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

Kleinman:

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You didn't read this paper either.

Taq:

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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.
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All you have to do is admit you don't understand why they saw these results and I will give you the explanations.

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As a bonus, why don't you tell us what the environmental condition was? Was it constant? Did they use a single selection condition or combination selection conditions? We all know that bacteria can easily evolve resistance to a single selection condition, that's the Kishony experiment. It is when the population has to evolve to 2 or more simultaneous selection conditions that replicators don't evolve so easily. If you can't answer these simple questions, I'll answer them for you.

They're very real and any fool can find them - except you. You're just flailing. Clearly not. He does. And so does everybody else who has looked at it honestly. There is no lack of transitional fossils. That has nothing to do with transitional fossils. The plethora of transitional fossils is enough evidence in itself to demonstrate UCD. So is the DNA evidence. So is the nested hierarchy based on gross anatomy. Why don't you look them up yourself? Any schoolboy can. A German General whom I never met? Maybe not. But to become a General, he must have been smart enough to accept evolution.

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

Kleinman:

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They are your imaginary links and you won't post them because they don't exist.

ringo:

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They're very real and any fool can find them - except you. You're just flailing.

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Yeah, right, I'm flailing because you don't post any links that explain how drugs evolve resistance and why cancer treatments fail. Let me help you with those links. For a single selection pressure:
The basic science and mathematics of random mutation and natural selection
And for multiple simultaneous selection pressures:
The mathematics of random mutation and natural selection for multiple simultaneous selection pressures and the evolution of antimicrobial drug resistance
See how easy that was ringo.

Kleinman:

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Then do it and show us how UCD is possible.

Taq:

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

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I understand thermodynamics (and probability theory) well enough to write out the mathematics of descent with modification. You are having a problem understanding how descent with modification works for sexual reproducers. Your understanding of probability theory is so poor that you think you will win when you go to a casino because they advertise some winner. What they don't advertise is all the losers. Sure you can post a link based on a single patient that appears to have failed HIV treatment due to recombination. But you fail to recognize that millions of people are successfully treated for HIV with three drug therapy. Every once in a while, someone wins two lotteries of the tens of millions of people that play lotteries and you think that everyone wins two lotteries. You really need to learn how to do the mathematics of biological evolution. 26 years of research and you should have learned something rather than everyone wins two lotteries.

Kleinman:

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That is complete BS. Energy and entropy don't even have the same units.

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

Taq:

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Like I said, you don't understand thermodynamics.

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Do you have a short-term memory problem or are you just stupid? You said the following:

Taq:

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What matters is the amount of energy available for work in the system which is entropy.

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Message 2458
Energy is not entropy. Your own reference says the units of entropy is energy/temperature. Your survey of physics course isn't helping you here and it hasn't helped you understand descent with modification.

Kleinman:

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So, you don't think that is accounted for in the relative fitness?

Taq:

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NO!!! Are you daft????
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How does relative fitness tell you the change in entropy when free nucleotides polymerize into a DNA strand?

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Not at all knucklehead. All the energy required for all chemical reactions must equal the carrying capacity of the environment in a biological competition process. If you want to compute the entropy when free nucleotides polymerize into a DNA strand, go for it. It's not necessary to know that value to do an "at least one calculation" or a Markov chain calculation, but if that's what you think is important, have at it.

Kleinman:

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Desai is using relative fitness to increase the frequencies of several of the more fit alleles by using a constant selection of a single selection pressure for 90 generations. He then induces sexual reproduction after 90 generations of amplification of the more fit alleles which are at high enough frequencies to give recombination of those alleles. If Desai had used varying environments with variable selection pressures, those alleles would not have been amplified.

Taq:

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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.

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Sure there was clonal interference in the asexual population because biological competition went to completion with fixation of the most fit variant, not variants. 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. Amplification of alleles occurs in both cases but only the most fit variant fixes with the asexual replicator. Do I have to remind you what the definition of fixation is because it appears you have forgotten the definition? You also have to learn that populations in "wild" environments aren't constant and don't have single selection pressures, not for 90 generations.

Kleinman:

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As a bonus, why don't you tell us what the environmental condition was? Was it constant? Did they use a single selection condition or combination selection conditions? We all know that bacteria can easily evolve resistance to a single selection condition, that's the Kishony experiment. It is when the population has to evolve to 2 or more simultaneous selection conditions that replicators don't evolve so easily. If you can't answer these simple questions, I'll answer them for you.

Taq:

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

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No stupid. Drug resistance to a single selection pressure works the same in all cases. It depends only on the mutation rate and population size just as it does in the Kishony experiment. The rate at which the population increases (improving the probability of an adaptive mutation occurring) depends on factors such as biological competition. Now, why don't you try to do the computation if your pea brain can handle it.

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.

These submissions have been rejected by the discipline. They are bogus.

It's either that, or he does and he's piling on the snake oil.I haven't met him, though, so at this stage, I'll stick with a probability of 0.5 on both options.

Kleinman:

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No stupid. Drug resistance to a single selection pressure works the same in all cases.

Taq:

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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?
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Sexual recombination and increased mutation rate expedite evolution of Escherichia coli in varied fitness landscapes - PMC

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Why don't you identify the population sizes, the selection conditions and whether they are constant or not, and the mutation rates for each experiment? If you have a constant environment, then recombination will increase the rate of evolution under these circumstances because competition (amplification) will happen. Just write the Python program and pretend it's one of your imaginary models. You are just too lazy to do the math, or you just don't know how to do it.

Kleinman:

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It depends only on the mutation rate and population size just as it does in the Kishony experiment.

Taq:

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The paper above proves you wrong.

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You are just too lazy to do the math and you continue to confuse descent with modification with recombination. Do the math you lazy twit.

Kleinman:

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I understand thermodynamics (and probability theory) well enough to write out the mathematics of descent with modification.

Taq:

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Your math has nothing to do with thermodynamics.

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All this reveals is how little you learned about thermodynamics in your survey of physics course.

Kleinman:

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You are having a problem understanding how descent with modification works for sexual reproducers.

Taq:

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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.

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So you are arguing that combination therapy doesn't work for the treatment of HIV, weeds, and insects. My, my, you virologists really understand how evolution works, especially when multiple selection pressures are acting on a population. Evolution only happens in a constant environment with a single selection pressure acting on a population. You are brilliant.

Kleinman:

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Sure you can post a link based on a single patient that appears to have failed HIV treatment due to recombination. But you fail to recognize that millions of people are successfully treated for HIV with three drug therapy.

Taq:

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People are successfully treated with antibiotics even though antibiotic resistance has evolved in bacteria many times.

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Have you ever treated a patient with single drug therapy that works only to find out a few days later when the bacterial cultures come back showing drug resistance? That's because the person has a functioning immune system and the lab test doesn't consider that in their testing. The drug is not being used in a single selection pressure environment in this case for the patient, it is being tested in a single selection pressure environment.

Kleinman:

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Energy is not entropy.

Taq:

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The availability of energy to do work in a system is the measure of entropy.

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Now Taq is an expert in thermodynamics. Compute the entropy and show us why UCD happened.

Kleinman:

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If you want to compute the entropy when free nucleotides polymerize into a DNA strand, go for it. It's not necessary to know that value to do an "at least one calculation" or a Markov chain calculation, but if that's what you think is important, have at it.

Taq:

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It is necessary for measuring entropy in biology.

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So, that's why biologists have failed to explain how drug resistance evolves and why cancer treatments fail. They are too busy computing entropy. Go for it, compute the entropy of a DNA segment.

Kleinman:

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Sure there was clonal interference in the asexual population because biological competition went to completion with fixation of the most fit variant, not variants. 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.

Taq:

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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.
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Wow, you really don't know how this works.

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Ok brainiac, how does Desai define fixation for his sexual replicators?

Kleinman:

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Amplification of alleles occurs in both cases but only the most fit variant fixes with the asexual replicator.

Taq:

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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.

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How do multiple alleles move to fixation? Here, I'll even help you with the definition of fixation:
Fixation - Wikipedia(population_genetics) Compare that definition with the definition that Desai uses in his paper for his sexual replicators.

Kleinman:

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Let me help you with those links.

AZPaul3:

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These submissions have been rejected by the discipline. They are bogus.

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You are dreaming and you are angry because your bubble has burst.

Taq:

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Wow, you really don't know how this works.

vimesey:

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It's either that, or he does and he's piling on the snake oil.
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I haven't met him, though, so at this stage, I'll stick with a probability of 0.5 on both options.

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Who needs snake oil? All you have to do is figure out the probabilities for two or more selection pressures. Taq is still trying to figure out how evolution works for a single selection pressure in a constant environment (with and without recombination).