The Theory of Evolution is Mathematically Irrational Round 2
Bill
Sorry for top posting, I'd just suggest that all the responses to
Dr.Dr.Dr. AK go into this thread. At least for those of us stuck with
Google Groups, once you hit 1000 posts the thread fragments. It's
entertaining and it would be nice to have it all in one place.
>
> You are wrong once again hersheyh. That s not my strange jargon,
> that s the jargon Tom Schneider of the National Cancer Institute uses.
> He does that on the same page of his web site where he claims that the
> multiplication rule of probabilities does not apply to biological
> evolution, a concept of his that you so ardently defended. But at
> least you finally understand that a trait must spread through a
> population, increasing in frequency as it spreads over generations so
> as to overcome the effect of the multiplication rule of probabilities.
> The process doesn t work so well when two or more traits must spread
> simultaneously as demonstrated by the example of combination therapy
> for HIV and for every other real, measurable and repeatable example of
> mutation and selection when combination selection pressures are used.
>
>
>
> > > This
> > > gives more players rolling the dice and more opportunities to roll the
> > > dice. What evolutionists don t understand is that the amplification
> > > process only works efficiently one gene at a time.
>
> > Really? Only if you imagine the spread of a trait as always being a
> > function of the *death* of individuals without the new trait resulting
> > in a large population size decrease. There certainly are examples of
> > selection conditions during which there is a large decrease in the
> > size of the population, e.g. selection of E. coli for strep
> > resistance. But again, take the Lenski experiment. There was at no
> > time any decrease in the size of the population. Rather there was,
> > during the spread of the new citrate-metabolizing trait, an *increase*
> > in the size of the population (because the bacteria could now use a
> > previously unavailable resource). So clearly it is not a *necessity*
> > that there be a significant change in population size for a trait to
> > spread thoughout a population.
>
> I have no idea what you are talking about with your statement e.g.
> selection of E. coli for strep
> resistance . Now if you had talked with Lenski, he should have told
> you he has to continually replenish his growth medium in order to
> prevent his populations from starving to death. Lenski had to give
> sufficient glucose so that his population would have time to become
> citrate metabolizers, something which no real environment would be so
> generous to do, that is to maintain extremely stable selection
> conditions for tens of thousands of generations.
>
> > So let's imagine a population of bunnies in a marginal environment
> > where it is cold and snowy. In one part of the population, some
> > animals mutate (or already have variants) such that the variants
> > restrict blood flow to extremities when the temperature drops. This
> > is selectively useful in the cold and animals with that variation
> > increase in the cold regions. In another part, some animals mutate
> > (or already have variants) that turn their coats white when the
> > temperature drops. This is also selectively useful in the cold and
> > animals with that variation increase. These are variations in
> > different genes and the spread of those genes is independent of the
> > other gene. At some point we will get via sexual recombination,
> > organisms with *both* useful traits for cold weather. Not
> > surprisingly, the bunnies with both traits are at a selective
> > advantage relative to those with only one. This is occurring
> > *simultaneously*, not "one gene at a time" like you claim is the only
> > possibility. Can you explain to me why you think it is impossible for
> > there to be such simultaneous accumulation of favorable variations?
>
> I have never said that it is impossible for there to be simultaneous
> accumulation of favorable variations (mutations). What I have said is
> that the multiplication rule of probabilities makes these events much,
> much less likely occurrences. In addition, the way populations
> overcome the multiplication rule of probabilities is by the
> amplification of beneficial alleles. And all the empirical evidence
> from real, measurable and repeatable examples of mutation and
> selection show that populations have a much more difficult time
> amplifying multiple beneficial alleles simultaneously. The mutation
> and selection phenomenon only works efficiently when selection targets
> a single gene at a time. When a beneficial mutation occurs on that
> gene, that allele can be amplified over generations setting the stage
> for the next beneficial mutation to occur.
>
>
>
> > > > That probability, however, does not hold when you roll 10 die, keep
> > > > all the ones that have a six and roll the remaining a second time,
> > > > repeating until all have all 6s. There the probability of all 6s on
> > > > the first roll (which is indeed 1/6^6) is the wrong question because
> > > > we are dealing with a different mechanism for obtaining all 6s, an
> > > > iterative mechanism. The right question is the probability that any
> > > > die will show at least one 6 on the first roll [about 67%]. That
> > > > probability is much higher than 1/6^6 and can be estimated by a
> > > > Poisson distribution for a mean chance of 1/6. Once you get one or
> > > > more 6s, then the next roll is of only 5 or fewer die. The number of
> > > > rolls of dice required to generate all 6s by this mechanism is much,
> > > > much, much, much smaller than the value determined by the first
> > > > mechanism.
>
> > > Ok hersheyh, now you are starting to play the game but now play the
> > > game with dice that have 17,000 sides like we have with HIV,
>
> > So, is it your claim that the evolution of HIV resistance to two drug
> > types requires 17,000 mutational changes? Or have you now gone on to
> > the "evolutionary biologists think that HIV is randomly assembled all
> > at once at random from random nucleotides"? That is, after all, what
> > every idiot creationist and his even dumber brother thinks. It is, of
> > course, really what *creationists* think. Namely that Dyslexic Dog in
> > his infinite loving wisdom intelligently designed HIV by intelligently
> > assembling all those nucleotides at one swell foop for the loving goal
> > of causing people to die a really, really, nasty and painful death.
> > Me, the *real* evolutionary biologist and not the strawman, thinks
> > that the human virus evolved from a quite similar ape virus by
> > mutation and selection (and probably not all at once) that improved
> > the ability of the virus to utilize a new environmental niche, aka,
> > humans. No 17000 sided dice. Only a few random changes, not 17000.
> > But you tell me what you mean with the number 17000 sides that doesn't
> > amount to the brain-dead idea that HIV appeared in a magical poof by
> > randomly assembling 17000 nucleotides in the right order all at once.
>
> Hersheyh, if you want, we can start a discussion on the incredibly
> stupid concept of abiogenesis. There is simply no physical, chemical,
> or mathematical evidence that it ever occurred. We only have the
> incredibly stupid evolutionist speculation that a primordial soup
> existed and from out of that soup popped a replicator. If you are
> smart, and I highly doubt that, you will stick with the concept of
> selection since that is the only physical phenomenon that you have
> that has any capability of overcoming the multiplication rule of
> probabilities. Without selection, your titanic theory of evolution
> hits the multiplication rule of probabilities iceberg and sinks into
> your primordial soup.
>
> > > or with
> > > about 500,000 sides that we have with the smallest genome free
> > > replicator, or with 3,000,000,000 billion sides like we have with
> > > humans.
>
> > See point above. The argument is just as stupid and brain-dead as the
> > same argument about HIV, just with larger numbers.
>
> I guess you aren t aware that Lenski s bacteria had sufficient numbers
> of mutations to occur at every locus several times over. Only a
> miniscule number of mutations found their way into the gene pool. But
> don t let empirical or mathematical evidence get in the way of your
> mathematically irrational belief system.
>
>
>
> > > And then add on the rule that if you don t get all your 6s in
> > > time, you die. That s the mathematics your irrational theory of
> > > evolution contradicts.
>
> > And that little paragraph or so demonstrates that you are the type of
> > utterly ignorant creationist nut who thinks that evolution involves
> > random assembly of entire organisms all at once that Tom Schnider was
> > complaining about. Keep in mind that it is you creationist nuts who
> > think that entire organisms are magically poofed into existence all at
> > once, not evolutionary biologists. The process of speciation is not
> > even the change of mongoose into a goose, it is more like the
> > conversion of H. erectus into archaic H. sapiens or Drosophila
> > simulans into D. melanogaster. But, you complain, both H. erectus and
> > archaic H. sapiens are Homo (humans)! And both Drosophila are still
> > Drosophilid fruit flies! Well, of course. That is what speciation
> > does.
>
> How many times can you be wrong in a single discussion? You have
> convinced me that evolutionism is a psychosis. You have lost contact
> with reality. And your failure to properly understand how mutation and
> selection works harms people suffering from diseases subject to the
> mutation and selection phenomenon.
>
>
>
> > > > *That*, of course, is what Tom Schnider is talking about. That every
> > > > creationist idiot and his even more dimwitted brother always assumes
> > > > that evolution works *all the time* by the first mechanism, when it
> > > > really works by the second nearly all the time [except for the rare
> > > > cases of *artificial* selection to eliminate or control organisms that
> > > > humans do not want].
>
> > > Hersheyh, do you want to start talking about abiogenesis instead of
> > > the theory of evolution?
>
> > Seems like you have already gone on to the creationist strawman
> > version of abiogenesis -- namely magical poofing of whole organisms
> > into existence by either pure random chance (which they falsely assume
> > is evolution) or, in their prefered version of magical creation, by
> > some invisible intelligent something who did the magical poofing with
> > design.
>
> Oh no, you have brought out the strawman argument. That s what
> evolutionists do when the mathematical and empirical evidence
> contradicts your irrational belief system. You have bungled the basic
> science and mathematics of the mutation and selection phenomenon and
> people are paying for it by suffering from multidrug resistant
> infections.
>
> > > Because in abiogenesis, you don t have
> > > selection to overcome the multiplication rule of probabilities.
>
> > False. You obviously have not read anything about abiogenesis. Life
> > is not a structure. It is a combination of functions. Specifically,
> > imperfect replication and the ability to extract energy and materials
> > from its environment to accomplish that imperfect replication.
> > Another definition of life is that which has the capacity to evolve by
> > imperfect replication by the ability to extract energy and materials
> > from its environment. Once chemistry produces a system capable of
> > imperfect replication by the ability to extract energy and materials
> > from its environment, you have conditions which favor evolution of
> > organisms better able to accomplish those functions.
>
> So let s see, you have the replicator HIV which can not evolve
> efficiently when selection pressures target two genes simultaneously
> and now you are going to tell us that there are selection conditions
> that operate on non-replicators. So let s hear your latest story from
> the SciFi channel.
>
> > > You
> > > know that rule; the one you think can be overcome by your equally
> > > irrational drift concept of evolution without selection.
>
> > No. I think that a lot of evolution that *matters*, that produces
> > difference in phenotype, is due to selection. I just don't think that
> > that involves changes involving thousands of changes. Nor does it
> > typically involve processes mathematically similar to that involving
> > multidrug selection against HIV.
>
> But in fact, there are at least 40,000,000 differences as claimed by
> John Harshman between humans and chimpanzees. It takes time for these
> differences to accumulate. You have about a million generations to do
> the accounting problem. Let s see you do it. I love seeing
> evolutionists paint themselves into corners.
>
>
>
> > > Actually,
> > > Schneider knows his computation on that page is wrong since he only
> > > considers L-amino acids in his mathematics. In your imaginary
> > > primordial soup, do you
r norman
<broger...@gmail.com> wrote:
>On Mar 16, 6:51 am, Alan Kleinman MD PhD <klein...@sti.net> wrote:
>
>Sorry for top posting, I'd just suggest that all the responses to
>Dr.Dr.Dr. AK go into this thread. At least for those of us stuck with
>Google Groups, once you hit 1000 posts the thread fragments. It's
>entertaining and it would be nice to have it all in one place.
I believe you, in a different thread, have been arguing against John
Wilkins about modifying traditional biological word usage just to
placate the creationists or at least to deny them the ability to twist
the meaning of the words to their purposes. Now you would have all
the rest of us modify traditional posting methods just to placate
those people who do not know how to use a real news reader and must
rely on Google Groups!
William Hughes
the good Dr. has been unable to note that he is confusing two
scenarios
1: A mutation A' causes an increase in reproductive
success, whether or not a mutation B' (which also
causes an increase in reproductive success) is present.
2: A mutation A' alone or a mutation B' alone does not cause an
increase
in reproductive success. Only both mutations together cause
an increase in reproductive success.
Only in case 2 is the multiplication rule for probabilities applicable
- William Hughes
Bill
> On Tue, 15 Mar 2011 16:59:52 -0700 (PDT), Bill
>
Ouch!! A hit, a very palpable hit, I do confess it.
jillery
> On Tue, 15 Mar 2011 16:59:52 -0700 (PDT), Bill
>
FWIW I rely on Google Groups not because I don't know how to use a
real newsreader. In fact I have used many. I rely on Google Groups
because it has the fastest propagation and the longest retention of
anything in its price class, which is no additional cost.
Of course TANSTAAFL, and enduring this design flaw is part of the cost
of using Google Groups. ISTM illustrating that point is one of the
reasons for pepetuating this topic.
John S. Wilkins
Ouch! :-)
--
John S. Wilkins, Associate, Philosophy, University of Sydney
http://evolvingthoughts.net
But al be that he was a philosophre,
Yet hadde he but litel gold in cofre
r norman
wrote:
I wasn't really criticizing -- just tweaking a little and the tweak
took exactly as intended. I would like Google Groups totally banned
to be replaced by a really useful and decent web-based news reader.
However I also recognize the utility of Google Groups and have been
forced into using it in past times and, no doubt, will again in the
future. I always regret it, but it is necessary.
That some threads go on for 1000 posts is the real problem that can be
solved by exercising some common sense.
jillery
> On Tue, 15 Mar 2011 21:18:56 -0700 (PDT), jillery <69jpi...@gmail.com>
I am glad to serve your purpose, as you have served mine by providing
an opportunity to point out the silliness of 1000-post topics.
> I would like Google Groups totally banned
> to be replaced by a really useful and decent web-based news reader.
> However I also recognize the utility of Google Groups and have been
> forced into using it in past times and, no doubt, will again in the
> future. I always regret it, but it is necessary.
>
> That some threads go on for 1000 posts is the real problem that can be
> solved by exercising some common sense.- Hide quoted text -
>
> - Show quoted text -
John McKendry
Oh, come on. The response to this kind of criticism is "a foolish
consistency is the hobgoblin of little minds". I'm surprised that
you don't know this already.
John
Bill
I always used to use that response in the past, but I decided I'd
change it up this time.
> John- Sembunyikan teks kutipan -
>
> - Perlihatkan teks kutipan -
Mitchell Coffey
Regarding 2: is it accepted by scientists that all mutations are
independent of each other in incidence?
Mitchell Coffey
Mike Lyle
wrote:
[...]
>
>
>FWIW I rely on Google Groups not because I don't know how to use a
>real newsreader. In fact I have used many. I rely on Google Groups
>because it has the fastest propagation and the longest retention of
>anything in its price class, which is no additional cost.
>
>Of course TANSTAAFL, and enduring this design flaw is part of the cost
>of using Google Groups. ISTM illustrating that point is one of the
>reasons for pepetuating this topic.
I admire and applaud GG for its retention, even though the parent
company isn't very conversant with the design of search engines. But
is its propagation really so reliable these days? It sometimes used to
take days; and sometimes used simply to stop for no discernible
reason.
--
Mike.
Friar Broccoli
> On Tue, 15 Mar 2011 21:18:56 -0700 (PDT), jillery <69jpi...@gmail.com>
.
True, but there are creationists in many of the threads.
Walter Bushell
jo...@wilkins.id.au (John S. Wilkins) wrote:
> r norman <r_s_n...@comcast.net> wrote:
>
> > On Tue, 15 Mar 2011 16:59:52 -0700 (PDT), Bill
> > <broger...@gmail.com> wrote:
> >
> > >On Mar 16, 6:51 am, Alan Kleinman MD PhD <klein...@sti.net> wrote:
> > >
> > >Sorry for top posting, I'd just suggest that all the responses to
> > >Dr.Dr.Dr. AK go into this thread. At least for those of us stuck with
> > >Google Groups, once you hit 1000 posts the thread fragments. It's
> > >entertaining and it would be nice to have it all in one place.
> >
> > I believe you, in a different thread, have been arguing against John
> > Wilkins about modifying traditional biological word usage just to
> > placate the creationists or at least to deny them the ability to twist
> > the meaning of the words to their purposes. Now you would have all
> > the rest of us modify traditional posting methods just to placate
> > those people who do not know how to use a real news reader and must
> > rely on Google Groups!
>
> Ouch! :-)
Anyway what's wrong with teleological language in science. We know that
people don't have teleological motivation because if they did
teleological phenomena would exist in nature.
--
The Chinese pretend their goods are good and we pretend our money
is good, or is it the reverse?
John S. Wilkins
Teleological thinking is perfectly approriate when you are dealing with
teleological systems, like humans and their societies/artifacts. There
*is* teleology in the world. Every time I go to the shop to buy milk,
such a system is in operation.
Alan Kleinman MD PhD
> On Mar 16, 6:51 am, Alan Kleinman MD PhD <klein...@sti.net> wrote:
>
> Sorry for top posting, I'd just suggest that all the responses to
> Dr.Dr.Dr. AK go into this thread. At least for those of us stuck with
> Google Groups, once you hit 1000 posts the thread fragments. It's
> entertaining and it would be nice to have it all in one place.
together some of my responses for a while. I know it upsets the
posters when I combine responses but unless you have a better
suggestion, that’s what I’m going to do so that the discussion doesn’t
fragment further.
==================================================================
Mark Isaak
> [...] When I went to the conference on H1N1 last year, [...]
>Why did you go to a conference? I thought you already know everything
>there is to know about everything. Your posts here leave no doubt that
>learning is the last thing you would ever want to do.
Mark, you are confusing me with evolutionists. It’s evolutionists who
claim they are the only ones who know anything about mutation and
selection when in reality evolutionists have completely bungled the
basic science and mathematics of mutation and selection. If
evolutionists knew anything about the mathematics of mutation and
selection, they would understand that the multiplication rule of
probabilities is the dominant mathematical principle governing this
phenomenon.
==================================================================
Mike Lyle
>I think the important thing for the slightly more sophisticated
>creationists is not to establish truth, but simply to keep the dispute
>churning over so they can give the public an impression of serious
>controversy. As is often pointed out, even if most of them are
>religiously sincere their aims and methods are essentially political.
Evolutionists could care less about how multidrug resistant microbes
occur. Evolutionist doctrine is far more important despite the fact
that this gross misrepresentation of the mutation and selection
phenomenon by evolutionists harms people.
==================================================================
Sandy
>Logical or not evolution is here to stay.
Feel free to find a quote where I said evolution doesn’t occur. The
only thing you will find is my claim and the evidence to substantiate
that claim that the theory of evolution is a mathematically irrational
belief system and that the gross misrepresentation of the mutation and
selection phenomenon by evolutionists has harmed and continues to harm
millions of people suffering from diseases subject to the mutation and
selection phenomenon.
>Evolution is the idea that under-girds all modern biology.
>And fits in well with archaeology, bio-chemistry, genetics,
>etc, etc.
No wonder so little progress has been made in addressing multidrug
resistant bacteria, multiherbicide resistant weeds, drug resistant
cancers and so on. Hey Sandy, how does the theory of evolution fit so
well with archaeology, biochemistry and genetics when the basic
science of mutation and selection has been so completely bungled by
evolutionists?
>So your post threatens a lot of rational research requiring
>tons of time, energy and money. So I think your thesis
>demands, not a short posting to talk.origins, but a
>book. Maybe a five or six volume work. With a lot of
>mathematical analysis and clear explanation thereof. An
>opportunity to make big bucks.
The only research my posts threaten is irrational research. The
pathway for dealing with drug resistance by mutation and selection is
very straight forward as shown by the success of combination therapy
for HIV. As long as policy makers at institutions like the Center for
Disease Control, the Sanford Guide and the National Cancer Institute
fail to understand the basic science and mathematics of mutation and
selection and recommend single drug therapy, the evolution of drug
resistance is going to be a major medical problem. This kind of
misunderstanding of a fundamental physical phenomenon (mutation and
selection) by these individuals only delays rational research.
Evolutionists are the ones who write volume after volume without
properly describing the mutation and selection phenomenon. The proper
description of the mutation and selection phenomenon only requires a
short posting on a web site.
==================================================================
hersheyh
>> So your post threatens a lot of rational research requiring
>> tons of time, energy and money. So I think your thesis
>> demands, not a short posting to talk.origins, but a
>> book. Maybe a five or six volume work. With a lot of
>> mathematical analysis and clear explanation thereof. An
>> opportunity to make big bucks.
>At minimum, if he had an actual intelligent argument against the *real*
> as opposed to his *imaginary* theory of evolution,
>he would be in line for a Nobel Prize in Medicine.
The Nobel Prize was already won; Edward Tatum won the prize in 1958.
He pointed out that the multiplication rule of probabilities was the
dominant mathematical feature of the mutation and selection
phenomenon. He is the one who should be honored. All I am doing is
reminding people of what he said about this important mathematical
principle that governs the mutation and selection phenomenon.
==================================================================
John Harshman
> Just because you evolutionists don’t want to
> discuss the basic science and mathematics of mutation and selection,
> that I have to enter your world of irrational speculations. We now
> have evolutionist expert Mark Isaak claiming that reducing the
> intensity of selection accelerates the mutation and selection
> phenomenon. This mathematical blunder ranks up there with the
> evolutionist blunder that selection increases the diversity of
> populations.
Bet he didn't actually say that. You aren't a very good reader. And
of
course selection can increase diversity under certain conditions,
some
of which have been explained to you.
Well let’s see exactly what Mark said in context to a comment I made:
Kleinman said:
>> Again, you repeat an old speculation that evolutionists like to use.
>> The intensity of selection has very specific mathematical effects on
>> the mutation and selection process. That effect is to slow the process
>> down. Reducing the intensity of selection is a two edged sword. On one
>> hand, reducing the intensity of selection reduces the chances that the
>> population will be driven to extinction. On the other hand, reducing
>> the intensity of selection slows the mutation and selection phenomenon.
Mark Isaak said in response:
>It is obvious to anyone with a smattering of knowledge of population
>genetics that you don't know what you're talking about. But it is also
>apparent (if not so blatant) that you *think* you know what you are
>talking about. I find that fascinating. It's like you are writing a
>travel book about a place you have never so much as heard of before, but
>are willing to swear to having lived there for years.
I am claiming that reducing the intensity of selection slows the
evolutionary process. Mark Isaak is claiming I don’t know what I’m
talking about. If either of you understood Haldane’s work, you would
have some idea how the intensity of selection affects the substitution
process. John, do you finally understand how population size affects
the probability that a beneficial mutation will occur at a particular
locus? That probability is not proportional to the population size.
You evolutionists are so confused on so many principles of the
mutation and selection phenomenon. Now wonder you draw so many
erroneous conclusions.
>> Lenski is starving his bacteria but leaving his population with an
>> out, ie citrate. You obviously have not read Lenski’s paper on the
>> quantitative results of his study. Hersheyh, get a copy of this paper
>> “Genome evolution and adaptation in a long-term experiment with
>> Escherichia coli”, Vol 461, October 29, 2009, Nature. In the adaptive
>> phase of his study, none of the mutations in the experiment were due
>> to drift (a crappy word to describe what populations do on a plateau
>> of a fitness landscape).
>Another very odd thing to say. Of course mutations aren't due to drift.
>Drift affects allele frequency, not mutation. And drift doesn't apply to
>populations; it applies to alleles. Perhaps you meant to say that none
>of the fixations were due to drift, which is true of the first 20,000
>generations. Many of the fixations by generation 40,000 were due to
>drift. The difference is that the mutation rate increased in the
>interim, and the rate of fixation due to drift equals the mutation rate.
All the mutations measured in the first 20,000 generations were found
in all populations, they were adaptive, not neutral. Only when his
populations reached a fitness plateau did more variants start to
appear. That is, his populations had adapted to the starvation
conditions and reduced the selection pressure allowing more variants
to appear after 20,000 generations. I question Lenski’s estimates for
the mutation rates. If Lenski is extrapolating backwards from the
number of mutations found in his populations, he could be getting
inaccurate estimates of the mutation rates.
However John, one of the many mathematical features of the mutation
and selection phenomenon that you don’t understand is that the
mutation rate has only a small effect on the behavior of the
phenomenon. Perhaps you want to claim that doubling the mutation rate
doubles the probability that a beneficial mutation will appear at a
particular locus? By far, the dominant mathematical principle of the
mutation and selection phenomenon is the multiplication rule of
probabilities. That is why the complexity of the selection conditions
dominates the behavior of the phenomenon.
Regardless, Lenski’s population fixed only a very small number of
mutations in more than 40,000 generations, only about 1 each 500
generations. Now you have done the mathematics for the number of
fixations required to transform humans and chimpanzees from a common
precursor. Your estimate is 67 fixations per generation. How do you do
that accounting problem?
>> Only when the populations evolved to improved
>> fitness did “neutral” mutations appear in his populations. In other
>> words, his population is diversifying on a fitness plateau. Still,
>> this population is limited by the amount of citrate available.
>You completely misunderstood his point. Which is not unexpected. There
>was in fact no fitness plateau. Advantageous mutations appeared
>throughout. What made the difference was the increase in mutation rate,
>as Lenski himself made clear in that paper.
The mutation rate has only a small effect on the mutation and
selection phenomenon. If you understood the mathematics of the
phenomenon, this would be clear to you. Do you think the mutation rate
will account for 67 fixations per generation?
>>> Now, if the glucose-only bacteria were more efficient at using glucose
>>> than the bacteria that could use both, we have a condition that could
>>> favor "specialization" to different niches, with some bacteria
>>> becoming specialized glucose users and others becoming more and more
>>> reliant on citrate. I.e., speciation (and because inability to use
>>> citrate is a key speciation-defining feature of E. coli, the new bug
>>> would not be E. coli, but perhaps E. citrusflavoreddietcoli.
>> I guess you haven’t read any of Lenski’s papers. The citrate
>> metobolizers no longer were efficient glucose metabolizers and these
>> citrate metabolizers were very sensitive to osmotic pressures.
>All adaptations are adaptive with respect to particular environments.
>Don't you understand that yet?
Give me a hint John; tell me how you can account for 67 fixations per
generation? Just what were the adaptive conditions for that primate
precursor?
>> Now
>> early on, you posted a paper that I wasted my time on reading. In this
>> paper, these evolutionist pseudo-scientists claim that evolution is
>> irreversible. Now do you think if you switched Lenski’s experiment and
>> put his citrate metabolizers in a glucose rich environment with sparse
>> citrate that his bacteria could evolve back to glucose metabolizers?
>That's not what "irreversible" means. We would expect adaptation to any
>environment, including a prior one. What we wouldn't expect is a
>reversion to exactly the same phenotype as the ancestral one. The reason
>is that there are many ways of achieving the same adaptive result.
Why not? So why would you say that reptile scales would turn into
feathers when there are many ways to achieve the same adaptive result?
Seems like a very difficult way for a reptile population to stay warm
when there are many other ways to accomplish the same result without
taking huge number of generations. The reptiles that live near my home
hibernate when the weather gets cold. They are not growing feathers.
>You haven't explained why that would be. Could you? And you might also
>explain where you think birds came from, if they didn't evolve from
>terrestrial reptiles.
It’s not my job here to tell you where birds came from. It’s my job to
properly describe how the mutation and selection phenomenon works. Do
you want to tell us how to account for 67 fixations per generation?
>> Even if you could describe the selection pressures that would
>> transform a reptile scale into a feather, sequentially it would take a
>> vast number of generations.
>How many? Show your work. By the way, you have been told many times that
>feathers evolved long before birds. Try to correct these simple errors.
Edward Max already gave us a citation which states that at least nine
genes would have to be transformed. If only one base substitution were
required for each gene, and the sequential selection pressures
existed, it would require around 300-500 generations per substitution.
That would give a bottom limit to the number of generations of
2700-4500 generations in the simplest case. This number would rapidly
go up if the number of base substitutions was greater and the number
would become huge if any of the beneficial mutation would have to
occur simultaneously. But this is all speculation. We know what the
genetic sequences are for humans and chimpanzees. How do you account
for 67 fixations per geneneration?
>> And remember, Lenski maintained constant
>> selection conditions over these tens of thousands of generations. What
>> to think would happen if he introduced other random selection
>> conditions into his experiment like temperature variations,
>> dehydration, predation, disease, do you think that would accelerate
>> the evolution of citrate metabolizers?
>No. So?
Any real “natural” environment would superimpose thermal stress,
starvation, predation, disease, dehydration and any other stress you
could imagine on your reptile population. Do you think your reptile
population was only subjected to thermal stress while it was evolving
scales into feathers? I don’t think so.
>> Real environments do this to
>> populations. Real environments don’t maintain constant selection
>> conditions for long periods of time. This is why your theory of
>> evolution is mathematically irrational.
>Why? Real environments do indeed maintain constant selection conditions
>for many factors. Constancy with respect to one feature doesn't require
>constancy with respect to all. And one adaptation can produce conditions
>in which the next becomes adaptive.
Challenging populations with a wide variety of selection conditions
which are always changing puts huge stress on the population. This is
why so many species have gone extinct. So what is that adaptive
environment that will fix 67 mutations per generation? Let’s try to
bring your evolutionist speculations back to reality.
>> Look what happens when self-deception is institutionalized in
>> evolutionism. We end up with a totally irrational misinterpretation of
>> the mutation and selection phenomenon and millions of people are
>> harmed by this irrational misinterpretation of mutation and selection
>> phenomenon.
>You really can't bring yourself to say "selection", can you? It always
>has to be "the mutation and selection phenomenon". Can anyone explain
>the psychology of such a twitch? A lot of creationists seem similarly
>inflexible, repeating the same phrases, even whole paragraphs, even when
>pointless.
Mutation and selection is the cycle of evolution. Mutation is the
source of diversity and selection is the source of order. This cycle
has a particular mathematical behavior that if you understand it can
use the principles by which it works to more effectively treat
diseases subject to this phenomenon. Evolutionists on the other hand
are obsessed with the concept that the mutation and selection
phenomenon can transform reptiles into birds and humans and
chimpanzees from a common precursor. Only this evolutionist obsession
can not account for 67 mutations fixed every generation and does not
recognize how combination therapy interferes with the evolution of
drug resistance. We have libraries full of this evolutionist
irrationality.
>> Do the math hersheyh, even with a viral load of 50/ml, you have a
>> population that is at least in the hundreds of thousands. There is
>> still replication of the virus even with effective three drug therapy.
>> If there wasn’t replication, RNAases would quickly clear the blood of
>> any viruses. I would be very surprised that in this replication
>> process that there were not mutations that would give benefit to one
>> drug or another.
>But does that increase their rate of replication in the presence of the
>other drugs? That's the question. If it doesn't, the mutation is
>neutral. If it does, it should increase in frequency. Multi-drug therapy
>works because it prevents resistance to a single drug from offering a
>selective advantage.
Of course combination therapy (in every circumstance which it is
tried) prevents an otherwise beneficial mutation from giving selective
advantage. That is why the example of the evolution of HIV to
combination therapy is not a special example of mutation and
selection, it is only a highly studied example of mutation and
selection. Any time selection pressures target more than a single
gene, a mutation beneficial to one or another selection pressure fails
to give significant selective advantage, the other selection pressures
continue to impair the reproduction of that member. That is why
combination therapy is successful. Not only does combination therapy
make use of the multiplication rule of probabilities which markedly
reduces the probability of simultaneous beneficial mutations, the
multiple selection pressures impair the amplification process so that
if a beneficial mutation does occur, it doesn’t get amplified. John
give us a single citation of a real, measurable and repeatable example
of mutation and selection where selection conditions target more than
a single gene and the amplification process is not impaired. Only in
your speculative mind does this event occur.
>> The problem for the population is amplifying these
>> variants so that there would be a reasonable probability that another
>> beneficial mutation for another drug would occur on one of these
>> variants. But if these are neutral mutations, shouldn’t they be fixed
>> in the population according to your drift theory?
>You really have no comprehension here. It's very unlikely for any single
>neutral mutation to be fixed. In fact, in your viral population, the
>initial probability is 1/N, where N is the population size. However,
>lots of mutations happen in the population, and the expected number of
>neutral mutations fixed in any generation is equal to the rate of
>neutral mutation. Most mutations just go extinct immediately. Some rise
>to a detectable frequency. And a few become fixed.
John, of course I comprehend that neutral mutations don’t get fixed in
populations. Without selection, the mutation and selection phenomenon
turns into the concept of abiogenesis. I hope you can imagine why the
multiplication rule of probabilities makes the concept of abiogenesis
irrational. I can understand why you find it more difficult to
comprehend why the multiplication rule of probabilities makes the
theory of evolution a mathematically irrational belief system because
in that concept, you have selection operating. Perhaps now you are
starting to understand the limits of selection. After all,
understanding how selection works is the key to understanding how to
prevent drug resistant microbes, herbicide resistant weeds, designing
more durable cancer treatments and so on.
>> So, do you think a thicker scale would not provide better insulation?
>Than what? Than a thinner scale? Yes, marginally. Than a covering of
>hair or feathers? No. Hint: it's trapped air that provides the best
>insulation.
So the population would wait tens of thousands of years to warm up
simply to produce feathers? The population could easily migrate to a
warmer climate and do that in a far shorter time.
>> But instead the reptile population would evolve feathers instead?
>That is clearly what happened. We may never know why, but knowing what
>is comparatively easy.
John let’s set your speculations aside for the moment and tell us how
67 mutations per generations can be fixed in the evolution of humans
and chimpanzees from a common precursor?
>> As
>> hersheyh likes to point out, selection always acts on the traits of a
>> population that already exists. Why wouldn’t a cooling of the climate
>> select for thicker scaled reptiles rather that the transformation of
>> numerous genes that takes who knows how many thousands of generations?
>> Of course from your point of view, only evolutionist speculations are
>> the only thing relevant to the mutation and selection phenomenon.
>This is not speculation. The evidence for feather evolution is
>excellent. The evidence for what selective regime made any given
>mutation in the pathway adaptive, not so much.
Sure it’s speculation. Now the number of genetic difference between
humans and chimpanzees is a measured value. Tell us how 67 mutations
per generations can be fixed.
>>>>>> It requires the
>>>>>> transformation of nine or more genes.
>>>>> What is your evidence that this cannot be done sequentially or
>>>>> concomitantly (in different parts of the same population and
>>>>> subsequently being joined by sexual processes) but must instead occur
>>>>> simultaneously in the same individual (which is the requirement you
>>>>> impose in the HIV case)? Be specific.
>>>> It is your job to prove your theory.
>>> No, it's your job to prove it can't be done, since that is your claim.
>>> The theory that reptiles (certain theropods, actually) evolved into
>>> birds is well supported by fossil evidence, and the theory that birds
>>> are archosaurs is well supported by molecular evidence as well. It seems
>>> to me that good evidence that something happened is also good evidence
>>> that it isn't impossible. Would you agree?
>> I have proved it but you evolutionists disregard the evidence.
>Apparently you disagree. I'd be interested in your reasoning, if any,
>for rejecting my claim above.
John, if you remember nothing else from this discussion, the
multiplication rule of probabilities is the dominant mathematical
principle of the mutation and selection phenomenon. No other variable
in this process has the profound mathematical effect as the
multiplication rule of probabilities.
>>>> If you believe there are targeted
>>>> selection pressures that would act on the genes in reptiles to
>>>> transform these genes from scale producers to feather producers
>>>> sequentially, go for it. Even for the sake of argument I could accept
>>>> such an outrageous speculation and you still wouldn’t have enough
>>>> generations to make such a transformation.
>>> Please present the math that shows you correct here.
>> I have, it’s called the multiplication rule of probabilities.
>You call that math? No, you would then have to show that the
>multiplication rule applies here. What conditions would make such a rule
>applicable? The obvious case under which the rule would apply is if all
>the mutations would have to happen at once, or at least that none of
>them would be advantageous unless all were present.
>Can you specify some other condition in which the rule would apply, and
>give an argument for why it should?
The multiplication rule applies whether the beneficial mutations have
to occur simultaneously or not. What selection does is that it allows
amplification of a beneficial allele so that one of the descendents of
the recipient of the first beneficial mutation can then get the next
beneficial mutation in the sequence. If the amplification process does
not occur, you don’t have the benefit of increased frequency of the
beneficial allele (and number of members with that beneficial allele)
and the number of generations to get that next beneficial mutation.
This is why the mutation and selection process is so slow and when it
does work the process can be easily disrupted when the population has
to amplify two or more beneficial alleles simultaneously to multiple
selection pressures. These combination pressures interfere with the
amplification process. This is what is demonstrated with the evolution
of HIV to combination selection pressures and the numerous other
empirical examples I have posted.
>> This
>> mathematics is well demonstrated by Thomas Schneider’s ev computer
>> algorithm of mutation and selection. The fundamental unit process of
>> evolution is the substitution of one allele for another. This process
>> is slow and arduous taking hundreds if not thousands of generations
>> per allele as demonstrated by Haldane’s mathematics and Lenski’s
>> empirical example. If you think a population of reptiles is going to
>> evolve feathers over millions of generations in order to adapt to a
>> cold climate rather than the population simply evolving thicker
>> scales, make your argument. Perhaps you don’t believe that thicker
>> scales would give better insulation?
>Only marginally. You apparently don't know much about the insulative
>properties of various integuments.
The mutation and selection phenomenon is a very slow way of adapting
to any selection pressure. This process requires consistent
application of the selection pressure for long periods of time without
driving the population to extinction. Imagining a thermal stress on a
population of reptiles without the population suffering the effects of
starvation, dehydration, predation, disease or any of a number of
other selection pressures acting on the population in a real
environment is not very realistic. Have you ever seen what thermal
stress does to range animals? If the population has to evolve to
multiple selection pressures simultaneously, the process becomes much,
much slower. The multiplication rule of probabilities will always
dominate this phenomenon.
>>>> This is why you have to
>>>> manufacture the concept of HARs to account for the huge number of
>>>> genetic differences between the different life forms.
>>> HARs aren't manufactured; they're observed. You may claim if you like
>>> that they couldn't have been produced by selection. But you would need
>>> to present some evidence for that. And there are actually quite few
>>> genetic differences between humans and chimps, a mere 40 million.
>> Evolutionists assume that humans and chimps came from a common
>> ancestor so you take these massive differences and call them HARs. Why
>> don’t you explain to us how these HARs work and arise?
>How they arise is pretty simple: through mutation and selection. What's
>causing the selection is a bit more difficult, but I'm sure there are
>people investigating the functions of these genes right now. And no, we
>don't assume common ancestry. We conclude that on the basis of
>overwhelming evidence.
Well John, by your own numbers, this transformation would require the
fixation of 67 mutations per generation. I would call that an
overwhelming number.
>> And let’s hear how you do your accounting for your claimed 40 million
>> differences between humans and chimpanzees if they came from common
>> ancestors 10 million years ago.
>6 million, actually. But remember the mutations are happening
>simultaneously in two lineages, so that would be around 12 million years
>of total time.
Fine, account for the fixation of 33 mutations per generations,
account for the fixation of a single beneficial mutation per
generation when the mathematical and empirical evidence shows that it
takes hundreds of generations to fix a single beneficial mutation.
>> 10 million years at let’s say 10 years
>> per generation gives about a million generations to perform the
>> transformation. That’s about 40 mutations being substituted per
>> generation. How do you line this up with Lenski’s experiment where
>> only 1 mutation is being substituted about every 500 generations? I
>> guess Lenski’s biological model does not have any HARs.
>Simple: the mutation rate per generation is much higher in humans than
>in Lenski's bacteria (especially the original population without the
>hypermutation allele). And Lenski's bacteria have much smaller genomes
>than humans. The number of neutral substitutions per generation is a
>function of both these factors. If I recall, the number of mutations per
>generation is a couple of hundred; that is, you differ from both your
>parents by about 200 germline mutations. And so we would expect about
>200 substitutions in the human lineage per generation.
John, what a lovely swan dive you’ve made down your evolutionist
rabbit hole. You still don’t understand how the substitution process
works and the significance of the multiplication rule of probabilities
on the behavior of the mutation and selection phenomenon.
Lenski’s bacteria tested billions of mutations and only a miniscule
number were fixed in his population in 50,000 generations taking
hundreds of generations for each fixation. And you have already said
“It's very unlikely for any single neutral mutation to be fixed.” And
now you are claiming that all 200 germline mutations are going to be
successfully substituted in the human lineage every generation?
Stabilizing selection prevents the vast majority of these mutations
from ever being fixed in the population. John you are contradicting
yourself.
>>>>>> If an animal has to adapt to an
>>>>>> environment to maintain body temperature, by turning a scales into a
>>>>>> feathers is a profoundly inefficient way of doing this.
>>>>> Hair also will do the job of maintaining body temperature.
>>>> What if the dinosaur has male pattern baldness? The poor dinosaur
>>>> holds his half limb, half wing over his head to try to keep his head
>>>> warm. He inadvertently covers his eyes not realizing that a T Rex is
>>>> about to celebrate the first Thanksgiving turkey dinner.
>>> Your descent into facetiousness suggests you have nothing to offer here.
>> What a minute John, there are bald eagles too!
>Down and down. Let me know when you hit bottom.
John, you need to evolve a humor gene.
==================================================================
Chris Thompson
>> The carrying capacity of his experiment is the selection pressure.
>Oh, goodness. As someone who spent quite of lot of time studying
>fisheries and wildlife, where carrying capacity is paramount, this
>sentence...offends. You do not understand carrying capacity at all, do
>you?
Yes I do and here is what Lenski and his co-authors had to say in
“Historical contingency and the evolution of a key innovation in an
experimental population of Escherichia coli”
“These populations were initially identical except for a neutral
marker that distinguished six lines from six others. They have since
been propagated by daily 1:100 serial transfer in DM25, a minimal
medium containing 25 mg/liter glucose as the limiting resource (2,
22). Environmental conditions have been controlled, constant, and
identical for all 12 lines.”
Chris, glucose was the limiting factor as clearly documented.
Starvation was the selection pressure Lenski is using. His population
became more efficient users of glucose and in one case became citrate
metobolizers thereby increasing the carrying capacity of the
environment for those strains.
Since you have “spent quite of lot of time studying fisheries and
wildlife, where carrying capacity is paramount” you should recognize
the similarities between what you do and what Lenski does. In your
case, you try to reduce the selection pressure on your populations by
providing clean fresh water minimizing contaminants, maintain
appropriate temperatures, adequate space, sufficient and appropriate
nutrients, and maintain a disease free environment and so on. By
reducing these selection pressures you obtain a healthy diverse
population. If you don’t do these things, you pressure your population
and only those fit to reproduce in your less than optimal environment
will pass their genetic information to the next generation thereby
reducing the diversity of the population.
>> Lenski is starving his bacteria but leaving his population with an
>> out, ie citrate. You obviously have not read Lenski s paper on the
>> quantitative results of his study. Hersheyh, get a copy of this paper
>> Genome evolution and adaptation in a long-term experiment with
>> Escherichia coli , Vol 461, October 29, 2009, Nature. In the adaptive
>> phase of his study, none of the mutations in the experiment were due
>> to drift (a crappy word to describe what populations do on a plateau
>> of a fitness landscape). Only when the populations evolved to improved
>> fitness did neutral mutations appear in his populations. In other
>> words, his population is diversifying on a fitness plateau. Still,
>> this population is limited by the amount of citrate available.
>I am curious about something. If a mutation is neutral, how do you
>stop it?
Chris, you can’t stop any mutation from occurring. What you can do to
stifle the mutation and selection phenomenon is to force the
population to evolve against multiple selection pressures
simultaneously. This forces the population to have multiple beneficial
mutations simultaneously which by the multiplication rule of
probabilities is a much less likely event. In addition, the
amplification process is impaired when a population has to amplify
multiple beneficial mutations simultaneously. If you remember nothing
else from this discussion, remember that the multiplication rule of
probabilities is the dominant mathematical principle governing the
mutation and selection phenomenon.
>Those bacteria never stopped metabolizing glucose. They evolved the
>ability to metabolize citrate in addition to the standard glucose
>metabolic pathways. Can you read?
Of course I can read. Here’s what Lenski and his co-authors had to say
in “Historical contingency and the evolution of a key innovation in an
experimental population of Escherichia coli”
“Although the Cit+ cells continued to use glucose, they did not drive
the Cit- subpopulation extinct
because the Cit- cells were superior competitors for glucose.”
The citrate metabolizers paid a price to achieve that function, that
price was the reduced ability to metabolize glucose. This is not an
unusual principle for the mutation and selection phenomenon.
Resistance to selection pressures often times put those members of the
population at a disadvantage with respects to other members of the
population when those selection pressures are removed. This is seen in
the case of drug resistant strains of HIV. These strains are often not
as good replicators as “wild” strains of the virus in low selection
pressure environments.
>Here we have an indicator that Dr.Dr.Dr.Dr.K believes in a young
>earth. I am open to correction here. But let's suppose that some
>reptile needs 32000 generations to generate a feather. Let's give
>Dr.Dr.Dr.Dr.K the benefit of the doubt, and assume the reptile in
>question breeds every other year. That would mean it would take 64000
>years to evolve a feather. An eyeblink compared to the age of the
>planet. But no one thinks feathers evolved all at once. Dr.Dr.Dr.Dr.K
>is fond of saying 9 genes had to change to produce feathers. This
>might be true for all I know. Nine times 64000 is ummmm 576000 years.
>Is the planet that old, Dr.Dr.Dr.Dr.K?
It doesn’t matter what I think the age of the earth is. I’ll use your
numbers for the age of the earth to show that your theory of evolution
is a mathematically irrational belief system. John Harshman has
computed the number of fixations required in the transformation of
humans and chimpanzees from a common precursor. John computed a value
of 67 mutations fixed every generation. How can that be done? Chris,
if you learn nothing else from this discussion, the multiplication
rule of probabilities is the dominant mathematical principle governing
the mutation and selection phenomenon, time, population size, mutation
rates and every other variable you can imagine have only a small
impact on the mutation and selection phenomenon. This is why the
complexity of the selection conditions is the dominant variable in the
mutation and selection process.
>> And remember, Lenski maintained constant
>> selection conditions over these tens of thousands of generations. What
>> to think would happen if he introduced other random selection
>> conditions into his experiment like temperature variations,
>What would be the selection pressure on a reptile evolving feathers if
>the planet got....cold?
By your numbers, that population would have a long, long, long, long
wait before it could evolve feathers and warm up.
==================================================================
John Harshman
> John Harshman
Very confused attributions. This was Kleinman:
>> Just because you evolutionists don’t want to
>> discuss the basic science and mathematics of mutation and selection,
>> that I have to enter your world of irrational speculations. We now
>> have evolutionist expert Mark Isaak claiming that reducing the
>> intensity of selection accelerates the mutation and selection
>> phenomenon. This mathematical blunder ranks up there with the
>> evolutionist blunder that selection increases the diversity of
>> populations.
This was me:
> Bet he didn't actually say that. You aren't a very good reader. And
> of course selection can increase diversity under certain conditions,
> some of which have been explained to you.
This was Kleinman again:
> Well let’s see exactly what Mark said in context to a comment I made:
> Kleinman said:
>>> Again, you repeat an old speculation that evolutionists like to use.
>>> The intensity of selection has very specific mathematical effects on
>>> the mutation and selection process. That effect is to slow the process
>>> down. Reducing the intensity of selection is a two edged sword. On one
>>> hand, reducing the intensity of selection reduces the chances that the
>>> population will be driven to extinction. On the other hand, reducing
>>> the intensity of selection slows the mutation and selection phenomenon.
> Mark Isaak said in response:
>> It is obvious to anyone with a smattering of knowledge of population
>> genetics that you don't know what you're talking about. But it is also
>> apparent (if not so blatant) that you *think* you know what you are
>> talking about. I find that fascinating. It's like you are writing a
>> travel book about a place you have never so much as heard of before, but
>> are willing to swear to having lived there for years.
> I am claiming that reducing the intensity of selection slows the
> evolutionary process. Mark Isaak is claiming I don’t know what I’m
> talking about.
I believe that was a general appreciation, not directed specifically at
some particular set of words. And so I'm right. You aren't a very good
reader.
[snip random insults]
>>> Lenski is starving his bacteria but leaving his population with an
>>> out, ie citrate. You obviously have not read Lenski’s paper on the
>>> quantitative results of his study. Hersheyh, get a copy of this paper
>>> “Genome evolution and adaptation in a long-term experiment with
>>> Escherichia coli”, Vol 461, October 29, 2009, Nature. In the adaptive
>>> phase of his study, none of the mutations in the experiment were due
>>> to drift (a crappy word to describe what populations do on a plateau
>>> of a fitness landscape).
>> Another very odd thing to say. Of course mutations aren't due to drift.
>> Drift affects allele frequency, not mutation. And drift doesn't apply to
>> populations; it applies to alleles. Perhaps you meant to say that none
>> of the fixations were due to drift, which is true of the first 20,000
>> generations. Many of the fixations by generation 40,000 were due to
>> drift. The difference is that the mutation rate increased in the
>> interim, and the rate of fixation due to drift equals the mutation rate.
> All the mutations measured in the first 20,000 generations were found
> in all populations, they were adaptive, not neutral.
Not true. You have again confused mutation with fixation. In order to be
assayed, mutations must reach an appreciable frequency. Most mutations
will become extinct after the first generation. There were almost
certainly many neutral mutations, but none of them reached any
appreciable frequency.
> Only when his
> populations reached a fitness plateau did more variants start to
> appear. That is, his populations had adapted to the starvation
> conditions and reduced the selection pressure allowing more variants
> to appear after 20,000 generations. I question Lenski’s estimates for
> the mutation rates. If Lenski is extrapolating backwards from the
> number of mutations found in his populations, he could be getting
> inaccurate estimates of the mutation rates.
You really can't read. The increase in mutation rates is both observed
and has a genetic mechanism (whose frequency in the population can
itself be tracked). It's fascinating that you take from Lenski whatever
you think serves your purpose and reject what doesn't, without even
attempting to justify the distinction.
> However John, one of the many mathematical features of the mutation
> and selection phenomenon that you don’t understand is that the
> mutation rate has only a small effect on the behavior of the
> phenomenon.
We were talking about drift, not selection.
> Perhaps you want to claim that doubling the mutation rate
> doubles the probability that a beneficial mutation will appear at a
> particular locus?
It certainly doubles the expected number of such mutations.
> By far, the dominant mathematical principle of the
> mutation and selection phenomenon is the multiplication rule of
> probabilities. That is why the complexity of the selection conditions
> dominates the behavior of the phenomenon.
Please show your work here. What's your math?
> Regardless, Lenski’s population fixed only a very small number of
> mutations in more than 40,000 generations, only about 1 each 500
> generations. Now you have done the mathematics for the number of
> fixations required to transform humans and chimpanzees from a common
> precursor. Your estimate is 67 fixations per generation. How do you do
> that accounting problem?
I have explained this at least twice, and Howard has done so at least
once, and you have so far ignored all of them. Briefly, in neutral
evolution, fixation rate (in the population) equals mutation rate (in an
individual). By any reasonable estimate of rates and times, 67 fixations
per generation is well within expectation.
>>> Only when the populations evolved to improved
>>> fitness did “neutral” mutations appear in his populations. In other
>>> words, his population is diversifying on a fitness plateau. Still,
>>> this population is limited by the amount of citrate available.
>> You completely misunderstood his point. Which is not unexpected. There
>> was in fact no fitness plateau. Advantageous mutations appeared
>> throughout. What made the difference was the increase in mutation rate,
>> as Lenski himself made clear in that paper.
> The mutation rate has only a small effect on the mutation and
> selection phenomenon. If you understood the mathematics of the
> phenomenon, this would be clear to you. Do you think the mutation rate
> will account for 67 fixations per generation?
Yes. We aren't talking about selection here. We're talking about neutral
evolution. You seem entirely blind to this point, to the degree that one
might imagine some form of psychosis. You can't even see the words.
>>>> Now, if the glucose-only bacteria were more efficient at using glucose
>>>> than the bacteria that could use both, we have a condition that could
>>>> favor "specialization" to different niches, with some bacteria
>>>> becoming specialized glucose users and others becoming more and more
>>>> reliant on citrate. I.e., speciation (and because inability to use
>>>> citrate is a key speciation-defining feature of E. coli, the new bug
>>>> would not be E. coli, but perhaps E. citrusflavoreddietcoli.
>>> I guess you haven’t read any of Lenski’s papers. The citrate
>>> metobolizers no longer were efficient glucose metabolizers and these
>>> citrate metabolizers were very sensitive to osmotic pressures.
>> All adaptations are adaptive with respect to particular environments.
>> Don't you understand that yet?
> Give me a hint John; tell me how you can account for 67 fixations per
> generation? Just what were the adaptive conditions for that primate
> precursor?
Adaptation is irrelevant. It's neutral evolution. Only a very tiny
minority of the observed differences have any phenotypic effect or are
subject to selection.
>>> Now
>>> early on, you posted a paper that I wasted my time on reading. In this
>>> paper, these evolutionist pseudo-scientists claim that evolution is
>>> irreversible. Now do you think if you switched Lenski’s experiment and
>>> put his citrate metabolizers in a glucose rich environment with sparse
>>> citrate that his bacteria could evolve back to glucose metabolizers?
>> That's not what "irreversible" means. We would expect adaptation to any
>> environment, including a prior one. What we wouldn't expect is a
>> reversion to exactly the same phenotype as the ancestral one. The reason
>> is that there are many ways of achieving the same adaptive result.
> Why not? So why would you say that reptile scales would turn into
> feathers when there are many ways to achieve the same adaptive result?
Because that's one of the ways, and it happens to be the one that arose.
I'm unable to penetrate the bizarre thought processes behind that question.
> Seems like a very difficult way for a reptile population to stay warm
> when there are many other ways to accomplish the same result without
> taking huge number of generations. The reptiles that live near my home
> hibernate when the weather gets cold. They are not growing feathers.
The reptiles that live near your home aren't endotherms, and aren't
evolving endothermy. Insulation is pointless in an ectotherm.
>> You haven't explained why that would be. Could you? And you might also
>> explain where you think birds came from, if they didn't evolve from
>> terrestrial reptiles.
> It’s not my job here to tell you where birds came from. It’s my job to
> properly describe how the mutation and selection phenomenon works. Do
> you want to tell us how to account for 67 fixations per generation?
It's not your job to take any position or defend your prior statements.
It's not your job to show any sort of intellectual integrity. But it
apparently is your job to ignore prior answers and repeat questions that
have been answered over and over.
>>> Even if you could describe the selection pressures that would
>>> transform a reptile scale into a feather, sequentially it would take a
>>> vast number of generations.
>> How many? Show your work. By the way, you have been told many times that
>> feathers evolved long before birds. Try to correct these simple errors.
> Edward Max already gave us a citation which states that at least nine
> genes would have to be transformed. If only one base substitution were
> required for each gene, and the sequential selection pressures
> existed, it would require around 300-500 generations per substitution.
> That would give a bottom limit to the number of generations of
> 2700-4500 generations in the simplest case.
So, a vanishingly short time in evolutionary terms: a few thousand
years. What, therefore, is the problem?
> This number would rapidly
> go up if the number of base substitutions was greater and the number
> would become huge if any of the beneficial mutation would have to
> occur simultaneously. But this is all speculation. We know what the
> genetic sequences are for humans and chimpanzees. How do you account
> for 67 fixations per geneneration?
I believe you are now acquainted with the answer, so will not repeat it.
>>> And remember, Lenski maintained constant
>>> selection conditions over these tens of thousands of generations. What
>>> to think would happen if he introduced other random selection
>>> conditions into his experiment like temperature variations,
>>> dehydration, predation, disease, do you think that would accelerate
>>> the evolution of citrate metabolizers?
>> No. So?
> Any real “natural” environment would superimpose thermal stress,
> starvation, predation, disease, dehydration and any other stress you
> could imagine on your reptile population. Do you think your reptile
> population was only subjected to thermal stress while it was evolving
> scales into feathers? I don’t think so.
I have no idea what you think your point is here. I agree that
starvation would not accelerate the evolution of flight. But what point
could there possibly be?
>>> Real environments do this to
>>> populations. Real environments don’t maintain constant selection
>>> conditions for long periods of time. This is why your theory of
>>> evolution is mathematically irrational.
>> Why? Real environments do indeed maintain constant selection conditions
>> for many factors. Constancy with respect to one feature doesn't require
>> constancy with respect to all. And one adaptation can produce conditions
>> in which the next becomes adaptive.
> Challenging populations with a wide variety of selection conditions
> which are always changing puts huge stress on the population. This is
> why so many species have gone extinct. So what is that adaptive
> environment that will fix 67 mutations per generation? Let’s try to
> bring your evolutionist speculations back to reality.
Adaptation has nothing to do with those 67 fixations. And most species
do not become extinct over the short term, so your imagination of this
constant holocaust is just silly.
>>> Look what happens when self-deception is institutionalized in
>>> evolutionism. We end up with a totally irrational misinterpretation of
>>> the mutation and selection phenomenon and millions of people are
>>> harmed by this irrational misinterpretation of mutation and selection
>>> phenomenon.
>> You really can't bring yourself to say "selection", can you? It always
>> has to be "the mutation and selection phenomenon". Can anyone explain
>> the psychology of such a twitch? A lot of creationists seem similarly
>> inflexible, repeating the same phrases, even whole paragraphs, even when
>> pointless.
> Mutation and selection is the cycle of evolution. Mutation is the
> source of diversity and selection is the source of order. This cycle
> has a particular mathematical behavior that if you understand it can
> use the principles by which it works to more effectively treat
> diseases subject to this phenomenon. Evolutionists on the other hand
> are obsessed with the concept that the mutation and selection
> phenomenon can transform reptiles into birds and humans and
> chimpanzees from a common precursor. Only this evolutionist obsession
> can not account for 67 mutations fixed every generation and does not
> recognize how combination therapy interferes with the evolution of
> drug resistance. We have libraries full of this evolutionist
> irrationality.
Your new obsession with "67 mutations" seems similarly pointless,
especially when you have consistently ignored every explanation.
>>> Do the math hersheyh, even with a viral load of 50/ml, you have a
>>> population that is at least in the hundreds of thousands. There is
>>> still replication of the virus even with effective three drug therapy.
>>> If there wasn’t replication, RNAases would quickly clear the blood of
>>> any viruses. I would be very surprised that in this replication
>>> process that there were not mutations that would give benefit to one
>>> drug or another.
>> But does that increase their rate of replication in the presence of the
>> other drugs? That's the question. If it doesn't, the mutation is
>> neutral. If it does, it should increase in frequency. Multi-drug therapy
>> works because it prevents resistance to a single drug from offering a
>> selective advantage.
> Of course combination therapy (in every circumstance which it is
> tried) prevents an otherwise beneficial mutation from giving selective
> advantage.
That means, by all reasonable definitions, that it isn't beneficial. You
are indeed talking about a system in which multiple simultaneous
mutations are necessary in order to confer benefit. This is indeed the
situation in which the multiplication rule applies. But it's the sole
situation. Your attempt to generalize this to all evolution is
unsupported by any argument.
> That is why the example of the evolution of HIV to
> combination therapy is not a special example of mutation and
> selection, it is only a highly studied example of mutation and
> selection.
Non sequitur.
> Any time selection pressures target more than a single
> gene, a mutation beneficial to one or another selection pressure fails
> to give significant selective advantage, the other selection pressures
> continue to impair the reproduction of that member.
Not true at all. First, let me remind you that you freely switch back
and forth between targeting multiple genes and multiple traits, as if
they were the same thing. But most genes, at least in multicellular
organisms, influence multiple traits, and most traits are influenced by
multiple genes. You can't equate the two at all.
Second, you have given no argument and provided no math that lets you
equate a situation in which no single mutation is beneficial with a more
typical situation in which mutations are independently beneficial.
> That is why
> combination therapy is successful. Not only does combination therapy
> make use of the multiplication rule of probabilities which markedly
> reduces the probability of simultaneous beneficial mutations, the
> multiple selection pressures impair the amplification process so that
> if a beneficial mutation does occur, it doesn’t get amplified.
That would be true only if the beneficial mutation were not in fact
beneficial in the multi-pressure environment. Let's at least use the
common scientific meanings of words.
> John
> give us a single citation of a real, measurable and repeatable example
> of mutation and selection where selection conditions target more than
> a single gene and the amplification process is not impaired. Only in
> your speculative mind does this event occur.
I repeat that any quantitative character shows this. For any phenotypic
character that's influenced by multiple genes, selection can operate on
all those genes at once to influence the character. If selection acts to
increase height, then height-increasing alleles at many loci will
increase in frequency.
>>> The problem for the population is amplifying these
>>> variants so that there would be a reasonable probability that another
>>> beneficial mutation for another drug would occur on one of these
>>> variants. But if these are neutral mutations, shouldn’t they be fixed
>>> in the population according to your drift theory?
>> You really have no comprehension here. It's very unlikely for any single
>> neutral mutation to be fixed. In fact, in your viral population, the
>> initial probability is 1/N, where N is the population size. However,
>> lots of mutations happen in the population, and the expected number of
>> neutral mutations fixed in any generation is equal to the rate of
>> neutral mutation. Most mutations just go extinct immediately. Some rise
>> to a detectable frequency. And a few become fixed.
> John, of course I comprehend that neutral mutations don’t get fixed in
> populations. Without selection, the mutation and selection phenomenon
> turns into the concept of abiogenesis.
What?
> I hope you can imagine why the
> multiplication rule of probabilities makes the concept of abiogenesis
> irrational.
No, I can't. Unless you are advancing the "tornado in a junkyard" argument.
> I can understand why you find it more difficult to
> comprehend why the multiplication rule of probabilities makes the
> theory of evolution a mathematically irrational belief system because
> in that concept, you have selection operating. Perhaps now you are
> starting to understand the limits of selection. After all,
> understanding how selection works is the key to understanding how to
> prevent drug resistant microbes, herbicide resistant weeds, designing
> more durable cancer treatments and so on.
I really don't know why I bother. You don't read, you just respond to
anything with your prefabricated mantra.
>>> So, do you think a thicker scale would not provide better insulation?
>> Than what? Than a thinner scale? Yes, marginally. Than a covering of
>> hair or feathers? No. Hint: it's trapped air that provides the best
>> insulation.
> So the population would wait tens of thousands of years to warm up
> simply to produce feathers? The population could easily migrate to a
> warmer climate and do that in a far shorter time.
You have no idea how selection works. Nobody is waiting for anything to
happen. Alleles that offer selective advantages increase in frequency in
the population. That's all. Nor does any population decide to migrate in
order to keep warm. Nor did feathers arise as a response to thermal
stress in some cold-blooded reptile.
>>> But instead the reptile population would evolve feathers instead?
>> That is clearly what happened. We may never know why, but knowing what
>> is comparatively easy.
> John let’s set your speculations aside for the moment and tell us how
> 67 mutations per generations can be fixed in the evolution of humans
> and chimpanzees from a common precursor?
Asked and answered, many times.
>>> As
>>> hersheyh likes to point out, selection always acts on the traits of a
>>> population that already exists. Why wouldn’t a cooling of the climate
>>> select for thicker scaled reptiles rather that the transformation of
>>> numerous genes that takes who knows how many thousands of generations?
>>> Of course from your point of view, only evolutionist speculations are
>>> the only thing relevant to the mutation and selection phenomenon.
>> This is not speculation. The evidence for feather evolution is
>> excellent. The evidence for what selective regime made any given
>> mutation in the pathway adaptive, not so much.
> Sure it’s speculation. Now the number of genetic difference between
> humans and chimpanzees is a measured value. Tell us how 67 mutations
> per generations can be fixed.
Ommmmm.
>>>>>>> It requires the
>>>>>>> transformation of nine or more genes.
>>>>>> What is your evidence that this cannot be done sequentially or
>>>>>> concomitantly (in different parts of the same population and
>>>>>> subsequently being joined by sexual processes) but must instead occur
>>>>>> simultaneously in the same individual (which is the requirement you
>>>>>> impose in the HIV case)? Be specific.
>>>>> It is your job to prove your theory.
>>>> No, it's your job to prove it can't be done, since that is your claim.
>>>> The theory that reptiles (certain theropods, actually) evolved into
>>>> birds is well supported by fossil evidence, and the theory that birds
>>>> are archosaurs is well supported by molecular evidence as well. It seems
>>>> to me that good evidence that something happened is also good evidence
>>>> that it isn't impossible. Would you agree?
>>> I have proved it but you evolutionists disregard the evidence.
>> Apparently you disagree. I'd be interested in your reasoning, if any,
>> for rejecting my claim above.
> John, if you remember nothing else from this discussion, the
> multiplication rule of probabilities is the dominant mathematical
> principle of the mutation and selection phenomenon. No other variable
> in this process has the profound mathematical effect as the
> multiplication rule of probabilities.
So you say. But you have never offered any sort of argument or
mathematical treatment showing that to be true.
No, I asked for an argument, not just a repetition of prior assertions.
>>> This
>>> mathematics is well demonstrated by Thomas Schneider’s ev computer
>>> algorithm of mutation and selection. The fundamental unit process of
>>> evolution is the substitution of one allele for another. This process
>>> is slow and arduous taking hundreds if not thousands of generations
>>> per allele as demonstrated by Haldane’s mathematics and Lenski’s
>>> empirical example. If you think a population of reptiles is going to
>>> evolve feathers over millions of generations in order to adapt to a
>>> cold climate rather than the population simply evolving thicker
>>> scales, make your argument. Perhaps you don’t believe that thicker
>>> scales would give better insulation?
>> Only marginally. You apparently don't know much about the insulative
>> properties of various integuments.
I see you have abandoned the bit about scales, perhaps realizing that
you know nothing about insulation.
> The mutation and selection phenomenon is a very slow way of adapting
> to any selection pressure. This process requires consistent
> application of the selection pressure for long periods of time without
> driving the population to extinction. Imagining a thermal stress on a
> population of reptiles without the population suffering the effects of
> starvation, dehydration, predation, disease or any of a number of
> other selection pressures acting on the population in a real
> environment is not very realistic. Have you ever seen what thermal
> stress does to range animals? If the population has to evolve to
> multiple selection pressures simultaneously, the process becomes much,
> much slower. The multiplication rule of probabilities will always
> dominate this phenomenon.
I grow tired of argument by naked assertion. Do you have anything else?
>>>>> This is why you have to
>>>>> manufacture the concept of HARs to account for the huge number of
>>>>> genetic differences between the different life forms.
>>>> HARs aren't manufactured; they're observed. You may claim if you like
>>>> that they couldn't have been produced by selection. But you would need
>>>> to present some evidence for that. And there are actually quite few
>>>> genetic differences between humans and chimps, a mere 40 million.
>>> Evolutionists assume that humans and chimps came from a common
>>> ancestor so you take these massive differences and call them HARs. Why
>>> don’t you explain to us how these HARs work and arise?
>> How they arise is pretty simple: through mutation and selection. What's
>> causing the selection is a bit more difficult, but I'm sure there are
>> people investigating the functions of these genes right now. And no, we
>> don't assume common ancestry. We conclude that on the basis of
>> overwhelming evidence.
> Well John, by your own numbers, this transformation would require the
> fixation of 67 mutations per generation. I would call that an
> overwhelming number.
Only because you don't have the slightest understanding of neutral
evolution. Once more: HARS arise through mutation and selection, but
there are very few of them; the great bulk of differences (the ones
requiring those 67 fixations/generation) are not HARS, are not under
selection at all, and evolved neutrally.
>>> And let’s hear how you do your accounting for your claimed 40 million
>>> differences between humans and chimpanzees if they came from common
>>> ancestors 10 million years ago.
>> 6 million, actually. But remember the mutations are happening
>> simultaneously in two lineages, so that would be around 12 million years
>> of total time.
> Fine, account for the fixation of 33 mutations per generations,
> account for the fixation of a single beneficial mutation per
> generation when the mathematical and empirical evidence shows that it
> takes hundreds of generations to fix a single beneficial mutation.
Nobody is claiming that any of the fixations in a typical generation are
beneficial. Unwillingness to even think about neutral evolution
completely cripples your ability to understand any of this.
>>> 10 million years at let’s say 10 years
>>> per generation gives about a million generations to perform the
>>> transformation. That’s about 40 mutations being substituted per
>>> generation. How do you line this up with Lenski’s experiment where
>>> only 1 mutation is being substituted about every 500 generations? I
>>> guess Lenski’s biological model does not have any HARs.
>> Simple: the mutation rate per generation is much higher in humans than
>> in Lenski's bacteria (especially the original population without the
>> hypermutation allele). And Lenski's bacteria have much smaller genomes
>> than humans. The number of neutral substitutions per generation is a
>> function of both these factors. If I recall, the number of mutations per
>> generation is a couple of hundred; that is, you differ from both your
>> parents by about 200 germline mutations. And so we would expect about
>> 200 substitutions in the human lineage per generation.
> John, what a lovely swan dive you’ve made down your evolutionist
> rabbit hole. You still don’t understand how the substitution process
> works and the significance of the multiplication rule of probabilities
> on the behavior of the mutation and selection phenomenon.
>
> Lenski’s bacteria tested billions of mutations and only a miniscule
> number were fixed in his population in 50,000 generations taking
> hundreds of generations for each fixation. And you have already said
> “It's very unlikely for any single neutral mutation to be fixed.” And
> now you are claiming that all 200 germline mutations are going to be
> successfully substituted in the human lineage every generation?
You understand that the 200 mutations mentioned there are per
individual, right? And that the 200 substitutions per generation are in
the entire population, right? If there are 200 mutations per individual,
then there are 200N in the population. If each one has a 1/N chance of
being fixed, then there are 200 fixations per generation. This is really
very simple math. I'm surprised that a double doctor such as yourself is
incapable of getting it.
> Stabilizing selection prevents the vast majority of these mutations
> from ever being fixed in the population. John you are contradicting
> yourself.
Stabilizing selection has no effect on neutral variation. Do you have
any clue what you are saying?
>>>>>>> If an animal has to adapt to an
>>>>>>> environment to maintain body temperature, by turning a scales into a
>>>>>>> feathers is a profoundly inefficient way of doing this.
>>>>>> Hair also will do the job of maintaining body temperature.
>>>>> What if the dinosaur has male pattern baldness? The poor dinosaur
>>>>> holds his half limb, half wing over his head to try to keep his head
>>>>> warm. He inadvertently covers his eyes not realizing that a T Rex is
>>>>> about to celebrate the first Thanksgiving turkey dinner.
>>>> Your descent into facetiousness suggests you have nothing to offer here.
>>> What a minute John, there are bald eagles too!
>> Down and down. Let me know when you hit bottom.
> John, you need to evolve a humor gene.
I'll only need one when you say something funny.
Stuart
<snip>
If you understood the mathematics of the
> > phenomenon, this would be clear to you. Do you think the mutation rate
> > will account for 67 fixations per generation?
>
> Yes. We aren't talking about selection here. We're talking about neutral
> evolution. You seem entirely blind to this point, to the degree that one
> might imagine some form of psychosis. You can't even see the words.
>
Kleinman offers one of the most clear examples of Morton's Deamon
I have ever seen. Its like having an argument with a windup doll.
Stuart
Garamond Lethe
> On Mar 15, 4:59 pm, Bill <brogers31...@gmail.com> wrote:
>> On Mar 16, 6:51 am, Alan Kleinman MD PhD <klein...@sti.net> wrote:
>>
>> Sorry for top posting, I'd just suggest that all the responses to
>> Dr.Dr.Dr. AK go into this thread. At least for those of us stuck with
>> Google Groups, once you hit 1000 posts the thread fragments. It's
>> entertaining and it would be nice to have it all in one place.
> Thanks Bill for continuing the thread. I’m going to have to patch
> together some of my responses for a while. I know it upsets the posters
> when I combine responses but unless you have a better suggestion, that’s
> what I’m going to do so that the discussion doesn’t fragment further.
Better suggestions:
1. Don't combine replies.
2. Post some math already.
3. Post the equations for at least the Moran and Wright-Fisher models,
so we know that you've at least looked at them.
4. Post the equations that would allow you to take frequency-dependent
selection and stabilizing selection into account.
5. Post the equations that describe what you think is correct.
6. Find an appropriate genetic dataset or simulation.
7. Post the error for your approach and for existing models (and show
your work).
8. Don't bother replying until you've done this. You've cemented your
reputation as "The guy who don't understand high-school probability".
Continuing to make math-free replies isn't going to make that any better
or worse.
9. No, really. Post some math already.
<snip>
Alan Kleinman MD PhD
> On Tue, 15 Mar 2011 16:59:52 -0700 (PDT), Bill
>
I think you are a bit confused here. I’ve only posted on this thread.
This discussion is centered on the mathematics of mutation and
selection, not on word usage. Evolutionists have abandoned mathematics
and embraced semantics as a means of substantiating the mathematically
irrational theory of evolution. Or has the “multiplication rule of
probabilities” become nothing more than a phrase that evolutionists
can counter semantically? “Population size”, “mutation rate”, “time
(number of generations)”, those are the semantic terms evolutionists
try to counter the “multiplication rule of probabilities” but all
these terms have specific mathematical behavior and none have the
mathematical weight to counter the dominant mathematical principle of
the mutation and selection phenomenon.
Alan Kleinman MD PhD
> On 3/15/2011 9:27 PM, William Hughes wrote:
>
>
>
>
>
> > It is rather interesting that in a> 1000 post thread
> > the good Dr. has been unable to note that he is confusing two
> > scenarios
>
> > 1: A mutation A' causes an increase in reproductive
> > success, whether or not a mutation B' (which also
> > causes an increase in reproductive success) is present.
>
> >2: A mutation A' alone or a mutation B' alone does not cause an
> > increase
> > in reproductive success. Only both mutations together cause
> > an increase in reproductive success.
>
>
> > - William Hughes
>
> Regarding2: is it accepted by scientists that all mutations are
> independent of each other in incidence?
>
>
> - Show quoted text -
Hi Mitchell, welcome to the discussion. For all practical purposes,
random mutations are essentially independent. The accumulation of
beneficial mutations depends on common descent. Lateral transmission
of beneficial mutations is a relatively rare event as demonstrated by
the failure of recombination of HIV from accelerating the mutation and
selection phenomenon. This is why the multiplication rule of
probabilities dominates the mutation and selection phenomenon.
Alan Kleinman MD PhD
> of using Google Groups. ISTM illustrating that point is one of the
>
> - Show quoted text -
I chose this Group because Edward Max, supervising medical doctor of
the Food and Drug Administration published an essay on this site
making irrational misrepresentations of how the mutation and selection
phenomenon works. With leadership like his, no wonder we live in a
world filled with multidrug resistant microbes. If Thomas Schneider of
the National Cancer Institute allowed me to post on his site, I would
tell him that his claim “The multiplication rule does not apply to
biological evolution” is a completely irrational claim and that in
fact, the multiplication rule is the central governing principle of
the mutation and selection phenomenon. Evolutionists have completely
bungled the basic science and mathematics of the mutation and
selection phenomenon and we have the multidrug resistant microbes and
less effective cancer treatments to show for it.
Alan Kleinman MD PhD
> It is rather interesting that in a > 1000 post thread
> the good Dr. has been unable to note that he is confusing two
> scenarios
>
> 1: A mutation A' causes an increase in reproductive
> success, whether or not a mutation B' (which also
> causes an increase in reproductive success) is present.
>
> 2: A mutation A' alone or a mutation B' alone does not cause an
> increase
> in reproductive success. Only both mutations together cause
> an increase in reproductive success.
>
>
> - William Hughes
William, the multiplication rule of probabilities always applies when
more than a single beneficial random mutation is required to adapt to
selection pressures. This is why the complexity of the selection
conditions is the dominant mathematical variable in the mutation and
selection phenomenon. Any evolutionary process which requires more
than a single beneficial mutation requires amplification of beneficial
mutations in order to improve the probabilities that the next
beneficial mutation in the sequence occurs. This is why when the
mutation and selection phenomenon works, it is arduous and slow. Any
combination of selection conditions which disrupts the amplification
process only makes the phenomenon work even more slowly.
Alan Kleinman MD PhD
> Walter Bushell <pr...@panix.com> wrote:
> > j...@wilkins.id.au (John S. Wilkins) wrote:
>
> > > r norman <r_s_nor...@comcast.net> wrote:
>
> > > > On Tue, 15 Mar 2011 16:59:52 -0700 (PDT), Bill
> > > > <brogers31...@gmail.com> wrote:
>
> > > > >On Mar 16, 6:51 am, Alan Kleinman MD PhD <klein...@sti.net> wrote:
>
> > > > >Sorry for top posting, I'd just suggest that all the responses to
> > > > >Dr.Dr.Dr. AK go into this thread. At least for those of us stuck with
> > > > >Google Groups, once you hit 1000 posts the thread fragments. It's
> > > > >entertaining and it would be nice to have it all in one place.
>
> > > > I believe you, in a different thread, have been arguing against John
> > > > Wilkins about modifying traditional biological word usage just to
> > > > placate the creationists or at least to deny them the ability to twist
> > > > the meaning of the words to their purposes. Now you would have all
> > > > the rest of us modify traditional posting methods just to placate
> > > > those people who do not know how to use a real news reader and must
> > > > rely on Google Groups!
>
> > > Ouch! :-)
>
> > Anyway what's wrong with teleological language in science. We know that
> > people don't have teleological motivation because if they did
> > teleological phenomena would exist in nature.
>
> Teleological thinking is perfectly approriate when you are dealing with
> teleological systems, like humans and their societies/artifacts. There
> *is* teleology in the world. Every time I go to the shop to buy milk,
> such a system is in operation.
> --
> But al be that he was a philosophre,
>
> - Show quoted text -
Evolutionists impose teleology in their thinking. Evolutionists claim
that reptiles evolved feathers to keep warm. This is a mathematically
irrational over extrapolation of the mutation and selection phenomenon.
Alan Kleinman MD PhD
> In article <1jy8cz7.5lgtk71u0n0lcN%j...@wilkins.id.au>,
>
> - Show quoted text -
What’s wrong with understanding that selection pressures impose
“evolutionary direction” on populations and that forcing the
population to take two or more evolutionary directions impairs the
population from evolving?
Alan Kleinman MD PhD
> On Mar 16, 1:17 am, r norman <r_s_nor...@comcast.net> wrote:
>
>
>
>
>
> > On Tue, 15 Mar 2011 21:18:56 -0700 (PDT), jillery <69jpi...@gmail.com>
> > wrote:
>
> > >On Mar 15, 9:08 pm, r norman <r_s_nor...@comcast.net> wrote:
> > >> On Tue, 15 Mar 2011 16:59:52 -0700 (PDT), Bill
>
> > >> <brogers31...@gmail.com> wrote:
> > >> >On Mar 16, 6:51 am, Alan Kleinman MD PhD <klein...@sti.net> wrote:
>
> > >> >Sorry for top posting, I'd just suggest that all the responses to
> > >> >Dr.Dr.Dr. AK go into this thread. At least for those of us stuck with
> > >> >Google Groups, once you hit 1000 posts the thread fragments. It's
> > >> >entertaining and it would be nice to have it all in one place.
>
> > >> I believe you, in a different thread, have been arguing against John
> > >> Wilkins about modifying traditional biological word usage just to
> > >> placate the creationists or at least to deny them the ability to twist
> > >> the meaning of the words to their purposes. Now you would have all
> > >> the rest of us modify traditional posting methods just to placate
> > >> those people who do not know how to use a real news reader and must
> > >> rely on Google Groups!
>
> > >FWIW I rely on Google Groups not because I don't know how to use a
> > >real newsreader. In fact I have used many. I rely on Google Groups
> > >because it has the fastest propagation and the longest retention of
> > >anything in its price class, which is no additional cost.
>
> > >of using Google Groups. ISTM illustrating that point is one of the
> > >reasons for pepetuating this topic.
>
> > I wasn't really criticizing -- just tweaking a little and the tweak
> > took exactly as intended. I would like Google Groups totally banned
> > to be replaced by a really useful and decent web-based news reader.
> > However I also recognize the utility of Google Groups and have been
> > forced into using it in past times and, no doubt, will again in the
> > future. I always regret it, but it is necessary.
>
> .
>
> > That some threads go on for 1000 posts is the real problem that can be
> > solved by exercising some common sense.
>
>
> - Show quoted text -
If you are waiting on evolutionists to give you any common sense on
the basic science and mathematics of the mutation and selection
phenomenon, this thread will go into eternity.
Mitchell Coffey
I wasn't asking you, I was asking someone with experience in the
relevant field. That you are unfamiliar even with the relevant
statistical concepts is demonstrated by your failure to realize you
haven't even answered my question: "is it accepted by scientists that
all mutations are independent of each other in incidence?"
Your "multiplication rule" rants appear to ignore the concept of
independence in several ways.
Of course, what kind of fool cites his state certifications for medicine
and engineering as reasons for his superior authority on issues of
evolutionary biology over people who actually have with PhDs in subjects
directly involved in evolutionary biology?!
Mitchell Coffey
Inez
> On Mar 15, 6:27 pm, William Hughes <wpihug...@gmail.com> wrote:
>
>
>
>
>
> > It is rather interesting that in a > 1000 post thread
> > the good Dr. has been unable to note that he is confusing two
> > scenarios
>
> > 1: A mutation A' causes an increase in reproductive
> > success, whether or not a mutation B' (which also
> > causes an increase in reproductive success) is present.
>
> > 2: A mutation A' alone or a mutation B' alone does not cause an
> > increase
> > in reproductive success. Only both mutations together cause
> > an increase in reproductive success.
>
> > Only in case2is the multiplication rule for probabilities applicable
>
> > - William Hughes
>
> William, the multiplication rule of probabilities always applies when
> more than a single beneficial random mutation is required to adapt to
> selection pressures.
Only if each step does not confer it's own little advantage. You
haven't even made an attempt to show that RL evolution is not made up
of such steps.
And your phrase "required to adapt to" implies that you think that
most adaptations are life or death, and that there can't be various
levels of "adaptedness," which probably stems from your monomaniacal
example of HIV vs. antiviral drugs. Water rolls off a duck's back,
but a cormorant has to dry himself after fishing. Is a cormorant "not
adapted?" They seem to do OK for themselves, even if they are
perfect.
> This is why the complexity of the selection
> conditions is the dominant mathematical variable in the mutation and
> selection phenomenon. Any evolutionary process which requires more
> than a single beneficial mutation requires amplification of beneficial
> mutations in order to improve the probabilities that the next
> beneficial mutation in the sequence occurs. This is why when the
> mutation and selection phenomenon works, it is arduous and slow. Any
> combination of selection conditions which disrupts the amplification
> process only makes the phenomenon work even more slowly.-
hersheyh
> On Mar 17, 9:15 pm, j...@wilkins.id.au (John S. Wilkins) wrote:
>
>
>
>
>
> > Walter Bushell <pr...@panix.com> wrote:
> > > In article <1jy8cz7.5lgtk71u0n0lcN%j...@wilkins.id.au>,
> > > j...@wilkins.id.au (John S. Wilkins) wrote:
>
> > > > r norman <r_s_nor...@comcast.net> wrote:
>
> > > > > On Tue, 15 Mar 2011 16:59:52 -0700 (PDT), Bill
> > > > > <brogers31...@gmail.com> wrote:
>
> > > > > >On Mar 16, 6:51 am, Alan Kleinman MD PhD <klein...@sti.net> wrote:
>
>
> > > Anyway what's wrong with teleological language in science. We know that
> > > people don't have teleological motivation because if they did
> > > teleological phenomena would exist in nature.
>
> > Teleological thinking is perfectly approriate when you are dealing with
> > teleological systems, like humans and their societies/artifacts. There
> > *is* teleology in the world. Every time I go to the shop to buy milk,
> > such a system is in operation.
> > --
> > John S. Wilkins, Associate, Philosophy, University of Sydneyhttp://evolvingthoughts.net
> > But al be that he was a philosophre,
> > Yet hadde he but litel gold in cofre- Hide quoted text -
>
> > - Show quoted text -
>
> Evolutionists impose teleology in their thinking. Evolutionists claim
> that reptiles evolved feathers to keep warm.
It would be teleology to claim that feathers evolved with the end goal
of producing flight feathers. The claim that the initial feathers
functioned to preserve warmth rather than for the goal of flight is
based on observation of the types of feathers that formed early. IOW,
it is working from what actually exists to try to determine its
functionality based on structure and observation of similar features
in living organisms. It is not making a claim of an end goal.
Alan Kleinman MD PhD
being presented like this to prevent further fragmentation of the
discussion. These are responses to messages 951-975
========================================================
R Norman
> This guy who loves to lecture to us about the multiplication rule in
> probability clearly does not believe at all in probability.
> The probability of having a male vs. a female child is 50:50. I have
> two brothers but no sisters. I have two daughters but no sons.
> Obviously the reason why the sex ratio changed so drastically in
> either direction in two generations in my own family is because of
> survival of the fittest. Stochastic processes had absolutely nothing
> to do with it. So says the good doctor who knows about probability so
> he must be right.
The reason why I lecture you on the multiplication rule of
probabilities is that it is the central governing mathematical
principle of the mutation and selection phenomenon. There is a reason
why I don’t go to casinos. It is not gambling in casinos. If you play
long enough, you will leave all your money there.
And
> The good doctor here totally ignores my several posts where I
> patiently explain to him the medical genetics is a different subject
> from evolutionary biology. Medical genetics is taught to medical
> students by medical geneticists and the thrust of the subject is not
> mutation and selection or evolution or even irrational views of
> evolutionism.
R norman, I haven’t ignored you. I just disagree with you. My medical
school genetics text discusses mutation and selection but does an
incompetent job of describing the phenomenon. I think most physicians
would agree that infectious diseases comprise a much greater fraction
of primary care medical practices than do genetic diseases. I would be
surprised if any medical geneticist said he wasn’t an evolutionist.
> But then the good doctor has always ignored my criticisms, especially
> those cogent ones he finds impossible to answer: his flawed use of
> Newton-Raphson methods to find the zeros of non-linear equations, his
> absurd claim that selection cannot increase diversity, his ridiculous
> posturing about how his claim of failures in medical practice are laid
> directly at the feet of evolutionary biologists, .....
Why don’t you try to take away my PhD by saying my thesis was wrong
where I used the Newton-Raphson method to find the zeros of six
simultaneous non-linear equations. And then why don’t you post any
mathematical or empirical evidence which shows that selection
increases the diversity of populations. Selection always removes
members of the population from contributing to the gene pool, which
always decreases the diversity of the gene pool. Now I lay the
responsibility for the failure to properly teach the basic science and
mathematics of the mutation and selection phenomenon on those who
control the educational system. And who controls the field of biology?
========================================================
Mark Issak
> You are bearing false witness. I never claimed that.
That sounds like some kind of religious belief. We need to keep that
kind of stuff out of our public school.
And
>> The good doctor here totally ignores my several posts where I patiently
>> explain to him the medical genetics is a different subject from
>> evolutionary biology. Medical genetics is taught to medical students
>> by medical geneticists and the thrust of the subject is not mutation
>> and selection or evolution or even irrational views of evolutionism.
>> But then the good doctor has always ignored my criticisms . . .
> I suspect he simply does not remember them. I am becoming increasingly
> persuaded that he is suffering from organic brain damage that affects his
> ability to form long-term memories. This would explain his abysmal
> reading comprehension, his complete inability to learn, and probably a
> lot of his belligerence, as a lot of people get defensive rather than
> admit the problem is with themselves. I would be curious to talk with
> one of his colleagues who sees him regularly to find out what they have
> noticed.
That’s why I put it in writing Mark. So Mark, do you believe that
selection pressures increase or decrease the diversity of populations?
We already know that you believe that if you decrease the intensity of
selection that you accelerate selection process. That’s mathematically
irrational.
========================================================
Hersheyh
>Reducing the intensity of selection has no effect on mutation rates.
>Mutagens and prevailing mutagenic conditions (the sum of positive
>causation of mutations decreased by repair capacity) will determine
>the rate of mutation. If I mutate or chemically inactivate repair
>systems, net mutagenesis will increase. If I add mutagens, net
>mutagenesis will increase. If I change selective conditions, I will
>almost never increase or decrease mutation rate. [There are a few
>exceptions where a specific genetic change is a response to
>environmental conditions, such as excision of integrated lambda phage
>under stress conditions. It is possible to consider these as
>"domesticated" mutagenesis events.]
Hersheyh, you don’t read my posts very carefully. What I have said is
that reducing the intensity of selection slows the evolutionary
process. The reason that reducing the intensity of selection slows the
evolutionary process is that the intensity of selection affects the
rate of substitution of a more beneficial allele for a less beneficial
allele. And the unit process of evolution is the substitution of a
more beneficial allele for a less beneficial allele. You evolutionists
are very confused on how each of the variables in the mutation and
selection phenomenon affects the behavior of this process. By far, the
complexity of the selection conditions is the dominant variable in
mutation and selection phenomenon. The reason is because this variable
is governed by the multiplication rule of probabilities. No other
variable in the mutation and selection phenomenon has the mathematical
leverage of the multiplication rule. Hersheyh, if you learn nothing
else from this discussion, learn that the multiplication rule of
probabilities is the dominant governing mathematical principle for the
mutation and selection phenomenon.
>> By your
>> twisted evolutionist logic, if you reduce the intensity of selection
>> to zero, evolution happens instantly.
>No. If you reduce the intensity of selection (positive or negative),
>you approach selective neutrality. I have described *in detail* what
>happens under conditions of selective neutrality -- a post that
>actually includes some math.
There is no such thing as selective neutrality. It’s a figment of an
evolutionist’s imagination. You can have neutral mutations but they
are not selected for or against. And you in your detailed description
includes rolls of a die which gives zero values.
>What happens is that any selectively neutral allele will undergo a
>"drunkard's walk" wrt its frequency in the population, with a certain
>probability of fixation. If it is a brand new allele, its initial
>frequency is 1/N (or 1/2N, depending on whether N stands for alleles
>or diploid organisms). The probability that it will exist for even
>one generation is a function of how much the population size decreases
>between zygote formation and reproduction. Since we have already
>assumed that the allele is selectively neutral, if only 10% of the
>zygotes reach reproductive age (and remember that, net, each fly that
>lays several hundred eggs will, on average, have only two of those
>eggs reach the egg-laying stage, so a 90% drop is not unusual -- in
>fact, it is probably not much different than what occurs in many
>mammals), then there is a 90% probability that that new allele will be
>lost that first generation.
Hersheyh, tell us, will a neutral allele increase in frequency by a
“drunkard’s walk” more quickly than a beneficial allele subject to
selection?
>But, let's say that the alternate selectively neutral allele already
>represents 30% of the allele population. Then, in the next
>generation, the Hardy-Weinberg idealized equilibrium would predict
>that the frequency of that allele in the next generation would also be
>30%. But in *real* organisms, we would not actually expect that
>*determinant* result. We would expect a plus/minus range of
>frequency. If in the *real* world, due to chance alone, the next
>generation is 29% rather than 30%, this would not be surprising
> (depending on population size). Anymore than getting 46 heads out of
>100 tosses would be surprising, despite the expectation of 50. But
>because chance has no memory, the H-W expectation for the next
>generation is 29% and not 30%. This is why there is a "drunkard's
>walk". In the case of the allele at 30%, we would expect that allele
>to drunkenly wander to the 100% level (fixation) 30% of the time and
>wander to the 0% level (loss or extinction) 70% of the time.
>In short, the probability that a new allele, initially at frequency 1/
>N, will go to fixation is 1/N. The probability that it will go to
>extinction is (1-1/N). Most of the time, a selectively neutral new
>allele will drift to extinction and do so quickly. Occasionally, it
>will drift to fixation.
>Now, if you have some new math that tells us a different story, please
>discuss it here. It would be most amusing and, for actually
>presenting math relevant to the population genetics of selectively
>neutral traits on your part, a first.
My math is the old math. It is the mathematics which states that
selection is the only principle available to the mutation and
selection phenomenon that can overcome the multiplication rule of
probabilities. What selection gives is amplification of beneficial
alleles which improves the fitness of populations to survive and
reproduce against selection pressures. It is this mathematics which
explains how to deal with the evolution of drug resistance, improve
cancer treatments and why the theory of evolution is a mathematically
irrational belief system. This mathematics has been tested with time
and empirical evidence. Neutral mutations do not explain the
evolutionary process by mutation and selection.
And
>So you think that the scientific evidence for the age of the earth and
>life on the earth is mere "speculation"? I don't.
That’s because you don’t understand the mathematics of mutation and
selection. If you did, you would understand that the number of
generations has only a small affect on the mutation and selection
process when compared to the multiplication rule of probabilities has
on two beneficial mutations occurring. This is why it requires both
many generations and a large increase in the frequency of a beneficial
mutation before there is a reasonable probability that the second
beneficial mutation will occur on a member with the first beneficial
mutation. Time is a minor variable in the mutation and selection
process. It’s the number of beneficial mutations required to adapt to
a set of selection conditions which dominates the behavior of this
phenomenon.
>> Just because you evolutionists don’t want to
>> discuss the basic science and mathematics of mutation and selection,
>I most certainly have been discussing the basic science and
>mathematics of mutation and selection. It is you who are fixated on
>the idea that all evolution involves traits that must arise via
>simultaneous mutations in a single individual to have any selective
>benefit. I recognize that such conditions can be arranged (and HIV
>multi-drug resistance is a good example), but reject your basic
>assumption that that is the only mechanism that exists.
The multiplication rule of probabilities governs the mutation and
selection phenomenon whether the mutations must occur simultaneously
or not. If an evolutionary process requires two simultaneously
mutations, then the evolutionary process is slowed even more. HIV is
not a special case of mutation and selection. In fact, it has every
variable in the process working in its favor. It has large
populations, high mutation rates, does recombination allowing for
lateral transfer of genetic material, short generation times and can
not be driven to extinction. Any time selection conditions target more
than a single gene, the mutation and selection phenomenon will be
stifled for the same reason the process is stifled when using
combination therapy for HIV.
>> that I have to enter your world of irrational speculations. We now
>> have evolutionist expert Mark Isaak claiming that reducing the
>> intensity of selection accelerates the mutation and selection
>> phenomenon. This mathematical blunder ranks up there with the
>> evolutionist blunder that selection increases the diversity of
>> populations.
>Selection *can* increase the diversity of populations (negative
>frequency dependent selection) measured as the number of alleles
>existing in a population at greater than, say, 1% frequency. That
>doesn't mean that it always does so and no one has claimed that. But
>you have not defined what you mean by "diversity" of populations and
>how you measure such diversity. A large population, say, of English
>sparrows, shows diversity in size and shape, with northern populations
>being stouter than southern populations. African populations of
>humans show diversity in some external features from human populations
>in northern Asia (as well as differences in blood types). Some
>species, unlike humans, even have subspecies in different localities
>that are distinctly different (say like the Bengal and Sumatran
>subspecies of tiger). But I don't know how you are defining
>"diversity" in a species. Until you tell us what you mean by
>"diversity", it is hard to argue the point.
What I mean by diversity is the number of genetic variants in a
population. Selection always reduces the number of genetic variants in
a population. The way to increase the diversity of a population is to
reduce the selection pressure on the population so that less fit
variants can still reproduce and pass their genetic information to the
next generation.
And
>When have I ever said differently? I agree that *when* there is no
>selective advantage to having only one mutation and there is *only* a
>selective advantage to an individual having two *simultaneous*
>mutations that the multiplication rule holds.
This is where you make a mathematical blunder; the multiplication rule
always applies whether the mutations occur simultaneously or not. The
way populations overcome the multiplication rule is by amplification
of a beneficial allele and by large numbers of generations working to
get that next beneficial mutation. Remember that population size and
the number of generations has less than an additive affect on the
probability of the next beneficial mutation occurring at the proper
locus.
>> But natural selections are
>> much more cooperative in your Twilight Zone world. They only target
>> one gene at a time and they occur sequentially in a very ordered
>> manner, kind of like sequential antimicrobial therapy which has given
>> us multidrug resistant microbes. I guess we can call that the natural
>> way of using antibiotics. That s good sound evolutionist training at
>> work.
>And, in fact, in nature, it is pretty unusual for a virus to be
>exposed to two antivirals at once. And, as you point out, *when*
>conditions expose the virus to one antiviral at a time, such that
>there is a selective advantage to each step, we get both steps
>occurring much faster than would be the case when conditions require
>an individual to have both mutations simultaneously.
But it is not unusual for the environment to cause thermal stress and
starvation on a population simultaneously, or disease, or dehydration,
or predation, or…
And
>Carrying capacity is not selection pressure.
It absolutely is a selection pressure. Once a population has reached a
size that the environment can no longer support an increasing
population, then the most fit members (efficient energy users) will
soon dominate the population.
>> Lenski is starving his bacteria but leaving his population with an
>> out, ie citrate.
>No more than humans are starving because we cannot use cellulose.
>Citrate is simply a niche that E. coli cannot utilize. There will
>certainly be "selective competition" within the E.coli population
>whether or not it contains any variant that can utilize citrate.
And Lenski’s E coli did two things. Most of his bacteria became more
efficient users of the glucose but one of his populations was able to
evolve a way to metabolize the citrate and increase the carrying
capacity of the environment. But even then, the most efficient
metabolizers of the citrate will come to dominate the citrate
environment as they reach the limits of their new carrying capacity in
their environment.
Of course, humans do use cellulose. We use it indirectly through
bacteria which can catabolize cellulose into glucose through bovines
and caprines. We also use cellulose for shelters, clothing and a
myriad of other purposes. Mutation and selection is not our main mode
of adaptation to environmental selection pressures. If it was, we’d
all be dead from exposure and starvation. Of course, perhaps you think
that we might respond to a cold environment by evolving feathers.
>> You obviously have not read Lenski s paper on the
>> quantitative results of his study. Hersheyh, get a copy of this paper
>> Genome evolution and adaptation in a long-term experiment with
>> Escherichia coli , Vol 461, October 29, 2009, Nature.
>I have read it, but it has been a couple of years.
You had better read it again if you want to understand the basic
science and mathematics of mutation and selection. Lenski’s
experimental model includes many of the features of mutation and
selection which we are talking about including neutral mutations which
you seem bent on using to try to save your mathematically irrational
theory of evolution.
>> In the adaptive
>> phase of his study, none of the mutations in the experiment were due
>> to drift (a crappy word to describe what populations do on a plateau
>> of a fitness landscape).
>Like I said, there will always be selective competition, regardless of
>whether or not any of the variants can utilize citrate. Drift is what
>happens when there is selective neutrality between variants.
Only when his population evolved to more efficient users of glucose
did neutral variants start showing up in the population. Only when his
population reached a fitness plateau did neutral variants start to
appear. As I have said many times in this discussion, reducing the
selection pressure on a population will allow an increase in diversity
of the population.
>> Only when the populations evolved to improved
>> fitness did neutral mutations appear in his populations.
>No. Neutral mutations, beneficial mutations, and detrimental
>mutations all occur independently of their selective advantage,
>disadvantage, or neutrality at a rate called the "mutation rate" for
>that particular change. There is no "waiting" until the selectively
>advantageous mutations all occur before there are neutral mutations.
>Mutation is not selection.
Lenski’s populations where subjected to directional selection pressure
(ie starvation). During that phase of evolution, no neutral mutations
were measurable in his population. Only when the population finally
adapted to the starvation selection conditions did the neutral
mutations become measurable in the population. It required a reduction
in selection pressure for these neutral mutations to occur in
measurable quantities. Needless to say, no detrimental mutations were
measured.
>> In other
>> words, his population is diversifying on a fitness plateau. Still,
>> this population is limited by the amount of citrate available.
>No. *Until* there are mutations that allow the bacteria to use
>citrate, the availability or amount of citrate is irrelevant. The
>population is limited by the amount of glucose available.
You had better read Lenski’s papers again. Most of his populations did
not become citrate metabolizers.
>> > Now, if the glucose-only bacteria were more efficient at using glucose
>> > than the bacteria that could use both, we have a condition that could
>> > favor "specialization" to different niches, with some bacteria
>> > becoming specialized glucose users and others becoming more and more
>> > reliant on citrate. I.e., speciation (and because inability to use
>> > citrate is a key speciation-defining feature of E. coli, the new bug
>> > would not be E. coli, but perhaps E. citrusflavoreddietcoli.
>> I guess you haven t read any of Lenski s papers. The citrate
>> metobolizers no longer were efficient glucose metabolizers and these
>> citrate metabolizers were very sensitive to osmotic pressures.
>Yet, relative to the original glucose metabolizers and at the osmotic
>pressures that existed, they were *selectively* favored in the
>experimental environment. Selection is always conditional to the
>specific local environment. That the citrate metabolizers may not do
>as well as the original strain in a *different* environment (one that
>lacks citrate or has a different osmotic pressure) is irrelevant.
>Evolution by selection does not select for a Neitzschean superbug. It
>selects for the organism that is best fit in a specific local
>environment.
And 11 of 12 populations have not become citrate metabolizers. You
have completely missed the point of the data produced by Lenski’s
experiments. But that’s not a surprise, you’ve missed the point that
the multiplication rule of probabilities is the dominant mathematical
feature of the mutation and selection phenomenon and that the
beneficial mutations do not have to occur simultaneously in order for
the multiplication rule of probabilities to still apply. Hersheyh, how
did you get to be so confused?
>> Now
>> early on, you posted a paper that I wasted my time on reading. In this
>> paper, these evolutionist pseudo-scientists claim that evolution is
>> irreversible.
>Rarely directly reversible.
Now how would you know that? Have you run the experiments? Do you have
the mathematical models? You think that if evolutionists repeat a
claim long enough it becomes true? I think it is the later. This kind
of claim is the evolutionist version of science, no data, no model,
only speculation.
>> Now do you think if you switched Lenski s experiment and
>> put his citrate metabolizers in a glucose rich environment with sparse
>> citrate that his bacteria could evolve back to glucose metabolizers?
>Yes (so long as they can survive in the new environment). However, it
>is unlikely that the bacteria became unable to utilize glucose, as
>opposed to not using it as efficiently. But they would not
>necessarily become better able to use glucose by direct reversion to
>the exact same organism that existed prior to the evolution of citrate-
>using E. coli.
His citrate metabolizers can still use glucose (though less
efficiently than there progenitors). Give his citrate metabolizers a
few tens of thousands of generations and they should be able to find
the genetic sequences that make efficient glucose metabolizers.
>> You really don t get it hersheyh. It took Lenski s bacteria about
>> 32,000 generations to become citrate metabolizers. When you
>> extrapolate your cases you describe above to a reptile transforming
>> into a bird, you have entered the realm of mathematical irrationality.
>Said with the utter certainty of someone who has refused to put any
>actual numbers down to demonstrate this "irrationality". It is easy
>to assert that "x is mathematically irrational" if you can do so
>without having to actually provide evidence other than your bogus
>assertion that all the changes have to occur simultaneously in the
>same individual.
What do you want me to do, I’ve already shown what the multiplication
rule of probabilities does with mutations with a probability of 10^-6.
The beta lactamase example requires five mutations. That would give a
probability of (10^-6)^5. Amplification and lots of generations can
overcome this kind of probability but it is slow and arduous process.
Neutral mutations do not have the benefit of selection so you are
dependent on generations alone to overcome these miniscule
probabilities. This is why you can’t do massive genetic
transformations by the mutation and selection phenomenon. This is why
John Harshman’s assertion of 40,000,000 differences between humans and
chimpanzees in a million generations can not be accounted for. The
multiplication rule of probabilities obliterates the concept of
abiogenesis and shows that the theory of evolution is a mathematically
irrational belief system. However, if you do understand how the
multiplication rule of probabilities dominates the mutation and
selection phenomenon, you can use this understanding to prevent the
evolution of multidrug resistant bacteria, develop more durable cancer
treatments, find safer and more rational uses of herbicides and
prevent herbicide resistant weeds and so on. This is what
evolutionists like you fail to understand.
>> Even if you could describe the selection pressures that would
>> transform a reptile scale into a feather, sequentially it would take a
>> vast number of generations.
>Which would be impossible if the earth were only 6000 years old like
>you believe. But quite possible in the millions of years during which
>feathers actually evolved.
Generations has only a minor effect on the mutation and selection
phenomenon. But you don’t understand how mutation and selection works
so why would you know this. Use Inez’s age for the earth, a jillion
years. Mutation and selection still can not accomplish what you claim
in the time available because the dominant mathematical principle
governing this phenomenon is the multiplication rule of probabilities.
>> And remember, Lenski maintained constant
>> selection conditions over these tens of thousands of generations. What
>> to think would happen if he introduced other random selection
>> conditions into his experiment like temperature variations,
>> dehydration, predation, disease, do you think that would accelerate
>> the evolution of citrate metabolizers?
>No. The generation of variants that can utilize citrate would be
>completely unaffected by other selective pressures.
Oh really? You don’t think any other selection pressures on this
population would affect the evolution of citrate metabolizers? What if
Lenski had changed the osmotic pressure of his solution?
>> Real environments do this to
>> populations. Real environments don t maintain constant selection
>> conditions for long periods of time. This is why your theory of
>> evolution is mathematically irrational.
>Depends. Real environments can change in persistent directions.
>E.g., Drier or wetter. Colder or warmer. If climate
>...
But real environments have nothing like the stability created in
Lenski’s laboratory. And that’s what is required for the mutation and
selection phenomenon to work well.
And
>> > > Don t confuse recombination and selection with mutation and selection.
>> > > This is a very common blunder on the part of evolutionists.
>> > Rather it is a common blunder of creationists who somehow think that
>> > selection doesn't involve the selection of existing variation, but
>> > only involves selection for non-existant variation that selection
>> > somehow *causes* to occur. *All* selection requires the pre-existence
>> > of actual variants. In all cases the selected variant phenotypes
>> > already exist in a population of organisms.
>> Oh really, did I make that claim?
>Yes, you did. You said one could not look at the selection of
>variants that already exist in a population because that is
>recombination and selection. My point remains. Selection always
>involves selection among variants that actually do exist in a
>population. Selection does not generate hypothetical solutions that
>might work.
I’ve never made that claim. What I have said is that selection reduces
the diversity of populations and that mutations increase the diversity
of populations. What directional selection pressures do is set a
direction for evolution of the population based on finding the fittest
replicators. Selection tests mutations in order for a population to
try to find a solution which does work. You in your contradictory
world of evolutionism claim that feathers are a hypothetical solution
for reptiles in order to keep them warm. But now you are claiming that
selection does not generate hypothetical solutions. I really wish you
evolutionists could make up your minds. On the other hand, I do claim
that selection tests hypothetical solutions for the solution of
environmental stressors on a population. Selection pressures define
evolutionary direction but the process must occur quickly enough for
the mutation and selection process to work without driving the
population to extinction.
>> I really would like to see your
>> breeding program where you take a population of reptiles and transform
>> them into a population of birds. That would really be something. Are
>> you now claiming that reptiles transformed into birds without mutation
>> and selection?
>Mutation first, to generate variation. Selection only among the
>variants that actually did occur and did exist.
Ok, now you are talking turkey (but that turkey didn’t evolve from a
reptile). The selection conditions of the environment determine which
variants are fit enough to reproduce. Then a change in selection
determines which variants survive and form the basis population for
the mutation and selection phenomenon to find a new fitness optimum
(unless you want to claim that every variant possible exists in a
population, 4^G becomes a huge number very quickly).
>> Do you think that the citrate metabolizers were just
>> variants of the glucose metabolizers and they already existed in
>> Lenski s experiment?
>In fact, the citrate metabolizers are indeed nothing but variants
>derived from and by mutations of genes that existed in the glucose
>metabolizers. But there was no selection for citrate metabolizing
>traits until they, by mutation, actually existed in the population.
Once again, ok. But now you open up a whole new can of worms for the
concept of evolutionism. What happened long ago in the evolutionist
fairy land when those traits did not exist in your primordial
replicator? In your settled science of evolutionism, how did this
transformation from non-replicator chemistry without selection form
all this function for the replicators to act upon by mutation and
selection? Did the original replicators “drift” into being?
>Are you claiming that the citrate metabolizers somehow came into
>existence by the magical poofing of entirely unknown genes into
>existence? That would indeed be a surprise.
Not a surprise at all. You have a set of functioning enzymes which can
transport and metabolize a carbohydrate. A few mutations in enzymes
already capable of operating on these chemicals and the enzymes have
the correct conformation to metabolize a different carbohydrate. You
evolutionists are the ones that claim that all these genes came about
by abiogenesis. That’s one of the silliest concepts to hit science
since the flat earth concept. You evolutionists find this plausible
despite all the mathematical and scientific evidence. You aren’t doing
much better with the mutation and selection phenomenon.
>> > > Recombination and selection is a selection process done on the basis
>> > > of already existing traits, it is a form of inbreeding. Mutation and
>> > > selection requires the evolution of new traits.
>See that above. You are explicitly saying that selection for existing
>traits is not evolution. Only selection for non-existing traits is
>evolution. Mutation, of course, does not *generate* new traits; it
>modifies old ones (some mutations producing larger modifications than
>others). Sometimes such mutations produce new (but often related)
>*functions* in the process. But most evolution is of quantitative
>features of organisms (e.g., size of braincase, shape of foot) in
>which there are always variants in most populations rather than the
>invention of new metabolic processes. For example, nearly all the
>differences between humans and chimp skeletons represent such
>quantitative modifications (the one exception is the complete loss of
>the already greatly reduced baculum in humans).
You are really squirming here. What I am saying is the mutation and
selection phenomenon is an extremely slow process for adapting to a
changing environment. And the reason the phenomenon is extremely slow
is the multiplication rule of probabilities. Now you can try what ever
semantic argument you like but the mathematical principles are the
truly explicit principle which we are describing here. I understand
that you are having trouble seeing this concept unless the mutations
must occur simultaneously but none the less, the multiplication rule
of probabilities dominates the mutation and selection phenomenon.
Without selection, the theory of evolution degenerates into the
concept of abiogenesis because selection is the only principle creates
an order in the theory of evolution.
>> > Variation (mutation) always occurs and always occurs independently of
>> > the selective conditions. The effect of variation is dependent on
>> > previous genetic history of the organism. But you have not defined
>> > what you call a "new trait". Does citrate metabolism in E. coli
>> > count? Does AZT resistance count? In both cases, selection only
>> > selected variants that actually existed in the population that could
>> > affect those stressors or opportunities.
>> I thought you evolutionist claim the selection increases the diversity
>> of populations?
>No. Unlike you we do not persistently deny that there are conditions
>in which selection increases diversity (measured as frequency and
>number of alternate alleles). But you have yet to define what you
>mean by "diversity of populations", so it is hard to say much about
>what you mean.
If you had an empirical example which demonstrates that selection
increases the diversity of a population, you would have posted that
example long ago. With respects to the concept of diversity, I prefer
a mathematical definition and that definition is given by the number
of genetic variants in a population. Selection always reduces the
number of genetic variants while mutations are the mechanism for
increasing the genetic diversity of a population. However, the only
way to increase the genetic diversity of a population is by reducing
the selection pressure on that population.
>> Are you finally realizing that mutations are the
>> source of variation? I ve never said that mutation and selection
>> doesn t occur. I m only saying the evolutionists make mathematically
>> irrational extrapolations of how this phenomenon works.
>Again, that is an assertion without even supporting math, much less a
>clear description of the assumptions you are making.
I make this assertion based on the probability of multiple independent
random mutations occurring in a population is governed by the
multiplication rule of probabilities. It doesn’t matter whether the
mutations are occurring simultaneously or not. This is why the
mutation and selection process is so slow and arduous when it does
work. Increasing the frequency of a beneficial allele takes many
generations because the population size and number of generations
required in an evolutionary process affect the probabilities less than
additively. There is no variable in the mutation and selection
phenomenon that has the profound affect on its behavior like the
complexity of the selection conditions because this is the variable
which is governed by the multiplication rule of probabilities. In
addition, if the population can not amplify beneficial mutations
efficiently as in the example of HIV evolution to combination therapy,
it is very highly unlikely that the evolutionary process will occur at
all. This is why the use of combination therapy stifles if not
suppress the evolutionary process when ever it is used.
> > > Now if you are
> > > claiming that you can carry out a breeding program with a population
> > > of reptiles and by inbreeding produce a bird, I would really like to
> > > see you do this.
>Feather buds from what would otherwise become foot scales (scutes).
>Both scale and feather are composed of the same materials (beta-
>keratins). Beta-keratin forms sheets of cross-linked fibers. Whether
>it forms a scale or a frayed scale or feathers or hair-like materials
> (as on a gecko's footpad) is something of a function of the extent of
>cross-linkage.
Our skin has keratin in it. Perhaps humans will evolve feathers?
>> So, populations in nature are never subject to weather selection
>> pressures, or diseases, or starvation, or drought, or any of a number
>> of selection conditions simultaneously. Nature simply cooperates with
>> populations and applies selection pressures in a nice convenient
>> sequence so that reptiles can transform into birds. Why is it that I
>> hear the Twilight Zone theme song whenever I hear you discuss the
>> theory of evolution?
>I cannot be responsible for the voices or theme songs you hear in
>your head. Organisms are subject to lots of selective pressures.
>Selection does a mini-max sorting job. All I can say is that nature
>*did* provide a viable pathway from reptiles to birds. There are
>intemediate organisms that show how that pathway occurred. That
>lineages also go extinct shows that nature does not always provide
>such a pathway.
Whenever you tell us that you can roll a die and get a zero; that’s a
pretty bizarre concept. Are you hitting your shoe on the table when
you tell us that “nature *did* provide a viable pathway from reptiles
to birds” because mutation and selection certainly could not have done
it. The process is far, far too slow. Mutation and selection can’t
even do the accounting between human and chimpanzee genomes.
40,000,000 differences between humans and chimpanzees and only a
million generations to do that transformation; it didn’t happen by
mutation and selection. Perhaps you can convince naïve school children
that neutral mutations which are fixed by chance occurs much more
quickly than beneficial mutations fixed by selection but then naïve
school children (and evolutionists) know nothing about the
multiplication rule of probabilities.
>> Nope hersheyh, you are wrong. You think when the selection intensity
>> is zero that neutral mutations are fixed in a population. This is one
>> of a number of mathematically irrational beliefs that evolutionists
>> hold.
>What I think is that when there is no selection, that selectively
>neutral changes *can* go to fixation by chance alone. I have
>explained why this is the case, giving actual numbers, before. It has
>to do with the "drunkard's walk" that occurs in the absence of
>anything but chance. For a new mutant selectively neutral allele, the
>probability of it going to fixation is 1/N. That is typically a small
>probability, meaning that most (nearly all) new selectively neutral
>traits will go to extinction. Learn a little neutral theory and
>proability theory, why don't you? It beats demonstrating your
>ignorance every time you post.
When there is no selection acting on a portion or all of DNA, any
variant has equal fitness to reproduce. Any stretch of DNA which is
not random has selection acting on that portion of DNA. Stabilizing
selection is what maintains the order of DNA in a population and the
vast majority of selection pressures acting on a population are these
stabilizing (or what you like to call “conservative”) selection
pressures.
Now at least I haven’t claimed that you can roll a die and get a zero.
========================================================
Inez
>> In your above statement.
>So you think that by recombining genes an antelope can develop a neck
>many feet longer than any extant antelope? Why do you think that?
I think you can do all kinds of morphological changes to a population
by inbreeding. Breeders can create all kinds of dogs by inbreeding for
particular traits. Do you think that growing feathers on a reptile is
the result of inbreeding?
>> > > Recombination and selection is a selection process done on the basis
>> > > of already existing traits, it is a form of inbreeding. Mutation and
>> > > selection requires the evolution of new traits.
>> > Well I would say that a giraffe is different than a non-giraffe
>> > ancestor, with many new traits, such as the famous neck thingy.
>> Don t confuse the change in expression of existing alleles with the
>> evolution of new alleles. They are completely different thingies. If
>> they weren t different, then you could transform reptiles into birds
>> by inbreeding.
>This seems like a strange claim with no substantiation.
You need the genes in the population if you are going to try to
express a particular trait. If those genes don’t exist in the
population, then you can’t express the trait. Reptiles don’t grow
feathers because they don’t have the correct genes (or alleles to
those genes). It would take mutation and selection to transform
existing reptile genes into genes capable of producing feathers.
Edward Max gave us a citation that points to which genes would have to
be transformed and there are at least nine genes. The mutation and
selection phenomenon does not work efficiently transforming large
numbers of genes as demonstrated by the inability of HIV to transform
two genes simultaneously with any efficiency by mutation and
selection.
>> > > Now if you are
>> > > claiming that you can carry out a breeding program with a population
>> > > of reptiles and by inbreeding produce a bird, I would really like to
>> > > see you do this.
>> > I'm pretty sure I didn't claim that, as such a project would likely
>> > take millions of years and even with eating my vegetables and liberal
>> > applications of Oil or Olay I don't plan to live that long.
>> Even if you didn t fry your vegetables in saturated fats and soaked in
>> a vat of Oil of Olay (hey, maybe that s what the primordial soup was)
>> for 4 billion years, once you understand how mutation and selection
>> works, you still wouldn t have enough time to make such a
>> transformation by mutation and selection.
>Can you demonstrate this with evidence?
I haven’t done the study with Oil of Olay but I did forget a container
of olive oil in the back of my refrigerator one time. There were signs
of replicators and it didn’t take billions of years. It must have been
the antioxidants in the olive oil that created this primitive
environment conducive to the origin of life.
><snip>
>> > Whoops! That's what I get for shooting my mouth off without knowing
>> > what I'm talking about. Except that now that I google around I find
>> > that HAART therapy has a failure rate which several papers quoted as
>> > around 14%. So it looks like maybe HIV does actually sometimes manage
>> > to mutate to resistance afterall.
>> Since you are not a physician, you probably don t understand about
>> patient compliance.
>So...you know that HIV never ever mutates to resistance in HAART, and
>it's always patient compliance? How do you know that? And what about
>patient non-compliance allows it to develop resistance? Are you
>claiming sometimes patients take one drug and then another? Or is it
>that patients who skip their drugs allow the population to increase
>enough so there will be triple-resistant mutants?
There are many factors which can cause HAART to fail. If the patient
already has resistant viruses to one or more of the drugs, the
treatment won’t be durable. If the patient is not compliant, the
treatment will fail. The underlying health of the patient is also a
factor. If the patient is debilitated and has a poor immune system
otherwise, it is much more difficult for treatment to work. Any
underlying diseases such as diabetes, cancer, and other viral
infections and so on make it more difficult to treat these patients.
What ever treatment is used, effective three drug therapy on an
otherwise healthy person give good chances for long term survival.
And
>> Inez, the point you are missing is that when HIV is subjected to
>> single drug therapy, the virus can evolve resistance to an individual
>> drug in a week. In three weeks, the virus can evolve resistance to
>> three drug therapy if used sequentially. On the other hand if the
>> drugs are used simultaneously, it takes years for the virus to mutate
>> and select to all the selection pressures simultaneously. Hersheyh
>> understands this; this is why he has retreated to the position that
>> reptiles turn into birds one gene at a time.
>And so by the demonstration of your own example, you admit that
>reptiles COULD evolve into birds as long as none of the steps are
>selected for in such a way that they must have all of them for any
>selective advantage to be realized, right?
You still don’t quite have the argument yet Inez. The main governing
mathematical principle for the mutation and selection phenomenon is
the multiplication rule of probabilities. That is the probability of
two beneficial mutations occurring is the product of the individual
probabilities for each beneficial mutations. Most of the evolutionists
can see this when both mutations must occur simultaneously on a
particular member of the population. What most evolutionists can’t see
is that this mathematical principle still governs the mutation and
selection phenomenon when the mutations do not occur simultaneously.
Here’s a simple example. Let’s say you buy a lottery ticket and you
happen to be the lucky player. Then you win the lottery and get the
money. But now let’s say you buy tickets in two different lotteries
and the only way you can win either is by winning both lotteries
simultaneously. That’s the case where evolutionists understand the
multiplication rule of probabilities. Now let’s say you are playing
two lotteries and you win one of the lotteries and in this case you
get the money. Now you can afford to raise a large family and your
family keeps buying tickets to the second lottery. As the generations
go on, your descendents become more and more numerous and they keep
buying tickets in the second lottery until finally your number of
descendents and the number of generations have passed that you now
have a reasonable probability of winning the second lottery. Many
generations and many descendents pass and finally one of your
descendents wins the second lottery. That’s how the mutation and
selection process works when it can. But anything which disrupts the
ability of you having large numbers of descendents interferes with
your family’s probabilities of winning the second lottery. That’s how
the multiplication rule of probability drives the mutation and
selection phenomenon.
>So now all you have to do is show that all the differences between
>birds and their predecessor had to arise at one go rather than
>slowly. Got any evidence like that? Because from what I'm told, the
>fossil record seems to show a step-wise development such as the one
>Mr. Hershey suggests.
I’ve never said that the mutation and selection process has to occur
at “one go”. I’ve always said that the mutation and selection is an
extremely slow and arduous process. Once you specify how many
beneficial mutations required for an evolutionary process to occur,
you’ve given an approximate number of generations required in order
for the entire process to occur. Since the evolution of reptiles into
birds can only be studied speculatively, consider the example of the
claimed evolution of humans and chimpanzees from a primate precursor.
We know the genetic sequences for both forms and we have the
evolutionist estimate that the divergence of the two forms occurred
about 10,000,000 years ago. That gives about a million generations to
achieve what ever genetic transformation can be done. John Harshman
has said there are 40,000,000 differences between humans and
chimpanzees. Now if that process occurs one gene at a time (which is
the only efficient way the mutation and selection phenomenon works),
it would require the substitution of 20,000,000 alleles (half in the
chimpanzee and half in the human population) in one million
generations or the substitution of 20 alleles per generation. Mutation
and selection simply can not substitute 20 alleles per generation. In
fact the substitution process for a single allele takes hundreds of
generations. There are simply far, far too many lotteries to win in
such a short time.
What ever evolutionists a claiming to see in the fossil record does
not coincide with the hard mathematics of how the mutation and
selection phenomenon works.
>>I have also proved that
>> the Ev-Men comic books to be works of fiction.
>Good for you, I'm sure your mommy is proud.
I wouldn’t be so sure, she would probably tell me to clean the old
olive oil out of by refrigerator, some life form might spontaneously
occur.
And
I admit to confusion. Apparently he thinks that antelopes might
become giraffes by recombining existing genes, but birds can't evolve
from reptiles. All mutations must be simultaneous, or else...I don't
know what. Whatever it is, it's either bad or laughable.
The reason why you are confused is that you are mixing two
phenomenons. Mutation and selection differs from recombination and
selection. Recombination without error can not make new alleles.
Recombination with selection can and does cause the loss of alleles
from a population. On the other hand mutation and selection is
required to make new alleles and I don’t think there are any
evolutionists here who think you can evolve a reptile population into
a bird population simply by a series of recombination events. The
reason is that the required alleles don’t exist in the reptile
population. The alleles would have to be generated by the mutation and
selection phenomenon. It’s bad for the theory of evolution but it’s
good for those who are suffering from diseases subject to the mutation
and selection phenomenon. Once you understand how mutation and
selection works, you can design drug treatments for infectious
diseases and cancers that are far more durable than the single drug
treatments that are the standard of care for the treatment of most
infectious diseases.
========================================================
John Harshman
>> This seems like a strange claim with no substantiation.
>I'll say. What does he think causes changes in expression of existing
>alleles? Magic? And what does he think is the result? Now in fact
>expression changes in evolution are the result of changes in DNA --
>mutations -- which can subsequently be selected. And these "mere"
>changes in expression can have major effects on morphology. What any of
>that has to do with inbreeding is a mystery.
Are you evolutionists still hung up on recombination and selection?
That phenomenon has a much smaller search space. In that case you are
recombining existing alleles and it doesn’t require amplification for
recombination. Recombination and selection is not governed by the
multiplication rule of probabilities. But any time one of you
evolutionists wants to demonstrate the evolution of a reptile to a
bird by an inbreeding program, I’d be thrilled to see that.
========================================================
Frank F Smith
>>>> Recombination and selection is a selection process done on the basis
>>>> of already existing traits, it is a form of inbreeding. Mutation and
>>>> selection requires the evolution of new traits.
>Also, recombination does sometimes produce new alleles.
>And once a mutation occurs, the new allele _is_ an existing allele
Recombination without error does not produce new alleles. You can get
chimeras but this is an error in the recombination process.
And once the mutation occurs and you have a new allele, it is subject
to the selection conditions of the environment. That new allele may or
may not be beneficial for the given environment or for any other
selection conditions the population is subject to. The Lenski
experiment should give you some sense of what new alleles will do for
a population and how long it takes these new alleles to be spread
throughout the population.
>> No. Unlike you we do not persistently deny that there are conditions
>> in which selection increases diversity (measured as frequency and
>> number of alternate alleles). But you have yet to define what you
>> mean by "diversity of populations", so it is hard to say much about
>> what you mean.
>IIRC he has specified Shannon index as his metric.
>Of course, it is _trivial_ to demonstrate that selection can increase
>Shannon diversity index. Such a demonstration takes only a few minutes
>with Excel (or equivalent). Of course, several posters (Richard Norman
>and Steve Carlip, and maybe others) have already demonstrated the math,
>in detail.
I have responded in greater detail why Steve Carlip is incorrect with
his example. I’m not the only one using the Shannon equation as my
metric. Edward Max of the FDA uses this as well, so does Thomas
Schneider of the NCI. If you are going to use the Shannon equation,
make sure you are comparing apples to apples. Evolutionists are so
used to comparing reptiles to birds, they have lost track of the
mathematics.
>One doesn't even need such relative esoterica as negative frequency
>dependent selection -- application of an antibiotic to an initially
>predominant susceptible strain with less than 100% effectiveness of the
>antibiotic is sufficient.
The reason why antibiotics with less than 100% effectiveness works is
that the antibiotics are not the only selection pressure acting on the
bacterial population. The individual’s immune system in most cases
provides sufficient additional selection pressure to cause extinction
of the bacterial population. In immune compromised hosts this is not
the case and resistant strains of bacteria can occur quite rapidly. It
is much more important to use combination therapy in these
circumstances.
And
Add his claim that there is no stochastic component to gametogenesis,
fertilization, fecundity, or mortality. (With, I think, an implicit
claim that there are no somatic cell mutations...)
Add some erroneous statements that someone who's been through high
school biology or math can readily recognize as just plain wrong.
Frank, do you think that increasing the randomness of the reproduction
process accelerates the evolutionary process? If you do, you must be a
mathematically incompetent evolutionist. Selection pressures are what
reduce fecundity and cause mortality but as an evolutionist, you
probably don’t understand this. And if you think there are no somatic
cell mutations, you are probably an evolutionist because somatic cell
mutations are the way cancers evolve resistance to therapies.
Now all we need is someone who has been through high school math who
understands the multiplication rule of probabilities so they can
explain to you evolutionists why your theory of evolution is a
mathematically irrational belief system and that evolutionists have so
bungled the basic science and mathematics of the mutation and
selection phenomenon that they have harmed and continue to harm
millions of people suffering from diseases subject to the mutation and
selection phenomenon.
========================================================
Steve Carlip
>> So, do you think a thicker scale would not provide better insulation?
>> But instead the reptile population would evolve feathers instead?
>You keep asking this. It's largely a question of physics, so here's
>an answer:
>The effectiveness of a substance as an insulator is determined by its
>thermal conductivity, which measures the rate at which energy passes
>through a given thickness. The higher the thermal conductivity, the
>faster heat passes through, and the worse the substance is as an
>insulator.
>Scales are made largely of keratin, which is a pretty poor insulator,
>having a thermal conductivity of about .2 W/K*m. This is about the
>same as plexiglass. If you poke around google scholar, you'll find
>that the thermal conductivity of crocodile skin has actually been
>measured, and is about twice as high, making it an even worse
>insulator (Drane, Comparative Biochemistry and Physiology A 68
> (1981) 107).
>Air, on the other hand, is a much better insulator, with a thermal
>conductivity of about .025 W/K*m. When you loose heat in cold
>air, it is mostly not through conduction, but through convection
>-- you warm a very thin layer of air near your skin, but it then
>moves away, giving you more cold air to warm. That's why cold
>weather is so much more dangerous when it's windy.
>Feathers -- specifically, down -- trap air, and prevent convection.
>As a result, their thermal conductivity is very close to that of air,
>rather than keratin. It's been measured; it's again about .025 W/K*m.
Steve, you’ve done a wonderful job explaining why there are no
reptiles in the arctic. Convective heat transfer without shelter does
markedly increase the transfer of heat. Perhaps that explains why
reptiles hibernate during the winter. I have never claimed that air is
not a better insulator than keratin but this notion that a reptile
population would take thousands if not tens of thousands of
generations to transform a scale into a feather in order to adapt to
the cold weather is nothing short of irrational. I doubt you
understand what thermal stress does to a population. A single cold
winter can kill large number of herd animals. If you superimpose
starvation, it is very likely to kill the entire population in one
season. Populations which are subjected to thermal stresses do not
have thousands of generations to adapt to these types of stresses.
>So, no, thicker scales won't provide better insulation. Specifically,
>to match the insulation of 3 mm of down, a reptile would need to
>have scales about 2.5 to 5 cm thick.
Only if the reptile doesn’t hibernate, migrate, shut down blood flow
to their skin surface, cluster together in groups to conserve heat or
do any of a myriad of other adaptive behaviors to avoid the thermal
stress. Thousands of generations to transform scales into feathers in
order to conserve heat only seems reasonable in the irrational mind of
an evolutionist. Most populations subject to thermal stress for
thousands of generations without adaptation would be long extinct.
>Now, try to imagine a sparrow covered with two inches of scales.
>Does that answer your question?
Steve, I know you are a physicist and probably have done little study
of the random mutation and natural selection phenomenon, but could you
tell us what the dominant mathematical principle of this phenomenon
is?
========================================================
J Astin
>> Perhaps in the evolutionist Twilight Zone, reducing the intensity of
>> selection accelerates the mutation and selection process. By your
>> twisted evolutionist logic, if you reduce the intensity of selection
>> to zero, evolution happens instantly.
>Alan, you are mistaken here.
>Reducing selection pressure does not reduce the rate of mutuation.
>Indeed, that rate should be unaffected. The total number of mutations
>in a population may increase if the lower selection pressure leads to
>a larger population, but the rate is independent of that.
J Astin, I’ve never said that reducing the selection pressure reduces
the mutation rate. What I have said is that reducing the selection
pressure increases the diversity of the population. Reducing the
selection pressure allows less fit variants to reproduce increasing
the size of the gene pool.
>Now, a reduced selection pressure may (and should) result in a more
>diverse population over time, such that more intense selection at a
>later time due to some change in the environment leads to speciation
>as a varied population exhibits different adaptations. That can be
>facilitated by a prior reduction in pressure. And please, lets avoid
>the strawman arguements as shown in your last sentence (that goes for
>all sides, of course). Logical fallacies have no place here.
Not only does reducing the intensity of selection cause an increase in
the diversity of the population, it also slows the substitution
process for more beneficial alleles for less beneficial alleles.
That’s a mathematical fact of life you evolutionists don’t appreciate.
>I'll float you one.
>Feathers may well have NOT had the functions at their earliest
>inception that they do now. Consider that the evidence is piling up
>for a number of species that are clearly dinosaurs to have been
>feathered. Developments leading towards flight feathers are ...
Ok, let’s fly with that speculation for a paragraph. So now the
feathers aren’t to keep warm, the dinosaur now has the feathers for
good looks. Since everyone knows that good looks attracts the opposite
sex, that’s worth thousands of generations to get a date. J Astin,
you’ve just won a feather in your cap.
========================================================
hersheyh
> On Mar 15, 6:27 pm, William Hughes <wpihug...@gmail.com> wrote:
>
>
>
>
>
> > It is rather interesting that in a > 1000 post thread
> > the good Dr. has been unable to note that he is confusing two
> > scenarios
>
> > 1: A mutation A' causes an increase in reproductive
> > success, whether or not a mutation B' (which also
> > causes an increase in reproductive success) is present.
>
> > 2: A mutation A' alone or a mutation B' alone does not cause an
> > increase
> > in reproductive success. Only both mutations together cause
> > an increase in reproductive success.
>
> > Only in case2is the multiplication rule for probabilities applicable
>
> > - William Hughes
>
> William, the multiplication rule of probabilities always applies when
> more than a single beneficial random mutation is required to adapt to
> selection pressures.
Only when the beneficial mutations must occur simultaneously in the
same *individual* to adapt to selection pressures. That is, when the
individual mutations have no selective benefit. You keep, however,
denying that the multiplication rule does NOT apply when those
conditions are not met.
> This is why the complexity of the selection
> conditions is the dominant mathematical variable in the mutation and
> selection phenomenon. Any evolutionary process which requires more
> than a single beneficial mutation requires amplification of beneficial
> mutations in order to improve the probabilities that the next
> beneficial mutation in the sequence occurs.
It requires spread of the variants in the population. An increase in
their *frequency*, not, in most cases, a major population decline and
restoration. I have presented actual data that you can apply that
shows the difference between your assumption of simultaneous in the
same individual (where the multiplication rule applies) and what
happens if one can engage in a serial (and parallel or partially
offset parallel) mutation and selection in a population using bacteria
and resistance to antibiotics. Perhaps you missed it.
If mutation to resistance to either antibiotic is 10^-8 and you add 1
ml of bacteria containing 10^9 bacteria to 9 mls of media containing
*both* antibiotics, the probability of mutation to both resistances
meet your requirement of being simultaneous and in the same
individual. That probability would be 10^-16. The probability that
the 10^9 bacteria added will have a double mutant is 10^-7, or quite
low.
OTOH, if you add the 1 ml of bacteria containing 10^9 bacteria to
media containing only *one* of the two antibiotics, the probability
rule says that there should be, as a mean, 10 bacteria in the 10^9
bacteria you added to the 9 mls of media that will be resistant to
that one antibiotic. After 30 generations, those 10 bacteria (the
survivors) will have grown back to 10^9 bacteria/ml. If you then add
1 ml of those bacteria already resistant to one antibiotic to 9 ml of
*both* antibiotics, you will, on average, have about 10 bacteria
resistant to both in the 10^9 bacteria you add. After another 30
generations, you will have a full population of double mutants.
The above is decidedly more common in evolution.
But let's take another example. Take a population of sensitive
bacteria that are F+ and expose them to one of the antibiotics and
another population of sensitive which is F- to the second antibiotic.
Grow overnight and then put them together in media without either
antibiotic for a couple of hours. Now when you add both antibiotics,
the probability of finding a bacteria with both antibiotics will be
much higher. Exactly how much higher will depend on where the F
factor starts and how far apart the two resistant alleles are. The
reason for the much higher probability is that recombination between
different bacteria can occur under those conditions. This would be
the bacterial form of parallel evolution.
The *only* case where the probability is low is the one that requires
your condition that both mutants be present simultaneously in the same
individual by chance alone.
> This is why when the
> mutation and selection phenomenon works, it is arduous and slow.
The second example above would take a grand total of two days. The
third will be somewhat faster.
John Stockwell
...unless there are two subpopulations in slightly different
environments, then they
diverge, which is the characteristic that your microorganism examples
do not address.
-John
John Harshman
> being presented like this to prevent further fragmentation of the
> discussion. These are responses to messages 951-975
Please stop doing this. And be aware that the numbers appear only in
Google Groups. The rest of us don't see them. And this post is way too
long to read. It may in some way be convenient to you, but it's a pain
in the ass to others. Have some consideration. Threading exists for a
reason.
> John Harshman
>>> This seems like a strange claim with no substantiation.
>> I'll say. What does he think causes changes in expression of existing
>> alleles? Magic? And what does he think is the result? Now in fact
>> expression changes in evolution are the result of changes in DNA --
>> mutations -- which can subsequently be selected. And these "mere"
>> changes in expression can have major effects on morphology. What any of
>> that has to do with inbreeding is a mystery.
> Are you evolutionists still hung up on recombination and selection?
> That phenomenon has a much smaller search space. In that case you are
> recombining existing alleles and it doesn’t require amplification for
> recombination. Recombination and selection is not governed by the
> multiplication rule of probabilities. But any time one of you
> evolutionists wants to demonstrate the evolution of a reptile to a
> bird by an inbreeding program, I’d be thrilled to see that.
This isn't a response at all. It appears that you didn't even read what
I wrote, especially the bit about "What any of this has to do with
inbreeding is a mystery." I'm going to stop arguing with you, because
you just don't pay attention.
r norman
It is often claimed that one of the major purposes of this site is to
allow crackpots like this one to have a place to vent their opinions
without garbaging up real scientific sites like Tom Schneider's of the
National Cancer Institute.
http://www.ccrnp.ncifcrf.gov/~toms/
To the extent that the good Dr. Dr. is busy posting here, he can't be
posting elsewhere. Let us hope that that practice works. It might
make all this worthwhile.
Stuart
> On Mar 15, 6:27 pm, William Hughes <wpihug...@gmail.com> wrote:
>
>
>
> > It is rather interesting that in a > 1000 post thread
> > the good Dr. has been unable to note that he is confusing two
> > scenarios
>
> > 1: A mutation A' causes an increase in reproductive
> > success, whether or not a mutation B' (which also
> > causes an increase in reproductive success) is present.
>
> > 2: A mutation A' alone or a mutation B' alone does not cause an
> > increase
> > in reproductive success. Only both mutations together cause
> > an increase in reproductive success.
>
> > Only in case2is the multiplication rule for probabilities applicable
>
> > - William Hughes
>
> William, the multiplication rule of probabilities always applies when
> more than a single beneficial random mutation is required to adapt to
> selection pressures.
For the umpteenth time, the multiplication rule only applies when the
mutations
must occur simultaneously in the same individual. This is the case
when we're talking
adapt or die.Either you get both mutations or you are dead.
That is far from the norm. Having less differential reproductive
success
is lot different than being dead.
Seriously, who do you you think you're fooling? You're only making a
fool of yourself.
Stuart
chris thompson
> Alan Kleinman MD PhD wrote:
>
> > The following is a compilation of responses to previous posts that are
> > being presented like this to prevent further fragmentation of the
> > discussion. These are responses to messages 951-975
>
> Please stop doing this. And be aware that the numbers appear only in
> Google Groups. The rest of us don't see them. And this post is way too
> long to read. It may in some way be convenient to you, but it's a pain
> in the ass to others. Have some consideration. Threading exists for a
> reason.
In the good Dr.Dr.Dr.'s defense, I believe he did this in response to
others agitating for a stop to him replying (he was accused of
spamming) to individual posts in multiple threads with the same
title.
The guilt resides with Gurgle Groups and their "feature" of
fragmenting any thread that reaches 1k posts. Whether Dr.^3 K. should
get a real news reader is another question entirely. Is there another
"good" solution to this issue? Sure, get Gurgle to fix their Usenet
software (not bloody likely).
"You can please some of the people all of the time..."
Chris
Mark Isaak
> William, the multiplication rule of probabilities always applies when
> more than a single beneficial random mutation is required to adapt to
> selection pressures.
Alan,
You do not know what the multiplication rule of probabilities is. I
quizzed you earlier to state where it does *not* apply, and you flunked
by not answering. But I'll give you a chance to retake the test. When
does the rule not apply?
--
Mark Isaak eciton (at) earthlink (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
richardal...@gmail.com
Actually, I suggest what will make this thread go on into eternity is
expecting creationists to demonstrate a basic understanding of
science, to offer evidence to support their assertions, and to take
note of the evidence from the real world which shows that their views
are wrong.
RF
hersheyh
Other than the fact that that is only the case under certain rather
unusual conditions (at least in nature)? Namely that you require
multiple mutations simultaneously in a single individual to have *any*
benefit.
hersheyh
wrote:
> On 3/15/2011 9:27 PM, William Hughes wrote:
>
>
>
>
>
> > It is rather interesting that in a> 1000 post thread
> > the good Dr. has been unable to note that he is confusing two
> > scenarios
>
> > 1: A mutation A' causes an increase in reproductive
> > success, whether or not a mutation B' (which also
> > causes an increase in reproductive success) is present.
>
> > 2: A mutation A' alone or a mutation B' alone does not cause an
> > increase
> > in reproductive success. Only both mutations together cause
> > an increase in reproductive success.
>
>
> > - William Hughes
>
> Regarding 2: is it accepted by scientists that all mutations are
> independent of each other in incidence?
In general, the answer is yes. The main exception is that a mutation
in the DNA repair or methylation system can differentially affect the
subsequent rate of mutation of the types of mutations they repair or
the sites they methylate. Another exception is that mutation rate at
a particular locus (say from a specific G to A) *is* affected by the
surrounding sequence. That is why there is a range of mutation rates
for, e.g., G to A mutations. So a mutation nearby that changes the
milieu can affect the mutation rate at the second nearby site. There
may be a few other exceptions. But note that the second mutation
involves merely a change in *mutation rate*.
> Mitchell Coffey
hersheyh
> The following is a compilation of responses to previous posts that are
> being presented like this to prevent further fragmentation of the
> discussion. These are responses to messages 951-975
> ========================================================
> R Norman> This guy who loves to lecture to us about the multiplication rule in
> > probability clearly does not believe at all in probability.
> > The probability of having a male vs. a female child is 50:50. I have
> > two brothers but no sisters. I have two daughters but no sons.
> > Obviously the reason why the sex ratio changed so drastically in
> > either direction in two generations in my own family is because of
> > survival of the fittest. Stochastic processes had absolutely nothing
> > to do with it. So says the good doctor who knows about probability so
> > he must be right.
>
> The reason why I lecture you on the multiplication rule of
> probabilities is that it is the central governing mathematical
> principle of the mutation and selection phenomenon.
Says who? Can you cite anyone aside from yourself who makes this
claim?
> There is a reason
> why I don’t go to casinos. It is not gambling in casinos. If you play
> long enough, you will leave all your money there.
I can certainly understand that you have very good reasons to avoid
all games of chance. Even ones where there is no "house" to take its
cut, like games of coin-flipping among friends, where your chances are
as good as any other player. Given your understanding of probability,
you probably think that every player would come out even in the end
because every player has a 50:50 chance of being right with each flip.
> And> The good doctor here totally ignores my several posts where I
> > patiently explain to him the medical genetics is a different subject
> > from evolutionary biology. Medical genetics is taught to medical
> > students by medical geneticists and the thrust of the subject is not
> > mutation and selection or evolution or even irrational views of
> > evolutionism.
>
> R norman, I haven’t ignored you. I just disagree with you. My medical
> school genetics text discusses mutation and selection but does an
> incompetent job of describing the phenomenon.
No. Although I am sure the text provides an *incomplete* description
of a complex subject, you undoubtedly think it is incompetent merely
because it doesn't agree with your brilliant insight about the
probability rule. Problem is, your insight is full of it.
> I think most physicians
> would agree that infectious diseases comprise a much greater fraction
> of primary care medical practices than do genetic diseases. I would be
> surprised if any medical geneticist said he wasn’t an evolutionist.
> > But then the good doctor has always ignored my criticisms, especially
> > those cogent ones he finds impossible to answer: his flawed use of
> > Newton-Raphson methods to find the zeros of non-linear equations, his
> > absurd claim that selection cannot increase diversity, his ridiculous
> > posturing about how his claim of failures in medical practice are laid
> > directly at the feet of evolutionary biologists, .....
>
> Why don’t you try to take away my PhD by saying my thesis was wrong
> where I used the Newton-Raphson method to find the zeros of six
> simultaneous non-linear equations.
SFW. Just because you can do that doesn't make you an expert in even
basic probability and population genetics. Just because William
Shockley won a Nobel Prize in physics did not make him competent in
human genetics (he was a notorious eugenicist promoter), although he
was probably more competent in that field than you are in
understanding how neutral allele frequencies change with time.
> And then why don’t you post any
> mathematical or empirical evidence which shows that selection
> increases the diversity of populations.
How do you define "diversity"? The number of alternate alleles at a
gene locus in a population that are above a frequency of, say, 10^-6?
> Selection always removes
> members of the population from contributing to the gene pool, which
> always decreases the diversity of the gene pool.
Selection differentially (and significantly) affects the reproductive
success of certain phenotypes relative to alternatives in a specified
environment. That neither requires "removal from the population" nor
does it prevent all "contribution to the gene pool." Several people
have already described selection which *favors* diversity. That which
occurs when "unusual" or "different" alleles are favored. I have
mentioned self-sterility in plants as a case where *selection* has
resulted in populations with over 200 alternate alleles.
> Now I lay the
> responsibility for the failure to properly teach the basic science and
> mathematics of the mutation and selection phenomenon on those who
> control the educational system. And who controls the field of biology?
If you were in charge, you would be teaching poor biology *and* false
mathematics.
> ========================================================
> Mark Issak> You are bearing false witness. I never claimed that.
>
> That sounds like some kind of religious belief. We need to keep that
> kind of stuff out of our public school.
> And>> The good doctor here totally ignores my several posts where I patiently
> >> explain to him the medical genetics is a different subject from
> >> evolutionary biology. Medical genetics is taught to medical students
> >> by medical geneticists and the thrust of the subject is not mutation
> >> and selection or evolution or even irrational views of evolutionism.
> >> But then the good doctor has always ignored my criticisms . . .
> > I suspect he simply does not remember them. I am becoming increasingly
> > persuaded that he is suffering from organic brain damage that affects his
> > ability to form long-term memories. This would explain his abysmal
> > reading comprehension, his complete inability to learn, and probably a
> > lot of his belligerence, as a lot of people get defensive rather than
> > admit the problem is with themselves. I would be curious to talk with
> > one of his colleagues who sees him regularly to find out what they have
> > noticed.
>
> That’s why I put it in writing Mark. So Mark, do you believe that
> selection pressures increase or decrease the diversity of populations?
It depends on the selective pressures and environmental conditions.
> We already know that you believe that if you decrease the intensity of
> selection that you accelerate selection process. That’s mathematically
> irrational.
>
> ========================================================
> Hersheyh>Reducing the intensity of selection has no effect on mutation rates.
> >Mutagens and prevailing mutagenic conditions (the sum of positive
> >causation of mutations decreased by repair capacity) will determine
> >the rate of mutation. If I mutate or chemically inactivate repair
> >systems, net mutagenesis will increase. If I add mutagens, net
> >mutagenesis will increase. If I change selective conditions, I will
> >almost never increase or decrease mutation rate. [There are a few
> >exceptions where a specific genetic change is a response to
> >environmental conditions, such as excision of integrated lambda phage
> >under stress conditions. It is possible to consider these as
> >"domesticated" mutagenesis events.]
>
> Hersheyh, you don’t read my posts very carefully. What I have said is
> that reducing the intensity of selection slows the evolutionary
> process.
In the absence of selection, we have neutral drift, which I have
already described as a process of change which is *slower* than any
form of selective allele *change*. Conservative selection is
selection against allele change, but that is a dynamic stasis.
> The reason that reducing the intensity of selection slows the
> evolutionary process is that the intensity of selection affects the
> rate of substitution of a more beneficial allele for a less beneficial
> allele.
Yes. The stronger the selection, the more rapidly we get substitution
for the allele that is beneficial in that specific environment.
> And the unit process of evolution is the substitution of a
> more beneficial allele for a less beneficial allele.
Neutral allele change is also evolution. The adjectives "beneficial"
and "detrimental" are not *inherent* properties of a gene sequence.
They are descriptives of how two alternate alleles compare in their
phenotypic effects in a particular environment. The terms are
*conditional*.
> You evolutionists
> are very confused on how each of the variables in the mutation and
> selection phenomenon affects the behavior of this process.
So you keep asserting, despite it being pointed out that you are
wrong.
> By far, the
> complexity of the selection conditions is the dominant variable in
> mutation and selection phenomenon. The reason is because this variable
> is governed by the multiplication rule of probabilities.
No. The conditions for anything to be "governed by the multiplication
rule of probabilities" is the requirement for *simultaneity* in a
single trial, or as in your case, *simultaneity* in a single
individual. We keep reminding you that evolution is most successful
when one or both of those requirements do not hold.
> No other
> variable in the mutation and selection phenomenon has the mathematical
> leverage of the multiplication rule. Hersheyh, if you learn nothing
> else from this discussion, learn that the multiplication rule of
> probabilities is the dominant governing mathematical principle for the
> mutation and selection phenomenon.
I refuse to learn errors. You have been expounding clear error. I
certainly agree with using the multiplication rule of probability
*when* the conditions for its use are present. I have never had any
problem with that. But your claim that all evolution occurs under
those conditions is the talk of someone that doesn't understand either
evolution or probability.
>> By your
> >> twisted evolutionist logic, if you reduce the intensity of selection
> >> to zero, evolution happens instantly.
> >No. If you reduce the intensity of selection (positive or negative),
> >you approach selective neutrality. I have described *in detail* what
> >happens under conditions of selective neutrality -- a post that
> >actually includes some math.
>
> There is no such thing as selective neutrality. It’s a figment of an
> evolutionist’s imagination. You can have neutral mutations but they
> are not selected for or against.
What the hell do you think "selective neutrality" means? It means you
have mutations that are not selected for or against.
> And you in your detailed description
> includes rolls of a die which gives zero values.
Liar. Why do you always omit what I actually say when you lie about
what I said? Guilty conscience? What I said is that if you roll a
die 18 times, there is a certain probabilty that you will get zero 5-
faces.
>What happens is that any selectively neutral allele will undergo a
> >"drunkard's walk" wrt its frequency in the population, with a certain
> >probability of fixation. If it is a brand new allele, its initial
> >frequency is 1/N (or 1/2N, depending on whether N stands for alleles
> >or diploid organisms). The probability that it will exist for even
> >one generation is a function of how much the population size decreases
> >between zygote formation and reproduction. Since we have already
> >assumed that the allele is selectively neutral, if only 10% of the
> >zygotes reach reproductive age (and remember that, net, each fly that
> >lays several hundred eggs will, on average, have only two of those
> >eggs reach the egg-laying stage, so a 90% drop is not unusual -- in
> >fact, it is probably not much different than what occurs in many
> >mammals), then there is a 90% probability that that new allele will be
> >lost that first generation.
>
> Hersheyh, tell us, will a neutral allele increase in frequency by a
> “drunkard’s walk” more quickly than a beneficial allele subject to
> selection?
>
A selectively neutral allele will *drift* neutrally in frequency by a
"drunkard's walk". The probability that a *new* mutant neutral allele
will go to fixation is 1/2N (diploid organism). If the neutral allele
is initially at 50% in the population, then the probability that it
will *increase* to fixation is 0.5. The probability that it will
*decrease* to loss is also 0.5. If the neutral allele is initially at
70% in the population, the probabilty that it will *increase* to
fixation is 0.7. The probability that it will *decrease* to loss is
0.3.
And I have *repeatedly* said that selection, *when* it leads to
fixation, is much faster than neutral drift. Stop lying about what I
say, or at least learn enough to understand what I am saying.
That is not a mathematical claim. Nor is it a reply that is at all
relevant to what I just said, which was about what happens in cases of
pure chance, of selective neutrality. Am I correct in my description
above or do even understand what I just wrote.
> What selection gives is amplification of beneficial
> alleles which improves the fitness of populations to survive and
> reproduce against selection pressures.
You are becoming incoherent. The above makes no sense. Selection at
the allele level occurs *when* one allele is differentially and
significantly favored in a particular environment. But selection
actually occurs at the phenotype level and only indirectly at the
allele level, although only changes at that level have evolutionary
import.
> It is this mathematics which
> explains how to deal with the evolution of drug resistance, improve
> cancer treatments and why the theory of evolution is a mathematically
> irrational belief system.
Anyone, like you, notice the complete absence of math in response to
my math?
> This mathematics has been tested with time
> and empirical evidence. Neutral mutations do not explain the
> evolutionary process by mutation and selection.
Of course not. Neutrality only exists in the absence of a selective
difference...by definition. But neutral changes over time account for
the vast majority of the genetic differences between organisms
(especially in eucaryotes, which have much more selectively neutral
sequence). Selective changes account for an insignificant fraction of
the differences between species. And the overwhelming number of the
selective differences are in regulatory sequences, which act in a
quantitative fashion.
> And>So you think that the scientific evidence for the age of the earth and
> >life on the earth is mere "speculation"? I don't.
>
> That’s because you don’t understand the mathematics of mutation and
> selection.
That wasn't an answer to the question asked. I asked if you agreed
with the scientific evidence for the age of the earth and the amount
of time that life has existed on the earth. Whether I understand the
mathematics of mutation and selection don't matter wrt that question.
> If you did, you would understand that the number of
> generations has only a small affect on the mutation and selection
> process when compared to the multiplication rule of probabilities has
> on two beneficial mutations occurring. This is why it requires both
> many generations and a large increase in the frequency of a beneficial
> mutation before there is a reasonable probability that the second
> beneficial mutation will occur on a member with the first beneficial
> mutation. Time is a minor variable in the mutation and selection
> process. It’s the number of beneficial mutations required to adapt to
> a set of selection conditions which dominates the behavior of this
> phenomenon.
Now, I have just recently described the difference, wrt double mutants
Show your math.
> The
> way populations overcome the multiplication rule is by amplification
> of a beneficial allele and by large numbers of generations working to
> get that next beneficial mutation.
30 generations of population doubling is not a "large number of
generations" in my book. Why is it in yours?
> Remember that population size and
> the number of generations has less than an additive affect on the
> probability of the next beneficial mutation occurring at the proper
> locus.
Bull. There is a direct correlation between population size and the
predicted *number* of mutants of any particular kind. The equation is
u*2N where N is number of diploid individuals and u is the mutation
rate for that particular type of mutation per haploid genome. Ditto
for number of generations. If each generation has N individuals, then
the predicted *number* of mutants per x generations would be x*u*2N.
Where did you learn the opposite? Now that is the *predicted* number
of mutants. In actuality, the probability that there will be any
individual *without* a mutant in any given generation or set of
generations will be distributed as a Poisson distribution (which is
really the limiting case of a binomial distribution). There will
always be a small probability that any given set will have zero
cases. The Poisson distribution for zero cases is = (lambda^k*e^-
lambda)/k!. In this case k = 0, the probability that there will be no
such mutants in a given set. Lambda is the predicted frequency of the
event, which is calculated, in this case as either u*2N or x*u*2N.
You, being the math genius, can figure out the probability if u =
10^-8 and N = 5 X 10^9 and x = 30. Note that in this case I assumed a
constant population instead of an exponentially growing one. Now if
you have different equations you pulled out of yer arse or somewhere
else, this would be a good time to present them.
[snip rest for now-- it's mostly re-re-re-re-assertions that the
multiplication rule is the end all and be all of mutation and
selection.]
hersheyh
> being presented like this to prevent further fragmentation of the
> discussion. These are responses to messages 951-975
> ========================================================
>
> The multiplication rule of probabilities governs the mutation and
> selection phenomenon whether the mutations must occur simultaneously
> or not.
No it doesn't. Show your mathematical reasoning. I have given you
(several times) a description using antibiotics and bacteria (assuming
a mutation rate to resistance of 10^-8 to either antibiotic) in which
I can generate 10^9/ml double mutant bacteria in two days (60
generations), using 20 ml of media by doing the deed serially
(selecting for one mutation at a time and allowing the population to
regrow inbetween) whereas it would take 10^17 liters and roughly the
same amount of time to do the same thing by demanding simultaneity of
the mutations (selecting for simultaneous mutations to both
resistances in a single individual). You tell me how you determine
that both are equally difficult.
> If an evolutionary process requires two simultaneously
> mutations, then the evolutionary process is slowed even more.
I agree that when you require simultaneity of mutation to have any
selectable effect that such an evolutionary event is less likely. See
my math above. You, however, in just the last sentence declared that
"The multiplication rule of probabilities governs the mutation and
selection phenomenon whether the mutations must occur simultaneously
or not." If that were so, how can your last sentence ("If an
evolutionary process requires two simultaneously mutations, then the
evolutionary process is slowed even more.") be correct?
> HIV is
> not a special case of mutation and selection.
Other than that its mutation rate is especially high because it is an
RNA virus. [RNA has no repair mechanism.]
> In fact, it has every
> variable in the process working in its favor. It has large
> populations, high mutation rates, does recombination allowing for
> lateral transfer of genetic material, short generation times and can
> not be driven to extinction. Any time selection conditions target more
> than a single gene, the mutation and selection phenomenon will be
> stifled for the same reason the process is stifled when using
> combination therapy for HIV.
And I have never disagreed that *when* "selection conditions target
more than a single gene" *and* requires *simultaneous* mutation to
resistance to both agents in the same individual, that it makes double
mutation less probable. But again, you have taken what Schneider said
out-of-context. Schneider was clearly talking about the brain dead
idea that whole proteins are randomly assembled.
>> that I have to enter your world of irrational speculations. We now
> >> have evolutionist expert Mark Isaak claiming that reducing the
> >> intensity of selection accelerates the mutation and selection
> >> phenomenon.
Liar. Mark said no such thing.
> > >This mathematical blunder ranks up there with the
> >> evolutionist blunder that selection increases the diversity of
> >> populations.
> >Selection *can* increase the diversity of populations (negative
> >frequency dependent selection) measured as the number of alleles
> >existing in a population at greater than, say, 1% frequency. That
> >doesn't mean that it always does so and no one has claimed that. But
> >you have not defined what you mean by "diversity" of populations and
> >how you measure such diversity. A large population, say, of English
> >sparrows, shows diversity in size and shape, with northern populations
> >being stouter than southern populations. African populations of
> >humans show diversity in some external features from human populations
> >in northern Asia (as well as differences in blood types). Some
> >species, unlike humans, even have subspecies in different localities
> >that are distinctly different (say like the Bengal and Sumatran
> >subspecies of tiger). But I don't know how you are defining
> >"diversity" in a species. Until you tell us what you mean by
> >"diversity", it is hard to argue the point.
>
> What I mean by diversity is the number of genetic variants in a
> population. Selection always reduces the number of genetic variants in
> a population.
Selection *and* chance both reduce the *number* of genes between
zygote and breeder or render the adult less fertile in some way. But
selection is about the *frequency* of alleles in a population, not the
number. If you are in the process of having an alternate allele sweep
through the population, the *number* of genetic variants is two during
the process and one at either end (before the alternate allele
appeared and after it becomes fixed). That is, *during* the process
of evolution, the *number* of alleles is higher than at either end.
During that same process, the frequency of the two alleles changes.
In the case of a balanced polymorphism, like sickle cell, the
selective advantage of the heterozygote in malarial areas leads to
selective pressures to *maintain* a certain frequency of both the HbA
and HbS alleles in the population.
Then there are frequency-dependent alleles like plant sterility
alleles or major histocompatibility alleles where selection favors
alleles that are currently less common.
And, of course, there are selectively neutral traits that can, by
chance, be fairly common. The ABO blood type system may have some
features of this and of balanced polymorphism and frequency-dependent
selection.
> The way to increase the diversity of a population is to
> reduce the selection pressure on the population so that less fit
> variants can still reproduce and pass their genetic information to the
> next generation.
In the absence of selective pressure, the frequency of alternate
alleles is governed by chance alone. And that means a "drunkard's
walk" for any new allele with the probability that that allele will
persist to fixation being set at 1/2N. Most new alleles will quickly
become extinct. A rare few will become relatively more frequent. 1/2N
will drift to fixation. The next time you lie about this, please show
your math and the assumptions you are making. In case you don't know,
the false assumptions you are making is that you have an infinitely
large population or that mating is deterministic rather than
stochastic in nature.
> >When have I ever said differently? I agree that *when* there is no
> >selective advantage to having only one mutation and there is *only* a
> >selective advantage to an individual having two *simultaneous*
> >mutations that the multiplication rule holds.
>
> This is where you make a mathematical blunder; the multiplication rule
> always applies whether the mutations occur simultaneously or not.
A lie repeated is still a lie. Or convince me by showing your math.
> The
> way populations overcome the multiplication rule is by amplification
> of a beneficial allele and by large numbers of generations working to
> get that next beneficial mutation.
Repeating a lie does not make it true.
> Remember that population size and
> the number of generations has less than an additive affect on the
> probability of the next beneficial mutation occurring at the proper
> locus.
Repeating a lie does not make it true.
>> But natural selections are
> >> much more cooperative in your Twilight Zone world. They only target
> >> one gene at a time and they occur sequentially in a very ordered
> >> manner, kind of like sequential antimicrobial therapy which has given
> >> us multidrug resistant microbes.
As a matter of fact, that is the case in nature, as a recent article
in Science demonstrates.
http://www.the-scientist.com/news/display/58097/
The reason why these bacteria in a quasi-natural system do not
accumulate resistances is because the mutations that produce phage
resistance also often impose a cost when the environment does not
contain the phage.
> > > I guess we can call that the natural
> >> way of using antibiotics. That s good sound evolutionist training at
> >> work.
> >And, in fact, in nature, it is pretty unusual for a virus to be
> >exposed to two antivirals at once. And, as you point out, *when*
> >conditions expose the virus to one antiviral at a time, such that
> >there is a selective advantage to each step, we get both steps
> >occurring much faster than would be the case when conditions require
> >an individual to have both mutations simultaneously.
>
> But it is not unusual for the environment to cause thermal stress and
> starvation on a population simultaneously, or disease, or dehydration,
> or predation, or…
And, relative to the wild type, *variants* resistant to heat alone
have a selective advantage. Relative to the wild-type, variants able
to utilize a food source that was either unavailable or not usable
that has increased in abundance during the increase in temperature (if
no such food source is available, there is no option but to have
reduced populations, which may require greater mobility to adapt to
reduced population density, but one cannot magically poof energy
sources where there are none) will also have a selective advantage.
Selection under these conditions will select for *either* variant
relative to the w.t. That is, you will have selection for *both*
types of variants relative to the w.t. in parallel. The *frequency*
of both types of variants will *increase*. The *frequency* of both
will increase until one gets, via reproduction, individuals with
*both* types of variants. The double variant will now be favored over
individuals with only one of the variations. The size of the
population likely will have decreased during the process, but this is
not a situation where one must *necessarily* have *both* variations in
a single individual to survive unless the change is so sudden and
great that it immediately exterminates *all* the w.t. organisms from
the environment.
> And>
Carrying capacity is not selection pressure.
> It absolutely is a selection pressure. Once a population has reached a
> size that the environment can no longer support an increasing
> population, then the most fit members (efficient energy users) will
> soon dominate the population.
That would be *more* fit. Fitness is a quantitative measure and term,
not an absolute one, and certainly not an inherent feature. There is
no such thing as an idealized "most" fit. Selection is always
comparative with the available alternatives.
>> Lenski is starving his bacteria but leaving his population with an
> >> out, ie citrate.
> >No more than humans are starving because we cannot use cellulose.
> >Citrate is simply a niche that E. coli cannot utilize. There will
> >certainly be "selective competition" within the E.coli population
> >whether or not it contains any variant that can utilize citrate.
>
> And Lenski’s E coli did two things. Most of his bacteria became more
> efficient users of the glucose but one of his populations was able to
> evolve a way to metabolize the citrate and increase the carrying
> capacity of the environment. But even then, the most efficient
> metabolizers of the citrate will come to dominate the citrate
> environment as they reach the limits of their new carrying capacity in
> their environment.
>
> Of course, humans do use cellulose. We use it indirectly through
> bacteria which can catabolize cellulose into glucose through bovines
> and caprines.
Well sure. But you know that I meant direct utilization by being able
to digest cellulose ourselves. Even ruminants don't directly digest
cellulose. They rely on a host of bacteria, archae, fungi, and
protozoa to do the job. Rabbits do the same thing, double digestion,
by eating their own shit rather than their vomit (cud). Unless humans
do one of these, I cannot see them evolving cellulose digestion
mechanisms. Our caecum has tended in the opposite direction of
decreasing size because we became better hunters of meat.
> We also use cellulose for shelters, clothing and a
> myriad of other purposes. Mutation and selection is not our main mode
> of adaptation to environmental selection pressures.
Just to look at cases of evolution in humans by mutation and selection
that have occurred in the last 20,000 years or so.
Lactose-digestion into adulthood is a clear example of adaptation of
humans to environmental selection pressure by mutation and selection.
In that case, the spread of this unusual variation (most mammals
greatly reduce lactase production after weaning), a dominant variation
due to a mutation on chromosome 2, occurred in countries which have
dairies. See map here:
http://en.wikipedia.org/wiki/Lactose_intolerance
Amylase gene copy number variation is another example of mutation and
evolution in modern humans. The selective pressure was the increasing
amount of plant starch in agricultural societies.
http://www.nature.com/ng/journal/v39/n10/abs/ng2123.html
Malaria resistance. This has been a strong selective pressure in a
number of tropical regions, strong enough to allow the spread of
traits that often have deleterious disease effects in the heterozygous
state. There are a number of genetic mutations that have increased in
frequency because they provide resistance to malaria in some genotype
combinations. This includes not only HbS, but also HbC and, in Asia,
HbE, alpha-thalassemia, ovalcytosis, and favism (G6PD-deficiency).
Perhaps the clearest example is a mutation in the Duffy antigen gene
that has a prevalence of 100% in sub-Saharan Africa and is virtually
absent outside Africa, that provides resistance to P. vivax malaria.
http://www.nature.com/scitable/topicpage/natural-selection-uncovering-mechanisms-of-evolutionary-adaptation-34539
The "thrifty" gene in Pima Indian culture that now accounts for their
high susceptibility to diabetes. This is less well documented than
the previous examples.
http://diabetes.niddk.nih.gov/dm/pubs/pima/genetic/genetic.htm
http://diabetes.niddk.nih.gov/dm/pubs/pima/obesity/obesity.htm
Several genetic diseases, including cystic fibrosis have been
associated with resistance to tuberculosis. The high frequency of CF
likely arose due to selection that occurred between 1600 and 1900.
http://www.newscientist.com/article/dn10013-cystic-fibrosis-gene-protects-against-tuberculosis.html
Even earlier local biological adaptations probably also include loss
of skin melanin production as humans moved to more northern latitudes
and body size and shape. Not all of the local body adaptations might
be due to "selection". Some could be due to founder effects or other
chance events.
> If it was, we’d
> all be dead from exposure and starvation. Of course, perhaps you think
> that we might respond to a cold environment by evolving feathers.
Humans have evolved by *both* cultural adaptation *and* by the
evolutionary mechanisms of mutation and/or selection. There is no
question that the latter is a slower process, although when the
selective pressure is high enough (say TB or malaria), the spread of
resistance variants can occur relatively quickly. But the point is
that humans *have* evolved biologically as well as via culture. In
fact, our ability to adapt culturally (via dairy farming, agriculture,
and entering new areas with new diseases or problems like getting
enough vitD) has *driven* most of the above local *biological*
evolution in humans by allowing humans to enter new biological niches.
>> You obviously have not read Lenski s paper on the
> >> quantitative results of his study. Hersheyh, get a copy of this paper
> >> Genome evolution and adaptation in a long-term experiment with
> >> Escherichia coli , Vol 461, October 29, 2009, Nature.
> >I have read it, but it has been a couple of years.
>
> You had better read it again if you want to understand the basic
> science and mathematics of mutation and selection. Lenski’s
> experimental model includes many of the features of mutation and
> selection which we are talking about including neutral mutations which
> you seem bent on using to try to save your mathematically irrational
> theory of evolution.
Actually, wrt neutral mutations, my claim is quite specific. Neutral
mutation accounts for the vast bulk of the 40 million point
differences between humans and chimps and accordingly larger or
smaller amounts of the differences between other species dependent on
when they diverged from a common ancestor. And that *because* such
neutral mutations become fixed in a stochastic fashion, it is possible
to estimate the rate of such changes. That rate is slightly to much
much slower than the rate of change due to positive selection for
change. Because selection rates vary widely, it is not possible to
give selection a single expected rate of change. [The neutral rate of
change is, of course, faster than the rate of change at sites
undergoing conservative selection.] The smaller the number of
differences between human and chimp that involve *selective* change,
the less problem there is to account for such selection. And, as a
matter of fact, the number of differences that can be clearly
identified as being due to selection rather than chance in the human
lineage (HARs), is quite small (in the range of a couple of hundred
sites, most of which are in regulatory sequences). And, unlike your
false assumption that such changes must occur simultaneously in the
same individual, we have fossil evidence that some of changes in the
human lineage occurred sequentially (e.g., bipedality and cranial
capacity) and some in parallel (bipedality and more 'premature'
birth).
[snip remainder, to be dealt with later]
hersheyh
[snip material previously replied to]
>> You obviously have not read Lenski s paper on the
> >> quantitative results of his study. Hersheyh, get a copy of this paper
> >> Genome evolution and adaptation in a long-term experiment with
> >> Escherichia coli , Vol 461, October 29, 2009, Nature.
> >I have read it, but it has been a couple of years.
>
> You had better read it again if you want to understand the basic
> science and mathematics of mutation and selection. Lenski’s
> experimental model includes many of the features of mutation and
> selection which we are talking about including neutral mutations which
> you seem bent on using to try to save your mathematically irrational
> theory of evolution.
I was never trying to use my *understanding* and your *ignorance*
about neutral mutations to any purpose but to explain to you how many
differences in two species DNA sequence are a function of neutral
drift rather than positive selection for change. It is a fact that
the vast majority of DNA sequence differences between humans and
chimps are selectively neutral (not surprising given the very small
fraction, about 3%, of the human genome that seem to be involved in
sequence-relevant protein or regulation coding). The *vast* majority
of the sequence differences between humans and chimps are selectively
neutral differences that have no effect on phenotype rather than
selectively relevant differences that are part of the phenotypic
difference between humans and chimps. The numbers of DNA sequences
that can be *demonstrated* to be likely due to selection (the HARs)
number in the few hundreds rather than in the millions. That is, a
rough ratio (ignoring selective differences due to single mutations)
of selective to neutral differences between humans and chimps is about
200/40 million or roughly 0.0005% of the total. Even if there were
4000 mutations selected for, with most of those mutants involving a
single mutational event, that would still be a ratio of selective to
neutral differences of 0.01%!
>> In the adaptive
> >> phase of his study, none of the mutations in the experiment were due
> >> to drift (a crappy word to describe what populations do on a plateau
> >> of a fitness landscape).
Fitness landscapes do not describe "what populations do." They
describe the effects of different genotypes in a particular
environment.
> >Like I said, there will always be selective competition, regardless of
> >whether or not any of the variants can utilize citrate. Drift is what
> >happens when there is selective neutrality between variants.
>
> Only when his population evolved to more efficient users of glucose
> did neutral variants start showing up in the population. Only when his
> population reached a fitness plateau did neutral variants start to
> appear.
You have not read the earlier papers. The big changes in fitness due
to increased efficiency in the particular environment the bacteria
were grown in occurred within 2,000 generations and in a *stepwise*
manner with no single step being more than a 10% improvement. The
overall 70% increase in fitness (in all 12 populations)
http://myxo.css.msu.edu/lenski/pdf/2003,%20JME,%20Lenski%20et%20al.pdf
"First, the populations have improved their fitness relative to the
ancestor by about 70%, on average, during the 20,000 generations
(Cooper and Lenski 2000). Based on the step-like dynamics of
adaptation during the first 2,000 generations, no substitution
accounted for more than about a 10% improvement, and the more gradual
later gains imply more mutations of smaller effect (Lenski et al.
1991; Lenski and Travisano 1994; Gerrish and Lenski 1998). Thus, there
must be at least 10, and perhaps 20 or so, beneficial substitutions in
each population. It is not surprising, however, that sequencing less
than 0.5% of the genome would have missed these beneficial
substitutions."
The Cooper and Lenski, 2000, paper is available here:
http://myxo.css.msu.edu/lenski/pdf/2000,%20Nature,%20Cooper%20&%20Lenski.pdf
Figure 1 shows that 50% of the 70% increase in fitness occurred during
the first 5000 generations. In fact, as pointed out in the above
quote, most of this parallel evolution occurred within the first 2000
generations, meaning that if it occurred serially, the estimated
change in the ten or so genes occurred once every 200 generations.
But when one actually sequences the genes involved in these parallel
changes in all twelve lines, there were only a few cases where the
specific mutations were the same.
http://www.pnas.org/content/103/24/9107.abstract (full text
available).
http://www.genetics.org/cgi/reprint/173/4/1851
http://myxo.css.msu.edu/lenski/pdf/2003,%20PNAS,%20Cooper%20et%20al.pdf
The above papers analyze the changes in protein expression and the
specific genes involved in the changes in that expression during the
parallel phase of evolution to adapt to the specific glucose
environment before the mutation that led to the ability to use
citrate. Note that four of the lines had become mutator strains by
this time.
The majority of this 2002 article is concerned with the expectations
and observations for synonymous (hence typically selectively neutral)
and nonsynonymous mutations (possibly, but not necessarily selective).
This is all about evolution that adapts the bacteria to the particular
environment of the experiment, but does not involve the evolution of
the capacity to use citrate at this point.
Let me summarize: Initially there is parallel evolution, involving
mutations in a limited number of genes, but NOT the same identical
mutations in each mutated gene, that produce E. coli that were 70%
more efficient in using glucose (but not citrate). This had largely
all been accomplished prior to 20,000 generations and most of it
before 2,000 generations had passed. Only at around 31,500
generations did they find a Cit+ variant. As they point out, there
are two possibilities for why it took this long and, unlike the case
for the evolution of more efficient growth in glucose, this variant
was not paralleled by similar Cit+ variants in the other 11 lines.
And it was not one of the mutator lines where this occurred.
As described in
http://myxo.css.msu.edu/lenski/pdf/2008,%20PNAS,%20Blount%20et%20al.pdf
"The long-delayed and unique evolution of this function might indicate
the involvement of some extremely rare mutation. Alternately, it may
involve an ordinary mutation, but one whose physical occurrence or
phenotypic expression is contingent on prior mutations in that
population. We tested these hypotheses in experiments that
‘‘replayed’’ evolution from differ- ent points in that population’s
history. We observed no Cit mutants among 8.4 1012 ancestral
cells, nor among 9 1012 cells from 60 clones sampled in the first
15,000 generations. However, we observed a significantly greater
tendency for later clones to evolve Cit, indicating that some
potentiating mutation arose by 20,000 generations. This potentiating
change increased the muta- tion rate to Cit but did not cause
generalized hypermutability."
IOW, unlike your claim that it was the requirement that Cit+ is due to
the multiple simultaneous mutations in one individual making it an
extremely rare mutation, we see that "the evolution of this phenotype
was contingent on the particular history of that population. More
generally, we suggest that historical contingency is especially
important when it facilitates the evolution of key innovations that
are not easily evolved by gradual, cumulative selection." That is,
what happened is that this particular line had undergone exaptation
(you might want to google the term).
As the authors point out:
"We demonstrated that the evolution of this new function was
contingent on the history of the population in which it arose. In
particular, we showed that one or more earlier mutations potentiated
the evolution of this function by increasing the mutation rate to Ci+,
although even the elevated rate is much lower than a typical mutation
rate. The potentiated cells are not generally hypermutable. Rather,
their potentiation appears to be specific to the C+ function, which
suggests two possible mechanisms. One mechanism is epistasis, whereby
the functional expression of the mutation that finally yielded the Cit
+ phenotype requires interaction with one or more mutations that
evolved earlier. A second possibility is that the physical production
of the mutation that produced the Cit+ phenotype requires some
previous mutation that allows the final sequence to be generated. For
example, the insertion of a mobile genetic element creates new
sequences at its junctures, and one of these new sequences might then
undergo a mutation that generates a final sequence that could not have
occurred without the inser- tion. The E. coli genome has many
insertion-sequence elements (53), some of which have been active in
the LTEE (54–56). Whatever the mechanism, this potentiation made the
Cit+ function mutationally accessible, and a weak Cit+ variant emerged
by 31,500 generations."
Moreover, the evolution of the Cit+ strain, because it was less
efficient at glucose-utilization, produced a new population which had
both the Cit+ and Cit- strains.
As the authors point out:
"Although the Ci+ cells continued to use glucose, they did not drive
the Cit+ subpopulation extinct because the Cit- cells were superior
competitors for glucose." That is, a mutational event has produced
the ability to use citrate, but at a cost. That is not unusual.
*That* is the equivalent of a speciation event and most definitely an
increase in diversity as you define it. Whether future mutations will
lead to further specialization of the two strains with both surviving
or will produce compensatory mutations in the Cit+ strain that allow
them to compete better against the Cit- strains for glucose (there are
examples of such compensatory mutations in other cases where an
initial adaptation has some maladaptive consequences that do not
outweigh the advantage of the mutation relative to the w.t. organism)
and thus lead to the 'extinction' of the Cit- strain is as yet
undetermined. So is, AFAICT, a determination of what specific prior
changes allowed the final mutation to Cit+. That is, what was the
cause of this historically contingent event?
http://www.microbemagazine.org/images/stories/images/jan2011/znw00111000030.pdf
The above more popular article mentions an early experiment by the
Rev. William Dallinger in 1878 to test evolution. "For several years,
he grew protozoa in an incubator, gradually raising their temperature.
The organisms he used to start the experiment struggled even at 73°F,
while those at the end tolerated 158°F but were unable to grow at the
initial temperature of 60°F."
[snip rest, which is mostly repetitive assertion without evidence,
which I may try to come back to]
hersheyh
> being presented like this to prevent further fragmentation of the
> discussion. These are responses to messages 951-975
> ========================================================
>
> Only when his population evolved to more efficient users of glucose
> did neutral variants start showing up in the population. Only when his
> population reached a fitness plateau did neutral variants start to
> appear.
Again, selection is rapid and neutral drift is slow. As was pointed
out, the Lenski experiment showed that the evolution to optimal
adaptation to glucose utilization occurred within, by and large, 2,000
to 5,000 generations. By that time the populations (all 12 of them)
showed a 50% increase in fitness over the original strain. The
remaining increases in adaptation to a roughly 70% increase in fitness
were smaller in effect. But the *specific* mutations that led to
these increases, although in the same gene, were typically not the
exact same mutations.
> As I have said many times in this discussion, reducing the
> selection pressure on a population will allow an increase in diversity
> of the population.
And you have been wrong every time you said it. Repeating a falsehood
does not make it true. Reducing selection pressure will have a very
modest effect on increasing diversity (mostly in not actively removing
new mutations more quickly) and certain conditions of selection lead
to an *increase* in diversity by your own definition. Clearly during
the transition from one allele to another that is replacing it, there
will be more diversity than at either extreme. There are also
balanced polymorphisms and negative frequency selection.
>> Only when the populations evolved to improved
> >> fitness did neutral mutations appear in his populations.
> >No. Neutral mutations, beneficial mutations, and detrimental
> >mutations all occur independently of their selective advantage,
> >disadvantage, or neutrality at a rate called the "mutation rate" for
> >that particular change. There is no "waiting" until the selectively
> >advantageous mutations all occur before there are neutral mutations.
> >Mutation is not selection.
>
> Lenski’s populations where subjected to directional selection pressure
> (ie starvation).
Actually they were subjected to pressures which favored more efficient
use of glucose when shaken in an Erlenmyer flask overnight. One of
the changes that was favored was a downshifting of flagella formation,
which is energy intensive and pretty much not needed in a shaken
flask.
> During that phase of evolution, no neutral mutations
> were measurable in his population.
Because rapid evolution by selection was noted.
> Only when the population finally
> adapted to the starvation selection conditions
The original population did not die under these "starvation"
conditions (actually conditions of limited glucose). It was selection
for optimal utilization of resources in that particular environment.
> did the neutral
> mutations become measurable in the population.
Neutral mutations undergo drift and replacement of one allele with a
neutral one is a function of time alone. The rate of change at
neutral positions would not be affected by the selective conditions.
In E. coli, there are only 4.6 X 10^6 nucleotides per haploid genome
(compared to the 3 X 10^9 of the human haploid genome) and a much
smaller fraction of the bacterial genome is "junk" that has no
sequence-dependent function. Moreover, E. coli has a lower rate of
mutation per gene (about 10^-8 per gene) compared to humans (between
10^-6 and 10^-5) on average. That means that the probability of any
genome having a mutation is u*N (not 2N, because E. coli is haploid)
or 4.6 X 10^-2 (0.046; 4.6%). But the probability of fixation of a
neutral mutation is still 1/N when that mutation first appears.
> It required a reduction
> in selection pressure for these neutral mutations to occur in
> measurable quantities.
No. NO. NO. Where did you learn this nonsense, this garbage, this
misinformation? The presence or absence of selection does not affect
the mutation rate. Every generation humans get new deleterious
mutants (say achondroplastic dwarfism, a dominant allele, that has a
particularly large mutation rate, occurring in the children of normal
parents who lack the allele. That is, the fact that the allele is
deleterious (both from a health and a 'reproductive fitness'
standpoint) with a selective disadvantage of about 0.8, makes
absolutely no difference in the mutation rate -- to new cases of
achondroplastic dwarfism to non-dwarf parents. Mutation rate can be
changed only by the addition of mutagens, the loss of repair systems,
or the activation of certain kinds of repair (the SOS system of
bacteria, for example). But *mutation rate* is not affected by
whether or not the particular allele formed by mutation will be
selected for, selected against, or will be neutral. That would
require the mutagenesis event to have foresight, to "know" what kind
of environment it would appear in and then to only produce mutants
that would be appropriate for the selective conditions. I don't know
of any system of mutagenesis that can do that. Do you?
> Needless to say, no detrimental mutations were
> measured.
Understandable. Since mutations that are "detrimental" in a
particular environment will be selected against. What do you think
"detrimental" means?
>> In other
> >> words, his population is diversifying on a fitness plateau. Still,
> >> this population is limited by the amount of citrate available.
> >No. *Until* there are mutations that allow the bacteria to use
> >citrate, the availability or amount of citrate is irrelevant. The
> >population is limited by the amount of glucose available.
>
> You had better read Lenski’s papers again. Most of his populations did
> not become citrate metabolizers.
That is *exactly* my point. *Until* there were mutations that allow
the bacteria to use citrate, and it appears that that requires a pre-
adaptive event, a previous change in the population that then permits
such a phenotype, the amount or availability of citrate (under
oxygenating conditions) is irrelevant. The population is limited to
utilizing glucose. The whole point of Lenski's finding is that the
evolution of Cit+ is affected by historical restraint; that is, it can
only occur *after* mutations have made some specific changes that are
not themselves capable of making the cells Cit+, but which prepare the
cells to respond with the Cit+ phenotype after another mutation.
>> > Now, if the glucose-only bacteria were more efficient at using glucose
> >> > than the bacteria that could use both, we have a condition that could
> >> > favor "specialization" to different niches, with some bacteria
> >> > becoming specialized glucose users and others becoming more and more
> >> > reliant on citrate. I.e., speciation (and because inability to use
> >> > citrate is a key speciation-defining feature of E. coli, the new bug
> >> > would not be E. coli, but perhaps E. citrusflavoreddietcoli.
> >> I guess you haven t read any of Lenski s papers. The citrate
> >> metobolizers no longer were efficient glucose metabolizers and these
> >> citrate metabolizers were very sensitive to osmotic pressures.
It is not uncommon for a new mutation to be "beneficial" in some ways
and "detrimental" in others. Selection favors it when the
"beneficial" effects outweigh the "detrimental" ones. In this case it
is still an open question, AFAK, whether there may be secondary
mutational changes that can counter the "detrimental" effects while
retaining the "beneficial" ones. There are examples of such. Or, if
that is not possible, it could lead to stable species formation in
which the Cit-/efficient glucose bacteria get a quick start in a new
flask (like the hare) and the slower growing Cit+ bacteria, because
they can also use citrate eventually outgrow them (like the tortoise)
as the glucose gets used up. Two species from one. Each specialized
to a particular niche. Produced by mutation and selection. Where I
have heard such ideas?
> >Yet, relative to the original glucose metabolizers and at the osmotic
> >pressures that existed, they were *selectively* favored in the
> >experimental environment. Selection is always conditional to the
> >specific local environment. That the citrate metabolizers may not do
> >as well as the original strain in a *different* environment (one that
> >lacks citrate or has a different osmotic pressure) is irrelevant.
> >Evolution by selection does not select for a Neitzschean superbug. It
> >selects for the organism that is best fit in a specific local
> >environment.
>
> And 11 of 12 populations have not become citrate metabolizers. You
> have completely missed the point of the data produced by Lenski’s
> experiments.
No I didn't. You did.
> But that’s not a surprise, you’ve missed the point that
> the multiplication rule of probabilities is the dominant mathematical
> feature of the mutation and selection phenomenon and that the
> beneficial mutations do not have to occur simultaneously in order for
> the multiplication rule of probabilities to still apply.
Since those two points are lies you refuse to support with evidence, I
have not missed the point at all. I have already given mathematical
examples that show that your claims are false even when using bacteria
and antibiotics. And pointed you to papers that also demonstrate the
falsity of your ideas. Including Lenski's experiments.
> Hersheyh, how
> did you get to be so confused?
I am not the one confused. You may not be either. You may simply be
delusional or blinded by ideology or, possibly, a knowing liar or even
a troll.
[snip rest for later]
hersheyh
[snip material covered previously]
>> You really don t get it hersheyh. It took Lenski s bacteria about
> >> 32,000 generations to become citrate metabolizers.
Do you have a point? They did evolve it in a relatively small
population in a constant environment within a time frame equaling your
IQ.
> >> When you
> >> extrapolate your cases you describe above to a reptile transforming
> >> into a bird,
That would be a feathered, bipedal, toothed, tailed theropod
transforming into a feathered, bipedal, toothed, and tailed bird,
wouldn't it? Or are you purposely trying to claim that modern birds
popped directly out of a modern lizard egg like the usual stupid
creationist does?
> > > you have entered the realm of mathematical irrationality.
> >Said with the utter certainty of someone who has refused to put any
> >actual numbers down to demonstrate this "irrationality". It is easy
> >to assert that "x is mathematically irrational" if you can do so
> >without having to actually provide evidence other than your bogus
> >assertion that all the changes have to occur simultaneously in the
> >same individual.
>
> What do you want me to do, I’ve already shown what the multiplication
> rule of probabilities does with mutations with a probability of 10^-6.
> The beta lactamase example requires five mutations. That would give a
> probability of (10^-6)^5.
You seem to prefer large numbers that fail in observations of the real
world. Actually it is more like you to think that everything from a
banana to a apple is a hammer because you want something to hammer a
nail with. The evolution of the ebg gene into a functional beta
lactamase in E. coli would not be *possible* for anyone to evolve beta
lactamase from ebg if it required the simultaneous occurrence of all
five mutations in the same individual. The probability of that would
indeed be (10^-6)^5 or 10^-30. If there are 10^9 bacteria per ml at
saturation in rich media, one would require (10^9bacteria/ml*10^3ml/l)/
10^-30mutants/per unit bacteria or 10^18 l of bacteria to expect a
*mean* of a single such mutant. [Of course, there is, because of the
Poisson distribution a 32% chance that even that large a volume would
come up with zero mutants.] The oceans of the world contain 10^21
liters and are not nearly the rich media needed to sustain that
population of bacteria. So, you are proposing rich media that
represents roughly one thousandth of all the surface water on this
planet be converted to rich media. One could deal with a smaller
Erlenmyer flask if one asked for the bacteria to grow for a number of
generations. Say, 10^4 generations like Lenski has done so far in
over a decade. I will ignore how you would actually restore the
nutrients in the media. Then you would "only" need 10^14 liters which
would need to be refreshed regularly.
Yet people in laboratories have no problem getting the ebg gene to
evolve into a functional beta lactamase gene in a matter of months or
even weeks. And without using Mediterranean seas worth of media. How
can this be if your math is right? Doesn't this mean, if you really
are a scientist, that you have generated a "beautiful theory" that has
been crushed by an "ugly fact"? Reality just doesn't seem to be
agreeing with your mathematical ideas. But then you haven't actually
presented any actual math. Just wishful thinking.
> Amplification and lots of generations can
> overcome this kind of probability but it is slow and arduous process.
> Neutral mutations do not have the benefit of selection so you are
> dependent on generations alone to overcome these miniscule
> probabilities. This is why you can’t do massive genetic
> transformations by the mutation and selection phenomenon.
From the above incomprehensible garbage, it appears that you *still*
do not understand what selective neutrality means. Think of a line
labelled from -1 to +1. The -1 is lethality for an allele relative to
the allele it is being compared to, the strongest possible selection
against a trait. The +1 is the opposite, an allele which survives
while the allele it is being compared to is lethal. Neutrality is the
region near 0. Specifically neutrality is when any selective
advantage/disadvantage is less than the chance variance from
generation to generation.
> This is why
> John Harshman’s assertion of 40,000,000 differences between humans and
> chimpanzees in a million generations can not be accounted for.
Except for the minor detail that John actually showed you the math and
demonstrated that the 40 X 10^6 differences *can* be accounted for
given reasonable assumptions about population size, generation time,
and mutation rate. But you might as well lie, since lying is all you
got.
> The
> multiplication rule of probabilities obliterates the concept of
> abiogenesis and shows that the theory of evolution is a mathematically
> irrational belief system.
Assertion again. Do you even know the difference between assertion
without evidence and argument with evidence? I see no evidence that
you do.
> However, if you do understand how the
> multiplication rule of probabilities dominates the mutation and
> selection phenomenon, you can use this understanding to prevent the
> evolution of multidrug resistant bacteria, develop more durable cancer
> treatments, find safer and more rational uses of herbicides and
> prevent herbicide resistant weeds and so on. This is what
> evolutionists like you fail to understand.
Except we do and always did understand it. You are simply lying about
this and distorting the arguments of Schneider and other to do so.
>> Even if you could describe the selection pressures that would
> >> transform a reptile scale into a feather, sequentially it would take a
> >> vast number of generations.
Not necessarily. But it depends on how many generations you consider
to be "vast".
> >Which would be impossible if the earth were only 6000 years old like
> >you believe. But quite possible in the millions of years during which
> >feathers actually evolved.
>
> Generations has only a minor effect on the mutation and selection
> phenomenon.
Yet another lie. If the mutation rate is u, the effect of population
on the predicted number of mutations occurring in a population is u*2N
(for diploid organisms) per generation. That is a linear effect in my
mathematics. The equation for predicted number of mutations occurring
in a population over x generations is x*u*2N. Also a linear effect.
I can only presume that you are talking about the probability that a
given population of size 2N and mutation rate u will have no mutants,
which is based on the Poisson distribution and is equal to e^-lambda,
where lambda is the predicted mean number of mutants expected. The
probability that a population will have at least one mutant, then,
would be 1-e^-lambda. But maybe you are just pulling these phrases
out of yer arse and wouldn't know a Poisson distribution from a fish
stew. But you tell me how you can claim that the number of
"generations has only a minor effect on the mutation and selection
phenomenon." Are you generating equations different from the ones I
just gave you? Where is your math and your working assumptions?
> But you don’t understand how mutation and selection works
> so why would you know this. Use Inez’s age for the earth, a jillion
> years. Mutation and selection still can not accomplish what you claim
> in the time available because the dominant mathematical principle
> governing this phenomenon is the multiplication rule of probabilities.
Typically, when one comes up with equations that say that x cannot
happen in a jillion years and then it is pointed out that x has
actually been observed to happen and happens repeatedly in far less
time and using far smaller populations and material, the scientific
thing to do is NOT to keep right on claiming that your math is right
and reality is wrong. It is to look for the erroneous assumptions in
your math. But then you are acting like a religious nut case, not a
scientist.
[snip, I am tired and have some other things to do]
Bill
>
> - Perlihatkan teks kutipan -
You keep talking about math, but you never actually do much. How about
showing some calculations. For example, consider a starting gene with
three sites in it, A, B, and C. Let's say that the older form is
[A,B,C] and a better adapted form is [a,b,c]. Assume that the mutation
rate for A->a or B->b or C->c is 10^-6 per generation and that the
mutations occur independently.. Assume a constant population size of
10^6. You are going to calculate the (expectation value for the)
number of generations required for the population to switch from all
[A,B,C] to all [a,b,c] under two assumptions about the relative
fitness of the various possible genotypes.
The first scenario is that the relative fitnesses of [A,B,C], [a,B,C],
[A,b,C], and all the other genotypes except [a,b,c] is 1.00, and the
relative fitness of [a,b,c] is 1.05.
The second scenario is that the relative fitness of [A,B,C] is 1.00,
the relative fitness of any of the single mutants, e.g. [A,b,C], is
1.01; the relative fitness of any of the double mutants, e.g.
[A,,b,c], is 1.03; and the relative fitness of [a,b,c] is 1.05, as in
the first scenario.
If you don't know where to begin to do such a calculation you have no
business telling anybody they don't understand the mathematics of "the
mutation selection process."
John Harshman
> On Apr 1, 6:00 pm, Alan Kleinman MD PhD <klein...@sti.net> wrote:
>> This is why
>> John Harshman’s assertion of 40,000,000 differences between humans and
>> chimpanzees in a million generations can not be accounted for.
>
> Except for the minor detail that John actually showed you the math and
> demonstrated that the 40 X 10^6 differences *can* be accounted for
> given reasonable assumptions about population size, generation time,
> and mutation rate. But you might as well lie, since lying is all you
> got.
Let me remind you that population size doesn't enter into the
calculations. I don't think he's lying, though. I think he's incapable
of reading for comprehension.
hersheyh
> hersheyh wrote:
> > On Apr 1, 6:00 pm, Alan Kleinman MD PhD <klein...@sti.net> wrote:
> >> This is why
> >> John Harshman’s assertion of 40,000,000 differences between humans and
> >> chimpanzees in a million generations can not be accounted for.
>
> > Except for the minor detail that John actually showed you the math and
> > demonstrated that the 40 X 10^6 differences *can* be accounted for
> > given reasonable assumptions about population size, generation time,
> > and mutation rate. But you might as well lie, since lying is all you
> > got.
>
> Let me remind you that population size doesn't enter into the
> calculations.
My bad.
> I don't think he's lying, though. I think he's incapable
> of reading for comprehension.
Possible. But when he repeats stuff that has been *explicitly*
pointed out again and again as a misreading of what was actually said,
I think it almost better to be considered an intelligent liar (for
Jesus, of course) than a complete and thorough ignoramus so utterly
incapable of reading for comprehension. Especially when one touts his
Dr. Dr. and mathematical competence.
r norman
<hers...@yahoo.com> wrote:
>On Apr 4, 11:29 am, John Harshman <jharsh...@pacbell.net> wrote:
>> hersheyh wrote:
>> > On Apr 1, 6:00 pm, Alan Kleinman MD PhD <klein...@sti.net> wrote:
>> >> This is why
>> >> John Harshman’s assertion of 40,000,000 differences between humans and
>> >> chimpanzees in a million generations can not be accounted for.
>>
>> > Except for the minor detail that John actually showed you the math and
>> > demonstrated that the 40 X 10^6 differences *can* be accounted for
>> > given reasonable assumptions about population size, generation time,
>> > and mutation rate. But you might as well lie, since lying is all you
>> > got.
>>
>> Let me remind you that population size doesn't enter into the
>> calculations.
>
>My bad.
>
A quibble. Doesn't population size first enter but then cancel out
so, say, fixation of a neutral allele becomes independent of
population size?
John Harshman
I'm sure he thinks he's mathematically competent. We know he isn't.
Perhaps it's better to consider him as lacking in the ability to
assimilate new information. Like the French aristocracy, he forgets
nothing and learns nothing.
John Harshman
You could think of it that way. I wouldn't. But we can agree that
population size is irrelevant to neutral evolution.
r norman
To some important aspects of neutral evolution. The time to fixation
of a particular allele is quite size dependent. Indeed, the classic
discussion of drift is that it dominates in small populations and is
absent in large ones. The same for the founders effect. These are
situations describing changes in gene frequency absent mutation.
John Harshman
I presume that by "absent" you don't really mean "absent". What you
probably meant to say is that drift swamps selection if the fitness
advantage and population are small enough, and the smaller the
population, the larger the fitness advantage swamped by drift.
> The same for the founders effect.
I will agree that founder effect doesn't apply very well to large
populations. (!?)
> These are
> situations describing changes in gene frequency absent mutation.
Or even present mutation.
Steven L.
"John Harshman" <jhar...@pacbell.net> wrote in message
news:UoKdne6ekNz...@giganews.com:
I have tried to argue with devout people of faith about some issues too.
It's impossible. They seem to have been trained from childhood to
disregard or tune out any arguments that might possibly call into
question some aspect of their faith. I guess they were warned against
being swayed.
-- Steven L.
hersheyh
> being presented like this to prevent further fragmentation of the
> discussion. These are responses to messages 951-975
[snip]
>
> Oh really? You don’t think any other selection pressures on this
> population would affect the evolution of citrate metabolizers? What if
> Lenski had changed the osmotic pressure of his solution?
Why not raise the temperature to 200 C? Why not add concentrated
sulfuric acid? It is, of course, clear from the experiment that
selection (or drift) in one of the 12 strains altered that strain, but
not the others, so that a subsequent mutation generated a Cit+
phenotype. *When* that mutation, which seems rare but not, probably,
via the mechanism of requiring multiple simultaneous mutations, did
occur in *that* background it changed the population into one which is
mostly Cit+ (with some Cit- surviving each generation because they are
more efficient at using the glucose available) very quickly. See Fig.
1 in
http://myxo.css.msu.edu/lenski/pdf/2008,%20PNAS,%20Blount%20et%20al.pdf
>> > Real environments do this to
> >> populations. Real environments don t maintain constant selection
> >> conditions for long periods of time. This is why your theory of
> >> evolution is mathematically irrational.
> >Depends. Real environments can change in persistent directions.
> >E.g., Drier or wetter. Colder or warmer. If climate
> >...
>
> But real environments have nothing like the stability created in
> Lenski’s laboratory. And that’s what is required for the mutation and
> selection phenomenon to work well.
No. As the Dallinger experiment of the late 1870s, which involved
gradually raising the temperature in protozoa showed
http://www.microbemagazine.org/images/stories/images/jan2011/znw00111000030.pdf
it is quite possible to change the ability of the organism to a
gradually changing environment with the organism becoming so well
adapted to the final environment that they no longer can grow in the
original environment. Similar such evolutionary changes have been
seen a number of times with a number of different organisms. In
bacteria, it is possible to evolve strains that only grow well in the
presence of an antibiotic that would have killed the original strain.
> And>> > > Don t confuse recombination and selection with mutation and selection.
> >> > > This is a very common blunder on the part of evolutionists.
> >> > Rather it is a common blunder of creationists who somehow think that
> >> > selection doesn't involve the selection of existing variation, but
> >> > only involves selection for non-existant variation that selection
> >> > somehow *causes* to occur. *All* selection requires the pre-existence
> >> > of actual variants. In all cases the selected variant phenotypes
> >> > already exist in a population of organisms.
> >> Oh really, did I make that claim?
> >Yes, you did. You said one could not look at the selection of
> >variants that already exist in a population because that is
> >recombination and selection. My point remains. Selection always
> >involves selection among variants that actually do exist in a
> >population. Selection does not generate hypothetical solutions that
> >might work.
>
> I’ve never made that claim.
No. You specifically said that selection among variants that already
exist in a population is not the mutation and selection process, but
is instead is recombination and selection. It certainly is
'selection', but it ain't recombination. And the source of *all*
genetic variation, both that which currently exist in a population and
that which are acquired later is still mutation. So it is still
mutation and selection. But selection can still only act on the
variation that actually exists in a population, not on possible future
mutations.
> What I have said is that selection reduces
> the diversity of populations and that mutations increase the diversity
> of populations.
Mutation certainly increases the diversity of populations. But
whether selection or drift leads to a decrease or increase in
diversity is a matter of the nature of the selection and the
environmental conditions (for selection) or chance (for drift). As
has been pointed out to you repeatedly. Some alleles are selected for
because they are rare. These are frequency-dependent selection. As a
consequence, diversity of alleles in that gene is increased.
> What directional selection pressures do is set a
> direction for evolution of the population based on finding the fittest
> replicators. Selection tests mutations in order for a population to
> try to find a solution which does work.
Selection actually tests *phenotypes* relative to each other on the
metric of net reproductive fitness. To the extent that the difference
in phenotype is heritable, *if* there is a significant difference on
the metric of net reproductive fitness, that environment selects for
the genotype or combination of genotypes that is more fit on that
metric. There is no requirement that the previous genotype be one
that "doesn't work" and only the new mutation be one that "does
work". That is absolutist nonsense. All that is required is an
improvement in net reproductive success. Lenski's E. coli, before the
Cit+ phenotype arose, grew perfectly well each generation. It is just
that those with the Cit+ phenotype, because they were able to utilize
a previously unavailable source of energy, were, on net, *more* fit
from the Cit+ phenotype than they were *less* fit in their use of the
glucose.
> You in your contradictory
> world of evolutionism claim that feathers are a hypothetical solution
> for reptiles in order to keep them warm.
So, undoubtedly, was hair (also made of keratin) when that evolved in
a "more reptile-like ancestor". The reason for thinking that the
earliest feathers found so far were used for warmth is because that is
*still* a common use for certain feathers (or haven't you heard of
'down'?) and the earliest feathers found in fossils were more like
downy feathers than flight feathers. IOW, the available *evidence*
(Ever hear of evidence? Scientists us that term a lot. It prevents
them from choosing a mathematical model that is in conflict with
observable reality, as you do when you claim that, regardless of
whether change must occur simultaneously in a single individual, or
could occur sequentially or in parallel is irrelevant to the necessity
of the use of the multiplication of probability rules.) points to the
first feathers being used for warmth rather than flight.
> But now you are claiming that
> selection does not generate hypothetical solutions.
It doesn't generate hypothetical solutions. Downy feathers are a real
solution that really did occur first in the history of history of
birds (actually in the preceding theropod dinosaurs). These feathers
occurred first on non-flying therapod dinosaurs. Flight feathers did
not occur until later. But "feathers" also occurred prior to the
evolution of such modern bird traits as beaks rather than teeth,
pygostyles instead of tails, and after the evolution of such modern
bird traits as bipedality. That is what the fossil record shows, not
some hypothetical end (teleological) goal predictable from knowledge
of avian ancestors. And the fossil record is also consistent with the
sequence record: living reptiles (specifically crocodilians) are the
closest living relative to modern birds.
> I really wish you
> evolutionists could make up your minds.
We have. Mutation does not generate hypothetical solutions only when
they are needed. Mutation produces genetic variants at a rate that is
independent of the environmental need for that mutation. Selection
can only work on phenotypes that actually exist in a population at the
time of selection. Selection does not cause a needed mutation to
occur.
> On the other hand, I do claim
> that selection tests hypothetical solutions for the solution of
> environmental stressors on a population.
Can you present *any* evidence for this assertion? The idea that
mutation produces variants only when they are needed has been well and
often tested ever since the Luria-Delbruck experiments of the mid
1940s, almost 70 years ago, and has come up a cropper. Do you even
know who Luria and Delbruck are?
> Selection pressures define
> evolutionary direction but the process must occur quickly enough for
> the mutation and selection process to work without driving the
> population to extinction.
Of course. But that is only a problem for idiots who think that there
is no existing variation in natural populations, no evolution without
massive death during selection, and the necessity that all evolution
involves the requirement for simultaneous multiple mutation to
different resistances to killing agents in a single individual. Can
you think of any such idiots?
> >> I really would like to see your
> >> breeding program where you take a population of reptiles and transform
> >> them into a population of birds. That would really be something. Are
> >> you now claiming that reptiles transformed into birds without mutation
> >> and selection?
> >Mutation first, to generate variation. Selection only among the
> >variants that actually did occur and did exist.
>
> Ok, now you are talking turkey (but that turkey didn’t evolve from a
> reptile). The selection conditions of the environment determine which
> variants are fit enough to reproduce.
And, to the extent that individual variations that already exist have
independent fitnesses, selection will increase all of those variants
in a population relative to their alternatives. In parallel. It is
only when the individual variations do not have any increased fitness
independent of another variations that you have the conditions
requiring the multiplication rule.
> Then a change in selection
> determines which variants survive and form the basis population for
> the mutation and selection phenomenon to find a new fitness optimum
> (unless you want to claim that every variant possible exists in a
> population, 4^G becomes a huge number very quickly).
No, I do not claim that every variant possible must exist in a given
population at the same time. But if the variations have *independent*
increased fitness, one can select them one after the other. And,
because fitness is also affected by past historical decisions,
variations that would have had low, zero, or even negative fitness
before a specific variant had established itself because of its
independent fitness advantage, would now be selectable. There are
many mutants that can be called "enhancer of" or "suppressor of" some
beneficial or deleterious phenotype that has one effect that is
positive, but others that are negative. What this means is that the
future evolution of an organism is dependent on or constrained by the
characteristics that already exist in the organism. That is,
evolution works via *pathways* rather than by *massive changes*. Brain-
dead creationists often demand that evolution must demonstrate a moden
bird emerging from a modern lizard egg or at least that one must be
able to generate a modern bird from a modern lizard via a program of
artificial selection. You don't know of any creationist who is that
ignorant of what evolution actually proposes, do you?
> >> Do you think that the citrate metabolizers were just
> >> variants of the glucose metabolizers and they already existed in
> >> Lenski s experiment?
> >In fact, the citrate metabolizers are indeed nothing but variants
> >derived from and by mutations of genes that existed in the glucose
> >metabolizers. But there was no selection for citrate metabolizing
> >traits until they, by mutation, actually existed in the population.
>
> Once again, ok. But now you open up a whole new can of worms for the
> concept of evolutionism. What happened long ago in the evolutionist
> fairy land when those traits did not exist in your primordial
> replicator?
Ever hear of duplication and divergence? As well as chimeric gene
formation? Point mutations are not the only mechanism by which
evolution is proposed. In fact, chimeric gene formation is probably
responsible for most new functions. Duplication and divergence is
*clearly* an important mechanism as well. Why do you propose that
genes involved in cascades are often so sequence similar? Ditto for
genes in gene families, like the various globins?
> In your settled science of evolutionism, how did this
> transformation from non-replicator chemistry without selection form
> all this function for the replicators to act upon by mutation and
> selection? Did the original replicators “drift” into being?
Abiogenesis is certainly an ongoing area of study, but is not
*biological evolution*, which already assumes the existence of
"life" (which, for this purpose, can be defined as a system that can
extract energy and/or materials from its environment and use that to
replicate a genetic system). And *chemical* selection in favor of
*chemical* replication is still selection.
> >Are you claiming that the citrate metabolizers somehow came into
> >existence by the magical poofing of entirely unknown genes into
> >existence? That would indeed be a surprise.
>
> Not a surprise at all. You have a set of functioning enzymes which can
> transport and metabolize a carbohydrate. A few mutations in enzymes
> already capable of operating on these chemicals and the enzymes have
> the correct conformation to metabolize a different carbohydrate.
Which is exactly what evolution proposes. In the case of citrate in
the Lenski experiment, there had to be some very specific initial
changes in the genome (by chance drift or selection for optimal
fitness to the specific environment) to allow some subsequent mutation
to produce sufficient ability to use citrate to provide a selective
advantage. This earlier exaptation mutation would have to be a change
that only occurred in one of the 12 lineages, but that could be as
simple as a specific point mutation in a gene that was different from
the chance point mutations that altered that gene in the other
lineages in ways that also produced a similar beneficial effect to the
mutation in the one lineage where that change allowed subsequent
mutation(s) to produce a significantly Cit+ individual.
> You
> evolutionists are the ones that claim that all these genes came about
> by abiogenesis.
No. Evolution claims that nearly all the genes in modern organisms
came about by modification of previously existing genes. In fact, the
very existence of gene families supports that idea. [Think
duplication and divergence or chimeric events.] It is creationists
who demand that the genes be made *independently* in different species
and in the same organism in one swell foop from scratch.
> That’s one of the silliest concepts to hit science
> since the flat earth concept. You evolutionists find this plausible
> despite all the mathematical and scientific evidence. You aren’t doing
> much better with the mutation and selection phenomenon.
The problem with your creationist idea of an abiogenesis that involves
magically poofing every gene in every species of organism that ever
existed from nothing instantaneously is that that idea *does* indeed
require the multiplication rule of probability. Ideas that involve
duplication and divergence (as in the blood globins), OTOH, do not
require that each gene be magically poofed from nothing all at the
same time. And I use the word "magic" to describe it, since no known
intelligent agent can do what is claimed by creationists and no known
natural mechanism, even one used by known intelligent agents, can do
it either. Evolution does not involve the "magic" production of the
entire of the biological world, past and present, in instantaneous
poofs of magic. That is precisely because change in DNA and protein
sequences by duplication and divergence is not an instantaneous or
simultaneous assembly event.
>> > > Recombination and selection is a selection process done on the basis
> >> > > of already existing traits, it is a form of inbreeding. Mutation and
> >> > > selection requires the evolution of new traits.
> >See that above. You are explicitly saying that selection for existing
> >traits is not evolution. Only selection for non-existing traits is
> >evolution. Mutation, of course, does not *generate* new traits; it
> >modifies old ones (some mutations producing larger modifications than
> >others). Sometimes such mutations produce new (but often related)
> >*functions* in the process. But most evolution is of quantitative
> >features of organisms (e.g., size of braincase, shape of foot) in
> >which there are always variants in most populations rather than the
> >invention of new metabolic processes. For example, nearly all the
> >differences between humans and chimp skeletons represent such
> >quantitative modifications (the one exception is the complete loss of
> >the already greatly reduced baculum in humans).
>
> You are really squirming here. What I am saying is the mutation and
> selection phenomenon is an extremely slow process for adapting to a
> changing environment.
And it often is. Just not as slow as you need/want it to be. I have
described mathematically how serial selection for double mutants to
antibiotic resistance can take place either in a couple of days (less
than 100 generations) in small volumes of media with relatively few
organisms or how, when conditions are made to require simultaneous
acquisition of the mutations in a single individual, the same double
mutants would either require truly massive populations or would
require, on average, very long time frames until the double mutant
would show up. Using exactly the same individual mutation rates to
resistance. You ignored that mathematical description and simply
repeated your assertion about the multiplication rule.
> And the reason the phenomenon is extremely slow
> is the multiplication rule of probabilities. Now you can try what ever
> semantic argument you like but the mathematical principles are the
> truly explicit principle which we are describing here. I understand
> that you are having trouble seeing this concept unless the mutations
> must occur simultaneously but none the less, the multiplication rule
> of probabilities dominates the mutation and selection phenomenon.
Except for the fact that that idea has been refuted by the evidence
that there are conditions in which the change can be quite rapid and
the fact that many of the features you claim could not possibly have
evolved did. For example, the optimization of Lenski's bacteria to
their growth conditions in glucose (a 70% increase in fitness) took
about 20,000 generations, with most of that change in fitness
occurring in the first 2000 generations. It was estimated that this
selection involved changes in roughly 10 genes as indicated by the
genes which changed. By your calculation, assuming that each of the
10 changes involved a single point mutation, if the mutation rate to
positive selective change was 10^-6 (probably higher than the real
rate) per gene, then the probability of all ten mutations occurring
simultaneously would be (10^6)^10 or 10^-600 (10^6 is ten with 600
zeros after it). The probability that such a 10 gene simultaneous
mutation would happen in a population of 10^9 bacteria (high in this
case) over 10,000 generations (long for most of the effect) would be
10^9*(2 X 10^4)*10^-600 = 2 X 10^-587. IOW, according to your
calculations, the 70% increase in fitness was impossible. Since that
increase in fitness actually happened, there *must* be a problem with
your assumptions. Yet here you are continually asserting that it
isn't your assumptions that are wrong; it is reality that is wrong.
[snip]
Alan Kleinman MD PhD
threads of March 15
========================================================
Mark Isaak
>> So let's go through step by step where Steve is incorrect with his half
>> computation. First of all, if a physician is really clever, you don't
>> want to take your population from a state of 1:1:5:1:1=> 1:1:0:1:1.
>To quote someone even cleverer than you, You can't always get what you
>want.
In this case, you don’t have to be clever; you simply have to
understand how mutation and selection works. And you won’t get the
proper understanding of this phenomenon from an evolutionist. This is
why we have the problem of multidrug resistant microbes,
multiherbicide resistant weeds, less than durable cancer treatments
and so on.
>> A really clever physician wants to take the population to a state of
>> 1:1:5:1:1=> 0:0:0:0:0. But since evolutionist training is more likely
>> to give Steve's case, let's complete his computation. The first mistake
>> Steve makes is that he assumes that the 1:1:0:1:1 state is the final
>> state of the system. It is actually simply an intermediary state due to
>> a new selection condition being applied to the population. And as any
>> physicist with knowledge and experience with the second law of
>> thermodynamics would know that any particular intermediary state can
>> have greater, lesser or equal entropy because entropy is not
>> conservative.
>Steve's assumption is, albeit in simplified form, entirely plausible;
>the state he calls final has as much right to be called final as any;
>and any physicist with knowledge and experience knows that the second law
>of thermodynamics does not give a damn whether or not a state is called
>intermediate.
The only absolute final state in the mutation and selection phenomenon
is extinction; otherwise populations continually try to improve
fitness. Steve presented a contrived example of selection and from his
contrived example I have demonstrated how selection actually works in
reality. There are more sophisticated models of mutation and selection
which demonstrate more rigorously what I’ve shown here.
>But I think I see your underlying problem now. When the world does not
>give the answers you want, you think the *world* is wrong. You are
>simply upset that everybody does not treat you as a God.
Mark, if you want to believe in the mathematically irrational theory
of evolution that is your prerogative. But it is not your prerogative
to misrepresent how the mutation and selection phenomenon actually
works. You are harming people who are suffering from diseases subject
to the mutation and selection phenomenon.
>> So let's see if we can complete Steve's computation
>> and demonstrate what real populations do. [...]
>Sorry, Steve already did that and showed that you are wrong. You give
>gods a bad name.
I doubt Steve knows very much about the mutation and selection
phenomenon but he does know something about entropy. Did you notice
that he is not defending his contrived example?
>> I've notice these responses and I dismiss them because the use of the
>> word "drift" does not properly describe what a population does when it
>> reaches a plateau on a fitness landscape. Populations diversify when
>> they reach these plateaus, they do not drift. I don't have to accept
>> sloppy evolutionist terminology any more than I have to accept sloppy
>> evolutionist speculations.
>And you, being God, get to dictate what technical terms are used in all
>specialized fields. Right?
Scientific terminology should adapt as more is known about how a
particular physical phenomenon works.
>Do you also reject chemical textbooks that use the sloppy terminology
>"atom", because the name means "uncuttable" but atoms can be split? I'm
>guessing you do; it would explain a lot.
An atom is the smallest component of a chemical element still having
the properties of that element. It doesn’t mean that an atom is
“uncuttable”. It just means that if you cut an atom, it will no longer
have the properties of the original chemical element. Mark, your
arguments about the theory of evolution are so weak and mathematically
irrational; you have to resort to splitting hairs in order to make any
point. Hey Mark, if you split a hair…
========================================================
Frank F. Smith
>> Did I ignore Steve s scenario?
>It certainly looked like it from here.
You need to take another look. I took Steve’s contrived example and
used it to show how selection actually works.
>> Or did Steve simply demonstrate his
>> misunderstanding of the mutation and selection phenomenon? I think it
>> was the second.
>I will give your opinion all of the consideration it deserves, based on
>my observations of your other posts.
We are not interested in opinions. We are interested in mathematical
and empirical facts. Evolutionists have been giving us their ill
conceived opinions for decades and we have multidrug resistant
microbes, multiherbicide resistant weeds and less than durable cancer
treatments to thank evolutionists for their ill conceived opinions.
>> Let s remind Steve and others with some understanding
>> of the second law of thermodynamics that entropy is not a conservative
>> property of a system. So let s review Steve s half computation.
>Of course diversity is not conserved. Has anyone suggested otherwise?
Neither entropy nor diversity are conservative properties. Now you are
starting to learn something about the mathematics of mutation and
selection. In fact, with respects to the mutation and selection
phenomenon, diversity and entropy are equivalent.
>> So let s go through step by step where Steve is incorrect with his
>> half computation. First of all, if a physician is really clever, you
>> don t want to take your population from a state of 1:1:5:1:1=>
>> 1:1:0:1:1. A really clever physician wants to take the population to a
>> state of 1:1:5:1:1=> 0:0:0:0:0.
>Fascinating. I never realized that clever physicians want to exterminate
>all life.
Now you are being silly Frank. However, if you have an infection and
don’t want to drive that bacterial agent causing that infection to
extinction, just follow evolutionist doctrine and you will have your
wish with a multidrug resistant infection.
>In case that's too obscure: note that Dr Carlip has not identified any
>particular species or population. It could be any population of any
>species. So your last comment amounts to "For any population of any
>species, a really clever physician wants to take the population to 0."
When you are dealing with an infection, the goal is to drive the
infecting agent to extinction. Why do you think there is still so much
work being done with HIV? That residual infection remains an ongoing
threat.
>> The
>> first mistake Steve makes is that he assumes that the 1:1:0:1:1 state
>> is the final state of the system. It is actually simply an
>> intermediary state due to a new selection condition being applied to
>> the population. And as any physicist with knowledge and experience
>> with the second law of thermodynamics would know that any particular
>> intermediary state can have greater, lesser or equal entropy because
>> entropy is not conservative. So let s see if we can complete Steve s
>> computation and demonstrate what real populations do. Let s say
>> variant B is the new most fit member of the population under Steve s
>> model.
>Why would one say that? You have added an additional assumption, an
>additional selection criterion not contained in Dr Carlip's model.
Steve’s assumption that a population reaches a final state is
incorrect. The only absolute final state in the mutation and selection
phenomenon is extinction. Otherwise populations continually try to
improve fitness.
>On the contrary, looking at the model he presented:
>"Now suppose that initially all of these variants occur, but C is
>somewhat more fit, so the initial ratio is 1:1:5:1:1."
>Note that the other four variants are present at equal proportions. So C
>is initially more fit than the other variants, but it is reasonable to
>conclude that {A, B, D, E} all have identical relative fitnesses.
>The only change in selection conditions is "the most widespread variant,
>C, cannot survive". That is, variant C and only variant C is targeted by
>the new selection conditions. There is no reason to _presume_ that the
>relative fitnesses of the other variants has changed.
Fitness always changes when populations change. The loss of variant C
opens up a niche for other variants to fill. Since Steve chose to talk
about bacterial infections, I related his example to what I have
observed with Staph infections. Removal of non-drug resistant strains
of these bacteria from the gene pool has been replaced with drug
resistant strains thanks to the failure of evolutionists to properly
describe the mutation and selection phenomenon. Frank, perhaps you
want to form the Society for Prevention of Cruelty to Bacteria for my
desire to drive these infectious agents to extinction in my patients.
The failure to drive these infectious agents to extinction has led to
multidrug resistant forms of bacteria.
>If instead we accept the conditions described, we are left with four
>variants that are selectively neutral under the current selection
>conditions. And as far as selection is concerned, 1:1:0:1:1 _IS_ the
>final state.
These simple examples are only correct if they properly describe
reality. Steve needs to do a more thorough analysis of his simple
examples before he presents them as examples of reality.
>The rest of your post is therefore irrelevant to Dr Carlip's example.
It is if you want to use Steve’s simple example as a demonstration of
what happens in reality.
>However, let's entertain the distinctly different selection regime that
>you propose.
> [edited]
> describes] in which one remaining variant is selectively favored over
> the other three.
>> At generation 1, we have the intermediary[sic] state [that Steve
>> 1:1:5:1:1=> 1:1:0:1:1
>> After some generations with selection we get the intermediary state:
>> 1:1:0:1:1=> 1:2:0:1:1
>> After more generations pass with selection we get the intermediary
>> state:
>> 1:2:0:1:1=> 1:3:0:1:1
>> After more generations pass with selection we get the intermediary
>> state:
>> 1:3:0:1:1=> 1:4:0:1:1
>> After more generations pass with selection we get the intermediary
>> state:
>> 1:4:0:1:1=> 1:5:0:1:1
>> After more generations pass with selection we get the adapted state:
>> 1:5:0:1:1=> 1:6:0:1:1
>Congratulations. You have described selection conditions that decrease
>the Shannon diversity index. Of course, I do not think anyone has argued
>that selection _never_ decreases diversity.
Frank, what you need to understand is that selection pressures either
kill or impair members of the population from passing on their genetic
information to future generations. This always decreases the diversity
of the gene pool. Only by mutation can you increase the diversity of
the gene pool. Now if you want to consider only the number of
variants, Steve’s example started with five variants and after
selection only had four variants. If you want to claim that is a more
diverse population after application of his selection condition, then
let’s see you defend that position. If you are trying to argue that
the quantum mechanical definition of the second law of thermodynamics
is not the correct equation for computing the diversity of a
population then Steve and you have made a point with his peculiar
example. However, there are many evolutionists who have embraced this
equation for describing the increase in information content in the
genetic code by selection. And selection conditions are simply
ordering rules for genetic codes. On the other hand, mutations are a
disordering phenomenon for genetic codes.
>However, showing that _some_ selection conditions decrease diversity
>does little to support your claim that _all_ selection conditions do so
>-- especially given how _trivially easy_ it is to describe a
>counterexample of selection that increases diversity.
So, you claim that five variants before selection and four variants
after selection represents a more diverse population? You
evolutionists have a strange way of describing increasing diversity in
populations. Do you claim that three variants represent a more diverse
population than four variants?
><snip remainder as irrelevant>
So now you claim that “One variant is the most diverse population you
can have”.
And
>Just a quick addendum, FWIW.
>I have noticed than AK's responses are typically delayed about three
>weeks from the post to which he is (nominally) responding. By the time
>he gets around to responding to my prior post, if ever, _my_ post will
>have expired from the NNTP server I'm using.
>Since I have concluded some time ago that he has nothing new or
>interesting to say, I do not read all (or even most) of his posts. I
>might well miss a response from him to _my_ post once that's no longer
>on my server.
>Hence the lack of further response from me should not be construed as
>anything other than failure to notice his response.
>Not that it matters.
>On 3/17/2011 7:56 PM, Frank F. Smith wrote:
><snip it all!>
Sorry I don’t respond more quickly but I’m responding to dozens of
other posters as well.
========================================================
John Harshman
>> I have read his text and I have extensive discussions with Schneider
>> about his model which I think is a good simulation of mutation and
>> selection.
>If the discussions are anything like the ones you have here, you are
>incapable of learning anything from them.
What I did is perform the study that Schneider suggested in the
original publication of his model. This study demonstrated what you
should now understand on how population size affect the probability of
a beneficial mutation occurs at a particular locus. What his model
does in that circumstance is accelerate the mutation and selection
phenomenon when you double small populations but as you keep doubling
population size, the rate of evolution asymptotically approaches a
rate which does not increase significantly with the doubling of
population size. His model also demonstrates that mutation rate has
only a small effect on the mutation and selection phenomenon. The
genome length has a significant effect on ability of his model to
evolve his selection conditions. If the genome length becomes too
long, his model will not converge. But by far, the dominant variable
in his model is the complexity of his selection conditions. His model
contains three selection conditions. If you set any two of the three
selection conditions to zero, the remaining selection condition can
sort and optimize very quickly, even on realistic length genomes. This
is the exact same behavior that HIV demonstrates with single drug
therapy vs combination therapy. Make the selection conditions simple
and the population has a reasonable chance that it can do the sorting
and optimization process by mutation and selection. Make the sorting
conditions complex and the process only works well on trivially short
genomes.
>> What Schneider is saying in his text is that amplification
>> of a beneficial allele is the way populations overcome the
>> multiplication rule of probabilities. The multiplication rule still
>> applies to biological evolution. This is why when evolutionists like
>> hersheyh claim that neutral mutations are important in the
>> evolutionary process, he neglects the fact that the multiplication
>> rule still applies. Schneider is wrong and he should either take his
>> claim off his web site or rephrase his claim. He knows that when he
>> does, his titanic theory of evolution hits the gigantic multiplication
>> rule of probabilities iceberg and the theory of evolution sinks into
>> the primordial soup.
>You have yet to explain any mechanism for why this "multiplication rule"
>should apply in any case other than when two mutations must happen
>simultaneously in one individual for an allele to be selectively
>advantageous.
John, you are still having a difficult time understanding what a
population must do in order for two mutations to end up on a single
member. There are two basic mechanisms available to a population in
order for two mutations to end up occurring on a single member of the
population. One mechanism if for that member and its descendents with
the first mutation to be able to reproduce over and until one of the
descendents is able to get that second beneficial mutation. Now if it
happens that the first mutation is beneficial and improves fitness of
that member, then the frequency of that variant will increase in the
population giving more and more descendents with that first beneficial
mutation and improving the probability that one of these descendents
will get the second mutation. If that first mutation is a neutral
mutation, you do not have selection available to increase the
frequency of that particular mutation. If the probability of the
second mutation occurring is let’s say one in a million, in a million
generations you will get one of those descendents finally getting the
second mutation. That’s why amplification is so important in the
mutation and selection phenomenon. Increasing the frequency of the
first mutation in the sequence over hundreds of generations gives many
more descendents who are candidates for the second mutation in the
sequence. Anything which disrupts this amplification process forces
that member with the first mutation in the sequence to go many, many
more generations before there is a reasonable probability that the
second mutation will occur. This is why combination therapy works for
HIV and in every other circumstance where it is tried.
>> Because if you keep doubling your population size and the probability
>> for that beneficial mutation occurring at a particular locus keeps
>> doubling, you will at some point have a probability greater than 1.
>You really can't read. Note that I'm talking about "expected number of
>mutations", not "probability of one mutation".
John, do you want me to quote you verbatim? You know what you said and
you were incorrect in a fundamental mathematical principle of the
mutation and selection phenomenon.
>> The probability for this event can get extremely close to 1 but it
>> will never have a probability of 1. There is always a small
>> probability that a particular mutation will not occur at a particular
>> locus no matter how large the population is. The effect of population
>> size on the mutation and selection phenomenon has less than an
>> additive effect on the phenomenon.
>That depends on whether multiple, identical mutations increase the
>probability of fixation. And of course they do. In the neutral case, the
>effect is exactly linear.
John, fixation is not a random process. Fixation occurs when you have
a more fit member in the population who is a better replicator than
other members of the population. Because that member and its
descendents are more fit replicators based on the selection
conditions, the number of descendents of that more fit replicator
increases over the generations.
>>>> In addition, John does not seem to recognize that
>>>> population size itself is a selection pressure. As population size
>>>> increases, the amount of resources available from a given environment
>>>> to the population becomes a limiting factor for survival and
>>>> reproduction, thus becoming a selection pressure on the population,
>>>> that selection pressure is called starvation.
>>> How is all that relevant to the occurrence of mutation?
>> As population size increases, at some point the population will reach
>> the carrying capacity of the environment. At that point, the most fit
>> reproducers and their alleles will start increasing in frequency.
>No, they will do that before the population reaches carrying capacity,
>though what's "most fit" may change as carrying capacity is neared.
John, as a population reaches the carrying capacity of the
environment, the less fit replicators will reduce in frequency because
the more fit replicators are more efficient users of the resources of
the environment.
>> Any
>> of the less fit members of the population who able to survive and
>> reproduce when there was excess resources in the environment will
>> reduce in frequency because of less availability of resources.
>> Increasing the size of populations in and of itself increase the
>> selection pressure on the population reducing the diversity of the
>> gene pool.
>Only if there is a fixed carrying capacity, which you have not specified.
There are always limits in an environment. There are limits on water
availability, light, food and so on. In Lenski’s experiment, his
environment was glucose limited until one of his strains became
citrate metabolizers. Lenski has to continually replenish glucose for
his bacteria so that they won’t starve out. Still, the most efficient
glucose metabolizers took over the environment in all his other cases.
>> Simply post an example of selection which increases the diversity of a
>> population.
>I have mentioned the major histocompatibility complex. That should do.
Your loosely mentioning something is not posting a real measurable
example.
>> I�ve notice these responses and I dismiss them because the use of the
>> word �drift� does not properly describe what a population does when it
>> reaches a plateau on a fitness landscape.
>So you're hung up on a single word? And for this you ignore a
>half-century (or more) of work in the field you claim to invalidate?
I don’t like the word “drift” because it doesn’t properly describe
what populations do on a fitness plateau. I can’t help the missteps
evolutionists have taken over the last 50 years. If evolutionists
hadn’t ignored what Edward Tatum said more than 50 years ago, perhaps
so many people would not have wasted so much time on a mathematically
irrational belief system.
>> Populations diversify when
>> they reach these plateaus, they do not drift. I don�t have to accept
>> sloppy evolutionist terminology any more than I have to accept sloppy
>> evolutionist speculations. You evolutionists have already bungled the
>> basic science and mathematics of mutation and selection. You have
>> already demonstrated that you don�t understand how the multiplication
>> rule of probabilities dominates this phenomenon. Why should I accept
>> your sloppy misinterpretation of what a population does on a plateau
>> of a fitness landscape?
>I know you don't actually read what I write, but I'll try again: drift
>doesn't apply to populations; it applies to alleles.
Certainly I read what you write. Tell me how you can separate alleles
from the population.
>>>> 5. Then we have r norman s blunder when he said the following: What
>>>> is being ignored is the possibility that two mutations can happen
>>>> quite separately but then assembled together by recombination
>>>> (bacterial or sexual). What r norman does not explain to us why his
>>>> claim does not work for HIV since HIV does recombination yet this
>>>> virus can not assemble two beneficial mutations together and overcome
>>>> combination therapy. What r norman does not realize is that the
>>>> shuffling of existing alleles has little effect on the creation of new
>>>> alleles. This is simply another example of the numerous mathematical
>>>> and scientific blunders that evolutionists make due to their obsession
>>>> that reptiles turn into birds by mutation and selection.
>>> That was so garbled as to be painful. Your HIV case is one in which no
>>> single mutation has a selective advantage, the only such advantage
>>> accruing to individuals with several necessary mutations. In that case,
>>> your "multiplication rule" applies. But that case is unusual. Generally
>>> single mutations are individually advantageous.
>> Are you sure this is an unusual case?
>Yes.
It’s very easy to find other examples of mutation and selection which
behave identically to the HIV case. I’ve already posted examples of
the treatment of malaria, examples from the field of oncology; I’ve
even posted an example of bacteria which produce multiple toxins to
mosquito larvae. You had better reconsider your answer since this is
how mutation and selection actually works.
>> Do you think it is very rare
>> that combination selection pressures suppress the mutation and
>> selection phenomenon?
>Yes, whatever you mean by that.
What I mean by that is the substitution of a more beneficial allele
for a less beneficial allele. After all, that is the unit process of
evolution.
And
>> John, let�s say that our population lives happily on this really huge
>> plateau on the fitness landscape with an infinite carrying capacity.
>> The population will continue to diversify until all variants on that
>> plateau are represented in the population distribution. As soon as you
>> introduce any kind of selection, you are removing some of those
>> variants from the distribution. Perhaps you believe that on the top of
>> Mt Everest, there is a gigantic plateau where all kinds of variants
>> live happily together. Most selection pressures prevent divergence.
>> Lenski�s experiment demonstrates that nicely.
>No it doesn't. You consistently misinterpret Lenski. And your first
>problem is your assumption of an infinite population. There is no such
>thing. In any finite population, drift will produce an equilibrium
>diversity, even without selection, and some sorts of selection will
>increase diversity above that equilibrium level.
So then are you now claiming that no new neutral mutations will occur?
========================================================
Inez
>> Are you sure this is an unusual case? Do you think it is very rare
>> that combination selection pressures suppress the mutation and
>> selection phenomenon? How about you post a single real, measurable and
>> repeatable example of mutation and selection where combination
>> selection pressures don t suppress the mutation and selection
>> phenomenon?
>Since you're so fond of HIV and drug resistance, how about single drug
>therapy and HIV?
HIV can very easily evolve resistance to single drug therapy. The
virus can do this in about a week. The amplification process for a
beneficial allele works very efficiently in this simple selective
environment.
>Here's another one, I think:
http://www.google.com/url?sa=D&q=http://www.annualreviews.org/doi/abs/10.1146/annurev.genet.37.110801.143820
>The ability of adults to digest lactose is apparently mostly linked to
>a single nucleotide change (it looks like there may be more
>complications, but the paywall came down on me).
The inability to digest milk can very easily be a selection pressure
where starvation is acting on a population. Dairy products are an
important food source for human populations.
>> Aside from the example of HIV, I ve posted examples from
>> the field of oncology, parasitology, and from bacteriology, all which
>> show that combination selection pressures suppress the mutation and
>> selection phenomenon. Why don t you put some mathematical and
>> empirical examples where your evolutionists speculations are?
>No one disagrees with that part, and you need to move past it. The
>actual point of disagreement is whether or not most selective
>pressures require multiple mutations to get any sort of benefit at
>all. Just having an example of an artificial selective environment
>that requires multiple mutations does nothing to show that such a
>situation is standard in nature, and all you have besides that is
>personal incredulity.
Why would I want to move past the way mutation and selection actually
works? The multiplication rule of probabilities is the dominant
governing mathematical principle of this phenomenon. Understanding
this principle gives the proper logical understanding of how to
prevent drug resistant microbes, herbicide resistant weeds and more
durable cancer treatments. Why would you want to move beyond that
other than it shows the theory of evolution to be a mathematically
irrational belief system?
And
>> > You seem not to have noticed any responses to this claim either. Have
>> > you ever read anything by Motoo Kimura, or for that matter any
>> > population genetics text?
>> I ve notice these responses and I dismiss them because the use of the
>> word drift does not properly describe what a population does when it
>> reaches a plateau on a fitness landscape. Populations diversify when
>> they reach these plateaus, they do not drift.
><snip>
>Really?
Yes, really.
>Let's say that you live on your own private island and have 4 breeding
>pairs of hamsters, with each pair having a different version of a gene
> (A, B, C and D). These genes have the same amino acids but different
>nucleotides, so no selective difference exists between them.
>Later in the day on which you purchased your hamsters you are killed
>by the exploding head of a tea-partier when Obama raises the top
>marginal rate by 0.1%, but your body is frozen cryogenically. A
>thousand years later you are revived and return to your island, which
>is now replete with hamsters. Using an ap on your futuristic Iphone
>you sequence all the hamsters genomes. What do you expect to find?
>An exact 25/25/25/25 distribution of the genes? What if I told you
>that right after you were frozen one of the hamster pairs was eaten by
>a snake while canoodling by your ficus? Would that throw your
>projection off, or would the hamsters be magically protected by your
>invincible mathematics? Would each breeding pair have to have litters
>of exactly the same size to protect the status quo? Do explain how
>drift doesn't happen.
Obama has said that he believes in the theory of evolution. I guess
that says something about his skills as a mathematician.
Now if your hamster pair had stuck with their caboodle and had some
stroodle they might not have ended up in an animal shaped like a
noodle.
Sounds like that snake did not allow your population to diversify. But
what does predation have to do with the theory of evolution?
========================================================
hersheyh
>> I have read his text and I have extensive discussions with Schneider
>> about his model which I think is a good simulation of mutation and
>> selection. What Schneider is saying in his text is that amplification
>> of a beneficial allele is the way populations overcome the
>> multiplication rule of probabilities.
>No he doesn't. He claims that most evolution that has happened does
>not involve the requisite conditions needed to require the
>multiplication rule, specifically in the context of arguing against
>the brain-dead idea that new functions arise by assembling a protein
>sequence all at once (the 747 in a tornado idea) from individual amino
>acids.
How could you get this so wrong? Any evolutionary process which
requires more than a single beneficial mutation to adapt to the
selection pressure will always be subject to the multiplication rule
of probabilities. This is a mathematical and empirical fact of life
you evolutionists can’t come to grips with.
>BTW, stop saying "amplification" of a beneficial allele. It shows
>your unfamilarity with the subject. We use the phrase "spread of the
>beneficial allele in the population". Again, this is because there is
>no necessary connection between population size and selection between
>alternate alleles, but there is a connection between selection and the
>relative frequency of the alleles. An alternate allele can spread
>throughout a population regardless of whether that population is
>decreased in size (as it is in the use of antivirals against HIV), or
>the population increases in size (as it does in the Lenski
>experiment), or the population remains constant or fluctuates for
>unrelated reasons.
I picked up the terminology “amplification” from Schneider and I
believe that he uses the terminology properly. What Schneider does not
do properly is his claim that the multiplication rule does not apply
to biological evolution when that rule is central to understanding the
behavior of the mutation and selection phenomenon. “Amplification” is
much easier to write than “spread of the beneficial allele in the
population” so when ever you see me use the term “amplification” you
will now know what I am talking about. I’m familiar enough with the
subject to know that the multiplication rule of probabilities is the
dominant mathematical feature of the mutation and selection
phenomenon. Now for once, I do believe you are correct when you state
that there is no direct correlation between population size and
selection between alternate alleles. The relevant variables with
regards to selection are the initial frequency of the beneficial
allele and the intensity of selection for each variant allele.
>> The multiplication rule still
>> applies to biological evolution.
>Only under conditions where there must be multiple *simultaneous*
>mutations in a single individual to have any selective impact.
You are wrong hersheyh. The mutations do not have to occur
simultaneously in order for the multiplication rule to still apply.
The only condition required for the multiplication rule of
probabilities to apply to the mutation and selection phenomenon is
that more than a single beneficial mutation is required for adaptation
to a selection condition. If the beneficial mutations don’t have to
occur simultaneously, they occur in a beneficial mutation/
amplification of beneficial mutation cycle in order to accumulate the
beneficial mutations on a single member because that’s the only way a
population can overcome the multiplication rule of probabilities. If
an evolutionary process requires two beneficial mutations
simultaneously, this disrupts the amplification process and this
occurs when more than a single gene is targeted by selection pressures
simultaneously. The amplification process does not work efficiently
when two or more alleles must be amplified simultaneously as
demonstrated by HIV when combination therapy is used.
>> This is why when evolutionists like
>> hersheyh claim that neutral mutations are important in the
>> evolutionary process, he neglects the fact that the multiplication
>> rule still applies.
>Not for selectively neutral variants. If the variants are selectively
>neutral, the spread of one allele in the population is always
>independent of the spread of the other. That is, unlike the
>conditions you need, where both variants must be present to have any
>selective benefit, since there is no selective benefit the alleles
>will either get lost or fixed solely by chance. What I claimed is
>that most of the allele *differences* (but not most of the
>phenotypically important *differences*) between species is due to
>random drift and fixation of selectively neutral variants. That is
>what analysis of sequence differences in humans and chimps, for
>example, points out -- that *most* of the sequence differences are not
>selective differences, but selectively neutral differences.
The mathematical problem with your claim is that there at least
40,000,000 differences between human and chimpanzee genomes by John
Harshman’s estimate. For example, John claims that the two amino acid
differences between human and chimpanzee preproinsulin are simply
neutral substitutions. If that were the case, we should find both
these variants in both populations. In addition, for this case, it
would require the fixation of dozens of alleles every generation in
both life forms. Why would dozens of neutral mutations fix in the
population every generation? You don’t have the benefit of selection
to force the spread of an allele. You need to read Lenski’s papers
where he and his co-authors describe how they determine which of his
measured mutations are neutral or not. Your mathematics and your
understanding of mutation and selection are irrational.
>> Schneider is wrong and he should either take his
>> claim off his web site or rephrase his claim.
>He is quite correct for the argument he *actually* makes. Evolution
>does not produce new protein functions from scratch by a process of
>randomly assembling nucleotides into a new gene. It does so by
>modifying pre-existing genes or duplicates (or chimeric duplicates) of
>pre-existing genes. In case you have somehow forgotten what Schneider
>was really arguing about in the paragraph that starts with the
>sentence "The multiplication rule does not apply to biological
>evolution.", it can be found below:
>"A common error in the non-scientific literature and poorly written
>papers is to assume that probabilities multiply for computing
>components of living things such as proteins. A typical argument notes
>that proteins are about 300 amino acids long and that there are 20
>different kinds of amino acids. If such a string were to be generated
>using independent selection of the amino acids, then the probability
>of generating any particular string is 20-300, a very small number
>indeed. While this may be true for random strings, it does not
>directly apply to proteins found in living organisms."
>My only comment is that by writing "The multiplication rule does not
>apply to biological evolution." Schneider opened himself up to some
>brain-dead idiot who did not read (or understand) the following few
>sentences from coming up with an example in evolution where the
>multiplication rule does hold, such as in multidrug treatment of HIV.
>Or perhaps that brain-dead idiot is using the same type of Biblical
>scholarship where a single comment stripped out of context can be used
>to declare that eating shellfish is an abomination or that drinking
>poison or handling poisonous snakes is fine if you really believed.
>In context, what Schneider is talking about is the common creationist
>argument about how they think new protein functions arise -- not by
>mutation and modification of pre-existing proteins but by simultaneous
>assembly by chance in a single individual.
It’s the brain dead evolutionists who are giving us dead people with
your gross misinterpretation of how mutation and selection actually
works. You can try to twist Schneider blunder any way you want but if
you are too mathematically incompetent to understand that the
multiplication rule of probabilities is the central governing
mathematical principle of the mutation and selection phenomenon, then
evolutionism should become a DSM-IV diagnosis.
>> He knows that when he
>> does, his titanic theory of evolution hits the gigantic multiplication
>> rule of probabilities iceberg and the theory of evolution sinks into
>> the primordial soup.
>So do you also think that the "probability" of a new protein function
>can be calculated by counting the number of nucleotides in the gene
> (n) and taking 4 to nth power? That would be the probability if that
>gene were created completely at random from a supply of nucleotides in
>a single step.
Hersheyh, you are really having trouble with this mathematics.
Actually, the only thing which distinguishes the mathematics of
abiogenesis (which shows this concept to be dumb to the nth power) and
the mathematics of the theory of evolution is selection (which shows
this concept to be just dumb). What selection does to random mutations
is give populations some mathematical leverage in limited cases to
overcome the multiplication rule of probabilities. Populations do this
by amplification of a beneficial allele and by using generations to
improve the probability of the next beneficial mutation occurring at
the proper locus. When you remove selection from the equation, you
have nothing more than the mathematics of abiogenesis a dumb to the
nth power concept. This is why Schneider is wrong with his claim that
the multiplication rule of probabilities does not apply to biological
evolution. The multiplication rule of probabilities is central to
understanding how and why mutation and selection does what it does.
>> > > 2. Then we John Harshman s claim about the probability of a particular
>> > > mutation occurring at a particular locus is proportional to population
>> > > size. Here is John s exact wording: Not true. If we're talking about
>> > > a given mutation, the probability of it happening is directly
>> > > proportional to population size. This is a mathematical and
>> > > scientific blunder. If John properly works out the mathematics for
>> > > this problem, he will find that doubling the population does not
>> > > double the probability that given mutation will occur at a given
>> > > locus. This probability for this event does not obey the additive rule
>> > > for probabilities.
>*******Please note that although John did incorrectly use the word
>"probability" rather than "number" if the "exact wording" you use
>above is correct, below he makes clear that he was talking about the
>*expected mean number* of mutants in a population of given size. That
>*expected mean number* of mutants is indeed calculated as 2nu and is
>indeed a linear function of population size.****
You evolutionists are as loose and sloppy with your grammar as you are
with your mathematics. The governing mathematical principles for the
mutation and selection phenomenon are given by probability theory.
Until you evolutionists recognize this, you will continue to make
irrational claims about how mutation and selection works. Hersheyh,
perhaps you should make a career out of spinning the blunders of
evolutionists so that they don’t appear so mathematically incompetent.
But wait, you have your own blunder to deal with. That is you claim “I
agree that *when* there is no
selective advantage to having only one mutation and there is *only* a
selective advantage to an individual having two *simultaneous*
mutations that the multiplication rule holds.” This is a mathematical
and scientific blunder. The multiplication rule of probabilities
applies to every circumstance of mutation and selection where more
than a single beneficial mutation is required to adapt to the
selection conditions. And because of this requirement, every
beneficial mutation must be amplified at a each step of the
evolutionary process before the next beneficial mutation has a
reasonable probability of occurring at the proper locus. This is why
the mutation and selection process is so slow and arduous as
demonstrated by Lenski’s experimental model. The process becomes
markedly slower when more than a single beneficial allele must be
amplified simultaneously.
>> > How so? If the gene population is 2N, and the mutation rate for that
>> > particular mutation is u, then why isn't the expected number of
>> > mutations of that type in that population not equal to 2Nu?
>> Because if you keep doubling your population size and the probability
>> for that beneficial mutation occurring at a particular locus keeps
>> doubling, you will at some point have a probability greater than 1.
>*****NOTE: John correctly was talking about the expected *number* just
>above your response to it. You apparently ignored his description of
>what he meant.****
Your expectations are not what govern the mathematical behavior of the
mutation and selection phenomenon. It is probability theory. Your
evolutionist indoctrinations have given you a set of expectations that
do not coincide with the actual behavior of the mutation and selection
phenomenon.
>If the mutation *rate* from A to G in a particular gene is 10^-8 and
>the population size is 10^9, then the probability that that population
>will have examples of that particular mutation approaches 1. That is
>because we *expect* 10 mutants in a population of that size given that
>rate of mutation. Ten is the mean expectation for number of mutants
>given that mutation rate and population size -- in actuality, the real
>numbers observed would be distributed as a Poisson distribution
>meaning that, although the mean expectation is 10, there is a small
>probability of a population having none, making the probability of
>finding any mutant in the population only very slightly less than a
>certainty. If the population size were 10^7, then the probability of
>a population that size having that mutation is 0.1, meaning that only
>one population in ten of that size would have a mutant.
Hersheyh, your calculation is wrong. You still don’t understand how to
do the computation of the probability of a beneficial mutation
occurring at a particular locus. I believe I can show you the proper
way to compute the probability that a particular mutation will occur
at a particular locus. You do the calculation as follows:
n -- is the population size
m -- the probability that in one organism in one generation, a
mutation will affect a specific locus in the genome
divide by four
m/4 -- the probability that in one organism in one generation, a
mutation will turn a specific locus into a specific nucleotide other
than the one it already is -- for instance, turn G, C, or T into A.
subtract that result from 1
1-(m/4) -- the probability that in one organism in one generation, the
specific mutation in question will NOT occur
raise that result to the power of n
(1-(m/4))^n -- the probability that in the entire population in one
generation, the specific mutation will NOT occur in ANY individual.
Then by the complementation rule of probabilities P(E) = 1 – P(Ec)
where P(E) is the probability that the specific mutation will occur at
a particular locus in one generation and P(Ec) is the probability that
a specific mutation will NOT occur at a particular locus. Then:
P(E) = 1 – ((1-(m/4))^n)
And for your case, m = 10^-8 and n = 10^7 and P(E) = 1 – ((1-((10^-8)/
4))^10^7) = 0.02469, not your value of 0.1.
The reason you have to do the computation in this manner is that you
are confusing mutually exclusive events (additive events) with
complementary events.
Consider a simpler example. Get a bunch of fair six-sided dice each
representing one individual. Say that any time a die rolls a 1, the
specific mutation in question has occurred in that individual. The
probability of the mutation not occurring for one die is 5/6. The
probability of the mutation not occurring anywhere in a roll of four
dice is (5/6)^4, or .482253.
It might appear correct to instead apply the additive rule to the
complement events, like this: "The probability of a die rolling a 1 is
1/6. Therefore the probability of rolling at least one 1 in a roll of
four dice is 1/6+1/6+1/6+1/6 = 2/3 (additive rule), and therefore the
probability of not rolling any 1s in a roll of four dice is 1/3." But
it's not. Try it. (One hint that that reasoning is incorrect is,
suppose you're rolling 7 dice. Is the probability of rolling at least
one 1 then 1/6+1/6+1/6+1/6+1/6+1/6+1/6 = 7/6? Having a probability
come out less than zero or greater than one is a sure sign of
incorrect application of the rules.) The additive rule only applies if
the individual events are mutually exclusive -- and rolling a 1 on one
die is not mutually exclusive with rolling a 1 on a different die.
You could do a similar analysis for how the number of generations
affects the probability that a beneficial mutation will occur at a
particular locus. If you assume that the additive rule applies, ie
that doubling the number of generations will double the probability
that a beneficial mutation will occur at a particular locus then at
some point your doubling of the number of generations will give you a
probability greater than one. Likewise for mutation rates, doubling
the mutation rate does not double the probability that a beneficial
mutation will occur at a particular locus because at some point,
continual doubling of the mutation will give you a probability greater
than one. The random mutation and natural selection phenomenon is a
complex probability problem with many variables. It is difficult to
recognize which events are mutually exclusive and which events are
complementary but with careful analysis, you can sort out how each
variable affects the probabilities involved. Clearly when we are
talking about random mutations which are independent events, the axiom
of probability which governs this event is the multiplication rule of
probabilities. The event does not have to occur on a single member in
a single generation simultaneously for the multiplication rule to
apply. In order for populations to have reasonable probabilities of
two beneficial mutations to occur (not simultaneously), the population
must amplify the first mutation over many generations. Anything which
disrupts that amplification process (such as forcing the population to
amplify two alleles simultaneously) causes the mutation and selection
phenomenon to break down.
>It was quite clear that John was talking about the expected *mean
>number* of mutant individuals in a population of given size. That
>*number* is calculated as 2Nu and is, thus, a *linear* function of N.
>The *probability* that a population of size 2N will have at least one
>mutant is calculated as 1-e^-m, where m is the mean expected number of
>mutants in a population of that size. The actual equation is a bit
>more complicated, but because 0! and m^0 are both = 1, I left them
>out. e is the base of the natural logarithm. When the mean expected
>number of mutants is 1 in populations of a given size, the probability
>that any given population of that size will have at least one mutant
>is 63%. When the mean expected number of mutants is 10 for a
>population, the probability that any given population will have at
>least one mutant is 99.995%.
Both you and John need to do some serious rethinking on your
computations. Expectations do not govern the behavior of the mutation
and selection phenomenon, probability theory does. Once you understand
how probability theory affects the mutation and selection phenomenon,
it will become quite clear how populations adapt by mutation and
selection and why combination selection pressures do what they do and
why sequences of single targeted selection pressures are so slow and
arduous. On one hand you will understand how prevent multidrug
resistant microbes, multiherbicide resistant weeds, and to develop
more durable cancer treatments. On the other hand, you will realize
that theory of evolution by mutation and selection is mathematically
irrational.
>> John, let s say that our population lives happily on this really huge
>> plateau on the fitness landscape with an infinite carrying capacity.
>No population of organisms lives in a perpetual state of infinite
>carrying capacity. Read Malthus or any ecologist since that time.
>Real populations always produce more offspring than can be
>indefinitely sustained, thus if there were an infinite carrying
>capacity (at least in terms of food resources -- nothing will prevent
>continued selection against genetic diseases and genetic infertility),
>you would have a continually increasing population. In the real
>world, states and times where resources are significantly greater than
>carrying capacity of a population of organisms are always transitory.
>The *best* that can happen is that ultimately a population reaches
>sustainability, where numbers and necessary renewable resources are in
>an equilibrium. Such a state *requires* that, in net, each generation
>only produces enough offspring such that there is just replacement of
>the breeders. For most organisms that requires producing tens to
>thousands of zygotes because of losses from all sorts of factors, both
>causal and chance. At *worst* the population overshoots and overuses
>the needed resources or overexploits a non-renewable resource, leading
>to a population crash and possibly even extinction (local or
>universal). In the *real* world, there are always constraints and
>selection and chance events occurring.
Of course there is no such thing as an infinite carrying capacity.
That’s why carrying capacity ultimately ends up being a selection
pressure on the population.
>Besides, the fitness landscape is one where we are comparing alleles,
>not populations.
The fitness landscape defines the trajectories available to the
population for improving fitness. Those trajectories require the
population to take a path of increasing fitness because each new
beneficial allele generated by a mutation must be amplified over
hundreds of generations before there is a reasonable probability that
the next beneficial mutation can occur.
>The situation you are assuming is equivalent to assuming an imaginary
>heaven where there is no death or need for resources because its
>organisms are ethereal souls who need nothing. You certainly can make
>such an assumption, but finding evidence for such a case on the earth
>will be hard. While you are at it, you can always "posit a ladder."
Nope hersheyh, we are talking about what happens here on earth and how
mutation and selection actually works.
>Even *if* you had a population that magically had infinite (or
>perpetually expanding) food resources, that would not prevent
>selection from occurring. It would merely shift the selection
>pressures toward those organisms with greater fertility or greater
>ability to generate offspring without defects that make them less able
>to use the food (e.g., Tay Sachs).
You don’t need to convince me that there are no infinite food
resources. But you do need to understand that the multiplication rule
of probabilities is the dominant mathematical principle of the
mutation and selection phenomenon.
>> The population will continue to diversify until all variants on that
>> plateau are represented in the population distribution.
>In reality, as I keep pointing out, under conditions of selective
>neutrality (which you are mistakenly calling 'infinite carrying
>capacity') any *new* allele will have only a 1/2N (N = number of
>diploid organisms in the population) chance of becoming fixed in the
>population. It will have a 1-(1/2N) chance of being lost. Given that
>N is typically a large number, the chances that a new selectively
>neutral allele will be lost is much greater than that it will go to
>fixation. What will NOT happen in any population that is not infinite
> (last I looked, that is all of them) and certainly not in any
>population with a stable population size is that, once such a mutant
>occurs, it will remain at that level in perpetuity. In a rapidly
>expanding population, the chance of retention of a new variant is
>greater, but no real population expands indefinitely.
How many times will you evolutionists miss the point?
>BTW, did you notice that I gave you some *real* math? The probability
>of fixation versus the probability of loss of a new allele. Those
>equations differ from your imaginary idea that new alleles are always
>perpetuated in perpetuity at some level after they occur. For your
>imaginary math to work, you would have to assume an infinite
>population and/or the idea that chance has a memory (the idea, one
>that has ruined many a gambler, that because you had a run of bad/good
>luck, that will somehow affect your next roll of the dice).
I think you better recheck your math and see whether it connects with
reality. Do you think your math will account for 40,000,000
differences between humans and chimpanzees according to John
Harshman’s numbers, that’s dozens of fixations per generation for
hundreds of thousands of generations?
>> As soon as you
>> introduce any kind of selection, you are removing some of those
>> variants from the distribution. Perhaps you believe that on the top of
>> Mt Everest, there is a gigantic plateau where all kinds of variants
>> live happily together.
>Actually, that seems to be what *you* think is happening in your
>imaginary landscape. I think that selectively neutral variants will
>undergo a random "drunkard's walk" with most of them eventually
>walking into the 0% ditch right near where they start as a % of the
>population (all new selectively neutral alleles start as a mutation at
>a frequency of 1/2N), but with 1/2N of them eventually stumbling into
>the '100%' ditch (actually, because mutation always produces new
>variants, complete and permanent fixation is not really possible;
>complete loss of a specific historical allele is possible, although
>some types of mutations recur). At any given time there will be
>typically 1 w.t. selectively neutral allele and a smattering of other
>selectively neutral alleles, but with some genes having, by chance
>alone, 2 (or more rarely more) common selectively neutral alleles with
>a smattering of other selectively neutral alleles. Not surprisingly,
>that is what is observed for selective neutrality.
Do you think your selective neutrality will account for dozens of
fixations every generation? You really need a better understanding of
the rules of probability which govern the mutation and selection
phenomenon. And no rule has the mathematical impact that the
multiplication rule of probability has which is the principle
governing factor in the mutation and selection phenomenon.
>> John, let s say that our population lives happily on this really huge
>> plateau on the fitness landscape with an infinite carrying capacity.
>Fitness landscapes are a way of visualizing the relationship between
>genotypes (or phenotypes) and reproductive success. There is no
>"population" living on a fitness landscape. And fitness landscapes
>have nothing to do with carrying capacity. Sites on the landscape
>represent genotypes (or phenotypes) and the surrounding sites around
>any point represent "similar" or "minimally variant" genotypes/
>phenotypes. The height of individual genotypes/phenotypes is a
>measure of the reproductive success of that genotype/phenotype
>relative to other genotypes/phenotypes surrounding it.
Every possible genotype represents a point on the fitness landscape
where the height of the point represents the relative fitness on that
genotype. The shape of the fitness landscape is determined by the
selection conditions and since carrying capacity represents the
ability of the environment to support the population, by its very
nature is a selection condition.
>Population mean genotypes move blindly on the surface from site to
>site stepwise following a few simple rules. If a change in genotype/
>phenotype (site on the surface) is higher than the current site, the
>new site is favored to the extent that it can be reached from the
>current site easily (that is, if mutation rate to that new site is a
>reasonable occurrence). If a change in an position is neutral (same
>height), movement of the mean genotype to that site is purely a matter
>of chance. If a change in position involves a drop in height, such a
>move is disfavored.
Good for you. You are now starting to understand something about
fitness landscapes except you are misusing terminology when you say
“mutation rate to that new site is a reasonable occurrence”.
>NONE of this tells us anything about the diversity of variants in a
>population or the rate of movement from site to site of mean genotypes/
>phenotypes when you are talking about selective neutrality. For that,
>you need to read about population genetics when there is no selective
>advantage. I have described that. For a new selectively neutral
>allele or mutation, the probability that it will go to extinction is 1-
> (1/2N), where N is the number of organisms in the population. Most
>selectively neutral mutations will go to extinction. A rare few
>selectively neutral mutations will randomly increase in frequency to
>significant levels in a population. And at a frequency of 1/2N, a new
>selectively neutral mutation will go to "fixation", replacing the
>original selectively neutral allele.
What you can say about the diversity of a population is that you can
increase the diversity by reducing the selection pressure. Reducing
the selection pressure on a population allows for less fit variants to
survive and reproduce increasing the diversity of the population.
>> The population will continue to diversify until all variants on that
>> plateau are represented in the population distribution. As soon as you
>> introduce any kind of selection, you are removing some of those
>> variants from the distribution. Perhaps you believe that on the top of
>> Mt Everest, there is a gigantic plateau where all kinds of variants
>> live happily together. Most selection pressures prevent divergence.
>> Lenski s experiment demonstrates that nicely.
>Lenski's experiment demonstrates that genotypes change and can even
>change significantly to produce novel biochemistry.
I’m not so sure you can claim that Lenski’s experiment is
demonstrating the production of novel biochemistry. What his
experiment demonstrates is that existing enzymes for transport and
metabolizing of the carbohydrate glucose can be modified for the
transport and metabolizing of the carbohydrate citrate. Regardless,
this modification process took tens of thousands of generations to
produce the small number of mutations necessary to carry out this
biological transformation. The reason it took tens of thousands of
generations is that the multiplication rule of probabilities required
that the population amplify each beneficial mutation over hundreds of
generations so that there was a reasonable probability that the next
beneficial mutation could occur at the proper locus. That’s the lesson
that Lenski’s experiment has to teach on the basic science and
mathematics of the mutation and selection phenomenon. If Lenski had
imposed additional selection pressure on his population, the process
would have gone much, much slower. That’s the lesson that combination
therapy for the treatment of HIV has to teach on the basic science and
mathematics of the mutation and selection phenomenon.
========================================================
John Astin
>This is a wrong assumption. Selection doesn't prevent divergence,
>though it can facilitate it given a combination of selection pressures
>in the environment.
>Are you still stuck on the "single gene selection" idea you were using
>before? I would hope you'd moved well past that by now, given how
>unrealistic it actually is.
Stabilizing selection does prevent divergence and most selection
pressures are stabilizing. Directional selection pressures will shift
the optimal phenotype.
The reality is that when more than a single gene is being selected
simultaneously, the ability of the population to amplify those
multiple alleles are markedly impaired. That’s why combination therapy
works for the treatment of HIV and combination therapy suppress the
mutation and selection process on every real measurable and repeatable
example of mutation and selection.
Alan Kleinman MD PhD
========================================================
Stuart
>> As long as evolutionists use terminology like drift to describe what
>> happens to populations on a plateau of a fitness landscape rather than
>> describing what actually happens, ie the population is diversifying,
>> they will continue to make the same blunders over and over.
>The genetic changes that occur as a result of fixation via drift
>greatly exceed those due to
>fixation becuase of selection. This is a simple statement of fact.
Very interesting Stuart, do you care to explain to us why this is a
fact? We wouldn’t want people to start believing that you are fixated
on fixation; we would have to fix that.
>Mutations occur at whatever rate they occur regardless of whether the
>population is
>at a peak, a plateau, in a valley or somewhere in between. Hence
>changes resulting from drift
>dwarf those from selection regardless.
So, now we no longer have the theory of evolution by mutation and
selection, it is now the theory of evolution by drift. Everything is
on one big happy plateau. There are no longer detrimental mutations
only reptiles drifting to birds.
>Its pretty clear now, that nothing will penetrate your self-worship
>and ego.
>You're a waste of alphabet soup and time.
Isn’t it the primordial alphabet soup and time which created life? How
could alphabet soup ever be a waste of time? Sometimes I feel like I’m
adrift on the alphabet soup of life. Hey Stuart, don’t you think
that’s a good way to describe the field of biology as it is presented
by evolutionists?
And
>> Wrong Stuart, survival of the fittest is a restatement of the first
>> law of thermodynamics. Members of the population which are the most
>> efficient at using the available energy in the environment can use
>> more energy for reproduction. Survival of the fittest is all about
>> efficiency.
>I don't use terms like *Survival of the Fittest". Try and read a book
>on evolution
>written in the 20th century or later.
So what is your theory of evolution supported by now, *Survival of the
Driftiest*?
>All that is required is differentail reproductive propensity. And to
>accomplish that,
>all an individual needs is a higher differential reproductive
>propensity than its cohorts.
So it is the *draftiest* that has the highest differential
reproductive propensity. Keep going Stuart; you are making some sense
here with way your letters are drifting in your alphabet soup.
>You are a waste of time. In one ear and at the other.
We haven’t even finished the alphabet soup. Don’t you even want to
consider the salad? Lettuce stop and think about this for a moment.
>> > Your challenge is to explain why feathered dinos existed, even though
>> > it is obvious that some, at least, never flew.
>> > But first, will you ever explain why birds have the genetic apparatus
>> > for making teeth,
>> > if they didn't evolve from dinos?
>> > Why do you not answer questions put to you?
>> If you put forth a question about the mutation and selection
>> phenomenon, I will attempt to answer it because it has importance to
>> the practice of medicine and it defines what this phenomenon can do.
>Your intellectual cowardice noted.
Now you are really taking a bite out of my argument, perhaps I’m just
trying to egg you on.
========================================================
r norman
>>The more selection conditions imposed on a population, the fewer
>>genetic variants are available with the fitness to reproduce.
>>Disruptive selection just allows a few more variants to survive and
>>reproduce than a simple directional selection pressure but either way,
>>the number of variants remaining after the selection process is
>>completed is fewer than before the selection process was imposed.
>Perhaps you fail to understand that some selection conditions select
>for more variability in the population. Perhaps you fail to realize
>that all measures of diversity including the Shannon informational
>definition which you systematicallly and stupidly continue to refer to
>as the "quantum mechanical" notion involves not simply the number of
>variants but the probability distribution among those variants and
>certain kinds of selection can alter the probability distribution to
>INcrease the diversity. Disruptive selection is one such process.
>Negative frequency dependent selection is another. You refuse to
>consider there cases because you are so pigheadedly convinced of the
>rectitude of your position.
r norman, it is you who fail to understand a fundamental principle of
selection which is that selection conditions always reduce the
diversity of populations. Selection removes variants from gene pools.
Now if you want to claim that if a population can adapt to selection
pressures and reach a plateau on the fitness landscape that more
variants with neutral mutations will appear, then you will start to
have an understanding how mutation and selection works.
Disruptive selection is only a special case of directional selection.
With disruptive selection, more than a single variant has fitness to
reproduce against the new selection conditions. Still, all the other
from the population are being killed or impaired from reproducing
reducing the diversity of the population by removing these variants
from the gene pool. Actually most real selection pressures are
disruptive.
Shannon Information is directly analogous to the quantum mechanical
definition of the second law of thermodynamics. If you want to see the
derivation of Shannon’s equation from the quantum mechanical
definition of the second law of thermodynamics, get the text
“Equilibrium Statistical Mechanics” by Andrews. He devotes an entire
chapter to the derivation of Shannon’s equation from the quantum
mechanical definition of the second law of thermodynamics.
Another lesson you need to learn from the basic science and
mathematics of mutation and selection is that the multiplication rule
of probabilities is the dominant mathematical principle governing the
behavior of the mutation and selection phenomenon. That is, the
probability of two beneficial mutations occurring on one member of a
population is equal to the product of the probability of the
individual probabilities. Everything done by a population to get this
event to occur (if it can occur) by selection is driven by this
mathematical principle.
And
>>Now the engineers I worked with in the aerospace industry had a
>>saying, put a big enough engine on anything and you can make it fly.
>>The problem for the theory of evolution is that the mutation and
>>selection phenomenon is not a big enough engine to make the theory of
>>evolution fly.
>If you had even the slightest clue as to what evolution is and how it
>works you would realize the enormous power in the engine of
>evolutionary mechanisms which do include but are not limited to
>mutation and selection. You would understand the engine not only
>allows the theory of evolution to fly, but lets it soar.
Mutation and selection is the engine for the theory of evolution and
this phenomenon can accomplish quite a bit as demonstrated by drug
resistant bacteria, drug resistant viruses, herbicide resistant weeds,
and cancers which can evolve resistance to the drugs used to treat
these diseases. However, when you understand how this engine works; it
is quite easy to shut down this engine so that it can barely sputter
if run at all. You can prevent drug resistant bacteria and viruses,
you can prevent herbicide resistant weeds, you can develop more
durable cancer treatments but the theory of evolution stalls. All you
have to do to understand this engine is to know that the dominant
mathematical principle of this engine is the multiplication rule of
probabilities.
And
>>There is no difference between “artificial” and “natural” selection
>>and your putting this false labeling does not somehow create a
>>difference.
>This is the same person who said the breeding of domestic animals and
>crops has nothing to do with evolution.
Feel free to quote me if I have said such a thing. I have drawn a
distinction between recombination and selection and mutation and
selection. I have also said that with inbreeding by recombination and
selection you can change the way genes are expressed, but I have also
said that recombination without error can not create new alleles and
that recombination with selection can and does cause the loss of
alleles. It requires mutations to create new alleles. Now how about if
I quote you r norman where you said the following: “What is being
ignored is the possibility that two mutations can happen quite
separately but then assembled together by recombination (bacterial or
sexual).” Now we know that HIV does recombination, yet HIV is not able
to assemble beneficial mutations together in order to overcome the
affects of combination selection pressures. Do you care to explain why
this doesn’t happen?
========================================================
John Harshman
>>John Harshman has noted that there are at
>> least 40,000,000 million differences between human and chimpanzee
>> genomes. That s far too many genetic differences to be accounted for
>> by mutation and selection in only a million generations by drift or
>> any other mechanism you can imagine.
>That was nonsensical. "Selection by drift"? Do you have any idea what
>you're saying. Now in fact that 40 million differencess could easily
>have been accomplished by drift. Remember (if you ever learned) that the
>rate of neutral fixation is equal to the rate of mutation. And the rate
>of mutation in humans is a couple hundred per generation. Do the math.
Perhaps if I put a comma between “generations, by drift” it would make
more sense to you. Now there are lots of zeros and commas in
40,000,000 differences in 1,000,000 generations. Do you want to
explain how this huge number of differences can be fixed in these
genomes in such a small number of generations when Haldane’s
computations and Lenski’s empirical evidence shows that it takes
hundreds of generations to fix a single mutation in a population?
>> And the selection conditions
>> required to carry out such transformations do not exist.
>Remember that most of those mutations have nothing to do with any
>phenotypic change, and are not subject to selection.
If these mutations are neutral, there is no selection to fix them into
the population.
>> For example,
>> humans and chimpanzees produce identical insulin however the
>> preproinsulin for the two species differ by two amino acids. What is
>> the selection condition that would make such a change?
>Probably none. It's probably neutral.
Are you claiming that if more chimpanzee genomes are sequenced that we
are going to find members with preproinsulin identical to human
preproinsulin? Why don’t you tell us why on chromosome 21 there are
large non-random differences between the two genomes? If the
differences were simply due to “drift” the differences would not be
non-random.
>> Even if the
>> selection condition existed, in would take around a thousand
>> generations to make such a genetic transformation by mutation and
>> selection for just that gene. The mutation and selection process is
>> too slow and the selection conditions don t exist to make such
>> transformations.
>You consistently refuse to believe that there's such a thing as neutral
>fixation. And that's your main error here.
Of course I find your claim that alleles without selective benefit
will increase in frequency in a population ridiculous. That’s a
mathematically irrational claim.
>>>> And no, I don t agree that most natural selection pressures target
>>>> single genes.
>>> I did not see that claim in any of the responses above. What I did see
>>> was "most real selection processes target many genes".
>> Selection processes which target many genes profoundly slow the
>> amplification process for any beneficial alleles.
>So you claim. Any evidence? No, your HIV example is not evidence of any
>such thing. By the way, you consistently confuse "many genes" with "many
>traits". Most traits are influenced by many genes, and most genes
>influence many traits. Your simplistic ideas of evolution are just plain
>wrong.
My evidence comes out of the mouths of evolutionists themselves when
they say things like “Indeed, multiple simultaneous intense selective
pressures can probably explain some of the many extinctions that have
occurred in the history of life on this planet—affecting perhaps 99%
of the species that lived on earth in the past. Many examples of such
selective pressures resulted from sudden changes in climate that
caused pleiotropic effects on supplies of food and water, as well as
extreme temperature shifts and changes in availability of shelter.”
And
>> As long as evolutionists use terminology like drift to describe what
>> happens to populations on a plateau of a fitness landscape rather than
>> describing what actually happens, ie the population is diversifying,
>> they will continue to make the same blunders over and over.
>Sigh. Drift doesn't describe what happens to populations. It describes
>what happens to alleles. It amazes me that you blame evolutionary
>biologists for the ignorance of doctors, when you have clearly never had
>a course in evolution.
I blame evolutionists for the bungled understanding and teaching of
the basic science and mathematics of mutation and selection. Do you
still believe that the probability of a beneficial mutation occurring
at a particular locus is proportional to the size of the population?
Do you still fail to understand that the principle governing
mathematical principle of the mutation and selection phenomenon is the
multiplication rule of probabilities? Why would I want to be
indoctrinated into evolutionism? I’m much more interested in a
mathematically rational explanation or reality. Mathematical
rationality and appropriate mathematical descriptions of physical
phenomenon give the logical tools for dealing with drug resistant
bacteria, drug resistant viruses, herbicide resistant weeds and better
more durable treatments for cancer. I’m not interested in evolutionist
irrationality. This irrationality has already penetrated the minds of
enough naïve school children.
>>> [snip further embarrassing ignorance]
We could talk more about your claim that the probability of a
beneficial mutation occurring at a particular locus is proportional to
the size of the population. They must love you at Las Vegas for your
superior understanding of probability theory.
>> Speaking of embarrassing ignorance, have you finally figured out how
>> population size affects the probability of a beneficial mutation
>> occurring at a particular locus. Or do you continue to believe that
>> there are probabilities greater than one. Before you talk about
>> embarrassing ignorance, the first thing you should do is take your
>> shorts off of your head.
>Settled long ago. I was speaking quite loosely, and corrected the error
>immediately. Yet you maintain your errors forever. You still refuse to
>believe that neutral fixation can happen, despite being directed to
>several references and shown several examples.
That’s the thing about mathematical precision; it doesn’t allow you to
get away with your loose sloppy speculations. You couple together some
mathematical precision like the dominant mathematical principle
governing the mutation and selection phenomenon is the multiplication
rule of probabilities and well measured empirical evidence, and you
find that the proper understanding of the basic science and
mathematics of the mutation and selection phenomenon gives one the
logical understanding of how to deal with drug resistant bacteria and
viruses, herbicide resistant weeds and make more durable treatments
for cancer. Oh yes, in addition it shows your theory of evolution to
be a mathematically irrational belief system despite the fact that you
have shifted into neutral.
And
>> Get a copy of Lenski�s paper �Phenotypic and Genomic Evolution during
>> a 20,000-Generation Experiment with the Bacterium Escherichia coli�
>> http://www.google.com/url?sa=D&q=http://myxo.css.msu.edu/lenski/pdf/2004,%2520Plant%2520Breeding%2520Reviews,%2520Lenski.pdf
>> where Lenski writes the following:
>> ��Thus, the total number of mutations per population during 20,000
>> generations is expected to be approximately 1.5 x 10^9 using the
>> higher mutation rate, and about 3 x 10^8 using the lower rate. That
>> is, several hundreds of million of point mutations have appeared in
>> each population, even after adjusting for the transfer bottleneck. In
>> addition to these point mutations, other types of spontaneous mutation
>> can also occur, including insertion, deletions, and inversions; many
>> of these larger events involve insertion sequences, or IS elements,
>> that are present in most bacteria.
>> That is certainly a lot of mutations. In fact, with a genome length of
>> 5 x 10^6 base-pairs and three alternative base-pairs per position,
>> only 1.5 x 10^7 point mutations are even possible. Thus, each
>> population has had most point mutations represented many times over.
>> Of course, this calculation does not imply that every possible
>> sequence has ever existed-far, far from it-because each mutation
>> occurs against a relatively few genetic backgrounds. The backgrounds
>> change as the population evolves, but as we shall see below, that the
>> vast majority of the genome does not change in the majority of cells.�
>I would have preferred a relevant quote, one that addressed my question.
>That didn't. And I understand why, since I don't believe you could have
>found a quote from that paper that supports your claims.
John, Lenski is clearly saying that stabilizing selection pressures
are the overwhelming dominant form of selection on his populations.
Perhaps you can find a quote from him where he says that neutral
mutations amplify far faster and simultaneously in his populations
than beneficial mutations with the benefit of selection because that’s
what you believe occurs in your fantasy world of evolutionism.
>> Lenski gives a variety of reasons why despite the huge number of
>> mutations that only a miniscule number of the mutations are fixed in
>> the population but clearly the vast number of loci in the genomes of
>> his populations remained stable despite the selection pressure he put
>> his population under. This is not an unusual principle. For example,
>> large portions of the hemoglobin molecule never have an amino acid
>> substitution. The reason being is that if any of the crucial amino
>> acids in this molecule are substituted, the molecule loses the
>> appropriate conformation and can not carry out its function as
>> hemoglobin. These stabilizing selection pressures are inherent in the
>> conformation of the molecules coded for by the genetic sequences. If
>> these molecules diverge too far by mutations, they no longer can carry
>> out their biologic function.
>None of which is relevant to your claim. The reason that so many
>mutations produced so few changes in Lenski's experiments isn't that all
>sites are under stabilizing selection. It's that the mutation rate was
>low enough that there were few fixations resulting from neutral
>evolution. This can be seen by the great increase in fixations when the
>hypermutability allele became fixed. Remember: the probability that a
>mutation will become fixed is its frequency, which is initially 1/N. If
>there's a population of 100,000,000, only 1 in 100,000,000 mutations
>will be fixed by drift. The great majority will be eliminated, by
>chance, within a generation or two.
John, I can see that your indoctrination into evolutionism and its
bizarre and twisted view of reality makes it hard for you to
understand the basic science and mathematics of mutation and
selection. In your world, neutral mutations spread through populations
thousands of times faster than beneficial mutations even without the
benefit of selection, probabilities greater than one exist in your
twisted world, selection increases the diversity of populations
despite the fact that selection kills or impairs members of the
population from passing their genetic information to future
generations, reducing the intensity of selection causes beneficial
mutations to be spread through populations more rapidly than stronger
selection pressures. All these are fundamental scientific and
mathematical blunders that evolutionists make in their loose and
irrational misinterpretation of reality. John, if you learn nothing
else here, learn this, the multiplication rule of probabilities is the
dominant and central mathematical principle which drives the mutation
and selection phenomenon. The variable which is governed by this
principle is the complexity of the selection conditions. There is no
other variable in this phenomenon that has the mathematical impact
which the complexity of the selection conditions does. This is why HIV
behaves the way it does when subject to combination selection
pressures, this is why cancer responds the way it does when
combination selection pressures are used, this is why weeds respond
the way they do when combination herbicides are used, this is why any
population subjected to combination selection pressures behaves the
way it does. Not mutation rates, not population size, not number of
generations; no other variable in the mutation and selection
phenomenon has the mathematical impact which the complexity of the
selection condition has. It’s time for you to come back to reality
John.
========================================================
hersheyh
>> There is no difference between artificial and natural selection
>> and your putting this false labeling does not somehow create a
>> difference.
>I made no such claim of an innate difference in the mechanism of
>selection aside from the definitional one that "artificial" selection
>involves environmental conditions that are arranged by humans and
>"natural" selection involves environmental conditions that are not
>arranged by humans. What I claim is that the environmental conditions
>*you* choose and which are definitely designed by humans (as is even
>single drug therapy) are rare in *nature*.
Humans aren’t the only once who design selection conditions which
target multiple sites. I’ve already given an example of Bacillus
thuringiensis which produces a multi-component toxin which targets
multiple sites in mosquito larvae. And the notion that thermal stress,
starvation and dehydration can not occur simultaneously to populations
is nothing more than direct ignorance of reality. If you want to
believe that a population or reptiles can be subject to thermal stress
for tens of thousands of years without any superimposed starvation,
dehydration, predation, disease or any other selection pressure you
could imagine, that’s fine by me. Just don’t indoctrinate naïve school
children with this irrational nonsense.
>> Selection pressures which target multiple genes always
>> slow the mutation and selection process whether you call them
>> artificial or natural selection pressures.
>And I have *repeatedly* said that when you arrange environmental
>conditions such that there is no selective advantage to a single
>mutational change, but only a selective advantage to multiple
>simultaneous changes in a single individual, that that reduces the
>probability of occurrence of that event by the multiplication rule. I
>only claim that 1) such conditions merely make the appearance of
>organisms with a selective advantage rarer (but not, even in your
>example, impossible) and 2) that such extreme conditions play little
>role in any actual evolutionary changes that have occurred in nature.
Hersheyh, the multiplication rule of probabilities applies whether the
mutations occur simultaneously or not. It takes a specialized
arrangement for the mutation and selection phenomenon to work
efficiently. It takes consistent application of a single targeted
selection pressure over long periods of time without the addition of
other selection pressures acting simultaneously. This occurs with the
uses of single drug therapy used in a sequential manner as done by the
existing standard of care in the medical field for treating most
infections. The consequence of this evolutionist inspired blunder is
multidrug resistant microbes. These are the conditions required for
the mutation and selection phenomenon to work efficiently.
>*Your* ignorance lies in the claim that *your* example is typical. It
>is, as even you have pointed out with other examples, possible to have
>conditions in which an organism can grow for tens of thousands of
>generations in an environment which has a rich niche available which
>it cannot use and then very quickly, once an individual has acquired
>the ability to exploit that environment, increase population size and
>change genetically (i.e., evolve) into a population that can now
>exploit a wider range of resources (the Lenski experiment; although
>this can happen in other cases, like ability to convert an E. coli
>with a deletion of its lacZ gene into one that can use lactose by
>virtue of modification of the ebg gene -- evolution, after all,
>involves the modification of existing structures to perform different
>functions not the generation of structures from scratch). And, in
>organisms that can undergo sexual recombination of some type, it is
>possible for independent mutants in different organisms, each with
>some selective advantage, to recombine to produce even more fit
>organisms with both variations without *your* requirement that the
>mutations occur simultaneously in the same individual. Again, in
>*nature* most selection that leads to change does not involve
>resistance to toxins that are always at lethal levels, requiring
>simultaneous mutations in a single individual. It usually takes the
>devious mind of man to arrange such double-lethal conditions. And, as
>you point out, any medication treatment modality that does NOT involve
>the requirement for multiple simultaneous mutation for any selective
>advantage will result in evolution of multiply resistant strains
>within the lifetime of the typical patient rather than, *when*
>conditions are arranged to require multiple simultaneous mutation in
>an individual to generate any selective advantage, the probability of
>evolution to multiple resistance can often occur in an individual's
>lifetime. Specifically, when the treatment modality (environmental
>conditions) allows the sequential evolution of resistance to multiple
>factors, it can occur quite quickly.
How many times can you evolutionists make the same blunders? R Norman
has made the same claim the recombination will allow beneficial
mutations to recombine laterally. HIV does recombination yet this does
not occur with any significant impact on the effects of combination
therapy. And the occurrence of multiple beneficial mutations is always
governed by the multiplication rule of probabilities. The mutations do
not have to occur simultaneously. The entire mutation and selection
phenomenon is geared for the population to try to overcome the
multiplication rule of probabilities by amplification of beneficial
alleles so that the population can improve the probability that the
next beneficial mutation will occur at the proper locus. Mutation and
selection is a very slow process when it works efficiently, anything
which would disrupt the amplification process only slows the
phenomenon much more.
>I am simply pointing out that your requirement for *multiple*
>*simultaneous* mutations in a single individual for there to be any
>significant selective advantage is actually pretty rare in nature when
>one is talking about traits that are the product of successful
>evolution. I am simply pointing out that you repeatedly claim that
>your unusual conditions are actually common.
Mutation and selection is all about getting the next beneficial
mutation on a descendent of the recipient of the first beneficial
mutation. This is how populations overcome the multiplication rule of
probabilities. If the population can not amplify that first beneficial
mutation through selection over hundreds of generations creating
millions of descendents with that beneficial mutation, the
multiplication rule of probabilities makes it very unlikely that the
next beneficial mutation will occur on the small number of descendents
that have the first beneficial mutation. All it takes is some other
cause of death besides thermal stress to disrupt the mutation and
selection process of evolving a reptile scale into a feather. You are
the one requiring rare selection conditions in order for your genetic
transformation to occur.
>> > It is only typical of selection for multiple
>> > toxicity resistance under conditions where resistance to one toxin
>> > does not significantly increase the selective advantage of the
>> > organism relative to no resistance at all. The entire designed (aka,
>> > artificial) intent of such selection schemes in medicine is to drive
>> > the organism attacked to extinction in its host or, at least, reduce
>> > its population to a level that renders the organism less harmful to
>> > the host. When *evolution*, as opposed to *extinction*, occurs in
>> > nature, it rarely involves some environment changing so dramatically
>> > on several different parameters so as to drive the population to
>> > extinction.
>> HIV is not driven to extinction, are you so thick skulled that you
>> don t recognize this simple fact?
>The entire goal of treatment is to reduce the replicative capacity of
>the endogenous virus to prevent it from spreading successfully to
>other (particularly immune) cells within the individual. Since, in
>multidrug therapy, only the double mutant has a selective reproductive
>advantage, the drugs keep the population of infective virus low which
>means that the probability of a double mutant occurring (which is
>different than the rate of double mutation in an individual, since it
>is the rate of double mutation times the effective population of
>infective particles) is quite low.
The population of viruses in effectively treated infected individuals
is in the hundreds of thousands. That’s more than enough population
for the mutation and selection phenomenon to work if only a single
selection pressure is applied. And the virus must be able to reproduce
sufficiently to maintain that population. Even a slight reduction in
fecundity of the selected viral population would drive the population
to extinction in a short period of time. The reason why combination
therapy works is that the population can not amplify beneficial
mutations to one drug or another due to the selection pressure of the
other drugs. The multiplication rule of probabilities makes it highly
unlikely that the double mutant will occur. The multiplication rule of
probabilities always applies with the mutation and selection
phenomenon whether the mutations occur simultaneously or not.
>This is in contrast to when conditions are arranged such that single
>mutations provide a selective advantage, such as serial use of drugs.
>In that case, the probability of mutation is affected by both the much
>increased rate of mutation to a selective advantage, given that
>resistance only requires resistance to a single drug and not both, and
>the somewhat larger population of infective particles, given that the
>virus only needs to, by chance, escape a single physiological drug-
>toxicity step to reach the stage of replication. Once the strain is
>resistant to the ...
The mutation rate is only a minor player in the mutation and selection
phenomenon. The dominant mathematical principle of the mutation and
selection phenomenon is the multiplication rule of probabilities.
That’s the lesson you evolutionists have yet to learn.
And
>> We’ve seen that process at work with the sequential use of
>> antibiotics. That’s how you obtain multidrug resistant microbes.
>Yes. IOW, there *are* conditions under which organisms can produce
>mutations resistant to one toxin that are selectively favored and
>subsequently select for resistance to a second toxin. In nature,
>which do you think is going to be more common? For a microbe to come
>across a single toxin at a time or two or more different independent
>toxins at once?
In the natural environment, a single toxin will usually be adequate to
suppress a bacterial population because there are many other selection
pressures already acting simultaneously such as thermal stress,
dehydration and so on. We actually see this effect in the use of
antibiotics. When bacterial specimens are sent to the lab, it is not
unusual for the in vitro results to show resistance to some
antibiotics while the in vivo results show otherwise. The bacteria are
grown in the lab under ideal conditions for the bacteria except for
the single antibiotic selection pressure. While the in vivo conditions
have the host immune system also putting selection pressure on the
bacteria. It is ludicrous to believe that natural environments don’t
have multiple selection pressures acting on populations
simultaneously. This is one of innumerable evolutionists’ fallacies.
>> I
>> understand what you are proposing. Perhaps in the Twilight Zone
>> selection pressures cooperate to give you these massive
>> transformations.
>I don't know what you mean by "massive transformations"? Massive
>transformation that *must* *necessarily* occur all at once, like a
>crocodile egg producing a duck all at once? Or massive transformation
>that occurs over long stretches of time with smaller intermediate
>transformations that have utility in and of themselves (like, say, a
>species of toothed, tailed, feathered, bipedal 'theropod' giving rise
>to a species of toothed, tailed, feathered, bipedal 'birds')?
When you understand what it takes for mutation and selection to
produce a small transformation such as transforming a glucose
metabolizing bacteria into a citrate metabolizing bacteria and the
tens of thousands of generations required to do such a transformation
under well controlled laboratory conditions that the number of
generations required to transform a reptile into a bird or even a
primate precursor into humans and chimpanzees is a mathematically
irrational occurrence. We now have John Harshman, the evolutionist who
believes in probabilities greater than one arguing that drift will fix
dozens of neutral mutations every generation for hundreds of thousands
of generations when selection takes hundreds of generations to fix a
single beneficial mutation with the assistance of selection. You
evolutionists are way past going down a rabbit hole.
>> But reality does not work that way.
>I agree that reality does not work to produce massive transformation
>by the crocodile laying an egg that produces a duck mechanism. It
>does work by the "species of toothed, tailed, feathered, bipedal
>'theropod' giving rise to a species of toothed, tailed, feathered,
>bipedal 'birds" mechanism. In fact, there may be quite some
>difficulty in determining what is a "theropod" and what is a "bird" at
>the early stages.
You can make up what ever fables you want and teach these fables to
naïve school children but you have no right to misrepresent how
mutation and selection actually works. This is too important an issue
for society that medical and agricultural decisions are made on the
basis of evolutionist fables.
>It may be impossible for me to walk 50 miles away from here in some
>direction in a single step, but it certainly is possible for me to
>walk that 50 mile distance in multiple steps, even if I do it
>blindfolded and drunk. I could probably do it even faster if there
>were some environmental factors guiding me.
Well then it’s about time for evolutionists to learn how quickly
mutation and selection works and according to John Harshman’s numbers,
you have 40,000,000 steps to make in about a million generations to
transform humans and chimpanzees from a primate precursor. Are you
going to jump on John Harshman’s band wagon and start claiming that
dozens of neutral mutations can be fixed every generation when it
takes hundreds of generations to fix a single beneficial mutation with
the assistance of selection? When you put numbers and measurements to
your logic, you find out that you can’t get there.
>> And you continue
>> to cling to your incorrect view of mutation and selection. Once you
>> define your selection conditions and you place your population on some
>> point of the fitness landscape, you have predetermined what
>> trajectories are available to your population. Read Lenski’s works and
>> you will find out that is what his populations did.
>It optimized its genome to its environmental conditions using whatever
>variants existed in the population at the time. But only to the
>extent that such variants were actually present in the population.
>Mutation is the ultimate source of variation. When a variation that
>allowed utilization of the previously unavailable resource came to be,
>that variant increased in frequency.
Mutation is the only source of genetic diversity.
>> That’s also what
>> HIV does when subjected to particular selection pressures, specific
>> mutations are selected for.
>It optimized its genome to its environmental conditions using whatever
>variants existed in the population at the time. But only to the
>extent that such variants were actually present in the population.
>Mutation is the ultimate source of variation. When the variations
>that allowed reproduction came to be in the same organism (since the
>conditions were specifically designed to provide no selective
>advantage to individual variants unless present in a single organism),
>those variants increased in frequency.
And the substitution of a more beneficial allele for a less beneficial
allele is the unit process of evolution and you need to learn that it
takes hundreds of generations for that event to occur. And this event
must occur for the process of evolution by mutation and selection to
occur because if the amplification process does not occur, the
multiplication rule of probabilities makes it highly unlikely that
another evolutionary step can occur.
>> Your empirically baseless claims are in
>> contradiction with reality.
>The fact that, in HIV, you tend to get the same specific mutations is
>more a function of the genetic simplicity of the organism than
>anything else. In vertebrates alone, for example, there have been
>multiple independent ways to generate "wings" (pterodactyl, bat,
>bird). The bones that form the wing differ. Or "swimming" organisms
> (fish, ichthyosaurs, seals, whales, penquins, snakes). Some of them
>use side to side motion, others use up and down, one uses undulation
>of the whole body). In every case, the *function* is produced by
>*modification* of a previously existing structure common to
>vertebrates, not by putting an extra set of wings on a pig.
So what? Evolution depends on the substitution of a more beneficial
allele for a less beneficial allele. If that substitution process can
not be carried out by a population, the evolutionary process by
mutation and selection is brought to a standstill. And that occurs
when multiple genes are targeted by multiple selection pressures.
>> Let’s see, I posted the example of HIV, and I have posted the example
>> of Bacillus thuringiensis which produces a combination toxin which
>> targets mosquito larvae, and I have posted examples from the field of
>> oncology, and I have posted examples from the field of parasitology,
>> all of which show that combination selection pressures stifle the
>> mutation and selection phenomenon. I have hundreds of more examples.
>Those are examples where evolution does not happen (or happens very
>slowly). What you have to do is show that those are the conditions
>that are *necessarily* present when evolution did happen. Again, I
>have no problem at all with the idea that the multiplication rule
>applies under certain conditions, namely when there is no *possible*
>selective advantage until all the variations exist in the same
>individual. That doesn't, of course, completely rule out the
>possibility of some change being due to a combination of selectively
>neutral fixation and selection or even of fixation of a slightly
>deleterious trait.
We all understand your argument, you claim that reptiles were under
constant thermal stress for thousands or tens of thousands of
generations and their scales turned into feathers. These reptiles
didn’t die for any other cause other than thermal stress. There were
no predators, there was no disease, there was no dehydration, you only
had thermal stress on the population which caused scales to be
transformed into feathers. This kind of irrational nonsense should not
be taught to naïve school children. These children should be taught
how mutation and selection actually works so that they will have some
logical strategy for dealing with drug resistant infections, herbicide
resistant weeds, develop more durable cancer treatments and so on.
>> Where is your real, measurable and repeatable example of mutation and
>> selection which shows that selection conditions which target more than
>> a single gene accelerates the mutation and selection phenomenon?
>I have given you the example where selection which can target more
>than one gene that independently provide some selective benefit can
>occur semi-simultaneously (or already be present) in different
>subpopulations and then increase in frequency until sexual
>recombination produces (at high and repeated frequency) the double
>variant. And I have pointed out that human bipedality and increases
>in human brain size occurred sequentially. Each was independently
>useful, but the increase in brain size may have become *more* useful
>after bipedality was common. That is, change in motility, beneficial
>in some environments all by itself, caused a change in selective
>conditions that made other changes more valuable. Neither of them
>require nor did they actually occur by the *necessary* *simultaneous*
>mutation occurring in a single individual. In fact, in the first
>example the mutations specifically occurred in different individuals
>and came to exist in the same individual by a process different from
>mutation and one that occurs with relatively high frequency relative
>to mutation.
That’s a crock hersheyh, you have not provided a single real,
measurable and repeatable example of mutation and selection which
demonstrates anything that you claim. You’ve been living with your
speculations for so long; you now believe that they are true.
>> All
>> we get from you is an endless stream of speculations.
>Like your completly evidenceless speculation that it is impossible for
>a reptile to evolve into a bird?
I haven’t given you much, only the correct basic science and
mathematics of mutation and selection and numerous real examples of
mutation which demonstrate that science. With that logic, you get the
proper strategy for dealing with drug resistant infections, herbicide
resistant weeds and more durable cancer treatments. All you have to
understand is that the multiplication rule of probabilities is the
dominant mathematical principle governing the mutation and selection
phenomenon. And you have argued that reptiles were subject only to
thermal stress in the past without any other selection conditions on
the population and because of this, reptiles grew feathers. That kind
of logic goes well with your claim that you can roll a die and get a
zero.
John Harshman
> threads of March 15
If you have the least consideration for other people, please stop doing
this.
The fact that genome size is so important makes me suspicious that there
is something wrong with the model. Logically, selection on a locus
should not be affected by the number of additional, irrelevant loci. And
it seems to me that Schneider mentioned this to you also.
>>> What Schneider is saying in his text is that amplification
>>> of a beneficial allele is the way populations overcome the
>>> multiplication rule of probabilities. The multiplication rule still
>>> applies to biological evolution. This is why when evolutionists like
>>> hersheyh claim that neutral mutations are important in the
>>> evolutionary process, he neglects the fact that the multiplication
>>> rule still applies. Schneider is wrong and he should either take his
>>> claim off his web site or rephrase his claim. He knows that when he
>>> does, his titanic theory of evolution hits the gigantic multiplication
>>> rule of probabilities iceberg and the theory of evolution sinks into
>>> the primordial soup.
>> You have yet to explain any mechanism for why this "multiplication rule"
>> should apply in any case other than when two mutations must happen
>> simultaneously in one individual for an allele to be selectively
>> advantageous.
> John, you are still having a difficult time understanding what a
> population must do in order for two mutations to end up on a single
> member. There are two basic mechanisms available to a population in
> order for two mutations to end up occurring on a single member of the
> population. One mechanism if for that member and its descendents with
> the first mutation to be able to reproduce over and until one of the
> descendents is able to get that second beneficial mutation.
Or the two mutations could appear independently in different
individuals, and both increase in frequency until, with recombination,
they are combined in a single individual. If both mutations are
selected, individuals in which both occur will increase in frequency
until both are fixed. Why do you ignore recombination?
>>> Because if you keep doubling your population size and the probability
>>> for that beneficial mutation occurring at a particular locus keeps
>>> doubling, you will at some point have a probability greater than 1.
>> You really can't read. Note that I'm talking about "expected number of
>> mutations", not "probability of one mutation".
> John, do you want me to quote you verbatim? You know what you said and
> you were incorrect in a fundamental mathematical principle of the
> mutation and selection phenomenon.
Yes, I misspoke. I've been trying to correct that misstatement ever
since to explain what I really meant. Can we get past that?
>>> The probability for this event can get extremely close to 1 but it
>>> will never have a probability of 1. There is always a small
>>> probability that a particular mutation will not occur at a particular
>>> locus no matter how large the population is. The effect of population
>>> size on the mutation and selection phenomenon has less than an
>>> additive effect on the phenomenon.
>> That depends on whether multiple, identical mutations increase the
>> probability of fixation. And of course they do. In the neutral case, the
>> effect is exactly linear.
> John, fixation is not a random process.
Sometimes it is, sometimes it isn't.
> Fixation occurs when you have
> a more fit member in the population who is a better replicator than
> other members of the population. Because that member and its
> descendents are more fit replicators based on the selection
> conditions, the number of descendents of that more fit replicator
> increases over the generations.
That's what happens under selection. Under neutrality, some alleles
still become fixed. At random. And in fact 1/2N of all neutral mutations
become fixed eventually.
>>>>> In addition, John does not seem to recognize that
>>>>> population size itself is a selection pressure. As population size
>>>>> increases, the amount of resources available from a given environment
>>>>> to the population becomes a limiting factor for survival and
>>>>> reproduction, thus becoming a selection pressure on the population,
>>>>> that selection pressure is called starvation.
>>>> How is all that relevant to the occurrence of mutation?
>>> As population size increases, at some point the population will reach
>>> the carrying capacity of the environment. At that point, the most fit
>>> reproducers and their alleles will start increasing in frequency.
>> No, they will do that before the population reaches carrying capacity,
>> though what's "most fit" may change as carrying capacity is neared.
> John, as a population reaches the carrying capacity of the
> environment, the less fit replicators will reduce in frequency because
> the more fit replicators are more efficient users of the resources of
> the environment.
Restating your claim isn't an argument. Selection happens both in
increasing and stable populations. Just different sorts of selection.
>>> Any
>>> of the less fit members of the population who able to survive and
>>> reproduce when there was excess resources in the environment will
>>> reduce in frequency because of less availability of resources.
>>> Increasing the size of populations in and of itself increase the
>>> selection pressure on the population reducing the diversity of the
>>> gene pool.
>> Only if there is a fixed carrying capacity, which you have not specified.
> There are always limits in an environment. There are limits on water
> availability, light, food and so on. In Lenski’s experiment, his
> environment was glucose limited until one of his strains became
> citrate metabolizers. Lenski has to continually replenish glucose for
> his bacteria so that they won’t starve out. Still, the most efficient
> glucose metabolizers took over the environment in all his other cases.
You understand that the limiting resource can change over time, often as
a result of evolution. Right?
>>> Simply post an example of selection which increases the diversity of a
>>> population.
>> I have mentioned the major histocompatibility complex. That should do.
> Your loosely mentioning something is not posting a real measurable
> example.
Look it up.
>>> I�ve notice these responses and I dismiss them because the use of the
>>> word �drift� does not properly describe what a population does when it
>>> reaches a plateau on a fitness landscape.
>> So you're hung up on a single word? And for this you ignore a
>> half-century (or more) of work in the field you claim to invalidate?
> I don’t like the word “drift” because it doesn’t properly describe
> what populations do on a fitness plateau. I can’t help the missteps
> evolutionists have taken over the last 50 years. If evolutionists
> hadn’t ignored what Edward Tatum said more than 50 years ago, perhaps
> so many people would not have wasted so much time on a mathematically
> irrational belief system.
Simply repeating a claim isn't an argument. Try to get past single words
and into the actual discussion. I repeat: drift isn't something that
happens to populations, whether at a fitness plateau or otherwise. It's
something that happens to alleles. Part of the genome can be under
intense selection while another part is evolving neutrally.
>>> Populations diversify when
>>> they reach these plateaus, they do not drift. I don�t have to accept
>>> sloppy evolutionist terminology any more than I have to accept sloppy
>>> evolutionist speculations. You evolutionists have already bungled the
>>> basic science and mathematics of mutation and selection. You have
>>> already demonstrated that you don�t understand how the multiplication
>>> rule of probabilities dominates this phenomenon. Why should I accept
>>> your sloppy misinterpretation of what a population does on a plateau
>>> of a fitness landscape?
>> I know you don't actually read what I write, but I'll try again: drift
>> doesn't apply to populations; it applies to alleles.
> Certainly I read what you write. Tell me how you can separate alleles
> from the population.
Independent assortment allows different loci to have different fates. Do
you know what independent assortment is?
>>>>> 5. Then we have r norman s blunder when he said the following: What
>>>>> is being ignored is the possibility that two mutations can happen
>>>>> quite separately but then assembled together by recombination
>>>>> (bacterial or sexual). What r norman does not explain to us why his
>>>>> claim does not work for HIV since HIV does recombination yet this
>>>>> virus can not assemble two beneficial mutations together and overcome
>>>>> combination therapy. What r norman does not realize is that the
>>>>> shuffling of existing alleles has little effect on the creation of new
>>>>> alleles. This is simply another example of the numerous mathematical
>>>>> and scientific blunders that evolutionists make due to their obsession
>>>>> that reptiles turn into birds by mutation and selection.
>>>> That was so garbled as to be painful. Your HIV case is one in which no
>>>> single mutation has a selective advantage, the only such advantage
>>>> accruing to individuals with several necessary mutations. In that case,
>>>> your "multiplication rule" applies. But that case is unusual. Generally
>>>> single mutations are individually advantageous.
>>> Are you sure this is an unusual case?
>> Yes.
> It’s very easy to find other examples of mutation and selection which
> behave identically to the HIV case. I’ve already posted examples of
> the treatment of malaria, examples from the field of oncology; I’ve
> even posted an example of bacteria which produce multiple toxins to
> mosquito larvae. You had better reconsider your answer since this is
> how mutation and selection actually works.
I doubt you are looking for cases that don't fit your model. Watch out
for selection bias.
>>> Do you think it is very rare
>>> that combination selection pressures suppress the mutation and
>>> selection phenomenon?
>> Yes, whatever you mean by that.
> What I mean by that is the substitution of a more beneficial allele
> for a less beneficial allele. After all, that is the unit process of
> evolution.
We call that "selection", not "the mutation and selection phenomenon".
> And
>
>>> John, let�s say that our population lives happily on this really huge
>>> plateau on the fitness landscape with an infinite carrying capacity.
>>> The population will continue to diversify until all variants on that
>>> plateau are represented in the population distribution. As soon as you
>>> introduce any kind of selection, you are removing some of those
>>> variants from the distribution. Perhaps you believe that on the top of
>>> Mt Everest, there is a gigantic plateau where all kinds of variants
>>> live happily together. Most selection pressures prevent divergence.
>>> Lenski�s experiment demonstrates that nicely.
>> No it doesn't. You consistently misinterpret Lenski. And your first
>> problem is your assumption of an infinite population. There is no such
>> thing. In any finite population, drift will produce an equilibrium
>> diversity, even without selection, and some sorts of selection will
>> increase diversity above that equilibrium level.
> So then are you now claiming that no new neutral mutations will occur?
No. Why? New mutations happen, increasing diversity, and old ones become
either fixed or extinct, reducing diversity. Eventually the system
reaches an equilibrium in which new diversity is added at the same rate
at which old diversity is lost. Is this hard to understand?
John Harshman
Please stop this. Do you care at all for the convenience of other people?
> ========================================================
> John Harshman
>>> John Harshman has noted that there are at
>>> least 40,000,000 million differences between human and chimpanzee
>>> genomes. That s far too many genetic differences to be accounted for
>>> by mutation and selection in only a million generations by drift or
>>> any other mechanism you can imagine.
>> That was nonsensical. "Selection by drift"? Do you have any idea what
>> you're saying. Now in fact that 40 million differencess could easily
>> have been accomplished by drift. Remember (if you ever learned) that the
>> rate of neutral fixation is equal to the rate of mutation. And the rate
>> of mutation in humans is a couple hundred per generation. Do the math.
> Perhaps if I put a comma between “generations, by drift” it would make
> more sense to you. Now there are lots of zeros and commas in
> 40,000,000 differences in 1,000,000 generations. Do you want to
> explain how this huge number of differences can be fixed in these
> genomes in such a small number of generations when Haldane’s
> computations and Lenski’s empirical evidence shows that it takes
> hundreds of generations to fix a single mutation in a population?
Yes. I have explaind this many, many times. Why, I even explained it in
the part you just quoted above. That's why I claim you don't read.
Haldane and Lenski were talking about selection. I'm talking about
neutral evolution. They're different.
>>> And the selection conditions
>>> required to carry out such transformations do not exist.
>> Remember that most of those mutations have nothing to do with any
>> phenotypic change, and are not subject to selection.
> If these mutations are neutral, there is no selection to fix them into
> the population.
That's right. They are fixed by drift, not by selection. 1/2N of all
neutral mutations become fixed by drift, and the rest (1 - 1/2N of them)
become extinct, usually in the first generation or two.
>>> For example,
>>> humans and chimpanzees produce identical insulin however the
>>> preproinsulin for the two species differ by two amino acids. What is
>>> the selection condition that would make such a change?
>> Probably none. It's probably neutral.
> Are you claiming that if more chimpanzee genomes are sequenced that we
> are going to find members with preproinsulin identical to human
> preproinsulin?
No. Why would you imagine that? It's another fixation of a neutral mutation.
> Why don’t you tell us why on chromosome 21 there are
> large non-random differences between the two genomes? If the
> differences were simply due to “drift” the differences would not be
> non-random.
You will have to explain what you mean here. In what way are the
differences non-random? What, in fact, are the differences you are
talking about?
>>> Even if the
>>> selection condition existed, in would take around a thousand
>>> generations to make such a genetic transformation by mutation and
>>> selection for just that gene. The mutation and selection process is
>>> too slow and the selection conditions don t exist to make such
>>> transformations.
>> You consistently refuse to believe that there's such a thing as neutral
>> fixation. And that's your main error here.
> Of course I find your claim that alleles without selective benefit
> will increase in frequency in a population ridiculous. That’s a
> mathematically irrational claim.
That's why I find it difficult to believe that you know anything about
mathematics. Do you know what a random walk is? Frequency increases and
decreases at random. The probability of eventual fixation (frequency 1)
for any point in a walk is the current frequency. Most mutations start
as a frequency of 1/2N, and thus all but a tiny number will become
extinct. But 1/2N of them eventually become fixed. This is simple
mathematics, and it's shocking you can't get this. Try flipping a coin.
Heads, add 1 to a total, and tails, subtract 1. Start from 1, and say
that you reach fixation if the total reaches 10, or extinction if it
reaches 0. I claim that 1/10 of trials will end in fixation, and 9/10
will end in extinction. Let me know what you get.
>>>>> And no, I don t agree that most natural selection pressures target
>>>>> single genes.
>>>> I did not see that claim in any of the responses above. What I did see
>>>> was "most real selection processes target many genes".
>>> Selection processes which target many genes profoundly slow the
>>> amplification process for any beneficial alleles.
>> So you claim. Any evidence? No, your HIV example is not evidence of any
>> such thing. By the way, you consistently confuse "many genes" with "many
>> traits". Most traits are influenced by many genes, and most genes
>> influence many traits. Your simplistic ideas of evolution are just plain
>> wrong.
> My evidence comes out of the mouths of evolutionists themselves when
> they say things like “Indeed, multiple simultaneous intense selective
> pressures can probably explain some of the many extinctions that have
> occurred in the history of life on this planet—affecting perhaps 99%
> of the species that lived on earth in the past. Many examples of such
> selective pressures resulted from sudden changes in climate that
> caused pleiotropic effects on supplies of food and water, as well as
> extreme temperature shifts and changes in availability of shelter.”
Who said this, and where? Note that it's completely irrelevant as a
response to what I said.
> And
>
>>> As long as evolutionists use terminology like drift to describe what
>>> happens to populations on a plateau of a fitness landscape rather than
>>> describing what actually happens, ie the population is diversifying,
>>> they will continue to make the same blunders over and over.
>> Sigh. Drift doesn't describe what happens to populations. It describes
>> what happens to alleles. It amazes me that you blame evolutionary
>> biologists for the ignorance of doctors, when you have clearly never had
>> a course in evolution.
> I blame evolutionists for the bungled understanding and teaching of
> the basic science and mathematics of mutation and selection. Do you
> still believe that the probability of a beneficial mutation occurring
> at a particular locus is proportional to the size of the population?
I never did.
> Do you still fail to understand that the principle governing
> mathematical principle of the mutation and selection phenomenon is the
> multiplication rule of probabilities?
Indeed I don't. Why don't you present some kind of argument to that
effect that doesn't involve mutations without benefit unless combined?
> Why would I want to be
> indoctrinated into evolutionism?
So you admit that you never had a course in it. How can you blame people
who never taught you for failing to teach you?
> I’m much more interested in a
> mathematically rational explanation or reality. Mathematical
> rationality and appropriate mathematical descriptions of physical
> phenomenon give the logical tools for dealing with drug resistant
> bacteria, drug resistant viruses, herbicide resistant weeds and better
> more durable treatments for cancer. I’m not interested in evolutionist
> irrationality. This irrationality has already penetrated the minds of
> enough naïve school children.
So you say it's spinach and to hell with it?
>>>> [snip further embarrassing ignorance]
> We could talk more about your claim that the probability of a
> beneficial mutation occurring at a particular locus is proportional to
> the size of the population. They must love you at Las Vegas for your
> superior understanding of probability theory.
Asked and answered. Move on.
>>> Speaking of embarrassing ignorance, have you finally figured out how
>>> population size affects the probability of a beneficial mutation
>>> occurring at a particular locus. Or do you continue to believe that
>>> there are probabilities greater than one. Before you talk about
>>> embarrassing ignorance, the first thing you should do is take your
>>> shorts off of your head.
>> Settled long ago. I was speaking quite loosely, and corrected the error
>> immediately. Yet you maintain your errors forever. You still refuse to
>> believe that neutral fixation can happen, despite being directed to
>> several references and shown several examples.
> That’s the thing about mathematical precision; it doesn’t allow you to
> get away with your loose sloppy speculations.
Oddly enough, I (along with similar efforts by Howard and a few others)
am the only one to apply any mathematics to this question. You have
never mentioned any mathematics at all. Feel free to refute neutral
theory, though.
> You couple together some
> mathematical precision like the dominant mathematical principle
> governing the mutation and selection phenomenon is the multiplication
> rule of probabilities and well measured empirical evidence, and you
> find that the proper understanding of the basic science and
> mathematics of the mutation and selection phenomenon gives one the
> logical understanding of how to deal with drug resistant bacteria and
> viruses, herbicide resistant weeds and make more durable treatments
> for cancer. Oh yes, in addition it shows your theory of evolution to
> be a mathematically irrational belief system despite the fact that you
> have shifted into neutral.
You always fall back on your mantra when you have nothing rational to say.
I never said or implied any such nonsense. Most neutral mutations become
extinct quickly. However, in the human genome there are so many of them
that even when fixation is unlikely, the total number of neutral
fixations greatly outnumbers those due to selection. The large amount of
neutrally evolving ("junk") DNA is one way in which eukaryote genomes
differ radically from prokaryote ones.
I never said or implied any such thing. Your ignorance drives you in odd
directions.
> probabilities greater than one exist in your
> twisted world,
Ditto.
> selection increases the diversity of populations
> despite the fact that selection kills or impairs members of the
> population from passing their genetic information to future
> generations,
Negative frequency-dependent selection. Look it up.
> reducing the intensity of selection causes beneficial
> mutations to be spread through populations more rapidly than stronger
> selection pressures.
Never said that either. I think you confused "soft selection" with
low-intensity selection.
> All these are fundamental scientific and
> mathematical blunders that evolutionists make in their loose and
> irrational misinterpretation of reality. John, if you learn nothing
> else here, learn this, the multiplication rule of probabilities is the
> dominant and central mathematical principle which drives the mutation
> and selection phenomenon.
So you claim. I see no mathematical argument, though.
> The variable which is governed by this
> principle is the complexity of the selection conditions. There is no
> other variable in this phenomenon that has the mathematical impact
> which the complexity of the selection conditions does. This is why HIV
> behaves the way it does when subject to combination selection
> pressures, this is why cancer responds the way it does when
> combination selection pressures are used, this is why weeds respond
> the way they do when combination herbicides are used, this is why any
> population subjected to combination selection pressures behaves the
> way it does. Not mutation rates, not population size, not number of
> generations; no other variable in the mutation and selection
> phenomenon has the mathematical impact which the complexity of the
> selection condition has. It’s time for you to come back to reality
> John.
I only wish you could read and respond to what I say, rather than using
it as an opportunity to repeat your canned rants for the nth time.
Stuart
> The following are a compilation of responses to messages 976-1000.
> ========================================================
> Stuart>> As long as evolutionists use terminology like drift to describe what
> >> happens to populations on a plateau of a fitness landscape rather than
> >> describing what actually happens, ie the population is diversifying,
> >> they will continue to make the same blunders over and over.
> >The genetic changes that occur as a result of fixation via drift
> >greatly exceed those due to
> >fixation becuase of selection. This is a simple statement of fact.
>
> Very interesting Stuart, do you care to explain to us why this is a
> fact? We wouldn t want people to start believing that you are fixated
> on fixation; we would have to fix that.
Yes, you seem to have a problem with anything that is demonstrably
true.
If you don't understand that mutations which do not affect selection
can get
fixed in the population by drift then I can't help you.
If you do understand that, and you understand the inherent redundancy
in the genetic code, you will realize that a large percentage of
mutations
don't result in any change.
>Mutations occur at whatever rate they occur regardless of whether the
> >population is
> >at a peak, a plateau, in a valley or somewhere in between. Hence
> >changes resulting from drift
> >dwarf those from selection regardless.
>
> So, now we no longer have the theory of evolution by mutation and
> selection, it is now the theory of evolution by drift.
To a large extent yes.. Drift best explains the bulk of the changes
that occur
in diverging lineages such as between Chimps
and Humans An example which Harshman has already used and
given the basics mathematics for. The changes which actually
result in phenotypic changes are numerically much smaller than those
fixed by drift.
That is all. This isn't rocket science.
Everything is
> on one big happy plateau. There are no longer detrimental mutations
Detrimental mutations are selected against. I'm not sure what they
have
to do with this particular argument. But I guess when you have run out
of arguments aimless flailing is all one has left.
Stuart
hersheyh
mathematical reasoning that results in his claim that the
"multiplication of probabilities" rule applies equally in all the
following cases In all the cases, the probability of interest is not
the individual probability of mutation to one of the resistances, but
the probability of both resistant mutations occurring in the same
individual.:
1) Selection for two antibiotic resistances, each able to kill all
individuals that are sensitive, when both antibiotics and bacteria are
added simultaneously to rich media. This is the only case where the
multiplication rule actually holds. Start with 10^9 bacteria added to
10 ml and the probability of mutation to resistance to either
antibiotic of 10^-8/bacteria/generation. The multiplication rule
applies here *because* the probability of both mutations occurring in
the same individual does, indeed, require that both occur
simultaneously in an individual that had neither mutation. This would
be like the probability of rolling two sixes in a simultaneous roll of
two dice.
2) Serial selection. Same number of bacteria and mutation rate, but
first select those individuals who are resistant to antibiotic A
(bacteria and antibiotic added simultaneously to rich media).
Survivors allowed to grow in rich media plus antibiotic A for 30
doublings (overnight growth for E. coli). Then 10^9 survivng bacteria
are added to 10 ml of fresh rich media with both antibiotics, for 30
doubling times. The multiplication rule does not apply here for the
probability we are asking about: the probability of *both* mutations
in the same individual. That is because the step that involves
selection for *both* mutations in the same individual is not occurring
on individuals with neither mutation, but rather in a population of
individuals that *already* have one of the mutations. This would be
like the probability of rolling two sixes by first rolling one die and
then, *if and *only if* that first die is a 6, do you then actually
roll the second die to try to get a second 6. The probability for
*both* mutations in the same individual (or both die showing a six) is
actually the probability of the second mutational step (or second die
showing a six) because the population which is undergoing selection
for *both* mutations in the same individual already has been chosen
(by the environment) to have the first. This is a problem of
conditional probability. The roll of the second die is conditional on
the result of the roll of the first die.
http://www.algebralab.org/lessons/lesson.aspx?file=Algebra_ConditionalProbability.xml
3) Parallel selection. Same number of bacteria and mutation rate. In
one tube select an F- strain of E. coli for resistance to antibiotic A
and in another tube select an F+ strain for resistance to antibiotic
B. Grow both overnight. Combine the strains (each resistant to one
of the antibiotics) for a few hours in media lacking either
antibiotic. Then add to media containing both antibiotics. In this
case, the probability of an individual having *both* mutations is
actually the probability of generating a double-mutant by
recombination from two populations each of which has already been
selected for resistance to one of the antibiotics. I am assuming,
correctly in this case, that that rate of recombination generating a
double-mutant is significantly higher than the probability of a second
independent mutation to resistance to the other antibiotic. This
would be like independently rolling two die on different tables until
each gives a six. Then moving the sixes to the same table with a high
probability that the moved die will still have both sixes facing up.
Of course, our dear Dr. Dr. may be unaware of what F- and F+ strains
imply. He should look it up. But I only ask that he explain exactly
why and where he introduces the "multiplication rule of probabilities"
in the last two examples wrt the probability of getting a *double
mutant* in the same individual. My guess is that he will simply
ignore it or just regurgitate the "its the multiplication of
probabilities" rule, as if that were the only rule in probability.
Probably never heard of the addition rule either.
Mark Isaak
> Alan Kleinman MD PhD wrote:
>> The following are a compilation of responses from the splinter threads
>> threads of March 15
If you're trying to respond to me, try again. I skip any post whose
line count gets into four digits.
Alan Kleinman MD PhD
========================================================
lucaspa
>> Since the concept of random mutation and natural
>> selection is a stochastic process dependent on random independent
>> events (random mutations), any selection conditions which require more
>> than a single beneficial mutation will be governed by the
>> multiplication rule of probabilities.
>Not necessarily. You are forgetting neutral mutations. What you have
>in the population are variations that are neutral in the current
>environment. However, using the antibiotic model, that neutral
>mutation would impart SOME resistance to antibiotic B. It does not
>have to be total resistance, but just some. Now your "multiplication
>rules of probability" are invalid because a significant proportion of
>the population already has has some resistance to antibiotic B. If
>the frequency of the neutral mutation for resistance to antibiotic B
>is 30%, what does that do to your "multiplication rules of
>probabilities"?
Welcome to the discussion lucaspa. You are correct to a point here.
Every population subjected to selection pressures must have some
variants that have sufficient fitness that they are still able to
reproduce otherwise the population would go extinct. But that doesn’t
invalidate the multiplication rule of probabilities. All you are
saying is that you have more players in your lottery for the next
beneficial mutation. You are just describing a scenario where you
already have some amplification of a beneficial allele before the new
selection pressure is applied.
>Now that the population already has a neutral mutation which is
>beneficial in the new environment -- antibiotic B -- the mutation for
>antibiotic A has put the population on a trajectory in the fitness
>landscape to get to resistance to simulataneous use of antibiotics A
>and B. The individual with resistance to both is going to be the one
>to give rise to the next generation of microbe. Now new mutations
>increasing resistance to either A or B is going to appear in an
>individual that already has some resistance to the other.
That’s why when treating HIV, you need three *effective* selection
pressures. If there are already resistant strains of the virus in the
host, you are not using three *effective* selection pressures if there
is already resistance to any of the three drugs.
And
>> That s why I don t want to get into your speculative games.
>> Evolutionists make a living by speculation. I make my living by doing
>> accurate computations and the multiplication rule of probabilities
>> shows that your speculations are wrong. Mutation and selection does
>> not work the way you claim.
> I strongly suggest you read Ronal Fisher's The Genetical Theory of
>Natural Selection (1930) ISBN 0-19-850440-3.
>It is as mathematical as you could wish.
That book was written long before there was any capability to gather
empirical evidence of mutation and selection like there is today. We
now have extensive empirical evidence how mutation and selection works
by the HIV example and many other real, measurable and repeatable
examples of mutation and selection. Selection pressures are precisely
identified and their targets known. The particular mutations which
give resistance to these selection pressures are known as well. And
the effects of multiple selection pressures acting simultaneously are
now better understood. If you think this book contradicts any point
that I am making, feel free to post the point. If you really have an
interest in studying population genetics, study Thomas Schneider’s ev
computer simulation of mutation and selection. This simple and elegant
model of the phenomenon allows you to easily change population size,
mutation rate, genome size and several other variables that allow you
to study how this phenomenon behaves. Incidentally, Ronal Fisher
believed that neutral mutations only had a minimal influence on the
evolutionary process.
>Your comment about "speculation" is apples and oranges. What is
>being discussed is the "selection pressure" or functionality of the
>new trait, not mathematics. As it turns out, the fossil record does
>show him to be correct about the reasons for the evolution of
>feathers. They started out as a few -- for display -- then evolved
>for a covering for thermoregulation. Dial's work then shows how
>feathers could be used for providing stability running up an incline,
>either to catch prey or get to a refuge to escape a predator:
> Kenneth P.Dial, Wing-Assisted Incline Running and the Evolution of
>Flight. Science, 299: 402-405, Jan 17, 2003.
There are very specific mathematical principles which govern the
mutation and selection phenomenon. These principles determine how
quickly the process can work when it does work and under what
conditions it does not work well or at all. Steve Carlip can give us
lectures on reptile scales, bird feathers and convective heat transfer
and Kenneth Dial can lecture how nice wings are in assisting incline
running. It would be nice to evolve eyes on the back of the head so
you could see predators coming from behind. But unless you have the
appropriate selection pressures and the number of generations
necessary to carry out the transformations, these concepts are nothing
but speculation. Why don’t you try a real mathematical problem? Try to
do the accounting for the 40,000,000 differences (per John Harshman)
between human and chimpanzee genomes in only a million generations.
That would require the fixing of dozens of alleles every generation
when the mathematical models and empirical evidence show that it takes
hundreds of generations to fix only a single beneficial allele by
mutation and selection. Perhaps you believe that neutral mutations can
spread through a population more quickly than beneficial mutations?
Show us the mathematical and empirical evidence which supports this
claim.
>For insect wings, the MATHEMATICS show that insect wings -- which are
>modified gills -- evolved as heat exchangers. When they reached the
>size for maximum efficiency as heat exchangers, that size was just
>below the size required to get the insect off the ground. Any
>reduction in body size by different selection pressure would then mean
>that the heat exchangers operated as wings. You want to look up the
>term "exaptation".
>Gould, "Not necessarily a wing" in Bully for Brontosaurus, pg.
>139-151, 1991.
>http://www.google.com/url?sa=D&q=ftp://128.32.118.46/pub/koehl/Kingsolver_Koehl_1994.pdf (for the peer-
>reviewed article)
No one is claiming that evolutionists haven’t written huge amounts of
speculation and by the sheer volume of this speculation you have been
convinced that it is true. That’s why I keep this discussion centered
on the mathematics of mutation and selection. Hard mathematics and the
precise measurement of empirical evidence is what are required to
understand how mutation and selection works. Once you understand this,
it will become clear that the transformation of gills into wings is
nothing more than rank speculation. It may be good material for the
SciFi channel but it doesn’t qualify as hard mathematical science.
Unless you can show how mutation and selection can do such a
transformation, you might as well save that literature for a fictional
writing course. Explain to us how dozens of mutations can be fixed
every generation for hundreds of thousands of generations in the
transformation of humans and chimpanzees from a common ancestor and
save your gills to wings and reptile scales to feathers for naïve
school children and your fellow indoctrinated evolutionists.
>> > > John, you have a hard time looking at
>> I ve done it in a previous post. If you missed that post I ll do it
>> again. I m responding to many posts and so I m a bit behind. I ve also
>> explained how the multiplication rule of probabilities still applies
>> to beneficial mutations even if they don t occur simultaneously.
>I'm afraid it doesn't. You are fogetting that, once a beneficial
>mutation appears, it spreads thru the population over generations.
>Eventually, it becomes "fixed". That is, EVERY member of the
>population has it. Therefore you don't multiply probabilities as tho
>each mutation is starting from scratch.
The amplification process must occur for there to be a reasonable
probability that the next beneficial mutation in the sequence to occur
at the proper locus, that’s what must occur for a population to
overcome the multiplication rule of probabilities. If there are
multiple selection pressures acting simultaneously, the ability of the
population to fix multiple alleles simultaneously is impaired if not
stopped. This is why combination therapy works for the treatment of
HIV.
>> The problem with your claims about bird evolution has to do with the
>> way mutation and selection works. I m trying to have a discussion
>> about the mathematics of mutation and selection, something which you
>> are having difficulty comprehending. I hope you understand why the
>> probability of a beneficial mutation occurring at a particular locus
>> is not proportional to the population size. That is an important
>> element of the mutation and selection phenomenon.
>You may be speaking different parts of the subject. While the
>probability of a particular mutation occurring at a particular site in
>DNA is independent of population size, the population size does
>influence the odds that the particular mutation will appear withing
>the population in any given generation.
That’s not totally correct lucaspa. The probability of a beneficial
mutation occurring at a particular locus is affected by population
size but the affect of population size on that probability of a
particular mutation occurring at a particular site is less than
additive. That’s why it takes so many generations with amplification
of a beneficial allele before there is a reasonable probability that
the next beneficial mutation will occur at the proper locus. That’s
what populations must do if they are going to overcome the
multiplication rule of probabilities. That’s what’s required of the
mutation and selection process for two beneficial mutations to occur
on a given member (not simultaneously).
>Are you considering that there are several mutations that will yield
>comparable phenotypes? Or do you think there is only one mutation
>that will give an given phenotype?
I believe that most non-stabilizing selection pressures are
disruptive. For example, there are many strains of MRSA. But this
doesn’t help the mutation and selection process because the different
strains will compete with other strains for resources in the
environment making it more difficult for each stain to amplify their
beneficial alleles.
========================================================
John Harshman
>> John, if you are talking about the evolutionist fantasy that reptiles
>> transform into birds, that’s your fiction and the only thing I have to
>> say about this is that it is a mathematically irrational concept only
>> suitable for the SciFi channel.
>How do you know it isn't true?
John, I know it is true because I know how mutation and selection
works and it doesn’t work the way evolutionist claim that it works.
Specific mathematical principles are followed by the mutation and
selection phenomenon and the dominant mathematical principle is the
multiplication rule of probabilities that two or more beneficial
mutations will occur on an individual (not simultaneously).
>>>> That’s an example of
>>>> recombination and selection. The environment is selecting for
>>>> different beak sizes based on the food availability. I have also
>>>> discussed the mathematical irrationality of the transformation of 9
>>>> signaling hormones in order to transform reptile scales into feathers.
>>> "Discussed" is a polite way to put it. You have in fact gone into
>>> data-free ridicule.
>> John, the random mutation and natural selection phenomenon is a
>> stochastic process and therefore the probability of random beneficial
>> mutations is governed by the multiplication rule of probabilities.
>Hard to tell, because what you're claiming isn't clear. Certainly the
>probability of two particular mutations happening is the product of
>their individual probabilities. But you supposedly aren't talking about
>mutation alone, but about fixation. And the probability of two mutations
>becoming fixed isn't the product of their individual probabilities of
>being fixed.
Fixation is how populations address the multiplication rule of
probabilities. It is already clear to you that it is highly unlikely
that two beneficial mutations will occur on a single individual in a
single generation. What fixation (which I actually prefer to call
*amplification*) does is increase in number the members of the
population with the first beneficial mutation so that you have many
players in the lottery for the second beneficial mutation. That’s how
populations overcome the multiplication rule of probabilities in order
to accumulate beneficial mutations in its members. The price
populations have to pay in order to do this is it costs many
generations. Haldane called this the “cost of natural selection”.
>> This is the dominant mathematical principle that determines whether an
>> evolutionary process has a reasonable chance of occurring or not. The
>> only time the mutation and selection process can work efficiently is
>> if the multiple beneficial mutations can occur in a sequence where
>> each of the beneficial mutations is separated by an amplification
>> process for that beneficial mutation. This is why when combination
>> therapy (selection pressures) works for HIV and for the treatment of
>> any other mutating and selection disease. You are forcing the
>> population to get two beneficial mutations simultaneously and/or
>> interfering with the amplification process of any single beneficial
>> mutations.
>And that does apply if a you need two simultaneous mutations in order
>for there to be a selective benefit. But not otherwise.
No John, it always applies. That’s why in every real, measurable and
repeatable example of mutation and selection where combination
selection pressures are applied, the mutation and selection process is
stifled if not stopped completely. The combined selection pressures
interfere with the amplification process for any beneficial mutation
which might occur. The mutation and selection process is very slow to
begin with taking hundreds of generations to fix (amplify) a single
beneficial mutation subject to a single selection pressure. As soon as
the population is forced to amplify more than a single beneficial
allele, the different selection conditions interfere with each other
in the amplification process. Remember, selection pressures are things
which kill or impair the reproduction of the members of a population.
Even if members of a population have a beneficial allele for one
selection pressure, the other selection pressure is still killing or
impairing the reproduction of those members preventing that allele
from being amplified and visa versa for the other beneficial alleles
to the other selection pressures.
>>>> I would rather avoid the evolutionists speculations about what
>>>> happened a hundred million years ago
>>> Why "speculation"? There's plenty of good evidence on the evolution of
>>> birds. But you refuse to discuss it.
>> Sure birds evolve, so do dogs, so do all living things, but the notion
>> that reptiles turn into birds is a mathematical irrationality. The
>> mutation and selection process is far, far too slow to make such
>> transformation and the selection conditions don’t exist which could
>> cause such a transformation.
>Please show your math on this one. How slow? What selection conditions
>would be needed that don't exist?
Last week I showed hersheyh how to compute the probability of a
beneficial mutation occurring at a particular locus as a function of
population size. Population has less than an additive affect on that
probability. The number of generations and the mutation rate also has
less than an additive affect on this probability. That’s why it takes
hundreds of generations with amplification of a beneficial allele in
order for the next step in the evolutionary process to occur. The
number of generations alone without amplification of beneficial
alleles would make the mutation process profoundly slow taking
millions of generations for the next beneficial mutation from
occurring on the member with a previous beneficial mutation. This is
why when you remove selection out of the equation as you do with the
drift concept, you don’t realize the mathematical corner you paint
yourself in. Selection is what differentiates the theory of evolution
from abiogenesis. I hope I don’t have to explain to you why
abiogenesis is mathematically irrational.
>> Evolutionists teach genetics to physicians, I hold those teachers of
>> evolutionism responsible for the failure to properly teach the basic
>> science and mathematics of the mutation and selection phenomenon.
>I'm pretty sure that geneticists teach genetics to physicians, and that
>hardly any physicians have ever had a single course in evolutionary
>biology. Clearly you haven't.
I’ve used my engineering skills and study to understand how mutation
and selection works. I’ve done a very careful study of Thomas
Schneider’s simple by elegant model of mutation and selection. His
model does properly describe the mathematics of population genetics
and does so with a minimum number of assumptions. Despite taking
courses in biology, microbiology, genetics and biochemistry, not a
single one of these courses attempted to properly describe the basic
science and mathematics of mutation and selection. Look what all your
studies in evolutionary biology have gotten you. You believe that the
probability of a beneficial mutation occurring at a particular locus
is proportional to population size. And you don’t understand how the
multiplication rule of probabilities drives the mutation and selection
phenomenon. I would rather use my engineering skills to analyze the
mutation and selection phenomenon properly and use that analysis to
prevent the evolution of multidrug resistant microbes than to learn
the mathematically irrational concepts that are being taught in
evolutionary biology today.
>> John, the multiplication rule of probabilities enters into every
>> example of mutation and selection unless that adaptation process only
>> requires a single mutation. As soon as the adaptation process requires
>> more than a single beneficial mutation, the multiplication rule enters
>> into the equation.
>Your fuzzy language is disguising the situation here. What do you mean
>by "adaptation process" and "requires more than a single"? Hard to say.
>If and only if a single mutation is not beneficial, and thus two
>mutations are required for any benefit, does that multiplication rule
>apply. If one mutation is good, but two mutations are even better, the
>multiplication rule is inapplicable.
As long as mutations are random independent events, the probability of
these events occurring is governed by the multiplication rule of
probabilities. It doesn’t matter whether the events occur
simultaneously or the events are separated by hundreds of generations
with amplification occurring between the events. If the amplification
process does not occur, the event of a second beneficial mutation
occurring on a member with the first beneficial mutation will be a
highly improbable occurrence due to the multiplication rule of
probabilities.
>>>> Apparently Edward Max
>>>> doesn’t know much about quantitative genetics, I guess it’s because he
>>>> was trained by an evolutionist.
>>> Such Christian charity.
>> We all know about evolutionist charity;
>How old are you? Are you really saying "Bobby hit me first"?
I’m old enough to know how mutation and selection works and I am sure
that Edward Max knows very little about how this process works. If
Edward Max understood how mutation and selection works, he would use
his position as supervising medical doctor of the Food and Drug
Administration to do something about antibiotic resistance. So far,
the only so called expert advice that primary care physicians get on
using antibiotics is to stop using these medicines so much so that the
selection of resistance doesn’t occur. My response to this is hell no.
Let those physicians who give that advice delay the giving of
antibiotics to their ill patients and let them die of pneumonia,
meningitis and sepsis. If these so called experts want to delay the
appearance of drug resistant microbes, let them learn the lesson given
by the use of combination therapy for HIV.
>> see what happens to the
>> careers of those biologists who question the validity of the theory of
>> evolution.
>What happens? Who are they?
Biologists who question the theory of evolution are denied faculty
positions, promotions, research money. This is because the inbred,
indoctrinated and mathematically irrational evolutionists can not take
any challenge to your irrational belief system.
>> The truth is that Edward Max because of his leadership in
>> the medical field has a responsibility to properly understand how
>> mutation and selection works. So far, he has written nothing which
>> shows that he properly understands how the mutation and selection
>> phenomenon works. This harms the people for which he has oversight.
>I doubt your ability to evaluate Max's knowledge.
If Edward Max wants to indoctrinate naïve school children with his
belief that reptiles turn into birds, that’s his prerogative. However,
someone in his position has a responsibility to properly understand
how the mutation and selection phenomenon works. He doesn’t and we
have multidrug resistant microbes and less than durable cancer
treatments to show for it.
>> John, you can read your fossil tea leaves any way you want. Just
>> explain to us how 67 mutations are fixed per generations in your
>> purported transformation of chimpanzees and humans from a common
>> precursor. You can make up any stories you want for the SciFi channel
>> but stop misrepresenting how mutation and selection works.
>I've explained this already. You don't read. In fact you seem to pay no
>attention whatsoever to anything that anyone says to you. Your mantras
>haven't changed by so much as a single word since we began this
>"discussion".
I saw your loose explanation. I put that explanation at a much lower
level of mathematical credibility than your loose claim that the
probability of a beneficial mutation occurring at a particular locus
is proportional to population size and that claim was wrong.
> [snip the great amount below that you didn't respond to, possibly
>because Google is such an inadequate platform, or possibly because you
>just forgot it was there]
I always say if it’s worth saying, it’s worth repeating. The governing
mathematical principle of the mutation and selection phenomenon is the
multiplication rule of probabilities and the mutations do not have to
occur simultaneously for the multiplication rule to apply.
And
>> That s why I don t want to get into your speculative games.
>> Evolutionists make a living by speculation. I make my living by doing
>> accurate computations and the multiplication rule of probabilities
>> shows that your speculations are wrong. Mutation and selection does
>> not work the way you claim.
>You make your living by doing accurate computations? What an odd sort of
>doctor you must be. And how can you say what evolutionary biologists do
>when you know nothing about evolutionary biology?
I certainly have to make accurate computations. When I specify the
amount of medication, I have to be very accurate. Now if you consider
yourself an evolutionary biologist, your loose approximations make for
sloppy computations. Do you still believe that the probability of a
beneficial mutation occurring at a particular locus is proportional to
population size? Do you think that the probability of a beneficial
mutation occurring at a particular locus is proportional to mutation
rate or the number of generations the population is able to reproduce?
Do you still believe that the multiplication rule of probabilities
does not apply in the mutation and selection process except when the
mutations must occur simultaneously? John you need a lot of work on
your computations to make them accurate.
>Do you think fossils have anything to tell us about past life? If so, what?
I think the mathematics of mutation and selection and the empirical
evidence which substantiates that mathematics has much more to tell us
about evolution than any evolutionist speculation about fossils.
>> I ve done it in a previous post. If you missed that post I ll do it
>> again. I m responding to many posts and so I m a bit behind. I ve also
>> explained how the multiplication rule of probabilities still applies
>> to beneficial mutations even if they don t occur simultaneously. If
>> you still have trouble understanding that mathematics and how
>> populations try to overcome the multiplication rule, I ll go over it
>> again.
>I think we would have resolved the mutation probability thing if you had
>read any of my posts. But I don't recall the explanation of that
>multiplication rule applying even without simultaneous mutations. Could
>you repeat that? Remember that I don't mean just simultaneous mutation,
>but mutations that must be together to have any selective advantage.
>They could happen sequentially provided that the first mutation alone
>conferred no advantage. The question is whether this rule applies even
>if a single mutation is advantageous, and why it should.
In order for a population to accumulate multiple beneficial mutations
by the mutation and selection process, it must do it in a cycle of
beneficial mutation/amplification of beneficial mutation before the
next mutation in the sequence has a reasonable probability of
occurring at the proper locus. If the population can not amplify the
particular allele, then the multiplication rule of probabilities makes
it highly unlikely that the next mutation in the sequence will occur
at the proper locus because so few members on which that mutation can
occur. Go back and look at the citation for the highly efficient beta
lactamase allele which requires five mutations to make the
transformation. Each mutation in the sequence must improve fitness to
reproduce so that that each allele in the sequence will amplify in the
population setting the stage for the next beneficial mutation in the
sequence. The population is using generations and amplification of the
beneficial allele in order to improve the probability that the next
beneficial allele will occur at the proper locus and thereby
overcoming the multiplication rule of probabilities.
>> The problem with your claims about bird evolution has to do with the
>> way mutation and selection works. I m trying to have a discussion
>> about the mathematics of mutation and selection, something which you
>> are having difficulty comprehending. I hope you understand why the
>> probability of a beneficial mutation occurring at a particular locus
>> is not proportional to the population size. That is an important
>> element of the mutation and selection phenomenon.
>So since you have no interest in discussing bird evolution, could you
>stop claiming it couldn't happen?
Ok, if you want to talk about reptiles turning into birds, tell us
what genes were targeted by which selection pressures and what
mutations were required to make the transformation. Then tell us how
many generations were required for the transformation. Perhaps you can
do better than your loose sloppy claims that dozens of alleles can be
fixed every generations for hundreds of thousands of generations in
the transformation of humans and chimpanzees from a common ancestor.
Let’s see how accurate a computation an evolutionary biologist can
make.
>> John, you are not prepared for this part of the discussion yet. Once
>> you have a better understanding of how mutation and selection works,
>> we can discuss how entropy relates to the mutation and selection
>> phenomenon. It s enough if you understand that mutations are a
>> disordering process and selection is and ordering process.
>Are you familiar with the Dunning-Kruger effect?
Go for it John, tell us how the Dunning-Kruger effect will overcome
the multiplication rule of probabilities of two beneficial mutations
occurring on a single member of the population (not simultaneously).
You throw every evolutionist idea and speculation against the wall
hoping that something will stick. Why don’t you learn the basic
science and mathematics of mutation and selection?
And
>> Ok, I agree with that. Every genetic sequence places that member on a
>> unique point on the fitness landscape. The starting point for the
>> trajectory impacts the possible trajectories that member can take.
>I accept your retraction.
John, do you even know what a retraction is? You simply claim you use
terms loosely. Have you figured out how to compute the effects of
population size on the probability that a beneficial mutation will
occur at a particular locus yet?
>>>> Recombination is not required
>>>> for there to be selection in a population.
>>> True but irrelevant to my point.
>> But you need to remember that selection reduces the diversity of the
>> population.
>Sometimes yes, sometimes no. Negative frequency-dependent selection, for
>example, increases diversity.
Give us a real example of this describing the gene and different
alleles for that gene both before and after selection has acted on the
population. Otherwise you are just blowing smoke.
>>>> Your drift concept is a
>>>> demonstration of poor use of vocabulary. When a population is able to
>>>> reach a plateau on a fitness landscape, the population does not drift
>>>> on this plateau, it diversifies.
>>> You really have no idea of elementary population genetics. It isn't the
>>> population that's drifting. It's allele frequencies. They undergo a
>>> random walk. Eventually, all random walks end either at 100% frequency
>>> (fixation) or at 0% (extinction). This happens to all neutrally evolving
>>> alleles. The probability of eventual fixation at any given moment is
>>> equal to the current frequency.
>> Oh really? So Lenski�s populations are all going to end up at 100%
>> fixation?
>They are for all neutral alleles they currently have. Of course new
>alleles arise in the meantime, so genetic diversity is replenished, and
>achieves an equilibrium level, given neutrality.
You haven’t read the paper where he describes his data, have you? Are
you just using your words loosely again?
>> He�s not allowing his populations to go extinct. Selection
>> does not allow for random walks. Selection is the principle that in
>> some cases allows a population to overcome the multiplication rule of
>> probabilities for multiple beneficial mutations. Fixation is not a
>> random process; it is a process dependent on the intensity of
>> selection which is not random. If you are trying to say that the
>> number of generations required in order for fixation to occur is
>> dependent on the current frequency of the beneficial allele, you�ve
>> just restated what Haldane stated with his model more than 50 years
>> ago.
>I wasn't talking about selection. I was talking about neutral evolution.
>You have already agreed that some alleles are equal in fitness; if all
>alleles are equally fit, there is no selection, but eventually one of
>them will become fixed.
Ok John, since you know so much about neutral evolution, tell us how
quickly neutral alleles are fixed in a population? And don’t use your
loose terminology.
>>> Note that some loci may be evolving neutrally at the same time as other
>>> loci are under selection. Whole organisms aren't the proper level at
>>> which to examine drift.
>> The fundamental unit process of evolution is the substitution of a
>> more beneficial allele for a less beneficial allele. That�s how
>> populations improve fitness. A neutral allele will not increase in
>> frequency because it offers no selective advantage. If this is your
>> idea of elementary population genetics, I�m glad I have no idea of
>> this mathematical irrationality.
>Yes, the willfully ignorant are often for some reason proud of their
>ignorance. I don't understand why, but it happens. Similarly, you don't
>understand anything about neutral evolution, and yet it happens.
Haldane is the one who made that statement. Read his paper. I realize
that there are many evolutionists who believe that neutral alleles are
randomly fixed in populations and that this occurs much more quickly
than selection could ever do it. You now need to demonstrate how
dozens of alleles can be fixed every generation randomly for hundreds
of thousands of generations to account for the 40,000,000 differences
you admit to between humans and chimpanzees. Just how do random
processes spread those dozens of alleles through a human and
chimpanzee populations every generation?
>But let's take it a little at a time. Do you agree that the frequency of
>a neutral allele (at a locus where all alleles have equal fitness) will
>undergo a random walk? If so, what do you think the result of a random
>walk will be?
What I believe is that neutral mutations primarily are going along for
the ride as the more fit members of a population increase in frequency
over generations. But let’s hear you explain how dozens of neutral
alleles can go on a random walk and spread through the human and
chimpanzee population every generation after generation for hundreds
of thousands of generations when selection takes hundreds of
generations to spread only a single allele thorough a population.
>>>> The reason why the population can
>>>> diversify is that there a number of variants possible (determined by
>>>> the size of the plateau) which survive and reproduce equally well to
>>>> other variants in this selection environment. Fixation or substitution
>>>> requires selection pressure and on a plateau, this pressure does not
>>>> exist, that is why the population can diversify.
>>> If you actually tried an experiment in this, you would find that one
>>> variant would eventually become fixed. Think of it as a lottery.
>>> Somebody has to win, and somebody has to lose, even though it's all random.
>> Amplification of an allele requires that it gives selective advantage
>> to that member. That member is a better replicator than other members
>> of the population and over time that allele will increase in
>> frequency. Mutations are random but selection is not.
>Selection is not but a random walk is, and that's what happens in
>neutral evolution. Surely you don't imagine that in a neutrally evolving
>locus the frequencies of all alleles will remain forever unchanged. Do you?
What I think is that you can not come up with a mathematically
rational explanation for how dozens of alleles are fixed every
generation based on a real mechanism of transformation of genomes. You
throw some loose terminology at us but it will not be mathematically
rational.
>>>> Remember selection
>>>> reduces diversity, mutations increase diversity and the way to
>>>> increase diversity of a population is to reduce the selection pressure
>>>> on the population.
>>> Sometimes true, sometimes not. You have no clue. Sorry.
>> Feel free to give us an example where selection increases the
>> diversity of a population. Pretty please, give us a clue.
>HLA is a good one. I've mentioned it before.
Tell us what the selection pressures are and what the alleles are
before and after the selection conditions applied.
And
>> Now it is true that the phenotype is an expression of the genotype but
>> ultimately evolution is played out on the genotype.
>Another of your problems is that you trot out stock phrases without
>regard to whether they actually respond to what was said. As in this
>case: your stock statement was irrelevant.
Perhaps you prefer I use some of your loose terminology?
>>>> I have collected hundreds of real, measurable and
>>>> repeatable examples of mutation and selection which all says that
>>>> combination selection pressures always suppress the mutation and
>>>> selection phenomenon.
>>> Hundreds? Can you try something other than HIV for a change?
>> John, did you miss the examples I posted from the field of oncology?
>Do you have anything non-medical? Perhaps something involving actual
>plants or animals? That would be more fun.
>I'm snipping the examples. In fact most of them seemed irrelevant to
>your point.
>> John, I have many more examples that I will continue to post all which
>> demonstrate what the multiplication rule of probabilities does to the
>> mutation and selection phenomenon, but I will also continue to post
>> examples from the evolution or lack thereof of HIV to combination
>> therapy.
>Try posting something relevant. And please, animals or plants would be
>nice. Just 'cause I like them.
Anything for you John.
http://www.inspection.gc.ca/english/plaveg/bio/resist/disdoce.shtml
"Herbicide Resistance Management Issues In Plants With Novel Traits
(PNT’s)" “There is a need to develop broadleaf combinations or
mixtures to control glyphosate and multiple HT volunteers pre-seed.
For example, 2,4-D, MCPA, bromoxynil and a low residual sulfonylurea
like tribenuron methyl in combination with glyphosate would provide
broad-spectrum pre-seed weed control including volunteer glyphosate HT
canola. In some situations amitrole and paraquat could provide
effective pre-seed control and resistance management for volunteer HT
canola.”
And
“Herbicide mixtures to manage volunteers and reduce selection pressure
could be a requirement for future HT crop releases.”
http://www.crcsalinity.com.au/newsletter/sea/articles/SEA_2102.html
"Social costs of herbicide resistance: the case of resistance to
glyphosate", “In this paper we discuss the case of the evolution in
weed species of resistance to glyphosate, a valuable and widely used
broad-spectrum non-selective herbicide first developed by Monsanto in
the early 1970s.”
and
“The authors conclude that “The use of glyphosate in combination with
other low risk herbicides for weed control with RR cotton provides an
opportunity to significantly reduce the risk of off-site herbicide
contamination in Australian cotton production” ”
http://www3.interscience.wiley.com/cgi-bin/abstract/112607405/ABSTRACT?CRETRY=1&SRETRY=0
"Possible methods of inhibiting or reversing the evolution of
insecticide resistance in mosquitoes" “The following possible methods
of minimising the risks of resistance are considered: (a) adjustment
of the dosage and frequency of spraying so that resistance genes are
effectively recessive; (b) detection and eradication of new foci of
resistance before they have a chance to spread; (c) spraying a mosaic
of unrelated insecticides with the intention that immigrants from one
sector of the mosaic to another will dilute the frequency of
resistance genes; (d) re-introduction of susceptibility genes into the
progeny of wild females by the release of heterozygous males with
resistance genes translocated on to their Y chromosome so that they
are protected from insecticidal killing but will pass susceptibility
to their female progeny; (e) replacement of a resistant by a
susceptible population by means of a negatively heterotic system such
as bidirectional cytoplasmic incompatibility. A plausible case can be
made for each of these methods based on theoretical models and
appropriate assumptions. However, an assessment of whether any of them
will really be of any value depends on the answers to certain
questions in the field. Therefore field projects have been initiated
on Anopheles culicifacies in Sri Lanka and Pakistan, Culex
quinquefasciatus in Tanzania and Anopheles arabiensis in Sudan. The
results so far are summarized.”
I have many more citations.
========================================================
r norman
>>I understand that probability theory is above the mathematical level
>>that most evolutionists learn in their dumbbell mathematics courses.
>>So let me give you a start in the mathematics of the random mutations
>>and natural selection, a stochastic process. The probability of two
>>independent beneficial mutations occurring is the product of the
>>probabilities of the individual beneficial mutations occurring. So if
>>the probability of mutation A occurring is P(A) and the probability of
>>mutation B occurring is P(B) then the probability of both mutations
>>occurring is P(A)*P(B). Did I go to fast for you?
>>- Hide quoted text -
>Wow, that went right over my head! Did I happen to mention that I
>took graduate level courses in probability theory and statistics? That
>I undoubtedly know far more mathematics and probability theory than
>you do?
Then why don’t you explain to the other evolutionists the difference
between events which are mutually exclusive and events which are
complementary. Evolutionists in this discussion seem to think that the
probability that a beneficial mutation occurring at a particular locus
is proportional to population size that is the additive rule of
probabilities applies. If you are the expert in probability theory,
why don’t you explain that to them that they are wrong? Also explain
to them that the additive rule does not apply to the probability for a
beneficial mutation at a particular locus to occur as a function of
the number of generations and that the additive rule does not apply to
the probability for a beneficial mutation to occur at a particular
locus as a function of mutation rate. These are all fundamental errors
evolutionists make in analyzing the mutation and selection phenomenon.
But the greatest error on the part of evolutionists is the failure to
recognize that the multiplication rule of probabilities is the
dominant mathematical principle which drives the mutation and
selection phenomenon that is the probability of two independent
beneficial mutations occurring is the product of the probabilities of
the individual beneficial mutations occurring.
>This, coming from somebody who has no idea in the world what quantum
>mechanics really is or how it differs from classical statistical
>thermodynamics.
Whatever.
========================================================
Frank J
>> Only those indoctrinated in evolutionism would make that claim.
> (snip)
>> I understand that probability theory is above the mathematical level
>> that most evolutionists learn in their dumbbell mathematics courses.
>While you were busy composing that and 100s of other posts you missed
>how we "indoctrinated dumbbells" were finally defeated by Tony Pagano,
>who succeeded where 150+ years of evolution-deniers failed.
>Now that "evolutionism" is dead, can we look forward to you
>elaborating on your incredulity of Tony's new theory? You can start
>with the geocentrist universe part.
Sorry, I’m too busy trying to correct the evolutionist bungling of the
basic science and mathematics of mutation and selection. This bungled
evolutionist understanding and teaching of mutation and selection has
harmed and continues to harm millions of people suffering from
diseases subject to the mutation and selection phenomenon.
> (snip)
========================================================
Prof Weird
>> Of course evolutionary biologists are not interested in preventing
>> drug resistance. That would require a proper interpretation of the
>> basic science and mathematics of the mutation and selection phenomenon
>> and would show that the theory of evolution is a mathematically
>> irrational belief system.
>Translation : "I have nothing of importance to say, so I'll insult
>evolutionists by accusing them of crimes against humanity !"
You evolutionist are insulted by the truth. What ever I say is nothing
compared to the harm you evolutionists have caused by improperly
understanding and teaching how the mutation and selection phenomenon
actually works.
>> Don t forget that ardent evolutionist Tom
>> Schneider works at the National Cancer Institute, an institution
>> dedicated to finding treatment and cures for cancer. Schneider has
>> made a scientific blunder by claiming that the multiplication rule of
>> probabilities does not apply to biological evolution.
>For evolution via SEQUENTIAL mutations, it doesn't.
It certainly does Prof Weird. Otherwise populations would not have to
amplify mutations before the next beneficial mutation has a reasonable
probability of occurring.
>As a hypothetical example :
>The odds of a bacterial population becoming resistant to antibiotic A,
>B or C is 1 in a million (10^-6)
>If you treat them with A AND B AND C at the same time, the odds of an
>ABC resistant strain showing up is
> (10^-6)^3, or 10^-18. As per the Mulplicative Rule.
>HOWEVER :
>If you treat bacteria with antibiotic A, then antibiotic B, then
>antibiotic C (switching drugs as
>soon as the population is resistant to the last treatment, ie
>SEQUENTIALLY), the odds of an
>ABC resistant strain arising is NOT (10^-6)^3 as the Mulplicative Rule
>suggests, but only 10^-6.
The point you evolutionists miss every time is that by using the drugs
sequentially, you are allowing the population to amplify the
beneficial mutations in order to overcome the 10^-18 probability. This
is the central point of the mutation and selection phenomenon, the
multiplication rule still applies but you are giving the population
generations and amplification of beneficial alleles in order to
overcome the multiplication rule in a step by step manner.
>EVERY TIME YOU SCREAM, WHINE AND FLATULATE ABOUT HOW DANGEROUS
>SEQUENTIAL
>DRUG SELECTION IS, YOU PROVE DR SCHNEIDER'S POINT !
Schneider is wrong with his claim that the multiplication rule of
probabilities doesn’t apply to biological evolution and the longer he
keeps that claim on his web site, the more he harms the people he is
paid to help ie those suffering from cancer. Schneider has made a
scientific blunder in describing the basic science and mathematics of
mutation and selection.
>> The
>> multiplication rule of probabilities is the governing mathematical
>> principle which determines why combination therapy improves the
>> durability of cancer treatments. Schneider s claim harms the very
>> people he is paid to help. Once the lawyers figure out that people are
>> being harmed by the irrational evolutionist teaching of mutation and
>> selection, we ll see where the blame ultimately falls.
>Schneider's claim is that evolution doesn't follow the mulplicative
>rule because THE STEPS ARE SEQUENTIAL.
The multiplication rule still applies when the steps are sequential.
What you evolutionists do not understand is that when the evolutionary
steps are sequential, the population can amplify beneficial mutations
over hundreds of generations improving the probability that the next
beneficial mutation can occur on a member with the previous beneficial
mutation. If the population can not amplify a mutation, then it should
be clear to you that it is highly unlikely that the next mutation in
the sequence will occur on a member with the previous beneficial
mutation and therefore have a very low probability of occurring on
that member or one of its descendents if the number of descendents
with that first beneficial mutation is small. Amplification is crucial
if the population will have any reasonable chance of overcoming the
multiplication rule of probabilities.
>You seem to have this pathological fixation on the idea that evolution
>REQUIRES the simultaneous fixation of several mutations in one
>individual all at once under hard selection (ie, 'have all the
>mutations or die !!!!!!!!')
No, fixation only occurs efficiently when only a single gene is
targeted by a single selection pressure. As soon as a population is
forced by selection conditions to fix multiple alleles simultaneously,
the different selection conditions interfere with the process of
fixing any of the beneficial mutations, that’s why combination therapy
works for HIV and why combination selection pressures always stifle
the mutation and selection phenomenon in every real, measurable and
repeatable example known.
>It doesn't; therefore, all your screaming about Haldane's 'dilemma'
>and 'mathematical irrationality of the ToE' is utterly misplaced.
Haldane’s work is not a dilemma to me. He properly described the
substitution process of a more beneficial allele for a less beneficial
allele. What Haldane did not address directly with his calculations
was the selection of multiple genes simultaneously. However Haldane
did comment on this in his discussion section. Read the paragraph
started with the sentence “Can this slowness be avoided by selecting
several genes at a time?” What I don’t believe that Haldane was aware
of was that selection of several genes at a time would not work
efficiently because the different selection conditions interfere with
the substitution process. Even if a member had an allele which was
beneficial for one selection condition, the other selection conditions
acting on the population will be killing or impairing the reproduction
of that member with that particular allele preventing the
amplification process.
>> > The "evolution of birds" in the context of everything that has
>> > transpired here on this discussion is the process by which birds
>> > appeared in the animal kingdom and their precursors., It does not
>> > mean how one species of finch changed into another species of finch.
>> > That latter is also an interesting question in evolution, but is not
>> > to the point. Tell us your theory/hypothesis/scenario about the
>> > origin of the group of animals now knows as "birds". Provide even a
>> > smidgeon of evidence for your story. Do not merely say it couldn't
>> > have happened your way because everybody knowledgeable in evolution
>> > says yes it could have and almost certainly did.
>> Only those indoctrinated in evolutionism would make that claim.
>Or anyone that actually knows anything about evolution, biology, and
>reality.
The evolutionist interpretation of mutation and selection is a far cry
from reality. The presence of multidrug resistant microbes, herbicide
resistant weeds and less than durable cancer treatments are a
testament to this.
>But you do seem to spend quite a bit of time evading the presentation
>of an alternative explanation;
>that is standard negative argumentation ('if I can complain about
>theory A loud enough long enough,
>my unstated theory B MUST be accepted as valid !!!!')
It’s not my job to give you an alternative explanation. It is my job
to show properly how mutation and selection works and it does not work
the way evolutionists claim.
>> Anyone
>> knowledgeable in the basic science and mathematics of mutation and
>> selection would say that claim is mathematically irrational.
>Only in YOUR version of evolution, where several mutations must arise
>in one individual all at once under hard selection.
The multiplication rule of probabilities applies to any evolutionary
process which requires more than a single beneficial mutation for the
adaptation process to occur. This is the mathematical and empirical
fact of life which you evolutionists have yet to come to grips.
>The REALITY-BASED version of evolution is sequential soft or neutral/
>near neutral selection.
The lower the intensity of selection, the greater the number of
generations required for the substitution of a more beneficial allele
for a less beneficial allele. Lowering the intensity of selection only
makes the evolutionary process slower. If you understood Haldane’s
work, that would be clear to you.
>For example, atrazine degradation. This is toxic to plants, but
>harmless to soil bacteria.
>Any bacteria that could digest atrazine would have access to a
>nutrient unavailable to the rest of the population,
>which gives them a reproductive advantage.
>BUT THE REST OF THE POPULATION WOULD NOT DIE OFF (as is required for
>Haldane's model to hold).
The substitution process does not require that the rest of the
population die off, it only requires that the number of members with
the beneficial allele be sufficient to overcome the multiplication
rule of probabilities. The beneficial allele only has to be amplified;
it doesn’t need to take over the population in order to improve the
probabilities for the next beneficial allele to occur at the proper
locus.
>Since the majority of the original population is not dying off,
>fixation of atz-utlizing mutations was fast, and FAR
>more likely than your 'all mutations MUST arise in the same bacterium
>at the same time !!' model.
Prof Weird, you still don’t get the point. Populations must amplify
beneficial alleles in order to accumulate multiple beneficial
mutations. If the population can not amplify an allele required for
the evolutionary process, the multiplication rule makes it very
unlikely that the next beneficial mutation in the sequence to occur at
the proper locus.
>> A while
>> back you made a claim: What is being ignored is the possibility that
>> two mutations can happen quite separately but then assembled together
>> by recombination (bacterial or sexual). HIV does recombination yet
>> your claim does not appear to be true. Would you explain why when HIV
>> does recombination; two beneficial mutations do not assemble together
>> by recombination? Or aren t you knowledgeable in evolution?
>This is a rare case where the mulplicative rule applies - the odds of
>resistance to A and B are required
>in the same virus at the same time.
The multiplication rule always applies whether the mutations have to
occur simultaneously in a single member in a single generation or
whether they occur in separate generations on descendents.
>In standard evolution, there is no requirement for A and B to arise in
>the same individual at the same time, so
>recombination works.
It doesn’t appear to have a significant affect on the evolution of HIV
when the virus is subjected to combination therapy. R norman thought
it should and now you are claiming that it should, however
recombination does not give significant help in the amplification of
beneficial mutations as demonstrated by the success of combination
therapy for the treatment of HIV.
>> > You have never discussed anything, especially not dealing with the
>> > evolution of birds or feathers or anything else. You merely parrot
>> > the same nonsense again and again the it is mathematically irrational
>> > without giving any mathematical calculations or references to those
>> > calculations to show that feathers could never have evolved. You
>> > present no argument for the origin of feathers (which is a very
>> > different story from the origin of birds).
>More evasive and petulant posturing :
Only the basic science and mathematics of mutation and selection which
shows that the theory of evolution is a mathematically irrational
belief system and that the failure of evolutionists to properly
describe this phenomenon has harmed and continues to harm millions of
people suffering from diseases subject to the mutation and selection
phenomenon.
========================================================
XaurreauX
>Evolution is for grownups.
Now I agree with that, we don’t need naïve school children being
indoctrinated with silly notions like “reptiles turn into birds”.
========================================================
Bob Berger
>And I would suggest (request) that Mr. Kleinman (MD PhD) publish here in very
>complete detail his mathematical model upon which Mr. Kleinman (MD PhD) bases
>his assertion that the theory of evolution is mathematically irrational.
>In the real world, mathematical models are expected to reflect reality; and when
>they don't, one corrects the model. Mr. Kleinman's (MD PhD) model, from what I
>have gathered from his posts, seems to be severely flawed. However, my
>impression is that Mr. Kleinman (MD PhD) leans more toward the "change reality"
>camp.
Bob, I know this will come to a complete surprise to you; I have
already published the mathematical principles here on this site. Let
me review the fundamental principle for you. The dominant mathematical
principle for the mutation and selection phenomenon is the
multiplication rule of probabilities. That is, the probability of two
beneficial mutations occurring on a single member of the population is
determined by the multiplication rule of probabilities. It doesn’t
matter whether the mutations occur simultaneously or not. All real
examples of mutation and selection are governed by this principle and
any properly written mathematical model is governed by this principle
as well. Now if you want to see how this is demonstrated, go to Thomas
Schneider’s web site sponsored by the National Cancer Institute and
study his ev computer simulation of mutation and selection. It’s a
very simple but elegant model of population genetics. You can run his
model online. I’ve done the study Schneider suggested in his original
publication and if you systematically vary the variables of his model,
you can easily see how the mutation and selection phenomenon works.
His model behaves in an analogous way to real examples of mutation and
selection as the numerous empirical examples I have posted
demonstrate.
And
>>> How would I know? How would anyone know? Why are you asking for the
>>> impossible here? It's enough for many purposes to know that it did
>>> happen. We will probably never be able to rigorously test why it
>>> happened. If I'm going to speculate, I would suggest that feathers
>>> evolved for thermoregulation, in parallel with the evolution of homeothermy.
>>That s why I don t want to get into your speculative games.
>>Evolutionists make a living by speculation.
>>I make my living by doing accurate computations
>And I have a five dollar calculator I bought at WalMart that makes its living
>doing accurate computations.
We have lots of computational tools and much more empirical evidence
of how mutation and selection works. There is a mathematical reason
why combination therapy works for the treatment of HIV. And that
mathematical reason is the multiplication rule of probabilities.
========================================================
Mark Isaak
>>> That's why I don't want to get into your speculative games.
>>> Evolutionists make a living by speculation. I make my living by doing
>>> accurate computations and the multiplication rule of probabilities
>>> shows that your speculations are wrong. Mutation and selection does
>>> not work the way you claim.
>> I strongly suggest you read Ronal Fisher's The Genetical Theory of
>> Natural Selection (1930) ISBN 0-19-850440-3. It is as mathematical as
>> you could wish.
>Lucaspa, you are new to this thread, so it is not obvious to you yet, but
>Dr. Kleinman already knows everything he ever needs to know about
>everything; learning something new -- anything new -- is beyond his
>consideration. Never mind that what he knows is wrong, he still will not
>learn.
Now Mark, I think you are a bit upset here. I know that it upsets you
that such a thing as the multiplication rule of probabilities sinks
your titanic theory. The waters were so smooth and you were making
such good time until you hit that iceberg. Who would have known that
the same mathematical principle which sunk the concept of abiogenesis
to the bottom of the primordial sea would also sink the unsinkable
theory of evolution? At least now with a rational understanding of how
mutation and selection actually works, logical strategies can be
developed for multidrug resistant microbes, herbicide resistant weeds
and the development of more durable cancer treatments. But I do want
to thank you evolutionists for giving me a lucrative medical practice
treating MRSA.
And
>> Mark, the multiplication rule of probabilities applies to every example
>> of mutation and selection which requires more than a single mutation to
>> adapt to the selection conditions.
>A quiz for you: Name the condition in which the multiplication rule of
>probabilities does *not* apply. I don't think you can do it.
I already have, the only case of mutation and selection where the
multiplication rule of probabilities does not apply is when only a
single beneficial mutation is required to adapt to the selection
condition.
>> Mark, you are so confused by your evolutionist indoctrination on this
>> topic; you think that selection increases the diversity of populations.
>Duh. We have both seen it. I am sane enough to admit that I have seen
>it.
So where is your real, measurable and repeatable example of a
selection condition which increases diversity? Are you going to join
with Frank Smith and claim that four variants are more diverse than
five variants?
>>> >> > 3. Then you have the flat fitness landscape advocate hersheyh who
>>> >> > is claiming that neutral mutations can be fixed (amplified) in a
>>> >> > population.
>>> >> Well, duh. Of course neutral mutations can be fixed. Only a
>>> >> cretin would think otherwise.
>>> > Oh really Mark?
>>> Yes, really.
>> You are wrong Mark, really.
>Wanna bet? I'll bet $100,000 of mine against an equal amount of yours.
>The only other conditions I will require is that the decision of winning
>be made by a sane person who is knowledgeable enough to judge, and that
>you must pay up whether you agree with that person or not.
Well that leaves out all evolutionists because they believe that
reptile scales turn into feathers when the weather gets cold and you
believe that evolution accelerates when the intensity of selection is
decreased.
>>> > You can fix neutral mutations without selection? Be a sport and tell
>>> > us how this is done,
>>> Why? You have been told multiple times already, and you paid no
>>> attention. Why should I expect that one more time would matter?
>>> Tell you what. If you send me $250, I will write a computer
>>> simulation that shows how it is done. Or, if any lurkers do not
>>> understand how alleles become fixed through neutral drift, I will
>>> explain for them.
>> Now you have hit upon why evolutionists fight so hard to support your
>> mathematically irrational theory. It's all about keeping a job.
>Look again. My money-making job is computer programming. As an
>evolutionist, I have made, net, approximately $0. You are writing
>fiction.
Evolutionists don’t make money by understanding how mutation and
selection works. Perhaps you think that if you write a sorting
algorithm for the computer, the more complex the sorting conditions
the faster the sorting process goes. If you do, that’s what it takes
to be an evolutionist.
>> Let's see you explain based on John Harshman's calculations how you
>> fix 67 mutations . . .
>I note that it is still impossible for *you* to say how reptiles turned
>into birds, if not by evolution. My hypothesis is that you cannot do so
>because you know, at some level, that evolution is the best explanation.
Mark, why don’t you write a computer algorithm which demonstrates how
dozens of neutral mutations are fixed every generation for hundreds of
thousands of generations because that is what has to be done to
account for the at least 40,000,000 differences between human and
chimpanzee genomes.
========================================================
Frank F. Smith
>> A better example woud be Ewens' works on mathematical population
>> genetics, as in
>> http://www.google.com/url?sa=D&q=http://www.springer.com/mathematics/applications/book/978-0-387-20191-7
>> Or check Ewens' lecture notes at
>> http://www.google.com/url?sa=D&q=http://www.math.cornell.edu/~durrett/CPSS2006/cornelllect.pdf
>Thanks for the link!
>Although I doubt Kleinman will read (or understand) it, I'm looking
>forward to giving it a few pleasant hours.
Why is it that evolutionists love to post URL’s but never quote from
their citations? Here are a couple of quotes from the lecture
reference.
“For each set of data we compute f, the observed homozygosity. Then
the exact neutral theory probability P (given in Table 2) that the
homozygosity is more extreme than its observed value may be calculated
(except for the D. simulans case where the computations are
prohibitive). The simulated probabilities Psim are also given in Table
2; these are in reasonable agreement with the exact values. The
conclusion that we draw is that significant evidence of selection
appears to exist in all species except D. tropicalis.” Pg 76
In this first quote, the authors are comparing Drosophila sample data
with the neutral theory of evolution. In all cases, the variations
were due to selection except in a single case, D. tropicalis.
“We next outline two procedures based on the sample "frequency
spectrum". ...
…A comparison of the observed ai values and the expected values
calculated from (196) is given in Table 3. It appears very difficult
to maintain the neutral theory in the light of this comparison.”
In the second quote, these authors again find that the neutral theory
of evolution does not apply.
So the mathematical evidence of the neutral theory is ambiguous at
best. If you are really interested in learning something about
population genetics, you should study Schneider’s ev model. In is
model, he makes very few assumptions, he allows for variation of
population size, mutation rate, genome size and a variety of other
variables. His model demonstrates how population size has very little
effect on the evolutionary rate once his population reaches a
particular level. His model has no limits on neutral mutations and
properly demonstrates how the evolutionary process works.
Now it remains for you evolutionists to present how dozens of alleles
can be fixed every generations for hundreds of thousands of
generations whether by selection or by your neutral drift theory in
order to explain the at least 40,000,000 differences between humans
and chimpanzee genomes. We already know that you evolutionists have
bungled the basic science and mathematics of mutation and selection.
By the way Frank, do you still believe that reducing the number of
variants in a population from five to four variants increases the
diversity of the population?
And
>>> If the population size is able to increase despite the
>>> selection pressure, the number of members with that beneficial allele
>>> will increase without increasing the frequency of that allele in the
>>> population.
>> Haven't you learned *any* population genetics wrt selectively neutral
>> traits yet.
>I _think_ he might be making a different claim above -- though I might
>well be missing the larger context. It appears to me that he is claiming
>that the frequency of a _beneficial_ allele remains constant as long as
>the population size is increasing. That the frequency of beneficial
>alleles only increases when the population size is static. (Perhaps he
>merely means that the frequency _might_ not increase.)
The point is the multiplication rule probability requires
amplification of the beneficial allele. This amplification can occur
without increase in frequency if the population size is increasing as
well.
>But then where's the "beneficial" allele? Isn't an allele whose expected
>change in frequency generation-to-generation neutral by definition? In
>which case the whole statement is intrinsically contradictory.
In order for a population to improve the probability of overcoming the
multiplication rule, the population can increase the number of members
on which the potential mutation can occur and/or try more generations
in order to obtain that next beneficial mutation. The mutation and
selection phenomenon uses both more members who are potential
recipients of the next beneficial mutation and generations of attempts
at getting that next beneficial mutation.
========================================================
hersheyh
>So will any selection that favors heterozygosity over homozygosity,
>that is, any balanced polymorphism. As is the case wrt the sickle
>cell allele. Again, Kleinman continually confuses the idea of
>differential reproductive success with changes in population size.
>That is, in his pea brain the only time selection occurs is when
>something toxic specifically kills most of a population. Or better
>yet, from his perspective, two or more toxic somethings independently
>and simultaneously kills off most of the population.
>He really seems confused about the concept of absolute number and
>ratio or percent.
I’m not nearly so confused as you are about how population size
affects the probability that a beneficial mutation will occur at a
particular locus or that the multiplication rule of probabilities is
the dominant mathematical principle governing the mutation and
selection phenomenon. Perhaps you would like to explain how dozens of
alleles can be fixed generation after generation to explain the
40,000,000 differences between human a chimpanzee genomes. Let’s hear
you accounting rules that accomplish this transformation. Hersheyh,
continue to impress us with your mathematical incompetence.
>And to give you the mathematics of it, since you are such a math
>genius, the probability that any new allele will go to fixation is 1/N
> (if N = number of alleles in the population). The probability that it
>will be lost is 1-(1/N). Furthermore, the average number of
>generations until fixation or loss depends on population size and the
>frequency of the allele. A graph would be a bullet-shaped arc that
>peaks when the frequency of the allele being examined for future loss/
>fixation is 0.5 (like my coin flipping experiment in another reply).
>When the initial frequency of an allele is 0.5, you would, on average
>reach fixation or loss in 2.8N generations. When the initial
>frequency of the allele being studied is 0.1, loss (more likely) or
>fixation (less likely) will occur, on average, in about 1.3N
>generations. For an initial frequency of 1/N, loss (more likely) or
>fixation (less likely) will, on average, be fairly quick. If you
>ignore the many cases where loss occurs, it takes about 4Ne
>generations for an originally rare selectively neutral variant to
>spread to the whole population (again, only in the 1/2Ne cases where
>fixation occurs).
Ok hersheyh, let’s run with your mathematics. Let’s say N=2. In 5.8
generations, one or the other allele will have been substituted for
the other by neutral drift. Can you explain to us how dozens of
neutral alleles can be substituted for to account for the 40,000,000
differences between the human and chimpanzee genome in less than a
million generations?
>> > He�s not allowing his populations to go extinct. Selection
>> > does not allow for random walks.
>Selection produces biased random walks in real populations because the
>genetic process is still a random process. Using the analogy of the
>drunkard's walk, starting right next to the 0% ditch, it would be like
>a road tilted toward the 100% ditch. The blind drunk will naturally
>tend to go downhill, but is not prevented from taking an uphill step.
>Even selectively favored alleles can be lost by chance alone,
>*especially* when they first appear at the smallest possible frequency
>of 1/N. [N = number of alleles in the population]
Is that so? Then why do people waste their time sequencing HIV to look
for particular mutations in order to identify drug resistant strains?
Why did Lenski’s populations have identical mutations for the first
20,000 generation? You are demonstrating why evolutionists are
bunglers of the basic science and mathematics of mutation and
selection.
>> > Selection is the principle that in
>> > some cases allows a population to overcome the multiplication rule of
>> > probabilities for multiple beneficial mutations.
>No. Selection also occurs under conditions under which the
>multiplication rule (which assumes necessary simultaneity) does not
>hold, like conditions where the evolutionary pathway has steps that
>can be selected sequentially or in parallel. You keep assuming that
>the multiplication rule always holds. You are wrong. Plain and
>simple, wrong.
Unless the population can amplify a beneficial allele, the
multiplication rule makes it highly unlikely that the next beneficial
mutation will occur on that member with the first beneficial mutation.
You blundered when you computed the how population size affects the
probability that a beneficial mutation will occur at a particular
locus and you are blundering when you claim that there are conditions
when the multiplication rule of probabilities does not apply unless
mutations occur simultaneously.
>> > Fixation is not a
>> > random process; it is a process dependent on the intensity of
>> > selection which is not random.
>Fixation (or loss) will occur regardless of whether or not there is
>selection. Fixation (or loss) in the absence of selection is slower,
>on average. The only conditions in which one has the appearance of an
>absence of change is when conditions favor conservative selection.
The vast majority of selection pressures are stabilizing pressures.
Lenski’s experiment demonstrates this. Why don’t you give us a real
example of your irrational claims? Why don’t you tell us how dozens of
neutral alleles can be fixed every generation for hundreds of
thousands of generations?
>> > If you are trying to say that the
>> > number of generations required in order for fixation to occur is
>> > dependent on the current frequency of the beneficial allele, you�ve
>> > just restated what Haldane stated with his model more than 50 years
>> > ago.
>Haldane's model was about selection. The number of generations to
>fixation/loss is affected by selection, but I have described the
>number of generations to fixation in the absence of selection above.
>You can look it up in any population genetics text. Or if you like to,
>read the original 1968 paper by Motoo Kimura and Tomoko Ohta. Their
>graphs are a little different than the one I described because they
>only looked at fixation rather than either fixation or loss. It is
>plenty mathematical, if you are actually interested.
Tell us how dozens of alleles can be fixed every generation for
hundreds of thousands of generations without selection. I’d be
interested in seeing you do that mathematics.
And
>> John, did you miss the examples I posted from the field of oncology?
>Again, an artificial situation exactly like that with HIV, where
>evolution works so long as the probability of reaching a state which
>has selective advantage is not too low. And where intelligent humans
>try to design such artificial conditions specifically to kill or
>retard the growth of specific entities.
>> How about the examples I posted on the treatment of Malaria? How about
>> the example of Bacillus thuringiensis which produces a multi-component
>> toxin used for killing Malaria larvae?
>First of all, Bacillus thuringiensis is not "used for killing malaria
>larvae". Malaria is a trypanosome that is unharmed by the bacteria,
>as far as I know. B. thuringiensis *is* used as an insecticide
>against mosquito larvae, mosquitos being a necessary vector for the
>trypanosome (although it is more commonly used against
>lepidopterans). And, of course, you are also wrong about this
>pesticide being immune to insects evolving resistance against it. The
>pink bollworm has become resistant to Bt transgenic cotton in parts of
>India, but that was a single Bt gene. But a Diamondback moth
>population has become resistant to the whole bacteria in spray form.
My mistake, Bacillus thuringiensis is used for killing mosquito
larvae. Do you evolutionists ever admit to making a mistake? Your
mistakes harm people yet you never take responsibility of your
blunders.
>Second, the use of the usually plasmid-borne Cry proteins Bt, when
>used as an insecticide, involves levels that are far above that seen
>in nature. It is likely that the true target of these proteins are
>nematodes (the insect targets are in the orders Lepidoptera, Diptera,
>Coleoptera, and Hymenoptera), which eat soil bacteria unlike the
>insects, rather than the insects (not uncommon: there are many toxins
>in spiders and octopi and other organisms that can kill humans that
>were clearly not evolved for that purpose). Insects die when they get
>a large enough dose because the alkaline pH of their digestive system
>activates these proteins, which then form a pore in the insect cell
>gut membrane resulting in cell lysis. Because of that mechanism, the
>only way to evolve resistance is to produce something or change gut
>conditions so as to prevent activation of the crystal proteins or
>prevent it from attaching to the gut's cell membrane.
Nature is so good, it never starves, freezes or dehydrates populations
to extinction. And nature never puts two selection pressures on a
population simultaneously.
>Third, the very success of transgenic Bt in cotton to combat bollworms
>has led to the opening of a potential niche that has led to secondary
>pests naturally resistant to the crystal proteins increasing in their
>destructive effects: mirids in China, mealy bugs in India.
Whatever happened to evolutionists claims that populations can always
find a way to evolve against selection pressures. I guess that’s only
true when they target a single gene at a time.
>It has been, using standard evolutionary ideas, common to plant
>refuges (non-transgenic plants) where sensitive insects can thrive and
>keep the population largely sensitive in the next generation and
>maintain the ability to use this insecticide. This can only work if
>resistance is recessive, as in loss of an activating protease.
>But the key feature is that this is, in fact, another example of
>artificial selection using toxins that would be largely ineffective in
>a natural setting (except against the real natural target, the
>nematodes). Toxin resistance is not where most evolution occurs.
I know, I know, it is a population evolving resistance to cold weather
that turns scales into feathers. I thought you evolutionists like to
avoid teleology?
>> Would you like some new
>> examples? Ok, here are some more examples, the first are mathematical
>> models:
>> http://www.google.com/url?sa=D&q=http://www.csiro.au/proprietaryDocuments/dobson_barnes.pdf.
>> "Computer models of parasite populations and anthelmintic resistance"
>> 2.4. Drug Combinations: Computer modelling has shown that the best
>> way to inhibit the development of drug resistance is by the
>> simultaneous applications of drugs (i.e. the use of combinations or
>> mixtures)[3,12].
>As I keep pointing out, that is exactly what evolutionary theory would
>predict. If you arrange conditions whereby any single mutation has no
>selective benefit and only the simultaneous mutation of several
>independent sites do, the multiplication rule holds. And, as I
>apparently have to keep reminding you, even you admit that that does
>not hold under conditions where single mutations do have a selective
>advantage. In those cases it is rather easier to generate multiply
>resistant strains. Those cases that do not involve the simultaneous
>requirement, but can be done via sequential or parallel mechanisms,
>are called "evolutionary pathways".
You keep making this blunder hersheyh, the multiplication rule of
probabilities always holds when an evolutionary process requires more
than a single beneficial mutation. Only if the population is able to
amplify a beneficial mutation is there a reasonable probability that
the next beneficial mutation in the sequence will occur.
And
>You can even test this out at home. Take 10 pennies. At the start,
>equivalent to the zygote stage, you have an all-surfaces population of
>10 heads and 10 tails. Now flip the coins and look at the surviving
>upward facing faces, equivalent to the breeding stage. Pure chance is
>responsible for this (unless you practice real hard at accurate coin
>flipping). You would predict, on average, that you should get 5
>upward-facing heads and 5 upward-facing tails, but instead you see 4
>tails and 6 heads. That is not a particularly surprising result, is
>it? Or do you think that you should always get *exactly* 5 heads and
>5 tails.
>But at breeding, we now have 60% heads breeding rather than the 50%
>heads we had on all surfaces. So now mark 2 tails on your 10 coins
>with red nail polish. Those tails are now regarded as heads. That
>gives you an all-surfaces population of 8 tails and 12 heads, the same
>60% ratio as the facing breeding population. Flip the coins again.
>Lets say that you got 4 tails and 6 heads. That would be *exactly*
>what you would expect to be the mean result. So don't change anything
>and flip again.
>This time, you get 3 tails and 7 heads. Again, not exactly a
>surprising result when you start with a flipping a all-surfaces
>population of 8 tails and 12 heads. Paint two more tails red. The
>population now has, all-surface, 6 tails and 14 heads, which is the
>same as the % seen facing up. Flip again. This time you got 4 tails
>and 6 heads. Again, not a surprising result when you start with a
>population of 8 tails and 12 heads on all surfaces. Scrape off the
>paint on 2 tails, giving an all-surfaces ratio identical to the ratio
>in the upward-facing (breeding) population.
>Repeat. This time you get 2 tails and 8 heads. Repeat until all the
>upward-facing features are heads (or tails).
>All this change is done solely by chance. Eventually, you will likely
>reach a point where all the coins facing up are either all heads or
>all tails. How quickly that happens will vary. The above is a
>description of a random walk using chance alone. The key difference
>between what Kleinman proposes for neutral change and the above is
>that I assume that "chance has no memory". That is, at each flip, the
>% heads is a function of the % heads in that specific parent
>generation, not in the original case where there was a 10:10 ratio of
>heads to tails (all-surface). Also, I do not think it unusual to get
>ratios of 6:4 or 7:3 in individual flips of 10 coins. Kleinman
>assumes that one will always get a 5:5 ratio of heads:tails. That is,
>he assumes that the 5:5 ratio is deterministic rather than one
>possible chance distribution.
>When you start with a population that is divided 10:10, the
>probability that you will wind up all heads is 50%. The probability
>that you will not reach fixation, but merely, by chance always wind up
>with equal heads or tails is essentially zero in a population this
>small (in the absence of selection for the maintenance of that ratio).
Do me a favor hersheyh, repeat your calculation with ten million
pennies. Then tell us what happens if you try this with two sets of
coins in order to amplify two sets of neutral alleles simultaneously.
========================================================
William Hughes
>>..., the multiplication rule of probabilities applies to every
>> example of mutation and selection which requires more than a single
>> mutation to adapt to the selection conditions.
>Nope, not when each mutation causes an increase in reproduction
>independently of the others. Whenever anyone points this out you
>stick your fingers in your ears and go WAH WAH WAH, but it is
>still true.
Simple William, post a real measurable and repeatable example where
this occurs. I’ve already posted numerous examples where this doesn’t
occur.
========================================================
Bill
What is faster, waiting for two beneficial mutations to occur in one
individual, or sequential selection? And how much faster? Please show
your math.
r norman
You have been told that your method of replying by joining together a
whole bunch of resonses is quite annoying. It makes more work for you
and it is irritating to us. Please stop doing this. Just respond
individually to separate posts.
Somehow you do not understand the same probability theory that those
professional biologists, including evolutionary biologists, understand
and are trying to explain to you. The probability that "some"
unspecified individual in a population will acquire a specific
beneficial mutation is, indeed, dependent on the population size. The
probability that "this specific" individual will acquire the mutation
is, of course, quite independent of the population size. Evolution
doesn't care who happens to end up with the mutation; only that it is
there.
Somehow, you totally lost me when you claimed that the probability
that a specific beneficial mutation can occur is independent of the
mutation rate. It seems quite trivial that if the mutation rate is
zero, the probability is zero but if the mutation rate is pretty
large, the probability is greater than zero. That looks like a
dependency to me. But I may be wrong. Feel free to correct me on
this issue. (I expect you will not perceive the sarcasm in this last
comment, but it will not be lost on others.)
Somehow, you also miss the point that the probability that two
independent beneficial mutations occuring within a population is NOT
the product of their separate occurrence. Read carefully. I did NOT
specify that the two mutations had to occur in the same individual.
Whether you think this last statement does not apploy to a particular
situation about HIV is quite irrelevant; it applies to the theory of
evolution which you claim requires the multiplication of
probabilitiies in each and every instance.
Far more important, you totally and willfully ignore the plain fact
that the problem of drug resistance to antibiotics and to antiviral
agents has long been known and that many people, including people
trained in evolutionary biology, have been yelling for about a half
century now to stop the inane and harmful practice of overusing
antibiotics and antiviral agents.
You totally and willfully ignore the plain fact that there are two
categories of people in the world. There are medical practitioners
who say, rightly, "My patient will die without the use of antibiotics
or antiviral agents. The potential danger of the development of
resistnace is real but is a small and future effect; the life of my
patient is immediate and real. I will prescribe the use of
antibiotics and antivirals in a cautious and responsible way to
mimimize the possibility of development of drug resistance so that the
immediate benefit to my patient far exceeds the potential future harm
in the development of drug resistance." In this way, many millions of
people have been saved from devastating bacterial and viral diseases.
Would you fail to administer an effective life-saving drug to a
patient because it is a single-action therapy that may in the long run
produce drug resistance and thereby condemn your patient to death?
On the other hand, there are venal and greedy people in the medical,
pharmaceutical, and animal husbandry fields who argue "the profit from
overprescribing antibiotics and antivirals is immediate; the harm is
potential and far distant. I will profit from continuing to ignore
the warmings and give my patients, sell my drugs, feed my animals
antibiotics and antivirals because if I don't others will anyway. The
same harm will result but this way I get the profit." These people
exist quite independent of what evolutionary biologists say or do.
Bill
Well, I asked you something like this already a few weeks ago, so I'll
just show the answer.
For a haploid organism in a stable population size of 10^6 organisms
and two mutations each of which occur at a rate of 10^-6 and provide
an independent fitness advantage of 4% compared to organisms without
the mutation...
You expect 1 of each mutation in the population in each generation,
but we'll take them one at a time (slower, even for haploid
organisms). It will take that mutation
Log[99 * 10^6]/Log[1.04] = 470 generations to go to 99% fixation.
It will then take another generation for the second mutant to arise in
an organism already bearing the first (except that once there got to
be a decent proportion of organisms bearing the first mutation, the
second could occur in one of them without waiting for the first to
reach fixation). Then it will take another 470 generations for the
double mutant to get fixed - though this is an overestimate, since it
would only take about 350 generations for half the population to be
made up of single mutants, so by generation 352 you should have your
first double mutant.
So, estimating very conservatively, it should take well under 1000
generations to get the double mutant by sequential selection.
On the other hand you would have to wait 10^6 generations, three logs
more, to expect to get a double mutant if neither single mutant had a
selective advantage.
This is a sloppy, but conservative calculation, that doesn't provide
variances on the estimates and doesn't take into account the fact that
mutations to both sites are occurring and undergoing selection
simultaneously. The corrections, however, would only shorten the time
required for sequential selection and magnify its difference from
simultaneous selection. And sex would make it faster still. Doubtless
a real population geneticist on t.o.(Master Harshman, I'm calling you)
will nitpick, I mean improve, this calculation, but the improved
estimate will be faster than this one.
Walter Bushell
"Steven L." <sdli...@earthlink.net> wrote:
<snip>
>
> I have tried to argue with devout people of faith about some issues too.
> It's impossible. They seem to have been trained from childhood to
> disregard or tune out any arguments that might possibly call into
> question some aspect of their faith. I guess they were warned against
> being swayed.
>
>
>
> -- Steven L.
Oh, yes, I myself was warned against losing the Faith and IIUC it's part
of all religious instruction.
--
The Chinese pretend their goods are good and we pretend our money
is good, or is it the reverse?
John Harshman
> Doubtless
> a real population geneticist on t.o.(Master Harshman, I'm calling you)
> will nitpick, I mean improve, this calculation, but the improved
> estimate will be faster than this one.
I'm not a population geneticist. I try to avoid population genetics
whenever possible. In fact I try to ignore intraspecific variation
altogether whenever I can, which is usually.
John Harshman
> of March 21
....forgets nothing, learns nothing.
> John Harshman
>>> John, if you are talking about the evolutionist fantasy that reptiles
>>> transform into birds, that’s your fiction and the only thing I have to
>>> say about this is that it is a mathematically irrational concept only
>>> suitable for the SciFi channel.
>> How do you know it isn't true?
> John, I know it is true because I know how mutation and selection
> works and it doesn’t work the way evolutionist claim that it works.
You have not demonstrated that even if evolution works the way you think
it's impossible for birds to evolve. And all the evidence that birds did
indeed evolve would seem to argue against your conclusion. Does any
evidence count other than your HIV stuff? Does evidence from fossils and
genomes count for nothing?
> Specific mathematical principles are followed by the mutation and
> selection phenomenon and the dominant mathematical principle is the
> multiplication rule of probabilities that two or more beneficial
> mutations will occur on an individual (not simultaneously).
How can two mutations occur on an individual without it being
simultaneous? And why is it required that two mutations happen in one
individual, rather than in separate individuals?
Why must the second mutation occur in an individual that already has the
first mutation?
>>> This is the dominant mathematical principle that determines whether an
>>> evolutionary process has a reasonable chance of occurring or not. The
>>> only time the mutation and selection process can work efficiently is
>>> if the multiple beneficial mutations can occur in a sequence where
>>> each of the beneficial mutations is separated by an amplification
>>> process for that beneficial mutation. This is why when combination
>>> therapy (selection pressures) works for HIV and for the treatment of
>>> any other mutating and selection disease. You are forcing the
>>> population to get two beneficial mutations simultaneously and/or
>>> interfering with the amplification process of any single beneficial
>>> mutations.
>> And that does apply if a you need two simultaneous mutations in order
>> for there to be a selective benefit. But not otherwise.
> No John, it always applies. That’s why in every real, measurable and
> repeatable example of mutation and selection where combination
> selection pressures are applied, the mutation and selection process is
> stifled if not stopped completely. The combined selection pressures
> interfere with the amplification process for any beneficial mutation
> which might occur.
Why? How?
> The mutation and selection process is very slow to
> begin with taking hundreds of generations to fix (amplify) a single
> beneficial mutation subject to a single selection pressure. As soon as
> the population is forced to amplify more than a single beneficial
> allele, the different selection conditions interfere with each other
> in the amplification process.
How? Why?
> Remember, selection pressures are things
> which kill or impair the reproduction of the members of a population.
Not necessarily. Selection may also operate by increasing the
reproduction of some members in an increasing population, while leaving
others unchanged.
..
> Even if members of a population have a beneficial allele for one
> selection pressure, the other selection pressure is still killing or
> impairing the reproduction of those members preventing that allele
> from being amplified and visa versa for the other beneficial alleles
> to the other selection pressures.
But that doesn't slow the spread of either favorable allele. Why should it?
I hope I don't have to explain to you why it's irrelevant to the
question. And how nonsensical your statements are. You didn't answer the
question either.
>>> Evolutionists teach genetics to physicians, I hold those teachers of
>>> evolutionism responsible for the failure to properly teach the basic
>>> science and mathematics of the mutation and selection phenomenon.
>> I'm pretty sure that geneticists teach genetics to physicians, and that
>> hardly any physicians have ever had a single course in evolutionary
>> biology. Clearly you haven't.
> I’ve used my engineering skills and study to understand how mutation
> and selection works. I’ve done a very careful study of Thomas
> Schneider’s simple by elegant model of mutation and selection. His
> model does properly describe the mathematics of population genetics
> and does so with a minimum number of assumptions. Despite taking
> courses in biology, microbiology, genetics and biochemistry,
So you admit you never had a course in evolution. You probably never had
a course taught by an evolutionary biologist. How then can you blame
evolutionary biologists for the teaching you got?
> not a
> single one of these courses attempted to properly describe the basic
> science and mathematics of mutation and selection.
Perhaps you should have taken that evolution course.
> Look what all your
> studies in evolutionary biology have gotten you. You believe that the
> probability of a beneficial mutation occurring at a particular locus
> is proportional to population size.
No I don't.
> And you don’t understand how the
> multiplication rule of probabilities drives the mutation and selection
> phenomenon.
Because it doesn't.
> I would rather use my engineering skills to analyze the
> mutation and selection phenomenon properly and use that analysis to
> prevent the evolution of multidrug resistant microbes than to learn
> the mathematically irrational concepts that are being taught in
> evolutionary biology today.
How do you even know what's being taught in evolutionary biology, when
you've never had a course in it?
>>> John, the multiplication rule of probabilities enters into every
>>> example of mutation and selection unless that adaptation process only
>>> requires a single mutation. As soon as the adaptation process requires
>>> more than a single beneficial mutation, the multiplication rule enters
>>> into the equation.
>> Your fuzzy language is disguising the situation here. What do you mean
>> by "adaptation process" and "requires more than a single"? Hard to say.
>> If and only if a single mutation is not beneficial, and thus two
>> mutations are required for any benefit, does that multiplication rule
>> apply. If one mutation is good, but two mutations are even better, the
>> multiplication rule is inapplicable.
> As long as mutations are random independent events, the probability of
> these events occurring is governed by the multiplication rule of
> probabilities.
The probability of both events occurring.
> It doesn’t matter whether the events occur
> simultaneously or the events are separated by hundreds of generations
> with amplification occurring between the events. If the amplification
> process does not occur, the event of a second beneficial mutation
> occurring on a member with the first beneficial mutation will be a
> highly improbable occurrence due to the multiplication rule of
> probabilities.
You are hopelessly confusing mutation and fixation. I will agree that if
A is never fixed, the joint probability of A and B both being fixed will
be rather low. So what? And why must mutation B happen in an individual
who already has mutation A?
>>>>> Apparently Edward Max
>>>>> doesn’t know much about quantitative genetics, I guess it’s because he
>>>>> was trained by an evolutionist.
>>>> Such Christian charity.
>>> We all know about evolutionist charity;
>> How old are you? Are you really saying "Bobby hit me first"?
> I’m old enough to know how mutation and selection works and I am sure
> that Edward Max knows very little about how this process works.
I know you're sure, but do you have any rational reason to be sure?
> If
> Edward Max understood how mutation and selection works, he would use
> his position as supervising medical doctor of the Food and Drug
> Administration to do something about antibiotic resistance. So far,
> the only so called expert advice that primary care physicians get on
> using antibiotics is to stop using these medicines so much so that the
> selection of resistance doesn’t occur. My response to this is hell no.
> Let those physicians who give that advice delay the giving of
> antibiotics to their ill patients and let them die of pneumonia,
> meningitis and sepsis. If these so called experts want to delay the
> appearance of drug resistant microbes, let them learn the lesson given
> by the use of combination therapy for HIV.
I'm not a doctor, so I have no with to argue medical policy with you.
But I can see there are more variables than you state, which make the
decision more complex than you claim.
>>> see what happens to the
>>> careers of those biologists who question the validity of the theory of
>>> evolution.
>> What happens? Who are they?
> Biologists who question the theory of evolution are denied faculty
> positions, promotions, research money. This is because the inbred,
> indoctrinated and mathematically irrational evolutionists can not take
> any challenge to your irrational belief system.
So you claim. Can you give any real examples? Maybe you saw "Expelled" once?
>>> The truth is that Edward Max because of his leadership in
>>> the medical field has a responsibility to properly understand how
>>> mutation and selection works. So far, he has written nothing which
>>> shows that he properly understands how the mutation and selection
>>> phenomenon works. This harms the people for which he has oversight.
>> I doubt your ability to evaluate Max's knowledge.
> If Edward Max wants to indoctrinate naïve school children with his
> belief that reptiles turn into birds, that’s his prerogative. However,
> someone in his position has a responsibility to properly understand
> how the mutation and selection phenomenon works. He doesn’t and we
> have multidrug resistant microbes and less than durable cancer
> treatments to show for it.
Since you refuse to examine the evidence for bird evolution, you have no
right to accuse those who have examined it of being naive.
>>> John, you can read your fossil tea leaves any way you want. Just
>>> explain to us how 67 mutations are fixed per generations in your
>>> purported transformation of chimpanzees and humans from a common
>>> precursor. You can make up any stories you want for the SciFi channel
>>> but stop misrepresenting how mutation and selection works.
>> I've explained this already. You don't read. In fact you seem to pay no
>> attention whatsoever to anything that anyone says to you. Your mantras
>> haven't changed by so much as a single word since we began this
>> "discussion".
> I saw your loose explanation.
But did you understand it? What, if anything, was wrong with it? And it
may be "loose" but it's more mathematics in one piece than the sum total
of all the mathematics you have managed to present in all your posts.
> I put that explanation at a much lower
> level of mathematical credibility than your loose claim that the
> probability of a beneficial mutation occurring at a particular locus
> is proportional to population size and that claim was wrong.
What's wrong with my explanation, then? If it's so bad, you should be
able to poke many holes in it.
>> [snip the great amount below that you didn't respond to, possibly
>> because Google is such an inadequate platform, or possibly because you
>> just forgot it was there]
> I always say if it’s worth saying, it’s worth repeating. The governing
> mathematical principle of the mutation and selection phenomenon is the
> multiplication rule of probabilities and the mutations do not have to
> occur simultaneously for the multiplication rule to apply.
So you claim. I see no math.
> And
>
>>> That s why I don t want to get into your speculative games.
>>> Evolutionists make a living by speculation. I make my living by doing
>>> accurate computations and the multiplication rule of probabilities
>>> shows that your speculations are wrong. Mutation and selection does
>>> not work the way you claim.
>> You make your living by doing accurate computations? What an odd sort of
>> doctor you must be. And how can you say what evolutionary biologists do
>> when you know nothing about evolutionary biology?
> I certainly have to make accurate computations. When I specify the
> amount of medication, I have to be very accurate. Now if you consider
> yourself an evolutionary biologist, your loose approximations make for
> sloppy computations. Do you still believe that the probability of a
> beneficial mutation occurring at a particular locus is proportional to
> population size?
Never did.
> Do you think that the probability of a beneficial
> mutation occurring at a particular locus is proportional to mutation
> rate or the number of generations the population is able to reproduce?
> Do you still believe that the multiplication rule of probabilities
> does not apply in the mutation and selection process except when the
> mutations must occur simultaneously? John you need a lot of work on
> your computations to make them accurate.
I will again note that you have never been observed to make a single
computation.
>> Do you think fossils have anything to tell us about past life? If so, what?
> I think the mathematics of mutation and selection and the empirical
> evidence which substantiates that mathematics has much more to tell us
> about evolution than any evolutionist speculation about fossils.
So what you're saying is that if your model conflicts with observation,
so much the worse for observation.
>>> I ve done it in a previous post. If you missed that post I ll do it
>>> again. I m responding to many posts and so I m a bit behind. I ve also
>>> explained how the multiplication rule of probabilities still applies
>>> to beneficial mutations even if they don t occur simultaneously. If
>>> you still have trouble understanding that mathematics and how
>>> populations try to overcome the multiplication rule, I ll go over it
>>> again.
>> I think we would have resolved the mutation probability thing if you had
>> read any of my posts. But I don't recall the explanation of that
>> multiplication rule applying even without simultaneous mutations. Could
>> you repeat that? Remember that I don't mean just simultaneous mutation,
>> but mutations that must be together to have any selective advantage.
>> They could happen sequentially provided that the first mutation alone
>> conferred no advantage. The question is whether this rule applies even
>> if a single mutation is advantageous, and why it should.
> In order for a population to accumulate multiple beneficial mutations
> by the mutation and selection process, it must do it in a cycle of
> beneficial mutation/amplification of beneficial mutation before the
> next mutation in the sequence has a reasonable probability of
> occurring at the proper locus.
Why?
> If the population can not amplify the
> particular allele, then the multiplication rule of probabilities makes
> it highly unlikely that the next mutation in the sequence will occur
> at the proper locus because so few members on which that mutation can
> occur.
This assumes that mutations must happen in a particular sequence and
that mutation B must happen in an individual that already has mutation
A. Why make those assumptions?
> Go back and look at the citation for the highly efficient beta
> lactamase allele which requires five mutations to make the
> transformation. Each mutation in the sequence must improve fitness to
> reproduce so that that each allele in the sequence will amplify in the
> population setting the stage for the next beneficial mutation in the
> sequence. The population is using generations and amplification of the
> beneficial allele in order to improve the probability that the next
> beneficial allele will occur at the proper locus and thereby
> overcoming the multiplication rule of probabilities.
Why are you assuming a particular sequence and a lack of recombination?
>>> The problem with your claims about bird evolution has to do with the
>>> way mutation and selection works. I m trying to have a discussion
>>> about the mathematics of mutation and selection, something which you
>>> are having difficulty comprehending. I hope you understand why the
>>> probability of a beneficial mutation occurring at a particular locus
>>> is not proportional to the population size. That is an important
>>> element of the mutation and selection phenomenon.
>> So since you have no interest in discussing bird evolution, could you
>> stop claiming it couldn't happen?
> Ok, if you want to talk about reptiles turning into birds, tell us
> what genes were targeted by which selection pressures and what
> mutations were required to make the transformation.
Why? Isn't the evidence that it happened good enough, without knowing
all the causes? To return to the stump and fallen tree analogy, I don't
have to know who cut it down, or when, or with what brand of chain saw.
I can still say that somebody cut down a tree. It would be silly to
claim that the stump and fallen tree were created in place, just as we
see them.
> Then tell us how
> many generations were required for the transformation. Perhaps you can
> do better than your loose sloppy claims that dozens of alleles can be
> fixed every generations for hundreds of thousands of generations in
> the transformation of humans and chimpanzees from a common ancestor.
> Let’s see how accurate a computation an evolutionary biologist can
> make.
That isn't a loose sloppy claim. It's standard neutral theory. What's
wrong with it?
>>> John, you are not prepared for this part of the discussion yet. Once
>>> you have a better understanding of how mutation and selection works,
>>> we can discuss how entropy relates to the mutation and selection
>>> phenomenon. It s enough if you understand that mutations are a
>>> disordering process and selection is and ordering process.
>> Are you familiar with the Dunning-Kruger effect?
> Go for it John, tell us how the Dunning-Kruger effect will overcome
> the multiplication rule of probabilities of two beneficial mutations
> occurring on a single member of the population (not simultaneously).
> You throw every evolutionist idea and speculation against the wall
> hoping that something will stick. Why don’t you learn the basic
> science and mathematics of mutation and selection?
Google in this case is your friend. Look up "Dunning-Kruger effect". It
isn't about evolutionary biology. But you are a victim.
> And
>
>>> Ok, I agree with that. Every genetic sequence places that member on a
>>> unique point on the fitness landscape. The starting point for the
>>> trajectory impacts the possible trajectories that member can take.
>> I accept your retraction.
> John, do you even know what a retraction is? You simply claim you use
> terms loosely. Have you figured out how to compute the effects of
> population size on the probability that a beneficial mutation will
> occur at a particular locus yet?
OK, so I reject your non-retraction.
>>>>> Recombination is not required
>>>>> for there to be selection in a population.
>>>> True but irrelevant to my point.
>>> But you need to remember that selection reduces the diversity of the
>>> population.
>> Sometimes yes, sometimes no. Negative frequency-dependent selection, for
>> example, increases diversity.
> Give us a real example of this describing the gene and different
> alleles for that gene both before and after selection has acted on the
> population. Otherwise you are just blowing smoke.
Here's the first one that came up in a search:
http://www.pnas.org/content/98/11/6253.short
>>>>> Your drift concept is a
>>>>> demonstration of poor use of vocabulary. When a population is able to
>>>>> reach a plateau on a fitness landscape, the population does not drift
>>>>> on this plateau, it diversifies.
>>>> You really have no idea of elementary population genetics. It isn't the
>>>> population that's drifting. It's allele frequencies. They undergo a
>>>> random walk. Eventually, all random walks end either at 100% frequency
>>>> (fixation) or at 0% (extinction). This happens to all neutrally evolving
>>>> alleles. The probability of eventual fixation at any given moment is
>>>> equal to the current frequency.
>>> Oh really? So Lenski�s populations are all going to end up at 100%
>>> fixation?
>> They are for all neutral alleles they currently have. Of course new
>> alleles arise in the meantime, so genetic diversity is replenished, and
>> achieves an equilibrium level, given neutrality.
> You haven’t read the paper where he describes his data, have you? Are
> you just using your words loosely again?
I read the paper. What's wrong with what I said, and why?
>>> He�s not allowing his populations to go extinct. Selection
>>> does not allow for random walks. Selection is the principle that in
>>> some cases allows a population to overcome the multiplication rule of
>>> probabilities for multiple beneficial mutations. Fixation is not a
>>> random process; it is a process dependent on the intensity of
>>> selection which is not random. If you are trying to say that the
>>> number of generations required in order for fixation to occur is
>>> dependent on the current frequency of the beneficial allele, you�ve
>>> just restated what Haldane stated with his model more than 50 years
>>> ago.
>> I wasn't talking about selection. I was talking about neutral evolution.
>> You have already agreed that some alleles are equal in fitness; if all
>> alleles are equally fit, there is no selection, but eventually one of
>> them will become fixed.
> Ok John, since you know so much about neutral evolution, tell us how
> quickly neutral alleles are fixed in a population? And don’t use your
> loose terminology.
That depends on population size. The mean time from mutation to fixation
of a neutral allele that does eventually become fixed (i.e. doesn't
become extinct) is 4N generations. (That's actually an approximation for
large populations; there are more complicated formulae if you really want.)
>>>> Note that some loci may be evolving neutrally at the same time as other
>>>> loci are under selection. Whole organisms aren't the proper level at
>>>> which to examine drift.
>>> The fundamental unit process of evolution is the substitution of a
>>> more beneficial allele for a less beneficial allele. That�s how
>>> populations improve fitness. A neutral allele will not increase in
>>> frequency because it offers no selective advantage. If this is your
>>> idea of elementary population genetics, I�m glad I have no idea of
>>> this mathematical irrationality.
>> Yes, the willfully ignorant are often for some reason proud of their
>> ignorance. I don't understand why, but it happens. Similarly, you don't
>> understand anything about neutral evolution, and yet it happens.
> Haldane is the one who made that statement. Read his paper. I realize
> that there are many evolutionists who believe that neutral alleles are
> randomly fixed in populations and that this occurs much more quickly
> than selection could ever do it.
No, nobody believes that. Selection is faster than drift.
> You now need to demonstrate how
> dozens of alleles can be fixed every generation randomly for hundreds
> of thousands of generations to account for the 40,000,000 differences
> you admit to between humans and chimpanzees. Just how do random
> processes spread those dozens of alleles through a human and
> chimpanzee populations every generation?
I have explained that. They don't spread in one generation. It's just
that dozens go from near-fixation to complete fixation in every
generation. Like I said, the probability that a neutral mutation will
eventually become fixed is only 1/2N. But there are a lot more neutral
mutations than beneficial ones, so that, even with the low individual
probability, most mutations that become fixed are neutral.
>> But let's take it a little at a time. Do you agree that the frequency of
>> a neutral allele (at a locus where all alleles have equal fitness) will
>> undergo a random walk? If so, what do you think the result of a random
>> walk will be?
> What I believe is that neutral mutations primarily are going along for
> the ride as the more fit members of a population increase in frequency
> over generations. But let’s hear you explain how dozens of neutral
> alleles can go on a random walk and spread through the human and
> chimpanzee population every generation after generation for hundreds
> of thousands of generations when selection takes hundreds of
> generations to spread only a single allele thorough a population.
I said nothing of the sort. You are comparing the number of alleles
fixed in one generation to the time it takes to go from mutation to
fixation. These are completely separate numbers.
>>>>> The reason why the population can
>>>>> diversify is that there a number of variants possible (determined by
>>>>> the size of the plateau) which survive and reproduce equally well to
>>>>> other variants in this selection environment. Fixation or substitution
>>>>> requires selection pressure and on a plateau, this pressure does not
>>>>> exist, that is why the population can diversify.
>>>> If you actually tried an experiment in this, you would find that one
>>>> variant would eventually become fixed. Think of it as a lottery.
>>>> Somebody has to win, and somebody has to lose, even though it's all random.
>>> Amplification of an allele requires that it gives selective advantage
>>> to that member. That member is a better replicator than other members
>>> of the population and over time that allele will increase in
>>> frequency. Mutations are random but selection is not.
>> Selection is not but a random walk is, and that's what happens in
>> neutral evolution. Surely you don't imagine that in a neutrally evolving
>> locus the frequencies of all alleles will remain forever unchanged. Do you?
> What I think is that you can not come up with a mathematically
> rational explanation for how dozens of alleles are fixed every
> generation based on a real mechanism of transformation of genomes. You
> throw some loose terminology at us but it will not be mathematically
> rational.
What was loose about my explanation? I've presented the math. You didn't
understand that. So I presented analogies to help you understand. But
you didn't understand them. You seem incapable of understanding the very
concept of a random walk.
>>>>> Remember selection
>>>>> reduces diversity, mutations increase diversity and the way to
>>>>> increase diversity of a population is to reduce the selection pressure
>>>>> on the population.
>>>> Sometimes true, sometimes not. You have no clue. Sorry.
>>> Feel free to give us an example where selection increases the
>>> diversity of a population. Pretty please, give us a clue.
>> HLA is a good one. I've mentioned it before.
> Tell us what the selection pressures are and what the alleles are
> before and after the selection conditions applied.
Well, in the modern population we see only the after, not the before.
But there are hundreds of alleles at intermediate frequencies, much more
variation than could be maintained by drift. Many alleles are shared
with chimps, which shows how long variation can be maintained by selection.
> And
>
>>> Now it is true that the phenotype is an expression of the genotype but
>>> ultimately evolution is played out on the genotype.
>> Another of your problems is that you trot out stock phrases without
>> regard to whether they actually respond to what was said. As in this
>> case: your stock statement was irrelevant.
> Perhaps you prefer I use some of your loose terminology?
No, I would prefer that you actually address the matter at hand rather
than repeat irrelevant mantras.
These quotes don't seem to be making any sort of point for you.
> http://www.crcsalinity.com.au/newsletter/sea/articles/SEA_2102.html
> "Social costs of herbicide resistance: the case of resistance to
> glyphosate", “In this paper we discuss the case of the evolution in
> weed species of resistance to glyphosate, a valuable and widely used
> broad-spectrum non-selective herbicide first developed by Monsanto in
> the early 1970s.”
> and
> “The authors conclude that “The use of glyphosate in combination with
> other low risk herbicides for weed control with RR cotton provides an
> opportunity to significantly reduce the risk of off-site herbicide
> contamination in Australian cotton production” ”
Now you're just quoting keyword searches without regard to anything.
> http://www3.interscience.wiley.com/cgi-bin/abstract/112607405/ABSTRACT?CRETRY=1&SRETRY=0
> "Possible methods of inhibiting or reversing the evolution of
> insecticide resistance in mosquitoes" “The following possible methods
> of minimising the risks of resistance are considered: (a) adjustment
> of the dosage and frequency of spraying so that resistance genes are
> effectively recessive; (b) detection and eradication of new foci of
> resistance before they have a chance to spread; (c) spraying a mosaic
> of unrelated insecticides with the intention that immigrants from one
> sector of the mosaic to another will dilute the frequency of
> resistance genes; (d) re-introduction of susceptibility genes into the
> progeny of wild females by the release of heterozygous males with
> resistance genes translocated on to their Y chromosome so that they
> are protected from insecticidal killing but will pass susceptibility
> to their female progeny; (e) replacement of a resistant by a
> susceptible population by means of a negatively heterotic system such
> as bidirectional cytoplasmic incompatibility. A plausible case can be
> made for each of these methods based on theoretical models and
> appropriate assumptions. However, an assessment of whether any of them
> will really be of any value depends on the answers to certain
> questions in the field. Therefore field projects have been initiated
> on Anopheles culicifacies in Sri Lanka and Pakistan, Culex
> quinquefasciatus in Tanzania and Anopheles arabiensis in Sudan. The
> results so far are summarized.”
> I have many more citations.
Are they all as irrelevant to your point at the ones you just quoted?
hersheyh
> The following are a compilation of responses from the splinter threads
> of March 21
[snip]
> ========================================================
> hersheyh
> >So will any selection that favors heterozygosity over homozygosity,
> >that is, any balanced polymorphism. As is the case wrt the sickle
> >cell allele. Again, Kleinman continually confuses the idea of
> >differential reproductive success with changes in population size.
> >That is, in his pea brain the only time selection occurs is when
> >something toxic specifically kills most of a population. Or better
> >yet, from his perspective, two or more toxic somethings independently
> >and simultaneously kills off most of the population.
> >He really seems confused about the concept of absolute number and
> >ratio or percent.
>
> I m not nearly so confused as you are about how population size
> affects the probability that a beneficial mutation will occur at a
> particular locus or that the multiplication rule of probabilities is
> the dominant mathematical principle governing the mutation and
> selection phenomenon.
At a *specific locus*, if a mutation rate is u/generation, the
expected *mean number* of such mutants in a population of N alleles is
uN individuals with that mutation. That is the *mean* expectation of
the number of mutants. This number can be greater than 1. The
probability that a given *population* of N individuals will have one
or more such mutant individuals is 1-e^-(uN) which is 1 minus the
probability that the population will have no such mutant individuals
(see Poisson distribution). If the mean expected number is exactly 1
in a population of size N, the probability that a population will have
no such mutant is about 36%, with the mean of one being a result of
populations that would be expected to have 2 or more such mutants by
chance alone. If you have a different calculation, let me know what
it is.
You have not demonstrated that the multiplication rule of
probabilities holds in all cases wrt calculating the probability of a
double-mutant in a single individual. In fact, it is dependent on the
assumption that there can never be any reason for the appearance of a
single-mutant in the absence of the second mutation. Can you explain
why you think the multiplication rule always holds rather than
idiotically repeating that mantra as an assertion?
> Perhaps you would like to explain how dozens of
> alleles can be fixed generation after generation to explain the
> 40,000,000 differences between human a chimpanzee genomes. Let s hear
> you accounting rules that accomplish this transformation. Hersheyh,
> continue to impress us with your mathematical incompetence.
Sure. I will give you a rough estimate. The rate of neutral fixation
per generation per locus is 1/2N for any new mutation at a locus
(where N is population size of a diploid organism). The expected
number of new mutations fixed by neutral fixation per generation per
locus is (u*2N)/2N or simply u per generation per locus. A reasonable
mutation rate for point mutations is about 10^-8 per locus per
generation. There are about 10 million years worth of divergence
between humans and chimps (5 million in each lineage since the last
common ancestor). Assuming 20 yrs/generation (which is likely a bit
long in the chimp lineage and most of the human one as well), that is
5X10^5 generations separating the two modern species. That gives a
probability of 5^10^-3 fixation difference per locus for any
comparable locus in human and chimp. There are about 6 X 10^9 loci
(nucleotides) in the diploid human (or chimp) genome, giving us an
expected about 30 X 10^6 fixation differences between humans and
chimps. That is certainly pretty close to the 40 X 10^6 differences
that are observed. A more accurate estimate of yrs/generation or
mutation rate could easily account for the discrepancy. But John
already did a rough calculation of this, which you simply ignored.
Have you actually tried to present an alternate calculation?
Or, if you want to calculate it differently, the rate of neutral
fixation per locus per generation is u (see above) or about 10^-8.
There are 6 X 10^9 loci in a human (or chimp) diploid genome, meaning
we would expect about 60 neutral fixations per generation per genome.
At 10^6 years of divergence and 20yrs/generation, that is 5 X 10^5
generations of difference. At 60 neutral fixation differences per
generation, we get 300 X 10^5 expected differences between human and
chimp. That is still, ta da, 30 X 10^6 differences, if you have
problems with exponents.
So, how would *you* calculate the expected number of differences
between human and chimp from the principles of selective neutrality?
Remember that neutral fixation is a much *slower* process of sequence
change than directional selection.
> >And to give you the mathematics of it, since you are such a math
> >genius, the probability that any new allele will go to fixation is 1/N
> > (if N = number of alleles in the population). The probability that it
> >will be lost is 1-(1/N). Furthermore, the average number of
> >generations until fixation or loss depends on population size and the
> >frequency of the allele. A graph would be a bullet-shaped arc that
> >peaks when the frequency of the allele being examined for future loss/
> >fixation is 0.5 (like my coin flipping experiment in another reply).
> >When the initial frequency of an allele is 0.5, you would, on average
> >reach fixation or loss in 2.8N generations. When the initial
> >frequency of the allele being studied is 0.1, loss (more likely) or
> >fixation (less likely) will occur, on average, in about 1.3N
> >generations. For an initial frequency of 1/N, loss (more likely) or
> >fixation (less likely) will, on average, be fairly quick. If you
> >ignore the many cases where loss occurs, it takes about 4Ne
> >generations for an originally rare selectively neutral variant to
> >spread to the whole population (again, only in the 1/2Ne cases where
> >fixation occurs).
>
> Ok hersheyh, let s run with your mathematics. Let s say N=2.
What is the original frequency of the alternate alleles? If it is
initially 0.5, meaning either that one of your 2 diploid individuals
is all A or all a, or that both are heterozygotes, there will be a
difference of one generation. The former will produce the second in
the first generation. So let's start with the generation in which
both individuals are heterozygous (there are four alleles in these two
individuals) and these two individuals produce exactly two offspring,
each with two alleles from their parents. The possibilities are that
you have all four alleles in the offspring be the same (all A or all
a), that half the alleles be A and half be a, and that 3 be one type
and the other the other. Starting with two heterozygotes, at
generation 1, there will be a 0.25:0.5:0.25 probability for *each*
individual being AA:Aa:aa. The probability that *both* progeny will
be AA in the first generation is 0.25*0.25 = 0.625. Same probability
for both progeny being aa. But we expect the classical probability
ratio from Mendelian genetics of 1 (AA & AA): 4 (AA & Aa) : 6 (Aa &
Aa) : 4 (aa & Aa) : 1 (aa & aa) in that first generation. [You have
to use the *addition rule* of probability to get those ratios. You do
know that there is an *addition rule* in probability, don't you? It
isn't all the *multiplication* rule.]
> In 5.8
> generations, one or the other allele will have been substituted for
> the other by neutral drift.
No. By roughly 6 generations or trials, one expects to have gotten
one trial in which the two progeny have either all A or all a. That
is, by that time it is more likely than not that one of the two
alleles, initially at a probability of 0.5, has become fixed and the
other has been lost by chance alone.
> Can you explain to us how dozens of
> neutral alleles can be substituted for to account for the 40,000,000
> differences between the human and chimpanzee genome in less than a
> million generations?
I have estimated the sum of the number of generations since divergence
of humans and chimps from the common ancestor at around 500,000
generations using 20 yr/generation and a sum of 10 million years
(equally divided between humans and chimps, since fixation of a change
in either lineage during the 5 million years since divergence would be
detectable as a difference between the two). That is probably
somewhat longer generation time than is really the case, particularly
in the chimp lineage, but also in most of the anthropoid ancestors to
modern humans. If the generation time were closer to 10 years, the
number of generations would be closer to the million years. Do you
have different estimates for generation times and years since
divergence from a common ancestor? 6000 years since "creation" or the
"flood", perhaps? Perhaps a generation time of 500 years, given
Methusalan ages? Could you present your assumptions and math?
>> > He s not allowing his populations to go extinct. Selection
> >> > does not allow for random walks.
> >Selection produces biased random walks in real populations because the
> >genetic process is still a random process. Using the analogy of the
> >drunkard's walk, starting right next to the 0% ditch, it would be like
> >a road tilted toward the 100% ditch. The blind drunk will naturally
> >tend to go downhill, but is not prevented from taking an uphill step.
> >Even selectively favored alleles can be lost by chance alone,
> >*especially* when they first appear at the smallest possible frequency
> >of 1/N. [N = number of alleles in the population]
>
> Is that so? Then why do people waste their time sequencing HIV to look
> for particular mutations in order to identify drug resistant strains?
Because, even though selectively favored alleles can be lost by
chance, they have a much higher probability of increasing to fixation
and a much faster speed to fixation than selectively neutral alleles
which, in turn, is more likely than the fixation of selectively
detrimental alleles, although that also can happen by a number of
different mechanisms, including chance. Again, when we say that there
is a certain mean probability of change in one direction, that does
not mean that that direction is the only possible one as long as
reproduction involves some element of chance.
> Why did Lenski s populations have identical mutations for the first
> 20,000 generation?
They *didn't* have identical *mutations*. They had (largely) non-
identical mutations affecting the same genes to produce similar
phenotypic effects. Read it again.
http://www.pnas.org/content/100/3/1072.abstract
"To examine further the extent of parallel evolutionary changes, we
sequenced spoT in clones from 10 other populations (besides the two
used in the arrays) that also had evolved for 20,000 generations under
the same conditions. Seven other evolved populations also had acquired
point mutations in spoT, causing amino acid replacements in all cases,
although no two mutations were identical (Fig. 3)."
> You are demonstrating why evolutionists are
> bunglers of the basic science and mathematics of mutation and
> selection.
Rather it is you who are demonstrating your incompetence and inability
to understand even simple probability.
>> > Selection is the principle that in
> >> > some cases allows a population to overcome the multiplication rule of
> >> > probabilities for multiple beneficial mutations.
> >No. Selection also occurs under conditions under which the
> >multiplication rule (which assumes necessary simultaneity) does not
> >hold, like conditions where the evolutionary pathway has steps that
> >can be selected sequentially or in parallel. You keep assuming that
> >the multiplication rule always holds. You are wrong. Plain and
> >simple, wrong.
>
> Unless the population can amplify a beneficial allele, the
> multiplication rule makes it highly unlikely that the next beneficial
> mutation will occur on that member with the first beneficial mutation.
And you assume that it is impossible to increase the frequency of a
beneficial mutation in a population in a reasonable number of
generations? Again, I have told you that bacteria can increase from a
single cell to essentially media saturation in 30 generation
doublings. Not thousands of generations. Thus, if you have a
population of 10^9 cells and a mutation rate to toxin resistance of
10^-8, *most* of the time if you add that toxin and your population
includes even one resistant mutant (and the probability of that is 1-
e^-m, where m = expected mean number of resistant bacteria in that
population) you will have a population of 10^9 resistant cells in
about 30 generations (which is roughly overnight in many rich media).
And killing all but one or a few cells out of a population of 10^9
cells is a *very* stringent selection.
> You blundered when you computed the how population size affects the
> probability that a beneficial mutation will occur at a particular
> locus and you are blundering when you claim that there are conditions
> when the multiplication rule of probabilities does not apply unless
> mutations occur simultaneously.
You keep asserting this without even trying to present your math or
any equation at all. The expected mean number of mutant individuals
is u*N where N = number of alleles (or 2N*u, where N = number of
diploid individuals) and u = specific mutation rate per site (be it
allele or nucleotide) per generation. And, yes, I do indeed point out
that the multiplication rule does not hold *except* when you are
talking about phenotypes which are only beneficial when two or more
mutations must have occurred in the same individual by chance alone
prior to the selective conditions being applied.
>> > Fixation is not a
> >> > random process; it is a process dependent on the intensity of
> >> > selection which is not random.
> >Fixation (or loss) will occur regardless of whether or not there is
> >selection. Fixation (or loss) in the absence of selection is slower,
> >on average. The only conditions in which one has the appearance of an
> >absence of change is when conditions favor conservative selection.
>
> The vast majority of selection pressures are stabilizing pressures.
> Lenski s experiment demonstrates this.
That is certainly more the case when one is looking a bacteria where
the percent of the genome that is directly involved in producing
proteins is a fairly high fraction of the total genome. It is less
the case in humans where roughly only 3% of the genome is involved in
producing proteins and most DNA has little or no sequence constraint.
Even in bacteria, a number of synonymous mutations (ones that produce
no change in the protein produced) are possible.
> Why don t you give us a real
> example of your irrational claims? Why don t you tell us how dozens of
> neutral alleles can be fixed every generation for hundreds of
> thousands of generations?
The math is rather simple. The expected mean number of new mutations
at a mutation rate of u/generation/site in a population of alleles of
size 2N is 2Nu. The probability that any of these new alleles will go
to fixation is 1/2N. Thus the fixation rate is 2Nu/2N = u/generation/
site. If u is 10^-8/generation/site and there are 3 X 10^9 nucleotide
sites in the haploid genome, the mean number of neutral fixations per
generation is 30 per haploid genome. Do you have some different
math? Different assumptions? What is your argument? The numbers of
mutations per genome, mutation rate, etc. are all within a factor of 2
of experimentally observed numbers. So if your numbers don't match,
you have to be able to explain the discrepancy between your numbers
and observed and observable reality.
>> > If you are trying to say that the
> >> > number of generations required in order for fixation to occur is
> >> > dependent on the current frequency of the beneficial allele, you ve
> >> > just restated what Haldane stated with his model more than 50 years
> >> > ago.
> >Haldane's model was about selection. The number of generations to
> >fixation/loss is affected by selection, but I have described the
> >number of generations to fixation in the absence of selection above.
> >You can look it up in any population genetics text. Or if you like to,
> >read the original 1968 paper by Motoo Kimura and Tomoko Ohta. Their
> >graphs are a little different than the one I described because they
> >only looked at fixation rather than either fixation or loss. It is
> >plenty mathematical, if you are actually interested.
>
> Tell us how dozens of alleles can be fixed every generation for
> hundreds of thousands of generations without selection. I d be
> interested in seeing you do that mathematics.
See above.
>
> And
>
> >> John, did you miss the examples I posted from the field of oncology?
> >Again, an artificial situation exactly like that with HIV, where
> >evolution works so long as the probability of reaching a state which
> >has selective advantage is not too low. And where intelligent humans
> >try to design such artificial conditions specifically to kill or
> >retard the growth of specific entities.
> >> How about the examples I posted on the treatment of Malaria? How about
> >> the example of Bacillus thuringiensis which produces a multi-component
> >> toxin used for killing Malaria larvae?
> >First of all, Bacillus thuringiensis is not "used for killing malaria
> >larvae". Malaria is a trypanosome that is unharmed by the bacteria,
> >as far as I know. B. thuringiensis *is* used as an insecticide
> >against mosquito larvae, mosquitos being a necessary vector for the
> >trypanosome (although it is more commonly used against
> >lepidopterans). And, of course, you are also wrong about this
> >pesticide being immune to insects evolving resistance against it. The
> >pink bollworm has become resistant to Bt transgenic cotton in parts of
> >India, but that was a single Bt gene. But a Diamondback moth
> >population has become resistant to the whole bacteria in spray form.
>
> My mistake, Bacillus thuringiensis is used for killing mosquito
> larvae. Do you evolutionists ever admit to making a mistake?
Yes. But, as you point out, this was *your* mistake, not mine. And
you have made many other mistakes and similarly ignorant statements.
> Your
> mistakes harm people yet you never take responsibility of your
> blunders.
I have not made the sort of blunders you claim. I agree that
evolution to a phenotype, when it involves a *joint* phenotype, such
as simultaneous prior resistance to multiple toxins in a single
individual does involve the multiplication rule. That is hardly news
to biologists or geneticists or anyone with a smattering of
understanding about probability. You responded with the falsehood
that *all* evolution involves the multiplication rule, even when it
can occur by mechanisms that do not involve the *joint* phenotype.
You refuse to show why we should believe that falsehood. That it is a
falsehood should be obvious even to someone as dense as you are, since
many of the very things that you claim cannot possibly evolve when
they are required to occur simultaneously do, in fact, occur in quite
reasonable time-frames and population sizes when that is not
necessary.
> >Second, the use of the usually plasmid-borne Cry proteins Bt, when
> >used as an insecticide, involves levels that are far above that seen
> >in nature. It is likely that the true target of these proteins are
> >nematodes (the insect targets are in the orders Lepidoptera, Diptera,
> >Coleoptera, and Hymenoptera), which eat soil bacteria unlike the
> >insects, rather than the insects (not uncommon: there are many toxins
> >in spiders and octopi and other organisms that can kill humans that
> >were clearly not evolved for that purpose). Insects die when they get
> >a large enough dose because the alkaline pH of their digestive system
> >activates these proteins, which then form a pore in the insect cell
> >gut membrane resulting in cell lysis. Because of that mechanism, the
> >only way to evolve resistance is to produce something or change gut
> >conditions so as to prevent activation of the crystal proteins or
> >prevent it from attaching to the gut's cell membrane.
>
> Nature is so good, it never starves, freezes or dehydrates populations
> to extinction.
When have I ever denied that extinction can occur or that particular
organisms can only exist in a narrow range of conditions?
> And nature never puts two selection pressures on a
> population simultaneously.
Populations are always under many different selection pressures. What
matters is whether different organismal phenotypes have independent
utility compared to the w.t. for that pressure or, as you claim, there
is no selective advantage of any individual different phenotype
relative to the w.t. unless all of the differences exist in the same
individual. You also seem to be claiming that all selective pressures
are lethal unless all of the changes occurred simultaneously in the
same individual. I find those assumptions bizarre in the extreme.
> >Third, the very success of transgenic Bt in cotton to combat bollworms
> >has led to the opening of a potential niche that has led to secondary
> >pests naturally resistant to the crystal proteins increasing in their
> >destructive effects: mirids in China, mealy bugs in India.
>
> Whatever happened to evolutionists claims that populations can always
> find a way to evolve against selection pressures. I guess that s only
> true when they target a single gene at a time.
False on both cases. Extinction happens. And I have suggested
parallel evolution of traits with recombination providing the
mechanism by which one gets both or all in the same individual.
Again, to be specific, the probability of two independent mutational
events being in the same individual, which is the probability you are
calculating, differs depending upon whether you are talking about both
mutations occurring simultaneously in the same individual or are
talking about the probability of the second mutation occurring in a
significant population already selected to have the first or are
talking about the probability of recombination producing individuals
with both from populations that have significant numbers of the two
mutations. The last, in particular, does not require that the two
traits be fully sequential, with the second only occurring when the
first has risen to a significant population frequency. The two traits
can appear in any relationship from simultaneous in different
individuals to nearly sequential but with the second mutation not
occurring in an individual having the first mutation.
> >It has been, using standard evolutionary ideas, common to plant
> >refuges (non-transgenic plants) where sensitive insects can thrive and
> >keep the population largely sensitive in the next generation and
> >maintain the ability to use this insecticide. This can only work if
> >resistance is recessive, as in loss of an activating protease.
> >But the key feature is that this is, in fact, another example of
> >artificial selection using toxins that would be largely ineffective in
> >a natural setting (except against the real natural target, the
> >nematodes). Toxin resistance is not where most evolution occurs.
>
> I know, I know, it is a population evolving resistance to cold weather
> that turns scales into feathers. I thought you evolutionists like to
> avoid teleology?
Feathers were, in fact, the solution that happened in the lineage that
produced birds. Hair was the solution that happened in the lineage
leading to us. Both feathers and hair (as well as inefficient
metabolism generating internal heat) can be and are used for warmth.
So is, in cetaceans and penguins and seals, a layer of insulating
fat. That is not teleology which requires foresight and
predestination. It is simply is what *did* happen. Similarly,
selection does not have any foresight. Selection increases the
frequency of alleles related to phenotypes that are more successful in
the parent generation *regardless* of whether or not those alleles or
phenotypes will be more successful in the offspring's generation.
That is, selection is backward-looking by one generation, not
teleologically forward-looking in anticipation of future environments
or possibilties.
>> Would you like some new
> >> examples? Ok, here are some more examples, the first are mathematical
> >> models:
> >>http://www.google.com/url?sa=D&q=http://www.csiro.au/proprietaryDocum....
> >> "Computer models of parasite populations and anthelmintic resistance"
> >> 2.4. Drug Combinations: Computer modelling has shown that the best
> >> way to inhibit the development of drug resistance is by the
> >> simultaneous applications of drugs (i.e. the use of combinations or
> >> mixtures)[3,12].
> >As I keep pointing out, that is exactly what evolutionary theory would
> >predict. If you arrange conditions whereby any single mutation has no
> >selective benefit and only the simultaneous mutation of several
> >independent sites do, the multiplication rule holds. And, as I
> >apparently have to keep reminding you, even you admit that that does
> >not hold under conditions where single mutations do have a selective
> >advantage. In those cases it is rather easier to generate multiply
> >resistant strains. Those cases that do not involve the simultaneous
> >requirement, but can be done via sequential or parallel mechanisms,
> >are called "evolutionary pathways".
> You keep making this blunder hersheyh, the multiplication rule of
> probabilities always holds when an evolutionary process requires more
> than a single beneficial mutation.
And you have utterly failed to justify this assertion. A lie repeated
is still a lie.
> Only if the population is able to
> amplify a beneficial mutation is there a reasonable probability that
> the next beneficial mutation in the sequence will occur.
Which *means* that there are conditions under which the multiplication
rule does not hold. You contradict your unsupported and
unsubstantiated assertion in the space of less than a paragraph.
What I said above still holds. The only difference in a large
population is that the variance is narrower. But chance still has no
memory, even in that large a population. That is, if I were to flip
ten million pennies, I would expect a *mean* value of 5 million heads
and 5 million tails (50.000% of each). But I would not be shocked to
actually get 5,000,500 heads and 4,999,500 tails. Then, after
painting 500 tails red to convert them to heads, flipping again I
would *predict* a *mean* value, in this second flip of 10 million
coins (with some having two heads), of 5,000,500 heads (50.005% heads;
49.995% tails), not the original 5 million heads. What I actually
get, however, will likely not be *exactly* 5,000,500 heads. Chance
plays a larger role in percentage terms in small populations. But it
is only in infinitely large populations that one would expect to get
exactly half of the flips be heads every trial. But that is only
because half of infinity is still infinity.
Feel free to explain what you think would be different in your
imaginary mathematical world? Does chance have a memory in your
world?
[snip]
Mark Isaak
I see from responses that you still have not figured out how and when
multiplication rule of probabilities apples. But I will give you one
last chance to give some indication that you are not totally incompetent
at mathematics. Simply explain when the multiplication of probabilities
applies and when it does not.
A lack of response will be considered an indication of incompetence, as
will any response more than 30 lines (including quoted lines).
John Harshman
"Locus" is a problematic term here, as it generally means a big
collection of sites. Better to use "site", which is what you mean.
> The expected
> number of new mutations fixed by neutral fixation per generation per
> locus is (u*2N)/2N or simply u per generation per locus. A reasonable
> mutation rate for point mutations is about 10^-8 per locus per
> generation. There are about 10 million years worth of divergence
> between humans and chimps (5 million in each lineage since the last
> common ancestor). Assuming 20 yrs/generation (which is likely a bit
> long in the chimp lineage and most of the human one as well), that is
> 5X10^5 generations separating the two modern species. That gives a
> probability of 5^10^-3 fixation difference per locus for any
> comparable locus in human and chimp. There are about 6 X 10^9 loci
> (nucleotides) in the diploid human (or chimp) genome, giving us an
> expected about 30 X 10^6 fixation differences between humans and
> chimps. That is certainly pretty close to the 40 X 10^6 differences
> that are observed.
A bit better than that. Only 35 x 10^6 of these are point mutations,
which is what your mutation rate is calculated on. The remaining 5 x
10^6 are indels and other rare events, which aren't included in your
rate estimate.
> A more accurate estimate of yrs/generation or
> mutation rate could easily account for the discrepancy. But John
> already did a rough calculation of this, which you simply ignored.
> Have you actually tried to present an alternate calculation?
He is handicapped by the fact that he apparently doesn't understand the
math, oddly enough, and even more by the fact that he thinks fixation
can result only from selection, never from drift. He is unable to
articulate why he thinks that, or in fact much else besides his
memorized mantras. He's too responsive for a bot, but not by much.
Inez
> On Mar 15, 9:18 pm, jillery <69jpi...@gmail.com> wrote:
>
>
>
>
>
> > On Mar 15, 9:08 pm, r norman <r_s_nor...@comcast.net> wrote:
>
> > > On Tue, 15 Mar 2011 16:59:52 -0700 (PDT), Bill
>
> > > <brogers31...@gmail.com> wrote:
> > > >On Mar 16, 6:51 am, Alan Kleinman MD PhD <klein...@sti.net> wrote:
>
> > > >Sorry for top posting, I'd just suggest that all the responses to
> > > >Dr.Dr.Dr. AK go into this thread. At least for those of us stuck with
> > > >Google Groups, once you hit 1000 posts the thread fragments. It's
> > > >entertaining and it would be nice to have it all in one place.
>
> > > I believe you, in a different thread, have been arguing against John
> > > Wilkins about modifying traditional biological word usage just to
> > > placate the creationists or at least to deny them the ability to twist
> > > the meaning of the words to their purposes. Now you would have all
> > > the rest of us modify traditional posting methods just to placate
> > > those people who do not know how to use a real news reader and must
> > > rely on Google Groups!
>
> > FWIW I rely on Google Groups not because I don't know how to use a
> > real newsreader. In fact I have used many. I rely on Google Groups
> > because it has the fastest propagation and the longest retention of
> > anything in its price class, which is no additional cost.
>
> > Of course TANSTAAFL, and enduring this design flaw ispartof the cost
> > of using Google Groups. ISTM illustrating that point is one of the
> > reasons for pepetuating this topic.- Hide quoted text -
>
> > - Show quoted text -
>
> I chose this Group because Edward Max, supervising medical doctor of
> the Food and Drug Administration published an essay on this site
> making irrational misrepresentations of how the mutation and selection
> phenomenon works. With leadership like his, no wonder we live in a
> world filled with multidrug resistant microbes. If Thomas Schneider of
> the National Cancer Institute allowed me to post on his site, I would
> tell him that his claim “The multiplication rule does not apply to
> biological evolution” is a completely irrational claim and that in
> fact, the multiplication rule is the central governing principle of
> the mutation and selection phenomenon.
Your own example shows that this is not necessarily so. If you give
HIV anti-viral drugs sequentially rather than at the same time they
mutate to resistance with no particular trouble, and soon you have
multiple resistant strains. In that case the multiplication rule does
not apply. You have yet even to attempt to show that your "all at
once" model is typical or most acts of selection.
Alan Kleinman MD PhD
========================================================
Peter Rathmann
>> The selection process can be very rapid if the initial frequency of
>> the beneficial allele is high. If the initial frequency is 50%, the
>> substitution process can occur in a single generation. However, when
>> you are talking about the mutation and selection phenomenon, by its
>> very nature, the initial frequency of the beneficial allele is going
>> to be extremely low and when that occurs, the substitution process
>> takes hundreds if not thousands of generations. If you understood
>> Haldane s mathematics, this principle would be readily apparent.
>> However evolutionists toss out any mathematical or empirical evidence
>> which contradicts your doctrine.
>Let's take a greatly simplified model to see if such substitution
>really needs to take so long. If it can work quickly in an extreme
>case then it is at least possible in principle for it to work rapidly
>in less extreme cases.
Welcome to the discussion Peter, let’s see what you are trying to
show.
>Assume a small population of 20 breeding pairs in an environment with
>a carrying capacity of 40 individuals (say scarcity of food). Each
>pair produces 10 offspring in a generation of which, on average, only
>2 survive. So the population remains constant. Now suppose there is
>a highly beneficial mutation 'a' in one individual which is so
>beneficial that anyone with it will out compete those without it,
>'b'. Also assume that the mutation is passed on in all offspring.
>Let's see what happens in subsequent generations:
You have already introduced a problem with the way you are formulating
your example of mutation and selection. When you are considering
random events with probabilities in the range of 10^-4 to 10^-8 or
smaller, populations of 40 are not reasonable size to accumulate
beneficial mutations and therefore advance the evolutionary process.
Even with a probability of a beneficial mutation of 10^-4, any
evolutionary process which requires only two beneficial mutations will
have a combined probability of 10^-8. This is a very unlikely
occurrence for a population size of 40 members.
>Gen. 0:
>40b 0a
>offspring:
>199b 1a (of these, only 39b and 1a survive due to the carrying
>capacity of the environment)
Ok
>Gen. 1:
>39b 1a
>offspring:
>190b 10a
Ok
>Gen. 2:
>30b 10a, paired as 11bb, 8ba, 1aa
>offspring:
>150b 50a
Ok
>Gen. 3:
>40a
Ok
>Doesn't seem to take many generations at all if the mutation is
>sufficiently beneficial and the number of offspring produced in each
>generation is well above the carrying capacity. With a larger
>population it will take a few more generations, but note that the
>population of the beneficial mutation is growing very quickly, so it
>won't take many generations to have it fixed in even a large
>population.
Not Ok. Reality shows that very small populations like this lack
diversity and are almost guaranteed to go to extinction. In addition,
as I said above, tiny populations do not give sufficient numbers of
members for the mutation and selection lottery to provide sufficient
numbers of winners for the evolutionary process to have reasonable
probabilities of working. Get the paper “The Cost of Natural Selection
Revisited” by Leonard Nunney. In that paper Nunney looked at the
effects of fecundity as a means of accelerating the selection process.
Nunney’s model could get the number of generations down to around 20
for very extreme cases but in many of his cases, his estimates for the
number of generations exceeded Haldane’s estimates.
The mutation and selection process requires large populations with the
previous beneficial mutation in order for the next beneficial mutation
to have a reasonable probability of occurring.
========================================================
hersheyh
>> The selection process can be very rapid if the initial frequency of
>> the beneficial allele is high. If the initial frequency is 50%, the
>> substitution process can occur in a single generation.
>http://www.google.com/url?sa=D&q=http://aac.asm.org/cgi/reprint/45/10/2877.pdf
>Let's instead take a clone from a bacteria sensitive to streptomycin
>and grow it up. Let's use Mycobacterium smegmatis, since streptomycin
>resistance is a factor in treating other mycobacteria, like M.
>tuberculosis. On average, spontaneous mutation to streptomycin
>resistance in wild type strain occurs at a frequency of 10^-8. That
>should actually probably be 5 X 10^-9 because there are two copies of
>the most common target gene (rrn, a ribosomal protein) in each
>bacteria. So the *frequency* of the allele that is beneficial in the
>presence of streptomycin is not 50%, but 0.0000005%, which, if my math
>is still there, is quite a bit less frequent than 50%.
>So plate 5 X 10^9 bacteria on brain heart infusion agar plates with
>streptomycin at 20ug/ml. You get about 2-10 colonies of resistant
>bacteria on each plate. The substitution, as a percent of the
>population that is resistant, is 10 out 10 colonies (each derived from
>a single cell) is 100%. As these colonies grow on the plate (or when
>removed to media with or without streptomycin) is now close to 100% in
>a single generation. Only close to 100% because reversion mutations
>do occur.
>I am amazed that you cannot even get this right at a conceptual
>level. Creationism must create brain damage.
I realize that mathematics is not your strong suit as an evolutionist
but how could you so completely bungle such a simple example of
substitution? In your case, you are killing 99.9999995% of your
population in a single (or very small number of generations). Your 5 X
10^9 population of bacteria has been reduced to about 25 bacteria. It
would take about 28 generations to reestablish your resistant
population. Of course the resistant population would not reestablish
if combination therapy was used. But you brilliant evolutionist fail
to properly understand and teach the basic science and mathematics of
mutation and selection. Your sloppy misunderstanding of how mutation
and selection works harms people.
>> However, when
>> you are talking about the mutation and selection phenomenon, by its
>> very nature, the initial frequency of the beneficial allele is going
>> to be extremely low and when that occurs, the substitution process
>> takes hundreds if not thousands of generations. If you understood
>> Haldane s mathematics, this principle would be readily apparent.
>> However evolutionists toss out any mathematical or empirical evidence
>> which contradicts your doctrine.
>> If you understood Haldane s model, you would recognize his
>> calculations are working with a fixed population size. I ve never said
>> that you need a change in population size in order for a substitution
>> process to occur. Increasing population size will increase the
>> probability that a beneficial mutation will occur at a particular
>> locus but only slightly.
>If the mutation *rate* is 10^-8, then we would expect (on average --
>it would actually be in a Poisson distribution) 1 mutant in a
>population the size of 10^8 individuals. In a population of 10^9
>individuals we would expect 10 mutants. Thus the *number* of expected
>mutants is N*u, where N is the population size and u is the rate of
>mutation. That is a *linear* increase in the *number* of mutants.
>The *rate* of mutation to a particular beneficial allele at a
>particular locus is unchanged (unless you add or subtract mutagens)
>regardless of the size of the population. It is selection (or chance)
>that determines the frequency of such mutants when they occur.
You still don’t get it. The probability of a particular mutation
occurring at a particular locus does not obey the additive rule of
probabilities. The probability that a particular mutation occur at a
particular locus is not a mutually exclusive event, it is a
complementary event. This is why doubling population size does not
double the probability that a particular beneficial mutation will
occur at a particular locus in any given generation. Doubling the
mutation rate also does not double the probability that a particular
mutation will occur at a particular locus in a given generation.
>As in the case of streptomycin described above, selection can change
>the frequency of alleles dramatically in one generation, but only by
>dramatically decreasing the population size. In many other cases of
>selection, population size can remain constant because the selective
>advantage is not like toxicity and all multicellular organisms have
>both random and selective losses between zygote and breeding and those
>losses can be massive compared to the changes due to selection. And
>in other cases of selection, as in Lenski's experiment, which involves
>opening up a new niche, the population size can actually increase
>during the spread of the allele.
But what you still don’t realize is that beneficial alleles must be
amplified before there is a reasonable probability that the next
beneficial mutation in an evolutionary process has a reasonable
probability of occurring on a member with the previous beneficial
mutation. That’s because the multiplication rule of probabilities is
the dominant mathematical principle governing the mutation and
selection phenomenon. It doesn’t matter what selection pressures do to
population size. If the beneficial allele can not be amplified, the
next beneficial mutation will have a very low probability of occurring
at the proper locus because there are so few members who are potential
recipients of the next beneficial mutation. This is the fundamental
principle of mutation and selection which is so difficult to get
through your thick evolutionist skull.
>> The selection process does not need to go to
>> completion in order to improve the probabilities that the next
>> beneficial mutation will occur at the proper locus, you only need to
>> have a sufficiently large number of members with the first beneficial
>> mutation for there to be a reasonable probability that the next
>> beneficial mutation in the sequence occur.
>Yes. The probability of the second mutation is still N*u2. If the
>first mutation is like the streptomycin resistance mutation described
>above, the probability of the second mutation occurring immediately
>after selection for streptomycin resistance is still described as
>N*u2. N, however, immediately after selection is perhaps 10 (if you
>plated 10^9 bacteria), while u2 is perhaps 10^-8. However, after the
>population has grown up to around 10^8 bacteria (almost all
>streptomycin resistant now), a process that would take less than 30
>generation with a population doubling time of 30 min. Say overnight
>growth (15 hrs or less) in rich medium with or without streptomycin,
>the same mutation rate, u2, in a population which now has more than
>10^9 bacteria nearly all of whom are streptomycin resistance, is still
>N*u2. It would be almost certain that one would find a double
>resistant bacteria in this case. Just as it would be almost certain
>that one would not find a double mutant if you did the selections
>*simultaneously* so that the single mutants in a population of 10^9
>bacteria (say 10 resistant to each antibiotic) are not selected for.
>Then, and *only* then, does the multiplication rule hold. The
>probability of a double mutant being present in a population of
>sensitive bacteria of size 10^9 would be N*u1*u2. That, and only that
>determines the probability of such a double mutant. If u for each
>individual mutation is 10^-8, then you would need a population size of
>10^16 cells to expect a mean of 1 double mutant. The difference is
>that I understand *when* the multiplication rule applies and when it
>doesn't. You don't know that difference. You *assume*, without
>evidence, that it always applies.
Perhaps now you are starting to understand why amplification of a
beneficial allele is crucial for a population to successfully carry
out a mutation and selection process but you still do not understand
completely. Amplification is what is required for a population to
overcome the multiplication rule of probabilities for two beneficial
mutations to occur on a single individual (not simultaneously). The
multiplication rule of probabilities always applies to beneficial
mutations occurring on the same individual whether they happen
simultaneously or not. Without amplification, the multiplication rule
of probabilities makes any evolutionary process requiring more than a
single beneficial mutation a highly unlikely event.
>> This is why any
>> evolutionary process that depends on a neutral allele will be a very
>> low probability event because without amplification, the mutation and
>> selection process is stymied by the multiplication rule of
>> probabilities.
>Again, this is based on your false ignoring of how *real* population
>genetics occurs. There is a certain probability of a selectively
>neutral allele spreading throughout a population by a random walk.
>You assume a perfect Hardy-Weinberg equilibrium which assumes an
>infinite or perfect population allele distribution from one generation
>to the next. Given the number of nucleotides in a human genome and
>the average mutation rate for point mutations, it is virtually certain
>that, over the course of a few million years, you would find the
>percentage of nucleotides that have changed by chance alone to be
>about that seen (actually a little less) in a comparison of chimps and
>humans.
Hersheyh, how would you know what *real* population genetics is? You
are not a population geneticist because any real population geneticist
would know that doubling population size does not double the
probability that a beneficial mutation will occur at a particular
locus. You have drifted so far from reality that you think that the
flipping of ten pennies explains your mathematically irrational
theory. Try flipping ten million pennies and see where your
mathematics leads you. Then try flipping two sets of ten pennies and
see if your populations can fix two neutral mutations simultaneously.
You have bungled the basic science and mathematics of mutation and
selection and clearly you are not a population geneticist.
And
>The *only* examples you have given have been artificial ones created
>by humans. Specifically designed environments by humans to lower the
>probability of a selective advantage. And every example you gave
>involves toxins that specifically reduce population size, thus
>reducing the probability of an individual with a needed mutation
>further. You repeatedly refuse to admit any other conditions of
>selection at the very same time that you accuse evolutionary biology
>of all sorts of evils by a false accusation that they are killing
>people by arranging conditions in which the same multiple resistances
>can occur -- either by arranging sequential resistance or allowing
>parallel resistances to accumulate in the same individual by sexual
>recombination. You need to get your story straight. If evolution of
>multiple resistance is mathematically impossible, why, exactly do you
>keep pointing out that it is possible and evolutionary biologists are
>to blaime?
So let’s see you design an experiment which shows something different.
Show us selection pressures which don’t kill or impair the
reproduction of member of a population. Are you now going to take the
stance that selection pressures don’t kill or impair the reproduction
of members of a population? You keep going further and further out on
you mathematically irrational limb.
Now with regards to when there is a reasonable mathematical
probability for a population to evolve to selection pressures by
mutation and selection depends on the complexity of the selection
conditions. The population must be able to amplify beneficial
mutations in order for there to be a reasonable probability that the
population can evolve to the selection conditions. Clearly from the
empirical examples I’ve presented, the amplification process does not
work efficiently when more than a single gene is targeted by selection
pressures.
>> That s why the amplification process
>> breaks down when combination selection pressures are used.
>*When* combination (i.e. simultaneous) selection pressures are
>arranged such that there is no selective advantage to individual
>variants. Even when selection pressures are arranged in combination,
>if there is a selective advantage for single variants, they will
>spread through the population. For example, if there is selective
>pressure for bipedality and selective pressure for ability to sweat,
>individuals with greater bipedality may have a selective advantage
>even in the absence of ability to sweat and ability to sweat may have
>a selective advantage even in the absence of bipedality. That leads
>to either sequential selection (where one appears first, perhaps
>thereby even increasing the selective advantage of the second, which
>then evolves to "catch up" more quickly) or parallel selection with an
>extra advantage to having both.
But that’s the basic science and mathematics of mutation and
selection. When two or more genes are targeted by selection pressures,
the amplification of any beneficial mutations which occur to one or
another selection pressure can not amplify because the other selection
pressures are killing or impairing the reproduction of that member. It
might be nice for living things to have all the properties you mention
above but mutation and selection takes thousands perhaps tens of
thousands of generations just to evolve resistance to single drug
antibiotic therapy or to transform a glucose metabolizer to a citrate
metabolizer. If you put additional selection pressures on these
populations, they have much, much more difficulty doing the sorting
and optimization process to these simultaneous selection pressures.
The reason these populations have much, much greater difficulty
evolving to these simultaneous selection pressures is these
populations can not amplify beneficial mutations efficiently.
>> If you have
>> an example where combination selection pressures do not stifle the
>> mutation and selection phenomenon,
>You cannot even correctly state what combination selection of the type
>you describe does. What your kind of simultaneity does is to decrease
>the probability of selectively favored genome by preventing
>selectively useful intermediacy. That is all it does. It does not
>change the individual mutation rates. Your conditions merely make the
>intermediate state of resistance to a single toxicity (which is the
>only kind of evolution you seem to think exists) nonselectable.
First of all hersheyh, you need to recognize that all a selection
pressure is a cause of death or something which impairs the
reproduction of members of a population. I have previously defined the
complexity of selection pressures by the number of mutations required
to adapt to the selection conditions and the number of genes targeted
by the selection conditions. Antimicrobial agents are unique amongst
selection pressures since they specifically target particular genes
(in most cases). Because of this, these types of selection pressures
are particularly amenable to the mutation and selection phenomenon
when used singly. The highly efficient beta lactamase example is good
example of how a population can use mutation and selection to adapt to
this type of selection pressure. Any selection pressures such as
thermal stressors or starvation tend to target many genes unless as in
Lenski’s example, he put a second carbohydrate in his medium which his
population was ultimately able to use based on a fairly small number
of mutations the population was able to amplify these small number of
mutations over some thirty thousand generations.
>> present it but you can t because
>> they don t exist. The examples of multidrug resistant organisms took
>> tens of thousands of generations to occur by the use of single drug
>> selection pressures sequentially over many years.
>Multidrug resistance does occur. Not surprisingly, it tends to occur
>in hospitals and other settings where both types of drug are used
>frequently (and especially if other conditions, like poor sterile
>technique by the doctors and nurses, exist and antibiotics are used to
>cover up their laxity). It is often the case that both resistances
>wind up on the same plasmid and then get transmitted horizontally as a
>unit. This is despite the often selective advantage of w.t. strains.
Multidrug resistance occurs because these selection pressures are used
singly in sequence allowing the microbial populations to amplify
beneficial alleles. The use of single drug therapy is standard of care
in the medical field. This clinical blunder has occurred because the
basic science and mathematics of mutation and selection has not been
well understood or explained to doctors or to anyone else as well.
>Even worse is the agricultural use of antibiotics as growth enhancers,
>since those are often used at low level for prolonged times.
I’ve heard this argument before. I live in farm country and I don’t
know of any farmers or ranchers doing this. In fact I don’t think it
is very smart to feed bovines or caprines antibiotics on a regular
basis since these animals depend on the bacteria in their gut to break
down cellulose. Even so, if a rancher or farmer can show that
antibiotics can safely improve growth in their animals, then they
should do it with combination antibiotics to impair the mutation and
selection process.
>>This allowed
>> amplification of beneficial alleles to produce these multidrug
>> resistant destructive organisms. This was a consequence of bungled
>> evolutionist teaching of how the mutation and selection phenomenon
>> works.
>So you claim based on an idiotically ignorant and biased reading of a
>heading on a single paragraph of Schneider's comment about the equally
>stupid creationist claim that evolution works by assembling new
>proteins by some unspecified random mechanism that randomly assembles
>new proteins from scratch using raw amino acids. But I presume you
>read the Bible the same way. Take sentences out-of-context to try to
>make the text agree with your beliefs.
Schneider should know better since this is his field but he didn’t
realize what happens to the amplification process when selection
pressures target multiple genes and how the multiplication rule of
probabilities stifles the evolutionary process. He does now. If he
would ever do a thorough analysis of his population genetics model, he
would have a much better understanding of the mutation and selection
phenomenon but you evolutionists just don’t seem to want to understand
how this phenomenon works in reality. This denial of reality on the
part of evolutionists has harmed and continues to harm millions of
people suffering from diseases subject to the mutation and selection
phenomenon.
>> Single drug therapy is still the standard of care for most
>> infectious diseases. This is a particularly bad strategy for
>> debilitated patients with impaired immune systems or when antibiotics
>> are used for long term prophylaxis. It s incredible how the stupid
>> evolutionists misperceptions of the mutation and selection phenomenon
>> have seeped into the medical system.
>So is treating debilitated patients with massive doses of multiple
>antibiotics, all of which have some side effects. And in many cases,
>the choice is to let patients die or treat them with the one
>antibiotic that is best for that condition. In other cases, multidrug
>therapy is indeed the correct way to go. But you seem to take an idea
>and automatically assume it is always the best.
The idea is to treat people with infections early so that they are not
debilitated by their infectious disease. If they have other underlying
health problems like cancer, diabetes, COPD, etc., all the more reason
to treat their infections with multiple selection pressures.
Debilitated patients tend to have poor functioning immune systems
which would normally act as a selection pressure on the microbes as
well. It is not unusual for someone with cancer to die of an
infection. My clinical experience has been that it is far superior to
give combination antibiotics to debilitated individuals.
But you do make a valid point. Every medicine is a little bit of
poison and if you do use combination antibiotics, potentially you
could do harm. Clearly, multidrug resistant bacteria are a big problem
which is only getting worse. The risks of using combination
antibiotics verses the risks of multidrug resistant bacteria must be
weighed. I explain these risks to my patients but since many of the
infections I deal with are due to MRSA, I’ve never had a patient
refuse combination therapy. I also have never had a serious adverse
result with using combination therapy.
>> Perhaps you believe that spores will evolve feathers if the
>> temperature drops?
>And that little bit of idiocy comes from what diseased portion of your
>brain? It makes no sense. Can you point to some evolutionary
>biologist who thinks that bacterial spores will magically produce
>feathers in your lifetime? We know about when "feathers" (downy ones)
>first evolved. And it wasn't in bacteria.
It must have come forth from the portion of my brain that
evolutionists have gotten too. Aren’t you the one who says not to
think of evolution as a teleological process?
> > > Mutation and selection only
> > > works well when a single gene is targeted by a single selection
> > > pressure. As soon as multiple genes are targeted, the mutation and
> > > selection process is stymied by the multiplication rule of
> > > probabilities.
>That is not true. There are several types of changes that will
>produce resistance to cold, including changes in body shape (to reduce
>surface area), changes in insulation (fat deposition, hair or
>feathers), changes in color to hide better in a cold ...
Produce the real, measurable and repeatable examples that mutation and
selection did all of this. All the real measurable and repeatable
examples that I have found demonstrate that as soon as more than a
single gene is targeted by selection pressures, the mutation and
selection process is stifled. I’ve found these examples thanks to
Google.
And
>> I don t get tired of telling evolutionists that the multiplication
>> rule of probabilities is the dominant mathematical principle of the
>> mutation and selection phenomenon.
>You mean asserting it again and again, without providing any
>justification for the assumptions you make.
Hersheyh, if you are going to play games of chance with bacteria,
viruses, parasites, cancer, weeds and so on, you had better learn the
rules of the game because the way you evolutionist would have us
understand the game would be no different than a casino owner posting
a picture of their latest big winner on a billboard so that you would
think you could be a big winner as well. The reality is that most
people leave their money at the casinos because they don’t understand
the probabilities of their game as you don’t understand the
probabilities of the mutation and selection phenomenon. And I support
my assertions with numerous empirical examples, all which demonstrate
that the multiplication rule of probabilities is the dominant
mathematical principle of the mutation and selection phenomenon.
>> Apparently, I m just going too fast
>> for you to understand this basic mathematical principle.
>No. You are not going too fast. You are quite repetitive. Boringly
>and ignorantly so. It is not enough to repeat your assertion over and
>over and over again. You need to provide some evidence that evolution
>*always* requires invoking the multiplication rule, despite our
>pointing out that that is not the case.
I understand that evolutionists are bored with the mathematical and
empirical facts of life of the mutation and selection phenomenon but
those of us who have to deal with the reality of this phenomenon have
a responsibility to properly describe how this phenomenon works. If
you want a more precise description of the probabilities of multiple
beneficial mutations occurring (not simultaneously), ie, computing the
probability of mutation B occurring after mutation A has occurred then
you have to compute the *conditional probability* which is denoted
mathematically P(B | A). Once you have mutation A, you have a new
(reduced) sample space and that probability is the fraction of P(A)
which corresponds to P(A)*P(B). Or to put it in equation form;
P(B | A) = (P(A)*P(B))/P(A) = (P(A)*P(B))/n where n is the number of
members with mutation A.
In order to get your conditional probability down to a reasonable
value, the population must increase n to a large number so that
mutation B has a reasonable chance of occurring on a member of the
population who already has mutation A. Note that the numerator of the
above equation is simply the multiplication rule of probabilities.
What selection does is allow populations to amplify a particular
mutation thereby increasing n so that P(B | A) has a reasonable chance
of occurring. I hope I’m not boring you.
>> But it is
>> worthwhile making the effort since the bungled evolutionist teaching
>> and understanding of this phenomenon has harmed and continues to harm
>> millions of people suffering from diseases subject to the mutation and
>> selection phenomenon. I think it is worthwhile to correct this
>> monumental evolutionist blunder.
>This is based on your ignorant misinterpretation of Schneider's
>article, which *correctly* points out that proteins, in evolution, are
>not assembled from scratch from a randomly assembled set of amino
>acids.
Both you and Schneider fail to understand that the multiplication rule
of probabilities is the central governing mathematical principle of
the mutation and selection phenomenon. The failure to understand this
principle has harmed and continues to harm millions of people
suffering from diseases subject to the mutation and selection
phenomenon.
========================================================
richardalanforrest
>> I don t get tired of telling evolutionists that the multiplication
>> rule of probabilities is the dominant mathematical principle of the
>> mutation and selection phenomenon.
>...but evidently too tired to read the well-informed responses to your
>post which explain why you are wrong.
Hello Richard. Just where do evolutionists get their well-informed
responses on how mutation and selection works, the SciFi channel? So
far, the only thing I have gotten from evolutionists is the incorrect
understanding how population size affect the probabilities that a
beneficial mutation will occur at a particular locus and a failure to
understand that the multiplication rule of probabilities is the
central governing mathematical principle of the mutation and selection
phenomenon.
>> Apparently, I m just going too fast
>> for you to understand this basic mathematical principle.
>I suggest that this is not the case.
When you are dealing with the evolutionist indoctrinated mind, you
can’t go too slowly.
>> But it is
>> worthwhile making the effort since the bungled evolutionist teaching
>> and understanding of this phenomenon has harmed and continues to harm
>> millions of people suffering from diseases subject to the mutation and
>> selection phenomenon.
>...an assertion for which you cannot provide any evidence.
So you don’t think that people die from infections due to multidrug
resistant bacteria and cancer treatments fail when the cancer cells
evolve resistance to the drugs used to suppress these cells. You
really need to come up to date Richard.
>> I think it is worthwhile to correct this
>> monumental evolutionist blunder.
>If this is the case, the place to do it is in the pages of academic
>journals, not internet forums.
Everything that I have posted is from academic journals or texts from
my science courses. I’m not the first to say that the multiplication
rule of probabilities is the dominant mathematical principle of the
mutation and selection phenomenon. Edward Tatum said this in his 1958
Nobel Laureate lecture. And what is wrong with Google? Edward Max,
ardent evolutionist, and supervising medical doctor of the Food and
Drug Administration posts his mathematically irrational understanding
of the mutation and selection phenomenon on this site.
========================================================
This is the last of the splinter threads, my next responses will be to
individual posts.
gdgu...@gmail.com
> The following are a compilation of responses from the splinter threads
> of March 23
> But that’s the basic science and mathematics of mutation and
> selection. When two or more genes are targeted by selection pressures,
> the amplification of any beneficial mutations which occur to one or
> another selection pressure can not amplify because the other selection
> pressures are killing or impairing the reproduction of that member.
Are they? Compared with what?
Suppose you have a population of prey animals. We'll call them
Gazelles for simplicity, but please let's not dwell on the properties
of real Gazelles. At the beginning of our thought experiment, none of
them possess any of the theoretical mutations I will propose below.
Now we'll sprinkle in a number of mutations. Each of them changes the
phenotype in a minor way, which produce things like slightly keener
night vision, slightly more acute hearing, slightly greater running
speed, cornering ability, changes in coloration, etc.
Let's further assume that each of these mutations provides its "owner"
with a slightly better chance of evading Cheetahs. First let us note
that none of the Gazelles has suffered any direct "impairment", except
in comparison with his fellows. But the "base-model" gazelles will be
at a disadvantage with respect to any of their enhanced brethren, and
will be eaten in greater proportions. Already we have a scenario in
which the "enhancements" are "amplified", even if no Gazelle has more
than one.
Over generations, assuming that some of the "enhancements" have
survived, some of the Gazelles will likely inherit more than one,
giving those individuals an advantage over their singly-enhanced
fellows. Thus will (some of) the enhancements spread through the
population, eventually becoming the dominant "model".
If there were two Cheetahs for each Gazelle, in a fenced-in area with
no cover, and three simultaneous mutations were required to produce
say , laser-cannon eyes, then I would agree that the Gazelles are
doomed. But in a scenario in which many of the Gazelles will survive
and reproduce despite selection (the Cheetahs), why couldn't several
beneficial mutations be "amplified" at the same time? Or, for that
matter, sequentially? No Gazelle needs all of the mutations to
survive, but each provides a benefit.
Greg Guarino
Alan Kleinman MD PhD
>
> If you understood the mathematics of the
>
> > > phenomenon, this would be clear to you. Do you think the mutation rate
> > > will account for 67 fixations per generation?
>
> > Yes. We aren't talking about selection here. We're talking about neutral
> >evolution. You seem entirely blind to this point, to the degree that one
> > might imagine some form of psychosis. You can't even see the words.
>
> Kleinman offers one of the most clear examples of Morton's Deamon
> I have ever seen. Its like having an argument with a windup doll.
Now Stuart, let’s not go overboard. How do you know that I’m not
battery powered? I might even be running on solar energy. Windup dolls
are so antique road show; let’s get you up to date.
>
> Stuart
Alan Kleinman MD PhD
>
> Very confused attributions. This was Kleinman:
>
> >> Just because you evolutionists don’t want to
> >> discuss the basic science and mathematics of mutation and selection,
> >> that I have to enter your world ofirrationalspeculations. We now
> >> have evolutionist expert Mark Isaak claiming that reducing the
> >> intensity of selection accelerates the mutation and selection
> >> phenomenon. This mathematical blunder ranks up there with the
> >> evolutionist blunder that selection increases the diversity of
> >> populations.
>
> This was me:
>
> > Bet he didn't actually say that. You aren't a very good reader. And
> > of course selection can increase diversity under certain conditions,
> > some of which have been explained to you.
>
> This was Kleinman again:
>
>
>
>
>
> > Well let’s see exactly what Mark said in context to a comment I made:
> > Kleinman said:
> >>> Again, you repeat an old speculation that evolutionists like to use.
> >>> The intensity of selection has very specific mathematical effects on
> >>> the mutation and selection process. That effect is to slow the process
> >>> down. Reducing the intensity of selection is a two edged sword. On one
> >>> hand, reducing the intensity of selection reduces the chances that the
> >>> population will be driven to extinction. On the other hand, reducing
> >>> the intensity of selection slows the mutation and selection phenomenon.
> > Mark Isaak said in response:
> >> It is obvious to anyone with a smattering of knowledge of population
> >> genetics that you don't know what you're talking about. But it is also
> >> apparent (if not so blatant) that you *think* you know what you are
> >> talking about. I find that fascinating. It's like you are writing a
> >> travel book about a place you have never so much as heard of before, but
> >> are willing to swear to having lived there for years.
> > I am claiming that reducing the intensity of selection slows the
> > evolutionary process. Mark Isaak is claiming I don’t know what I’m
> > talking about.
>
> I believe that was a general appreciation, not directed specifically at
> some particular set of words. And so I'm right. You aren't a very good
> reader.
>
> [snip random insults]
>
>
>
>
>
> >>> Lenski is starving his bacteria but leaving his population with an
> >>> out, ie citrate. You obviously have not read Lenski’s paper on the
> >>> quantitative results of his study. Hersheyh, get a copy of this paper
> >>> “Genomeevolutionand adaptation in a long-term experiment with
> >>> Escherichia coli”, Vol 461, October 29, 2009, Nature. In the adaptive
> >>> phase of his study, none of the mutations in the experiment were due
> >>> to drift (a crappy word to describe what populations do on a plateau
> >>> of a fitness landscape).
> >> Another very odd thing to say. Of course mutations aren't due to drift.
> >> Drift affects allele frequency, not mutation. And drift doesn't apply to
> >> populations; it applies to alleles. Perhaps you meant to say that none
> >> of the fixations were due to drift, which is true of the first 20,000
> >> generations. Many of the fixations by generation 40,000 were due to
> >> drift. The difference is that the mutation rate increased in the
> >> interim, and the rate of fixation due to drift equals the mutation rate.
> > All the mutations measured in the first 20,000 generations were found
> > in all populations, they were adaptive, not neutral.
>
> Not true. You have again confused mutation with fixation. In order to be
> assayed, mutations must reach an appreciable frequency. Most mutations
> will become extinct after the first generation. There were almost
> certainly many neutral mutations, but none of them reached any
> appreciable frequency.
Well John, what do you think the Lenski team was measuring?
>
> > Only when his
> > populations reached a fitness plateau did more variants start to
> > appear. That is, his populations had adapted to the starvation
> > conditions and reduced the selection pressure allowing more variants
> > to appear after 20,000 generations. I question Lenski’s estimates for
> > the mutation rates. If Lenski is extrapolating backwards from the
> > number of mutations found in his populations, he could be getting
> > inaccurate estimates of the mutation rates.
>
> You really can't read. The increase in mutation rates is both observed
> and has a genetic mechanism (whose frequency in the population can
> itself be tracked). It's fascinating that you take from Lenski whatever
> you think serves your purpose and reject what doesn't, without even
> attempting to justify the distinction.
John, you have gotten so used to making irrational extrapolations, you
don’t even recognize when you are doing it anymore.
>
> > However John, one of the many mathematical features of the mutation
> > and selection phenomenon that you don’t understand is that the
> > mutation rate has only a small effect on the behavior of the
> > phenomenon.
>
> We were talking about drift, not selection.
So do you want to continue your claim that dozens of neutral mutations
are fixed every generation in the evolution of humans and chimpanzees
from a common ancestor? How do so many neutral mutations get fixed
simultaneously by chance alone when even with the benefit of selection
it takes hundreds of generations to fix a single mutation? John, I
think your brain is in neutral with this claim.
>
> > Perhaps you want to claim that doubling the mutation rate
> > doubles the probability that a beneficial mutation will appear at a
> > particular locus?
>
> It certainly doubles the expected number of such mutations.
Where did you learn probability theory, UMI, The University of the
Mathematically Incompetent? So now I suppose that when you double the
mutation rate, you double the probability that a particular mutation
will occur at a particular locus? Just keep doubling the mutation rate
and you will find that the probability will at some point be greater
than one. John, you don’t know how to apply probability theory to a
stochastic process and you do not have the capability to learn. You
need to learn how to distinguish between mutually exclusive events
which obey the additive rule of probabilities and complementary events
which require the use of the complementation rule of probabilities to
compute the probabilities. Until you learn these mathematical
principles, you will continue to bungle the basic science and
mathematics of the mutation and selection phenomenon.
>
> > By far, the dominant mathematical principle of the
> > mutation and selection phenomenon is the multiplication rule of
> > probabilities. That is why the complexity of the selection conditions
> > dominates the behavior of the phenomenon.
>
> Please show your work here. What's your math?
I posted the mathematics in a response to hersheyh previously but I
will do it again here for you because of the importance of this
principle in understanding how and why mutation and selection does
what it does. In addition, I made a mathematical error in my post to
hersheyh.
If you want a more precise description of the probabilities of
multiple beneficial mutations occurring (not simultaneously), ie,
computing the probability of mutation B occurring after mutation A has
occurred then you have to compute the *conditional probability* which
is denoted mathematically P(B | A). Once you have mutation A, you have
a new (reduced) sample space and that probability is the fraction of
P(A) which corresponds to P(A)*P(B). Or to put it in equation form;
P(B | A) = (P(A)*P(B))/P(A)
And P(A) = (n/N) where n is the number of members with mutation A and
N is the total population.
In by original post of this equation, I left N out of the equation.
In order to get your conditional probability down to a reasonable
value, the population must increase n to a large number so that
mutation B has a reasonable chance of occurring on a member of the
population who already has mutation A. Note that the numerator of the
above equation is simply the multiplication rule of probabilities.
What selection does is allow populations to amplify a particular
mutation thereby increasing n so that P(B | A) has a reasonable chance
of occurring.
>
> > Regardless, Lenski’s population fixed only a very small number of
> > mutations in more than 40,000 generations, only about 1 each 500
> > generations. Now you have done the mathematics for the number of
> > fixations required to transform humans and chimpanzees from a common
> > precursor. Your estimate is 67 fixations per generation. How do you do
> > that accounting problem?
>
> I have explained this at least twice, and Howard has done so at least
> once, and you have so far ignored all of them. Briefly, in neutralevolution, fixation rate (in the population) equals mutation rate (in an
> individual). By any reasonable estimate of rates and times, 67 fixations
> per generation is well within expectation.
We already know what evolutionist expectations are and that they are
mathematically irrational. You’ve abandoned probability theory for
expectation theory (whatever that means to an evolutionist). Now you
are telling us that every member of a population gets 67 neutral
mutations spread through the population simultaneously every
generation and this happens for hundreds of thousands of generations.
You have very high expectations but very low probabilities. I’m really
starting to believe that evolutionism is a form of folie a deux.
>
> >>> Only when the populations evolved to improved
> >>> fitness did “neutral” mutations appear in his populations. In other
> >>> words, his population is diversifying on a fitness plateau. Still,
> >>> this population is limited by the amount of citrate available.
> >> You completely misunderstood his point. Which is not unexpected. There
> >> was in fact no fitness plateau. Advantageous mutations appeared
> >> throughout. What made the difference was the increase in mutation rate,
> >> as Lenski himself made clear in that paper.
> > The mutation rate has only a small effect on the mutation and
> > selection phenomenon. If you understood the mathematics of the
> > phenomenon, this would be clear to you. Do you think the mutation rate
> > will account for 67 fixations per generation?
>
> Yes. We aren't talking about selection here. We're talking about neutralevolution. You seem entirely blind to this point, to the degree that one
> might imagine some form of psychosis. You can't even see the words.
I think we are talking about some form of psychosis and I do see your
words.
>
> >>>> Now, if the glucose-only bacteria were more efficient at using glucose
> >>>> than the bacteria that could use both, we have a condition that could
> >>>> favor "specialization" to different niches, with some bacteria
> >>>> becoming specialized glucose users and others becoming more and more
> >>>> reliant on citrate. I.e., speciation (and because inability to use
> >>>> citrate is a key speciation-defining feature of E. coli, the new bug
> >>>> would not be E. coli, but perhaps E. citrusflavoreddietcoli.
> >>> I guess you haven’t read any of Lenski’s papers. The citrate
> >>> metobolizers no longer were efficient glucose metabolizers and these
> >>> citrate metabolizers were very sensitive to osmotic pressures.
> >> All adaptations are adaptive with respect to particular environments.
> >> Don't you understand that yet?
> > Give me a hint John; tell me how you can account for 67 fixations per
> > generation? Just what were the adaptive conditions for that primate
> > precursor?
>
> Adaptation is irrelevant. It's neutralevolution. Only a very tiny
> minority of the observed differences have any phenotypic effect or are
> subject to selection.
I see John, now you don’t need selection any more. All these neutral
mutations fix themselves in the population by random chance. You do
have great expectations.
>
> >>> Now
> >>> early on, you posted a paper that I wasted my time on reading. In this
> >>> paper, these evolutionist pseudo-scientists claim thatevolutionis
> >>> irreversible. Now do you think if you switched Lenski’s experiment and
> >>> put his citrate metabolizers in a glucose rich environment with sparse
> >>> citrate that his bacteria could evolve back to glucose metabolizers?
> >> That's not what "irreversible" means. We would expect adaptation to any
> >> environment, including a prior one. What we wouldn't expect is a
> >> reversion to exactly the same phenotype as the ancestral one. The reason
> >> is that there are many ways of achieving the same adaptive result.
> > Why not? So why would you say that reptile scales would turn into
> > feathers when there are many ways to achieve the same adaptive result?
>
> Because that's one of the ways, and it happens to be the one that arose.
> I'm unable to penetrate the bizarre thought processes behind that question.
And I suppose this all happened because of neutral mutations?
>
> > Seems like a very difficult way for a reptile population to stay warm
> > when there are many other ways to accomplish the same result without
> > taking huge number of generations. The reptiles that live near my home
> > hibernate when the weather gets cold. They are not growing feathers.
>
> The reptiles that live near your home aren't endotherms, and aren't
> evolving endothermy. Insulation is pointless in an ectotherm.
You are getting awfully teleological here aren’t you?
>
> >> You haven't explained why that would be. Could you? And you might also
> >> explain where you think birds came from, if they didn't evolve from
> >> terrestrial reptiles.
> > It’s not my job here to tell you where birds came from. It’s my job to
> > properly describe how the mutation and selection phenomenon works. Do
> > you want to tell us how to account for 67 fixations per generation?
>
> It's not your job to take any position or defend your prior statements.
> It's not your job to show any sort of intellectual integrity. But it
> apparently is ...
From my first post I have claimed that the multiplication rule of
probabilities is the dominant mathematical feature of the mutation and
selection phenomenon. I have posted numerous empirical examples of
this and given you the equations which describe these probabilities.
Sorry that this mathematics does not meet your evolutionist
expectations.
>
> read more »- Hide quoted text -
>
> - Show quoted text -- Hide quoted text -
Alan Kleinman MD PhD
> On Wed, 30 Mar 2011 08:08:18 -0700, Alan Kleinman MD PhD wrote:
>
> > On Mar 15, 4:59 pm, Bill <brogers31...@gmail.com> wrote:
> >> On Mar 16, 6:51 am, Alan Kleinman MD PhD <klein...@sti.net> wrote:
>
> >> Sorry for top posting, I'd just suggest that all the responses to
> >> Dr.Dr.Dr. AK go into this thread. At least for those of us stuck with
> >> Google Groups, once you hit 1000 posts the thread fragments. It's
> >> entertaining and it would be nice to have it all in one place.
> > together some of my responses for a while. I know it upsets the posters
> > when I combine responses but unless you have a better suggestion, that’s
> > what I’m going to do so that the discussion doesn’t fragment further.
>
> Better suggestions:
>
> 1. Don't combine replies.
Sorry, I either would have to deal with dozens of splinter threads or
combine posts.
> 2. Post some math already.
Check my post to John Harshman where I show how the multiplication
rule of probabilities relates to conditional probabilities (where
beneficial mutations do not occur simultaneously).
> 3. Post the equations for at least the Moran and Wright-Fisher models,
> so we know that you've at least looked at them.
I read the lecture notes recommended by lucaspa and at best these
models are ambiguous. If you want to look at a good model of
population genetics, study Schneider’s ev model of mutation and
selection. It gives you a good mathematical platform to study the
effects of population size, mutation rates, genome size and of course
the complexity of the selection conditions on the evolutionary
process.
As far as I know, Schneider's model does not preclude neutral
mutations.
> 4. Post the equations that would allow you to take frequency-dependent
> selection and stabilizing selection into account.
It’s up to you evolutionists to show how any particular selection
condition would have a significant affect on the mutation and
selection process. By far the dominant mathematical principle in the
mutation and selection phenomenon is the multiplication rule of
probabilities.
Schneider's model demonstrates stabilizing selection.
> 5. Post the equations that describe what you think is correct.
I’ve done it already. Instead we have evolutionists who believe that
you can have probabilities greater than one, don’t understand the
principles of conditional probabilities and developed a new
mathematical theory called expectation theory.
> 6. Find an appropriate genetic dataset or simulation.
Schneider’s ev model is a good simulation which contains all the
essential features of the mutation and selection phenomenon. Too bad
that Schneider has only done a superficial analysis of his model
because then he wouldn’t be making claims that the multiplication rule
of probabilities does not apply to biological evolution.
> 7. Post the error for your approach and for existing models (and show
> your work).
Now I do agree that Schneider’s model does not include recombination
and only includes point mutations. The empirical evidence shows that
recombination has very little effect on the creation of new alleles
and other forms of mutations such as insertions and deletions are much
more destructive causing frame shifts. I’ve only found a few empirical
examples of frame shifts which give benefit to those members.
Regardless, no matter what form of mutations, if more than a single
beneficial mutation is required the multiplication rule of probability
holds. That is what dominates the mutation and selection phenomenon.
> 8. Don't bother replying until you've done this. You've cemented your
> reputation as "The guy who don't understand high-school probability".
> Continuing to make math-free replies isn't going to make that any better
> or worse.
> 9. No, really. Post some math already.
I’ve already posted the probabilities for a beneficial mutation to
occur as a function of population size and I have posted the
conditional probability that two beneficial mutations occur (not
simultaneously). The first example shows that the effect of population
size is less than additive on the probability that a beneficial
mutation will occur at a particular locus and the second example shows
that the multiplication rule of probabilities is embedded in the
conditional probability of two beneficial mutations occurring (not
simultaneously). If you can’t find the calculations in this
evolutionist morass, I’ll repost the calculations to you directly.
>
> <snip>
John Harshman
They were measuring alleles that had reached a high enough frequency to
be detected. They would have detected every mutation only if they had
sampled every individual in every population. And of coruse that would
have ended the experiment right there.
>>> Only when his
>>> populations reached a fitness plateau did more variants start to
>>> appear. That is, his populations had adapted to the starvation
>>> conditions and reduced the selection pressure allowing more variants
>>> to appear after 20,000 generations. I question Lenski’s estimates for
>>> the mutation rates. If Lenski is extrapolating backwards from the
>>> number of mutations found in his populations, he could be getting
>>> inaccurate estimates of the mutation rates.
>> You really can't read. The increase in mutation rates is both observed
>> and has a genetic mechanism (whose frequency in the population can
>> itself be tracked). It's fascinating that you take from Lenski whatever
>> you think serves your purpose and reject what doesn't, without even
>> attempting to justify the distinction.
> John, you have gotten so used to making irrational extrapolations, you
> don’t even recognize when you are doing it anymore.
I see you aren't going to get into specifics. Lenski observed a
particular mutation that resulted in heightened mutation rates in
individual that possessed it, and he watched it grow from low frequency
to fixation.
>>> However John, one of the many mathematical features of the mutation
>>> and selection phenomenon that you don’t understand is that the
>>> mutation rate has only a small effect on the behavior of the
>>> phenomenon.
>> We were talking about drift, not selection.
> So do you want to continue your claim that dozens of neutral mutations
> are fixed every generation in the evolution of humans and chimpanzees
> from a common ancestor?
Why not? What's wrong with that claim? Show your work.
> How do so many neutral mutations get fixed
> simultaneously by chance alone when even with the benefit of selection
> it takes hundreds of generations to fix a single mutation?
Because there are billions and billions of neutral mutations in every
generation. A very few of them become fixed, and for those that do it
takes on average millions of generations. But the system has been
running for a long time, and so mutations that are many millions of
years old are just now becoming fixed. Of course, most of their cohort
became extinct many millions of years ago. This is only a tiny
percentage of those that arose. Why can't you understand any of this?
> John, I
> think your brain is in neutral with this claim.
You lost me at "I think". I see no signs that you ever do.
>>> Perhaps you want to claim that doubling the mutation rate
>>> doubles the probability that a beneficial mutation will appear at a
>>> particular locus?
>> It certainly doubles the expected number of such mutations.
> Where did you learn probability theory, UMI, The University of the
> Mathematically Incompetent?
Do you disagree with my claim?
> So now I suppose that when you double the
> mutation rate, you double the probability that a particular mutation
> will occur at a particular locus?
For low mutation rates, yes. But of course that's not what I'm saying.
Have you noticed that? I'm talking about the expected number, not the
probability of at least one happening.
> Just keep doubling the mutation rate
> and you will find that the probability will at some point be greater
> than one.
True, if you were so stupid as to do such a thing.
> John, you don’t know how to apply probability theory to a
> stochastic process and you do not have the capability to learn.
You accuse me of being unable to learn? You still haven't figured out
what I'm actually claiming, which isn't what you keep bringing up.
> You
> need to learn how to distinguish between mutually exclusive events
> which obey the additive rule of probabilities and complementary events
> which require the use of the complementation rule of probabilities to
> compute the probabilities. Until you learn these mathematical
> principles, you will continue to bungle the basic science and
> mathematics of the mutation and selection phenomenon.
What do you know about the mathematics of random walks?
>>> By far, the dominant mathematical principle of the
>>> mutation and selection phenomenon is the multiplication rule of
>>> probabilities. That is why the complexity of the selection conditions
>>> dominates the behavior of the phenomenon.
>> Please show your work here. What's your math?
> I posted the mathematics in a response to hersheyh previously but I
> will do it again here for you because of the importance of this
> principle in understanding how and why mutation and selection does
> what it does. In addition, I made a mathematical error in my post to
> hersheyh.
>
> If you want a more precise description of the probabilities of
> multiple beneficial mutations occurring (not simultaneously), ie,
> computing the probability of mutation B occurring after mutation A has
> occurred then you have to compute the *conditional probability* which
> is denoted mathematically P(B | A). Once you have mutation A, you have
> a new (reduced) sample space and that probability is the fraction of
> P(A) which corresponds to P(A)*P(B). Or to put it in equation form;
>
> P(B | A) = (P(A)*P(B))/P(A)
I don't think that's what you intended, since that ends up with
P(B|A)=P(B), and the frequency of A doesn't enter into that equation.
> And P(A) = (n/N) where n is the number of members with mutation A and
> N is the total population.
> In by original post of this equation, I left N out of the equation.
Considering that it cancels out in the equation you give here, that's
not unreasonable.
> In order to get your conditional probability down to a reasonable
> value, the population must increase n to a large number so that
> mutation B has a reasonable chance of occurring on a member of the
> population who already has mutation A. Note that the numerator of the
> above equation is simply the multiplication rule of probabilities.
> What selection does is allow populations to amplify a particular
> mutation thereby increasing n so that P(B | A) has a reasonable chance
> of occurring.
Your equation is garbage, since according to it P(A) is irrelevant to
the outcome. It's garbage for another reason too. Why do you assume that
mutation B must occur in an individual that already has mutation A?
>>> Regardless, Lenski’s population fixed only a very small number of
>>> mutations in more than 40,000 generations, only about 1 each 500
>>> generations. Now you have done the mathematics for the number of
>>> fixations required to transform humans and chimpanzees from a common
>>> precursor. Your estimate is 67 fixations per generation. How do you do
>>> that accounting problem?
>> I have explained this at least twice, and Howard has done so at least
>> once, and you have so far ignored all of them. Briefly, in neutralevolution, fixation rate (in the population) equals mutation rate (in an
>> individual). By any reasonable estimate of rates and times, 67 fixations
>> per generation is well within expectation.
> We already know what evolutionist expectations are and that they are
> mathematically irrational. You’ve abandoned probability theory for
> expectation theory (whatever that means to an evolutionist). Now you
> are telling us that every member of a population gets 67 neutral
> mutations spread through the population simultaneously every
> generation and this happens for hundreds of thousands of generations.
> You have very high expectations but very low probabilities. I’m really
> starting to believe that evolutionism is a form of folie a deux.
You appear to have no comprehension of what I'm claiming. Every
generation, in every individual (assuming a mutation rate for the sake
of argument of 10^-8/site/individual) there are around 60 mutations.
That is of course the mean of a distribution of actual numbers. Almost
all these mutations are neutral, and almost all will eventually be lost.
Now it happens, because population size appears in both the numerator
and denominator of the calculation of the probability of neutral
fixation, it cancels out. All that's left is the mutation rate itself.
And so around 60 mutations are fixed in the population each generation.
These are not mutations that happened recently in the population. On
average, they are mutations that happened 4N generations ago. Takes a
long time for drift to fix a mutation, and the probability for each
individual one to be fixed eventually is extremely low (1/2N). But there
are so many neutral mutations that the number of fixations per
generation is appreciable. What's wrong with that claim, exactly?
>>>>> Only when the populations evolved to improved
>>>>> fitness did “neutral” mutations appear in his populations. In other
>>>>> words, his population is diversifying on a fitness plateau. Still,
>>>>> this population is limited by the amount of citrate available.
>>>> You completely misunderstood his point. Which is not unexpected. There
>>>> was in fact no fitness plateau. Advantageous mutations appeared
>>>> throughout. What made the difference was the increase in mutation rate,
>>>> as Lenski himself made clear in that paper.
>>> The mutation rate has only a small effect on the mutation and
>>> selection phenomenon. If you understood the mathematics of the
>>> phenomenon, this would be clear to you. Do you think the mutation rate
>>> will account for 67 fixations per generation?
>> Yes. We aren't talking about selection here. We're talking about
>> neutral evolution. You seem entirely blind to this point, to the
>> degree that one might imagine some form of psychosis. You can't
>> even see the words.
> I think we are talking about some form of psychosis and I do see your
> words.
Then why do you keep talking about selection when I'm talking about
neutral evolution? Why don't you actually address my claims instead of
repeating your canned rants?
>>>>>> Now, if the glucose-only bacteria were more efficient at using glucose
>>>>>> than the bacteria that could use both, we have a condition that could
>>>>>> favor "specialization" to different niches, with some bacteria
>>>>>> becoming specialized glucose users and others becoming more and more
>>>>>> reliant on citrate. I.e., speciation (and because inability to use
>>>>>> citrate is a key speciation-defining feature of E. coli, the new bug
>>>>>> would not be E. coli, but perhaps E. citrusflavoreddietcoli.
>>>>> I guess you haven’t read any of Lenski’s papers. The citrate
>>>>> metobolizers no longer were efficient glucose metabolizers and these
>>>>> citrate metabolizers were very sensitive to osmotic pressures.
>>>> All adaptations are adaptive with respect to particular environments.
>>>> Don't you understand that yet?
>>> Give me a hint John; tell me how you can account for 67 fixations per
>>> generation? Just what were the adaptive conditions for that primate
>>> precursor?
>> Adaptation is irrelevant. It's neutralevolution. Only a very tiny
>> minority of the observed differences have any phenotypic effect or are
>> subject to selection.
> I see John, now you don’t need selection any more. All these neutral
> mutations fix themselves in the population by random chance. You do
> have great expectations.
No, not all of them. Only 1/2N of them. 1/2N is a very tiny proportion.
However, since there are 2Nu of them happening in each generation, there
are u of them being fixed every generation. Note that the ones being
fixed are not the same ones happening in that generation. The ones being
fixed happened, on average, a very long time ago, and took a very long
time to get to high frequencies.
>>>>> Now
>>>>> early on, you posted a paper that I wasted my time on reading. In this
>>>>> paper, these evolutionist pseudo-scientists claim thatevolutionis
>>>>> irreversible. Now do you think if you switched Lenski’s experiment and
>>>>> put his citrate metabolizers in a glucose rich environment with sparse
>>>>> citrate that his bacteria could evolve back to glucose metabolizers?
>>>> That's not what "irreversible" means. We would expect adaptation to any
>>>> environment, including a prior one. What we wouldn't expect is a
>>>> reversion to exactly the same phenotype as the ancestral one. The reason
>>>> is that there are many ways of achieving the same adaptive result.
>>> Why not? So why would you say that reptile scales would turn into
>>> feathers when there are many ways to achieve the same adaptive result?
>> Because that's one of the ways, and it happens to be the one that arose.
>> I'm unable to penetrate the bizarre thought processes behind that question.
> And I suppose this all happened because of neutral mutations?
Of course not. It's clearly the result of selection.
>>> Seems like a very difficult way for a reptile population to stay warm
>>> when there are many other ways to accomplish the same result without
>>> taking huge number of generations. The reptiles that live near my home
>>> hibernate when the weather gets cold. They are not growing feathers.
>> The reptiles that live near your home aren't endotherms, and aren't
>> evolving endothermy. Insulation is pointless in an ectotherm.
> You are getting awfully teleological here aren’t you?
Do you know what a metaphor is?
>>>> You haven't explained why that would be. Could you? And you might also
>>>> explain where you think birds came from, if they didn't evolve from
>>>> terrestrial reptiles.
>>> It’s not my job here to tell you where birds came from. It’s my job to
>>> properly describe how the mutation and selection phenomenon works. Do
>>> you want to tell us how to account for 67 fixations per generation?
>> It's not your job to take any position or defend your prior statements.
>> It's not your job to show any sort of intellectual integrity. But it
>> apparently is ...
> From my first post I have claimed that the multiplication rule of
> probabilities is the dominant mathematical feature of the mutation and
> selection phenomenon. I have posted numerous empirical examples of
> this and given you the equations which describe these probabilities.
> Sorry that this mathematics does not meet your evolutionist
> expectations.
Your mathematics, such as they are, merely repeat a multiplication of
probabilities, which requires simultaneous mutations in a single
individual. Your application to sequential mutations is primitive and
mathematically just plain wrong. And you haven't managed to explain why
mutations have to happen sequentially, or why mutation B can only happen
Stuart
> On Mar 30, 9:00 am, John Harshman <jharsh...@pacbell.net> wrote:
>
> > Alan Kleinman MD PhD wrote:
>
> > > John Harshman
>
>
> I posted the mathematics in a response to hersheyh previously but I
> will do it again here for you because of the importance of this
> principle in understanding how and why mutation and selection does
> what it does. In addition, I made a mathematical error in my post to
> hersheyh.
>
> If you want a more precise description of the probabilities of
> multiple beneficial mutations occurring (not simultaneously), ie,
> computing the probability of mutation B occurring after mutation A has
> occurred then you have to compute the *conditional probability* which
> is denoted mathematically P(B | A). Once you have mutation A, you have
> a new (reduced) sample space and that probability is the fraction of
> P(A) which corresponds to P(A)*P(B). Or to put it in equation form;
>
> P(B | A) = (P(A)*P(B))/P(A)
>
> And P(A) = (n/N) where n is the number of members with mutation A and
> N is the total population.
>
> In by original post of this equation, I left N out of the equation.
>
> In order to get your conditional probability down to a reasonable
> value, the population must increase n to a large number so that
> mutation B has a reasonable chance of occurring on a member of the
> population who already has mutation A. Note that the numerator of the
> above equation is simply the multiplication rule of probabilities.
> What selection does is allow populations to amplify a particular
> mutation thereby increasing n so that P(B | A) has a reasonable chance
> of occurring.
>
Why must mutation B occur in an individual that
already has mutation A ? If an individual with mutation B produces
offspring
with an indvidual that has mutation A, the offsrping have a 1 in 4
chance of receiving
both A & B. These two mutations do not necessarily have to arrive in a
AB or BA order.
Stuart
Garamond Lethe
> On Mar 30, 7:31 pm, Garamond Lethe <cartographi...@gmail.com> wrote:
>> On Wed, 30 Mar 2011 08:08:18 -0700, Alan Kleinman MD PhD wrote:
>>
>> > On Mar 15, 4:59 pm, Bill <brogers31...@gmail.com> wrote:
>> >> On Mar 16, 6:51 am, Alan Kleinman MD PhD <klein...@sti.net> wrote:
>>
>> >> Sorry for top posting, I'd just suggest that all the responses to
>> >> Dr.Dr.Dr. AK go into this thread. At least for those of us stuck
>> >> with Google Groups, once you hit 1000 posts the thread fragments.
>> >> It's entertaining and it would be nice to have it all in one place.
>> > Thanks Bill for continuing the thread. I’m going to have to patch
>> > together some of my responses for a while. I know it upsets the
>> > posters when I combine responses but unless you have a better
>> > suggestion, that’s what I’m going to do so that the discussion
>> > doesn’t fragment further.
>>
>> Better suggestions:
>>
>> 1. Don't combine replies.
> Sorry, I either would have to deal with dozens of splinter threads or
> combine posts.
You have a few other options:
a) Reply selectively.
b) Use the right tool for the job.
Usenet has been around a long time. Certain conventions have been agreed
to that make posting, reading and replying pretty efficient. You lose
most of that with google groups.
I don't know how much your time is worth these days, but I assume cutting
and pasting articles was not how you were planning on spending a
significant chunk of your retirement. I'm pleased that you've chosen to
spend so much time here, and I think you'll find that time far more
enjoyable if you let software handle the boring details of organizing
replies.
http://en.wikipedia.org/wiki/List_of_Usenet_newsreaders
>> 2. Post some math already.
> Check my post to John Harshman where I show how the multiplication rule
> of probabilities relates to conditional probabilities (where beneficial
> mutations do not occur simultaneously).
I know your advisor taught you to cite better than that. You've written
a lot of responses to John. I can't say I've skimmed all of them, but
none that I've seen contain anything that I'd recognize as math. Which
article did you have in mind? Google provides per-article URLs, or you
can point me to a message ID in the header.
>> 3. Post the equations for at least the Moran and Wright-Fisher models,
>> so we know that you've at least looked at them.
> I read the lecture notes recommended by lucaspa and at best these models
> are ambiguous.
That's the kind of reply I'd expect from an undergraduate who didn't
quite get around to the reading assignment.
Which article? Which page? Which equation? How is it ambiguous? How
does the ambiguity invalidate the model?
> If you want to look at a good model of population
> genetics, study Schneider’s ev model of mutation and selection. It gives
> you a good mathematical platform to study the effects of population
> size, mutation rates, genome size and of course the complexity of the
> selection conditions on the evolutionary process.
Did you decide that it was a good model of population genetics because
the paper does not contain the words "population genetics"? Or was it
because it was published in a journal that doesn't do population
genetics? Or was it the fact that when you googled for population
genetics simulation software, this model was nowhere to be found?
Here are a couple of actual population genetics simulations:
F. Balloux, EASYPOP (Version 1.7): A Computer Program for Population
Genetics Simulations. J Hered (2001) 92 (3): 301-302.
http://jhered.oxfordjournals.org/content/92/3/301.short
Frédéric Guillaume and Jacques Rougemont, Nemo: an evolutionary and
population genetics programming framework. Bioinformatics (2006) 22
(20): 2556-2557.
http://bioinformatics.oxfordjournals.org/content/22/20/2556.short
As I've told you before, Schneider's model is a toy that's useful for
thinking about the evolution of information. Even if you were completely
correct that its population genetics are horribly wrong, all you
demonstrated is that models designed for one area need not perform well
in a completely different area.
>
> As far as I know, Schneider's model does not preclude neutral mutations.
>> 4. Post the equations that would allow you to take frequency-dependent
>> selection and stabilizing selection into account.
> It’s up to you evolutionists to show how any particular selection
> condition would have a significant affect on the mutation and selection
> process.
Not if you're offering a mathematical critique of evolution.
(See, "Post some math already", above.)
I have to admit, demanding evidence is a lot easier than critiquing
existing evidence, and given your track record with critiquing that's
probably a good transition to make.
> By far the dominant mathematical principle in the mutation and
> selection phenomenon is the multiplication rule of probabilities.
That may be. But you haven't show that either by citation or
mathematical demonstration, and seeing as how you don't know enough about
population genetics to understand when it's being simulated, I kinda
doubt that you've stumbled on to any great truth here.
>
> Schneider's model demonstrates stabilizing selection.
>> 5. Post the equations that describe what you think is correct.
> I’ve done it already.
No, you haven't.
You've posted words, which, in your words, are "ambiguous". In fact,
you've posted piles upon piles of words. I find mathematics to be a much
less ambiguous method of communication, don't you?
Let's start with an easy one that I've posted before.
"The probability that a single copy of an allele with selective
advantage s will be fixed in a population of effective size N_e
is 2s(N_e/N)/(1-exp(-4N_es)), where N is the actual number of
individuals."
Show me how you get from your "multiplication of probabilities" to the
above. No words, just math. (And yes, I think it's doable in a half-
dozen steps; I just don't think you have the chops to do it.)
> Instead we have evolutionists who believe that you
> can have probabilities greater than one, don’t understand the principles
> of conditional probabilities and developed a new mathematical theory
> called expectation theory.
>> 6. Find an appropriate genetic dataset or simulation.
> Schneider’s ev model is a good simulation
Not for population genetics it isn't.
But I'm willing to be convinced. Find me a population genetics paper
that uses it. (Schneider's paper has only been cited about a hundred
times, shouldn't take you too long.)
> which contains all the
> essential features of the mutation and selection phenomenon. Too bad
> that Schneider has only done a superficial analysis of his model because
> then he wouldn’t be making claims that the multiplication rule of
> probabilities does not apply to biological evolution.
>> 7. Post the error for your approach and for existing models (and show
>> your work).
> Now I do agree that Schneider’s model does not include recombination and
> only includes point mutations.
"Error" involves numbers. You don't have any.
> The empirical evidence shows that
> recombination has very little effect on the creation of new alleles and
> other forms of mutations such as insertions and deletions are much more
> destructive causing frame shifts. I’ve only found a few empirical
> examples of frame shifts which give benefit to those members.
> Regardless, no matter what form of mutations, if more than a single
> beneficial mutation is required the multiplication rule of probability
> holds. That is what dominates the mutation and selection phenomenon.
>> 8. Don't bother replying until you've done this. You've cemented your
>> reputation as "The guy who don't understand high-school probability".
>> Continuing to make math-free replies isn't going to make that any
>> better or worse.
And here we are at the end of another math-free post.
Would you like to discuss mathematics outside of evolution?
I picked up Frederick Mosteller's _Fifty Challenging Problems in
Probability_ on a lark. It's pretty uneven, but the first problem was
particularly good. Here's the generalization:
"The probability of pulling $r$ red marbles in a row out of an urn is $p
$. What is the minimum number of red marbles in the urn?"
That's assuming no fractional marbles, of course.
Care to have a go?
>> 9. No, really. Post some math already.
> I’ve already posted the probabilities for a beneficial mutation to occur
> as a function of population size and I have posted the conditional
> probability that two beneficial mutations occur (not simultaneously).
But no math. No equations. No models. No results. No comparative
error.
Just words.
Would you consider writing your own simulation? I think that would force
you to formalize your ideas and give the rest of us something concrete to
comment on.
> The first example shows that the effect of population size is less than
> additive on the probability that a beneficial mutation will occur at a
> particular locus and the second example shows that the multiplication
> rule of probabilities is embedded in the conditional probability of two
> beneficial mutations occurring (not simultaneously). If you can’t find
> the calculations in this evolutionist morass, I’ll repost the
> calculations to you directly.
Well, it can't hurt. Go ahead and repost.
>>
>> <snip>
alextangent
Which I understood to be one of the best reasons for sexual
recombination. Is that still considered the case?
Garamond Lethe
> On Mar 30, 7:31 pm, Garamond Lethe <cartographi...@gmail.com> wrote:
>> On Wed, 30 Mar 2011 08:08:18 -0700, Alan Kleinman MD PhD wrote:
>>
>> > On Mar 15, 4:59 pm, Bill <brogers31...@gmail.com> wrote:
>> >> On Mar 16, 6:51 am, Alan Kleinman MD PhD <klein...@sti.net> wrote:
>>
>> >> Sorry for top posting, I'd just suggest that all the responses to
>> >> Dr.Dr.Dr. AK go into this thread. At least for those of us stuck
>> >> with Google Groups, once you hit 1000 posts the thread fragments.
>> >> It's entertaining and it would be nice to have it all in one place.
>> > Thanks Bill for continuing the thread. I’m going to have to patch
>> > together some of my responses for a while. I know it upsets the
>> > posters when I combine responses but unless you have a better
>> > suggestion, that’s what I’m going to do so that the discussion
>> > doesn’t fragment further.
>>
>> Better suggestions:
>>
>> 1. Don't combine replies.
> Sorry, I either would have to deal with dozens of splinter threads or
> combine posts.
>> 2. Post some math already.
> Check my post to John Harshman
You mean this?
P(B | A) = (P(A)*P(B))/P(A)
P(A) = (n/N)
Ok, I do need to credit you for writing an equation. Well done --- I
just wish you had done this a thousand posts ago.
What you're trying (and failing) to describe is the probability that a
mutation occurs in a single generation of a subpopulation that already
has another mutation.
What you've completely failed to grasp is this isn't a one-off: given $n$
generations, what is probability of not just the mutations occurring, but
fixation as well. That depends on the effective population size, the
mutation rate and the selective advantage of the mutation. You don't
list any of those terms above, but you'll find them in the equation I
provided to you in my other reply.
Still and all, I think this is progress. It's much easier for people here
to point out how equations are wrong rather than work from your verbal
descriptions of equations.
hersheyh
> >http://www.google.com/url?sa=D&q=http://aac.asm.org/cgi/reprint/45/10...
Yes. That is exactly what I am saying, although I used the smaller
expected number of resistant bacteria after the first selection by
ignoring the fact that this bacteria has two copies of the target
gene.
> It
> would take about 28 generations to reestablish your resistant
> population.
I said about 30. And given that mycobacteria typically grow more
slowly than E. coli, it may take a few days to a week or so to get 28
or 30 generations. But 28 or 30 generations is NOT thousands and
millions of generations. It is your utterly false claim that there
are NO conditions under which the multiplication of probabilities does
not hold. The multiplication rule only applies when the two mutations
must both occur simultaneously in the same individual. If it applied
in the process I described above, I would have almost no chance of
finding a double mutant. Yet in the process I described, it was
virtually certain that I would find a double mutant without either
starting with a massive swimming pool of bacteria or going thousands
of generations.
> Of course the resistant population would not reestablish
> if combination therapy was used.
What do you mean by "reestablish"? I am showing a process of
"establishing" a population of double-mutants, not "re-establishing"
anything.
> But you brilliant evolutionist fail
> to properly understand and teach the basic science and mathematics of
> mutation and selection. Your sloppy misunderstanding of how mutation
> and selection works harms people.
No. Your math is fine when and *only* when the conditions do involve
the requirement for double-mutation occurring in a single individual
in order to have selective value.
> >> However, when
> >> you are talking about the mutation and selection phenomenon, by its
> >> very nature, the initial frequency of the beneficial allele is going
> >> to be extremely low and when that occurs, the substitution process
> >> takes hundreds if not thousands of generations.
Since when is 28-30 now "hundreds if not thousands of generations".
Is that an example of your math prowress?
> >> If you understood
> >> Haldane s mathematics, this principle would be readily apparent.
> >> However evolutionists toss out any mathematical or empirical evidence
> >> which contradicts your doctrine.
> >> If you understood Haldane s model, you would recognize his
> >> calculations are working with a fixed population size. I ve never said
> >> that you need a change in population size in order for a substitution
> >> process to occur. Increasing population size will increase the
> >> probability that a beneficial mutation will occur at a particular
> >> locus but only slightly.
> >If the mutation *rate* is 10^-8, then we would expect (on average --
> >it would actually be in a Poisson distribution) 1 mutant in a
> >population the size of 10^8 individuals. In a population of 10^9
> >individuals we would expect 10 mutants. Thus the *number* of expected
> >mutants is N*u, where N is the population size and u is the rate of
> >mutation. That is a *linear* increase in the *number* of mutants.
> >The *rate* of mutation to a particular beneficial allele at a
> >particular locus is unchanged (unless you add or subtract mutagens)
> >regardless of the size of the population. It is selection (or chance)
> >that determines the frequency of such mutants when they occur.
>
> You still don’t get it. The probability of a particular mutation
> occurring at a particular locus does not obey the additive rule of
> probabilities.
If you were capable of actual reading for comprehension, you would see
that I said absolutely nothing about the "additive rule of
probability" or even the *probability* of finding a mutant. I
calculated the *mean* or *expected* *number* of mutants in a
population of a given size. That *number* can be less than one (for
example, if the mutation rate is 10^-8/generation and N = 10^6) or
more than one (for example, if the mutation rate is 10^-8/generation
and N = 10^9). I have also given you the math for the *probability*
that a population of a given size will have one or more mutant
individuals. That is 1-e^-m, where m is the mean or expected number
of mutants in a population of that size (see Poisson distribution).
*That* value will always be between 0 and 1. As m increases above the
number 1, the probability of a population of the given size having a
mutant will approach 1.
> The probability that a particular mutation occur at a
> particular locus is not a mutually exclusive event, it is a
> complementary event.
The probability of a particular mutation occurring at a particular
site is called the mutation rate. The mutation rate at any given site
is typically *independent* of the mutation rate at any other site.
The *rate* of a particular mutation at a particular site can be
changed by changing the levels of mutagen present or by changing the
rate of repair. But that is like a "tide that lifts [or lowers] all
boats" rather than a change in a specific site.
> This is why doubling population size does not
> double the probability that a particular beneficial mutation will
> occur at a particular locus in any given generation.
Do you not read? Or is it that you simply don't know the difference
between mean or expected *number* and *probability*? Doubling the
population doubles the mean expected *number* of mutants at a
particular site (whether that is beneficial or not). It does so
without any change in the *probability* of a particular mutation
occurring at that site (aka, mutation rate at that site) at all.
> Doubling the
> mutation rate also does not double the probability that a particular
> mutation will occur at a particular locus in a given generation.
Doubling the mutation rate for a particular mutation does, in fact,
double the probability that a particular mutation will occur at a site
where the rate is doubled. Mutation rate for a site, is, in fact, the
measured *probability* of a mutation occurring at that site. You
obviously don't know what "mutation rate" means (and yet you pretend
to understand evolution)!
> >As in the case of streptomycin described above, selection can change
> >the frequency of alleles dramatically in one generation, but only by
> >dramatically decreasing the population size. In many other cases of
> >selection, population size can remain constant because the selective
> >advantage is not like toxicity and all multicellular organisms have
> >both random and selective losses between zygote and breeding and those
> >losses can be massive compared to the changes due to selection. And
> >in other cases of selection, as in Lenski's experiment, which involves
> >opening up a new niche, the population size can actually increase
> >during the spread of the allele.
>
> But what you still don’t realize is that beneficial alleles must be
> amplified before there is a reasonable probability that the next
> beneficial mutation in an evolutionary process has a reasonable
> probability of occurring on a member with the previous beneficial
> mutation.
It is true, for organisms that can only reproduce *only* asexually or
vegetatively, that one mutation must typically spread through the
population by replacement of its alternative until there is a large
enough population of single mutant individuals to have a reasonable
probability of the second. But it is false for organisms that can
reproduce sexually or have other mechanisms for genetic exchange.
If phenotype A and phenotype B both increase reproductive fitness
independently of the presence or absence of the other (say white coat
rather than brown is A and thicker fur is B in colder climates) and
either mutation occurs at a probability of 10^-6, you will still get
both variations initially appearing in any population greater than
10^8. In fact, you would expect about 10 individuals with A and 10
with B each generation, but you would also expect no individual with
both by simultaneous double mutation (when the multiplication rule
holds). Individuals with A but not B are still beneficial relative to
the majority of individuals with neither. Individuals with B but not
A are also still beneficial to the majority of individuals with
neither. Thus both the A phenotype and the B phenotype will
*increase* in the population since either alone is better than
neither. At some point, sexual recombination will produce individuals
with both A and B, which will have greater fitness than either alone;
this will lead to selection of individuals with both traits in a much
faster mechanism than via the sequential mechanism for completely
asexual organisms.
> That’s because the multiplication rule of probabilities is
> the dominant mathematical principle governing the mutation and
> selection phenomenon.
So you keep asserting. But a lie repeated does not become truth.
> It doesn’t matter what selection pressures do to
> population size. If the beneficial allele can not be amplified,
You keep slipping in the assumption that single mutations cannot have
any independent beneficial effect in order to proclaim your lie that
all evolution requires simultaneous multiple mutation as truth. Even
though you have been given alternate mechanisms where that is not the
case. Even though you have resorted to proclaiming that 30
generations is now "hundreds and even thousands of generations" in
order to argue your point.
> the
> next beneficial mutation will have a very low probability of occurring
> at the proper locus because there are so few members who are potential
> recipients of the next beneficial mutation.
What you have to do, then, is demonstrate that no beneficial feature
has any possible stepwise mechanism of increasing beneficial utility.
You haven't done that. In fact, you specifically point out that there
*are* such stepwise mechanisms and that those stepwise mechanisms are
what has led to double mutants that are the "fault" of evolutionary
biology (rather than stupid doctors relying too much on antibiotics).
> This is the fundamental
> principle of mutation and selection which is so difficult to get
> through your thick evolutionist skull.
> >> The selection process does not need to go to
> >> completion in order to improve the probabilities that the next
> >> beneficial mutation will occur at the proper locus, you only need to
> >> have a sufficiently large number of members with the first beneficial
> >> mutation for there to be a reasonable probability that the next
> >> beneficial mutation in the sequence occur.
> >Yes. The probability of the second mutation is still N*u. If the
> >first mutation is like the streptomycin resistance mutation described
> >above, the probability of the second mutation occurring immediately
> >after selection for streptomycin resistance is still described as
> >N*u. N, however, immediately after selection is perhaps 10 (if you
> >plated 10^9 bacteria), while u is perhaps 10^-8. However, after the
> >population has grown up to around 10^8 bacteria (almost all
> >streptomycin resistant now), a process that would take less than 30
> >generation with a population doubling time of 30 min. Say overnight
> >growth (15 hrs or less) in rich medium with or without streptomycin,
> >the same mutation rate, u, in a population which now has more than
> >10^9 bacteria nearly all of whom are streptomycin resistance, is still
> >N*u. It would be almost certain that one would find a double
> >resistant bacteria in this case. Just as it would be almost certain
> >that one would not find a double mutant if you did the selections
> >*simultaneously* so that the single mutants in a population of 10^9
> >bacteria (say 10 resistant to each antibiotic) are not selected for.
> >Then, and *only* then, does the multiplication rule hold. The
> >probability of a double mutant being present in a population of
> >sensitive bacteria of size 10^9 would be N*u1*u2. That, and only that
> >determines the probability of such a double mutant. If u for each
> >individual mutation is 10^-8, then you would need a population size of
> >10^16 cells to expect a mean of 1 double mutant. The difference is
> >that I understand *when* the multiplication rule applies and when it
> >doesn't. You don't know that difference. You *assume*, without
> >evidence, that it always applies.
>
> Perhaps now you are starting to understand why amplification of a
> beneficial allele is crucial for a population to successfully carry
> out a mutation and selection process but you still do not understand
> completely.
Selection ensures the spread of any independently beneficial allele
ithroughout a population.
> Amplification is what is required for a population to
> overcome the multiplication rule of probabilities for two beneficial
> mutations to occur on a single individual (not simultaneously).
Yet, that spread of allele in the extreme case of lethality/survival
led to the generation of a population large enough to, with near
certainty, produce the second mutation in a cell with the first in a
mere 30 generations. Non-lethal spread of a variant would certainly
be slower depending on the selective advantage. But keep in mind that
*even* a very small 1% selective advantage of a dominant or codominant
trait would lead to half the alleles in the population being the
dominant one in less than 600 generations (the actual curve of
replacement is S-shaped). 600 generations for long-generation time
humans (20 yrs) would be 12,000 yrs. Fixation of a beneficial
recessive trait would be slower. Local inbreeding would speed the
process (as is evident from the examples of localized lactose-
tolerance, increased amylase gene number, and other examples of
selection in humans that have occurred since the 'invention' of
agriculture and herding). Consistent directional change of 1%
increase in a quantitative trait like size could, in principle,
generate an elephant-sized organism from a rabbit-sized one in 10,000
yrs. Since it is rare to have a fossil record with fossils that close
in time, that would make it hard to see fossils of intermediate size.
> The
> multiplication rule of probabilities always applies to beneficial
> mutations occurring on the same individual whether they happen
> simultaneously or not.
No. The probability of a *second* mutation in an individual depends
upon whether that individual has the first mutation or not. If he
already has the first mutation, the probability of the second is
simply that mutation's rate of occurrence. If he does not already
have the first mutation and *must* have both to exist, then and only
then is does the multiplication rule hold for that individual.
> Without amplification, the multiplication rule
> of probabilities makes any evolutionary process requiring more than a
> single beneficial mutation a highly unlikely event.
Without the need for simultaneity in a single individual, the
multiplication rule does not hold.
> >> This is why any
> >> evolutionary process that depends on a neutral allele will be a very
> >> low probability event because without amplification, the mutation and
> >> selection process is stymied by the multiplication rule of
> >> probabilities.
> >Again, this is based on your false ignoring of how *real* population
> >genetics occurs. There is a certain probability of a selectively
> >neutral allele spreading throughout a population by a random walk.
> >You assume a perfect Hardy-Weinberg equilibrium which assumes an
> >infinite or perfect population allele distribution from one generation
> >to the next. Given the number of nucleotides in a human genome and
> >the average mutation rate for point mutations, it is virtually certain
> >that, over the course of a few million years, you would find the
> >percentage of nucleotides that have changed by chance alone to be
> >about that seen (actually a little less) in a comparison of chimps and
> >humans.
>
> Hersheyh, how would you know what *real* population genetics is?
By studying and going to legitimate sources rather than ignorant ones.
> You
> are not a population geneticist because any real population geneticist
> would know that doubling population size does not double the
> probability that a beneficial mutation will occur at a particular
> locus.
And you apparently cannot even read. You keep confusing *probability*
with *number* even when I use **s to point out the difference. The
expected mean *number* of mutants doubles with a doubling of
population. The mutation rate, which is the *probability* of a
mutation (mutation rate is calculated as number of mutants observed/
population size after all) occurring does not change at all with
population size unless you add or subtract mutagens or change repair
rates.
>You have drifted so far from reality that you think that the
> flipping of ten pennies explains your mathematically irrational
> theory. Try flipping ten million pennies and see where your
> mathematics leads you.
It would lead me to expect a *mean* or *expected* value of 5 million
heads with a variance. In any *actual* flip of 10,000,000 coins, I
would not expect to *actually* get *exactly* the mean value of 5
million heads. I would expect to get within two standard deviations
of that number 95% of the time. [Roughly.]
> Then try flipping two sets of ten pennies and
> see if your populations can fix two neutral mutations simultaneously.
Where have I ever presented that? You cannot make up lies about what
I actually said and then not expect to be called on it.
> You have bungled the basic science and mathematics of mutation and
> selection and clearly you are not a population geneticist.
And someone who doesn't know the difference between a *mean* number
and a *probability* is worse than a poor population geneticist.
>
> And
>
> >The *only* examples you have given have been artificial ones created
> >by humans. Specifically designed environments by humans to lower the
> >probability of a selective advantage. And every example you gave
> >involves toxins that specifically reduce population size, thus
> >reducing the probability of an individual with a needed mutation
> >further. You repeatedly refuse to admit any other conditions of
> >selection at the very same time that you accuse evolutionary biology
> >of all sorts of evils by a false accusation that they are killing
> >people by arranging conditions in which the same multiple resistances
> >can occur -- either by arranging sequential resistance or allowing
> >parallel resistances to accumulate in the same individual by sexual
> >recombination. You need to get your story straight. If evolution of
> >multiple resistance is mathematically impossible, why, exactly do you
> >keep pointing out that it is possible and evolutionary biologists are
> >to blaime?
>
> So let’s see you design an experiment which shows something different.
> Show us selection pressures which don’t kill or impair the
> reproduction of member of a population.
Selection is about *differential* reproduction, not necessarily by
killing or impaired reproduction. In the case of evolution that
allows using a new niche, there need not be any change in the number
of individuals with the old phenotype. Just an increase in the number
of individuals with the new phenotype. It is when there is direct
competition between individuals with different phenotypes for the same
niche, that one phenotype must decrease (in a relative sense only,
that is, as a % of the total, not necessarily in absolute numbers
which is typically more affected by changes in the availablility of
resources). For example, in bacteria one thing that can affect
*relative* fitness is speed of reproduction. If you add rich media to
a culture, those bacteria that reproduce faster will have a selective
advantage and increase as a % of the population even if there is no
change in the number of bacteria that grow slower. That, in fact, is
why there is a dual population in Lenski's cultures after the
evolution of citrate metabolizers while the total density increased.
> Are you now going to take the
> stance that selection pressures don’t kill or impair the reproduction
> of members of a population?
Sometimes selection pressures do kill or impair reproduction.
Sometimes they don't. They do in all your artificial examples. But
that is due to your cherry picking of your examples.
> You keep going further and further out on
> you mathematically irrational limb.
>
> Now with regards to when there is a reasonable mathematical
> probability for a population to evolve to selection pressures by
> mutation and selection depends on the complexity of the selection
> conditions. The population must be able to amplify beneficial
> mutations in order for there to be a reasonable probability that the
> population can evolve to the selection conditions. Clearly from the
> empirical examples I’ve presented, the amplification process does not
> work efficiently when more than a single gene is targeted by selection
> pressures.
To translate into reality: *When* simultaneous multiple mutation is
required for any selective advantage, the multiplication rule of
probabilities hold for the probability and likelihood of generation of
a double mutant. *When* that condition does not hold, the
multiplication rule does not hold and does not describe the
probability or likelihood of double mutants.
>> That s why the amplification process
> >> breaks down when combination selection pressures are used.
> >*When* combination (i.e. simultaneous) selection pressures are
> >arranged such that there is no selective advantage to individual
> >variants. Even when selection pressures are arranged in combination,
> >if there is a selective advantage for single variants, they will
> >spread through the population. For example, if there is selective
> >pressure for bipedality and selective pressure for ability to sweat,
> >individuals with greater bipedality may have a selective advantage
> >even in the absence of ability to sweat and ability to sweat may have
> >a selective advantage even in the absence of bipedality. That leads
> >to either sequential selection (where one appears first, perhaps
> >thereby even increasing the selective advantage of the second, which
> >then evolves to "catch up" more quickly) or parallel selection with an
> >extra advantage to having both.
>
> But that’s the basic science and mathematics of mutation and
> selection. When two or more genes are targeted by selection pressures,
> the amplification of any beneficial mutations which occur to one or
> another selection pressure can not amplify because the other selection
> pressures are killing or impairing the reproduction of that member.
No. Selection cares about the net (or summary) effect in a comparison
of organism. The environment does not care whether an individual is
favored by 10% because of a difference in phenotype A or phenotype B.
Individuals with either of those two phenotypes will increase in
frequency relative to their respective alternative alleles. And
(because the selective advantage is the same 10%) they will increase
at about the same rate. That is what having an independent selective
advantage means.
> It
> might be nice for living things to have all the properties you mention
> above but mutation and selection takes thousands perhaps tens of
> thousands of generations just to evolve resistance to single drug
> antibiotic therapy
So 30 generations is yet again "thousands of generations" in your
math. In reality, mutation and selection to resistance, in this case,
occurred in a single generation, with the 30 generations being the
time to restore population size to the previous level, not the time it
took to mutate and select a population which is 100% resistant from
one that was 0.000001% resistant.
> or to transform a glucose metabolizer to a citrate
> metabolizer.
This experiment actually demonstrates two different kinds of
evolution. First, we have *all* the 12 lineages accumulating
phenotypically similar, but not identical mutations in about 10
*different* genetic loci that made them more efficient in the
environment the cells were grown in. That stepwise evolution had been
largely completed by 2-5,000 generations. That was at least 10
*different* mutational events, each with a mutation rate that is
probably in the range of 10^-5 (because the mutation is to phenotype
and need not be identical in all the lineages, but rather several
different mutations in a gene can produce the same phenotypic
effect). But, according to your argument, this should be completely
impossible, since the probability of the end result, using your misuse
of the multiplication rule, should be (10^-5)^10 or 10^-50! Yet that
change happened, not in quadrillions of generations, but in a couple
of thousand. Again, the rule in science is that if reality differs
from your expectation, you question the assumptions of your
expectation and not reality. That is a rule you seem not to
understand.
> If you put additional selection pressures on these
> populations, they have much, much more difficulty doing the sorting
> and optimization process to these simultaneous selection pressures.
> The reason these populations have much, much greater difficulty
> evolving to these simultaneous selection pressures is these
> populations can not amplify beneficial mutations efficiently.
The reason why citrate metabolism occurred only in one lineage is
currently unknown. The likely reasons include either a need to be a
couple of steps, selective or not, some of which need to have occurred
before the step to citrate metabolism in order for there to be a step
that generates selectively significant citrate metabolism. In
evolution, such a situation is called exaptation and basically tells
us that there is some historical constraint involved, that the final
step requires the pre-existence (either by chance or selection for
other reasons) of some feature in the organism. Flight feathers could
not have evolved if downy feathers were not present in an ancestor.
>> > If you have
> >> an example where combination selection pressures do not stifle the
> >> mutation and selection phenomenon
,
> >You cannot even correctly state what combination selection of the type
> >you describe does. What your kind of simultaneity does is to decrease
> >the probability of selectively favored genome by preventing
> >selectively useful intermediacy. That is all it does. It does not
> >change the individual mutation rates. Your conditions merely make the
> >intermediate state of resistance to a single toxicity (which is the
> >only kind of evolution you seem to think exists) nonselectable.
> First of all hersheyh, you need to recognize that all a selection
> pressure is a cause of death or something which impairs the
> reproduction of members of a population.
A lie repeated is still a lie. All that is required is that a new
trait be differentially *better* in some way.
> I have previously defined the
> complexity of selection pressures by the number of mutations required
> to adapt to the selection conditions and the number of genes targeted
> by the selection conditions. Antimicrobial agents are unique amongst
> selection pressures since they specifically target particular genes
> (in most cases). Because of this, these types of selection pressures
> are particularly amenable to the mutation and selection phenomenon
> when used singly.
Antimicrobials are useful in studies because they provide clear cut
and definitive ways of identifying that selection has occurred because
they are so lethal. It is also possible to get toxin resistance that
occurs in a quantitative fashion. Methotrexate resistance is a good
example. So is DDT resistance. So is herbicide resistance. The
initial resistance is to the low levels used with organisms still
being sensitive to higher levels.
> The highly efficient beta lactamase example is good
> example of how a population can use mutation and selection to adapt to
> this type of selection pressure. Any selection pressures such as
> thermal stressors or starvation tend to target many genes unless as in
> Lenski’s example, he put a second carbohydrate in his medium which his
> population was ultimately able to use based on a fairly small number
> of mutations the population was able to amplify these small number of
> mutations over some thirty thousand generations.
More likely the *phenotype* of sufficient ability to use citrate to
outweigh the disadvantages of slower utilization of glucose required
either a couple of changes (possibly regulatory changes, which tend to
be quantitative in nature), or it required certain *specific* site
mutations affecting some aspect of more efficient glucose
utilization. Other possibilities could include the at least temporary
transitional state involving a gene duplication. Again, that has yet
to be worked out AFAIK. I don't expect the change to be due to a
miracle of creation. I expect it will be a known form of mutation and
gene modification.
> >> present it but you can t because
> >> they don t exist. The examples of multidrug resistant organisms took
> >> tens of thousands of generations to occur by the use of single drug
> >> selection pressures sequentially over many years.
> >Multidrug resistance does occur. Not surprisingly, it tends to occur
> >in hospitals and other settings where both types of drug are used
> >frequently (and especially if other conditions, like poor sterile
> >technique by the doctors and nurses, exist and antibiotics are used to
> >cover up their laxity). It is often the case that both resistances
> >wind up on the same plasmid and then get transmitted horizontally as a
> >unit. This is despite the often selective advantage of w.t. strains.
>
> Multidrug resistance occurs because these selection pressures are used
> singly in sequence allowing the microbial populations to amplify
> beneficial alleles.
> The use of single drug therapy is standard of care
> in the medical field. This clinical blunder has occurred because the
> basic science and mathematics of mutation and selection has not been
> well understood or explained to doctors or to anyone else as well.
Actually I might agree that it has occurred because the doctors
*didn't* understand the basic science. You sure don't. Bacterial
antibiotic resistance in hospitals occurs largely via horizontal
plasmid transfer rather than by independent mutation to resistance in
different bacterial genes. The same mechanism, horizontal plasmid
transfer is also responsible for the killer E. coli strain O157:H7.
This strain is a harmless gut bacteria in cattle because cattle lack
the appropriate cell protein that allows the bacteria to adhere to
intestinal cells.
>Even worse is the agricultural use of antibiotics as growth enhancers,
> >since those are often used at low level for prolonged times.
>
> I’ve heard this argument before. I live in farm country and I don’t
> know of any farmers or ranchers doing this. In fact I don’t think it
> is very smart to feed bovines or caprines antibiotics on a regular
> basis since these animals depend on the bacteria in their gut to break
> down cellulose. Even so, if a rancher or farmer can show that
> antibiotics can safely improve growth in their animals, then they
> should do it with combination antibiotics to impair the mutation and
> selection process.
"Drugs are used in animals that are used as human food, such as cows,
pigs, chickens, fish, etc., and these drugs can affect the safety of
the meat, milk, and eggs produced from those animals and can be the
source of superbugs. For example, farm animals, particularly pigs, are
believed to be able to infect people with MRSA.[22] The resistant
bacteria in animals due to antibiotic exposure can be transmitted to
humans via three pathways, those being through the consumption of
meat, from close or direct contact with animals, or through the
environment.[23]
The World Health Organization concluded that antibiotics as growth
promoters in animal feeds should be prohibited (in the absence of risk
assessments). In 1998, European Union health ministers voted to ban
four antibiotics widely used to promote animal growth (despite their
scientific panel's recommendations). Regulation banning the use of
antibiotics in European feed, with the exception of two antibiotics in
poultry feeds, became effective in 2006.[24] In Scandinavia, there is
evidence that the ban has led to a lower prevalence of antimicrobial
resistance in (non-hazardous) animal bacterial populations.[25] In the
USA federal agencies do not collect data on antibiotic use in animals
but animal to human spread of drug resistant organisms has been
demonstrated in research studies. Antibiotics are still used in U.S.
animal feed—along with other ingredients which have safety concerns.[5]
[26]
Growing U.S. consumer concern about using antibiotics in animal feed
has led to a niche market of "antibiotic-free" animal products, but
this small market is unlikely to change entrenched industry-wide
practices.[27]
In 2001, the Union of Concerned Scientists estimated that greater than
70% of the antibiotics used in the US are given to food animals (for
example, chickens, pigs and cattle) in the absence of disease.[28] In
2000 the US Food and Drug Administration (FDA) announced their
intention to revoke approval of fluoroquinolone use in poultry
production because of substantial evidence linking it to the emergence
of fluoroquinolone resistant campylobacter infections in humans. The
final decision to ban fluoroquinolones from use in poultry production
was not made until five years later because of challenges from the
food animal and pharmaceutical industries.[29] Today, there are two
federal bills (S. 549[30] and H.R. 962[31]) aimed at phasing out "non-
therapeutic" antibiotics in US food animal production."
http://en.wikipedia.org/wiki/Antibiotic_resistance#Role_of_other_animals
That is the reality. >70% of all the antibiotics used in the US are
given to farm animals in the absence of disease. I have no problem
with antibiotic use to treat sick animals.
>>This allowed
> >> amplification of beneficial alleles to produce these multidrug
> >> resistant destructive organisms. This was a consequence of bungled
> >> evolutionist teaching of how the mutation and selection phenomenon
> >> works.
> >So you claim based on an idiotically ignorant and biased reading of a
> >heading on a single paragraph of Schneider's comment about the equally
> >stupid creationist claim that evolution works by assembling new
> >proteins by some unspecified random mechanism that randomly assembles
> >new proteins from scratch using raw amino acids. But I presume you
> >read the Bible the same way. Take sentences out-of-context to try to
> >make the text agree with your beliefs.
> Schneider should know better
You think Schneider is responsible for writing a heading that some
idiot creationist would take out of context? Idiot creationists
*always* take things out of context. That is the only evidence they
can have.
> since this is his field but he didn’t
> realize what happens to the amplification process when selection
> pressures target multiple genes and how the multiplication rule of
> probabilities stifles the evolutionary process.
Again, that is NOT what the rest of the paragraph is about. The rest
of the paragraph is about the idiot creationist idea that proteins are
supposed to assemble in one magical poof and randomly from raw amino
acids. That actually describes what *they* think happens, not what
evolution thinks happen. A lie repeated is still a lie. And you are
repeating a lie when you claim that what you are talking about is what
Schneider was talking about.
> He does now. If he
> would ever do a thorough analysis of his population genetics model, he
> would have a much better understanding of the mutation and selection
> phenomenon but you evolutionists just don’t seem to want to understand
> how this phenomenon works in reality. This denial of reality on the
> part of evolutionists has harmed and continues to harm millions of
> people suffering from diseases subject to the mutation and selection
> phenomenon.
Rather it is you who are denying reality. According to your
mathematical model, Lenski should not have gotten the 10 or so
mutations that increased the fitness of his 12 strains by 70% in 2000
generations. Reality says your math is wrong on that. According to
your argument that regardless of whether two mutations must occur
simultaneously or can occur with intermediate selection, the
multiplication rule holds, it shouldn't matter if one used antibiotics
singly or in combination, since evolution would be equally difficult
in both cases due to the required multiplication of probabilties.
Reality says differently. Radically differently. According to your
understanding of probability, if I toss dice 12 times, I should get
*exactly* 2 of each type of face upward. According to your
understanding of probability, the mean *number* of expected mutants
(which you mislabel as a "probability") is barely related to
population size and will never be larger than 1 mutant no matter the
size of the population.
>> Single drug therapy is still the standard of care for most
Looking at what *actually* happened in the past is not teleology. And
the historical record (aka, fossils) is what tells me that downy
feathers came before flight feathers. No teleological assumption
needed.
> > > Mutation and selection only
> > > > works well when a single gene is targeted by a single selection
> > > > pressure. As soon as multiple genes are targeted, the mutation and
> > > > selection process is stymied by the multiplication rule of
> > > > probabilities.
> >That is not true. There are several types of changes that will
> >produce resistance to cold, including changes in body shape (to reduce
> >surface area), changes in insulation (fat deposition, hair or
> >feathers), changes in color to hide better in a cold ...
>
> Produce the real, measurable and repeatable examples that mutation and
> selection did all of this.
Are you claiming that organisms do not vary wrt such features as body
shape, fat deposition, hirsuteness? Or are you claiming that there is
no genetic basis for those variations? Or are you claiming that those
variations do not affect an animal's ability to survive the cold? Has
to be one of those. If organisms do vary in those features and if
those features have a hereditary component and if variation in those
features affect reproductive success in colder environments, what else
do you need to show?
> All the real measurable and repeatable
> examples that I have found demonstrate that as soon as more than a
> single gene is targeted by selection pressures, the mutation and
> selection process is stifled. I’ve found these examples thanks to
> Google.
>
> And
>
> >> I don t get tired of telling evolutionists that the multiplication
> >> rule of probabilities is the dominant mathematical principle of the
> >> mutation and selection phenomenon.
> >You mean asserting it again and again, without providing any
> >justification for the assumptions you make.
>
> Hersheyh, if you are going to play games of chance with bacteria,
> viruses, parasites, cancer, weeds and so on, you had better learn the
> rules of the game because the way you evolutionist would have us
> understand the game would be no different than a casino owner posting
> a picture of their latest big winner on a billboard so that you would
> think you could be a big winner as well. The reality is that most
> people leave their money at the casinos because they don’t understand
> the probabilities of their game as you don’t understand the
> probabilities of the mutation and selection phenomenon. And I support
> my assertions with numerous empirical examples, all which demonstrate
> that the multiplication rule of probabilities is the dominant
> mathematical principle of the mutation and selection phenomenon.
No. You cherry pick examples that do or might involve the
multiplication rule and ignore the ones that don't.
>> Apparently, I m just going too fast
> >> for you to understand this basic mathematical principle.
> >No. You are not going too fast. You are quite repetitive. Boringly
> >and ignorantly so. It is not enough to repeat your assertion over and
> >over and over again. You need to provide some evidence that evolution
> >*always* requires invoking the multiplication rule, despite our
> >pointing out that that is not the case.
>
> ========================================================
[snip]
hersheyh
> of March 23
> ========================================================
> >You need to provide some evidence that evolution
> >*always* requires invoking the multiplication rule, despite our
> >pointing out that that is not the case.
>
> I understand that evolutionists are bored with the mathematical and
> empirical facts of life of the mutation and selection phenomenon but
> those of us who have to deal with the reality of this phenomenon have
> a responsibility to properly describe how this phenomenon works. If
> you want a more precise description of the probabilities of multiple
> beneficial mutations occurring (not simultaneously), ie, computing the
> probability of mutation B occurring after mutation A has occurred then
> you have to compute the *conditional probability* which is denoted
> mathematically P(B | A). Once you have mutation A, you have a new
> (reduced) sample space and that probability is the fraction of P(A)
> which corresponds to P(A)*P(B). Or to put it in equation form;
>
> P(B | A) = (P(A)*P(B))/P(A) = (P(A)*P(B))/n where n is the number of
> members with mutation A.
>
> In order to get your conditional probability down to a reasonable
> value, the population must increase n to a large number so that
> mutation B has a reasonable chance of occurring on a member of the
> population who already has mutation A. Note that the numerator of the
> above equation is simply the multiplication rule of probabilities.
> What selection does is allow populations to amplify a particular
> mutation thereby increasing n so that P(B | A) has a reasonable chance
> of occurring. I hope I’m not boring you.
>
Of course the problem with your reiteration of the multiplication rule
is that you are completely ignoring the difference between a process
with intemediate selection steps and one without intermediate
selection steps and are falsely assuming that there is never any
intermediate selection (which is a non-random event) even when there
is. Let me phrase the question we are asking a bit more precisely and
calculate the probabilities *correctly* under two different
conditions.
"How many generations (or its equivalent, "How many organisms") are
required to generate a double mutant under each given set of
conditions?"
I will use a bacterial population of 10^9 bacteria as the "population
size" each generation. The probability of mutants resistant to
antibiotic A is 10^-8 mutants/total population/generation. The
probability of mutants resistant to antibiotic B is 10^-8 mutants/
total population/generation.
In case 1, there is no selection until I select for double mutants by
adding both antibiotics. This is the case in which we *both* agree
that the multiplication rule does hold, since only a double mutant
will survive.
If I have a population of 10^9 bacteria, the probability that that
population will have one or more bacteria resistant to A is 1-(e^-m)
at the start of the experiment (in one generation), where m is the
expected mean *number* (note: that is *number* not probability) of
mutants in a population of size 10^9. ' m' is calculated as uN, which
in this case is 10^-8mutants/total population/generation * 10^9 total
population, which = 10mutants/generation. That is, I would expect 10
of the 10^9 bacteria to be resistant to A. I would also expect, in
the same population of 10^9 cells using the same argument and
formulas, 10 bacteria that are resistant to B. But what I need is the
number of bacteria resistant to *both* A and B. The probability of a
bacteria resistant to *both* A and B is the joint probability, or the
multiplication of both their individual probabilities. That is, the
probability of a bacteria resistant to both is 10^-8*10^-8 = 10^-16.
That means that the expected mean *number* of double mutants in a
population of 10^9 is uN = 10^9*10^-16 = 10^-7. And that means that
the probability that my population of 10^9 bacteria will have a double
mutant is 1- (e^-10^-7), which, of course is a very low probability.
Now, to get a 63% probability that there will be a double mutant in a
population, you need to have an m = 1. Since m = uN, and u, the
mutation rate, does not change, that means either one must have a
population of 10^16 bacteria or one must have a population of 10^9
bacteria for 10^7 generations in order to produce 10^16 bacteria.
[Technically, because resistance is toxic, you would double the number
of bacteria in non-selective conditions from 10^9 to 2 X 10^9 and test
half of the bacteria by adding both antibiotics. Each doubling is a
generation.]
So, in the absence of selection, I must either have a population of
size 10^16 bacteria or I must grow a population of 10^9 bacteria for
10^7 generations to have only a 63% chance of finding a double
mutant. I am going to ignore the number of generations it will take
to grow any double resistant bacteria to 10^9 cells because that would
be insignificant compared to the average of 10^7 generations required
to produce a 63% chance of even one double mutant.
But now we go to a *different* mechanism, one that involves three
different steps: 1) Select only for resistance to antibiotic A. 2)
Grow the survivors to 10^9 cells. 3) Add both antibiotics to find a
double mutant. This is serial selection.
The probability of my having one or more resistant bacteria when I add
only antibiotic A is still 1-(e^-m) and m is still uN. In this case,
however, I am not selecting for *both* antibiotics, but only for
bacteria resistant to A. That m = uN = 10^-8 * 10^9 = 10. [Note that
this is quite a bit different than the m of 10^-7 of the previous non-
selective mechanism.] 1-e^-10 > 0.99 (actually closer to 0.99995).
That is, the *probability* of my getting one or more mutants resistant
to A in a single generation is quite high; not quite 1.0, but quite
close to it. The "probability" that a population that has only A-
resistant bacteria will grow into a larger population of A-resistant
bacteria is also near certainty, regardless of whether or not I have
the antibiotic A present during the 30 doubling growth phase (because
the selection step killed the non-resistant cells). So let's call the
*probability* of growth of a culture having one or more resistant
bacteria into 10^9 A-resistant bacteria in 30 generations to also be
equal to 0.99. Now we are at the third step where we add both
antibiotics to a culture already resistant to A. The *probability*
that a mutation in one of the A-resistance bacteria will have produced
a double mutant that can be selected is 10^-8. In a population of
10^9 A-resistant bacteria, I would expect uN = 10^-8*10^9 = 10 double
mutants. The *probability* that any given population of 10^9 A-
resistant bacteria will have one or more double mutants also resistant
to B is 1-(e^-m), which, in this case is = 1-e^-10 > 0.99.
Thus the *joint probability* of all three steps producing a double
mutant is at least (0.99)(0.99)(0.99) =0.97. And that is an
underestimate of the probability. The real probability value is
closer to 0.9999.
Now let's compare the two probabilities:
In example 1's mechanism, to get a probability of a double mutant of
only 63%, I would need either 10^16 bacteria or 10^7 generations of a
steady state population of 10^9 bacteria.
In example 2's mechanism, I got a probability of a double mutant of
(greater than) 97% with only a population of 2 X 10^9 bacteria (the
10^9 initial population plus the 10^9 of the selected A-resistant
bacteria) and 31 generations (I will even toss in another 30
generations to grow the double mutant to 10^9 cells and make that 61).
Compare, in particular, the number of bacteria required (10^16 to 2 X
10^9) or the number of generations required (10^7 to 31) to get a
given probability of one or more double mutants (63% compared to near
certainty).
That is the *real* way to calculate probabilities in this case.
Now, I have not calculated the probability of generating a double
mutant in the case where we have two populations (one F-, one F+) one
of which we select for resistance to A and the other for resistance to
B and then ask what the probability of a double mutant is after we mix
the two cultures together. Partly because of the unidirectionality of
"sex" in bacteria, it would be easier to use diploid organisms where
sex is more regularized and quantiatively predictable. But that also
would result in much higher probabililty of double-mutant appearance
with much smaller numbers or generations than your mechanism.
[snip]
Inez
> The following are a compilation of responses from the splinter threads
> of March 23
> ========================================================
> >> low probability event because without amplification, the mutation and
> >> selection process is stymied by the multiplication rule of
> >> probabilities.
> >Again, this is based on your false ignoring of how *real* population
> >genetics occurs. There is a certain probability of a selectively
> >neutral allele spreading throughout a population by a random walk.
> >You assume a perfect Hardy-Weinberg equilibrium which assumes an
> >infinite or perfect population allele distribution from one generation
> >to the next. Given the number of nucleotides in a human genome and
> >the average mutation rate for point mutations, it is virtually certain
> >that, over the course of a few million years, you would find the
> >percentage of nucleotides that have changed by chance alone to be
> >about that seen (actually a little less) in a comparison of chimps and
> >humans.
>
> Hersheyh, how would you know what *real* population genetics is? You
> are not a population geneticist because any real population geneticist
> would know that doubling population size does not double the
> probability that a beneficial mutation will occur at a particular
> locus. You have drifted so far from reality that you think that the
> flipping of ten pennies explains your mathematically irrational
> theory. Try flipping ten million pennies and see where your
> mathematics leads you. Then try flipping two sets of ten pennies and
> see if your populations can fix two neutral mutations simultaneously.
Is that supposed to be a model of neutral evolution? Because even a
mathmatical nitwit like myself can see that it isn't a good one. Try
flipping ten million pennies, then having them reproduce (passing on
their "heads" or "tails" to their descendents), with pennies being
randomly removed from the table to keep the total around 10 million.
Eric Root
I am beginning to suspect a blow-up doll.
Eric Root
Alan Kleinman MD PhD
> On Apr 1,2:23 pm, Alan Kleinman MD PhD <klein...@sti.net> wrote:
>
>
>
>
>
> > On Mar 15, 6:27 pm, William Hughes <wpihug...@gmail.com> wrote:
>
> > > It is rather interesting that in a > 1000 post thread
> > > the good Dr. has been unable to note that he is confusing two
> > > scenarios
>
> > > 1: A mutation A' causes an increase in reproductive
> > > success, whether or not a mutation B' (which also
> > > causes an increase in reproductive success) is present.
>
> > >2: A mutation A' alone or a mutation B' alone does not cause an
> > > increase
> > > in reproductive success. Only both mutations together cause
> > > an increase in reproductive success.
>
> > > Only in case2is the multiplication rule for probabilities applicable
>
> > > - William Hughes
>
> > William, the multiplication rule of probabilities always applies when
> > more than a single beneficial random mutation is required to adapt to
> > selection pressures.
>
> Only if each step does not confer it's own little advantage. You
> haven't even made an attempt to show that RLevolutionis not made up
> of such steps.
Actually Inez, the multiplication rule of probabilities applies to the
calculation of the probabilities of a single beneficial mutation
occurring as well as multiple beneficial mutations.
>
> And your phrase "required to adapt to" implies that you think that
> most adaptations are life or death, and that there can't be various
> levels of "adaptedness," which probably stems from your monomaniacal
> example of HIV vs. antiviral drugs. Water rolls off a duck's back,
> but a cormorant has to dry himself after fishing. Is a cormorant "not
> adapted?" They seem to do OK for themselves, even if they are
> perfect.
Selection pressures are life or death issues for those members of the
population who are not adapted to those selection pressures. After all
what makes a selection pressure a selection pressure? A selection
pressure is nothing more than something which kills or impairs the
reproduction of members of a population preventing their genetic
information from passing on to future generations. Shouldn’t you be
calling me polymaniacal since I have presented examples from all areas
of medicine besides the example of HIV such as examples of mutation
and selection from agriculture, mosquito control and other areas of
science which demonstrate the same behavior to HIV evolution to
combination selection pressures? And what they all demonstrate is the
mutation and selection process is stifled when combination selection
pressures are applied to populations.
>
>
>
> > This is why the complexity of the selection
> > conditions is the dominant mathematical variable in the mutation and
> > selection phenomenon. Any evolutionary process which requires more
> > than a single beneficial mutation requires amplification of beneficial
> > mutations in order to improve the probabilities that the next
> > beneficial mutation in the sequence occurs. This is why when the
> > mutation and selection phenomenon works, it is arduous and slow. Any
> > combination of selection conditions which disrupts the amplification
> > process only makes the phenomenon work even more slowly.-- Hide quoted text -
Alan Kleinman MD PhD
> On 4/1/2011 5:25 PM, Alan Kleinman MD PhD wrote:
>
>
>
>
>
> > On Mar 16, 8:00 am, Mitchell Coffey<mitchell.cof...@gmail.com> wrote:
> >> On 3/15/2011 9:27 PM, William Hughes wrote:
>
> >>> It is rather interesting that in a> 1000 post thread
> >>> the good Dr. has been unable to note that he is confusing two
> >>> scenarios
>
> >>> 1: A mutation A' causes an increase in reproductive
> >>> success, whether or not a mutation B' (which also
> >>> causes an increase in reproductive success) is present.
>
> >>>2: A mutation A' alone or a mutation B' alone does not cause an
> >>> increase
> >>> in reproductive success. Only both mutations together cause
> >>> an increase in reproductive success.
>
> >>> Only in case2is the multiplication rule for probabilities applicable
>
> >>> - William Hughes
>
> >> independent of each other in incidence?
>
> >> Mitchell Coffey- Hide quoted text -
>
> >> - Show quoted text -
>
> > random mutations are essentially independent. The accumulation of
> > beneficial mutations depends on common descent. Lateral transmission
> > of beneficial mutations is a relatively rare event as demonstrated by
> > the failure of recombination of HIV from accelerating the mutation and
> > selection phenomenon. This is why the multiplication rule of
> > probabilities dominates the mutation and selection phenomenon.
>
> I wasn't asking you, I was asking someone with experience in the
> relevant field. That you are unfamiliar even with the relevant
> statistical concepts is demonstrated by your failure to realize you
> haven't even answered my question: "is it accepted by scientists that
> all mutations are independent of each other in incidence?"
Who was that *someone*? Was it a evolutionist *someone* who’s lack of
knowledge of the basic science and mathematics of mutation and
selection that has led the world into a state of multidrug resistant
microbes, multiherbicide resistant weeds and less than effective
cancer treatments?
>
> Your "multiplication rule" rants appear to ignore the concept of
> independence in several ways.
Tell us Mitchell how my rants about the "multiplication rule" ignore
the concept of independence?
>
> Of course, what kind of fool cites his state certifications for medicine
> and engineering as reasons for his superior authority on issues of
> evolutionary biology over people who actually have with PhDs in subjects
> directly involved in evolutionary biology?!
I’ll tell you exactly how my state certifications in medicine and
engineering are reasons for superior authority on evolutionary
biology. I’m held accountable for my decisions based in engineering
and medicine by the state. If I incorrectly apply the principles of
science, my decisions can cause me to lose the ability to practice my
profession. Evolutionists like Schneider who claims that the
multiplication rule of probability does not apply to biological
evolution and harm the very people he is paid to help ie those
suffering from cancer and no one stops him from practicing his
profession. If I am wrong, the state can take away my ability to
practice my livelihood. Why don’t you file a complaint with the
California State Medical Board or Engineering Board and try to take
away my licenses? Let’s see how far your mathematical incompetence
gets you? Why don’t you check with the California medical board and
see what their latest recommendation is for the treatment of Neisseria
gonorrhoeae?
>
> Mitchell Coffey- Hide quoted text -
Alan Kleinman MD PhD
> On Apr 1, 5:27 pm, Alan Kleinman MD PhD <klein...@sti.net> wrote:
>
>
>
>
>
> > On Mar 17, 9:15 pm, j...@wilkins.id.au (John S. Wilkins) wrote:
>
> > > Walter Bushell <pr...@panix.com> wrote:
> > > > In article <1jy8cz7.5lgtk71u0n0lcN%j...@wilkins.id.au>,
> > > > j...@wilkins.id.au (John S. Wilkins) wrote:
>
> > > > > r norman <r_s_nor...@comcast.net> wrote:
>
> > > > > > <brogers31...@gmail.com> wrote:
>
> > > > > > >On Mar 16, 6:51 am, Alan Kleinman MD PhD <klein...@sti.net> wrote:
>
> [snip]
>
> > > > Anyway what's wrong with teleological language in science. We know that
> > > > people don't have teleological motivation because if they did
> > > > teleological phenomena would exist in nature.
>
> > > Teleological thinking is perfectly approriate when you are dealing with
> > > teleological systems, like humans and their societies/artifacts. There
> > > *is* teleology in the world. Every time I go to the shop to buy milk,
> > > such a system is in operation.
> > > --
> > > John S. Wilkins, Associate, Philosophy, University of Sydneyhttp://evolvingthoughts.net
> > > But al be that he was a philosophre,
> > > Yet hadde he but litel gold in cofre- Hide quoted text -
>
> > > - Show quoted text -
>
> > that reptiles evolved feathers to keep warm.
>
> It would be teleology to claim that feathers evolved with the end goal
> of producing flight feathers. The claim that the initial feathers
> functioned to preserve warmth rather than for the goal of flight is
> based on observation of the types of feathers that formed early. IOW,
> it is working from what actually exists to try to determine its
> functionality based on structure and observation of similar features
> in living organisms. It is not making a claim of an end goal.
I see, so escaping from the cold is not imposing teleology and
escaping from a predator is imposing teleology.
>
>
>
> > This is a mathematically
> >irrationalover extrapolation of the mutation and selection phenomenon.- Hide quoted text -
>
> - Show quoted text -- Hide quoted text -
Alan Kleinman MD PhD
> On Apr 1, 5:23 pm, Alan Kleinman MD PhD <klein...@sti.net> wrote:
>
>
>
>
>
> > On Mar 15, 6:27 pm, William Hughes <wpihug...@gmail.com> wrote:
>
> > > It is rather interesting that in a > 1000 post thread
> > > the good Dr. has been unable to note that he is confusing two
> > > scenarios
>
> > > 1: A mutation A' causes an increase in reproductive
> > > success, whether or not a mutation B' (which also
> > > causes an increase in reproductive success) is present.
>
> > >2: A mutation A' alone or a mutation B' alone does not cause an
> > > increase
> > > in reproductive success. Only both mutations together cause
> > > an increase in reproductive success.
>
> > > Only in case2is the multiplication rule for probabilities applicable
>
> > > - William Hughes
>
> > more than a single beneficial random mutation is required to adapt to
> > selection pressures.
>
> same *individual* to adapt to selection pressures. That is, when the
> individual mutations have no selective benefit. You keep, however,
> denying that the multiplication rule does NOT apply when those
> conditions are not met.
Hersheyh, the multiplication rule of probabilities is used in the
calculation of the probabilities of a single beneficial mutation
how the calculation is done.
>
> > This is why the complexity of the selection
> > conditions is the dominant mathematical variable in the mutation and
> > selection phenomenon. Any evolutionary process which requires more
> > than a single beneficial mutation requires amplification of beneficial
> > mutations in order to improve the probabilities that the next
> > beneficial mutation in the sequence occurs.
>
> their *frequency*, not, in most cases, a major population decline and
> restoration. I have presented actual data that you can apply that
> shows the difference between your assumption of simultaneous in the
> same individual (where the multiplication rule applies) and what
> happens if one can engage in a serial (and parallel or partially
> offset parallel) mutation and selection in a population using bacteria
> and resistance to antibiotics. Perhaps you missed it.
Actually, the mutation and selection process does not require increase
in frequency of beneficial alleles; it requires amplification of
beneficial alleles for the process to proceed. In many if not most
cases this is associated with an increase in frequency of those
beneficial alleles but is not a requirement. When you are talking
about accumulation of events which occur with probabilities of the
order of 10^-4 to 10^-9, you need lots of members playing the
lotteries. This is why mutation and selection does not work well if at
all with small subpopulations.
>
> If mutation to resistance to either antibiotic is 10^-8 and you add 1
> ml of bacteria containing 10^9 bacteria to 9 mls of media containing
> *both* antibiotics, the probability of mutation to both resistances
> meet your requirement of being simultaneous and in the same
> individual. That probability would be 10^-16. The probability that
> the 10^9 bacteria added will have a double mutant is 10^-7, or quite
> low.
Before you try tackling the calculation of the probabilities of a
double beneficial mutation occurring, you should learn how to
calculate the probabilities that a single beneficial mutation occurs
as a function of population size. Then you can try to do the
calculation of two beneficial mutations occurring whether simultaneous
or not because your numbers are way off.
>
> OTOH, if you add the 1 ml of bacteria containing 10^9 bacteria to
> media containing only *one* of the two antibiotics, the probability
> rule says that there should be, as a mean, 10 bacteria in the 10^9
> bacteria you added to the 9 mls of media that will be resistant to
> that one antibiotic. After 30 generations, those 10 bacteria (the
> survivors) will have grown back to 10^9 bacteria/ml. If you then add
> 1 ml of those bacteria already resistant to one antibiotic to 9 ml of
> *both* antibiotics, you will, on average, have about 10 bacteria
> resistant to both in the 10^9 bacteria you add. After another 30
> generations, you will have a full population of double mutants.
I’ve already shown the mathematics for the calculation of the
probability of a single beneficial mutation occurring at a particular
locus as a function of population size. Why don’t you take that
calculation and try to calculate the probability that a second
beneficial mutation will occur as a function of population size? Let’s
see if you are willing and able to learn some hard mathematical
science about the mutation and selection phenomenon.
>
> The above is decidedly more common inevolution.
It may be so in your evolutionist belief system but in the hard
mathematical science of reality, the multiplication rule of
probabilities always enters into the calculation of the probabilities
of beneficial mutations occurring whether singly in sequence or
simultaneously. Let’s see if you are willing and able to learn that
mathematical skill.
>
> But let's take another example. Take a population of sensitive
> bacteria that are F+ and expose them to one of the antibiotics and
> another population of sensitive which is F- to the second antibiotic.
> Grow overnight and then put them together in media without either
> antibiotic for a couple of hours. Now when you add both antibiotics,
> the probability of finding a bacteria with both antibiotics will be
> much higher. Exactly how much higher will depend on where the F
> factor starts and how far apart the two resistant alleles are. The
> reason for the much higher probability is that recombination between
> different bacteria can occur under those conditions. This would be
> the bacterial form of parallelevolution.
Bacteriophages can short circuit the amplification process but
recombination does not help HIV in adapting to combination selection
pressures. Combination therapy also works with bacteria that can
amplify resistance genes with bacteriophages is you are using
effective combination selection pressures because the population must
still evolve the resistance genes by mutation and selection and that
process is stifled when combination therapy is used.
>
> The *only* case where the probability is low is the one that requires
> your condition that both mutants be present simultaneously in the same
> individual by chance alone.
If you are really serious about learning how the mutation and
selection phenomenon actually works, take the calculation I presented
showing the probability of a beneficial mutation occurring at a
particular locus as a function of population size and extend that
calculation to find the probability of a second beneficial mutation
occurring as a function of population size. Then you will start
understanding something about the basic science and mathematics of the
mutation and selection phenomenon. You won’t have to speculate or
approximate what you think the probabilities are.
>
> > This is why when the
> > mutation and selection phenomenon works, it is arduous and slow.
>
> third will be somewhat faster.
You are speculating that it would happen in two days. Lenski’s
populations took years to accumulate the small number of beneficial
mutations to transform a glucose metabolizer to a citrate metabolizer.
Learn how to calculate the probabilities of two beneficial mutations
occurring (whether simultaneous or not) as a function of population
size and it will become clear why Lenski’s experiment works the way it
does.
>
>
>
> > Any
> > combination of selection conditions which disrupts the amplification
Alan Kleinman MD PhD
> On Apr 1, 11:23 am, Alan Kleinman MD PhD <klein...@sti.net> wrote:
>
>
>
>
>
> > On Mar 15, 6:27 pm, William Hughes <wpihug...@gmail.com> wrote:
>
> > > It is rather interesting that in a > 1000 post thread
> > > the good Dr. has been unable to note that he is confusing two
> > > scenarios
>
> > > 1: A mutation A' causes an increase in reproductive
> > > success, whether or not a mutation B' (which also
> > > causes an increase in reproductive success) is present.
>
> > >2: A mutation A' alone or a mutation B' alone does not cause an
> > > increase
> > > in reproductive success. Only both mutations together cause
> > > an increase in reproductive success.
>
> > > Only in case2is the multiplication rule for probabilities applicable
>
> > > - William Hughes
>
> > William, the multiplication rule of probabilities always applies when
> > more than a single beneficial random mutation is required to adapt to
> > selection pressures.
>
> mutations
> must occur simultaneously in the same individual. This is the case
> when we're talking
> adapt or die.Either you get both mutations or you are dead.
Here’s the challenge for you evolutionists. Compute the probability
that two beneficial mutations occur sequentially as a function of
population size. If you are able to do this computation, you will
understand how the multiplication rule of probabilities enters into
the computation and why amplification of beneficial alleles is so
important for there to be a reasonable probability of this event to
occur.
>
> That is far from the norm. Having less differential reproductive
> success
> is lot different than being dead.
>
> Seriously, who do you you think you're fooling? You're only making a
> fool of yourself.
Do the probability calculation Stuart and we will see who is correct.
>
> Stuart- Hide quoted text -
Alan Kleinman MD PhD
> On Apr 1, 3:26 pm, Alan Kleinman MD PhD <klein...@sti.net> wrote:
>
>
>
>
>
> > On Mar 17, 3:54 pm, Walter Bushell <pr...@panix.com> wrote:
>
> > > In article <1jy8cz7.5lgtk71u0n0lcN%j...@wilkins.id.au>,
> > > j...@wilkins.id.au (John S. Wilkins) wrote:
>
> > > > r norman <r_s_nor...@comcast.net> wrote:
>
> > > > > On Tue, 15 Mar 2011 16:59:52 -0700 (PDT), Bill
> > > > > <brogers31...@gmail.com> wrote:
>
>
> > > > > >Sorry for top posting, I'd just suggest that all the responses to
> > > > > >Dr.Dr.Dr. AK go into this thread. At least for those of us stuck with
> > > > > >Google Groups, once you hit 1000 posts the thread fragments. It's
> > > > > >entertaining and it would be nice to have it all in one place.
>
> > > > > Wilkins about modifying traditional biological word usage just to
> > > > > placate the creationists or at least to deny them the ability to twist
> > > > > the meaning of the words to their purposes. Now you would have all
> > > > > the rest of us modify traditional posting methods just to placate
> > > > > those people who do not know how to use a real news reader and must
> > > > > rely on Google Groups!
>
>
> > > Anyway what's wrong with teleological language in science. We know that
> > > people don't have teleological motivation because if they did
> > > teleological phenomena would exist in nature.
>
> > > The Chinese pretend their goods are good and we pretend our money
> > > is good, or is it the reverse?- Hide quoted text -
>
> > > - Show quoted text -
>
> > “evolutionary direction” on populations and that forcing the
> > population to take two or more evolutionary directions impairs the
> > population from evolving?
>
> ...unless there are two subpopulations in slightly different
> environments, then they
> diverge, which is the characteristic that your microorganism examples
> do not address.
John, the central tool that populations have for improving the
probabilities of the next beneficial mutation occurring is
amplification of the previous beneficial allele. Reducing the size of
a population by breaking it into subpopulations reduces the number of
players in the lottery. When you are talking about accumulation of
events which occur with probabilities of the order of 10^-4 to 10^-9,
you need lots of members playing the lotteries. This is why mutation
and selection does not work well if at all with small subpopulations.
probabilities of two beneficial mutations occurring (whether
>
> -John- Hide quoted text -
Alan Kleinman MD PhD
> > being presented like this to prevent further fragmentation of the
> > discussion. These are responses to messages 951-975
>
> Please stop doing this. And be aware that the numbers appear only in
> Google Groups. The rest of us don't see them. And this post is way too
> long to read. It may in some way be convenient to you, but it's a pain
> in the ass to others. Have some consideration. Threading exists for a
> reason.
I didn’t want this thread to splinter into numerous splinter threads.
So unless you have a better suggestion, stop whining.
>
> > John Harshman
> >>> This seems like a strange claim with no substantiation.
> >> I'll say. What does he think causes changes in expression of existing
> >> alleles? Magic? And what does he think is the result? Now in fact
> >> expression changes inevolutionare the result of changes in DNA --
> >> mutations -- which can subsequently be selected. And these "mere"
> >> changes in expression can have major effects on morphology. What any of
> >> that has to do with inbreeding is a mystery.
> > Are you evolutionists still hung up on recombination and selection?
> > That phenomenon has a much smaller search space. In that case you are
> > recombining existing alleles and it doesn’t require amplification for
> > recombination. Recombination and selection is not governed by the
> > multiplication rule of probabilities. But any time one of you
> > evolutionists wants to demonstrate theevolutionof a reptile to a
> > bird by an inbreeding program, I’d be thrilled to see that.
>
> This isn't a response at all. It appears that you didn't even read what
> I wrote, especially the bit about "What any of this has to do with
> inbreeding is a mystery." I'm going to stop arguing with you, because
> you just don't pay attention.
What arguments have you made? Are you talking about your claim that
the probability of a beneficial mutation occurring at a particular
mathematics that showed you are wrong and you said you were just
speaking loosely. Why don’t you extend the calculation I presented and
show us how population size affects the probability of two beneficial
mutations occurring (whether simultaneously or not) and you will see
how the multiplication rule of probabilities always enters into the
calculation.
Alan Kleinman MD PhD
> On Fri, 1 Apr 2011 14:24:48 -0700 (PDT), Alan Kleinman MD PhD
>
> >> > On Tue, 15 Mar 2011 16:59:52 -0700 (PDT), Bill
>
> >> > <brogers31...@gmail.com> wrote:
> >> > >On Mar 16, 6:51 am, Alan Kleinman MD PhD <klein...@sti.net> wrote:
>
> >> > >Sorry for top posting, I'd just suggest that all the responses to
> >> > >Dr.Dr.Dr. AK go into this thread. At least for those of us stuck with
> >> > >Google Groups, once you hit 1000 posts the thread fragments. It's
> >> > >entertaining and it would be nice to have it all in one place.
>
> >> > I believe you, in a different thread, have been arguing against John
> >> > Wilkins about modifying traditional biological word usage just to
> >> > placate the creationists or at least to deny them the ability to twist
> >> > the meaning of the words to their purposes. Now you would have all
> >> > the rest of us modify traditional posting methods just to placate
> >> > those people who do not know how to use a real news reader and must
> >> > rely on Google Groups!
>
> >> real newsreader. In fact I have used many. I rely on Google Groups
> >> because it has the fastest propagation and the longest retention of
> >> anything in its price class, which is no additional cost.
>
> >> Of course TANSTAAFL, and enduring this design flaw ispartof the cost
> >> of using Google Groups. ISTM illustrating that point is one of the
>
> >> - Show quoted text -
>
> >the Food and Drug Administration published an essay on this site
> >phenomenon works. With leadership like his, no wonder we live in a
> >world filled with multidrug resistant microbes. If Thomas Schneider of
> >the National Cancer Institute allowed me to post on his site, I would
> >tell him that his claim “The multiplication rule does not apply to
> >fact, the multiplication rule is the central governing principle of
> >the mutation and selection phenomenon. Evolutionists have completely
> >bungled the basic science and mathematics of the mutation and
> >selection phenomenon and we have the multidrug resistant microbes and
> >less effective cancer treatments to show for it.
>
> It is often claimed that one of the major purposes of this site is to
> allow crackpots like this one to have a place to vent their opinions
> without garbaging up real scientific sites like Tom Schneider's of the
> National Cancer Institute.
> http://www.ccrnp.ncifcrf.gov/~toms/
>
> To the extent that the good Dr. Dr. is busy posting here, he can't be
> posting elsewhere. Let us hope that that practice works. It might
> make all this worthwhile.
R norman, you claim that you have taken graduate level courses in
probability theory. I have already presented the calculation of the
probability that a beneficial mutation will occur at a particular
training in probability theory go to work and calculate the
probability of two beneficial mutations occurring as a function of
population size (whether simultaneous or not) and you will see that
the multiplication rule of probabilities always enters into the
claim that the multiplication rule of probabilities does not apply to
biological evolution and Schneider harms the very people he is paid to
help with his mathematically irrational claim. R norman, I don’t
believe you have the mathematical training or skills to calculate the
probability of two beneficial mutations occurring sequentially. Let’s
see if you can prove me wrong. However, if you do prove me wrong on
this point, you will find that the multiplication rule of
probabilities always enters into this calculation and you will see
Schneider’s blunder.
Alan Kleinman MD PhD
> On Fri, 01 Apr 2011 14:23:44 -0700, Alan Kleinman MD PhD wrote:
>
> > William, the multiplication rule of probabilities always applies when
> > more than a single beneficial random mutation is required to adapt to
> > selection pressures.
>
>
> You do not know what the multiplication rule of probabilities is. I
> quizzed you earlier to state where it does *not* apply, and you flunked
> by not answering. But I'll give you a chance to retake the test. When
> does the rule not apply?
Mark, here’s the challenge. Calculate the probability of two
beneficial mutations occurring (not simultaneously) as a function of
population size. If you do the computation properly, you will see how
the multiplication rule of probabilities always enters into the
important to the mutation and selection phenomenon.
>
> --
> Mark Isaak eciton (at) earthlink (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
> On Apr 1, 5:26 pm, Alan Kleinman MD PhD <klein...@sti.net> wrote:
>
>
>
>
>
> > On Mar 17, 3:54 pm, Walter Bushell <pr...@panix.com> wrote:
>
> > > In article <1jy8cz7.5lgtk71u0n0lcN%j...@wilkins.id.au>,
> > > j...@wilkins.id.au (John S. Wilkins) wrote:
>
>
> > > > > On Tue, 15 Mar 2011 16:59:52 -0700 (PDT), Bill
> > > > > <brogers31...@gmail.com> wrote:
>
> > > > > >On Mar 16, 6:51 am, Alan Kleinman MD PhD <klein...@sti.net> wrote:
>
> > > > > >Sorry for top posting, I'd just suggest that all the responses to
> > > > > >Dr.Dr.Dr. AK go into this thread. At least for those of us stuck with
> > > > > >Google Groups, once you hit 1000 posts the thread fragments. It's
> > > > > >entertaining and it would be nice to have it all in one place.
>
> > > > > I believe you, in a different thread, have been arguing against John
> > > > > Wilkins about modifying traditional biological word usage just to
> > > > > placate the creationists or at least to deny them the ability to twist
> > > > > the meaning of the words to their purposes. Now you would have all
> > > > > the rest of us modify traditional posting methods just to placate
> > > > > those people who do not know how to use a real news reader and must
> > > > > rely on Google Groups!
>
>
> > > Anyway what's wrong with teleological language in science. We know that
> > > people don't have teleological motivation because if they did
> > > teleological phenomena would exist in nature.
>
> > > --
> > > The Chinese pretend their goods are good and we pretend our money
>
> > > - Show quoted text -
>
> > “evolutionary direction” on populations and that forcing the
> > population to take two or more evolutionary directions impairs the
> > population from evolving?
>
> unusual conditions (at least in nature)? Namely that you require
> multiple mutations simultaneously in a single individual to have *any*
> benefit.
Really, so you think that disruptive selection pressures are rare?
Hersheyh, here’s the challenge. Calculate the probability of two
beneficial mutations occurring (not simultaneously) as a function of
population size. If you do the computation properly, you will see how
the multiplication rule of probabilities always enters into the
computation and why amplification of beneficial alleles is so
important to the mutation and selection phenomenon.
Alan Kleinman MD PhD
> > > being presented like this to prevent further fragmentation of the
> > > discussion. These are responses to messages 951-975
>
> > Please stop doing this. And be aware that the numbers appear only in
> > Google Groups. The rest of us don't see them. And this post is way too
> > long to read. It may in some way be convenient to you, but it's a pain
> > in the ass to others. Have some consideration. Threading exists for a
> > reason.
>
> others agitating for a stop to him replying (he was accused of
> spamming) to individual posts in multiple threads with the same
> title.
>
> The guilt resides with Gurgle Groups and their "feature" of
> fragmenting any thread that reaches 1k posts. Whether Dr.^3 K. should
> get a real news reader is another question entirely. Is there another
> "good" solution to this issue? Sure, get Gurgle to fix their Usenet
> software (not bloody likely).
>
> "You can please some of the people all of the time..."
Thanks Chris, that’s exactly why the compilation of responses. I hope
this thread won’t go to 2000 and I’m trying to prevent this by
challenging you evolutionists with the following probability problem.
Calculate the probability of two beneficial mutations occurring (not
simultaneously) as a function of population size. If you do the
computation properly, you will see how the multiplication rule of
probabilities always enters into the computation and why amplification
of beneficial alleles is so important to the mutation and selection
phenomenon.
>
>
>
>
>
>
> > > John Harshman
> > >>> This seems like a strange claim with no substantiation.
> > >> I'll say. What does he think causes changes in expression of existing
> > >> alleles? Magic? And what does he think is the result? Now in fact
> > >> expression changes inevolutionare the result of changes in DNA --
> > >> mutations -- which can subsequently be selected. And these "mere"
> > >> changes in expression can have major effects on morphology. What any of
> > >> that has to do with inbreeding is a mystery.
> > > Are you evolutionists still hung up on recombination and selection?
> > > That phenomenon has a much smaller search space. In that case you are
> > > recombining existing alleles and it doesn’t require amplification for
> > > recombination. Recombination and selection is not governed by the
> > > multiplication rule of probabilities. But any time one of you
> > > evolutionists wants to demonstrate theevolutionof a reptile to a
> > > bird by an inbreeding program, I’d be thrilled to see that.
>
> > This isn't a response at all. It appears that you didn't even read what
> > I wrote, especially the bit about "What any of this has to do with
> > inbreeding is a mystery." I'm going to stop arguing with you, because
Alan Kleinman MD PhD
> On Apr 1, 6:00 pm, Alan Kleinman MD PhD <klein...@sti.net> wrote:
>
>
>
>
>
> > The following is a compilation of responses to previous posts that are
> > being presented like this to prevent further fragmentation of the
> > discussion. These are responses to messages 951-975
> > R Norman> This guy who loves to lecture to us about the multiplication rule in
> > > probability clearly does not believe at all in probability.
> > > The probability of having a male vs. a female child is 50:50. I have
> > > two brothers but no sisters. I have two daughters but no sons.
> > > Obviously the reason why the sex ratio changed so drastically in
> > > either direction in two generations in my own family is because of
> > > survival of the fittest. Stochastic processes had absolutely nothing
> > > to do with it. So says the good doctor who knows about probability so
> > > he must be right.
>
> > The reason why I lecture you on the multiplication rule of
> > probabilities is that it is the central governing mathematical
> > principle of the mutation and selection phenomenon.
>
> Says who? Can you cite anyone aside from yourself who makes this
> claim?
You would if you knew how to compute the probability that two
beneficial mutations were to occur as a function of population size.
>
> > There is a reason
> > why I don’t go to casinos. It is not gambling in casinos. If you play
> > long enough, you will leave all your money there.
>
> I can certainly understand that you have very good reasons to avoid
> all games of chance. Even ones where there is no "house" to take its
> cut, like games of coin-flipping among friends, where your chances are
> as good as any other player. Given your understanding of probability,
> you probably think that every player would come out even in the end
> because every player has a 50:50 chance of being right with each flip.
I recall a group of excellent mathematicians (I believe they were from
MIT) studied the probabilities of blackjack associated with the
counting of cards which shifted the probabilities of winning to their
favor. The casinos responded by using more decks in the game and
ultimately by preventing these players from playing. If you are so
knowledgeable of probability theory, compute the probability that two
beneficial mutations were to occur as a function of population size.
When you are able to do this computation, then you will know how the
multiplication rule of probabilities always governs the probability of
two beneficial mutations occurring even when the mutations do not
occur simultaneously but sequentially.
>
> > And> The good doctor here totally ignores my several posts where I
> > > patiently explain to him the medical genetics is a different subject
> > > from evolutionary biology. Medical genetics is taught to medical
> > > students by medical geneticists and the thrust of the subject is not
> > > mutation and selection orevolutionor evenirrationalviews of
> > > evolutionism.
>
> > R norman, I haven’t ignored you. I just disagree with you. My medical
> > school genetics text discusses mutation and selection but does an
> > incompetent job of describing the phenomenon.
>
> No. Although I am sure the text provides an *incomplete* description
> of a complex subject, you undoubtedly think it is incompetent merely
> because it doesn't agree with your brilliant insight about the
> probability rule. Problem is, your insight is full of it.
Let’s see how full of insight you are by computing the probability of
two beneficial mutations occurring in a population sequentially.
>
> > I think most physicians
> > would agree that infectious diseases comprise a much greater fraction
> > of primary care medical practices than do genetic diseases. I would be
> > surprised if any medical geneticist said he wasn’t an evolutionist.
> > > But then the good doctor has always ignored my criticisms, especially
> > > those cogent ones he finds impossible to answer: his flawed use of
> > > Newton-Raphson methods to find the zeros of non-linear equations, his
> > > absurd claim that selection cannot increase diversity, his ridiculous
> > > posturing about how his claim of failures in medical practice are laid
> > > directly at the feet of evolutionary biologists, .....
>
> > Why don’t you try to take away my PhD by saying my thesis was wrong
> > where I used the Newton-Raphson method to find the zeros of six
> > simultaneous non-linear equations.
>
> SFW. Just because you can do that doesn't make you an expert in even
> basic probability and population genetics. Just because William
> Shockley won a Nobel Prize in physics did not make him competent in
> human genetics (he was a notorious eugenicist promoter), although he
> was probably more competent in that field than you are in
> understanding how neutral allele frequencies change with time.
Hersheyh, compute the probability of two beneficial mutations
occurring in a population sequentially.
>
> > And then why don’t you post any
> > mathematical or empirical evidence which shows that selection
> > increases the diversity of populations.
>
> gene locus in a population that are above a frequency of, say, 10^-6?
Let’s forget about our side bar argument of what defines diversity.
Our central argument is whether the multiplication rule of
probabilities is involved in the probabilities of two beneficial
mutations occurring. Hersheyh, compute the probability of two
beneficial mutations occurring in a population sequentially.
>
> > Selection always removes
> > members of the population from contributing to the gene pool, which
> > always decreases the diversity of the gene pool.
>
> Selection differentially (and significantly) affects the reproductive
> success of certain phenotypes relative to alternatives in a specified
> environment. That neither requires "removal from the population" nor
> does it prevent all "contribution to the gene pool." Several people
> have already described selection which *favors* diversity. That which
> occurs when "unusual" or "different" alleles are favored. I have
> mentioned self-sterility in plants as a case where *selection* has
> resulted in populations with over 200 alternate alleles.
We can debate the issue of diversity later. Do the calculation of the
probability of two beneficial mutations occurring as a function of
population size. I already gave you a good hint how to do this
computation by posting the computation of the probability of a single
beneficial mutation occurring in a population as a function of
population size.
>
> > Now I lay the
> > responsibility for the failure to properly teach the basic science and
> > mathematics of the mutation and selection phenomenon on those who
> > control the educational system. And who controls the field of biology?
>
> If you were in charge, you would be teaching poor biology *and* false
> mathematics.
At least what I teach about mutation and selection gives consistent
results with both the mathematical and empirical evidence and perhaps
if you could compute the probability of two beneficial mutations
occurring in a population sequentially as a function of population
size, you would too.
>
>
>
>
>
> > ========================================================
> > Mark Issak> You are bearing false witness. I never claimed that.
>
> > That sounds like some kind of religious belief. We need to keep that
> > kind of stuff out of our public school.
> > And>> The good doctor here totally ignores my several posts where I patiently
> > >> explain to him the medical genetics is a different subject from
> > >> evolutionary biology. Medical genetics is taught to medical students
> > >> by medical geneticists and the thrust of the subject is not mutation
> > >> and selection orevolutionor evenirrationalviews of evolutionism.
> > >> But then the good doctor has always ignored my criticisms . . .
> > > I suspect he simply does not remember them. I am becoming increasingly
> > > persuaded that he is suffering from organic brain damage that affects his
> > > ability to form long-term memories. This would explain his abysmal
> > > reading comprehension, his complete inability to learn, and probably a
> > > lot of his belligerence, as a lot of people get defensive rather than
> > > admit the problem is with themselves. I would be curious to talk with
> > > one of his colleagues who sees him regularly to find out what they have
> > > noticed.
>
> > That’s why I put it in writing Mark. So Mark, do you believe that
> > selection pressures increase or decrease the diversity of populations?
>
> It depends on the selective pressures and environmental conditions.
>
>
>
>
>
> > We already know that you believe that if you decrease the intensity of
> > selection that you accelerate selection process. That’s mathematically
> >irrational.
>
> > ========================================================
> > Hersheyh>Reducing the intensity of selection has no effect on mutation rates.
> > >Mutagens and prevailing mutagenic conditions (the sum of positive
> > >causation of mutations decreased by repair capacity) will determine
> > >the rate of mutation. If I mutate or chemically inactivate repair
> > >systems, net mutagenesis will increase. If I add mutagens, net
> > >mutagenesis will increase. If I change selective conditions, I will
> > >almost never increase or decrease mutation rate. [There are a few
> > >exceptions where a specific genetic change is a response to
> > >environmental conditions, such as excision of integrated lambda phage
> > >under stress conditions. It is possible to consider these as
> > >"domesticated" mutagenesis events.]
>
> > Hersheyh, you don’t read my posts very carefully. What I have said is
> > that reducing the intensity of selection slows the evolutionary
> > process.
>
> already described as a process of change which is *slower* than any
> form of selective allele *change*. Conservative selection is
> selection against allele change, but that is a dynamic stasis.
Well then you will have to come up with yet another mathematically
irrational theory to account for the at least 40,000,000 genetic
differences between humans and chimpanzees in only about a million
generations.
>
> > The reason that reducing the intensity of selection slows the
> > evolutionary process is that the intensity of selection affects the
> > rate of substitution of a more beneficial allele for a less beneficial
> > allele.
>
> Yes. The stronger the selection, the more rapidly we get substitution
> for the allele that is beneficial in that specific environment.
If the selection pressure does not drive the population to extinction
first.
>
> > And the unit process ofevolutionis the substitution of a
> > more beneficial allele for a less beneficial allele.
>
> Neutral allele change is alsoevolution. The adjectives "beneficial"
> and "detrimental" are not *inherent* properties of a gene sequence.
> They are descriptives of how two alternate alleles compare in their
> phenotypic effects in a particular environment. The terms are
> *conditional*.
I think I’m going to diverge from Haldane’s definition of the unit
process of evolution. Haldane’s definition is that the unit process of
evolution is the substitution of a more beneficial allele for a less
beneficial allele. I think that the unit process of evolution is the
ability of a population to amplify a beneficial mutation because
amplification of a beneficial allele is how a population overcomes the
multiplication rule of probabilities for two beneficial mutations to
>
> > You evolutionists
> > are very confused on how each of the variables in the mutation and
> > selection phenomenon affects the behavior of this process.
>
> So you keep asserting, despite it being pointed out that you are
> wrong.
If you are not confused, compute the probability of two beneficial
mutations occurring in a population sequentially as a function of
population size.
>
> > By far, the
> > complexity of the selection conditions is the dominant variable in
> > mutation and selection phenomenon. The reason is because this variable
> > is governed by the multiplication rule of probabilities.
>
> No. The conditions for anything to be "governed by the multiplication
> rule of probabilities" is the requirement for *simultaneity* in a
> single trial, or as in your case, *simultaneity* in a single
> individual. We keep reminding you thatevolutionis most successful
> when one or both of those requirements do not hold.
Compute the probability of two beneficial mutations occurring in a
population sequentially as a function of population size. The
multiplication rule of probabilities always applies even if the
mutations do not occur simultaneously.
>
> > No other
> > variable in the mutation and selection phenomenon has the mathematical
> > leverage of the multiplication rule. Hersheyh, if you learn nothing
> > else from this discussion, learn that the multiplication rule of
> > probabilities is the dominant governing mathematical principle for the
> > mutation and selection phenomenon.
>
> I refuse to learn errors. You have been expounding clear error. I
> certainly agree with using the multiplication rule of probability
> *when* the conditions for its use are present. I have never had any
> problem with that. ...
No hersheyh, you refuse to learn probability theory. Try to compute
the probability of two beneficial mutations occurring in a population
sequentially as a function of population size.
>
> read more »- Hide quoted text -
>
> - Show quoted text -- Hide quoted text -
>
> - Show quoted text -- Hide quoted text -
Alan Kleinman MD PhD
> On Apr 1, 6:00 pm, Alan Kleinman MD PhD <klein...@sti.net> wrote:
>
> > The following is a compilation of responses to previous posts that are
> > being presented like this to prevent further fragmentation of the
> > discussion. These are responses to messages 951-975
> > ========================================================
>
> > The multiplication rule of probabilities governs the mutation and
> > selection phenomenon whether the mutations must occur simultaneously
> > or not.
>
> No it doesn't. Show your mathematical reasoning. I have given you
> (several times) a description using antibiotics and bacteria (assuming
> a mutation rate to resistance of 10^-8 to either antibiotic) in which
> I can generate 10^9/ml double mutant bacteria in two days (60
> generations), using 20 ml of media by doing the deed serially
> (selecting for one mutation at a time and allowing the population to
> regrow inbetween) whereas it would take 10^17 liters and roughly the
> same amount of time to do the same thing by demanding simultaneity of
> the mutations (selecting for simultaneous mutations to both
> resistances in a single individual). You tell me how you determine
> that both are equally difficult.
Hersheyh, your mathematical reasoning is wrong. If you want to get
back on the right track you need to solve this probability problem.
You need to be able to compute the probability of two beneficial
mutations occurring in a population as a function of population size.
I have already given you a good hint by showing you how to compute the
probability of a single beneficial mutation occurring in a population
foundation for computing the probability of two beneficial mutations
occurring in a population as a function of population size. Let’s see
if we can put some hard mathematical science through the evolutionist
cob webs in your brain.
>
> > If an evolutionary process requires two simultaneously
> > mutations, then the evolutionary process is slowed even more.
>
> I agree that when you require simultaneity of mutation to have any
> selectable effect that such an evolutionary event is less likely. See
> my math above. You, however, in just the last sentence declared that
> "The multiplication rule of probabilities governs the mutation and
> selection phenomenon whether the mutations must occur simultaneously
> or not." If that were so, how can your last sentence ("If an
> evolutionary process requires two simultaneously mutations, then the
> evolutionary process is slowed even more.") be correct?
When you solve the probability problem I presented to you above, you
will understand how important amplification of the first beneficial
mutation is for the population to overcome the multiplication rule
which always appears in the equation. Anytime a stochastic process is
dependent on independent random events, you can be sure that the
multiplication rule will show up some how.
>
> > HIV is
> > not a special case of mutation and selection.
>
> Other than that its mutation rate is especially high because it is an
> RNA virus. [RNA has no repair mechanism.]
Mutation rate does not obey the additive rule of probabilities either.
The mutation rate is not the variable which has the mathematical
capability to overcome the multiplication rule of probabilities. It is
the ability of a population to amplify the first beneficial mutation
in a sequence which determines if a population will get the second
beneficial mutation.
>
> > In fact, it has every
> > variable in the process working in its favor. It has large
> > populations, high mutation rates, does recombination allowing for
> > lateral transfer of genetic material, short generation times and can
> > not be driven to extinction. Any time selection conditions target more
> > than a single gene, the mutation and selection phenomenon will be
> > stifled for the same reason the process is stifled when using
> > combination therapy for HIV.
>
> And I have never disagreed that *when* "selection conditions target
> more than a single gene" *and* requires *simultaneous* mutation to
> resistance to both agents in the same individual, that it makes double
> mutation less probable. But again, you have taken what Schneider said
> out-of-context. Schneider was clearly talking about the brain dead
> idea that whole proteins are randomly assembled.
Schneider’s claim is a clear mathematical and scientific blunder. If
Schneider understood how to compute the probability of two beneficial
mutations occurring sequentially in a population as a function of
population size, he would understand how bad his blunder is.
>
> >> that I have to enter your world ofirrationalspeculations. We now
> > >> intensity of selection accelerates the mutation and selection
> > >> phenomenon.
>
> Liar. Mark said no such thing.
Here’s the exact exchange between Mark and I.
Kleinman wrote:
“> Again, you repeat an old speculation that evolutionists like to
use.
> The intensity of selection has very specific mathematical effects on
> the mutation and selection process. That effect is to slow the process
> down. Reducing the intensity of selection is a two edged sword. On one
> hand, reducing the intensity of selection reduces the chances that the
> population will be driven to extinction. On the other hand, reducing
> the intensity of selection slows the mutation and selection phenomenon.”
And Mark Isaak wrote in response:
“It is obvious to anyone with a smattering of knowledge of population
genetics that you don't know what you're talking about. But it is
also
apparent (if not so blatant) that you *think* you know what you are
talking about. I find that fascinating. It's like you are writing a
travel book about a place you have never so much as heard of before,
but
are willing to swear to having lived there for years.”
Hersheyh, you don’t know the truth from a lie and you don’t know how
to do the probability calculations associated with the mutation and
selection process. If you don’t want to be a totally mathematically
incompetent dim wit, compute the probabilities of two beneficial
mutations occurring (not simultaneously) and show us that
multiplication rule of probabilities does not apply.
>
>
>
>
>
> > > >This mathematical blunder ranks up there with the
> > >> evolutionist blunder that selection increases the diversity of
> > >> populations.
> > >Selection *can* increase the diversity of populations (negative
> > >frequency dependent selection) measured as the number of alleles
> > >existing in a population at greater than, say, 1% frequency. That
> > >doesn't mean that it always does so and no one has claimed that. But
> > >you have not defined what you mean by "diversity" of populations and
> > >how you measure such diversity. A large population, say, of English
> > >sparrows, shows diversity in size and shape, with northern populations
> > >being stouter than southern populations. African populations of
> > >humans show diversity in some external features from human populations
> > >in northern Asia (as well as differences in blood types). Some
> > >species, unlike humans, even have subspecies in different localities
> > >that are distinctly different (say like the Bengal and Sumatran
> > >subspecies of tiger). But I don't know how you are defining
> > >"diversity" in a species. Until you tell us what you mean by
> > >"diversity", it is hard to argue the point.
>
> > What I mean by diversity is the number of genetic variants in a
> > population. Selection always reduces the number of genetic variants in
> > a population.
>
> Selection *and* chance both reduce the *number* of genes between
> zygote and breeder or render the adult less fertile in some way. But
> selection is about the *frequency* of alleles in a population, not the
> number. If you are in the process of having an alternate allele sweep
> through the population, the *number* of genetic variants is two during
> the process and one at either end (before the alternate allele
> appeared and after it becomes fixed). That is, *during* the process
> ofevolution, the *number* of alleles is higher than at either end.
> During that same process, the frequency of the two alleles changes.
Actually it is more accurate to say that selection is about
amplification of beneficial alleles because it is much more important
to increase the number of members with the beneficial allele than to
increase the frequency of the allele. In the calculation of the
probabilities of two beneficial mutations occurring in a population,
the frequency of the beneficial alleles does not show up in the
probability equations, it is the number of members with the first
beneficial allele which shows up in the equation. Hersheyh, you do not
understand the simpler probability calculation for the probability of
a single beneficial occurring in a population as a function of
population size. Previously you and John Harshman claimed that that
probability was proportional to population size which was incorrect.
If you don’t understand that simpler problem, you will not be able to
do the more complex problem for two beneficial mutations to occur (not
simultaneously) which is governed by the multiplication rule of
probabilities.
>
> In the case of a balanced polymorphism, like sickle cell, the
> selective advantage of the heterozygote in malarial areas leads to
> selective pressures to *maintain* a certain frequency of both the HbA
> and HbS alleles in the population.
>
> Then there are frequency-dependent alleles like plant sterility
> alleles or major histocompatibility alleles where selection favors
> alleles that are currently less common.
>
> And, of course, there are selectively neutral traits that can, by
> chance, be fairly common. The ABO blood type system may have some
> features of this and of balanced polymorphism and frequency-dependent
> selection.
Just tell us what the probability of two beneficial mutations
occurring in a population (not simultaneously) is as a function of
population size.
>
> > The way to increase the diversity of a population is to
> > reduce the selection pressure on the population so that less fit
> > variants can still reproduce and pass their genetic information to the
> > next generation.
>
> In the absence of selective pressure, the frequency of alternate
> alleles is governed by chance alone. And that means a "drunkard's
> walk" for any new allele with the probability that that allele will
> persist to fixation being set at 1/2N. Most new alleles will quickly
> become extinct. A rare few will become relatively more frequent. 1/2N
> will drift to fixation. The next time you lie about this, please show
> your math and the assumptions you are making. In case you don't know,
> the false assumptions you are making is that you have an infinitely
> large population or that mating is deterministic rather than
> stochastic in nature.
You have already admitted previously that fixing an allele by chance
is slower than by selection. Now you need to understand why selection
is so slow. And if you learn how to compute the probability of two
beneficial mutations occurring (not simultaneously) in a population as
a function of population size, you will learn that this probability is
governed by the multiplication rule of probabilities.
>
> > >When have I ever said differently? I agree that *when* there is no
> > >selective advantage to having only one mutation and there is *only* a
> > >selective advantage to an individual having two *simultaneous*
> > >mutations that the multiplication rule holds.
>
> > This is where you make a mathematical blunder; the multiplication rule
> > always applies whether the mutations occur simultaneously or not.
>
> A lie repeated is still a lie. Or convince me by showing your math.
I’ve already shown you a part of the probability calculation by
showing you how to compute the probability of a single beneficial
mutation occurring at a particular locus as a function of population
size. Study and understand that calculation. Once you understand that
calculation then consider what would happen if a second beneficial
mutation were to happen after the first beneficial mutation in a
population. I’ll give you a hint. The members of the population with
the first beneficial mutation form a subset of the total population.
Then think how you would calculate the probability of the second
beneficial mutation occurring on the subset of the total population.
If neither you nor the other evolutionists posting on this thread are
able to do the calculation, I’ll post the answer. And remember, we
have evolutionists like r norman who have taken graduate level courses
in probability theory so this person should know how to do the
calculation and will recognize that the multiplication rule of
probabilities governs this calculation.
>
> > The
> > way populations overcome the multiplication rule is by amplification
> > of a beneficial allele and by large numbers of generations working to
> > get that next beneficial mutation.
>
> Repeating a lie does not make it true.
It’s not a lie hersheyh, you are just ignorant of probability theory.
>
> > Remember that population size and
> > the number of generations has less than an additive affect on the
> > probability of the next beneficial mutation occurring at the proper
> > locus.
>
> Repeating a lie does not make it true.
Hersheyh, what are you trying to prove, that you are ignorant^2. You
need to learn to recognize the difference between mutually exclusive
events which obeys the additive rule of probabilities and
complementary events which do not obey the additive rule. A simple way
to test this concept is if can continue to double your variable and
think the probabilities double than at some point your probabilities
will be greater than one, you don’t have mutually exclusive events,
and the use of the additive rule is a mathematically irrational
concept that you seem insistent upon doing.
>
> >> But natural selections are
> > >> much more cooperative in your Twilight Zone world. They only target
> > >> one gene at a time and they occur sequentially in a very ordered
> > >> manner, kind of like sequential antimicrobial therapy which has given
> > >> us multidrug resistant microbes.
>
> As a matter of fact, that is the case in nature, as a recent article
> in Science demonstrates.
>
> http://www.the-scientist.com/news/display/58097/
>
> The reason why these bacteria in a quasi-natural system do not
> accumulate resistances is because the mutations that produce phage
> resistance also often impose a cost when the environment does not
> contain the phage.
>
> > > > I guess we can call that the natural
> > >> way of using antibiotics. That s good sound evolutionist training at
> > >> work.
> > >And, in fact, in nature, it is pretty unusual for a virus to be
> > >exposed to two antivirals at once. And, as you point out, *when*
> > >conditions expose the virus to one antiviral at a time, such that
> > >there is a selective advantage to each step, we get both steps
> > >occurring much faster than would be the case when conditions require
> > >an individual to have both mutations simultaneously.
>
> > But it is not unusual for the environment to cause thermal stress and
> > starvation on a population simultaneously, or disease, or dehydration,
> > or predation, or…
>
> And, relative to the wild type, *variants* resistant to heat alone
> have a selective advantage. Relative to the wild-type, variants able
> to utilize a food source that was either unavailable or not usable
> that has increased in abundance during the increase in temperature (if
> no such food source is available, there is no option but to have
> reduced populations, which may require greater mobility to adapt to
> reduced population density, but one cannot magically poof energy
> sources where there are none) will also have a selective advantage.
> Selection under these conditions will select for *either* variant
> relative to the w.t. That is, you will have selection for *both*
> types of variants relative to the w.t. in parallel. The *frequency*
> of both types of variants will *increase*. The *frequency* of both
> will increase until one gets, via reproduction, individuals with
> *both* types of variants. The double variant will now be favored over
> individuals with only one of the variations. The size of the
> population likely will have decreased during the process, but this is
> not a situation where one must *necessarily* have *both* variations in
> a single individual to survive unless ...
Hersheyh, learn how to do the probability of two beneficial mutations
occurring as a function of population size. When you learn how to do
this computation, you will learn that the multiplication rule of
probabilities governs the occurrence of these two events. You will
then understand why amplification is crucial to the mutation and
selection process if more than a single beneficial mutation is
required for adaptation to the selection conditions. I have high hopes
for you hersheyh that some day you will learn something of the basic
science and mathematics of mutation and selection.