USPharmacist.com; Protective Role of Vitamin D on the Cardiovascular System
Heart disease is a broad term that describes a range of diseases that affect the cardiovascular system and result in approximately 630,000 deaths annually in the United States.1 Cardiovascular disease (CVD) is the leading cause of death of both men and women above the age of 35 among all racial and ethnic groups.2 While risk factors such as increased age, male gender, and family history are nonmodifiable, others, such as smoking, high cholesterol, hypertension, physical inactivity, obesity, diabetes mellitus, and stress are preventable.2 Another possible modifiable risk factor, vitamin D deficiency, has been identified and has caused debates in the literature as the protective role of vitamin D on the cardiovascular system continues to be investigated. This article will expand on this proposed phenomenon, providing deeper insight into recently published literature, as well as discuss the pharmacist’s role in preventing vitamin D deficiency.
Vitamin D: The Basics
Vitamin D refers to two biologically inactive precursors: vitamin D3 (cholecalciferol), produced mainly in the skin post exposure to ultraviolet (UV) radiation, and vitamin D2 (ergocalciferol), produced exogenously and entering the circulation solely after gastrointestinal absorption.3 Both vitamin D2 and D3 require hydroxylation reactions in the liver and kidney, closely regulated by the parathyroid hormone (PTH), to form the biologically active metabolite of vitamin D, 1,25(OH)2D (calcitriol).4 Vitamin D status is best measured by 25(OH)D concentrations or levels and not calcitriol levels for several reasons, including longer half-life (~3 weeks compared to ~8 hours for calcitriol), higher circulating serum concentrations, and tight regulation of calcitriol by PTH, resulting in falsely elevated calcitriol levels despite vitamin D deficiency.5 Currently, there is no universally accepted “normal” measure of 25(OH)D levels; however, it has been suggested that concentrations above 30 ng/mL are associated with decreased fracture rates and maximal parathyroid suppression.6
Although the classic function of vitamin D has been to increase the intestinal absorption of calcium for proper bone health, its role in health maintenance is beginning to expand with the finding of vitamin D receptors (VDRs) in many cells throughout the body, including cardiomyocytes, vascular smooth muscle, and endothelium.5,7 Additionally, recent studies have found that individuals with vitamin D deficiency have increased incidence of CVD.7
Article mentions Vitamin D and its effects on:
Atherosclerosis and Inflammation
Hypertension
Diabetes and Metabolic Syndrome
Heart disease is a broad term that describes a range of diseases that affect the cardiovascular system and result in approximately 630,000 deaths annually in the United States.1 Cardiovascular disease (CVD) is the leading cause of death of both men and women above the age of 35 among all racial and ethnic groups.2 While risk factors such as increased age, male gender, and family history are nonmodifiable, others, such as smoking, high cholesterol, hypertension, physical inactivity, obesity, diabetes mellitus, and stress are preventable.2 Another possible modifiable risk factor, vitamin D deficiency, has been identified and has caused debates in the literature as the protective role of vitamin D on the cardiovascular system continues to be investigated. This article will expand on this proposed phenomenon, providing deeper insight into recently published literature, as well as discuss the pharmacist’s role in preventing vitamin D deficiency.
Vitamin D: The Basics
Vitamin D refers to two biologically inactive precursors: vitamin D3 (cholecalciferol), produced mainly in the skin post exposure to ultraviolet (UV) radiation, and vitamin D2 (ergocalciferol), produced exogenously and entering the circulation solely after gastrointestinal absorption.3 Both vitamin D2 and D3 require hydroxylation reactions in the liver and kidney, closely regulated by the parathyroid hormone (PTH), to form the biologically active metabolite of vitamin D, 1,25(OH)2D (calcitriol).4 Vitamin D status is best measured by 25(OH)D concentrations or levels and not calcitriol levels for several reasons, including longer half-life (~3 weeks compared to ~8 hours for calcitriol), higher circulating serum concentrations, and tight regulation of calcitriol by PTH, resulting in falsely elevated calcitriol levels despite vitamin D deficiency.5 Currently, there is no universally accepted “normal” measure of 25(OH)D levels; however, it has been suggested that concentrations above 30 ng/mL are associated with decreased fracture rates and maximal parathyroid suppression.6
Although the classic function of vitamin D has been to increase the intestinal absorption of calcium for proper bone health, its role in health maintenance is beginning to expand with the finding of vitamin D receptors (VDRs) in many cells throughout the body, including cardiomyocytes, vascular smooth muscle, and endothelium.5,7 Additionally, recent studies have found that individuals with vitamin D deficiency have increased incidence of CVD.7
Article mentions Vitamin D and its effects on:
Atherosclerosis and Inflammation
Hypertension
Diabetes and Metabolic Syndrome
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