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Table of Contents    
Year : 2022  |  Volume : 70  |  Issue : 4  |  Page : 1726-1727

Low Vitamin D is Linked to Cardiac Dysfunction in Parkinson's Disease

1 Disciplina de Neurociência. Universidade Federal de São Paulo/Escola Paulista de Medicina (UNIFESP/EPM), São Paulo, Brazil
2 Laboratório de Neurociência Experimental e Computacional, Departamento de Engenharia de Biossistemas, Universidade Federal de São João del-Rei (UFSJ), Brazil
3 Krankenanstalt Rudolfstiftung, Messerli Institute, Vienna, Austria
4 Programa de Estudos Pós-Graduado em Fonoaudiologia, Pontifícia Universidade Católica de São Paulo (PUC-SP), Departamento de Fonoaudiologia, Escola Paulista de Medicina/Universidade Federal de São Paulo (EPM/UNIFESP), São Paulo, Brazil
5 Departamento de Ginecologia. Núcleo de Avaliação de Tecnologias em Saúde, Escola Paulista de Medicina/Universidade Federal de São Paulo (EPM/UNIFESP), São Paulo, Brazil

Date of Submission05-Jun-2020
Date of Decision22-Jun-2020
Date of Acceptance15-Jun-2020
Date of Web Publication30-Aug-2022

Correspondence Address:
Fulvio A Scorza
Rua Pedro de Toledo, 669 – 10 andar, CEP: 04039-032. São Paulo - SP
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0028-3886.355174

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How to cite this article:
Scorza CA, de Almeida ACG, Finsterer J, Fiorini AC, M Fonseca MC, Scorza FA. Low Vitamin D is Linked to Cardiac Dysfunction in Parkinson's Disease. Neurol India 2022;70:1726-7

How to cite this URL:
Scorza CA, de Almeida ACG, Finsterer J, Fiorini AC, M Fonseca MC, Scorza FA. Low Vitamin D is Linked to Cardiac Dysfunction in Parkinson's Disease. Neurol India [serial online] 2022 [cited 2022 Oct 2];70:1726-7. Available from: https://www.neurologyindia.com/text.asp?2022/70/4/1726/355174


Always on the lookout for articles from Neurology India, one in particular[1] has attracted a lot of attention because the results are really important. In this context, Ozturk and colleagues addressed a priority issue in clinical research demonstrating that bone mineral density and vitamin D (VitD) levels are decreased at the early stages of Parkinson's disease (PD) and they were adversely affected with the progression of the disease.[1] Considering the effectiveness of VitD in many organs and its significant role in maintaining general health, we applaud the authors for pursuing this topic.[1] Moreover, the possibility of relating VitD concentrations as a biological indicator for possible cardiac abnormalities in patients with PD also deserves some reflections.

PD is one of the most frequent age-related neurodegenerative disorders that affects millions of people globally and has no cure, the prevalence of which will double by 2030.[2] Thereby, several studies have shown that patients with PD have a higher risk of mortality compared with the general population.[2] Sudden unexpected death in PD (SUDPAR), a rare but fatal event, contributes to the increased risk of mortality in patients with PD.[2] While the specific causes of SUDPAR are still unknown, the results of translational studies suggest that cardiac abnormalities and autonomic dysfunction play a possible “direct” role in SUDPAR, since ~60% of PD patients have cardiovascular disturbances because of frequent autonomic disturbances in PD.[2] Despite the formidable progress made in relation to PD, much still needs to be done.[2] At least in the last decade, it is well discussed that low VitD levels and PD are considered bad fellows.[1] Importantly, studies have also been shown that VitD is involved in the regulation of the cardiovascular system.[3] Thus, several studies clearly indicate that VitD deficiency is related to the genesis of coronary heart disease, cardiovascular dysfunction, and hence, sudden cardiac death.[3] Furthermore, low VitD levels are also associated with arterial hypertension, left ventricular hypertrophy, congestive heart failure, and chronic vascular inflammation.[3] Experimentally, our research group recently demonstrated a link between cardiac tissue changes and cardiac functional abnormalities early after the intrastriatal 6-hydroxydopamine (6-OHDA) lesion models of PD.[4]

Considering that PD is a systemic disease, we will also have to explore the specific mechanisms of action that vitamin D plays in order to improve cardiac function and prevent possible cardiac abnormalities present in patients with PD.


Our studies are supported by the following grants: FAPESP (Fundação de Amparo à Pesquisa do Estado de São Paulo) and CNPq (Conselho Nacional de Desenvolvimento Científico e Tecnológico) e Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES).

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

  References Top

Ozturk EA, Gundogdu I, Tonuk B, Umay E, Kocer BG, Cakci A. Bone mineral density and serum vitamin D status in Parkinson's disease: Are the stage and clinical features of the disease important? Neurol India 2020;68:394-400.  Back to cited text no. 1
[PUBMED]  [Full text]  
Scorza FA, Fiorini AC, Scorza CA, Finsterer J. Cardiac abnormalities in Parkinson's disease and Parkinsonism. J Clin Neurosci 2018;53:1-5.  Back to cited text no. 2
Lee JH, O'Keefe JH, Bell D, Hensrud DD, Holick MF. Vitamin D deficiency an important, common, and easily treatable cardiovascular risk factor? J Am Coll Cardiol 2008;52:1949-56.  Back to cited text no. 3
Nejm MB, Guimarães-Marques MJ, Oliveira LF, Damasceno L, Andersen ML, Tufik S, et al. Assessment of vitamin D and inflammatory markers profile in cardiac tissue on Parkinson disease animal model. Pharmacol Rep 2020;72:296-304.  Back to cited text no. 4


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