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

There hasn't been enough time or enough selective pressure over a large enough percentage of the population to drive them to fixation across the entire population. Also, pathogens change so past adaptations may not apply to modern pathogens. There's lots of reasons, but not included in those reasons is the requirement for those mutations to reoccur in each lineage when there are possibilities of mating between lineages.This is what we keep coming back to. You are making the false claim that in human evolution we can't combine mutations from different lineages. You have claimed that mutation A has to reach a high enough percentage within the population so that you can have mutation B occur. You then try to multiply these chances together, and also claim that they have to happen in sequence. Do you see why this is wrong? Do you understand why sexual reproduction gets around this hurdle?

Kleinman:

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This equation is applicable to any two genetic loci in any replicator, human or otherwise.

Taq:

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I've already shown this isn't the case. You are now saying that as someone with a new mutation has offspring with any other person the equation no longer applies.

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Don't be silly Taq. If we use your logic that multiple adaptive mutations go to fixation simultaneously, no one should ever die from infectious disease because anyone with an adaptive allele to that disease should have that allele go to fixation. Last I checked, people still die from infectous diseases. And when a new mutation occurs, just add a variable to include that variant in the frequency equation. But the sum of the frequencies of all the variants will still equal 1.

Kleinman:

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Biologists just don't recognize how to apply this math and in your case, very slow to learn.

Taq:

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I followed your equation exactly and it failed.

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Is that so? Where's the biologists' explanation of why combination therapy for the treatment of HIV isn't defeated by recombination?

Kleinman:

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The AB variants will increase in frequency because the AB variant will have greater reproductive fitness than either the A or B variants so those variants will decrease in frequency.

Taq:

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The A only and B only variants can mate and have children that have both mutations, right?
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The A and B mutations are still on separate chromosomes and are being passed on as independent entities. They are not linked.
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As you yourself are now saying, A does not outcompete B. The frequency of B on chromosome 2 can increase in frequency alongside the frequency of A on chromosome 1. Both increasing in frequency even though they aren't on the same chromosome or closely linked on the same chromosome.​

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You are the one claiming that the A and B variants have exactly the same reproductive fitness. And there are survivors of virtually every infectious disease you can imagine. Why haven't all these adaptive alleles that allow survival to all these diseases gone to fixation in the population?

Kleinman:

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Are you going to explain to us how a member of the population with beneficial allele A from North Africa meets a member of the population with beneficial allele B from South Africa?

Taq:

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What if both mutations are in North Africa?

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Yeah, what if? That's the biologist's version of science. Why don't you try doing your explanations with mathematical and experimental evidence?

1. You falsely assume that there exists an allele for immunity for all pathogens.2. You falsely assume that the pathogen has been around long enough to drive the alleles to fixation.3. You falsely assume that the entire human population is experiencing infections from the same pathogen. Once you admit that your equation has failed we can discuss HIV. Already have. You can't even wrap your head around diploidy, sexual reproduction, meiosis, and separate chromosomes.

Kleinman:

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So, why isn't everyone resistant to malaria, tuberculosis, influenza, covid, ...

Taq:

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There hasn't been enough time or enough selective pressure over a large enough percentage of the population to drive them to fixation across the entire population. Also, pathogens change so past adaptations may not apply to modern pathogens. There's lots of reasons, but not included in those reasons is the requirement for those mutations to reoccur in each lineage when there are possibilities of mating between lineages.
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This is what we keep coming back to. You are making the false claim that in human evolution we can't combine mutations from different lineages. You have claimed that mutation A has to reach a high enough percentage within the population so that you can have mutation B occur. You then try to multiply these chances together, and also claim that they have to happen in sequence. Do you see why this is wrong? Do you understand why sexual reproduction gets around this hurdle?

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Is that so? Are all these infectious diseases something new? Don't you think that all these diseases existed before humans and chimps ever appeared on the scene?So what in your imagination do you think are these adaptive alleles that give humans the reproductive fitness advantage over chimps?

Many are. For example, HIV entered into the human population for the first time in the 20th century. For other diseases there is no single mutation that will confer immunity.A great example is SARS-CoV-2 which evolves faster than any human population could. The spike protein on the surface of the virus attaches to the ACE2 protein on the surface of our cells. If there are alleles that reduce spike protein binding the virus will evolve new strategies in a matter of months compared to the 25 year generation time for humans. Even our adaptive immune systems which can change in just days to weeks can't keep up with this virus.Oh, and by the way, I do research on infectious diseases, mainly on Gram positives and adenovirus. I have actually modified the genomes of many of these pathogens, and studied both the innate and adaptive immune responses to these pathogens. You sure you want to lecture me on this subject?Better yet, why don't you explain to us why the map of the distribution for the sickle cell trait happens to match the distribution of endemic malaria. click hereWe can add another false assumption to the list. You assume that alleles conferring higher immunity to pathogens is either beneficial or neutral in the absence of the pathogen. We could also add the false assumption that homozygotes and heterozygotes face the same selective pressures. You have already stated that humans are fitter than chimps, haven't you? Why do you think that is? Is it because of the traits we have that chimps do not?

Kleinman:

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If we use your logic that multiple adaptive mutations go to fixation simultaneously, no one should ever die from infectious disease because anyone with an adaptive allele to that disease should have that allele go to fixation.

Taq:

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1. You falsely assume that there exists an allele for immunity for all pathogens.

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Don't be silly, there isn't a single allele that gives immunity to all pathogens. In fact, there are multiple different alleles that give some immunity to malaria. How much time will it take for all these alleles to go to fixation?

Taq:

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2. You falsely assume that the pathogen has been around long enough to drive the alleles to fixation.

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None of the malaria alleles have gone to fixation, nowhere close. Do you think malaria just appeared on the scene in the last few generations?

Taq:

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3. You falsely assume that the entire human population is experiencing infections from the same pathogen.

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You are the one claiming that multiple adaptive alleles go to fixation simultaneously.

Kleinman:

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Where's the biologists' explanation of why combination therapy for the treatment of HIV isn't defeated by recombination?

Taq:

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Once you admit that your equation has failed we can discuss HIV.

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Let us note that Taq doesn't want to discuss why recombination doesn't cause combination therapy to fail for the treatment of HIV.

Kleinman:

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Yeah, what if? That's the biologist's version of science. Why don't you try doing your explanations with mathematical and experimental evidence?

Taq:

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Already have. You can't even wrap your head around diploidy, sexual reproduction, meiosis, and separate chromosomes.

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Why does the Desai experiment using sexually reproducing yeast demonstrate the same kind of evolutionary behavior as the Lenski experiment?

I never said there was. I said you are falsely assuming there is an allele that confers immunity for all pathogens. This includes any number of different alleles for different pathogens. As long as there are humans living in regions without malaria, those alleles will never reach fixation. If we are talking about the classic sickle cell trait, even that allele will not reach fixation in regions with malaria. Can you figure out why? I never claimed they all do. Let us note that Kleinman won't address the abject failure of his mathematic equations.By the way, I have already covered this in previous posts. Show that it does. Show us that in sexually reproducing populations in the Desai experiment that beneficial mutations are not inherited in a way where multiple beneficial mutations can be found in the same individuals through inheritance instead of separate mutational events in each lineage.

Kleinman:

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Is that so? Are all these infectious diseases something new?

Taq:

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Many are. For example, HIV entered into the human population for the first time in the 20th century. For other diseases there is no single mutation that will confer immunity.

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Give us a list of diseases that killed people in the past but no longer kill people today because the adaptive allele(s) for these diseases have gone to fixation.

Kleinman:

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So what in your imagination do you think are these adaptive alleles that give humans the reproductive fitness advantage over chimps?

Taq:

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You have already stated that humans are fitter than chimps, haven't you? Why do you think that is? Is it because of the traits we have that chimps do not?

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You need some help with this question. What alleles do humans have that enable humans to do industrial farming which has increased the carrying capacity of our environment that chimps don't have?

I don't know of any because those pathogens would have died out before the advent of modern science.We can also add another false assumption to your growing list. You assume that pathogens will always remain pathogenic. You ignore the possibility of evolution towards a symbiotic relationship, such as all of the bacteria found in our guts. Those would be the alleles responsible for our increased intelligence, whatever those alleles are. Do you agree that our increased intelligence is due to alleles we have that chimps do not have?

Kleinman:

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Don't be silly, there isn't a single allele that gives immunity to all pathogens.

Taq:

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I never said there was. I said you are falsely assuming there is an allele that confers immunity for all pathogens. This includes any number of different alleles for different pathogens.

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Thank you for your clarification.

Kleinman:

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In fact, there are multiple different alleles that give some immunity to malaria. How much time will it take for all these alleles to go to fixation?

Taq:

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As long as there are humans living in regions without malaria, those alleles will never reach fixation. If we are talking about the classic sickle cell trait, even that allele will not reach fixation in regions with malaria. Can you figure out why?

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Have these alleles reached fixation in malaria-endemic regions?

Kleinman:

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You are the one claiming that multiple adaptive alleles go to fixation simultaneously.

Taq:

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I never claimed they all do.

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Which alleles have given humans the reproductive fitness advantage over chimps?

Kleinman:

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Let us note that Taq doesn't want to discuss why recombination doesn't cause combination therapy to fail for the treatment of HIV.

Taq:

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Let us note that Kleinman won't address the abject failure of his mathematic equations.
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By the way, I have already covered this in previous posts.

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The equations I've presented fit the experimental and empirical evidence. What equations do you have? Have you figured out how to use the addition rule yet?

Kleinman:

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Why does the Desai experiment using sexually reproducing yeast demonstrate the same kind of evolutionary behavior as the Lenski experiment?

Taq:

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Show that it does. Show us that in sexually reproducing populations in the Desai experiment that beneficial mutations are not inherited in a way where multiple beneficial mutations can be found in the same individuals through inheritance instead of separate mutational events in each lineage.

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Phenotypic and molecular evolution across 10,000 generations in laboratory budding yeast (with asexual reproduction and sexual reproduction) populations

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We find that some aspects of evolution in our system are broadly consistent with the conclusions of the LTEE and other long-term evolution experiments. For example, the dynamics of fitness increase are largely repeatable between replicate lines and show a pattern of declining adaptability over time even while the rate of molecular evolution remains relatively constant. However, there are also key differences: we find no evidence of stably coexisting lineages or widespread evolution of mutator phenotypes. As the first laboratory evolution of this length in a eukaryotic system, our study provides an important test of the generality of conclusions from earlier work (primarily the LTEE), as well as a novel opportunity to observe evolutionary dynamics over long timescales across many replicate populations in multiple environmental conditions.

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Not the classic sickle cell allele. Do you know why? The alleles responsible for the physical differences between humans and chimps. No, they don't.Then let's look at achondroplasia which is caused by mutations in the FGFR3 gene and cystic fibrosis which is caused by mutations in the CFTR gene. More than 99% of people have the healthy allele for both and only an extreme few have both cystic fibrosis and dwarfism. So let's do the math:
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0.99A + 0.99B + 0.0000001C != 1
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Just remember, this is the equation you gave:
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Define the following variables:
n – is the total population size.
nA – is the number of members in the population with beneficial allele A.
nB – is the number of members in the population with beneficial allele B.
nC – is the number of members in the population that have neither beneficial allele A nor beneficial allele B.
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In addition, we have the following condition: nA + nB + nC = n.
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And the frequency of each of the variants are:
f_A = nA/n
f_B = nB/n
f_C = nC/n

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Phenotypic and molecular evolution across 10,000 generations in laboratory budding yeast (with asexual reproduction and sexual reproduction) populations
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We find that some aspects of evolution in our system are broadly consistent with the conclusions of the LTEE and other long-term evolution experiments. For example, the dynamics of fitness increase are largely repeatable between replicate lines and show a pattern of declining adaptability over time even while the rate of molecular evolution remains relatively constant. However, there are also key differences: we find no evidence of stably coexisting lineages or widespread evolution of mutator phenotypes. As the first laboratory evolution of this length in a eukaryotic system, our study provides an important test of the generality of conclusions from earlier work (primarily the LTEE), as well as a novel opportunity to observe evolutionary dynamics over long timescales across many replicate populations in multiple environmental conditions.

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It says "some aspects", so which aspects are those? What differed between the sexual and asexual populations? What was the pattern of allele fixation in the sexual population?

Wow!Nobody who actually understands evolution would say anything that foolish.You do not understand evolution.Your "mathematics of evolution" is actually the mathematics of your gross misunderstanding of evolution. It is worthless.

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Phenotypic and molecular evolution across 10,000 generations in laboratory budding yeast (with asexual reproduction and sexual reproduction) populations
We find that some aspects of evolution in our system are broadly consistent with the conclusions of the LTEE and other long-term evolution experiments. For example, the dynamics of fitness increase are largely repeatable between replicate lines and show a pattern of declining adaptability over time even while the rate of molecular evolution remains relatively constant. However, there are also key differences: we find no evidence of stably coexisting lineages or widespread evolution of mutator phenotypes. As the first laboratory evolution of this length in a eukaryotic system, our study provides an important test of the generality of conclusions from earlier work (primarily the LTEE), as well as a novel opportunity to observe evolutionary dynamics over long timescales across many replicate populations in multiple environmental conditions.

Taq:

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It says "some aspects", so which aspects are those? What differed between the sexual and asexual populations? What was the pattern of allele fixation in the sexual population?

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Read the quote: "the dynamics of fitness increase are largely repeatable between replicate lines and show a pattern of declining adaptability over time even while the rate of molecular evolution remains relatively constant"And read the entire paper and see if they found that multiple adaptive alleles fix simultaneously in any of their replicate lines.The following img "B" gives the number of fixations as a function of number of generations. I suggest you read the paper carefully so that you understand how they define fixation. You should also note that they are working with much smaller population sizes than Lenski does with his experiment. Descent with modification and adaptation, DNA evolution, works essentially the same for asexual replicators and sexual replicators. This experiment does not support your claim of universal common descent, it contradicts that notion.

Kleinman:

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If we use your logic that multiple adaptive mutations go to fixation simultaneously, no one should ever die from infectious disease because anyone with an adaptive allele to that disease should have that allele go to fixation.

nwr:

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Wow!
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Nobody who actually understands evolution would say anything that foolish.
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You do not understand evolution.
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Your "mathematics of evolution" is actually the mathematics of your gross misunderstanding of evolution. It is worthless.

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See Taq, even nwr, the mathematician that doesn't do the mathematics of biological evolution understands that multiple adaptive alleles don't go to fixation simultaneously.nwr, you can go back to storing nuts in your cheeks.

You jumped to a wrong conclusion. This further illustrates your failed understanding of evolution.