Creationists: Explain your understanding of microevolution and macroevolution

[Alan Kleinman]

"Macroevolutionists"? Don't you mean biologists?

Sadly, most biologists are macroevolutionists. That explains why they can't explain the physics and mathematics of microevolutionary adaptation.

 

[pitabread]

Sadly, most biologists are macroevolutionists. That explains why they can't explain the physics and mathematics of microevolutionary adaptation.

"Sadly"?

Why do you care whether biologists accept common ancestry?

 

[Alan Kleinman]

Please, let's deal with your errors first. You will never learn as long as you duck and dodge and try to shift the burden of proof.

And yes, though all journals tend to charge something, some try to get their money more from subscriptions than from the person publishing. The most reliable journals rely on subscriptions. Open access journals can publish valid articles, but there are quite a few of them out there that will publish almost anything. If a nobody that does not know what he is talking about wants to get published he will go to an open access source. If a person that knows nothing is afraid of being exposed even from the vanity press he or she will go to an off topic journal. No one is taking your articles seriously since they have been refuted and you do not even appear to understand the refutations.

So, where is the mathematical explanation of the Kishony and Lenski experiments in your "reliable" journals? And I think you will find that the editors and peer reviewers of "Statistics in Medicine" are not only reliable able to understand the mathematics of microevolutionary adaptation. Only macroevolutionists try to refute this math, sadly they don't have their own explanation other than algae forming colonies and transposon as the way reptiles evolve into birds and fish evolve into mammals.

 

[FrumiousBandersnatch]

Well, I'm confused - if AK's maths, when applied correctly to the genetics of human evolution, means we couldn't possibly have a common ancestor with chimps, why is there so much genetic evidence that we do?

For example, why do we share over 200 endogenous retrovirus insertions (ERV) for a certain retrovirus group at the exact same points in our genomes, vs single figure counts for non-shared (unique) ERVs of that virus group?

If there are around 10 million possible insertion points, what are the odds of sharing over 200 identical insertions by chance?

Would that be greater or less than the odds AK is suggesting?

Someone told me that if the observational data contradict your model, you should revise or abandon your model. What should AK do?

 

[Alan Kleinman]

What happened when you submitted your paper to Science, for example? Surely with a discovery of such an astounding scale you were accepted immediately. Why didn't you publish there?

Their peer reviewers had the paper for several months. They didn't say it was wrong, they said it needed to be submitted to a more specialized journal. So I submitted it to "Statistics in Medicine"" because of their expertise in the math and that they would realize the importance of explaining the evolution of drug resistance properly, something which macroevolutionist haven't done.

 

[Phred]

Then why ask Hans, "So how does his equation fit the data?"

And thank you very much, this math very nicely fits the data, it fits it so well that it predicted the behavior of the Kishony experiment before it was performed.

Because you're under the impression your limited equation explains what you're trying oh so desperately to say. It doesn't. But if you keep on blustering eventually we'll all give up and you can tell your cat you won.

I asked Hans because I actually respect his opinion. A model is something that helps explain a system. And it's been awhile since I've done any complex math. You have a limited equation that has a small number of variables and can't begin to model evolution, as you keep claiming. It models ONE gene. ONE mutation.

It's useless. So I wanted to know if I was missing something before I vomited all over it.

 

[Alan Kleinman]

Well, I'm confused - if AK's maths, when applied correctly to the genetics of human evolution, means we couldn't possibly have a common ancestor with chimps, why is there so much genetic evidence that we do?

For example, why do we share over 200 endogenous retrovirus insertions (ERV) for a certain retrovirus group at the exact same points in our genomes vs single figure counts for non-shared (unique) ERVs of that virus group?

If there are around 10 million possible insertion points, what are the odds of sharing over 200 identical insertions by chance?

Would that be greater or less than the odds AK is suggesting?

Someone told me that if the observational data contradict your model, you should revise or abandon your model. What should AK do?

You are good a seeing the similarities but unable to see the differences.

 

[Phred]

Their peer reviewers had the paper for several months. They didn't say it was wrong, they said it needed to be submitted to a more specialized journal. So I submitted it to "Statistics in Medicine"" because of their expertise in the math and that they would realize the importance of explaining the evolution of drug resistance properly, something which macroevolutionist haven't done.

You still can't define the difference between micro and macro but you love to use the terms...

 

[Alan Kleinman]

I asked Hans because I actually respect his opinion. A model is something that helps explain a system. And it's been awhile since I've done any complex math. You have a limited equation that has a small number of variables and can't begin to model evolution, as you keep claiming. It models ONE gene. ONE mutation.

That's the way microevolutionary adaptation works. For a single selection pressure process, it is one adaptive mutation at a time and the joint probability for more than a single adaptive mutation requires the multiplication rule. Study the Kishony experiment, you can watch the process actually happening.

 

[pitabread]

Well, I'm confused - if AK's maths, when applied correctly to the genetics of human evolution, means we couldn't possibly have a common ancestor with chimps, why is there so much genetic evidence that we do?

For example, why do we share over 200 endogenous retrovirus insertions (ERV) for a certain retrovirus group at the exact same points in our genomes, vs single figure counts for non-shared (unique) ERVs of that virus group?

If there are around 10 million possible insertion points, what are the odds of sharing over 200 identical insertions by chance?

Would that be greater or less than the odds AK is suggesting?

Someone told me that if the observational data contradict your model, you should revise or abandon your model. What should AK do?

Haven't you been following along? Math and physics refutes common ancestry because the joint probability of Kishony and Lenski doing an experiment involves the multiplication rule that refutes the idea that birds evolved from reptiles.

Something like that, anyway.

 

[Alan Kleinman]

You still can't define the difference between micro and macro but you love to use the terms...

I can do the mathematics for DNA microevolutionary adaptation and if the process requires more than a single adaptive mutation, you need to compute the joint probability using the multiplication rule.

 

[Alan Kleinman]

Haven't you been following along? Math and physics refutes common ancestry because the probability of Kishony and Lenski doing an experiment involving the multiplication rule that refutes the idea that birds evolved from reptiles.

Something like that, anyway.

All you need is a single selection pressure environment with a billion replications for each adaptation step and there you go, reptiles evolving into birds and fish evolving into mammals. So, what do you think the selection pressure is that would do this?

 

[pitabread]

All you need is a single selection pressure environment with a billion replications for each adaptation step and there you go, reptiles evolving into birds and fish evolving into mammals. So, what do you think the selection pressure is that would do this?

As I said earlier:

1) Either you are absolutely correct and you've just overturned the entire paradigm of common ancestry in modern biology. At which point your Nobel Prize awaits.

Or,

2) Your model is wrong.

I know where I am putting my money.

 

[Phred]

That's the way microevolutionary adaptation works. For a single selection pressure process, it is one adaptive mutation at a time and the joint probability for more than a single adaptive mutation requires the multiplication rule. Study the Kishony experiment, you can watch the process actually happening.

That's cute. That's a pointshift mutation that changes a single nucleotide. Now what about a mutation that requires a change in chromosome structure? Or a frameshift mutation that has a deletion of a nucleotide? Or maybe a deletion and an addition? Your simplistic high-school equation can't handle any of that.

Study freakin' BIOLOGY and forget the math. You're locked into something that doesn't represent reality.

 

[Alan Kleinman]

As I said earlier:

1) Either you are absolutely correct and you've just overturned the entire paradigm of common ancestry in modern biology. At which point your Nobel Prize awaits.

Or,

2) Your model is wrong.

I know where I am putting my money.

Big mistake for you to take up gambling, you should study and understand introductory probability theory first.

 

[Phred]

Big mistake for you to take up gambling, you should study and understand introductory probability theory first.

No, that's irrelevant.

 

[SelfSim]

@Alan Kleinman;
I haven't yet read the two papers you refer to, so please excuse me if this is already covered, but I have some issues/questions which aren't immediately obvious from your commentaries on the information models.

i) The first is that the information sequences passed onto offspring are not all conserved ..
How is this taken into account in the calculations of subsequent generation information 'measures'?

ii) My second comment is along similar lines, in that (from your descriptions), this model doesn't seem to take into account the principles of autocatalysis, in as far as there is other relevant information to consider with each successive generation. We aren't dealing with a closed system here, y'know(?)

 

[Alan Kleinman]

That's cute. That's a pointshift mutation that changes a single nucleotide. Now what about a mutation that requires a change in chromosome structure? Or a frameshift mutation that has a deletion of a nucleotide? Or maybe a deletion and an addition? Your simplistic high-school equation can't handle any of that.

Study freakin' BIOLOGY and forget the math. You're locked into something that doesn't represent reality.

I've only seen one real example of a frameshift mutation that didn't completely change the protein coded for. It was an HIV mutant that had a frameshift mutation near the end of the coding sequence and only changed a few amino acids. But if you think that frameshift mutations are the way reptiles evolve into birds and fish evolve into mammals, oh well.

 

[pitabread]

Big mistake for you to take up gambling, you should study and understand introductory probability theory first.

Given my current profession, I think I'm covered.

 

[Alan Kleinman]

No, that's irrelevant.

Las Vegas loves people like you.