vironment” study. First they took cerebral spinal fluid from 132 juvenile rhesus monkeys and analyzed it for a serotonin metabolite, called 5-HIAA, that’s considered a reliable indicator of how much serotonin the nervous system is processing. Lesch’s studies had already shown that depressed people with the short/long serotonin-transporter allele had lower 5-HIAA levels, reflecting less-efficient serotonin processing. He and Suomi wanted to see if the finding would hold true in monkeys. If it did, it would provide more evidence for the genetic dynamic shown in Lesch’s studies. And finding such a dynamic in rhesus monkeys would confirm their value as genetic and behavioral models for studying human behavior.

After Suomi, Lesch, and Higley had grouped the monkeys’ 5-HIAA levels according to their serotonin genotype (short/long or long/long, but not short/short, which was too rare to be of use), they also sorted the results by whether the monkeys had been raised by their mothers or as orphans with only same-aged peers. When their colleague Allison Bennett charted the results on a bar graph showing 5-HIAA levels, all of the mother-reared monkeys, no matter which allele they had, showed serotonin processing in the normal range. The metabolite levels of the peer-raised monkeys, however, diverged sharply by genotype: the short/long monkeys in that group processed serotonin highly inefficiently (a risk factor for depression and anxiety), whereas the long/long monkeys processed it robustly. When Suomi saw the results, he realized that he finally had proof of a behaviorally relevant gene-by-environment interaction in his monkeys. “I took one look at that graph,” he told me, “and said, ‘Let’s go pop some champagne.’”

Suomi and Lesch published their results in 2002 in Molecular Psychiatry, a relatively new journal about behavioral genetics. The paper formed part of a surge of gene-by-environment studies of mood and behavioral disorders. That same year, two psychologists at King’s College, London, Avshalom Caspi and Terrie Moffitt, published the first of two large longitudinal studies (both drawing on life histories of hundreds of New Zealanders) that would prove particularly influential. The first, published in Science, showed that the short allele of another major neurotransmitter-processing gene (known as the MAOA gene) sharply increased the chance of antisocial behavior in human adults who’d been abused as children. The second, in 2003 and also in Science, showed that people with short/short or short/long serotonin-transporter alleles, if exposed to stress, faced a higher-than-normal risk of depression.

These and dozens of similar studies were critical to establishing the vulnerability hypothesis over the last few years. Yet many of these studies also contained data that supported the orchid hypothesis—but went unnoticed or unremarked at the time. (Jay Belsky, the child-dev

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