Vitamin D and cardiovascular health Article

Full Text via DOI: 10.1016/j.clnu.2020.12.025 Web of Science: 000654716700012
International Collaboration

Cited authors

  • de la Guia-galipienso F, Martinez-Ferran M, Vallecillo N, Lavie CJ, Sanchis-Gomar F, Pareja-Galeano H


  • The principal source of vitamin D in humans is its biosynthesis in the skin through a chemical reaction dependent on sun exposure. In lesser amounts, the vitamin can be obtained from the diet, mostly from fatty fish, fish liver oil and mushrooms. Individuals with vitamin D deficiency, defined as a serum level of 25 hydroxyvitamin D < 20 ng/dl, should be supplemented. Vitamin D deficiency is a prevalent global problem caused mainly by low exposure to sunlight. The main role of 1,25 dihydroxyvitamin D is the maintenance of calcium and phosphorus homeostasis. However, vitamin D receptors are found in most human cells and tissues, indicating many extra-skeletal effects of the vitamin, particularly in the immune and cardiovascular (CV) systems. Vitamin D regulates blood pressure by acting on endothelial cells and smooth muscle cells. Its deficiency has been associated with various CV risk factors and appears to be linked to a higher mortality and incidence of CV disease (CVD). Several mechanisms have been proposed relating vitamin D deficiency to CV risk factors such as renin-angiotensin-aldosterone system activation, abnormal nitric oxide regulation, oxidative stress or altered inflammatory pathways. However, in the latest randomized controlled trials no benefits of vitamin D supplementation for CVD have been confirmed. Although more work is needed to establish the protective role of vitamin D in this setting, according to current evidences vitamin D supplements should not be recommended for CVD prevention. (c) 2020 Elsevier Ltd and European Society for Clinical Nutrition and Metabolism. All rights reserved.

Publication date

  • 2021

Published in

International Standard Serial Number (ISSN)

  • 0261-5614

Number of pages

  • 12

Start page

  • 2946

End page

  • 2957


  • 40


  • 5