a1 Department of Psychology, Virginia Commonwealth University, Richmond, VA, USA
a2 Department of Pediatrics, Virginia Commonwealth University, Richmond, VA, USA
a3 Virginia Institute for Psychiatric & Behavioral Genetics, Virginia Commonwealth University, Richmond, VA, USA
a4 Departments of Psychiatry and Nutrition, University of North Carolina, Chapel Hill, NC, USA
a5 Department of Psychiatry, Virginia Commonwealth University, Richmond, VA, USA
a6 Department of Human Genetics, Virginia Commonwealth University, Richmond, VA, USA
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.
(Received May 06 2008)
(Revised February 28 2009)
(Accepted March 03 2009)
(Online publication October 12 2009)