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Objective: This study aimed to determine the associations among paternal alcohol problems, separation, and educational attainment in European American and African American offspring and whether offspring early alcohol/tobacco/marijuana use influenced these associations.Method: Families with offspring ages 13-19 years at intake were selected from state birth records and screened by telephone to determine high-risk or low-risk status (with/without paternal heavy drinking). Families of men with two or more driving-under-the-influence offenses were added as a very-high-risk group. Data from 340 African American and 288 European American offspring who were not enrolled in school at their last interview were analyzed. Educational attainment was modeled as less than high school, high school only (reference category), and some college or higher. Separation was defined as offspring report of not having lived continuously in the same household with their biological father from birth to age 14. Analyses were stratified by race.Results: In European Americans, neither family risk status nor early alcohol/tobacco/marijuana use was associated with educational outcomes. However, paternal separation significantly elevated the likelihood of not completing high school in all models (relative risk ratios [RRRs] = 6.0-8.1, p <.001). For African American offspring, likelihoods of high school noncompletion were elevated marginally for paternal separation in only one model, but significantly for early marijuana use (RRRs = 2.8-3.2, p < .05). Very-high-risk status significantly reduced the likelihood of post-high school education in an adjusted model (RRR = 0.4, p < .05).Conclusions: High school noncompletion was significantly associated with paternal separation in European Americans and with early marijuana use in African American offspring. In addition, very-high-risk status reduced the likelihood of post-high school education in African American offspring only, suggesting that research with ethnically diverse samples yields important differences when examining outcomes of both separation and substance use on offspring education. [ABSTRACT FROM AUTHOR]

Objective: Cannabis use, particularly at an early age, has been linked to suicidal thoughts and behavior, but minimal work has examined the association between cannabis use and lifetime nonsuicidal self-injury (NSSI). The current study aims to characterize the overlap between lifetime and early cannabis use and NSSI and to examine genetic and environmental mechanisms of this association.Method: Adult male and female twins from the Australian Twin Registry (N = 9,583) were used to examine the odds of NSSI associated with lifetime cannabis use and early cannabis use (i.e., <17 years of age). These associations were also examined within monozygotic (MZ) twins discordant for cannabis use and MZ twins discordant for early cannabis use. Analyses were replicated in an independent sample of female twins (n = 3,787) accounting for the age at onset of cannabis use and NSSI.Results: Lifetime cannabis use (odds ratio [OR] = 2.84, 95% CI [2.23, 3.61]) and early cannabis use were associated with increased odds of NSSI (OR = 2.15, 95% CI [1.75, 2.65]), and this association remained when accounting for covariates. The association was only significant, however, in MZ twin pairs discordant for early cannabis use (OR = 3.20, 95% CI [1.17, 8.73]). Replication analyses accounting for the temporal ordering of cannabis use and NSSI yielded similar findings of nominal significance.Conclusions: Results suggest that NSSI is associated with cannabis involvement via differing mechanisms. For lifetime cannabis use, the lack of association in discordant pairs suggests the role of shared genes and family environment. However, in addition to such shared familial influences, person-specific and putatively causal factors contribute to the relationship between early cannabis use and NSSI. Therefore, delaying the onset of cannabis use may reduce exposure to influences that exacerbate vulnerabilities to NSSI. [ABSTRACT FROM AUTHOR]

Objective: The alcoholism research literature has long reported a significant, reliable, and inverse association between alcohol use disorders and religion/spirituality (R/S), and this is also evident in the period of highest risk--adolescence and young adulthood. In the treatment area, both clinical and mutual-help programs for alcohol use disorders often include a spiritual component, and outcome studies validate the efficacy of such programs. Even so, the alcoholism-R/S relationship is little understood. Method: The current study examined data from an existing sample of 4,002 female adolescents/young adults and their families. Data analyses examined five demographic, nine R/S, and eight risk-factor variables as predictors of five alcohol milestones: initial drink, first intoxication, regular use, heavy consumption, and alcohol dependence. Results: Results affirmed the known association between alcoholism risk factors and alcohol use milestones and also found moderate to strong associations between most R/S variables and these risk factors and milestones. A multivariate model simultaneously examining both sets of variables found that specific risk factors and specific R/S variables remained significant predictors of alcohol use milestones after accounting for all other variables. Mediation and moderation tests did not find evidence that R/S accounted for or qualified the relationship between alcohol risk factors and alcohol milestones. Conclusions: This study confirmed the multidimensional role of R/S influences within the etiological network of alcoholism risk and protective factors in adolescents/young adults and found R/S dimensions to be independent and substantial influences on alcohol use disorders rather than mediators or moderators of other risks. [ABSTRACT FROM AUTHOR]

Objective: The aim of this study was to examine the relationships between body mass index (BMI) and alcohol use and misuse in young adulthood in a sample of black and white female twins. Method: Cox proportional hazards and logistic regression models were used to examine the relationships between BMI category and first alcohol use, current weekly alcohol use, and current weekly heavy episodic drinking in 3,514 (14.06% black) young adult female twins. Analyses were conducted separately in black and white women. Results: After adjusting for relevant covariates, in white women obesity was protective against alcohol use (hazard ratio = 0.83; 95% confidence interval [CI]: 0.73-0.93) and against weekly drinking (odds ratio [OR] = 0.36; 95% CI: 0.24-0.53) and weekly heavy episodic drinking (OR = 0.51; 95% CI: 0.31-0.82) among ever drinkers compared with women of ideal weight. Overweight women living with their parents were less likely to be weekly drinkers (OR = 0.31; 95% CI: 0.16-0.61), whereas overweight women who were not living with their parents were less likely to be weekly heavy episodic drinkers (OR = 0.51; 95% CI: 0.31-0.82). Among black women, obesity was not associated with any of the drinking outcomes; however, black women who were overweight and who reported that the majority of their friends were not weekly drinkers had greater odds of reporting weekly drinking than those of ideal weight (OR = 2.91; 95% CI: 1.33-6.39). Conclusions: Obese white women were less likely to ever use alcohol, be weekly drinkers, or be weekly heavy episodic drinkers than their ideal-weight peers. Body weight may affect drinking behavior in young women, and this effect may differ by race. Future research is needed to identify mediators and moderators of this relationship as well as to explore racial differences in the effect of body weight on drinking behavior. [ABSTRACT FROM AUTHOR]

Objective: The purpose of this study was to develop a quantitative measure of alcohol consumption for gene-mapping studies. Method: Using a sample of 3,787 young-adult twin women and an independent sample of 489 men and women from a college drinking study, we developed an alcohol-consumption factor score indexed by (1) maximum typical consumption (log-transformed quantity frequency [LQNTFRQ]), (2) maximum drinks in a 24-hours period (LMAXALC), (3) frequency of drinking five or more drinks per day (FIVE), and (4) frequency of drinking to intoxication (INTOX). We tested (I) for factorial and psychometric equivalence across samples and genders; (2) for construct validity and its equivalence, across samples and genders, using measures of tobacco and cannabis use and family history of alcoholism; and (3) to determine the heritability of the alcohol-consumption factor score using a genetic psychometric model. Results: A single-factor model fit well with factor loadings ranging from .60 to .90. With rare exception, we found support for measurement invariance across the two samples and across genders. Measures of nicotine and cannabis use as well as family history of alcoholism were associated, to a similar extent across samples and genders, with the underlying alcohol-consumption factor. Psychometric twin modeling revealed that each of the alcohol-consumption measures (h² = 34%-47%) and the underlying factor score (h² = 50%) were heritable, with the remainder of the variance attributable to individual-specific environmental factors. This moderately heritable alcohol-consumption factor also accounted for a majority of the genetic variance in LQNTFRQ, LMAXALC, FIVE, and INTOX. Conclusions: Quantitative measures of alcohol consumption with the favorable attributes of measurement invariance, construct validity, and moderate heritability can greatly enhance future gene-mapping efforts, supplementing information afforded by conventional diagnostic measures of alcohol abuse/dependence. [ABSTRACT FROM AUTHOR]

Objective: Research indicates that low parental monitoring increases the risk for early substance use. Because low parental monitoring tends to co-occur with other familial and neighborhood factors, the specificity of the association is challenging to establish. Using logistic regression and propensity score analyses, we examined associations between low parental monitoring and early substance use in European American (EA) and African American (AA) girls, controlling for risk factors associated with low parental monitoring.Method: Participants were 3,133 EA and 523 AA girls from the Missouri Adolescent Female Twin Study with data on parental monitoring assessed via self-report questionnaire, and with ages at first use of alcohol, tobacco, and cannabis queried in at least one of three diagnostic interviews (median ages = 15, 22, and 24 years).Results: The rate of early alcohol use was greater in EA than AA girls, whereas the proportion of AA girls reporting low parental monitoring was higher than in EA girls. EA girls who experienced low parental monitoring were at elevated risk for early alcohol, tobacco, and cannabis use, findings supported in both logistic regression and propensity score analyses. Evidence regarding associations between low parental monitoring and risk for early substance use was less definitive for AA girls.Conclusions: Findings highlight the role of parental monitoring in modifying risk for early substance use in EA girls. However, we know little regarding the unique effects, if any, of low parental monitoring on the timing of first substance use in AA girls. [ABSTRACT FROM AUTHOR]

OBJECTIVE: Childhood sexual abuse (CSA) is associated with elevated risk of early marijuana use and cannabis use disorder (CUD). Both the prevalence of CSA and the course of marijuana use differ between African Americans and European Americans. The current study aimed to determine whether these differences manifest in racial/ ethnic distinctions in the association of CSA with early and problem use of marijuana. METHOD: Data were derived from female participants in a female twin study and a high-risk family study of substance use (n = 4,193, 21% African-American). Cox proportional hazard regression analyses using CSA to predict initiation of marijuana use and progression to CUD symptom(s) were conducted separately by race/ethnicity. Sibling status on the marijuana outcome was used to adjust for familial influences. RESULTS: CSA was associated with both stages of marijuana use in African-American and European-American women. The association was consistent over the risk period (hazard ratio [HR] = 1.57, 95% confidence interval [CI] [1.37, 1.79] for initiation; HR = 1.51, 95% CI [1.21, 1.88] for CUD symptom onset) in European-American women. In African-American women, the HRs for initiation were 2.52 (95% CI [1.52, 4.18]) before age 15, 1.82 (95% CI [1.36, 2.44]) at ages 15-17, and nonsignificant after age 17. In the CUD symptom model, CSA predicted onset only at age 21 and older (HR = 2.17, 95% CI [1.31, 3.59]). CONCLUSIONS: The association of CSA with initiation of marijuana use and progression to problem use is stable over time in European-Ameri-can women, but in African-American women, it varies by developmental period. FINDINGS suggest the importance of considering race/ethnicity in prevention efforts with this high-risk population. [ABSTRACT FROM AUTHOR]

Objective: Rates of alcohol dependence are elevated in women with eating disorders who engage in binge eating or compensatory behaviors compared with women with eating disorders who do not report binge eating or compensatory behaviors and with healthy controls. Alcohol dependence, binge eating, and compensatory behaviors are heritable; however, it is unclear whether a shared genetic liability contributes to the phenotypic association among these traits, and little information exists regarding this shared liability in men. We investigated genetic and environmental correlations among alcohol dependence, binge eating, and compensatory behaviors in male and female twins. Method: Participants included 5,993 same- and opposite-sex twins from the Australian Twin Registry who completed a modified version of the Semi-Structured Assessment for the Genetics of Alcoholism that assessed lifetime alcohol dependence and binge eating as defined in the Diagnostic and Statistical Manual of Mental Disorders, Third Edition, Revised. Compensatory behaviors were assessed via a general health questionnaire in women only. Biometrical twin models estimated genetic and environmental influences on alcohol dependence, binge eating, and compensatory behaviors. Results: In women, the multivariate twin model suggested that additive genetic and nonshared environmental effects influenced alcohol dependence, binge eating, and compensatory behaviors, with heritability estimates ranging from 38% to 53%. The best-fitting sex-limitation model was a common effects model that equated all genetic and nonshared environmental influences in men and women. The heritability estimates were 50% and 38% for alcohol dependence and binge eating, respectively. Overall, there were significant genetic correlations between alcohol dependence and binge eating, alcohol dependence and compensatory behaviors, and binge eating and compensatory behaviors. Conclusions: These findings indicate that common genetic factors may underlie the vulnerability to alcohol dependence and the liability to binge eating and compensatory behaviors. [ABSTRACT FROM AUTHOR]

Objective: Not only are substance-use disorders and externalizing disorders frequently comorbid, they often co-occur in families across generations. The current study examined the role of genetic and environmental influences in the relationship between paternal histories of drug dependence or alcohol dependence and offspring conduct disorder using an offspring-of-twins design. Method: Participants were male twins (n = 1,774) from the Vietnam Era Twin Registry, their offspring (n = 1,917), and mothers of the offspring (n = 1,202). Twins had a history of drug dependence, alcohol dependence, or neither. Based on the father's and his co-twin's drug-dependence or alcohol-dependence history and zygosity, risk groups were constructed to reflect different levels of genetic and environmental risk that were then used to predict offspring conduct disorder. Results: After controlling for potentially confounding variables, the offspring of men with a history of drug dependence or alcohol dependence had significantly higher rates of conduct disorder, compared with offspring of men without this history. Offspring at higher genetic risk had higher rates of conduct disorder. High-risk offspring at lower environmental risk had lower rates of conduct disorder but only in the case of paternal drug-dependence risk. Lower environmental risk did not influence rates of offspring conduct disorder when the father had an alcohol-dependence history. Conclusions: Genetic risk associated with both paternal drug-dependence and paternal alcohol-dependence histories predicted offspring conduct-disorder risk, but only risk associated with paternal drug-dependence history was mitigated by having a low-risk environment. These results demonstrated a significant gene-environment interaction effect. [ABSTRACT FROM AUTHOR]

Objective: It is not known if parental psychiatric disorders have an independent effect on offspring smoking after controlling for genetic and environmental vulnerability to nicotine dependence. We tested if parental alcohol, drug, or conduct disorders; antisocial personality disorder; depression; and anxiety disorders remained significant predictors of offspring smoking initiation, regular smoking, and nicotine dependence before and after adjusting for genetic and environmental risk for nicotine dependence. Method: Data were obtained via semi-structured interviews with 1,107 twin fathers, 1,919 offspring between the ages of 12 and 32, and 1,023 mothers. Genetic and environmental liability for smoking outcomes was defined by paternal and maternal nicotine dependence. Multinomial logistic regression models were computed to estimate the risk for offspring trying cigarettes, regular smoking, and the Fagerstrom Test for Nicotine Dependence (FTND) as a function of parental psychopathology and sociodemographics before and after adjusting for genetic and environmental vulnerability to nicotine dependence. Results: Before adjusting for genetic and environmental risk for nicotine dependence, ever trying cigarettes was associated with maternal depression, regular smoking was associated with maternal alcohol dependence and maternal conduct disorder, and FTND was associated with paternal and maternal conduct disorder and antisocial personality disorder. No parental psychopathology remained significantly associated with regular smoking and FTND after adjusting for genetic and environmental vulnerability to nicotine dependence in a multivariate model. Conclusions: The association between parental psychopathology and offspring smoking outcomes is partly explained by genetic and environmental risk for nicotine dependence. Point estimates suggest a trend for an association between parental antisocial personality disorder and offspring regular smoking and nicotine dependence after adjusting for genetic and environmental vulnerability. Studies in larger samples are warranted. [ABSTRACT FROM AUTHOR]