Home » Health » A study in Nature Microbiology analyzed the association between the intestinal microbiome and anorexia nervosa, finding a probable role of the microbiome in AN-associated changes of satiety and metabolism. The results indicate that gut microbial disruptions may contribute to the pathogenesis of anorexia nervosa.

A study in Nature Microbiology analyzed the association between the intestinal microbiome and anorexia nervosa, finding a probable role of the microbiome in AN-associated changes of satiety and metabolism. The results indicate that gut microbial disruptions may contribute to the pathogenesis of anorexia nervosa.

Anorexia nervosa is a complex and devastating eating disorder characterized by a severely restricted diet and an intense fear of gaining weight. The causes of anorexia are multifactorial and include both biological and environmental factors. Recently, there has been a growing interest in the potential role of the gut microbiota in the pathogenesis of this disorder. The gut microbiota is a diverse community of microorganisms that reside in the human gut, playing a crucial role in regulating metabolism, immune function, and brain health. In this article, we will explore the emerging evidence suggesting that a disrupted gut microbiota could contribute to the development and maintenance of anorexia nervosa.


Anorexia nervosa (AN) is a serious mental health condition that can cause significant mortality, particularly among women. Although multiple environmental and genetic factors appear to contribute to AN development, therapies informed by scientific evidence are rare. Researchers have focused on determining whether disruptions to the gut microbiota could be involved in AN pathogenesis, as previous studies have detected microbial dysbiosis among affected individuals. However, these studies had small sample sizes, and they relied on amplicon sequencing to analyze genus-level microbial changes. In a new study published in Nature Microbiology, scientists investigated the potential links between the gut microbiome and AN, using metabolomic and shotgun metagenomic analyses on serum and fecal samples obtained from women with AN and age- and sex-matched healthy controls. The researchers also transplanted fecal microbiota from AN cases to mice fed calorie-limited diets to simulate AN eating behavior for in vivo analysis. They used the eating disorder inventory-3 and an insulin resistance assessment tool to gauge eating behaviors and insulin resistance, respectively. Linear regression modeling was also employed, adjusting for age, smoking status, medications, and body mass index (BMI).

The study’s results revealed changes in bacterial organisms, particularly Clostridium, among AN-affected individuals, and these changes were associated with mental well-being and eating behavior measures. The researchers also found several bacterial functional-type modules related to neurotransmitter degradation enriched among those with AN. Furthermore, alterations in structural variants in bacterial organisms were associated with AN metabolic characteristics, which indicates that the gut microbiome probably plays a role in AN-associated changes related to satiety and the metabolism of secondary bile acids.

The study’s findings indicated a causal relationship between serological bacterial metabolites and gut microbial alterations in AN. At the phylum level, AN microbiome samples had lowered Actinobacteriota and Bacteroidota counts, while at the genus level, AN microbiota had an elevated Lactobacillus count, with a more prevalent Ruminococcacea-enterotype. Linear regression modeling revealed greater β-diversity among AN-affected women at the species level, with depleted Roseburia inulinivorans and Roseburia intestinalis, and increased Erysipelatoclostridium ramosum, Blautia species CAG, and Enterocloster bolteae innocuum (Clostridium) levels in AN patients. Interestingly, Clostridium counts correlated positively with eating disorder scores. The abundance of Bifidobacterium, Parasutterella, and Brachyspira showed positive correlations with perfectionism, body dissatisfaction, and ‘drive for thinness’ markers in AN, respectively. Among AN subjects, bacterial organisms with significant growth retardation included Alistipes finegoldii, Akkermansia muciniphila, Eubacterium siraeum, Coprococcus catus, SS3/4, and Odoribacter splanchnicus.

Overall, the study finds that the gut microbiome probably disrupts AN pathogenesis given the molecular, microbial, and viral alterations observed in AN women. However, further research is necessary to understand more about how gut microbiota interacts with AN pathogenesis to identify effective therapies to improve outcomes.


In conclusion, the relationship between the gut microbiota and anorexia nervosa pathogenesis is increasingly becoming a subject of intense scientific inquiry. While there is still limited empirical evidence to establish a definitive cause-and-effect link between gut dysbiosis and anorexia nervosa, the recent studies suggest that the potential correlation between the two is worth exploring further. By understanding the complex interplay between gut health and eating disorders, clinicians and researchers are hopeful that new strategies for diagnosis, prevention, and treatment of anorexia nervosa could emerge in the future.

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