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.

Higher 25‐hydroxyvitamin D levels are associated with greater odds of remission with anti‐tumour necrosis factor‐α medications among patients with inflammatory bowel diseases

“…Vitamin D can be acquired either by endogenous production or through consumption of foods containing vitamin D. Vitamin D is produced when the skin comes in contact with ultraviolet light, and can also be found in egg yolks, as well as certain seafood and dairy products . Some foods such as orange juice may be supplemented with Vitamin D which is absorbed in the small intestine . The vitamin D that is produced or absorbed is metabolised in the liver to produce 25‐hydroxyvitamin D (25‐OH vitamin D), which is activated by the kidney to form 1,25 dihydroxyvitamin D. The primary circulating form of vitamin D is 25‐OH vitamin D, which is often measured clinically to determine vitamin D sufficiency …”

“…While there are insufficient data regarding treatment of IBD with vitamin D, studies have shown that patients who are vitamin D deficient are also likely to have complications of IBD including increased risk of hospitalisation, stricturing disease, surgical resection, pancolitis in UC and use of steroids earlier after diagnosis. 8,9 In addition, higher vitamin D levels have been associated with a higher quality of life among patients with IBD, as measured by the short IBD questionnaire. 10 Compared to placebo, treatment with vitamin D was associated with decreased risk of relapse.…”

Pharmacology of bile acid receptors: Evolution of bile acids from simple detergents to complex signaling molecules

“…Numerous clinical studies and basic research support a role of intestine VDR signaling in the pathogenesis and treatment of inflammatory bowel diseases [116]. Vitamin D deficiency was associated with higher risk of inflammatory bowel diseases, while higher vitamin D intake lowers this risk.…”

Lack of Vitamin D Receptor Causes Dysbiosis and Changes the Functions of the Murine Intestinal Microbiome

“…11,12 Vitamin D supplementation has been reported to have clinical benefit in reducing IBD occurrence and relapse and in improving outcomes. 12 VDR regulates the expression of cathelicidin antimicrobial peptides (CAMPs), β-defensins, and autophagy regulator ATG16L1 [13][14][15] and therefore possesses some antibiotic properties. For example, [1,25(OH) 2 D 3 ] leads to up-regulation of CAMPs and the killing of intracellular Mycobacterium tuberculosis in human monocytes.…”