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

Conman.

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

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.

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.

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.

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.

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?

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.

I didn't use a selection factor.FOR THE MILLIONTH TIME!!!!All I am showing you is that two mutations at unlinked loci can be at any percentage and still add up to one in your stupid addition rule. For example, two mutations can both be at a frequency of 0.9 (or 0.01) and still add up to 1 in your equation. You claimed this wasn't possible, and I showed you it was. Multiple beneficial mutations can go to fixation if they are in the same genetic background. However, if they are in different genetic backgrounds then clonal interference will prevent the less fit beneficial mutations from reaching fixation. This doesn't happen in sexual populations because of recombination which moves beneficial mutations from different genetic backgrounds onto the same genetic background.This is like the millionth time I've explained this. THAT'S BECAUSE THE E. COLI IN THE LENSKI EXPERIMENT WERE ASEXUAL!!!!!My god, man. I have shown multiple alleles independently increasing in frequency over time. For example, this figure from the Desai paper:Notice on the left, the asexual populations, that mutations come in waves? Notice how that does not occur in the sexual populations? Notice how there are many different mutations at different stages of moving towards fixation in the sexual populations with no apparent waves of mutations? That's just a distraction you are conning people into paying attention to. You don't have to have a constant environment in order for selection to occur. There are no generations in the program. Do you even understand how math works? It's like you don't even remember saying this:"You continue to cling to the notion that all evolutionary processes occur in constant environment, with single selection pressures that are only found in laboratories."You fucking hypocrite. "50,000 generations of constant selection in the Lenski experiment and about 75 different biological competitions as adaptive mutations accumulated. This more than demonstrates how descent with modification works."--KleinmanYou fucking hypocrite.

You are the one who introduced the addition rule. Now you are criticizing other people for using it. You fucking hypocrite. Then why are you even discussing fixation?Does a mutation have to a frequency of 1 in order to be beneficial? No.
Does a mutation have to reach a frequency of 1 in order for evolution to occur? No.What does have to happen is an increase in frequency. What we see in the Desai experiment is just that, and there is no clonal interference. You still won't address the lack of clonal interference in the sexual populations. Which is why I have always said "moving towards fixation". "50,000 generations of constant selection in the Lenski experiment and about 75 different biological competitions as adaptive mutations accumulated. This more than demonstrates how descent with modification works."--Kleinman
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You fucking hypocrite.

I am using the addition rule you put forward, you fucking hypocrite. How in the world would there be evolution without competition?????? The one thing that would stop evolution is a lack of competition. Amplification does occur in the Kishony experiment. The mutations for chloramphenicol are amplified as the bacteria move up in the drug gradient. Prove it. Show us the evolving genomes of every single species that lives in a varying environment and demonstrate to us that this isn't happening. Yes, for asexual populations. Not for sexual populations. That doesn't model every possible changing environment. You can't make the sweeping conclusions you are trying to make. Extremely harsh selection regimes are not the normal situation in nature. You first. You are the one who is trying to make sweeping conclusions about evolution based on very artificial selection regimes that are very different from what is found in nature. We have the fucking experimental results!!! You have to take into account sexual reproduction.

You claimed that the addition rule meant that the frequencies of two mutations at different loci could not add up to more than 1. Remember that?Care to retract that claim? Or is it you that doesn't understand math? No, it isn't. Bacteria were continually competing with each other for food in that experiment. Now you are demonstrating you don't know how the Kishony experiment works.You are now claiming that evolution works the fastest when there is no competition. That's false. No evolution takes place if there is no competition. It is competition that drives evolution. Prove it. Prove that there are no beneficial mutations being amplified in these populations. No it doesn't, you fucking moron.

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We find that sex alters the molecular signatures of adaptation. We observe similar proportions of synonymous, nonsynonymous, and intergenic mutations segregating in sexual and asexual lines (Fig. 1b). Consistent with earlier work21, in asexual populations these types of mutation are roughly equally likely to fix, conditional on reaching observable frequency (Fig. 1b and Extended Data Table 3). This indicates that natural selection cannot efficiently distinguish between their effects. In contrast, fewer mutations fix in sexual populations, and these mutations are overwhelmingly nonsynonymous. These observations suggest that sex improves the efficiency of selection, so that only beneficial mutations fix.
Sex speeds adaptation by altering the dynamics of molecular evolution | Nature

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And you are such a fucking moron that you even get this easy part wrong. You think the rate of adaptive mutations is equal to the mutation rate. IT ISN'T. The rate of adaptive mutations changes with the number of possible beneficial mutations in a given environment, something that is never a part of your math. You fail to understand that it isn't a fact in sexually reproducing populations. That doesn't fucking matter you fucking moron.

You fucking moron. I showed you my calculations with the addition rule and you thought the numbers represented number of generations and selection. You don't have an inkling what the addition rule is. The stupid. It burns. There is no descent with modification when there is no competition. There was competition in the Kishony experiment. There was competition in the Lenski experiment. You don't even have a grasp on the basics of reality. I already did. You refuse to address them. You fucking moron. I just showed you multiple papers that describe how sexual reproduction changes descent with modification. Read the fucking papers. Your publication assumes there is only one possible beneficial mutation in any given genome. That is not true for all genomes. That's the part you can't seem to get through your thick fucking skull. If those two or more beneficial mutations occur in unlinked loci then they will be moved into the same genetic background, you fucking moron.

The last universal common ancestor already had protein synthesis. Nothing at all would be changed in the theory of evolution if God created the first life and then all the biodiversity we see today evolved from that first created life.You might as well argue against our understanding of how germs cause disease because we don't understand where the first life came from. Or claim that we can't know how clouds form because we don't understand where the energy found at the start of the Big Bang came from. How many do they save? No one is saying that doctors are perfect. How would you determine that Haeckel is wrong without using the scientific method?