My grandparents were immigrants from Eastern Europe who owned a small necktie factory on the outskirts of Montreal. While visiting them one weekend, I found my grandfather on the factory floor, cutting shapes out of irregular stacks of cloth with a fabric saw. He explained that by carving up the remnants that were left over when the neckties had been cut out and stitching them together in places that didn't show, he could get a few extra ties out of each sheet of cloth. I asked him why he was doing this himself rather than leaving it to his employees. He shrugged, tapped his forehead, and said, "Goyishe kop," a term of condescension that literally means "gentile head."
He wasn't exactly serious, but he wasn't exactly not serious either. Jews have long had an ambivalent attitude toward their own intelligence, and toward their reputation for intelligence. There is an ethnic pride at the prevalence of Jews in occupations that reward brainpower. A droll e-mail called "New Words to Add to Your Jewish Vocabulary" includes "jewbiliation, N: pride in finding out that one's favorite celebrity is Jewish" and "meinstein, N: My son, the genius." Many Jews subscribe to a folk theory that attributes Jewish intelligence to what would have to be the weirdest example of sexual selection in the living world: that for generations in the shtetl, the brightest yeshiva boy was betrothed to the daughter of the richest man, thereby favoring the genes, if such genes there are, for Talmudic pilpul.
But pride has always been haunted by fear that public acknowledge of Jewish achievement could fuel the perception of "Jewish domination" of institutions. And any characterization of Jews in biological terms smacks of Nazi pseudoscience about "the Jewish race." A team of scientists from the University of Utah recently strode into this minefield with their article "Natural History of Ashkenazi Intelligence," which was published online in the Journal of Biosocial Science a year ago, and was soon publicized in The New York Times, The Economist, and on the cover of New York magazine.
The Utah researchers Gregory Cochran, Jason Hardy, and Henry Harpending (henceforth CH&H) proposed that Ashkenazi Jews have a genetic advantage in intelligence, and that the advantage arose from natural selection for success in middleman occupations (moneylending, selling, and estate management) during the first millennium of their existence in northern Europe, from about 800 C.E. to 1600 C.E. Since rapid selection of a single trait often brings along deleterious by-products, this evolutionary history also bequeathed the genetic diseases known to be common among Ashkenazim, such as Tay-Sachs and Gaucher's.
The CH&H study quickly became a target of harsh denunciation and morbid fascination. It raises two questions. How good is the evidence for this audacious hypothesis? And what, if any, are the political and moral implications?
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. In his autobiography, the eminent social psychologist Stanley Schachter wrote that
I went to Yale much against my father's wishes. He couldn't have cared less about higher education and wanted me to go to a one-year laundry college (no kidding) out in the Midwest and join him then in the family business. I never have understood what this intellectually driven Jewish immigrant business is all about. It wasn't true of my family, and I know very few families for which it was true…. To me, Jewish love of learning has always seemed a myth perpetrated by a few rabbis' sons who weren't good at anything much but going to school and then spending the rest of their lives writing novels about it.
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.
CH&H, then, have provided prima facie evidence for each of the hypotheses making up their theory. But all the hypotheses would have to be true for the theory as a whole to be true--and much of the evidence is circumstantial, and the pivotal hypothesis is the one for which they have the least evidence. Yet that hypothesis is also the most easily falsifiable. By that criterion, the CH&H story meets the standards of a good scientific theory, though it is tentative and could turn out to be mistaken.
But is it good for the Jews? More to the point, is it good for ideals of tolerance and ethnic amity? On one interpretation, perhaps it is. Jewish achievement is obvious; only the explanation is unclear. The idea of innate Jewish intelligence is certainly an improvement over the infamous alternative generalization, a worldwide Jewish conspiracy. And attention to the talents needed in the middleman niche (whether they are biological or cultural) could benefit other middleman minorities, such as Armenians, Lebanese, Ibos, and overseas Chinese and Indians, who have also been targets of vicious persecution because of their economic success.
And yet the dangers are real. Like intelligence, personality traits are measurable, heritable within a group, and slightly different, on average, between groups. Someday someone could test whether there was selection for personality traits that are conducive to success in money-lending and mercantilism, traits that I will leave to the reader's imagination. One can also imagine how a finding of this kind would be interpreted in, say, Cairo, Tehran, and Kuala Lumpur. And the CH&H study could lower people's resistance to more invidious comparisons, such as groups who historically score lower, rather than higher, on IQ tests.
What can be done? In recent decades, the standard response to claims of genetic differences has been to deny the existence of intelligence, to deny the existence of races and other genetic groupings, and to subject proponents to vilification, censorship, and at times physical intimidation. Aside from its effects on liberal discourse, the response is problematic. Reality is what refuses to go away when you do not believe in it, and progress in neuroscience and genomics has made these politically comforting shibboleths (such as the non-existence of intelligence and the non-existence of race) untenable.
Rather than legislating facts, could we adopt a policy of agnosticism, and recommend that we "don't go there"? Scientists routinely avoid research that may have harmful consequences, such as injuring human subjects or releasing dangerous microorganisms. The problem with this line of thought is that it would restrict research based on its intellectual content rather than on its physical conduct. Ideas are connected to other ideas, often in unanticipated ways, and restrictions on content could cripple freedom of inquiry and distort the intellectual landscape.
Also, there are positive reasons to study the genetics of groups. Until the day that every person is issued a CD containing his or her genome, medicine will need the statistical boost of data on group differences when targeting tests and treatments to those most likely to benefit from them. Remember that the CH&H study grew out of research aimed at reducing the enormous suffering caused by genetic diseases. Many have effects on the nervous and endocrine systems, and connections with the psychological traits of sufferers and carriers may be unavoidable. And of course the tests could refute claims of group differences as easily as they could confirm them.
The genetics of groups is also an exciting frontier in the study of history. Many Jews have been thrilled by the discoveries of a common Y-chromosome among many of today's kohanim (believed to be descendants of the priestly caste in ancient Judea, who were themselves the descendants of Aaron), of genetic commonalities between the Ashkenazic and Sephardic Jews traceable to a common ancestry in the Middle East, and of the presence of these genes in isolated communities in Africa and Asia that retain some Jewish rituals. Studies of the genes of African, American, and Australian populations could shed light on their prehistory, filling in pages that are sadly missing from the history of our species, as well as enlightening curious individuals about their genealogy.
In theory, we have the intellectual and moral tools to defuse the dangers. "Is" does not imply "ought." Group differences, when they exist, pertain to averages, not to individual men and women. There are geniuses and dullards, saints and sinners, in every race, ethnicity, and gender. Political equality is a commitment to universal human rights, and to policies that treat people as individuals rather than as representatives of groups; it is not an empirical claim that people are indistinguishable. Many commentators seem unwilling to grasp these points.
The revolution in human genomics has spawned profuse commentary about the perils of cloning and human genetic enhancement. But these fears may be misplaced. When people realize that cloning is just forgoing a genetically unique child for an identical twin of one of the parents, rather than resurrecting a soul or investing in an organ farm, I suspect no one will want to do it. And when they realize that most genes have costs as well as benefits (a gene might raise a child's IQ but also predispose him to a genetic disease), "designer babies" will lose whatever appeal they have. In contrast, the power to uncover genetic and evolutionary roots of group differences in psychological traits is both more likely to materialize and more incendiary in its consequences. And it is a prospect that we are, intellectually and emotionally, very poorly equipped to confront.
Steven Pinker is Johnstone Professor of Psychology at Harvard and the author of The Stuff of Thought.
"Groups and Genes" (June 26) mistakenly claimed that the sickle-cell gene leads to malaria resistance in homozygotes and anemia in heterozygotes. In fact, heterozygotes are resistant to malaria while homozygotes have sickle-cell anemia.