create counter
Vitamin D and MS: Vieth


Professor at the University of Toronto in the Department of of Laboratory Medicine and Pathobiology, as well as in the Department of Nutritional Sciences, Faculty of Medicine, University of Toronto, Toronto, Canada M5S 3E2
T +1 416 978 2747

Prof. Reinhold Vieth recently retired as director of the Bone and Mineral Group Laboratory at Mount Sinai Hospital, and remains active as a Professor at the University of Toronto in the Department of Laboratory Medicine and Pathobiology, as well as in the Department of Nutritional Sciences. He is an expert on the clinical nutrition, pharmacology and safety of vitamin D, and he has served as an expert adviser on vitamin D-related matters for the Institutes of Medicine, the Centers for Disease Control in Washington, the American Geriatric Society and Health Canada. he has been the principal investigator on many clinical trials involving vitamin D, ranging from osteoporosis, to multiple sclerosis and prostate dancer. Currently, his work relates to the utility of higher doses of vitamin D in health maintenance.

Pharmacology of vitamin D: dosing regimes and toxicity
Pharmacological principles of the dosage, efficacy and therapeutic index of ergocalciferol and cholecalciferol [vitamin D2 and D3 respectively] are rarely addressed. Vitamin D is a pro-drug, activated within the body into its major circulating metabolite, 25-hydroxyvitamin D [25(OH)D], the inactive compound measured to indicate vitamin D adequacy. Vitamin D2 is not physiological, because it exhibits different pharmacology and it is normally present in minimal amounts compared to vitamin D3. The biologically useful half-life for the combination of vitamin D3 and 25(OH)D3 is approximately 8 wk. Therefore, at a sustained vitamin D3 dose, the plateau concentration is reached after about 24 wk of treatment, and that assumes no change to its metabolic clearance. Implications of the unique, 1st-order (below Km) enzyme kinetics of the vitamin D system are usually ignored, but they can explain adverse effects of vitamin D treatment. Changes in dose need to be accompanied by adaptation of the enzymes of the vitamin D system. Large, intermittent doses of vitamin D can elicit signs of both vitamin D excess and, ironically, deficiency. Evidence regarding a suitable dosing interval remains limited. The time interval between maintenance doses of vitamin D should probably be no longer than 1 mo.

Google Scholar: R Vieth
PubMed: Veith R

Prospects for Vitamin D Nutrition
Vitamin D - Q&A with Dr. Reinhold Vieth

Clinical trials
Start Date: January 2010
Supplementation of VigantOL® Oil Versus Placebo as Add-on in Patients With Relapsing Remitting Multiple Sclerosis Receiving Rebif® Treatment (SOLAR)
>> NCT01285401

Start Date: August 2009 - completed
Vitamin D3 Supplementation and the T Cell Compartment in Multiple Sclerosis (MS)

>> NCT00940719

Start Date: July 2006 - completed
Safety Trial of High Dose Oral Vitamin D3 With Calcium in Multiple Sclerosis (VitD4MS)
>> NCT00644904

Research Interests
Current research focuses on the roles played by vitamin D in osteoporosis, and cancers of the breast and prostate.

Vitamin D Nutrition
Our research focuses on clinical trails involving vitamin D intakes that correct for the lack of vitamin D caused by the Canadian environment. The aim is to find out if health benefits that are implied from basic science and from epidemiological investigations can be realized by consuming more vitamin D. Our clinical goal is to find out whether postmenopausal bone loss can be minimized, and osteoporosis prevented. The goal of our basic science research is to find out what genes are induced by improved vitamin D nutrition. Some recent publications reflecting these interests are listed below.

Vitamin D levels in MS patients and their families
Reinhold Vieth, PhD, University of Toronto; A. Dessa Sadovnick, PhD, University of British Columbia; and George Ebers, MD, University of Oxford
$276,000 (April 1, 2006 – March 31, 2008)
There is growing evidence that the interplay between genes and the environment determines susceptibility to MS. One very striking clue about a role for the environment is that MS increases the farther away one lives from the equator. In Australia, the incidence of MS in temperate Tasmania is five times greater than in subtropical Queensland, despite the similar ethnic origins of the
inhabitants. Very few foods contain vitamin D so geographical location would definitely influence vitamin D levels because people living further away from the equator don’t get enough sunlight (UVB) for the skin to make vitamin D during winter months. The focus of the research is to compare vitamin D levels in people with and without a risk for MS. The researchers are measuring the levels of vitamin D in identical and fraternal twins, in people with MS and their families (3,500 individuals in total), and in mothers with multiple children having MS. Improving vitamin D nutrition could be implemented fairly easily and safely, and in a costeffective way. If they find a link between vitamin D and MS, then the research may provide the evidence needed to begin clinical studies of vitamin D-based strategies to prevent MS.

A phase I dose escalation study of vitamin D3 with calcium supplementation in patients with multiple sclerosis
M.R. Ursell, R. Vieth, P.W. O'Connor, B. Gray, S. Kimball (Toronto, CAN)
Background: There is growing epidemiological and biological evidence to suggest that vitamin D3 status may play a role in the development and/or progression of multiple sclerosis. In support, a recent large observational study showed an inverse relationship between vitamin D3 supplementation and the risk of developing MS. Unfortunately, the recommended adequate intake (AI) of vitamin D3 is targeted towards calcium homeostasis, and doses required for the treatment of non-bone disease remain unknown, although they are hypothesized to be much higher than currently recommended doses used for the prevention of Rickets and osteoporosis. Due to concerns of causing hypercalcemia, no study has been conducted to assess the effect of larger doses of vitamin D3 on implicated diseases such as MS. Objective: In order to characterize the therapeutic safety of higher doses of vitamin D3 in multiple sclerosis, we conducted a phase I dose-escalation study in 12 patients. Design: Escalating doses of vitamin D3 (4,000–40,000 IU/d) were given orally over 28 weeks to 12 patients with clinically definite MS. MRI scans with gadolinium were obtained at baseline and trial completion to assess for radiological evidence of disease exacerbation. Expanded Disability Status Scores (EDSS), Ambulation Indices (AI) and relapse rates were assessed for each participant. Vitamin D3 nutritional status and calcium homeostasis were assessed by measuring 25-hydroxyvitamin D3 (25(OH)D) levels, parathyroid hormone (PTH), serum calcium and urine calcium:creatinine ratios. Results: Mean serum 25(OH)D concentrations increased significantly from 79.4 to 452.6 nmol/L (p<0.02). The highest serum vitamin D3 level attained was 800 nmol/L. PTH levels declined from a basal mean concentration of 2.76 to 1.28 pmol/L (p<0.03). Serum and urine calcium levels remained within normal ranges (2.2-2.6mmol/L) for all participants. MRI and clinical data is being analyzed and will be presented for the 12 participants. Conclusions: Despite attaining serum levels that well exceeded the traditionally accepted “toxic” level for vitamin D3 nutritional status (>250 nmol/L), no participant developed hypercalcemia or adverse clinical effects on doses of vitamin D3 as high as 40,000 IU/day. This data provides a new perspective on the safety of vitamin D3 supplementation for the treatment and/or prevention of diseases such as MS, and will be used to help determine an optimal dose of vitamin D3 in a phase II efficacy trial.

Terms of Use