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Author Topic:   Rebuttal To Creationists - "Since We Can't Directly Observe Evolution..."
Taq
Member
Posts: 9972
Joined: 03-06-2009
Member Rating: 5.5


(1)
Message 316 of 2926 (898948)
10-04-2022 10:55 AM
Reply to: Message 314 by Kleinman
10-03-2022 12:33 PM


Re: Taq's random recombination model and the trinomial distribution
Kleinman writes:
I thought that we were assuming that each member of the population were homogeneous at these two loci.
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.
Do you want to show us how to compute the joint probability of one Aa parent mating with a second Bb parent to give an AB offspring from your population of 20,000 as a function of the distribution of different frequencies of variants? That is a multinomial distribution calculation with lots of different possible outcomes. Start with AA, BB, CC, Ab, AC,... You have a few permutations to compute.
I already did that in a previous post.
Apparently, I've confused you. Adaptive allele A occurs at one genetic locus, adaptive allele B occurs at a different genetic locus, and the C alleles are the subset of all alleles that don't give an improvement in fitness at either genetic loci.
Your math doesn't add up. Here is what you presented before:
quote:
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.

In addition, we have the following condition: nA + nB + nC = n.

And the frequency of each of the variants are:
f_A = nA/n
f_B = nB/n
f_C = nC/n
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 = 1
Does that math add up? Nope.
Taq, have you thought about what would happen in the fixation process if either the A adaptive allele or B adaptive allele gave greater reproductive fitness than the other?
A would reach fixation in fewer generations than B. If fitness were additive then carriers of both A and B would be the fittest.
In the biological evolutionary competition, wouldn't the variant with the adaptive allele that gives greater reproductive fitness go to a frequency of 1 and the variant that gives a lower degree of improvement in reproductive fitness go to a frequency of 0?
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.

This message is a reply to:
 Message 314 by Kleinman, posted 10-03-2022 12:33 PM Kleinman has replied

Replies to this message:
 Message 318 by Kleinman, posted 10-04-2022 12:54 PM Taq has replied

  
Taq
Member
Posts: 9972
Joined: 03-06-2009
Member Rating: 5.5


(1)
Message 317 of 2926 (898949)
10-04-2022 11:04 AM
Reply to: Message 315 by Kleinman
10-03-2022 1:50 PM


Re: Keeps going and.going
Kleinman writes:
Let's say that every time you flap your arms, you generate a small amount of lift. I then take the laws of physics and formulate a computer simulation that determines the amount of lift as a function of the number of times you flap your arms. I plug in a number of times you flap your arms that is sufficient to generate a lift to get you off the ground. Does that mean you can actually fly?
If the simulation is used on birds and it shows that they can fly, is that an accurate simulation?
But that leaves 1% still able to reproduce because they have the alleles that enable them to do so.
Where in human evolution do you think there was a point where 99% of the population died off because they lacked a specific allele?
And in the case of HIV, this virus can do recombination. The problem for the HIV virus is that it cannot increase the frequency of any of the single drug-resistant variants to give a reasonable probability of an advantageous recombination event occurring.
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?
All these drugs inhibit the reproduction of the virus, they don't kill the virus. Recombination in the 2 drug environment might well get a two-drug resistant variant but the addition of a third drug (third selection condition) affects the mathematics of DNA (RNA in this case) evolution and random recombination for the virus to adapt.
In the presence of the HIV drug, do the HIV resistant viruses reproduce better than the drug sensitive HIV viruses?
The point you are missing is that these bottlenecks select for variants with some degree of resistance to these selection conditions. For example, the black plague killed between 75-200 million people when the world population was about 450 million at that time.
Which is all beside the point. All I said is that bottlenecks aren't necessary, not that they never happen.
You can't have different mutations fixing simultaneously unless you have hitchhikers. Haldane's math applies to the fixation of a single allele. You want to consider two different adaptive alleles at two different genetic loci fixing simultaneously. But that only allows for a frequency of 0.5 for each variant.
That is only for alleles at the same genetic locus, not for mutations at different genetic loci.
So the frequency of the A variant is 1 in the population and the frequency of the B variant is 1? You need to check your math.
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?

This message is a reply to:
 Message 315 by Kleinman, posted 10-03-2022 1:50 PM Kleinman has not replied

  
Kleinman
Member (Idle past 335 days)
Posts: 2142
From: United States
Joined: 10-06-2016


Message 318 of 2926 (898950)
10-04-2022 12:54 PM
Reply to: Message 316 by Taq
10-04-2022 10:55 AM


Re: Taq's random recombination model and the trinomial distribution
Kleinman:
Taq:


Kleinman:
I thought that we were assuming that each member of the population were homogeneous at these two loci.
Taq:
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.

Any time you are ready to get beyond Mendelian Genetics, let us know.
Kleinman:
Do you want to show us how to compute the joint probability of one Aa parent mating with a second Bb parent to give an AB offspring from your population of 20,000 as a function of the distribution of different frequencies of variants? That is a multinomial distribution calculation with lots of different possible outcomes. Start with AA, BB, CC, Ab, AC,... You have a few permutations to compute.
Taq:
I already did that in a previous post.

Are we to understand that in your population of 20,000, the only possible inheritance in that population is Aa bb x aa Bb? aa bb x aa bb can't occur? Doesn't this inheritance pattern depend on the frequencies of different variants in the population?
Kleinman:
Apparently, I've confused you. Adaptive allele A occurs at one genetic locus, adaptive allele B occurs at a different genetic locus, and the C alleles are the subset of all alleles that don't give an improvement in fitness at either genetic loci.
Taq:
Your math doesn't add up. Here is what you presented before:
Kleinman:
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.

In addition, we have the following condition: nA + nB + nC = n.

And the frequency of each of the variants are:
f_A = nA/n
f_B = nB/n
f_C = nC/n
Taq:
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 = 1

Does that math add up? Nope.



You should know better than this Taq. You can only add frequencies (probabilities) if they are mutually exclusive.
Kleinman:
Taq, have you thought about what would happen in the fixation process if either the A adaptive allele or B adaptive allele gave greater reproductive fitness than the other?
Taq:
A would reach fixation in fewer generations than B. If fitness were additive then carriers of both A and B would be the fittest.

The A variant would drive the B variant to extinction unless there happened to be a B mutation hitchhiking along with an A variant but that AB variant would have better reproductive fitness than either the A or B variants. The B variant would be part of the cost of natural selection. That's what the Lenski experiment and Haldane's mathematics demonstrate.
Kleinman:
In the biological evolutionary competition, wouldn't the variant with the adaptive allele that gives greater reproductive fitness go to a frequency of 1 and the variant that gives a lower degree of improvement in reproductive fitness go to a frequency of 0?
Taq:
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.

"disease alleles" would drive to fixation? And only one non-disease allele? Are "disease alleles" increasing in frequency in the population?
I don't ignore the fact that A and B adaptive alleles can be inherited by an offspring in a sexually reproducing population. I'm saying that the probability of that happening depends on the frequency of those individual variants in the population. The strange claim that you are making is that both the A and B variants can go to fixation simultaneously.
Kleinman:
Let's say that every time you flap your arms, you generate a small amount of lift. I then take the laws of physics and formulate a computer simulation that determines the amount of lift as a function of the number of times you flap your arms. I plug in a number of times you flap your arms that is sufficient to generate a lift to get you off the ground. Does that mean you can actually fly?
Taq:
If the simulation is used on birds and it shows that they can fly, is that an accurate simulation?

This is a point you still have to learn about mathematical modeling and computer simulations. You have to test your model against experimental data to test the veracity of your model or simulation.
Kleinman:
But that leaves 1% still able to reproduce because they have the alleles that enable them to do so.
Taq:
Where in human evolution do you think there was a point where 99% of the population died off because they lacked a specific allele?

It is not necessary. You only have a billion replications available to explain human DNA evolution. Bacteria and viruses have the capability of population recovery for DNA evolution to occur. The populations that microbes achieve are many orders of magnitude larger even when considering the limited population sizes of the Kishony and Lenski laboratory experiments compared to the entire history of human reproduction.
Kleinman:
And in the case of HIV, this virus can do recombination. The problem for the HIV virus is that it cannot increase the frequency of any of the single drug-resistant variants to give a reasonable probability of an advantageous recombination event occurring.
Taq:
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?

Are you claiming that combination therapy for the treatment of HIV doesn't work?
Kleinman:
All these drugs inhibit the reproduction of the virus, they don't kill the virus. Recombination in the 2 drug environment might well get a two-drug resistant variant but the addition of a third drug (third selection condition) affects the mathematics of DNA (RNA in this case) evolution and random recombination for the virus to adapt.
Taq:
In the presence of the HIV drug, do the HIV resistant viruses reproduce better than the drug sensitive HIV viruses?

Do the single drug-resistant variants increase in frequency? If they did, that would improve the probability of giving double drug-resistant variants by recombination, and ultimately those double drug-resistant variants should increase in frequency and give 3 drug-resistant variants and cause the treatment to fail. How many years has Magic Johnson been under treatment?
Kleinman:
The point you are missing is that these bottlenecks select for variants with some degree of resistance to these selection conditions. For example, the black plague killed between 75-200 million people when the world population was about 450 million at that time.
Taq:
Which is all beside the point. All I said is that bottlenecks aren't necessary, not that they never happen.

We can agree on this point for different reasons. The human population size is too small for any significant DNA adaptive evolution, bottlenecks or no bottlenecks.
Kleinman:
You can't have different mutations fixing simultaneously unless you have hitchhikers. Haldane's math applies to the fixation of a single allele. You want to consider two different adaptive alleles at two different genetic loci fixing simultaneously. But that only allows for a frequency of 0.5 for each variant.
Taq:
That is only for alleles at the same genetic locus, not for mutations at different genetic loci.

Are you now claiming that a parent only passes a single genetic locus, not an entire genome?
Kleinman:
So the frequency of the A variant is 1 in the population and the frequency of the B variant is 1? You need to check your math.
Taq:
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?

The numbers I've heard are that humans have in common over 99% of our DNA. But if you are going to add frequencies, make sure they are mutually exclusive.

This message is a reply to:
 Message 316 by Taq, posted 10-04-2022 10:55 AM Taq has replied

Replies to this message:
 Message 319 by Taq, posted 10-04-2022 3:05 PM Kleinman has replied

  
Taq
Member
Posts: 9972
Joined: 03-06-2009
Member Rating: 5.5


(1)
Message 319 of 2926 (898960)
10-04-2022 3:05 PM
Reply to: Message 318 by Kleinman
10-04-2022 12:54 PM


Re: Taq's random recombination model and the trinomial distribution
Kleinman writes:
Any time you are ready to get beyond Mendelian Genetics, let us know.
When you are ready to stop rejecting Mendelian genetics, let me know.
Are we to understand that in your population of 20,000, the only possible inheritance in that population is Aa bb x aa Bb? aa bb x aa bb can't occur?
Already explained it in the other post.
You should know better than this Taq. You can only add frequencies (probabilities) if they are mutually exclusive.
Then you should know better, too. So why are you using this equation for mutations in different genes when it clearly does not apply?
The A variant would drive the B variant to extinction unless there happened to be a B mutation hitchhiking along with an A variant but that AB variant would have better reproductive fitness than either the A or B variants.
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.
I don't ignore the fact that A and B adaptive alleles can be inherited by an offspring in a sexually reproducing population. I'm saying that the probability of that happening depends on the frequency of those individual variants in the population. The strange claim that you are making is that both the A and B variants can go to fixation simultaneously.
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?
This is a point you still have to learn about mathematical modeling and computer simulations. You have to test your model against experimental data to test the veracity of your model or simulation.
The computer simulation has been tested against experimental data:
MetaPopGen 2.0: A multilocus genetic simulator to model populations of large size
The human population size is too small for any significant DNA adaptive evolution, bottlenecks or no bottlenecks.
Assertion without evidence.
Are you now claiming that a parent only passes a single genetic locus, not an entire genome?
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.
The numbers I've heard are that humans have in common over 99% of our DNA. But if you are going to add frequencies, make sure they are mutually exclusive.
A million irony meters just exploded.

This message is a reply to:
 Message 318 by Kleinman, posted 10-04-2022 12:54 PM Kleinman has replied

Replies to this message:
 Message 320 by Kleinman, posted 10-04-2022 5:36 PM Taq has replied

  
Kleinman
Member (Idle past 335 days)
Posts: 2142
From: United States
Joined: 10-06-2016


Message 320 of 2926 (898965)
10-04-2022 5:36 PM
Reply to: Message 319 by Taq
10-04-2022 3:05 PM


Re: Taq's random recombination model and the trinomial distribution
Kleinman:
Any time you are ready to get beyond Mendelian Genetics, let us know.
Taq:
When you are ready to stop rejecting Mendelian genetics, let me know.

When did I reject Mendelian genetics? Do you think Mendelian genetics only applies to adaptive alleles?
Kleinman:
Are we to understand that in your population of 20,000, the only possible inheritance in that population is Aa bb x aa Bb? aa bb x aa bb can't occur?
Taq:
Already explained it in the other post.

You really don't want to do the mathematics of random recombination in a population. Then you would have to admit that not only is the mathematics of DNA adaptive evolution correct, but so is the mathematics of random recombination in a population. You can include Mendelian genetics in the calculation but you will have to use a multinomial distribution instead of the simpler case with the trinomial distribution.
Kleinman:
You should know better than this Taq. You can only add frequencies (probabilities) if they are mutually exclusive.
Taq:
Then you should know better, too. So why are you using this equation for mutations in different genes when it clearly does not apply?

Why can't you add these frequencies? You have 3 subsets in the population. One subset has allele A at one genetic locus. Another subset has allele B at a different genetic locus and a third subset has neither allele. Unless there is an intersection of any of these three subsets, they are mutually exclusive. Each of these 3 subsets has a subpopulation size associated with their corresponding subset and if you add up these subpopulation sizes, you get the total population size. And if you divide the individual subpopulation sizes by the total population size, you get the frequencies for each of the subset variants. If you want to include Mendelian genetics in the math, don't make the assumption that these alleles are homogeneous at their respective genetic loci and include more subsets for the different possible variants. I suggest you master the simpler case first since you are having so much difficulty with the math.
Kleinman:
The A variant would drive the B variant to extinction unless there happened to be a B mutation hitchhiking along with an A variant but that AB variant would have better reproductive fitness than either the A or B variants.
Taq:
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.

I only repeated a fundamental axiom of probability theory. The A and B variants are separate subsets that don't intersect and therefore, you can use the addition rule to compute the sum of the frequencies. If the A and B subsets intersect means that you have variants in the population with both an adaptive allele A at one genetic locus and an adaptive allele B at the second genetic locus. That can only happen by DNA evolution or recombination. These are mathematical facts of life.
Kleinman:
I don't ignore the fact that A and B adaptive alleles can be inherited by an offspring in a sexually reproducing population. I'm saying that the probability of that happening depends on the frequency of those individual variants in the population. The strange claim that you are making is that both the A and B variants can go to fixation simultaneously.
Taq:
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?

Fixation by selection involves the most fit allele going to a frequency of 1. Other adaptive alleles that give a smaller increase in fitness are not increasing in frequency. They are decreasing in frequency. And when did I say that non-disease alleles are "being" near fixation? Fixation at a genetic locus occurs when 100% of the population has the same allele.
Kleinman:
This is a point you still have to learn about mathematical modeling and computer simulations. You have to test your model against experimental data to test the veracity of your model or simulation.
Taq:
The computer simulation has been tested against experimental data:

MetaPopGen 2.0: A multilocus genetic simulator to model populations of large size

Ask the authors of this paper to explain why combination therapy works for the treatment of HIV despite the fact that the virus does recombination.
Kleinman:
The human population size is too small for any significant DNA adaptive evolution, bottlenecks or no bottlenecks.
Taq:
Assertion without evidence.

How about every real, measurable, and repeatable empirical example of DNA evolution? Start with the Kishony and Lenski experiments, then go on with the success of combination herbicides, pesticides, and rodenticides inhibiting the evolution of selection pressure resistant variants. How about mathematical models that predict and simulate the behaviors of these evolutionary processes? All this data has forced you into a position of making strange claims about fixation. Taq, do you think you could take a population of chimpanzees, selectively breed them and get a breed of chimpanzees that can do industrial farming, build computers, aircraft, automobiles,...? You are attributing an awful lot to selective recombination.
Kleinman:
Are you now claiming that a parent only passes a single genetic locus, not an entire genome?
Taq:
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.

Don't be silly, I haven't made a claim like that. And of course, frequencies are always less than or equal to 1. Frequencies range from 0 to 1. Why do believe that there can be frequencies greater than 1?
Kleinman:
The numbers I've heard are that humans have in common over 99% of our DNA. But if you are going to add frequencies, make sure they are mutually exclusive.
Taq:
A million irony meters just exploded.

Why? Because you believe that the frequency of all the different alleles shared by eveyone adds up to a number greater than 1? Is this really the way you do your math?

This message is a reply to:
 Message 319 by Taq, posted 10-04-2022 3:05 PM Taq has replied

Replies to this message:
 Message 841 by Taq, posted 10-26-2022 3:17 PM Kleinman has replied

  
Kleinman
Member (Idle past 335 days)
Posts: 2142
From: United States
Joined: 10-06-2016


Message 321 of 2926 (899037)
10-07-2022 9:53 AM


The multiplication rule and universal common descent
It appears that Taq has left the building but who can blame him? He's one of the few on this forum with any understanding of the mathematics and its application to biological evolution. I think there aren't any biologists that understand the physics (thermodynamics) of biological evolution. Taq has done his best to try and recover the concept of universal common descent using sexual replication and recombination. Taq tries to do this by making hand-waving arguments such as claiming that different alleles at different genetic loci can fix simultaneously in a population when none of the biologists' models of fixation model or make that claim. And Taq knows that using the concept of neutral evolution to explain the genetic differences between humans and chimpanzees falls flat on its face when confronted with the mathematical fact that there are over 7 billion humans on earth living in almost every environment possible while there are only about 300,000 chimps alive today in only a limited environment. So, where is the fundamental flaw in the theory of evolution in the way that biologists teach this theory to naive school children? That flaw is "universal common descent". This concept is a gross over-extrapolation of descent with modification as demonstrated by the mathematical and experimental evidence of how adaptive common descent operates.
The mathematical explanation for the reason that universal common descent is not possible is the multiplication rule of probabilities. The effect of this mathematical rule on DNA adaptive evolution is that each adaptive step in a lineage requires about 1/(mutation rate) replications. That is, for each step improvement (each adaptive mutation), for a mutation rate of 1e-9, a billion replications. And that is in a single selection pressure environment. In a multi-selection pressure environment, the population size becomes exponentially larger for each adaptive step because it takes more than a single mutation to improve reproductive fitness. The classic empirical example that demonstrates this is the adaptive evolution of HIV in a 3-drug environment, even when this virus has a mutation rate of 1e-5.
The multiplication rule also impacts random recombination and increasing reproductive fitness. The probability of an adaptive random recombination event occurring in a population is proportional to the product of the frequencies of the adaptive alleles in that population. This is why Taq is forced into the position of claiming that biological competition can cause the fixation of multiple adaptive alleles simultaneously. Taq does this when the mathematical and experimental evidence contradicts his claim.
The simple mathematical fact of life is that humans and chimpanzees could not have come from a common ancestor. You don't have sufficient population size to account for the reproductive fitness differences. I understand that the zealots and atheist readers of this forum won't buy this mathematical fact of life. Just understand that your belief does not make any scientific sense.
I hope this discussion gives some points to consider when hearing stories from fossil tea-leaf readers. Paleontologists should have transitional forms coming out of their ears considering that each DNA adaptive step requires 1/(mutation rate) replications.
If biologists took their field seriously, they would teach naive schoolchildren the correct physics and mathematics of biological evolution. Then these children would have the preparation for dealing with drug-resistant microbes, herbicide-resistant weeds, and pesticide-resistant insects and why cancer treatments fail, not these mathematically irrational ideas that reptiles evolve into birds and fish evolve into mammals. Biologists do a disservice to society when they teach children these types of myths as scientific facts. It wouldn't hurt biologists to take the same mathematics and physics courses required of math, chemistry, engineering, and physics majors. Then biologists might have the skill to correctly do the physics and mathematics of biological evolution, a subject they claim as their own private domain.

Replies to this message:
 Message 322 by nwr, posted 10-07-2022 12:41 PM Kleinman has replied

  
nwr
Member
Posts: 6408
From: Geneva, Illinois
Joined: 08-08-2005
Member Rating: 5.1


(3)
Message 322 of 2926 (899041)
10-07-2022 12:41 PM
Reply to: Message 321 by Kleinman
10-07-2022 9:53 AM


It appears that Taq has left the building but who can blame him?
Taq is probably tired of responding to your nonsense.
The mathematical explanation for the reason that universal common descent is not possible is the multiplication rule of probabilities.
When your mathematical model does not match reality, you are supposed to abandon that broken model. Instead, you are abandoning reality and sticking with your failed model.
Evolution doesn't work the way that you think it does. Your arguments should have shown you that. But you trust your own beliefs rather than the actual evidence.
This is the failure of your creationism.

Fundamentalism - the anti-American, anti-Christian branch of American Christianity

This message is a reply to:
 Message 321 by Kleinman, posted 10-07-2022 9:53 AM Kleinman has replied

Replies to this message:
 Message 323 by Kleinman, posted 10-07-2022 1:17 PM nwr has replied
 Message 328 by Tanypteryx, posted 10-10-2022 2:09 PM nwr has seen this message but not replied

  
Kleinman
Member (Idle past 335 days)
Posts: 2142
From: United States
Joined: 10-06-2016


Message 323 of 2926 (899042)
10-07-2022 1:17 PM
Reply to: Message 322 by nwr
10-07-2022 12:41 PM


Kleinman:
It appears that Taq has left the building but who can blame him?
nwr:
Taq is probably tired of responding to your nonsense.

Taq has already admitted that my mathematical model is correct for DNA adaptive evolution with asexual replicators. And I am sure Taq is tired but not because I'm giving him nonsense. It is because I know how to formulate the mathematics of random recombination and Taq knows that I'm correct. It is very fatiguing to argue again the mathematical and physical facts of life. Only zealots and atheists would do this, not someone that understands something about mathematics and physics.
Kleinman:
The mathematical explanation for the reason that universal common descent is not possible is the multiplication rule of probabilities.
nwr:
When your mathematical model does not match reality, you are supposed to abandon that broken model. Instead, you are abandoning reality and sticking with your failed model.

Evolution doesn't work the way that you think it does. Your arguments should have shown you that. But you trust your own beliefs rather than the actual evidence.

This is the failure of your creationism.

Why does it take a Creationist to correctly explain the physics and mathematics of the Kishony and Lenski biological evolutionary experiments? Where is the biologist's explanation of these experiments? They are still trying to figure out why biological competition slows descent with modification. As I said in my previous post, I don't expect my argument to convince the zealots and atheists posting on this forum, only those with some knowledge of physics and mathematics. I don't include you in that group, I do include Taq. Of course, Taq needs to do a little more study and work on the mathematics of random recombination to get a good understanding of that aspect of biological evolution.

This message is a reply to:
 Message 322 by nwr, posted 10-07-2022 12:41 PM nwr has replied

Replies to this message:
 Message 324 by nwr, posted 10-07-2022 2:43 PM Kleinman has replied

  
nwr
Member
Posts: 6408
From: Geneva, Illinois
Joined: 08-08-2005
Member Rating: 5.1


(1)
Message 324 of 2926 (899045)
10-07-2022 2:43 PM
Reply to: Message 323 by Kleinman
10-07-2022 1:17 PM


Taq has already admitted that my mathematical model is correct for DNA adaptive evolution with asexual replicators.
I'm doubting that. You have interpreted Taq as making such an admission, but I don't think he agree. He has spent a lot of effort trying to explain your mistakes to you, but you repeatedly ignore his explanations.
It is because I know how to formulate the mathematics of random recombination and Taq knows that I'm correct.
More accurately, Taq knows that you are wrong, but has given up on trying to explain this to you.
Just by the way, I am a mathematician, so I do know something about mathematics and physics. I haven't looked closely at your mathematical claims, but it is quite possible that you have correctly modeled your absurdly false understanding of evolution.
Maybe you should try looking at the actual empirical evidence.

Fundamentalism - the anti-American, anti-Christian branch of American Christianity

This message is a reply to:
 Message 323 by Kleinman, posted 10-07-2022 1:17 PM Kleinman has replied

Replies to this message:
 Message 325 by Kleinman, posted 10-07-2022 3:41 PM nwr has replied

  
Kleinman
Member (Idle past 335 days)
Posts: 2142
From: United States
Joined: 10-06-2016


Message 325 of 2926 (899046)
10-07-2022 3:41 PM
Reply to: Message 324 by nwr
10-07-2022 2:43 PM


Kleinman:
Taq has already admitted that my mathematical model is correct for DNA adaptive evolution with asexual replicators.
nwr:
I'm doubting that. You have interpreted Taq as making such an admission, but I don't think he agree. He has spent a lot of effort trying to explain your mistakes to you, but you repeatedly ignore his explanations.

Here's the exchange where Taq admits my math is correct for asexual replicators:
Kleinman:
This is the paper that explains how to compute the probability of adaptive mutations occurring at two or more genetic loci.
Taq:
Those are asexual populations under extremely stringent selection conditions, both of which are not true for human evolution.

Taq never tells us what is so stringent about the selection conditions in the Kishony and Lenski experiments. But he does go on to try and show that recombination can explain the improved reproductive fitness that humans have over chimps. He does this by claiming that multiple alleles can fix simultaneously in a population. Of course, a layman like you with no scientific training wouldn't recognize this blunder.
Kleinman:
It is because I know how to formulate the mathematics of random recombination and Taq knows that I'm correct.
nwr:
More accurately, Taq knows that you are wrong, but has given up on trying to explain this to you.

Just by the way, I am a mathematician, so I do know something about mathematics and physics. I haven't looked closely at your mathematical claims, but it is quite possible that you have correctly modeled your absurdly false understanding of evolution.

Maybe you should try looking at the actual empirical evidence.

Taq thinks that multiple alleles can fix simultaneously in a population. Taq knows he is wrong and that's why he has left the discussion. Taq has left the discussion because he understands this is a blunder.
Oh really? You are a mathematician and you have some understanding of physics? Let's see your mathematical model of the Kishony and Lenski experiments. After you do that, you can give us a mathematical explanation of why 3 drug therapy works for the treatment of HIV when single drug therapy rapidly fails. And then you can show us your mathematical model of random recombination. And we've seen your empirical evidence, fossil tea-leaf reading. Is this where you start claiming I move the goalposts, or you post some silly picture of a fossil and say it is a reptile growing feathers or a fish turning into a mammal? Or perhaps you trot out the claim that with enough time and random processes anything can happen? It is a lot more fun debating the varsity. When they bring out the JV or in this case the C team, it gets really boring really fast. Maybe nwr will surprise us and actually show us how to do some applied mathematics. Given enough time and random chance, anything can happen.

This message is a reply to:
 Message 324 by nwr, posted 10-07-2022 2:43 PM nwr has replied

Replies to this message:
 Message 326 by nwr, posted 10-07-2022 4:26 PM Kleinman has replied

  
nwr
Member
Posts: 6408
From: Geneva, Illinois
Joined: 08-08-2005
Member Rating: 5.1


(1)
Message 326 of 2926 (899047)
10-07-2022 4:26 PM
Reply to: Message 325 by Kleinman
10-07-2022 3:41 PM


Taq never tells us what is so stringent about the selection conditions in the Kishony and Lenski experiments.
If you don't already understand that, then you should not be pontificating.
Of course, a layman like you with no scientific training wouldn't recognize this blunder.
Oh, I recognize the blunder. But you keep on making it, even though this has been repeatedly explained to you.
Taq thinks that multiple alleles can fix simultaneously in a population. Taq knows he is wrong and that's why he has left the discussion. Taq has left the discussion because he understands this is a blunder.
I'll put you down as being as incompetent at reading Taq's mind as you are at understanding evolution.
Let's see your mathematical model of the Kishony and Lenski experiments.
I'm not a biologist. I'll leave the modeling to the real biologists.
I do know enough biology to recognize that you badly misunderstand evolution.

Fundamentalism - the anti-American, anti-Christian branch of American Christianity

This message is a reply to:
 Message 325 by Kleinman, posted 10-07-2022 3:41 PM Kleinman has replied

Replies to this message:
 Message 327 by Kleinman, posted 10-07-2022 4:53 PM nwr has seen this message but not replied

  
Kleinman
Member (Idle past 335 days)
Posts: 2142
From: United States
Joined: 10-06-2016


Message 327 of 2926 (899049)
10-07-2022 4:53 PM
Reply to: Message 326 by nwr
10-07-2022 4:26 PM


nwr's Blah, blah, blah
Kleinman:
Let's see your mathematical model of the Kishony and Lenski experiments.
nwr:
I'm not a biologist. I'll leave the modeling to the real biologists.

I do know enough biology to recognize that you badly misunderstand evolution.

It figures. A mathematician that can't do the mathematics of biological evolution. This isn't even the C-team. Where's the biologist's mathematical explanation of the evolution of antimicrobial drug resistance?

This message is a reply to:
 Message 326 by nwr, posted 10-07-2022 4:26 PM nwr has seen this message but not replied

  
Tanypteryx
Member
Posts: 4344
From: Oregon, USA
Joined: 08-27-2006
Member Rating: 5.9


(3)
Message 328 of 2926 (899213)
10-10-2022 2:09 PM
Reply to: Message 322 by nwr
10-07-2022 12:41 PM


nwr writes:
Kleinman writes:
It appears that Taq has left the building but who can blame him?
Taq is probably tired of responding to your nonsense.
Nonsense indeed. It's interesting to see how Kleinman. a supposed scientist, has refined the Gish Gallop, with a sprinkling of "something, something thermodynamics" and "atheist" thrown in. Taq handed him his ass, but Kleinman was so busy coming up with belittling comments to get it.
Once in a while I have encountered people like him, who apparently took advanced scientific courses and yet failed to understand some basic concepts and then doubled down on their errors when they were pointed out. Taking conclusions from narrow lab experiments on single species of bacteria and applying them as universal rules for all of biology and the evolution of all complex multicellular organisms, when they are obviously incorrect is not going to convince scientists seeing something different in the field.
The funny thing is, this guy's arrogant ignorance alienates all the people who can appreciate the correct parts of his argument. I have noticed these guys being shunned when I've encountered them at scientific meetings.
Competent scientists, in my experience, seek criticism of their ideas, want the holes in their arguments pointed out and self correct when it is appropriate.
Kleinman writes:
The mathematical explanation for the reason that universal common descent is not possible is the multiplication rule of probabilities.
I note also that he has offered no explanation for the patterns of descent we see in cladograms based on genetics and other molecular comparisons and morphology. His whole argument is really the same as Dredge's, "If you don't know the answer to my question, then you can't know anything at all."

Stop Tzar Vladimir the Condemned!

What if Eleanor Roosevelt had wings? -- Monty Python

One important characteristic of a theory is that is has survived repeated attempts to falsify it. Contrary to your understanding, all available evidence confirms it. --Subbie

If evolution is shown to be false, it will be at the hands of things that are true, not made up. --percy

The reason that we have the scientific method is because common sense isn't reliable. -- Taq


This message is a reply to:
 Message 322 by nwr, posted 10-07-2022 12:41 PM nwr has seen this message but not replied

Replies to this message:
 Message 329 by Kleinman, posted 10-10-2022 5:38 PM Tanypteryx has replied

  
Kleinman
Member (Idle past 335 days)
Posts: 2142
From: United States
Joined: 10-06-2016


Message 329 of 2926 (899218)
10-10-2022 5:38 PM
Reply to: Message 328 by Tanypteryx
10-10-2022 2:09 PM


Tanypteryx explains the physics and mathematics of biological evolution
Kleinman:
It appears that Taq has left the building but who can blame him?
nwr:
Taq is probably tired of responding to your nonsense.
Tanypteryx:
Nonsense indeed. It's interesting to see how Kleinman. a supposed scientist, has refined the Gish Gallop, with a sprinkling of "something, something thermodynamics" and "atheist" thrown in. Taq handed him his ass, but Kleinman was so busy coming up with belittling comments to get it.


I never heard of the Gish gallop, so I looked it up:
Gish gallop - Wikipedia
quote:
The Gish gallop /ˈɡɪʃ ˈɡæləp/ is a rhetorical technique in which a person in a debate attempts to overwhelm their opponent by providing an excessive number of arguments with no regard for the accuracy or strength of those arguments.
Did I confuse you with my explanation of the physics (thermodynamics) of Darwinian Evolution?
The Physics of Darwinian Evolution
Kleinman:
Darwinian Evolution gives the correct qualitative framework to understand important examples of
biological evolution. Darwin identified two of the important processes that occur with this biological phenomenon. From his “Origin of Species”[2]:
Darwin:
For it should be remembered that the competition will generally be most severe between those forms which are most nearly related to each other in habits, constitution, and structure. Hence all the intermediate forms between the earlier and later states, that is between the less and more improved state of a species, as well as the original parent-species itself, will generally tend to become extinct. So it probably will be with many whole collateral lines of descent, which will be conquered by later and improved lines of descent. If, however, the modified offspring of a species get into some distinct country, or become quickly adapted to some quite new station, in which child and parent do not come into competition, both may continue to exist.
Kleinman:
Darwin, in the above paragraph, is describing two biological processes. The first process is “competition”, the struggle for existence of different lineages in a population in the given environment. The second process is “adaptation”, modification of some offspring in a given lineage that gives improved reproductive fitness for that new variant to the given selection conditions of the particular environment. These two biological processes are governed by different laws of thermodynamics.


I then go on to describe how the first law of thermodynamics applies to biological competition and the second law of thermodynamics applies to adaptation (descent with modification). You must forgive me if my rhetorical technique overwhelms you. I wrote this paper so that it could be understood by laymen and biologists. It appears that I have failed you. Try reading the article and point out to me what is overwhelming you.
Tanypteryx:
Once in a while I have encountered people like him, who apparently took advanced scientific courses and yet failed to understand some basic concepts and then doubled down on their errors when they were pointed out. Taking conclusions from narrow lab experiments on single species of bacteria and applying them as universal rules for all of biology and the evolution of all complex multicellular organisms, when they are obviously incorrect is not going to convince scientists seeing something different in the field.
Is that a tacit admission that I've done the mathematics of the Kishony and Lenski experiments correctly? Taq made the same type of claim and nwr thinks I'm mind reading when I say that is an admission that I got that math and physics correct. If you say I got the math and physics wrong, feel free to point out where. I'm open to that discussion. Tell me where I got some basic concepts wrong.
Tanypteryx:
The funny thing is, this guy's arrogant ignorance alienates all the people who can appreciate the correct parts of his argument. I have noticed these guys being shunned when I've encountered them at scientific meetings.

Competent scientists, in my experience, seek criticism of their ideas, want the holes in their arguments pointed out and self correct when it is appropriate.
Go ahead and criticize. Point out the error in the math or physics I've presented and present what you think is the correct mathematical and physical explanation of the Kishony and Lenski experiments. nwr claims to be a mathematician with a little knowledge of physics and he doesn't point out any errors in the papers I've presented. You won't either.
Kleinman:
The mathematical explanation for the reason that universal common descent is not possible is the multiplication rule of probabilities.
Tanypteryx:
I note also that he has offered no explanation for the patterns of descent we see in cladograms based on genetics and other molecular comparisons and morphology. His whole argument is really the same as Dredge's, "If you don't know the answer to my question, then you can't know anything at all."

Have you ever done a careful analysis of Joe Felsenstein's work on inferential phlogenetics? Here's a simple explanation of how it's done.
How to build a phylogenetic tree
quote:
The first thing to do is align the two DNA sequences together that you’re going to compare. Make sure you’re comparing the same gene! (Or other sequence.) Otherwise you are comparing apples to oranges.
There are two mathematical problems when doing this kind of statistical analysis. The first is that in order to get an accurate model, you have to use the correct statistical distribution. That's a minor problem. There is a much larger problem in this type of analysis. It really isn't a problem, it is a lower-division, undergraduate-level blunder. Can you see what that blunder is and why doing this can't be used to construct clades?

This message is a reply to:
 Message 328 by Tanypteryx, posted 10-10-2022 2:09 PM Tanypteryx has replied

Replies to this message:
 Message 330 by Tanypteryx, posted 10-10-2022 8:17 PM Kleinman has replied

  
Tanypteryx
Member
Posts: 4344
From: Oregon, USA
Joined: 08-27-2006
Member Rating: 5.9


(2)
Message 330 of 2926 (899223)
10-10-2022 8:17 PM
Reply to: Message 329 by Kleinman
10-10-2022 5:38 PM


Re: Tanypteryx explains the physics and mathematics of biological evolution
Kleinman writes:
Tanypteryx explains the physics and mathematics of biological evolution
Now see, this is why I doubt your credibility. You behave like an obnoxious jerk rather than a scientist with something interesting to say.
Did I confuse you with my explanation of the physics (thermodynamics) of Darwinian Evolution?
Nope, because your explanation doesn't describe the evolution of the organisms I study.
Is that a tacit admission that I've done the mathematics of the Kishony and Lenski experiments correctly?
Nope, I'm saying that you alienate many of the only people who could appreciate your work.
And that you are mistaken to try and extrapolate what was learned from those narrow experiments to rules for how mutation and selection occur in all complex, sexually reproducing, multicellular organisms. You ignore that every individual organism acquire numerous mutations that can be passed on to their descendants along with thousands of other mutations that they each inherited from their ancestors.
Taq explained your lower-division, undergraduate-level blunders, but you have far too lofty an intellect to learn anything from him.
I await your Nobel acceptance speech for medicine.

Stop Tzar Vladimir the Condemned!

What if Eleanor Roosevelt had wings? -- Monty Python

One important characteristic of a theory is that is has survived repeated attempts to falsify it. Contrary to your understanding, all available evidence confirms it. --Subbie

If evolution is shown to be false, it will be at the hands of things that are true, not made up. --percy

The reason that we have the scientific method is because common sense isn't reliable. -- Taq


This message is a reply to:
 Message 329 by Kleinman, posted 10-10-2022 5:38 PM Kleinman has replied

Replies to this message:
 Message 331 by Kleinman, posted 10-10-2022 9:25 PM Tanypteryx has replied

  
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