Annoying creationists

[kjkent1]

Yes, I think so. And I was a bit quick to jump on you about mistakes, since certainly mistakes can be reintroduced once they evolve away.






~~ PaulOK, now that we're in reasonable alignment, and in anticipation of Dr. Kleinman's attempt to claim differently, I have taken it upon myself to do a little experiment using ev. My hypotheses are as follows:(1) The number of generations required to evolve an ev binding-site region are dependent upon the selective forces acting simultaneously on the region, and (2) said evolutionary generations are normally distributed with the maximum number of selective forces residing at the mean average.In order to test the above hypothesis,

1) I ran ev using the default parameters, except, that I changed the setting for ties to randomly select a creature for survival. The purpose of this change was to maintain the maximum amount of randomness in the results possible.

2) I repeated the experiment using 10 different random seeds (0 through 9), in order to diminish the possibility that any particular random seed would cause a biased outcome.

3) While using each random seed, I repeated the experiment and sequenced through the eight available combinations of the three available mistake weights (missing bindings, spurious bindings inside the binding-site region, spurious bindings outside the binding-site region) using weights of either 1 or 100. The objective was to maximize or minimize the effect of each of the selective forces that can be manipulated in ev.

The result of this experiment is reported here (http://www.geocities.com/kjkent1/ev_average_results_with_random_seeds.pdf).

As shown from the results, the average fastest evolution (558 generations) occurs by maximizing the selective effect of missing bindings while simultaneously minimizing the selective effect of all spurious bindings, and the average slowest evolution (983 generations) occurs by maximizing the selective effect of all spurious bindings, while minimizing the selective effect of missing bindings.

The mean average evolution is 834 generations, which lies between maximizing the effect of both missing bindings and spurious bindings, and maximizing the effect of missing bindings and spurious bindings outside the binding-site region, while minimizing the effect of spurious bindings inside the binding-site region.

The experimental findings strongly suggest that the effect of multiple selective forces is to average out the number of generations necessary for evolution to occur. This makes sense in view of what we see in nature, i.e., living organisms are subjected to an uncountable number of selective forces, all of which combine to cause one average evolutionary outcome.

The results also suggest that creationist claims of conflicting selective forces slowing or halting evolution are not supported by the ev model.

Additionally, the normalized graph of the eight different combinations of ev selective forces, while certainly not a perfect bell-shaped curve, shows a definite tendency toward a normalized, or perhaps parabolic distribution. However, without more selective forces to plot, it's difficult to tell whether there is a clear tendency toward one or the other.

The conclusion is clear in at least one respect: multiple selective forces do not impair/halt evolution, but rather center around a mean average of possible outcomes.

[kleinman]

Your missing the point Taffer, by using multiple antimicrobials (that is multiple selection pressures) such as done when treating HIV, prevents or impairs the emergence of multiple resistant microbes. It is when using single antimicrobials (that is single selection pressures) that resistant microbes are much more likely to emerge.Er, no kleinman. Using a single antimicrobial (antibacterials used in HIV treatment are, AFAIK, not for the treatment of the virus itself, but for treatment of other bacterial agents) drug can result in a microbe resistant to that drug. The use of multiple antimicrobial drugs can result in a microbe resistant to all of the drugs. You can't use a single antibacterial agent, for example, and expect the bacteria to become resistant to a completely different antibacterial. Yes, multiple selective pressures will make it 'harder' for the bacteria to become resistant to all of the drugs, but it is not an impossibility, as it has been observed to happen many times. I have, personally, created, using selective pressures alone, multiple resistant bacteria.
You’ve got this wrong Taffer. The standard of care for treating HIV now calls for the use of three antiviral agents simultaneously. This is done to prevent the emergence of resistant strains of the virus. You do have it correct when you say it is ‘harder’ for bacteria to become resistant to multiple drugs when the drugs are used simultaneously. You are much more likely to create multiple drug resistant bacteria when you subject the bacteria to one drug at a time. This is exactly what ev is showing and it shows why the theory of evolution is mathematically impossible. Multiple selection pressures slow and ultimately stop evolution. Selection pressures acting in parallel slow and ultimately stop evolution.
It is amazing that so many academicians can be wrong. It is an observable fact that theory of evolution is mathematically impossible. Multiple selection pressures slow and then ultimately stop evolution. This is shown by ev and observed in reality. So you're right, and everyone else is wrong? You wonder why no-one takes you seriously? You can't even admit that you could be wrong. Reality shows that evolution is a fact. I have personally observed evolution at work, kleinman.
Taffer, ev does a precise mathematical analysis of mutation and selection and shows an important and fatal flaw in your theory. The reason why ev fails to converge is that parallel selection processes slows and ultimately stop the evolutionary process. You have observed this effect when using multiple antimicrobials. Unless you are going to propose that genes evolve in a serial manner to individual selection pressures, you are going to encounter this mathematical fact the ev reveals. Anyone who understands the mathematics of ev and understands why multiple antiviral agents are used in the treatment of HIV will have to take this fact seriously. Multiple selection pressures acting in parallel stop evolution.

[delphi_ote]

Same tired arguments? Here’s a little lesson in the nonlinear mathematics of mutation and selection that is shown by ev.
Quick! Ignore the context and jump to another one of your irrelevant, tired arguments! Then everyone can play wack-a-mole for another 82 pages.
This is also observed in reality.
Care to point me to a reference for that lie interesting claim?

[delphi_ote]

Multiple selection pressures slow and ultimately stop evolution. Selection pressures acting in parallel slow and ultimately stop evolution.
I keep trying to type a response, but words fail me every time. It's times like these when we must turn to literature.
Anything approaching the change that came over his features I have never seen before, and hope never to see again. Oh, I wasn't touched. I was fascinated. It was as though a veil had been rent. I saw on that ivory face the expression of sombre pride, of ruthless power, of craven terror--of an intense and hopeless despair. Did he live his life again in every detail of desire, temptation, and surrender during that supreme moment of complete knowledge? He cried in a whisper at some image, at some vision--he cried out twice, a cry that was no more than a breath:

`The horror! The horror!'

[Taffer]

You’ve got this wrong Taffer. The standard of care for treating HIV now calls for the use of three antiviral agents simultaneously.

I stand corrected.

This is done to prevent the emergence of resistant strains of the virus.

Citation, please.

You do have it correct when you say it is ‘harder’ for bacteria to become resistant to multiple drugs when the drugs are used simultaneously. You are much more likely to create multiple drug resistant bacteria when you subject the bacteria to one drug at a time. This is exactly what ev is showing and it shows why the theory of evolution is mathematically impossible. Multiple selection pressures slow and ultimately stop evolution. Selection pressures acting in parallel slow and ultimately stop evolution.

No, it is not. All this shows is that, in the presence of multiple selective pressures, it takes longer for an organism to evolve to a predetermined value. But evolution does not work like this in the real world. There is no "predetermined value"

Also, please show where evolution ever stops.

Taffer, ev does a precise mathematical analysis of mutation and selection and shows an important and fatal flaw in your theory. The reason why ev fails to converge is that parallel selection processes slows and ultimately stop the evolutionary process. You have observed this effect when using multiple antimicrobials.

No, it doesn't, kleinman. You make the mistake of assuming the organism which an individual is going to evolve into. Evolution does not work like that.

Unless you are going to propose that genes evolve in a serial manner to individual selection pressures, you are going to encounter this mathematical fact the ev reveals.

Of course not. But, and this is very important kleinman, this effect is only observable if the selective pressures are binary. If the selective pressures are "evolve or die", then of course multiple selective pressures will slow evolution. But, in the real world, it is not a matter of black-and-white. As I've already tried to explain to you, not all deletarious mutations are fatal. The same goes for everything, selective pressures included.

Anyone who understands the mathematics of ev and understands why multiple antiviral agents are used in the treatment of HIV will have to take this fact seriously.

Right. Everyone else is wrong, and you are right. Got it. :rolleyes:

Multiple selection pressures acting in parallel stop evolution.

No they don't, otherwise multiple antibacterial resistant bacteria could not evolve. They do, therefore you are wrong.

[kleinman]

The results also suggest that creationist claims of conflicting selective forces slowing or halting evolution are not supported by the ev model.
Why don’t you explain why ev stops converging as you lengthen the genome? And then when you eliminate two of the three selection pressures, ev then will converge with all other parameters held fixed.
Same tired arguments? Here’s a little lesson in the nonlinear mathematics of mutation and selection that is shown by ev. Quick! Ignore the context and jump to another one of your irrelevant, tired arguments! Then everyone can play wack-a-mole for another 82 pages.
If you are looking for someone who has tired arguments, try an evolutionist. Mutation and selection is a worn out slogan that ev shows stops evolution when you have multiple selection processes. Anyway, I’m playing wack-a-worn out theory and annoy and evolutionist.
This is also observed in reality.Care to point me to a reference for that lie interesting claim?
For you Delphi, any time. The use of multiple drugs (triple antiviral medications) to prevent selection and evolution of drug resistant strains of HIV is extensively documented in the http://aidsinfo.nih.gov/contentfiles/AdultandAdolescentGL.pdf (http://aidsinfo.nih.gov/contentfiles/AdultandAdolescentGL.pdf) guidelines for the treatment of this disease.
Multiple selection pressures slow and ultimately stop evolution. Selection pressures acting in parallel slow and ultimately stop evolution. I keep trying to type a response, but words fail me every time. It's times like these when we must turn to literature. Anything approaching the change that came over his features I have never seen before, and hope never to see again. Oh, I wasn't touched. I was fascinated. It was as though a veil had been rent. I saw on that ivory face the expression of sombre pride, of ruthless power, of craven terror--of an intense and hopeless despair. Did he live his life again in every detail of desire, temptation, and surrender during that supreme moment of complete knowledge? He cried in a whisper at some image, at some vision--he cried out twice, a cry that was no more than a breath:

`The horror! The horror!'
That makes sense, quote from fiction to defend your mathematically impossible theory.
This is done to prevent the emergence of resistant strains of the virus. Citation, please.
http://aidsinfo.nih.gov/contentfiles/AdultandAdolescentGL.pdf (http://aidsinfo.nih.gov/contentfiles/AdultandAdolescentGL.pdf)
You do have it correct when you say it is ‘harder’ for bacteria to become resistant to multiple drugs when the drugs are used simultaneously. You are much more likely to create multiple drug resistant bacteria when you subject the bacteria to one drug at a time. This is exactly what ev is showing and it shows why the theory of evolution is mathematically impossible. Multiple selection pressures slow and ultimately stop evolution. Selection pressures acting in parallel slow and ultimately stop evolution.No, it is not. All this shows is that, in the presence of multiple selective pressures, it takes longer for an organism to evolve to a predetermined value. But evolution does not work like this in the real world. There is no "predetermined value"

Also, please show where evolution ever stops.
Ev does stop converging. Paul is trying to attribute this to his Rcapacity factor but it is easily seen that the failure of ev to converge is due to the multiple selection factors. Read the link I provide to the guidelines for treatment of HIV and you will see the treatment strategy is identical to what ev is demonstrating. If you can ever describe a selection pressure to evolve a gene from the beginning, imagine what would happen with a multitude of selection pressures evolving genes from the beginning would have to overcome.
Taffer, ev does a precise mathematical analysis of mutation and selection and shows an important and fatal flaw in your theory. The reason why ev fails to converge is that parallel selection processes slows and ultimately stop the evolutionary process. You have observed this effect when using multiple antimicrobials.No, it doesn't, kleinman. You make the mistake of assuming the organism which an individual is going to evolve into. Evolution does not work like that.
Ev does accurately model mutation and selection. It shows that multiple selection pressures slow and ultimately stop evolution and that principle is used to treat HIV.
Unless you are going to propose that genes evolve in a serial manner to individual selection pressures, you are going to encounter this mathematical fact the ev reveals. Of course not. But, and this is very important kleinman, this effect is only observable if the selective pressures are binary. If the selective pressures are "evolve or die", then of course multiple selective pressures will slow evolution. But, in the real world, it is not a matter of black-and-white. As I've already tried to explain to you, not all deletarious mutations are fatal. The same goes for everything, selective pressures included.
Not every mutation in ev causes a creature to die, yet ev demonstrates that multiple selection pressures slow and ultimately stop evolution. Ev is showing what happens mathematically with multiple selection pressures, which is evolution slows down and ultimately stops. Ev is not doing this as a matter of black-and-white. If you think that ev is doing this as a matter of black-and-white, correct the model and show us how multiple selection pressures work.
Anyone who understands the mathematics of ev and understands why multiple antiviral agents are used in the treatment of HIV will have to take this fact seriously. Right. Everyone else is wrong, and you are right. Got it.
Very few people have studied ev and what it shows due to its multiple selection pressures. This is why ev fails to converge and this is the reason triple antiviral drugs are used to treat HIV. I doubt any evolutionist ever considered what happens when multiple selection pressures occur simultaneously and how it affects the rate of evolution. Now that ev is available and its behavior has been studied, it is becoming apparent why the theory of evolution is mathematically impossible. It is not just that there are no selection pressures that can evolve a gene from the beginning; it is also that multiple selection pressures slow and then stop evolution.
Multiple selection pressures acting in parallel stop evolution. No they don't, otherwise multiple antibacterial resistant bacteria could not evolve. They do, therefore you are wrong.
Taffer, multiple antibacterial resistant bacteria occurs much more quickly when the bacteria are subjected to the antibiotics in a serial manner, one antibiotic at a time. If the bacteria are subject to the antibiotics in parallel, they are much less likely to evolve. So what are the selection pressures that evolved the hundreds of genes necessary for the simplest free living organism and how did this happen in parallel?

[kjkent1]

Why don’t you explain why ev stops converging as you lengthen the genome? And then when you eliminate two of the three selection pressures, ev then will converge with all other parameters held fixed.Your first question relates to no part of my experiment or my conclusion, so your raising it here is irrelevant.

Re your second question, until you show me the specific evidence supporting your conclusion, I have no comment.

While you're at it, why don't you explain why my experimental results directly contradict your conclusion that multiple selective forces slow/halt evolution.

[Taffer]

http://aidsinfo.nih.gov/contentfiles/AdultandAdolescentGL.pdf (http://aidsinfo.nih.gov/contentfiles/AdultandAdolescentGL.pdf)

Did you actually read your source? If you did, then perhaps you can point it out to me where it says that multiple drugs are used to stop resistance developing in the HIV virus. Because I could not find it.

Ev does stop converging. Paul is trying to attribute this to his Rcapacity factor but it is easily seen that the failure of ev to converge is due to the multiple selection factors. Read the link I provide to the guidelines for treatment of HIV and you will see the treatment strategy is identical to what ev is demonstrating. If you can ever describe a selection pressure to evolve a gene from the beginning, imagine what would happen with a multitude of selection pressures evolving genes from the beginning would have to overcome.

*Sigh* You obviously do not understand evolution in the slightest, or you would know this is complete bollocks. List, kleinman, this is very important. Selective pressures are not positive.

And please demonstrate how what happens in the ev model translates to what happens in the real world? Even if ev shows the stopping of evolution, this does not mean it actually happens in real life. Since evolutioni is an observable fact it obviously does not stop, does it?

Your continued claim that there are no selection pressures to evolve a gene "from the beginning" is a false dichotomy. A functional gene need not be the lowest form of life.

Lastly, please demonstrate that the failure in ev for convergence is due to multiple selective pressures, and not Rcap.

Ev does accurately model mutation and selection.

It accurately enough models mutation and selection of a single binding site, with a 'perfect' creature already established. It does not accurately model evolution in the real world. Get over it.

It shows that multiple selection pressures slow and ultimately stop evolution...

No, it doesn't. You just claim that it does.

...and that principle is used to treat HIV.

No, it isn't. Multiple antiretroviral agents are used because restance arrises. Using more then one does not slow the evolution of the resistance of any single antiretroviral agent, but rather prolongs the course of treatment before the HIV virus becomes resistant to all three. You need to understand, kleinman, that not all selective pressures are do or die.

Not every mutation in ev causes a creature to die, yet ev demonstrates that multiple selection pressures slow and ultimately stop evolution.

You have no evidence that evolution has stopped, so stop claiming that it has.

Ev is showing what happens mathematically with multiple selection pressures, which is evolution slows down and ultimately stops. Ev is not doing this as a matter of black-and-white. If you think that ev is doing this as a matter of black-and-white, correct the model and show us how multiple selection pressures work.

I don't have to show how multiple selective pressures work, because I have observed them working myself. Remember those bacteria I've created? They were multiple resistant bacteria. Three, to be exact. We spontaniously generated resistant bacteria from non-resistant bacteral cultures. Wow, evolution! Oh, but that's right, it's "mathematically impossible". :rolleyes:

Very few people have studied ev and what it shows due to its multiple selection pressures. This is why ev fails to converge and this is the reason triple antiviral drugs are used to treat HIV. I doubt any evolutionist ever considered what happens when multiple selection pressures occur simultaneously and how it affects the rate of evolution.

You are a pompous git. We already have models for multiple selective pressures!

Now that ev is available and its behavior has been studied, it is becoming apparent why the theory of evolution is mathematically impossible. It is not just that there are no selection pressures that can evolve a gene from the beginning; it is also that multiple selection pressures slow and then stop evolution.

And anyone who disagrees with you is wrong. Because you are right. Not the people who actually understand the material. You. Right. :rolleyes:

You have failed to show anything, kleinman, except your own ignorance and arrogance towards the subject.

Taffer, multiple antibacterial resistant bacteria occurs much more quickly when the bacteria are subjected to the antibiotics in a serial manner, one antibiotic at a time. If the bacteria are subject to the antibiotics in parallel, they are much less likely to evolve. So what are the selection pressures that evolved the hundreds of genes necessary for the simplest free living organism and how did this happen in parallel?

You do not understand at all. Selection for antibacterial resistance occurs at the organism level. Take three loci, all of which give a different antibacterial reistance. Put bacteria on media in series, and you will evolve triple-resistant bacteria. Put the bacteria on media which contains all three antibiotics, and you will evolve triple-resistant bacteria. I have done this myself. So your claims that multiple selection pressures stop evolution are stupid, ignorant, and above all, false. The only reason why it seems to be harder to evolve triple-resistant bacteria in "parallel", is because their resistance has to evolve at once. But the probability is the same. 1+1+1 is the same as 3X1.

[Paul C. Anagnostopoulos]

Paul, in case you haven’t noticed, ev can easily evolve binding sites despite your Rcapacity condition when you set the weight factors for spurious binding sites to 0.
Alan, you simply refuse to pay any attention, don't you? I'm going to say this one more time and then give up:

Rcapacity is the number of bits of information required to distinguish binding sites from the rest of the genome. If you are not distinguishing binding sites from the rest of the genome, Rcapacity is irrelevant.


Oh really, why? Paul, ev can easily evolve all three of the selection conditions when done separately on a genome where your Rcapacity value equals Rfrequency. The failure of ev to converge when using all three selection conditions simultaneously is due to the competition of these conditions. It has nothing to do with being able to identify the binding sites. Binding sites are easily identified. This is shown by setting the weight factors for spurious bindings to zero.
Binding sites are easily identified because the program knows where they are. Locating the binding sites is not interesting. What is interesting is distinguishing binding sites from other sites using the transcription factor modeled by the weight matrix and threshold.


Not only does setting two of the three selection conditions to zero affect the number of generations to evolve a perfect creature, it is the only way to evolve a perfect creature when you lengthen the genome in ev.
You do not know this, because you have never run an experiment where evolution "stops dead" when Rcapacity is not an issue. And apparently you never will, because you do not believe that the width of the binding sites puts a limit on Rsequence. I'm not sure I've ever had a conversation with someone who installed a belief system on top of mathematics.

~~ Paul

[Paul C. Anagnostopoulos]

Excellent experiment, Kjkent. Thanks.


While you're at it, why don't you explain why my experimental results directly contradict your conclusion that multiple selective forces slow/halt evolution.
Because your genome is not large enough, obviously! Increase its size so that Rfrequency > Rsequence and try again. You silly goose.

~~ Paul

[delphi_ote]

For you Delphi, any time. The use of multiple drugs (triple antiviral medications) to prevent selection and evolution of drug resistant strains of HIV is extensively documented in the guidelines for the treatment of this disease.
Thanks for the 121 page document you haven't read. Another smokescreen. Why am I not suprised?

Adding multiple drugs... each of which would cause selection... prevents selection? Are you really typing these things?

Also, I note that you've dodged away from your original position...
In fact, ev will not converge at all in many cases when all the selection processes are acting simultaneously. This is also observed in reality.
You said multiple selection pressures stop evolution, and that this has been observed in nature. You've repeated this fiction several times. That's obviously not the case here, as HIV and AIDS are still a problem. The only way to "stop" evolution is to put the entire population under too stringent a selection pressure (i.e. kill them all off.)

[Dr Adequate]

Lie #1. Truth #1.

[Taffer]

Truth #1.

:D

[kleinman]

Why don’t you explain why ev stops converging as you lengthen the genome? And then when you eliminate two of the three selection pressures, ev then will converge with all other parameters held fixed.Your first question relates to no part of my experiment or my conclusion, so your raising it here is irrelevant.
Once again, you miss the point. The reason why ev stops converging is that the multiple competing selection process stop evolution. Why don’t you perform some relevant experiments?
Re your second question, until you show me the specific evidence supporting your conclusion, I have no comment.
The evidence couldn’t be simpler. Choose any case you want and lengthen the genome until ev no longer converges with each of the weight factors set to 1. Then take any two of the three weight factors and set them to zero and behold, ev converges with a single selection condition. It is the multiple selection conditions that prevents ev from converging.
While you're at it, why don't you explain why my experimental results directly contradict your conclusion that multiple selective forces slow/halt evolution.
Your explanation is incomprehensible. Post your experimental results and I’ll comment on them.
http://aidsinfo.nih.gov/contentfiles/AdultandAdolescentGL.pdf (http://aidsinfo.nih.gov/contentfiles/AdultandAdolescentGL.pdf) Did you actually read your source? If you did, then perhaps you can point it out to me where it says that multiple drugs are used to stop resistance developing in the HIV virus. Because I could not find it.
Take that paper and do a word search on the words “resistant” and “resistance” and you will find hundreds of occurrences of these words in this guideline. The main point of this guideline for the treatment of HIV is to prevent the emergence drug resistant strains. Here is a typical quote from the guidelines:
Simultaneously stopping all drugs in a regimen containing these agents may result in functional monotherapy with the NNRTIs, because their half-lives are longer than other agents. This may increase the risk of selection of NNRTI-resistant mutations.
Ev does stop converging. Paul is trying to attribute this to his Rcapacity factor but it is easily seen that the failure of ev to converge is due to the multiple selection factors. Read the link I provide to the guidelines for treatment of HIV and you will see the treatment strategy is identical to what ev is demonstrating. If you can ever describe a selection pressure to evolve a gene from the beginning, imagine what would happen with a multitude of selection pressures evolving genes from the beginning would have to overcome. *Sigh* You obviously do not understand evolution in the slightest, or you would know this is complete bollocks. List, kleinman, this is very important. Selective pressures are not positive.
So let’s hear your convoluted logic of how genes arose.
And please demonstrate how what happens in the ev model translates to what happens in the real world? Even if ev shows the stopping of evolution, this does not mean it actually happens in real life. Since evolutioni is an observable fact it obviously does not stop, does it?
Be glad to do that for you Taffer. Now you other evolutionists don’t complain that I am repeating myself because Taffer has asked.

Ev has three selection conditions; they are the identification of binding sites where they should occur, the prevention of spurious binding sites in the gene region and the prevention of spurious binding sites outside of the gene. As one lengthens the genome length parameter in ev, the generations for convergence becomes greater and greater until ev fails to converge at all. If you take that case that fails to converge, and remove any two of the three selection pressures, ev will successfully evolve that sequence based on that selection condition which would not evolve when applying all three selection conditions. This is exactly analogous to the strategy used in the treatment of HIV. By using multiple drug regimens, you apply multiple selection pressures and reduce the ability of the virus to evolve. Monotherapy treatment markedly increases the likelihood of evolving resistant strains of the virus.
Your continued claim that there are no selection pressures to evolve a gene "from the beginning" is a false dichotomy. A functional gene need not be the lowest form of life.
Genes came from somewhere, explain to us how an original gene arose.
Lastly, please demonstrate that the failure in ev for convergence is due to multiple selective pressures, and not Rcap.
Take Dr Schneider’s baseline case and keep doubling the genome length until ev fails to converge to a perfect creature. Then go to the advanced features of ev and set any two of the three weight factors for the selection conditions to 0 and you will see that ev very rapidly converges to a perfect creature. Setting two of the three weight factors to 0 is equivalent to eliminating two of the three selection pressures. This is exactly analogous to what we see with the use of multi-drug regimens for the treatment of HIV. Single drug regimens (single selection pressures) quickly lead to resistant strains of the virus while multi-drug regimens (multiple selection pressures) markedly reduce the emergence of drug resistant strains of HIV.
Ev does accurately model mutation and selection.It accurately enough models mutation and selection of a single binding site, with a 'perfect' creature already established. It does not accurately model evolution in the real world. Get over it.
Dr Schneider has very effectively captured the mathematics of multiple selection pressures. What his model demonstrates due to the multiple selection pressure accurately reflects what happens in reality. Now his selection conditions do not accurately model the evolution of a gene from the beginning but that is because there is no such selection condition.
It shows that multiple selection pressures slow and ultimately stop evolution... No, it doesn't. You just claim that it does.
Run that example I’ve described above and give yourself a lesson in the mathematics of mutation and selection with single and multiple selection pressures.
...and that principle is used to treat HIV.No, it isn't. Multiple antiretroviral agents are used because restance arrises. Using more then one does not slow the evolution of the resistance of any single antiretroviral agent, but rather prolongs the course of treatment before the HIV virus becomes resistant to all three. You need to understand, kleinman, that not all selective pressures are do or die.
Which do you think happens more quickly, evolving a strain of HIV resistant to three drugs when the drugs are administered serially or administering the drugs simultaneously?
Not every mutation in ev causes a creature to die, yet ev demonstrates that multiple selection pressures slow and ultimately stop evolution.You have no evidence that evolution has stopped, so stop claiming that it has.
Ask Paul whether evolution stops in ev. Paul knows it stops; his problem is that he has concocted a convoluted explanation with his Rcapacity concept. How unusual that an evolutionist comes up with a concocted, convoluted explanation.
Ev is showing what happens mathematically with multiple selection pressures, which is evolution slows down and ultimately stops. Ev is not doing this as a matter of black-and-white. If you think that ev is doing this as a matter of black-and-white, correct the model and show us how multiple selection pressures work.I don't have to show how multiple selective pressures work, because I have observed them working myself. Remember those bacteria I've created? They were multiple resistant bacteria. Three, to be exact. We spontaniously generated resistant bacteria from non-resistant bacteral cultures. Wow, evolution! Oh, but that's right, it's "mathematically impossible".
Tell us, what occurs more quickly, creating multi-drug resistant bacteria using one drug at a time or using all the drugs simultaneously?
Very few people have studied ev and what it shows due to its multiple selection pressures. This is why ev fails to converge and this is the reason triple antiviral drugs are used to treat HIV. I doubt any evolutionist ever considered what happens when multiple selection pressures occur simultaneously and how it affects the rate of evolution. You are a pompous git. We already have models for multiple selective pressures!
Then why don’t you understand your own models? If you did, you would understand that multiple selection pressures slow down the evolutionary process. If you are so smart, explain to Dr Schneider and Paul your selection pressure models and fix what ev shows.
Now that ev is available and its behavior has been studied, it is becoming apparent why the theory of evolution is mathematically impossible. It is not just that there are no selection pressures that can evolve a gene from the beginning; it is also that multiple selection pressures slow and then stop evolution.And anyone who disagrees with you is wrong. Because you are right. Not the people who actually understand the material. You. Right.
You are wrong if you think that multiple selection pressures does not slow down the evolutionary process. Why don’t you give us an example where multiple selection pressures which speed up evolution. I’ve already shown how ev demonstrates that multiple selection pressures slow and ultimately stop evolution and I have given a real example of this phenomena. So give us some math and a real example of your convoluted thinking.
Taffer, multiple antibacterial resistant bacteria occurs much more quickly when the bacteria are subjected to the antibiotics in a serial manner, one antibiotic at a time. If the bacteria are subject to the antibiotics in parallel, they are much less likely to evolve. So what are the selection pressures that evolved the hundreds of genes necessary for the simplest free living organism and how did this happen in parallel? You do not understand at all. Selection for antibacterial resistance occurs at the organism level. Take three loci, all of which give a different antibacterial reistance. Put bacteria on media in series, and you will evolve triple-resistant bacteria. Put the bacteria on media which contains all three antibiotics, and you will evolve triple-resistant bacteria. I have done this myself. So your claims that multiple selection pressures stop evolution are stupid, ignorant, and above all, false. The only reason why it seems to be harder to evolve triple-resistant bacteria in "parallel", is because their resistance has to evolve at once. But the probability is the same. 1+1+1 is the same as 3X1.
That’s right, when you apply your selection pressures simultaneously; it slows the evolutionary process because you must get all three random mutations simultaneously. This is why evolution slows with multiple selection pressures. Ev demonstrates this and it is the reason why this model shows that evolution by random point mutation and natural selection is profoundly slow, so slow that the theory of evolution is mathematically impossible. You may be able evolve three loci to get drug resistant bacteria but you have no selection condition that would evolve the thousands of bases to make a gene, especially when other selection conditions would interfere with this process.
Paul, in case you haven’t noticed, ev can easily evolve binding sites despite your Rcapacity condition when you set the weight factors for spurious binding sites to 0. Alan, you simply refuse to pay any attention, don't you? I'm going to say this one more time and then give up:

Rcapacity is the number of bits of information required to distinguish binding sites from the rest of the genome. If you are not distinguishing binding sites from the rest of the genome, Rcapacity is irrelevant.
Paul, you are in denial. Ev easily recognizes binding sites no matter how long the genome is. Set any two of the three selection conditions to 0 and you will evolve the binding condition specified by that third condition. It doesn’t matter whether ev is locating the desired binding sites or preventing the spurious binding sites. Ev can do each no matter how long the genome is. Ev just can’t evolve all three selection conditions simultaneously when the genome gets too long. It is the competing selection pressures that stop evolution in ev. I listen to your explanation at it is convoluted and confused.
Oh really, why? Paul, ev can easily evolve all three of the selection conditions when done separately on a genome where your Rcapacity value equals Rfrequency. The failure of ev to converge when using all three selection conditions simultaneously is due to the competition of these conditions. It has nothing to do with being able to identify the binding sites. Binding sites are easily identified. This is shown by setting the weight factors for spurious bindings to zero.Binding sites are easily identified because the program knows where they are. Locating the binding sites is not interesting. What is interesting is distinguishing binding sites from other sites using the transcription factor modeled by the weight matrix and threshold.
And ev can’t do all three selection conditions when the genome becomes too long.
Not only does setting two of the three selection conditions to zero affect the number of generations to evolve a perfect creature, it is the only way to evolve a perfect creature when you lengthen the genome in ev. You do not know this, because you have never run an experiment where evolution "stops dead" when Rcapacity is not an issue. And apparently you never will, because you do not believe that the width of the binding sites puts a limit on Rsequence. I'm not sure I've ever had a conversation with someone who installed a belief system on top of mathematics.
Yes I have Paul, I’ll post the series again here.
The case I used consists of G=16384, binding sites=6, weight width=5, Rfreq=10, Paul’s infamous Rcapacity=2*site width=10. With the weights for each mistake, (missed site, spurious binding in gene, spurious binding outside gene), set to 1, this case fails to converge. But for varying weights you get the following results:
missed site/spurious binding-gene/spurious binding outside gene/gens to perfect creature
1/0/0/7
0/1/0/223
0/0/1/233
So, a case with three different selection conditions will not converge when all three conditions must be satisfied simultaneously. While if you select based on one condition at a time it takes only 7 generations to evolve the binding sites, 223 generations to eliminate spurious binding within the gene and only 233 generations to eliminate spurious binding outside the gene. These cases take so few generations to evolve, it is instructive to step through the evolution and watch the mistakes go to zero.
Choose any case you want that doesn’t converge and try the same concept. Set any two of the three selection conditions to 0 and watch ev evolve the remaining condition.
While you're at it, why don't you explain why my experimental results directly contradict your conclusion that multiple selective forces slow/halt evolution. Because your genome is not large enough, obviously! Increase its size so that Rfrequency > Rsequence and try again. You silly goose.
Paul, any length genome will evolve in ev if you use only one of the three selection conditions.
For you Delphi, any time. The use of multiple drugs (triple antiviral medications) to prevent selection and evolution of drug resistant strains of HIV is extensively documented in the guidelines for the treatment of this disease. Thanks for the 121 page document you haven't read. Another smokescreen. Why am I not suprised?

Adding multiple drugs... each of which would cause selection... prevents selection? Are you really typing these things?
The whole guide is about the prevention of the evolution of drug resistant strains of HIV. I’ll again post a quote from the guide:
Simultaneously stopping all drugs in a regimen containing these agents may result in functional monotherapy with the NNRTIs, because their half-lives are longer than other agents. This may increase the risk of selection of NNRTI-resistant mutations.
I guess you were the one who didn’t read the guide.
Also, I note that you've dodged away from your original position...
Also, I note that you've dodged away from your original position...
Are you whining about moving goal posts again? My position has always been that ev shows that the theory of evolution is mathematically impossible. The reason why ev shows this is that the competing selection conditions slow and ultimately stop evolution.
In fact, ev will not converge at all in many cases when all the selection processes are acting simultaneously. This is also observed in reality. You said multiple selection pressures stop evolution, and that this has been observed in nature. You've repeated this fiction several times. That's obviously not the case here, as HIV and AIDS are still a problem. The only way to "stop" evolution is to put the entire population under too stringent a selection pressure (i.e. kill them all off.)
What I said is that ev shows that with increasing genome lengths, the multiple selection pressures slow and then ultimately stop the evolutionary process. Multiple selection pressures on the HIV virus slow the evolution of resistant strains sufficiently to allow people to live for years with the virus.

[Paul C. Anagnostopoulos]

Paul, you are in denial. Ev easily recognizes binding sites no matter how long the genome is. Set any two of the three selection conditions to 0 and you will evolve the binding condition specified by that third condition. It doesn’t matter whether ev is locating the desired binding sites or preventing the spurious binding sites. Ev can do each no matter how long the genome is. Ev just can’t evolve all three selection conditions simultaneously when the genome gets too long. It is the competing selection pressures that stop evolution in ev. I listen to your explanation at it is convoluted and confused.
You are the poster child for denial, Alan. Ev recognizes binding sites no matter what parameters you specify, because it knows precisely where they are. But if you set any of the mistake counts to zero, then the gene does not distinguish the binding sites from the rest of the genome. Do you see the difference? Please answer yes or no.


And ev can’t do all three selection conditions when the genome becomes too long.
How long would that be?


Yes I have Paul, I’ll post the series again here.
The case I used consists of G=16384, binding sites=6, weight width=5, Rfreq=10, Paul’s infamous Rcapacity=2*site width=10. With the weights for each mistake, (missed site, spurious binding in gene, spurious binding outside gene), set to 1, this case fails to converge. But for varying weights you get the following results:
missed site/spurious binding-gene/spurious binding outside gene/gens to perfect creature
1/0/0/7
0/1/0/223
0/0/1/233
But obviously I was not talking about the scenario where any of the mistake counts are zero, so your answer is irrelevant. Please run an experiment with mistake counts of 1, where Rcapacity is not an issue, and evolution "stops dead."

~~ Paul

[kjkent1]

***Deleted***

I'll leave Paul's comments undisturbed. Alan doesn't seem to comprehend that setting mistake weights to zero yields meaningless results.

[kleinman]

Paul, you are in denial. Ev easily recognizes binding sites no matter how long the genome is. Set any two of the three selection conditions to 0 and you will evolve the binding condition specified by that third condition. It doesn’t matter whether ev is locating the desired binding sites or preventing the spurious binding sites. Ev can do each no matter how long the genome is. Ev just can’t evolve all three selection conditions simultaneously when the genome gets too long. It is the competing selection pressures that stop evolution in ev. I listen to your explanation at it is convoluted and confused.You are the poster child for denial, Alan. Ev recognizes binding sites no matter parameters you specify, because it know precisely where they are. But if you set any of the mistake counts to zero, then the gene does not distinguish the binding sites from the rest of the genome. Do you see the difference? Please answer yes or no.
Paul, I’m not the one whose evaluation of ev has gone from it represents reality, to it represents a tiny fraction of the evolutionary landscape to it represents a stylized model of mutation and natural selection.

Paul, you have just changed you position on what ev does. I have said that the weight matrix always recognizes a binding site no matter how long the genome. When you set any of the weight counts to zero, all you are doing is not including that selection condition in the evolutionary process. Paul, there is no gene in ev, there is just a region of the genome that you set aside to evolve binding sites. If you set the weight condition for missed sites to 1, and spurious sites inside and outside the binding site region to 0, you will evolve the binding sites where they should be according to the model but still have spurious bindings elsewhere on the genome. Here is another example: G=100,000, binding site width=4, weight width is 3, Rfrequency is 13.61, Rcapacity=8, gamma=8, mutation rate=1 per genome per generation.
Missed sites/spurious gene/spurious non-gene/Gens convergence PC
1/0/0/1
0/1/0/54
0/0/1/2192
Here is a case where Rfrequency is much greater than Rcapacity. Ev has no problem locating the binding sites where they should be when that weight factor is set to 1, ev has no problem eliminating spurious binding sites in the gene region when that weight condition is set to 1, and ev has no problem eliminating spurious binding sites outside the gene region when that weight factor is set to 1. This is all done in a case with Rfrequency is almost twice the value of your Rcapacity value. The ev computation cycles through a mutation/selection process. When you have too many selection conditions on too long of a gene, evolution stops. Eliminate 2 of the 3 selection conditions and ev starts evolving that portion of the genome.

When you say “gene does not distinguish the binding sites from the rest of the genome”, what are you talking about? If you are talking about the weight matrix which represents the binding protein, the above example once again shows that the weight matrix has no trouble locating binding sites whether they are missed sites where they should have occurred or spurious sites where they should not occur no matter how large the genome is.
And ev can’t do all three selection conditions when the genome becomes too long. How long would that be?
I just did an example above with a genome length of 100,000 and a binding site width of only 4 bases. Even the elimination of the spurious binding sites in the non-binding site region of the genome took only a couple of thousand cycles. I believe you can do a genome length of 3 gigabases and get convergence if you only have a single selection condition, but more than one selection condition and you can only evolve tiny nonrealistic length genomes.
Yes I have Paul, I’ll post the series again here.
The case I used consists of G=16384, binding sites=6, weight width=5, Rfreq=10, Paul’s infamous Rcapacity=2*site width=10. With the weights for each mistake, (missed site, spurious binding in gene, spurious binding outside gene), set to 1, this case fails to converge. But for varying weights you get the following results:
missed site/spurious binding-gene/spurious binding outside gene/gens to perfect creature
1/0/0/7
0/1/0/223
0/0/1/233 But obviously I was not talking about the scenario where any of the mistake counts are zero, so your answer is irrelevant. Please run an experiment with mistake counts of 1, where Rcapacity is not an issue, and evolution "stops dead."
Paul, it is not Rcapacity which stops ev from converging, it is the conflicting selection processes that stops evolution. This mathematical effect that ev is demonstrating is the exact principle that is used for treating HIV. This is totally relevant because this is the reason why ev takes huge numbers of generations to converge (if it can converge at all) when you try to evolve binding sites and eliminate spurious binding sites on longer genomes. When your model has this much trouble evolving binding sites and eliminating spurious binding, what do you think will happen when you try to model the evolution of an entire gene (if you could ever model a selection process that would do this) when you have “millions” of other selection processes acting at the same time?

Your Rcapacity concept is useless for estimating which cases will converge unless you include all three selection conditions in ev.
I'll leave Paul's comments undisturbed. Alan doesn't seem to comprehend that setting mistake weights to zero yields meaningless results.
You know more about your string cheese theory of evolution than you do about ev. Setting a weight to zero is simply eliminating that particular selection process.

[Paul C. Anagnostopoulos]

Paul, I’m not the one whose evaluation of ev has gone from it represents reality, to it represents a tiny fraction of the evolutionary landscape to it represents a stylized model of mutation and natural selection.
That is neither a yes nor a no.


Paul, you have just changed you position on what ev does. I have said that the weight matrix always recognizes a binding site no matter how long the genome.
If by "recognizes" you mean matches, that is not correct.


When you set any of the weight counts to zero, all you are doing is not including that selection condition in the evolutionary process.
I presume you mean mistake counts. That is correct, setting a mistake count to zero removes that selection pressure, rendering Rcapacity et al moot.


Paul, there is no gene in ev, there is just a region of the genome that you set aside to evolve binding sites.
The weight matrix and threshold are referred to as the gene.


If you set the weight condition for missed sites to 1, and spurious sites inside and outside the binding site region to 0, you will evolve the binding sites where they should be according to the model but still have spurious bindings elsewhere on the genome.
I presume you mean mistake count. You are correct.


Here is another example: G=100,000, binding site width=4, weight width is 3, Rfrequency is 13.61, Rcapacity=8, gamma=8, mutation rate=1 per genome per generation.
Missed sites/spurious gene/spurious non-gene/Gens convergence PC
1/0/0/1
0/1/0/54
0/0/1/2192
Here is a case where Rfrequency is much greater than Rcapacity.
Rfrequency and Rcapacity are irrelevant here. They only matter when attempting to evolve creatures who distinguish binding sites from other sites, that is, when all three mistake counts are positive. Let me try to make this simple:

Measures of information capacity, requirement, and current state are only relevant when distinguishing binding sites from other sites. If you are not trying to distinguish them, then the amount of information required to do so is irrelevant.


Ev has no problem locating the binding sites where they should be when that weight factor is set to 1, ev has no problem eliminating spurious binding sites in the gene region when that weight condition is set to 1, and ev has no problem eliminating spurious binding sites outside the gene region when that weight factor is set to 1.
Correct.


This is all done in a case with Rfrequency is almost twice the value of your Rcapacity value.
See above.


The ev computation cycles through a mutation/selection process. When you have too many selection conditions on too long of a gene, evolution stops.
You have not demonstrated this.


Eliminate 2 of the 3 selection conditions and ev starts evolving that portion of the genome.
Correct.


When you say “gene does not distinguish the binding sites from the rest of the genome”, what are you talking about?
See above.


If you are talking about the weight matrix which represents the binding protein, the above example once again shows that the weight matrix has no trouble locating binding sites whether they are missed sites where they should have occurred or spurious sites where they should not occur no matter how large the genome is.
That is not what I am talking about.


And ev can’t do all three selection conditions when the genome becomes too long.
...
I just did an example above with a genome length of 100,000 and a binding site width of only 4 bases.
But you did it with two of the selection pressures turned off, so your experiment has nothing to do with the first statement you made here.


Even the elimination of the spurious binding sites in the non-binding site region of the genome took only a couple of thousand cycles. I believe you can do a genome length of 3 gigabases and get convergence if you only have a single selection condition, but more than one selection condition and you can only evolve tiny nonrealistic length genomes.
Please demonstrate this claim.


Paul, it is not Rcapacity which stops ev from converging, it is the conflicting selection processes that stops evolution.
Please demonstrate this.


Your Rcapacity concept is useless for estimating which cases will converge unless you include all three selection conditions in ev.
No kidding, Sherlock. That is because Rcapacity is completely irrelevant unless all three selection pressures are present.


You know more about your string cheese theory of evolution than you do about ev. Setting a weight to zero is simply eliminating that particular selection process.
Which renders the information measures meaningless, as Kjkent said.

~~ Paul

[kleinman]

Paul, I’m not the one whose evaluation of ev has gone from it represents reality, to it represents a tiny fraction of the evolutionary landscape to it represents a stylized model of mutation and natural selection.That is neither a yes nor a no.
The answer to your question is the gene distinguishes nothing and your Rcapacity concept is hogwash. The reason why ev does not converge with longer genomes is that the competing selection processes in the model stop the evolution. Eliminate 2 of the three selection conditions and ev will start evolving again.
Paul, you have just changed you position on what ev does. I have said that the weight matrix always recognizes a binding site no matter how long the genome.If by "recognizes" you mean matches, that is not correct.
Exceeds the threshold Mr Rcapacity. The weight matrix can do this no matter how long the genome is.
When you set any of the weight counts to zero, all you are doing is not including that selection condition in the evolutionary process.I presume you mean mistake counts. That is correct, setting a mistake count to zero removes that selection pressure, rendering Rcapacity et al moot.
Are you paying attention kjkent1?
Paul, there is no gene in ev, there is just a region of the genome that you set aside to evolve binding sites. The weight matrix and threshold are referred to as the gene.
And that weight matrix has no trouble locating binding sites which exceed the threshold no matter how long the genome is. The reason ev fails to converge is conflicting selection conditions.
If you set the weight condition for missed sites to 1, and spurious sites inside and outside the binding site region to 0, you will evolve the binding sites where they should be according to the model but still have spurious bindings elsewhere on the genome.I presume you mean mistake count. You are correct.
Again, are you paying attention kjkent1?
Here is another example: G=100,000, binding site width=4, weight width is 3, Rfrequency is 13.61, Rcapacity=8, gamma=8, mutation rate=1 per genome per generation.
Missed sites/spurious gene/spurious non-gene/Gens convergence PC
1/0/0/1
0/1/0/54
0/0/1/2192
Here is a case where Rfrequency is much greater than Rcapacity.Rfrequency and Rcapacity are irrelevant here. They only matter when attempting to evolve creatures who distinguish binding sites from other sites, that is, when all three mistake counts are positive. Let me try to make this simple:

Measures of information capacity, requirement, and current state are only relevant when distinguishing binding sites from other sites. If you are not trying to distinguish them, then the amount of information required to do so is irrelevant.
Paul, Dr Schneider’s definition for Rfrequency is:
Rfrequency = -log2(gamma/G)
Rfrequency depends only on the number of binding sites and the length of the genome. The selection process(es) does not change the computed value of Rfrequency. Your definition for Rcapacity is:
Rcapacity = 2*binding site width
Your definition for Rcapacity has no relationship to selection process(es). It is an interesting coincidence that your equation gives a fairly good estimate when ev will stop converging when including all three selection conditions in ev but your equation is useless for estimating when ev will fail to converge for different selection conditions. In particular, if you have only a single selection condition, ev will evolve sequences of bases that will satisfy that condition no matter how long the genome is. It is the multiple selection conditions that stop ev from converging.
Ev has no problem locating the binding sites where they should be when that weight factor is set to 1, ev has no problem eliminating spurious binding sites in the gene region when that weight condition is set to 1, and ev has no problem eliminating spurious binding sites outside the gene region when that weight factor is set to 1. Correct.
You paying attention kjkent1?
This is all done in a case with Rfrequency is almost twice the value of your Rcapacity value. See above.
Paul, your Rcapacity value is meaningless. See above, see the results from ev, see the reality revealed by the treatment of HIV using multiple drugs (multiple selection pressures).
The ev computation cycles through a mutation/selection process. When you have too many selection conditions on too long of a gene, evolution stops.You have not demonstrated this.
Paul, I have already done two cases, one with a G > 16,000 and another with G = 100,000 and both with Rfrequency > Rcapacity which won’t converge with all three of ev’s selection conditions imposed but will converge for all three conditions if done one at a time. If you want, I will start doing hundreds of cases to further demonstrate this.
Eliminate 2 of the 3 selection conditions and ev starts evolving that portion of the genome. Correct.
Paying attention kjkent1?
When you say “gene does not distinguish the binding sites from the rest of the genome”, what are you talking about? See above.
We know that the weight matrix easily finds matches which exceeds the threshold no matter how long the genome is.
If you are talking about the weight matrix which represents the binding protein, the above example once again shows that the weight matrix has no trouble locating binding sites whether they are missed sites where they should have occurred or spurious sites where they should not occur no matter how large the genome is. That is not what I am talking about.
Paul, I looked above, and the weight matrix has no trouble locating sites which exceed the threshold no matter how long the gene is.
And ev can’t do all three selection conditions when the genome becomes too long.
...
I just did an example above with a genome length of 100,000 and a binding site width of only 4 bases. But you did it with two of the selection pressures turned off, so your experiment has nothing to do with the first statement you made here.
Paul, that’s the point. Ev fails to converge with all three selection conditions imposed in the model. When you turn off two of the three selection conditions, ev will evolve one selection condition at a time without any problem. Multiple selection conditions slow and ultimately stop the evolutionary process in ev. What ev is demonstrating here is a real phenomena. I’ll go around with you on this issue as many times as you want because Dr Schneider got this effect right.
Even the elimination of the spurious binding sites in the non-binding site region of the genome took only a couple of thousand cycles. I believe you can do a genome length of 3 gigabases and get convergence if you only have a single selection condition, but more than one selection condition and you can only evolve tiny nonrealistic length genomes. Please demonstrate this claim.
You want me to do the 3 gigabase case? Hey kjkent1, you ready to get out of your cubicle and get your company’s parallel processor system crunching on this case. We’ll get that one done. Hey, what is the Rcapacity value for this case?
Paul, it is not Rcapacity which stops ev from converging, it is the conflicting selection processes that stops evolution. Please demonstrate this.
Paul, I’ve already demonstrated this on a 16k genome and a 100k genome. I’ll start posting hundreds of cases that demonstrate this. This thread is going to be longer than an ev run with Rfrequency greater than Rcapacity and all three selection conditions turned on.
Your Rcapacity concept is useless for estimating which cases will converge unless you include all three selection conditions in ev.No kidding, Sherlock. That is because Rcapacity is completely irrelevant unless all three selection pressures are present.
Your Rcapacity definition is also useless with Unnamed’s selection process.
You know more about your string cheese theory of evolution than you do about ev. Setting a weight to zero is simply eliminating that particular selection process. Which renders the information measures meaningless, as Kjkent said.
Kjkent1 is now your expert on ev? He’s also an expert on the string cheese theory of evolution.

Paul, I really like Dr Schneider’s computer model and you have done a wonderful job on programming the online version of the model. It is interesting studying the mathematics of mutation and selection.

[delphi_ote]

Simultaneously stopping all drugs in a regimen containing these agents may result in functional monotherapy with the NNRTIs, because their half-lives are longer than other agents. This may increase the risk of selection of NNRTI-resistant mutations.
This is evidence that if you ease overall selection pressure, the probability of mutants adapting to the remaining selection pressure increases. If more of the virus can survive, obviously there's a greater danger that one of them will develop resistance.

This is not evidence that multiple selection pressures "stop evolution". It has nothing to do with the number of selection mechanisms. It's simply a matter of the population size! Multiple selection pressures do not make evolution impossible. As I stated before (and you compeltely ignored) if that were the case, HIV and AIDS would be cured for good by these drugs. Two of them would be enough to guarantee that HIV never developed resistance. Simply carrying through your own logic on your own example shows you're wrong. Christ eating babyback ribs, kleinman. THINK FOR A CHANGE!

[kjkent1]

Kjkent1 is now your expert on ev? He’s also an expert on the string cheese theory of evolution.Evidently, I understand ev a hell of a lot better than you do.

If a "perfectly ordered" deck of cards is 1 through 13, hearts, clubs diamonds and spades, and you try to sort the deck without considering numerical order, how long do you think it will take to "converge" on, or produce a "perfectly ordered" deck?

And if you don't consider suits, how long do you think it will take to sort it to perfection?

The answer is that it will take less time to sort for either of the above conditions, because you're ignoring the other condition.

In the first case you will have four suits with random numbers. In the second you will have ordered numbers and random suits.

So, the RESULT of your sort is crap, because in neither circumstance do you produce a perfectly ordered deck.

By turning off the mistake weights, your experiment is not evolving anything close to a perfect creature. Ev is, however, reporting a perfect creature, because it doesn't recognize that it can't sort correctly due to the zeroed mistake weight.

[Paul C. Anagnostopoulos]

The answer to your question is the gene distinguishes nothing and your Rcapacity concept is hogwash.
So once a perfect creature has evolved, the gene is not distinguishing the binding sites from the rest of the genome? Wow, that's interesting. That means that Ev does absolutely nothing.


The reason why ev does not converge with longer genomes is that the competing selection processes in the model stop the evolution.
Please demonstrate this.


Exceeds the threshold Mr Rcapacity. The weight matrix can do this no matter how long the genome is.
But you said "the weight matrix always recognizes a binding site." That is not true until a perfect creature evolves.


Are you paying attention kjkent1?
Wait, are you agreeing with my entire statement: "That is correct, setting a mistake count to zero removes that selection pressure, rendering Rcapacity et al moot."


And that weight matrix has no trouble locating binding sites which exceed the threshold no matter how long the genome is. The reason ev fails to converge is conflicting selection conditions.
Please demonstrate this.


Paul, Dr Schneider’s definition for Rfrequency is:
Rfrequency = -log2(gamma/G)
Rfrequency depends only on the number of binding sites and the length of the genome. The selection process(es) does not change the computed value of Rfrequency. Your definition for Rcapacity is:
Rcapacity = 2*binding site width
Your definition for Rcapacity has no relationship to selection process(es).
It has a relationship. You mean the math does not refer to the selection process. But that does not mean that Rfrequency and Rcapacity are relevant to all those selection combinations, does it? In fact, I have on my to-do list an item to flag the R values when they are not relevant to the chosen selection process.


It is an interesting coincidence that your equation gives a fairly good estimate when ev will stop converging when including all three selection conditions in ev but your equation is useless for estimating when ev will fail to converge for different selection conditions.
Well, at least you're beginning to understand something. Now, if Rcapacity has nothing to do with the information capacity of binding sites, what do you think would happen if a binding site width of 1 is specified? Do you think this could allow a gene that distinguishes the binding sites from all other sites?


Paul, I have already done two cases, one with a G > 16,000 and another with G = 100,000 and both with Rfrequency > Rcapacity which won’t converge with all three of ev’s selection conditions imposed but will converge for all three conditions if done one at a time. If you want, I will start doing hundreds of cases to further demonstrate this.
But that is not your claim, is it? Your claim is that evolution stops when all three mistake counts are positive and Rcapacity is not an issue. Please demonstrate this.


You want me to do the 3 gigabase case? Hey kjkent1, you ready to get out of your cubicle and get your company’s parallel processor system crunching on this case. We’ll get that one done. Hey, what is the Rcapacity value for this case?
Thank you for acknowledging that you have not demonstrated your claim.


Paul, I’ve already demonstrated this on a 16k genome and a 100k genome.
You're absolutely sure that evolution had stopped in those experiments and that Rcapacity was not an issue? If so, present the parameters.


Your Rcapacity definition is also useless with Unnamed’s selection process.
Thank you for acknowledging that you were previously applying Rcapacity to irrelevant cases. However, Rcapacity is relevant to Unnamed's selection process.

~~ Paul

[kleinman]

Kjkent1 is now your expert on ev? He’s also an expert on the string cheese theory of evolution. Evidently, I understand ev a hell of a lot better than you do.
You do understand the string cheese theory of evolution far better than I do.
By turning off the mistake weights, your experiment is not evolving anything close to a perfect creature. Ev is, however, reporting a perfect creature, because it doesn't recognize that it can't sort correctly due to the zeroed mistake weight.
Kjkent1, you didn’t pay attention to Paul’s answers.

Anyway, let’s run that 3 gigabase genome case with a single selection condition on your company’s computer. Maybe then you and Paul will understand that it is the competing selection conditions that slows then ultimately stops the evolutionary process.

[Paul C. Anagnostopoulos]

By turning off the mistake weights, your experiment is not evolving anything close to a perfect creature. Ev is, however, reporting a perfect creature, because it doesn't recognize that it can't sort correctly due to the zeroed mistake weight.
Indeed, and so now on my to-do list are items to clarify these issues in the user interface.

~~ Paul

[Paul C. Anagnostopoulos]

Kjkent1, you didn’t pay attention to Paul’s answers.
Why do you think so?

~~ Paul

[kjkent1]

You do understand the string cheese theory of evolution far better than I do.A little more humility and the ability to learn from your mistakes would serve you well.

[kleinman]

The answer to your question is the gene distinguishes nothing and your Rcapacity concept is hogwash. So once a perfect creature has evolved, the gene is not distinguishing the binding sites from the rest of the genome? Wow, that's interesting. That means that Ev does absolutely nothing.
When you have one selection condition, ev evolves for that one condition, when you have two or more conditions, ev will evolve for those selection conditions if the genome is short enough. What is interesting is that you cling on to this Rcapacity concept when you admit it only has application to Dr Schneider’s selection process. Why don’t you define Rcapacity for Unnamed’s selection process.
The reason why ev does not converge with longer genomes is that the competing selection processes in the model stop the evolution.Please demonstrate this.
Already have done this for you twice.
Exceeds the threshold Mr Rcapacity. The weight matrix can do this no matter how long the genome is.But you said "the weight matrix always recognizes a binding site." That is not true until a perfect creature evolves.
The weight matrix finds many matches for binding sites which exceed the threshold long before the perfect creature evolves. You call them spurious binding sites.
Are you paying attention kjkent1? Wait, are you agreeing with my entire statement" "That is correct, setting a mistake count to zero removes that selection pressure, rendering Rcapacity et al moot."
Paul, your observation that with Dr Schneider’s selection conditions lead to a point where ev stops converging when Rfrequency approaches 2*binding site width is an interesting coincidence but does not explain why ev stops converging. I doubt you will find any simple algebraic expression which allows you to estimate when ev will converge based on the number of selection conditions. If you modified ev to evolve two sets of binding sites rather than the one set as done now, I doubt you could apply your Rcapacity equation to that situation.
And that weight matrix has no trouble locating binding sites which exceed the threshold no matter how long the genome is. The reason ev fails to converge is conflicting selection conditions.Please demonstrate this.
I’ve already done two cases that demonstrate this. I’m checking with kjkent1 to see if we can use his company’s computer to do the 3 gigabase case.
Paul, Dr Schneider’s definition for Rfrequency is:
Rfrequency = -log2(gamma/G)
Rfrequency depends only on the number of binding sites and the length of the genome. The selection process(es) does not change the computed value of Rfrequency. Your definition for Rcapacity is:
Rcapacity = 2*binding site width
Your definition for Rcapacity has no relationship to selection process(es).Correct, but that does not mean that Rfrequency is relevant to all those selection combinations, does it? In fact, I have on my to-do list an item to flag the R values when they are not relevant to the chosen selection process.
Paul, Rfrequency is dependent on gamma and G. gamma and G are independent of the selection process. Unless Dr Schneider improperly defined Rfrequency, this value is independent of the selection process.
It is an interesting coincidence that your equation gives a fairly good estimate when ev will stop converging when including all three selection conditions in ev but your equation is useless for estimating when ev will fail to converge for different selection conditions. Well, at least you're beginning to understand something. Now, if Rcapacity has nothing to do with the information capacity of binding sites, what do you think would happen if a binding site width of 1 is specified? Do you think this could allow a gene that distinguishes the binding sites from all other sites?
A binding site width of 1 means that particular base will always be recognized as a binding site. What ev should do is evolve so that all binding sites will be of that base in the binding site region and eliminate that base from causing spurious binding inside and outside the gene.
Paul, I have already done two cases, one with a G > 16,000 and another with G = 100,000 and both with Rfrequency > Rcapacity which won’t converge with all three of ev’s selection conditions imposed but will converge for all three conditions if done one at a time. If you want, I will start doing hundreds of cases to further demonstrate this. But that is not your claim, is it? Your claim is that evolution stops when all three mistake counts are positive and Rcapacity is not an issue. Please demonstrate this.
Paul, that’s what these examples do. These examples do not evolve when all three selection conditions are turned on yet when you set two of the three to 0, the non-zero condition evolves sequences that satisfy the remaining selection condition.
You want me to do the 3 gigabase case? Hey kjkent1, you ready to get out of your cubicle and get your company’s parallel processor system crunching on this case. We’ll get that one done. Hey, what is the Rcapacity value for this case?Thank you for acknowledging that you have not demonstrated your claim.
Paul, I never said I demonstrated the 3 gigabase case. What I said is that I believe that with a single selection condition, the 3 gigabase case will converge. Now if we can get kjkent1 to get his company’s computer in action, I could show the results for this case. As it stands, we’ll have to live with the results of the 100k case which converges for all three selection conditions in less than three thousand cycles.
Paul, I’ve already demonstrated this on a 16k genome and a 100k genome. You're absolutely sure that evolution had stoppped in those experiments and that Rcapacity was not an issue?
The 16k case was one from a series I did last year and it did not converge. The 100k case, I chose parameters much worse than many of the other cases which failed to converge. I chose a small site width of 4 and a larger genome length than many of the other cases which failed to converge. Feel free to burn up some clock cycles on your computer on this 100k case and prove me wrong and that this case will converge with all three selection conditions acting.
Your Rcapacity definition is also useless with Unnamed’s selection process. Thank you for acknowledging that you were previously applying Rcapacity to irrelevant cases. However, Rcapacity is relevant to Unnamed's selection process.
Just what good is your Rcapacity concept? Let’s see you apply it to Unnamed’s selection process.
Kjkent1, you didn’t pay attention to Paul’s answers.Why do you think so?
Because he doesn’t realize that setting a mistake weight to 0 is equivalent to turning off that particular selection condition
You do understand the string cheese theory of evolution far better than I do. A little more humility and the ability to learn from your mistakes would serve you well.
Evidently, I understand ev a hell of a lot better than you do.

[kjkent1]

Because he doesn’t realize that setting a mistake weight to 0 is equivalent to turning off that particular selection condition.What you don't recognize is that an ev "perfect creature" is defined as a genome substantially absent missed or spurious bindings. So, when you turn off a selection condition, ev reports a perfect creature when no perfect creature has yet evovled according to the ev definition of perfection. Thus, the report is an error -- as is your conclusion based on the error.

[Taffer]

kleinman, I can honestly not be bothered wading through your response to me anymore. Either clean up your formatting, or I'm not going to bother responding to specific points. Perhaps later, when I'm not in "a mood".

One specific point, though. The time to create a triple-resistant mutant is the same in both cases you provided. If you disagree, provide evidence and citations. Until you do, I will trust my own studies, thank you.

[Paul C. Anagnostopoulos]

When you have one selection condition, ev evolves for that one condition, when you have two or more conditions, ev will evolve for those selection conditions if the genome is short enough. What is interesting is that you cling on to this Rcapacity concept when you admit it only has application to Dr Schneider’s selection process. Why don’t you define Rcapacity for Unnamed’s selection process.
I did not say it was relevant only to Ev's selection process. I said it was only relevant when the width of the binding sites are fixed, as they are in Ev. Rcapacity works the same with Unnamed's selection process, assuming that the mistake counts are all positive.


The weight matrix finds many matches for binding sites which exceed the threshold long before the perfect creature evolves. You call them spurious binding sites.
Ah, okay. You called them "binding sites," which confused me.


Paul, your observation that with Dr Schneider’s selection conditions lead to a point where ev stops converging when Rfrequency approaches 2*binding site width is an interesting coincidence but does not explain why ev stops converging.
It explains why it has stopped converging in all the experiments I've seen. You claim to have two experiments that stop converging even when Rcapacity is not an issue. Please present the parameters of those experiments.


I’ve already done two cases that demonstrate this. I’m checking with kjkent1 to see if we can use his company’s computer to do the 3 gigabase case.
Please present the parameters of those experiments.


Paul, Rfrequency is dependent on gamma and G. gamma and G are independent of the selection process. Unless Dr Schneider improperly defined Rfrequency, this value is independent of the selection process.
Alan, what is Rfrequency? Could you define it for us?


A binding site width of 1 means that particular base will always be recognized as a binding site. What ev should do is evolve so that all binding sites will be of that base in the binding site region and eliminate that base from causing spurious binding inside and outside the gene.
And so as Rfrequency climbs above Rcapacity (2 in this case), the number of bits required to distinguish binding sites from other sites exceeds the available number of bits in the binding sites. This happens quickly when Rcapacity = 2.


Paul, that’s what these examples do. These examples do not evolve when all three selection conditions are turned on yet when you set two of the three to 0, the non-zero condition evolves sequences that satisfy the remaining selection condition.
Which examples? Please present the parameters.


Paul, I never said I demonstrated the 3 gigabase case.
I know you haven't. What I want to see are the two examples you claim "stopped."


The 16k case was one from a series I did last year and it did not converge. The 100k case, I chose parameters much worse than many of the other cases which failed to converge. I chose a small site width of 4 and a larger genome length than many of the other cases which failed to converge. Feel free to burn up some clock cycles on your computer on this 100k case and prove me wrong and that this case will converge with all three selection conditions acting.
I can't burn any cycles until you specify the parameters.


Just what good is your Rcapacity concept? Let’s see you apply it to Unnamed’s selection process.
It isn't any good! It just explains why certain Ev experiments will not converge. You claim evolution stops for a different reason. I just want you to demonstrate your claim. Is this really so hard to understand?


Because he doesn’t realize that setting a mistake weight to 0 is equivalent to turning off that particular selection condition.
He doesn't?

~~ Paul

[Cuddles]

Can I just see if I've got this straight? Is Kleinman really now arguing that the evolution of drug resistance proves that evolution doesn't happen? I didn't think it was possible to prove yourself quite so spectatularly wrong without actually imploding.

[Taffer]

Can I just see if I've got this straight? Is Kleinman really now arguing that the evolution of drug resistance proves that evolution doesn't happen? I didn't think it was possible to prove yourself quite so spectatularly wrong without actually imploding.

As far as I can tell, he is arguing that using three drugs on one microbe culture at once causes them to evolve resistances to all three drugs slower then if the drugs were applied one-by-one.

This is, of course, complete bollocks.

[Paul C. Anagnostopoulos]

Wait, I thought he was saying that multiple selection pressures causes evolution to stop. Well, with a sufficiently large genome, anyway.

~~ Paul

[Mercutio]

Wait, I thought he was saying that multiple selection pressures causes evolution to stop. Well, with a sufficiently large genome, anyway.

~~ Paul
Well, yes and no. He claims "stop", but when he speaks of specific examples like HIV treatment, reality creeps in a bit: This is exactly analogous to the strategy used in the treatment of HIV. By using multiple drug regimens, you apply multiple selection pressures and reduce the ability of the virus to evolve. Monotherapy treatment markedly increases the likelihood of evolving resistant strains of the virus. [color highlighting mine]

In the real world, he cannot demonstrate evolution coming to a stop. His interpretation of evolution in ev is made possible by an a priori definition of success; certainly, if there is only one way into a room, and you block the door, you have stopped entry. But in the real world, evolution cannot be stopped by some Maginot line; there is more than one way to respond to any given selection pressure. Some interesting reading here (http://www.greythumb.org/blog/index.php?/archives/7-T.M.T.O.W.T.D.I..html), about TMTOWTDI (There's More Than One Way To Do It). An appropriate excerpt: This is why a lot of computer programmers, mathematicians, and engineers seem to have a hard time intuitively grasping both evolution and the possibility of abiogenesis. They think that things have to be just one way in order to work, and then they wonder how evolution can possibly find such a tiny target in such a large field of possibilities. This is also a point harped on by evolution's critics, and I am willing to believe that at least some of them honestly think they are onto something here (especially the mathematicians and computer scientists for the aforementioned reasons).

[delphi_ote]

In the real world, he cannot demonstrate evolution coming to a stop... But in the real world, evolution cannot be stopped by some Maginot line...
It can be stopped by complete extinction. If you wipe out all of the relevant life, there won't be anymore evolution.

[Mercutio]

It can be stopped by complete extinction. If you wipe out all of the relevant life, there won't be anymore evolution.
True--thus the "Maginot Line" reference (if not a great analogy). If there is a way around, over, under, or through, then blocking one of those routes is not enough. Nor two, nor three. While there is life, there is the possibility that something will stumble upon the solution. If, instead of the Maginot Line, the French had simply exterminated the Germans...

[kleinman]

Because he doesn’t realize that setting a mistake weight to 0 is equivalent to turning off that particular selection condition.What you don't recognize is that an ev "perfect creature" is defined as a genome substantially absent missed or spurious bindings. So, when you turn off a selection condition, ev reports a perfect creature when no perfect creature has yet evovled according to the ev definition of perfection. Thus, the report is an error -- as is your conclusion based on the error.
“Perfect creature” is only a label used by Paul and Dr Schneider to indicate a creature that has satisfied all three of their selection conditions. If you turn off two of the three selection conditions then a “perfect creature” is one that satisfies that selection condition.
One specific point, though. The time to create a triple-resistant mutant is the same in both cases you provided. If you disagree, provide evidence and citations. Until you do, I will trust my own studies, thank you.
Taffer, read the guidelines for treating HIV and why triple medications are used. I posted a specific quote from the guidelines and I repost it again here:
Simultaneously stopping all drugs in a regimen containing these agents may result in functional monotherapy with the NNRTIs, because their half-lives are longer than other agents. This may increase the risk of selection of NNRTI-resistant mutations.
With respects to your argument that you can achieve triple resistance as quickly using triple antimicrobials in parallel as when the antimicrobials serially, provide your evidence and citations. You argue that 1+1+1=3 give the same results as 1*3=3. Do you think this argument extends to millions of selection conditions? If so, you are in disagreement with the results from ev.
When you have one selection condition, ev evolves for that one condition, when you have two or more conditions, ev will evolve for those selection conditions if the genome is short enough. What is interesting is that you cling on to this Rcapacity concept when you admit it only has application to Dr Schneider’s selection process. Why don’t you define Rcapacity for Unnamed’s selection process.I did not say it was relevant only to Ev's selection process. I said it was only relevant when the width of the binding sites are fixed, as they are in Ev. Rcapacity works the same with Unnamed's selection process, assuming that the mistake counts are all positive.
Really? I don’t recall Unnamed running any cases with a short site width.
Paul, your observation that with Dr Schneider’s selection conditions lead to a point where ev stops converging when Rfrequency approaches 2*binding site width is an interesting coincidence but does not explain why ev stops converging.It explains why it has stopped converging in all the experiments I've seen. You claim to have two experiments that stop converging even when Rcapacity is not an issue. Please present the parameters of those experiments.
Rcapacity doesn’t explain why ev converges when you eliminate two of the three selection conditions no matter what the site width is.
I’ve already done two cases that demonstrate this. I’m checking with kjkent1 to see if we can use his company’s computer to do the 3 gigabase case.Please present the parameters of those experiments.
1st case: Population 64, gamma=16, site width=6, G=16384, mutation rate=1/G/generation, weight width=5, Rfreq=10, Paul’s infamous Rcapacity=2*site width=10. With the weights for each mistake, (missed site, spurious binding in gene, spurious binding outside gene), set to 1, this case fails to converge. But for varying weights you get the following results:
missed site/spurious binding-gene/spurious binding outside gene/gens to perfect creature
1/0/0/7
0/1/0/223
0/0/1/233
2nd case: G=100,000, binding site width=4, weight width is 3, Rfrequency is 13.61, Rcapacity=8, gamma=8, mutation rate=1/G/generation.
Missed sites/spurious gene/spurious non-gene/gens to perfect creature
1/0/0/1
0/1/0/54
0/0/1/2192
Paul, Rfrequency is dependent on gamma and G. gamma and G are independent of the selection process. Unless Dr Schneider improperly defined Rfrequency, this value is independent of the selection process. Alan, what is Rfrequency? Could you define it for us?
Rfrequency=-log2(gamma/G) where gamma is the number of binding sites and G is the number of sites in the genome. Do you want to define Rcapacity for us?
A binding site width of 1 means that particular base will always be recognized as a binding site. What ev should do is evolve so that all binding sites will be of that base in the binding site region and eliminate that base from causing spurious binding inside and outside the gene. And so as Rfrequency climbs above Rcapacity (2 in this case), the number of bits required to distinguish binding sites from other sites exceeds the available number of bits in the binding sites. This happens quickly when Rcapacity = 2.
Paul, run those cases I’ve listed above. Single step through the cases and watch what happens to the mistake counts.
Paul, that’s what these examples do. These examples do not evolve when all three selection conditions are turned on yet when you set two of the three to 0, the non-zero condition evolves sequences that satisfy the remaining selection condition. Which examples? Please present the parameters.
I’ve presented them above for the third time. Do you want me to post the parameters again?
Paul, I never said I demonstrated the 3 gigabase case. I know you haven't. What I want to see are the two examples you claim "stopped."
And the reason they “stopped” is that there was only one selection condition acting. This condition was achieved by setting to of the three weight factors to 0 thereby eliminating two of the three selection conditions. Once you run these cases, it should become clear to you that the reason these cases are able to converge is there is only a single selection condition.
The 16k case was one from a series I did last year and it did not converge. The 100k case, I chose parameters much worse than many of the other cases which failed to converge. I chose a small site width of 4 and a larger genome length than many of the other cases which failed to converge. Feel free to burn up some clock cycles on your computer on this 100k case and prove me wrong and that this case will converge with all three selection conditions acting. I can't burn any cycles until you specify the parameters.
Don’t worry; you won’t burn very many clock cycles with these cases. If fact, you should run the 16k case using the step button.
Just what good is your Rcapacity concept? Let’s see you apply it to Unnamed’s selection process. It isn't any good! It just explains why certain Ev experiments will not converge. You claim evolution stops for a different reason. I just want you to demonstrate your claim. Is this really so hard to understand?
Paul, I have posted the parameters three times now. If you don’t run the cases after reading this post, you have no other excuse than denial.
Because he doesn’t realize that setting a mistake weight to 0 is equivalent to turning off that particular selection condition. He doesn't?
He seems to think that you can only have a perfect creature when you satisfy all three of your selection conditions. Who knows what is going on in his mind, he thinks string cheese explains evolution.
Can I just see if I've got this straight? Is Kleinman really now arguing that the evolution of drug resistance proves that evolution doesn't happen? I didn't think it was possible to prove yourself quite so spectatularly wrong without actually imploding.
You didn’t get it quite right Cuddles. What I said was that multiple selection processes slow and then ultimately stop evolution. This is what ev shows and it is this principle which is used to treat HIV. Monotherapy treatment of HIV quickly leads to resistant strains of the virus to that drug, so standard of care now for HIV is triple antiviral drugs to reduce the evolution of drug resistance strains. Multiple selection processes slow and ultimately stop evolution. This is a mathematical fact revealed by ev and it occurs in reality.
Wait, I thought he was saying that multiple selection pressures causes evolution to stop. Well, with a sufficiently large genome, anyway.
Paul, that is in fact what your model shows.
Wait, I thought he was saying that multiple selection pressures causes evolution to stop. Well, with a sufficiently large genome, anyway.Well, yes and no. He claims "stop", but when he speaks of specific examples like HIV treatment, reality creeps in a bit:
The mutations that give drug resistance in HIV are usually single base substitutions which are much simpler than the evolution example described by ev and therefore don’t require multiple mutations to a sequence of bases yet three drugs (selection pressures) are enough to prevent the evolution of resistant strains for years. If resistant strains do start appearing, I suspect the strategy will be to add a fourth drug. To you want to explain how you can have a selection processes evolving the ancestral insulin gene, the ancestral hemoglobin gene, the ancestral genes for the DNA replicase system… all acting simultaneously?
This is exactly analogous to the strategy used in the treatment of HIV. By using multiple drug regimens, you apply multiple selection pressures and reduce the ability of the virus to evolve. Monotherapy treatment markedly increases the likelihood of evolving resistant strains of the virus. In the real world, he cannot demonstrate evolution coming to a stop. His interpretation of evolution in ev is made possible by an a priori definition of success; certainly, if there is only one way into a room, and you block the door, you have stopped entry. But in the real world, evolution cannot be stopped by some Maginot line; there is more than one way to respond to any given selection pressure. Some interesting reading here, about TMTOWTDI (There's More Than One Way To Do It). An appropriate excerpt:
Add a fourth drug to the HIV treatment regimen, it will only slow the evolution of resistant strains more so. As Paul said previously, there are millions of selection pressures acting simultaneously on living things. Ev shows that three selection pressures are enough to stop evolution. Ev presents you with a humungous mathematical problem. The reason why ev takes so many generations to evolve binding sites is that the three selection conditions in the model interfere with each other. This principle is used to treat HIV to prevent the evolution of drug resistant strains of the virus.
In the real world, he cannot demonstrate evolution coming to a stop... But in the real world, evolution cannot be stopped by some Maginot line...It can be stopped by complete extinction. If you wipe out all of the relevant life, there won't be anymore evolution.
Is the HIV virus relevant?
It can be stopped by complete extinction. If you wipe out all of the relevant life, there won't be anymore evolution. True--thus the "Maginot Line" reference (if not a great analogy). If there is a way around, over, under, or through, then blocking one of those routes is not enough. Nor two, nor three. While there is life, there is the possibility that something will stumble upon the solution. If, instead of the Maginot Line, the French had simply exterminated the Germans...
Your “Maginot Line” is a perfect analogy. The Maginot line was a single selection pressure. The French might have done better if they used multiple selection pressures such as an Air Force and mobile armor.

[kjkent1]

“Perfect creature” is only a label used by Paul and Dr Schneider to indicate a creature that has satisfied all three of their selection conditions. If you turn off two of the three selection conditions then a “perfect creature” is one that satisfies that selection condition.Nope. You're wrong, and you need to drop your superiority complex and recognize that you're wrong, so we can move on, because you're spewing out nonsense with this current argument.

A perfect creature in ev is a creature which is substantially free of missed and/or spurious bindings, and which has evolved information such that Rseq is approaching Rfreq. There's an easy way to prove this:

1. Use the default settings, and pick a random seed that produce a perfect creature. Whenever you do this, the perfect creature will also show that Rseq is approaching Rfreq, because that is the measure of an evolved genome that ev uses to prove that evolution is possible by RMNS.

2. Use the same settings, but set one of the mistake weights to zero, and pick a random seed that produces a perfect creature. Under no circumstances will Rseq come anywhere near Rfreq.

Under your required conditions, with mistake weights at zero, there is no requirement that the final genome represent anything remotely resembling an evolved genetic sequence. You will consistently obtain a perfect creature in one generation with a genome that's random gibberish.

All you need do is look at the sequence to see that it's still filled with errors. So, just open your eyes and look.

[Paul C. Anagnostopoulos]

“Perfect creature” is only a label used by Paul and Dr Schneider to indicate a creature that has satisfied all three of their selection conditions. If you turn off two of the three selection conditions then a “perfect creature” is one that satisfies that selection condition.
This is arguable, but not really worth the effort to argue it.


Really? I don’t recall Unnamed running any cases with a short site width.
What does this have to do with whether Rcapacity is relevant to Unnamed's selection process? Rcapacity is relevant when all three mistake counts are nonzero.


Rcapacity doesn’t explain why ev converges when you eliminate two of the three selection conditions no matter what the site width is.
That is correct. As I have now said a half dozen times: Rcapacity is irrelevant when any mistake counts are zero.


1st case: Population 64, gamma=16, site width=6, G=16384, mutation rate=1/G/generation, weight width=5, Rfreq=10, Paul’s infamous Rcapacity=2*site width=10. With the weights for each mistake, (missed site, spurious binding in gene, spurious binding outside gene), set to 1, this case fails to converge.
Actually, Rcapacity = 12. How do you know it fails to converge, or simply takes a long time?


Rfrequency=-log2(gamma/G) where gamma is the number of binding sites and G is the number of sites in the genome. Do you want to define Rcapacity for us?
I know the math. I want you to define what Rfrequency means.


And the reason they “stopped” is that there was only one selection condition acting. This condition was achieved by setting to of the three weight factors to 0 thereby eliminating two of the three selection conditions. Once you run these cases, it should become clear to you that the reason these cases are able to converge is there is only a single selection condition.
On and on you go, without actually demonstrating what you claim: Evolution stopping with all mistake counts nonzero and Rcapacity not an issue.


Paul, I have posted the parameters three times now. If you don’t run the cases after reading this post, you have no other excuse than denial.
I don't need to run the cases. I am not claiming that you are lying. How do you know your experiment won't produce a perfect creature?


He seems to think that you can only have a perfect creature when you satisfy all three of your selection conditions. Who knows what is going on in his mind, he thinks string cheese explains evolution.
Alan, this is simply a question of the definition of perfect creature, isn't it? As the person who coined the term, I get to specify the definition. Would you like it to mean (a) a creature who perfectly distinguishes binding sites from other sites; or (b) a creature with zero mistakes?


Paul, that is in fact what your model shows.
Demonstration, please.

~~ Paul

[kleinman]

“Perfect creature” is only a label used by Paul and Dr Schneider to indicate a creature that has satisfied all three of their selection conditions. If you turn off two of the three selection conditions then a “perfect creature” is one that satisfies that selection condition. Nope. You're wrong, and you need to drop your superiority complex and recognize that you're wrong, so we can move on, because you're spewing out nonsense with this current argument.
Well, Paul is going to run the cases I have suggested so prepare yourself for a shock.
A perfect creature in ev is a creature which is substantially free of missed and/or spurious bindings, and which has evolved information such that Rseq is approaching Rfreq. There's an easy way to prove this:
You need to take a few courses in mathematical modeling of physical systems.
All you need do is look at the sequence to see that it's still filled with errors. So, just open your eyes and look.
So what? The ev model won’t converge with all three selection conditions imposed. Turn off two of the three selection conditions and you can evolve that condition in the genome. It is the competing selection conditions which slow and ultimately stop evolution in ev. This effect is seen in reality. This principle is used to slow if not stop the evolution of resistant strains of HIV viruses. Not only do you not have a selection process to evolve a gene from the beginning, multiple selection pressures slow and ultimately stop evolution. This is what ev shows mathematically and this is what is seen in the treatment of HIV. This is why the theory of evolution is mathematically impossible.

[Taffer]

Taffer, read the guidelines for treating HIV and why triple medications are used. I posted a specific quote from the guidelines and I repost it again here:

I have read enough of that document to know it does not say what you are claiming. Multiple drugs are used, primarily as far as I can tell from your source, because if resistance to one drug evolves, you can replace it with another drug while continuing treatment.

Simultaneously stopping all drugs in a regimen containing these agents may result in functional monotherapy with the NNRTIs, because their half-lives are longer than other agents. This may increase the risk of selection of NNRTI-resistant mutations.

They are talking about specific drugs, and not he overall drug regeme. Did you even read your own source? Just doing a word search isn't going to cut it, especially if you do not understand microbiology.

Secondly, it is stating that there is an increased risk of resistance arrisal because of the increased half-life of those specific drugs. Read your own bloody source.

With respects to your argument that you can achieve triple resistance as quickly using triple antimicrobials in parallel as when the antimicrobials serially, provide your evidence and citations.

My own experiments. Provide your citations and evidence that they are wrong. Can't? Didn't think so.

You argue that 1+1+1=3 give the same results as 1*3=3. Do you think this argument extends to millions of selection conditions?

Yes. In fact, I think multiple selective pressures increase variation within a population, and ultimately lead to more diversity (and thus more evolution).

If so, you are in disagreement with the results from ev.

I'm in disagreement with a model of one specific section of evolution when it is compared to the whole of evolution? Oh noes, the horror! :rolleyes:

[kleinman]

Paul, you better check your arithmetic, that 16384 base case has an Rfrequency of 10 according to your computer model.

[Paul C. Anagnostopoulos]

Well, Paul is going to run the cases I have suggested so prepare yourself for a shock.
If I run anything, it will be the experiment with all three mistakes counts set to 1. I don't care about the other cases.


You need to take a few courses in mathematical modeling of physical systems.
Cripes, Alan, you're such a condescending jerk. The term perfect creature is just one I made up. There is no mathematical/scientific definition of the term.


So what? The ev model won’t converge with all three selection conditions imposed.
Demonstration, please.

~~ Paul

[Paul C. Anagnostopoulos]

Paul, you better check your arithmetic, that 16384 base case has an Rfrequency of 10 according to your computer model.
Yes, Alan, it does. What I said was that Rcapacity = 12.

~~ Paul

[kleinman]

Paul, you better check your arithmetic, that 16384 base case has an Rfrequency of 10 according to your computer model. Yes, Alan, it does. What I said was that Rcapacity = 12.
Oh, I’m sorry, so let’s do the case of G=16384 and site width=4, all other parameters the same:
missed site/spurious binding-gene/spurious binding outside gene/gens to perfect creature
1/0/0/104
0/1/0/114
0/0/1/14
Rfrequency=10, and your famous Rcapacity value =8. Let’s try a site width of 3.
missed site/spurious binding-gene/spurious binding outside gene/gens to perfect creature
1/0/0/12
0/1/0/1
0/0/1/36
Rfrequeny=10, Rcapacity=6
Paul, it is the competing selection processes that prevent ev from evolving all the selection conditions simultaneously.

[Paul C. Anagnostopoulos]

Paul, it is the competing selection processes that prevent ev from evolving all the selection conditions simultaneously.
Alan, read my fingers: I don't care about experiments with mistake counts of zero. The only reason you've moved the goalpost to that red herring is because you can contrast it with experiments in which you claim that evolution stopped completely. But that isn't interesting if it didn't actually stop, is it? And you don't have no compelling data to show they stopped, do you? So we don't give a crap, do we?

Prove that evolution stops in the normal case and then we have something to talk about.

Edited to add: And you can do it with high mutation rates, because if evolution stops, then it stops no matter the mutation rate.

~~ Paul

[delphi_ote]

Is the HIV virus relevant?
Definitely. If you can find any treatment to which it cannot adapt, do let the world know. A cure for HIV/AIDS would probably be a big deal.

[Mercutio]

Your “Maginot Line” is a perfect analogy. The Maginot line was a single selection pressure. The French might have done better if they used multiple selection pressures such as an Air Force and mobile armor.

Ok, then let me expand on it a bit. Suppose the French did use an Air Force and mobile armor, and nerve agents, blister gases, poisoned saurkraut, and a hermetically sealed geodesic dome over the entire country. Let us further suppose that these successfully kept the Nazis out of France. Have they stopped the Third Reich from successfully evolving? Not as long as there are other countries--other sources of energy to exploit.

If we define success as "invading France", and our selection pressures prevent that outcome, we can "stop evolution". But in the real world, we don't get to define an outcome a priori. We have to come up with a new flu vaccine each year, because even though we provided a selection pressure in the form of last year's vaccine, we could not predict which direction(s), if any, the Nazi Flu Germs would take around our Maginot Line, or even whether they would give up on France and head for Canada instead. Ev does not model that. Sorry.

[kleinman]

Paul, it is the competing selection processes that prevent ev from evolving all the selection conditions simultaneously. Alan, read my fingers: I don't care about experiments with mistake counts of zero. The only reason you've moved the goalpost to that red herring is because you can contrast it with experiments in which you claim that evolution stopped completely. But that isn't interesting if it didn't actually stop, is it? And you don't have no compelling data to show they stopped, do you? So we don't give a crap, do we?
You forgot your strawman argument as well. Only two of the three selection conditions are set to zero. There are no moving goalposts here Paul. I started this discussion stating that your computer model shows that evolution is mathematically impossible. The only thing that has been added is the explanation why your computer model shows it is impossible. It is the competing selection processes that slow down and ultimately stop ev from converging. It is not due to the weight matrix not being able to match (surpass the threshold). The last two cases I presented had Rcapacity values much less than Rfrequency yet they rapidly converge if you have only one selection condition. In fact all three selection conditions will converge if done one at a time. This accurately models the situation of using three drugs (three selection conditions) to prevent the evolution of resistant strains of the HIV virus. You are in denial about what the data from ev shows. With respects to having compelling data to show that ev slows down and stops converging with the three selection conditions imposed, the G=8192 case took over 700,000 generations to converge. The G=16,384 case takes only about 100 generations to converge each of the individual selection conditions and that is with small site widths than what your Rcapacity condition would allow.
Prove that evolution stops in the normal case and then we have something to talk about.
Paul, there is no “normal” case. You have three selection conditions defined in ev and can weight each condition from 0 to what ever value you have allow. If you think that it requires your three selection conditions to be imposed in order to have a “normal” case, what do you think would happen to your model if you evolve two different sets of binding sites simultaneously? In this case you would have 6 selection conditions, 2 selection conditions for missed binding sites, 2 selection conditions for spurious binding in the gene and 2 selection conditions for spurious binding outside the gene. Do you think this model will converge more quickly than your present model? Paul, it is the competing selection conditions that slow down and ultimately stop ev from converging. This effect would be worse with more selection conditions.
And you can do it with high mutation rates, because if evolution stops, then it stops no matter the mutation rate.
Paul, it is the multiple selection conditions which slows down the convergence of ev. I’ll start posting series of cases which make it more apparent to you. This is a real phenomena that Dr Schneider’s model has captured. Why don’t you put a two binding site set model on your to do list? Then you can evolve perfect creatures that satisfy 6 selection conditions. This would make kjkent1 happy except I doubt this model would ever converge no matter what the genome length.
Is the HIV virus relevant? Definitely. If you can find any treatment to which it cannot adapt, do let the world know. A cure for HIV/AIDS would probably be a big deal.
There already is a good strategy for treating this disease. 3 drug therapy can extend life for years. The biggest problem with these multi-drug regimens is the adverse reactions from the drugs. If more low side effect drugs can be developed that target more viral proteins then you can put more selective pressure on the virus than just 3. The more selective pressures you can put on the virus, the less likely resistant strains will evolve. Multiple selective pressures slow the evolutionary process.

[kjkent1]

So what? The ev model won’t converge with all three selection conditions imposed. Turn off two of the three selection conditions and you can evolve that condition in the genome.No, you can't, because the other condition is physically present and its hosts are never selected against. You can produce a "perfect creature," but it's not evolved in any meaningful sense, according to the mathematics upon which ev is postulated.

It is the competing selection conditions which slow and ultimately stop evolution in ev.Laughably incorrect conclusion.This effect is seen in reality.BZZZZ! Incorrect!This principle is used to slow if not stop the evolution of resistant strains of HIV viruses. Is it? Let's test this spectacular logic. In the real world there are countless environmental stresses on every creature, and evolution is generally slow but inexorable. Along comes the mighty Alan Kleinman and he subjects one of these creatures, the HIV virus, to one more selective pressure, and the creature starts to evolve more slowly. Then he does it with one more stress, and the creature's evolution really starts to slow. Finally, he applies the third stroke, and HIV's evolution comes to a practical halt. Remarkable -- the first 10 billion odd environmental stresses had no perceivable effect, and in fact, HIV evolved OUT of this huge number of stresses. Then suddenly, just by coincidence, the application of three more stresses brings evolution to a dead stop -- just like Mr. Logic says that it should.

Makes sense huh? Of course a reasonable person might just conjecture that the reason why HIV was slowing down in the lab is because the anti-virals were killing most of the virus off entirely, or that the drugs were targeted in a manner which would be more likely to destroy the virus -- not necessarily because of the coincidence of environmental stresses.

I'm sure you'll have a startling explanation for why my logical analogy is wrong and your ridiculous conclusion is correct -- and I can't wait to read it in the next episode of: "When the wine cork turns."

[Paul C. Anagnostopoulos]

You forgot your strawman argument as well. Only two of the three selection conditions are set to zero. There are no moving goalposts here Paul. I started this discussion stating that your computer model shows that evolution is mathematically impossible. The only thing that has been added is the explanation why your computer model shows it is impossible. It is the competing selection processes that slow down and ultimately stop ev from converging.
But you have not proved that it stops, so the entire argument has no basis.

I am running the following experiment:

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

These are identical to your parameters, except for 4 mutations per generation instead of 1. This should make no difference, since your argument has nothing to do with mutation rate. After 800,000 generations the mistake count is 4. It hasn't "stopped" yet. I'll let you know if it does.


Paul, it is the multiple selection conditions which slows down the convergence of ev. I’ll start posting series of cases which make it more apparent to you.
Alan, really, you're wasting your time and ours. I agree that less stringent selection pressures will allow faster evolution. That is not what I am arguing with. I am arguing with the word STOP.


Why don’t you put a two binding site set model on your to do list? Then you can evolve perfect creatures that satisfy 6 selection conditions. This would make kjkent1 happy except I doubt this model would ever converge no matter what the genome length.
So your current thesis is what? That the maximum number of selection pressures that can converge is three? Four? Five selection pressure and suddenly no convergence?

You do realize that you are saying that no evolution has ever taken place in the real world. That is a pretty extraordinary claim.

~~ Paul

[Paul C. Anagnostopoulos]

Finally, he applies the third stroke, and HIV's evolution comes to a practical halt. Remarkable -- the first 10 billion odd environmental stresses had no perceivable effect, and in fact, HIV evolved OUT of this huge number of stresses.
The only conclusion I can reach from this remarkable logic is that no evolution has ever occurred at all.

~~ Paul

[Taffer]

Alan, really, you're wasting your time and ours. I agree that less stringent selection pressures will allow faster evolution. That is not what I am arguing with. I am arguing with the word STOP.

In reality, stronger selective pressures increase the rate of evolution.

This is modeled by the time to fixation of a new mutant allele at a specific loci. The stronger the selection against that allele, the faster the ratios of that allele change (either to fixation, equilibrium or loss, depending on the type of selection).

[Paul C. Anagnostopoulos]

In reality, stronger selective pressures increase the rate of evolution.

This is modeled by the time to fixation of a new mutant allele at a specific loci. The stronger the selection against that allele, the faster the ratios of that allele change (either to fixation, equilibrium or loss, depending on the type of selection).
Yes, what I should say is that fewer selection pressures in Ev mean that the mistake count can reach zero faster. After all, the mistake count includes fewer sorts of mistakes.

~~ Paul

[delphi_ote]

In reality, stronger selective pressures increase the rate of evolution.

This is modeled by the time to fixation of a new mutant allele at a specific loci. The stronger the selection against that allele, the faster the ratios of that allele change (either to fixation, equilibrium or loss, depending on the type of selection).
Unless we're talking about a real population. High enough selection pressure will slow the rate of evolution because the population will die off.

Also, if you think about it, it's possible the earlier mutations in a series of smooth mutations to adapt to one selection pressure might be maladaptive to a different selection pressure. This is possible, but I can't think of a natural case where this is likely.

In the end, the number of selection pressures don't matter. It's the shape of the resulting fitness landscape that matters. We can only really talk about fitness landscape in a concrete way in terms of simulations like ev.

[Paul C. Anagnostopoulos]

I am running the following experiment:

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

These are identical to your parameters, except for 4 mutations per generation instead of 1. This should make no difference, since your argument has nothing to do with mutation rate. After 800,000 generations the mistake count is 4. It hasn't "stopped" yet. I'll let you know if it does.
Well, it doesn't. After 1,083,137 generations, a creature with zero mistakes has emerged from the primordial depths. It has an Rsequence of 11.13, higher than the Rfrequency of 10 and lower than the Rcapacity of 12. The sequence logo is ACGACA.

Let the goalpost moving continue ...

~~ Paul

[Taffer]

Unless we're talking about a real population. High enough selection pressure will slow the rate of evolution because the population will die off.

Evolution is defined as a change in allele frequences. Strong selection pressures cause a fast change in allele frequences, leading ultimately to fixation or loss (generally the latter). Thus, strong selection pressures cause evolution to occur more quickly.

Also, if you think about it, it's possible the earlier mutations in a series of smooth mutations to adapt to one selection pressure might be maladaptive to a different selection pressure. This is possible, but I can't think of a natural case where this is likely.

It is possible. But, as noted above, strong selective pressures will cause beneficial alleles to quickly fix, thereby speeding up evolution. (I know what you're saying, btw, but I'm making a point with regard to kleinman.)

In the end, the number of selection pressures don't matter. It's the shape of the resulting fitness landscape that matters. We can only really talk about fitness landscape in a concrete way in terms of simulations like ev.

Very true. Although there are plenty of pop gene simulations which model fitness landscapes.

I wonder what a 50 dimensional fitness landscape would look like? :D

[kjkent1]

The only conclusion I can reach from this remarkable logic is that no evolution has ever occurred at all.

~~ PaulWell, that's Kleinman's base conclusion -- there is no evolution -- every significant change in an organism is caused by a miracle of God.

I wonder how a miracle looks, up close, when it produces a macro-evolutionary change? Would we see a little index finger appear out of nowhere, flipping alleles? Or, would it just look like a random accidental occurrence (better known in the legal profession as an "Act of God")?

The irony of the theistic view is, that even were God actually involved in macro-evolutionary change, the most devout believer would observe nothing more than evolution.

[kleinman]

So what? The ev model won’t converge with all three selection conditions imposed. Turn off two of the three selection conditions and you can evolve that condition in the genome. No, you can't, because the other condition is physically present and its hosts are never selected against. You can produce a "perfect creature," but it's not evolved in any meaningful sense, according to the mathematics upon which ev is postulated.
Physically present? Do you think a creature with a 256 bases is physically present? Kjkent1, this is a mathematical simulation. Reducing the number of selection conditions in ev still produces meaningful base sequences that satisfy the remaining selection conditions. All ev does is a random point mutation and selection condition(s) and shows that sequences of bases can evolve that satisfy those selection condition(s) (under very restricted circumstances).
It is the competing selection conditions which slow and ultimately stop evolution in ev.Laughably incorrect conclusion.
Not as laughable as your string cheese theory of evolution but let’s see if ev shows this. The following series is based on Dr Schneider’s published case. Starting with G=256 and a mutation rate of 1 mutation per 256 bases per generation (used for all cases in this series) and initially all weight factors for binding site mistakes, spurious binding in gene mistakes and spurious binding outside of gene set to 1. All other parameters in the model use default values.
G/ Generations to Perfect Creature
256/ 662
512/ 1251
1024/ 2991
2048/ 5382
4096/ 7715
8192/ 20237
16384/ 49963
32768/ 140958
65536/ Yours Paul
Well, what happens when we set two of the three selection conditions to 0? Let’s see what ev has to say.
G/Gens PC/bind mist/spur bind gene/spur outside gene
65536/ 1/ 1/ 0/ 0/
65536/ 5/ 0/ 1/ 0/
65536/ 18/ 0/ 0/ 1/
131072/1/ 1/ 0/ 0/
131072/17/ 0/ 1/ 0/
131072/27/ 0/ 0/ 1/
262144/3/ 1/ 0/ 0/ pop 32
262144/1/ 0/ 1/ 0/
262144/15/ 0/ 0/ 1/
In order to get the G=262144 case to run, I had to reduce the population to 32 but this case still rapidly converges for single selection conditions.

So what does this data say? It says that with three selection conditions the number of generations for convergence to a perfect creature (all selection conditions satisfied) rapidly increases as genome length increases. When you reduce the number of selection conditions to 1, even with genome lengths that are much larger than what Paul’s Rcapacity value says should converge, rapidly converge to a perfect creature for that selection condition. Multiple selection conditions slow and ultimately stop evolution in ev.
This effect is seen in reality. BZZZZ! Incorrect!
Ask the infectious disease experts why triple antiviral agents are used to treat HIV.
This principle is used to slow if not stop the evolution of resistant strains of HIV viruses. Is it? Let's test this spectacular logic. In the real world there are countless environmental stresses on every creature, and evolution is generally slow but inexorable. Along comes the mighty Alan Kleinman and he subjects one of these creatures, the HIV virus, to one more selective pressure, and the creature starts to evolve more slowly. Then he does it with one more stress, and the creature's evolution really starts to slow. Finally, he applies the third stroke, and HIV's evolution comes to a practical halt. Remarkable -- the first 10 billion odd environmental stresses had no perceivable effect, and in fact, HIV evolved OUT of this huge number of stresses. Then suddenly, just by coincidence, the application of three more stresses brings evolution to a dead stop -- just like Mr. Logic says that it should.
Hey, that is what ev shows and that is what the use of triple antiviral agents shows when treating HIV.
Makes sense huh? Of course a reasonable person might just conjecture that the reason why HIV was slowing down in the lab is because the anti-virals were killing most of the virus off entirely, or that the drugs were targeted in a manner which would be more likely to destroy the virus -- not necessarily because of the coincidence of environmental stresses.
It does make sense. What the results from ev show is that you must have multiple random mutations occurring at the right loci at the same time in order to satisfy the multiple selection conditions for the evolutionary process to proceed. This is very unlikely to happen as the selection conditions become more complex.
I'm sure you'll have a startling explanation for why my logical analogy is wrong and your ridiculous conclusion is correct -- and I can't wait to read it in the next episode of: "When the wine cork turns."
The explanation is not startling, it is very simple.
You forgot your strawman argument as well. Only two of the three selection conditions are set to zero. There are no moving goalposts here Paul. I started this discussion stating that your computer model shows that evolution is mathematically impossible. The only thing that has been added is the explanation why your computer model shows it is impossible. It is the competing selection processes that slow down and ultimately stop ev from converging. But you have not proved that it stops, so the entire argument has no basis.

I am running the following experiment:

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

These are identical to your parameters, except for 4 mutations per generation instead of 1. This should make no difference, since your argument has nothing to do with mutation rate. After 800,000 generations the mistake count is 4. It hasn't "stopped" yet. I'll let you know if it does.
Paul, there are many ways to stop the evolutionary process. You’ve just demonstrated that an extremely high mutation rate stops evolution. Another reason that evolution stops is multiple selection conditions. Try your case and see whether a using a single selection condition allows evolution to proceed more quickly.
Paul, it is the multiple selection conditions which slows down the convergence of ev. I’ll start posting series of cases which make it more apparent to you.Alan, really, you're wasting your time and ours. I agree that less stringent selection pressures will allow faster evolution. That is not what I am arguing with. I am arguing with the word STOP.
Paul, why should I STOP when it is your own program that shows that evolution is mathematically impossible? And the reason why the theory of evolution is mathematically impossible is that multiple selection conditions STOP evolution.
Why don’t you put a two binding site set model on your to do list? Then you can evolve perfect creatures that satisfy 6 selection conditions. This would make kjkent1 happy except I doubt this model would ever converge no matter what the genome length. So your current thesis is what? That the maximum number of selection pressures that can converge is three? Four? Five selection pressure and suddenly no convergence?
Paul, your own program shows this. When you lengthen the genome beyond what your Rcapacity value says will converge, still converges if you eliminate any two of the three selection conditions but only for that one nonzero selection condition.
You do realize that you are saying that no evolution has ever taken place in the real world. That is a pretty extraordinary claim.
No macroevolution has ever taken place in the real world.
Finally, he applies the third stroke, and HIV's evolution comes to a practical halt. Remarkable -- the first 10 billion odd environmental stresses had no perceivable effect, and in fact, HIV evolved OUT of this huge number of stresses. The only conclusion I can reach from this remarkable logic is that no evolution has ever occurred at all.
No macroevolution has ever occurred, that is what your computer model shows and that is what triple antiviral medications for the treatment of HIV shows. Care to describe the selection process that evolved the original HIV virus. If you say simian virus, I’ll ask how the simian virus evolved.
Alan, really, you're wasting your time and ours. I agree that less stringent selection pressures will allow faster evolution. That is not what I am arguing with. I am arguing with the word STOP.In reality, stronger selective pressures increase the rate of evolution.
That is correct Taffer, so what is the selective pressure that evolved the original HIV virus?
This is modeled by the time to fixation of a new mutant allele at a specific loci. The stronger the selection against that allele, the faster the ratios of that allele change (either to fixation, equilibrium or loss, depending on the type of selection).
So you think that three new mutant alleles can evolve simultaneously as quickly as three new mutant alleles evolving one after another?
In reality, stronger selective pressures increase the rate of evolution.

This is modeled by the time to fixation of a new mutant allele at a specific loci. The stronger the selection against that allele, the faster the ratios of that allele change (either to fixation, equilibrium or loss, depending on the type of selection).Yes, what I should say is that fewer selection pressures in Ev mean that the mistake count can reach zero faster. After all, the mistake count includes fewer sorts of mistakes.
It is only a mistake if there is a selection pressure. For example, if the selection pressure is due to the lack of an essential nutrient in the diet, addition of that nutrient removes that selective pressure.
Unless we're talking about a real population. High enough selection pressure will slow the rate of evolution because the population will die off.

Also, if you think about it, it's possible the earlier mutations in a series of smooth mutations to adapt to one selection pressure might be maladaptive to a different selection pressure. This is possible, but I can't think of a natural case where this is likely.

In the end, the number of selection pressures don't matter. It's the shape of the resulting fitness landscape that matters. We can only really talk about fitness landscape in a concrete way in terms of simulations like ev.
Well said.
I am running the following experiment:

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

These are identical to your parameters, except for 4 mutations per generation instead of 1. This should make no difference, since your argument has nothing to do with mutation rate. After 800,000 generations the mistake count is 4. It hasn't "stopped" yet. I'll let you know if it does.Well, it doesn't. After 1,083,137 generations, a creature with zero mistakes has emerged from the primordial depths. It has an Rsequence of 11.13, higher than the Rfrequency of 10 and lower than the Rcapacity of 12. The sequence logo is ACGACA.

Let the goalpost moving continue ...
Don’t think of it as moving goalposts; just think of this as an evolving discussion. Try your example with two of the three selection conditions set to 0 and see what happens.
Unless we're talking about a real population. High enough selection pressure will slow the rate of evolution because the population will die off.Evolution is defined as a change in allele frequences. Strong selection pressures cause a fast change in allele frequences, leading ultimately to fixation or loss (generally the latter). Thus, strong selection pressures cause evolution to occur more quickly.
Taffer, you are confusing recombination and natural selection with mutation and natural selection.
Also, if you think about it, it's possible the earlier mutations in a series of smooth mutations to adapt to one selection pressure might be maladaptive to a different selection pressure. This is possible, but I can't think of a natural case where this is likely. It is possible. But, as noted above, strong selective pressures will cause beneficial alleles to quickly fix, thereby speeding up evolution. (I know what you're saying, btw, but I'm making a point with regard to kleinman.)
The mutations that occur with HIV are usually single base substitutions. In order to achieve resistance to three antiviral agents simultaneously, you must have all three random mutations appear simultaneously. If a particular virus manages to become resistant to one agent, it still must content with the selective pressure of the other two agents which is slowing down the reproduction of this strain resistant to the one drug. The net result either way is that multiple selective pressures slow down the evolutionary process.
In the end, the number of selection pressures don't matter. It's the shape of the resulting fitness landscape that matters. We can only really talk about fitness landscape in a concrete way in terms of simulations like ev.Very true. Although there are plenty of pop gene simulations which model fitness landscapes.

I wonder what a 50 dimensional fitness landscape would look like?
Dr Schneider’s 3 dimensional fitness landscape already shows bad news for the theory of evolution. I suggested to Paul to modify ev to evolve two sets of binding sites with 6 selection conditions. I doubt he will do this because it is now quite apparent what ev does with 3 selection conditions. He knows I will co-opt this work.

[kjkent1]

Physically present? Do you think a creature with a 256 bases is physically present? Kjkent1, this is a mathematical simulation. Reducing the number of selection conditions in ev still produces meaningful base sequences that satisfy the remaining selection conditions. All ev does is a random point mutation and selection condition(s) and shows that sequences of bases can evolve that satisfy those selection condition(s) (under very restricted circumstances).You're still missing the important point. Schneider's model is predicated on showing how Rseq approaches Rfreq over many generations of RMNS, because Rseq is found to approach Rfreq in living organisms. When you shut off one of the mistake weights, Rseq never approaches Rfreq. Instead, you get a perfect creature, nearly immediately. But the genome of this creature is not "evolved" according to Schneider's math.

In short, what you are doing by zeroing out a mistake weight is introducing design into the algorithm, i.e., you have created a perfect creature via a MIRACLE! If you could find a living organism with huge numbers of spurious and missing bindings in the real world, now THAT might convince someone of the possibility of divine intervention. What you're doing by shutting off the mistake weights is roughly equivalent to taking all of the parts of the proverbial Boeing 747, laying them next to each other on the tarmac, and then shouting "FLY!"

It's a ridiculous proposition -- what is the matter with you?

Not as laughable as your string cheese theory of evolution but let’s see if ev shows this. The following series is based on Dr Schneider’s published case. Starting with G=256 and a mutation rate of 1 mutation per 256 bases per generation (used for all cases in this series) and initially all weight factors for binding site mistakes, spurious binding in gene mistakes and spurious binding outside of gene set to 1. All other parameters in the model use default values.
G/ Generations to Perfect Creature
256/ 662
512/ 1251
1024/ 2991
2048/ 5382
4096/ 7715
8192/ 20237
16384/ 49963
32768/ 140958
65536/ Yours Paul
Well, what happens when we set two of the three selection conditions to 0? Let’s see what ev has to say.
G/Gens PC/bind mist/spur bind gene/spur outside gene
65536/ 1/ 1/ 0/ 0/
65536/ 5/ 0/ 1/ 0/
65536/ 18/ 0/ 0/ 1/
131072/1/ 1/ 0/ 0/
131072/17/ 0/ 1/ 0/
131072/27/ 0/ 0/ 1/
262144/3/ 1/ 0/ 0/ pop 32
262144/1/ 0/ 1/ 0/
262144/15/ 0/ 0/ 1/
In order to get the G=262144 case to run, I had to reduce the population to 32 but this case still rapidly converges for single selection conditions.

So what does this data say? It says that with three selection conditions the number of generations for convergence to a perfect creature (all selection conditions satisfied) rapidly increases as genome length increases. When you reduce the number of selection conditions to 1, even with genome lengths that are much larger than what Paul’s Rcapacity value says should converge, rapidly converge to a perfect creature for that selection condition. Multiple selection conditions slow and ultimately stop evolution in ev.What it says, is, that you can't admit that you're conclusion is based on a false premise, so you're gonna keep on telling everyone you're right.

Earlier in this thread, I thought that a zero mistake weight was useful. But, after a quick post from Paul, I realized that zero mistake weights cause ev to malfunction. Then I created an experiment to test the various mistake behaviors without introducing the zero mistake. I had no idea what that experiment would show. But, the result is that missed bindings have more selective power than do spurious bindings, and spurious bindings have less selective power than missed bindings and spurious bindings in combination (see results (http://www.geocities.com/kjkent1/ev_average_results_with_random_seeds.pdf)). Also, when all the possible combinations are considered, we find that the combinations fit reasonably within a normalized distribution. Which makes a great deal of sense, because most behaviors of living things do in fact observe normal distributions, so why should selective effects be any different.

This also aligns itself with your view that adding selective effects slow down ev. This is true. What is not true, is that the effect of aggregate seletive forces is cumulative without end. Reality is that selective effects center around a mean average dependent upon their respective selective powers. The problem for the geneticist is to be able to quantify any particular selective effect in the real world. In ev, it's easy, because there are only three available selective effects, and my experiment shows exactly what happens for every one of the possible combinations.

You just don't want to recognize that you are only looking at one tail of the curve -- you're ignoring the other tail, because that tail falsifies your conclusion.

[kleinman]

Physically present? Do you think a creature with a 256 bases is physically present? Kjkent1, this is a mathematical simulation. Reducing the number of selection conditions in ev still produces meaningful base sequences that satisfy the remaining selection conditions. All ev does is a random point mutation and selection condition(s) and shows that sequences of bases can evolve that satisfy those selection condition(s) (under very restricted circumstances).You're still missing the important point. Schneider's model is predicated on showing how Rseq approaches Rfreq over many generations of RMNS, because Rseq is found to approach Rfreq in living organisms. When you shut off one of the mistake weights, Rseq never approaches Rfreq. Instead, you get a perfect creature, nearly immediately. But the genome of this creature is not "evolved" according to Schneider's math.
Selection in this model is based on mistakes, whether they be failed identification of binding sites or spurious identification of binding sites. Dr Schneider’s selection process shows a coincidental finding where Rsequence approaches Rfrequency when using all three of his selection conditions and the genome length is short enough. Selection is not based on this condition. I don’t know whether this coincidental finding has any real physical significance. Bottom line is that Dr Schneider’s model shows more than just this mathematical peculiarity when you do the parametric studies that he suggested be done. The most significant finding is that multiple selection processes slow and ultimately stop evolution in his model. This finding does have real physical significance.
In short, what you are doing by zeroing out a mistake weight is introducing design into the algorithm, i.e., you have created a perfect creature via a MIRACLE! If you could find a living organism with huge numbers of spurious and missing bindings in the real world, now THAT might convince someone of the possibility of divine intervention. What you're doing by shutting off the mistake weights is roughly equivalent to taking all of the parts of the proverbial Boeing 747, laying them next to each other on the tarmac, and then shouting "FLY!"
I remove selection conditions from Dr Schneider’s computer model and I have introduced design into the model? Your analogy of Dr Schneider’s computer model and a Boeing 747 is strange considering how highly designed a 747 is.
It's a ridiculous proposition -- what is the matter with you?
Hey, it is your proposition comparing ev with a Boeing 747.
Not as laughable as your string cheese theory of evolution but let’s see if ev shows this. The following series is based on Dr Schneider’s published case. Starting with G=256 and a mutation rate of 1 mutation per 256 bases per generation (used for all cases in this series) and initially all weight factors for binding site mistakes, spurious binding in gene mistakes and spurious binding outside of gene set to 1. All other parameters in the model use default values.What it says, is, that you can't admit that you're conclusion is based on a false premise, so you're gonna keep on telling everyone you're right.
Kjkent1, don’t confuse the fact that you don’t understand my premise as it being a false premise. Ev is a stylized model of random point mutation and natural selection and under certain circumstances you can evolve sequences of bases that satisfy its three selection conditions. Under more realistic circumstances (realistic genome lengths) ev fails to converge with its three selection conditions but still can evolve sequences of bases that satisfy one selection condition. The conclusion is that multiple selection conditions slow and ultimately stop evolution. This what ev shows and this effect is seen in reality.
Earlier in this thread, I thought that a zero mistake weight was useful. But, after a quick post from Paul, I realized that zero mistake weights cause ev to malfunction. Then I created an experiment to test the various mistake behaviors without introducing the zero mistake. I had no idea what that experiment would show. But, the result is that missed bindings have more selective power than do spurious bindings, and spurious bindings have less selective power than missed bindings and spurious bindings in combination (see results). Also, when all the possible combinations are considered, we find that the combinations fit reasonably within a normalized distribution. Which makes a great deal of sense, because most behaviors of living things do in fact observe normal distributions, so why should selective effects be any different.
The only thing that ev shows malfunctioning is the theory of evolution by mutation and natural selection because multiple selection conditions slow and ultimately stop evolution. Since you have trouble understanding this concept, why don’t you ask Paul to modify ev to evolve two sets of binding sites with 6 selection conditions, two conditions for missed binding sites, two conditions for spurious binding the gene and two conditions for spurious binding outside the gene. What do you think will happen in this simulation?
This also aligns itself with your view that adding selective effects slow down ev. This is true. What is not true, is that the effect of aggregate seletive forces is cumulative without end. Reality is that selective effects center around a mean average dependent upon their respective selective powers. The problem for the geneticist is to be able to quantify any particular selective effect in the real world. In ev, it's easy, because there are only three available selective effects, and my experiment shows exactly what happens for every one of the possible combinations.
Explain this to Paul so he can put this in ev.
You just don't want to recognize that you are only looking at one tail of the curve -- you're ignoring the other tail, because that tail falsifies your conclusion.
Which alternative universe are you telling your tale from?

[Paul C. Anagnostopoulos]

Don’t think of it as moving goalposts; just think of this as an evolving discussion. Try your example with two of the three selection conditions set to 0 and see what happens.
Are you ever going to acknowledge that you are a *********** liar? You said, multiple times, that those particular parameters cause evolution to stop, halt, hang up, never happen. I just showed that you are wrong. In fact, you never ran that particular case long enough to find out whether a perfect creature evolved. And then you wasted our time blathering on about multiple selection pressures causing evolution to halt.


You’ve just demonstrated that an extremely high mutation rate stops evolution.
Are you seriously going to argue that dropping the mutation rate by a factor of 4 would stop the perfect creature from evolving? You recall that we ran a series of experiments that showed that generations to perfection varies linearly with mutation rate.

Notice how you just moved the goalpost to include mutation rate.

~~ Paul

[kjkent1]

Selection in this model is based on mistakes, whether they be failed identification of binding sites or spurious identification of binding sites. Dr Schneider’s selection process shows a coincidental finding where Rsequence approaches Rfrequency when using all three of his selection conditions and the genome length is short enough. Selection is not based on this condition. I don’t know whether this coincidental finding has any real physical significance.According to the ev paper, "The average distance betwen accetor sites is the average size of introns plus exons, or ~812 bases, so the information needed to find the acceptors is Rfrequency = log2812 = 9.7. By comparison, Rseqence = 9.4 bits, so in this and other genetic systems, Rsequence is close to Rfrequency."

Schneider's ev paper is intended to "demonstrate that Rseqence can indeed evolve to match Rfrequency." You're the person who throughout this thread has advocated that ev is an accurate model of evolution. If true, then you cannot now argue that it is mere coincidence that Rseq approaches Rfreq, because to do so, is to reject the accuracy of the ev model. This is incredibly disingenuous, and it frankly suggests that I've got you up against the ropes, because you're so obviously wrong right now, and you know you are. Bottom line is that Dr Schneider’s model shows more than just this mathematical peculiarity when you do the parametric studies that he suggested be done. The most significant finding is that multiple selection processes slow and ultimately stop evolution in his model. This finding does have real physical significance.If this were actually true, then based on your findings of evolution producing perfect creatures long before there is any reasonable convergence from Rseq to Rfreq, we would find no creatures in nature with DNA sequences wherein Rseq is found to approach Rfreq. And, if this is true, then Schneider would never have written ev or the paper because he would not have found this measurement apparent in living organisms.

Checkmate.

Your experiments which produce perfect creatures wherein there is no approach of Rseq to Rfreq do not model real life. Therefore, your experiments cannot be used to extrapolate to real-world evolution. The genomes of your proposed perfect creatures are not viable, according to the principles of evolution stated in the ev paper.I remove selection conditions from Dr Schneider’s computer model and I have introduced design into the model? Your analogy of Dr Schneider’s computer model and a Boeing 747 is strange considering how highly designed a 747 is.No, you set a selective condition to zero and thereby create a "perfect creature" whose genome is completely inconsistent with any known living organism.

Your creature is magical, because it did not evolve -- it was designed -- by you.

[kleinman]

Schneider's ev paper is intended to "demonstrate that Rseqence can indeed evolve to match Rfrequency." You're the person who throughout this thread has advocated that ev is an accurate model of evolution. If true, then you cannot now argue that it is mere coincidence that Rseq approaches Rfreq, because to do so, is to reject the accuracy of the ev model. This is incredibly disingenuous, and it frankly suggests that I've got you up against the ropes, because you're so obviously wrong right now, and you know you are.
You may have me up against the string cheese but not the ropes. I love it when you evolutionists want to argue if ev is an accurate model of evolution. I have always called this a plausible model which captures some elements of reality. But let’s let Dr Schneider speak for himself.
The following quotes were taken from Dr Schneider’s blog web page: http://www.lecb.ncifcrf.gov/~toms/paper/ev/blog-ev.html (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 (http://www.lecb.ncifcrf.gov/~toms/paper/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 (http://www.discovery.org/scripts/viewDB/index.php?command=view&id=51&isFellow=true).

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.
I don’t go quite as far as Dr Schneider has gone but his model does properly simulate the effects of multiple selection conditions.
Bottom line is that Dr Schneider’s model shows more than just this mathematical peculiarity when you do the parametric studies that he suggested be done. The most significant finding is that multiple selection processes slow and ultimately stop evolution in his model. This finding does have real physical significance.If this were actually true, then based on your findings of evolution producing perfect creatures long before there is any reasonable convergence from Rseq to Rfreq, we would find no creatures in nature with DNA sequences wherein Rseq is found to approach Rfreq. And, if this is true, then Schneider would never have written ev or the paper because he would not have found this measurement apparent in living organisms.
We all know that evolutionists never misinterpret their measurements.
Checkmate.
The only problem here is you are playing checkers.
Your experiments which produce perfect creatures wherein there is no approach of Rseq to Rfreq do not model real life. Therefore, your experiments cannot be used to extrapolate to real-world evolution. The genomes of your proposed perfect creatures are not viable, according to the principles of evolution stated in the ev paper.
If you want to model real life, tell us what the selection process is that evolved the original HIV virus.
I remove selection conditions from Dr Schneider’s computer model and I have introduced design into the model? Your analogy of Dr Schneider’s computer model and a Boeing 747 is strange considering how highly designed a 747 is.No, you set a selective condition to zero and thereby create a "perfect creature" whose genome is completely inconsistent with any known living organism.
You’ve just proved that ev also models abiogenesis.
Your creature is magical, because it did not evolve -- it was designed -- by you.
Are you sure I didn’t create it, just to annoy you.

[kjkent1]

You may have me up against the string cheese but not the ropes.

(kleinman follows with a cacophony of irrelevancy designed to obfuscate from the fact that his argument is completely destroyed -- redacted to protect the sanity of the audience.)Alan, your arguments are "a tale full of sound and fury, signifying nothing." Shakespeare, Macbeth, Act 5, Scene 5.

If you decide to come back to reality, let me know. Your current argument is frivolous.

[Mercutio]

Alan, your arguments are "a tale full of sound and fury, signifying nothing." Shakespeare, Macbeth, Act 5, Scene 5.
Um... you left out 4 words. Whether you were being polite or ironic is left for the reader to discover.


:D :D :D :D

[kleinman]

Don’t think of it as moving goalposts; just think of this as an evolving discussion. Try your example with two of the three selection conditions set to 0 and see what happens. Are you ever going to acknowledge that you are a *********** liar? You said, multiple times, that those particular parameters cause evolution to stop, halt, hang up, never happen. I just showed that you are wrong. In fact, you never ran that particular case long enough to find out whether a perfect creature evolved. And then you wasted our time blathering on about multiple selection pressures causing evolution to halt.
Paul, it is your theory of evolution which is the lie. Your own computer model shows this. Paul you can list lots of other ways of stopping ev from converging but it is the multiple selection pressures which explains why ev stops evolving as you lengthen the genome not your silly Rcapacity. This issue is not going away because it is the explanation why the theory of evolution is mathematically impossible. It is easily shown by eliminating two of the three selection conditions that ev will then evolve the third condition. The theory of evolution is mathematically impossible because competing selection conditions slow and ultimately stop evolution. There are no mutation mechanisms that will change this mathematical fact. You need to learn to live with this mathematical fact, your own computer model shows this. By the way, did I tell you how good a job you did on programming ev?
You’ve just demonstrated that an extremely high mutation rate stops evolution. Are you seriously going to argue that dropping the mutation rate by a factor of 4 would stop the perfect creature from evolving? You recall that we ran a series of experiments that showed that generations to perfection varies linearly with mutation rate.
Your experiments examining the effect of mutation rate are incomplete. If you examine a wider range of mutation rates you will find the mutation rate/generations for convergence curve is actually paraboloid, not linear. If you want, I’ll repost the data that shows this. Notice how you just moved the goalpost to include mutation rate.
Stop whining Paul; it is unbecoming for a moderator on the James Randi forum. You should be proud that your own computer program proves the theory of evolution to be mathematically impossible and the reason it is impossible is that conflicting selection conditions slow and then ultimately stop evolution.

[Paul C. Anagnostopoulos]

Paul, it is your theory of evolution which is the lie. Your own computer model shows this. Paul you can list lots of other ways of stopping ev from converging but it is the multiple selection pressures which explains why ev stops evolving as you lengthen the genome not your silly Rcapacity.
Alan, you must have been quite good at dodgeball. Let's cease talking about the reasons why evolution stops, and ponder the more fundamental question of whether it stops at all. Could you present a complete list of the experiments you ran that you think stopped? In addition to the parameters, please tell us how many generations you ran before you concluded that evolution had stopped.


Your experiments examining the effect of mutation rate are incomplete. If you examine a wider range of mutation rates you will find the mutation rate/generations for convergence curve is actually paraboloid, not linear. If you want, I’ll repost the data that shows this.
Yes, please do. I ran a series of experiments with a genome size of 1000 and mutation rates from 1/1,000,000 bases down to 1/200 bases. The results fit g = 8.7 m^1.0 with r = .996.

~~ Paul

[kleinman]

Paul, it is your theory of evolution which is the lie. Your own computer model shows this. Paul you can list lots of other ways of stopping ev from converging but it is the multiple selection pressures which explains why ev stops evolving as you lengthen the genome not your silly Rcapacity.Alan, you must have been quite good at dodgeball. Let's cease talking about the reasons why evolution stops, and ponder the more fundamental question of whether it stops at all. Could you present a complete list of the experiments you ran that you think stopped? In addition to the parameters, please tell us how many generations you ran before you concluded that evolution had stopped.
Ok, let’s talk about whether evolution really stops. Clearly extinction stops the evolution of that genetic line. If a genetic line does not go extinct, microevolutionary process don’t stop. These are the type of events that are seen for example with the evolution of drug resistance in the HIV virus. What ev shows is that macroevolutionary processes can not succeed because of the competing selection conditions. So how do you get microevolutionary processes to accumulate to make a macroevolutionary change? The answer to that question is you don’t. There are no selection processes that lead to macroevolutionary changes and if there were, they would be slowed profoundly by competing selection conditions as shown by your computer model. Evolutionists have mistakenly extrapolated microevolutionary processes to macroevolution. There are no selection processes to do this.
Your experiments examining the effect of mutation rate are incomplete. If you examine a wider range of mutation rates you will find the mutation rate/generations for convergence curve is actually paraboloid, not linear. If you want, I’ll repost the data that shows this. Yes, please do. I ran a series of experiments with a genome size of 1000 and mutation rates from 1/1,000,000 bases down to 1/200 bases. The results fit g = 8.7 m^1.0 with r = .996.
Ok, here is a typical series, G=1024, population=64, binding site width=6
Muts/G Generations
1 / 10108
2 / 6669
3 / 3432
4 / 2546
5 / 1268
6 / 1874
7 / 2147
8 / 3626
9 / 15351
10 / 81112

Try 1 mutation per 100 bases in your series and I think you will see the paraboloid behavior of the curve.

Here’s another series, G=2048
Mut/G Generations
1 / 35486
2 / 21666
3 / 8697
4 / 6001
5 / 7501
6 / 6143
7 / 3425
8 / 4998
9 / 4154
10 / 4043
11 / 8250
12 / 3570
13 / 4278
14 / 3650
15 / 5546
16 / 9424
17 / 38333
18 / 11250
19 / did not converge
You may get a linear fit in the range that you examined but if you increase the mutation rate further than what you examined you will see the paraboloid nature of the curve.

[Taffer]

No macroevolution has ever taken place in the real world.

Macroevolution is not a meaningful distinction in evolutionary theory.

No macroevolution has ever occurred, that is what your computer model shows and that is what triple antiviral medications for the treatment of HIV shows. Care to describe the selection process that evolved the original HIV virus. If you say simian virus, I’ll ask how the simian virus evolved.

Triple antiretrovirals have nothing to do with 'macroevolution', nor do they have anything to do with the subject at hand. They are used because three antiretrovirals kill faster then one. They also decrease the risk of any one resistance evolving at a particular time, but it does not decrease the probability of triple resistance mutants arising

That is correct Taffer, so what is the selective pressure that evolved the original HIV?

I believe there is lots of evidence for the evolution of the HIV virus. See here (http://en.wikipedia.org/wiki/AIDS_origin#Possible_spread_from_animal_to_human_p opulations) for a very brief run down on the origins of HIV.

So you think that three new mutant alleles can evolve simultaneously as quickly as three new mutant alleles evolving one after another?

Yes, of course. The chance of a mutant allele arrising at any one loci is fixed and independant on the number of other mutations arrising on the genome.

Taffer, you are confusing recombination and natural selection with mutation and natural selection.

No, I am not. Given that I am, in essence, a population geneticist (ok, a phylogeneticist, but same difference :o), I trust my own studies over what you say. Secondly, evolution is defined as the change in alleles over time. There is no difference between "recombination and natural selection" from "mutation and natural selection". Natural selection works on any existing variation in a population, no matter how that variation arose.

The mutations that occur with HIV are usually single base substitutions. In order to achieve resistance to three antiviral agents simultaneously, you must have all three random mutations appear simultaneously. If a particular virus manages to become resistant to one agent, it still must content with the selective pressure of the other two agents which is slowing down the reproduction of this strain resistant to the one drug. The net result either way is that multiple selective pressures slow down the evolutionary process.

No it isn't, and you obviously do not understand how antivirals work. Most, if not all, antivirals do not lead to a complete death of the virus. The slow the rate of viral infection, but not 100% of viruses are killed. Thus, a virus which evolves resistance to a single antiretroviral agent will have an advantage over its peers, as it is only being selected for by two selection pressures, not three. Stop thinking in black-and-whites. Biology does not work that way.

Dr Schneider’s 3 dimensional fitness landscape already shows bad news for the theory of evolution. I suggested to Paul to modify ev to evolve two sets of binding sites with 6 selection conditions. I doubt he will do this because it is now quite apparent what ev does with 3 selection conditions. He knows I will co-opt this work.

Whatever, kleinman. Since you have shown to have little to know understanding of even basic microbiology, evolutionary theory or population theory, I will trust population and evolutionary genetics over what you claim anyday. Since I have done the maths myself, I know 3 dimensional fitness landscapes work.

[delphi_ote]

Anyone interested in HIV evolution should check out the March 16th issue of Science. There's a fantastic publication on recent discoveries using phylogenetic analysis concluding that, "Virus variability may not be as predictable as first thought, making it harder to cover the variation of HIV by vaccines."

Taffer, you'd probably really dig it, what with your being a phylogeneticist and all. The idea that the virus has a phylogeny within a host and between hosts is definitely interesting. If you have experience with that type of thing, I'd love to hear about it!

The Science publication makes this whole discussion about multiple selection pressures seem silly. In the summary of this cutting edge research by the greatest minds of our day on the very topic we're discussing, we read that, "the extraordinary power of viruses like HIV and HCV to escape almost any means of host attack remains a daunting hurdle to overcome."

[Taffer]

Anyone interested in HIV evolution should check out the March 16th issue of Science. There's a fantastic publication on recent discoveries using phylogenetic analysis concluding that, "Virus variability may not be as predictable as first thought, making it harder to cover the variation of HIV by vaccines."

Taffer, you'd probably really dig it, what with your being a phylogeneticist and all. The idea that the virus has a phylogeny within a host and between hosts is definitely interesting. If you have experience with that type of thing, I'd love to hear about it!

The Science publication makes this whole discussion about multiple selection pressures seem silly. In the summary of this cutting edge research by the greatest minds of our day on the very topic we're discussing, we read that, "the extraordinary power of viruses like HIV and HCV to escape almost any means of host attack remains a daunting hurdle to overcome."

I had a quick look at it online, and it looks really interesting! Tomorrow I will go to the uni and see if I can nab a copy to read over. Thanks for pointing it out to me.

Oh, and FWIW, I'm not a phylogeneticist yet, only a grad student in genetics. But I have specialized into phylogenetics and evolution, and my research project is a phylogenetics one (we are doing the phylogenetics of a certain family of native New Zealand snails at the genra level, and also interspecifically, using several genes). :o

[Taffer]

No, I am not. Given that I am, in essence, a population geneticist (ok, a phylogeneticist, but same difference :o), I trust my own studies over what you say. Secondly, evolution is defined as the change in alleles over time. There is no difference between "recombination and natural selection" from "mutation and natural selection". Natural selection works on any existing variation in a population, no matter how that variation arose.

I take back the bolded section. I am a phylogenetics grad student, not an actual phylogeneticist. However, over the course of my studies, I have delt with a lot of population genetics (and phylogenetics, obviously), and so, while I do not claim to be an expert by any stretch of the imagination, at least I am familiar with the subject material. I apologize to anyone who got the impression that I am a practicing phylogeneticist. :o

[The Great Hairy One]

I've forgotten most of the population genetics I did at uni. Sooo long ago. I do remember calculating allele frequencies in populations, and all that stuff. Anyway, I preferred the more lab orientated stuff. Breeding Drosophila and stuff.

Cheers,
TGHO

[Paul C. Anagnostopoulos]

Try 1 mutation per 100 bases in your series and I think you will see the paraboloid behavior of the curve.
Oh yes, I see. You're cranking the rate up so high that you're introducing some sort of mutational overload. I think I saw that when I increased the rate above 1 mutation per 180 bases or so.

However, I'm talking about 4 mutations per genome vs. your 1 mutation per genome. I don't think the overload comes into consideration then. How many generations did you run that experiment before you concluded that evolution had stopped?


Evolutionists have mistakenly extrapolated microevolutionary processes to macroevolution. There are no selection processes to do this.
This claim is meaningless until you define macroevolution.

~~ Paul

[Mr. Scott]

This [Kleinman's] claim is meaningless until you define macroevolution.

I'd been thinking about this and want to provide an example as food for thought for Dr. Kleinman.

I once read that it was discovered that the cat family branched from its ancestors (more dog-like IIRC) when the gene that allowed them to taste sweetness was damaged (I guess by a point mutation). Scientists found a gene necessary for the sensing of sugars to be complete in the cat family except for a mutation that completely crippled it. The parent mammals had a sweet tooth and were omniverous. The child had no sweet tooth and was completely disinterested in eating anything but meat -- almost purely carniverous.

Here we had a point mutation microevolutionary step that profoundly affected the lifestyle of the animal -- the kind of step Dr. Kleinman asserts gives no problem to the Ev program or to a literal interpretation of Bible.

Now, if we have an omnivore that's lost its taste for everything but meat, we have a creature that better become a good predator, and better get most of its dietary needs from it. While not a fatal mutation at first, it obviously engaged selective pressures towards prefecting its predatory skills.

In each microevolutionary step, a random mutation could have modified our proto-cat's ability to hunt. A microevolution to the ear shape so it could hear its prey better, to its eye shape to see, its binocular vision to lock on to a target, its paw shape to walk more stealthily, and so on, and so forth. Many, many microevolutionary steps later, and we have a mammal that appears to bronze age men to be not at all related to similar predators, and it accumulated too many microevolutionary changes to mate with it's distant cousins (I presume -- has anyone tried to make a cog or a dat?). The cat, because of its perfection as a meat eater without backup of eating plants, became that most perfect predator on land. It's easy to understand intuitively how this run of micro-evolutionary changes, each of which Dr. Kleinman couldn't dispute as "mathematically impossible," would add up to a macroevolutionary transformation after millions of years.

OK, Dr. Kleinman, prove mathematically that dogs and cats could not have diverged from a common ancestor. Apparently, there is evidence that they did. I don't think extrapolating from the HIV antiviral drug treatments or a partial computer simulation of evolution could do this. You'll need more than that.

http://forums.randi.org/imagehosting/6736460bc65e14986.jpg

[kleinman]

No macroevolution has ever taken place in the real world.Macroevolution is not a meaningful distinction in evolutionary theory.
That’s obvious.
No macroevolution has ever occurred, that is what your computer model shows and that is what triple antiviral medications for the treatment of HIV shows. Care to describe the selection process that evolved the original HIV virus. If you say simian virus, I’ll ask how the simian virus evolved. Triple antiretrovirals have nothing to do with 'macroevolution', nor do they have anything to do with the subject at hand. They are used because three antiretrovirals kill faster then one. They also decrease the risk of any one resistance evolving at a particular time, but it does not decrease the probability of triple resistance mutants arising
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. 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. 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.
That is correct Taffer, so what is the selective pressure that evolved the original HIV? I believe there is lots of evidence for the evolution of the HIV virus. See here (http://en.wikipedia.org/wiki/AIDS_origin#Possible_spread_from_animal_to_human_p opulations) for a very brief run down on the origins of HIV.
So, how did the simian virus evolve?
So you think that three new mutant alleles can evolve simultaneously as quickly as three new mutant alleles evolving one after another?Yes, of course. The chance of a mutant allele arrising at any one loci is fixed and independant on the number of other mutations arrising on the genome.
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?
Taffer, you are confusing recombination and natural selection with mutation and natural selection. No, I am not. Given that I am, in essence, a population geneticist (ok, a phylogeneticist, but same difference ), I trust my own studies over what you say. Secondly, evolution is defined as the change in alleles over time. There is no difference between "recombination and natural selection" from "mutation and natural selection". Natural selection works on any existing variation in a population, no matter how that variation arose.
Ok expert in phylogenetics, how did the first allele arise?
The mutations that occur with HIV are usually single base substitutions. In order to achieve resistance to three antiviral agents simultaneously, you must have all three random mutations appear simultaneously. If a particular virus manages to become resistant to one agent, it still must content with the selective pressure of the other two agents which is slowing down the reproduction of this strain resistant to the one drug. The net result either way is that multiple selective pressures slow down the evolutionary process. No it isn't, and you obviously do not understand how antivirals work. Most, if not all, antivirals do not lead to a complete death of the virus. The slow the rate of viral infection, but not 100% of viruses are killed. Thus, a virus which evolves resistance to a single antiretroviral agent will have an advantage over its peers, as it is only being selected for by two selection pressures, not three. Stop thinking in black-and-whites. Biology does not work that way.
Triple antiretrovirals have nothing to do with 'macroevolution', nor do they have anything to do with the subject at hand. They are used because three antiretrovirals kill faster then one. They also decrease the risk of any one resistance evolving at a particular time, but it does not decrease the probability of triple resistance mutants arising
I added the color. Could you get your story straight.
Dr Schneider’s 3 dimensional fitness landscape already shows bad news for the theory of evolution. I suggested to Paul to modify ev to evolve two sets of binding sites with 6 selection conditions. I doubt he will do this because it is now quite apparent what ev does with 3 selection conditions. He knows I will co-opt this work.Whatever, kleinman. Since you have shown to have little to know understanding of even basic microbiology, evolutionary theory or population theory, I will trust population and evolutionary genetics over what you claim anyday. Since I have done the maths myself, I know 3 dimensional fitness landscapes work.
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.
The Science publication makes this whole discussion about multiple selection pressures seem silly. In the summary of this cutting edge research by the greatest minds of our day on the very topic we're discussing, we read that, "the extraordinary power of viruses like HIV and HCV to escape almost any means of host attack remains a daunting hurdle to overcome."
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.
Simultaneously stopping all drugs in a regimen containing these agents may result in functional monotherapy with the NNRTIs, because their half-lives are longer than other agents. This may increase the risk of selection of NNRTI-resistant mutations.
So Delphi, why don’t you give us a quote from your Science publication that shows that multiple selection pressures for treating the virus seem silly?
No, I am not. Given that I am, in essence, a population geneticist (ok, a phylogeneticist, but same difference ), I trust my own studies over what you say. Secondly, evolution is defined as the change in alleles over time. There is no difference between "recombination and natural selection" from "mutation and natural selection". Natural selection works on any existing variation in a population, no matter how that variation arose. I take back the bolded section. I am a phylogenetics grad student, not an actual phylogeneticist. However, over the course of my studies, I have delt with a lot of population genetics (and phylogenetics, obviously), and so, while I do not claim to be an expert by any stretch of the imagination, at least I am familiar with the subject material. I apologize to anyone who got the impression that I am a practicing phylogeneticist.
Apology accepted.
Try 1 mutation per 100 bases in your series and I think you will see the paraboloid behavior of the curve. Oh yes, I see. You're cranking the rate up so high that you're introducing some sort of mutational overload. I think I saw that when I increased the rate above 1 mutation per 180 bases or so.
What is your problem? If you want to study the parametric behavior of ev, you go through the range of values and see what kind of curve is obtained. You don’t think a mutation rate of 1 mutation per 256 bases per generation will give mutational overload to any real living thing?
However, I'm talking about 4 mutations per genome vs. your 1 mutation per genome. I don't think the overload comes into consideration then. How many generations did you run that experiment before you concluded that evolution had stopped?
I’m no longer sure which experiment you are talking about. Choose a series you want to look at, (genome length, mutation rate, etc.) and we will show everyone when ev converges and when ev stops converging. Then I will show you on the case where ev does not converge, eliminating any two of the three selection conditions will allow ev to evolve that particular condition. It is the multiple conflicting selection conditions that stops ev from converging.
Evolutionists have mistakenly extrapolated microevolutionary processes to macroevolution. There are no selection processes to do this.This claim is meaningless until you define macroevolution.
Paul, I’ve defined it by example. I’ll repeat some of the examples here. The evolution of a gene from the beginning, the transformation of a gene from some original function to some totally new function and the evolution of humans and chimpanzees from a primate ancestor. Here are some examples of microevolution. The evolution of drug resistant strains of HIV, Sickle cell hemoglobin and recombination events are all examples of microevolution.
This [Kleinman's] claim is meaningless until you define macroevolution.OK, Dr. Kleinman, prove mathematically that dogs and cats could not have diverged from a common ancestor. Apparently, there is evidence that they did. I don't think extrapolating from the HIV antiviral drug treatments or a partial computer simulation of evolution could do this. You'll need more than that.
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.

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? That is a cute picture though.

[delphi_ote]

So Delphi, why don’t you give us a quote from your Science publication that shows that multiple selection pressures for treating the virus seem silly?
You've changed your claim from "slowing/stopping evolution" to "treating the virus." Any particular reason for that?

Also, it's not my Science publication.

[kleinman]

So Delphi, why don’t you give us a quote from your Science publication that shows that multiple selection pressures for treating the virus seem silly?You've changed your claim from "slowing/stopping evolution" to "treating the virus." Any particular reason for that?
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. 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.
Also, it's not my Science publication.
That’s right, your niche is gene duplication but you still won’t tell us how the original gene appeared.

You appeared to start to understand why multiple selection pressures slow evolution. This is the very heart of the theory of evolution. Ev shows mathematically why multiple selection pressures slow this process. 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. 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? 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. 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.

[Paul C. Anagnostopoulos]

What is your problem? If you want to study the parametric behavior of ev, you go through the range of values and see what kind of curve is obtained. You don’t think a mutation rate of 1 mutation per 256 bases per generation will give mutational overload to any real living thing?
I have no idea, but we are talking about the way Ev behaves, not the way the real world behaves. At some point, mutation overload occurs. Meanwhile, generations appears to be linear with mutation rate until that point.

Alan, not only are you claiming that evolution in Ev stops dead, but then you are extrapolating this to the real world.


I’m no longer sure which experiment you are talking about. Choose a series you want to look at, (genome length, mutation rate, etc.) and we will show everyone when ev converges and when ev stops converging. Then I will show you on the case where ev does not converge, eliminating any two of the three selection conditions will allow ev to evolve that particular condition. It is the multiple conflicting selection conditions that stops ev from converging.
I'm talking about these parameters:

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

How long did you run that before you concluded that it had stopped evolving?


You appeared to start to understand why multiple selection pressures slow evolution. This is the very heart of the theory of evolution. Ev shows mathematically why multiple selection pressures slow this process.
Wait, a bit ago you were claiming that multiple pressures stop the process.

~~ Paul

[Dr Adequate]

Lie #1. Truth #1.

Come back when you have some new lies, you boring whining little freak.

[Dr Richard]

This claim is meaningless until you define macroevolution.



Good luck Paul! I suspect that this question is futile until you define goalposts

If you ever get an answer, could you then ask Kleinman whether a 491 base-pair difference between genes is a "micro-" or "macro-" evolutionary event?

http://www.genetics.org/cgi/content/abstract/175/3/1071

(In fruit flies, a wandering "selfish" gene inserted itself upstream of a gene that is able to confer resistance to insecticides such as DDT, and left behind some of itself. The residual DNA (a 491 base pair long terminal repeat) doubles the expression of said gene in tissues useful for breaking down ingested toxins (such as the gut), and perhaps not suprisingly is now the dominant allele).

[kleinman]

What is your problem? If you want to study the parametric behavior of ev, you go through the range of values and see what kind of curve is obtained. You don’t think a mutation rate of 1 mutation per 256 bases per generation will give mutational overload to any real living thing? I have no idea, but we are talking about the way Ev behaves, not the way the real world behaves. At some point, mutation overload occurs. Meanwhile, generations appears to be linear with mutation rate until that point.
Well Paul, your retreat from your previous statement is complete. Recall when you said this on http://forums.randi.org/showthread.php?t=48008&page=6 (http://forums.randi.org/showthread.php?t=48008&page=6) ?
There are plenty of examples of A-life evolving. I think Ev rankles the IDers because it is a model of actual life, and also because Schneider is fairly good at advertising it.
So how many years have you spent modeling unreality? By the way, I consider myself a creationist, maybe that is why ev doesn’t rankle me. In fact, I really enjoy this model. Do you have any other models you are planning to do, I really like your work. Talk about moving goalposts. I think you just entered one of kjkent1’s alternative universes.

You can put linear curve fits to a portion of the mutation/generation for convergence curve.
Alan, not only are you claiming that evolution in Ev stops dead, but then you are extrapolating this to the real world.
The example of the evolution of HIV drug resistance is not extrapolation. You know that ev stops dead when you reach what you call the Rcapacity value. It is very easy to show that if you remove two of the three selection conditions that the third condition will evolve despite exceeding your Rcapacity value.
I’m no longer sure which experiment you are talking about. Choose a series you want to look at, (genome length, mutation rate, etc.) and we will show everyone when ev converges and when ev stops converging. Then I will show you on the case where ev does not converge, eliminating any two of the three selection conditions will allow ev to evolve that particular condition. It is the multiple conflicting selection conditions that stops ev from converging. I'm talking about these parameters:

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

How long did you run that before you concluded that it had stopped evolving?
I stopped this case at 400,000 generations because no selection was occurring. Feel free to run this case for a longer period. I notice your case with 4 mutations/G has run 800,000 generations and appears to be converging which is ok with me because even with only 1 mutation/G, this case will evolve individual selection conditions in:
missed site/spurious binding-gene/spurious binding outside gene/gens to perfect creature
1/0/0/7
0/1/0/223
0/0/1/233
When you get your case to converge, you can do the G=64k, 128k, 256k… with three selection conditions and I’ll show how quickly the individual selection conditions converge for the cases.

When you get finished with those cases, would you do a version of ev that evolves two sets of binding sites simultaneously? Let’s see if six selection conditions can evolve simultaneously on a 256 base genome.
You appeared to start to understand why multiple selection pressures slow evolution. This is the very heart of the theory of evolution. Ev shows mathematically why multiple selection pressures slow this process. Wait, a bit ago you were claiming that multiple pressures stop the process.
The HIV case shows the slowing of evolution with multiple selection pressures. Ev shows both the slowing and ultimately the stopping of evolution with multiple selection pressures. When you do the two sets of binding sites version of ev, you can show how much more quickly evolution stops with 6 selection conditions.
This claim is meaningless until you define macroevolution. Good luck Paul! I suspect that this question is futile until you define goalposts

If you ever get an answer, could you then ask Kleinman whether a 491 base-pair difference between genes is a "micro-" or "macro-" evolutionary event?
There you go Paul, put transposons in your model and that solves your mathematical conundrum. Hey Dr Richard, when are you going to tell us how the ancestral insulin gene evolved from the beginning? Paul, maybe you should ask Dr Richard this question, it appears he is not talking with me any more. Dr Richard, I don’t care if you dropped out of Sesame Street, I’ll still talk with you.

Goalposts? Paul originally said ev models actual life, but now he says ev does not behave the way the real world behaves. Well, I told Dr Schneider that once people understood his model, they would discredit the model. Now his own programmer is doing this. Dr Schneider, I am still with you and your model.

[kjkent1]

Dr Schneider, I am still with you and your model.LOL! This is a riot. You contradict yourself in just about every other post.

I'm still trying to avoid sitting down at Dr. Adequate's table, but the only other seat available appears to be one with a view of you sitting on a bus bench wearing an aluminum hat!

I will give you this: you've managed to convince just about everyone here that ev works pretty much as advertised.

When will we see your paper rebutting ev? Certainly the Discovery Institute would pay you big bucks to publish your findings.

[kleinman]

Dr Schneider, I am still with you and your model.LOL! This is a riot. You contradict yourself in just about every other post.
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.
I will give you this: you've managed to convince just about everyone here that ev works pretty much as advertised.
You did read the fine print in the advertisement?
When will we see your paper rebutting ev? Certainly the Discovery Institute would pay you big bucks to publish your findings.
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.

[kjkent1]

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.Write a research proposal detailing your hypothesis and experiment, the resources you believe will be necessary to prove your experiment, and the rationale for why the experiment is important to the general scientific community.

Both you and Dr. Schneider must agree, in writing, that the experiment, as proposed will resolve a fundamental scientific question concerning evolutionary biology, and that you each reasonably believe that this experiment is important enough to command the attention of major scientific publications (Nature, Science, etc.).

Alternatively, you may construct and wear an aluminum hat.

[Paul C. Anagnostopoulos]

I stopped this case at 400,000 generations because no selection was occurring. Feel free to run this case for a longer period. I notice your case with 4 mutations/G has run 800,000 generations and appears to be converging ...
I think you missed the big news in post #3306:

After 1,083,137 generations, a creature with zero mistakes has emerged from the primordial depths. It has an Rsequence of 11.13, higher than the Rfrequency of 10 and lower than the Rcapacity of 12. The sequence logo is ACGACA.
So you were running an experiment that should take at least four times as long, and you quit at 400,000 generations?! From this you concluded that evolution can stop.


Ev shows both the slowing and ultimately the stopping of evolution with multiple selection pressures. [emphasis mine]
Not according to that experiment, it doesn't.

~~ Paul

[kleinman]

I stopped this case at 400,000 generations because no selection was occurring. Feel free to run this case for a longer period. I notice your case with 4 mutations/G has run 800,000 generations and appears to be converging ...I think you missed the big news in post #3306:
Well, let’s repeat that post here:
I am running the following experiment:

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

These are identical to your parameters, except for 4 mutations per generation instead of 1. This should make no difference, since your argument has nothing to do with mutation rate. After 800,000 generations the mistake count is 4. It hasn't "stopped" yet. I'll let you know if it does.Well, it doesn't. After 1,083,137 generations, a creature with zero mistakes has emerged from the primordial depths. It has an Rsequence of 11.13, higher than the Rfrequency of 10 and lower than the Rcapacity of 12. The sequence logo is ACGACA.
So with a mutation 4 times higher than I used, you can get all three selection condition to converge in a little more than a million generations. For the same length genome and a mutation rate of 1 per genome per generation you get the following:
missed site/spurious binding-gene/spurious binding outside gene/gens to perfect creature
1/0/0/7
0/1/0/223
0/0/1/233
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.
After 1,083,137 generations, a creature with zero mistakes has emerged from the primordial depths. It has an Rsequence of 11.13, higher than the Rfrequency of 10 and lower than the Rcapacity of 12. The sequence logo is ACGACA.
Were having so much fun with this, let’s do the 32k, 64k, 128k and 256k genomes. My data is for 1 mutation per 256 bases per generation for all these cases. Other parameters are the same as your case except where noted.
G /Gens PC/bind/spur gen/spur out gen
65536 /1/ 1/ 0/ 0
65536 /5/ 0/ 1/ 0
65536 /18/ 0/ 0/ 1
131072/1/ 1/ 0/ 0
131072/17/ 0/ 1/ 0
131072/27/ 0/ 0/ 1
262144/3/ 1/ 0/ 0/ pop 32
262144/1/ 0/ 1/ 0
262144/15/ 0/ 0/ 1
In order to run the 256k case, I had to reduce population to 32. I’ll let you run these cases with all three selection processes operating and you can refute my argument the evolution doesn’t stop.
So you were running an experiment that should take at least four times as long, and you quit at 400,000 generations?! From this you concluded that evolution can stop.
I’ll remember this, I won’t give up so easily next time.
Ev shows both the slowing and ultimately the stopping of evolution with multiple selection pressures. [emphasis mine] Not according to that experiment, it doesn't.
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.

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:

(4 billion years)*(365days/year)*(1 generation/day) = 1,460,000,000,000 generations.

If you want to use the reproductive rate for bacteria, feel free to run you simulation a little longer.

This is fun!

[kjkent1]

Well, let’s repeat that post here:

So with a mutation 4 times higher than I used, you can get all three selection condition to converge in a little more than a million generations. For the same length genome and a mutation rate of 1 per genome per generation you get the following:
missed site/spurious binding-gene/spurious binding outside gene/gens to perfect creature
1/0/0/7
0/1/0/223
0/0/1/233
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.

Were having so much fun with this, let’s do the 32k, 64k, 128k and 256k genomes. My data is for 1 mutation per 256 bases per generation for all these cases. Other parameters are the same as your case except where noted.
G /Gens PC/bind/spur gen/spur out gen
65536 /1/ 1/ 0/ 0
65536 /5/ 0/ 1/ 0
65536 /18/ 0/ 0/ 1
131072/1/ 1/ 0/ 0
131072/17/ 0/ 1/ 0
131072/27/ 0/ 0/ 1
262144/3/ 1/ 0/ 0/ pop 32
262144/1/ 0/ 1/ 0
262144/15/ 0/ 0/ 1
In order to run the 256k case, I had to reduce population to 32. I’ll let you run these cases with all three selection processes operating and you can refute my argument the evolution doesn’t stop.

This is fun!Yes it is fun. Observe exactly how fun this is, Alan.

The first creature appeared in the first generation, because it was first. Therefore, no selective pressures could have existed.

Your experiments confirm that the first creature could have easily appeared instantly from the primordial soup, regardless of the length of its genome, because low and behold, it routinely appears in the first generation of your ev experiments.

Congratulations Alan! You've demonstrated abiogenesis via ev.

You may now collect your Nobel Prize. Alternatively, you may construct and wear an aluminum hat.

[kleinman]

This is fun!Yes it is fun. Observe exactly how fun this is, Alan.

The first creature appeared in the first generation, because it was first. Therefore, no selective pressures could have existed.
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.

[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]

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]

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? :rolleyes:

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. :rolleyes:

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 (http://www.stellaralchemy.com/ice/) 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 (http://en.wikipedia.org/wiki/Ribozyme) 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. :D


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]

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

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

[kjkent1]

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

~~ PaulPaul,

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

[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]

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 (http://www.stellaralchemy.com/ice/) 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 (http://en.wikipedia.org/wiki/Ribozyme) 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 (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 (http://www.lecb.ncifcrf.gov/~toms/paper/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 (http://www.discovery.org/scripts/viewDB/index.php?command=view&id=51&isFellow=true).

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

A gene not need be the first thing to evolve. See the irreducible complexity evolver (http://www.stellaralchemy.com/ice/). 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 (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15130825). 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. :rolleyes:

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.



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

[quote]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.[quote]

Poor, inprecise, definition. But acceptible for now.

[quote]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? :rolleyes:

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 (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 (http://www.discovery.org/scripts/viewDB/index.php?command=view&id=51&isFellow=true).



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]

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 (http://www.stellaralchemy.com/ice/). 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 (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 (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]

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]

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 (http://en.wikipedia.org/wiki/Gut_flora), 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]

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.

[Paul C. Anagnostopoulos]

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.
Yes, I agree with that, for the specific selection pressures that Ev models. I believe "more time" covers a factor of a million.


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.
Let's run some population experiments, shall we? I'll use these parameters:

genome size 8K
binding sites 16
weight/site width 5/6
1 mutation per genome
pause on perfect creature

population, generations
64, 710152
256, 300000 (est.)

Stay tuned ...

~~ Paul

REQUEST FOR CYCLES: If anyone has a fast machine with lots of RAM, please run some large cases, for example, a population of 16,384 or 20,480. Remember, a cycle lost is gone forever.

[delphi_ote]

In a nutshell:

I can demonstrate that a process I believe to be theoretically impossible takes an implausible amount of time using a simulation I believe is totally inaccurate.

The number of levels on which this argument eats itself is just spectacular.

[kleinman]

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.Let's run some population experiments, shall we? I'll use these parameters:

genome size 8K
binding sites 16
weight/site width 5/6
1 mutation per genome
pause on perfect creature

population, generations
64, 710152
256, 300000 (est.)

Stay tuned ...
This is going to be fun. One thing Paul, with your 1 gig of memory on your machine, you are going to be limited to about 256k population but we should see a rapid drop in the slope of the generations for convergence/population curve.
REQUEST FOR CYCLES: If anyone has a fast machine with lots of RAM, please run some large cases, for example, a population of 16,384 or 20,480. Remember, a cycle lost is gone forever.
Paul, there are also memory limitations to the Java version of ev. The Pascal version of ev can run larger population cases. You also have the capability of breaking up a case into a series of shorter runs that can be restarted from a given state. This allows running a case over multiple nights for example. If I remember correctly, the 1k genome length, 1meg population case took around 300meg of memory and 100 hours of computer time on a 2.7gigaHz machine.
I can demonstrate that a process I believe to be theoretically impossible takes an implausible amount of time using a simulation I believe is totally inaccurate.
Delphi, you have demonstrated nothing. What I have demonstrated with ev is that mutation and selection becomes profoundly slow as you lengthen the genome in the model. I have also shown that increasing population decreases the generations for convergence at a rapidly decreasing rate (Paul is going to demonstrate this again with the series he is now to running). I have also shown that reducing the selection conditions in ev to one condition markedly accelerates the rate of convergence of the model. I have also given a real example where multiple selection pressures slow the evolutionary process. So unless you are going to subscribe to the view that life evolved on tiny genome creatures that no longer exist that could sustain much higher mutation rates than living things do now, and were only subject to one selection condition at a time (whatever that selection condition could be), you are done in by the mathematics of mutation and selection.
The number of levels on which this argument eats itself is just spectacular.
This mathematics is not going to disappear. You have no selection process to evolve a gene from the beginning. You have no mathematical basis for your theory. You have no chemistry to explain abiogenesis. You do have speculations, extrapolations and denial as a basis for your pseudoscience.

Hey Delphi, would you tell us how the gene came to be that you use in your gene duplication story?

[kjkent1]

This mathematics is not going to disappear. You have no selection process to evolve a gene from the beginning.False. You have proved this up yourself. With all selection conditions turned off, as they would have been before the first gene existed, a gene ab initio appears in the first generation. Must be a huge bummer to have your own proof used against you. Either your proof is irrational, or your entire theory is wrong. Good thing for you I'm giving you the benefit of the doubt, that you realize by now, that zero mistake weights in ev produce nothing but a bug. Otherwise, you would have to choose between being wrong and being wrong.You have no mathematical basis for your theory. You have no chemistry to explain abiogenesis. LOL! Riiight. See above.You do have speculations, extrapolations and denial as a basis for your pseudoscience.Let's see now. We have the theory of evolution wihch appears to answer the majority of questions about how life developed, using observations of the physical world.

Contrast that with the theory of God, which answers all questions about all subjects, using blind faith in what must, by definition, always remain unknown.

Given the two alternatives, it's no wonder that you would choose the latter.

You really must to remember to wear your aluminum hat.

[Paul C. Anagnostopoulos]

Paul, there are also memory limitations to the Java version of ev. The Pascal version of ev can run larger population cases. You also have the capability of breaking up a case into a series of shorter runs that can be restarted from a given state. This allows running a case over multiple nights for example. If I remember correctly, the 1k genome length, 1meg population case took around 300meg of memory and 100 hours of computer time on a 2.7gigaHz machine.
Great, thanks for volunteering to run the population 16,384 case.

~~ Paul

[kleinman]

Paul, there are also memory limitations to the Java version of ev. The Pascal version of ev can run larger population cases. You also have the capability of breaking up a case into a series of shorter runs that can be restarted from a given state. This allows running a case over multiple nights for example. If I remember correctly, the 1k genome length, 1meg population case took around 300meg of memory and 100 hours of computer time on a 2.7gigaHz machine.Great, thanks for volunteering to run the population 16,384 case.
There are a couple issues here Paul. The first is that a G=8192, population 16,384 case will not run in your online version of ev. Even if it could run in evjava, it would have to run continuously until converged and I can’t run my computer 24 hour a day. I’ll run this case on the Pascal version of ev but it will take me a while to get this case done.

And stop whining, all the largest population data we have I generated months ago. I sent you a compiled version of Pascal ev that would run a 2 meg population on a G=1000 and you have yet to run this case (this case requires too much memory to run on my machine).

I do commend you though because at least you are starting to look at the data from ev again.

One question for this post with respects to a comment you wrote a few posts back.
I agree that evolving a distinguishing binding site requires more time than evolving a nondistinguishing gene threshold.
Are you abandoning your Rcapacity concept?

[Paul C. Anagnostopoulos]

There are a couple issues here Paul. The first is that a G=8192, population 16,384 case will not run in your online version of ev. Even if it could run in evjava, it would have to run continuously until converged and I can’t run my computer 24 hour a day. I’ll run this case on the Pascal version of ev but it will take me a while to get this case done.
It'll run fine if you tweak your Java run-time parameters. Press the Pause button if you want to stop it for awhile. By all means, run it with the Pascal version.


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

Are you abandoning your Rcapacity concept?
All I get from this is a non sequitur.

~~ Paul

[delphi_ote]

Hey Delphi, would you tell us how the gene came to be that you use in your gene duplication story?
Can put together an argument that doesn't derive inferences from the negation of the premise? (hint: If you want to convince people that evolution is impossible, you probably shouldn't use observations of evolution happening in nature and a simulation to make your case.)

[kleinman]

I agree that evolving a distinguishing binding site requires more time than evolving a nondistinguishing gene threshold.Are you abandoning your Rcapacity concept?All I get from this is a non sequitur.
Let’s see if I can put this in sequence for you. You said the following concerning the series we had just been working on.
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.
What do you predict the number of generations for the perfect creature for the G=64k case? Binding site width is 6 for this case.
Hey Delphi, would you tell us how the gene came to be that you use in your gene duplication story?Can put together an argument that doesn't derive inferences from the negation of the premise? (hint: If you want to convince people that evolution is impossible, you probably shouldn't use observations of evolution happening in nature and a simulation to make your case.)
I have always said that microevolution occurs. It is evolutionists who extrapolate these microevolutionary processes to a macroevolutionary theory. There are no selection processes that take a series of microevolutionary processes to accomplish a macroevolutionary change. If there was, you would describe the selection process that takes a duplicated gene and transforms this gene to some totally new function. Darwin did this when he observed variations in finch beaks which is a recombination and natural selection phenomena, which is a microevolutionary process. Stephen J. Gould did this with his concept of punctuated equilibrium which he inappropriately applied to mutation and selection but does appropriately fits recombination and natural selection.

If you think the evolution of drug resistant HIV viruses is a macroevolutionary change, then I’ll have to disagree with you. The slowing of the evolution of drug resistant HIV viruses by using three selection pressures is analogous to what ev show with it’s three selection conditions. Anything more than a single selection condition profoundly slows the mutation and selection process. That is what the mathematics of ev is showing and that is what happens in reality.

Delphi, your theory of evolution is mathematically impossible.

[delphi_ote]

I have always said that microevolution occurs... Anything more than a single selection condition profoundly slows the mutation and selection process.
So adaptation occurs, but is stopped as soon as it encounters too many selection pressures, which prevents speciation? Is this your hypothesis? If so, what is the maximum number of selection pressures to which an organism can adapt? How did you arrive at this number? Can you point me to biological literature that lists this number?

[kleinman]

I have always said that microevolution occurs... Anything more than a single selection condition profoundly slows the mutation and selection process.So adaptation occurs, but is stopped as soon as it encounters too many selection pressures, which prevents speciation? Is this your hypothesis? If so, what is the maximum number of selection pressures to which an organism can adapt? How did you arrive at this number? Can you point me to biological literature that lists this number?
The use of multiple antimicrobials is not limited to the treatment of HIV. Combination antibiotics are also often used in the treatment of bacterial infections. These are the most obvious use of multiple selective pressures to prevent the evolution of drug resistant microbes.

I don’t know of any evolutionist who ever considered that multiple selection pressures would interfere with the evolutionary process. This fact only became apparent when studying the behavior of ev. When I saw this type of mathematical behavior, I started looking for real examples of this phenomena.

Perhaps evolutionists will reconsider their interpretations of their observations in the light of this mathematical finding and the real examples of this finding.

Remember, these are examples of how multiple selective pressures prevent microevolution. Macroevolution requires huge numbers of mutation and selection events. These evolutionary events would be easily confounded by multiple selection conditions. If Paul modified ev to evolve two different sets of binding sites simultaneously with six selection conditions, I would be very surprised if this model would ever converge no matter what length genome was used.

[mijopaalmc]

Please forgive if this me if this has already asked this question:

Does any one know where I can find the primary literature on Ev?

[delphi_ote]

<Text which does not answer my questions.>
That's all very interesting, but I need three one word answers and one expository answer:

1. So adaptation occurs, but is stopped as soon as it encounters too many selection pressures, which prevents speciation? Is this your hypothesis?
2. If so, what is the maximum number of selection pressures to which an organism can adapt?
3. How did you arrive at this number?
4. Can you point me to biological literature that lists this number?

[kjkent1]

Please forgive if this me if this has already asked this question:

Does any one know where I can find the primary literature on Ev?http://www.lecb.ncifcrf.gov/~toms/paper/ev/

[Taffer]

I see, as Dr. A has been saying for some time, that kleinman continues to spout what has shown to be false premises and conclusions. HIV antiretrovirals are not using to slow evolution, but to provide a broad spectrum antiviral agent which, if resistance to one or more drugs is developed, can be "hotswapped" for different antiretroviral agents without completely stopping treatment. Yet he continues to claim it is because it slows evolution. He, when asked, has failed to provide any citations nor evidence that slowing evolution is the reason for multiple antiretrovirals. He has failed to provide any citations or evidence that evolution slows down in reality. He has misinterpreted the reasons behind different results gained from ev. When this is pointed out to him, he then makes the strawman and false dichotemic argument that either ev perfectly models reality, or ev doesn't model reality at all. He then goes on to claim that anyone questioning ev is questioning its validity as a model for point mutation and natural selection in the evolution of a binding site. He continues to claim that evolution slows down, and/or stops entirely (depending on his mood), yet provides no evidence that this happens in reality. Paul has continued to bravely explain, over and over again, why kleinman's assumptions about ev are false, and why his conclusions are false. Kleinman continues to claim that ev shows that evolution is impossible, despite the fact that ev is not a model for the entire evolutionary process. He continues to ignore the entire field of population and evolutionary genetics, which clearly show why he is wrong.

In conclusion, I am forced to find that either kleinman is a liar and/or a troll, or too unable/unwilling to learn and understand his falsity to be worth interacting with.

Good day, kleinman. I may return when you have come up with some different lies.

[Dr Adequate]

Well, at least he was constructing grammatical sentences ... ... about "string cheese".

[Dr Adequate]

Lie #1. Truth #1.

[Paul C. Anagnostopoulos]

What do you predict the number of generations for the perfect creature for the G=64k case? Binding site width is 6 for this case.
Now Rfrequency = Rcapacity, so I think it will take a very long time. No idea.

~~ Paul

[Paul C. Anagnostopoulos]

If Paul modified ev to evolve two different sets of binding sites simultaneously with six selection conditions, I would be very surprised if this model would ever converge no matter what length genome was used.
The problem with this idea is that we know precisely how such a creature would converge: Both transcription factors would evolve to recognize exactly the same binding site sequence. The model would have to be much more complex to force the transcription factors to be independent. In particular the binding sites would have to control genes that performed life-sustaining functions, so that when one transcription factor started interfering with the other's binding site, selection pressure would stop it from doing so. This would allow the two transcription factors to evolve independently.

If Kleinman is correct, then no transcription factors have ever evolved. They were all poofed into existence.

~~ Paul

[kleinman]

Does any one know where I can find the primary literature on Ev?
No problem, the computer model was developed by Dr Tom Schneider, the head of computational molecular biology at the National Cancer Institute. The program can be accessed at:

http://www.ccrnp.ncifcrf.gov/~toms/paper/ev/evj/evjava/index.html (http://www.ccrnp.ncifcrf.gov/~toms/paper/ev/evj/evjava/index.html)

Dr Schneider has published this model and this paper is available on the following page:

http://www.ccrnp.ncifcrf.gov/~toms/paper/ev/ev.html

You can search around the site and find a blog page, glossary and a variety of other helpful information. The only thing lacking on these pages is any data from the model based on realistic parameters. This you can easily obtain by changing the input parameters to the model and you will find that the theory of evolution is mathematically impossible.

Paul C. Anagnostopoulos wrote the java version of ev for Dr Schneider. Paul and I have been having a friendly discussion about this model and the theory of evolution for about a year. Initially this discussion was done by email and included Dr Schneider in the discussion. I wanted to take the discussion public and started a thread on the Evolutionisdead forum http://www.evolutionisdead.com/forum/viewforum.php?f=1&sid=dab46a8a655e24347ad4f45a2efa181f (http://www.evolutionisdead.com/forum/viewforum.php?f=1&sid=dab46a8a655e24347ad4f45a2efa181f) . I chose this forum because Dr Schneider had used this forum previously to discuss his model publicly. As far as I know, other than a brief mention of me on his ev blog page, Dr Schneider has refused to talk about his model publicly since this thread was started.

Welcome to this discussion.

That's all very interesting, but I need three one word answers and one expository answer:

1. So adaptation occurs, but is stopped as soon as it encounters too many selection pressures, which prevents speciation? Is this your hypothesis?
2. If so, what is the maximum number of selection pressures to which an organism can adapt?
3. How did you arrive at this number?
4. Can you point me to biological literature that lists this number?
1. Yes, and not only do multiple selection pressures slow and ultimately stop evolution, natural selection actually impedes the transformation of genes from one to another because it prevents the gene from diverging too far from its functional form. You can counter this argument by telling us what the selection process is that would transform an existing gene from one form to another.
2. That depends on the severity of the selection pressures. A single profound selection pressure can cause extinction. When multiple non-fatal selection pressures are acting, it can vary on the severity of the selection pressures. The three drug therapy for HIV is very close to being sufficient.
3. Ev uses three selection conditions and the treatment of HIV uses three selection pressures. Both of these situations show how much only three selection conditions profoundly slow the evolutionary process.
4. I already posted the URL to the guidelines for treatment of HIV and posted a quote from these guidelines which describes why monotherapy is not used to treat this disease with the existing drugs available. That’s not to say that somebody won’t develop a single drug that puts sufficient selective pressure on the virus to make it go extinct.
In conclusion, I am forced to find that either kleinman is a liar and/or a troll, or too unable/unwilling to learn and understand his falsity to be worth interacting with.
Taffer, you are a graduate student in the theory of evolution and you don’t understand the fundamentals of your own theory. You demonstrated this when said this:
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.
Fitness is measured by the ability of a creature to reproduce. You remember “survival of the fittest”? Ev and the example of treatment of HIV both demonstrate how multiple selection pressures slow evolution. I don’t mind discussing these issues with evolutionists who don’t understand the fundamentals of their own theory.
What do you predict the number of generations for the perfect creature for the G=64k case? Binding site width is 6 for this case.Now Rfrequency = Rcapacity, so I think it will take a very long time. No idea.
Well, when you go to extrapolate the population data to genomes where Rfrequency >= Rcapacity, how do you propose to estimate the generations for convergence for these cases.

I propose that we do a series where we see if population can overcome the Rcapacity effect. The only possible cases we can run require relatively short genomes. Perhaps if we did a series with binding site width of 3 or 4 would give us short enough genomes that we can see whether larger populations will overcome the Rcapacity effect.
If Paul modified ev to evolve two different sets of binding sites simultaneously with six selection conditions, I would be very surprised if this model would ever converge no matter what length genome was used.The problem with this idea is that we know precisely how such a creature would converge: Both transcription factors would evolve to recognize exactly the same binding site sequence. The model would have to be much more complex to force the transcription factors to be independent. In particular the binding sites would have to control genes that performed life-sustaining functions, so that when one transcription factor started interfering with the other's binding site, selection pressure would stop it from doing so. This would allow the two transcription factors to evolve independently.
That’s an interesting argument, Delphi argues the exact opposite. He says that selection pressures exist that transform identical genes into different genes. You are saying that your selection conditions will evolve two identical set of binding sites.
If Kleinman is correct, then no transcription factors have ever evolved. They were all poofed into existence.
If I am correct about what ev shows and the real life example of the treatment of HIV, what I have shown is that your theory is mathematically impossible. I have said nothing about how transcriptions factors came to be, other than I’m the annoying creationist.

[Paul C. Anagnostopoulos]

Well, when you go to extrapolate the population data to genomes where Rfrequency >= Rcapacity, how do you propose to estimate the generations for convergence for these cases.
Rcapacity is not an issue in the real world. I don't propose to extrapolate such data with Ev.


I propose that we do a series where we see if population can overcome the Rcapacity effect. The only possible cases we can run require relatively short genomes. Perhaps if we did a series with binding site width of 3 or 4 would give us short enough genomes that we can see whether larger populations will overcome the Rcapacity effect.
I suspect a large enough population will overcome it. Eventually you win by sheer luck.


That’s an interesting argument, Delphi argues the exact opposite. He says that selection pressures exist that transform identical genes into different genes. You are saying that your selection conditions will evolve two identical set of binding sites.
Yes, if the selection pressures for the two transcription factors are identical, I'm guessing Ev would effectively evolve two identical genes that match twice as many binding sites. That's why I said the model would have to be more complex, with multiple conflicting pressures. Also, we would have to decide whether to let the two genes coevolve from the beginning, or let one evolve first and then model a duplication event.

~~ Paul

[Ichneumonwasp]

Why so much emphasis on HIV? Triple therapy is designed to prevent transcription, such that one escape is prevented from allowing another mechanism to take over. I don't know of any other selection pressures in nature that work like that. If we use a vertebrate example there may well be three predators trying to eat a goat but they generally do not act at precisely the same time to prevent that goat from reproducing. If the goat escapes the lion it can still have offspring before the jaguar gets it.

Triple therapy for HIV seems like an awful example of three selection pressures as they appear in the real world. Triple therapy is specifically designed. We also might find that the virus mutates to escape all three mechanisms over time. It really hasn't been that long that we have been using it.

Another issue with selection pressures in the model -- while I see that you can weight them, can you alter the weighting of the pressures at different times as the simulation is running? That would seem a more realistic model.

ETA
Technically, shouldn't we think of triple therapy for HIV not as three selection pressures, but as one very effective pressure? I mean, there are three drugs, but aren't they really all the same pressure? Or how do we define what constitutes a pressure?

[kjkent1]

Why so much emphasis on HIV?It's a red herring, thrown into the mix by kleinman to try to maintain what he already knows: multiple selective pressures on an organism create one average evolutionary result.

If the above conclusion were not true, then neither HIV nor any other organic life form could have evolved in the first place, because the same multiple selection pressures that kleinman claims cause a halt to evolution would have prevented the original evolution of HIV. After all, there were untolled natural random selective pressures acting on HIV prior to the moment that any human-created selective pressures were applied to the virus.

Where kleinman want to take you with his "logic," is that we must conclude that the HIV triple therapy conducted by humans is actually the first time multiple selective pressures were applied to the organism, BECAUSE prior to that the HIV virus was created by an "Act of God."

The problem with kleinman's logic, however, is the same as for every creationist who has or will ever live: he has only his faith to support that prior to the triple therapy, HIV was produced by God's almighty plan. There is no direct evidence in support of this conclusion, nor could such evidence ever exist, because God will not suffer being limited by the evidence of mere mortals.

So, what we have is just the same ****, different day. There is either a scientific answer to the riddle of life, or the answer is that magic rules the universe. If the former is true, then science can and eventually will resolve the gaps in evolutionary theory -- even if the final result is to invoke anthropic principle and state that, "We are here as the result of natural processes, because otherwise we would not be here to consider the question."

And, if the latter is true, then all scientific activities are a profound waste of resources, because prayer is the overwhelmingly superior solution to every human problem.

All of which causes me to wonder why kleinman bothered to go to medical school. Based on his own logic, he, and the rest of the world would be far better off without medical physicians.

[kleinman]

Well, when you go to extrapolate the population data to genomes where Rfrequency >= Rcapacity, how do you propose to estimate the generations for convergence for these cases.Rcapacity is not an issue in the real world. I don't propose to extrapolate such data with Ev.
Here is the series from which you are selecting the G=8192 for a study of population.
G / Gens for Perfect Creature
256 / 675
512 / 2,925
1024 / 10,108
2048 / 35,486
4096 / 162,892
8192 / 710,152
16384 / 6,894,433
32768 / ? (Paul’s prediction 18,000,000)
Now the increase in generations between G=8192 and G=16384 is almost a factor of 10 greater, not the factor of 3 greater that you are estimating. If the rate of increase in generations is by a factor of 10, you get the following table for the generations of convergence for larger genomes:
Genome size/generations for convergence
16k/6,000,000
32k/60,000,000
64k/600,000,000
128k/6,000,000,000
256k/60,000,000,000
512k/600,000,000,000
My, my, my. Almost 600 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/6,000,000,000,000
2048k/60,000,000,000,000
4096k/600,000,000,000,000
That’s 600 trillion generations to evolve 96 loci. Hey Dr Richard, what is your gut feeling about that number of generations. Got enough bacteria in the gut to do that? Paul, how many orders of magnitude do huge populations have to drop the generations of convergence to make your theory feasible?
I propose that we do a series where we see if population can overcome the Rcapacity effect. The only possible cases we can run require relatively short genomes. Perhaps if we did a series with binding site width of 3 or 4 would give us short enough genomes that we can see whether larger populations will overcome the Rcapacity effect.I suspect a large enough population will overcome it. Eventually you win by sheer luck.
Paul, it is your theory that depends on luck. The problem is that when you look at the mathematics of your theory, it is a really bad bet.
That’s an interesting argument, Delphi argues the exact opposite. He says that selection pressures exist that transform identical genes into different genes. You are saying that your selection conditions will evolve two identical set of binding sites.Yes, if the selection pressures for the two transcription factors are identical, I'm guessing Ev would effectively evolve two identical genes that match twice as many binding sites. That's why I said the model would have to be more complex, with multiple conflicting pressures. Also, we would have to decide whether to let the two genes coevolve from the beginning, or let one evolve first and then model a duplication event.
I understand what you are saying. It again points to a major flaw in the theory of evolution. There are no selection processes that do these things. Natural selection can only select for a given mutation at a given generation. There is no direction associated with natural selection. Dr Schneider’s selection process puts direction in the model where it does not exist in reality.
Why so much emphasis on HIV? Triple therapy is designed to prevent transcription, such that one escape is prevented from allowing another mechanism to take over. I don't know of any other selection pressures in nature that work like that. If we use a vertebrate example there may well be three predators trying to eat a goat but they generally do not act at precisely the same time to prevent that goat from reproducing. If the goat escapes the lion it can still have offspring before the jaguar gets it.
HIV treatment is an ideal example of how mutation and selection works for the very reason that three selection pressures are being applied simultaneously.
Triple therapy for HIV seems like an awful example of three selection pressures as they appear in the real world. Triple therapy is specifically designed. We also might find that the virus mutates to escape all three mechanisms over time. It really hasn't been that long that we have been using it.
It’s only an awful example if you are an evolutionist trying to argue the mathematics of mutation and natural selection. Whether the therapy is designed or induced by other environmental factors does not matter. It demonstrates mutation and selection quite well.
Another issue with selection pressures in the model -- while I see that you can weight them, can you alter the weighting of the pressures at different times as the simulation is running? That would seem a more realistic model.
I don’t believe you can alter the weights in the java version of ev during a run. I don’t know whether you can vary weights in the Pascal version of ev. If you can vary weights in the Pascal version then you should be able to vary weights during a run (unless Dr Schneider’s data checking routines prevents you from altering parameters in the middle of a run). How do you propose to vary the weights and what do you expect to achieve by this? It would be interesting to see what would happen if you sequentially set two of the three selection conditions to zero, evolve the third condition and then see if you can evolve each condition serially to make a perfect creature that satisfies all three selection conditions.
Technically, shouldn't we think of triple therapy for HIV not as three selection pressures, but as one very effective pressure? I mean, there are three drugs, but aren't they really all the same pressure? Or how do we define what constitutes a pressure?
No, the drugs target different sites.
Why so much emphasis on HIV?It's a red herring, thrown into the mix by kleinman to try to maintain what he already knows: multiple selective pressures on an organism create one average evolutionary result.
Red herring goes much better with string cheese and whine.

[Paul C. Anagnostopoulos]

Now the increase in generations between G=8192 and G=16384 is almost a factor of 10 greater, not the factor of 3 greater that you are estimating.
Why would you use just the last two points to determine the rate of increase? Especially when you're so concerned about extrapolating at all. Those points fit gens = .004 G^2.13 with r=0.996. For G=32768, it gives 16.6 million generations.


I understand what you are saying. It again points to a major flaw in the theory of evolution. There are no selection processes that do these things.
What things? Provide conflicting selection pressures? Isn't that your current goalpost theory on why evolution doesn't work?

~~ Paul

[Ichneumonwasp]

It’s only an awful example if you are an evolutionist trying to argue the mathematics of mutation and natural selection. Whether the therapy is designed or induced by other environmental factors does not matter. It demonstrates mutation and selection quite well.


I'm not so sure about "quite well". Perhaps you have other examples similar to this. I can't think of any other situation outside of multiple drug cocktails for other infectious diseases in which selection pressures in nature attack the same basic mechanism. How does this mimic what we would have seen in nature during the early development of genetic material?

I suppose you could argue that the combos using 2 transcription inhibitors and the protease inhibitor hit distinctly different targets, but the triple reverse transcriptases essentially hit the same mechanism, though in slightly different ways and at slightly different sites. What exactly does this model in nature?

A better example, I think, of HIV and multiple selection pressures would be the way AIDS used to act in the 80's and early 90's and the introduction of the early drugs we used to treat the disease. We kept a few people alive a bit longer with Pneumocystis protocols, treated some with steroids, began using AZT, etc. AIDS patients died quickly back then, some very quickly. It was a very different virus only 30 years ago.

I don’t believe you can alter the weights in the java version of ev during a run. I don’t know whether you can vary weights in the Pascal version of ev. If you can vary weights in the Pascal version then you should be able to vary weights during a run (unless Dr Schneider’s data checking routines prevents you from altering parameters in the middle of a run). How do you propose to vary the weights and what do you expect to achieve by this? It would be interesting to see what would happen if you sequentially set two of the three selection conditions to zero, evolve the third condition and then see if you can evolve each condition serially to make a perfect creature that satisfies all three selection conditions.

Oh, well, just thought I'd ask. This seems like a serious limitation of the program, since having three selection pressures produce the same effect without change over the course of numerous generations, even with the ability to weight them, does not approximate real world conditions. Are there any plans to change the code and make a variable feature available?

No, the drugs target different sites.


Yes, I'm aware of the drugs and their mechanisms. But "different sites" can be taken specifically or generally. In general, the reverse transcriptases act in very similar ways. Technically, yes, they target different sites. I suppose it depends on exactly how we define "differing selection pressures". If we define it in this narrow sense, then that's OK with me.

[kleinman]

Now the increase in generations between G=8192 and G=16384 is almost a factor of 10 greater, not the factor of 3 greater that you are estimating.Why would you use just the last two points to determine the rate of increase? Especially when you're so concerned about extrapolating at all. Those points fit gens = .004 G^2.13 with r=0.996. For G=32768, it gives 16.6 million generations.
Paul, when have any of your curve fits to data from ev been useful for extrapolation? If you are so sure that your estimate is correct, run the 32k case and see what you get.
I understand what you are saying. It again points to a major flaw in the theory of evolution. There are no selection processes that do these things.What things? Provide conflicting selection pressures? Isn't that your current goalpost theory on why evolution doesn't work?
Dr Schneider’s selection conditions are a contrivance that does not occur in reality. Binding sites don’t evolve this way genes don’t evolve this way, none of these things evolve this way. What Dr Schneider’s selection conditions are useful for is demonstrating the mathematics of mutation and selection which shows your theory is mathematically impossible.

Haven’t you learned yet that the moving goalpost defense doesn’t work. Try kjkent1’s red herring, string cheese and whine defense. It’s a hearty meal fit for any evolutionist.
It’s only an awful example if you are an evolutionist trying to argue the mathematics of mutation and natural selection. Whether the therapy is designed or induced by other environmental factors does not matter. It demonstrates mutation and selection quite well.I'm not so sure about "quite well". Perhaps you have other examples similar to this. I can't think of any other situation outside of multiple drug cocktails for other infectious diseases in which selection pressures in nature attack the same basic mechanism. How does this mimic what we would have seen in nature during the early development of genetic material?
Other examples of multiple selective pressures can be seen when essential nutrients are missing from the diet, or combinations of environmental stresses and so on. But none are so nicely delineated as the effects of antimicrobials on microbes.
I suppose you could argue that the combos using 2 transcription inhibitors and the protease inhibitor hit distinctly different targets, but the triple reverse transcriptases essentially hit the same mechanism, though in slightly different ways and at slightly different sites. What exactly does this model in nature?
This is exactly what happens in nature. The mold that produces penicillin target the bacteria’s ability to crosslink proteins in cell walls. Many antimicrobials are based on chemicals found in living things which specifically target a step in the metabolic pathway of a microbe.
A better example, I think, of HIV and multiple selection pressures would be the way AIDS used to act in the 80's and early 90's and the introduction of the early drugs we used to treat the disease. We kept a few people alive a bit longer with Pneumocystis protocols, treated some with steroids, began using AZT, etc. AIDS patients died quickly back then, some very quickly. It was a very different virus only 30 years ago.
That early strategies had no way of applying selective pressure on the HIV virus itself. These strategies attempted to deal with the secondary consequences of a failing immune system.
I don’t believe you can alter the weights in the java version of ev during a run. I don’t know whether you can vary weights in the Pascal version of ev. If you can vary weights in the Pascal version then you should be able to vary weights during a run (unless Dr Schneider’s data checking routines prevents you from altering parameters in the middle of a run). How do you propose to vary the weights and what do you expect to achieve by this? It would be interesting to see what would happen if you sequentially set two of the three selection conditions to zero, evolve the third condition and then see if you can evolve each condition serially to make a perfect creature that satisfies all three selection conditions.Oh, well, just thought I'd ask. This seems like a serious limitation of the program, since having three selection pressures produce the same effect without change over the course of numerous generations, even with the ability to weight them, does not approximate real world conditions. Are there any plans to change the code and make a variable feature available?
Ask Paul, if you can make a good case that you will improve the rate of convergence of ev, he may do it.
No, the drugs target different sites.Yes, I'm aware of the drugs and their mechanisms. But "different sites" can be taken specifically or generally. In general, the reverse transcriptases act in very similar ways. Technically, yes, they target different sites. I suppose it depends on exactly how we define "differing selection pressures". If we define it in this narrow sense, then that's OK with me.
If the drug is selecting for a different mutation at a different locus, it is a different selection pressure. That is not a narrow definition.

[Ichneumonwasp]

Other examples of multiple selective pressures can be seen when essential nutrients are missing from the diet, or combinations of environmental stresses and so on. But none are so nicely delineated as the effects of antimicrobials on microbes.


You have well-described examples of three nutrients missing at the same time from the diet of organisms? OK, I'd love to hear about them. But that isn't what I asked. I asked about nature generally hitting organisms with three selection pressures on the same system at the same time. What examples do you have of that if this is such a terrific example of multiple selection pressures? Since you seem so convinced that this is a terrific example to exploit I assume that you have others to back that claim. Otherwise, I must conclude that this example is extraordinarily artificial and does not mimic the reality of selection pressures in the wild.

This is exactly what happens in nature. The mold that produces penicillin target the bacteria’s ability to crosslink proteins in cell walls. Many antimicrobials are based on chemicals found in living things which specifically target a step in the metabolic pathway of a microbe.


I know how antimicrobials work (well, most of them, since I don't keep up with the latest ones unless I have a need), but, again, this is not what I was asking. You are arguing that triple therapy's effect on HIV mimics multiple selection pressures as we would have seen in real world. I question this. At the bare minimum we are speaking of more than three selection pressures on HIV because there are other host effects that act as selection pressures as well -- the rapidity or slowness of death; the effect of disease on transmission possibilities, etc. There are probably twenty or so selection pressures operative on that virus when it infects a host and the host is treated. So, at a bare minimum, your proposal that this mimics what you see in the computer is simply wrong.

The other issue, which you still have not addressed, is that the triple therapy programs that we use all target one or, at most, two systems in the virus. Other approaches are being addressed, but we have a situation with triple therapy in which the first transcription inhibitor may not work, but the next will for any given clone. How is that applicable to the real world? Is the proper example an organism that lacks glucose and iron and lactose all at the same time? Such an organism would die. Those are very profound selection pressures. They do not mimic the real world types of selection pressures that I would want to see modelled. But that is essentially what we get with HIV triple therapy.

That early strategies had no way of applying selective pressure on the HIV virus itself. These strategies attempted to deal with the secondary consequences of a failing immune system.


What? What exactly, then, is the definition of "selection pressure"? Several of those strategies worked by keeping people alive longer. Longer survival means more chance to spread infection. The rapid deaths of folks who initially contracted the infection was itself a selection pressure. The virulence of this agent is not the same as it was back then. Yes, it took years for the clinical manifestations to show, but, once present, people died quickly. This was largely due to the fact that we didn't know the best ways to care for them, but by the late 80s we had a pretty good idea what to do in most cases. Folks still died quickly. People with the virus today who opt out of treatment or who stop because they want to hasten the end do not die as quickly as they did in the past with the same range of CD4 counts (and this is not all due to improved medical care). This is simply a different form of virus now than in the late 80s and early 90s.

Ask Paul, if you can make a good case that you will improve the rate of convergence of ev, he may do it.


Why would we want anyone to design a program with a set outcome? I would like to see it simply because it would more closely mimic the natural world.

If the drug is selecting for a different mutation at a different locus, it is a different selection pressure. That is not a narrow definition.

OK, that's fine if you wish to define things in that way. But you must then admit that HIV has many more than three selection pressures when it invades a host who is treated with triple therapy.

[Paul C. Anagnostopoulos]

Oh, well, just thought I'd ask. This seems like a serious limitation of the program, since having three selection pressures produce the same effect without change over the course of numerous generations, even with the ability to weight them, does not approximate real world conditions. Are there any plans to change the code and make a variable feature available?
No such plans. The purpose of Ev is to show information increase as a result of evolution.

~~ Paul

[kleinman]

Other examples of multiple selective pressures can be seen when essential nutrients are missing from the diet, or combinations of environmental stresses and so on. But none are so nicely delineated as the effects of antimicrobials on microbes.You have well-described examples of three nutrients missing at the same time from the diet of organisms? OK, I'd love to hear about them. But that isn't what I asked. I asked about nature generally hitting organisms with three selection pressures on the same system at the same time. What examples do you have of that if this is such a terrific example of multiple selection pressures? Since you seem so convinced that this is a terrific example to exploit I assume that you have others to back that claim. Otherwise, I must conclude that this example is extraordinarily artificial and does not mimic the reality of selection pressures in the wild.
Examples of nutrient deficiencies are so commonplace that I didn’t think I had to give any examples. In humans, multiple nutrient deficiencies are very common, for example in alcoholism, starvation, fad dieting and so on. Dietary nutrient deficiencies also occur in the wild.

So, you are taking the position that only a single selection condition drives evolution at any given moment. Do you want to describe to us what the selection condition that evolves a gene from the beginning?
This is exactly what happens in nature. The mold that produces penicillin target the bacteria’s ability to crosslink proteins in cell walls. Many antimicrobials are based on chemicals found in living things which specifically target a step in the metabolic pathway of a microbe.I know how antimicrobials work, but, again, this is not what I was asking. You are arguing that triple therapy's effect on HIV mimics multiple selection pressures as we would have seen in real world. I question this. At the bare minimum we are speaking of more than three selection pressures on HIV because there are other host effects that act as selection pressures as well -- the rapidity or slowness of death; the effect of disease on transmission possibilities, etc. There are probably twenty or so selection pressures operative on that virus when it infects a host and the host is treated. So, at a bare minimum, your proposal that this mimics what you see in the computer is simply wrong.
You are correct that there are more than three selection pressures when using three antiretroviral medicines simultaneously. You have the person’s immune system which if given time will also mount a response to the virus. There are even rare cases of individuals who are infected with HIV and get no immune suppression but the vast majority of people infected with HIV rapidly proceed to AIDS if not given antiretroviral medications despite the twenty or so selection pressures that you postulate.
The other issue, which you still have not addressed, is that the triple therapy programs that we use all target one or, at most, two systems in the virus. Other approaches are being addressed, but we have a situation with triple therapy in which the first transcription factor may not work, but the next will for any given clone. How is that applicable to the real world? Is the proper example an organism that lacks glucose and iron and lactose all at the same time? Such an organism would die. Those are very profound selection pressures. They do not mimic the real world types of selection pressures that I would want to see modelled. But that is essentially what we get with HIV triple therapy.
Just because antiretroviral drugs primarily target reverse transcriptase does not mean that each drug works in the same way. Ultimately, the strategy for the using multiple drugs is to slow the reproduction of the virus and minimize the appearance of drug resistant strains of the virus.

So tell us, what was the selection pressure that gives rise to the hemoglobin gene and molecule? If it is as Paul previously suggested, the presence of oxygen in the atmosphere, describe that selection pressure so that it can be put in ev and evolve the hemoglobin gene.
That early strategies had no way of applying selective pressure on the HIV virus itself. These strategies attempted to deal with the secondary consequences of a failing immune system.What? What exactly, then, is the definition of "selection pressure"? Several of those strategies worked by keeping people alive longer. Longer survival means more chance to spread infection. The rapid deaths of folks who initially contracted the infection was itself a selection pressure. The virulence of this agent is not the same as it was back then. Yes, it took years for the clinical manifestations to show, but, once present, people died quickly. This was largely due to the fact that we didn't know the best ways to care for them, but by the late 80s we had a pretty good idea what to do in most cases. Folks still died quickly. People with the virus today who opt out of treatment or who stop because they want to hasten the end do not die as quickly as they did in the past with the same range of CD4 counts (and this is not all due to improved medical care). This is simply a different form of virus now than in the late 80s and early 90s.
It is the secondary infection that usually kills the person infected with HIV so treating the secondary infection prolonged life slightly. It wasn’t until combination therapy was introduced that real selective pressure was put on the virus (unless you count the 20 or so selective pressures you speculate are placed on the virus by the person’s own immune system). This selective pressure has altered the HIV virus. Mutated HIV reproduces at a slow rate than the wild virus.
Ask Paul, if you can make a good case that you will improve the rate of convergence of ev, he may do it.Why would we want anyone to design a program with a set outcome? I would like to see it simply because it would more closely mimic the natural world.
You asked, I told you could do this. I doubt Paul wants to do any more programming on the theory of evolution. He knows I will co-opt his work.
If the drug is selecting for a different mutation at a different locus, it is a different selection pressure. That is not a narrow definition.OK, that's fine if you wish to define things in that way. But you must then admit that HIV has many more than three selection pressures when it invades a host who is treated with triple therapy.
It’s not the way I define it, it is the way reality works. Certainly there is an immune response to the virus, antibodies to the virus are detected. However, this immune response is almost universally ineffective. Once the retroviral therapy is initiated, it would not surprise me that the person’s own immune system contributes to the suppression of the virus.

[kleinman]

I told you Ichneumonwasp, Paul has no interest in doing any more mathematical modeling of the theory of evolution. He is still trying to extract himself out of the quicksand that ev has put him into.

[Paul C. Anagnostopoulos]

Paul, when have any of your curve fits to data from ev been useful for extrapolation? If you are so sure that your estimate is correct, run the 32k case and see what you get.
If you won't extrapolate, then your entire thesis is a load of crap. Notice how you've drawn conclusions about real life by extrapolating from Ev.


Dr Schneider’s selection conditions are a contrivance that does not occur in reality.
Then why are you drawing any conclusions whatsoever about real life?


Binding sites don’t evolve this way genes don’t evolve this way, none of these things evolve this way. What Dr Schneider’s selection conditions are useful for is demonstrating the mathematics of mutation and selection which shows your theory is mathematically impossible.
You just ate your entire thesis with those two sentences.

Not only is it time for new lies, it's time for a new dance routine.

~~ Paul

[Paul C. Anagnostopoulos]

Paul, when have any of your curve fits to data from ev been useful for extrapolation? If you are so sure that your estimate is correct, run the 32k case and see what you get.
Remember when we were running the population experiment with the genome size 1024? After running populations from 4 through 65,536, I extrapolated a population of 92,680 and estimated 702 generations. It took 718. I extrapolated a population of 1,000,000 and estimated 273 generations. You ran that case and it took 438. Not bad, huh?

It will never be perfect, because we know there is significant variance in the number of generations given different random number seeds.

~~ Paul

[kleinman]

Paul, when have any of your curve fits to data from ev been useful for extrapolation? If you are so sure that your estimate is correct, run the 32k case and see what you get. If you won't extrapolate, then your entire thesis is a load of crap. Notice how you've drawn conclusions about real life by extrapolating from Ev.
Paul, I said your extrapolations have never been useful. If you look at my earliest extrapolations done on the Evolutionisdead forum, they are still valid.
Dr Schneider’s selection conditions are a contrivance that does not occur in reality.Then why are you drawing any conclusions whatsoever about real life?
Just because Dr Schneider’s selection process is a contrivance does not mean that you can’t learn something about the mathematics of mutation and selection. In reality, evolution would proceed far more slowly than what ev shows because there are no selection processes that can evolve genes from the beginning or transform genes from one form to another. Dr Schneider’s model gives an upper limit on the rate at which information could be gained.
Binding sites don’t evolve this way genes don’t evolve this way, none of these things evolve this way. What Dr Schneider’s selection conditions are useful for is demonstrating the mathematics of mutation and selection which shows your theory is mathematically impossible.You just ate your entire thesis with those two sentences.
You wish these sentences ate my thesis. Mathematical modeling is often time used to define limits on physical processes. Ev show that even with a contrive selection process, evolution proceeds far too slowly to be mathematically possible. Without a real selection process, evolution does not proceed at all. You ready to tell us the selection process that would evolve a gene from the beginning?
Not only is it time for new lies, it's time for a new dance routine.
We have all kinds of new dance routines from you. Your dance routine started with ev representing reality, to ev representing a small portion of the evolutionary landscape, to ev is a stylized model of mutation and selection.

Sorry to bore you guy but I am doing the same old routine, ev shows that the theory of evolution is mathematically impossible. The reason why this routine works is that it is true.

By the way, how is your population series coming? The generations for convergence/population curve dropping off rapidly? Every series I have done does this.
Paul, when have any of your curve fits to data from ev been useful for extrapolation? If you are so sure that your estimate is correct, run the 32k case and see what you get.Remember when we were running the population experiment with the genome size 1024? After running populations from 4 through 65,536, I extrapolated a population of 92,680 and estimated 702 generations. It took 718. I extrapolated a population of 1,000,000 and estimated 273 generations. You ran that case and it took 438. Not bad, huh?
I guess you consider to be in error by 50% as a good extrapolation especially since the generations for convergence/population curve appears to be approaching an asymoptote.
It will never be perfect, because we know there is significant variance in the number of generations given different random number seeds.
So do you think that your estimate in the following case is going to be accurate?
G / Gens for Perfect Creature
256 / 675
512 / 2,925
1024 / 10,108
2048 / 35,486
4096 / 162,892
8192 / 710,152
16384 / 6,894,433
32768 / ? (Paul’s prediction 18,000,000)
It sure looks like the slope of this curve is increasing much more rapidly than the curve fit you used. Between G=4096 and G=8192, the generations for convergence has gone up by a factor of greater than 4. Between G=8192 and G=16384, the generations for convergence increases by almost a factor of 10. Your curve fit has missed the trends in this data if you think that the next increase in the generations for converges goes by a factor of 2.6.

[Paul C. Anagnostopoulos]

Paul, I said your extrapolations have never been useful. If you look at my earliest extrapolations done on the Evolutionisdead forum, they are still valid.
Aha, it's just me. Got it.


You wish these sentences ate my thesis. Mathematical modeling is often time used to define limits on physical processes. Ev show that even with a contrive selection process, evolution proceeds far too slowly to be mathematically possible. Without a real selection process, evolution does not proceed at all. You ready to tell us the selection process that would evolve a gene from the beginning?
You're still eating yourself.


I guess you consider to be in error by 50% as a good extrapolation especially since the generations for convergence/population curve appears to be approaching an asymoptote.
Yes, since the variance in number of generations from one random seed to another is sometimes 100% or more, I'd say that was a pretty good estimate. There is an asymptote: 0. It is possible that a randomly-generated genome could be perfect immediately.


So do you think that your estimate in the following case is going to be accurate?
Don't know. I'm not planning on running the 32K case. Either are you. You'll just have to base your mathematical rejection of evolution on guesses.

~~ Paul

[kjkent1]

Dr Schneider’s selection conditions are a contrivance that does not occur in reality. Binding sites don’t evolve this way genes don’t evolve this way, none of these things evolve this way. What Dr Schneider’s selection conditions are useful for is demonstrating the mathematics of mutation and selection which shows your theory is mathematically impossible.This is really funny material, Alan! Earlier in the thread you stated that you don't know if Rfreq's convergence to Rseq is a real measurement or merely a "coincidence." Now you are claiming that ev's selection conditions are contrived and that niether binding sites nor genes evolve in the manner that ev proposes.

This raises the issue of why you would argue that ev proves or disproves anything, as you are now claiming that nothing that ev simulates has anything to do with reality.

If ev doesn't model evolutionary processes, then you cannot rationally conclude that evolution is mathematically impossible based upon what ev models, because in your view, ev doesn't model evolution.

Why don't you just be honest with everyone. Your entire argument is nothing more than: evolution is false because if it's true, then Jesus was just a nice guy.

[kleinman]

Paul, I said your extrapolations have never been useful. If you look at my earliest extrapolations done on the Evolutionisdead forum, they are still valid.Aha, it's just me. Got it.
G / Gens for Perfect Creature
256 / 675
512 / 2,925
1024 / 10,108
2048 / 35,486
4096 / 162,892
8192 / 710,152
16384 / 6,894,433
32768 / ? (Paul’s prediction 18,000,000)
Do the 32k case in this series and prove me wrong.
You wish these sentences ate my thesis. Mathematical modeling is often time used to define limits on physical processes. Ev show that even with a contrive selection process, evolution proceeds far too slowly to be mathematically possible. Without a real selection process, evolution does not proceed at all. You ready to tell us the selection process that would evolve a gene from the beginning? You're still eating yourself.
Paul, it is you evolutionists who are the cannibals. I told Dr Schneider once it was revealed what his model really showed, his work would be discredited. That’s what has happened in this thread. His model even has been attributed to me.

So tell us, does Dr Schneider still say that his model simulates reality?
I guess you consider to be in error by 50% as a good extrapolation especially since the generations for convergence/population curve appears to be approaching an asymoptote. Yes, since the variance in number of generations from one random seed to another is sometimes 100% or more, I'd say that was a pretty good estimate. There is an asymptote: 0. It is possible that a randomly-generated genome could be perfect immediately.
So, do you still believe that Dr Schneider’s model shows how a human genome could evolve in a billion years give or take a 100% or more? (Let’s not forget world wide populations, interspecies gene transfers and panspermia.)
So do you think that your estimate in the following case is going to be accurate? Don't know. I'm not planning on running the 32K case. Either are you. You'll just have to base your mathematical rejection of evolution on guesses.
How do you know whether I am planning to run this 32k case? Let’s see, your guess is 18,000,000 generations and my guess is 60,000,000 generations. I’m starting to think this is a good case to run. I’ll have to do this one with the Pascal version of ev. It will probably take about 3 or 4 weeks to run, maybe more since I won’t be able to run the case every day. It would be fun to post intermediate results, kind of like a horse race.

[delphi_ote]

a single profound selection pressure can cause extinction
Evidence contrary to your thesis that the number of selection pressures imposes a limit on evolution by natural selection..
Ev uses three selection conditions and the treatment of HIV uses three selection pressures. Both of these situations show how much only three selection conditions profoundly slow the evolutionary process.
Every triangle has three corners,
Every triangle has three sides,
No more, no less.
You don't have to guess.
When it's three you can see
It's a magic number.
I already posted the URL to the guidelines for treatment of HIV and posted a quote from these guidelines which describes why monotherapy is not used to treat this disease with the existing drugs available.
Which is not what I asked for: a scientific biological source claiming there is a limit on the number of selection pressures to which an organism can adapt through natural selection.

[Ichneumonwasp]

Examples of nutrient deficiencies are so commonplace that I didn’t think I had to give any examples. In humans, multiple nutrient deficiencies are very common, for example in alcoholism, starvation, fad dieting and so on. Dietary nutrient deficiencies also occur in the wild.


And these somehow limit evolution? How? Your argument was that these multiple pressures limit or eliminate evolution, was it not?

I've seen plenty of multiple minor deficiencies. They tend to do fairly little clinically, but may have effects on reproduction (obviously important for the evolutionary process). I've seen plenty of multiple major deficiencies. They tend to do one thing -- lead to death. Death seems to me to be a very big part of evolution. Those who do survive the process of these multiple deficiencies tend to do so for only one reason -- variability or new mutation that allows them to survive. Funny, that.

So, you are taking the position that only a single selection condition drives evolution at any given moment. Do you want to describe to us what the selection condition that evolves a gene from the beginning?


OK, I'll spell it out.......what you are describing with the antiretrovirals are selection pressures that tend to lead to the death of species. The pressures are immense for this particular virus. The fact that they work tells us something important -- that we have found a significantly profound pressure that has beaten back this virus somewhat. If you provide significant enough pressures you can kill or beat back anything. The number of pressures is not necessarily the magic ingredient. If we have a bacterium that uses glucose but has a pathway that can activate galactose metabolism, then the absence of glucose will not kill it. But if we remove glucose and galactose then the bacterium is in serious trouble and will likely go extinct unless there is a variant that uses another food source and takes over. If we have a bacterium that will not produce quite as many offspring if glucose is not present and not as many offspring if galactose is not present, then this will not be absolutely fatal, even in the presence of both deficiencies. It is likely that some variant will arise in that situation to use another energy source eventually though. Of course this process will take longer than the deficiencies that tend to be fatal. While multiple pressures may be fatal or severely limiting, other variants of different types of pressures will not. It depends critically on the type of pressures involved. Concentrating on the number and thinking of it magically is silly. These pressures are generally not absolute -- we see relative deficiences of certain foodstuffs rather than complete deficiences. The situation with multiple reverse trancscriptase inhibitors is most akin to a complete or near complete deficiency of some resource that keeps the organism near the brink of extinction. Or, rather, it is like a severe hit on the gonads of any vertebrate -- eliminate the possibility of reproduction. This should eradicate the organism, but it hasn't in this case (damn retroviruses). HIV is a special case in many respects. I don't think you can draw many conclusions from the type of pressure being placed on this virus except that if you slow reproduction, then you slow reproduction. I see nothing that tells me that other pressures would have the same effect.

And, no, I have no number of selection pressures in mind. I don't think it even makes sense to think that way as an absolute. There were undoubtedly times when one pressure for early organisms was important and other times when multiple pressures came into play.

Just because antiretroviral drugs primarily target reverse transcriptase does not mean that each drug works in the same way. Ultimately, the strategy for the using multiple drugs is to slow the reproduction of the virus and minimize the appearance of drug resistant strains of the virus.


Um, yes, in the broad sense it does. That is what we mean when we use the term "mechanism of action". They all target the same enzyme system. They have different sites of action, so one drug may continue to work when resistance to the others forms. Eventually this will mean that none of these drugs will work. Eventually the virus is going to win. We already know it will win. It's beginning to win already.

So tell us, what was the selection pressure that gives rise to the hemoglobin gene and molecule? If it is as Paul previously suggested, the presence of oxygen in the atmosphere, describe that selection pressure so that it can be put in ev and evolve the hemoglobin gene.

I'm sorry, but what does this have to do with anything I have said or your use of HIV as the example par excellence? I do not pretend to knowledge that I do not have. I would need to study the problem before even beginning to suggest alternatives. I do not know the history of the molecule and its progenitors well enough to say.

It is the secondary infection that usually kills the person infected with HIV so treating the secondary infection prolonged life slightly. It wasn’t until combination therapy was introduced that real selective pressure was put on the virus (unless you count the 20 or so selective pressures you speculate are placed on the virus by the person’s own immune system). This selective pressure has altered the HIV virus. Mutated HIV reproduces at a slow rate than the wild virus.


I know the history, I watched it happen. Support for the secondary infections initially prolonged life only for short periods of time. As time progressed and before triple therapy was begun people were already living longer. The virus was already becoming less virulent before triple therapy was introduced. It mutated because it killed people too fast and less virulent strains were able to be transmitted to others. AZT caused a huge pressure on the virus to mutate. That pressure alone resulted in big changes, not all of which have or can be quantified. Triple therapy has produced changes as well. It continues to do so. Evolution has stopped, though?

It’s not the way I define it, it is the way reality works. Certainly there is an immune response to the virus, antibodies to the virus are detected. However, this immune response is almost universally ineffective. Once the retroviral therapy is initiated, it would not surprise me that the person’s own immune system contributes to the suppression of the virus.

I'm sorry again, but I cannot understand what would possess anyone to think that the immune response is the only host reaction to the presence of the virus and the only selection pressure.

Bottom line........HIV is a bad example.

[delphi_ote]

He says that selection pressures exist that transform identical genes into different genes.
When one gene is performing a function, it is under selection pressure not to adapt to another function. An unused duplicate copy of that gene, on the other hand, is free to adapt to some other function.

If, however, having two copies of the same gene is more beneficial than one, the duplicate copy is not likely to adapt to a new use. The second copy is then under selection pressure to perform the same function as the original gene! I know for a fact there are tandem duplicates of tRNA genes in populus trichocarpa and arabidopsis thaliana that maintain their original function for exactly this reason.

[kjkent1]

Paul, it is you evolutionists who are the cannibals. I told Dr Schneider once it was revealed what his model really showed, his work would be discredited. That’s what has happened in this thread. His model even has been attributed to me.

So tell us, does Dr Schneider still say that his model simulates reality?Thus far, after 100s of posts, the only thing that you've credibly demonstrated, is that you don't know a for-next loop from a fruit loop.

[delphi_ote]

Thus far, after 100s of posts, the only thing that you've credibly demonstrated, is that you don't know a for-next loop from a fruit loop.
http://i71.photobucket.com/albums/i133/delphi_ote/awinnerisyou-37081.jpg

[kleinman]

a single profound selection pressure can cause extinctionEvidence contrary to your thesis that the number of selection pressures imposes a limit on evolution by natural selection..
Really? A single fatal selection pressure precludes multiple non-fatal selection pressures from slowing evolution? Then explain why the emergence of drug resistance HIV is slowed when multiple drug therapy is used.
Ev uses three selection conditions and the treatment of HIV uses three selection pressures. Both of these situations show how much only three selection conditions profoundly slow the evolutionary process.Every triangle has three corners,
Every triangle has three sides,
No more, no less.
You don't have to guess.
When it's three you can see
It's a magic number.
Oh no, three is not a magic number, four selection pressures will slow evolution even further, five more so… It shows that only as few as three selection pressures slow evolution profoundly. Only a single selection condition evolves quickly in ev. Monotherapy quickly leads to strains of HIV resistant to that strain.
I already posted the URL to the guidelines for treatment of HIV and posted a quote from these guidelines which describes why monotherapy is not used to treat this disease with the existing drugs available. Which is not what I asked for: a scientific biological source claiming there is a limit on the number of selection pressures to which an organism can adapt through natural selection.
Ev shows this, the guidelines for the treatment of HIV shows this. What evolutionist publication has ever considered that selection pressures actually slow evolution? This is a mathematical fact. Evolutionist have assumed that there is no limit to what natural selection can do. Ev and the HIV treatment strategy plainly demonstrate this phenomena. One from a mathematical viewpoint and the other from a clinical medical view point. Next time you publish in Science you can publish this finding.
Examples of nutrient deficiencies are so commonplace that I didn’t think I had to give any examples. In humans, multiple nutrient deficiencies are very common, for example in alcoholism, starvation, fad dieting and so on. Dietary nutrient deficiencies also occur in the wild. And these somehow limit evolution? How? Your argument was that these multiple pressures limit evolution, was it not?

I've seen plenty of multiple minor deficiencies. They tend to do fairly little clinically, but may have effects on reproduction. I've seen plenty of multiple major deficiencies. They tend to do one thing -- lead to death. Death seems to me to be a very big part of evolution. Those who do survive the process of these multiple deficiencies tend to do so for only one reason -- variability or new mutation that allows them to survive. Funny, that.
Another evolutionist who doesn’t realize his own theory measures fitness by the ability to reproduce.
So, you are taking the position that only a single selection condition drives evolution at any given moment. Do you want to describe to us what the selection condition that evolves a gene from the beginning?OK, I'll spell it out.......what you are describing with the antiretrovirals are selection pressures that tend to lead to the death of organisms. The fact that HIV is still around should be telling you the exact opposite of what you think it does. These pressures are immense for this particular virus. The fact that they work tells us something important -- that we have found a significantly profound pressure that has beaten back this virus somewhat. If you provide significant enough pressures you can kill or beat back anything. The number of pressures is not necessarily the magic ingredient. If we have a bacterium that uses glucose but has a pathway that can activate galactose metabolism, then the absence of glucose will not kill it. But if we remove glucose and galactose then the bacterium is in serious trouble and will likely go extinct. If we have a bacterium that will not produce quite as many offspring if glucose is not present and not as many offspring if galactose is not present, then this will not be absolutely fatal, even in the presence of both deficiencies. It is likely that some variant will arise in that situation to use another energy source eventually though. While multiple pressures may be fatal or severely limiting, other variants of different types of pressures will not. It depends critically on the type of pressures involved. Concentrating on the number and thinking of it magically is silly.
None of the treatments for HIV lead to death of the virus, these treatments only limit reproduction of the virus. So why don’t you tell us what the selection pressure is that evolves a gene from the beginning. I keep asking this question of you evolutionists and you never answer it.
And, no, I have no number of selection pressures in mind. I don't think it even makes sense to think that way as an absolute. There were undoubtedly times when one pressure for early organisms was important and other times when multiple pressures came into play.
What you don’t seem to realize is that multiple selection conditions even if not fatal confound the evolutionary process. In a simple sense, what happens if you get a beneficial mutation for one selection condition and a harmful mutation for another selection condition on the same creature. Is that creature selected for or selected against? What happens when you have numerous selection conditions? Ev shows this mathematically. Evolution becomes profoundly slow.
Just because antiretroviral drugs primarily target reverse transcriptase does not mean that each drug works in the same way. Ultimately, the strategy for the using multiple drugs is to slow the reproduction of the virus and minimize the appearance of drug resistant strains of the virus.Um, yes, in the broad sense it does. That is what we mean when we use the term "mechanism of action". They all target the same enzyme system. They have different sites of action, so one drug may continue to work when resistance to the others forms. Eventually this will mean that none of these drugs will work. Eventually the virus is going to win. We already know it will win. It's beginning to win already. The fact that it remains viable within people who cannot stop the cocktails tells us all we need to know about how thoroughly "powerful" these drugs are. They are going to fail.
The net result is that evolution is slowed. The virus doesn’t have to win.
So tell us, what was the selection pressure that gives rise to the hemoglobin gene and molecule? If it is as Paul previously suggested, the presence of oxygen in the atmosphere, describe that selection pressure so that it can be put in ev and evolve the hemoglobin gene. I'm sorry, but what does this have to do with anything I have said or your use of HIV as the example par excellence? I do not pretend to knowledge that I do not have. I would need to study the problem before even beginning to suggest alternatives. I do not know the history of the molecule and its progenitors well enough to say.
It has everything to do with the theory of evolution. Choose any gene, how does any gene evolve from the beginning. How do you select for something before it exists. Natural selection only can act on something that exists. Since I doubt you have carefully read this thread, I’ll explain to you what there are no selection pressures that evolve a gene from the beginning.

A gene is to evolve. The first base in the sequence for the gene is laid down on the genome. One base codes for nothing so there is nothing for natural selection to act upon. A second base added by random chance is laid down in the sequence. Still nothing to code for, natural selection can not act on this sequence. A third base in the sequence is laid down. You now have enough bases to form a codon for a single amino acid. A single amino acid has no functional use so there is still nothing for natural selection to act upon. So bases must be added randomly until you have a long enough sequence of bases to produce a functional polypeptide and then natural selection can act. Adding bases randomly yield probabilities so infinitesimally small that evolution is mathematically impossible.
It is the secondary infection that usually kills the person infected with HIV so treating the secondary infection prolonged life slightly. It wasn’t until combination therapy was introduced that real selective pressure was put on the virus (unless you count the 20 or so selective pressures you speculate are placed on the virus by the person’s own immune system). This selective pressure has altered the HIV virus. Mutated HIV reproduces at a slow rate than the wild virus. I know the history, I watched it happen. Support for the secondary infections initially prolonged life only for short periods of time. As time progressed and before triple therapy was begun people were already living longer. The virus was already becoming less virulent before triple therapy was introduced. It mutated because it killed people too fast and less virulent strains were able to be transmitted to others. AZT caused a huge pressure on the virus to mutate. That pressure alone resulted in big changes, not all of which have or can be quantified. Triple therapy has produced changes as well. It continues to do so. Evolution has stopped, though?
Evolution has slowed sufficiently for people who suffer from HIV to live years longer. More effective and additional selection pressures on the virus may cause the virus to go extinct.
It’s not the way I define it, it is the way reality works. Certainly there is an immune response to the virus, antibodies to the virus are detected. However, this immune response is almost universally ineffective. Once the retroviral therapy is initiated, it would not surprise me that the person’s own immune system contributes to the suppression of the virus.I'm sorry again, but I cannot understand what would possess anyone to think that the immune response is the only host reaction to the presence of the virus and the only selection pressure.

Bottom line........HIV is a bad example.
What????? What other response does a host have beside an immune response to the presence of a virus? Maybe you are talking about the sudden urge a host has to have a cup of chicken soup when exposed to a virus?
He says that selection pressures exist that transform identical genes into different genes. When one gene is performing a function, it is under selection pressure not to adapt to another function. An unused duplicate copy of that gene, on the other hand, is free to adapt to some other function.
If the unused gene is not functioning, there is no selection.
If, however, having two copies of the same gene is more beneficial than one, the duplicate copy is not likely to adapt to a new use. The second copy is then under selection pressure to perform the same function as the original gene! I know for a fact there are tandem duplicates of tRNA genes in populus trichocarpa and arabidopsis thaliana that maintain their original function for exactly this reason.
So in one case you have no selection and in the other case selection is preventing divergence.

Paul, I did a preliminary study of the 32k case. This case does about 1,000 generations per minute. If this case takes 60,000,000 generations to converge, that would be over 40 days of cpu time. Since I can’t run my computer 24 hours/day, it would take about three months to run this case. Maybe I’ll start running this case a little at a time, just for fun. But that will have to wait until next week.

You all have a Happy Passover and joyous Easter.

[Dr Adequate]

Another evolutionist who doesn’t realize his own theory measures fitness by the ability to reproduce. He evidently understands that perfectly well, you whining lying little freak. You on the other hand, seem to have overlooked the subtle little fact that it's not possible to reproduce when you're dead.

Still, congratulations on thinking of a new lie, it was most entertaining. Got any more?

[Dr Adequate]

Now I come to think of it, there are things which reproduce when they're dead.

Creationist arguments.

[Mercutio]

Now, now. They aren't dead. They smell that way naturally.










Ok, yeah, dead.

[delphi_ote]

Really? A single fatal selection pressure precludes multiple non-fatal selection pressures from slowing evolution? Then explain why the emergence of drug resistance HIV is slowed when multiple drug therapy is used.
As I've repeated many times, it's not the number of selection pressures (you can't really count selection pressures anyway!) The shape of the fitness landscape is what you think you're talking about here. It is possible that the topology of a fitness landscape is too steep (e.g. throwing a population of monkeys in the middle of the Pacific,) but there is no limit to the number of selection pressures to which an organism can adapt. Your theory that eventually there is a limit to the number of selection pressures to which an organism can adapt is total bunk.
Evolutionist have assumed that there is no limit to what natural selection can do.
No, they haven't.
If the unused gene is not functioning, there is no selection.
Which is why I never said the unused gene was nonfunctional. You seem to be grasping at strawmen a lot in this post.

[joobz]

Now I come to think of it, there are things which reproduce when they're dead.


resurrection is a central theme to ID isn't it?

[Ichneumonwasp]

Another evolutionist who doesn’t realize his own theory measures fitness by the ability to reproduce.


No. The point is that you are focusing on a system which has very special characteristics. Fitness may be affected in many ways. Let's say we have selection pressure one -- wolf. And we have selection pressure two -- big gonads. Little mousie with big gonads who escapes wolf long enough to reproduce before being eaten is fit. Particularly if those big gonads get him into selection pressure three, big colony of sister mice wearing white robes, promising oral sex, and lighting Grail shaped beacons.

Triple therapy for HIV is a very special case. That therapy directly targets replication -- the direct means by which the virus reproduces. There is no way for the virus to escape easily when we specifically target its ability to reproduce directly, not through the indirect means of impacting fitness through depleted resources, or whatever, that we see in nature. That is what Taffer was trying to tell you. That is why I entered this silly exchange in the first place. Triple therapy for HIV does not mimic what we tend to see in nature. It is not an issue of us not understanding what fitness means. It is an issue of us seeing that you are loading the dice in your favor and calling you on it.

None of the treatments for HIV lead to death of the virus, these treatments only limit reproduction of the virus.

And you will need to excuse me for using examples that are not directly applicable to this case in an effort to explain things within a larger context. The whole point of mentioning death scenarios is an attempt to re-orient the discussion toward a more realistic scenario. You cannot use three pressures that directly act on the molecular machinery for reproduction of an organism and pretend that this in some way replicates the natural history of three selection pressures as it relates to evolutionary change (except in very peculiar circumstances).

So why don’t you tell us what the selection pressure is that evolves a gene from the beginning. I keep asking this question of you evolutionists

I've already told you that I'm not playing that game. This discussion concerns your use of a particular example and what you think it shows. Why do you continue to try and switch the emphasis? This is a narrow discussion. You stated that triple therapy for HIV is directly analogous to what occurs in the ev program and by extension to what happens in real life when multiple pressures are put on an organism. I disagree with you. Please stay focused on the issue at hand.

What you don’t seem to realize is that multiple selection conditions even if not fatal confound the evolutionary process.

Confound the evolutionary process? What in the world could that even possibly mean?

In a simple sense, what happens if you get a beneficial mutation for one selection condition and a harmful mutation for another selection condition on the same creature. Is that creature selected for or selected against?

There is simply no way to answer that question based on the information you have provided. It depends on the actual selection pressures involved and chance.

The net result is that evolution is slowed. The virus doesn’t have to win.


What does that mean? Evolution is slowed? I don't see a stop sign sitting over Evolution. There is no slowing of evolution. There is perhaps slowing of this virus. That, in and of itself, is evolution. Your contention is nonsensical and utterly dependent on a teleological framework.

The virus will win. It already is winning. If we do not devise new strategies in the next few decades, then it will prove to be a bigger problem. Thankfully it is not as virulent now. But, there are already people in whom the virus escapes all three therapies, even when the triple therapy approach is changed and they are given a different cocktail. People still die of this disease. Most of them are so sick before the virus "gets through" that they do not spread the infection, though. So we do not currently have a crop of completely drug resistant organisms traipsing about.

It has everything to do with the theory of evolution.

Need I remind you again that we are discussing your emphasis on HIV and triple therapy. Nothing else. I am not playing that game. If we conclude this discussion, then perhaps we may move on to another topic. We need, however, to finish this topic first.

Evolution has slowed sufficiently for people who suffer from HIV to live years longer. More effective and additional selection pressures on the virus may cause the virus to go extinct.


Of course the virus could go extinct. It almost assuredly isn't, but that is beside the point. Please explain to me how the virus going extinct is not "evolution". There is no such thing as "slowing evolution". We can slow an organism down by attacking it. If it survives it may remain relatively dormant, dead, or virulent beyond anything we dreaded because it escapes our selection pressures. Slowing evolution? I have no idea what you are talking about.

What????? What other response does a host have beside an immune response to the presence of a virus? Maybe you are talking about the sudden urge a host has to have a cup of chicken soup when exposed to a virus?


You haven't bothered to notice that HIV is a parasite? Host death is a fairly significant selective pressure on parasites. Host alive means transmission opportunities. Host dead means parasite dead. Rapid host death means limited transmission while long refractory periods means more chances to replicate. Didn't you get the message of why I was speaking about the early years of this disease? We see the same thing with other infectious agents. Syphilis was an absolute scourge before it became less virulent.

[Ichneumonwasp]

Since this is getting so unweildy, even for a very limited discussion, here are the main points:

You claim that HIV triple therapy is a good analogy for the three selection pressures seen in the ev program.

I counter with:
1. In human hosts HIV has more than 3 selection pressures. At minimum there is triple therapy (by your definition -- 3 pressures), the host immune response, host longevity. That is a minimum of 5 pressures (167% of your stated 3). I have not even mentioned the competition for transcription and translation within the host between the reverse transcriptase and the normal host machinery -- another set of selection pressures. The reason I mentioned "probably 20", as an underestimate of, selection pressures is because, by your definition, each and every attempt at host transcription that competes with the reverse transcriptase serves as an independent selection pressure. Not a big pressure, but a pressure nonetheless.

2. The peculiar selection pressure(s) exerted by triple therapy do not mimic the typical selection pressures one would see in the wild. These are three very specific selection pressures designed to attack one (really two) specific systems. These systems are directly involved in replication of the virion. Typical selection pressures act indirectly on reproduction and affect fitness through those indirect means. These are also not independent selection pressures as I would assume is modeled in ev. They are linked together specifically by humans to attack the same system. The analogy I made earlier with death of organisms was the closest we see in nature to this paradigm. I can't think of anything else, in nature, that directly affects fitness so thoroughly as immediate death.

ETA
3. Evolution doesn't stop when a species becomes extinct (well, it stops for that species, but evolution itself does not stop). Extinction is a key ingredient in the mix. Multiple synergistic selection pressures, like triple therapy for HIV, have a high chance of leading to extinction of an organism, especially higher organisms. {It won't work for HIV because of the nature of the virus. We need another means of attacking the virus in order to promote its extinction, including better means of preventing infection.} Slowing an organism is not slowing evolution; it is part oand parcel of evolution. If you specifically target an organism's ability to produce offspring, then it will not produce as many offspring and so not produce as many distinct varieties. That is not a slowing of evolution, but an instance of evolution from the host/prey side. It means that the attack on the predator/parasite is effective and nothing else. There is nothing special about the number three. There is something special about directly attacking reproduction. Your example actually argues for the natural selection paradigm -- a perfect instance of fewer offspring, fewer varieties, so less chance for that organism to change over time. It isn't three selection presures that perform this feat. It is a synergistic effect of pressures specifically designed to stop viral replication. We might have been able to do it with one agent if they dang virus weren't so mutable to begin with. We use three not because there is something magical about the number three but because the three agents represent a compromise between toxicity and efficacy.

Therefore, HIV triple therapy is a bad example of a real-world analog to the modelling in ev.

[Paul C. Anagnostopoulos]

So, do you still believe that Dr Schneider’s model shows how a human genome could evolve in a billion years give or take a 100% or more? (Let’s not forget world wide populations, interspecies gene transfers and panspermia.)
I believe that's lie #12. You always forget to quote the part where he said "at this rate."


How do you know whether I am planning to run this 32k case? Let’s see, your guess is 18,000,000 generations and my guess is 60,000,000 generations. I’m starting to think this is a good case to run. I’ll have to do this one with the Pascal version of ev. It will probably take about 3 or 4 weeks to run, maybe more since I won’t be able to run the case every day. It would be fun to post intermediate results, kind of like a horse race.
By all means, run it. Rfrequency is getting close to Rcapacity, so it might take longer than my estimate. I certainly don't understand the behavior as Rfrequency approaches Rcapacity. Make sure you don't reach any definitive conclusion unless you run it three or four times, because of the variance.

~~ Paul

[kjkent1]

I believe that's lie #12. You always forget to quote the part where he said "at this rate."


By all means, run it. Rfrequency is getting close to Rcapacity, so it might take longer than my estimate. I certainly don't understand the behavior as Rfrequency approaches Rcapacity. Make sure you don't reach any definitive conclusion unless you run it three or four times, because of the variance.

~~ PaulPaul,

This "Rcapacity" problem that you and Alan keep coming back to is unclear to me. Can you clarify?

[Dr Richard]

Since this is getting so unweildy, even for a very limited discussion, here are the main points:

You claim that HIV triple therapy is a good analogy for the three selection pressures seen in the ev program.

I counter with:
1. In human hosts HIV has more than 3 selection pressures...

I would say WAY more than 20 selection pressures acting on HIV.

HIV itself codes for 15 proteins. 15 selection pressures acting immediately as a positive or negative mutation in any gene coding for an expressed protein will affect overall fitness of the virus.

Then consider the basic life cycle of the virus:

HIV Binding to cell membrane
Penetration
Uncoating
Reverse Transcriptase
Integration
Transcription
Translation
Assembly
Extrusion
Maturation

Many of these steps will be affected by the host cell - cell membrane binding for instance, plus, as you mentioned, transcription.

If we assume every HIV protein function has only one host counterpart, that doubles us to 30 selection pressures.

Now consider the host immune response. Diffeerences in host immune response to HIV affect clinical outcome (many refs, see http://www.pnas.org/cgi/content/abstract/94/1/254 for an example) so the human immune system is a selection factor acting upon HIV. We know for instance that some individuals are naturally resistant to HIV (http://www.hhs.gov/news/press/1996pres/960926.html).

So, how many genes are involved in the function of the human immune system? I have to admit I don't know; 3000 seems like a reasonable estimate (http://arjournals.annualreviews.org/doi/pdf/10.1146/annurev.immunol.18.1.829?cookieSet=1).

This takes us up to 3030 selection pressures.

Now we have to see what happens when the virus spreads. As already pointed out, if the virus kills the host before being allowed to spread, the virus dies. Plus the virus must be secreted into transmissable fluids, and survive in them. Plus the virus must survive directed attempts to stop spread (abstinence, condom use, blood screening). And then it must be able to breach an epithelial membrane and survive in a new host bloodstream.

A conservative estimate now would be about 3050 selection factors.

Compared to Kleinman's three, 3050 would certainly halt evolution dead.

No questions, stops evolution in its tracks.

Which is probably why HIV continues to evolve.

Which is probably why 1% of all newly diagnosed HIV sufferers in the UK are resistant to three antiretrovirals at the time of diagnosis. (http://www.bmj.com/cgi/content/abstract/331/7529/1368).

Which is probably why Kleinman has to endlessly whine about his "mathematecal proof" that evolution does not exist because the real world demonstrates it ocurring every day.

[Paul C. Anagnostopoulos]

This "Rcapacity" problem that you and Alan keep coming back to is unclear to me. Can you clarify?
Rcapacity is a measure of the information carrying capacity of the binding sites. An n-base site can carry 2n bits of information.

Rsequence is a measure of the amount of information required to distinguish the binding sites from the rest of the genome. It is based on the size of the genome and number of binding sites. As the creatures evolve, Rsequence, the measure of the amount of information actually in their binding sites, approaches Rfrequency and then hovers there. The genetic pattern in the binding sites is illustrated by the sequence logo, and the amount of information in the sequence logo is equal to Rsequence.

If Rcapacity < Rfrequency, it becomes very difficult for Rsequence to approach Rfrequency, since the binding sites can't carry Rfrequency bits of information. It's not impossible, just more difficult. All these R variables are irrelevant if any of the mistake count parameters are set to 0, since then you are not trying to distinguish the binding sites from the rest of the genome.

Running Ev experiments where Rcapacity < Rfrequency throws another factor into the model that makes it tenuous to draw conclusions about the number of generations required to evolve a perfect creature.

~~ Paul

[Ichneumonwasp]

Thanks Dr. Richard. I was trying to be extremely conservative because of the nature of the debate, but that is an excellent way of explaining it.

I suppose I should keep up on HIV more, but since I don't have to deal with it on a daily basis any longer I don't or I might have know the actual drug resistance info. Thanks again for the excellent post.

[delphi_ote]

resurrection is a central theme to ID isn't it?
Easter is right around the corner!

[Paul C. Anagnostopoulos]

A little known fact: No evolution happens on Easter Sunday.

~~ Paul

[Mr. Scott]

A little known fact: No evolution happens on Easter Sunday.

~~ Paul

Do you mean we probably won't hear from our resident lying creationist, considering his known patterns, until Sunday night?

I recall learning about the HIV "three strikes and it's out" principle too long ago to remember where, so I'm going from memory, but based on my recollections, I think Kleinman is wrong in his interpretation and extrapolation. It's fallacious anyway to extrapolate from a simple virus to evolution of higher life forms (as it is to extrapolate from the misuse of an incomplete model of evolution to assert proof of its impossibility), but even if such extrapolation is valid, he has a fatal problem with the initial point he extrapolates from.

Here's my recollection about 3-strike HIV treatments. Someone correct me if I'm wrong.

We have three anti-HIV drugs. Each of them corresponds to a different point on the same HIV gene. This HIV gene is capable of mutating to defeat each specific attack point of each of these drugs. However, if the gene mutates at all three points of all three anti-HIV drugs, then that gene ceases to perform it's critical reproductive function.

Now, this does not show that three of any selection pressures against any organism stops its evolution. It shows the result of three carefully prepared drugs carefully targeted to three specific points in one specific gene in a specific virus for a specific, carefully planned supression effect. It is intelligently designed, not by god but by scientists who I suspect believe in evolution (oh, the irony). Real world evolution involves a helter-skelter array of selection pressures, not an intelligently designed biochemically choreographed attack.

So, I assert Dr. Kleinman's specious extrapolation of HIV treatments to all of evolution is not evidence that multiple selective pressures halt evolution. It's evidence that a species can be overwhelmed by selective pressures and become extinct. It just so happens that such extinction scenerios are a foundational principle of the theory of evolution (last I heard).

ETA: I see Ichneumonwasp has made this same basic point, which had been on my mind for months now, but decided to express before Kleinman got too carried away. Wish I had time to read every posting to this incredible thread. My regards to Ichneumonwasp, with no intent to steal thunder.

[Dr Adequate]

Perhaps he has some sort of primitive taboo against lying during religious holidays.

[kleinman]

Did you all have a Happy Passover and joyous Easter?

Really? A single fatal selection pressure precludes multiple non-fatal selection pressures from slowing evolution? Then explain why the emergence of drug resistance HIV is slowed when multiple drug therapy is used.As I've repeated many times, it's not the number of selection pressures (you can't really count selection pressures anyway!) The shape of the fitness landscape is what you think you're talking about here. It is possible that the topology of a fitness landscape is too steep (e.g. throwing a population of monkeys in the middle of the Pacific,) but there is no limit to the number of selection pressures to which an organism can adapt. Your theory that eventually there is a limit to the number of selection pressures to which an organism can adapt is total bunk.
Too bad your point is not supported by the results from ev or the example of using three selection pressures to treat HIV. Both the theoretical and real examples show that three non-fatal selection pressures profoundly slow the rate of evolution.
Evolutionist have assumed that there is no limit to what natural selection can do.No, they haven't.
Ok, what is the limit?
If the unused gene is not functioning, there is no selection.Which is why I never said the unused gene was nonfunctional. You seem to be grasping at strawmen a lot in this post.
So your unused gene is functioning? You tend to use contradictory logic quite often to defend your theory of evolution. The only thing made out of straw in this discussion is your theory of evolution and it is being blown to bits by the mathematics of ev.
Another evolutionist who doesn’t realize his own theory measures fitness by the ability to reproduce.No. The point is that you are focusing on a system which has very special characteristics. Fitness may be affected in many ways. Let's say we have selection pressure one -- wolf. And we have selection pressure two -- big gonads. Little mousie with big gonads who escapes wolf long enough to reproduce before being eaten is fit. Particularly if those big gonads get him into selection pressure three, big colony of sister mice wearing white robes, promising oral sex, and lighting Grail shaped beacons.

Triple therapy for HIV is a very special case. That therapy directly targets replication -- the direct means by which the virus reproduces. There is no way for the virus to escape easily when we specifically target its ability to reproduce directly, not through the indirect means of impacting fitness through depleted resources, or whatever, that we see in nature. That is what Taffer was trying to tell you. That is why I entered this silly exchange in the first place. Triple therapy for HIV does not mimic what we tend to see in nature. It is not an issue of us not understanding what fitness means. It is an issue of us seeing that you are loading the dice in your favor and calling you on it.
If the causative factor does not affect reproduction, then it is not a selection pressure. It doesn’t matter whether the causative factor affects reproduction directly or indirectly for it to be a selection pressure. An environmental temperature change does not need to directly effect the temperature of a bird’s egg in order to affect the ability of the bird to reproduce.

If you think that multiple selection pressures can speed up evolution, give us some examples.
None of the treatments for HIV lead to death of the virus, these treatments only limit reproduction of the virus.And you will need to excuse me for using examples that are not directly applicable to this case in an effort to explain things within a larger context. The whole point of mentioning death scenarios is an attempt to re-orient the discussion toward a more realistic scenario. You cannot use three pressures that directly act on the molecular machinery for reproduction of an organism and pretend that this in some way replicates the natural history of three selection pressures as it relates to evolutionary change (except in very peculiar circumstances).
Again, give us examples of multiple selection pressures that speed up evolution. Give us an example of the selection pressure that would evolve a gene from the beginning.
So why don’t you tell us what the selection pressure is that evolves a gene from the beginning. I keep asking this question of you evolutionistsI've already told you that I'm not playing that game. This discussion concerns your use of a particular example and what you think it shows. Why do you continue to try and switch the emphasis? This is a narrow discussion. You stated that triple therapy for HIV is directly analogous to what occurs in the ev program and by extension to what happens in real life when multiple pressures are put on an organism. I disagree with you. Please stay focused on the issue at hand.
No evolutionist will play that game because there are no selection pressures that evolve a gene from the beginning. The issue at hand is the mathematics of mutation and selection. If evolutionists are going to use the slogan “mutation and selection” as the mechanism that leads reptiles to morph into birds and humans and chimpanzees to morph from a primate precursor and claim this is scientific, then you need to describe the selection mechanism(s) that can do this.
What you don’t seem to realize is that multiple selection conditions even if not fatal confound the evolutionary process.Confound the evolutionary process? What in the world could that even possibly mean?
Confound-to mingle so that the elements cannot be distinguished or separated. Hey Paul, does that sound like your definition for Rcapacity?
In a simple sense, what happens if you get a beneficial mutation for one selection condition and a harmful mutation for another selection condition on the same creature. Is that creature selected for or selected against?There is simply no way to answer that question based on the information you have provided. It depends on the actual selection pressures involved and chance.
You need to study ev, you will get an education on this topic.
The net result is that evolution is slowed. The virus doesn’t have to win.What does that mean? Evolution is slowed? I don't see a stop sign sitting over Evolution. There is no slowing of evolution. There is perhaps slowing of this virus. That, in and of itself, is evolution. Your contention is nonsensical and utterly dependent on a teleological framework.

The virus will win. It already is winning. If we do not devise new strategies in the next few decades, then it will prove to be a bigger problem. Thankfully it is not as virulent now. But, there are already people in whom the virus escapes all three therapies, even when the triple therapy approach is changed and they are given a different cocktail. People still die of this disease. Most of them are so sick before the virus "gets through" that they do not spread the infection, though. So we do not currently have a crop of completely drug resistant organisms traipsing about.
You affect evolution by reducing the fitness of the creature. That fitness is measured by the ability of the creature to reproduce. The virus always wins? No viruses go extinct?
It has everything to do with the theory of evolution.Need I remind you again that we are discussing your emphasis on HIV and triple therapy. Nothing else. I am not playing that game. If we conclude this discussion, then perhaps we may move on to another topic. We need, however, to finish this topic first.
The use of triple antiviral medications to treat HIV is a very nice example of how mutation and selection works. I’m simply playing the evolutionist game by the evolutionist rules. The evolutionist computer model ev shows mathematically the same results as the real example of the treatment of HIV. These examples also show why multiple selection pressures slow evolution.
Evolution has slowed sufficiently for people who suffer from HIV to live years longer. More effective and additional selection pressures on the virus may cause the virus to go extinct.Of course the virus could go extinct. It almost assuredly isn't, but that is beside the point. Please explain to me how the virus going extinct is not "evolution". There is no such thing as "slowing evolution". We can slow an organism down by attacking it. If it survives it may remain relatively dormant, dead, or virulent beyond anything we dreaded because it escapes our selection pressures. Slowing evolution? I have no idea what you are talking about.
Extinction does not lead to evolution, extinction is the end of a genetic line. The reason you have no idea what I’m talking about is that you don’t understand the mathematics of ev. Ev is an evolutionist written, peer reviewed and published model of random point mutation and natural selection. Once you have an understanding of this model, you will understand my arguments, that is if you don’t go into denial like Paul has.
What????? What other response does a host have beside an immune response to the presence of a virus? Maybe you are talking about the sudden urge a host has to have a cup of chicken soup when exposed to a virus?You haven't bothered to notice that HIV is a parasite? Host death is a fairly significant selective pressure on parasites. Host alive means transmission opportunities. Host dead means parasite dead. Rapid host death means limited transmission while long refractory periods means more chances to replicate. Didn't you get the message of why I was speaking about the early years of this disease? We see the same thing with other infectious agents. Syphilis was an absolute scourge before it became less virulent.
If parasites kill their host before they can complete their life cycle then they will go extinct. Syphilis is no longer an absolute scourge because of the advent of antibiotics, also the selective pressure on the host has selected out those who can’t mount a strong immune response against the bacteria.
You claim that HIV triple therapy is a good analogy for the three selection pressures seen in the ev program.

I counter with:
1. In human hosts HIV has more than 3 selection pressures. At minimum there is triple therapy (by your definition -- 3 pressures), the host immune response, host longevity. That is a minimum of 5 pressures (167% of your stated 3). I have not even mentioned the competition for transcription and translation within the host between the reverse transcriptase and the normal host machinery -- another set of selection pressures. The reason I mentioned "probably 20", as an underestimate of, selection pressures is because, by your definition, each and every attempt at host transcription that competes with the reverse transcriptase serves as an independent selection pressure. Not a big pressure, but a pressure nonetheless.
Any of the selection pressures you allege are so weak that the sum of all pressures have no affect on the outcome of the disease when compared to the affect of triple antiviral therapy.
2. The peculiar selection pressure(s) exerted by triple therapy do not mimic the typical selection pressures one would see in the wild. These are three very specific selection pressures designed to attack one (really two) specific systems. These systems are directly involved in replication of the virion. Typical selection pressures act indirectly on reproduction and affect fitness through those indirect means. These are also not independent selection pressures as I would assume is modeled in ev. They are linked together specifically by humans to attack the same system. The analogy I made earlier with death of organisms was the closest we see in nature to this paradigm. I can't think of anything else, in nature, that directly affects fitness so thoroughly as immediate death.
You are making a distinction where none exists. A selection pressure by definition is one which affects the ability of a creature to reproduce. Ultimately, all these pressures act somewhere at the genetic level. Whether the pressure acts directly on enzymes involved in reproduction of the genome or at some other metabolic step which is required for the creature to survive, they all affect the fitness of a creature to reproduce. If you starve a creature, you deprive the creature of the required energy and materials needed to reproduce. This is an example of multiple selection pressures. If you deprive a creature of a single essential nutrient, you impair the reproduction of that creature with a single selection pressure.
3. Evolution doesn't stop when a species becomes extinct (well, it stops for that species, but evolution itself does not stop). Extinction is a key ingredient in the mix. Multiple synergistic selection pressures, like triple therapy for HIV, have a high chance of leading to extinction of an organism, especially higher organisms. {It won't work for HIV because of the nature of the virus. We need another means of attacking the virus in order to promote its extinction, including better means of preventing infection.} Slowing an organism is not slowing evolution; it is part oand parcel of evolution. If you specifically target an organism's ability to produce offspring, then it will not produce as many offspring and so not produce as many distinct varieties. That is not a slowing of evolution, but an instance of evolution from the host/prey side. It means that the attack on the predator/parasite is effective and nothing else. There is nothing special about the number three. There is something special about directly attacking reproduction. Your example actually argues for the natural selection paradigm -- a perfect instance of fewer offspring, fewer varieties, so less chance for that organism to change over time. It isn't three selection presures that perform this feat. It is a synergistic effect of pressures specifically designed to stop viral replication. We might have been able to do it with one agent if they dang virus weren't so mutable to begin with. We use three not because there is something magical about the number three but because the three agents represent a compromise between toxicity and efficacy.

Therefore, HIV triple therapy is a bad example of a real-world analog to the modelling in ev.
As I said previously to Delphi, there is nothing special about three selection pressures other than it only takes three selection pressures to profoundly slow evolution. This is what ev shows and this is what the example of triple therapy for HIV shows. Four or more selection pressures only slow the process more so. The more ways you try to select and sort on, the more slowly the process occurs.
So, do you still believe that Dr Schneider’s model shows how a human genome could evolve in a billion years give or take a 100% or more? (Let’s not forget world wide populations, interspecies gene transfers and panspermia.)I believe that's lie #12. You always forget to quote the part where he said "at this rate."
Silly Paul, “at this rate”, didn’t you forget to mention that this rate is based on a genome only 256 bases long with a mutation rate 100 times faster than you see in HIV. The latest case you ran which evolved the same number of binding sites and loci took over 6 million generations. Plug those numbers into Dr Schneider’s equations an you get 6 trillion years to evolve a human genome. Of course, that still only a 16k genome. What happens when you compute the rate of information gain on a 500k genome?
How do you know whether I am planning to run this 32k case? Let’s see, your guess is 18,000,000 generations and my guess is 60,000,000 generations. I’m starting to think this is a good case to run. I’ll have to do this one with the Pascal version of ev. It will probably take about 3 or 4 weeks to run, maybe more since I won’t be able to run the case every day. It would be fun to post intermediate results, kind of like a horse race.By all means, run it. Rfrequency is getting close to Rcapacity, so it might take longer than my estimate. I certainly don't understand the behavior as Rfrequency approaches Rcapacity. Make sure you don't reach any definitive conclusion unless you run it three or four times, because of the variance.
I know you don’t understand the mathematics of ev. It is the multiple selection pressures which slow the convergence of the model. As I said previously, this is analogous to a large database sorting problem. The more conditions you try to sort on and the larger the database, the slower the sorting process occurs. Ev can select and sort when the genome is small (a relatively small database) but as the genome is lengthened, the slower the select and sort occurs. If you reduce the number of sorting conditions (reduce the number of selection pressures) you can markedly speed up the process. That is what the mathematics of ev is saying and that effect is demonstrated by the use of triple antiviral medications for the treatment of HIV.
By all means, run it. Rfrequency is getting close to Rcapacity, so it might take longer than my estimate. I certainly don't understand the behavior as Rfrequency approaches Rcapacity. Make sure you don't reach any definitive conclusion unless you run it three or four times, because of the variance.This "Rcapacity" problem that you and Alan keep coming back to is unclear to me. Can you clarify?
Yes Paul, explain Rcapacity to all of us. If you want, you can use the definition for “confound”.
Compared to Kleinman's three, 3050 would certainly halt evolution dead.
3050 selection pressures? Do you want to explain why 3053 selection pressures works so well at slowing the reproduction of the virus?
Which is probably why 1% of all newly diagnosed HIV sufferers in the UK are resistant to three antiretrovirals at the time of diagnosis..

Which is probably why Kleinman has to endlessly whine about his "mathematecal proof" that evolution does not exist because the real world demonstrates it ocurring every day.
So Dr Richard, are you advocating monotherapy for the treatment of HIV?
This "Rcapacity" problem that you and Alan keep coming back to is unclear to me. Can you clarify? Rcapacity is a measure of the information carrying capacity of the binding sites. An n-base site can carry 2n bits of information.

Rsequence is a measure of the amount of information required to distinguish the binding sites from the rest of the genome. It is based on the size of the genome and number of binding sites. As the creatures evolve, Rsequence, the measure of the amount of information actually in their binding sites, approaches Rfrequency and then hovers there. The genetic pattern in the binding sites is illustrated by the sequence logo, and the amount of information in the sequence logo is equal to Rsequence.

If Rcapacity < Rfrequency, it becomes very difficult for Rsequence to approach Rfrequency, since the binding sites can't carry Rfrequency bits of information. It's not impossible, just more difficult. All these R variables are irrelevant if any of the mistake count parameters are set to 0, since then you are not trying to distinguish the binding sites from the rest of the genome.

Running Ev experiments where Rcapacity < Rfrequency throws another factor into the model that makes it tenuous to draw conclusions about the number of generations required to evolve a perfect creature.
Set the weight factors for spurious binding sites to 0 and ev has no trouble evolving sequences of bases that satisfy the threshold for the weight matrix no matter how long the genome is. Your binding sites are evolved but you still have spurious binding sites. You haven’t satisfied the other selection conditions. It is the multiple selection conditions which confounds the evolutionary process.

This is a database sorting problem, the more sorting conditions and the larger the database, the slower the process goes. That’s the mathematics that ev demonstrates for the slogan “mutation and natural selection”. This is why the theory of evolution is mathematically impossible. Well that and the fact that there are no selection processes to evolve genes from the beginning.
A little known fact: No evolution happens on Easter Sunday.Do you mean we probably won't hear from our resident lying creationist, considering his known patterns, until Sunday night?
Mr Scott, I neither need to nor want to lie about this. I have the Dr Schneider’s mathematics, peer reviewed and published which shows exactly why macroevolution does not occur, Easter Sundays or any other day of the week. Ev shows that multiple selection pressures slow and ultimately stop evolution and there are no selection pressures which can evolve a gene from the beginning. The treatment of HIV demonstrates the former and no evolutionists can refute the later.
We have three anti-HIV drugs. Each of them corresponds to a different point on the same HIV gene. This HIV gene is capable of mutating to defeat each specific attack point of each of these drugs. However, if the gene mutates at all three points of all three anti-HIV drugs, then that gene ceases to perform it's critical reproductive function.
That’s not quite right. If the virus succeeds in mutating at all three points, the resultant strain of the HIV virus is a slower reproducing virus than the wild strain of the virus.
Now, this does not show that three of any selection pressures against any organism stops its evolution. It shows the result of three carefully prepared drugs carefully targeted to three specific points in one specific gene in a specific virus for a specific, carefully planned supression effect. It is intelligently designed, not by god but by scientists who I suspect believe in evolution (oh, the irony). Real world evolution involves a helter-skelter array of selection pressures, not an intelligently designed biochemically choreographed attack.
Dr Richard says there are a helter-skelter of 3050 selection pressures against the virus. Doesn’t seem to slow the reproduction of the virus very much. They must not be much of selection pressures. By definition, selection pressures affect the ability of the virus to reproduce. It doesn’t matter whether they are intelligently designed or environmental in origin. The example of the use of triple antiviral therapy for the treatment of HIV is a perfect example how mutation and selection works.

So Mr Scott, do you want to show us how a helter-skelter array of selection pressures speed up evolution?
So, I assert Dr. Kleinman's specious extrapolation of HIV treatments to all of evolution is not evidence that multiple selective pressures halt evolution. It's evidence that a species can be overwhelmed by selective pressures and become extinct. It just so happens that such extinction scenerios are a foundational principle of the theory of evolution (last I heard).
That’s right, multiple selection pressures slow the evolutionary process and can and do lead to extinction. So do you want to explain how a helter-skelter array of selection pressures speed up evolution? Maybe you want to define three different selection conditions that Paul can put into ev and evolve three different sequences of bases that satisfy those conditions. The process is profoundly slow with the selection conditions that Dr Schneider intelligently designed.

What you and the other evolutionists are having trouble seeing is that mutation and selection is analogous to sorting a database. The larger the database and the more sorting conditions, the slower the process goes. It doesn’t matter whether you intelligently design the sorting conditions or whether the sorting conditions are helter-skelter, except that the helter-skelter conditions will be slower. That is what the mathematics of ev is showing and that is what the real example of the treatment of HIV is showing.
I see Ichneumonwasp has made this same basic point, which had been on my mind for months now, but decided to express before Kleinman got too carried away. Wish I had time to read every posting to this incredible thread. My regards to Ichneumonwasp, with no intent to steal thunder.
You are not stealing his thunder, you are stealing his blunder.

[kjkent1]

If setting ev mistake weights to zero proves that evolution is sped up by the absence of competing selective pressure (and slowed by the introduction of competing selective pressure), then the natural extension of this is that zero mistake weights for all selective pressures should increase the speed of evolution to the maximum.

And, ev does indeed prove this, because with all mistake weights set to zero, ev generates a perfect creature in the first generation every time, regardless of the genome length.

Which proves abiogenesis -- and falsifies the existence of a divine creator.

That's right folks. Kleinman demonstrates that, based on ev, any and all random genomes instantly produce viable life forms without selection!

Absolutely amazing logic.

[Paul C. Anagnostopoulos]

That's right folks. Kleinman demonstrates that, based on ev, any and all random genomes instantly produce viable life forms without selection!
And the really cool part is that it's all based on the interpretation of the word perfect. Now who made up the term perfect creature? Why, yours truly. By a mere flick of the terminology wrist, I have solved the problem of abiogenesis and discovered the core concept of evolution: Abiogenesis and evolution are instantaneous; everything else just slows them down. I'll let y'all know when the Nobel committee contacts me.

~~ Paul

[delphi_ote]

Too bad your point is not supported by the results from ev or the example of using three selection pressures to treat HIV. Both the theoretical and real examples show that three non-fatal selection pressures profoundly slow the rate of evolution.
Both results support my claim. You just haven't bothered to understand the fitness landscape concept. I'll give you a link where you can read about it in plain English. Click on these words. (http://en.wikipedia.org/wiki/Fitness_landscape)

[Ichneumonwasp]

If the causative factor does not affect reproduction, then it is not a selection pressure. It doesn’t matter whether the causative factor affects reproduction directly or indirectly for it to be a selection pressure. An environmental temperature change does not need to directly effect the temperature of a bird’s egg in order to affect the ability of the bird to reproduce.


That is not the point I was making. If you had read what I wrote you would not respond in this way. The point I made concerned a directed (man-made, directed) and direct attack on the ability to reproduce a virus. If the machinery for viral reproduction is completely shut off, then there is no possibility for reproduction and fitness drops to zero. End of story. If an indirect attack affects fitness it can serve as a pressure but not leave fitness at zero. Those are different scenarios.

The number of selection pressures is not necessarily the important factor that translates to a fitness of zero. A single pressure can translate into a fitness of zero.

If you think that multiple selection pressures can speed up evolution, give us some examples.


This is now the third time that I must tell you that I am not playing that game.

So, let's get this out of the way. I'm not playing that game. I'm not playing that game.I'm not playing that game.I'm not playing that game.I'm not playing that game.I'm not playing that game.I'm not playing that game.I'm not playing that game.I'm not playing that game.I'm not playing that game.

Got it? We are discussing your analogy. Once we finish with your analogy we can move on.

Again, give us examples of multiple selection pressures that speed up evolution. Give us an example of the selection pressure that would evolve a gene from the beginning.


Hello? Hello? Are you not even capable of sticking to the topic at hand? Hello? Hello?

Your analogy. That is what we are discussing. Nothing else. I asked a simple question about the use of this analogy and you responded. We are discussing your analogy. Your analogy. I'm hoping it will stick in your mind if I repeat it enough.

No evolutionist will play that game because there are no selection pressures that evolve a gene from the beginning.

Um, gosh, and all this time I thought it was because we started along a certain line of argument, and I didn't want any distractions from that line of argument. So, really, I have ulterior motives? That's nice. What am I having for lunch since you know so much about me and my motives?

Once and for all -- we are discussing your analogy. Stick to the topic at hand. No obfuscation.

The issue at hand is the mathematics of mutation and selection.

Not with me it isn't. You can argue whatever you want with other people. I asked a simple question. You returned with a snarky comment and have continued in the same vein. We -- you and I -- are discussing your use of a metaphor. Nothing else.

You affect evolution by reducing the fitness of the creature. That fitness is measured by the ability of the creature to reproduce. The virus always wins? No viruses go extinct?


Please pay attention. We are discussing HIV, not any virus. I have made no claims about any other virus or any other organism. I have used other analogies to make my points.

The use of triple antiviral medications to treat HIV is a very nice example of how mutation and selection works. I’m simply playing the evolutionist game by the evolutionist rules. The evolutionist computer model ev shows mathematically the same results as the real example of the treatment of HIV. These examples also show why multiple selection pressures slow evolution.


Of course it is a nice example of how certain types of selection pressures and mutation works. That is not the issue. The issue is that you made a very specific claim about it -- that it represents three selection pressures. I assume that you mean an actual three, as in not two and not four or more. That claim is wrong. There are many more than three selection pressures at work. And that particular selection pressure is very specific and not like the typical selection pressures one sees in nature or, again, I would assume are modelled in ev. That's all I'm saying. I'm saying your analogy is poor.

Extinction does not lead to evolution, extinction is the end of a genetic line

Whoa, extinction is the end of the line? Really?

Give me a break. This is not first grade. Please stop preteding that no one knows what words mean but you.

Evolution is not a process affecting a single entity or one species. Last time I checked, there was a great big world out there with numerous competing species, competing individuals. They change over time. That is evolution. It is simply stupid to say that evolution ends when one species dies. Evolution doesn't end. It isn't slowed. It continues. Certain pressures lead to extinction. Fact.

The reason you have no idea what I’m talking about is that you don’t understand the mathematics of ev.

I have a very good idea what you are talking about. You are simply wrong. Your metaphor is wrong.

Do you still want to defend this metaphor?

If parasites kill their host before they can complete their life cycle then they will go extinct. Syphilis is no longer an absolute scourge because of the advent of antibiotics, also the selective pressure on the host has selected out those who can’t mount a strong immune response against the bacteria.


Good, so you now agree that early host death is a selection pressure on a parasite? If you haven't bothered reading the literature on syphilis I suggest you do so. The spirochete became less virulent long before the use of antibiotics. Or do you want to deny this reality as well?

Any of the selection pressures you allege are so weak that the sum of all pressures have no affect on the outcome of the disease when compared to the affect of triple antiviral therapy.


What difference does that make? You can't model weak selection pressures? The whole point is that if you give an organism a selection pressure or pressures that they cannot overcome, then they will become extinct. Nothing magical there. It isn't the number that matters. It is the type of pressure. If you haven't noticed that is what I have been going on about for these several posts that are becoming increasingly boring and repetitious.

You are making a distinction where none exists. A selection pressure by definition is one which affects the ability of a creature to reproduce. Ultimately, all these pressures act somewhere at the genetic level. Whether the pressure acts directly on enzymes involved in reproduction of the genome or at some other metabolic step which is required for the creature to survive, they all affect the fitness of a creature to reproduce. If you starve a creature, you deprive the creature of the required energy and materials needed to reproduce. This is an example of multiple selection pressures. If you deprive a creature of a single essential nutrient, you impair the reproduction of that creature with a single selection pressure.


You continue to focus on the wrong issue. No one claims that the site (molecular vs organism as a whole) of the selection pressure is the absolute critical entity. The point is that a selection pressure that directly affects fitness and will not allow any reproduction is different from a relative pressure that still allows some reproduction. The number of factors is not critical. The critical issue is how effective the pressure is in preventing reproduction. Strong effect -- big effect on fitness. Weak effect -- weak effect on fitness. Completely stop reproduction and the organism will go extinct. But that is not the reality of most selection pressures in the wild (except, of course, for the rally big ones that do cause extinction). Most selection pressures are relatively weak. They affect fitness but do not generally completely stop reproduction. Even when they are present in large numbers, as you seem to agree is the case with the very large number of selection pressures affecting HIV. You did agree above that there are many selection pressures affecting HIV did you not?

As I said previously to Delphi, there is nothing special about three selection pressures other than it only takes three selection pressures to profoundly slow evolution.

Where is your evidence? It cannot be HIV. HIV has many more than three selection pressures. You have already admitted that most of those selection pressures are rather weak. Good, we agree. That is my point. Three selection pressures do not profoundly slow evolution. There is nothing special about the number three in slowing evolution (again, whatever that phrase means).

There can very easily be something special about certain types of pressures that slow the process of change in a particular organism because that (or those) pressure(s) significantly hit fitness for that organism. But that is the critical issue -- the particular effect on fitness of the pressure involved. There could be several hundred weak selection pressures that help to create changes in organisms. That is, in fact, what I would expect from nature.

You can say that three selection pressures profoundly slow evolution. But you would be wrong. That statement must be qualified. It is not the case that the number three is in any way important. It is the types of pressures that matter.

ETA

Or, to make the point again, we seem to have identifed hundreds, if not thousands, of selection pressures working on HIV -- all of which existed before the introduction of triple therapy -- during which time the virus was reproducing and mutating into many different forms. So, it cannot be the case that three selection pressures (or an increasing number of selection pressures) necessarily profoundly slows "evolution". Once again, it is not the number, but the type of selection pressure that is critical.

[delphi_ote]

Now who made up the term perfect creature?
Definition:
http://i71.photobucket.com/albums/i133/delphi_ote/NataliePortmanPicture.jpg

[kleinman]

That's right folks. Kleinman demonstrates that, based on ev, any and all random genomes instantly produce viable life forms without selection!And the really cool part is that it's all based on the interpretation of the word perfect. Now who made up the term perfect creature? Why, yours truly. By a mere flick of the terminology wrist, I have solved the problem of abiogenesis and discovered the core concept of evolution: Abiogenesis and evolution are instantaneous; everything else just slows them down. I'll let y'all know when the Nobel committee contacts me.
Paul, you seem to be right at home in one of kjkent1’s 10^500 alternative universes.
Too bad your point is not supported by the results from ev or the example of using three selection pressures to treat HIV. Both the theoretical and real examples show that three non-fatal selection pressures profoundly slow the rate of evolution.Both results support my claim. You just haven't bothered to understand the fitness landscape concept. I'll give you a link where you can read about it in plain English. Click on these words. (http://en.wikipedia.org/wiki/Fitness_landscape)
I did click on these words and here are some of them:
Fitness landscapes are often conceived of as ranges of mountains. There exist local peaks (points from which all paths are downhill, i.e. to lower fitness) and valleys (regions from which most paths lead uphill). A fitness landscape with many local peaks surrounded by deep valleys is called rugged.
Apart from the field of evolutionary biology, the concept of a fitness landscape has also gained importance in evolutionary optimization (http://en.wikipedia.org/wiki/Evolutionary_algorithm) methods such as genetic algorithms (http://en.wikipedia.org/wiki/Genetic_algorithm) or evolutionary strategies. In evolutionary optimization, one tries to solve real-world problems (e.g., engineering (http://en.wikipedia.org/wiki/Engineering) or logistics (http://en.wikipedia.org/wiki/Logistics) problems) by imitating the dynamics of biological evolution. For example, a delivery truck with a number of destination addresses can take a large variety of different routes, but only very few will result in a short driving time. In order to use evolutionary optimization, one has to define for every possible solution (http://en.wikipedia.org/wiki/Solution_point) s to the problem of interest (i.e., every possible route in the case of the delivery truck) how 'good' it is. This is done by introducing a scalar (http://en.wikipedia.org/wiki/Scalar_%28mathematics%29)-valued function (http://en.wikipedia.org/wiki/Function_%28mathematics%29) f(s) (scalar valued means that f(s) is a simple number, such as 0.3, while s can be a more complicated object, for example a list of destination addresses in the case of the delivery truck), which is called the fitness function (http://en.wikipedia.org/wiki/Fitness_function) or fitness landscape. A high f(s) implies that s is a good solution. In the case of the delivery truck, f(s) could be the number of deliveries per hour on route s. The best, or at least a very good, solution is then found in the following way. Initially, a population of random solutions is created. Then, the solutions are mutated and selected for those with higher fitness, until a satisfying solution has been found.
Evolutionary optimization techniques are particularly useful in situations in which it is easy to determine the quality of a single solution, but hard to go through all possible solutions one by one (it is easy to determine the driving time for a particular route of the delivery truck, but it is almost impossible to check all possible routes once the number of destinations grows to more than a handful).
What ev is demonstrating that once the number of selection conditions (truck routes) becomes three or more, it becomes virtually impossible to evolve all three conditions (check all truck routes) simultaneously. When there is a single selection condition (truck route) it is easy to converge that solution (optimize that particular truck route).

Delphi, not only does your link to Wikipedia fitness landscape not support your claims, it explains in evolutionist terms what ev is showing. That is, multiple selection conditions are almost impossible to evolve. Thank you for this reference, I think I will co-opt it for my proof that the theory of evolution is mathematically impossible.
If the causative factor does not affect reproduction, then it is not a selection pressure. It doesn’t matter whether the causative factor affects reproduction directly or indirectly for it to be a selection pressure. An environmental temperature change does not need to directly effect the temperature of a bird’s egg in order to affect the ability of the bird to reproduce.That is not the point I was making. If you had read what I wrote you would not respond in this way. The point I made concerned a directed (man-made, directed) and direct attack on the ability to reproduce a virus. If the machinery for viral reproduction is completely shut off, then there is no possibility for reproduction and fitness drops to zero. End of story. If an indirect attack affects fitness it can serve as a pressure but not leave fitness at zero. Those are different scenarios.

The number of selection pressures is not necessarily the important factor that translates to a fitness of zero. A single pressure can translate into a fitness of zero.
Read Delphi’s link to Wikipedia and fitness landscape. It doesn’t matter whether the selection pressures are man-made or from environmental sources. The mathematics is identical.
If you think that multiple selection pressures can speed up evolution, give us some examples.This is now the third time that I must tell you that I am not playing that game.

So, let's get this out of the way. I'm not playing that game. I'm not playing that game.I'm not playing that game.I'm not playing that game.I'm not playing that game.I'm not playing that game.I'm not playing that game.I'm not playing that game.I'm not playing that game.I'm not playing that game.

Got it? We are discussing your analogy. Once we finish with your analogy we can move on.
Of course you are not going to play this game. Evolutionists already know that multiple selection pressures slow evolution. The treatment of HIV with three selective pressures slows the evolution of the virus. This is what ev shows and this is what the Wikipedia definition for fitness landscape shows.
Again, give us examples of multiple selection pressures that speed up evolution. Give us an example of the selection pressure that would evolve a gene from the beginning.Hello? Hello? Are you not even capable of sticking to the topic at hand? Hello? Hello?

Your analogy. That is what we are discussing. Nothing else. I asked a simple question about the use of this analogy and you responded. We are discussing your analogy. Your analogy. I'm hoping it will stick in your mind if I repeat it enough.
Well tell us, do you believe multiple selection pressures speed up or slow down evolution? Ev shows that multiple selection pressures slow down evolution, The Wikipedia definition for fitness landscape shows that multiple selection pressures slow down evolution and the use of triple selection pressures on HIV shows that multiple selection pressures slow down evolution.
No evolutionist will play that game because there are no selection pressures that evolve a gene from the beginning.Um, gosh, and all this time I thought it was because we started along a certain line of argument, and I didn't want any distractions from that line of argument. So, really, I have ulterior motives? That's nice. What am I having for lunch since you know so much about me and my motives?

Once and for all -- we are discussing your analogy. Stick to the topic at hand. No obfuscation.
Ichneumonwasp, I do not obfuscate, I annoy evolutionists.
The issue at hand is the mathematics of mutation and selection.Not with me it isn't. You can argue whatever you want with other people. I asked a simple question. You returned with a snarky comment and have continued in the same vein. We -- you and I -- are discussing your use of a metaphor. Nothing else.
Of course evolutionists do not want to talk about the mathematics of mutation and selection, it shows your theory to be impossible.
You affect evolution by reducing the fitness of the creature. That fitness is measured by the ability of the creature to reproduce. The virus always wins? No viruses go extinct? Please pay attention. We are discussing HIV, not any virus. I have made no claims about any other virus or any other organism. I have used other analogies to make my points.
Oh yes, that’s right, we are talking about the evolution of the HIV virus. That example shows that triple selection pressures slow down the evolution of the virus.
The use of triple antiviral medications to treat HIV is a very nice example of how mutation and selection works. I’m simply playing the evolutionist game by the evolutionist rules. The evolutionist computer model ev shows mathematically the same results as the real example of the treatment of HIV. These examples also show why multiple selection pressures slow evolution.Of course it is a nice example of how certain types of selection pressures and mutation works. That is not the issue. The issue is that you made a very specific claim about it -- that it represents three selection pressures. I assume that you mean an actual three, as in not two and not four or more. That claim is wrong. There are many more than three selection pressures at work. And that particular selection pressure is very specific and not like the typical selection pressures one sees in nature or, again, I would assume are modelled in ev. That's all I'm saying. I'm saying your analogy is poor.
Oh, that’s right, our Sesame Street drop out, Dr Richard, says there are thousands of selection pressures acting on HIV. I wonder if he would care to describe the fitness landscape mathematically. Then Paul could mathematically model the evolution of the HIV virus from the beginning.
Extinction does not lead to evolution, extinction is the end of a genetic lineWhoa, extinction is the end of the line? Really?

Give me a break. This is not first grade. Please stop preteding that no one knows what words mean but you.

Evolution is not a process affecting a single entity or one species. Last time I checked, there was a great big world out there with numerous competing species, competing individuals. They change over time. That is evolution. It is simply stupid to say that evolution ends when one species dies. Evolution doesn't end. It isn't slowed. It continues. Certain pressures lead to extinction. Fact.
Extinction represents the loss of genetic information.
The reason you have no idea what I’m talking about is that you don’t understand the mathematics of ev.I have a very good idea what you are talking about. You are simply wrong. Your metaphor is wrong.

Do you still want to defend this metaphor?
Certainly I will continue to defend this metaphor. Delphi has helped me with this defense when he gave the link to Wikipedia fitness landscape.
If parasites kill their host before they can complete their life cycle then they will go extinct. Syphilis is no longer an absolute scourge because of the advent of antibiotics, also the selective pressure on the host has selected out those who can’t mount a strong immune response against the bacteria.Good, so you now agree that early host death is a selection pressure on a parasite? If you haven't bothered reading the literature on syphilis I suggest you do so. The spirochete became less virulent long before the use of antibiotics. Or do you want to deny this reality as well?
Really? What was the most common cause for aortic arch aneurysm before the use of antibiotics? Untreated syphilis is still a profoundly destructive disease.
Any of the selection pressures you allege are so weak that the sum of all pressures have no affect on the outcome of the disease when compared to the affect of triple antiviral therapy.What difference does that make? You can't model weak selection pressures? The whole point is that if you give an organism a selection pressure or pressures that they cannot overcome, then they will become extinct. Nothing magical there. It isn't the number that matters. It is the type of pressure. If you haven't noticed that is what I have been going on about for these several posts that are becoming increasingly boring and repetitious.
If your alleged selection pressures have no affect on reproduction then they have no effect on evolution. You need to learn the basics of your own theory.
You are making a distinction where none exists. A selection pressure by definition is one which affects the ability of a creature to reproduce. Ultimately, all these pressures act somewhere at the genetic level. Whether the pressure acts directly on enzymes involved in reproduction of the genome or at some other metabolic step which is required for the creature to survive, they all affect the fitness of a creature to reproduce. If you starve a creature, you deprive the creature of the required energy and materials needed to reproduce. This is an example of multiple selection pressures. If you deprive a creature of a single essential nutrient, you impair the reproduction of that creature with a single selection pressure. You continue to focus on the wrong issue. No one claims that the site (molecular vs organism as a whole) of the selection pressure is the absolute critical entity. The point is that a selection pressure that directly affects fitness and will not allow any reproduction is different from a relative pressure that still allows some reproduction. The number of factors is not critical. The critical issue is how effective the pressure is in preventing reproduction. Strong effect -- big effect on fitness. Weak effect -- weak effect on fitness. Completely stop reproduction and the organism will go extinct. But that is not the reality of most selection pressures in the wild (except, of course, for the rally big ones that do cause extinction). Most selection pressures are relatively weak. They affect fitness but do not generally completely stop reproduction. Even when they are present in large numbers, as you seem to agree is the case with the very large number of selection pressures affecting HIV. You did agree above that there are many selection pressures affecting HIV did you not?
Ev’s selection conditions don’t allow for extinction and shows how slow the evolutionary process is with only three selection conditions. If a selection condition is so weak to have little effect on reproduction, it will have little effect on evolution. The mathematical point is that selection increases the frequency of sequences of bases in the population. The mathematical conundrum that evolutionist have to face is that multiple selection pressures confound this process.
As I said previously to Delphi, there is nothing special about three selection pressures other than it only takes three selection pressures to profoundly slow evolution. Where is your evidence? It cannot be HIV. HIV has many more than three selection pressures. You have already admitted that most of those selection pressures are rather weak. Good, we agree. That is my point. Three selection pressures do not profoundly slow evolution. There is nothing special about the number three in slowing evolution (again, whatever that phrase means).
Ev shows that three selection conditions profoundly slow evolution. The treatment strategy for HIV using three selection pressures slow the evolutionary process and now Delphi has given us the Wikipedia definition for fitness landscape which shows that multiple selection conditions slow evolution.

If you think that multiple selection conditions speed up evolution, give us some mathematical proof or a physical example of your contention. I have given you both for my contention.
There can very easily be something special about certain types of pressures that slow the process of change in a particular organism because that (or those) pressure(s) significantly hit fitness for that organism. But that is the critical issue -- the particular effect on fitness of the pressure involved. There could be several hundred weak selection pressures that help to create changes in organisms. That is, in fact, what I would expect from nature.
There is nothing special about the selection conditions used in ev. Give Paul a set of selection conditions to use in ev to speed up evolution.
You can say that three selection pressures profoundly slow evolution. But you would be wrong. That statement must be qualified. It is not the case that the number three is in any way important. It is the types of pressures that matter.
I have qualified my statement mathematically with ev, by physical example with the case of treatment of HIV by triple selection pressures and now thanks to Delphi, have the Wikipedia definition of fitness landscape. How have you qualified your position?
Or, to make the point again, we seem to have identifed hundreds, if not thousands, of selection pressures working on HIV -- all of which existed before the introduction of triple therapy -- during which time the virus was reproducing and mutating into many different forms. So, it cannot be the case that three selection pressures (or an increasing number of selection pressures) necessarily profoundly slows "evolution". Once again, it is not the number, but the type of selection pressure that is critical.
Only those pressures that affect reproduction are selection pressures. Before the advent of antiretroviral medications, the only selective pressures a person could mount against HIV was the production of immunoglobins and cell mediated immunity. There were not thousands of selective pressures mounted against the virus. Neither of these selective pressures were sufficient to impair reproduction of the virus significantly. That why the vast majority of the people with HIV died from the consequences of their disease.

[Ichneumonwasp]

Read Delphi’s link to Wikipedia and fitness landscape. It doesn’t matter whether the selection pressures are man-made or from environmental sources. The mathematics is identical.


For the nth figgin' time, I am not claiming that the issue is man-made vs environmental. The issue is a pressure that completely blocks any possibility of reproduction and one that does not. How many time must I repeat the same thing?

Of course you are not going to play this game. Evolutionists already know that multiple selection pressures slow evolution. The treatment of HIV with three selective pressures slows the evolution of the virus. This is what ev shows and this is what the Wikipedia definition for fitness landscape shows.


No. Please follow. I am not playing the obfuscation game. We are discussing one matter and one matter alone right now. Deal with the issue at hand. The rest can wait until after this issue is resolved.

Well tell us, do you believe multiple selection pressures speed up or slow down evolution?

I'm sorry, but are you brain-damaged or something? IS this now the twentieth time for me to tell you that I'm not playing that game. Deal with your analogy in this series of posts, nothing else. The rest waits for later.

That example shows that triple selection pressures slow down the evolution of the virus.


How? You seemed to agree up above that there were other selection pressures. Do you retract that implication? There were host selection pressures from the immune system, host selection pressures from early death once the diseae course began, selection pressures related to transcription rates and competition for transcription, etc. Those are all selection pressures. There are more than three. No slowing of evolution.

Extinction represents the loss of genetic information.


Yeah, so? And when new organisms replace the extinct species?

Really? What was the most common cause for aortic arch aneurysm before the use of antibiotics? Untreated syphilis is still a profoundly destructive disease.


Who said it wasn't? It wasn't the same disease as when it first appeared, though. It allowed the infected to survive and reproduce instead of killing them quickly. Rapid death of a host is a selective pressure on parasites. Parasites that kill quickly, like syphilis when it first appeared, tend to become less deadly over time because those variants that allow the host to survive longer can make more copies.

If your alleged selection pressures have no affect on reproduction then they have no effect on evolution. You need to learn the basics of your own theory.


They do. Rapid death of a host has a distinct effect on the reproduction ability of a parasite. As does anything that can potentially interfere with transcription when a retrovirus is at play. As can the immune response that tires to keep the retrovirus out of its target cell of choice, so that it cannot reproduce. Those are all selection pressures. They all existed before triple therapy became available.

If a selection condition is so weak to have little effect on reproduction, it will have little effect on evolution.

Thank you. Finally. So, you agree that it is not the number but the type of selection pressure that is important?

The mathematical conundrum that evolutionist have to face is that multiple selection pressures confound this process.


Wait, you just agreed that selection conditions that have little effect on reproduction will have little effect on evolution. You just said that up above. Multiple little effects does not mean one bi