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

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I don't need much of an excuse for something so simple. Why it confuses you is really a mystery.

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There is no mystery at all. You chose to use unclear notation and didn’t explain it in the posts here,

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Whose fault is it that you don't see the obvious?

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It’s your fault that you failed to see the obvious. That’s the problem.

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You make the error and you should get the credit for your error, it's only fair enough.

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Funny how you expect everyone else to accept the blame for your errors then.

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My notation was clear enough to anyone who can read, perhaps your problem is that you can't read.

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Only to those who read the explanation - which you didn’t post here.Of course it was perfectly clear that my point didn’t depend on heterozygosity but you somehow missed that.

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That's correct in a constant environment. What happens when the environment is changing? An allele might be advantageous in one environment but disadvantageous in another environment

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Might be is hardly a guarantee. Many environmental conditions are relatively constant, or changing in a way that makes the advantageous allele more advantageous. Human intelligence is obviously useful in a wide range of terrestrial environments. Malaria maintains the frequency of sickle cell and doesn’t seem to be going away any time soon - for all our efforts. Hospital conditions are constant enough to make multiply-resistant bacteria a problem.That something might happen is not proof that it did or would.

Tanypteryx:

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So, you still have no evidence refuting the patterns of ERVs in the genomes of sexually reproducing species. We can all see you flailing, Bullshit Peddler.

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You still don't understand that you have to sample data randomly.
Statistics for Dummies

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How do you select a statistical sample in a way that avoids bias? The key word is random. A random sample is a sample selected by equal opportunity; that is, every possible sample of the same size as yours had an equal chance to be selected from the population. What random really means is that no subset of the population is favored in or excluded from the selection process.

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Non-random (in other words bad) samples are samples that were selected in such a way that some type of favoritism and/or automatic exclusion of a part of the population was involved, whether intentional or not.

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You are a dummy.

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Of course, they don't make UCD possible. It also is a demonstration of biologists wrongly doing non-random sampling and introducing bias into their math. But if that is all you have, what else can you do.

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I guess that lies and scorn for science are all you have.

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So anything you don't understand is junk. No wonder you are so slow in understanding.

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The evidence for junk DNA is rather more than that it isn’t understood. But of course you can’t be bothered to understand that. So you call it junk.

Kleinman:

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Tell us how sexual reproduction makes UCD possible, this should be entertaining.

Tanypteryx:

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Tell us how sexual reproduction works, this should be entertaining.

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Tany can't explain the Kishony or Lenski experiments and now he can't explain how sexual reproduction works. He's a fake.

So, still nothing but bullshit. Not a single paper refuting the ERV data. You are flailing.

Kleinman:

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I don't need much of an excuse for something so simple. Why it confuses you is really a mystery.

PaulK:

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There is no mystery at all. You chose to use unclear notation and didn’t explain it in the posts here,

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It's only unclear to you. To the peer reviewers, it was obvious.

Kleinman:

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Whose fault is it that you don't see the obvious?

PaulK:

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It’s your fault that you failed to see the obvious. That’s the problem.

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It is obvious to me and obvious to the peer reviewers. Why it isn't obvious to you is because you are confused.

Kleinman:

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You make the error and you should get the credit for your error, it's only fair enough.

PaulK:

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Funny how you expect everyone else to accept the blame for your errors then.

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I think you should take responsibility for your own errors. Why don't you take responsibility for your own errors?

Kleinman:

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My notation was clear enough to anyone who can read, perhaps your problem is that you can't read.

PaulK:

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Only to those who read the explanation - which you didn’t post here.
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Of course it was perfectly clear that my point didn’t depend on heterozygosity but you somehow missed that.

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Don't blame me if you don't read.

Kleinman:

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That's correct in a constant environment. What happens when the environment is changing? An allele might be advantageous in one environment but disadvantageous in another environment

PaulK:

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Might be is hardly a guarantee. Many environmental conditions are relatively constant, or changing in a way that makes the advantageous allele more advantageous. Human intelligence is obviously useful in a wide range of terrestrial environments. Malaria maintains the frequency of sickle cell and doesn’t seem to be going away any time soon - for all our efforts. Hospital conditions are constant enough to make multiply-resistant bacteria a problem.
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That something might happen is not proof that it did or would.

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Now that's a claim. When is the environment constant over the lifespan of a human? And hospital conditions include a population that is immune compromised. In case you didn't know, they have sick people in hospitals. That's why there is a higher concentration of drug-resistant infections in hospitals than out in the community. Perhaps you very stupidly believe that they use too many antibiotics in the hospital. You have some really stupid ideas.

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It's only unclear to you. To the peer reviewers, it was obvious

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Because you explained it in the paper. The only mystery is how you fail to see the obvious.

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I think you should take responsibility for your own errors. Why don't you take responsibility for your own errors?

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I do. I just won’t take responsibility for yours.

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Now that's a claim. When is the environment constant over the lifespan of a human?

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I guess that you can’t read. I said that aspects of the environment can remain sufficiently constant. I even offered an example - the presence of malaria in some regions seems quite constant, for instance.

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And hospital conditions include a population that is immune compromised. In case you didn't know, they have sick people in hospitals. That's why there is a higher concentration of drug-resistant infections in hospitals than out in the community.

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By which you mean that I was correct. The environment in hospitals is sufficiently stable to permit the evolution of multiply resistant bacteria. Which is all I said on the subject.So please, please take responsibility for this gross error on your part.

Kleinman:

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It's only unclear to you. To the peer reviewers, it was obvious

PaulK:

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Because you explained it in the paper. The only mystery is how you fail to see the obvious.

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I'll have to remember to put a special engraved invitation for you. We wouldn't want you to miss the obvious.

Kleinman:

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I think you should take responsibility for your own errors. Why don't you take responsibility for your own errors?

PaulK:

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I do. I just won’t take responsibility for yours.

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Why is it my fault that you didn't read the paper?

Kleinman:

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Now that's a claim. When is the environment constant over the lifespan of a human?

PaulK:

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I guess that you can’t read. I said that aspects of the environment can remain sufficiently constant. I even offered an example - the presence of malaria in some regions seems quite constant, for instance.

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Since when does one particular selection condition make the entire environment constant? Did the weather remain constant? Were there no droughts or floods? Did they have any wars? Any famines? Other diseases? I don't think you have thought through your argument.

Kleinman:

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And hospital conditions include a population that is immune compromised. In case you didn't know, they have sick people in hospitals. That's why there is a higher concentration of drug-resistant infections in hospitals than out in the community.

PaulK:

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By which you mean that I was correct. The environment in hospitals is sufficiently stable to permit the evolution of multiply resistant bacteria. Which is all I said on the subject.
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So please, please take responsibility for this gross error on your part.

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You clearly aren't thinking through your argument. You are posing an argument based on a particular environment and a particular population. These are ideal conditions for drug-resistant infections to appear and therefore, combination antibiotics should be used. In this way, resistant infections will be more likely defeated because resistance to one drug will be defeated by another drug with a different mode of action.

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Since when does one particular selection condition make the entire environment constant? Did the weather remain constant? Were there no droughts or floods? Did they have any wars? Any famines? Other diseases? I don't think you have thought through your argument.

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No, you haven’t thought through my argument. It is not necessary that the environment remains absolutely constant, only that it does not change in ways that make the new allele disadvantageous before it fixes. You will note that none of these things have removed the advantages of the sickle cell allele.Of course if you had thought though your argument you would realise that it assumes that such is the case. You are arguing that recombination does not give an advantage in fixing two advantageous alleles. If either of the two alleles cease to be advantageous your argument is moot.

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You clearly aren't thinking through your argument. You are posing an argument based on a particular environment and a particular population

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No, I am offering an actual example of an environment staying stable enough to allow cumulative evolutionary change. Which demonstrates that such is possible.

Kleinman:

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Since when does one particular selection condition make the entire environment constant? Did the weather remain constant? Were there no droughts or floods? Did they have any wars? Any famines? Other diseases? I don't think you have thought through your argument.

PaulK:

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No, you haven’t thought through my argument. It is not necessary that the environment remains absolutely constant, only that it does not change in ways that make the new allele disadvantageous before it fixes. You will note that none of these things have removed the advantages of the sickle cell allele.

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The sickle cell allele is not advantageous in the non-malaria environment. Otherwise, it would fix. Your example is not valid.

PaulK:

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Of course if you had thought though your argument you would realise that it assumes that such is the case. You are arguing that recombination does not give an advantage in fixing two advantageous alleles. If either of the two alleles cease to be advantageous your argument is moot.

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You make the same mistake that Taq makes that multiple alleles can fix simultaneously. That is by definition is not possible. That's what the Desai experiment shows. The adaptive alleles increase in frequencies but before fixation occurs, they induce sexual reproduction. If they had waited longer, only a single allele would have fixed and all the other alleles would have been eliminated by the competition and fixation process.

Kleinman:

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You clearly aren't thinking through your argument. You are posing an argument based on a particular environment and a particular population

PaulK:

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No, I am offering an actual example of an environment staying stable enough to allow cumulative evolutionary change. Which demonstrates that such is possible.

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Then everyone would have the sickle cell allele. It only has benefit in malaria endemic regions. In non-malaria regions it is not a beneficial allele.

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The sickle cell allele is not advantageous in the non-malaria environment. Otherwise, it would fix. Your example is not valid

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On the contrary - it is valid for that exact reason. We know an environmental change - eliminating malaria - could wipe out the advantage. But it hasn’t happened - despite all the other changes that have gone on. That is the point.Indeed if my point were invalid sickle cell shouldn’t exist - or should be very rare. It has remained advantageous - in malarial regions - for many human lifetimes. That is why it is as common as it is in the world

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You make the same mistake that Taq makes that multiple alleles can fix simultaneously.

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They can certainly increase in frequency simultaneously - in a sexually reproducing species - which is all I am claiming.

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That's what the Desai experiment shows. The adaptive alleles increase in frequencies but before fixation occurs, they induce sexual reproduction. If they had waited longer, only a single allele would have fixed and all the other alleles would have been eliminated by the competition and fixation process.

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So the Desai experiment shows that you are wrong.

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Then everyone would have the sickle cell allele. It only has benefit in malaria endemic regions. In non-malaria regions it is not a beneficial allele.

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Mixing up examples made to illustrate different points is not going to help you. Multiply-resistant bacteria demonstrate that cumulative evolution is possible. Sickle cell demonstrates only that environments can be constant enough to maintain allele frequencies - and I am not claiming any more for it.(Besides that you are wrong. Even if malaria was everywhere, we wouldn’t all have the sickle cell allele. As predicted by the mathematics of evolution).

Kleinman:

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The sickle cell allele is not advantageous in the non-malaria environment. Otherwise, it would fix. Your example is not valid

PaulK:

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On the contrary - it is valid for that exact reason. We know an environmental change - eliminating malaria - could wipe out the advantage. But it hasn’t happened - despite all the other changes that have gone on. That is the point.

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Sure, but it isn't advantageous outside the malaria environment. It gives no advantage to those living in northern Europe.

PaulK:

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Indeed if my point were invalid sickle cell shouldn’t exist - or should be very rare. It has remained advantageous - in malarial regions - for many human lifetimes. That is why it is as common as it is in the world

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It isn't as common in northern Europe where malaria is not endemic. And if it is homozygous for the sickle cell allele, it is harmful. I treated a patient many years ago who was homozygous for sickle cell and this patient was hospitalized many times for sickle cell crisis.

Kleinman:

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You make the same mistake that Taq makes that multiple alleles can fix simultaneously.

PaulK:

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They can certainly increase in frequency simultaneously - in a sexually reproducing species - which is all I am claiming.

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Only in a constant environment will they increase and only within a limit. If an adaptive recombination event doesn't occur, competition and fixation will eliminate all but one of the adaptive alleles. If the environment is not constant, who knows what alleles will increase in frequencies.

Kleinman:

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That's what the Desai experiment shows. The adaptive alleles increase in frequencies but before fixation occurs, they induce sexual reproduction. If they had waited longer, only a single allele would have fixed and all the other alleles would have been eliminated by the competition and fixation process.

PaulK:

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So the Desai experiment shows that you are wrong.

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You are confused. The Desai experiment behaves exactly as expected. 90 generations of a constant environment with asexual replication gives increases in frequencies of adaptive alleles, then at 90 generations, sexual reproduction is induced and adaptive recombination events occur. Sexual reproduction is induced before fixation has occurred.

Kleinman:

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Then everyone would have the sickle cell allele. It only has benefit in malaria endemic regions. In non-malaria regions it is not a beneficial allele.

PaulK:

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Mixing up examples made to illustrate different points is not going to help you. Multiply-resistant bacteria demonstrate that cumulative evolution is possible. Sickle cell demonstrates only that environments can be constant enough to maintain allele frequencies - and I am not claiming any more for it.

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(Besides that you are wrong. Even if malaria was everywhere, we wouldn’t all have the sickle cell allele. As predicted by the mathematics of evolution).

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I didn't bring up the Malaria example, you did. Multiply resistant bacteria requires a population size much greater than that for singly resistant bacteria. It take much larger populations because they have to diverge more to get variants with double mutants. And to get triple mutants requires such large populations that even HIV does not achieve such population size. That's why 3-drug therapy works. Learn how to do this math. You can find it here, and read the paper so you don't make any excuses.
The mathematics of random mutation and natural selection for multiple simultaneous selection pressures and the evolution of antimicrobial drug resistance

You've got me there, blondie.

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Sure, but it isn't advantageous outside the malaria environment. It gives no advantage to those living in northern Europe

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Which does not change the fact that it is advantageous in malarial regions, and that that advantage is constant enough to spread the allele there.

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It isn't as common in northern Europe where malaria is not endemic. And if it is homozygous for the sickle cell allele, it is harmful. I treated a patient many years ago who was homozygous for sickle cell and this patient was hospitalized many times for sickle cell crisis.

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Which still does not change the facts.

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Only in a constant environment will they increase and only within a limit. If an adaptive recombination event doesn't occur, competition and fixation will eliminate all but one of the adaptive alleles. If the environment is not constant, who knows what alleles will increase in frequencies.

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As usual you haven’t thought out your argument. If the two alleles do not come into contact they cannot interfere. If they do then recombination becomes a possibility - and the greater the contact the greater the probability of it occurring.It does not require an absolutely constant environment, only that the alleles remain advantageous which is implicit in your original argument.

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You are confused

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Not at all. As you admit the Desai experiment proves the point:

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The Desai experiment behaves exactly as expected. 90 generations of a constant environment with asexual replication gives increases in frequencies of adaptive alleles, then at 90 generations, sexual reproduction is induced and adaptive recombination events occur. Sexual reproduction is induced before fixation has occurre

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I didn't bring up the Malaria example, you did.

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I see. I am it supposed to bring up valid examples because you’ll make stupid mistakes?

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Multiply resistant bacteria requires a population size much greater than that for singly resistant bacteria. It take much larger populations because they have to diverge more to get variants with double mutants. And to get triple mutants requires such large populations that even HIV does not achieve such population size. That's why 3-drug therapy works.

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Which does not change the fact that hospitals are a stable enough environment for the evolution of multiply-resistant bacteria.

Over 1500 posts into your thread... and all you've done is shown a complete misunderstanding of physics and mathematics in anything you've posted.And you think you have the ability to judge other people's math work?
I think you need to work on yourself a bit.