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Background:Previous studies examined caffeine use and caffeine dependence and risk for the symptoms, or diagnosis, of psychiatric disorders. The current study aimed to determine if generalized anxiety disorder (GAD), panic disorder, phobias, major depressive disorder (MDD), anorexia nervosa (AN), or bulimia nervosa (BN) shared common genetic or environmental factors with caffeine use, caffeine tolerance, or caffeine withdrawal.Method:Using 2,270 women from the Virginia Adult Twin Study of Psychiatric and Substance Use Disorders, bivariate Cholesky decomposition models were used to determine if any of the psychiatric disorders shared genetic or environmental factors with caffeine use phenotypes.Results:GAD, phobias, and MDD shared genetic factors with caffeine use, with genetic correlations estimated to be 0.48, 0.25, and 0.38, respectively. Removal of the shared genetic and environmental parameter for phobias and caffeine use resulted in a significantly worse fitting model. MDD shared unique environmental factors (environmental correlation = 0.23) with caffeine tolerance; the genetic correlation between AN and caffeine tolerance and BN and caffeine tolerance were 0.64 and 0.49, respectively. Removal of the genetic and environmental correlation parameters resulted in significantly worse fitting models for GAD, phobias, MDD, AN, and BN, which suggested that there was significant shared liability between each of these phenotypes and caffeine tolerance. GAD had modest genetic correlations with caffeine tolerance, 0.24, and caffeine withdrawal, 0.35.Conclusions:There was suggestive evidence of shared genetic and environmental liability between psychiatric disorders and caffeine phenotypes. This might inform us about the etiology of the comorbidity between these phenotypes.

The multiple risk factors for alcohol use (AU) and alcohol use disorders (AUDs) are interrelated through poorly understood pathways, many of which begin in childhood. In this report, the authors seek to develop an empirical, broad-based developmental model for the etiology of AU and AUDs in men. We assessed 15 risk factors in four developmental tiers in 1,794 adult male twins from the Virginia population based twin registry. The best fitting model explained 39% of the variance in late adolescent AU, and 30% of the liability to lifetime symptoms of AUD. AU and AUDs can be best understood as arising from the action and interaction of two pathways reflecting externalizing genetic/temperamental and familial/social factors. Peer group deviance was important in each pathway. Internalizing symptoms played a more minor role. Familial/social factors were especially important influences on AU, while genetic/temperamental factors were more critical for AUDs. We conclude that AU and AUDs in men are complex traits influenced by genetic, family, temperamental, and social factors, acting and interacting over developmental time.

AbstractWe seek to identify factors that facilitate or inhibit transmission of drug abuse (DA) from high-risk parents to their children. In 44,250 offspring of these parents, ascertained from a Swedish national sample for having a mother and/or father with DA, we explored, using Cox models, how the prevalence of DA was predicted by potentially malleable risk factors in these high-risk parents, their spouses and the rearing environment they provided. Analyses of offspring of discordant high-risk siblings and offspring of discordant sibling-in-laws and step-parents aided causal inference. Risk for DA in the children was associated with high-risk and married-in parental externalizing psychopathology, a range of other features of these parents (e.g., low education and receipt of welfare), and aspects of the rearing environment (e.g., neighborhood deprivation and number of nearby drug dealers). Offspring of discordant high-risk siblings, siblings-in-laws and step-parents suggested that nearly all these associations were partly causal. A multivariate analysis utilizing offspring of discordant high-risk siblings identified the six most significant potentially malleable risk factors for offspring DA: (1) criminal behavior (CB) in married-in parent, (2) community peer deviance, (3) broken family, (4) DA in high-risk parent, (5) CB in high-risk parent and (6) number of family moves. Children in the lowest decile of risk had a 50% reduction in their DA prevalence, similar to that seen in the general population. We conclude that transmission of DA from high-risk parents to children partly results from a range of potentially malleable risk factors that could serve as foci for intervention.

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.

Background: Few studies examining the genetic architecture of cigarette smoking have focused on adolescents or examined developmental changes in additive genetic, shared environment, and unique environmental influences on liability to initiate cigarette smoking and quantity of cigarettes smoked. The aim of this study was to add to the literature on liability to initiate and use cigarettes during adolescence using a nationally representative sample. Method: Data for this study came from adolescent and young adult twin pairs (aged 14–33 years) from the National Longitudinal Study of Adolescent to Adult Health. We ran a series of developmental causal–contingent–common pathway models to examine whether additive genetic, shared, and unique environmental influences on liability to the initiation of cigarette use are shared with those on smoking quantity, and whether their contributions change across development. Results: We found evidence for a developmental shift in genetic and shared environmental contributions to cigarette use. Early in adolescence, genetic and environmental influences work independently on liability to cigarette smoking initiation and quantity of cigarettes smoked, but liability to these behaviors becomes correlated as individuals age into young adulthood. Conclusions: These findings provide insight into the causal processes underlying the liability to smoke cigarettes. With age, there is greater overlap in the genetic and environmental factors that influence the initiation of cigarette smoking and quantity of cigarettes smoked.

AbstractWeb-based studies have become increasingly common in the social sciences, but have been rare in genetic epidemiology in general and twin studies in particular. We here review the methods, validity checks and preliminary correlational data from an on-line questionnaire collected from 2005–2008. During this time period, 44,112 individuals completed the questionnaire. This sample was 65.3% female, 85.4% 18 years or older, 72.0% Caucasian and had a mean educational level of 12.2 years. The sample included 609 twin, 333 sibling and 201 parent-offspring pairs as well as 342 dating partners, 313 'significant other' pairs, 327 spouses and 2,316 friend pairs. A range of checks suggested low levels of invalid data. Correlations for personality, substance use and misuse, lifetime major depression, social attitudes, educational status, and height and weight were broadly similar to those obtained previously using conventional assessment methods. Web-based studies are a relatively easy and inexpensive way to ascertain large numbers of individuals, although obtaining twin pairs is more difficult, and female and monozygotic pairs are overrepresented. The sample is diverse and pair resemblance is generally similar to that obtained using interviews or mailed questionnaires.

AbstractThe relative proportions of genetic and environmental variance in behavioral measures have been studied extensively. A growing body of literature has examined changes in heritability measures over time, but we are unaware of any prior efforts to assess developmental heritability changes for multiple behavioral phenotypes using multiple data sources. We have chosen to explore the proportional genetic influences on a variety of behaviors during the genetically and environmentally labile adolescent and young adult years. This meta-analysis examined 8 behavioral domains and incorporated only primary research articles reporting two or more heritability time points in order to minimize the age-to-age error variability. Linear regression analyses revealed significant cross-time heritability increases for externalizing behaviors, anxiety symptoms, depressive symptoms, IQ, and social attitudes and nonsignificant increases for alcohol consumption, and nicotine initiation, but no evidence of heritability changes for attention-deficit/hyperactivity disorder. A variety of mechanisms may underlie these findings including the rising importance of active genotype-environment correlation, an increase in gene expression, or proportional reductions in environmental variance. Additional longitudinal studies and the inclusion of measures of total variance in primary research reports will aid in distinguishing between these possibilities. Further studies exploring heritability changes beyond young adulthood would also benefit our understanding of factors influencing heritability of behavioral traits over the lifespan.

To determine the relationship between the genetic and environmental risk factors for externalizing psychopathology and mental wellbeing, we examined detailed measures of emotional, social and psychological wellbeing, and a history of alcohol-related problems and smoking behavior in the last year in 1,386 individual twins from same-sex pairs from the MIDUS national US sample assessed in 1995. Cholesky decomposition analyses were performed withthe Mx program. The best fit model contained one highly heritable common externalizing psychopathology factor for both substance use/abuse measures, and one strongly heritable common factor for the three wellbeing measures. Genetic and environmental risk factors for externalizing psychopathology were both negatively associated with levels of mental wellbeing and accounted for, respectively, 7% and 21% of its genetic and environmental influences. Adding internalizing psychopathology assessed in the last year to the model, genetic risk factors unique for externalizing psychopathology were nowpositivelyrelated to levels of mental wellbeing, although accounting for only 5% of the genetic variance. Environmental risk factors unique to externalizing psychopathology continued to be negatively associated with mental wellbeing, accounting for 26% of the environmental variance. When both internalizing psychopathology and externalizing psychopathology are associated with mental wellbeing, the strongest risk factors for low mental wellbeing are genetic factors that impact on both internalizing psychopathology and externalizing psychopathology, and environmental factors unique to externalizing psychopathology. In this model, genetic risk factors for externalizing psychopathology predict, albeit weakly, higher levels of mental wellbeing.

Using information from Swedish population registries, we attempt to decompose the shared environment (C) into four subcomponents: close family, family, household, and community. Among pairs differing in their genetic and geographical/household relationships, we examine three externalizing syndromes: drug abuse (DA), criminal behavior (CB), and alcohol use disorders (AUD). The best-fitting common pathway model suggested that total estimates for C were higher for DA (21% for males and 18% for females) than for AUD (16% and 14%) and CB (17% and 10%). Concerning syndrome-specific influences in males, close family effects were stronger for CB and AUD, while community effects were stronger for DA. The two C components in between community experiences and close family experiences (family and household) were estimated to almost entirely derive from the common latent factor. In females, among the four components of C, the community experiences were just slightly above zero, while the C components referred to as the household effect were almost zero. The total close family experiences were similar and most important across syndromes were also divided into common and specific components. For all syndromes, for both males and females, the effects of additive genetic factors were 2–4 times the size of the total effect of the shared environment. Applying standard methods to novel relationships, we expand our understanding of how the shared environment contributes to individual differences in three externalizing syndromes.

Our aim was to test the direction of causation between self-report parental monitoring (PM) and the liability to illicit drug initiation (DI) as indicated by cannabis, cocaine, and stimulants. We fitted a multiple indicator model to test causal and non-causal models based on a large, genetically informative cross-sectional sample of male twins. The sample comprised 1,778 males aged 24–62 years from the Virginia Adult Twin Study of Psychiatric and Substance Use Disorders. Data came from self-report measures of lifetime cannabis, stimulants, and cocaine initiation, and retrospective assessment of PM between ages 8–17 years. Multivariate modeling showed that familial aggregation in PM and DI were both explained by a combination of additive genetic and shared environmental effects. Moreover, the significant association between PM and DI was best explained by a correlated liability model versus causal models. PM has typically been assumed to be an environmental, causal risk factor for drug use and has been shown to be among the more salient environmental risk factors for illicit DI. Our data were not consistent with this causal hypothesis. Instead, a correlated liability model in which PM and risk of DI share common genetic and environmental risks provided a better fit to the data.

AbstractMany studies of human behavior and psychological constructs rely on subjects' willingness to disclose information about themselves. This is problematic for phenotypes that require the disclosure of sensitive information, such as sexual behavior or illicit drug use, which are likely to be underreported. We describe a method for evaluating how sensitive variance component estimates are to underreporting. The method involves estimating, by maximum likelihood, the original population proportions of the response classes, and adjusting them for a set of hypothesized underreporting parameters. If the true values of the underreporting parameters were known, the researcher could estimate the variance components based on these values. Usually, underreporting levels are not known with certainty. However, it is possible to assume a specific value for the underreporting rate, obtain response pattern proportions adjusted for this rate, and then to conduct the analyses on these revised estimates. By repeating the procedure across the range of plausible underreporting values, the researcher can assess how sensitive the variance component estimates are to variation in underreporting. We apply this method to a sample of male-male twin pairs who reported on themselves and their co-twins for illicit drug abuse and dependence (DAD). We show how underreporting influences estimates of additive genetic, common environment, and specific environment variance components (A, C, and E) obtained for DAD in a classical twin design.