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26th Aug, 2026 12:00 AM
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Eating Disorder Genetics Go Beyond BMI

The genetic factors underlying anorexia nervosa and binge eating are largely distinct from those that influence body weight.

Results of a large genetic study showed that nearly 90% of the genetic variation associated with both conditions could not be explained by BMI-related genetics.

The analysis also revealed that binge eating and anorexia nervosa share genetic links with several psychiatric conditions but differ markedly in their genetic relationships with body weight and other traits, pointing to both shared and distinct underlying biology.

“This research confirms on a genetic level that eating disorders are not just about body weight; many of the versions of genes linked to these conditions are different from the versions of genes that are linked to how much someone weighs,” study investigator Helena Davies, PhD, postdoctoral research fellow at the Institute of Psychiatry, Psychology and Neuroscience (IoPPN) at King’s College London, London, England, said in a statement.

Article Key Points
  • AN, binge eating genetics largely distinct from BMI genetics.
  • ~90% genetic variation unexplained by BMI-related genetics.
  • Shared psychiatric links: MDD, bipolar, schizophrenia, anxiety phenotypes.
  • Binge eating: ADHD, risk-taking, alcohol use, smoking genetic links.
  • Polygenic scores modest; not ready for clinical use.
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The findings could also help counter the perception that eating disorders are primarily behavioral or driven by body weight. “It is enormously helpful for people with eating disorders and their loved ones to understand that there is a biological component to these illnesses,” study investigator Cynthia M. Bulik, PhD, professor of eating disorders at The University of North Carolina at Chapel Hill School of Medicine and founding director of the UNC Center of Excellence for Eating Disorders, told Medscape Medical News. 

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The study was published online on August 19 in Nature Mental Health.

Shared and Distinct Genetic Links

The genomic meta-analysis of case-control studies included nearly 40,000 individuals with binge eating behavior and roughly 24,000 individuals with anorexia nervosa. These groups were compared with more than 1.2 million control individuals.

The researchers identified six genomic regions associated with binge eating and eight with anorexia nervosa, including two anorexia loci not previously identified.

Binge eating and anorexia nervosa showed moderate genetic overlap and broadly similar positive genetic correlations with psychiatric disorders, including major depressive disorder, bipolar disorder, schizophrenia, and anxiety-related phenotypes.

But there were also notable differences. The genetic correlation with attention-deficit/hyperactivity disorder was stronger for binge eating, whereas the association with obsessive-compulsive disorder was stronger for anorexia nervosa.

Binge eating also showed genetic associations with risk-taking, problematic alcohol use, and smoking, consistent with the loss-of-control component of the behavior, the researchers noted.

Some of the clearest differences involved body weight. Genetic factors associated with higher body weight were linked to greater susceptibility to binge eating but lower susceptibility to anorexia nervosa.

One of the genetic signals associated with binge-eating behavior was located near the FTO gene, which has long been associated with higher body weight, suggesting that binge eating may partly explain the relationship between this gene and higher BMI.

However, BMI-related genetic variation accounted for only about 12% of the genetic variance in binge eating and 10% in anorexia nervosa, suggesting that most of the genetic signal underlying both conditions is independent of body weight, the researchers noted.

They also developed polygenic risk scores for binge eating and anorexia nervosa, but their ability to predict either condition was modest.

“These scores alone won’t tell us who will develop binge eating, and they are not currently ready for clinical use. However, as their accuracy improves, we hope that further research could show them to be useful alongside known risk factors like personal and family medical history,” said study co-investigator Jonathan Coleman, PhD, senior lecturer in statistical genetics at the IoPPN.

Few Treatment Options

Coleman added that this research may also help identify future drug targets, which, he said are “desperately needed in eating disorders.”

Bulik agreed. “Our pharmacologic toolbox for eating disorders is still extremely limited,” she said. There are currently no medications that are effective or FDA approved for either anorexia nervosa or avoidant/restrictive food intake disorder (ARFID), and medications used for bulimia nervosa and binge-eating disorder were originally developed for other conditions, Bulik said.

“Genetics gives us an opportunity to work in the other direction: start with the biology of the eating disorder, identify the pathways that are disrupted, and ultimately develop or repurpose medications that actually target those pathways,” Bulik said.

“The goal is to tailor treatment to biology, and these results suggest that it will not be a one-treatment-fits-all across eating disorders. The underlying genetic differences that we observed mean that we will have to take into account both their genetic similarities and their genetic differences as we move toward those precision treatments,” she added.

The investigators plan to expand the research to other eating disorders and presentations, including ARFID and atypical eating disorders, and to more diverse global populations. They noted that these efforts will be important for identifying additional genetic signals and ensuring that future genomic approaches are relevant across populations.

This research had no commercial funding. Author disclosures are available with the original study publication.

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