Background Individual differences in impulsivity and early adversity are known to be strong predictors of adolescent antisocial behavior. However, the neurobiological bases of impulsivity and their relation to antisocial behavior and adversity are poorly understood. Methods Impulsivity was estimated with a temporal discounting task. Voxel-based morphometry was used to determine the brain structural correlates of temporal discounting in a large cohort (n = 1830) of 14- to 15-year-old children. Mediation analysis was then used to determine whether the volumes of brain regions associated with temporal discounting mediate the relation between adverse life events (e.g., family conflict, serious accidents) and antisocial behaviors (e.g., precocious sexual activity, bullying, illicit substance use). Results Greater temporal discounting (more impulsivity) was associated with 1) lower volume in frontomedial cortex and bilateral insula and 2) greater volume in a subcortical region encompassing the ventral striatum, hypothalamus and anterior thalamus. The volume ratio between these cortical and subcortical regions was found to partially mediate the relation between adverse life events and antisocial behavior. Conclusions Temporal discounting is related to regions of the brain involved in reward processing and interoception. The results support a developmental imbalance model of impulsivity and are consistent with the idea that negative environmental factors can alter the developing brain in ways that promote antisocial behavior. ; This work received support from the European Union-funded FP6 Integrated Project IMAGEN (Grant No. LSHM-CT- 2007-037286), the FP7 project IMAGEMEND and the Innovative Medicine Initiative Project EU-AIMS (Grant No. 115300-2), the National Institute on Drug Abuse (Grant No. 1R21DA03838), the National Institutes of Health (Grant No. 1P20GM103644-01A1 awarded to the Vermont Center on Behavior and Health), a Medical Research Council Programme Grant (Grant No. 93558), the Swedish funding agency FORMAS, the Wellcome Trust (University of Cambridge), the National Institute for Health Research Biomedical Research Centre at South London and Maudsley National Health Service Foundation Trust and King’s College London, the Department of Health United Kingdom, the Bundesministerium für Bildung und Forschung (Grant Nos. 01GS08152; 01EV0711; eMED Grant No. SysAlc01ZX1311A; Forschungsnetz AERIAL), and the Fondation de France.