As part of the special issue of Development and Psychopathology honoring the remarkable contributions of Dr Dante Cicchetti, the current paper attempts to describe the recent contributions that a developmental psychopathology perspective has made in understanding the development of alcohol use and alcohol-related problems over the lifespan. The paper also identifies some of the future challenges and research directions. Because the scope of this task far exceeds the confines of a journal length article this paper does not attempt a comprehensive review. Rather, it builds on an earlier review and commentary that was published in Development and Psychopathology in 2013, with a similar goal.)Building on that work and updating its conclusions and suggestions for future directions, the current paper emphasizes findings from the research areas that were identified for further study in 2013 and the findings that have been published since that time.

There is evidence for intergenerational transmission of substance use and disorder. However, it is unclear whether separation from a parent with substance use disorder (SUD) moderates intergenerational transmission, and no studies have tested this question across three generations. In a three-generation study of families oversampled for familial SUD, we tested whether separation between father (G1; first generation) and child (G2; second generation) moderated the effect of G1 father SUDs on G2 child SUDs. We also tested whether separation between father (G2) and child (G3; third generation) moderated the effect of G2 SUDs on G3 drinking. Finally, we tested whether G1-G2 or G2-G3 separation moderated the mediated effect of G1 SUDs on G3 drinking through G2 SUDs. G1 father-G2 child separation moderated intergenerational transmission. In families with G1-G2 separation, there were no significant effects of father SUD on G2 SUD or G3 drinking. However, in nonseparated families, greater G1 father SUDs predicted heightened G2 SUDs and G3 grandchild drinking. In nonseparated families, G1 father SUDs significantly predicted G2 SUDs, which predicted G3 drinking. However, G2-G3 separation predicted heightened G3 drinking regardless of G2 and G1 SUDs. Parental separation may introduce risk for SUDs and drinking among youth with lower familial risk.

While prior literature has largely focused on marriage effects during young adulthood, it is less clear whether these effects are as strong in middle adulthood. Thus, we investigated age differences in marriage effects on problem-drinking reduction. We employed parallel analyses with two independent samples (analytic-sample Ns of 577 and 441, respectively). Both are high-risk samples by design, with about 50% of participants having a parent with lifetime alcohol use disorder. Both samples have been assessed longitudinally from early young adulthood to the mid-to-late 30s. Separate parallel analyses with these two samples allowed evaluation of the reproducibility of results. Growth models of problem drinking tested marriage as a time-varying predictor and thereby assessed age differences in marriage effects. For both samples, results consistently showed marriage effects to be strongest in early young adulthood and to decrease somewhat monotonically thereafter with age, reaching very small (and nonsignificant) magnitudes by the 30s. Results may reflect that role transitions like marriage have more impact on problem drinking in earlier versus later adulthood, thereby highlighting the importance of life span developmental research for understanding problem-drinking desistance. Our findings can inform intervention strategies aimed at reducing problem drinking by jumpstarting or amplifying natural processes of adult role adaptation.

Poor family cohesion and elevated adolescent aggression are associated with greater alcohol use in adolescence and early adulthood. In addition, evocative gene–environment correlations (rGEs) can underlie the interplay between offspring characteristics and negative family functioning, contributing to substance use. Gene–environment interplay has rarely been examined in racial/ethnic minority populations. The current study examined adolescents’ polygenic risk scores for aggression in evocative rGEs underlying aggression and family cohesion during adolescence, their contributions to alcohol use in early adulthood (n = 479), and differences between Mexican American and European American subsamples. Results suggest an evocative rGE between polygenic risk scores, aggression, and low family cohesion, with aggression contributing to low family cohesion over time. Greater family cohesion was associated with lower levels of alcohol use in early adulthood and this association was stronger for Mexican American adolescents compared to European American adolescents. Results are discussed with respect to integration of culture and racial/ethnic minority samples into genetic research and implications for alcohol use.

The current study used data from two longitudinal samples to test whether self-regulation, depressive symptoms, and aggression/antisociality were mediators in the relation between a polygenic score indexing serotonin (5-HT) functioning and alcohol use in adolescence. The results from an independent genome-wide association study of 5-hydroxyindoleacetic acid in the cerebrospinal fluid were used to create 5-HT polygenic risk scores. Adolescents and/or parents reported on adolescents’ self-regulation (Time 1), depressive symptoms (Time 2), aggression/antisociality (Time 2), and alcohol use (Time 3). The results showed that 5-HT polygenic risk did not predict self-regulation. However, adolescents with higher levels of 5-HT polygenic risk showed greater depression and aggression/antisociality. Adolescents’ aggression/antisociality mediated the relation between 5-HT polygenic risk and later alcohol use. Deficits in self-regulation also predicted depression and aggression/antisociality, and indirectly predicted alcohol use through aggression/antisociality. Pathways to alcohol use were especially salient for males from families with low parental education in one of the two samples. The results provide insights into the longitudinal mechanisms underlying the relation between 5-HT functioning and alcohol use (i.e., earlier aggression/antisociality). There was no evidence that genetically based variation in 5-HT functioning predisposed individuals to deficits in self-regulation. Genetically based variation in 5-HT functioning and self-regulation might be separate, transdiagnostic risk factors for several types of psychopathology.

Alcohol use disorders and internalizing disorders are highly comorbid, but how this comorbidity unfolds over development is not well understood. The present study investigated effects of internalizing symptoms in late childhood on speed of transition between three alcohol involvement milestones: first drink, first binge, and onset of first alcohol dependence symptom. Greater early internalizing symptoms were expected to predict a later age of first drink, a slower transition from first drink to first binge, and a faster transition from first binge to first dependence symptom. The effects of age and moderating effects of gender were also examined. Data were from a longitudinal study of children of alcoholics and matched controls (N = 454) followed from late childhood to midlife. Generally, stage-specific hypotheses were not supported; rather, greater internalizing symptoms predicted an earlier age of first drink and a faster transition through the full interval from first drink to first dependence symptom. Regarding gender moderation, internalizing significantly predicted a faster transition between each milestone as well as through the full interval among women but not men. These results suggest that early internalizing problems confer risk for a rapid transition through all stages of alcohol involvement, and this risk may be limited to women.

Previous research suggests that mothers’ and fathers’ parenting may be differentially influenced by marital and child factors within the family. Some research indicates that marital stress is more influential in fathers’ than mothers’ parenting, whereas other research shows that children's difficult behavior preferentially affects mothers’ parenting. The present study examined marital stress and children's externalizing behavior in middle childhood as predictors of mothers’ versus fathers’ consistency, monitoring, and support and care in early adolescence, and the subsequent associations of these parenting behaviors with externalizing behavior 1.5 years later. Pathways were examined within a longitudinal mediation model testing for moderation by parent gender (N = 276 mothers, N = 229 fathers). Children's externalizing behavior in middle childhood was found to more strongly inversely predict mothers’ versus fathers’ monitoring in early adolescence. In contrast, marital stress more strongly predicted low monitoring for fathers than for mothers. Regardless of parent gender, marital stress predicted lower levels of parental consistency, and children's externalizing behavior predicted lower levels of parental support. Mothers’ monitoring and fathers’ support in early adolescence predicted lower levels of externalizing behavior 1.5 years later. The results are discussed with respect to family transactions relative to parent gender and implications for intervention.

Deviance proneness models propose a multilevel interplay in which transactions among genetic, individual, and family risk factors place children at increased risk for substance use. We examined bidirectional transactions between impulsivity and family conflict from middle childhood to adolescence and their contributions to substance use in adolescence and emerging adulthood (n = 380). Moreover, we examined children's, mothers’, and fathers’ polygenic risk scores for behavioral undercontrol, and mothers’ and fathers’ interparental conflict and substance disorder diagnoses as predictors of these transactions. The results support a developmental cascade model in which children's polygenic risk scores predicted greater impulsivity in middle childhood. Impulsivity in middle childhood predicted greater family conflict in late childhood, which in turn predicted greater impulsivity in late adolescence. Adolescent impulsivity subsequently predicted greater substance use in emerging adulthood. Results are discussed with respect to evocative genotype–environment correlations within developmental cascades and applications to prevention efforts.

The present study utilizes longitudinal data from a high-risk community sample to examine the unique effects of genetic risk, parental knowledge about the daily activities of adolescents, and peer substance use on emerging adult substance use disorders (SUDs). These effects are examined over and above a polygenic risk score. In addition, this polygenic risk score is used to examine gene–environment correlation and interaction. The results show that during older adolescence, higher adolescent genetic risk for SUDs predicts less parental knowledge, but this relation is nonsignificant in younger adolescence. Parental knowledge (using mother report) mediates the effects of parental alcohol use disorder (AUD) and adolescent genetic risk on risk for SUD, and peer substance use mediates the effect of parent AUD on offspring SUD. Finally, there are significant gene–environment interactions such that, for those at the highest levels of genetic risk, less parental knowledge and more peer substance use confers greater risk for SUDs. However, for those at medium and low genetic risk, these effects are attenuated. These findings suggest that the evocative effects of adolescent genetic risk on parenting increase with age across adolescence. They also suggest that some of the most important environmental risk factors for SUDs exert effects that vary across level of genetic propensity.

In the current study, we examined continuity in conflict across generations and explored potential mediators and moderators that could explain this continuity. We followed 246 targets from adolescence to adulthood and examined family conflict as reported by multiple reporters in targets' family of origin and current families. Results showed that conflict in the current family was strongly correlated with that of the family of origin in women but not in men. Continuity in family conflict across generations was mediated by patterns of elevated adolescent externalizing behavior in members of the second generation (G2). In addition, analyses revealed an interaction between both G2 partners' externalizing behavior such that if one partner in the G2 family demonstrated high levels of externalizing behavior, elevated levels of family conflict resulted. Potential explanations and implications of these findings are considered.

Impulse control and future orientation increase across adolescence, but little is known about how contextual factors shape the development of these capacities. The present study investigates how stress exposure, operationalized as exposure to violence, alters the developmental pattern of impulse control and future orientation across adolescence and early adulthood. In a sample of 1,354 serious juvenile offenders, higher exposure to violence was associated with lower levels of future orientation at age 15 and suppressed development of future orientation from ages 15 to 25. Increases in witnessing violence or victimization were linked to declines in impulse control 1 year later, but only during adolescence. Thus, beyond previous experiences of exposure to violence, witnessing violence and victimization during adolescence conveys unique risk for suppressed development of self-regulation.

The last 25 years have seen significant advances in our conceptualization of alcohol use and alcohol use disorders within a developmental framework, along with advances in our empirical understanding that have been potentiated by advances in quantitative methods. These include advances in understanding the heterogeneity of trajectories of alcohol outcomes; new insights about early childhood antecedents, and adolescence and emerging adulthood as important developmental periods for alcohol outcomes; a more nuanced understanding of the influences of developmental transitions, and their timing and contexts; a greater appreciation for the importance of considering multiple levels of analysis (including an increasing number of genetically informative studies); a continuing focus on studying multiple pathways underlying alcohol outcomes; and an increasing focus on studying the effects of alcohol exposure on future development. The current paper reviews these advances and suggests directions for future study.

Research has shown a developmental process of “maturing out” of alcohol involvement beginning in young adulthood, but the precise nature of changes characterizing maturing out is unclear. We used latent transition analysis to investigate these changes in a high-risk sample from a longitudinal study of familial alcoholism (N = 844; 51% children of alcoholics; 53% male, 71% non-Hispanic Caucasian, 27% Hispanic). Analyses classified participants into latent drinking statuses during late adolescence (ages 17–22), young adulthood (ages 23–28), and adulthood (ages 29–40), and characterized transitions among these statuses over time. The resulting four statuses were abstainers, low-risk drinkers who typically drank less than weekly and rarely binged or showed drinking problems, moderate-risk drinkers who typically binged less than weekly and showed moderate risk for drinking problems, and high-risk drinkers who typically binged at least weekly and showed high risk for drinking problems. Maturing out between late adolescence and young adulthood was most common among initial high-risk drinkers, but they typically declined to moderate-risk drinking rather than to nonrisky drinking statuses. This suggests that the developmental phenomenon of maturing out pertains primarily to relatively high-risk initial drinkers and that many high-risk drinkers who mature out merely reduce rather than eliminate their risky drinking.

This study examined the interplay between the influence of peers who promote alcohol use and μ-opioid receptor M1 (OPRM1) genetic variation in the intergenerational transmission of alcohol use disorder (AUD) symptoms while separating the “traitlike” components of AUD symptoms from their age-specific manifestations at three ages from emerging adulthood (17–23 years) to adulthood (29–40 years). The results for males were consistent with genetically influenced peer selection mechanisms as mediators of parent alcoholism effects. Male children of alcoholics were less likely to be carriers of the G allele in single nucleotide polymorphism A118G (rs1799971), and those who were homozygous for the A allele were more likely to affiliate with alcohol use promoting peers who increased the risk for AUD symptoms at all ages. There was evidence for women of an interaction between OPRM1 variation and peer affiliations but only at the earliest age band. Peer influences had stronger effects among women who were G-carriers. These results illustrate the complex ways in which the interplay between influences at multiple levels of analysis can underlie the intergenerational transmission of alcohol disorders as well as the importance of considering age and gender differences in these pathways.

Using a high-risk community sample (N = 405), the current study examined developmental cascades among substance use, affiliation with substance use promoting peers, and academic achievement over an 18-year period and tested whether these pathways mediated the influence of parental alcoholism on adult alcohol and drug use disorders. Results showed that the influence of parental alcoholism on adult drug disorders was mediated by developmental cascades across all three domains, whereas the influence of parental alcoholism on adult alcohol disorders was mediated through affiliation with substance use promoting peers and persistence in binge drinking. Adolescent drug use had more implications for adult outcomes than did adolescent alcohol use, which was less likely to spill over into other domains of functioning. Findings indicated that adolescent risk factors had indirect rather than unique effects on adult substance use disorders, suggesting that adolescent risk is not immutable and is largely mediated by later influences.

The current study tested the impact of the transition to parenthood on growth in alcohol consumption from early adolescence through emerging adulthood. We measured age-related discontinuity in trajectories of alcohol consumption associated with timing of the parenthood transition, above and beyond the effects of accrued educational status, gender, and time-varying marital status. We also examined the impact of a familial selection factor for the transmission of alcohol use problems, family history density of alcoholism (FHD), on both risk for adolescent parenthood and risk for adolescent parents' continuity in alcohol consumption after the parent transition within a mediation structural equation model. Premature timing of parenthood had a distinct effect on emerging adult alcohol trajectories. Although participants who became parents as emerging adults showed role-related decline in alcohol consumption, those who became parents during adolescence showed a role-related rise in emerging adult alcohol consumption. Gender moderated adolescent parents' role-related growth in emerging adult alcohol consumption. Adolescent fathers showed an adverse rise in alcohol consumption after becoming parents, whereas adolescent mothers' alcohol consumption did not change significantly. FHD was related to high adolescent alcohol consumption, which mediated risk for the incidence of early parenthood. Finally, the adverse effect of FHD on trajectories of emerging adult alcohol use was mediated by a dual pathway: (a) developmental continuity of conduct problems and (b) early transition to parenthood.

Adopting a developmental epidemiology perspective, the current study examines sources of risk heterogeneity for internalizing symptomatology among children of alcoholic parents (COAs). Parent-based factors, including comorbid diagnoses and the number of alcoholic parents in the family, as well as child-based factors, namely child gender, formed the indicators of heterogeneity. Following a novel approach to cross-study methods, we present a three-stage analysis involving measurement development using item response theory, examination of study effects on latent trajectories over time using latent curve modeling, and prediction of these latent trajectories testing our theoretically derived hypotheses in two longitudinal investigations across both mother- and self-reported symptomatology. Specifically, we replicated previous findings that parent alcoholism has a unique effect on child internalizing symptoms, above and beyond those of both parent depression and antisocial personality disorder. However, we also found important subgroup differences, explaining heterogeneity within COAs' risk profile in terms of the number of alcoholic parents in the family, comorbid diagnoses for the alcoholic parent and, for self-reported symptoms, child gender. Such factors serve to refine the definition of risk among COAs, suggesting a more severely impaired target group for preventive interventions, identifying the significance of familial alcoholism in individual differences underlying internalizing symptoms over time, and further specifying the distal risk matrix for an internalizing pathway to alcohol involvement.

The relations of children's coping strategies and coping efficacy to parent socialization and child adjustment were examined in a sample of school-age children that included families in which some of the grandparents and/or parents had an alcoholism diagnosis. Parents and older children reported on the children's coping strategies; parents reported on their parenting behavior; and teachers reported on children's externalizing and internalizing problems. Measures of parent socialization were associated with parents' and children's reports of active coping strategies and parents' reports of both support-seeking coping and coping efficacy. Some of these relations were moderated by familial alcohol status. Children higher in parent-reported active/support-seeking coping and coping efficacy were rated lower in teacher-reported externalizing and internalizing adjustment problems. The findings were consistent with the view that active/support-seeking coping and coping efficacy mediated the association of parent socialization to children's psychological adjustment and that this relation was sometimes moderated by parental alcohol status.This research was supported by a grant from the National Institute of Drug Abuse (DA05227; Laurie Chassin, Principle Investigator, Nancy Eisenberg, Co-Principal Investigator).

The transition to young adulthood is both a time when risky health behaviors such as substance misuse peak and a time of opportunity for growth and development through the acquisition of adult roles. In this transition, coping styles include responses to the stressors and opportunities associated with the emergence of adulthood. The extent to which such coping styles are skillfully employed in part determines adjustment into adulthood. The current study used a high-risk, longitudinal design to examine the development of coping styles over adolescence, continuity in these coping styles from adolescence to adulthood, the impact of coping on adult stress and substance misuse, the ability of coping to buffer effects of stress on substance use, and differences in coping between at-risk youth (i.e., children of alcoholics [COAs]) and their peers. A sample of 340 adolescents completed four assessments over ages 11–23. We used latent trajectory models to examine interindividual and intraindividual change in coping over time. Evidence for both change and continuity in the development of coping from adolescence to adulthood was found, although adolescent coping had limited impact on stress and substance use in adulthood. Support was also found for complex stress-buffering and stress-exacerbating effects of coping on the relations between major life events and adult drug use and between stress associated with the new roles of adulthood and heavy alcohol use. Implications of these findings for development and adjustment in the transition to adulthood are discussed.