Infusing Neuroscience Into the Study and Prevention of Drug Misuse and Co-Occurring Aggressive Behavior

Abstract

The etiology of behavioral precursors to substance misuse and aggression is viewed from the perspective of a developmental, multifactorial model of complex disorders. Beginning at conception, genetic and environmental interactions have potential to produce a sequence of behavioral phenotypes during development that bias the trajectory toward high-risk outcomes. One pathway is theorized to emanate from a deviation in neurological development that predisposes children to affective and cognitive delays or impairments that, in turn, generate dysregulatory behaviors. The plasticity of these neurobiological systems is highly relevant to the prevention sciences; their functions are reliant upon environmental inputs and can be altered, for better or for worse, contingent upon the nature of the inputs. Thus, social contextual factors confer significant influence on the development of this neural network and behavioral outcomes by increasing risk for, or protecting against, dysregulatory outcomes. A well-designed intervention can exploit the brain's plasticity by targeting biological and social factors at sensitive time points to positively influence emergent neurobiological functions and related behaviors. Accordingly, prevention research is beginning to focus on perturbations in developmental neural plasticity during childhood that increase the likelihood of risky behaviors and may also moderate intervention effects on behavior. Given that the more complex features of neurobiological functions underlying drug misuse and aggression (e.g., executive cognitive function, coping skills, affect regulation) do not coalesce until early adulthood when prefrontal-limbic brain networks consolidate, it is critical that mechanisms underlying developmental risk factors are identified. An empirically driven prevention approach, thus, may benefit from consideration of (i) the type, effect, and developmental timing of the environmental impact on the brain, and (ii) the type and effect on brain function, and developmental timing of the intervention. This translational approach promises to eventually offer some direction for the design of effective interventions to prevent drug misuse and concomitant aggression.

Keywords:

• Drug misuse
• aggressiveness
• neuroscience
• prevention
• plasticity

Notes

¹The reader is reminded that these two concepts, which are often noted in the literature, are all -too often inadequately delineated in terms of their dimensions (linear, nonlinear), their “demands,” the critical necessary conditions (endogenous as well as exogenous ones, and both micro and macro) which are necessary for either of them to operate (begin, continue, become anchored and integrate, change as de facto realities change, cease, etc.) or not to and whether their underpinnings are theory-driven, empirically based, individual, and/or systemic stakeholder bound, based upon “principles of faith,” etc. Such understanding is necessary if these posited processes are not to remain as yet additional shibboleths in a field of many stereotypes. Hills's criteria for causation are a useful consideration. These were developed in order to help assist researchers and clinicians determine if risk factors were causes of a particular disease or outcomes or merely associated. Editor's note

²The often used nosology “drugs of abuse” is both unscientific and misleading in that (1) it mystifies and empowers selected active chemicals into a category whose underpinnings are neither theoretically anchored nor evidence-informed and is based upon “principles of faith” held and transmitted by a range of stakeholders representing a myriad of agendas and goals, and (2) active chemical substances of any types—“drugs”—are used or misused; living organisms can be and are all –too often abused. Editor's note