Codevelopment Between Key Personality Traits and Alcohol Use Disorder From Adolescence Through Young Adulthood

ObjectivePersonality traits related to negative emotionality and low constraint are strong correlates of alcohol use disorder (AUD), but few studies have evaluated the prospective interplay between these traits and AUD symptoms from adolescence to young adulthood.MethodThe Minnesota Twin Family Study (N = 2,769) was used to examine the developmental interplay between AUD symptoms and three personality measures of constraint, negative emotionality, and aggressive undercontrol from ages 17 to 29.ResultsResults from random‐intercept, cross‐lagged panel models showed that low constraint and aggressive undercontrol predicted subsequent rank‐order increases in AUD symptoms from ages 17 to 24. AUD symptoms did not predict rank‐order change in these traits from ages 17 to 24. There was support for both cross‐effects from ages 24 to 29. Biometric analysis of the twin data showed genetic influences accounted for most of the phenotypic correlations over time.ConclusionResults are consistent with the notion that personality traits related to low constraint and aggressive undercontrol are important vulnerability/predisposition factors for the development of early adult AUD. In later young adulthood, there is more evidence for the simultaneous codevelopment of personality and AUD. Implications are addressed with attention to personality‐based risk assessments and targeted AUD prevention approaches.Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/142935/1/jopy12311.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/142935/2/jopy12311_am.pd

A Genetic Epidemiological Mega Analysis of Smoking Initiation in Adolescents

Introduction. Previous studies in adolescents were not adequately powered to accurately disentangle genetic and environmental influences on smoking initiation across adolescence. Methods. Mega-analysis of pooled genetically informative data on smoking initiation was performed, with structural equation modeling, to test equality of prevalence and correlations across cultural backgrounds, and to estimate the significance and effect size of genetic and environmental effects according to the classical twin study, in adolescent male and female twins from same-sex and opposite-sex twin pairs (N=19 313 pairs) between age 10 and 19, with 76 358 longitudinal assessments between 1983 and 2007, from 11 population-based twin samples from the US, Europe and Australia. Results. Although prevalences differed between samples, twin correlations did not, suggesting similar etiology of smoking initiation across developed countries. The estimate of additive genetic contributions to liability of smoking initiation increased from approximately 15% to 45% from age 13 to 19. Correspondingly, shared environmental factors accounted for a substantial proportion of variance in liability to smoking initiation at age 13 (70%) and gradually less by age 19 (40%). Conclusions. Both additive genetic and shared environmental factors significantly contribute to variance in smoking initiation throughout adolescence. The present study, the largest genetic epidemiological study on smoking initiation to date, found consistent results across 11 studies for the etiology of smoking initiation. Environmental factors, especially those shared by siblings in a family, primarily influence smoking initiation variance in early adolescence, while an increasing role of genetic factors is seen at later ages, which has important implications for prevention strategies. IMPLICATIONS: This is the first study to find evidence of genetic factors in liability to smoking initiation at ages as young as 12. It also shows the strongest evidence to date for decay of effects of the shared environment from early adolescence to young adulthood. We found remarkable consistency of twin correlations across studies reflecting similar etiology of liability to initiate smoking across different cultures and time periods. Thus familial factors strongly contribute to individual differences in who starts to smoke with a gradual increase in the impact of genetic factors and a corresponding decrease in that of the shared environment

The Developmental Progression of Age 14 Behavioral Disinhibition, Early Age of Sexual Initiation, and Subsequent Sexual Risk-taking Behavior

Background: Research has demonstrated a consistent relationship between early sexual experience and subsequent sexual risk-taking behaviors. We hypothesized that this relationship is due to a general predisposition toward behavioral disinhibition (BD), and that relationships among BD, early sex, and subsequent risky sexual behavior may be influenced by common genetic influences for males and common environmental influences for females. Methods: A prospective sample of 1,512 same-sex adolescent twins (50.2% female) was used. Adolescent BD was measured by clinical symptom counts of conduct disorder, oppositional defiant disorder, and self-reported delinquent behavior (age 14). Age of sexual initiation was defined as first age of consensual oral or penetrative sex (mean age ~17). Adult risky sexual behavior was defined by sexual behaviors under the influence of drugs and alcohol and number of casual sexual partners in the past year (age 24). Results: Multivariate analyses showed evidence for substantial common genetic variance among age 14 BD, age at sexual initiation, and adult risky sexual behavior for males, but not females. There was no significant difference in the degree of common environmental influence on these variables for females compared to males. Notably, age of sexual initiation was not significantly correlated with age 24 risky sexual behavior for females. Conclusion: The relationship between early sex and later risky sex can be better understood through a general liability toward BD, which is influenced primarily by genetic factors for males. The association between age 14 BD and age of sexual initiation was influenced through a combination of genetic and environmental factors for females; however, age of sexual initiation does not appear to be a salient predictor of adult women\u27s sexual risk-taking behavior. Findings suggest that prevention programs aimed at reducing sexual risk behavior might target youth exhibiting BD by age 14, particularly males. More research is needed on what predicts adult sexual risk-taking behavior for females

Co‐development of alcohol use problems and antisocial peer affiliation from ages 11 to 34: selection, socialization and genetic and environmental influences

Background and aimsSocial context is an important factor in determining the developmental trajectory of alcohol use. We examined the co‐development between alcohol use problems and antisocial peer affiliation. We also estimated the genetic and environmental influences on alcohol use problems, antisocial peer affiliation and their co‐development over time.DesignLongitudinal study using bivariate latent basis models with structured residuals (LBM‐SR). A biometric model was then fitted to estimate the genetic and environmental influences on the growth factors and their covariances.SettingThe United States mid‐west region.ParticipantsMembers of the Minnesota Twin Family Study (MTFS), an ongoing, longitudinal study of 3762 (52% female) twins (1881 pairs).MeasurementsAlcohol use problems were assessed using a composite measure of average number of drinks per occasion in the past 12 months, maximum number of drinks in 24 hours and DSM‐III‐R symptoms of alcohol abuse and dependence. Antisocial peer affiliation was measured by self‐report of the proportion of one’s friends who exhibited types of antisocial behaviors.FindingsThe LBM‐SR model revealed that there was a large correlation between the growth factors for alcohol use problems and antisocial peer affiliation [r = 0.78, 95% confidence interval (CI) = 0.76, 0.80] and cross‐lagged effects consistent with both selection and socialization effects. Additionally, antisocial peer affiliation in adolescence was associated with greater increases in alcohol use problems over time (r = 0.57, 95% CI = 0.54, 0.60). Genetic influences largely accounted for the association between antisocial peer affiliation in pre‐adolescence and growth in alcohol use problems, while shared environmental influences accounted for the correlation between antisocial peer affiliation and alcohol use problems growth factors.ConclusionsAntisocial peer affiliation in adolescence appears to be a salient, genetically influenced risk factor for early alcohol use and increase in alcohol use from adolescence to young adulthood.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/168476/1/add15402_am.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/168476/2/add15402.pd