Genome-wide association studies of binge eating behaviour and anorexia nervosa yield insights into the unique and shared biology of eating disorder phenotypes
Research output: Preprint/Documentation/Report › Preprint
Contributors
- Division of Psychological and Social Medicine and Developmental Neurosciences
- Department of Child and Adolescent Psychiatry and Psychotherapy
- Karolinska Institutet
- Mental Health Services in the Capital Region of Denmark
- South London and Maudsley NHS Foundation Trust
- NIHR Maudsley Biomedical Research Centre (BRC)
- King's College London (KCL)
- University of British Columbia
- DRK Kliniken Berlin
- University of North Carolina at Chapel Hill
- Texas Tech University
- University Hospital Essen
- University of Texas at Austin
- Icahn School of Medicine at Mount Sinai
- University College London
- Quantitative Genomic Medicine Laboratories, S.L. (qGenomics)
- Aarhus University
- University of Oslo
- University of Bristol
- University of Tartu
- Vanderbilt University Medical Center
- University of Helsinki
- Broad Institute of Harvard University and MIT
- Equip Health
- Rutgers - The State University of New Jersey, Newark
- University of Split
- Ludwig Maximilian University of Munich
- Oberberg Specialist Clinic
- University of Padua
- Altrecht Mental Health Institute
- LVR University Hospital Essen
- Seattle University
- Université de Nantes
- University of Medical Sciences Poznan
- Stanford University
- Reinier van Arkel Group
- University Hospital Carl Gustav Carus Dresden
- German Center for Mental Health (DZPG)
- Charité – Universitätsmedizin Berlin
Abstract
Eating disorders -including anorexia nervosa (AN), bulimia nervosa, and binge eating disorder-are clinically distinct but exhibit symptom overlap and diagnostic crossover. Genomic analyses have mostly examined AN. We conducted the first genomic meta-analysis of binge eating behaviour (BE; 39,279 cases, 1,227,436 controls), alongside new analyses of AN (24,223 cases, 1,243,971 controls) and its subtypes (all European ancestries). We identified six loci associated with BE, including loci associated with higher body mass index (BMI) and impulse-control behaviours. AN GWAS yielded eight loci, validating six loci. Subsequent polygenic risk score analysis demonstrated an association with AN in two East Asian ancestry cohorts. BE and AN exhibited similar positive genetic correlations with psychiatric disorders, but opposing genetic correlations with anthropometric traits. Most of the genetic signal in BE and AN was not shared with BMI. We have extended eating disorder genomics beyond AN; future work will incorporate multiple diagnoses and global ancestries.
Details
| Original language | English |
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| Publication status | Published - 8 May 2025 |
External IDs
| PubMedCentral | PMC12083633 |
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| ORCID | /0000-0003-2132-4445/work/188858302 |
| ORCID | /0000-0001-8333-867X/work/188860284 |