Sunday, November 05, 2006

The IQ of the Ashkenazi Jews in Israel   posted by Darth Quixote @ 11/05/2006 11:59:00 PM
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In press at The Journal of Biosocial Science is a paper by Hanna David and Richard Lynn reviewing several Israeli studies comparing the IQs of the Ashkenazim to those of Jews from non-European backgrounds. A virtue of the paper is that it brings to light many studies that had originally been published in Hebrew and thus been obscured from the attention of Western differential psychologists.

The results, compiled over the last half century, are so stark that even as notorious a number bumbler as Lynn could not possibly have manufactured the signal. David and Lynn conclude that the Ashkenazim enjoy an IQ advantage of roughly 14 points over their fellow Jews.

Related: Recall that N-acetylaspartate (NAA), a brain metabolite found to correlate positively with IQ and often employed as a marker (by its absence) of brain insult or dysfunction, leads to Canavan disease when an individual is homozygous for a mutation knocking out the enzyme that breaks it down. This mutation is more common among the Ashkenazi Jews than in any other population--an observations that led Cochran, Hardy, and Harpending (2006) to hypothesize that the mutant is in fact an IQ booster. I have found an extremely thorough review of NAA by the neurochemist Morris Baslow (2003). Much of it is over my head, but perhaps the biochemists and neuroscientists among us can make something of it. My impression is that there are several plausible pathways by which NAA might affect the information-processing capacity of neurons and neural networks.

NAA is indeed an important intracellular osmolyte and storage form for brain Asp and Ac. It also participates in the formation of NAAG, supplies Ac to oligodendrocytes that may be incorporated into myelin, and has the potential for functioning as an intercellular signaling molecule, along with its derivative NAAG. However, as a hypothesis that encompasses most of these observations, it is proposed that the NAA cycle serves primarily as a neuronal mechanism to remove large amounts of metabolic water generated in performing its interneuronal and intercellular signaling tasks.

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