Nature-Nuture: The Orchid Hypothesis

Few things have captured my interest so completely for so long as questions of nature and nurture. That is, to what extent are our behaviors, our very personalities, temperaments, aptitudes, successes and failures a function of our genetic prescriptions, predispositions or environmental trigger mechanisms. And, to what extent are they a function of what we learn, our acculturation, how we are shaped by our family, community and education experiences. In college, I was intensely focused on psychology, learning theory, classical and operant conditioning--but only as balanced by a secondary focus on biology and genetics, the brain, neurological and endocrine systems. And little about that has changed for me--except the notable, even illuminating, advances in genome research and evolutionary psychology. And I'd like to share with you one of the more fascinating and useful implications of recent research: The Orchid Hypothesis.
As reported in The Atlantic:

Most of us have genes that make us as hardy as dandelions: able to take root and survive almost anywhere. A few of us, however, are more like the orchid: fragile and fickle, but capable of blooming spectacularly if given greenhouse care. So holds a provocative new theory of genetics, which asserts that the very genes that give us the most trouble as a species, causing behaviors that are self-destructive and antisocial, also underlie humankind's phenomenal adaptability and evolutionary success. With a bad environment and poor parenting, orchid children can end up depressed, drug-addicted, or in jail—but with the right environment and good parenting, they can grow up to be society's most creative, successful, and happy people.  

Introduction, "The Science of Success," by David Dobbs, The Atlantic (December 2009)

The story begins with some genetics basics: there are certain key genes affecting our behavior that have variations called "alleles." Such genes are called "polymorphisms." As the article notes, it has long been known that variants of these genes "affect either brain development or the processing of the brain's chemical messengers, making people more vulnerable to certain mood, psychiatric, or personality disorders." Such variants are known as "risk alleles"--in contradistinction to the more normal, more prevalent "protective alleles"--because they increase our likelihood of developing a behavioral problem. And according to this article, based on many studies over the last decade or so,

...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 became known as the "stress diathesis" or "genetic vulnerability" model. And most of the research advancing this hypothesis was focused on the presence or absence of the risk allele in individuals and the resulting effect of childhood stress or trauma on the individuals' behavior. What was affirmed again and again was that having a risk allele did not mean that you would necessarily exhibit these various behavioral problems, only that you were vulnerable to them if you had suffered oppressive levels of stress or trauma. But because of the focus on behavioral dysfunction, no one was looking for whether there were other possible results--upsides, perhaps, in cases of particularly supportive environments.

But that has changed in the last few years. New research directions and initial results have offered a broader and deeper understanding of the range of circumstances and results that obtain from the presence of these risk alleles. In fact, these risk alleles are, in certain circumstances, "possibility alleles." From the Atlantic article:

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.

There are apparently references in Swedish folk wisdom to "dandelion children": normal, healthy, resilient children who adapt and thrive almost anywhere. In noting this, Bruce Ellis and W. Thomas Boyce, offer that their research now suggests that there are also "orchid children," children who "will wilt if ignored or maltreated but bloom spectacularly with greenhouse care."

That's all well enough, even exciting, if like me you are fascinated by such things. But what does it all mean for our understanding of human potential, behavioral management or remediation, even for our understandings of evolutionary processes? More from the article:

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.

The article returns to a recent study comparing children with and without the risk allele. In this study, there is a risk allele control group and a group where parents of children with the risk allele were trained to intervene in constructive and supportive ways. The author notes that both the "vulnerability hypothesis" and the "orchid hypothesis" would predict that the control group with the risk allele would exhibit worse behaviors than the the group with the protective allele. And they did. But the surprise came with the risk allele group that received parental interventions. The "vulnerability hypothesis" would suggest that they would improve, but not achieve the same level of normative behavior as the group with the protective allele. Wrong. The Atlantic article, in conclusion:

As it turned out, the toddlers with the risk allele blew right by their counterparts. They cut their externalizing scores by almost 27 percent, while the protective-allele kids cut theirs by just 12 percent (improving only slightly on the 11 percent managed by the protective-allele population in the control group). The upside effect in the intervention group, in other words, was far larger than the downside effect in the control group. Risk alleles, the Leiden team concluded, really can create not just risk but possibility.  

Can liability really be so easily turned to gain? The pediatrician W. Thomas Boyce, who has worked with many a troubled child in more than three decades of child-development research, says the orchid hypothesis "profoundly recasts the way we think about human frailty." He adds, "We see that when kids with this kind of vulnerability are put in the right setting, they don't merely do better than before, they do the best—even better, that is, than their protective-allele peers."

A long article, it is nonetheless worth reading in full for those with an appetite for more depth of coverage. Complementary, affirming research with Rhesus monkeys is also examined at length. And the author's personal examinations and reflections on his own risk allele raise another set of very human considerations and decisions.
http://www.theatlantic.com/doc/print/200912/dobbs-orchid-gene