On Mathematical Anti-Evolutionism

[jillery]

In Jason Rosenhouse's review of "Undeniable", he cites one of his own
papers, which he claims mathematically refutes the mathematical
arguments of IDiots and other evolution-haters:

<http://link.springer.com/article/10.1007/s11191-015-9801-7>

From the abstract:

**********************************
The teaching of evolution in American high schools has long been a
source of controversy. The past decade has seen an important shift in
the rhetoric of anti-evolutionists, toward arguments of a strongly
mathematical character. These mathematical arguments, while different
in their specifics, follow the same general program and rely on the
same underlying model of evolution. We shall discuss the nature and
history of this program and model and describe general reasons for
skepticism with regard to any anti-evolutionary arguments based upon
them. We shall then survey the major arguments used by
anti-evolutionists, to show how our general considerations make it
possible to quickly identify their weakest points.
*********************************

I am intrigued by the comprehensive reference list he claims. Given
that T.O. is occasionally visited by such types, my impression is such
a paper would be a useful reference.

However, I am uncomfortable shelling out $40 only to find it to be an
arcane tome comprehensible only to other mathematicians. If anybody
in T.O. has read this paper, will you post an opinion about it,
whether it does what it claims to do in an way understandable to those
who have only a superficial familiarity with mathematical jargon?
--
This space is intentionally not blank.

[rsNorman]

jillery <69jp...@gmail.com> Wrote in message:

I now have the paper and it seems quite excellent. It is 17
pages, not counting the bibliography and I don't have the time
now to summarize it but I will try to get to it later
today.

There are several pages devoted to the Wistar Conference as well
as sections about Dembski's Complex Specified Information and
Behe's "Edge of Evolution."

The major "mathematical" proof employed by the creationists
involves, as we already all too well know, the identification of
a specific target that evolution must hit in order to produce
what we see. The "proof" then shows that the probability of any
random search algorithm could not possibly find that target
because the probability is so minute. I haven't gone deeply
enough into the paper to see the comments about the problem of
"creating" information.

Unfortunately I don't see that the author, Jason Rosenhouse, has
posted the paper on his James Madison University Web site.
Incidentally, he is a mathematician, not a biologist, but
interested in ensuring that mathematics is taught and interpreted
correctly.


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[Glenn]

"jillery" <69jp...@gmail.com> wrote in message news:110s0c9rs5mnftjfg...@4ax.com...

> In Jason Rosenhouse's review of "Undeniable", he cites one of his own
> papers, which he claims mathematically refutes the mathematical
> arguments of IDiots and other evolution-haters:
>
> <http://link.springer.com/article/10.1007/s11191-015-9801-7>
>
> From the abstract:
>
> **********************************
> The teaching of evolution in American high schools has long been a
> source of controversy. The past decade has seen an important shift in
> the rhetoric of anti-evolutionists, toward arguments of a strongly
> mathematical character. These mathematical arguments, while different
> in their specifics, follow the same general program and rely on the
> same underlying model of evolution. We shall discuss the nature and
> history of this program and model and describe general reasons for
> skepticism with regard to any anti-evolutionary arguments based upon
> them. We shall then survey the major arguments used by
> anti-evolutionists, to show how our general considerations make it
> possible to quickly identify their weakest points.
> *********************************
>

Who is "we"?

[Alan Kleinman MD PhD]

I don't have any problem teaching evolution in school. A proper understanding of the basic science and mathematics of rmns is the key for dealing with drug-resistant infections and less than durable cancer treatments. Rosenhouse has no expertise in this particular stochastic problem. If he had, he would have solved this problem long ago.
-
I do have a problem with teaching the theory of evolution which makes an irrational extrapolation of the rmns phenomenon when it is claimed that rmns transforms reptiles into birds. This type of pseudo-scientific mythology only confuses naive school children.

[jillery]

That's another reason why his paper should be useful, as contrasted to
for example DrDr's spam. Thank you for sharing the above.

[John Harshman]

Why the obsession with reptiles and birds? And why does this obsession
not extend to the particular reptiles and birds that provide evidence of
the transformation in question?

What about, to pick a random example, a transformation between brown
bears and polar bears? How far are you willing to go?

[jillery]

On Mon, 24 Oct 2016 06:50:10 -0700, "Glenn" <g...@invalid.invalid>
wrote:

If it really matters to you, ask Rosenhouse.

[Alan Kleinman MD PhD]

It's not my obsession, it's the evolutionist claim.

>
> What about, to pick a random example, a transformation between brown
> bears and polar bears? How far are you willing to go?

Clearly not as far as you would go. That's because I understand how rmns works and you don't.

[John Harshman]

It's one claim among thousands. Why that one specifically?

>> What about, to pick a random example, a transformation between brown
>> bears and polar bears? How far are you willing to go?

> Clearly not as far as you would go. That's because I understand how rmns works and you don't.

Once more you avoid answering the question in favor of an irrelevant insult.

[Alan Kleinman MD PhD]

What you call an irrelevant insult is the truth. rmns is a fundamental mechanism of genetic transformation and a cause of problems in medicine, agriculture, pest control... As a biologist, you have been an utter failure in describing how this mechanism works. This kind of failure would be analogous to an engineer not understanding Newton's laws or conservation of energy. That's what people like you have done to the field of biology.

[John Harshman]

Rather than simply repeat your canned rant another time, why not answer
the questions?

[Alan Kleinman MD PhD]

What you like to call a rant is also true, you don't understand how rmns operates. Why do you want me to speculate on whether brown bears and polar bears are related? Do the genetic analysis and measure whether they are related or not and that's not finding a genetic sequence here and there showing similarities, that involves taking into account the entire genome and the mechanisms of genetic transformation and looking for a MRCA. That's how science is done.

[rsNorman]

I have now read it thoroughly, but just once. It really is quite
excellent and has an awful lot to say about arguments we go
through regularly on this forum. In particular, to stay right on
post with your reference to Dr Dr material, it even covers this
specific argument quite nicely.

However there is an awful lot of material in it and I would like
to do a rather thorough and well thought out summary so it will
take me a little time to get to it. It is worth far more than a
quick "here are one or two highlights." So it will take me a day
or two. In the meantime, anyone else with good library access is
welcome to pipe in.





--

[eridanus]

"We" is anyone Jillery presumes would think is right his argument.

I can present myself voluntarily for this category of "we".

eri

[eridanus]

I presume there is a lot of bogus mathematics applied to genetic mutations.

To apply mathematics to mutations we need to know a lot about the nature,
the conditions and the mechanics of them. I do not think anyone knows so
much about this subject to create a valid mathematical analysis.

It is a bogus argument. I recall from primary school some advanced student
proving me that 1+2 were not 4, or something of this style. My maths were
too poor to understand what trick he was applying in his argument. The same
happens here. Someone presents here a bogus mathematical argument to prove
"evolution is an intellectual hoax". But the "intellectual hoax" is his
mathematical argument.

I do not need to be very intelligent to be an atheist. I simple ask myself
"what was the reason for god
after an infinite amount of time
had decided to create a universe
of the huge size we figure it has."

Or why he decided,
what was the reason,
to creating living beings,
some of them so undesirable,
including in this category
some human beings.

I can also wonder, why
of there is an unique god
it has been hidden by the existence
of previous fake gods
in the brief period of history
we know.

Discarding a lot of absurd theories about the existence
of a god... the theory of evolution, even if it is not yet fully
developed and mature, it is the best theory we can think off to explain
the existence of living beings around us.

Eri

[eridanus]

The best theory of the planet can have detractors. People that accept
evolution can presume, perhaps, to know more than he knows. If we can
explain in detail how a reptile converted into any sort of bird, it is
easily understood as we have not yet clear fossil clues to understand it.

Our fossil record is fragmentary and we only have small parts of the
past history. If we speculate with scarce data there is a great probability
that of being wrong.

Then, any argument referring on "how a species came from another" is merely
speculative. The global theory of evolution cannot be rejected because most
of changes from some species to another, cannot be explained in detail.

Eri

[eridanus]

try to explain this <rmns> thing to see if the logic of the argument
is leaking oil or not. Because by using an unfamiliar "acronym" you can
impress some naive people with a jargon word, but to a skeptic.

To me, the frequent use of acronyms only pretend to impress naive gullible
people.

Eri

[Alan Kleinman MD PhD]

We have mathematically incompetent bunglers like John and we have mathematically competent (at least you admit to taking a graduate level course in probability theory) bunglers like you. So let's see Rosenhouse prove that rmns in not simply a set of nested binomial problems linked by the multiplication rule of probabilities.

>
> However there is an awful lot of material in it and I would like
> to do a rather thorough and well thought out summary so it will
> take me a little time to get to it. It is worth far more than a
> quick "here are one or two highlights." So it will take me a day
> or two. In the meantime, anyone else with good library access is
> welcome to pipe in.

I doubt Rosenhouse would ever join in this debate. rmns is too elementary of a stochastic process for him to waste his time. I think you will only find those who think that doubling population size doubles the probability of beneficial mutation occurring will support your argument.

[John Harshman]

I don't think you have any clue about what evidence would be necessary
or sufficient to show relatedness. I doubt you have ever thought about
it for more than the time it took you to write that paragraph. All you
appear to have is pride in your ignorance.

How exactly would you look for a MRCA? Fossils? You reject those. Among
living populations? But the MRCA was a long time ago; that population is
dead. No, that demand is just an excuse for you to reject the evidence
we do have.

And so is your apparent demand for complete genome sequences.

And of course you reject the main mechanism of genetic transformation,
if we are considering sheer prevalence in the bulk of the genome, which
is drift. Yet another excuse.

[John Harshman]

Actually, we have pretty clear fossil clues. When is the last time you
looked at the literature? You radically underestimate what we know and
what we can conclude from it.

[Alan Kleinman MD PhD]

I don't have to do the retrospective mathematics of genetic relatedness, Charles Brenner can do that. And he would have to be crazy to give you any support in your argument. Why would he want to undermine his own work? I'll do the prospective mathematics of rmns, a mechanism of genetic transformation. You do know what that is, that's what you ignore when drawing your clades.

>
> How exactly would you look for a MRCA? Fossils? You reject those. Among
> living populations? But the MRCA was a long time ago; that population is
> dead. No, that demand is just an excuse for you to reject the evidence
> we do have.

John, I reject the stories you make up about fossils just like I reject tea leaf readers for telling us the future. You don't understand how rmns works in todays' populations, why should I believe you or any other evolutionist when you claim rmns can transform reptiles into birds; that population is dead.

>
> And so is your apparent demand for complete genome sequences.

You can't get the complete genomes for polar and brown bears? Last I heard, we still have polar and brown bears.

>
> And of course you reject the main mechanism of genetic transformation,
> if we are considering sheer prevalence in the bulk of the genome, which
> is drift. Yet another excuse.

Wait a minute!!! Are you claiming that populations which are drifting will transform into birds? Is that any population that's drifting will turn into birds? John, you really have some weird ideas. Have you ever thought about becoming a science fiction writer? Wait another minute, you already are a science fiction writer!

[rsNorman]

Alan Kleinman MD PhD <klei...@sti.net> Wrote in message:

I did say to give me time to compose a response.

But in the meantime you might try to stop simply regurgitating
garbage because it sounds good to you. Doubling population size
does, to a very good approximation, actually double the
probability of a beneficial mutation occurring to at least one
individual in that population. Knowing the conditions under
which the approximation is valid ensures that you only make that
statement when those conditions are met. That is what anybody
with even an elementary knowledge of probability knows. I guess
you are not included in that.

[Alan Kleinman MD PhD]

On Monday, October 24, 2016 at 12:00:03 PM UTC-7, rsNorman wrote:
> Alan Kleinman MD PhD Wrote in message:

How many decades do you want? You have been arguing that rmns transforms reptiles into birds for more than half a century. When are you going to understand the rudimentary probability theory that governs the rmns phenomenon?

>
> But in the meantime you might try to stop simply regurgitating
> garbage because it sounds good to you. Doubling population size
> does, to a very good approximation, actually double the
> probability of a beneficial mutation occurring to at least one
> individual in that population. Knowing the conditions under
> which the approximation is valid ensures that you only make that
> statement when those conditions are met. That is what anybody
> with even an elementary knowledge of probability knows. I guess
> you are not included in that.

Really, doubling the population size doubles the probability that a beneficial mutation will occur is a good approximation? So if the population size is N and the probability of mutation A occurring is P(A)=0.6, then doubling the population to 2N gives a probability of mutation A occurring P(A)=1.2? You really need to rethink your use of linearized equations.
-
And I will continue to regurgitate, spew, rant, spam,... the correct way to understand the basic science and mathematics of random mutation and natural selection. rmns is too important of a phenomenon to be left to science fiction writers.
-
Why not get Rosenhouse to join your argument, he blogs? Let's see if he squirms as much as you. Do you still think that natural selection works by altering natural frequencies of populations? What happened in the primordial soup when there was only the first replicator? How does natural selection work when there is only one replicator?

[John Harshman]

Again, when questioned, you merely retreat to your mantra. I don't think
you have any clue what you mean by "retrospective mathematics of genetic
relatedness".

>> How exactly would you look for a MRCA? Fossils? You reject those. Among
>> living populations? But the MRCA was a long time ago; that population is
>> dead. No, that demand is just an excuse for you to reject the evidence
>> we do have.

> John, I reject the stories you make up about fossils just like I
> reject tea leaf readers for telling us the future. You don't
> understand how rmns works in todays' populations, why should I
> believe you or any other evolutionist when you claim rmns can
> transform reptiles into birds; that population is dead.

And again you ignore the question and retreat to your mantra.

>> And so is your apparent demand for complete genome sequences.

> You can't get the complete genomes for polar and brown bears? Last I heard, we still have polar and brown bears.

Even in the modern age, complete genome sequences are not simple to get.
I realize you have no idea of the necessary effort, but again, you
shouldn't be proud of your ignorance. Fortunately you don't need
complete sequences. Are you familiar with the concept of statistical
sampling?

>> And of course you reject the main mechanism of genetic transformation,
>> if we are considering sheer prevalence in the bulk of the genome, which
>> is drift. Yet another excuse.

> Wait a minute!!! Are you claiming that populations which are drifting
> will transform into birds? Is that any population that's drifting
> will turn into birds? John, you really have some weird ideas. Have
> you ever thought about becoming a science fiction writer? Wait
> another minute, you already are a science fiction writer!

Hiding your ignorance with jokes doesn't actually hide your ignorance.
You also seem to have forgotten that we were talking about bears, not
birds, and about whole genomes, not phenotypes. That's probably because
your obsessions keep pulling you away from any other subject.

[Alan Kleinman MD PhD]

It's not my job to speculate if polar and brown bears are related. Now if you tell us what that selection pressure is which transforms reptiles into birds, that is your job since that is your claim.

>
> >> And so is your apparent demand for complete genome sequences.
>
> > You can't get the complete genomes for polar and brown bears? Last I heard, we still have polar and brown bears.
>
> Even in the modern age, complete genome sequences are not simple to get.
> I realize you have no idea of the necessary effort, but again, you
> shouldn't be proud of your ignorance. Fortunately you don't need
> complete sequences. Are you familiar with the concept of statistical
> sampling?

So not only are you in the math is hard crowd, you are also in the science is hard crowd. It is much easier to speculate, nothing to measure, nothing to prove. So what do you know about statistical sampling? Statistics is based in the principles of probability theory which you know nothing. Give us an example of biased sampling.

>
> >> And of course you reject the main mechanism of genetic transformation,
> >> if we are considering sheer prevalence in the bulk of the genome, which
> >> is drift. Yet another excuse.
>
> > Wait a minute!!! Are you claiming that populations which are drifting
> > will transform into birds? Is that any population that's drifting
> > will turn into birds? John, you really have some weird ideas. Have
> > you ever thought about becoming a science fiction writer? Wait
> > another minute, you already are a science fiction writer!
>
> Hiding your ignorance with jokes doesn't actually hide your ignorance.
> You also seem to have forgotten that we were talking about bears, not
> birds, and about whole genomes, not phenotypes. That's probably because
> your obsessions keep pulling you away from any other subject.

This thread is about mathematics and "anti-evolutionism". So if you want to to the mathematics of polar and brown bear relatedness, be my guest. My position on this subject is that evolution does occur but the mathematics of rmns does not support the theory of evolution(ism).

[John Harshman]

So it isn't your job to do the work, just to tell me how to do it. No,
you don't get to do that. I know how to test phylogenetic hypotheses,
and it doesn't involve figuring out selection pressure.

>>>> And so is your apparent demand for complete genome sequences.
>>
>>> You can't get the complete genomes for polar and brown bears? Last I heard, we still have polar and brown bears.
>>
>> Even in the modern age, complete genome sequences are not simple to get.
>> I realize you have no idea of the necessary effort, but again, you
>> shouldn't be proud of your ignorance. Fortunately you don't need
>> complete sequences. Are you familiar with the concept of statistical
>> sampling?

> So not only are you in the math is hard crowd, you are also in the
> science is hard crowd. It is much easier to speculate, nothing to
> measure, nothing to prove. So what do you know about statistical
> sampling? Statistics is based in the principles of probability theory
> which you know nothing. Give us an example of biased sampling.

I'm going to take that as a "yes" to my question. So, if you know about
statistical sampling, why are you claiming we have to compare whole
genomes rather than sampling those genomes? Do you have any evidence
that existing sampling is biased? Do you even know what existing
sampling consists of for any phylogenetic question you care to name?

Again, being proud of your ignorance is not a valid argument.

>>>> And of course you reject the main mechanism of genetic transformation,
>>>> if we are considering sheer prevalence in the bulk of the genome, which
>>>> is drift. Yet another excuse.
>>
>>> Wait a minute!!! Are you claiming that populations which are drifting
>>> will transform into birds? Is that any population that's drifting
>>> will turn into birds? John, you really have some weird ideas. Have
>>> you ever thought about becoming a science fiction writer? Wait
>>> another minute, you already are a science fiction writer!
>>
>> Hiding your ignorance with jokes doesn't actually hide your ignorance.
>> You also seem to have forgotten that we were talking about bears, not
>> birds, and about whole genomes, not phenotypes. That's probably because
>> your obsessions keep pulling you away from any other subject.

> This thread is about mathematics and "anti-evolutionism". So if you
> want to to the mathematics of polar and brown bear relatedness, be my
> guest. My position on this subject is that evolution does occur but
> the mathematics of rmns does not support the theory of
> evolution(ism).

And again you deflect. You just say it's spinach and to hell with it.

[AlwaysAskingQuestions]

On Mon, 24 Oct 2016 12:23:14 -0700 (PDT), Alan Kleinman MD PhD
<klei...@sti.net> wrote:

[...]

>Really, doubling the population size doubles the probability that a beneficial mutation will occur is a good approximation? So if the population size is N and the probability of mutation A occurring is P(A)=0.6, then doubling the population to 2N gives a probability of mutation A occurring P(A)=1.2? You really need to rethink your use of linearized equations.

Can you give an example of anyone anywhere stating the probability of
any mutation at 0.6 or anywhere remotely near that?

[AlwaysAskingQuestions]

Eri seems to have these weird notions that if he can't understand
something then nobody can and if he doesn't believe something then it
simply isn't true.

[John Harshman]

All anyone has said is that if the probability is small, then doubling
the population size comes very close to doubling the probability. Even
better, regardless of the probability, it does exactly double the
expected number of mutations, which might be a more reasonable number to
consider.

[Alan Kleinman MD PhD]

I've done the mathematical work of explaining how rmns works and the flaws of population genetics. So now your phylogenetics does not depend on the mechanism of genetic transformation and you don't need to know the selection pressures which would transform reptiles into birds. This is why I compare phylogenetics to tea leaf reading.

>
> >>>> And so is your apparent demand for complete genome sequences.
> >>
> >>> You can't get the complete genomes for polar and brown bears? Last I heard, we still have polar and brown bears.
> >>
> >> Even in the modern age, complete genome sequences are not simple to get.
> >> I realize you have no idea of the necessary effort, but again, you
> >> shouldn't be proud of your ignorance. Fortunately you don't need
> >> complete sequences. Are you familiar with the concept of statistical
> >> sampling?
>
> > So not only are you in the math is hard crowd, you are also in the
> > science is hard crowd. It is much easier to speculate, nothing to
> > measure, nothing to prove. So what do you know about statistical
> > sampling? Statistics is based in the principles of probability theory
> > which you know nothing. Give us an example of biased sampling.
>
> I'm going to take that as a "yes" to my question. So, if you know about
> statistical sampling, why are you claiming we have to compare whole
> genomes rather than sampling those genomes? Do you have any evidence
> that existing sampling is biased? Do you even know what existing
> sampling consists of for any phylogenetic question you care to name?

And I'll take that as a "no", you don't what biased sampling is.

>
> Again, being proud of your ignorance is not a valid argument.

John, have you learned anything in all our discussions? Do you still think that doubling population size doubles the probability of a beneficial mutation occurring?

>
> >>>> And of course you reject the main mechanism of genetic transformation,
> >>>> if we are considering sheer prevalence in the bulk of the genome, which
> >>>> is drift. Yet another excuse.
> >>
> >>> Wait a minute!!! Are you claiming that populations which are drifting
> >>> will transform into birds? Is that any population that's drifting
> >>> will turn into birds? John, you really have some weird ideas. Have
> >>> you ever thought about becoming a science fiction writer? Wait
> >>> another minute, you already are a science fiction writer!
> >>
> >> Hiding your ignorance with jokes doesn't actually hide your ignorance.
> >> You also seem to have forgotten that we were talking about bears, not
> >> birds, and about whole genomes, not phenotypes. That's probably because
> >> your obsessions keep pulling you away from any other subject.
>
> > This thread is about mathematics and "anti-evolutionism". So if you
> > want to to the mathematics of polar and brown bear relatedness, be my
> > guest. My position on this subject is that evolution does occur but
> > the mathematics of rmns does not support the theory of
> > evolution(ism).
>
> And again you deflect. You just say it's spinach and to hell with it.

Nobody is stopping you from doing the mathematics of genetic relatedness of polar and brown bears, I just don't care to get into a speculation contest with someone who makes a living off of speculation.

[Alan Kleinman MD PhD]

On Monday, October 24, 2016 at 1:35:02 PM UTC-7, AlwaysAskingQuestions wrote:
> On Mon, 24 Oct 2016 12:23:14 -0700 (PDT), Alan Kleinman MD PhD

> wrote:
>
> [...]
>
> >Really, doubling the population size doubles the probability that a beneficial mutation will occur is a good approximation? So if the population size is N and the probability of mutation A occurring is P(A)=0.6, then doubling the population to 2N gives a probability of mutation A occurring P(A)=1.2? You really need to rethink your use of linearized equations.
>
> Can you give an example of anyone anywhere stating the probability of
> any mutation at 0.6 or anywhere remotely near that?

Now don't get the mutation rate confused with the probability of a beneficial mutation occurring. If the population is large enough, the probability of at least one member getting a beneficial mutation will be almost 1. If you double that population size, the probability of at least one member getting a beneficial mutation will be slightly higher but still an itsy bit less than 1.

[John Harshman]

I grow bored.

>>>>>> And so is your apparent demand for complete genome sequences.
>>>>
>>>>> You can't get the complete genomes for polar and brown bears? Last I heard, we still have polar and brown bears.
>>>>
>>>> Even in the modern age, complete genome sequences are not simple to get.
>>>> I realize you have no idea of the necessary effort, but again, you
>>>> shouldn't be proud of your ignorance. Fortunately you don't need
>>>> complete sequences. Are you familiar with the concept of statistical
>>>> sampling?
>>
>>> So not only are you in the math is hard crowd, you are also in the
>>> science is hard crowd. It is much easier to speculate, nothing to
>>> measure, nothing to prove. So what do you know about statistical
>>> sampling? Statistics is based in the principles of probability theory
>>> which you know nothing. Give us an example of biased sampling.
>>
>> I'm going to take that as a "yes" to my question. So, if you know about
>> statistical sampling, why are you claiming we have to compare whole
>> genomes rather than sampling those genomes? Do you have any evidence
>> that existing sampling is biased? Do you even know what existing
>> sampling consists of for any phylogenetic question you care to name?
> And I'll take that as a "no", you don't what biased sampling is.
>>
>> Again, being proud of your ignorance is not a valid argument.
> John, have you learned anything in all our discussions? Do you still
> think that doubling population size doubles the probability of a
> beneficial mutation occurring?

I have indeed learned nothing from you, since you have nothing to teach.
Nor did I ever think that doubling population size doubles the
probability of a mutation, except as a good approximation if the
mutation rate is small. Isn't the expected number of mutations a better
figure anyway? Do you even consider the probability of a mutation
occurring two or more times?

>>>>>> And of course you reject the main mechanism of genetic transformation,
>>>>>> if we are considering sheer prevalence in the bulk of the genome, which
>>>>>> is drift. Yet another excuse.
>>>>
>>>>> Wait a minute!!! Are you claiming that populations which are drifting
>>>>> will transform into birds? Is that any population that's drifting
>>>>> will turn into birds? John, you really have some weird ideas. Have
>>>>> you ever thought about becoming a science fiction writer? Wait
>>>>> another minute, you already are a science fiction writer!
>>>>
>>>> Hiding your ignorance with jokes doesn't actually hide your ignorance.
>>>> You also seem to have forgotten that we were talking about bears, not
>>>> birds, and about whole genomes, not phenotypes. That's probably because
>>>> your obsessions keep pulling you away from any other subject.
>>
>>> This thread is about mathematics and "anti-evolutionism". So if you
>>> want to to the mathematics of polar and brown bear relatedness, be my
>>> guest. My position on this subject is that evolution does occur but
>>> the mathematics of rmns does not support the theory of
>>> evolution(ism).
>>
>> And again you deflect. You just say it's spinach and to hell with it.

> Nobody is stopping you from doing the mathematics of genetic
> relatedness of polar and brown bears, I just don't care to get into a
> speculation contest with someone who makes a living off of
> speculation.

Been done, so I don't have to. You think it's speculation, but that's
because you know nothing about it.

Here, for example:
https://www.ncbi.nlm.nih.gov/pubmed/24477675

[Alan Kleinman MD PhD]

On Monday, October 24, 2016 at 1:45:03 PM UTC-7, John Harshman wrote:
> On 10/24/16 1:34 PM, AlwaysAskingQuestions wrote:
> > On Mon, 24 Oct 2016 12:23:14 -0700 (PDT), Alan Kleinman MD PhD

> > wrote:
> >
> > [...]
> >
> >> Really, doubling the population size doubles the probability that a beneficial mutation will occur is a good approximation? So if the population size is N and the probability of mutation A occurring is P(A)=0.6, then doubling the population to 2N gives a probability of mutation A occurring P(A)=1.2? You really need to rethink your use of linearized equations.
> >
> > Can you give an example of anyone anywhere stating the probability of
> > any mutation at 0.6 or anywhere remotely near that?
> >
> All anyone has said is that if the probability is small, then doubling
> the population size comes very close to doubling the probability. Even
> better, regardless of the probability, it does exactly double the
> expected number of mutations, which might be a more reasonable number to
> consider.

John, you should do this exercise. Take the correct equation which calculates the probability of a beneficial mutation occurring, put the equation into a spreadsheet and plot out the equation. You will find that this is a highly non-linear equation. And the expected number of members who get beneficial mutations is totally unimportant, it is the first member to get that beneficial mutation which is important because amplification of that variant by replication will be much, much more important in the amplification process than any new members created by mutation.

[John Harshman]

On 10/24/16 2:02 PM, Alan Kleinman MD PhD wrote:
> On Monday, October 24, 2016 at 1:45:03 PM UTC-7, John Harshman wrote:
>> On 10/24/16 1:34 PM, AlwaysAskingQuestions wrote:
>>> On Mon, 24 Oct 2016 12:23:14 -0700 (PDT), Alan Kleinman MD PhD
>>> wrote:
>>>
>>> [...]
>>>
>>>> Really, doubling the population size doubles the probability that a beneficial mutation will occur is a good approximation? So if the population size is N and the probability of mutation A occurring is P(A)=0.6, then doubling the population to 2N gives a probability of mutation A occurring P(A)=1.2? You really need to rethink your use of linearized equations.
>>>
>>> Can you give an example of anyone anywhere stating the probability of
>>> any mutation at 0.6 or anywhere remotely near that?
>>>
>> All anyone has said is that if the probability is small, then doubling
>> the population size comes very close to doubling the probability. Even
>> better, regardless of the probability, it does exactly double the
>> expected number of mutations, which might be a more reasonable number to
>> consider.

> John, you should do this exercise. Take the correct equation which
> calculates the probability of a beneficial mutation occurring, put
> the equation into a spreadsheet and plot out the equation. You will
> find that this is a highly non-linear equation.

No need. I know how it works. You seem to think that you invented 1 -
(1-p)^n. You did not.

> And the expected
> number of members who get beneficial mutations is totally
> unimportant, it is the first member to get that beneficial mutation
> which is important because amplification of that variant by
> replication will be much, much more important in the amplification
> process than any new members created by mutation.

Why would that be? If two mutations happen, won't amplification be twice
as fast? Of course you don't consider time, do you? You don't even
consider amplification. You just assume it happens.

[Alan Kleinman MD PhD]

Now don't fall asleep in class.

Doesn't surprise me that polar bears and brown bears are related. It's those clades in that paper which show cats, dogs, polecats and bears all coming from a common ancestor. At least they aren't showing birds and reptiles in those clades.

[Alan Kleinman MD PhD]

On Monday, October 24, 2016 at 2:15:02 PM UTC-7, John Harshman wrote:
> On 10/24/16 2:02 PM, Alan Kleinman MD PhD wrote:
> > On Monday, October 24, 2016 at 1:45:03 PM UTC-7, John Harshman wrote:
> >> On 10/24/16 1:34 PM, AlwaysAskingQuestions wrote:
> >>> On Mon, 24 Oct 2016 12:23:14 -0700 (PDT), Alan Kleinman MD PhD
> >>> wrote:
> >>>
> >>> [...]
> >>>
> >>>> Really, doubling the population size doubles the probability that a beneficial mutation will occur is a good approximation? So if the population size is N and the probability of mutation A occurring is P(A)=0.6, then doubling the population to 2N gives a probability of mutation A occurring P(A)=1.2? You really need to rethink your use of linearized equations.
> >>>
> >>> Can you give an example of anyone anywhere stating the probability of
> >>> any mutation at 0.6 or anywhere remotely near that?
> >>>
> >> All anyone has said is that if the probability is small, then doubling
> >> the population size comes very close to doubling the probability. Even
> >> better, regardless of the probability, it does exactly double the
> >> expected number of mutations, which might be a more reasonable number to
> >> consider.
>
> > John, you should do this exercise. Take the correct equation which
> > calculates the probability of a beneficial mutation occurring, put
> > the equation into a spreadsheet and plot out the equation. You will
> > find that this is a highly non-linear equation.
>
> No need. I know how it works. You seem to think that you invented 1 -
> (1-p)^n. You did not.

Of course, I didn't invent this formula, I first saw this formula in elementary school. But the mathematically incompetent don't investigate the behavior of equations. They linearize them because the math is too hard. What I did do is show how this formula is linked with other similar formulas like this by the multiplication rule. I do admit this mathematics is quite rudimentary but it is the correct way to do the mathematics of rmns.

>
> > And the expected
> > number of members who get beneficial mutations is totally
> > unimportant, it is the first member to get that beneficial mutation
> > which is important because amplification of that variant by
> > replication will be much, much more important in the amplification
> > process than any new members created by mutation.
>
> Why would that be? If two mutations happen, won't amplification be twice
> as fast? Of course you don't consider time, do you? You don't even
> consider amplification. You just assume it happens.

Of course, amplification would not occur twice as fast. I'll try and do this mathematics nice and slow so even you will understand.
.
Consider the ideal case where every member is able to replicate and therefore double every generation successfully. And then let's say instead of one member with a beneficial mutation, you start with two members with beneficial mutations. What you have done is reduce the number of generations of doubling by 1. But to reduce the generations of doubling again, you need to start with four members with beneficial mutations. And then to reduce the generations of doubling again, you need to start with eight members who get beneficial mutations.
.
Doubling (generations) time is only very, very slightly reduced when you start with more than a single member with a beneficial mutation. If you need e9 members for there to be a reasonable probability of the next beneficial mutation, here's a table which gives "n" initial members with the beneficial mutation and the number of generations "Ng" necessary to achieve a population size of e9
n Ng
1 30
2 29
4 28
8 27
16 26
32 25
64 24
Do I need to do more or do you see the pattern? Be fruitful and multiply. I hope this doesn't bore you John and you have learned something.

[Bill Rogers]

On Monday, October 24, 2016 at 5:55:03 PM UTC-4, Alan Kleinman MD PhD wrote:
> On Monday, October 24, 2016 at 2:15:02 PM UTC-7, John Harshman wrote:

<snip>

> > No need. I know how it works. You seem to think that you invented 1 -
> > (1-p)^n. You did not.
> Of course, I didn't invent this formula, I first saw this formula in elementary school. But the mathematically incompetent don't investigate the behavior of equations. They linearize them because the math is too hard.

Guffaw. I thought you knew something about physics. Whole areas of physics commonly use the judicious linearization of non-linear equations. Judicious meaning that they, like John, understand enough about the math to know when linearization introduces quantitatively important errors, and when it does not. A good deal of "mathematical competence" in the physical sciences involves knowing when approximations and linearizations are good enough, and when they are not.

[erik simpson]

On Monday, October 24, 2016 at 2:55:03 PM UTC-7, Alan Kleinman MD PhD wrote:
> <...>

Why does anyone continue to respond to this guy?

[Alan Kleinman MD PhD]

Of course, linearization is used in the solution of many physics problems but the smart scientists check out the validity of their linear approximations. And sometimes, there is no way to avoid the non-linearity, you have to solve the problem the hard way and deal with the non-linearity. Have you ever published solutions to mathematical problems where you couldn't get rid of the non-linearity? I doubt it.
.
Are you going to join John and claim that amplification is doubled if you start with 2 members with beneficial mutations? Or perhaps you think that rmns works twice as fast when you have two selection pressures?

[Alan Kleinman MD PhD]

Because I got the basic science and mathematics of rmns right. This mathematics gives guidance in how to deal with drug-resistant infections, less than durable cancer treatment, herbicide resistant weeds, pesticide resistant insects... and it also shows why the theory of evolution is a mathematically irrational belief system.

You won't enjoy this discussion if you are mathematically challenged which includes most evolutionists.

[John Harshman]

There are other papers using similar methods that do. I suppose you
accept the validity of the methods for bears but not for other things,
right?

Now, if brown bears and polar bears are related, how did bears
transform? Polar bears have denser fur than brown bears, white fur, and
a fully carnivorous diet. Did all three transformations happen
sequentially, acting on a single gene each time, or is it possible they
all happened concurrently, acting on multiple genes in each case?

[jillery]

On Mon, 24 Oct 2016 12:23:14 -0700 (PDT), Alan Kleinman MD PhD
<klei...@sti.net> wrote:

>Why not get Rosenhouse to join your argument, he blogs?

Rosenhouse no longer blogs. HTH but I seriously doubt it.

[jillery]

On Mon, 24 Oct 2016 10:43:48 -0700 (PDT), eridanus
<leopoldo...@gmail.com> wrote:

>El lunes, 24 de octubre de 2016, 14:55:02 (UTC+1), Glenn escribió:
>> "jillery" <69jp...@gmail.com> wrote in message news:110s0c9rs5mnftjfg...@4ax.com...

>> > In Jason Rosenhouse's review of "Undeniable", he cites one of his own
>> > papers, which he claims mathematically refutes the mathematical
>> > arguments of IDiots and other evolution-haters:
>> >
>> > <http://link.springer.com/article/10.1007/s11191-015-9801-7>
>> >
>> > From the abstract:
>> >
>> > **********************************
>> > The teaching of evolution in American high schools has long been a
>> > source of controversy. The past decade has seen an important shift in
>> > the rhetoric of anti-evolutionists, toward arguments of a strongly
>> > mathematical character. These mathematical arguments, while different
>> > in their specifics, follow the same general program and rely on the
>> > same underlying model of evolution. We shall discuss the nature and
>> > history of this program and model and describe general reasons for
>> > skepticism with regard to any anti-evolutionary arguments based upon
>> > them. We shall then survey the major arguments used by
>> > anti-evolutionists, to show how our general considerations make it
>> > possible to quickly identify their weakest points.
>> > *********************************
>> >

>> Who is "we"?
>
>"We" is anyone Jillery presumes would think is right his argument.
>
>I can present myself voluntarily for this category of "we".
>
>eri


In your haste to post your gratuitous insults against me, you failed
to notice that it was not me who posted "we", but the person whom I
quoted. That makes your insult not just gratuitous, but stupid.

[Alan Kleinman MD PhD]

On Monday, October 24, 2016 at 3:35:02 PM UTC-7, John Harshman wrote:
> On 10/24/16 2:28 PM, Alan Kleinman MD PhD wrote:
> > On Monday, October 24, 2016 at 2:05:02 PM UTC-7, John Harshman wrote:
> >> On 10/24/16 1:51 PM, Alan Kleinman MD PhD wrote:
>
> >>> Nobody is stopping you from doing the mathematics of genetic
> >>> relatedness of polar and brown bears, I just don't care to get into a
> >>> speculation contest with someone who makes a living off of
> >>> speculation.
> >>
> >> Been done, so I don't have to. You think it's speculation, but that's
> >> because you know nothing about it.
> >>
> >> Here, for example:
> >> https://www.ncbi.nlm.nih.gov/pubmed/24477675
>
> > Doesn't surprise me that polar bears and brown bears are related.
> > It's those clades in that paper which show cats, dogs, polecats and
> > bears all coming from a common ancestor. At least they aren't showing
> > birds and reptiles in those clades.
>
> There are other papers using similar methods that do. I suppose you
> accept the validity of the methods for bears but not for other things,
> right?

You don't recall the discussion from a few years ago with Charles Brenner when we talked about his mathematics. It is not just a few genetic matches here and there which determine genetic relatedness, there must be large numbers genetic similarity. Peter found the discussion and reposted it recently.

>
> Now, if brown bears and polar bears are related, how did bears
> transform? Polar bears have denser fur than brown bears, white fur, and
> a fully carnivorous diet. Did all three transformations happen
> sequentially, acting on a single gene each time, or is it possible they
> all happened concurrently, acting on multiple genes in each case?

I've never said that you could not have large phenotypic changes based on recombination. But the alleles have to exist in the population before recombination can change the expression of the given alleles. We discussed dog breeding and how recombination can give Great Danes and Chihuahuas.
.
On the other hand, if the alleles don't exist in the gene pool and have to come about by rmns, it will be glacially slow and laborious process to create those new alleles. Even if only a single gene is targeted at a time. If the selection pressure(s) target more than a single gene, forget about it.

[Bill Rogers]

On Monday, October 24, 2016 at 6:20:02 PM UTC-4, Alan Kleinman MD PhD wrote:
> On Monday, October 24, 2016 at 3:05:02 PM UTC-7, Bill Rogers wrote:
> > On Monday, October 24, 2016 at 5:55:03 PM UTC-4, Alan Kleinman MD PhD wrote:
> > > On Monday, October 24, 2016 at 2:15:02 PM UTC-7, John Harshman wrote:
> > <snip>
> > > > No need. I know how it works. You seem to think that you invented 1 -
> > > > (1-p)^n. You did not.
> > > Of course, I didn't invent this formula, I first saw this formula in elementary school. But the mathematically incompetent don't investigate the behavior of equations. They linearize them because the math is too hard.
> >
> > Guffaw. I thought you knew something about physics. Whole areas of physics commonly use the judicious linearization of non-linear equations. Judicious meaning that they, like John, understand enough about the math to know when linearization introduces quantitatively important errors, and when it does not. A good deal of "mathematical competence" in the physical sciences involves knowing when approximations and linearizations are good enough, and when they are not.
> Of course, linearization is used in the solution of many physics problems but the smart scientists check out the validity of their linear approximations. And sometimes, there is no way to avoid the non-linearity, you have to solve the problem the hard way and deal with the non-linearity. Have you ever published solutions to mathematical problems where you couldn't get rid of the non-linearity? I doubt it.

http://jid.oxfordjournals.org/content/193/3/467.long

and

http://repository.unhas.ac.id/bitstream/handle/123456789/9281/A%20MODEL%20FOR%20TRANSMISSION%20OF%20PARTIAL%20RESISTANCE%20TO.pdf?sequence=1

> .
> Are you going to join John and claim that amplification is doubled if you start with 2 members with beneficial mutations? Or perhaps you think that rmns works twice as fast when you have two selection pressures?

What I will say is that for np<<1, (1-p)^n is well approximated by 1-np.

[Alan Kleinman MD PhD]

On Monday, October 24, 2016 at 3:50:02 PM UTC-7, jillery wrote:
> On Mon, 24 Oct 2016 12:23:14 -0700 (PDT), Alan Kleinman MD PhD

> wrote:
>
> >Why not get Rosenhouse to join your argument, he blogs?
>
>
> Rosenhouse no longer blogs. HTH but I seriously doubt it.

I guess we'll have to depend on Norman to defend Rosenhouse's claims. Anyway, I'm not defending intelligent design, I'm explaining rmns and why the theory of evolution is a mathematical belief system.

[John Harshman]

I don't actually recall anything about genetic relatedness, but I doubt
he was talking about anything like what you suppose.

>> Now, if brown bears and polar bears are related, how did bears
>> transform? Polar bears have denser fur than brown bears, white fur, and
>> a fully carnivorous diet. Did all three transformations happen
>> sequentially, acting on a single gene each time, or is it possible they
>> all happened concurrently, acting on multiple genes in each case?

> I've never said that you could not have large phenotypic changes
> based on recombination. But the alleles have to exist in the
> population before recombination can change the expression of the
> given alleles. We discussed dog breeding and how recombination can
> give Great Danes and Chihuahuas.

I think you're using words whose meaning you don't know again, like
"expression". I doubt you can get from brown bears to polar bears with
recombination of existing alleles. If that were so, polar bears would
presumably not have any alleles not present in brown bears.

> On the other hand, if the alleles don't exist in the gene pool and
> have to come about by rmns, it will be glacially slow and laborious
> process to create those new alleles. Even if only a single gene is
> targeted at a time. If the selection pressure(s) target more than a
> single gene, forget about it.

The polar bears would seem to contradict your claims here, based on the
evidence of transformation in multiple characters.

[Alan Kleinman MD PhD]

On Monday, October 24, 2016 at 3:55:02 PM UTC-7, Bill Rogers wrote:
> On Monday, October 24, 2016 at 6:20:02 PM UTC-4, Alan Kleinman MD PhD wrote:
> > On Monday, October 24, 2016 at 3:05:02 PM UTC-7, Bill Rogers wrote:
> > > On Monday, October 24, 2016 at 5:55:03 PM UTC-4, Alan Kleinman MD PhD wrote:
> > > > On Monday, October 24, 2016 at 2:15:02 PM UTC-7, John Harshman wrote:
> > > <snip>
> > > > > No need. I know how it works. You seem to think that you invented 1 -
> > > > > (1-p)^n. You did not.
> > > > Of course, I didn't invent this formula, I first saw this formula in elementary school. But the mathematically incompetent don't investigate the behavior of equations. They linearize them because the math is too hard.
> > >
> > > Guffaw. I thought you knew something about physics. Whole areas of physics commonly use the judicious linearization of non-linear equations. Judicious meaning that they, like John, understand enough about the math to know when linearization introduces quantitatively important errors, and when it does not. A good deal of "mathematical competence" in the physical sciences involves knowing when approximations and linearizations are good enough, and when they are not.
> > Of course, linearization is used in the solution of many physics problems but the smart scientists check out the validity of their linear approximations. And sometimes, there is no way to avoid the non-linearity, you have to solve the problem the hard way and deal with the non-linearity. Have you ever published solutions to mathematical problems where you couldn't get rid of the non-linearity? I doubt it.
>
> http://jid.oxfordjournals.org/content/193/3/467.long
>
> and
>
> http://repository.unhas.ac.id/bitstream/handle/123456789/9281/A%20MODEL%20FOR%20TRANSMISSION%20OF%20PARTIAL%20RESISTANCE%20TO.pdf?sequence=1
>

You show me yours, I'll show you mine:
https://www.ncbi.nlm.nih.gov/pubmed/6632825
http://onlinelibrary.wiley.com/doi/10.1002/aic.690260516/full
and I worked on many other non-linear problems when I worked as an engineer and taught engineering at the undergraduate and graduate levels before I decided to go to medical school. I have not forgotten how to do a mathematics problem, I just hadn't done any until I decided to look at the physics and mathematics of rmns and random recombination.

> > .
> > Are you going to join John and claim that amplification is doubled if you start with 2 members with beneficial mutations? Or perhaps you think that rmns works twice as fast when you have two selection pressures?
>
> What I will say is that for np<<1, (1-p)^n is well approximated by 1-np.

So what, I do the problem without the approximation, the math works correctly for all values of n and p. And starting with 2 or more members with beneficial mutations rather than 1 has little effect on the number of generations for amplification and of course, rmns doesn't work twice as fast when the population is evolving to multiple simultaneous selection pressures.

[J. J. Lodder]

Glenn <g...@invalid.invalid> wrote:

> "jillery" <69jp...@gmail.com> wrote in message news:110s0c9rs5mnftjfgahc0g3r1
2s9i...@4ax.com...

> > In Jason Rosenhouse's review of "Undeniable", he cites one of his own
> > papers, which he claims mathematically refutes the mathematical
> > arguments of IDiots and other evolution-haters:
> >
> > <http://link.springer.com/article/10.1007/s11191-015-9801-7>
> >
> > From the abstract:
> >
> > **********************************
> > The teaching of evolution in American high schools has long been a
> > source of controversy. The past decade has seen an important shift in
> > the rhetoric of anti-evolutionists, toward arguments of a strongly
> > mathematical character. These mathematical arguments, while different
> > in their specifics, follow the same general program and rely on the
> > same underlying model of evolution. We shall discuss the nature and
> > history of this program and model and describe general reasons for
> > skepticism with regard to any anti-evolutionary arguments based upon
> > them. We shall then survey the major arguments used by
> > anti-evolutionists, to show how our general considerations make it
> > possible to quickly identify their weakest points.
> > *********************************
> >
> Who is "we"?

The scientific plural 'we'
should be understood as 'the reader and I'.

Jan

[RonO]

On 10/24/2016 1:15 PM, Alan Kleinman MD PhD wrote:
> On Monday, October 24, 2016 at 10:45:02 AM UTC-7, rsNorman wrote:
>> jillery <69jp...@gmail.com> Wrote in message:
>>> On Mon, 24 Oct 2016 09:17:33 -0400 (EDT), rsNorman
>>> <r_s_n...@comcast.net> wrote:
>>>
>>>> jillery <69jp...@gmail.com> Wrote in message:

>>>>> In Jason Rosenhouse's review of "Undeniable", he cites one of his own
>>>>> papers, which he claims mathematically refutes the mathematical
>>>>> arguments of IDiots and other evolution-haters:
>>>>>
>>>>> <http://link.springer.com/article/10.1007/s11191-015-9801-7>
>>>>>
>>>>> From the abstract:
>>>>>
>>>>> **********************************
>>>>> The teaching of evolution in American high schools has long been a
>>>>> source of controversy. The past decade has seen an important shift in
>>>>> the rhetoric of anti-evolutionists, toward arguments of a strongly
>>>>> mathematical character. These mathematical arguments, while different
>>>>> in their specifics, follow the same general program and rely on the
>>>>> same underlying model of evolution. We shall discuss the nature and
>>>>> history of this program and model and describe general reasons for
>>>>> skepticism with regard to any anti-evolutionary arguments based upon
>>>>> them. We shall then survey the major arguments used by
>>>>> anti-evolutionists, to show how our general considerations make it
>>>>> possible to quickly identify their weakest points.
>>>>> *********************************
>>>>>

>>>>> I am intrigued by the comprehensive reference list he claims. Given
>>>>> that T.O. is occasionally visited by such types, my impression is such
>>>>> a paper would be a useful reference.
>>>>>
>>>>> However, I am uncomfortable shelling out $40 only to find it to be an
>>>>> arcane tome comprehensible only to other mathematicians. If anybody
>>>>> in T.O. has read this paper, will you post an opinion about it,
>>>>> whether it does what it claims to do in an way understandable to those
>>>>> who have only a superficial familiarity with mathematical jargon?
>>>>> --
>>>>

>>>> I now have the paper and it seems quite excellent. It is 17
>>>> pages, not counting the bibliography and I don't have the time
>>>> now to summarize it but I will try to get to it later
>>>> today.
>>>>
>>>> There are several pages devoted to the Wistar Conference as well
>>>> as sections about Dembski's Complex Specified Information and
>>>> Behe's "Edge of Evolution."
>>>>
>>>> The major "mathematical" proof employed by the creationists
>>>> involves, as we already all too well know, the identification of
>>>> a specific target that evolution must hit in order to produce
>>>> what we see. The "proof" then shows that the probability of any
>>>> random search algorithm could not possibly find that target
>>>> because the probability is so minute. I haven't gone deeply
>>>> enough into the paper to see the comments about the problem of
>>>> "creating" information.
>>>>
>>>> Unfortunately I don't see that the author, Jason Rosenhouse, has
>>>> posted the paper on his James Madison University Web site.
>>>> Incidentally, he is a mathematician, not a biologist, but
>>>> interested in ensuring that mathematics is taught and interpreted
>>>> correctly.
>>>
>>>
>>> That's another reason why his paper should be useful, as contrasted to
>>> for example DrDr's spam. Thank you for sharing the above.
>>> --
>>
>> I have now read it thoroughly, but just once. It really is quite
>> excellent and has an awful lot to say about arguments we go
>> through regularly on this forum. In particular, to stay right on
>> post with your reference to Dr Dr material, it even covers this
>> specific argument quite nicely.
> We have mathematically incompetent bunglers like John and we have mathematically competent (at least you admit to taking a graduate level course in probability theory) bunglers like you. So let's see Rosenhouse prove that rmns in not simply a set of nested binomial problems linked by the multiplication rule of probabilities.

Projection is stupid and I don't know why it is so common among IDiots.
It is likely all the defense they have left.

Your own example of multiple antibiotic resistance is a case in point.
You cannot pick a target and calculate the probabilities for "your"
version of what should have happened. You know that "your" version is
not likely, but you also know that there are obviously other means of
evolving the same thing because you can watch it evolve and it has
evolved in the past. Multiple antibiotic resistance is fact. It has
already occurred and we have watched it happen when we add a new antibiotic.

When you know that something can occur by other means you have no
argument. It is just fact that organisms do not have to be resistant to
three different antibiotics at once. Your scenario is useless, and your
argument is obviously bogus.

Talk about mathematical bunglers, you are king. You have no examples
where your impossible events ever had to happen. What does that mean?

What are the facts about antibiotic resistance? What are the facts
about DNA replication? Why are feather keratins related to other
keratins that do other things in the organism? Where are your
impossible events in feather evolution? What good is your mathematics?

Ron Okimoto

>> However there is an awful lot of material in it and I would like
>> to do a rather thorough and well thought out summary so it will
>> take me a little time to get to it. It is worth far more than a
>> quick "here are one or two highlights." So it will take me a day
>> or two. In the meantime, anyone else with good library access is
>> welcome to pipe in.
> I doubt Rosenhouse would ever join in this debate. rmns is too elementary of a stochastic process for him to waste his time. I think you will only find those who think that doubling population size doubles the probability of beneficial mutation occurring will support your argument.
>>
>>
>>
>>
>>
>> --
>>
>>
>> ----Android NewsGroup Reader----
>> http://usenet.sinaapp.com/
>
>

[jillery]

Sight unseen, my impression is Rosenhouse defends Rosenhouse's claims
just fine. Perhaps you should get a copy of his paper for yourself.

In any case, the issue here isn't Rosenhouse's claims, or even
rnorman's claims, but your claims, that the theory of evolution is a
mathematical belief system. Apparently you don't know what you're
talking about.

[Glenn]

"J. J. Lodder" <nos...@de-ster.demon.nl> wrote in message news:1mvn9k0.4rr...@de-ster.xs4all.nl...

As in preaching to the choir.

[Glenn]

"jillery" <69jp...@gmail.com> wrote in message news:av3t0ctcdk9em8af4...@4ax.com...

Mistaking your misattributed quote as your own words is not stupid or gratuitous.
Eradinus has you both pegged to a tee.

[J. J. Lodder]

Glenn <g...@invalid.invalid> wrote:

> "J. J. Lodder" <nos...@de-ster.demon.nl> wrote in message news:1mvn9k0.4rr3j91
lx5...@de-ster.xs4all.nl...

Feel free to feel yourself excluded,

Jan

[Glenn]

"J. J. Lodder" <nos...@de-ster.demon.nl> wrote in message news:1mvohqw.167ojnjojujtqN%nos...@de-ster.demon.nl...

You're so magnanimous.

[jillery]

On Tue, 25 Oct 2016 04:55:52 -0700, "Glenn" <g...@invalid.invalid>
wrote:

Big words coming from someone who doesn't know who "we" is.

>Eradinus has you both pegged to a tee.

Thanks for sharing.

[Alan Kleinman MD PhD]

Ron, I'm going to explain this so that even the mathematically incompetent can understand this. Multi-drug resistance occurs most commonly when single-drug therapy is used in a sequential manner. When the first drug fails, a second drug is used, when the second drug fails, on to the third drug and so on. This is how MRSA came about. Now multi-drug therapy can still lead to resistant variants but it requires very large populations. The populations must be large enough for there to be a reasonable probability that there are members with beneficial mutations to each of the drugs used. Each additional drug requires a much, much larger population. This is why 3 drug therapy is required for the treatment of HIV and why Bill Rogers saw the emergence of resistance when only 2 drugs where used to treat Malaria which can achieve huge populations. If you want to understand the mathematics, read my peer reviewed and published papers on rmns. And also learn that rmns can't cause feathers to grow on reptiles.
<snip>

[Alan Kleinman MD PhD]

On Tuesday, October 25, 2016 at 4:40:03 AM UTC-7, jillery wrote:
> On Mon, 24 Oct 2016 15:56:33 -0700 (PDT), Alan Kleinman MD PhD

> wrote:
>
> >On Monday, October 24, 2016 at 3:50:02 PM UTC-7, jillery wrote:
> >> On Mon, 24 Oct 2016 12:23:14 -0700 (PDT), Alan Kleinman MD PhD
> >> wrote:
> >>
> >> >Why not get Rosenhouse to join your argument, he blogs?
> >>
> >>
> >> Rosenhouse no longer blogs. HTH but I seriously doubt it.
> >I guess we'll have to depend on Norman to defend Rosenhouse's claims. Anyway, I'm not defending intelligent design, I'm explaining rmns and why the theory of evolution is a mathematical belief system.
>
>
> Sight unseen, my impression is Rosenhouse defends Rosenhouse's claims
> just fine. Perhaps you should get a copy of his paper for yourself.

I'm not interested in defending intelligent design, I'd much rather do the mathematics of rmns which explains how drug resistance occurs and cancer treatments fail and incidentally also shows why the theory of evolution is a mathematically irrational belief.

>
> In any case, the issue here isn't Rosenhouse's claims, or even
> rnorman's claims, but your claims, that the theory of evolution is a
> mathematical belief system. Apparently you don't know what you're
> talking about.

The theory of evolution is a mathematically irrational belief system. rmns will not allow reptiles to grow feathers, the multiplication rule of probabilities precludes this.
.
And forgive me, I forgot to thank you for starting a thread on mathematics and evolutionism. Sometimes you hit on and interesting topic.

[John Harshman]

Hey, Alan actually had a point there. This is one case in which his
canned rant was appropriate for a change, up until the last sentence.

[Alan Kleinman MD PhD]

John, do you understand why if two members get the same beneficial mutation that it has no significant effect on amplification? Multiplication works much faster than addition.
.
And anytime you are willing to tell us what the selection pressures are and the targeted genes to transform scales into feathers, we'll, whoops, I'll do the mathematics for you.

[Bill Rogers]

On Tuesday, October 25, 2016 at 10:40:03 AM UTC-4, Alan Kleinman MD PhD wrote:
<snip>

> Ron, I'm going to explain this so that even the mathematically incompetent can understand this. Multi-drug resistance occurs most commonly when single-drug therapy is used in a sequential manner. When the first drug fails, a second drug is used, when the second drug fails, on to the third drug and so on. This is how MRSA came about. Now multi-drug therapy can still lead to resistant variants but it requires very large populations. The populations must be large enough for there to be a reasonable probability that there are members with beneficial mutations to each of the drugs used. Each additional drug requires a much, much larger population. This is why 3 drug therapy is required for the treatment of HIV and why Bill Rogers saw the emergence of resistance when only 2 drugs where used to treat Malaria which can achieve huge populations.

No surprise that you misunderstood my paper. I did not see the "emergence" of drug resistance. I saw the spread of previously existing resistant strains into a new area. There's evidence that the two drug therapy selected for pre-existing resistance over the course of therapy, but no evidence at all that resistance emerged de novo in patients in course of the study. That's all laid out pretty clearly in the paper, so I can only guess that your obsession prevents you from understanding what you read. In the case of malaria, the emergence of multiply resistant strains (which is documented in other papers than the one by me you keep mentioning) is more similar to emergence of multiple resistance following sequential single drug therapies. It's not due to spontaneous double mutants arising in a huge parasite population within single individuals.

[RSNorman]

On Mon, 24 Oct 2016 08:36:51 -0400, jillery <69jp...@gmail.com>
wrote:

I have the paper and it is indeed something that would be of great
interest here. I am responding with this summary of its contents as a
response to jillery's original posting of it in order to eliminate
some of the later irrelevancies in other posts.

For the record, the paper is
On Mathematical Anti-Evolutionism
Jason Rosenhouse
Science & Education
March 2016, Volume 25, Issue 1, pp 95–114
http://link.springer.com/article/10.1007/s11191-015-9801-7

Fair use interpretation of copyright law might allow me to distribute
copies to my colleagues and students for academic study but certainly
does not allow copying it here so I will describe/review it in some
detail. If you have questions about the original, please email me
directly by removing the two underscores in my listed email address.
The full abstract was made available above by jillery (that is legal).

The paper opens with a brief history of mathematical approaches to
"disproving" evolution. This goes back to a 1925 book by WA Williams:
"The Evolution of Man Scientifically Disproved." However most earlier
works before the early 2000's were based on scientific or
philosophical objections to evolution. These include Phillip Johnson,
Michael Behe, William Dembski, and Jonathan Wells. Although Dembski's
works included mathematics, that was not the major subject.

Since 2005 it seems that mathematical objectins have come to the fore.
The major recent anti-evolution works based on mathematical arguments
are cited and a number of references given to debunking the works. It
is possible that mathematic proofs that evolution can't work carries
great weight among the uninitated because of the sophistication and
precision attributed to math. Indeed we scientists often claim that
science "can't actually prove anything" but mathematicians regularly
produce proofs that are incontrovertible and undeniable. So math
carries a special cachet for those who can't follow the details.


It should be noted that this paper does not pretend to be a thorough
cataloging of all the ills of the anti-evolutionists nor a complete
review of all the debunking arguments. However it does do an
excellent job of reviewing many of the more important anti-evolution
works and describes the major flaws on those arguments.

There is a general pattern to the anti-evolution argument based on the
notion of evolution as a "search" through a set or space of possible
alternatives. Existing complex biological structures are specific
points in this space. Mathematics demonstrates that it is extremely
implausible (impossibly small probability) that any naturalistic
process or algorithmic procedure could ever find those target points.

The seach space may be composed of genes, proteins, whole genomes or
phenotypes. It does matter. The same argument is applied: how can
you reach a complex tiny target in the vastness of the space of
unsuccessful or unlivable alternatives? This whole concept suffers
from the problem that human problems such as those in computer science
or its applications has predifined targets that serve our own goals.
Biological evolution, on the other hand, is undirected and explores
genetic space where the only criterion is producing something that
works.

As an alternative, the target may not be an existing biological
structure/organism/species but rather an optimum fitness value. Here
the mathematical or computational model fails because biological
fitness is an incredibly complex result of a large number of
variables, not a simple function defined across the space. Further,
fitness is not predefined but itself "evolves" along with the changing
environment which includes all the living things in it.

There are two major ways of developing the mathematics to disprove
evolution: compute a probability value of reaching the target that is
incredibly small or produce a general principle or theorem to show
that the target is unreachable.

The first, calculation of a probability, is based on combinatorics;
that is, counting the number of possibilities. Four example there are
four bases so a DNA segment n characters long has 4^n possibilities.
Similarly a protein n amino acids long has 20^n possibilities. For
even rather small values of n, these are enormous numbers. Evolution
manages to find a small target in this enormous space, either by
random assembly or by some search strategy (algorithm) that threads
its way through the space until finding the target. Both of these are
easily "proven" to be essentially impossible.

To develop the model with any mathematical rigor, though, you need to
understand the topology and the metric of the space of possibilities.
That means knowing what points are in the "neighborhood" of eacdh
point and also how to measure how far apart two points are. You also
need to know the probability distribution over the space. The simple
fact is that in real life "protein space is vast, but its probability
distribution is hi8ghly non-uniform. Natural selection has the
consequence that enormous swaths of the space receive a probability
very close to zero, while the probability of the regions of
functionality will be relatively large." (quoted from the paper). A
second simple fact is that even though "every modern endpoint of
evolution is highly improbable, but that this by itself does not count
against the theory." This quote is cited as being developed at length
by Sober.)

The algorithmic search strategy, finding a pathway through the space
to the target, But the topology of the search space is unspecified. To
demonstrate a failure in random walks through the space (hill climbing
algorithms, for example) requires that functional points (proteins,
genomes) are highly isolated so that evolution would have to cross
vast non-functional regions to move. We do know that neutral amino
acid substitutions and neutral mutations are common and therefore
around each functional point there is a rather large swatch of
functionality. Search arguments must address these issues properly or
else are meaningless.

Rosenhouse then turns his attention to the now infamous 1966 Wistar
Conference as serving as the foundation for the framework of
subsequent developments. There were two main presentations, Murray
Eden, a EE from MIT, and Marcel-Paul Schutzenberger, a mathematician
from U. Paris.

Eden's argument was based on naive combinatorics, counting
possibilities and calculating probabilities. The space of possible
proteins is vast: there are some 10^325 possible proteins of length
250 or less but the total number of protein molecules that could have
ever existed is only about 10^52. So how could evolution have
"explored" any significant portion of that space to arrive at the
successes we see? Eden could see no mechanistic, naturalistic
constraint to would produce the result. Eden has left out the biology
in his notion of random construction. Once you have abiogenesis, some
form of initial life, then you only need search the protein space in
the vicinity of the starting point. The seach branches out like a
spider-web pattern and "natural selection has the consequence that we
stay on the threads of the web and do not stray into the regions of
non-functional proteins." Denton's book "Evolution: A Theory in
Crisins" and "Meyer's book "Darwin's Doubt" rebroadcast Eden's
argument.

The problem with abiogenesis is somewhat different because it is still
an unsolved problem. Still an awful lot more is known now that was in
1966. In any event, the works under consideration attacking evolution
usually deal with the impossibility of biological evolution following
the initial formation of life. Abiogenesis is a separate topic, as we
try to point out here.

Schutzenberger bases his objections to evolution by comparison to
computer code or formal language (in the mathematical logic sense).
The code is a string of characters that results in a phenotype. Random
typographical changes in computer code destroy the program completely.
The chances of random change producing functional results is
impossibly small. Here, too, the argument ignores the biology.
Changes in a functional protein usually do not "halt the program" but
rather produce a protein with a different or altered function
(including a non-function). And we have decades of subsequent work in
"genetic algorithms" that produce very successful computer code based
on exactly the procedures that are claimed to make evolution
impossible.

The legacy of the Wistar conference, as Rosenhouse describes it, has
three components. First, evolution is modeled as a combinatorial
process. Second, following Eden, a calculation is made not based on
biological constraints, producing ridiculously small probabilities for
evolutionary success. Third, following Schutzenberger, a general
principle is searched for that denies evolution's plausibility, again
failing to recognize biological constraints.

I have only covered the first eight pages of Rosenhouse's paper. He
continues with five pages on the probability arguments including long
sections on Dembski's "Complex Specified Information" and Behe's "Edge
of Evolution". Then follows three pages on the general principles
argument including a discussion of the Dembski's "No Free Lunch" book
based on the "no free lunch" arguments about search strategy in the
computer science literature by Wolpert ande MacReady. It also
considers the "conservation of information" argument.

I have no idea whether anybody is at all interested in those details
(or even in any of my current summary). So I will leave that to
another day. Sorry, Dr. Dr. Kleinman, you will have to wait. Your
argument is essentially Behe's in "Edge of Evolution" about evolution
of chloroquine resistance in malaria.

The conclusion is actually rather simple and simple minded. The
so-called mathematical disproofs of evolution are based entirely on
unfounded assumptions about how evolution works. These assumptions
are unstated, yet implicit in the models. Given the assumptions, the
models might well be derived correctly in the mathematical sense. But
if the assumptins are false then no proper conclusion can be drawn
from the correct mathematics. And examining and testing the
assumptions can well be done without all the mathematical formalism
piled on top. However the mathematical formalism is so "impressive"
as to completely overshadow the assumptions which are only implicit
and hidden.

As an example I quote: "Behe's 'edge of evolution' calculations were
based on the assumption that certain protein complexes could only
evolve via the occurrence of multiple, simultaneous mutations. This
assumption does all the work in his argument. If the assumption were
true, the challenge to evolution would be clear: a probability
calculation would be unnecessary. Since the assumption is not true, or
is at least ungrounded, the calculation has no value."

In the Wistar conference, one participant wrote "I do really think
that if they [the mathematicians and engineers and computer
scientists] want us to take these things seriously, they have to
present them in a way in which not only do we understand them but in
which they make biological sense." Rosenhouse ends saying "That is a
perfect description of modern mathematical anti-evolutionism."

[This is more than enough for one go. Also I am rather pressed for
time and so forego effective proof-reading and correction of egregious
misphrasings. I will leave that for you.]

[Alan Kleinman MD PhD]

Why would you be so dumb to use drugs where there is already existing drug-resistant variants in the populations you are treating? And why would you use the word "emergence" so many times in your paper? If you read my paper, you would see that I acknowledge the possibility of what you are claiming but went on to explore the possibility that you are actually seeing the de novo evolution of drug resistance. And if you would continue doing the math that you did in med school, you would find that there is a realistic probability that this is exactly what happened in your study.

[Alan Kleinman MD PhD]

To summarize this long and the total lack of any mathematics post is that evolutionists believe that the multiplication rule of probabilities does not apply to biological evolution. This is why evolutionism is a mathematically irrational belief system. Abiogenesis and the theory of evolution, the dumb and dumber of the field of biology.

[Burkhard]

Published with Springer and older than 6 month? Might allow
self-archiving, let's see...

Ahh, yes, indeed:
http://educ.jmu.edu/~rosenhjd/sewell.pdf

:o)

I knew all the meetings in our open access committee would pay off
sometime.

[rsNorman]

Burkhard <b.sc...@ed.ac.uk> Wrote in message:

Thank you very much for that. Now instead of trying to summarize
the rest of it or making you all actually read through my first
go at it I can just say
Read the damn thing for yourself!

It is really worth the read.

[eridanus]

He is hoaxing ignorants with his mathematical bogus jargon.
Eri

[eridanus]

what does mean < Eradinus has you both pegged to a tee.>?
English is not my mother tongue.
eri

[Alan Kleinman MD PhD]

It appears the Rosenhouse doesn't address the multiplication rule of probabilities. At least you recognize the problem and try to find some evidence that mutations aren't random events. The multiplication rule, the reason that hard mathematical scientists are anti-evolutionism. And the empirical evidence justifies this stand.

[rsNorman]

Alan Kleinman MD PhD <klei...@sti.net> Wrote in message:

>> March 2016, Volume 25, Issue 1, pp 95?114

For the record, the last several paragraphs of my post were
written very much with you in mind. The antepenultimate
paragraph is especially appropriate. Read carefully "a
probability calculation would be unnecessary". Also read
carefully "the calculation has no value."

Your mathematics is correct. You argument about the
multiplicative law of probability is correct. It is simply that
the assumptions in your model of evolution do not apply to
evolution generally except in a small number of very specialized
and artificial cases. Those cases are very important in medicine
and other applications requiring extermination of unwanted living
things using a variety of highly toxic chemicals. Those cases
are not at all important in understanding evolution in general
and evolution of lizards to birds in particular.

[Alan Kleinman MD PhD]

Sure it's worth the read to find Rosenhouse's error. Here's where he makes his error:
"Part one is a simple empirical fact. Part two is the realm of chance; the genetic variations exhibited by an organism are random with respect to the needs of that organism. But part three is the antithesis of chance. Natural selection is a lawlike process. It is this aspect of Darwinism that gets left out of the BAI."
What Rosenhouse's blunder is that he neglects the multiplication rule of probabilities and its effect on natural selection. He should have seen this long ago with the success of combination therapy for the treatment of HIV.

[Alan Kleinman MD PhD]

On Tuesday, October 25, 2016 at 10:35:03 AM UTC-7, rsNorman wrote:
> Alan Kleinman MD PhD Wrote in message:

Where is the empirical evidence which supports your claim? What makes you think that the multiplication rule will work differently in nature than it does in the laboratory? It's not just toxins, Lenski's starvation stress experiment performs the same way. What selection pressures exist in your mind that somehow don't invoke the multiplication rule?

[eridanus]

the main way to hoax people with an argument is by way of using some
abstract word that is not explain in detail. Then by using jargon, abstract
words we are not sure of the meaning for a particular case... we can easily
hoax anyone that is easily impressed with jargon, of whatever sort.
Thus, for me to accept the importance of this multiplication that is so
important you must explain what damn is this multiplication with a handful
of examples.
By considering a number of examples, we would see if this multiplication
is worthy of consideration of it is a hoax. I had heard a number of people
using maths to prove any shit whatever. Specially in the field of economics.

In this case, it must be the same circumstance. Anyone that is pissed off
with evolution because of his creationist faith would think the mathematical
argument is good.

I was raised in a catholic religious school since 9 years old till 16. But
when I was like 12 years old, I do not believed in god anymore. Why?
Because it make not any sense to me, that god had put us in this planet
to sing the praises of the god. This gave to me the impression of something
preposterous. Then, the question of "god loves you" resulted absurd
considering the chronic hunger I was suffering. Why an almighty god was
making to suffer hunger? Does god hated me or what?
To me, the question of god became a philosophical problem. And the main
argument was, why god made the universe? Why he made so huge, just to make
some stupid creatures to sing his praises? Then, if god wanted us to sing
his praises why he do not gives sort sort of pleasure, like a light orgasm,
when we were obliged to sing religious hymns? On the other hand, why god
needed that stupid human beings would sing his praises? This would had meant
some shrinking of the power of god. It implied he needed humans. This is
absurd. Then, one day another boy o my age came with the idea, he had heard
in some place, that humans are a evolution from some monkeys. I was a little
shocked for a second and asked him, "how do you know?" He said, "I heard
that to my uncle." He said "if you go to a zoo and watch a chimp, you would
see how similar it is us. Imagine you are a chimp, then your head grows a
little, and you loose all your hair of monkey, and grow up in size 50%, well
you would look like a human. You only need a few more changes and to
develop a memory. Then, you had passed from being a chimp to be a human."
"Can this occur too fast?" I asked him. "No," he said, "it would take some
millions of years." I was thinking about this question, and the most I
thought about the most I believe we had evolved from some monkey. Why?
I could not believe that "a god that loves me would be so sadistic."
When I was living with my aunt, that was a poor woman that sawed clothes
I was not feeling any hunger. If god would had been a weak god, it would
make sense to explain my hunger. He had not any power to give the nuns
enough food to feed the children. But I had heard a lot of times that god
was almighty.

Then, what philosophical problems can I have to believe in evolution?
Even if do not understand in a minimal detail how the evolution works. For
my lack of understanding only means the problem is very complex and we
have only a faint idea.

You cannot have a faint idea why god made the universe, so huge, after an
infinity delay of time. You cannot explain to me, even faintly, why an
almighty good need us to sing his praises. You cannot explain why a loving
almighty god, made me suffer so much hunger, while my aunt that was poor
feed me alright, and I do no suffered hunger.

You cannot reply to all those questions any better that I would explain
how a monkey became a human being. Of course, evolution has some flavor
of being miraculous. For we have problems to explain how things occurred.

Then, evolution is natural, but difficult to explain. Not only because some
cases like a monkey becoming human occurred more than 15 million years ago,
but because we barely can explain in detail why a baby was born blind, or
deaf or with Down syndrome. We have a few ideas, some mutations occurred
here or there, in this chromosome or in other chromosome. But we are yet
unable to explain in detail why this had occurred.
Any way, ask Ron about this question. Perhaps he knows how these sort of
things occur.
Anyway, if we are yet unable to explain in detail why a child is born with
some rare genetic anomaly, how can we pretend to extrapolated from the
highs of our ignorance the future of some mutations applying mathematics.
How can we apply mathematical probabilities to the realm of our ignorance?

Eri

[Alan Kleinman MD PhD]

Here is the perfect example how evolutionists have confused naive school children with their mathematically irrational indoctrination.

[rsNorman]

eridanus <leopoldo...@gmail.com> Wrote in message:

Eri, your skepticism has gotten well out of hand here. I know you
enjoy reveling in how much we don't know and how science has been
wrong in the past so you can't believe what it says today and
that it is all just appeals to authority.

The fact is that we do know an awful lot about mathematics. We do
know an awful lot about science. People trained in mathematics
and in science know how to use both. The "law of multiplication
of probabilities" is elementary probability theory which
absolutely must be applied in the proper circumstances. People
versed in population genetics, the foundation of modern
evolutionary theory since the 1950's, know probability theory.
We also know evolutionary biology. We also know an awful lot
about ecology and molecular biology and physiology and genetics
and development and all divisions of biology. This knowledge of
biology is critical in applying a mathematical model to study it.
A truly major problem of physicists and mathematicians and
computer scientists trying to "do" biology or "fix the serious
problems" biologists have in theorizing is the result of their
not understanding biology.

You, personally, lack a great deal of this education. I do NOT
claim that you lack intelligence or imagination or creativity or
value, just that you were not trained in the details of
mathematics and science. Some of us were. So some of your ideas
about how ignorant we are really are not very accurate.

[eridanus]

It does not make any sense your argument. I was brain washed by the nuns
in a religious boarding school. But I rejected the brain wash for I could
not believe in a sadist god. It made not any sense. But, later when I was
in a zoo, I was then 20 years old, I realized how close were our body
structures were. The chimps only needed some touches, some changes, and
they would had become a sort of close to human beings.
Then, I thought this idea of evolution made sense. Anyway, I never read
the book of Darwin or any other book defending evolution. I do not needed
more arguments. The arguments I developed when I was 12 years old were
basis enough to disbelieve in a god creator, and to accept evolution. I do
not needed farther arguments. Just a little childish philosophy.
I had only read some loose leaves about evolution, sometimes in a newspaper.

Try to present me some philosophy to prove I must believe in god.
As for evolution, I do not need farther arguments. I am totally ignorant
about the details of evolution. But I do not need bogus arguments.
My idea is that we are basically ignorant we we have only a light
understanding of evolution. Then the attacks of creationist asking for
explanations about this matter make not any logical sense.

eri

[eridanus]

I have not any reasons to object to your arguments. Basically I think
that some problems are difficult to solve. And when they are difficult
we can easily get the argument wrong. It is a theoretical argument
that do not pretend to finger concrete arguments

Another problem you do not presented, in your interest to defend
how much science knows, is the argument of Doc Kleinman telling he
has mathematical arguments to prove evolution wrong. This looks to
rather preposterous. For in spite of your arguments about how much
we understand of genetics, I am sort of skeptic. But not totally to
negate any knowledge, but to think we do not know yet enough.

And this do not need farther argumentation. Being an ignorant, I guide
myself by subjective meanings. No by any certainties.
eri

[Alan Kleinman MD PhD]

Eri, I am presenting mathematical and empirical evidence why the theory of evolution is wrong. It requires training and practice to understand these arguments. If you want to try and understand these arguments, watch these videos: https://www.youtube.com/watch?v=uzkc-qNVoOk&list=PLC58778F28211FA19

[Glenn]

"jillery" <69jp...@gmail.com> wrote in message news:a1qu0c9kquri7dsc6...@4ax.com...

We is.

[jillery]

On Tue, 25 Oct 2016 18:07:51 +0100, Burkhard <b.sc...@ed.ac.uk>
wrote:

Thank you for that link. As grateful as I am to Rosenhouse for
writing it, I hope he understands that I need that $40 more than he
does.

[jillery]

Yes, it is. IMO anybody who passed Noor's Coursera course will find
it understandable and informative.

[jillery]

On Tue, 25 Oct 2016 07:44:27 -0700 (PDT), Alan Kleinman MD PhD
<klei...@sti.net> wrote:

>On Tuesday, October 25, 2016 at 4:40:03 AM UTC-7, jillery wrote:
>> On Mon, 24 Oct 2016 15:56:33 -0700 (PDT), Alan Kleinman MD PhD
>> wrote:
>>
>> >On Monday, October 24, 2016 at 3:50:02 PM UTC-7, jillery wrote:
>> >> On Mon, 24 Oct 2016 12:23:14 -0700 (PDT), Alan Kleinman MD PhD
>> >> wrote:
>> >>
>> >> >Why not get Rosenhouse to join your argument, he blogs?
>> >>
>> >>
>> >> Rosenhouse no longer blogs. HTH but I seriously doubt it.
>> >I guess we'll have to depend on Norman to defend Rosenhouse's claims. Anyway, I'm not defending intelligent design, I'm explaining rmns and why the theory of evolution is a mathematical belief system.
>>
>>
>> Sight unseen, my impression is Rosenhouse defends Rosenhouse's claims
>> just fine. Perhaps you should get a copy of his paper for yourself.
>I'm not interested in defending intelligent design, I'd much rather do the mathematics of rmns which explains how drug resistance occurs and cancer treatments fail and incidentally also shows why the theory of evolution is a mathematically irrational belief.

That's not it. From your posts, my impression is all you're
interested in is posting spam.

>> In any case, the issue here isn't Rosenhouse's claims, or even
>> rnorman's claims, but your claims, that the theory of evolution is a
>> mathematical belief system. Apparently you don't know what you're
>> talking about.
>The theory of evolution is a mathematically irrational belief system. rmns will not allow reptiles to grow feathers, the multiplication rule of probabilities precludes this.
>.
>And forgive me, I forgot to thank you for starting a thread on mathematics and evolutionism. Sometimes you hit on and interesting topic.

You're welcome. I wish I could say the same about you.

[Ray Martinez]

Can you please name three of these scientists?

Ray

[Alan Kleinman MD PhD]

On Tuesday, October 25, 2016 at 3:45:03 PM UTC-7, jillery wrote:
> On Tue, 25 Oct 2016 07:44:27 -0700 (PDT), Alan Kleinman MD PhD

> wrote:
>
> >On Tuesday, October 25, 2016 at 4:40:03 AM UTC-7, jillery wrote:
> >> On Mon, 24 Oct 2016 15:56:33 -0700 (PDT), Alan Kleinman MD PhD
> >> wrote:
> >>
> >> >On Monday, October 24, 2016 at 3:50:02 PM UTC-7, jillery wrote:
> >> >> On Mon, 24 Oct 2016 12:23:14 -0700 (PDT), Alan Kleinman MD PhD
> >> >> wrote:
> >> >>
> >> >> >Why not get Rosenhouse to join your argument, he blogs?
> >> >>
> >> >>
> >> >> Rosenhouse no longer blogs. HTH but I seriously doubt it.
> >> >I guess we'll have to depend on Norman to defend Rosenhouse's claims. Anyway, I'm not defending intelligent design, I'm explaining rmns and why the theory of evolution is a mathematical belief system.
> >>
> >>
> >> Sight unseen, my impression is Rosenhouse defends Rosenhouse's claims
> >> just fine. Perhaps you should get a copy of his paper for yourself.
> >I'm not interested in defending intelligent design, I'd much rather do the mathematics of rmns which explains how drug resistance occurs and cancer treatments fail and incidentally also shows why the theory of evolution is a mathematically irrational belief.
>
>
> That's not it. From your posts, my impression is all you're
> interested in is posting spam.

I understand that I'm giving you a message evolutionists don't want to receive.

>
>
> >> In any case, the issue here isn't Rosenhouse's claims, or even
> >> rnorman's claims, but your claims, that the theory of evolution is a
> >> mathematical belief system. Apparently you don't know what you're
> >> talking about.
> >The theory of evolution is a mathematically irrational belief system. rmns will not allow reptiles to grow feathers, the multiplication rule of probabilities precludes this.
> >.
> >And forgive me, I forgot to thank you for starting a thread on mathematics and evolutionism. Sometimes you hit on and interesting topic.
>
>
> You're welcome. I wish I could say the same about you.

I can always count on you to say something sweet. That's what I like about you, you are so predictable, just like rmns is predictable.

[Alan Kleinman MD PhD]

Norman named them when he posted this:

"In the Wistar conference, one participant wrote "I do really think
that if they [the mathematicians and engineers and computer
scientists] want us to take these things seriously, they have to
present them in a way in which not only do we understand them but in
which they make biological sense." Rosenhouse ends saying "That is a
perfect description of modern mathematical anti-evolutionism." "
>

> Ray

[RonO]

On 10/25/2016 9:35 AM, Alan Kleinman MD PhD wrote:

> On Tuesday, October 25, 2016 at 4:25:02 AM UTC-7, Ron O wrote:
>> On 10/24/2016 1:15 PM, Alan Kleinman MD PhD wrote:
>>> On Monday, October 24, 2016 at 10:45:02 AM UTC-7, rsNorman wrote:
>>>> jillery <69jp...@gmail.com> Wrote in message:

>>>>> On Mon, 24 Oct 2016 09:17:33 -0400 (EDT), rsNorman
>>>>> <r_s_n...@comcast.net> wrote:
>>>>>
>>>>>> jillery <69jp...@gmail.com> Wrote in message:

> Ron, I'm going to explain this so that even the mathematically incompetent can understand this. Multi-drug resistance occurs most commonly when single-drug therapy is used in a sequential manner. When the first drug fails, a second drug is used, when the second drug fails, on to the third drug and so on. This is how MRSA came about. Now multi-drug therapy can still lead to resistant variants but it requires very large populations. The populations must be large enough for there to be a reasonable probability that there are members with beneficial mutations to each of the drugs used. Each additional drug requires a much, much larger population. This is why 3 drug therapy is required for the treatment of HIV and why Bill Rogers saw the emergence of resistance when only 2 drugs where used to treat Malaria which can achieve huge populations. If you want to understand the mathematics, read my peer reviewed and published papers on rmns. And also learn that rmns can't cause feathers to grow on reptiles.
> <snip>
>

You shouldn't snip and run from reality and you should stop belittling
your meager understanding of what the math that you are pushing can
actually do with the stupid projection of your own inadequacy. You
likely are not stupid just insanely willfully ignorant.

Snipping out the fact that you are obviously missing with multidrug
resistance is mental incompetence where insanity is an issue. On some
level you might understand that, but you may be too far gone to retain
that ability.

It doesn't matter if you can devise some way to thwart the evolution of
something. You have to claim that your way is the way for your
mathematical argument to mean anything. Just think for a couple of
seconds and it may dawn on you if your willful ignorance would just
crack for a moment.

You are trying to claim that evolution of some type is impossible, but
you have no examples of that type of evolution being needed. Even your
own antibiotic example, as you point out yourself, can evolve by a
different path. You aren't identifying any impossible evolutionary
mechanisms. All you can identify is what is actually known to work.

It doesn't matter if there is some way that it might not happen, what
matters is how it does happen. I cannot state the obvious any more
plainly than that. If you still don't get it, insanity is about your
only excuse.

Ron Okimoto

[Ray Martinez]

Your main argument is mathematical probabilities. You've basically said, over and over, that the multiplication rule invalidates or falsifies cumulative selection as used to explain and conclude for macroevolution. So you're saying mathematics falsifies the theory of evolution. What about the material evidence used to conclude for macroevolution? You seem to have given preeminence to mathematics instead of the material. Do you really think this is a logical and thus valid falsification model?

Ray

[Alan Kleinman MD PhD]

Ray, the mathematics I derived for rmns is based on real, measurable and repeatable examples of rmns. It's not just mathematics, it is mathematics which correlates with every real, measurable and repeatable example of rmns. Why do you think that combination therapy works for the treatment of HIV? It is the multiplication rule of probabilities which does this. The mathematics is correct and the physics is correct.

[Ray Martinez]

So your answer confirms the well know fact that your falsification model grants preeminence to mathematics, namely the multiplication rule of probabilities. But the evolution of primary phenomena, species and higher taxa, grants preeminence to nested hierarchies, the material evidence itself, and the ensuing mathematics is but a representation of the material. So one cannot expect evolutionary biologists to accept a falsification model of primary phenomena based on an external niche in medicine that grants preeminence to mathematics. Just saying. Your model, based solely on the fact that you grant preeminence to a non-material line of evidence, is illogical.

Ray

[Burkhard]

Ray Martinez wrote:
> So your answer confirms the well know fact that your falsification model grants preeminence to mathematics, namely the multiplication rule of probabilities. But the evolution of primary phenomena, species and higher taxa, grants preeminence to nested hierarchies, the material evidence itself, and the ensuing mathematics is but a representation of the material. So one cannot expect evolutionary biologists to accept a falsification model of primary phenomena based on an external niche in medicine that grants preeminence to mathematics. Just saying. Your model, based solely on the fact that you grant preeminence to a non-material line of evidence, is illogical.
>
> Ray
>

That is sort of fascinating. To a degree, I agree with you - if a
mathematical model contradicts what we observe, chances are the model is
simply flawed. (OK, in reality it is more difficult, a back and forth
between the two to find an equilibrium).

But mathematics is just logic plus a few equally self-evident (apart
from maybe the axiom of choice, if you need it) axioms. So his reasoning
and yours are ultimately pretty much identical. Just you call it logic
and he mathematics, but the same thing, really.

[jillery]

I might regret not fulfilling your expectations, if only you expected
them of others as well.

>That's what I like about you, you are so predictable, just like rmns is predictable.

Your spam is a practical certainty.

[Alan Kleinman MD PhD]

On Tuesday, October 25, 2016 at 10:30:04 PM UTC-7, Ray Martinez wrote:
> So your answer confirms the well know fact that your falsification model grants preeminence to mathematics, namely the multiplication rule of probabilities. But the evolution of primary phenomena, species and higher taxa, grants preeminence to nested hierarchies, the material evidence itself, and the ensuing mathematics is but a representation of the material. So one cannot expect evolutionary biologists to accept a falsification model of primary phenomena based on an external niche in medicine that grants preeminence to mathematics. Just saying. Your model, based solely on the fact that you grant preeminence to a non-material line of evidence, is illogical.
>
> Ray

Ray, my model falsifies the theory of evolution by correctly describing how rmns works. Since mutations are random independent events, the joint probability of beneficial mutations occurring is done using the multiplication rule.

[Alan Kleinman MD PhD]

On Tuesday, October 25, 2016 at 11:10:04 PM UTC-7, Burkhard wrote:
> Ray Martinez wrote:
> > So your answer confirms the well know fact that your falsification model grants preeminence to mathematics, namely the multiplication rule of probabilities. But the evolution of primary phenomena, species and higher taxa, grants preeminence to nested hierarchies, the material evidence itself, and the ensuing mathematics is but a representation of the material. So one cannot expect evolutionary biologists to accept a falsification model of primary phenomena based on an external niche in medicine that grants preeminence to mathematics. Just saying. Your model, based solely on the fact that you grant preeminence to a non-material line of evidence, is illogical.
> >
> > Ray
> >
> That is sort of fascinating. To a degree, I agree with you - if a
> mathematical model contradicts what we observe, chances are the model is
> simply flawed. (OK, in reality it is more difficult, a back and forth
> between the two to find an equilibrium).

The mathematics I've presented doesn't contradict any real, measurable and repeatable examples of rmns. It only contradicts your imaginary genetic transformation required for the theory of evolution to work.

>
> But mathematics is just logic plus a few equally self-evident (apart
> from maybe the axiom of choice, if you need it) axioms. So his reasoning
> and yours are ultimately pretty much identical. Just you call it logic
> and he mathematics, but the same thing, really.

Mathematical logic is the most precise form of logic. Every step is measurable and testable.

[rsNorman]

Alan Kleinman MD PhD <klei...@sti.net> Wrote in message:

Dr. Dr. Alan, the probability of one mutation of any kind
happening is about 10^-8. The probability of one individual
getting a dozen mutations of any kind simultaneously has a joint
probability of (10^-8)^12 according to the law of multiplication
of probabilities. That is around 10^-100. So how does it turn
out that every human in existence possesses several dozen
mutations? Your model showing how rmns works proves this to be
impossible. Somehow biology does not work the way your version
of "rmns" does.

Also you should know that introductory biology students are taught
about the Hardy-Weinberg equilibrium in population genetics. If
the relative frequency (yes, that awful concept) of a dominant
allele is p and the relative frequency of the recessive
alternative is q = 1-p then, with random mating, the proportion
(again relative frequency) of phenotypes showing the recessive
trait will be q^2. That is the law of multiplication of
probabilities in action and is part of the teaching of the theory
of evolution. That idea is used to point out that if the
recessive trait is found in more than 25% of the population then
the recessive allele is actually more common in the gene pool
than the dominant allele. It is important to teach that
"recessive" does not mean "rare" or "uncommon." All of
population genetics, all counting of fruit fly genetics
experiments results, is based on the law of multiplication of
probabilities. It is just that in biology we do it
right.

[Alan Kleinman MD PhD]

On Wednesday, October 26, 2016 at 4:25:02 AM UTC-7, jillery wrote:
> On Tue, 25 Oct 2016 17:06:41 -0700 (PDT), Alan Kleinman MD PhD

What should you expect when you tell evolutionists that they have lost contact with reality and present the mathematical and empirical evidence which confirms this?

>
>
> >That's what I like about you, you are so predictable, just like rmns is predictable.
>
>
> Your spam is a practical certainty.

I like to be practical.

[Alan Kleinman MD PhD]

On Wednesday, October 26, 2016 at 7:20:03 AM UTC-7, rsNorman wrote:
> Alan Kleinman MD PhD Wrote in message:

> > On Tuesday, October 25, 2016 at 10:30:04 PM UTC-7, Ray Martinez wrote:
> >> So your answer confirms the well know fact that your falsification model grants preeminence to mathematics, namely the multiplication rule of probabilities. But the evolution of primary phenomena, species and higher taxa, grants preeminence to nested hierarchies, the material evidence itself, and the ensuing mathematics is but a representation of the material. So one cannot expect evolutionary biologists to accept a falsification model of primary phenomena based on an external niche in medicine that grants preeminence to mathematics. Just saying. Your model, based solely on the fact that you grant preeminence to a non-material line of evidence, is illogical.
> >>
> >> Ray
> >
> > Ray, my model falsifies the theory of evolution by correctly describing how rmns works. Since mutations are random independent events, the joint probability of beneficial mutations occurring is done using the multiplication rule.
> >
> >
>
> Dr. Dr. Alan, the probability of one mutation of any kind
> happening is about 10^-8. The probability of one individual
> getting a dozen mutations of any kind simultaneously has a joint
> probability of (10^-8)^12 according to the law of multiplication
> of probabilities. That is around 10^-100. So how does it turn
> out that every human in existence possesses several dozen
> mutations? Your model showing how rmns works proves this to be
> impossible. Somehow biology does not work the way your version
> of "rmns" does.

rmns does not operate on every mutation. If every human shared the same several dozen mutations every generation, then your calculation would be kinda correct. Remember, selection reduces the diversity of populations and mutations increase the diversity of populations.

>
> Also you should know that introductory biology students are taught
> about the Hardy-Weinberg equilibrium in population genetics. If
> the relative frequency (yes, that awful concept) of a dominant
> allele is p and the relative frequency of the recessive
> alternative is q = 1-p then, with random mating, the proportion
> (again relative frequency) of phenotypes showing the recessive
> trait will be q^2. That is the law of multiplication of
> probabilities in action and is part of the teaching of the theory
> of evolution. That idea is used to point out that if the
> recessive trait is found in more than 25% of the population then
> the recessive allele is actually more common in the gene pool
> than the dominant allele. It is important to teach that
> "recessive" does not mean "rare" or "uncommon." All of
> population genetics, all counting of fruit fly genetics
> experiments results, is based on the law of multiplication of
> probabilities. It is just that in biology we do it
> right.

Norman, don't get me wrong. I don't object to using the concept of relative frequencies of variants in populations, that's the correct variable to use when computing random recombination. It's when relative frequencies are used to describe how natural selection works, that's not correct, especially when doing the mathematics of rmns. And there are many instances when the Hardy-Weinberg equilibrium does not give correct frequencies of alleles.
.
Do you want to explain how the Hardy-Weinberg principle applies to rmns? Perhaps you want to take a shot at doing the mathematics for rmns for sexually reproducing replicators. I think you would have to include not only the mathematics of nested binomial probability problems of clonal replicators with the mathematics of the Hardy-Weinberg principle.

[Charles Brenner]

On Monday, October 24, 2016 at 2:00:03 PM UTC-7, Alan Kleinman MD PhD wrote:

> On Monday, October 24, 2016 at 1:35:02 PM UTC-7, AlwaysAskingQuestions wrote:
> > On Mon, 24 Oct 2016 12:23:14 -0700 (PDT), Alan Kleinman MD PhD
> > wrote:
> >

> > [...]
> >
> > >Really, doubling the population size doubles the probability that a beneficial mutation will occur is a good approximation? So if the population size is N and the probability of mutation A occurring is P(A)=0.6, then doubling the population to 2N gives a probability of mutation A occurring P(A)=1.2? You really need to rethink your use of linearized equations.
> >
> > Can you give an example of anyone anywhere stating the probability of
> > any mutation at 0.6 or anywhere remotely near that?
> Now don't get the mutation rate confused with the probability of a beneficial mutation occurring.

Ironically Alan now commits exactly the confusion he warns against.

> If the population is large enough, the probability of at least one member getting a beneficial mutation will be almost 1.

Right -- so that nearly 1 number; could be 0.6 for example; isn't the mutation rate (which would be a very small number), but is "the probability of a beneficial mutation occurring" anywhere in the population.

His earlier argument against using the linear np approximation for 1-(1-p)^n amounts to a population size of n=2 and a per-individual chance of the beneficial mutation arising being p=0.6.

The probability of a beneficial mutation arising is small for each individual, but perhaps large for a large population. That's why the linear approximation might be reasonable. For example if the per-individual probability is 1 per thousand and the population size is 500, the linear approximation gives 50% as the chance the mutation arises in the population as opposed to 40% by the more tedious formula. (So even with this extreme example where np is unrealistically large, the approximation is good enough for biology.)

Aside: In a previous incarnation of these Alan threads 5 or so years ago, I noted that the 1-(1-p)^n trick seems to be the entirety of Alan's claim to mathematical sophistication. Still true.

[Alan Kleinman MD PhD]

On Wednesday, October 26, 2016 at 8:05:03 AM UTC-7, Charles Brenner wrote:
> On Monday, October 24, 2016 at 2:00:03 PM UTC-7, Alan Kleinman MD PhD wrote:
> > On Monday, October 24, 2016 at 1:35:02 PM UTC-7, AlwaysAskingQuestions wrote:
> > > On Mon, 24 Oct 2016 12:23:14 -0700 (PDT), Alan Kleinman MD PhD
> > > wrote:
> > >
> > > [...]
> > >
> > > >Really, doubling the population size doubles the probability that a beneficial mutation will occur is a good approximation? So if the population size is N and the probability of mutation A occurring is P(A)=0.6, then doubling the population to 2N gives a probability of mutation A occurring P(A)=1.2? You really need to rethink your use of linearized equations.
> > >
> > > Can you give an example of anyone anywhere stating the probability of
> > > any mutation at 0.6 or anywhere remotely near that?
> > Now don't get the mutation rate confused with the probability of a beneficial mutation occurring.
>
> Ironically Alan now commits exactly the confusion he warns against.

Hi Charles, are you going to clarify this confusion? Or are you going to start up your circular logic again?

>
> > If the population is large enough, the probability of at least one member getting a beneficial mutation will be almost 1.
>
> Right -- so that nearly 1 number; could be 0.6 for example; isn't the mutation rate (which would be a very small number), but is "the probability of a beneficial mutation occurring" anywhere in the population.

Let's do this calculation with some rigor and start by defining mutation rate: http://www.nature.com/scitable/definition/mutation-rate-131
"Frequency with which a gene changes from the wild-type to a specific mutant; generally expressed as the number of mutations per biological unit (i.e., mutations per cell division, per gamete, or per round of replication)."
That nearly 1 probability of a beneficial mutation occurring could be 0.6 for a lower mutation rate.

>
> His earlier argument against using the linear np approximation for 1-(1-p)^n amounts to a population size of n=2 and a per-individual chance of the beneficial mutation arising being p=0.6.
>
> The probability of a beneficial mutation arising is small for each individual, but perhaps large for a large population. That's why the linear approximation might be reasonable. For example if the per-individual probability is 1 per thousand and the population size is 500, the linear approximation gives 50% as the chance the mutation arises in the population as opposed to 40% by the more tedious formula. (So even with this extreme example where np is unrealistically large, the approximation is good enough for biology.)

In some circumstances, the linearization will work ok, such as when n*p << 1, but with rmns, we are interested to know when the value when n*p goes to 1. So you have to use the correct equation. Let's apply this concept to a real example. Let's say someone is suffering from cancer. And let's say that we can estimate the mutation rate for the cancer cells and the number of cancer cells using radiological and pathological techniques. If 1-(1-p)^n ~= 1, you had better use more than one drug if you want to have a durable treatment. The same calculation applies to infectious diseases, herbicide usage, pesticide usage,... you need to use the correct formula to get an accurate value.

>
> Aside: In a previous incarnation of these Alan threads 5 or so years ago, I noted that the 1-(1-p)^n trick seems to be the entirety of Alan's claim to mathematical sophistication. Still true.

It doesn't take much mathematical sophistication to do the mathematics of rmns correctly. rmns is nothing more than nested binomial probability problems where each of the binomial probability problems are linked by the multiplication rule of probabilities. With all your mathematical sophistication, you didn't see the obvious.

[jillery]

Since you have presented neither mathematical nor empirical evidence
which confirms that evolutionists have lost contact with reality, I
consider your question a rhetorical non sequitur.

And no, repeating your spam doesn't change anything.

[Charles Brenner]

On Wednesday, October 26, 2016 at 8:45:03 AM UTC-7, Alan Kleinman MD PhD wrote:
> On Wednesday, October 26, 2016 at 8:05:03 AM UTC-7, Charles Brenner wrote:
> > On Monday, October 24, 2016 at 2:00:03 PM UTC-7, Alan Kleinman MD PhD wrote:
> > > On Monday, October 24, 2016 at 1:35:02 PM UTC-7, AlwaysAskingQuestions wrote:
> > > > On Mon, 24 Oct 2016 12:23:14 -0700 (PDT), Alan Kleinman MD PhD
> > > > wrote:
> > > >
> > > > [...]
> > > >
> > > > >Really, doubling the population size doubles the probability that a beneficial mutation will occur is a good approximation? So if the population size is N and the probability of mutation A occurring is P(A)=0.6, then doubling the population to 2N gives a probability of mutation A occurring P(A)=1.2? You really need to rethink your use of linearized equations.
> > > >
> > > > Can you give an example of anyone anywhere stating the probability of
> > > > any mutation at 0.6 or anywhere remotely near that?
> > > Now don't get the mutation rate confused with the probability of a beneficial mutation occurring.
> >
> > Ironically Alan now commits exactly the confusion he warns against.
> Hi Charles, are you going to clarify this confusion? Or are you going to start up your circular logic again?
> >
> > > If the population is large enough, the probability of at least one member getting a beneficial mutation will be almost 1.
> >
> > Right -- so that nearly 1 number; could be 0.6 for example; isn't the mutation rate (which would be a very small number), but is "the probability of a beneficial mutation occurring" anywhere in the population.
> Let's do this calculation with some rigor and start by defining mutation rate: http://www.nature.com/scitable/definition/mutation-rate-131
> "Frequency with which a gene changes from the wild-type to a specific mutant; generally expressed as the number of mutations per biological unit (i.e., mutations per cell division, per gamete, or per round of replication)."
> That nearly 1 probability of a beneficial mutation occurring could be 0.6 for a lower mutation rate.
>
> >
> > His earlier argument against using the linear np approximation for 1-(1-p)^n amounts to a population size of n=2 and a per-individual chance of the beneficial mutation arising being p=0.6.
> >
> > The probability of a beneficial mutation arising is small for each individual, but perhaps large for a large population. That's why the linear approximation might be reasonable. For example if the per-individual probability is 1 per thousand and the population size is 500, the linear approximation gives 50% as the chance the mutation arises in the population as opposed to 40% by the more tedious formula. (So even with this extreme example where np is unrealistically large, the approximation is good enough for biology.)
> In some circumstances, the linearization will work ok, such as when n*p << 1,

I just showed that the approximation is adequate even when np=0.5 which is emphatically NOT "<<1."

> but with rmns, we are interested to know when the value when n*p goes to 1.

Nonsense. When np is close to 1, np is essentially a meaningless quantity because after all np comes into our discussion only as an approximation to something (namely to your "exact" formula) and when np is close to 1 you would be correct that the approximation is likely inadequate. (Did you know that when np=1, the chance of the mutation arising with any of n individuals is essentially 0.63...=1-1/e?

Perhaps you meant to say we are interested to know when 1-(1-p)^n goes to 1. Maybe, maybe not -- that gets us back to R Norman's original point that our communication ("our" = Alan on the one hand and those arguing against him on the other) may be at cross purposes. In the context of eradicating an infection, we might be interested in when 1-(1-p)^n is nearly 1. From the perspective of evolution of species in history, criteria of interest are not nearly so extreme.