Abstract

Epidemiological and experimental studies have suggested that diet is one of the environmental factors that contributes to the onset and pathophysiology of ulcerative colitis. Although many patients suffering from ulcerative colitis attribute their symptoms or disease relapse to dietary factors, only a few well-designed randomized controlled trials have been done to investigate the role of diet in the management of ulcerative colitis. Here, we review the potential mechanisms of the relationship between diet and pathogenesis of ulcerative colitis and summarize randomized controlled dietary interventions that have been conducted in ulcerative colitis patients.

Highlights

  • Ulcerative colitis (UC)—a subtype of inflammatory bowel disease (IBD)—is a chronic, idiopathic inflammatory disease that affects the colon and is characterized by relapsing and remitting mucosal inflammation [1]

  • Early-life events such as mode of birth, breastfeeding, and exposure to antibiotics and other factors such as air pollution, smoking, psychological state, exercise, and diet are among the potential environmental contributors of IBD development or disease activity [3]

  • It has been suggested that environmental factors including diet play an important role in the pathophysiology of IBD and especially in UC, a chronic colonic inflammation

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Summary

Introduction

Ulcerative colitis (UC)—a subtype of inflammatory bowel disease (IBD)—is a chronic, idiopathic inflammatory disease that affects the colon and is characterized by relapsing and remitting mucosal inflammation [1]. UC patients mostly present blood in the stool and diarrhea [1]. UC is associated with major morbidity in Western countries, and its incidence is increasing in developing countries [2]. It has been suggested that environmental factors play a major role in the pathogenesis of IBD. Early-life events such as mode of birth, breastfeeding, and exposure to antibiotics and other factors such as air pollution, smoking, psychological state, exercise, and diet are among the potential environmental contributors of IBD development or disease activity [3]

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