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:
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.