Annoying creationists

[Mercutio]

Mr Scott, I’ve already proved mathematically that ev can’t evolve binding sites on a realistic length genome because of the multiple selection conditions. If you can’t evolve simple binding sites, what makes you think you can evolve the huge number of genetic differences between cats and dog from a common ancestor? Do you want to tell us what the selection conditions that do this? Paul can then put it in ev and end this discussion.

Kleinman, a little question for you: Do you realize that if some powerful being were actually able to precisely replicate the selection conditions that gave rise to cats and dogs from a common ancestor, it would still be highly unlikely that the creatures which arose from this replication would be exactly like our cats and dogs? Any selection pressure may be overcome in many different ways; the random variation that is selected for might have gone a different direction than it did. You will still get divergence (as with ring species) to the point where they are separate species, then more divergence such that even you would call them different "kinds", to where perhaps even you would call it macroevolution and challenge someone to replicate it precisely.

You have drawn a small circle around a wildly-shot bullet that landed a mile away in some random patch of dirt, and challenged a marksman to hit the same target again. If you do not understand this, you are wholly ignorant of the process of natural selection; if you do understand it, you are being dishonest in what you are asking for proof.

This is the problem with your argument (you remember, "a gene is to evolve..."?); you are specifying a target in advance. As with the Maginot Line example, you are attempting, by saying that the Germans could not cross that line, to prove that they could not expand anywhere at all. It is a limitation of ev, since it had to specify a particular outcome in order to answer the question it was trying to answer. As such, though, ev had to be an incomplete model, ironically in precisely the area where your understanding of natural selection is either deficient or deceitful.

As an aside--have you given up on the idea of writing out your idea from the beginning (as it were) in one document? It appears that you are back at full throttle in this thread instead. Should I be asking about your own evidence again?

 

[kjkent1]

In case no one's noticed, Kleinman never posts on Friday. Based on past history, his workweek (and posting period) appears to be from Sunday night to Thursday afternoon.

 

[Paul C. Anagnostopoulos]

I finished running Alan's El Stoppo Experimento:

population 64
genome size 16,384
binding sites 16
weight/site widths 5/6
1 mutation per generation

The perfect creature evolved after 6,894,433 generations. Its sequence logo is CAtGCGC.

~~ Paul

 

[kleinman]

Annoying Creationists

Delphi, you already answered this question yourself, so I point to you.

Nice effort, but I'm afraid you'll have to get all of the parts of your claim in one go if you want full credit on this assignment.

1. Evolution stopping
2. Observed in nature
3. Caused by multiple selection pressures

You can't pick and choose.

1. Evolution does stop, it is called extinction which is,
2. observed in nature which can be caused by
3. one or more selection pressures.

You aren’t going to say that extinction doesn’t occur?
As we continue to discuss ev, the mathematics of this phenomena will become more apparent to you.

That’s obvious.

It doesn't seem to be to you. Macro and micro evolution is not a real distinction. The distinction is not needed for evolutionary theory to be correct.

So, explain how a series of microevolutionary processes can lead to the evolution of a gene from the beginning.

Second, the mutations seen which lead to drug resistance in HIV change the molecular structure of the particular enzyme sufficiently that the drug can no longer act effectively. There are no new enzymes being produced.

Define "new".

Existing genes are modified only slightly and these genes to perform the same basic function. Neither a new gene evolved from the beginning nor a new function from the existing gene occurs.

Third, I have no idea how you compute the probability that resistance will occur one drug at a time vs resistance to three drugs simultaneously.

It's called population genetics. The probability of a mutation occuring at a particular loci is fixed. For example, let us pretend that the probability is 1x10^-8. The probability of getting all three resistances in sequence is, thus, (1*10^-8)+(1*10^-8)+(1*10^-8). The probability of getting all three resistances in parallel is (1*10^-8)*3. Tell me, how are the probabilities different?

You’ve got some big problems with this mathematics. First is that ev shows that this mathematics does not work. Then, how do you address the condition in the real world if the three selection pressures together cause extinction while the single selection pressures alone are not sufficient to cause extinction?

So, how did the simian virus evolve?

I can see where this is going. You want me to provide a clear pathway from the first pseudo-gene to the HIV genome, correct?

These things have to come from somewhere.

Too bad the mathematics of ev doesn’t show this and why are the infectious disease experts subjecting people with HIV to all the adverse drug reactions of multiple drug therapy?

Firstly, the mathematics of ev doesn't simulate reality. Get over it. Secondly, as I've already explained, to my understanding it is because three drugs are more effective at controlling the virus then one, and also because when resistance to a particular drug does arise, one drug can easily be replaced when there are two others still functioning.

Really? This is a peer reviewed and published model of random point mutation and natural selection by the head of computational molecular biology at the National Cancer Institute. The author of this program for years has defended this as a simulation of reality and the programmer of the online version of this model said this modeled actual life, that is until he saw what the mathematics really shows.

One of the key reasons that three drugs control the virus more effectively is that monotherapy leads to faster emergence of strains of the virus resistant to that drug.

Ok expert in phylogenetics, how did the first allele arise?

Firstly, that is not a meaningful question. An allele is just a specific sequence at any particular loci which is common in a population over a certain value (generally a single base pair). An allele does not require a gene. Secondly, you have completely ignored my answer to your question. Thirdly, you need to stop thinking that a gene is the simplest possible unit for life. It is not.

So what is the simplest possible unit for life?

I added the color. Could you get your story straight.

Of course, argue against my rhetoric, and not the actual meaning of my words.

Kleinman, I am using "kill" in the second sentence as a figurative device. Replace it with "suppress" if you wish, and then answer the meaning of the words.

Rewrite your question without using figurative devices otherwise let’s stick strictly with mathematics.

Really, do you know how fitness landscapes work as well as how antiretrovirals work? In one sentence you say they kill the virus and the next you say they don’t.

Ad hominem. Yes, I do understand how fitness landscapes work. I have calculated my own. Yes, I do understand how antiretrovirals (and antivirals in general) work. Yes, I know I said that, and as I've explained, it was for rhetorical effect. If you couldn't see that, then I give you more credit then I should. Answer the points raised, not the way they were raised.

Really? You have your own mathematical model of mutation and natural selection? It is peer reviewed and published like ev is? You know, the mathematical model that you say is wrong.

Really, I posted a quote from the guidelines for treating HIV that monotherapy increases risk of the evolution resistant strains. I’ll repost it here since your drinking seems to be impairing your memory.

Um, kleinman? Risk and probability are different things.

So is microevolution and macroevolution.

You evolutionists have such weak arguments that you have to parse words to try to find anything to argue. HIV is treated by using multiple selection pressures.

Define "selection pressures".

Your are an evolutionist and you don’t know what a “selection pressure” is? Oh well, I’ll give you a definition that we can argue about for a while. A selection pressure is a stress on a creature which affects it’s ability to reproduce.

These multiple selection pressures slow the evolution of drug resistant strains because it either requires that multiple beneficial mutations occur simultaneously or if a single beneficial mutation occurs, the other drugs suppress the reproduction of the virus, either way it slows evolution. There is a distinction between treating and curing a disease.

Nonsense. If there are three selection pressures acting on the virus, and it gains immunity to one of those selection pressure, now there are only two selection pressures. Evolution has not stopped or even slowed down, as the new selection pressure immune virus can replicate more effectively then others. You misunderstand, thinking that each antiretroviral agent acts to the maximum ability. There are three antiretrovirals because the overall effect of all three is to more effectively inhibit the replication of the viron, not to slow evolution. You are completely misunderstanding pretty much everything.

Did you know that drug resistant strains of HIV can’t reproduce as rapidly as wild strains of the virus?

That’s right, your niche is gene duplication but you still won’t tell us how the original gene appeared.

You first need to stop thinking that a gene is the most basic form of genetic structure.

So, tell us what the fundamental unit of life is.

You appeared to start to understand why multiple selection pressures slow evolution.

They don't.

Oh, that’s right the peer reviewed and published model random point mutation and natural selection is wrong and your mathematics of mutation and natural selection is correct and inhibiting the replication of the viron does not slow evolution. I thought your theory said that the ability to reproduce determines the fitness of a population.

This is the very heart of the theory of evolution.

No, it isn't.

So the ability to reproduce is not the condition that natural selection acts on? What theory are we now talking about?

Ev shows mathematically why multiple selection pressures slow this process.

No, it doesn't.

The difference here is that I have posted data from the model that show my statement to be true. What data from the model have you posted?

It is now obvious that when you have multiple selection conditions, the only way you can advance all the selection conditions simultaneously is that a given creature have nothing but beneficial mutations.

That is not the case. Selection is not black-and-white. Any beneficial mutation will be selected for. Actually, that is not quite correct. Any negative mutation will be selected against, and any beneficial mutation will be selected against less. Natural selection only works in the negative sense. It selects against things, not for things.

You need to spend some time studying ev. It will educate you on the mathematics of mutation and selection.

Otherwise, combinations of good and bad mutations confound the evolutionary process. How do you evolve all the genes that code for the enzymes of the Krebs cycle?

You could evolve them by having the enzymes play a different role before the Krebs cycle is fully developed, or by having some other beneficial function. Proteins often do not have just one use. You seem to be arguing against irreducible complexity. See the

irreducible complexity evolver as an example of why this is wrong.

Why don’t you apply this argument to the DNA replicase system and tell us what the function of the components of this system were doing before the system evolved, especially since DNA can not be replicated without this system. What were helicase and gyrase doing before DNA was replicated?

Even more incomprehensible is how do you evolve all the genes required for the DNA replicase system, especially since without these enzymes you can’t replicate DNA? What are the selection processes that would accomplish such events? How can these events occur serially when parallel selection conditions (if you could describe them) slow if not completely stop the evolutionary process.

They do not slow or completely stop. You are wrong. See

ribozymes as an example of a non-protein enzyme. Also, you are arguing that DNA polymerase (replicase is a RNA encoded polymerase, for the self replication of single stranded RNA, not DNA) did not exist before DNA did. Or are you claiming that not protein existed before DNA? That is an absurd position.

My position is absurd? How did the RNA replicase system form and what were the components of this system doing before RNA could be replicated? How does ribose form nonezymatically?

Mutation and selection is a much more limited phenomena than you evolutionist like to make it. The mathematics shown by ev reveals this and there are real examples of this.

The mathematics of ev simulate a very limited situation, not all of real life. Get over it.

Also, please show an example of evolution stopping in real life due to multiple selection pressures.

Sure, we all now know that your mathematics of mutation and selection is superior to the peer reviewed and published mathematics of Dr Schneider.

Many species have gone extinct from selection pressures. I have give a specific example of the treatment of HIV with multiple drugs which you have already admitted slows the reproduction of the viron. Of course reproduction has nothing to do with the theory of evolution. Continue to apply selection pressures to the HIV virus and it will go extinct. If you are not happy with this example, consider the small pox virus. It is virtually extinct since it’s ability to reproduce has been suppressed so effectively that it only exists in laboratories.

You got this confused. It is ev that contradicts the theory of evolution. Why do you think that Paul now says ev does not behave the way the real world behaves. Perhaps he is in one of you 10^500 alternative universes.

Ev has never simulated the real world. It simulates a very limited situation, using simplified evolutionary theories, to show something in principle. You are the only one clinging to it to try to disprove all of evolutionary theory with a simple model. The amount of evidence for evolution is overwhelming. You might as well deny atomic theory.

I’ll let Dr Schneider’s own words defend his model.
The following quotes were taken from Dr Schneider’s blog web page: http://www.lecb.ncifcrf.gov/~toms/paper/ev/blog-ev.html

The following are Dr Schneider’s responses to a critique of his paper Evolution of biological information by Dr Stephen E Jones.

"Schneider's paper is misleadingly titled: "Evolution of biological information". But it is just a *computer* simulation. No actual *biological* materials (e.g. genomes of nucleic acids, proteins, etc) were used, nor does Schneider propose that his simulation be tested with *real* genomes or proteins

Actual biological materials were used to determine the original hypothesis. Read the literature: Schneider1986

It only becomes *real* biological information and random mutation and natural selection, when the simulation is tested in the *real* world, using *real* DNA, proteins, with *real* mutations and a *real* environment does the selecting. It is significant that Schneider does not propose this, presumably because he knows it wouldn't work.

You are very bad at reading my mind, I have considered doing this experiment. Given the right conditions, it WILL WORK. Do you have th gumption to do the experiment yourself? That's the way real science works! FURTHERMORE, if you read the literature, you will recognize that related experiments have been repeatedly done for 20 years. Look up SELEX.

In the rest of the paper he uses the single word "selection". I take this as a tacit admission that his model is not a simulation of *real* biological natural selection.

No. A rose is a rose by any other name. Selection is selection whether it be natural (generally meaning the environment of earth), breeding (by humans usually, though perhaps some ants select their fungi), SELEX or in a computer simulation. Of COURSE it is a simulation of natural selection! The paper would not be relevant to biology and would not have been published in a major scientific journal if it were not!

Schneider lets slip that there is another unrealistic element in his (and indeed all) computer simulations in that it (they) "does not correlate with time":

So? Run the program slower if you want. Make one generation per 20 minutes to match rapid bacterial growth. THIS WILL NOT CHANGE THE FINIAL RESULT!

Well, when Schneider's simulation is actually tested with *real* "life" (e.g. a bacterium), and under *real* mutation and natural selection it gains information, then, and only then, would "creationists" be favourably impressed. But if they are like me, they would already be impressed (but unfavourably) that Schneider does not mention in his paper that his simulation should now be so tested in the *real* "biological" world.

1. The simulation was of phenomena in the "real" world.
2. Dr. Jones is invited yet again to do an experiment.

The following is a response Dr Schneider made to a statement made by David Berlinski.

Where attempts to replicate Darwinian evolution on the computer have been successful, they have not used classical Darwinian principles, and where they have used such principles, they have not been successful.

The ev program disproves this statement since it uses classical Darwinian principles and was successful.

The previous statements are clear that Dr Schneider believes that ev simulates the real world.

When will we see you present a marketing plan to your company so we can do cases with realistic genome lengths and large populations. We still haven’t completely driven that nail in the theory of evolution coffin.

Except that you tirelessly shout from your soapbox that evolution has been proven impossible. It hasn't, you haven't done that, and even if ev showed that evolution was impossible, the overwhelming amount of supportive evidence for evolution would highly suggest that the model was wrong, not that theory.

When you learn to understand the mathematics shown by ev, you will understand my arguments.

There is still so much annoying to do.

If your only goal is to annoy "evolutionists", then simply say so and we shall put you on ignore.

Of course annoying “evolutionists” is not my only goal. In fact annoying “evolutionists” has never been my goal. It is only an additional bonus in revealing the truth of the mathematics of mutation and selection.

If you get tired of trying to figure this out, you can explain what the selection process is that would evolve a gene from the beginning. If you get tired of that, you can explain what the components of the DNA replicase system were doing before the DNA replicase system existed. Seems you have a few minor gaps in your theory.

God, you are ignorant. A gene is not the simplest form of a genetic grouping. DNA polymerase is not likely to have sprung up magically when DNA first appeared, and it need not have. Yes, there are gaps in our knowledge of evolution. A gap is not evidence that the theory is wrong. Only conclusive falsification of the theory can prove it is wrong. You have not done this, and so far, it has never been done. The theory of evolution has so much evidence supporting it that to deny it is paramount to denying atomic theory.

God?

Present treatment strategies already are extending life for years. With safer drugs, even more selection pressures can be put on the virus and effectively stop the evolution of the virus. The more selection pressures, the slower evolution proceeds.

Wrong. The stronger the selective pressures, the faster evolution proceeds. I have explained this many times to you, but you choose to ignore it because it does not conform to your version of reality.

Oh yes, you have said that multiple drug therapy is used to slow the replication of the virus and that has nothing to due with the theory of evolution. Affecting the fitness of the virus to reproduce has everything to do with the theory of evolution Taffer.

Putting more selection pressures on the virus can effectively stop the evolution of the virus. By the way, this is what ev shows.

No it can't and no it doesn't.

In that case which should stop treating HIV, all we are doing is making the virus evolve more quickly according to your logic.

Isn’t this your Rcapacity argument? Then can you explain why single selection conditions can evolve on much longer genomes than your Rcapacity equation allows.

I've explained it half a dozen times now, but you're not getting it. I'll try one more time:

Rsequence is the approximate number of bits of information required to distinguish binding sites from other loci. Distinguish, as in tell them apart: bind at the binding sites but not at any other loci. Rcapacity is the maximum number of bits of information that a binding site can contain. If you have set the mistake counts so that you are not trying to distinguish bindings sites from other loci, then both of these numbers are irrelevant.

I’ll have to think about your definition for a while. What I’ll probably do is study the effects of varying the different weights on each selection condition. There is something that does not sound right in your definition. The problem I have with this is how do extend this concept to evolving a gene. Ultimately, it is your Rcapacity concept which I think will prove irrelevant because the individual selection conditions can evolve no matter how long the genome is and the combined selection conditions is what stops the evolution. Another way to view your concept is by considering what would happen if you evolved two sets of binding sites simultaneously. Do you still retain your definitions for Rfrequency and Rcapacity? What happens to the rate of information accumulation with the six selection conditions?

Do you want to explain why single selection conditions can still evolve on ev when Rfrequency is much larger than Rcapacity? That includes genome lengths of 64k, 128k and 256k with binding site widths of 6.

Same question, same answer.

Ok, what happens with the evolution of two sets of binding sites simultaneously.

Really, evolution has many other ways to get things done? Like what? Do you have something other than mutation and selection?

Nature has something other than single point mutation and selection.

So let’s see you evolve two sets of binding sites simultaneously with six selection conditions operating simultaneously using whatever mutation mechanism you want.

I'm running Alan's El Stoppo Experimento:

population 64
genome size 16,384
binding sites 16
weight/site widths 5/6
1 mutation per generation

After 3,853,200 generations, we're down to 10 mistakes and counting ...

You are going to run the 32k genome size aren’t you? That’s the evolution El Stoppo Experimento.

Mr Scott, I’ve already proved mathematically that ev can’t evolve binding sites on a realistic length genome because of the multiple selection conditions. If you can’t evolve simple binding sites, what makes you think you can evolve the huge number of genetic differences between cats and dog from a common ancestor? Do you want to tell us what the selection conditions that do this? Paul can then put it in ev and end this discussion.

…

Why, Dr. Kleinman, do you insist that an incomplete model of evolution can be used to prove that evolution is impossible?

Random point mutations are the least destructive of mutations. Phase shift mutation are more harmful to living things. Ultimately, there is no selection process that can evolve a gene from the begin despite the mechanism of mutation. The most serious blow that ev does to the theory of evolution is that it reveals the multiple selection conditions confound the evolutionary process. No mutation mechanism can overcome this mathematical fact.

By the way, do you consider a picture of a dog and cat with similar markings as your evidence that they evolved from a common ancestor?

Faith in the bible comes from the gut, not from evidence. Sometimes, a picture illustrating the similarities between species, such that you can actually see how accumulations of microevolutionary steps can have a macroevolutionary result, can make an impression at a gut level and therefore influence how one interprets the mathematics of evolution. It's clear your gut faith in the bible has impeded your ability to objectively acknowledge mathematical truths.

Really? Evolutionists only questioned ev when it was revealed what the model really shows. Ev is a good model of random point mutation and natural selection and is instructive for teaching the mathematics of this concept. Unfortunately for proponents of the theory of evolution, it teaches that the theory is mathematically impossible.

Paul, you can answer this question about binding sites better than I can. Is this Ev-able?

What? Enhancing Ev to evolve cats and dogs from a common ancestor? I think that would be a lot of work.

Let’s see if ev can evolve two sets of binding sites simultaneously.

Mr Scott, I’ve already proved mathematically that ev can’t evolve binding sites on a realistic length genome because of the multiple selection conditions.

You have proven no such thing, since you have no idea what realistic genome lengths, mutation rates, and populations are. And even if you did know, you have not presented the mathematics of your proof.

Paul, why don’t you tell us what a realistic mutation rate and genome length is? And don’t try to hide behind the argument that you have no idea what the genome lengths and mutation rates were when you speculate that life started evolving. Ignorance is not the basis for a scientific proof of a theory. We know what the genome sizes are for the smallest free living organisms. We also know what the mutation rates are for living things. Despite all this evidence against your theory, it is the lack of selection conditions that can evolve a gene from the beginning and that ev shows that multiple selection conditions slow and ultimately stop evolution that are the fatal blows to the theory of evolution.

As an aside--have you given up on the idea of writing out your idea from the beginning (as it were) in one document? It appears that you are back at full throttle in this thread instead. Should I be asking about your own evidence again?

No, no, yes.

I finished running Alan's El Stoppo Experimento:

population 64
genome size 16,384
binding sites 16
weight/site widths 5/6
1 mutation per generation

The perfect creature evolved after 6,894,433 generations. Its sequence logo is CAtGCGC.

So let’s see, the rate of evolution of the perfect creature has slowed from the 256 base genome case 662 generations to more than 10,000 times slower for the 16k genome. So, Paul, you have proved that evolution is slowing. Now are you going to do the 32k genome case, the evolution El Stoppo Experimento?

 

[Taffer]

So, explain how a series of microevolutionary processes can lead to the evolution of a gene from the beginning.

False Dichotomy^WP

A gene not need be the first thing to evolve. See the irreducible complexity evolver. You need to stop thinking that a gene is the most basic form of life, or you will never grasp deeper evolutionary theory.

As for a method, let me first ask you a question. What is the simplest currently recognized gene?

Existing genes are modified only slightly and these genes to perform the same basic function. Neither a new gene evolved from the beginning nor a new function from the existing gene occurs.

One second on google found me this. To quote:

Duplication of genes increases the amount of genetic material on which evolution can work and has been considered of major importance for the development of biological novelties or to explain important transitions that have occurred during biological evolution. Recently, much research has been devoted to the study of the evolutionary and functional divergence of duplicated genes. Since the majority of genes are part of gene families, there is considerable interest in predicting differences in function between duplicates and assessing the functional redundancy of genes within gene families. In this review, we discuss the strengths and limitations of both older and novel approaches to investigate the evolution of duplicated genes in silico.

For your own studies, I suggest you research the HOX gene complex.

You’ve got some big problems with this mathematics. First is that ev shows that this mathematics does not work.

Nope, it is your assumption of the cause behind the phenomenon you are seeing in ev that is at fault. You have already made up your mind. That is not the way to do science. You have to show that it is, indeed, the evolutionary pressure which slows evolution in ev, and not a fragment of coding a simple model onto a computer.

Then, how do you address the condition in the real world if the three selection pressures together cause extinction while the single selection pressures alone are not sufficient to cause extinction?

Evidence? Do you have a citation where this has occured?

From my own studies, three antimicrobial agents (in this case, they were three antibacterials) lead to extinction not because of a slowing of the evolution of resistance, but because they are three agents working on three different molecular pathways in the microbe, which is always going to be more efficient at killing microbes then one. You have no evidence that evolution slowing is the cause of this. Furthermore, population genetics provides us with an accurate model wherein increased selective pressures increase the rate of evolutionary change.

These things have to come from somewhere.

So you would not be happy until the entire evolutionary history of all organisms is obtained? Careful, kleinman, your bias is starting to show.

Really? This is a peer reviewed and published model of random point mutation and natural selection by the head of computational molecular biology at the National Cancer Institute. The author of this program for years has defended this as a simulation of reality and the programmer of the online version of this model said this modeled actual life, that is until he saw what the mathematics really shows.

I mistyped. It simulates reality. It does not simulate the entire evolutionary process.

One of the key reasons that three drugs control the virus more effectively is that monotherapy leads to faster emergence of strains of the virus resistant to that drug.

Evidence.

So what is the simplest possible unit for life?

I would say self replicating molecules, depending on the defintion. Abiogenesis is far more hypothetical then evolution is. Please stop conflating the two.

[quote[Rewrite your question without using figurative devices otherwise let’s stick strictly with mathematics.[/quote]

Replace the word "kill" with suppress and you have my question. I already told you this. And get over the litirary device. They happen.

Really? You have your own mathematical model of mutation and natural selection? It is peer reviewed and published like ev is? You know, the mathematical model that you say is wrong.

I never said it was wrong. I said your interpretation of it was wrong.

And no, I personally do not have a model. However, the entirety of population and evolutionary genetics does, and they are well respected. This is what ev is based upon.

So is microevolution and macroevolution.

No, they are not. That is not a meaningful distinction. Or perhaps you would like to define the two terms? Then we shall see how well those definitions fit to reality.

Your are an evolutionist and you don’t know what a “selection pressure” is? Oh well, I’ll give you a definition that we can argue about for a while. A selection pressure is a stress on a creature which affects it’s ability to reproduce.

Poor, inprecise, definition. But acceptible for now.

Did you know that drug resistant strains of HIV can’t reproduce as rapidly as wild strains of the virus?

A) What does that have to do with your misinterpretation of pretty much everything?
B) Citation?

So, tell us what the fundamental unit of life is.

I would like to say "information", but that is not a currently accepted definition. The most fundamental unit of life is a self replicating molecule.

Oh, that’s right the peer reviewed and published model random point mutation and natural selection is wrong and your mathematics of mutation and natural selection is correct and inhibiting the replication of the viron does not slow evolution. I thought your theory said that the ability to reproduce determines the fitness of a population.

Wow, that is perhaps the biggest strawman I've seen in ages.

1) I never said their mathematics was wrong.
2) I said your interpretation is wrong.
3) You have provided no evidence that evolution slows in reality.
4) You have provided no evidence that multiple drugs are use specifically to slow evolution.
5) Fitness is determined, quite often, as the number of offspring the creature could theoretically produce. Although there is much debate as to the exact definition of "fitness".

So the ability to reproduce is not the condition that natural selection acts on? What theory are we now talking about?

Liar. You know very well what this was responding two. The heart of the matter, as claimed by you, is that evolution slows with multiple selective pressures.

The difference here is that I have posted data from the model that show my statement to be true. What data from the model have you posted?

I don't need data to know your interpretation is wrong. So many posters have shown you why it's just getting a bit silly. Please, by all means, continue to stick your fingers in your ears and sing "lalala, I can't HEAR you!".

You need to spend some time studying ev. It will educate you on the mathematics of mutation and selection.

You need to spend time studying population and evolutionary genetics. It will educate you on the mathematics of mutation and selection that ev is based upon, and show you why your interpretation is incorrect.

Why don’t you apply this argument to the DNA replicase system and tell us what the function of the components of this system were doing before the system evolved, especially since DNA can not be replicated without this system. What were helicase and gyrase doing before DNA was replicated?

Considering I've never studied that before, I don't know. But ICE clearly demonstrates that your basic assertion that irreducible complexity cannot evolve is false.

My position is absurd? How did the RNA replicase system form and what were the components of this system doing before RNA could be replicated? How does ribose form nonezymatically?

So, because we do not understand everything, the theory is false?

Sure, we all now know that your mathematics of mutation and selection is superior to the peer reviewed and published mathematics of Dr Schneider.

Considering I never said that, I am forced to call you a liar.

Many species have gone extinct from selection pressures. I have give a specific example of the treatment of HIV with multiple drugs which you have already admitted slows the reproduction of the viron. Of course reproduction has nothing to do with the theory of evolution. Continue to apply selection pressures to the HIV virus and it will go extinct. If you are not happy with this example, consider the small pox virus. It is virtually extinct since it’s ability to reproduce has been suppressed so effectively that it only exists in laboratories.

You are dishonest. You should be well aware that antiretrovirals do not slow evolution, but cause the virus to produce fewer numbers. If evolution is slowed, then how come increased selective pressures speed up evolution?

I’ll let Dr Schneider’s own words defend his model.[/SIZE][/FONT]
The following quotes were taken from Dr Schneider’s blog web page: http://www.lecb.ncifcrf.gov/~toms/paper/ev/blog-ev.html

The following are Dr Schneider’s responses to a critique of his paper Evolution of biological information by Dr Stephen E Jones.











The following is a response Dr Schneider made to a statement made by David Berlinski.



The previous statements are clear that Dr Schneider believes that ev simulates the real world.

Since I never said his model was incorrect, I am once again forced to call you a liar.

When you learn to understand the mathematics shown by ev, you will understand my arguments.

When you understand population and evolutionary genetics, you will understand why your arguments are false. Increased selective pressures lead to a faster time to loss or fixation of a novel allele. Thus, evolution is sped up.

Of course annoying “evolutionists” is not my only goal. In fact annoying “evolutionists” has never been my goal. It is only an additional bonus in revealing the truth of the mathematics of mutation and selection.

Considering you are wrong, you are not annoying, merely diluded.

God?

I see you cannot even understand basic figures of speech, anymore.

Oh yes, you have said that multiple drug therapy is used to slow the replication of the virus and that has nothing to due with the theory of evolution. Affecting the fitness of the virus to reproduce has everything to do with the theory of evolution Taffer.

Of course it does. But your claim that the reson behind it is to slow evolution is false. Evolution is not slowed, as each individual viron has exactly the same chance of developing any antibiotic resistance.

In that case which should stop treating HIV, all we are doing is making the virus evolve more quickly according to your logic.

Once resistance arises, it will spread throughout the population much quicker, yes. Not allowing it to arise, but using multiple drugs which are able to function as a broad spectrum inhibitor, does not constitute slowing of evolution.

You need to understand the difference between slowing the change in alleles in a population, and simply killing the population. The later conveys the former, but that does not mean what you think it does.

 

[Paul C. Anagnostopoulos]

So let’s see, the rate of evolution of the perfect creature has slowed from the 256 base genome case 662 generations to more than 10,000 times slower for the 16k genome. So, Paul, you have proved that evolution is slowing. Now are you going to do the 32k genome case, the evolution El Stoppo Experimento?

No, Alan, I'm not. I've wasted enough time chasing your moving goalpost. No matter what I do, you will say that a larger genome will finally stop evolution. What this proves is that you don't understand how Ev works. Why would there come a point at which random changes to a genome would not eventually result in a creature with zero mistakes? Is the random number generator suddenly incapable of producing random numbers that cover the entire length of the genome? Does it know where the binding sites are and avoid generating those indices?

If you do run the 32K genome, I predict it will take about 18 million generations. Note that these experiments have both an increasing genome size and a decreasing rate of mutation.

~~ Paul

 

[delphi_ote]

3. one or more selection pressures.

Great. So you admit the number of selection pressures has nothing to do with it. Rather than stringing us along for pages with this fiction, you could've just been honest about your mistake.

 

[kleinman]

Annoying Creationists

So, explain how a series of microevolutionary processes can lead to the evolution of a gene from the beginning.

False Dichotomy

You are the one who says there is no distinction between microevolution and macroevolution. If genes don’t arise by evolution, tell us how they do arise.

A gene not need be the first thing to evolve. See the

irreducible complexity evolver. You need to stop thinking that a gene is the most basic form of life, or you will never grasp deeper evolutionary theory.

I see, the first thing to evolve was a computer game.

As for a method, let me first ask you a question. What is the simplest currently recognized gene?

This link http://www.sanger.ac.uk/Info/Press/2005/050316-numbers.shtml gives a base pair size of 114. Do you want to tell how this gene arose from the beginning?

Existing genes are modified only slightly and these genes to perform the same basic function. Neither a new gene evolved from the beginning nor a new function from the existing gene occurs.

One second on google found me this. To quote:

Link doesn’t work so let’s work from your quote.

Duplication of genes increases the amount of genetic material on which evolution can work and has been considered of major importance for the development of biological novelties or to explain important transitions that have occurred during biological evolution. Recently, much research has been devoted to the study of the evolutionary and functional divergence of duplicated genes. Since the majority of genes are part of gene families, there is considerable interest in predicting differences in function between duplicates and assessing the functional redundancy of genes within gene families. In this review, we discuss the strengths and limitations of both older and novel approaches to investigate the evolution of duplicated genes in silico.

Do you want to tell us how the original gene appeared?

You’ve got some big problems with this mathematics. First is that ev shows that this mathematics does not work.

Nope, it is your assumption of the cause behind the phenomenon you are seeing in ev that is at fault. You have already made up your mind. That is not the way to do science. You have to show that it is, indeed, the evolutionary pressure which slows evolution in ev, and not a fragment of coding a simple model onto a computer.

It is not my assumption that ev fails to converge 3 simultaneous selection condition yet will easily converge a single selection condition with all other parameters held constant, it is easily demonstrated. You have no selection conditions that can evolve a gene from the beginning and now the mathematics of mutation and selection shows that multiple selection conditions slow and ultimately stop evolution. These are the mathematical facts that show your theory to be impossible.

Then, how do you address the condition in the real world if the three selection pressures together cause extinction while the single selection pressures alone are not sufficient to cause extinction?

Evidence? Do you have a citation where this has occured?

The HIV example is a perfect demonstration of this. Of course you think that the more you suppress the replication of the viron has nothing to do with fitness of the viron and evolution. You don’t understand the basics of your own theory. It is the ability of a population to reproduce which determines its fitness. Selection pressures act on a population to reduce its fitness to reproduce. If your thesis advisors ask questions about fitness and reproduction, you had better not answer them the way you are answering here.

So let’s see, the rate of evolution of the perfect creature has slowed from the 256 base genome case 662 generations to more than 10,000 times slower for the 16k genome. So, Paul, you have proved that evolution is slowing. Now are you going to do the 32k genome case, the evolution El Stoppo Experimento?

No, Alan, I'm not. I've wasted enough time chasing your moving goalpost. No matter what I do, you will say that a larger genome will finally stop evolution. What this proves is that you don't understand how Ev works. Why would there come a point at which random changes to a genome would not eventually result in a creature with zero mistakes? Is the random number generator suddenly incapable of producing random numbers that cover the entire length of the genome? Does it know where the binding sites are and avoid generating those indices?

The only thing that has moved in this discussion is your evaluation of ev. The following is from my first post from the Evolutionisdead forum:

The significance of this mathematical behavior in the ev program demonstrates the huge number of generations necessary for any real genome to theoretically evolve by a random mutation/natural selection process. The number of generations needed to complete a single evolutionary step for a bacterium reproducing every 20 minutes with genome length of 5,000,000 base pairs exceeds the age of the earth. For a genome the length of a human, approximately 3,000,000,000 base pairs in length, his program demonstrates that the 1,000,000 generations which evolutionists propose separate us from our closest related primate relative could not occur by a random mutation/natural selection process.

We now know from your good programming skills that the reason it takes so many generation is the competing selection conditions. There are no moving goalposts here, there is only increasing understanding of the mathematics of ev.

If you do run the 32K genome, I predict it will take about 18 million generations. Note that these experiments have both an increasing genome size and a decreasing rate of mutation.

So let’s see, a 32k genome is going to take 18 million generations to evolve 96 loci. The smallest free living organism has a genome size of about 500k. If we assume that doubling the genome size causes a tripling of the generations of convergence you get:
Genome size/generations for convergence
16k/6,000,000
32k/18,000,000
64k/54,000,000
128k/162,000,000
256k/486,000,000
512k/1,458,000,000
My, my, my. Almost 1.5 billion generations to evolve 96 loci. What happens when we extrapolate your estimate to an e coli size genome? Let’s do the arithmetic.
1024k/4,374,000,000
2048k/13,122,000,000
4096k/39,366,000,000
Why that’s 40 billion generations to evolve the same number of binding sites on an e coli size genome that Dr Schneider’s published case took less than a thousand generations on a 256 base genome. Something is slowing down here Paul and it is your theory of evolution. Why don’t you evolutionists go back to the Evolutionisdead forum and see what my estimates were to evolve these binding sites on an e coli size genome. There are no moving goalposts. With respects to your whining about increasing genome sizes and decreasing mutation rates, both will reach realistic values after the 500k genome size. Of course you have evidence that the original life forms you speculate had smaller genomes than this and could sustain higher mutation rates than life forms today. That’s really solid evolutionary science.

3. one or more selection pressures.

Great. So you admit the number of selection pressures has nothing to do with it. Rather than stringing us along for pages with this fiction, you could've just been honest about your mistake.

No, a single fatal selection pressure can cause extinction or combinations of individually non-fatal selection pressures can be sufficient to cause extinction. Even if the individually non-fatal selection pressures do not cause extinction, they reduce the rate of reproduction and slow the evolutionary process.

The only fiction we are dealing with here is the theory of evolution. You are starting to understand the mathematics of mutation and selection and why multiple selection conditions confound the evolutionary process. This is why ev takes billions of generations to evolve less than 100 loci. You can evolve these loci in a tiny fraction of the number of generations when using individual selection conditions done serially. This is the same phenomena that is used to treat HIV. Put as many selective pressures on the virus you can and you slow the evolution of the virus. You combine this mathematical fact with the fact there are no selection processes to evolve a gene from the beginning and your theory of evolution is proved to be mathematically impossible.

 

[delphi_ote]

No, a single fatal selection pressure can cause extinction or combinations of individually non-fatal selection pressures can be sufficient to cause extinction. Even if the individually non-fatal selection pressures do not cause extinction, they reduce the rate of reproduction and slow the evolutionary process.

I'm glad you continue to admit the error of your claim that multiple selection pressures stop evolution. It's a refreshing change in your behavior.

The only fiction we are dealing with here is the theory of evolution.

How exactly do you propose to have real evidence this fictional process stops?

 

[Dr Adequate]

You are the one who says there is no distinction between microevolution and macroevolution. If genes don’t arise by evolution, tell us how they do arise.

I see, the first thing to evolve was a computer game.

This link http://www.sanger.ac.uk/Info/Press/2005/050316-numbers.shtml gives a base pair size of 114. Do you want to tell how this gene arose from the beginning?

Link doesn’t work so let’s work from your quote.

Do you want to tell us how the original gene appeared?

It is not my assumption that ev fails to converge 3 simultaneous selection condition yet will easily converge a single selection condition with all other parameters held constant, it is easily demonstrated. You have no selection conditions that can evolve a gene from the beginning and now the mathematics of mutation and selection shows that multiple selection conditions slow and ultimately stop evolution. These are the mathematical facts that show your theory to be impossible.

The HIV example is a perfect demonstration of this. Of course you think that the more you suppress the replication of the viron has nothing to do with fitness of the viron and evolution. You don’t understand the basics of your own theory. It is the ability of a population to reproduce which determines its fitness. Selection pressures act on a population to reduce its fitness to reproduce. If your thesis advisors ask questions about fitness and reproduction, you had better not answer them the way you are answering here.

The only thing that has moved in this discussion is your evaluation of ev. The following is from my first post from the Evolutionisdead forum:

We now know from your good programming skills that the reason it takes so many generation is the competing selection conditions. There are no moving goalposts here, there is only increasing understanding of the mathematics of ev.

So let’s see, a 32k genome is going to take 18 million generations to evolve 96 loci. The smallest free living organism has a genome size of about 500k. If we assume that doubling the genome size causes a tripling of the generations of convergence you get:
Genome size/generations for convergence
16k/6,000,000
32k/18,000,000
64k/54,000,000
128k/162,000,000
256k/486,000,000
512k/1,458,000,000
My, my, my. Almost 1.5 billion generations to evolve 96 loci. What happens when we extrapolate your estimate to an e coli size genome? Let’s do the arithmetic.
1024k/4,374,000,000
2048k/13,122,000,000
4096k/39,366,000,000
Why that’s 40 billion generations to evolve the same number of binding sites on an e coli size genome that Dr Schneider’s published case took less than a thousand generations on a 256 base genome. Something is slowing down here Paul and it is your theory of evolution. Why don’t you evolutionists go back to the Evolutionisdead forum and see what my estimates were to evolve these binding sites on an e coli size genome. There are no moving goalposts. With respects to your whining about increasing genome sizes and decreasing mutation rates, both will reach realistic values after the 500k genome size. Of course you have evidence that the original life forms you speculate had smaller genomes than this and could sustain higher mutation rates than life forms today. That’s really solid evolutionary science.

No, a single fatal selection pressure can cause extinction or combinations of individually non-fatal selection pressures can be sufficient to cause extinction. Even if the individually non-fatal selection pressures do not cause extinction, they reduce the rate of reproduction and slow the evolutionary process.

The only fiction we are dealing with here is the theory of evolution. You are starting to understand the mathematics of mutation and selection and why multiple selection conditions confound the evolutionary process. This is why ev takes billions of generations to evolve less than 100 loci. You can evolve these loci in a tiny fraction of the number of generations when using individual selection conditions done serially. This is the same phenomena that is used to treat HIV. Put as many selective pressures on the virus you can and you slow the evolution of the virus. You combine this mathematical fact with the fact there are no selection processes to evolve a gene from the beginning and your theory of evolution is proved to be mathematically impossible.

There don't seem to be any new lies here, unless we count your witless crap about "computer games".

I presume that, handicapped though you are, you are not stupid enough to think that anyone claimed that "the first thing to evolve was a computer game". Your pretense that someone has done so is not going to fool anyone.

 

[Paul C. Anagnostopoulos]

Why that’s 40 billion generations to evolve the same number of binding sites on an e coli size genome that Dr Schneider’s published case took less than a thousand generations on a 256 base genome.

And so, even with this ridiculous population of only 64, E. coli could pull this off in about 1.5 million years.

Notice how we're back to evolution taking a whole big really long time, rather than evolution stopping dead.

~~ Paul

 

[Mr. Scott]

When I asked, "Why, Dr. Kleinman, do you insist that an incomplete model of evolution can be used to prove that evolution is impossible?"

Random point mutations are the least destructive of mutations. Phase shift mutation are more harmful to living things. Ultimately, there is no selection process that can evolve a gene from the begin despite the mechanism of mutation. The most serious blow that ev does to the theory of evolution is that it reveals the multiple selection conditions confound the evolutionary process. No mutation mechanism can overcome this mathematical fact.

But there is a well-known mutation mechanism that can overcome your purported mathematic fact, and one that you seem to ignore like a child humming while his ears are covered. It's gene duplication, which Ev does not model.

Even if, as you assert, three mutations will permanently disable any gene, if there's a duplicate present, the 3x mutated gene could continue mutating while the organism can survive just fine with the working copy while the scratch copy could find a use advantagous to the organism's reproduction. That would make it a "new gene" evolved from an existing gene. Cases of this actually happening have been verified. Deal with this point, Dr. Kleinman, instead of the "first gene on Earth" retreat.

So, you are wrong on both counts. Evolution of new genes is a documented fact resulting from gene duplication, and since the Ev program does not model this, your proof, using Ev, is mathematically invalid.

 

[kleinman]

Annoying Creationists

No, a single fatal selection pressure can cause extinction or combinations of individually non-fatal selection pressures can be sufficient to cause extinction. Even if the individually non-fatal selection pressures do not cause extinction, they reduce the rate of reproduction and slow the evolutionary process.

I'm glad you continue to admit the error of your claim that multiple selection pressures stop evolution. It's a refreshing change in your behavior.

Oh, I didn’t admit that but I am glad you admit you have no idea how the original gene arose in your gene duplication hypothesis. That’s just a minor gap in your theory.

The only fiction we are dealing with here is the theory of evolution.

How exactly do you propose to have real evidence this fictional process stops?

Are you proposing there is no such thing as extinction now? Are you going to concur with Taffer that multiple drug therapy for the treatment of HIV slows the reproduction of the virus more effectively than monotherapy but has nothing to do with fitness and evolution? There is now plenty of mathematical evidence of how mutation and selection works and multiple selection processes slow evolution and sufficient selection pressures causes extinction.

Why that’s 40 billion generations to evolve the same number of binding sites on an e coli size genome that Dr Schneider’s published case took less than a thousand generations on a 256 base genome.

And so, even with this ridiculous population of only 64, E. coli could pull this off in about 1.5 million years.

Well run the case with the largest population you want a prove me wrong. But we already have a good idea what huge populations do in ev so I doubt you will waste your time on this case, you know I will co-opt the results.

Notice how we're back to evolution taking a whole big really long time, rather than evolution stopping dead.

You know I love quoting you Paul, so do you remember this question?

Just a question to finish this post. If the number of generations required to converge your cases exceeds the time available in the age of the universe, does that qualify as evolution stopping? That’s ok with me, so you can stop your cases when they exceed: ...

No, but it does make evolution impractical. Fortunately, real evolution has many other ways to get things done, so no conclusion can be drawn from Ev alone.

What conclusion can you draw from ev Mr Rcapacity?

Random point mutations are the least destructive of mutations. Phase shift mutation are more harmful to living things. Ultimately, there is no selection process that can evolve a gene from the begin despite the mechanism of mutation. The most serious blow that ev does to the theory of evolution is that it reveals the multiple selection conditions confound the evolutionary process. No mutation mechanism can overcome this mathematical fact.

But there is a well-known mutation mechanism that can overcome your purported mathematic fact, and one that you seem to ignore like a child humming while his ears are covered. It's gene duplication, which Ev does not model.

None of you evolutionists will tell us where the original gene came from and if you think gene duplication is what drives the theory of evolution, add the feature to ev and evolve new genes from the existing genes. I wonder what the selection process is that would accomplish such a thing?

You evolutionist need to take your slogan “mutation and selection” and demonstrate mathematically how it works. Ev shows that random point mutation with multiple selection conditions doesn’t do it, you think that gene duplication does it, put in the model and demonstrate how it works. I especially look forward to you demonstrating how the original gene came to be.

Even if, as you assert, three mutations will permanently disable any gene, if there's a duplicate present, the 3x mutated gene could continue mutating while the organism can survive just fine with the working copy while the scratch copy could find a use advantagous to the organism's reproduction. That would make it a "new gene" evolved from an existing gene. Cases of this actually happening have been verified. Deal with this point, Dr. Kleinman, instead of the "first gene on Earth" retreat.

Describe to us the selection process that is morphing this copy of a gene to a new gene because this is the crucial mechanism that needs to be mathematically modeled.

So, you are wrong on both counts. Evolution of new genes is a documented fact resulting from gene duplication, and since the Ev program does not model this, your proof, using Ev, is mathematically invalid.

Examples of so called new genes have been presented in this thread but these examples started as proteases and remained proteases. What kind of examples to you have?

The mathematical fact that ev shows that multiple selection conditions slow and ultimately stop evolution will be independent of the mechanism of mutation. It is obvious that the more different ways you try to sort things the slower the process occurs. Well it’s obvious to everyone except evolutionists.

 

[Paul C. Anagnostopoulos]

The mathematical fact that ev shows that multiple selection conditions slow and ultimately stop evolution will be independent of the mechanism of mutation. It is obvious that the more different ways you try to sort things the slower the process occurs. Well it’s obvious to everyone except evolutionists.

Now you're just babbling, man.

~~ Paul

 

[Dr Adequate]

Now he's just babbling?

And prior to this, he was doing ... what?

 

[Dr Adequate]

None of you evolutionists will tell us where the original gene came from ...

I think I'll call that one Lie #2.

Truth #2: We have shown you not merely how genes, but also entire genomes are produced de novo. Hysterical denial of reality won't make it go away, you crawling whimpering little liar.

 

[kleinman]

Annoying Creationists

The mathematical fact that ev shows that multiple selection conditions slow and ultimately stop evolution will be independent of the mechanism of mutation. It is obvious that the more different ways you try to sort things the slower the process occurs. Well it’s obvious to everyone except evolutionists.

Now you're just babbling, man.

Really Mr Rcapacity? You wish it was babbling. Just when did you last work on a sorting problem when increasing the number of ways you are sorting makes the sort go faster? Don’t you have any experience with databases? Ev shows that sorting on three selection conditions is profoundly slower than sorting on a single selection condition. So set up ev to evolve two sets of binding sites with six selection conditions and show us how much faster evolution proceeds. I’d love to co-opt this work. Of course you can always claim that this is a stylized model of mutation and selection that only models a small part of the evolutionary landscape.

I’ve got a question for you. Has Dr Schneider done any new advertising of ev recently?

 

[Paul C. Anagnostopoulos]

Now he's just babbling?

And prior to this, he was doing ... what?

Well, at least he was constructing grammatical sentences.

Really Mr Rcapacity? You wish it was babbling. Just when did you last work on a sorting problem when increasing the number of ways you are sorting makes the sort go faster? Don’t you have any experience with databases? Ev shows that sorting on three selection conditions is profoundly slower than sorting on a single selection condition.

You mean selecting, not sorting, right? I think those are database terms.

I agree that evolving a distinguishing binding site requires more time than evolving a nondistinguishing gene threshold.

~~ Paul

 

[Dr Richard]

And so, even with this ridiculous population of only 64, E. coli could pull this off in about 1.5 million years.

Notice how we're back to evolution taking a whole big really long time, rather than evolution stopping dead.

~~ Paul

Only 40 billion generations? I assume Kleinman means 40x10^9 generations each comprising 64 bacteria.

Given that there are approximately 1x10^14 microorganisms in the gut , if we assume E coli make up just one 1% of this, that is 10000000000000 E coli inside each and every one of us, all dividing up to three times an hour.

Kleinman has claimed that evolution "stops" when a realistic gene size is used. In fact, he has proved that with a realistic population size, evolution is inevitable.

Kleinman, congratulations on your faeculent proof!

 

[kleinman]

Annoying Creationists

Really Mr Rcapacity? You wish it was babbling. Just when did you last work on a sorting problem when increasing the number of ways you are sorting makes the sort go faster? Don’t you have any experience with databases? Ev shows that sorting on three selection conditions is profoundly slower than sorting on a single selection condition.

You mean selecting, not sorting, right? I think those are database terms.

The problems are analogous except the mutation and selection problem is more complex because the data is being randomly modified as it is being sorted. The point is the selection conditions define the sort and the more selection conditions you have, the more difficult it is to do the sort. This applies to whether your talking about a database or the theory of evolution.

I agree that evolving a distinguishing binding site requires more time than evolving a nondistinguishing gene threshold.

Are you saying that it take more time for ev to satisfy all three selection conditions simultaneously than it takes to satisfy any single selection condition alone? If that is what you are saying, that is a bit of an understatement. It is about a million times slower on the 16k genome case.

And so, even with this ridiculous population of only 64, E. coli could pull this off in about 1.5 million years.

Notice how we're back to evolution taking a whole big really long time, rather than evolution stopping dead.

Only 40 billion generations? I assume Kleinman means 40x10^9 generations each comprising 64 bacteria.

Given that there are approximately 1x10^14 microorganisms in the gut , if we assume E coli make up just one 1% of this, that is 10000000000000 E coli inside each and every one of us, all dividing up to three times an hour.

Kleinman has claimed that evolution "stops" when a realistic gene size is used. In fact, he has proved that with a realistic population size, evolution is inevitable.

Kleinman, congratulations on your faeculent proof!

Dr Richard, once you finish Sesame Street, we’ll start you on the mathematics of ev. You evolutionists think that huge populations markedly accelerate evolution. Ev is showing otherwise and if you realized that increasing populations affect the probabilities in less than an additive manner, the results from ev become understandable.