Annoying creationists

[kjkent1]

Is that what you think this data says? What is says it is very easy for sequences of bases to satisfy the threshold for the weight matrix. It is so easy that there were no mistakes in identifying binding sites. The weight matrix is able to recognizes binding sites starting with a random genome. Now getting rid of the many spurious binding sites takes a few generations but it doesn’t take long. If you want to learn something about the behavior of ev, run these cases in the step mode and watch what happens to the mistake counts. I don’t suggest using the step method when doing cases with three selection conditions. You will get a repetitive use injury of your index finger long before these cases converge (if they ever will converge).

Now there is another explanation, your string cheese theory of evolution and we are running these cases in one of your 10^500 alternative universes.

If you turn off all three selection conditions, you will instantly create a perfect creature in the first generation, regardless of what other conditions are specified. This means:

1. Ev simulates abiogenesis with mistake weights of all zero.
2. Mistake weights of zero, break ev and produce invalid results.
3. Kleinman constructs and wears an aluminum hat.

I pick #2. You pick your nose.

 

[Paul C. Anagnostopoulos]

So far, evolution hasn’t stopped for three selection conditions on a 16,384 base genome but I think you can say that it has slowed down a bit since each individual selection condition converges more than a thousand times faster.

By all means, it slows down. What I'm quite confident it does not do is stop, which is what you've been claiming for weeks now.

I’ll remember this, I won’t give up so easily next time.

Excellent.

Now don’t you give up so easily, you have the 32k case to run. Isn’t that one where Rcapacity=Rfrequency? Then when you finish that one, you have the 64k, 128k and 256k genomes to do. So enjoy your fleeting victory because I’ve already shown that these other cases easily converge when using only a single selection condition.

The 32K would certainly require a huge number of generations to converge, if it ever did. That's because Rfrequency is getting close to Rcapacity, and it becomes difficult to match binding sites without also matching other loci. You can fix this by setting one or more mistake counts to zero, whereby Rcapacity is no longer a limitation and mistakes can drop to zero quite easily. Even with Rcapacity in play, I would bet that, given sufficient time, even 32K and 64K genomes could reach perfection. Fortuntately, there is no artificial limitation on binding site width in nature.

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.

~~ Paul

 

[delphi_ote]

HIV is treated by using multiple selection pressures. 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.

That makes zero sense, but it's okay. I'm going to ignore it for now. You've already got a claim on the table. Are you retreating from your "stopping evolution" claim without admitting error? That's not very honest of you.

There is a distinction between treating and curing a disease.

The fact that we can't stop the evolution of HIV is precisely why our best medicine to date can only treat it, not cure it.

 

[kleinman]

Annoying Creationists

So far, evolution hasn’t stopped for three selection conditions on a 16,384 base genome but I think you can say that it has slowed down a bit since each individual selection condition converges more than a thousand times faster.

By all means, it slows down. What I'm quite confident it does not do is stop, which is what you've been claiming for weeks now.

Perhaps you would be willing to explain this statement you made on the Evolutionisdead Forum?

It is certainly not the crux of your 4^n objection. The problem is that the information capacity of the binding sites limits the length of the genome that can converge on a perfect creature. At some point the number of generations required to converge goes to infinity (not 4^n). The problem can be postponed by increasing the capacity of the binding sites without increasing the length of the genome.

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’ll remember this, I won’t give up so easily next time.

Excellent.

There is still so much annoying to do.

Now don’t you give up so easily, you have the 32k case to run. Isn’t that one where Rcapacity=Rfrequency? Then when you finish that one, you have the 64k, 128k and 256k genomes to do. So enjoy your fleeting victory because I’ve already shown that these other cases easily converge when using only a single selection condition.

The 32K would certainly require a huge number of generations to converge, if it ever did. That's because Rfrequency is getting close to Rcapacity.

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.

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.

Really, evolution has many other ways to get things done? Like what? Do you have something other than mutation and selection? If you do, you really need to put this feature in ev because as it stands, the data from ev is showing that your theory is mathematically impossible. The reason it is mathematically impossible is that the competing selection conditions slow and then ultimately stop evolution. You think it is your Rcapacity concept but reduce the number of selection conditions and the model converges again.

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.

HIV is treated by using multiple selection pressures. 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.

What part of "the extraordinary power of viruses like HIV and HCV to escape almost any means of host attack remains a daunting hurdle to overcome" do you not understand?

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.

There is a distinction between treating and curing a disease.

The fact that we can't stop the evolution of HIV is precisely why our best medicine to date can only treat it, not cure it.

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

 

[delphi_ote]

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.

You claimed evidence exists in the natural world that evolution stops under multiple selection pressures. If that is the case, it should be very easy to point me to some kind of expert stating precisely that. Back this up with some kind of science.

 

[kleinman]

Annoying Creationists

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.

You claimed evidence exists in the natural world that evolution stops under multiple selection pressures. If that is the case, it should be very easy to point me to some kind of expert stating precisely that. Back this up with some kind of science.

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

It can be stopped by complete extinction. If you wipe out all of the relevant life, there won't be anymore evolution.

 

[delphi_ote]

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.

 

[Taffer]

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.

First of all, there are no antiretrovirals that kill the virus. Antiretrovirals impair a particular metabolic step whether it be in reproduction of the virus or some other step in the life cycle of the virus. Once you have HIV, you always have HIV.

Yes, klienman, I know.

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".

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?

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?

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.

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.

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.

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

Um, kleinman? Risk and probability are different things.

 

[Taffer]

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".

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.

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.

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

They don't.

This is the very heart of the theory of evolution.

No, it isn't.

Ev shows mathematically why multiple selection pressures slow this process.

No, it doesn't.

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.

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.

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.

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.

 

[Taffer]

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.

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.

 

[Taffer]

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.

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.


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.[/quote]

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.

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.

 

[Paul C. Anagnostopoulos]

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.

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.

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.

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 ...

~~ Paul

 

[Mr. Scott]

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.

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

My own way to answer is, if any binding site can evolve in a finite amount of time, then we only have to do the math to see if cats and dogs could have had a common ancestor. We pretty much can know how far back the split may have occured because we can count the genetic differences -- perhaps even mitochondrial DNA would suffice -- between present day animals. Remember that the genetic difference between the standard cat and dog will be twice the difference between their common ancestor and each. Note also that many individuals would be evolving binding sites in parallel, not just in series. A cat that eats well because a microevolutionary step lets its ears hear prey better could mate with one who's paws were the beneficiaries of their own, independent microevolutionary step that let it stalk prey more silently. The changes don't have to be sequential, as, I understand, is an Ev limitation. In populations of thousands of dogs and thousands of cats over thousands of generations mixing their genes by sexual reproduction thousands of times, it's easy to see how macroevolution would occur after such a huge accumulation of microevolutionary steps. Why can't multitudes of microevolutions add up to macroevolution?

In fact, by tracing the fossil records, such diversions of one species into many over time have been verified countless times.

The evidence provided by a partial model of evolution can lend support for the theory, but can never be relied on to prove such a theory "impossible." Only a complete model/simulation can do that, and there presently is no such computer model capable of proving evolution to be impossible.

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

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.

That is a cute picture though.

It is cute. My first choice would have been a picture of the cartoon character "catdog," but that was too cute. My second choice was one of the photos I found of cats humping dogs. That would have been too un-cute for a bible thumper. The photo I settled on seemed to express the heart of cat/dog divergence, but you can't let that into your heart. There's an ignorant holy book blocking its path.

Don't forget my important questions:

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

Why can't multitudes of microevolutions add up to macroevolution?

 

[Paul C. Anagnostopoulos]

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.

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

 

[Paul C. Anagnostopoulos]

4,074,800 generations, 4 mistakes, and counting ...

~~ Paul

 

[Mr. Scott]

Annoying Incomplete Simulations

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

Well, make it snappy. The K-man is waiting for more proof of his faith, which he seems delighted you are providing.

 

[kjkent1]

4,074,800 generations, 4 mistakes, and counting ...

~~ Paul

Paul,

Although I would argue that 4 mistakes is close enough considering the size of the genome, and although you may already have completed the experiment, it's worth mentioning that pseudo-random number generators repeat their pattern, usually in less than 10 million cycles. I can easily envision many situations with ev where the program will have accessed the random function many millions of times, and how this could lead to a misleading result causing the appearance of a halt to evolution.

The only way to ensure really large random simulations is to use a real random number generator. Just ask any slot machine manufacturer.

 

[cyborg]

It is however slightly problematic to do this given that real randomness requires special hardware - like something that uses radioactive decay.

 

[Dr Adequate]

You claimed evidence exists in the natural world that evolution stops under multiple selection pressures. If that is the case, it should be very easy to point me to some kind of expert stating precisely that. Back this up with some kind of science.

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

It can be stopped by complete extinction. If you wipe out all of the relevant life, there won't be anymore evolution.

So, kleinman, are you:

(a) So mentally crippled that you don't know the difference between "multiple selection pressures" and "complete extinction"?

(b) So socially crippled that you think this drivel is going to fool someone?

(c) So morally crippled that you just love puking out stupid lies even when you know that they're not going to fool anyone --- just out of sheer hatred of truth and decency?

So far as I can tell, you are crippled in all three respects --- I'm just wondering which of your handicaps made you drivel this particular load of crap from your incontinent orifice.

 

[Paul C. Anagnostopoulos]

Although I would argue that 4 mistakes is close enough considering the size of the genome, and although you may already have completed the experiment, it's worth mentioning that pseudo-random number generators repeat their pattern, usually in less than 10 million cycles. I can easily envision many situations with ev where the program will have accessed the random function many millions of times, and how this could lead to a misleading result causing the appearance of a halt to evolution.

Even without a decrease in the number of mistakes, I don't think that Ev could be in the same state after billions of random numbers go by. The best creature would still have a different genome content.

~~ Paul