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Objectives. Our aim was to determine if the decrease in drug use disorders with age is attributable to changes in persistence, as implied by the notion of maturing out. Also, we examined the association between role transitions and persistence, recurrence, and new onset of drug use disorders. Methods. We performed secondary analysis of the 2 waves of the National Epidemiologic Survey on Alcohol and Related Conditions data (baseline assessment 2001-2002, follow-up conducted 2004-2005). We conducted logistic regressions and multinomial logistic regression to determine the effect of age on wave 2 diagnosis status, as well as the interaction between age and role transitions. Results. Rates of persistence were stable over the life span, whereas rates of new onset and recurrence decreased with age. Changes in parenthood, marital, and employment status were associated with persistence, new onset, and recurrence. We found an interaction between marital status and age. Conclusions. Our findings challenge commonly held notions that the age-related decrease in drug use disorders is attributable to an increase in persistence, and that the effects of role transitions are stronger during young, compared with middle and older, adulthood. [ABSTRACT FROM AUTHOR]

Clinical and population-based samples show high comorbidity between Substance Use Disorders (SUDs) and Axis II Personality Disorders (PDs). However, Axis II disorders are frequently comorbid with each other, and existing research has generally failed to distinguish the extent to which SUD/PD comorbidity is general or specific with respect to both specific types of PDs and specific types of SUDs. We sought to determine whether ostensibly specific comorbid substance dependence-Axis II diagnoses (e.g., alcohol use dependence and borderline personality disorder) are reflective of more pervasive or general personality pathology or whether the comorbidity is specific to individual PDs. Face-to-face interview data from Wave 1 and Wave 2 of the National Epidemiologic Survey on Alcohol and Related Conditions were analyzed. Participants included 34,653 adults living in households in the United States. We used hierarchical factor models to statistically partition general and specific personality disorder dimensions while simultaneously testing for specific PD-substance dependence relations. Results indicated that substance dependence-Axis II comorbidity is characterized by general (pervasive) pathology and by Cluster B PD pathology over and above the relationship to the general PD factor. Further, these relations between PD factors and substance dependence diagnoses appeared to largely account for the comorbidity among substance dependence diagnoses in the younger but not older participants. Our findings suggest that a failure to consider the general PD factor, which we interpret as reflecting interpersonal dysfunction, can lead to potential mischaracterizations of the nature of certain PD and SUD comorbidities. [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]

This study provides findings to assist in identifying factors that contribute to the current clinical and public health debate of the obesity epidemic. The study examined the genetics of adult-onset weight change in middle-aged male-male twins controlling for weight in early adulthood, lifetime history of tobacco use and alcohol dependence, and aimed to estimate the proportion of genetic factors that influence weight change between early adulthood and middle age in white middle-class males. The study was a classic longitudinal twin design and used Body Mass Index (BMI) for three waves of data collection from the Vietnam Era Twin Registry--induction physicals (approximately 1968), 1987 and 1990--or periods corresponding between young adulthood and middle age. Univariate heritability estimates for BMI at all three data periods were conducted as well as a Cholesky longitudinal genetic analysis for weight change controlling for BMI at military induction, smoking and alcohol use. Frequency data indicated that the sample was on average classified as normal BMI in their 20s; but BMI gradually increased during the next twenty years. Univariate data for each data period indicated that additive genetic factors accounted for between 63% and 69% of total variance in BMI. The Cholesky longitudinal genetic analysis of BMI87 and BMI90, controlling for BMI at military induction, indicated that more than half of the change in BMI from early adulthood to middle age remains heritable. No shared environmental factors were identified, thus the remainder of the variance was accounted for by nonshared, or unique, environmental factors and error. The data analysis suggests that treatments and public health interventions need to recognize the magnitude of genetic factors if short-term and long-term interventions are to be effective.

Many studies have found strong peer correlations for a variety of problem behaviors that begin in adolescence (e.g. substance use). Such correlations are commonly attributed to peer influences, but could also be explained by selective ('assortative') friendship: the tendency for those with similar patterns of behavior to become friends. Here we show how, under certain assumptions, cross-sectional data from pairs of siblings or twins and their peers may be used to resolve the contributions of peer selection and reciprocal peer environmental influences to peer resemblance. We performed power calculations to determine necessary sample sizes for rejecting with 80% power, at the 5% significance level, the hypothesis of only peer selection effects, or only reciprocal peer environmental effects. A false hypothesis of only selective friendship effects was always easier to reject than a false hypothesis of only reciprocal peer environmental influences. Limitations of these simulations, including uncertainty about the most appropriate way to model peer selection, are discussed.