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

No, it isn't. Asexual reproduction is what causes clonal interference. You have changed my mind on that one. You don't even know what descent with modification is. Darwin is the guy who coined the term, and he called it "descent with modification through natural selection". Descent with modification includes natural selection.I have already shown you how descent with modification differs between asexual and sexual populations. You refuse to accept reality. I don't. I have referenced many papers and many examples. You ignore them, and then try to claim that I am saying multidrug therapy doesn't work.Here is another one:

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The potential contribution of recombination to the development of HIV-1 resistance to multiple drugs was investigated. Two distinct viruses, one highly resistant to a protease inhibitor (SC-52151) and the other highly resistant to zidovudine, were used to coinfect T lymphoblastoid cells in culture. The viral genotypes could be distinguished by four mutations conferring drug resistance to each drug and by other sequence differences specific for each parental virus. Progeny virions recovered from mixed infection were passaged in the presence and absence of both zidovudine and SC-52151. Dually resistant mutants emerged rapidly under selective conditions, and these viruses were genetic recombinants. These results emphasize that genetic recombination could contribute to high-level multiple-drug resistance and that this process must be considered in chemotherapeutic strategies for HIV infection.
Recombination leads to the rapid emergence of HIV-1 dually resistant mutants under selective drug pressure. - PMC

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So you can't tell us how antibiotic resistance evolved in those experiments. Figures.

Yes you do. If you can't measure entropy then you can't demonstrate that entropy has changed. It's a pretty simple concept. DNA is chemistry. If your mathematics don't include the entropy of the chemical interactions then it is meaningless. What matters is the amount of energy available for work in the system which is entropy. In order to make those comparisons you have to incorporate the chemistry of DNA and and the movement of energy during the replication of DNA. What you are ignoring is the change between free individual nucleotide bases and a string of nucleotide bases. Then why was there clonal interference in the asexual organisms in a constant environment but no clonal interference in the sexual organisms that were in the same constant environment?

I did read them. I would be glad to explain why the evolution of chloramphenicol resistance benefitted from sexual recombination while the evolution of trimethoprim resistance did not benefit from sexual recombination. As a bonus, I could also throw in a discussion on the evolution of glycerol utilization as it relates to sexual recombination and epistasis.All you have to do is admit you don't understand why they saw these results and I will give you the explanations.

Then you admit you have no idea how to apply thermodynamics to evolution.

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Entropy, in fact, is the ratio of heat energy over temperature. This definition has very important applications in chemistry and engineering, where heat is used to do work. But for most people, this definition of entropy—heat divided by temperature—is a non-intuitive concept.
Understanding Entropy in Terms of Energy

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Like I said, you don't understand thermodynamics. NO!!! Are you daft????How does relative fitness tell you the change in entropy when free nucleotides polymerize into a DNA strand? The beneficial alleles in the asexual populations were also amplified by the same constant environment. There was clonal interference in the asexual populations. There was not clonal interference in the sexual populations. How do you explain the difference between the asexual and sexual populations that are in the very same environment? It can't be the amplification of beneficial alleles because that happened in both cases.

Is this an admission that you can't explain how antibiotic resistance evolved in this experiment?Sexual recombination and increased mutation rate expedite evolution of Escherichia coli in varied fitness landscapes - PMC

Then why did they get different results for the evolution of chloramphenicol and trimethoprim resistance? Why did they get different results for asexual and sexual populations? Why did they get different results for the evolution of glycerol utilization between sexual and asexual populations?Sexual recombination and increased mutation rate expedite evolution of Escherichia coli in varied fitness landscapes - PMC The paper above proves you wrong.

Your math has nothing to do with thermodynamics. The problem lies with you. You think a constant environment is what alleviated clonal interference in the Desai experiment. The asexual populations were in a constant environment, and they experienced clonal interference. People are successfully treated with antibiotics even though antibiotic resistance has evolved in bacteria many times. The availability of energy to do work in a system is the measure of entropy. It is necessary for measuring entropy in biology. The individuals in the sexual population were still competing with one another. Competition is what drove the beneficial mutations towards fixation in the sexual population. It is what drives fixation in all sexual populations.Wow, you really don't know how this works. And in the sexual populations, all of the fitter alleles move towards fixation. That's the difference. Also, deleterious mutations do not hitchhike with the fittest allele in the sexual populations like they do in the asexual populations. Yet another difference in how descent with modification occurs in these populations.

Nowhere in any physics course did they teach what you are claiming. Are you arguing that multidrug resistance never occurs in HIV? But people are successfully treated with antibiotics, so by your logic that means resistance never evolves. Now you are trying to change the subject to hide your ignorance.You actually think that sexual reproduction eliminates competition. That's what you said. This means that there is no competition in the hundreds of thousands of vertebrate species that sexually reproduce, according to your absurd claims. Apparently, you don't know.

All you have to do is figure out how genetics works in sexual reproduction.

They were physics classes, not biology classes. And no, they never taught what you are claiming, probably because you're wrong. And you are wrong. For example, in the Lederberg paper they saw a 1,000 fold difference in the adaptive mutation rate for two different phenotypes even though the mutation rate was the same in both populations. The mutation rate is not the adaptive mutation rate. Never has been. It isn't a single case. There are many, many, many examples where an adaptive phenotype can be reached by more than one mutation. Every time I show you how multidrug resistance has evolved in HIV you turn around and try to claim that I am telling people triple drug treatments should not be used. Care to reverse your course? You once again try to change the subject.You claimed that sexual reproduction prevents competition. Care to correct yourself on this one? Yes, they do.

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To investigate how sex improves the efficiency of selection, we analysed the dynamics of adaptation. As in earlier studies21,22, asexual populations exhibit signatures of hitchhiking and clonal interference (Fig. 2a–d). Groups of functionally unrelated mutations, linked within the same genetic background, change in frequency together as clonal cohorts. The outcomes of evolution are determined by competition between these cohorts. In contrast, sexual populations are not characterized by cohorts of linked mutations (Fig. 2e–h). Instead, the dynamics of each mutation is largely independent of other variation in the population. In these populations, mutations that occur on different backgrounds fix independently, while others briefly hitchhike to moderate frequencies where they persist or are eliminated from the population.
Sex speeds adaptation by altering the dynamics of molecular evolution | Nature

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Are you done being a liar?

And now you are trying to distract people away from the evidence that disproves your claims.What you can't seem to wrap your head around is that there can be more than one mutation that is adaptive. Therefore, you can't use the mutation rate as the adaptive mutation rate. You claimed multidrug resistance has never evolved in HIV. Obviously, you are very wrong. Conman. Conman.

Let's take just a few examples of how wrong your math is.1. The mutation rate is the adaptive mutation rate. That's false because more than one mutation can be adaptive.2. Sexual reproduction eliminates competition. That's so ludicrous I don't even need to explain it further.3. You don't think the polymerization of DNA impacts changes in entropy.4. You claim that multiple alleles can not move towards fixation at the same time, even though they are observed to do so in sexual populations. All you can do is shift the conversations to definitions of fixation.

You are still getting the basic maths wrong. You are claiming that the chances of getting an adaptive phenotype is the mutation rate. That is wrong because there can be multiple mutations that are adaptive. It isn't that hard to figure out.If there are 10 possible mutations that confer antibiotic resistance then the rate of adaptive mutations would be 10*mutation rate. "Desai let his sexual replicators carry out 90 generations of amplification of the beneficial alleles but stopped the competition process at that point by inducing sexual reproduction before fixation occurred."--KleinmanYou claimed that sexual reproduction stops competition. Thank you for admitting that you can't do the entropy calculations. Moving towards fixation is just increasing in frequency.You claim that multiple alleles can not move towards fixation at the same time, even though they are observed to do so in sexual populations. All you can do is shift the conversations to definitions of fixation. You mean the one that allows any number of beneficial alleles to be any frequency whatsoever?

It doesn't apply to multiple beneficial alleles in unlinked genes within sexual populations. That's what you have failed to understand from the very beginning.Here is a section from one of my previous posts.By your own admission, the addition rule is:fA + (fB-(fA*fB)) + fC = TpWhere
fA = frequency of variant A
fB = frequency of variant B
fC = frequency of no A or B = ((1-fA)*(1-fB))
Tp = Total population, should be equal to 1I contend that your made up version of the addition rule, invented to try and explain away your misapplication to variants at different loci, allows A and B to be whatever number I want. In fact, I can have them increasing in frequency in lock stop together, from a frequency of 0.01 on up to a frequency of 1 for each. Your new made up addition (i.e. subtraction) rule allows the very thing you claimed couldn't happen.If I am right then I should be able to increase both A and B and still have the equation equal 1. I will be using the assumption of equal distribution for each variant. I will be using a crude population curve that starts with frequencies of 0.01 to 0.05 in increments of 0.01, and then to speed things up I will change the frequency by 0.05 to 1 by increments of 0.05.I will be using n to represent census numbers and fX to represent the frequencies of each variant.A = n * fA
B = n * fB
AandB = n * (fA * fB)
C = (1-fA) * (1-fB)So for the whole equation:(fA) + (fB - (fA*fB)) + ((1-fA)*(1-fB)) = TpI will use a population of 100,000The code looks like this (adding window scroll to reduce size):

n = 100000

for i in range(1, 6):
    f = i*0.01
    fA = f
    fB = f
    A = int(n * f)
    B = int(n * f)
    AandBn = int(n * (fA * fB))
    C = int(n*((1-fA)*(1-fB)))
    Tp = (fA) + (fB - (fA*fB)) + ((1-fA)*(1-fB))
    print(f'{f} = frequency of A and frequency of B')
    print(f'{A} = number of offspring with A or B')
    print(f'{AandBn} = number of offspring with AB')
    print(f'{C} = number of offspring with neither A nor B')
    print(f'{Tp} = normalized total population')
    print('\n')

for i in range(1, 21):
    f= round(i*0.05, 2)
    fA = f
    fB = f
    A = int(n * f)
    B = int(n * f)
    AandBn = int(n * (fA * fB))
    C = int(n*((1-fA)*(1-fB)))
    Tp = (fA) + (fB - (fA*fB)) + ((1-fA)*(1-fB))
    print(f'{f} = frequency of A and frequency of B')
    print(f'{A} = number of offspring with A or B')
    print(f'{AandBn} = number of offspring with AB')
    print(f'{C} = number of offspring with neither A nor B')
    print(f'{Tp} = normalized total population')
    print('\n')

If you run it on an online python interpreter you will see that the normalized population size (Tp) remains at 1.0 throughout (0.9 repeating is a python glitch). You can also see that the number of AB individuals increases through time.My results:

0.01 = frequency of A and frequency of B
1000 = number of offspring with A or B
10 = number of offspring with AB
98010 = number of offspring with neither A nor B
1.0 = normalized total population

0.02 = frequency of A and frequency of B
2000 = number of offspring with A or B
40 = number of offspring with AB
96039 = number of offspring with neither A nor B
0.9999999999999999 = normalized total population

0.03 = frequency of A and frequency of B
3000 = number of offspring with A or B
90 = number of offspring with AB
94090 = number of offspring with neither A nor B
1.0 = normalized total population

0.04 = frequency of A and frequency of B
4000 = number of offspring with A or B
160 = number of offspring with AB
92160 = number of offspring with neither A nor B
1.0 = normalized total population

0.05 = frequency of A and frequency of B
5000 = number of offspring with A or B
250 = number of offspring with AB
90250 = number of offspring with neither A nor B
1.0 = normalized total population

0.05 = frequency of A and frequency of B
5000 = number of offspring with A or B
250 = number of offspring with AB
90250 = number of offspring with neither A nor B
1.0 = normalized total population

0.1 = frequency of A and frequency of B
10000 = number of offspring with A or B
1000 = number of offspring with AB
81000 = number of offspring with neither A nor B
1.0 = normalized total population

0.15 = frequency of A and frequency of B
15000 = number of offspring with A or B
2250 = number of offspring with AB
72249 = number of offspring with neither A nor B
0.9999999999999999 = normalized total population

0.2 = frequency of A and frequency of B
20000 = number of offspring with A or B
4000 = number of offspring with AB
64000 = number of offspring with neither A nor B
1.0 = normalized total population

0.25 = frequency of A and frequency of B
25000 = number of offspring with A or B
6250 = number of offspring with AB
56250 = number of offspring with neither A nor B
1.0 = normalized total population

0.3 = frequency of A and frequency of B
30000 = number of offspring with A or B
9000 = number of offspring with AB
48999 = number of offspring with neither A nor B
1.0 = normalized total population

0.35 = frequency of A and frequency of B
35000 = number of offspring with A or B
12249 = number of offspring with AB
42250 = number of offspring with neither A nor B
1.0 = normalized total population

0.4 = frequency of A and frequency of B
40000 = number of offspring with A or B
16000 = number of offspring with AB
36000 = number of offspring with neither A nor B
1.0 = normalized total population

0.45 = frequency of A and frequency of B
45000 = number of offspring with A or B
20250 = number of offspring with AB
30250 = number of offspring with neither A nor B
1.0 = normalized total population

0.5 = frequency of A and frequency of B
50000 = number of offspring with A or B
25000 = number of offspring with AB
25000 = number of offspring with neither A nor B
1.0 = normalized total population

0.55 = frequency of A and frequency of B
55000 = number of offspring with A or B
30250 = number of offspring with AB
20249 = number of offspring with neither A nor B
1.0 = normalized total population

0.6 = frequency of A and frequency of B
60000 = number of offspring with A or B
36000 = number of offspring with AB
16000 = number of offspring with neither A nor B
1.0 = normalized total population

0.65 = frequency of A and frequency of B
65000 = number of offspring with A or B
42250 = number of offspring with AB
12249 = number of offspring with neither A nor B
0.9999999999999999 = normalized total population

0.7 = frequency of A and frequency of B
70000 = number of offspring with A or B
48999 = number of offspring with AB
9000 = number of offspring with neither A nor B
1.0 = normalized total population

0.75 = frequency of A and frequency of B
75000 = number of offspring with A or B
56250 = number of offspring with AB
6250 = number of offspring with neither A nor B
1.0 = normalized total population

0.8 = frequency of A and frequency of B
80000 = number of offspring with A or B
64000 = number of offspring with AB
3999 = number of offspring with neither A nor B
1.0 = normalized total population

0.85 = frequency of A and frequency of B
85000 = number of offspring with A or B
72249 = number of offspring with AB
2250 = number of offspring with neither A nor B
1.0 = normalized total population

0.9 = frequency of A and frequency of B
90000 = number of offspring with A or B
81000 = number of offspring with AB
999 = number of offspring with neither A nor B
1.0 = normalized total population

0.95 = frequency of A and frequency of B
95000 = number of offspring with A or B
90250 = number of offspring with AB
250 = number of offspring with neither A nor B
1.0 = normalized total population

1.0 = frequency of A and frequency of B
100000 = number of offspring with A or B
100000 = number of offspring with AB
0 = number of offspring with neither A nor B
1.0 = normalized total population