Remarkable article about how our social experience and the way we come to frame our lives influences gene-expression.
I would’ve bet my eyeteeth that we’d get a lot of noisy results that are inconsistent from one realm to another. And at the level of individual genes that’s kind of true—there is some noise there.” But the kinds of genes that get dialed up or down in response to social experience, he said, and the gene networks and gene-expression cascades that they set off, “are surprisingly consistent—from monkeys to people, from five-year-old kids to adults, from Vancouver teenagers to 60-year-olds living in Chicago.”
The principal pathway through which this works appears to be the immune system.
Normally, a healthy immune system works by deploying what amounts to a leashed attack dog. It detects a pathogen, then sends inflammatory and other responses to destroy the invader while also activating an anti-inflammatory response—the leash—to keep the inflammation in check. The lonely Chicagoans’ immune systems, however, suggested an attack dog off leash—even though they weren’t sick. Some 78 genes that normally work together to drive inflammation were busier than usual, as if these healthy people were fighting infection. Meanwhile, 131 genes that usually cooperate to control inflammation were underactive. The underactive genes also included key antiviral genes.
This opened a whole new avenue of insight. If social stress reliably created this gene-expression profile, it might explain a lot about why, for instance, the lonely HIV carriers in Cole’s earlier studies fell so much faster to the disease. 1
The effects of these at times remarkably rapid shifts in gene-expression are not only physical, but also mental. A 2004 study examined 57 children “who were so badly abused that state social workers had removed them from their homes.”
Kaufman looked first to see whether the kids’ mental health tracked their SERT 2 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.
I was stunned when I read this. Not because it doesn’t make sense (in many ways, it makes all too much sense), but because it opens up such a vista of both hope and sadness; so much misery about for want of a deeply trusted connection.
A later study concluded “3he main thing driving screwy immune responses appeared to be not poverty, but whether the child saw the social world as scary.” Not that poverty is irrelevant, of course, but it seems much of its negative effect comes from the social environment it tends to create. An environment where the world, and other people, are far more often viewed as threatening.
The message tentatively coming out of all of this is by no means straightforward. It could easily be construed as deterministic with our environment heavily shaping how we see the world and also, therefore, how we, and our bodies, react. On the other hand, our perceptions seem to be astonishingly important
To an extent that immunologists and psychologists rarely appreciate, we are architects of our own experience. Your subjective experience carries more power than your objective situation. If you feel like you’re alone even when you’re in a room filled with the people closest to you, you’re going to have problems. If you feel like you’re well supported even though there’s nobody else in sight; if you carry relationships in your head; if you come at the world with a sense that people care about you, that you’re valuable, that you’re okay; then your body is going to act as if you’re okay—even if you’re wrong about all that.”
In some ways this all seems a little Norman Vincent Pealish. Only superficially though, I think. Two things make it different. First, a recognition of the bootstrapping dilemma is inherent in the dominant gene-expression processes now known to be at work; if the world seems scary, and you feel alone in facing it, no amount of exhortations to think positively is likely to work. You’re more or less nobbled from day one. Secondly, the value of individual, trusting connections is made heartbreakingly clear. One, it seems, can sometimes be enough, no matter how appalling an individual’s circumstances otherwise.
- These mechanisms might also, on the flip side, go a long way towards explaining the placebo effect.
- “the so-called depression risk gene—the serotonin transporter gene”