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Heritability of obsessive-compulsive symptom dimensions

Authors

  • Daniël S. van Grootheest,

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    1. Department of Biological Psychology, Vrije Universiteit Amsterdam, Amsterdam, The Netherlands
    2. Department of Psychiatry, VU University Medical Center, Amsterdam, The Netherlands
    • Vrije Universiteit, Department of Biological Psychology, Van der Boechorststraat 1, 1081 BT Amsterdam, The Netherlands.
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  • Dorret I. Boomsma,

    1. Department of Biological Psychology, Vrije Universiteit Amsterdam, Amsterdam, The Netherlands
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  • John M. Hettema,

    1. Department of Psychiatry, Virginia Institute for Psychiatric and Behavioral Genetics, Virginia Commonwealth University, Richmond, Virginia
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  • Kenneth S. Kendler

    1. Department of Psychiatry, Virginia Institute for Psychiatric and Behavioral Genetics, Virginia Commonwealth University, Richmond, Virginia
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  • Please cite this article as follows: van Grootheest DS, Boomsma DI, Hettema JM, Kendler KS. 2007. Heritability of Obsessive-Compulsive Symptom Dimensions. Am J Med Genet Part B 147B:473–478.

Abstract

Recent research has shown that obsessive-compulsive symptoms (OCS) differ remarkably among patients and can be divided into several symptom dimensions. OCS are influenced by genetic components, but it is unknown to what extent these symptom dimensions are heritable. The phenotypic heterogeneity also raises the question to what extent the symptom dimensions are influenced by specific or shared genetic factors. We studied a population sample of 1,383 female twins from the Virginia Twin Registry. OCS was measured by a questionnaire with 20 items from the Padua Inventory. After factor analysis, three reliable OC symptom dimensions were retained: Rumination, Contamination, and Checking. These OC dimensions were analyzed with multivariate genetic models to investigate both the overlap and uniqueness of genetic and environmental contributions underlying OC symptom dimensions. The multivariate common pathway model provided the best description of the data. All symptom dimensions share variation with a latent common factor, that is, OC behavior. Variation in this common factor was explained by both genes (36%) and environmental factors (64%). Only the Contamination dimension was influenced by specific genes and seemed to be a relatively independent dimension. The results suggest that a broad OC behavioral phenotype exists, influenced by both genes and nonshared environment. In addition, we found evidence for specific genetic and environmental factors underlying the Contamination dimension. Use of the Contamination dimension could therefore provide a powerful approach for the detection of genetic susceptibility loci that contribute to OCS. © 2007 Wiley-Liss, Inc.

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