Developmental change in the association between adolescent depressive symptoms and the home environment: results from a longitudinal, genetically informative investigation

Background: Depression is already highly prevalent by late adolescence, indicating that research into its developmental emergence should consider earlier risk factors and environmental contexts. The home environment is a key context for children and adolescents throughout development. However, the nature of relationships that exist between aspects of the home environment and the development of depressive symptoms cannot be assumed. Genetically informative studies have been used to provide insights about the aetiology of such relationships, often finding them to be partly confounded by the influence of children's genes. Here, we investigate developmental change in the aetiology of the association between aspects of the home environment and depressive symptoms at the onset of adolescence. Methods: We used longitudinal child‐ and parent‐report data from >5,000 twin pairs enrolled in the UK‐representative Twins Early Development Study. Multivariate, genetically sensitive structural equation models were used to decompose latent variance and covariance in depressive symptoms (measured at 12 and 16 years) and aspects of the home environment (at 9 and 14 years) into genetic and environmental influences. Results: Going from childhood to adolescence, genetic influences accounted for an increasing proportion of the association [30% (16–42) of r = .44 in childhood; 40% (25–61) of r = .43 in adolescence], at the expense of shared environmental influences, which decreased from 70% (58–83) to 48% (29–62). Unique environmental influences accounted for a significant proportion of the association in adolescence only [12% (06–18)]. Developmental changes could largely be attributed to subtle shifts in the relative importance of stable aetiological factors, rather than the emergence of influences unique to adolescence. Conclusions: These findings emphasise the importance of developmental and aetiological context in interpreting associations between aspects of the home environment and child emotional outcomes

Etiological influences on perceptions of parenting: A longitudinal, multi-informant twin study

Children and their parents often differ in their perception of the relationship they share. As this relationship changes developmentally, the nature of these differences may also change. Longitudinal genetic designs can be used to investigate the developmental etiologies of shared and distinct perceptions. In this study, we used longitudinal psychometric models to analyze child and parent reports of negative parenting for 6417 twin pairs from the Twins Early Development Study at ages 9, 12 and 14 years. Within-time cross-reporter correlations, indicating the degree to which children and parents perceived negative parenting behaviors similarly at each age, were moderate (r = .44 − .46). Longitudinal genetic analyses revealed these shared perceptions to be relatively stable during the transition into adolescence, with this stability driven by a combination of children’s genetic factors and family-wide environmental factors. In contrast, child- and parent-specific perceptions of parenting were predominantly age-specific, a developmental pattern underpinned by child genetic factors and a combination of family-wide and unique environmental influences. These results and their implications are discussed in the context of interplay between reciprocal interactions, subjective insight and developmental behavioral change in the parent–child relationship

The parent play questionnaire: development of a parent questionnaire to assess parent–child play and digital media use

We introduce the Parent Play Questionnaire (PPQ), a parent-report measure designed to assess frequency of parent–infant play, parents’ attitudes towards play with their infant, and infants’ use of digital media. We describe measure development and empirical data across three samples of parent–infant dyads (total N = 414, offspring aged 0.3–2.5 years). Three latent factors explain the PPQ, corresponding with theoretically defined subscales. Summary scores showed good internal consistency and normally distributed results. Weak to moderate correlations were found between the frequency and attitude play scales, and with standardized measures of family social and emotional characteristics. Overall, frequency of digital media use was not correlated with play or broader family variables. Results suggest that the PPQ will be a useful tool for researchers interested in assessing parent–child play during early childhood

Causal inference methods for intergenerational research using observational data

Identifying early causal factors leading to the development of poor mental health and behavioral outcomes is essential to design efficient preventive interventions. The substantial associations observed between parental risk factors (e.g., maternal stress in pregnancy, parental education, parental psychopathology, parent-child relationship) and child outcomes point toward the importance of parents in shaping child outcomes. However, such associations may also reflect confounding, including genetic transmission-that is, the child inherits genetic risk common to the parental risk factor and the child outcome. This can generate associations in the absence of a causal effect. As randomized trials and experiments are often not feasible or ethical, observational studies can help to infer causality under specific assumptions. This review aims to provide a comprehensive summary of current causal inference methods using observational data in intergenerational settings. We present the rich causal inference toolbox currently available to researchers, including genetically informed and analytical methods, and discuss their application to child mental health and related outcomes. We outline promising research areas and discuss how existing approaches can be combined or extended to probe the causal nature of intergenerational effects. (PsycInfo Database Record (c) 2023 APA, all rights reserved)

Early Puberty Is Associated With Higher Academic Achievement in Boys and Girls and Partially Explains Academic Sex Differences

Purpose: On average, boys have lower academic achievement than girls. We investigated whether the timing of puberty is associated with academic achievement, and whether later puberty among boys contributes to the sex difference in academic achievement. Method: Examination scores at age 16 were studied among 13,477 British twins participating in the population-based Twins Early Development Study. A pubertal development scale, a height based proxy of growth spurt, and age at menarche were used as indicators of puberty. Associations between puberty, sex, and academic achievement were estimated in phenotypic mediation models and biometric twin models. Results: Earlier puberty was associated with higher academic achievement both in boys and girls. The exception was early age at menarche in girls, which associated with lower academic achievement. More than half of the sex differences in academic achievement could be linked to sex differences in pubertal development, but part of this association appeared to be rooted in prepubertal differences. The biometric twin modelling indicated that the association between puberty and academic achievement was due to shared genetic risk factors. Genetic influences on pubertal development accounted for 7%-8% of the phenotypic variation in academic achievement. Conclusions: Pubertal maturation relates to the examination scores of boys and of girls. This can give genes related to pubertal maturation an influence on outcomes in education and beyond. Sex differences in pubertal maturation can explain parts of the sex difference in academic achievement. Grading students when they are immature may not accurately measure their academic potential. (c) 2021 Society for Adolescent Health and Medicine. Published by Elsevier Inc. All rights reserved. This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).Peer reviewe

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

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

The Genesis 12–19 (G1219) Study: A Twin and Sibling Study of Gene–Environment Interplay and Adolescent Development in the UK

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

Maternal prenatal depressive symptoms and risk for early-life psychopathology in offspring: results from a genetically-informative, population-based sample

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

Associations between socioeconomic factors and depression in Sri Lanka: The role of gene-environment interplay

Background: Low socioeconomic status is a risk factor for depression. The nature and magnitude of associations can differ cross-culturally and is influenced by a range of contextual factors. We examined the aetiology of 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