Evidence for God from Science

DBowling wrote: ↑Sat Dec 04, 2021 12:16 pm

Nils wrote: ↑Wed Dec 01, 2021 6:48 pm Sorry, I don’t follow you argument and what empirically observed behaviour you refer to.

The empirically observed behavior I am referring to is...
1. In the malaria example, the 2 coordinated mutations (substitutions) that provide resistance to chloroquine occurs at an exponential rate as opposed to the linear rate presumed for and required by current evolutionary theory.
2. In Lenski's experiments the overwhelming majority of beneficial mutations degrade genetic information instead of adding genetic information. So even when you get to the small subset of beneficial mutations you still haven't reached a level that is capable (at least through random processes) of generating the substitutions and adds required to generate what we see in the fossil record and the DNA of life today

Who says that? Who has given a measure of the level of “substitutions and adds” and who has come to the conclusion that this level isn’t what is “required to generate what we see in the fossil record and the DNA of life today”. Certainly not Lenski.

3. As Behe points out, genetic analysis of observed evolutionary activity in nature today confirms what we see in Lenski's experiments. Beneficial mutations in nature overwhelmingly degrade genetic information insteading of adding new genetic information.

But again, this says nothing about the mutation rate in higher organisms.

First, you seem to presume that the proportion of beneficial mutations relatively to the total number of mutations is constant in some species or between species. This is far from true. As I said earlier the Lemski experiment clearly shows that the rate of beneficial mutation varies. (See the Wikipedia article about Lemski’s experiment)

I agree that while the mutation rate is relatively constant for an organism, a larger number of those mutations will need to be beneficial in order for an organism to thrive in a changing environment.

Secondly, what is important is not the number of mutations per base pair per generation which is shown in the diagram but the total number of mutation in the genome per generation. Now, as you say in the last post: “The smallest genomes, belonging to primitive, single-celled organisms, contain just over half a million base pairs of DNA. Humans have around 3.2 billion base pairs of DNA.” That gives that the total mutation rate is higher in humans than in bacteria.

I'm not quite sure what you are saying here...
the mutation rate is mutations per base pair per generation

But this is a definition question. There is a mutation rate per base pair and there is a mutation rate per individual. The latter is much much higher in complex species. Back in post #62 you wrote

“You are referring to the "presumed" rate of evolution based on reverse engineering the rate of evolution from the fossil record and genetic analysis of currently existing life forms.

The big problem is the empirically observed behavior of mutation at the genetic level in the lab and in nature is a far cry from the reverse engineered "presumed" rate of mutation required to generate the tree of life.”

Because you referred to the rate of mutation required to generate the tree of life I assumed that you was talking about the number of mutations per individual. Now it seems that you all the time has been talking of the number of mutations per base pair. Why you have done that I don’t understand but it is irrelevant.
From this follows that most of the discussion since post # 62 is just based on a misunderstanding.

However
- a larger genome will have more base pairs.
- a smaller genome has a much larger population
- a generation for a smaller genome occurs much more rapidly than for a larger genome.

This is why we are actually able to empirically observe the behavior of evolution in organisms with a smaller genome, because evolution occurs much more rapidly in small genomes than in large genomes.
Hence Lenski's evolution experiment with e.coli.

Thirdly, the importance of mutations is to introduce a variability in the genome on which natural selection can work but there is another way to increase variability namely sexual reproduction. This is an important source of variability in higher organisms. The reason why sexual reproduction is developed is to increase the variability of the inherited genome to increase the evolutionary speed. Mutations isn’t the only one. (I have mentioned this several times but you have never commented this).

I haven't commented on it because...
Sexual reproduction passes on genetic information (including mutations) from a progenitor to an offspring.
But sexual reproduction (in and of itself) does not cause mutations.
"Mutations can result from DNA copying mistakes made during cell division, exposure to ionizing radiation, exposure to chemicals called mutagens, or infection by viruses."

So sexual reproduction is neither causal (mutation) or selective (natural selection).
Sexual reproduction is a means of propagating genetic information (including mutations) throughout a population.

If sexual reproduction were ONLY a means of propagation there would be no reason for sexual reproduction. The behaviour of a species depends not only of the specific codons but also of combinations of several. Sexual reproduction where genes and parts of genes are a mix of the parents genes can give new capabilities. This is an import developing feature.

I did smile when I read this
"The reason why sexual reproduction is developed is to increase the variability of the inherited genome"
That almost sounds like there was a "purpose" behind the development of sexual reproduction.

Well, I used this short form of “developed by the evolution process” or better “evolved”. Usually when discussing evolution such a mistake is harmless but perhaps not in this forum

This shows that it is impossible to find some general figure of beneficial mutations per individual. It is highly dependent of for instance the actual environment.

One thing to note.
The observed behavior of "beneficial mutations" in and of themselves is not adequate to support evolutionary theory.
In order to create the tree of life and the DNA in life today you need specific types of beneficial mutations (not just any beneficial mutation), namely adds and substitutions, and even more importantly you need coordinated adds and substitution to generate new genetic information.

Definitely not. But this discussion is a bit complex because it is crucial to have exact definitions of “coordinated” and “information” which you haven’t supported. I plan to come back to this later.

This is why examining the behavior of "beneficial mutations" in nature and in the lab is so important.
And when beneficial mutations are empirically observed, we see that beneficial mutations overwhelmingly degrade existing genetic information and do not generate new genetic information.

So "beneficail mutations" don't get the job done. You need lots and lots of beneficial adds and substitutions (which we just don't see in either the lab or nature).
Now lots and lots of beneficial adds and substitutions be impossible for "random mutations"

Nothing of what you have said supports that beneficial mutations don’t get the job done. Some of them increase information and some degrade it but that doesn’t say that there isn’t a long term evolution.

When you refer to what is seen in the lab and nature you all the time refer (sometimes erroneously) to just two experiments/ observations. Aren’t you aware of the science of evolution is done by thousands of scientists since Darwin 150 years ago. What do you think they are doing?

But they would be well within the skill set of the causal agent for the big bang and the physical laws of our universe.

Of course you can define some entity that is able to do anything.

To summarize our dicussion about the mutation speed. You have not showed (not even showed any indications) that the mutation rate per individual is low. You haven't showed that it is lower than the speed that is required for the evolution theory.

I will not be able to comment for a while so I wish you and the readers of this post a Merry Christmas.

Nils wrote: ↑Sat Dec 18, 2021 2:31 am

DBowling wrote: ↑Sat Dec 04, 2021 12:16 pm

Nils wrote: ↑Wed Dec 01, 2021 6:48 pm Sorry, I don’t follow you argument and what empirically observed behaviour you refer to.

The empirically observed behavior I am referring to is...
1. In the malaria example, the 2 coordinated mutations (substitutions) that provide resistance to chloroquine occurs at an exponential rate as opposed to the linear rate presumed for and required by current evolutionary theory.
2. In Lenski's experiments the overwhelming majority of beneficial mutations degrade genetic information instead of adding genetic information. So even when you get to the small subset of beneficial mutations you still haven't reached a level that is capable (at least through random processes) of generating the substitutions and adds required to generate what we see in the fossil record and the DNA of life today

Who says that? Who has given a measure of the level of “substitutions and adds” and who has come to the conclusion that this level isn’t what is “required to generate what we see in the fossil record and the DNA of life today”. Certainly not Lenski.

That is demonstrated by the Malaria example that we have discussed many times regarding the exponentially decreasing nature of coordinated beneficial substitutions.
(once again... Coordinated mutations are multiple mutations that are required to perform a specific beneficial function)

Beneficial adds are much more rare than beneficial substitutions.
So back to what we've discussed earlier...
If six coordinated substitutions exceed the capability of all life that has ever existed on our planet.
Then the billions of coordinated adds and substitutions required to create the tree of life far exceeds the capability of all life that has ever existed on our planet.

The only example on the table of empirically observed coordinated substitutions is the malaria example.
Evolutionary theory depends on the majority of beneficial substitutions (and adds) to be linear in nature and thus much more rapid than the exponential rate we see in malaria.
The problem is you have yet to produce a single empirically observed example of coordinated substitutions or adds occurring at this linear rate which allegedly should occur at a rate that is orders of magnitude faster than the exponentially decreasing rate observed in malaria.

There is a mutation rate per base pair and there is a mutation rate per individual. The latter is much much higher in complex species. Back in post #62 you wrote

“You are referring to the "presumed" rate of evolution based on reverse engineering the rate of evolution from the fossil record and genetic analysis of currently existing life forms.

The big problem is the empirically observed behavior of mutation at the genetic level in the lab and in nature is a far cry from the reverse engineered "presumed" rate of mutation required to generate the tree of life.”

Because you referred to the rate of mutation required to generate the tree of life I assumed that you was talking about the number of mutations per individual. Now it seems that you all the time has been talking of the number of mutations per base pair.

The rate that is key to evolution is mutations within a population PER TIME
Even though higher genome organisms have a larger number of base pairs per individual, smaller genomes have a much larger number of individuals in their population, and the generation span of small genome organisms is much shorter than the generation span of large genome organisms.

So due to their population size and the time span of a generation...
The number of mutations per time within a small genome population exceeds (by orders of magnitude) the number of mutations per time within a large genome population.

This is is why Lenski chose bacteria instead of elephants when he wanted to empirically observe evolution.

If sexual reproduction were ONLY a means of propagation there would be no reason for sexual reproduction. The behaviour of a species depends not only of the specific codons but also of combinations of several. Sexual reproduction where genes and parts of genes are a mix of the parents genes can give new capabilities. This is an import developing feature.

Agreed...
Like I said...
That almost sounds like there was a "purpose" behind the development of sexual reproduction.

This is why examining the behavior of "beneficial mutations" in nature and in the lab is so important.
And when beneficial mutations are empirically observed, we see that beneficial mutations overwhelmingly degrade existing genetic information and do not generate new genetic information.

So "beneficail mutations" don't get the job done. You need lots and lots of beneficial adds and substitutions (which we just don't see in either the lab or nature).
Now lots and lots of beneficial adds and substitutions be impossible for "random mutations"

Nothing of what you have said supports that beneficial mutations don’t get the job done. Some of them increase information and some degrade it but that doesn’t say that there isn’t a long term evolution.

My point was that specific types of beneficial mutations (not just any beneficial mutation) are required to "get the job done". Generating the tree of life requires coordinated mutations that add information (adds and substitutions) and Lenski's experiments and observing beneficial mutations in nature demonstrates that beneficial mutations degrade genetic information at a much faster rate than they add information.

When you refer to what is seen in the lab and nature you all the time refer (sometimes erroneously) to just two experiments/ observations. Aren’t you aware of the science of evolution is done by thousands of scientists since Darwin 150 years ago. What do you think they are doing?

They are studying and exploring the nature of evolution. And as these studies have progressed, and our understanding of mutations and genetics has increased over time, then our understanding of how evolution works has also increased greatly since the time of Darwin.

I will not be able to comment for a while so I wish you and the readers of this post a Merry Christmas.

Thank you
And a Merry Christmas and a Happy Holiday season to you and your loved ones as well.

DBowling wrote: ↑Mon Jul 26, 2021 7:00 am In this 8 minute episode of Science Uprising, Michael Behe discusses how the observed behavior of mutations fails to invent
https://www.youtube.com/watch?v=_ivgQFIST1g

As you all know I'm against evolution but sometimes it is hard to explain why evolution is a myth.Well I now I am much better at explaining why evolution is a myth and I will answer your question too. Can mutation invent? First off,it is important to understand that Evolution is a case of stating the obvious namely that there is variation in all populations but variation in a population is limited.As you all may know,for thousands of years before Chrles Darwin plant and animal breeders have proven variation in populations but also what evolutionists ignore and overlook that variation in populations is limited.Well Evolution demonstrates and proves to us what we already knew there is variation in the populations and it is limited. So to answer your question can mutations invent? They can only invent enough for "normal and limited" variation in populations.Such as a new dog breed or a new virus variant, for example.

abelcainsbrother wrote: ↑Sat Dec 18, 2021 11:28 am

DBowling wrote: ↑Mon Jul 26, 2021 7:00 am In this 8 minute episode of Science Uprising, Michael Behe discusses how the observed behavior of mutations fails to invent
https://www.youtube.com/watch?v=_ivgQFIST1g

As you all know I'm against evolution but sometimes it is hard to explain why evolution is a myth.Well I now I am much better at explaining why evolution is a myth and I will answer your question too. Can mutation invent? First off,it is important to understand that Evolution is a case of stating the obvious namely that there is variation in all populations but variation in a population is limited.As you all may know,for thousands of years before Chrles Darwin plant and animal breeders have proven variation in populations but also what evolutionists ignore and overlook that variation in populations is limited.Well Evolution demonstrates and proves to us what we already knew there is variation in the populations and it is limited. So to answer your question can mutations invent? They can only invent enough for "normal and limited" variation in populations.Such as a new dog breed or a new virus variant, for example.

What you are saying is that evolution is a myth because it is “obvious” that genetic variation is limited (from which follows that macro evolution isn’t possible). Very convincing.

As I got some time to read our discussion from the beginning it seem that we perhaps are coming close to a point where it’s of no use continuing the discussion. It has been interesting and I have learnt a lot, especially on E coli and Lenski’s experiment. We have had some problems to understand each other but I think now that I understand your position. To me, you trust Behe far to much and make the same mistakes as he makes, mainly extrapolating from the data about evolution of some bacteria to the general evolution. In post #12 I tried to clarify that by structuring your position and showing that one argument, 6. was missing. But you ignored my point.

You bring up a few arguments again and again in spite of me giving reasons to refute them but you don’t discuss my reasons. Instead you come back to your argument again later. I will exemplify the most important now.

Issue 1. The malaria case.
You mention often the malaria case where two non-beneficial mutations is needed to provide resistance to chloroquine. From that you (following Behe) argue that if four or more non-beneficial mutations is needed to get a function the probability would be so low that it is virtual impossible that it would ever happen. That is correct but the problem with the argument is that yours (and Behe’s) conclusion “that six coordinated mutations exceeds the capability of the number of life forms that have ever existed on this planet.” (for instance #69 and #77)) doesn’t follow. Perhaps there was a typing error, that you intended to write “coordinated non-beneficial mutations”. Then it were correct but as the evolution theory is about how the evolution is done in small steps by beneficial mutations your conclusion is irrelevant. Why then do you bring up the malaria example again and again and again?.

Issue 2. “Coordinated mutations”
The problem with Issue 1 may be your use of the term “coordinated mutations”. You say for example “(once again... Coordinated mutations are multiple mutations that are required to perform a specific beneficial function)” (#77). I have asked several times how you define “function” but got no answer. Is getting a bigger E Coli as in Lensk’s experiment a new function or is something like a functioning eye a new function? In the Nilsson’s article on a model for eye development (https://www.cs.bgu.ac.il/~ben-shahar/Te ... Evolve.pdf) he estimated the number of steps (beneficial mutations) to be less than
80 129 540 over some three hundred thousand years. Are these mutations “coordinated”? (You referred indirectly to this article in #18).

Also, the use of the term “coordinated” seems to presume that someone has actively coordinated the mutations. This is contradictory to the evolution theory so using the term in this discussion is confusing.

Issue 3. Lenski’s experiment
show according to you that “the overwhelming majority of beneficial mutations that do occur in nature and in the lab degrade genetic information” (#58). Assuming you are correct it still doesn’t follow what you continue with: “I think it is even more "wrong" to expect a high rate of beneficial mutations to add genetic information.” I don’t know what you mean by a “high” rate and even less how you can infer a reasonable rate in higher animals from Lenski’s bacteria experiment, something Lenski don’t. In Nilsson’s calculations he assumed a rate of beneficial mutations that in average gave a better performance of 0.005% per generation. Is that “high”?

What is completely missing is an explanation of how the results of Lenski’s experiments on bacteria can be transformed to evolution in vertebrates which for instance Nilsson discusses.

In #77 you make a stronger statement: “Lenski's experiments and observing beneficial mutations in nature demonstrates that beneficial mutations degrade genetic information at a much faster rate than they add information”. This is discussed in the Wikipedia reference to Lenski’s experiments and the conclusion isn’t clear. Lenski himself says (quoted in #10): “"Behe points to many examples of evolution in which genes and their functions have been degraded, but he largely ignores the ways that evolution generates new functions and thereby produces complexity.”

Issue 4. The mutation rate generally.
In post #69 you referred to a diagram that showed the number of mutations per base pair per generation and that is higher in simple organisms than in higher organisms. I remarked that the interesting speed is per individual and the number of base pairs in higher organism well compensate for the lower speed per base pair. Your answer is not to comment but saying: “The rate that is key to evolution is mutations within a population PER TIME. Even though higher genome organisms have a larger number of base pairs per individual, smaller genomes have a much larger number of individuals in their population, and the generation span of small genome organisms is much shorter than the generation span of large genome organisms.” But you don’t show that the mutation rate per generation is much slower in higher organisms and more important that the speed isn’t sufficient for the assumed evolution of for example eye evolution.

Issue 5. Burden of proof
You have now and then asked for evidence for my position which I haven’t tried to give because the discussion is about your view. You have the burden of proof. In our discussion in this thread the positions aren’t symmetrical. The burden of proof is more heavily on you than on me. The reason is that on your side is only Behe and a few supporters that have written only a few scientific peer reviewed articles (as far as I know only Behe). On my side I have hundreds or perhaps thousands of professional scientist that have written bookshelves with books and peer reviewed articles. You deviate from the common understanding and therefore the burden of proof is mainly on your side.

Moreover, being an amateur in biology I have no possibility to cover the extensive literature on evolution. You ask for examples of small step evolution evolving new functions. This depends of how you define “function” but also a deep knowledge of evolutionary research that I don’t have. However I think that I have a reasonable understanding of the basic mechanisms of the evolution by reading some books and lots of articles, for example about computer simulations of the evolutionary algorithm. Together with some basic data that gives an intuitive picture of how evolution works. My arguments in our debate come from this general understanding rather than from some specific references.

Issue 6 Irreducible complexity
This issue we haven’t discussed in this thread even if you a few times have referred to it indirectly. My intension was to come to it when we had finished the other issues but that has taken so long time. I guess that this issue is part of the explanation of your interest in this debate.


---

We have discussed the issues above at length. It’s not meaningful to continue the discussion if your argument is:

1. “It has been shown in nature and the lab” referring to the Malaria case and E Coli experiment.

and from that you make a giant leap to the conclusion:

2. “Then the billions of coordinated adds and substitutions required to create the tree of life far exceeds the capability of all life that has ever existed on our planet.” (#77) (or something similar which you repeat again and again).

You have to in some way show how 2. follows from 1. If you don't do that the discussion is meaningless.

This has become a long post and if you want to comment (which I assume) and go into details it would be preferable if we can concentrate on one of the issues above each time. That is the only way to come forward as I see.

Happy New Year!
I hope you had an enjoyable Holiday season

Let me address a couple of your comments and come back to the rest later.

Nils wrote: ↑Wed Jan 05, 2022 8:48 pm As I got some time to read our discussion from the beginning it seem that we perhaps are coming close to a point where it’s of no use continuing the discussion. It has been interesting and I have learnt a lot, especially on E coli and Lenski’s experiment.

It is very possible where we have reached a point where no new data is being introduced in our discussion.
But I would like to note that I too have learned a lot from this very interesting discussion.

We have had some problems to understand each other but I think now that I understand your position. To me, you trust Behe far to much and make the same mistakes as he makes, mainly extrapolating from the data about evolution of some bacteria to the general evolution. In post #12 I tried to clarify that by structuring your position and showing that one argument, 6. was missing. But you ignored my point.

I believe I responded in detail to your post #12 (and point 6 in particular) in my responses in post #13 and #15.

You bring up a few arguments again and again in spite of me giving reasons to refute them but you don’t discuss my reasons. Instead you come back to your argument again later. I will exemplify the most important now.

Yes... you provide argumentation to support your position (and I understand your reasoning), but I have not seen any empirical evidence to rebut my position.
So with no empirical data rebutting my position... yes I will continue to come back (repeatedly) to a position that is founded on empirical data.

Issue 1. The malaria case.
You mention often the malaria case where two non-beneficial mutations is needed to provide resistance to chloroquine. From that you (following Behe) argue that if four or more non-beneficial mutations is needed to get a function the probability would be so low that it is virtual impossible that it would ever happen. That is correct but the problem with the argument is that yours (and Behe’s) conclusion “that six coordinated mutations exceeds the capability of the number of life forms that have ever existed on this planet.” (for instance #69 and #77)) doesn’t follow. Perhaps there was a typing error, that you intended to write “coordinated non-beneficial mutations”. Then it were correct but as the evolution theory is about how the evolution is done in small steps by beneficial mutations your conclusion is irrelevant. Why then do you bring up the malaria example again and again and again?.

I do (and did) stipulate to your definition of "coordinated non-beneficial mutations".
But as we have discussed a number of times, the empirical evidence does not support the premise that small beneficial steps produce coordinated beneficial mutations (specifically substitutions and adds) any faster than "coordinated non-beneficial" mutations do.

We have an example on the table (malaria) of empirically observed "coordinated non-beneficial mutations" (substitutions) creating a new function.
According to your premise, small beneficial steps will create new functions at an exponentially faster rate than "coordinated non-beneficial mutations".

We have an empirically observed example of two "coordinated non-beneficial mutations" (substitutions) creating a new function.
Where are the corresponding millions of empirically observed examples of two "small beneficial mutations" (substitutions) creating a new function?

If this is an accurate premise, then where is the empirical evidence to support that premise?
I understand the premise. I just haven't seen any empirical evidence to support the premise.

Issue 2. “Coordinated mutations”
The problem with Issue 1 may be your use of the term “coordinated mutations”. You say for example “(once again... Coordinated mutations are multiple mutations that are required to perform a specific beneficial function)” (#77). I have asked several times how you define “function” but got no answer. Is getting a bigger E Coli as in Lensk’s experiment a new function or is something like a functioning eye a new function? In the Nilsson’s article on a model for eye development (https://www.cs.bgu.ac.il/~ben-shahar/Te ... Evolve.pdf) he estimated the number of steps (beneficial mutations) to be less than
80 129 540 over some three hundred thousand years. Are these mutations “coordinated”? (You referred indirectly to this article in #18).

Also, the use of the term “coordinated” seems to presume that someone has actively coordinated the mutations. This is contradictory to the evolution theory so using the term in this discussion is confusing.

Function
a. an activity or purpose natural to or intended for a person or thing.
b. a relationship or expression involving one or more variables.

Coordinated - bring the different elements of (a complex activity or organization) into a relationship that will ensure efficiency or harmony.

Nils wrote: ↑Wed Jan 05, 2022 8:48 pm We have discussed the issues above at length. It’s not meaningful to continue the discussion if your argument is:

1. “It has been shown in nature and the lab” referring to the Malaria case and E Coli experiment.

and from that you make a giant leap to the conclusion:

2. “Then the billions of coordinated adds and substitutions required to create the tree of life far exceeds the capability of all life that has ever existed on our planet.” (#77) (or something similar which you repeat again and again).

You have to in some way show how 2. follows from 1. If you don't do that the discussion is meaningless.

I think my statement below demonstrates how my conclusion follows logically from my premise very clearly and simply.

"If six coordinated substitutions exceed the capability of all life that has ever existed on our planet.
Then the billions of coordinated adds and substitutions required to create the tree of life far exceeds the capability of all life that has ever existed on our planet."

Nils wrote: ↑Wed Jan 05, 2022 8:48 pm Issue 3. Lenski’s experiment
show according to you that “the overwhelming majority of beneficial mutations that do occur in nature and in the lab degrade genetic information” (#58). Assuming you are correct it still doesn’t follow what you continue with: “I think it is even more "wrong" to expect a high rate of beneficial mutations to add genetic information.” I don’t know what you mean by a “high” rate and even less how you can infer a reasonable rate in higher animals from Lenski’s bacteria experiment, something Lenski don’t. In Nilsson’s calculations he assumed a rate of beneficial mutations that in average gave a better performance of 0.005% per generation. Is that “high”?

Nilsson's 'estimate' is purely speculative.
That doesn't mean he is right or wrong. It just means that his path is speculative and the rate is speculative.
Even if we accept Nilsson's path and rate are accurate, that still doesn't address the question at hand.

Is Nilsson's 'estimated' rate consistent with the empirically observed rate for RANDOM mutations that we see in the real world and in the lab?
If the empirically observed rate for RANDOM mutations in the real world is not consistent with Nilsson's estimated mutation rate, then the logical conclusion is that Nilsson's speculated process and rate requires a causal factor that exceeds the observed capability of RANDOM mutation... possibly GUIDED mutation

In #77 you make a stronger statement: “Lenski's experiments and observing beneficial mutations in nature demonstrates that beneficial mutations degrade genetic information at a much faster rate than they add information”. This is discussed in the Wikipedia reference to Lenski’s experiments and the conclusion isn’t clear. Lenski himself says (quoted in #10): “"Behe points to many examples of evolution in which genes and their functions have been degraded, but he largely ignores the ways that evolution generates new functions and thereby produces complexity.”

I think it is interesting that in your quote Lenski does not contradict any of Behe's conclusions.
Lenski even has to qualify 'ignores' with 'largely' because Behe does in fact address the infrequent instances where adds and substitutions did occur. However, I am unaware of any case where Lenski's experiments resulted in any coordinated adds and/or substitutions.
I would love to see any examples of coordinated adds or substitutions.

Issue 5. Burden of proof
You have now and then asked for evidence for my position which I haven’t tried to give because the discussion is about your view. You have the burden of proof.

I disagree...
Your primary premise makes a huge unverified presumption regarding the capability of RANDOM mutation.

Every empirically observed example of RANDOM mutation that we have discussed so far is inconsistent with the unverified presumptions that are required for RANDOM mutation to generate the changes we see in the fossil record and in the DNA of life today.

Therefore, the burden of proof is upon those who assert a capability for RANDOM mutation that is inconsistent with the empirically observable examples of RANDOM mutation in nature and in the lab.

If RANDOM mutation is truly a capable cause then there should be millions of empirically observed examples to demonstrate the capability of RANDOM mutation.
I just want to see some empirically observable examples.

Happy New Year to you too!

You discuss Issue 1 so let’s concentrate on that.
I wrote:
“Issue 1. The malaria case.
You mention often the malaria case where two non-beneficial mutations is needed to provide resistance to chloroquine. From that you (following Behe) argue that if four or more non-beneficial mutations is needed to get a function the probability would be so low that it is virtual impossible that it would ever happen. That is correct but the problem with the argument is that yours (and Behe’s) conclusion “that six coordinated mutations exceeds the capability of the number of life forms that have ever existed on this planet.” (for instance #69 and #77)) doesn’t follow. Perhaps there was a typing error, that you intended to write “coordinated non-beneficial mutations”. Then it were correct but as the evolution theory is about how the evolution is done in small steps by beneficial mutations your conclusion is irrelevant. Why then do you bring up the malaria example again and again and again?.”

My intension with Issue 1 was to discuss only what follows directly from the malaria case:

The malaria case shows that six non-beneficial coordinated mutations exceeds the capability of the number of life forms that have ever existed on this plan.

Do you agree?

If you agree that is what I think is important in Issue1

In your response you argue like this (assuming you agree)

1) Six non-beneficial coordinated mutations exceeds the capability …
2) Any sequence of beneficial mutations exceeds the capability …
therefore
3) Any sequence of mutations exceeds the capability….

My purpose with Issue 1 was only to come to an agreement on 1), which we have done if you agree above.

Now you added 2) which is another issue and which is highly contentious and is questioning the base of the evolution theory.

To be able to have a constructive discussion, please let’s argue in small steps (like evolution ) so let’s agree on non-beneficial mutations ( 1) ) first.

So a question to be sure that I understand you: Do you think that the malaria case says anything about the evolutionary possibilities with beneficial mutations? If so, please explain how and why.

Nils wrote: ↑Thu Jan 06, 2022 10:12 am Happy New Year to you too!

You discuss Issue 1 so let’s concentrate on that.
I wrote:
“Issue 1. The malaria case.
You mention often the malaria case where two non-beneficial mutations is needed to provide resistance to chloroquine. From that you (following Behe) argue that if four or more non-beneficial mutations is needed to get a function the probability would be so low that it is virtual impossible that it would ever happen. That is correct but the problem with the argument is that yours (and Behe’s) conclusion “that six coordinated mutations exceeds the capability of the number of life forms that have ever existed on this planet.” (for instance #69 and #77)) doesn’t follow. Perhaps there was a typing error, that you intended to write “coordinated non-beneficial mutations”. Then it were correct but as the evolution theory is about how the evolution is done in small steps by beneficial mutations your conclusion is irrelevant. Why then do you bring up the malaria example again and again and again?.”

My intension with Issue 1 was to discuss only what follows directly from the malaria case:

The malaria case shows that six non-beneficial coordinated mutations exceeds the capability of the number of life forms that have ever existed on this plan.

Do you agree?

Absolutely

If you agree that is what I think is important in Issue1

In your response you argue like this (assuming you agree)

1) Six non-beneficial coordinated mutations exceeds the capability …
2) Any sequence of beneficial mutations exceeds the capability …
therefore
3) Any sequence of mutations exceeds the capability….

Very close...
My slight modification would be

1) Six non-beneficial coordinated mutations (adds/substitutions) exceeds the capability …
1b) I am unaware of any empirical evidence that any sequence of coordinated beneficial mutations (adds/substitutions) exceeds the capability of "non-beneficial coordinated mutations" (adds/substitutions)
2) Therefore any sequence of six beneficial coordinated mutations (adds/substitutions) also exceeds the capability
3) And finally... Any sequence of six or more beneficial or non-beneficial coordinated mutations (adds/substitutions) also exceeds the capability

My purpose with Issue 1 was only to come to an agreement on 1), which we have done if you agree above.

Now you added 2) which is another issue and which is highly contentious and is questioning the base of the evolution theory.

To be able to have a constructive discussion, please let’s argue in small steps (like evolution ) so let’s agree on non-beneficial mutations ( 1) ) first.

So a question to be sure that I understand you: Do you think that the malaria case says anything about the evolutionary possibilities with beneficial mutations? If so, please explain how and why.

Yes... the malaria example establishes an empirically observable rate for two coordinated substitutions working together together to provide a new function (ie resistance to chloroquine)

Based on the exponential nature of the rate of this mutation I have stipulated to your premise that this mutation most likely involves two non-beneficial coordinated mutations.
The outstanding unverified assumption is that two beneficial substitutions would work together to form a new function at a rate orders of magnitude faster than two non-beneficial substitutions.
However, we do not see that assumption verified in real life.
In fact I have not seen any case where two substitutions (beneficial or non-beneficial) work together to produce a new function any more rapidly than the malaria example.
So until I see something that works faster than the malaria example, I have no reason to believe that any process will work faster than the malaria example... much less orders of magnitude faster than the malaria example.

DBowling wrote: ↑Thu Jan 06, 2022 2:20 pm

Nils wrote: ↑Thu Jan 06, 2022 10:12 am
The malaria case shows that six non-beneficial coordinated mutations exceeds the capability of the number of life forms that have ever existed on this plan.

Do you agree?

Absolutely

If you agree that is what I think is important in Issue1

In your response you argue like this (assuming you agree)

1) Six non-beneficial coordinated mutations exceeds the capability …
2) Any sequence of beneficial mutations exceeds the capability …
therefore
3) Any sequence of mutations exceeds the capability….

Very close...
My slight modification would be

1) Six non-beneficial coordinated mutations (adds/substitutions) exceeds the capability …
1b) I am unaware of any empirical evidence that any sequence of coordinated beneficial mutations (adds/substitutions) exceeds the capability of "non-beneficial coordinated mutations" (adds/substitutions)
2) Therefore any sequence of six beneficial coordinated mutations (adds/substitutions) also exceeds the capability
3) And finally... Any sequence of six or more beneficial or non-beneficial coordinated mutations (adds/substitutions) also exceeds the capability

Not “very close”. Your change makes the result opposite to the original.

To start with you refer to what you are “aware of”. This is a very weak argument. As far as I know you aren’t an expert in biology or evolution.

Leaving that aside it seems that you don’t understand the implications of the difference between beneficial and non-benficial mutations. I tried to explain that in post post #31, didn’t you understand? I’ll try to explain more related to the malaria case with resistance to chloroquine. The resistance is dependent of two specific mutations occurring at the same time, the probability of that is very low but occurs now and then. Suppose the chance that the any of the mutations occurs in one individual is 1 in 10^12. The chance that the other mutation occurs in the same individual will then be 1 in 10^24. If one of these mutations occur in an individual it will be inherited to the descendents for some generations until it disappears because of a new mutation, by genetic drift or perhaps because it is unfavourable to those individuals having it. But it will still exist for some generations so the probability to get the two mutations in one individual is a bit higher, 1 in 10^20.

If they happen to occur in an environment with chloroquine the combination of the two mutations is beneficial and the descendents with those mutations will be more adapted to this environment. They will thrive and the property will spread through the population. If the chloroquine disappears there will be no advantage with the two mutations and they will disappear in the long run through new mutations and genetic drift.

If it were the case that one of the mutations was beneficial it would spread to all individuals in the population. That is the definition of a beneficial mutation. If the other mutation were non-beneficial the chance that the two mutations occurred in one individual would then be 1 in 10^12. So only about 10^12 individuals was needed to get the two mutations. If both mutations were beneficial then both would continue to be present after they once had occurred, independent of the presence of chloroquine, that is the probability would be 1.

The conclusion is that the frequency of the combination of non-beneficial mutations (for instance in the malaria bacteria) says nothing about the frequencies of combinations of beneficial mutations.

In the posts following my post #31 you made some objections that were irrelevant.

-You asked me to show an example of two beneficial mutations producing a new “function”. My response was that I’m no expert on every evolutionary experiment and observation done. I later noted the Lempski’s experiment showed exactly how several beneficial mutations in combinations lead to bigger E Coli bacteria. Also it is much more difficult to experiment on the difference between populations with and without that mutations because if there is a possible beneficial mutation in a population it has occurred long ago and spread to the whole population. This was handled in Lempski’s experiment but that experiment is as I understand it extraordinary in many ways. Finally even if there is no example, it is theoretically clear, as I show above, that for instance six beneficial mutations may work together. Six non-beneficial mutations can’t.

- You said that “there are a host of documented irreducibly complex biological organisms in nature that cannot be produced through a series of single beneficial mutations” (#43). Even if that were true, which I don’t think (see Issue 6), it’s not an argument against that some biological functions can be produced through a series (more than 6 for example) of single beneficial mutations.

Nils wrote: ↑Fri Jan 07, 2022 8:43 pm

DBowling wrote: ↑Thu Jan 06, 2022 2:20 pm

Nils wrote: ↑Thu Jan 06, 2022 10:12 am
The malaria case shows that six non-beneficial coordinated mutations exceeds the capability of the number of life forms that have ever existed on this plan.

Do you agree?

Absolutely

If you agree that is what I think is important in Issue1

In your response you argue like this (assuming you agree)

1) Six non-beneficial coordinated mutations exceeds the capability …
2) Any sequence of beneficial mutations exceeds the capability …
therefore
3) Any sequence of mutations exceeds the capability….

Very close...
My slight modification would be

1) Six non-beneficial coordinated mutations (adds/substitutions) exceeds the capability …
1b) I am unaware of any empirical evidence that any sequence of coordinated beneficial mutations (adds/substitutions) exceeds the capability of "non-beneficial coordinated mutations" (adds/substitutions)
2) Therefore any sequence of six beneficial coordinated mutations (adds/substitutions) also exceeds the capability
3) And finally... Any sequence of six or more beneficial or non-beneficial coordinated mutations (adds/substitutions) also exceeds the capability

Leaving that aside it seems that you don’t understand the implications of the difference between beneficial and non-benficial mutations. I tried to explain that in post post #31, didn’t you understand? I’ll try to explain more related to the malaria case with resistance to chloroquine. The resistance is dependent of two specific mutations occurring at the same time, the probability of that is very low but occurs now and then. Suppose the chance that the any of the mutations occurs in one individual is 1 in 10^12. The chance that the other mutation occurs in the same individual will then be 1 in 10^24. If one of these mutations occur in an individual it will be inherited to the descendents for some generations until it disappears because of a new mutation, by genetic drift or perhaps because it is unfavourable to those individuals having it. But it will still exist for some generations so the probability to get the two mutations in one individual is a bit higher, 1 in 10^20.

If they happen to occur in an environment with chloroquine the combination of the two mutations is beneficial and the descendents with those mutations will be more adapted to this environment. They will thrive and the property will spread through the population. If the chloroquine disappears there will be no advantage with the two mutations and they will disappear in the long run through new mutations and genetic drift.

If it were the case that one of the mutations was beneficial it would spread to all individuals in the population. That is the definition of a beneficial mutation. If the other mutation were non-beneficial the chance that the two mutations occurred in one individual would then be 1 in 10^12. So only about 10^12 individuals was needed to get the two mutations. If both mutations were beneficial then both would continue to be present after they once had occurred, independent of the presence of chloroquine, that is the probability would be 1.

The conclusion is that the frequency of the combination of non-beneficial mutations (for instance in the malaria bacteria) says nothing about the frequencies of combinations of beneficial mutations.

I understand the premise perfectly well...
Here are the assumptions...
A string of non-beneficial mutations (substitutions/adds) work together to form a new function at an inverse exponential rate.
A string of beneficial mutations (substitutions/adds) will hypothetically work together to form a new function at a linear rate.
==>
A string of beneficial mutations (substitutions/adds) will hypothetically work together to form new functions at a rate that is exponentially faster than non-beneficial mutations work together to form new functions.
and
We should be able to empirically observe orders of magnitude more strings of beneficial mutations working together to form a new function than non-beneficial mutations working together to form a new function.
...
That's the premise
The problem is that is NOT what we see in real life.

We have the empirically observable malaria example of two non-beneficial mutations working together to form a new function (resistance to chloroquine)
If the above premise is true there should be millions of empirically observable examples of two beneficial mutations (substitutions/adds) working together to form a new function.

Where are those hypothetical empirically observable examples of two beneficial mutations (substitutions/adds) working together to form a new function?.
I think the answer is probably they simply don't exist...
And millions of empirically observable examples most definitely do not exist, or someone would have already brought them forward to shut up those pesky ID folks.

Neither the frequency or quantity of empirically observed examples of two beneficial mutations (substitutions/adds) working together to form a new function verifies your premise.
Therefore the empirically observable data indicates there is an error of some sort in your premise.

There are two possibilities that I can think of.
1. There is another factor of some sort that prevents benificial mutations from working together to form new functions at a rate that is substantially faster than non-benificial mutations.
2. Or possibly the overwhelming majority of coordinated mutations cannot be formed by strings of beneficial mutations, and non-beneficial mutations are the predominant type of mutation required for mutations (substitutions/adds) to work together to form a new function.

DBowling wrote: ↑Sat Jan 08, 2022 12:33 pm

Nils wrote: ↑Fri Jan 07, 2022 8:43 pm The conclusion is that the frequency of the combination of non-beneficial mutations (for instance in the malaria bacteria) says nothing about the frequencies of combinations of beneficial mutations.

I understand the premise perfectly well...
Here are the assumptions...
1. A string of non-beneficial mutations (substitutions/adds) work together to form a new function at an inverse exponential rate.
2. A string of beneficial mutations (substitutions/adds) will hypothetically work together to form a new function at a linear rate.

I am not certain what your intension is with some of your terminology, what do you mean by “string”, why do you talk specifically about “substitution/adds” when mentioning mutation and your definition of function is unclear, but perhaps that isn’t problem so let’s go on. In 1. and 2. you talk about exponential and linear rates but that may be misleading, see below.

==>
3. A string of beneficial mutations (substitutions/adds) will hypothetically work together to form new functions at a rate that is exponentially faster than non-beneficial mutations work together to form new functions
and
4. we should be able to empirically observe orders of magnitude more strings of beneficial mutations working together to form a new function than non-beneficial mutations working together to form a new function.

...
That's the premise

First 1. and 2. above ( I have inserted the numbering in you text) are not my premises. I write about my them in my post #31:

My presumptions are:
- Mutations occur randomly and the probability of one specific mutation to occur in some specific DNA point during the lifetime of one individual is a fixed value P.
-Then the time (number of generations) until there is a will be a mutation depends on the value P and the population size. The more individuals there are in a population, the faster the mutation will occur (fewer generations are needed).
-If a mutation is beneficial it spreads to the whole population after some time. If it isn’t beneficial the mutation generally doesn’t spread. It slowly disappears.

From that follows my conclusions 1. and 2. above. For details see post #31.

Now 3. doesn’t follow from 1 and 2 !!

You can’t determine the rates only from the kind of mutation because there are also other aspects. It is quite possible that in a population there are only few or no beneficial mutations possible. Even if there are point mutations in all position beneficial mutation may not occur. In Lenski’s experiment with the bacteria E Coli they changed the environment and then new beneficial mutations occurred but after a while there were fewer and fewer. In a fixed environment the rate may go down towards zero.

Your statement 4. is based on your statement 3 so it is also wrong.

The rest of your post is based on these erroneous statements.

My conclusion persists:
The frequency of the combination of non-beneficial mutations (for instance in the malaria bacteria) says nothing about the frequencies of combinations of beneficial mutations.
Therefore there is no use to bring up the malaria case (Issue #1) and your conclusion based on it doesn’t follow:

“Then the billions of coordinated adds and substitutions required to create the tree of life far exceeds the capability of all life that has ever existed on our planet.”

Nils wrote: ↑Sun Jan 09, 2022 12:31 pm

DBowling wrote: ↑Sat Jan 08, 2022 12:33 pm

Nils wrote: ↑Fri Jan 07, 2022 8:43 pm The conclusion is that the frequency of the combination of non-beneficial mutations (for instance in the malaria bacteria) says nothing about the frequencies of combinations of beneficial mutations.

I understand the premise perfectly well...
Here are the assumptions...
1. A string of non-beneficial mutations (substitutions/adds) work together to form a new function at an inverse exponential rate.
2. A string of beneficial mutations (substitutions/adds) will hypothetically work together to form a new function at a linear rate.

I am not certain what your intension is with some of your terminology, what do you mean by “string”

I meant nothing more or less than referring to a series of mutations...

why do you talk specifically about “substitution/adds” when mentioning mutation

This is a deliberate clarification on my part.
The specific types of mutations required to generate complex new information in DNA are adds and substitutions.
Since the overwhelming majority of beneficial mutations degrade existing genetic information, I am focusing on the miniscule percentage of beneficial mutations that are actually capable of contributing new information to DNA.

==>
3. A string of beneficial mutations (substitutions/adds) will hypothetically work together to form new functions at a rate that is exponentially faster than non-beneficial mutations work together to form new functions
and
4. we should be able to empirically observe orders of magnitude more strings of beneficial mutations working together to form a new function than non-beneficial mutations working together to form a new function.

...
That's the premise

First 1. and 2. above ( I have inserted the numbering in you text) are not my premises. I write about my them in my post #31:

Here is your quote from post #31 that I was basing my statement on

M1 will occur after G1 number of generations (in average) where G1 is depending on P and the population size, perhaps millions of individuals. If the M1 mutation isn’t beneficial it will not spread through the population and will be limited to a few individuals for the generations to come. That means that the population that is useful to get a mutation M2 is very small. From that follows that the number of generations until M2 occurs will be a great number (very approximatively G1 x G1)

On the other hand, if M1 is beneficial, the population of individuals the have the mutation M1 will spread and finally reach almost the total population. Then the number of generations until M2 occurs will be about the same magnitude as G1. If the time for spreading is Gs, the total time will very approximatively be G1 + Gs + G1. If G1 is a big number 2xG1+Gs is much smaller than G1xG1.

G1 + Gs + G1 is linear
G1xG1 is exponential

My conclusion persists:
The frequency of the combination of non-beneficial mutations (for instance in the malaria bacteria) says nothing about the frequencies of combinations of beneficial mutations.

That is not quite true.

Do you agree with this statement?
The frequency of the combination of x benificial mutations exceeds (by orders of magnitude) the frequency of the combination of x non-beneficial mutations.
Therefore...
The number of empirically observable examples of combinations of x beneficial mutations should also exceed (by orders of magnitude) the number of empirically observable examples of combinations of x non-beneficial mutations.

DBowling wrote: ↑Sun Jan 09, 2022 8:02 pm

==>
3. A string of beneficial mutations (substitutions/adds) will hypothetically work together to form new functions at a rate that is exponentially faster than non-beneficial mutations work together to form new functions
and
4. we should be able to empirically observe orders of magnitude more strings of beneficial mutations working together to form a new function than non-beneficial mutations working together to form a new function.

...
That's the premise

First 1. and 2. above ( I have inserted the numbering in you text) are not my premises. I write about my them in my post #31:

Here is your quote from post #31 that I was basing my statement on

M1 will occur after G1 number of generations (in average) where G1 is depending on P and the population size, perhaps millions of individuals. If the M1 mutation isn’t beneficial it will not spread through the population and will be limited to a few individuals for the generations to come. That means that the population that is useful to get a mutation M2 is very small. From that follows that the number of generations until M2 occurs will be a great number (very approximatively G1 x G1)

On the other hand, if M1 is beneficial, the population of individuals the have the mutation M1 will spread and finally reach almost the total population. Then the number of generations until M2 occurs will be about the same magnitude as G1. If the time for spreading is Gs, the total time will very approximatively be G1 + Gs + G1. If G1 is a big number 2xG1+Gs is much smaller than G1xG1.

G1 + Gs + G1 is linear
G1xG1 is exponential

My conclusion persists:
The frequency of the combination of non-beneficial mutations (for instance in the malaria bacteria) says nothing about the frequencies of combinations of beneficial mutations.

That is not quite true.

Do you agree with this statement?
The frequency of the combination of x benificial mutations exceeds (by orders of magnitude) the frequency of the combination of x non-beneficial mutations.
Therefore...
The number of empirically observable examples of combinations of x beneficial mutations should also exceed (by orders of magnitude) the number of empirically observable examples of combinations of x non-beneficial mutations.

You apparently didn’t read the following in my last post:

You can’t determine the rates only from the kind of mutation because there are also other aspects. It is quite possible that in a population there are only few or no beneficial mutations possible. Even if there are point mutations in all position beneficial mutation may not occur. In Lenski’s experiment with the bacteria E Coli they changed the environment and then new beneficial mutations occurred but after a while there were fewer and fewer. In a fixed environment the rate may go down towards zero.

When you quoted from my post #31 above you unfortunately didn’t quote the two lines preceding your quote:

Assume that two different mutations M1 and M2 are needed to get a specific function (and assume they have to occur in that order) . Assume that both have the mutation rate P.

What I wrote about was an imagined example where there is one case with possible non-beneficial mutations and one case with possible beneficial mutations and I compared the rate between these two specific cases. The motive for this example was to show that there are two different mechanisms, one linear and one exponential (to which you agree). That doesn’t mean that every case with beneficial mutations is more rapid than some case with non-beneficial mutations. There has to be possible mutations as well.

So please comment my post #88 again.