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Annual Research Review: Phenotypic and causal structure of conduct disorder in the broader context of prevalent forms of psychopathology
Article first published online: 23 DEC 2011
© 2011 The Authors. Journal of Child Psychology and Psychiatry © 2011 Association for Child and Adolescent Mental Health
Journal of Child Psychology and Psychiatry
Special Issue: Annual Research Review issue
Volume 53, Issue 5, pages 536–557, May 2012
How to Cite
Lahey, B. B. and Waldman, I. D. (2012), Annual Research Review: Phenotypic and causal structure of conduct disorder in the broader context of prevalent forms of psychopathology. Journal of Child Psychology and Psychiatry, 53: 536–557. doi: 10.1111/j.1469-7610.2011.02509.x
- Issue published online: 4 APR 2012
- Article first published online: 23 DEC 2011
- Accepted for publication: 8 November 2011 Published online: 23 December 2011
- Conduct disorder;
- oppositional defiant disorder;
- homotypic and heterotypic continuity.
Background: A better understanding of the nature and etiology of conduct disorder (CD) can inform nosology and vice versa. We posit that any prevalent form of psychopathology, including CD, can be best understood if it is studied in the context of other correlated forms of child and adolescent psychopathology using formal models to guide inquiry.
Methods: Review of both cross-sectional and longitudinal studies of the place of CD in the phenotypic and causal structure of prevalent psychopathology, with an emphasis on similarities and differences between CD and oppositional defiant disorder (ODD). Papers were located using Web of Science by topic searches with no restriction on year of publication.
Results: Although some important nosologic questions remain unanswered, the dimensional phenotype of CD is well defined. CD differs from other disorders in its correlates, associated impairment, and course. Nonetheless, it is robustly correlated with many other prevalent dimensions of psychopathology both concurrently and predictively, including both other ‘externalizing’ disorders and some ‘internalizing’ disorders. Based on emerging evidence, we hypothesize that these concurrent and predictive correlations result primarily from widespread genetic pleiotropy, with some genetic factors nonspecifically influencing risk for multiple correlated dimensions of psychopathology. In contrast, environmental influences mostly act to differentiate dimensions of psychopathology from one another both concurrently and over time. CD and ODD share half of their genetic influences, but their genetic etiologies are distinct in other ways. Unlike most other dimensions of psychopathology, half of the genetic influences on CD appear to be unique to CD. In contrast, ODD broadly shares nearly all of its genetic influences with other disorders and has little unique genetic variance.
Conclusions: Conduct disorder is a relatively distinct syndrome at both phenotypic and etiologic levels, but much is revealed by studying CD in the context of its causal and phenotypic associations with other disorders over time. Advancing and refining formal causal models that specify the common and unique causes and biological mechanisms underlying each correlated dimension of psychopathology should facilitate research on the fundamental nature and nosology of CD.