Laurie John Hannigan

Aetiological influences on stability and change in emotional and behavioural problems across development: a systematic review

Emotional and behavioural problems in childhood and adolescence can be chronic and are predictive of future psychiatric problems. Understanding what factors drive the development and maintenance of these problems is therefore crucial. Longitudinal behavioural genetic studies using twin, sibling or adoption data can be used to explore the developmental aetiology of stability and change in childhood and adolescent psychopathology. We present a systematic review of longitudinal, behavioural genetic analyses of emotional and behavioural problems between ages 0 to 18 years. We identified 58 studies, of which 19 examined emotional problems, 30 examined behavioural problems, and 9 examined both. In the majority of studies, stability in emotional and behavioural problems was primarily genetically influenced. Stable environmental factors were also widely found, although these typically played a smaller role. Both genetic and environmental factors were involved in change across development. We discuss the findings in the context of the wider developmental literature and make recommendations for future research.

Widespread covariation of early environmental exposures and trait-associated polygenic variation

Significance Environmental exposures are among the best predictors of health and educational outcomes. Models that estimate the effect of environmental exposures on developmental outcomes typically ignore genetic factors or focus on gene–environment interaction (whether individuals’ response to environmental exposures depends on their genotype). Here we test gene–environment correlation (whether individuals’ exposure to environments depends on their genotype). Using a method that tests specific genetic effects while controlling for background genetic effects, we estimate covariation between children’s genetic liability/propensity for core developmental outcomes and a wide range of environmental exposures. Findings suggest that genetic variants associated with traits, such as educational attainment, body mass index, and schizophrenia, also capture environmental risk and protective factors. Although gene–environment correlation is recognized and investigated by family studies and recently by SNP-heritability studies, the possibility that genetic effects on traits capture environmental risk factors or protective factors has been neglected by polygenic prediction models. We investigated covariation between trait-associated polygenic variation identified by genome-wide association studies (GWASs) and specific environmental exposures, controlling for overall genetic relatedness using a genomic relatedness matrix restricted maximum-likelihood model. In a UK-representative sample (n = 6,710), we find widespread covariation between offspring trait-associated polygenic variation and parental behavior and characteristics relevant to children’s developmental outcomes—independently of population stratification. For instance, offspring genetic risk for schizophrenia was associated with paternal age (R2 = 0.002; P = 1e-04), and offspring education-associated variation was associated with variance in breastfeeding (R2 = 0.021; P = 7e-30), maternal smoking during pregnancy (R2 = 0.008; P = 5e-13), parental smacking (R2 = 0.01; P = 4e-15), household income (R2 = 0.032; P = 1e-22), watching television (R2 = 0.034; P = 5e-47), and maternal education (R2 = 0.065; P = 3e-96). Education-associated polygenic variation also captured covariation between environmental exposures and children’s inattention/hyperactivity, conduct problems, and educational achievement. The finding that genetic variation identified by trait GWASs partially captures environmental risk factors or protective factors has direct implications for risk prediction models and the interpretation of GWAS findings.

The stability of educational achievement across school years is largely explained by genetic factors

Little is known about the etiology of developmental change and continuity in educational achievement. Here, we study achievement from primary school to the end of compulsory education for 6000 twin pairs in the UK-representative Twins Early Development Study sample. Results showed that educational achievement is highly heritable across school years and across subjects studied at school (twin heritability ~60%; SNP heritability ~30%); achievement is highly stable (phenotypic correlations ~0.70 from ages 7 to 16). Twin analyses, applying simplex and common pathway models, showed that genetic factors accounted for most of this stability (70%), even after controlling for intelligence (60%). Shared environmental factors also contributed to the stability, while change was mostly accounted for by individual-specific environmental factors. Polygenic scores, derived from a genome-wide association analysis of adult years of education, also showed stable effects on school achievement. We conclude that the remarkable stability of achievement is largely driven genetically even after accounting for intelligence.Learning: High stability of school achievementTwin studies have shown that individual differences in school achievement are to a large extent (around 60%) explained by genetic differences. However, little is known about age-to-age stability and change in school achievement. A team led by Kaili Rimfeld used school achievement data from primary school to the end of compulsory education for 6000 twin pairs in the UK-representative Twins Early Development Study sample. Results showed that school achievement is highly heritable across the school years and across subjects studied at school, that school achievement is highly stable, and that this stability is largely explained by genetic factors. The finding of genetically driven stability of school achievement should provide additional motivation to identify children in need of interventions as early as possible, as the problems are likely to remain throughout the school years.

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 childrens 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.

Parent- and child-driven effects during the transition to adolescence: a longitudinal, genetic analysis of the home environment

Abstract Theoretical models of child development typically consider the home environment as a product of bidirectional effects, with parent‐ and child‐driven processes operating interdependently. However, the developmental structure of these processes during the transition from childhood to adolescence has not been well studied. In this study we used longitudinal genetic analyses of data from 6646 UK‐representative twin pairs (aged 9–16 years) to investigate stability and change in parenting and household chaos in the context of parent–child bidirectional effects. Stability in the home environment was modest, arising mainly from parent‐driven processes and family‐wide influences. In contrast, change over time was more influenced by child‐driven processes, indicated by significant age‐specific genetic influences. Interpretations of these results and their implications for researchers are discussed.

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

Common genetic influences offer a partial explanation for comorbidity between different psychiatric disorders1–3. 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.Analyses of twin and genomic data show a significant influence of genetic factors on the co-development of conduct and emotional problems from childhood to adolescence. Those with co-developing symptoms may represent a clinical subgroup with higher genetic risk.

Shared genetic influences do not explain the association between parent-offspring relationship quality and offspring internalizing problems: results from a Children-of-Twins study

Background Associations between parenting and child outcomes are often interpreted as reflecting causal, social influences. However, such associations may be confounded by genes common to children and their biological parents. To the extent that these shared genes influence behaviours in both generations, a passive genetic mechanism may explain links between them. Here we aim to quantify the relative importance of passive genetic v. social mechanisms in the intergenerational association between parent–offspring relationship quality and offspring internalizing problems in adolescence. Methods We used a Children-of-Twins (CoT) design with data from the parent-based Twin and Offspring Study of Sweden (TOSS) sample [909 adult twin pairs and their offspring; offspring mean age 15.75 (2.42) years], and the child-based Swedish Twin Study of CHild and Adolescent Development (TCHAD) sample [1120 adolescent twin pairs; mean age 13.67 (0.47) years]. A composite of parent-report measures (closeness, conflict, disagreements, expressions of affection) indexed parent–offspring relationship quality in TOSS, and offspring self-reported internalizing symptoms were assessed using the Child Behavior Checklist (CBCL) in both samples. Results A social transmission mechanism explained the intergenerational association [r = 0.21 (0.16–0.25)] in our best-fitting model. A passive genetic transmission pathway was not found to be significant, indicating that parental genetic influences on parent–offspring relationship quality and offspring genetic influences on their internalizing problems were non-overlapping. Conclusion These results indicate that this intergenerational association is a product of social interactions between children and parents, within which bidirectional effects are highly plausible. Results from genetically informative studies of parenting-related effects should be used to help refine early parenting interventions aimed at reducing risk for psychopathology.