Aims Adolescents with substance use disorders (SUD) have difficulties with cognitive, behavioral and affective regulation. White matter (WM) disorganization has been observed in adolescents with SUD and may be related to psychological dysregulation. This study compared adolescents with SUD and control adolescents to investigate relationships among psychological dysregulation, WM disorganization, and SUD symptoms. Design Cross-sectional observation. Setting Adolescents with SUD were recruited from SUD treatment programs. Controls were recruited from the community. Participants The 55 participants were ages 14–19; 35 with SUD, 20 controls without SUD. Measurements Psychological dysregulation was characterized by the Behavior Rating Inventory of Executive Function. WM disorganization was measured by diffusion tensor imaging, and fractional anisotropy, radial diffusivity and axial diffusivity were examined within cortical regions of interest. Findings Compared to controls, SUD adolescents showed significantly greater psychological dysregulation and prefrontal and parietal WM disorganization. WM disorganization was positively correlated with psychological dysregulation and cannabis-related symptoms. In multivariate mediation models, the results were consistent with both the Neurodevelopmental Immaturity model, in which WM disorganization leads to psychological dysregulation and cannabis-related symptoms, and with the Substance Effects Model, in which cannabis-related symptoms lead to WM disorganization and psychological dysregulation. Conclusions In adolescents, substance use disorder and psychological dysregulation appear to be associated with reduced frontoparietal network white matter maturation.

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Background Resilience has been shown to be protective against alcohol use disorders (AUD), but the magnitude and nature of the relationship between these two phenotypes is not clear. The aim of this study is to examine the strength of this relationship and the degree to which it results from common genetic or common environmental influences. Methods Resilience was assessed on a nine-point scale during a personal interview in 1,653,721 Swedish men aged 17–25 years. AUD was identified based on Swedish medical, legal, and pharmacy registries. The magnitude of the relationship between resilience and AUD was examined using logistic regression. The extent to which the relationship arises from common genetic or common environmental factors was examined using a bivariate Cholesky decomposition model. Results The five single items that comprised the resilience assessment (social maturity, interest, psychological energy, home environment, and emotional control) all reduced risk for subsequent AUD, with social maturity showing the strongest effect. The linear effect by logistic regression showed that a one-point increase on the resilience scale was associated with a 29% decrease in odds of AUD. The Cholesky decomposition model demonstrated that the resilience-AUD relationship was largely attributable to overlapping genetic and shared environmental factors (57% and 36%, respectively). Conclusion Resilience is strongly associated with a reduction in risk for AUD. This relationship appears to be the result of overlapping genetic and shared environmental influences that impact resilience and risk of AUD, rather than a directly causal relationship.

Offspring of parents with AUD are at increased risk for externalizing psychopathology. Maternal and paternal AUD differentially affected sons' vs. daughters' risks for AUD, drug abuse, and criminal behavior. The transmission of psychopathology within the externalizing spectrum appears to have sex-specific elements.

Background: Peer drinking is one of the most robust predictors of college students' alcohol use and can moderate students' genetic risk for alcohol use. Peer effect research generally suffers from 2 problems: selection into peer groups and relying more on perceptions of peer alcohol use than peers' selfreport. The goal of the present study was to overcome those limitations by capitalizing on a genetically informed sample of randomly assigned college roommates to examine multiple dimensions of peer influence and the interplay between peer effects and genetic predisposition on alcohol use, in the form of polygenic scores.Methods: We used a subsample (n = 755) of participants from a university-wide, longitudinal study at a large, diverse, urban university. Participants reported their own alcohol use during fall and spring and their perceptions of college peers' alcohol use in spring. We matched individuals into their rooms and residence halls to create a composite score of peer-reported alcohol use for each of those levels. We examined multiple dimensions of peer influence and whether peer influence moderated genetic predisposition to predict college students' alcohol use using multilevel models to account for clustering at the room and residence hall level.Results: We found that polygenic scores (b = 0.12), perceptions of peer drinking (b = 0.37), and roommates' self-reported drinking (b = 0.10) predicted alcohol use (all ps < 0.001), while average alcohol use across residence hall did not (b = À0.01, p = 0.86). We found no evidence for interactions between peer influence and genome-wide polygenic scores for alcohol use.Conclusions: Our findings underscore the importance of genetic predisposition on individual alcohol use and support the potentially causal nature of the association between peer influence and alcohol use.