Alcohol use disorder (AUD) causes immense global burden and has a significant impact on economic and societal functioning. Efficacious treatments for AUDs have been well-established within the literature, however the most commonly accessed treatments for AUD are alcohol-related services, such as self-help groups, outpatient clinics, and detoxification centers. Though studies suggest these services are effective at treating AUDs, there are numerous differences between individuals who receive alcohol-related services and individuals who do not, causing selection bias. Furthermore, current studies of alcohol-related services frequently define recovery outcomes as abstinence, which reduces variability in viable recovery outcomes, such as reduction of drinking behaviors. In addition, reduction in drinking and alcohol-related problems should theoretically have an impact on broader aspects of functioning, such as familial functioning. Improved familial context may reduce risk to family members, who are otherwise at heightened risk for emotional and behavioral problems when living with a family member with AUD. The current study investigated the effect of alcohol-related services on binary and continuous drinking outcomes after eliminating selection bias using multiple propensity score approaches, to identify the best methodology for a high-risk community sample of individuals with AUD. Propensity scores were created using logistic regression approaches and boosted regression trees. Matching, weighting, and subclassification were used, and matching was performed both using greedy and global approaches. Results suggested subclassification was the most successful method for real world alcohol-related services samples with moderate sample size. Moreover, findings demonstrated that boosted regression approaches were less successful than logistic regression approaches at minimizing the effects of selection bias on known confounding variables that are highly related to group selection. In addition, after removing the effects of selection bias, there were no significant difference between participants who received alcohol-related services and the comparison control group on drinking or family functioning, though both groups reduced drinking from pre- to post-alcohol-related services receipt. Findings suggest careful selection of quasi-experimental methods is warranted in real-world samples, to ensure optimal removal of selection bias. Moreover, future studies should continue to clarify the profile of individual that benefits from alcohol-related services to inform intervention efforts.

Despite the established co-prevalence of substance use (SU) and disordered eating (DE), few longitudinal studies have sought to examine their shared development. Findings have been inconsistent within the extant literature. This may be attributable in part to several methodological aspects, including overlooking distinct psychopharmacological properties of common substances of abuse, examining only between-person relations, and failing to account for shared risk factors. The current study sought to address these gaps by applying latent curve models with structured residuals (LCM-SR) to a preexisting, national sample of adolescent girls followed into adulthood, Add Health. In Aim 1, between-person effects examined the simultaneous development of alcohol, tobacco, and marijuana use and DE behaviors in substance-specific models. In Aim 2, bivariate latent curve models were expanded to account for within-person effects (LCM-SR) in order to examine the potentially bidirectional, prospective relationship between use of a specific substance and DE. Lastly, models accounted for shared developmental risk factors. Findings of the current study demonstrate preliminary evidence of substance-specific effects with DE emerging in adolescence. Across model-building steps, DE engagement in early adolescence was significantly associated with growth in tobacco use and marginally associated with marijuana use. Appetitive side-effects of both substances may link use with DE behaviors and enhance instrumental use for weight control. Significant associations did not emerge between alcohol and DE, and results of the conditional model indicate this co-occurrence is best explained by third variable mechanisms. Implications for prevention are discussed.

Alcohol use remains a major public health concern and economic burden. Extant literature suggests that young adulthood is a particularly high-risk developmental period for heavy drinking. Given this, it is imperative to understand possible risk and protective factors for heavy drinking and related consequences during this risky developmental period. Prior research has shown that both drinking history and alcohol response (AR) are consistent predictors of future drinking outcomes. However, it is unclear how they may work together to confer this risk. The current study aimed to fill this gap in the literature by examining how alcohol use trajectories across adolescence and early adulthood impacted relations between AR after an alcohol challenge and drinking outcomes over a 2-year period in a sample of young adult moderate to heavy drinkers. Results showed that both drinking history and AR were independently predictive of alcohol outcomes at the 6-month follow-up such that a more extensive drinking history, greater high arousal positive effects, and lesser low arousal negative effects predicted greater drinking and alcohol-related problems 6-months later. However, drinking history and AR were largely not predictive of change in drinking outcomes over time. Finally, AR did not mediate the relationship between drinking history and later alcohol-related outcomes. This is the first study to address relations among drinking history, AR, and later drinking outcomes using a longitudinal alcohol challenge design with a full account of early drinking history. Future research would benefit from inclusion of a broad range of drinkers and longer follow-up assessments to better understand the complex pathways of risk from early drinking history and AR to future drinking outcomes. Such efforts may increase the understanding of who is at greatest risk and/or would benefit most from specific intervention programs.

Excessive drinking in adolescence is a public health issue with major consequences on both an individual and societal level. Elucidating genetic and environmental influences could be particularly informative for prevention efforts. One potential source of genetic influence is sensitivity to environmental influences. It was hypothesized that parent knowledge would interact with genetic sensitivity to the environment to indirectly reduce risk for alcohol problems through less adolescent rule breaking behavior. Participants (N=316) provided genetic data and reported their rule breaking behavior and past year frequency of heavy drinking, and participants’ custodial parents reported their perceived knowledge of their child’s activities. A novel index of genetic sensitivity to environmental influence was created using published methylation quantitative trait locus data from the frontal lobe. Study hypotheses were mostly not supported. The study results likely reflect the poor distribution of study variables and the limitations of the current study’s sensitivity gene score. The current study underscored the importance of adhering to methodological rigor and explored alternate conceptualizations and methods that future research could use to elucidate the role of inherited to sensitivity to environmental influences in adolescent drinking.

Prior research suggests that African American adults are more likely than White adults to experience negative alcohol use outcomes such as alcohol use disorder (AUD) despite reporting lower rates of alcohol consumption. Research also shows that African Americans experience higher rates of depression, which can increase risk for alcohol consumption and AUD through drinking to cope. The current study examined the role of depressive symptoms and drinking to cope in alcohol consumption and AUD symptoms among White and Black/African American college students. Participants completed an online survey during the fall (T1) and spring semester (T2) of their first year of college (N = 2,168, 62.8% female, 75.8% White). Path analyses were conducted to examine whether depressive symptoms and drinking to cope mediated the association between race/ethnicity and alcohol consumption and AUD symptoms, as well as whether race/ethnicity moderated the associations between depressive symptoms, drinking to cope, and alcohol use outcomes. Results indicated that White participants had higher levels of depressive symptoms and alcohol consumption than African American participants. Drinking to cope at T1 was also associated with more depressive symptoms at T1, higher levels of alcohol consumption at T2, and higher levels of AUD symptoms at T2. Also, there was an indirect effect of depressive symptoms on AUD symptoms via drinking to cope. Results from multigroup path analyses suggested that depressive symptoms were more strongly associated with drinking to cope for White students than African American students. There were no significant racial/ethnic differences in the associations between depressive symptoms or drinking to cope and alcohol use outcomes. Future research should examine the roles of race, depression, and drinking to cope in alcohol use outcomes for college students.

This study aimed to advance understanding of the relation between social media and adolescent alcohol use while accounting for offline peer alcohol use, exploring offline peer alcohol use separately as a covariate and as a moderator, with an additional exploratory analysis of the relation between social media and alcohol use without offline peer alcohol use in the model. A total of 868 students (55% female) in grade 7 (n = 468) and grade 8 (n = 400) at wave 1, self-reported on alcohol use, binge drinking, and social media use as well as nominated friends from their school and grade. Data from nominated peers who also completed the questionnaires were used for peer-report of alcohol use. Data were collected annually from students at grades 8, 9, 10, and 11 were used in analyses. Final structural models consisted of a cross-lagged panel design with saved factor scores for social media and peer alcohol use predicting a categorical alcohol use variable or a binary binge drinking variable. With offline peer alcohol use as a covariate in the model, social media did not prospectively relate to subsequent grade alcohol use or binge drinking. However, without offline peer alcohol use, the path from social media use to subsequent grade alcohol use was significant but not the path to binge drinking. Offline peer alcohol use did not significantly moderate the relation between social media and subsequent grade alcohol use or binge drinking.

Past research suggests that both Alcohol Expectancies and Subjective Response are strong predictors of drinking. However, most studies do not account for the shared variance or relations between the two. Social cognitive and expectancy theories suggest that cognitions may distort reality, creating a discrepancy between expected and subjective effects. Only one study has tested the effects of such discrepancies (Morean et al., 2015), but that study was cross-sectional, making it impossible to determine the direction of effects. As such, the present study sought to test prospective associations between expectancy-subjective response interactions and future drinking behavior. Participants (N=448) were randomly assigned to receive alcohol (target blood alcohol alcohol =.08 g%) or placebo, with 270 in the alcohol condition. Alcohol expectancies and subjective response were assessed across the full range of affective space of valence by arousal. Hierarchical regression tested whether expectancies, subjective response, and their interaction predicted follow-up drinking in 258 participants who reached a blood alcohol curve of >.06 (to differentiate blood alcohol curve limbs). Covariates included gender, age, drinking context, and baseline drinking. High arousal subjective response was tested on the ascending limb and low arousal subjective response on the descending limb. High arousal positive expectancies and subjective response interacted to predict future drinking, such that mean and low levels of high arousal positive subjective response were associated with more drinking when expectancies were higher. High arousal negative expectancies and subjective response also interacted to predict future drinking, such that high levels of high arousal negative subjective response marginally predicted more drinking when expectancies were lower. There were no interactions between low arousal positive or low arousal negative expectancies and subjective response. Results suggest that those who expected high arousal positive subjective response but did not receive many of these effects drank more, and those who did not expect to feel high arousal negative subjective response but did in fact feel these effects also drank more. The results suggest that challenging inaccurate positive expectancies and increasing awareness of true negative subjective response may be efficacious ways to reduce drinking.

Substance use during adolescence is a significant predictor of developing a later substance use disorder. An encouraging trend is that there have been recent declines in rates of adolescent substance use, including alcohol and marijuana. However, these two substances may be decreasing differently from one another as a result of age, period, and cohort effects. Therefore, the overall trend of decreased substance use in more recent generations of adolescents may be greater for one substance than the other. The current study tested declines in adolescent alcohol and marijuana use across two generations measured in 1988-1990 and 2006-2012. Methodological strengths include controls for demographic characteristics and for parental alcohol disorder (as a proxy for genetic risk). Moreover, we tested whether findings would replicate using two methods—first comparing all assessed members of one generational cohort with all assessed members of the other generational cohort, and then comparing only matched parent-child pairs. Testing this second matched sample removes some potential demographic and risk confounds that might occur across cohorts in typical epidemiological studies. Results demonstrated that the younger cohort of adolescents used both substances less than the older cohort, and this effect was stronger for alcohol than for marijuana. These results were replicated in both samples over and above demographic variables. The parent-child sample showed that children used less alcohol and marijuana than did their parent during the same age period, suggesting that these trends cannot simply be due to changes in the demographics of the adolescent population over time. Taken together with epidemiological studies, these findings suggest encouraging declines in adolescent substance use rates but also indicate less decline in marijuana use compared to alcohol use. This prompts further surveillance to determine if marijuana use rates may start increasing among adolescents in the future.

Family disruption, or the separation of children from caregivers, has been well-established in prior literature as a risk factor for child maladjustment; however, little is known about how family disruption impacts youth into adulthood, particularly how it influences children’s later parenting of their own offspring. The present study examined whether cumulative family disruption (i.e., parental hospitalization, death, incarceration, divorce) in childhood exerts effects on children’s parenting of their own offspring in adulthood, beyond other demographic characteristics and risk factors. Further, several potential mechanisms were hypothesized to underlie the association between family disruption in the first and second generation (G1-G2) family and later parenting provided from second-generation (G2) adults to third-generation (G3) children. Mediators included conflict and disorganization in the G1-G2 family and dysregulation in the G2 child.

Participants (N = 236 in models that included multiple G2 siblings; N = 110 in models without siblings) were drawn from a larger sample of at-risk (i.e., alcoholic) and comparison families followed longitudinally for over 30 years and across three generations. Four mediation models were estimated to examine effects of two separate G1-G2 family disruption components (deviance-related and health-related disruption) on parenting of G3, mediated by family conflict, family disorganization, and G2 dysregulation. Results indicated that health-related disruption impairs consistency of parenting provided to G3 offspring through conflict in the G1-G2 family. A direct effect of health-related disruption was also seen on parental monitoring. There were no direct or mediated effects of deviance-related disruption on parenting. Implications and future directions will be discussed.

The tendency for psychopathology to aggregate within families is well-documented, though little is known regarding the level of specificity at which familial transmission of symptomology occurs. The current study first tested competing higher-order structures of psychopathology in adolescence, indexing general and more specific latent factors. Second, parent-offspring transmission was tested for broadband domain specificity versus transmission of a general liability for psychopathology. Lastly, genetic and environmental mechanisms underlying the familial aggregation of psychopathology were examined using nuclear twin-family models. The sample was comprised of five hundred adolescent twin pairs (mean age 13.24 years) and their parents drawn from the Wisconsin Twin Project. Twins and parents completed independent diagnostic interviews. For aim 1, correlated factors, bifactor, and general-factor models were tested using adolescent symptom count data. For aim 2, structural equation modeling was used to determine whether broadband domain-specific transmission effects were necessary to capture parent-offspring resemblance in psychopathology above and beyond a general transmission effect indexed by the latent correlation between a parental internalizing factor and offspring P-factor. For aim 3, general factor models were fitted in both generations, and factor scores were subsequently extracted and used in nuclear twin-family model testing. Results indicated that the bifactor model exhibited the best fit to the adolescent data. Familial aggregation of psychopathology was sufficiently accounted for by the transmission of a general liability. Lastly, the best fitting reduced nuclear twin-family model indicated that additive genetic, sibling-specific shared environmental, and nonshared environmental influences contributed to general psychopathology. Parent-offspring transmission was accounted for by shared genetics only, whereas co-twin aggregation was additionally explained by sibling-specific shared environmental factors. Results provide novel insight into the specificity and etiology of the familial aggregation of psychopathology.