Vitamin D and cardiovascular health

Abstract

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.

Vitamin D Deficiency in Children With Vasovagal Syncope Is Associated With Impaired Circadian Rhythm of Blood Pressure

“…Secondly, the active form of vitamin D plays a critical role in the proliferation of vascular smooth muscle cells and endothelial cells. Vitamin D regulates blood pressure by acting on vascular smooth muscle cells and endothelial cells (de la Guia-Galipienso et al, 2021). Endothelium-derived nitric oxide-evoked dilation was decreased in arteries from vitamin D deficient rats (Tare et al, 2011), suggesting vitamin D deficiency prompts endothelial vasodilator dysfunction.…”

The Obesity Paradox in Infections and Implications for COVID-19

“…There are several other implications of interest regarding obesity in COVID-19. First, low serum 25-hydroxyvitamin D levels on hospital admission have been correlated with COVID-19 disease severity and mortality, 17 and obese patients are known to have lower levels of vitamin D. 18 Vitamin D is essential to a host of immune functions, control of inflammation, and modulation of the coagulation cascade. Vitamin D may be involved in decreasing the replication and survival of the SARS-CoV-2 through the induction of cathelicidins and defensins, major host antimicrobial defense proteins.…”

Association of Serum 25-Hydroxyvitamin D Concentrations With All-Cause and Cause-Specific Mortality Among Adult Patients With Existing Cardiovascular Disease

“…The cardiovascular system appears to be highly sensitive to vitamin D deficiency ( 38 ). In humans, vitamin D deficiency could be linked to vascular dysfunction, arterial stiffness, reduced coronary flow, subclinical atherosclerosis, and left ventricular hypertrophy ( 44 , 45 ). All the mentioned studies demonstrate that vitamin D treatment could have salutary effects in the development of CVD.…”