Using epidemiologic methods to test hypotheses regarding causal influences on child and adolescent mental disorders

• Authors: Benjamin B. Lahey, University of Chicago; Brian M. D'Onofrio, Indiana University; Irwin Waldman, Emory University
• Journal Title: Journal of Child Psychology and Psychiatry
• Volume: Volume 50, Number 1-2
• Publisher: Wiley: 12 months | 2009-01-01, Pages 53-62
• Type of Work: Article | Post-print: After Peer Review
• Publisher DOI: http://doi.org/10.1111/j.1469-7610.2008.01980.x
• Subjects: Psychology, Clinical; Health Sciences, Epidemiology
• Keywords: Adolescent; Child; Diagnostic and Statistical Manual of Mental Disorders; Epidemiologic Methods; Humans; International Classification of Diseases; Mental Disorders; Phenotype; Risk Factors; Terminology as Topic

Abstract

Epidemiology uses strong sampling methods and study designs to test refutable hypotheses regarding the causes of important health, mental health, and social outcomes. Epidemiologic methods are increasingly being used to move developmental psychopathology from studies that catalogue correlates of child and adolescent mental health to designs that can test rival hypotheses regarding causal genetic and environmental influences. A two-part strategy is proposed for the next phase of epidemiologic research. First, to facilitate the most informed tests of causal hypotheses, it is necessary to develop and test models of the structure of hypothesized genetic and environmental influences on mental health phenotypes. This will involve testing the related hypotheses that there are both (a) dimensions of psy- chopathology that are distinct in the sense of having at least some unique genetic and/or environmental influences, and (b) higher-order domains of correlated dimensions that are all apparently influenced in part by the same genetic and/or environmental factors. The resulting causal taxonomy would organize tests of causal hypotheses regarding both factors that may broadly increase risk for multiple dimensions of psychopathology and factors that may specifically increase risk for each individual dimension. Second, it is necessary to make greater use of a number of powerful epidemiologic designs that allow rigorous tests of rival hypotheses regarding genetic and environmental causes.