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any particular mutation among Ashkenazim. Of course, they may be
waiting a long time as positive selection is a notoriously hard thing
to prove.
The reader may say, Yes, yes, this is all well and good, but isn t the
selection-versus-drift-in-Ashkenazim debate really just a minor tiff
of interest only to a few pointy-headed geneticists? Until recently,
I might have agreed. In 2005, however, the media picked up on a
paper by anthropologists Gregory Cochran, Jason Hardy, and Henry
Harpending that has effectively moved the argument from the realm
of science to that of sociology. Now we geneticists have a genuine
kerfuffle on our hands.
What Cochran, Hardy, and Harpending proposed is that the unique
demographic and sociological history of Ashkenazim in medieval Eu-
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rope created an environment that made intelligence a highly advanta-
geous trait. As part of this process, they hypothesized, certain gene
variants that conferred intelligence were selected for in Ashkenazim.
In particular, carriers for mutations in lysosomal storage genes were
likely to exhibit increased intelligence. In other words, not only were
lysosomal storage diseases selected for but they gave Ashkenazi Jews
an intellectual advantage.
Just as two copies of a mutant globin gene will cause sickle-cell
anemia, Cochran, Hardy, and Harpending noted, two mutant copies
of a lysosomal enzyme gene will cause Tay-Sachs disease, Gaucher,
Niemann-Pick disease, and mucolipidosis type IV. No one argues that
point. But the authors went further: just as one copy of the same glo-
bin gene will protect the carrier against malaria, they contended, so too
does one copy of the lysosomal enzyme gene enhance intelligence.
As one can imagine, the paper caused quite a stir. To support their
claims, Cochran, Hardy, and Harpending pointed to the fate of Ash-
kenazim in medieval Europe. Banned from guilds and forbidden to
own land, Jews were forced to be resourceful in order to make a living.
Because Christians were prohibited from engaging in usury, a large
proportion of Jews wound up working as moneylenders. Without
question, the job required intelligence and mathematical literacy.
Could it be that the main occupation Jews were consigned to acted
as a selective force favoring intelligence?
In addition to presumptive selection and the idea that four lyso-
somal storage diseases prevalent among Ashkenazim cannot be coinci-
dental, the other leg of the Cochran-Hardy-Harpending argument is a
contemporary one: a relatively large number of Jews are prize-winners
and chess champs, score very well on standardized tests, and so on.
Referring to the preponderance of lysosomal storage diseases among
Ashkenazim and to the large number of Ashkenazi Nobel laureates,
Cochran wondered aloud to New York magazine why 27 percent of
Nobel Prize winners have been Jewish.
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What about the biological evidence? Cochran, Hardy, and Harpen-
ding cited numerous studies of brains from individuals with lysosomal
storage diseases showing anatomical differences, involving neuronal
dendrites in particular, that might be suggestive of more intercon-
nections among neurons.5 The implication? Patients with lysosomal
storage diseases have diseased but potentially more highly developed
brains. The director of a Gaucher clinic in Jerusalem reported that
nearly one-third of his patients held jobs that, according to Cochran,
Hardy, and Harpending, required an IQ of 120 or better.
Their paper, published in a journal not frequently read by the hu-
man genetics community, is tantalizing, circumstantial, politically in-
correct in the extreme, and entirely speculative. In my view, the pos-
sibility that glycosphingolipids have something to do with intelligence
cannot be ruled out. But that s a very long way from being able to
confidently invoke the carrier status of lysosomal storage disease muta-
tions as an explanation for Ashkenazi intellect, if that s even what we re
measuring. Consequently, there s nothing to say that it s the lysosomal
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