“[T]here have probably always been wide differences among the peoples of the world in average intellectual ability,” one of the pioneers of population genetics, Sewall Wright, wrote in Evolution and the Genetics of Populations, Volume 4: Variability Within and Among Natural Populations (Univ of Chicago Press: 1978, p. 456), in a chapter that was pointedly titled, ‘Racial Differentiation in Mankind’. ‘The capacity to anticipate and plan for the future is a mental attribute’, he continued, ‘that would be favored under northern conditions and selected for insofar as it has a genetic basis.’ Not only was the modern industrial world the creation of biologically superior brains, according to Wright, so was domestication of plants and animals:
The initiation of agriculture and livestock breeding was a revolutionary advance from the hunting and gathering way of life, which could hardly occur until the genetic basis for intelligence had reached an advanced grade. It is fair to assume that the regions in which these appeared first were at the peaks in the genetic basis for intelligence.
This is classic high racialism. But note the late date: Sewall is writing not before 1950, which is what we would expect if we bought the standard narrative that privileges the UNESCO statement on race as dividing line between the very bad, terrible, no good racist world of before from the enlightened world after. A lot of “historians” have convinced themselves that the Statement ‘signaled the triumph of antiracist anthropology’. As Hazard relays:
The 1950 UNESCO Statement on Race looms large in the historical study of “race” in the 20th century. Historians, sociologists, anthropologists and others point to the 1950 Statement on Race as the key moment in which science was harnessed in the political battle to combat racism and overturn the philosophical underpinnings of European colonialism and Jim Crow. These scholars recognize how the UNESCO Statement was doubly significant because the newly formed United Nations called for such an effort along with its 1948 Universal Declaration of Human Rights, and because the Statement apparently signaled the triumph of anti‐racist anthropology over the science that had defined social Darwinism, eugenics, and the Holocaust (Baker 1998; Banton 2002; Barkan 1992; Graves 2001; Kohn 1995; Patterson 2001; Shipman 2002; Tucker 1994; Zack 2002).
It was nothing of the sort. The 1950 UNESCO statement on race was authored by Montagu and a small coterie of Boasians without any input whatsoever from physical anthropologists, who continued to believe in the applicability, indeed the supreme importance, of the biological race concept to the human species for the rest of the century — as Ann Morning has documented. Indeed, Sewall was writing 16 years after Coon’s confrontation with Dobansky and Montagu on the pages of Current Anthropology, that marked the triumph of Boasian antiracism in Proctor’s reading. It was again, nothing of the sort. The confrontation amounted to Coon giving the two a lecture in professional standards; particularly ‘the junior author’. Nor was Wright marginal to modern biology. To the contrary, in the late-1970s and early-1980s, Wright was at the height of his influence. With Fisher and Haldane having given up the ghost in the early-1960s, Wright reigned as the last living father of population genetics.
Sewall Wright died in 1988; too early for the revolutions that were to come in population genetics and molecular anthropology. These revolutions would raise the specter of furnishing incontrovertible evidence for the speculations of Wright in particular and scientific high racialism in general. Many a racialist jumped the gun.
An army of psychometricians, lead by Rushton, kept up a steady stream of research documenting racial differences in cognitive test scores on the one hand and estimating the heritability of general intelligence on the other. None of them bothered to test whether these population differences were evidence of differences in health status; it was simply assumed that the causal vector pointed in the ‘right’ direction. After the violent reception of The Bell Curve in 1994, Herrnstein kicked the bucket, but Murray would forever be hounded by Boasian antiracists for replicating known results on racial differences in test scores in one of the chapters. No critic, not one among the many thousands who surfaced to skin Murray, bothered to challenge the main thrust of their argument — that the social order was a function of class differences in cognitive ability. Meanwhile, the amateur and semi-professional soldiers of Rushton’s army were driven underground. They were to reemerge later as neoracialism, once advances in DNA reignited hopes for molecular evidence for biological reductionism. Richard Lynn’s The Global Bell Curve: Race, IQ, and Inequality Worldwide (Washington Summit Publishers: 2008) was studiously ignored by the cognicenti; even as it became a bible for Rushton’s army.
It was a long time in the making, but Nicholas Wade crossed the Rubicon with the publication of A Troublesome Inheritance: Genes, Race, and Human History (Penguin: 2014). Wade seems to have convinced himself that clustering algorithms proved the existence of geographic races in our species — they don’t; more precisely, they cannot. But it was not simply Wade’s fault. The geneticists pretending to be anthropologists were themselves using a racialized reference frame. Before long their neat phylogenetic trees with their immaculate branches (corresponding to continental populations) would get destabilized; lots of dotted lines (indicating gene flow) would emerge between the branches; and, finally, ancient DNA would demolish easy assumptions about the genotypic integrity and historic continuity of continental populations. The attention of molecular anthropologists would shift dramatically to introgressions (gene flow between “species”) from Neanderthals, Denisovans, and all manner of vanished ghost populations in Asia and Africa; and to fine-scale population structure. In other words, molecular anthropology would recapitulate the path of scientific racialism — then as now, the uncontrolled proliferation of races and subraces would test the validity of the dominant reference frame of systematics. The modern picture that emerged towards the end of the decade would not be kind to the easy certainties of the beginning of the decade. But we are digressing.
In what he called his more speculative chapters, Wade pulled the full monty of sociobiology. Behavioral differences are mobilized to explain world order and differences in genomic endowment are mobilized to explain said behavioral differences. Interestingly, unlike high racialism, neoracialism, from Rushton through Wade, holds the Chinese in high regard. It doesn’t take long to see why. The Chinese are now held in high regard for the same reason that the Japanese were admitted as ‘a vigorous race’ at the turn of the century. For racialism is nothing more than an explanatory schema for world order. Now that Chinese power cannot be dismissed, the ranking of the races must be reshuffled so as to continue the explanatory work. Whether this is consistent with the assumed stability of racial genotypes is a question best avoided if faith in racialism is to be maintained.
The double reduction — world order to individual behavioral propensities and individual behavioral propensities to genetic differences in populations — is the classic move of racialism. How much water can it hold? What, in particular, is the genetic basis for cognitive ability? and what is the distribution of said gene frequencies?
The heritability of cognitive ability is around 0.5. This means that 25 percent of the variation in cognitive test scores (or its proxies like GPA, GRE, GMAT, LSAT et cetera) is due to all the stuff that is inherited, including genes and economic and social capital. Twin studies have shown that much of it is indeed genetic. There are also well established differences in population means in test scores. But that does not mean that these differences are due to genetics. And even if some of the difference is genetic, that does not mean that the associated gene frequencies are stable. Indeed, we know that if population differences in IQ are genetic, then the associate gene frequencies cannot be stable. The reason is that IQ has been increasing rapidly — what’s called the Flynn effect. A good comparison can be made with height. Now, height is even more heritable than IQ. It’s heritability coefficient is 0.8. Both height and IQ rose across the board is every single nation that modernized in the 20th century, and for the same reason. In as much as they are under genetic control, both of these traits are highly polygenic — they depend of thousands of genes. These gene frequencies get constantly reshuffled under the continuous action of natural selection in a relentlessly changing environment, neutral drift, and even changing cultural mores that affect fitness in the sexual economy.
Putting all these facts together, the most compelling explanation of patterns that have been documented is that cognitive ability is simply a measure of health status accounting for both nutrition and disease burdens. As living standards and health has improved in the fortunate parts of the world and in the fortunate strata of societies, people have grown taller, live longer, are healthier, and perform better at cognitively challenging tasks such as taking IQ tests. We don’t know if genes corresponding to intelligence have become more frequent in such fortunate populations. It is a fair bet that they have. In any case, the fundamental issue is the health status of populations; the gene frequencies will take care of themselves.
A few years ago there was much fuss about ‘polygenic scores’. Basically, innovations in DNA sequencing dramatically reduced the cost of whole genome mapping, so that one could do it at scale. After the 1990s dream of finding a single gene for every disorder and trait had been dashed, geneticists began to study the correlations between the traits under investigation, say schizophrenia, and thousands of genetic markers. Each single locus turned out to be very weakly correlated with any single trait; but together they provided some handle on complex polygenic traits — and almost everything interesting turned out to be polygenic.
Polygenic scores may be of some use in medical screening. But they were both theoretically and practically unsatisfying. There was some excitement when some workers reported that the genetic basis of IQ had been identified. But it turned out to be a dud. Polygenic scores explained a mere 5 percent of the variation in cognitive test scores. I can do better by talking to someone for 2 minutes.
At the same time as excitement about polygenic scores was crashing, a new approach began to yield more promising results. This approach would end up completely upending the fundamental basis of biological reductionism. It is my discovery of this body of work that prompted this essay.
Genes are functional regions of the genome — that is, they control something or the other, usually protein production. Gene variants are called alleles. There are usually just two alleles, say A and a. When we talk about gene frequencies; we are really talking about allele frequencies. X and Y are sex chromosomes, which are inherited differently. The bulk of the genetic code is autosomal; at each locus (“gene”), we get one allele from each parent. If they are identical, say AA or aa, we are homozygous on that locus; if they are different, ie Aa, we are heterozygous. Heterozygosity, the frequency of heterozygotes, the Aa type, is a measure of genetic diversity. We can average these frequencies over all loci to obtain a generic measure of genetic variability for any population. When a small population breaks off from a large parent population, as in the Out-of-Africa dispersal, it only takes away a small portion of the total genetic variation with it. We therefore expect it’s average heterozygosity to be lower. More generally, heterozygosity may be even lower for geographic isolates due to the serial-founder effect whereby the breakaway population splits further into even smaller populations, taking with them an even smaller sample of the genetic variability of the mother population. The evidence that this happened in our Out-of-Africa dispersal is simply overwhelming.
If the number of breeding individuals in a relatively isolated population is small, ie the effective population size is small, alleles are likelier to reach fixation. That is to say, the population may lose alleles simply due to random fluctuations in allele frequencies; a process called drift. When this happens, the allele is forever lost to the population — unless it can be reacquired by gene flow. The loss of variation by drift is dangerous. Since most harmful alleles are recessive — dominant lethal alleles are self-annihilating — heterozygosity, that is genetic variation, protects us against genetic disorders. A high degree of homozygosity is dangerous for the exact same reason that inbreeding is dangerous. Conversely, heterozygosity is beneficial. The evidence is overwhelming that it protects us against genetic disorders.
So much for preliminaries. Now, what has been discovered recently is that, not only does heterozygosity provide insurance against genetic disorders, heterozygosity is strongly correlated with things like height, IQ and lung capacity. This is not the straightforward mean of heterozygosity at multiple loci that we plotted above. Instead, what seems to matter is what is called ‘runs of homozygosity’ (ROH). Basically, boring long strings of homozygous loci, are strongly negatively correlated with things like height, IQ and lung capacity.
The distribution of ROH obeys the same Out-of-Africa pattern as mean heterozygosity: The further you go, the greater the ROH.
The evidence that ROH has a very strong influence on the genetic component of IQ, height and lung capacity is overwhelming. In a paper published in Nature, Joshi et al. (2015) examined ROH in 354,224 individuals from 102 cohorts. Their estimates boggle the mind. A one unit increase in ROH decreases height by 2.9 standard deviation units or 20cm, cognitive ability by 4.6 standard deviation units, educational attainment by 4.7 standard units or 12.9 months, and lung capacity by 3.5 standard units or 137ml. And all these fixed-effects are highly statistically significant.
This is quite simply the most significant result to come out of population genetics that I have seen. The bottom line could not be clearer. Not only is world order not reducible to biology, if biological reductionism is true, the polarization of the world is exactly the wrong way around. Mean ROH is 124Mb in Europe and 143Mb in East Asia; in Africa it is 64Mb. If biological reductionism were true, Africa would be rich and powerful and the two extremities of Eurasia would be peripheral.
The plot thickens, as they say.