To what extent do specific genes determine our behavior? Although the jury is still out, the answer for intricate illnesses like bipolar disorder seems to be much more complicated than originally anticipated. Often in studies in which researchers scan the whole genome looking for associations between genes and a neuropsychiatric illness, spirits flare when a risk gene pops up in a one study only to drop when many times the finding is not replicated in subsequent studies.
While some argue that the difficulty arises from studies being underpowered (having too small a pool of subjects), one interesting possibility is that these genes might be difficult to detect because they are only “activated” when exposed to a certain environment. For example, let’s take an analogy in which a person’s genes interact with the environment in a similar manner to the way a car’s parts interact with the road. If the car was put together with tires that have no tread (a risk gene), the car will drive just fine if the sun is out and the road is smooth and dry. However, if the car goes driving in a heavy rain or snow, all of a sudden the tread-less tires make it more likely than if it had treads that the car will get into an accident; the tread-less tire confers a risk for an accident only when exposed to a specific, adverse environment like hazardous weather.
If the importance of environmental interaction turns out to be a general rule with risk genes, then by controlling our environments we may be able to have more control over our “risky genes” than we previously thought. The best evidence that it takes an adverse environment to activate bad genes, however, comes from research on a fascinating Dutch family, a cohort of New Zealand school children, and a gene called MAOA.