by Therese Johansson, Karolinska Institutet

Eating disorders arise from a combination of genetic and environmental factors. Eating disorders affect millions of people around the world, are life-disrupting, and in some cases can be life-threatening. Unfortunately, no easy test exists, like a blood test, that can tell us if someone has an eating disorder. Likewise, we have no way of predicting who might recover after a brief illness or who is at risk of developing a chronic illness. If we could identify people who are at high risk of a chronic eating disorder at an earlier stage, we could tailor treatments to the individual. 

Recent studies led by Karolinska Institutet, UNC CEED, and King’s College London compared the DNA of people with and without (typical) anorexia nervosa and identified regions in the human DNA that differ between individuals with anorexia nervosa and those without [1]. This has helped us understand the underlying biology of the disorder and has the potential to further help us identify people at risk for poor outcomes. Another somewhat surprising result of these studies was that low body mass index (BMI)** and anorexia nervosa share genetics, indicating that people who are genetically prone to a low BMI might be at higher risk for developing low weight anorexia nervosa [2].

**An important note to readers** We know that there are many problems with BMI as a measure. We also acknowledge that this work focused on typical anorexia nervosa and clarify that teams around the world (including at Karolinska Institutet in Sweden) are doing similar work with atypical anorexia nervosa; however, those studies are not yet complete.

Our study examined whether we could identify individuals with anorexia nervosa who are at high risk for a protracted course of illness [3]. To do this, we compared the genetic makeup of individuals with a severe and enduring eating disorder (meaning those who had not recovered within five years after their first treatment attempt) and individuals who had recovered within these five years. We observed that patients with a severe and enduring eating disorder had a different genetic makeup than those who had recovered, and the difference was that they were more genetically prone to higher BMI. This could mean that they were more likely to engage in more severe eating disorder behaviours that could lead to their illness becoming more entrenched.

This study was the first of its kind to show that an individual’s DNA may be useful as an adjunct tool in clinical care. More specifically, if findings from genetic studies become more robust through larger sample sizes, genetic information may help us identify individuals who are at greatest risk for developing a severe or enduring illness.

To generate clinically meaningful tools for treatment, we need to understand the underlying biology of eating disorders better. Our one-size-fits-all approach to eating disorder treatment does not recognize the vast differences that exist across individuals with the same diagnosis. Genetics might be a promising tool to make finer distinctions among individuals with eating disorders to tailor our treatment approach toward each individual or groups of individuals.  

1.        Watson HJ, Yilmaz Z, Thornton LM, Hübel C, Coleman JRI, Gaspar HA, et al. Genome-wide association study identifies eight risk loci and implicates metabo-psychiatric origins for anorexia nervosa. Nat Genet. 2019;51: 1207–1214. doi:10.1038/s41588-019-0439-2

2.        Hübel C, Gaspar HA, Coleman JRI, Hanscombe KB, Purves K, Prokopenko I, et al. Genetic correlations of psychiatric traits with body composition and glycemic traits are sex- and age-dependent. Nat Commun. 2019;10: 5765. doi:10.1038/s41467-019-13544-0

3.        Johansson T, Birgegård A, Zhang R, Bergen SE, Landén M, Petersen L V, et al. Polygenic association with severity and long-term outcome in eating disorder cases. Transl Psychiatry. 2022;12: 61. doi:10.1038/s41398-022-01831-2