Vitamin D Therapy and Cardiovascular Health

Abstract

Vitamin D belongs to the family of nuclear steroid hormones, which has pleiotropic effects on several organ systems. Different vitamin D compounds have been studied as potential cardioprotective agents over the past 20 years. The results of these clinical studies vary based on the form and dosage of vitamin D administered during the trial. In the past 5 years, many have described an association of vitamin D compounds and cardiovascular health through reduction in blood pressure, reduction in inflammatory biomarkers, improved insulin sensitivity, and reduction in cardiovascular disease complications and death. Because there are several vitamin D compounds, it is important to consider the full breadth of the literature when examining vitamin D and cardiovascular health, to assist in hypothesis generation and understanding of the current state of the science. Although a growing body of evidence suggests that nutritional vitamin D supplementation and potentially even treatment with synthetic analogues of vitamin D may be cardioprotective, relatively few studies have examined either of these compounds in a randomized, controlled fashion. Studies examining the benefit of vitamin D supplementation are now beginning, but future studies considering calcitriol and analogue therapy also seem warranted.

The role of vitamin D in regulating the iron-hepcidin-ferroportin axis in monocytes

“…Optimal vitamin D status is important in patients with CKD to regulate parathyroid hormone (PTH) concentrations [3], [4], [5] for optimal bone health and prevention of osteomalacia and for potential cardioprotective effects [3], [6], [7]. Recent reports have established an association between vitamin D insufficiency and anemia in patients with CKD [8], [9], [10]; however, the role for vitamin D in the regulation of anemia has not been fully explained.…”

Diabetic CVD – Focus on Vitamin D

“…Activated T cells increase oxidative stress followed by accelerated angiotensin II secretion [26]. Vitamin D as an anti inflammatory factor can eventually reduce angiotensin II concentration [26,27].…”

“…Vitamin D as an anti inflammatory factor can eventually reduce angiotensin II concentration [26,27]. A study on patients with chronic kidney disease reported that treatment with intravenous calcitriol can cause left ventricle hypertrophy regression, plasma rennin activity reduction and angiotensin II level decline [28].…”

“…Antiatherosclerosis, protection against vascular injury Immunosuppressive effects, inhibition of lymphocyte proliferation and inflammatory cytokine production, down regulation of NF (nuclear factor)-K activity and expression of the tissue matrix metalloproteinase (MMPs), stimulation of IL10 as an anti-inflammatory cytokine, reduces vascular smooth muscle cells replication, up regulates thrombomodulin expression, increases fibrinolysis and vascular relaxation [15][16][17][18] Prevention of cardiac hypertrophy Increases myotrophin expression, inhibition of the N terminal proatrial natriuretic peptide and c-myc level, Vitamin D deficiency influences the distribution of both V1 and V3 myosin chains with predominant V1 isotype and reduces cardiac inothropy and increases the heart weight and collagen content [19][20][21] Regulation of renin-angiotensin system and blood pressure (VDR) null mice have increased renin gene expression, Active form of vitamin D disrupts the cAMP signaling pathway that involved in rennin biosynthesis, regression of left ventricle hypertrophy and reduces plasma renin activity and the angiotensin II level, has regulatory effects on natriuretic peptide receptor [22][23][24][25][26][27] Reduction in Insulin resistance and improvement of insulin secretion Vitamin D regulates calcium pool that is essential for insulin action; stimulate insulin receptor expression, improvement of insulin action in peripheral tissues, anti-inflammatory effects.Increases insulin response to glucose stimulation [37][38][39][40][41][42][45][46][47][48] Effects of vitamin D on obesity and metabolic syndrome D deficiency induces obesity through activation of Oxidative stresses and systemic inflammation and increase in PTH level [63][64][65][66][67][68] Reduction of albuminuria Suppression of renin transcription, angiotensin 2 production, podocyte loss, glumerulosclerosis and albuminuria, improvement of blood pressure [73][74]…”

Treatment of patients with intermediate cardiovascular risk: Are clinical measures enough?

“…Long term studies of the population of Framingham, MA 3,4 have provided valuable insights into CVD risk, and the Framingham score 3 continues to be a highly useful tool for assessing risk in populations represented by the original Framingham studies. In recent years, several other measures have been proposed for refining the predictive accuracy of the Framingham score, and all require additional laboratory testing, [5][6][7][8] radiographic imaging of the coronary arteries, 9,10 or ultrasound imaging of the carotid arteries. 11,12 While additional refinement of risk is possible with these advanced methodologies, their use in large populations is prohibitive because of cost.…”