title: 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.
  
  
  METHODS
  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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Neurology, Katsushika Medical Center and the Division of Molecular Epidemiology, Jikei University School of Medicine, Tokyo, Japan.
authors.forename: Masahiko
authors.initials: M
authors.lastname: Suzuki
authors.forename: Masayuki
authors.initials: M
authors.lastname: Yoshioka
authors.forename: Masaya
authors.initials: M
authors.lastname: Hashimoto
authors.forename: Maiko
authors.initials: M
authors.lastname: Murakami
authors.forename: Miki
authors.initials: M
authors.lastname: Noya
authors.forename: Daisuke
authors.initials: D
authors.lastname: Takahashi
authors.forename: Mitsuyoshi
authors.initials: M
authors.lastname: Urashima
mesh_terms: D000368:Aged; D001794:Blood Pressure; D015992:Body Mass Index; D002136:Calcium, Dietary / Q000097:blood; D002762:Cholecalciferol / Q000008:administration & dosage* / Q000097:blood; D019587:Dietary Supplements; D018450:Disease Progression; D004311:Double-Blind Method; D023381:Endpoint Determination; D005260:Female; D005500:Follow-Up Studies; D005838:Genotype; D006801:Humans; D008297:Male; D008875:Middle Aged; D010281:Parathyroid Hormone / Q000097:blood; D010300:Parkinson Disease / Q000188:drug therapy* / Q000235:genetics; D018167:Receptors, Calcitriol / Q000235:genetics / Q000378:metabolism; D011795:Surveys and Questionnaires
chemical_list: D002136:Calcium, Dietary; D010281:Parathyroid Hormone; D018167:Receptors, Calcitriol; D002762:Cholecalciferol