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.

Keywords: Cardiovascular disease; Coronary heart disease; Endothelial function; Hypertension; Supplements.

Fig. 1

Diagram showing how cholecalciferol (vitamin D3) is synthesized in the human epidermis. In a two-stage process, 7-dehydrocholesterol (7-DHC) present in the cell membranes of keratinocytes is converted into 9,10-secosteroid (pre-cholecalciferol) by UV-B radiation in sunlight (wavelengths of 290–320 nm). Then, through thermal isomerization at body temperature, pre-cholecalciferol is transformed into cholecalciferol (vitamin D3).

Fig. 2

Diagram showing the synthesis of 1,25-hydroxy-cholecalciferol (1,25-hydroxyvitamin D3) in humans. Cholecalciferol (vitamin D3) is converted into 25-hydroxycholecalciferol by 25-hydroxylase, and this 25-hydroxyvitamin D3 is then transformed into 1,25-hydroxycholecalciferol (1,25-hydroxyvitamin D3) by 1α-hydroxylase in the liver and kidney, respectively. Both reactions can nevertheless take place in the epidermis.

Fig. 3

Diagram showing how vitamin D from the diet and sun exposure can improve skeletal function and prevent several cardiovascular problems. AHT (arterial hypertension), CAD (coronary artery disease), CV (cardiovascular), HF (heart failure), RAAS (renin–angiotensin–aldosterone system), UV (ultraviolet), VED (vascular endothelial dysfunction).