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Am J Psychiatry 162:2256-2262, December 2005
doi: 10.1176/appi.ajp.162.12.2256
© 2005 American Psychiatric Association
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* Eating Disorders
* Genetics

Association Between the Insulin-Like Growth Factor 2 Gene (IGF2) and Scores on the Eating Attitudes Test in Nonclinical Subjects: A Family-Based Study

Rachel Bachner-Melman, M.A., Ada H. Zohar, Ph.D., Lubov Nemanov, M.D., Uriel Heresco-Levy, M.D., Inga Gritsenko, M.S., and Richard P. Ebstein, Ph.D.

OBJECTIVE: An interesting candidate gene for eating disorders is the gene for insulin-like growth factor 2 (IGF2). Located on chromosome 11p15.5, IGF2 is a member of the insulin family of polypeptide growth factors that is involved in development and growth. Consistent with its profile of metabolic actions, an association has been reported between a single nucleotide polymorphism (SNP) in the 3' untranslated region of the IGF2 gene (ApaI) and body mass index. This investigation extended these studies and investigated the psychological and behavioral implications of this hormone’s impact on metabolism and body composition. METHOD: The authors tested nonclinical subjects from 376 families for three IGF2 SNPs and for eating disorders, as reflected in scores on the 26-item Eating Attitudes Test, a self-report questionnaire widely used as a screening instrument. RESULTS: A highly significant association was observed between the IGF2 ApaI G allele and scores on the Eating Attitudes Test overall and each of its subscales (bulimia, dieting, and oral control). Additionally, a significant association was observed between this polymorphism and body mass index. CONCLUSIONS: The current finding that the IGF2 ApaI G polymorphism, which predisposes to weight gain, may also contribute to the pathology of eating disorders is intriguing. Neurotransmitter modulation of appetitive behavior is the focus of most hypotheses regarding the etiology of severe eating disorders. The current results to some measure challenge this view, and inborn metabolic tendencies to weight gain in some women may trigger constant dieting, which in predisposed individuals eventually leads to severe eating disorders.







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