Blood Matters Page 3
Current scientific wisdom, often couched in much additional information aimed at masking the study authors’ discomfort, is that intelligence is, to a large extent, genetically determined. Studies of siblings reared together and apart, studies of twins, and studies of adopted children and their biological and adoptive parents show that the genetic component in determining intelligence is strong—and that it gets stronger as a child ages, suggesting that inherited ability is more important than all the early development strategies contemporary parents can produce (or fail to produce). How exactly intelligence is passed on from generation to generation is an open question; many scientists are working on genetic models of intelligence, often focusing on genetic causes of mental retardation, on the assumption that this trail may lead them to understanding the genetic mechanisms of intellectual ability in general. But if intelligence is inherited like genes—or like surnames—then the explanation for Ashkenazi Jews’ high average IQ may also be either selective advantage or genetic drift.
The Utah researchers argued that it was selective advantage. Before the diaspora era, they pointed out, written accounts made no mention of Jews’ unusual intelligence, but once in exile, Ashkenazim tended to find themselves in financial and managerial occupations. Those who excelled had significantly more success reproducing—and thus more children who survived to adulthood and themselves went on to reproduce—thereby passing on whatever intellectual ability allowed the parents to succeed in their middleman occupations. Presumably, these were verbal and mathematical abilities, while spatiovisual aptitude played no role in the Ashkenazi model of success. That would explain the contemporary Ashkenazi Jews’ lopsided test scores, the researchers argued.
This was not exactly a new theory. The debate on the origins of Jewish success dates back at least to the turn of the twentieth century—with future fascist propagandists arguing the biological line alongside Jewish theoreticians. The Jewish historian Joseph Jacobs attributed the Jews’ intellectual leadership to what was then widely known as the “germ-plasm.” He wrote, presciently, “There is a certain probability that a determinate number of Jews at the present time will produce a larger number of ‘geniuses’...than any equal number of men of other races. It seems highly probable, for example, that German Jews at the present moment are quantitatively (not necessarily qualitatively) at the head of European intellect.” Therefore, he concluded, “the desirability of further propagation of the Jewish germ-plasm is a matter not merely of Jewish interest.”
But the Utah researchers went further. They argued that selection for intelligence also explained the Jewish diseases. Those who carry only one copy of the genes that cause one of the lipid-storage diseases have an altered chemistry affecting the brain and the central nervous system, and the effects of this change may actually facilitate learning. To bolster their argument, the researchers used the case of Gaucher’s disease—the only one of these illnesses that does not always kill people before they reach adulthood. A list of 322 adult Gaucher’s patients—basically all the affected adults in Israel—showed that a disproportionately high number were engaged in intellectually challenging professions such as the academe, the sciences, engineering, law, and medicine. Five of the patients were physicists. On the other hand, these numbers were disproportionate when compared to the general U.S. or Israeli population, where the smart Ashkenazim do not constitute a majority, whereas the Gaucher’s patients were Ashkenazim virtually by definition. The researchers did not compare the Gaucher’s patients’ occupational profile to a general picture of Israeli Ashkenazim—whether because such statistics were not available, because the comparison would not have been as dramatic, or because they were getting into politically charged and potentially distasteful territory, I do not know.
They did, however, discuss two other diseases. Torsion dystonia shows up as painful muscle spasms that can spread and become so severe that sufferers are confined to a wheelchair and unable to dress or feed themselves. The disease is dominant—only one copy of the gene is required for symptoms to appear—but only 30 percent of carriers show symptoms. Roughly one in nine hundred Ashkenazim is a carrier, and carrier status seems to correlate with a higher IQ Nonclassic congenital adrenal hyperplasia is a recessive disorder in which an enzyme deficiency causes a hormonal imbalance that can manifest itself in symptoms ranging from negligible, such as hirsutism in women, to severe, such as infertility and the failure to develop breasts. One in five Ashkenazi Jews may be a carrier, and most of them have higher-than-average IQ.
But that is not all. The researchers argued that mutations like mine—disorders of DNA repair that cause cancer or untreatable anemia (a recessive condition known as Fanconi’s anemia) or a number of physical changes and increased susceptibility to infections and cancers (a recessive disorder called Bloom syndrome)—may also be related to intelligence. Perhaps, they suggested, the same deficiency in the BRCA gene that makes it ineffectual at preventing cancer may encourage neural growth and thereby enhance intelligence.
The paper had all the hallmarks of a promising scientific theory: However wacky the premise seemed, the story was well told and internally coherent. The authors admitted their theory was unproven, made their case, and suggested further investigation. A perfect study would involve many pairs of siblings who were heterozygotes—genetically different—for the genes implicated in Ashkenazi diseases. If it could be demonstrated that the siblings who carried a deleterious mutation were on average more intelligent than their unaffected brothers or sisters, the we-are-so-sick-because-we-are-so-smart theory would be all but proved.
The media loved the study. I liked it, too, in part because it affirmed my new world view: It seemed there was a basis for my sense that I inherited my mother’s intelligence, her verbal ability, and her cancer gene as a package. But, probably like most people, I found the discussion of Jewish intelligence uncomfortable, the way an inappropriate remark that elicits giggles at a dinner table can make one uncomfortable. It is not that I do not think that Jews are smarter, on average, than other people. Indeed, thinking that way is part of my cultural heritage: My grandmother, a principled cosmopolitan, always told me in a stage whisper that Jewish intelligence and the envy it engendered were the cause of anti-Semitism. But you could make that argument and then fall back upon cultural explanations, such as a tradition of literacy and a premium placed on education, even if you secretly suspected that Jews were just born smarter. So what made me uncomfortable about the Utah paper was what always makes people uncomfortable about genetic research: It takes private facts and makes them a matter of public discourse. This is the essence of obscenity.
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Less than a year later an Israeli study purported to debunk the natural selection theory and to establish genetic drift as the cause of all the Ashkenazi illnesses and genetic advantages. The researchers claimed to show that nearly half of all contemporary Ashkenazim were the descendants of just four women who lived some fifteen hundred years ago. That settles the argument because, the logic goes, if Ashkenazi started that small, anything could happen. When a population starts with just a few people—or, at the extreme, with one woman—geneticists call this the “founder effect,” meaning that the entire population or a large proportion of it will carry the genetic traits that happened to characterize that one person or small group of founders.
I went to see the authors of the study in Haifa. Doron Behar, listed first among twenty authors—the spot usually reserved for the graduate student who does the bulk of the research—had defended his Ph.D. dissertation less than a year earlier (“a recent founder event,” he joked), and his skyrocketing career in genetics had been a matter of drift.
Doron was a critical-care doctor at Rambam, the large medical center right next to the Port of Haifa. In an age when doctors the world over are criticized for cookie-cutter care, critical-care doctors exemplify the assembly-line approach. Unlike general practitioners and most specialists, they do not get to know their patients. They com
e in when the patient’s condition is dire and exit if he improves. In the absence of familiarity and communication, they use standard measurements as their guide—and they cannot help noticing that just as the same trigger causes reactions of varying severity in different people, so the same treatment can be more or less effective. Doron Behar wondered what sort of knowledge might allow a doctor to administer a test that would tell him which approach would work best for the person with systemic inflammatory response syndrome who has just been wheeled in. The term “personalized medicine,” just coming into use as Behar was developing his interest in genetics, usually refers to complex, often long-term procedures, such as chemotherapy for cancer or medicating a patient for a major surgery, but it stands to reason that a doctor involved in the least personalized practice of medicine would want to find a shortcut to knowing his patients.
In addition to being a critical-care doctor, Doron Behar was also an inveterate people-watcher and a shameless picture-taker. The walls of his home office were covered with pictures of faces seen in China, Tibet, India, and elsewhere—the faces of strangers, ad nauseam. Behar was a man obsessed. His being a Jew, and an Israeli, made his obsession perhaps less socially suspect than it might otherwise have seemed. He really wanted to know what it is that causes the members of one tribe to have necks, noses, and skin color markedly different from the members of a tribe who live half a mile away. He also wanted to know what causes people to develop medical reactions of varying severity in response to identical triggers. And he talked about this a lot.
He happened to talk about this to Karl Skorecki, the head of the nephrology department at Rambam. Skorecki’s own foray into genetics, quite accidental, happened about a decade earlier. One day in the midnineties Skorecki let his mind wander in the synagogue. Just at that moment a Cohen was called to the Torah reading. Skorecki was a Cohen himself; his mind still not focused on the service, he wondered what it was that connected all the Cohanim. Being a religious man and a learned man, he knew: The Cohanim are a priestly caste endowed with a set of particular privileges in synagogue and burdened with a set of restrictions in ordinary life. The Cohen lineage is paternal: The son of a Cohen is a Cohen and his son is a Cohen, and so on. All the Cohanim are sons of Aaron, brother of Moses. If that is the case, thought Skorecki, then he, a Jew of Ashkenazic roots, and the man of apparently North African extraction who was just then making his way to the front of the congregation, would carry the traces of their common forefather. And they would carry them most evidently where all men store the traces of their fathers and their fathers’ fathers: in the DNA of the Y chromosome.
Skorecki, who had no research background in genetics, contacted an Arizona geneticist named Michael Hammer, who had distinguished himself in Y-chromosome research, and told him of his idea. It was a perfect research hypothesis: simple and obvious but for the fact that no one had thought of it before, and eminently verifiable. Hammer loved it, and together they conducted a study showing that, indeed, a majority of Jewish men who have been told by their fathers that they are members of the high priesthood are the descendants of a single male. Whether that man was named Aaron and had a brother named Moses, the DNA will not tell us—or, it will not tell us definitively. The signs did match. To determine when the common ancestor had lived, the researchers looked at the level of relatedness—or, rather, the degree of difference—among the Y-chromosome DNA of his various descendants. The difference is measured in mutations. Using estimates of the average time it takes a mutation to occur, the researchers calculated that the common ancestor had lived 106 generations, or roughly 2,650 years, ago, give or take a few hundred years. In other words, the man may have been alive during the exodus from Egypt. Furthermore, genetic signs place the father of most Cohens (Cohns, Kagans, Koches, Cheneys, and others) unambiguously in the Middle East.
The study of genetic heritage combines science that is staggeringly precise with what are at best decent estimates and respectable probabilities. Contemporary equipment allows scientists to decipher segments of DNA and compare them to each other. Some of these segments, which are shared among many individuals, are called haplotypes (short for “haploid genotypes”), a sort of DNA signature of a given population. The greatest variety of haplotypes is found in Africa, which establishes Africa as the common homeland of all humankind: People have been there the longest—roughly 150,000 years, it is believed—and in that time have achieved the greatest diversity. As people migrated to other parts of the world, and as some of them then migrated again, different haplotypes came to be predominant in different places. This knowledge has engendered a number of projects, both commercial and nonprofit, that aim to place a person’s ancestors by looking at his or her haplotypes. But the results are mere probabilities: If a given haplotype is seen frequently in, say, the Middle East, infrequently in Europe, and never anywhere else, then there is a greater probability—but no certainty—that the person’s ancestors hail from the Middle East and a slight possibility that they lived in Europe.
Time estimates are even less precise. To calculate the number of years that have elapsed since a group’s common ancestor lived, geneticists look at the diversity within the group, essentially counting the number of mutations that have appeared in a particular segment of the genome. They estimate the number of generations required to acquire that many mutations, then multiply that number by twenty-five to get the number of years. There are two fallible assumptions here: the number of generations required for a mutation to appear, which is based on current statistics but can be skewed or imprecise, or inapplicable to the particular mutations in question; and the equation of a generation with 25 years. If the number of years in a generation is adjusted down from 25 to 15 years—an obvious biological probability given that Jewish girls, for example, could be as young as twelve when they started having children—the number of years that have elapsed since the common Cohanim ancestor will shrink from 2,650 to 1,590.
Consider families you know. Take mine. My father was twenty-two when I was born; his mother was just twenty when she had him. I have two uncles who are roughly my age; their parents were in their forties when they were born. I am thirty-five years older than my youngest brother; my father was fifty-seven when this son was born. Twenty-five years is a bit more than a generation lasts in my particular lineage and a lot less than it does in the case of my brother or my uncles. Whether the twenty-five-year estimate gets any truer when spread out over many generations is debatable: My great-great-grandfather, for one, did not start having children until after he was discharged from the czar’s army around the age of sixty; other men in his lineage also tended to live a long time and have children late. Which brings us to the problem of sample size: the smaller the sample—and sometimes a haplotype grouping examined in a particular paper includes just a couple of people—the larger the “confidence interval,” or the margin of error. It is not unusual to see a table in a genetics paper that lists a number like 1,500—say, years to common ancestor—followed, in parenthesis, by a confidence interval of 1,000, meaning that the person may have lived 2,500 or 500 years ago. The numbers are all blinks in genetic time, but in our understanding of history they are huge.
Still, the magical quality of studies like Skorecki’s overshadows their imprecise nature. The media loved his study; his colleagues—for Skorecki suddenly found he was a star in the field of genetics, and geneticists were his colleagues—loved it. Scientists generally love a question well asked, and this is why Skorecki’s study appealed to them. And everyone loves a question well answered, which is why the media, and the public, ate it up. Skorecki himself thought his question was “parochial,” as he put it, and the study would not draw much attention. Instead, it generated endless press and continued to have reverberations—and, it seems fair to say, to draw fans—nearly ten years later.
It made for a great story. On the one hand, it proved something quite improbable: that people from entirely different parts of the world, people who look com
pletely different—just as Skorecki, fairskinned, tall, and slim, must have looked completely different from the North African Cohen who gave him the idea for the study that morning at the synagogue—can be related. At the same time, this incredible discovery confirms, and is confirmed by, the most believed story of all time, which is the story contained in religious texts. It also offered a chance at the reconciliation for which the modern world yearns: the agreement between hard science and religious tradition. Here was scientific evidence that the Cohanim, as a group, existed and that they were who they said they were.
“I always give this example,” Skorecki said when I interviewed him at Rambam, in an eleventh-floor corner office overlooking the Mediterranean shore in Haifa: a military base, the port, blue-gray water, and a chunk of Lebanon in the not-too-great distance (in about a month, Lebanese rockets started falling within yards of the building). “If you have a male who gave his son a secret word and he transferred this secret word to male offspring only, and so on and so forth, and we go into the future a hundred generations, to the extent that the secret is kept, any male on the planet who knows this secret word, their Y-chromosome DNA markers should be closer, more related, than the Y-chromosome DNA markers of any two males on the planet. That’s the idea. The secret word is an oral tradition. It’s a simple idea.”