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Vitamin D Defficientcy and Cardiovascular Disease

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Effects of Vitamin D Deficiency:

Correlation to the Increased Risk of Cardiovascular Disease

Word count: 1078



Vitamin D deficiencies occur in approximately 30 to 50% of people in developed countries (Lips, 2010), and one billion people globally (Holick, 2011). Vitamin D is responsible for calcium homeostasis, cell proliferation and cell differentiation (Kato, 200) and an absence of this may result in several chronic diseases such as autoimmune, neurological and cardiovascular diseases (Forrest, 2011. Gonzalez-Parra, 2012. Tare, 2011). This is because the calcitriol receptor (Vitamin D receptor) is distributed across a broad spectrum of tissue including the vascular muscles, kidneys, immune cells, brain and muscles (Gonzalez-Parra, 2012). Hence, the presence vitamin D is believed to have anti-hypertrophic effects in the cardiovascular system, while deficiencies are related to the increased risk of developing hypertension (Michael, 2010. Simpson, 2011)

The constriction and dilation of blood vessels in the cardiovascular system is regulated by the release of vasodilator substances such as nitric acid endothelium-derived relaxing factors by the endothelium. Endothelial dysfunction, an early indicator of cardiovascular disease, occurs when there is an imbalance between vasoconstriction and vasodilating substances. Hence, as nitric acid production is reduced with age or diseases, so does the blood vessel’s ability to dilate (Vanhoutte, 2009). However, vitamin D is believed to increase the production of nitric acid and therefore maintain this balance.


Vitamin D also acts as an inhibitor to the Renin Angiotensin System, which is a hormonal system that regulates arterial blood pressure. Without calcitriol (1,25-dihydroxycholecalciferol or 1,25-dihydroxyvitamin D3), a metabolite of vitamin D, the increase in activity in this system would result in hypertension, heart failure and kidney failure.

Keywords: calcitriol receptor, hypertrophic, hypertension, endothelium-derived relaxing factors, endothelial dysfunction, vasoconstriction, vasodilating, renin angiotensin system, calcitriol, metabolite

The first study that establishes a correlation between vitamin D and cardiovascular dysfunction was conducted by Marianne Tare on male and female rats and their off spring. Two groups of female pregnant and non-pregnant rats were given two different type of food sources, one with added Vitamin D and the other without. The off springs were then kept on the same diet as their mothers until 7-8 weeks of age. Observations in the off spring indicated the harmful effects of Vitamin D deficiency to the vasodilation function of arteries, resulting in the increase in blood pressure. While nitric acid regulated vasodilation was found to have partially decreased in the arteries in infertile males and females, endothelium-derived relaxing factors were found to be completely removed from tissues in females in their period of fertility. In males, blood pressure rose by 11mmHg while in females it rose by 20mmHg (Tare, 2011). For human analysis, the increase by 10-11mmHg in blood pressure increases the risk of cardiovascular diseases by 2 (Chobanian, 2003).


Early animal studies demonstrated a correlation between Vitamin D and a variety of cardiovascular dysfunctions. In these studies, vitamin D insufficiencies induced ventricle muscle mass vasocontraction functions were shown to be enhanced along with the increase in production of renin which induced a significantly higher systolic blood pressure (Simpson, 2011). Renin is a hormone produced in the renin-angiotensin system. It converted from prorenin (a protein) in the kidneys and excreted into the circulatory system where it induces constriction in arterial pressures. These results are used to demonstrate the action of calcitriol on vitamin D receptors and their effect on regulating cardiovascular homeostasis.

Evidence that insufficient vitamin D levels had direct correlation to the increase risk of cardiovascular disease originated from patients who suffered from end stage renal disease, also known as chronic kidney disease. This is when the kidneys are no longer functional for daily requirements. The kidney can no longer convert 25-Hydroxyvitamin D to 1,25-Dihydroxyvitamin D which results in a severe vitamin D deficiency. This deficiency induces an excess of parathyroid hormones to be released into the bloodstream. Over a long period of time, the stress on the cardiac tissue results in heart failure and hypertrophy. Further research has also revealed a link between the increased levels of parathyroid hormones in the bloodstream and hyperlipidaemia (Gafter, 2008). Hyperlipidaemia occurs when the concentration of triglycerides and cholesterol in the blood is too high. These substances can deposit adipose tissue into cells and is one of the causes to hypertrophy in organs. Blood vessels are also effected as these substances can also effect vessel walls and restrict blood flow. This in turn increases the risk of heart attacks and strokes.




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