BACKGROUND:Psychiatric research is increasingly embracing a paradigm shift from categorical diagnoses to neurobiologically meaningful dimensions that cross current diagnostic boundaries. This transposition calls for redefining endophenotypes to accommodate transdiagnostic vulnerabilities. We sought to identify shared and disorder-specific neurocognitive endophenotypes for schizophrenia, bipolar I disorder (BD-I) and a broad psychosis/BD-I phenotype in a mega-analysis of twin/sibling data. STUDY DESIGN:We performed genetic model fitting to intelligence (IQ) and computerised neurocognitive data derived from 1050 twins/siblings from three research centres in the UK, Denmark and the Netherlands, affected (n = 257) or unaffected (n = 793) by schizophrenia, other primary psychoses and BD-I. We examined the endophenotypic status of IQ, spatial working memory (SWM), visual recognition, sustained attention/rapid visual processing (RVP), mental flexibility, and spatial planning/problem solving (all validated as endophenotypes for schizophrenia in previous studies) in relation to schizophrenia, BD-I and the broad phenotype. STUDY RESULTS:After covarying for age, gender, education and research centre, IQ and SWM emerged as transdiagnostic endophenotypes, showing statistically significant heritabilities (h2 67-75% and 28-30%, respectively), phenotypic correlations (rph |0.14|-|0.25|) and genetic correlations (rg |0.18|-|0.42|) with all diagnostic phenotypes. Additionally, all remaining cognitive domains received validation as endophenotypes for the broad phenotype, and all, but RVP, for schizophrenia. CONCLUSIONS:IQ and SWM tap into transdiagnostic elements of the genetic vulnerabilities to psychosis and BD-I. Our findings add to emergent evidence which spurs cautious optimism that a psychiatric nosology based on aetiology rather than phenotypical classifications may be feasible in the future, enabling biotyping and novel approaches to treatment.

Abstract Polygenic scores are imperfect measures of the additive genetic effects of common genetic variants. The resulting measurement error biases estimates of quantities of interest in epidemiological analyses integrating polygenic scores. For example, how much of an exposure-outcome association is genetically confounded can be substantially underestimated when using polygenic scores alone. Here we present extensions to Gsens , a genetic sensitivity analysis, which aims to correct for such measurement error using both polygenic scores and heritability estimates. Gsens now allows for multiple exposures and estimates several quantities of interest, i.e. genetic confounding, adjusted residual association (net of genetic confounding), genetic overlap and environmentally mediated genetic effects. We present derivations and simulations showing how Gsens accounts for measurement error in the polygenic score; we also show how estimation may be affected by misspecifications of the causal structure between exposures. Applying Gsens in the Norwegian Mother, Father and Child Cohort Study (MoBa), we uncover, among other results, substantial genetic confounding in the associations between multiple known risk factors for attention deficit hyperactivity disorder (ADHD), such as low birth weight and temperament, and measures of ADHD in childhood. The updated Gsens R package offers multiple options, including for missing data handling and customisable syntax. Our extended version of Gsens is applicable to a broad range of substantive questions in multiple disciplines.

Background Poor dietary habits and insufficient nutrient intake pose significant global challenges. This study examines the nutrient intake of Sri Lankan adults and its association with selected socio-demographic characteristics during the economic crisis from 2020 to 2023. It also examines the validity of a subjective 24-hour dietary recall (24HDR) questionnaire using blood and urine biomarkers. Methods Data were collected from 164 twins and 138 adult offspring of the twins in the Colombo District of Sri Lanka. Nutrient intake was calculated using a 24HDR and, then compared with the recommended dietary allowances (RDA) in Sri Lanka. Blood and urine samples were analyzed for biomarker detection to assess dietary validity. Results Participants did not reach the recommended energy intake (mean for females: 1954.93 Kcal; mean for males:2507.04 Kcal). Participants also failed to meet the RDA for fat and dietary fiber. However, 71% of participants achieved the recommended carbohydrate intake. Micronutrient deficits were also evident; for example, most participants had low intakes of vitamins B2, B3, B12, C, and calcium. Regression analysis comparing questionnaire-based nutrient intake with biomarker data showed positive associations between serum beta-carotene, zeaxanthin, and vitamin D intake, as well as between urinary phenolic content, serum zeaxanthin, and vitamin A intake. Age significantly influenced portion size and the intake of energy, fat, and vitamins. Conclusion Our findings support the validity of the 24HDR as a dietary and nutritional assessment tool in Sri Lanka. These results offer valuable insights for public health policymakers, highlighting the importance of revising dietary recommendations to enhance dietary diversity and promote routine nutritional assessments in Sri Lanka.

BackgroundPositive, negative and disorganised psychotic symptom dimensions are associated with clinical and developmental variables, but differing definitions complicate interpretation. Additionally, some variables have had little investigation.AimsTo investigate associations of psychotic symptom dimensions with clinical and developmental variables, and familial aggregation of symptom dimensions, in multiple samples employing the same definitions.MethodWe investigated associations between lifetime symptom dimensions and clinical and developmental variables in two twin and two general psychosis samples. Dimension symptom scores and most other variables were from the Operational Criteria Checklist. We used logistic regression in generalised linear mixed models for combined sample analysis (n = 875 probands). We also investigated correlations of dimensions within monozygotic (MZ) twin pairs concordant for psychosis (n = 96 pairs).ResultsHigher symptom scores on all three dimensions were associated with poor premorbid social adjustment, never marrying/cohabiting and earlier age at onset, and with a chronic course, most strongly for the negative dimension. The positive dimension was also associated with Black and minority ethnicity and lifetime cannabis use; the negative dimension with male gender; and the disorganised dimension with gradual onset, lower premorbid IQ and substantial within twin-pair correlation. In secondary analysis, disorganised symptoms in MZ twin probands were associated with lower premorbid IQ in their co-twins.ConclusionsThese results confirm associations that dimensions share in common and strengthen the evidence for distinct associations of co-occurring positive symptoms with ethnic minority status, negative symptoms with male gender and disorganised symptoms with substantial familial influences, which may overlap with influences on premorbid IQ.

Background The use of cannabis in adolescence and early adulthood, critical phases for brain development, is linked to psychotic-like experiences (PLEs). The underlying mechanisms, however, remain unclear. This research examined the relationship between recreational cannabis use and PLEs, emphasizing the connectivity of the salience network (SN), which plays a role in salience processing and psychosis. To determine whether this relationship reflects shared genetic or environmental contributions, twin modeling was used.Methods We included 232 healthy adolescent Turkish twins who underwent diffusion MRI and psychometric assessment. SN connectivity was quantified using graph theory metrics. Linear mixed models were used to examine the associations among cannabis use, SN factors, and PLEs. Mediation analyses assessed whether SN parameters explained the cannabis-PLEs association. Twin models disentangle genetic and environmental contributions to these traits and their covariation.Results Cannabis use was significantly associated with higher overall PLE frequency. A specific SN factor predicted both total and positive PLEs. However, SN connectivity did not mediate the cannabis-PLEs relationship. Twin modeling showed that cannabis use and PLEs were mainly influenced by unique environmental factors. No significant phenotypic covariations were found among cannabis use, PLEs, and SN parameters.Conclusions Recreational cannabis use during adolescence and young adulthood is associated with heightened PLEs, although this association is not mediated by SN connectivity. The environment plays an important role during adolescence in shaping these traits independently. The findings underscore the need for longitudinal and genetically informed studies to clarify the mental health effects of adolescent cannabis use.

Globally, most children and adolescents live in low- and middle-income (LAMI) countries. Despite the high and under-recognized mental health burden in these settings, there is little systematic research to inform cost-effective mental health interventions. Identifying causal risk and protective mechanisms is important to inform such interventions. Longitudinal genetically informative designs can help identify potentially causal environmental mechanisms in the etiology of childhood psychopathology but few have been carried out in LAMI settings. We tested the feasibility of a twin-family study in a semi-urban setting in South-Western Nigeria. We recruited 320 family units, each comprising at least one parent and both twins aged 2.5–5.9 (x̄ = 4.0 ± 0.92) years from two towns using five strategies: direct and indirect contacts, radio adverts, cluster sampling (based on local administrative units) and snowball sampling. Participants were asked about their willingness to participate in future research including providing biological samples. These were supplemented with participant engagement activities before and after data collection. Snowball sampling was the most effective strategy while cluster sampling was the least effective (recruiting 46.3

BACKGROUND:Interpersonal violence, for example bullying and intimate partner violence, affects millions of people worldwide and is related to mental health problems. However, research methodologies which allow us to study mechanisms of this association, such as longitudinal and twin studies, overrepresent populations in the global north. METHODS:The Colombo Twin and Singleton Study collected data between 2005 and 2007 as well as 2012-2015. First, linear models were used to assess risks factors for exposure to interpersonal violence. Second, they were used to test the associations between exposure to interpersonal violence and the outcomes - depression and suicidal ideation. Further, the quasi-causal monozygotic twin differences design was used to test the associations between exposure and outcome. A bivariate twin moderation model was applied to investigate gene-environment interactions. RESULTS:There was a heightened risk of experiencing interpersonal violence among those previously affected by armed conflict (β = 0.13, 95 % CI = 0.06, 0.20) or natural disasters (β = 0.11, 95 % CI = 0.02, 0.19), in men (β = 0.23, 95 % CI = 0.17, 0.30) and those of lower socioeconomic status (β = 0.05, 95 % CI = 0.01, 0.08). Experiencing interpersonal violence was associated with depression symptoms after accounting for confounding familial factors (β = 0.23, 95 % CI = 0.10, 0.36). Twin model fitting showed that interpersonal violence moderated the genetic and non-shared environmental influences on depression symptoms. CONCLUSIONS:Exposures to natural disasters and civil conflict are associated with experiencing interpersonal violence. Being affected by interpersonal violence is linked to depressive difficulties, and those with genetic and environmental vulnerabilities may be more likely to be negatively affected.

Sensory symptoms are highly prevalent amongst autistic individuals and are now considered in the diagnostic criteria. Whilst evidence suggests a genetic relationship between autism and sensory symptoms, sensory symptoms are neither universal within autism nor unique to autism. One explanation for the heterogeneity within autism and commonality across conditions with respect to sensory symptoms, is that it is alexithymia (a condition associated with difficulties identifying and describing one’s own emotions) that has a genetic relationship with sensory symptoms, and that alexithymia commonly co-occurs with autism and with several other conditions. Using parent-reports of symptoms in a sample of adolescent twins, we sought to examine the genetic association between autism, alexithymia and sensory symptoms. Results showed that the genetic correlation between autism and sensory symptoms was not significant after controlling for alexithymia. In contrast, after controlling for variance in alexithymia explained by autism, the genetic correlation between alexithymia and sensory symptoms was significant (and the proportion of variance explained by genetic factors remained consistent after controlling for autism). These results suggest that 1) alexithymia and sensory symptoms share aetiology that is not accounted for by their association with autism and 2) that the genetic association between sensory symptoms and autism may be, in part or wholly, a product of alexithymia. Future research should seek to examine the contribution of alexithymia to sensory symptoms across other conditions.

We estimate whether risk preferences are affected by traumatic events by using a unique survey of Sri Lankan twins which contains information on individual's exposure to the 2004 Indian Ocean Tsunami, validated measures of mental health and risk preferences, and a rich set of control variables. Our estimation strategy utilizes variation in experiences within twin pairs and allows us to explore wealth shocks and/or changes in mental health as mechanisms. We find that exposure to the tsunami lead to less risk aversion, a result that is not explained by mental health.

Background. ADHD symptoms are associated with emotional problems such as depressive and anxiety symptoms from early childhood to adulthood, with the association increasing with age. A shared aetiology and/or a causal relationship could explain their correlation. In the current study, we explore these explanations for the association between ADHD symptoms and emotional problems from childhood to adulthood. Methods. Data were drawn from the Twins Early Development Study (TEDS), including 3675 identical and 7063 non-identical twin pairs. ADHD symptoms and emotional symptoms were reported by parents from childhood to adulthood. Self-report scales were included from early adolescence. Five direction of causation (DoC) twin models were fitted to distinguish whether associations were better explained by shared aetiology and/or causal relationships in early childhood, mid-childhood, early adolescence, late adolescence, and early adulthood. Followup analyses explored associations for the two subdomains of ADHD symptoms, hyperactivity-impulsivity and inattention, separately. Results. The association between ADHD symptoms and emotional problems increased in magnitude from early childhood to adulthood. In the best-fitting models, positive genetic overlap played an important role in this association at all stages. A negative causal effect running from ADHD symptoms to emotional problems was also detected in early childhood and mid-childhood. When distinguishing ADHD subdomains, the apparent protective effect of ADHD symptoms on emotional problems in childhood was mostly driven by hyperactivity-impulsivity. Conclusions. Genetic overlap plays an important role in the association between ADHD symptoms and emotional problems. Hyperactivity-impulsivity may protect children from emotional problems in childhood, but this protective effect diminishes after adolescence.

Aims To determine: i. the nature of the associations between three domains of psychopathology (depressive, hyperactivity and conduct symptoms) and cognitive/academic performance among adolescents i.e., whether these reflect causal processes and/or common genetic effects; ii. The extent to which these associations vary by comorbidity. Methods The sample comprised participants in the UK Twins Early Development Study (TEDS; n≈12,000 individuals) assessed for depressive, hyperactivity and conduct symptoms using standardised questionnaires. Cognitive and academic performance were assessed using Standard Progressive Matrices and GCSE scores respectively. Comorbidity was derived as a count of borderline/high psychopathology scores present per individual. Twin modelling was used to investigate preliminary correlations and moderation effects. Genetic models were further used to determine the most likely direction of causal effects with/without genetic correlations. Results There were small to moderate negative correlations between adolescent psychopathology domains and cognitive performance (−0.01 ≤ r≤−0.15) and academic performance (−0.06 ≤ r≤−0.23). Correlations were smallest for depressive symptoms and larger for hyperactivity/conduct symptoms. The correlation between hyperactivity symptoms and cognitive performance was significantly more negative as comorbidities increased (moderation coefficient – βmod = 0.07, 95% CI: 0.02, 0.12). Similarly, the association between depressive symptoms and academic performance also became more negative as comorbidities increased (βmod = −0.08, 95% CI: −0.11, −0.05). Twin modelling indicated that hyperactivity symptoms were causally associated with poorer cognitive and academic performance. In contrast, poorer cognitive performance was causally associated with conduct symptoms. Conclusion These preliminary findings indicate the impact of comorbidity on the functioning of adolescents with hyperactivity and depressive symptoms. They further suggest the need to specifically recognise these comorbidities during assessment and treatment planning to promote optimal functioning. Our findings also suggest differential mechanisms for the links between different psychopathology domains and impaired functioning. Further analyses will investigate moderation of the causal links and/or genetic correlations and whether these associations vary by indicators of marginalisation (sex and ethnicity).

Childhood victimization is a key risk factor for poor mental and physical health. In order to prevent childhood victimization, it is important to better understand its underlying etiological factors. Childhood victimization is not randomly distributed in the population but occurs more often in the context of certain characteristics of the child, the family, and the broader environment. These characteristics may be both genetically and environmentally influenced, making genetically informative designs valuable to disentangle the etiological factors. Here we performed meta-analyses of the genetic and environmental influences on childhood victimization based on twin studies. We also tested whether genetic and environmental influences on childhood victimization vary depending on key features of victimization experiences including the reporter of victimization experiences, the type of victimization, and the age at exposure. Following PRISMA guidelines, a search for relevant literature was conducted using MEDLINE, APA PsycInfo, and Embase databases until September 2023. A meta-analysis based on 21 studies with 62,794 participants showed that genetic influences accounted for 40% of the variance in childhood victimization, shared environmental influences for 20%, and non-shared environmental influences for 40%. In addition, we found that genetic and environmental influences on victimization varied based on the reporter and the type of victimization, and the age at victimization. The quantitative summary of genetic and environmental influences provided by this study advances our understanding of the mechanisms underlying risk for childhood victimization and points to prevention targets for victimization and its health effects.

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.

Existing evidence indicates genetic and non-genetic influences on sexual orientation; however, the possibility of gene-environment interplay has not been previously formally tested despite theories indicating this. Using a Finnish twin cohort, this study investigated whether childhood gender nonconformity and early-life adversities independently moderated individual differences in sexual orientation and childhood gender nonconformity, the relationship between them, and the etiological bases of the proposed moderation effects. Sexual orientation, childhood gender nonconformity, and early-life adversities were assessed using standard questionnaires. Structural equation twin model fitting was carried out using OpenMx. Childhood gender nonconformity was significantly associated with reduced phenotypic variance in sexual orientation (β = − 0.14, 95

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

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.

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

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

Abstract 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.

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