Science of Success

One of the most amazing power of the ongoing genome research et al is at times it reinstates some of the old wisdom and sometimes it completely rewrites the stereotypes and conventional wisdome we are imbibed in.
Starting for religion, caste, fedualism, Darwin, DNA, Blank Slate and human genome project, its been an evolving process and there isn't an end in sight of discovering why and how we become who we are. Ever since the human genome project, there seems to a consensus as well disparity between all these ideas. Cacophony of current political scene and all the fancy economic theories are primed to balance the imbalance in the evolutionary lottery - our genes. Paradoxically, geneome studies have been pointing to an alternate direction - Genome Plasticity. Success is not only defined by birth but by nuture (and ad infinitum). David Dobbs chronicles the ground breaking research of Marian Bakermans Kranenburg - Orchid Hypothesis (audio):

"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.

Of special interest to the team was a new interpretation of one of the most important and influential ideas in recent psychiatric and personality research: that certain variants of key behavioral genes (most of which affect either brain development or the processing of the brain’s chemical messengers) make people more vulnerable to certain mood, psychiatric, or personality disorders. Bolstered over the past 15 years by numerous studies, this hypothesis, often called the “stress diathesis” or “genetic vulnerability” model, has come to saturate psychiatry and behavioral science. During that time, 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. It casts them as products not of nature or nurture but of complex “gene-environment interactions.” Your genes don’t doom you to these disorders. But if you have “bad” versions of certain genes and life treats you ill, you’re more prone to them.

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.

The evidence for this view is mounting. Much of it has existed for years, in fact, but the focus on dysfunction in behavioral genetics has led most researchers to overlook it. This tunnel vision is easy to explain, according to Jay Belsky, a child-development psychologist at Birkbeck, University of London. “Most work in behavioral genetics has been done by mental-illness researchers who focus on vulnerability,” he told me recently. “They don’t see the upside, because they don’t look for it. It’s like dropping a dollar bill beneath a table. You look under the table, you see the dollar bill, and you grab it. But you completely miss the five that’s just beyond your feet.”

Though this hypothesis is new to modern biological psychiatry, it can be found in folk wisdom, as the University of Arizona developmental psychologist Bruce Ellis and the University of British Columbia developmental pediatrician W. Thomas Boyce pointed out last year in the journal Current Directions in Psychological Science. The Swedes, Ellis and Boyce noted in an essay titled “Biological Sensitivity 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-tended garden. Ellis and Boyce offer that there are also “orchid” children, who will wilt if ignored or maltreated but bloom spectacularly with greenhouse care.

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.

This is a transformative, even startling view of human frailty and strength. For more than a decade, proponents of the vulnerability hypothesis have argued that certain gene variants underlie some of humankind’s most grievous problems: despair, alienation, cruelties both petty and epic. The orchid hypothesis accepts that proposition. But it adds, tantalizingly, that these same troublesome genes play a critical role in our species’ astounding success.

The orchid hypothesis—sometimes called the plasticity hypothesis, the sensitivity hypothesis, or the differential-susceptibility hypothesis—is too new to have been tested widely. Many researchers, even those in behavioral science, know little or nothing of the idea. A few—chiefly those with broad reservations about ever tying specific genes to specific behaviors—express concerns. But as more supporting evidence emerges, the most common reaction to the idea among researchers and clinicians is excitement. A growing number of psychologists, psychiatrists, child-development experts, geneticists, ethologists, and others are beginning to believe that, as Karlen Lyons-Ruth, a developmental psychologist at Harvard Medical School, puts it, “It’s time to take this seriously.”"

David Dobbs has a phenomenal personal story to tell as well:

"Suomi, Lesch, and NIH colleague J. Dee Higley set about doing a type of study now recognized as a classic “gene-by-environment” study. First they took cerebral spinal fluid from 132 juvenile rhesus monkeys and analyzed it for a serotonin metabolite, called 5-HIAA, that’s considered a reliable indicator of how much serotonin the nervous system is processing. Lesch’s studies had already shown that depressed people with the short/long serotonin-transporter allele had lower 5-HIAA levels, reflecting less-efficient serotonin processing. He and Suomi wanted to see if the finding would hold true in monkeys. If it did, it would provide more evidence for the genetic dynamic shown in Lesch’s studies. And finding such a dynamic in rhesus monkeys would confirm their value as genetic and behavioral models for studying human behavior.

After Suomi, Lesch, and Higley had grouped the monkeys’ 5-HIAA levels according to their serotonin genotype (short/long or long/long, but not short/short, which was too rare to be of use), they also sorted the results by whether the monkeys had been raised by their mothers or as orphans with only same-aged peers. When their colleague Allison Bennett charted the results on a bar graph showing 5-HIAA levels, all of the mother-reared monkeys, no matter which allele they had, showed serotonin processing in the normal range. The metabolite levels of the peer-raised monkeys, however, diverged sharply by genotype: the short/long monkeys in that group processed serotonin highly inefficiently (a risk factor for depression and anxiety), whereas the long/long monkeys processed it robustly. When Suomi saw the results, he realized that he finally had proof of a behaviorally relevant gene-by-environment interaction in his monkeys. “I took one look at that 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 formed part of a surge of gene-by-environment studies of mood and behavioral disorders. That same year, two psychologists at King’s College, London, Avshalom Caspi and Terrie Moffitt, published the first of two large longitudinal studies (both drawing on life histories of hundreds of New Zealanders) that would prove particularly influential. The first, published in Science, showed that the short allele of another major neurotransmitter-processing gene (known as the MAOA gene) sharply increased the chance of antisocial behavior in human adults who’d been abused as children. The second, in 2003 and also in Science, showed that people with short/short or short/long serotonin-transporter alleles, if exposed to stress, faced a higher-than-normal risk of depression.

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.

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."

This changes everything, no one can find solace and excuse from their faulty gene - Dr.Fallon didn't become a psychopath and David Dobbs has never been affected with manic depression.