[Paleopsych] NYT: Researchers Say Intelligence and Diseases May Be Linked in Ashkenazic Genes

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Researchers Say Intelligence and Diseases May Be Linked in Ashkenazic Genes
New York Times, 5.6.3


    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

    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

    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

    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

    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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