Hammer2002 - S C I E N C E S C O M PA S S 65 64 63 62 61 60...

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65 64 63 62 61 60 59 58 57 56 55 54 53 52 51 50 49 48 47 46 45 44 43 42 41 40 39 38 37 36 35 34 33 32 31 30 29 28 27 26 25 24 23 22 21 20 19 18 17 16 15 14 13 12 11 10 9 8 7 6 5 4 3 2 1 www.sciencemag.org SCIENCE VOL 298 4 OCTOBER 2002 71 SCIENCE ’ S COMPASS CREDIT: KATHARINE SUTLIFF/ SCIENCE T he first 100 years spent studying the genetics of behavior were straightfor- ward. The aim was to determine the extent to which individual differences in the way people think, feel, and behave are due to variations in their genetic makeup. The basic approaches, first described by Sir Francis Galton in the late 1800s, were to compare identical and fraternal twins, other family members, and adoptees that had been raised together or apart. The results were consistently striking, albeit slow to be accepted. Genes were shown to influence virtually every aspect of human personality, temperament, cognitive style, and psychiatric disorder. The effects of heredity were substantial, typically rep- resenting 30 to 70% of total variation, and highly replicable across societies and cul- tures. The long reach of genes extended from a friendly disposition to xenophobia, from bipolar disease to bedwetting, from getting married to keeping a job. About the only characteristics that seemed not to be at least partially heritable were purely learned traits such as the particular language one spoke or the religion one believed in ( 1 ). The second century of behavior genet- ics has gotten off to a less satisfying start. The current aim is to identify the specific genes that contribute to individual differ- ences and determine what they do in the brain. The approach is to search for DNA sequence variations that correlate with be- havioral and personality traits, either by tracking anonymous markers close to the genes of interest in family members (link- age analysis) or by directly comparing the coding and regulatory sequences of candi- date genes (association analysis). The results have been disappointing and inconsistent. Large and well-funded linkage studies of the major psychiatric disorders including schizophrenia, alcoholism, Tourette syndrome, and bipolar disorder have come up empty-handed; not a single new gene has been conclusively identified. Most candidate gene findings have failed consistent replication, and even those that have been verified account for only a small fraction of total variation. Meanwhile, the statisticians who are supposed to be guiding and evaluating the research are unable to agree on how to design experiments or to interpret the results; their advice has proven as faddish (and useful) as the Hula-Hoop. What’s the problem? It’s not the basic premise of linkage and candidate gene analy- sis; these approaches have identified dozens of genes involved in inherited diseases. Nor is it the lack of DNA sequence information; virtually the entire code of the human genome is now known. The real culprit is the assumption that the rich complexity of hu-
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Hammer2002 - S C I E N C E S C O M PA S S 65 64 63 62 61 60...

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