Aims: This study explored whether the density of family history (FH) of substance use disorders relates to post-treatment substance use outcomes in adolescents, with the primary aim of determining whether FH exerts a relatively stronger influence on longer-term outcomes. Method: The present investigation examined adolescents (ages 12-18, n= 366) from two independent samples who were treated for alcohol/substance use disorder (ASUD) and re-assessed during the eight years following treatment with identical methodology. Primary substance use outcomes were assessed at 1, 2, 4, 6, and 8 years post-treatment and included total drinks, days using marijuana, and days using other drugs. Results: In hierarchical linear models there were significant FH density × linear time interactions for total drinks (z= 12.75, p< 0.001) and marijuana use days (z= 4.39, p<. 0.001); greater FH density predicted more total drinks and more marijuana use days, with both associations becoming stronger over time. The increasing linkage between FH and other drug use was not significant over time. Conclusions: Findings are consistent with previous research indicating that the risk associated with FH increases over time, especially in relation to quantity/frequency measures of alcohol and marijuana use. By extending these findings to an adolescent clinical sample, the current study highlights that FH density of alcohol and drug dependence is a risk factor for poorer long-term outcomes for adolescent-onset ASUD youth as they transition into adulthood. Future work should explore the mechanisms underlying greater post-treatment substance use for adolescents/young adults with greater FH density.

Recent research highlights the role of peer victimization in students’ adjustment across a variety of domains (e.g., academic, social), but less often identifies potential mediating variables. In the current study, we tested for direct effects from peer victimization to adolescents’ academic behavior and alcohol use, as well as indirect effects through school belonging. Adolescents from two large samples (middle school: N = 2,808; high school: N = 6,821) self-reported on peer victimization, school belonging, academic outcomes (GPA, school truancy), and alcohol use (lifetime, past 30 days). Two-group structural equation models revealed (a) direct and indirect paths from peer victimization to academic functioning; (b) indirect, but not direct, effects through school belonging for lifetime drinking; and (c) direct and indirect effects from peer victimization to current drinking. Findings implicate school belonging as a mediator between peer victimization and important outcomes in adolescence.

The age- and time-dependent effects of binge drinking on adolescent brain development have not been well characterized even though binge drinking is a health crisis among adolescents. The impact of binge drinking on gray matter volume (GMV) development was examined using 5 waves of longitudinal data from the National Consortium on Alcohol and NeuroDevelopment in Adolescence study. Binge drinkers (n = 166) were compared with non-binge drinkers (n = 82 after matching on potential confounders). Number of binge drinking episodes in the past year was linked to decreased GMVs in bilateral Desikan-Killiany cortical parcellations (26 of 34 with P < 0.05/34) with the strongest effects observed in frontal regions. Interactions of binge drinking episodes and baseline age demonstrated stronger effects in younger participants. Statistical models sensitive to number of binge episodes and their temporal proximity to brain volumes provided the best fits. Consistent with prior research, results of this study highlight the negative effects of binge drinking on the developing brain. Our results present novel findings that cortical GMV decreases were greater in closer proximity to binge drinking episodes in a dose-response manner. This relation suggests a causal effect and raises the possibility that normal growth trajectories may be reinstated with alcohol abstinence.

Cannabis is the most widely produced and consumed illicit psychoactive substance worldwide. Occasional cannabis use can progress to frequent use, abuse and dependence with all known adverse physical, psychological and social consequences. Individual differences in cannabis initiation are heritable (40-48%). The International Cannabis Consortium was established with the aim to identify genetic risk variants of cannabis use. We conducted a meta-analysis of genome-wide association data of 13 cohorts (N=32 330) and four replication samples (N=5627). In addition, we performed a gene-based test of association, estimated single-nucleotide polymorphism (SNP)-based heritability and explored the genetic correlation between lifetime cannabis use and cigarette use using LD score regression. No individual SNPs reached genome-wide significance. Nonetheless, gene-based tests identified four genes significantly associated with lifetime cannabis use: NCAM1, CADM2, SCOC and KCNT2. Previous studies reported associations of NCAM1 with cigarette smoking and other substance use, and those of CADM2 with body mass index, processing speed and autism disorders, which are phenotypes previously reported to be associated with cannabis use. Furthermore, we showed that, combined across the genome, all common SNPs explained 13-20% (P<0.001) of the liability of lifetime cannabis use. Finally, there was a strong genetic correlation (rg=0.83; P=1.85 × 10(-8)) between lifetime cannabis use and lifetime cigarette smoking implying that the SNP effect sizes of the two traits are highly correlated. This is the largest meta-analysis of cannabis GWA studies to date, revealing important new insights into the genetic pathways of lifetime cannabis use. Future functional studies should explore the impact of the identified genes on the biological mechanisms of cannabis use.

Background

The Adolescent Brain Cognitive Development ™ Study (ABCD Study®) is an open-science, multi-site, prospective, longitudinal study following over 11,800 9- and 10-year-old youth into early adulthood. The ABCD Study aims to prospectively examine the impact of substance use (SU) on neurocognitive and health outcomes. Although SU initiation typically occurs during teen years, relatively little is known about patterns of SU in children younger than 12.

Methods

This study aims to report the detailed ABCD Study® SU patterns at baseline (n = 11,875) in order to inform the greater scientific community about cohort's early SU. Along with a detailed description of SU, we ran mixed effects regression models to examine the association between early caffeine and alcohol sipping with demographic factors, externalizing symptoms and parental history of alcohol and substance use disorders (AUD/SUD).

Primary results

At baseline, the majority of youth had used caffeine (67.6 %) and 22.5 % reported sipping alcohol (22.5 %). There was little to no reported use of other drug categories (0.2 % full alcohol drink, 0.7 % used nicotine, <0.1 % used any other drug of abuse). Analyses revealed that total caffeine use and early alcohol sipping were associated with demographic variables (p's<.05), externalizing symptoms (caffeine p = 0002; sipping p = .0003), and parental history of AUD (sipping p = .03).

Conclusions

ABCD Study participants aged 9-10 years old reported caffeine use and alcohol sipping experimentation, but very rare other SU. Variables linked with early childhood alcohol sipping and caffeine use should be examined as contributing factors in future longitudinal analyses examining escalating trajectories of SU in the ABCD Study cohort.