transcriptase inhibitor. Isn’t that
which is required to accelerate the evolutionary process by
recombination?

>
> > >Not relevant.
> > John, you shouldn�t be making this argument until you derive the
> > probability function for random recombination. I�m not going to give
> > the derivation of that probability function now but consider this.
> > What if in your population every member has allele A except the member
> > which has allele B, that is A has a frequency close to 1 in the
> > population? That member with allele B that is B has a frequency very
> > close to 0. What is the chance that a member with allele A will meet
> > and recombine with the member with allele B?
>
> This again shows your confusion about the difference between the term 'allele' and the term 'gene' or your confusion between the 'probability of mutation' and the 'probability of recombination'.  You treat A and B here as if they were alternate alleles of the same gene.  And given your confusion between a 'gene locus' and a 'nt site', you are probably treating the two,  A and B, as different nts at the same nt site.  If that is what you mean, then recombination will not produce anything but the same two alleles (unless the two alleles contain *different* mutations at *different* nt sites from each other rather, in which case a rare recombination between those two independent mutations will produce a double-mutant and a non-mutant).

What makes you think I’m confused about what a gene and an allele are?
You are the one who has been using the wrong probability distribution
for years without ever going through the derivation of the equation
and determining when the equation is valid to use. Why should I
believe that you understand what a gene and an allele is?

>
> Ordinarily, recombination refers to recombination between *gene loci*, not recombination within a gene, and recombination between alleles that differ by having different nt's at a single nt site is impossible because a nt site is the limit for recombination.

The mathematics I will present will give the probability function for
recombination between gene loci.

>
> So tell us what you mean when you talk about *recombination*.  Are you concerned with eucaryotic recombination, which occurs each and every generation?  Or are you concerned with some type of gene exchange that goes on in procaryotes or viruses?  When you use the term 'allele' in your discussion above, are you talking about different forms of a specific gene locus (the actual definition) or are you talking about differences in nt's at a single nt site or are you talking about two *different* unlinked genetic loci, each of which has alternate alleles?  Or do you not understand what I am talking about?

The equation I will derive for you will include multiple
recombinatorial events, not just a single recombination event. I’ll
give you the equation which shows how many recombinatorial trials must
occur before you get a reasonable probability that alleles A and B
will recombine on a single member.

>
> [snip stupidity about the Poisson, which is irrelevant]

You’re the one who so stupidly uses the Poisson distribution. Do you
want me to give you the name of the lower division mathematics text I
used when I was a freshman in college that gives the derivation of the
Poisson equation?

>
> > >It's really quite simple. Given various simple assumptions, such as
> > >independent assortment, panmixis, a constant population, and frequencies
> > >p and q for the two alleles, the expected frequency of AB individuals is
> > >just pq. As p and q increase, pq increases. We have already specified
> > >that p and q are increasing. If AB phenotypes are favored over A, B, and
> > >"wild type" phenotypes, p and q will increase faster than they would in
> > >the absence of that advantage.
>
> John is possibly falsely thinking that you were talking about eucaryotic recombination involving organisms with a meiotic cycle and also are thinking of A and B as alternate alleles of the same gene.  I think you are probably thinking of A and B as different *genes* rather than alleles of the same gene.  But it is hard to tell what you mean since you have *repeatedly* refused to clarify what you mean.  Probably because you don't understand the criticisms, in this case don't know the difference between "allele" and "gene locus" and "nt site".

If I confused John on this point, I apologize. It should not be that
confusing. You evolutionists are claiming that recombination will
somehow accelerate the mutation and selection process by combining a
beneficial mutation in an allele of one gene with a beneficial
mutation in another allele of a different gene giving our double
mutant. I’m going to derive for you the mathematics which describes
this process and show you why you are wrong with your claim.

>
> > John, the only thing that the Hardy-Weinberg law gives you is that the
> > frequency of alleles remains constant when the population is in
> > equilibrium (selection is not acting).
>
> And the H-W equilibrium only really exists when the population is of infinite size.

The equation I will derive for you is based on a finite population and
applies to equilibrium and non-equilibrium conditions.

>
> But if you consider A and B to be two different unlinked *genes*, each with certain *frequency* of alternate alleles in the population, say p for A and q for A's alternate allele, a, and r for B and s for b, then you can use the expansion to determine the frequencies of any kind of diploid offspring assuming randomness.  The frequency, in the population, of gametes with the *haploid genotype* A;B would be pr.  The frequency of A;b would be ps.  Of a;B would be qr.  [As an exercise to show that the frequencies of the gametes add up to 1, which is the whole population of possibilities: pr+ps+qr+qs = p(r+s)+q(r+s) = (p+q)(r+s) = (1)(1) = 1]  And of a;b would be qs.  
>

This is not how to do the computation in general because a population
can have A, B and C alleles where the C alleles are not A and not B
alleles. What you need to accelerate the mutation and selection
process is for one parent with the A allele and another parent with
the B allele to recombine those two alleles into a descendent with
both A and B alleles to give the more fit replicator, not A and C or B
and C.

> Using a Punnet Square and crossing the gametes to each other along with the appropriate frequency of the gametes in the population will generate the frequencies of different genotypes in the progeny population.
>
> But that is assuming that A and B are two different unlinked genes in a eucaryotic population.

The equation I will derive for you will degenerate to the mathematics
of the Punnett Square if you eliminate C alleles and have only two
members with A alleles and two members with B alleles or if you are
talking about diploid, a single member with some combination of A and
B and another member with some combination of A and B. You can set up
that circumstance in reality with a breeding experiment but now we are
talking about random recombination such as would be seen with HIV
where you have more than two possible alleles.

>
> > If you want to estimate the
> > probability of two alleles randomly recombining, you need to write the
> > probability function for that stochastic process. Once you do that,
> > you can consider how selection will change the probabilities over
> > generations as the frequencies and population sizes of the alleles
> > change.
>
> Selection increases the relative frequency of the allele of a gene which has the selectively advantageous phenotype.  It will do so each generation relative to the alternative allele.   That is the very definition of selection.  So the relevant question is "What is the *frequency* of the alleles in reproducing individuals is there at the generation I am looking at?"  Not, for recombination in sexually reproducing eucaryotes, "How many, numbers, of allele a are present in reproducing members of the population?"

Of course selection changes the frequency of alleles or more correctly
causes the amplification of the beneficial allele, so how does this
affect the random recombination process? You have to derive the
probability function which describes this stochastic process to
understand this.

>
> Of course, you could be talking about recombination in procaryotes or viruses, which are mostly growing in a clonal fashion.  Until you choose to actually respond intelligently, it is hard to parse out what you are talking about here.

You are going to have a hard time understanding me until you
understand the mathematics and you are ever so slowly understanding
the mathematics.

>
> [snip major material which I will try to cover in smaller chunks and re-label the subject heading]- Hide quoted text -

[Vincent Maycock]

"Alan Kleinman MD PhD" <klei...@sti.net> wrote in message
news:5cd53d5f-497f-4bdd...@t16g2000yqm.googlegroups.com...

snip

> Evolutionists will never admit they have bungled the basic science and
> mathematics of the mutation and selection phenomenon. It would reveal
> that they have developed a mathematically irrational belief system
> around a physical phenomenon that doesn’t work the way they claim.

Did creationists who believe in microevolution (but not macroevolution) also
bungle this basic science?

[hersheyh]

On Thursday, October 6, 2011 7:44:51 PM UTC-4, Alan Kleinman MD PhD wrote:

[Can't you respond to posts individually anymore?]

>
> From: John Harshman <jhar...@pacbell.net>
> Date: Thu, 08 Sep 2011 16:15:55 -0700
> Local: Thurs, Sep 8 2011 4:15 pm
> Subject: Re: The Theory of Evolution is Mathematically Irrational
> Round 2
> > On Aug 4, 5:41 pm, "Vincent Maycock" <vam...@aol.com> wrote:

> >> "Alan Kleinman MD PhD" <klei...@sti.net> wrote in messagehttp://groups.google.com/groups?as_umsgid=c26c3472-eef4-471d...@m6g2000prh.googlegroups.com...

> >>>> On Jul 11, 9:19 am, John Harshman <jhar...@pacbell.net> wrote:
> >>>>> hersheyh wrote:

The immune system recognizes *self* and distinguishes that from *nonself*. If a human had fly cytochrome c instead of human cytochrome c since conception, the immune system would recognize that sequence as *self*. So the only real question is whether or not there is a significant *functional* difference between fly and human cytochrome c that makes fly sequence incompatible with the *function* of cytochrome c in humans. In many cases, the answer to such a question is no, there is no significant functional difference. There may be a *quantitative* effect (e.g., some temperature or other quantitative effects) and, in a few cases of co-evolution of interacting parts, incompatability. But fly cytochrome basically functions just like human cytochrome.

If you mean that the immune system can be made to recognize the difference between human and fly cytochromes, the answer is probably yes. But the immune system can also recognize the difference between A, B, and O antigens from different humans.

>
> >> What makes you think that humans and chimpanzees came from a
> >> common progenitor when so many genes differ and you have less than a
> >> million generations to make this transformation of tens of thousands
> >> of genes?

That would be about 23,000 total protein-coding genes (accounting for only about 1.5% of the genome), and of which 30% do not differ at all and most of the rest differ by only one or two amino acids (the average difference is two). 16,000 is not "tens of thousands of genes". Only about 600 proteins show any indication of strong positive selection and many of those are in the immune system where there is often frequency-dependent selection.

Given that protein-coding sequences undergo neutral drift at a somewhat slower rate than non-coding sequences because of evolutionary constraint, the number of aa differences per protein is about what one would expect given the rate of neutral drift and the number of generations separating human and chimpanzee.

> From: John Harshman <jhar...@pacbell.net>

> Date: Thu, 08 Sep 2011 16:19:28 -0700
> Local: Thurs, Sep 8 2011 4:19 pm
> Subject: Re: The Theory of Evolution is Mathematically Irrational
> Round 2
> >>>> On Jul 13, 1:29 am, G<g...@nowhere.invalid> wrote:

Can you tell us how you identify that a mutation has occurred given that you don't know what the original nt was nor whether or not it has changed from that original nt to some other nt? ESP? God tells you?

> >> You don’t need
> >> to know what the original base was to compute the probability of a
> >> particular mutation occurring.
> >Of course you do, even at the molecular level. For one thing,
> >transitions are much more common than transversions. It's much more
> >likely that C will change to T than that G will change to T.
>
> Can you tell us how this was measured and why this happens? In fact,
> give us a table of frequencies of mutations of one base to another.

You determine that transitions (that is, purine to purine mutations or pyrimidine to pyrimidine mutation) by identifying *change* from a known wt sequence to a *mutant* sequence. Typically this is done by distinguishing mutant phenotypes from non-mutant phenotypes and subsequently sequencing the spontaneous mutants that occur. Then you compare the number of *changes* from, say, G to A and compare that to the number of changes from G to either C or T. Of course, the historical reason why it was thought that transitions would outnumber transversions (despite there being twice as many possible transversions) is chemistry. It is simply easier to make a Pu to Pu error than a Pu to Py error. Transversions usually occur after ionizing radiation and certain large and bulky alkylating agents. Transitions, OTOH, can occur by oxidative deamination and tautomerization. This is especially the case for 5-methylcytosine in CpG pairs.

When you look at SNPs (single nucleotide polymorphisms) in humans, about 2/3 are transition changes. But this seems to be, to some extent, species specific. Which again points out that mutation rates/frequencies cannot be generated as a hypothetical by making assumptions that all sites have the same mutation rate and that all three types of change are equally likely to happen (one can generate a hypothetical ratio for an honest pair of dice). Mutation frequency can only be measured empirically by knowing the original and changed genetic states and actually measuring the frequency of the mutant state in a population that is initially non-mutant.

>
> >>>> That would be insane and thus fit perfectly with the rest of your
> >>>> "math". G, 2 + 2 = 4, not 12. Now your bit of mathematical illogic
> >>>> may impress a mathematically incompetent evolutionist like John
> >>>> Harshman who has no idea how to apply the principles of probability
> >>>> theory but it will impress few others.
> >>> Do you understand that he was making fun of you? Probably not.
> >> John, I find you evolutionists amusing when you make your serious
> >> claims like reptiles can be transformed into birds by the mutation and
> >> selection phenomenon. I find it particularly amusing when you claim
> >> that selective evolution occurs more rapidly than neutral evolution
> >> and then you claim that a couple hundred neutral mutations are fixed
> >> every generation, generation after generation for hundreds of
> >> thousands of generations when the selective evolution of a single
> >> beneficial mutation takes hundreds of generations.
> >You may find it amusing, but it's amusement occasioned by your own
> >ignorance. I've explained all this many times before.
>
> Then would you explain to us how hundreds of neutral mutations can be
> transferred from one family line to an unrelated family line?

Sex. The same reason why the term "racial purity" is an oxymoron. The same reason why the genes you have include genes from different family lines (unless, of course, you are from Kentucky or some completely inbred line). Frankly, it is much more likely that you are a mongrel than your pet is.

> >> It’s weird
> >> discussing hard mathematical science with mathematically irrational
> >> evolutionist dogmatists. It’s like talking with someone with a drug
> >> addictive personality.
> >We all think that way of you. The difference is that we're right.
> >Where's your hard math here, by the way?
>
> I’ve already given you the hard mathematical science of mutation and
> selection and substantiated this mathematics with empirical evidence.

Ha. Ha. Ha. Ha. Snicker.

> On the other hand you give us rank and gross over extrapolation of a
> model which describes fixation of one of two neutral allele and claim
> that it happens a couple hundred times per generation, generation
> after generation for hundreds of thousands of generations.

That is what the math says. After you calculate the rate of fixation per nt pair, to get the rate of fixation per genome, you have to multiply the rate of fixation per nt pair by the number of nt pairs in the genome. That is what the math requires.

> The hard
> math that argues against your mathematically irrational claim is the
> multiplication rule of probabilities.

Multiplying the probability of fixation per nt pair by itself n times gives the probability that *every* pair of the n pairs has become neutrally fixed. That is not the relevant number.

> Of course if you can explain how
> hundreds of neutral mutations can be transferred from one family line
> to an unrelated family line, we would be amused by your folklore.

The mutations that become fixed *spread* throughout the population by sex.

>
> John Harshman Sep 8, 4:25 pm
> Newsgroups: talk.origins

> From: John Harshman <jhar...@pacbell.net>

> Date: Thu, 08 Sep 2011 16:25:14 -0700
> Local: Thurs, Sep 8 2011 4:25 pm
> Subject: Re: The Theory of Evolution is Mathematically Irrational
> Round 2
>

> >> On Aug 4, 4:37 pm, John Harshman <jhar...@pacbell.net> wrote:
> >>> Alan Kleinman MD PhD wrote:

> >>>> On Jul 11, 9:19 am, John Harshman <jhar...@pacbell.net> wrote:
> >>>>> hersheyh wrote:

So you keep stupidly and blindly asserting while demonstrating no grasp of what the multiplication rule really does nor how to use it.

[snip]

[Inez]

On Oct 7, 11:08�am, Alan Kleinman MD PhD <klein...@sti.net> wrote:
> On Sep 16, 2:35 pm, Inez <savagemouse...@hotmail.com> wrote:
>
> > <snip rat king of replies>
>
> > So I have a question for you. I'm studying a certain sort of fungus,
> > and have discovered that it has 100 neutral fixations per generation
> > and only 10 selected mutations. How fast did each of these types of
> > mutations spread throughout the population? Can you show me how to
> > calculate that using only those numbers? John Harshman tells me that
> > you need other information, but you seem to be able to just look at
> > the final numbers and tell the speed that the genes spread at, so I
> > turn to you for illumination.
>
> Well mouse queen of mathematical incompetence.

That's not actually a sentence.

> What I can tell you is
> that as Haldane s calculations of more than 50 years ago showed, it
> takes about 300 generations to do the substitution of a more
> beneficial allele than a less beneficial allele.

Really? So if I dump some antibiotics into a tube of bacteria the
resistant strains won't emerge for 300 generations?

> So if an evolutionary
> process requires 10 selected mutations, you can figure that the
> beneficial mutation/amplification of beneficial mutation cycle will
> take about 3000 generations. And that s if you have a subpopulation
> size sufficient to give the necessary trials for the beneficial
> mutation. That s why hersheyh uses population sizes of 10^9 when the
> mutation rate is 10^-8. If the population is small like 10^4 or 10^5,
> you can forget it. The mutation and selection process will die on the
> vine due to the lack of trials for the beneficial mutation. Now for
> your hypothetical claim that you have 100 neutral fixations per
> generation, that s a crocrich of evolutionist mathematical
> irrationality.

So what you're saying is that you can't tell, right? Or if you can
tell, why don't you do the math for us?

[Inez]

On Oct 7, 11:38�am, Alan Kleinman MD PhD <klein...@sti.net> wrote:
> On Sep 21, 10:36 am, Inez <savagemouse...@hotmail.com> wrote:> The splintering effect of your thread only happens in Google Groups
> > when the thread hits 1000 posts. People with real newsreaders are not
> > patient with working around the vagueries of Googles Groups, and it is
> > unlikely that many people will respond to your massive cut-and-paste
> > threads.
>
> That s not my problem. I m here to properly describe the basic science
> and mathematics of the mutation and selection phenomenon and I am
> willing to work within the limitations of the forum.

When are you going to start doing that? Just curious.

> > What you migh try is reading people's posts for comprehension and
> > responding to what they actually say, which might get the thread
> > wrapped up on under 1,000 (or in this case 2,000) posts.
>
> We are already well into our first hundred of the third round and I am
> only now responding to individual posts again. You are dreaming if you
> think this discussion will end in 3000 posts. You evolutionists are
> just very slow learners.
>

Oh, I think it will end as soon as people get bored with your
nonsense, which may be soon.

You don't read counter arguments.

> > > So you want to know if
> > > a neutral mutation could spread through a population by chance? Your
> > > own evolutionist computations show that there is a very small chance
> > > that this will happen equal to the frequency of that allele. And that
> > > model only applies when you only have two neutral alleles for a single
> > > gene. Now what s the probability of two neutral mutations being fixed
> > > by chance? Shouldn t that joint probability of that event be governed
> > > by the multiplication rule of probabilities?
>
> > No. The question isn't what the odds are of two *specific* mutations
> > being fixed is, the question is what the odds are of *any* two (or
> > more) mutations being fixed.
>
> So present your mathematical model which demonstrates your claim.

It's common sense, which apparently you do not have. Deal out two
bridge hands, and calculate the odds of you getting those exact
hands. How was that possible? If your math doesn't describe the real
world, the trouble is with your math.

>You
> are using the model for the fixation of a single neutral allele from a
> gene that has only two neutral alleles. What makes you think that you
> can extrapolate that model to the fixation of any two (or more)
> mutations being fixed simultaneously? Are you one of those
> evolutionists who don t think that the multiplication rule applies to
> the joint probability of two or more events occurring in a random
> process? You must be if you are making the above claim.
>
> > > >> Now I have shown you mathematically why neutral mutations do not
> > > >> spread through populations rapidly if at all.
> > > >No one claims they spread rapidly.
>
> > > They better if you want to do the accounting to explain the 40,000,000
> > > differences between human and chimpanzee genomes in 500,000
> > > generations.
>
> > Why does it have to be 500,000 generations?
>
> This should be clear to you, I m using evolutionist numbers.
>

No you're not.

The math is similar.

[hersheyh]

On Friday, October 7, 2011 2:30:15 PM UTC-4, Alan Kleinman MD PhD wrote:
> On Sep 18, 12:00�pm, hersheyh <hers...@yahoo.com> wrote:

> > On Friday, September 16, 2011 4:34:53 PM UTC-4, Alan Kleinman MD PhD wrote:
> >
> > [snip]
> >
> > Wherein I reduce the Dear Dr.Dr.'s garbage to its crucial elements.
> >
> >
> >
> > > The probability function I derived to compute the probability of two
> > > mutations occurring is applicable to detrimental, neutral or
> > > beneficial mutations.
> >
> > It is appropriate only when and if the Dear Dr. Dr. could actually understand the conditions where it
> > is correct. �And the division by 4 part of his "derivation" of the binomial probability distribution
> > (for that *is* what he derived although he apparently is unaware of that fact) is wrong under any
> > conditions.
>
> As I said in my previous post, evolutionists are slow learners. There
> is more than one possible outcome from a point mutation and unless you
> know what the base was before the mutation occurred, you can only be

> certain that it is one of four possible outcomes.

Unless you know what the base was before the mutation occurs, you have no way to know you *have* a
mutation.

> > > What distinguishes whether the mutation is
> > > detrimental, neutral or beneficial is how the subpopulation with the
> > > particular mutation responds over generations.
> >
> > Agreed. One uses the terms "beneficial" or "detrimental" to describe statistically significant changes
> > in the fraction of the population with a particular genetic state from generation to generation
> > relative to its alternative genetic state under specific environmental conditions. Such changes only
> > occur when the two genetic states produce a *phenotypic difference* that matters wrt relative
> > reproductive success. One uses the term "neutral" to describe the state when either the different
> > genetic states produce no phenotypic difference that the environment can use to discriminate
> > between the genetic states on the metric of relative reproductive success or when the phenotypic
> > difference produced is irrelevant on the metric of relative reproductive success. Empirically, this is
> > identified by the fact that the generation to generation changes in fraction of the population having
> > a particular state varies by no more than the expected amount of variance due to chance alone. The

> > percentage amount of expected chance variance is a function of population size. Typically the 95%

> > confidence level is used to distinguish chance differences generation to generation from
> > statistically significant differences generation to generation.

> The point you are missing hersheyh is that the same probability

> function for two mutations accumulating in a population applies
> whether the mutations are beneficial, neutral or detrimental.

And you don't understand that the *probability* of a mutation in a population does depend on whether that variant is beneficial. When a variation is beneficial relative to the alternative in a particular environment, the *probability* or *frequency* of that 'beneficial' variant will increase above the frequency of mutation from the original state to the variant state because the 'beneficial' variant will have a reproductive advantage over the original state.

> When
> mutations are neutral, you don't have the benefit of amplification to
> improve the probability that the next mutation will occur on a member

> with the previous mutation. This is why when John Harshman argues that

> hundreds of neutral mutations are being fixed in the population

> simultaneously every generation; you are requiring that hundreds of
> neutral mutations are accumulating simultaneously. The multiplication

> rule of probabilities makes John's claim mathematically irrational
> nonsense.
>
> >
> > > If the mutation is
> > > beneficial, the subpopulation will increase in number,

> > More important than number is the change in fractional distribution. Take antibiotic resistance.
> > Upon selection (the addition of the antibiotic), the population size drastically decreases because of
> > the deaths of the sensitive cells. What matters is that the fraction of the population with the genetic
> > state of antibiotic resistance increases from 10^-8 to 1.0. Whether or not one continues with the
> > selective condition, subsequent growth (and growth is all that is required to increase numbers at
> > this point) will not change the fraction of the population that has the 'genetic resistant state'
> > significantly until there is mutation to a different genetic state that has a significant reproductive
> > advantage over the resistant state under the environmental conditions at these post-selection
> > times.

> That�s not correct hersheyh. It is not the frequency of a beneficial

> allele which determines the number of trials for the beneficial
> mutation;

It is *both* the frequency and the number of trials (individuals tested) that is important. The expected mean number of individuals with a particular state (used to calculate the probability of one or more mutants) is the product of the frequency of that state times the number of individuals tested. But you seem to think that the number of trials is something other than the number of individuals tested for the mutant state. I have no idea what you call a 'trial'. If the probability of a given state per trial (individual) is 10^-8 and the number of trials is 10^9, we get a subpopulation having the state = 10 individuals. OTOH, if the probability of a given state per trial is 0.9999999999 and the population is 10^9, we get a subpopulation having the state of 9.99999999 x 10^8.

> it's the number of members in the subpopulation who are able
> to reproduce which determine the number of trials for the next
> beneficial mutation.

How is that different from what I said? Except, of course, that in some cases the subpopulation in question is at a frequency of 1.00 rather than a frequency of 10^-8. Again, what matters is *both* the frequency and number, or, rather, the product of those two numbers (the expected mean number of individuals with a particular genetic state.

> And as the Weinreich experiment demonstrates, you
> can have multiple variants, each with their own subpopulations which
> have to amplify their own particular beneficial mutations.

And how many times do I have to point out that, because the bacteria in these experiments do not undergo recombination, the only mechanism for generating double-mutants involves serial steps.

> > > The mathematical significance of this
> > > relates to the probability of the next beneficial mutation occurring
> > > at the proper locus (position on the genome).
> >
> > The probability of any subsequent or second mutation occurring is a function of the rate of
> > mutation to that state and the number of individuals in a population that have the needed previous
> > genetic state. The number of individuals in a population that have the requisite genetic state is a
> > function of both selection for that state and the number of generations of growth under selective
> > conditions for that state.
>
> You still don't understand how little the mutation rate contributes to
> the behavior of the mutation and selection phenomenon. HIV has a
> mutation rate 3 or 4 orders of magnitude larger than the rate you like
> to use yet this virus still can not evolve efficiently to selection
> pressures which target two genes simultaneously.

That is, when you impose two strongly reproduction-inhibiting selective conditions simultaneously. This means that you are applying conditions where only viruses with the double-mutants can replicate efficiently. Viruses with single resistance mutations have no significant advantage over viruses with none. In fact, viruses with single resistance mutations may even be at a slight disadvantage over viruses with none. This means that your "event" is the "presence of both mutations" and, I certainly agree, that if your event is the presence of both mutations in the viruses before you change the selective conditions, that that event probability is the joint probability of the two independent mutations. The expected mean number of individuals with both mutations would be the product of the probability of the double-mutant times the number of viruses present at the time of selection.

The reason why double-mutant probability is small is *precisely* because, in the non-selective conditions, neither mutant state is "beneficial". Because neither is "beneficial" in the non-selective conditions, the frequency of the mutant state is going to be (unless there has been a long period of directional drift in the case of selective neutrality) essentially the mutation rate. *If* one or both mutants were "beneficial" in the non-selective environment, both mutations would have increased in frequency relative to the non-mutant state and could be as high as a frequency of 1.0.

> The mutation rate
> only determines the frequency at which trials are done for a
> particular mutation.

This is particularly stupid misunderstanding of probability theory. It makes no sense mathematically.

What is your "mutation rate" and how is it determined empirically?

[I say that "mutation rate" or "mutation frequency" (the latter is actually more important, but is typically not much different if the mutation is neutral or deleterious in the non-selective conditions) is empirically measured by counting the number of "mutant" organisms and dividing that by the total number of organisms one has examined for the "mutant" state. This requires that one both know and be able to distinguish the "mutant" state from the "non-mutant state". In most cases, this is done by looking at mutant and non-mutant phenotypes. In our particular case, it is done by counting the number of cells that survive the presence of antibiotic and the total number of cells present initially. This is done by plating serial dilutions on both selective and non-selective plates.]

In probability theory, "trials" refers to the number of times one tests for the presence of the "event". So, in dice flipping, it is the number of times one flips an honest die (whether one is flipping the same die n times or flipping n dice). In coin flipping, it is the number of times one flips an honest coin (whether one is flipping the same coin n times or flipping n coins). In mutation, the number of trials is the number of individuals one tests for the presence of the "mutant state" (and, necessarily, one must also be able to determine the non-mutant state to distinguish between the two).

You seem to be under the delusion that the *number* of trials is actually a ratio, as the mutation rate in fact is. How do you go from determining the "mutation rate" (and how do you calculate it) to determining the number of trials? Your sentence "The mutation rate only determines the frequency at which trials are done for a particular mutation," makes no sense. The *event* we are interested in is the "number of mutants". The mutation rate (actually frequency) is the "number of mutants observed" divided by the "total number of individuals examined". That is how mutation rates are determined.

Your claim, apparently, is that you can determine mutation rates without any knowledge of *anything* about the "mutant" and "non-mutant" states and then use that rate to determine the number (although you say 'frequency' at which trials are done, which makes no sense at all) of trials. Can you explain how you do this in the case of antibiotic resistance?

> When selection pressures target more than a
> single gene,

Simultaneously. Never forget that. Selection which targets more than a single gene in a serial fashion has a different math.

> you need exponentially more trials for the two beneficial

> mutations and larger mutation rates only increase the number of trials

> additively and improve the probability of the events less than
> additively.
>
> >
> > Thus, the precise order of selective events matters. �
>
> And now you should understand why the canned binomial distribution is

> not the correct mathematical formulation for the mutation and

> selection process because in the derivation of that function, the
> order of events was not important and because of that a combinatorial
> term appears in the equation.

As I have shown, your equation is nothing but the "canned binomial distribution" probability distribution used to calcuate the probability of one or more mutants appearing.

>
> > If the genetic state of antibiotic resistance is selectively neutral or detrimental under conditions where there is no antibiotic, then the steady-state fraction of the population having that state is essentially equal to the mutation rate assuming that there has not been sufficient time for a drunkard's walk to, by chance, having increased the frequency. �And in the examples we have been using, where the initial population was grown from a double-sensitive organism, there hasn't been sufficient time for a significant amount of drift. �Thus the *number* of individuals with resistance to the antibiotic is equal to the mutation rate to that genetic state times the population size examined for that genetic state. �At generation one of selection for the genetic state of antibiotic resistance, the *number* of individuals with the resistant genetic state has not changed. �But the *fraction* of the population with the resistant state has changed dramatically und
> >
> > er these conditions, from 10^-8 to 1.0. �After 30 generations of population doubling, almost regardless of whether or not one continues to use the selective conditions of antibiotic present, the *fraction* of the population resistant to the antibiotic remains essentially unchanged (1.0, with only back mutation providing the sensitive genetic state), but the *number* has increased.
>
> Hersheyh, you are conflating your ideas before you even properly
> understand mutation and selection. You first need to understand that
> it is not the fraction of population which determines the number of
> trials for a particular mutation; it is the absolute size of the
> subpopulation. This is why recovery of the subpopulation size must

> occur first before there is a reasonable probability that the next

> beneficial mutation in an evolutionary sequence will occur. Even if
> the fraction of the population with the first beneficial mutation is
> 1, the population size still must be large enough to do sufficient
> trials that the next beneficial mutation will occur at the proper
> locus.

Haven't I just pointed that out? If the fraction of the population having the mutant is 1.0 after selection, it takes about 30 doublings to produce a population of 10^9 individuals, essentially all of whom will have that first mutant. Are you claiming that if I start with 10 individuals with the mutant state that, after 30 doublings, the frequency of that mutant in the population will be 10^-8?

> >
> > I certainly agree that the probability of finding a double-mutant is importantly a function of the number of individuals with the first mutation selected for. �The odds of finding a double-mutant for a second mutation in the cells selected for resistance to the first antibiotic is low if you do that selection in the first few generations after selection. �But it becomes increasingly possible in larger cells precisely because the size of the population with the first genetic resistant state is now large. �It is large precisely because of the earlier selection changing the fraction of cells with the first resistant state and subsequent selective growth of that subfraction.
>
> Why does the �size� of the cell have anything to do with this?

Sorry, that should read "cell population". AKA cell numbers.

> It is
> the size of the subpopulation with the first beneficial mutation which
> drives the probabilities of the second beneficial mutation occurring.

Which is *exactly* what I am saying. And I also use the *correct* multiplication of probabilities when I do so. For the first selection step, where I select for resistance to one antibiotic and don't care whether the genetic state of the other gene is mutant or non-mutant because my selective conditions don't involve selection for or against that gene, I use only the probability of there being a mutant capable of resisting the one antibiotic to calculate the probability of one or more cells resistant to that antibiotic. And I also correctly use a probability of 1.00 (or close to it) for the frequency of that antibiotic in the third step when I select for double-mutants. Would you use 10^-8 for the third step?

> Any of the remaining population that is not on the same fitness
> trajectory only represents competitors for the resources of the
> environment and slows the growth of the subpopulation that is trying
> to amplify its first beneficial mutation. This is why in the Lenski
> experiment it takes hundreds of generations to amplify a beneficial
> mutation, not your estimate of 30 generations of clonal doubling.
> Lenski�s diverse populations are competing for the limiting resource,
> glucose.
>

It took about 200 generations per mutational step. The reason it took longer has to do with the relative fitness of the mutant compared to non-mutants. To take 30 generations, the mutant strain would have to grow twice as fast as the w.t. For a 10% increase in fitness, it takes longer for the frequency of the population having that variant (or any variant with any of the more beneficial traits) to be large enough for there to be a high probability of a second beneficial mutation in one of the cells having any of the other beneficial mutations. I certainly agree that 30 generations is roughly the minimum time to restore a population where the w.t. has all died.

> >
> > [snip]
> >
> > > Evolutionists for decades have used the Poisson distribution function
> > > in an attempt to describe the mutation and selection phenomenon. I
> > > believe this is not the correct probability distribution to use
> > > because the random mutation is not a Poisson random variable.
> >
> > The Poisson is only used as an estimate of the binomial probability distribution when certain conditions apply. �They apply in the cases I used it in. �So your real problem is that you disagree with the use of the binomial probability distribution. �You do so even though, with the exception of the division of 4, the equation you "derived" is nothing but the binomial probability distribution and is based on its assumptions.
>
> And for the conditions of the mutation and selection phenomenon, the
> Poisson distribution is not a good approximation for the binomial
> distribution. I pointed this out to explicitly why the Poisson
> distribution is not correct here.

No you haven't. You have repeatedly asserted that the Poisson distribution is incorrect, but you have never, not even once, given any reason why it is incorrect other than that you divide the mutation rate by 4 so the numbers don't match what you calculate. The problem, of course, is your stupid division by 4. I have it on good authority, one competent in probability theory, that under the conditions used, the Poisson is quite accurate.

> In the mutation and selection
> process, the number of trials is actually quite small (only 10 per
> generation using your numbers) and the probability of the beneficial
> event is much larger than zero.

Gee. And here I was under the delusion that the number 10 was the *expected mean number* of mutants when the mutation rate was 10^-8 and the population size was 10^9. If, under those conditions, the number of *trials* is 10, what is the mutation rate? I say that the mutation rate is the number of mutants observed/total number of individuals examined. That is the number of "events" seen divided by the number of "trials" in my understanding. If 10 is indeed both the *expected mean number of mutants* under these conditions *and* the *number of trials under these conditions*, doesn't that make the mutation rate equal to one? Which you then divide by 4?

> If you use my numbers the probability
> of the beneficial event is 1/4 when the trial occurs.

So the "mutation rate" is not, in your bizarro teminology, the number of mutants seen divided by the total number of individuals examined, but instead is always 1/4? Or is it 10/4? The number of trials divided by the number of different nt's in DNA? And how do you identify a "beneficial event"? And aren't you assuming that only 1 of the 4 nts can ever be a "beneficial event"? How do you identify when a 'trial' has occurred?

> If you want to
> claim that there are only three possible outcomes from a point
> mutation then the probability of the beneficial event is 1/3 from a
> single trial.

How do you identify that a trial has occurred without any knowledge of the starting genetic state or the end genetic state? Pull a number out of your *ss? I know how I calculate, empirically, the mutation frequency. How do you do it?

> Either way, the probability is much larger than zero and
> the Poisson distribution is not the correct approximation for either
> the binomial distribution or the correct probability function which

> describes the mutation and selection phenomenon in this case.

Oh, dear Dr. Dr. Genius, brilliant omnipotent mathematician, on bended knee, I pray thee to explain exactly what you think m/4 means in your equation. Specifically, how do you calculate and/or empirically determine m?

> And you
> should recall that I never said that the binomial distribution was a
> bad approximation for the mutation and selection phenomenon, I said
> the Poisson distribution was a bad approximation for the process and I
> have provided the mathematical justification for this reasoning.

No, you haven't. You have repeatedly asserted both that your equation was not a binomial distribution calculation, yet by simply replacing m/4 by p, we can easily observe that it is identical to a binomial distribution calculation (specifically calculating the probability of finding one or more mutants in a given population assuming certain conditions - in your case, assuming that you use simultaneous selection against two mutant traits that would only be present in the population at roughly the mutation frequency from w.t.). Now you are claiming that n or n*g (whichever calculates the total number of organisms tested) is NOT the number of trials that we examine for the presence or absence of the mutant state. Instead the number of trials is the mean expected number of mutants given an arbitrary mutation rate and a population size of n. Yet you never show how you can get the value of mutation rate = m/4 = 10^8/4 from that number of trials.

> But
> there are also two significant differences between the binomial
> probability function and the correct probability function for mutation
> and selection. The first is there are four possible outcomes from a
> point mutation, not two.

So? First, there are not four possible outcomes from a point mutation if you know you have had a point mutation. The only way to know you have a point mutation is to know the initial nt at that site. And that means that you cannot identify a G (assuming that is the initial nt) to G as a point mutation because there has been no *change*. For something to be a mutation, there must be a *change* in genetic state that is identified somehow. No detectable change, no mutation. Period. Second, you are assuming that only one other nt of the three produces a *mutant* state. And also assume that the other three nts are all equally likely to occur by point mutation. But the main problem is that you have *already* stated that the mutation rate is m, since m is the probability that a mutation or change, has occurred at this nt. That makes m/4 just the mutation rate divided by 4.

> The second is the binomial distribution was
> derived without consideration of the order of events. The order of
> events is crucial in the mutation and selection process as you have
> now finally acknowledged above.
>

I have repeatedly pointed out that the order of events (history) is crucial in determining the probability of a double mutant and how quickly one can obtain same. That is exactly why I point out the difference in probability of the three-step sequential process producing a double-mutant compared to your single-step simultaneous selection process. History can change the frequency of different alleles in a population. You just rant on about joint probability without even asking questions about the difference in allele frequency that can occur when selection is working. You talk as if the frequency or probability of a variant in a population is *always* equal to the mutation frequency.

> >
> > > In
> > > addition, the Poisson distribution does not properly relate population
> > > size, number of generations and mutation rate for computing the number
> > > of trials for a particular mutation.

Of course the Poisson properly discusses the total number of trials as well as the number of events/trial. It calculates probability differently than the binomial probability distribution, but, given that the number of trials is the total number of individuals examined, it certainly takes both mean population size examined per generation and number of generations into account. As pointed out, the term lambda in the Poisson exponent is the same as p*(n*g), where p is the event rate per trial and n*g is the total number of trials.

This is no different than using the two different equations for exponential growth. y = a*b^x = a*e^bx.

> > > I have derived what I believe is
> > > the correct probability function for computing the probability of two

> > > mutations A and B to occur. I�ll repeat the derivation here for you.

> >
> > > Probability of two beneficial mutations occurring (not simultaneously)
> > > at two loci as a function of population size and number of
> > > generations.
> >
> > > The following are the definition of the variables used.
> > > n -- is the total population size
> > > nA -- is the fraction of the total population size with mutation A

> > > nGA � is the number of generations for beneficial mutation A to occur
> > > nGB � is the number of generations for beneficial mutation B to occur

> > > mA -- the probability that in one organism in one generation, a
> > > mutation A will affect a specific locus in the genome
> >
> > Ordinarily this would be considered the "mutation rate." �But the Dr. Dr. does not
> > ...
> >

> > read more �- Hide quoted text -

[hersheyh]

On Friday, October 7, 2011 3:00:51 PM UTC-4, Alan Kleinman MD PhD wrote:

> On Sep 23, 12:19�pm, hersheyh <hers...@yahoo.com> wrote:
> > On Tuesday, September 20, 2011 2:42:19 PM UTC-4, Alan Kleinman MD PhD wrote:
> >
> >
> >
> >
> >
> > > The following replies are from a splinter threads

> > > Virgil � Sep 14, 1:35 pm

> > > Newsgroups: talk.origins
> > > From: Virgil <vir...@ligriv.com>
> > > Date: Wed, 14 Sep 2011 14:35:43 -0600
> > > Local: Wed, Sep 14 2011 1:35 pm
> > > Subject: Re: The Theory of Evolution is Mathematically Irrational
> > > Round 2
> > > In article

> > > <7f7ca969-1...@x11g2000prb.googlegroups.com>,

> > > �Alan Kleinman MD PhD <kle...@sti.net> wrote:
> > > >> On Aug 10, 7:42 pm, Mark Isaak <eci...@curioustaxonomyNOSPAM.net>
> > > >> wrote:
> > > >> > On 8/10/11 2:21 PM, Alan Kleinman MD PhD wrote:
> > > >> > > On Jul 14, 8:58 am, Mark Isaak<eci...@earthlink.net> wrote:
> > > >> > >> On Tue, 12 Jul 2011 18:18:51 -0700, Alan Kleinman MD PhD wrote:
> > > >> > >>> On Jun 7, 2:45 pm, Mark Isaak<eci...@earthlink.net> wrote:
> > > >> > >>>> On Mon, 06 Jun 2011 17:47:21 -0700, Alan Kleinman MD PhD wrote:
> >
> > [snip]
> >
> > > What makes you think that I am not
> > > dedicated to figuring out how mutation and selection works?
> >
> > Everything you have posted on the subject and your complete refusal to do any research into the

> > math, try to actually discuss your bogus assumptions, or even try to listen. �You come across as
> > both profoundly arrogant and ignorant. �And I don't think that is just my opinion.
>
> Hersheyh, you are the one who doesn�t do research into the equations

> you use. You have used the Poisson equation incorrectly for the
> mutation and selection phenomenon without ever studying the derivation
> of the equation and knowing the limitations of the use of the
> equation.

In fact, I have repeatedly pointed you to math sites, and directly quoted from it, the conditions under which the Poisson distribution is a good estimator of the binomial probability distribution, which is the equation you "derived". But, then, you seem to think the number of trials in your equation is the same as the number of mutants expected rather than the number of individuals examined for the mutant state. But, then, you also think you can calculate the mutation frequency without being able to identify a mutant or distinguish it from a non-mutant. You seem not to understand that the word mutant means changed.

> Evolutionists always think that anyone who claims they are
> wrong are arrogant and ignorant but it is not my teaching which has
> led to the occurrence of multidrug resistant microbes, multiherbicide
> resistant weeds, multipesticide resistant insects and less than
> durable cancer treatments.

Nor is it mine. But your equation is still just so much GIGO bullshit.

> > > The correct probability
> > > function for random recombination does not require that you consider
> > > selection. The affects of selection on random recombination only
> > > affects the probabilities implicitly by altering the number of members
> > > with each of the particular alleles.
> >
> > The probability of *recombination*, in random sexually reproducing eucaryotes (organisms that go
> > through a meiotic cycle), is determined by the *frequencies* of the alleles in the parent generation
> > and is described by the logic of the Punnet Square, which makes it about as old as modern

> > genetics. �Note that I said frequencies in the parent generation and not the *frequency of mutation*
> > from w.t. to mutant allele. �The *frequency* of alleles in any particular generation is a function of

> > its history, specifically the selective pressures that have historically acted upon different

> > phenotypes produced by the genotypes and/or the chance history of neutral drift. �Again, it is the

> > *relative frequency* of different alleles in a randomly sexually reproducing population that
> > determines the probability of recombination, NOT the absolute number of members NOR the
> > mutation probability.
>
> The Punnett square is only useful for predicting the results of a
> breeding experiment.

The Hardy-Weinberg equation says otherwise. The H-W involves the consequencess of random sexual reproduction from generation to generation.

> It is not useful for predicting the results of
> random recombination. To do that prediction, you have to apply the
> principles of probability theory correctly and you have already shown

> that you can�t do that.

Which is exactly what H-W does.

> You do have some idea of what the variables
> are including the frequencies of the alleles. Since no evolutionist
> has derived the correct probability function that would describe

> random recombination here, I�ll do the derivation for you in a week or

> two. Then you can say how amateurish the derivation is and whine about

> some feature of the calculation before you finally admit it�s correct.
>
At best, you will come up with the H-W. At worst you will probably assume that bacteria and viruses engage in sexual reproduction every generation.

> >
> > In procaryotes and viruses, recombination is a rarer event, as these organisms generally reproduce
> > clonally, and one has to define what mechanism of genetic exchange one is talking about:
> > exchange resulting from double infection of different viruses, transmission via plasmids and other
> > extra-chromosomal agents, transformation, or by viral transduction.
>
> Do you think it is the rarity of recombination for HIV that prevents
> the lateral transmission of beneficial alleles?

Yes.

> Why don�t you present

> the mathematics to substantiate your claim?

Because I would need to know values for some variables that cannot be simply arbitrarily assumed. Like the frequency of double infection of a cell in natural HIV infections (rather than in cell cultures).

> > > >> What happens to the probabilities of the random
> > > >> recombination of A and B if only one of the two all alleles amplify?
> >

> > So, are A and B different alleles of the same gene or are they different genes? �Do you know the
> > difference? �And why it makes a difference?

>
> Let A be a resistance allele to a protease inhibitor and B be a

> resistance allele to a reverse transcriptase inhibitor. Isn�t that

> which is required to accelerate the evolutionary process by
> recombination?

So, you *are* talking about variant alleles of different, unlinked genes, then. Right?
Yes. But, again, the frequency of recombination in HIV in natural infections is not nearly as easy to determine as the frequency of recombination in humans and other sexually reproducing organisms.

> > > >Not relevant.
> > > John, you shouldn�t be making this argument until you derive the
> > > probability function for random recombination. I�m not going to give
> > > the derivation of that probability function now but consider this.
> > > What if in your population every member has allele A except the member
> > > which has allele B, that is A has a frequency close to 1 in the
> > > population? That member with allele B that is B has a frequency very
> > > close to 0. What is the chance that a member with allele A will meet
> > > and recombine with the member with allele B?
> >
> > This again shows your confusion about the difference between the term 'allele' and the term 'gene'

> > or your confusion between the 'probability of mutation' and the 'probability of recombination'. �You
> > treat A and B here as if they were alternate alleles of the same gene. �And given your confusion
> > between a 'gene locus' and a 'nt site', you are probably treating the two, �A and B, as different nts at
> > the same nt site. �If that is what you mean, then recombination will not produce anything but the

> > same two alleles (unless the two alleles contain *different* mutations at *different* nt sites from
> > each other rather, in which case a rare recombination between those two independent mutations
> > will produce a double-mutant and a non-mutant).
>

> What makes you think I�m confused about what a gene and an allele are?

Because of your awkward and unclear use of the terms.

> You are the one who has been using the wrong probability distribution
> for years without ever going through the derivation of the equation
> and determining when the equation is valid to use. Why should I
> believe that you understand what a gene and an allele is?

Because I am also right about the use of the Poisson. And the binomial probability distribution. And the Luria-Delbruck distribution. And you have been wrong about each and every one of them. In fact, you have been wrong even about the meaning of terms like "trial" and "event", wrong about the meaning of p^n as opposed to p*n, wrong about what the word "mutation" means, wrong about what "beneficial" means. I think that almost covers everything you have been wrong about.

> > Ordinarily, recombination refers to recombination between *gene loci*, not recombination within a
> > gene, and recombination between alleles that differ by having different nt's at a single nt site is
> > impossible because a nt site is the limit for recombination.
>
> The mathematics I will present will give the probability function for
> recombination between gene loci.

Unlinked gene loci? For sexually reproducing organisms or for bacteria or for the various kinds of viruses? There is no "the" probability function for recombination between gene loci.

> > So tell us what you mean when you talk about *recombination*. �Are you concerned with eucaryotic
> > recombination, which occurs each and every generation? �Or are you concerned with some type of
> > gene exchange that goes on in procaryotes or viruses? �When you use the term 'allele' in your

> > discussion above, are you talking about different forms of a specific gene locus (the actual
> > definition) or are you talking about differences in nt's at a single nt site or are you talking about

> > two *different* unlinked genetic loci, each of which has alternate alleles? �Or do you not understand

> > what I am talking about?
>
> The equation I will derive for you will include multiple

> recombinatorial events, not just a single recombination event. I�ll

> give you the equation which shows how many recombinatorial trials must
> occur before you get a reasonable probability that alleles A and B
> will recombine on a single member.
>
> >
> > [snip stupidity about the Poisson, which is irrelevant]
>

> You�re the one who so stupidly uses the Poisson distribution. Do you

> want me to give you the name of the lower division mathematics text I
> used when I was a freshman in college that gives the derivation of the
> Poisson equation?

Giving me the name of a text doesn't mean you know how and when to use it.

> > > >It's really quite simple. Given various simple assumptions, such as
> > > >independent assortment, panmixis, a constant population, and frequencies
> > > >p and q for the two alleles, the expected frequency of AB individuals is
> > > >just pq. As p and q increase, pq increases. We have already specified
> > > >that p and q are increasing. If AB phenotypes are favored over A, B, and
> > > >"wild type" phenotypes, p and q will increase faster than they would in
> > > >the absence of that advantage.
> >
> > John is possibly falsely thinking that you were talking about eucaryotic recombination involving
> > organisms with a meiotic cycle and also are thinking of A and B as alternate alleles of the same

> > gene. �I think you are probably thinking of A and B as different *genes* rather than alleles of the
> > same gene. �But it is hard to tell what you mean since you have *repeatedly* refused to clarify what
> > you mean. �Probably because you don't understand the criticisms, in this case don't know the

> > difference between "allele" and "gene locus" and "nt site".
>
> If I confused John on this point, I apologize. It should not be that
> confusing. You evolutionists are claiming that recombination will
> somehow accelerate the mutation and selection process by combining a
> beneficial mutation in an allele of one gene with a beneficial
> mutation in another allele of a different gene giving our double

> mutant. I�m going to derive for you the mathematics which describes

> this process and show you why you are wrong with your claim.

The above shows how awkward your use of "allele" and "gene" is. Geneticists would claim that recombination can produce new combination of alleles in sexually reproducing individuals that would otherwise only occur by sequential mutation. They would never describe a mutation as "beneficial" unless they specified the environment in which it is beneficial.

Specifically, they would say that if the frequency of two alleles, A and A', of gene coding for function M, and the frequency of two alleles, B and B', of an unlinked gene coding for function N are present in the population in frequencies p, for A, q, for A' (p + q = 1), r for B and s for B' (r + s = 1) and the population mates at random, the frequencies of different gametes produced will be pr A;B, ps A;B', qr A';B, and qs A';B'. Multiplying these through a Punnet square will give you the population frequencies of the various genotypes expected. Multiplying those frequencies by the population size will give you the mean expected number of each genotype.

> > > John, the only thing that the Hardy-Weinberg law gives you is that the
> > > frequency of alleles remains constant when the population is in
> > > equilibrium (selection is not acting).

Actually the assumption also is that neutral drift is not acting or is not significant in the time-frame used.

It also tells you the expected frequencies of each genotype produced. Of course, if you are talking about alleles of a single gene, you cannot get recombination. You can only get homozygosity and heterozygosity.

> > And the H-W equilibrium only really exists when the population is of infinite size.
>
> The equation I will derive for you is based on a finite population and
> applies to equilibrium and non-equilibrium conditions.
>
> >
> > But if you consider A and B to be two different unlinked *genes*, each with certain *frequency* of
> > alternate alleles in the population, say p for A and q for A's alternate allele, a, and r for B and s for
> > b, then you can use the expansion to determine the frequencies of any kind of diploid offspring

> > assuming randomness. �The frequency, in the population, of gametes with the *haploid genotype*
> > A;B would be pr. �The frequency of A;b would be ps. �Of a;B would be qr. �[As an exercise to show

> > that the frequencies of the gametes add up to 1, which is the whole population of possibilities:

> > pr+ps+qr+qs = p(r+s)+q(r+s) = (p+q)(r+s) = (1)(1) = 1] �And of a;b would be qs. �

>
> This is not how to do the computation in general because a population
> can have A, B and C alleles where the C alleles are not A and not B
> alleles.

A gene (I assume you are now talking about different alleles of a single gene, although it is hard to tell because of your limited knowledge of genetic terminology) can have three alternate alleles, as does the ABO blood type gene. In that case, you have a gene with three frequencies that add up to 1. If the frequency of the A allele is p, the frequency of the B allele of that gene is q, and the frequency of the C allele of that same gene is r, then the Punnet Square would show frequencies of p^2 AA, Q^2 BB, R^2 CC, 2pq AB, 2pr AC, and 2qr BC.

OTOH, if you are talking about alternate alleles in different unlinked genes (A and A'; B and B'; C and C'), the argument would be an expansion of that given for two unlinked genes above. Choose one, whichever one you actually meant.

> What you need to accelerate the mutation and selection
> process is for one parent with the A allele and another parent with
> the B allele to recombine those two alleles into a descendent with
> both A and B alleles to give the more fit replicator, not A and C or B
> and C.

You seem to be assuming that the organism is haploid. Although there are sexually reproducing organisms that spend most of their lives in the haploid state and only undergo meiosis during a sexual stage, that is not the anthropocentric model of sex.

>
> > Using a Punnet Square and crossing the gametes to each other along with the appropriate
> > frequency of the gametes in the population will generate the frequencies of different genotypes in
> > the progeny population.
> >
> > But that is assuming that A and B are two different unlinked genes in a eucaryotic population.
>
> The equation I will derive for you will degenerate to the mathematics
> of the Punnett Square if you eliminate C alleles and have only two
> members with A alleles and two members with B alleles or if you are
> talking about diploid, a single member with some combination of A and
> B and another member with some combination of A and B. You can set up
> that circumstance in reality with a breeding experiment but now we are
> talking about random recombination such as would be seen with HIV
> where you have more than two possible alleles.

As I showed above, the cases you mention are merely an extension of the Punnet Square. I am quite certain that the Punnet Square can be put into an equation form. But I am most certainly NOT talking about recombination as would be seen in HIV, since I have no idea how frequent or infrequent recombination is in natural human infections. Perhaps you do?

> > > If you want to estimate the
> > > probability of two alleles randomly recombining, you need to write the
> > > probability function for that stochastic process. Once you do that,
> > > you can consider how selection will change the probabilities over
> > > generations as the frequencies and population sizes of the alleles
> > > change.
> >
> > Selection increases the relative frequency of the allele of a gene which has the selectively

> > advantageous phenotype. �It will do so each generation relative to the alternative allele. � That is the
> > very definition of selection. �So the relevant question is "What is the *frequency* of the alleles in
> > reproducing individuals is there at the generation I am looking at?" �Not, for recombination in

> > sexually reproducing eucaryotes, "How many, numbers, of allele a are present in reproducing
> > members of the population?"
>
> Of course selection changes the frequency of alleles or more correctly
> causes the amplification of the beneficial allele,

"Change in frequency" is more correct than "amplification". Amplification assumes that the population size increases beyond some point. That is not necessarily true. The rate of replication of the mutant can be lower in the selective conditions than the rate of replication of the non-mutant in non-selective conditions, such that maximum population size is lower. Again, there is a "change in frequency" and change in population size are not the same thing.

> so how does this
> affect the random recombination process? You have to derive the
> probability function which describes this stochastic process to
> understand this.

I await with bated breath your "stochastic process", oh genius one.

> > Of course, you could be talking about recombination in procaryotes or viruses, which are mostly

> > growing in a clonal fashion. �Until you choose to actually respond intelligently, it is hard to parse

> > out what you are talking about here.

> You are going to have a hard time understanding me until you
> understand the mathematics and you are ever so slowly understanding
> the mathematics.
>

I understand the GIGO that arises when someone who thinks he is a mathematical genius tries his/her hand at deriving equations. You get things like his "deriving" the idea that the number of "trials" is the same as the "mean expected number of events". That the "mutation rate" is not actually the "mutation rate", but 4 times the "mutation rate".

[hersheyh]

On Thursday, October 6, 2011 7:49:35 PM UTC-4, Alan Kleinman MD PhD wrote:
> The following are the remainder of responses to posts 976-1001 and
> splinter threads.
> Mark Isaak Sep 10, 5:12 pm
> Newsgroups: talk.origins
> From: Mark Isaak <eci...@curioustaxonomyNOSPAM.net>
> Date: Sat, 10 Sep 2011 17:12:16 -0700
> Local: Sat, Sep 10 2011 5:12 pm
> Subject: Re: The Theory of Evolution is Mathematically Irrational
> Round 2
>
> >On 9/9/11 5:34 PM, Charles Brenner wrote:
> >> On Sep 9, 1:36 pm, Mark Isaak<eci...@curioustaxonomyNOSPAM.net>
> >> wrote:
> >>> On 9/9/11 7:59 AM, Alan Kleinman MD PhD wrote:

> >>>> On Aug 10, 1:45 pm, Inez<savagem...@hotmail.com> wrote:

> >>>>> On Aug 4, 4:05 pm, Alan Kleinman MD PhD<klei...@sti.net> wrote:
> >>>>> <snippers>
> >>>>>> What I would like to hear from either of you evolutionists is a
> >>>>>> reasonable explanation how neutral mutations can spread through a
> >>>>>> population faster than beneficial mutations which have selection
> >>>>>> assisting in the spread of these beneficial mutations.
> >>>>> You are tediously thick headed. No one made that claim.
> >>>> You had better tell that to John Harshman because he has claimed that
> >>>> a couple hundred neutral mutations are fixed every generation,
> >>>> generation after generation for hundreds of thousands of generations.
> >>>> Would you care to compute the joint probability of all those neutral
> >>>> mutations being fixed?
> >>> The chance of any one new neutral mutation being fixed is 1/2N. The
> >>> number of new neutral mutations per person is about 50. The number of
> >>> people is N. You can do the math from there. Don't forget to multiply.

> >> This simplistic argument is driving me nuts.
> >> What have you in mind for N?

Yet the only thing you apparently would change is that you somehow think that if the probability of mutation and fixation per nucleotide is u, then you think the probability of 30 fixations must be calculated as u^30 or something. That would be the probability of 30 arbitrarily picked, but very specific, nts out of 3 X 10^9 all being mutated and fixed this generation. That, however, is not the question asked. The question asked is "How many of the 3X10^9 nts in the genome will have undergone mutation and final fixation this generation?" In that question, we are not looking at 30 specific nts and asking for the probability that those 30 had become mutated and fixed this generation. We are asking a different question. It is the difference between flipping 600 dice, knowing that the probability of a 6-face is 1/6 and asking whether flips 1 through 100 [or any 100 dice chosen at random before flipping them] all had a 6-face. The probability of that would be (1/6)^100. Or, instead, asking the question, h

ow many dice, out of 600 flipped and regardless of which ones, should show a 6-face (probability of that would be (1/6)*600 = 100.

> >Doesn't matter. Notice that the Ns cancel. The result is the same
> >whether the population is in the hundreds, as may have been the case
> >shortly after the human-chimp split, or in the billions, as today. The
> >equation does *not* handle quickly growing or shrinking populations, but
> >those are probably relatively few generations out of millions.
>
> I see, so our social engineer thinks that mutation and selection works
> efficiently with populations of hundreds.

There is no selection in selective neutrality. By definition. [Also, there is no crying in baseball.] Mutation occurs less frequently when the population is small, but drift is significantly faster when populations are small (chance % swings are larger). The reverse holds when populations are large. That is why the Ns cancels out.

> Mark, I like hearing a good
> evolutionist fairytale, tell us how humans got a different number of
> chromosomes from chimpanzees and tell us how both a male and female
> both got the same chromosome number when the change occurred and the
> lucky bride and groom met each other?

Organisms with different chromosome arrangements, including Robertsonian events that change chromosome number, can mate with each other to produce heterozygous, but balanced, progeny. In fact this is the case in about 0.2% of live births. Even individuals with ring chromosomes (but balanced) are not uncommon. Unbalanced rearrangements with chromosome 21 is a cause of hereditary Down's syndrome. The fertility of these heterozygous progeny (including balanced translocations and inversions) is not necessarily much worse than the w.t. (although multiple rearrangements are) and the new arrangement can spread in a local population. If the local population has a benefit over the larger population, in fact, this can drive the accumulation of multiple rearrangements to prevent gene exchange between the two populations. Aka, speciation.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1684876/pdf/ajhg00361-0046.pdf

>
> >> If you are thinking billions, then you
> >> are thinking modern humans and Dr. Dr.'s confused picture of mutations
> >> propagating among living people like a plague is what you have.
> >Neutral mutations, by definition, cannot be plague-like, unless you are
> >counting invisible, inconsequential plagues.
>
> So Mark, tell us how these neutral mutations in one family line find
> there way into unrelated family lines?

By the same mechanism by which DNA from your mate's family finds its way into your children and their mate's DNA finds its way into your grandchildren. It's called sexual reproduction. Unless your children and grandchildren are clones, of course. Are they?

>
> >> So what should our model be?
> >> What does the bottleneck at which human and monkey separated look
> >> like?
> >> Note that fixation isn't really the issue - fortunately as absolute
> >> fixation of neutral single nucleotide mutations rarely happens. 10^8
> >> human births per year times 10^-8 mutation rate means that just when
> >> you think the last surviving rare type is about to die, a backmutation
> >> in a newborn somewhere extends the the persistence of the type.
> >> So what is the data that the supposed 35 million SNP differences
> >> between man an monkey comes from, and what does it really mean? I
> >> don't know. Even if it's a matter of comparing sequences (rather than
> >> e.g. extrapolating based on assumptions about population histories) I
> >> think it's more statistical that just counting -- humans too have many
> >> neutral differences from one another. Lots of definitional
> >> complications.
> >I'm not sure, but I'm pretty sure the number of differences does come
> >from comparing the sequences and counting. After all, both genomes have
> >been sequenced, and the comparing and counting is pretty easy to do by
> >computer.
> >As to what they all mean, that is why there are still geneticists working.
>
> Mark, you actually hit the nail on the head here. One of the main
> reasons evolutionists are fighting so hard here is job security. How
> many people would want to hear hersheyh’s babble once they understand
> he knows nothing about how mutation and selection actually works?

Arrogance and ignorance from someone who most certainly cannot even define "mutation" much less tell us how to distinguish between a "mutation" and a "non-mutation".

>
> John Harshman Sep 14, 2:24 pm
> Newsgroups: talk.origins

> From: John Harshman <jhar...@pacbell.net>

> Date: Wed, 14 Sep 2011 14:24:24 -0700
> Local: Wed, Sep 14 2011 2:24 pm
> Subject: Re: Trying to salvage something from this Re: The Theory of
> Evolution
>
> >Alan Kleinman MD PhD wrote:

> >> On Aug 11, 7:16 am, John Harshman <jhar...@pacbell.net> wrote:
> >>> Alan Kleinman MD PhD wrote:

> >>>> On Jul 13, 1:56 pm, John Harshman <jhar...@pacbell.net> wrote:

The human *absence* of 47 and 48 is because, in humans, the two chromosomes present in chimpanzees underwent a Robertsonian fusion. That is evident from the order of genes on the chromosomes.

> You are not doing a base by base comparison of
> the two genomes. Evolutionists look for stretches in the two genomes
> that have some similarity and line these stretches up.

That used to be the case. It isn't anymore. But keep in mind that there is no such thing as "the" human or "the" chimp genome. Genomes are much more fluid in structure than that, as evidenced by the length polymorphisms that are used in DNA fingerprinting. That is especially the case when it comes to retroviral and LINE and SINE elements expanding or contracting in number.

See below for the entire human and chimp genome data.

http://www.nature.com/nature/journal/v437/n7055/full/nature04072.html

See this for chromosome 21 specifically:

http://www.sciencemag.org/content/295/5552/131.full
http://www.pnas.org/content/100/14/8331.full

> Your 98.7%
> similarity is a load of evolutionist crap. Why don’t you line up
> chromosome 21 and tell us how similar these chromosomes are?

In coding sequences, the references say
"The BESs mapped with high confidence (13) were used to calculate the difference between the chimpanzee and human genomes at the nucleotide level. The number of sites in valid alignments (nucleotide sites that have PHRED quality values q ≧ 30) was 19,813,086. Out of this number, 19,568,394 sites were identical to their human counterparts for a mean percent identity of 98.77."

http://etd.lsu.edu/docs/available/etd-08302006-100849/unrestricted/Han_dis.pdf

> >> This data is presented for those areas which can be matched and the
> >> match is not close at all.
> >It isn't? 98.7% identity isn't close? What would constitute close, then?
>
> You evolutionists are cherry picking data out of the two chromosomes.
> Your claim is an evolutionist fabrication and is a totally
> untrustworthy estimate. Have you gotten your subscription to “Science”
> yet? Read the full article
> http://www.sciencemag.org/content/295/5552/131.abstract&usg=AFQjCNF6LJDM3GHffyRjXPABtkVjwnfm9w
> and tell us how similar chromosome 21 is for humans and chimpanzees.

See the quote from the same article you cited, just above. As for differences, they say:

"We identified 18 STSs that amplified products from human DNA but not from that of chimpanzee (shown as circles inFig. 2). Because we used genomic DNA isolated from three chimpanzee individuals, two males and one female, the effects of relatively larger polymorphisms among the chimpanzee genomes should be minimized. These 18 primer sets, together with the flanking STSs, were further tested with other primates including gorilla. Out of these, amplification products appeared exclusively in humans from seven primer pairs (filled green circles in Fig. 2 whose positions in human chr21 are about 7.2, 8.5, 10.0, 11.6, 11.8, 18.1, and 29.3 Mb from the centromeric end, respectively) (16,17), suggesting that these loci might correspond to insertions that are specific to the human lineage. Nonhuman primate specific deletions cannot be ruled out but seem less likely because this deletion would have had to occur in all primates but humans. The remaining 11 primer pairs fail to amplify any products from chimpanzee DNAs bu

t showed positive signals in some of the other primates, suggesting the existence of deletions or mutation sites at those positions in the chimpanzee genome."

What that means is that they found seven sites on chromosome 21 that were human specific, probably because of insertions (likely of retroviruses or retrotransposon-like element migration after divergence), inversions, deletions or other small chromosome rearrangements (in both genic regions, within 10kb of a coding sequence and its introns, and non-genic ones -- although only rarely in coding sequences).

http://genome.cshlp.org/content/13/3/341.full.pdf+html

>
> In this URL, they studied chromosome 21. They report “We detected
> candidate positions, including two clusters on human chromosome 21
> that suggest large, nonrandom regions of difference between the two
> genomes.” Nonrandom means these are selective differences.

You need to read the whole article rather than just the abstract. They attribute the large differences to chromosome rearrangements. And that has been amply demonstrated by the above 2011 paper. They point out that
"To date, it has commonly been thought that single-basepair changes between the human and chimpanzee genomes would underlie the majority of these postulated regulatory differences. However,
the data we present in this study demonstrate that genomic rearrangements are a significant source of DNA variation between humans and chimpanzees, as well as other nonhuman primates. These rear- rangements provide excellent start- ing points for focused studies of gene expression differences in humans and chimpanzees as part of an effort to identify the genetic differences responsible for the biological, physiological, and behavior differences between these species."

It is hardly surprising that there are mutations other than point mutations that can accumulate either by chance alone (neutral drift) or by selection.

> Perhaps you
> want to claim these differences are due to a retrotransposon, from
> where?

From retroviruses and defective retroviruses in the germ line. Including many with multiple copies and that can and have switched or added new or lost old positions within a lineage.

>
> >> Evolutionists claim that humans and
> >> chimpanzees come from a common progenitor. Now you are claiming that
> >> many of these differences are neutral which is typical evolutionist
> >> speculation.

> >Simple observation of how proteins work.
>
> More like simple minded evolutionist speculation. Why don’t you
> explain to us why humans and chimpanzees produce identical insulin
> molecules but do not produce identical preproinsulin molecules?

Easy. There has been neutral drift replacing an Ala with a Ser in the chimp lineage at position 23 and a Val for an Ala at position 13. Both are conservative amino acid change and probably functionally neutral changes. Given that human and gorilla preproinsulin are identical, the changes likely occurred in the chimp lineage rather than in the human lineage. 2 conservative and probably functionally neutral amino acid differences in a part of the 110 amino acid protein that gets clipped off and is not strongly conserved is hardly outside the expected mean number of changes per 100 aa's. Here is a figure showing a number of preproinsulins from organisms as distant as the zebrafish.

http://www.springerimages.com/Images/MedicineAndPublicHealth/1-10.1007_s11154-010-9151-3-3

>
> > Tell us which are neutral differences and which are
> > selective differences.

> Well, it seldom matters whether a protein has leucine, isoleucine, or
> phenylalanine in a particular spot.

And alanine, leucine, and serine are also conservative changes.

>
> You are not answering. The authors of the study of chromosome 21 said
> there are long non-random stretches of bases. You have claimed that
> you don’t need selection to get non-random sequences. Tell us how you
> distinguish neutral differences from selective differences in a
> genome.

The most common method is their rate of change.

>
> > And then compute the joint probability of two
> > neutral mutations being fixed in a population.

> Are you still on about that? Your joint probability is irrelevant. We
> don't care about the joint probability of some particular set of
> mutations being fixed, only about the probability that any set of
> mutations will be fixed. Different, no?
>
> John, we all know that you don’t know how to analyze a stochastic
> process and both mutation and selection and mutation without selection
> are stochastic processes.

Selection is the opposite of a stochastic process. It is directional. Mutation without selection (that is, with drift) is a completely stochastic process. Mutation is a stochastic process. Selection is not.

> The joint probability of events occurring in
> a stochastic process has been and always will be governed by the
> multiplication rule of probabilities. The accumulation of mutations
> must always occur by common descent unless you have some lateral form
> of transfer of mutations. The probability of these mutations
> accumulating will always be governed by the multiplication rule of
> probabilities.

No. The probability of a mutation or two mutations "accumulating" (i..e., increasing in frequency beyond the mutation frequency) is governed by its (or their combined) relative selective advantage. Selection is not a random process. It is directional.

>
> >>>>>> How many with other known functions? How much "junk"?
> >>>>> Almost all is junk, just as almost all the genome is junk. Non-coding,
> >>>>> functional regions are just another few percent of the genome.
> >>>> This is the type of stupidity that evolutionist perpetuate. If they
> >>>> don’t know what a portion of the genome does, it is junk.
> >>> No, that's not how it works. We recognize junk by the fact that it
> >>> evolves at the rate of mutation.

> >> Take a look at this URL: http://www.google.com/url?sa=D&q=http://www.sciencemag.org/content/295/5552/131.abstract&usg=AFQjCNF6LJDM3GHffyRjXPABtkVjwnfm9w
> >> In this URL, they studied chromosome 21. They report “We detected
> >> candidate positions, including two clusters on human chromosome 21
> >> that suggest large, nonrandom regions of difference between the two
> >> genomes.” Nonrandom means these are selective differences

> >No it doesn't.

It means there have been significant, non-point changes in sequence. As they said in the actual article. You probably only read the creationist site's explanation or the abstract (which is probably all the creationist that wrote this read.:
http://www.godandscience.org/evolution/sld072.html

> This is the second time you have made this claim. So tell us how you
> distinguish selective genetic differences from non-selective. You go
> around claiming that most of the differences between human and
> chimpanzee genomes are neutral. Tell us how you have come to this
> conclusion. Or don’t you think that explaining how you come to your
> conclusions is relevant? You have claimed that 98.7% of the human and
> chimpanzee genomes are identical yet these authors studied chromosome
> 21 and found large non-random differences between the two chromosomes.

A chromosomal rearrangement, no matter how large, is a single mutational event. Even large changes can be quite compatible with life (see Down's syndrome) and, in some cases, even without important functional import.

>
> >> and we all
> >> should know by now that selective differences take hundreds of
> >> generations per base substitution. But you claim that neutral
> >> mutations fix at the rate of a couple of hundred per generation,
> >> thousands of times faster than selection can fix a beneficial
> >> mutation.

> >Once again you confuse numbers with rates.
>
> No I haven’t John.

Yes you have. Repeatedly.

> Even Charles Brenner is using the word “plague” to
> describe what you are claiming.
>
> >>>> If they
> >>>> don’t understand how to do a mathematical computation it is junk.
> >>>> John, just because you are ignorant what a non-coding region of a
> >>>> genome does, don’t impose your ignorance on us by claiming this is
> >>>> junk. If a region of DNA has no coding function for proteins but
> >>>> remains non-random, it does so because it has stabilizing selection
> >>>> acting on those sequences.

If a region of DNA has no coding function but is more conserved than, say, pseudogene sequences that can be eliminated without consequence, it likely has a function related to its sequence. Otherwise, even if it has a function, that function is not related significantly to sequence.

> >>> True. Which has nothing to do with what I'm talking about. Stabilizing
> >>> selection makes loci evolve at less than the neutral rate. Such loci are
> >>> only a few percent of the genome. By the way, evolution isn't so fast as
> >>> to randomize sequences in 5 million years.

> >> Just what are you talking about? I guess you missed the study I posted
> >> above about the large non-random differences on chromosome 21 between
> >> humans and chimpanzees.

> >So? How is that relevant? Do you have access to the whole article? I don't.

Anyone can access these older articles by signing up with Science. A bit more spam is the cost.

>
> It is relevant because you have claimed that the human and chimpanzee
> genomes are 98.7% similar and here is data from chromosome 21 which
> shows you are wrong. Yes I have access to the whole article and I told
> you how you could get access to the article without cost. Don’t use
> ignorance as a defense to your irrational claims.
>
> > 70% of genes code for different proteins,
> ....if by "different" you mean having at least one different amino
> acid.
>
> At least one amino acid different.

That is one or two aa in 350 or so. But that varies. Small proteins tend to be more highly conserved because they tend to have a larger fraction of their aa's involved in function. Other sequences, such as those that get clipped off and discarded (like the B section of preproinsulin or fibrinogen peptide) have more changes over the same time frame.

>
> >> large stretches of non-random differences between human and chimpanzee
> >> genomes yet neutral evolution will fix all these differences a rate of
> >> a couple of hundred per generation, thousands of times faster than a
> >> single beneficial mutation can be fixed in a population. What you are
> >> talking about is mathematical irrationality.

> >I've become convinced that you know almost nothing about mathematics
> >beyond the scraps rote learning you have displayed here.
>
> John, I am not the one who has thrown out the multiplication rule of
> probabilities.

Neither have I. I just know when to use it and when not to. And I don't think that the probability of a mutation is a fixed constant.

> This is the governing rule of the joint probability of
> events for a stochastic process. And every time you claim that I know
> almost nothing about mathematics, I’m going to remind you about how
> population size affects the probabilities of events. If you continue
> in this discussion, I’m going to teach you something about the
> practice of hard mathematical science and show you why your theory of
> evolution is a mathematically irrational belief system.

That would be a first for you.

>
> >>>> And the reason it has stabilizing selection
> >>>> pressures acting on those sequences is that it has some type of
> >>>> important function on maintaining the life and reproductive capability
> >>>> of that member. The only junk in this discussion is the evolutionist
> >>>> junk science which fails to properly explain how mutation and
> >>>> selection works.
> >>> You mistake evolution at the rate of mutation for stabilizing selection,
> >>> presumably because you have a false understanding of the mutation rate.
> >>> Neutral evolution produces only a bit more than 1% difference over 5
> >>> million years, not a randomization of sequences.

> >> You will only get randomization of sequences if there is no selection
> >> acting on that sequence. Your mathematics is faulty because 5 million
> >> years only represents about 500,000 generations and you can not fix
> >> 40,000,000 differences in two divergent populations in such a short
> >> period of time. It is mathematical irrationality to believe this.

Only if one is so stupid as not to understand the effect of sexual reproduction, which allows a second mechanism for generating new combinations of alleles beyond repeated serial mutation.

> >You seem to have stopped even pretending to have an argument and are
> >just repeating your mantra regardless of what you are supposedly
> >responding to.
>
> Here’s your big opportunity to show us how my mantra is wrong. Show us
> how 40,000,000 neutral or selective mutations sweep through or spread
> like a plague through the two populations.

We have shown you the math. It is your religious belief that all mutation and selection must involve serial mutation in a clonal organism that is the problem. That, and your failure to understand the difference between "What is the probability that 100 *specified* dice (whether specified before or ex post facto without reference to what was rolled) out of 600 all come up 6-face?" and "How many 6-faces do I expect if I roll 600 dice?" The first answer, mathematically, is (1/6)^100. The second answer gives the expected mean number as (1/6)*600. You think the answer to all such questions is (1/6)^100.

>
> >>>>>> Of the ones that are in coding areas, how many are thought to make
> >>>>>> significant "interesting" morphological differences rather than minor,
> >>>>>> possibly non-function-altering changes to a protein?
> >>>>> Again, very few. The vast majority of differences in coding regions are
> >>>>> silent, i.e. making no difference in the protein being coded for.
> >>>> Really John? Is that why over 70% of the genes in humans and
> >>>> chimpanzees code for different proteins? I can’t tell what you are
> >>>> worse at, mathematics or the interpretation of data.
> >>> This is silly. "Over 70% of the genes code for different proteins" is a
> >>> reasonable expectation for neutral evolution. Few of these differences
> >>> mean anythng.

> >> We all know about evolutionist expectations, they are mathematically
> >> irrational. But if you want to show your work and compute the joint
> >> probability of two neutral mutations being fixed in a population, that
> >> would be some interesting evolutionist folklore to hear.
> >Mantra. At least your mantra does evolve over time, though it seems to
> >be randomly so.
>
> My mantras are selective John. They are based on hard mathematical and
> empirical evidence. Even hersheyh now agrees that I’ve derived the
> correct probability function for the mutation and selection phenomenon
> except he is whining about the 4 in the denominator of the mutation
> rate. Hersheyh still hasn’t figured out that there is more than a
> single possible outcome from a mutation.

There are two, and only two, possible outcomes: mutant and not mutant. That is what makes what you 'derived' as being based on a *binary* probability. You might want to look at what "binary" means. [There are other assumptions that go into binary probability theory, such as the assumption that each trial has an equal probability of being an event, that are violated.]

> So I guess you are not going
> to derive for us the probability of two neutral mutations being fixed
> in a population.

If the probability of a point mutation per site per generation somewhere in the entire population is u*2N and the probability of that specific mutation going to fixation is 1/2N, then the probability of mutation and fixation per site per generation is u. If there are 3 X10^9 nt sites per genome, then the probability of mutation and fixation per *genome* (all 3X10^9 sites) is around 30 if u = 10^-8. I cannot specify which 30 out of the 3X10^9 sites will have had the mutation and will have had it reached fixation. But that is the expected number of fixations per generation. Since 30, the expected mean number of fixations, is significantly larger than 2, the probability of at least 2 fixations per generation is essentially 1. Now if I wanted to know the probability that the nt at position 375 and the nt at position 2.5X10^8 in the genome had both undergone mutation and fixation, that probability would be u^2. But I am not interested in that. I can figure out which specific nt's had, in fact, changed rath

er easily ex post facto. But I cannot predict which ones will change beforehand.

>
> >>>>>> I assume this is ongoing research; perhaps the answers are not yet
> >>>>>> clear.
> >>>>> Oh, no. They're quite clear. What isn't clear is the exact number and
> >>>>> identities of the comparatively few functional differences.
> >>>> John, your irrational speculations don’t form a scientific basis for
> >>>> any of your claims. You don’t know how mutation and selection works
> >>>> and you can’t explain why over 70% of the genes code for different
> >>>> proteins in humans and chimpanzees.
> >>> By "different" you merely mean -- though you probably don't know it --
> >>> that there is at least one amino acid difference, i.e. one point
> >>> mutation. Trivial.
> >> Tens of thousands of different proteins between humans and chimpanzees
> >> fixed in 500,000 generations, that’s what a mathematically irrational
> >> evolutionist would call “trivial”. Maybe these proteins diverged
> >> during the pre-split period, you know, the banana split period.
> >>> [mantra snipped]
> >> Repeat after me, reptiles transform into birds, reptiles transform
> >> into birds, reptiles transform into birds…
> >That is indeed what the data show. Care to discuss it?
>
> So John, are you now going to claim that 98.7% of the data shows that
> reptiles transform into birds?
>

[snip]

[hersheyh]

On Thursday, October 6, 2011 7:44:51 PM UTC-4, Alan Kleinman MD PhD wrote:
> The following are a compilation or responses to posts 976-1001 and
> splinter posts. Sorry for any inconvenience.
>

[snip]

>
> hersheyh Sep 8, 8:53 pm
> Newsgroups: talk.origins

> From: hersheyh <hers...@yahoo.com>

> Date: Thu, 8 Sep 2011 20:53:01 -0700 (PDT)
> Local: Thurs, Sep 8 2011 8:53 pm
> Subject: Re: The Theory of Evolution is Mathematically Irrational
> Round 2
>
> > [snip]
> >> >>> Perhaps this is a good time
> >> >>> for me to go over the fact that dice rolling is a very good metaphor
> >> >>> for the mutation and selection process.

> >> >> Only if the die has a few billion faces, almost all of which have the original allele on them. (the
> >> >> rest wouldn't be equally distributed either, would they?)

> >> > Greg, the die has only four faces for a point mutation, A, C, G and T.
> >> > If you think the die has billions of faces why don t you tell us what
> >> > a few of them are?

> >The die, to properly produce the ratio of the 'event' to 'trials', which is what your dice analogy does,
> > has to have as many faces as the minimum number of 'trials' needed to produce one 'event'. In
> > dice, that would be six faces with only one of those faces being the 'event'; that is what will give
> > you the 1 to 6 ratio. [The assumption is that the die are fair.] The 'event' in our case is a
> > *mutation*, which is any change from an identifiable non-mutant genetic state to an identifiable
> > different mutant state. That does mean, given a ratio of mutant (the 'event') to trials of 10^-8 that
> > the "die" have 10^8 faces, all but one of which is labelled not-mutant and the other face being
> > labelled "mutant". When you roll such a die, the probability that it will come up "mutant" is 10^-8,
> > isn't it?
>
> Hersheyh, how did you get so confused on this topic? Here is a quote

> from �Advanced Engineering Mathematics� by Kreyszig. �The statement �E

> has the probability P(E) then means that if we perform the experiment
> very often, it is practically certain that the relative frequency f(E)

> is approximately equal to P(E)� If we are flipping a coin and do it a

> large number of times, half the time we will get heads and half the
> time we will get tails. If we are rolling a die many times, 1/6 the
> time we will get a 1, 1/6 the time we will get a 2 and so on.

That is *exactly* what I said. You seem too stupid to even understand that the 1/2 of coin flips
(frequency of heads per flips) and the 1/6 of die rolls (frequency of 6-faces per roll) are the exact
counterpart to the 10^-8 of mutation frequency (frequency of observed mutants per tested individual).
All of them are P(E) or f(E), the ratio of the number of events divided by the number of trials. That gives
us a ratio that is the probability of the event per trial.

> In the mutation and selection phenomenon, the trial is the mutation.
> Consider if the mutation rate was 0 and the DNA replicated perfectly
> each time.

A "rate", "probability", or "frequency" is a "ratio", not a "number". To have a "mutation rate", "mutation
probability", or "mutation frequency" of 0, you would still have to divide the *number* of mutants (zero)
by the number of trials. You do know the difference between a "number" and a "ratio", don't you?

> No mutations gives no trials.

No mutations means that there are no trials (individuals tested) that had a mutation. That would make
the mutation *rate* or *frequency* or *probability*, obtained by dividing zero by the number of trials,
zero as well. But it would also then be an actual ratio rather than a number. Apparently you really don't
know the difference between a ratio and a number.

If the number of "mutations" is the number of trials, how do you calculate the "mutation frequency" or
"mutation rate"? Divide the number of "mutations" by the number of "mutations"? That would always
produce a "mutation rate" of 1.0.

> The mutation rate is simply
> the frequency which the die is rolled at a particular locus and with a
> mutation rate of 10^-8, the die is not rolled at that locus very
> often.

Most intelligent people would say that the mutation rate is rate or frequency at which one observes a
mutation in a population of cells. That allows us to actually measure a mutation rate. You seem to be
pulling the number 10^-8 out of your ass. How did you identify and measure the "frequency at which a
die is rolled at a particular locus" if you have no way to identify a mutant nor whether the die has
actually been rolled? Why don't you define what you mean by mutation *rate* and come up with an
actual rate rather than the number of mutations? IOW, try again.

> That�s why you need such large populations with this tiny

> mutation rate. You need a large population like 10^9 so that at least
> a few members will roll the die at that locus. But when those members
> do roll the die, there are four possible outcomes, A, C, T or G. I

> know this sticks in the craw of evolutionists because you can�t have a
> mutation from the original base to the original base but you don�t

> know what the original base is before the point random mutation
> occurs.

And you have not told us how one identifies the cases where "the four-sided die" was rolled.

> You can only say with certainty after the mutation occurs it
> will be one of the four bases. There are not 10^8 faces on the die,
> there are four faces on the die and the die is only rolled once in
> 10^8 replications when the mutation rate is 10^-8.

How does one measure the "mutation rate"? How does one identify a "mutant"? And what does
"mutation rate" mean if it isn't an actual rate but merely the expected mean number of "mutants" if one
arbitrarily decides that the "mutation rate" and the "number of trials" are the same number?

>
> >> Nearly all would be the original base, wouldn't they? The rest (a
> >> handful) would be labeled with the other bases, in numerical proportion
> >> to their empirically-determined probability. Surely you don't imagine
> >> that a four-sided die, with a 25% chance of landing on any letter, is a
> >> good model.

> >Actually, as a creationist, he probably does think that because he thinks that genes are assembled
> > by scratch by randomly choosing each nt from equimolar pools of the four nt's. Yeah, I know that
> > is a ridiculous description of evolution, but the "747 formed by a tornado" scenario seems to be
> > stuck in the creationist brain. It is what allows them to say that a 900 nt gene has the probability
> > of forming "randomly" of 1 in 4^900. Pure GIGO.
>

> Don�t be silly hersheyh, I don�t believe in abiogenesis. The concept

> of abiogenesis is more mathematically irrational than the theory of
> evolution and the theory of evolution is really mathematically
> irrational.

Says someone who cannot distinguish between a rate and a number.
>
[snip]

[hersheyh]

On Thursday, October 6, 2011 7:44:51 PM UTC-4, Alan Kleinman MD PhD wrote:

[snip]

>
> hersheyh Sep 9, 11:59 am
> Newsgroups: talk.origins

> From: hersheyh <hers...@yahoo.com>

> Date: Fri, 9 Sep 2011 11:59:21 -0700 (PDT)
> Local: Fri, Sep 9 2011 11:59 am
> Subject: Re: The Theory of Evolution is Mathematically Irrational
> Round 2
>

> > > > only when a specific n.t. change occurs or whether all three produce the effect or only 2 of the 3 produce A-resistance. We know

> > > > none of that since we are not observing where the mutations occur (1 site or many) and which mutations produce the effect. But
> > > > we *do* describe what we *are* using to test the *genetic change* that is behind the *phenotypic* change we can see.
>
>
> >> You can’t necessarily distinguish the new genetic state from the old
> >> genetic state phenotypically, you can only distinguish the change by
> >> sequencing.

Not if you are interested in mutations that have a selective effect. In that case, the mutation *must* have a phenotypic effect. Having a phenotypic effect is necessary but not sufficient condition for there to be selection (a mutant *can* be both neutral and have a phenotypic effect). Mutations that have no phenotypic effect are necessarily selectively neutral.

> >Being able to empirically identify the nt present at a site is a "phenotype". It is "observed" by some form of sequencing. But *we*
> > (meaning anyone that has ever taken and understood an undergrad genetics class) are not using sequence to
> > identify a mutant genetic state. *We* are using 'mutation' to describe a genetic change that produces a specific
> > phenotype (antibiotic resistance) from a different original specific phenotype (antibiotic sensitive). By *your*
> > argument, geneticists cannot determine that a phenotypic change is due to a change at the genotype level unless
> > we sequence. That would be a surprise to the generations of geneticists that existed before the 1980s.
> > Biologists have been able to identify genetic variants since before Mendel, although they did not call these
> > variants "mutants" until Hugo DeVries coined it to describe heritable (non-point mutation; the changes were
> > actually chromosomal mutations) changes in the Evening Primrose in 1901, when he published _Die

> > Mutationstheorie. And, of course, they were able to follow the Mendelian pattern of simple identifiable allelic

> > changes after Mendel's rediscovery. You essentially are telling us that all this previous history of what genes and
> > mutation are should be tossed out the window.
>
> The gold standard for identifying a nucleotide at a particular locus
> is genetic sequencing.

And, indeed, geneticists often *sequence* mutants *after* they are identified in order to determine what kinds of
sequence changes produce the mutant state. But sequencing is not how mutants (especially mutants that have
selective consequences) are identified. Moreover, sequencing mutants does not ever
produce equal numbers of nucleotides. And the fact remains that you cannot even identify that there is a mutant
unless you know what the original genetic state is (regardless of whether you identify the genetic state by its
phenotype or by its sequence).

I *define* mutation as a *change* in a gene. In order to identify a *change*, you need to know and be able to identify
the original state and the changed state. How do you define and operationally identify a "mutation"?

Even when geneticists look at selectively neutral events, they start out with a knowledge of the initial genetic state.
For example, one can use a genetic probe's affinity for a sequence as a way to identify a *change* in genetic sequence
in an organism. This can be used to identify mutants that have no phenotypic effect. So can, in some cases, changes
in restriction enzyme sites. But you always have to know the starting state and be able to identify some type of
change in that starting state. Otherwise, you cannot determine that a mutation has occurred and your numbers
become worthless GIGO using meaningless numbers pulled out of your ass.

> Before DNA could be sequenced, people studying
> genetics were limited to observing phenotype changes to determine when
> a mutation occurred but the science has advanced and you refuse to do
> the advancement.

Since, and especially in cases where selection is relevant, it is phenotypic difference that matters, people studying
genetics still use phenotypic *change* as a way to identify genetic *change*. After they have identified mutation, they
then often, now, sequence to discover what sorts of changes produce the phenotypic difference. But, except when
changes in features that can be directly reflective of sequence changes, like changes in restriction fragment sites or
numbers of repeats, or binding a probe can be used, mutation is still usefully determined by change in phenotype.
And in *every* case, one needs to know both the initial state and be able to distinguish that from a changed state in
order to identify a mutation. Regardless of how that is done.

Can you tell me how you identify that a "mutation" has occurred without any knowledge about either the original
phenotype or genotype or sequence nor any way of identifying a change from that original state? ESP?

How do you identify "mutants" when you determine the "mutation rate", m, in your so-called equation?
Remember that this must be done without your having any knowledge of the original sequence, given the fact
that you divide by 4 precisely because you don't know the original sequence and don't use any other way of identifying
the original state or that there has been a change in that state.

> What I am telling you is that the Poisson
> distribution is the wrong mathematics to describe the mutation and
> selection phenomenon

I only use the Poisson to descibe the stochastic mutation part of the process. Selection is a non-random, directional
event that is described by a different math. One that involves things like differential reproductive success as measured by relative fitness and describes changes in frequency over time.

> and you are failing to recognize how the
> multiplication rule of probabilities dominates the joint probability
> of events in the mutation and selection phenomenon.

No. I have always used the correct values for the *probability* or *frequency* of a particular genetic state in a
population. It is just that that *probability* or *frequency* is not always the *mutation probability* in a population
that initially was non-mutant. Depending on past history, the *frequency* of a variant and the size of a population
containing that variant can change dramatically and rather quickly.

>
> >> What I am stating is that when a point mutation occurs at
> >> a locus, you have four possible bases which can occur at that locus.

You still haven't told me how you identify that a "point mutation has occurred at a locus". Especially since you claim
that the only gold standard way to identify a "mutant" is by sequencing and that means that you can't identify whether
or not there has been a *change* in sequence.

> >As has been pointed out many times to you, but you appear to be too dense to understand it, a point mutation
> > occurs when, and only when, there is a *change* of the original nt at that site to one of the three others.

> > Mutation requires *change*, not the same thing. You do not have *change* when a C at a particular site produces

> > a C in that site in its progeny. C to C is a non-mutant event and one that happens almost all the time (in our
> > example, non-mutation happens with a frequency of (1 - 10^-8)). Moreover, the probability of *change* is not
> > equal even for the three possible *changes* (mutation means "change", not existence of a site). That alone means
> > that division by 4 is GIGO nonsense. Moreover,>it is always possible that some of the possible nt changes, even > > at a site, do not produce any change in phenotype.
>
> If you are so smart hersheyh, tell us what the base was before the
> mutation occurred. But you are not so smart because you can’t.

If I am defining "mutation," in this case, as a *change* in DNA sequence, I would have to sequence this region of DNA
in the original organism used to start the population to know what the original genetic state was. Otherwise, I would
not be able to identify that a mutation has occurred. Then I would have to have some way of sequencing every cell in
the population to determine how many have had a "mutation event", identified as a *change* in sequence to *any*
other nt. Every single organism that has had a change in *sequence* is a mutant. Organisms that have the original nt
is not a mutant. That is the dichotomy that produces the binary probability function: Mutant (changed state) and non-
mutant (unchanged state).

If I do not know the original nt was and cannot sequence or otherwise identify a change from that original nt (and
cannot use other ways of distinguishing mutant from non-mutant), then I have no way of identifying that a mutation has occurred. All the cells would look the same.

> That’s
> why when you formulate the mathematics, you must allow for all four
> bases as possible outcomes when a point mutation occurs because that’s
> the only thing you know with certainty is that after a point mutation
> occurs, you only know for sure that it will be one of the four bases.

I also know that the DNA has two antiparallel strands, but I don't divide by 2. How can I know "when a point mutation has occurred (to use the correct tense)" if I cannot distinguish mutant from non-mutant?

> Someday you might learn how to actually do a calculation using
> probability theory rather than plugging numbers into the wrong
> probability distribution.

I cannot use probability theory when I cannot calculate the *actual* mutation rate or frequency rather than use some
number pulled out of someone's ass. Especially when that someone doesn't know that mutation rate or frequency is a
ratio and not a number and keeps trying to claim that the number of trials is 10 (the mean expected number of
mutants in a population of 10^9 individuals when the mutation rate is 10^-8) and that is the divisor of the event
(which is also the number of mutants seen in a population of 10^9 individuals). And then tells me that he cannot even
identify these mutants in the population. That is absurdity piled on absurdity.

> >> The change from one base to another does not imply that the change
> >> will be beneficial.

> >Well, duh. That is because the terms "beneficial", "neutral", and "detrimental" are conditional and are descriptions
> > of the effects of particular genetically caused phenotypes. That is why I use the correct description of "antibiotic-
> > resistant" or "antibiotic-sensitive" to describe the different genetic states. Those are the genetic states of the cell
> > described whether that cell is in media with an antibiotic where being resistant is "strongly beneficial" or is in an
> > environment without the antibiotic where it is likely that the same genetic state is "neutral" or "weakly
> > detrimental". Unless you are claiming that>most of the time antibiotic resistance is an environmentally induced
> > or non-genetic state.
>
> And this is why you can not properly formulate the mutation and
> selection phenomenon as a strictly binomial process. The mutation and
> selection process is more than a beneficial or not beneficial mutation
> process. You are failing to make this distinction. It is you that is
> claiming that antibiotic resistance is already present in the
> population before the toxin is ever introduced.

Indeed I am. Selection can only work on variants that actually exist. In the case of lethal antibiotics, if the resistance
mutation does not exist in the population *before* addition of the antibiotic, the whole population will die. If the
selective condition is not lethal, then the selective conditions can still only have a *differential effect* on variants after
mutation produces the variant and it actually exists in the population. Are you seriously proposing that selection
works on non-existent variants? Absurdity piled on absurdity!

> >>> The change can be neutral or detrimental as well.
> >>>The simple observable fact of *change* is insufficient to determine whether that *change* is beneficial, neutral, >>> > or detrimental. You also need to know the environmental conditions. Again, applying these terms can only be
>>> > done empirically by examining the differential reproductive success of the identifiable traits in pairwise
>>> >comparisons in a specified environment.

> >> The effect of selection on that change will only be identifiable based
> >> on the reproductive capabilities of that member for the given
> >> environmental conditions. If the change is beneficial, this will be
> >> seen in the increase in subpopulation size with this beneficial
> >> mutation, that is the change will be amplified.

> >Again, the *change* is not inherently 'beneficial'. It is only beneficial when you describe the specified
> > environment. Using the word "beneficial" without describing the environment it is beneficial in is intentionally

> >misleading. Antibiotic-resistance is not a "beneficial mutation" unless you add the phrase "in environments with

> > antibiotic" each and every time. If antibiotic resistance is *also* "beneficial" in the absence of antibiotic (likely not
> >the case), you can use the phrase "in environments with or without antibiotic".
>
> You are only misled by your confusion of how the mutation and
> selection phenomenon works. Populations have no trouble identifying
> whether a particular mutation is beneficial, neutral or detrimental.
> Populations also don’t need to be instructed on the selection
> conditions they are forced to respond to. You are having trouble
> understanding the mathematical behavior of populations when they are
> responding to selection conditions.

When there is positive selection, the variant which has a reproductive advantage will tend to increase in frequency
toward fixation. When there is negative selection, the variant which has a selective disadvantage will tend to decrease
until the minimum frequency of spontaneous new mutation. When there is no selection (selective neutrality), the
frequency will, from generation to generation, be close to the immediate past frequency in large populations (small
populations will have greater generation to generation variance). Because any new mutation is typically present in a
small frequency, most of the time the drunkard's walk will lead to loss of that specific mutation and its progeny. Over
longer time frames, there will be neutral drift of frequencies as described by a drunkard's walk because chance has no
memory. That is the effect of selection and nonselection.

>
> >> On the other hand, if
> >> the change is neutral or detrimental, that will be reflected in the
> >> subpopulation size as staying relatively constant or decreasing over
> >> generations respectively.

> >Only if you *specify* the environment. When I use "antibiotic-resistant" to refer to a genetic and phenotypic state, > > you automatically know the condition in which that variant is "beneficial".
>
> I’m the only one posting on this thread who gives empirical examples
> which “specify” the environment and the populations’ response to the
> environment. On the other hand, you claim that mutation and selection
> occurs in parallel without ever specifying the environment or
> providing any measurements.

Of course I have done exactly that several times. The problem with your "empirical" examples is that you seem to pull your "mutation rate" out of thin air, given that you have no way of identifying when a mutation has occurred.

> Instead, evolutionists claim that reptiles
> turn into birds and humans and chimpanzees come from a common
> progenitor without ever specifying the environment which would cause
> such a massive genetic transformation.

There was no "massive genetic transformation" involving selection. The number of selectively relevant differences between human and chimp is quite small relative to the total number of differences (most of which are the expected amount of selectively neutral changes for populations that have been reproductively isolated for 5-6 million years).

> This is why evolutionists have
> to come up with the junk science of neutral evolution. Hersheyh, you
> are in dire need of training in the hard mathematical sciences, your
> indoctrination into evolutionism just doesn’t cut it.
>
> >> > Mutation A is defined as the change from a genetic state which produces a cell resistant to antibiotic A from a
> > > > cell which was sensitive to antibiotic A. Again, mutation means change. In order to identify change, you
> > > > have to be able to identify both the start point (state before change) and the changed state. In our case, A-
> > > > sensitive is the starting genetic point and A-resistance is the changed genetic state.

> >> Not necessarily so.

What isn't necessarily so? That our starting genetic state was A-sensitive? That it was mutation to A-resistance from A-sensitive that is relevant? That you can identify "mutation" or change of any kind without knowing the initial and end states?

> > > Mutation A can be beneficial and give improve
> >> fitness to reproduce for that member but mutation A can also be
> >> neutral or detrimental.

What is that relevant to? Are you claiming that "mutation A" is not mutation from the A-sensitive to the A-resistant state? I have already repeatedly pointed out that the terms "beneficial", "detrimental", or "neutral" are conditional descriptions and that the actual genetic state is the change that makes the organism A-resistant. A-resistance is an inherent or hereditary property of that variant. It is, in fact, passed on to its offspring.

> > > You measure that effect by changes in
> >> subpopulation size with the particular mutation.

> >You identify antibiotic-resistant cells by virtue of their resistant to (certain specified levels of) the antibiotic as
> > opposed to>the sensitivity of the original cells to that level. You do not identify antibiotic resistance by
> > sequencing the entire genome and looking for changes in nt sequence. How do you plan to identify cells with a
> > genetic mutation that causes the cell to >be antibiotic resistant in your world? Would you identify a mutant
> > white-eyed fruit fly (red-eye is the w.t.) by asking a blind man to do it visually? Or would you sequence the entire
> > genome to identify sequence differences first? Me. I would, like Thomas Hunt Morgan, look for white eyes to
> > identify the white-eye mutants (this was the first sex-linked mutation found in Drosophila, in 1910).
>
> Apparently you are blind to genetic sequencing because that is the
> most accurate way of identifying an error in genetic replication.

I am not "blind to genetic sequencing". In fact, I find the results of sequencing mutants (usually identified by other means) quite informative. As in the cases below.

>
> >In this case, like in the case of cystic fibrosis and unlike achondroplastic dwarfism, there are a number of different
> > alleles of the gene that can produce the same mutant phenotype. Some are deletions or frameshifts. Others are > > point mutations at different sites in that gene. I may, after identifying the gene, sequence it and all the various

> > mutations in that gene that produce [a common effect].

>
> And Weinreich’s experiment identified several different variants of
> the highly resistant beta-lactamase bacteria and these variants were
> identified by genetic sequencing. And not only were the variants
> identified, the sequence in which the mutations had to occur

That was sequences, not sequence, by which the maximally resistant sequence involving 5 point mutations could have
occurred.

> was
> identified as well. You don’t do this type of measurement by simply
> identifying a phenotype change, you must sequence the DNA.

And the way he identified the intermediate levels of resistance particular combinations of the 5 mutations had was by observing their ability to grow in different levels of antibiotic. That is, by examining the phenotype caused by the genotype. I have absolutely no problem with sequencing. I am just pointing out that, especially when one is talking about selectively relevant change, phenotype is what selection *directly* works on, not sequence.

> You are
> teaching genetics from the 19th century. Hersheyh, you need to bring
> your teaching up to the 21st century.

I taught 21st century genetics. You are simply producing mathematical garbage.
>
[snip]

[hersheyh]

On Friday, September 16, 2011 9:09:40 AM UTC-4, Alan Kleinman MD PhD wrote:
[snip]

> >For *any* kind of mutation, there are only two outcomes: mutant and not-mutant. There most
> > certainly are not four possible outcomes. Mutation *means* change from one defined genetic state
> > to a different genetic state. Typically this change in state is defined by a change in phenotype
> > rather than genotype. In all the cases we have been discussing with HIV, bacteria, pesticide
> > resistance, etc., the change in genetic state has been defined phenotypically, usually by
> > distinguishing between a toxin-sensitive and a toxin-resistant state. In other bacterial cases, the
> > distinction is between ability to use a resource or inability to use a resource (e.g. citrate), the
> > amount of resistance to an antibiotic, or the ability to grow efficiently in defined conditions as
> > measured by population produced per unit time. In some cases, the genetic changes are directly
> > known (e.g., a change from a C to a T), but in other cases they are not known.
>
> You have used phenotypic change as the definition of mutation, I have
> not.

No, I most certainly have NOT used phenotypic change as the definition of mutation. Just above here I
said that mutation means "change from one defined genetic state to a different genetic state." But I
point out that, especially for changes with selective impact, the changed genetic state must also involve
a change in phenotype, since selection works directly on phenotype and only indirectly on genotype or
sequence. But the important part of that definition is *change*. You have to be able to identify a
change. That means you have to be able to distinguish between an initial state and a changed state. If
you cannot do that, mutation is a meaningless term.

> It is not my fault that this is not clear to you. I made my
> definitions of variables explicitly clear.

Then why am I just finding out that you think that the number of "trials" in your equation is the same as
the mean expected number of mutants (10 in our example). What do you think the "event" is? And do
you know what the term "rate" or "frequency" or "probability" means? To me, it implies a ratio and not a
number.

> And your definition is the
> wrong mathematical definition for mutation. With your sloppy
> definition, there is no such thing as a neutral mutation because there
> is no phenotypic change.

Where do you get that from what I said!!!! First you complain that I use phenotype to *identify* the
changed genetic state. Now you are saying that I deny the existence of mutations that, in at least some
environment, are selectively neutral. I have pointed out that some mutations that produce detectable
phenotypic differences can be selectively neutral. And also that some mutations only affect genotype
(sequence) without having any phenotypic effect. Those mutations can only be identified by a *change*
in sequence. But to identify any kind of *change* you have to know the starting state and end state.

> I’ll stick with the correct definitions and
> probability function to describe the mutation and selection phenomenon
> and you can stick with your sloppy incorrect definition of a mutation
> and the wrong probability distribution (Poisson).

First, you have not provided an operational definition of mutation. Operational means you can actually
identify a mutation and distinguish it from non-mutation. I have. Mutation is a change in genetic state.
That means that one identifies a mutant by observing some kind difference between the original genetic
state and the mutant genetic state. What is your definition of "mutation"? And how do you distinguish
a mutant from a non-mutant? Don't say sequence change, since you repeatedly claim that you divide by
4 specifically because you don't know the sequence -- either before mutation or after.

Second, the probability functions can only be used to describe the mutation process. Only mutation is a stochastic or random event. Selection is neither stochastic nor random. It is directional.

> >>And the reason why there is four, not
> >> three possible outcomes is that a priori you do not know what the base
> >> was at that locus before the mutation occurred.

> >If you don't know the initial genetic state or the final genetic state, you cannot even say whether or
> > not there has been a mutation or change in that state. And four would still not be the correct
> > number since, obviously, at least one of the nts represents no change. Basically, unless I am
> > specifically calling a change from C (which I have to know is the w.t. nt at that position) to A, G, or
> > T or only one or only two other nt's the mutation of interest, the genetic nature of the change
> > (which need not be at a single site or be a point mutation) is irrelevant. Mutation has *always*
> > been defined as a change in genetic state from one state (often the w.t. state) to a different state as
> > evidenced by a change in phenotype. When I measure mutation rate, I have to be able to
> > distinguish the mutant state from the non-mutant state in some way. That means I need to be able
> > to empirically determine a change. I can do that with resistant to A or sensitive to A.
>
> You don’t need to know what a particular coin flip gives to write a
> probability function which describes coin tossing. You don’t need to
> know what a particular roll of the dice gives to write a probability
> function to describe dice rolling.

Only because you assume the coins and dice are honest, unweighted, and equal sided. That allows you to make a theoretical or a priori estimate of the frequency of the event (the frequency of heads or tails per coin flip, frequency of specific number-face per dice roll, or the frequency of mutants per individual tested -- although you seem to think it is the number of mutations in a certain population per number of mutants in a certain population using a frequency you pull out of your ass).

The frequency of mutants per trial (individual tested) does not have any theoretical basis. It must be determined by actually counting the number of mutants in a population and dividing that number by the size of the population tested.

> What a probability function gives
> you is a mathematical representation of the frequency of events if you
> were to do the experiment many times. I have used the most general
> mathematical definition of a point mutation at a locus. Your
> definition ignores other possible outcomes.

There is only one "event" that needs to be identified. Change from the original state. You count the number of such changes and divide that number by the size of the population you examined for such changes. If you have discovered a theoretical value for mutation frequency that involves dividing something you call an event by 10 trials, please describe it here.

> >> This has nothing to do with distinguishing a mutant state from a non-
> >> mutant state.
> >You don't seem to understand what "mutation" means. Being able to distinguish between the
> > mutant state and the non-mutant state has everything to do with determination of the mutation
> > rate. Namely, you cannot determine mutation rate if you cannot identify and distinguish between
> > the mutant and non-mutant states.

[snip]
>
> You are simply are unable to derive the correct mathematical equations
> to describe the mutation and selection phenomenon. You don’t
> understand what a probability function is.

I certainly understand that mutation rate is a ratio and not a number.

> You have used the wrong
> probability function to describe the mutation and selection phenomenon
> your entire career and can’t comprehend the fact that when a point
> mutation occurs at a particular locus, the only thing that you can say
> with certainty is that you have one of four possible outcomes.

You keep saying "when a point mutation occurs" as if you had some way of determining "when a point mutation occurs". How do you determine that a point mutation *has* occurred if you don't know what the original nt at that site was? ESP?

> I am
> not going to use your definition because you limit your ability to
> measure whether a mutation occurs based on a phenotypic change.

I am perfectly happy to say that *when* one observes a change from a known nt to some other nt in a
sequence, you are observing a point mutation. If you don't know the original nt, you cannot observe
any *change*. By definition, then, you can't observe mutation. To observe *change*, you need to know
both the starting and end states. Otherwise there is nothing to observe that would be recognizable as
the necessary change in state. It is like saying that you know the frequency of heads on a coin that you don't know is honest, don't know if it has been flipped, and no one will tell you whether heads or tails are up, but only that you should divide the answer by 2 because there are two sides to the coin.

> Yours
> is a wrong definition for mutation and it has led you to draw a series
> of mathematically irrational conclusions.

> >For example, the spontaneous rate of mutation to achondroplastic dwarfism to normal parents is known because >achondroplastic dwarfism is a dominant mutation that is fully penetrant.
> >http://www.google.com/url?sa=D&q=http://omim.org/entry/100800
> >The mutation rate from the normal, non-achondroplastic allele to the achondroplasia allele can thus be calculated by >counting the number of children born to 'normal' parents (normal in this context means that the parents are not >achondroplastic dwarfs) who are achondroplastic dwarfs and dividing this by 2 times the total number of children born to >'normal' parents in the same area and time. That is: u = Na/2Nt where Na is the number of children with achondroplasia >born to 'normal' parents and Nt is the total number of children born to 'normal' parents. The factor 2 here has *nothing* >to do with nucleotides. It is due to the fact that every human child is diploid and the mutation rate is the rate of mutation >from the 'nonachondroplasia' allele to the 'achondroplasia' allele, so we have to count the number of new mutant alleles >and divide it by the total number of alleles examined. Each achondroplastic child has only one dominant >'achondroplasia' allele (the new mutant allele, since the parents

we
>
> re 'normal') yet every child has two alleles.
> >Now, to me it makes sense that we call Na/2Nt the mutation rate for the conversion of the normal allele to the >achondroplasia (ACH) allele. BTW, this rate is in the order of 10^-5. There have been several studies and the rates >differ in the different studies. Some of this difference may be due to diagnostic confusions by the doctor involved. >There are some other traits that have similar diagnostic features. After all this is data that has to be collected from a >large number of births attended to by many doctors, some of whom may have the competence shown here by our Dr. Dr. > [There would now be a DNA diagnostic test that could, with 99% accuracy, confirm diagnoses, but most of these studies >only involved phenotypic diagnosis by the attending physician.] The mutation rates from normal allele to ACH allele >range from around 0.5 to 1.5 X 10^-5/per allele. BTW, because, in this measurement (unlike the bacterial cases) all the >starting alleles are w.t., there is no Luria-Delbruck skew because i

t
>
> is the case that every event has the same probability >of occurring. [There might be a minor effect due if the same normal parents give rise to ACH siblings, since this is more >likely due to a parent's gametic mosaicism than to independent mutation.
> >Such siblings (and monozygotic twins) should probably only be counted once.)
> >But that rate is not one Dr. Dr. would agree to. In his mind, the true mutation rate is not the actual rate at which the >normal allele mutates to an allele that causes ACH. His 'true mutation rate' is that rate divided by 4. Because there are >four possible nucleotides at any nucleotide site. Exactly why the fact that any nt site can have one of 4 possible nt's >means one has to divide that actual rate at which
> >ACH alleles arise by mutation from w.t. alleles I have not been able to discern. Certainly no logical reason has been >given, aside from some mumbling about loci and randomness.

> You are correct here, I do not agree with your definition of mutation
> rate. If you want to measure the mutation rate correctly, you would
> need to sequence numerous parent and child genomes and compare the
> sequences for differences in the replication process.

How the hell do you think they determined that achondroplastic dwarfism was due to a change at a
specific nt? We know, from phenotypic analysis, that the trait is a dominant and fully penetrant state.
We also knew where the gene responsible is in the genome from genetic analysis. Then we sequence
the gene to see what mutations produce the phenotype. Every case is due to a change in a specific nt.
That *means*, for achondroplastic dwarfism, that seeing the phenotype is essentially the same as
seeing the change in sequence of a specific nt. That is the way its done. No division by 4 (which
obviously wouldn't work, since almost all the changes seen are transitions). Instead you determine the mutation rate by dividing the number of observed mutants (which, in this case, are clearly distinguishable from normal individuals) by the total number of individuals examined for that mutant state. That is a real example of the type of case you are interested in.

> That’s the
> mathematically correct way to measure the frequency of mutation. This
> is no different than flipping a coin to determine the frequencies of
> heads and tails.

With the minor exception that you have no idea that the coin has or has not been flipped and no way to
identify whether the up face is heads or tails in your argument. That's your problem. You say you can recognize "when a mutation event has occurred" but never tell us how you can do that without knowing either the original state or the changed state.

> If you depend on phenotype changes as your measure,
> you will miss all the neutral mutations that are occurring and you
> will have a mathematically incorrect value for the mutation rate.

[snip]

[Charles Brenner]

On Oct 7, 11:06 am, Alan Kleinman MD PhD <klein...@sti.net> wrote:
> On Sep 16, 7:46 am, Charles Brenner <cbren...@berkeley.edu> wrote:> On Sep 16, 6:09 am, Alan Kleinman MD PhD <klein...@sti.net> wrote:
>
> > > Google has again splintered this thread so I am restarting this thread
> > > again as round three and reposting responses from posts 851 through
> > > 875 as a single post. Please continue your posts on this thread and
> > > not on the splinter threads as I will not follow the splinter threads.
> > > I will post the rest of my responses to posts from round 2 in bulk on
> > > this thread. Sorry for any inconvenience.
>
> > [snip many pages randomly running one topic after another, leaving it
> > to the less important readers who have scads more time than the self-
> > important and pompous author to sort out what is what]
>

> You
> do have a search feature in your software?

That's exactly why I mocked you Alan, because of your expectation that
others work so you don't have to.

> > I wonder how an intelligent person would have handled the problem?
>
> Instead of whining, offer a different solution.

Not whining; maybe sarcasm. And the question was rhetorical. The
obvious answer had already been given to you: Just make separate
posts. If you'd like make them all subsidiary to one new master
thread, even that would be better organized than what you did although
I don't see the point. Inventing new topic headings would also be
helpful and courteous.

> And you actually made an intelligent comment when you used the term
> bottleneck but you let John Harshman bully you out of the term. If you
> are going to argue that chimpanzees and humans came from a common
> progenitor, when a population goes through a selective bottleneck, not
> only will the beneficial alleles which allowed the population to
> survive the selection pressure be amplified after the population
> recovers, so will all the neutral alleles be amplified that these
> members are carrying at all their gene loci. This idea that tens of
> millions of neutral mutations will amplify and fix in a population
> without the aid of selection is mathematically irrational evolutionist
> crap.

A lot of very smart population geneticists with great mathematical
talent have shown why the opposite is true. In a vacuum, neither you
nor any person is credible in mathematics merely because you claim to
be so without support. In your case, even worse you affirmatively
reveal yourself to lack mathematical understanding time and again. Two
specifics that are definitive and indicative, respectively:

Bill posed a very good aptitude question many months back. I think it
was to show that any loop on a terrain must include two points of
equal altitude. I was impressed that you even attempted to answer but
your attempt didn't even begin to work. You made some excuse that
Bill's problem was in a totally different domain than the mathematics
at issue in arguing population genetics and that is true. But the
point for me is that by giving a totally wrong answer and not even
realizing it, you proved that you lack the most basic mathematical
prerequisite of a sense of rigor - the ability to discern correct
mathematical thinking. Even if you were brilliant, none of your
mathematical claims would be worth listening to if you have no
conception of rigor.

Second, I once looked up the engineering work that you repeated
boasted of, giving a solution to some partial differential equations.
It seems that your contribution was a new solution to a problem for
which several other solutions already existed. I believe you used a
standard method not particularly well suited to the problem and
obtained therefore a clumsy solution useful only for getting a PhD. Is
that a fair summary? I did study partial differential equations long
ago (Stanford, by invitation before I graduated high school; grade of
A) so I have some understanding though not much interest. Certainly
they are practically important, but to an extent one can solve
differential equations by routine, without much sense about the fabric
of mathematics, e.g. rigor. They are so far divorced from population
genetics that your excuse reasonably applies in this case; competence
with differential equations does not give your mathematical claims any
credibility.

[Bill]

On 10 Okt, 08:05, Charles Brenner <cbren...@berkeley.edu> wrote:
<snip>

>
> A lot of very smart population geneticists with great mathematical
> talent have shown why the opposite is true. In a vacuum, neither you
> nor any person is credible in mathematics merely because you claim to
> be so without support. In your case, even worse you affirmatively
> reveal yourself to lack mathematical understanding time and again. Two
> specifics that are definitive and indicative, respectively:

.

>
> Bill posed a very good aptitude question many months back. I think it
> was to show that any loop on a terrain must include two points of
> equal altitude.

Given a smooth contour map, prove that an arbitrary circle drawn on
the map must contain at least two points that are 180 degrees apart on
the circle and are at the same altitude.

> I was impressed that you even attempted to answer but
> your attempt didn't even begin to work. You made some excuse that
> Bill's problem was in a totally different domain than the mathematics
> at issue in arguing population genetics and that is true. But the
> point for me is that by giving a totally wrong answer and not even
> realizing it, you proved that you lack the most basic mathematical
> prerequisite of a sense of rigor - the ability to discern correct
> mathematical thinking. Even if you were brilliant, none of your
> mathematical claims would be worth listening to if you have no
> conception of rigor.
>

<snip>

[hersheyh]

[snip]
>
> hersheyh Sep 8, 8:53 pm

> Newsgroups: talk.origins
> From: hersheyh <hers...@yahoo.com>

> Date: Thu, 8 Sep 2011 20:53:01 -0700 (PDT)
> Local: Thurs, Sep 8 2011 8:53 pm

> Subject: Re: The Theory of Evolution is Mathematically Irrational
> Round 2
>

Yes. And if we look at at specific nt in billions of individuals we will get a *different* nt (for a site that has an average point mutation rate of 10^-8) about once in every 10^8 individuals. Is that or is that
not the value of the mutation rate or frequency of mutation, m, in your equation? The value, m, in your
equation is the frequency at which one finds mutants in a total examined population of size n, is it not?

If you actually calculate m differently, say by dividing the number of events (mutations) seen in a total examined population of size n (what I would call the number of trials) by what you now call the number of trials (10, which I assume you calculated by multiplying 10^9 as n by 10^-8 as mutation rate), you will always get a value of 1. Which means that value m/4 is always 1/4. Are you really *sure* that you want to call the mean expected number of mutants as the number of trials?

Now think (for once) about what you would need in order to actually calculate a "mutation frequency" and what that term actually means. Because mutation is a *change* in genetic state, a *change* from one state to another, you *must* be able to identify when there has been a *change* in genetic state in order to get the ratio of mutants observed/total number of genetic states examined. That *requires* you to be able to identify both the initial genetic state and the different genetic state. Does it or does it not?

This is simple. Can you tell me how you plan to measure the mutation frequency, m, without being able
to distinguish between "mutant" and "not mutant"? Again, 10^-8 was used in our experiments not
because it is always correct, but because it is a typical or average value that was calculated empirically
by dividing the number of point mutation changes per generation over a large number of nt sites.

Unlike coin flips and dice rolls where we can generate a theoretical expectation of frequency based on
honest coins, honest dice, and random flips, there is no such theoretical mutation rate. Only measured
mutation rates or frequencies. Measured as a frequency by counting number of organisms examined
which are mutant and dividing by the number of organisms examined. If you have some other way of
measuring the mutation rate, let us know. Otherwise your m is a mystery number that you simply pull out of some place where the sun don't shine.

If you are using point mutation at a specific site as the "phenotype" you are using to determine the mutation rate, that means you need to know the non-mutant state you are starting with and must be able to distinguish it from the mutant or changed state(s). In this example, any single nt change from the original nt at that site is classified as a "mutation" BY DEFINITION OF MUTATION. That is, the mutation rate that you actually calculate is the rate of change from a specific known nt to *any* other nt. Again, if you can measure a mutation rate

> In the mutation and selection phenomenon, the trial is the mutation.

No it isn't. We don't calculate the mutation rate, m, by dividing the number of mutants we find by the number of mutants we find. That would always be 1. We calculate it by dividing the number of mutants we find by the number of cells we had to search through to find those mutants. The number of examined organisms is the number of trials.

> Consider if the mutation rate was 0 and the DNA replicated perfectly

> each time. No mutations gives no trials. The mutation rate is simply

> the frequency which the die is rolled at a particular locus and with a
> mutation rate of 10^-8, the die is not rolled at that locus very

> often. That�s why you need such large populations with this tiny

> mutation rate. You need a large population like 10^9 so that at least
> a few members will roll the die at that locus. But when those members
> do roll the die, there are four possible outcomes, A, C, T or G. I
> know this sticks in the craw of evolutionists because you can�t have a
> mutation from the original base to the original base but you don�t
> know what the original base is before the point random mutation

> occurs. You can only say with certainty after the mutation occurs it

> will be one of the four bases. There are not 10^8 faces on the die,
> there are four faces on the die and the die is only rolled once in

> 10^8 replications when the mutation rate is 10^-8.

The above is all the evidence one needs to know that you don't even understand your own equation!

The term you call m is the *mutation rate*, aka mutation *frequency*, aka mutation *probability* and is
presented as if it were a well-known constant. We have, for the sake of argument, been using the
average rate for point mutation in man, E. coli and many other organisms (but not HIV) of about 10^-8.
But if we were to actually use the equation in a real situation, we would need to know the *real*
mutation rate or mutation frequency for that particular site, not some hypothetical or average value.
That's because there are both mutational hotspots (e.g., achondroplasia is due to a mutational hot spot)
and mutational cold spots and the variance is several orders of magnitude either way.

That means you have to know how the mean mutation frequency was determined and know how to
apply that kind of measurement to a specific nt. Do you? Can you do it if you don't know the initial nt at any site nor even whether it has been changed to a different one? If so, please explain how.

This was elegantly shown by Seymour Benzer in the 1950s using classical genetic techniques on the
phage T4. This work also demonstrated that the gene was not an indivisible unit and that there could
be recombination within as well as between genes. As well as identifying the smallest unit of
recombination, which *later* work showed to be between two nts. IOW, he "discovered" the nt as the
indivisible unit of a gene without sequencing, using phenotypic effects to identify genotypic changes.

http://www.sbs.utexas.edu/genetics/genweb/images/cistmap.gif

biuforums.com/attachment.php?aid=3657 - Israel

The *real* mutation rate, m, must be determined empirically and not assumed. We have just been using an average value that, in any actual case, would have to be calculated as *number of mutants seen in n organisms divided by n organisms* where you actually and in the real world count real mutants and real organisms. And since *any* change in a nt from the original base present counts as a mutation, that would mean that dividing by 4 is meaningless because the *actual* *observed* number of mutants
includes all 3 possible different nts that could represent a *change* in genetic state from the w.t. nt at
that site.

The question is how you measure m and what you think the term m means. For that matter, what you think the term "mutation" means. If you are unhappy with my definition, namely that mutation is a
*change* (I often add the word permanent, to distinguish changes in the actual nts from short-term
modifications like methylations that can work over several generations; there are quasi-mutations) from
one genetic state to a different genetic state. That is a more inclusive (and accurate) definition than
your apparent claim that mutation can only mean a point mutation from some unknown nt to some
unknown nt and that mutations in a gene that produce the same selective phenotype has no relevance to the selection process. But feel free to give your own definition of mutation. In my definition, the
word *change* is quite important operationally. But you apparently can put your hand to your head (or
somewhere else) and devine a mutation rate out of thin air that you can apply to a nt without knowing either the starting or mutant state(s).
>
[snip]

[hersheyh]

On Friday, September 30, 2011 12:42:44 PM UTC-4, hersheyh wrote:

This is a pared down repeat that demonstrates that all that the Dr. Dr. did was re-invent the wheel (well, re-invent binomial probability distribution).

[snip]
>
> > That’s why you have to use the correct
> > probability function to describe the phenomenon and the Poisson
> > distribution is not the correct equation. And I expect you still
> > haven’t studied the derivation of the Poisson distribution yet. You
> > use the equation blindly without understanding what is being
> > calculated.
>
> I understand when it can be used as a good estimate of the binomial probability distribution. And the
> binomial probability distribution is what you have "derived", despite your division of the actual
> mutation probability by 4.

> Your equation that calculates the probability that one or more individuals with mutation A will be
> present in a population of total size, n, is:
>
> P(A) = 1 - (1-(mA/4))^(n*nGA)


This *is* your equation, is it not?

> Now I am going to simplify the symbols of that equation to demonstrate that it is nothing more than the
> binomial probability distribution solved to answer the question "What is the probability that there will be
> one or more A mutants in a total examined population of n*nGA?" where n = number of trials per
> generation and nGA = number of generations or times in which n trials are conducted or examined?
>
> First, I will change n to the mean total number of individuals examined. In most binomial probability
> equations n, in standard terminology is "the total number of trials". And the total number of organisms
> examined for the presence or absence of mutation *is* the total number of trials. Thus n is a simple
> replacement for your n*nGA
>
> That makes your equation now:
>
> P(A) = 1 - (1-(mA/4))^(n*nGA)
 = 1 - (1-(mA/4))^n)
>
> Now I claim that the "real" mutation probability is mA per trial and you think the "real" mutation
> probability per trial is mA/4 per trial. [The per trial clause is needed for the equation to actually work
> out as an equation. Any *frequency* or *probability* is always a division of something by something.
> For mA to be the mutation *rate*, it must be the minimum frequency of the mutant that you get when
> the mutant state is either deleterious or is neutral without enough time for there to have been
> substantial drift. I will instead call mA the mutation *frequency*. The *frequency* of a mutant can be
> any value between the mutation rate and 1.0 depending on the mutant's selective value and past history.
>
> Our discussion of mA versus (mA/4) is merely a quantitative disagreement and not a qualitative one. So
> I will coin a term I will call pA, which symbolizes the "real" mutation probability per trial for A. I would
> plug in a number mA for pA. You would plug in a number that is 1/4 that. But pA can still stand for the
> "real" probability of the 'event' (real presence of mutation A) per trial. That makes your equation now
>
> P(A) = 1 - (1-(mA/4))^(n*nGA)
 = 1 - (1-(mA/4))^n = 
 1 - (1-pA)^n
>
> In other words, your "derived" equation can be symbolized as
>
> P(A) = 1 - (1-pA)^n
>
> where P(A) is the probability of one or more A events in n trials.

> More generally,

> P(E) = 1 - (1-pE)^n
>
> Are you following this math so far? Do you agree with it?
>
> Now, what exactly does the term (1-pE)^n mean? (1-pE) is the probability of not-E per trial. And that
> makes (1-pE)^n the probability that *every* trial of the n trials done will come up as not-E. IOW, (1-
> pE)^n is the probability of seeing exactly zero 'events' in n 'trials'. Thus, 1 - (1-pE)^n = 1 - the
> probability of seeing exactly zero events in n trials = the probability of seeing one or more events in n
> trials, P(E).

>The above was your argument and I never had any problem with that argument.
>
> Now, if we had a way of directly determining the probability of exactly zero events in n trials, we could
> use that instead of (1-pE)^n, right? Well, *if* the above equation (your equation) is the same as the
> equation for one or more events from a binomial probability distribution, I should be able to show it.
> The mass probability function for a binomial distribution with the parameters n (total number of trials)
> and p (probability of the event per trial) is [n!/k!(n-k)!]*p^k((1-p)^(n-k)). k = the exact number of
> events being examined.
>
> http://en.wikipedia.org/wiki/Binomial_distribution
>
> Since we have shown above that your equation = 1 - the probability of seeing exactly zero events in n
> trials, that means that P(E) should = 1 - [n!/k!(n-k)!]*pE^k(1-pE)^n-k when k = 0 if we are looking at a
> binomial probability distribution. And, if I am correct that your 'derivation' is nothing but a binomial
> probability distribution, then when k = 0,
>
> 1 - [n!/k!(n-k)!]*pE^k(1-pE)^n-k = 1 - (1-pE)^n
>
> Now, since k! = 0! = 1, the [n!/k!(n-k)!] part above reduces to [n!/0!(n-0)!] = n!/n! = 1. Moreover p^0
> = 1 too.
>
> That reduces the left side of the equal sign to 1 - [1*1*(1-pE)^(n-0)] = 1 - (1-pE)^n
> That is:
>
> 1 - (1-pE)^n (your equation) = 1 - (1-pE)^n (binomial mass probability equation)
>
> The above sure looks like an equality to me. This demonstrates that what you derived in calculating the
> probability of there being one or more mutants in a population of size n is (drumroll please) nothing but
> the binomial probability distribution.
>
> Moreover, because "the binomial distribution converges towards the Poisson distribution as the number
>of trials goes to infinity while the product np remains fixed. Therefore the Poisson distribution with
> parameter λ = np can be used as an approximation to B(n, p) of the binomial distribution if n is
> sufficiently large and p is sufficiently small. According to two rules of thumb, this approximation is good > if n ≥ 20 and p ≤ 0.05, or if n ≥ 100 and np ≤ 10."
>
> That means that, assuming the above conditions are met, 1 - (1-pE)^n should also approximately equal 1 - the Poisson probability when k = 0.
>
> That is:
>
> http://en.wikipedia.org/wiki/Poisson_distribution
>
> 1 - (1-pE)^n should roughly equal [((p*n)^k)(e^(-p*n))]/k! when k = 0. I have switched the lambda in the equation (expected mean number of occurrences of E in n trials with p*n, which is the same thing).
>
> Because k! = 1 and (p*n)^k = 1 when k = 0, the Poisson in this case simplifies to e^-(p*n). Which
> means (again assuming that n ≥ 20 and p ≤ 0.05, or if n ≥ 100 and np ≤ 10, which it is in all the cases
> we have looked at) that
>
> 1-e^(np) =~ 1 - (1-pE)^n

> Remember that, by the form of this equation, n is the total number of individuals examined for mutant
> or not mutant state. 10^9 is a large number > 20. And p, in this case the mutation frequency, was
> 10^-8, which is certainly less than 0.05.

> Lately you have been making the absurd claim that n is not the number of trials. Instead, you claim that
> np (the mean number of mutants, given a population of n and mutant frequency of p) is the number of
> trials. Yet you have been accepting the idea that m, the mutation frequency (the frequency at which a
> mutation occurs), which is defined as observed # individuals that are mutants/total # of observed
> individuals (n) is 10^-8 (as it would be if you observed 10 mutants in 10^9 cells).
> Where do you divide the number of events by the number of trials if the the number of trials is 10?
> Which symbol in your equation represents the number of events per number of trials if the number of
> trials is 10?

> So, unless you can find something wrong with my math, stop pretending that your probability
> distribution is something different from the binomial probability distribution. It isn't. That you are not
> aware of that fact is your problem, not mine.
>
> At this point, let's talk about the equation you claim gives the joint probability or something. Your
> language is so muddled, it is hard to tell what you think you are saying.

> This is a direct quote from you:
>
> "And finally, the probability that mutation B will fall on a member of
the subpopulation with mutation A
> by the multiplication rule of
probabilities is:
> P(A)*P(B) = {1 - (1-(mA/4))^(n*nGA)} * {1 – ((1-(mB/4))^(nA*nGB)}
> 
This is the correct probability function for two point mutations A 
then mutation B occurring not
> simultaneously as a function of
population and subpopulation size and the number of generations for

> each event for given mutation rates."
>
> In actuality, the above is the multiplication of the binomial probability that there will be one or more A
> mutants in a population of total size n times the binomial probability
> there there will one or more B mutants in a population of total *size* nA, where nA is the number of
> individuals that have mutation A. Note that nowhere in this equation is there any requirement
> that the B mutations must actually occur in an *organism* that has an A mutation. Only that it occur in
> population of the same *size* as the population containing A. I strongly suspect that is not the equation
> you thought you were writing. I suspect you wanted to calculate the joint probability of *both* A and B > occurring in a single trial (that is, jointly in a single individual). That equation would be written
> (using the simplified terminology of binomial probability distributions:
>
> P(A,B) = 1 - (1-pA*pB)^n
>
> Note that this is just the general binomial probability distribution calculating the probability of one or
> more 'events' in n 'trials', P(E) = 1 - (1-pE)^n. The difference is that the 'event' is now the *joint*
> probability of both A and B being present per trial. The probability of that 'event' (the joint event) is
> pA*pB per trial, assuming that the A and B events are independent events.
>
> At this point, it is worth reminding you that pA and pB are not constants and are not always equal to the
> mutation probability to A or B from the non-mutant state. Again, the mutation probability is the
> *minimum* probability that a trial will have that mutant. *When* we directly select for cells that have
> both mutant state A and mutant state B *from* cells that were initially neither A nor B, the mutation
> probability is, in fact, a reasonable estimate of the probability that any given trial will have that mutant.
>
> However, if I first select for A mutants and grow up a population that is 100% A mutant, the mutation
> probability of A from not-A no longer holds. Instead the probability of A in that population is 1.0 per
> trial or close to it. That is, pA and pB are not constants but depend crucially on the past history of the
> organism.
>
> I would be interested in seeing how you deal with the above that shows that all you have derived is the
> binomial probability distribution. Please go through it step by step. The math isn't all that hard.
>
> [snip]

[hersheyh]

[snip]

> >> > With recombination, you add the possibility of lateral
> >> > transfer of a beneficial mutation but that event has probabilities
> >> > associated with this occurrence. So let s say your population of
> >> > animals starts accumulating beneficial mutations for your cold
> >> > environment. One member gets a mutation which gives thicker fur.
> >> > Another member gets a mutation which allows for fat storage, another
> >> > member gets a mutation that gives beneficial effects on metabolism,
> >> > another member gets a beneficial mutation which affects size giving a
> >> > better surface to volume ratio for the environment. There are any
> >> > number of mutations that are occurring throughout the population.
> >> Firstly, do you have any doubt that scenarios like this exist?
> >> How
> >> do you recombine all these traits into one descendent? Do the math.
> >Any organism which has *any* of those traits is selectively favored. *All* of those traits can
> > increase in parallel in frequency in the population relative to the w.t. organism with none.
> > Eventually some of them will be frequent enough to, after recombination, produce organisms with
> > more than one trait. That organism will now have two such traits and have a selective advantage
> > over organisms with only one.
> >Again, the frequency of such organisms can easily be determined by using a Punnet square.
>
> The Punnett square is used to compute the outcome from a breeding
> program not random recombination.

The logic is easily extended to a randomly breeding sexually-reproducing population. I have shown you how to do it. If you look at a randomly breeding sexually-reproducing population, looking at a single gene with alternate alleles A and a, with A being at frequency p in the population and allele a being at frequency q in the population, the frequency of genotypes in the diploid population (p + q = 1) will be a^2AA + 2pq Aa + q^2 aa = 1. If you have three alleles of the same gene, the logic is easily extended to include that. Think p + q + r = 1

If you look at two unlinked genes, each with a two alternate alleles -- say A and a for one and B and b for the other. And the frequency of A = p, a = q, B = s, and b = t and under the assumption of random mating in the population, the gametes produced will be in the ratio ps A;B, pt A;b, qs a;B, qt a;b. ps+pt+qs+qt = 1 Using the Punnet square with these ratios, you can determine the expected *frequency* of individuals that will be a;b/a;b in the population. It will be qt^2. For A;B/A;B individuals it will be ps^2. For A;B/a;b and A;b/a:B (both types of double heterozygotes), it will be 4(pt*qs). And so forth. I will leave the calculations of the exact frequencies to you. You should get a 1:1:1:1:1:1:2:2:2:4 ratio of types. You may consider this a "breeding experiment" involving the entire population in random breeding, if that makes you happier.

> And you keep making the claim that
> “traits” can increase in parallel. Give us a real, measurable and
> repeatable example where that happens with the mutation and selection
> process, not your ever present hypothetical examples.

Rather, why don't you explain, mathematically, why only one mutation can increase in frequency if you have two mutations (in different individuals) that are both more reproductively fit than the w.t. in a particular environment? Assume that both are equally fit over the w.t. individuals. Selection, to remind you, is NOT a stochastic process. It is a directional process. Why do you think that only one of these beneficial mutations will increase in frequency?

[snip]

[William Morse]

Granting your being correct in your malpractice case, you still appear
to be incorrect with your statements here.

>> Note: I wouldn't want to cut off all such claims -- there is more
>> than enough medical incompetence going around that the medical
>> profession itself seems unwilling or unable to control internally.
>> Still, a little common sense in throwing out really frivolous claims
>> would be in order. People do get worse and die for mysterious reasons
>> and, often enough, for no known reason. Doctors can't stop it, merely
>> stem the tide.
> And if you want to stem the tide of drug resistant microbes, learn the
> empirical lesson taught by the use of combination therapy for HIV and
> the mathematical lesson I am giving you evolutionists now. And you
> evolutionists need to start teaching the basic science and mathematics
> of the mutation and selection phenomenon correctly despite the

> questions it will raise in the minds of naïve school children about

> the theory of evolution. Or is that what you fear? Do you fear anyone
> who would question your mathematically irrational beliefs?

Combination antibiotic therapies have in fact been tried, with mixed
results. You might also want to take a look at the article on page 1713
of the 23 September Science magazine. Regardless of whatever you think
your mathematics leads to, if it doesn't conform to observed data it is
wrong.

[Alan Kleinman MD PhD]

On Sep 23, 12:30�pm, John Harshman <jharsh...@pacbell.net> wrote:
> hersheyh wrote:

> > On Tuesday, September 20, 2011 2:42:19 PM UTC-4, Alan Kleinman MD PhD wrote:
> >>> It's really quite simple. Given various simple assumptions, such as
> >>> independent assortment, panmixis, a constant population, and frequencies
> >>> p and q for the two alleles, the expected frequency of AB individuals is
> >>> just pq. As p and q increase, pq increases. We have already specified
> >>> that p and q are increasing. If AB phenotypes are favored over A, B, and
> >>> "wild type" phenotypes, p and q will increase faster than they would in
> >>> the absence of that advantage.
>
> > John is possibly falsely thinking that you were talking about
> > eucaryotic recombination involving organisms with a meiotic cycle and
> > also are thinking of A and B as alternate alleles of the same gene.

> > I think you are probably thinking of A and B as different *genes*

> > rather than alleles of the same gene. �But it is hard to tell what

> > you mean since you have *repeatedly* refused to clarify what you
> > mean. �Probably because you don't understand the criticisms, in this
> > case don't know the difference between "allele" and "gene locus" and
> > "nt site".
>

> No, John is possibly falsely thinking that he was talking about
> eukaryotic recombination with A and B as alleles at two unlinked loci.- Hide quoted text -

>
> - Show quoted text -

That�s the random recombination probability function you can�t derive.

[Alan Kleinman MD PhD]

On Sep 23, 3:35�pm, hersheyh <hershe...@yahoo.com> wrote:
> On Wednesday, September 21, 2011 7:27:54 PM UTC-4, Alan Kleinman MD PhD wrote:
> [snip]
>
>
>
>
>
> > hersheyh �Aug 24, 12:59 pm
> > >> On Jul 22, 9:18 pm, hersheyh <her...@yahoo.com> wrote:
> > >> > The figure here
> > >> >http://www.google.com/url?sa=D&q=http://en.wikipedia.org/wiki/File:Ra...
> > >> > which can be found in this article
> > >> >http://www.google.com/url?sa=D&q=http://en.wikipedia.org/wiki/Genetic...
> > >> > shows the relationship between fixation of one of two alleles at a
> > >> > single gene locus that started out at 50% in a population and the size
> > >> > of the population. For populations of size 20, it is very clear that
> > >> > completely random variation from generation to generation can lead to
> > >> > fixation of one or the other allele rather quickly. For larger
> > >> > populations, the neutral drift away from the starting point is slower,
> > >> > but is still significant after a mere 50 generations. What this graph
> > >> > does not show is that the probability of mutation per generation also
> > >> > increases with population size. We have gone thru that math several
> > >> > times, and each time you have ignored it because you don't understand
> > >> > it. Why would it be any different this time?
> > >> I ve read this page previously. Your gross over-extrapolation of this
> > >> mathematics demonstrates your evolutionist bias.
>
> So tell us why the math is a "gross over-extrapolation" due to "evolutionist bias".

It�s very simple to see your �gross over-extrapolation� and
�evolutionist bias�. You take a mathematical model of a single gene
with two neutral alleles and the random probability that one of the
two alleles being fixed and then claim that tens of millions of
neutral alleles can be randomly fixed simultaneously. John Harshman
likens it to the dealing of a bridge hand randomly from a deck of
cards. The probability of any particular bridge hand being dealt is
vanishingly small but those hands are dealt when the game is played.
But if you are going to do this analogy, what John is claiming is that
hundreds of millions or billions of card players are each dealt 30
cards randomly from a deck that contains an astronomical number of
cards and after 500,000 generations without selection, you end up with
generations that have billions of card players with tens of millions
of identical cards in their hands. Random mutation without selection
is not going to put tens of millions of identical neutral mutations
into the genomes of millions of members of a population in 500,000
generations or any number of generations you want to use in your
calculations.

>
> > >So, exactly what is wrong with the math, mathematically? �Is it the statement that the probability of
> > > a neutral mutation that has just occurred at a nt site becoming fixed in a population = 1/(2Ne),
> > > where Ne is the effective population size? �Is it the statement that the probability of a mutation at
> > > that nt site occurring being 2Ne*u, where u is the mutation rate for that site (again, assuming
> > > selective neutrality or near neutrality)? �Are you claiming that there are not 3 X 10^9 nt sites in
> > >the haploid human genome? �Are you claiming that the vast majority of those sites are selectively
> > > crucial (a statement that is contrary to evidence since the mean mutation rate for point mutation is
> > > around 10^-8), or do you agree that most mutation is selectively neutral?
> > There is nothing wrong with the mathematics. What is wrong is your
> > extrapolation of this mathematics to multiple neutral mutations
> > simultaneously being fixed in the population.
>
> So, are you saying, then, that there is nothing wrong with the calculation that the probability of fixation �per nt site is u, the mutation rate? �That your problem then comes from the multiplication of the probability of fixation per nt site by the total number of nt sites per haploid genome to get the rate of fixation per generation per haploid genome? �Exactly how is that mathematically wrong or an extrapolation? �The terms do come out to give the rate of fixation per generation per haploid genome, don't they? �It is no different from saying that if the probability of a 6 per roll is 1/6, in 600 independent rolls I would expect to see 100 6's. �Or saying, if I line up 100 coins and the odds of heads is 1/2 per coin flip, that I would expect, over all 100 coins flipped to see 50 heads. �Are those irrational mathematical extrapolations?
>

What I am saying is that your model is not a good model of reality.
You are trying to take a special case of a single gene with only two
neutral alleles and generalize this to situations where you actually
have multiple alleles at a single gene loci and furthermore claiming
that this random process will happen simultaneously at multiple
different gene loci simultaneously and with each gene loci having its
multiple neutral alleles. This is the gross over-extrapolation that
you are doing with this model. Now I�m going to help you with your
argument but I don�t believe it will be sufficient to make your theory
of evolution mathematically rational. Neutral evolution needs
selection but the selection comes from the selection of beneficial
alleles. Charles Brenner alluded to the concept. He brought up the
term �bottleneck�. When a population is subject to selection, not
only are the beneficial alleles amplified over generations but so are
any of the neutral alleles that the subpopulation with beneficial
allele happens to be carrying. That�s how you can achieve
amplification of neutral alleles.

> > You have this enormous
> > mathematical blind spot in your thinking. You somehow throw out the

> > multiplication rule of probabilities for computing the joint

> > probability of multiple independent events for every stochastic
> > process you see fit. This is not mathematically based science you are
> > practicing. This is evolutionist mathematical irrationality.
>
> Exactly where, in the above, did I "throw out the multiplication rule of probabilities" or use it incorrectly? �Are you claiming that, if the probability of heads per coin flip is 1/2, that if I flip a hundred coins I should multiply the probability of heads in each coin flip together to get (1/2)^100? �Is that what you think the *correct* use of the multiplication rule implies? �It sure seems like you are claiming that the *correct* use of the multiplication rule in the above equations would involve u^3000000000, that is, multiplying the probability of fixation per nt by itself 3 billion times. �Again, that would be like claiming that the probability of getting heads in flips in 100 coins is (1/2)^100.
>

Study the probability function that I derived for you which shows how
two mutations will show up on a single descendent. That probability
function shows how the multiplication rule comes into play and that in
order for the two mutations to have a reasonable probability of
appearing on a descendent that selection (amplification) must come
into play in order for there to be a reasonable probability that the
two events will occur. Amplification is what changes the probability
of events in the mutation and selection phenomenon and when you claim
that you can get tens of millions of neutral mutations to amplify
without the benefit of selection, your thinking becomes mathematically
irrational.

> > What I am saying is that whether the genetic differences are selective
> > or neutral makes no real difference in the mathematics of evolution.
> > Let all the genetic differences between humans and chimpanzees be
> > selective which gives the most rapid fixation of mutations. You are
> > still no where close to being able to do the mathematical accounting
> > for these differences in 500,000 generations.
>
> Show your math here: �Ooops. �All we get is your WAG.
>

I can easily show how the probability function I derived for two
mutations can be extended to any number of mutations you want. And I
have presented empirical examples which demonstrate this mathematical
behavior. You on the other hand give us an unrealistic simplification
and no empirical examples. Your mathematical skills are limited to
plugging number into the Poisson distribution (the wrong probability
distribution to describe mutation and selection) and using the Punnett
square to describe recombination. The probability function for random
recombination is not hard to derive if you know the basics of
probability theory but apparently evolutionists don�t even know the
basics of probability theory.

>
>
>
>
> > You can be as derisive
> > as possible but that will not give you any scientific or mathematical
> > evidence to support your mathematically irrational belief system and
> > in the meantime you have bungled the basic science and mathematics of
> > the mutation and selection phenomenon and harmed millions of people in
> > the process.
>
> > >> You try to take this
> > >> model and impose the results derived on John Harshman s 40,000,000
> > >> differences between human and chimpanzee genomes.
> > >Quite successfully.
> > If you want to call it a mathematically irrational extrapolation that
> > throws out the multiplication rule of probabilities for the joint
> > probabilities of multiple independent events for a stochastic process,
> > it�s a perfect fit for your mathematically irrational belief system.
>
> > >> On average, to
> > >> account for these differences requires the fixation of dozens of
> > >> neutral mutations generation after generation for hundreds of
> > >> thousands of generations.
> > >Yes. �But fixation is actually a fuzzy boundary when you have a population of 6 billion people because that size almost >guarantees new point mutation at every site. �Basically, all that is required for fixation is that the last step from Ne-1 (or >several) individuals having an originally new mutant allele that was first acquired long ago become Ne - 0 by loss of the >few individuals having the original w.t. allele. �When you look at the chimp compared to human genome and the time >available since last divergence, the amount of difference seen is that expected if most of the genome is selectively >neutral. �That is, the mathematics appears to work in the real world under the assumption that most of the nt's in the >human and chimp genome are selectively neutral (any of the 4 possibilities will have the same functional effect). �We >*know* that not all the sequence differences are due to drift (the slowest mechanism for producing a difference). �Some >(small) fraction of difference is of selective impor

ta
>
> nc
>
>
>
> > e.
> > Hersheyh, you play fast and loose with population sizes. Do you think
> > that five million years ago there was a population of 6 billion
> > progenitors?
>
> Not at all. �In fact, the best estimate is that during most of its existence, human populations were closer to 10,000 individuals. �But I was just commenting on the difficulty of defining "fixation" in a large population. �I wasn't using the number 6 billion anywhere in any equation. �Can you possibly try to read for comprehension?
>

You have just sealed the mathematical irrationality of your theory of
evolution. What happens to your mathematics of mutation and selection
when you have a population of 10^4? How do you get two beneficial
mutations to show up on a descendent? What happens to your
probabilities of a single beneficial mutation occurring? Can you
possibly do your mathematics more irrationally?

> > This is why your analysis is a crock of hot steaming bs.
> > Why don�t you try doing the analysis of the fixation of two neutral
> > mutations in a similar manner as the fixation of a single neutral
> > mutation and present the algebra to us? Oh, I forgot, all you know how
> > to do is blah, blah, blah and plug in numbers in the wrong probability
> > distribution.
>
> No probability distribution. �But if I correctly calculated the probability of fixation for a single nt site, the probability for fixation in one of two nt sites would be twice the probability of fixation for a single nt site. �I am not interested in the probability that both of the two nts have a fixation. �I am interested in how many fixation events there will be if I look at N nts. �That is equivalent to asking the probability of getting a six in six flips of the dice. �That answer is one, and that is an answer to a different question than asking the probability of getting a six in all six flips of the dice, which is the question you are asking. �The mathematical answer to the first is (1/6)(probability of a six per flip)*6(number of flips) = 1 six per six flips. �The mathematical answer to the second is (1/6)^6 = 0.0000214 the probability that 6 flips will give a 6 every time.
>

So you believe the probability of two random events occurring is
governed by the addition rule of probabilities? Let�s see what happens
when we continue with your mathematical irrationality. The probability
of fixation of two nt sites is twice the probability of a single nt
site. So the probability of fixation of three nt sites will be three
times the probability of fixation of a single nt site and the
probability of fixing N nt sites is N times the probability of
fixation of a single nt site. If you keep this up, we can have
probabilities in the millions. Hersheyh, I don�t know how you could
have done this but you started this discussion with no understanding
of probability theory and now you actually know less than nothing
about the theory.

> > >> This drift model only takes into account the
> > >> fixation of one of two alleles as you describe above, not the fixation
> > >> of dozens of neutral alleles every generation and when in reality, you
> > >> have more than two possible alleles at a single locus.
>
> It is just correctly multiplying the probability of an event per trial times the number of trials to get the expected mean number per that many trials. �Like multiplying the probability of a 6 per dice throw by the number of dice throws to get the expected mean number of 6's in that larger number of throws.
>

The joint probability of multiple independent events is not governed
by the addition rule of probabilities; it is governed by the
multiplication rule.

>
>
> > >We are talking about point mutational changes in nt's, not alleles or alternate forms of genes. �Learn
> > > the meaning of genetic terminology, why don't you -- at least before you say more ignorant things? �
> > > In most genes (say, a coding sequence for a 300 aa protein, thus 900 nt), neutral drift is 1) less
> > > likely since the protein must function and there is more constraint on nt sequences, 2) when it
> > > occurs, is more likely to be a point mutation that does not change the aa sequence encoded, 3)
> > > when an aa is changed by neutral fixation, it will tend to be similar in characteristics (e.g.,
> > >hydrophobicity) or in an unnecessary part of the protein, 4) will, given the time of divergence
> > > between chimps and humans, produce an average of somewhat less than one aa change per
> > > average
>
> ...
>
> read more �- Hide quoted text -
>
> - Show quoted text -- Hide quoted text -
>
> - Show quoted text -- Hide quoted text -

[Alan Kleinman MD PhD]

On Sep 24, 11:12 am, hersheyh <hershe...@yahoo.com> wrote:
> On Friday, September 23, 2011 3:45:07 PM UTC-4, Alan Kleinman MD PhD wrote:> The following are a compilation of responses to posts 926-950
> > presented in this manner to prevent splinter threads.
>
> > hersheyh  Aug 26, 8:53 am

> > Newsgroups: talk.origins
> > From: hersheyh <hers...@yahoo.com>

> > Date: Fri, 26 Aug 2011 08:53:04 -0700 (PDT)
> > Local: Fri, Aug 26 2011 8:53 am

> > Subject: Re: The Theory of Evolution is Mathematically Irrational
> > Round 2
>
> [snip]
>

> > >> What a surprising piece of wisdom an evolutionist crank is coming
> > >> forth with. Single drug therapy for HIV leads to rapid selection of
> > >> drug resistance. Who would have guessed this?
> > >Every single virologist and evolutionary biologist would have guessed this.  I certainly would have.  
> > > Based on my understanding of mutation and selection and my understanding of how toxic agents
> > > work (by interacting with and interfering with some normal biologic function).
>
> > This was not mainstream thinking before the 1990s when HIV hit. Read
> > the literature from the 1990s about the treatment of HIV and the use
> > of combination therapy. There was a lot of debate for and against.
>
> As, of course, there should have been.  Not every type of combination therapy will work without too much toxicity to the patients.  Sometimes the cure can indeed be worse than the disease.  Note that there was *debate for and against*, not uniform claims from the scientific community that "combination therapy cannot work".

Of course medicines have toxicities and of course there was debate but
ultimately it required combination selection pressures to stifle the
evolution of HIV and combination selection pressures stifle the
mutation and selection process in every real, measurable and
repeatable example of mutation and selection. There is absolutely no
empirical evidence that mutation and selection can occur in parallel
with any efficiency.

>
> > However, if virologists and evolutionary biologists had read Edward
> > Tatum’s 1958 Nobel Laureate lecture, and understood what he was saying
> > about using combination therapy, the debate would have been much
> > shorter.
>
> Tatum was a biologist and a geneticist.  He was also, as any competent biologist is, fully accepting of evolution.
>

Tatum understood the effects of the multiplication rule of
probabilities and what it would do to the mutation and selection
process. And now you are not only a mind reader, you can read the mind
of the dead. I wonder if Tatum would believe that the addition rule of
probabilities is the governing rule of the joint probability of events
occurring as you claim?

>
>
> > >> I suppose the next thing
> > >> you are going to tell us is that combination therapy suppresses the
> > >> mutation and selection process.
> > >Of course it does, as any biologist would have told you.  But in the early days of antivirals directed
> > >against HIV -- when only AZT was available, there was no choice but to use single-gene therapy.  
> > > The other option was to intentionally not treat patients.  When other antivirals came on-line, they
> > > were used.  The initial 'other antivirals' were also anti-reverse transcriptases, so there was a
> > > possibility of cross-interaction (non-independence) of action, which would render combination
> > > therapy much less useful.
> > That’s a line of crap and you know it.
>
> No.  It is the truth.  It is your interpretation of HIV/AIDS treatment history that is crap.  The full recognition that AIDS was due to a virus didn't occur until after 1984.  But as the virus was a retrovirus and there was no good way to screen for it on a commercial scale early on, it wasn't clear that the virus was replicating between infection and the onset of immune deficiency syndrome.  AZT clinical trials did not start until 1986.
>
> The results of ACTG019, a trial, using AZT, still the only drug available and an extremely expensive drug at that, about *when* to start treating patients, before or only after they exhibit symptoms of AIDS were announced in 1989.  It showed that using AZT early slowed progression to AIDS.  But cost was still a factor.  It is only in 1999 that a second drug, ddI, also a reverse transcriptase inhibitor, became available.
>
> At this point, in the early 1990s, it was still unclear what the best way to treat patients was.  Do you wait until they show symptoms of disease?  Do you treat with AZT early and hope for some other drug that will be useful latter?  In 1991, we see the introduction of a third reverse transcriptase inhibitor, ddC.  Now, *because* all three available drugs attack the same enzyme, it is not at all clear that they would have additive effects.  That is, if you treat with AZT *and* ddI, you may not get much additional inhibitory effect from the ddI.  In that case, it might indeed be better to use one of the reverse transcriptase inhibitors until resistance to that builds up and then switch to the second.  That is because the two drugs may not have *independent* effects and combining them might have no positive effect and could have negative effects.
>
> In 1992, the FDA approved the use of ddC *and* AZT for advanced patients with advanced HIV who were continuing to show signs of clinical or immunological deterioration.  So, the idea of using drugs in combination was not something biologists did not think of.  In fact, given that ddC was just introduced in 1991, trials using the drugs as *possible* combination therapy started almost immediately.  As in most trials, the initial population tested were those in which current therapy was ineffective.
>
> The *real* argument about therapy (I am ignoring the idiotic claims of HIV/AIDS denialists and religious extremists who prevented good public health ideas like teaching condom use and having needle exchanges) in the early 1990s was not so much about combination therapy as it was about *when* to start treating with these then very expensive drugs (although cost was certainly a factor).  Do you only start treatment when you start to see clinical effects or do you start treatment when a person is classified as HIV+, but is otherwise healthy?
>
> The initial discovery of the *spread* of AZT-resistant HIV was in early 1993.  Also, in 1993, preliminary results from a clinical trial of AZT indicated that it was NOT useful therapy for patients without clinical symptoms.  Again, the real argument in the early 1990s was about *when* to start treating, not whether combination therapy (again all the drugs available, most introduced less than 1-2 years ago, were reverse transcriptase inhibitors and, without trials, one could not predict that combination therapy would be better, worse, or of the same effectiveness).
>
> In 1993, a number of *trials* were underway comparing the effectiveness of AZT alone or in combination with ddI and ddC.  Again, because these drugs act on the same enzyme, it is not necessarily the case that combination therapy would be significantly more effective than serial use of the drugs.  Hence trials to actually test whether combination therapy works.
>
> The first protease inhibitor. saquinavir, was approved in 1995.  This would be the first drug that could reasonably be used in combination therapy and which we would *know* would likely be acting independently to the reverse transcriptase inhibitors.  But you still need to run *trials* to see if there would be any unforeseen interactions.
>
> In 1996, the first drug that was a non-nucleoside reverse transcriptase inhibitor was approved (Viramune -- nevirapine).  And it is only now that we see the introduction of the viral load test, which is used to provide information about the risk of disease progression.  And it is only now that you start seeing real optimism about treatment, especially in people taking combination therapy.  That was THE excitement in 1996.  But such combination therapies, again combination therapy was being used almost as soon as one had two drugs to combine in such therapy, still needed to be fully vetted by future work.  What combinations worked best?  Had the least side effects?  Were less expensive so that these treatments might be used in communities with high rates of infection -- Africa, Asia, IV drug users, sex workers -- that don't have the resources of the wealthy?  Again, should treatment start early in HIV infection or should one wait for symptoms?  At that time, these questions still had no answers.
>
> By spring 1997, the use of combination therapy was having its expected (by evolutionary biologists) effects and we were seeing declines in deaths, declines in children born with HIV, but were also seeing some of the early detrimental consequences of combination therapy:  unpleasant and sometimes serious side effects and resistance, even when 3 antivirals were being taken (mostly because of complex schedules with many pills needed each day leading to less than stellar adherence by patients.  Note to the Dr. Dr.:  this failure of adherence would lead to viruses resistant not just to one antiviral, but to three, despite your claims that this would be "mathematically irrational".
>
> But, still, there was argument about *when* to start treatment (with the U.S. doctors being more likely to start treatment upon HIV identification and U.K. doctors only when symptoms start).  The hope of the U.S. strategy of "hit early, hit hard" was that HIV could be totally eradicated.  They found that it could not be eradicated, but the strategy had important public health effects by reducing the probability of spread of the virus to others.  But that determination was still for the future.
>
> In 1998, patients taking combination therapy (now the standard treatment) were showing signs of long term effects like lipodystrophy (fat redistribution) that might be indicators of long-term safety issues.  By this time it was clear that *single drug therapy* with AZT (administered to the mother before birth), combined with Cesarian birth, could drastically reduce mother to child transmission to less than 1%.  AZT was becoming significantly cheaper at this time.
>
> In 1999, we start to trace the *evolutionary history* of the HIV-1 virus from its origin in chimpanzees to humans.  Nevirapine, in a single dose, is also found to be an affordable and effective block to mother-child transmission.
>
> In 2003, a new class of drugs that prevent fusion of the virus with cell membranes (Fuzeon, enfuvirtide, T-20) became available.  Unfortunately it can only be administered by injection and thus is given primarily in combination therapy to patients who have become resistant to other drugs.
>
> Since that time, the main changes in treatment has been finding out which kinds of combination therapy work best and have the ...
>

Why don’t you read the interview with the scientist credited with
developing combination therapy?
http://www.pbs.org/wgbh/pages/frontline/aids/interviews/ho.html
"In 1994, Dr. David Ho discovered that what was then thought of as a
latency phase -- when a person was infected with HIV but not
experiencing any symptoms -- was in fact a period of continuous
onslaught, in which the virus and the immune system are engaged in a
pitched battle. Once he was able to measure the amount of virus in the
blood, he learned that in fact billions of HIV particles were being
produced every day. This breakthrough allowed Ho and his collaborators
to come up with the idea for combination therapy -- treating a person
with several drugs at once to suppress the virus down to undetectable
levels. Patients near death rebounded dramatically after beginning
what was called "triple cocktail" therapy, and Ho was named Time
magazine's "Man of the Year" in 1996 for his work. In this wide-
ranging interview, Ho recounts his breakthrough discoveries and his
battles against the virus over the years. He also talks about the
implications of combination therapy on the future of the epidemic and
the importance of prevention efforts. "We have to bear in mind that
during the years where this concerted treatment effort took place,
approximately 2 million were treated. But during those years, another
15 million or so got newly infected." Currently Ho is executive
director of the Aaron Diamond AIDS Research Center, where he is
working on potential vaccine approaches, which he also discusses here.
This transcript is drawn from four interviews conducted in New York
and China in April and June 2005, and March 2006. "

And in the Ho interview:

"The consequence of that obviously is central to thinking about how
HIV destroys the immune system, but also it has great ramifications
for therapy, because HIV is an error-prone virus. As it replicates it
makes mistakes. Now, that may not be all bad, because mistakes allow
HIV to generate new variants, some of which will allow it to survive
in the presence of drugs, survive in the presence of immune attack, so
that's actually an advantage to HIV. When we know how much virus
replication is going on and we know the error rate with which the
virus makes mistakes, then we could begin to calculate what HIV would
do if we applied drug pressure, and from those type of calculations
came to the conclusion that it's inevitable for HIV to develop drug
resistance if you give it one drug at a time. However, if you start to
combine the drugs and try to force the virus into a corner using
multiple drugs, it is exceedingly difficult or statistically
improbable for HIV to become resistant to all the drugs
simultaneously. That for us formed the foundation of thinking about
combination therapy. "

David Ho was made Time Magazine “Man of the Year” for rediscovering
what Edward Tatum said more than thirty years earlier. The failure of
evolutionists to properly teach how the mutation and selection sorting
process actually works has and continues to contribute to the
premature death of millions of people suffering from diseases subject
to mutation and selection phenomenon. This same blunder to understand
immediately that HIV needed to be treated with combination therapy to
stifle evolution by the mutation and selection sorting/optimization
process is being repeated today with Tamiflu and the influenza virus.
This very useful anti-influenza medicine is already being dissipated
by using this medicine as monotherapy and resistance is already
appearing. The blunder of using monotherapy not only did not give any
long term survival benefit to people suffering from HIV, it introduce
huge number of resistant viruses into the gene pool making it far more
difficult to find effective combination therapy.

Evolutionists are in complete denial of how the mutation and selection
sorting/optimization process actually works and their dominance in the
field of biology prevents the proper teaching of the basic science and
mathematics of this phenomenon. Instead, evolutionists would rather
indoctrinate naïve school children with irrational and illogical
speculations.

Hersheyh, you can attempt to rewrite history to try to mitigate the
evolutionist culpability for the harm done to people by your failure
to describe how mutation and selection actually works but the truth of
your scientific failure and blunders are too great to obscure.


> read more »

[Alan Kleinman MD PhD]

On Sep 24, 6:32 am, "Robert Carnegie: Fnord: cc talk-
orig...@moderators.isc.org" <rja.carne...@excite.com> wrote:

> On Sep 23, 4:13 pm, "Steven L." <sdlit...@earthlink.net> wrote:
>
>
>
>
>
> > "r norman" <r_s_nor...@comcast.net> wrote in message
>
> >news:46l777pqufop933rv...@4ax.com:
>

> > Maybe Dr. Kleinman, M.D., can't deal with the fact that it's *doctors*
> > (and patients), not evolutionists, who bear such responsibility for the
> > rise of antibiotic-resistant bacteria.  
>

> And farmers.  Feeding antibiotics labelled as "growth promoters" to
> meat animals and thereby depriving human beings of their use as
> effective cures is extremely wicked, in my opinion.

Welcome to the discussion Robert. The cattle ranchers I know do not
feed antibiotics to their cattle as “growth promoters” since these
ranchers run their cattle on range lands and primarily feed their
animals grass. Perhaps you are not aware that ruminants require
bacteria in their guts to digest cellulose since mammals do not have
the enzymes necessary to decompose cellulose. Now perhaps there are
cattlemen who do use antibiotics on there cattle when they feed their
animals starch such as corn and grain for which their animals do have
the necessary enzymes to digest these chains of sugar molecules. I
understand the logic of these cattlemen that they don’t want to share
the feed resources for their cattle with bacteria and I understand
your argument that the use of antibiotic selection pressures like this
will lead to drug resistance. On one hand you have cattlemen who want
to produce protein less expensively and on the other hand you don’t
want to squander antibiotic resources.

I think the term “wicked” is too strong for this behavior. One of the
key reasons we have an increasing lifespan and a more healthy
population is the easy and generally inexpensive access to nutritious
food. A good functioning immune system requires energy and the farmers
and ranchers in our society I think do a good job providing that
service to us. If your concern is the wide spread use of antibiotics
in cattle feed will select for resistant antibiotics and deprive
humans of there treatments for infection then don’t use the
antibiotics as single selection pressures because there is already
abundant evidence that combination selection pressures stifles the
mutation and selection process.

Perhaps you want to argue that farmers should not use herbicides or
pesticides in their production of food because it will cause the
selection of resistance for these chemicals? I think if you did call
for this and these decisions were forced on farmers then the cost for
food would go up and it would foment societal unrest. I think
selection pressures should be used wisely based on a good scientific
understanding of the mutation and selection phenomenon and the costs
and benefits of using these chemicals be weighed based on sound
mathematical logic. You won’t get this sound mathematical logic from
the evolutionist teachings of how mutation and selection works.

>
> I gather that the very first patient treated with penicillin got an
> inadequate dose - as much as they could manufacture of it - and he
> ended up with a thriving and fatal infection of resistant microbes,
> and died.  So then it's not a big secret.

Certainly intensity of selection is important when understanding how
selection works. When treating infection, you always want to try to
put adequate pressure on the microbial population and drive that
population to extinction and the quicker you do that to the microbial
population, the better for the welfare of the patient. In the case of
HIV, you can not drive the population to extinction but you can
suppress the viral population sufficiently that sufferers of the
disease can survive for decades. What should be clear by now in this
discussion is that multiple selection pressures do not help
populations evolve to these pressures simultaneously. What multiple
selection pressures do to a population is drive the populations down
more than a single selection pressure would and then force the
population to get multiple beneficial mutations simultaneously in
order to evolve to these simultaneous selection pressures. The
multiplication rule of probabilities shows that the occurrences of
these events is a low probability occurrence, that’s why combination
therapy works for HIV and for every other mutating and selecting
population that it is tried on.
>
> The modern problem arises from drug companies that want doctors to
> prescribe one product, theirs.  Not a combination.  Somewhat
> corrective to this is seeing House, M.D., on television prescribing
> several pills at once for diseases that the semi-diagnosed patient may
> be dying of, possibly simultaneously, but the episodes I've seen (till
> about series four) still tend to be one treatment for one disease.

There are already combination antibiotics out there; one of the oldest
is Trimethoprim-Sulfamethoxazole. This has been a very successful
antibiotic and continues to be despite a period when resistance to
this drug was high. Its use fell out of favor for a while and the
resistance disappeared. It didn’t take legislation to make doctors
stop using this drug. They stopped because it wasn’t working. So when
the wide spread use of sulfa drugs died out for a decade or so, the
resistant microbial populations evolved back to their wild strains and
this combination drug again became useful again. Of course drug
companies want you to buy their products just like google want people
to buy their product. You just have to be a discerning buyer. And when
google posts essays like Edward Max’s irrational claims about mutation
and selection, you have to decide what is correct or not. I’ve watched
a couple episodes of House over the years and thought it was a silly
program. You will learn about as much about the practice of medicine
from watching an episode of House as going to an evolutionist lecture
on how mutation and selection works.

[Alan Kleinman MD PhD]

On Sep 24, 2:08�pm, hersheyh <hershe...@yahoo.com> wrote:
> On Friday, September 23, 2011 3:45:07 PM UTC-4, Alan Kleinman MD PhD wrote:
>
> > The following are a compilation of responses to posts 926-950
> > presented in this manner to prevent splinter threads.
>

> > hersheyh �Aug 26, 8:53 am

> > Newsgroups: talk.origins
> > From: hersheyh <hers...@yahoo.com>
> > Date: Fri, 26 Aug 2011 08:53:04 -0700 (PDT)
> > Local: Fri, Aug 26 2011 8:53 am
> > Subject: Re: The Theory of Evolution is Mathematically Irrational
> > Round 2
>

> > On Friday, August 26, 2011 9:29:16 AM UTC-4, Alan Kleinman MD PhD
> > wrote:
> > > On Jul 26, 12:06 pm, hersheyh <her...@yahoo.com> wrote:
>
> [snip]
>
> > >> And then I suppose you are going to
> > >> tell us these are unnatural selection pressures
> > >They are. �Population-wide (in this case, the infected individual) instantaneous appearance of large
> > > amount of toxic compounds are novel selection pressures that typically are artificially introduced
> > > by humans for their purposes.
>
> > Oh, I see, no populations ever went extinct until humans came along.
>
> Irrelevant since I did not say that. �
>
> > There was just single targeted selection pressures in nature targeting
> > one gene at a time and �poof� reptiles transformed into birds.
>
> It is your myth that selection can only target one gene at a time. �Selection in procaryotes and viruses, because those organisms are most often clonal in nature, does require either serial selection for changes to accumulate in a single organism or that there either be a gene exchange event of the type seen occasionally in procaryotes and viruses. �Selection in eucaryotes is greatly speeded up by the fact that these organisms engage in recombination every generation. �But in both cases, there is nothing preventing the selection at more than one locus at a time. �It is just that in the procaryotic and viral cases, there is not a regular mechanism for introducing the two genes into the same organism.

You are on the road to making another mathematical and scientific
blunder. Do you think that combination herbicides and pesticides are
being applied to viruses and prokaryotes? These selection pressures
are being applied to eukaryotes which regularly do recombination. And
they demonstrate the same mathematical behavior as does the viral and
prokaryotic examples. Do you want me to repost these empirical
examples for you? And you have yet to provide us with the probability
function which describes random recombination. You are still working
with your century old Punnett square. Your lecture notes must be old
and frayed.

>
> > > This is
> > the mathematically and empirically irrational crap that forms the
> > basis of evolutionism.
>
> You keep claiming that evolution is mathematically irrational, yet you are the one presenting mathematical garbage and calling it a "derivation" of the "correct probability distribution".

How would you know what the correct probability distribution for the
mutation and selection phenomenon is? You use the Poisson distribution
without ever going through the derivation of the equation and I have
shown you previously why it not even a good approximation for the
phenomenon. And now you are using the addition rule of probabilities
to compute the joint probability of events. There�s enough methane gas
coming out of your brain to power a city.

>
[snip another of hersheyh�s hypothetical examples, still waiting for a
real measurable and repeatable example]

[Alan Kleinman MD PhD]

On Sep 24, 5:58�pm, Charles Brenner <cbren...@berkeley.edu> wrote:
> On Sep 24, 11:12�am, hersheyh <hershe...@yahoo.com> wrote:
>

> > > >�But in the early days of antivirals directed
> > > >against HIV...
>
> > At this point, in the early 1990s, it was still unclear ...
>
> Thanks, very good lecture. I enjoyed it.

Too bad hersheyh left out the part from the scientist credited with
developing combination therapy where he (David Ho) describes how he is
using the multiplication rule of probabilities to stifle the mutation
and selection process.

[Alan Kleinman MD PhD]

On Sep 27, 10:00�am, hersheyh <hershe...@yahoo.com> wrote:
> [snip]

>
>
>
>
>
>
>
> > On Friday, August 26, 2011 9:29:16 AM UTC-4, Alan Kleinman MD PhD
> > wrote:
> > > On Jul 26, 12:06 pm, hersheyh <her...@yahoo.com> wrote:

> > > > On Jul 25, 8:56 pm, Alan Kleinman MD PhD <kle...@sti.net> wrote:
> > > > > On Jun 19, 3:28 pm, hersheyh <her...@yahoo.com> wrote:> On Jun 13, 8:57 am, Alan Kleinman MD PhD <kle...@sti.net> wrote:
> > > > > > > On Jun 1, 12:57 pm, hersheyh <her...@yahoo.com> wrote:> On Jun 1, 10:33 am, Alan Kleinman MD PhD <kle...@sti.net> wrote:
> > [snip]
>
> > >> We understand the
> > >> evolutionist philosophy, which is blizzards turn lizards into buzzards
> > >> with gizzards.
> > >Lizards (specifically and relevantly, alligators and crocodiles, the closest living relatives to
> > > dinosaurs) have gizzards. �As, likely, did a number of plant-eating dinosaurs (based on gizzard
> > > stones found near their fossils; meat-eating birds, and >probably dinosaurs, also have gizzards,
> > > but don't often swallow stones and gizzards themselves don't fossilize). �So buzzards certainly
> > > inherited their gizzards from their lizard ancestors. �Blizzards have nothing to do with gizzards. �
> > >They may have something to do with the selective pressures for *feathers*, which initially (and still
> > > today) are often functionally >relevant as air- and heat-trapping insulation.
>
> > Well my, my, are you going to tell us that cold-blooded alligators and
> > crocodiles without feathers, wings or beaks are closely related to
> > birds because they have gizzards.
>
> Obviously taxonomy and anatomy are also not your strong points.
>
> No. Cold-blooded crocodilians and birds are the sole surving groups in the Division Archosauria, the group of diapsid amniotes (within the class Reptilia, which is where Aves should also be) that also included the now extinct dinosaurs and pterosaurs.

I�m so disappointed, I though crocodiles and ostriches were closely
related, after all they both have gizzards and that the missing link
was crocriches.

[snip evolutionist folklore]

[Alan Kleinman MD PhD]

On Sep 27, 3:46�pm, hersheyh <hershe...@yahoo.com> wrote:
> hersheyh �Aug 26, 12:53 pm

> Newsgroups: talk.origins
> From: hersheyh <hers...@yahoo.com>

> Date: Fri, 26 Aug 2011 12:53:47 -0700 (PDT)
> Local: Fri, Aug 26 2011 12:53 pm

> Subject: Re: The Theory of Evolution is Mathematically Irrational
> Round 2
>

> On Friday, August 26, 2011 9:33:02 AM UTC-4, Alan Kleinman MD PhD
> wrote:
> [snip]
>
> > >If you want evidence for parallel evolution in organisms that do engage in regular and frequent
> > > recombination (aka eucaryotes), pick any multigenic trait in a eucaryote (height, weight, fruit size,
> > > egg production, bristle number in Drosophila) where we use heritability to describe the results and > > follow selection in those cases. �There will be change in the trait until one hits the point where
>
> [snip]
>
> > >http://www.google.com/url?sa=D&q=http://www.ncbi.nlm.nih.gov/pmc/arti...
> > >http://www.google.com/url?sa=D&q=http://www.ncbi.nlm.nih.gov/pmc/arti...
> > >http://www.google.com/url?sa=D&q=http://www.ncbi.nlm.nih.gov/pmc/arti...
> > If you are trying to convince me that Chihuahuas and Great Danes can
> > be created by recombination, don�t waste my time because that�s all
> > you�ve demonstrated with these examples. Here�s a quote from your
> > first citation.
>
> Yet producing differences as large as that between Chihuahuas and Great Danes from *existing* variation in a population is exactly what can be accomplished by *recombination and selection* alone. �According to your so-called "mathematical" argument, the *only* way I should be able to generate the two breeds is by serial mutation and selection of one trait at a time. �I am well aware of the fact that all genetic variation starts as mutation.

So is your claim now that you can transform reptiles into birds by a
breeding program? All you can do with a breeding program is change the
expression of existing genes and this only works properly with
homologous members of a population. Evolutionists gloss over the
differences in homology between different life forms. To an
evolutionist fictionalized view of reality, chromosome number is no
barrier at all to the evolutionary process. Non-homologous life forms
cross breed all the time giving fertile offspring and more fit
replicators. There is no limit to evolutionist speculations are
irrationality.

>

[snip more evolutionist speculations]

>
> > You write so much and say so little. Amplification is the requirement
> > for a population to overcome the multiplication rule of probabilities.
> > If the population can not amplify the allele, there is a very low
> > probability that the next beneficial mutation will occur at the proper
> > locus.
>
> If by "amplification" you mean that the *frequency* of particular alleles in the population changes, sure. �That is the definition of what happens during selection.
>

When are you going to learn that it is not �frequency� which drives
the mutation and selection process, it is the subpopulation size which
drives the probabilities of events occurring?

>
>
> > >With the assumption of random mating, we would expect 0.35 for the frequency of Aa, 0.0 for the frequency of AA, and >0.65 for aa in the next generation (because we are crossing Aa X aa). �Similarly, we would expect 0.15 Bb and 0.85 bb >individuals. �Since the genes are assumed to be unlinked and *using* the multiplication rule of probabilities (correctly), >then I would expect the progeny of this mating to be (0.65)*(0.85) = 0.55 �aa, bb; (0.65)*(0.15) = 0.10 aa, Bb; >(0.35)*(0..85) = 0.30 Aa, bb; and (0.35)*(0.15) = 0.05 Aa, Bb individuals. �That adds up to 1.0.
>
> > You still haven�t figured out how to write the probability function
> > for random recombination. This is reasonable since it has taken months
> > for you to get any understanding of the probability function for
> > mutation and selection.
>
> No. �I have understood what mutation does, what selection does, and what recombination does. �You, OTOH, have repeatedly and stupidly presented your messed up derivation of the binomial probability, where you divide the mutation rate by 4, all the while claiming that that stupidity is a work of genius.
>

You are wrong hersheyh and it should be obvious to you why you are
wrong. Even Inez realizes there should be at least 3 outcomes from a
point mutation. What evolutionists like you who don�t comprehend is
that when you don�t know what the base was before the mutation
occurred requires that you consider that any of the four bases must be
taken into account as possible outcomes.

[snip more of hersheyh�s inability to comprehend the mathematics of
mutation and selection]

[Charles Brenner]

On Oct 9, 6:39�pm, Bill <brogers31...@gmail.com> wrote:
> On 10 Okt, 08:05, Charles Brenner <cbren...@berkeley.edu> wrote:

> > Bill posed a very good aptitude question many months back. I think it
> > was to show that any loop on a terrain must include two points of
> > equal altitude.
>
> Given a smooth contour map, prove that an arbitrary circle drawn on
> the map must contain at least two points that are 180 degrees apart on
> the circle and are at the same altitude.

Thanks; I forgot the 180 degree stipulation which is an interesting
condition in that it reminds me of an Einstein anecdote. About 1946
Einstein interviewed (graduate student) Ernst Straus to be Einstein's
mathematical assistant. Asked for an example of his mathematical
discoveries, Straus mentioned this theorem: Given any closed curve in
a plane, there are three points on the curve which form an equilateral
triangle. Einstein replied that he didn't like the theorem at all
because it combined two concepts, topology and geometry, which are
inimical to one another. (But Straus did get the job.)