Dr. Halima Phelps, DC, ND. This study demonstrated that cholecalciferol at a dose of 40,000 IU per week for a period of four weeks significantly reduced neuropathy severity and inflammation and improved skin microcirculation in participating diabetics.
Vitamin D is commonly known as the “sunshine vitamin,” but is more accurately classified as a steroid hormone due to its biological effects 1. It has far-reaching implications in various organs and systems in the body, as well as regulatory potential in diseases such as autoimmunity and diabetes mellitus types 1 and 2 1. Commonly-known medical associations that are made with a deficiency of vitamin D are osteomalacia and rickets 1. However, further research is also revealing potential associations between adequate vitamin D levels and the potential mitigation of the development of diabetes, as well as the alleviation of neuropathic pain associated with the advanced state of the condition.
Diabetes mellitus is a global problem, and is estimated by the World Health Organization to continue to rise as time progresses 1. Diabetic peripheral neuropathy (DPN) is a common symptom of the disease and half of patients suffering from diabetes experience this circulatory deficit, which is a primary cause of fatal complications from the disease; it is a very significant concern 1,2. Unfortunately, DPN has also been difficult to treat; partially due to a comprehension deficit concerning its disease mechanisms 1-3 . A couple of factors that are believed to contribute to the disease progression are the presence of glycated hemoglobin (measured in a hemoglobin A1c test [HbA1c]) and inflammation 1,3. This study examines the therapeutic effects of low and high-dose vitamin D in the form of cholecalciferol on DPN and inflammation over a period of 24 weeks.
This prospective randomized trial included a group of 67 males and females ages 18-65 (n=33 and n=34 respectively), with an average BMI measured at 30.2 kg/m2, and a pre-existing minimum 5 year diagnosis of type 2 diabetes mellitus (T2DM), as well as DPN. Patients maintained their previous diabetic medication intake status. They were randomized into two groups, wherein Group I (n=34) was assigned 5,000 IU of oral cholecalciferol per week, and Group II (n=33) was assigned 40,000 IU of oral cholecalciferol per week. Baseline data on each participant was obtained, including patient demographics, disease and social history and treatments, as well as body measurements. They were also tested for DPN using the neuropathic symptomatic and disability scores (NSS/NDS), and the visual analogue scale (VAS). Blood work was obtained at baseline and at the end of therapies for assessment, which included serum total cholesterol (TC), C-reactive protein (CRP), HbA1c, vitamin D levels (serum 25(OH)D), parathyroid hormone (PTH), interleukin (IL) testing (via enzyme-linked immunosorbent assay [ELISA]), and tumor necrosis factor-α (TNF-α). Skin microcirculation was also tested at the trial’s start and finish via laser Doppler flowmetry (LDF) to assess circulatory sufficiency.
Study results revealed that vitamin D levels were augmented in both trial groups at the conclusion of the therapies: however, 100% of the patients assigned the high dose of 40,000 IU (Group II) vitamin D obtained normal vitamin D levels compared to only 48.4% of the participants in Group I. It was also noticed at the treatment conclusion that Group II experienced significant improvements in lowering BMI, HbA1c, and IL-6 levels, and higher IL-10 levels (p=0.001, p=0.004, p<0.001, and p<0.001 respectively) and 61% of the cohort lost weight; none of which applied to the 5,000 IU (Group I) cohort. Neither cohort experienced significant benefits with total cholesterol, PTH, IL-1β, or CRP levels; however, Group II experienced significantly-lowered HbA1c levels with vitamin D intake (p=0.031), and it was noted that the lowering of HbA1c possessed a relationship with decreased neurological pathology. Neurological deficiencies improved in Group II by decreasing from a score of 8 to 6, p=0.001, pain levels decreased from 50 to 47 on the VAS scale (p=0.001), and neuropathies declined from 5 to 4 (p=0.001); these changes did not apply to Group I. Finally, microcirculation in Group II improved, whereas there was no significant improvement in Group I (p<0.001) at treatment conclusion.
This study confirms a positive association between high-dose vitamin D supplementation and the mitigation of diabetic symptomology. As a simple measure, such an effective remedy should be considered for implementation in routine diabetic therapies. Further considerations should include assessment of potential risks from taking high dose vitamin-D for extended periods of time as it is a fat-soluble supplement; as well as an evaluation of a time limitation that is possibly safe to dose the supplement for therapeutic benefits. Also, further studies should conclude whether cholecalciferol will have to be dosed periodically following the preliminary treatment to maintain the health benefits, and how often testing should be performed.
Source: Karonova T, Stepanova A, Bystrova A, Jude EB. High-Dose Vitamin D Supplementation Improves Microcirculation and Reduces Inflammation in Diabetic Neuropathy Patients. Nutrients. 2020; 12(9):2518.
© 2020 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/)
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Posted November 24, 2020.
References:
- Qu GB, Wang LL, Tang X, Wu W, Sun YH. The association between vitamin D level and diabetic peripheral neuropathy in patients with type 2 diabetes mellitus: An update systematic review and meta-analysis. J Clin Transl Endocrinol. 2017;9:25-31.
- Pop-Busui R, Ang L, Holmes C, Gallagher K, Feldman EL. Inflammation as a Therapeutic Target for Diabetic Neuropathies. Curr Diab Rep. 2016;16(3):29.
- Pop-Busui R, Boulton AJ, Feldman EL, et al. Diabetic Neuropathy: A Position Statement by the American Diabetes Association. Diabetes Care. 2017;40(1):136-154.
