Modifiable Environmental Factors in Inflammatory Bowel Disease

• Published in: Current gastroenterology reports Vol. 19; no. 5; p. 21
• Main Authors: Burke, Kristin E., Boumitri, Christine, Ananthakrishnan, Ashwin N.
• Format: Journal Article
• Language: English
• Published: New York Springer US 01-05-2017; Springer Nature B.V
• Subjects: Cohort analysis; Crohns disease; Diet; Diet - adverse effects; Dietary Supplements; Enteral nutrition; Enteral Nutrition - methods; Environment; Gastroenterology; Humans; Inflammation; Inflammatory bowel disease; Inflammatory Bowel Disease (S Hanauer; Inflammatory Bowel Diseases - etiology; Inflammatory Bowel Diseases - therapy; Influence; Medicine; Medicine & Public Health; Nicotine; Nutrition research; Pathogenesis; Pediatrics; Remission (Medicine); Risk Factors; Section Editor; Sleep Wake Disorders - complications; Smoking - adverse effects; Smoking cessation; Stress, Psychological - complications; Tobacco; Topical Collection on Inflammatory Bowel Disease; Environment; Diet; Crohn’s disease; Ulcerative colitis; Smoking
• ISSN: 1522-8037; 1534-312X
• DOI: 10.1007/s11894-017-0562-0

Purpose of Review
Environmental factors may influence predisposition to develop inflammatory bowel diseases (Crohn’s disease, ulcerative colitis) or alter its natural history by modification of both the host immune response and intestinal microbial composition. The purpose of this review is to translate such evidence into clinical practice by a focus on interventional studies that have modified such environmental influences to improve disease outcomes.
Recent Findings
Several environmental influences have been identified in the recent literature including tobacco use, diet, antibiotics, vitamin D deficiency, stress, appendectomy, and oral contraceptive use. Some risk factors have similar influences on both Crohn’s disease and ulcerative colitis while others are disease-specific or have divergent effects.
Summary
Emerging epidemiologic evidence has confirmed the association of many of these factors with incident disease using prospective data. In addition, laboratory data has supported their mechanistic plausibility and relevance to intestinal inflammation.