Randomized, double-blind, placebo-controlled trial of vitamin D supplementation in Parkinson disease

doi:10.3945/ajcn.112.051664

The American Journal of Clinical Nutrition

Volume 97, Issue 5, May 2013, Pages 1004-1013

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ABSTRACT

Background:

In our previous study, higher serum 25-hydroxyvitamin D [25(OH)D] concentrations and the vitamin D receptor (VDR) FokI CC genotype were associated with milder Parkinson disease (PD).

Objective:

We evaluated whether vitamin D₃ supplementation inhibits the progression of PD on the basis of patient VDR subgroups.

Design:

Patients with PD (n = 114) were randomly assigned to receive vitamin D₃ supplements (n = 56; 1200 IU/d) or a placebo (n = 58) for 12 mo in a double-blind setting. Outcomes were clinical changes from baseline and the percentage of patients who showed no worsening of the modified Hoehn and Yahr (HY) stage and Unified Parkinson’s Disease Rating Scale (UPDRS).

Results:

Compared with the placebo, vitamin D₃ significantly prevented the deterioration of the HY stage in patients [difference between groups: P = 0.005; mean ± SD change within vitamin D₃ group: +0.02 ± 0.62 (P = 0.79); change within placebo group: +0.33 ± 0.70 (P = 0.0006)]. Interaction analyses showed that VDR FokI genotypes modified the effect of vitamin D₃ on changes in the HY stage (P-interaction = 0.045), UPDRS total (P-interaction = 0.039), and UPDRS part II (P-interaction = 0.021). Compared with the placebo, vitamin D₃ significantly prevented deterioration of the HY stage in patients with FokI TT [difference between groups: P = 0.009; change within vitamin D₃ group: -0.38 ± 0.48 (P = 0.91); change within placebo group, +0.63 ± 0.77 (P = 0.009)] and FokI CT [difference between groups: P = 0.020; change within vitamin D₃ group: ±0.00 ± 0.60 (P = 0.78); change within placebo group: +0.37 ± 0.74 (P = 0.014)] but not FokI CC. Similar trends were observed in UPDRS total and part II.

Conclusion:

Vitamin D₃ supplementation may stabilize PD for a short period in patients with FokI TT or CT genotypes without triggering hypercalcemia, although this effect may be nonspecific for PD. This trial was registered at UMIN Clinical Trials Registry as UMIN000001841.

Cited by (0)

^¹: From the Department of Neurology, Katsushika Medical Center (MS, MY, MH, MM, and MN) and the Division of Molecular Epidemiology (MN, DT, and MU), Jikei University School of Medicine, Tokyo, Japan.

^²: Funders had no role in the study design, data collection and analysis, decision to publish, or preparation of the manuscript.

^³: Supported by the Ministry of Education, Culture, Sports, Science and Technology in the Japan-Supported Program for the Strategic Research Foundation at Private Universities and the Jikei University School of Medicine.

^⁴: Address correspondence and reprint requests to M Urashima, Division of Molecular Epidemiology, Jikei University School of Medicine, 3-25-8 Nishi-shimbashi, Minato-ku, Tokyo 105-8461, Japan. E-mail: [email protected].

^⁵: Abbreviations used: EQ-5D, EuroQol 5 Dimension; HY, Hoehn and Yahr; LED, levodopa equivalency dose; MMSE, Mini-Mental State Examination; PD, Parkinson disease; PDQ39, Parkinson’s Disease Questionnaire-39; UPDRS, Unified Parkinson’s Disease Rating Scale; VDR, vitamin D receptor; 1,25(OH)D, 1,25-dihydroxyvitamin D; 25(OH)D, 25-hydroxyvitamin D.