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Biosocial studies of antisocial and violent behavior in children and adults: a review - 1

Journal of Abnormal Child Psychology,  August, 2002  by Adrian Raine

<< Page 1  Continued from page 13.  Previous | Next

Neurotransmitters and Toxins

Neurotransmitter and toxin research is also beginning to provide evidence of interactions with social and environmental processes. Moffitt et al. (1997) found that although violent offenders had higher blood serotonin levels than controls, those with both high blood serotonin and a conflicted family background were over three times more likely to become violent by age 21 compared to men with only high serotonin or only conflicted family background. Similarly, Masters, Hone, and Doshi (1998) in an analysis of violent crime rates in 1,242 counties in the United States found a three-way interaction between environmental lead or manganese exposure, high population density, and alcoholism rates, with highest rates of violence in counties with high densities, exposure to toxins, and alcoholism. As with research on hormones, there is a dearth of empirical data to support or refute a biosocial interaction hypothesis of antisocial and violent behavior with respect to toxins, and further tests of this proposition are required.

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CONCLUSIONS AND RECOMMENDATIONS

Summarizing the key findings of this review, there has in recent years been growing evidence for replicable interactions between biological and social factors in relation to antisocial and violent behavior. In the last review of this area (Brennan & Raine, 1997), only nine studies could be drawn on to illustrate biosocial interactions. In the current review, 39 studies have been outlined that illustrate interactions between biological and social factors in relation to antisocial and violent behavior. Clearly, there is recent, growing evidence that social and biological processes do interact in predisposing to antisocial behavior. To date, the best-replicated biosocial effect appears to consist of birth complications interacting with negative home environments in predisposing to adult violence, and there is also evidence that this effect particularly characterizes life-course persistent antisocial behavior.

Although these findings give reason to take biosocial perspectives on antisocial behavior seriously, study counts and documentation of findings by themselves will not advance knowledge within a field. The establishment of interaction effects is not an end process, but merely the end of a beginning in understanding antisocial behavior. Interaction effects need to be explained with respect to their underlying mechanisms. For example, birth complications consistently interact with negative home environments in predisposing to adult violence, and this effect seems specific to violence, and to violence with an early onset--but why? What are the processes that operate in negative home environments, which trigger the deleterious effects of birth complications? Do birth complications predispose to violence by mild impairment to brain functioning, or does family adversity instead predispose to both birth complications such as pregnancy-induced hypertension and also childhood conduct disorder? That is, are birth compli cations merely a marker of a third factor and are by themselves unrelated to violence? Although these questions are difficult to answer, the next generation of biosocial research needs to go beyond simple interaction effects and research the fundamental mechanisms and processes underlying the interactions.