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.

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.

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).

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.

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.

Associations Between Anxiety Symptoms and Health-Related Quality of Life: A Population-Based Twin Study in Sri Lanka.

Anxiety not only concerns mental wellbeing but also negatively impacts other areas of health. Yet, there is limited research on (a) the genetic and environmental aetiology of such relationships; (b) sex differences in aetiology and (c) non-European samples. In this study, we investigated the genetic and environmental variation and covariation of anxiety symptoms and eight components of health-related quality of life (QoL), as measured by the short form health survey (SF-36), using genetic twin model fitting analysis. Data was drawn from the Colombo Twin and Singleton Study (COTASS), a population-based sample in Sri Lanka with data on twins (N = 2921) and singletons (N = 1027). Individual differences in anxiety and QoL traits showed more shared environmental (family) effects in women. Men did not show familial effects. Anxiety negatively correlated with all eight components of QoL, mostly driven by overlapping unique (individual-specific) environmental effects in both sexes and overlapping shared environmental effects in women. This is the first study in a South Asian population supporting the association between poor mental health and reduced QoL, highlighting the value of integrated healthcare services. Associations were largely environmental, on both individual and family levels, which could be informative for therapy and intervention.

Associations between maternal depressive symptoms and risk for offspring early-life psychopathology: the role of genetic and non-genetic mechanisms.

BACKGROUND: Although maternal depressive symptoms are robustly associated with offspring early-life psychopathology symptoms, it is not clear which potential mechanisms are at play. We aimed to estimate the relative importance of genetic transmission and direct environmental exposure in these associations on three occasions in early childhood. METHODS: Biometric modeling of maternal sisters and their offspring from the Norwegian Mother and Child Cohort Study. The analyzed sample comprised 22 316 mothers and 35 589 offspring. Mothers reported their own depressive symptoms using the Symptom checklist, and offspring's concurrent symptoms of psychopathology using the Child Behavior Checklist at 1.5, 3, and 5 years postpartum. RESULTS: Associations between maternal symptoms of depression and offspring emotional problems were predominantly explained by passive genetic transmission at 1.5 and 3 years postpartum. At age 5, associations were more due to direct environmental exposure. For offspring behavioral problems, there was no net increase in the importance of direct environmental exposure across occasions. CONCLUSIONS: Associations between maternal depressive symptoms and offspring psychopathology symptoms remained after accounting for shared genes, consistent with a small, causal effect. For offspring emotional problems, this effect appeared to increase in importance over time. Our findings imply that treatment of maternal depressive symptoms could also benefit the offspring, and that genetic confounding should be considered in future studies of such mother-offspring associations.

Parental Prenatal Symptoms of Depression and Offspring Symptoms of ADHD: A Genetically Informed Intergenerational Study.

Objective: The primary aim of the present study was to separate the direct effect of maternal prenatal depression on offspring ADHD from the passive transmission of genetic liability. Method: A children-of-twins and siblings design including 17,070 extended-family units participating in the Norwegian Mother and Child Cohort Study was used. Self-ratings were obtained from parents using the Symptom Checklist during pregnancy. Maternal ratings using Conner's Parent Rating Scale were obtained when the children were 5 years of age. Results: Genetic influences were important for explaining similarity between parents and offspring. There was also evidence for a maternal effect after accounting for genetic transmission (m = 0.06, 95% confidence interval [CI] = [0.02, 0.09]). Conclusion: Our results were consistent with hypotheses suggesting that maternal prenatal depression influences symptoms of ADHD in offspring. However, the effect was weak and a substantial portion of the association could be accounted for by shared genetic influences.

Cyber-victimisation and mental health in young people: a co-twin control study.

BACKGROUND: The rise of social media use in young people has sparked concern about the impact of cyber-victimisation on mental health. Although cyber-victimisation is associated with mental health problems, it is not known whether such associations reflect genetic and environmental confounding. METHODS: We used the co-twin control design to test the direct association between cyber-victimisation and multiple domains of mental health in young people. Participants were 7708 twins drawn from the Twins Early Development Study, a UK-based population cohort followed from birth to age 22. RESULTS: Monozygotic twins exposed to greater levels of cyber-victimisation had more symptoms of internalising, externalising and psychotic disorders than their less victimised co-twins at age 22, even after accounting for face-to-face peer victimisation and prior mental health. However, effect sizes from the most stringent monozygotic co-twin control analyses were decreased by two thirds from associations at the individual level [pooled ß across all mental health problems = 0.06 (95% CI 0.03-0.10) v. 0.17 (95% CI 0.15-0.19) in individual-level analyses]. CONCLUSIONS: Cyber-victimisation has a small direct association with multiple mental health problems in young people. However, a large part of the association between cyber-victimisation and mental health is due to pre-existing genetic and environmental vulnerabilities and co-occurring face-to-face victimisation. Therefore, preventative interventions should target cyber-victimisation in conjunction with pre-existing mental health vulnerabilities and other forms of victimisation.

Twins and Causal Inference: Leveraging Nature's Experiment.

In this review, we discuss how samples comprising monozygotic and dizygotic twin pairs can be used for the purpose of strengthening causal inference by controlling for shared influences on exposure and outcome. We begin by briefly introducing how twin data can be used to inform the biometric decomposition of population variance into genetic, shared environmental, and nonshared environmental influences. We then discuss how extensions to this model can be used to explore whether associations between exposure and outcome survive correction for shared etiology (common causes). We review several analytical approaches that can be applied to twin data for this purpose. These include multivariate structural equation models, cotwin control methods, direction of causation models (cross-sectional and longitudinal), and extended family designs used to assess intergenerational associations. We conclude by highlighting some of the limitations and considerations that researchers should be aware of when using twin data for the purposes of interrogating causal hypotheses.

Higher Anxiety Is Associated with Lower Cardiovascular Autonomic Function in Female Twins.

Anxiety symptoms co-occur with cardiovascular health problems, with increasing evidence suggesting the role of autonomic dysfunction. Yet, there is limited behavior genetic research on underlying mechanisms. In this twin study, we investigated the phenotypic, genetic and environmental associations between a latent anxiety factor and three cardiovascular autonomic function factors: interbeat interval (IBI, time between heart beats), heart rate variability (HRV, overall fluctuation of heart-beat intervals) and baroreflex sensitivity (BRS, efficiency in regulating blood pressure [BP]). Multivariate twin models were fit using data of female twins (N = 250) of the Twin Interdisciplinary Neuroticism Study (TWINS). A significant negative association was identified between latent anxiety and BRS factors (r = -.24, 95% CI [-.40, -.07]). Findings suggest that this relationship was mostly explained by correlated shared environmental influences, and there was no evidence for pleiotropic genetic or unique environmental effects. We also identified negative relationships between anxiety symptoms and HRV (r = -.17, 95% CI [-.34, .00]) and IBI factors (r = -.13, 95% CI [-.29, .04]), though these associations did not reach statistical significance. Findings implicate that higher anxiety scores are associated with decreased efficiency in short-term BP regulation, providing support for autonomic dysfunction with anxiety symptomatology. The baroreflex system may be a key mechanism underlying the anxiety-cardiovascular health relationship.

The relationship between independent and dependent life events and depression symptoms in Sri Lanka: a twin and singleton study.

PURPOSE: Life events have been associated with a variety of mental health conditions including depression. There is a scarcity of research in South Asia exploring the aetiology of independent and dependent life events and their relationship with depression symptoms. This study aimed, in a Sri Lankan population, to identify the socio-demographic correlates and genetic and environmental influences on independent and dependent life events and their relationship with depression. METHODS: Questionnaire data came from the Colombo Twin and Singleton Follow-up Study, CoTaSS-2 (N = 3969), a population study of Sri Lankan twins and singletons. Lifetime-ever independent and dependent life events were measured using a questionnaire and depressive symptoms using the Revised Beck's Depression Inventory. Structural Equation Model-fitting analyses explored the genetic and environmental influences on life events and depression. RESULTS: Living in a rural environment and financial hardship were associated with greater reporting of independent and dependent life events. Sex differences were evident in the aetiology of life events and depression symptoms. Independent and dependent life events, but not depression symptoms, were heritable in males. Independent life events and depression symptoms, but not dependent life events, were heritable in females. Non-shared environmental influences explained phenotypic associations between independent life events and depression symptoms in both males and females. Genetic and non-shared environmental influences explained the phenotypic associations between dependent life events and depression symptoms in males. Only non-shared environment explained the covariation between dependent life events and depression symptoms in females. CONCLUSIONS: Socio-demographic correlates of independent and dependent life events were similar to those reported in Western populations. Life events were associated with increased depression symptoms. Contrary to research in Western populations, we found that non-shared environmental, rather than genetic, influences explained much of the covariation between life events and depression symptoms. This suggests that whilst independent LEs may be heritable, the relationship is unlikely to be confounded by genetic influences and has significant implications for possible interventions for depression.

The narrow-sense and common single nucleotide polymorphism heritability of early repolarization.

BACKGROUND: Early repolarization (ER) is a risk marker for sudden cardiac death. Higher risk is associated with horizontal/descending ST-segment ER in the inferior or inferolateral ECG leads. Studies in family cohorts have demonstrated substantial heritability for the ER pattern, but genome-wide association studies (GWAS) have failed to identify statistically significant and replicable genetic signals. METHODS AND RESULTS: We assessed the narrow-sense and common single nucleotide polymorphism (SNP) heritability of ER and ER subtypes using ECG data from 5829 individuals (TwinsUK, BRIGHT and GRAPHIC cohorts). ER prevalence was 8.3%. In 455 monozygous vs 808 dizygous twin pairs, concordances and twin correlations for ER subtypes (except horizontal/descending ST-segment ER) were higher and familial resemblance (except notched ER) was significant. Narrow-sense heritability estimates derived from 1263 female twin pairs using the structural equation program Mx ranged from 0.00-0.47 and common SNP heritability estimates derived from 4009 unrelated individuals of both sexes using Genome-wide Restricted Maximum Likelihood (GREML) ranged from 0.00-0.36, but none were statistically significant. CONCLUSION: From our data, ER shows limited genetic predisposition. There appears to be significant environmental influence and these modest narrow-sense and common SNP heritability estimates may explain why previous GWAS have been unsuccessful.

Maternal prenatal depressive symptoms and risk for early-life psychopathology in offspring: genetic analyses in the Norwegian Mother and Child Birth Cohort Study.

BACKGROUND: Maternal prenatal depression is a known risk factor for early-life psychopathology among offspring; however, potential risk transmission mechanisms need to be distinguished. We aimed to test the relative importance of passive genetic transmission, direct exposure, and indirect exposure in the association between maternal prenatal depressive symptoms and early-life internalising and externalising psychopathology in offspring. METHODS: We used structural equation modelling of phenotypic data and genetically informative relationships from the families of participants in the Norwegian Mother and Child Birth Cohort Study (MoBa). The analytic subsample of MoBa used in the current study comprises 22 195 mothers and 35 299 children. We used mothers' self-reported depressive symptoms during pregnancy, as captured by the Symptom Checklist, and their reports of symptoms of psychopathology in their offspring during the first few years of life (measured at 18, 36, and 60 months using the Child Behavior Checklist). FINDINGS: Maternal prenatal depressive symptoms were found to be associated with early-life psychopathology primarily via intergenerationally shared genetic factors, which explained 41% (95% CI 36-46) of variance in children's internalising problems and 37% (30-44) of variance in children's externalising problems. For internalising problems, phenotypic transmission also contributed significantly, accounting for 14% (95% CI 5-19) of the association, but this contribution was found to be explained by exposure to concurrent maternal depressive symptoms, rather than by direct exposure in utero. INTERPRETATION: Associations between maternal prenatal depressive symptoms and offspring behavioural outcomes in early childhood are likely to be at least partially explained by shared genes. This genetic confounding should be considered when attempting to quantify risks posed by in-utero exposure to maternal depressive symptoms. FUNDING: UK Economic and Social Research Council, Norwegian Research Council, Norwegian Ministries of Health and Care Services, and Education & Research, Wellcome Trust, Royal Society, and National Institute for Health Research.

Revisiting the Children-of-Twins Design: Improving Existing Models for the Exploration of Intergenerational Associations.

Datasets comprising twins and their children can be a useful tool for understanding the nature of intergenerational associations between parent and offspring phenotypes. In the present article we explore structural equation models previously used to analyse Children-of-Twins data, highlighting some limitations and considerations. We then present new variants of these models, showing that extending the models to include multiple offspring per parent addresses several of the limitations discussed. Accompanying the updated models, we provide power calculations and demonstrate with application to simulated data. We then apply to intergenerational analyses of height and weight, using a sub-study of the Norwegian Mother and Child Cohort (MoBa); the Intergenerational Transmission of Risk (IToR) project, wherein all kinships in the MoBa data have been identified (a children-of-twins-and-siblings study). Finally, we consider how to interpret the findings of these models and discuss future directions.

Genetics of co-developing conduct and emotional problems during childhood and adolescence.

Common genetic influences offer a partial explanation for comorbidity between different psychiatric disorders1-3. However, the genetics underlying co-development-the cross-domain co-occurrence of patterns of change over time-of psychiatric symptoms during childhood and adolescence has not been well explored. Here, we show genetic influence on joint symptom trajectories of parent-reported conduct and emotional problems (overall N = 15,082) across development (4-16 years) using both twin- and genome-wide polygenic score analyses (genotyped N = 2,610). Specifically, we found seven joint symptom trajectories, including two characterized by jointly stable and jointly increasing symptoms of conduct and emotional problems, respectively (7.3% of the sample, collectively). Twin modelling analyses revealed substantial genetic influence on trajectories (heritability estimates range of 0.41-0.78). Furthermore, individuals' risk of being classified in the most symptomatic trajectory classes was significantly predicted by polygenic scores for years-of-education-associated alleles and depressive symptoms-associated alleles. Complementary analyses of child self-reported symptoms across late childhood and early adolescence yielded broadly similar results. Taken together, our results indicate that genetic factors are involved in the co-development of conduct and emotional problems across childhood and adolescence, and that individuals with co-developing symptoms across multiple domains may represent a clinical subgroup characterized by increased levels of genetic risk.

Associations between the parent-child relationship and adolescent self-worth: a genetically informed study of twin parents and their adolescent children.

BACKGROUND: Low self-worth during adolescence predicts a range of emotional and behavioural problems. As such, identifying potential sources of influence on self-worth is important. Aspects of the parent-child relationship are often associated with adolescent self-worth but to date it is unclear whether such associations may be attributable to familial confounding (e.g. genetic relatedness). We set out to clarify the nature of relationships between parental expressed affection and adolescent self-worth, and parent-child closeness and adolescent self-worth. METHODS: We used data from the Twin and Offspring Study in Sweden, a children-of-twins sample comprising 909 adult twin pairs with adolescent children. Using these data we were able to apply structural equation models with which we could examine whether associations remained after accounting for genetic transmission. RESULTS: Results demonstrated that parent-child closeness and parental-expressed affection were both phenotypically associated with adolescent self-worth. Associations could not be attributed to genetic relatedness between parent and child. CONCLUSIONS: Parent-child closeness and parental affection are associated with adolescent self-worth above and beyond effects attributable to genetic relatedness. Data were cross-sectional, so the direction of effects cannot be confirmed but findings support the notion that positive parent-child relationships increase adolescent self-worth.

A Longitudinal Twin and Sibling Study of Associations between Insomnia and Depression Symptoms in Young Adults.

STUDY OBJECTIVES: To estimate genetic and environmental influences on the associations between insomnia and depression symptoms concurrently and longitudinally. METHODS: Behavioral genetic analyses were conducted on data from the British longitudinal G1219 twin/sibling study. One thousand five hundred fiftysix twins and siblings participated at Time 1 (mean age = 20.3 years, SD = 1.76). Eight hundred sixty-two participated at Time 2 (mean age = 25.2 years, SD = 1.73 years). Participants completed the Insomnia Symptoms Questionnaire and the Short Mood and Feelings Questionnaire to assess symptoms of insomnia and depression respectively. RESULTS: Genetic effects accounted for 33% to 41% of the variance of the phenotypes. The phenotypic correlations were moderate (r = 0.34 to r = 0.52). The genetic correlations between the variables were high (0.73-1.00). Genetic effects accounted for a substantial proportion of the associations between variables (50% to 90%). Non-shared environmental effects explained the rest of the variance and covariance of the traits. CONCLUSIONS: While genetic effects play a modest role in insomnia and depression symptoms separately, they appear to play a more central role in concurrent and longitudinal associations between these phenotypes. This should be acknowledged in theories explaining these common associations.