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

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.

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  • Authors+Show Affiliations

    ,

    Department of Neurology, Katsushika Medical Center and the Division of Molecular Epidemiology, Jikei University School of Medicine, Tokyo, Japan.

    , , , , ,

    Source

    MeSH

    Aged
    Blood Pressure
    Body Mass Index
    Calcium, Dietary
    Cholecalciferol
    Dietary Supplements
    Disease Progression
    Double-Blind Method
    Endpoint Determination
    Female
    Follow-Up Studies
    Genotype
    Humans
    Male
    Middle Aged
    Parathyroid Hormone
    Parkinson Disease
    Questionnaires
    Receptors, Calcitriol

    Pub Type(s)

    Journal Article
    Randomized Controlled Trial
    Research Support, Non-U.S. Gov't

    Language

    eng

    PubMed ID

    23485413

    Citation

    TY - JOUR T1 - Randomized, double-blind, placebo-controlled trial of vitamin D supplementation in Parkinson disease. AU - Suzuki,Masahiko, AU - Yoshioka,Masayuki, AU - Hashimoto,Masaya, AU - Murakami,Maiko, AU - Noya,Miki, AU - Takahashi,Daisuke, AU - Urashima,Mitsuyoshi, Y1 - 2013/03/13/ PY - 2013/3/13/aheadofprint PY - 2013/3/15/entrez PY - 2013/3/15/pubmed PY - 2013/6/19/medline SP - 1004 EP - 13 JF - The American journal of clinical nutrition JO - Am. J. Clin. Nutr. VL - 97 IS - 5 N2 - 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. SN - 1938-3207 UR - https://www.unboundmedicine.com/medline/citation/23485413/full_citation L2 - http://www.ajcn.org/cgi/pmidlookup?view=long&pmid=23485413 ER -