It’s fascinating to examine these studies with the orchid hypothesis in mind. 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—even though, as Jay Belsky points out, the studies were designed and analyzed primarily to spot negative vulnerabilities. Belsky suspects that as researchers start to design studies that test for gene sensitivity rather than just risk amplification, and as they increasingly train their sights on positive environments and traits, the evidence for the orchid hypothesis will only grow.
Suomi gathered plenty of that evidence himself in the years after his 2002 study. He found, for example, that monkeys who carried the supposedly risky serotonin-transporter allele, and who had nurturing mothers and secure social positions, did better at many key tasks—creating playmates as youths, making and drawing on alliances later on, and sensing and responding to conflicts and other dangerous situations—than similarly blessed monkeys who held the supposedly protective allele. They also rose higher in their respective dominance hierarchies. They were more successful.
Suomi made another remarkable discovery. He and others assayed the serotonin-transporter genes of seven of the 22 species of macaque, the primate genus to which the rhesus monkey belongs. None of these species had the serotonin-transporter polymorphism that Suomi was beginning to see as a key to rhesus monkeys’ flexibility. Studies of other key behavioral genes in primates produced similar results; according to Suomi, assays of the SERT gene in other primates studied to date, including chimps, baboons, and gorillas, turned up “nothing, nothing, nothing.” The science is young, and not all the data is in. But so far, among all primates, only rhesus monkeys and human beings seem to have multiple polymorphisms in genes heavily associated with behavior. “It’s just us and the rhesus,” Suomi says.
This discovery got Suomi thinking about another distinction we share with rhesus monkeys. Most primates can thrive only in their specific environments. Move them and they perish. But two kinds, often called “weed” species, are able to live almost anywhere and to readily adapt to new, changing, or disturbed environments: human beings and rhesus monkeys. The key to our success may be our weediness. And the key to our weediness may be the many ways in which our behavioral genes can vary.
One morning this past May, Elizabeth Mallott, a researcher working at Suomi’s lab, arrived to start her day at the main rhesus enclosure and found a half-dozen monkeys in her parking spot. They were huddling close together, bedraggled and nervous. As Mallott got out of her car and moved closer, she saw that some had bite wounds and scratches. Most monkeys who jump the enclosure’s double electrified fences (it happens now and then) soon want to get back in. These monkeys did not. Neither did several others that Mallott found between the two fences.
After caging the escapees in an adjacent building, Mallott, now joined by Matthew Novak, another researcher who knew the colony well, entered through the double gates. The colony, numbering about 100-odd monkeys, had been together for about 30 years. Changes in its hierarchy usually came slowly and subtly. But when Novak and Mallott started looking around, they realized that something big had happened. “Animals were in places they weren’t supposed to be,” Novak would later tell me. “Animals who don’t hang out together were sitting together. Social rules were suspended.”
It soon became apparent that the family group called Family 3, which for decades had ranked second to a group called Family 1, had staged a coup. Family 3 had grown larger than Family 1 several years before. But Family 1, headed by a savvy matriarch named Cocobean, had retained incumbency through authority, diplomacy, and momentum. A week or so before the coup, however, one of Cocobean’s daughters, Pearl, had been moved from the enclosure to the veterinary facility because her kidneys seemed to be failing. Family 1’s most formidable male, meanwhile, had grown old and arthritic. Pearl was especially close to Cocobean and, as the only daughter without children of her own, was particularly likely to defend her. Her absence, along with the male’s infirmity, created a vulnerable moment for Family 1.
“This may have been in the works for a couple weeks,” Novak says. “But as far as we can reconstruct, the actual event, the night before we found the monkeys in the parking lot, started when a young female named Fiona”—a 3-year-old Family 1 member, a borderline bully known to have initiated many a scuffle—“started something with someone in Family 3. It escalated. Family 3 saw its chance. And they just started to take Family 1 out. You could see it from who was wounded and who wasn’t, and who was sitting in preferred places, and who was run out of the colony, and who was suddenly extremely deferential. One other female in Family 1, Quark, was killed; another, Josie, was hurt so badly we had to put her down. They’d gone after all of Cocobean’s other daughters, too. Somebody had bitten the big male in Family 1 so badly he couldn’t use his arm. Fiona got roughed up pretty bad. It was a very systematic scuffle. They went right at the head of the group and worked their way down.”
Soon after Novak described all this to me, he and I walked around the enclosure. Though it was the middle of a broiling July day, downtime for the monkeys, you could see hints of the new order. Family 3 calmly occupied what seemed to be the new center of power, a corncrib near the pond (one of several corncribs set out for shelter). They groomed one another, napped, and evenly stared at us as we stared at them. A more nervous bunch clustered in another crib down the hill. When we got within 30 feet, the largest monkey in the group shot up onto the cage bars. From 10 feet up it screamed at me, rattled the bars, and showed some nasty teeth.
From there I went to Suomi’s office and asked him what he thought had happened. Suomi has thought a lot about this coup, and it’s easy to see why. All of the important threads he’d been weaving together in his research were on display in this revolt: the importance of early experience; the interplay of environment, parenting, and genetic inheritance; the maddening primacy of family and social bonds; the repercussions of different traits in different circumstances. And now, in light of the orchid hypothesis, he was beginning to see that the threads might be woven together in a new way.
“About 15 years ago,” he said, “Carol Berman, a monkey researcher at SUNY-Buffalo, spent a lot of time watching a large rhesus-monkey colony that lives on an island in Puerto Rico. She wanted to see what happened as the groups changed size over time. They’d start at about 30 or 40 individuals—a group that had split off from another—and then expand. At a certain point, often somewhere near a hundred, the group would reach its limit, and it, too, would split into smaller troops.”
Such size limits, which vary among social species, are sometimes called “Dunbar numbers,” after Robin Dunbar, a British evolutionary psychologist who argues that a species’ group limit reflects how many social relationships its individuals can manage cognitively. Berman’s observations suggested that the Dunbar number of a species reflects not just its cognitive powers but its temperamental and behavioral range as well.
Berman saw that when rhesus troops are small, the mothers can let their young play freely, because strangers rarely approach. But as a troop grows and the number of family groups rises, strangers or semi-strangers more often come near. The adult females become more vigilant, defensive, and aggressive. The kids and adult males follow suit. More and more monkeys receive upbringings that draw out the less sociable sides of their behavioral potentials; fights grow more common; rivalries grow more tense. Things finally get so bad that the troop must split. “And that’s what happened here,” Suomi said. “It’s a very extensive feedback system. What happens at the dyadic level, between mother and infant, ultimately affects the very nature and survival of the larger social group.”
Studies by Suomi and others show that such differences in early experience can wildly alter how genes express themselves—that is, whether, when, and how strongly the genes switch themselves on and off. Suomi suspects that early experiences may affect later patterns of gene expression and behavior as well, including how flexible and reactive an animal is, by helping to set the sensitivity level of key alleles. A tense upbringing, he says, will produce watchful caution or vigilant aggression in any monkey (the parents’ way of preparing the offspring for tough times)—but this effect may be especially pronounced in monkeys with particularly plastic behavioral alleles.
That’s what Suomi thinks may have happened in the run-up to what he calls the Palace Revolt. Fiona’s injudicious aggression proved disastrous for her and Family 1. But Family 3, a group that had been diplomatically deferring to Family 1 for years, dramatically improved its fortunes by mounting an uncharacteristically aggressive and sustained counterattack. Suomi speculates that in the tenser, more crowded conditions of the large colony, gene-environment interactions had made some of the monkeys in Family 3, particularly those with more-reactive “orchid” alleles, not more aggressive but more potentially aggressive. During the period when they could not afford to challenge the hierarchy—the period before Pearl’s departure—aggressiveness would have led them into unwinnable, possibly fatal conflicts. But in Pearl’s absence the odds changed—and the Family 3 monkeys exploited a rare and decisive opportunity by unleashing their aggressive potential.
The coup also showed something more straightforward: that 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 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.
As the evolutionary anthropologists Gregory Cochran and Henry Harpending have pointed out, in The 10,000 Year Explosion (2009), the past 50,000 years—the period in which orchid genes seem to have emerged and expanded—is also the period during which Homo sapiens started to get seriously human, and during which sparse populations in Africa expanded to cover the globe in great numbers. Though Cochran and Harpending don’t explicitly incorporate the orchid-gene hypothesis into their argument, they make the case that human beings have come to dominate the planet because certain key mutations allowed human evolution to accelerate—a process that the orchid-dandelion hypothesis certainly helps explain.
How this happened must have varied from context to context. If you have too many aggressive people, for example, conflict runs rampant, and aggression is selected out, because it becomes costly; when aggression decreases enough to be less risky, it becomes more valuable, and its prevalence again rises. Changes in environment or culture would likewise affect an allele’s prevalence. The orchid variant of the DRD4 gene, for instance, increases risk of ADHD (a syndrome best characterized, Cochran and Harpending write, “by actions that annoy elementary-school teachers”). Yet attentional restlessness can serve people well in environments that reward sensitivity to new stimuli. The current growth of multitasking, for instance, may help select for just such attentional agility. Complain all you want that it’s an increasingly ADHD world these days—but to judge by the spread of DRD4’s risk allele, it’s been an increasingly ADHD world for about 50,000 years.
Even if you accept that orchid genes may grant us flexibility crucial to our success, it can be startling to ponder their dynamics up close and personal. After I FedExed away my vial of saliva for genotyping, I told myself more or less to forget it. To my surprise, I managed to. The e-mail that eventually arrived with the results, promised for a Monday, turned up three days early, during a Friday evening when I was simultaneously half-watching Monsters, Inc. with my kids and distractedly scanning the messages on my iPhone. At first I didn’t really register what I was reading.
“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.”
When I finished reading the message, the house seemed quieter, though it was not. As I looked out the window at our pear tree, its blossoms fallen but its fruit only nubbins, I felt a chill spread through my torso.
I hadn’t thought it would matter.
Yet as I sat absorbing this information, the chill came to seem less the coldness of fear than a shiver of abrupt and inverted self-knowledge—of suddenly knowing with certainty something I had long suspected, and finding that it meant something other than I thought it would. 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.