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.
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