Objectives: Tests the hypothesis that the social adversity-antisocial behavior relationship is partly mediated by a biological mechanism, low heart rate. Method: 18 indicators of social adversity and heart rate measured at rest and in anticipation of a speech stressor were assessed alongside nine measures of antisocial behavior including delinquency (Youth Self-Report [YSR] and Child Behavior Checklist [CBCL]), conduct disorder (Conduct Disorder and Oppositional Defiant Disorder Questionnaire), and child psychopathy (Antisocial Process Screening Device [APSD]) in a community sample of 388 children aged 11 to 12 years. PROCESS was used to test mediation models. Results: Low heart rate was a partial mediator of the adversity-antisocial behavior relationship, explaining 20.35 percent and 15.40 percent of the effect of social adversity on delinquency and overall antisocial behavior, respectively. Conclusions: Findings are, to the authors’ knowledge, one of the first to establish any biological risk factor as a mediator of the social adversity-antisocial behavior relationship and suggest that social processes alter autonomic functioning in a way to predispose to antisocial behavior. While not definitive, results give rise to a social neurocriminology theory that argues that the social environment influences biological risk factors in a way to predispose to antisocial and criminal behavior.

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Researchers increasingly recognize that biological risk factors contribute to the development of antisocial behavior. Although academic dishonesty is a pervasive problem, this type of antisocial behavior has not been investigated in biosocial research. This article addresses this limitation by examining the relationship between academic dishonesty and resting heart rate in a sample of undergraduates (N = 149, 65.69% female, M age = 19.62 years). Subjects completed self-report academic dishonesty questionnaires, and heart rate was measured during a resting period. Low resting heart rate was associated with more frequent and varied academic dishonesty in females, but not in males. Self-control and sensation seeking, but not fearlessness, mediated this relationship in females. To our knowledge, this is the first study to examine a biological risk factor for academic dishonesty. This is also the first study to examine self-control as a possible mediator of the resting heart rate-antisocial behavior relationship in adults. Findings suggest a potential pathway in young adults through which low resting heart rate may affect antisocial behavior.

Research into the biological underpinnings of antisocial behavior has not only been increasingly integrated into criminological research, but has also expanded its scope to focus on antisocial behavior that develops during childhood. Many of the biological risk factors that are associated with antisocial behavior during adulthood have also been found to characterize young antisocials. Structural and functional brain imaging studies have implicated several brain regions in the development of antisocial behavior in children, including the amygdala, the ventromedial prefrontal cortex, and the temporal region. Neuropsychological studies indicate that antisocial children display multiple behavioral indices of brain dysfunction, including executive dysfunction and IQ de fi cits. Psychophysiological studies have revealed that antisocial children are characterized by underarousal and diminished responses to stimuli and stressors. Early health factors, including minor physical anomalies and prenatal nicotine exposure, both independently and in interaction with social risk factors are associated with antisocial behavior in children. Future research should focus on incorporating a life-course criminological perspective into the study of the biology of childhood crime and antisocial behavior. Longitudinal studies that measure both biological and social risk factors over time will be critical to advancing our understanding of the development of antisocial behavior both during childhood and throughout the life-course.