RISK TAKING AND SUBSTANCE ABUSE
Epidemiological studies clearly point to the fact that adolescents are more likely to experiment with controlled substances than any other age-group. Do any of the statistics reflect underlying mental health issues? Certainly some forms of substance abuse are associated with behavioral anomalies during childhood. Are any of these anomalies associated with mental disorders?
Research into questions like these can be difficult to perform and for a single reason: from lemurs to humans, typical, normally developing adolescence is associated with a rich increase in novelty-seeking and risk-taking behaviors. There are certainly evolutionary reasons why this might be so. Creating behavioral firewalls between otherwise well-associated groups is a great way to keep newly reproductively competent adolescents from mating within the natal clan. (A willingness to leave the group and find other non-consanguineous clans with whom to mate would ensure greater genetic diversity). The probability of actually exiting the safety of home would be greatly aided by a healthy desire for novelty seeking and risk taking. That, in turn, would increase the genetic diversity of mating opportunities.
If that were the case, you might hypothesize that the activity of regions of the brain involved in rewarding risk taking might be more active in adolescents than in adults. And that those adolescents who were born with a pathologically heightened need for thrill seeking might be more susceptible to dangerous behavior of any kind, including substance abuse.
Are there any genetic explanations for these ideas? There certainly is a gene that has over the years become associated with risk-taking behavior. The sequence is called neuroD2 and is expressed in various regions of the brain, including the amygdala. Its relationship with specific alterations in teenaged behavior in humans is ambiguous, however, and awaits further research. And perhaps clarification.
One way to think of changes in behavioral risk is not to think of neuroD2-like behaviors at all. One could just as easily speculate that adolescents have less aversive reactions to the negative biological consequences of their behaviors—such as drugs normally associated with substance abuse.
Such changes are certainly true in laboratory animals. Adolescent mice are astonishingly more insensitive to the motor impairments normally associated with alcohol(Drug information on alcohol) ingestion than are older animals. They are not as easily sedated as adult controls and get less of a hangover too. There is evidence that the developmental immaturity of our familiar GABAA receptor in adolescent mice brains is in part responsible for these changes.
Researchers have also looked to noninvasive imaging experiments in an attempt to explain increases in risk-taking behavior. Deploying a series of monetary-reward tasks in conjunction with fMRI, some initially promising work examining both adolescent and adult subjects was done. Specifically, adolescents possess greater reward feedback–related activity than older persons. The focus was initially on the nucleus accumbens, which as you may recall, is largely associated with reward behavior. The researchers found greater activity in response to monetary gains in adolescents than they did in young adults.
Unfortunately, not all researchers were able to replicate these findings. Indeed, some investigators showed just the opposite: that nucleus accumbens activity is actually reduced in adolescents in response to financial-gain experiments when compared with controls.
How to think about these data? It is reasonable to assume that certain neural alterations occurring during adolescence would predispose those populations to risky behavior. But exactly what those differences are is a matter of great debate. In most cases, the jury is out—way out—in both applying what we see in mice to humans and to understanding exactly what is occurring in the adolescent brain when it is being imaged. From a research perspective, the devil is in the midpubertal details.
And that, perhaps, is a lesson. No one will argue that adolescence is a time of great change. Powerful hormones unleashing equally powerful behavioral forces get to accomplish the brain’s ultimate reason for living: to supply humanity’s next generation with a next generation. But as I hoped to have illustrated here, we are a long way from being able to understand exactly what those changes are. We are even further from understanding how those changes link to observable behavior and how that understanding will help us explain the NCS-R age-onset data.
At the end of the day, the most important contribution these data give us is to provide a reassuring—even tantalizing—framework for asking the right research questions. Something is going on in a brain under assault by puberty. If we could only just discover what the psychiatric anomalies were telling us, we might have greater insight into what happens normally. Finally, we might begin to understand what is going on in the minds of our adolescents—a hope no doubt echoed by every researcher interested in the biological basis of puberty.
And, perhaps, by every family who has ever had to experience the mixed blessing of sharing a household with an adolescent.