Sickle Cell, Tay Sachs and some European Jews

[GeneW]

Some European Jews were limited during Medieval times to careers as money changers and bankers. The most successful bankers and moneychangers had large families. Jews were not encouraged to marry Gentiles and vice versa.

Over the course of a few centuries the smartest Jews had more kids. They paid for this increased brilliance by getting nasty genetic diseases.

However the only time that kids suffered is when both parents carried the mutations. If only parent had the mutation the kid got a lot smarter, was a carrier but did not suffer too many genetic problems.

Our general hypothesis is that high IQ test scores of Ashkenazim, along with their unusual pattern of abilities, are a product of natural selection, stemming from their occupation of an unusual social niche. All the required preconditions–low inward gene flow and unusually high reproductive reward for certain cognitive skills, over a long-enough period–did exist. These preconditions are both necessary and sufficient, so such a selective process would almost inevitably have this kind of result. The pattern of high
achievement among Ashkenazi Jews and the observed psychometric results are certainly consistent with this hypothesis.

Our more specific prediction is that some or most of the characteristic Ashkenazi genetic diseases are by-byproducts of this strong selection for IQ. In particular we think that this is the most likely explanation of the sphingolipid mutations. The improbably high frequency and observed effects of the storage compounds of axonal and dendritic growth are very suggestive of selection for some neurological trait. We predict that heterozygotes
for the sphingolipid storage mutations should have higher scores on psychometric tests of verbal and mathematical abilities than their non-carrier sibs. In the case of Gaucher disease, homozygotes for mild mutations such as N370S may also have elevated scores, and the occupational profile of the sample of Gaucher patients supports the hypothesis.

Considering the reports of elevated IQ in torsion dystonia and CAH heterozygotes, we think that carriers of other common Ashkenazi mutations should also be studied, including the DNA repair mutations but also carriers of mutations with neurological effects such as familial dysautonomia and Canavan disease.

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From http://homepage.mac.com/harpend/.Pub...jbiosocsci.pdf

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