<unk>  is a complex disease which arises as a result of the interaction of environmental and genetic factors leading to immunological responses and inflammation in the intestine. Diet A 2022 study found that diets with increased intake of fruits and vegetables, reduction of processed meats and refined carbohydrates, and preference of water for hydration were associated with lower risk of active symptoms with<unk> , although increased intake of fruits and vegetables alone did not reduce risk of symptoms with Crohn's disease. Dietary patterns are associated with a risk for ulcerative colitis. In particular, subjects who were in the highest tertile of the healthy dietary pattern had a 79% lower risk of ulcerative colitis. Gluten sensitivity is common in<unk>  and associated with having flareups. Gluten sensitivity was reported in 23.6 and 27.3% of Crohn's disease and ulcerative colitis patients, respectively. A diet high in protein, particularly animal protein, and/or high in sugar may be associated with increased risk of<unk>  and relapses. Microbiota As a result of microbial symbiosis and immunity, alterations in the gut microbiome may contribute to<unk>  gut diseases.<unk> -affected individuals have been found to have 30–50 percent reduced biodiversity of commensal bacteria, such as decreases in Bacillota (namely Lachnospiraceae) and Bacteroidota. Further evidence of the role of gut flora in the cause of<unk>  is that<unk> -affected individuals are more likely to have been prescribed antibiotics in the 2–5 year period before their diagnosis than unaffected individuals. The enteral bacteria can be altered by environmental factors, such as concentrated milk fats (a common ingredient of processed foods and confectionery) or oral medications such as antibiotics and oral iron preparations. The mucosal microbiota in the large intestine of<unk>  patients with active inflammation was found to be associated with pro-inflammatory changes to the host epigenome. However, large international studies have failed to identify a single microbial biomarker of<unk>  indicating it's not driven by any single micro-organism. Breach of intestinal barrier Loss of integrity of the intestinal epithelium plays a key pathogenic role in<unk> . Dysfunction of the innate immune system as a result of abnormal signaling through immune receptors called toll-like receptors (TLRs)—which activates an immune response to molecules that are broadly shared by multiple pathogens—contributes to acute and chronic<unk>  processes in<unk>  colitis and associated cancer. Changes in the composition of the intestinal microbiota are an important environmental factor in the development of<unk> . Detrimental changes in the intestinal microbiota induce an inappropriate (uncontrolled) immune response that results in damage to the intestinal epithelium. Breaches in this critical barrier (the intestinal epithelium) allow further infiltration of microbiota that, in turn, elicit further immune responses.<unk>  is a multifactorial disease that is nonetheless driven in part by an exaggerated immune response to gut microbiota that causes defects in epithelial barrier function. Oxidative stress and DNA damage Pereira et al. reviewed evidence from numerous studies indicating that oxidative stress and DNA damage likely have a role in the pathophysiology of<unk> . Oxidative DNA damage as measured by 8-OHdG levels was found to be significantly increased in patients with<unk>  compared to control patients, and in inflamed mucosa compared with non-inflamed mucosa.
Inflammatory bowel disease
Coeliac disease
Crohn's disease
Irritable bowel syndrome
Gastroenteritis
Ulcerative colitis
Anorexia nervosa
Chemical colitis