Atheist question

[DBowling]

Here is an interesting one, not from Meyer:

https://www.claremont.org/crb/article/giving-up-darwin/

As I wrote in #202:
"Another source of information is a current article: https://quillette.com/2019/09/09/david- ... ng-darwin/ by Jerry A. Coyne where he discusses https://www.claremont.org/crb/article/giving-up-darwin/ by David Gelernter.

I read Coyne's article...
It makes a lot of fallacious fact free assertions about ID (maybe that's why you like it)

But I didn't see anything in your link that rebutted the following from Gerlenter's article.

What proportion of these many polypeptides are useful proteins? Douglas Axe did a series of experiments to estimate how many 150-long chains are capable of stable folds—of reaching the final step in the protein-creation process (the folding) and of holding their shapes long enough to be useful. (Axe is a distinguished biologist with five-star breeding: he was a graduate student at Caltech, then joined the Centre for Protein Engineering at Cambridge. The biologists whose work Meyer discusses are mainly first-rate Establishment scientists.) He estimated that, of all 150-link amino acid sequences, 1 in 10^74 will be capable of folding into a stable protein. To say that your chances are 1 in 10^74 is no different, in practice, from saying that they are zero. It’s not surprising that your chances of hitting a stable protein that performs some useful function, and might therefore play a part in evolution, are even smaller. Axe puts them at 1 in 10^77.

If you want to demonstrate that Meyer is wrong then you need to find evidence to demonstrate that Douglas Axe's experiments mentioned in Gerlenter's article above are factually incorrect.

Here is a short video where Doug Axe gives a very high level overview of his methodology and results.
https://www.youtube.com/watch?v=qwFi_2YZa_c

Meyer explains it here (less than 8 minutes)
https://www.youtube.com/watch?v=JQ3hUlU0vR4

you don’t have to go to any library to read it.

The library is your friend...
You might want to try it sometime.

[Nils]

I have seen nothing to indicate that Meyer's statement is factually incorrect.

The statement is correct but explain to me how it is possible to come from the statement to the conclusion. How does he reason?

Meyer's reasoning from the quote above is factually accurate...
If the probability of finding a new protein is 1 in 10^70 then he is correct that the age of the earth isn't long enough to generate a new protein.

If you wish to prove Meyer is wrong you only need to demonstrate that the possibility of finding a new protein is significantly less than 1 in 10^70.
That would support your assertion.
Again... data free assertions do nothing to help out your argument.

OK, I have to repeat. Meyer’s reasoning is correct if we talk about creating a new protein from scratch. If that was a correct description of how evolution is assumed to function his conclusion would be correct, Darwinian evolution would not be possible. Now, evolution theory assumes that new proteins are created by small changes in old proteins or, long ago, in simpler structures. This makes the probability of finding a new protein considerable bigger than 1 in 10^70. That also makes Meyer’s conclusion erroneous and he certainly knows that. Why he still argues as he does I don’t know but it is remarkable.

I stop here today.

Nils

But Nils, that's not what the last article says (new proteins from scratch). It says the creation of useful proteins. Here's the quote again:

What proportion of these many polypeptides are useful proteins? Douglas Axe did a series of experiments to estimate how many 150-long chains are capable of stable folds—of reaching the final step in the protein-creation process (the folding) and of holding their shapes long enough to be useful. (Axe is a distinguished biologist with five-star breeding: he was a graduate student at Caltech, then joined the Centre for Protein Engineering at Cambridge. The biologists whose work Meyer discusses are mainly first-rate Establishment scientists.) He estimated that, of all 150-link amino acid sequences, 1 in 10^74 will be capable of folding into a stable protein. To say that your chances are 1 in 10^74 is no different, in practice, from saying that they are zero. It’s not surprising that your chances of hitting a stable protein that performs some useful function, and might therefore play a part in evolution, are even smaller. Axe puts them at 1 in 10^77.

Note the italicized, bolded, and underlined. The idea here is not that proteins are being created from scratch but that errors (mutations) are largely useless and the probability of a mutation turning the protein into a different but useful protein is 10^74.

I must say I have no ax to grind on either side of the debate (to some extent, obviously). But I just wanted to clarify this point.

carry on.

Yes, Byblos, I know. The problem with Meyer, Axe and Gelernter is that evolution doesn’t work as they assume. Certainly if there were no way to bridge the gap between two stable proteins evolution would be impossible and the evolution theory would be dead. But evolution doesn’t work that way. Here is a quote from Coyne’s article that comments Gelernter ( References: https://quillette.com/2019/09/09/david- ... ng-darwin/ by Jerry A. Coyne and https://www.claremont.org/crb/article/giving-up-darwin/ by David Gelernter).

“Gelernter then tells us not only that macroevolution wasn’t seen to happen, but is also theoretically impossible. These claims have also been discredited.
First, he argues that the chance that useful proteins could evolve is close to zero, asserting that “random mutation plus natural selection” are insufficient to create new protein shapes. That’s equivalent to the claim that these processes aren’t sufficient to explain new protein sequences.
The fallacy here is obvious. Gelernter assumes there is a useful, pre-specified target protein that must be reached from a “nonsense” sequence of amino acids. Then he multiplies together the small probabilities needed to convert each amino acid in the starting “gibberish protein” into the ones in the final target. The resulting probability is so minuscule that, he concludes, the Darwinian evolution of useful proteins is impossible.
This argument rests on several big errors. First, evolution doesn’t start with “gibberish proteins”; it continues with what it had before: useful proteins that evolved via natural selection from earlier sequences, but can still improve further. Second, evolution doesn’t drive proteins toward pre-specified target sequences. All that’s required for evolution to work is a mutation changing a gene (and its protein product) in such a way that the new gene leaves more copies than its antecedent. It’s an incremental form of improvement, not a narrowing-in on a specified target.
In fact, we have plenty of examples, in our species and others, in which a small change in an existing protein leads to a better protein. This has occurred, for instance, in proteins adapting human cultures to diving in water, enzymes for making fatty acids in populations that are largely vegetarian, in genes controlling armor plating that reduces predation on marine stickleback fish, and in proteins conferring an attraction to human odor in mosquitoes that invaded urban areas.
There are many similar examples, all showing that a small change in an already useful protein sequence can make it extra useful in new environments. This is the way evolution has worked from the very first Ur-protein.”
Nils

[Philip]

There are serious limits to mutations!

A molecular biologist talks mutations and microevolution: https://www.reasons.org/explore/blogs/t ... they-favor

"The fact that rapid selection of mutations provides fitness advantages is an uncontested idea at the level of single-cell microorganisms."

"But the scientific mechanisms of such inheritance and spread within multicellular organisms and populations are much more complex and less frequent than for single-cell organisms."

"Significantly, however, somatic mutations in sexual, diploid organisms are not passed on to offspring. In order for a mutation to be inherited, the mutation must occur in a gamete, the haploid cell of a sperm or egg.1 If the mutation occurs within a gamete (sperm or egg), upon fusion with the corresponding unmutated gamete (egg or sperm, respectively) the resulting diploid progeny becomes heterozygous (occurring in one chromosome) for the mutation. If a mutation is heterozygous but not dominant in its phenotype, it must occur independently and concurrently in both individual gametes of the reproductive pair in order to have a phenotypic effect in offspring and for subsequent positive selection to occur within a population. In fact, it would almost certainly need to have spontaneously occurred in multiple germ-line cells of each individual to result in a likely fertilization of a mutated sperm with a mutated egg. Therefore, in multicellular organisms, in order for a single change to be passed to progeny, such fitness mutations must be heterozygous dominant or they must occur independently and concurrently in multiple cells in each member of a reproductive pair."

[DBowling]

The statement is correct but explain to me how it is possible to come from the statement to the conclusion. How does he reason?

Meyer's reasoning from the quote above is factually accurate...
If the probability of finding a new protein is 1 in 10^70 then he is correct that the age of the earth isn't long enough to generate a new protein.

If you wish to prove Meyer is wrong you only need to demonstrate that the possibility of finding a new protein is significantly less than 1 in 10^70.
That would support your assertion.
Again... data free assertions do nothing to help out your argument.

OK, I have to repeat. Meyer’s reasoning is correct if we talk about creating a new protein from scratch. If that was a correct description of how evolution is assumed to function his conclusion would be correct, Darwinian evolution would not be possible. Now, evolution theory assumes that new proteins are created by small changes in old proteins or, long ago, in simpler structures. This makes the probability of finding a new protein considerable bigger than 1 in 10^70. That also makes Meyer’s conclusion erroneous and he certainly knows that. Why he still argues as he does I don’t know but it is remarkable.

I stop here today.

Nils

But Nils, that's not what the last article says (new proteins from scratch). It says the creation of useful proteins. Here's the quote again:

What proportion of these many polypeptides are useful proteins? Douglas Axe did a series of experiments to estimate how many 150-long chains are capable of stable folds—of reaching the final step in the protein-creation process (the folding) and of holding their shapes long enough to be useful. (Axe is a distinguished biologist with five-star breeding: he was a graduate student at Caltech, then joined the Centre for Protein Engineering at Cambridge. The biologists whose work Meyer discusses are mainly first-rate Establishment scientists.) He estimated that, of all 150-link amino acid sequences, 1 in 10^74 will be capable of folding into a stable protein. To say that your chances are 1 in 10^74 is no different, in practice, from saying that they are zero. It’s not surprising that your chances of hitting a stable protein that performs some useful function, and might therefore play a part in evolution, are even smaller. Axe puts them at 1 in 10^77.

Note the italicized, bolded, and underlined. The idea here is not that proteins are being created from scratch but that errors (mutations) are largely useless and the probability of a mutation turning the protein into a different but useful protein is 10^74.

I must say I have no ax to grind on either side of the debate (to some extent, obviously). But I just wanted to clarify this point.

carry on.

Yes, Byblos, I know. The problem with Meyer, Axe and Gelernter is that evolution doesn’t work as they assume. Certainly if there were no way to bridge the gap between two stable proteins evolution would be impossible and the evolution theory would be dead. But evolution doesn’t work that way. Here is a quote from Coyne’s article that comments Gelernter ( References: https://quillette.com/2019/09/09/david- ... ng-darwin/ by Jerry A. Coyne and https://www.claremont.org/crb/article/giving-up-darwin/ by David Gelernter).

“Gelernter then tells us not only that macroevolution wasn’t seen to happen, but is also theoretically impossible. These claims have also been discredited.
First, he argues that the chance that useful proteins could evolve is close to zero, asserting that “random mutation plus natural selection” are insufficient to create new protein shapes. That’s equivalent to the claim that these processes aren’t sufficient to explain new protein sequences.
The fallacy here is obvious. Gelernter assumes there is a useful, pre-specified target protein that must be reached from a “nonsense” sequence of amino acids. Then he multiplies together the small probabilities needed to convert each amino acid in the starting “gibberish protein” into the ones in the final target. The resulting probability is so minuscule that, he concludes, the Darwinian evolution of useful proteins is impossible.

You are again factually inaccurate...
The probabilities in Gelernter's article are based on actual experiments by Douglas Axe who manipulates proteins in an effort to get them to evolve from one functional state to another.

Here are a couple of short videos on Doug Axe's experiments on proteins
https://www.youtube.com/watch?v=mKUMH1vEkmU
https://youtu.be/8ZiLsXO-dYo
https://youtu.be/jJy2oRxPrlg?list=PLR8e ... oU5v2poZKf

[Nils]

There are serious limits to mutations!

A molecular biologist talks mutations and microevolution: https://www.reasons.org/explore/blogs/t ... they-favor

"The fact that rapid selection of mutations provides fitness advantages is an uncontested idea at the level of single-cell microorganisms."

"But the scientific mechanisms of such inheritance and spread within multicellular organisms and populations are much more complex and less frequent than for single-cell organisms."

"Significantly, however, somatic mutations in sexual, diploid organisms are not passed on to offspring. In order for a mutation to be inherited, the mutation must occur in a gamete, the haploid cell of a sperm or egg.1 If the mutation occurs within a gamete (sperm or egg), upon fusion with the corresponding unmutated gamete (egg or sperm, respectively) the resulting diploid progeny becomes heterozygous (occurring in one chromosome) for the mutation. If a mutation is heterozygous but not dominant in its phenotype, it must occur independently and concurrently in both individual gametes of the reproductive pair in order to have a phenotypic effect in offspring and for subsequent positive selection to occur within a population. In fact, it would almost certainly need to have spontaneously occurred in multiple germ-line cells of each individual to result in a likely fertilization of a mutated sperm with a mutated egg. Therefore, in multicellular organisms, in order for a single change to be passed to progeny, such fitness mutations must be heterozygous dominant or they must occur independently and concurrently in multiple cells in each member of a reproductive pair."

Sorry Philips, I’m not able to dig into this also.
Nils

[PaulSacramento]

Of cource he can't, natural science isn't about proof, it is about evidence. Nobody can prove that there is gravity everywhere on the earth but still everyone assumes that the gravitation theory is correct. The evidence is total. The same with evolution.

Wow.
So Gravity is a LAW.
We can replicate, in real time, gravity, we even have a formula for gravity:
There is a gravitational constant even.

Don't compare the too, that is a bad move.

It is true that Gravity is regarded as a law. But still, it is not possible to prove it. If you experiment on it you just add evidence but still you don’t prove it. Natural scientist don’t talk about proofs, they talk about evidence.
Nils

Evidence leads to proof, and we have empirical proof of gravity, do you deny that?

[Nils]

Re #211

Here is an interesting one, not from Meyer:
https://www.claremont.org/crb/article/giving-up-darwin/

As I wrote in #202:
"Another source of information is a current article: https://quillette.com/2019/09/09/david- ... ng-darwin/ by Jerry A. Coyne where he discusses https://www.claremont.org/crb/article/giving-up-darwin/ by David Gelernter.

I read Coyne's article...
It makes a lot of fallacious fact free assertions about ID (maybe that's why you like it)

I would prefer not to widen the discussion now.

But I didn't see anything in your link that rebutted the following from Gerlenter's article.

What proportion of these many polypeptides are useful proteins? Douglas Axe did a series of experiments to estimate how many 150-long chains are capable of stable folds—of reaching the final step in the protein-creation process (the folding) and of holding their shapes long enough to be useful. (Axe is a distinguished biologist with five-star breeding: he was a graduate student at Caltech, then joined the Centre for Protein Engineering at Cambridge. The biologists whose work Meyer discusses are mainly first-rate Establishment scientists.) He estimated that, of all 150-link amino acid sequences, 1 in 10^74 will be capable of folding into a stable protein. To say that your chances are 1 in 10^74 is no different, in practice, from saying that they are zero. It’s not surprising that your chances of hitting a stable protein that performs some useful function, and might therefore play a part in evolution, are even smaller. Axe puts them at 1 in 10^77.

See the citation that I included in post #212

If you want to demonstrate that Meyer is wrong then you need to find evidence to demonstrate that Douglas Axe's experiments mentioned in Gerlenter's article above are factually incorrect.

Here is a short video where Doug Axe gives a very high level overview of his methodology and results.
https://www.youtube.com/watch?v=qwFi_2YZa_c

Meyer explains it here (less than 8 minutes)
https://www.youtube.com/watch?v=JQ3hUlU0vR4

you don’t have to go to any library to read it.

The library is your friend...
You might want to try it sometime.

I understand what they say, that several mutations are needed to come from one beneficial (functional) state to another. When Axe talks I get the feeling that he thinks of a long wandering in the desert until one finally comes to the goal. This is not the evolution theory. Generally it is assumed that every mutation is beneficial.
Talking about libraries Meyer’s works are not available in any university or city library in Sweden. Now I prefer reading the original article and I’ve found Axe’s article from 2004 on Google Scholar and I will read and perhaps understand some things. Interesting is the links to articles that refer to Axe’s article. For instance Romero et al, https://www.pnas.org/content/pnas/early ... 0.full.pdf
“Second, within this vast space, functional proteins are extremelyscarce, with estimates that range from a high of 1 in 10^11to as little as 1 in 10^77 (4, 5)” where (5) refers to Axe’s article.
---------------- ---------------------------------------------------------

Re #210

OK, I have to repeat. Meyer’s reasoning is correct if we talk about creating a new protein from scratch.

And I have to repeat, you don't know what you are talking about (as Byblos points out in his post) ... again.

Your argumentation in this thread has two significant problems.
1. You simply do not understand Meyer's position (or possibly are deliberately misrepresenting it)
2. You choose not to do the research necessary to understand Meyer's position even when you are given specific references.

If you don't want to go through the effort to actually understand Meyer's position then don't pretend that you have the knowledge to rebut a position that you don't even understand.

See my comment to #211 above

So to support your assertion with data, you need to demonstrate that Doug Axe's research on folding proteins is incorrect and the probability of finding a new protein is significantly less than 1 in 10^70.

See the citation from Romero et el. above.
----- ---------------------------------------------------------

Re #214

…….
The problem with Meyer, Axe and Gelernter is that evolution doesn’t work as they assume. Certainly if there were no way to bridge the gap between two stable proteins evolution would be impossible and the evolution theory would be dead. But evolution doesn’t work that way. Here is a quote from Coyne’s article that comments Gelernter ( References: https://quillette.com/2019/09/09/david- ... ng-darwin/ by Jerry A. Coyne and https://www.claremont.org/crb/article/giving-up-darwin/ by David Gelernter).

“Gelernter then tells us not only that macroevolution wasn’t seen to happen, but is also theoretically impossible. These claims have also been discredited.
First, he argues that the chance that useful proteins could evolve is close to zero, asserting that “random mutation plus natural selection” are insufficient to create new protein shapes. That’s equivalent to the claim that these processes aren’t sufficient to explain new protein sequences.
The fallacy here is obvious. Gelernter assumes there is a useful, pre-specified target protein that must be reached from a “nonsense” sequence of amino acids. Then he multiplies together the small probabilities needed to convert each amino acid in the starting “gibberish protein” into the ones in the final target. The resulting probability is so minuscule that, he concludes, the Darwinian evolution of useful proteins is impossible.

You are again factually inaccurate...

This wasn’t my words, it was a quote from Coyne.

The probabilities in Gelernter's article are based on actual experiments by Douglas Axe who manipulates proteins in an effort to get them to evolve from one functional state to another.

Here are a couple of short videos on Doug Axe's experiments on proteins
https://www.youtube.com/watch?v=mKUMH1vEkmU
https://youtu.be/8ZiLsXO-dYo
https://youtu.be/jJy2oRxPrlg?list=PLR8e ... oU5v2poZKf

These clips and the earlier you quoted repeat the same thing over and over. Nothing new. He think he has shown that there is no way to form new or adjust old proteins in the way that is normally assumed in the evolution theory, that is by many single mutations that each make a change that is beneficial.
I haven’t read Axe’s article in detail yet but he admits in the clips above that the result of his results he found are valid “at least in the cases we examined”. And as far as I read the article there are lot of assumption in the text and it based only on a few experiments.
Even if Axe’s figure were correct it doesn’t mean that he has proved anything. He also has to prove that his method suggested for evolution is the only possible one. As Coyne's article shows there are other strategies for evolution, and he is not alone. One interesting question is that if Axe was right about his (and Meyer’s) conclusion 2004 when he wrote his article why have no others tried to verify his experiment. If he believed in his own article why didn’t he follow up his research publishing new articles? I can’t find any. It’s now fifteen years since he wrote his article. If his result and conclusion had been worth considering it had been a tremendous challenge to the evolution theory. But it is not even mentioned for instance in Wikipedia and neither have I read about it in books about the evolution theory.

Generally, one can discuss the seriousness of Meyer. The evolution theory is not controversial among biologist, there are lot of discussions ongoing about details in the theory but the main principles are not discussed (see below). Then, it seems dangerous to dismiss it based on a single 15 years old article. That is not serious. It can be said that there are reasons to dismiss evolution but in the first clip by Meyer (https://www.youtube.com/watch?v=7c9PaZzsqEg ) he states that the conclusion of the article is that evolution is false.

A citations from https://en.wikipedia.org/wiki/Talk:Evolution: “The fact that evolution occurs and the ability of modern evolutionary theory to explain why it occurs are not controversial amongst biologists. Indeed, numerous respectable scientific societies, such as the American Association for the Advancement of Science and the National Academy of Sciences, have issued statements supporting evolution and denouncing creationism and/or ID.[1] In 1987 only about 0.15% of American Earth and life scientists supported creationism.[2] “

This is not an argument from authority. It’s just an argument that you need more than a single article to dismiss an established theory.
Nils

[DBowling]

But I didn't see anything in your link that rebutted the following from Gerlenter's article.

What proportion of these many polypeptides are useful proteins? Douglas Axe did a series of experiments to estimate how many 150-long chains are capable of stable folds—of reaching the final step in the protein-creation process (the folding) and of holding their shapes long enough to be useful. (Axe is a distinguished biologist with five-star breeding: he was a graduate student at Caltech, then joined the Centre for Protein Engineering at Cambridge. The biologists whose work Meyer discusses are mainly first-rate Establishment scientists.) He estimated that, of all 150-link amino acid sequences, 1 in 10^74 will be capable of folding into a stable protein. To say that your chances are 1 in 10^74 is no different, in practice, from saying that they are zero. It’s not surprising that your chances of hitting a stable protein that performs some useful function, and might therefore play a part in evolution, are even smaller. Axe puts them at 1 in 10^77.

See the citation that I included in post #212

I looked again and I still don't see anything that rebuts the analysis in the quote above
It would be helpful if you could hilight the specific quote that you had in mind.

If you want to demonstrate that Meyer is wrong then you need to find evidence to demonstrate that Douglas Axe's experiments mentioned in Gerlenter's article above are factually incorrect.

Here is a short video where Doug Axe gives a very high level overview of his methodology and results.
https://www.youtube.com/watch?v=qwFi_2YZa_c

Meyer explains it here (less than 8 minutes)
https://www.youtube.com/watch?v=JQ3hUlU0vR4

I understand what they say, that several mutations are needed to come from one beneficial (functional) state to another. When Axe talks I get the feeling that he thinks of a long wandering in the desert until one finally comes to the goal. This is not the evolution theory. Generally it is assumed that every mutation is beneficial.

I think you are wrong on that assumption...
We know from experience that most mutations are harmful to organisms, That is why evolution assumes long periods of time between each beneficial or functional mutation.

This is exactly what Matheson was acknowledging when he said the following in his discussion with Meyer
"It is surely an open question about whether that whole tree can be navigated through function all the way through.
I certainly can't prove it's the case."

So to support your assertion with data, you need to demonstrate that Doug Axe's research on folding proteins is incorrect and the probability of finding a new protein is significantly less than 1 in 10^70.

See the citation from Romero et el. above.

I looked through Romero's article and I was unable to find a discussion of the probability of moving from one functional protein to another functional protein which was the subject of Axe's experiments.

Could you please provide the quote you had in mind that rebuts Axe's results?

The probabilities in Gelernter's article are based on actual experiments by Douglas Axe who manipulates proteins in an effort to get them to evolve from one functional state to another.

Here are a couple of short videos on Doug Axe's experiments on proteins
https://www.youtube.com/watch?v=mKUMH1vEkmU
https://youtu.be/8ZiLsXO-dYo
https://youtu.be/jJy2oRxPrlg?list=PLR8e ... oU5v2poZKf

These clips and the earlier you quoted repeat the same thing over and over. Nothing new. He think he has shown that there is no way to form new or adjust old proteins in the way that is normally assumed in the evolution theory, that is by many single mutations that each make a change that is beneficial.

And Axe has experimental empirical evidence to support his conclusion.
While the 'assumptions' about proteins ability to evolve from one functional state to another are just that... assumptions... with no empirical evidence to support those assumptions.

Generally, one can discuss the seriousness of Meyer. The evolution theory is not controversial among biologist, there are lot of discussions ongoing about details in the theory but the main principles are not discussed (see below). Then, it seems dangerous to dismiss it based on a single 15 years old article. That is not serious. It can be said that there are reasons to dismiss evolution but in the first clip by Meyer (https://www.youtube.com/watch?v=7c9PaZzsqEg ) he states that the conclusion of the article is that evolution is false.

And based on empirical evidence, Meyer is correct.
But I think it would be helpful to understand what Meyer means when he says evolution is false.

At a high level, there are three components of Darwinian Evolutionary Theory.
1. Common Descent
2. Random Mutation
3. Natural Selection

Intelligent Design does not question some sort of shared ancestry (Common Descent), Natural Selection, or even the process of Mutation.
Intelligent Design uses empirical evidence to show that random mutation is incapable of generating the information that we see in the fossil record and in the DNA of life today.

ID even acknowledges that random mutations do occur and Behe has done a lot of work in understanding the upper limits of what the Darwinian process of random mutation is capable of in the lab and in nature. Thus the difference between micro-evolution, an established scientific fact which functions within the observed capability of random mutation, and macro-evolution which exceeds the observed capability of random mutation.

This is not an argument from authority. It’s just an argument that you need more than a single article to dismiss an established theory.

You need empirical evidence to support or dismiss any theory.
And Meyer is basing his position on empirical evidence from numerous sources regarding the capabilities of 'random' mutation and the known causes of information.

[DBowling]

DB: One example of empirical evidence involves comparing the ability of malaria to develop resistance to atovaquone (which requires one amino acid change) and chloroquine (which requires 2 coordinated amino acid changes).
The observed rate of malaria to adapt to atovaquone (which requires 2 coordinated amino acid changes) is 1 in 10^20 cells.

Nils: It seems that you cite some scientific article. Do you have the reference?

DB: Meyer discusses that (with references) in...
Darwin's Doubt.
Chapter 12 Complex Adaptations and the Neo-Darwinian Math

Nils: I would prefer to have a reference from some independent source.

DB: lets try another source.
The Edge of Evolution Chapter 3
The Mathematical Limits of Darwinism

Since you don't have access to The Edge of Evolution in a library, here's a lecture by Behe that I found online where he discusses this topic in detail.
https://www.youtube.com/watch?v=Y6j8Yp6s6E8

[Nils]

But I didn't see anything in your link that rebutted the following from Gerlenter's article.

What proportion of these many polypeptides are useful proteins? Douglas Axe did a series of experiments to estimate how many 150-long chains are capable of stable folds—of reaching the final step in the protein-creation process (the folding) and of holding their shapes long enough to be useful. (Axe is a distinguished biologist with five-star breeding: he was a graduate student at Caltech, then joined the Centre for Protein Engineering at Cambridge. The biologists whose work Meyer discusses are mainly first-rate Establishment scientists.) He estimated that, of all 150-link amino acid sequences, 1 in 10^74 will be capable of folding into a stable protein. To say that your chances are 1 in 10^74 is no different, in practice, from saying that they are zero. It’s not surprising that your chances of hitting a stable protein that performs some useful function, and might therefore play a part in evolution, are even smaller. Axe puts them at 1 in 10^77.

See the citation that I included in post #212

I looked again and I still don't see anything that rebuts the analysis in the quote above
It would be helpful if you could hilight the specific quote that you had in mind.

If you want to demonstrate that Meyer is wrong then you need to find evidence to demonstrate that Douglas Axe's experiments mentioned in Gerlenter's article above are factually incorrect.

Here is a short video where Doug Axe gives a very high level overview of his methodology and results.
https://www.youtube.com/watch?v=qwFi_2YZa_c

Meyer explains it here (less than 8 minutes)
https://www.youtube.com/watch?v=JQ3hUlU0vR4

I understand what they say, that several mutations are needed to come from one beneficial (functional) state to another. When Axe talks I get the feeling that he thinks of a long wandering in the desert until one finally comes to the goal. This is not the evolution theory. Generally it is assumed that every mutation is beneficial.

I think you are wrong on that assumption...
We know from experience that most mutations are harmful to organisms, That is why evolution assumes long periods of time between each beneficial or functional mutation.

This is exactly what Matheson was acknowledging when he said the following in his discussion with Meyer
"It is surely an open question about whether that whole tree can be navigated through function all the way through.
I certainly can't prove it's the case."

So to support your assertion with data, you need to demonstrate that Doug Axe's research on folding proteins is incorrect and the probability of finding a new protein is significantly less than 1 in 10^70.

See the citation from Romero et el. above.

I looked through Romero's article and I was unable to find a discussion of the probability of moving from one functional protein to another functional protein which was the subject of Axe's experiments.

Could you please provide the quote you had in mind that rebuts Axe's results?

The probabilities in Gelernter's article are based on actual experiments by Douglas Axe who manipulates proteins in an effort to get them to evolve from one functional state to another.

Here are a couple of short videos on Doug Axe's experiments on proteins
https://www.youtube.com/watch?v=mKUMH1vEkmU
https://youtu.be/8ZiLsXO-dYo
https://youtu.be/jJy2oRxPrlg?list=PLR8e ... oU5v2poZKf

These clips and the earlier you quoted repeat the same thing over and over. Nothing new. He think he has shown that there is no way to form new or adjust old proteins in the way that is normally assumed in the evolution theory, that is by many single mutations that each make a change that is beneficial.

And Axe has experimental empirical evidence to support his conclusion.
While the 'assumptions' about proteins ability to evolve from one functional state to another are just that... assumptions... with no empirical evidence to support those assumptions.

Generally, one can discuss the seriousness of Meyer. The evolution theory is not controversial among biologist, there are lot of discussions ongoing about details in the theory but the main principles are not discussed (see below). Then, it seems dangerous to dismiss it based on a single 15 years old article. That is not serious. It can be said that there are reasons to dismiss evolution but in the first clip by Meyer (https://www.youtube.com/watch?v=7c9PaZzsqEg ) he states that the conclusion of the article is that evolution is false.

And based on empirical evidence, Meyer is correct.
But I think it would be helpful to understand what Meyer means when he says evolution is false.

At a high level, there are three components of Darwinian Evolutionary Theory.
1. Common Descent
2. Random Mutation
3. Natural Selection

Intelligent Design does not question some sort of shared ancestry (Common Descent), Natural Selection, or even the process of Mutation.
Intelligent Design uses empirical evidence to show that random mutation is incapable of generating the information that we see in the fossil record and in the DNA of life today.

ID even acknowledges that random mutations do occur and Behe has done a lot of work in understanding the upper limits of what the Darwinian process of random mutation is capable of in the lab and in nature. Thus the difference between micro-evolution, an established scientific fact which functions within the observed capability of random mutation, and macro-evolution which exceeds the observed capability of random mutation.

This is not an argument from authority. It’s just an argument that you need more than a single article to dismiss an established theory.

You need empirical evidence to support or dismiss any theory.
And Meyer is basing his position on empirical evidence from numerous sources regarding the capabilities of 'random' mutation and the known causes of information.

Your way to cut away parts of my argument when you reference me and intermix different argument makes it tiresome to discuss with you but I’ll do my best.

To try to structure the debate:

1. The main thing I want to discuss is Meyers argument in the clip https://www.youtube.com/watch?v=7c9PaZzsqEg. He says that Axe’s article shows that random mutations isn’t enough to move from one functional protein to another and therefore the evolution theory is false.
I claim (and it is generally accepted) that you can’t dismiss an established scientific theory by reference to one single article and that Meyer should know that. Further support for this is that the article is old 2004 and there has as far as I know been no follow up, neither by Axe or some other.

2. Axes article if far from conclusive.
- The probability he mentions is 1 in 10^77 but there are at least on other reference that mentions 1 in 10^11
Romero’s article says in the first page: “Second, within this vast space, functional proteins are extremely scarce, with estimates that range from a high of 1 in 10^11to as little as 1 in 10^77 (4, 5)” where (5) refers to Axe’s article. (https://www.pnas.org/content/pnas/early ... 0.full.pdf)

- There are lot of presumptions in his article that don’t seem self-evident to me. For instance he assumes that the proteins are evenly distributed in the space of possible alternatives. More probable is that they are clustered which will make it much more easy to go from one protein to another.
- There are more probable mechanisms than the several step random walk that Axe discusses, for instance successive steps where each step is functional. This is what Coyne discusses in the citation I supported in #212. He first discusses the methodology and then gives some examples.
- - - -
You also bring up some other questions that aren’t central to this discussion but I anyhow will try to comment even if I prefer not to discuss those things before we have discussed 1 and 2.
3. You say: This is exactly what Matheson was acknowledging when he said the following in his discussion with Meyer "It is surely an open question about whether that whole tree can be navigated through function all the way through. I certainly can't prove it's the case."
I have commented this before and what you don’t understand is the use of the word “proof”. Wikipedia has a good explanation of this: https://en.wikipedia.org/wiki/Talk:Evolution Q4: But isn't evolution unproven?
4. You say: “Intelligent Design uses empirical evidence to show that random mutation is incapable of generating the information that we see in the fossil record and in the DNA of life today.”
This is really a bold statement. How can that be shown? Behe has used the concept of irreducible complexity (IC) which says that there are designs that are so complex that it isn’t possible to achieve them by small steps which all are beneficial. But how can that be shown? Behe supports some examples that he claims is IC, for instance the mousetrap and the design of the human eye. Most (at least) of these examples are rebutted. About the mousetrap you can search on the net. About the eye see https://www.cs.bgu.ac.il/~ben-shahar/Te ... Evolve.pdf
There may be other examples that aren’t rebutted but that only show that we don’t know everything in biology. Behe’s argument is a God of the gaps argument.
--- --
Finally
“And Meyer is basing his position on empirical evidence from numerous sources regarding the capabilities of 'random' mutation and the known causes of information”
According to his video clip he dismisses evolution relying on Axe’s article only. However, further on in the clip he argues from causes of information. It is an obvious faulty statement but I will discuss that later.
Nils

[DBowling]

To try to structure the debate:

1. The main thing I want to discuss is Meyers argument in the clip https://www.youtube.com/watch?v=7c9PaZzsqEg. He says that Axe’s article shows that random mutations isn’t enough to move from one functional protein to another and therefore the evolution theory is false.
I claim (and it is generally accepted) that you can’t dismiss an established scientific theory by reference to one single article and that Meyer should know that. Further support for this is that the article is old 2004 and there has as far as I know been no follow up, neither by Axe or some other.

Fine...
If you want to make a claim then provide some empirical support for your claim.
The basis of Axe's claims are real live experiments.
You have yet to provide any data that disproves the results of Axe's experiments on the evolution of proteins.

Yes, I will absolutely take empirical data more seriously than unsubstantiated claims

2. Axes article if far from conclusive.
- The probability he mentions is 1 in 10^77 but there are at least on other reference that mentions 1 in 10^11
Romero’s article says in the first page: “Second, within this vast space, functional proteins are extremely scarce, with estimates that range from a high of 1 in 10^11 to as little as 1 in 10^77 (4, 5)” where (5) refers to Axe’s article. (https://www.pnas.org/content/pnas/early ... 0.full.pdf)

Romero is not disputing Axe's conclusions. As you already pointed out, he actually references Axe's findings in his article.
Here is the complete paragraph

Identifying such optimized sequences is extremely challenging
for several reasons. First, the space of possible protein sequences is
incomprehensibly large and will never be searched exhaustively by
any means, naturally, in the laboratory, or computationally (2, 3).
Second, within this vast space, functional proteins are extremely
scarce, with estimates that range from a high of 1 in 10^11 to as little
as 1 in 10^77 (4, 5). Of the sequences that are functional, most have
poor fitness and their numbers decrease exponentially with higher
levels of fitness (6, 7). Thus, highly fit sequences are vanishingly
rare and overwhelmed by nonfunctional and mediocre sequences.

The final sentence of this paragraph actually supports the position of Axe and Meyer.

Here is a link to Keefe's article which Romero also references
https://www.researchgate.net/publicatio ... ce_library
For the sake of argument, even if we assume Keefe's number of 1 in 10^11, I found the final paragraph of Keefe's conclusion interesting

In conclusion, we suggest that functional proteins are sufficiently common in protein sequence space (roughly 1 in 10^11) that they may be discovered by entirely stochastic means, such as presumably operated when proteins were first used by living organisms. However, this frequency is still low enough to emphasize the magnitude of the problem faced by those attempting de novo protein design.

One final observation... It is interesting to note that Axe's work is more recent (2004) than Keefe's (2001).

Here's a brief article that compares the work of Axe and Keefe with others who have examined the evolution of protein folds.
https://uncommondescent.com/intelligent ... ein-folds/

- There are lot of presumptions in his article that don’t seem self-evident to me. For instance he assumes that the proteins are evenly distributed in the space of possible alternatives. More probable is that they are clustered which will make it much more easy to go from one protein to another.

If you have any empirical evidence to support your presumption I would be glad to see it.
But again, unproven presumptions are not data and they are not evidence.

4. You say: “Intelligent Design uses empirical evidence to show that random mutation is incapable of generating the information that we see in the fossil record and in the DNA of life today.”
This is really a bold statement. How can that be shown? Behe has used the concept of irreducible complexity (IC) which says that there are designs that are so complex that it isn’t possible to achieve them by small steps which all are beneficial. But how can that be shown?

Behe explains it in this video
https://www.youtube.com/watch?v=Y6j8Yp6s6E8
(specific empirical evidence is given in minutes 21-46)

Behe’s argument is a God of the gaps argument.

I have never heard Behe or Meyer refer to their argument as "God of the gaps"
The only people I see using the term "God of the gaps" are opponents of Meyer and Behe who are unable to support their position with actual empirical data, so they are forced to revert to their standby "God of the gaps" rhetoric to gloss over the known gaps in their position.

The positions of Meyer and Behe are based on empirical evidence regarding the known capabilities of "random" mutation, the known information demonstrated in the DNA of life today, and known sources of information.
It is a position that is based on empirical evidence regarding known processes from beginning to end.

[DBowling]

One final observation... It is interesting to note that Axe's work is more recent (2004) than Keefe's (2001).

Here is a link to Axe's paper (2004)
Estimating the Prevalence of Protein Sequences Adopting Functional Enzyme Folds
http://citeseerx.ist.psu.edu/viewdoc/do ... 1&type=pdf

Here is a link to Keefe's paper (2001)
Functional proteins from a random-sequence library
https://www.researchgate.net/publicatio ... ce_library

Axe does address Keefe's paper in his study
(Reference #3 is Keefe's paper)

This is a difficult problem to approach experimentally, however, and no clear picture has yet emerged. A number of studies have suggested that
functional sequences are not extraordinarily rare,1–5 while others have suggested that they are.6–9

And the goal of of Axe's study was to empirically address the question about whether functional protein sequences are extraordinarily rare or not.

[PaulSacramento]

God of the gaps? science of the gaps...

Difference is that when we say GOD we are referring to an actual ANSWER to the question, whereas the "science of the gap" argument is an expression of hope and faith.
See, in GOD we see the driving force of creation and sustainability AND the very attributes that rationally and reasonably CAN create and sustain the universe.
That is why the God of the Gaps argument fails.

[Nils]

Sorry DB, for late response.

To try to structure the debate:

1. The main thing I want to discuss is Meyers argument in the clip https://www.youtube.com/watch?v=7c9PaZzsqEg. He says that Axe’s article shows that random mutations isn’t enough to move from one functional protein to another and therefore the evolution theory is false.
I claim (and it is generally accepted) that you can’t dismiss an established scientific theory by reference to one single article and that Meyer should know that. Further support for this is that the article is old 2004 and there has as far as I know been no follow up, neither by Axe or some other.

Fine...
If you want to make a claim then provide some empirical support for your claim.
The basis of Axe's claims are real live experiments.
You have yet to provide any data that disproves the results of Axe's experiments on the evolution of proteins.

Yes, I will absolutely take empirical data more seriously than unsubstantiated claims

You misunderstand me completely. My claim above isn’t about Axe’s article. My claim is a general claim that one (or a few) single article isn’t enough to dismiss an established theory.

2. Axes article if far from conclusive.
- The probability he mentions is 1 in 10^77 but there are at least on other reference that mentions 1 in 10^11
Romero’s article says in the first page: “Second, within this vast space, functional proteins are extremely scarce, with estimates that range from a high of 1 in 10^11 to as little as 1 in 10^77 (4, 5)” where (5) refers to Axe’s article. (https://www.pnas.org/content/pnas/early ... 0.full.pdf)

Romero is not disputing Axe's conclusions. As you already pointed out, he actually references Axe's findings in his article.
Here is the complete paragraph

Identifying such optimized sequences is extremely challenging
for several reasons. First, the space of possible protein sequences is
incomprehensibly large and will never be searched exhaustively by
any means, naturally, in the laboratory, or computationally (2, 3).
Second, within this vast space, functional proteins are extremely
scarce, with estimates that range from a high of 1 in 10^11 to as little
as 1 in 10^77 (4, 5). Of the sequences that are functional, most have
poor fitness and their numbers decrease exponentially with higher
levels of fitness (6, 7). Thus, highly fit sequences are vanishingly
rare and overwhelmed by nonfunctional and mediocre sequences.

The final sentence of this paragraph actually supports the position of Axe and Meyer.

Here is a link to Keefe's article which Romero also references
https://www.researchgate.net/publicatio ... ce_library
For the sake of argument, even if we assume Keefe's number of 1 in 10^11, I found the final paragraph of Keefe's conclusion interesting

In conclusion, we suggest that functional proteins are sufficiently common in protein sequence space (roughly 1 in 10^11) that they may be discovered by entirely stochastic means, such as presumably operated when proteins were first used by living organisms. However, this frequency is still low enough to emphasize the magnitude of the problem faced by those attempting de novo protein design.

One final observation... It is interesting to note that Axe's work is more recent (2004) than Keefe's (2001).

Here's a brief article that compares the work of Axe and Keefe with others who have examined the evolution of protein folds.
https://uncommondescent.com/intelligent ... ein-folds/

- There are lot of presumptions in his article that don’t seem self-evident to me. For instance he assumes that the proteins are evenly distributed in the space of possible alternatives. More probable is that they are clustered which will make it much more easy to go from one protein to another.

If you have any empirical evidence to support your presumption I would be glad to see it.
But again, unproven presumptions are not data and they are not evidence.

The main problem with your (and Meyers) reasoning is that evidence for a problem being difficult and having no known solution, isn’t evidence that the problem is not solvable. During the history of evolution, since 1859, there has been so many problems solved, problems that seemed unsolvable beforehand. Why do you think that all the problems that are unsolved exactly 160 years after the Darwin will remain unsolved?
Because I’m not an expert I can’t point at any specific research but what you cut away from my last post (the reference to Coyne). Also, if the problem with protein folding has that importance that you think. Why isn’t that problem highlighted in Wikipedia or other current literature?

4. You say: “Intelligent Design uses empirical evidence to show that random mutation is incapable of generating the information that we see in the fossil record and in the DNA of life today.”
This is really a bold statement. How can that be shown? Behe has used the concept of irreducible complexity (IC) which says that there are designs that are so complex that it isn’t possible to achieve them by small steps which all are beneficial. But how can that be shown?

Behe explains it in this video
https://www.youtube.com/watch?v=Y6j8Yp6s6E8
(specific empirical evidence is given in minutes 21-46)

Behe’s argument is a God of the gaps argument.

I have never heard Behe or Meyer refer to their argument as "God of the gaps"
The only people I see using the term "God of the gaps" are opponents of Meyer and Behe who are unable to support their position with actual empirical data, so they are forced to revert to their standby "God of the gaps" rhetoric to gloss over the known gaps in their position.

The positions of Meyer and Behe are based on empirical evidence regarding the known capabilities of "random" mutation, the known information demonstrated in the DNA of life today, and known sources of information.
It is a position that is based on empirical evidence regarding known processes from beginning to end.

Of course, Behe and Meyer don’t mention the God of the gaps argument but that doesn’t make the argument false. More important, in the video you refer to above Behe states that “that Darwinism cannot make complex functional system” 46:19, and that there “is an observation that it does not”.
However, his logic is false. He does the following reasoning in minutes 26 to 46:
1. He shows that a single mutation has the probability of 1 in 10^10
2. He shows that two independent mutations have the probability of 1 in 10^20
This is based on evidence of the malaria parasite and is uncontroversial
3. He concludes that the probability of four independent mutations would be 1 in 10^40
This is also uncontroversial.
4. He says that the probability of 1 in 10^40 is so small that four independent mutations will never occur during the existence of Earth.
Also uncontroversial.
5. He states that because 4. “Darwinism cannot make complex functional system”

The problem with 5. is that it doesn’t follow from 4. There is a hidden assumption:
4.1. In Darwinian evolution four independent mutations are necessary.
But he has no evidence at all for 4.1. It’s only assumption. The evolution theory assumes that complex structures evolve in small steps (probably with not more than two independent mutations in each step) where each step is beneficial. It may be the case that it is not known how, for instance new proteins are developed but that isn’t any evidence for 4.1. If you say “that we don’t know is an argument for 4.1” then is is exactly a God of the gaps argument.
What Meyer and Behe would have to do is to show that there is at least one example of small step evolution that isn’t possible. However, that is virtually impossible, how can you prove that there is no solution possible? It doesn’t suffice to say that it’s not known today. Biological knowledge and the evolution theory have developed extremely the last 160 years and there no sign that it will stop in the near future. May be much that is unknown today will be more clear in another 160 years but I doubt everything will be explained then. So you have to wait till then, at least, to speculate about gaps of knowledge.
The bottom line is that there is no evidence at all for the impossibility of evolution. Meyer and Behe are completely wrong.
Nils

[DBowling]

Sorry DB, for late response.

No problem

You misunderstand me completely. My claim above isn’t about Axe’s article. My claim is a general claim that one (or a few) single article isn’t enough to dismiss an established theory.

I don't believe Behe, Meyer, and Axe are dismissing an established theory.
They are questioning one part of a theory that has not been empirically established.
And the specific part that has not been empirically established is the alleged ability of "random" mutation to infuse new information into the biosphere that we see in the fossil record and in the DNA of life today.

They are not questioning natural selection or that mutation of some sort has played role.
They are saying that empirical evidence demonstrates that what we see in the fossil record and in the DNA of life today is beyond the capability of the observed limits of "random" mutation.

The main problem with your (and Meyers) reasoning is that evidence for a problem being difficult and having no known solution, isn’t evidence that the problem is not solvable. During the history of evolution, since 1859, there has been so many problems solved, problems that seemed unsolvable beforehand. Why do you think that all the problems that are unsolved exactly 160 years after the Darwin will remain unsolved?

This is where you are misunderstanding Meyer's position.
Meyer is proposing that there is an empirically known cause of design and information.
And that known cause is intelligence.

A solution exists and is apparent based on known causes of design and information.

in the video you refer to above Behe states that “that Darwinism cannot make complex functional system” 46:19, and that there “is an observation that it does not”.
He does the following reasoning in minutes 26 to 46:
1. He shows that a single mutation has the probability of 1 in 10^10
2. He shows that two independent mutations have the probability of 1 in 10^20
This is based on evidence of the malaria parasite and is uncontroversial
3. He concludes that the probability of four independent mutations would be 1 in 10^40
This is also uncontroversial.
4. He says that the probability of 1 in 10^40 is so small that four independent mutations will never occur during the existence of Earth.
Also uncontroversial.

So far so good

5. He states that because 4. “Darwinism cannot make complex functional system”
The problem with 5. is that it doesn’t follow from 4. There is a hidden assumption:
4.1. In Darwinian evolution four independent mutations are necessary.
But he has no evidence at all for 4.1. It’s only assumption.

That's not accurate...
In his first book, Darwin's Black Box, Behe provides a number of examples of irreducibly complex biological systems that require much more than 4 independent mutations.

In Behe's video, he also discusses the behavior of Darwinian evolution, and he notes that observed beneficial mutations do not involve adding information to DNA, instead observed beneficial mutations involve some replacements but mostly deletions.
Which again speaks to the inability of "random" mutation to add new information to life.

The evolution theory assumes that complex structures evolve in small steps (probably with not more than two independent mutations in each step) where each step is beneficial.

And that particular assumption has not been empirically validated.
Despite your issue with the semantics of the word prove, I still think Matheson's quote is relevant here, because he acknowledges that this is still an "open question".
"It is surely an open question about whether that whole tree can be navigated through function all the way through.
I certainly can't prove it's the case."

The bottom line is that there is no evidence at all for the impossibility of evolution. Meyer and Behe are completely wrong.

No... you are completely wrong here.

Behe has provided empirical evidence in nature and in the lab regarding the limits of Darwinian Evolution.
Behe has provided numerous examples of irreducibly complex biological systems that require much more than 4 independent mutations at the molecular level.

It is you who have provided zero empirical evidence to support the "assumption" that random mutation is capable of generating the information that we see in the fossil record and in the DNA of life today.