Many parents and teachers are familiar with cases already—children are constantly in detention, isolated outside of the principal’s office, can barely pay attention unless it is something that they really want to do, and peers avoid them like the plague. Today, biological and cognitive neuro-scientists offer a completely new way to think about genetics and human behavior—perhaps your child is an orchid and needs a greenhouse in order to thrive.

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 orchids: fragile and fickle, but capable of blooming spectacularly if given greenhouse care. In truth, we all have the same genes, but because some genes are polymorphic in their make-up, variant expressions can occur outside of our control, which can have very powerful bearing on our lives and livelihoods.

Researchers have identified a dozen or so gene variants that can increase a person’s susceptibility to depression, anxiety, attention-deficit hyperactivity disorder (ADHD), 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. In other words, the person must have the particular variant of the gene and be traumatized in youth. The genes in question are numerous, but we focus on a few that can modulate mood, affect learning, and enable happiness. Polymorphism is a critical assay of genetics that contributes to understanding of orchid versus dandelion in humans. Polymorphism is the presence of genetic variation within a gene population, upon which natural selection can operate.

If your child has risky variants—expressions of certain genes combined with life hardships, then and only then, we are more prone to end up badly. For instance, there is evidence to suggest that adolescent orchid children who, in addition experience ACEs, will have a less than 20% chance of making it through high school without getting into serious trouble, dropping out, or ending up in the juvenile justice system.

**Dandelion **children possess “resilient” genes. They do pretty well almost anywhere, whether raised in the equivalent of a sidewalk crack or a well-tended garden. However, “orchid” children will wilt if ignored or maltreated, but bloom spectacularly with greenhouse care. We refer to dandelion children as individuals with the “protective” allele and we refer to orchids as children with the “risky” allele.

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Genetic Expressions say a lot About You

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 orchids: fragile and fickle, but capable of blooming spectacularly if given greenhouse care. In truth, we all have the same genes, but because some genes are polymorphic in their make-up, variant expressions can occur outside of our control, which can have very powerful bearing on our lives and livelihoods.

Today, biological and cognitive neuro-scientists offer a completely new way to think about genetics and human behavior.

Researchers have identified a dozen or so gene variants that can increase a person’s susceptibility to depression, anxiety, attention-deficit hyperactivity disorder (ADHD), 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. In other words, the person must have the particular variant of the gene and be traumatized in youth. The genes in question are numerous, but we focus on a few that can modulate mood, affect learning, and enable happiness. Polymorphism is a critical assay of genetics that contributes to understanding of orchid versus dandelion in humans. Polymorphism is the presence of genetic variation within a gene population, upon which natural selection can operate.

Polymorphism Selects

Neurotransmitters like serotonin, norepinephrine, dopamine and others are prime contenders for polymorphism—several choices of expression. For instance, the serotonin transporter gene has three variants (short/short, short/long, and long/long alleles). Significantly, the two shorter versions (short/short, short/long) magnify the risk for depression, anxiety, anti-social behavior, and other problems.

Knowing one’s predisposition to stressors and a probable reaction to adversity can change everything. But that is only half the picture. Just as we know through evidence of neural plasticity, dendritic arbors that have shrunk because of adverse environmental conditions can be optimally reversed with care and attention, so too we describe optimal neural plasticity when orchids receive greenhouse attention that supports and fosters. In particular, parents, teachers, managers and leaders of industry are in a much better position to make informed decisions about their children, their co-workers, and their colleagues when armed with the kind of scientific knowledge that springs from neural plasticity. Hence, the importance of stress diagnostics in schools, work place settings and homes—to explore genetic predispositions and probable trait characteristics.

But it is not all bad. These 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 (ACEs or adverse childhood experiences), 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. Imagine children accessing mental models that mapped their journey.

Am I Doomed to my Genetic Expression?

Doom and predisposition are not the same. Our genes don’t doom us to the negative disorders described above—depression, drug-addiction, or jail. But if one discovers that they have risky variants—expressions of certain genes combined with life hardships, then and only then, we are more prone to end up badly. For instance, there is evidence to suggest that adolescent orchid children who, in addition experience ACEs, will have a less than 20% chance of making it through high school without getting into serious trouble, dropping out, or ending up in the juvenile justice system. Many parents and teachers are familiar with cases already—children are constantly in detention, isolated outside of the principal’s office, can barely pay attention unless it is something that they really want to do, and peers avoid them like the plague.

Dandelion children possess “resilient” genes. They do pretty well almost anywhere, whether raised in the equivalent of a sidewalk crack or a well-tended garden. However, “orchid” children will wilt if ignored or maltreated, but bloom spectacularly with greenhouse care. We refer to dandelion children as individuals with the “protective” allele and we refer to orchids as children with the “risky” allele.

Yes, risk-expressed genes can create dysfunction in unfavorable contexts—but the opposite is also true. These same genes can also enhance function in favorable contexts. The genetic sensitivities to negative experience are just one aspect—the downside, of a bigger phenomenon: a heightened genetic sensitivity to all experience. Heightened sensitivity is a good thing in certain situations and is vital for not only personal survival but (lucky for us) for species survival. So why do we look with aversion to our orchid kids, why do we see them as troublemakers and outsiders? In order to understand the paradigm from which we have emerged, we might want to go back to the growth of state systems in education and unpack the idea of behaviorism with a capital B.

Behaviorism Ruled my Day

In the 1930s, the study of childhood development was dominated by a ruthlessly mechanistic behaviorism. The movement’s leading figure in the United States, John Watson, considered mother love “a dangerous instrument.” He urged parents to leave crying babies alone; to never hold them to give pleasure or comfort; and to kiss them only occasionally, on the forehead. Mothers were important less for their affection than as conditioners of behavior. Although, most of us will recognize this parenting style, we were probably better cared for by our own mothers. Yet, the central behaviorist outcome from schooling continued to be rewards and punishments in a stimulus response environment that attempted to treat all children the same. It was easy to isolate troublemakers, and just as easy to label and stratify children with measuring criteria that ignored genetic makeup or environmental considerations of stress and/or enrichment. Plasticity was not a concept that entered into teacher training thinking or parental preparatory courses.

When tools for the study of genes first became available, in the late 1990s, scientists were quick to use them to more directly examine the balance between genes and environment in shaping human development. Today, cognitive neuroscientists are translating these findings into meaningful practice and processes in classrooms, workplaces, and in the home.

Serotonin Transporter enhances Mood

Serotonin is a very important neurotransmitter. Commonly, it transmits impulses between nerve cells, and regulates cyclic body processes. But most important it is critical for contributing to wellbeing and happiness. Increasingly, serotonin is regarded by researchers as a chemical that is responsible for maintaining mood balance, and that a deficit of serotonin leads to depression. The short/long expression of this gene typically processes serotonin highly inefficiently and is thus a risk factor for depression and anxiety. At the same time, the long/long expression processes serotonin robustly. There is ample evidence of this kind of contextualized result. An article published in Science (2002), 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 neglected/abused as children. Similarly, a paper in Science (2003) showed that people with short/short or short/long serotonin-transporter alleles, if exposed to stress, faced a higher-than-normal risk of depression. Yet, there is plenty evidence that parental affection and attentive rearing for infants (greenhouse effect) with the risky serotonin-transporter allele were able to process serotonin 10 percent more efficiently than even mother-raised infants who had the supposedly protective allele.

In a supportive environment (greenhouse effect – no ACEs), teenagers with the risky allele (short/short or short/long serotonin-transporter gene) show lower rates of conduct disorder than do non-abused teens with the protective allele (long/long expression). Non-abused teens with the risky serotonin-transporter allele suffer less depression than do non-abused teens with the protective allele.

Evolutionary Success

Individuals who carried the risky (short/short or short/long expression) of the 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 individuals who held the supposedly protective allele (long/long expression). They also rose higher in their respective societies. They were more successful.

Early experiences affect later patterns of gene expression and behavior, including how flexible and reactive an individual is, by helping to set the sensitivity level of key alleles. A tense upbringing will produce watchful caution or vigilant aggression in any person (the parents’ way of preparing the offspring for tough times)—but this effect may be especially pronounced in individuals with particularly plastic behavioral alleles.

A genetic trait, tremendously maladaptive in one situation, can prove highly adaptive in another. We needn’t look far to see such phenomena 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 have only emerged in humans 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.

Following is a description of awareness. What if we were able to measure children and ascertain the nature of their genetic predispositions?

I have the short/short expression of the Serotonin Transporter Gene

*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.

As the evolutionary anthropologists Gregory Cochran and Henry Harpending have pointed out, (The 10,000 Year Explosion), 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. 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.

Changes in environment or culture would 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.


DAVID DOBBS The Atlantic – the Science of Success was a source for much of the thinking behind this article.