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Introduction: Substance use and mood disorders account for about 10% of the global burden of disease and, among adolescents, are a significant source of disability. The present study examined whether additive genetic or shared environmental factors influenced the covariance of internalizing symptoms and cigarette use during adolescence when both of these problems begin to increase.Aims and Methods: We used data (n = 1230 pairs of twins) from the Virginia Twin Study of Adolescent Behavioral Development (mean age = 15.3) to decompose the variance of internalizing symptoms, cigarette initiation, and quantity of cigarettes smoked in a variance decomposition model that included a beta coefficient to allow for estimates of cigarette initiation to influence quantity of cigarettes smoked.Results: In biometric models we were able to equate all parameter estimates by sex. After identifying the best fitting model, parameter estimates were calculated and the significance of overlapping paths between internalizing symptoms and cigarette initiation were tested. After accounting for the genetic architecture of cigarette initiation and quantity smoked, the covariance between internalizing symptoms and cigarette use was accounted for by sex-specific shared and unique environmental factors.Conclusions: Among adolescents, the overlap in risk factors between internalizing symptoms and cigarette use is because of non-genetic, environmental factors. Further exploration of the environmental sources of variance involved in the onset of adolescents internalizing symptoms and cigarette use is warranted.Implications: We find that during adolescence common environmental factors influence the association between internalizing symptoms and cigarette use. Correlated vulnerabilities because of environmental sources between internalizing and cigarette use may be open to intervention and likely will influence the progression of internalizing and cigarette use. [ABSTRACT FROM AUTHOR]

Background: Shared experiences within families play an important role in the initiation of cigarette use among adolescents. Behavioral genetic studies using various samples have implicated that the shared environment that twins experience is an important source of influence on whether adolescents initiate cigarette use. Whether the special twin environment, in addition to the shared environment, contributes significantly to making twin siblings more similar in cigarette initiation, and whether the influence of the special twin environment persists into adulthood, is less clear.Methods: Data for this study came from the National Longitudinal Survey of Adolescent Health. Twin, full-, and half-sibling pairs between the ages of 12 and 33 were separated into three age groups, with about 3,000 individuals in each age group. The proportion of variance in cigarette use initiation explained by genetic, shared, special twin, and unique environmental factors were examined.Results: The results of separate age-moderated univariate variance decomposition models indicate that the special twin environment does not significantly contribute to the variance in cigarette use initiation in adolescence or young adulthood.Conclusion: Factors shared by individuals in a family, but that are not specific to being a twin, are important in determining whether adolescents will initiate the use of cigarettes. [ABSTRACT FROM AUTHOR]

Several “genetic” item-response theory (IRT) models are fitted to the responses of 1086 adolescent female twins to the 33 multi-category item Mood and Feeling Questionnaire relating to depressive symptomatology in adolescence. A Markov-chain Monte Carlo (MCMC) algorithm is used within a Bayesian framework for inference using Gibbs sampling, implemented in the program WinBUGS 1.4. The final model incorporated separate genetic and non-shared environmental traits (“A and E”) and item-specific genetic effects. Simpler models gave markedly poorer fit to the observations judged by the deviance information criterion (DIC). The common genetic factor showed major loadings on melancholic items, while the environmental factor loaded most highly on items relating to self-deprecation. The MCMC approach provides a convenient and flexible alternative to Maximum Likelihood for estimating the parameters of IRT models for relatively large numbers of items in a genetic context. Additional benefits of the IRT approach are discussed including the estimation of latent trait scores, including genetic factor scores, and their sampling errors. [ABSTRACT FROM AUTHOR]

The purpose of this study was to determine whether the observed phenotypic stability in static strength during adolescence, as measured by interage correlations in arm pull, is mainly caused by genetic and/or environmental factors. Subjects were from the Leuven Longitudinal Twin Study (n = 105 pairs, equally divided over 5 zygosity groups). Arm-pull data were aligned on age at peak height velocity to attenuate the temporal fluctuations in interage correlations caused by differences in timing of the adolescent growth spurt. Developmental genetic models were fitted using structural equation modeling. After the data were aligned on age at peak height velocity, the annual interage correlations conformed to a quasi-simplex structure over a 4-yr interval. The best-fitting models included additive genetic and unique environmental sources of variation. Additive genetic factors that already explained a significant amount of variation at previous measurement occasions explained 44.3 and 22.5% of the total variation at the last measurement occasion in boys and girls, respectively. Corresponding values for unique environmental sources of variance are 31.2 and 44.5%, respectively. In conclusion, the observed stability of static strength during adolescence is caused by both stable genetic influences and stable unique environmental influences in boys and girls. Additive genetic factors seem to be the most important source of stability in boys, whereas unique environmental factors appear to be more predominant in girls. [ABSTRACT FROM AUTHOR]

Purpose: To determine whether the observed phenotypic stability in explosive strength during adolescence, as measured by inter-age correlations in vertical jump (VTJ), is mainly caused by genetic and/or environmental factors. Methods: Subjects are from the Leuven Longitudinal Twin Study (LLTS) ( n = 105 pairs, equally divided over five zygosity groups). VTJ data were aligned on age at peak height velocity (APHV) to attenuate the temporal fluctuations in inter-age correlations caused by differences in timing of the adolescent growth spurt. Simplex models were fitted using structural equation modelling. Results: After aligning the data on APHV, the annual inter-age correlations show a clear simplex structure over a 4 year interval. The best fitting models included additive genetic and unique environmental sources of variation. Heritability estimates ranged between 60.8% (CI 37.7%–77.2%) and 87.3% (CI 74.2%–94.0%) for boys and between 76.5% (CI 56.7%–89.0%) and 88.6% (CI 77.8%–94.1%) for girls. Up to 56.4% and 62.8% of the total variation at the last measurement occasion is explained by additive genetic factors that already explained a significant amount of variation at previous measurement occasions in boys and girls respectively. It thus can be concluded that the observed stability of explosive strength during adolescence is mainly caused by a stable genetic influence in boys and girls. Conclusions: Additive genetic factors seem to be the main cause of the observed phenotypic stability in VTJ performance in boys and girls during adolescence. [ABSTRACT FROM AUTHOR]

Univariate and multivariate analyses of the genetic and environmental contributions to variance in adipose tissue and adipose tissue distribution were carried out in early adolescents. Stature, weight, body mass index (BMI), and five subcutaneous skinfolds were measured at half-yearly intervals in 105 MZ and DZ twin pairs from 10 to 14 years. The most parsimonious model, which provided an adequate explanation for variation in the BMI, five skinfolds, and the T/E ratio, included additive genetic and specific environmental factors. Multivariate analyses of the genetic architecture of subcutaneous fat indicated a general skinfold genetic factor, an extremity skinfold genetic factor, and skinfold specific genetic factors. This implies that all skinfolds are under control of the same set of genes, that a different set of genes partly controls extremity skinfolds, and that other genes have a small skinfold specific impact. Environmental contributions included a general skinfold environmental factor and skinfold specific environmental factors. BMI is under control of the same set of genes as skinfolds and shows high genetic correlations with trunk skinfolds, which implies that nearly the same genes may influence trunk skinfolds and the BMI. All models were fairly consistent across the age range. [ABSTRACT FROM AUTHOR]

Little is known about the contribution of genetic and environmental factors to risk for juvenile psychopathology. The Virginia Twin Study of Adolescent Behavioral Development allows these contributions to be estimated. A population-based, unselected sample of 1412 Caucasian twin pairs aged 8-16 years was ascertained through Virginia schools. Assessment of the children involved semi-structured face-to-face interviews with both twins and both parents using the Child and Adolescent Psychiatric Assessment (CAPA). Self-report questionnaires were also completed by parents, children, and teachers. Measures assessed DSM-III-R symptoms of Attention Deficit Hyperactivity Disorder (ADHD), Conduct Disorder, Oppositional Defiant Disorder, Overanxious Disorder, Separation Anxiety, and Depressive Disorder. Factorially derived questionnaire scales were also extracted. Scores were normalized and standardized by age and sex. Maximum likelihood methods were used to estimate contributions of additive and nonadditive genetic effects, the shared and unique environment, and sibling imitation or contrast effects. Estimates were tested for heterogeneity over sexes. Generally, monozygotic (MZ) twins correlated more highly than dizygotic (DZ) twins, parental ratings more than child ratings, and questionnaire scales more highly than interviews. DZ correlations were very low for measures of ADHD and DZ variances were greater than MZ variances for these variables. Correlations sometimes differed between sexes but those for boy-girl pairs were usually similar to those for like-sex pairs. Most of the measures showed small to moderate additive genetic effects and moderate to large effects of the unique individual environment. Measures of ADHD and related constructs showed marked sibling contrast effects. Some measures of oppositional behavior and conduct disorder showed shared environmental effects. There were marked sex differences in the genetic contribution to separation anxiety, otherwise similar genetic effects appear to be expressed in boys and girls. Effects of rater biases on the genetic analysis are considered. The study supports a widespread influence of genetic factors on risk to adolescent psychopathology and suggests that the contribution of different types of social influence may vary consistently across domains of measurement. [ABSTRACT FROM AUTHOR]