Abstract
Eating disorders (EDs) are common, complex psychiatric disorders thought to be caused by both genetic and environmental factors. They share many symptoms, behaviors, and personality traits, which may have overlapping heritability. The aim of the present study is to perform a genome-wide association scan (GWAS) of six ED phenotypes comprising three symptom traits from the Eating Disorders Inventory 2 [Drive for Thinness (DT), Body Dissatisfaction (BD), and Bulimia], Weight Fluctuation symptom, Breakfast Skipping behavior and Childhood Obsessive-Compulsive Personality Disorder trait (CHIRP). Investigated traits were derived from standardized self-report questionnaires completed by the TwinsUK population-based cohort. We tested 283,744 directly typed SNPs across six phenotypes of interest in the TwinsUK discovery dataset and followed-up signals from various strata using a two-stage replication strategy in two independent cohorts of European ancestry. We meta-analyzed a total of 2,698 individuals for DT, 2,680 for BD, 2,789 (821 cases/1,968 controls) for Bulimia, 1,360 (633 cases/727 controls) for Childhood Obsessive-Compulsive Personality Disorder trait, 2,773 (761 cases/2,012 controls) for Breakfast Skipping, and 2,967 (798 cases/2,169 controls) for Weight Fluctuation symptom. In this GWAS analysis of six ED-related phenotypes, we detected association of eight genetic variants with P < 10−5. Genetic variants that showed suggestive evidence of association were previously associated with several psychiatric disorders and ED-related phenotypes. Our study indicates that larger-scale collaborative studies will be needed to achieve the necessary power to detect loci underlying ED-related traits. © 2012 Wiley Periodicals, Inc.
Highlights
Eating disorders (EDs) are complex psychiatric disorders involving both genetic and environmental factors
The aim of the present study is to carry out a genome-wide association scan (GWAS) of six ED-related phenotypes consisting of four ED-related symptom measures, Breakfast Skipping behavior and Obsessive-Compulsive Personality Disorder (OCPD) traits in a population-based twin cohort of British origin and a follow-up of interesting signals in two independent cohorts of European origin
For the OCPD traits, the Childhood Retrospective Perfectionism Questionnaire (CHIRP) was used. 1/squared root transformation was applied to normalize the distribution of Drive for Thinness (DT) scores and was analyzed together with Body Dissatisfaction (BD) as a quantitative phenotype, whereas Bulimia, Weight Fluctuation (WF), Breakfast Skipping, and OCPD phenotypes were dichotomized because their distribution could not be transformed to normality
Summary
Eating disorders (EDs) are complex psychiatric disorders involving both genetic and environmental factors. EDs are not likely to be etiologically separate from each other, as patients can move from one diagnosis to another over time (e.g., from AN to BN), they share many symptoms and environmental risk factors, and have overlapping heritability, most likely from shared genetic susceptibility loci [Strober et al, 2000; Wade et al, 2000; Helder and Collier, 2011]. Many candidate genes, such as BDNF and HTR2A, have been examined for association with EDs, mainly for AN [Pinheiro et al, 2010; Rask-Andersen et al, 2010]. Genome-wide significance of these findings has not yet been achieved, partly because of the paucity of available datasets of sufficient sample size (and power) for replication studies
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