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This study explores the relationship between alcohol dependence and humor styles based on a large data set of 2752 adults. Participants completed a humor styles questionnaire, assessing four dimensions: affiliative, self-enhancing, aggressive, and self-defeating. Participants also completed a telephone survey assessing their lifetime use and problems with alcohol. The survey classified individuals as meeting or failing to meet the DSM-IV definition of alcohol dependence. Logistic regression analyses in predicting alcohol dependence categorization resulted in a 95.6% correct classification and two significant predictors: being a man and aggressive humor style scores. These results show that those who characteristically engage in an aggressive humor style, are more likely to meet the criteria for alcohol dependence., Author(s): Julie Aitken Schermer [sup.1] , Marisa L. Kfrerer [sup.2] , Michael T. Lynskey [sup.3] Author Affiliations: (1) grid.39381.30, 0000 0004 1936 8884, Management and Organizational Studies, Faculty of Social [...]

Liability to alcohol dependence (AD) is heritable, but little is known about its complex polygenic architecture or its genetic relationship with other disorders. To discover loci associated with AD and characterize the relationship between AD and other psychiatric and behavioral outcomes, we carried out the largest genome-wide association study to date of DSM-IV-diagnosed AD. Genome-wide data on 14,904 individuals with AD and 37,944 controls from 28 case-control and family-based studies were meta-analyzed, stratified by genetic ancestry (European, n = 46,568; African, n = 6,280). Independent, genome-wide significant effects of different ADH1B variants were identified in European (rs1229984; P = 9.8 × 10-13) and African ancestries (rs2066702; P = 2.2 × 10-9). Significant genetic correlations were observed with 17 phenotypes, including schizophrenia, attention deficit-hyperactivity disorder, depression, and use of cigarettes and cannabis. The genetic underpinnings of AD only partially overlap with those for alcohol consumption, underscoring the genetic distinction between pathological and nonpathological drinking behaviors.

The mu1 opioid receptor gene, OPRM1, has long been a high-priority candidate for human genetic studies of addiction. Because of its potential functional significance, the non-synonymous variant rs1799971 (A118G, Asn40Asp) in OPRM1 has been extensively studied, yet its role in addiction has remained unclear, with conflicting association findings. To resolve the question of what effect, if any, rs1799971 has on substance dependence risk, we conducted collaborative meta-analyses of 25 datasets with over 28,000 European-ancestry subjects. We investigated non-specific risk for "general" substance dependence, comparing cases dependent on any substance to controls who were non-dependent on all assessed substances. We also examined five specific substance dependence diagnoses: DSM-IV alcohol, opioid, cannabis, and cocaine dependence, and nicotine dependence defined by the proxy of heavy/light smoking (cigarettes-per-day >20 vs. ≤ 10). The G allele showed a modest protective effect on general substance dependence (OR = 0.90, 95% C.I. [0.83-0.97], p value = 0.0095, N = 16,908). We observed similar effects for each individual substance, although these were not statistically significant, likely because of reduced sample sizes. We conclude that rs1799971 contributes to mechanisms of addiction liability that are shared across different addictive substances. This project highlights the benefits of examining addictive behaviors collectively and the power of collaborative data sharing and meta-analyses.

BackgroundCannabis users are highly likely to also be tobacco cigarette smokers and a proportion of this comorbidity is attributable to shared genetic influences. Three large meta-analyses of genomewide association studies (GWAS) of tobacco smoking have identified multiple genomewide significant (p

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.

Earlier studies have found an elevated risk for psychopathology and suicidal behavior associated with childhood sexual abuse (CSA); however, the degree to which risk is mediated by depression and posttraumatic stress disorder (PTSD) in women and men remains unclear. We examined these issues in data from a family study of childhood maltreatment (N = 2,559). We found significant CSA-associated risk for depression, PTSD, and suicidal behavior for women and men. In survival analyses controlling for these disorders, we observed persistent but somewhat reduced CSA-associated risk for suicidal ideation and suicide attempt. Our findings suggest that these disorders partially mediate CSA-associated risk.

Objective: To provide an overview of the genetic epidemiology of substance use and misuse in adolescents. Method: A selective review of genetically informative research strategies, their limitations, and key findings examining issues related to the heritability of substance use and substance use disorders in children and adolescents is presented. Results: Adoption, twin, and extended-family designs have established there is a strong heritable component to liability to nicotine, alcohol, and illicit drug dependence in adults. However, shared environmental influences are relatively stronger in youth samples and at earlier stages of substance involvement (e.g., use). There is considerable overlap in the genetic influences associated with the abuse/dependence across drug classes, and shared genetic influences contribute to the commonly observed associations between substance-use disorders and externalizing and, to a lesser extent, internalizing psychopathology. Rapid technologic advances have made the identification of specific gene variants that influence risks for substance-use disorders feasible, and linkage and association (including genomewide association studies) have identified promising candidate genes implicated in the development of substance-use disorders. Conclusions: Studies using genetically informative research designs, including those that examine aggregate genetic factors and those examining specific gene variants, individually and in interaction with environmental influences, offer promising avenues not only for delineating genetic effects on substance-use disorders but also for understanding the unfolding of risk across development and the interaction between environmental and genetic factors in the etiology of these disorders. (Contains 2 figures.)

Background and Aims: Previous studies have demonstrated associations between substance use and reduced educational attainment; however, many were unable to account for potential confounding factors like genetics and the rearing environment. In the few studies that controlled for these factors, the substances assessed were limited to alcohol, cannabis, and tobacco. To address these limitations, we examined the relationship between adolescent use of seven kinds of substances, the number of additional substances used, and high school noncompletion within a large sample of Australian twins. Design: A series of two‐level generalized mixed effects logistic regressions were conducted to examine associations between adolescent substance use and high school noncompletion. Setting: Australia. Participants: A total of 9579 adult Australian twins from two cohorts of the Australian Twin Registry. Measurements Assessments of high school completion, childhood major depression, conduct disorder symptoms, substance use initiation, demographics, and parental educational attainment using the Australian version of the Semi‐Structured Assessment for the Genetics of Alcoholism. Findings There were unique within‐twin‐pair effects of use of sedatives (odds ratio [OR] = 22.39 [95% confidence interval (CI) = 1.18–423.48]) and inhalants/solvents (OR = 10.46 [95% CI = 1.30–84.16]) on high school noncompletion. The number of substances used in adolescence was strongly associated with high school noncompletion across all discordant twin models (ORs from 1.50–2.32, Ps < 0.03). Conclusions: In Australia, adolescent substance use appears to be associated with early school dropout, with the effects of any given substance largely because of the confounding factors of parental education, childhood conduct disorder symptoms, and use of other substances. Sedatives and inhalants/solvents have effects on high school noncompletion that cannot be explained by polysubstance use or familial factors. [ABSTRACT FROM AUTHOR]