Is There a Smart Gene in Ashkenazis?
The idea that some ethnic groups may, on average, be more intelligent than others is one of those hypotheses that dare not speak its name. But Gregory Cochran, a noted scientific iconoclast, is prepared to say it anyway. He is that rare bird, a scientist who works independently of any institution.
He helped popularize the idea that some diseases not previously thought to have a bacterial cause were actually infections, which ruffled many scientific feathers when it was first suggested. And more controversially still, he has suggested that homosexuality is caused by an infection.
Even he, however, might tremble at the thought of what he is about to do. Together with Jason Hardy and Henry Harpending of the University of Utah, he is publishing in a forthcoming edition of the Journal of Biosocial Science a paper that not only suggests that one group of humanity is more intelligent than the others, but explains the process that has brought this about.
The group in question is Ashkenazi Jews. The process is natural selection.
History before science.
Ashkenazim generally do well in IQ tests, scoring 12-15 points above the mean value of 100, and have contributed disproportionately to the intellectual and cultural life of the West, as the careers of Freud, Einstein and Mahler affirm. They also suffer more often than most people from a number of nasty genetic diseases, such as Tay-Sachs and breast cancer.
These facts, however, have previously been thought unrelated. The former has been put down to social effects, such as a strong tradition of valuing education. The latter was seen as a consequence of genetic isolation. Even now, Ashkenazim tend to marry among themselves. In the past they did so almost exclusively.
Cochran, however, suspects that the intelligence and the diseases are intimately linked. His argument is that the unusual history of the Ashkenazim has subjected them to unique evolutionary pressures that have resulted in this paradoxical state of affairs.
Ashkenazi history begins with the Jewish rebellion against Roman rule in the first century CE. When this was crushed, Jewish refugees fled in all directions. The descendants of those who fled to Europe became known as Ashkenazim.
In the Middle Ages, European Jews were subjected to legal discrimination, one effect of which was to drive them into money-related professions, such as banking and tax farming, which were often disdained by, or forbidden to, Christians. This, along with the low level of intermarriage with their non-Jewish neighbors (which modern genetic analysis confirms was the case), is Cochran’s starting point.
He argues that the professions occupied by European Jews were all ones that put a premium on intelligence. Of course, it is hard to prove that this intelligence premium existed in the Middle Ages, but it is certainly true that it exists in the modern versions of those occupations. Several studies have shown that intelligence, as measured by IQ tests, is highly correlated with income in jobs such as banking.
What can, however, be shown from the historical records is that European Jews at the top of their professions in the Middle Ages raised more children to adulthood than those at the bottom. Of course, that was true of successful non-Jews, as well. But in the Middle Ages, success in Christian society tended to be violently aristocratic (warfare and land), rather than peacefully meritocratic (banking and trade).
Put these two things together — a correlation of intelligence and success and a correlation of success and fecundity — and you have circumstances that favor the spread of genes that enhance intelligence. The questions are, do such genes exist and what are they if they do? Cochran thinks they do exist, and that they are exactly the genes that cause the inherited diseases that afflict Ashkenazi society.
That small, reproductively isolated groups of people are susceptible to genetic disease is well known. Constant mating with even distant relatives reduces genetic diversity, and some disease genes will thus randomly become more common. But the very randomness of this process means there should be no discernible pattern about which disease genes increase in frequency.
In the case of Ashkenazim, Cochran argues, this is not the case. Most of the dozen or so disease genes that are common in them belong to one of two types: They are involved either in the storage in nerve cells of special fats called sphingolipids, which form part of the insulating outer sheaths that allow nerve cells to transmit electrical signals, or in DNA repair. The former genes cause neurological diseases, such as Tay-Sachs, Gaucher’s and Niemann-Pick. The latter cause cancer.
That does not look random. And what is even less random is that in several cases the genes for particular diseases come in different varieties, each the result of an independent original mutation. This really does suggest the mutated genes are being preserved by natural selection. But it does not answer the question of how evolution can favor genetic diseases. However, in certain circumstances, evolution can.
West Africans and people of West African descent are susceptible to a disease called sickle-cell anemia that is virtually unknown elsewhere. The anemia develops in those whose red blood cells contain a particular type of hemoglobin, the protein that carries oxygen.
But the disease occurs only in those who have two copies of the gene for the disease-causing hemoglobin (one copy from each parent). Those who have only one copy have no symptoms. They are, however, protected against malaria, one of the biggest killers in that part of the world.
Thus, the theory goes, the pressure to keep the sickle-cell gene in the population because of its malaria-protective effects balances the pressure to drive it out because of its anemia-causing effects. It therefore persists without becoming ubiquitous.
Cochran argues that something similar happened to the Ashkenazim. Genes that promote intelligence in an individual when present as a single copy create disease when present as a double copy. His thesis is not as strong as the sickle-cell/malaria theory, because he has not proved that any of his disease genes do actually affect intelligence. But the area of operation of some of them suggests that they might.
The sphingolipid-storage diseases, Tay-Sachs, Gaucher’s and Niemann-Pick, all involve extra growth and branching of the protuberances that connect nerve cells together. Too much of this (as caused in those with double copies) is clearly pathological. But it may be that those with single copies experience a more limited, but still enhanced, protuberance growth. That would yield better linkage between brain cells, and might thus lead to increased intelligence.
Indeed, in the case of Gaucher’s disease, the only one of the three in which people routinely live to adulthood, there is evidence that those with full symptoms are more intelligent than the average. An Israeli clinic devoted to treating people with Gaucher’s has vastly more engineers, scientists, accountants and lawyers on its books than would be expected by chance.
Why a failure of the DNA-repair system should boost intelligence is unclear, and is, perhaps, the weakest part of the thesis, although evidence is emerging that one of the genes in question is involved in regulating the early growth of the brain. But the thesis also has a strong point: It makes a clear and testable prediction. This is that people with a single copy of the gene for Tay-Sachs, or that for Gaucher’s, or that for Niemann-Pick should be more intelligent than average.
Cochran and his colleagues predict they will be so by about five IQ points. If that turns out to be the case, it will strengthen the idea that, albeit unwillingly, Ashkenazi Jews have been part of an accidental experiment in eugenics.
It has brought them some advantages. But, like the deliberate eugenics experiments of the 20th century, it has also exacted a terrible price.
This article is reprinted with permission from The Economist magazine.