Vitamin D is a specific group of fat-soluble molecules which can bind with certain elements, ultimately giving its functionality in humans. Vitamin D deficiency (VDD) has increased significantly in recent years, a change seemingly largely due to lack of sunlight exposure. The potential mechanisms by which VDD increases the prevalence of many forms of cardiovascular disease such as heart failure, hypertension and coronary artery disease have been determined and will be discussed further in this essay.

Vitamin D (VD) is mostly produced via UV radiation. UV rays with a wavelength between 290 and 315 nm are able to penetrate the skin and with the help of intermediate previtamin D, transform 7-dehydrocholesterol [7-DHC] to 25-hydroxycholecalciferol [25-(OH)D3] vitamin D3. 25-(OH)D is then converted to the vitamin D (VD) hormone [1α,25(OH)2D] which is metabolically active (Gröber et al. 2013, p. 331). The active hormone binds to the VD receptor in most cells and tissues, allowing it to exert its biological effects (Kunadian et al. 2014, p. 284).

Synthesising VD is primarily controlled by the 25(OH)D levels (Gröber et al. 2013, p. 331). VDD has been defined by the Institute of Medicine (IOM) as a value of 20 ng/mL for 25-(OH)D. However Heaney (2012) argues that these values are not definite, due to different diseases having different VD risk (VDR) levels. Furthermore, Gröber et al. (2013) uses different VDD values, further showing how a specific value for VDD is yet to be agreed upon. However, most cardiovascular diseases have clearly defined VD concentrations where the disease is not manifested (Kunadian et al. 2014, p. 284) and the end points used in this essay will reflect those used in the referencing material.

Hypertension is a medical condition where blood pressure in the arteries is elevated to dangerous levels, which has VD as a risk factor. In a comparison of 25(OH)D levels of 30 (ng/mL), those who had former VD concentrations had significantly higher levels of hypertension, according to the Intermountain Heart Collaborative Study (Gröber et al. 2013, p. 335). The study showed that VD reduced diastolic pressure by 3.1 mmHg and systolic blood pressure by 6.18 mmHg, demonstrating an inversely proportional relationship in VD levels and blood pressure. One potential mechanism in which this is achieved is the suppression of the parathyroid hormone (PTH) by VD. PTH is associated with hyperparathyroidism, which can cause hyper contractility of the heart muscle, resulting from calcification (Gröber et al. 2013, p. 336). This causes the heart to contract rapidly in order to maintain blood flow to the body (Ulu et al. 2013, p. 52). This is further clarified in a study of 80 cardiac insufficient infants, where those given daily VD supplementation resulted in significant cardiac improvement compared to the placebo group (Gröber et al. 2013, p. 336). PTH levels were also lowered in the non-placebo group, showing an inverse relationship between VD and PTH levels, presumed to be achieved through PTH binding to the VD receptor, effectively suppressing it via 1,25(OH)2D3 (Ritter et al. 2006, p. 657). Although the exact molecular mechanics of PTH suppression are not clear, the importance of VD to prevent hypertension and the risk of VDD is unambiguous.

Similar to hypertension, coronary artery disease prevalence is reduced by VD. Coronary artery disease (CAD) refers to when the blood vessels in the heart who supply oxygen narrow via plaque build-up (Nordqvist 2013, n.p.). A recent study found that the slow coronary flow rate incidence was higher in the VDD group compared with those who had sufficient VD levels in former CAD patients (Gröber et al. 2013, p. 336). Another study with 119 patients determined a 5.8 odds ratio of being affected with CAD if one had VDD, after risk factors adjustment (Siadat et al. 2012, p. 1053). One possible mechanism by which VD can assist in the prevention of CAD is its