Objective. The transmission of anxiety within families is well-recognised, but the underlying processes are poorly understood. Twin studies of adolescent anxiety demonstrate both genetic and environmental influence, and multiple aspects of parenting are associated with offspring anxiety. To date, the Children-ofTwins design has not been used to evaluate the relative contributions of genetic versus direct transmission of anxiety from parents to their offspring. Method. Anxiety and neuroticism measures were completed by 385 monozygotic and 486 dizygotic same-sex twin families (37% male twin pair families) from the Twin and Offspring Study in Sweden (TOSS). Structural equation models tested for the presence of both genetic and environmental transmission from one generation to the next. Results. For both anxiety and neuroticism the models provide support for significant direct environmental transmission from parents to their adolescent offspring. In contrast there was no evidence of significant genetic transmission. Conclusions. The association between parental and offspring anxiety largely arises due to a direct association between parents and their children independent of genetic confounds. The lack of genetic transmission may reflect there being different genetic effects on these traits in adolescence and adulthood. Direct environmental transmission is in line with developmental theories of anxiety suggesting that children and adolescents learn anxious behaviours from their parents via a number of pathways such as modelling. Future analyses should combine children-of-twins data with child twin data in order to examine whether this direct effect solely represents parental influences on the offspring or whether it also includes child/adolescent anxiety evoking parental anxiety.

This study presents an extended children-of-twins model, allowing us to test the direction of the association between parenting and child adjustment. Three mechanisms can be examined: direct phenotypic influence of parenting on child behavior (controlling for both parental and child genotype), passive genotype-environment correlation and evocative genotype-environment correlation. This model has been tested using Monte-Carlo simulations. We generated datasets consisting of 1000 twin parent pairs together with their children, and 1000 twin children pairs together with their parents. These simulated datasets were then used to estimate the model and the procedure was repeated 1000 times. The simulation results showed that our model recovered the true values of parameters with high precision. The model was also applied to an observed dataset to analyze, as a first example, the association between maternal emotional overinvolvement and child internalizing problems. The results showed that this association was best explained by evocative genotype-environment correlation.

Parental psychopathology, parenting style, and the quality of intra-familial relationships are all associated with child mental health outcomes. However, most research can say little about the causal pathways underlying these associations. This is because most studies are not genetically informative and are therefore not able to account for the possibility that associations are confounded by gene-environment correlation. That is, biological parents provide not only a rearing environment for their child but also contribute 50% of their genes. Any associations between parental phenotype and child phenotype are therefore potentially confounded. One technique for disentangling genetic from environmental effects is the Children-of-Twins (CoT) method. This involves using datasets comprising twin parents and their children to distinguish genetic from environmental associations between parent and child phenotypes. The CoT technique has grown in popularity in the last decade and we predict that this surge in popularity will continue. In the present article we explain the CoT method for those unfamiliar with its use. We present the logic underlying this approach, discuss strengths and weaknesses and highlight important methodological considerations for researchers interested in the CoT method. We also cover variations on basic CoT approaches, including the extended-CoT method, capable of distinguishing forms of geneenvironment correlation. We then present a systematic review of all of the behavioral CoT studies published to date. These studies cover such diverse phenotypes as psychosis, substance abuse, internalizing, externalizing, parenting and marital difficulties. In reviewing this literature we highlight past applications, identify emergent patterns, and suggest avenues for future research.Keywords: children-of-twins; gene-environment correlation; intergenerational transmission; parenting; psychiatric epidemiology.Theories of parenting propose that parents impact the development of their children in a variety of ways: At one level parental characteristics are predictive of child characteristics -many traits tend to run in families and this is often interpreted as evidence for the impact of parent behavior on child development. For example, anxious parents often rear anxious children (Murray et al., 2008) and it has been suggested that this is because children learn such behavior from their parents (Murray et al., 2008;Rachman, 1977;. Proponents of social learning theory (Bandura, 1977) might suggest that this learning occurs via processes of imitation and modelling, and evidence also indicates that the learning process can be more direct and involve the verbal transmission of information from parent to child (Field & Purkis, 2011).Although children may learn behaviors through imitating and listening to their parents, parents often seek to influence their children's behavior in more direct ways, through the parenting behaviors that they direct towards their child. For example, the punishment and praise of chil...

Background Parental depressive symptoms are associated with emotional and behavioural problems in offspring. However, genetically informative studies are needed to distinguish potential causal effects from genetic confounds, and longitudinal studies are required to distinguish parent-to-child effects from child-to-parent effects. Method We conducted cross-sectional analyses on a sample of Swedish twins and their adolescent offspring (n = 876 twin families), and longitudinal analyses on a US sample of children adopted at birth, their adoptive parents, and their birth mothers (n = 361 adoptive families). Depressive symptoms were measured in parents, and externalizing and internalizing problems measured in offspring. Structural equation models were fitted to the data. Results Results of model fitting suggest that associations between parental depressive symptoms and offspring internalizing and externalizing problems remain after accounting for genes shared between parent and child. Genetic transmission was not evident in the twin study but was evident in the adoption study. In the longitudinal adoption study child-to-parent effects were evident. Conclusions We interpret the results as demonstrating that associations between parental depressive symptoms and offspring emotional and behavioural problems are not solely attributable to shared genes, and that bidirectional effects may be present in intergenerational associations.

BackgroundPrevious studies of risk factors for disability pension (DP) have mainly focused on psychosocial, or environmental, factors, while the relative importance of genetic effects has been less studied. Sex differences in biological mechanisms have not been investigated at all.MethodsThe study sample included 46,454 Swedish twins, consisting of 23,227 complete twin pairs, born 1928–1958, who were followed during 1993–2008. Data on DP, including diagnoses, were obtained from the National Social Insurance Agency. Within-pair similarity in liability to DP was assessed by calculating intraclass correlations. Genetic and environmental influences on liability to DP were estimated by applying discrete-time frailty modeling.ResultsDuring follow-up, 7,669 individuals were granted DP (18.8% women and 14.1% men). Intraclass correlations were generally higher in MZ pairs than DZ pairs, while DZ same-sexed pairs were more similar than opposite-sexed pairs. The best-fitting model indicated that genetic factors contributed 49% (95% CI: 39–59) to the variance in DP due to mental diagnoses, 35% (95% CI: 29–41) due to musculoskeletal diagnoses, and 27% (95% CI: 20–33) due to all other diagnoses. In both sexes, genetic effects common to all ages explained one-third, whereas age-specific factors almost two-thirds, of the total variance in liability to DP irrespective of diagnosis. Sex differences in liability to DP were indicated, in that partly different sets of genes were found to operate in women and men, even though the magnitude of genetic variance explained was equal for both sexes.ConclusionsThe findings of the study suggest that genetic effects are important for liability to DP due to different diagnoses. Moreover, genetic contributions to liability to DP tend to differ between women and men, even though the overall relative contribution of genetic influences does not differ by sex. Hence, the pathways leading to DP might differ between women and men.