The Theory of Evolution is a mathematically irrational belief part 4

[Alan Kleinman MD PhD]

So here we are again, passing another 1000 post mile stone. Let's pick
up here:

It appears that our self-proclaimed professional forensic
mathematician and our graduate student of probability theory and the
other mathematically incompetent dim bulbs of evolutionism who can’t
or won’t properly do the mathematics for mutation and selection when
mutations other than point mutations are included in the calculation
so it is left to us to do this mathematics. We start with the
following definition:

P(-∞ < X < +∞) = 1,

which simply corresponds to all possible outcomes in the entire sample
space. Initially in the derivation of the probability that a
particular mutation will occur at a specific locus; we only considered
point substitutions in the sample space for possible outcomes for a
mutation at a specific locus. We then obtained the following:

P(-∞ < X < +∞) = P(Ad) + P(Cy) + P(Gu) + P(Th) = 1

We weighted each possible point substitution equally (that is they
occur with equal frequency) and we obtain the following equality:

P(Ad) = P(Cy) = P(Gu) = P(Th) = 1/4,

This is where the weight factor of 1/4 comes when computing the
probability that a particular mutation will occur at a specific locus.

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 Gu, Cy, or Th into
Ad.

Based on these principles, one can do the analogous derivation of the
possible outcomes for a mutation including not only point mutations
but any other mutation you wish to consider such as insertions and
deletions.

For example a base can be inserted at the locus. Let an i preceding
the base denote an insertion. Then P(iAd) means the probability that
an Ad base will be inserted at the particular locus and so on for the
other bases. Then the equation that would describe the probabilities
for the sample space for a point mutation and any possible single base
insertion mutation becomes:

P(-∞ < X < +∞) = P(Ad) + P(Cy) + P(Gu) + P(Th) + P(iAd) + P(iCy) +
P(iGu) + P(iTh) = 1

One could think of these outcomes as equivalent to an unfair die where
a roll of this die is more likely to give a substitution mutation
rather than an insertion of a base. Then as an approximation of the
values for the point mutations P(Ad) = P(Cy) = P(Gu) = P(Th) = (1 – x)/
4 and for the insertion mutations P(iAd) = P(iCy) = P(iGu) = P(iTh) =
x/4.

x, the frequency for which a base insertion occurs as well as the
mutation rate itself are experimentally determined values but as we
will see, x can only fall between a certain range of values.

Then the probability of a particular beneficial mutation including
both point mutations and insertions becomes:

mA*(1-x)/4 -- the probability that in one organism in one generation,
a base substitution mutation A will turn a specific locus into a
specific nucleotide other than the one it already is -- for instance,
turn Gu, Cy, or Th into Ad if the beneficial mutation is a base
substitution. Or if the beneficial mutation is a base insertion:

mA*x/4 -- the probability that in one organism in one generation, an
insertion mutation A will give a more fit replicator than the
progenitor -- for instance, inserting Gu, Cy, Th or Ad into the
genetic sequence.

The rest of the computation for the probability of a particular
mutation occurring at a specific locus as a function of population
size and number of generations remains the same. This applies as well
to computing the joint probability of two beneficial mutations
accumulating in a subpopulation. This continues the mathematical
explanation why combination therapy works and why the theory of
evolution is a mathematically irrational belief system. In the next
few weeks, we will include deletions in the mathematics of the
mutation and selection phenomenon which will again show why the type
of beneficial mutation has virtually no affect on the mathematics of
mutation and selection and that the dominant mathematical feature of
mutation and selection is the multiplication rule of probabilities.

I'll bundle responses to the last posts later.

[David Hare-Scott]

Alan Kleinman MD PhD wrote:
> So here we are again, passing another 1000 post mile stone. Let's pick
> up here:
>

Let's not. If you haven't made your case by now the chances are you never
will.

Instead of these interminable arguments of the form

tis
tisn't
tis
tisn't

why not get some suitably qualified people to review your work.

If you are serious submit it to the appropriate learned journal for peer
review. You know how to do that. If you have something you will be famous
as the man who slew evolution, there ought to be a prize for that, maybe
even fame and fortune. There is every chance you will be showered with more
degrees, how cool would Dr Dr Dr Dr be? I could tell my grandchildren "yes
I knew him when he was just Dr Dr".

If your paper is tossed we avoid another 1000 post thread, seems like a
win-win to me.

If you are a crank just keep regurgitating on TO and never ever get
seriously reviewed.

David

[hersheyh]

Just to make sure AK reads it.

On Wednesday, January 18, 2012 2:13:33 PM UTC-5, Alan Kleinman MD PhD wrote:
> On Jan 17, 9:25 pm, hersheyh <her...@yahoo.com> wrote:
> > On Tuesday, January 17, 2012 6:22:05 PM UTC-5, Alan Kleinman MD PhD wrote:
> >
> >
> >
> >
> >
> > > On Jan 16, 7:31 pm, Charles Brenner <cbr...@berkeley.edu> wrote:
> > > > On Jan 16, 6:33 pm, hersheyh <her...@yahoo.com> wrote:
> >
> > > > > On Friday, January 13, 2012 12:46:08 PM UTC-5, Alan Kleinman MD PhD wrote:
> >
> > > > > > On Jan 11, 3:07 am, Charles Brenner <cbr...@berkeley.edu> wrote:
> > > > > > > On Jan 10, 1:28 pm, Alan Kleinman MD PhD <kle...@sti.net> wrote:
> >
> > > > > > > > It is clear that no evolutionist posting on this thread understands
> > > > > > > > how to do the mathematics of mutation and selection
> >
> > > > > > > "the"? I do not think you understand the meaning of the definite
> > > > > > > article in English.
> >
> > > > > > > And it is also certain that you mean nothing by the word "selection."
> > > > > > > Whatever else may be said of your trivial probability comments alleged
> > > > > > > to be an answer, they in no way relate to selection. (I am not the
> > > > > > > first to note this.)
> >
> > > > > > > > We start with the following definition P(-∞ < X < +∞) = 1.
> >
> > > > > Can you please parse what you think you are saying here?
> > > > > If you are saying that the probability of an event X, when X
> > > > > is any value between minus and plus infinity, is always equal
> > > > > to one seems like a strange thing to say. The event of rolling
> > > > > a 6 with a die lies between minus and plus infinity, but the
> > > > > probability of rolling it is (for an honest die) about 1/6, not 1.
> >
> > > > The notation is ok. Realize that P(E) means that E is a statement
> > > > (which can be either true or false), and P(E) is the probability that
> > > > it is true. Alan has written -∞ < X < +∞ for his E. The event isn't X;
> > > > it's the whole statement inside the parentheses. We interpret the
> > > > statement E as meaning that X is a random variable (meaning a function
> > > > that takes on different values at different times), and X is claimed
> > > > to lie in the range from negative to positive infinite -- in other
> > > > words, E is the statement "X is a number on the real line". To say
> > > > that P(E)=1 then means saying that X is always on the real line, i.e.
> > > > it is just a fancy way to say "Let X be a real number".
> >
> > > Here are some simple examples which demonstrate this notation if X is
> > > the number that turns up in rolling a fair die, P(X = 1) = 1/6, P(X =
> > > 2) = 1/6 etc., P(1 < X < 2) = 0, P(1 ≤ X ≤ 2) = 1/3, P(0 ≤ X ≤ 3.2) =
> > > 1/2, P(X > 4) = 1/3, etc. And if we write P(-∞ < X < +∞), we are
> > > including all possible outcomes from a random trial.
> >
> > Apparently you are using the terms plus and minus infinity
> > metaphorically. What you really mean is:
> > P(all possible results) = 1. Or the sum of the probabilities of
> > every possible result = 1.
>
> I’m using the term both metaphorically and mathematically.

No. It only makes sense metaphorically (and not even that).
Mathematically it makes no sense to talk about the probability
of a number between -∞ and +∞.

> > > However, X is not a real number. X is the label we assign to the
> > > outcomes. If we took our six sided fair die and instead of labeling
> > > the sides with a 1, 2, 3, 4, 5, and 6 we used the labels Ad, Gu, Cy,
> > > Th, hersheyh, and Charles Brenner, then P(X = Ad) = 1/6, P(X = Gu) =
> > > 1/6 … P(X = hersheyh) = 1/6, P(X = Charles Brenner) = 1/6.
> >
> > How does P(-∞ < Kleinman < +∞) = 1 make any mathematical
> > sense at all? I certainly agree that Kleinman is not a real number
> > or any number at all. It is a name applied to an event or a set of
> > events with certain properties, just like "mutant" is a name applied
> > to an event or a set of events with certain properties.
>
> X is simply any possible outcome for a trial.

Even metaphorically, X would have to be *all* (not *any*) possible outcome[s]
for a trial. You do know that there is a difference between saying "any" and
saying "all", don't you? But then why wrap it between two infinities, instead
of just saying P(X), where X is all possible categories = 1?

> We can label those
> outcomes any way you want without affecting the mathematical behavior
> of the stochastic process. We could label the sides of dice with 10,
> 20, 30, 40, 50, and 60 but the probabilities for a particular side
> appearing remain the same.

My problem is that if you are going to be claiming something mathematical,
it should make mathematical sense. That is, what you claim you mean and
the mathematical representation you present should say the same thing
rather than different or nonsensical things.

> > If you want to say that the sum of the probabilities of all possible
> > results = 1, that would make sense. That is, if there are 6 possible
> > different results from tossing a die, the sum of their individual
> > probabilities would = 1. That is the addition rule of probability.
> > That would be true regardless of whether the individual probabilities
> > are equal to each other or not.

> And that is correct way to use the addition rule because now we are
> talking about mutually exclusive events.

I *know* what *I* said (and what you probably *meant*) is the correct
way to use the addition rule. But that isn't what P(-∞ < X < +∞) = 1
says. It says that the probability of *any* single *number*, X, between
-∞ and +∞ always = 1. That is not math. It is the arrogant pseudomath
of someone who thinks he can write an equation and make it mean
whatever he wants it to mean.

> > If I took a fair six-sided die, and labelled one side 1, two sides 2
> > and three sides 3, the probability of a 1 would be 1/6, the
> > probability of a 2 would be 2/6 = 1/3, and the probability of
> > a 3 would be 3/6 = 1/2. And the sum of the individual
> > probabilities would be 1/6 + 2/6 + 3/6 = 1.

> Again, that is the correct way to use the addition rule. And as I
> showed previously, if you weight the die so that you increase the
> probability that a particular face will show, you will decrease the
> probabilities of the other faces appearing.

I understand that. Which is also why, given that new mutations
are rare events, that *nearly* all the time, the face you see would
be the "not-mutant" face. That "not-mutant" face will have one
of the four bases, if you insist on defining mutation as an event
at a particular nt site. Absent past selection or past drift, the
probability of point or any other kind of "mutant(s)" at a nt site
in a population will be quite small relative to the probability of
not-mutants. That is quite unlike your expectation that the probability
of point mutation will be 1/4 with the presence of bases in equal proportion.

> > Just as the sum of the probability of a "mutant-of-interest" (one
> > event or set of events with certain properties) and "not-mutants"
> > (another event or set of events with different properties) = 1.
> > Note that, for example, if you define "mutant" as being the set
> > of possible point mutants, there would be three possible point
> > mutations (changes from the non-mutant base) in that set.
>
> Hersheyh, you continually try to force the mathematics of mutation and
> selection into the binomial model.

I am not "forcing" the math of mutation (selection has a different math)
into a binomial framework. That is the most natural and parsimonious
and elegant way of presenting the math of mutation. You do it by classifying
everything one sees as either having the properties you are interested in
(the mutation(s)-of-interest) or not having the properties you are interested
in (the not-mutation(s)-of-interest).

Very simple yes/no rule determined for each trial: Mutant-of-interest
or not-mutant-of-interest.

> Because of this, you are unable to
> do the accounting for all the different possible forms of mutation.

Nope. I can account for all possible forms of mutation by defining
what I consider a "mutation". For determining the probability of
'point mutation', for example, the original base in the population is
considered to be a "not-mutation-of-interest" and the three bases
that the "not-mutant-base" can change to are, collectively, the
"mutation(s)-of-interest". Mutations other than the change to the
three other bases are also included as "not-mutation-of-interest"
because they are not point mutations. Thus, you easily have two
categories: point mutations and not-point-mutations. To determine
the probability of point mutations in a population, you count the
number of individual organisms that have a point mutation and
divide it by the population size. You don't have to make any
stupid false assumptions about equal distributions. You don't
have to consider deletion mutations, because we know the
number of point mutations and the population size and know
that p(u) + p(~u) = 1. p(u) is the sum of the probabilities of
all the changes we have defined as being the "mutant(s) of
interest" and p(~u) is the probability of everything else.

If I define (as you seem to do) the mutation I am interested in
as "a change from the original base at a specific nt site to one
specific different base that causes a change in phenotype which
is called beneficial in a specified environment", then only that
specific change represents the "mutation-of-interest" and the
original base at that nt and all other kinds of mutation, including
point mutations other than one described as beneficial are
classified in the "not-mutation-of-interest" binary category.

If I define the "mutation-of-interest" as *any* mutation in a
specified *gene* (or codon or even nt) that makes the organism
better fit in a specified environment, then any mutation in that
gene that has that effect is classified as the "mutant(s)-of-interest"
and those that don't are classified as "not-mutant(s)-of-interest".

If I define the "mutation-of-interest" as *any* mutation that makes
the organism better fit (or just different) in a specified environment,
then any mutation anywhere in the genome that has that effect is classified
as a "mutant-of-interest" and all other mutations in that genome
are classified with the non-mutant sequences as "not-mutant-of-interest".

The probability of a mutant per trial, p, is the # of "mutant(s) of interest"
divided by the # of genes or nts or organisms examined for "mutant", as
clearly defined. This probability, p, is different than the mass probability
of one or more mutants in a population of n trials when the probability
of the mutant is p.

That probability, the probability of one or more mutants in a population
is 1 - (1-p)^n.

> > But if that is what you meant, you have a very strange way of saying it.
>
> It only sounds strange to you because you have never heard the
> mathematics on mutation and selection described properly before.

And anyone who thinks *you* are correctly describing it is a fool.
Your math of random mutation is incorrect in many places and
your math doesn't describe selection at all.

> You
> have gotten hung up on the first step of the derivation of the
> probability of a particular mutation occurring at a specific locus by
> the weight factor of 1/4 on the mutation rate when considering only
> point mutations in the mathematics. That weight factor will change
> depending on the particular mutation being considered.

Scientists are interested in the *real* probability of mutants (and new
mutation in particular) in a population, not an airy-fairy hypothetical
probability making false assumptions about the nature of mutation.
Your assumption that point mutations somehow does not involve
a *change* from the "not-mutant" base to one of three "mutant" bases
is one such false assumption. The assumption that mutation always
is described as a change at a nt site and that probability is representative
of all mutation is another.

[Eric Root]

On Jan 20, 7:15 pm, Alan Kleinman MD PhD <klein...@sti.net> wrote:
> So here we are again, passing another 1000 post mile stone. Let's pick
> up here:
>
> It appears that our self-proclaimed professional forensic
> mathematician and our graduate student of probability theory and the
> other mathematically incompetent dim bulbs of evolutionism

Bzzt! No evolutionism in evidence here.

[Richard Norman]

This "graduate student of probability theory" is waiting to see some
probability theory that actually applies to the way the biology of
genetics and evolution really works, including properly considering
the meaning of a mutation that changes, for example, a 'G' into a 'G'
and the determination of exactly what is meant by a 'beneficial'
mutation in a discussion where fitness is never mentioned, not to
mention the mechanisms of horizontal gene transfer to which
microorganisms seem rather prone.

[Alan Kleinman MD PhD]

>nando_r...@yahoo.com Jan 20, 7:31 am
>Newsgroups: talk.origins
>From: "nando_rontel...@yahoo.com" <nando_rontel...@yahoo.com>
>Date: Fri, 20 Jan 2012 07:31:37 -0800 (PST)
>Local: Fri, Jan 20 2012 7:31 am
>Subject: Re: The Theory of Evolution is a mathematically irrational belief
>
>On Jan 20, 4:12 pm, Alan Kleinman MD PhD <klein...@sti.net> wrote:
>
>> On Jan 19, 10:10 am, "nando_rontel...@yahoo.com"
>
>> <nando_rontel...@yahoo.com> wrote:
>> > On Jan 19, 6:17 pm, "Jim T." <x...@y.z> wrote:
>
>> > > On Wed, 18 Jan 2012 15:44:26 -0800 (PST), hersheyh
>> > > >You are hilarious! When are you going to tell us the truth -- that you are a troll?
>> > > >Only a troll could present your mathematical ignorance and high arrogance
>> > > >in all seriousness.
>
>> > > Surely he suffering from some sort of mental illness. I have suspected
>> > > so for months.
>
>> > 100 percent of anti-evolutionists on talk.origins are "accused" of a
>> > mental disorder. That is because evolutionists can't deal with forming
>> > a subjective opinion about another. Evolutionists can only deal with
>> > people by making it into a matter of objective fact about a brain
>> > state, instead of forming a subjective opinion. It is your science
>> > induced pathology that you can't accept the existence of anything
>> > subjectively, that you need to be forced by evidence in everything.
>
>> > All you evolutionists are insulting everybody on a continuous basis
>> > because you don't properly relate free will of yourself, to free will
>> > of the other. You don't properly subjectively acknowledge the people
>> > you are conversing with as the owner of their choices. Alan could go
>> > on a TV show presenting his finding, all you evolutionists couldn't
>> > because of your obvious social deficiency.
>
>> > Again the study....
>> > Prosocial Benefits of Feeling Free: Disbelief in Free Will Increases
>> > Aggression and Reduces Helpfulnesshttp://psp.sagepub.com/content/35/2/260.abstract
>
>> Nando, this is what evolutionists do when they don’t have any
>> empirical or mathematical evidence to support their theory. If Charles
>> Brenner, self proclaimed professional forensic mathematician had any
>> mathematical evidence to support the theory of evolution, he would
>> have posted it long ago. If Bill had any empirical evidence to support
>> the theory of evolution, he would have posted it long ago. And we have
>> evolutionist bureaucrats like Thomas Schneider at National Cancer
>> Institute who makes a major scientific blunder by claiming that the
>> multiplication rule does not apply to biological evolution and harms
>> the very people he is paid to help. Instead, we have multidrug
>> resistant microbes, multiherbicide resistant weeds, multipesticide
>> resistant insects and less than durable cancer treatments as the
>> legacy of the mathematically irrational theory of evolution.
>> Evolutionists have embraced the mathematically irrational theory of
>> evolution with religious fervor and the consequence of this scientific
>> bungling dogmatism is harm to millions of people. It is evolutionists
>> who have lost contact with reality.
>
>You say it yourself, religious fervor. The theory of evolution is tied
>up with how they view free will, values etc. It requires a big
>personal change for them to acknowledge they are wrong, which is why
>they won't do it. Darwinists denied Mendel for up to 72 years, then
>they turned around and said Mendel findings support Darwinism, while
>Mendellism indicates stasis. The most likely outcome of it is that
>they will adopt the change in mathematics, fudge the issue about how
>come they were wrong, and simply say those mathematics support
>evolution theory.

Nando, evolutionists will have a hard time fudging this one. Mutation
and selection only works efficiently one mutation at a time and the
amplification of that mutation takes hundreds of generations before
you have a reasonable probability that the next beneficial mutation
will occur on a member with the previous beneficial mutation.
Evolutionists simply don’t have enough generations to transform a
reptile into a bird. That is a mathematical and empirical fact of
life. So unless the evolutionist dominated field of biology comes to
grips with these mathematical facts of life, we will be faced with
more multidrug resistant microbes, multiherbicide resistant weeds,
multipesticide resistant insects and less than durable cancer
treatments.

[Alan Kleinman MD PhD]

On Jan 21, 1:05 pm, "David Hare-Scott" <sec...@nospam.com> wrote:
> Alan Kleinman MD PhD wrote:
>
> > So here we are again, passing another 1000 post mile stone. Let's pick
> > up here:
>
> Let's not.  If you haven't made your case by now the chances are you never
> will.
>
> Instead of these interminable arguments of the form
>
> tis
> tisn't
> tis
> tisn't
>
> why not get some suitably qualified people to review your work.

David, we have hersheyh who claims he is suitably qualified even
though it is quite evident that he suffers from EMDD (Evolutionist
Mathematical Deficit Disorder). And then we have rnorman, graduate
student of probability theory who suffers from EMHD (Evolutionist
Mathematical Hypoactivity Disorder) or Charles Brenner, Self-
proclaimed Professional Forensic Mathematician who also suffers from a
variant of EMHD which includes SAD (Semantic Addiction Disability)
which prevents him from having amusement from word games but he is
compelled to play them.

>
> If you are serious submit it to the appropriate learned journal for peer
> review.  You know how to do that.  If you have something you will be famous
> as the man who slew evolution, there ought to be a prize for that, maybe
> even fame and fortune.  There is every chance you will be showered with more
> degrees, how cool would Dr Dr Dr Dr be?  I could tell my grandchildren "yes
> I knew him when he was just Dr Dr".

You don’t need to go to a “learned journal” to find someone who
understands this mathematics. It only requires taking and passing an
introductory course in probability theory (which leaves hersheyh out).
And this particular example of a probability problem (mutation and
selection) doesn’t require any skill in calculus or differential
equations to understand, it only requires an understanding of basic
algebra (which again leaves hersheyh out).

>
> If your paper is tossed we avoid another 1000 post thread, seems like a
> win-win to me.

This is the correct forum to present the mathematics of mutation and
selection because we have the Supervising Medical Doctor Edward Max
MD, PhD of the Food and Drug Administration using this forum to put
forth the mathematically irrational beliefs of evolutionism. We find
Edward Max’s mathematically irrational claims posted here on Talk
Origins in the following essay http://www.talkorigins.org/faqs/fitness/
where he says the following:

“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.”

There is a reason why there are individuals with training in the hard
mathematical sciences find Dr. Max’s claims difficult to accept. Dr.
Max has demonstrated a complete ignorance of the basic science and
mathematics of the mutation and selection phenomenon. I have had two
communications with Dr. Max and pointed out his blunder in his
understanding of the mutation and selection phenomenon. If Dr. Max
believes that reptiles can be transformed into birds by mutation and
selection, it must be one gene at a time. When Dr. Max presented me
with a paper which attempted to argue how a reptile scale could be
transformed into a feather, his own reference contained over eight
different genes would have to be transformed. My simple question to
him was, how could a reptile transform eight genes at a time when the
fastest evolving replicator known can not transform two genes at a
time effectively? Dr. Max has remained silent on this issue since his
blunder was pointed out and his silence harms people that he is paid
to help.

>

> If you are a crank just keep regurgitating on TO and never ever get
> seriously reviewed.

It is evolutionists like Dr. Max at the FDA and Thomas Schneider at
the National Cancer Institute who claims that the multiplication rule
does not apply to biological evolution who are mathematically
incompetent evolutionist pseudoscientists. This failure on the part of
these evolutionists to properly describe the basic science and
mathematics of the mutation and selection phenomenon harm the people
they are paid to help by perpetuating multidrug resistant microbial
infections and less than durable cancer treatments.

>
> David

[Alan Kleinman MD PhD]

>Steven L. Jan 20, 7:44 am
>Newsgroups: talk.origins
>From: "Steven L." <sdlit...@earthlink.net>
>Date: Fri, 20 Jan 2012 15:44:37 +0000
>Local: Fri, Jan 20 2012 7:44 am
>Subject: Re: The Theory of Evolution is a mathematically irrational belief
>
>"Alan Kleinman MD PhD" <klein...@sti.net> wrote in message
>news:89feea55-7ef1-41e7...@k9g2000pbc.googlegroups.com:

>
>> Nando, this is what evolutionists do when they don't have any
>> empirical or mathematical evidence to support their theory. If Charles
>> Brenner, self proclaimed professional forensic mathematician had any
>> mathematical evidence to support the theory of evolution, he would
>> have posted it long ago. If Bill had any empirical evidence to support
>> the theory of evolution, he would have posted it long ago. And we have
>> evolutionist bureaucrats like Thomas Schneider at National Cancer
>> Institute who makes a major scientific blunder by claiming that the
>> multiplication rule does not apply to biological evolution and harms
>> the very people he is paid to help. Instead, we have multidrug
>> resistant microbes, multiherbicide resistant weeds, multipesticide
>> resistant insects and less than durable cancer treatments as the
>> legacy of the mathematically irrational theory of evolution.
>

>You don't have to keep repeating it:
>The Theory of Evolution is a mathematically irrational belief
>talk.origins - 449 posts - 29 authors - Last post: Nov 14, 2011
>And your sloppy evolutionist junk science has given us multidrug

>resistant microbes, multiherbicide resistant weeds, multipesticide resistant

>insects and less ...
>
>http://groups.google.com/g/c9c7fef4/t/97d3bac032a2ed51/.../73a30e9601......
>The Theory of Evolution is Mathematically Irrational Round 2
>talk.origins - 716 posts - 44 authors - Last post: Jul 19, 2011
>The reality of multidrug resistant microbes, multiherbicide resistant
>weeds, multipesticide resistant insects and less than durable cancer treatments
>is a testament ...
>
>http://groups.google.com/g/c9c7fef4/t/db3f6763b7616fbd/d/a8ea0bf6a258......
>The Theory of Evolution is a mathematically irrational belief system
>talk.origins - 2 posts - 2 authors - Last post: Mar 15, 2011
>.... phenomenon works leads to drug resistant microbes, herbicide
>resistant weeds, pesticide resistant insects, reduced durability of cancer
>treatments and so on. ...
>
>http://groups.google.com/g/c9c7fef4/t/3964b88e0f9b2e58/d/bfacf50960f7......
>The Theory of Evolution is a mathematically irrational belief
>talk.origins - 2 posts - 2 authors - Last post: Mar 21, 2011
>It is not just multidrug resistant bacteria that's a problem, it
>multi-herbicide resistant weeds, multi-pesticide resistant insects, and drug resistant
>cancers. Farmers ...
>
>http://groups.google.com/g/c9c7fef4/t/2ed6cf2b11893a93/d/ae72e624c7fd......
>Trying to salvage something from this Re: The Theory of Evolution
>talk.origins - 1 post - 1 author - Last post: Sep 14, 2011
>You've bungled the mathematics of mutation and selection and given us

>multidrug resistant microbes, multiherbicide resistant weeds,

>multipesticide resistant ...
>
>http://groups.google.com/g/c9c7fef4/t/c99c95ee7f90ebef/d/74d86c30a695......
>The Theory of Evolution is a mathematically irrational belief
>talk.origins - 1 post - 1 author - Last post: Mar 23, 2011
>No wonder we live in a world with multidrug resistant bacteria,
>multi-herbicide resistant weeds, multi-pesticide resistant insects. Evolutionists have
>taken us into ....
>
>http://groups.google.com/g/c9c7fef4/t/791d4747b8934600/d/6f9a4aa1c9ea......
>Trying to salvage something from this Re: The Theory of Evolution
>talk.origins - 1 post - 1 author - Last post: Sep 14, 2011
>The end result of this evolutionist blunder is multidrug resistant

>microbes, multiherbicide resistant weeds, multipesticide resistant insects and

>less than durable ...
>
>http://groups.google.com/g/c9c7fef4/t/f058224d55f65df4/d/3952b710b5fa......
>The Theory of Evolution is a mathematically irrational belief
>talk.origins - 1 post - 1 author - Last post: Mar 15, 2011
>.... phenomenon works, we would not have the problems we have today with
>multidrug resistant microbes, multiherbicide resistant weeds, multipesticide resistant ...
>
>http://groups.google.com/g/c9c7fef4/t/7a538320e0eaa9d3/d/bc5cfdde1072......
>The Theory of Evolution is Mathematically Irrational Round 2
>talk.origins - 1 post - 1 author - Last post: Sep 14, 2011
>.... to prevent drug resistant microbes, herbicide resistant weed,
>pesticide resistant .... multiherbicide resistant weeds, multipesticide resistant insects
>and produce ...
>
>http://groups.google.com/g/c9c7fef4/t/6c621df006fbbad9/d/3210a9371c5f......
>Insane "logic" from Ron O.
>talk.origins - 6 posts - 4 authors - Last post: Sep 23, 2011
>And the end result of this scientific and educational failure is the
>spread of multidrug resistant microbes, multiherbicide resistant weeds,
>multipesticide resistant ...
>
>http://groups.google.com/g/c9c7fef4/t/ae189dac2e081315/d/7bb5c61dda11......
>We hear you.
>You don't have to keep repeating it like a mantra.
>Have you defined a hotkey that keeps spitting out "multidrug resistant

>microbes, multiherbicide resistant weeds, multipesticide resistant

>insects and less than durable cancer treatments"
>or do you just retype it over and over?

Quit whining Steven, it makes you sound like an evolutionist. This

multidrug resistant microbes, multiherbicide resistant weeds,

multipesticide resistant insects and less than durable cancer
treatments defines the utter failure of evolutionism and the harm it
has done to society and you better get used to hearing it because this

[Alan Kleinman MD PhD]

On Jan 22, 9:28 am, Richard Norman <r_s_nor...@comcast.net> wrote:
> On Sun, 22 Jan 2012 09:16:22 -0800 (PST), Eric Root
>

Richard, are you telling us that you actually want to try to apply
some mathematics to the mutation and selection phenomenon? Let’s take
your points one by one starting with how to address the mathematics of
a mutation “for example, a 'G' into a 'G'”. Start by going back to the
fundamental principles of probability theory where we consider only
base substitutions as possible outcomes for a mutation since the
formulation for this type of mutation is what you object to. I wrote
the equation for the possible outcomes for a base substitution as:

P(-∞ < X < +∞) = P(Ad) + P(Cy) + P(Gu) + P(Th) = 1

You object because Gu -> Gu does not represent a mutation. I have
pointed out numerous times that unless you know a priori the base at a
particular locus; you must consider all four bases as a possible
outcome from a base substitution. This still does not satisfy you. So
let’s rewrite the above equation and include the condition that the
base before the mutation occurs can not equal the base afterwards and
write out the possible base substitutions which can occur at a
particular locus.

P(-∞ < X < +∞) = P(i) + P(j) + P(k) = 1, where i, j, k = the three
bases not found at that locus before the mutation occurs.

How does this change the weight factor for the mutation rate? Instead
of a weight factor of 1/4, you have a weight factor of 1/3 (if the
base substitutions are weighted equally) on the mutation rate for a
particular mutation to occur at a specific locus. Ultimately, this has
virtually no affect on the mathematical behavior of the mutation and
selection phenomenon. Base insertions, deletions and other types of
mutations can be included in the sample space as described previously.

Now we come to the issue of what it means for there to be a
“beneficial mutation”. A mutation is only beneficial in the context of
the selection conditions of the environment. The way a member with a
particular mutation expresses whether the mutation is beneficial or
not is determined physically by what happens to the subpopulation
started by the progenitor with that particular mutation. If that
progenitor has a beneficial mutation, it becomes a more fit replicator
in the particular environment that it resides in. This means that the
number of members with that particular mutation will increase over
generations. When the subpopulation descended from that original
progenitor becomes large enough, then the probabilities improve for
the next beneficial mutation in an evolutionary sequence to occur on a
member who has the previous beneficial mutation. When that next
beneficial mutation occurs, that member becomes a progenitor for a new
population that is more fit than the previous subpopulation and over
generations, this subpopulation will increase in number setting the
stage for the next beneficial mutation in the evolutionary sequence to
occur at the proper locus. This is how the mutation and selection
cycle operates. When selection pressures target more than a single
gene at a time, this process is stifled. This is why combination
therapy for HIV works and for any other example of mutation and
selection known where multiple selection pressures are applied to a
population.

The last issue you raise in your post is “mechanisms of horizontal
gene transfer to which microorganisms seem rather prone”. This is not
an issue of mutation and selection but rather recombination. I take it
that you are talking about phages and other forms of genetic
transformation (see http://en.wikipedia.org/wiki/Antibiotic_resistance
) where antibiotic resistance does not occur by mutation and selection
but by the transmission of resistance genes to the microbe by one form
or another. The formation of these resistance genes must still occur
by mutation and selection and with microbes that already have the
capability of transmitting resistance genes to other members of the
population, it is all the more important to understand how mutation
and selection works. What lateral transfer of resistance genes does is
short circuits the mutation and selection process. It negates the need
of a subpopulation to spend hundreds of generations to amplify a
beneficial mutation. It makes it all the more important to use
combination therapy against populations which are capable of
transmitting genes laterally. You do remember now how to do the
mathematics of random recombination?

[John Stockwell]

Where can we read your papers on the subject of mathematics of
evolution?

-John

[Davej]

On Jan 20, 6:15 pm, Alan Kleinman MD PhD <klein...@sti.net> wrote:
> [...]

> It appears that our self-proclaimed professional forensic

> mathematician and our graduate student of probability theory...


Since evolution does not even require the rate of change observed in
domesticated animals we can safely discard your bogus calculations.

[Greg Guarino]

A simple "yes" would have been more succinct.

[Alan Kleinman MD PhD]

Greg is that how you answer a question with the word “or” in it or is
this your way of avoiding the junk science and mathematics of neutral
evolution? I’ll give you a question for which you can answer “no”. Are
you going to tell us how many neutral mutations in each member of the
population in the third generation and how many of those neutral
mutations show up in every member of the population?

And you evolutionists are not going to get a free ride on this major
scientific blunder you have made.

[John Harshman]

Alan Kleinman MD PhD wrote:

> I wrote
> the equation for the possible outcomes for a base substitution as:
>
> P(-∞ < X < +∞) = P(Ad) + P(Cy) + P(Gu) + P(Th) = 1
>
> You object because Gu -> Gu does not represent a mutation. I have
> pointed out numerous times that unless you know a priori the base at a
> particular locus; you must consider all four bases as a possible
> outcome from a base substitution. This still does not satisfy you. So
> let’s rewrite the above equation and include the condition that the
> base before the mutation occurs can not equal the base afterwards and
> write out the possible base substitutions which can occur at a
> particular locus.
>
> P(-∞ < X < +∞) = P(i) + P(j) + P(k) = 1, where i, j, k = the three
> bases not found at that locus before the mutation occurs.
>
> How does this change the weight factor for the mutation rate? Instead
> of a weight factor of 1/4, you have a weight factor of 1/3 (if the
> base substitutions are weighted equally) on the mutation rate for a
> particular mutation to occur at a specific locus.

Sign of the apocalypse: Dr. Dr. has finally understood an objection to
his math, and has corrected it! I suspect this is just a passing phase,
though. And it was the least of all his errors, too.

[Alan Kleinman MD PhD]

John, it’s been a while since you posted on this thread. I recall one
of your last posts on April 20, 2011, 1:23pm
http://groups.google.com/group/talk.origins/browse_thread/thread/db3f6763b7616fbd/732a25d1a2bd5ea6?q=
when you said the following in a response to a challenge I gave you:

Kleinman said:
>> John, perhaps you would like to take a shot at computing the
>> probabilities of two beneficial mutations occurring (whether
>> simultaneous or not) as a function of population size?
John Stockwell responded
>Obviously it is not possible to make such a calculation in general.

Perhaps you are starting to understand how to do such a calculation in
general.

My papers are on my computer. I’ve done some other calculations that I
haven’t discussed here including a complete analysis of Thomas
Schneider’s ev numerical simulation of mutation and selection
http://www.lecb.ncifcrf.gov/~toms/paper/ev/ which requires a
completely different approach from the one shown here using
probability theory. Schneider’s computer simulation is a good model of
mutation and selection. And I have done an exact solution to Haldane’s
Cost of Natural Selection equations. It turns out that Haldane’s
approximation using integral calculus and the method of
underdetermined coefficients gives a very accurate solution to the
equations.


>
> -John

[Kleuskes & Moos]

Mendel has answered the last question, the other requires some definition
of "neutral" and a well defined "population" all can agree on. Lacking
those, it's a meaningless question.

> And you evolutionists are not going to get a free ride on this major
> scientific blunder you have made.

What scientific blunder?

-------------------------------------------------------------------------------
_____________________________
< I like your SNOOPY POSTER!! >
-----------------------------
\
\
___
{~._.~}
( Y )
()~*~()
(_)-(_)
-------------------------------------------------------------------------------

[David Hare-Scott]

You claim that following evolutionary principles leads to negative
consequences for the drug treatment of patients but you are not prepared to
genuinely do anything about it. You have tested the waters here in TO and
clearly it ain't going anywhere but you don't have the courage of your
convictions to take it anywhere else.

I am glad you are not my doctor as clearly you place your own ego in front
of your patient's welfare and public health. Don't all doctors have a duty
towards public health? If you thought you had a chance of precipitating a
paradigm revolution and saving all those problems that you claim exist you
would take it, instead you hide here where you can bluster on and on, and
where there are no real consequences if the debate is never resolved. Try
addressing the issue of patient welfare and public health instead of spewing
more debating tactics and name calling.

David

[hersheyh]

On Monday, January 23, 2012 1:18:14 PM UTC-5, Alan Kleinman MD PhD wrote:

> On Jan 22, 9:28 am, Richard Norman <r_s_n...@comcast.net> wrote:
> > On Sun, 22 Jan 2012 09:16:22 -0800 (PST), Eric Root
> >

> > <eric...@gmail.com> wrote:

Actually the objection is that the above equation tells us nothing of interest.
All it says is that (ignoring a small error for deletions) the sum of the
probabilities of all four bases at a nt site in a haploid genome equals 1
(actually close to it).

Well duh! The sum of the probability of all four bases is always going
to equal 1. Of course, *one* of those four probabilities, the one with
the non-mutant base, will be vastly more probable than the other three.
In what world and under what conditions would the probability of all
four bases, the non-mutant base and the three mutant bases,
actually be expected to be equal?

In a population of n haploid genomes, P(A), the probability of Ad at the
specified nt site in that population would be determined by calculated by
dividing the # of A's seen at that nt site in the genome by
n, the number of those nt sites examined. Thus the above equation
is equivalent to saying:

#Ad's/n + #Cy/n + #Gu/n + # Th/n = 1

I am again ignoring a minor discrepancy for deletions or other changes
at that nt site, but that can be easily accounted for by simply adding
a #O/n term (where O stands for any other state at that nt site).

> I have
> pointed out numerous times that unless you know a priori the base at a
> particular locus; you must consider all four bases as a possible
> outcome from a base substitution.

In *real* science if the correct value or chemical is an unknown, it is
treated as an unknown rather than a known. If we do not know which
base is the non-mutant base, to write the correct mathematics
of mutation, rather than the wrong math, we must treat the non-mutant
base as an unknown base, x, and the three possible point mutations
*from* that base as y1, y2, and y3 (and o for other, if you want to be
complete). We don't pretend that all these probabilities are equal. In
fact, pretending that all four bases are equally likely is nonsense.

That would mean that the equation above would be:

p(x) + p(y1) + p(y2) +p(y3) +p(O) =1

and also equals:

#x/n +#y1/n +#y2/n +#y3/n +#O/n = 1

where #x, etc., is the number of the examined haploid genomes that have that
base at the specified nt site (or the absence of the specified nt site in the case of O).

> This still does not satisfy you. So
> let’s rewrite the above equation and include the condition that the
> base before the mutation occurs can not equal the base afterwards and
> write out the possible base substitutions which can occur at a
> particular locus.
>
> P(-∞ < X < +∞) = P(i) + P(j) + P(k) = 1, where i, j, k = the three
> bases not found at that locus before the mutation occurs.

Well that would require, to be mathematically true, that the probabilities be the number
of each "mutant base" divided by a population of all "mutated" sites at the specified nt
site in the haploid genome. Yet you keep saying that each of these probabilities is the
probability of the "mutant base" in a population of n*NgA (or n, if n is the total
examined population of haploid genomes). That is, you would be saying that P(i)
is the probability of that specific base per *mutated* base, not the probability of the
mutation in the population. Those are two quite different things. If n is the
total population of haploid genomes (each having one of the specified nt sites -- or
in the case of deletion, missing that site), then #i/n is the probability of that
base in the population and would be a very small number because the base not
included is the non-mutant base and most of the population will have that base.

However, if m, the total number of "mutants" (a small fraction of the total population
size), then what you are actually saying above is that if:

P(i) + P(j) + P(k) = 1

is to be true, it really means (again you ignore deletions):

#i/m + #j/m + #k/m = 1, not #i/n + #j/n + #k/n = 1

where n is the total examined population size and m is only those
cells that have a "mutation".

But the probability determined by #i/m is NOT the probability of
of that mutation occurring in a population. It is the relative probability
of that mutation among other possible mutations.

It is the probability of mutation occurring in a population that is relevant
to your claim that mutation is too rare to support evolution. That is
the probability any sensible person uses when they talk about the
probability of mutation and is why I say that the probability of
point mutation at a nt site is 10^-8. That is most certainly NOT
the probability of an A at the site assuming that a point mutation
has occurred.

> How does this change the weight factor for the mutation rate? Instead
> of a weight factor of 1/4, you have a weight factor of 1/3 (if the
> base substitutions are weighted equally) on the mutation rate for a
> particular mutation to occur at a specific locus. Ultimately, this has
> virtually no affect on the mathematical behavior of the mutation and
> selection phenomenon. Base insertions, deletions and other types of
> mutations can be included in the sample space as described previously.

I am perfectly happy to say that the probability of all possible *events* and
*non-events* at a nt site can be stated as:

p(x) + p(y1) + p(y2) + p(y3) + p(O) = 1

where x is the non-mutant state and the other three are changed from that
non-mutant state. If I am interested in all possible "mutants",
the probability of that would be p(y1) + p(y2) + p(y3) + p(O) and would
be less than 1. If I am only interested in point mutations, the probability
of that would be p(y1) + p(y2) + p(y3), also less than 1, and the probability
of events I am not interested in would be p(x) + p(O). If the
probability of only mutation to y2 is of interest, perhaps because it
would have a different phenotype than the other mutations and the
not-mutant, then the probability of the mutation-of-interest would
be p(y2) and all the other possible events would be considered to not
be mutants-of-interest.

> Now we come to the issue of what it means for there to be a
> “beneficial mutation”. A mutation is only beneficial in the context of
> the selection conditions of the environment. The way a member with a
> particular mutation expresses whether the mutation is beneficial or
> not is determined physically by what happens to the subpopulation
> started by the progenitor with that particular mutation. If that
> progenitor has a beneficial mutation, it becomes a more fit replicator
> in the particular environment that it resides in. This means that the
> number of members with that particular mutation will increase over
> generations. When the subpopulation descended from that original
> progenitor becomes large enough, then the probabilities improve for
> the next beneficial mutation in an evolutionary sequence to occur on a
> member who has the previous beneficial mutation. When that next
> beneficial mutation occurs, that member becomes a progenitor for a new
> population that is more fit than the previous subpopulation and over
> generations, this subpopulation will increase in number setting the
> stage for the next beneficial mutation in the evolutionary sequence to
> occur at the proper locus. This is how the mutation and selection
> cycle operates. When selection pressures target more than a single
> gene at a time, this process is stifled. This is why combination
> therapy for HIV works and for any other example of mutation and
> selection known where multiple selection pressures are applied to a
> population.

No problem. Serial mutation is quite true for asexual reproduction.
But when the selection pressure is not lethal or produces no major
population decline, serial mutation merely slows the evolution of double
mutants; it doesn't "stifle" it.

In sexually reproducing organisms, the process of sexual recombination
allows new combination of alleles to occur without the requirement
for serial mutation.

But you have not mentioned the math of selection here -- or anywhere
for that matter.

[Alan Kleinman MD PhD]

John, I’ve always understood your objection on this point. What you
have not understood is that you are objecting to something which has
no significant affect on the mathematical behavior of the mutation and
selection phenomenon. The reason why is has no significant affect on
the mathematical behavior of the mutation and selection phenomenon is
that the dominant governing mathematical principle for the mutation
and selection phenomenon is the multiplication rule of probabilities.
You entered this discussion understanding little about the mathematics
of mutation and selection and you have actually managed to go down
from there.

[Alan Kleinman MD PhD]

> >http://www.talkorigins.org/faqs/fitness/where he says the following:

David, you think so little of the Talk Origins forum. Edward Max,
Supervising Medical Doctor of the FDA doesn’t seem to think that this
forum is worthless. Edward Max thinks that reptiles can be transformed
into birds by mutation and selection. I think that belief is
mathematically irrational and present the basic science and
mathematics of the mutation and selection phenomenon. And Max’s gross
misunderstanding of the basic science and mathematics of the mutation
and selection phenomenon prevents the development of a rational
strategy for dealing with and preventing multidrug resistant microbes.

>
> I am glad you are not my doctor as clearly you place your own ego in front
> of your patient's welfare and public health.  Don't all doctors have a duty
> towards public health?   If you thought you had a chance of precipitating a
> paradigm revolution and saving all those problems that you claim exist you
> would take it, instead you hide here where you can bluster on and on, and
> where there are no real consequences if the debate is never resolved.   Try
> addressing the issue of patient welfare and public health instead of spewing
> more debating tactics and name calling.

If you think I’m engaging in this discussion to recruit more patients,
you are entirely wrong. My medical practice is already intensely busy.
And one of the reasons my practice is so busy is that 50% of the soft
tissue infections I have to treat are MRSA. If evolutionists did their
job and properly described the basic science and mathematics of the
mutation and selection phenomenon, this problem would not be nearly so
severe today, but evolutionists haven’t done their job. In fact
evolutionists have bungled the basic science and mathematics of the
mutation and selection phenomenon and the result of this evolutionist
failure are multidrug resistant microbes, multiherbicide resistant
weeds, multipesticide resistant insects and less than durable cancer
treatments. Evolutionists have harmed millions of people with there
bungled misinterpretation of the mutation and selection phenomenon.

>
> David- Hide quoted text -
>
> - Show quoted text -

[John Stockwell]

> of your last posts on April 20, 2011, 1:23pmhttp://groups.google.com/group/talk.origins/browse_thread/thread/db3f...

> when you said the following in a response to a challenge I gave you:
>
> Kleinman said:>> John, perhaps you would like to take a shot at computing the
> >> probabilities of two beneficial mutations occurring (whether
> >> simultaneous or not) as a function of population size?
>
> John Stockwell responded
>
> >Obviously it is not possible to make such a calculation in general.
>
> Perhaps you are starting to understand how to do such a calculation in
> general.

You aren't doing anything in general. You are proposing toy problems
that
have little to do with biology.

>
> My papers are on my computer. I’ve done some other calculations that I
> haven’t discussed here including a complete analysis of Thomas
> Schneider’s ev numerical simulation of mutation and selection

>http://www.lecb.ncifcrf.gov/~toms/paper/ev/which requires a

> completely different approach from the one shown here using
> probability theory. Schneider’s computer simulation is a good model of
> mutation and selection. And I have done an exact solution to Haldane’s
> Cost of Natural Selection equations. It turns out that Haldane’s
> approximation using integral calculus and the method of
> underdetermined coefficients gives a very accurate solution to the
> equations.

Schneider's work do not invalidate the notion of evolution by any
means.

So, you don't have any papers. You are just a blow hard. Having 2 Ph
D's just
means that you are an educated blow hard.


>
>
>
> > -John

-John

[John Harshman]

Alan Kleinman MD PhD wrote:
> On Jan 23, 12:34 pm, John Harshman <jharsh...@pacbell.net> wrote:
>> Alan Kleinman MD PhD wrote:
>>
>>
>>
>>
>>
>>> I wrote
>>> the equation for the possible outcomes for a base substitution as:
>>> P(-∞ < X < +∞) = P(Ad) + P(Cy) + P(Gu) + P(Th) = 1
>>> You object because Gu -> Gu does not represent a mutation. I have
>>> pointed out numerous times that unless you know a priori the base at a
>>> particular locus; you must consider all four bases as a possible
>>> outcome from a base substitution. This still does not satisfy you. So
>>> let’s rewrite the above equation and include the condition that the
>>> base before the mutation occurs can not equal the base afterwards and
>>> write out the possible base substitutions which can occur at a
>>> particular locus.
>>> P(-∞ < X < +∞) = P(i) + P(j) + P(k) = 1, where i, j, k = the three
>>> bases not found at that locus before the mutation occurs.

As Howard has pointed out, this is wrong for many reasons, but I do
consider it an improvement. All it tells us is that if there's a
mutation, it will be to a different base than the one that was there
before. Well, duh. That's what a mutation is. This has nothing to do
with mutation rates, or with any rate of advantageous mutation. And how
would you measure the values of P(i, j, k)? There's no way.

>>> How does this change the weight factor for the mutation rate? Instead
>>> of a weight factor of 1/4, you have a weight factor of 1/3 (if the
>>> base substitutions are weighted equally) on the mutation rate for a
>>> particular mutation to occur at a specific locus.
>> Sign of the apocalypse: Dr. Dr. has finally understood an objection to
>> his math, and has corrected it! I suspect this is just a passing phase,
>> though. And it was the least of all his errors, too.
>
> John, I’ve always understood your objection on this point. What you
> have not understood is that you are objecting to something which has
> no significant affect on the mathematical behavior of the mutation and
> selection phenomenon. The reason why is has no significant affect on
> the mathematical behavior of the mutation and selection phenomenon is
> that the dominant governing mathematical principle for the mutation
> and selection phenomenon is the multiplication rule of probabilities.
> You entered this discussion understanding little about the mathematics
> of mutation and selection and you have actually managed to go down
> from there.
>

Now if you could only be convinced that "the mutation and selection
phenomenon" makes about as much sense as "the peanut butter and
spaghetti phenomenon".

[Mark Isaak]

On 1/23/12 10:14 AM, Alan Kleinman MD PhD wrote:
> [snip preliminary blather]

> If Dr. Max
> believes that reptiles can be transformed into birds by mutation and
> selection, it must be one gene at a time.

Why?

> When Dr. Max presented me
> with a paper which attempted to argue how a reptile scale could be
> transformed into a feather, his own reference contained over eight
> different genes would have to be transformed.

So? Even if those had to happen one gene at a time, what's the problem?


--
Mark Isaak eciton (at) curioustaxonomy (dot) net
"It is certain, from experience, that the smallest grain of natural
honesty and benevolence has more effect on men's conduct, than the most
pompous views suggested by theological theories and systems." - D. Hume

[Alan Kleinman MD PhD]

The only thing that I am doing is showing how subpopulations under the
right circumstances accumulate beneficial mutations and that is the
basic science and mathematics of the mutation and selection
phenomenon. This is something which evolutionists have failed to do.
And the consequence of this failure to understand the basic science
and mathematics of the mutation and selection phenomenon is multidrug

resistant microbes, multiherbicide resistant weeds, multipesticide

resistant insects and less than durable cancer treatments. You may
consider these toy problems but to the people who suffer from these
evolutionist blunders, they are anything but toys.

>
>
>
> > My papers are on my computer. I’ve done some other calculations that I
> > haven’t discussed here including a complete analysis of Thomas
> > Schneider’s ev numerical simulation of mutation and selection

> >http://www.lecb.ncifcrf.gov/~toms/paper/ev/whichrequires a

> > completely different approach from the one shown here using
> > probability theory. Schneider’s computer simulation is a good model of
> > mutation and selection. And I have done an exact solution to Haldane’s
> > Cost of Natural Selection equations. It turns out that Haldane’s
> > approximation using integral calculus and the method of
> > underdetermined coefficients gives a very accurate solution to the
> > equations.
>
> Schneider's work do not invalidate the notion of evolution by any
> means.

The National Cancer Institute pays for a website to instruct people
about this mathematics. Schneider believes that his model includes all
the essential features of the mutation and selection phenomenon and so
do I. Do a thorough analysis of his model and learn to understand why
it behaves the way it does. Schneider has not done the analysis but if
he did, he would find out why the theory of evolution is
mathematically irrational. Why is it that evolutionists belittle
mathematical models for which they have neither studied nor
understood? John, just because you don’t understand how to do this
mathematics, do not lay your ignorance on others.

>
> So, you don't have any papers. You are just a blow hard. Having 2 Ph
> D's just
> means that you are an educated blow hard.

It’s an MD and PhD degrees, not 2 PhD’s. And the correct mathematics
of the mutation and selection phenomenon blows the theory of evolution
to smithereens. But this mathematics also shows you how to deal with

multidrug resistant microbes, multiherbicide resistant weeds,

multipesticide resistant insects, and produce more durable cancer
treatments. If evolutionists weren’t so mathematically incompetent,
the basic science and mathematics of the mutation and selection
phenomenon would have been elucidated long ago. Sadly, you
evolutionists blew it and continue to blow it.


>
>
>
> > > -John
>
> -John- Hide quoted text -

[Alan Kleinman MD PhD]

On Jan 23, 3:14 pm, John Harshman <jharsh...@pacbell.net> wrote:
> Alan Kleinman MD PhD wrote:
>
>
>
>
>
> > On Jan 23, 12:34 pm, John Harshman <jharsh...@pacbell.net> wrote:
> >> Alan Kleinman MD PhD wrote:
>
> >>>  I wrote
> >>> the equation for the possible outcomes for a base substitution as:
> >>> P(-∞ < X < +∞) = P(Ad) + P(Cy) + P(Gu) + P(Th) = 1
> >>> You object because Gu -> Gu does not represent a mutation. I have
> >>> pointed out numerous times that unless you know a priori the base at a
> >>> particular locus; you must consider all four bases as a possible
> >>> outcome from a base substitution. This still does not satisfy you. So
> >>> let’s rewrite the above equation and include the condition that the
> >>> base before the mutation occurs can not equal the base afterwards and
> >>> write out the possible base substitutions which can occur at a
> >>> particular locus.
> >>> P(-∞ < X < +∞) = P(i) + P(j) + P(k) = 1, where i, j, k = the three
> >>> bases not found at that locus before the mutation occurs.
>
> As Howard has pointed out, this is wrong for many reasons, but I do
> consider it an improvement. All it tells us is that if there's a
> mutation, it will be to a different base than the one that was there
> before. Well, duh. That's what a mutation is. This has nothing to do
> with mutation rates, or with any rate of advantageous mutation. And how
> would you measure the values of P(i, j, k)? There's no way.

Hersheyh doesn’t know right from wrong when it comes to this
mathematics. And you also don’t understand this mathematics either.
You are showing this by writing P(i, j, k). What you have just written
there is a probability involving 3 random variables. If you want to
see an example of probabilities with multiple random variables, go
back and study the distribution function I derived for random
recombination. Measuring mutation rates and particular outcomes for
mutations will always be difficult. Charles Brenner many posts ago
gave the correct theoretical way of doing such a measurement. But what
you still don’t understand is that the mutation rate is a minor
variable in the mutation and selection phenomenon. What can be
measured easily is the behavior of populations when subjected to a
single selection pressure and multiple selection pressures
simultaneously. What you will find is that when a population is
subjected to a single selection pressure at a time, it can fix
beneficial mutations one at a time at a rate of about 1 mutation per
300 generations. When you subject a population to multiple selection
pressures simultaneously, the mutation and selection process is
brought to a standstill.

>
>
>
>
>
> >>> How does this change the weight factor for the mutation rate? Instead
> >>> of a weight factor of 1/4, you have a weight factor of 1/3 (if the
> >>> base substitutions are weighted equally) on the mutation rate for a
> >>> particular mutation to occur at a specific locus.
> >> Sign of the apocalypse: Dr. Dr. has finally understood an objection to
> >> his math, and has corrected it! I suspect this is just a passing phase,
> >> though. And it was the least of all his errors, too.
>
> > John, I’ve always understood your objection on this point. What you
> > have not understood is that you are objecting to something which has
> > no significant affect on the mathematical behavior of the mutation and
> > selection phenomenon. The reason why is has no significant affect on
> > the mathematical behavior of the mutation and selection phenomenon is
> > that the dominant governing mathematical principle for the mutation
> > and selection phenomenon is the multiplication rule of probabilities.
> > You entered this discussion understanding little about the mathematics
> > of mutation and selection and you have actually managed to go down
> > from there.
>
> Now if you could only be convinced that "the mutation and selection
> phenomenon" makes about as much sense as "the peanut butter and
> spaghetti phenomenon".

John, you should know by now that it doesn’t bother me to play word
games, in fact I have fun with them. In fact you evolutionists have
gone nuts and are off your noodle.

[Alan Kleinman MD PhD]

On Jan 23, 3:51 pm, Mark Isaak <eci...@curioustaxonomyNOSPAM.net>
wrote:

> On 1/23/12 10:14 AM, Alan Kleinman MD PhD wrote:
>
> > [snip preliminary blather]
> > If Dr. Max
> > believes that reptiles can be transformed into birds by mutation and
> > selection, it must be one gene at a time.
>
> Why?

Mark Isaak, social engineer. Where have you been?

It must be one gene at a time because that’s the only way mutation and
selection can work efficiently. When selection is acting on two or
more genes simultaneously, the mutation and selection process is
brought to a standstill. That’s why combination therapy works for the
treatment of HIV and any other population on which combination
selection pressures are applied.

>
> > When Dr. Max presented me
> > with a paper which attempted to argue how a reptile scale could be
> > transformed into a feather, his own reference contained over eight
> > different genes would have to be transformed.
>
> So?  Even if those had to happen one gene at a time, what's the problem?

You have at least two problems. The first is to have selection
pressures which target only one gene at a time. We have this with
targeted selection pressures such as antimicrobial agents, herbicides
and pesticides but selection pressures in nature such as starvation,
dehydration, thermal stress and so on will target many genes
simultaneously. The second problem you encounter is the number of
generations required in order to do such a transformation even if the
selection pressures existed. If you have a sufficiently large
population such as seen with microbes, the process will take about 300
generations per mutation. That’s why the Lenski experiment takes tens
of thousands of generations to fix only a few dozen mutations.

[John Stockwell]

I believe that Schneider has basically shown that there is no
"information problem"
which is something that creationists and other near scientists say
there is.

>
>
>
> > So, you don't have any papers. You are just a blow hard. Having 2 Ph
> > D's just
> > means that you are an educated blow hard.
>
> It’s an MD and PhD degrees, not 2 PhD’s. And the correct mathematics
> of the mutation and selection phenomenon blows the theory of evolution
> to smithereens. But this mathematics also shows you how to deal with
> multidrug resistant microbes, multiherbicide resistant weeds,
> multipesticide resistant insects, and produce more durable cancer
> treatments. If evolutionists weren’t so mathematically incompetent,
> the basic science and mathematics of the mutation and selection
> phenomenon would have been elucidated long ago. Sadly, you
> evolutionists blew it and continue to blow it.

The modern understanding of evolution is empirical, based on a large
collection
of observations. So you make up a mathematical model. You claim that
evolution
is false because your mathematical model fails to describe the
phenomenon that
is observed through biology paleontology, etc. You have not explained
those ideas
with your model, nor have you "disproven evolution". You have merely
disproven
your own model of evolution.

Now, in itself toy models are not bad. Sometimes science begins with
toy models.
So publish. Put your stuff out to the community of scientists.

You are aware that Talk.Origins is best described as "crank flypaper".
People like
myself read it as a form of entertainment. So, if you plan on sticking
around, then
you really revealing yourself as one of the many, many, cranks who
have come
waltzing in here claiming to have "disproved evolution" by some model
or other
and who have chosen to defend their egos, at the expense of their
credibility.

If you want to impress us: Publish. Be the change, as they say.


-John

[hersheyh]

On Monday, January 23, 2012 5:48:25 PM UTC-5, Alan Kleinman MD PhD wrote:

Other than that you are assuming that all bases are equally likely in a population
when the original or non-mutant base is much more frequent than the
mutants unless there has been past selection or that there is no drift. There
can be no real population that would have equimolar amounts of the four
possible bases (with the possible extremely unlikely case where there is
frequency-dependent selection and all four bases are equally fit). Ever.
Any real population would typically have one base that would be overwhelmingly
dominant with only a scattering frequency of the other three regardless of
whether the bases had selective differences or not. Certainly, in the case
of bacteria grown from a single colony, the base in that initial colony would
be overwhelmingly dominant as a fraction of the population in the absence
of selection over any short number of generations. Why do you think that
the probability of *all three* possible point mutations at a nt site is
well estimated as being 10^-8? Meaning the probability of the not-point-mutation
base would be 1 - 10^-8. That is nowhere near being equimolar.

And that you are surreptitiously or ignorantly changing how you calculate
the probability of the event -- from measuring the probability of a mutation
in a population to measuring the probability of a mutation relative to other
mutations.

> The reason why is has no significant affect on
> the mathematical behavior of the mutation and selection phenomenon is
> that the dominant governing mathematical principle for the mutation
> and selection phenomenon is the multiplication rule of probabilities.

Both of the above dramatically affects the calculated probability. The assumption that
the probability of mutation is = 1/4, as if there were no difference between the
probability of the not-mutant-of-interest and any of the other three possible
point mutation differences is absurd.

Moreover, the difference between calculating point mutation probabilities as
the number of such mutants divided by the total population you look through
to find them and the number of such mutants divided by the total number
of point mutations measure two different things.

> You entered this discussion understanding little about the mathematics
> of mutation and selection and you have actually managed to go down
> from there.

Actually, you are the one who looks the fool here. You have a very
sloppy mind when it comes to the use of mathematical symbols and seem to
believe that whatever symbols you use necessarily reflect whatever you meant
them to say. Your inability to think clearly about probability is embarrassing.
Your inability to even try to define mutation is worse. Your inability to
understand the meaning of the probabilities you calculate is yet worse again.
And, of course, I excuse you from your failure to describe selection, since you
haven't done so.

[Ray Martinez]

"[U]tter failure of evolutionism" yet you accept the main empirical
claims: natural selection, species mutability.

Ray (species immutabilist)

[John Harshman]

Don't care. You know what I meant, and I was too lazy to write P(i),
P(j), P(k). Stop hiding behind formalism.

> What you have just written
> there is a probability involving 3 random variables. If you want to
> see an example of probabilities with multiple random variables, go
> back and study the distribution function I derived for random
> recombination. Measuring mutation rates and particular outcomes for
> mutations will always be difficult.

No it won't, not if the mutation is defined by phenotype. You just
count. Here, it isn't just different, it's impossible. You don't know
what bases i, j, and k are, you don't know what phenotypes if any
they're associated with, and you don't know which ones (note that it may
be anything from none of them to all three) are advantageous.

[snip repetitive bloviation]

>> Now if you could only be convinced that "the mutation and selection
>> phenomenon" makes about as much sense as "the peanut butter and
>> spaghetti phenomenon".
>
> John, you should know by now that it doesn’t bother me to play word
> games, in fact I have fun with them.

Yes, that's one of your major faults. Instead of real discussion, you
prefer word games.

[Richard Norman]

>P(-? < X < +?) = P(Ad) + P(Cy) + P(Gu) + P(Th) = 1

>
>You object because Gu -> Gu does not represent a mutation. I have
>pointed out numerous times that unless you know a priori the base at a
>particular locus; you must consider all four bases as a possible
>outcome from a base substitution. This still does not satisfy you. So
>let’s rewrite the above equation and include the condition that the
>base before the mutation occurs can not equal the base afterwards and
>write out the possible base substitutions which can occur at a
>particular locus.
>

>P(-? < X < +?) = P(i) + P(j) + P(k) = 1, where i, j, k = the three

I am still waiting to see probability theory based on the way real
biology works. John Harshman has already commented on your reversal
on the "divide by four" vs. "divide by three" issue, something that
was pointed out to you repeatedly several thousand posts ago. The
difference in the mathematics is, as you say, not terribly
significant. The difference as an indication of your lack of
understanding of biology is enormous.

You tell John Stockwell "The only thing that I am doing is showing how

subpopulations under the right circumstances accumulate beneficial

mutations" yet you do not account for the benefit of these beneficial
mutations in any calculation you show. Now you describe what you mean
by beneficial but that concept appears absolutely nowhere in your
work. You also argue that recombination must be totally irrelevant
without seeming to understand that it is an important mechanism in
producing organisms that show multiple mutations, the separate
mutations arising separately. That fact, alone, destroys your
argument about multiplication of probabilities when applied in the
trivial way you seem to insist.

You constant harp on the inability of evolutionary biologists to
understand the basic mathematics of mutation and selection but now you
claim " What lateral transfer of resistance genes does is
short circuits the mutation and selection process." There goes your
argument about mutation and selection being too slow! Which way is
it, really?

I am not the only person here complaining about the total absence of
biological relevance to your claims. Please come back when you are
prepared to discuss quantitative issues in the proper context of what
really happens in the real world.

[chris thompson]

On Jan 23, 6:57 pm, Alan Kleinman MD PhD <klein...@sti.net> wrote:

snip

How old is planet Earth?

How old is the universe?

Chris

[David Hare-Scott]

What is the mechanism that medicine makes progress? It isn't by restricting
publication to TO. You are playing dodge ball. Why won't you publish in
the journals?

>>
>> I am glad you are not my doctor as clearly you place your own ego in
>> front of your patient's welfare and public health. Don't all doctors
>> have a duty towards public health? If you thought you had a chance
>> of precipitating a paradigm revolution and saving all those problems
>> that you claim exist you would take it, instead you hide here where
>> you can bluster on and on, and where there are no real consequences
>> if the debate is never resolved. Try addressing the issue of patient
>> welfare and public health instead of spewing more debating tactics
>> and name calling.
>
> If you think I’m engaging in this discussion to recruit more patients,
> you are entirely wrong.

I said nothing of the kind please don't make things up.

My medical practice is already intensely busy.
> And one of the reasons my practice is so busy is that 50% of the soft
> tissue infections I have to treat are MRSA. If evolutionists did their
> job and properly described the basic science and mathematics of the
> mutation and selection phenomenon, this problem would not be nearly so
> severe today, but evolutionists haven’t done their job. In fact
> evolutionists have bungled the basic science and mathematics of the
> mutation and selection phenomenon and the result of this evolutionist
> failure are multidrug resistant microbes, multiherbicide resistant
> weeds, multipesticide resistant insects and less than durable cancer
> treatments. Evolutionists have harmed millions of people with there
> bungled misinterpretation of the mutation and selection phenomenon.
>

You claim all these horid consequence yet you do nothing effective about a
remedy and instead waste hours in pointless debates. What kind of medical
professional is that? Stop dodging, why won't you publish?

D

[Greg Guarino]

On 1/23/2012 3:24 PM, Alan Kleinman MD PhD wrote:
> And you evolutionists are not going to get a free ride on this major
> scientific blunder you have made.

That's where you're wrong. Repeating the same phrases over and over in a
sort of OCD Ostinato is very, very odd. You really can't see that? It
makes you look like a crank, a zealot or perhaps a politician; certainly
anything but a scientist.

I am convinced that you have no coherent understanding of the things you
claim to debunk. But if you do have some worthwhile point to make, no
one will ever know. You stick exclusively to the talking points and
avoid giving straight answers; thereby sabotaging any chance you might
have of being taken seriously.

Looks like a "free ride" to me.

[hersheyh]

On Monday, January 23, 2012 7:36:27 PM UTC-5, John Harshman wrote:
> Alan Kleinman MD PhD wrote:

The most hilarious part is that that carp comes from someone who claims
that P(-∞ < X < +∞) means something other than the probability
of a number between -∞ and +∞. He, in fact, actually claims that
X isn't a number or even a single thing (which makes "between
-∞ and +∞" a bit of a puzzler).


Mostly he claims it "really" means (or, rather, what he intended it to
mean) was the sum of the probabilities of all possible "events" in a
population of "trials", although he cannot even be consistent with that.

[Frank Smith]

He is evidently unfamiliar with the distinction between quantitative
and qualitative (specifically, nominative) variables.

Is anyone surprised?

>
> Mostly he claims it "really" means (or, rather, what he intended it to
> mean) was the sum of the probabilities of all possible "events" in a
> population of "trials", although he cannot even be consistent with that.

<snip>

--
Frank F. Smith

[Richard Norman]

On Tue, 24 Jan 2012 09:12:23 -0800 (PST), Frank Smith
<smith...@gmail.com> wrote:

>On Jan 24, 11:54 am, hersheyh <hershe...@yahoo.com> wrote:
>> On Monday, January 23, 2012 7:36:27 PM UTC-5, John Harshman wrote:
>> > Alan Kleinman MD PhD wrote:
>> > > On Jan 23, 3:14 pm, John Harshman <jhar...@pacbell.net> wrote:
>> > >> Alan Kleinman MD PhD wrote:
>>
>> > >>> On Jan 23, 12:34 pm, John Harshman <jhar...@pacbell.net> wrote:
>> > >>>> Alan Kleinman MD PhD wrote:
>> > >>>>>  I wrote
>> > >>>>> the equation for the possible outcomes for a base substitution as:

>> > >>>>> P(-? < X < +?) = P(Ad) + P(Cy) + P(Gu) + P(Th) = 1

>> > >>>>> You object because Gu -> Gu does not represent a mutation. I have
>> > >>>>> pointed out numerous times that unless you know a priori the base at a
>> > >>>>> particular locus; you must consider all four bases as a possible
>> > >>>>> outcome from a base substitution. This still does not satisfy you. So
>> > >>>>> let’s rewrite the above equation and include the condition that the
>> > >>>>> base before the mutation occurs can not equal the base afterwards and
>> > >>>>> write out the possible base substitutions which can occur at a
>> > >>>>> particular locus.

>> > >>>>> P(-? < X < +?) = P(i) + P(j) + P(k) = 1, where i, j, k = the three

>> > >>>>> bases not found at that locus before the mutation occurs.
>> > >> As Howard has pointed out, this is wrong for many reasons, but I do
>> > >> consider it an improvement. All it tells us is that if there's a
>> > >> mutation, it will be to a different base than the one that was there
>> > >> before. Well, duh. That's what a mutation is. This has nothing to do
>> > >> with mutation rates, or with any rate of advantageous mutation. And how
>> > >> would you measure the values of P(i, j, k)? There's no way.
>>
>> > > Hersheyh doesn’t know right from wrong when it comes to this
>> > > mathematics. And you also don’t understand this mathematics either.
>> > > You are showing this by writing P(i, j, k).
>>
>> > Don't care. You know what I meant, and I was too lazy to write P(i),
>> > P(j), P(k). Stop hiding behind formalism.
>>
>> The most hilarious part is that that carp comes from someone who claims

>> that P(-? < X < +?) means something other than the probability
>> of a number between -? and +?.  He, in fact, actually claims that

>> X isn't a number or even a single thing (which makes "between

>> -? and +?" a bit of a puzzler).

>
>He is evidently unfamiliar with the distinction between quantitative
>and qualitative (specifically, nominative) variables.
>
>Is anyone surprised?
>
>>
>> Mostly he claims it "really" means (or, rather, what he intended it to
>> mean) was the sum of the probabilities of all possible "events" in a
>> population of "trials", although he cannot even be consistent with that.
>
><snip>

Somebody who has studied probability theory might write Pr(S) = 1
where S is the sample space. It still wouldn't mean anything but at
least it would be standard notation.

[Frank Smith]

On Jan 24, 12:35 pm, Richard Norman <r_s_nor...@comcast.net> wrote:
> On Tue, 24 Jan 2012 09:12:23 -0800 (PST), Frank Smith
>
>
>
>
>
>
>
>
>

<snip>

> >He is evidently unfamiliar with the distinction between quantitative
> >and qualitative (specifically, nominative) variables.
>
> >Is anyone surprised?
>
> >> Mostly he claims it "really" means (or, rather, what he intended it to
> >> mean) was the sum of the probabilities of all possible "events" in a
> >> population of "trials", although he cannot even be consistent with that.
>
> ><snip>
>
> Somebody who has studied probability theory might write Pr(S) = 1
> where S is the sample space.  It still wouldn't mean anything but at
> least it would be standard notation.

Well... meaningful in that it's one of the criteria for a valid
probability measure.

[Mark Isaak]

On 1/23/12 4:12 PM, Alan Kleinman MD PhD wrote:
> On Jan 23, 3:51 pm, Mark Isaak<eci...@curioustaxonomyNOSPAM.net>
> wrote:
>> On 1/23/12 10:14 AM, Alan Kleinman MD PhD wrote:
>>
>>> [snip preliminary blather]
>>> If Dr. Max
>>> believes that reptiles can be transformed into birds by mutation and
>>> selection, it must be one gene at a time.
>>
>> Why?
>
> Mark Isaak, social engineer. Where have you been?

Huh?

> It must be one gene at a time because that’s the only way mutation and
> selection can work efficiently. When selection is acting on two or
> more genes simultaneously, the mutation and selection process is
> brought to a standstill.

Don't be stupid. That is not even possible, except in extinctions and
in very artificially contrived situations.

>>> When Dr. Max presented me
>>> with a paper which attempted to argue how a reptile scale could be
>>> transformed into a feather, his own reference contained over eight
>>> different genes would have to be transformed.
>>
>> So? Even if those had to happen one gene at a time, what's the problem?
>
> You have at least two problems. The first is to have selection
> pressures which target only one gene at a time.

That's *your* constraint; it has nothing to do with nature. In the real
world, working on several things simultaneously gets the lot of them
done sooner.

> The second problem you encounter is the number of
> generations required in order to do such a transformation even if the
> selection pressures existed. If you have a sufficiently large
> population such as seen with microbes, the process will take about 300
> generations per mutation. That’s why the Lenski experiment takes tens
> of thousands of generations to fix only a few dozen mutations.

So you didn't know that the length of time to fixation depends on
population size, among other things. Now you do, so you can forget that
300 generation number.

[Rolf]

You keep denying natural selection. Do you know any scientifc defintion of
natural selection?

Are you denying artificial selection too?

And what would the main difference between the two be, in your opinion?

> Ray (species immutabilist)

[hersheyh]

On Monday, January 23, 2012 7:12:33 PM UTC-5, Alan Kleinman MD PhD wrote:
> On Jan 23, 3:51 pm, Mark Isaak <eci...@curioustaxonomyNOSPAM.net>
> wrote:
> > On 1/23/12 10:14 AM, Alan Kleinman MD PhD wrote:
> >
> > > [snip preliminary blather]
> > > If Dr. Max
> > > believes that reptiles can be transformed into birds by mutation and
> > > selection, it must be one gene at a time.
> >
> > Why?
>
> Mark Isaak, social engineer. Where have you been?
>
> It must be one gene at a time because that’s the only way mutation and
> selection can work efficiently. When selection is acting on two or
> more genes simultaneously, the mutation and selection process is
> brought to a standstill. That’s why combination therapy works for the
> treatment of HIV and any other population on which combination
> selection pressures are applied.
>
> >
> > > When Dr. Max presented me
> > > with a paper which attempted to argue how a reptile scale could be
> > > transformed into a feather, his own reference contained over eight
> > > different genes would have to be transformed.
> >
> > So?  Even if those had to happen one gene at a time, what's the problem?
>
> You have at least two problems. The first is to have selection
> pressures which target only one gene at a time.

No we don't. We only need to have selection pressures that target one gene
at a time when those pressures are lethal and greatly reduce population
numbers. Most *natural* selection pressures an organism faces are nowhere
near strong enough to reduce population numbers below their present levels.

> We have this with
> targeted selection pressures such as antimicrobial agents, herbicides
> and pesticides but selection pressures in nature such as starvation,
> dehydration, thermal stress and so on will target many genes
> simultaneously.

Real organisms are already evolved to be adapted to current levels
of starvation, dehydration, thermal stress, etc. It is only major and
significant *change* in those stresses that would cause the population
to crash.

> The second problem you encounter is the number of
> generations required in order to do such a transformation even if the
> selection pressures existed. If you have a sufficiently large
> population such as seen with microbes, the process will take about 300
> generations per mutation. That’s why the Lenski experiment takes tens
> of thousands of generations to fix only a few dozen mutations.

That is in microbes reproducing asexually, where new combinations of
alleles must involve serial mutation. But in eucaryotes that reproduce
sexually, recombination allows new combinations of alleles that arise
independently in different organisms. I have already discussed this in
my *correct* analysis of the probability of one or more double-mutants.

[Alan Kleinman MD PhD]

Ray, I accept that life forms have mutations when they replicate and
selection will act on those mutations but I don’t accept that random
mutation and natural selection will transform reptiles into birds. If
you understand the basic science and mathematics of mutation and
selection, you would find that to be a mathematically irrational
belief.

[Alan Kleinman MD PhD]

The formalism of mathematical notation is what allows you to work with
these abstract concepts. It is what shows you why that doubling
population size does not double the probability that a beneficial
mutation will occur. Don’t be sloppy in your mathematical notation. It
introduces unnecessary confusion and ambiguity to the discussion. Stop
hiding behind your laziness.

>
> > What you have just written
> > there is a probability involving 3 random variables. If you want to
> > see an example of probabilities with multiple random variables, go
> > back and study the distribution function I derived for random
> > recombination. Measuring mutation rates and particular outcomes for
> > mutations will always be difficult.
>
> No it won't, not if the mutation is defined by phenotype. You just
> count. Here, it isn't just different, it's impossible. You don't know
> what bases i, j, and k are, you don't know what phenotypes if any
> they're associated with, and you don't know which ones (note that it may
> be anything from none of them to all three) are advantageous.

If you base your measurement of mutation rate by a change in
phenotype, you will only be able to measure beneficial and detrimental
mutations because only these types of mutation will cause a change in
phenotype. You will miss counting all the neutral mutations. In
addition can not identify the locus at which the mutation occurs.
Phenotype does not give enough detail to do an accurate accounting of
mutation rate (and type of mutation), you must do this counting at the
genotype.

>
> [snip repetitive bloviation]

John you’re getting too much of your vocabulary from watching TV.

>
> >> Now if you could only be convinced that "the mutation and selection
> >> phenomenon" makes about as much sense as "the peanut butter and
> >> spaghetti phenomenon".
>
> > John, you should know by now that it doesn’t bother me to play word
> > games, in fact I have fun with them.
>
> Yes, that's one of your major faults. Instead of real discussion, you
> prefer word games.

If you are tired of the word games, let’s have a mathematical game and
you can learn the mathematics of the mutation and selection phenomenon.

[Alan Kleinman MD PhD]

What Schneider has shown is that information is simply a measure of
order of the system. Selection pressures order the genetic sequences,
mutations disorder the genetic sequence. What Schneider’s model shows
is that random sequences of bases can be ordered by selection
conditions. Some mutations will increase the order (these are called
beneficial mutations) for those selection conditions. When Schneider
turns off selection in his model after his model has sorted for
beneficial mutations, the sequences revert to random over time and the
information (order) decreases.

Information theory is not the way to explain the basic science and
mathematics of the mutation and selection phenomenon, probability
theory gives you the mathematical tools to explain mutation and
selection.

>
>
>
>
>
>
>
> > > So, you don't have any papers. You are just a blow hard. Having 2 Ph
> > > D's just
> > > means that you are an educated blow hard.
>
> > It’s an MD and PhD degrees, not 2 PhD’s. And the correct mathematics
> > of the mutation and selection phenomenon blows the theory of evolution
> > to smithereens. But this mathematics also shows you how to deal with
> > multidrug resistant microbes, multiherbicide resistant weeds,
> > multipesticide resistant insects, and produce more durable cancer
> > treatments. If evolutionists weren’t so mathematically incompetent,
> > the basic science and mathematics of the mutation and selection
> > phenomenon would have been elucidated long ago. Sadly, you
> > evolutionists blew it and continue to blow it.
>
> The modern understanding of evolution is empirical, based on a large
> collection
> of observations. So you make up a mathematical model. You claim that
> evolution
> is false because your mathematical model fails to describe the
> phenomenon that
> is observed through biology paleontology, etc. You have not explained
> those ideas
> with your model, nor have you "disproven evolution". You have merely
> disproven
> your own model of evolution.

I claim that the theory of evolution is mathematically irrational, not
that mutation and selection is false. Mutation and selection has a
specific behavior that is governed by mathematical rules. Those rules
are the axioms of probability theory. When these axioms are applied
correctly, you obtain a mathematical model which closely correlates
with the empirical data. You have not explained why combination
therapy works to suppress the evolution of HIV. The probability
function for two mutations occurring that I derived for you does
explain this. Until you do that, you know nothing about how the
mutation and selection phenomenon operates.

>
> Now, in itself toy models are not bad. Sometimes science begins with
> toy models.

> So publish. Put Put your stuff out to the community of scientists.

I have put this out to people who call themselves scientists. I’ve
discussed this topic extensively with Thomas Schneider at the National
Cancer Institute. I’ve also discussed this on a much smaller scale
with Edward Max at the Food and Drug Administration. Schneider
comprehends that combination therapy suppresses the mutation and
selection process but refuses to acknowledge that the reason this
happens is the multiplication rule of probabilities, the very rule
that he claims does not apply to biological evolution. Edward Max
understood this when I pointed out to him that his argument for
transforming a reptile scale into a feather requires the
transformation of eight or more genes. When I pointed out to him that
HIV can not transform two genes simultaneously with any efficiency
despite being one of the most rapid evolving life forms known, Max
ended the discussion.

>You are aware that Talk.Origins is best described as "crank flypaper".
>People like myself read it as a form of entertainment. So, if you plan on sticking
>around, then you really revealing yourself as one of the many, many, cranks who
>have come waltzing in here claiming to have "disproved evolution" by some model
>or other and who have chosen to defend their egos, at the expense of their
>credibility.

There was a time when Edward Max would engage in debate about the
theory of evolution on Talk Origins. So what if there are cranks
posting. Anyone who thinks I’m wrong or crazy can report me to the
California Medical Board where I hold my medical license or the
California Department of Consumer Affairs where I hold my professional
engineering license. If you think that mutation and selection works
any way other than described by the probability functions I derived
for you, point out the error but you can’t because the mathematics is
correct and the empirical evidence verifies the mathematics.

>If you want to impress us: Publish. Be the change, as they say.

Are you trying to say that this mathematics will only be correct when
it is published and that anything that is published is true? The
mathematics is published. It is published here on Talk Origins. The
same forum which publishes Edward Max’s mathematically irrational
claims which harms people that he has responsibility for. It probably
has a greater readership than any of the journals you think I should
try to publish in. And where else would I have the opportunity to show
that the theory of evolution is a mathematically irrational belief
system and the failure of evolutionists to properly describe the basic
science and mathematics of the mutation and selection phenomenon has
harmed and continues to harm millions of people from diseases subject
to the mutation and selection phenomenon.

[Alan Kleinman MD PhD]

There is absolutely nothing wrong with the notation P(-∞ < X < +∞) = 1
and it is totally equivalent to P(S) = 1. You should know that Richard
as a graduate student of probability theory.

[Alan Kleinman MD PhD]

> >transformation (seehttp://en.wikipedia.org/wiki/Antibiotic_resistance

> >) where antibiotic resistance does not occur by mutation and selection
> >but by the transmission of resistance genes to the microbe by one form
> >or another. The formation of these resistance genes must still occur
> >by mutation and selection and with microbes that already have the
> >capability of transmitting resistance genes to other members of the
> >population, it is all the more important to understand how mutation
> >and selection works. What lateral transfer of resistance genes does is
> >short circuits the mutation and selection process. It negates the need
> >of a subpopulation to spend hundreds of generations to amplify a
> >beneficial mutation. It makes it all the more important to use
> >combination therapy against populations which are capable of
> >transmitting genes laterally. You do remember now how to do the
> >mathematics of random recombination?
>
> I am still waiting to see probability theory based on the way real
> biology works.  John Harshman has already commented on your reversal
> on the "divide by four" vs. "divide by three" issue, something that
> was pointed out to you repeatedly several thousand posts ago.  The
> difference in the mathematics is, as you say, not terribly
> significant.  The difference as an indication of your lack of
> understanding of biology is enormous.

Richard, “divide by four” vs. “divide by three” is not a reversal. A
reversal is when you are shown that the mathematics and empirical
evidence of mutation and selection can not operate efficiently at all
in parallel. That takes the theory of evolution from mathematically
rational to mathematically irrational. That is what a reversal is.

>
> You tell John Stockwell "The only thing that I am doing is showing how
> subpopulations under the right circumstances accumulate beneficial
> mutations" yet you do not account for the benefit of these beneficial
> mutations in any calculation you show.  Now you describe what you mean
> by beneficial but that concept appears absolutely nowhere in your
> work.  You also argue that recombination must be totally irrelevant
> without seeming to understand that it is an important mechanism in
> producing organisms that show multiple mutations, the separate
> mutations arising separately.  That fact, alone, destroys your
> argument about multiplication of probabilities when applied in the
> trivial way you seem to insist.

Richard pay attention. I have shown many times where the concept of
beneficial and detriment mutation enters into the mathematics of
mutation and selection. I’ll repeat it once again for you here. Here
once again is the equation which describes the probabilities of two
beneficial mutations occurring in a subpopulation:

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

The variable in the above equation which reflects whether mutation B
will have a reasonable probability of occurring on a member with
mutation A is nA, the number of members with mutation A. If mutation A
is beneficial, nA will amplify over generations, increasing in number
so as to improve the probability that mutation B will occur on one of
the members of this subpopulation. If mutation A is neutral or
detrimental so that the subpopulation size with that mutation remains
constant or decreases, the only other variable which can improve the
probability that mutation B will occur on a member with mutation A is
nGB, the number of generations which that subpopulation with mutation
A is able to replicate.

Your theory of evolution remains mathematically irrational, a reversal
of your belief system.

>
> You constant harp on the inability of evolutionary biologists to
> understand the basic mathematics of mutation and selection but now you
> claim " What lateral transfer of resistance genes does is
> short circuits the mutation and selection process."  There goes your
> argument about mutation and selection being too slow!  Which way is
> it, really?

Don’t be silly Richard, resistance genes must still be formed one by
one sequentially by mutation and selection. These resistance genes
were selected for by use of single drug therapy in a sequential
manner. If you want to stop the lateral transfer of resistance genes,
don’t use your selection pressures one at a time in a sequential
manner and give these microbes reasonable opportunities to evolve
these resistance genes. This is a simple mathematical fact of life
that you and evolutionary biologists have failed to recognize.

>
> I am not the only person here complaining about the total absence of
> biological relevance to your claims.  Please come back when you are
> prepared to discuss quantitative issues in the proper context of what
> really happens in the real world.

Richard Norman, graduate student of probability theory, if you want to
play probability games with microbes as doctors do with their
antimicrobial selection pressures, you better learn the rules of the
game if you want to have a good chance of winning the game.
Evolutionists have demonstrated that they have no idea of the rules of
the game. On the other hand, you as a graduate student of probability
theory have the basic tools to understand the rules of the game. Apply
these principles correctly and learn how to deal with multidrug

resistant microbes, multiherbicide resistant weeds, multipesticide

resistant weeds and less than durable cancer treatments and understand
why your theory of evolution is mathematically irrational.

[Alan Kleinman MD PhD]

> >>>http://www.talkorigins.org/faqs/fitness/wherehe says the following:

I’m countering the mathematically irrational claims that Edward Max,
Supervising Medical Doctor of the Food and Drug Administration has
posted on this forum. This is the appropriate place to post the basic
science and mathematics of the mutation and selection phenomenon if
Edward Max is willing to learn it.

I am publishing this mathematics here on the Talk Origins forum. If
Edward Max and the other evolutionists on this forum can not
understand this simple mathematics and the empirical evidence which
verifies this mathematics then we will be stuck with more multidrug

resistant microbes, multiherbicide resistant weeds, multipesticide
resistant insects and less than durable cancer treatments.

>

> D- Hide quoted text -

[Alan Kleinman MD PhD]

And it gives the correct way of formulating the mathematics of
outcomes for a mutation, a set of mutually exclusive outcomes. It also
gives the correct starting point for computing the probability of a
particular mutation occurring at a specific locus and the probability
of two mutations occurring in a subpopulation.

[John Harshman]

That would be a more defensible position if your math were indeed
correct as a rule.

>>> What you have just written
>>> there is a probability involving 3 random variables. If you want to
>>> see an example of probabilities with multiple random variables, go
>>> back and study the distribution function I derived for random
>>> recombination. Measuring mutation rates and particular outcomes for
>>> mutations will always be difficult.
>> No it won't, not if the mutation is defined by phenotype. You just
>> count. Here, it isn't just different, it's impossible. You don't know
>> what bases i, j, and k are, you don't know what phenotypes if any
>> they're associated with, and you don't know which ones (note that it may
>> be anything from none of them to all three) are advantageous.
>
> If you base your measurement of mutation rate by a change in
> phenotype, you will only be able to measure beneficial and detrimental
> mutations because only these types of mutation will cause a change in
> phenotype. You will miss counting all the neutral mutations. In
> addition can not identify the locus at which the mutation occurs.
> Phenotype does not give enough detail to do an accurate accounting of
> mutation rate (and type of mutation), you must do this counting at the
> genotype.

If you have to go by the genotype, then how is it possible that you
don't know the original base? You are highly self-contradictory.

>> [snip repetitive bloviation]
>
> John you’re getting too much of your vocabulary from watching TV.

H.L. Mencken, actually.

>>>> Now if you could only be convinced that "the mutation and selection
>>>> phenomenon" makes about as much sense as "the peanut butter and
>>>> spaghetti phenomenon".
>>> John, you should know by now that it doesn’t bother me to play word
>>> games, in fact I have fun with them.
>> Yes, that's one of your major faults. Instead of real discussion, you
>> prefer word games.
>
> If you are tired of the word games, let’s have a mathematical game and
> you can learn the mathematics of the mutation and selection phenomenon.

There is no "mutation and selection phenomenon". Get this at much
correct. Mutation and selection are two separate phenomena.

[Alan Kleinman MD PhD]

John, if you evolutionists could find an exception to the mathematical
rules that I’ve applied to the mutation and selection phenomenon, you
would have posted them long ago.

>
>
>
>
>
> >>> What you have just written
> >>> there is a probability involving 3 random variables. If you want to
> >>> see an example of probabilities with multiple random variables, go
> >>> back and study the distribution function I derived for random
> >>> recombination. Measuring mutation rates and particular outcomes for
> >>> mutations will always be difficult.
> >> No it won't, not if the mutation is defined by phenotype. You just
> >> count. Here, it isn't just different, it's impossible. You don't know
> >> what bases i, j, and k are, you don't know what phenotypes if any
> >> they're associated with, and you don't know which ones (note that it may
> >> be anything from none of them to all three) are advantageous.
>
> > If you base your measurement of mutation rate by a change in
> > phenotype, you will only be able to measure beneficial and detrimental
> > mutations because only these types of mutation will cause a change in
> > phenotype. You will miss counting all the neutral mutations. In
> > addition can not identify the locus at which the mutation occurs.
> > Phenotype does not give enough detail to do an accurate accounting of
> > mutation rate (and type of mutation), you must do this counting at the
> > genotype.
>
> If you have to go by the genotype, then how is it possible that you
> don't know the original base? You are highly self-contradictory.

You don’t know what the original base is because you don’t know a
priori where a random mutation will occur before it occurs.

>
> >> [snip repetitive bloviation]
>
> > John you’re getting too much of your vocabulary from watching TV.
>
> H.L. Mencken, actually.
>
> >>>> Now if you could only be convinced that "the mutation and selection
> >>>> phenomenon" makes about as much sense as "the peanut butter and
> >>>> spaghetti phenomenon".
> >>> John, you should know by now that it doesn’t bother me to play word
> >>> games, in fact I have fun with them.
> >> Yes, that's one of your major faults. Instead of real discussion, you
> >> prefer word games.
>
> > If you are tired of the word games, let’s have a mathematical game and
> > you can learn the mathematics of the mutation and selection phenomenon.
>
> There is no "mutation and selection phenomenon". Get this at much
> correct. Mutation and selection are two separate phenomena.

Mutations are occurrences and selection determines the consequences of
these occurrences. The two concepts are coupled together to allow
adaptation to environmental stressors governed by specific
mathematical rules.

[Garamond Lethe]

On Tue, 24 Jan 2012 21:59:38 -0800, Alan Kleinman MD PhD wrote:


> John, if you evolutionists could find an exception to the mathematical
> rules that I’ve applied to the mutation and selection phenomenon, you
> would have posted them long ago.
>

Like this?

Richard Durrett, _Probability Models for DNA Sequence Evolution_, 2nd
ed. Springer, 2008.

Section 2.6 on the McDonald-Kreitman test is as good a place as any to
start (pg 78-82).

If you want to go back to the original paper, it's here:

McDonald, H. H., and Kreitman, M. (1991) Adaptive protein evoution at
the /Adh/ locus in /Drosophila/. Nature. 351, 652-654.

Enjoy!

<snip>

[David Hare-Scott]

You repeatedly claim that following current evolutionary principles will
result in considerable harm in the fields of medicine and agriculture. You
claim to have a solution to the problem or at least an alert that there is a
problem. Your method of dealing with the issue is to not publish in a
journal where it might actually do some good.

Either you have no concept of public good and the responsibility of a doctor
towards public health, or you are afraid that your theory will go down in
flames if exposed to the real world of peer review. So is it that you lack
integrity or courage?

David

[Mark Isaak]

Your notation makes sense if X is necessarily a scalar. As you used it,
X was not a scalar. If P(-∞< X< +∞) = 1, then the probability that X
= adenine or cytosine or guanine or thymine is zero, because none of
nucleic acid bases are on the number line. In short, there is
absolutely nothing right with your notation.

Anyone should know this who took any graduate-level classes in
probability. Or any mathematics, computer science, biology, chemistry,
physics, or probably a variety of other courses.

[John Harshman]

Alan Kleinman MD PhD wrote:
> On Jan 24, 9:38 pm, John Harshman <jharsh...@pacbell.net> wrote:
>> Alan Kleinman MD PhD wrote:
>>
>>
>>
>>
>>
>>> On Jan 23, 4:36 pm, John Harshman <jharsh...@pacbell.net> wrote:
>>>> Alan Kleinman MD PhD wrote:
>>>>> On Jan 23, 3:14 pm, John Harshman <jharsh...@pacbell.net> wrote:
>>>>>> Alan Kleinman MD PhD wrote:
>>>>>>> On Jan 23, 12:34 pm, John Harshman <jharsh...@pacbell.net> wrote:
>>>>>>>> Alan Kleinman MD PhD wrote:
>>>>>>>>> I wrote
>>>>>>>>> the equation for the possible outcomes for a base
substitution as:

>>>>>>>>> P(-? < X < +?) = P(Ad) + P(Cy) + P(Gu) + P(Th) = 1

>>>>>>>>> You object because Gu -> Gu does not represent a mutation. I have
>>>>>>>>> pointed out numerous times that unless you know a priori the
base at a
>>>>>>>>> particular locus; you must consider all four bases as a possible
>>>>>>>>> outcome from a base substitution. This still does not satisfy
you. So
>>>>>>>>> let’s rewrite the above equation and include the condition
that the
>>>>>>>>> base before the mutation occurs can not equal the base
afterwards and
>>>>>>>>> write out the possible base substitutions which can occur at a
>>>>>>>>> particular locus.

>>>>>>>>> P(-? < X < +?) = P(i) + P(j) + P(k) = 1, where i, j, k = the

So far you have posted absolutely nothing about selection.

>>>>> What you have just written
>>>>> there is a probability involving 3 random variables. If you want to
>>>>> see an example of probabilities with multiple random variables, go
>>>>> back and study the distribution function I derived for random
>>>>> recombination. Measuring mutation rates and particular outcomes for
>>>>> mutations will always be difficult.
>>>> No it won't, not if the mutation is defined by phenotype. You just
>>>> count. Here, it isn't just different, it's impossible. You don't know
>>>> what bases i, j, and k are, you don't know what phenotypes if any
>>>> they're associated with, and you don't know which ones (note that
it may
>>>> be anything from none of them to all three) are advantageous.
>>> If you base your measurement of mutation rate by a change in
>>> phenotype, you will only be able to measure beneficial and detrimental
>>> mutations because only these types of mutation will cause a change in
>>> phenotype. You will miss counting all the neutral mutations. In
>>> addition can not identify the locus at which the mutation occurs.
>>> Phenotype does not give enough detail to do an accurate accounting of
>>> mutation rate (and type of mutation), you must do this counting at the
>>> genotype.
>> If you have to go by the genotype, then how is it possible that you
>> don't know the original base? You are highly self-contradictory.
>
> You don’t know what the original base is because you don’t know a
> priori where a random mutation will occur before it occurs.

That makes no sense. In order to know that a mutation has occurred, you
need to know what the original base was, so you can know that the
current base is different.

>>>> [snip repetitive bloviation]
>>> John you’re getting too much of your vocabulary from watching TV.
>> H.L. Mencken, actually.
>>
>>>>>> Now if you could only be convinced that "the mutation and selection
>>>>>> phenomenon" makes about as much sense as "the peanut butter and
>>>>>> spaghetti phenomenon".
>>>>> John, you should know by now that it doesn’t bother me to play word
>>>>> games, in fact I have fun with them.
>>>> Yes, that's one of your major faults. Instead of real discussion, you
>>>> prefer word games.
>>> If you are tired of the word games, let’s have a mathematical game and
>>> you can learn the mathematics of the mutation and selection phenomenon.
>> There is no "mutation and selection phenomenon". Get this at much
>> correct. Mutation and selection are two separate phenomena.
>
> Mutations are occurrences and selection determines the consequences of
> these occurrences. The two concepts are coupled together to allow
> adaptation to environmental stressors governed by specific
> mathematical rules.

Yes, and a car needs both wheels and an engine. But there is no such
thing as "the wheels and engine phenomenon". They're two separate things.

[Kermit]

On Jan 23, 4:12 pm, Alan Kleinman MD PhD <klein...@sti.net> wrote:
> On Jan 23, 3:51 pm, Mark Isaak <eci...@curioustaxonomyNOSPAM.net>
> wrote:
>

> > On 1/23/12 10:14 AM, Alan Kleinman MD PhD wrote:
>
> > > [snip preliminary blather]

> > > If Dr. Max
> > > believes that reptiles can be transformed into birds by mutation and
> > > selection, it must be one gene at a time.
>

> > Why?
>
> Mark Isaak, social engineer. Where have you been?
>
> It must be one gene at a time because that’s the only way mutation and
> selection can work efficiently. When selection is acting on two or
> more genes simultaneously, the mutation and selection process is
> brought to a standstill.

Nonsense. Why would it?

Natural selection is acting on the phenotype all the time, for every
organism that's alive. To the degree that the phenotype is an
expression of genes, then *all of those genes are being acted on
simultaneously, forever and ever amen.

> That’s why combination therapy works for the
> treatment of HIV and any other population on which combination
> selection pressures are applied.

Showing clearly that natural selection (in the form of death) is
acting on all genes having to do with resistance to those drugs
simultaneously. It would require a bacterium resistant to all of them
to survive exposure, yes?

>
>
>
> > > When Dr. Max presented me
> > > with a paper which attempted to argue how a reptile scale could be
> > > transformed into a feather, his own reference contained over eight
> > > different genes would have to be transformed.
>

> > So?  Even if those had to happen one gene at a time, what's the problem?
>
> You have at least two problems. The first is to have selection

> pressures which target only one gene at a time.

Why are your unsupported claims a problem for reality?
Neither the math, the evidence, nor the experts in the field suggest
this. Why should I, a layman, believe someone who is contrary to
mainstream theory, has not published, and rejects evidence?

> We have this with
> targeted selection pressures such as antimicrobial agents, herbicides
> and pesticides but selection pressures in nature such as starvation,
> dehydration, thermal stress and so on will target many genes
> simultaneously.

Yes. And all the alleles interacting with each other and the
environment are being selected for or against or neither all the time.

In organisms which exchange genes, two individuals with two separate
advantages can exchange those genes with each other (if bacteria) or
pass them on (for sexually dimorphic critters).

> The second problem you encounter is the number of
> generations required in order to do such a transformation even if the
> selection pressures existed. If you have a sufficiently large
> population such as seen with microbes, the process will take about 300
> generations per mutation. That’s why the Lenski experiment takes tens
> of thousands of generations to fix only a few dozen mutations.

Yet altering the digestive system of lizards only takes a few dozen
generations.
http://www.sciencedaily.com/releases/2008/04/080417112433.htm

If multiple advantages show up, they will be processed in parallel.

> > --
> >   Mark Isaak          eciton (at) curioustaxonomy (dot) net
> > "It is certain, from experience, that the smallest grain of natural
> >   honesty and benevolence has more effect on men's conduct, than the most
> >   pompous views suggested by theological theories and systems." - D. Hume

Kermit

[hersheyh]

On Wednesday, January 25, 2012 12:05:12 AM UTC-5, Alan Kleinman MD PhD wrote:

> On Jan 23, 6:41 pm, Richard Norman <r_s_n...@comcast.net> wrote:
> > On Mon, 23 Jan 2012 10:18:14 -0800 (PST), Alan Kleinman MD PhD
> >

[snip]

>
> >
> > You tell John Stockwell "The only thing that I am doing is showing how
> > subpopulations under the right circumstances accumulate beneficial
> > mutations" yet you do not account for the benefit of these beneficial
> > mutations in any calculation you show.  Now you describe what you mean
> > by beneficial but that concept appears absolutely nowhere in your
> > work.  You also argue that recombination must be totally irrelevant
> > without seeming to understand that it is an important mechanism in
> > producing organisms that show multiple mutations, the separate
> > mutations arising separately.  That fact, alone, destroys your
> > argument about multiplication of probabilities when applied in the
> > trivial way you seem to insist.
>
> Richard pay attention. I have shown many times where the concept of
> beneficial and detriment mutation enters into the mathematics of
> mutation and selection. I’ll repeat it once again for you here. Here
> once again is the equation which describes the probabilities of two
> beneficial mutations occurring in a subpopulation:
>
> P(A)*P(B) = {1 - (1-(mA/4))^(n*nGA)} * {1 – ((1-(mB/4))^(nA*nGB)}

The above is a GIGO equation on many levels.

First, 1 - (1-pA)^n (which is the algebraic equivalent of your equation)
does not calculate the probability of A in a population. It calculates
the probability of one or more A's in a population of size n when
the probability of A is pA. pA is the probability (frequency) of A
in the population.

Second, the second term in the equation is NOT the probability of
B in cells that already have mutation A. It is the probability of B
in the number of cells that have A, whether they actually have A
or not.

Third, it is not a calculation of the joint probability of A and B.
That would be pA*pB if mutation were like dice rolling. The calculation
of joint probability gives us the probability of a double-mutant,
which is the "event" of interest. You then use that *joint probability*
to calculate the probability of one or more such double-mutants
in a population of size n when the joint probability of double-mutants
is pA*pB. IOW:
Probability of one or more double-mutants = 1 - (1-pA*pB)^n

However, serial mutation is not like dice rolling in this sense: In
dice rolling both dice are completely independent events and the
probability of any one face is set in stone (well, ivory or plastic).
In serial mutation, the probability of any single mutant can be affected by
past selection or drift and can be any value between the mutation
rate/frequency/probability and 1. But in organisms without recombination
the only way to get a double-mutant is either simultaneous mutation or
a second mutation in a lineage that is derived from a previous mutation
at the other site.

I have given Kleinman a *correct* description of that probability by pointing
out that there are four ways a cell can have one or more new double-mutant
(prior to selection for double-mutants). The frequency of A and the frequency of B can
be any value between the mutation probability and 1 in a population due to
prior selection and/or drift. Let's call this the *observed*
probability of A, pAo, and call the *mutation* probability of A, pAm. Then the
probability of A present due to past history of A (due to selection or drift rather
than new mutation; this would be the probability in excess of the pAm) =
pA0 - pAm = pAd (the probability of A in the population by descent rather
than new mutation). Similarly for B, we get pBo, pBm, and pBd.

Unlike dice, where the probability of any given face is always *observed* to
be 1/6, the probability of double-mutant does not equal pAo*pBo in the
absence of recombination each generation.

The four ways that a cell can have a new double-mutant are:
1) A new B mutation in a cell that inherited an A mutation by descent.
That probability is pAd*pBm.
2) A new A mutation in a cell that inherited a B mutation by descent.
That probability is pAm*pBd
3) Simultaneous new mutation to A and B in a cell that had neither mutant allele.
4) Random recombination of pre-exisiting A and B alleles (A and B by descent).
This term is a function of the frequency of recombination per generation, fr, and
the frequency of the alleles of interest by descent, pAd and pBd. The
frequency of recombination can be any value between 0 and 1.
Bacteria in these experiments typically have an fr = 0. Sexually-reproducing
multicellular eucaryotes like us have fr = 1. Other organisms can
have intermediate levels of random recombination.

The general equation, including all four mechanisms, would be:

Probability of one or more double-mutants in a population of size n when
the probability of A is pAo and the probability of B is pBo in the population =
[1 - (1-pAm*pBd)^n] + [1 - (1-pAd*pBm)^n] + [1 - (1-pAm*pBm)^n] + [fr*pAd*pBd]

These terms calculate mutation in the haploid state rather than the diploid state.
Diploid states complicate things and requires an understanding of dominance
and recessiveness if phenotype matters.

Note that each of the four terms has an actual *joint probability* of A and B
double-mutants in it. Which make them an immediate improvement over
Kleinman's garbage. All four terms measure the *joint probability* of A and
B in the same trial rather than in a given number of trials.

Moreover, the importance of the various terms is related to the reality. If
the frequency of recombination is 0, the last term drops out. If the probability
of both A and B in the population are their respective mutation frequencies,
the first two terms drop out. If pAo (or pBo) is significantly higher than pAm
(or pBm), then that term is the most important one. If both pAo and pBo are
higher than their respective mutation probabilities, which is quite possible
if each has independent selective utility above their respective w.t., then
both of the first two terms are the important ones. If random recombination
between existing alleles is occurring at a frequency of once per generation
and both pAd and pBd are larger than the respective mutation probabilities,
then that recombination term will largely determine the probability of new
double-mutant in such a population of size n and pAo and pBo.

> The variable in the above equation which reflects whether mutation B
> will have a reasonable probability of occurring on a member with
> mutation A is nA, the number of members with mutation A. If mutation A
> is beneficial, nA will amplify over generations, increasing in number
> so as to improve the probability that mutation B will occur on one of
> the members of this subpopulation. If mutation A is neutral or
> detrimental so that the subpopulation size with that mutation remains
> constant or decreases, the only other variable which can improve the
> probability that mutation B will occur on a member with mutation A is
> nGB, the number of generations which that subpopulation with mutation
> A is able to replicate.

Kleinman's GIGO is based, probably, on the false idea that what he is
calculating is the joint probability of a double-mutation rather than
the probability of one or more double-mutants. Mine is based on
knowing that pAo and pBo are the observed probability of A and B
in the population.

I have described both why I think Kleinman's equation is GIGO and
presented an alternative equation based on a more correct understanding
of both what mutation is, what the probability of a mutant in a population
is and how it differs from the mass probability equation. Now it is up to
Herr Kleinman to do both and let the best equation win.

[snip]

[Kermit]

On Jan 23, 10:06 am, Alan Kleinman MD PhD <klein...@sti.net> wrote:
> >nando_rontel...@yahoo.com   Jan 20, 7:31 am
> >Newsgroups: talk.origins
> >From: "nando_rontel...@yahoo.com" <nando_rontel...@yahoo.com>
> >Date: Fri, 20 Jan 2012 07:31:37 -0800 (PST)
> >Local: Fri, Jan 20 2012 7:31 am
> >Subject: Re: The Theory of Evolution is a mathematically irrational belief
>
> >On Jan 20, 4:12 pm, Alan Kleinman MD PhD <klein...@sti.net> wrote:
>
> >> On Jan 19, 10:10 am, "nando_rontel...@yahoo.com"
>
> >> <nando_rontel...@yahoo.com> wrote:
> >> > On Jan 19, 6:17 pm, "Jim T." <x...@y.z> wrote:
>
> >> > > On Wed, 18 Jan 2012 15:44:26 -0800 (PST), hersheyh
> >> > > >You are hilarious!  When are you going to tell us the truth -- that you are a troll?
> >> > > >Only a troll could present your mathematical ignorance and high arrogance
> >> > > >in all seriousness.
>
> >> > > Surely he suffering from some sort of mental illness. I have suspected
> >> > > so for months.
>
> >> > 100 percent of anti-evolutionists on talk.origins are "accused" of a
> >> > mental disorder. That is because evolutionists can't deal with forming
> >> > a subjective opinion about another. Evolutionists can only deal with
> >> > people by making it into a matter of objective fact about a brain
> >> > state, instead of forming a subjective opinion. It is your science
> >> > induced pathology that you can't accept the existence of anything
> >> > subjectively, that you need to be forced by evidence in everything.
>
> >> > All you evolutionists are insulting everybody on a continuous basis
> >> > because you don't properly relate free will of yourself, to free will
> >> > of the other. You don't properly subjectively acknowledge the people
> >> > you are conversing with as the owner of their choices.  Alan could go
> >> > on a TV show presenting his finding, all you evolutionists couldn't
> >> > because of your obvious social deficiency.
>
> >> > Again the study....
> >> > Prosocial Benefits of Feeling Free: Disbelief in Free Will Increases
> >> > Aggression and Reduces Helpfulnesshttp://psp.sagepub.com/content/35/2/260.abstract

>
> >> Nando, this is what evolutionists do when they don’t have any
> >> empirical or mathematical evidence to support their theory. If Charles
> >> Brenner, self proclaimed professional forensic mathematician had any
> >> mathematical evidence to support the theory of evolution, he would
> >> have posted it long ago. If Bill had any empirical evidence to support
> >> the theory of evolution, he would have posted it long ago. And we have
> >> evolutionist bureaucrats like Thomas Schneider at National Cancer
> >> Institute who makes a major scientific blunder by claiming that the
> >> multiplication rule does not apply to biological evolution and harms

> >> the very people he is paid to help. Instead, we have multidrug

> >> resistant microbes, multiherbicide resistant weeds, multipesticide

> >> resistant insects and less than durable cancer treatments as the
> >> legacy of the mathematically irrational theory of evolution.

> >> Evolutionists have embraced the mathematically irrational theory of
> >> evolution with religious fervor and the consequence of this scientific
> >> bungling dogmatism is harm to millions of people. It is evolutionists
> >> who have lost contact with reality.
>
> >You say it yourself, religious fervor. The theory of evolution is tied
> >up with how they view free will, values etc. It requires a big
> >personal change for them to acknowledge they are wrong, which is why
> >they won't do it. Darwinists denied Mendel for up to 72 years, then
> >they turned around and said Mendel findings support Darwinism, while
> >Mendellism indicates stasis. The most likely outcome of it is that
> >they will adopt the change in mathematics, fudge the issue about how
> >come they were wrong, and simply say those mathematics support
> >evolution theory.
>
> Nando, evolutionists will have a hard time fudging this one. Mutation
> and selection only works efficiently one mutation at a time and the
> amplification of that mutation takes hundreds of generations before
> you have a reasonable probability that the next beneficial mutation
> will occur on a member with the previous beneficial mutation.
> Evolutionists simply don’t have enough generations to transform a
> reptile into a bird. That is a mathematical and empirical fact of
> life. So unless the evolutionist dominated field of biology comes to
> grips with these mathematical facts of life, we will be faced with

> more multidrug resistant microbes, multiherbicide resistant weeds,
> multipesticide resistant insects and less than durable cancer
> treatments.

This non-mathematician is not impressed by your treating Nando as an
ally. Do you agree with him that rocks make decisions?

Kermit

[Richard Norman]

In short, Kleinman does not understand the biology of the "mutation
and selection" process and hence is totally incapable of calculating
anything related to it.

[Kermit]

On Jan 23, 6:41 pm, chris thompson <chris.linthomp...@gmail.com>
wrote:
> On Jan 23, 6:57 pm, Alan Kleinman MD PhD <klein...@sti.net> wrote:
>
> snip
>
> How old is planet Earth?

Now you've done it. We're going to get math that shows that geology is
an irrational science.

>
> How old is the universe?

Crap. And cosmology.

>
> Chris

Kermit

[hersheyh]

On Wednesday, January 25, 2012 12:21:41 PM UTC-5, Kermit wrote:
> On Jan 23, 10:06 am, Alan Kleinman MD PhD <klei...@sti.net> wrote:
> > >nando_r...@yahoo.com   Jan 20, 7:31 am

[snip]

> This non-mathematician is not impressed by your treating Nando as an
> ally. Do you agree with him that rocks make decisions?

Kleinman is happy to get support from any nut he can. Do you expect
someone sane to support him?
>
> Kermit

[Alan Kleinman MD PhD]

The edition of “Probability Models for DNA Sequence Evolution”
available to me discusses the McDonald-Kreitman statistical test in
section 4 starting on page 181. What they found when they examined the
evolutionary dynamics of alcohol dehydrogenase gene in three species
of Drosophila was their test provides strong evidence for positive
selection and against neutral mutation-random drift.

How does this contradict the mathematical and empirical facts of life
that mutation and selection does not operate in parallel? Of course it
doesn’t.


>
> <snip>

[Alan Kleinman MD PhD]

[snip]

>
> If multiple advantages show up, they will be processed in parallel.

When you have multiple selection pressures targeting multiple genes,
you don’t have multiple advantages. That is why combination therapy
works for the treatment of HIV and for all real, measurable and
repeatable examples of mutation and selection this is a fact of life.

>
> > > --
> > >   Mark Isaak          eciton (at) curioustaxonomy (dot) net
> > > "It is certain, from experience, that the smallest grain of natural
> > >   honesty and benevolence has more effect on men's conduct, than the most
> > >   pompous views suggested by theological theories and systems." - D. Hume
>

> Kermit- Hide quoted text -

[Alan Kleinman MD PhD]

> >>>>>http://www.talkorigins.org/faqs/fitness/wherehesays the

My response is to try to correct Edward Max, Supervising Medical
Doctor of the Food and Drug Administration and publisher of essays on
this forum when his essays claim a mathematically irrational
misinterpretation of the mutation and selection phenomenon. Edward Max
has a responsibility to properly understand how mutation and selection
works because his failure to do so harms millions of people. Max is in
the position to do something about it if he wishes to prevent the
formation of more multidrug resistant organisms.

>
> Either you have no concept of public good and the responsibility of a doctor
> towards public health, or you are afraid that your theory will go down in
> flames if exposed to the real world of peer review.  So is it that you lack
> integrity or courage?

Who peer reviewed Max’s mathematically irrational claims about
mutation and selection when he posted his essay here on this forum?
Max and people like Thomas Schneider at the National Cancer Institute
would rather see people suffer from diseases subject to mutation and
selection rather than understanding the basic science and mathematics
of the mutation and selection phenomenon. If Max thinks I’m wrong then
let him explain why combination therapy suppresses the evolution of
HIV and for every other real, measurable and repeatable example of
mutation and selection where combination selection pressures are used.
It’s not just the mathematical derivations I’ve done for you; it’s all
the empirical evidence which substantiates the mathematics.

>
> David- Hide quoted text -

[Alan Kleinman MD PhD]

Hersheyh has not taken an introductory course in probability theory
let alone passed such a course. Hersheyh thinks that the addition rule
of probabilities is the governing axiom for the joint probability of
events. Richard, if you read hersheyh’s equations you will see his
obvious blunder. Now you Richard are a graduate student of probability
theory and almost derived the correct probability function for random
recombination. Now you need to try to understand why combination
therapy works for the treatment of HIV because the correct application
of the axioms of probability theory will explain the mathematical and
empirical facts of life how mutation and selection works.

[Alan Kleinman MD PhD]

On Jan 25, 6:50 am, Mark Isaak <eci...@curioustaxonomyNOSPAM.net>
wrote:

> On 1/24/12 9:07 PM, Alan Kleinman MD PhD wrote:
>
> > On Jan 24, 9:35 am, Richard Norman<r_s_nor...@comcast.net>  wrote:
>
> >>> <snip>
>
> >> Somebody who has studied probability theory might write Pr(S) = 1
> >> where S is the sample space.  It still wouldn't mean anything but at
> >> least it would be standard notation.
>
> > There is absolutely nothing wrong with the notation P(-∞<  X<  +∞) = 1
> > and it is totally equivalent to P(S) = 1. You should know that Richard
> > as a graduate student of probability theory.
>
> Your notation makes sense if X is necessarily a scalar.  As you used it,
> X was not a scalar.  If P(-∞<  X<  +∞) = 1, then the probability that X
> = adenine or cytosine or guanine or thymine is zero, because none of
> nucleic acid bases are on the number line.  In short, there is
> absolutely nothing right with your notation.
>
> Anyone should know this who took any graduate-level classes in
> probability.  Or any mathematics, computer science, biology, chemistry,
> physics, or probably a variety of other courses.

Mark, what difference does it make in the probabilities if you label
the faces on a die Ad, Cy, Gu, Th, Mark and John instead of 1, 2, 3,
4, 5, and 6? Even a social engineer should understand this.

[Alan Kleinman MD PhD]

Didn’t you read the post I made to rnorman on this issue? I’ll repeat
it here for you:

John pay attention and don’t be lazy. I have shown many times where
the concept of beneficial and detrimental mutation enters into the

mathematics of mutation and selection. I’ll repeat it once again for
you here. Here once again is the equation which describes the
probabilities of two beneficial mutations occurring in a
subpopulation:

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

The variable in the above equation which reflects whether mutation B
will have a reasonable probability of occurring on a member with
mutation A is nA, the number of members with mutation A. If mutation A
is beneficial, nA will amplify over generations, increasing in number
so as to improve the probability that mutation B will occur on one of
the members of this subpopulation. If mutation A is neutral or
detrimental so that the subpopulation size with that mutation remains
constant or decreases, the only other variable which can improve the
probability that mutation B will occur on a member with mutation A is
nGB, the number of generations which that subpopulation with mutation
A is able to replicate.


>

Certainly you need to know what the original base was before the
mutation occurred but you don’t know this a priori. Why does Lenski
freeze samples from his experiment? He does this so he can determine
how the genetic sequences change with time. He does not know where the
mutations will occur. He must sequence before and after replication in
order to determine this. Unless you know before hand what the base is
at a particular site before the mutation occurs, you must consider all
bases as possible substitution outcomes in the probability
calculations.

>
>  >>>> [snip repetitive bloviation]
>  >>> John you’re getting too much of your vocabulary from watching TV.
>  >> H.L. Mencken, actually.
>  >>
>  >>>>>> Now if you could only be convinced that "the mutation and selection
>  >>>>>> phenomenon" makes about as much sense as "the peanut butter and
>  >>>>>> spaghetti phenomenon".
>  >>>>> John, you should know by now that it doesn’t bother me to play word
>  >>>>> games, in fact I have fun with them.
>  >>>> Yes, that's one of your major faults. Instead of real discussion, you
>  >>>> prefer word games.
>  >>> If you are tired of the word games, let’s have a mathematical game and
>  >>> you can learn the mathematics of the mutation and selection phenomenon.
>  >> There is no "mutation and selection phenomenon". Get this at much
>  >> correct. Mutation and selection are two separate phenomena.
>  >
>  > Mutations are occurrences and selection determines the consequences of
>  > these occurrences. The two concepts are coupled together to allow
>  > adaptation to environmental stressors governed by specific
>  > mathematical rules.
>
> Yes, and a car needs both wheels and an engine. But there is no such
> thing as "the wheels and engine phenomenon". They're two separate things.

The engine drives the wheels and the theory of evolution no longer has
an engine.

[Alan Kleinman MD PhD]

Didn’t you read the post I made to rnorman on this issue? I’ll repeat
it here for you:

John pay attention and don’t be lazy. I have shown many times where
the concept of beneficial and detrimental mutation enters into the
mathematics of mutation and selection. I’ll repeat it once again for
you here. Here once again is the equation which describes the
probabilities of two beneficial mutations occurring in a
subpopulation:

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

The variable in the above equation which reflects whether mutation B
will have a reasonable probability of occurring on a member with
mutation A is nA, the number of members with mutation A. If mutation A
is beneficial, nA will amplify over generations, increasing in number
so as to improve the probability that mutation B will occur on one of
the members of this subpopulation. If mutation A is neutral or
detrimental so that the subpopulation size with that mutation remains
constant or decreases, the only other variable which can improve the
probability that mutation B will occur on a member with mutation A is
nGB, the number of generations which that subpopulation with mutation
A is able to replicate.


>

Certainly you need to know what the original base was before the
mutation occurred but you don’t know this a priori. Why does Lenski
freeze samples from his experiment? He does this so he can determine
how the genetic sequences change with time. He does not know where the
mutations will occur. He must sequence before and after replication in
order to determine this. Unless you know before hand what the base is
at a particular site before the mutation occurs, you must consider all
bases as possible substitution outcomes in the probability
calculations.

>

>  >>>> [snip repetitive bloviation]
>  >>> John you’re getting too much of your vocabulary from watching TV.
>  >> H.L. Mencken, actually.
>  >>
>  >>>>>> Now if you could only be convinced that "the mutation and selection
>  >>>>>> phenomenon" makes about as much sense as "the peanut butter and
>  >>>>>> spaghetti phenomenon".
>  >>>>> John, you should know by now that it doesn’t bother me to play word
>  >>>>> games, in fact I have fun with them.
>  >>>> Yes, that's one of your major faults. Instead of real discussion, you
>  >>>> prefer word games.
>  >>> If you are tired of the word games, let’s have a mathematical game and
>  >>> you can learn the mathematics of the mutation and selection phenomenon.
>  >> There is no "mutation and selection phenomenon". Get this at much
>  >> correct. Mutation and selection are two separate phenomena.
>  >
>  > Mutations are occurrences and selection determines the consequences of
>  > these occurrences. The two concepts are coupled together to allow
>  > adaptation to environmental stressors governed by specific
>  > mathematical rules.
>
> Yes, and a car needs both wheels and an engine. But there is no such
> thing as "the wheels and engine phenomenon". They're two separate things.

[John Harshman]

I will just point out that none of the math there has anything to do
with selection. The only bit about selection is the couple of sentences
where you talk about what happens to nA over time. But that isn't in the
math at all.

None of that has anything to do with the proper math.

> Why does Lenski
> freeze samples from his experiment? He does this so he can determine
> how the genetic sequences change with time. He does not know where the
> mutations will occur. He must sequence before and after replication in
> order to determine this. Unless you know before hand what the base is
> at a particular site before the mutation occurs, you must consider all
> bases as possible substitution outcomes in the probability
> calculations.

No you mustn't. If you do that you get a wrong answer. Your math is just
plain wrong and biologically meaningless. You further assume, may I
point out, that only a single mutation at a given site is advantageous.

>> >>>> [snip repetitive bloviation]
>> >>> John you’re getting too much of your vocabulary from watching TV.
>> >> H.L. Mencken, actually.
>> >>
>> >>>>>> Now if you could only be convinced that "the mutation and selection
>> >>>>>> phenomenon" makes about as much sense as "the peanut butter and
>> >>>>>> spaghetti phenomenon".
>> >>>>> John, you should know by now that it doesn’t bother me to play word
>> >>>>> games, in fact I have fun with them.
>> >>>> Yes, that's one of your major faults. Instead of real discussion, you
>> >>>> prefer word games.
>> >>> If you are tired of the word games, let’s have a mathematical game and
>> >>> you can learn the mathematics of the mutation and selection phenomenon.
>> >> There is no "mutation and selection phenomenon". Get this at much
>> >> correct. Mutation and selection are two separate phenomena.
>> >
>> > Mutations are occurrences and selection determines the consequences of
>> > these occurrences. The two concepts are coupled together to allow
>> > adaptation to environmental stressors governed by specific
>> > mathematical rules.
>>
>> Yes, and a car needs both wheels and an engine. But there is no such
>> thing as "the wheels and engine phenomenon". They're two separate things.
>
> The engine drives the wheels and the theory of evolution no longer has
> an engine.

Having no argument, you fall back on word games. As usual.

[David Hare-Scott]

More dodgeball. I'm done with your evasions.

D

[Ray Martinez]

On Jan 24, 8:59 pm, Alan Kleinman MD PhD <klein...@sti.net> wrote:
> On Jan 23, 4:31 pm, Ray Martinez <pyramid...@yahoo.com> wrote:
>
>
>
>
>
> > On Jan 23, 10:08 am, Alan Kleinman MD PhD <klein...@sti.net> wrote:
>
> > > >Steven L.  Jan 20, 7:44 am
> > > >Newsgroups: talk.origins
> > > >From: "Steven L." <sdlit...@earthlink.net>
> > > >Date: Fri, 20 Jan 2012 15:44:37 +0000
> > > >Local: Fri, Jan 20 2012 7:44 am

> > > >Subject: Re: The Theory of Evolution is a mathematically irrational belief
>

> > > >"Alan Kleinman MD PhD" <klein...@sti.net> wrote in message
> > > >news:89feea55-7ef1-41e7...@k9g2000pbc.googlegroups.com:

>
> > > >> Nando, this is what evolutionists do when they don't have any
> > > >> empirical or mathematical evidence to support their theory. If Charles
> > > >> Brenner, self proclaimed professional forensic mathematician had any
> > > >> mathematical evidence to support the theory of evolution, he would
> > > >> have posted it long ago. If Bill had any empirical evidence to support
> > > >> the theory of evolution, he would have posted it long ago. And we have
> > > >> evolutionist bureaucrats like Thomas Schneider at National Cancer
> > > >> Institute who makes a major scientific blunder by claiming that the
> > > >> multiplication rule does not apply to biological evolution and harms

> > > >> the very people he is paid to help. Instead, we have multidrug

> > > >> resistant microbes, multiherbicide resistant weeds, multipesticide

> > > >> resistant insects and less than durable cancer treatments as the
> > > >> legacy of the mathematically irrational theory of evolution.
>

> > > >You don't have to keep repeating it:

> > > >The Theory of Evolution is a mathematically irrational belief

> > > >talk.origins  -  449 posts  -  29 authors  - Last post:  Nov 14, 2011
> > > >And your sloppy evolutionist junk science has given us multidrug

> > > >resistant microbes, multiherbicide resistant weeds, multipesticide resistant

> > > >insects and less ...
>
> > > >http://groups.google.com/g/c9c7fef4/t/97d3bac032a2ed51/.../73a30e9601......
> > > >The Theory of Evolution is Mathematically Irrational Round 2
> > > >talk.origins  -  716 posts  -  44 authors  - Last post:  Jul 19, 2011
> > > >The reality of multidrug resistant microbes, multiherbicide resistant

> > > >weeds, multipesticide resistant insects and less than durable cancer treatments

> > > >is a testament ...
>
> > > >http://groups.google.com/g/c9c7fef4/t/db3f6763b7616fbd/d/a8ea0bf6a258......
> > > >The Theory of Evolution is a mathematically irrational belief system
> > > >talk.origins  -  2 posts  -  2 authors  - Last post:  Mar 15, 2011
> > > >.... phenomenon works leads to drug resistant microbes, herbicide
> > > >resistant weeds, pesticide resistant insects, reduced durability of cancer
> > > >treatments and so on. ...
>
> > > >http://groups.google.com/g/c9c7fef4/t/3964b88e0f9b2e58/d/bfacf50960f7......

> > > >The Theory of Evolution is a mathematically irrational belief

> > > >talk.origins  -  2 posts  -  2 authors  - Last post:  Mar 21, 2011
> > > >It is not just multidrug resistant bacteria that's a problem, it
> > > >multi-herbicide resistant weeds, multi-pesticide resistant insects, and drug resistant
> > > >cancers. Farmers ...
>
> > > >http://groups.google.com/g/c9c7fef4/t/2ed6cf2b11893a93/d/ae72e624c7fd......
> > > >Trying to salvage something from this Re: The Theory of Evolution
> > > >talk.origins  -  1 post  -  1 author  - Last post:  Sep 14, 2011
> > > >You've bungled the mathematics of mutation and selection and given us

> > > >multidrug resistant microbes, multiherbicide resistant weeds,

> > > >multipesticide resistant ...
>
> > > >http://groups.google.com/g/c9c7fef4/t/c99c95ee7f90ebef/d/74d86c30a695......

> > > >The Theory of Evolution is a mathematically irrational belief

> > > >talk.origins  -  1 post  -  1 author  - Last post:  Mar 23, 2011
> > > >No wonder we live in a world with multidrug resistant bacteria,
> > > >multi-herbicide resistant weeds, multi-pesticide resistant insects. Evolutionists have
> > > >taken us into ....
>
> > > >http://groups.google.com/g/c9c7fef4/t/791d4747b8934600/d/6f9a4aa1c9ea......
> > > >Trying to salvage something from this Re: The Theory of Evolution
> > > >talk.origins  -  1 post  -  1 author  - Last post:  Sep 14, 2011
> > > >The end result of this evolutionist blunder is multidrug resistant

> > > >microbes, multiherbicide resistant weeds, multipesticide resistant insects and

> > > >less than durable ...
>
> > > >http://groups.google.com/g/c9c7fef4/t/f058224d55f65df4/d/3952b710b5fa......

> > > >The Theory of Evolution is a mathematically irrational belief

> > > >talk.origins  -  1 post  -  1 author  - Last post:  Mar 15, 2011
> > > >.... phenomenon works, we would not have the problems we have today with
> > > >multidrug resistant microbes, multiherbicide resistant weeds, multipesticide resistant ...
>
> > > >http://groups.google.com/g/c9c7fef4/t/7a538320e0eaa9d3/d/bc5cfdde1072......
> > > >The Theory of Evolution is Mathematically Irrational Round 2
> > > >talk.origins  -  1 post  -  1 author  - Last post:  Sep 14, 2011
> > > >.... to prevent drug resistant microbes, herbicide resistant weed,
> > > >pesticide resistant .... multiherbicide resistant weeds, multipesticide resistant insects
> > > >and produce ...
>
> > > >http://groups.google.com/g/c9c7fef4/t/6c621df006fbbad9/d/3210a9371c5f......
> > > >Insane "logic" from Ron O.
> > > >talk.origins  -  6 posts  -  4 authors  - Last post:  Sep 23, 2011
> > > >And the end result of this scientific and educational failure is the
> > > >spread of multidrug resistant microbes, multiherbicide resistant weeds,
> > > >multipesticide resistant ...
>
> > > >http://groups.google.com/g/c9c7fef4/t/ae189dac2e081315/d/7bb5c61dda11......
> > > >We hear you.
> > > >You don't have to keep repeating it like a mantra.
> > > >Have you defined a hotkey that keeps spitting out "multidrug resistant

> > > >microbes, multiherbicide resistant weeds, multipesticide resistant
> > > >insects and less than durable cancer treatments"

> > > >or do you just retype it over and over?
>
> > > Quit whining Steven, it makes you sound like an evolutionist. This

> > > multidrug resistant microbes, multiherbicide resistant weeds,
> > > multipesticide resistant insects and less than durable cancer

> > > treatments defines the utter failure of evolutionism and the harm it
> > > has done to society and you better get used to hearing it because this

> > > is a mathematical and empirical fact of life.
>

> > "[U]tter failure of evolutionism" yet you accept the main empirical
> > claims: natural selection, species mutability.
>
> > Ray (species immutabilist)
>
> Ray, I accept that life forms have mutations when they replicate and
> selection will act on those mutations....

In other words you accept the **concepts** of random mutation and
natural selection to exist in nature, like all Darwinists/Atheists.

> ....but I don’t accept that random
> mutation and natural selection will transform reptiles into birds.

Since you accept conceptual existence your denial of cumulation is
meaningless and contradictory. Your arguments against the veracity of
ToE are completely undermined.

> If you understand the basic science and mathematics of mutation and
> selection, you would find that to be a mathematically irrational
> belief.

I completely agree. Darwinism is irrational and illogical on every
level. Your inability to perceive the contradiction and undermining
effect in your position dictates, at the very least, knowledge
limitations in the relevant disciplines of logic, philosophy and the
histories of Creationism/Darwinism. Natural selection is a mutually
exclusive claim. If it exists, then the God hypothesis (arguments from
design) is refuted.

Ray (Old Earth Paleyan IDist-species immutabilist)

[hersheyh]

On Wednesday, January 25, 2012 7:18:50 PM UTC-5, Alan Kleinman MD PhD wrote:
> On Jan 25, 6:50 am, Mark Isaak <eci...@curioustaxonomyNOSPAM.net>
> wrote:
> > On 1/24/12 9:07 PM, Alan Kleinman MD PhD wrote:
> >

> > > On Jan 24, 9:35 am, Richard Norman<r_s_n...@comcast.net>  wrote:

> >
> > >>> <snip>
> >
> > >> Somebody who has studied probability theory might write Pr(S) = 1
> > >> where S is the sample space.  It still wouldn't mean anything but at
> > >> least it would be standard notation.
> >
> > > There is absolutely nothing wrong with the notation P(-∞<  X<  +∞) = 1
> > > and it is totally equivalent to P(S) = 1. You should know that Richard
> > > as a graduate student of probability theory.
> >
> > Your notation makes sense if X is necessarily a scalar.  As you used it,
> > X was not a scalar.  If P(-∞<  X<  +∞) = 1, then the probability that X
> > = adenine or cytosine or guanine or thymine is zero, because none of
> > nucleic acid bases are on the number line.  In short, there is
> > absolutely nothing right with your notation.
> >
> > Anyone should know this who took any graduate-level classes in
> > probability.  Or any mathematics, computer science, biology, chemistry,
> > physics, or probably a variety of other courses.
>
> Mark, what difference does it make in the probabilities if you label
> the faces on a die Ad, Cy, Gu, Th, Mark and John instead of 1, 2, 3,
> 4, 5, and 6? Even a social engineer should understand this.

It makes a difference if what you claim is an actual mathematical
equation is complete bullshit and doesn't say what you claim it means.
That goes to your supposed (hypothetical)
competence. In fact, it wouldn't matter in this case, since the
claim that the probability of any *number* between - and + infinity
(except one, of course) always equals one is just as absurd as the
claim that any *symbol* or *category* between - and + infinity makes
any sense.

We are objecting to a set of symbols that don't mean what you
claim they mean. P(-∞< X< +∞) = 1 is nonsense.

What is the probability of the number 100? Is it 1? 100 clearly is
an X that exists between - and + infinity. So what is its probability?

What is the probability of gold? Is it 1? I don't even know what
the claim, "gold lies between - and + infinity" means.

Besides, in mutation analysis, *one* of the bases will be the "not-mutant"
state. That base has a probability close to, but not equal to 1.

If you want to say that sum of probabilities of all possible categories
observed in n trials = 1, then say that. Don't pretend that
P(-∞< X< +∞) = 1 says that.

[hersheyh]

On Wednesday, January 25, 2012 7:27:25 PM UTC-5, Alan Kleinman MD PhD wrote:

> On Jan 25, 9:38 am, Richard Norman <r_s_n...@comcast.net> wrote:
> > On Wed, 25 Jan 2012 09:20:07 -0800 (PST), hersheyh
> >
> >
> >
> >
> >
> > <hers...@yahoo.com> wrote:
> > >On Wednesday, January 25, 2012 12:05:12 AM UTC-5, Alan Kleinman MD PhD wrote:

Since no one else here is as brilliant a mathematician as you are
why don't you dazzle us by SHOWING me up to be the idiot you
seem to think I am rather than pleading for poor Richard to do
it for you?

I am *correctly* using the addition rule to add mutually exclusive
probabilities together, since all four of the mechanisms I described
for generating new double-mutants are mutually exclusive.

I am *correctly* using the multiplication rule for multiplying
the probabilities of the two mutations in each of those
mechanisms to get the probability of double-mutation
attributable to that mechanism.

Now, do you have something intelligent to say, or are you
going to whine for your mommy or Richard to save your
sorry ass?

[Bill]

On Jan 26, 11:55 am, hersheyh <hershe...@yahoo.com> wrote:

>
> It makes a difference if what you claim is an actual mathematical
> equation is complete bullshit and doesn't say what you claim it means.
> That goes to your supposed (hypothetical)
> competence.  In fact, it wouldn't matter in this case, since the
> claim that the probability of any *number* between - and + infinity
> (except one, of course) always equals one is just as absurd as the
> claim that any *symbol* or *category* between - and + infinity makes
> any sense.
>
> We are objecting to a set of symbols that don't mean what you
> claim they mean.  P(-∞<  X<  +∞) = 1 is nonsense.
>
> What is the probability of the number 100?   Is it 1?  100 clearly is
> an X that exists between - and + infinity.  So what is its probability?
>
> What is the probability of gold?  Is it 1?  I don't even know what
> the claim, "gold lies between - and + infinity" means.
>
> Besides, in mutation analysis, *one* of the bases will be the "not-mutant"
> state.  That base has a probability close to, but not equal to 1.

.
>
> If you want to say that sum of probabilities of all possible categories
> observed in n trials = 1, then say that.  Don't pretend that
>  P(-∞<  X<  +∞) = 1 says that.

Although Dr.Dr. is wrong about most everything he writes, this
notation does not bother me. Given any random, real number variable X,
and any probability distribution, the probability that X falls within
the range from negative infinity to positive infinity is indeed
1.Given a standard normal distribution he could write P(X<0)= 0.5.

He's being sloppy if he thinks that that notation applies directly to
categorical variables (e.g. "gold").

It's trivial. It says no more than that given a trial, some outcome
will occur.

[hersheyh]

On Wednesday, January 25, 2012 7:22:23 PM UTC-5, Alan Kleinman MD PhD wrote:

> On Jan 25, 7:57 am, John Harshman <jhar...@pacbell.net> wrote:
> > Alan Kleinman MD PhD wrote:

> >  > On Jan 24, 9:38 pm, John Harshman <jhar...@pacbell.net> wrote:
> >  >> Alan Kleinman MD PhD wrote:
> >  >>
> >  >>
> >  >>
> >  >>
> >  >>
> >  >>> On Jan 23, 4:36 pm, John Harshman <jhar...@pacbell.net> wrote:
> >  >>>> Alan Kleinman MD PhD wrote:

> >  >>>>> On Jan 23, 3:14 pm, John Harshman <jhar...@pacbell.net> wrote:
> >  >>>>>> Alan Kleinman MD PhD wrote:

You have indicated that there is such a thing as selection and that
it does affect the probability of an allele in a population by increasing
the frequency of that allele generation after generation so long as
the selective conditions remain. But you haven't presented the
mathematics of such change. Presenting a concept is not presenting
a mathematical model.

> I’ll repeat it once again for
> you here. Here once again is the equation which describes the
> probabilities of two beneficial mutations occurring in a
> subpopulation:
>
> P(A)*P(B) = {1 - (1-(mA/4))^(n*nGA)} * {1 – ((1-(mB/4))^(nA*nGB)}
>
> The variable in the above equation which reflects whether mutation B
> will have a reasonable probability of occurring on a member with
> mutation A is nA, the number of members with mutation A.

The above only says that if selection for A has happened in the past, the
probability of A in a population will be higher than the probability of
new mutation to A. It does not present the math of selection at all.

Moreover, I have pointed out that the second term does NOT include
a joint probability term for the "event" you are interested in, the
joint probability of A and B in the same trial. As written it only
presents the probability of one or more new B mutation in a
population the size of the number of the number of individuals
in the population that had an A mutation (your nA*nGB term; my n)
and a probability of new B mutation of your mB/4 term (my p term).

Joint probability requires that the p term in the general mass probability
equation be changed from the probability of one event to the probabilty
of a double-event per trial.

Moreover, your P(A) is NOT the probability of an A event per trial.
The probability of an A event per trial is mA/4 in your terminology,
not that that terminology makes any sense.

> If mutation A
> is beneficial, nA will amplify over generations, increasing in number
> so as to improve the probability that mutation B will occur on one of
> the members of this subpopulation.

The math of selection would tell you how fast and with what mathematical
relationship will the fraction of the population with A increase. You have
not presented that math in your equation. That math is the math of
differential increase in frequency. There is no such math in your
equation.

> If mutation A is neutral or
> detrimental so that the subpopulation size with that mutation remains
> constant or decreases,

The *minimum* frequency/probability of an allele in a population is the
mutation rate, the rate of change to the mutation-of-interest per generation.
In general, the frequency of a detrimental or neutral allele will be close to
the mutation rate. The probability or frequency of a selectively beneficial
allele will increase over time by a rate determined by its relative fitness
(selective advantage). But a selectively neutral allele can also increase
in frequency by chance alone because "chance has no memory", although
more rarely and more slowly than an increase due to positive selection.

You fail to accurately distinguish between the *observed* probability or
frequency of an allele in a population and the probability of new mutation
to that allele in your equation. I don't make that mistake in my equation.
I also actually perform a joint probability of the two alleles of interest
in each of the terms in my equation. The terms themselves represent
the mutually exclusive ways a cell can acquire a new double-mutant
state and thus use the addition rule.

If you don't know which base was the original one, you create a
mathematical model that treats that base as an unknown. You
don't pretend that the non-mutant base is actually a mutant base
as likely as any other base. Then when you know what the original
*non-mutant* base was, you can then *correctly* calculate the
frequency of the *mutant* bases.

> Why does Lenski
> freeze samples from his experiment? He does this so he can determine
> how the genetic sequences change with time.

But not to calculate the mutation frequency.

> He does not know where the
> mutations will occur.

True. But he is not interested in that. He is interested in where the
mutations *did* occur and the different mutational pathways different
lineages went down to reach the end state.

> He must sequence before and after replication in
> order to determine this.

Yes, because he did not know, beforehand, what selective pressures
he was presenting to his cells. OTOH, if I present a cell with an
antibiotic, I can reason that any mutation of interest will be in a
gene(s) that allow the cell to survive that level of antibiotic. I
still won't know what genes and what mutations produced this
effect until I sequence the results. Often, I will, however, be able
to guess which genes will need to mutate and only will need to
sequence those genes. That doesn't mean I will always be right.
I may find an "antibiotic resistant" cell that doesn't have any
mutation in the genes where most such resistance mutations are
located. That would be interesting because it would lead me to
a previously unknown gene that can affect the phenotype of
"antibiotic resistance". I would then use the techniques of
genetics (recombination being one) to isolate and locate this
previously unknown site of antibiotic resistance.

> Unless you know before hand what the base is
> at a particular site before the mutation occurs, you must consider all
> bases as possible substitution outcomes in the probability
> calculations.

No. If you don't know what the base is at a particular site that
is the "not-mutant" base, you treat it as an unknown base and
derive a mathematical model that treats it as an unknown, but
*non-mutant* base. Your pseudomathimatical model treats
all four bases as if they were all "mutant" bases. That
is not the math of *mutation* because it pretends that there is
no such thing as a "non-mutant" base.

Again, the probability that any real population of organisms
(barring a rare frequency-dependent selection) would have
25% of each base is essentially nil.

[Mark Isaak]

On 1/25/12 4:23 PM, Alan Kleinman MD PhD wrote:
> [snip]
>>
>> If multiple advantages show up, they will be processed in parallel.
>
> When you have multiple selection pressures targeting multiple genes,
> you don’t have multiple advantages.

Yes you do. You can see it happening.

> That is why combination therapy
> works for the treatment of HIV and for all real, measurable and
> repeatable examples of mutation and selection this is a fact of life.

No it isn't. Combination therapy works because of multiple weaknesses.

Why can you not get that simple fact -- or any fact, for that matter --
through your skull?

N.B.: That last question is the one you should be addressing.

[Mark Isaak]

On 1/25/12 4:18 PM, Alan Kleinman MD PhD wrote:
> On Jan 25, 6:50 am, Mark Isaak<eci...@curioustaxonomyNOSPAM.net>
> wrote:
>> On 1/24/12 9:07 PM, Alan Kleinman MD PhD wrote:
>>
>>> On Jan 24, 9:35 am, Richard Norman<r_s_nor...@comcast.net> wrote:
>>
>>>>> <snip>
>>
>>>> Somebody who has studied probability theory might write Pr(S) = 1
>>>> where S is the sample space. It still wouldn't mean anything but at
>>>> least it would be standard notation.
>>
>>> There is absolutely nothing wrong with the notation P(-∞< X< +∞) = 1
>>> and it is totally equivalent to P(S) = 1. You should know that Richard
>>> as a graduate student of probability theory.
>>
>> Your notation makes sense if X is necessarily a scalar. As you used it,
>> X was not a scalar. If P(-∞< X< +∞) = 1, then the probability that X
>> = adenine or cytosine or guanine or thymine is zero, because none of
>> nucleic acid bases are on the number line. In short, there is
>> absolutely nothing right with your notation.
>>
>> Anyone should know this who took any graduate-level classes in
>> probability. Or any mathematics, computer science, biology, chemistry,
>> physics, or probably a variety of other courses.
>
> Mark, what difference does it make in the probabilities if you label
> the faces on a die Ad, Cy, Gu, Th, Mark and John instead of 1, 2, 3,
> 4, 5, and 6? Even a social engineer should understand this.

So it's a die now, where it used to be a measuring tape? That makes a
huge difference. Consult probability textbooks for the reasons why.

[Tim Anderson]

On Jan 21, 11:15 am, Alan Kleinman MD PhD <klein...@sti.net> wrote:
> So here we are again, passing another 1000 post mile stone. Let's pick
> up here:
>

> It appears that our self-proclaimed professional forensic
> mathematician and our graduate student of probability theory and the
> other mathematically incompetent dim bulbs of evolutionism who can’t
> or won’t properly do the mathematics for mutation and selection when
> mutations other than point mutations are included in the calculation
> so it is left to us to do this mathematics. We start with the
> following definition:

>
> P(-∞ < X < +∞) = 1,
>

> which simply corresponds to all possible outcomes in the entire sample
> space. Initially in the derivation of the probability that a
> particular mutation will occur at a specific locus; we only considered
> point substitutions in the sample space for possible outcomes for a
> mutation at a specific locus. We then obtained the following:
>
> P(-∞ < X < +∞) = P(Ad) + P(Cy) + P(Gu) + P(Th) = 1
>
> We weighted each possible point substitution equally (that is they
> occur with equal frequency) and we obtain the following equality:
>
> P(Ad) = P(Cy) = P(Gu) = P(Th) = 1/4,
>
> This is where the weight factor of 1/4 comes when computing the
> probability that a particular mutation will occur at a specific locus.
>
> 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 Gu, Cy, or Th into
> Ad.
>
> Based on these principles, one can do the analogous derivation of the
> possible outcomes for a mutation including not only point mutations
> but any other mutation you wish to consider such as insertions and
> deletions.
>
> For example a base can be inserted at the locus. Let an i preceding
> the base denote an insertion. Then P(iAd) means the probability that
> an Ad base will be inserted at the particular locus and so on for the
> other bases. Then the equation that would describe the probabilities
> for the sample space for a point mutation and any possible single base
> insertion mutation becomes:
>
> P(-∞ < X < +∞) = P(Ad) + P(Cy) + P(Gu) + P(Th) + P(iAd) + P(iCy) +
> P(iGu) + P(iTh) = 1
>
> One could think of these outcomes as equivalent to an unfair die where
> a roll of this die is more likely to give a substitution mutation
> rather than an insertion of a base. Then as an approximation of the
> values for the point mutations P(Ad) = P(Cy) = P(Gu) = P(Th) = (1 – x)/
> 4 and for the insertion mutations P(iAd) = P(iCy) = P(iGu) = P(iTh) =
> x/4.
>
> x, the frequency for which a base insertion occurs as well as the
> mutation rate itself are experimentally determined values but as we
> will see, x can only fall between a certain range of values.
>
> Then the probability of a particular beneficial mutation including
> both point mutations and insertions becomes:
>
> mA*(1-x)/4 -- the probability that in one organism in one generation,
> a base substitution mutation A will turn a specific locus into a
> specific nucleotide other than the one it already is -- for instance,
> turn Gu, Cy, or Th into Ad if the beneficial mutation is a base
> substitution. Or if the beneficial mutation is a base insertion:
>
> mA*x/4 -- the probability that in one organism in one generation, an
> insertion mutation A will give a more fit replicator than the
> progenitor -- for instance, inserting Gu, Cy, Th or Ad into the
> genetic sequence.
>
> The rest of the computation for the probability of a particular
> mutation occurring at a specific locus as a function of population
> size and number of generations remains the same. This applies as well
> to computing the joint probability of two beneficial mutations
> accumulating in a subpopulation. This continues the mathematical
> explanation why combination therapy works and why the theory of
> evolution is a mathematically irrational belief system. In the next
> few weeks, we will include deletions in the mathematics of the
> mutation and selection phenomenon which will again show why the type
> of beneficial mutation has virtually no affect on the mathematics of
> mutation and selection and that the dominant mathematical feature of
> mutation and selection is the multiplication rule of probabilities.
>
> I'll bundle responses to the last posts later.

I beseech you, in the bowels of Christ, think it possible you may be
mistaken in continuing this thread.

[Alan Kleinman MD PhD]

Increasing nA over time is what Schneider calls “amplification”. That
is what is required of a subpopulation to overcome the multiplication
rule of probabilities for joint probability of events to have a
reasonable probability of occurring. If nA is not able to increase
over time, P(A)*P(B) will remain small (though slowly increasing
because nGB will also increase the number of trials for the beneficial
mutation).

If you don’t know which base was at the particular locus before the
substitution occurs, how do you know which base to eliminate as a
possible outcome in the probability calculation?

>
> > Why does Lenski
> > freeze samples from his experiment? He does this so he can determine
> > how the genetic sequences change with time. He does not know where the
> > mutations will occur. He must sequence before and after replication in
> > order to determine this. Unless you know before hand what the base is
> > at a particular site before the mutation occurs, you must consider all
> > bases as possible substitution outcomes in the probability
> > calculations.
>
> No you mustn't. If you do that you get a wrong answer. Your math is just
> plain wrong and biologically meaningless. You further assume, may I
> point out, that only a single mutation at a given site is advantageous.

I don’t make that assumption at all John. There may be more than a
single mutational outcome at a particular locus which will improve
fitness but you don’t know which fitness trajectory each particular
mutation will take those progenitors of the new more fit
subpopulations. Do you want to do the mathematics for this case? If
you can’t do it, I’ll show you how to do such a calculation.

>
>
>
>
>
> >>  >>>> [snip repetitive bloviation]
> >>  >>> John you’re getting too much of your vocabulary from watching TV.
> >>  >> H.L. Mencken, actually.
>
> >>  >>>>>> Now if you could only be convinced that "the mutation and selection
> >>  >>>>>> phenomenon" makes about as much sense as "the peanut butter and
> >>  >>>>>> spaghetti phenomenon".
> >>  >>>>> John, you should know by now that it doesn’t bother me to play word
> >>  >>>>> games, in fact I have fun with them.
> >>  >>>> Yes, that's one of your major faults. Instead of real discussion, you
> >>  >>>> prefer word games.
> >>  >>> If you are tired of the word games, let’s have a mathematical game and
> >>  >>> you can learn the mathematics of the mutation and selection phenomenon.
> >>  >> There is no "mutation and selection phenomenon". Get this at much
> >>  >> correct. Mutation and selection are two separate phenomena.
>
> >>  > Mutations are occurrences and selection determines the consequences of
> >>  > these occurrences. The two concepts are coupled together to allow
> >>  > adaptation to environmental stressors governed by specific
> >>  > mathematical rules.
>
> >> Yes, and a car needs both wheels and an engine. But there is no such
> >> thing as "the wheels and engine phenomenon". They're two separate things.
>
> > The engine drives the wheels and the theory of evolution no longer has
> > an engine.
>
> Having no argument, you fall back on word games. As usual.

If mutation and selection wasn’t the engine for the theory of
evolution, what is the engine which would transform a reptile into a
bird now that we know that mutation and selection can not work in
parallel with any efficiency?

[Alan Kleinman MD PhD]

[snip]

> More dodgeball. I'm done with your evasions.

David, you quit too easily.

[Alan Kleinman MD PhD]

> seem to think I am rather than ...
>

Hersheyh, I don’t think you are an idiot, I think you don’t have any
training or skill in the hard mathematical sciences. But that has been
my experience with most people trained in evolutionism. These
mathematical principles can be well understood by anyone who has put
the time and effort into learning them. You have never put the time
and effort into learning these principles. If fact, you put great
effort into not learning these principles. Thousands of posts ago I
asked you if you had ever gone through the derivation of the Poisson
distribution. You had not done this. If you had, you would have
understood clearly why this distribution was not appropriate for
describing the mutation and selection phenomenon. A random mutation is
not a Poisson random variable.

[Alan Kleinman MD PhD]

Bill you must really enjoy having your “oops” moments because you have
so many of them. There is no intrinsic order to the faces on a die but
for convenience or tradition, we label them 1, 2, 3, 4, 5, and 6. We
could just as easily label the faces on the die Ad, Cy, Gu, Th, Bill
and hersheyh and that will have no affect on the probabilities of a
particular face appearing. Any probability problem where X is a
discrete variable such as dice rolling or card drawing involves
categorical variables until conditions impose that they become ordinal
variables. If you are rolling dice and ask what is the probability of
rolling a 7 with two dice? You have imposed the condition that the sum
of the two faces equals 7. If you are playing poker and ask what is
the probability of drawing a straight flush? You have imposed the
condition that the cards have all the same suit and are sequential in
number. If you are talking about mutation and selection, what is the
sequence of bases which will satisfy a particular selection condition?
The probability calculations are all done in the same manner governed
by the same axioms. You define the sample space, trial and outcomes
for the trials and determine the probabilities for an event and joint
probabilities for multiple events occurring by applying the
appropriate principles. The selection conditions determine the order
of events.

>
> It's trivial. It says no more than that given a trial, some outcome
> will occur.

Once you have properly defined the probability problem, the
mathematics is actually quite simple. For some reason, you
evolutionists have never done this.

Any time you are dealing with a probability problem with discrete
variable X, you will obtain an f(x) probability function which will be
represented as a bar graph where each outcome will have some
probability value when a particular outcome occurs and be zero between
the intervals of the outcomes. The distribution function F(x) will be
a step function (piecewise constant function) which will have a jump
in value of P(X=a) at x=a and will be constant between subsequent
discrete outcomes. That is the categorical part of the problem. When
you require two or more categorical events to occur, you have imposed
that the categorical events occur in an ordinal sequence, which is
what is happening in the mutation and selection process when selection
conditions require that the sequence of mutations give increasing
fitness.

[Alan Kleinman MD PhD]

On Jan 26, 10:28 am, Mark Isaak <eci...@curioustaxonomyNOSPAM.net>
wrote:

> On 1/25/12 4:23 PM, Alan Kleinman MD PhD wrote:
>
> > [snip]
>
> >> If multiple advantages show up, they will be processed in parallel.
>
> > When you have multiple selection pressures targeting multiple genes,
> > you don’t have multiple advantages.
>
> Yes you do.  You can see it happening.

What exactly are you seeing Mark. Give us an empirical example where
you are seeing this. I’ve posted dozens of empirical examples where
this doesn’t happen. If what you claim did happen, combination therapy
would not work for the treatment of HIV.

>
> > That is why combination therapy
> > works for the treatment of HIV and for all real, measurable and
> > repeatable examples of mutation and selection this is a fact of life.
>
> No it isn't.  Combination therapy works because of multiple weaknesses.

Mark, that’s what selection pressures do, they expose genetic weakness
in populations. Adaptation by mutation and selection only works
efficiently when a single gene is targeted by a single selection
pressure.

>
> Why can you not get that simple fact -- or any fact, for that matter --
> through your skull?
>
> N.B.:  That last question is the one you should be addressing.

Sadly, I have to deal with the facts in my medical practice, and one
of those facts is multidrug resistant microbes. So I looked at this
problem of mutation and selection and ask how do these problems come
about and what can one do to deal with these problems. Evolutionism
only offers the suggestion to stop using selection pressures. This
simple minded approach may reduce selection of resistant microbes but
at the risk of injury and death to my patients. Why can’t you get that
through your skull?

[Steven L.]

"Alan Kleinman MD PhD" <klei...@sti.net> wrote in message
news:8a0a5b23-a5ab-4541...@q7g2000pbg.googlegroups.com:

> Evolutionists simply don't have enough generations to transform a
> reptile into a bird. That is a mathematical and empirical fact of
> life.

No it's not.

The first therapod dinosaurs date back to the Late Triassic.
The first birds, like Archaeopteryx, date back about 150 million years
ago.

That's about 70 million years, or a few million generations.

You don't think that's enough?
How different do you think birds are from theropod dinosaurs?




-- Steven L.

[Steven L.]

"Alan Kleinman MD PhD" <klei...@sti.net> wrote in message

news:8fac320a-b5ef-4221...@pt5g2000pbb.googlegroups.com:

> is a mathematical and empirical fact of life.

I don't like the way you're trying to scapegoat1 evolutionists for the
ills of society.

I've had to struggle with some serious infections myself that proved
resistant to multiple antibiotics. But I got to see firsthand how that
antibiotic resistance came about. And it didn't happen the way you're
suggesting.

After all your mathematical arguments are over and done with, you're no
different from the Bible thumpers who claim that all the ills of modern
society are caused by the acceptance of the ToE.




-- Steven L.

[Steven L.]

"Greg Guarino" <gdgu...@gmail.com> wrote in message
news:jfmhp3$5tj$1...@dont-email.me:

> On 1/23/2012 3:24 PM, Alan Kleinman MD PhD wrote:
> > And you evolutionists are not going to get a free ride on this major
> > scientific blunder you have made.
>
> That's where you're wrong. Repeating the same phrases over and over in a
> sort of OCD Ostinato is very, very odd. You really can't see that? It
> makes you look like a crank, a zealot or perhaps a politician; certainly
> anything but a scientist.

It's also factually wrong.

In America, the Centers for Disease Control has worked hard on the
problem of microbial resistance to anti-infectives.

They NEVER blame evolutionists for any of that.

If there's anyone they blame, it's health care providers for inadequate
anti-infective protocols, overuse or misuse of antibiotics, etc.

When nurses don't wash their hands (spreading MRSA around), when doctors
prescribe antibiotics for viral infections "just in case," when doctors
prescribe the wrong antibiotic because they didn't take the time and
money to do a culture and sensitivity analysis, it's not because of
anything Darwin wrote or anything Dawkins said. Rather, it's a
combination of carelessness and being penny-wise and pound-foolish where
economic cost of infections is concerned.

I have told Kleinman that; I've given him references to the CDC website;
he ignores them and comes right back with his antimicrobial mantra.
Typical of creationists (though less so of ID proponents): They ignore
rebuttals and come right back with the same argument as if it's brand
new.

And Kleinman really is a creationist. Because when I pointed out that
the evolution of species is a FACT confirmed by the fossil record and
the distribution of life forms on Earth--regardless of what mechanisms
are responsible for that evolution--he denied that too.



-- Steven L.

[John Harshman]

None of which addresses my point.

Doesn't matter, since your probability calculation is meaningless. Not
only don't you know which base was there before, you don't know which
base (or bases) would be advantageous or deleterious (if any). That's
why it would be more useful just to consider the mutation rate to equal
the expected number of advantageous mutations per individual, best
estimated by examining a population, counting the number that occur in
that population over some time, and dividing by the total number of
individuals.

>>> Why does Lenski
>>> freeze samples from his experiment? He does this so he can determine
>>> how the genetic sequences change with time. He does not know where the
>>> mutations will occur. He must sequence before and after replication in
>>> order to determine this. Unless you know before hand what the base is
>>> at a particular site before the mutation occurs, you must consider all
>>> bases as possible substitution outcomes in the probability
>>> calculations.
>> No you mustn't. If you do that you get a wrong answer. Your math is just
>> plain wrong and biologically meaningless. You further assume, may I
>> point out, that only a single mutation at a given site is advantageous.
>
> I don’t make that assumption at all John. There may be more than a
> single mutational outcome at a particular locus which will improve
> fitness but you don’t know which fitness trajectory each particular
> mutation will take those progenitors of the new more fit
> subpopulations. Do you want to do the mathematics for this case? If
> you can’t do it, I’ll show you how to do such a calculation.

If the past is any guide, you'll show me something unrelated to the
question. If you don't make that assumption, then why do you divide the
mutation rate by 4?

More word games. I'm growing tired of this again. I may not respond to
the next repetition of the same old nonsense.

[Kermit]

On Jan 27, 5:45 am, Alan Kleinman MD PhD <klein...@sti.net> wrote:
> On Jan 26, 10:28 am, Mark Isaak <eci...@curioustaxonomyNOSPAM.net>
> wrote:
>
> > On 1/25/12 4:23 PM, Alan Kleinman MD PhD wrote:
>
> > > [snip]
>
> > >> If multiple advantages show up, they will be processed in parallel.
>
> > > When you have multiple selection pressures targeting multiple genes,
> > > you don’t have multiple advantages.
>
> > Yes you do.  You can see it happening.
>
> What exactly are you seeing Mark. Give us an empirical example where
> you are seeing this. I’ve posted dozens of empirical examples where
> this doesn’t happen. If what you claim did happen, combination therapy
> would not work for the treatment of HIV.

Why not? The odds of any microorganisms having resistance to multiple
new toxins are less likely than any of them having resistance to just
one. But if they are exposed to all of them in prolonged weak doses,
or one at a time in succession, you end up with the same result -
multiple drug-resistant strains.

The mutations do not happen *in order to* respond to the environment.

>
>
>
> > > That is why combination therapy
> > > works for the treatment of HIV and for all real, measurable and
> > > repeatable examples of mutation and selection this is a fact of life.
>
> > No it isn't.  Combination therapy works because of multiple weaknesses.
>
> Mark, that’s what selection pressures do, they expose genetic weakness
> in populations.

They also expose strengths. And they are acting *all the time*. I am
extremely nearsighted. A thousand years ago, it would have been a
major handicap. Ten thousand years ago i would not have reached
adulthood - I'd have been eaten by a smilodon or somesuch. Now it's
barely an annoyance.

> Adaptation by mutation and selection only works
> efficiently when a single gene is targeted by a single selection
> pressure.

All genes are always under pressure all the time. How could they not
be?

If circumstances changed (e.g. civilization broke down and
optometrists were unavailable), then my myopia would become suddenly
very important to me. The pressure is on, all the time. But organisms
are generally pretty well adapted to their current circumstances. When
those circumstances *change, then those organisms are under greater
pressure, almost always on multiple fronts (behaviors and physical
characteristics), and those normally involve multiple genes.

If it were to become colder on the average, then a mammal would be
challenged in numerous respects. It would be losing body heat faster
than normal, it would require more calories than normal, it might have
trouble moving around, it may no longer be camoflauged, etc. a mammal
in such circumstances that was larger (and therefore lost body heat
more slowly and one that had slightly larger paws (and therefore
walked more easily in the snow), would each have survival (and
therefore reproductive) advantages. They could easily mate and produce
offspring which would carry those traits and pass them on. The gene
pool would see these two traits spread simultaneously.

You keep making this contrary assertion which is refuted by facts and
makes no sense.

>
>
>
> > Why can you not get that simple fact -- or any fact, for that matter --
> > through your skull?
>
> > N.B.:  That last question is the one you should be addressing.
>
> Sadly, I have to deal with the facts in my medical practice, and one
> of those facts is multidrug resistant microbes. So I looked at this
> problem of mutation and selection and ask how do these problems come
> about and what can one do to deal with these problems. Evolutionism
> only offers the suggestion to stop using selection pressures.

The closest I have seen to this claim are microbiologists who suggest
that we start taking steps to stop breeding resistant bacteria. Why do
you take issue with this?

[...]

You think that multiple antibiotic use cannot breed multiple resistant
strain strains, don't you? And therefore you don't take appropriate
precautions...

> This
> simple minded approach may reduce selection of resistant microbes but
> at the risk of injury and death to my patients. Why can’t you get that
> through your skull?

How many have been killed by multiply resistant bacteria? I have never
heard any in the medical field who suggested not using what's
necessary to cure the patient. If the infection is beaten back enough
that the patient's immune system can clear the infection, then there
isn't much in the way of resistant bugs to spread, is there? But those
that do, are resistant to some degree to what they have been exposed
to.

The problem is largely use of antibiotics inappropriately, such as
prescribing them for viral infections, or patients stopping their
antibiotics when the symptoms reduce, rather than going through the
full course, etc. The prevalence of antibiotics in the environment is
a problem, and it is difficult to assess the damage from various
practices such as using antibotics in animal feed.

>
> > --
> >   Mark Isaak          eciton (at) curioustaxonomy (dot) net
> > "It is certain, from experience, that the smallest grain of natural
> >   honesty and benevolence has more effect on men's conduct, than the most
> >   pompous views suggested by theological theories and systems." - D. Hume

Kermit

[Kermit]

On Jan 27, 7:04 am, "Steven L." <sdlit...@earthlink.net> wrote:
> "Greg Guarino" <gdguar...@gmail.com> wrote in message

I suspect I know what's happening out there. Kleinman thinks that a
genepool (like an infection of bacteria, who have a pretty
enthusiastic horizontal gene transfer process going) cannot adapt more
than one characteristic at a time (which also helps him cling to his
creationist model). Therefore, using all available antibiotics
simultaneously is *safe, and he doesn't need to take the precautions
that are recommended. (Such as not using more when less is enough.)

Far be it from me to imply any malpractice, but I wonder if his
judgement has been questioned by other doctors? To seriously consider
their criticisms would require:
1. Risking the admission that he is wrong, and
2. Accepting a model that would provide enough time for evolution of
the species to have occurred, and he is currently comforted by the
idea that it is impossible.

Kermit

[Mark Isaak]

On 1/27/12 5:45 AM, Alan Kleinman MD PhD wrote:
> On Jan 26, 10:28 am, Mark Isaak<eci...@curioustaxonomyNOSPAM.net>
> wrote:
>> On 1/25/12 4:23 PM, Alan Kleinman MD PhD wrote:
>>
>>> [snip]
>>
>>>> If multiple advantages show up, they will be processed in parallel.
>>
>>> When you have multiple selection pressures targeting multiple genes,
>>> you don’t have multiple advantages.
>>
>> Yes you do. You can see it happening.
>
> What exactly are you seeing Mark. Give us an empirical example where
> you are seeing this.

Every existing population on the planet. They all have multiple
selection pressures on them, and somehow life is not extinct.

If you want examples where the selection and its effects are measured
quantitatively, look at plant breeding.

> I’ve posted dozens of empirical examples where
> this doesn’t happen.

You have posted essentially the same example multiple times. You are
incapable of learning that the world is bigger than what you have
already seen.

> If what you claim did happen, combination therapy
> would not work for the treatment of HIV.

You have been corrected on this myriad times, yet you keep repeating it.
WHY?

Combination therapy works because the selection is strong enough to
eliminate essentially all of the alleles that are being selected, and
because there is little or no crossover. If selection is not strong
and/or if there is sex, however, it won't work like you think. All the
alleles being selected are likely to increase in frequency.

>>> That is why combination therapy
>>> works for the treatment of HIV and for all real, measurable and
>>> repeatable examples of mutation and selection this is a fact of life.
>>
>> No it isn't. Combination therapy works because of multiple weaknesses.
>
> Mark, that’s what selection pressures do, they expose genetic weakness
> in populations. Adaptation by mutation and selection only works
> efficiently when a single gene is targeted by a single selection
> pressure.

And yet selection works even when targeting a single gene is impossible.
Why do you think the world is so against you?

>> Why can you not get that simple fact -- or any fact, for that matter --
>> through your skull?
>>
>> N.B.: That last question is the one you should be addressing.
>
> Sadly, I have to deal with the facts in my medical practice, and one
> of those facts is multidrug resistant microbes. So I looked at this
> problem of mutation and selection and ask how do these problems come
> about and what can one do to deal with these problems. Evolutionism
> only offers the suggestion to stop using selection pressures. This
> simple minded approach may reduce selection of resistant microbes but
> at the risk of injury and death to my patients. Why can’t you get that
> through your skull?

I don't believe a word of it. I bet you hated evolution long before you
ever heard of multidrug resistance, and you have just been itching to
find a problem to blame on it. Answer honestly: How old do you think
the world is, and how old is mankind?

[Alan Kleinman MD PhD]

On Jan 27, 6:44 am, "Steven L." <sdlit...@earthlink.net> wrote:

> "Alan Kleinman MD PhD" <klein...@sti.net> wrote in messagenews:8a0a5b23-a5ab-4541...@q7g2000pbg.googlegroups.com:
>
> > Evolutionists simply don't have enough generations to transform a
> > reptile into a bird. That is a mathematical and empirical fact of
> > life.
>
> No it's not.
>
> The first therapod dinosaurs date back to the Late Triassic.
> The first birds, like Archaeopteryx, date back about 150 million years
> ago.
>
> That's about 70 million years, or a few million generations.

Let’s give you a generation per year, at 300 generations per fixation,
which gives you about 250,000 mutations you can fix over that number
of generations. Tell us what the selection pressures were that would
make such a transformation. It’s been a while since I’ve heard an
evolutionist fairytale.

>
> You don't think that's enough?
> How different do you think birds are from theropod dinosaurs?

A lot different, so much different that birds didn’t evolve from
theropod dinosaurs. http://www.science20.com/news_articles/theropod_dinosaurs_evolved_birds_not_likely_says_study


>
> -- Steven L.

[Alan Kleinman MD PhD]

On Jan 27, 6:49 am, "Steven L." <sdlit...@earthlink.net> wrote:

I’m only blaming evolutionists for failing to properly understand and
teach the basic science and mathematics of the mutation and selection
phenomenon and causing the evolution of multidrug resistant microbes,

multiherbicide resistant weeds, multipesticide resistant insects and

less than durable cancer treatments. As long as we have evolutionists
making the following claims:

Doctor Edward Max MD, PhD of the Food and Drug Administration using
this forum to put forth the mathematically irrational beliefs of
evolutionism. We find Edward Max’s mathematically irrational claims
posted here on Talk Origins in the following essay http://www.talkorigins.org/faqs/fitness/

where he says the following:

“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.”

And Thomas Schneider of the National Cancer Institute claiming on
http://www-lmmb.ncifcrf.gov/~toms/paper/ev/AND-multiplication-error.html
“The multiplication rule does not apply to biological evolution.”,
when he knows very well that mutations are random independent events
subject to the multiplication rule of probabilities that I’m going to
hang these blunders around the necks of you pseudo-scientist
evolutionists.

>
> I've had to struggle with some serious infections myself that proved
> resistant to multiple antibiotics.  But I got to see firsthand how that
> antibiotic resistance came about.  And it didn't happen the way you're
> suggesting.

Considering I’ve treated tens of thousands of infections, I’ll take
your one personal experience and weight it appropriately. Why is it
that hospital acquired strains of MRSA demonstrate resistance to more
drugs than community acquired strains of MRSA? Do you think that it
might be due to the fact that hospitalized patients are more
debilitated and do not have a good functioning immune system? The more
selection pressure you put on a population, the less likely the
population will evolve resistance to all those selection pressures
simultaneously. Use the selection pressures sequentially and allow the
population time to replicate and then when the particular treatment
fails go on to the next drug and you have your formula for multidrug
resistant microbes. I suppose you think that combination therapy is
not the correct way to treat HIV? Perhaps we should withhold and
reduce the usage of drugs in this case to prevent the evolution of
resistant strains of the virus?

>
> After all your mathematical arguments are over and done with, you're no
> different from the Bible thumpers who claim that all the ills of modern
> society are caused by the acceptance of the ToE.

Steven, I’m not thumping you with the Bible, I’m thumping you with the
mathematics of probability theory and the empirical evidence of how
mutation and selection works. I’m doing the job that evolutionists
should have done decades ago.

>
> -- Steven L.- Hide quoted text -

[Alan Kleinman MD PhD]

That’s because you don’t understand the basic science and mathematics

of the mutation and selection phenomenon.


>
>
>
>
>

Populations know and they show this by amplifying the beneficial
mutation. And once the mutation has been amplified sufficiently then
that subpopulation has a reasonable probability of a member having a
trial at another proper locus for the next beneficial mutation and if
the outcome is the beneficial mutation then you have a new
subpopulation with two beneficial mutations. This is what Lenski
measured after the fact in his experiment.

>
>
>
>
>
> >>> Why does Lenski
> >>> freeze samples from his experiment? He does this so he can determine
> >>> how the genetic sequences change with time. He does not know where the
> >>> mutations will occur. He must sequence before and after replication in
> >>> order to determine this. Unless you know before hand what the base is
> >>> at a particular site before the mutation occurs, you must consider all
> >>> bases as possible substitution outcomes in the probability
> >>> calculations.
> >> No you mustn't. If you do that you get a wrong answer. Your math is just
> >> plain wrong and biologically meaningless. You further assume, may I
> >> point out, that only a single mutation at a given site is advantageous.
>
> > I don’t make that assumption at all John. There may be more than a
> > single mutational outcome at a particular locus which will improve
> > fitness but you don’t know which fitness trajectory each particular
> > mutation will take those progenitors of the new more fit
> > subpopulations. Do you want to do the mathematics for this case? If
> > you can’t do it, I’ll show you how to do such a calculation.
>
> If the past is any guide, you'll show me something unrelated to the
> question. If you don't make that assumption, then why do you divide the
> mutation rate by 4?

The factor of 1/4 on the mutation rate takes into account that not
every mutation is the beneficial mutation. If you have four equally
probable base substitution outcomes for a mutation then the weight
factor is 1/4. If you have more possible outcomes such as base
insertions, deletions and whatever other type of mutation you can
imagine, then the weight factor will be smaller than 1/4. On the other
hand, if two of the possible base substitutions give a more fit
replicator, the weight factor would be closer to 1/2. But one
substitution may put that subpopulation on a different fitness
landscape trajectory than the other substitution. One thing that
should be clear to you is that the weight factor can never be greater
than 1.

[Alan Kleinman MD PhD]

On Jan 27, 9:31 am, Kermit <unrestrained_h...@hotmail.com> wrote:
> On Jan 27, 5:45 am, Alan Kleinman MD PhD <klein...@sti.net> wrote:
>
>
>
>
>
> > On Jan 26, 10:28 am, Mark Isaak <eci...@curioustaxonomyNOSPAM.net>
> > wrote:
>
> > > On 1/25/12 4:23 PM, Alan Kleinman MD PhD wrote:
>
> > > > [snip]
>
> > > >> If multiple advantages show up, they will be processed in parallel.
>
> > > > When you have multiple selection pressures targeting multiple genes,
> > > > you don’t have multiple advantages.
>
> > > Yes you do.  You can see it happening.
>
> > What exactly are you seeing Mark. Give us an empirical example where
> > you are seeing this. I’ve posted dozens of empirical examples where
> > this doesn’t happen. If what you claim did happen, combination therapy
> > would not work for the treatment of HIV.
>
> Why not? The odds of any microorganisms having resistance to multiple
> new toxins are less likely than any of them having resistance to just
> one.  But if they are exposed to all of them in prolonged weak doses,
> or one at a time in succession, you end up with the same result -
> multiple drug-resistant strains.
>
> The mutations do not happen *in order to* respond to the environment.

You are dreaming Kermit. There is absolutely no evidence of your
claim. You evolutionists have been speculating like this for so many
years, you’ve convinced yourselves of this mathematically irrational
nonsense. Reducing selection intensity slows the mutation and
selection process.

>
>
>
> > > > That is why combination therapy
> > > > works for the treatment of HIV and for all real, measurable and
> > > > repeatable examples of mutation and selection this is a fact of life.
>
> > > No it isn't.  Combination therapy works because of multiple weaknesses.
>
> > Mark, that’s what selection pressures do, they expose genetic weakness
> > in populations.
>
> They also expose strengths. And they are acting *all the time*. I am
> extremely nearsighted. A thousand years ago, it would have been a
> major handicap. Ten thousand years ago i would not have reached
> adulthood - I'd have been eaten by a smilodon or somesuch. Now it's
> barely an annoyance.

When a population is subjected to a selection pressure, the first
thing that happens is all the members that do not have sufficient
fitness either are killed or fail to reproduce. Any of the remaining
members become progenitors for subpopulations that are candidates for
the further beneficial mutations. But these subpopulations have to
amplify their alleles sufficiently so there is a reasonable
probability that a beneficial mutation will occur at the proper locus.

>
> > Adaptation by mutation and selection only works
> > efficiently when a single gene is targeted by a single selection
> > pressure.
>
> All genes are always under pressure all the time. How could they not
> be?

Most selection pressures are stabilizing which prevents divergence of
their genetic sequence. The selection pressures which transform and
create new alleles are directional selection pressures and mutation
and selection does not work efficiently when two or more directional
pressures are applied to the population simultaneously.

>
> If circumstances changed (e.g. civilization broke down and
> optometrists were unavailable), then my myopia would become suddenly
> very important to me. The pressure is on, all the time. But organisms
> are generally pretty well adapted to their current circumstances. When
> those circumstances *change, then those organisms are under greater
> pressure,  almost always on multiple fronts (behaviors and physical
> characteristics), and those normally involve multiple genes.

What you are having trouble seeing is that adaptation by mutation and
selection can not work efficiently when multiple genes are targeted
simultaneously. This is why combination therapy works. And it requires
mutations to create new alleles.

>
> If it were to become colder on the average, then a mammal would be
> challenged in numerous respects. It would be losing body heat faster
> than normal, it would require more calories than normal, it might have
> trouble moving around, it may no longer be camoflauged, etc. a mammal
> in such circumstances that was larger (and therefore lost body heat
> more slowly and one that had slightly larger paws (and therefore
> walked more easily in the snow), would each have survival (and
> therefore reproductive) advantages. They could easily mate and produce
> offspring which would carry those traits and pass them on. The gene
> pool would see these two traits spread simultaneously.
>
> You keep making this contrary assertion which is refuted by facts and
> makes no sense.

What thermal stress will do to a population is select out any variants
that don’t have sufficient fitness to reproduce but thermal stress
won’t cause mutation and selection to transform a reptile scale into a
feather as suggested by Edward Max. There are too many genes which
would require new alleles that don’t exist in the population.

>
>
>
> > > Why can you not get that simple fact -- or any fact, for that matter --
> > > through your skull?
>
> > > N.B.:  That last question is the one you should be addressing.
>
> > Sadly, I have to deal with the facts in my medical practice, and one
> > of those facts is multidrug resistant microbes. So I looked at this
> > problem of mutation and selection and ask how do these problems come
> > about and what can one do to deal with these problems. Evolutionism
> > only offers the suggestion to stop using selection pressures.
>
> The closest I have seen to this claim are microbiologists who suggest
> that we start taking steps to stop breeding resistant bacteria. Why do
> you take issue with this?

I take issue with this because I’ve seen what happens to people with
infections when antibiotic usage is delayed. I understand the argument
being put forth. Reduce the use of antibiotics and reduce the use of
selection for resistance. Do you think that three drug therapy is
appropriate for the treatment of HIV? Do you think that everyone with
HIV should be treated? By your argument, we should reduce the
treatment of HIV so as to reduce the selection of resistant strains of
the virus.

Kermit, the message we get from the treatment of HIV is that selection
occurring at two or more genes simultaneously impairs the mutation and
selection process. This principle applies for selection of resistance
of microbes, weeds, insects and cancer treatment as well. The
difference is the time scales because each of these life forms have
different generation times. And the mathematical reason for this is
given by the correct application of the axioms of probability theory.
Forcing a population to get two beneficial mutations simultaneously to
improve fitness is a low probability event. Populations must have time
(generations) to amplify the first beneficial mutation before there is
a reasonable probability that the next beneficial mutation will occur
at the proper locus.

>
> [...]
>
> You think that multiple antibiotic use cannot breed multiple resistant
> strain strains, don't you? And therefore you don't take appropriate
> precautions...

I’m not the only one who thinks this. I get messages from the
California Medical Board and CDC to use combination therapy for the
treatment of multidrug resistant Gonorrhea. And I’ve posted dozens of
other examples of the use of combination selection pressures to
suppress the mutation and selection phenomenon. If you want to breed
multidrug resistant organisms, use your selection pressures one at a
time in a sequential manner and you have the formula for producing
MRSA.

>
> > This
> > simple minded approach may reduce selection of resistant microbes but
> > at the risk of injury and death to my patients. Why can’t you get that
> > through your skull?
>
> How many have been killed by multiply resistant bacteria? I have never
> heard any in the medical field who suggested not using what's
> necessary to cure the patient. If the infection is beaten back enough
> that the patient's immune system can clear the infection, then there
> isn't much in the way of resistant bugs to spread, is there? But those
> that do, are resistant to some degree to what they have been exposed
> to.

The standard of care for treating infections was developed 60 years
ago. In medical school and post graduate training you are instructed
to use single drug therapy for the treatment of infections. The
consequence of this ill-advised strategy is multidrug resistant
infections. Evolutionists have failed to properly describe the basic
science and mathematic of the mutation and selection phenomenon. If
you think things have changed, get a copy of the “Sanford Guide”. This
handbook is published every year and is used world-wide. Every care
provider is using the same selection pressure to treat the same
infections. This is the easiest selection problem for microbes to
solve. When that treatment fails, the second line drug is used and the
end result is multidrug resistant microbes. Combination therapy will
become the standard of care in microbes which already show a
predisposition to evolve resistance to the drugs being used and in
patients with suppressed immune systems. It’s only a matter of time
and painful experience before this becomes universally understood. The
failure of evolutionists to properly understand and teach the basic
science and mathematics of the mutation and selection phenomenon only
slows the advancement of science and harms people.

>
> The problem is largely use of antibiotics inappropriately, such as
> prescribing them for viral infections, or patients stopping their
> antibiotics when the symptoms reduce, rather than going through the
> full course, etc. The prevalence of antibiotics in the environment is
> a problem, and it is difficult to assess the damage from various
> practices such as using antibotics in animal feed.

I know plenty of cattle ranchers and none of them feed antibiotics to
their animals unless they are ill. It would be stupid to do this since
ruminants do not have the capability to digest cellulose without the
bacteria in their gut. Kermit, you have a superficial and clichéd
understanding of this issue.

[Alan Kleinman MD PhD]

On Jan 27, 9:56 am, Mark Isaak <eci...@curioustaxonomyNOSPAM.net>

wrote:
> On 1/27/12 5:45 AM, Alan Kleinman MD PhD wrote:
>
> > On Jan 26, 10:28 am, Mark Isaak<eci...@curioustaxonomyNOSPAM.net>
> > wrote:
> >> On 1/25/12 4:23 PM, Alan Kleinman MD PhD wrote:
>
> >>> [snip]
>
> >>>> If multiple advantages show up, they will be processed in parallel.
>
> >>> When you have multiple selection pressures targeting multiple genes,
> >>> you don’t have multiple advantages.
>
> >> Yes you do.  You can see it happening.
>
> > What exactly are you seeing Mark. Give us an empirical example where
> > you are seeing this.
>
> Every existing population on the planet.  They all have multiple
> selection pressures on them, and somehow life is not extinct.
>
> If you want examples where the selection and its effects are measured
> quantitatively, look at plant breeding.
>
> > I’ve posted dozens of empirical examples where
> > this doesn’t happen.
>
> You have posted essentially the same example multiple times.  You are
> incapable of learning that the world is bigger than what you have
> already seen.

You asked for it Mark.

http://nobelprize.org/nobel_prizes/medicine/laureates/1958/tatum-lecture.html
"Edward Tatum, Nobel Lecture, December 11, 1958" “In microbiology the
roles of mutation and selection in evolution are coming to be better
understood through the use of bacterial cultures of mutant strains. In
more immediately practical ways, mutation has proven of primary
importance in the improvement of yields of important antibiotics -
such as in the classic example of penicillin, the yield of which has
gone up from around 40 units per ml of culture shortly after its
discovery by Fleming to approximately 4,000, as the result of a long
series of successive experimentally produced mutational steps. On the
other side of the coin, the mutational origin of antibiotic-resistant
micro-organisms is of definite medical significance. The therapeutic
use of massive doses of antibiotics to reduce the numbers of bacteria
which by mutation could develop resistance, is a direct consequence of
the application of genetic concepts. Similarly, so is the increasing
use of combined antibiotic therapy, resistance to both of which would
require the simultaneous mutation of two independent characters.

As an important example of the application of these same concepts of
microbial genetics to mammalian cells, we may cite the probable
mutational origin of resistance to chemotherapeutic agents in leukemic
cells 44, and the increasing and effective simultaneous use of two or
more chemotherapeutic agents in the treatment of this disease.”

And

http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1863594
"The Cancer Treatment Revolution by David G. Nathan, M.D." “Single
agent therapy is unlikely to be successful for very long because the
emergence of resistant strains of tumor cells is almost the rule in
such circumstances. Only combination therapy using different types of
drugs that attack a target at different sites on a molecule or attack
other key molecules can prevent resistance in most cases.”

http://www.dissectmedicine.com/resistance
"Combination therapy with aromatase inhibitors: the next era of breast
cancer treatment?" "Long-term endocrine therapy with either aromatase
inhibitors (AIs) or tamoxifen may lead to endocrine resistance and
disease progression. Recent years have seen advances in our
understanding of the complex biological mechanisms associated with
resistance. Growth factor signaling pathways appear to be upregulated
in hormone-resistant tumours and interact with oestrogen-receptor (ER)
signaling, which remains functional even after long-term endocrine
deprivation. Signaling through the human epidermal and insulin-like
growth-factor receptor (HER and IGFR, respectively) pathways may
promote ligand-independent ER gene transcription and stimulate growth
factor signaling. Therapeutic agents that inhibit these signal
transduction pathways, when combined with AIs, may offer breast cancer
patients new hope for more robust, longer-term remissions. Preliminary
data from phase II studies of combination therapies are encouraging.
There is a large programme of ongoing randomised, controlled trials,
the results of which should pave the way for integrating combination
therapies into clinical practice. To identify which patients will
respond best to particular combinations of treatments, biomarkers and
gene expression profiles are being investigated as predictors of
sensitivity or resistance. In time, breast cancer treatment will
become truly individualised because physicians will be able to match
patients with a variety of disease phenotypes to optimal combination
therapies." British Journal of Cancer (2006) 95, 661-666.”

http://www.bentham.org/cdt/contabs/cdt3-4.htm
"The Means to an End of Tumor Cell Resistance to Chemotherapeutic
Drugs Targeting Thymidylate Synthase: Shoot the Messenger" “Recent
preclinical and clinical studies have addressed the resistance problem
by using combinations of different drugs that target TS, or by
combining TS-targeting and non-TS-targeting drugs.”
And
"Distinctive cellular responses to targeting of specific TS mRNA
regions provide exciting therapeutic opportunities. Antisense ODN
treatment to modulate TS activity, in combination with TS-targeting
chemotherapeutic drugs, has the potential to be an effective anti-
tumor therapy.”

http://cancerres.aacrjournals.org/cgi/reprint/22/11_Part_1/1290.pdf
"The Prediction of Growth-inhibitory Drug Combinations Showing
Enhanced Differential Toxicity and Collateral Sensitivity" “The
possible application to chemotherapy of factors affecting the
regulatory systems of cells has been considered. The extensive
coordinate changes in intracellular enzyme concentrations which result
from exposure to compounds interfering with the normal regulatory
mechanisms suggest the possibility of combination therapy based upon
the selective induction of quantitative changes in enzymatic
activities. Such approaches would appear to be useful in circumventing
two major problems of chemotherapy: finding sufficient metabolic
differences between host and parasite to provide targets for selective
drug toxicity, and preventing the eventual development of drug
resistance.

It is concluded that a combination of two compounds affecting the same
metabolic pathway, one producing feedback inhibition and the other
effective through lethal synthesis, will show an enhanced differential
toxicity greater than that from either drug alone. Similarly, pairs of
compounds in which one member produces enzyme repression and the other
is active through lethal synthesis should produce collateral
sensitivity and thus prevent the development of drug-resistant
populations.”

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12803854&dopt=Abstract
"The chemotherapy of rodent malaria. LXI. Drug combinations to impede
the selection of drug resistance, part 4: the potential role of 8-
aminoquinolines." ”The influence of combinations containing the blood
schizontocides chloroquine (CQ) or mefloquine (MEF), together with the
8-aminoquinolines (8AQ) primaquine (PQ) or the new, long-acting
compound, tafenoquine (TAF), on the rate of selection of resistance to
the individual compounds was examined using the asexual, intra-
erythrocytic stages in rodent malaria models.”
and
"It is concluded that, whereas use of an 8AQ alone carries a high risk
of selecting resistance, combinations containing 8AQ may have a place
in the protection of blood schizontocides that are to be deployed in
endemic areas.”

http://www.rff.org/rff/Documents/RFF-Resources-160-malaria.pdf
"Malaria among African Children" “The hope is that combined drug
therapies can be implemented more widely in affected areas. Like the
AIDS “cocktail” that has transformed that illness from an automatic
death sentence to something that can be aggressively managed, at least
in industrialized countries, the new malaria combination therapies are
believed to be more effective at delaying the emergence of resistance
when compared to single drugs used as stand-alone treatments, which
are rapidly losing their effectiveness.”

http://www.ajtmh.org/cgi/reprint/68/5/608.pdf
"EFFICACY OF MEFLOQUINE AND A MEFLOQUINE-ARTESUNATE COMBINATION
THERAPY FOR THE TREATMENT OF UNCOMPLICATED PLASMODIUM FALCIPARUM
MALARIA IN THE AMAZON BASIN OF PERU" “Based on the results of this
study and with the objective of slowing the development of resistance,
the Peruvian Ministry of Health has decided to revise its malaria
treatment policy and recommend combination therapy with MQ-AS as the
new first-line treatment of uncomplicated P. falciparum malaria in the
Amazon region.”

http://www.ajtmh.org/cgi/content/full/72/2/163 .
"THE SEARCH FOR EFFECTIVE AND SUSTAINABLE TREATMENTS FOR PLASMODIUM
FALCIPARUM MALARIA IN AFRICA: A MODEL OF THE SELECTION OF RESISTANCE
BY ANTIFOLATE DRUGS AND THEIR COMBINATIONS" “The goal of combination
therapy (CT) is to delay the emergence and spread of drug resistance.
The strategy is supported empirically by the success of CT in treating
tuberculosis and human immunodeficiency virus infections, and by
mathematical models.1 The rationale for CT is simple. If two drugs
have independent mechanisms of action, mutations that confer
resistance to each drug will only rarely co-exist in the same
parasite. By this logic, drug combinations should both improve
treatment cure rate, and delay the emergence of drug resistance.2”
And
"These equations enable the frequencies of dhfr mutations to be
tracked over the time course of the evolution of resistance as
described in more detail elsewhere.4”

http://www.journals.uchicago.edu/JID/journal/issues/v192n7/34874/34874.html
"Reply to Hastings and Ward" “There is consensus that combination
therapy in general and ACT in particular is the way forward in
antimalarial chemotherapy. Maybe the optimal future combination will
be a 3-drug ACT including 2 intersynergistic quinoline drugs with
similar, relatively long half-lives, protecting each others'
efficacies after the fast elimination of the artemisinine derivative.
Additionally, the expected complex multigenic mechanism needed for
quinolone-based antimalarial resistance would be expected to slow down
the emergence of this resistance to these drugs.”

And I have many, many more examples from the fields of agriculture,
pest control, parasitology, virology, …

>
> > If what you claim did happen, combination therapy
> > would not work for the treatment of HIV.
>
> You have been corrected on this myriad times, yet you keep repeating it.
>   WHY?
>
> Combination therapy works because the selection is strong enough to
> eliminate essentially all of the alleles that are being selected, and
> because there is little or no crossover.  If selection is not strong
> and/or if there is sex, however, it won't work like you think.  All the
> alleles being selected are likely to increase in frequency.

Your evolutionist folklore no longer cuts it Mark. You don’t
understand how mutation and selection works and you don’t understand
the mathematics of random recombination. And your evolutionist
blunders have caused multidrug resistant microbes, multiherbicide

resistant weeds, multipesticide resistant insects and less than
durable cancer treatments.

>

You are silly Mark and a mathematically incompetent evolutionist who
has no idea how the mutation and selection phenomenon works. And you
and your fellow evolutionists harm people by not properly
understanding or teaching how mutation and selection works.

[Frank J]

On Jan 24, 11:59 pm, Alan Kleinman MD PhD <klein...@sti.net> wrote:
> On Jan 23, 4:31 pm, Ray Martinez <pyramid...@yahoo.com> wrote:
>
>
>
>
>

> > On Jan 23, 10:08 am, Alan Kleinman MD PhD <klein...@sti.net> wrote:
>
> > > >Steven L.  Jan 20, 7:44 am
> > > >Newsgroups: talk.origins
> > > >From: "Steven L." <sdlit...@earthlink.net>
> > > >Date: Fri, 20 Jan 2012 15:44:37 +0000
> > > >Local: Fri, Jan 20 2012 7:44 am
> > > >Subject: Re: The Theory of Evolution is a mathematically irrational belief
>
> > > >"Alan Kleinman MD PhD" <klein...@sti.net> wrote in message
> > > >news:89feea55-7ef1-41e7...@k9g2000pbc.googlegroups.com:
>
> > > >> Nando, this is what evolutionists do when they don't have any
> > > >> empirical or mathematical evidence to support their theory. If Charles
> > > >> Brenner, self proclaimed professional forensic mathematician had any
> > > >> mathematical evidence to support the theory of evolution, he would
> > > >> have posted it long ago. If Bill had any empirical evidence to support
> > > >> the theory of evolution, he would have posted it long ago. And we have
> > > >> evolutionist bureaucrats like Thomas Schneider at National Cancer
> > > >> Institute who makes a major scientific blunder by claiming that the
> > > >> multiplication rule does not apply to biological evolution and harms

> > > >> the very people he is paid to help. Instead, we have multidrug

> > > >> resistant microbes, multiherbicide resistant weeds, multipesticide

> > > >> resistant insects and less than durable cancer treatments as the
> > > >> legacy of the mathematically irrational theory of evolution.
>
> > > >You don't have to keep repeating it:
> > > >The Theory of Evolution is a mathematically irrational belief
> > > >talk.origins  -  449 posts  -  29 authors  - Last post:  Nov 14, 2011

> > > >And your sloppy evolutionist junk science has given us multidrug

> > > >resistant microbes, multiherbicide resistant weeds, multipesticide resistant

> > > >insects and less ...
>
> > > >http://groups.google.com/g/c9c7fef4/t/97d3bac032a2ed51/.../73a30e9601......
> > > >The Theory of Evolution is Mathematically Irrational Round 2
> > > >talk.origins  -  716 posts  -  44 authors  - Last post:  Jul 19, 2011
> > > >The reality of multidrug resistant microbes, multiherbicide resistant
> > > >weeds, multipesticide resistant insects and less than durable cancer treatments
> > > >is a testament ...
>
> > > >http://groups.google.com/g/c9c7fef4/t/db3f6763b7616fbd/d/a8ea0bf6a258......
> > > >The Theory of Evolution is a mathematically irrational belief system
> > > >talk.origins  -  2 posts  -  2 authors  - Last post:  Mar 15, 2011
> > > >.... phenomenon works leads to drug resistant microbes, herbicide
> > > >resistant weeds, pesticide resistant insects, reduced durability of cancer
> > > >treatments and so on. ...
>
> > > >http://groups.google.com/g/c9c7fef4/t/3964b88e0f9b2e58/d/bfacf50960f7......
> > > >The Theory of Evolution is a mathematically irrational belief
> > > >talk.origins  -  2 posts  -  2 authors  - Last post:  Mar 21, 2011
> > > >It is not just multidrug resistant bacteria that's a problem, it
> > > >multi-herbicide resistant weeds, multi-pesticide resistant insects, and drug resistant
> > > >cancers. Farmers ...
>
> > > >http://groups.google.com/g/c9c7fef4/t/2ed6cf2b11893a93/d/ae72e624c7fd......
> > > >Trying to salvage something from this Re: The Theory of Evolution
> > > >talk.origins  -  1 post  -  1 author  - Last post:  Sep 14, 2011

> > > >You've bungled the mathematics of mutation and selection and given us

> > > >multidrug resistant microbes, multiherbicide resistant weeds,

> > > >multipesticide resistant ...
>
> > > >http://groups.google.com/g/c9c7fef4/t/c99c95ee7f90ebef/d/74d86c30a695......
> > > >The Theory of Evolution is a mathematically irrational belief
> > > >talk.origins  -  1 post  -  1 author  - Last post:  Mar 23, 2011
> > > >No wonder we live in a world with multidrug resistant bacteria,
> > > >multi-herbicide resistant weeds, multi-pesticide resistant insects. Evolutionists have
> > > >taken us into ....
>
> > > >http://groups.google.com/g/c9c7fef4/t/791d4747b8934600/d/6f9a4aa1c9ea......
> > > >Trying to salvage something from this Re: The Theory of Evolution
> > > >talk.origins  -  1 post  -  1 author  - Last post:  Sep 14, 2011

> > > >The end result of this evolutionist blunder is multidrug resistant

> > > >microbes, multiherbicide resistant weeds, multipesticide resistant insects and

> > > >less than durable ...
>
> > > >http://groups.google.com/g/c9c7fef4/t/f058224d55f65df4/d/3952b710b5fa......
> > > >The Theory of Evolution is a mathematically irrational belief
> > > >talk.origins  -  1 post  -  1 author  - Last post:  Mar 15, 2011
> > > >.... phenomenon works, we would not have the problems we have today with
> > > >multidrug resistant microbes, multiherbicide resistant weeds, multipesticide resistant ...
>
> > > >http://groups.google.com/g/c9c7fef4/t/7a538320e0eaa9d3/d/bc5cfdde1072......
> > > >The Theory of Evolution is Mathematically Irrational Round 2
> > > >talk.origins  -  1 post  -  1 author  - Last post:  Sep 14, 2011
> > > >.... to prevent drug resistant microbes, herbicide resistant weed,
> > > >pesticide resistant .... multiherbicide resistant weeds, multipesticide resistant insects
> > > >and produce ...
>
> > > >http://groups.google.com/g/c9c7fef4/t/6c621df006fbbad9/d/3210a9371c5f......
> > > >Insane "logic" from Ron O.
> > > >talk.origins  -  6 posts  -  4 authors  - Last post:  Sep 23, 2011
> > > >And the end result of this scientific and educational failure is the
> > > >spread of multidrug resistant microbes, multiherbicide resistant weeds,
> > > >multipesticide resistant ...
>
> > > >http://groups.google.com/g/c9c7fef4/t/ae189dac2e081315/d/7bb5c61dda11......
> > > >We hear you.
> > > >You don't have to keep repeating it like a mantra.

> > > >Have you defined a hotkey that keeps spitting out "multidrug resistant

> > > >microbes, multiherbicide resistant weeds, multipesticide resistant

> > > >insects and less than durable cancer treatments"
> > > >or do you just retype it over and over?
>
> > > Quit whining Steven, it makes you sound like an evolutionist. This

> > > multidrug resistant microbes, multiherbicide resistant weeds,
> > > multipesticide resistant insects and less than durable cancer

> > > treatments defines the utter failure of evolutionism and the harm it
> > > has done to society and you better get used to hearing it because this
> > > is a mathematical and empirical fact of life.
>

> > "[U]tter failure of evolutionism" yet you accept the main empirical
> > claims: natural selection, species mutability.
>
> > Ray (species immutabilist)
>
> Ray, I accept that life forms have mutations when they replicate and

> selection will act on those mutations but I don’t accept that random
> mutation and natural selection will transform reptiles into birds. If

> you understand the basic science and mathematics of mutation and
> selection, you would find that to be a mathematically irrational

> belief.- Hide quoted text -

>
> - Show quoted text -

So do you think that reptiles (or whatever you call their Paleozoic or
Mezozoic ancestors) transformed into birds (or whatever you call their
Paleozoic or Mezozoic ancestors) by another in-vivo process, whether
or not designer-controlled?

[John Harshman]

We've already established that there are only three possible point
mutations at any site, and, worse, you don't know how many of them, if
any, are advantageous or deleterious. So this calculation just shows
your ignorance.

> If you have four equally
> probable base substitution outcomes for a mutation then the weight
> factor is 1/4.

Of course you don't have 4. You have 3. And they aren't equally
probable. Transitions are much more common than transversions. Your
"weight factor" is biological nonsense on a great many grounds.

> If you have more possible outcomes such as base
> insertions, deletions and whatever other type of mutation you can
> imagine, then the weight factor will be smaller than 1/4.

There is no "weight factor". You're assuming that a gene first decides
to mutate, and then picks a particular mutation out of a bag. That's
biological nonsense. Each sort of mutation has some probability of
occurrence. Point mutations are of course mutually exclusive at any one
site. But you could have both a point mutation and an indel in the same
area, so there goes your summation to 1.

> On the other
> hand, if two of the possible base substitutions give a more fit
> replicator, the weight factor would be closer to 1/2.

GIGO.

> But one
> substitution may put that subpopulation on a different fitness
> landscape trajectory than the other substitution. One thing that
> should be clear to you is that the weight factor can never be greater
> than 1.

One thing that's clear to me is that a weight factor is a biologically
meaningless bit of nonsense. It models no real process.

[Mark Isaak]

On 1/27/12 11:50 AM, Alan Kleinman MD PhD wrote:
> [cowardice snipped]

Answer honestly: How old do you think the world is, and how long do you
think mankind has been in existence?

[Alan Kleinman MD PhD]

On Jan 27, 12:13 pm, Frank J <f...@verizon.net> wrote:

>
> So do you think that reptiles (or whatever you call their Paleozoic or
> Mezozoic ancestors) transformed into birds (or whatever you call their
> Paleozoic or Mezozoic ancestors) by another in-vivo process, whether
> or not designer-controlled?

I think that birds evolved from a prehistoric ancestor called a bird.
And it happened by a process called common descent.

Actually Frank shouldn’t it be what came first, two chickens or the
egg?

[Alan Kleinman MD PhD]

On Jan 27, 12:38 pm, John Harshman <jharsh...@pacbell.net> wrote:
> Alan Kleinman MD PhD wrote:
>
> > On Jan 27, 7:59 am, John Harshman <jharsh...@pacbell.net> wrote:
> >> If the past is any guide, you'll show me something unrelated to the
> >> question. If you don't make that assumption, then why do you divide the
> >> mutation rate by 4?
>
> > The factor of 1/4 on the mutation rate takes into account that not
> > every mutation is the beneficial mutation.
>
> We've already established that there are only three possible point
> mutations at any site, and, worse, you don't know how many of them, if
> any, are advantageous or deleterious. So this calculation just shows
> your ignorance.

Which three bases are they?

>
> > If you have four equally
> > probable base substitution outcomes for a mutation then the weight
> > factor is 1/4.
>
> Of course you don't have 4. You have 3. And they aren't equally
> probable. Transitions are much more common than transversions. Your
> "weight factor" is biological nonsense on a great many grounds.

Your understanding of mutation and selection is mathematically
irrational nonsense. Do you think a mutation is more likely to occur
at a purine site or a pyrimidine site? If the mutation requires a
transversion, then the weight factor for the mutation rate will be
less than 1/4. You got yourself a weighted die.

>
> > If you have more possible outcomes such as base
> > insertions, deletions and whatever other type of mutation you can
> > imagine, then the weight factor will be smaller than 1/4.
>
> There is no "weight factor". You're assuming that a gene first decides
> to mutate, and then picks a particular mutation out of a bag. That's
> biological nonsense. Each sort of mutation has some probability of
> occurrence. Point mutations are of course mutually exclusive at any one
> site. But you could have both a point mutation and an indel in the same
> area, so there goes your summation to 1.

No I’m not. Mutations are random independent events and to compute the
probability that two beneficial mutations will occur in a
subpopulation requires the use of the multiplication rule of
probabilities for random independent events. And the sum of
probabilities for all possible outcomes for a random mutation will be
1 even if you include any type of mutation you can imagine.

>
> > On the other
> > hand, if two of the possible base substitutions give a more fit
> > replicator, the weight factor would be closer to 1/2.
>
> GIGO.

You are confusing this with a course in evolutionism.

>
> > But one
> > substitution may put that subpopulation on a different fitness
> > landscape trajectory than the other substitution. One thing that
> > should be clear to you is that the weight factor can never be greater
> > than 1.
>
> One thing that's clear to me is that a weight factor is a biologically
> meaningless bit of nonsense. It models no real process.

I understand you now. You believe that every mutation is beneficial no
matter where they occur.

[Alan Kleinman MD PhD]

On Jan 27, 1:05 pm, Mark Isaak <eci...@curioustaxonomyNOSPAM.net>
wrote:

> On 1/27/12 11:50 AM, Alan Kleinman MD PhD wrote:
>  > [cowardice snipped]
>
> Answer honestly: How old do you think the world is, and how long do you
> think mankind has been in existence?

Not old enough to make your theory of evolution a mathematically
rational belief system.