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Nutritional Neuroscience
An International Journal on Nutrition, Diet and Nervous System
Volume 25, 2022 - Issue 6
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Research Article

Clinical correlates of serum 25-hydroxyvitamin D in Parkinson’s disease

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Pages 1128-1136 | Published online: 05 Nov 2020
 

ABSTRACT

Background

Parkinson’s disease (PD) patients have lower levels of serum 25-hydroxyvitamin D (25(OH)D) than the general population. Previous studies have suggested a negative association between 25(OH)D and clinical features of PD, but the data are inconsistent.

Materials and Methods

We conducted a cross-sectional, observational study. Serum 25(OH)D, disease (Hoehn-Yahr stage [HY]) and clinical symptom (Unified Parkinson Disease Rating Scale [UPDRS]) severity and global cognitive functions (Mini-Mental State Examination [MMSE]) were studied in 500 consecutive PD patients not using vitamin D supplements. Information on sunlight exposure and dietary intakes (using a 66-item food frequency questionnaire) were also collected. A convenient sample of age and sex-matched community healthy controls (N = 100) was included as a control group.

Results

PD patients had lower 25(OH)D serum levels than controls. Deficiency status (<20 ng/mL) was found in 65.6% of patients. 25(OH)D levels were independently correlated to sunlight exposure (P = .002) and vitamin D intake (P = .009). In multivariate models, using a Mendelian randomization approach, lower serum 25(OH)D was associated with more severe disease (HY, P = .035), worse clinical symptoms (UPDRS Part-III total score [P = .006] and dopaminergic [P = .033] and non-dopaminergic subscores [P = .001]) and greater global cognitive function impairment (P = .041). Neither cognitive functions nor clinical features were associated with reduced intake of vitamin D and sunlight exposure.

Conclusion

: Serum 25(OH)D was negatively correlated with disease and symptoms severity, as well as with global cognitive functions. Our study adds to the evidence that low 25(OH)D may affect the progression of PD negatively. Intervention studies in this area are required.

Acknowledgements

This work was supported by ‘Fondazione Grigioni per il Morbo di Parkinson’ and ‘Brain and Malnutrition in Chronic Disease Association Onlus’. Dr Cereda had full access to all of the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis. All the authors have participated sufficiently in the work to fulfill the criteria for authorship. Particularly, the contributions were as follows: study concept and design: Barichella, Cereda; acquisition of data: Barichella, Bolliri, Caronni, Cassani, Colombo, Del Sorbo, Esposito, Ferri, Giana, Iorio, Monti Guarnieri, Pinelli, Pusani, Quacci, Schiaffino; analysis and interpretation of data: Barichella, Cereda, Pezzoli; drafting of the manuscript: Cereda; critical revision of the manuscript for important intellectual content: Barichella, Cereda, Cilia, Pezzoli, Riboldazzi, Sacilotto, Zecchinelli; statistical analysis: Cereda; obtained funding: Barichella, Pezzoli; administrative, technical or material support: Barichella, Pezzoli, Zecchinelli; study supervision: Barichella, Pezzoli, Zecchinelli. The authors wish to thank the Osservatorio Grana Padano for the online food frequency questionnaire (software use and management) and Dr Jennifer S Hartwig for assistance in editing the manuscript.

Disclosure statement

Emanuele Cereda has received consultancy honoraria and investigator grants from Nutricia Italia, Akern s.r.l., Wunder s.r.l. and the ‘Fondazione Grigioni per il Morbo di Parkinson’.

Data availability statement

Data described in the manuscript, code book and analytic code will not be made available because a specific note was not included in the informed consent at the time of protocol approval and recruitment. Therefore, data sharing was not approved by the Ethics Committees.

Additional information

Funding

This work was supported by the ‘Fondazione Grigioni per il Morbo di Parkinson’ and ‘Brain and Malnutrition in Chronic Disease Association Onlus’.

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