not a reality under rabbinic law," Cohen observes._
Ethnic origins and hereditary priesthoods have opened two windows on Jewish history; a third has been created by the study of genetic diseases. Every population has its own particular set of genetic diseases, but those of Jewish communities in the United States and Israel have come under particular medical scrutiny, which is one reason why so many have been documented. The diseases are known as Mendelian, because they are caused by a single mutation and inherited in an obvious pattern; this stands in contrast with the so-called complex diseases, like cancer or diabetes, which can be caused by many contributing genes and are not inherited in any clear pedigree.
So far at least 40 different Mendelian diseases have been detected in Jewish 322
populations. Some of these diseases occur in non-Jewish populations as well, some are common to several Jewish communities, and some are restricted just to the Jews of a single community. The diseases are of course studied so as to help the patients but incidentally they yield many interesting clues to population history.
A disease called familial Mediterranean fever is caused by an errant gene that occurs among Ashkenazi, Iraqi and Moroccan Jews. It is also found in Armenians, the Muslim Druze sect and Turks. All present versions of the gene seem to be descended from a single ancestor who must have lived about 4,000 years ago in the ancient Middle Eastern population from which Jews and other ethnic groups are descended.
Later, the Jewish religion was founded and its adherents developed their own genetic history as they started to marry among themselves. The Jewish population may have grown to about a million people before suffering a terrible decline in AD 70, the year of the destruction of the temple in Jerusalem by a Roman army. That event began the diaspora, the dispersal of Jewish populations around the Mediterranean world. The largest Jewish community, the Ashkenazim of central and eastern Europe, may have reached 150,000 or so people by AD 1095, the year of the first crusade and the beginning of the persecution of Jews by Christians.
The Ashkenazi Jewish population is of particular interest because it has produced many individuals of high intellectual achievement, both in Europe and among the Ashkenazim who fled to the United States and elsewhere in the wake of Nazi persecution. Another attribute is a distinctive set of Mendelian diseases. The mutations that cause these diseases can hit at random anywhere in the genome, so would not be expected to favor any particular category of gene. But no fewer than four of the Ashkenazic Mendelian diseases affect the cell's management of chemicals known as sphingolipids, so called because their discoverer could not resolve the sphinxlike riddle of what they did. The four sphingolipid diseases are Tay-Sachs, Gaucher, Niemann-Pick and mucolipidosis type IV. Another cluster of four diseases affects the cell's system for repairing DNA. These are the BRCA1 and BRCA2 mutations which can cause breast and ovarian cancer, Fanconi's anemia Type C and Bloom syndrome. The sphingolipid diseases in particular are reminiscent of the group of mutations that cause blood disorders like sickle cell anemia, and which are now recognized as defenses against malaria. When malaria suddenly became a threat some 5,000 years ago, natural selection favored any mutation that offered protection, even if it carried serious disadvantages. Diseases like sickle cell anemia are the result of that quick fix. The sickle cell mutation, though devastating for individuals unlucky enough to inherit a copy from each parent, offers substantial protection against malaria for the much larger number in the population who inherit just a single copy.
Evolution has probably engineered many quick fixes like this in the human genome. Later, as the generations pass and better mutations turn up, evolution is generally able to improve on the quick fix or favor variant genes that diminish the side effects of the first mutation. This is why a batch of harmful mutations affecting a common pathway is the fingerprint of a recent evolutionary response to some sudden selective pressure.
Turning back to the four sphingolipid diseases, they look awfully like an evolutionary quick fix, a set of mutations selected because of some advantage gained by disrupting sphingolipid metabolism. So if that advantage was protection against disease, what disease could it have been? The puzzle is that carriers of the sphingolipid mutations don't seem to enjoy unusual immunity to any specific disease.
"A second hypothesis," writes Jared Diamond, after discussing the idea that the variant genes conferred greater resistance to tuberculosis, "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
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