Systematic Review of the Relationship between Vitamin D and Parkinson’s Disease
Journal of Parkinson's Disease, Preprint, pp. 1-9, 2016, DOI: 10.3233/JPD-150615
Rimmelzwaan, Lisanne M.a | van Schoor, Natasja M.b | Lips, Paula | Berendse, Henk W.c | Eekhoff, Elisabeth M.W.a; *
[a] Department of Internal Medicine section Endocrinology, VU University Medical Centre, Amsterdam, The Netherlands |
[b] Department of Epidemiology and Biostatistics, EMGO Institute for Health and Care Research, VU University Medical Centre, Amsterdam, The Netherlands |
[c] Department of Neurology, VU University Medical Centre, Amsterdam, The Netherlands
Correspondence: [*] Correspondence to: Dr. E.M.W. Eekhoff, Department of Endocrinology, VU University Medical Centre (VUmc), De Boelelaan 1117, 1081 HV Amsterdam, The Netherlands. Tel.:+31 20 4444444 (tracer 729); Fax:+31 20 4440588; emw.eekhoff at vumc.nl.
Background: Although vitamin D may have both protective and symptomatic effects in Parkinson’s disease (PD), the evidence is scarce and not well understood. Also, 25-hydroxyvitamin D (vitamin D) is suggested to play a neuroprotective and neurotrophic role in the brain. Therefore, this review investigates the relationship between vitamin D and PD.
Objective: Investigate the evidence for a relationship between vitamin D and PD by summarizing observational and interventional studies in humans, as well as relevant experimental studies.
Methods: A systematic search was made in the Medline, Cochrane and Embase databases (from inception to March 2014). All identified titles were independently evaluated by two reviewers. Articles were selected based on the presence of PD-related outcome data. Included were observational studies (including genetic studies) and interventional studies in humans, as well as relevant animal studies.
Results: A total of 20 studies (
- 14 observational,
- 1 interventional and
- 5 rodent studies)
were selected for analysis. Eight observational studies showed that serum 25(OH) D levels tend to be low in PD. One observational study indicated that low serum 25(OH) D may worsen automatic postural responses and one interventional study suggested that vitamin D supplementation can prevent worsening (based on the Hoehn and Yahr rating scale). Studies in rodent models of PD showed a protective effect of vitamin D treatment on dopaminergic neurons in the substantia nigra. Results of genetic studies on the association between vitamin D receptor polymorphisms and the risk of PD were contradictory.
Conclusion: The literature supports possible protective and symptomatic effects of vitamin D in PD. However, more observational and interventional studies in humans are needed to confirm and further elucidate the suggested beneficial effect of vitamin D on PD.
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