Genetic and environmental influences on the familial transmission of externalizing disorders in adoptive and twin offspring.
- Authors
- Hicks, Brian M; Foster, Katherine T; Iacono, William G; McGue, Matt
- Year
- 2013
- Journal
- JAMA psychiatry
- PMID
- 23965950
- DOI
- 10.1001/jamapsychiatry.2013.258
- PMCID
- PMC3790867
IMPORTANCE: Twin-family studies have shown that parent-child resemblance on substance use disorders and antisocial behavior can be accounted for by the transmission of a general liability to a spectrum of externalizing disorders. Most studies, however, include only biological parents and offspring, which confound genetic and environmental transmission effects. OBJECTIVE: To examine the familial transmission of externalizing disorders among both adoptive (genetically unrelated) and biological relatives to better distinguish genetic and environmental mechanisms of transmission. DESIGN: Family study design wherein each family included the mother, father, and 2 offspring, including monozygotic twin, dizygotic twin, nontwin biological, and adoptive offspring. Structural equation modeling was used to estimate familial transmission effects and their genetic and environmental influences. SETTING: Participants were recruited from the community and assessed at a university laboratory. PARTICIPANTS: A total of 1590 families with biological offspring and 409 families with adoptive offspring. Offspring participants were young adults (mean age, 26.2 years). MAIN OUTCOMES AND MEASURES: Symptom counts of conduct disorder, adult antisocial behavior, and alcohol, nicotine, and drug dependence. RESULTS There was a medium effect for the transmission of the general externalizing liability for biological parents (r = 0.27-0.30) but not for adoptive parents (r = 0.03-0.07). In contrast, adoptive siblings exhibited significant similarity on the general externalizing liability (r = 0.21). Biometric analyses revealed that the general externalizing liability was highly heritable (a2 = 0.61) but also exhibited significant shared environmental influences (c2 = 0.20). CONCLUSIONS AND RELEVANCE: Parent-child resemblance for substance use disorders and antisocial behavior is primarily due to the genetic transmission of a general liability to a spectrum of externalizing disorders. Including adoptive siblings revealed a greater role of shared environmental influences on the general externalizing liability than previously detected in twin studies and indicates that sibling rather than parent-child similarity indexes important environmental risk factors for externalizing disorders.
EXT = Externalizing factor; AAB = adult antisocial behavior; CD = conduct disorder; ALD = alcohol dependence; NCD = nicotine dependence; DRG = drug dependence. The three numbers listed above the paths linking the specific disorders across sibling 1 and 2 refer to the effects for MZ twins, DZ twins and biological siblings, and adoptive siblings, respectively. All path coefficients are standardized and the weighted mean across the family types. All paths greater than 0.10 are significant at p < 0.01. The latent externalizing variables represent the general liability factors that contribute to each disorder. The smaller circular variables associated with each disorder are the residual variances, and represent all liability factors that are specific to each disorder and unrelated to the general externalizing liability. The double-headed arrows linking the mother and father externalizing factors to the offspring (sibling) externalizing factors represent the general transmission effects. The double-headed arrows linking the sibling 1 and sibling 2 externalizing factors indexes sibling similarity for the general externalizing liability, and was allowed to vary across MZ twins, DZ twins and non-twin biological siblings, and adoptive siblings. The double-headed arrows linking the residual variances for conduct disorder and alcohol, nicotine, and drug dependence across siblings represent disorder specific liability factors that increase sibling similarity, but that are independent of the general externalizing factor. Correlations among the residual variances are from left to right for MZ twins, DZ twins and non-twin biological siblings, and adoptive siblings. To reduce the figure's complexity, we did not depict a small but statistically significant specific effect for maternal nicotine dependence (biological mothers r = 0.11, 95% CI = 0.06-0.17; adoptive mothers r = 0.03). If included, this would be a double-headed arrow linking the residual variance of maternal nicotine dependence to residual variance of sibling 1 and sibling 2 nicotine dependence.
All path coefficients are standardized and 95% confidence intervals are shown in parentheses beneath each coefficient. All coefficients that do not include zero are significant. The percentage of variance accounted for by a given variable in another variable can be determined by squaring the path coefficient on the path connecting the first variable to the second variable. The sum of the squared loadings (effects from the general externalizing factor as well as the specific ACE loadings) equals 1.0. The total effect for A, C, and E can be calculated by summing the general effect (squared loading for a given disorder multiplied by the squared A, C, and E loadings on the externalizing factor) and the specific effect (squared A, C, or E specific effect on a given disorder). Using conduct disorder as an example, a2 = general (0.612 × 0.502) + specific (0.492) = 0.33; c2 = general(0.452 × 0.502) + specific(0.432) = 0.24; e2 = general(0.442 × 0.502) + specific(0.622) = 0.43. A = additive genetic; C = shared environment; E = nonshared environment; EXT = Externalizing factor; AAB = adult antisocial behavior; CD = conduct disorder; ALD = alcohol dependence; NCD = nicotine dependence; DRG = drug dependence.
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