• Quick note - the problem with Youtube videos not embedding on the forum appears to have been fixed, thanks to ZiprHead. If you do still see problems let me know.

Annoying creationists

Status
Not open for further replies.
Kleinman said:
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
 
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?
 
Last edited:
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.
 
Annoying Creationists

Kleinman said:
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.
Paul said:
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?
Kleinman said:
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.
Paul said:
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.
Kleinman said:
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.
Paul said:
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.
Ichneumonwasp said:
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.
Ichneumonwasp said:
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.
Ichneumonwasp said:
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.
Ichneumonwasp said:
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.
Ichneumonwasp said:
Why so much emphasis on HIV?
kjkent1 said:
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.
 
Kleinman said:
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
 
Kleinman said:
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.
 
Annoying Creationists

Kleinman said:
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.
Paul said:
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.
Kleinman said:
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.
Paul said:
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.
Kleinman said:
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.
Ichneumonwasp said:
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.
Ichneumonwasp said:
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.
Ichneumonwasp said:
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.
Kleinman said:
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.
Ichneumonwasp said:
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.
Kleinman said:
No, the drugs target different sites.
Ichneumonwasp said:
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.
 
Kleinman said:
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.
 
Last edited:
Ichneumonwasp said:
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
 
Annoying Creationists

Kleinman said:
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.
Ichneumonwasp said:
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?
Kleinman said:
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.
Ichneumonwasp said:
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.
Ichneumonwasp said:
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.
Kleinman said:
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.
Ichneumonwasp said:
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.
Kleinman said:
Ask Paul, if you can make a good case that you will improve the rate of convergence of ev, he may do it.
Ichneumonwasp said:
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.
Kleinman said:
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 said:
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.
 
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.
 
Kleinman said:
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
 
Kleinman said:
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
 
Annoying Creationists

Kleinman said:
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.
Paul said:
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.
Kleinman said:
Dr Schneider’s selection conditions are a contrivance that does not occur in reality.
Paul said:
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.
Kleinman said:
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.
Paul said:
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?
Paul said:
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.
Kleinman said:
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.
Paul said:
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.
Paul said:
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.
 
Kleinman said:
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
 
Last edited:
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.
 
Annoying Creationists

Kleinman said:
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.
Paul said:
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.
Kleinman said:
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?
Paul said:
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?
Kleinman said:
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.
Paul said:
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.)
Kleinman said:
So do you think that your estimate in the following case is going to be accurate?
Paul said:
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.
 
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.
 
Kleinman said:
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.

Kleinman said:
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.
 
Last edited:
you know who said:
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.
 
Status
Not open for further replies.

Back
Top Bottom