Low butyrate availability in anorexia nervosa disrupts the intestinal barrier by causing inflammation, and as carbohydrate-fermenting microorganisms decrease, mucin-degrading organisms tend to increase. They slowly grow and expand due to delayed colonic transit, allowing them to digest the intestine's protective mucus layer to survive in a malnourished gut environment. These changes may increase intestinal permeability and allow bacterial products to enter systemic circulation, becoming a potential risk factor for autoimmune diseases and other atypical immune responses in anorexia nervosa patients and possibly contributing to appetite dysregulation and psychopathology. Increased levels of pro-inflammatory cytokines and autoantibodies against appetite-modulating neuropeptides like α-melanocyte-stimulating hormone (α-MSH) have been found in patients. α-MSH autoantibodies are thought to react with proteins in the intestinal barrier, potentially causing anorexia nervosa by impairing satiety pathways.