Abstract

In past decades, the primary focus on vitamin D was the recognition and treatment of deficiency as it related to metabolic bone disease (rickets, osteomalacia, and secondary hyperparathyroidism). In the last 10 years, however, with the discovery of vitamin D receptors in multiple tissue types has come the recognition that the role of vitamin D extends beyond the musculoskeletal system.1 The presence of abundant vitamin D receptors in myocardial tissue and vasculature and the observation that hypertension may be ameliorated with vitamin D suggest a greater role for vitamin D in the cardiovascular system.2 Presently, large numbers of people are found to have hypovitaminosis D (a term chosen for this review to indicate any concentration below normal under substrate-saturated conditions) resulting in part from more indoor activities and the purposeful avoidance of sunshine. This review first describes why vitamin D, parathyroid hormone (PTH), and the skeleton are important to the heart and vasculature, then outlines why the epidemic of hypovitaminosis D deserves further scrutiny by the cardiovascular community, and finally suggests why treatment options for reducing hypovitaminosis D may favorably affect the morbidity and mortality of common cardiovascular disorders. Vitamin D is both a nutrient and a hormone. It is an essential precursor of calcitriol, 1,25-hydroxyvitamin D3 [1,25(OH)2D], which is necessary for bone development, growth, and mineralization and the maintenance of skeletal integrity. A cascade of steps is needed to cause progression of lesser active nutritionally ingested or synthesized vitamin D to more biologically active forms as depicted in Figure 1.1 The cascade starts with the photolysis of 7 dehydrocholesterol in the epidermis by solar ultraviolet B (UVB) radiation to previtamin D3, which then undergoes thermal isomerization to vitamin D3. Vitamin D3 undergoes primary hydroxylation in the liver to 25-hydroxyvitamin D [25(OH)D] and then …

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