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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]

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]

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]

Background: Stressful life events (SLEs) are associated with psychotic experiences. SLEs might act as an environmental risk factor, but may also share a genetic propensity with psychotic experiences.Aims: To estimate the extent to which genetic and environmental factors influence the relationship between SLEs and psychotic experiences.Method: Self- and parent reports from a community-based twin sample (4830 16-year-old pairs) were analysed using structural equation model fitting.Results: SLEs correlated with positive psychotic experiences (r = 0.12-0.14, all P<0.001). Modest heritability was shown for psychotic experiences (25-57%) and dependent SLEs (32%). Genetic influences explained the majority of the modest covariation between dependent SLEs and paranoia and cognitive disorganisation (bivariate heritabilities 74-86%). The relationship between SLEs and hallucinations and grandiosity was explained by both genetic and common environmental effects.Conclusions: Further to dependent SLEs being an environmental risk factor, individuals may have an underlying genetic propensity increasing their risk of dependent SLEs and positive psychotic experiences. [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]

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]