An interesting article:
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.
If there wasn't an upside to this gene would the author have had his genes assayed?
As I researched this story, I thought about such questions a lot, including how they pertained to my own temperament and genetic makeup. Having felt the black dog’s teeth a few times over the years, I’d considered many times having one of my own genes assayed—specifically, the serotonin-transporter gene, also called the SERT gene, or 5-HTTLPR. This gene helps regulate the processing of serotonin, a chemical messenger crucial to mood, among other things. The two shorter, less efficient versions of the gene’s three forms, known as short/short and short/long (or S/S and S/L), greatly magnify your risk of serious depression—if you hit enough rough road. The gene’s long/long form, on the other hand, appears to be protective.
In the end, I’d always backed away from having my SERT gene assayed. Who wants to know his risk of collapsing under pressure? Given my family and personal history, I figured I probably carried the short/long allele, which would make me at least moderately depression-prone. If I had it tested I might get the encouraging news that I had the long/long allele. Then again, I might find I had the dreaded, riskier short/short allele. This was something I wasn’t sure I wanted to find out.
...“David,” the message began. “I ran the assay on the DNA from your saliva sample today. The assay ran well and your genotype is S/S. Good thing neither of us think of these things as deterministic or even having a fixed valence. Let me know if you want to talk about your result or genetic issues.”
... The orchid hypothesis suggested that this particular allele, the rarest and riskiest of the serotonin-transporter gene’s three variants, made me not just more vulnerable but more plastic. And that new way of thinking changed things. I felt no sense that I carried a handicap that would render my efforts futile should I again face deep trouble. In fact, I felt a heightened sense of agency. Anything and everything I did to improve my own environment and experience—every intervention I ran on myself, as it were—would have a magnified effect. In that light, my short/short allele now seems to me less like a trapdoor through which I might fall than like a springboard—slippery and somewhat fragile, perhaps, but a springboard all the same.
I don’t plan to have any of my other key behavioral genes assayed. I don’t plan on having my kids’ genes done, either. What would it tell me? That I shape them in every encounter? I know this. Yet I do like thinking that when I take my son trolling for salmon, or listen to his younger brother’s labyrinthine elaborations of his dreams, or sing “Sweet Betsy of Pike” with my 5-year-old daughter as we drive home from the lake, I’m flipping little switches that can help light them up. I don’t know what all those switches are—and I don’t need to. It’s enough to know that together we can turn them on.
We have survived not despite these alleles but becauseof 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. Rhesus monkeys and human beings split from their common lineage about 25 million to 30 million years ago, so these polymorphisms must have mutated and spread on separate tracks in the two species. Yet in both species, these new alleles proved so valuable that they spread far and wide.