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Researchers Say Intelligence and Diseases May Be Linked in Ashkenazic Genes
By NICHOLAS WADE

A team of scientists at the University of Utah has proposed that the unusual pattern of genetic diseases seen among Jews of central or northern European origin, or Ashkenazim, is the result of natural selection for enhanced intellectual ability.

The selective force was the restriction of Ashkenazim in medieval Europe to occupations that required more than usual mental agility, the researchers say in a paper that has been accepted by the Journal of Biosocial Science, published by Cambridge University Press in England. ["The Natural History of Ashkenazi Intelligence"]

The hypothesis advanced by the Utah researchers has drawn a mixed reaction among scientists, some of whom dismissed it as extremely implausible, while others said they had made an interesting case, although one liable to raise many hackles.

"It would be hard to overstate how politically incorrect this paper is," said Steven Pinker, a cognitive scientist at Harvard, noting that it argues for an inherited difference in intelligence between groups. Still, he said, "it's certainly a thorough and well-argued paper, not one that can easily be dismissed outright."

"Absolutely anything in human biology that is interesting is going to be controversial," said one of the report's authors, Dr. Henry Harpending, an anthropologist and a member of the National Academy of Sciences.

He and two colleagues at the University of Utah, Gregory Cochran and Jason Hardy, see the pattern of genetic disease among the Ashkenazi Jewish population as reminiscent of blood disorders like sickle cell anemia that occur in populations exposed to malaria, a disease that is only 5,000 years old.

In both cases, the Utah researchers argue, evolution has had to counter a sudden threat by favoring any mutation that protected against it, whatever the side effects. Ashkenazic diseases like Tay-Sachs, they say, are a side effect of genes that promote intelligence.

The explanation that the Ashkenazic disease genes must have some hidden value has long been accepted by other researchers, but no one could find a convincing infectious disease or other threat to which the Ashkenazic genetic ailments might confer protection.

A second suggestion, wrote Dr. Jared Diamond of the University of California, Los Angeles, in a 1994 article, "is selection in Jews for the intelligence putatively required to survive recurrent persecution, and also to make a living by commerce, because Jews were barred from the agricultural jobs available to the non-Jewish population."

The Utah researchers have built on this idea, arguing that for some 900 years Jews in Europe were restricted to managerial occupations, which were intellectually demanding, that those who were more successful also left more offspring, and that there was time in this period for the intelligence of the Ashkenazi population as a whole to become appreciably enhanced.

But the Utah researchers' analysis comes at a time when some geneticists have suggested natural selection is not the reason for the Ashkenazic diseases after all. Two years ago, Dr. Neil Risch, a geneticist now at the University of California, San Francisco, proposed a different genetic mechanism known as a founder effect, which occurs when a population is reduced for a time.

He found that all the Ashkenazic diseases had similar properties, including having arisen within the last 1,100 years. Therefore they had all arisen through the same cause, he argued, which must be founder effects, because it was unlikely that all could be due to natural selection. Last year, Dr. Montgomery Slatkin of the University of California, Berkeley, came to much the same conclusion for different reasons.

The Utah team agrees with Dr. Risch that the diseases all arose in historical times from the same cause but say natural selection is more likely because none of the non-disease Ashkenazic genes they tested showed any sign of a founder effect. They say the clustering of four of the diseases in the same biochemical pathway could only have arisen under the influence of natural selection, and calculate that the odds of a founder effect producing such a cluster are vanishingly low.

The four diseases, all of which are caused by mutations that affect the cell's management of chemicals known as sphingolipids, are Tay-Sachs, Niemann-Pick, Gaucher, and mucolipidosis type IV. A second cluster of diseases affects repair of DNA.

Turning to the possibility that some infection was the cause of the selective effect, the Utah researchers noted that Ashkenazim and Europeans lived together in the same cities and were exposed to the same microbes. If disease were the agent of selection, the Utah team argues, the European population would have developed a similar genetic response.

Ashkenazi Jews occupied a different social niche from their European hosts, and that is where any selective effect must have operated, the Utah researchers say. From A.D. 800, when the Ashkenazi presence in Europe is first recorded, to about 1700, Ashkenazi Jews held a restricted range of occupations, which required considerable intellectual acumen. In France, most were moneylenders by A.D. 1100. Expelled from France in 1394, and from parts of Germany in the 15th century, they moved eastward and were employed by Polish rulers first as moneylenders and then as agents who paid a large tax to a noble and then tried to collect the amount, at a profit, from the peasantry. After 1700, the occupational restrictions on Jews were eased.

As to how the disease mutations might affect intelligence, the Utah researchers cite evidence that the sphingolipid disorders promote the growth and interconnection of brain cells. Mutations in the DNA repair genes, involved in second cluster of Ashkenazic diseases, may also unleash growth of neurons.

In describing what they see as the result of the Ashkenazic mutations, the researchers cite the fact that Ashkenazi Jews make up 3 percent of the American population but won 27 percent of its Nobel prizes, and account for more than half of world chess champions. They say that the reason for this unusual record may be that differences in Ashkenazic and northern European I.Q. are not large at the average, where most people fall, but become more noticeable at the extremes; for people with an I.Q. over 140, the proportion is 4 per 1,000 among northern Europeans but 23 per 1,000 with Ashkenazim.

The Utah researchers describe their proposal as a hypothesis. Unlike many speculations, it makes a testable prediction: that people who carry one of the sphingolipid or other Ashkenazic disease mutations should do better than average on I.Q. tests.

The researchers have identified two reasonably well accepted issues, the puzzling pattern of diseases inherited by the Ashkenazi population and the population's general intellectual achievement. But in trying to draw a link between them they have crossed some fiercely disputed academic territories, including whether I.Q. scores are a true measure of intelligence and the extent to which intelligence can be inherited.

The authors "make pretty much all of the classic mistakes in interpreting heritability," said Dr. Andrew Clark, a population geneticist at Cornell University, and the argument that the sphingolipid gene variants are associated with intelligence, he said, is "far-fetched."

In addition, the genetic issue of natural selection versus founder effects is far from settled. Dr. Risch, whose research supports founder effects, said he was not persuaded by the Utah team's arguments. Dr. David Goldstein, a geneticist at Duke University who was not connected with either Dr. Risch's or the Utah study, was more open on the issue, saying Dr. Risch had made "quite a strong case" that founder effects could be the cause, but had not ruled out the possibility of selection.

Dr. Slatkin, though favoring a founder effect over all, said he agreed with the Utah team that this would not account for the cluster of sphingolipid diseases.

As for the Utah researchers' interpretation of Jewish medieval history, Paul Rose, professor of Jewish studies at Pennsylvania State University, said, "I think that some of their conclusions may be right though they still need a lot of work to be persuasive to historians and others."

Dr. Gregory Cochran, the first author on the Utah team's paper and a physicist who took up biology, said he became interested in the subject upon learning that patients with a particular Ashkenazic disease known as torsion dystonia were told by their physicians that "the positive thing is that this makes you smart."

"When you're in a hurry and have strong selection, you have a lot of genes with bad side effects," he said. The Ashkenazi Jewish population seemed to fit this pattern, he said, since they married only inside the community, making selection possible, and they had an urgent need for greater intelligence. Evolution had therefore selected every possible mutation that worked in this direction, despite their harmful side effects when inherited from both parents. "In a sense, I consider this a very boring paper since it raises no new principles of genetics," Dr. Cochran said.
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