Finding genes involved in complex behavioral outcomes, and understanding the pathways by which they confer risk, is a challenging task, necessitating large samples that are phenotypically well characterized across time. We describe an effort to create a university-wide research project aimed at understanding how genes and environments impact alcohol use and related substance use and mental health outcomes across time in college students. Nearly 70% of the incoming freshman class (N = 2715) completed on-line surveys, with 80% of the students from the fall completing spring follow-ups. 98% of eligible participants also gave DNA. The participants closely approximated the university population in terms of gender and racial/ethnic composition. Here we provide initial results on alcohol use outcomes from the first wave of the sample, as well as associated predictor variables. We discuss the potential for this kind of research to advance our understanding of genetic and environment influences on substance use and mental health outcomes.

In this project, we aimed to bring large-scale gene-identification findings into a developmental psychopathology framework. Using a family-based sample, we tested whether polygenic scores for externalizing disorders—based on single nucleotide polymorphism weights derived from genome-wide association study results in adults (n = 1,249)—predicted externalizing disorders, subclinical externalizing behavior, and impulsivity-related traits among adolescents (n = 248) and young adults (n = 207) and whether parenting and peer factors in adolescence moderated polygenic risk to predict externalizing disorders. Polygenic scores predicted externalizing disorders in adolescents and young adults, even after we controlled for parental externalizing-disorder history. Polygenic scores also predicted subclinical externalizing behavior and impulsivity traits in the adolescents and young adults. Adolescent parental monitoring and peer substance use moderated polygenic scores to predict externalizing disorders. This illustrates how state-of-the-science genetics can be integrated with psychological science to identify how genetic risk contributes to the development of psychopathology.

This study adopted a developmental perspective on recovery from conflict in romantic relationships. Participants were 73 young adults (target participants), studied since birth, and their romantic partners. A novel observational coding scheme was used to evaluate each participant’s degree of conflict recovery, operationalized as the extent to which the participant disengaged from conflict during a 4-min “cool-down” task immediately following a 10-min conflict discussion. Conflict recovery was systematically associated with developmental and dyadic processes. Targets who were rated as securely attached more times in infancy recovered from conflict better, as did their romantic partners. Concurrently, having a romantic partner who displayed better recovery predicted more positive relationship emotions and greater relationship satisfaction. Prospectively, target participants’ early attachment security and their partners’ degree of conflict recovery interacted to predict relationship stability 2 years later, such that having a partner who recovered from conflict better buffered targets with insecure histories.

Alcohol problems represent a classic example of a complex behavioral outcome that is likely influenced by many genes of small effect. A polygenic approach, which examines aggregate measured genetic effects, can have predictive power in cases where individual genes or genetic variants do not. In the current study, we first tested whether polygenic risk for alcohol problems—derived from genome-wide association estimates of an alcohol problems factor score from the age 18 assessment of the Avon Longitudinal Study of Parents and Children (ALSPAC; n = 4304 individuals of European descent; 57% female)—predicted alcohol problems earlier in development (age 14) in an independent sample (FinnTwin12; n = 1162; 53% female). We then tested whether environmental factors (parental knowledge and peer deviance) moderated polygenic risk to predict alcohol problems in the FinnTwin12 sample. We found evidence for both polygenic association and for additive polygene-environment interaction. Higher polygenic scores predicted a greater number of alcohol problems (range of Pearson partial correlations 0.07–0.08, all p-values ≤ 0.01). Moreover, genetic influences were significantly more pronounced under conditions of low parental knowledge or high peer deviance (unstandardized regression coefficients (b), p-values (p), and percent of variance (R²) accounted for by interaction terms: b = 1.54, p = 0.02, R² = 0.33%; b = 0.94, p = 0.04, R² = 0.30%, respectively). Supplementary set-based analyses indicated that the individual top single nucleotide polymorphisms (SNPs) contributing to the polygenic scores were not individually enriched for gene-environment interaction. Although the magnitude of the observed effects are small, this study illustrates the usefulness of polygenic approaches for understanding the pathways by which measured genetic predispositions come together with environmental factors to predict complex behavioral outcomes.