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

Sexual selection does change your math. All of your math is based on one beneficial mutation reaching fixation at a time. That's ridiculous. That is not how it works in sexually reproducing populations. The earliest populations wouldn't have to be fully adapted to the open savanna. They could live at the edges of their arboreal range and only venture out a bit into the savanna. As they acquired more an more adaptations to the savanna they could move further out into the savanna which would remove them from competition with other arboreal apes. This is nothing like antibiotic selection. Again, there is more than one gene in a genome.Parent One is homozygous for a beneficial mutation in gene A. Parent Two is homozygous for a beneficial mutation in gene B. All offspring will be heterozygous for both beneficial mutations. There's no need for another random trial to get the 2nd mutation in each parent. The same for phage resistance, as shown in both the Lederberg plate replica experiment and the Luria and Delbruck fluctuation assay. In those experiments, they start with a single bacterium and grow a population. They then expose that population to antibiotics or phage. They find resistant bacteria that already had the resistance mutation before being exposed to either challenge. However, as discussed in the Lederberg paper, antibiotic resistance appeared 1,000 times less often than phage resistance.How do you explain this difference in the appearance of resistance in both cases? That is only for alleles of the same gene. This is not true for different genes in a sexually reproducing population. Again, a genome has more than one gene. If there are two beneficial alleles for two different genes then they will both increase in frequency unless there is an interaction between the genes that lowers fitness. For example, the two mutations in different genes that I spoke about earlier, one for lighter skin and one for lactase persistence. They are both beneficial on their own, and they don't compete with one another because the mutations are on different genes.Eukaryotes have more than one chromosome. Genes on separate chromosomes are not linked in any way. They independently disperse through the population.
Even then, meiosis will switch alleles across the paired chromosomes so you will have different linkages between alleles of different genes on the same chromosome through time. There is about 1 cross over event per chromosome per offspring, at least in humans. There is more than one gene in the genome. Those are asexual populations under extremely stringent selection conditions, both of which are not true for human evolution. YES, IN AN ASEXUAL POPULATION. What are you not getting here? Just to repeat . . .Parent One is homozygous for a beneficial mutation in gene A. Parent Two is homozygous for a beneficial mutation in gene B. All offspring will be heterozygous for both beneficial mutations. There's no need for another random trial to get the 2nd mutation in each parent.

Billions of replications would put beneficial mutations in many different genes. You keep asserting that those mutations on separate genes stay separate from one another. They don't. Actually, hybridization was a big part of the process:

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Introgressive hybridization, i.e. hybridization with backcrossing, can lead to the fusion of two species, but it can also lead to evolution of a new trajectory through an enhancement of genetic variation in a new or changed ecological environment. On Daphne Major Island in the Galápagos archipelago, ~1–2% of Geospiza fortis finches breed with the resident G. scandens and with the rare immigrant species G. fuliginosa in each breeding season. Previous research has demonstrated morphological convergence of G. fortis and G. scandens over a 30-year period as a result of bidirectional introgression. Here we examine the role of hybridization with G. fuliginosa in the evolutionary trajectory of G. fortis. Geospiza fuliginosa (~12 g) is smaller and has a more pointed beak than G. fortis (~17 g). Genetic variation of the G. fortis population was increased by receiving genes more frequently from G. fuliginosa than from G. scandens (~21 g). A severe drought in 2003–2005 resulted in heavy and selective mortality of G. fortis with large beaks, and they became almost indistinguishable morphologically from G. fuliginosa. This was followed by continuing hybridization, a further decrease in beak size and a potential morphological fusion of the two species under entirely natural conditions.
Introgressive hybridization and natural selection in Darwin's finches | Biological Journal of the Linnean Society | Oxford Academic

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This was an increase in genetic variation. It was the mixture of mutations from different lineages that resulted in adaptation, something you can't seem to get your head wrapped around. The only reason you are saying this is because you only allow one beneficial mutation to move towards fixation at a time, which is ridiculous.

Parent One is homozygous for a beneficial mutation in gene A. Parent Two is homozygous for a beneficial mutation in gene B. All offspring will be heterozygous for both beneficial mutations. There's no need for another random trial to get the 2nd mutation in each parent.Please show me how this is wrong. Human ancestors weren't plucked from their arboreal environment and placed smack dab in the middle of the savanna. That's not what happened. That is what happens in the analogous Kishony experiment. The Kishony experiment requires adaptation in almost a single generation, something our human ancestors would not have had to do. Parent One is homozygous for a beneficial mutation in gene A. Parent Two is homozygous for a beneficial mutation in gene B. All offspring will be heterozygous for both beneficial mutations. There's no need for another random trial to get the 2nd mutation in each parent.Please show me how this is wrong. The same way streptomycin gets antibiotic resistance. Do cancer drugs get drug resistance?It is the bacteria that are phage resistant. The phage aren't phage resistant. That makes no sense. The bacteria had already evolved phage resistance before they came into contact with phage, so it wasn't the phage that gave the bacteria a resistance allele.So I will ask again. As discussed in the Lederberg paper, antibiotic resistance appeared 1,000 times less often than phage resistance.
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How do you explain this difference in the appearance of resistance in both cases? Please address what I wrote:you: Doesn't relative fitness differences of different variants determine which variants increase in frequency and which decrease?me: That is only for alleles of the same gene. This is not true for different genes in a sexually reproducing population. Again, a genome has more than one gene. If there are two beneficial alleles for two different genes then they will both increase in frequency unless there is an interaction between the genes that lowers fitness. For example, the two mutations in different genes that I spoke about earlier, one for lighter skin and one for lactase persistence. They are both beneficial on their own, and they don't compete with one another because the mutations are on different genes.
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Eukaryotes have more than one chromosome. Genes on separate chromosomes are not linked in any way. They independently disperse through the population.
Even then, meiosis will switch alleles across the paired chromosomes so you will have different linkages between alleles of different genes on the same chromosome through time. There is about 1 cross over event per chromosome per offspring, at least in humans. There is more than one gene in the genome. You don't need population bottlenecks in order for beneficial mutations in different genes to all reach fixation in parallel.

1. Each of the two beneficial mutations must be under positive selection.
2. Free interbreeding within the population.
3. Positive selection lasts long enough so that both beneficial mutations reach a small percentage of the population.If 5% of the population is heterozygous for one of the two beneficial mutations then 2.5% of births will have parents where each one has one of the two beneficial mutations. If they are heterozygous, 12.5% of their children will have both mutations.Dual carriers will only increase as each mutation increases in frequency until 100% of the population has both mutations if the benefice of each mutation is strong enough. I'm not aware of very many environments where only a few individuals survive out of billions in a single generation. Again, they are asexual organisms. That's why there are steps. If they are reproducing sexually then multiple steps could occur in one set of 30 generations and be combined into a single genome. Bottlenecks do occur, they just aren't necessary. So I will ask again. As discussed in the Lederberg paper, antibiotic resistance appeared 1,000 times less often than phage resistance.
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How do you explain this difference in the appearance of resistance in both cases? In a single replication the odds are low. Across hundreds of millions of replications in humans, the odds are extremely high that there will be different beneficial mutations in a whole host of different genes.You want to make the claim that only the fittest mutation out of all them will move towards fixation at the demise of all those other mutations in other genes. THIS ISN'T TRUE. All of those mutations will have their frequencies changed by comparison to the other alleles for that gene, not the frequency of alleles in other genes. Speculation mode??????Are you once again denying this scenario?Parent One is homozygous for a beneficial mutation in gene A. Parent Two is homozygous for a beneficial mutation in gene B. All offspring will be heterozygous for both beneficial mutations. There's no need for another random trial to get the 2nd mutation in each parent.
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Please show me how this is wrong.This would have happened in the chimp lineage as well. The difference is that the chimp lineage and the human lineage adapted to different environments, so they had different mutations reach fixation. It's one of the basic concepts in evolution.

It's simply math. If you agree that selection increases the frequency of beneficial alleles then the outcome I described is inevitable.And I already showed you the real world example:

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The allele frequencies at the neutral locus remained relatively stable during the simulation, showing small fluctuations due to genetic drift and gene flow between demes (Figure 5a-d, “LocusD”). The allele frequencies at the adaptive loci showed monotonic increasing or decreasing trends depending on the value of the selective environmental variable in the deme (salinity). For example, in deme 1 (high salinity, x = 38.5; Figure 5b), the frequency of the salinity-tolerant alleles increased and reached unity at all three adaptive loci in about 50 years (Figure 6). In deme 69 (low salinity, x = 32.4), the frequency of the salinity-tolerant alleles decreased to about 0.2 in the same time (Figure 6). These dynamics were driven by strong directional selective pressure at the adaptive loci due to extreme salinity values. Different replicates of the simulations produced the same results (not shown).

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If you put human ancestors in an environment where only a few out of billions survived in each generation then they would go extinct. However, that is not what happened in the evolution of humans. It is the extremely harsh environment that makes your HIV model irrelevant to human evolution. I fully agree that if the founding population of the human lineage was put in a similar extreme environment that we would not be here today. But it didn't happen in human evolution. Parent One is homozygous for a beneficial mutation in gene A. Parent Two is homozygous for a beneficial mutation in gene B. All offspring will be heterozygous for both beneficial mutations. There's no need for another random trial to get the 2nd mutation in each parent.
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Please show me how this is wrong. Are you remembering that they are on different genes? I'm guessing you forgot that part.Are you also forgetting about separate chromosomes and meiosis? I am asking you to explain.So I will ask again. As discussed in the Lederberg paper, antibiotic resistance appeared 1,000 times less often than phage resistance.
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How do you explain this difference in the appearance of resistance in both cases? Where are the units on these rates? Bullshit.From message 246:"The math is way beyond you. 20 million beneficial mutations * 300 generations/fixation = 6 billion generations"You have one beneficial moving to fixation at a time, and no other beneficial mutations are even allowed to occur or move towards fixation while one beneficial mutation is moving towards fixation. That's ridiculous.This is ALL about how different mutations in different genes move towards fixation. All you can seem to do is see one gene and one beneficial mutation at a time. You simply can't wrap your head around the idea that there can be more than one possible beneficial mutation in more than one gene. You also can't seem to understand that these mutations are spread over many chromosomes. It may take a long time. The most recent history of humans has seen isolated subpopulations. This doesn't seem to be the case for most of our history where we were found in Africa. It demonstrates the very thing you claim can't happen, the combination of different beneficial mutations into a single genome.

I don't need any help. We have two genes with two alleles, Aa and Bb. Parent A is Aa bb, Parent B is aa Bb. Half of the children will be Aa and half will be Bb. The odds of being Aa and Bb are the product of those probabilities, 0.25 or 25%. You are calculating 3 alleles at the same gene, not 3 mutations in 3 different genes. The frequency of each mutation can be 90%, and that obviously does not add up to the total population size. In other words, you are modeling AA, Aa, and aa. You are not modeling the combination of Aa and Bb. Perhaps you should try modeling mutations in different genes instead of alleles of a single gene.You are also stopping your modelling at one generation and not factoring in all of the incoming mutations that occur while those mutations are moving towards fixation.

It's a computer simulation of a real population of fish, and the simulation matched the distribution of 3 alleles in 3 different genes associated with high salinity adaptations. Read the paper:

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Dalongeville et al. (2018) identified three loci significantly associated with water salinity in M. surmuletus, thus potentially implicated in mechanisms of salinity tolerance and adaptation. Accordingly, we simulated four biallelic loci, among which three loci under selection from salinity (adaptive loci) and one neutral locus to track neutral genetic differentiation. Since no explicit test for linkage was conducted in Dalongeville et al. (2018), we assumed that the four simulated loci were unlinked (r = 0.5). We further assumed a mutation probability mu = 10–6 per locus. As each biallelic locus can give rise to three genotypes, with L = 3 unlinked loci under selection, the number of multilocus adaptive genotypes is 3L = 33 = 27 (Box 2, Equation B4). At the three loci under selection, we assumed that one allele reduced the phenotypic value (the “−” allele) while the other increased it (the “+” allele). This gives rise to seven different combinations of number of “+” alleles per genotype. We assigned to each combination an optimal salinity ranging from 36 to 39 practical salinity units (PSU) at intervals of 0.5, according to the range of water salinity in the Mediterranean Sea.
Just a moment...

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More than 99% of bacteria die or fail to reproduce in concentrations of antibiotics above the minimal inhibitory concentration. If the drugs don't reduce the replication rate of HIV without the resistance mutation then what does the drug do and what is resistance? Which one of those wiped out more than 99% of humans? In what way were the post bottleneck environments stable enough to induce adaptation to them? You tell me, you are the one who keeps talking about recombination events. How does Haldane's model apply to different mutations on different genes in a diploid sexually replicating species? They reach fixation independently of each other if they are not close to each other on the same chromosome, which is called linkage disequilibrium.If we take your 300 generation number, then in generation 1 there are 5 adaptation mutations and they reach fixation at generation 301. In generation 2 there are 5 beneficial mutations, and they reach fixation at generation 302. In generation 3 there are 5 beneficial mutations, and they reach fixation in generation 303. At no time does evolution just stop and wait for the previous beneficial mutations to reach fixation while ignoring all of the beneficial mutations that happen in the mean time. It would depend on gene flow.

Doesn't matter. For Aa bb x aa Bb, 25% of the children will be Aa Bb. That is true no matter how many other heterozygous or homozygous parents there are at the two genetic loci. I already did that in a previous post. Your math doesn't add up. Here is what you presented before:

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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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Non-disease alleles should serve this example well. There are disease alleles like achondroplasia (dwarfism), hemophilia, and cystic fibrosis. The non-disease alleles greatly outnumber the disease alleles. Let's say that each is at 0.99 frequency, and we will call them A, B, and C. So does your math make sense?0.99A + 0.99B + 0.99C = 1Does that math add up? Nope. A would reach fixation in fewer generations than B. If fitness were additive then carriers of both A and B would be the fittest. No. If that were the case then there would only be one non-disease allele and the rest of the disease alleles would drive towards fixation.You also ignore the fact, once again, that A and B can be put into the same genome in sexually reproducing species unlike what is seen in asexual organisms. You also apply the wrong formula which is meant for alleles of the same gene.

If the simulation is used on birds and it shows that they can fly, is that an accurate simulation? Where in human evolution do you think there was a point where 99% of the population died off because they lacked a specific allele? One parent is Aa bb and the other parent is aa Bb. 25% of their children are Aa Bb, carrying one copy of each beneficial dominant mutation. Do you describe this as recombination? In the presence of the HIV drug, do the HIV resistant viruses reproduce better than the drug sensitive HIV viruses? Which is all beside the point. All I said is that bottlenecks aren't necessary, not that they never happen. That is only for alleles at the same genetic locus, not for mutations at different genetic loci. Are you saying there is no base in the human genome where nearly 100% of humans have the same base? What are the frequencies of the wild type allele for genes where there are known Mendelian diseases like achondroplasia or hemophilia?

When you are ready to stop rejecting Mendelian genetics, let me know. Already explained it in the other post. Then you should know better, too. So why are you using this equation for mutations in different genes when it clearly does not apply? Are you the same person who wrote this?"You should know better than this Taq. You can only add frequencies (probabilities) if they are mutually exclusive."A variant and B variant are not mutually exclusive in the same way that the non-disease alleles are not mutually exclusive. What is so strange about that if the mutations are in different genes? You already accept the non-disease alleles all being near fixation, so why not mutations A and B found in different genes? The computer simulation has been tested against experimental data: MetaPopGen 2.0: A multilocus genetic simulator to model populations of large size
Assertion without evidence. That's what you are claiming, not me.You claim that the frequency of any two mutations anywhere in the genome can not add up to more than 1. Obviously, that is false. A million irony meters just exploded.

You reject Mendelian genetics when you require the percentage distribution of alleles in different genes to add up to 1. You keep doing this. I bet you do it later in this post. And there it is. You still don't understand basic Mendelian genetics, at least at the time you wrote this post.Let's see how this works out. Let's use 3 hypothetical disease alleles (e.g. cystic fibrosis, achondroplasia). Let's say 1 out of 1,000 people carries the diseases allele, or 0.1% of the population. This would mean that 99.9% of people don't carry the disease allele but the healthy allele. Let's call these Aa, Bb, and Cc alleles for genes A, B, C. According to you, I should be able to add up the number of people with the A, B, and C allele and get an accurate population count. Is that true?NO!!!If I do as you suggest I will get about 3x the actual population number. Do you know why? You still don't understand how sexual reproduction works. How about learning how genetics works? Why don't you start there?You seem to think that there is just one gene per genome. Perhaps you could start by learning how meiosis works, or perhaps what a chromosome is. Maybe you could learn that there are multiple genes in a genome, each with it's own set of alleles. So you claim you don't make that claim, and then make that very claim in the next sentence. You effing moron.

Quiz for Kleinman:Why are gene 1 and 2 linked in the first example but not in the other two examples?What effects does linkage have on relative allele distributions between linked genes compared to unlinked genes?

We are getting more distant from the actual genetic system that got this all going.Kleinman is claiming that if we add up all of the allele frequencies for all genes in a genome that we will get 1. That's ridiculous. That shows a massive misunderstanding of the basic mathematics of genetics.Let's just say that there are two alleles for each of the ~30,000 genes in the human genome, and the frequency of each allele is 0.5, or 1.0 for each gene. If we add them up like Kleinman claims we can then we get 30,000, not 1.

We could start here:

Bullshit, K-man. Life happens, and I got busy elsewhere.Let's revisit this classic you used in post 311

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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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Do you still stand by this? Do you add the allele frequencies for alleles in different genes?What about the healthy alleles for 3 different genes associated with a genetic disease, each with a frequency of 0.999?0.999A + 0.999B + 0.999C != 1OOOOOPPPPPSSS!!!! Your math doesn't work.