title: Vitamin D improves inflammatory bowel disease outcomes: basic science and clinical review.
abstract: Vitamin D deficiency is commonly diagnosed among patients with inflammatory bowel disease (IBD). Patients with IBD are at risk of low bone density and increased fractures due to low vitamin D levels, long standing disease, and frequent steroid exposures; as a result, it is well established that vitamin D supplementation in this population is important. There is increasing support for the role of vitamin D in strengthening the innate immune system by acting as an immunomodulator and reducing inflammation in experimental and human IBD. The active form of vitamin D, 1,25(OH)D3, acts on T cells to promote T helper (Th)2/regulatory T responses over Th1/Th17 responses; suppresses dendritic cell inflammatory activity; induces antibacterial activity; and regulates cytokine production in favor of an anti-inflammatory response. Murine and human IBD studies support a therapeutic role of vitamin D in IBD. Risk factors for vitamin D deficiency in this population include decreased sunlight exposure, disease duration, smoking, and genetics. Vitamin D normalization is associated with reduced risk of relapse, reduced risk of IBD-related surgeries, and improvement in quality of life. Vitamin D is an inexpensive supplement which has been shown to improve IBD outcomes. However, further research is required to determine optimal serum vitamin D levels which will achieve beneficial immune effects, and stronger evidence is needed to support the role of vitamin D in inducing disease response and remission, as well as maintaining this improvement in patients' disease states.
authors.affiliation: Krista M Reich, Richard N Fedorak, Karen Madsen, Karen I Kroeker, Division of Gastroenterology, University of Alberta, Edmonton, Alberta T6G 2X8, Canada.
authors.forename: Krista M
authors.initials: KM
authors.lastname: Reich
authors.affiliation: Krista M Reich, Richard N Fedorak, Karen Madsen, Karen I Kroeker, Division of Gastroenterology, University of Alberta, Edmonton, Alberta T6G 2X8, Canada.
authors.forename: Richard N
authors.initials: RN
authors.lastname: Fedorak
authors.affiliation: Krista M Reich, Richard N Fedorak, Karen Madsen, Karen I Kroeker, Division of Gastroenterology, University of Alberta, Edmonton, Alberta T6G 2X8, Canada.
authors.forename: Karen
authors.initials: K
authors.lastname: Madsen
authors.affiliation: Krista M Reich, Richard N Fedorak, Karen Madsen, Karen I Kroeker, Division of Gastroenterology, University of Alberta, Edmonton, Alberta T6G 2X8, Canada.
authors.forename: Karen I
authors.initials: KI
authors.lastname: Kroeker
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use*; D019587:Dietary Supplements; D004195:Disease Models, Animal; D005765:Gastrointestinal Agents / Q000627:therapeutic use*; D006801:Humans; D015212:Inflammatory Bowel Diseases / Q000150:complications / Q000175:diagnosis / Q000188:drug therapy* / Q000276:immunology; D016896:Treatment Outcome; D014807:Vitamin D / Q000097:blood / Q000627:therapeutic use*; D014808:Vitamin D Deficiency / Q000097:blood / Q000150:complications / Q000175:diagnosis / Q000188:drug therapy* / Q000276:immunology
chemical_list: D000893:Anti-Inflammatory Agents; D005765:Gastrointestinal Agents; D014807:Vitamin D
keywords: Cytokines; Immune response; Inflammation; Inflammatory bowel disease; Supplementation; Vitamin D