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Creationists: Explain your understanding of microevolution and macroevolution

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Ponderous Curmudgeon

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Why don't you tell us what that fundamental error is and then tell us the correct way to mathematically model DNA evolution. Explain why it takes a billion replications for each adaptive microevolutionary step in the Kishony experiment. You can't and you won't.

The math I presented predicted that it would take a billion replications for each adaptive microevolutionary step and it was published years before Kishony ran his experiment. Where is the error in that?
Because at best your probability model is a retrospective analysis of "a great chain of being" resulting in us. The sequence of events (mutations) that resulted in human beings is basically irrelevant to evolutionary biology. We are not a goal or determined endpoint in any evolutionary sense, rather just the result of the many branches that have occurred in the past. And yes, if you wanted to calculate the forward odds of the specific path from our LCA with chimps you would have a tiny number, but that doesn't make it useful math in evolutionary biology.

You are basically calculating what are the odds that you exist relative to the number of sperm and eggs produced by all of your ancestors. A pointless calculation.

Your math to the degree that it is correct, has some validity in determining the probability of a few specific mutations occurring in a defined scenario, and thus will give possibly reasonable numbers in something like the mega plate where there are only a few quick solutions available before the population dies of starvation or whatever. However as a general answer, it is not a description of evolution in general.
 
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Ponderous Curmudgeon

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Definition of MACRO

You are not going to get reptiles evolving into birds and fish evolving into mammals by microevolution. The multiplication rule of probabilities requires far too large populations for this kind of genetic transformation.
Your point, large quantities of micro = macro.

As to this multiplication rule, the way you are using it is not relevant to evolution without your false understanding of evolution.
 
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tas8831

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In a couple decades of debating science and creationism on the internet, I don't think I've ever seen someone chronically linking to their own published works in this way. It's very odd.
John A. Davison
 
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Ponderous Curmudgeon

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Do you think that humans and bacteria evolved from a common ancestor by neutral evolution? And of course, Swamidass's blunder was using neutral evolution to explain the genetic differences between humans and chimpanzees. So, how many beneficial mutations did humans get in order to have our reproductive fitness advantage over chimps? Which mutations gave humans the ability to do industrial farming, build aircraft, make computers,...?
No Felsenstein was explaining the difference between neutral evolution and neutral mutations that were later useful as several were making errors in their use of the terms.
 
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tas8831

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You are not going to get reptiles evolving into birds and fish evolving into mammals by microevolution. The multiplication rule of probabilities requires far too large populations for this kind of genetic transformation.
:sleep:
This is absolutely hilarious.

This is the sort of bare assertion someone makes when they literally have zero understanding of how genotype affects phenotype.

Tell us - do you believe that there is some kind of 1-to-1 relationship between a mutation and phenotype? Because this nonsense about probabilities tells me that you are clueless about that relationship.

Are you aware of things like segmental duplications? Polyploidy? Gene duplications? Transposition?

Unless I missed it, yo never did explain that this is impossible because math:

2002 Sep 27;297(5590):2253-6.
doi: 10.1126/science.1074170.
A single p450 allele associated with insecticide resistance in Drosophila
Abstract
Insecticide resistance is one of the most widespread genetic changes caused by human activity, but we still understand little about the origins and spread of resistant alleles in global populations of insects. Here, via microarray analysis of all P450s in Drosophila melanogaster, we show that DDT-R, a gene conferring resistance to DDT, is associated with over-transcription of a single cytochrome P450 gene, Cyp6g1. Transgenic analysis of Cyp6g1 shows that over-transcription of this gene alone is both necessary and sufficient for resistance. Resistance and up-regulation in Drosophila populations are associated with a single Cyp6g1 allele that has spread globally. This allele is characterized by the insertion of an Accord transposable element into the 5' end of the Cyp6g1 gene.
 
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Ponderous Curmudgeon

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:sleep:
This is absolutely hilarious.

This is the sort of bare assertion someone makes when they literally have zero understanding of how genotype affects phenotype.

Tell us - do you believe that there is some kind of 1-to-1 relationship between a mutation and phenotype? Because this nonsense about probabilities tells me that you are clueless about that relationship.

Are you aware of things like segmental duplications? Polyploidy? Gene duplications? Transposition?

Unless I missed it, yo never did explain that this is impossible because math:

2002 Sep 27;297(5590):2253-6.
doi: 10.1126/science.1074170.
A single p450 allele associated with insecticide resistance in Drosophila
Abstract
Insecticide resistance is one of the most widespread genetic changes caused by human activity, but we still understand little about the origins and spread of resistant alleles in global populations of insects. Here, via microarray analysis of all P450s in Drosophila melanogaster, we show that DDT-R, a gene conferring resistance to DDT, is associated with over-transcription of a single cytochrome P450 gene, Cyp6g1. Transgenic analysis of Cyp6g1 shows that over-transcription of this gene alone is both necessary and sufficient for resistance. Resistance and up-regulation in Drosophila populations are associated with a single Cyp6g1 allele that has spread globally. This allele is characterized by the insertion of an Accord transposable element into the 5' end of the Cyp6g1 gene.
His argument is not that it is particular mutations per se, his math is even relevant for a case like yours. He is arguing that a specific series of mutations is necessary for the evolution of the LCA of us and chimps and thus the probabilities multiply. Thus the probability of humans as seen at the time of the LCA is miniscule and math and little numbers, it must be wrong. It is rather laughable.
 
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pitabread

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His argument is not that it is particular mutations per se, his math is even relevant for a case like yours. He is arguing that a specific series of mutations is necessary for the evolution of the LCA of us and chimps and thus the probabilities multiply. Thus the probability of humans as seen at the time of the LCA is miniscule and math and little numbers, it must be wrong. It is rather laughable.

It's basically just the "waiting time" problem. I think he even mentioned Haldane earlier in this thread.

Which IIRC hasn't been a problem for evolution and common ancestry since the 1960's?
 
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Alan Kleinman

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That didn't answer my question. I asked if you reject common ancestry.

Let's try again:

Do you reject common ancestry of species? Are you rejecting the notion of theropods evolving into birds, etc.?

A simple yes/no will suffice.
The multiplication rule precludes this possibility. No.
 
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pitabread

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John A. Davison

Huh. Hadn't heard of him either. Sounds like a real character, though.

Towards the end of his life Davison would spend hours spamming websites and blogs about how Darwin's theory of evolution was wrong and unscientific and how the neo-Darwinists had ruined science. Davison was banned from many forums and even banned from intelligent design websites for his constant trolling. He was known for sending abusive emails to scientists who he claimed were "brainwashed" by Darwinism.

John A. Davison - RationalWiki
 
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Alan Kleinman

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Because at best your probability model is a retrospective analysis of "a great chain of being" resulting in us. The sequence of events (mutations) that resulted in human beings is basically irrelevant to evolutionary biology. We are not a goal or determined endpoint in any evolutionary sense, rather just the result of the many branches that have occurred in the past. And yes, if you wanted to calculate the forward odds of the specific path from our LCA with chimps you would have a tiny number, but that doesn't make it useful math in evolutionary biology.

You are basically calculating what are the odds that you exist relative to the number of sperm and eggs produced by all of your ancestors. A pointless calculation.

Your math to the degree that it is correct, has some validity in determining the probability of a few specific mutations occurring in a defined scenario, and thus will give possibly reasonable numbers in something like the mega plate where there are only a few quick solutions available before the population dies of starvation or whatever. However as a general answer, it is not a description of evolution in general.
This math was published before Kishony ran his experiment and correctly predicted his experimental results. The multiple simultaneous selection pressure model also predicts what his two drug model will do, if he ever gets it to work. There is no scenario where DNA microevolutionary adaptation operates different. Feel free to post an experimental example of DNA microevolutionary adaptation operates differently if you can find an example. You won't.
 
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Alan Kleinman

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:sleep:
This is absolutely hilarious.

This is the sort of bare assertion someone makes when they literally have zero understanding of how genotype affects phenotype.

Tell us - do you believe that there is some kind of 1-to-1 relationship between a mutation and phenotype? Because this nonsense about probabilities tells me that you are clueless about that relationship.

Are you aware of things like segmental duplications? Polyploidy? Gene duplications? Transposition?

Unless I missed it, yo never did explain that this is impossible because math:

2002 Sep 27;297(5590):2253-6.
doi: 10.1126/science.1074170.
A single p450 allele associated with insecticide resistance in Drosophila
Abstract
Insecticide resistance is one of the most widespread genetic changes caused by human activity, but we still understand little about the origins and spread of resistant alleles in global populations of insects. Here, via microarray analysis of all P450s in Drosophila melanogaster, we show that DDT-R, a gene conferring resistance to DDT, is associated with over-transcription of a single cytochrome P450 gene, Cyp6g1. Transgenic analysis of Cyp6g1 shows that over-transcription of this gene alone is both necessary and sufficient for resistance. Resistance and up-regulation in Drosophila populations are associated with a single Cyp6g1 allele that has spread globally. This allele is characterized by the insertion of an Accord transposable element into the 5' end of the Cyp6g1 gene.
How did the allele come about in the first place to be duplicated?
 
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Alan Kleinman

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His argument is not that it is particular mutations per se, his math is even relevant for a case like yours. He is arguing that a specific series of mutations is necessary for the evolution of the LCA of us and chimps and thus the probabilities multiply. Thus the probability of humans as seen at the time of the LCA is miniscule and math and little numbers, it must be wrong. It is rather laughable.
And you do not have the population sizes necessary for humans and chimpanzees to evolve from a common ancestor. Only about 100 billion humans have existed in all time and 99% in the last 10,000 years. That gives a population size for adaptive evolution of a lineage to accumulate about 5 adaptive mutations, and that under ideal circumstances. So, what are the 5 magical mutations that give humans the intellect to do industrial farming, produce aircraft, make computers,... and chimps only able to gather ants and termites with a stick for food?
 
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Alan Kleinman

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Your point, large quantities of micro = macro.

As to this multiplication rule, the way you are using it is not relevant to evolution without your false understanding of evolution.
As long as mutations are random events, the joint probability of adaptive mutations accumulating in a lineage will be computed by the multiplication rule. All empirical experimental evidence substantiates this claim. Feel free to post an empirical example that demonstrates otherwise, if you can. You won't.
 
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Subduction Zone

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As long as mutations are random events, the joint probability of adaptive mutations accumulating in a lineage will be computed by the multiplication rule. All empirical experimental evidence substantiates this claim. Feel free to post an empirical example that demonstrates otherwise, if you can. You won't.

Your question appears to be poorly formed. You have a phrase in it that indicates you do not understand what you are arguing about. What do you mean by the phrase "joint probability of adaptive mutations"? It appears by that question that you think that there is a goal to evolution.
 
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Alan Kleinman

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It's basically just the "waiting time" problem. I think he even mentioned Haldane earlier in this thread.

Which IIRC hasn't been a problem for evolution and common ancestry since the 1960's?
Haldane's "cost of natural selection" model is a model of competition, not DNA adaptive microevolution. If you want to do the mathematics for the Lenski experiment, you have to superimpose a variation of the Haldane model onto the DNA adaptive evolution model that I've presented. If you want to see how you do this mathematics, you can read about it here:
Fixation and Adaptation in the Lenski E. coli Long Term Evolution Experiment

Per your suggestion, I've sent this paper to Lenski. This paper explains why competition slows DNA adaptive evolution, something which the Lenski team does not understand.
 
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pitabread

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Not by microevolution. That is the only scientific answer I can give.

I'm not asking for a scientific answer necessarily.

How do you think species arose if not via evolution?
 
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pitabread

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Per your suggestion, I've sent this paper to Lenski. This paper explains why competition slows DNA adaptive evolution, something which the Lenski team does not understand.

Be sure to let us know their response.
 
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