The geneticists propose that one or more of the Khazar converts may have become levites, accounting for the R1a1 signature among today’s Ashkenazic levites. But Shaye Cohen, an expert on Jewish religious history, believes it unlikely that converts would become levites, let alone founding members of the levite community in Europe. The Khazar connection is “all hypothesis,” in his view.
The genetic findings about cohen and levite ancestry are just genetics; they have no bearing on who is or is not considered to be a cohen or a levite. “Genetics is not a reality under rabbinic law,” Cohen observes.321
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 populations.322 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 jobs available to the non-Jewish population.”323
The suggestion that one group of people may be genetically more intelligent than another is a sensitive subject, not least because it opens the door to the argument that if some groups are smarter, others may be less so. The idea Diamond floated was not followed up, and indeed the geneticists who next looked at the sphingolipid diseases suggested they had grown common not through natural selection but because of a quite different mechanism known as a founder effect.
If a population gets squeezed down to small numbers by some calamity, and then expands, its gene pool will be an amplified version of that of the few individuals who survived the disaster. If one of the survivors carried a generally rare mutation, the mutation will be much commoner in the new expanded population than it is in the general human population. The relatively high incidence of the usually rare mutation in the expanded population is called a founder effect, after the founder who carried the mutation.
Recently Neil Risch, now of the University of California, San Francisco, concluded that the four sphingolipid diseases must have become common among the Ashkenazi Jewish population because of founder effects. He noted that the four diseases had similar properties to the other Ashkenazic Mendelian diseases, such as having arisen very recently, in the last 1,100 years. Because all the Mendelian diseases seemed therefore to have arisen through the same cause, he argued, that cause must be founder effects, since natural selection wouldn’t favor such a miscellany of different mutations. 324
A similar conclusion was reached for different reasons by Montgomery Slatkin of the University of California, Berkeley.325 He calculated that if there had been two bottlenecks in the Jewish population, at AD 70 following the destruction of the temple, and at sometime after AD 1100, the founder effects caused by these two population reductions could explain how the Ashkenazic disease genes had gotten to be so common. Slatkin’s calculation did not rule out natural selection, but since a founder effect was possible, that provided the most economical explanation, in his view.
But a new and substantially buttressed case for natural selection, with the need for extra intelligence posited as the driving force, has now been advanced by Gregory Cochran, a physicist turned population geneticist, and Henry Harpending, an anthropologist at the University of Utah.326 They agree with Risch that all the diseases arose from the same cause and at about the same time. But the cause must have been natural selection, not founder effects, because in testing other, non-disease causing Ashkenazic genes, Cochran and Harpending could see no evidence for any of the reductions in population size required to cause Risch’s founder effects. Nor is there any clear historical evidence, they say, that the Ashkenazi Jewish population ever dwindled to the low numbers needed to generate a founder effect.
Having argued that natural selection must therefore have been the reason that the Ashkenazic mutations bec
ame so common, Cochran and Harpending next ruled out disease as the agent of selection. The Ashkenazic population, they note, lived in the same cities as their European hosts and suffered from the same diseases, yet Europeans show no similar pattern of mutations.
But there was a significant difference between Ashkenazim and Europeans, Cochran and Harpending argue, and it lay in the special range of occupations to which Ashkenazi Jews were restricted by their Christian hosts.
The origin of the Ashkenazi Jews is obscure but they were established in northern France by shortly after AD 900. Most had become moneylenders by AD 1100 because Christians forbade usury, and this continued for several centuries. Moneylending was an intellectually demanding profession, not least because the Indian numerals in use today, and specifically the concept of zero, did not become widespread in Europe until around 1500. Figuring out xvii percent of cccl, without the use of zero, is not a straightforward computation.
Jewish communities became subject to particular persecution after the First Crusade, launched in AD 1095. They were expelled from England in 1290, from France in 1394, and from various regions of Germany in the fifteenth century. Many migrated to Poland, where they lived first as moneylenders and then served as the managerial class for the Polish authorities, particularly in such roles as tax farming. (The tax farmer would pay a nobleman the tax due, then try to recoup the sum, with profit, from the peasantry.) Being frequently uprooted and forced to start over again, there was continual pressure on families to survive and find ways of being useful to their unpredictable hosts. “From roughly 800 AD to 1650 or 1700 AD, the great majority of the Ashkenazi Jews had managerial and financial jobs, jobs of high complexity, and were neither farmers nor craftsmen. In this they differed from all other settled peoples of which we have knowledge,” Cochran and colleagues write.
Restrictions on Ashkenazi employment were lifted around 1700, bringing to an end a period of some 900 years during which most of the population would have had to earn a living in occupations requiring more mental ability than most. Given what is known about the heritability of intelligence, the Cochran team calculates that even in as little as 500 years there would have been time for the intelligence of the Ashkenazi population to have been raised appreciably.
The authors cite evidence suggesting that sphingolipid mutations serve to foster the growth and interconnectedness of neurons, sometimes by lifting natural restraints. They believe that all the Ashkenazic disease mutations, in ways that remain to be discovered, serve to promote the extra cognitive skills that the Ashkenazic population needed in order to survive.
The outcome, they say, is that Ashkenazim have an average IQ of 115, one standard deviation above that of northern Europeans, although some measurements put it at only half a standard deviation higher. This is the highest average IQ of any ethnic group for which reliable data exist. Such an advantage may not make much difference at the average, where most people are situated, but it translates into a significant difference at the extremes. The proportion of northern Europeans with IQs greater than 140 is 4 per thousand but the figure for Ashkenazim is 23 per thousand, a sixfold difference.
This may have something to do with the fact that Ashkenazim make up only 3% of the U.S. population but have won 27% of U.S. Nobel prizes. Ashkenazim account for more than half of world chess champions. “Jews and half Jews, who make up about 0.2 percent of the world’s population, have won a total of 155 Nobel prizes in all fields, 117 in physics, chemistry and medicine,” writes the anthropologist Melvin Konner.327
Jewish folklore holds that intelligence was fostered not by occupation but by channeling the cleverest children to become rabbis. The rabbis were able to have more children, the folklore explanation holds, because they were sought as husbands for the daughters of wealthy families. “Talmudic academies served as systems of selection,” writes Konner. “Whatever we think of what was studied, the process culled the best minds in every generation of Jews for more than a thousand years. Rising stars among these bright young men would board with successful merchants, and matches would be made between them and the merchants’ daughters.”
But the Cochran team gives short shrift to this explanation, saying there were not enough rabbis—only 1% of the population—to make a genetically significant difference. As further proof of their thesis, they cite the fact that the two other main branches of the Jewish community, Oriental Jews and Sephardim, lived mostly under Muslim rulers who often forced them into menial jobs, not the intellect-demanding ones imposed on Ashkenazim. Oriental Jews and Sephardim score similarly to northern Europeans with no elevation in IQ, as would be predicted under the Cochran team’s thesis.
Among Ashkenazim, some 15% carry one of the sphingolipid or DNA repair mutations, and up to 60% carry one or other of all the disease mutations. (Most of these diseases are only harmful if a mutated gene is inherited from both parents, and some others are not fully “penetrant,” a geneticist’s term meaning a person can carry the mutation but doesn’t necessarily have the disease.)
In summary, the Cochran group has taken two well accepted phenomena—the odd pattern of Ashkenazic Mendelian diseases and the notable intellectual achievement of Ashkenazim—and has attempted to establish a link between them. The argument is necessarily extended, but is carefully developed at each stage. “It’s certainly a thorough and well argued paper, not one that can easily be dismissed outright,” said Steven Pinker, a cognitive scientist at Harvard. Though several aspects of the argument cross disputed academic territory—it assumes that intelligence is heritable and that IQ scores are a reliable measure of it—it has the virtue of making a clear and testable prediction: that people carrying one of the Ashkenazic mutations should do better than average on IQ tests. As of this writing, the test has not been conducted.
Despite the existence of genetic diseases that can be called Jewish, in the broader context Jews are doubtless highly similar to other populations in the west Eurasian or Caucasian branch of the human family. Their genesis as a distinctive group resembles that of Icelanders. Just as Jews appear to be a mixture of Middle Easterners with various European or other Middle Eastern populations, Icelanders also are probably a mix of two Caucasian populations, Norwegians and Celts. Both Jews and Icelanders have practiced endogamy, the necessary step for keeping one’s gene pool to oneself, Jews for religious reasons, Icelanders for geographic ones. Icelanders have been genetically separate for 1,000 years, but are still so similar to other Europeans that they can serve as a test bed for discovering European disease genes; Jews have been separate for just 2,000 years longer.
DNA and the Secret Family of Thomas Jefferson
Leading American historians for years denied a startling circumstance that was clearly attested to in the historical record: Thomas Jefferson, the third president of the United States, fathered an unacknowledged family with his slave mistress Sally Hemings.
Here is some of the evidence that historians of Jefferson found reason to disbelieve:
“It is well known,” the journalist James T. Callender wrote in the Rich mond Recorder on September 1, 1802, the second year of Jefferson’s first presidency, “that the man, whom it delighteth the people to honor, keeps, and for many years past has kept, as his concubine, one of his own slaves. Her name is SALLY. The name of her eldest son is TOM. His features are said to bear a striking although sable resemblance to those of the president himself.”
In 1873 a son of Sally Hemings, Madison Hemings, gave a long biographical statement to an Ohio newspaper, the Pike County Republican. He told how his mother, then aged around 13, had been sent to Paris, where Jefferson, then a widower, was American ambassador. Sally’s role was to be a servant to Maria, one of Jefferson’s two daughters.
“Their stay (my mother and Maria’s) was about eighteen months,” Madison Hemings related. “But during that time my mother became Mr. Jefferson’s concubine, and when he was called back home she was enceinte by him. He desired to bring my mother back to Virginia w
ith him but she demurred. She was just beginning to understand the French language well, and in France she was free, while if she returned to Virginia she would be re-enslaved. So she refused to return with him. To induce her to do so he promised her extraordinary privileges, and made a solemn pledge that her children should be freed at the age of twenty-one years. In consequence of this promise, on which she implicitly relied, she returned with him to Virginia.
“Soon after their arrival, she gave birth to a child, of whom Thomas Jefferson was the father. It lived but a short time. She gave birth to four others, and Jefferson was the father of them all. Their names were Beverly, Harriet, Madison (myself) and Eston—three sons and one daughter. We all became free, agreeably to the treaty entered into by our parents before we were born.”
It is difficult to believe that a 68-year-old Ohio carpenter, as Madison Hemings then was, would be moved on chance encounter with a journalist to invent an account of such specificity and poignancy. It contained many details that could be independently checked. Jefferson freed very few slaves, but he let all of Sally’s children go free. Winthrop Jordan, a historian at the University of Mississippi, documented in 1968 that Jefferson, despite his many absences from Monticello, was present at the time of conception of all Hemings’s known children.
But apart from Jordan, who stated that a liaison between Jefferson and Hemings was a possibility, a long line of Jefferson historians dismissed Madison Hemings’s account. Merrill Peterson, the first historian to give it scholarly study, conceded that Madison’s recollection “checks remarkably well with the data accumulated by scholars on Jefferson’s domestic life and the Monticello slaves.” But he chose to reject its central claim, that Madison was Jefferson’s son, with the defective argument that since Jefferson’s enemies wanted the story to be true, it must be false. The Jefferson-Hemings liaison was a legend, he wrote, sustained by the hatred of the Federalists, the propaganda of the British, “the Negroes’ pathetic wish for a little pride,” and the cunning of slave auctioneers thinking they would “get a better price for a Jefferson than for a Jones.” The “overwhelming evidence of Jefferson’s domestic life refuted the legend,” Peterson assured his readers in 1960.328
Before the Dawn: Recovering the Lost History of Our Ancestors Page 31