Race and intelligence

I'm gonna get more fire on this one. I'm not going to talk about this from a comparative standpoint but am going to present general information; I am not going to talk about this in controversial terms until I'm a professor and I've got tenure, because I know who probably reads this blog and I need to make it clear, in no uncertain terms, that I am an individual of no significant prejudices. ('No prejudices' would be a misnomer, because everybody's got them.)

Race is undoubtedly a factor in intelligence because members of certain cultural groups tend to mate with people of their own cultural group - interracial offspring are becoming more common, yes, but there is still a strong trend in organisms to stick to their own. An example of selection for intelligence is Steven Pinker's article in The New Republic (admittedly a conservative paper which I usually will not read because of its sheer stupidity, but Steven Pinker writes mostly good stuff, though I still thoroughly disagree with him on his rather sexist defense of Larry Summers) about selection for intelligence in individuals of Ashkenazi Hebrew background ('Jewish' is a misnomer; 'Jewish' describes an adherent of a religion, not a member of an ethnicity.) Pinker writes:

The appearance of an advantage in average intelligence among Ashkenazi Jews is easier to establish than its causes. Jews are remarkably over-represented in benchmarks of brainpower. Though never exceeding 3 percent of the American population, Jews account for 37 percent of the winners of the U.S. National
Medal of Science, 25 percent of the American Nobel Prize winners in literature,
40 percent of the American Nobel Prize winners in science and economics, and so
on. On the world stage, we find that 54 percent of the world chess champions have had one or two Jewish parents.
Does this mean that Jews are a nation of meinsteins? It does not. Their average IQ has been measured at 108 to 115, one-half to one standard deviation above the mean. But statisticians have long known that a moderate difference in the means of two distributions translates into a large difference at the tails. In the simplest case, if we have two groups of the same size, and the average of Group A exceeds the average of Group B by fifteen IQ points (one standard deviation), then among people with an IQ of 115 or higher the As will outnumber the Bs by a ratio of three to one,
but among people with an IQ of 160 or higher the As will outnumber the Bs by a ratio of forty-two to one. Even if Group A was a fraction of the size of Group B to begin with, it would contribute a substantial proportion of the people who had the highest scores.

The CH&H theory can be divided into seven hypotheses. The first is that the Ashkenazi advantage in intelligence is genetic in the first place. Many intellectuals dismiss this possibility out of hand, having been convinced by Stephen Jay Gould's book The Mismeasure of Man that general intelligence does not exist and that there is no evidence for its heritability. But a decade ago, the American Psychological Association commissioned an ideologically and racially diverse panel of scientists to review the evidence. They reported that IQ tests measure a stable property of the
person; that general intelligence reflects a real phenomenon (namely, that measures of different aspects of intelligence intercorrelate); that it predicts a variety of positive life outcomes; and that it is highly heritable among individuals within a group. This does not imply that differences between groups are also genetic, since one group may experience a difference across the board, such as in wealth, discrimination, or social and cultural capital.
The most obvious test of a genetic cause of the Ashkenazi advantage would be a cross-adoption study that measured the adult IQ of children with Ashkenazi biological parents and gentile adoptive parents, and vice versa. No such study exists, so CH&H's evidence is circumstantial. The Ashkenazi advantage has been found in many decades, countries, and levels of wealth, and the IQ literature shows no well-understood environmental factors capable of producing an advantage of that magnitude. It remains possible that the advantage is caused by some poorly understood environmental cause. Environmental hypotheses tend to get a free pass in intellectual life, but they must be scrutinized as well. The possibility that Jewish mothers produce smarter children is unlikely in light of abundant evidence that families have no lasting effect on intelligence. Siblings reared together are no more correlated in IQ than siblings who were separated at birth, and adopted siblings are not correlated at all. Growing up in a given home within a culture seems to leave no
lasting stamp on intelligence.
But parents are just one aspect of the environment, and the cultural milieu is surely more important. Yet it cannot be taken for granted that Jewish culture favors achievement in physics, philosophy, or chess. ...

Also worth remembering is the saying that if wishes were horses, beggars would ride. Mere expectations cannot produce a brilliant mind. So an environmental explanation of the Ashkenazi advantage in intelligence is also unproven, though it certainly cannot be ruled out.

The second hypothesis is that Ashkenazim tended to marry their own during most of their formative history. This is necessary, because natural selection cannot change the genetic composition of a population if new genes are constantly flowing in from the neighbors and diluting its effects. CH&H cite the Jewish traditions of avoiding intermarriage, proselytization, or conquest. They mention historical accounts attesting that intermarriage was indeed rare, and genetic evidence pointing to an admixture of about 0.5 to 1 percent of neighboring genes per generation. Note that over many centuries this is enough to make Ashkenazim genetically similar to their European neighbors, so the notion of a distinct "Jewish race" is indeed nonsense. But the two populations are not identical: the genetic overlap due to interbreeding is around one-third to one-half, depending on which genes you look at.

The third hypothesis is that Ashkenazim were concentrated in mercantile, managerial, and financial occupations at a time when their neighbors were likely to be peasant farmers, craftsmen, or soldiers. Jews presumably had an accidental head start in these occupations because of their religious obligation of literacy, their ability to network with one another across far-flung communities, and their role as a go-between amid Christian and Islamic civilizations. In the Middle Ages they were funneled into middlemen professions by their exclusion from guilds, their inability to own land, and the niche opened up by the Christian prohibition of usury. CH&H cite historians who have documented that a majority of Jews were middlemen during the Middle Ages, many of them moneylenders.
The fourth hypothesis is that in traditional Ashkenazi occupations higher intelligence led to greater economic success. CH&H cite contemporary data that IQ predicts income and occupational success in every profession, and that the minimum IQ requirements for financial and managerial occupations are higher than those for farming, crafts, and the military. Presumably, numeracy, verbal skill, problem solving, and social intelligence are invaluable in calculating slim profits and interest
rates, in assessing creditworthiness, in anticipating trends, and in meeting other cognitive demands of the middleman niche. Cultural historians have noticed that these skills seem to be cultivated among contemporary middleman minorities.
The fifth hypothesis is that richer people had more surviving children during the centuries in which Ashkenazim were middlemen. Today the wealthy tend to have fewer children, but before the demographic transition (which began with the industrial revolution) wealth brought better nutrition and healthier surroundings, and hence more children who survived to adulthood. CH&H cite historians who made this point about the Ashkenazim in particular.
The sixth hypothesis is that the common Ashkenazi diseases are a product of natural selection rather than genetic drift, the other mechanism of evolutionary change. In any finite population, some genes can go extinct and others can take over the population by sheer chance. Imagine an island on which a lightning bolt happened to kill everyone but the redheads; the descendants would found a redheaded race, despite the lack of any advantage to redheadedness. As the example suggests, drift is most potent in small populations. It can leave a genetic stamp on an inbred community that was founded by a small number of pioneers, or that suffered a bottleneck in population size and subsequently rebounded, multiplying copies of whatever genes were possessed by the few lucky survivors.
Most medical geneticists believe that drift is to blame for Ashkenazic genetic diseases. CH&H respond with two lines of evidence, based on the logic that drift affects all genes equally, be they advantageous, neutral, or deleterious. Bottlenecks tend to reduce heterozygosity, or the state of having different versions of a gene from one's mother and father. That is because if only a few ancestors were around at some point in the past, they would have had fewer gene variants to leave to their descendants, increasing the chance that a gene would meet a copy of itself when a couple conceives a child. CH&H adduce evidence that Ashkenazim, unlike other small populations, have degrees of heterozygosity similar to their more numerous European neighbors. They also suggest that Ashkenazim have a distribution of neutral genes similar to that of Europeans in general. A problem in evaluating this hypothesis is that arguments for and against genetic bottlenecks are often sensitive to assumptions built into the models, and we can expect CH&H to be debating their critics for some time.
Perhaps the most interesting biological fact addressed by CH&H is that Ashkenazi
genetic diseases tend to cluster in a small number of metabolic pathways. Genes involved in different stages of a single biochemical assembly line are often scattered throughout the genome. The presence of mutations in a set of these genes is a fingerprint of natural selection, because the only common denominator is their effect on the organism, which is what selection, and selection alone, can "see." Random drift is unlikely to collect genes scattered hither and yon that just happen to take part in the same biochemical process.
It has long been known that Ashkenazi diseases cluster in groups with a common
metabolic pathway. They include disorders of storing sphingolipids ("sphinx-like fats"), such as Tay-Sachs and Gaucher's, and disorders of DNA repair, including the BRCA1 gene, which increases the odds of breast cancer. Using a functional genomic database, CH&H try to calculate the a priori probability that these clusterings could have arisen at random, and dismiss it as infinitesimal.


The seventh and really pivotal hypothesis is that the common Ashkenazi diseases are by-products of genes that were selected because they enhance intelligence. The alternative is that they were selected for something else, such as resistance to infectious disease. CH&H discount disease resistance for most of the genes in question because the genes are not shared by other Europeans, who must have been victims of the same germs.
Harmful genetic by-products can arise in two major ways. In heterozygote advantage, a gene confers an advantage on possessors of one copy (heterozygotes or carriers), which outweighs the disadvantage it encumbers on possessors of two copies (homozygotes). The best-known example is the sickle cell gene, prevalent in malaria-ridden parts of Africa, which leads to malaria resistance in homozygotes but to anemia in heterozygotes. CH&H suggest that a similar trade-off could have produced the Ashkenazi diseases, though the evidence is paltry. They note that increased levels of sphingolipids foster neural growth in developing rodent brains, and that the normal version of the BRCA1 gene inhibits neural growth; but that is a long way from human intelligence.
The other kind of by-product comes from antagonistic pleiotropy: a single copy of a gene has multiple effects, the good ones outweighing the bad ones on average. The
evidence here is a bit better. People with the genes for torsion dystonia,
non-classical congenital adrenal hyperplasia, and Gaucher's disease tend to have higher average IQs, or tend to be concentrated in professions such as physics and engineering. But the numbers are small. So the evidence that Ashkenazi disease genes boost intelligence is extremely iffy. Still, the hypothesis is testable: compare the IQs in a large sample of sibling pairs, one of whom is a carrier of a disease gene, the other a non-carrier. If the carriers are not smarter, the hypothesis is wrong. The study could easily be done in Israel, with its centralized records of health care, education, and military service.

Pinker's hypotheses seem to state that certain genes are going to be selected for in certain populations and some populations are more prone to select for intelligent genes. So there are, certainly, some mild genetic correlations, but I have to issue a warning: this does not mean one race has superior intelligence to another. Even if one race has a higher average IQ, you cannot generalize from a population to an individual. The mean is not the median. People of different races are very spread out among the continuum of IQ.

One of my favorite academics in my field is J. Philippe Rushton, an evolutionary neurogeneticist at the University of Western Ontario. Dr. Rushton nearly lost his job because of his article 'Evolutionary Biology and Heritable Traits (With Reference to Oriental-White-Black Differences)' . Pinker and Rushton make the point that there are clearly differences between people of different ethnic backgrounds, but that there is potential for misuse. Intelligence researchers will have to deal with - and I am absolutely afraid of having to deal with this in the future, but I will need to deal with this - human rights groups such as the NAACP. Their purpose is noble and I am a LOUD supporter of civil rights for folks, but censoring science because they may not want to know information gathered in an ethical, honest way is going too far - and they will most likely misinterpret it, because frankly, not too many people in most human rights groups about anything lately have any science background, and people in general are also morons.

Before we tackle race and intelligence, though, we still have to figure out the neurological basis of it. As I said, I aim to be one of the researchers who does significant work in this area. We have a tiny list of genes, and a comprehensive neurologic model of intelligence is not going to be possible until we have the rest of the genes.

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