Annoying creationists

[Paul C. Anagnostopoulos]

Kjkent and others: I am not ignoring your posts, but I'm off to New Jersey for a model car show. First things first.

~~ Paul

 

[Dr Adequate]

Lie #1.

Truth #1.

 

[Paul C. Anagnostopoulos]

OK, meanwhile, perhaps Paul will provide his own opinion. If I'm wrong, that's fine, but it seems pretty obvious to me that setting any of the mistake weights to zero allows the program to introduce mistakes in the genome and then fail to select for those errors. This is nearly the same as turning selection off.

Mistakes are not "introduced," they are there to begin with. Otherwise, yes, there is no selection pressure to cause binding at binding sites, and/or no pressure to eliminate spurious bindings, depending on which mistake counts are set to zero.

The various combinations of zero mistake counts are certainly going to effect the number of generations to a perfect creature, not only because it might be "easier" to evolve a creature with fewer selection constaints, but also because the idea of a perfect creature doesn't even make sense in those scenarios. That is why Rcapacity, Rfrequency, and Rsequence are irrelevant.

~~ Paul

 

[Myriad]

I see you’ve added a new button since I last used your java version of ev.

LMAO! So much for Kleinman's claims to have performed a parametric analysis of ev. He apparently didn't even bother to find out what all the parameters are.

Respectfully,
Myriad

 

[kjkent1]

Mistakes are not "introduced," they are there to begin with. Otherwise, yes, there is no selection pressure to cause binding at binding sites, and/or no pressure to eliminate spurious bindings, depending on which mistake counts are set to zero.

The various combinations of zero mistake counts are certainly going to effect the number of generations to a perfect creature, not only because it might be "easier" to evolve a creature with fewer selection constaints, but also because the idea of a perfect creature doesn't even make sense in those scenarios. That is why Rcapacity, Rfrequency, and Rsequence are irrelevant.

~~ Paul

Thanks. I think we're saying pretty much the same thing using different words.

 

[Paul C. Anagnostopoulos]

Thanks. I think we're saying pretty much the same thing using different words.

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.

~~ Paul

 

[kleinman]

Annoying Creationists

With missing binding sites set to 0, spurious bindings inside the gene set to 1 and spurious binding outside the gene set to 0, and set “pause on perfect creature” does not yield a random binding site region. It yields a binding site region without spurious bindings. The non-binding site region remains random. Likewise, with missing binding sites set to 0, spurious binding inside the gene set to 0 and spurious bindings outside the gene set to 1, and set “pause on perfect creature” does not yield a random non-binding site region. It yields a non-binding site region without spurious bindings. The binding site region in this case does remain random. …

OK, meanwhile, perhaps Paul will provide his own opinion. If I'm wrong, that's fine, but it seems pretty obvious to me that setting any of the mistake weights to zero allows the program to introduce mistakes in the genome and then fail to select for those errors. This is nearly the same as turning selection off.

I’m also interested in hearing how Paul is going to explain this result from ev away.

I definitely don’t want to get into a pissing contest with someone who always needs a drink, I concede that honor to you.

After reading your same tired arguments couched in the same mathematical word salad in the same annoying formatting while you make the same lame joke about drinking for pages on end, even Muhammad would need a drink.

Same tired arguments? Here’s a little lesson in the nonlinear mathematics of mutation and selection that is shown by ev. You can not separate the individual selection process in ev, allow the individual selection processes to evolve their gene sequences and then superimpose the solutions and get the same results as running ev with all selection processes acting simultaneously. 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.

Do you want to explain how the overall fitness will evolve a gene from the beginning? How do you include what you have just said in a mathematical model of mutation and selection?

What ev reveals about competing selection processes is demonstrated with the use of multiple antimicrobials. Evolution is slowed if not halted in the HIV by using the three antimicrobials. The prevention of the changes in the genotype prevent the change in the phenotype.

Did I say anything about ev? Or abiogenesis? No. I was simply pointing out that you were wrong in your conception of natural selection.

Really, then why is ev showing that simultaneous selection pressures stop evolution and why are multiple antimicrobials often used to treat infections?

Let’s see if I can understand your logic. Genes arose in abiogenesis and given enough time these genes evolved into evolutionists. I will try not to confuse genes and evolutionists. In addition, I will try not to confuse abiogenesis with the theory of evolution. One is utter nonsense, the other is simply mathematically impossible. You can guess which one is which.

Abiogenesis and evolution are two completely different things. Now I think I am beginning to understand why you fail to grasp this. You are using a popular definition of a gene, not one that actual geneticists use.

Yes, abiogenesis is utter nonsense and the theory of evolution by mutation and selection is mathematically impossible as show by ev and observed in reality.

Paul, Dr Schneider uses the following definition for Rfrequency:

Rfreqency = -log2(gamma/G)

Rfrequency is dependent only the number of binding sites and the length of the genome. The selection process is not in the definition of Rfrequency.

Sigh. Rfrequency is a calculation of how many bits of information are required to uniquely identify the binding sites from among the rest of the genome. Implicit in this calculation is the idea that you are actually going to identify the binding sites from among the rest of the genome. If you are not, Rfrequency is irrelevant. Setting any of the three mistake counts to zero means you are not identifying the binding sites.

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.

Your definition for Rcapacity is as follows:

Rcapacity = 2*binding site width

The selection process is not in your definition of Rcapacity.

Rcapacity is only interesting when compared to Rfrequency. Since Rfrequency is irrelevant in your scenarios, so is Rcapacity.

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.

OK, meanwhile, perhaps Paul will provide his own opinion. If I'm wrong, that's fine, but it seems pretty obvious to me that setting any of the mistake weights to zero allows the program to introduce mistakes in the genome and then fail to select for those errors. This is nearly the same as turning selection off.

Mistakes are not "introduced," they are there to begin with. Otherwise, yes, there is no selection pressure to cause binding at binding sites, and/or no pressure to eliminate spurious bindings, depending on which mistake counts are set to zero.

Well said. Setting a particular mistake weight factor to zero is simply eliminating that selection pressure.

The various combinations of zero mistake counts are certainly going to effect the number of generations to a perfect creature, not only because it might be "easier" to evolve a creature with fewer selection constaints, but also because the idea of a perfect creature doesn't even make sense in those scenarios. That is why Rcapacity, Rfrequency, and Rsequence are irrelevant.

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.

I see you’ve added a new button since I last used your java version of ev.

LMAO! So much for Kleinman's claims to have performed a parametric analysis of ev. He apparently didn't even bother to find out what all the parameters are.

Hey Myriad, you don’t have to giggle, whoops jiggle the weight factors in order to get ev to converge more quickly, all you have to do is eliminate two of the three selection condition and ev will converge. It is the competing selection conditions that slows and then ultimately stops convergence of ev. You know that happens in reality.

 

[Taffer]

Really, then why is ev showing that simultaneous selection pressures stop evolution and why are multiple antimicrobials often used to treat infections?

Um...kleinman? Multiple resistant bacteria are evidence of evolution. It is also a simple fact that a the overall fitness of an organism depends on the sum of all fitnesses at individual loci. It is also a fact that not all deleterious mutations are fatal.

Yes, abiogenesis is utter nonsense and the theory of evolution by mutation and selection is mathematically impossible as show by ev and observed in reality.

I'm sorry, kleinman, but the rest of the academic world does not agree with you. Evolution is an observable fact.

 

[kleinman]

Annoying Creationists

Really, then why is ev showing that simultaneous selection pressures stop evolution and why are multiple antimicrobials often used to treat infections?

Um...kleinman? Multiple resistant bacteria are evidence of evolution. It is also a simple fact that a the overall fitness of an organism depends on the sum of all fitnesses at individual loci. It is also a fact that not all deleterious mutations are fatal.

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.

Yes, abiogenesis is utter nonsense and the theory of evolution by mutation and selection is mathematically impossible as show by ev and observed in reality.

I'm sorry, kleinman, but the rest of the academic world does not agree with you. Evolution is an observable fact.

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.

 

[Taffer]

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.

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.

 

[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.






~~ Paul

OK, 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.

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]

Annoying Creationists

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.

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]

Annoying Creationists

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 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

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

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".

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.

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