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

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

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.

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

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

Socioeconomic status and risk for child psychopathology: exploring gene-environment interaction in the presence of gene-environment correlation using extended families in the Norwegian Mother, Father and Child Birth Cohort Study.

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.

Genetic architecture of Environmental Sensitivity reflects multiple heritable components: a twin study with adolescents.

Humans differ substantially in how strongly they respond to similar experiences. Theory suggests that such individual differences in susceptibility to environmental influences have a genetic basis. The present study investigated the genetic architecture of Environmental Sensitivity (ES) by estimating its heritability, exploring the presence of multiple heritable components and its genetic overlap with common personality traits. ES was measured with the Highly Sensitive Child (HSC) questionnaire and heritability estimates were obtained using classic twin design methodology in a sample of 2868 adolescent twins. Results indicate that the heritability of sensitivity was 0.47, and that the genetic influences underlying sensitivity to negative experiences are relatively distinct from sensitivity to more positive aspects of the environment, supporting a multi-dimensional genetic model of ES. The correlation between sensitivity, neuroticism and extraversion was largely explained by shared genetic influences, with differences between these traits mainly attributed to unique environmental influences operating on each trait.

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.

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

Bullying-victimisation has been associated with sleep disturbances. This study investigated the degree to which subtypes of bullying-victimisation in adolescence are linked with sleep disturbances. Genetic and environmental contributions underlying bullying-victimisation and sleep disturbances were investigated. Participants (3,242-5,076 pairs) from a longitudinal community twin study reported on their bullying-victimisation at the age of 14 years, and sleep quality and insomnia symptoms at age 16. Regression analyses were used, accounting for the role of individual and family factors. Structural equation twin model fitting was conducted. Bullying-victimisation was modestly associated with sleep quality and insomnia symptoms (r = 0.22-0.23) and a similar strength of associations was found across bullying-victimisation subtypes (r = 0.11-0.22). Bullying-victimisation, sleep quality and insomnia symptoms were predominantly influenced by genes (25-59%) and non-shared environments (40-62%). The association between bullying-victimisation and sleep quality was explained by genetic and non-shared environmental influences. For insomnia symptoms and sleep quality, the association with bullying-victimisation was in part explained by a genetic overlap. Associations between bullying-victimisation and sleep disturbances are not limited to specific aspects of bullying-victimisation but appear to exist for all subtypes. These findings stimulate research questions regarding the mechanisms underlying these links. For example, could certain heritable traits, such as temperament, increase vulnerability to experiencing sleep disturbances and being bullied? Research on bullying and sleep should aim to take the role of genetic predisposition into account, while also noting that it is not the only causal influence. Understanding more about these pathways could strengthen the development of techniques to prevent these difficulties from occurring.

Why do depression, conduct, and hyperactivity symptoms co-occur across adolescence? The role of stable and dynamic genetic and environmental influences.

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.

Genetic Overlap Between Type 2 Diabetes and Depression in a Sri Lankan Population Twin Sample.

OBJECTIVE: Results from twin studies examining the genetic overlap between type 2 diabetes and depression are currently inconclusive. This question has not been addressed in non-Western populations. We aimed to examine whether there are common genetic factors between type 2 diabetes and depression in a Sri Lankan population using genetic model-fitting analysis. METHOD: The Colombo Twin and Singleton Study-Phase 2 consists of 2019 singletons, and 842 monozygotic and 578 dizygotic twin pairs. The primary outcomes were self-reported type 2 diabetes diagnosis and Beck Depression Inventory scores. Standard bivariate twin models were fitted to estimate the genetic and environmental (co)variance of type 2 diabetes and depression. RESULTS: In the best-fitting model, the phenotypic correlation between type 2 diabetes and depression was significant in female individuals only (r = 0.15 [0.08-0.21]). This association was primarily attributed to a significant genetic correlation between the traits (rA = 0.53 [0.19-0.98]). CONCLUSIONS: In female individuals, but not male individuals, we found a significant genetic overlap between type 2 diabetes and depression in the context of a modest phenotypic correlation.

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 Colombo Twin and Singleton Follow-up Study: a population based twin study of psychiatric disorders and metabolic syndrome in Sri Lanka.

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.

In the eye of the beholder: Perceptions of neighborhood adversity and psychotic experiences in adolescence.

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.

Association between stressful life events and psychotic experiences in adolescence: evidence for gene-environment correlations.

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.

Etiology of Pervasive Versus Situational Antisocial Behaviors: A Multi-Informant Longitudinal Cohort Study.

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

Why some children with externalising problems develop internalising symptoms: testing two pathways in a genetically sensitive cohort study.

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.

A twin and molecular genetics study of sleep paralysis and associated factors.

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.

A multivariate twin study of trait mindfulness, depressive symptoms, and anxiety sensitivity.

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.

The prevalence and correlates of alcohol use and alcohol use disorders: a population based study in Colombo, Sri Lanka.

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.

Measuring adolescents' exposure to victimization: The Environmental Risk (E-Risk) Longitudinal Twin Study.

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.

Trauma, post-traumatic stress disorder and psychiatric disorders in a middle-income setting: prevalence and comorbidity.

BACKGROUND: Most studies of post-traumatic stress disorder (PTSD) in low- and middle-income countries (LMICs) have focused on 'high-risk' populations defined by exposure to trauma. AIMS: To estimate the prevalence of post-traumatic stress disorder (PTSD) in a LMIC, the conditional probability of PTSD given a traumatic event and the strength of associations between traumatic events and other psychiatric disorders. METHOD: Our sample contained a mix of 3995 twins and 2019 non-twins. We asked participants about nine different traumatic exposures, including the category 'other', but excluding sexual trauma. RESULTS: Traumatic events were reported by 36.3% of participants and lifetime PTSD was present in 2.0%. Prevalence of non-PTSD lifetime diagnosis was 19.1%. Of people who had experienced three or more traumatic events, 13.3% had lifetime PTSD and 40.4% had a non-PTSD psychiatric diagnosis. CONCLUSIONS: Despite high rates of exposure to trauma, this population had lower rates of PTSD than high-income populations, although the prevalence might have been slightly affected by the exclusion of sexual trauma. There are high rates of non-PTSD diagnoses associated with trauma exposure that could be considered in interventions for trauma-exposed populations. Our findings suggest that there is no unique relationship between traumatic experiences and the specific symptomatology of PTSD.