Lewontin's legacy

 

Lewontin assumed that genetic diversity between populations is qualitatively similar to genetic diversity within populations. So comparing the two would be like comparing apples with apples. He was wrong. The second kind of diversity is less functionally significant.

 

 

The geneticist Richard Lewontin died last Sunday at the age of 92. He became prominent during the 1970s, particularly through his 1972 paper "The Apportionment of Human Diversity." Using data from blood groups, serum proteins, and red blood cell enzymes, he found far more genetic diversity within human populations than between them:

 

The results are quite remarkable. The mean proportion of the total species diversity that is contained within populations is 85.4%, with a maximum of 99.7% for the Xm gene, and a minimum of 63.6% for Duffy. Less than 15% of all human genetic diversity is accounted for by differences between human groups!

 

It is clear that our perception of relatively large differences between human races and subgroups, as compared to the variation within these groups, is indeed a biased perception and that, based on randomly chosen genetic differences, human races and populations are remarkably similar to each other, with the largest part by far of human variation being accounted for by the differences between individuals.

 

His reasoning seems sound. It ignores, however, two aspects of population genetics:

 

1. Genetic differences between populations are qualitatively different from genetic differences within populations. A population boundary is usually a boundary between different environments, either natural environments or cultural environments. It is thus a boundary between different pressures of natural selection and, hence differences in adaptation. An allele may work just fine on one side of the boundary, but not so well on the other side. Conversely, genetic diversity within a population is less meaningful because the end result tends to be the same. Everyone is adapting to the same environment. Genetic differences are less likely to produce real functional differences.

 

2. Genetic differences vary considerably in their functional significance, with the overwhelming majority having little or none. Many of these differences are found in junk DNA.

 

Lewontin discovered the obvious. Most genetic differences have little or no functional significance, and such differences account for most of the diversity within human populations. The more a genetic difference has real consequences, the less likely it will be found within a population because that is where the pressures of selection are uniform. It will more likely be found at a population boundary where the pressures of selection are different.

 

We see this, for example, in dog breeds. Although they differ considerably in anatomy and behavior, they are barely discernable in the genetic data. There is much more diversity within breeds than between them:

 

... genetic and biochemical methods ... have shown domestic dogs to be virtually identical in many respects to other members of the genus. ... Greater mtDNA differences appeared within the single breeds of Doberman pinscher or poodle than between dogs and wolves. ... there is less mtDNA difference between dogs, wolves, and coyotes than there is between the various ethnic groups of human beings, which are recognized as a single species. (Coppinger & Schneider 1995)

 

Well, dog breeds have been created through human-directed selection. What about subspecies that have arisen through natural selection? We see the same fuzziness, not only between subspecies but also between many sibling species that are anatomically distinct. In the deer family, genetic diversity is greater within some species than between some genera (Cronin 1991). Some masked shrew populations are genetically closer to prairie shrews than they are to other masked shrews (Stewart et al. 1993). Only a minority of mallards cluster together on an mtDNA tree, the rest being scattered among black ducks (Avise et al. 1990). All six species of Darwin's ground finches seem to form a genetically homogeneous genus while showing very little concordance between mtDNA, nuclear DNA, and morphology (Freeland & Boag 1999). In terms of genetic distance, redpoll finches from the same species are not significantly closer to each other than they are to sibling species (Seutin et al. 1995). Different species of haplochromine cichlids cannot be easily told apart by means of nuclear or mitochondrial genes, yet they are well differentiated morphologically and behaviorally (Klein et al., 1998). Neither mtDNA nor allozyme alleles can distinguish the various species of Lycaedis butterflies, despite clear differences in morphology (Nice & Shapiro 1999). An extreme example is a dog tumor that spreads through sexual contact: canine transmissible venereal sarcoma. It looks and acts like an infectious pathogen, yet its genes would show it to be a canid, and some beagles may be genetically more similar to it than they are to Great Danes (Yang 1996; see Frost 2011 for a full discussion).

 

When populations diverge under the impact of divergent pressures of natural selection, changes initially occur only within a fraction of the genome. Later, with the passage of time, the two populations will drift apart over the rest of the genome. But the human species is still young. The genetic split between Africans and non-Africans goes back only 60,000 years, and other splits are younger still.

 

This doesn't mean that genetic diversity between human populations is trivial. In fact, almost the opposite is true. It is the diversity within populations that is largely trivial.

 

 

References

 

Avise, J.C., C.D. Ankney, and W.S. Nelson. (1990). Mitochondrial gene trees and the evolutionary relationship of mallard and black ducks. Evolution 44: 1109-1119.

https://doi.org/10.1111/j.1558-5646.1990.tb03829.x

 

Coppinger, R. and R. Schneider (1995). Evolution of working dogs. In: J. Serpell (ed.) The Domestic Dog: Its Evolution, Behaviour and Interactions with People. Cambridge: Cambridge University Press, pp. 21-47.

https://books.google.ca/books?id=4fB7DQAAQBAJ&printsec=frontcover&hl=fr&source=gbs_ge_summary_r&cad=0#v=onepage&q&f=false

 

Cronin, M. (1991). Mitochondrial-DNA phylogeny of deer (Cervidae). Journal of Mammalogy 72: 533-566.

https://doi.org/10.2307/1382139

 

Freeland, J.R. and P.T. Boag. (1999). The mitochondrial and nuclear genetic homogeneity of the phenotypically diverse Darwin's ground finches. Evolution 53: 1553-1563.

https://doi.org/10.1111/j.1558-5646.1999.tb05418.x

 

Frost, P. (2011). Human nature or human natures? Futures 43: 740-748.

https://www.researchgate.net/profile/Peter_Frost2/publication/251725125_Human_nature_or_human_natures/links/004635223eaf8196f0000000.pdf  

 

Klein, J., A. Sato, S. Nagl, and C. O'hUigin. (1998). Molecular trans-species polymorphism. Annual Review of Ecology and Systematics 29: 1-21.

https://doi.org/10.1146/annurev.ecolsys.29.1.1

 

Lewontin, R.C. (1972). The apportionment of human diversity. Evolutionary Biology 6: 381-398.

https://emilkirkegaard.dk/en/wp-content/uploads/Lewontin-1972-The-Apportionment-of-Human-Diversity.pdf

 

Nice, C.C. and A.M. Shapiro. (1999). Molecular and morphological divergence in the butterfly genus Lycaeides (Lepidoptera: Lycaenidae) in North America: evidence of recent speciation. Journal of Evolutionary Biology 12: 936-950.

https://doi.org/10.1046/j.1420-9101.1999.00111.x

 

Seutin, G., L.M. Ratcliffe, and P.T. Boag. (1995). Mitochondrial DNA homogeneity in the phenotypically diverse redpoll finch complex (Aves: Carduelinae: Carduelis flammea-hornemanni). Evolution 49: 962-973.

https://doi.org/10.1111/j.1558-5646.1995.tb02331.x

 

Stewart, D.T., A.J. Baker, and S.P. Hindocha. (1993). Genetic differentiation and population structure in Sorex Haydeni and S. Cinereus. Journal of Mammalogy 74: 21-32.

https://doi.org/10.2307/1381902

 

Yang, T.J. (1996). Parasitic protist of metazoan origin. Evolutionary Theory 11: 99-103.

A modern myth

 

Your blood group cannot reliably identify your ethnicity, your race ... or even your species (Wikicommons, Etan Tal).

 

What sort of ideas will guide our elites twenty years from now? You can find out by observing university students, especially those in the humanities and social sciences. One popular idea is that race doesn't exist, except as a social construct. Its proponents include Eula Biss, a contributor to the New York Times Magazine:

Whiteness is not a kinship or a culture. White people are no more closely related to one another, genetically, than we are to black people. [...] Which is why it is entirely possible to despise whiteness without disliking yourself. (Biss, 2015, h/t to Steve Sailer)

The last sentence needs little explanation. It's possible to like yourself a lot while despising your own people. Such individuals have existed since time immemorial. But what about the second sentence? One often hears it among the educated, even those who dislike genetics and biology. Where does it come from?

From a study by geneticist Richard Lewontin, in 1972. He looked at human genes with more than one variant, mostly blood groups but also serum proteins and red blood cell enzymes. His conclusion:

The results are quite remarkable. The mean proportion of the total species diversity that is contained within populations is 85.4%, with a maximum of 99.7% for the Xm gene, and a minimum of 63.6% for Duffy. Less than 15% of all human genetic diversity is accounted for by differences between human groups! Moreover, the difference between populations within a race accounts for an additional 8.3%, so that only 6.3% is accounted for by racial classification.

[...] It is clear that our perception of relatively large differences between human races and subgroups, as compared to the variation within these groups, is indeed a biased perception and that, based on randomly chosen genetic differences, human races and populations are remarkably similar to each other, with the largest part by far of human variation being accounted for by the differences between individuals. (Lewontin, 1972)

The problem here is the assumption that genetic variation within a human group is comparable to genetic variation between human groups. In fact, the two are qualitatively different. When a gene varies between two groups the cause is more likely a difference in natural selection, since the group boundary also tends to separate different natural environments (vegetation, climate, topography) or, more often, different cultural environments (diet, means of subsistence, sedentism vs. nomadism, gender roles, state monopoly of violence, etc.). Conversely, when a gene varies within a population, the cause is more likely a random factor without adaptive significance. That kind of variation is less easily flattened out by the steamroller of similar selection pressures.

This point isn't merely theoretical. In other animals, as Lewontin himself noted, we often see the same genetic overlap between races of one species. But we also see it between many species that are nonetheless anatomically and behaviorally distinct. Some two decades after Lewontin’s study, this apparent paradox became known when geneticists looked at how genes vary within and between dog breeds:

[...] genetic and biochemical methods ... have shown domestic dogs to be virtually identical in many respects to other members of the genus. [...] Greater mtDNA differences appeared within the single breeds of Doberman pinscher or poodle than between dogs and wolves. Eighteen breeds, which included dachshunds, dingoes, and Great Danes, shared a common haplotype and were no closer to wolves than poodles and bulldogs.

[...] there is less mtDNA difference between dogs, wolves, and coyotes than there is between the various ethnic groups of human beings, which are recognized as a single species. (Coppinger and Schneider, 1995)

Initially, this paradox was put down to the effects of artificial selection. Kennel clubs insist that each breed should conform to a limited set of criteria. All other criteria, particularly those not readily visible, end up being ignored. So artificial selection targets a relatively small number of genes and leaves the rest of the genome alone.

But is natural selection any different? When a group buds off from a population and moves into a new environment, its members too have to conform to a new set of selection pressures that act on a relatively small number of genes. So the new group will diverge anatomically and behaviorally from its parent population, and yet remain similar to it over most of the genome. This is either because most of the genes respond similarly to the new environment—as with those that do the same housekeeping tasks in a wide range of species—or because they respond weakly to natural selection in general. Many genes are little more than "junk DNA"—they change slowly over time, not through the effects of natural selection but through gradual accumulation of random mutations.

With the extension of population studies to nonhuman species, geneticists have often encountered this paradox: a gene will vary much less between two species than within each of them. This is notably the case with sibling species that have emerged since the last ice age, when many new and different environments came into being.

Thus, the genetic overlap between dog breeds also appears between many natural species. In the deer family, genetic variability is greater within some species than between some genera (Cronin, 1991). Some masked shrew populations are genetically closer to prairie shrews than they are to other masked shrews (Stewart et al., 1993). Only a minority of mallards cluster together on an mtDNA tree, the rest being scattered among black ducks (Avise et al., 1990). All six species of Darwin's ground finches form a genetically homogeneous genus with very little concordance between mtDNA, nuclear DNA, and morphology (Freeland and Boag, 1999). In terms of genetic distance, redpoll finches from the same species are not significantly closer to each other than they are to redpolls from different species (Seutin et al., 1995). The haplochromine cichlids of Lake Victoria are extremely difficult to identify as species when one looks at their nuclear or mitochondrial genes, despite being well differentiated anatomically and behaviorally (Klein et al., 1998). Neither mtDNA nor allozyme alleles can distinguish the various species of Lycaedis butterflies, despite clear differences in morphology (Nice and Shapiro, 1999). An extreme example is a dog tumor that has developed the ability to spread to other dogs through sexual contact. It looks and acts like an infectious microbe, yet its genes would show it to be a canid and, conceivably, some beagles may be genetically more similar to it than they are to Great Danes (Cochran, 2001; Yang, 1996).

We see this genetic overlap not only between sibling species, but even between some species that have long been separated, like humans and other primates. This is the case with ABO blood groups:

Remarkably, the A, B, and H antigens exist not only in humans but in many other primates [...], and the same two amino acids are responsible for A and B enzymatic specificity in all sequenced species. Thus, primates not only share their ABO blood group, but also the same genetic basis for the A/B polymorphism. O alleles, in contrast, result from loss-of-function alleles such as frame-shift mutations and appear to be species specific. (Segurel et al., 2012)

Just think. Lewontin used the same blood group polymorphisms for his study. While the O alleles are specific to each primate species, the A and B alleles show considerable overlap between primates that have been separated for millions of years. So it's not surprising that this polymorphism should vary much more within human races than between them, as Lewontin found. Little did he know that the same pattern can continue above the species level.

Some have argued that this genetic overlap between humans and apes is only apparent. In other words, the same antigens have evolved independently in each species. Well, no. It seems that this polymorphism has survived one speciation event after another for millions of years:

That different species share the same two A/B alleles could be the result of convergent evolution in many lineages or of an ancestral polymorphism stably maintained for millions of years and inherited across (at least a subset of) species. The two possibilities have been debated for decades, with a consensus emerging that A is ancestral and the B allele has evolved independently at least six times in primates (in human, gorilla, orangutan, gibbon/siamang, macaque, and baboon), in particular, that the human A/B polymorphism arose more recently than the split with chimpanzee. We show instead that the remarkable distribution of ABO alleles across species reflects the persistence of an old ancestral polymorphism that originated at least 20 million years (My) ago and is shared identical by descent by humans and gibbons as well as among distantly related Old World monkeys. (Segurel et al., 2012)

Are blood groups a special case? Perhaps. But there seem to be quite a few trans-species polymorphisms, at least between humans and chimpanzees:

Instances in which natural selection maintains genetic variation in a population over millions of years are thought to be extremely rare. We conducted a genome-wide scan for long-lived balancing selection by looking for combinations of SNPs shared between humans and chimpanzees. In addition to the major histocompatibility complex, we identified 125 regions in which the same haplotypes are segregating in the two species, all but two of which are noncoding. In six cases, there is evidence for an ancestral polymorphism that persisted to the present in humans and chimpanzees. (Leffler et al., 2013)

Many of these appear to be "disease polymorphisms." If an epidemic sweeps through a community, it pays to have surface antigens that differ somewhat from your neighbor’s. The result is selection that inflates within-group variability, especially for the sort of structural proteins that are easy to collect and examine for studies on population genetics.

If such polymorphisms can remain intact despite millions of years of separation, how many more persist among human populations that have been separated for only tens of thousands of years?

In sum, if we are to believe blood groups and other genetic markers, it seems that Eula Biss may have more in common with certain apes than with the white folks she despises. Let’s hope she feels gratified.

When I discuss Richard Lewontin's study with antiracists, preferably those with some background in biology, they often agree that he misunderstood his findings. They nonetheless go on to say that their position has many other justifications, particularly moral ones. Fine. But it is above all Lewontin who gave antiracism a veneer of scientific objectivity. He still impresses people who are less impressed by academics who attack racism by attacking objectivity, like Stephen Jay Gould. "I criticize the myth that science itself is an objective enterprise, done properly only when scientists can shuck the constraints of their culture and view the world as it really is" (Gould, 1996, p. 53). It was in this spirit that he impugned the integrity of long-dead scholars who could not defend themselves—or point out that Gould himself was manipulating the data to suit his preconceived views (Frost, 2013).

When one takes Lewontin and Gould out of the picture, who is left? A lot of people, to be sure. Followers for the most part—those like Eula Biss who believe because everyone else in their milieu seems to believe, at least anyone with moral authority.

References 

Avise, J.C., C.D. Ankney, and W.S. Nelson. (1990). Mitochondrial gene trees and the evolutionary relationship of mallard and black ducks, Evolution, 44, 1109-1119.

http://www.jstor.org/stable/2409570?seq=1#page_scan_tab_contents 

Biss, E. (2015). White Debt, The New York Times Magazine, December 2

http://www.nytimes.com/2015/12/06/magazine/white-debt.html?_r=1

Cochran, G. (2001). Personal communication. 

Coppinger, R. and R. Schneider (1995). Evolution of working dogs. In J. Serpell (ed.), The Domestic Dog: Its Evolution, Behaviour and Interactions with People. Cambridge: Cambridge University Press, pp. 21-47.

https://books.google.ca/books?hl=fr&lr=&id=I8HU_3ycrrEC&oi=fnd&pg=PA21&dq=evolution+of+working+dogs&ots=BccrPzh5v3&sig=Cy-uz8gKk_epZRPTP58-k-1D9wg#v=onepage&q=evolution%20of%20working%20dogs&f=false 

Cronin, M. (1991). Mitochondrial-DNA phylogeny of deer (Cervidae), Journal of Mammalogy, 72, 533-566.

http://jmammal.oxfordjournals.org/content/72/3/553.abstract 

Freeland, J.R. and P.T. Boag. (1999).The mitochondrial and nuclear genetic homogeneity of the phenotypically diverse Darwin's ground finches, Evolution, 53, 1553-1563.

https://www.researchgate.net/profile/Peter_Boag/publication/233529125_The_mitochondrial_and_nuclear_genetic_homogeneity_of_the_phenotypically_diverse_Darwins_Ground_finches/links/0deec514a004f3a887000000.pdf 

Frost, P. (2013). Not getting the point, Evo and Proud, June 22

http://evoandproud.blogspot.ca/2013/06/not-getting-point.html  

Gould, S.J. (1996). The Mismeasure of Man, New York: W.W. Norton & Co.

http://www.amazon.com/The-Mismeasure-Man-Revised-Expanded/dp/0393314251 

Klein, J., A. Sato, S. Nagl, and C. O’hUigin. (1998). Molecular trans-species polymorphism, Annual Review of Ecology and Systematics, 29, 1-21.

http://www.jstor.org/stable/221700?seq=1#page_scan_tab_contents

Leffler, E.M., Z. Gao, S. Pfeifer, L. Ségurel, A. Auton, O. Venn, R. Bowden, R. Bontrop, J.D. Wall, G. Sella, P. Donnelly, G. McVean, and M. Przeworski. (2013). Multiple instances of ancient balancing selection shared between humans and chimpanzees, Science, 339 (6127), 1578-1582.

http://www.sciencemag.org/content/339/6127/1578.short  

Lewontin, R. (1972). The apportionment of human diversity, Evolutionary Biology, 6, 381-398.

http://www.philbio.org/wp-content/uploads/2010/11/Lewontin-The-Apportionment-of-Human-Diversity.pdf  

Nice, C.C. and A.M. Shapiro. (1999). Molecular and morphological divergence in the butterfly genus Lycaeides (Lepidoptera: Lycaenidae) in North America: evidence of recent speciation, Journal of Evolutionary Biology, 12, 936-950.

http://onlinelibrary.wiley.com/doi/10.1046/j.1420-9101.1999.00111.x/full 

Sailer, S. (2015). White Debt, The Unz Review, December 5

http://www.unz.com/isteve/white-debt/  

Ségurel, L.,  E.E. Thompson, T. Flutre, J. Lovstad, A. Venkat, S.W. Margulis, J. Moyse, S. Ross, K. Gamble, G. Sella, C. Ober, and M. Przeworski. (2012). The ABO blood group is a trans-species polymorphism in primates, Proceedings of the National Academy of Sciences U.S.A., 109, 18493-18498

http://www.pnas.org/content/109/45/18493.abstract  

Seutin, G., L.M. Ratcliffe, and P.T. Boag. (1995). Mitochondrial DNA homogeneity in the phenotypically diverse redpoll finch complex (Aves: Carduelinae: Carduelis flammea-hornemanni), Evolution, 49, 962-973.

http://www.jstor.org/stable/2410418?seq=1#page_scan_tab_contents 

Stewart, D.T., A.J. Baker, and S.P. Hindocha. (1993). Genetic differentiation and population structure in Sorex Haydeni and S. Cinereus, Journal of Mammalogy, 74, 21-32.

http://jmammal.oxfordjournals.org/content/74/1/21.abstract 

Yang, T.J. (1996). Parasitic protist of metazoan origin, Evolutionary Theory, 11, 99-103.

Another Robert Chambers?

 

Robert Chambers (1802-1871). His anonymously published book, Vestiges of the Natural History of Creation (1844), helped pave the way for public acceptance of Darwin’s theory of evolution. (source)

 

I haven't yet read Nicholas Wade's book A Troublesome Inheritance. I will venture to say, however, that it will be remembered less for its actual content than for its role in encouraging discussion of a difficult topic. In particular, it will familiarize a broad audience with the following points:

1. Biological evolution did not slow down with the advent of cultural evolution. In fact, it speeded up, particularly when farming began to replace hunting and gathering some 10,000 years ago. At that time, the pace of genetic change may have risen a hundred-fold.

2. Cultural evolution diversified the range of human environments. Instead of adapting only to differences in climate or food sources, like other animals, our species also adapted to differences in social structure, in the division of labor, in the means of subsistence, in unwritten or codified norms of conduct, in the degree of sedentary living, and in many other human-made phenomena. Our ancestors reshaped their environments, and these human-made environments reshaped them via gene-culture co-evolution.

3. This gene-culture co-evolution persisted into modern times. The English population, for instance, evolved between the twelfth and nineteenth centuries in terms of certain behavioral traits, particularly future time orientation and distaste for violence as a means to settle personal disputes. As Gregory Clark has shown, this behavioral change resulted from a demographic change—the relative reproductive success of the middle and upper classes—which altered the composition of the English gene pool. So the mantra that "we, too, were once savages" does not, in fact, deny the reality of biological evolution. It affirms it.

4. Human populations thus differ not only anatomically but also in various mental and behavioral predispositions. These differences are statistical and often apparent only when one compares large numbers of people. But even a weak statistical difference can profoundly affect how a society will develop and organize itself.

5. Finally, Richard Lewontin was right when he reported that genes vary much more within populations than between populations. He was unaware, however, that genetic variability between populations is qualitatively different from genetic variability within a population. The more a gene has value, the more it will vary across a population boundary, since such boundaries usually coincide with barriers that separate different habitats, different environments, different means of subsistence and, hence, different selection pressures. Conversely, the less a gene has value, the more it will vary within a population, that is, among individuals who share similar conditions of life. The selection pressure is uniform but this uniformity will not level out the variability of such genes within the population—much as a steam iron will smooth a rumpled shirt—since this variability is less phenotypically significant, i.e., it produces fewer functional differences that natural selection can act on. 

 

Are there questionable points in Wade's book? Undoubtedly. But we should not wait until all issues are settled before we put pen to paper. Writing is a process where ideas are shared with a broader audience for debate. We may forget that The Origin of Species was written without any knowledge of Mendelian genetics. We may also forget, or simply not know, that Darwin’s path to public acceptance was cleared by an earlier book: Vestiges of the Natural History of Creation (1844). Although its anonymous author, Robert Chambers, had no understanding of natural selection, he nonetheless played a key role in familiarizing the public with the fossil record and the reality of biological change over time. As one historian pointed out:

It is customary among biographers of Darwin to speak of the excitement which greeted the appearance of the Origin and of Huxley's able defense of Darwin at Oxford in his clash with Bishop Wilberforce. Actually, however, by the time Darwin published, Robert Chambers had drawn much of the first wrath of the critics and the intelligent public was at least reasonably prepared to consider a more able, scientific presentation of the subject.

[…] The attacks which the scientific world launched upon the Vestiges have, in retrospect, a quite unreal character. They belabor minutiae and amateurish minor errors as though there was some subconscious recognition that the heart of the thesis was unassailable.

[…] With its publication and success as a best seller, the world of fashion discovered evolution. The restricted professional worlds of science and of theology both lost their ability to suppress or intimidate public thinking upon the matter.

[…] By 1859, when the Origin of Species was published, an aroused and eager audience was considerably prepared for the revelations of Charles Darwin. The great amateur disputant and the great professional scholar should always be remembered as having together won the public mind to evolution. (Eiseley, 1958, pp. 134, 138, 139)

References 

Chambers, R. (1844). Vestiges of the Natural History of Creation, London: John Churchill

http://darwin-online.org.uk/content/frameset?itemID=A2&viewtype=text&pageseq=1

Eiseley, L. (1958). Darwin's Century. Evolution and the Men Who Discovered It, New York: Anchor Books.

Wade, N. (2014). A Troublesome Inheritance. Genes, Race and Human History, Penguin Books.

 

 

Burakumin, Paekchong, and Cagots

This is the first of a series of ebooks. You can access an Epub version here or a PDF here. Below is the foreword.

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Foreword

 

The Burakumin of Japan, the Paekchong of Korea, and the Cagots of France … What do they have in common? All three were despised castes—closed groups of people who married among themselves. A despised caste is not just a low class. Otherwise, it would always be gaining and losing members, with some moving up and out and others down and in. As Gregory Clark has shown, the English lower class is descended largely from people who were middle or even upper class a few centuries before. This may seem strange if you equate the middle class with voluntary childlessness, but until the late 19th century they were the ones who had the most children—even more so if we look only at children who lived to adulthood. The resulting demographic overflow continually spilled over into the lower class.

In contrast, not much new blood flows into a despised caste, at least not on an ongoing basis. Social stigma discourages people from marrying out or marrying in. Nor does one enter simply by virtue of being poor, since the fear of losing caste keeps out most of the downwardly mobile. Despite this lack of new blood, a despised caste can perpetuate itself indefinitely because its members usually have enough resources—through their monopoly over equally despised occupations—to get married, form families, and have enough children to replace themselves. This was not the case with urban lower classes of pre-industrial times, which typically had large numbers of childless single men.

Because a caste is closed and self-perpetuating, it may preserve genetic traits that disappear everywhere else. It thus becomes more and more different not because it is changing but because its host population is changing.

But how can a population change over a few centuries? Didn’t human nature assume its present form back in the Pleistocene when cultural evolution took over from genetic evolution? In reality, these two evolutionary processes have reinforced each other. Human genetic evolution actually accelerated 40,000 years ago and even more so 10,000 years ago, apparently in response to a growing diversity of cultural environments.

What about Richard Lewontin’s finding that human genes vary much more within populations than between populations? Isn’t that proof that genetic evolution stagnated while humans were spreading over the earth and forming the many populations we see today? Lewontin’s finding is correct but does not mean what it seems to mean. Indeed, the same genetic overlap has been found between many species that are nonetheless distinct anatomically, morphologically, and behaviorally. Genetic variation between populations differs qualitatively from genetic variation within populations. In the first case, genes vary across a boundary that separates different environments and, thus, different selection pressures. This kind of genetic variation is shaped by selection and gives rise to real phenotypic differences. The situation is something else entirely when genes vary among individuals who belong to the same population and face similar selection pressures. That kind of variation matters much less, the actual phenotypic differences often being trivial or nonexistent.

Human evolution is a logarithmic curve where most of the interesting changes have happened since the advent of farming and complex societies. Homo sapiens was not a culmination but rather a beginning … of gene-culture co-evolution. There are many ways to study this co-evolution, but one way is to look at the different evolutionary trajectories followed by castes and their host populations.

Apples, oranges, and genes

Publicly funded misinformation. Source: PBS website

In human genetics, a ‘population’ is a group of individuals who share ancestry and hence genes. This sharing is not absolute. There is always some gene flow from outside, and sometimes “outside” means another species. We humans, for example, have received genes not only from Neanderthals and Denisovans but also from … viruses.

In addition, new gene variants are constantly arising through mutation. Most of them are harmful or useless. But some are useful and will thus spread through the population.

So below the species level, and often even at the species level, population boundaries tend to be fuzzy. Genes vary both between and within populations.

You’ve undoubtedly heard that there is much more genetic variation within human populations than between them, this being true even for the large continental populations we used to call ‘races.’ This was the finding of the geneticist Richard Lewontin (1972), and others have concluded likewise. You’ve probably not heard, however, that the same kind of genetic overlap exists between many sibling species that are nonetheless distinct in anatomy and behavior (Frost, 2011).

How come? First, keep in mind that genes vary a lot in adaptive value. Some are little more than ‘junk DNA.’ Others code for structural proteins that form the building blocks of flesh and blood. Others still are very important because they code for regulatory proteins that control how other genes behave and, hence, the way an organism grows and develops. The last kind of gene accounts for only a tiny fraction of the genome. Most genes have modest effects, or none at all.

Second, keep in mind that different populations occupy different environments and are thus exposed to differences in natural selection. In most species, these differences are due to physical environments that differ in climate, vegetation, and wildlife. Humans also have to adapt to cultural environments that differ in social structure, belief systems, and technology. In either case, when a gene varies between two populations the cause is probably a difference in natural selection, since the population boundary also separates different selection pressures. Conversely, when a gene varies within a population this variation is less likely to have adaptive significance. It hasn’t been flattened out by the steamroller of similar selection pressures.

This is one aspect of “Lewontin’s fallacy.” Within-population variation isn’t comparable to between-population variation. It’s like comparing apples and oranges.

Another aspect of Lewontin’s fallacy is that natural selection within a population exercises a leveling effect only on phenotypes, and not on genotypes. If two gene variants have a similar phenotypic effect, natural selection will take longer to replace one with the other. Sometimes, this sort of diversity will persist indefinitely because epidemics often spare individuals whose surface proteins are somewhat different from those of their neighbors.

Thus, within-population variation tends to consist of different gene variants at different loci whose effects nonetheless point in the same general direction. To some degree, these variants can stand in for each other. If one is absent, another one might do the trick. This is probably why population differences are more sharply defined if several gene loci are compared simultaneously. If we chart how each gene varies geographically and then superimpose these maps on top of each other, the resulting composite map will show population differences in sharper relief (Edwards, 2003; Mitton, 1977; Mitton, 1978; Sesardic, 2010).

This point has been made by Emmanuel Milot, the principal author of the paper I reviewed in my last post. His research team found that the time between marriage and first birth steadily shrank among succeeding generations of French Canadians on Île aux Coudres (Milot et al., 2011). In the land-rich environment of the New World, there was strong selection for married women to get pregnant faster. A genetic difference has thus developed between French Canadians and the French who remained in France.

But this difference is not due to a few genes. As Milot points out, natural selection tends to produce effects at many different genes:

“We should not think that there are genes that code specifically for age at first reproduction. In fact, this type of trait is probably influenced by hundreds, even thousands, of genes. These genes act on other characteristics, like body weight at birth, age at first menstruation, or even personality traits, which impact on age at first birth” (Bourdon, 2011)

This point is important. If two populations differ at one gene, and if the difference is sensitive to natural selection, they probably also differ at many other genes. The same selection pressure that caused one difference has almost certainly caused others. Typically, we see only the tip of the iceberg—a gene variant that produces an obvious effect in affected individuals, such as illness. Most gene variants, however, don’t cause medically recognized illnesses, and their effects also tend to be subtler.

References

Bourdon, M-C. (2011). L’espèce humaine. Toujours en évolution. UQAM. Entrevues
http://www.uqam.ca/entrevues/entrevue.php?id=965

Edwards, A.W.F. (2003). Human genetic diversity: Lewontin’s fallacy. BioEssays, 25, 798-801.

Frost, P. (2011). Human nature or human natures? Futures, 43, 740-748. http://dx.doi.org/10.1016/j.futures.2011.05.017

Lewontin, R.C. (1972). The apportionment of human diversity. Evolutionary Biology, 6, 381-398.

Milot, E., F.M. Mayer, D.H. Nussey, M. Boisvert, F. Pelletier, and D. Réale. (2011). Evidence for evolution in response to natural selection in a contemporary human population, Proceedings of the National Academy of Sciences (USA), early view

Mitton, J.B. (1977). Genetic differentiation of races of man as judged by single-locus and multilocus analyses, American Naturalist, 111, 203-212.

Mitton, J.B. (1978). Measurement of differentiation: reply to Lewontin, Powell, and Taylor, American Naturalist, 112, 1142-1144.

Sesardic, N. (2010). Race: a social destruction of a biological concept, Biology and Philosophy, 25(2), 143-162.

Arroseur arrosé?

Stephen Jay Gould in a 1997 Simpsons episode (Pagepulp). Gould enjoys an almost iconic status in American culture.

Who was the greatest evolutionary scientist of recent times? Most people would answer “Stephen J. Gould,” at least on this side of the Atlantic. With the possible exception of L.L. Cavalli-Sforza, he was the one best known to non-biologists, partly because he wrote well but also because he said the sorts of things that people in the humanities and social sciences wished to hear. My anthropology department was no exception. When I presented my dissertation proposal, one committee member launched into a criticism that he supported with a quote from one of Gould’s works. I didn’t understand the relevance of the quote—other than the banal point that many scholars are unconscious liars. But it hit home among the other people present.

And why not? When Gould died, in 2002, his reputation was unshakable. You might have disagreed with his conclusions, but his methodology seemed sound. This was particularly so with his 1978 Science paper on 19th-century physical anthropologist Samuel George Morton, which showed how a reputedly objective scientist had unconsciously fudged his data to make Europeans look larger-brained than sub-Saharan Africans.

These findings were later carried over into The Mismeasure of Man (1981), a bestseller and now required reading in many undergrad social science courses. Gould also brought up his 1978 paper in public lectures, making it a centerpiece of his attacks on the “myth of scientific objectivity.” In reviewing a posthumous Gould anthology, Richard Lewontin, underlined this point as “the one that is most important to the public understanding of science”:

Despite the myth of detached objectivity that scientists propagate, their motivations are as messy as everyone else's. In particular, they have political, social, and personal concerns that may influence what they do, how they do it, and what they say about it. Putting aside deliberate fraud, of which we have an embarrassment of examples, the gathering of data, their statistical representation, and their interpretation offer many opportunities for unconscious bias toward conclusions that we already "knew" to be true. (Lewontin, 2008)

By the time of his death, Gould had become an icon of popular culture:

Dr. Gould achieved a fame unprecedented among modern evolutionary biologists. The closest thing to a household name in the field, he became part of mainstream iconography when he was depicted in cartoon form on "The Simpsons." Renovations of his SoHo loft in Manhattan were featured in a glowing article in Architectural Digest. (Yoon, 2002)

The Simpsons episode aired in 1997 and is worth summarizing:

Lisa Simpson wants to stop a huge mall development from proceeding at "Sabertooth Ravine" because the ravine is a fossil site. As a compromise, the mall developers decide to let Lisa dig for fossils while they continue to build the mall. While digging, Lisa finds an almost human fossil. Almost, but not quite: in place of arms the fossil has wings. "It's an angel" declare the naive and religiously motivated townfolk. Lisa, who plays the scientific naturalist, will have none of it. She therefore enlists Gould to prove that the fossil is nothing of the sort. Gould claims that the DNA tests he performed proved inconclusive.

[…] In the closing scene, Lisa asks Gould why his test failed to detect that the angel fossil was a fraud. Gould (and mind you, this was Gould's actual voice--he is listed explicitly in the credits) admits that in fact he never did perform the test--even though he claimed he did earlier. (Dembski, 1997)

The Simpsons episode raised a few eyebrows. Was Gould guilty of the sort of shenanigans he had accused others of doing?

Arroseur arrosé

Yes indeed. A team of physical anthropologists recently located half of the skulls that Samuel George Morton had measured more than a century and a half ago. When they remeasured the skulls they found very few errors in Morton’s measurements. More to the point, the errors were distributed randomly. There was, in fact, a non-significant tendency to overestimate African skull size (Lewis et al., 2011).

It is also doubtful whether Morton considered Africans to be less “evolved” than Europeans. His Crania Americana was published in 1839, long before the first attempts to apply evolutionary theory to human races. Morton was in fact a devout Christian who wished to find out whether different human populations were separate species resulting from multiple divine creations or a single species created but once. He had little if any interest in research on human intelligence, which anyhow was embryonic at the time.

Needless to say, Gould never remeasured any of Morton’s skulls. His paper was at best a clumsy re-analysis of Morton’s published data. I say “at best” because Gould bolstered his argument by creating facts out of thin air. It is a wonder that he managed to get published in a first-tier journal like Science, which as a rule publishes only original data.

Further thoughts

There is another disturbing element in this affair. Many of the flaws in Gould’s paper had already been pointed out … twenty-three years ago (Michael, 1988). And they were pointed out in a first-tier journal (Current Anthropology). Yet that other paper was studiously ignored. Gould owed his reputation not so much to the quality of his work as to an academic milieu that covered for him, acting more as cheerleaders than as responsible critics. He was shielded by a personality cult. Without it, he would have been just another biology professor.

What now? Academia will likely enter a long and painful process of “de-Gouldization.” Long, because many other academics were in on the collective lying. Painful, because the lies were far from trivial.

References

Dembski, W.A. (1997). An Analysis of Homer Simpson and Stephen Jay Gould, Access Research Network.

http://www.arn.org/docs/dembski1129.htm

Gould S.J. (1981). The mismeasure of man. New York: W. W. Norton and Company.

Gould , S.J. (1978). Morton’s ranking of races by cranial capacity: unconscious manipulation of data may be a scientific norm, Science, 200, 503–509.

Lewis, J.E., D. DeGusta, M.R. Meyer, J.M. Monge, A.E. Mann, R.L. Holloway. (2011). The Mismeasure of Science: Stephen Jay Gould versus Samuel George Morton on Skulls and Bias, PLoS Biology, 9(6) e1001071

Lewontin, R.C. (2008). The Triumph of Stephen Jay Gould, New York Review of Books, 55(2), 39-41, February 14, 2008.

Michael, J.S. (1988). A new look at Morton’s craniological research, Current Anthropology, 29, 349–354.

Pagepulp (2011). The literary world of the Simpsons, April 24
http://www.pagepulp.com/176/the-literary-world-of-the-simpsons/

Yoon, C.K. (2002). Stephen Jay Gould, Biologist and Theorist on Evolution, Dies at 60, New York Times, May 20, 2002,
http://www.nytimes.com/2002/05/20/obituaries/20CND-GOULD.html

The fast runners of evolution

In the deer family, genetic variability is greater within some species than between some genera. Does Fst tell us what we think it tells us?

At almost any genetic marker (blood types, serum proteins, enzymes, mtDNA, etc.), a typical gene varies much more within than between human populations. And this is true not only for large continental populations but also for small local ones. The geneticist Richard Lewontin found that 85% of our genetic variation exists among individuals and only 15% between ‘races.’ He concluded:

It is clear that our perception of relatively large differences between human races and subgroups, as compared to the variation within these groups, is indeed a biased perception and that, based on randomly chosen genetic differences, human races and populations are remarkably similar to each other, with the largest part by far of human variation being accounted for by the differences between individuals. (Lewontin, 1972)

Was Lewontin right? Some geneticists have remained unconvinced, their doubts focusing on three points:

1. A small genetic difference can still make a big cultural difference

Even if human populations differ only slightly at certain gene loci, these slight differences can still have big effects.

For instance, the historical economist Gregory Clark has argued that the slow but steady demographic expansion of the English middle class from the 12th century onward gradually raised the population mean for predispositions to non-violence, deferment of pleasure, and other future-oriented behavior. Although the nascent middle class was initially a small minority in medieval England, its descendants grew in number and gradually replaced the lower class through downward mobility. By the 1800s, its lineages accounted for most of the English population.

There then came the triumph of Victorian morality—a relatively sudden cultural change due to a genetic change that had slowly reached a point of critical mass. The English middle class could now impose its behavioral norms on the whole population, thereby abandoning the ‘two-tier morality’ of other class-stratified societies (Clark, 2007, pp. 124-129, 182-183; Clark, 2009).

2. Lewontin’s finding is true only if we look at one gene at a time

Genes vary much more within than between human populations only if we look at one gene at a time. The pattern reverses if we aggregate variation at several gene loci. The more we aggregate, the more the genetic variation will exist between populations and not within them. This point was first made by Cavalli-Sforza back in 1966 and later by Mitton (1977, 1978), Edwards (2003), and Sesardic (2010).

3. A big chunk of inter-individual genetic variation is actually intra-individual

Although only 15% of human genetic variation is composed of population differences, the remaining 85% is not necessarily between individuals. Since we are diploid organisms, some genetic variation is actually intra-individual—the differences between the genes you inherited from your mother and the genes you inherited from your father. If we factor out this kind of variation, population differences actually account for a third of all human genetic variation (Sarich and Miele, 2004).

How valid are these three points?

The first one was true historically and, presumably, prehistorically. A slight genetic advantage could indeed leverage very disproportionate benefits. “Winner takes all.” This kind of dynamic, however, is no longer legitimate in modern societies, at least not to the same extent. Although we accept that losers should lose, we don’t accept that they should lose everything. Our societies provide a wide array of redistributionist mechanisms to ensure that slight advantages don’t snowball into big ones.

The second point is certainly true. Clearly, two groups are easier to tell apart with several criteria than with one. With enough criteria, any overlap will shrink to zero and all individuals can be unambiguously assigned to either group. This is basic logic. But all this proves is that human populations are identifiable. It doesn’t prove that the differences between them are greater than the differences within them.

The third point invites the same reply of “So what?” If our intra-population variation is inflated by intra-individual variation, the same would be true for all species, and not just our own. Remove intra-individual variation, and you’ll certainly get a higher estimate of inter-population variation. But this will be true across the board. Human races will still look relatively unimportant.

In all this, a more fundamental criticism is being ignored. How meaningful is the ratio of inter-population to intra-population variation? Just what exactly does it tell us?

This ratio, called Fst, is not as meaningful as one might think:

Fst isn’t a good measure of genetic-phenotypic mediation. As a case example, Long and Kittles (2003) found a between human population Fst of 11% based on their sample; when they added chimpanzees, the between population Fst increased only to 18% [3]. Mountain and Risch (2004), citing this example, note that ‘‘a low FST estimate implies little about the degree to which genes contribute to between-group differences.’
(Occidentalist, 2011)

Indeed, some sibling species show the same kind of genetic overlap that we see between human races. And yet these species are anatomically, physiologically, and behaviorally distinct (Frost, 2008).

Remember, when two populations differentiate under the impact of diverging selection pressures, this differentiation concerns only a tiny fraction of the genome. Why? There are two reasons:

(a) Much genetic variation is of low selective value, often being little more than "junk" variability, and thus responds weakly to changes in selection pressure.

(b) Much genetic variation is equally adaptive in both of the new adaptive landscapes. There are many cases of genetic polymorphisms that widely occur not only among different populations of one species, but also among related species (Klein et al., 1998).

Fst cannot tell us how much populations really differ from each other within a species—and by ‘really’ we’re talking about adaptive differences that show up in anatomy, physiology, and behavior. It basically tells us how long these populations have been separated from each other, with some adjustment for ongoing gene flow. In our case, Fst tells us that human races are young, very young.

But this we know already. The past 40,000 years have seen our ancestors spread into a multitude of natural environments—from tropical rain forest to arctic tundra. And the past 10,000 years have seen humans enter an even greater variety of cultural and social environments—from simple horticulture to complex societies with class differentiation, State formation, urbanization, systematized religion, and the ability to store, accumulate, and exchange information via writing.

We also know that these same years have seen an accelerating pace of genetic change. Natural selection has altered at least 7% of our genome over the last 40,000 years. In particular, the speed of genetic change rose over a hundred-fold with the advent of agriculture some 10,000 years ago (Hawks et al., 2007).

The correlation is very weak between the passage of time and the degree of evolutionary change. Some organisms have remained virtually the same for millions of years. Others have changed very quickly. We, humans, are the fast runners of evolution.

References

Cavalli-Sforza, L.L. (1966). Population Structure and Human Evolution, Proceedings of the Royal Society of London. Series B, Biological Sciences, 164, 362-379.

Cavalli-Sforza, L.L., P. Menozzi, and A. Piazzi. (1994). The History and Geography of Human Genes, Princeton: Princeton University Press.

Clark, G. (2007). A Farewell to Alms. A Brief Economic History of the World, Princeton University Press, Princeton and Oxford.

Clark, G. (n.d.). The indicted and the wealthy: surnames, reproductive success, genetic selection and social class in pre-industrial England, http://www.econ.ucdavis.edu/faculty/gclark/Farewell%20to%20Alms/Clark%20-Surnames.pdf

Edwards, A.W.F. (2003). Human genetic diversity: Lewontin’s fallacy. BioEssays, 25, 798-801.

Frost, P. (2008). The 85% truism, Evo and Proud, January 4

Hawks, J., E.T. Wang, G.M. Cochran, H.C. Harpending, and R.K. Moyzis. (2007). Recent acceleration of human adaptive evolution, Proceedings of the National Academy of Sciences USA. 104, 20753-20758.

Jorde, L.B., W.S. Watkins, M.J. Bamshad, M.E. Dixon, C.E. Ricker, M.T. Seielstad, and M. A. Batzer. (2000). The Distribution of Human Genetic Diversity: A Comparison of Mitochondrial, Autosomal, and Y-Chromosome Data, American Journal of Human Genetics, 66, 979–988.

Klein, J., A. Sato, S. Nagl, and C. O’hUigin. (1998). Molecular trans-species polymorphism, Annual Review of Ecology and Systematics, 29, 1-21.

Lewontin, R. (1972). The apportionment of human diversity, Evolutionary Biology, 6, 381-398.

Long, J.C. and R.A. Kittles. (2003). Human Genetic Diversity and the Nonexistence of Biological Races, Human Biology, 81, 777-798.

Mitton, J.B. (1977). Genetic differentiation of races of man as judged by single-locus and multilocus analyses, American Naturalist, 111, 203-212.

Mitton, J.B. (1978). Measurement of differentiation: reply to Lewontin, Powell, and Taylor, American Naturalist, 112, 1142-1144.

Mountain, J.L. and N. Risch. (2004). Assessing genetic contributions to phenotypic differences among ‘racial’and ‘ethnic’groups, Nature Genetics, 36, S48 - S53.

Occidentalist (2011). Did Sarich Get It Right? Occidentalist, April 14
http://occidentalascent.wordpress.com/2011/04/14/did-sarich-get-it-right/

Sarich, V. and F. Miele. (2004). Race: The Reality of Human Differences, Basic Books.

Sesardic, N. (2010). Race: a social destruction of a biological concept, Biology and Philosophy, 25, 143-162.