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The ‘Random Genetic Drift’ Fallacy

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I finished reading Provine’s last book a few weeks ago, and have meant to post something about it ever since.

In his book, The ‘Random Genetic Drift’ Fallacy, Provine hammers his main thesis over and over: that is, that genetic changes in small populations occur not because of “random genetic drift,” but because of “inbreeding.”

The entire book is meant to show that the entirety of population genetics is based on a basic misunderstanding by Sewell Wright of what was happening in populations, a misunderstanding that allowed R.A. Fisher’s analysis to prevail, a model of alleles mutating around a specific gene location, or locus, which, IIRC, he called F.

Provine says over and over again that descendants don’t inherit this locus F and its mutants, but actual chromosomes.

Because of a lack of clarity in his central claim, I would advise anyone reading the book to read Chapter Six after Chapter One, and then to go back and read the intervening chapters, and then the final chapter.

I was planing out laying out Provine’s fundamental assertions, and the implications that go with it, but while looking around for some reviews of Provine’s work I found one that was so keen, and that captured all the elements of the book—a review by a population geneticist who knew Provine—that I’ll just include a link.

Here it is. You can see that Provine thinks that the fundamental assertion of the Modern Synthesis, made by Fisher, misses the mark.

Bob: Most distributions are a version or other of the gaussian, as is the binomial. See here for example. PaV
The broad picture of evolution may be right but it is untestable and because of that outside of science. Virgil Cain
Neil - your idea about small population looks rather like Wright's shifting balance idea, although he invokes drift rather than inbreeding. I can't see why population genetics wouldn't be useful in this situation - indeed, Coyne, Barton & Turelli developed a model for precisely that and showed that Wright's verbal model only worked in a narrow parameter range). PaV - the “statistical filtering” in genetic drift invokes binomial (and multinonial) distributions, rather than Gaussian. Bob O'H
Neil: I'm not a mathematician, but have studied a fair amount of it here and there. I have an intuitive sense of what you mean by "statistical filtering," and am assuming that this invokes Gaussian distributions and such. From this sense, I think I would agree with you, and find the very same problem: adaptation=microevolution (with NS passively involved) is reasonable; but no one has made a case, as far as I can see, for macroevolution. I think as a mathematician you might like Hoyle's book. He uses a path-integral approach---which is more a technique used by physicists (or, in Hoyle's case, astrophysics) than mathematicians---but he does get interesting results, many of which are the very same that standard pop. gen. comes up with. And his final numbers suggest that a genome can move a few 'steps' in either direction, but must fluctuate around some norm---which sounds a lot like your 'statistical filtering.' Give it a read. PaV
Replying to PaV:
But, bottom line, pop. gen. needs to be rethought almost in its entirety.
I agree with that. I'm a mathematician. So when I first heard of evolution (in high school), I tried some amateur population genetics. It did not seem persuasive to me. The kind of statistical filtering that it requires seemed too weak to account for the diversity we find in the biosphere. A few years later, I read Watson's "The Double Helix". That's what convinced that the broad picture of evolution was right. But I still had doubts about the neo-Darwinian account, which is why I don't consider myself a Darwinist. My current view is that the statistical filtering of NS can account for some of the change, such as gradual change in horses. But it cannot, by itself, account for all of the diversity we see. It seems to me that the diversity depends a great deal on small populations which happen to be successful. That's where inbreeding would be involved. And I don't see population genetics as giving a useful account of that. Neil Rickert
vjtorley: The reason I bought and read Provine's book was because of Larry Moran's review. The crux of the matter comes down to how we interpret the following, and, in particular, the bolded section: (from Moran's review, quoting Suzuki and Griffiths)
If a population is finite in size (as all populations are) and if a given pair of parents have only a small number of offspring, then even in the absence of all selective forces, the frequency of a gene will not be exactly reproduced in the next generation because of sampling error. If in a population of 1000 individuals the frequency of "a" is 0.5 in one generation, then it may by chance be 0.493 or 0.505 in the next generation because of the chance production of a few more or less progeny of each genotype. In the second generation, there is another sampling error based on the new gene frequency, so the frequency of "a" may go from 0.505 to 0.501 or back to 0.498. This process of random fluctuation continues generation after generation, with no force pushing the frequency back to its initial state because the population has no "genetic memory" of its state many generations ago. Each generation is an independent event. The final result of this random change in allele frequency is that the population eventually drifts to p=1 or p=0. After this point, no further change is possible; the population has become homozygous. A different population, isolated from the first, also undergoes this random genetic drift, but it may become homozygous for allele "A", whereas the first population has become homozygous for allele "a". As time goes on, isolated populations diverge from each other, each losing heterozygosity. The variation originally present within populations now appears as variation between populations.
Random genetic drift, per the bolded section, is, as Provine says, a measure of 'inbreeding,' or, equivalently, a reduction in variation. Wright and Haldane, conforming their thought to Fisher's model, all insist that this reduction of variation is caused directly by RGD (random genetic drift). Provine is saying, "Wait a second. Let's look at the actual experiments that were done and which, purportedly, support the view that RGD is at work. When we do this, we are really seeing something else at work. We're seeing the reduction of variation due to the 'inbreeding' taking place in the studied populations. This is exactly what 'inbreeding' does: it brings about 'fixation' of genes through the loss of chromosomes which are "different" from the line being 'inbred.'" Provine goes through all of these experiments. He is right in what he says principally because of this: everyone knows, especially breeders, that 'inbreeding' causes a loss of 'vigor,' and will cause inbred populations to collapse. The tell-tale indicator that Provine uses in analyzing these historical experiments is this 'collapse' of populations. When you look at the studies, we find 'fixation;' but we also find that a great number of the populations being studied simply died off; i.e., they "collapsed" due to a lack of vigor. IOW, 'inbreeding.' This central and critical interpretation of the entire history of pop. gen. (Provine's specialty) and the foundational experimental studies that undergird it (and Provine is well-informed here; more so than perhaps anyone else) undermines the entire structure of modern day pop. gen.. Again from Moran's review, quoting Provine:
Having no "random genetic drift" in evolution harms the neutral theories, No matter how we approach the neutral theories, "random genetic drift" is the crucial variable, and does not exist. I can see no way to preserve the neutral theory in population genetics."
If someone wants to impugn Provine, then they need to look through these experiments and tell us why Provine's insistence that they can only be interpreted as 'inbreeding' is wrong. PaV
Neil Rickert: I agree 100% with what Virgil Cain says about "contingent serendipity." Without NS, you have to believe life happened completely by chance. This, of course, requires a much greater amount of faith than is required by a theist. I would agree with you, Neil, that Provine doesn't talk much about 'meiosis.' I scratched my head some, and said: "Why doesn't he make this more explicit?" This is why I suggested reading chapter six after chapter one--you get a better idea of what Provine means. I think Provine takes this tack because he feels he doesn't have to say more than, "this is not random genetic drift; this is inbreeding," or something to that effect, which becomes his mantra. Provine book helped me in two ways, with one being related to the other. First, he helped clarify why I find population genetics so confusing at times. It's because the model they use is defective, and, also because this model has been employed---wrongly per Provine---from the very beginning. Second, it helped make sense of Fred Hoyle's abandonment of population genetics entirely. He said that none of it made sense to him. So, in The Mathematics of Evolution, he began from scratch. The problem with the 'allele' model that pop. gen. uses is that it treats it as if it is completely independent of the chromosome---a point you make. In my mind, there is something terribly wrong with pop. gen., and it has a huge part to due with R.A. Fisher. He was a mathematician, not a biologist, and the model he employed is almost completely devoid of any biological facts. With each passing year, his model becomes even more problematic. In a nutshell, here's the problem: Fisher considers "fitness" in terms of the organism as a whole, and does not mathematically make any provision for the reality of 'meiosis.' This is Provine's principal point: Fisher was wrong from the beginning; Sewell Wright bought the package, and applied his knowledge of inheritance to build a model based on Fisher's, and that his model is fundamentally flawed. So, in particular, here is the problem as I see it: EACH chromosome has a 'fitness' of its own. This is a simple, yet profound statement. Rather, per Fisher, treating the entire 'organism' as a 'jar of marbles,' EACH chromosome should be treated in this fashion. Now, various parts of the chromosome can be changed around via recombination, which does have a 'fitness' effect, but is, IMHO, only a secondary reason for recombination, the 'conservation' of genetic information being the primary reason why recombination takes place. When viewed in this way, then we're right back to what modern biology seems to be saying to us: 'Adapation' involves a lowering of 'fitness.' (cf. Behe's First Rule of Adaptation). Further, if we consider that for humans, e.g., there are considered to be 10,000 coding sections in the genome, then dividing by 23 (one part of the genome from each parent), we get around 400 genes per chromosome, and this suggests that the 'fitness' of each chromosome involves the 'relative fitness' of each of these 400 genes. Presumably, these genes osciallate around some mean value of 'fitness,' so then the, let's say, "average fitness" of the chromosome should be the sum of the individual 'fitness' divided by 400. Viewed this way, of course, it becomes quite clear why any one gene would be, let us say, almost 'nearly neutral' in its effect. There is more to be said, having to do with the fundamental limitations of Fisher's model, limitations which point to a conservation of genetic information, and not to increased genetic variation, which is the hallmark of Fisher's Fundamental Theorem of Natural Selection. Perhaps we'll leave that for another OP. But, bottom line, pop. gen. needs to be rethought almost in its entirety. PaV
Meiosis- another cellular process that unguided evolution cannot account for. BTW Neil, unguided evolution is all contingency- contingent serendipity. Also natural selection is still the only proposed mechanism capable of producing the appearance of design. However reality has failed to demonstrate that is true. So where does Neil want Neil want to put the emphasis? Is it magic, Neil? Virgil Cain
I read Provine's book a while ago, and posted a review. I found it interesting. However, I'm not at all sure why Pav thought it relevant to what is usually discussed at UD. And it is still not entirely clear why Provine wrote this book. He clearly has strong views on the issue, but he did not explain his motivation. Some evolutionists deny that they are darwinists. I am one of those deniers. Some of those who separate themselves from Darwinism, argue that most evolution is due to random genetic drift, though that's not my reason for not being a Darwinist. (I just want to put the emphasis somewhere other than natural selection). Presumably Provine thinks that there's a problem for those who say that most evolution is neutral drift. Perhaps Provine is a pan-selectionist, but I could not tell that from the book. Those who say that evolution is mostly random drift are often motivated by Gould's mention of "contingency". But if evolution is driven by small populations becoming reproductively isolated, and then inbreeding, that would still be due to contingencies. So whether we call it "inbreeding" or "neutral drift" would not seem to be very important. For me, the more important part of Provine's book is toward the end where he criticizes population genetics. I think he is correct there, though I have not kept up with the literature on population genetics. It is common when doing mathematical modeling, to make simplifications that make it easier to model. I would guess that population geneticists are well aware that they are doing this. The test is how well their predictions work. Provine seems to believe that there is a problem there. Provine also mentions meiosis, but he does not spend a lot of time on that. I think that's unfortunate, for I agree with Provine that meiosis is important in mixing up the genes and maintaining variation in a population. The population geneticists probably see this mixing up as being the basis for talking of a gene pool, from which selections are made. But what happens, due to meiosis, is that a pair of genes that are close together on the chromosome will usually be inherited as a pair, while when the two genes are further apart, they are more likely to be separated in a crossover event, so inherited more independently. This suggests some importance of the way that genes are organized into chromosomes. Neil Rickert
Hi PaV, Thanks for this very interesting post. Apparently Professor Larry Moran has reviewed the book as well: http://sandwalk.blogspot.jp/2015/08/william-provine-doesnt-like-random.html vjtorley
While I have not read Provine's objection to neutral genetic drift, I have read the critique by Jensen and the comments here particularly focusing on recombination. So I really don't know what Provine was trying to get across. What follows is my take on the situation following the lead of what I have just read and (think) I know. If, for example, a phenotype change requires two adjacent amino acids to be changed in an exon, can recombination effectively move the changes that might arise in two separate lines into the same exon (within the same chromosome) in a single line? Or, must the two changes arise in the same line to be paired up, effectively meaning that one of the two changes is irrelevant (since it may never get paired with the other necessary amino acid change. What if several nearby changes are required on a single exon? Does that render all but one change in a single line, the one that is eventually complemented by all the other required changes, irrelevant? How about when a new phenotype requires a chromosome have multiple nearby genes to have multiple exons that have multiple nearby amino acid changes? If the latter is the case, does the math supporting the neutral genetic drift theory, in its current form, take the effect of that situation into account at all? If it does, does it do it sufficiently and correctly? Has the theory been properly challenged by empirical studies? From what I (think I) know, I find it hard to believe that the situation where a new phenotype requires a number of gene modifications that none (or so few as to make the point mute) of them would require multiple amino acid changes in relatively close proximity or that recombination would have no difficulty completely unlinking close amino acid changes so that the "marbles in a jar" would be an accurate representation of the situation. Was Provine thinking along the same lines? If so, I can see his point. Has the issue been adequately considered and properly addressed in the current theory but Provine was not up to speed? Does invoking recombination, something I find hard to believe Provine was unaware of, really cover the situation so well as to make Provine's point (if I am not off track here) absurd? Do any of the naysayers to Provine's point (if I am on point) have any further information or comment? Stephen SteRusJon
Provine was talking about fixation of 'alleles', which, as far as I know, is the way pop. gen. says is how speciation takes place. But why don't you read the book and find out exactly what Provine wrote? From the review:
[Provine] chronicles numerous experiments that claim to have produced allelic fixation via random genetic drift but which are clearly examples of inbreeding leading to loss of chromosomal diversity. Interestingly many of these studies were performed in Drosophila, which often maintain unusually high rates of recombination. Provine also wants to make it clear that the shadow of pop-gen’s founding fathers is long. He devotes a chapter to Kimura and Ohta, the founding father and mother of neutral theory, showing that Kimura’s contribution was to extend random genetic drift thinking by applying Kolmogorov‘s diffusion equations to the problem of gene fixation. Like his predecessors, Kimura treated each gene locus as if it existed on its very own chromosome. Again, this over-simplification allowed the application of models that would not otherwise apply to a more nuanced depiction of genetic inheritance. In 1975 Kimura and Ohta published a paper in which they explained their rationale by insisting: …linkage is important only in small and transient populations such as those at the time of speciation, and not in large and stable populations. Provine suggests that Kimura’s neutral theory is the updated foundation of population genetics, and like its predecessor is a shaky and unrealistic platform on which to base our understanding of genetic evolution. If Provine is right about the flaws of population genetics, we have some serious problems with the way that we depict the processes of evolutionary change.
Shouldn't you, as a population geneticist, be concerned about Provine's critiques? Or, is the very fact that he would come out and criticize pop. gen. already an indication that he is "confused," and not worthy of being paid attention to? Long live the prevailing dogma!! (Which, per Provine, has been dogma since the early 1920's. Shall we look and see how Haldane personally ran Barbara McClintock out of science?) PaV
I'm pretty sure meosis is well enough established as a concept that it doesn't need the scare quotes. If provine says speciation (hardly the only outcome of drift...) is the result of the loss of whole-chromosome haplotypes then he's even more confused than I thought. Recombination happens, after all. wd400
wd400: You're not being specific about what, exactly, pop. gen. says about "meiosis"; but, Provine is not saying that pop. gen. doesn't in any way deal with "meiosis," rather, he's saying that what it calls "neutral genetic drift," it's very foundation, is mistaken; and, that potential for speciation is brought about by a 'chromosomal' effect; viz., a loss of variability through the loss of 'chromosomes,' and not by 'shifting alleles.' There's more that can be said about the "marbles in the jar" model pop. gen. uses. PaV
The intra-chromosomal shuffling is called recombination.
Recombination happens by design- see Spetner "Not BY Chance" 1997 Virgil Cain
No. But reviews like the one linked in the OP make it look like Provine was very confused. As described in 4, it's simply wrong to say that modern pop. gen. ignores the effects of meiosis. wd400
wd400: Have you read the book? PaV
That much is clear from the title. Doesn't answer the question though. wd400
So I’m a little lost as to what Provine is on about.
He's saying that "neutral genetic drift" is not real. PaV
"According to Provine, random genetic drift is a classic case of a theory that was so good that it did not merit testing" Mung
"...the realities of biology were subjugated to the convenience of theory." Mung
I haven't read Provine's book, so I'm curious to know how he thinks inbreeding occurs in haploid organisms, or in the mitechondria, chloroplasts etc. Bob O'H
The intra-chromosomal shuffling is called recombination. I'm a little surprised you an know how much recombination "helps this problem" when you literally don't know the first thing about it. The process of a benificial mutation dragging along nearby sequences is called "genetic hitchiking". It can only really happen under strong selection (because it a gene is at an intermediate frequency for a long time it will recombine plenty), so finding tracts of low diversity is actually one way we detect such rapid evolution in genomic data. Evolutionary biologists understand all of this, the extend of "linkage disequlibrium" in populations and influence of recombination on evolution are all parts of mainstream pop. gen. So I'm a little lost as to what Provine is on about. wd400
Y'know when I put my evolutionary hat on, I always think of genes as the fundamental unit of inheritance. This isn't correct at all. The chromosome is the fundamental unit of inheritance. Each chromosome passes on about 1/23 of the genes. The good is passed with the bad. If a "beneficial mutation" happens in a gene, it is inextricably glued to all of the other genes in that chromosome. I don't think that this is totally true, as I think there is some mechanism of intra-chromosome shuffling. However, this capacity helps the problem -- but not by much. Please Zachriel, Larry Moran, any of you evolutionary gurus, rescue my image of a new level of idiocy in your theory. bFast
Thanks for the observations, BA77. PaV
here is a gem from the link:
Review of William B. Provine’s “The ‘Random Genetic Drift’ Fallacy” - 05 Nov 2015 Excerpt: What about experiments? Certainly if random genetic drift has been an integral facet of population genetic theory, it should have been empirically demonstrated dozens of time by now, right? According to Provine, random genetic drift is a classic case of a theory that was so good that it did not merit testing:
"For decades after this, including the present, evolutionists or geneticists quote these three papers by Kerr and Wright as demonstrating the efficacy of “random genetic drift” in small populations. In my opinion, what Kerr and Wright showed was that intense inbreeding shows the results of inbreeding, not “random genetic drift.” The genes used were simply to mark the chromosomes and to add problems with selection. All the mechanisms were at the chromosomal level. Beyond general invocation, which happens everywhere in population genetics and biology, few other experiments demonstrating “random genetic drift” in eukaryotes have occurred in the laboratory since 1957."
He chronicles numerous experiments that claim to have produced allelic fixation via random genetic drift but which are clearly examples of inbreeding leading to loss of chromosomal diversity. Interestingly many of these studies were performed in Drosophila, which often maintain unusually high rates of recombination. http://www.christopherxjjensen.com/2015/11/05/review-of-william-b-provines-the-random-genetic-drift-fallacy
Which reminds me of this quote:
Lynn Margulis Criticizes Neo-Darwinism in Discover Magazine (Updated) - Casey Luskin April 12, 2011 Excerpt: Population geneticist Richard Lewontin gave a talk here at UMass Amherst about six years ago, and he mathemetized all of it--changes in the population, random mutation, sexual selection, cost and benefit. At the end of his talk he said, "You know, we've tried to test these ideas in the field and the lab, and there are really no measurements that match the quantities I've told you about." This just appalled me. So I said, "Richard Lewontin, you are a great lecturer to have the courage to say it's gotten you nowhere. But then why do you continue to do this work?" And he looked around and said, "It's the only thing I know how to do, and if I don't do it I won't get grant money." - Lynn Margulis - biologist http://www.evolutionnews.org/2011/04/lynn_margulis_criticizes_neo-d045691.html

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