Dandelions, Orchids and Destiny
I just read a fascinating article in the December edition of The Atlantic. David Dobb’s The Science of Success relates the genetics of behavioral plasticity to weeds and hothouse plants:
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.
Today most of us agree that behavior arises from a complex interaction of nature and nurture. The goal of behavioral genetics is to understand the complex interaction between genetic and environmental contributions to behavior, and it’s not an easy job. First of all it can be difficult simply to define exactly what the specific behavior one wants to study involves. Toss in the additional complicating factors that arise because the expression of behavior, like all complex traits, is born from an intricate dance between genetic heritage, upbringing and epigenetic factors — and you discover that even creatures as outwardly similar as identical twins are as unique as snowflakes.
One of the hot areas of research in behavioral genetics is centered around the idea that specific polymorphisms affecting key behavioral genes can increase our vulnerability to specific mood, psychiatric, or personality disorders. As Dobbs writes in The Atlantic, genetic polymorphisms have been found that affect our susceptibility to depression, anxiety, attention-deficit hyperactivity disorder (ADHD), heightened risk-taking, 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. According to Dobbs’ article:
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.
Although the science of behavioral genetics has been around since the 1960’s, the idea that Dobbs refers to as the orchid hypothesis is a new way to think about genetics and human behavior. It points out that it’s not correct to think of the genes we inherit as being good or bad. Genes represent potential, and like investments, some are low risk / low reward while others are high risk / high reward. In a balanced genetic portfolio a species wants to hold investments in both sectors.
Some of the key areas where researchers have found behavioral genetic tradeoffs are in the serotonin and dopamine transmission and uptake systems. In the 1990’s Klaus-Peter Lesch discovered that there were three different variants to the human serotonin-transporter gene (the short/short, short/long, and long/long alleles). He found that the two shorter versions of the gene were related to a higher risk of being affected by depression, anxiety and related problems.
At the same time that Lesch was working on serotonin-transporter genes, Stephen Suomi was studying personality types in Rhesus monkeys. Dobbs writes:
Very early in his work, Suomi identified two types of monkeys that had trouble managing these relations. One type, which Suomi calls a “depressed” or “neurotic” monkey, accounted for about 20 percent of each generation. These monkeys are slow to leave their mothers’ sides when 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”: an unusually and indiscriminately aggressive monkey. These monkeys accounted for 5 to 10 percent of each generation. “Rhesus monkeys are fairly aggressive in general, even when young,” Suomi says, “and their play involves a lot of rough-and-tumble. But usually no one gets hurt—except with these guys. They do stupid things most other monkeys know not to. They repeatedly confront dominant monkeys. They get between moms and their kids. They don’t know how to calibrate their aggression, and they don’t know how to read signs they should back off. Their conflicts tend to always escalate.”
Suomi saw early on that each of these monkey types tended to come from a particular type of mother. Bullies came from harsh, censorious mothers who restrained their children from socializing. Anxious monkeys came from anxious, withdrawn, distracted mothers. The heritages were pretty clear-cut. But how much of these different personality types passed through genes, and how much derived from the manner in which the monkeys were raised?
To find out, Suomi split the variables. He took nervous infants of nervous mothers—babies who in standardized newborn testing were already jumpy themselves—and gave them to especially nurturing “supermoms.” These babies turned out very close to normal. Meanwhile, Dario Maestripieri of the University of Chicago took secure, high-scoring infants from secure, nurturing mothers and had them raised by abusive mothers. This setting produced nervous monkeys.
The lesson seemed clear. Genes played a role—but environment played an equally important one.
Lesch collaborated with Suomi on genotyping monkeys from the different behavioral groups identified. They were excited to discover that the same three serotonin-transporter gene variants that were known to be important in human behavioral genetics were also present in Suomi’s rhesus monkeys.
The next step in the work was a study conducted by Suomi, Lesch and J. Dee Higley on a serotonin metabolite that indicates how much serotonin an animal’s nervous system is processing. The results of this work showed that regardless of which serotonin-transporter genotype a monkey inherited, all of the monkeys reared by nurturing mothers processed serotonin in the normal range. This pointed to the vital importance of nurture’s affect on nature. It also made Suomi wonder if this genetic sensitivity to upbringing was a common feature in all primates.
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.
This talk of “weediness”, of course, immediately made me think of dogs. The domestic dog is a brilliantly adaptive species, cheerfully surviving anywhere humans do. From the arctic to the tropics, free ranging feral or pampered house pet, the dog lives in a wider range of habitats than almost any other animal.
So of course I wondered if anyone had studied the SERT gene and serotonin metabolites in dogs. I surfed the googles and almost immediately hit pay dirt.
I discovered that breed-specific patterns of a number of coding single nucleotide polymorphisms of behavior-related genes have been identified in different breeds of dogs. I read that repeat polymorphisms associated with human attention deficit disorder appear to have the same effect in the Belgian Tervueren. And I found that the same polymorphism in SLC6A4 found to be important in Suomi, Lesch and Higley’s work on the weediness of rhesus monkeys – has also been found in dogs.
One of the most interesting studies was Våge and Lingaas’ “Single Nucleotide Polymorphisms (SNPs) in Coding Regions of Canine Dopamine- and Serotonin-Related Genes” where they the important relationship in dogs between breed traits like size, color and conformation and behavioral phenotypes was described:
The large number of canine breeds exhibits an extreme between-breed variation in traits like size, colour, conformation and behaviour. For many of these breeds, behavioural characteristics represent an important part of the breed definition and description. Certain behavioural phenotypes are associated with specific breeds as a result of long-term, systematic selection and limited genetic variation. In a behavioural context, dog breeds are evidence for the considerable impact of genetics on behavioural traits. They are therefore valuable models for genetic studies aimed at revealing basic biological knowledge of genetic regulation of behavioural traits. This can be efficiently performed through crossbreeding and backcrosses of these isolates with strong between-breed contrasts in specific behaviours.
There’s a lot more out there and it is absolutely fascinating stuff… but don’t hold your breath waiting for a genetic test that will tell you if Fifi suffers from clinical depression or Rover is a budding psychopath. According to the DOE’s Human Genome Project website:
“No single gene determines a particular behavior. Behaviors are complex traits involving multiple genes that are affected by a variety of other factors. This fact often gets overlooked in media reports hyping scientific breakthroughs on gene function, and, unfortunately, this can be very misleading to the public.”
Beyond any media hype, these studies point out the vital importance of early socialization, care and training on human and canine youngsters. Your genes don’t make you who you are, they just lay out a general, and rather fuzzy, template for your environment to shape. Having the gene variant that can predispose you to ADHD doesn’t mean that you’re doomed to suffer from it. The other genes in your DNA and specific environmental factors can suppress or increase the chance that a trait will develop. And as the orchid hypothesis points out, there are also cases where having a what is commonly seen as a problematic gene presents an adaptive advantage.
With apologies to the Greeks, we aren’t born with a single, immutable, predetermined destiny. We’re born with potential, and the genes we inherit aren’t good or bad, some are just more adaptive in certain situations than others. The range of adaptiveness that “weedy” genes give species like rhesus monkeys, humans and dogs allows us to adapt to a broader range of environments – while possibly also leaving us more vulnerable to certain behavioral disorders than less weedy species.
Resilient dandelion or fragile orchid – it’s not your destiny, it’s just a phenotype that affects your individual potential and increases the adaptiveness of your species as a whole.