The Science of Success - The Atlantic (December 2009)

The Science of Success
In 2004, Marian Bakermans-Kranenburg,a professor of child and family studies at Leiden University, startedcarrying a video camera into homes of families whose 1-to-3-year-oldsindulged heavily in the oppositional, aggressive, uncooperative, andaggravating behavior that psychologists call “externalizing”: whining,screaming, whacking, throwing tantrums and objects, and willfullyrefusing reasonable requests. Staple behaviors in toddlers, perhaps.But research has shown that toddlers with especially high rates ofthese behaviors are likely to become stressed, confused children whofail academically and socially in school, and become antisocial andunusually aggressive adults.
At the outset of their study, Bakermans-Kranenburg and hercolleagues had screened 2,408 children via parental questionnaire, andthey were now focusing on the 25 percent rated highest by their parentsin externalizing behaviors. Lab observations had confirmed theseparental ratings.
Bakermans-Kranenburg meant to change the kids’ behavior. In anintervention her lab had developed, she or another researcher visitedeach of 120 families six times over eight months; filmed the mother andchild in everyday activities, including some requiring obedience orcooperation; and then edited the film into teachable moments to show tothe mothers. A similar group of high-externalizing children received nointervention.
To the researchers’ delight, the intervention worked. The moms,watching the videos, learned to spot cues they’d missed before, or torespond differently to cues they’d seen but had reacted to poorly.Quite a few mothers, for instance, had agreed only reluctantly to readpicture books to their fidgety, difficult kids, saying they wouldn’tsit still for it. But according to Bakermans-Kranenburg, when thesemothers viewed the playback they were “surprised to see how muchpleasure it was for the child—and for them.” Most mothers began readingto their children regularly, producing what Bakermans-Kranenburgdescribes as “a peaceful time that they had dismissed as impossible.”
And the bad behaviors dropped. A year after the intervention ended,the toddlers who’d received it had reduced their externalizing scoresby more than 16 percent, while a nonintervention control group improvedonly about 10 percent (as expected, due to modest gains in self-controlwith age). And the mothers’ responses to their children became morepositive and constructive.
Few programs change parent-child dynamics so successfully. Butgauging the efficacy of the intervention wasn’t the Leiden team’s onlygoal, or even its main one. The team was also testing a radical newhypothesis about how genes shape behavior—a hypothesis that stands torevise our view of not only mental illness and behavioral dysfunctionbut also human evolution.
Of special interest to the team was a new interpretation of one ofthe most important and influential ideas in recent psychiatric andpersonality research: that certain variants of key behavioral genes(most of which affect either brain development or the processing of thebrain’s chemical messengers) make people more vulnerable to certainmood, psychiatric, or personality disorders. Bolstered over the past 15years by numerous studies, this hypothesis, often called the “stressdiathesis” or “genetic vulnerability” model, has come to saturatepsychiatry and behavioral science. During that time, researchers haveidentified a dozen-odd gene variants that can increase a person’ssusceptibility to depression, anxiety, attention-deficit hyperactivitydisorder, heightened risk-taking, and antisocial, sociopathic, orviolent behaviors, and other problems—if, and only if, the personcarrying the variant suffers a traumatic or stressful childhood orfaces particularly trying experiences later in life.
This vulnerability hypothesis, as we can call it, has alreadychanged our conception of many psychic and behavioral problems. Itcasts them as products not of nature or nurture but of complex“gene-environment interactions.” Your genes don’t doom you to thesedisorders. But if you have “bad” versions of certain genes and lifetreats you ill, you’re more prone to them.
Recently, however, an alternate hypothesis has emerged from this oneand is turning it inside out. This new model suggests that it’s amistake to understand these “risk” genes only as liabilities. Yes, thisnew thinking goes, these bad genes can create dysfunction inunfavorable contexts—but they can also enhance function in favorablecontexts. The genetic sensitivities to negative experience that thevulnerability hypothesis has identified, it follows, are just thedownside of a bigger phenomenon: a heightened genetic sensitivity to all experience.
The evidence for this view is mounting. Much of it has existed foryears, in fact, but the focus on dysfunction in behavioral genetics hasled most researchers to overlook it. This tunnel vision is easy toexplain, according to Jay Belsky, a child-development psychologist atBirkbeck, University of London. “Most work in behavioral genetics hasbeen done by mental-illness researchers who focus on vulnerability,” hetold me recently. “They don’t see the upside, because they don’t lookfor it. It’s like dropping a dollar bill beneath a table. You lookunder the table, you see the dollar bill, and you grab it. But youcompletely miss the five that’s just beyond your feet.”
Though this hypothesis is new to modern biological psychiatry, itcan be found in folk wisdom, as the University of Arizona developmentalpsychologist Bruce Ellis and the University of British Columbiadevelopmental pediatrician W. Thomas Boyce pointed out last year in thejournal Current Directions in Psychological Science. TheSwedes, Ellis and Boyce noted in an essay titled “BiologicalSensitivity 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-tendedgarden. Ellis and Boyce offer that there are also “orchid” children,who will wilt if ignored or maltreated but bloom spectacularly withgreenhouse care.
At first glance, this idea, which I’ll call the orchid hypothesis,may seem a simple amendment to the vulnerability hypothesis. It merelyadds that environment and experience can steer a person up instead ofdown. Yet it’s actually a completely new way to think about geneticsand human behavior. Risk becomes possibility; vulnerability becomesplasticity 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 ashighly leveraged evolutionary bets, with both high risks and highpotential rewards: gambles that help create a diversified-portfolioapproach to survival, with selection favoring parents who happen toinvest in both dandelions and orchids.
In this view, having both dandelion and orchid kids greatly raises afamily’s (and a species’) chance of succeeding, over time and in anygiven environment. The behavioral diversity provided by these twodifferent types of temperament also supplies precisely what a smart,strong species needs if it is to spread across and dominate a changingworld. The many dandelions in a population provide an underlyingstability. The less-numerous orchids, meanwhile, may falter in someenvironments but can excel in those that suit them. And even when theylead troubled early lives, some of the resulting heightened responsesto adversity that can be problematic in everyday life—increasednovelty-seeking, restlessness of attention, elevated risk-taking, oraggression—can prove advantageous in certain challenging situations:wars, tribal or modern; social strife of many kinds; and migrations tonew environments. Together, the steady dandelions and the mercurialorchids offer an adaptive flexibility that neither can provide alone.Together, they open a path to otherwise unreachable individual andcollective achievements.
This orchid hypothesis also answers a fundamental evolutionaryquestion that the vulnerability hypothesis cannot. If variants ofcertain genes create mainly dysfunction and trouble, how have theysurvived natural selection? Genes so maladaptive should have beenselected out. Yet about a quarter of all human beings carry thebest-documented gene variant for depression, while more than a fifthcarry the variant that Bakermans-Kranenburg studied, which isassociated with externalizing, antisocial, and violent behaviors, aswell as ADHD, anxiety, and depression. The vulnerability hypothesiscan’t account for this. The orchid hypothesis can.
This is a transformative, even startling view of human frailty andstrength. For more than a decade, proponents of the vulnerabilityhypothesis have argued that certain gene variants underlie some ofhumankind’s most grievous problems: despair, alienation, cruelties bothpetty and epic. The orchid hypothesis accepts that proposition. But itadds, tantalizingly, that these same troublesome genes play a criticalrole in our species’ astounding success.
The orchid hypothesis—sometimes called the plasticity hypothesis,the sensitivity hypothesis, or the differential-susceptibilityhypothesis—is too new to have been tested widely. Many researchers,even those in behavioral science, know little or nothing of the idea. Afew—chiefly those with broad reservations about ever tying specificgenes to specific behaviors—express concerns. But as more supportingevidence emerges, the most common reaction to the idea amongresearchers and clinicians is excitement. A growing number ofpsychologists, psychiatrists, child-development experts, geneticists,ethologists, and others are beginning to believe that, as KarlenLyons-Ruth, a developmental psychologist at Harvard Medical School,puts it, “It’s time to take this seriously.”
With the data gathered in the video intervention, the Leiden teambegan to test the orchid hypothesis. Could it be, they wondered, thatthe children who suffer most from bad environments also profit the mostfrom good ones? To find out, Bakermans-Kranenburg and her colleagueMarinus van Ijzendoorn began to study the genetic makeup of thechildren in their experiment. Specifically, they focused on oneparticular “risk allele” associated with ADHD and externalizingbehavior. (An allele is any of the variants of a gene that takes morethan one form; such genes are known as polymorphisms. A risk allele,then, is simply a gene variant that increases your likelihood ofdeveloping a problem.)
Bakermans-Kranenburg and van Ijzendoorn wanted to see whether kidswith a risk allele for ADHD and externalizing behaviors (a variant of adopamine-processing gene known as DRD4) would respond as much topositive environments as to negative. A third of the kids in the studyhad this risk allele; the other two-thirds had a version considered a“protective allele,” meaning it made them less vulnerable to badenvironments. The control group, who did not receive the intervention,had a similar distribution.
Both the vulnerability hypothesis and the orchid hypothesis predictthat in the control group the kids with a risk allele should do worsethan those with a protective one. And so they did—though only slightly.Over the course of 18 months, the genetically “protected” kids reducedtheir externalizing scores by 11 percent, while the “at-risk” kids cuttheirs by 7 percent. Both gains were modest ones that the researchersexpected would come with increasing age. Although statisticallysignificant, the difference between the two groups was probablyunnoticeable otherwise.
The real test, of course, came in the group that got theintervention. How would the kids with the risk allele respond?According to the vulnerability model, they should improve less thantheir counterparts with the protective allele; the modest upgrade thatthe video intervention created in their environment wouldn’t offsettheir general vulnerability.
As it turned out, the toddlers with the risk allele blew right bytheir counterparts. They cut their externalizing scores by almost 27percent, while the protective-allele kids cut theirs by just 12 percent(improving only slightly on the 11 percent managed by theprotective-allele population in the control group). The upside effectin the intervention group, in other words, was far larger than thedownside effect in the control group. Risk alleles, the Leiden teamconcluded, really can create not just risk but possibility.
Can liability really be so easily turned to gain? The pediatricianW. Thomas Boyce, who has worked with many a troubled child in more thanthree decades of child-development research, says the orchid hypothesis“profoundly recasts the way we think about human frailty.” He adds, “Wesee that when kids with this kind of vulnerability are put in the rightsetting, they don’t merely do better than before, they do the best—evenbetter, that is, than their protective-allele peers. “Are there anyenduring human frailties that don’t have this other, redemptive side tothem?”
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’dconsidered many times having one of my own genes assayed—specifically,the serotonin-transporter gene, also called the SERTgene, or 5-HTTLPR. This gene helps regulate the processing ofserotonin, 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 magnifyyour risk of serious depression—if you hit enough rough road. Thegene’s long/long form, on the other hand, appears to be protective.
In the end, I’d always backed away from having my SERTgene assayed. Who wants to know his risk of collapsing under pressure?Given my family and personal history, I figured I probably carried theshort/long allele, which would make me at least moderatelydepression-prone. If I had it tested I might get the encouraging newsthat I had the long/long allele. Then again, I might find I had thedreaded, riskier short/short allele. This was something I wasn’t sure Iwanted to find out.
But as I looked into the orchid hypothesis and began to think interms of plasticity rather than risk, I decided maybe I did want tofind out. So I called a researcher I know in New York who doesdepression research involving the serotonin-transporter gene. The nextday, FedEx left a package on my front porch containing a specimen cup.I spat into it, examined what I’d produced, and spat again. Then Iscrewed the cap tight, slid the vial into its little shipping tube, andput it back on the porch. An hour later, the FedEx guy took it away.
Of all the evidence supporting the orchid-gene hypothesis, perhapsthe most compelling comes from the work of Stephen Suomi, arhesus-monkey researcher who heads a sprawling complex of labs andmonkey habitats in the Maryland countryside—the National Institutes ofHealth’s Laboratory of Comparative Ethology. For 41 years, first at theUniversity of Wisconsin and then, beginning in 1983, in the Marylandlab the NIH built specifically for him, Suomi has been studying theroots of temperament and behavior in rhesus monkeys—which share about95 percent of our DNA, a number exceeded only in apes. Rhesus monkeysdiffer from humans in obvious and fundamental ways. But their closeresemblance to us in crucial social and genetic respects reveals muchabout the roots of our own behavior—and has helped give rise to theorchid hypothesis.
Suomi learned his trade as a student and protégé of,and then a direct successor to, Harry Harlow, one of the 20th century’smost influential and problematic behavioral scientists. When Harlowstarted his work, in the 1930s, the study of childhood development wasdominated by a ruthlessly mechanistic behavioralism. The movement’sleading figure in the United States, John Watson, considered motherlove “a dangerous instrument.” He urged parents to leave crying babiesalone; to never hold them to give pleasure or comfort; and to kiss themonly occasionally, on the forehead. Mothers were important less fortheir affection than as conditioners of behavior.
With a series of ingenious but sometimes disturbingly cruelexperiments on monkeys, Harlow broke with this cool behavioralism. Hismost famous experiment showed that baby rhesus monkeys, raised alone orwith same-age peers, preferred a foodless but fuzzy terryclothsurrogate “mother” over a wire-mesh version that freely dispensedmeals. He showed that these infants desperately wanted to bond, andthat depriving them of physical, emotional, and social attachment couldcreate a near-paralyzing dysfunction. In the 1950s this work providedcritical evidence for the emerging theory of infant attachment: atheory that, with its emphasis on rich, warm parent-child bonds andhappy early experiences, still dominates child-development theory (andparenting books) today.
In the years since Suomi took over Harlow’s Wisconsin lab as a28-year-old wunderkind, he has both broadened and sharpened the inquiryHarlow started. New tools now let Suomi examine not just his monkeys’temperaments but also the physiological and genetic underpinnings oftheir behavior. His lab’s naturalistic environment allows him to focusnot just on mother-child interactions but also on the family and socialenvironments that shape and respond to the monkeys’ behavior. “Life ina rhesus-monkey colony is very, very complicated,” Suomi says. Themonkeys must learn to navigate a social system that is highly nuancedand hierarchical. “Those who can manage this, do well,” Suomi told me.“Those who don’t, don’t.”
Rhesus monkeys typically mature at about four or five years and liveto about 20 in the wild. Their development parallels our own at afairly neat 1-to-4 ratio: a 1-year-old monkey is much like a 4-year-oldhuman being, a 4-year-old monkey is like a 16-year-old human being, andso on. A mother typically gives birth annually, starting at around age4. Though the monkeys copulate all year, the females’ fertility seasonsare only a couple of months long. Since they tend to occur together, atroop usually produces crops of babies that have same-age peers.
For the first month, the mother keeps the baby attached to her orwithin arm’s reach. At about two weeks, the baby starts to explore, atfirst within only a few feet of its mother. These forays grow infrequency, duration, and distance over the next six to seven months,but rarely do the babies pass out of the mother’s sight line orearshot. If the young monkey gets frightened, it scampers back to themother. Often she’ll see trouble coming and pull the infant close.
When the monkey is about eight months old—a rhesus preschooler—itsmother’s mating time arrives. Anticipating another child, the motherallows the youngster to spend more and more time with its cousins, witholder siblings in the maternal line, and with occasional visitors fromother families or troops. The youngster’s family group, friends, andallies still provide protection when necessary.
A maturing female will stay with this group all her life. A male,however, will leave—often under pressure from the females as he getsrowdier and rougher—when he’s 4 or 5, or roughly the equivalent of a16-to-20-year-old person. At first he’ll join an all-male gang thatlives more or less separately. After a few months to a year, he’llleave the gang and try to charm, push, or sidle his way into a newfamily or troop. If he succeeds, he becomes one of several adult malesto serve as mate, companion, and muscle for the several females. Butonly about half the males make it that far. Their transition periodexposes them to attacks from other young males, attacks from rivalgangs, attacks from new troop members if they play their cards wrong,and predation during any time they lack a gang’s or troop’s protection.Many die in the transition.
Very early in his work, Suomi identified two types of monkeys thathad trouble managing these relations. One type, which Suomi calls a“depressed” or “neurotic” monkey, accounted for about 20 percent ofeach generation. These monkeys are slow to leave their mothers’ sideswhen young. As adults they remain tentative, withdrawn, and anxious.They form fewer bonds and alliances than other monkeys do.
The other type, generally male, is what Suomi calls a “bully”: anunusually and indiscriminately aggressive monkey. These monkeysaccounted for 5 to 10 percent of each generation. “Rhesus monkeys arefairly aggressive in general, even when young,” Suomi says, “and theirplay involves a lot of rough-and-tumble. But usually no one getshurt—except with these guys. They do stupid things most other monkeysknow not to. They repeatedly confront dominant monkeys. They getbetween moms and their kids. They don’t know how to calibrate theiraggression, and they don’t know how to read signs they should back off.Their conflicts tend to always escalate.” These bullies also scorepoorly in tests of monkey self-control. For instance, in a “cocktailhour” test that Suomi sometimes uses, monkeys get unrestricted accessto a neutral-tasting alcoholic drink for an hour. Most monkeys havethree or four drinks and then stop. The bullies, Suomi says, “drinkuntil they drop.”
The neurotics and the bullies meet quite different fates. Theneurotics mature late but do okay. The females become jumpy mothers,but how their children turn out depends on the environment in which themothers raise them. If it’s secure, they become more or less normal; ifit’s insecure, they become jumpy too. The males, meanwhile, stay withintheir mothers’ family circles an unusually long time—up to eight years.They’re allowed to do so because they don’t make trouble. And theirlonger stay lets them acquire enough social savvy and diplomaticdeference so that when they leave, they usually work their way into newtroops more successfully than do males who break away younger. Theydon’t get to mate as prolifically as more confident, more assertivemales do; they seldom rise high in their new troops; and their lowstatus can put them at risk in conflicts. But they’re less likely todie trying to get in the door. They usually survive and pass on theirgenes.
The bullies fare much worse. Even as babies and youths, they seldommake friends. And by the time they’re 2 or 3, their extreme aggressionleads the troop’s females to simply run them out, by group force ifnecessary. Then the male gangs reject them, as do other troops.Isolated, most of them die before reaching adulthood. Few mate.
Suomi saw early on that each of these monkey types tended to comefrom a particular type of mother. Bullies came from harsh, censoriousmothers who restrained their children from socializing. Anxious monkeyscame from anxious, withdrawn, distracted mothers. The heritages werepretty clear-cut. But how much of these different personality typespassed through genes, and how much derived from the manner in which themonkeys were raised?
To find out, Suomi split the variables. He took nervous infants ofnervous mothers—babies who in standardized newborn testing were alreadyjumpy themselves—and gave them to especially nurturing “supermoms.”These babies turned out very close to normal. Meanwhile, DarioMaestripieri of the University of Chicago took secure, high-scoringinfants from secure, nurturing mothers and had them raised by abusivemothers. This setting produced nervous monkeys.
The lesson seemed clear. Genes played a role—but environment played an equally important one.
When tools for the study of genes first became available, in thelate 1990s, Suomi was quick to use them to more directly examine thebalance between genes and environment in shaping his monkeys’development. He almost immediately struck gold, with a project hestarted in 1997 with Klaus-Peter Lesch, a psychiatrist from theUniversity of Würzburg. The year before, Lesch had published datarevealing, for the first time, that the human serotonin-transportergene had three variants (the previously mentioned short/short,short/long, and long/long alleles) and that the two shorter versionsmagnified risk for depression, anxiety, and other problems. Askedto genotype Suomi’s monkeys, Lesch did so. He found that they had thesame three variants, though the short/short form was rare.
Suomi, Lesch, and NIH colleague J. Dee Higley set about doing a typeof study now recognized as a classic “gene-by-environment” study. Firstthey took cerebral spinal fluid from 132 juvenile rhesus monkeys andanalyzed it for a serotonin metabolite, called 5-HIAA, that’sconsidered a reliable indicator of how much serotonin the nervoussystem is processing. Lesch’s studies had already shown that depressedpeople with the short/long serotonin-transporter allele had lower5-HIAA levels, reflecting less-efficient serotonin processing. He andSuomi wanted to see if the finding would hold true in monkeys. If itdid, it would provide more evidence for the genetic dynamic shown inLesch’s studies. And finding such a dynamic in rhesus monkeys wouldconfirm their value as genetic and behavioral models for studying humanbehavior.
After Suomi, Lesch, and Higley had grouped the monkeys’ 5-HIAAlevels according to their serotonin genotype (short/long or long/long,but not short/short, which was too rare to be of use), they also sortedthe results by whether the monkeys had been raised by their mothers oras orphans with only same-aged peers. When their colleague AllisonBennett charted the results on a bar graph showing 5-HIAA levels, allof the mother-reared monkeys, no matter which allele they had, showedserotonin processing in the normal range. The metabolite levels of thepeer-raised monkeys, however, diverged sharply by genotype: theshort/long monkeys in that group processed serotonin highlyinefficiently (a risk factor for depression and anxiety), whereas thelong/long monkeys processed it robustly. When Suomi saw the results, herealized that he finally had proof of a behaviorally relevantgene-by-environment interaction in his monkeys. “I took one look atthat graph,” he told me, “and said, ‘Let’s go pop some champagne.’”
Suomi and Lesch published their results in 2002 in Molecular Psychiatry,a relatively new journal about behavioral genetics. The paper formedpart of a surge of gene-by-environment studies of mood and behavioraldisorders. That same year, two psychologists at King’s College, London,Avshalom Caspi and Terrie Moffitt, published the first of two largelongitudinal studies (both drawing on life histories of hundreds of NewZealanders) that would prove particularly influential. The first,published in Science, showed that the short allele of anothermajor neurotransmitter-processing gene (known as the MAOA gene) sharplyincreased the chance of antisocial behavior in human adults who’d beenabused as children. The second, in 2003 and also in Science,showed that people with short/short or short/long serotonin-transporteralleles, if exposed to stress, faced a higher-than-normal risk ofdepression.
These and dozens of similar studies were critical to establishingthe vulnerability hypothesis over the last few years. Yet many of thesestudies also contained data that supported the orchid hypothesis—butwent unnoticed or unremarked at the time. (Jay Belsky, thechild-development psychologist, has recently documented more than twodozen such studies.) Both of Caspi and Moffitt’s seminal papers in Science, for example, contain raw data and graphs showing that for people who did not face severe or repeated stress, the risk alleles in question heightened resistance to aggression or depression. And the data in Suomi and Lesch’s 2002 Molecular Psychiatrypaper, in which peer-reared monkeys with the riskyserotonin-transporter allele appeared to process serotonininefficiently, also showed that mother-reared infants with that sameallele processed serotonin 10 percent more efficiently than even mother-raised infants who had the supposedly protective allele.
It’s fascinating to examine these studies with theorchid 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 thanthe protective ones. Securely raised 7-year-old boys with the DRD4 riskallele for ADHD, for instance, show fewer symptoms than their securelyraised protective-allele peers. Non-abusedteenagers with that same risk allele show lower rates of conductdisorder. Non-abused teens with the risky serotonin-transporter allelesuffer less depression than do non-abused teens with the protectiveallele. Other examples abound—even though, as Jay Belsky points out,the studies were designed and analyzed primarily to spot negativevulnerabilities. Belsky suspects that as researchers start to designstudies that test for gene sensitivity rather than just riskamplification, and as they increasingly train their sights on positiveenvironments and traits, the evidence for the orchid hypothesis willonly grow.
Suomi gathered plenty of that evidence himself in the years afterhis 2002 study. He found, for example, that monkeys who carried thesupposedly risky serotonin-transporter allele, and who had nurturingmothers and secure social positions, did better at many keytasks—creating playmates as youths, making and drawing on allianceslater on, and sensing and responding to conflicts and other dangeroussituations—than similarly blessed monkeys who held the supposedlyprotective allele. They also rose higher in their respective dominance hierarchies. They were more successful.
Suomi made another remarkable discovery. He and others assayed theserotonin-transporter genes of seven of the 22 species of macaque, theprimate genus to which the rhesus monkey belongs. None of these specieshad the serotonin-transporter polymorphism that Suomi was beginning tosee as a key to rhesus monkeys’ flexibility. Studies of other keybehavioral genes in primates produced similar results; according toSuomi, assays of the SERTgene in other primates studied to date, including chimps, baboons, andgorillas, turned up “nothing, nothing, nothing.” The science is young,and not all the data is in. But so far, among all primates, only rhesusmonkeys and human beings seem to have multiple polymorphisms in genesheavily associated with behavior. “It’s just us and the rhesus,” Suomisays.
This discovery got Suomi thinking about another distinction we sharewith rhesus monkeys. Most primates can thrive only in their specificenvironments. Move them and they perish. But two kinds, often called“weed” species, are able to live almost anywhere and to readily adaptto new, changing, or disturbed environments: human beings and rhesusmonkeys. The key to our success may be our weediness. And the key toour weediness may be the many ways in which our behavioral genes canvary.
One morning this past May, Elizabeth Mallott, a researcher workingat Suomi’s lab, arrived to start her day at the main rhesus enclosureand found a half-dozen monkeys in her parking spot. They were huddlingclose together, bedraggled and nervous. As Mallott got out of her carand moved closer, she saw that some had bite wounds and scratches. Mostmonkeys who jump the enclosure’s double electrified fences (it happensnow and then) soon want to get back in. These monkeys did not. Neitherdid several others that Mallott found between the two fences.
After caging the escapees in an adjacent building, Mallott, nowjoined by Matthew Novak, another researcher who knew the colony well,entered through the double gates. The colony, numbering about 100-oddmonkeys, had been together for about 30 years. Changes in its hierarchyusually came slowly and subtly. But when Novak and Mallott startedlooking around, they realized that something big had happened. “Animalswere in places they weren’t supposed to be,” Novak would later tell me.“Animals who don’t hang out together were sitting together. Socialrules were suspended.”
It soon became apparent that the family group called Family 3, whichfor decades had ranked second to a group called Family 1, had staged acoup. Family 3 had grown larger than Family 1 several years before. ButFamily 1, headed by a savvy matriarch named Cocobean, had retainedincumbency through authority, diplomacy, and momentum. A week or sobefore the coup, however, one of Cocobean’s daughters, Pearl, had beenmoved from the enclosure to the veterinary facility because her kidneysseemed to be failing. Family 1’s most formidable male, meanwhile, hadgrown old and arthritic. Pearl was especially close to Cocobean and, asthe only daughter without children of her own, was particularly likelyto defend her. Her absence, along with the male’s infirmity, created avulnerable 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 beforewe found the monkeys in the parking lot, started when a young femalenamed Fiona”—a 3-year-old Family 1 member, a borderline bully known tohave initiated many a scuffle—“started something with someone in Family3. It escalated. Family 3 saw its chance. And they just started to takeFamily 1 out. You could see it from who was wounded and who wasn’t, andwho was sitting in preferred places, and who was run out of the colony,and who was suddenly extremely deferential. One other female in Family1, Quark, was killed; another, Josie, was hurt so badly we had to puther 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 usehis arm. Fiona got roughed up pretty bad. It was a very systematicscuffle. They went right at the head of the group and worked their waydown.”
Soon after Novak described all this to me, he and I walked aroundthe enclosure. Though it was the middle of a broiling July day,downtime for the monkeys, you could see hints of the new order. Family3 calmly occupied what seemed to be the new center of power, a corncribnear the pond (one of several corncribs set out for shelter). Theygroomed one another, napped, and evenly stared at us as we stared atthem. A more nervous bunch clustered in another crib down the hill.When we got within 30 feet, the largest monkey in the group shot uponto the cage bars. From 10 feet up it screamed at me, rattled thebars, and showed some nasty teeth.
From there I went to Suomi’s office and asked him what he thoughthad happened. Suomi has thought a lot about this coup, and it’s easy tosee why. All of the important threads he’d been weaving together in hisresearch were on display in this revolt: the importance of earlyexperience; the interplay of environment, parenting, and geneticinheritance; the maddening primacy of family and social bonds; therepercussions of different traits in different circumstances. And now,in light of the orchid hypothesis, he was beginning to see that thethreads 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 onan island in Puerto Rico. She wanted to see what happened as the groupschanged size over time. They’d start at about 30 or 40 individuals—agroup that had split off from another—and then expand. At a certainpoint, 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 sometimescalled “Dunbar numbers,” after Robin Dunbar, a British evolutionarypsychologist who argues that a species’ group limit reflects how manysocial relationships its individuals can manage cognitively. Berman’sobservations suggested that the Dunbar number of a species reflects notjust its cognitive powers but its temperamental and behavioral range aswell.
Berman saw that when rhesus troops are small, the mothers can lettheir young play freely, because strangers rarely approach. But as atroop grows and the number of family groups rises, strangers orsemi-strangers more often come near. The adult females become morevigilant, defensive, and aggressive. The kids and adult males followsuit. More and more monkeys receive upbringings that draw out the lesssociable sides of their behavioral potentials; fights grow more common;rivalries grow more tense. Things finally get so bad that the troopmust split. “And that’s what happened here,” Suomi said. “It’s a veryextensive feedback system. What happens at the dyadic level, betweenmother and infant, ultimately affects the very nature and survival ofthe larger social group.”
Studies by Suomi and others show that such differences in earlyexperience 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 geneexpression and behavior as well, including how flexible and reactive ananimal is, by helping to set the sensitivity level of key alleles. Atense upbringing, he says, will produce watchful caution or vigilantaggression in any monkey (the parents’ way of preparing the offspringfor tough times)—but this effect may be especially pronounced inmonkeys with particularly plastic behavioral alleles.
That’s what Suomi thinks may have happened in the run-up to what hecalls the Palace Revolt. Fiona’s injudicious aggression proveddisastrous for her and Family 1. But Family 3, a group that had beendiplomatically deferring to Family 1 for years, dramatically improvedits fortunes by mounting an uncharacteristically aggressive andsustained counterattack. Suomi speculates that in the tenser, morecrowded conditions of the large colony, gene-environment interactionshad made some of the monkeys in Family 3, particularly those withmore-reactive “orchid” alleles, not more aggressive but more potentiallyaggressive. During the period when they could not afford to challengethe hierarchy—the period before Pearl’s departure—aggressiveness wouldhave led them into unwinnable, possibly fatal conflicts. But in Pearl’sabsence the odds changed—and the Family 3 monkeys exploited a rare anddecisive opportunity by unleashing their aggressive potential.
The coup also showed something more straightforward: that a genetictrait tremendously maladaptive in one situation can prove highlyadaptive in another. We needn’t look far to see this in human behavior.To survive and evolve, every society needs some individuals who aremore aggressive, restless, stubborn, submissive, social, hyperactive,flexible, solitary, anxious, introspective, vigilant—and even moremorose, irritable, or outright violent—than the norm.
All of this helps answer that fundamental evolutionary questionabout how risk alleles have endured. We have survived not despite thesealleles 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 onlyduring 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 beganrapidly proliferating. Rhesus monkeys and human beings split from theircommon lineage about 25 million to 30 million years ago, so thesepolymorphisms must have mutated and spread on separate tracks in thetwo species. Yet in both species, these new alleles proved so valuablethat 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 tohave emerged and expanded—is also the period during which Homo sapiensstarted to get seriously human, and during which sparse populations inAfrica expanded to cover the globe in great numbers. Though Cochran andHarpending don’t explicitly incorporate the orchid-gene hypothesis intotheir argument, they make the case that human beings have come todominate the planet because certain key mutations allowed humanevolution to accelerate—a process that the orchid-dandelion hypothesiscertainly helps explain.
How this happened must have varied from context to context. If youhave too many aggressive people, for example, conflict runs rampant,and aggression is selected out, because it becomes costly; whenaggression decreases enough to be less risky, it becomes more valuable,and its prevalence again rises. Changes in environment or culture wouldlikewise affect an allele’s prevalence. The orchid variant of the DRD4gene, for instance, increases risk of ADHD (a syndrome bestcharacterized, Cochran and Harpending write, “by actions that annoyelementary-school teachers”). Yet attentional restlessness can servepeople well in environments that reward sensitivity to new stimuli. Thecurrent growth of multitasking, for instance, may help select for justsuch attentional agility. Complain all you want that it’s anincreasingly ADHD world these days—but to judge by the spread of DRD4’srisk allele, it’s been an increasingly ADHD world for about 50,000years.
Even if you accept that orchid genes may grant us flexibilitycrucial to our success, it can be startling to ponder their dynamics upclose and personal. After I FedExed away my vial of saliva forgenotyping, I told myself more or less to forget it. To my surprise, Imanaged to. The e-mail that eventually arrived with the results,promised for a Monday, turned up three days early, during a Fridayevening 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 yoursaliva sample today. The assay ran well and your genotype is S/S. Goodthing neither of us think of these things as deterministic or evenhaving a fixed valence. Let me know if you want to talk about yourresult 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, itsblossoms fallen but its fruit only nubbins, I felt a chill spreadthrough my torso.
I hadn’t thought it would matter.
Yet as I sat absorbing this information, the chill came to seem lessthe coldness of fear than a shiver of abrupt and invertedself-knowledge—of suddenly knowing with certainty something I had longsuspected, and finding that it meant something other than I thought itwould. The orchid hypothesis suggested that this particular allele, therarest and riskiest of the serotonin-transporter gene’s three variants,made me not just more vulnerable but more plastic. And that new way ofthinking changed things. I felt no sense that I carried a handicap thatwould render my efforts futile should I again face deep trouble. Infact, I felt a heightened sense of agency. Anything and everything Idid to improve my own environment and experience—every intervention Iran 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 throughwhich I might fall than like a springboard—slippery and somewhatfragile, perhaps, but a springboard all the same.
I don’t plan to have any of my other key behavioral genes assayed. Idon’t plan on having my kids’ genes done, either. What would it tellme? That I shape them in every encounter? I know this. Yet I do likethinking that when I take my son trolling for salmon, or listen to hisyounger brother’s labyrinthine elaborations of his dreams, or sing“Sweet Betsy of Pike” with my 5-year-old daughter as we drive home fromthe lake, I’m flipping little switches that can help light them up. Idon’t know what all those switches are—and I don’t need to. It’s enoughto know that together we can turn them on.