Familial Transmission and Heritability of Childhood Disruptive Disorders

Department of Psychology, University of Minnesota, Minneapolis, USA.
American Journal of Psychiatry (Impact Factor: 13.56). 09/2010; 167(9):1066-74. DOI: 10.1176/appi.ajp.2010.09091272
Source: PubMed

ABSTRACT There is substantial evidence of a link between parental substance use disorders and antisocial behavior and childhood disruptive disorders in offspring, but it is unclear whether this transmission is specific to particular disorders or if a general liability accounts for familial resemblance. The authors examined whether the association between parental externalizing disorders and childhood disruptive disorders in preadolescent offspring is a result of the transmission of general or disorder-specific liabilities and estimated the genetic and environmental contributions to variation in these general and specific liability indicators.
Participants were 1,069 families consisting of 11-year-old twins and their biological mother and father. Structural equation modeling was used to simultaneously estimate the general and specific transmission effects of four parental externalizing disorders (conduct disorder, adult antisocial behavior, alcohol dependence, and drug dependence) on childhood disruptive disorders (attention deficit hyperactivity disorder, conduct disorder, and oppositional defiant disorder).
Parent-child resemblance was accounted for by the transmission of a general liability to externalizing disorders, and this general liability was highly heritable. Specific effects were also detected, but for sibling rather than parental transmission. Specific genetic and nonshared environmental effects were detected for each childhood disruptive disorder, but only conduct disorder exhibited a significant shared environmental effect.
A highly heritable general liability accounts for the parent-child transmission of externalizing psychopathology from parents to their preadolescent offspring. This general liability should be a focus of research for both etiology and intervention.


Available from: Brian M Hicks, May 29, 2015
  • [Show abstract] [Hide abstract]
    ABSTRACT: Although heritable, externalizing disorders have a number of robust associations with several environmental risk factors, including family, school and peer contexts. To account for these associations, we integrate a behavioral genetic perspective with principles of a developmental cascade theory of antisocial behavior. The major environmental contexts associated with child externalizing problems are reviewed, as are the processes of gene–environment interplay underlying these associations. Throughout, we discuss implications for prevention and intervention. Three major approaches designed to reduce child externalizing behavior are reviewed. Prevention and intervention programs appear to be most successful when they target individuals or communities most at risk for developing externalizing disorders, rather than applied universally. We end by commenting on areas in need of additional research concerning environmental influences on persistent externalizing behaviors.
    09/2014; 11(5):537. DOI:10.2217/cpr.14.47
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Background Antisocial personality disorder (ASPD) is characterised by elevated impulsive aggression and increased risk for criminal behaviour and incarceration. Deficient activity of the monoamine oxidase A (MAOA) gene is suggested to contribute to serotonergic system dysregulation strongly associated with impulsive aggression and antisocial criminality. Aims To elucidate the role of epigenetic processes in altered MAOA expression and serotonin regulation in a population of incarcerated offenders with ASPD compared with a healthy non-incarcerated control population. Method Participants were 86 incarcerated participants with ASPD and 73 healthy controls. MAOA promoter methylation was compared between case and control groups. We explored the functional impact of MAOA promoter methylation on gene expression in vitro and blood 5-HT levels in a subset of the case group. Results Results suggest that MAOA promoter hypermethylation is associated with ASPD and may contribute to downregulation of MAOA gene expression, as indicated by functional assays in vitro, and regression analysis with whole-blood serotonin levels in offenders with ASPD. Conclusions These results are consistent with prior literature suggesting MAOA and serotonergic dysregulation in antisocial populations. Our results offer the first evidence suggesting epigenetic mechanisms may contribute to MAOA dysregulation in antisocial offenders. Royal College of Psychiatrists.
    The British journal of psychiatry: the journal of mental science 12/2014; 206(3). DOI:10.1192/bjp.bp.114.144964 · 7.34 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: The study focuses on the analysis of the contribution of sociodemographic, clinical, academic and family variables to the likelihood of the presence of disruptive behaviour disorder (DBD). Ex post facto, retrospective, transversal, comparative study in two groups (cases of DBD and clinical controls) is used. Ages range 6 to 16 years. Sample of 1,847 clinical cases. Cases and controls are defined by clinical interview according to DSM-IV-TR criteria. A descriptive phase and an estimated logistic regression procedure are included. The proposed model is significant and correctly classified 87.2% of cases. The variables male sex (OR = 1.82, p = .00), comorbidity (OR = 7.68, p = .00), borderline intellectual functioning (OR = 3.15, p = .00), less educated mothers (OR = 1.57, p = .04) and repeat the course (OR = 2, p = .00), significantly increased the probability for DBD. The variables age, psychiatric history, divorced parents and fathers' educational level are not significant in the model. DBD has multidimensional association with clinical, academic and family variables, being eligible for the inclusion in prevention programs. KEY WORDS. Disruptive behaviour disorder. Conduct disorder. Oppositional defiant disorder. Ex post facto study.