Re: The Reason the Theory of Evolution is Not True

[Alan Kleinman MD PhD]

On Thursday, August 25, 2016 at 6:11:22 AM UTC-7, Bill Rogers wrote:
> On Thursday, August 25, 2016 at 8:51:23 AM UTC-4, Steady Eddie wrote:
> > On Thursday, 25 August 2016 04:31:23 UTC-6, Bill Rogers wrote:
> > > On Wednesday, August 24, 2016 at 10:16:23 PM UTC-4, Steady Eddie wrote:
> > > > On Wednesday, 24 August 2016 09:01:25 UTC-6, Greg Guarino wrote:
> > > > > On 8/23/2016 6:13 PM, Steady Eddie wrote:
> > > > > >>> Sure evolution occurs and it occurs in a mathematically
> > > > > >>> predictable fashion. It doesn't matter whether the selection
> > > > > >>> pressures are antimicrobial agents, or starvation or thermal
> > > > > >>> stress or any kind of stressor you can imagine. The rmns
> > > > > >>> phenomenon only works efficiently when the stressor targets a
> > > > > >>> single genetic locus at a time. The reason is that rmns must
> > > > > >>> operate in a cycle of beneficial mutation followed by
> > > > > >>> amplification of the mutation so that there are sufficient
> > > > > >>> numbers of members with this beneficial mutation for another
> > > > > >>> beneficial mutation to occur on one of the members.
> > > > > >>>
> > > > > >>> This statement is obviously false.
> > > > >
> > > > > > LOL! You obviously don't understand Dr. K's perfectly clear
> > > > > > statement. He said "The rmns phenomenon only works efficiently when
> > > > > > the stressor targets a single genetic locus at a time."
> > > > >
> > > > > A statement can be both clear, and wrong. Why don't you explain in your
> > > > > own words what you think Kleinman's reasoning is, and why you agree with
> > > > > it.
> > > > > >
> > > > > > He is fully aware, and it goes without saying that real-world
> > > > > > populations are obviously under multiple selective stressors.
> > > > > >
> > > > > > That means that the RMNS phenomenon DOESN'T WORK EFFICIENTLY ENOUGH
> > > > > > FOR MACRO-EVOLUTION TO OCCUR, in the real world of multiple selective
> > > > > > stressors.
> > > > >
> > > > > Apparently all life forms are actually extinct, then.
> > > >
> > > > Astonishingly, all extant life forms exist! That's because they were produced by an intelligent designer.
> > > > What part of that do you not get?
> > > >
> > > > > > What part of that do you not get?
> > > > >
> > > > > This is not our first go-round with Kleinman. Many of us "get" his
> > > > > meaning just fine, but dispute that he is correct, at least as regards
> > > > > scenarios that do not involve lethal agents that kill all but a handful
> > > > > of lucky mutants.
> > > >
> > > > Oh, okay, so any subject of research is acceptable, except "scenarios that ... involve lethal agents that
> > > > kill all but a handful of lucky mutants".
> > > >
> > > > What a coincidence - that's just what Dr. K has...
> > >
> > > The drug resistance scenarios certainly are cases of natural selection. Nobody disputes that. What we keep disputing is the claim that such "scenarios that involve lethal agents that kill all but a handful of lucky mutants" are typical of the selections at work in nature most of the time. His examples are real examples, sure, and examples we all understand. It's perfectly fine and useful to do research on those situations. What is entirely unreasonable is to think that those examples represent the only possible form of natural selection, or even a common form.
> >
> > LOL!
> > The only entirely unreasonable thing here is your refusal to accept the best-studied examples of REAL
> > RMNS at work in the REAL world, just because it doesn't support your philosophy.
>
> Who doesn't accept them? Of course I accept them. What I don't accept is Alan's totally unsupported claim that *all* natural selection involves lethal selection pressures that wipe out every member of a species except for a handful who happen to have lucky mutations. Rare examples, usually from medical treatments, *do* indeed work that way. Most don't.

Bill, study my math carefully. What you will see is that rmns consists of nested binomial probability problems. Lineages must accumulate beneficial mutations to adapt to selection pressures and they do this by a cycle of beneficial mutation/amplification of beneficial mutation in order to improve the probability for the next binomial probability condition. I used your malaria publication as an example but the mathematics is applicable to any selection pressure(s). Unless a particular lineage can amplify (increase in number), the probability that another beneficial mutation will occur on some member of that lineage will be small. The only exception to this rule is if a small size population can replicate for a sufficient number of generations (without an increase in number) then enough trials will occur for there to be a reasonable probability that another beneficial mutation occurs on one of its members.

But feel free to try and give us an example of a selection pressure which requires a population to accumulate mutations in order to adapt that doesn't require amplification. Perhaps you can give us a formula for improving our probability of winning a lottery without buying more tickets.

[Alan Kleinman MD PhD]

Post move from original thread

=Really? Why not explain why Kleinman's argument is applicable to
=selection conditions in general. In your own words. I invited you to do
=so a couple of posts back, but you gave us the universal symbol of
=capitulation instead ("LOL!")

Greg, why don't you give us a single real, measurable and repeatable example of rmns that doesn't obey my math? I may have used real examples to give context to my derivations but the mathematics is quite general.

[Rolf]

"Alan Kleinman MD PhD" <klei...@sti.net> wrote in message
news:173e77b6-833e-4574...@googlegroups.com...

Since evolution is a fact, it is safe to draw the conclusion that evolution
doesn't obey toe the claims of your math. That's easy to see, isn't it? You
don't have evidence on your side, math notwithstanding.

[Steady Eddie]

Test... losing lots of posts

[Steady Eddie]

You're starting to go Jillery on us, Bill.
Dr. K doesn't claim that "*all* natural selection involves lethal selection pressures". He doesn't have to.

Why do you claim that HIV undergoing lethal selection pressures is not a representative example of how
RMNS works in the real world?

[Vincent Maycock]

On Sun, 28 Aug 2016 06:08:43 -0700 (PDT), Steady Eddie
<1914o...@gmail.com> wrote:

>On Thursday, 25 August 2016 17:21:22 UTC-6, Alan Kleinman MD PhD wrote:
>> On Thursday, August 25, 2016 at 6:11:22 AM UTC-7, Bill Rogers wrote:

snip

>> > Who doesn't accept them? Of course I accept them. What I don't accept is Alan's totally unsupported claim that *all* natural selection involves lethal selection pressures that wipe out every member of a species except for a handful who happen to have lucky mutations. Rare examples, usually from medical treatments, *do* indeed work that way. Most don't.
>
>You're starting to go Jillery on us, Bill.
>Dr. K doesn't claim that "*all* natural selection involves lethal selection pressures". He doesn't have to.
>
>Why do you claim that HIV undergoing lethal selection pressures is not a representative example of how
>RMNS works in the real world?

Because that's how combination therapy works; if one selection
pressure (anti-viral drug) doesn't kill the organism, the other drug
in the combination therapy will.

The point is, though, that this is only true if the selection
pressures are lethal; if they're not, no simultaneous beneficial
mutations are required for natural selection to work.

[riskys...@gmail.com]

But he resolutely refuses to show us any "math" that involves any other scenario. Apply his math to an animal population in which there are two "competing" alleles at two different loci. Let's call one pair A1 and A2, the other B1 and B2. In each case the "1" variety is the wild type, and is in the majority. But also in each case, the "2" type confers a selective advantage.

Members with A2/B1 leave 5% more surviving progeny in the next generation than A1/B1. "A1/B2" members leave 2% more surviving progeny than A1/B1. And any A2/B2 members that may be produced have a 10% advantage over A1/B1. The population remains fairly constant.

Alan's argument depends (at least) on the idea that only one beneficial bit of genetics can "amplify" at a time, but he usually also adds in that the population is reduced to a tiny fraction of it's original size with each selective episode.

To be fair, he also means that even if the population is not decimated, only the progeny of the original mutated member will have the first mutation, thus greatly lowering the population that can create the second beneficial mutation. But this is also why he refuses to apply his math to sexual species.

I see no obvious reason why both A2 and B2 in the scenario above cannot amplify simultaneously and, once both have reached significant proportions in the population, we should not expect A2/B2 members to appear, and eventually become the the majority.

> Why do you claim that HIV undergoing lethal selection pressures is not a representative example of how
> RMNS works in the real world?

I doubt that you understand Kleinman's argument; you merely "agree" with it. If you did understand it, you'd have a better chance of being able to understand Bill's objection.

The numbers you choose to use matter. Can electricity be dangerous? Nope. I have dozens AA batteries in my house. Not one of them has ever given me a shock.

[Steve L]

On Sun, 28 Aug 2016 06:08:43 -0700 (PDT), Steady Eddie
<1914o...@gmail.com> wrote:

>Why do you claim that HIV undergoing lethal selection pressures is not a representative example of how
>RMNS works in the real world?

Go to a park or the woods. Every plant or animal you see is under an
uncountable number of selection pressures, yet very few are dead.

[jillery]

On Sun, 28 Aug 2016 06:08:43 -0700 (PDT), Steady Eddie
<1914o...@gmail.com> wrote:

>You're starting to go Jillery on us, Bill.

Yes, I have noticed that Bill often makes the same comments I do, not
that he has ever admitted it. And you don't understand what either
one of us posts, so that's something else he and I have in common.
Thanks for pointing that out.
--
This space is intentionally not blank.

[Steady Eddie]

On Sunday, 28 August 2016 10:45:02 UTC-6, Vincent Maycock wrote:
> On Sun, 28 Aug 2016 06:08:43 -0700 (PDT), Steady Eddie
> <1914o...@gmail.com> wrote:
>
> >On Thursday, 25 August 2016 17:21:22 UTC-6, Alan Kleinman MD PhD wrote:
> >> On Thursday, August 25, 2016 at 6:11:22 AM UTC-7, Bill Rogers wrote:
>
> snip
>
> >> > Who doesn't accept them? Of course I accept them. What I don't accept is Alan's totally unsupported claim that *all* natural selection involves lethal selection pressures that wipe out every member of a species except for a handful who happen to have lucky mutations. Rare examples, usually from medical treatments, *do* indeed work that way. Most don't.
> >
> >You're starting to go Jillery on us, Bill.
> >Dr. K doesn't claim that "*all* natural selection involves lethal selection pressures". He doesn't have to.
> >
> >Why do you claim that HIV undergoing lethal selection pressures is not a representative example of how
> >RMNS works in the real world?
>
> Because that's how combination therapy works; if one selection
> pressure (anti-viral drug) doesn't kill the organism, the other drug
> in the combination therapy will.

Yes, and that's why combination therapy works - because that's how RMNS works in the wild - in fact,
that's how it works in all life.

Do you have reason to doubt this?

> The point is, though, that this is only true if the selection
> pressures are lethal; if they're not, no simultaneous beneficial
> mutations are required for natural selection to work.

That's not the point of the research.

The point of Dr. K's research is to quantify just how likely the RMNS process is to have created and
selected any of a vast variety of different machines, traits, processes, organisms and/or body plans we see
in nature.

To do so, you have to start from the beginning - how likely is any given functional piece of DNA to mutate
into some other sequence that codes for a different functional protein?

I'm sure this number is floating around; does anybody have a reference handy?

[Steady Eddie]

Thanks for the nature walk, Steve.

Yes, look at all the plants and animals that are all working with the same DNA as HIV!

Isn't it wonderful how all of life's DNA mutates at mathematically predictable rates!

[jillery]

On Wed, 31 Aug 2016 12:19:56 -0700 (PDT), Steady Eddie

Of course, the answer to your question depends on your definition of
"different functional protein". Are you willing to provide one?

>> >> Bill, study my math carefully. What you will see is that rmns consists of nested binomial probability problems. Lineages must accumulate beneficial mutations to adapt to selection pressures and they do this by a cycle of beneficial mutation/amplification of beneficial mutation in order to improve the probability for the next binomial probability condition. I used your malaria publication as an example but the mathematics is applicable to any selection pressure(s). Unless a particular lineage can amplify (increase in number), the probability that another beneficial mutation will occur on some member of that lineage will be small. The only exception to this rule is if a small size population can replicate for a sufficient number of generations (without an increase in number) then enough trials will occur for there to be a reasonable probability that another beneficial mutation occurs on one of its members.
>> >>
>> >> But feel free to try and give us an example of a selection pressure which requires a population to accumulate mutations in order to adapt that doesn't require amplification. Perhaps you can give us a formula for improving our probability of winning a lottery without buying more tickets.
>

[Steady Eddie]

Well, what is the consensus definition of "functional protein"?

My idea of a functional protein is any protein that could plausibly be expected to perform a function in the cell in which it originated.
Basically, I'm talking about mutational changes in existing, functional proteins which result in a different functional proteins - I don't mean proteins originating from scratch.

[Greg Guarino]

I think that we have excellent reasons to doubt that any current, living
animal lineage was subject at some point to two or more simultaneous
selective agents either one of which would kill practically the whole
population; whose only chance of survival would depend on two saving
mutations occurring in the same individual.

>
>> The point is, though, that this is only true if the selection
>> pressures are lethal; if they're not, no simultaneous beneficial
>> mutations are required for natural selection to work.
>
> That's not the point of the research.
>
> The point of Dr. K's research is to quantify just how likely the RMNS
> process is to have created and selected any of a vast variety of
> different machines, traits, processes, organisms and/or body plans we
> see in nature.

Nope.

His claim, in brief, is that "amplification" (his term for the spread of
a new beneficial mutation through a population over time) can
effectively only happen one genetic change at a time as the "next"
mutation has to wait for a large enough population of the "previous" one
to build up in order to have a reasonable chance of occurring on an
individual who is already equipped with the "first" one.

The necessary "cyclic" nature of the process means there would not be
enough time to accumulate all of the genetic changes necessary to turn a
"reptile" into a bird, or the common ancestor of humans and chimps into
humans and chimps, to use the two examples he most often cites. He says
that "evolutionist numbers" count the necessary changes in the tens of
millions (for the human-chimp case).

There are several flaws with those arguments, but that is what his
claims are about.

[jillery]

On Wed, 31 Aug 2016 13:20:48 -0700 (PDT), Steady Eddie

That's not it. In order to say that a protein has a different
function, one must be clear what protein functions qualify as
different. For example, when Lenski's E.coli evolved the ability to
metabolize citrate in oxic conditions, many supporters of ID claimed
that it wasn't a different function. Does your definition of
"different functional protein" include Lenski's E.coli mutation?

[Steady Eddie]

Of course. That's one of the technical questions that science is there to find an answer to.

> For example, when Lenski's E.coli evolved the ability to
> metabolize citrate in oxic conditions, many supporters of ID claimed
> that it wasn't a different function. Does your definition of
> "different functional protein" include Lenski's E.coli mutation?

My memory fails me.
Reference please.

[Glenn]

"Steady Eddie" <1914o...@gmail.com> wrote in message news:e2cf078a-9305-45a8...@googlegroups.com...

Looks like you got a real experimentalist by the tail in Jillery.

"We conclude that the rarity of the LTEE mutant was an artifact of the experimental conditions and not a unique evolutionary event. No new genetic information (novel gene function) evolved."
http://www.ncbi.nlm.nih.gov/pubmed/26833416

http://www.evolutionnews.org/2016/05/richard_lenski102839.html

[eridanus]

I remember of a video I watched about some mutation somewhere in a particle
related to Immune system. A doc whose brother died of AIDS started to study
the case of the Black Death in Britain. Why? Because it appeared a few cases
of people with aid positive markers, that do not developed the sickness. He
went to a village in rural England where according to the story most of
the inhabitants survived the plague. So, this concept, some little mutations
that got unnoticed only provided immunity against plague or other serious
illness like AIDS. The doc discovered that most of the people in this village
of England had the same type of... I do not remember now the name, that a few
guys in California that got the virus of AIDS but do not developed the
sickness. We know they got infected because some serum test declared them
positive for AIDS. Just some mutations in some part of the immune system.
eri

[Peter Nyikos]

On Wednesday, August 31, 2016 at 4:25:03 PM UTC-4, Steady Eddie wrote:
> On Wednesday, 31 August 2016 14:10:02 UTC-6, jillery wrote:
> > On Wed, 31 Aug 2016 12:19:56 -0700 (PDT), Steady Eddie
> > <1914o...@gmail.com> wrote:
> >
> > >On Sunday, 28 August 2016 10:45:02 UTC-6, Vincent Maycock wrote:
> > >> On Sun, 28 Aug 2016 06:08:43 -0700 (PDT), Steady Eddie
> > >> <1914o...@gmail.com> wrote:
> > >>
> > >> >On Thursday, 25 August 2016 17:21:22 UTC-6, Alan Kleinman MD PhD wrote:
> > >> >> On Thursday, August 25, 2016 at 6:11:22 AM UTC-7, Bill Rogers wrote:
> > >>
> > >> snip
> > >>
> > >> >> > Who doesn't accept them? Of course I accept them. What I don't accept is Alan's totally unsupported claim that *all* natural selection involves lethal selection pressures that wipe out every member of a species except for a handful who happen to have lucky mutations. Rare examples, usually from medical treatments, *do* indeed work that way. Most don't.
> > >> >
> > >> >You're starting to go Jillery on us, Bill.

Touche. Jillery talks out of both sides of her mouth on the "That's
not what I said" theme. I could show you a real doozy where she
did the same thing Bill is doing, INTENTIONALLY, and then when I
pointed out her double standards, she did a snip-n-deceive by
snipping out my entire refutation, then indulged in diabolical
disingenuousness with a "someone may have spoofed your account"
to hide the fact that she was being hypocritical.

But why am I telling you all this, Eddie? You don't seem to take real note
of evidence for what a totally untrustworthy person this or that
Internet Hellion is. You seem to prefer simple "rebuttals" like "LOL."

Anyway, to give Bill the benefit of the doubt: he may just have
been innocently misled by an ambiguity in what Alan had said.
Internet Hellions typically leave out qualifying adjectives like
"some," "many" "most" "all" etc. because their case rests
to a greater or lesser extent on equivocation. Ray Martinez
is a huge offender on this score.

> > >> >Dr. K doesn't claim that "*all* natural selection involves lethal selection pressures". He doesn't have to.
> > >> >
> > >> >Why do you claim that HIV undergoing lethal selection pressures is not a representative example of how
> > >> >RMNS works in the real world?
> > >>
> > >> Because that's how combination therapy works; if one selection
> > >> pressure (anti-viral drug) doesn't kill the organism, the other drug
> > >> in the combination therapy will.
> > >
> > >Yes, and that's why combination therapy works - because that's how RMNS works in the wild - in fact,
> > >that's how it works in all life.

I tuned in late. What does RMNS stand for.

> > >Do you have reason to doubt this?

Don't hold your breath waiting for an answer from Vincent, what with
jillery running interference for him by speaking out of one side of
her mouth about the concept of a function.

You disappeared from the thread where I congratulated you on your
use of the word "propulsion." Jillery, talking out of the other
side of her mouth about "function," has been indulging in
snip-n-deceive about that, and you need to get back there,
pronto, while her deceit is still front and center. Start here,
and look at what jillery is up to in her "rebuttal":

https://groups.google.com/forum/#!original/talk.origins/ys8ynNDx1U0/TlNf7nS7AQAJ
Message-ID: <2eb14284-fb0c-41ba...@googlegroups.com>
Subject: Re: Origin of the Flagellum ON TRIAL, Continued
Date: Mon, 29 Aug 2016 12:48:11 -0700 (PDT)

> > >> The point is, though, that this is only true if the selection
> > >> pressures are lethal; if they're not, no simultaneous beneficial
> > >> mutations are required for natural selection to work.
> > >
> > >That's not the point of the research.
> > >
> > >The point of Dr. K's research is to quantify just how likely the RMNS process is to have created and
> > >selected any of a vast variety of different machines, traits, processes, organisms and/or body plans we see
> > >in nature.
> > >
> > >To do so, you have to start from the beginning - how likely is any given functional piece of DNA to mutate
> > >into some other sequence that codes for a different functional protein?
> > >
> > >I'm sure this number is floating around; does anybody have a reference handy?
> >
> >
> > Of course, the answer to your question depends on your definition of
> > "different functional protein". Are you willing to provide one?
>
> Well, what is the consensus definition of "functional protein"?

It may bar "junk DNA". Anti-ID zealots love to discount or even
ignore the many non-coding-for-protein functions that are being
discovered for some of it. They are trying to make a game of it,
making up their rules as they go along, and "disqualifying"
the ID folks who say ID theory predicted a function for
a lot of "junk DNA".

> My idea of a functional protein is any protein that could plausibly be expected to perform a function in the cell in which it originated.
> Basically, I'm talking about mutational changes in existing, functional proteins which result in a different functional proteins - I don't mean proteins originating from scratch.

<long wraparound spiel by "Dr. Dr. Kleinman" snipped here>

Peter Nyikos
Professor, Dept. of Mathematics -- standard disclaimer--
University of South Carolina

[jillery]

On Wed, 31 Aug 2016 19:09:14 -0700 (PDT), Steady Eddie

A failed memory is not your problem here. It's likely you never
learned about the example to which I referred, and you're too lazy to
look it up for yourself.

[jillery]

>I remember of a video I watched about some mutation somewhere in a particle
>related to Immune system. A doc whose brother died of AIDS started to study
>the case of the Black Death in Britain. Why? Because it appeared a few cases
>of people with aid positive markers, that do not developed the sickness. He
>went to a village in rural England where according to the story most of
>the inhabitants survived the plague. So, this concept, some little mutations
>that got unnoticed only provided immunity against plague or other serious
>illness like AIDS. The doc discovered that most of the people in this village
>of England had the same type of... I do not remember now the name, that a few
>guys in California that got the virus of AIDS but do not developed the
>sickness. We know they got infected because some serum test declared them
>positive for AIDS. Just some mutations in some part of the immune system.
>eri

You might find interesting the results from a Google search using "HIV
immunity gene".

[jillery]

On Wed, 31 Aug 2016 23:10:34 -0700, "Glenn" <g...@invalid.invalid>
wrote:

You say that like it's a Bad Thing (c).

>"We conclude that the rarity of the LTEE mutant was an artifact of the experimental conditions and not a unique evolutionary event. No new genetic information (novel gene function) evolved."
>http://www.ncbi.nlm.nih.gov/pubmed/26833416
>
>http://www.evolutionnews.org/2016/05/richard_lenski102839.html

Let's see if Steadly even bothers to read your cite, nevermind
understand it. Care to bet on it?

[jillery]

On Thu, 1 Sep 2016 07:52:29 -0700 (PDT), Peter Nyikos
<nyi...@bellsouth.net> wrote:

>On Wednesday, August 31, 2016 at 4:25:03 PM UTC-4, Steady Eddie wrote:
>> On Wednesday, 31 August 2016 14:10:02 UTC-6, jillery wrote:
>> > On Wed, 31 Aug 2016 12:19:56 -0700 (PDT), Steady Eddie
>> > <1914o...@gmail.com> wrote:
>> >
>> > >On Sunday, 28 August 2016 10:45:02 UTC-6, Vincent Maycock wrote:
>> > >> On Sun, 28 Aug 2016 06:08:43 -0700 (PDT), Steady Eddie
>> > >> <1914o...@gmail.com> wrote:
>> > >>
>> > >> >On Thursday, 25 August 2016 17:21:22 UTC-6, Alan Kleinman MD PhD wrote:
>> > >> >> On Thursday, August 25, 2016 at 6:11:22 AM UTC-7, Bill Rogers wrote:
>> > >>
>> > >> snip
>> > >>
>> > >> >> > Who doesn't accept them? Of course I accept them. What I don't accept is Alan's totally unsupported claim that *all* natural selection involves lethal selection pressures that wipe out every member of a species except for a handful who happen to have lucky mutations. Rare examples, usually from medical treatments, *do* indeed work that way. Most don't.
>> > >> >
>> > >> >You're starting to go Jillery on us, Bill.
>
>Touche. Jillery talks out of both sides of her mouth on the "That's
>not what I said" theme. I could show you a real doozy where she
>did the same thing Bill is doing, INTENTIONALLY, and then when I
>pointed out her double standards, she did a snip-n-deceive by
>snipping out my entire refutation, then indulged in diabolical
>disingenuousness with a "someone may have spoofed your account"
>to hide the fact that she was being hypocritical.

Of course, your rant above is entirely irrelevant to this topic, this
thread, this context, and anything anybody posted to it. It just
shows what you do, to ejaculate his Big Lies about me into as many
threads as you can. One can only wonder how you think that makes you
look clever.

Since you brought it up, I post it again: Since you don't like your
comments snipped, then don't snip mine. It's as simple as that. One
can only wonder why you haven't figured that out yet.

[Peter Nyikos]

On Thursday, September 1, 2016 at 1:45:03 PM UTC-4, jillery wrote:
> On Thu, 1 Sep 2016 07:52:29 -0700 (PDT), Peter Nyikos
> <nyi...@bellsouth.net> wrote:
>
> >On Wednesday, August 31, 2016 at 4:25:03 PM UTC-4, Steady Eddie wrote:
> >> On Wednesday, 31 August 2016 14:10:02 UTC-6, jillery wrote:
> >> > On Wed, 31 Aug 2016 12:19:56 -0700 (PDT), Steady Eddie
> >> > <1914o...@gmail.com> wrote:
> >> >
> >> > >On Sunday, 28 August 2016 10:45:02 UTC-6, Vincent Maycock wrote:
> >> > >> On Sun, 28 Aug 2016 06:08:43 -0700 (PDT), Steady Eddie
> >> > >> <1914o...@gmail.com> wrote:
> >> > >>
> >> > >> >On Thursday, 25 August 2016 17:21:22 UTC-6, Alan Kleinman MD PhD wrote:
> >> > >> >> On Thursday, August 25, 2016 at 6:11:22 AM UTC-7, Bill Rogers wrote:
> >> > >>
> >> > >> snip
> >> > >>
> >> > >> >> > Who doesn't accept them? Of course I accept them. What I don't accept is Alan's totally unsupported claim that *all* natural selection involves lethal selection pressures that wipe out every member of a species except for a handful who happen to have lucky mutations. Rare examples, usually from medical treatments, *do* indeed work that way. Most don't.
> >> > >> >
> >> > >> >You're starting to go Jillery on us, Bill.
> >
> >Touche. Jillery talks out of both sides of her mouth on the "That's
> >not what I said" theme. I could show you a real doozy where she
> >did the same thing Bill is doing, INTENTIONALLY, and then when I
> >pointed out her double standards, she did a snip-n-deceive by
> >snipping out my entire refutation, then indulged in diabolical
> >disingenuousness with a "someone may have spoofed your account"
> >to hide the fact that she was being hypocritical.
>
>
> Of course, your rant above is entirely irrelevant to this topic, this
> thread, this context, and anything anybody posted to it.

Of course, you are lying again. Just look at Eddie's line to which
I was replying.

Besides, you aren't the least bit interested in reviving "this
topic" or "this thread." NOTHING from you here promoting them.

And just look at my on-topic comments that
you've completely ignored in your single-minded revenge against
me for letting people know what kind of person you are.

> It just
> shows what you do, to ejaculate his Big Lies about me into as many
> threads as you can.

I told the truth, and you aren't even trying to refute it.

> One can only wonder how you think that makes you
> look clever.

Disingenuous crack to hide the fact that you are lying. Just like
when you posted that patently insincere crack about "spoofed."

>
> >But why am I telling you all this, Eddie? You don't seem to take real note
> >of evidence for what a totally untrustworthy person this or that
> >Internet Hellion is. You seem to prefer simple "rebuttals" like "LOL."

You, jillery, call Eddie and me a "tag team" but that is because you
act as though you'd never seen criticism like the above.

A real tag team -- a MAJOR one -- here is you and Casanova. I'd be absolutely
astounded if you said anything so critical to him, or he to you,
as what I've said to Eddie just now. You and he have been working
hand in glove for about two weeks not.

"The exception that proves the rule": five or more years ago, you
and Casanova had a minor tiff, but that was well before you two
found out how ideally suited to each other you are.

One can only wonder why you make this sickeningly disingenuous
claim after I so thoroughly demolished it in a post that you
cannot pretend to have missed:

https://groups.google.com/forum/#!original/talk.origins/ys8ynNDx1U0/LaaaDEzvAQAJ

Subject: Re: Origin of the Flagellum ON TRIAL, Continued

Date: Tue, 30 Aug 2016 04:38:01 -0700 (PDT)
Message-ID: <382d0c27-826d-490d...@googlegroups.com>

Why don't you go the whole hog and tell me the following?

Since you don't like to be accused of dishonesty, then
don't accuse me of dishonesty. It's as simple as that. One

can only wonder why you haven't figured that out yet.

Of course, the answer is that I can thoroughly document how
dishonest you are, and have started to do it to your main
tag team partner, while your accusations of my dishonesty
are devoid of reality, and only go to show how little truth
and justice mean to you.

>
> >> > >> The point is, though, that this is only true if the selection
> >> > >> pressures are lethal; if they're not, no simultaneous beneficial
> >> > >> mutations are required for natural selection to work.
> >> > >
> >> > >That's not the point of the research.
> >> > >
> >> > >The point of Dr. K's research is to quantify just how likely the RMNS process is to have created and
> >> > >selected any of a vast variety of different machines, traits, processes, organisms and/or body plans we see
> >> > >in nature.
> >> > >
> >> > >To do so, you have to start from the beginning - how likely is any given functional piece of DNA to mutate
> >> > >into some other sequence that codes for a different functional protein?
> >> > >
> >> > >I'm sure this number is floating around; does anybody have a reference handy?
> >> >
> >> >
> >> > Of course, the answer to your question depends on your definition of
> >> > "different functional protein". Are you willing to provide one?
> >>
> >> Well, what is the consensus definition of "functional protein"?
> >
> >It may bar "junk DNA". Anti-ID zealots love to discount or even
> >ignore the many non-coding-for-protein functions that are being
> >discovered for some of it. They are trying to make a game of it,
> >making up their rules as they go along, and "disqualifying"
> >the ID folks who say ID theory predicted a function for
> >a lot of "junk DNA".

Naturally, you had nothing to say to this on-topic comment of mine.
Like your erstwhile tag-team partner, Ron O, you aren't the least bit
interested in discussing on-topic matters with me in an adult manner;
all you want is to fling as much mud at me as you can.

Peter Nyikos
Professor, Dept. of Mathematics -- standard disclaimer--

U. of South Carolina

[Peter Nyikos]

Piggybacking, because both attempted replies to riskys... failed to post.

On Sunday, August 28, 2016 at 1:05:03 PM UTC-4, riskys...@gmail.com wrote:

> On Sunday, August 28, 2016 at 9:10:03 AM UTC-4, Steady Eddie wrote:
> > On Thursday, 25 August 2016 17:21:22 UTC-6, Alan Kleinman MD PhD wrote:
> > > On Thursday, August 25, 2016 at 6:11:22 AM UTC-7, Bill Rogers wrote:
> > > > On Thursday, August 25, 2016 at 8:51:23 AM UTC-4, Steady Eddie wrote:
> > > > > On Thursday, 25 August 2016 04:31:23 UTC-6, Bill Rogers wrote:
> > > > > > On Wednesday, August 24, 2016 at 10:16:23 PM UTC-4, Steady Eddie wrote:

> > > > > > > Oh, okay, so any subject of research is acceptable, except "scenarios that ... involve lethal agents that
> > > > > > > kill all but a handful of lucky mutants".
> > > > > > >
> > > > > > > What a coincidence - that's just what Dr. K has...
> > > > > >
> > > > > > The drug resistance scenarios certainly are cases of natural selection. Nobody disputes that. What we keep disputing is the claim that such "scenarios that involve lethal agents that kill all but a handful of lucky mutants" are typical of the selections at work in nature most of the time. His examples are real examples, sure, and examples we all understand. It's perfectly fine and useful to do research on those situations. What is entirely unreasonable is to think that those examples represent the only possible form of natural selection, or even a common form.
> > > > >
> > > > > LOL!
> > > > > The only entirely unreasonable thing here is your refusal to accept the best-studied examples of REAL
> > > > > RMNS at work in the REAL world, just because it doesn't support your philosophy.
> > > >
> > > > Who doesn't accept them? Of course I accept them. What I don't accept is Alan's totally unsupported claim that *all* natural selection involves lethal selection pressures that wipe out every member of a species except for a handful who happen to have lucky mutations. Rare examples, usually from medical treatments, *do* indeed work that way. Most don't.
> >
> > You're starting to go Jillery on us, Bill.
> > Dr. K doesn't claim that "*all* natural selection involves lethal selection pressures". He doesn't have to.
>

> But he resolutely refuses to show us any "math" that involves any other scenario.

Nevertheless, that doesn't make what Bill wrote correct. A genotype
could be at a disadvantage that could make it disappear over thousands
generations in competition with a mutant, but that is not a lethal
selection pressure.

> Apply his math to an animal population in which there are two "competing" alleles at two different loci. Let's call one pair A1 and A2, the other B1 and B2. In each case the "1" variety is the wild type, and is in the majority. But also in each case, the "2" type confers a selective advantage.
>
> Members with A2/B1 leave 5% more surviving progeny in the next generation than A1/B1. "A1/B2" members leave 2% more surviving progeny than A1/B1. And any A2/B2 members that may be produced have a 10% advantage over A1/B1. The population remains fairly constant.
>
> Alan's argument depends (at least) on the idea that only one beneficial bit of genetics can "amplify" at a time, but he usually also adds in that the population is reduced to a tiny fraction of it's original size with each selective episode.

But is that a necessary part of his theory? And why the original population?
Why could not that tiny fraction be of a much smaller "daughter" population
that split off from the original, as is a staple in the theory of Punctuated
Equilibrium?

> To be fair, he also means that even if the population is not decimated, only the progeny of the original mutated member will have the first mutation, thus greatly lowering the population that can create the second beneficial mutation. But this is also why he refuses to apply his math to sexual species.
>
> I see no obvious reason why both A2 and B2 in the scenario above cannot amplify simultaneously and, once both have reached significant proportions in the population, we should not expect A2/B2 members to appear, and eventually become the the majority. >
>

> > Why do you claim that HIV undergoing lethal selection pressures is not a representative example of how
> > RMNS works in the real world?
>

> I doubt that you understand Kleinman's argument; you merely "agree" with it.

I'd need to see more of it before understanding it; people addressing my
points up there and answering my questions may be a good place to start.

I ran into Kleinman a number of years ago, and his thread shattered
the 1000 post "glass ceiling" of Google Groups several times. Then he
disappeared for a long time, and so I felt that I had wasted a lot
of time on him.

And so, I have avoided looking at threads by him, and
the only reason I made an exception for this one is that I hadn't
seen anything by Vincent Maycock all year and wondered whether he
was still around. So I clicked "Show activity" on a post by him from
last year and came across this thread.

> If you did understand it, you'd have a better chance of being able to understand Bill's objection.

This makes me wonder whether YOU understand Bill's objection.

Peter Nyikos
Professor, Dept. of Mathematics -- standard disclaimer--

University of South Carolina
http://people.math.sc.edu/nyikos/

> The numbers you choose to use matter. Can electricity be dangerous? Nope. I have dozens AA batteries in my house. Not one of them has ever given me a shock.

[Alan Kleinman MD PhD]

On Sunday, August 28, 2016 at 9:45:02 AM UTC-7, Vincent Maycock wrote:
> On Sun, 28 Aug 2016 06:08:43 -0700 (PDT), Steady Eddie

> wrote:
>
> >On Thursday, 25 August 2016 17:21:22 UTC-6, Alan Kleinman MD PhD wrote:
> >> On Thursday, August 25, 2016 at 6:11:22 AM UTC-7, Bill Rogers wrote:
>
> snip
>
> >> > Who doesn't accept them? Of course I accept them. What I don't accept is Alan's totally unsupported claim that *all* natural selection involves lethal selection pressures that wipe out every member of a species except for a handful who happen to have lucky mutations. Rare examples, usually from medical treatments, *do* indeed work that way. Most don't.
> >
> >You're starting to go Jillery on us, Bill.
> >Dr. K doesn't claim that "*all* natural selection involves lethal selection pressures". He doesn't have to.
> >
> >Why do you claim that HIV undergoing lethal selection pressures is not a representative example of how
> >RMNS works in the real world?
>
> Because that's how combination therapy works; if one selection
> pressure (anti-viral drug) doesn't kill the organism, the other drug
> in the combination therapy will.

None of the anti-viral medications "kill" the virus, they only inhibit the reproduction of the virus. What combination anti-viral therapy does is inhibit the amplification of any beneficial mutations for one drug or another. Without amplification, the probability of another beneficial mutation occurring on the particular lineage remains small.

>
> The point is, though, that this is only true if the selection
> pressures are lethal; if they're not, no simultaneous beneficial
> mutations are required for natural selection to work.

Vincent, give us one real, measurable and repeatable example of a population evolving efficiently by rmns to more than a single non-lethal selection pressure.

[Alan Kleinman MD PhD]

On Sunday, August 28, 2016 at 3:40:02 PM UTC-7, Steve L wrote:
> On Sun, 28 Aug 2016 06:08:43 -0700 (PDT), Steady Eddie

> wrote:
>
> >Why do you claim that HIV undergoing lethal selection pressures is not a representative example of how
> >RMNS works in the real world?
>
> Go to a park or the woods. Every plant or animal you see is under an
> uncountable number of selection pressures, yet very few are dead.

They also aren't evolving by rmns. When selection pressures are random, you get genetic drift, but you aren't going to transform reptiles into birds that way.

[Alan Kleinman MD PhD]

On Wednesday, August 31, 2016 at 12:25:03 PM UTC-7, Steady Eddie wrote:
> On Sunday, 28 August 2016 10:45:02 UTC-6, Vincent Maycock wrote:
> > On Sun, 28 Aug 2016 06:08:43 -0700 (PDT), Steady Eddie

> > wrote:
> >
> > >On Thursday, 25 August 2016 17:21:22 UTC-6, Alan Kleinman MD PhD wrote:
> > >> On Thursday, August 25, 2016 at 6:11:22 AM UTC-7, Bill Rogers wrote:
> >
> > snip
> >
> > >> > Who doesn't accept them? Of course I accept them. What I don't accept is Alan's totally unsupported claim that *all* natural selection involves lethal selection pressures that wipe out every member of a species except for a handful who happen to have lucky mutations. Rare examples, usually from medical treatments, *do* indeed work that way. Most don't.
> > >
> > >You're starting to go Jillery on us, Bill.
> > >Dr. K doesn't claim that "*all* natural selection involves lethal selection pressures". He doesn't have to.
> > >
> > >Why do you claim that HIV undergoing lethal selection pressures is not a representative example of how
> > >RMNS works in the real world?
> >
> > Because that's how combination therapy works; if one selection
> > pressure (anti-viral drug) doesn't kill the organism, the other drug
> > in the combination therapy will.
>
> Yes, and that's why combination therapy works - because that's how RMNS works in the wild - in fact,
> that's how it works in all life.
>
> Do you have reason to doubt this?
>
> > The point is, though, that this is only true if the selection
> > pressures are lethal; if they're not, no simultaneous beneficial
> > mutations are required for natural selection to work.
>
> That's not the point of the research.
>
> The point of Dr. K's research is to quantify just how likely the RMNS process is to have created and
> selected any of a vast variety of different machines, traits, processes, organisms and/or body plans we see
> in nature.

It's even more basic than that Eddie, my research shows how a lineage accumulates mutations to adapt to a single selection pressure and to multiple selection pressures simultaneously. The best empirical examples happen to be to antimicrobial agents because the time scale is fast enough to be observed due to their rapid life cycle. Now if these agents were lethal, nothing would ever evovle to these pressures even when used as single drug therapy. If you want a single selection pressure that microbes can not evolve resistance to, bleach.

Now the selection pressures which would evolve all the complex biological mechanisms we see in the living cells only exist in the imaginations of evolutionists.

[Alan Kleinman MD PhD]

On Wednesday, August 31, 2016 at 1:10:02 PM UTC-7, jillery wrote:
> On Wed, 31 Aug 2016 12:19:56 -0700 (PDT), Steady Eddie

> wrote:
>
> >On Sunday, 28 August 2016 10:45:02 UTC-6, Vincent Maycock wrote:
> >> On Sun, 28 Aug 2016 06:08:43 -0700 (PDT), Steady Eddie

What is that selection pressure for hemoglobin or for insulin or for the DNA replicase system or for...?
<snip>

[Alan Kleinman MD PhD]

On Wednesday, August 31, 2016 at 1:50:03 PM UTC-7, Greg Guarino wrote:
> On 8/31/2016 3:19 PM, Steady Eddie wrote:
> > On Sunday, 28 August 2016 10:45:02 UTC-6, Vincent Maycock wrote:
> >> On Sun, 28 Aug 2016 06:08:43 -0700 (PDT), Steady Eddie

Tell us why thermal stress is never accompanied by starvation. What is that single selection pressure that would transform reptiles into birds? And explain why HIV can not evolve efficiently to three drug therapy despite that well treated patients still harbor hundreds of thousands of replicating viruses.

[Alan Kleinman MD PhD]

On Thursday, September 1, 2016 at 7:55:04 AM UTC-7, Peter Nyikos wrote:
> On Wednesday, August 31, 2016 at 4:25:03 PM UTC-4, Steady Eddie wrote:
> > On Wednesday, 31 August 2016 14:10:02 UTC-6, jillery wrote:
> > > On Wed, 31 Aug 2016 12:19:56 -0700 (PDT), Steady Eddie

> > > wrote:
> > >
> > > >On Sunday, 28 August 2016 10:45:02 UTC-6, Vincent Maycock wrote:
> > > >> On Sun, 28 Aug 2016 06:08:43 -0700 (PDT), Steady Eddie

> > > >> wrote:
> > > >>
> > > >> >On Thursday, 25 August 2016 17:21:22 UTC-6, Alan Kleinman MD PhD wrote:
> > > >> >> On Thursday, August 25, 2016 at 6:11:22 AM UTC-7, Bill Rogers wrote:
> > > >>
> > > >> snip
> > > >>
> > > >> >> > Who doesn't accept them? Of course I accept them. What I don't accept is Alan's totally unsupported claim that *all* natural selection involves lethal selection pressures that wipe out every member of a species except for a handful who happen to have lucky mutations. Rare examples, usually from medical treatments, *do* indeed work that way. Most don't.
> > > >> >
> > > >> >You're starting to go Jillery on us, Bill.
>
> Touche. Jillery talks out of both sides of her mouth on the "That's
> not what I said" theme. I could show you a real doozy where she
> did the same thing Bill is doing, INTENTIONALLY, and then when I
> pointed out her double standards, she did a snip-n-deceive by
> snipping out my entire refutation, then indulged in diabolical
> disingenuousness with a "someone may have spoofed your account"
> to hide the fact that she was being hypocritical.
>
> But why am I telling you all this, Eddie? You don't seem to take real note
> of evidence for what a totally untrustworthy person this or that
> Internet Hellion is. You seem to prefer simple "rebuttals" like "LOL."
>
> Anyway, to give Bill the benefit of the doubt: he may just have
> been innocently misled by an ambiguity in what Alan had said.
> Internet Hellions typically leave out qualifying adjectives like
> "some," "many" "most" "all" etc. because their case rests
> to a greater or lesser extent on equivocation. Ray Martinez
> is a huge offender on this score.

Just what ambiguity did I say? There is no ambiguity in my mathematics and my mathematics correctly describes all real, measurable and repeatable examples of rmns.

>
> > > >> >Dr. K doesn't claim that "*all* natural selection involves lethal selection pressures". He doesn't have to.
> > > >> >
> > > >> >Why do you claim that HIV undergoing lethal selection pressures is not a representative example of how
> > > >> >RMNS works in the real world?
> > > >>
> > > >> Because that's how combination therapy works; if one selection
> > > >> pressure (anti-viral drug) doesn't kill the organism, the other drug
> > > >> in the combination therapy will.
> > > >
> > > >Yes, and that's why combination therapy works - because that's how RMNS works in the wild - in fact,
> > > >that's how it works in all life.
>
> I tuned in late. What does RMNS stand for.

Random mutation and natural selection.
<snip>

[jillery]

So that's a "no". BTW, are you Steadly?

[jillery]

On Thu, 1 Sep 2016 11:32:14 -0700 (PDT), Peter Nyikos
<nyi...@bellsouth.net> ranted on:

Yes, just look at Steadly's line, as meaningful as his typical "LOL".
Of course, you have no idea what it means, because Steadly has never
said what he means by it.

>Besides, you aren't the least bit interested in reviving "this
>topic" or "this thread." NOTHING from you here promoting them.

It's not possible to revive this dead horse while you continue beating
it.

>And just look at my on-topic comments that
>you've completely ignored in your single-minded revenge against
>me for letting people know what kind of person you are.

Even if you had any on-topic comments, they are overwhelmed by your
irrelevant noise. Unlike the porn publishers of yore, you don't get
to claim redeeming social value just because you throw in a line or
two to justify your anile ejaculations.

>> It just
>> shows what you do, to ejaculate his Big Lies about me into as many
>> threads as you can.
>
>I told the truth, and you aren't even trying to refute it.

What's to refute? Your rants aren't relevant to anything.

>> One can only wonder how you think that makes you
>> look clever.
>
>Disingenuous crack to hide the fact that you are lying. Just like
>when you posted that patently insincere crack about "spoofed."

Really? Then right here would have been a good place for you to show
how your rants make you look clever.

>> >But why am I telling you all this, Eddie? You don't seem to take real note
>> >of evidence for what a totally untrustworthy person this or that
>> >Internet Hellion is. You seem to prefer simple "rebuttals" like "LOL."
>
>You, jillery, call Eddie and me a "tag team" but that is because you
>act as though you'd never seen criticism like the above.

Apparently you think Hermann Goring would have been acquitted if he
had criticized the Fuhrer for wearing white after Labor Day.

>A real tag team -- a MAJOR one -- here is you and Casanova. I'd be absolutely
>astounded if you said anything so critical to him, or he to you,
>as what I've said to Eddie just now. You and he have been working
>hand in glove for about two weeks not.

Cite an instance where Casanova behaved Steadly Stupid. Failing that,
you're just blowing smoke out of your puckered sphincter.

>"The exception that proves the rule": five or more years ago, you
>and Casanova had a minor tiff, but that was well before you two
>found out how ideally suited to each other you are.

So you admit you and Steadly are well-suited. That's what I said. So
what are you complaining about?

Since you have no interest in posting anything relevant to this
thread, right here would have been a good place for you to say how the
post you cite above "thoroughly demolishes" anything but what remains
of your credibility.

>Why don't you go the whole hog and tell me the following?
>
> Since you don't like to be accused of dishonesty, then
> don't accuse me of dishonesty. It's as simple as that. One
> can only wonder why you haven't figured that out yet.

You post a false equivalence. That's something else you have in
common with your strange bedfellows. I made no accusations. I noted
your explicit and habitual behavior. Or do you deny that you snipped
my comments?

>Of course, the answer is that I can thoroughly document how
>dishonest you are, and have started to do it to your main
>tag team partner, while your accusations of my dishonesty
>are devoid of reality, and only go to show how little truth
>and justice mean to you.

Don't forget "the American Way"; wannabe superheroes like you have to
recite the whole thing, or you don't get a gold star.

>> >> > >> The point is, though, that this is only true if the selection
>> >> > >> pressures are lethal; if they're not, no simultaneous beneficial
>> >> > >> mutations are required for natural selection to work.
>> >> > >
>> >> > >That's not the point of the research.
>> >> > >
>> >> > >The point of Dr. K's research is to quantify just how likely the RMNS process is to have created and
>> >> > >selected any of a vast variety of different machines, traits, processes, organisms and/or body plans we see
>> >> > >in nature.
>> >> > >
>> >> > >To do so, you have to start from the beginning - how likely is any given functional piece of DNA to mutate
>> >> > >into some other sequence that codes for a different functional protein?
>> >> > >
>> >> > >I'm sure this number is floating around; does anybody have a reference handy?
>> >> >
>> >> >
>> >> > Of course, the answer to your question depends on your definition of
>> >> > "different functional protein". Are you willing to provide one?
>> >>
>> >> Well, what is the consensus definition of "functional protein"?
>> >
>> >It may bar "junk DNA". Anti-ID zealots love to discount or even
>> >ignore the many non-coding-for-protein functions that are being
>> >discovered for some of it. They are trying to make a game of it,
>> >making up their rules as they go along, and "disqualifying"
>> >the ID folks who say ID theory predicted a function for
>> >a lot of "junk DNA".
>
>Naturally, you had nothing to say to this on-topic comment of mine.
>Like your erstwhile tag-team partner, Ron O, you aren't the least bit
>interested in discussing on-topic matters with me in an adult manner;
>all you want is to fling as much mud at me as you can.

Apparently you think I'm a terrible person that I missed your stupid
comment about the topic in order to address your stupid comments about
me. Tu quoque back atcha, bozo.

>Peter Nyikos
>Professor, Dept. of Mathematics -- standard disclaimer--
>U. of South Carolina
>
>> >> My idea of a functional protein is any protein that could plausibly be expected to perform a function in the cell in which it originated.
>> >> Basically, I'm talking about mutational changes in existing, functional proteins which result in a different functional proteins - I don't mean proteins originating from scratch.
>> >
>> ><long wraparound spiel by "Dr. Dr. Kleinman" snipped here>
>> >

[Alan Kleinman MD PhD]

On Friday, September 2, 2016 at 5:10:03 AM UTC-7, jillery wrote:
> On Thu, 1 Sep 2016 18:04:47 -0700 (PDT), Alan Kleinman MD PhD

Of course that's a "no" because these selection pressures do not exist. Let me check at the top of the post. That's a no also, are you having a private conversation. Better be careful, the Russians may hack this.

[Greg Guarino]

On 9/1/2016 9:11 PM, Alan Kleinman MD PhD wrote:
>>> I think that we have excellent reasons to doubt that any

>>> **current, living** animal lineage was subject at some point to two

>>> or more simultaneous selective agents either one of which would
>>> kill practically the whole population; whose only chance of
>>> survival would depend on two saving mutations occurring in the
>>> same individual.

> Tell us why thermal stress is never accompanied by starvation.

I'm sure those two conditions have occurred simultaneously. But if two
such "pressures" were suddenly visited on an animal population, and if
they had the destructive efficiency of the cases you never stray from,
that population would be very very unlikely to have "current" "living"
descendants.

> What is that single selection pressure that would transform reptiles
> into birds?

Why would it need to be "single"? And why can't one selective issue
(better gliding, for example) simultaneously favor multiple genetic
changes?

> And explain why HIV can not evolve efficiently to three drug
> therapy despite that well treated patients still harbor hundreds of
> thousands of replicating viruses.

Because - obviously - the required triple mutant to defeat the three
drugs is prohibitively unlikely to occur in a population of that size,
(at least not for a long time), a population that is what, a tenth of a
percent of the norm? And also because no none of the three (I assume)
required genetic changes does much to increase reproductive success
without the other two.

[Tim Norfolk]

I am trying to make sense of the arguments here.

Suppose that there are two independent point mutations, each with a probability of 1 in a million. Given a population of 10 billion individuals, what is the probability that none of the individuals experiences both mutations?

[Alan Kleinman MD PhD]

On Friday, September 2, 2016 at 6:40:03 AM UTC-7, Greg Guarino wrote:
> On 9/1/2016 9:11 PM, Alan Kleinman MD PhD wrote:
> >>> I think that we have excellent reasons to doubt that any
> >>> **current, living** animal lineage was subject at some point to two
> >>> or more simultaneous selective agents either one of which would
> >>> kill practically the whole population; whose only chance of
> >>> survival would depend on two saving mutations occurring in the
> >>> same individual.
>
> > Tell us why thermal stress is never accompanied by starvation.
>
> I'm sure those two conditions have occurred simultaneously. But if two
> such "pressures" were suddenly visited on an animal population, and if
> they had the destructive efficiency of the cases you never stray from,
> that population would be very very unlikely to have "current" "living"
> descendants.

What you are having trouble understanding is that the intensity of selection pressures does not alter the evolutionary trajectory. Study the Lenski experimental model. Lenski uses both starvation and thermal stress to measure the ability of his populations to adapt but he doesn't use the stresses simultaneously. And the most studied example of rmns is the evolution of HIV to protease and reverse transcriptase inhibitors. Even with populations in the hundreds of thousands and many generations of replication, this virus can not efficiently amplify any beneficial mutations for one drug or another. And random recombination does not help this virus evolve resistance.

Beneficial mutations are bottlenecks in the evolutionary path. Unless that lineage can amplify, the probability of another beneficial mutation occurring on some member of that lineage remains small. It's all about the multiplication rule for random independent events. And beneficial mutations are random independent events.

>
> > What is that single selection pressure that would transform reptiles
> > into birds?
>
> Why would it need to be "single"? And why can't one selective issue
> (better gliding, for example) simultaneously favor multiple genetic
> changes?

The key to your question is the phrase "multiple genetic changes". Each genetic change imposes its own instance of the multiplication rule. If you have huge populations, you can have a reasonable probability of two beneficial mutations. I demonstrate this by doing the mathematics of Bill Rodgers'paper on the failure of combination therapy for treating Malaria. Malaria can achieve populations of 10^12 or more in an infected individual. With populations that size and mutations rates of 10^-8, double beneficial mutations have realistic probabilities. That's why, my math shows that for durable treatment of Malaria, it will require at least 3 effective drugs to disrupt the rmns phenomenon.

>
> > And explain why HIV can not evolve efficiently to three drug
> > therapy despite that well treated patients still harbor hundreds of
> > thousands of replicating viruses.
>
> Because - obviously - the required triple mutant to defeat the three
> drugs is prohibitively unlikely to occur in a population of that size,
> (at least not for a long time), a population that is what, a tenth of a
> percent of the norm? And also because no none of the three (I assume)
> required genetic changes does much to increase reproductive success
> without the other two.

Again, you miss the key point. The improved fitness variant represents a bottleneck in the evolutionary process. Unless that variant can amplify sufficiently (from a probability point of view do the replication trials necessary to improve the probability of the next beneficial mutation(s) occurring on that lineage), the rmns phenomenon is suppressed.

But you do get it right when you recognize that a small population (lineage) that is able to replicate for many generations can do enough replication trials to get another beneficial mutation(s). But this will take huge numbers of generations for this small population.

[Alan Kleinman MD PhD]

Tim, welcome to the discussion.

It depends on the kind of mutation you are talking about. If you are talking about any type of mutation (beneficial, neutral or detrimental), then the probability of these events occurring is very high. For example for a human size genome of 3e9 bases and a mutation of e-6, you will have about 3e3 mutations.

On the other hand, if you are talking only about beneficial mutations which improve fitness to replicate, I did that math in the following publication:
http://www.ncbi.nlm.nih.gov/pubmed/27501057
The mutation rates for Malaria are in the e-8 to e-9 range but the population sizes can be e12 or more.

If you have trouble understanding the math, ask me a question and I'll try to make it clear for you.

[Greg Guarino]

On 9/2/2016 10:35 AM, Alan Kleinman MD PhD wrote:

> Again, you miss the key point.

I don't miss it; it's simple, everyone gets it. I contend that it is a
special case of the examples you (invariably) choose.

> The improved fitness variant
> represents a bottleneck in the evolutionary process. Unless that
> variant can amplify sufficiently (from a probability point of view do
> the replication trials necessary to improve the probability of the
> next beneficial mutation(s) occurring on that lineage), the rmns
> phenomenon is suppressed.

Which lineage am *I* in, exactly? Or any other sexually-reproducing
creature? Lots of them, right?

Try to think for a moment. If there are two alleles at each of two loci
in a given population, and selection *modestly* or even *slightly*
favors one allele at each locus, what is there to "suppress" the spread
of both of them through the population? And once they have spread to
enough of the population, what is to prevent individuals who possess one
of the favored alleles from reproducing with individuals who possess the
other one and creating offspring with both?

Any example that uses either very strong selection or posits that
neither allele is individually beneficial will (again) miss the point.

[Alan Kleinman MD PhD]

On Friday, September 2, 2016 at 8:15:03 AM UTC-7, Greg Guarino wrote:
> On 9/2/2016 10:35 AM, Alan Kleinman MD PhD wrote:
>
> > Again, you miss the key point.
>
> I don't miss it; it's simple, everyone gets it. I contend that it is a
> special case of the examples you (invariably) choose.

Simple Greg, post a real, measurable and repeatable example that contradicts my claims.

>
> > The improved fitness variant
> > represents a bottleneck in the evolutionary process. Unless that
> > variant can amplify sufficiently (from a probability point of view do
> > the replication trials necessary to improve the probability of the
> > next beneficial mutation(s) occurring on that lineage), the rmns
> > phenomenon is suppressed.
>
> Which lineage am *I* in, exactly? Or any other sexually-reproducing
> creature? Lots of them, right?

It depends on your ancestry. If your ancestry lived around the Mediterranean, you many be carrying mutations which are beneficial for resisting Malaria.

>
> Try to think for a moment. If there are two alleles at each of two loci
> in a given population, and selection *modestly* or even *slightly*
> favors one allele at each locus, what is there to "suppress" the spread
> of both of them through the population? And once they have spread to
> enough of the population, what is to prevent individuals who possess one
> of the favored alleles from reproducing with individuals who possess the
> other one and creating offspring with both?

I've done the math for this problem but you don't seem to want to do it. For your recombination scenario to work, there must be high relative frequencies for both alleles in the population. That is both variants (alleles) must amplify. But empirical evidence shows that this "double" amplification does not happen when there are combination selection pressures acting on a population. This is why random recombination does not help HIV to evolve to combination therapy even though the population is in the hundreds of thousands in well treated patients. This is also why combination herbicides work for suppressing the evolution of herbicide resistant weeds despite weeds sexually reproduce. Of course, feel free to present any real, measurable and repeatable empirical evidence which contradicts this.

>
> Any example that uses either very strong selection or posits that
> neither allele is individually beneficial will (again) miss the point.

Post your real, measurable and repeatable examples which support your claim. There is no empirical evidence which supports your claim, only your speculation. And you refuse to understand how the multiplication rule affects random recombination as well as rmns.

[Greg Guarino]

On 9/2/2016 12:16 PM, Alan Kleinman MD PhD wrote:
> On Friday, September 2, 2016 at 8:15:03 AM UTC-7, Greg Guarino
> wrote:
>> On 9/2/2016 10:35 AM, Alan Kleinman MD PhD wrote:
>>
>>> Again, you miss the key point.
>>
>> I don't miss it; it's simple, everyone gets it. I contend that it
>> is a special case of the examples you (invariably) choose.

> Simple Greg, post a real, measurable and repeatable example that
> contradicts my claims.

Are you disputing that "gentler" selection happens? I'm not conversant
with the literature, but I did a little looking and found this:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3918505/

That page mentions quite a few measured selection coefficients. The
highest I saw was .52; the lowest .0017. (now I'm interested to know how
17 parts in 10000 can be separated from the "noise" of drift)

>>
>>> The improved fitness variant represents a bottleneck in the
>>> evolutionary process. Unless that variant can amplify
>>> sufficiently (from a probability point of view do the replication
>>> trials necessary to improve the probability of the next
>>> beneficial mutation(s) occurring on that lineage), the rmns
>>> phenomenon is suppressed.
>>
>> Which lineage am *I* in, exactly? Or any other sexually-reproducing
>> creature? Lots of them, right?

> It depends on your ancestry. If your ancestry lived around the
> Mediterranean, you many be carrying mutations which are beneficial
> for resisting Malaria.

That's not what I meant, but yes, my ancestors until very recently were
very familiar with two pats of the Mediterreanean.

>> Try to think for a moment. If there are two alleles at each of two
>> loci in a given population, and selection *modestly* or even
>> *slightly* favors one allele at each locus, what is there to
>> "suppress" the spread of both of them through the population? And
>> once they have spread to enough of the population, what is to
>> prevent individuals who possess one of the favored alleles from
>> reproducing with individuals who possess the other one and creating
>> offspring with both?

> I've done the math for this problem but you don't seem to want to do
> it. For your recombination scenario to work, there must be high
> relative frequencies for both alleles in the population. That is both
> variants (alleles) must amplify.

Of course. Now, unless the selection is quite severe, what would stop
both of them from doing so?

But empirical evidence shows that
> this "double" amplification does not happen when there are
> combination selection pressures acting on a population.

Empirical evidence taken from studies in which the selection coefficient
is much higher than any on the page I mention - very close to "1" in
fact - right?

This is why
> random recombination does not help HIV to evolve to combination
> therapy even though the population is in the hundreds of thousands in
> well treated patients. This is also why combination herbicides work
> for suppressing the evolution of herbicide resistant weeds despite
> weeds sexually reproduce. Of course, feel free to present any real,
> measurable and repeatable empirical evidence which contradicts this.
>>
>> Any example that uses either very strong selection or posits that
>> neither allele is individually beneficial will (again) miss the
>> point.

Point missed.

[Tim Norfolk]

Not necessary. I was asking with those numbers. What is the probability?

[Bob Casanova]

On Fri, 02 Sep 2016 08:04:51 -0400, the following appeared
in talk.origins, posted by jillery <69jp...@gmail.com>:

Direct questions seem to repeatedly result in that sort of
"response" from him. I wouldn't be surprised to learn that
he's contracted with IHOP to generate waffles.
--

Bob C.

"The most exciting phrase to hear in science,
the one that heralds new discoveries, is not
'Eureka!' but 'That's funny...'"

- Isaac Asimov

[Steady Eddie]

On Thursday, 1 September 2016 00:15:03 UTC-6, Glenn wrote:
> "Steady Eddie" <1914o...@gmail.com> wrote in message news:e2cf078a-9305-45a8...@googlegroups.com...

> > On Wednesday, 31 August 2016 19:40:02 UTC-6, jillery wrote:
> >> On Wed, 31 Aug 2016 13:20:48 -0700 (PDT), Steady Eddie
> >> <1914o...@gmail.com> wrote:

> >> >Well, what is the consensus definition of "functional protein"?
> >> >

> >> >My idea of a functional protein is any protein that could plausibly be expected to perform a function in the cell in which it originated.
> >> >Basically, I'm talking about mutational changes in existing, functional proteins which result in a different functional proteins - I don't mean proteins originating from scratch.
> >>
> >>

> >> That's not it. In order to say that a protein has a different
> >> function, one must be clear what protein functions qualify as
> >> different.
> >
> > Of course. That's one of the technical questions that science is there to find an answer to.
> >
> >> For example, when Lenski's E.coli evolved the ability to
> >> metabolize citrate in oxic conditions, many supporters of ID claimed
> >> that it wasn't a different function. Does your definition of
> >> "different functional protein" include Lenski's E.coli mutation?
> >
> > My memory fails me.
> > Reference please.
> >
> Looks like you got a real experimentalist by the tail in Jillery.

A true Darwinist, and a rhetorical specialist; she pulled off a cite-bluff without even providing a cite, then
assigned the job to me LOL!

> "We conclude that the rarity of the LTEE mutant was an artifact of the experimental conditions and not a unique evolutionary event. No new genetic information (novel gene function) evolved."
> http://www.ncbi.nlm.nih.gov/pubmed/26833416
>
> http://www.evolutionnews.org/2016/05/richard_lenski102839.html

Yup, pretty much dispenses with her cite-bluff. She probably never even read it; just parroted some
spoon-feeding from some Darwinist site.

[Steady Eddie]

EXACTLY!
Organisms in the wild are endowed with intricate, irreducibly complex systems to safely provide a huge
range of phenotypic variation within the created kind.
It's called ADAPTABILITY. It works, by design, to PRESERVE the kind, not to CREATE it or any other life
form.
To propose that this entire system came about by RMNS, and is proceeding to create new kinds of life
forms by RMNS, is just laughable.

[Alan Kleinman MD PhD]

On Friday, September 2, 2016 at 10:30:04 AM UTC-7, Greg Guarino wrote:
> On 9/2/2016 12:16 PM, Alan Kleinman MD PhD wrote:
> > On Friday, September 2, 2016 at 8:15:03 AM UTC-7, Greg Guarino
> > wrote:
> >> On 9/2/2016 10:35 AM, Alan Kleinman MD PhD wrote:
> >>
> >>> Again, you miss the key point.
> >>
> >> I don't miss it; it's simple, everyone gets it. I contend that it
> >> is a special case of the examples you (invariably) choose.
>
> > Simple Greg, post a real, measurable and repeatable example that
> > contradicts my claims.
>
> Are you disputing that "gentler" selection happens? I'm not conversant
> with the literature, but I did a little looking and found this:
>
> http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3918505/

That's a paper on real, measurable and repeatable examples of rmns? The authors present more questions than answers: "There are many fundamental questions that remain largely unanswered, including: Where do most adaptive genetic variants come from—ancestral variation or de novo mutation? How strong is selection, on average, and does its strength vary for different types of phenotypic traits? Does the strength of selection change in a predictable way as mutations are fixed and populations approach phenotypic optima? Do most adaptations involve a small number of genes with large phenotypic effects or many genes of small effect? To what extent do competing ecological demands, genetic linkage, and pleiotropy constrain adaptation? Finally, how often does natural selection rely on the same genes and/or mutations to drive convergent evolution? Answering these questions is challenging because it requires knowing the precise phenotypic targets of selection, identifying the genetic loci contributing to those adaptive traits, and measuring the strength of selection acting on both phenotypes and genotypes."

>
> That page mentions quite a few measured selection coefficients. The
> highest I saw was .52; the lowest .0017. (now I'm interested to know how
> 17 parts in 10000 can be separated from the "noise" of drift)

So tell us what genes they are talking about and what mutations they are talking about. I think I see where you are getting confused on this topic. Natural selection can act on multiple genetic loci simultaneously. For example, selection can act on the best adapted for thermal stress and also the fastest runner against predation simultaneously but those traits must already exist in those variants in order for them to survive and reproduce. For variants without those traits, selection removes them from the population. It does not require new alleles to appear by rmns in these cases. If it does require rmns adaptation to evolve to the selection pressures at multiple genetic loci simultaneously, your paper does not show this.

It's the multiplication rule Greg. The random recombination problem is nothing more than a random card drawing problem. Take a deck of cards where some cards are labeled A, other cards are labeled B, and the rest of the cards are labeled C. If most of the cards are C's and you have only a few A's and B's in the deck and you pull 2 cards, most of the time you will pull 2 C's, less of the time you will pull a C and A or a C and B and rarely you will pull an A and a B.

>
> But empirical evidence shows that
> > this "double" amplification does not happen when there are
> > combination selection pressures acting on a population.
>
> Empirical evidence taken from studies in which the selection coefficient
> is much higher than any on the page I mention - very close to "1" in
> fact - right?

What makes you think that the evolutionary trajectory for a selection pressure changes with intensity of selection? What makes you think that the probability of a beneficial mutation occurring on a member of a lineage is not governed by a binomial probability problem? Do you think that HIV or E Coli will have different sets of adaptation mutations dependent on the intensity of selection pressure?

>
> This is why
> > random recombination does not help HIV to evolve to combination
> > therapy even though the population is in the hundreds of thousands in
> > well treated patients. This is also why combination herbicides work
> > for suppressing the evolution of herbicide resistant weeds despite
> > weeds sexually reproduce. Of course, feel free to present any real,
> > measurable and repeatable empirical evidence which contradicts this.
> >>
> >> Any example that uses either very strong selection or posits that
> >> neither allele is individually beneficial will (again) miss the
> >> point.
>
> Point missed.
>
> > Post your real, measurable and repeatable examples which support your
> > claim. There is no empirical evidence which supports your claim, only
> > your speculation. And you refuse to understand how the multiplication
> > rule affects random recombination as well as rmns.

Still no empirical example of rmns which shows that a population can evolve efficiently to multiple selection pressures simultaneously. Why don't you contact Lenski and ask him to run his E Coli experiment with both his starvation selection pressure and thermal stress experiment with both selection pressures simultaneously? See whether his already glacially slow experiment will speed up with a little heat.

[Alan Kleinman MD PhD]

I did the computation already and it is published in the above link but I did it in general terms. You can compute your probability for any mutation rate, population size and number of generations. If you have trouble with the math, I put graphical solutions in the paper.

[Alan Kleinman MD PhD]

On Friday, September 2, 2016 at 12:15:03 PM UTC-7, Steady Eddie wrote:
> On Thursday, 1 September 2016 00:15:03 UTC-6, Glenn wrote:

> > "Steady Eddie" wrote in message news:e2cf078a-9305-45a8...@googlegroups.com...

> > > On Wednesday, 31 August 2016 19:40:02 UTC-6, jillery wrote:
> > >> On Wed, 31 Aug 2016 13:20:48 -0700 (PDT), Steady Eddie

> > >> wrote:
> > >>
> > >> >On Wednesday, 31 August 2016 14:10:02 UTC-6, jillery wrote:
> > >> >> On Wed, 31 Aug 2016 12:19:56 -0700 (PDT), Steady Eddie

> > >> >> wrote:
> > >> >>
> > >> >> >On Sunday, 28 August 2016 10:45:02 UTC-6, Vincent Maycock wrote:
> > >> >> >> On Sun, 28 Aug 2016 06:08:43 -0700 (PDT), Steady Eddie

I believe the citrate metabolizer Lenski obtained occurred because that lineage got a mutation which caused a defective cell wall (spherical form) and because of this the citrate was able to be transported into the cell more easily making the citrate available for the Krebs cycle.

[Alan Kleinman MD PhD]

Eddie, it is also sad because the people who believe this also control the field of biology which is foundational training for the practice of medicine. The end result of this is multidrug resistant microbes and less than durable cancer treatments.

[Vincent Maycock]

On Thu, 1 Sep 2016 17:53:19 -0700 (PDT), Alan Kleinman MD PhD
<klei...@sti.net> wrote:

>On Sunday, August 28, 2016 at 3:40:02 PM UTC-7, Steve L wrote:
>> On Sun, 28 Aug 2016 06:08:43 -0700 (PDT), Steady Eddie
>> wrote:
>>
>> >Why do you claim that HIV undergoing lethal selection pressures is not a representative example of how
>> >RMNS works in the real world?
>>
>> Go to a park or the woods. Every plant or animal you see is under an
>> uncountable number of selection pressures, yet very few are dead.
>
>They also aren't evolving by rmns.

Not even by microevolution?

[Vincent Maycock]

On Thu, 1 Sep 2016 17:38:01 -0700 (PDT), Alan Kleinman MD PhD
<klei...@sti.net> wrote:

>On Sunday, August 28, 2016 at 9:45:02 AM UTC-7, Vincent Maycock wrote:
>> On Sun, 28 Aug 2016 06:08:43 -0700 (PDT), Steady Eddie
>> wrote:
>>
>> >On Thursday, 25 August 2016 17:21:22 UTC-6, Alan Kleinman MD PhD wrote:
>> >> On Thursday, August 25, 2016 at 6:11:22 AM UTC-7, Bill Rogers wrote:
>>
>> snip
>>
>> >> > Who doesn't accept them? Of course I accept them. What I don't accept is Alan's totally unsupported claim that *all* natural selection involves lethal selection pressures that wipe out every member of a species except for a handful who happen to have lucky mutations. Rare examples, usually from medical treatments, *do* indeed work that way. Most don't.
>> >
>> >You're starting to go Jillery on us, Bill.
>> >Dr. K doesn't claim that "*all* natural selection involves lethal selection pressures". He doesn't have to.
>> >
>> >Why do you claim that HIV undergoing lethal selection pressures is not a representative example of how
>> >RMNS works in the real world?
>>
>> Because that's how combination therapy works; if one selection
>> pressure (anti-viral drug) doesn't kill the organism, the other drug
>> in the combination therapy will.
>None of the anti-viral medications "kill" the virus, they only inhibit the reproduction of the virus.

Which is much like killing them. If one drug won't prevent their
reproduction, then the other one can still prevent it, leading to the
evolutionary death of the viruses.

>What combination anti-viral therapy does is inhibit the amplification of any beneficial mutations for one drug or another. Without amplification, the probability of another beneficial mutation occurring on the particular lineage remains small.
>>
>> The point is, though, that this is only true if the selection
>> pressures are lethal; if they're not, no simultaneous beneficial
>> mutations are required for natural selection to work.
>Vincent, give us one real, measurable and repeatable example of a population evolving efficiently by rmns to more than a single non-lethal selection pressure.

In the fossil record, we find horses becoming more cursorial, (adapted
for running in the open plains) at the same time as their teeth became
adapted to eating tougher plant foods (like grass).

[Alan Kleinman MD PhD]

On Friday, September 2, 2016 at 1:25:03 PM UTC-7, Vincent Maycock wrote:
> On Thu, 1 Sep 2016 17:53:19 -0700 (PDT), Alan Kleinman MD PhD

> wrote:
>
> >On Sunday, August 28, 2016 at 3:40:02 PM UTC-7, Steve L wrote:
> >> On Sun, 28 Aug 2016 06:08:43 -0700 (PDT), Steady Eddie
> >> wrote:
> >>
> >> >Why do you claim that HIV undergoing lethal selection pressures is not a representative example of how
> >> >RMNS works in the real world?
> >>
> >> Go to a park or the woods. Every plant or animal you see is under an
> >> uncountable number of selection pressures, yet very few are dead.
> >
> >They also aren't evolving by rmns.
>
> Not even by microevolution?
>
> >When selection pressures are random, you get genetic drift, but you aren't going to transform reptiles into birds that way.

You are getting small genetic changes but not the kind of changes which would turn a reptile population into birds. That type of evolutionary change requires directional selection pressures which operate by rmns. And those kind of changes are subject to the multiplication rule.

[Greg Guarino]

On 9/2/2016 3:53 PM, Alan Kleinman MD PhD wrote:
> On Friday, September 2, 2016 at 10:30:04 AM UTC-7, Greg Guarino
> wrote:
>> On 9/2/2016 12:16 PM, Alan Kleinman MD PhD wrote:
>>> On Friday, September 2, 2016 at 8:15:03 AM UTC-7, Greg Guarino
>>> wrote:
>>>> On 9/2/2016 10:35 AM, Alan Kleinman MD PhD wrote:
>>>>
>>>>> Again, you miss the key point.
>>>>
>>>> I don't miss it; it's simple, everyone gets it. I contend that
>>>> it is a special case of the examples you (invariably) choose.
>>
>>> Simple Greg, post a real, measurable and repeatable example that
>>> contradicts my claims.
>>
>> Are you disputing that "gentler" selection happens? I'm not
>> conversant with the literature, but I did a little looking and
>> found this:
>>
>> http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3918505/

> That's a paper on real, measurable and repeatable examples of rmns?

It's a compilation that shows that "gentler" selection not only exists,
but is the typical case. The rest is just math and logic.

> The authors present more questions than answers: "There are many
> fundamental questions that remain largely unanswered, including:
> Where do most adaptive genetic variants come from—ancestral variation
> or de novo mutation? How strong is selection, on average, and does
> its strength vary for different types of phenotypic traits? Does the
> strength of selection change in a predictable way as mutations are
> fixed and populations approach phenotypic optima? Do most adaptations
> involve a small number of genes with large phenotypic effects or many
> genes of small effect? To what extent do competing ecological
> demands, genetic linkage, and pleiotropy constrain adaptation?
> Finally, how often does natural selection rely on the same genes
> and/or mutations to drive convergent evolution? Answering these
> questions is challenging because it requires knowing the precise
> phenotypic targets of selection, identifying the genetic loci
> contributing to those adaptive traits, and measuring the strength of
> selection acting on both phenotypes and genotypes."



>> That page mentions quite a few measured selection coefficients.
>> The highest I saw was .52; the lowest .0017. (now I'm interested to
>> know how 17 parts in 10000 can be separated from the "noise" of
>> drift)


> So tell us what genes they are talking about and what mutations they
> are talking about.

It doesn't matter. You say you are making a mathematical argument.

I think I see where you are getting confused on
> this topic. Natural selection can act on multiple genetic loci
> simultaneously. For example, selection can act on the best adapted
> for thermal stress and also the fastest runner against predation
> simultaneously but those traits must already exist in those variants
> in order for them to survive and reproduce. For variants without
> those traits, selection removes them from the population.

You act as if it's always a binary option: well-suited or dead.

It does not
> require new alleles to appear by rmns in these cases. If it does
> require rmns adaptation to evolve to the selection pressures at
> multiple genetic loci simultaneously, your paper does not show this.

Every variation was originally a mutation, but that really doesn't
matter. We're dealing with math, right? As long as we know there is
"gentle" selection, we can proceed.

Jeez, you repeat this elementary nonsense over and over and over as if
there is anyone on the planet that doesn't understand it. If cards could
reproduce, and if A and B each conferred an advantage, why wouldn't A
and B "amplify" until an "AB" combination is virtually guaranteed?

[Of course, since each organism has more than one "trait" and more then
one variation at each trait, the cards are an inaccurate analogy]

>>
>> But empirical evidence shows that
>>> this "double" amplification does not happen when there are
>>> combination selection pressures acting on a population.
>>
>> Empirical evidence taken from studies in which the selection
>> coefficient is much higher than any on the page I mention - very
>> close to "1" in fact - right?

> What makes you think that the evolutionary trajectory for a selection
> pressure changes with intensity of selection?

I think it's obvious that when multiple selection pressures each kill
nearly the whole population AND when no one mutation confers any real
benefit without the others, no significant "amplification" will occur.
But you have not, and have never, addressed why it would be that in the
more typical case, with selection coefficients of .1 or .01, several
individually-beneficial genetic variants could not "amplify" at the same
time. What would stop them? Unless the variations involved were in some
way directly opposed to each other, what would the (small) selective
effect at one locus do to retard the amplification of another variant at
another locus?

What makes you think
> that the probability of a beneficial mutation occurring on a member
> of a lineage is not governed by a binomial probability problem?

I think that the "second" mutation has no need to occur on a member of
the lineage that produced the "first" one in any population whose
lineages regularly cross. Do we need significant numbers of each
beneficial mutation in the population? Of course. But what's to stop
that from happening if 1. Selection favors both and 2. there is no
extreme selection at work at any locus.

Do
> you think that HIV or E Coli will have different sets of adaptation
> mutations dependent on the intensity of selection pressure?

Huh? Where in the world did that come from?

>> This is why
>>> random recombination does not help HIV to evolve to combination
>>> therapy even though the population is in the hundreds of
>>> thousands in well treated patients. This is also why combination
>>> herbicides work for suppressing the evolution of herbicide
>>> resistant weeds despite weeds sexually reproduce. Of course, feel
>>> free to present any real, measurable and repeatable empirical
>>> evidence which contradicts this.
>>>>
>>>> Any example that uses either very strong selection or posits
>>>> that neither allele is individually beneficial will (again)
>>>> miss the point.
>>
>> Point missed.
>>
>>> Post your real, measurable and repeatable examples which support
>>> your claim. There is no empirical evidence which supports your
>>> claim, only your speculation. And you refuse to understand how
>>> the multiplication rule affects random recombination as well as
>>> rmns.
>
> Still no empirical example of rmns which shows that a population can
> evolve efficiently to multiple selection pressures simultaneously.

You tell us over and over that math is what prevents it. Show us the
math with typical selection coefficients.

[John Stockwell]

BZZT. Actually, you aren't talking about "improved fitness" at all. "Fitness"
in a population genetics sense, is genetic diversity, not the sort of
genetic bottleneck world that you are describing.

So in the 3 drug cocktail bottleneck, the population keeps bouncing around
inside a deep hole with three minima. The HIV mutates enough to keep jumping
between basins, but not enough to leap out of the region that contains the
separate minima. So, evolution is contained, in that situation, but, note that the HIV doesn't become extinct, so it is doing what biology does, which is "stayin' alive". Everything is fine until there is a major change to
where the virus jumps out of the larger basin. To our knowledge that hasn't
happened with HIV yet. However, consider when viruses jump species. That is
a major shift.

-John

When we look at larger populations of organisms in the wild, there is
a diversity of environments and most species have gone extinct, but a few
populations have broken out of past environments. We're a breakout species
ourselves. We have runaway diversity, which means we have runaway fitness---for now---until something happens that bombs us back to the paleolithic.

[Vincent Maycock]

On Fri, 2 Sep 2016 13:39:56 -0700 (PDT), Alan Kleinman MD PhD
<klei...@sti.net> wrote:

>On Friday, September 2, 2016 at 1:25:03 PM UTC-7, Vincent Maycock wrote:
>> On Thu, 1 Sep 2016 17:53:19 -0700 (PDT), Alan Kleinman MD PhD
>> wrote:
>>
>> >On Sunday, August 28, 2016 at 3:40:02 PM UTC-7, Steve L wrote:
>> >> On Sun, 28 Aug 2016 06:08:43 -0700 (PDT), Steady Eddie
>> >> wrote:
>> >>
>> >> >Why do you claim that HIV undergoing lethal selection pressures is not a representative example of how
>> >> >RMNS works in the real world?
>> >>
>> >> Go to a park or the woods. Every plant or animal you see is under an
>> >> uncountable number of selection pressures, yet very few are dead.
>> >
>> >They also aren't evolving by rmns.
>>
>> Not even by microevolution?
>>
>> >When selection pressures are random, you get genetic drift, but you aren't going to transform reptiles into birds that way.
>
>You are getting small genetic changes but not the kind of changes which would turn a reptile population into birds.

If you wait long enough, what would prevent the small changes from
adding up to large changes like the dinosaur-bird transition?

[Steady Eddie]

On Friday, 2 September 2016 14:25:03 UTC-6, Vincent Maycock wrote:
> On Thu, 1 Sep 2016 17:53:19 -0700 (PDT), Alan Kleinman MD PhD
> <klei...@sti.net> wrote:
>
> >On Sunday, August 28, 2016 at 3:40:02 PM UTC-7, Steve L wrote:
> >> On Sun, 28 Aug 2016 06:08:43 -0700 (PDT), Steady Eddie
> >> wrote:
> >>
> >> >Why do you claim that HIV undergoing lethal selection pressures is not a representative example of how
> >> >RMNS works in the real world?
> >>
> >> Go to a park or the woods. Every plant or animal you see is under an
> >> uncountable number of selection pressures, yet very few are dead.
> >
> >They also aren't evolving by rmns.
>
> Not even by microevolution?

Of course, by microevolution.
Its called ADAPTATION, and it is a process designed to provide a generous spectrum of variability within
a created kind to preserve the integrity and fitness of the kind.

Here, you are attempting to perpetrate the same fraudulent equivocation committed by Mo Noor (discussed in the post "Darwinian Indoctrination 101", which I will bump to the top presently for the benefit
of any newcomers), where he first defines "Evolution" as simply change over time throughout a population (simple adaptation), then "demonstrates" the "mathematical inevitability" of Evolution via the tried-and-true asphalt-phobic squirrel story (no, I'm not kidding-you gotta see it).

After securing consensus among his students of the "mathematical inevitability" of Evolution, Mo
proceeds to re-define "Evolution" from simple adaptation to the origination of new kinds of life forms,
such as land animals turning into whales.

There you have it-
It's a mathematical inevitability that whales originated from land mammals without any intelligent design!

I've explained this a few times now on different threads - time to give this shuffle a name.

How bout "The Tandoori Triplet"?
It consists of three parts:

1. Define Evolution as simple adaptation within kinds.
2. Declare Evolution, defined as adaptation, to be "mathematically inevitable" (or insert similar Darwinian rhetoric)
3. Change the definition of "Evolution" back to what Darwinists like Mo REALLY mean by it- the process of
unintelligent processes doing stuff like turning land animals into whales.

Presto! there you have it - just as surely as asphalt-phobic squirrels out-compete their oblivious cousins,
land animals can do such things as turn into whales with no involvement of any intelligent agent.

One rhetorical advantage of the Tandoori Triplet is built-in plausible deniability:
Because you use equivocation and insinuation, rather than just saying what you mean forthrightly, you
build yourself an escape hatch in literalism - you didn't ACTUALLY SAY that land animals are able to turn
themselves into whales with mathematical inevitability - it's not YOUR FAULT if your students come away
with that DISTINCT IMPRESSION, which impression must be so deep in the psyche of a Darwinist that it
distorts their view of reality.
Only with this distorted view of reality can people plausibly conclude that "Evolution" can build new life
forms, let alone originate life in the first place, without an intelligent designer.

[Alan Kleinman MD PhD]

On Friday, September 2, 2016 at 1:40:03 PM UTC-7, Vincent Maycock wrote:
> On Thu, 1 Sep 2016 17:38:01 -0700 (PDT), Alan Kleinman MD PhD

> wrote:
>
> >On Sunday, August 28, 2016 at 9:45:02 AM UTC-7, Vincent Maycock wrote:
> >> On Sun, 28 Aug 2016 06:08:43 -0700 (PDT), Steady Eddie
> >> wrote:
> >>
> >> >On Thursday, 25 August 2016 17:21:22 UTC-6, Alan Kleinman MD PhD wrote:
> >> >> On Thursday, August 25, 2016 at 6:11:22 AM UTC-7, Bill Rogers wrote:
> >>
> >> snip
> >>
> >> >> > Who doesn't accept them? Of course I accept them. What I don't accept is Alan's totally unsupported claim that *all* natural selection involves lethal selection pressures that wipe out every member of a species except for a handful who happen to have lucky mutations. Rare examples, usually from medical treatments, *do* indeed work that way. Most don't.
> >> >
> >> >You're starting to go Jillery on us, Bill.
> >> >Dr. K doesn't claim that "*all* natural selection involves lethal selection pressures". He doesn't have to.
> >> >
> >> >Why do you claim that HIV undergoing lethal selection pressures is not a representative example of how
> >> >RMNS works in the real world?
> >>
> >> Because that's how combination therapy works; if one selection
> >> pressure (anti-viral drug) doesn't kill the organism, the other drug
> >> in the combination therapy will.
> >None of the anti-viral medications "kill" the virus, they only inhibit the reproduction of the virus.
>
> Which is much like killing them. If one drug won't prevent their
> reproduction, then the other one can still prevent it, leading to the
> evolutionary death of the viruses.

The viruses are still replicating, they just can not improve fitness by rmns.

>
> >What combination anti-viral therapy does is inhibit the amplification of any beneficial mutations for one drug or another. Without amplification, the probability of another beneficial mutation occurring on the particular lineage remains small.
> >>
> >> The point is, though, that this is only true if the selection
> >> pressures are lethal; if they're not, no simultaneous beneficial
> >> mutations are required for natural selection to work.
> >Vincent, give us one real, measurable and repeatable example of a population evolving efficiently by rmns to more than a single non-lethal selection pressure.
>
> In the fossil record, we find horses becoming more cursorial, (adapted
> for running in the open plains) at the same time as their teeth became
> adapted to eating tougher plant foods (like grass).

Evolutionists read fossil tea leaves to fit their belief system. If you want to practice hard mathematical science, study and learn how rmns operates and correlate this with the empirical evidence.

[Tim Norfolk]

And the article is behind a paywall. What is your equation?

[Alan Kleinman MD PhD]

On Friday, September 2, 2016 at 1:50:03 PM UTC-7, Greg Guarino wrote:
> On 9/2/2016 3:53 PM, Alan Kleinman MD PhD wrote:
> > On Friday, September 2, 2016 at 10:30:04 AM UTC-7, Greg Guarino
> > wrote:
> >> On 9/2/2016 12:16 PM, Alan Kleinman MD PhD wrote:
> >>> On Friday, September 2, 2016 at 8:15:03 AM UTC-7, Greg Guarino
> >>> wrote:
> >>>> On 9/2/2016 10:35 AM, Alan Kleinman MD PhD wrote:
> >>>>
> >>>>> Again, you miss the key point.
> >>>>
> >>>> I don't miss it; it's simple, everyone gets it. I contend that
> >>>> it is a special case of the examples you (invariably) choose.
> >>
> >>> Simple Greg, post a real, measurable and repeatable example that
> >>> contradicts my claims.
> >>
> >> Are you disputing that "gentler" selection happens? I'm not
> >> conversant with the literature, but I did a little looking and
> >> found this:
> >>
> >> http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3918505/
>
> > That's a paper on real, measurable and repeatable examples of rmns?
>
> It's a compilation that shows that "gentler" selection not only exists,
> but is the typical case. The rest is just math and logic.

But this is not a paper about rmns, it's a paper only about natural selection.

>
> > The authors present more questions than answers: "There are many
> > fundamental questions that remain largely unanswered, including:
> > Where do most adaptive genetic variants come from—ancestral variation
> > or de novo mutation? How strong is selection, on average, and does
> > its strength vary for different types of phenotypic traits? Does the
> > strength of selection change in a predictable way as mutations are
> > fixed and populations approach phenotypic optima? Do most adaptations
> > involve a small number of genes with large phenotypic effects or many
> > genes of small effect? To what extent do competing ecological
> > demands, genetic linkage, and pleiotropy constrain adaptation?
> > Finally, how often does natural selection rely on the same genes
> > and/or mutations to drive convergent evolution? Answering these
> > questions is challenging because it requires knowing the precise
> > phenotypic targets of selection, identifying the genetic loci
> > contributing to those adaptive traits, and measuring the strength of
> > selection acting on both phenotypes and genotypes."
>
>
>
> >> That page mentions quite a few measured selection coefficients.
> >> The highest I saw was .52; the lowest .0017. (now I'm interested to
> >> know how 17 parts in 10000 can be separated from the "noise" of
> >> drift)
>
>
> > So tell us what genes they are talking about and what mutations they
> > are talking about.
>
> It doesn't matter. You say you are making a mathematical argument.

It's a mathematical argument that describes the physical phenomenon of rmns. Your citation is not addressing random mutations.

>
> I think I see where you are getting confused on
> > this topic. Natural selection can act on multiple genetic loci
> > simultaneously. For example, selection can act on the best adapted
> > for thermal stress and also the fastest runner against predation
> > simultaneously but those traits must already exist in those variants
> > in order for them to survive and reproduce. For variants without
> > those traits, selection removes them from the population.
>
> You act as if it's always a binary option: well-suited or dead.

It is a binary option for rmns. Does the beneficial mutation occur or does it not. And the vast majority of times, it does not. And the probability is even lower if amplification does not occur.

>
> It does not
> > require new alleles to appear by rmns in these cases. If it does
> > require rmns adaptation to evolve to the selection pressures at
> > multiple genetic loci simultaneously, your paper does not show this.
>
> Every variation was originally a mutation, but that really doesn't
> matter. We're dealing with math, right? As long as we know there is
> "gentle" selection, we can proceed.

That's not necessarily so. You are making that claim based on the assumption that every genetic sequence came about by rmns. If your assumption is true, your should be able to tell us what the selection pressure was to create hemoglobin or the selection pressure which created insulin or the selection pressure was to create the DNA replicase system... What was that selection pressure that created the original replicator in the primordical soup?

It's simple but it is correct. Perhaps you think Mendelian genetics is elementary nonsense. A and B don't amplify because the selection pressure which selected for A is interfering with the amplification of B and the selection pressure which created B interferes with the amplification of A.

>
> [Of course, since each organism has more than one "trait" and more then
> one variation at each trait, the cards are an inaccurate analogy]

For someone who understands probability theory, the card analogy is totally accurate. But we are all ready to hear what your reason is that random recombination is not contributing to the evolution of drug resistance in HIV.

> >>
> >> But empirical evidence shows that
> >>> this "double" amplification does not happen when there are
> >>> combination selection pressures acting on a population.
> >>
> >> Empirical evidence taken from studies in which the selection
> >> coefficient is much higher than any on the page I mention - very
> >> close to "1" in fact - right?
>
> > What makes you think that the evolutionary trajectory for a selection
> > pressure changes with intensity of selection?
>
> I think it's obvious that when multiple selection pressures each kill
> nearly the whole population AND when no one mutation confers any real
> benefit without the others, no significant "amplification" will occur.
> But you have not, and have never, addressed why it would be that in the
> more typical case, with selection coefficients of .1 or .01, several
> individually-beneficial genetic variants could not "amplify" at the same
> time. What would stop them? Unless the variations involved were in some
> way directly opposed to each other, what would the (small) selective
> effect at one locus do to retard the amplification of another variant at
> another locus?

I have given you the reason and that reason is that the intensity of selection does not affect the evolutionary trajectory. Consider the Weinreich experiment http://isites.harvard.edu/fs/docs/icb.topic440346.files/Papers/Weinreich-et-al-2006.pdf
Do you think if Weinreich altered his concentration of cefotaxime in his experiment that he would get different sets of mutations for resistance to that drug? No matter what the intensity of selection is, the evolutionary process by rmns will consist of sets of binomial probability problems linked by the multiplication rule of probabilities.

>
> What makes you think
> > that the probability of a beneficial mutation occurring on a member
> > of a lineage is not governed by a binomial probability problem?
>
> I think that the "second" mutation has no need to occur on a member of
> the lineage that produced the "first" one in any population whose
> lineages regularly cross. Do we need significant numbers of each
> beneficial mutation in the population? Of course. But what's to stop
> that from happening if 1. Selection favors both and 2. there is no
> extreme selection at work at any locus.

Recombination without error does not create new alleles. The transformation of reptiles into birds would require new alleles and those alleles must be created by mutations. Of course you might try to argue that the alleles that generate feathers already exist in reptile populations. Then all you have to do is start a breeding program that would transform reptile into birds. Our government would probabily fund this.

>
> Do
> > you think that HIV or E Coli will have different sets of adaptation
> > mutations dependent on the intensity of selection pressure?
>
> Huh? Where in the world did that come from?

It came from your claim. Do you think that the intensity of selection alters the mutations which would allow a lineage to adapt to a given selection pressure? Take test tubes of bacteria and put different concentrations of an antibiotic in it. Do you think the mutations that give resistance to that drug will vary with the concentration of the antibiotic solution?

>
> >> This is why
> >>> random recombination does not help HIV to evolve to combination
> >>> therapy even though the population is in the hundreds of
> >>> thousands in well treated patients. This is also why combination
> >>> herbicides work for suppressing the evolution of herbicide
> >>> resistant weeds despite weeds sexually reproduce. Of course, feel
> >>> free to present any real, measurable and repeatable empirical
> >>> evidence which contradicts this.
> >>>>
> >>>> Any example that uses either very strong selection or posits
> >>>> that neither allele is individually beneficial will (again)
> >>>> miss the point.
> >>
> >> Point missed.
> >>
> >>> Post your real, measurable and repeatable examples which support
> >>> your claim. There is no empirical evidence which supports your
> >>> claim, only your speculation. And you refuse to understand how
> >>> the multiplication rule affects random recombination as well as
> >>> rmns.
> >
> > Still no empirical example of rmns which shows that a population can
> > evolve efficiently to multiple selection pressures simultaneously.
>
> You tell us over and over that math is what prevents it. Show us the
> math with typical selection coefficients.

The selection coefficients only affect the rate of amplification, not the fundamental mathematics of rmns. My math shows that for a given selection pressure and mutation rate that you need a certain number of trials (replications) before you have a reasonable probability of a beneficial mutation occurring. You speculate about the rate of amplification and refuse to look at any real empirical examples. What is the selection coefficient for Lenski's E Coli starvation selection pressure experiment?

[Alan Kleinman MD PhD]

I disagree with you John and so does Google: "genetic fitness n. The reproductive success of a genotype, usually measured as the number of offspring produced by an individual that survive to reproductive age relative to the average for the population."

>
> So in the 3 drug cocktail bottleneck, the population keeps bouncing around
> inside a deep hole with three minima. The HIV mutates enough to keep jumping
> between basins, but not enough to leap out of the region that contains the
> separate minima. So, evolution is contained, in that situation, but, note that the HIV doesn't become extinct, so it is doing what biology does, which is "stayin' alive". Everything is fine until there is a major change to
> where the virus jumps out of the larger basin. To our knowledge that hasn't
> happened with HIV yet. However, consider when viruses jump species. That is
> a major shift.

And the reason why HIV can not get out of the hole in the fitness landscape is that it can not amplify any of the beneficial mutations for one drug or another. In order to get out of that hole, some member of the population must get 3 beneficial mutations simultaneously a very low probability outcome.

[Alan Kleinman MD PhD]

On Friday, September 2, 2016 at 2:00:03 PM UTC-7, Vincent Maycock wrote:
> On Fri, 2 Sep 2016 13:39:56 -0700 (PDT), Alan Kleinman MD PhD

> wrote:
>
> >On Friday, September 2, 2016 at 1:25:03 PM UTC-7, Vincent Maycock wrote:
> >> On Thu, 1 Sep 2016 17:53:19 -0700 (PDT), Alan Kleinman MD PhD
> >> wrote:
> >>
> >> >On Sunday, August 28, 2016 at 3:40:02 PM UTC-7, Steve L wrote:
> >> >> On Sun, 28 Aug 2016 06:08:43 -0700 (PDT), Steady Eddie
> >> >> wrote:
> >> >>
> >> >> >Why do you claim that HIV undergoing lethal selection pressures is not a representative example of how
> >> >> >RMNS works in the real world?
> >> >>
> >> >> Go to a park or the woods. Every plant or animal you see is under an
> >> >> uncountable number of selection pressures, yet very few are dead.
> >> >
> >> >They also aren't evolving by rmns.
> >>
> >> Not even by microevolution?
> >>
> >> >When selection pressures are random, you get genetic drift, but you aren't going to transform reptiles into birds that way.
> >
> >You are getting small genetic changes but not the kind of changes which would turn a reptile population into birds.
>
> If you wait long enough, what would prevent the small changes from
> adding up to large changes like the dinosaur-bird transition?
>

Just how long do you have to wait? The Lenski experiment using starvation as the selection pressure takes thousands of generations per benficial mutation and that's with just a single selection pressure acting (which targets several genetic loci) and a population size of e7 to e8. Putting any other stress on his populations would only slow the process further.

[Alan Kleinman MD PhD]

Sorry, I'm a primary care physician and not working for an institution that would pay the $5000 open source fee (for each paper). Go to your university library and get a copy for free which shows a step by step derivation of the equations. The fundamental equation for a single beneficial mutation A is given by:
P(A) = 1 − (1 − P(BeneficialA)𝜇)^(n∗nGA)
P(BeneficialA) is a term which takes into account that not all mutations at a particular site are beneficial, 𝜇 is the mutation rate, n is the population size and nGA is the number of generations that variant replicates. Note that (n∗nGA) is simply the total number of replications.

The next beneficial mutation B would have a similar type of equation with the joint probability of A and B occurring computed using the multiplication rule of probabilities.

[Alan Kleinman MD PhD]

On Friday, September 2, 2016 at 2:00:03 PM UTC-7, Vincent Maycock wrote:
> On Fri, 2 Sep 2016 13:39:56 -0700 (PDT), Alan Kleinman MD PhD

> wrote:
>
> >On Friday, September 2, 2016 at 1:25:03 PM UTC-7, Vincent Maycock wrote:
> >> On Thu, 1 Sep 2016 17:53:19 -0700 (PDT), Alan Kleinman MD PhD
> >> wrote:
> >>
> >> >On Sunday, August 28, 2016 at 3:40:02 PM UTC-7, Steve L wrote:
> >> >> On Sun, 28 Aug 2016 06:08:43 -0700 (PDT), Steady Eddie
> >> >> wrote:
> >> >>
> >> >> >Why do you claim that HIV undergoing lethal selection pressures is not a representative example of how
> >> >> >RMNS works in the real world?
> >> >>
> >> >> Go to a park or the woods. Every plant or animal you see is under an
> >> >> uncountable number of selection pressures, yet very few are dead.
> >> >
> >> >They also aren't evolving by rmns.
> >>
> >> Not even by microevolution?
> >>
> >> >When selection pressures are random, you get genetic drift, but you aren't going to transform reptiles into birds that way.
> >
> >You are getting small genetic changes but not the kind of changes which would turn a reptile population into birds.
>
> If you wait long enough, what would prevent the small changes from
> adding up to large changes like the dinosaur-bird transition?

The multiplication rule of probabilities would prevent this. This evolutionary process would require the transformation of far to many genes. Just the transformation of scales to feathers would require the transformation of at least eight genes. HIV can not efficiently transform two genes subject to selection by just 3 selection pressures.

[Vincent Maycock]

On Fri, 2 Sep 2016 14:54:04 -0700 (PDT), Alan Kleinman MD PhD
<klei...@sti.net> wrote:

>On Friday, September 2, 2016 at 1:40:03 PM UTC-7, Vincent Maycock wrote:
>> On Thu, 1 Sep 2016 17:38:01 -0700 (PDT), Alan Kleinman MD PhD
>> wrote:
>>
>> >On Sunday, August 28, 2016 at 9:45:02 AM UTC-7, Vincent Maycock wrote:
>> >> On Sun, 28 Aug 2016 06:08:43 -0700 (PDT), Steady Eddie
>> >> wrote:
>> >>
>> >> >On Thursday, 25 August 2016 17:21:22 UTC-6, Alan Kleinman MD PhD wrote:
>> >> >> On Thursday, August 25, 2016 at 6:11:22 AM UTC-7, Bill Rogers wrote:
>> >>
>> >> snip
>> >>
>> >> >> > Who doesn't accept them? Of course I accept them. What I don't accept is Alan's totally unsupported claim that *all* natural selection involves lethal selection pressures that wipe out every member of a species except for a handful who happen to have lucky mutations. Rare examples, usually from medical treatments, *do* indeed work that way. Most don't.
>> >> >
>> >> >You're starting to go Jillery on us, Bill.
>> >> >Dr. K doesn't claim that "*all* natural selection involves lethal selection pressures". He doesn't have to.
>> >> >
>> >> >Why do you claim that HIV undergoing lethal selection pressures is not a representative example of how
>> >> >RMNS works in the real world?
>> >>
>> >> Because that's how combination therapy works; if one selection
>> >> pressure (anti-viral drug) doesn't kill the organism, the other drug
>> >> in the combination therapy will.
>> >None of the anti-viral medications "kill" the virus, they only inhibit the reproduction of the virus.
>>
>> Which is much like killing them. If one drug won't prevent their
>> reproduction, then the other one can still prevent it, leading to the
>> evolutionary death of the viruses.
>The viruses are still replicating, they just can not improve fitness by rmns.

They may be still replicating, but the drug treatment would presumably
have a catastrophic effect on the virus population, which wouldn't be
the case for milder forms of natural selection.

>> >What combination anti-viral therapy does is inhibit the amplification of any beneficial mutations for one drug or another. Without amplification, the probability of another beneficial mutation occurring on the particular lineage remains small.
>> >>
>> >> The point is, though, that this is only true if the selection
>> >> pressures are lethal; if they're not, no simultaneous beneficial
>> >> mutations are required for natural selection to work.
>> >Vincent, give us one real, measurable and repeatable example of a population evolving efficiently by rmns to more than a single non-lethal selection pressure.
>>
>> In the fossil record, we find horses becoming more cursorial, (adapted
>> for running in the open plains) at the same time as their teeth became
>> adapted to eating tougher plant foods (like grass).
>Evolutionists read fossil tea leaves to fit their belief system.

https://en.wikipedia.org/wiki/Evolution_of_the_horse#/media/File:Horseevolution.png

These pictures of the changes to the early horses definitely look
clearer than tea-leaf reading to me.

Maybe paleontologists' pattern recognition is better than yours, and
that's why you think they're "tea leaf reading."

[Vincent Maycock]

On Fri, 2 Sep 2016 16:11:07 -0700 (PDT), Alan Kleinman MD PhD
<klei...@sti.net> wrote:

>On Friday, September 2, 2016 at 2:00:03 PM UTC-7, Vincent Maycock wrote:
>> On Fri, 2 Sep 2016 13:39:56 -0700 (PDT), Alan Kleinman MD PhD
>> wrote:
>>
>> >On Friday, September 2, 2016 at 1:25:03 PM UTC-7, Vincent Maycock wrote:
>> >> On Thu, 1 Sep 2016 17:53:19 -0700 (PDT), Alan Kleinman MD PhD
>> >> wrote:
>> >>
>> >> >On Sunday, August 28, 2016 at 3:40:02 PM UTC-7, Steve L wrote:
>> >> >> On Sun, 28 Aug 2016 06:08:43 -0700 (PDT), Steady Eddie
>> >> >> wrote:
>> >> >>
>> >> >> >Why do you claim that HIV undergoing lethal selection pressures is not a representative example of how
>> >> >> >RMNS works in the real world?
>> >> >>
>> >> >> Go to a park or the woods. Every plant or animal you see is under an
>> >> >> uncountable number of selection pressures, yet very few are dead.
>> >> >
>> >> >They also aren't evolving by rmns.
>> >>
>> >> Not even by microevolution?
>> >>
>> >> >When selection pressures are random, you get genetic drift, but you aren't going to transform reptiles into birds that way.
>> >
>> >You are getting small genetic changes but not the kind of changes which would turn a reptile population into birds.
>>
>> If you wait long enough, what would prevent the small changes from
>> adding up to large changes like the dinosaur-bird transition?
>The multiplication rule of probabilities would prevent this. This evolutionary process would require the transformation of far to many genes. Just the transformation of scales to feathers would require the transformation of at least eight genes.

And how many millions of years would it take for this transformation
to occur (with consecutive steps rather than simultaneous ones -- if
necessary, in your view)?

[Bill Rogers]

On Friday, September 2, 2016 at 6:45:02 PM UTC-4, Alan Kleinman MD PhD wrote:

> > You tell us over and over that math is what prevents it. Show us the
> > math with typical selection coefficients.
> The selection coefficients only affect the rate of amplification, not the fundamental mathematics of rmns. My math shows that for a given selection pressure and mutation rate that you need a certain number of trials (replications) before you have a reasonable probability of a beneficial mutation occurring. You speculate about the rate of amplification and refuse to look at any real empirical examples. What is the selection coefficient for Lenski's E Coli starvation selection pressure experiment?

OK. Let's do the math here. I trust you still remember how to set up numerical solutions for differential equations in matlab or mathematica or even excel.

Let's consider an organism with four genotypes, ab, aB, Ab, and AB. Let's call ab the wild type. The mutations a to A and b to B are independent and rare. Each one alone gives the organism a small reproductive advantage, and together they combine to give a small combined advantage.

Let's say that the fitnesses of the genotypes are as follows ab:.90, aB: .95, Ab: .95, and AB: 1.0.

Let's say that the mutations are independent, and that the frequency of each is 10^-8 per generation. So that, by the multiplication rule of probabilities, the frequency of ab to AB mutations is 10^-16 per generation. Let's also assume, just to be fair that the mutation rate is symmetric, that is that of aB to ab is the same as the rate of ab to aB (it does not actually effect the model much to include the reversion rate, but why not throw it in there).

Now you set up differential (or difference) equations to describe the changes in genotype frequencies.

For each genotype x(i) the time rate of change of the frequency of x(i) is ...

dx(i)/dt = SUM(over j)[x(j)f(j)Q(ij)] - avg(f)*x(i)

where Q(ij) is the frequency of mutation from the ith genotype to the jth genotype and the avg(f) is the population weighted average of the fitness.

You, of course, know this already, but this is the well known quasispecies equation, and anyone who, unlike you, is not an expert on the mathematics of RMNS can look it up in Martin Nowak's lovely book, Evolutionary Dynamics, or on line.

It simply says that the change in frequency of any given genotype equals the sum over all genotypes of each genotypes fitness times its frequency in the population times the rate at which it yields mutants to that given genotype, not forgetting that the rate of mutation from x(i) to x(i) is close to 1.

Just to be clear, mutation rates are

ab to aB 10^-8
ab to Ab 10^-8
ab to AB 10^-16
ab to ab 1-(2*10^-8 + 10^-16) this counts as a "mutation" in the "mutation matrix" even though there's no change in the allele. Necessary for proper bookkeeping.

Then you pick your initial conditions and do a numerical solution. The steps are so small that a straight Euler's method will do, but I've done a modified Euler's method and the results are essentially the same, the only differences being minor changes in the oscillations around the final equilibrium state (dominated by the AB genotype regardless of the numerical method used).

So, starting with a pure population of genotype ab, with the mutation rates and fitnesses I mentioned above, it takes 435 generations for the double mutant AB to reach a frequency of 99%.

There's no problem whatsoever with the two beneficial mutants amplifying simultaneously. Nothing gets disrupted.

[Bill Rogers]

A couple of additional points.

1. Obviously there's no sexual reproduction in this model. If there were, the double mutants would take over faster.

2. I used the "multiplication law of probabilities" to get the low frequency of direct ab -> AB double mutations: 10^-8 times 10^-8 gives 10^-16. But the model is not driven by simultaneous mutations anyway. The results are not significantly different if you set the probability of simultaneous double mutations all the way to zero.

3. I can't put plots up here, but just to give an idea of how the population changes over time..... For the first 200 generations the wild type, ab, dominates and stays at frequencies over 99%, with the double mutants essentially at zero and the single mutants creeping up slowly. Then from generations 200 - 300 the single mutants take off and overtake the wild type, and a low percentage of the double mutants appear (by mutations occurring in the now abundant single mutants). Finally, from generations 300-435 the double mutants gradually take over and the single mutants and wild type fall off to negligible frequencies, maintained only by the reversion rate.

[Alan Kleinman MD PhD]

On Friday, September 2, 2016 at 5:50:02 PM UTC-7, Vincent Maycock wrote:
> On Fri, 2 Sep 2016 14:54:04 -0700 (PDT), Alan Kleinman MD PhD

The virus can still maintain populations in the hundreds of thousands and can replicate for many, many generations. How many replication trials are needed until some member improves fitness?

>
> >> >What combination anti-viral therapy does is inhibit the amplification of any beneficial mutations for one drug or another. Without amplification, the probability of another beneficial mutation occurring on the particular lineage remains small.
> >> >>
> >> >> The point is, though, that this is only true if the selection
> >> >> pressures are lethal; if they're not, no simultaneous beneficial
> >> >> mutations are required for natural selection to work.
> >> >Vincent, give us one real, measurable and repeatable example of a population evolving efficiently by rmns to more than a single non-lethal selection pressure.
> >>
> >> In the fossil record, we find horses becoming more cursorial, (adapted
> >> for running in the open plains) at the same time as their teeth became
> >> adapted to eating tougher plant foods (like grass).
> >Evolutionists read fossil tea leaves to fit their belief system.
>
> https://en.wikipedia.org/wiki/Evolution_of_the_horse#/media/File:Horseevolution.png
>
> These pictures of the changes to the early horses definitely look
> clearer than tea-leaf reading to me.
>
> Maybe paleontologists' pattern recognition is better than yours, and
> that's why you think they're "tea leaf reading."

We are presenting hard mathematical science here and the empirical evidence which correlates with this mathematics, not reading Rorschach tests.

[Alan Kleinman MD PhD]

On Friday, September 2, 2016 at 6:00:03 PM UTC-7, Vincent Maycock wrote:
> On Fri, 2 Sep 2016 16:11:07 -0700 (PDT), Alan Kleinman MD PhD

I'll let you try to do that math yourself. To give you a sense of your problem, Lenski's E Coli starvation selection pressure experiment takes thousands of generation for each beneficial mutation. That's only a single selection pressure which targets several genetic loci. What if Lenski used thermal stress in combination with starvation. Do you think the evolutionary process would go faster?

[Mark Isaak]

Kleinman claims that simultaneous selective pressures only slow down the
evolutionary process. I doubt that. How many generations it would take
to go from ab to 99% Ab (with no selection for b/B), followed
immediately by selection on B to go to AB?

--
Mark Isaak eciton (at) curioustaxonomy (dot) net
"The evil that is in the world always comes of ignorance, and good
intentions may do as much harm as malevolence, if they lack
understanding." - Albert Camus, _The Plague_

[jillery]

On Fri, 2 Sep 2016 06:27:53 -0700 (PDT), Alan Kleinman MD PhD
<klei...@sti.net> wrote:

>On Friday, September 2, 2016 at 5:10:03 AM UTC-7, jillery wrote:
>> On Thu, 1 Sep 2016 18:04:47 -0700 (PDT), Alan Kleinman MD PhD
>> wrote:
>>
>> >On Wednesday, August 31, 2016 at 1:10:02 PM UTC-7, jillery wrote:
>> >> On Wed, 31 Aug 2016 12:19:56 -0700 (PDT), Steady Eddie

>> >> wrote:
>> >>
>> >> >On Sunday, 28 August 2016 10:45:02 UTC-6, Vincent Maycock wrote:
>> >> >> On Sun, 28 Aug 2016 06:08:43 -0700 (PDT), Steady Eddie
>> >> >> wrote:
>> >> >>

>> >> >> >On Thursday, 25 August 2016 17:21:22 UTC-6, Alan Kleinman MD PhD wrote:
>> >> >> >> On Thursday, August 25, 2016 at 6:11:22 AM UTC-7, Bill Rogers wrote:
>> >> >>
>> >> >> snip
>> >> >>
>> >> >> >> > Who doesn't accept them? Of course I accept them. What I don't accept is Alan's totally unsupported claim that *all* natural selection involves lethal selection pressures that wipe out every member of a species except for a handful who happen to have lucky mutations. Rare examples, usually from medical treatments, *do* indeed work that way. Most don't.
>> >> >> >
>> >> >> >You're starting to go Jillery on us, Bill.
>> >> >> >Dr. K doesn't claim that "*all* natural selection involves lethal selection pressures". He doesn't have to.
>> >> >> >

>> >> >> >Why do you claim that HIV undergoing lethal selection pressures is not a representative example of how
>> >> >> >RMNS works in the real world?
>> >> >>

>> >> >> Because that's how combination therapy works; if one selection
>> >> >> pressure (anti-viral drug) doesn't kill the organism, the other drug
>> >> >> in the combination therapy will.
>> >> >

>> >> >Yes, and that's why combination therapy works - because that's how RMNS works in the wild - in fact,
>> >> >that's how it works in all life.
>> >> >
>> >> >Do you have reason to doubt this?
>> >> >

>> >> >> The point is, though, that this is only true if the selection
>> >> >> pressures are lethal; if they're not, no simultaneous beneficial
>> >> >> mutations are required for natural selection to work.
>> >> >

>> >> >That's not the point of the research.
>> >> >
>> >> >The point of Dr. K's research is to quantify just how likely the RMNS process is to have created and
>> >> >selected any of a vast variety of different machines, traits, processes, organisms and/or body plans we see
>> >> >in nature.
>> >> >
>> >> >To do so, you have to start from the beginning - how likely is any given functional piece of DNA to mutate
>> >> >into some other sequence that codes for a different functional protein?
>> >> >
>> >> >I'm sure this number is floating around; does anybody have a reference handy?
>> >>
>> >>
>> >> Of course, the answer to your question depends on your definition of
>> >> "different functional protein". Are you willing to provide one?

>> >What is that selection pressure for hemoglobin or for insulin or for the DNA replicase system or for...?
>>
>>
>> So that's a "no". BTW, are you Steadly?
>Of course that's a "no" because these selection pressures do not exist. Let me check at the top of the post. That's a no also, are you having a private conversation. Better be careful, the Russians may hack this.


It's no surprise that you misrepresent what I posted. Even you should
be able to recognize that the veracity of Steadly's point depends on
Steadly's opinion, which is something nobody but Steadly can
rightfully provide. I absolutely encourage you to share your
opinions, but not to give Steadly cover for evading my question.
--
This space is intentionally not blank.

[jillery]

On Fri, 2 Sep 2016 12:10:57 -0700 (PDT), Steady Eddie
<1914o...@gmail.com> wrote:

>On Thursday, 1 September 2016 00:15:03 UTC-6, Glenn wrote:

>> "Steady Eddie" <1914o...@gmail.com> wrote in message news:e2cf078a-9305-45a8...@googlegroups.com...

>> > On Wednesday, 31 August 2016 19:40:02 UTC-6, jillery wrote:
>> >> On Wed, 31 Aug 2016 13:20:48 -0700 (PDT), Steady Eddie

>> >> <1914o...@gmail.com> wrote:

>> >> >Well, what is the consensus definition of "functional protein"?
>> >> >
>> >> >My idea of a functional protein is any protein that could plausibly be expected to perform a function in the cell in which it originated.
>> >> >Basically, I'm talking about mutational changes in existing, functional proteins which result in a different functional proteins - I don't mean proteins originating from scratch.
>> >>
>> >>
>> >> That's not it. In order to say that a protein has a different
>> >> function, one must be clear what protein functions qualify as
>> >> different.
>> >
>> > Of course. That's one of the technical questions that science is there to find an answer to.
>> >
>> >> For example, when Lenski's E.coli evolved the ability to
>> >> metabolize citrate in oxic conditions, many supporters of ID claimed
>> >> that it wasn't a different function. Does your definition of
>> >> "different functional protein" include Lenski's E.coli mutation?
>> >
>> > My memory fails me.
>> > Reference please.
>> >
>> Looks like you got a real experimentalist by the tail in Jillery.
>
>A true Darwinist, and a rhetorical specialist; she pulled off a cite-bluff without even providing a cite, then
>assigned the job to me LOL!

A cite bluff is where one refers to a nonexistent event. Lenski's
E.col have been around since the 1980s, as the most trivial Google
search demonstrates, like the one below:

>> "We conclude that the rarity of the LTEE mutant was an artifact of the experimental conditions and not a unique evolutionary event. No new genetic information (novel gene function) evolved."
>> http://www.ncbi.nlm.nih.gov/pubmed/26833416
>>
>> http://www.evolutionnews.org/2016/05/richard_lenski102839.html
>
>Yup, pretty much dispenses with her cite-bluff. She probably never even read it; just parroted some
>spoon-feeding from some Darwinist site.

Since the above shows that Lenski's E.coli are real, and that
supporters of ID claimed they evolved no new function, right here
would have been a good place for you to say how you think the above
cite "dispenses" with my cite-bluff. Don't be insulted that I don't
wait for a coherent reply.

[jillery]

On Fri, 2 Sep 2016 13:06:02 -0700 (PDT), Alan Kleinman MD PhD
<klei...@sti.net> wrote:


<mercy snip>

>I believe the citrate metabolizer Lenski obtained occurred because that lineage got a mutation which caused a defective cell wall (spherical form) and because of this the citrate was able to be transported into the cell more easily making the citrate available for the Krebs cycle.

You believe incorrectly. All of Lenksi's E.coli populations evolved
rounded forms, as compared to wild E.coli's rod shape. This isn't a
defect, but a positive response to the artificial environment. The
mutations caused changes to the proteins which transport citrate
through the cell wall.

[Alan Kleinman MD PhD]

On Saturday, September 3, 2016 at 9:50:02 AM UTC-7, jillery wrote:
> On Fri, 2 Sep 2016 13:06:02 -0700 (PDT), Alan Kleinman MD PhD

> wrote:
>
>
> <mercy snip>
>
>
> >I believe the citrate metabolizer Lenski obtained occurred because that lineage got a mutation which caused a defective cell wall (spherical form) and because of this the citrate was able to be transported into the cell more easily making the citrate available for the Krebs cycle.
>
>
> You believe incorrectly. All of Lenksi's E.coli populations evolved
> rounded forms, as compared to wild E.coli's rod shape. This isn't a
> defect, but a positive response to the artificial environment. The
> mutations caused changes to the proteins which transport citrate
> through the cell wall.

Really? So all of Lenski's population became citrate metabolizers?
http://rationalwiki.org/wiki/Richard_Lenski
"They reported that, as a result of several beneficial mutations, his organisms had acquired the ability to metabolize citrate - or more correctly an ability to transport it through the cell wall prior to metabolizing it."

[Alan Kleinman MD PhD]

Anybody know why TO won't post my response to Bill Rogers mathematics post?

[jillery]

On Sat, 3 Sep 2016 10:09:11 -0700 (PDT), Alan Kleinman MD PhD
<klei...@sti.net> wrote:

>On Saturday, September 3, 2016 at 9:50:02 AM UTC-7, jillery wrote:
>> On Fri, 2 Sep 2016 13:06:02 -0700 (PDT), Alan Kleinman MD PhD
>> wrote:
>>
>>
>> <mercy snip>
>>
>>
>> >I believe the citrate metabolizer Lenski obtained occurred because that lineage got a mutation which caused a defective cell wall (spherical form) and because of this the citrate was able to be transported into the cell more easily making the citrate available for the Krebs cycle.
>>
>>
>> You believe incorrectly. All of Lenksi's E.coli populations evolved
>> rounded forms, as compared to wild E.coli's rod shape. This isn't a
>> defect, but a positive response to the artificial environment. The
>> mutations caused changes to the proteins which transport citrate
>> through the cell wall.
>Really? So all of Lenski's population became citrate metabolizers?

Rounded form has nothing to do with the mutation to metabolize
citrate. All of Lenski's E.coli populations created lots of
mutations. Only one population became predominately (not exclusively)
citrate metabolizers.

>http://rationalwiki.org/wiki/Richard_Lenski
>"They reported that, as a result of several beneficial mutations, his organisms had acquired the ability to metabolize citrate - or more correctly an ability to transport it through the cell wall prior to metabolizing it."

That's what I said. And to be even more complete, transporting
citrate in the presence of oxygen is the new function which
distinguishes that particular population from the others. It's that
subtle yet significant distinction which throws most ID supporters.

[jillery]

You keep asking that question. Will you make explicit what you mean
by "thermal stress", and how you would apply both in combination?

[Alan Kleinman MD PhD]

On Saturday, September 3, 2016 at 12:05:03 PM UTC-7, jillery wrote:
> On Sat, 3 Sep 2016 08:37:08 -0700 (PDT), Alan Kleinman MD PhD

That's an easy one. Lenski has run at least two major experiments. In one experiment which we have talked about is the limited glucose (starvation) selection pressure but the other is an experiment where he subjects E Coli to thermal stress http://bio.classes.ucsc.edu/bioe200b/pdf%20files/Lenski_%26_Bennett_AmNat_1993.pdf
To impose both starvation and thermal stress simultaneously, take the starvation selection pressure experiment and run the experiment at non-optimal temperatures. What my mathematics predicts is that even if a beneficial mutation occurs for the starvation pressure, the thermal stress will inhibit the amplification of that variant and likewise if a beneficial mutation occurs for the thermal stress, the starvation pressure will inhibit the amplification of that variant.

On another issue, have you ever had TO not post a particular response? TO will not post my response to Bill Rogers mathematical model. His model is based on a physically incorrect assumption.

[Steady Eddie]

On Saturday, 3 September 2016 12:15:02 UTC-6, Alan Kleinman MD PhD wrote:
> Anybody know why TO won't post my response to Bill Rogers mathematics post?

I have noticed that when I open a reply and take a long time to finish my response, T.O. somehow
times out, and my whole reply gets lost. Frustrating!
(when I re-do my reply, it always seems inferior to my original).

What I do now, for long replies, is:

-open a reply box
-select ALL and paste it into a notepad program
-close the reply box
-take my time and formulate my replies in notepad, as if it were in the reply box
-When I'm done, I select ALL of my notepad file, and copy it.
-Then I re-open the original reply box (reply to the original post)
-select ALL of the reply box contents
-Paste my entire notepad contents into the reply box, replacing the entire contents of the reply box with the notepad contents
-post the reply.

This way, I have a copy of my complete reply in case it gets lost, and T.O. seems to accept it just fine.

Hope this helps.

[Bill Rogers]

On Saturday, September 3, 2016 at 2:15:02 PM UTC-4, Alan Kleinman MD PhD wrote:
> Anybody know why TO won't post my response to Bill Rogers mathematics post?

The Evil Atheist Conspiracy is working assiduously to prevent the appearance of your devastating response. Alas, though, you have both an MD and a PhD, so you'll probably be able to figure out a way to get the post through in the end.

[Vincent Maycock]

If evolutionary changes are not due to catastrophic environmental
factors, it seems that amplification and eventual fixation can occur
simultaneously.

For example, take the evolutionary horse series I posted.

If a horse becomes slightly better adapted for running over the
plains, but still has low-crowned teeth more useful for eating soft
forest foliage rather than tough grass, the low-crowned teeth are not
going to "slow down the amplification" of the cursorial types'
mutation -- if the stresses are not too great.

Instead, the speedier low-crowned horses' mutation will amplify
despite their low-crowned teeth, and when the taller teeth for eating
grass come into the picture, the mutations for faster, tall-toothed
types of horses will amplify the best of all.

>> >> >What combination anti-viral therapy does is inhibit the amplification of any beneficial mutations for one drug or another. Without amplification, the probability of another beneficial mutation occurring on the particular lineage remains small.
>> >> >>
>> >> >> The point is, though, that this is only true if the selection
>> >> >> pressures are lethal; if they're not, no simultaneous beneficial
>> >> >> mutations are required for natural selection to work.
>> >> >Vincent, give us one real, measurable and repeatable example of a population evolving efficiently by rmns to more than a single non-lethal selection pressure.
>> >>
>> >> In the fossil record, we find horses becoming more cursorial, (adapted
>> >> for running in the open plains) at the same time as their teeth became
>> >> adapted to eating tougher plant foods (like grass).
>> >Evolutionists read fossil tea leaves to fit their belief system.
>>
>> https://en.wikipedia.org/wiki/Evolution_of_the_horse#/media/File:Horseevolution.png
>>
>> These pictures of the changes to the early horses definitely look
>> clearer than tea-leaf reading to me.
>>
>> Maybe paleontologists' pattern recognition is better than yours, and
>> that's why you think they're "tea leaf reading."
>We are presenting hard mathematical science here and the empirical evidence which correlates with this mathematics, not reading Rorschach tests.

What may seem like a Rorschach test to you turns out to be a wealth of
knowledge about life on earth in the past to an expert paleontologist.
Here's the horses again:


https://en.wikipedia.org/wiki/Evolution_of_the_horse#/media/File:Horseevolution.png

[Alan Kleinman MD PhD]

On Saturday, September 3, 2016 at 2:45:02 PM UTC-7, Vincent Maycock wrote:
> On Sat, 3 Sep 2016 08:30:14 -0700 (PDT), Alan Kleinman MD PhD

Therefore reptiles can turn into birds?

[Öö Tiib]

On Saturday, 3 September 2016 21:15:02 UTC+3, Alan Kleinman MD PhD wrote:
> Anybody know why TO won't post my response to Bill Rogers mathematics post?

Are you posting with the Google? Google initially bought Usenet archives
and online posting software from DejaNews. Posting software was nowhere
as good like real NNTP client (for example Microsoft's Outlook Express)
but still relatively decent.

However then Google rewrote everything using some novice programmers and
named the resulting crap "google groups". Now it only sometimes does work.
Other times it runs into some sort of limits internally but instead of
reporting being crap it throws your post silently away.

[jillery]

Thank your for your clear reply to my question. However, you should
consider the following points:

1. You don't say what you mean by "beneficial". The same mutation can
be beneficial or detrimental to an organism, depending on the
environment. Do you constrain your meaning of beneficial mutation
here to only the one particular environment you described above? If
so, how do you reasonably apply that specific case to conclusions
about RMNS for all environments in general?

2. Lenski's LTEE populations developed numerous mutations throughout
the experiment, as would any biological population. What they were
very unlikely to do was produce a particular mutation on demand, as
the results clearly show. That's not how random mutations work.

A fatal flaw in your expressed methodology above is that you're
looking for a particular kind of mutation, ex. one that improves
response to thermal stress, while literally ignoring all the other
mutations that are created. You're not testing how RMNS actually
works.

>On another issue, have you ever had TO not post a particular response? TO will not post my response to Bill Rogers mathematical model. His model is based on a physically incorrect assumption.

As has been pointed out semi-regularly, and quite recently, the
problem you mention above almost certainly isn't caused by T.O., but
instead by Google Groups (GG) you use, which is known to limit the
total number of posts to any one particular thread (thread is not the
same as topic/subject). If you're determined to stick with GG, there
are some workarounds, one of them is described here:

<https://groups.google.com/forum/#!original/talk.origins/BJnTtClSVtM/tCaKMoHAAwAJ>

[Alan Kleinman MD PhD]

On Saturday, September 3, 2016 at 3:50:03 PM UTC-7, jillery wrote:
> On Sat, 3 Sep 2016 12:50:16 -0700 (PDT), Alan Kleinman MD PhD

A beneficial mutation improves fitness to reproduce. And true, a beneficial mutation for one variant may not be a beneficial mutation for another variant. The environment is tightly tied to whether a mutation is beneficial or not. For example, a drug resistant variant may be most fit in an environment with the drug selection pressure but in the drug free environment, the non-drug resistant variant may be more fit to reproduce.

>
> 2. Lenski's LTEE populations developed numerous mutations throughout
> the experiment, as would any biological population. What they were
> very unlikely to do was produce a particular mutation on demand, as
> the results clearly show. That's not how random mutations work.

It's been a while since I read his papers but if I recall, all ten of his populations followed the same evolutionary trajectory (except for his special case of the citrate metabolizer).

>
> A fatal flaw in your expressed methodology above is that you're
> looking for a particular kind of mutation, ex. one that improves
> response to thermal stress, while literally ignoring all the other
> mutations that are created. You're not testing how RMNS actually
> works.

Adaptation by rmns to stressors requires beneficial mutations. Neutral and detrimental mutations are also occurring. But a detrimental mutation to a variant which is evolving to the particular selection pressure only reduces the population size which is on that evolutionary trajectory. Neutral mutations are not contributing to fitness by definition but they do increase diversity of the population. My mathematics was framed by real, measurable and repeatable examples of rmns.

Now what do you think would happen if Lenski ran his experiment with both starvation and thermal stress? With starvation stress alone it takes a thousand generations per beneficial mutation. Under ideal circumstances, it would only take 30 doublings to give e9 variants with a particular beneficial mutation.

>
>
> >On another issue, have you ever had TO not post a particular response? TO will not post my response to Bill Rogers mathematical model. His model is based on a physically incorrect assumption.
>
>
> As has been pointed out semi-regularly, and quite recently, the
> problem you mention above almost certainly isn't caused by T.O., but
> instead by Google Groups (GG) you use, which is known to limit the
> total number of posts to any one particular thread (thread is not the
> same as topic/subject). If you're determined to stick with GG, there
> are some workarounds, one of them is described here:
>
> <https://groups.google.com/forum/#!original/talk.origins/BJnTtClSVtM/tCaKMoHAAwAJ>

I'll try that.

[Alan Kleinman MD PhD]

On Friday, September 2, 2016 at 7:45:03 PM UTC-7, Bill Rogers wrote:
> On Friday, September 2, 2016 at 6:45:02 PM UTC-4, Alan Kleinman MD PhD wrote:
>
> > > You tell us over and over that math is what prevents it. Show us the
> > > math with typical selection coefficients.
> > The selection coefficients only affect the rate of amplification, not the fundamental mathematics of rmns. My math shows that for a given selection pressure and mutation rate that you need a certain number of trials (replications) before you have a reasonable probability of a beneficial mutation occurring. You speculate about the rate of amplification and refuse to look at any real empirical examples. What is the selection coefficient for Lenski's E Coli starvation selection pressure experiment?
>
> OK. Let's do the math here. I trust you still remember how to set up numerical solutions for differential equations in matlab or mathematica or even excel.

I'll do my best.

>
> Let's consider an organism with four genotypes, ab, aB, Ab, and AB. Let's call ab the wild type. The mutations a to A and b to B are independent and rare. Each one alone gives the organism a small reproductive advantage, and together they combine to give a small combined advantage.
>
> Let's say that the fitnesses of the genotypes are as follows ab:.90, aB: .95, Ab: .95, and AB: 1.0.
>
> Let's say that the mutations are independent, and that the frequency of each is 10^-8 per generation. So that, by the multiplication rule of probabilities, the frequency of ab to AB mutations is 10^-16 per generation. Let's also assume, just to be fair that the mutation rate is symmetric, that is that of aB to ab is the same as the rate of ab to aB (it does not actually effect the model much to include the reversion rate, but why not throw it in there).
>
> Now you set up differential (or difference) equations to describe the changes in genotype frequencies.
>
> For each genotype x(i) the time rate of change of the frequency of x(i) is ...
>

> dx(i)/dt = SUM(over j)[x(j)f(j)Q(ij)] – avg(f)*x(i)
Bill, do something for me here, put the dimensions on each of the variables in your differential equation.

>
> where Q(ij) is the frequency of mutation from the ith genotype to the jth genotype and the avg(f) is the population weighted average of the fitness.
>
> You, of course, know this already, but this is the well known quasispecies equation, and anyone who, unlike you, is not an expert on the mathematics of RMNS can look it up in Martin Nowak's lovely book, Evolutionary Dynamics, or on line.

Since the quasispecies equation was designed to study the evolution of HIV, why don't you apply your model to this case and do the math. You have two genetic loci (protease and reverse transcriptase). You have different alleles, put fitness values to each of the different combinations of alleles and show us that 3 drug combination therapy does not work.

>
> It simply says that the change in frequency of any given genotype equals the sum over all genotypes of each genotypes fitness times its frequency in the population times the rate at which it yields mutants to that given genotype, not forgetting that the rate of mutation from x(i) to x(i) is close to 1.

There is an implicit assumption you are using here. It is the same assumption that Haldane uses in his cost of natural selection model and Kimura uses in his probability of fixation model. This implicit assumption is physically incorrect. As a hint, this assumption is how natural selection works.

>
> Just to be clear, mutation rates are
>
> ab to aB 10^-8
> ab to Ab 10^-8
> ab to AB 10^-16
> ab to ab 1-(2*10^-8 + 10^-16) this counts as a "mutation" in the "mutation matrix" even though there's no change in the allele. Necessary for proper bookkeeping.
>
> Then you pick your initial conditions and do a numerical solution. The steps are so small that a straight Euler's method will do, but I've done a modified Euler's method and the results are essentially the same, the only differences being minor changes in the oscillations around the final equilibrium state (dominated by the AB genotype regardless of the numerical method used).

I don't doubt your skills in plugging numbers into equations. I doubt your skills in understanding the equations you are working with and whether your equations correctly correlate with reality. A major reason my papers got published was that the editors of the journal were looking for mathematical papers which correlate with real empirical data. You should study these papers because they will give you insight into why 2 drug therapy for the treatment of Malaria can still allow for emergence of resistance.

>
> So, starting with a pure population of genotype ab, with the mutation rates and fitnesses I mentioned above, it takes 435 generations for the double mutant AB to reach a frequency of 99%.

You and Schneider, you take mathematical models using invalid assumptions and draw incorrect conclusions. So your calculations show that combination therapy does not work for the treatment of HIV. You have advanced evolutionism.

>
> There's no problem whatsoever with the two beneficial mutants amplifying simultaneously. Nothing gets disrupted.

Sure something has been disrupted, it is mathematical logic you are disrupting by using an incorrect assumption to derive your model. Let's see if you can figure out what that incorrect assumption is.

[Bill Rogers]

On Saturday, September 3, 2016 at 7:55:02 PM UTC-4, Alan Kleinman MD PhD wrote:
> On Friday, September 2, 2016 at 7:45:03 PM UTC-7, Bill Rogers wrote:
> > On Friday, September 2, 2016 at 6:45:02 PM UTC-4, Alan Kleinman MD PhD wrote:
> >
> > > > You tell us over and over that math is what prevents it. Show us the
> > > > math with typical selection coefficients.
> > > The selection coefficients only affect the rate of amplification, not the fundamental mathematics of rmns. My math shows that for a given selection pressure and mutation rate that you need a certain number of trials (replications) before you have a reasonable probability of a beneficial mutation occurring. You speculate about the rate of amplification and refuse to look at any real empirical examples. What is the selection coefficient for Lenski's E Coli starvation selection pressure experiment?
> >
> > OK. Let's do the math here. I trust you still remember how to set up numerical solutions for differential equations in matlab or mathematica or even excel.
> I'll do my best.
> >
> > Let's consider an organism with four genotypes, ab, aB, Ab, and AB. Let's call ab the wild type. The mutations a to A and b to B are independent and rare. Each one alone gives the organism a small reproductive advantage, and together they combine to give a small combined advantage.
> >
> > Let's say that the fitnesses of the genotypes are as follows ab:.90, aB: .95, Ab: .95, and AB: 1.0.
> >
> > Let's say that the mutations are independent, and that the frequency of each is 10^-8 per generation. So that, by the multiplication rule of probabilities, the frequency of ab to AB mutations is 10^-16 per generation. Let's also assume, just to be fair that the mutation rate is symmetric, that is that of aB to ab is the same as the rate of ab to aB (it does not actually effect the model much to include the reversion rate, but why not throw it in there).
> >
> > Now you set up differential (or difference) equations to describe the changes in genotype frequencies.
> >
> > For each genotype x(i) the time rate of change of the frequency of x(i) is ...
> >
> > dx(i)/dt = SUM(over j)[x(j)f(j)Q(ij)] – avg(f)*x(i)

> Bill, do something for me here, put the dimensions on each of the variables in your differential equation.

Sure, Alan, it's just that as an MD PhD expert in the hard mathematics of rmns, I thought it would be obvious to you. But OK....

x(i) is dimensionless, it's a number of organisms of genotype "i" divided by a total number of organisms.

dx(i)/dt therefore has dimensions of 1/time

f(i), the fitness is also a dimensionless proportion

the entries in the mutation matrix Q(ij) are, likewise, dimensionless proportions.

So the dimensions of each side of the equation are 1/time.

> >
> > where Q(ij) is the frequency of mutation from the ith genotype to the jth genotype and the avg(f) is the population weighted average of the fitness.
> >
> > You, of course, know this already, but this is the well known quasispecies equation, and anyone who, unlike you, is not an expert on the mathematics of RMNS can look it up in Martin Nowak's lovely book, Evolutionary Dynamics, or on line.
> Since the quasispecies equation was designed to study the evolution of HIV, why don't you apply your model to this case and do the math. You have two genetic loci (protease and reverse transcriptase). You have different alleles, put fitness values to each of the different combinations of alleles and show us that 3 drug combination therapy does not work.

I'm not talking about HIV. Three drug therapy does work. So what? The fitnesses of the wild type and single and even double mutants are abysmal under triple drug treatment.

> >
> > It simply says that the change in frequency of any given genotype equals the sum over all genotypes of each genotypes fitness times its frequency in the population times the rate at which it yields mutants to that given genotype, not forgetting that the rate of mutation from x(i) to x(i) is close to 1.
> There is an implicit assumption you are using here. It is the same assumption that Haldane uses in his cost of natural selection model and Kimura uses in his probability of fixation model. This implicit assumption is physically incorrect. As a hint, this assumption is how natural selection works.

Sorry, I have no interest in trying to guess what you think is an incorrect assumption. Either you have an argument to make or you don't. If not, suit yourself.

> >
> > Just to be clear, mutation rates are
> >
> > ab to aB 10^-8
> > ab to Ab 10^-8
> > ab to AB 10^-16
> > ab to ab 1-(2*10^-8 + 10^-16) this counts as a "mutation" in the "mutation matrix" even though there's no change in the allele. Necessary for proper bookkeeping.
> >
> > Then you pick your initial conditions and do a numerical solution. The steps are so small that a straight Euler's method will do, but I've done a modified Euler's method and the results are essentially the same, the only differences being minor changes in the oscillations around the final equilibrium state (dominated by the AB genotype regardless of the numerical method used).

> I don't doubt your skills in plugging numbers into equations. I doubt your skills in understanding the equations you are working with and whether your equations correctly correlate with reality. A major reason my papers got published was that the editors of the journal were looking for mathematical papers which correlate with real empirical data. You should study these papers because they will give you insight into why 2 drug therapy for the treatment of Malaria can still allow for emergence of resistance.

I suspect I'm aware of more practical, real world reasons why two drug therapy for malaria can still allow the emergence of resistance than you are. But I'm not talking about malaria here.

> >
> > So, starting with a pure population of genotype ab, with the mutation rates and fitnesses I mentioned above, it takes 435 generations for the double mutant AB to reach a frequency of 99%.

> You and Schneider, you take mathematical models using invalid assumptions and draw incorrect conclusions. So your calculations show that combination therapy does not work for the treatment of HIV. You have advanced evolutionism.

My calculation, at least, shows no such thing about HIV and triple drug therapy. There is no doubt that it is possible to exert strong enough selective pressure on an organism that no attainable combination of mutations will save it. Throw it in an autoclave, for example, or drop a 10 km wide asteroid on it.

The point of the model here is simply that multiple beneficial mutations can easily and rapidly combine under weak selection pressures without the need for each individual mutation to go to fixation before the next arises.

> >
> > There's no problem whatsoever with the two beneficial mutants amplifying simultaneously. Nothing gets disrupted.
> Sure something has been disrupted, it is mathematical logic you are disrupting by using an incorrect assumption to derive your model. Let's see if you can figure out what that incorrect assumption is.

As I said, you can either make your argument or not, up to you; I'm not going to guess at what it might be.

[Bill Rogers]

Sorry, typed too fast. Above on the dimensions... it should read

fitness is a dimensionless proportion per unit time.

[jillery]

I stipulate for argument's sake your "adaptation by rmns to stressors
requires beneficial mutations". However, that comment evades the
point I made, that your expressed argument focuses on a single
"adaptation" from a single kind of random mutation, and handwaves away
all other adaptations and random mutations. That's one reason why
your "mathematics" give invalid results, because you ignore almost all
of the data.

If stressors worked by making mutations which only improved
organisms' responses to that stressor, then your methodology would be
valid. But that's an IDiot concept. Random mutations don't work that
way. That's why they're called "random"; their appearance is *not*
directed to the stressor.

Your expressed methodology ignores all of the other adaptations
resulting from all the other random mutations, and so doesn't support
your conclusions about the chances of adaptations generally.

Your argument is logically similar to Steadly's argument that
biological functions have to appear at just the right time and place,
another IDiot concept. It's as if anti-evolutionist brains are wired
to recognize only intentional causes, and be blind to unguided natural
processes.

>Now what do you think would happen if Lenski ran his experiment with both starvation and thermal stress? With starvation stress alone it takes a thousand generations per beneficial mutation. Under ideal circumstances, it would only take 30 doublings to give e9 variants with a particular beneficial mutation.

Even if what you say above is factually correct as stated, and I don't
know that's the case, it doesn't apply to RMNS generally. By analogy,
it's as if you claimed to prove the odds of being dealt a "beneficial"
hand of five cards by counting only royal flushes.

[gkaplan]

On 9/2/2016 11:33 AM, Bob Casanova wrote:
> On Fri, 02 Sep 2016 08:04:51 -0400, the following appeared
> in talk.origins, posted by jillery <69jp...@gmail.com>:
>
>> On Thu, 1 Sep 2016 18:04:47 -0700 (PDT), Alan Kleinman MD PhD
>> <klei...@sti.net> wrote:
>>
>>> On Wednesday, August 31, 2016 at 1:10:02 PM UTC-7, jillery wrote:
>>>> On Wed, 31 Aug 2016 12:19:56 -0700 (PDT), Steady Eddie

>>>> wrote:
>>>>
>>>>> On Sunday, 28 August 2016 10:45:02 UTC-6, Vincent Maycock wrote:
>>>>>> On Sun, 28 Aug 2016 06:08:43 -0700 (PDT), Steady Eddie
>>>>>> wrote:
>>>>>>

>>>>>>> On Thursday, 25 August 2016 17:21:22 UTC-6, Alan Kleinman MD PhD wrote:
>>>>>>>> On Thursday, August 25, 2016 at 6:11:22 AM UTC-7, Bill Rogers wrote:
>>>>>>
>>>>>> snip
>>>>>>
>>>>>>>>> Who doesn't accept them? Of course I accept them. What I don't accept is Alan's totally unsupported claim that *all* natural selection involves lethal selection pressures that wipe out every member of a species except for a handful who happen to have lucky mutations. Rare examples, usually from medical treatments, *do* indeed work that way. Most don't.
>>>>>>>
>>>>>>> You're starting to go Jillery on us, Bill.
>>>>>>> Dr. K doesn't claim that "*all* natural selection involves lethal selection pressures". He doesn't have to.
>>>>>>>

>>>>>>> Why do you claim that HIV undergoing lethal selection pressures is not a representative example of how
>>>>>>> RMNS works in the real world?
>>>>>>

>>>>>> Because that's how combination therapy works; if one selection
>>>>>> pressure (anti-viral drug) doesn't kill the organism, the other drug
>>>>>> in the combination therapy will.
>>>>>

>>>>> Yes, and that's why combination therapy works - because that's how RMNS works in the wild - in fact,
>>>>> that's how it works in all life.
>>>>>
>>>>> Do you have reason to doubt this?
>>>>>

>>>>>> The point is, though, that this is only true if the selection
>>>>>> pressures are lethal; if they're not, no simultaneous beneficial
>>>>>> mutations are required for natural selection to work.
>>>>>

>>>>> That's not the point of the research.
>>>>>
>>>>> The point of Dr. K's research is to quantify just how likely the RMNS process is to have created and
>>>>> selected any of a vast variety of different machines, traits, processes, organisms and/or body plans we see
>>>>> in nature.
>>>>>
>>>>> To do so, you have to start from the beginning - how likely is any given functional piece of DNA to mutate
>>>>> into some other sequence that codes for a different functional protein?
>>>>>
>>>>> I'm sure this number is floating around; does anybody have a reference handy?
>>>>
>>>>
>>>> Of course, the answer to your question depends on your definition of
>>>> "different functional protein". Are you willing to provide one?
>

>>> What is that selection pressure for hemoglobin or for insulin or for the DNA replicase system or for...?
>
>> So that's a "no". BTW, are you Steadly?
>

> Direct questions seem to repeatedly result in that sort of
> "response" from him. I wouldn't be surprised to learn that
> he's contracted with IHOP to generate waffles.
>

Are you Jillery? :)

[gkaplan]

LOL! You asked me if I was Steadly too!

[Bob Casanova]

On Sun, 4 Sep 2016 09:19:48 -0700, the following appeared in
talk.origins, posted by gkaplan <georg....@gmail.com>:

No.
--

Bob C.

"The most exciting phrase to hear in science,
the one that heralds new discoveries, is not
'Eureka!' but 'That's funny...'"

- Isaac Asimov

[gkaplan]

I would like to know how this relates to my thread on the number of
mutations we see in modern history with a human population of 7 billion.
In the 14th century there were as many mutations in humans as in the
entire 5MY which are said to have taken a primate to a modern human.
There are some 35M single point mutations that need to be changed alone,
and that does not include other differences.

In the 15th century it was higher and in the 20th century every 5 years
there are as many mutations as a population of 10,000 5 million years ago.

I am being told that it takes a million years for 1000s of mutations to
become fixed and that other things need to be in place for this to
happen as well.

But you appear to say that mutations do not need to appear at a
particular time for them to be fixed.

[gkaplan]

I am not Martin Smart either :)

[jillery]

On Sun, 4 Sep 2016 10:27:51 -0700, gkaplan <georg....@gmail.com>
wrote:

>I would like to know how this relates to my thread on the number of
>mutations we see in modern history with a human population of 7 billion.
> In the 14th century there were as many mutations in humans as in the
>entire 5MY which are said to have taken a primate to a modern human.
>There are some 35M single point mutations that need to be changed alone,
>and that does not include other differences.
>
>In the 15th century it was higher and in the 20th century every 5 years
>there are as many mutations as a population of 10,000 5 million years ago.
>
>I am being told that it takes a million years for 1000s of mutations to
>become fixed and that other things need to be in place for this to
>happen as well.
>
>But you appear to say that mutations do not need to appear at a
>particular time for them to be fixed.

I don't just appear to say it, I said it explicitly. And I stand by
it. And AIUI it's an uncontroversial fact, as contrasted to some
anti-evolutionists' claims that mutations are created with intent as
the need arises.

And I might not understand what you mean by what you say you're being
told, but I don't see how what I said conflicts with that. Regardless
of how long it takes a mutation to become fixed, they will become
fixed, or not, regardless of when they originated.

Perhaps you mean to say that certain mutations are fixed *now*, and in
order for that to be, they had to have originated at a specific time
in the past? If so, then your real concern is with *how long* it
takes mutations to become fixed, not when.

IIUC the good DrDr claims there hasn't been enough time for most
mutations to become fixed. My objection to his claim is that his
expressed methodology is flawed, and so his conclusions based on that
flawed methodology is incorrect.

[jillery]

On Sun, 4 Sep 2016 09:18:49 -0700, gkaplan <georg....@gmail.com>
wrote:


<snip for focus>

>LOL! You asked me if I was Steadly too!

No, I didn't. That's a figment of your imagination. The only thing I
posted which comes even remotely close to what you say above is where
I posted a conditional case to note similarities in your posting
styles.

[jillery]

On Sun, 4 Sep 2016 10:30:56 -0700, gkaplan <georg....@gmail.com>
wrote:

Do you really think it's unreasonable to note a poster's habit of
answering questions as if they were answering for some other poster?

[gkaplan]

One poster said that when mutations and genetic drift were at
equilibrium (or words to that effect) that the mutations would be lost
as fast as they happened.

Others have said that there needs to be a environmental need so that the
mutation gives a sufficient advantage in order to be selected.

That is what I meant by "when" they originated.

> Perhaps you mean to say that certain mutations are fixed *now*, and in
> order for that to be, they had to have originated at a specific time
> in the past? If so, then your real concern is with *how long* it
> takes mutations to become fixed, not when.
>
> IIUC the good DrDr claims there hasn't been enough time for most
> mutations to become fixed. My objection to his claim is that his
> expressed methodology is flawed, and so his conclusions based on that
> flawed methodology is incorrect.

I read through the posts and absorbed a bit. It appears to me that the
good DrDr has verifiable evidence based on real observable examples in
the micro world but that evolutionists say that this may not be relevant
to other life forms but have no evidence.

[gkaplan]

But do you know who Martin Smart is?