Randomized, double-blind, placebo-controlled trial of vitamin D supplementation in Parkinson disease.
What this study found
Vitamin D3 generally favored slower Parkinson disease progression, with benefit most apparent in patients with VDR FokI TT or CT genotypes. Hoehn and Yahr stage changed less in the vitamin D3 group than in placebo (+0.02 ± 0.62 vs +0.33 ± 0.70; P = 0.005), and more vitamin D3 participants had no worsening or improvement in HY stage (29.1% vs 12.3%; RR 2.37, 95% CI 1.06-5.31; P = 0.028). UPDRS total did not differ significantly (P = 0.11), but UPDRS part II and several PDQ-39 domains favored vitamin D3, including no worsening or improvement in UPDRS part II (47.3% vs 28.1%; RR 1.68, 95% CI…
- Study & population
- Randomized, double-blind, placebo-controlled trial in adults with Parkinson disease aged 45-85 years at Katsushika Medical Center in Tokyo, Japan.
- Intervention
- Vitamin D3 (cholecalciferol) was given orally as a tablet at 1200 IU/day for 12 months.
- Key limitation
- The trial was relatively small, and the genotype-specific conclusion limits generalizability.
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Open PDFOriginal 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.