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A twin study of specific bulimia nervosa symptoms

Published online by Cambridge University Press:  12 October 2009

S. E. Mazzeo*
Affiliation:
Department of Psychology, Virginia Commonwealth University, Richmond, VA, USA Department of Pediatrics, Virginia Commonwealth University, Richmond, VA, USA Virginia Institute for Psychiatric & Behavioral Genetics, Virginia Commonwealth University, Richmond, VA, USA
K. S. Mitchell
Affiliation:
Department of Psychology, Virginia Commonwealth University, Richmond, VA, USA Virginia Institute for Psychiatric & Behavioral Genetics, Virginia Commonwealth University, Richmond, VA, USA
C. M. Bulik
Affiliation:
Departments of Psychiatry and Nutrition, University of North Carolina, Chapel Hill, NC, USA
S. H. Aggen
Affiliation:
Virginia Institute for Psychiatric & Behavioral Genetics, Virginia Commonwealth University, Richmond, VA, USA Department of Psychiatry, Virginia Commonwealth University, Richmond, VA, USA
K. S. Kendler
Affiliation:
Virginia Institute for Psychiatric & Behavioral Genetics, Virginia Commonwealth University, Richmond, VA, USA Department of Psychiatry, Virginia Commonwealth University, Richmond, VA, USA
M. C. Neale
Affiliation:
Virginia Institute for Psychiatric & Behavioral Genetics, Virginia Commonwealth University, Richmond, VA, USA Department of Psychiatry, Virginia Commonwealth University, Richmond, VA, USA Department of Human Genetics, Virginia Commonwealth University, Richmond, VA, USA
*
*Address for correspondence: Dr S. E. Mazzeo, Department of Psychology, Virginia Commonwealth University, PO Box 842018, Richmond, VA23284–2018, USA. (Email: semazzeo@vcu.edu)

Abstract

Background

Twin studies have suggested that additive genetic factors significantly contribute to liability to bulimia nervosa (BN). However, the diagnostic criteria for BN remain controversial. In this study, an item-factor model was used to examine the BN diagnostic criteria and the genetic and environmental contributions to BN in a population-based twin sample. The validity of the equal environment assumption (EEA) for BN was also tested.

Method

Participants were 1024 female twins (MZ n=614, DZ n=410) from the population-based Mid-Atlantic Twin Registry. BN was assessed using symptom-level (self-report) items consistent with DSM-IV and ICD-10 diagnostic criteria. Items assessing BN were included in an item-factor model. The EEA was measured by items assessing similarity of childhood and adolescent environment, which have demonstrated construct validity. Scores on the EEA factor were used to specify the degree to which twins shared environmental experiences in this model.

Results

The EEA was not violated for BN. Modeling results indicated that the majority of the variance in BN was due to additive genetic factors. There was substantial variability in additive genetic and environmental contributions to specific BN symptoms. Most notably, vomiting was very strongly influenced by additive genetic factors, while other symptoms were much less heritable, including the influence of weight on self-evaluation. These results highlight the importance of assessing eating disorders at the symptom level.

Conclusions

Refinement of eating disorder phenotypes could ultimately lead to improvements in treatment and targeted prevention, by clarifying sources of variation for specific components of symptomatology.

Type
Original Articles
Copyright
Copyright © Cambridge University Press 2009

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