Earlier this week, WBUR’s Here and Now ran a taped interview with me about “Beautiful Brains,” my recent National Geographic article on teen brain and behavior. (You can listen to the interview here.) It’s only six minutes long, but nicely edited to highlight, from a high-altitude evolutionary point of view, what distinguishes adolescence, when we peak in our pursuits of risk, novelty, and same-age peers even as our brains consolidate gains while remaining especially plastic. The adolescent brain, as researcher Jay Giedd likes to say, is not a defective adult brain, but a nicely tuned teen brain. The show also squeezes in some Shakespeare, some fast driving, and a bit of Steve Jobs. Not bad for six minutes.
A couple of the write-ups about the show, however, carry headlines that make a mistake too often made about behavioral genetics:
Reckless Teen Behavior May Be Evolutionary Advantage | Here & Now
Know a risky teenager? Evolutionarily speaking, that’s good behavior | PRI.ORG
I don’t want to beat up too badly on these press releases; doubtless they were written quickly, and in any case the headlines are the worst of it. But perhaps because they were written quickly, they offer a teachable moment by embedding a common misconception. They mistake behaviors for traits.
This is too bad, for especially in behavioral genetics, it’s important to distinguish the two. When considering the behavioral genetics, we best view a trait as a sort of broad inclination — and behaviors as actions rising from those inclinations. Traits (from this evo perspective) exist because they’re selected for over long stretches of time, while behaviors rise as their current, context-sensitive expressions. So curiosity (aka “novelty-seeking”) is a trait, and if you’re a curious type you might express that in behaviors ranging from reading a book or inventing the wheel to riding a skateboard off a skyscraper. Or, to put it all in one basket, you might explore a new valley — and discover either death or a rich new hunting ground. Some of these actions are obviously more adaptive than others — but any or all might rise (partly) from a single trait. Their form and value depend depends on context, personal history, and what other traits you have. If you’re curious but sensitive to signs of danger, for instance, you’re more likely to survive your trip into that valley. (Get as metaphorical with that one as you like. As useful in marriage as in hunting.)
Hence the problem with the above headlines: Reckless teen behavior is not really adaptive, almost by definition (my son’s quibbles in the NatGeo story notwithstanding), but it can rise from traits — tastes for risk and novelty — that are adaptive overall, which is to say, valuable more often than not.
By failing to distinguish traits from behaviors, we court confusion over how evolution works — and how underlying traits can mix with experience or other traits to lead to a huge variety of behavior. Yet countless stories about behavioral genetics make just this mistake. Look at coverage of the dopamine-processing gene called DRD4, for instance. One variant of this gene, DRD4-7R (the “long repeat” version), is associated in many studies with traits such as increased novelty seeking, increased risk-taking, and what you might call either greater distractibility or attentional fluidity, though some elementary school administrators and drug companies like to call it ADHD. (A passage about this gene variant opens my Atlantic story about the genetics of temperament.)
Novelty-seeking and risk-taking are traits. Yet many individual studies have tied DRD4-7R to specific behaviors such as drinking, doing drugs, or sleeping around, and these studies, many of which are perfectly sound, have spawned scores of facepalm-worthy news write-ups about “the drinking gene,” “the ADHD gene,” and, God save us, the “slut gene.”
Must be a really bad gene! But wait: the the same variant has also been associated with traveling and reading more widely, having more friends, doing more for other people, exploring more interests, and migrating farther out of Africa; plus it’s being actively selected for. So we have overdrinking, sleeping around, and hyperactivity on one hand, and on the other, exploration and the migration that put humanity all over the globe. (Plus curiosity and vigilance in horses. Ride that.) Ponder all that and you’ll see how silly it is to think of a gene coding for all these behaviors — or for any one of them. This gene is not making people drink and distractedly have lots of sex! It’s creating a curiosity and openness to new experience. The rest is experience, context, and opportunity.
Another story published just last night, meanwhile, claimed researchers had discovered “the brat gene.” (Gah! Tonstant Weader fwowed up.) This is an incredibly bad read on that study, which found that the gene in question, a variant of the serotonin transporter gene, or SERT, frequently mislabeled “the depression gene,” creates not brattiness but extra responsiveness to parenting, good our bad; yet the story is spreading through the parenting-site world as I write.
This greater sensitivity to environment is known as “differential susceptibility,” and the differential susceptibility hypothesis — the recognition of a heightened responsiveness to environment in people carrying certain gene variants — is the subject of the book I’m writing. Its power lies partly in its focus on foundational traits rather than overlying outcomes — social sensitivity rather than depression, for instance, or curiosity rather than distractibility.
Stories that conflate behaviors and traits miss all that. They also encourage a oversimplified view of one gene creating one behavior. This ignores our maddening but wonderful multigenic complexity. Individual genes almost never generate particular behaviors, and individual genes in fact seldom if ever generate, on their own, highly specific behavioral traits. They almost always work in concert with other genes to create fairly broad traits; the blend gives even broadly defined traits a lot of nuance in individuals. Thus my curiosity differs from yours.
To be fair, this clunky, over-reductive press coverage occurs partly because so many behavioral genetics studies link one gene to one behavior. Sometimes researchers do this (and over-reduce the finding) because they think simplistically. Many, however, do single gene/single trait studies of necessity, because behavioral genetics is still at an early stage and needs to define basic effects of individual genes before exploring multigenic effects. But this is changing as some researchers, with single-gene effects well-established in some cases, look at how multiple genes interact. They’re finding some snazzy stuff.
One study three years ago, for instance, found that two particular genes that individually create deficits partially erase each other’s deficits if you have both of them. One gene was the short SERT variant mentioned above, which puts creates greater depression risk because if you carry it and go through really tough times, you tend to absorb more deeply the negative lessons that troubled times seem to offer. (This is the dreaded “negative bias.”) It’s as if your skin is thinner, so when the feces hits the fan and then you, you absorb it more readily.
The other gene involved is the “bad” version of a gene known as BNDF, for brain-derived neurotrophic factor, which plays a role in growing and sustaining neurons. The “bad” BDNF version doesn’t build or maintain neurons as well. This makes you a bit slower in learning certain types of things. It gives you a particular, limited form of stupid. (So many forms of stupid!) But here’s the cool: If you have this bad BDNF gene, one of the things you don’t learn as well is negative bias; so if you have the bad BNDF, it actually protects you against becoming depressed in response to trouble even if you have the short SERT variant, the so-called depression gene. Bad BNDF disables the badness in the short SERT. Its particular form of stupid covers your thin skin like Teflon, so the fan-flung feces slides off.
Now, I don’t remember hearing a peep about this extremely cool study when it was published in 2008, nor when any of several follow-ups were published; I heard about it directly from Daniel Weinberger, one of the authors. Maybe I was asleep all those times; but it seems these studies received little attention. Why? Was this too difficult a concept? Was it not novel enough? Actually it was novel — far newer than another story accusing DRD4-7R of creating sluts, rakes, or drunkards. Yet … no play.
Enough, eh? I call on science writers everywhere, writing about behavioral genetics, to put at the top of your list that eternal to-do item: Do Better.
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Image: eskimo_jo
There’s definitely a lot at play here – genetic determinism and its splintered interpretations, media misrepresentations of findings, clearly gendered assumptions of sexual behavior, and a general scientific and lay need to explain behaviors through evolutionary utility. It’s fascinating that both realms of thinkers have so much trouble wrestling with socialized behaviors. I.e., we can’t empirically write up the fact that risk is entirely relative – how adolescents push boundaries necessarily implies that there are boundaries that we all, as members of society, agree on. And the fringe populations that push these arbitrary, constructed boundaries are the ones that invite the most scientific anxiety. Hence our ceaseless search for the impossible “gay gene.”
I guess it’s no surprise to me that we need there to be a slut gene so we’re at ease about this behavior – and it’s no surprise that we’re anxious about females exhibiting this behavior – and it’s no surprise that we have normative standards of sexual behavior. But that the ever-present (albeit oversimplified) debate between nature and nurture seems to be quickly tipping towards the former so we can all wear a “born this way” tee shirt propagates exactly the kind of scientific misconception you’re talking about – a clunky watering down of genetic science.