“I have always believed that the smartest people in the world are Asians,” declares Ed Koch, former mayor of New York (and, let’s face it, a pretty smart Ashkenazi Jew). “If you look at the special schools in New York City, they have so many. I think Stuyvesant’s 40 percent Asian now, and Bronx Science is 50”—actually, 53 and 49 percent—“so this paper is something I question.”
Jews have long debated the origin and nature of intelligence. In Kaddish, his beautiful book of aphorisms and ruminations about the rite of mourning, Leon Wieseltier notes that Rabbi Akiva postulated in the second century that sons inherit not just wealth, beauty, and strength from their fathers, but wisdom. Centuries later, Maimonides came to the opposite conclusion: It’s “great exertion” that makes us who we are. To attribute it to anything in our blood would trivialize our own agency, our hard work, our humanity. Wieseltier can’t even countenance another point of view. “The important question is, even if there is an Ashkenazi gene, what does it explain and what does it not explain?” he asks, when I reach him by phone. “The idea that it explains intellectuality seems empirically and philosophically spurious. The world is riddled—riddled!—with dumb Ashkenazi Jews, so it’s empirically false, and it’s philosophically spurious because it flies in the face of human freedom and the belief in human freedom.”
He thinks. “We’re living in a new golden age of scientism—the idea that there are scientific answers to all human questions,” he says. “People are so rattled by the speed and complexity of their lives that they need rock-solid certainty. They cannot bear to live inconclusively. Religion provides one definitive answer; science provides another. The important thing for most people is to feel that the way they live is an inevitable outcome.”
“I probably have a lot to say about this,” he concludes, “because I’m an Ashkenazi. So I must be really smart.”
Harpending and Cochran are hardly the first scientists to suggest that the diseases of the Ashkenazim are the product of genetic selection. Until fairly recently, many geneticists believed these mutations may have helped protect Jews from tuberculosis, because the disease so frequently surfaced in ghettos, though no one has been able to show how these mutations protected Jews—or why neighboring non-Jewish populations didn’t develop the same immunity.
If geneticists are disinclined to believe a trait is the result of natural selection, they attribute it instead to something called genetic drift, a process by which a mutation, for some random reason, evolves in one population but not in another. The smaller the population, the more glaring this mutation will seem. Geographic isolation, for instance, can explain radical genetic differences—if two groups evolve in separate places with little intermingling, different mutations are bound to pop up and spread in each. Natural disasters are another explanation—a rock slide could kill off a species of purple petunias, say. Or—in the case of Jews—one of the founders of a small settlement has a lot of children, and these children have lots of children. What the founder doesn’t know is that he or she has a gene mutation, like the one for Tay-Sachs. It takes hold and spreads, like an epidemic. (Geneticists call this “the founder effect.”)
“Ashkenazi neurological diseases are hints of ways in which one could supercharge intelligence, so it seems likely we could develop pharmaceutical agents that had similar effects.”
The problem with this theory, as Cochran and Harpending rather forcefully argue using mathematical models and a long disquisition about medieval Jewish economic history (starting from the expulsion of the Jews by King Dagobert of the Franks in 629), is that Tay-Sachs is just one of four sphingolipid diseases common to Jews, which seems like a rather unlikely coincidence. It suggests they all evolved for a reason, a similar reason. How could random mutations account for such a closely related cluster of ailments?
“That’s one of the ways this paper is actually strong,” says Sheila Rothman, a Columbia professor of public health who specializes in questions about genetics and group identity. “Geneticists don’t have a great grasp of Jewish history. They often tend to cite each other. Sometimes they cite themselves.”
It’s not just social scientists who concede this part of the paper is strong. So, too, do many mainstream geneticists, who’ve never been entirely comfortable with the theory of genetic drift to explain so many interrelated diseases among Jews.
“If these genes were shuffling randomly,” says Gregory Pastores, director of the neurogenetics unit at NYU, “then why is it that we see the clustering of four diseases in Jews—Gaucher, Niemann-Pick, mucolipidosis type IV, and Tay-Sachs—when the genes are in different chromosomes entirely? They’re not even next to one another.”
But this doesn’t mean that Pastores buys the message of the paper, and neither do most of his colleagues. Ostrer, from NYU, points out what he believes is a major flaw: The authors assume Jews are selected for sphingolipid diseases, and not for some other gene that may happen to be passed along with these diseases. “Blocks of the genome are inherited together,” he explains. “They’re saying heterozygotes carrying these sphingolipid mutations are smarter. Fine. But who’s to say it’s that gene and not the gene next door? Or down the street?”