Creationists: Explain your understanding of microevolution and macroevolution

[Hans Blaster]

What makes someone a biologist?

They studied the basics of biology and are engaged in a rigorous study of a biological system or organism.

Do they have to believe that reptiles evolve into birds and fish evolve into mammals?

Biology is a science, not a belief system. Do try to understand.

What makes a person an engineer is that they can explain the physics and mathematics of engineering systems. Biologists should be able to explain the physics and mathematics of biological systems.

I thought to be an Engineer you needed a certification from the state.

Take your time. The Lenski paper may be easier to understand if you study and understand Haldane's "Cost of Natural Selection" paper.

This "new" paper of yours isn't any more complicated that the previous.

 

[Yttrium]

This math isn't based on looking for a specific outcome. When a variant does 1/(mutation rate) replications, that on average will give some member of that population a mutation at every possible site in the genome. If the variant does about 4/(mutation rate) replications, every possible base substitution is randomly tried. There are no other possible outcomes that could occur (unless you want to consider frameshift mutations).

See, that's why I'd like you to start a new thread. You need to step back and explain what you mean by all this. No doubt it's scattered over a number of pages, but I don't know where to put it all together.

 

[Yttrium]

Don't be silly, you just want to change the subject because you can give us an experimental example of macroevolution.

It seems to me that for every creationist (with the exception of AV1611VET), the definition of macroevolution is the amount of evolution that can't be demonstrated under laboratory conditions. So yeah, we can't provide something that can't exist.

 

[tas8831]

The Lenski paper may be easier to understand if you study and understand Haldane's "Cost of Natural Selection" paper.

Here is Ewens, in an interview in 2004:

A second form of the load concept was introduced by the British biologist-mathematician Haldane who claimed, in 1957, that substitutions in a Darwinian evolutionary process could not proceed at more than a certain comparatively slow rate, because if they were to proceed at a faster rate, there would be an excessive “substitutional load.” Since Haldane was so famous, that concept attracted a lot of attention. In particular, Crow and Kimura made various substitutional load calculations around 1960, that is at about that time that I was becoming interested in genetics.
Perhaps the only disagreement I ever had with Crow concerned the substitutional load, because I never thought that the calculations concerning this load, which he and others carried out, were appropriate. From the very start, my own calculations suggested to me that Haldane’s arguments were misguided and indeed erroneous, and that there is no practical upper limit to the rate at which substitutions can occur under Darwinian natural selection.​

And further:

AP: Can I follow that up? Can you, in layman’s terms, explain why you think that there is no upper limit in the way that Haldane suggested?


WE: I can, but it becomes rather mathematical. Let me approach it this way. Suppose that you consider one gene locus only, at which a superior allele is replacing an inferior allele through natural selection. In broad terms, what this requires is that individuals carrying the superior allele have on average somewhat more offspring than the mean number of offspring per parent, otherwise the frequency of the superior allele would not increase. This introduces a concept of a “one-locus substitutional load,” and a formal numerical value for this load is fairly easily calculated. However, the crux of the problem arises when one considers the many, perhaps hundreds or even thousands, substitution processes that are being carried out at any one time. In his mathematical treatment of this “multi-locus” situation, Kimura, for example, in effect simply multiplied the loads at the various individual substituting loci to arrive at an overall total load. The load so calculated was enormous. This uses a reductionist approach to the load question, and to me, this reductionist approach is not the right way of doing things. Further, the multiplicative assumption is, to me, unjustified. It is the selectively favored individuals, carrying a variety of different genes at different loci, who are reproducing and being required to contribute more offspring than the average. If you consider load arguments from that individual-based, non-reductionist basis, the mathematical edifice which Kimura built up just evaporates, and in my view the very severe load calculations which he obtained by his approach became irrelevant and misleading. The individual-based calculations that I made indicated to me that there is no unbearable substitutional load.​

 

[tas8831]

I don't have a scientific explanation but I can give you a story that sounds much more logical

Actually, it seems you can NOT do this.

 

[tas8831]

I did that math in this paper:
Fixation and Adaptation in the Lenski E. coli Long Term Evolution Experiment

Let us know when it gets cited in an interesting paper. At 0 right now.

 

[Alan Kleinman]

They studied the basics of biology and are engaged in a rigorous study of a biological system or organism.

Been there, done that, somewhere in my collection of diplomas, I have a degree in biology. But in those studies, not one lecture on the physics and mathematics of microevolutionary adaptation, and they didn't explain that competition was a first law of thermodynamics process. That I figured out with my training in thermodynamics in engineering school. Note that Warden didn't understand this either, no biologist I know or have debated understand the relationship between the first law and competition. I take that back, Kimura had a slight idea about this and I did come across one paper that showed that Haldane's work is a conservation of energy process.

I thought to be an Engineer you needed a certification from the state.

I got that. I can tell you a cute story about that. When I was doing my post-graduate training in medicine in Detroit, I got a call from the Franchise Tax Board in California asking me why I hadn't paid my taxes in California. I told them that I was living in Michigan. The tax person says to me, "Our records show that you are licensed in California!" I said, no I'm not, I'm licensed in Michigan. The tax person says, "I have the records right in front of me and it says you are licensed in California". Then it came to me, they were talking about my engineering license, not my medical license. So I said, Oh, you are talking about my engineering license, I was talking about my medical license. And the tax person says, "You are licensed in both engineering and medicine?" I said, yeah, I'm educated, not smart. The tax person laughed and left me alone, no California taxes that year.

This "new" paper of yours isn't any more complicated that the previous.

That's the thing I've found out about engineering problems, once you understand the solution, the complexity seems to disappear. It takes me a lot of studies to see solutions but interestingly, I only finally saw these solutions in a dream. Same thing with my PhD dissertation, I saw that solution in a dream. Imagine that!

 

[Alan Kleinman]

Let us know when it gets cited in an interesting paper. At 0 right now.

Maybe one day Lenski will be interested in knowing how his own experiment works and why competition slows adaptation in his experiment.

 

[FrumiousBandersnatch]

There's lots of literature on the subject, here's an example:
Secondary bacterial infections in influenza virus infection pathogenesis - PubMed
It is not unusual for those that die with influenza don't die from the virus but from secondary bacterial pneumonia and sepsis.

I would expect a competent GP to be able to assess the probability that he was diagnosing influenza with a secondary bacterial infection or a high probability of one (knowing the patient helps). Flu isn't the only viral infection for which doctors have been pestered by patients for antibiotics, and until the recommendation of (and reasons for) minimising unnecessary use were clear, many would pander to their patient's wishes.

However, I am not a GP or one of the people you need to persuade, and this forum has little weight in the biological and medical communities

 

[Alan Kleinman]

Here is Ewens, in an interview in 2004:

A second form of the load concept was introduced by the British biologist-mathematician Haldane who claimed, in 1957, that substitutions in a Darwinian evolutionary process could not proceed at more than a certain comparatively slow rate, because if they were to proceed at a faster rate, there would be an excessive “substitutional load.” Since Haldane was so famous, that concept attracted a lot of attention. In particular, Crow and Kimura made various substitutional load calculations around 1960, that is at about that time that I was becoming interested in genetics.
Perhaps the only disagreement I ever had with Crow concerned the substitutional load, because I never thought that the calculations concerning this load, which he and others carried out, were appropriate. From the very start, my own calculations suggested to me that Haldane’s arguments were misguided and indeed erroneous, and that there is no practical upper limit to the rate at which substitutions can occur under Darwinian natural selection.​

And further:

AP: Can I follow that up? Can you, in layman’s terms, explain why you think that there is no upper limit in the way that Haldane suggested?


WE: I can, but it becomes rather mathematical. Let me approach it this way. Suppose that you consider one gene locus only, at which a superior allele is replacing an inferior allele through natural selection. In broad terms, what this requires is that individuals carrying the superior allele have on average somewhat more offspring than the mean number of offspring per parent, otherwise the frequency of the superior allele would not increase. This introduces a concept of a “one-locus substitutional load,” and a formal numerical value for this load is fairly easily calculated. However, the crux of the problem arises when one considers the many, perhaps hundreds or even thousands, substitution processes that are being carried out at any one time. In his mathematical treatment of this “multi-locus” situation, Kimura, for example, in effect simply multiplied the loads at the various individual substituting loci to arrive at an overall total load. The load so calculated was enormous. This uses a reductionist approach to the load question, and to me, this reductionist approach is not the right way of doing things. Further, the multiplicative assumption is, to me, unjustified. It is the selectively favored individuals, carrying a variety of different genes at different loci, who are reproducing and being required to contribute more offspring than the average. If you consider load arguments from that individual-based, non-reductionist basis, the mathematical edifice which Kimura built up just evaporates, and in my view the very severe load calculations which he obtained by his approach became irrelevant and misleading. The individual-based calculations that I made indicated to me that there is no unbearable substitutional load.​

Haldane's estimates for the number of generations needed for fixation underestimate those measured in the Lenski experiment. But you biologists still don't get it that fixation is not required for adaptation to occur if there is sufficient carrying capacity in the environment. Competition slows adaptation!

 

[Alan Kleinman]

I would expect a competent GP to be able to assess the probability that he was diagnosing influenza with a secondary bacterial infection or a high probability of one (knowing the patient helps). Flu isn't the only viral infection for which doctors have been pestered by patients for antibiotics, and until the recommendation of (and reasons for) minimising unnecessary use were clear, many would pander to their patient's wishes.

However, I am not a GP or one of the people you need to persuade, and this forum has little weight in the biological and medical communities

Influenza isn't the only viral infection that is subject to co-infection. It wouldn't surprise me at all that Covid be found to have a high incidence of coinfection causing death. That may be the reason why people were seeing good responses when treating Covid with azithromycin.

And in my 30+ years of practicing primary care medicine, it was rare in my 150,000 or so patient visits that I had patients pester me for antibiotics. Most people don't like going to the doctor, it cost money, it usually requires long waits sitting in a waiting room filled with other sick people, and sometimes you need to get a shot or some other uncomfortable treatment. You should check out where drug-resistance is a bigger problem, that's in the hospital. Maybe the ER docs and hospitalists need to reduce their usage of antibiotics. Or maybe the problem is that they are dealing with sicker people with compromised immune systems.

My view in dealing with the problem is giving the correct explanation of the evolution of drug resistance and developing solutions based on that understanding. But trying to give that explanation to people trained by biologists telling them that evolution causes reptiles to transform into birds and fish to transform into mammals isn't an easy task.

 

[Yttrium]

.

Awright, correct me if I'm wrong, but you seem to be assuming a macroevolution happening after one continuous selection event over many generations. Personally, I have a hard time imagining this happening myself. But that's not the kind of thing we're going to see in nature, as far as macroevolution is concerned. We're going to see a variety of selection events, favoring entirely different advantages. We could have predators moving in. Changes in temperature. Changes in food supply. Etc. In this case, the advantages are not necessarily cumulative. What may be an advantage for a while may become unimportant later on, as new and different advantages are selected. With each different selection event, changes occur.

 

[Hans Blaster]

Haldane's estimates for the number of generations needed for fixation underestimate those measured in the Lenski experiment. But you biologists still don't get it that fixation is not required for adaptation to occur if there is sufficient carrying capacity in the environment. Competition slows adaptation!

What makes you think you are talking to biologists? Most of us are no more biologists than you are. (That is -- not at all.) I think tas8831 is a biologist of some sort. Perhaps someone else is as well.

The only thing you can easily identify about us is our religious affiliation (and in some cases political party). Biologist is not something that falls under either of those labels.

 

[Alan Kleinman]

Awright, correct me if I'm wrong, but you seem to be assuming a macroevolution happening after one continuous selection event over many generations. Personally, I have a hard time imagining this happening myself. But that's not the kind of thing we're going to see in nature, as far as macroevolution is concerned. We're going to see a variety of selection events, favoring entirely different advantages. We could have predators moving in. Changes in temperature. Changes in food supply. Etc. In this case, the advantages are not necessarily cumulative. What may be an advantage for a while may become unimportant later on, as new and different advantages are selected. With each different selection event, changes occur.

That's not it at all. It's all about computing the joint probability of one or more adaptive mutations accumulating in a lineage. If you have minimal skills in probability theory, this paper explains how you do that calculation:
The basic science and mathematics of random mutation and natural selection

This paper gives the fundamental mathematics of the evolution of a lineage of replicators to a single selection pressure. Read it and see if it makes sense to you.

 

[FrumiousBandersnatch]

My view in dealing with the problem is giving the correct explanation of the evolution of drug resistance and developing solutions based on that understanding. But trying to give that explanation to people trained by biologists telling them that evolution causes reptiles to transform into birds and fish to transform into mammals isn't an easy task.

Why not try the commercial sector ('Big Pharma') where the dogmatic ideology of macroevolution will take a distant second place to the prospect of financial advantage ('Greed')?

 

[Alan Kleinman]

What makes you think you are talking to biologists? Most of us are no more biologists than you are. (That is -- not at all.) I think tas8831 is a biologist of some sort. Perhaps someone else is as well.

You have already said that you are not a biologist but does that mean you can't understand anything about biology? Actually, I think the fundamental principles of biological evolution are pretty simple, it's the biochemistry of a cell that is difficult. It's pretty incredible that a strand of DNA constructs and controls all of that.

The only thing you can easily identify about us is our religious affiliation (and in some cases political party). Biologist is not something that falls under either of those labels.

Actually, I don't assume anything about the academic training of anyone I debate with. I just find it curious that anyone that is not a biologist would complain when I say that biologists are not doing the physics and mathematics of biological evolution correctly.

 

[FrumiousBandersnatch]

What makes you think you are talking to biologists? Most of us are no more biologists than you are. (That is -- not at all.) I think tas8831 is a biologist of some sort. Perhaps someone else is as well.

The only thing you can easily identify about us is our religious affiliation (and in some cases political party). Biologist is not something that falls under either of those labels.

I'm a biologist, by qualification & early career

But you don't need to be a biologist to see that Kleinman's claims about macroevolution are not consistent with the evidence.

 

[Frank Robert]

I'm not the one that thinks that bacteria can evolve into humans.

It's a bit more complicated.
Meet Luca, the Ancestor of All Living Things

 

[Alan Kleinman]

Why not try the commercial sector ('Big Pharma') where the dogmatic ideology of macroevolution will take a distant second place to the prospect of financial advantage ('Greed')?

Explain to me why Big Pharma would want their drug treatments to be more durable? They make their money when their drugs are under patent. If you can treat infections with combinations of generic antibiotics that only cost 5 bucks, why would you spend hundreds for drugs that are under patent protection?

 

[Alan Kleinman]

I'm a biologist, by qualification & early career

But you don't need to be a biologist to see that Kleinman's claims about macroevolution are not consistent with the evidence.

Is any of that evidence experimental, and I mean repeatable, not this silly idea that an observation is an experiment. If so, now is the time to post that experimental evidence. And while you are at it, why don't you give the correct mathematical explanation of microevolutionary adaptation. Start with the mathematical explanation of how drug resistance evolves in the Kishony experiment.