Passive Gene-environment Correlation Research Articles

Integrating the family stress model within a longitudinal sibling-adoption study of adolescent externalizing behavior.

Using a sample of linked adopted children, adoptive and birth parents (N = 561), and biological siblings residing in the birth parent home (N = 191), we examined the role of genetics within family stress processes. We tested parental hostility (7 years) as a mediator of the associations between socioeconomic strain and rearing parent psychopathology (4 years) and adolescent externalizing behaviors (11 years) in adoptive and biological parent homes. Next, we examined parent social support (4 years) as a moderator of paths from socioeconomic strain and parent psychopathology to parental hostility. Parental hostility significantly mediated effects of socioeconomic strain and parent psychopathology on adolescent externalizing behaviors in biological and adoptive parent homes, respectively. Equivalence testing of the paths to adolescent externalizing behaviors across family types indicated a negligible role of passive gene-environment correlation. Parent social support significantly attenuated the effect of parent psychopathology on parental hostility in biological families. Birth parent externalizing behaviors were not significantly associated with adoptee externalizing behaviors nor adoptive parent hostility, suggesting negligible heritable risk or evocative gene-environment processes. Full- and half-sibling correlations indicated that children's unique rearing contexts contributed to the parenting they received and the externalizing behavior they exhibited. Implications for intervention are discussed.

Using a polygenic score in a family design to understand genetic influences on musicality

To further our understanding of the genetics of musicality, we explored associations between a polygenic score for self-reported beat synchronization ability (PGSrhythm) and objectively measured rhythm discrimination, as well as other validated music skills and music-related traits. Using family data, we were able to further explore potential pathways of direct genetic, indirect genetic (through passive gene–environment correlation) and confounding effects (such as population structure and assortative mating). In 5648 Swedish twins, we found PGSrhythm to predict not only rhythm discrimination, but also melody and pitch discrimination (betas between 0.11 and 0.16, p < 0.001), as well as other music-related outcomes (p < 0.05). In contrast, PGSrhythm was not associated with control phenotypes not directly related to music. Associations did not deteriorate within families (N = 243), implying that indirect genetic or confounding effects did not inflate PGSrhythm effects. A correlation (r = 0.05, p < 0.001) between musical enrichment of the family childhood environment and individuals' PGSrhythm, suggests gene–environment correlation. We conclude that the PGSrhythm captures individuals' general genetic musical propensity, affecting musical behavior more likely direct than through indirect or confounding effects.

Exploring the possibility of parents' broad internalizing phenotype acting through passive gene-environment correlations on daughters' disordered eating.

Twin studies demonstrate significant environmental influences and a lack of genetic effects on disordered eating before puberty in girls. However, genetic factors could act indirectly through passive gene-environment correlations (rGE; correlations between parents' genes and an environment shaped by those genes) that inflate environmental (but not genetic) estimates. The only study to explore passive rGE did not find significant effects, but the full range of parental phenotypes (e.g., internalizing symptoms) that could impact daughters' disordered eating was not examined. We addressed this gap by exploring whether parents' internalizing symptoms (e.g., anxiety, depressive symptoms) contribute to daughters' eating pathology through passive rGE. Participants were female twin pairs (aged 8-14 years; M = 10.44) in pre-early puberty and their biological parents (n = 279 families) from the Michigan State University Twin Registry. Nuclear twin family models explored passive rGE for parents' internalizing traits/symptoms and twins' overall eating disorder symptoms. No evidence for passive rGE was found. Instead, environmental factors that create similarities between co-twins (but not with their parents) and unique environmental factors were important. In pre-early puberty, genetic factors do not influence daughters' disordered eating, even indirectly through passive rGE. Future research should explore sibling-specific and unique environmental factors during this critical developmental period.

Associations between parenting characteristics and adolescent substance use: A genetically informed, longitudinal adoption study.

The present study examined putative environmental predictors of adolescent substance use, using a prospective adoption design to distinguish between environmental mediation (i.e., parenting influencing adolescent substance use), passive gene-environment correlation (i.e., parental genetic predisposition influencing the association between parenting characteristics and adolescent substance use), and evocative gene-environment correlation (i.e., children's genetic predisposition influencing parenting). Longitudinal data from the Colorado Adoption Project (395 adoptees, 491 nonadoptees, 485 adoptive parents, and 490 biological parents) were examined. Children (48% girls) were assessed at ages 1 to 17 years. Over 90% of the sample were non-Hispanic White. Associations between parenting and adolescent substance use were compared between adoptive and nonadoptive families. Positive, negative, and inconsistent parenting measures in early childhood through adolescence were not consistently associated with adolescent substance use, with only 6% of correlations being statistically significant (r = -0.152 to .207). However, parent-child relationship quality assessed from childhood to adolescence and orientation to parents assessed during adolescence were significantly, negatively associated with adolescent substance use, with 71% of correlations being statistically significant (r = -0.88 to -0.11). There was little evidence of sex differences in the associations. Environmental mediation, rather than passive or evocative gene-environment correlation, explained most associations.

Maternal stress in pregnancy and child autism spectrum disorder: evaluating putative causal associations using a genetically informed design

AimsPrenatal adversity is hypothesized to increase risk of Autism Spectrum Disorder (ASD) via epigenetic changes. Maternal stress in late pregnancy may alter offspring neurodevelopmental outcomes by disrupting a unique period of rapid neurogenesis. Observational studies reporting an environmentally mediated programming pathway face challenges in drawing causal inferences including passive gene-environment correlation. This project aims to use a quasi-experimental genetically informed design to assess if reported correlations between maternal prenatal stress and offspring ASD traits were due to maternally inherited factors or consistent with a potentially causal prenatal exposure effect. No previous cross-fostering studies have assessed the effects of prenatal stress on childhood ASD.MethodThis study used an in-vitro fertilization cross-fostering sample with pregnant mothers related (n = 365) or unrelated (n = 111) to their offspring (mean age = 9.84 years). Prenatal stress was assessed using a subjective Likert scale during pregnancy. Questionnaires examined maternally rated offspring ASD traits using the Social and Communication Disorders Checklist. Birth weight and gestational age from medical records were used as comparison outcomes to validate the measure of stress as evidence suggests they are influenced by environmental factors. Correlations from multiple regression models were examined in relation to magnitude of effect size as well as significance. This is partly due to small sample size and that cross-fostering designs rely on comparing magnitudes of associations between related and unrelated groups. An interaction term was used to test the difference in the strength of association between related and unrelated mother-child groups.ResultSubjective assessment of prenatal maternal stress showed construct validity as it was associated with low birth weight (β = –0.297, p = 0.005) and reduced gestational age (β= –0.320, p = 0.001). Subjective late pregnancy stress was associated with increased offspring ASD traits in the whole sample (β = 0.089, p = 0.073) and in the related (β=0.045, p = 0.424) and unrelated mother-child (β=0.233, p = 0.029) subgroups. Non-significant interaction terms demonstrated that the mechanisms underlying the association between maternal stress and ASD and birth outcomes are likely to be similar and environmentally driven in the different conception groups.ConclusionFindings demonstrate the utility of genetically informed designs in disentangling inherited factors from environmental influences in the study of prenatal risk factors. Correlations between maternal prenatal stress and offspring ASD being present in both related and unrelated mother-child groups indicate an environmental link that is consistent with a potential causal effect. Associations detected are of imperative use for clinicians and policymakers, as they can guide the implementation of early psychosocial care for families at high liability.

Genetic and environmental sources of familial resemblance in anxiety: a nuclear twin family design.

A dominant feature of anxiety disorders is familial aggregation. However, the underlying mechanisms of between- and within-generational anxiety resemblance remain poorly understood. By disentangling the genetic v. environmental sources of familial resemblance in anxiety, we can help prevent within-family transmission of anxiety disorders. Therefore, data from both parents and twins are needed to obtain unbiased and detailed estimations of genetic and environmental sources of similarity between family members. We examined data from 991 families with same-sex twins. Trait anxiety in twins was assessed via self-report and parent report, while parental trait anxiety was assessed via self-report. We established a nuclear twin family model and estimated genetic and environmental variances using two survey waves. The results suggested that additive genetic (A), dominant genetic (D), and non-shared environmental (E) influences significantly contributed to trait anxiety, whereas familial environmental influences (F) and passive gene-environment correlations (rGE) did not. Sibling environmental influences (S) were only found in self-report data, and increased when genetic influences decreased from Wave 1 to Wave 2. Our study highlights the important role of broad heritability in intrafamilial trait anxiety similarity. Parent-child resemblance occurred primarily due to shared genetic makeup rather than direct environmental transmission. Sibling-specific environments, as the only source of shared environments, need further investigation. These findings have both theoretical and practical significance for anxiety disorders. Future research can expand our understanding by examining the gene-environment interplay and sex differences.

No Evidence for Passive Gene-Environment Correlation or the Influence of Genetic Risk for Psychiatric Disorders on Adult Body Composition via the Adoption Design

The relationship between genetic and environmental risk is complex and for many traits, estimates of genetic effects may be inflated by passive gene-environment correlation. This arises because biological offspring inherit both their genotypes and rearing environment from their parents. We tested for passive gene-environment correlation in adult body composition traits using the ‘natural experiment’ of childhood adoption, which removes passive gene-environment correlation within families. Specifically, we compared 6165 adoptees with propensity score matched non-adoptees in the UK Biobank. We also tested whether passive gene-environment correlation inflates the association between psychiatric genetic risk and body composition. We found no evidence for inflation of heritability or polygenic scores in non-adoptees compared to adoptees for a range of body composition traits. Furthermore, polygenic risk scores for anorexia nervosa, attention-deficit/hyperactivity disorder and schizophrenia did not differ in their influence on body composition traits in adoptees and non-adoptees. These findings suggest that passive gene-environment correlation does not inflate genetic effects for body composition, or the influence of psychiatric disorder genetic risk on body composition. Our design does not look at passive gene-environment correlation in childhood, and does not test for ‘pure’ environmental effects or the effects of active and evocative gene-environment correlations, where child genetics directly influences home environment. However, these findings suggest that genetic influences identified for body composition in this adult sample are direct, and not confounded by the family environment provided by biological relatives.

Genetic and environmental variation in political orientation in adolescence and early adulthood: A Nuclear Twin Family analysis.

Political orientation is often assumed to be shaped by socialization processes; however, previous studies have shown substantial genetic variance components in party affiliation, political attitudes and behaviors, or closely related personality traits. The majority of these studies have relied on the Classical Twin Design, which comes with restrictive assumptions, some of which are easily violated. Moreover, most analyses lack a perspective of age-group differences. In this study, we investigated political orientation in adolescents (age: 16-18) and young adults (age: 21-25) in a cross-sectional Nuclear Twin Family Design. We used data of the German TwinLife project, including data from same-sex twins reared together, their biological parents, and nontwin full siblings. We found genetic variation in political orientation, which was significant in the older cohort, possibly indicating an increasing importance of active gene-environment correlation from adolescence to adulthood. Individual differences in political orientation because of passive gene-environment correlation and shared environmental effects were larger in the younger cohort, substantiating the same theoretical consideration and the importance of shared socialization contexts for adolescents' political views. By running Nuclear Twin Family model analyses, and considering age-group differences, as well as the relationship of political orientation with the Big Five personality traits, our study extended previous work, and resulted in more robust and fine-grained estimates of genetic and environmental sources of variance in political orientation. Therefore, it contributed to a better understanding of the complex nature-nurture interplay that forms political orientation in emerging adulthood. (PsycINFO Database Record (c) 2020 APA, all rights reserved).

Elucidating factors underlying parent-offspring similarity in eating pathology in pre- and early puberty: Exploring the possibility of passive gene-environment correlation.

Familial resemblance in eating pathology is typically attributed to parents providing an environment that leads to the development of eating pathology. However, offspring raised by biological parents receive both their environment and genes from their parents, raising the possibility that genetic influences, environmental influences, and/or gene-environment interplay may account for familial resemblance. Past studies have not explored the possibility of parents' genes influencing the environment they provide (i.e., passive gene-environment correlations or "passive rGE"). If present, passive rGE is most likely to "hide" in estimates of shared environmental influence in classical twin models. The current study used a nuclear twin family design to explore the possibility of passive rGE during pre- and early puberty when past studies have demonstrated the importance of shared environmental influence. Additionally, the present study explored whether sibling-specific (i.e., influences specific to the twin generation) or family-specific (i.e., "cultural" influences within the home) environmental influences account for shared environmental influences found in past studies. Participants included preearly pubertal same-sex female twins and their biological parents (N = 547 families) from the Minnesota Twin Family Study and the Michigan State University Twin Registry. Disordered eating was assessed with self-report measures in the twins and parents. Pubertal status was determined using an established cut-off on a self-report measure. Passive rGE was not indicated in this study of pre- and early pubertal twins. Instead, sibling-specific shared environmental and nonshared environmental influences were most influential. Future research should work to identify the sibling-specific environmental influences that contribute to sibling similarity in disordered eating. (PsycINFO Database Record (c) 2019 APA, all rights reserved).

Longitudinal examination of pathways to peer problems in middle childhood: A siblings-reared-apart design.

To advance research from Dishion and others on associations between parenting and peer problems across childhood, we used a sample of 177 sibling pairs reared apart since birth (because of adoption of one of the siblings) to examine associations between parental hostility and children's peer problems when children were ages 7 and 9.5 years (n = 329 children). We extended conventional cross-lagged parent-peer models by incorporating child inhibitory control as an additional predictor and examining genetic contributions via birth mother psychopathology. Path models indicated a cross-lagged association from parental hostility to later peer problems. When child inhibitory control was included, birth mother internalizing symptoms were associated with poorer child inhibitory control, which was associated with more parental hostility and peer problems. The cross-lagged paths from parental hostility to peer problems were no longer significant in the full model. Multigroup analyses revealed that the path from birth mother internalizing symptoms to child inhibitory control was significantly higher for birth parent-reared children, indicating the possible contribution of passive gene-environment correlation to this association. Exploratory analyses suggested that each child's unique rearing context contributed to his or her inhibitory control and peer behavior. Implications for the development of evidence-based interventions are discussed.

Supplemental Material for Elucidating Factors Underlying Parent–Offspring Similarity in Eating Pathology in Pre- and Early Puberty: Exploring the Possibility of Passive Gene–Environment Correlation

Supplemental Material for Elucidating Factors Underlying Parent–Offspring Similarity in Eating Pathology in Pre- and Early Puberty: Exploring the Possibility of Passive Gene–Environment Correlation

Contributions of mothers' and fathers' parenting to children's self-regulation: Evidence from an adoption study.

The origins of top-down self-regulation are attributed to genetic and socialization factors as evidenced by high heritability estimates from twin studies and the influential role of parenting. However, recent evidence suggests that parenting behavior itself is affected by parents' own top-down self-regulation. Because children's top-down self-regulation is influenced by genetic factors and parenting is influenced by top-down self-regulation, the effects of parenting on children's top-down self-regulation identified in prior studies may partially reflect passive gene-environment correlation. The goal of this study was to examine parenting influences on children's top-down self-regulation using a longitudinal, adoption-at-birth design, a method of identifying parenting influences that are independent of the role of shared genetic influences on children's characteristics because adoptive parents are genetically unrelated to their adopted child. Participants (N = 361) included adoptive families and biological mothers of adopted children. Adoptive mothers' and fathers' harsh/negative parenting were assessed when children were 27 months of age and biological mothers' top-down self-regulation was assessed when children were 54 months of age. Adopted children's top-down self-regulation was assessed when they were 54 and 72 months of age. Results, accounting for child gender, biological mother top-down self-regulation, and the potential evocative effects of adopted child anger, provide evidence that inherited influences and socialization processes uniquely contribute to children's top-down self-regulation. Furthermore, findings demonstrate the importance of both mother's and father's parenting behavior as an influence on young children's top-down self-regulation. The implications of these findings for understanding the complex mechanisms that influence children's top-down self-regulation are discussed.

Disentangling Child-Specific and Family-Wide Processes Underlying Negative Mother-Child Transactions.

The current study examines the transactional processes between maternal negativity and child disruptive behavior during early childhood, using a sibling comparison design. This design allows for a more sophisticated test of the behavioral training hypothesis than is possible when only one child per family is included in the analysis as it excludes two confounders (passive gene-environment correlation and family-wide environmental influence). Three hundred and ninety-seven families were visited on three occasions when the target child was 1.5, 3 and 4.5years old (920 children, 51.5% female). The target child and up to three older siblings per family were included in data collection and analysis. Mothers and fathers reported on children's disruptive behavior and mothers reported on their negativity to children. Within-family cross-lag pathways, as well as a significant indirect effect through which children increased their own disruptive behavior via maternal negativity confirmed a behavioral training effect. Family level maternal negativity and sibling disruptive behavior showed high levels of stability over three to four years and no context effect for maternal negativity or sibling disruptive behavior was seen. The theoretical and clinical implications of these findings are discussed.

Passive rGE or Developmental Gene-Environment Cascade? An Investigation of the Role of Xenobiotic Metabolism Genes in the Association Between Smoke Exposure During Pregnancy and Child Birth Weight.

There is considerable evidence that smoke exposure during pregnancy (SDP) environmentally influences birth weight after controlling for genetic influences and maternal characteristics. However, maternal smoking during pregnancy-the behavior that leads to smoke exposure during pregnancy-is also genetically-influenced, indicating the potential role of passive gene-environment correlation. An alternative to passive gene-SDP correlation is a cascading effect whereby maternal and child genetic influences are causally linked to prenatal exposures, which then have an 'environmental' effect on the development of the child's biology and behavior. We describe and demonstrate a conceptual framework for disentangling passive rGE from this cascading GE effect using a systems-based polygenic scoring approach comprised of genes shown to be important in the xenobiotic (substances foreign to the body) metabolism pathway. Data were drawn from 5044 families from the Avon Longitudinal Study of Parents and Children with information on maternal SDP, birth weight, and genetic polymorphisms in the xenobiotic pathway. Within a k-fold cross-validation approach (k=5), we created weighted maternal and child polygenic scores using 18 polymorphisms from 10 genes that have been implicated in the xenobiotic metabolism pathway. Mothers and children shared variation in xenobiotic metabolism genes. Amongst mothers who smoked during pregnancy, neither maternal nor child xenobiotic metabolism polygenic scores were associated with a higher likelihood of smoke exposure during pregnancy, or the severity of smoke exposure during pregnancy (and therefore, neither proposed mechanism was supported), or with child birth weight. SDP was consistently associated with lower child birth weight controlling for the polygenic scores, maternal educational attainment, social class, psychiatric problems, and age. Limitations of the study design and the potential of the framework using other designs are discussed.

Why does parental language input style predict child language development? A twin study of gene–environment correlation

There are well-established correlations between parental input style and child language development, which have typically been interpreted as evidence that the input style causes, or influences the rate of, changes in child language. We present evidence from a large twin study (TEDS; 8395 pairs for this report) that there are also likely to be both child-to-parent effects and shared genetic effects on parent and child. Self-reported parental language style at child age 3 and age 4 was aggregated into an ‘informal language stimulation’ factor and a ‘corrective feedback’ factor at each age; the former was positively correlated with child language concurrently and longitudinally at 3, 4, and 4.5 years, whereas the latter was weakly and negatively correlated. Both parental input factors were moderately heritable, as was child language. Longitudinal bivariate analysis showed that the correlation between the language stimulation factor and child language was significantly and moderately due to shared genes. There is some suggestive evidence from longitudinal phenotypic analysis that the prediction from parental language stimulation to child language includes both evocative and passive gene–environment correlation, with the latter playing a larger role.Learning outcomes: The reader will understand why correlations between parental language and rate of child language are by themselves ambiguous, and how twin studies can clarify the relationship. The reader will also understand that, based on the present study, at least two aspects of parental language style – informal language stimulation and corrective feedback – have substantial genetic influence, and that for informal language stimulation, a substantial portion of the prediction to child language represents the effect of shared genes on both parent and child. It will also be appreciated that these basic research findings do not imply that parental language input style is unimportant or that interventions cannot be effective.

Parent involvement, sibling companionship, and adolescent substance use: A longitudinal, genetically informed design.

A large literature shows that parent and sibling relationship factors are associated with an increased likelihood of adolescent substance use. Less is known about the etiology of these associations. Using a genetically informed sibling design, we examined the prospective associations between parent involvement, sibling companionship, and adolescent substance use at 2 points in mid- and late-adolescence. Adolescents were adopted (n = 568) or the biological offspring of both parents (n = 412). Cross-lagged panel results showed that higher levels of parent involvement in early adolescence were associated with lower levels of substance use later in adolescence. Results did not significantly differ across adoption status, suggesting this association cannot be due to passive gene-environment correlation. Adolescent substance use at Time 1 was not significantly associated with parent involvement at Time 2, suggesting this association does not appear to be solely due to evocative (i.e., "child-driven") effects either. Together, results support a protective influence of parent involvement on subsequent adolescent substance use that is environmental in nature. The cross-paths between sibling companionship and adolescent substance use were significant and negative in direction (i.e., protective) for sisters, but positive for brothers (in line with a social contagion hypothesis). These effects were consistent across genetically related and unrelated pairs, and thus appear to be environmentally mediated. For mixed gender siblings, results were consistent with environmentally driven, protective influence hypothesis for genetically unrelated pairs, but in line with a genetically influenced, social contagion hypothesis for genetically related pairs. Implications are discussed.

General and specific predictors of nicotine and alcohol dependence in early adulthood: genetic and environmental influences.

This study builds on previous work delineating a hierarchical model of family environmental risk in relation to a hierarchical model of externalizing disorders (EXTs) by evaluating for gene-environment interplay in these relationships. The associations between parent-child relationship quality (conflict, bonding, and management) and substance-specific adolescent family environments (parental/sibling tobacco/alcohol use) in relation to young adult EXTs (age ∼22 years nicotine, alcohol, and other drug dependence; antisocial and risky sexual behavior) were evaluated. The sample included 533 adopted offspring and 323 biological offspring. Because adopted youth do not share genes with their parents, a significant association between parent-child relationship quality and EXTs would provide evidence against passive gene-environment correlation (rGE). Significant associations between parental tobacco/alcohol use in relation to offspring nicotine/alcohol dependence in the adopted offspring support common environmental influence. Significant associations detected for the biological offspring only suggest common genetic influence. For both adoptive and biological offspring, there was a significant association between parent-child relationship quality and EXTs. Parental tobacco/alcohol use was unrelated to EXTs. Sibling tobacco/alcohol use was related to EXTs, but only for the biological siblings. Parental tobacco use was associated with the residual variance in nicotine dependence in adopted offspring. Findings replicate a long-term influence of adolescent parent-child relationship quality on adult EXTs. Findings extend previous research by providing evidence against passive rGE in this association. The association between parental tobacco use and adult nicotine dependence appears to be environmentally mediated, but caution is warranted as we found this relationship only for adopted youth.

Do dopamine gene variants and prenatal smoking interactively predict youth externalizing behavior?

Externalizing behaviors (encompassing antisocial, impulsive, and substance use behaviors) are pervasive and impairing across a multitude of settings and developmental contexts. These behaviors, though often investigated separately, are highly comorbid. Prenatal tobacco exposure in interaction with various genetic influences has predicted later externalizing behavior, and recent evidence supports investigating sex differences in these patterns. In the current study, we extend this work by (a) examining two functional genetic markers in the dopamine system: the transporter gene (DAT1) and the dopamine receptor D4 gene (DRD4) in interaction with prenatal tobacco exposure to predict a latent composite of externalizing behavior and (b) testing whether these patterns differ by sex of youth in a community sample of adolescents (n=176). The relatively small sample is partially offset by high quality, multi-method prospective measurement. We assessed prenatal tobacco exposure using prospective repeated cotinine-corrected reports and externalizing behaviors were assessed utilizing multiple measures across three waves. The interaction between DAT1 (but not DRD4) and prenatal tobacco exposure was statistically significant in boys, and patterns appeared to differ by sex. Risk for externalizing behaviors for exposed boys increased linearly as a function of the 10r DAT1 allele. For exposed girls, there was a trend such that DAT1 heterozygotes had a marginally higher risk than homozygotes. This pattern was not explained by passive gene-environment correlation. Elucidating sex-specific pathways through which early adverse exposures and genetic susceptibilities contribute to externalizing behavior can inform early targeted prevention efforts for those children at highest risk.

Understanding the relative contributions of direct environmental effects and passive genotype–environment correlations in the association between familial risk factors and child disruptive behavior disorders

Previous work reports an association between familial risk factors stemming from parental characteristics and offspring disruptive behavior disorders (DBDs). This association may reflect (a) the direct effects of familial environment and (b) a passive gene-environment correlation (r(GE)), wherein the parents provide both the genes and the environment. The current study examined the contributions of direct environmental influences and passive r(GE) by comparing the effects of familial risk factors on child DBDs in genetically related (biological) and non-related (adoptive) families. Participants were 402 adoptive and 204 biological families. Familial environment was defined as maternal and paternal maladaptive parenting and antisociality, marital conflict and divorce; offspring DBDs included attention deficit hyperactivity disorder (ADHD), conduct disorder (CD) and oppositional defiant disorder (ODD). Mixed-level regressions estimated the main effects of familial environment, adoption status and the familial environment by adoption status interaction term, which tested for the presence of passive r(GE). There was a main effect of maternal and paternal maladaptive parenting and marital discord on child DBDs, indicating a direct environmental effect. There was no direct environmental effect of maternal or paternal antisociality, but maternal and paternal antisociality had stronger associations with child DBDs in biological families than adoptive families, indicating the presence of a passive r(GE). Many familial risk factors affected children equally across genetically related and non-related families, providing evidence for direct environmental effects. The relationship of parental antisociality and offspring DBDs was best explained by a passive r(GE), where a general vulnerability toward externalizing psychopathology is passed down by the parents to the children.

Genes of Experience: Explaining the Heritability of Putative Environmental Variables Through Their Association with Behavioural and Emotional Traits

An increasing body of evidence shows that many ‘environmental’ measures are heritable, indicating genetic involvement in environmental exposure (or gene–environment correlation). In the present study we attempt to clarify why three such ‘environmental’ measures (maternal negativity, paternal negativity and negative life events) are consistently found to be heritable. Through multivariate genetic analysis of a sample of adolescent twins from the UK we show that the heritability of these putative environmental measures can be explained via their association with five behavioural phenotypes: oppositionality, delinquency, physical aggression, depression and anxiety. This is consistent with the notion that being genetically susceptible to certain behavioural difficulties could lead to exposure to certain life events, and this may account for the reported heritability of ‘environmental’ measures. Results are discussed in the context of possible active, evocative and passive gene–environment correlations.