Much research has focused on executive function (EF) impairments in psychopathy, a severe personality disorder characterized by a lack of empathy, antisocial behavior, and a disregard for social norms and moral values. However, it is still unclear to what extent EF deficits are present across psychopathy factors and, more importantly, which EF domains are impaired. The current meta-analysis answers these questions by synthesizing the results of 50 studies involving 5,694 participants from 12 different countries. Using multilevel random-effects models, we pooled effect sizes (Cohen's d) for five different EF domains: overall EF, inhibition, planning, shifting, and working memory. Moreover, differences between psychopathy factors were evaluated. Our analyses revealed small deficits in overall EF, inhibition, and planning performance. However, a closer inspection of psychopathy factors indicated that EF deficits were specific to lifestyle/antisocial traits, such as disinhibition. Conversely, interpersonal/affective traits, such as boldness, showed no deficits and in some cases even improved EF performance. These findings suggest that EF deficits are not a key feature of psychopathy per se, but rather are related to antisociality and disinhibitory traits. Potential brain correlates of these findings as well as implications for future research and treatment are discussed.

Substance use disorders among juveniles are a major public health concern and are often intertwined with other psychosocial risk factors including antisocial behavior. Identifying etiological risks and mechanisms promoting substance use disorders remains a high priority for informing more focused interventions in high-risk populations. The present study examined brain gray matter structure in relation to substance use severity among n = 152 high-risk, incarcerated boys (aged 14–20). Substance use severity was positively associated with gray matter volume across several frontal/striatal brain regions including amygdala, pallidum, putamen, insula, and orbitofrontal cortex. Effects were apparent when using voxel-based-morphometric analysis, as well as in whole-brain, data-driven, network-based approaches (source-based morphometry). These findings support the hypothesis that elevated gray matter volume in striatal reward circuits may be an endogenous marker for vulnerability to severe substance use behaviors among youth.

We study why suffering a negative economic shock, i.e., a significant loss, may trigger a change in other-regarding behavior. We conjecture that people trade off concern for money with a conditional preference to follow social norms and that suffering a shock makes extrinsic motivation more salient, leading to more norm violation. This hypothesis is grounded on the premise that preferences are norm-dependent. We study this question experimentally: after administering losses on the earnings from a real-effort task, we analyze choices in prosocial and antisocial settings. To derive our predictions, we elicit social norms for each context analyzed in the experiments. We find evidence that shock increases deviations from norms.

Adverse environments are linked to elevated youth antisocial behavior. However, this relation is thought to depend, in part, on genetic susceptibility. The present study investigated whether polygenic risk for antisociality moderates relations between hostile environments and stable as well as dynamic antisocial behaviors across adolescence. We derived two antisocial-linked polygenic risk scores (PRS) (N = 721) based on previous genome-wide association studies. Forms of antisocial behavior (nonaggressive conduct problems, physical aggression, social aggression) and environmental hostility (harsh parenting and school violence) were assessed at age 13, 15, and 17 years. Relations to individual differences stable across adolescence (latent stability) vs. time-specific states (timepoint residual variance) of antisocial behavior were assessed via structural equation models. Higher antisocial PRS, harsh parenting, and school violence were linked to stable elevations in antisocial behaviors across adolescence. We identified a consistent polygenic-environment interaction suggestive of differential susceptibility in late adolescence. At age 17, harsher parenting was linked to higher social aggression in those with higher antisocial PRS, and lower social aggression in those with lower antisocial PRS. This suggests that genetics and environmental hostility relate to stable youth antisocial behaviors, and that genetic susceptibility moderates home environment-antisocial associations specifically in late adolescence.

Research has suggested that childhood-onset conduct problems (CPs) are more strongly related to individual predispositions, whereas adolescent-onset CP is more strongly associated with social factors, such as peer delinquency. Neighborhood disadvantage (ND) increases the risk for associating with deviant peers. Thus, peer delinquency could mediate the relationship between ND and adolescent-onset CP. This mediational hypothesis has not been tested previously. We tested this hypothesis in 1,127 justice-involved adolescent males using self-reported delinquency and official arrest records over 3 years after the youth’s first arrest as outcomes. Predictors were self-reported and census-derived indicators of ND and self-reported peer delinquency. Age of onset moderated the associations between self-reported ND and arrests and between self-report of peer delinquency and arrests. In both cases, the association was stronger for those with adolescent-onset CP. Peer delinquency mediated all relationships between ND and CP. Our results also showed some unexpected differences in associations depending on whether self-reported ND or census-derived indicators were used as predictors. Specifically, census-derived ND was negatively related to self-reported offending, which could be due to the use of an arrested sample and the need for youth in more advantaged neighborhoods to show a more severe pattern of antisocial behavior to be arrested.

While many studies have identified risk and protective factors of substance use (SU), few have assessed the reciprocal associations of child conduct problems (CP) and parenting practices and behaviors in the prediction of SU across development. A greater understanding of how these factors relate over time is needed to improve the timing of targeted prevention efforts. This study examined how child CP, parenting behaviors, and parents’ own antisocial behavior relate from preschool to adolescence and eventuate in SU. Participants included 706 youth (70.6% male; 89.7% white) enrolled in the Michigan Longitudinal Study. Data from waves 1 (ages 3–5), 2 (ages 6–8), 3 (ages 9–11), 4 (ages 12–14), and 5 (ages 15–17) were included. A random intercept cross-lagged panel model (RI-CLPM) examined reciprocal associations between parenting practices, parents’ antisocial behavior, and child CP over time (waves 1–4) and how these factors contribute to adolescent alcohol, cigarette, and marijuana use (wave 5). At the within-person level, negative parenting and parents’ own antisocial behavior had a strong influence in late childhood/early adolescence. Only child CP emerged as a significant predictor of SU. Results highlight the importance of early intervention and the potential influence of parenting and child factors throughout development in the prevention of SU.

Antisocial behavior can be contagious, spreading from individual to individual and rippling through social networks. Moreover, it can spread not only through third-party influence from observation, just like innovations or individual behavior do, but also through direct experience, via “pay-it-forward” retaliation. Here, we distinguish between the effects of observation and victimization for the contagion of antisocial behavior by analyzing large-scale digital trace data. We study the spread of cheating in more than a million matches of an online multiplayer first-person shooter game, in which up to 100 players compete individually or in teams against strangers. We identify event sequences in which a player who observes or is killed by a certain number of cheaters starts cheating and evaluate the extent to which these sequences would appear if we preserve the team and interaction structure but assume alternative gameplay scenarios. The results reveal that social contagion is only likely to exist for those who both observe and experience cheating, suggesting that third-party influence and “pay-it-forward” reciprocity interact positively. In addition, the effect is present only for those who both observe and experience more than once, suggesting that cheating is more likely to spread after repeated or multi-source exposure. Approaching online games as models of social systems, we use the findings to discuss strategies for targeted interventions to stem the spread of cheating and antisocial behavior more generally in online communities, schools, organizations, and sports.

Neuropsychological evidence supports the developmental taxonomy theory of antisocial behavior, suggesting that abnormal brain development distinguishes life-course-persistent from adolescence-limited antisocial behavior. Recent neuroimaging work confirmed that prospectively-measured life-course-persistent antisocial behavior is associated with differences in cortical brain structure. Whether this extends to subcortical brain structures remains uninvestigated. This study compared subcortical gray-matter volumes between 672 members of the Dunedin Study previously defined as exhibiting life-course-persistent, adolescence-limited or low-level antisocial behavior based on repeated assessments at ages 7–26 years. Gray-matter volumes of 10 subcortical structures were compared across groups. The life-course-persistent group had lower volumes of amygdala, brain stem, cerebellum, hippocampus, pallidum, thalamus, and ventral diencephalon compared to the low-antisocial group. Differences between life-course-persistent and adolescence-limited individuals were comparable in effect size to differences between life-course-persistent and low-antisocial individuals, but were not statistically significant due to less statistical power. Gray-matter volumes in adolescence-limited individuals were near the norm in this population-representative cohort and similar to volumes in low-antisocial individuals. Although this study could not establish causal links between brain volume and antisocial behavior, it constitutes new biological evidence that all people with antisocial behavior are not the same, supporting a need for greater developmental and diagnostic precision in clinical, forensic, and policy-based interventions.

The triarchic model was advanced as an integrative, trait-based framework for investigating psychopathy using different assessment methods and across developmental periods. Recent research has shown that the triarchic traits of boldness, meanness, and disinhibition can be operationalized effectively in youth, but longitudinal research is needed to realize the model's potential to advance developmental understanding of psychopathy. We report on the creation and validation of scale measures of the triarchic traits using questionnaire items available in the University of Southern California Risk Factors for Antisocial Behavior (RFAB) project, a large-scale longitudinal study of the development of antisocial behavior that includes measures from multiple modalities (self-report, informant rating, clinical-diagnostic, task-behavioral, physiological). Using a construct-rating and psychometric refinement approach, we developed triarchic scales that showed acceptable reliability, expected intercorrelations, and good temporal stability. The scales showed theory-consistent relations with external criteria including measures of psychopathy, internalizing/externalizing psychopathology, antisocial behavior, and substance use. Findings demonstrate the viability of measuring triarchic traits in the RFAB sample, extend the known nomological network of these traits into the developmental realm, and provide a foundation for follow-up studies examining the etiology of psychopathic traits and their relations with multimodal measures of cognitive-affective function and proneness to clinical problems.