Rebuttal To Creationists - "Since We Can't Directly Observe Evolution..."

Kleinman:

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What's the matter, in 26 years of research you never tried to model a real example?

Taq:

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What's the matter, can't address the math I presented?

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I've done the mathematics for real, measurable, and repeatable experiments. The Lenski experiment has been going on for 30 years, the Kishony experiment has been performed with multiple different drugs. What point are you trying to make with your mathematics of imaginary models? Are you trying to show that adaptive recombination can occur if the adaptive mutations can amplify? I already showed that can happen and published that result. In Message 2564, I show how to do the probability calculation when there are multiple possible adaptive mutations and it has a slight effect on the evolutionary process but nothing like the multiplication rule has. And sure, there may be a few cases of HIV treated with 3 drug therapy that is defeated by recombination (or descent with modification) but at the same time, tens of millions of people are successfully treated with 3 drug therapy. That's because these are stochastic processes and when you have millions of cases, somebody is going to win two lotteries. If you want me to address your mathematics, take one of the real examples that you think contradicts the model I've presented and formulate your model and mathematics, and show that my model is incorrect. That mathematics, I will address, but your imaginary models are a waste of time.

Yes, in asexual populations, not in sexual populations. I am showing you that your addition rule allows for beneficial alleles at different loci in sexual populations to move towards fixation together. These alleles can be at any frequency and still add up to 1 in your equation.This also refutes your multiplication rule in sexual populations when those mutations are at unlinked loci. You don't have to repeat the same mutations in one genetic background. Instead, beneficial alleles in different genetic backgrounds are moved into the same genetic background through recombination. This is what is seen in real populations in real experiments:

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Together, our results show that sex increases the rate of adaptation both by combining beneficial mutations into the same background and by separating deleterious mutations from advantageous backgrounds that would otherwise drive them to fixation. In other words, sex makes natural selection more efficient at sorting beneficial from deleterious mutations. This alters the rate and molecular signatures of adaptation.
Sex speeds adaptation by altering the dynamics of molecular evolution | Nature

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You won't address anything that is outside of your conman script.

Kleinman:

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I've done the mathematics for real, measurable, and repeatable experiments.

Taq:

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Yes, in asexual populations, not in sexual populations.

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You really are a stupid ass. What do you think my paper about recombination was all about?

Kleinman:

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What point are you trying to make with your mathematics of imaginary models? Are you trying to show that adaptive recombination can occur if the adaptive mutations can amplify?

Taq:

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I am showing you that your addition rule allows for beneficial alleles at different loci in sexual populations to move towards fixation together. These alleles can be at any frequency and still add up to 1 in your equation.
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This also refutes your multiplication rule in sexual populations when those mutations are at unlinked loci. You don't have to repeat the same mutations in one genetic background. Instead, beneficial alleles in different genetic backgrounds are moved into the same genetic background through recombination. This is what is seen in real populations in real experiments:

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What, do you want to celebrate that you finally figured out how to use the addition rule when there are intersections of the subsets? You should have learn that long ago, but you are an extremely slow learner. And in your delusional mind you think that multiple different alleles can fix in a population. So, fA = 0 and fB = 0, and fAB = 1. Your only problem is that it doesn't happen with real examples of evolution. And the frequency equation is not my equation, stupid.

Kleinman:

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That mathematics, I will address, but your imaginary models are a waste of time.

Taq:

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You won't address anything that is outside of your conman script.

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Oh really, your script that reptiles evolve into birds and fish evolve into mammals, and evolution always behaves like the Desai experiment is the correct script. You are too stupid to do the mathematics of a real example. You are an idiot virologist that can't explain how drug resistance evolves and why cancer treatments fail. You are too busy doing imaginary problems. You dummy.

Then lets see your math in a real population. Why can't they? You are the one who claimed that only the fittest beneficial mutation out of all beneficial mutations could reach fixation and the fittest mutation would drive the others to extinction. You based this on the addition rule. This is obviously false in a sexual population.You are also avoiding the fact that your multiplication rule is busted. Mutation A and Mutation B can happen in different individuals, and those mutations can be combined in offspring. You don't have to wait for those with Mutation A to replicate a further X number of times until Mutation B happens in the same genetic background.

Kleinman:

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What do you think my paper about recombination was all about?

Taq:

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Then lets see your math in a real population.

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You are a blithering inattentive idiot.
Random recombination and evolution of drug resistance
You inattentive dummy.

Kleinman:

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And in your delusional mind you think that multiple different alleles can fix in a population.

Taq:

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Why can't they?

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It is because when an allele fixes, it is in 100% of the population.
Fixation - Wikipedia(population_genetics) How many times do I have to post this before it gets through your thick skull.

Kleinman:

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And the frequency equation is not my equation, stupid.

Taq:

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You are the one who claimed that only the fittest beneficial mutation out of all beneficial mutations could reach fixation and the fittest mutation would drive the others to extinction. You based this on the addition rule. This is obviously false in a sexual population.
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You are also avoiding the fact that your multiplication rule is busted. Mutation A and Mutation B can happen in different individuals, and those mutations can be combined in offspring. You don't have to wait for those with Mutation A to replicate a further X number of times until Mutation B happens in the same genetic background.

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I don't claim that about fixation, that's how biologists define fixation. It is in the Wikipedia definition, it is in my biology text, the only place that definition doesn't apply is in your thick skull. And you don't know anything about the multiplication rule. That's why you can't explain how drug resistance evolves and why cancer treatments fail. You are a mathematically incompetent virologist that doesn't understand the physics and mathematics of biological evolution. And you are too stupid to understand that adaptive recombination only occurs when the individual alleles can amplify. The successful treatment of HIV with 3 drug therapy and combination therapy for weed and insect control demonstrates that these alleles don't always amplify. Only in your mathematically irrational imagination is adaptive recombination a commonplace occurrence. In your mind, all environments are constant single selection pressure environments. You dummy.

That's a made up population. Show us the math for a real population. So why can't you have a fixed allele in multiple genes? I did explain it. Sexual recombination can speed up antibiotic resistance when beneficial mutations occur in unlinked loci. I already gave you that paper:Sexual recombination and increased mutation rate expedite evolution of Escherichia coli in varied fitness landscapes - PMCMutations that confer chloramphenicol resistance can occur in different genes. If these different mutations exist on different genetic backgrounds they can be combined into a single genetic background through recombination which would speed up adaptation by avoiding the multiplication rule.How many times do I need to point this out? It happens in every generation in all sexually reproducing species.

Kleinman:

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You are a blithering inattentive idiot.

Taq:

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That's a made up population. Show us the math for a real population.

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Now the brilliant virologist thinks that HIV isn't real.

Kleinman:

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It is because when an allele fixes, it is in 100% of the population.

Taq:

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So why can't you have a fixed allele in multiple genes?

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Now the brilliant virologist thinks the entire population is identical, with no variation at all. Why did Haldane and Kimura even bother writing papers on fixation?

Kleinman:

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And you don't know anything about the multiplication rule. That's why you can't explain how drug resistance evolves and why cancer treatments fail.

Taq:

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I did explain it. Sexual recombination can speed up antibiotic resistance when beneficial mutations occur in unlinked loci. I already gave you that paper:
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Sexual recombination and increased mutation rate expedite evolution of Escherichia coli in varied fitness landscapes - PMC
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Mutations that confer chloramphenicol resistance can occur in different genes. If these different mutations exist on different genetic backgrounds they can be combined into a single genetic background through recombination which would speed up adaptation by avoiding the multiplication rule.
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How many times do I need to point this out?

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Why don't you do the model and mathematics of chloramphenicol resistance? Oh, that's right, it isn't imaginary and you only do the mathematics of imaginary problems.You will need to point this out until you correctly do the mathematics which means forever. Too bad they didn't show you how to do the math in your survey of math course.And you need to understand a topic before you can explain the topic. Try doing the math.

Kleinman:

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Only in your mathematically irrational imagination is adaptive recombination a commonplace occurrence.

Taq:

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It happens in every generation in all sexually reproducing species.

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Now the brilliant virologist claims that every recombination event is an adaptive recombination event. No wonder he can't explain the evolution of drug resistance and why cancer treatments fail. Good job virologist.

Yes, he is full of it. He is also a truck driver in the Philippines who has collected a lot of YEC rubbish and posted it in one long run-on -- consider the ID nonsense posted by his compatriot, MrIntelligentDesign. The best that he accomplishes is to demonstrate that US and Australian YECs have been successful in polluting the rest of the world with their nonsense.And, like with all creationists, nobody will ever collect his offer of a reward to anyone refuting his page because he will not honor that offer. Like trying to collect on a MAGAt reward for finding a case of voter fraud -- what few cases could be found were all Republicans voting more than once for Trump, not what that Texan MAGAt expected.So much garbage there to wade through, plus most of it consists of bald assertions without any backing, hence giving us nothing to work with. But let's look at his section on population growth, which is perhaps one of the stupidest YEC claims out there.The main thrust of his claim is to argue that by using "reasonable" population growth rates the current world population could have resulted within 6000 years from the Biblical First Family. However, that does not limit the length of time, such that humans could have existed for 300,000 years before our population's growth spurt.His "response" is to assert the standard YEC population claim:

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If scientists are right by claiming animals and humans appeared millions of years ago, even if millions die annually from natural causes and diseases, there will be trillions upon trillions of animals and people today, stacking 200 feet high on all of Earth’s surface.

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Even if dogs and pigs perform %90 abortions, out of their 20 offspring every few months, the population will reach billions in a few years.

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People and animals crowded together such that they cover all the earth's surface (including the oceans making up about 75% of our planet's surface)? Absolutely impossible! And incredibly stupid!The problem is that Dr. Henry Morris, the source of this YEC claim (he presented it in his 1961 The Genesis Flood and continued to develop it over the years; see my CompuServe library article, THE BUNNY BLUNDER (or What's Up, Doc Morris?). Morris used the highly simplistic pure-birth model which is the exponential growth of a population with no constraints (eg, the initial population growth from that first fruit fly couple you put into the jar in high school biology). The truth of the matter is that you need to use something like the logistic model of population growth in which that initial exponential turns into a logarithmic curve as it approaches the environment's carrying capacity somewhat asymptotically. IOW, no environment will support a population which is larger than what it can support.For example, consider a population of human hunter-gatherers living in something like the Kalahari Desert (population density of about 1 per square mile). Let's take that as how many people a square mile area in that environment can support. Now let's assume that this population will range five miles in any direction, so they must draw from an area of 100 square miles for sustenance. That would set their maximum population at 100 individuals. Below that population limit and there's enough to eat and their population can grow. But above that population limit there's not enough food, and the more you go past that population limit the more the lack of food will be felt, including death by starvation.So then, if an environment can only support 100 individuals, what should we expect the population size to be after 100 years? Or 1000? Or 100,000? Or a million? Or millions? About 100. That creationists would expect that population to be in the millions just demonstrates how mind-bogglingly stupid creationism is.BTW, their human population growth claim is called "The Bunny Blunder" because applying their model to rabbits "proves" that the current world population of rabbits originated from two bunnies about 100 years ago, therefore the earth cannot be any older than one century.Nothing to see there. Unless one wishes to see what kind of nonsense creationists are pushing.

You are using a made up population of HIV. Use a real population. Now the conman is avoiding the question.So why can't you have a fixed allele in multiple genes? I already have the data, which you are avoiding:Sexual recombination and increased mutation rate expedite evolution of Escherichia coli in varied fitness landscapes - PMC You already said it yourself."Now the brilliant virologist thinks the entire population is identical, with no variation at all. Why did Haldane and Kimura even bother writing papers on fixation?"--KleinmanSo do you think all genomes in sexually reproducing populations are identical. If not, then there are going to be recombination events that are more beneficial than others. So says the person who can't explain drug resistance. Why is chloramphenicol resistance aided by sexual recombination while trimethoprim resistance is not? Can you answer that question? No, because it isn't part of your conman script, and you have no idea how antibiotic resistance or sexual reproduction works.

Kleinman:

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Now the brilliant virologist thinks that HIV isn't real.

Taq:

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You are using a made up population of HIV. Use a real population.

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You are having trouble understanding the model. I use various frequencies of adaptive alleles to determine the probability of an adaptive recombination event occurring. The probability of an adaptive recombination event occurring depends on the frequencies of the adaptive alleles in the population. In your case, you choose a selection factor that insures that the frequencies of the adaptive alleles will be high. In the case of HIV, weeds, and insects, the selection factor(s) do not give high frequencies of the adaptive allele. The Desai experiment gives a situation where the selection factor will be high enough and constant for a long enough duration for the frequencies of the adaptive alleles to increase to give a reasonable probability of an adaptive recombination event occurring. And that is a constant environment with only a single selection condition. That's why your model and the Desai experiment only apply in very limited circumstances, certainly not the wild. You take the results of a limited experiment and try to apply this to all evolution. This is why you don't understand biological evolution.

Kleinman:

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Now the brilliant virologist thinks the entire population is identical, with no variation at all. Why did Haldane and Kimura even bother writing papers on fixation?

Taq:

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Now the conman is avoiding the question.
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So why can't you have a fixed allele in multiple genes?

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Go back to the original problem, the evolution of humans and chimps from a common ancestor. What are you assuming? Are they arising from a common gene pool? If so, why do humans have reproductive fitness over chimps? Are humans just lucky and the shuffling of existing alleles was just better than the shuffling of existing alleles for chimps? Or were new alleles generated that gave that increase in fitness? You think that in a single biological competition process multiple alleles can be fixed simultaneously. Even Desai's experiment doesn't show that. Tell us what environment and what selection condition did this for humans and chimps because it certainly doesn't happen for HIV, weeds, and insects.

Kleinman:

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Why don't you do the model and mathematics of chloramphenicol resistance?

Taq:

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I already have the data, which you are avoiding:
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Sexual recombination and increased mutation rate expedite evolution of Escherichia coli in varied fitness landscapes - PMC

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You are a liar. Their population size varied. You assumed a constant population size of n = 100,000, a selection value of 0.01 which forces fA and fB to increase, and your calculation uses 6 generations when their experiment collected data over 250 generations. You haven't modeled their experiment, you have modeled what is in your imagination. Your calculation is garbage and you are a liar.

Kleinman:

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Now the brilliant virologist claims that every recombination event is an adaptive recombination event.

Taq:

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You already said it yourself.
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"Now the brilliant virologist thinks the entire population is identical, with no variation at all. Why did Haldane and Kimura even bother writing papers on fixation?"--Kleinman
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So do you think all genomes in sexually reproducing populations are identical. If not, then there are going to be recombination events that are more beneficial than others.

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You are really stupid. Recombination does occur, if you have siblings, you know that. But you know nothing about reproductive fitness except by the number of offspring. And that number varies for many reasons. So, why are there only about 300,000 chimps and 8e9 humans today? What recombination events give humans the capability to do industrial farming, build and fly aircraft, build dams and power plants, while chimps still haven't figured out fire and the wheel? Was it a constant environment and single selection pressure? If so, why didn't it happen for chimps?

Kleinman:

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No wonder he can't explain the evolution of drug resistance and why cancer treatments fail. Good job virologist.

Taq:

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So says the person who can't explain drug resistance. Why is chloramphenicol resistance aided by sexual recombination while trimethoprim resistance is not? Can you answer that question? No, because it isn't part of your conman script, and you have no idea how antibiotic resistance or sexual reproduction works.

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This is your example of drug resistance and so far your model is crap, but it does fit your script. Why don't you do the model for chloramphenicol resistance correctly instead of doing your garbage? Did it ever enter your mind that they did 55 generations of selection in a constant environment? Stop being a dumbass and doing this model like a lower-division undergraduate. Perhaps you are just too stupid to do the math correctly.

That's what I did too, but you refused to even comment on it because it was not a "real population". So you have to meet your own requirements.Show me your math based on a real data from a real population of sexually reproducing organisms. How is that any different than the Lenski and Kishony experiments? Can you show why they can't? The Desai experiment demonstrated that many different beneficial alleles were moving towards fixation at once. What would stop them from all reaching fixation over time? HIV, weeds, and insects have not been evolving for 5 million years an environment containing man made challenges of drugs and pesticides. That's one massive difference you are ignoring. What the fuck are you even talking about?????? The stupid burns.It is the mutations that differ between our species. It is sexual recombination that put the beneficial mutations into the same background. If you want to know where to look for those beneficial mutations, they are the mutations that differ between the genomes of our species. Not that hard to figure out. The model is right here:Sexual recombination and increased mutation rate expedite evolution of Escherichia coli in varied fitness landscapes - PMC Have you forgotten once again that the Lenski and Kishony experiment used constant environments?

Kleinman:

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You are having trouble understanding the model. I use various frequencies of adaptive alleles to determine the probability of an adaptive recombination event occurring.

Taq:

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That's what I did too, but you refused to even comment on it because it was not a "real population". So you have to meet your own requirements.
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Show me your math based on a real data from a real population of sexually reproducing organisms.

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You are a liar. You used a selection factor of 0.01 for all your examples. That insures that the frequencies will all be high after just 6 generations of selection. If you think your model represents all cases of recombination, get it published. You won't because it doesn't. On the other hand, my model tells something very important about adaptive recombination, it depends on the frequencies of the alleles in the population. And that relationship can be explained by a trinomial distribution.

Kleinman:

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The Desai experiment gives a situation where the selection factor will be high enough and constant for a long enough duration for the frequencies of the adaptive alleles to increase to give a reasonable probability of an adaptive recombination event occurring. And that is a constant environment with only a single selection condition. That's why your model and the Desai experiment only apply in very limited circumstances, certainly not the wild.

Taq:

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How is that any different than the Lenski and Kishony experiments?

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If Desai didn't use a constant environment with constant selection with a single selection pressure, he wouldn't have gotten amplification of his alleles and you should know that. Why don't you write your model with varying selection conditions so that A and B won't be amplified but some other alleles will be, say C and D. And as soon as they start to amplify, change the selection condition so that different alleles are amplified, say E and F. What do you think your model would tell you? Which alleles are being amplified in a varying environment with varying selection conditions?

Kleinman:

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You think that in a single biological competition process multiple alleles can be fixed simultaneously.

Taq:

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Can you show why they can't?

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I don't have to, Haldane and Kimura already did that. Of course, you think they are wrong. You should publish your work that shows that they are wrong. Make sure you tell everyone that when an allele reaches 40% frequency in a population, it is fixed.

Kleinman:

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Even Desai's experiment doesn't show that.

Taq:

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The Desai experiment demonstrated that many different beneficial alleles were moving towards fixation at once. What would stop them from all reaching fixation over time?

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Those alleles are amplified because there is constant selection for 90 generations in a single selection pressure environment. What would stop them from amplifying is there is a new most fit variant starting another cycle of competition. Of course, your sloppy use of mathematics would say they would continue amplifying.

Kleinman:

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Tell us what environment and what selection condition did this for humans and chimps because it certainly doesn't happen for HIV, weeds, and insects.

Taq:

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HIV, weeds, and insects have not been evolving for 5 million years an environment containing man made challenges of drugs and pesticides. That's one massive difference you are ignoring.

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You are avoiding the question. What environment and selection condition give the selective advantage of humans over chimps? You and Desai are using a single selection pressure constant environment. What constant environment and what selection condition gives the selective advantage that humans have over chimps? You should say "I don't know". Then I would ask you, is there any constant environment, single selection pressure environment that gives selection advantage of humans over chimps and you can use your numbers, 6 generations? There is no such thing and you should know it.

Kleinman:

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You assumed a constant population size of n = 100,000, a selection value of 0.01 which forces fA and fB to increase, and your calculation uses 6 generations when their experiment collected data over 250 generations. You haven't modeled their experiment, you have modeled what is in your imagination.

Taq:

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What the fuck are you even talking about??????

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You are such an idiot. You don't even know what numbers you are using. From Message 2553

Taq:

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I will use a population of 100,000

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and your selection factor from your Python program where you increment i:

Taq:

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f = i*0.01
fA = f
fB = f

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and from your paper, they have many references to the number of generations they ran their experiment, here's just one:
Sexual recombination and increased mutation rate expedite evolution of Escherichia coli in varied fitness landscapes - PMC Why don't you try reading your own papers?

Kleinman:

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Recombination does occur, if you have siblings, you know that. But you know nothing about reproductive fitness except by the number of offspring. And that number varies for many reasons. So, why are there only about 300,000 chimps and 8e9 humans today? What recombination events give humans the capability to do industrial farming, build and fly aircraft, build dams and power plants, while chimps still haven't figured out fire and the wheel? Was it a constant environment and single selection pressure? If so, why didn't it happen for chimps?

Taq:

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The stupid burns.
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It is the mutations that differ between our species. It is sexual recombination that put the beneficial mutations into the same background. If you want to know where to look for those beneficial mutations, they are the mutations that differ between the genomes of our species. Not that hard to figure out.

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Everyone knows you can't answer the question. All you know is that if you write a computer program with selection and apply it to a couple of alleles, their frequencies increase. So it must happen to all populations. You are a simpleton.

Kleinman:

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Why don't you do the model for chloramphenicol resistance correctly instead of doing your garbage?

Taq:

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The model is right here:
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Sexual recombination and increased mutation rate expedite evolution of Escherichia coli in varied fitness landscapes - PMC

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You claimed you wrote a computer simulation of the experiment. All you did is write a model of selection and increased the frequencies of A and B. You didn't even use the same population sizes they used, they same number of generations they used, or the same selection condition they used. You haven't modeled their experiment.

Kleinman:

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Did it ever enter your mind that they did 55 generations of selection in a constant environment? Stop being a dumbass and doing this model like a lower-division undergraduate. Perhaps you are just too stupid to do the math correctly.

Taq:

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Have you forgotten once again that the Lenski and Kishony experiment used constant environments?

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That's right dumdum, and I was able to derive the equation for descent with modification and explain how biological competition affects adaptive evolution. I also wrote a paper which explains the mathematical behavior of recombination and that it depends of the frequencies of alleles. You are just too dumb to do the math in an experiment that does recombination and in order to get their results, they did 55 generations of selection in a constant environment. They did the same thing that Desai did in his experiment. Adaptive recombination needs those 55 generations of constant selection to increase the probability of an adaptive recombination event occurring in a single selection pressure environment. But you are too dumb to do the math so you don't understand this.

Yes, you may be having hallucinations. That would explain your blindness to reality.

I've recommended to him that he go see Psych, but he's too far gone to realize that he should.I've come across at least one anti-theist who defined religion as a mental illness. I normally would not go that far, but specimens like Kleinman, Dredge, and candle2 just make such an incredibly strong case of their religions being mental illnesses.

I didn't use any selection factors. What in the world are you talking about?Also, you still haven't supplied any math for sexual reproduction from real populations. Where is it? What I presented was so mundane as to be elementary. If 1% of a population of 1 million heterozygous carriers of either mutation A or mutation B then that would mean 0.01*0.01*1E6*0.5*0.5.01 offspring will carry both mutations, or 25 in total for random mating. It's a basic formula that isn't worth publishing on.What are you on about? Do you think it is impossible for a beneficial mutation to increase in frequency? How is that any different than the Lenski and Kishony experiments? They have been shown to be wrong in the peer reviewed literature.

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As stated above, Haldane (1957) argued that the costs of natural selection accumulate over loci, i.e., the reproductive cost of allele substitution at two loci would be twice the cost at a single locus. Consequently, the time required for substitution should be twice as long. In general, if it takes t generations for a gene substitution at a single locus, it should take Lt generations for substitutions at L loci. Applying this logic to our model, given that it takes 400 generations for allelic substitution at one locus, it should take 40 000 generations for substitutions at 100 loci. This prediction is in stark contrast to our finding that it takes only 400 generations for allelic substitution at all 100 loci (see Fig. 2F). How can we explain this major difference between Haldane’s prediction and our findings?
Clearly, Haldane’s scenario does not explain our simulation results as shown in Fig. 2. The reason for the discrepancy is, we believe, that Haldane’s argument assumed that the optimal genotypic combination had to be already present in the initial population and that genotypes could be considered as fixed entities that reproduce themselves from one generation to the next. But these assumptions do not hold for a sexually outbreeding population. First, the population is usually not large enough to contain even a single individual with the vanishingly rare optimal genotypic combination; this fact has already been pointed out by Ewens (1972) and Maynard Smith (1976). Second, specific genotypes are broken down by recombination each generation and replaced by other genotypic combinations (Hickey and Golding 2018). The process of recombination involves the continual disassembly of existing genotypes and reassembly of new genotypes from one generation to the next. Because of this process, however, those genotypes that are expected to be vanishingly rare when the allele frequencies are low will be automatically generated through recombination once the allele frequencies begin to rise in response to selection (Muller 1964; Hickey and Golding 2018). Consequently, there is no need for the massive culling that would be required in a very large initial population that contained an extremely rare optimal genotype. Thus, in an outbreeding sexual population, recombination solves the perceived problem of costs that are cumulative over different genetic loci. In Haldane’s scenario, it is necessary to “grow” the optimal genotypic combination from an initial, vanishingly rare frequency to fixation. In practice, however, this optimal combination is produced by recombination only near the end of the process. This avoids the huge cumulative cost of natural selection.
Canadian Science Publishing

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Before you complain about this not being based on real populations, you also have to remember that Haldane's work was also not based on real populations but on simulations. There was 50,000 generations of constant selection in the Lenski experiment, and yet you think this is a valid experiment.Also, as I have said many, many, many times, both the asexual and sexual populations were under the very same constant conditions, and yet there was only clonal interference in the asexual population. You STILL won't address this. Open savanna, as I have stated over and over and over. I never used 6 generations. What a liar. That's not a selection factor. That's the percentage of the population that carries either mutation A or mutation B. What I am showing is that your addition rule allows those mutations to be any frequency from 0 to 1, something you claimed couldn't happen. What does that have to do with anything? I did answer it, you liar. If you don't think the mutations that differ between humans and chimps are responsible for the physical differences between chimps and humans, then what in the world are we discussing here? The model is in the paper. READ IT!!! But those same calculations don't apply when looking at the Desai experiment because the Desai experiment used a constant environment? What a fucking hypocrite.