I'm not vulnerable, just especially plastic. Risk genes, environment, and evolution, in the Atlantic

The video interview above, with NIH primatologist Stephen Suomi, is embedded within a feature of mine that that appeared today at The Atlantic website -- and is in the December 2009 issue now shipping -- about a new hypothesis in behavioral genetics.

This emerging hypothesis, which draws on substantial data, much of which has gone simply unnoticed or unremarked, I call the "orchid-gene hypothesis," for lack of a better name. Some of the researchers have other offerings. It's been around for several years but is now blooming as evidence accumulates. When I came across it at a conference this spring -- gaggles of scientists talking excitedly in the halls -- it immediately struck me as a deeply transformative and powerful idea. It recasts the genes we now see simply as 'risk alleles' for things such as depression or ADHD as 'sensitivity' genes that create greater responsiveness not just to bad environments (creating the well-documented risk) but good environments -- creating an upside to these genes that has gone largely unnoticed.

It is thus

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 view is mounting. Much of it has existed for years, in fact, but the focus on dysfunction in behavioral genetics has led most researchers to overlook it. This tunnel vision is easy to explain, according to Jay Belsky, a child-development psychologist at Birkbeck, University of London. "Most work in behavioral genetics has been done by mental-illness researchers who focus on vulnerability," he told me recently. "They don't see the upside, because they don't look for it. It's like dropping a dollar bill beneath a table. You look under the table, you see the dollar bill, and you grab it. But you completely miss the five that's just beyond your feet."

Though this hypothesis is new to modern biological psychiatry, it can be found in folk wisdom, as the University of Arizona developmental psychologist Bruce Ellis and the University of British Columbia developmental pediatrician W. Thomas Boyce pointed out last year in the journal Current Directions in Psychological Science. The Swedes, Ellis and Boyce noted in an essay titled "Biological Sensitivity to Context," have long spoken of "dandelion" children. These dandelion children--equivalent to our "normal" or "healthy" children, with "resilient" genes--do pretty well almost anywhere, whether raised in the equivalent of a sidewalk crack or a well-tended garden. Ellis and Boyce offer that there are also "orchid" children, who will wilt if ignored or maltreated but bloom spectacularly with greenhouse care.

At first glance, this idea, which I'll call the orchid hypothesis, may seem a simple amendment to the vulnerability hypothesis. It merely adds that environment and experience can steer a person up instead of down. Yet it's actually a completely new way to think about genetics and human behavior. Risk becomes possibility; vulnerability becomes plasticity and responsiveness. It's one of those simple ideas with big, spreading implications. Gene variants generally considered misfortunes (poor Jim, he got the "bad" gene) can instead now be understood as highly leveraged evolutionary bets, with both high risks and high potential rewards: gambles that help create a diversified-portfolio approach to survival, with selection favoring parents who happen to invest in both dandelions and orchids.

In this view, having both dandelion and orchid kids greatly raises a family's (and a species') chance of succeeding, over time and in any given environment. The behavioral diversity provided by these two different types of temperament also supplies precisely what a smart, strong species needs if it is to spread across and dominate a changing world. The many dandelions in a population provide an underlying stability. The less-numerous orchids, meanwhile, may falter in some environments but can excel in those that suit them. And even when they lead troubled early lives, some of the resulting heightened responses to adversity that can be problematic in everyday life--increased novelty-seeking, restlessness of attention, elevated risk-taking, or aggression--can prove advantageous in certain challenging situations: wars, tribal or modern; social strife of many kinds; and migrations to new environments. Together, the steady dandelions and the mercurial orchids offer an adaptive flexibility that neither can provide alone. Together, they open a path to otherwise unreachable individual and collective achievements.

This orchid hypothesis also answers a fundamental evolutionary question that the vulnerability hypothesis cannot. If variants of certain genes create mainly dysfunction and trouble, how have they survived natural selection? Genes so maladaptive should have been selected out. Yet about a quarter of all human beings carry the best-documented gene variant for depression, while more than a fifth carry the variant that Bakermans-Kranenburg studied, which is associated with externalizing, antisocial, and violent behaviors, as well as ADHD, anxiety, and depression. The vulnerability hypothesis can't account for this. The orchid hypothesis can.

This is a transformative, even startling view of human frailty and strength. For more than a decade, proponents of the vulnerability hypothesis have argued that certain gene variants underlie some of humankind's most grievous problems: despair, alienation, cruelties both petty and epic. The orchid hypothesis accepts that proposition. But it adds, tantalizingly, that these same troublesome genes play a critical role in our species' astounding success.

Do read the whole thing at the Atlantic, where you'll also find a video interview with primatologist Stephen Suomi, whose work is featured heavily.

I'm traveling today but hope to post some related links in a day or two -- sources, papers, and a video of Suomi's long but stunning lecture. Till then, happy reading.


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This is a really sticky field. But extremely fascinating. I appreciate the balance you provided throughout and although there are criticisms that can be leveled at much of this research, it is important to make sure we are not so critical that we squash a nascent field.

My only disappointment with the piece was the treatment of the Caspi/Moffitt work in Science regarding the link between the serotonin transporter and depression. Neil Risch has recently published large, careful meta-analyses exploring this link and fails to find strong evidence to support the original Caspi/Moffitt finding. In addition, the link has never been replicated since that 2003 finding. These days, such gene/bahavior connections need to be replicated in multiple cohorts *prior* to publication, hence making this research area an exciting but dangerous minefield. In short, it would have been nice to have at least referred to these important new analyses which should help to shape this field as it continues to grow.

Otherwise, Bravo!

Very interesting. Being the mother of an adopted child with ADHD I have taken quite an interest in the subject. I have found that a high percentage of the adopted children I know of also have ADHD and or other learning and behavioral problems. I have often wondered if there wasn't something inherent in the adoption process, removing a baby even at birth from it's birthmother might have a detrimental effect on the developing brain. Have there been any studies on this?

This is a very important article and is fascinating. The "plasticity genes" hypothesis is something that J.Belsky has been talking about for some time but it has only been recently that we were able to pull together some very important findings in the GxE literature demonstrating the "for better or for worse" concept.

Please take a peak at this review to find out more about gene plasticity and what it might mean for human psychological and behavioral traits such as depression.
Belsky, J. et al. 2009. Vulnerability genes or plasticity genes? Molecular Psychiatry (2009) 14, 746â754.

Dear Dobbs, Please read Steven Rose's tome "Lifelines: Life Beyond The Gene" before writing/attempting to write/conceptualsing about 'specific genes' that control behaviour, the brain, mood swings et al.

Neelu Chitrapu

By Neelu Chitrapu (not verified) on 17 Nov 2009 #permalink

It seemed to me more that the video was about intergenerational transmission of secure vs insecure attachment rather than the orchid hypothesis. Suomi hints very briefly that securely attached monkeys with the short allele may develop superior function, but he mostly sticks to the idea that they can turn out just as well as long-alleled, securely-attached monkeys.

Does he further elaborate on the specific notion of superior psychological function in the context of a nurturing environment elsewhere?

By Meat Robot (not verified) on 18 Nov 2009 #permalink

Outstanding article. Thank you for your work on this! As additional evidence for the orchid hypothesis, here's a quote from my 1998 doctoral thesis about a 10-year followup study to the Finnish adoption study of schizophrenia (Wahlberg et al., 1997, in the Amer Journal of Psychiatry):

"In a 10-year update of the Finnish adoption study, Wahlberg (1997) found that index offspring (with schizophrenic mothers), who were raised by adoptive parents with low communication deviance, exhibited an even lower proportion of thought disordered responses to a Rorschach stimulus than did control offspring raised by adoptive parents with similarly low communication deviance. Only when the communication deviance of adoptive parents was high did the index offspring have a greater proportion of thought-disordered responses than their control group counterparts. Such a wide and inconsistent range of values of concordance and aggregation among these studies indicates that environmental effects profoundly influence any genetic contribution."