Evolving Diverse Fragility

Over the last 50,000 years humans have evolved many fragile features – features that in the wrong situations fail badly, but in the right situations gain greatly.  Apparently, in previous environments the cost of failure was too high to tolerate such fragile features, but our larger denser societies somehow magnify the gains while minimizing the losses, enough to make such features useful.

I’m not entirely clear how this works, but it does suggest even more diverse fragility in our future, and the importance of supporting such diversity.  Some details:

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. …

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. …  Recently, however, an alternate hypothesis has emerged from this one and is turning it inside out. … 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. …

Focus on just the bad-environment results, and you see only vulnerability. Focus on the good-environment results, and you see that the risk alleles usually produce better results than the protective ones. Securely raised 7-year-old boys with the DRD4 risk allele for ADHD, for instance, show fewer symptoms than their securely raised protective-allele peers. Non-abused teenagers with that same risk allele show lower rates of conduct disorder. Non-abused teens with the risky serotonin-transporter allele suffer less depression than do non-abused teens with the protective allele. Other examples abound …

A genetic trait tremendously maladaptive in one situation can prove highly adaptive in another. We needn’t look far to see this in human behavior. To survive and evolve, every society needs some individuals who are more aggressive, restless, stubborn, submissive, social, hyperactive, flexible, solitary, anxious, introspective, vigilant—and even more morose, irritable, or outright violent—than the norm.

All of this helps answer that fundamental evolutionary question about how risk alleles have endured. We have survived not despite these alleles but because of them. And those alleles haven’t merely managed to slip through the selection process; they have been actively selected for. Recent analyses, in fact, suggest that many orchid-gene alleles, including those mentioned in this story, have emerged in humans only during the past 50,000 or so years. Each of these alleles, it seems, arose via chance mutation in one person or a few people, and began rapidly proliferating.

Hat tip to Tyler.