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The aim of the study was to examine associations between life events and self-assessed loneliness in adolescence. We used data from a Norwegian population-based twin sample including seven birth cohorts (N = 2,879, 56% females). The participants completed self-report questionnaires three times throughout adolescence, with 2 years in between (i.e., 12–18 years old at Wave 1). By using a random intercept cross-lagged panel model (RI-CLPM), we were able to separate stable influences in the measured constructs from the within-person changes at each measurement occasion. In addition, using data from twins allowed us to examine to what degree the associations between life events and loneliness were genetic and/or environmental in nature. The results showed moderate stability of both loneliness and aggregation scores of life events throughout adolescence. The life events were assigned to clusters based on their independence (i.e., events considered dependent or independent on a person's behavior) and desirability (i.e., positive or negative). The time-stable between-person variance in all three measures, loneliness and person-dependent positive and negative life events, could almost exclusively be accounted for by genetic factors. However, as expected, also shared environmental factors influenced person-independent life events. The associations between time-stable between-person variance in loneliness and life events were small, and nearly exclusively due to shared genetic influences. Furthermore, life events do not seem to predict changes in loneliness or vice versa. In conclusion, the self-reported levels of loneliness throughout adolescence seems to be independent of life events. Public Significance Statement: This study suggests that life events do not influence levels of loneliness in adolescence. The weak associations between life events and loneliness were mainly due to shared genetic influences. Additionally, the results showed that levels of loneliness are moderately stable throughout this period of life, mainly due to genetic influences. Importantly, the study highlights the need of using genetically informative designs, also when studying the effects of assumed "environmental" measures. [ABSTRACT FROM AUTHOR]

Although previous studies have identified negative relationships between cognitive ability and emotional problems (EP), mechanism explaining these relationships remained unclear. This study evaluated two explanatory models using bivariate moderation model-fitting analysis in a twin design. The resilience model suggests that high cognitive ability decreases the risk of EP in adverse settings, and the scarring model suggests that EP symptoms lead to persistent cognitive deficits following onset. The Standard Progressive Matrices Plus (SPM) and EP scale were administered to a sample of 3,202 twins (mean age = 14.62 ± 1.74 years) attending public schools in Nigeria. The results of bivariate moderation model-fitting analyses only supported the resilience model. Moderation effects were not significant in the scarring model when genetic and environmental influences were incorporated. The best-fitting bivariate moderation model assuming the resilience model yielded a genetic correlation of − 0.57 (95% CI = − 0.40, − 0.84) with no significant environmental correlations. Moreover, the SPM moderated the environmental, not genetic, influences on EP, such that environmental influences were strong when protective factors were absent (low SPM) and weak when these were present (high SPM). These results indicate the need to develop targeted prevention and intervention strategies for EP in adolescents displaying low cognitive ability in deprived settings. [ABSTRACT FROM AUTHOR]

Background: Stress is a universal phenomenon and one of the most common precipitants of insomnia. However, not everyone develops insomnia after experiencing a stressful life event. This study aims to test aspects of Spielman's '3P model of insomnia' (during adolescence) by exploring the extent to which: (a) insomnia symptoms are predicted by polygenic scores (PGS); (b) life events predict insomnia symptoms; (c) the interaction between PGS and life events contribute to the prediction of insomnia symptoms; (d) gene–environment interaction effects remain after controlling for sex. Methods: The sample comprised 4,629 twins aged 16 from the Twin Early Development Study who reported on their insomnia symptoms and life events. PGS for insomnia were calculated. In order to test the main hypothesis of this study (a significant interaction between PGS and negative life events), we fitted a series of mixed effect regressions. Results: The best fit was provided by the model including sex, PGS for insomnia, negative life events, and their interactions (AIC = 26,158.7). Our results show that the association between insomnia symptoms and negative life events is stronger for those with a higher genetic risk for insomnia. Conclusions: This work sheds light on the complex relationship between genetic and environmental factors implicated for insomnia. This study has tested for the first time the interaction between genetic predisposition (PGS) for insomnia and environmental stressors (negative life events) in adolescents. This work represents a direct test of components of Spielman's 3P model for insomnia which is supported by our results. [ABSTRACT FROM AUTHOR]

Background: Twin studies have demonstrated shared genetic and environmental effects between eating disorders and alcohol involvement in adults and middle adolescents. However, fewer studies have focused on late adolescents or investigated a wide range of eating disorder dimensions and alcohol involvement subscales in both sexes. We examined genetic and environmental correlations among three eating disorder dimensions and two alcohol involvement subscale scores in late adolescent twins using bivariate twin models. Methods: Participants were 3568 female and 2526 male same‐sex twins aged 18 years old from the Child and Adolescent Twin Study in Sweden. The Eating Disorder Inventory‐2 (EDI) assessed the drive for thinness, bulimia, and body dissatisfaction. Alcohol involvement was assessed with the Alcohol Use Disorder Identification Test consumption (AUDIT‐C) and problem (AUDIT‐P) subscales. Results: Only phenotypic and twin correlations in female twins met our threshold for twin modeling. The proportion of total variance for each trait accounted for by additive genetic factors ranged from 0.50 to 0.64 in female twins, with the rest explained by nonshared environmental factors and measurement error. Shared environmental factors played a minimal role in the variance of each trait. The strongest genetic correlation (ra) emerged between EDI bulimia and AUDIT‐P (ra = 0.46, 95% confidence interval: 0.37, 0.55), indicating that the proportion of genetic variance of one trait that was shared with the other trait was 0.21. Nonshared environmental correlations between eating disorder dimensions and alcohol involvement ranged from 0.03 to 0.13. Conclusions: We observed distinct patterns of genetic and environmental effects for co‐occurring eating disorder dimensions and alcohol involvement in female vs. male twins, supporting sex‐specific treatment strategies for late adolescents with comorbid eating disorders and alcohol use disorder. Our findings emphasize the importance of assessing family history of multiple eating disorder dimensions while treating late adolescents with problematic alcohol use, and vice versa, to improve detection and treatment. [ABSTRACT FROM AUTHOR]

Background : Heritability of alcohol use disorders (AUDs) varies widely, with reported estimates of 30–78% in twin studies. This variation might be due to methodological differences (e.g., using different thresholds for AUDs, age differences between samples). Aim : To investigate the heritability of AUDs in a nation-wide sample of male and female twins in late adolescence (18 years). Participants : The study is based on data from 8,330 18-year-old Swedish monozygotic (MZ) and dizygotic (DZ) twins from the Child and Adolescent Twin Study (Sweden). Method : Univariate sex-limitation twin analyses were performed using (a) total AUDIT score, (b) different AUDIT cut-offs (AUDIT-10: potentially harmful alcohol use and most likely alcohol dependent ; AUDIT-C: potential hazardous alcohol consumption/active alcohol use disorders), and (c) a risk-group classification for alcohol dependence based on AUDIT total score. Results : Prevalence of potential hazardous alcohol consumption/active alcohol use was 57.1%, and for potentially harmful alcohol use prevalence was 26.5%. Prevalence was higher among females (59.0% and 31.1% respectively) than males (54.4% and 20.0% respectively). Overall, the results of the univariate model fitting indicated that there were qualitative sex differences in the genetic and environmental influences on AUDs, with generally moderate heritability estimates ranging between 0.37 and 0.50. Discussion : At odds with previous research, a harmful/hazardous drinking pattern was more common in this age group among females than a low-risk drinking pattern (where males were overrepresented). Heritability estimates were moderate throughout all measures and cut-offs, with equally high contributions from shared and non-shared environment. Sex-limitation models revealed qualitative sex differences for AUDs, suggesting that different genetic and/or environmental factors influence variation in AUDs in males and females. [ABSTRACT FROM AUTHOR]

Children from lower-income households are at increased risk for poor health, educational failure, and behavioral problems. This social gradient is one of the most reproduced findings in health and social science. How people view their position in social hierarchies also signals poor health. However, when adolescents' views of their social position begin to independently relate to well-being is currently unknown. A cotwin design was leveraged to test whether adolescents with identical family backgrounds, but who viewed their family's social status as higher than their same-aged and sex sibling, experienced better well-being in early and late adolescence. Participants were members of the Environmental Risk Longitudinal Twin Study, a representative cohort of British twins (n = 2,232) followed across the first 2 decades of life. By late adolescence, perceptions of subjective family social status (SFSS) robustly correlated with multiple indicators of health and well-being, including depression; anxiety; conduct problems; marijuana use; optimism; not in education, employment, or training (NEET) status; and crime. Findings held controlling for objective socioeconomic status both statistically and by cotwin design after accounting for measures of childhood intelligence (IQ), negative affect, and prior mental health risk and when self-report, informant report, and administrative data were used. Little support was found for the biological embedding of adolescents' perceptions of familial social status as indexed by inflammatory biomarkers or cognitive tests in late adolescence or for SFSS in early adolescence as a robust correlate of well-being or predictor of future problems. Future experimental studies are required to test whether altering adolescents' subjective social status will lead to improved well-being and social mobility.

Background and Aims: Previous studies have demonstrated associations between substance use and reduced educational attainment; however, many were unable to account for potential confounding factors like genetics and the rearing environment. In the few studies that controlled for these factors, the substances assessed were limited to alcohol, cannabis, and tobacco. To address these limitations, we examined the relationship between adolescent use of seven kinds of substances, the number of additional substances used, and high school noncompletion within a large sample of Australian twins. Design: A series of two‐level generalized mixed effects logistic regressions were conducted to examine associations between adolescent substance use and high school noncompletion. Setting: Australia. Participants: A total of 9579 adult Australian twins from two cohorts of the Australian Twin Registry. Measurements Assessments of high school completion, childhood major depression, conduct disorder symptoms, substance use initiation, demographics, and parental educational attainment using the Australian version of the Semi‐Structured Assessment for the Genetics of Alcoholism. Findings There were unique within‐twin‐pair effects of use of sedatives (odds ratio [OR] = 22.39 [95% confidence interval (CI) = 1.18–423.48]) and inhalants/solvents (OR = 10.46 [95% CI = 1.30–84.16]) on high school noncompletion. The number of substances used in adolescence was strongly associated with high school noncompletion across all discordant twin models (ORs from 1.50–2.32, Ps < 0.03). Conclusions: In Australia, adolescent substance use appears to be associated with early school dropout, with the effects of any given substance largely because of the confounding factors of parental education, childhood conduct disorder symptoms, and use of other substances. Sedatives and inhalants/solvents have effects on high school noncompletion that cannot be explained by polysubstance use or familial factors. [ABSTRACT FROM AUTHOR]

Background: A dominant feature of anxiety disorders is familial aggregation. However, the underlying mechanisms of between- and within-generational anxiety resemblance remain poorly understood. By disentangling the genetic v. environmental sources of familial resemblance in anxiety, we can help prevent within-family transmission of anxiety disorders. Therefore, data from both parents and twins are needed to obtain unbiased and detailed estimations of genetic and environmental sources of similarity between family members. Methods: We examined data from 991 families with same-sex twins. Trait anxiety in twins was assessed via self-report and parent report, while parental trait anxiety was assessed via self-report. We established a nuclear twin family model and estimated genetic and environmental variances using two survey waves. Results: The results suggested that additive genetic (A), dominant genetic (D), and non-shared environmental (E) influences significantly contributed to trait anxiety, whereas familial environmental influences (F) and passive gene–environment correlations (rGE) did not. Sibling environmental influences (S) were only found in self-report data, and increased when genetic influences decreased from Wave 1 to Wave 2. Conclusions: Our study highlights the important role of broad heritability in intrafamilial trait anxiety similarity. Parent–child resemblance occurred primarily due to shared genetic makeup rather than direct environmental transmission. Sibling-specific environments, as the only source of shared environments, need further investigation. These findings have both theoretical and practical significance for anxiety disorders. Future research can expand our understanding by examining the gene–environment interplay and sex differences. [ABSTRACT FROM AUTHOR]

Socio-environmental factors play an important role in adolescent well-being, but potential genetic contributions to these associations are rarely assessed. To address this gap in the literature, associations between well-being and family conflict and functioning, number of friends, friendship importance and satisfaction, and leisure time variables were studied in N = ~ 4700 twin pairs from the Netherlands Twin Register, us ing generalized estimating equations and twin-difference scores. When twin-difference scores indicated a role for genetic factors, we used bivariate genetic models to quantify genetic and environmental contributions to these associations. We identify significant associations between well-being and family functioning, family conflict, different leisure time activities, number of friends, and satisfaction with friendships. Additionally, we find evidence for large (73–91%) genetic influence on the associations between well-being and family conflict and functioning, leisure time sport/scouting clubs, and satisfaction with friendships. Finally, findings support the hypothesis of a causal association between well-being and family conflict and functioning. These findings have important implications for research into the social correlates of well-being in adolescence, as not taking genetic factors into account leads to overestimations of the influence of identified correlates and consequently to recommendations of these correlates as intervention targets. [ABSTRACT FROM AUTHOR]

Aims: The extent to which maternal transmission of primary dysmenorrhoea is genetically determined in adolescents and young women has yet to be determined. We aimed to assess heritability and associations relevant to primary pain syndromes using a twin family study. Methods: Participants were young menstruating female twins, and their oldest sisters and mothers, whose families were registered with Twins Research Australia and previously participated in a twin family study of primary paediatric pain disorders. Questionnaire packs were mailed, assessing current maximum and average menstrual pain intensity, current pain interference with activities and retrospective dysmenorrhea secondary symptoms. Results: The sample comprised 206 twin individuals (57 monozygous (MZ) and 46 dizygous (DZ) pairs) aged 10–22 years, eldest siblings (n = 38) aged 13–28 years and mothers (n = 101) aged 32–61 years. The estimated regression coefficient of the relationship between mother–daughter and twin–sibling dyads indicated significant associations for the measures of dysmenorrhea and supported heritability. Adjusted for age, the within twin‐pair correlation for MZ twins was generally more than twice that of DZ twins. Heritability estimates were maximal pain intensity 0.67 (P = 3.8 × 10−11), average pain intensity 0.63 (P = 3.7 × 10−10), pain interference 0.57 (P = 1.8 × 10−8) and retrospective symptoms 0.57 (P = 1.8 × 10−8). Twin individuals with a lifetime (three‐month) history of iron deficiency and those with painless restless legs syndrome (RLS) were significantly more likely to have more intense pain associated with menstruation. Conclusion: Primary dysmenorrhea in adolescents and young women was shown to be relatively strongly genetically influenced and associated especially with a history of iron deficiency and painless RLS which have potential therapeutic implications. [ABSTRACT FROM AUTHOR]

Background: We sought to clarify the impact of adolescent alcohol misuse on adult physical health and subjective well‐being. To do so, we investigated both the direct associations between adolescent alcohol misuse and early midlife physical health and life satisfaction and the indirect effects on these outcomes attributable to subsequent alcohol problems. Method: The sample included 2733 twin pairs (32% monozygotic; 52% female) from the FinnTwin16 study. Adolescent alcohol misuse was a composite of frequency of drunkenness, frequency of alcohol use, and alcohol problems at ages 16, 17, and 18.5. The early midlife outcomes included somatic symptoms, self‐rated health, and life satisfaction at age 34. The mediators examined as part of the indirect effect analyses included alcohol problems from the Rutgers Alcohol Problem Index at ages 24 and 34. Serial mediation and co‐twin comparison models were applied and included covariates from adolescence and early midlife. Results: There were weak direct associations between adolescent alcohol misuse and early midlife physical health and life satisfaction. However, there was stronger evidence for indirect effects, whereby young adult and early midlife alcohol problems serially mediated the relationship between adolescent alcohol misuse and early midlife somatic symptoms (β = 0.03, 95% CI [0.03, 0.04]), self‐rated health (β = −0.02, 95% CI [−0.03, −0.01]), and life satisfaction (β = −0.03, CI [−0.04, −0.02]). These serial mediation effects were robust in co‐twin comparison analyses. Conclusions: These results provide evidence that alcohol problems are a primary driver linking adolescent alcohol misuse and poor health outcomes across the lifespan. [ABSTRACT FROM AUTHOR]

Accumulating evidence suggests that individuals exposed to victimization at key developmental stages may have different epigenetic fingerprints compared to those exposed to no/minimal stressful events, however results are inconclusive. This study aimed to strengthen causal inference regarding the impact of adolescent victimization on the epigenome by controlling for genetic variation, age, gender, and shared environmental exposures. We conducted longitudinal epigenome-wide association analyses (EWAS) on DNA methylation (DNAm) profiles of 118 monozygotic (MZ) twin pairs from the Environmental Risk study with and without severe adolescent victimization generated using buccal DNA collected at ages 5, 10 and 18, and the Illumina EPIC array. Additionally, we performed cross-sectional EWAS on age-18 blood and buccal DNA from the same individuals to elucidate tissue-specific signatures of severe adolescent victimization. Our analyses identified 20 suggestive differentially methylated positions (DMPs) (P

Feeling inhibited and socially not at ease is reflected in the trait social inhibition (SI). SI is associated with psychopathology that arises in young adulthood, such as anxiety. We aim for a better insight into the genetic and environmental contributions to SI across the life span, and as such examine their contributions to SI stability and change across adolescent and adult life span. We analyzed cohort-sequential longitudinal data from the Netherlands Twin Register (NTR), spanning a period of 25 years (Men (N, %): 17855,37.4%; Age (Median, IQR): 19 years, 16-26 years: 7474 complete MZ twins and 8799 complete DZ twins). The data were organized into 7 age groups: <14 (preadolescence), 15-16 (early adolescence), 17-18 (mid adolescence), 19-20 Cite adolescence), 21-30 (young adulthood), 31-40 (adulthood), 41+ (middle-age--older adulthood). SI was assessed with the ASEBA-based proxy questionnaire. Phenotypic stability was established across the entire age range. Next, a longitudinal genetic simplex model was fitted to estimate the genetic and environmental contributions to the observed phenotypic stability. Results showed SI correlated well across follow-up of a single decade (.44 ≤ r ≤ .59) and moderately across the 25 years (.23 - .32) from adolescence to middle-age and older. Broad-sense heritability (h² was between 40 and 48% across the 7 age groups, Additive and nonadditive genetic effects together explained most of the stability of SI across the life span (about 60-90% of the phenotypic correlation between ages), whereas environmental effects played a lesser role (about 10-40%). Concluding, SI, known to increase the risk of internalizing psychopathology, is phenotypically stable across the life span, which is largely attributable to genetic contributions to individual differences in SI. [ABSTRACT FROM AUTHOR]

Background: Previous research indicates that body dysmorphic disorder (BDD) is associated with risk of suicidality. However, studies have relied on small and/or specialist samples and largely focussed on adults, despite these difficulties commonly emerging in youth. Furthermore, the aetiology of the relationship remains unknown. Methods: Two independent twin samples were identified through the Child and Adolescent Twin Study in Sweden, at ages 18 (N = 6027) and 24 (N = 3454). Participants completed a self-report measure of BDD symptom severity. Young people and parents completed items assessing suicidal ideation/behaviours. Logistic regression models tested the association of suicidality outcomes with: (a) probable BDD, classified using an empirically derived cut-off; and (b) continuous scores of BDD symptoms. Bivariate genetic models examined the aetiology of the association between BDD symptoms and suicidality at both ages. Results: Suicidal ideation and behaviours were common among those with probable BDD at both ages. BDD symptoms, measured continuously, were linked with all aspects of suicidality, and associations generally remained significant after adjusting for depressive and anxiety symptoms. Genetic factors accounted for most of the covariance between BDD symptoms and suicidality (72.9 and 77.7% at ages 18 and 24, respectively), but with significant non-shared environmental influences (27.1 and 22.3% at ages 18 and 24, respectively). Conclusions: BDD symptoms are associated with a substantial risk of suicidal ideation and behaviours in late adolescence and early adulthood. This relationship is largely explained by common genetic liability, but non-shared environmental effects are also significant and could provide opportunities for prevention among those at high-risk. [ABSTRACT FROM AUTHOR]

There is considerable variability in the extent to which young people with developmental language disorder (DLD) experience mental health difficulties. What drives these individual differences remains unclear. In the current article, data from the Twin Early Development Study were used to investigate the genetic and environmental influences on psychopathology in children and adolescents with DLD (n = 325) and those without DLD (n = 865). Trivariate models were fitted to investigate etiological influences on DLD and psychopathology, and bivariate heterogeneity and homogeneity models were fitted and compared to investigate quantitative differences in etiological influences on psychopathology between those with and without DLD. The genetic correlation between DLD and internalizing problems in childhood was significant, suggesting that their co-occurrence is due to common genetic influences. Similar, but nonsignificant effects were observed for externalizing problems. In addition, genetic influences on internalizing problems, but not externalizing problems, appeared to be higher in young people with DLD than those without DLD, suggesting that the presence of DLD may exacerbate genetic risk for internalizing problems. These findings indicate that genetic influences on internalizing problems may also confer susceptibility to DLD (or vice versa) and that DLD serves as an additional risk factor for those with a genetic predisposition for internalizing problems. [ABSTRACT FROM AUTHOR]

Parents are known to provide a lasting basis for their children's social development. Understanding parent-driven socialization is particularly relevant in adolescence, as an increasing social independence is developed. However, the relationship between key parenting styles of care and control and the microlevel expression of daily-life social interactions has been insufficiently studied. Adolescent and young adult twins and their nontwin siblings (N = 635; mean age = 16.6: age range = 14.2-21.9; 58.6% female; 79.5% in or having completed higher secondary/tertiary education; 2.8% speaking language other than Dutch at home) completed the Parental Bonding Instrument (PBI) on parental care and control. Participants also completed a 6-day experience sampling period (10 daily beeps, mean compliance = 68.0%) to assess daily-life social interactions. Higher overall parental bonding quality (of both parents) related to more positive social experiences in daily life (e.g., belonging in company), but not to more social behaviors (e.g., being with others). Factor analysis indicated a three-factor structure of the PBI, with care, denial of psychological autonomy, and encouragement of behavioral freedom. Paternal care was uniquely predictive of better social experiences. These findings demonstrate how parenting styles [ABSTRACT FROM AUTHOR]

STUDY QUESTION Does adolescent attachment to parents and peers differ between singletons and twins born with ART or natural conception (NC)? SUMMARY ANSWER Adolescent attachment anxiety with the father was higher among NC singletons than among ART and NC twins, whereas attachment avoidance with the father was higher in ART singletons than in NC singletons and NC twins. No differences were found in attachment to the mother, best friend or romantic partner. WHAT IS KNOWN ALREADY Most studies have not found differences between ART and NC singletons in parent–adolescent relationships, but twin relationships may be more at risk. No previous study has examined all four groups in the same study, or specifically looked at attachment relationships. STUDY DESIGN, SIZE, DURATION This was an 18-year, prospective and controlled longitudinal study with families of 496 ART singletons, 101 ART twin pairs, 476 NC singletons and 22 NC twin pairs. Families were recruited during the second trimester of pregnancy; the ART group was recruited from five infertility clinics in Finland and the control group was recruited from a hospital outpatient clinic during a routine visit. PARTICIPANTS/MATERIALS, SETTING, METHODS Mothers and fathers gave background information for this study during pregnancy, and during the child's first year and early school age (7–8 years). For the ART group, infertility characteristics and prenatal medical information was also obtained from the patient registry of the infertility clinics. Children (originally 50% girls) filled in electronic questionnaires related to their attachment to mother, father, best friend and romantic partner (Experiences in Close Relationships—Relationship Structures) at 17–19 years of age. MAIN RESULTS AND THE ROLE OF CHANCE Adolescent attachment anxiety to father was higher in NC singletons than in ART twins, P  = 0.004 and marginally higher than in NC twins, P  = 0.06. Adolescent attachment avoidance to father was higher in ART singletons than in NC singletons, P  = 0.006 and marginally higher than in NC twins, P  = 0.055. LIMITATIONS, REASONS FOR CAUTION The sample size was small especially in the NC twin group and there was drop-out over the 18-year time period, especially among boys and families with lower parental education level. The study only included native Finnish-speaking families. The results could differ in a more diverse population. ART singletons were younger and had fewer siblings than ART twins and NC children, and ART and NC twins had more newborn health risks than ART and NC singletons. WIDER IMPLICATIONS OF THE FINDINGS The study adds to a growing body of evidence that neither ART treatments nor being a twin places mother–child relationships or peer relationships at long-term risk. However, in our study, which was the first to examine both ART and twinhood simultaneously, we found that there may be more problems in father–adolescent relationships, but only in ART singletons and only related to attachment avoidance. Our findings suggest that men, as well as women, should receive enough support in pre- and peri-natal health care during and after infertility treatments. STUDY FUNDING/COMPETING INTEREST(S) This study was funded by Academy of Finland (grant number 2501308988), the Juho Vainio Foundation and the Finnish Cultural Foundation. The authors report no conflict of interest. TRIAL REGISTRATION NUMBER N/A. [ABSTRACT FROM AUTHOR]

Abstract: Data on the etiological factors underlying the co-occurrence of common adolescent pain with anxiety and depression symptoms are very limited. Opioid prescriptions for adolescent pain problems are on the rise in North America and constitute a risk factor for diversion, misuse, and substance use. In this study, we aimed to investigate the phenotypic and etiological association among pain, depression, and anxiety and to test their link to substance use in adolescents. By taking advantage of the Italian National Twin Registry and of the relatively low incidence of opioid prescriptions in Italy, we applied multivariate modelling analyses to 748 Italian adolescent twins (374 pairs, mean age 16 ± 1.24 years). Twins' responses to the Achenbach Youth Self-Report questionnaire were used to build a composite adolescent pain index and to measure anxiety, depression, and substance use. All monozygotic within-pair correlations were higher than the dizygotic correlations, indicating genetic influences for adolescent pain, anxiety, and depressive problems. A common latent liability factor influenced by genetic and environmental elements shared among pain, depression, and anxiety provided the best fit to explain the co-occurrence of adolescent pain, anxiety, and depression problems. A common phenotypic factor capturing all 3 phenotypes was positively associated (β = 0.19, P < 0.001, confidence interval: 0.10-0.27) with substance use. These findings indicate that several intertwined mechanisms, including genetic factors, can explain a shared liability to common adolescent pain, anxiety, and depression problems. Their association with substance use remains traceable even in societies with relatively low prevalence of opioid prescriptions. [ABSTRACT FROM AUTHOR]

Background: Shame is considered a maladaptive self‐conscious emotion that commonly co‐occurs alongside depression and anxiety. Little is known, however, about the aetiology of shame and its associations with depression and anxiety. We estimated, for the first time, genetic and environmental influences on shame and on its associations with depression and anxiety in adolescence. Methods: The sample was twin and sibling pairs from the Genesis 1219 Study (Time 1, N = 2,685; males 42.8%, Mage = 14.95, SD = 1.67, age range: 12–21; Time 2, N = 1618; males 39.7%, Mage = 16.97, SD = 1.64, age range: 14–23). Participants completed validated questionnaires to measure shame (at Time 1), depression and anxiety (at Times 1 and 2). Results: Shame was moderately to strongly associated with concurrent depression and anxiety. Prospectively, shame was significantly associated with an increase in depression, but not anxiety. Genetic analyses revealed that shame was moderately heritable with substantial nonshared environmental influence. The associations between shame and concurrent depression and anxiety were primarily accounted for by overlapping genetic influences. Prospectively, the association between shame and later depression was primarily accounted for by genetic and nonshared environmental influences shared with earlier depression. The unique association between shame and later depression was mostly explained by common nonshared environmental influences. Conclusions: The findings offer novel evidence regarding aetiology of shame—although moderately heritable, shame in adolescents may also result from nonshared environmental factors. Genetic and nonshared environmental influences contribute to the co‐occurrence of shame with depression and anxiety. [ABSTRACT FROM AUTHOR]

The goal of the present study was to replicate Burt et al. (2009) and Hou et al. (2013) findings by determining the contribution of peers' deviance to changes in participants' (monozygotic [MZ] twins') self-reported delinquency from mid- to late adolescence while controlling for possible gene-environment correlations (rGE) through the use of the cotwin method in the context of a cross-lagged design. Two separate samples were used to this purpose. The first sample included 289 MZ-twin pairs (48.42% female, 65.5% of European descent, 2 1,7% of African descent, 12.8% other; average age at first assess- ment = 16.20 years) and relied on perceived measures of peer deviance, as in the two original studies. The second sample comprised 181 MZ-twin pairs (50.67% female; 84% of European descent, 3% of African descent. 2% of Asian descent, 2% Native North Americans, and 9% unspecified: average age at first assessment = 13.05 years) and used direct measures to assess peers' deviance. Participants in the first sample were part of a large representative sample of American adolescents. whereas the second sample included families with twins born in a large Canadian city. Results showed that within-pair differences in self-reported delinquency were stable from midadolescence to late adolescence in both samples. As in Burt et al. (2009) and Hou et al. (2013) within-pair differences in peer deviance did not predict changes in within-pair differences in self-reported delinquency in both samples (i.e., no socialization effect). In contrast to Burt et al. (2009) and Hou et al. (2013), however. we found no predictive link from twins' self-reported delinquency to peers' deviance (i.e., no selection effect). Finally, as in Burt et al. (2009) we found that peers' deviance was stable from middle to late adolescence and that peers' deviance and participants' delinquency were cross-sectionally correlated in the first sample, but not in the second sample. These results are interpreted in the context of the ongoing debate in regard to peers' socialization vs selection effects. [ABSTRACT FROM AUTHOR]

Accumulating evidence suggests that individuals exposed to victimization at key developmental stages may have different epigenetic fingerprints compared to those exposed to no/minimal stressful events, however results are inconclusive. This study aimed to strengthen causal inference regarding the impact of adolescent victimization on the epigenome by controlling for genetic variation, age, gender, and shared environmental exposures. We conducted longitudinal epigenome-wide association analyses (EWAS) on DNA methylation (DNAm) profiles of 118 monozygotic (MZ) twin pairs from the Environmental Risk study with and without severe adolescent victimization generated using buccal DNA collected at ages 5, 10 and 18, and the Illumina EPIC array. Additionally, we performed cross-sectional EWAS on age-18 blood and buccal DNA from the same individuals to elucidate tissue-specific signatures of severe adolescent victimization. Our analyses identified 20 suggestive differentially methylated positions (DMPs) (P < 5e-05), with altered DNAm trajectories between ages 10–18 associated with severe adolescent victimization (∆Beta range = −5.5%−5.3%). Age-18 cross-sectional analyses revealed 72 blood (∆Beta range = −2.2%−3.4%) and 42 buccal (∆Beta range = −3.6%−4.6%) suggestive severe adolescent victimization-associated DMPs, with some evidence of convergent signals between these two tissue types. Downstream regional analysis identified significant differentially methylated regions (DMRs) in LGR6 and ANK3 (Šidák P = 5e-09 and 4.07e-06), and one upstream of CCL27 (Šidák P = 2.80e-06) in age-18 blood and buccal EWAS, respectively. Our study represents the first longitudinal MZ twin analysis of DNAm and severe adolescent victimization, providing initial evidence for altered DNA methylomic signatures in individuals exposed to adolescent victimization. [ABSTRACT FROM AUTHOR]

Bullying‐victimisation has been associated with sleep disturbances. This study investigated the degree to which subtypes of bullying‐victimisation in adolescence are linked with sleep disturbances. Genetic and environmental contributions underlying bullying‐victimisation and sleep disturbances were investigated. Participants (3,242–5,076 pairs) from a longitudinal community twin study reported on their bullying‐victimisation at the age of 14 years, and sleep quality and insomnia symptoms at age 16. Regression analyses were used, accounting for the role of individual and family factors. Structural equation twin model fitting was conducted. Bullying‐victimisation was modestly associated with sleep quality and insomnia symptoms (r = 0.22–0.23) and a similar strength of associations was found across bullying‐victimisation subtypes (r = 0.11–0.22). Bullying‐victimisation, sleep quality and insomnia symptoms were predominantly influenced by genes (25–59%) and non‐shared environments (40–62%). The association between bullying‐victimisation and sleep quality was explained by genetic and non‐shared environmental influences. For insomnia symptoms and sleep quality, the association with bullying‐victimisation was in part explained by a genetic overlap. Associations between bullying‐victimisation and sleep disturbances are not limited to specific aspects of bullying‐victimisation but appear to exist for all subtypes. These findings stimulate research questions regarding the mechanisms underlying these links. For example, could certain heritable traits, such as temperament, increase vulnerability to experiencing sleep disturbances and being bullied? Research on bullying and sleep should aim to take the role of genetic predisposition into account, while also noting that it is not the only causal influence. Understanding more about these pathways could strengthen the development of techniques to prevent these difficulties from occurring. [ABSTRACT FROM AUTHOR]

Externalizing behavior is substantially affected by genetic effects, which are moderated by environmental exposures. However, little is known about whether these moderation effects differ depending on individual characteristics, and whether moderation of environmental effects generalizes across different environmental domains. With a large sample (N = 1,441 individuals) of early adolescent twins (ages 11 and 13), using a longitudinal multi-informant design, we tested interaction effects between negative emotionality and both positive and negative aspects of three key social domains: parents, peers, and schools, on the phenotypic variance as well as the etiology of externalizing. Negative emotionality moderated some of the environmental effects on the phenotypic, genetic, and environmental variance in externalizing, with adolescents at both ends of the negative emotionality distribution showing different patterns of sensitivity to the tested environmental influences. This is the first use of gene-environment interaction twin models to test individual differences in environmental sensitivity, offering a new approach to study such effects. [ABSTRACT FROM AUTHOR]

Depression, conduct, and hyperactivity symptoms are chronic and frequently co-occur in adolescence. Common genetic and environmental vulnerability to these conditions have previously been demonstrated, however, the manner in which common versus disorder-specific etiological influences operate across development and maintain symptom co-occurrence is unclear. Thus, the current study investigated the role of common genetic and environmental influences in the comorbidity of depression, conduct, and hyperactivity across adolescence. Over 10,000 twins and their parents reported adolescents' symptoms at mean ages 11 and 16 years. Biometric independent pathway models were fitted to estimate genetic and environmental contributions to the continuity of symptom co-occurrence over time, as well as time‐ and symptom‐specific influences. Results found that a common stable genetic factor accounted for the concurrent and longitudinal co-occurrence of depression, conduct, and hyperactivity symptoms. New genetic influences common to these three symptom scales emerged at 16 years, and further contributed to symptom co-occurrence. Conversely, environmental influences largely contributed to the time-specific associations. The findings were generally consistent for self- and parent-reported symptoms. Overall, the results suggest that stable, overlapping genetic influences contribute to the co-occurrence of depression, conduct, and hyperactivity symptoms across adolescence. The results are in line with hierarchical causal models of psychopathology, which posit that much of the developmental co-occurrence between different symptoms is due to common liability. Specifically, current findings indicate that only genetic influences constitute common liability over time. Future studies should identify genetically influenced transdiagnostic risk and maintenance factors to inform prevention and treatment of comorbid internalizing and externalizing symptoms in adolescence. [ABSTRACT FROM AUTHOR]

Background: Research has demonstrated that individuals who identify as a sexual minority (e.g., gay/lesbian, bisexual) are at increased risk for suicidality‐related outcomes. However, previous research is primarily limited by the lack of adjustment for unmeasured (i.e., genetic and environmental) confounding factors and previous psychopathology. Methods: Using the Child and Adolescent Twin Study in Sweden, we employed a co‐twin control design to examine the extent to which the association between sexual orientation and adolescent suicide attempt and self‐harm (SA/SH) was independent of genetic and environmental factors shared by twins, as well as measured symptoms of childhood psychopathology. Results: Adolescents who identified as a sexual minority (i.e., gay/lesbian, bisexual, or other sexual orientation) were at two‐fold increased odds for SA/SH (OR, 2.01 [95% confidence interval, 1.63–2.49) compared to heterosexual adolescents. When adjusting for all genetic and shared environmental factors that make twins similar and for measured childhood psychopathology, the association remained positive but attenuated to OR, 1.55 (1.11–2.16). Conclusions: Identifying as a sexual minority was associated with approximately 50% increased odds of SA/SH in adolescence after adjusting for unmeasured genetic and environmental factors shared by twins and for childhood psychopathology. The results support that environmental factors specifically associated with identifying as a sexual minority likely increase risk for SA/SH. Our findings highlight the need to monitor suicidality risk among this group. [ABSTRACT FROM AUTHOR]

Brain structural covariance norms capture the coordination of neurodevelopmental programs between different brain regions. We develop and apply anatomical imbalance mapping (AIM), a method to measure and model individual deviations from these norms, to provide a lifespan map of morphological integration in the human cortex. In cross-sectional and longitudinal data, analysis of whole-brain average anatomical imbalance reveals a reproducible tightening of structural covariance by age 25 y, which loosens after the seventh decade of life. Anatomical imbalance change in development and in aging is greatest in the association cortex and least in the sensorimotor cortex. Finally, we show that interindividual variation in whole-brain average anatomical imbalance is positively correlated with a marker of human prenatal stress (birthweight disparity between monozygotic twins) and negatively correlated with general cognitive ability. This work provides methods and empirical insights to advance our understanding of coordinated anatomical organization of the human brain and its interindividual variation. [ABSTRACT FROM AUTHOR]

Clarifying longitudinal, behavioral predictors for adolescent suicidality could enhance prediction and treatment efforts. We examined whether childhood attentional focusing, persistence, and problem-solving behavior are associated with risk for adolescent suicidal ideation. Participants were 116 twins, 40 of whom endorsed active suicidal ideation (i.e., probands), probands' cotwins, and matched controls. Higher scores on a composite measure derived at mean age 7.7 years of (1) effort and work duration during two childhood problem-solving tasks (untangling yarn and attempting to solve an unsolvable puzzle), (2) mother reported attentional focusing, and (3) observer reported persistence predicted decreased risk for suicidal ideation at mean age 14.4 years. This prediction held when comparing probands with controls (B = -1.01, SE = 0.38, p = 0.01, OR = 0.37) and with their cotwins (B = -0.86, SE = 0.38, p = 0.02, OR = 0.42). Our findings indicate that childhood problem-solving behavior relates meaningfully to risk for suicidal thoughts approximately 7 years later, on average. These results underscore how longitudinal behavioral risk factors could enhance prediction and treatment of adolescent suicidal ideation. [ABSTRACT FROM AUTHOR]

The synergic interaction of risk genes and environmental factors has been thought to play a critical role in mediating emotion-related brain circuitry function and dysfunction in depression and anxiety disorders. Little, however, is known regarding neurodevelopmental bases underlying how maternal negative parenting affects emotion-related brain circuitry linking to adolescent internalizing symptoms and whether this neurobehavioral association is heritable during adolescence. The effects of maternal parenting on amygdala-based emotional circuitry and internalizing symptoms were examined by using longitudinal functional magnetic resonance imaging among 100 monozygotic twins and 78 dizygotic twins from early adolescence (age 13 years) to mid-adolescence (age 16 years). The mediation effects among variables of interest and their heritability were assessed by structural equation modeling and quantitative genetic analysis, respectively. Exposure to maternal negative parenting was positively predictive of stronger functional connectivity of the amygdala with the ventrolateral prefrontal cortex. This neural pathway mediated the association between negative parenting and adolescent depressive symptoms and exhibited moderate heritability (21%). These findings highlight that maternal negative parenting in early adolescence is associated with the development of atypical amygdala-prefrontal connectivity in relation to internalizing depressive symptoms in mid-adolescence. Such abnormality of emotion-related brain circuitry is heritable to a moderate degree. [ABSTRACT FROM AUTHOR]

Hoarding disorder (HD) is hypothesized to originate in childhood/adolescence but little is known about the presentation of hoarding symptoms in youth and their natural history. In this longitudinal study, we tracked and conducted in-depth psychiatric interviews with twins who participated in an epidemiological survey and screened positive on a measure of hoarding symptoms at age 15. Twins screening positive for clinically significant hoarding symptoms at age 15 (n = 42), their co-twins (n = 33), a group of screen negative twins (n = 49), and their parents underwent a clinical assessment a median of 3 years after the initial screening. The assessment included psychiatric screening, hoarding symptoms and cognitions, in-home or photographic assessment of clutter levels, parental accommodation and familial burden. None of the participants had significant levels of clutter at follow-up and thus did not meet strict criteria for HD. However, twins meeting partial criteria (i.e., DSM-5 criteria A and B) for HD (n = 28) had more psychiatric disorders and scored significantly higher on all measures of hoarding symptoms including researcher-rated levels of clutter in their homes, compared to twins who did not meet partial criteria for HD (n = 46). As currently defined in DSM-5, HD may be rare in young people. A non-negligible proportion of young people who were screen positive on hoarding symptoms at age 15 had substantial hoarding symptoms and other psychopathology at follow-up. Whether and how many of these individuals will develop full-blown HD is unknown but the results offer unique insights about the probable origins of HD in adolescence. [ABSTRACT FROM AUTHOR]

Background: Whereas short and problematic sleep are associated with psychological problems in adolescence, causality remains to be elucidated. This study therefore utilized the discordant monozygotic cotwin design and cross‐lagged models to investigate how short and problematic sleep affect psychological functioning. Methods: Adolescent twins (N = 12,803, 13–20 years, 42% male) completed questionnaires on sleep and psychological functioning repeatedly over a two‐year interval. Monozygotic twin pairs were classified as concordant or discordant for sleep duration and trouble sleeping. Resulting subgroups were compared regarding internalizing problems, externalizing problems, and subjective well‐being. Results: Cross‐sectional analyses indicated associations of worse psychological functioning with both short sleep and problematic sleep, and cross‐lagged models indicate bidirectional associations. Longitudinal analyses showed that an increase in sleep problems experienced selectively by one individual of an identical twin pair was accompanied by an increase of 52% in internalizing problem scores and 25% in externalizing problem scores. These changes were significantly different from the within‐subject changes in cotwins with unchanged sleep quality (respectively, 3% increase and 5% decrease). Psychological functioning did, however, not worsen with decreasing sleep duration. Conclusions: The findings suggest that sleep quality, rather than sleep duration, should be the primary target for prevention and intervention, with possible effect on psychological functioning in adolescents. [ABSTRACT FROM AUTHOR]

Study Objectives: To investigate the influence of genetic and environmental factors on sleep-wake behaviors across adolescence. Methods: Four hundred and ninety-five participants (aged 9-17; 55% females), including 93 monozygotic and 117 dizygotic twin pairs, and 75 unmatched twins, wore an accelerometry device and completed a sleep diary for 2 weeks. Results: Individual differences in sleep onset, wake time, and sleep midpoint were influenced by both additive genetic (44%-50% of total variance) and shared environmental (31%-42%) factors, with a predominant genetic influence for sleep duration (62%) and restorative sleep (43%). When stratified into younger (aged 9-14) and older (aged 16-17) subsamples, genetic sources were more prominent in older adolescents. The moderate correlation between sleep duration and midpoint (rP = -.43, rG = .54) was attributable to a common genetic source. Sleep-wake behaviors on school and nonschool nights were correlated (rP = .44-.72) and influenced by the same genetic and unique environmental factors. Genetic sources specific to night-type were also identified, for all behaviors except restorative sleep. Conclusions: There were strong genetic influences on sleep-wake phenotypes, particularly on sleep timing, in adolescence. Moreover, there may be common genetic influences underlying both sleep and circadian rhythms. The differences in sleep-wake behaviors on school and nonschool nights could be attributable to genetic factors involved in reactivity to environmental context. [ABSTRACT FROM AUTHOR]

Family connectedness is key for the development of self-control in early and middle childhood. But is family connectedness still important during the transitional phase of adolescence, when adolescents demand more independence from their parents and rely more on their peers? The aim of the present study was to investigate the association between family connectedness and self-control, and whether it still holds in adolescence using a genetically sensitive design. Data were used from a large sample of twins aged 14 (N = 11,260) and aged 16 (N = 8175), all enrolled in the Netherlands Twin Register. We applied bivariate twin models and monozygotic twin difference models to investigate the association between family connectedness and self-control and to unravel to what extent genetic and environmental factors explain this association. The results showed that more family connectedness is significantly related to better self-control in adolescence, albeit with a small effect size. Twin analyses revealed that this association was mainly explained by common genetic factors and that the effects of environmental factors were small. The current findings confirm the role of family connectedness in adolescent self-control. Importantly, however, the results demonstrate that phenomena we see within families seem the product of parent and children sharing the same genes rather than being exclusively attributable to environmental processes. [ABSTRACT FROM AUTHOR]

Background: Social support has been shown to be associated with a reduced likelihood of developing psychotic experiences in the general population and even amongst those at high risk due to exposure to multiple forms of victimisation (poly-victimised). However, it is unclear whether this association is merely due to the confounding effects of shared environmental and genetic influences, or reverse causality. Therefore, we investigated whether social support has a unique environmentally mediated effect on adolescent psychotic experiences after accounting for familial factors, including genetic factors, and also prior psychopathology. Methods: Participants were from the Environmental Risk (E-Risk) Longitudinal Twin Study, a nationally-representative cohort of 2232 UK-born twins. Adolescents were interviewed at age 18 about psychotic experiences and victimisation exposure since age 12, and their perceptions of social support. Prior childhood mental health problems and psychotic symptoms were assessed at age 12. The discordant twin method was used to disentangle the relative family-wide and unique-environmental effects of social support on psychotic experiences in the general population and among poly-victimised adolescents. Results: Perceived social support, particularly from friends, was found to have a unique environmentally mediated buffering effect on adolescent psychotic experiences in the whole sample and in the high-risk poly-victimised group. Conclusions: The protective effects of social support on adolescent psychotic experiences cannot be accounted for by shared environmental or genetic factors, nor by earlier psychopathology. Our findings suggest that early intervention programmes focused on increasing perceptions of social support have the potential to prevent the emergence of psychotic experiences amongst adolescents. [ABSTRACT FROM AUTHOR]

Background: Adolescence is critical to intercept chronic/persistent pain and decipher its association with anxiety. We ascertained adolescent pain trajectories, their demographic and clinical correlates, the longitudinal association with opiate prescriptions at age 19, and the etiology of the covariation between adolescent pain problems and anxiety symptoms.Methods: Longitudinal assessment of: 6 common pain problems at age 12, 13, 14, 15, and 17 years; 7 common anxiety symptoms at age 12, 13, and 14 years; opiates' prescriptions at age 19, in the Quebec Newborn Twin Study birth cohort of 667 twin pairs born between 1995-1998.Results: Analyses yielded three trajectories of: "none-to-minimal" (34.3%), "sporadic" (56.7%), and "frequent" (9.0%) pain problems between age 12-17. Anxiety (odds ratios [OR] ORage12 : 2.38; confidence interval [CI]: 1.26-4.47; ORage13 : 3.96; CI: 1.73-9.05; ORage14 : 5.45; CI: 2.67-11.11), the female sex (OR: 3.69; CI: 2.20-6.21), and lower socioeconomic status (OR: 0.87; CI: 0.77-0.98) were associated with the "frequent" compared to the "none-to-minimal" pain trajectory. Only the "frequent" pain trajectory predicted opioid prescriptions at age 19 (OR: 4.14; CI: 1.16-14.55). A twin bivariate latent growth curve model and a cross-lagged model showed that genetic factors and non-shared environmental factors common to both phenotypes influence the longitudinal association between anxiety and adolescent pain problems.Conclusions: The relatively common, adolescent "frequent pain" trajectory predicts early opioid prescriptions, and anxiety and adolescent pain share multiple etiological components. These data can inform diagnostic reasoning, clinical practice, and help reducing opioid prescriptions and abuse. [ABSTRACT FROM AUTHOR]

Background Childhood psychotic symptoms have been associated with various psychiatric disorders in adulthood but their role as early markers of poor outcomes during the crucial transition to adulthood is largely unknown. Therefore, we investigated associations between age-12 psychotic symptoms and a range of mental health problems and functional outcomes at age 18. Methods Data were used from the Environmental Risk Longitudinal Twin Study, a nationally representative birth cohort of 2232 twins born in 1994–1995 in England and Wales, followed to age 18 with 93% retention. Childhood psychotic symptoms were assessed in structured interviews at age 12. At age 18, study members' mental health problems, functional outcomes, risky behaviors, and offending were measured using self-reports and official records. Results Children with psychotic symptoms (N = 125, 5.9%) were more likely to experience a range of mental health problems in young adulthood than children without such symptoms. They were also more likely to be obese, smoke cigarettes, be lonely, be parents, and report a lower quality of life, but not more likely to commit crimes. Childhood psychotic symptoms predicted these poor outcomes over and above other emotional and behavioral problems during childhood. Nevertheless, twin analyses indicated that these associations were largely accounted for by shared family factors. Conclusions Psychotic symptoms in childhood signal risk for pervasive mental health and functional difficulties in young adulthood and thus may provide a useful screen for an array of later problems. However, early psychotic symptoms and poor outcomes may be manifestations of shared environmental and genetic risks. [ABSTRACT FROM AUTHOR]

Life-course experiences have been postulated to program hypothalamus-pituitary-adrenal (HPA) axis activity, suggesting that HPA axis activity is, at least partially, stable over time. Yet, there is paucity of data on the long-term stability of cortisol production and metabolism. We performed a prospective follow-up study in twins recruited from a nationwide register to estimate the stability of cortisol production and metabolism over time, and the contribution of genetic and environmental factors to this stability. In total, 218 healthy mono- and dizygotic twins were included. At the ages of 9, 12 and 17 years, morning urine samples were collected for assessment (by gas chromatography-tandem mass spectrometry) of cortisol metabolites, enabling the calculation of cortisol metabolite excretion rate and cortisol metabolism activity. Our results showed a low stability for both cortisol metabolite excretion rate (with correlations <.20) and cortisol metabolism activity indices (with correlations of .25 to .46 between 9 and 12 years, -.02 to .15 between 12 and 17 years and .09 to .28 between 9 and 17 years). Because of the low stability over time, genetic and environmental contributions to this stability were difficult to assess, although it seemed to be mostly determined by genetic factors. The low stability in both cortisol production and metabolism between ages 9 and 17 years reflects the dynamic nature of the HPA axis. [ABSTRACT FROM AUTHOR]

Attention-deficit/hyperactivity disorder (ADHD) is a highly heritable neurodevelopmental disorder. However, no study has examined genetic and environmental influences in the longitudinal developmental course of ADHD symptoms in a non-Western population. This study investigated changes of genetic and environmental influences and their contributions to the stability and change of ADHD symptoms of hyperactivity/impulsivity and inattention in Chinese adolescent twins. A prospective sample of 602 twin pairs (48% male) self-reported both DSM-IV ADHD symptom subscales three times at the approximate age of 12, 13, and 15 years. Longitudinal multivariate genetic analyses through structural equation modelling examined genetic and environmental contributions to the developmental course of ADHD symptoms. From early (time 1 and 2) to middle adolescence (time 3), both symptoms showed modest and non-significant genetic influences that became substantial and significant, whereas shared environmental influences were substantial and significant and became modest and non-significant. The same genetic factors influenced ADHD symptoms throughout adolescence, while shared and non-shared environmental influences largely came from new emerging factors. In early adolescence, genetic factor contributed to the stability of inattention, whereas shared environmental factor contributed to the stability of hyperactivity/impulsivity. Genetic influences of ADHD tended to be smaller, whereas shared environmental influences tended to be larger in Chinese than in Western populations. Genetic factors played a large role in the stability of ADHD throughout adolescence, while shared and non-shared environment primarily contributed to its change. Findings highlight the importance of shared family, neighbourhood, and community experiences on child psychopathology in a collectivistic culture such as the Chinese society. [ABSTRACT FROM AUTHOR]

Objective: Family conflict is associated with low self-control in adolescence. Thus far research about the direction of this association is inconclusive. In this study, we sort out whether this association reflects a causal effect or whether it is explained by a common underlying cause, including genetic factors.Method: In twin data, we fitted a series of causal models, and compared models for the association of family conflict and self-control including reciprocal causation, unidirectional causation from family conflict to low self-control, unidirectional causation from low self-control to family conflict, and common genetic susceptibility. We included data from a large sample of twins aged 14 years (N = 9,173), all enrolled in the Netherlands Twin Register.Results: The results suggested a unidirectional pathway model in which family conflict leads to low self-control in adolescence, with genetic factors also playing a role in explaining the association.Conclusion: Adolescents experiencing family conflict are at risk for showing hampered self-control capacities, with family conflict being a robust predictor of low self-control through common genetic factors but also through direct causal influences. [ABSTRACT FROM AUTHOR]

Objective: Despite established comorbidity between anxiety and disordered eating (DE), and a plethora of research using various methodologies to examine this overlap, use of twin modeling to expose whether a shared genetic liability underpins these conditions remains rare. Method: Data from a longitudinal sample of female twins were selected: measures of risk for DE from Wave 1 (N = 699, 351 pairs, aged 12–15 years), and the Eating Disorder Examination (EDE) and Children's Anxiety Sensitivity Index (CASI) from Wave 2 (N = 669, 338 pairs, aged 16–19 years). At this time, they also completed Children's Anxiety Sensitivity Index (CASI). Bivariate Cholesky decomposition models adjusting for age and body mass index centile investigated the covariance structure between the CASI and EDE. Results: Modeling both genetic and nonshared environmental influences parsimoniously fit these data. All paths were significant. Additive genetic influences were notable for CASI and EDE phenotypes; 14% of the heritable variance was contributed by CASI to the expression of EDE. There was also a smaller but significant contribution of nonshared environmental influences. A multinomial logistic regression indicated body dissatisfaction (RRR = 1.53; 95% CI = 1.07–2.18) differentiated groups with highest EDE scores from the highest CASI scores. Discussion: Shared genetic and environmental influences appear to underpin the relationship, and potentially the observed comorbidity, between anxiety sensitivity and DE. The age of onset is typically earlier for anxiety than DE, suggesting a significant opportunity for early intervention work to reduce the likelihood of subsequent development of DE. [ABSTRACT FROM AUTHOR]

Growing use of in vitro fertilization (IVF) has resulted in an elevated twin birth rate, and a burgeoning population of IVF twins who are now aging into adolescence and beyond. This study tests a model examining whether parental conformity expectations have differential effects on twins' versus singletons' parent–adolescent relationship satisfaction, and if this effect is indirectly associated with relative changes in twins' and singletons' internalizing and externalizing behavior from middle childhood to adolescence. Using a sample of 278 IVF twins and singletons, path models demonstrate that twin status and conformity expectations interact to influence parent–adolescent relationships. Although there was an association between twin status and mother–adolescent relationship satisfaction among parents with high conformity expectations (r = .25, p < .01), this relationship was nonsignificant among parents with low conformity expectations (r = .05, p = .85). The differential effect of conformity expectations on parent–adolescent relationship satisfaction for twins and singletons was indirectly associated with relative changes in twins' and singletons' externalizing behavior from middle childhood to adolescence. Results demonstrate that higher levels of parental conformity expectations may not have the same effect on adolescent twins and singletons. [ABSTRACT FROM AUTHOR]

Neurodevelopment is sensitive to genetic and pre/postnatal environmental influences. These effects are likely mediated by epigenetic factors, yet current knowledge is limited. Longitudinal twin studies can delineate the link between genetic and environmental factors, epigenetic state at birth and neurodevelopment later in childhood. Building upon our study of the Peri/postnatal Epigenetic Twin Study (PETS) from gestation to 6 years of age, here we describe the PETS 11-year follow-up in which we will use neuroimaging and cognitive testing to examine the relationship between early-life environment, epigenetics and neurocognitive outcomes in mid-childhood. Using a within-pair twin model, the primary aims are to (1) identify early-life epigenetic correlates of neurocognitive outcomes; (2) determine the developmental stability of epigenetic effects and (3) identify modifiable environmental risk factors. Secondary aims are to identify factors influencing gut microbiota between 6 and 11 years of age to investigate links between gut microbiota and neurodevelopmental outcomes in mid-childhood. Approximately 210 twin pairs will undergo an assessment at 11 years of age. This includes a direct child cognitive assessment, multimodal magnetic resonance imaging, biological sampling, anthropometric measurements and a range of questionnaires on health and development, behavior, dietary habits and sleeping patterns. Data from complementary data sources, including the National Assessment Program - Literacy and Numeracy and the Australian Early Development Census, will also be sought. Following on from our previous focus on relationships between growth, cardiovascular health and oral health, this next phase of PETS will significantly advance our understanding of the environmental interactions that shape the developing brain. [ABSTRACT FROM AUTHOR]

This article reviews the Southern Illinois Twins/Triplets and Siblings Study (SITSS) and describes some of the findings related to recent projects that were completed using this sample. At this time, the SITSS has enrolled 375 twin pairs, 12 triplet families, 1 family of quadruplets, 98 nontwin sibling pairs and 287 singletons. Testing begins for twins and triplets as young as age 1 and then occurs yearly on their birthdays until 5 years of age. Through age 20, various follow-up studies have been conducted on the SITSS sample to examine their social, emotional, and cognitive development across childhood and adolescence from a behavioral genetic perspective. A variety of methodologies have been used to investigate gene-environment correlations (rGE) and gene-environment interactions (GxE). Advanced statistical procedures (e.g., genetic likelihood indices and multilevel modeling) have been utilized to further investigate genetic underpinnings of behavior. Recent results have indicated genetic influences on the aggressiveness of preschoolers' media preferences, increased problem behaviors related to young children's overestimation of self-competence, and the influence of early life temperament and internalizing problems on adolescent health behaviors. Additionally, the SITSS has provided evidence for evocative rGE for various behaviors (aggression, prosocial and play), as well as findings supporting interactions between the dopamine receptor D4 gene (DRD4) and the environment (peer victimization, prenatal birth complications and parental sensitivity). Together, by use of multitrait and multimethodological investigations, this behavior genetic data set assists in furthering our understanding of biological and environmental influences on children's development. [ABSTRACT FROM AUTHOR]

Background: Prior work has indicated both theoretical and empirical overlap between social and physical aggression. The extent to which their covariance can be explained by the same underlying genetic or environmental factors, however, remains unclear. It is also uncertain whether or how the origins of their covariance might vary across sex. The current study sought to fill these gaps in the literature. Methods: We examined maternal and teacher reports of youth physical and social aggression in over 1000 6–10 years old (mean age = 8.02 years) twin pairs from the Michigan State University Twin Registry. We made use of the bivariate correlated factors model to clarify the origins of their association. We further tested both sex difference and no-sex difference versions of that model to determine whether there are sex differences in the association between social and physical aggression, as often assumed. Results: The covariation between social and physical aggression was due to overlapping genetic factors and common environmental conditions. Specifically, 50–57% of the genetic factors, 74–100% of the shared environmental factors, and 28–40% of the unique environmental factors influencing physical aggression also influenced social aggression according to both mother and teacher reports. These shared etiological factors did not differ across sex. Conclusions: These findings argue against the common assumption that social aggression is the 'female version' of male physical aggression, and instead suggest that social aggression may be best conceptualized as a form of antisocial behavior that shares developmental pathways with other manifestations of externalizing pathology. [ABSTRACT FROM AUTHOR]

Background Little is known about adolescent mental health problems, including social phobia, as risk factors for future work incapacity. The aim of this study was to investigate the association between social phobia in adolescence and unemployment and sickness absence (SA) in early adulthood, also evaluating the role of familial factors (genetics and shared environment). Methods A sample of 2845 Swedish twins born in 1985–86 in Sweden was followed longitudinally in the population-based and prospective Twin study of CHild and Adolescent Development. Information on twins' social phobia was collected at ages 13–4, 16–7 and 19–20 years. Logistic regression providing odds ratios (OR) with 95% confidence intervals (95% CI) was used to analyze the associations between social phobia, unemployment and SA during the follow-up 2006–12. The influence of familial factors was evaluated by conditional logistic regression. Results Presence of social phobia during adolescence was associated with increased odds for unemployment and SA in young adulthood. For unemployment, the highest OR was at the age of 13–4 years (1.58 [95% CI: 1.22–2.06]), and the associations became null after adjusting for familial factors. For SA, the highest OR was at the age of 19–20 years (1.73 [95% CI: 1.13–2.65]), and the estimates changed slightly after adjusting for familial factors. Conclusions : Results suggest that social phobia experienced in adolescence contribute to early adulthood unemployment and SA. Familial factors seemed to explain the association between social phobia and unemployment. [ABSTRACT FROM AUTHOR]

Adolescent alcohol use demonstrates distinct developmental trajectories with different times of onset, levels, and rates of growth. Twin research on adolescent alcohol use has shown that genetic influences are consistent with a gradual growth of risks, whereas non-shared environmental influences are more consistent with an accumulation of risks over time. The current study investigated the relative contributions of genetic and environmental influences on shaping different developmental trajectories of alcohol use through adolescence. Self-reported past year alcohol use was collected from 877 Canadian twins (47.1% males) at age 13, 14, 15, and 17 years. Growth mixture models were fit to examine different developmental trajectories of alcohol use, and biometric liability threshold models were fit to investigate genetic and environmental influences on the liability of belonging to identified trajectories. Three trajectories were identified: low (15.1%), early onset (8.2%), and normative increasing (76.7%). Memberships in the low and early-onset group were under genetic (27.6% and 34.7%), shared (42.4% and 21.5%), and non-shared environment influences (30.0% and 43.8%). Membership in the normative increasing group was under genetic (37.7%) and non-shared environment influences (62.3%). Non-shared environmental influences were significantly larger for the normative increasing trajectory than for the low trajectory. These findings provide a more refined picture of genetic and environmental influences in the development of alcohol use in subgroups of adolescents. Genetic and environmental influences both matter, but to different degrees in different trajectories. Future research should identify specific shared and non-shared environmental experiences that distinguish different trajectories. [ABSTRACT FROM AUTHOR]

To get additional insight into the phenotype of attentional problems, we examined to what extent genetic and environmental factors explain covariation between lack of dispositional mindfulness and attention-deficit/hyperactivity disorder (ADHD) traits in youth, and explored the incremental validity of these constructs in predicting life satisfaction. We used data from a UK population-representative sample of adolescent twins (N = 1092 pairs) on lack of dispositional mindfulness [Mindful Attention Awareness Scale (MAAS)], ADHD traits [Conners' Parent Rating Scale-Revised (CPRS-R): inattentive (INATT) and hyperactivity/impulsivity (HYP/IMP) symptom dimensions] and life satisfaction (Students' Life Satisfaction Scale). Twin model fitting analyses were conducted. Phenotypic correlations (rp) between MAAS and CPRS-R (INATT: rp = 0.18, HYP/IMP: rp = 0.13) were small, but significant and largely explained by shared genes for INATT (% rp INATT–MAAS due to genes: 93%, genetic correlation rA = 0.37) and HYP/IMP (% rp HYP/IMP–MAAS due to genes: 81%; genetic correlation rA = 0.21) with no significant contribution of environmental factors. MAAS, INATT and HYP/IMP significantly and independently predicted life satisfaction. Lack of dispositional mindfulness, assessed as self-reported perceived lapses of attention (MAAS), taps into an aspect of attentional functioning that is phenotypically and genetically distinct from parent-rated ADHD traits. The clinically relevant incremental validity of both scales implicates that MAAS could be used to explore the underlying mechanisms of an aspect of attentional functioning that uniquely affects life satisfaction and is not captured by DSM-based ADHD scales. Further future research could identify if lack of dispositional mindfulness and high ADHD traits can be targeted by different therapeutic approaches resulting in different effects on life satisfaction. [ABSTRACT FROM AUTHOR]

Peer victimization impacts 13% of adolescents worldwide (Currie et al. 2012). Despite its prevalence and associated adverse outcomes, global cognitive processes that could be affected by peer victimization have not been thoroughly investigated. Using a monozygotic (MZ) twin difference design that rigorously controls for the influence of genetic and familial level confounders, we examined the relation between peer victimization exposure and selective attention processes during an affective go/no go task. Twins who experienced more severe peer victimization were biased towards detecting goal relevant stimuli during the task. Our findings suggest an environmentally salient relation between peer victimization and goal oriented selective attention. Future work should investigate how this process might serve to enhance or buffer risk of peer victimization exposure for developing later adverse outcomes. [ABSTRACT FROM AUTHOR]

The present study used a genetically informed design of twins raised in the same family (375 monozygotic and 290 dizygotic twins; 50.2% girls) to examine the association between adolescents' genetic risk for depressive symptoms and the course of the parent-child relationship quality throughout adolescence. Depressive symptoms and the quality of the parent-adolescent relationships were measured through adolescents' self-reports from ages 13 to 17. Group-based trajectory modeling revealed that most adolescents experienced high-quality relationships with both of their parents, characterized by high levels of warmth and low levels of conflict, and marked by gradual changes over adolescence. However, 3% of adolescents showed a trajectory of high and increasing conflict with their mothers and 16% of adolescents showed a trajectory of low warmth with their fathers, which decreased until mid-adolescence before increasing thereafter. Moreover, in line with an evocative gene- environment correlation process, a higher genetic vulnerability to depressive symptoms increased the likelihood of following a more problematic relationship trajectory with parents. This rGE was mediated by adolescents' actual depressive behavior symptoms. Results also suggest that adolescents' depression symptoms may affect girls' and boys' relationship with their parents in a similar way, with specific sex-patterns revolving more around the sex of the parent. [ABSTRACT FROM AUTHOR]

Background: Longitudinal studies enhance understanding of the complex reciprocal relationship between smoking and depression from adolescence to young adulthood. Examining bi-directional associations between cigarette smoking and depressive symptoms in a genetically informative twin design can help to understand whether the associations are independent of shared genetic and environmental factors.Methods: We analyzed longitudinal data on smoking and depressive symptoms in twins participating in the adolescent (mean age 17.5) and young adult (mean age 21.9) surveys of the FinnTwin12 study (maximum N = 2,954 individuals; 1,154 twin pairs). At both waves, self-reported depressive symptoms, assessed with the 10-item version of the General Behavior Inventory (GBI), and smoking status were analyzed. The bi-directional associations were first studied among individuals and then within monozygotic and dizygotic twin pairs.Results: When adjusted for multiple covariates and baseline depressive symptoms, daily smokers at age 17 had higher depressive symptom scores at age 22 than never smokers (Incidence Rate Ratio = 1.17, 95% CI: 1.03-1.33). Similarly, when adjusted for covariates and baseline smoking, higher score in GBI at age 17 was associated with an increased likelihood of being a non-daily (Relative Risk Ratio (RRR) = 1.06, 95% CI: 1.01-1.11) or daily (RRR = 1.05, 95% CI: 1.00-1.10) smoker at age 22. No associations were found in within-pair analyses, suggesting that the individual-level association is explained by shared familial liabilities.Conclusion: During the developmental period from adolescence to adulthood, cigarette smoking and depressive symptoms are reciprocally associated. However, these associations are confounded by shared genetic and other familial liabilities. [ABSTRACT FROM AUTHOR]