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Background and aimsCannabis is one of the most commonly used substances among adolescents and young adults. Earlier age at cannabis initiation is linked to adverse life outcomes, including multi-substance use and dependence. This study estimated the heritability of age at first cannabis use and identified associations with genetic variants.MethodsA twin-based heritability analysis using 8055 twins from three cohorts was performed. We then carried out a genome-wide association meta-analysis of age at first cannabis use in a discovery sample of 24 953 individuals from nine European, North American and Australian cohorts, and a replication sample of 3735 individuals.ResultsThe twin-based heritability for age at first cannabis use was 38% [95% confidence interval (CI) = 19-60%]. Shared and unique environmental factors explained 39% (95% CI = 20-56%) and 22% (95% CI = 16-29%). The genome-wide association meta-analysis identified five single nucleotide polymorphisms (SNPs) on chromosome 16 within the calcium-transporting ATPase gene (ATP2C2) at P  0.8), with the strongest association at the intronic variant rs1574587 (P = 4.09E-09). Gene-based tests of association identified the ATP2C2 gene on 16q24.1 (P = 1.33e-06). Although the five SNPs and ATP2C2 did not replicate, ATP2C2 has been associated with cocaine dependence in a previous study. ATP2B2, which is a member of the same calcium signalling pathway, has been associated previously with opioid dependence. SNP-based heritability for age at first cannabis use was non-significant.ConclusionAge at cannabis initiation appears to be moderately heritable in western countries, and individual differences in onset can be explained by separate but correlated genetic liabilities. The significant association between age of initiation and ATP2C2 is consistent with the role of calcium signalling mechanisms in substance use disorders.

Behavioral disinhibition (BD) is a quantitative measure designed to capture the heritable variation encompassing risky and impulsive behaviors. As a result, BD represents an ideal target for discovering genetic loci that predispose individuals to a wide range of antisocial behaviors and substance misuse that together represent a large cost to society as a whole. Published genome-wide association studies (GWAS) have examined specific phenotypes that fall under the umbrella of BD (e.g. alcohol dependence, conduct disorder); however no GWAS has specifically examined the overall BD construct. We conducted a GWAS of BD using a sample of 1,901 adolescents over-selected for characteristics that define high BD, such as substance and antisocial behavior problems, finding no individual locus that surpassed genome-wide significance. Although no single SNP was significantly associated with BD, restricted maximum likelihood analysis estimated that 49.3 % of the variance in BD within the Caucasian sub-sample was accounted for by the genotyped SNPs (p = 0.06). Gene-based tests identified seven genes associated with BD (p ≤ 2.0 × 10(-6)). Although the current study was unable to identify specific SNPs or pathways with replicable effects on BD, the substantial sample variance that could be explained by all genotyped SNPs suggests that larger studies could successfully identify common variants associated with BD.

Executive functions (EFs) and impulsivity are dimensions of self-regulation that are both related to psychopathology. However, self-report measures of impulsivity and laboratory EF tasks typically display small correlations, and existing research indicates that impulsivity and EFs may tap separate aspects of self-regulation that independently statistically predict psychopathology in adulthood. However, relationships between EFs, impulsivity, and psychopathology may be different in childhood compared to adulthood. Here, we examine whether these patterns hold in the baseline assessment of the Adolescent Brain and Cognitive Development (ABCD) sample, a national sample of over 11,000 children (including 749 twin pairs) ages 9–10 years. We examine the phenotypic and genetic relationships among latent variables for different components of EFs and multiple facets of impulsivity. Additionally, we assess how EFs and impulsivity relate to composite measures and latent variables of psychopathology derived from parent report. EFs were weakly correlated with impulsivity, and the strength varied by impulsivity facet, emphasizing their separability. We did not identify significant genetic and environmental correlations between EFs and impulsivity. Moreover, controlling for their small relationships with each other, both EFs and some facets of impulsivity statistically predicted an Externalizing factor, attention problems, and social problems, and twin analyses suggested these relationships were genetic in origin. These findings indicate that EFs and impulsivity represent phenotypically and genetically separable aspects of self-regulation that are both transdiagnostic correlates of psychopathology in childhood. [ABSTRACT FROM AUTHOR]

Executive functions (EFs) and intelligence (IQ) are phenotypically correlated. In twin studies, latent variables for EFs and IQ display moderate to high heritability estimates; however, they show variable genetic correlations in twin studies spanning childhood to middle age. We analyzed data from over 11,000 children (9‐ to 10‐year‐olds, including 749 twin pairs) in the Adolescent Brain Cognitive Development (ABCD) Study to examine the phenotypic and genetic relations between EFs and IQ in childhood. We identified two EF factors—Common EF and Updating‐Specific—which were both related to IQ (rs = 0.64–0.81). Common EF and IQ were heritable (53%–67%), and their genetic correlation (rG = 0.86) was not significantly different than 1. These results suggest that EFs and IQ are phenotypically but not genetically separable in middle childhood, meaning that this phenotypic separability may be influenced by environmental factors. [ABSTRACT FROM AUTHOR]

The ABCD twin study will elucidate the genetic and environmental contributions to a wide range of mental and physical health outcomes in children, including substance use, brain and behavioral development, and their interrelationship. Comparisons within and between monozygotic and dizygotic twin pairs, further powered by multiple assessments, provide information about genetic and environmental contributions to developmental associations, and enable stronger tests of causal hypotheses, than do comparisons involving unrelated children. Thus a sub-study of 800 pairs of same-sex twins was embedded within the overall Adolescent Brain and Cognitive Development (ABCD) design. The ABCD Twin Hub comprises four leading centers for twin research in Minnesota, Colorado, Virginia, and Missouri. Each site is enrolling 200 twin pairs, as well as singletons. The twins are recruited from registries of all twin births in each State during 2006–2008. Singletons at each site are recruited following the same school-based procedures as the rest of the ABCD study. This paper describes the background and rationale for the ABCD twin study, the ascertainment of twin pairs and implementation strategy at each site, and the details of the proposed analytic strategies to quantify genetic and environmental influences and test hypotheses critical to the aims of the ABCD study. [ABSTRACT FROM AUTHOR]

This study examined the extent to which rumination and depression share genetic and environmental influences in a community sample of adult twins (N= 663). Twins completed multiple rumination questionnaires, a depressive symptoms questionnaire and a diagnostic interview. Rumination was moderately heritable (h2= .37–.41 for the latent variable) and substantially influenced by nonshared environmental factors, and these results were consistent across different measures. Nonshared environmental influences on rumination were larger for women than men. Depressive symptoms and diagnosis were influenced by genetic and nonshared environmental factors (h2= .30–.45). The genetic correlations between rumination and depression were moderate to large (rA= .40–.82), suggesting that a substantial proportion of the genetic influences on rumination overlap with those on depression. Results were similar when examining self-reported depressive symptoms and interview-based diagnosis of major depressive disorder. These results highlight the importance of rumination in the integration of cognitive and genetic models of depression risk. [ABSTRACT FROM PUBLISHER]

Human facial attractiveness and facial sexual dimorphism (masculinity-femininity) are important facets of mate choice and are hypothesized to honestly advertise genetic quality. However, it is unclear whether genes influencing facial attractiveness and masculinity-femininity have similar, opposing, or independent effects across sex, and the heritability of these phenotypes is poorly characterized. To investigate these issues, we assessed facial attractiveness and facial masculinity-femininity in the largest genetically informative sample ( n = 1,580 same- and opposite-sex twin pairs and siblings) to assess these questions to date. The heritability was ~0.50-0.70 for attractiveness and ~0.40-0.50 for facial masculinity-femininity, indicating that, despite ostensible selection on genes influencing these traits, substantial genetic variation persists in both. Importantly, we found evidence for intralocus sexual conflict, whereby alleles that increase masculinity in males have the same effect in females. Additionally, genetic influences on attractiveness were shared across the sexes, suggesting that attractive fathers tend to have attractive daughters and attractive mothers tend to have attractive sons. [ABSTRACT FROM AUTHOR]

Background: Previous studies have demonstrated that the heritability of alcohol-related phenotypes depends upon the social background in which it is measured (e.g., urbanicity, marital status, and religiosity). The aim of the current study was to identify whether religiosity moderated the genetic variance of problem alcohol use in men and women at two time points: adolescence and early adulthood. Method: Participants were 312 male MZ pairs, 379 female MZ pairs, 231 male DZ pairs, 235 female DZ pairs, and 275 opposite sex DZ pairs participating in the University of Colorado Center on Antisocial Drug Dependence. Religiosity was measured using the Value on Religion Scale ( Jessor and Jessor, 1977 ), and problem alcohol use was measured using the Composite International Diagnostic Interview–Substance Abuse Module ( Cottler et al., 1989 ). Data were analyzed using a model-fitting approach to the twin data. Results: In adolescence, genetic variance of problem alcohol use decreased significantly with increasing levels of religiosity in both men and women, whereas in early adulthood, religiosity did not moderate the genetic variance of problem alcohol use in either men or women. Conclusion: Religiosity appears to moderate the genetic effects on problem alcohol use during adolescence, but not during early adulthood. The reduced genetic variance for problem alcohol use in adolescence may be the consequence of greater social control in adolescence than in young adulthood. [ABSTRACT FROM AUTHOR]

Associations between smoking behavior and polymorphisms in the dopaminergic genes (DAT1 and DRD2) were tested by using within- and between-family measures of allelic transmission in 2,448 young adults from the National Longitudinal Study of Adolescent Health. The 9-repeat allele of the dopamine transporter gene polymorphism (DAT1) was inversely associated with smoking in samples that included all subjects and only those who had initiated smoking, accounting for approximately 1% of the variance. Never smokers and current nonsmokers had an excess transmission of the 9-repeat allele compared with regular smokers, suggesting a protective effect of the 9-repeat allele, which is hypothesized to alter synaptic dopamine levels. [ABSTRACT FROM AUTHOR]

ABSTRACT Objective Method Results Discussion Pediatric loss‐of‐control (LOC) eating is associated with high BMI and predicts binge‐eating disorder and obesity onset with age. Research on the etiology of this common comorbidity has not explored the potential for shared genetic risk. This study examined genetic and environmental influences on LOC eating and its shared influence with BMI.Participants were 499 monozygotic and 398 same‐sex dizygotic twins (age = 17.38 years ± 0.67, BMIz = 0.03 ± 1.03, 54% female) from the Colorado Center for Antisocial Drug Dependence Study. LOC eating was assessed dichotomously. Self‐reported height and weight were converted to BMIz. Univariate and bivariate twin models estimated genetic and environmental influences on LOC eating and BMIz.More girls (21%) than boys (9%, p < 0.001) reported LOC eating. The phenotypic correlation with BMIz was 0.03 in girls and 0.18 in boys. Due to the nonsignificant phenotypic correlation in girls, bivariate twin models were fit in boys only. Across all models, the best‐fitting model included genetic and unique environmental effects. Genetic factors accounted for 0.51 (95% CI: 0.23, 0.73) of the variance of LOC eating in girls and 0.54 (0.18, 0.90) in boys. The genetic correlation between LOC eating and BMIz in boys was 0.45 (0.15, 0.75).Findings indicate moderate heritability of LOC eating in adolescence, while emphasizing the role of unique environmental factors. In boys, LOC eating and BMIz share a proportion of their genetic influences. [ABSTRACT FROM AUTHOR]

Previous research has suggested that individual differences in procrastination are tied to everyday goal-management abilities, but little research lias been conducted on specific cognitive abilities that may underlie tendencies for procrastination, such as executive functions (EFs). In this study, we used behavioral genetics methodology to investigate 2 hypotheses about the relationships between procrastination and EF ability: (a) that procrastination is negatively correlated with general EF ability, and (b) that this relationship is due to the genetic components of procrastination that are most related to other everyday goal-management abilities. The results confirmed both of these hypotheses. Procrastination was related to worse general EF ability at both the phenotypic and genetic levels, and this relationship was due to the component of procrastination shared with self-report measures of everyday goal-management failures. These results were observed even after controlling for potential self-report biases stemming from the urge to respond in a socially desirable manner. Together, these findings provide strong evidence for growing theories of procrastination emphasizing the importance of goal-related cognitive abilities and further highlight important genetic influences that underlie procrastination. [ABSTRACT FROM AUTHOR]

Previous research has revealed a moderate and positive correlation between procrastination and impulsivity. However, little is known about why these two constructs are related. In the present study, we used behavior-genetics methodology to test three predictions derived from an evolutionary account that postulates that procrastination arose as a by-product of impulsivity: (a) Procrastination is heritable, (b) the two traits share considerable genetic variation, and (c) goal-management ability is an important component of this shared variation. These predictions were confirmed. First, both procrastination and impulsivity were moderately heritable (46% and 49%, respectively). Second, although the two traits were separable at the phenotypic level (r = .65), they were not separable at the genetic level (rgenetic = 1.0). Finally, variation in goal-management ability accounted for much of this shared genetic variation. These results suggest that procrastination and impulsivity are linked primarily through genetic influences on the ability to use high-priority goals to effectively regulate actions. [ABSTRACT FROM AUTHOR]

Individual differences in music traits are heritable and correlated with the development of cognitive and communication skills, but little is known about whether diverse modes of music engagement (e.g., playing instruments vs. singing) reflect similar underlying genetic/environmental influences. Moreover, the biological etiology underlying the relationship between musicality and childhood language development is poorly understood. Here we explored genetic and environmental associations between music engagement and verbal ability in the Colorado Adoption/Twin Study of Lifespan behavioral development & cognitive aging (CATSLife). Adolescents (N = 1,684) completed measures of music engagement and intelligence at approximately age 12 and/or multiple tests of verbal ability at age 16. Structural equation models revealed that instrument engagement was highly heritable (a² = .78), with moderate heritability of singing (a² = .43) and dance engagement (a² = .66). Adolescent self-reported instrument engagement (but not singing or dance engagement) was genetically correlated with age 12 verbal intelligence and still was associated with age 16 verbal ability, even when controlling for age 12 full-scale intelligence, providing evidence for a longitudinal relationship between music engagement and language beyond shared general cognitive processes. Together, these novel findings suggest that shared genetic influences in part accounts for phenotypic associations between music engagement and language, but there may also be some (weak) direct benefits of music engagement on later language abilities. [ABSTRACT FROM AUTHOR]

Meta-analytic findings suggest that antisocial behavior, broadly defined, may relate to a Common Executive Function (EF) factor that captures covariance across response inhibition, working memory updating, and mental set shifting tasks. However, it is unclear whether this common factor, which is isomorphic with individual differences in response inhibition, accounts for all of the EF variance in antisocial behavior and psychopathy, or if they also relate to updating- and shifting-specific abilities. Moreover, findings that antisocial behavior and lower cognitive ability are particularly associated with the psychopathy dimension reflecting impulsivity and irresponsibility, compared to the dimension reflecting affective–interpersonal functioning, raise the possibility that EF relates to the variance shared between the impulsive–irresponsible psychopathy dimension and antisocial personality disorder. We examined these questions in a young adult twin sample (N = 765) with measures of multiple EF latent variables, Levenson Self-Report Psychopathy (LSRP) Primary (affective–interpersonal) and Secondary (impulsive–irresponsible) scales, and antisocial personality disorder symptoms (ASPDsx). Phenotypically, higher ASPDsx and LSRP Secondary psychopathy, but not LSRP Primary psychopathy, were associated with lower Common EF. Moreover, both psychopathy dimensions were negatively correlated with Updating-Specific ability, which was unrelated to ASPDsx. Results from twin models indicated that the association between LSRP Secondary psychopathy and ASPDsx was due to both genetic and nonshared environmental influences; however, Common EF's association with ASPDsx was primarily genetic, whereas its association with LSRP Secondary psychopathy had a significant environmental component. Thus, the interrelations among these constructs may reflect heterogeneous etiological pathways. • Common Executive Function (EF) relates to lower secondary but not primary psychopathy. • Common EF relates to lower antisocial personality disorder (ASPD) symptoms. • Common EF is genetically related to ASPD but environmentally related to psychopathy. • Working memory updating genetically relates to lower secondary & primary psychopathy. • The interrelations among these constructs may reflect somewhat different etiologies. [ABSTRACT FROM AUTHOR]

The relationship of verbal fluency to executive functions (EFs) remains somewhat unclear. Verbal fluency is sometimes considered an EF ability, but is not often included in the same models as other well-studied EFs (inhibition, shifting, and working memory updating). We examined the associations between verbal fluency and EFs at 2 ages with the unity/diversity model, which includes common and domain-specific EF factors. Participants were 813 adolescent twins from the Colorado Longitudinal Twin Sample (mean age 17 years) and 1,290 middle-aged twins from the Vietnam Era Twin Study of Aging (mean age 56 years) who completed multiple measures of EFs, verbal fluency, vocabulary, and nonverbal cognitive ability. Results revealed that, in both samples, a General Fluency factor (i.e., comprising both phonemic and semantic fluency measures) was associated with the Common EF factor, but also with variance unique to working memory updating, working memory span, and set-shifting. In adolescents, semantic fluency also had unique associations with shifting beyond its shared variance with phonemic fluency and Common EF. After accounting for EFs and other cognitive abilities, there were unique genetic and environmental influences on the General Fluency and Semantic-Specific latent factors. These results suggest that verbal fluency ability may best be viewed as an amalgamation of general EF variance (i.e., Common EF ability), variance shared with other EFs (e.g., Updating-Specific ability), and multiple sources of unique genetic/environmental variance (i.e., General Fluency and Semantic-Specific abilities). These associations between verbal fluency and EFs generalize to populations that differ in age by approximately 40 years. [ABSTRACT FROM AUTHOR]

Highlights • Genetic influences uniting impulsivity facets strongly related to goal management. • Unique genetic and environmental influences on all facets lead to separability. • Sensation seeking was entirely genetically distinct from other impulsivity facets. • Urgency was more strongly related to psychopathology than lack of premeditation. • Lack of perseverance was more similar to urgency than lack of premeditation. Abstract In this study, we characterized the genetic/environmental commonality and heterogeneity of impulsivity facets and tested the hypothesis that goal-management is central to their common variance. 764 young-adult twins completed the UPPS-P Impulsive Behavior Scale and measures of goal management, personality, and psychopathology. We found common genetic influences across all impulsivity facets except sensation seeking. These impulsivity genetic influences explained 40.0% of variance in goal-management ability. Other results supported three hypotheses concerning heterogeneity: that sensation seeking is independent of other facets, that urgency is more related to psychopathology than lack of premeditation, and that lack of perseverance is more similar to urgency than lack of premeditation. Thus, impulsivity facets show considerable heterogeneity in addition to common variation related to goal-management abilities. [ABSTRACT FROM AUTHOR]

Executive functions (EFs)--the higher level cognitive abilities that enable us to control our own thoughts and actions--continue to develop into early adulthood, yet no longitudinal study has examined their stability during the important life transition from late adolescence to young adulthood. In this twin study (total N = 840 individuals from 424 families), we examined the stability of individual differences in 3 EF components across a 6-year period, from approximately age 17 years (Wave 1) to 23 years (Wave 2). Specifically, we address the following questions: (a) How stable are individual differences in multiple EFs across this time period? and (b) What (genetic and/or environmental) influences affect stability and change in EFs? Results indicated that individual differences in EFs are quite stable across this 6-year period (phenotypic latent variable correlations ranged from 0.86 to 1.0). However, there was evidence for change, particularly in the factor common to multiple EFs (Common EF). Multivariate twin models suggested that stability was due almost entirely to high genetic correlations across time; there was no new genetic variance at Wave 2. Change in Common EF was due to small but significant nonshared environmental influences at Wave 2 (15%). The results suggest that individual differences in EFs are quite heritable and stable by late adolescence, yet are still sensitive to environmental influences. [ABSTRACT FROM AUTHOR]

Recent psychological and neuropsychological research suggests that executive functions--the cognitive control processes that regulate thought and action--are multifaceted and that different types of executive functions are correlated but separable. The present multivariate twin study of 3 executive functions (inhibiting dominant responses, updating working memory representations, and shifting between task sets), measured as latent variables, examined why people vary in these executive control abilities and why these abilities are correlated but separable from a behavioral genetic perspective. Results indicated that executive functions are correlated because they are influenced by a highly heritable (99%) common factor that goes beyond general intelligence or perceptual speed, and they are separable because of additional genetic influences unique to particular executive functions. This combination of general and specific genetic influences places executive functions among the most heritable psychological traits. These results highlight the potential of genetic approaches for uncovering the biological underpinnings of executive functions and suggest a need for examining multiple types of executive functions to distinguish different levels of genetic influences. [ABSTRACT FROM AUTHOR]

Many putative environmental risks correlate with individuals' genotypes. The association between delinquent peer affiliation and conduct problems may occur because of shared genetic liability. Five hundred fifty three monozygotic and 558 dizygotic twin pairs, aged 11 to 18 years, were assessed for delinquent peer affiliation and conduct problems. The authors investigated whether genes contribute to both delinquent peer affiliation and the correlation between delinquent peer affiliations and conduct problems. Delinquent peer affiliation was influenced by genetic, shared environmental, and nonshared environmental factors; genetic factors also contributed to the correlation between delinquent peer affiliations and conduct problems, providing evidence for genotype-environment correlation. The magnitude of the genetic variance of conduct problems was contextually dependent on levels of delinquent peer affiliation and was greater at higher levels of delinquent peer affiliation. [ABSTRACT FROM AUTHOR]

Objective: To explore the genetic and environmental influences on DSM-IV conduct disorder (CD) aggressive and nonaggressive subscales, taking into account age and sex differences.Method: A community sample of 1,100 twin pairs (ages 11-18) was interviewed using the Diagnostic Interview Schedule for Children. Bivariate analyses, using variable threshold models accounting for age and sex differences, were used to determine the extent to which the genetic and environmental influences on aggressive and nonaggressive CD domains are shared or unique.Results: The phenotypic correlation between aggressive and nonaggressive CD domains was 0.32. The most parsimonious bivariate model included additive genetic effects and nonshared environmental effects only (AE model).Conclusions: The results of behavior genetic model fitting suggest that the DSM-IV CD domains are influenced by unique genetic and environmental factors, but also share some common genetic and environmental influences. A large percentage of the covariation (61%) is caused by genetic factors. These results are consistent with a previous report on the bivariate heritability of aggressive and nonaggressive antisocial behavior, but extend the findings to DSM-IV domains. [ABSTRACT FROM AUTHOR]

We report a longitudinal genetic analysis that combines twins and adoptive and nonadoptive siblings to investigate continuity and change in the etiology of general cognitive ability from infancy through the transition to adolescence. Research in childhood suggests that heritability increases and shared environmental influence decreases, that genetic factors contribute to change as well as continuity, that shared environment contributes entirely to continuity, and that nonshared environment contributes entirely to change. Twins from the Longitudinal Twin Study (LTS; 224 MZ pairs, 189 same-sex DZ pairs at 1 year) and adoptive (genetically unrelated) and nonadoptive (biological) siblings from the Colorado Adoption Project (CAP; 107 and 87 pairs, respectively, at 1 year) were assessed again at 2, 3, 4, 7, 9, and 10 years, and nontwin siblings were also assessed at 12 years. Longitudinal model fitting supported the above hypotheses derived from research in childhood with two exceptions. Nonshared environmental influences contribute to continuity as well as change in middle childhood. The most striking exception is that during the transition to adolescence, genetic factors no longer contribute to change, just to continuity. [Copyright &y& Elsevier]

Abstract: Background: We investigated the etiological nature of comorbid alcohol, tobacco, and cannabis DSM-IV dependence symptoms in late adolescence and young adulthood while accounting for gender differences in the magnitude of genetic and environmental influences. Methods: Univariate and multivariate twin modeling was used to determine the heritability of each substance and the etiology of multiple drug problems in a sample of 2484 registrants of the Center for Antisocial Drug Dependence who provided data at the second wave of an ongoing longitudinal study. We report on mean and prevalence levels of whole-life DSM-IV dependence symptoms that were assessed with the Composite International Diagnostic Interview-Substance Abuse Module. Biometrical analyses were limited to age-adjusted DSM-IV dependence symptom counts from a subset of twins that reported using alcohol, tobacco, or cannabis in their lifetime. Results: Male and female alcohol, tobacco, and cannabis DSM-IV symptoms are indicators of a heritable unidimensional latent continuous trait. Additive genetic factors explain more than 60% of the common liability to drug dependence. A larger proportion of the variation in each substance is attributable to substance-specific genetic and environmental factors. Conclusions: These data suggest that both common and substance-specific genetic and environmental factors contribute to individual differences in the levels of DSM-IV alcohol, tobacco, and cannabis dependence symptoms. [Copyright &y& Elsevier]