Recent scientific interest has focused on abnormalities in mineral metabolism and the role those abnormalities may play in the pathogenesis of cardiovascular disease (CVD). Many vascular biologists believe that arterial calcification, rather than a passive product of aging, is an active process mediated by signaling molecules, such as osteocalcin, osteopontin, bone morphogenic protein, matrix Gla protein, and fibroblast growth factor, among others (1). These signals are induced by inflammatory and lipid mediators that have established roles in atherothrombosis, including transforming growth factor-β and oxidized low-density lipoprotein cholesterol, and lead to transformation of vascular smooth-muscle cells into osteoblast-type cells (2–3). Traditional mediators of calcium metabolism, such as parathyroid hormone, vitamin D, and phosphate, all seem to be central to this process. Epidemiologic studies have reported associations between markers of mineral metabolism, which include phosphorus, the calcium–phosphorus product, and parathyroid hormone, and incident CVD (4–6). Several recent studies have also reported an association between low dietary intake of vitamin D or low serum levels of vitamin D and incident CVD (7–10).