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Since Watson and Crick deduced the structure of DNA in 1953, our genes have captured our imagination as little else about our bodies. It seemed, after decades of interest in heredity, that we could now unlock the mystery of human variety, or, as the title of the first newspaper article on the discovery put it: “Why you are you: Nearer secret of life” (Calder, 1953). Along with the purely scientific excitement, however, the discovery also stoked fantasies of perfectibility. Genetic research might let us learn what endows some with the attributes to seemingly race through life, while others, bedeviled by illness and infirmity, can't seem to get even off the blocks. In the ensuing half-century, researchers learned that certain chromosomal or single-gene mutations could exert a devastating effect on the human organism—in Down's syndrome, Fragile X syndrome, cystic fibrosis, and Huntington's Disease, to name just a few conditions. Certainly, then, other, subtler single-gene mutations must be responsible for other, subtler forms of human pathology? In this context, the hunt to identify “bad genes” has carried on at full throttle.
However, outside of oncology and immunology, the past half-century's human and financial investment in genetic research has paid limited dividends in clinical medicine. In psychiatry, despite decades of hunting for gene loci controlling risk for illness, few candidates have been found with a confirmed association with illness risk, and controversy over findings is the rule, not the exception. One research group's