Anorexia nervosa and bulimia nervosa are two severe eating disorders associated with high premature mortality, suicidal risk and serious medical complications. Transition between anorexia nervosa and bulimia nervosa over the illness course and familial co-aggregation of the two eating disorders imply aetiological overlap. However, genetic and environmental liabilities to the overlap are poorly understood. Quantitative genetic research using clinical diagnosis is needed.

We acquired a clinical diagnosis of anorexia nervosa (prevalence = 0.90%) and bulimia nervosa (prevalence = 0.48%) in a large population-based sample (N = 782 938) of randomly selected full-sisters and maternal half-sisters born in Sweden between 1970 and 2005. Structural equation modelling was applied to quantify heritability of clinically diagnosed anorexia nervosa and bulimia nervosa and the contributions of genetic and environmental effects on their overlap.

The heritability of clinically diagnosed anorexia nervosa and bulimia nervosa was estimated at 43% [95% confidence interval (CI) (36–50%)] and 41% (31–52%), respectively, in the study population, with the remaining variance explained by variance in unique environmental effects. We found statistically significant genetic [0.66, 95% CI (0.49–0.82)] and unique environmental correlations [0.55 (0.43–0.66)] between the two clinically diagnosed eating disorders; and their overlap was about equally explained by genetic and unique environmental effects [co-heritability 47% (35–58%)].

Our study supports shared mechanisms for anorexia nervosa and bulimia nervosa and extends the literature from self-reported behavioural measures to clinical diagnosis. The findings encourage future molecular genetic research on both eating disorders and emphasize clinical vigilance for symptom fluctuation between them.

The phenotypic and aetiological architecture of depression symptomatology has been mostly studied in Western samples. In this study, we conducted a genetically informed factor analysis to elucidate both the phenotypic and aetiological architectures of self-reported depression among a Japanese adult twin sample.

Depressive symptoms assessed by Zung's Self-rating Depression Scale were self-rated by 425 twin pairs (301 monozygotic and 124 dizygotic twin pairs) in a community sample in Japan.

An exploratory factor analysis extracted three symptom domains representing cognitive, affective and somatic symptomatology. A confirmatory factor analysis demonstrated that a bi-factor solution fitted better than the alternative solutions, implying that depression may be defined as a combination of a single general construct and three factors specific to each of the three symptom domains. A multivariate genetic analysis with the bi-factor solution showed that the general factor was substantially heritable (47%), and that only the affective symptom domain was significantly heritable (29%) among the three specific factors, their remaining variance being explained by non-shared environmental influences.

Depression symptomatology appears to be adequately captured by a substantially heritable general factor. The heritability of this factor (47%) in a Japanese adult sample is in line with commonly reported heritability estimates for depression. The three specific factors – cognitive, affective and somatic – are mostly explained by non-shared environmental factors, which include measurement error. The extent to which these specific factors are uniquely associated with correlates of depression when the general factor is accounted for should be investigated in future studies.

The genetic component of Cannabis Use Disorder may overlap with influences acting more generally on early stages of cannabis use. This paper aims to determine the extent to which genetic influences on the development of cannabis abuse/dependence are correlated with those acting on the opportunity to use cannabis and frequency of use.

A cross-sectional study of 3303 Australian twins, measuring age of onset of cannabis use opportunity, lifetime frequency of cannabis use, and lifetime DSM-IV cannabis abuse/dependence. A trivariate Cholesky decomposition estimated additive genetic (A), shared environment (C) and unique environment (E) contributions to the opportunity to use cannabis, the frequency of cannabis use, cannabis abuse/dependence, and the extent of overlap between genetic and environmental factors associated with each phenotype.

Variance components estimates were A = 0.64 [95% confidence interval (CI) 0.58–0.70] and E = 0.36 (95% CI 0.29–0.42) for age of opportunity to use cannabis, A = 0.74 (95% CI 0.66–0.80) and E = 0.26 (95% CI 0.20–0.34) for cannabis use frequency, and A = 0.78 (95% CI 0.65–0.88) and E = 0.22 (95% CI 0.12–0.35) for cannabis abuse/dependence. Opportunity shares 45% of genetic influences with the frequency of use, and only 17% of additive genetic influences are unique to abuse/dependence from those acting on opportunity and frequency.

There are significant genetic contributions to lifetime cannabis abuse/dependence, but a large proportion of this overlaps with influences acting on opportunity and frequency of use. Individuals without drug use opportunity are uninformative, and studies of drug use disorders must incorporate individual exposure to accurately identify aetiology.

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.

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.

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.

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.

Many psychological traits become increasingly influenced by genetic factors throughout development, including several that might intuitively be seen as purely environmental characteristics. One such trait is the parent–child relationship, which is associated with a variety of socially significant outcomes, including mental health and criminal behavior. Genetic factors have been shown to partially underlie some of these associations, but the changing role of genetic influence over time remains poorly understood.

Over 1000 participants in a longitudinal twin study were assessed at three points across adolescence with a self-report measure regarding the levels of warmth and conflict in their relationships with their parents. These reports were analyzed with a biometric growth curve model to identify changes in genetic and environmental influences over time.

Genetic influence on the child-reported relationship with parent increased throughout adolescence, while the relationship's quality deteriorated. The increase in genetic influence resulted primarily from a positive association between genetic factors responsible for the initial relationship and those involved in change in the relationship over time. By contrast, environmental factors relating to change were negatively related to those involved in the initial relationship.

The increasing genetic influence seems to be due to early genetic influences having greater freedom of expression over time whereas environmental circumstances were decreasingly important to variance in the parent–child relationship. We infer that the parent–child relationship may become increasingly influenced by the particular characteristics of the child (many of which are genetically influenced), gradually displacing the effects of parental or societal ideas of child rearing.