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Background and aimsAdolescents with conduct and substance use problems are at increased risk for premature mortality, but the extent to which these risk factors reflect family- or individual-level differences and account for shared or unique variance is unknown. This study examined common and independent contributions to mortality hazard in adolescents ascertained for conduct disorder (CD) and substance use disorder (SUD), their siblings and community controls, hypothesizing that individual differences in CD and SUD severity would explain unique variation in mortality risk beyond that due to clinical/control status and demographic factors.DesignMortality analysis in a prospective study (Genetics of Antisocial Drug Dependence Study) that began in 1993.SettingMulti-site sample recruited in San Diego, California and Denver, Colorado, USA.ParticipantsA total of 1463 clinical probands were recruited through the juvenile correctional system, court-mandated substance abuse treatment programs and correctional schools, along with 1399 of their siblings, and 904 controls.MeasurementsMortality and cause-of-death were assessed via National Death Index search (released October, 2017).FindingsThere were 104 deaths documented among 3766 (1168 female) adolescents and young adults (average age 16.79 years at assessment, 32.69 years at death/censoring). Mortality hazard for clinical probands and their siblings was 4.99 times greater than that of controls (95% confidence interval = 2.40-10.40; P

Although psychological symptoms are broadly considered to be risk factors for substance use, internalizing symptoms may be associated with lower risk for adolescent substance use after controlling for co-occurring externalizing symptoms. The present study explored two potential mediators of this protective association between internalizing symptoms and adolescent substance use: popularity and harm avoidance. The study used data from the Colorado Longitudinal Twin Study (LTS) and Colorado Adoption Project (CAP). Annual assessments of internalizing and externalizing symptoms and social competence were completed by parents and teachers at participant ages 7 to 16. Harm avoidance and substance use were assessed at age 17. In this sample, internalizing symptoms were associated with less frequent substance use, controlling for externalizing symptoms. We did not find evidence that popularity or harm avoidance account for the protective association of internalizing symptoms with adolescent substance use. Teacher-reported popularity was associated with less frequent substance use, suggesting that social connectedness in the school context may be a protective factor for adolescent substance use. Harm avoidance was not associated with substance use after accounting for internalizing and externalizing symptoms. [ABSTRACT FROM AUTHOR]

Externalizing psychopathology is a strong risk factor for substance use, whereas the role of internalizing manifestations of distress, and anxiety in particular, in predicting substance use remains unclear. Studies have suggested that anxiety may be either a protective or risk factor for substance use. The present study aimed to clarify evidence for anxiety-specific associations with substance use, examining sex and developmental period (adolescence vs. adulthood) as potential moderators that may help explain conflicting results in the literature. In a longitudinal twin sample, cross-sectional associations of anxiety with substance use differed in adolescents and adults and in girls/women and boys/men. Controlling for externalizing psychopathology and depression, anxiety was associated with reduced substance use in adolescent girls and increased substance use in adult women. In contrast, anxiety-specific associations with substance use were not significant in boys and men. Possible explanations for these contrasting results across development and sex are discussed. [ABSTRACT FROM AUTHOR]

Introduction: Parental monitoring is a key intervention target for adolescent substance use, however this practice is largely supported by causally uninformative cross-sectional or sparse-longitudinal observational research designs. Methods: We therefore evaluated relationships between adolescent substance use (assessed weekly) and parental monitoring (assessed every two months) in 670 adolescent twins for two years. This allowed us to assess how individual-level parental monitoring and substance use trajectories were related and, via the twin design, to quantify genetic and environmental contributions to these relationships. Furthermore, we attempted to devise additional measures of parental monitoring by collecting quasi-continuous GPS locations and calculating a) time spent at home between midnight and 5am and b) time spent at school between 8am-3pm. Results: ACE-decomposed latent growth models found alcohol and cannabis use increased with age while parental monitoring, time at home, and time at school decreased. Baseline alcohol and cannabis use were correlated (r=.65) and associated with baseline parental monitoring (r= -.24 to -.29) but not with baseline GPS measures (r= -.06 to -.16). Longitudinally, changes in substance use and parental monitoring were not significantly correlated. Geospatial measures were largely unrelated to parental monitoring, though changes in cannabis use and time at home were highly correlated (r=-.53 to -.90), with genetic correlations suggesting their relationship was substantially genetically mediated. Due to power constraints, ACE estimates and biometric correlations were imprecisely estimated. Most of the substance use and parental monitoring phenotypes were substantially heritable, but genetic correlations between them were not significantly different from 0. Discussion: Overall, we found developmental changes in each phenotype, baseline correlations between substance use and parental monitoring, co-occurring changes and mutual genetic influences for time at home and cannabis use, and substantial genetic influences on many substance use and parental monitoring phenotypes. However, our geospatial variables were mostly unrelated to parental monitoring, suggesting they poorly measured this construct. Furthermore, though we did not detect evidence of genetic confounding, changes in parental monitoring and substance use were not significantly correlated, suggesting that, at least in community samples of mid-to-late adolescents, the two may not be causally related. [ABSTRACT FROM AUTHOR]

The data release of Adolescent Brain Cognitive Development® (ABCD) Study represents an extensive resource for investigating factors relating to child development and mental wellbeing. The genotype data of ABCD has been used extensively in the context of genetic analysis, including genome-wide association studies and polygenic score predictions. However, there are unique opportunities provided by ABCD genetic data that have not yet been fully tapped. The diverse genomic variability, the enriched relatedness among ABCD subsets, and the longitudinal design of the ABCD challenge researchers to perform novel analyses to gain deeper insight into human brain development. Genetic instruments derived from the ABCD genetic data, such as genetic principal components, can help to better control confounds beyond the context of genetic analyses. To facilitate the use genomic information in the ABCD for inference, we here detail the processing procedures, quality controls, general characteristics, and the corresponding resources in the ABCD genotype data of release 4.0. [ABSTRACT FROM AUTHOR]

Aims: To estimate interactions and unique effects of behavioral approach and behavioral control on alcohol involvement hypothesized by dual‐systems models, during adolescence and emerging adulthood. Design In a longitudinal study, behavioral approach and behavioral control were examined in relation to alcohol involvement, cross‐sectionally and prospectively. Setting and participants: A total of 846 general population twins born in Colorado, USA were assessed twice (mean = 17.3 and 22.8 years; female = 51.4%; white = 91.8%). Measurements Behavioral approach was measured by self‐report questionnaires of sensation‐seeking and subjective effects of alcohol. Behavioral control was measured by self‐reported lack of planning and nine executive functioning (EF) tasks. Interviewers administered semi‐structured clinical interviews to assess alcohol use and disorder (AUD). Findings None of 36 interaction effects was statistically significant (β = −0.16–0.14, P > 0.06), suggesting that dual systems are additively related to alcohol involvement. In multiple regression models, behavioral approach and behavioral control explained independent variance in alcohol use quantity (β = 0.09–0.33, P < 0.04) and frequency (β = −0.11–0.29, P < 0.03) at both waves. During adolescence, only subjective effects (β = 0.27–0.28, P < 0.001) explained independent variance in AUD. Moreover, measures of the same construct explained independent variance in alcohol involvement: for behavioral control, lack of planning and EF were associated with alcohol frequency in adolescence (β = −0.11–0.25, P < 0.02) and AUD in emerging adulthood (β = −0.09–0.16, P < 0.03). For the behavioral approach, subjective effects were associated with all measures at both waves (β = 0.20–0.33, P < 0.01) and sensation‐seeking was associated with all measures in emerging adulthood (β = 0.09–0.11, P < 0.04). In prospective models, adolescent alcohol involvement was associated with later lack of planning (β = 0.12–0.18, P < 0.03) and lack of planning in adolescence was associated with later alcohol involvement (β = 0.12–0.14, P < 0.02). Conclusions: Both the behavioral approach and behavioral control components of dual‐systems models explain alcohol involvement during adolescence and adulthood, and different measures of the same system assess separate risk processes. The relations between alcohol involvement and the dual systems appear to be bidirectional. [ABSTRACT FROM AUTHOR]

Objective: We examined the etiology of two disordered eating characteristics. Method: Participants included 1,470 female adolescent and young adult twins and their female nontwin siblings. Phenotypic factor analyses of a seven-item eating pathology screening tool yielded two factors: weight and shape concerns and behaviors (WSCB) and binge eating (BE). Univariate and bivariate extended twin analyses (including cotwins and nontwin siblings) were used to estimate the magnitude of genetic and environmental influences on these characteristics. Results: Analyses indicated that individual differences in WSCB and BE could be explained by additive genetic influences (a² = 0.43 (95% CI: 0.33-0.52) and 0.49 (95% CI: 0.36-0.58), respectively), with the remaining variance due to nonshared environmental influences. The genetic correlation between WSCB and BE was estimated at 0.64; the nonshared environmental correlation was estimated at 0.27. Discussion: These results corroborate previous findings on genetic and environmental influences on disordered eating characteristics and suggest that findings can be extended to nontwin populations. [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]

Characterizing the interactions among attention, cognitive control, and emotion during adolescence may provide important insights into why this critical developmental period coincides with a dramatic increase in risk for psychopathology. However, it has proven challenging to develop a single neurobehavioral task that simultaneously engages and differentially measures these diverse domains. In the current study, we describe properties of performance on the Emotional Word-Emotional Face Stroop (EWEFS) task in the Adolescent Brain Cognitive Development (ABCD) Study, a task that allows researchers to concurrently measure processing speed/attentional vigilance (i.e., performance on congruent trials), inhibitory control (i.e., Stroop interference effect), and emotional information processing (i.e., difference in performance on trials with happy as compared to angry distracting faces). We first demonstrate that the task manipulations worked as designed and that Stroop performance is associated with multiple cognitive constructs derived from different measures at a prior time point. We then show that Stroop metrics tapping these three domains are preferentially associated with aspects of externalizing psychopathology and inattention. These results highlight the potential of the EWEFS task to help elucidate the longitudinal dynamics of attention, inhibitory control, and emotion across adolescent development, dynamics which may be altered by level of psychopathology. • ABCD's Emotional Word-Emotional Face Stroop task manipulations worked as designed. • Task measures processing speed, inhibition, and emotion information processing. • Stroop performance is associated with cognitive ability at baseline. • Performance is associated with externalizing symptom dimensions. [ABSTRACT FROM AUTHOR]

The evidence for common genetic and environmental influences on conduct disorder (CD) and major depressive disorder (MDD) in adolescents was examined. A sample of 570 monozygotic twin pairs, 592 dizygotic twin pairs, and 426 non-twin siblings, aged 12-18 years, was recruited from the Colorado Twin Registry. For the past year data, there was a significant correlation between the genetic influences on MDD and CD and, for the lifetime data, there was a significant correlation between the genetic influences on MDD and CD, and a significant correlation between the nonshared environmental influences on MDD and CD. Our results suggest that some genetic factors will increase an individual's vulnerability to both MDD and CD in adolescence. [ABSTRACT FROM AUTHOR]

Background: While college attendance has been shown to be associated with increased drinking behaviors, there are no studies to our knowledge that have examined whether college attendance moderates genetic influences for drinking. We first tested for changes in alcohol consumption in adolescents who did and did not subsequently attend college, and then tested for variation of the genetic and environmental determinants of drinking in these 2 groups. Methods: Participants eligible for this study were selected from 2 samples from the National Longitudinal Study of Adolescent Health (Add Health), a national probability sample ( n=7,083) and a sample of sibling pairs ( n=855 pairs). Participants were assessed for measures of drinking behaviors as adolescents (wave I) and reinterviewed at 1 (wave II) and 6 years (wave III) following the initial survey. Changes in binge drinking and average quantity of alcohol consumed in the past year were estimated among 4 groups (2-year college students, 4-year college students, college withdrawers, noncollege participants) in sequential cohorts which spanned the ages of 13 to 24 across the 3 Add Health waves. Gene by environment interactions were then tested at wave III using biometrical models in the genetically informative pairs. Results: Participants who did not attend college reported more binge drinking and consumed greater quantities of alcohol as adolescents than participants who subsequently attended college. However, the college students not only surpassed their noncollege peers in alcohol use as young adults, but also exhibited a greater genetic influence on quantity of alcohol consumed per drinking episode. Conclusions: Exposure to a college environment acts as an environmental moderator, supporting the hypothesis that the magnitude of genetic influence on certain aspects of alcohol consumption is greater in environments where drinking behaviors are more likely to be promoted. [ABSTRACT FROM AUTHOR]

Abstract: Background: Knowledge regarding the causes of comorbidity among substance use disorders can have significant impact on future research examining the etiology of these disorders. Unfortunately, the conclusions of past studies examining the comorbidity among substance use disorders are conflicting; some studies emphasize familial influences common to multiple substances, while others emphasize substance-specific influences. Discrepancies in results may reflect different analytical approaches or differences in the samples. Here, we examine the causes of comorbidity between alcohol dependence and illicit drug dependence in adolescents. Methods: We ascertained a clinical sample of adolescents treated for antisocial behavior and substance use disorders and their siblings and a matched control sample. A model fitting approach was used to test 13 alternative hypotheses for the causes of comorbidity. Results: The best supported hypothesis for the comorbidity between alcohol dependence and illicit drug dependence was a model hypothesizing that comorbid disorders are alternate forms of a single underlying liability. The next best fitting models were two of the correlated liabilities models (correlated risk factors and reciprocal causation). Discussion: The results suggest that the best hypotheses explaining the comorbidity between alcohol and illicit drug dependence in adolescents are that alcohol dependence and illicit drug dependence are manifestations of a single general liability to develop substance dependence or that there are separate liabilities that are highly correlated. [Copyright &y& Elsevier]

This study examined the utility of Cloninger's tridimensional personality theory (1986, 1987a) in predicting preferred substance of abuse and self-reported motivations for use among a sample of 200 adolescent substance abusers and 200 matched community control adolescents. Two primary hypotheses were tested: (1) Cloninger's type II profile is more strongly associated with stimulant use, and his type I profile is more strongly associated with substances having sedative-hypnotic effects; and 2) type II individuals will report motivations for use that focus primarily on obtaining positive rewards, whereas type I individuals will report motivations primarily concerning negative reinforcement or the avoidance of problems and negative life experiences. Our results did not show strong associations between Cloninger's Harm Avoidance and Reward Dependence dimensions and preferred substance or motivations for use. However, in partial support of the hypotheses examined here, we did find that individuals low in novelty seeking (NS) tended to prefer alcohol and marijuana, whereas those high in NS endorsed a wider range of preferred substances. High NS was associated with significantly greater stimulant use and motivations focused on obtaining positive rewards, whereas low NS was associated with greater sedative use and motivations related to avoiding negative emotions or negative life experiences. [ABSTRACT FROM AUTHOR]

We introduce an overlapping cohort sequential longitudinal study of behavioral development and psychopathology in a representative sample of 1412 pairs of twins aged 8 through 16 years. Multiple phenotypic assessments involve a full psychiatric interview with each child and each parent, and supplementary parental, teacher, and child interview material and questionnaires. For the first wave of assessments, the numbers of reported DSM-III-R symptoms of Major Depressive Disorder (MDD), Separation Anxiety Disorder (SAD), Overanxious Disorder (OAD), Oppositional Defiant Disorder (ODD), Conduct Disorder (CD), and Attention Deficit Hyperactivity Disorder (ADHD), assessed through interviews, confirm patterns of age and sex trends found in other epidemiological samples, but underscore their dependence on whether the child or the parent is the informant. Correlations across domains for symptoms reported by the same informant are often as large as correlations across informants for the same domain of symptoms. Factor analyses of these symptom counts, taking account of informant view and unreliability of assessment, show the high degree of correlation between SAD and OAD, between MDD and OAD, and between CD and ODD. ADHD symptoms are relatively independent of the other domains, but show moderate correlations with CD, ODD, and MDD. Factorially derived dimensional questionnaire scales, based on child, parental, and teacher reports, show patterns of relationship to symptom counts consistent with both convergent and discriminant validity as indices of liability to clinical symptoms. Across informants, questionnaire scales provide as good a prediction of symptoms as do clinical interviews. Multitrait-multimethod confirmatory factor analysis reveals the patterns of relationship between symptoms of psychiatric disorder in children taking due account of informant and unique sources of variance. Gender differences are consistent within the correlated clusters of ODD/CD and MDD/SAD/OAD, although there are disorder-specific age trends. There are large informant-specific influences on the reporting of symptoms in clinical interviews. Dimensional questionnaire scales provide a useful source of additional information. In subsequent analyses of genetic and environmental etiology of childhood psychopathology we must expect that results may differ by informant and method of assessment. Multivariate and developmental analyses that explore the sources of these differences will shed new light on the relationship between genetic and environmentally influenced vulnerability and the manifestation of psychopathology in specific circumstances. [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]

This study describes results from a genome-wide search for quantitative trait loci (QTL) influencing substance dependence vulnerability in adolescence. We utilized regression-based multipoint (and single-point) QTL mapping procedures designed for selected sibpair samples. Selected sibling pairs included 250 proband-sibling pairs from 192 families. Clinical probands (13–19 years of age) were drawn from consecutive admissions to substance abuse treatment facilities in the Denver metropolitan area; siblings of probands ranged in age from 12 to 25 years. In addition to the selected sample, a community-based sample of 3676 adolescents and young adults were utilized to define a clinically-significant, heritable, age- and sex-normed index of substance dependence vulnerability—a priori and independent of our linkage results. Siblings and their parents were genotyped for 374 STR micro-satellite markers distributed across the 22 autosomes (average inter-marker distance=9.2 cM). Non-parametric single-point linkage results indicated 17 markers on 11 chromosomes with nominally significant tests of linkage; six markers with LOD scores greater than 1.0 and one marker (D3S1614) with a LOD score of 2.2. Multipoint mapping corroborated two locations and provided preliminary evidence for linkage to regions on chromosome 3q24-25 (near markers D3S1279 and D3S1614) and chromosome 9q34 (near markers D9S1826 and D9S1838). [Copyright &y& Elsevier]

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]

Youth with loss of control eating (LOC) have poorer social relationships than youth without LOC. However, perceived family functioning among youth reporting LOC is relatively unexplored. We examined perceived family functioning among 990 twins (age = 17.47 ± 0.71 years, 53% female) from the Colorado Center for Antisocial Drug Dependence with (n = 158) and without (n = 832) LOC. LOC was assessed with one binary item. Associations between family functioning and LOC were examined using general linear models that accounted for dependence in twin data. Girls with greater family conflict had higher odds of endorsing LOC (p = .02), but not after accounting for depressive symptoms (p = .26). Further analysis indicated that depressive symptoms mediated the association between LOC and family conflict (p = .04). This finding is consistent with an interpersonal model, which proposes that interpersonal difficulties lead to negative emotional states, which promotes LOC as a method of coping with negative affect. Family cohesion and expressiveness were not associated with LOC in girls, and none of the family functioning variables were associated with LOC in boys (ps > .05). Future studies are needed to clarify these relations and to determine any relevant treatment indications. [ABSTRACT FROM AUTHOR]

The literature on the association between subjective effects (SEs; i.e., how an individual perceives their physiological and psychological reactions to a drug) and substance use disorders (SUDs) is largely limited to community samples. The present study addressed the following aims in a clinical sample: whether SEs predict general versus substance-specific SUD in adolescence and adulthood after controlling for conduct disorder symptoms (CDsymp); whether SEs predict SUDs across drug classes; whether SEs predict change in SUD from adolescence to adulthood; and whether there are racial/ethnic differences in associations. Longitudinal analyses were conducted using data from a sample of 744 clinical probands recruited from residential and outpatient SUD treatment facilities in CO during adolescence (M age = 16.26) and re-assessed twice in adulthood (M ages = 22.56 and 28.96), approximately seven and twelve years after first assessment. SEs and CDsymp were assessed in adolescence. SUD severity was assessed at adolescence and twice during adulthood. SEs assessed in adolescence robustly predicted general SUD for legal and illegal substances in adolescence and adulthood, whereas CDsymp predicted SUD primarily in adolescence. Higher positive and negative SEs in adolescence were associated with greater SUD severity after controlling for CDsymp, with similar magnitudes. Results indicated cross-substance effects of SEs on SUD. We found no evidence for racial/ethnic differences in associations. We investigated the progression of SUD in a high-risk sample with greater odds of sustained SUD. In contrast to CDsymp, both positive and negative SEs consistently predicted general SUD across substances in adolescence and adulthood. • Adolescent subjective effects predicted general SUD for legal and illegal substances. • Results were robust from adolescence through adulthood. • Conduct disorder predicted SUD primarily in adolescence. • Both positive and negative subjective effects positively predicted SUD. • Subjective effects predicted SUDs across substances. [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]

Variation in the composition of the human oral microbiome in health and disease has been observed. We have characterized inter- and intra-individual variation of microbial communities of 107 individuals in one of the largest cohorts to date (264 saliva samples), using culture-independent 16S rRNA pyrosequencing. We examined the salivary microbiome in up to three time-points during 10 yr spanning adolescence, and determined the influence of human genotype, gender, age, and weight class. Participants, including 27 monozygotic and 18 dizygotic twin pairs, were sampled mainly at ages 12--13, 17--18, and 22--24, with a few sampled as early as 8 yr of age. In contrast to gut or skin microbiomes, there is a core genuslevel salivary microbiome. Individuals are more similar to themselves and their co-twins in the 12--17 and in the 17--22 cohorts than to the whole sample population, but not over the 10 yr from 12 to 22; and monozygotic twin pairs are statistically not more similar than dizygotic twin pairs. The data are most consistent with shared environment serving as the main determinant of microbial populations. Twins resemble each other more closely than the whole population at all time-points, but become less similar to each other when they age and no longer cohabit. Several organisms have agespecific abundance profiles, including members of the genera Veillonella, Actinomyces, and Streptococcus. There is no clear effect of weight class and gender. The results of this work will provide a basis to further study oral microbes and human health. [ABSTRACT FROM AUTHOR]

Abstract: Objective: Cannabis is the most frequently abused illicit substance among adolescents and young adults. Genetic risk factors account for part of the variation in the development of cannabis dependence symptoms; however, no linkage studies have been performed for cannabis dependence symptoms. This study aimed to identify such loci. Method: Three hundred and twenty-four sibling pairs from 192 families were assessed for cannabis dependence symptoms. Probands (13–19 years of age) were recruited from consecutive admissions to substance abuse treatment facilities. The siblings of the probands ranged in age from 12 to 25 years. A community-based sample of 4843 adolescents and young adults was utilized to define an age- and sex-corrected index of cannabis dependence vulnerability. DSM-IV cannabis dependence symptoms were assessed in youth and their family members with the Composite International Diagnostic Instrument-Substance Abuse Module. Siblings and parents were genotyped for 374 microsatellite markers distributed across the 22 autosomes (average inter-marker distance=9.2cM). Cannabis dependence symptoms were analyzed using Merlin-regress, a regression-based method that is robust to sample selection. Results: Evidence for suggestive linkage was found on chromosome 3q21 near marker D3S1267 (LOD=2.61), and on chromosome 9q34 near marker D9S1826 (LOD=2.57). Conclusions: This is the first reported linkage study of cannabis dependence symptoms. Other reports of linkage regions for illicit substance dependence have been reported near 3q21, suggesting that this region may contain a quantitative trait loci influencing cannabis dependence and other substance use disorders. [Copyright &y& Elsevier]

Abstract: Objective:: To examine genetic and environmental influences on drinking in a nationally representative study of genetically informative adolescents followed into young adulthood. Method:: The average quantity of alcohol used per drinking episode during the past year was analyzed in 4432 youth assessed during adolescence (mean age of 16) and then 1 and 6 years later. The variance of quantity of alcohol consumed was decomposed into three components: additive genetic (a 2), shared environmental (c 2), non-shared environmental (e 2). Four candidate genes were tested for association. Results:: Wave (1) a 2 −0.52e 2 −0.48, Wave (2) a 2 −0.28e 2 −0.72, Wave (3) a 2 −0.30e 2 −0.70. Genetic correlations between Waves 1 and 2 were 0.85, Waves 1 and 3 were 0.34. The DAT1 440 allele was associated at Wave 1 (p =0.007). DRD2 TaqI A1/A2 was associated at Wave 3 (p =0.007). DRD4 and 5HTT were not associated. The DAT1 and DRD2 polymorphisms accounted for 3.1% and 2.0% of the variation, respectively. Conclusion:: Genetic influence on drinking behavior was common in adolescents longitudinally assessed 1 year apart, but was less correlated between these adolescents and their assessment as young adults at a subsequent time point. Polymorphisms in genes of the dopaminergic system appear to influence variation in drinking behavior. [Copyright &y& Elsevier]

Background: It is unclear whether cannabis use causes cognitive decline; several studies show an association between cannabis use and cognitive decline, but quasi-experimental twin studies have found little support for a causal effect. Here, we evaluate the association of cannabis use with general cognitive ability and executive functions (EFs) while controlling for genetic and shared environmental confounds in a longitudinal twin study.Methods: We first examined the phenotypic associations between cannabis initiation, frequency, and use disorder with cognitive abilities, while also controlling for pre-use general cognitive ability and other substance involvement. We tested the concurrent association between the cannabis use variables and cognitive abilities in late adolescence and young adulthood and the longitudinal association between cannabis use variables during adolescence and young adulthood cognitive abilities. Next, we used multilevel models to test whether these relations reflect between- and/or within-twin pair associations.Results: Phenotypically, cannabis use was related to poorer cognitive functioning, although most associations were negligible after accounting for other substance use. Nevertheless, there were few significant within-family twin-specific associations, except that age 17 cannabis frequency was associated with worse age 23 Common EF and general cognitive ability.Conclusions: We found little support for a potential causal effect of cannabis use on cognition, consistent with previous twin studies. Results suggest that cannabis use may not cause decline in cognitive ability among a normative sample of cannabis users. [ABSTRACT FROM AUTHOR]

Background: Limited evidence suggests that early cannabis use is associated with sleep problems. Research is needed to understand the developmental impact of early regular cannabis use on later adult sleep duration.Methods: In a sample of 1656 adult twins (56% female, Mean age = 25.79yrs), linear mixed effects models were used to analyze the influence of retrospectively assessed age of onset of regular cannabis use on adult sleep duration controlling for sex, depression, and current substance use. Twin analyses provided genetic and environmental variance estimates as well as insights into the association and potential casual relationships between these traits.Results: Earlier age of onset for regular cannabis use was significantly associated with shorter adult sleep duration on both weekdays (β = -0.13, 95% CI = [-0.23, -0.04]) and weekends (β = -0.18, 95% CI = [-0.27, -0.08]). Additive genetics significantly contributed to the onset of regular cannabis use (a2 = 76%, 95% CI = [68, 85]) and adult weekend sleep duration (a2 = 20%, 95% CI = [11, 32]). We found evidence of a significant genetic correlation (rA = -0.31, 95% CI = [-0.41, -0.15]) between these two traits and our best fitting model was consistent with early onset of regular cannabis use causing shorter adult weekend sleep duration (β = -0.11, 95% CI = [-0.18, -0.03]).Conclusions: Our results are consistent with the hypothesis that early onset of regular cannabis use may have a negative impact on adult sleep duration. [ABSTRACT FROM AUTHOR]