ir 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 person’s susceptibility to depression, anxiety, attention-deficit hyperactivity disorder, heightened risk-taking, and antisocial, sociopathic, or violent behaviors, and other problems—if, and only if, the person carrying the variant suffers a traumatic or stressful childhood or faces particularly trying experiences later in life.

This vulnerability hypothesis, as we can call it, has already changed our conception of many psychic and behavioral problems. It casts them as products not of nature or nurture but of complex “gene-environment interactions.” Your genes don’t doom you to these disorders. But if you have “bad” versions of certain genes and life treats you ill, you’re more prone to them.

Recently, however, an alternate hypothesis has emerged from this one and is turning it inside out. This new model suggests that it’s a mistake to understand these “risk” genes only as liabilities. Yes, this new thinking goes, these bad genes can create dysfunction in unfavorable contexts—but they can also enhance function in favorable contexts. The genetic sensitivities to negative experience that the vulnerability hypothesis has identified, it follows, are just the downside of a bigger phenomenon: a heightened genetic sensitivity to all experience.

The evidence for this v

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