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Turning to race, we must begin with the fraught question of whether it even exists, or whether it is instead a social construct. The Harvard geneticist Richard Lewontin originated the idea of race as a social construct in 1972, arguing that the genetic differences across races were so trivial that no scientist working exclusively with genetic data would sort people into blacks, whites, or Asians. In his words, “racial classification is now seen to be of virtually no genetic or taxonomic significance.”
Lewontin’s position, which quickly became a tenet of political correctness, carried with it a potential means of being falsified. If he was correct, then a statistical analysis of genetic markers would not produce clusters corresponding to common racial labels.
In the last few years, that test has become feasible, and now we know that Lewontin was wrong. Several analyses have confirmed the genetic reality of group identities going under the label of race or ethnicity. In the most recent, published this year, all but five of the 3,636 subjects fell into the cluster of genetic markers corresponding to their self-identified ethnic group. When a statistical procedure, blind to physical characteristics and working exclusively with genetic information, classifies 99.9 percent of the individuals in a large sample in the same way they classify themselves, it is hard to argue that race is imaginary.
The above is from an article by Charles Murray in Commentary, “The Inequality Taboo.” It apparently refers to an earlier article on ‘Lewontin’s Fallacy’ by Edwards (2003).
Murray is right in believing that human genetic variation does cluster geographically and that these clusters are adaptively significant —be they ‘races’, ‘geographical populations’ or whatever.
But is this point proven by the above line of reasoning? Lewontin never argued that human genetic variation is random. He simply affirmed that human races, however they may be defined, account for only a small percentage of total variation. Hence, there is far more variability within than between human populations. Murray counters that this conclusion is false because Lewontin looked at only one genetic trait at a time.
Clearly, if two groups overlap, they are more easily told apart with several criteria than with just one. If we use enough criteria, the overlap will shrink to zero: individuals will be assignable to either group with no ambiguity. But none of this means that within-group variability has decreased. In fact, it has actually increased. The only difference now is that this variability consists of combinations of genes that are unique to each group. How does this fact invalidate Lewontin’s contention that “the largest part by far of human variation [is] accounted for by the differences between individuals.”?
One might object that Charles Murray was talking about genes that contribute to intelligence and that such a contribution is almost certainly polygenic. Yes, but we’re not looking at several genes that display one form in one group and another form in the other. The two groups are still very heterogeneous whether you’re looking at any one gene or at gene combinations.
To find the flaw in Lewontin’s argument, we must examine his initial assumption: a random sample of genes should tell us how important race differences are. True, a large enough sample of genes will tell us whether a species has begun to differentiate into identifiable subpopulations. It will also tell us, roughly, when these subpopulations began to differentiate from each other.
But it won’t tell us how important between-population differences are in relation to within-population differences. It’s an apples and oranges comparison. The two groups of genes are qualitatively different.
First, when genes vary between populations, it’s usually because these populations inhabit different environments with different sets of selection pressures. Genes that differ across this environmental boundary are necessarily genes that make a difference, i.e., that have selective value.
In contrast, when genes vary within a population, despite similar selection pressures, it’s usually because they have little or no selective value (or because they form a balanced polymorphism, but that’s another topic!).
Second, the genetic markers used by population geneticists (blood groups, enzymes, mtDNA, etc.) tend to be selectively less important. This is partly because that is how population geneticists want them to be. Researchers will often choose markers that are close to selective neutrality because such markers change at a predictable rate (through random mutations) and can thus provide a time clock of a population’s history.
Such markers are also chosen because their protein products are easier to find and measure in body tissues. These ‘structural proteins’ are usually similar when we compare different species or even different genera. Humans and chimps, for instance, look very much alike when it comes to the protein building blocks that make up their body tissues. We have diverged from other apes largely through evolutionary changes at a higher level. i.e., regulatory genes that control development and other higher-order processes.
This point was grasped by Stephen J. Gould (1977, 406). He explained how we distort our understanding of genetic variation by relying on data from structural genes:
The most important event in evolutionary biology during the past decade has been the development of electrophoretic techniques for the routine measurement of genetic variation in natural populations. Yet this imposing edifice of new data and interpretation rests upon the shaky foundation of its concentration on structural genes alone (faute de mieux, to be sure; it is notoriously difficult to measure differences in genes that vary only in the timing and amount of their products in ontogeny, while genes that code for stable proteins are easily assessed).
Edwards, A.W.F. (2003). Human genetic diversity: Lewontin’s fallacy. BioEssays, 25, 798-801.
Gould, S.J. (1977). Ontogeny and Phylogeny. Belknap Press: Cambridge (Mass.)
Lewontin, R.C. (1972). The apportionment of human diversity. Evolutionary Biology, 6,381-398.
Murray, C. (2005). The inequality taboo. Commentary, September.