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Old June 6th, 2005, 12:21 PM
Fred H. Fred H. is offline
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Default Natural selection—the good, the bad, & the ugly

Evidence corroborating selection, but it’s politically incorrect—

Quote:
Study links diseases to intelligence, Paper explores successes of European Jews, By Nicholas Wade, The New York Times, Posted June 3 2005

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

The selective force was the restriction of Ashkenazis 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 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, 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 the 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, disease-causing genes represent an evolutionary quick fix, in which any mutation at hand is favored in order to counter a sudden threat. 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 Ashkenazi 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 Ashkenazi genetic ailments might confer protection.

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 Ashkenazis 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 AD 800, when the Ashkenazi presence in Europe is first recorded, until about 1700, Ashkenazi Jews held a restricted range of occupations, which required considerable intellectual acumen. In France, most were moneylenders by AD 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 Ashkenazi 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 Ashkenazi and north European IQ are not large at the average, where most people fall, but become more noticeable at the extremes; for people with an IQ over 140, the proportion is 4 per 1,000 among northern Europeans but 23 per 1,000 with Ashkenazis.

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 Ashkenazi disease mutations should do somewhat better than average on IQ tests.

The Utah researchers have identified two reasonably well-accepted issues, the puzzling pattern of Ashkenazi inherited diseases 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 IQ 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."
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