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E-mail this The evolution of intelligence Natural genius? Jun 2nd 2005 From The Economist print edition Corbis - Getty Images Corbis - Getty Images The high intelligence of Ashkenazi Jews may be a result of their persecut ed past THE idea that some ethnic groups may, on average, be more intelligent tha n others is one of those hypotheses that dare not speak its name. But Gr egory Cochran, a noted scientific iconoclast, is prepared to say it anyw ay. He is that rare bird, a scientist who works independently of any ins titution. He helped popularise the idea that some diseases not previousl y thought to have a bacterial cause were actually infections, which ruff led many scientific feathers when it was first suggested. And more contr oversially still, he has suggested that homosexuality is caused by an in fection. 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 Ut ah, he is publishing, in a forthcoming edition of the Journal of Biosoci al Science, a paper which not only suggests that one group of humanity i s more intelligent than the others, but explains the process that has br ought this about.
Ashkenazim generally do well in IQ tests, scoring 12-15 points above the mean value of 100, and have contributed disproportionately to the intell ectual and cultural life of the West, as the careers of Freud, Einstein and Mahler, pictured above, affirm. They also suffer more often than mos t people from a number of nasty genetic diseases, such as Tay-Sachs and breast cancer. These facts, however, have previously been thought unrela ted. The former has been put down to social effects, such as a strong tr adition of valuing education. The latter was seen as a consequence of ge netic isolation. Dr Cochran, however, suspects that the intelligence and the diseases are intimately linked. His argument is that the unusual history of the Ashke nazim has subjected them to unique evolutionary pressures that have resu lted in this paradoxical state of affairs. Ashkenazi history begins with the Jewish rebellion against Roman rule in the first century AD. 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 su ch as banking and tax farming which were often disdained by, or forbidde n to, Christians. This, along with the low level of intermarriage with t heir gentile neighbours (which modern genetic analysis confirms was the case), is Dr Cochran's starting point. He argues that the professions occupied by European Jews were all ones th at put a premium on intelligence. Of course, it is hard to prove that th is 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 highl y 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 chil dren to adulthood than those at the bottom. Of course, that was true of successful gentiles as well. But in the Middle Ages, success in Christia n society tended to be violently aristocratic (warfare and land), rather than peacefully meritocratic (banking and trade). Put these two things togethera correlation of intelligence and success, and a correlation of success and fecundityand you have circumstances th at favour the spread of genes that enhance intelligence. The questions a re, do such genes exist, and what are they if they do? Dr Cochran thinks they do exist, and that they are exactly the genes that cause the inher ited diseases which afflict Ashkenazi society. That small, reproductively isolated groups of people are susceptible to g enetic disease is well known. Constant mating with even distant relative s 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, Dr Cochran argues, this is not the case. Most of the dozen or so disease genes that are common in them bel ong to one of two types: they are involved either in the storage in nerv e cells of special fats called sphingolipids, which form part of the ins ulating outer sheaths that allow nerve cells to transmit electrical sign als, or in DNA repair. The former genes cause neurological diseases, suc h as Tay-Sachs, Gaucher's and Niemann-Pick. And what is even less random is that in severa l cases the genes for particular diseases come in different varieties, e ach the result of an independent original mutation. This really does sug gest the mutated genes are being preserved by natural selection. But it does not answer the question of how evolution can favour genetic disease s However, in certain circumstances, evolution can. West Africans, and people of West African descent, are susceptible to a d isease called sickle-cell anaemia that is virtually unknown elsewhere. T he anaemia develops in those whose red blood cells contain a particular type of haemoglobin, the protein that carries oxygen. But the disease oc curs only in those who have two copies of the gene for the disease-causi ng haemoglobin (one copy from each parent). They are, however, protected against malaria, one of the biggest killers in that part of the world. Thus, the theory goes, th e pressure to keep the sickle-cell gene in the population because of its malaria-protective effects balances the pressure to drive it out becaus e of its anaemia-causing effects. Dr Cochran argues that something similar happened to the Ashkenazim. Gene s that promote intelligence in an individual when present as a single co py create disease when present as a double copy. His thesis is not as st rong as the sickle-cell/malaria theory, because he has not proved that a ny 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 connec t 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 c opies experience a more limited, but still enhanced, protuberance growth . That would yield better linkage between brain cells, and might thus le ad to increased intelligence. Indeed, in the case of Gaucher's disease, the only one of the three in which people routinely live to adulthood, t here 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 uncle arand is, perhaps, the weakest part of the thesis, although evidence is emerging that one of the genes in question is involved in regulating th e 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 Niem ann-Pick should be more intelligent than average. Dr Cochran and his col leagues predict they will be so by about five IQ points. If that turns o ut to be the case, it will strengthen the idea that, albeit unwillingly, Ashkenazi Jews have been part of an accidental experiment in eugenics. But, like the deliberate eugenics e xperiments of the 20th century, it has also exacted a terrible price.
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