Bozur
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Post by Bozur on Jul 4, 2005 0:43:38 GMT -5
NATIONAL DESK | June 3, 2005, Friday Researchers Say Intelligence and Diseases May Be Linked in Ashkenazic Genes By NICHOLAS WADE (NYT) 1637 words
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Bozur
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Post by Bozur on Jul 4, 2005 0:44:34 GMT -5
Researchers Say Intelligence and Diseases May Be Linked in Ashkenazic Genes
By NICHOLAS WADE Published: June 3, 2005 nytimes.com
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 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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Bozur
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Post by Bozur on Jan 18, 2006 2:04:40 GMT -5
New Light on Origins of Ashkenazi in Europe
By NICHOLAS WADE Published: January 14, 2006
A new look at the DNA of the Ashkenazi Jewish population has thrown light on its still mysterious origins.
Until now, it had been widely assumed by geneticists that the Ashkenazi communities of Northern and Central Europe were founded by men who came from the Middle East, perhaps as traders, and by the women from each local population whom they took as wives and converted to Judaism.
But the new study, published online this week in The American Journal of Human Genetics, suggests that the men and their wives migrated to Europe together.
The researchers, Doron Behar and Karl Skorecki of the Technion and Ramban Medical Center in Haifa, and colleagues elsewhere, report that just four women, who may have lived 2,000 to 3,000 years ago, are the ancestors of 40 percent of Ashkenazis alive today. The Technion team's analysis was based on mitochondrial DNA, a genetic element that is separate from the genes held in the cell's nucleus and that is inherited only through the female line. Because of mutations - the switch of one DNA unit for another - that build up on the mitochondrial DNA, people can be assigned to branches that are defined by which mutations they carry.
In the case of the Ashkenazi population, the researchers found that many branches coalesced to single trees, and so were able to identify the four female ancestors.
Looking at other populations, the Technion team found that some people in Egypt, Arabia and the Levant also carried the set of mutations that defines one of the four women. They argue that all four probably lived originally in the Middle East.
A study by Michael Hammer of the University of Arizona showed five years ago that the men in many Jewish communities around the world bore Y chromosomes that were Middle Eastern in origin. This finding is widely accepted by geneticists, but there is less consensus about the women's origins.
David Goldstein, now of Duke University, reported in 2002 that the mitochondrial DNA of women in Jewish communities around the world did not seem to be Middle Eastern, and indeed each community had its own genetic pattern. But in some cases the mitochondrial DNA was closely related to that of the host community.
Dr. Goldstein and his colleagues suggested that the genesis of each Jewish community, including the Ashkenazis, was that Jewish men had arrived from the Middle East, taken wives from the host population and converted them to Judaism, after which there was no further intermarriage with non-Jews.
The Technion team suggests a different origin for the Ashkenazi community: if the women too are Middle Eastern in origin, they would presumably have accompanied their husbands. At least the Ashkenazi Jewish community might have been formed by families migrating together.
Dr. Hammer said the new study "moves us forward in trying to understand Jewish population history." His own recent research, he said, suggests that the Ashkenazi population expanded through a series of bottlenecks - events that squeeze a population down to small numbers - perhaps as it migrated from the Middle East after the destruction of the Second Temple in A.D. 70 to Italy, reaching the Rhine Valley in the 10th century.
But Dr. Goldstein said the new report did not alter his previous conclusion. The mitochondrial DNA's of a small, isolated population tend to change rapidly as some lineages fall extinct and others become more common, a process known as genetic drift. In his view, the Technion team has confirmed that genetic drift has played a major role in shaping Ashkenazi mitochondrial DNA. But the linkage with Middle Eastern populations is not statistically significant, he said.
Because of genetic drift, Ashkenazi mitochondrial DNA's have developed their own pattern, which makes it very hard to tell their source. This differs from the patrilineal case, Dr. Goldstein said, where there is no question of a Middle Eastern origin.
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