Free The Best American Science and Nature Writing 2014 by Deborah Blum Page A

serotonin transporter gene, or SERT —which comes in both long and short forms. Any single gene’s impact on mood or behavior is limited, of course, and these single-gene or “candidate gene” studies must be viewed with that in mind. Yet many studies have found that SERT ’s short form seems to render many people (and rhesus monkeys) more sensitive to environment; according to those studies, people who carry the short SERT are more likely to become depressed or anxious if faced with stress or trauma.
    Kaufman looked first to see whether the kids’ mental health tracked their SERT variants. It did: the kids with the short variant suffered twice as many mental-health problems as those with the long variant. The double whammy of abuse plus short SERT seemed to be too much.
    Then Kaufman laid both the kids’ depression scores and their SERT variants across the kids’ levels of “social support.” In this case, Kaufman narrowly defined social support as contact at least monthly with a trusted adult figure outside the home. Extraordinarily, for the kids who had it, this single, modest, closely defined social connection erased about 80 percent of the combined risk of the short SERT variant and the abuse. It came close to inoculating kids against both an established genetic vulnerability and horrid abuse.
    Or, to phrase it as Cole might, the lack of a reliable connection harmed the kids almost as much as abuse did. Their isolation wielded enough power to raise the question of what’s really most toxic in such situations. Most of the psychiatric literature essentially views bad experiences—extreme stress, abuse, violence—as toxins, and “risk genes” as quasi-immunological weaknesses that let the toxins poison us. And abuse is clearly toxic. Yet if social connection can almost completely protect us against the well-known effects of severe abuse, isn’t the isolation almost as toxic as the beatings and neglect?
    The Kaufman study also challenges much conventional Western thinking about the state of the individual. To use the language of the study, we sometimes conceive of “social support” as a sort of add-on, something extra that might somehow fortify us. Yet this view assumes that humanity’s default state is solitude. It’s not. Our default state is connection. We are social creatures, and have been for eons. As Cole’s colleague John Cacioppo puts it in his book
Loneliness
, Hobbes had it wrong when he wrote that human life without civilization was “solitary, poor, nasty, brutish, and short.” It may be poor, nasty, brutish, and short. But seldom has it been solitary.
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    Toward the end of the dinner I shared with Cole, after the waiter took away the empty platters and we sat talking over green tea, I asked him if there was anything I should have asked but had not. He’d been talking most of three hours. Some people run dry. Cole does not. He spoke about how we are permeable fluid beings instead of stable unitary isolates; about recursive reconstruction of the self; about an engagement with the world that constantly creates a new you, only you don’t know it, because you’re not the person you would have been otherwise—you’re a one-person experiment that has lost its control.
    He wanted to add one more thing: he didn’t see any of this as deterministic.
    We were obviously moving away from what he could prove at this point, perhaps from what is testable. We were in fact skirting the rabbit hole that is the free-will debate. Yet he wanted to make it clear he does not see us as slaves to either environment or genes.
    â€œYou can’t change your genes. But if we’re even half right about all this, you can change the way your genes behave—which is almost the same thing. By adjusting your environment you can adjust your gene activity. That’s what we’re doing as we move through life.