The Colombo Twin and Singleton Study (COTASS): Piloting the Feasibility of Collecting Nutritional Data and Extension of the Sample to Include Children of Twins.

Nutrition and diet are key modifiable risk factors for the rising burden of non-communicable diseases like cardio-vascular diseases and diabetes in low- and middle- income countries (LMICs). The nutritional transition in dietary behaviours in LMICs has most likely contributed to this problem. Although traditionally assumed to be environmental, dietary choices are also genetically influenced. Twin study designs can be used to investigate the relative influence of genes and environment on nutrition intake, eating behaviours and associated psychological health. The overall aim of this project is to: provide proof-of-concept for the feasibility of using dietary (biomarker) data within the Children-of-Twin design in nutrition studies, develop laboratory skills and statistical genetic skills and establish a Sri Lankan-specific food composition database. Currently, a pilot study is being conducted with 304 individuals (38 Monozygotic twin pairs, 38 Dizygotic twin pairs and their male or female adult offspring). Questionnaire data on nutritional intake, eating behaviours, psychological well-being, physical health, and bio-specimens are being collected. A Sri Lankan-specific food composition database was developed, training sessions on macro and micro element analysis in biological samples and statistical genetics skills development were conducted and Community Engagement and Involvement programs were carried out in two districts of Sri Lanka.

Genetic and Environmental Influences on Sexual Orientation: Moderation by Childhood Gender Nonconformity and Early-Life Adversity.

Existing evidence indicates genetic and non-genetic influences on sexual orientation; however, the possibility of gene-environment interplay has not been previously formally tested despite theories indicating this. Using a Finnish twin cohort, this study investigated whether childhood gender nonconformity and early-life adversities independently moderated individual differences in sexual orientation and childhood gender nonconformity, the relationship between them, and the etiological bases of the proposed moderation effects. Sexual orientation, childhood gender nonconformity, and early-life adversities were assessed using standard questionnaires. Structural equation twin model fitting was carried out using OpenMx. Childhood gender nonconformity was significantly associated with reduced phenotypic variance in sexual orientation (ß = - 0.14, 95% CI - 0.27, - 0.01). A breakdown of the underlying influences of this moderation effect showed that this was mostly due to moderation of individual-specific environmental influences which significantly decreased as childhood gender nonconformity increased (ßE = - 0.38; 95% CI - 0.52, - 0.001) while additive genetic influences were not significantly moderated (ßA = 0.05; 95% CI - 0.30, 0.27). We also observed that the relationship between sexual orientation and childhood gender nonconformity was stronger at higher levels of childhood gender nonconformity (ß = 0.10, 95% CI 0.05, 0.14); however, significance of the underlying genetic and environmental influences on this relationship could not be established in this sample. The findings indicate that beyond a correlation of their genetic and individual-specific environmental influences, childhood gender nonconformity is further significantly associated with reduced individual-specific influences on sexual orientation.

Frequency of Consumption of Food Groups and Cardio-Metabolic Risk Factors: A Genetically Informative Twin Study in Sri Lanka.

Low- and middle-income countries (LMICs) globally have undergone rapid urbanisation, and changes in demography and health behaviours. In Sri Lanka, cardio-vascular disease and diabetes are now leading causes of mortality. High prevalence of their risk factors, including hypertension, dysglycaemia and obesity have also been observed. Diet is a key modifiable risk factor for both cardio-vascular disease and diabetes as well as their risk factors. Although typically thought of as an environmental risk factor, dietary choice has been shown to be genetically influenced, and genes associated with this behaviour correlate with metabolic risk indicators. We used Structural Equation Model fitting to investigate the aetiology of dietary choices and cardio-metabolic phenotypes in COTASS, a population-based twin and singleton sample in Colombo, Sri Lanka. Participants completed a Food Frequency Questionnaire (N = 3934) which assessed frequency of intake of 14 food groups including meat, vegetables and dessert or sweet snacks. Anthropometric (N = 3675) and cardio-metabolic (N = 3477) phenotypes were also collected including weight, blood pressure, cholesterol, fasting plasma glucose and triglycerides. Frequency of consumption of most food items was found to be largely environmental in origin with both the shared and non-shared environmental influences indicated. Modest genetic influences were observed for some food groups (e.g. fruits and leafy greens). Cardio-metabolic phenotypes showed moderate genetic influences with some shared environmental influence for Body Mass Index, blood pressure and triglycerides. Overall, it seemed that shared environmental effects were more important for both dietary choices and cardio-metabolic phenotypes compared to populations in the Global North.

Assessing aetiological overlap between child and adult attention-deficit hyperactivity disorder symptoms in an extended family design.

BACKGROUND: Several longitudinal studies have cast doubt on the aetiological overlap between child and adult attention-deficit hyperactivity disorder (ADHD). However, a lack of genetically sensitive data following children across adulthood precludes direct evaluation of aetiological overlap between child and adult ADHD. AIMS: We circumvent the existing gap in longitudinal data by exploring genetic overlap between maternal (adult) and offspring (child) ADHD and comorbid symptoms in an extended family cohort. METHOD: Data were drawn from the Norwegian Mother, Father and Child Cohort Study, a Norwegian birth registry cohort of 114 500 children and their parents. Medical Birth Registry of Norway data were used to link extended families. Mothers self-reported their own ADHD symptoms when children were aged 3 years; reported children's ADHD symptoms at age 5 years; and children's ADHD, oppositional defiant disorder (ODD), conduct disorder, anxiety and depression symptoms at age 8 years. Genetic correlations were derived from Multiple-Children-of-Twins-and-Siblings and extended bivariate twin models. RESULTS: Phenotypic correlations between adult ADHD symptoms and child ADHD, ODD, conduct disorder, anxiety and depression symptoms at age 8 years were underpinned by medium-to-large genetic correlations (child ADHD: rG = 0.55, 95% CI 0.43-0.93; ODD: rG = 0.80, 95% CI 0.46-1; conduct disorder: rG = 0.44, 95% CI 0.28-1; anxiety: rG = 0.72, 95% CI 0.48-1; depression: rG = 1, 95% CI 0.66-1). These cross-generational adult-child genetic correlations were of a comparable magnitude to equivalent child-child genetic correlations with ADHD symptoms at age 5 years. CONCLUSIONS: Our findings provide genetically sensitive evidence that ADHD symptoms in adulthood share a common genetic architecture with symptoms of ADHD and four comorbid disorders at age 8 years. These findings suggest that in the majority of cases, ADHD symptoms in adulthood are not aetiologically distinct from in childhood.

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 4000 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.

Associations between socioeconomic factors and depression in Sri Lanka: The role of gene-environment interplay.

BACKGROUND: Low socioeconomic status is a risk factor for depression. The nature and magnitude of associations can differ cross-culturally and is influenced by a range of contextual factors. We examined the aetiology of socioeconomic indicators and depression symptoms and investigated whether socioeconomic indicators moderate genetic and environmental influences on depression symptoms in a Sri Lankan population. METHODS: Data were from a population-based sample of twins (N = 2934) and singletons (N = 1035) in Colombo, Sri Lanka. Standard of living, educational attainment, and financial strain were used to index socioeconomic status. Depression symptoms were assessed using the Revised Beck Depression Inventory. Structural equation modelling explored genetic and environmental influences on socioeconomic indicators and depression symptoms and moderation of aetiological influences on depression symptoms by socioeconomic status. RESULTS: Depression symptoms were associated with lower standard of living, lower educational attainment, and financial strain. Sex differences were evident in the aetiology of standard of living, with a small contribution of genetic influences in females. Educational attainment was moderately heritable in both males and females. Total variance in depression was greater among less socioeconomically advantaged individuals. Modest evidence of moderation of the aetiology of depression by standard of living and education was observed. LIMITATIONS: While the sample is representative of individuals living in Colombo District, it may not be representative of different regions of Sri Lanka. CONCLUSIONS: The aetiology of depression varies across socioeconomic contexts, suggesting a potential mechanism through which socioeconomic disadvantage increases the risk for depression in Sri Lanka. Findings have implications for cross-cultural investigations of the role of socioeconomic factors in depression and for identifying targets for social interventions.

The Etiological and Predictive Association Between ADHD and Cognitive Performance From Childhood to Young Adulthood.

OBJECTIVE: Evidence about the etiology of the predictive associations between a diagnosis of ADHD and cognitive performance over time is scarce. Here, we examine these predictive and etiological patterns using a cross-lagged model design in a sample of 404 participants (74% males) from ADHD and control sibling pairs aged 6 to 17 years at baseline and 12 to 24 years at follow-up. METHODS: Data included IQ, short-term and working memory measures, and response speed and variability from a four-choice reaction-time task. RESULTS: ADHD and IQ predicted each other over time. ADHD at baseline predicted lower working memory performance at follow-up. Stable etiological influences emerged in the association between ADHD and cognitive variables across time. CONCLUSION: Whether early interventions can reduce negative interference with learning at school requires further study.

Gene-environment interplay linking perceived parental supervision and peer drunkenness with Chinese adolescent alcohol initiation.

Following 602 Chinese twin pairs (48% male, all Han ethnicity) from primarily lower-than-average socioeconomic status families from early to mid-adolescence (Ms  = 12 and 15 in 2006 and 2009), this study investigated gene-environment interplay between perceived parental supervision, peer drunkenness, and adolescent alcohol initiation. For alcohol initiation, shared environmental influences were initially negligible but became substantial. Genetic factors largely explained the links between both correlates with alcohol initiation. Parental supervision amplified genetic risks for alcohol initiation in early adolescence but suppressed it in mid-adolescence. Peer drunkenness augmented genetic and environmental influences at both times. Peer drunkenness showed stronger links and moderating potential than parental supervision. Chinese adolescents show dynamic gene-environment interplay patterns involving parent-child and peer processes in alcohol initiation.

Causal Influences of Same-Sex Attraction on Psychological Distress and Risky Sexual Behaviors: Evidence for Bidirectional Effects.

Although health disparities among same-sex attracted compared to heterosexual individuals are typically explained by minority stress, there is limited evidence for a causal effect. This study investigated whether same-sex attraction was causally associated with psychological distress and risky sexual behavior using sociosexual behavior as a proxy. The sample comprised monozygotic and dizygotic twins and their non-twin siblings (n = 2036, 3780 and 2356, respectively) genotyped and assessed for same-sex attraction, psychological distress (anxiety and depressive symptoms), and risky sexual behavior. Causal influences were investigated with same-sex attraction as the predictor and psychological distress and risky sexual behavior as the outcomes in two separate Mendelian Randomization-Direction of Causation (MRDoC) models using OpenMx in R. The MRDoC model improves on the Mendelian Randomization and Direction of Causation twin models by allowing analyses of variables with similar genetic architectures, incorporating polygenic scores as instrumental variables and specifying pleiotropy and residual covariance. There were significant causal influences flowing from same-sex attraction to psychological distress and risky sexual behavior (standardized coefficients = 0.13 and 0.16; 95% CIs 0.03-0.23 and 0.08-0.25, respectively). Further analyses also demonstrated causal influences flowing from psychological distress and risky sexual behavior toward same-sex attraction. Causal influences from same-sex attraction to psychological distress and risky sexual behavior may reflect minority stress, which reinforces ongoing measures to minimize social disparities. Causal influences flowing in the opposite direction may reflect rejection sensitivity, stigma-inducing outcomes of risky sexual behavior, and recall bias; however, further research is required to specifically investigate these processes.

A genetically informed Registered Report on adverse childhood experiences and mental health.

Children who experience adversities have an elevated risk of mental health problems. However, the extent to which adverse childhood experiences (ACEs) cause mental health problems remains unclear, as previous associations may partly reflect genetic confounding. In this Registered Report, we used DNA from 11,407 children from the United Kingdom and the United States to investigate gene-environment correlations and genetic confounding of the associations between ACEs and mental health. Regarding gene-environment correlations, children with higher polygenic scores for mental health problems had a small increase in odds of ACEs. Regarding genetic confounding, elevated risk of mental health problems in children exposed to ACEs was at least partially due to pre-existing genetic risk. However, some ACEs (such as childhood maltreatment and parental mental illness) remained associated with mental health problems independent of genetic confounding. These findings suggest that interventions addressing heritable psychiatric vulnerabilities in children exposed to ACEs may help reduce their risk of mental health problems.

Bidirectional Causal Associations Between Same-Sex Attraction and Psychological Distress: Testing Moderation and Mediation Effects.

Only one study has examined bidirectional causality between sexual minority status (having same-sex attraction) and psychological distress. We combined twin and genomic data from 8700 to 9700 participants in the UK Twins Early Development Study cohort at ≈21 years to replicate and extend these bidirectional causal effects using separate unidirectional Mendelian Randomization-Direction of Causation models. We further modified these models to separately investigate sex differences, moderation by childhood factors (retrospectively-assessed early-life adversity and prospectively-assessed childhood gender nonconformity), and mediation by victimization. All analyses were carried out in OpenMx in R. Same-sex attraction causally influenced psychological distress with significant reverse causation (beta = 0.19 and 0.17; 95% CIs = 0.09, 0.29 and 0.08, 0.25 respectively) and no significant sex differences. The same-sex attraction → psychological distress causal path was partly mediated by victimization (12.5%) while the reverse causal path was attenuated by higher childhood gender nonconformity (moderation coefficient = -0.09, 95% CI: -0.13, -0.04).

Different trajectories of depression, anxiety and anhedonia symptoms in the first 12 months of the COVID-19 pandemic in a UK longitudinal sample.

BACKGROUND: While studies from the start of the COVID-19 pandemic have described initial negative effects on mental health and exacerbating mental health inequalities, longer-term studies are only now emerging. METHOD: In total, 34 465 individuals in the UK completed online questionnaires and were re-contacted over the first 12 months of the pandemic. We used growth mixture modelling to identify trajectories of depression, anxiety and anhedonia symptoms using the 12-month data. We identified sociodemographic predictors of trajectory class membership using multinomial regression models. RESULTS: Most participants had consistently low symptoms of depression or anxiety over the year of assessments (60%, 69% respectively), and a minority had consistently high symptoms (10%, 15%). We also identified participants who appeared to show improvements in symptoms as the pandemic progressed, and others who showed the opposite pattern, marked symptom worsening, until the second national lockdown. Unexpectedly, most participants showed stable low positive affect, indicating anhedonia, throughout the 12-month period. From regression analyses, younger age, reporting a previous mental health diagnosis, non-binary, or self-defined gender, and an unemployed or a student status were significantly associated with membership of the stable high symptom groups for depression and anxiety. CONCLUSIONS: While most participants showed little change in their depression and anxiety symptoms across the first year of the pandemic, we highlight the divergent responses of subgroups of participants, who fared both better and worse around national lockdowns. We confirm that previously identified predictors of negative outcomes in the first months of the pandemic also predict negative outcomes over a 12-month period.

Cardiometabolic risk profiles in a Sri Lankan twin and singleton sample.

INTRODUCTION: Prevention of cardiovascular disease and diabetes is a priority in low- and middle-income countries, especially in South Asia where these are leading causes of morbidity and mortality. The metabolic syndrome is a tool to identify cardiometabolic risk, but the validity of the metabolic syndrome as a clinical construct is debated. This study tested the existence of the metabolic syndrome, explored alternative cardiometabolic risk characterisations, and examined genetic and environmental factors in a South Asian population sample. METHODS: Data came from the Colombo Twin and Singleton follow-up Study, which recruited twins and singletons in Colombo, Sri Lanka, in 2012-2015 (n = 3476). Latent class analysis tested the clustering of metabolic syndrome indicators (waist circumference, high-density lipoprotein cholesterol, triglycerides, blood pressure, fasting plasma glucose, medications, and diabetes). Regression analyses tested cross-sectional associations between the identified latent cardiometabolic classes and sociodemographic covariates and health behaviours. Structural equation modelling estimated genetic and environmental contributions to cardiometabolic risk profiles. All analyses were stratified by sex (n = 1509 men, n = 1967 women). RESULTS: Three classes were identified in men: 1) "Healthy" (52.3%), 2) "Central obesity, high triglycerides, high fasting plasma glucose" (40.2%), and 3) "Central obesity, high triglycerides, diabetes" (7.6%). Four classes were identified in women: 1) "Healthy" (53.2%), 2) "Very high central obesity, low high-density lipoprotein cholesterol, raised fasting plasma glucose" (32.8%), 3) "Very high central obesity, diabetes" (7.2%) and 4) "Central obesity, hypertension, raised fasting plasma glucose" (6.8%). Older age in men and women, and high socioeconomic status in men, was associated with cardiometabolic risk classes, compared to the "Healthy" classes. In men, individual differences in cardiometabolic class membership were due to environmental effects. In women, genetic differences predicted class membership. CONCLUSION: The findings did not support the metabolic syndrome construct. Instead, distinct clinical profiles were identified for men and women, suggesting different aetiological pathways.

Investigating the causal risk factors for self-harm by integrating Mendelian randomisation within twin modelling.

Previous genetically informed studies have uncovered likely causal relationships between mental health problems and self-harm but resulting causal estimates may be biased due to unmediated pleiotropy. By fitting Mendelian Randomization - Direction of Causation (MR-DoC) models that explicitly model pleiotropy, we investigated the effect of four quantitatively measured mental health problems - major depressive disorder (MDD), schizophrenia, attention-deficit hyperactivity disorder (ADHD), and insomnia, on non-suicidal self-harm (NSSH) and suicidal self-harm (SSH), separately. We used data of 12,723 twins (56.6% females) in the Twins Early Development Study. Besides substantial pleiotropy, we found effects from child-rated depressive symptoms to both NSSH (ß = 0.194, 95% CIs: 0.131, 0.257) and SSH (ß = 0.210, 95% CIs: 0.125, 0.295). Similarly, effects flowed from parent-rated depressive symptoms to NSSH (ß = 0.092, 95% CIs: 0.004, 0.181) and SSH (ß = 0.165, 95% CIs: 0.051, 0.281). We did not find evidence of aetiological difference between NSSH and SSH.

The aetiological relationship between depressive symptoms and health-related quality of life: A population-based twin study in Sri Lanka.

OBJECTIVE: Depression often co-occurs with poor health-related quality of life (HRQL). Twin studies report genetic and individual-level environmental underpinnings in the aetiology of both depression and HRQL, but there is limited twin research exploring this association further. There is also little evidence on sex differences and non-Western populations are underrepresented. In this paper we explored the phenotypic and aetiological relationship between depressive symptoms and HRQL and possible sex differences in a low-middle-income Sri Lankan population. METHOD: Data for 3,948 participants came from the Colombo Twin and Singleton Follow-up Study (CoTaSS-2). Using self-report measures of depressive symptoms and HRQL, we conducted univariate and bivariate sex-limitation twin analyses. RESULTS: Depressive symptoms showed moderate genetic (33%) and strong nonshared environmental influences (67%). Nonshared environment accounted for the majority of variance in all the subscales of HRQL (ranging from 68 to 93%), alongside small genetic influences (ranging from 0 to 23%) and shared environmental influences (ranging from 0 to 28%). Genetic influences were significant for emotional wellbeing (23%). Shared environmental influences were significant for four out of the eight HRQL variables (ranging from 22-28%), and they were more prominent in females than males. Depressive symptoms were significantly associated with lower HRQL scores. These correlations were mostly explained by overlapping nonshared environmental effects. For traits related to emotional functioning, we also detected substantial overlapping genetic influences with depressive symptoms. CONCLUSIONS: Our study confirmed previous findings of a negative association between depressive symptoms and HRQL. However, some of the aetiological factors of HRQL differed from Western studies, particularly regarding the effects of shared environment. Our findings highlight the importance of cross-cultural research in understanding associations between psychological wellbeing and HRQL.

Research Review: How to interpret associations between polygenic scores, environmental risks, and phenotypes.

BACKGROUND: Genetic influences are ubiquitous as virtually all phenotypes and most exposures typically classified as environmental have been found to be heritable. A polygenic score summarises the associations between millions of genetic variants and an outcome in a single value for each individual. Ever lowering costs have enabled the genotyping of many samples relevant to child psychology and psychiatry research, including cohort studies, leading to the proliferation of polygenic score studies. It is tempting to assume that associations detected between polygenic scores and phenotypes in those studies only reflect genetic effects. However, such associations can reflect many pathways (e.g. via environmental mediation) and biases. METHODS: Here, we provide a comprehensive overview of the many reasons why associations between polygenic scores, environmental exposures, and phenotypes exist. We include formal representations of common analyses in polygenic score studies using structural equation modelling. We derive biases, provide illustrative empirical examples and, when possible, mention steps that can be taken to alleviate those biases. RESULTS: Structural equation models and derivations show the many complexities arising from jointly modelling polygenic scores with environmental exposures and phenotypes. Counter-intuitive examples include that: (a) associations between polygenic scores and phenotypes may exist even in the absence of direct genetic effects; (b) associations between child polygenic scores and environmental exposures can exist in the absence of evocative/active gene-environment correlations; and (c) adjusting an exposure-outcome association for a polygenic score can increase rather than decrease bias. CONCLUSIONS: Strikingly, using polygenic scores may, in some cases, lead to more bias than not using them. Appropriately conducting and interpreting polygenic score studies thus requires researchers in child psychology and psychiatry and beyond to be versed in both epidemiological and genetic methods or build on interdisciplinary collaborations.

Do psychosocial factors mediate sexual minorities' risky sexual behaviour? A twin study.

OBJECTIVES: Risky sexual behavior among sexual minorities (lesbian, gay, and bisexual individuals) are partly attributed to mental health and other social disparities; but this may be confounded by correlated genetic and environmental influences. As preregistered, the present study investigated indirect associations between sexual minority status and increased lifetime sexual partners through increased psychosocial adversity (depressive and anxiety symptoms, intimate partner violence, and early life adversities) and substance use (alcohol, cannabis, and other illicit drugs), confounding by correlated genetic and environmental influences, and sex differences in these relationships. METHOD: The sample comprised sexual minority and heterosexual twins who participated in the first and second phases of the latest wave of data collection in the U.K. population-based Twins Early Development study cohort (June 2017 through February 2019; n = 9,697 and 8,718, respectively, Mage = 22.3 ± .92 years). Structural equation modeling was used to specify psychosocial adversity and substance use as mediators while genetic and environmental confounding was further determined by biometrical genetic analyses in which similarities in identical and nonidentical twins were compared. RESULTS: Increased psychosocial adversity and substance use fully mediated increased lifetime sexual partners in sexual minority women while this effect was partial (31.1%) in men. The best-fitting genetic models indicated that these relationships were not confounded by correlated genetic and environmental influences. CONCLUSIONS: The relationships between sexual minority status, psychosocial adversity, substance use, and sexual health disparities appeared independent of genetic and environmental influences. Individual and systemic interventions to reduce psychosocial disadvantage and substance use can also decrease sexual health disparities among sexual minorities. (PsycInfo Database Record (c) 2022 APA, all rights reserved).

Quality of life, functional impairment and continuous performance task event-related potentials (ERPs) in young adults with ADHD and autism: A twin study.

Background: Young adulthood is a key developmental period for understanding outcomes of childhood onset attention-deficit/hyperactivity disorder (ADHD) and autism. Measurement of functional impairment and quality of life (QoL) can provide important information on the real-life challenges associated with these conditions. Event-related potential (ERP) measures from the continuous performance task (CPT) have long been identified as altered in ADHD and autism but the role of these functions in the aetiological pathway to the disorders and associated impact on quality of life in young adulthood is unknown. Method: We investigated the relationships between ADHD and autism, functional impairment, quality of life, and ERP measures from the cued CPT (CPT-OX) in a young adult twin sample (566 participants aged 22.43 ± 0.96 years old). Results: We observed significant phenotypic correlations between ADHD/autism and lower quality of life with specific genetic overlap between ADHD and physical health, psychological, and environmental aspects. We found significant phenotypic and genetic correlations between ADHD and functional impairment in all domains, as well as between autism and impairment in social functioning and lower impairment in risk-taking. Both ADHD and autism were associated with attenuated amplitude of inhibitory and proactive control ERPs, with large genetic contributions to the overlap. We also found significant phenotypic correlations between these ERP measures and Weiss Functional Impairment Rating Scale (WFIRS) and QoL. Conclusion: This is the first study to investigate the phenotypic and genetic relationships between ADHD and autism, functional impairment, quality of life and ERP measures in young adulthood. Our findings could represent a step towards identifying ERP measures that are related to behaviour in the absence of overt symptoms.

The association between body dysmorphic symptoms and suicidality among adolescents and young adults: a genetically informative study.

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.