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Some sources report increases in alcohol use have been observed since the start of the COVID-19 pandemic, particularly among women. Cross-sectional studies suggest that specific COVID-19-related stressful experiences (e.g., social disconnection) may be driving such increases in the general population. Few studies have explored these topics among individuals with a history of Alcohol Use Disorders (AUD), an especially vulnerable population. Drawing on recent data collected by the Collaborative Study on the Genetics of Alcoholism (COGA; COVID-19 study N = 1651, 62% women, age range: 30-91) in conjunction with AUD history data collected on the sample since 1990, we investigated associations of COVID-19 related stressors and coping activities with changes in drunkenness frequency since the start of the pandemic. Analyses were conducted for those without a history of AUD (N: 645) and three groups of participants with a history of AUD prior to the start of the pandemic: (1) those experiencing AUD symptoms (N: 606), (2) those in remission who were drinking (N: 231), and (3) those in remission who were abstinent (had not consumed alcohol for 5+ years; N: 169). Gender-stratified models were also examined. Exploratory analyses examined the moderating effects of 'problematic alcohol use' polygenic risk scores (PRS) and neural connectivity (i.e., posterior interhemispheric alpha EEG coherence) on associations between COVID-19 stressors and coping activities with changes in the frequency of drunkenness. Increases in drunkenness frequency since the start of the pandemic were higher among those with a lifetime AUD diagnosis experiencing symptoms prior to the start of the pandemic (14% reported increased drunkenness) when compared to those without a history of AUD (5% reported increased drunkenness). Among individuals in remission from AUD prior to the start of the pandemic, rates of increased drunkenness were 10% for those who were drinking pre-pandemic and 4% for those who had previously been abstinent. Across all groups, women reported nominally greater increases in drunkenness frequency when compared with men, although only women experiencing pre-pandemic AUD symptoms reported significantly greater rates of increased drunkenness since the start of the pandemic compared to men in this group (17% of women vs. 5% of men). Among those without a prior history of AUD, associations between COVID-19 risk and protective factors with increases in drunkenness frequency were not observed. Among all groups with a history of AUD (including those with AUD symptoms and those remitted from AUD), perceived stress was associated with increases in drunkenness. Among the remitted-abstinent group, essential worker status was associated with increases in drunkenness. Gender differences in these associations were observed: among women in the remitted-abstinent group, essential worker status, perceived stress, media consumption, and decreased social interactions were associated with increases in drunkenness. Among men in the remitted-drinking group, perceived stress was associated with increases in drunkenness, and increased relationship quality was associated with decreases in drunkenness. Exploratory analyses indicated that associations between family illness or death with increases in drunkenness and increased relationship quality with decreases in drunkenness were more pronounced among the remitted-drinking participants with higher PRS. Associations between family illness or death, media consumption, and economic hardships with increases in drunkenness and healthy coping with decreases in drunkenness were more pronounced among the remitted-abstinent group with lower interhemispheric alpha EEG connectivity. Our results demonstrated that only individuals with pre-pandemic AUD symptoms reported greater increases in drunkenness frequency since the start of the COVID-19 pandemic compared to those without a lifetime history of AUD. This increase was more pronounced among women than men in this group. However, COVID-19-related stressors and coping activities were associated with changes in the frequency of drunkenness among all groups of participants with a prior history of AUD, including those experiencing AUD symptoms, as well as abstinent and non-abstinent participants in remission. Perceived stress, essential worker status, media consumption, social connections (especially for women), and relationship quality (especially for men) are specific areas of focus for designing intervention and prevention strategies aimed at reducing pandemic-related alcohol misuse among this particularly vulnerable group. Interestingly, these associations were not observed for individuals without a prior history of AUD, supporting prior literature that demonstrates that widespread stressors (e.g., pandemics, terrorist attacks) disproportionately impact the mental health and alcohol use of those with a prior history of problems.

BackgroundResearchers have identified genetic and neural risk factors for externalizing behaviors. However, it has not yet been determined if genetic liability is conferred in part through associations with more proximal neurophysiological risk markers.MethodsParticipants from the Collaborative Study on the Genetics of Alcoholism, a large, family-based study of alcohol use disorders were genotyped and polygenic scores for externalizing (EXT PGS) were calculated. Associations with target P3 amplitude from a visual oddball task (P3) and broad endorsement of externalizing behaviors (indexed via self-report of alcohol and cannabis use, and antisocial behavior) were assessed in participants of European (EA; N = 2851) and African ancestry (AA; N = 1402). Analyses were also stratified by age (adolescents, age 12-17 and young adults, age 18-32).ResultsThe EXT PGS was significantly associated with higher levels of externalizing behaviors among EA adolescents and young adults as well as AA young adults. P3 was inversely associated with externalizing behaviors among EA young adults. EXT PGS was not significantly associated with P3 amplitude and therefore, there was no evidence that P3 amplitude indirectly accounted for the association between EXT PGS and externalizing behaviors.ConclusionsBoth the EXT PGS and P3 amplitude were significantly associated with externalizing behaviors among EA young adults. However, these associations with externalizing behaviors appear to be independent of each other, suggesting that they may index different facets of externalizing.

We tested whether aspects of the childhood/adolescent home environment mediate genetic risk for alcohol problems within families across generations. Parental relationship discord and parental divorce were the focal environments examined. The sample included participants of European ancestry (N = 4806, 51% female) and African ancestry (N = 1960, 52% female) from the high-risk Collaborative Study on the Genetics of Alcoholism. Alcohol outcomes in the child generation included lifetime criterion counts for DSM-5 Alcohol Use Disorder (AUD), lifetime maximum drinks in 24 h, age at initiation of regular drinking, and age at first alcohol intoxication. Predictors in the parent generation included relationship discord, divorce, alcohol measures parallel to those in the child generation, and polygenic scores for alcohol problems. Parental polygenic scores were partitioned into alleles that were transmitted and non-transmitted to the child. The results from structural equation models were consistent with genetic nurture effects in European ancestry families. Exposure to parental relationship discord and parental divorce mediated, in part, the transmission of genetic risk for alcohol problems from parents to children to predict earlier ages regular drinking (βindirect = -0.018 [-0.026, -0.011]) and intoxication (βindirect = -0.015 [-0.023, -0.008]), greater lifetime maximum drinks (βindirect = 0.006 [0.002, 0.01]) and more lifetime AUD criteria (βindirect = 0.011 [0.006, 0.016]). In contrast, there was no evidence that parental alleles had indirect effects on offspring alcohol outcomes via parental relationship discord or divorce in the smaller number of families of African ancestry. In conclusion, parents transmit genetic risk for alcohol problems to their children not only directly, but also indirectly via genetically influenced aspects of the home environment. Further investigation of genetic nurture in non-European samples is needed.

Substance use disorders (SUDs) incur serious social and personal costs. The risk for SUDs is complex, with risk factors ranging from social conditions to individual genetic variation. We examined whether models that include a clinical/environmental risk index (CERI) and polygenic scores (PGS) are able to identify individuals at increased risk of SUD in young adulthood across four longitudinal cohorts for a combined sample of N = 15,134. Our analyses included participants of European (NEUR = 12,659) and African (NAFR = 2475) ancestries. SUD outcomes included: (1) alcohol dependence, (2) nicotine dependence; (3) drug dependence, and (4) any substance dependence. In the models containing the PGS and CERI, the CERI was associated with all three outcomes (ORs = 01.37-1.67). PGS for problematic alcohol use, externalizing, and smoking quantity were associated with alcohol dependence, drug dependence, and nicotine dependence, respectively (OR = 1.11-1.33). PGS for problematic alcohol use and externalizing were also associated with any substance dependence (ORs = 1.09-1.18). The full model explained 6-13% of the variance in SUDs. Those in the top 10% of CERI and PGS had relative risk ratios of 3.86-8.04 for each SUD relative to the bottom 90%. Overall, the combined measures of clinical, environmental, and genetic risk demonstrated modest ability to distinguish between affected and unaffected individuals in young adulthood. PGS were significant but added little in addition to the clinical/environmental risk index. Results from our analysis demonstrate there is still considerable work to be done before tools such as these are ready for clinical applications.

ObjectiveTo examine associations between alcohol use disorder (AUD), its psychiatric comorbidities, and their interactions, with marital outcomes in a diverse high-risk, genetically informative sample.MethodParticipants included European ancestry (EA; n = 4,045) and African ancestry (AA; n = 1,550) individuals from the multigenerational Collaborative Study on the Genetics of Alcoholism (COGA) sample (56% female, Mage ∼ 41 years). Outcomes were lifetime marriage and divorce. Predictors included lifetime AUD, an alcohol problems polygenic score (PRS), and AUD comorbidities, including conduct or antisocial personality disorder (ASP), cannabis dependence/abuse (CAN), frequent tobacco use (TOB), and major depressive disorder (MDD). Mixed effect Cox models and generalized linear mixed effects models were fit.ResultsAmong EA participants, those with AUD and CAN were less likely to marry (hazard ratios [HRs] 0.70-0.83, ps < 0.01). Among AA participants, those with AUD and TOB were less likely to marry (HRs 0.66-0.82, ps < 0.05) and those with MDD were more likely to marry (HR = 1.34, ps < 0.01). Among EA participants, AUD, CAN, TOB, and MDD were associated with higher odds of divorce (odds ratios [ORs] 1.59-2.21, ps < 0.01). Among AA participants, no predictors were significantly associated with divorce. Significant random effects indicated genetic and environmental influences on marriage, but only environmental factors on divorce.ConclusionsIn a high-risk sample, AUD was associated with reduced likelihood of marriage in EA and AA individuals and increased risk of divorce in EA individuals. These associations were largely independent of comorbidities. Genetic and environmental background factors contributed to marriage, while only environmental background factors contributed to divorce. (PsycInfo Database Record (c) 2022 APA, all rights reserved).

ObjectiveGenome-wide association studies (GWASs) of the Alcohol Use Disorders Identification Test (AUDIT), a 10-item screen for alcohol use disorder (AUD), have elucidated novel loci for alcohol consumption and misuse. However, these studies also revealed that GWASs can be influenced by numerous biases (e.g., measurement error, selection bias), which may have led to inconsistent genetic correlations between alcohol involvement and AUD, as well as paradoxically negative genetic correlations between alcohol involvement and psychiatric disorders and/or medical conditions. The authors used genomic structural equation modeling to elucidate the genetics of alcohol consumption and problematic consequences of alcohol use as measured by AUDIT.MethodsTo explore these unexpected differences in genetic correlations, the authors conducted the first item-level and the largest GWAS of AUDIT items (N=160,824) and applied a multivariate framework to mitigate previous biases.ResultsThe authors identified novel patterns of similarity (and dissimilarity) among the AUDIT items and found evidence of a correlated two-factor structure at the genetic level ("consumption" and "problems," rg=0.80). Moreover, by applying empirically derived weights to each of the AUDIT items, the authors constructed an aggregate measure of alcohol consumption that was strongly associated with alcohol dependence (rg=0.67), moderately associated with several other psychiatric disorders, and no longer positively associated with health and positive socioeconomic outcomes. Lastly, by conducting polygenic analyses in three independent cohorts that differed in their ascertainment and prevalence of AUD, the authors identified novel genetic associations between alcohol consumption, alcohol misuse, and health.ConclusionsThis work further emphasizes the value of AUDIT for both clinical and genetic studies of AUD and the importance of using multivariate methods to study genetic associations that are more closely related to AUD.

Genetic predispositions and environmental influences both play an important role in adolescent externalizing behavior; however, they are not always independent. To elucidate gene-environment interplay, we examined the interrelationships between externalizing polygenic risk scores, parental knowledge, and peer substance use in impacting adolescent externalizing behavior across two time-points in a high-risk longitudinal sample of 1,200 adolescents (764 European and 436 African ancestry; Mage = 12.99) from the Collaborative Study on the Genetics of Alcoholism. Results from multivariate path analysis indicated that externalizing polygenic scores were directly associated with adolescent externalizing behavior but also indirectly via peer substance use, in the European ancestry sample. No significant polygenic association nor indirect effects of genetic risk were observed in the African ancestry group, likely due to more limited power. Our findings underscore the importance of gene-environment interplay and suggest peer substance use may be a mechanism through which genetic risk influences adolescent externalizing behavior.

BackgroundSuicidal thoughts and behaviors (STBs) and nonsuicidal self-injury (NSSI) behaviors are moderately heritable and may reflect an underlying predisposition to depression, impulsivity, and cognitive vulnerabilities to varying degrees.ObjectivesWe aimed to estimate the degrees of association between genetic liability to depression, impulsivity, and cognitive performance and STBs and NSSI in a high-risk sample.MethodsWe used data on 7,482 individuals of European ancestry and 3,359 individuals of African ancestry from the Collaborative Study on the Genetics of Alcoholism to examine the links between polygenic scores (PGSs) for depression, impulsivity/risk-taking, and cognitive performance with 3 self-reported indices of STBs (suicidal ideation, persistent suicidal ideation defined as ideation occurring on at least 7 consecutive days, and suicide attempt) and with NSSI.ResultsThe PGS for depression was significantly associated with all 4 primary self-harm measures, explaining 0.6-2.5% of the variance. The PGS for risk-taking behaviors was also associated with all 4 self-harm behaviors in baseline models, but was no longer associated after controlling for a lifetime measure of DSM-IV alcohol dependence and abuse symptom counts. Polygenic predisposition for cognitive performance was negatively associated with suicide attempts (q = 3.8e-4) but was not significantly associated with suicidal ideation nor NSSI. We did not find any significant associations in the African ancestry subset, likely due to smaller sample sizes.ConclusionsOur results encourage the study of STB as transdiagnostic outcomes that show genetic overlap with a range of risk factors.

BackgroundAlcohol consumption and problems are increasing among older adults, who are at elevated risk for alcohol-related accidents and medical problems. This paper describes a pilot follow-up of older adults with a history of alcohol dependence that was designed to determine the feasibility of conducting a more extensive investigation.MethodsThe sample consisted of previously assessed subjects in the Collaborative Studies on the Genetics of Alcoholism who: (i) were age 50+; (ii) had lifetime DSM-IV AD; and (iii) had DNA available. Individuals were located through family contacts, Internet searches, and death registries. A brief telephone interview assessed demographics, health, and alcohol involvement.ResultsOf the total sample (N = 2,174), 36% were contacted, 24% were deceased, and 40% were not yet located. Most (89%) contacted subjects were interviewed, and 99% of them agreed to future evaluation. Thirty percent of interviewed subjects reported abstinence for 10+ years, 56% reported drinking within the past year, and 14% last drank between >1 and 10 years ago. There were no age-related past-year differences in weekly consumption (overall sample mean: 16 drinks), number of drinking weeks (30.8), maximum number of drinks in 24 hours (8.1), or prevalence of weekly risky drinking (19%). Among those who drank within the past 5 years, the 3 most common alcohol-related problems were spending excessive time drinking or recovering (49%), drinking more/longer than intended (35%), and driving while intoxicated (35%); and about a third (32%) received some form of treatment.ConclusionsOver a 1-year period, we located 60% of individuals last seen an average of 23 years ago. The majority of contacted individuals were interviewed and willing to be evaluated again. Although the proportion of individuals currently drinking diminished with age, subjects exhibited troublesome levels of alcohol consumption and problems. Our findings suggest the importance and feasibility of a more comprehensive follow-up.

Background and aimsFew studies have explored how polygenic propensity to cannabis use unfolds across development, and no studies have yet examined this question in the context of environmental contributions such as peer cannabis use. Outlining the factors that contribute to progression from cannabis initiation to problem use over time may ultimately provide insights into mechanisms for targeted interventions. We sought to examine the relationships between polygenic liability for cannabis use, cannabis use trajectories from ages 12-30 years and perceived peer cannabis use at ages 12-17 years.DesignMixed-effect logistic and linear regressions were used to examine associations between polygenic risk scores, cannabis use trajectory membership and perceived peer cannabis use.SettingUnited States.ParticipantsFrom the Collaborative Study on the Genetics of Alcoholism (COGA) study, a cohort of 1167 individuals aged 12-26 years at their baseline (i.e. first) interview.MeasurementsKey measurements included life-time cannabis use (yes/no), frequency of past 12-month cannabis use, maximum life-time frequency of cannabis use, cannabis use disorder (using DSM-5 criteria) and perceived peer cannabis use. Polygenic risk scores (PRS) were created using summary statistics from a large (n = 162 082) genome-wide association study (GWAS) of cannabis use.FindingsThree trajectories reflecting no/low (n = 844), moderate (n = 137) and high (n = 186) use were identified. PRS were significantly associated with trajectory membership [P = 0.002-0.006, maximum conditional R2  = 1.4%, odds ratios (ORs) = 1.40-1.49]. Individuals who reported that most/all of their best friends used cannabis had significantly higher PRS than those who reported that none of their friends were users [OR = 1.35, 95% confidence interval (CI) = 1.04, 1.75, P = 0.023]. Perceived peer use itself explained up to 11.3% of the variance in trajectory class membership (OR = 1.50-4.65). When peer cannabis use and the cannabis use PRS were entered into the model simultaneously, both the PRS and peer use continued to be significantly associated with class membership (P

A multistage model of drug addiction in which individuals' motivations for use change as they develop problems is widely accepted; however, the evidence for this model comes mostly from animal work and cross-sectional studies. We used longitudinal data to test whether positive and negative reinforcement associated with alcohol consumption differed as a function of alcohol dependence (AD). Specifically, we tested whether (a) positive reinforcement is more strongly associated with alcohol consumption than is negative reinforcement among individuals without AD, (b) negative reinforcement is more strongly associated with AD than is positive reinforcement, and (c) in the presence of AD, the association between positive reinforcement and alcohol consumption becomes weaker, whereas the association with negative reinforcement becomes stronger. We included assessments between Ages 18 and 30 years from participants who indicated they ever had a drink (N = 2,556; 51.6% female) from the Collaborative Study on the Genetics of Alcoholism Prospective Study. Results from generalized estimating equations indicated that positive, but not negative, reinforcement was associated with alcohol consumption among individuals without AD. Both positive and negative reinforcement were associated with AD, but the association was stronger with negative reinforcement. Results from the multilevel growth model indicated that the association between negative reinforcement and alcohol consumption became stronger with the presence of AD, whereas the association between positive reinforcement and alcohol consumption did not differ as a function of AD. We provide empirical evidence that positive and negative reinforcement are differentially associated with alcohol consumption as a function of AD. (PsycINFO Database Record (c) 2019 APA, all rights reserved).

Genetic predispositions play an important role in the development of internalizing and externalizing behaviors. Understanding the mechanisms through which genetic risk unfolds to influence these developmental outcomes is critical for developing prevention and intervention efforts, capturing key elements of Irv's research agenda and scientific legacy. In this study, we examined the role of parenting and personality in mediating the effect of genetic risk on adolescents' major depressive disorder and conduct disorder symptoms. Longitudinal data were drawn from a sample of 709 European American adolescents and their mothers from the Collaborative Studies on Genetics of Alcoholism. Results from multivariate path analysis indicated that adolescents' depressive symptoms genome-wide polygenic scores (DS_GPS) predicted lower parental knowledge, which in turn was associated with more subsequent major depressive disorder and conduct disorder symptoms. Adolescents' DS_GPS also had indirect effects on these outcomes via personality, with a mediating effect via agreeableness but not via other dimensions of personality. Findings revealed that the pattern of associations was similar across adolescent gender. Our findings emphasize the important role of evocative gene-environment correlation processes and intermediate phenotypes in the pathways of risk from genetic predispositions to complex adolescent outcomes.

Background and aimsParental alcohol use disorders (AUDs) and parental separation are associated with increased risk for early use of alcohol in offspring, but whether they increase risks for early use of other substances and for early sexual debut is under-studied. We focused on associations of parental AUDs and parental separation with substance initiation and sexual debut to (1) test the strength of the associations of parental AUDs and parental separation with time to initiation (age in years) of alcohol, tobacco and cannabis use and sexual debut and (2) compare the strength of association of parental AUD and parental separation with initiation.DesignProspective adolescent and young adult cohort of a high-risk family study, the Collaborative Study on the Genetics of Alcoholism (COGA).SettingSix sites in the United States.ParticipantsA total of 3257 offspring (aged 14-33 years) first assessed in 2004 and sought for interview approximately every 2 years thereafter; 1945 (59.7%) offspring had a parent with an AUD.MeasurementsDiagnostic interview data on offspring substance use and sexual debut were based on first report of these experiences. Parental life-time AUD was based on their own self-report when parents were interviewed (1991-2005) for most parents, or on offspring and other family member reports for parents who were not interviewed. Parental separation was based on offspring reports of not living with both biological parents most of the time between ages 12 and 17 years.FindingsParental AUDs were associated with increased hazards for all outcomes, with cumulative hazards ranging from 1.19 to 2.71. Parental separation was also an independent and consistent predictor of early substance use and sexual debut, with hazards ranging from 1.19 to 2.34. The strength of association of parental separation with substance initiation was equal to that of having two AUD-affected parents, and its association with sexual debut was stronger than the association of parental AUD in one or both parents.ConclusionsParental alcohol use disorders (AUDs) and parental separation are independent and consistent predictors of increased risk for early alcohol, tobacco and cannabis use and sexual debut in offspring from families with a high risk of parental AUDs.

Cytochrome P450 2A6 (CYP2A6) encodes the enzyme responsible for the majority of nicotine metabolism. Previous studies support that slow metabolizers smoke fewer cigarettes once nicotine dependent but provide conflicting results on the role of CYP2A6 in the development of dependence. By focusing on the critical period of young adulthood, this study examines the relationship of CYP2A6 variation and smoking milestones. A total of 1209 European American young adults enrolled in the Collaborative Study on the Genetics of Alcoholism were genotyped for CYP2A6 variants to calculate a previously well-validated metric that estimates nicotine metabolism. This metric was not associated with the transition from never smoking to smoking initiation nor with the transition from initiation to daily smoking (P > 0.4). But among young adults who had become daily smokers (n = 506), decreased metabolism was associated with increased risk of nicotine dependence (P = 0.03) (defined as Fagerström Test for Nicotine Dependence score ≥4). This finding was replicated in the Collaborative Genetic Study of Nicotine Dependence with 335 young adult daily smokers (P = 0.02). Secondary meta-analysis indicated that slow metabolizers had a 53 percent increased odds (OR = 1.53, 95 percent CI 1.11-2.11, P = 0.009) of developing nicotine dependence compared with normal metabolizers. Furthermore, secondary analyses examining four-level response of time to first cigarette after waking (>60, 31-60, 6-30, ≤5 minutes) demonstrated a robust effect of the metabolism metric in Collaborative Study on the Genetics of Alcoholism (P = 0.03) and Collaborative Genetic Study of Nicotine Dependence (P = 0.004), illustrating the important role of this measure of dependence. These findings highlight the complex role of CYP2A6 variation across different developmental stages of smoking behaviors.

Background and aimsStudies that have included family history of alcohol use disorder (AUD) as a predictor of remission from AUD have yielded few significant results. The goals of this study were to estimate the association of persistent AUD, non-abstinent remission and abstinent remission ('AUD/remission status') in a proband with AUD/remission status in a relative and to test whether this association differed in related and unrelated proband-relative pairs.DesignHigh-risk family study of alcohol dependence. Probands were recruited from treatment settings and relatives were invited to participate. Baseline assessments occurred between 1991 and 1998 with follow-up between 1996 and 2005. Half of probands were matched with a biological 1st-degree relative with life-time AUD (related group) and half of probands were paired with an unrelated individual with life-time AUD (unrelated group).SettingBrooklyn, New York; Indianapolis, Indiana; Iowa City, Iowa; San Diego, California; Farmington, Connecticut; and St Louis, Missouri, USA.ParticipantsA total of 606 probands (25.7% female, mean age 37.7) with baseline and follow-up data and 606 of their 1st-degree relatives who had life-ime AUDs (45.8% female, mean age 36.2 years).MeasurementsPersistent AUD, non-abstinent remission and abstinent remission were based on self-report interview data on most recent AUD symptoms and alcohol consumption. Dependent variable was relatives' AUD/remission status. Independent variable was probands' AUD/remission status.FindingsA total of 34.6% of probands and 20.6% of relatives were abstinent and 11.1% of probands and 22.8% of relatives were in non-abstinent remission. AUD/remission status was correlated significantly in related (r = 0.23, P = 0.0037) but not in unrelated pairs. A significant interaction of probands' abstinent remission with a variable representing related (versus unrelated, P = 0.003) pairs suggested a familial association for abstinent remission. In related pairs, individuals with an abstinent proband were more likely to be abstinent themselves than were individuals whose proband had persistent AUD [relative risk ratio = 3.27, 95% confidence interval (CI) = 1.56-6.85, P = 0.002]; this association was not significant in unrelated pairs.ConclusionsThe likelihood of abstinent remission among people with alcohol use disorder appears to be more than three times greater for individuals who are related to an abstinent proband versus those related to a proband with persistent alcohol use disorder.

BackgroundAll stages of development of alcohol use disorder (AUD) have not been equally studied. While initiation of drinking has been given considerable attention, other stages have not been as thoroughly investigated. It is not clear whether the same factors are associated consistently across early and late transitions in AUD involvement. High-risk family samples that are enriched for AUD vulnerability and transitions in AUD development offer an opportunity to examine influences across multiple stages of AUD development.MethodsData from adolescents and young adults from high-risk families were used to study 4 transitions in AUD development-time to first drink, first drink to first problem, first drink to first diagnosis, and first problem to first diagnosis. Cox modeling was used to compare associations of parental AUD, parental separation, peer substance use, offspring ever-use of cannabis, trauma exposures, and internalizing and externalizing psychopathology across transitions.ResultsHazards of most transitions were elevated for those who had ever used cannabis, those who attributed substance use to their peers, those with externalizing disorders, and those with parents with AUD. Many risk factors were linked to early initiation of alcohol, particularly cannabis use. Internalizing disorders were associated with later stages. Nonassaultive trauma was associated only with early initiation; assaultive trauma was not associated with any transition.ConclusionsIn this large, ethnically diverse sample of high-risk youth, significant influences across transitions were fairly consistent, with externalizing disorders and cannabis ever-use elevating the likelihood of each stage, and peer and parental (and especially maternal AUD) influences linked to initiation and some later stages. Finally, in light of the increasingly permissive legal and social stances toward cannabis in the United States, the marked elevations of all alcohol outcomes observed for cannabis use underscore the importance of studying the underpinnings of this relationship.

Classical guitar ensembles are increasing in the United States as popular alternatives to band, choir, and orchestra. Classical guitar ensembles are offered at many middle and high schools as fine arts electives as one of the only options for classical guitarists to participate in ensembles. The purpose of this study was to explore the development of self-perceptions and skill acquisition of students in classical guitar ensembles. Participants included 14 classical guitar students ages 7-15 years in a university music outreach program. All students took weekly private classical guitar lessons and guitar ensemble classes from graduate music students. Systematic observation of 220 minutes of video data collected over a 12-week period was used to determine whether students demonstrated music skills associated with good tone and playing in time in an ensemble. All students took either the Self-Perception Profile for Children (Harter, 1985) for ages 7-13 years or the Self-Perception Profile for Adolescents (Harter, 1988) for ages 14-18 years. These surveys were administered at the end of the 12-week period. Participants answered approximately 40 questions using a forced-choice four-point Likert-like scale. All students answered questions related to student perceptions of their scholastic competence, social acceptance, athletic competence, physical appearance, behavioral conduct, and global self-worth. Results were compared to similar questions students answered about the importance of each subscale to determine discrepancies between their competence, importance and global self-worth scores. Ensemble instructors answered similar questions on their perceptions of their students for reliability purposes. Students also took a short multiple-choice questionnaire designed by the researcher on their musical experience, practicing behaviors and musical preferences. [Paper presented at the Annual Meeting of the Texas Music Educators Association (San Antonio, TX, Feb 2012).]

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 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 controlling 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.

BackgroundAdolescent drinking is an important public health concern, one that is influenced by both genetic and environmental factors. The functional variant rs1229984 in alcohol dehydrogenase 1B (ADH1B) has been associated at a genome-wide level with alcohol use disorders in diverse adult populations. However, few data are available regarding whether this variant influences early drinking behaviors and whether social context moderates this effect. This study examines the interplay between rs1229984 and peer drinking in the development of adolescent drinking milestones.MethodsOne thousand five hundred and fifty European and African American individuals who had a full drink of alcohol before age 18 were selected from a longitudinal study of youth as part of the Collaborative Study on the Genetics of Alcoholism (COGA). Cox proportional hazards regression, with G × E product terms in the final models, was used to study 2 primary outcomes during adolescence: age of first intoxication and age of first DSM-5 alcohol use disorder symptom.ResultsThe minor A allele of rs1229984 was associated with a protective effect for first intoxication (HR = 0.56, 95% CI 0.41 to 0.76) and first DSM-5 symptom (HR = 0.45, 95% CI 0.26 to 0.77) in the final models. Reporting that most or all best friends drink was associated with a hazardous effect for first intoxication (HR = 1.81, 95% CI 1.62 to 2.01) and first DSM-5 symptom (HR = 2.17, 95% 1.88 to 2.50) in the final models. Furthermore, there was a significant G × E interaction for first intoxication (p = 0.002) and first DSM-5 symptom (p = 0.01). Among individuals reporting none or few best friends drinking, the ADH1B variant had a protective effect for adolescent drinking milestones, but for those reporting most or all best friends drinking, this effect was greatly reduced.ConclusionsOur results suggest that the risk factor of best friends drinking attenuates the protective effect of a well-established ADH1B variant for 2 adolescent drinking behaviors. These findings illustrate the interplay between genetic and environmental factors in the development of drinking milestones during adolescence.

BackgroundMeasures of social context, such as marriage and religious participation, are associated with remission from alcohol use disorders (AUDs) in population-based and treatment samples, but whether these associations hold among individuals at high familial risk for AUD is unknown. This study tests associations of measures of social context and treatment with different types of remission from DSM-5 AUD in a high-risk sample.MethodsSubjects were 686 relatives of probands (85.7% first-degree) who participated in a high-risk family study of alcohol dependence. All subjects met criteria for AUD at baseline and were re-interviewed 5 years later. Follow-up status was categorized as persistent AUD, high-risk drinking, remitted low-risk drinking, and abstinence. Social context measures were defined as stable or changing from baseline to follow-up, and their bivariate and multivariate associations with follow-up status were tested.ResultsAt follow-up, 62.8% of subjects had persistent AUD, 6.4% were high-risk drinkers, 22.2% were remitted low-risk drinkers, and 8.6% were abstinent. Birth of first child during the interval was the only measure of social context associated with remitted low-risk drinking and was significant for women only. Abstinent remission was characterized by being stably separated or divorced for women, new marriage for both sexes, experiencing low levels of family support and high levels of friend support, and receiving treatment. High-risk drinkers were more likely than individuals with persistent AUD to have a stable number of children and to have been recently unemployed.ConclusionsThe social contexts accompanying different types of remission in this high-risk sample resemble those found in population-based and clinical samples. Low-risk drinkers resemble natural remitters from population-based samples who change their drinking habits with life transitions. Abstainers resemble clinical samples in marital context, support from friends, and treatment. High-risk drinkers appear to continue to experience negative consequences of heavy drinking.

BackgroundWe explore the factor structure of DSM-5 cannabis use disorders, examine its prevalence across European- and African-American respondents as well as its genetic underpinnings, utilizing data from a genome-wide study of single nucleotide polymorphisms (SNPs). We also estimate the heritability of DSM-5 cannabis use disorders explained by these common SNPs.MethodsData on 3053 subjects reporting a lifetime history of cannabis use were utilized. Exploratory and confirmatory factor analyses were conducted to create a factor score, which was used in a genome-wide association analysis. p-values from the single SNP analysis were examined for evidence of gene-based association. The aggregate effect of all SNPs was also estimated using Genome-Wide Complex Traits Analysis.ResultsThe unidimensionality of DSM-5 cannabis use disorder criteria was demonstrated. Comparing DSM-IV to DSM-5, a decrease in prevalence of cannabis use disorders was only noted in European-American respondents and was exceedingly modest. For the DSM-5 cannabis use disorders factor score, no SNP surpassed the genome-wide significance testing threshold. However, in the European-American subsample, gene-based association testing resulted in significant associations in 3 genes (C17orf58, BPTF and PPM1D) on chromosome 17q24. In aggregate, 21% of the variance in DSM-5 cannabis use disorders was explained by the genome-wide SNPs; however, this estimate was not statistically significant.ConclusionsDSM-5 cannabis use disorder represents a unidimensional construct, the prevalence of which is only modestly elevated above the DSM-IV version. Considerably larger sample sizes will be required to identify individual SNPs associated with cannabis use disorders and unequivocally establish its polygenic underpinnings.

Background: Researchers have identified genetic and neural risk factors for externalizing behaviors. However, it has not yet been determined if genetic liability is conferred in part through associations with more proximal neurophysiological risk markers. Methods: Participants from the Collaborative Study on the Genetics of Alcoholism, a large, family-based study of alcohol use disorders were genotyped and polygenic scores for externalizing (EXT PGS) were calculated. Associations with target P3 amplitude from a visual oddball task (P3) and broad endorsement of externalizing behaviors (indexed via self-report of alcohol and cannabis use, and antisocial behavior) were assessed in participants of European (EA; N = 2851) and African ancestry (AA; N = 1402). Analyses were also stratified by age (adolescents, age 12–17 and young adults, age 18–32). Results: The EXT PGS was significantly associated with higher levels of externalizing behaviors among EA adolescents and young adults as well as AA young adults. P3 was inversely associated with externalizing behaviors among EA young adults. EXT PGS was not significantly associated with P3 amplitude and therefore, there was no evidence that P3 amplitude indirectly accounted for the association between EXT PGS and externalizing behaviors. Conclusions: Both the EXT PGS and P3 amplitude were significantly associated with externalizing behaviors among EA young adults. However, these associations with externalizing behaviors appear to be independent of each other, suggesting that they may index different facets of externalizing. [ABSTRACT FROM AUTHOR]

This review describes the genetic approaches and results from the family‐based Collaborative Study on the Genetics of Alcoholism (COGA). COGA was designed during the linkage era to identify genes affecting the risk for alcohol use disorder (AUD) and related problems, and was among the first AUD‐focused studies to subsequently adopt a genome‐wide association (GWAS) approach. COGA's family‐based structure, multimodal assessment with gold‐standard clinical and neurophysiological data, and the availability of prospective longitudinal phenotyping continues to provide insights into the etiology of AUD and related disorders. These include investigations of genetic risk and trajectories of substance use and use disorders, phenome‐wide association studies of loci of interest, and investigations of pleiotropy, social genomics, genetic nurture, and within‐family comparisons. COGA is one of the few AUD genetics projects that includes a substantial number of participants of African ancestry. The sharing of data and biospecimens has been a cornerstone of the COGA project, and COGA is a key contributor to large‐scale GWAS consortia. COGA's wealth of publicly available genetic and extensive phenotyping data continues to provide a unique and adaptable resource for our understanding of the genetic etiology of AUD and related traits. [ABSTRACT FROM AUTHOR]

Retrospective childhood attention-deficit/hyperactivity disorder (ADHD) symptoms are required to diagnosis adult ADHD, but the validity of self-rated symptoms across time is questionable. Here, boys with ADHD-related problems, their brothers without ADHD, and former schoolmates rated themselves during young adulthood for ages 9, 14, and 19. Brothers rated probands retrospectively at the same ages. The young adults referred as children for ADHD (a) acknowledged childhood symptoms; (b) described improvement over time; (c) did not differ from brothers or controls on most self-ratings of young adult symptoms; (d) rated themselves as more symptomatic at age 9, but less symptomatic at age 19, than their brothers rated them; and (e) agreed only to some degree with brothers' ratings of probands' aggression (median correlation = 0.22). Probands' ratings showed limited agreement with judges' symptom ratings (median correlation = 0.16) and young adult follow-up examiners' ratings (median correlation = 0.14). These findings are not accounted for solely by changes in informants, nor by the course of ADHD psychopathology. They suggest some stability but limited internal consistency and validity for retrospective ADHD ratings by probands and brothers.

Objective: The aim of this study was to examine the abbreviated Desires for Alcohol Questionnaire (DAQ) with respect to component structure and concurrent validity. Method: The DAQ was administered to 2,960 adults participating in the Collaborative Studies on the Genetics of Alcohol. Rotated principal components analysis was conducted on 1,500 subjects with an alcohol-use disorder (AUD) and on 1,460 non-AUD subjects. Total DAQ scores were compared for these two subsamples. In addition, correlations were computed between DAQ scores and the following: (1) a sum of alcohol symptoms, and (2) endorsement of a single interview craving question. Results: Similar solutions emerged in the AUD and non-AUD subsamples, with dimensions characterized by (1) strong desires/intentions to drink, (2) negative reinforcement, and (3) positive reinforcement + ability to control drinking. Each component was significantly correlated with the alcohol symptom scale in both subsamples ([r.sub.s] = .25-.64 and .31-.40, respectively, p < .0001) and with the interview craving item in the AUD subsample ([r.sub.s] = .22-.55, p < .0001). Total DAQ score was significantly higher for AUD subjects (40.5) than for non-AUD subjects (23.1, p < .0001) and exhibited significant correlations with the alcohol symptom scale in the AUD and non-AUD subsamples ([r.sub.s] = .61 and .39, respectively, p < .0001) and with the interview craving item in the AUD subsample ([r.sub.s] = .51, p < .0001). Conclusions: The DAQ is an appropriate measure of alcohol craving, as demonstrated by similar component structures across two samples as well as its concurrent validity. (J. Stud. Alcohol Drugs, 71, 150-155, 2010), CRAVING HAS LONG BEEN CONSIDERED central to alcohol dependence (Drummond, 2001). It is the first criterion listed for International Classification of Diseases-10 alcohol dependence syndrome (World Health Organization, 1992), and [...]

Objective: The aim of this study was to compare the prevalence of psychiatric diagnoses when the Semi-Structured Assessment for the Genetics of Alcoholism (SSAGA-II) interview was administered in person with the prevalence when the SSAGA-II was conducted by telephone. Method: As part of the Collaborative Studies on the Genetics of Alcoholism, SSAGAs were administered either by telephone (n = 1,294) or in person (n = 1,484) to adult relatives of probands (42.3% male). The two modes of interview were compared with respect to reported lifetime prevalence of (1) Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV) alcohol dependence; (2) other DSM-IV substance-dependence diagnoses (nicotine, marijuana, cocaine, opioid, stimulant, sedative); and (3) DSM-IV nonsubstance diagnoses (i.e., antisocial personality disorder, major depressive disorder, mania, panic, social phobia, obsessive-compulsive disorder, and generalized anxiety disorder). These analyses took into account the potential confounds of gender, age, race, education, income, marital status, and potential within-family correlation. Results: Diagnostic prevalence rates for alcohol dependence and major depressive disorder were lower for telephone interviews than for in-person interviews (7% and 2%, respectively); there were no other significant differences. Conclusions: When circumstances dictate (e.g., subject out of area, subject preference), telephone administration of the SSAGA should be considered., AN INTERVIEW CONDUCTED BY TELEPHONE costs less than one administered in person (Weeks et al., 1983), and the accumulated savings can be considerable for large-scale research projects. In addition, the [...]

Objective: The goal of this study was to identify predictors of problematic young adult alcohol use. Method: The sample consisted of 141 subjects (81 females) participating in a national study of genetic risk factors for alcoholism. All subjects were evaluated first as children or adolescents, then approximately 5 years later as young adults. Outcome consisted of the number of alcohol symptoms (0-10) endorsed at this second time point. Predictors of outcome were drawn from five domains representing: (1) Demographic Characteristics, (2) Child/Adolescent Problematic Alcohol Use, (3) Biological Risk, (4) Externalizing Behaviors, and (5) Family Environment. A two-stage analytic strategy was used in which (1) separate multiple regression analyses were conducted within each of the five domains and (2) statistically significant predictors of problematic alcohol use from each domain were combined into one regression model to determine which remained significant. Results: In the final model, 31% of the variance in the number of alcohol symptoms in young adulthood was predicted by a high number of alcohol symptoms in childhood and adolescence, low initial sensitivity to alcohol, and a negative child/adolescent relationship with the father. Conclusions: These results demonstrated that GABRA2--originally associated with a diagnosis of alcohol dependence in adults--also predicted the onset of symptoms among subjects in their 20s, confirmed specific hypotheses about three other predictors in the final model, and suggested the utility of incorporating biological and nonbiological predictors to optimally predict young adult alcohol problems., ALCOHOL-USE DISORDERS (AUDs; American Psychiatric Association, 2000) are complex phenomena, with a wide range of contributing factors. Twin studies suggest that approximately half of the variance in alcohol dependence is [...]

Objective: The aim of this study was to compare psychiatric diagnoses based on interview information with those based on best-estimate procedures, to evaluate information used in such procedures, and to use 5-year follow-up data to determine whether the best-estimate diagnosis is an improvement over the interview-based diagnosis. Method: Psychiatric diagnoses were based on interview reports from 373 probands and 2,615 relatives participating in a high-risk family study of alcoholism. The diagnosis also included clinician ratings in a best-estimate procedure of this study. Results: For most diagnoses, both sensitivity and specificity, using the best-estimate diagnosis (BED) as the gold standard, were excellent, in both relatives and probands. Substance abuse was an exception, with very low sensitivity, although specificity rates were excellent. For nonsubstance diagnoses, specificity was high, but sensitivity ranged from 59% to 84% across relatives and probands. In general, BED procedures led to higher prevalence estimates than those from the interview only. In the BED process, family history data were especially useful for conduct and antisocial personality disorders. Follow-up interview data supported the fact that BED procedures led to both enhancements of, as well as errors in, diagnosis. Conclusions: Our data attest to the utility of family history information, particularly for antisocial personality disorder and conduct disorder, and indicate that, for the phenotype of substance-dependence disorder, an interview-based diagnosis alone is adequate in classifying individuals with a minimum of error. These results should be reassuring for research studies in which costs and resources required for best-estimate procedures are not affordable., THE BEST-ESTIMATE DIAGNOSTIC PROCEDURE has been recognized as an important element in the assessment protocol of a psychiatric genetics study (Baron et al., 1990; Merikangas et al., 1989; Weissman et [...]