Evidence for God from Science

DBowling wrote: ↑Wed Sep 01, 2021 5:21 pm I understand your premise, but I don't see any empirical evidence to support your premise.

Which premise are you talking about?

Your premise presumes that sequential mutations will produce a new function involving coordinated mutations at a faster rate than coordinated simultaneous mutations.

Now you introduce new terminology even before you explained the old. What is your definition of “sequential mutations”. I can guess but we apparently need to be exact here. You use the term “coordinated” without explaining in spite of I clearly asked for it. “simultaneous” how do you define that? Few thing in biology are exactly simultaneous.

You also presume that the observed 1 in 10^20 rate of 2 coordinated mutations is due to it being a simultaneous mutation.

I certainly don’t. I even don’t know what it would mean.

And you also presume that two sequential selectable mutations that produce a new function will occur at a rate that is much faster than the 1 in 10^20 rate for resistance to chloroquine.

If your assumptions are factually accurate then we should have expected to observe many sequential coordinated mutations producing a new function at a much faster rate within the time it took us to observe malaria developing resistance to chloroquine.
The other possibility is that sequential mutations may not produce new a new function involving coordinated mutations any faster than simultaneous mutations.

This takes us back to the question I asked in post #4 in this thread.
- -

I will now again try to make my argument clearer, showing which assumptions I make, without using any new terminology.

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.
Do you agree?

From that the following it is simple logic. It can be simulated by a simple computer program.

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.

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.

If four mutations is needed for a function and all the mutations are beneficial the number of generations will be G1+ Gs+ G1 + Gs + G1+ Gs+G1 = 4x G1 +3 x Gs. If they aren’t beneficial the number of generation will be of the magnitude of G1 x G1 x G1 x G1. If G1 for instance is 10^10 this number will be 10^40, so four specific non-beneficial nutations will never occur in one individual.

Here I don’t use any of your terminology: coordinated, selectable, sequential or simultaneous mutations. When you comment I ask you not to use those terms, at least without exact definitions.

Nils wrote: ↑Sat Sep 11, 2021 2:42 am I will now again try to make my argument clearer, showing which assumptions I make, without using any new terminology.

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.
Do you agree?

Yes... I pretty much agree...

From that the following it is simple logic. It can be simulated by a simple computer program.

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.

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.

I think reality is probably a bit more complicated, but I will stipulate to your basic premise.

If four mutations is needed for a function and all the mutations are beneficial the number of generations will be G1+ Gs+ G1 + Gs + G1+ Gs+G1 = 4x G1 +3 x Gs. If they aren’t beneficial the number of generation will be of the magnitude of G1 x G1 x G1 x G1. If G1 for instance is 10^10 this number will be 10^40, so four specific non-beneficial nutations will never occur in one individual.

I agree with your basic premise...
It would never occur in one individual using "random" mutations.
However, if we were to observe that four non-beneficial mutations did occur in one individual, then that would be evidence that something other than random mutation was at work.

Getting back to the malaria example
Since the observed difference between malaria developing resistance to atovaquone and chloroquine is exponential, then using your logic, that would indicate that malaria's resistance to chloroquine involved 'non-beneficial' mutations of some sort.
Would you agree?

We would also expect that a new function involving two beneficial mutations would occur at a rate orders of magnitude faster than the observed rate at which malaria developed resistance to chloroquine (1 in 10^20).
Would you agree?

So within the same time that it took malaria to adapt resistance to chloroquine, we would expect to see a host of new functions produced by two beneficial mutations.

We have an observed real world example of two non-beneficial mutations producing resistance to chloroquine.
Where are the expected host of observable real world examples of new functions being produced by two beneficial mutations?

DBowling wrote: ↑Sat Sep 11, 2021 4:46 am

Nils wrote: ↑Sat Sep 11, 2021 2:42 am I will now again try to make my argument clearer, showing which assumptions I make, without using any new terminology.

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.
Do you agree?

Yes... I pretty much agree...

From that the following it is simple logic. It can be simulated by a simple computer program.

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.

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.

I think reality is probably a bit more complicated, but I will stipulate to your basic premise.

If four mutations is needed for a function and all the mutations are beneficial the number of generations will be G1+ Gs+ G1 + Gs + G1+ Gs+G1 = 4x G1 +3 x Gs. If they aren’t beneficial the number of generation will be of the magnitude of G1 x G1 x G1 x G1. If G1 for instance is 10^10 this number will be 10^40, so four specific non-beneficial nutations will never occur in one individual.

I agree with your basic premise...
It would never occur in one individual using "random" mutations.
However, if we were to observe that four non-beneficial mutations did occur in one individual, then that would be evidence that something other than random mutation was at work.

Yes, but the problem is how to know that a mutation is non-beneficial

Getting back to the malaria example
Since the observed difference between malaria developing resistance to atovaquone and chloroquine is exponential, then using your logic, that would indicate that malaria's resistance to chloroquine involved 'non-beneficial' mutations of some sort.
Would you agree?

Yes, but as I understand it, in this case they have observed the single mutation and know that it isn’t spreading.

We would also expect that a new function involving two beneficial mutations would occur at a rate orders of magnitude faster than the observed rate at which malaria developed resistance to chloroquine (1 in 10^20).
Would you agree?

Not for sure. Malaria is a fairly old sickness so if the environment is stable there are probably very few possible mutations (if any) that are beneficial. However if the environment changes, many more mutations will become beneficial and a (relatively) rapid evolution will follow.

So within the same time that it took malaria to adapt resistance to chloroquine, we would expect to see a host of new functions produced by two beneficial mutations.
We have an observed real world example of two non-beneficial mutations producing resistance to chloroquine.
Where are the expected host of observable real world examples of new functions being produced by two beneficial mutations?

No. Because of what I said above I disagree with your conclusions.
(I assume that you above refer to development in malaria)

Nils wrote: ↑Sun Sep 12, 2021 2:56 pm

DBowling wrote: ↑Sat Sep 11, 2021 4:46 am

Nils wrote: ↑Sat Sep 11, 2021 2:42 am I will now again try to make my argument clearer, showing which assumptions I make, without using any new terminology.

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.
Do you agree?

Yes... I pretty much agree...

From that the following it is simple logic. It can be simulated by a simple computer program.

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.

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.

I think reality is probably a bit more complicated, but I will stipulate to your basic premise.

If four mutations is needed for a function and all the mutations are beneficial the number of generations will be G1+ Gs+ G1 + Gs + G1+ Gs+G1 = 4x G1 +3 x Gs. If they aren’t beneficial the number of generation will be of the magnitude of G1 x G1 x G1 x G1. If G1 for instance is 10^10 this number will be 10^40, so four specific non-beneficial nutations will never occur in one individual.

I agree with your basic premise...
It would never occur in one individual using "random" mutations.
However, if we were to observe that four non-beneficial mutations did occur in one individual, then that would be evidence that something other than random mutation was at work.

Yes, but the problem is how to know that a mutation is non-beneficial

Getting back to the malaria example
Since the observed difference between malaria developing resistance to atovaquone and chloroquine is exponential, then using your logic, that would indicate that malaria's resistance to chloroquine involved 'non-beneficial' mutations of some sort.
Would you agree?

Yes, but as I understand it, in this case they have observed the single mutation and know that it isn’t spreading.

I hadn't heard that, but it sounds intriguing...
I'd be interested in where you heard that.

We would also expect that a new function involving two beneficial mutations would occur at a rate orders of magnitude faster than the observed rate at which malaria developed resistance to chloroquine (1 in 10^20).
Would you agree?

Not for sure. Malaria is a fairly old sickness so if the environment is stable there are probably very few possible mutations (if any) that are beneficial. However if the environment changes, many more mutations will become beneficial and a (relatively) rapid evolution will follow.

The environment did change with the introduction of atovaquone and chloroquine to fight malaria.
But Malaria is not alone. There are many diseases out there in the world, and scientists are constantly developing new drugs to fight these diseases.

If multiple beneficial mutations are able to create new functions exponentially faster than multiple non-beneficial mutations (like malaria developing resistance to chloroquine).
Then why don't we regularly observe thousands and thousands of examples of multiple beneficial mutations creating new functions in the medical field as diseases are constantly forced to adapt to these new drugs?

DBowling wrote: ↑Sun Sep 12, 2021 5:26 pm

Nils wrote: ↑Sun Sep 12, 2021 2:56 pm

DBowling wrote: ↑Sat Sep 11, 2021 4:46 am
Getting back to the malaria example
Since the observed difference between malaria developing resistance to atovaquone and chloroquine is exponential, then using your logic, that would indicate that malaria's resistance to chloroquine involved 'non-beneficial' mutations of some sort.
Would you agree?

Yes, but as I understand it, in this case they have observed the single mutation and know that it isn’t spreading.

I hadn't heard that, but it sounds intriguing...
I'd be interested in where you heard that.

I don't know. Perhaps only a conclusion. When they studied Malaria they should have noticed whether the mutation was spreading.

We would also expect that a new function involving two beneficial mutations would occur at a rate orders of magnitude faster than the observed rate at which malaria developed resistance to chloroquine (1 in 10^20).
Would you agree?

Not for sure. Malaria is a fairly old sickness so if the environment is stable there are probably very few possible mutations (if any) that are beneficial. However if the environment changes, many more mutations will become beneficial and a (relatively) rapid evolution will follow.

The environment did change with the introduction of atovaquone and chloroquine to fight malaria.
But Malaria is not alone. There are many diseases out there in the world, and scientists are constantly developing new drugs to fight these diseases.

If multiple beneficial mutations are able to create new functions exponentially faster than multiple non-beneficial mutations (like malaria developing resistance to chloroquine).
Then why don't we regularly observe thousands and thousands of examples of multiple beneficial mutations creating new functions in the medical field as diseases are constantly forced to adapt to these new drugs?

But we do. As you say, virus and bacteria adapt through mutations for instance to new penicillins all the time. They achieve the function to be resistant to penicillin A and B and C etc.

Nils wrote: ↑Mon Sep 13, 2021 12:32 am

DBowling wrote: ↑Sun Sep 12, 2021 5:26 pm But Malaria is not alone. There are many diseases out there in the world, and scientists are constantly developing new drugs to fight these diseases.

If multiple beneficial mutations are able to create new functions exponentially faster than multiple non-beneficial mutations (like malaria developing resistance to chloroquine).
Then why don't we regularly observe thousands and thousands of examples of multiple beneficial mutations creating new functions in the medical field as diseases are constantly forced to adapt to these new drugs?

But we do. As you say, virus and bacteria adapt through mutations for instance to new penicillins all the time. They achieve the function to be resistant to penicillin A and B and C etc.

Technically speaking, viruses are not living organisms, and they mutate at a faster rate than living organisms.
So I would expect to find specific examples of multiple beneficial mutations producing new functions in viruses at a faster rate than in living organisms.
We see mutations in viruses all the time (as Covid shows us), but I am unaware of empirically observed examples of multiple beneficial mutations creating a new function in a virus. But I would be very interested in seeing an example if you are aware of one.

Bacteria are living organisms, and they are the subject of Lenski's long term experiments of evolution in the lab.
To the best of my knowledge Lenski has yet to see multiple beneficial mutations producing a new function.
As Behe points out, Lenski's experiments demonstrate that beneficial mutations overwhelmingly degrade existing genetic information instead of creating new complex genetic information.

With all the examples of evolution that we have observed in nature and in the lab, we still have no empirical evidence to support the unverified premise that a series of billions of unguided beneficial mutations is capable of creating the complex genetic code and biological functions that we find in life today.

DBowling wrote: ↑Mon Sep 13, 2021 4:23 am

Nils wrote: ↑Mon Sep 13, 2021 12:32 am

DBowling wrote: ↑Sun Sep 12, 2021 5:26 pm But Malaria is not alone. There are many diseases out there in the world, and scientists are constantly developing new drugs to fight these diseases.

If multiple beneficial mutations are able to create new functions exponentially faster than multiple non-beneficial mutations (like malaria developing resistance to chloroquine).
Then why don't we regularly observe thousands and thousands of examples of multiple beneficial mutations creating new functions in the medical field as diseases are constantly forced to adapt to these new drugs?

But we do. As you say, virus and bacteria adapt through mutations for instance to new penicillins all the time. They achieve the function to be resistant to penicillin A and B and C etc.

Technically speaking, viruses are not living organisms, and they mutate at a faster rate than living organisms.
So I would expect to find specific examples of multiple beneficial mutations producing new functions in viruses at a faster rate than in living organisms.
We see mutations in viruses all the time (as Covid shows us), but I am unaware of empirically observed examples of multiple beneficial mutations creating a new function in a virus. But I would be very interested in seeing an example if you are aware of one.

Bacteria are living organisms, and they are the subject of Lenski's long term experiments of evolution in the lab.
To the best of my knowledge Lenski has yet to see multiple beneficial mutations producing a new function.
As Behe points out, Lenski's experiments demonstrate that beneficial mutations overwhelmingly degrade existing genetic information instead of creating new complex genetic information.

With all the examples of evolution that we have observed in nature and in the lab, we still have no empirical evidence to support the unverified premise that a series of billions of unguided beneficial mutations is capable of creating the complex genetic code and biological functions that we find in life today.

It seems that we are not using “function” in the same way. To me anything useful is a function. For instance if a bacteria achieves resistance to penicillin A and B and C because of three beneficial mutations it has achieved a new function namely: Having resistance to penicillin A, B, and C.

Summarising the discussion so far it seems that you now understand that several beneficial mutations can give new functions faster than several non-beneficial mutations.
Now, it seems that you doubt that many beneficial mutations can produce complex functions.

But first, there is an enormous amount of evidence of multiple beneficial mutations (which by definition give new functions). So the question is whether a lot of these small increments of functions can produce complex functions. The Intelligent Design theory claims that there are some cases which are too complex. The evolutionists ask for proof.

Nils wrote: ↑Fri Sep 17, 2021 1:52 pm Summarising the discussion so far it seems that you now understand that several beneficial mutations can give new functions faster than several non-beneficial mutations.
Now, it seems that you doubt that many beneficial mutations can produce complex functions.

Oh I understand the premise that several 'beneficial mutations' can presumably give new functions faster than several 'non=beneficial mutations'.
The fundamental point of the OP is that there is no observable empirical evidence to support that presumption.
In fact the observable empirical evidence shows a glaring absence of several (or even 2) beneficial mutations working together to provide a new function.

We do have an example of two mutations working together to provide a new function at a rate of 1 in 10^20 with malaria developing resistance to chloroquine.
There is a presumption that two beneficial mutations working together could produce a new function at an exponentially faster rate than the rate at which malaria develops resistance to chloroquine.
So since we have an observable example of two non-beneficial mutations working together to provide a new function, where are the thousands and thousands of empirically observable examples of two beneficial mutations working together to provide a new function.

You make a claim that is fundamental to current evolutionary theory
"several beneficial mutations can give new functions faster than several non-beneficial mutations."
If this is true, where are the thousands of examples of 2 beneficial mutations working together to provide a new function?
I ask the evolutionist...
Where's the proof?

DB: I ask the evolutionist...
Where's the proof?

Yes, the proof has apparently gone...

DBowling wrote: ↑Sat Sep 18, 2021 3:54 am

Nils wrote: ↑Fri Sep 17, 2021 1:52 pm Summarising the discussion so far it seems that you now understand that several beneficial mutations can give new functions faster than several non-beneficial mutations.
Now, it seems that you doubt that many beneficial mutations can produce complex functions.

Oh I understand the premise that several 'beneficial mutations' can presumably give new functions faster than several 'non=beneficial mutations'.
The fundamental point of the OP is that there is no observable empirical evidence to support that presumption.
In fact the observable empirical evidence shows a glaring absence of several (or even 2) beneficial mutations working together to provide a new function.

We do have an example of two mutations working together to provide a new function at a rate of 1 in 10^20 with malaria developing resistance to chloroquine.
There is a presumption that two beneficial mutations working together could produce a new function at an exponentially faster rate than the rate at which malaria develops resistance to chloroquine.
So since we have an observable example of two non-beneficial mutations working together to provide a new function, where are the thousands and thousands of empirically observable examples of two beneficial mutations working together to provide a new function.

You make a claim that is fundamental to current evolutionary theory
"several beneficial mutations can give new functions faster than several non-beneficial mutations."
If this is true, where are the thousands of examples of 2 beneficial mutations working together to provide a new function?
I ask the evolutionist...
Where's the proof?

Why don’t you comment my last paragraph in #37? There is an answer to your question.

Regarding the OP, I commented it in #4 but your comment in #5 didn’t answer my question. Actually, it sustained it. Do we have to go through this again?

Nils wrote: ↑Sat Sep 18, 2021 1:25 pm

DBowling wrote: ↑Sat Sep 18, 2021 3:54 am

Nils wrote: ↑Fri Sep 17, 2021 1:52 pm Summarising the discussion so far it seems that you now understand that several beneficial mutations can give new functions faster than several non-beneficial mutations.
Now, it seems that you doubt that many beneficial mutations can produce complex functions.

Oh I understand the premise that several 'beneficial mutations' can presumably give new functions faster than several 'non=beneficial mutations'.
The fundamental point of the OP is that there is no observable empirical evidence to support that presumption.
In fact the observable empirical evidence shows a glaring absence of several (or even 2) beneficial mutations working together to provide a new function.

We do have an example of two mutations working together to provide a new function at a rate of 1 in 10^20 with malaria developing resistance to chloroquine.
There is a presumption that two beneficial mutations working together could produce a new function at an exponentially faster rate than the rate at which malaria develops resistance to chloroquine.
So since we have an observable example of two non-beneficial mutations working together to provide a new function, where are the thousands and thousands of empirically observable examples of two beneficial mutations working together to provide a new function.

You make a claim that is fundamental to current evolutionary theory
"several beneficial mutations can give new functions faster than several non-beneficial mutations."
If this is true, where are the thousands of examples of 2 beneficial mutations working together to provide a new function?
I ask the evolutionist...
Where's the proof?

Why don’t you comment my last paragraph in #37? There is an answer to your question.

I did...
Very directly in post 38

But to spell it out explicitly...

Nills said...
But first, there is an enormous amount of evidence of multiple beneficial mutations (which by definition give new functions). So the question is whether a lot of these small increments of functions can produce complex functions.

There is an enormous amount of evidence of beneficial mutations providing new functions. There is no disagreement there.

However, the outstanding question is... is there any evidence of multiple (2 or more) beneficial mutations working together to produce a new function.
That is the proof that I have requested multiple times that you have yet to produce.

If you are unable to produce any examples of two or three beneficial mutations working together to produce a new function,
Then the presumption that billions of small beneficial mutations can somehow produce complex functions is simply non-credible based on the empirically observed behavior of evolution in nature and in the lab.

Especially when the overwhelming majority of observed beneficial mutations degrade or remove genetic information instead of altering (like the malaria examples) or even more infrequently adding genetic information.

DBowling wrote: ↑Sat Sep 18, 2021 4:58 pm But to spell it out explicitly...

Nills said...
But first, there is an enormous amount of evidence of multiple beneficial mutations (which by definition give new functions). So the question is whether a lot of these small increments of functions can produce complex functions.

There is an enormous amount of evidence of beneficial mutations providing new functions. There is no disagreement there.

However, the outstanding question is... is there any evidence of multiple (2 or more) beneficial mutations working together to produce a new function.
That is the proof that I have requested multiple times that you have yet to produce.

This is as I said in #38 a question about the definition of “function”.
You say

However, the outstanding question is... is there any evidence of multiple (2 or more) beneficial mutations working together to produce a new function.

Here you ask for functions based “multiple (2 or more) beneficial mutations working together” where none of the multiple beneficial mutation produces a function. But there isn’t any. Beneficial mutations produce things that are beneficial, i.e. functions that are beneficial.
I don’t remember that even Behe has asked for such mutations you ask for.

If you are unable to produce any examples of two or three beneficial mutations working together to produce a new function,
Then the presumption that billions of small beneficial mutations can somehow produce complex functions is simply non-credible based on the empirically observed behavior of evolution in nature and in the lab.

How can you say this "based on the empirically observed behavior of evolution in nature and in the lab.”
What empirical behaviour or observations in nature and in the lab do you refer to? The Lemski experiment certainly doesn’t have any implications about this.

About examples, sorry, I’m not a professional evolutionist scientist, so I don’t have knowledge about all findings but when I searched for multiple beneficial mutations I found this for example: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4429600/ It touches on the subject in several places. But the science of evolution is about building complex functions by several mutations. Probably you will find examples is lot of scientific articles about mutations.

Especially when the overwhelming majority of observed beneficial mutations degrade or remove genetic information instead of altering (like the malaria examples) or even more infrequently adding genetic information.

This statement seems to be based on a misunderstanding. Beneficial mutations are indeed very uncommon. Especially when the environment isn’t changing. It’s not a law that there always are possible mutations that are beneficial. That’s why Behes statement in the OP is so astounding. The e coli bacteria has existed in more than one hundred million years. How could there be a lot of possible beneficial mutations that have never occurred long time ago appearing now in Lemski’s thirty year experiment.
Agree?

Nils wrote: ↑Sun Sep 19, 2021 4:50 am

DBowling wrote: ↑Sat Sep 18, 2021 4:58 pm But to spell it out explicitly...

Nills said...
But first, there is an enormous amount of evidence of multiple beneficial mutations (which by definition give new functions). So the question is whether a lot of these small increments of functions can produce complex functions.

There is an enormous amount of evidence of beneficial mutations providing new functions. There is no disagreement there.

However, the outstanding question is... is there any evidence of multiple (2 or more) beneficial mutations working together to produce a new function.
That is the proof that I have requested multiple times that you have yet to produce.

This is as I said in #38 a question about the definition of “function”.
You say

However, the outstanding question is... is there any evidence of multiple (2 or more) beneficial mutations working together to produce a new function.

Here you ask for functions based “multiple (2 or more) beneficial mutations working together” where none of the multiple beneficial mutation produces a function. But there isn’t any. Beneficial mutations produce things that are beneficial, i.e. functions that are beneficial.

You are totally missing my point...

We have a real life example on the table of two mutations working together to form a new function in malaria's resistance to chloroquine.
Due to the exponential nature of the two mutations occurring, you presume that this particular example involves two non-beneficial mutations working together to perform a specific function.
And for the sake of argument I will stipulate to your presumption that malaria's resistance to chloroquine involves two non-beneficial mutations.

You also presume that two beneficial mutations will work together to perform a new function more rapidly and more frequently than two non-beneficial mutations working together to perform a new function.
I am asking for empirical evidence of this presumption. I am not saying it doesn't exist. I just want to see an example, so we can compare the rate at which two beneficial mutations produce a new function with the rate at which two non-beneficial mutations produce a new function.

We would start by finding a new function of some sort that requires two mutations working together (similar to malaria's resistance to chloroquine).
Then we would see if there is a midpoint where either of those two mutations produces a beneficial function by itself.
- If one of those two mutations provides a beneficial function by itself.
- And then a second mutation works together with that first mutation to provide a different beneficial function.
==> Then we will have our example and we can determine the rate at which two beneficial mutations are able to produce a new function.

Especially when the overwhelming majority of observed beneficial mutations degrade or remove genetic information instead of altering (like the malaria examples) or even more infrequently adding genetic information.

Beneficial mutations are indeed very uncommon. Especially when the environment isn’t changing. It’s not a law that there always are possible mutations that are beneficial. That’s why Behes statement in the OP is so astounding. The e coli bacteria has existed in more than one hundred million years. How could there be a lot of beneficial mutations that have never occurred long time ago appearing now in Lemski’s thirty year experiment.
Agree?

But if the observed behavior of evolution in nature and in the lab demonstrates that 5 or 6 non-beneficial mutations working together to perform a new function exceeds the capability of all life that has ever existed on this planet.
And if there are a host of documented irreducibly complex biological organisms in nature that cannot be produced through a series of single beneficial mutations.
Then, the observed behavior of evolution in nature and the lab does demonstrate that unguided evolution is incapable of producing the complex genetic code found in the DNA of life on our planet.

DBowling wrote: ↑Sun Sep 19, 2021 5:40 am
We have a real life example on the table of two mutations working together to form a new function in malaria's resistance to chloroquine.
Due to the exponential nature of the two mutations occurring, you presume that this particular example involves two non-beneficial mutations working together to perform a specific function.
And for the sake of argument I will stipulate to your presumption that malaria's resistance to chloroquine involves two non-beneficial mutations.

You also presume that two beneficial mutations will work together to perform a new function more rapidly and more frequently than two non-beneficial mutations working together to perform a new function.
I am asking for empirical evidence of this presumption. I am not saying it doesn't exist. I just want to see an example, so we can compare the rate at which two beneficial mutations produce a new function with the rate at which two non-beneficial mutations produce a new function.

We would start by finding a new function of some sort that requires two mutations working together (similar to malaria's resistance to chloroquine).
Then we would see if there is a midpoint where either of those two mutations produces a beneficial function by itself.
- If one of those two mutations provides a beneficial function by itself.
- And then a second mutation works together with that first mutation to provide a different beneficial function.
==> Then we will have our example and we can determine the rate at which two beneficial mutations are able to produce a new function.

Probably you can find somewhere in the vast literature on evolution something similar. However as I write in post #31 I base my conclusion on three presumptions. Is any of these false? If not, the conclusion follows directly without any experiment. Besides, any experiment would require lot of things. For instance, you had to compare two experiments with the same probability P, one with two non-beneficial mutations and one with two beneficial mutations. Would be very difficult to attain and for what purpose?

Besides, again, the argument you have forwarded all the time is that the result of Lemski’s experiment with two non-benefical mutations blocks evolution with a great number of beneficial mutations. That is clearly false. The actual speed is of little interest.

Especially when the overwhelming majority of observed beneficial mutations degrade or remove genetic information instead of altering (like the malaria examples) or even more infrequently adding genetic information.

Beneficial mutations are indeed very uncommon. Especially when the environment isn’t changing. It’s not a law that there always are possible mutations that are beneficial. That’s why Behes statement in the OP is so astounding. The e coli bacteria has existed in more than one hundred million years. How could there be a lot of beneficial mutations that have never occurred long time ago appearing now in Lemski’s thirty year experiment.
Agree?

You didn’t answer my question.

(Below I added “A” and “B” for clarity)

But if, A, the observed behavior of evolution in nature and in the lab demonstrates that 5 or 6 non-beneficial mutations working together to perform a new function exceeds the capability of all life that has ever existed on this planet.
And if, B, there are a host of documented irreducibly complex biological organisms in nature that cannot be produced through a series of single beneficial mutations.

Yes.

Then, the observed behavior of evolution in nature and the lab does demonstrate that unguided evolution is incapable of producing the complex genetic code found in the DNA of life on our planet.

You say: If A then “unguided evolution is incapable of producing the complex genetic code found in the DNA of life on our planet.” That is quite misleading.

The correct wording is: If A and B then “unguided evolution is incapable of producing the complex genetic code found in the DNA of life on our planet.”

Now B is false. Show me any “documented irreducibly complex biological organisms in nature that cannot be produced through a series of single beneficial mutations” that is proven.

If B is false then your conclusion: “unguided evolution is incapable of producing the complex genetic code found in the DNA of life on our planet” also is false.

Nils wrote: ↑Sun Sep 19, 2021 2:16 pm

DBowling wrote: ↑Sun Sep 19, 2021 5:40 am
We have a real life example on the table of two mutations working together to form a new function in malaria's resistance to chloroquine.
Due to the exponential nature of the two mutations occurring, you presume that this particular example involves two non-beneficial mutations working together to perform a specific function.
And for the sake of argument I will stipulate to your presumption that malaria's resistance to chloroquine involves two non-beneficial mutations.

You also presume that two beneficial mutations will work together to perform a new function more rapidly and more frequently than two non-beneficial mutations working together to perform a new function.
I am asking for empirical evidence of this presumption. I am not saying it doesn't exist. I just want to see an example, so we can compare the rate at which two beneficial mutations produce a new function with the rate at which two non-beneficial mutations produce a new function.

We would start by finding a new function of some sort that requires two mutations working together (similar to malaria's resistance to chloroquine).
Then we would see if there is a midpoint where either of those two mutations produces a beneficial function by itself.
- If one of those two mutations provides a beneficial function by itself.
- And then a second mutation works together with that first mutation to provide a different beneficial function.
==> Then we will have our example and we can determine the rate at which two beneficial mutations are able to produce a new function.

Probably you can find somewhere in the vast literature on evolution something similar.

I haven't been able to find any examples.
And based on the malaria examples of resistance to atovaquone (1 in 10^12) and chloroquine (1 in 10^20), somewhere around 10^8 (or 100 million) examples of two beneficial mutations working together to provide a new function should have been produced within the timeframe that two non-beneficial mutations produced resistance to chloroquine.

However as I write in post #31 I base my conclusion on three presumptions. Is any of these false?

I believe I have already stipulated to those three premises.

If not, the conclusion follows directly without any experiment.

No it doesn't...
You still have the unverified presumption that the complex code found in the DNA of life today can be created by billions of single beneficial mutations.
We already have one example on the table that contradicts that that presumption.
We agree that malaria's resistance to chloroquine involves two non-beneficial mutations working together to perform a new function.

And if your presumption was true, there should be around 100 million examples of two beneficial mutations working together to provide a new function
for every single example of two non-beneficial mutations working together to provide a new function.

Since we have yet to see a single example of two beneficial mutations working together to provide a new function (where we would expect to see millions of examples), that demonstrates that the path to producing new functions with multiple mutations does not typically involve multiple beneficial mutations.
In fact... The only example we have on the table at the moment involves multiple non-beneficial mutations (not multiple beneficial mutations).

(Below I added “A” and “B” for clarity)

But if, A, the observed behavior of evolution in nature and in the lab demonstrates that 5 or 6 non-beneficial mutations working together to perform a new function exceeds the capability of all life that has ever existed on this planet.
And if, B, there are a host of documented irreducibly complex biological organisms in nature that cannot be produced through a series of single beneficial mutations.

Yes.

Then, the observed behavior of evolution in nature and the lab does demonstrate that unguided evolution is incapable of producing the complex genetic code found in the DNA of life on our planet.

You say: If A then “unguided evolution is incapable of producing the complex genetic code found in the DNA of life on our planet.” That is quite misleading.

The correct wording is: If A and B then “unguided evolution is incapable of producing the complex genetic code found in the DNA of life on our planet.”

I'll agree with your wording there

Now B is false. Show me any “documented irreducibly complex biological organisms in nature that cannot be produced through a series of single beneficial mutations” that is proven.

No it's not...

"Behe's original examples of irreducibly complex mechanisms included the bacterial flagellum of E. coli, the blood clotting cascade, cilia, and the adaptive immune system."
And there are many more examples, but for this discussion we don't need to go any farther than Behe's four original examples.

The only way to prove Behe is wrong is to provide a path of single beneficial mutations for all of Behe's examples of irreducibly complex biological mechanisms.
Show me where any scientist has produced a path of single beneficial mutations for any of Behe's original four examples of irreducibly complex mechanisms.
You won't find any examples of a path of single beneficial mutations producing an irreducibly complex biological mechanism, because no one has been able to come up with one.

Which brings me back to my conclusion,
(And I will defer to your wording)

But if, A, the observed behavior of evolution in nature and in the lab demonstrates that 5 or 6 non-beneficial mutations working together to perform a new function exceeds the capability of all life that has ever existed on this planet.
And if, B, there are a host of documented irreducibly complex biological organisms in nature that cannot be produced through a series of single beneficial mutations.
Then “unguided evolution is incapable of producing the complex genetic code found in the DNA of life on our planet.”