Neurology · Medical Literature
Effect of vitamin D supplementation on clinical outcomes of patients with Parkinson disease: A randomized controlled study.
Abstract
Vitamin D deficiency is linked to Parkinson disease (PD) pathogenesis; however, clinical trial results remain inconclusive. Thus, in this study, we aimed to evaluate the prevalence of vitamin D deficiency in Thai patients with PD and the efficacy of vitamin D3 supplementation on clinical outcomes in a tropical, sun-abundant region. In this randomized controlled trial, we enrolled 60 patients with PD and 60 healthy controls. Patients with PD were randomized 1:1 to receive 2000 IU/d of vitamin D3 or no additional treatment (control) for 12 weeks. Primary outcomes included changes in MDS-UPDRS, Hoehn and Yahr (mH&Y), Thai Mini-Mental State Examination, and PDQ-39 scores. The secondary outcome was the prevalence of vitamin D deficiency (25(OH)D < 20 ng/mL). At baseline, vitamin D deficiency was significantly more prevalent in patients with PD than in healthy controls (23.2% vs 10.0%, P = .046). After 12 weeks, the vitamin D group showed a significant increase in serum 25(OH)D levels compared to the control group (P < .001, successfully normalizing levels in the deficiency subgroup (30.96 ± 3.18 ng/mL). Although Thai Mini-Mental State Examination scores improved significantly within the vitamin D group (mean difference 1.37, P < .001), a similar improvement occurred in the control group (mean difference 0.93, P = .010), with no significant difference between groups (P = .378). No significant improvements were observed in motor function (MDS-UPDRS, mH&Y) or quality of life (PDQ-39). Vitamin D deficiency is common among Thai patients with PD, despite equatorial proximity. While 2000 IU/d of vitamin D3 safely corrected nutritional deficiency, it provided no significant short-term motor or cognitive benefits.
Clinical relevance
Vitamin D deficiency has been implicated in Parkinson disease (PD) pathogenesis, yet evidence from clinical trials regarding supplementation benefits remains inconclusive. This RCT is clinically relevant because it challenges the assumption that geographic sun exposure confers adequate vitamin D status, demonstrating significant deficiency even in a tropical Thai cohort. Neurologists managing PD patients should be aware that correcting vitamin D deficiency, while safe, may not translate into meaningful short-term motor or cognitive gains.
Key findings
1. Vitamin D deficiency (25(OH)D < 20 ng/mL) was significantly more prevalent in PD patients than healthy controls at baseline (23.2% vs. 10.0%; P = .046), despite residence in a sun-abundant equatorial region. 2. Twelve weeks of vitamin D3 supplementation at 2000 IU/day produced a statistically significant increase in serum 25(OH)D levels compared to controls (P < .001), successfully normalizing levels in the deficiency subgroup (mean post-treatment 25(OH)D: 30.96 ± 3.18 ng/mL). 3. Thai Mini-Mental State Examination (TMSE) scores improved significantly within the vitamin D group (mean difference +1.37; P < .001); however, the control group also demonstrated significant within-group improvement (mean difference +0.93; P = .010), with no statistically significant between-group difference (P = .378), suggesting a practice or placebo effect. 4. No significant between-group improvements were observed in motor function as measured by MDS-UPDRS or modified Hoehn and Yahr (mH&Y) staging after 12 weeks of supplementation. 5. Health-related quality of life, assessed by PDQ-39, showed no significant improvement in the vitamin D supplementation group versus controls over the 12-week treatment period. 6. The supplementation regimen of 2000 IU/day was safe and well-tolerated, effectively correcting nutritional deficiency without reported adverse outcomes in this 60-patient PD cohort.
Practice implications
Clinicians should screen PD patients for vitamin D deficiency regardless of geographic latitude or assumed sun exposure, as deficiency is disproportionately prevalent in this population even in tropical regions. Supplementation with 2000 IU/day of vitamin D3 is appropriate and safe for correcting documented deficiency in PD patients, but prescribers should counsel patients that this dose over 12 weeks does not provide demonstrable short-term improvements in motor performance, cognition, or quality of life. Longer-duration trials with higher doses or in severely deficient subgroups may be warranted before vitamin D supplementation can be recommended as a neuroprotective or disease-modifying adjunct in PD management.