Eating disorders can dramatically affect body weight, but a major new genetic study suggests weight is far from the whole story.
Researchers studying anorexia nervosa and binge-eating behavior found that the genetic patterns associated with these conditions were not simply the same ones associated with body mass index, or BMI. The findings add to evidence that eating disorders involve a complex mix of biological and psychological factors rather than being conditions that can be understood by body size alone.
“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,” said Dr. Helena Davies, a postdoctoral research fellow at King’s College London and joint-first author of the study.
Published in Nature Mental Health, the observational study brought together genetic information from people participating in studies around the world. Researchers compared nearly 40,000 people with a history of binge eating with more than 1.2 million people without the behavior. They also analyzed about 24,000 people with anorexia nervosa.
For the binge-eating portion, researchers studied the behavior itself rather than binge-eating disorder specifically. That's an important distinction because binge eating can occur in several eating disorders, including binge-eating disorder, bulimia nervosa and some cases of anorexia nervosa.
Researchers looked for places in the genome where genetic differences appeared more often among people with anorexia or binge eating than among people without those conditions. They identified six such regions associated with binge eating and eight associated with anorexia nervosa in the main analysis of people with European genetic ancestry.
But the more revealing finding came from looking at how those genetic patterns related to other traits.
Anorexia nervosa and binge eating showed some similar genetic connections with psychiatric conditions, even though their relationships with body weight and metabolism often pointed in opposite directions.
In other words, two eating-related conditions that may look very different when viewed through the lens of weight could still share some underlying biological vulnerability.
“We've been making important progress in understanding the genetics of anorexia nervosa for several years, but that’s only one of several eating disorders that have major impacts on people's lives,” said Dr. Jonathan Coleman, senior lecturer in statistical genetics at King’s College London and lead senior author. “This work is really important - we go beyond anorexia nervosa and start to understand the genetics of binge eating, which affects many people with eating disorders. We're hopeful that our findings will allow future research to improve the lives of people with all eating disorders.”
The study also found a connection between binge eating and a region near FTO, a gene that has been extensively studied in relation to body weight. Previous research has linked variations around FTO with higher BMI.
The new results raise the possibility that eating behavior could be one part of that relationship. But they do not show that FTO causes binge eating or that binge eating explains why any individual has a higher body weight.
That distinction applies to the study as a whole.
Genes can contribute to vulnerability, but they do not determine whether someone will develop an eating disorder. The study cannot tell an individual their eating-disorder risk, explain why a particular person developed anorexia or binge eating or establish that the genetic differences identified directly caused either condition.
It also does not mean body weight is irrelevant in eating-disorder care. Instead, the findings suggest that weight alone cannot capture the underlying complexity of these conditions.
The study has other limitations. The researchers combined data from many different studies that did not all identify eating disorders or binge eating in exactly the same way. Some relied on medical diagnoses, while others used questionnaires or self-reported histories. The supplementary material also notes that some control groups had not been specifically screened for anorexia nervosa.
The strongest genetic findings were also based primarily on people with European genetic ancestry. The researchers said future work will include more globally diverse populations as well as other eating disorders, including avoidant/restrictive food intake disorder, or ARFID, and atypical presentations.
For now, the research offers a broader way of thinking about eating disorders: what is visible on the scale may be only one part of what is happening underneath.
This was a large international consortium study that combined information from many previously established research projects, so its funding came from a wide range of sources.
The Psychiatric Genomics Consortium, which coordinated the work, is supported by the U.S. National Institutes of Health. Individual researchers and participating datasets also received funding from numerous public agencies, universities and nonprofit foundations in the United States, United Kingdom, Europe, Australia, Canada and Asia. Major supporters included NIH and the National Institute of Mental Health, the U.K. National Institute for Health and Care Research, Wellcome, the Klarman Family Foundation and national research councils and health agencies in several countries.
Some of the datasets included in the analysis had also received industry support. A binge-eating dataset drawn from an earlier clinical trial was funded by Johnson & Johnson Pharmaceutical Research & Development. FinnGen, another contributing research resource, reports funding from AbbVie, AstraZeneca, Biogen, Celgene, Genentech, GSK, MSD, Pfizer and Sanofi, along with public funding. Genetic data generation for one U.K. cohort received support from 23andMe, and another contributing cohort reported partial industry funding from Cogir Immobilier. These companies did not necessarily fund or participate in the new analysis itself.
Several study authors also disclosed financial relationships outside this research. These included consulting, speaking fees, advisory roles, employment, stock ownership or other financial ties involving Novo Nordisk, Janssen, Lilly, Lundbeck, Otsuka, Boehringer Ingelheim, Roche, Rovi, Neumora Therapeutics, Myriad Neuroscience, Orbimed and other organizations. One author was a Janssen employee when the work was completed and holds company equity.