Gut-brain axis in eating disorders offers new treatment potential

By Dr. Sanchari Sinha Dutta, Ph.D.Reviewed by Lauren HardakerJul 16 2025

Could a disrupted gut be fueling eating disorders? This study explains the gut-brain hormone loop behind anorexia, binge eating, and more, and how restoring microbial balance may unlock better recovery.

Study: Gut Microbiota in Women with Eating Disorders: A New Frontier in Pathophysiology and Treatment. Image credit: Pormezz/Shutterstock.com

A review article published in the journal Nutrients described the involvement of gut microbiota in the pathophysiology of eating disorders in women. The review also provided an overview of microbiota-targeted therapies that may complement conventional psychological and pharmacological treatments.

Background

Eating disorders are a group of disorders characterized by changes in eating-related behaviors that can potentially affect both physical and mental health. Anorexia nervosa, bulimia nervosa, and binge eating disorder are the most common eating disorders, which predominantly affect women. These disorders are also marked by psychological symptoms such as body image disturbances, intense fear of weight gain, and compensatory behaviors.

The gut microbiota regulates various physiological functions and is closely related to human health and disease. Significant alterations in the gut microbiota composition and functioning have been observed in women with eating disorders. Hormonal fluctuations related to menstruation, pregnancy, and menopause have also been found to alter the gut microbial composition, potentially increasing the risk of eating disorders in women.

Gut microbiota changes in eating disorders

Gut microbiota alterations can substantially contribute to the complex pathogenesis of eating disorders. These alterations may arise from viral, bacterial, or parasitic infections that interfere with the gut-brain axis and potentially increase the risk of eating disorders.

Reduced microbial diversity and compositional shifts toward specific bacterial populations have increased production of inflammatory cytokines, which cross the blood-brain barrier and cause alterations in neurotransmitter signaling in the brain.

GABA is an inhibitory neurotransmitter that can directly influence eating behavior through interactions with gut-derived microbial metabolites that modulate appetite-regulating hormones such as GLP-1, PYY, and CCK. GABA-producing bacteria in the gut, particularly from the genus Bacteroides, have been identified as key modulators of host appetite.

It has been observed that dysregulation of appetite-related gut peptides potentially contributes to reduced hunger, impaired satiety signaling, and disrupted gastrointestinal motility, which subsequently increases the risk of developing anorexia nervosa, an eating disorder characterized by restricted energy intake relative to the body’s physiological demands, accompanied by significant weight loss and psychological symptoms.

Psychotropic drugs used to treat patients with eating disorders, or prolonged caloric restriction in patients with anorexia nervosa, have been found to reduce gut microbiota diversity and trigger a compositional shift from beneficial bacteria towards harmful bacteria.

Emerging evidence highlights a multifactorial crosstalk between immune–inflammatory pathways, disordered eating behaviors, and mood-related psychopathology. In patients with anorexia nervosa, a reduced abundance of short-chain fatty acid (SCFA)- producing bacteria has been observed. This disrupts intestinal permeability and facilitates the blood's translocation of microbes and microbial metabolites. This cascade subsequently increases pro-inflammatory cytokine levels and impacts neuroimmune signaling and brain functioning.

Gut microbiota-derived SCFAs are crucial in regulating appetite and maintaining metabolic homeostasis by increasing satiety hormones leptin, glucagon-like peptide-1 (GLP-1), and peptide YY. 

SCFAs primarily influence brain activities by altering neuroinflammation, promoting microglial maturation, and regulating the synthesis of neurotransmitters and neurotrophic factors. Inflammatory activity in the brain has been found to increase anorexia nervosa risk by suppressing the appetite-stimulating hormone ghrelin, leading to early satiety and reduced food intake. However, evidence also suggests that SCFAs may have context-dependent effects on appetite and behavior, influenced by dietary composition, microbial taxa, and host physiology.

Hormonal influence in women with eating disorder

Female sex hormones, especially estrogen and progesterone, have a significant impact on the gut and vaginal microbiota. High levels of estrogen metabolites have been linked to microbial diversity, whereas high levels of unmetabolized parent estrogens have been linked to breast cancer development.

The estrogenome in the intestine refers to bacterial genes involved in deconjugating estrogens and recirculating estrogens in the blood. Estrogens are essential in regulating intestinal motility and permeability, promoting gut microbiota diversity, and increasing the abundance of beneficial bacteria. The gut microbiota, on the other hand, plays a crucial role in regulating estrogen metabolism. Disruptions in this estrogen-microbiota axis may contribute to the development of hormone-sensitive disorders, including those with psychological and metabolic components.  

The cyclical fluctuations of estrogen and progesterone during the menstrual cycle, pregnancy, and menopause have been found to affect the balance of the microbial ecosystem, leading to changes in the composition and stability of the gut microbiota. These changes are associated with mood fluctuations, appetite alterations, and food cravings, which are also common in eating disorders. In individuals with pre-existing psychological vulnerabilities, such hormone-driven microbial shifts may exacerbate disordered eating behaviors, especially during hormonally sensitive periods such as puberty, pregnancy, and menopause.

Gut microbiota-targeted interventions

Conventional psychological and pharmacological treatments for eating disorders have shown only modest success. Given the significant involvement of gut microbiota in the pathogenesis of these disorders, researchers are currently aiming to develop microbiota-targeted interventions, such as probiotics, prebiotics, dietary modulation, and fecal microbiota transplantation, that could complement conventional therapies.

Several animal studies have suggested that probiotics can improve eating behavior by regulating satiety, attenuating compulsive eating patterns, and modulating food addiction. These improvements are associated with the beneficial impact of probiotics on the gut microbiota composition and the production of metabolites, hormones, and neurotransmitters that exert beneficial effects on the gut-brain axis.

In human clinical trials, probiotic supplementation, cognitive behavioral therapy, and a weight loss program have been found to improve anthropometric measures, reduce food addiction, and regulate eating behavior. In obese adults, probiotic supplementation, together with dietary modification, has been found to alleviate binge eating behaviors, mood symptoms, and metabolic indices.

Fecal microbiota transplantation (FMT) is a promising strategy for restoring gut microbial homeostasis. In anorexic patients, FMT has been found to improve body weight, body fat percentage, gut microbiota diversity, and microbial metabolite levels. However, these findings are based on small-scale or pilot studies, and the long-term safety and efficacy of FMT in eating disorder populations remain to be fully established.

Precision nutrition and personalized microbiome-based interventions are gaining attention in the medical field for managing eating disorders. These interventions primarily focus on the specific needs of single patients, including dietary plans, psychobiotics (a probiotic), and supplementation customized to individuals’ microbiota and nutritional profiles. These interventions are crucial for restoring healthy guts and improving outcomes.

Although promising, these approaches are still considered exploratory and require further clinical validation before widespread application.

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