Genetic and Environmental Contributions to Antisocial Personality Disorder

Antisocial personality disorder (ASPD) is a clinically heterogeneous psychiatric condition marked by persistent violations of social norms, impulsivity, aggression, and impaired interpersonal functioning. With an estimated prevalence of 1–4% in the general population and substantially higher rates in forensic contexts, ASPD contributes to considerable public health and societal burden. This review synthesizes evidence on the developmental risk architecture of ASPD across genetic, environmental, and epigenetic domains. Behavioral genetic research (twin, family, and adoption studies) indicates moderate heritability for antisocial behavior and ASPD-related traits, with genetic influences tending to increase from childhood into adolescence and varying by sex and behavioral phenotype. Molecular studies support a polygenic liability model in which many variants of small effect—implicating dopaminergic and serotonergic signaling, neurodevelopmental processes, and immune-related pathways—contribute to externalizing risk, although ASPD-specific associations remain limited. Longitudinal evidence identifies robust environmental predictors, including childhood maltreatment, adverse family climates, deviant peer affiliation, socioeconomic disadvantage, and community violence, which shape trajectories from early conduct problems to adult antisocial outcomes. Emerging work suggests that epigenetic processes, particularly DNA methylation, may help explain how early adversity becomes biologically embedded by altering gene regulation in neural systems relevant to impulse control and emotion regulation. Overall, the literature supports a developmental framework in which ASPD reflects cumulative, context-dependent risk arising from genetic liability interacting with environmental exposures, highlighting prevention-focused implications and the importance of early intervention on modifiable pathways.