Clients frequently ask me if their mental and emotional struggles are a result of their genes or their environment. My answer is always the same - "yes". Of course, my simplistic response refers to the interaction between genes and environment that characterizes nearly all mental health conditions, but it clearly belies the centuries of debate on this fundamental and contentious topic. In recent decades, the Cartesian dualism that has traditionally dominated the nature-nurture debate has given way to scientific theories that describe complex, bi-directional relations between genes and environment. These theories of human development have also furthered our understanding of "neural plasticity" the exciting notion that our brains are more malleable and open to change than we once thought.
First, a brief historical regression may be helpful. In the early part of the twentieth century, psychoanalysis was the dominant perspective in psychology and its guardians were particularly keen on environmental influences. In fact, parents of the baby-boomer generation were likely told that schizophrenia was entirely caused by cold, unresponsive mothering (i.e., so-called "schizophrenigenic mothers"). Behaviorism, which rose to prominence in the early-to-middle part of the century, saw human development as a process of learning based on stimulus-response interactions between an organism and its environment. By the nineteen-sixties, the "cognitive-revolution", with its emphasis on internal mental states and the promise of neuroscience advances, largely eclipsed these theories, but still had relatively little to say about the role of genetics.
In the second half of the twentieth century, geneticists began conducting large twin and adoption studies and found that a number of psychiatric conditions showed evidence of genetic heritability. For example, studies showed that schizophrenia occurs in 1% of the general population, but this increases to 6% if a parent is affected and 48% if an identical twin is affected. Findings such as these clearly showed that genetics play a role in many forms of mental illness. However, by the end of the twentieth century, the pendulum had swung too far in the direction of genetic influence, with some researchers claiming that single genes could be wholly responsible for complex phenomena like depression, violence and even suicide (e.g., one research group claimed to have found "the suicide gene").
At the turn of the twenty-first century, genetic theories relying on simple one-to-one relations between a single gene and a psychiatric condition were supplanted by "diathesis-stress" models, which posited that genetic diatheses or "vulnerabilities" could interact with environmental stressors to produce deleterious outcomes. The most prominent study of this genre was published by Caspi et al. in 2002 and showed that the relation between childhood maltreatment and later-occurring antisocial behavior was much stronger for individuals who had the less efficient form of the MAOA gene (a gene that improves the function of nerve transmission in the brain). In other words, genetics alone didn't predict poor outcomes; it was the combination of a genetic predisposition and the stress of childhood maltreatment that led to an increase in antisocial behavior.
Although this particular gene-environment interaction has been replicated a number of times, some researchers have questioned whether the diathesis-stress model tells the whole story. In the last decade, researchers began noticing that when individuals with a genetic "vulnerability" experienced lower levels of environmental stress, they often fared better than those with individuals with the "favorable" form of the gene. For example, in the graph from the Caspi (2002) study (see above), under conditions of no childhood maltreatment, individuals with the "inefficient" form of the gene (red line) actually had lower levels of antisocial behavior than individuals with the "efficient" form of the gene (blue line). In the Caspi study, this difference wasn't statistically significant, but it raised questions about whether it could be a significant finding if studies were designed to see the phenomenon more clearly.
Jay Belsky, a professor of mine at the University of California at Davis, was one of the first to propose that particular genes (like MAOA) may confer risk or benefit, depending on the environment. Instead of thinking of certain genes as merely a liability, he argued that these genes might increase susceptibility to environmental conditions, "for better or for worse". Belsky and colleagues" theory of "Differential Susceptibility" is rooted in an evolutionary argument that, under circumstances where the future is uncertain, it makes sense to have some offspring that are less sensitive, and other offspring that are more sensitive, to environmental conditions. Like a well-diversified financial portfolio with some money in conservative, robust holdings and some money in high-risk stocks that can respond dramatically to market swings (too close to home for some of us), differential susceptibility posits that some people have a more "fixed" genetic makeup that is less vulnerable to environmental conditions, while others have a more plastic or malleable genetic makeup that is more susceptible to the environment, whether it be positive or negative.
Of course, this theory comes with the exciting possibility that reducing environmental stress (e.g., child maltreatment and relational trauma) may be particularly meaningful for individuals with genetic susceptibilities. In a study published in 2008, Bakermans-Kranenburg and her colleagues tested this hypothesis by investigating 157 families with toddlers who showed elevated levels of externalizing problems (e.g., hyperactivity, oppositional behavior, aggression, etc.) They found that their Positive Parenting and Sensitive Discipline intervention program was most effective in reducing externalizing behaviors in those children who had a version of the dopamine gene (DRD4) that has been linked to externalizing behavior and attention-deficit hyperactivity disorder. That is, children who would have traditionally been thought of as carrying a dopamine-related genetic "vulnerability" were in fact most responsive to the positive environmental changes associated with the parenting intervention program.
The results of this study, and many others like it, suggest that improving environmental conditions during childhood can drastically enhance developmental outcomes, especially for those children who are genetically susceptible to environmental influences. However, these findings might also apply to adults - especially considering recent research showing that the brain remains plastic or malleable well into adulthood. For adults with adverse life experiences who are recovering from conditions like depression, addiction, and post-traumatic stress, the genetic susceptibilities that previously contributed to their sensitivity to adverse environmental conditions may also facilitate their responsiveness to the positive changes associated with recovery treatment. In other words, by improving environmental conditions, what was once considered a vulnerability may actually become the very means for plasticity and growth.
As the Serenity Prayer suggests, it takes courage to improve our environmental conditions and there is much of our day-to-day circumstances that remains beyond our control. However, even when we cannot change our external environment, we can always alter our perspective of it. Approaching ourselves, our fellow beings, and the world with a greater measure of acceptance and compassion can literally change the subjective experience of our environment, and in many cases it can also lead to objective changes in the environment. This shift in perspective is bound to feed back into the biology of our being, perhaps most noticeably for those individuals who at one time may have been considered genetically vulnerable, but who might actually be predisposed to resiliency, especially if the right environmental conditions are established.