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Author Notes:

Corresponding Author: Benjamin B. Lahey, Department of Health Studies (MC 2007), University of Chicago, Chicago, IL 60637. blahey@uchicago.edu..

Dr. Lahey had full access to all data and takes responsibility for the integrity of the data and the accuracy of the data analysis.

The authors have no financial disclosures.


Research Funding:

This study was supported by grant R01 MH59111 to Benjamin Lahey and R21 MH086099 to Paul Rathouz.


  • Adolescent
  • Agoraphobia
  • Anxiety Disorders
  • Attention Deficit Disorder with Hyperactivity
  • Attention Deficit and Disruptive Behavior Disorders
  • Child
  • Conduct Disorder
  • Cross-Sectional Studies
  • Depressive Disorder, Major
  • Diseases in Twins
  • Factor Analysis, Statistical
  • Female
  • Genetic Pleiotropy
  • Genetic Predisposition to Disease
  • Genetic Variation
  • Humans
  • Incidence
  • Internal-External Control
  • Male
  • Mental Disorders
  • Models, Psychological
  • Obsessive-Compulsive Disorder
  • Phenotype
  • Phobic Disorders
  • Risk Factors
  • Social Environment

Higher-order genetic and environmental structure of prevalent forms of child and adolescent psychopathology


Journal Title:

Archives of General Psychiatry


Volume 68, Number 2


, Pages 181-189

Type of Work:

Article | Final Publisher PDF


Context: It is necessary to understand the etiologic structure of child and adolescent psychopathology to advance theory and guide future research. Objective: To test alternative models of the higher-order structure of etiologic effects on 11 dimensions of child and adolescent psychopathology using confirmatory factor analyses of genetic and environmental covariances. Design: Representative sample of twins. Setting: Home interviews. Participants: A total of 1571 pairs of 9- to 17-year-old twins. Main Outcome Measures: Structured assessments of psychopathology using adult caregivers and youth as informants. Results: The best-fitting genetic model revealed that most genetic factors nonspecifically influence risk for either all 11 symptom dimensions or for dimensions of psychopathology within 1 of 2 broad domains. With some notable exceptions, dimension-specific genetic influences accounted for modest amounts of variance. Conclusions: To inform theory and guide molecular genetic studies, an etiologic model is offered in which 3 patterns of pleiotropy are hypothesized to be the principal modes of genetic risk transmission for common forms of child and adolescent psychopathology. Some common environmental influences were found, but consistent with a "generalist genes, specialist environments" model, there was little sharing of environmental influences. This implies that prevalent dimensions of child and adolescent psychopathology mostly share their genetic liabilities but are differentiated by nonshared experiences.

Copyright information:

©2011 American Medical Association. All rights reserved.

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