The safety and efficacy of Vitamin D and probiotic therapy in mild-to-moderate ulcerative colitis

Excerpt from the ACNEM Journal (June 2021)

 

BY CHLOE WORTHINGTON 

Chloe is an ACNEM student member with a special interest in digestive health and patient-centred, evidence-based integrative healthcare and nutraceutical research. Chloe is passionate about exploring the power of optimal nutrition and nature connectedness for healing, vitality, and wellness.

 

INTRODUCTION

Environmental influences exert important roles on the pathogenesis of inflammatory bowel disease [ IBD] (Vedamurthy, 2019). Ulcerative colitis [UC] is a chronic, relapsing and remitting IBD affecting the colonic mucosa. Globally, the incidence and prevalence of IBD and UC are increasing and associated with economic burden and reduced quality of life [QOL] (Naghavi, 2020, p. 18). Vitamin D [VitD] is anti-inflammatory and has been shown to support nnate immune functionality. Probiotics mediate microbial diversity, correct dysbiosis and restore epithelial integrity. A comprehensive literature search was conducted online with strict inclusion/exclusion criteria. Published randomized controlled trials (RCTs) were included from electronic databases (Embase, PubMed, Web of Science, Cochrane library and so forth). This paper methodically examines 4 Systematic Reviews [SRs] and Meta-Analyses [MAs] and 4 randomised controlled trials [RCTs] pertaining to the safety/efficacy of VitD and probiotics in UC. Please refer to appendix 1 for the inclusion criteria.

 

ULCERATIVE COLITIS

Pathophysiology

The etiopathogenesis of UC is complex, progressive and involves defective colonic mucin and tight junction protein expression. Impaired epithelial integrity alters microbiota composition and induces unfavourable, abnormal dendritic and T-helper [Th] cell activity (Lynch & Hsu, 2021). This provokes leukocyte recruitment, adhesion and extravasation, and tumour necrosis factor alpha [TNFα] and interleukin [IL]-13 cytokine release. These conditions perpetuate diffuse inflammation, friability and superficial erosions, which presents as diarrhoea, abdominal pain, tenesmus and rectal bleeding.

Aetiology

UC is multifactorial and idiopathic. Colonic inflammation (from dysbiosis and autoimmunity) is believed to originate from genetic, microbial, psychological and environmental risk factors. External environmental factors such as geography and urban living, latitude of residence, cigarette smoking and air pollution play a role in hypovitaminosis, in particular the synthesis of VitD (Manicourt, 2008; Barrea, 2017). Other internal environmental factors such as diet, family history, ethnicity (European and North American), pathogenic exposure, pharmaceutical use (oral contraceptives, nonsteroidal anti-inflammatory drugs, antibiotics) and single-nucleotide polymorphisms (interleukin genes and human leukocyte class II antigens) (Li et al., 2018, p. 126; Vedamurthy, 2019) also play a role. Sarlos et al., (2014, p. 316) identified that UC progression is exacerbated/sustained by chronic stress, unhygienic lifestyle, VitD deficiency and poor nutrition. A Nurses Health Study identified physical activity to decrease the risk of the disease, highlighting the importance of a person-centered approach to UC care (Khakiki, 2013).

Read Chloe’s full article here which includes proposed nutritional therapeutics, a literature review and case studies.

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