Adolescent Irritability: Phenotypic Associations and Genetic Links With Depressed Mood

OBJECTIVE: Irritability has been proposed to underlie the developmental link between oppositional problems and depression. However, little is known about the genetic and environmental influences on irritability and its overlap with depression. This paper tests the hypothesis that the association between irritability and depression is accounted for by genetic factors. As such, it draws on the notion of “generalist genes” i.e., genes of general effect that underlie phenotypic overlap between disorders. METHOD: The G1219 study, a UK-based twin sample (N=2651), was used in a cross-sectional and longitudinal design. Irritable and headstrong/hurtful dimensions of oppositional behavior were derived using factor analysis. Regression was used to estimate the association between depression and delinquency. Multivariate genetic analyses were used to estimate the genetic overlap between irritability versus headstrong/hurtful behaviors with depression and delinquency respectively. RESULTS: Irritability showed a significantly stronger phenotypic relationship with depression than delinquency, whereas headstrong/hurtful behaviors were more strongly related to delinquency than depression. In multivariate genetic analyses, the genetic correlation between irritability and depression (0.70; CI: 0.59-0.82) was significantly higher than that between irritability and delinquency (0.57; CI: 0.45-0.69); conversely, the genetic correlation between headstrong/hurtful behaviors and delinquency (0.80; CI: 0.72-0.86) was significantly higher than that between headstrong/hurtful behaviors and depression (0.46; CI: 0.36-0.57). In longitudinal models, the phenotypic association between irritability at Time 1 and depression at Time 2 was accounted for by the genetic association between irritability and depression at Time1. CONCLUSIONS: The findings are consistent with the theory that genes with general effects underlie the relationship between irritability and depression

The association between bullying‐victimisation and sleep disturbances in adolescence: Evidence from a twin study

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

The relationship between weight-related indicators and depressive symptoms during adolescence and adulthood: results from two twin studies

Background: The association between weight and depressive symptoms is well established, but the direction of effects remains unclear. Most studies rely on body mass index (BMI) as the sole weight indicator, with few examining the aetiology of the association between weight indicators and depressive symptoms. // Methods: We analysed data from the Twins Early Development Study (TEDS) and UK Adult Twin Registry (TwinsUK) (7658 and 2775 twin pairs, respectively). A phenotypic cross-lagged panel model assessed the directionality between BMI and depressive symptoms at ages 12, 16, and 21 years in TEDS. Bivariate correlations tested the phenotypic association between a range of weight indicators and depressive symptoms in TwinsUK. In both samples, structural equation modelling of twin data investigated genetic and environmental influences between weight indicators and depression. Sensitivity analyses included two-wave phenotypic cross-lagged panel models and the exclusion of those with a BMI <18.5. // Results: Within TEDS, the relationship between BMI and depression was bidirectional between ages 12 and 16 with a stronger influence of earlier BMI on later depression. The associations were unidirectional thereafter with depression at 16 influencing BMI at 21. Small genetic correlations were found between BMI and depression at ages 16 and 21, but not at 12. Within TwinsUK, depression was weakly correlated with weight indicators; therefore, it was not possible to generate precise estimates of genetic or environmental correlations. // Conclusions: The directionality of the relationship between BMI and depression appears to be developmentally sensitive. Further research with larger genetically informative samples is needed to estimate the aetiological influence on these associations

Initiation and Stability of Self-Harm in Adolescence and Early Adulthood: Investigating Social and Aetiological Factors in Twins

Background: Almost one in five (18.8%) UK adolescents are estimated to self-harm and many young people initiate self-harm early (average age 13 years). Prevention of self-harm should be informed by knowledge about risk factors (e.g., socio-demographic indices), characteristics (i.e., motivation for self-harm and help-seeking behaviours), as well as relative aetiological genetic and environmental processes. Previous twin studies evidence both genetic and environmental influences on self-harm. However, to date, there has been no genetically informed research on self-harm aetiology across development, nor studies identifying risk factors for initiating self-harm at a younger age.Methods: We examined self-harm in the Twins Early Development Study, a birth cohort twin study. Using clustered regression models we tested associations of socio-demographic factors and victimisation with lifetime self-harm and age of self-harm initiation, both reported at 21. To investigate stability and/or change in genetic and environmental influences on self-harm we interpreted a multivariate Cholesky decomposition across ages ≤16, 21, and 26.Results: Self-harm was more common in adolescence than early adulthood, and incidence of self-harm in early adulthood was low (1.4%). The most common motivation for self-harm was “to get relief from a terrible state of mind” (83.4%). Independent predictors of self-harm and earlier initiation of self-harm were being female, belonging to a gender and/or sexual minority group, and experience of bullying victimisation. Sexual minority status was still significantly associated with self-harm after controlling for familial factors in co-twin control analyses. The Cholesky decomposition showed stability in genetic influences and innovation in non-shared environmental influences on self-harm. Conclusions: Adolescence should be a key period for self-harm interventions. Women, sexual and gender minorities, and those experiencing victimisation may need targeted support early in adolescence. Furthermore, it should be acknowledged that different individuals can be at risk at different stages as environmental factors influencing self-harm change across time

Relative Age Effects on Attention-Deficit/Hyperactivity Disorder Symptoms and Educational Achievement:A Longitudinal UK Cohort Study

ObjectiveBeing among the youngest in a school class increases the risk for worse educational outcomes and attention-deficit/hyperactivity disorder (ADHD) symptoms, but questions remain about the nature and persistence of such effects. We investigated this “relative age effect” on educational achievement at age 15 to 16 years and on ADHD symptoms from age 7 to age 21 years. Furthermore, we examined whether being young-in-class is linked to a greater reduction in ADHD symptoms from childhood to adulthood and a lower genetic propensity to ADHD.MethodWe identified 3,928 young-in-class and 4,580 old-in-class participants from the Twins’ Early Development Study. Educational achievement was measured with mathematics and English examination grades at age 15 to 16 years, and ADHD symptoms were measured using 2 different scales and different raters, from age 7 to 21 years, with effects tested using regression.ResultsA relative age effect emerged for English but not mathematics examination grades, and for the majority of parent and teacher ratings on ADHD symptoms, most consistently in middle childhood. Being young-in-class was associated with a greater reduction in parent-rated ADHD symptoms from childhood to adulthood when measured with a brief scale, but the comparable result from a longer scale was non-significant (after multiple testing correction). No interaction emerged between relative age and ADHD polygenic scores.ConclusionOur results emphasise the need to improve support for the children who start school younger than most, and to ensure that developmental comparisons take children’s precise age into account. Future research would benefit from in-depth analyses of individual trajectories and their variability among the young-in-class children.</div

Etiology of pervasive versus situational antisocial behaviors:a multi-informant longitudinal cohort study

The aim of this study was to disentangle pervasive from situational antisocial behaviors using multiple informants, and to investigate their genetic and environmental etiologies in preadolescence and across time. Antisocial behaviors were assessed in 2,232 twins from the Environmental Risk (E‐Risk) Longitudinal Twin Study at ages 5 and 12. Pervasive antisocial behaviors were defined as behaviors that mothers, teachers, interviewers, and twins themselves agreed on. Results from a psychometric model indicated that the variation in children's pervasive antisocial behaviors was mostly accounted for by familial influences that originated in childhood, whereas situational behaviors were explained by newly emerging nonshared environmental and genetic influences. This study shows that children's pervasive and situational antisocial behaviors have distinct etiologies that could guide research and treatment

Sub-types of insomnia in adolescents: insights from a quantitative/ molecular twin study

Background: Insomnia with short sleep duration has been postulated as more severe than that accompanied by normal/long sleep length. While the short duration subtype is considered to have greater genetic influence than the other subtype, no studies have addressed this question. This study aimed to compare these subtypes in terms of: 1) the heritability of insomnia symptoms; 2) polygenic scores (PGS) for insomnia symptoms and sleep duration; 3) the associations between insomnia symptoms and a wide variety of traits/disorders. Methods: The sample comprised 4,000 pairs of twins aged 16 from the Twins Early Development Study. Twin models were fitted to estimate the heritability of insomnia in both groups. PGS were calculated for self-reported insomnia and sleep duration and compared among participants with short and normal/long sleep duration. Results: Heritability was not significantly different in the short sleep duration group (A=0.13 [95%CI=0.01, 0.32]) and the normal/long sleep duration group (A=0.35 [95%CI=0.29, 0.40]). Shared environmental factors accounted for a substantial proportion of the variance in the short sleep duration group (C=0.19 [95%CI= 0.05, 0.32]) but not in the normal/long sleep duration group (C=0.00 [95%CI=0.00, 0.04]). PGS did not differ significantly between groups although results were in the direction expected by the theory. Our results also showed that insomnia with short (as compared to normal/long) sleep duration had a stronger association with anxiety and depression (p<.05) - although not once adjusting for multiple testing. Conclusions: We found mixed results in relation to the expected differences between the insomnia subtypes in adolescents. Future research needs to further establish cut-offs for ‘short’ sleep at different developmental stages and employ objective measures of sleep

The Genesis 12–19 (G1219) Study: A Twin and Sibling Study of Gene–Environment Interplay and Adolescent Development in the UK

The Genesis 12–19 (G1219) Study is an ongoing longitudinal study of a sample of UK twin pairs, non-twin sibling pairs, and their parents. G1219 was initially designed to examine the role of gene–environment interplay in adolescent depression. However, since then data have continued to be collected from both parents and their offspring into young adulthood. This has allowed for longitudinal analyses of depression and has enabled researchers to investigate multiple phenotypes and to ask questions about intermediate mechanisms. The study has primarily focused on emotional development, particularly depression and anxiety, which have been assessed at multiple levels of analysis (symptoms, cognitions, and relevant environmental experiences). G1219 has also included assessment of a broader range of psychological phenotypes ranging from antisocial behaviors and substance use to sleep difficulties, in addition to multiple aspects of the environment. DNA has also been collected. The first wave of data collection began in the year 1999 and the fifth wave of data collection will be complete before the end of 2012. In this article, we describe the sample, data collection, and measures used. We also summarize some of the key findings to date