The strange case of John Sanford, creationist

[tas8831]

An old discussion between @leroy and myself lead me to search the forum for older discussions on the number of mutations between humans and chimps and the like, and in a couple year old post Leroy referred to John Sanford.
Sanford is a former legitimate scientist, who had worked as a research horticulturist at Cornell and had a couple of patents. Then he became a creationist. And man, creationists love patents for some reason.
Anyway, he eventually wrote a book (as all such folk usually do) that made a splash a few years ago (I will not name it for I do not want to generate any publicity for it), and someone on a forum I was on at the time quoted from it. I couldn't believe the quote was real, so I Googled it and found a web site had hosted a couple of chapters for an advertisement, I guess, available to read for free on it for a while when it came out. I read those, found the quote, and chuckled (on p. 128-9):

"Selection for 1,000 specific and adjacent mutations could not happen in 6 million years because that specific sequence of adjacent mutations would never arise, not even in 6 billion years."​

Think about that for a moment. Really think about it -

"...1,000 specific and adjacent mutations could not happen in 6 million years because that specific sequence of adjacent mutations would never arise..."


Surely I am not the only one who, upon reading that, immediately thought "STRAWMAN!!!"?

I mean, does he REALLY think that Haldane (or anyone else, ever) actually posited that new genes are needed in evolution, and that new genes are made 1 beneficial mutation at a time, right next to each other???


Now, some may think that I am taking him out of context to make another creationist look like an incompetent fool (which, it turns out, is actually pretty easy). I thought about this, and so searched for the quote again, and was able to find the entire book online (a plain text version, to be sure) for free under a different name. So, with context:

Waiting on “Haldane’s dilemma”.
Once that first mutation destined to become fixed within the population has finally occurred, it needs time to undergo selective amplification. A brand new mutation within a population of 10,000 people exists as only one nucleotide out of 20,000 alternatives (there are 20,000 nucleotides at that site, within the whole population). The mutant nucleotide must “grow” gradually within the population, either due to drift or due to natural selection. Soon there might be two copies of the mutant, then four, then 100, and eventually 20,000. How long does this process take? For dominant mutations, assuming very strong unidirectional selection, the mutant might conceivably grow within the population at a rate of 10% per generation. At this very high rate, it would still take roughly 105 generations (2,100 years) to increase from 1 to 20,000 copies (1.1 105 = 20,000).
However, mutation fixation takes much longer than this because selection is generally very weak, and most mutations are recessive and very subtle. When the mutation is recessive, or when selection is not consistently unidirectional or strong, this calculation is much more complex, but it is obvious that the fixation process would be dramatically slower. For example, an entirely recessive beneficial mutation, even if it could increase fitness by as much as 1%, would require at least 100,000 generations to fix (Patterson, 1999).

Haldane (1957), calculated that it would take (on average) 300 generations (>6,000 years) to select a single new mutation to fixation, given what he considered a “reasonable” mixture of recessive and dominant mutations. Selection at this rate is so slow that it is essentially the same as no selection at all. This problem
has classically been called “Haldane’s dilemma”. At this rate of selection, one could only fix 1,000 beneficial nucleotide mutations within the whole genome in the time since we supposedly evolved from chimps (6 million years). This simple fact has been confirmed independently by Crow and Kimura (1970), and ReMine (1993,2005). The nature of selection is such that selecting for one nucleotide reduces our ability to select for other nucleotides (selection interference). Simultaneous selection does not help.

NOTE - Interesting that he provided citations for the rate of fixation according to Haldane, even though this is not controversial, but for his mere assertion re: simultaneous selection, he offers...... Nothing....ReMine did the same thing thoughout his book - all sorts of citations for trivial issues, not a one for his zany creationist claims.


Can Natural Selection Create?

At first glance, the above calculation seems to suggest that one might at least be able to select for the creation of one small gene (of up to 1,000 nucleotides) in the time since we reputedly diverged
from chimpanzee. There are two reasons why this is not true. First, Haldane’s calculations were only for independent, unlinked mutations. Selection for 1,000 specific and adjacent mutations could not happen in 6 million years because that specific sequence of adjacent mutations would never arise, not even in 6 billion
years. One cannot select mutations that have not happened. Second, the vast bulk of a gene’s nucleotides are near-neutral and cannot be selected at all—not in any length of time. The bottom line of Haldane’s dilemma is selection to fix new beneficial mutations occurs at glacial speeds, and the more nucleotides under selection, the slower the progress. This severely limits progressive selection. Within reasonable evolutionary timeframes, we can only select for an extremely limited number of unlinked nucleotides. In the last 6 million years, selection could maximally fix 1,000 unlinked beneficial mutations, creating less new information than is on this page of text.* There is no way that such a small amount of information could transform an ape into a human....​

As the kids say, WHOOMP there it is! Context seals the deal (see the text in red).

How do we classify that - sleight of hand? Bait and switch? Strawman? Lie? Confusion factor?

To sum up - Haldane's model was about the time needed to fix beneficial mutations (i.e., mutant alleles, or genes that had acquired novel function via mutation) given the understanding at the time (1957). IF all of Haldane's parameters were 100% applicable to all large, slowly reproducing populations, he calculated that it would take 300 generations for that mutant allele to reach fixation (be present in all members) of a population. That is all. It was not REMOTELY about making a brand new gene one mutation at a time, so why did Sanford take the time to set up a scenario indicating how impossible THAT would be?
This was considered a 'dilemma' at the time due to the current beliefs/understandings - that humans had more than 100,000 genes, that evolution occurred only or primarily via selection, etc.

And a mere 1000 or so such mutations since we split from chimps? PREPOSTEROUS! Humans are so special and so different from the apes that there HAD to have been much much larger changes to explain it all! Or so Sanford's hero ReMine claimed (without evidence), and so Sanford perpetuates.

Couple of problems....

1. Not all population geneticists accepted Haldane's model as accurate or universally applicable. Warren Ewens, for example, said in an interview (italics mine):

"...There was an interest in two load concepts. The first was the mutational load, and interest in that concept came from the concern about genetic damage caused by atomic bombs. This was discussed in detail by the great geneticist Muller in 1950. Jim Neal and Jack Schull had gone to Japan shortly after the 1939-45 war to conduct an examination of the mutational effects of the atomic bomb. Their work on this matter was very well known, and so the question of how much genetic damage had been produced by the bomb was uppermost in many people’s minds. That damage became analyzed mathematically as a mutational load.

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

Interestingly, ReMine had interviewed Ewens for his 1993 book, but did not seem to care much about his disagreement with Haldane and Crow, for what are obvious reasons.

2. Experiments demonstrated that Haldane's model had flaws, 1 example:

Proc. Nat. Acad. Sci. USA Vol. 71, No. 10, pp. 3863-3865, October 1974
Solutions to the Cost-of-Selection Dilemma
(substitutional load/gene substitution/evolutionary rate)​

3. The notion that some large number of genetic changes is required to produced notable phenotypic change is false:

Am J Hum Genet. 1998 Sep;63(3):711-6.
Mutations in Fibroblast Growth-Factor Receptor 3 in Sporadic Cases of Achondroplasia Occur Exclusively on the Paternally Derived Chromosome

Abstract
More than 97% of achondroplasia cases are caused by one of two mutations (G1138A and G1138C) in the fibroblast growth factor receptor 3 (FGFR3) gene, which results in a specific amino acid substitution, G380R. ..​

I present that only to show that a single mutation can affect all limbs as well as the skull and other structures. No huge suite of mutations required.

I am shocked that Sanford would not have had the sense to do a lit review prior to writing his creationist pap.

 

[leroy]

An old discussion between @leroy and myself lead me to search the forum for older discussions on the number of mutations between humans and chimps and the like, and in a couple year old post Leroy referred to John Sanford.
Sanford is a former legitimate scientist, who had worked as a research horticulturist at Cornell and had a couple of patents. Then he became a creationist. And man, creationists love patents for some reason.
Anyway, he eventually wrote a book (as all such folk usually do) that made a splash a few years ago (I will not name it for I do not want to generate any publicity for it), and someone on a forum I was on at the time quoted from it. I couldn't believe the quote was real, so I Googled it and found a web site had hosted a couple of chapters for an advertisement, I guess, available to read for free on it for a while when it came out. I read those, found the quote, and chuckled (on p. 128-9):

"Selection for 1,000 specific and adjacent mutations could not happen in 6 million years because that specific sequence of adjacent mutations would never arise, not even in 6 billion years."​

Think about that for a moment. Really think about it -

"...1,000 specific and adjacent mutations could not happen in 6 million years because that specific sequence of adjacent mutations would never arise..."


Surely I am not the only one who, upon reading that, immediately thought "STRAWMAN!!!"?

I mean, does he REALLY think hat Haldane (or anyone else, ever) actually posited that new genes are needed in evolution, and that new genes are made 1 beneficial mutation at a time, right next to each other???


Now, some may think that I am taking him out of context to make another creationist look like an incompetent fool (which, it turns out, is actually pretty easy). I thought about this, and so searched for the quote again, and was able to find the entire book online (a plain text version, to be sure) for free under a different name. So, with context:

Waiting on “Haldane’s dilemma”.
Once that first mutation destined to become fixed within the population has finally occurred, it needs time to undergo selective amplification. A brand new mutation within a population of 10,000 people exists as only one nucleotide out of 20,000 alternatives (there are 20,000 nucleotides at that site, within the whole population). The mutant nucleotide must “grow” gradually within the population, either due to drift or due to natural selection. Soon there might be two copies of the mutant, then four, then 100, and eventually 20,000. How long does this process take? For dominant mutations, assuming very strong unidirectional selection, the mutant might conceivably grow within the population at a rate of 10% per generation. At this very high rate, it would still take roughly 105 generations (2,100 years) to increase from 1 to 20,000 copies (1.1 105 = 20,000).
However, mutation fixation takes much longer than this because selection is generally very weak, and most mutations are recessive and very subtle. When the mutation is recessive, or when selection is not consistently unidirectional or strong, this calculation is much more complex, but it is obvious that the fixation process would be dramatically slower. For example, an entirely recessive beneficial mutation, even if it could increase fitness by as much as 1%, would require at least 100,000 generations to fix (Patterson, 1999).

Haldane (1957), calculated that it would take (on average) 300 generations (>6,000 years) to select a single new mutation to fixation, given what he considered a “reasonable” mixture of recessive and dominant mutations. Selection at this rate is so slow that it is essentially the same as no selection at all. This problem
has classically been called “Haldane’s dilemma”. At this rate of selection, one could only fix 1,000 beneficial nucleotide mutations within the whole genome in the time since we supposedly evolved from chimps (6 million years). This simple fact has been confirmed independently by Crow and Kimura (1970), and ReMine (1993,2005). The nature of selection is such that selecting for one nucleotide reduces our ability to select for other nucleotides (selection interference). Simultaneous selection does not help.

NOTE - Interesting that he provided citations for the rate of fixation according to Haldane, even though this is not controversial, but for his mere assertion re: simultaneous selection, he offers...... Nothing....ReMine did the same thing thoughout his book - all sorts of citations for trivial issues, not a one for his zany creationist claims.


Can Natural Selection Create?

At first glance, the above calculation seems to suggest that one might at least be able to select for the creation of one small gene (of up to 1,000 nucleotides) in the time since we reputedly diverged
from chimpanzee. There are two reasons why this is not true. First, Haldane’s calculations were only for independent, unlinked mutations. Selection for 1,000 specific and adjacent mutations could not happen in 6 million years because that specific sequence of adjacent mutations would never arise, not even in 6 billion
years. One cannot select mutations that have not happened. Second, the vast bulk of a gene’s nucleotides are near-neutral and cannot be selected at all—not in any length of time. The bottom line of Haldane’s dilemma is selection to fix new beneficial mutations occurs at glacial speeds, and the more nucleotides under selection, the slower the progress. This severely limits progressive selection. Within reasonable evolutionary timeframes, we can only select for an extremely limited number of unlinked nucleotides. In the last 6 million years, selection could maximally fix 1,000 unlinked beneficial mutations, creating less new information than is on this page of text.* There is no way that such a small amount of information could transform an ape into a human....​

As the kids say, WHOOMP there it is! Context seals the deal (see the text in red).

How do we classify that - sleight of hand? Bait and switch? Strawman? Lie? Confusion factor?

To sum up - Haldane's model was about the time needed to fix beneficial mutations (i.e., mutant alleles, or genes that had acquired novel function via mutation) given the understanding at the time (1957). IF all of Haldane's parameters were 100% applicable to all large, slowly reproducing populations, he calculated that it would take 300 generations for that mutant allele to reach fixation (be present in all members) of a population. That is all. It was not REMOTELY about making a brand new gene one mutation at a time.
This was considered a 'dilemma' at the time due to the current beliefs/understandings - that humans had more than 100,000 genes, that evolution occurred only or primarily via selection, etc.

And a mere 1000 or so such mutations since we split from chimps? PREPOSTEROUS! Humans are so special and so different from the apes that there HAD to have been much much larger changes to explain it all! Or so Sanford's hero ReMine claimed (without evidence), and so Sanford perpetuates.

Couple of problems....

1. Not all population geneticists accepted Haldane's model as accurate or universally applicable. Warren Ewens, for example, said in an interview (italics mine):

"...There was an interest in two load concepts. The first was the mutational load, and interest in that concept came from the concern about genetic damage caused by atomic bombs. This was discussed in detail by the great geneticist Muller in 1950. Jim Neal and Jack Schull had gone to Japan shortly after the 1939-45 war to conduct an examination of the mutational effects of the atomic bomb. Their work on this matter was very well known, and so the question of how much genetic damage had been produced by the bomb was uppermost in many people’s minds. That damage became analyzed mathematically as a mutational load.

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

Interestingly, ReMine had interviewed Ewens for his 1993 book, but did not seem to care much about his disagreement with Haldane and Crow, for what are obvious reasons.

2. Experiments demonstrated that Haldane's model had flaws, 1 example:

Proc. Nat. Acad. Sci. USA Vol. 71, No. 10, pp. 3863-3865, October 1974
Solutions to the Cost-of-Selection Dilemma
(substitutional load/gene substitution/evolutionary rate)​

3. The notion that some large number of genetic changes is required to produced notable phenotypic change is false:

Am J Hum Genet. 1998 Sep;63(3):711-6.
Mutations in Fibroblast Growth-Factor Receptor 3 in Sporadic Cases of Achondroplasia Occur Exclusively on the Paternally Derived Chromosome

Abstract
More than 97% of achondroplasia cases are caused by one of two mutations (G1138A and G1138C) in the fibroblast growth factor receptor 3 (FGFR3) gene, which results in a specific amino acid substitution, G380R. ..​

I present that only to show that a single mutation can affect all limbs as well as the skull and other structures. No huge suite of mutations required.

I am shocked that Sanford would not have had the sense to do a lit review prior to writing his creationist pap.

Ok if creationist can only do strawmans and false assumptions.... Why don you provide your own correct model with correct assumptions, and show that humans and chimps could have evolved from a common ancestor 5Mya through the mechanism of random mutations and natural selection.

Or you can simply admit that such model doesn't exist

 

[shunyadragon]

Ok if creationist can only do strawmans and false assumptions.... Why don you provide your own correct model with correct assumptions, and show that humans and chimps could have evolved from a common ancestor 5Mya through the mechanism of random mutations and natural selection.

Or you can simply admit that such model doesn't exist

The assumption that 'the whole process of evolution is random,' is an old fallacy used by Creationist for many years. There calculations of Creationists assume that the statistically probability of the whole process over a long period of time can be assumed as random, and the probability of the whole process in time is calculated as random, and that is not the case. The only thing that is random in the genetics of evolution is the outcome of the timing of individual mutations 'within a limited range of outcomes.The natural process of the outcome of the chain of cause and effect outcomes of mutation are determined by the Laws of Nature, the environment and natural chain of cause and effect mutations limited by the nature of the chemistry of genetics. I have provided sources in the past that demonstrated that the statistics of Creationist is as phony as frogs hair and bull from wings.

If what the describe as randomness as the Creationist believe is true life could not evolve even on the micro scale. The observed randomness in recent history and the genetic evidence in recent geologic history demonstrates the Creationist assumptions are false, and a bogus ENRON Probability game to justify their agenda..

The two articles addressed this, so I put it in simple blunt words.

 

[leroy]

The assumption that 'the whole process of evolution is random,' is an old fallacy used by Creationist for many years. There calculations of Creationists assume that the statistically probability of the whole process over a long period of time can be assumed as random, and the probability of the whole process in time is calculated as random, and that is not the case. The only thing that is random in the genetics of evolution is the outcome of the timing of individual mutations 'within a limited range of outcomes.The natural process of the outcome of the chain of cause and effect outcomes of mutation are determined by the Laws of Nature, the environment and natural chain of cause and effect mutations limited by the nature of the chemistry of genetics. I have provided sources in the past that demonstrated that the statistics of Creationist is as phony as frogs hair and bull from wings.

If what the describe as randomness as the Creationist believe is true life could not evolve even on the micro scale. The observed randomness in recent history and the genetic evidence in recent geologic history demonstrates the Creationist assumptions are false, and a bogus ENRON Probability game to justify their agenda..

Ok creationist don't know how to calculate probabilities....


That is why I am giving you the opportunity to do your own math and your own probabilities and show that the mechanism of random mutation + natural selection can explain the differences of chimps and humans

 

[shunyadragon]

Ok if creationist can only do strawmans and false assumptions...

Yes, it more than that. It the unethical use of statistics and. Why don you provide your own correct model with correct assumptions, and show that humans and chimps could have evolved from a common ancestor 5Mya through the mechanism of random mutations and natural selection.

Or you can simply admit that such model doesn't exist

First, you lack the education in genetics and paleontology to understand the science and models you are requesting and the scientific references supporting evolution have been provided,\ Second, you have a religious agenda that up front rejects the science of abiogenesis and evolution.

Again . . . What are your qualifications in the sciences that apply to abiogenesis and evolution to even understand the answers to the questions you repeated ask, but reject the references provided?

 

[tas8831]

Ok if creationist can only do strawmans and false assumptions..

If you say so. I do not find it OK at all. I find it sad.

.. Why don you provide your own correct model with correct assumptions, and show that humans and chimps could have evolved from a common ancestor 5Mya through the mechanism of random mutations and natural selection.

Sure - right after you stop relying on long-ago refuted nonsense and present an evidence-backed model for 'Intelligent Design' of both chimps and humans with an explanation of why there are so many shared unique mutations between them.

Or you can simply admit that such model doesn't exist

Yes, I fully admit that your model does not exist.


So... nothing on topic?

 

[leroy]

First, you lack the education in genetics and paleontology to understand the science and models you are requesting and the scientific references supporting evolution have been provided,\ Second, you have a religious agenda that up front rejects the science of abiogenesis and evolution.

Again . . . What are your qualifications in the sciences that apply to abiogenesis and evolution to even understand the answers to the questions you repeated ask, but reject the references provided?

Really? More excuses to avoid an answer?

 

[shunyadragon]

Ok creationist don't know how to calculate probabilities....


That is why I am giving you the opportunity to do your own math and your own probabilities and show that the mechanism of random mutation + natural selection can explain the differences of chimps and humans

You have refused to acknowledge the long list of references in the past you apparently do not understand, and reject up front base don your religious agenda.

Simply evolution takes place under natural environment selective pressure in the genetic diversity within a populations developed over time by genetic drift in the populations. The individual mutations only contribute to the genetic diversity, and they do not cause the changes in the populations that lead to change due to adaptive pressures of the environment.

 

[shunyadragon]

Really? More excuses to avoid an answer?

Again . . . What are your qualifications in the sciences that apply to abiogenesis and evolution to even understand the answers to the questions you repeated ask, but reject the references provided?

You have refused to acknowledge the long list of references in the past you apparently do not understand, and reject up front base don your religious agenda.

Simply evolution takes place under natural environment selective pressure in the genetic diversity within a populations developed over time by genetic drift in the populations. The individual mutations only contribute to the genetic diversity, and they do not cause the changes in the populations that lead to change due to adaptive pressures of the environment.

 

[leroy]

If you say so. I do not find it OK at all. I find it sad.

Sure - right after you stop relying on long-ago refuted nonsense and present an evidence-backed model for 'Intelligent Design' of both chimps and humans with an explanation of why there are so many shared unique mutations between them.

Yes, I fully admit that your model does not exist.


So... nothing on topic?

Sure, sure, and when are you going to provide your proof?

 

[leroy]

Again . . . What are your qualifications in the sciences that apply to abiogenesis and evolution to even understand the answers to the questions you repeated ask, but reject the references provided?

You have refused to acknowledge the long list of references in the past you apparently do not understand, and reject up front base don your religious agenda.

Simply evolution takes place under natural environment selective pressure in the genetic diversity within a populations developed over time by genetic drift in the populations. The individual mutations only contribute to the genetic diversity, and they do not cause the changes in the populations that lead to change due to adaptive pressures of the environment.

Ok you explained how is evolution suppose to work..... Now can you show that the mechanism that you described can account for the differences between chimps and humans?

 

[tas8831]

Ah, what the heck - it only took 2 minutes to find some references...

Estimated mammalian mutation rate:

2.2x10^-9/site/year =

(2.2x10^-9)x 3,000,000 sites = 6.6/yr x 5 million years = 33,000,000


Isn't that amazing!!??

Now, it is not as simple as all that, of course, but given the numbers YOU put forth, it looks like plain old nature 'explains' it.

Now, that is based on your number that we are 99% similar genetically. True, in most genes we are on the order of 99% similar, but in noncoding DNA we are less than that, so closer to 96% overall (where we can do site-by-site analyses).

So that means more like a difference of 120 million. Uh oh! Big trouble for evolution, right?

Not really.
1. Humans and chimps have the same general mutation rate, so we have to divide that by 2:

60 million.

Still trouble, right?

2. Not really - that mutation rate is only for SNPs. Indel polymorphisms likely represent up to ~2 million indels, some of which can be up to several kB in length.

3. Then there are transposons, which account for around 33 megabases. Many of these are shared between humans and chimps, but those that are not round out the overall difference generally.

4. AND transposons tend to insert in genes, promoters, etc., likely due to site recognition (sequence similarity), so they can account for some phenotypic change as well.


This is not a scholarly work - as I indicated, it took me just a couple of minutes to find a few relevant sources, glean a few numbers, and patch together a plain old evolution-safe numerical explanation. Some of the refs were on the older side, so some specific numbers are likely not up to date, but so what?

YOUR "argument" is based on just multiplying genome size by a percent and demanding that we explain it. At least I am not relying on the documented (see the OP) farce that is creation 'science' fake news.

Still waiting for YOUR 'proof.'

 

[shunyadragon]

Ok you explained how is evolution suppose to work..... Now can you show that the mechanism that you described can account for the differences between chimps and humans?

Supposed to work? That is how evolution is observed to work.

There is no change from Chimps to humans. They share common ancestors. The changes in the environments in Africa from foerst to open plains favored upright posture being able to walk large distances and run, larger intelligent brains, and ultimately cooperative tribal behavior.

 

[tas8831]

Ok you explained how is evolution suppose to work..... Now can you show that the mechanism that you described can account for the differences between chimps and humans?

Can you show your evidence-supported model for how IDCreation made humans and chimps?

 

[shunyadragon]

Ok creationist don't know how to calculate probabilities.

Well, ah . . . they know how to calculate probabilities very well. The problem is the assumptions that they based calculations on their desire to justify their religious creationist beliefs, and not science..

 

[leroy]

Ah, what the heck - it only took 2 minutes to find some references...

Estimated mammalian mutation rate:

2.2x10^-9/site/year =

(2.2x10^-9)x 3,000,000 sites = 6.6/yr x 5 million years = 33,000,000

Your math seems wrong (or perhaps I am the one who cant understand what you are trying to represent)

But assuming a mutation rate of 2.2x10^-9/site/year you need 23M years to accumulate 30,000,000 mutations (or 1% of the human/ape genome)

but irrelevant lets simply agree on that the "human line" evolved faster that average ¿ok? (answer yes or no)

Now, it is not as simple as all that, of course, but given the numbers YOU put forth, it looks like plain old nature 'explains' it.

Now, that is based on your number that we are 99% similar genetically. True, in most genes we are on the order of 99% similar, but in noncoding DNA we are less than that, so closer to 96% overall (where we can do site-by-site analyses).

So that means more like a difference of 120 million. Uh oh! Big trouble for evolution, right?

Not really.
1. Humans and chimps have the same general mutation rate, so we have to divide that by 2:

60 million.

Still trouble, right?

2. Not really - that mutation rate is only for SNPs. Indel polymorphisms likely represent up to ~2 million indels, some of which can be up to several kB in length.


This is not a scholarly work - as I indicated, it took me just a couple of minutes to find a few relevant sources, glean a few numbers, and patch together a plain old evolution-safe numerical explanation. Some of the refs were on the older side, so some specific numbers are likely not up to date, but so what?

YOUR "argument" is based on just multiplying genome size by a percent and demanding that we explain it. At least I am not relying on the documented (see the OP) farce that is creation 'science' fake news.

Still waiting for YOUR 'proof.'

The relevant point is that you don’t seem to understand my point, yes sure we both agree that humans and chimps evolved from a common ancestor and that all mammals share a common ancestor, and given the “molecular clocks” described in the paper, the average speed of evolution would be 2.2x10^-9/site/year.

The point is that you have to show that the mechanism of random mutation natural selection and genetic drift (Darwinism) are mainly responsible for this “evolution” my point is and has always been that given that the speed of evolution is much faster than the speed that would be possible by the mechanism of random mutation natural selection and genetic drift, there must be other nonrandom mechanisms that made mayor contributions to the process of evolution (being Darwinism just a minor contributor)

But feel free to prove me wrong, my statement is testable, all you have to do is show that “Darwinism” can account for such a fast speed of evolution in mammals.

3. Then there are transposons, which account for around 33 megabases. Many of these are shared between humans and chimps, but those that are not round out the overall difference generally.

4. AND transposons tend to insert in genes, promoters, etc., likely due to site recognition (sequence similarity), so they can account for some phenotypic change as well.

Yes, that is part of my point “transposons” while the can contribute to the diversity of the genome and can create very fast changes in the phenotype in a very small little amount of time, this mechanism is not random

My point is and has always been that organism changing and adapt mainly by nonrandom mechanism (being random mutations just a minor contributor) Trasposons is just 1 of many other non random mechanism that could have played a mayor role.

Given that you seem to believe that organisms evolve mainly by random mutations and natural selection (Darwinism) you have to show that this mechanism is enough to account for the speed of evolution in mammals describe in your paper. (or correct me if I am misrepresenting your view)

 

[leroy]

Can you show your evidence-supported model for how IDCreation made humans and chimps?

Can you show your evidence-supported model for how IDCreation made humans and chimps?

No, I cant,

But the evidence seems to be consistent with the idea that evolution was caused mainly by non random variation, if you would affirm the opposite (random mutations are the mayor contributor) we can have a discussion where you present your arguments and I present mine.



By this is what I mean by random (just anticipating possible semantic games from your part)

Factors in the environment are thought to influence the rate of mutation but are not generally thought to influence the direction of mutation. For example, exposure to harmful chemicals may increase the mutation rate, but will not cause more mutations that make the organism resistant to those chemicals. In this respect, mutations are random — whether a particular mutation happens or not is generally unrelated to how useful that mutation would be.
Mutations are random

 

[leroy]

Well, ah . . . they know how to calculate probabilities very well. The problem is the assumptions that they based calculations on their desire to justify their religious creationist beliefs, and not science..

Ok, then make the correct assumptions and calculate the correct probabilities.

 

[leroy]

Supposed to work? That is how evolution is observed to work.

There is no change from Chimps to humans. They share common ancestors. The changes in the environments in Africa from foerst to open plains favored upright posture being able to walk large distances and run, larger intelligent brains, and ultimately cooperative tribal behavior.

Well then show that random mutations (rather than othe rmechanisms) where mainly responsible for larger brains, upright posture, cooperative behavior etc.

 

[Dan From Smithville]

An old discussion between @leroy and myself lead me to search the forum for older discussions on the number of mutations between humans and chimps and the like, and in a couple year old post Leroy referred to John Sanford.
Sanford is a former legitimate scientist, who had worked as a research horticulturist at Cornell and had a couple of patents. Then he became a creationist. And man, creationists love patents for some reason.
Anyway, he eventually wrote a book (as all such folk usually do) that made a splash a few years ago (I will not name it for I do not want to generate any publicity for it), and someone on a forum I was on at the time quoted from it. I couldn't believe the quote was real, so I Googled it and found a web site had hosted a couple of chapters for an advertisement, I guess, available to read for free on it for a while when it came out. I read those, found the quote, and chuckled (on p. 128-9):

"Selection for 1,000 specific and adjacent mutations could not happen in 6 million years because that specific sequence of adjacent mutations would never arise, not even in 6 billion years."​

Think about that for a moment. Really think about it -

"...1,000 specific and adjacent mutations could not happen in 6 million years because that specific sequence of adjacent mutations would never arise..."


Surely I am not the only one who, upon reading that, immediately thought "STRAWMAN!!!"?

I mean, does he REALLY think that Haldane (or anyone else, ever) actually posited that new genes are needed in evolution, and that new genes are made 1 beneficial mutation at a time, right next to each other???


Now, some may think that I am taking him out of context to make another creationist look like an incompetent fool (which, it turns out, is actually pretty easy). I thought about this, and so searched for the quote again, and was able to find the entire book online (a plain text version, to be sure) for free under a different name. So, with context:

Waiting on “Haldane’s dilemma”.
Once that first mutation destined to become fixed within the population has finally occurred, it needs time to undergo selective amplification. A brand new mutation within a population of 10,000 people exists as only one nucleotide out of 20,000 alternatives (there are 20,000 nucleotides at that site, within the whole population). The mutant nucleotide must “grow” gradually within the population, either due to drift or due to natural selection. Soon there might be two copies of the mutant, then four, then 100, and eventually 20,000. How long does this process take? For dominant mutations, assuming very strong unidirectional selection, the mutant might conceivably grow within the population at a rate of 10% per generation. At this very high rate, it would still take roughly 105 generations (2,100 years) to increase from 1 to 20,000 copies (1.1 105 = 20,000).
However, mutation fixation takes much longer than this because selection is generally very weak, and most mutations are recessive and very subtle. When the mutation is recessive, or when selection is not consistently unidirectional or strong, this calculation is much more complex, but it is obvious that the fixation process would be dramatically slower. For example, an entirely recessive beneficial mutation, even if it could increase fitness by as much as 1%, would require at least 100,000 generations to fix (Patterson, 1999).

Haldane (1957), calculated that it would take (on average) 300 generations (>6,000 years) to select a single new mutation to fixation, given what he considered a “reasonable” mixture of recessive and dominant mutations. Selection at this rate is so slow that it is essentially the same as no selection at all. This problem
has classically been called “Haldane’s dilemma”. At this rate of selection, one could only fix 1,000 beneficial nucleotide mutations within the whole genome in the time since we supposedly evolved from chimps (6 million years). This simple fact has been confirmed independently by Crow and Kimura (1970), and ReMine (1993,2005). The nature of selection is such that selecting for one nucleotide reduces our ability to select for other nucleotides (selection interference). Simultaneous selection does not help.

NOTE - Interesting that he provided citations for the rate of fixation according to Haldane, even though this is not controversial, but for his mere assertion re: simultaneous selection, he offers...... Nothing....ReMine did the same thing thoughout his book - all sorts of citations for trivial issues, not a one for his zany creationist claims.


Can Natural Selection Create?

At first glance, the above calculation seems to suggest that one might at least be able to select for the creation of one small gene (of up to 1,000 nucleotides) in the time since we reputedly diverged
from chimpanzee. There are two reasons why this is not true. First, Haldane’s calculations were only for independent, unlinked mutations. Selection for 1,000 specific and adjacent mutations could not happen in 6 million years because that specific sequence of adjacent mutations would never arise, not even in 6 billion
years. One cannot select mutations that have not happened. Second, the vast bulk of a gene’s nucleotides are near-neutral and cannot be selected at all—not in any length of time. The bottom line of Haldane’s dilemma is selection to fix new beneficial mutations occurs at glacial speeds, and the more nucleotides under selection, the slower the progress. This severely limits progressive selection. Within reasonable evolutionary timeframes, we can only select for an extremely limited number of unlinked nucleotides. In the last 6 million years, selection could maximally fix 1,000 unlinked beneficial mutations, creating less new information than is on this page of text.* There is no way that such a small amount of information could transform an ape into a human....​

As the kids say, WHOOMP there it is! Context seals the deal (see the text in red).

How do we classify that - sleight of hand? Bait and switch? Strawman? Lie? Confusion factor?

To sum up - Haldane's model was about the time needed to fix beneficial mutations (i.e., mutant alleles, or genes that had acquired novel function via mutation) given the understanding at the time (1957). IF all of Haldane's parameters were 100% applicable to all large, slowly reproducing populations, he calculated that it would take 300 generations for that mutant allele to reach fixation (be present in all members) of a population. That is all. It was not REMOTELY about making a brand new gene one mutation at a time, so why did Sanford take the time to set up a scenario indicating how impossible it would be?
This was considered a 'dilemma' at the time due to the current beliefs/understandings - that humans had more than 100,000 genes, that evolution occurred only or primarily via selection, etc.

And a mere 1000 or so such mutations since we split from chimps? PREPOSTEROUS! Humans are so special and so different from the apes that there HAD to have been much much larger changes to explain it all! Or so Sanford's hero ReMine claimed (without evidence), and so Sanford perpetuates.

Couple of problems....

1. Not all population geneticists accepted Haldane's model as accurate or universally applicable. Warren Ewens, for example, said in an interview (italics mine):

"...There was an interest in two load concepts. The first was the mutational load, and interest in that concept came from the concern about genetic damage caused by atomic bombs. This was discussed in detail by the great geneticist Muller in 1950. Jim Neal and Jack Schull had gone to Japan shortly after the 1939-45 war to conduct an examination of the mutational effects of the atomic bomb. Their work on this matter was very well known, and so the question of how much genetic damage had been produced by the bomb was uppermost in many people’s minds. That damage became analyzed mathematically as a mutational load.

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

Interestingly, ReMine had interviewed Ewens for his 1993 book, but did not seem to care much about his disagreement with Haldane and Crow, for what are obvious reasons.

2. Experiments demonstrated that Haldane's model had flaws, 1 example:

Proc. Nat. Acad. Sci. USA Vol. 71, No. 10, pp. 3863-3865, October 1974
Solutions to the Cost-of-Selection Dilemma
(substitutional load/gene substitution/evolutionary rate)​

3. The notion that some large number of genetic changes is required to produced notable phenotypic change is false:

Am J Hum Genet. 1998 Sep;63(3):711-6.
Mutations in Fibroblast Growth-Factor Receptor 3 in Sporadic Cases of Achondroplasia Occur Exclusively on the Paternally Derived Chromosome

Abstract
More than 97% of achondroplasia cases are caused by one of two mutations (G1138A and G1138C) in the fibroblast growth factor receptor 3 (FGFR3) gene, which results in a specific amino acid substitution, G380R. ..​

I present that only to show that a single mutation can affect all limbs as well as the skull and other structures. No huge suite of mutations required.

I am shocked that Sanford would not have had the sense to do a lit review prior to writing his creationist pap.

By old discussion, it appears you mean where @leroy claims science is wrong and ID is right, but refuses to support that while doing everything to shift the burden of proof. That is what I see growing here.