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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. [ABSTRACT FROM AUTHOR]

Background: Previous studies have shown associations between major depression and C-reactive protein (CRP) levels. Few studies have considered the extent to which shared genetic and environmental factors contribute to this association, nor have they considered the relationship outside of European populations. We examined the association between CRP levels and depression and their aetiology in a Sri Lankan population.Methods: Data were collected from 2577 twins and 899 singletons in Colombo, Sri Lanka. Depression symptoms were assessed using the revised Beck Depression Inventory (BDI-II). High-sensitive CRP blood levels were assessed using immunoturbidimetry. Linear regressions were performed to test the association between CRP and depression. The heritability of CRP levels was estimated using Structural Equation Modelling.Results: CRP was significantly associated with BMI (p < 0.01) but not depression (p > 0.05). In males, variance in CRP levels was explained by shared environment (51% 95%CIs: 13-62) and non-shared environment (45% 95%CIs: 36-54). In contrast, in females, CRP variance was explained by genetic (41% 95%CIs: 10-52) and non-shared environment (56% 95%CIs: 47-67). A genetic correlation between CRP and BMI was observed in females only.Limitations: CRP level was based on a single data collection point, longer term data collection would give a more accurate picture of an individual's state of inflammation.Conclusions: The lack of association between depression and CRP strengthens the hypothesis that inflammation might contribute to the development of some, but not all types of depression. CRP levels were moderated by the environment, suggesting interventions aimed at reducing CRP levels and risk for inflammatory conditions, particularly in males. [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]

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. [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]

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. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

This study investigated associations between mindfulness and symptoms of insomnia, depression and anxiety. Mindfulness was disaggregated into five subscales: 'nonreactivity to inner experience', 'observing', 'acting with awareness', 'describing' and 'nonjudging of inner experience'. Twin models were used to examine genetic and environmental influences on mindfulness, symptoms of insomnia, depression and anxiety and on their associations. Data came from a longitudinal twin/sibling study (G1219) comprising 862 individuals (age range 22–32 years, 66% females). Less mindfulness was associated with greater symptoms of insomnia, depression and anxiety (r =.22-.48). Of the mindfulness subscales, 'nonjudging of inner experience' was most strongly associated with the other traits. Overall mindfulness was largely influenced by non-shared environmental factors (E =.72) although familial influences played a role for overall mindfulness, as well as for the 'acting with awareness' and 'describing' subscales. The genetic correlations between overall mindfulness and symptoms of insomnia, depression and anxiety ranged from.32 to.75 (but were non-significant), while the shared environmental correlations ranged from −.78 to.79 (also non-significant). The non-shared environmental influences between these three variables were moderately, significantly correlated (r E =.21-.55). [ABSTRACT FROM AUTHOR]

Objective: Only a minority of trauma-exposed individuals go on to develop post traumatic stress disorder (PTSD). Previous studies in high income countries suggest that maladaptive family functioning adversities (MFFA) in childhood may partially explain individual variation in vulnerability to PTSD following trauma. We test in a lower middle-income setting (Sri Lanka) whether: (1) MFFA is associated with trauma exposure; (2) MFFA moderates the association between exposure to trauma and later (a) PTSD (b) other psychiatric diagnoses; and (3) any association between MFFA and PTSD is explained by experiences of interpersonal violence, cumulative trauma exposure or comorbid psychopathology.Methods: We conducted a population study of 3995 twins and 2019 singletons residing in Colombo, Sri Lanka. Participants completed the Composite International Diagnostic Interview, including nine traumatic exposures and a questionnaire on MFFA.Results: 23.4% of participants reported exposure to MFFA. We found that (1) MFFA was strongly associated with trauma exposure (2) MFFA moderates the association between trauma exposure and both (a) PTSD and (b) other DSM psychiatric diagnosis. (3) This was not explained by interpersonal violence, cumulative trauma exposure or other psychopathology.Conclusions: MFFA moderates the association between trauma and PTSD, and the association between trauma and non-PTSD psychopathology. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

Background: Alcohol use is increasing in non-Western countries. However, the effects of this increase on the prevalence of alcohol use disorders (AUD) remains unknown, particularly in South Asia. This study aimed to estimate the prevalence of alcohol use and AUD in the Colombo District, Sri Lanka. Environmental risk factors and psychiatric correlates were also examined. Methods: The Composite International Diagnostic Interview was used to assess alcohol use and psychiatric disorders in a population based sample of 6014 twins and singletons in the Colombo region of Sri Lanka. Results: Lifetime alcohol use on 12 or more occasions was estimated at 63.1% (95% CI: 61.3-64.9) in men and 3.7% (95% CI: 3.0-4.3) in women. Prevalence of lifetime alcohol abuse and alcohol dependence in men was 6.2% (95% CI: 5.3-7.1) and 4.0% (95% CI: 3.3-4.7) respectively. Lower standard of living was independently associated with alcohol use and dependence but not abuse. Significant associations between lifetime AUD and other psychiatric disorders were observed. Conclusions: Lower prevalence of alcohol use and AUD was observed compared to Western countries. Prevalence of alcohol use and AUD were higher than previous reports. Socio-demographic and environmental risk factors appear to be similar across cultures as were associations between AUD and other psychiatric disorders. [ABSTRACT FROM AUTHOR]

Background Children with externalising problems are at risk of developing internalising problems as they grow older. The pathways underlying this developmental association remain to be elucidated. We tested two processes that could explain why some children with externalising problems develop internalising symptoms in preadolescence: a mediation model whereby the association between early externalising and later new internalising symptoms is explained by negative experiences; and a genetic model, whereby genes influence both problems. Methods We used data from the Environmental Risk (E-Risk) Study, a 1994-1995 birth cohort of 2,232 twins born in England and Wales. We assessed externalising and internalising problems using combined mothers' and teachers' ratings at age 5 and 12. We measured bullying victimisation, maternal dissatisfaction and academic difficulties between age 7 and 10 and used linear regression analyses to test the effects of these negative experiences on the association between early externalising and later internalising problems. We employed a Cholesky decomposition to examine the genetic influences on the association. Results Children with externalising problems at age 5 showed increased rates of new internalising problems at age 12 ( r = .24, p < .001). Negative experiences accounted for some of the association between early externalising and later internalising problems. Behavioural-genetic analyses indicated that genes influencing early externalising problems also affected later internalising problems. Conclusions Our findings highlight the role of genetic influences in explaining why some children with externalising problems develop internalising symptoms in preadolescence. Negative experiences also contribute to the association, possibly through gene-environment interplay. Mental health professionals should monitor the development of internalising symptoms in young children with externalising problems. [ABSTRACT FROM AUTHOR]

Cannabis users are more likely to have psychotic experiences (PEs). The degree to which these associations are driven by genetic or environmental influences in adolescence is unknown. This study estimated the genetic and environmental contributions to the relationship between cannabis use and PEs. Specific PEs were measured in a community-based twin sample (4830 16-year-old pairs) using self-reports and parent-reports. Adolescents reported on ever using cannabis. Multivariate liability threshold structural equation model-fitting was conducted. Cannabis use was significantly correlated with PEs. Modest heritability (37%), common environmental influences (55%) and unique environment (8%) were found for cannabis use. For PEs, modest heritability (27–54%), unique environmental influences ( E =12–50%) and little common environmental influences (11–20%), with the exception of parent-rated Negative Symptoms (42%), were reported. Environmental influences explained all of the covariation between cannabis use and paranoia, cognitive disorganization and parent-rated negative symptoms (bivariate common environment=69–100%, bivariate unique environment=28–31%), whilst the relationship between cannabis use and hallucinations indicated familial influences. Cannabis use explains 2–5% of variance in positive, cognitive, and negative PEs. Cannabis use and psychotic experience co-occur due to environmental factors. Focus on specific environments may reveal why adolescent cannabis use and psychotic experiences tend to ‘travel together’. [ABSTRACT FROM AUTHOR]

Background Mindfulness-based therapies have been shown to be effective in treating depression and reducing cognitive biases. Anxiety sensitivity is one cognitive bias that may play a role in the association between mindfulness and depressive symptoms. It refers to an enhanced sensitivity toward symptoms of anxiety, with a belief that these are harmful. Currently, little is known about the mechanisms underpinning the association between mindfulness, depression, and anxiety sensitivity. The aim of this study was to examine the role of genetic and environmental factors in trait mindfulness, and its genetic and environmental overlap with depressive symptoms and anxiety sensitivity. Methods Over 2,100 16-year-old twins from a population-based study rated their mindfulness, depressive symptoms, and anxiety sensitivity. Results Twin modeling analyses revealed that mindfulness is 32% heritable and 66% due to nonshared environmental factors, with no significant influence of shared environment. Genetic influences explained over half of the moderate phenotypic associations between low mindfulness, depressive symptoms, and anxiety sensitivity. About two-thirds of genetic influences and almost all nonshared environmental influences on mindfulness were independent of depression and anxiety sensitivity. Conclusions This is the first study to show that both genes and environment play an important role in the etiology of mindfulness in adolescence. Future research should identify the specific environmental factors that influence trait mindfulness during development to inform targeted treatment and resilience interventions. Shared genetic liability underpinning the co-occurrence of low mindfulness, depression, and anxiety sensitivity suggests that the biological pathways shared between these traits should also be examined. [ABSTRACT FROM AUTHOR]

Chronic pain syndromes (CPS) are highly prevalent in the general population, and increasingly the evidence points to a common etiological pathway. Using a large cohort of twins (n = 8564) characterized for chronic widespread musculoskeletal pain (CWP), chronic pelvic pain (PP), migraine (MIG), dry eye disease, and irritable bowel syndrome (IBS), we explored the underlying genetic and environmental factors contributing to CPS and the correlation between them. The sample was predominantly female (87.3%), with a mean age of 54.7 (±14.7) years. Prevalence of the different CPS ranged from 7.4% (PP) to 15.7% (MIG). For all CPS the within-twin correlation in monozygotic twin pairs was higher than in dizygotic pairs, suggesting a heritable component. Estimated heritability ranged from 19% (IBS) to 46% (PP). Except for MIG, we found significant pairwise phenotypic correlations between the CPS. The phenotypic correlation was highest between CWP and IBS (0.40; 95% confidence interval: 0.27 to 0.46). Excluding MIG from further analyses, cross-twin cross-trait correlations were higher in monozygotic compared with dizygotic twin pairs, suggestive of shared genetic factors between CWP, PP, IBS, and dry eye disease. Twin modeling analysis revealed the common pathway model as the model best explaining the observed pattern of correlation between the traits, with an estimated heritability of 66% of the underlying latent variable. These results are evidence of shared genetic factors in conditions manifesting chronic pain and justify the search for underlying genetic variants. [ABSTRACT FROM AUTHOR]

Little is known about the prevalence and etiology of tobacco use in Asian populations. This study aims to test whether the finding of substantial heritability for tobacco-related phenotypes in Western populations is generalizable to developing countries. The twin method was used to estimate the relative contribution of genetic and environmental influences on nicotine-related phenotypes. Participants were selected from the population based Sri Lankan Twin Registry. The Composite International Diagnostic Interview was administered to 1,804 male individuals to assess five phenotypes: nicotine use; desire and unsuccessful attempts to quit smoking; subjective feeling of being tobacco dependent; and two DSM-IV diagnoses; nicotine dependence and nicotine withdrawal. Almost one-third of the male twins were life-time smokers. The genetic results were consistent with the previously reported findings from Western and Chinese populations, in that the nicotine use traits were significantly heritable, with environmental influences being of the non-shared nature. The results derived from the Causal Contingent Common pathway model (CCC) supported previous findings that show that liabilities to regular smoking and subsequent problem smoking have both shared and specific genetic influences. [ABSTRACT FROM AUTHOR]

The current study sought to examine the direction of influences on longitudinal associations between anxiety sensitivity, anxiety and depression. The continuity of genetic and environmental influences on these traits over adolescence was also investigated. Self reports of anxiety sensitivity, anxiety and depression were collected from approximately 1,300 twin and sibling pairs, on two occasions (mean ages 15 and 17). The direction and etiology of the associations between these traits were examined using longitudinal genetic cross-lagged models. All traits were stable over time and this stability accounted for the largest proportion of variance at time 2. There was, however, also evidence of reciprocal associations between variables over time. Genetic effects were fairly stable across time, although new genetic influences were evident at the second time point. Environmental effects tended to be more time specific. This study adds to our understanding of the direction of effects between anxiety sensitivity, anxiety and depression in adolescence, and the risks underlying their associations. [ABSTRACT FROM AUTHOR]

Background Cognitive biases have long been hypothesized to influence the development and maintenance of symptoms of internalizing problems. Anxiety sensitivity represents one such bias and refers to sensitivity to the physical and emotional symptoms of anxiety and the belief that these are harmful. Twin studies indicate a role for both environmental and genetic influences on anxiety sensitivity. However, little work has been done specifying environments or genes involved in this phenotype. In light of this, we looked at the association between stressful life events, the serotonin transporter gene polymorphism (5HTTLPR), and anxiety sensitivity in a longitudinal sample of adolescents. Methods Stressful life events and anxiety sensitivity were measured in over 1,500 individuals at three time points (mean ages 15, 17, and 20 years). 5HTTLPR was genotyped in 1,109 participants. Results There was consistent evidence for an association between stressful life events and both anxiety sensitivity and change in anxiety sensitivity over time. Although the effect of independent stressful life events was relatively short lived, dependent stressful life events were associated with anxiety sensitivity over time. There was no evidence for a main effect of 5HTTLPR on anxiety sensitivity. 5HTTLPR genotype did not moderate the effect of stressful life events on anxiety sensitivity. Conclusions The current study extends previous work by showing that stressful life events, independent of the individual, explained change in cognitions associated with anxiety and depression. This effect does not, however, appear to be moderated by genotype. [ABSTRACT FROM AUTHOR]

Anxiety sensitivity is associated with both anxiety and depression and has been shown to be heritable. Little, however, is known about the role of genetic influence on continuity and change of symptoms over time. The authors' aim was to examine the stability of anxiety sensitivity during adolescence. By using a genetically sensitive design, the authors were also able to investigate the extent to which genetic and environmental factors influence anxiety sensitivity over time. Self-reports of anxiety sensitivity were obtained for over 1,300 twin and sibling pairs at 3 time points. Data were analyzed using multivariate genetic models. Anxiety sensitivity was moderately heritable at all time points with substantial nonshared environmental contributions. Time 1 genetic factors accounted for continuity of symptoms at Times 2 and 3. New genetic factors at Time 2 also influenced Time 3 symptoms. New nonshared environmental influences emerged at each time point. Analysis of a latent factor of trait anxiety sensitivity revealed some stable nonshared environmental influences. Genetic effects were generally stable over time, with new genetic influences emerging in late adolescence. Environmental influences on anxiety sensitivity were, on the whole, more time specific; however, some stable environmental influences were also found. [ABSTRACT FROM AUTHOR]

We examined the aetiology of anxiety symptoms in an unselected population at ages 7 and 9, a period during which anxiety disorders first begin to develop (mean age at onset is 11 years). Specifically, the aim of the study was to investigate genetic and environmental continuity and change in components of anxiety in middle childhood. Parents of over 3,500 twin pairs completed the Anxiety-Related Behaviours Questionnaire (ARBQ) when twins were 7 and 9 years old. Multivariate-longitudinal analyses were conducted to examine genetic and environmental influences on stability and change in four anxiety scales: Negative Cognition, Negative Affect, Fear and Social Anxiety. We found moderate temporal stability in all four scales from 7 to 9 years (correlations ranging from 0.45 to 0.54) and moderate heritability (average 54%). Both shared and non-shared environmental influences were modest (average 18%-28% respectively). Genetic factors (68%) explained most of the homotypic continuity in anxiety. We show that homotypic continuity of Anxiety-Related Behaviours (i.e. the continuation of one specific type of anxiety over time) was largely driven by genetic factors. In contrast, though more varied, heterotypic continuity between some traits (i.e. the change from one type of anxiety-related behaviour into another over time) was mainly due to shared-environmental factors. [ABSTRACT FROM AUTHOR]

Objective: Irritability has been proposed to underlie the developmental link between oppositional problems and depression. Little is known, however, about the genetic and environmental influences on irritability and its overlap with depression. Drawing on the notion of "generalist genes" (genes of general effect that underlie phenotypic overlap between disorders), the authors test the hypothesis that the association between irritability and depression is accounted for by genetic factors. Method: Data from the G1219 study, a U.K. twin/sibling sample (N=2,651), were used in a cross-sectional and longitudinal design. The 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 overlaps between the two components of oppositionality (irritability and headstrong/hurtful behaviors) and depression and delinquency. Results: Irritability showed a significantly stronger phenotypic relationship with depression than with delinquency, whereas headstrong/hurtful behaviors were more strongly related to delinquency than to depression. In multivariate genetic analyses, the genetic correlation between irritability and depression (rA=0.70, 95% CI=0.59-0.82) was significantly higher than that between irritability and delinquency (rA=0.57, 95% CI=0.45-0.69); conversely, the genetic correlation between headstrong/hurtful behaviors and delinquency (rA=0.80, 95% CI=0.72-0.86) was significantly higher than that between headstrong/hurtful behaviors and depression (rA=0.46, 95% CI=0.36-0.57). In longitudinal models, the phenotypic association between irritability at wave 2 and depression at wave 3 was accounted for by the genetic association between irritability and depression at wave 2. Conclusions: These findings are consistent with the theory that genes with general effects underlie the relationship between irritability and depression. [ABSTRACT FROM AUTHOR]

Abstract: Background: There is a substantial overlap between genes affecting anxiety and depression. Both anxiety and depression are associated with cognitive biases such as anxiety sensitivity and attributional style. Little, however, is known about the relationship between these variables and whether these too are genetically correlated. Methods: Self-reports of anxiety sensitivity, anxiety symptoms, attributional style and depression symptoms were obtained for over 1300 adolescent twin and sibling pairs at two time points. The magnitude of genetic and environmental influences on the measures was examined. Results: Strongest associations were found between anxiety sensitivity and anxiety ratings at both measurement times (r =.70, .72) and between anxiety and depression (r =.62 at both time points). Correlations between the cognitive biases were modest at time 1 (r =−.12) and slightly larger at time 2 (r =−.31). All measures showed moderate genetic influence. Generally genetic correlations reflected phenotypic correlations. Thus the highest genetic correlations were between anxiety sensitivity and anxiety ratings (.86, .87) and between anxiety and depression ratings (.77, .71). Interestingly, depression ratings also showed a high genetic correlation with anxiety sensitivity (.70, .76). Genetic correlations between the cognitive bias measures were moderate (−.31, −.46). Limitations: The sample consists primarily of twins, there are limitations associated with the twin design. Conclusions: Cognitive biases associated with depression and anxiety are not as genetically correlated as anxiety and depression ratings themselves. Further research into the cognitive processes related to anxiety and depression will facilitate understanding of the relationship between bias and symptoms. [Copyright &y& Elsevier]

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. [ABSTRACT FROM AUTHOR]

Background: Low socioeconomic status (SES) is associated with increased risk for emotional and behavioural problems among children. Evidence from twin studies has shown that family SES moderates genetic and environmental influences on child mental health. However, it is also known that SES is itself under genetic influence and previous gene–environment interaction (G×E) studies have not incorporated the potential genetic overlap between child mental health and family SES into G×E analyses. We applied a novel approach using extended family data to investigate the moderation of aetiological influences on child emotional and behavioural problems by parental socioeconomic status in the presence of modelled gene–environment correlation. Methods: The sample comprised >28,100 children in extended‐family units drawn from the Norwegian Mother, Father and Child Cohort Study (MoBa). Mothers reported children's emotional and behavioural symptoms. Parents' income and educational attainment were obtained through linkage to administrative register data. Bivariate moderation Multiple‐Children‐of‐Twins‐and‐Siblings (MCoTS) models were used to analyse relationships between offspring outcomes (emotional and behavioural symptom scores) and parental socioeconomic moderators (income rank and educational attainment). Results: The aetiology of child emotional symptoms was moderated by maternal and paternal educational attainment. Shared environmental influences on child emotional symptoms were greater at lower levels of parents' education. The aetiology of child behavioural symptoms was moderated by maternal, but not paternal, socioeconomic factors. Genetic factors shared between maternal income and child behavioural symptoms were greater in families with lower levels maternal income. Nonshared environmental influences on child behavioural symptoms were greater in families with higher maternal income and education. Conclusions: Parental socioeconomic indicators moderated familial influences and nonshared environmental influences on child emotional and behavioural outcomes. Maternal SES and child mental health share aetiological overlap such that shared genetic influence was greater at the lower end of the socioeconomic distribution. Our findings collectively highlight the role that family socioeconomic factors play in shaping the origins of child emotional and behavioural problems. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

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. 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. 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. While the sample is representative of individuals living in Colombo District, it may not be representative of different regions of Sri Lanka. 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. • Higher depression scores were associated with lower standard of living, lower educational attainment, and financial strain • Significant genetic influences were observed for standard of living in females, and for educational attainment in both males and females • Shared and non-shared environmental influences were also apparent for both standard of living and educational attainment • Total variance in depression was greater among less socioeconomically advantaged individuals • The aetiology of depression varies across socioeconomic contexts [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

Introduction. Biobanks are a valuable resource for creating advancements in science through cutting-edge omics research. Twin research methods allow us to understand the degree to which genetics and environmental factors contribute to health outcomes. Methods. The Sri Lankan Twin Registry biobank (SLTR-b) was established in 2015 as part of Colombo Twin and Singleton Follow-up Study. Venous blood and urine were collected from twins and comparative sample of singletons for clinical investigations and biobanking. Results. The SLTR-b currently houses 3369 DNA and serum samples. Biobank specimens are linked to longitudinal questionnaire data, clinical investigations, anthropometric measurements, and other data. Discussion. The SLTR-b aims to address gaps in health and genetics research. It will provide opportunities for academic collaborations, local and international, and capacity building of future research leaders in twin and omics research. This paper provides a cohort profile of the SLTR-b and its linked data, and an overview of the strategies used for biobanking. [ABSTRACT FROM AUTHOR]

Objective/background: Many patients find cognitive behavioral therapy for insomnia (CBT-I) useful. However, it is currently unknown if those with sub-threshold insomnia also benefit. Here we assessed whether CBT-I is both feasible and acceptable in participants with sub-threshold insomnia. The primary aims were to evaluate participation rates and treatment acceptability, and to establish an effect size for symptom improvement.Patients/methods: A total of 199 female participants (Mage 20 ± 5 years) took part. Following baseline assessments, participants were randomly allocated to either a six-week digital CBT-I intervention or a six-week control group receiving puzzles. Additional assessments were performed three-weeks, six-weeks, and six-months later.Results: Participation rates at each survey assessment wave did not differ between the groups (ps > 0.140), though adherence to completing each weekly task was lower in the CBT-I group, p = 0.02. Treatment acceptability was high (M (SD) = 33.61 (4.82), theoretical range 6-42). The CBT-I group showed greater improvement in insomnia symptoms at the end of the intervention compared to the control group (p = 0.013, d = 0.42), with significant variation in outcome (M = 4.69, SD = 5.41). Sub-threshold participants showed a similar pattern of results, whilst those meeting insomnia criteria showed a smaller between-group difference. CBT-I led to improvements in anxiety, paranoia and perceived stress between baseline and end of intervention. Changes in insomnia symptoms were mediated by cognitions about sleep and somatic pre-sleep arousal.Conclusions: CBT-I provides a benefit even in sub-threshold insomnia. CBT-I may be useful to tackle insomnia symptoms even when they are sub-threshold. [ABSTRACT FROM AUTHOR]

This study investigated the genetic and environmental contributions to emotional overeating (EOE) and depressive symptoms, and their covariation, in a Sri-Lankan population, using genetic model-fitting analysis. In total, 3957 twins and singletons in the Colombo Twin and Singleton Study-Phase 2 rated their EOE behaviour and depressive symptoms, which were significantly associated (men: r = 0.11, 95% confidence interval (CI) 0.06-0.16, women: r = 0.12, 95% CI 0.07-0.16). Non-shared environmental factors explained the majority of variance in men (EOE e² = 87%, 95% CI 78-95%; depressive symptoms e² = 72%, 95% CI 61-83%) and women (EOE e² = 76%, 95% CI 68-83%; depressive symptoms e² = 64%, 95% CI 55-74%). Genetic factors were more important for EOE in women (h² = 21%, 95% CI 4-32%) than men (h² = 9%, 95% CI 0-20%). Shared-environmental factors were more important for depressive symptoms in men (c² = 25%, 95% CI 10-36%) than women (c² = 9%, 95% CI 0-35%). Non-shared environmental factors explained the overlap between depressive symptoms and EOE in women but not in men. Results differed from high-income populations, highlighting the need for behavioural genetic research in global populations. [ABSTRACT FROM AUTHOR]

Background: The disease burden related to mental disorders and metabolic syndrome is growing in low-and middle-income countries (LMIC). The Colombo Twin and Singleton Study (COTASS) is a population-based sample of twins and singletons in Colombo, Sri Lanka. Here we present prevalence estimates for metabolic syndrome (metS) and mental disorders from a follow-up (COTASS-2) of the original study (COTASS-1), which was a mental health survey.Methods: In COTASS-2, participants completed structured interviews, anthropometric measures and provided fasting blood and urine samples. Depressive disorder, depressive symptoms, anxiety symptoms, post-traumatic stress disorder (PTSD) and hazardous alcohol use were ascertained with structured psychiatric screens (Composite International Diagnostic Interview (CIDI), Beck Depression Inventory (BDI-II), Generalised Anxiety Disorder Questionnaire (GAD-7), PTSD Checklist - Civilian Version (PCL-C), and Alcohol Use Disorders Identification Test (AUDIT)). We defined metS according to the International Diabetes Federation (IDF) criteria and the revised National Cholesterol Education Programme Adult Treatment Panel (NCEP ATP III) criteria. We estimated the prevalence of psychiatric disorders and metS and metS components, and associations with gender, education and age.Results: Two thousand nine hundred thirty-four twins and 1035 singletons were followed up from COTASS-1 (83.4 and 61.8% participation rate, respectively). Prevalence estimates for depressive disorder (CIDI), depressive symptoms (BDI ≥ 16), anxiety symptoms (GAD-7 ≥ 10) and PTSD (PCL-C DSM criteria) were 3.8, 5.9, 3.6, and 4.5% respectively for twins and 3.9, 9.8, 5.1 and 5.4% for singletons. 28.1 and 30.9% of male twins and singletons respectively reported hazardous alcohol use. Approximately one third met the metS criteria (IDF: 27.4% twins, 44.6% singletons; NCEP ATP III: 30.6% twins, 48.6% singletons). The most prevalent components were central obesity (59.2% twins, 71.2% singletons) and raised fasting blood glucose or diabetes (38.2% twins, 56.7% singletons).Conclusion: MetS was highly prevalent in twins, and especially high in singletons, whereas the prevalence of mental disorders was low, but consistent with local estimates. The high levels of raised fasting plasma glucose and central obesity were particularly concerning, and warrant national diabetes prevention programmes. [ABSTRACT FROM AUTHOR]

Adolescent psychotic experiences increase risk for schizophrenia and other severe psychopathology in adulthood. Converging evidence implicates urban and adverse neighborhood conditions in the etiology of adolescent psychotic experiences, but the role of young people's personal perceptions of disorder (i.e., physical and social signs of threat) in their neighborhood is unknown. This was examined using data from the Environmental Risk Longitudinal Twin Study, a nationally representative birth cohort of 2,232 British twins. Participants were interviewed at age 18 about psychotic phenomena and perceptions of disorder in the neighborhood. Multilevel, longitudinal, and genetically sensitive analyses investigated the association between perceptions of neighborhood disorder and adolescent psychotic experiences. Adolescents who perceived higher levels of neighborhood disorder were significantly more likely to have psychotic experiences, even after accounting for objectively/independently measured levels of crime and disorder, neighborhood- and family-level socioeconomic status, family psychiatric history, adolescent substance and mood problems, and childhood psychotic symptoms: odds ratio = 1.62,95% confidence interval [1.27,2.05], p < .001. The phenotypic overlap between adolescent psychotic experiences and perceptions of neighborhood disorder was explained by overlapping common environmental influences, rC = .88, 95% confidence interval [0.26, 1.00]. Findings suggest that early psychological interventions to prevent adolescent psychotic experiences should explore the role of young people's (potentially modifiable) perceptions of threatening neighborhood conditions. [ABSTRACT FROM AUTHOR]

This paper presents multilevel findings on adolescents' victimization exposure from a large longitudinal cohort of twins. Data were obtained from the Environmental Risk (E-Risk) Longitudinal Twin Study, an epidemiological study of 2,232 children (1,116 twin pairs) followed to 18 years of age (with 93% retention). To assess adolescent victimization, we combined best practices in survey research on victimization with optimal approaches to measuring life stress and traumatic experiences, and introduce a reliable system for coding severity of victimization. One in three children experienced at least one type of severe victimization during adolescence (crime victimization, peer/sibling victimization, Internet/mobile phone victimization, sexual victimization, family violence, maltreatment, or neglect), and most types of victimization were more prevalent among children from low socioeconomic backgrounds. Exposure to multiple victimization types was common, as was revictimization; over half of those physically maltreated in childhood were also exposed to severe physical violence in adolescence. Biometric twin analyses revealed that environmental factors had the greatest influence on most types of victimization, while severe physical maltreatment from caregivers during adolescence was predominantly influenced by heritable factors. The findings from this study showcase how distinct levels of victimization measurement can be harmonized in large-scale studies of health and development. [ABSTRACT FROM AUTHOR]

Sleep paralysis is a relatively common but under-researched phenomenon. In this paper we examine prevalence in a UK sample and associations with candidate risk factors. This is the first study to investigate the heritability of sleep paralysis in a twin sample and to explore genetic associations between sleep paralysis and a number of circadian expressed single nucleotide polymorphisms. Analyses are based on data from the Genesis1219 twin/sibling study, a community sample of twins/siblings from England and Wales. In total, data from 862 participants aged 22-32 years (34% male) were used in the study. This sample consisted of monozygotic and dizygotic twins and siblings. It was found that self-reports of general sleep quality, anxiety symptoms and exposure to threatening events were all associated independently with sleep paralysis. There was moderate genetic influence on sleep paralysis (53%). Polymorphisms in the PER2 gene were associated with sleep paralysis in additive and dominant models of inheritance-although significance was not reached once a Bonferroni correction was applied. It is concluded that factors associated with disrupted sleep cycles appear to be associated with sleep paralysis. In this sample of young adults, sleep paralysis was moderately heritable. Future work should examine specific polymorphisms associated with differences in circadian rhythms and sleep homeostasis further in association with sleep paralysis. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

The Sri Lankan Twin Registry (SLTR), established in 1997, is a unique resource for twin and genetic research in a low- and middle-income country (LMIC). It comprises of a volunteer cohort of 14,120 twins (7,060 pairs) and 119 sets of triplets, and a population-based cohort of 19,040 (9,520 pairs) twins and 89 sets of triplets. Several studies have been conducted using this registry, including the Colombo Twin and Singleton Study (CoTaSS 1; 4,387 twins, 2,311 singletons), which have explored the prevalence and heritability of a range of psychiatric disorders as well as gene-environmental interplay. Currently, a follow-up study (CoTaSS 2) of the same cohort is underway, looking at the prevalence and interrelationship of key cardiovascular and metabolic risk markers (e.g., metabolic syndrome). A significant feature of CoTaSS 2 is the establishment of a biobank. Current SLTR work is extending beyond mental health and the interface between mental and physical health to new horizons, extending collaborations with the wider global twin research community. Ethics and governance have been given special emphasis in the initiative. Capacity building and public engagement are two crucial components. Establishment of a state-of-the-art genetic laboratory was a major accomplishment. SLTR is a classic showcase of successful North–South partnership in building a progressive research infrastructure in a LMIC. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

Background Separation anxiety disorder ( SAD) and separation anxiety symptoms ( SA) have been studied both epidemiologically and genetically; however, large between-studies discrepancies emerge relative to the role of genetic, shared-, and nonshared environmental influences on these conditions. Methods Based upon available literature, 18 cohorts and 31,859 subjects belonging to twin samples in Europe, the United States, and Australia were included in three meta-analytic estimations of: the standardized variance components of etiological influences on SAD/ SA, and on the effect of sex and rater. Results Meta-analytic estimations carried out on all cohorts showed that within-family (genetic 43% and shared environmental 17%) factors explain most of individual differences for SAD/ SA. Meta-heritability estimates were higher among females (.52) than males (.26), whereas nonshared environmental effects were stronger for the latter (.74) than for the former (.41). When SAD/ SA was rated by parents, the shared environmental influences were higher than those obtained with self-assessment instruments (.23 versus .05), but this may reflect an age difference between subsamples. Conclusions A shared environmental effect is present and important in SAD/ SA. Our results support at an etiological level the involvement of parents in treating SAD/ SA in children, and the provision of specific strategies to parents to manage their own anxiety. Depression and Anxiety 00:1-8, 2012. © 2012 Wiley Periodicals, Inc. [ABSTRACT FROM AUTHOR]