BACKGROUND: Previous cross-sectional studies have shown that Parkinson's disease (PD) patients have lower serum 25-hydroxy vitamin D (25(OH)D) concentrations than controls. Vitamin D deficiency was associated with increased disease severity and cognitive impairment in prevalent PD patients.
OBJECTIVE: The aim of the study was to determine 25(OH)D in newly diagnosed PD and age-matched controls and to assess if there was an association with clinical outcomes (disease severity, cognition and falls) over the 36-month follow up period.
METHODS: A prospective observational study of newly diagnosed PD patients in the North East of England with age-matched controls (PD, n = 145; control, n = 94). Serum 25(OH)D was assessed at baseline and 18 months. Participants underwent clinical assessment at baseline, 18 and 36 months. One hundred and ten participants with PD also took part in a prospective falls study.
RESULTS: Mean serum 25(OH)D concentrations were lower in PD than control participants at baseline (44.1±21.7 vs. 52.2±22.1 nmol/L, p < 0.05) and 18 months (44.2±23.6 vs. 55.7±28.8 nmol/L, p < 0.05). Baseline serum 25(OH)D concentration, age, motor score and dosage of dopaminergic medication were significant predictors of variance of motor severity at 36 months ((ΔR2 = 0.039, F = 6.6, p < 0.01). Serum 25(OH)D was not associated with cognition or falls during the follow up period.
CONCLUSIONS: Patients with incident PD had significantly lower serum 25(OH)D concentrations than age-matched controls, which may have implications in terms of bone health and fracture risk. There was a small but significant association between vitamin D status at baseline and disease motor severity at 36 months.
Bibliographical noteThe authors acknowledge the study funders, Parkinson’s UK (J-0802), Newcastle University
Lockhart Parkinson’s Disease fund and the Newcastle Biomedical Research Centre. The research was supported by the National Institute of Health Research (NIHR) Newcastle Biomedical Research Unit based at Newcastle upon Tyne Hospitals NHS Foundation Trust/Newcastle University. The research was also supported by NIHR Newcastle CRF Infrastructure funding. Newcastle University acknowledge the support of the NIHR, through the Dementias and Neurodegenerative Diseases Research Network. IS was supported by a NIHR clinical fellowship. The authors would like to thank Sarah Meadows and her colleagues Nutritional Biomarker Analysis laboratory at MRC Elsie Widdowson Laboratory for the analyses of 25 hydroxyvitamin D. The views expressed are those of the authors and
not necessarily those of the NHS, the NIHR, or the Department of Health.
- disease progression
- 25-hydroxy vitamin D
- Parkinson's disease
- vitamin D