eluctantly to read picture books to their fidgety, difficult kids, saying they wouldn’t sit still for it. But according to Bakermans-Kranenburg, when these mothers viewed the playback they were “surprised to see how much pleasure it was for the child—and for them.” Most mothers began reading to their children regularly, producing what Bakermans-Kranenburg describes as “a peaceful time that they had dismissed as impossible.” And the bad behaviors dropped. A year after the intervention ended, the toddlers who’d received it had reduced their externalizing scores by more than 16 percent, while a nonintervention control group improved only about 10 percent (as expected, due to modest gains in self-control with age). And the mothers’ responses to their children became more positive and constructive. Few programs change parent-child dynamics so successfully. But gauging the efficacy of the intervention wasn’t the Leiden team’s only goal, or even its main one. The team was also testing a radical new hypothesis about how genes shape behavior—a hypothesis that stands to revise our view of not only mental illness and behavioral dysfunction but also human evolution. Of special interest to the team was a new interpretation of one of the most important and influential ideas in recent psychiatric and personality research: that certain variants of key behavioral genes (most of which affect either brain development or the processing of the brain’s chemical messengers) make people more vulnerable to certain mood, psychiatric, or personality disorders. Bolstered over the past 15 years by numerous studies, this hypothesis, often called the “stress diathesis” or “genetic vulnerability” model, has come to saturate psychiatry and behavioral science. During that time, researchers have identified a dozen-odd gene variants that can increase a

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