Too Soon to Turn Out the Lights?
The interest level among practitioners and investigators alike in linking vitamin D deficiency with cardiovascular outcomes has hardly subsided, despite the consistent lack of clear evidence supporting the relationship. Why does there continue to be such feverish interest in the subject matter? Despite our best efforts during the past half century to understand and modify known risk factors, cardiovascular disease remains one of the most common causes of death among women and men worldwide.1 The major outcomes of interest, such as myocardial infarction and stroke, have substantial morbidity, and the number of individuals newly affected by these conditions is not likely to diminish. As with the outcomes, the exposure of interest is easily quantified although with various cut points that constitute normal and abnormal levels. Circulating levels of 25 hydroxyvitamin D (25OHD), unlike biomarkers for most other vitamins, can be measured routinely using widely accessible automated platforms. Global population studies would argue that vitamin D deficiency has reached almost epidemic proportions.2 Furthermore, and most importantly, correcting vitamin D deficiency is not only possible (and quantifiable) but also fairly inexpensive. Finally, experimental studies strongly suggest a myriad of biological pathways linking cardiovascular disease and vitamin D deficiency, thus supporting the plausibility that treatment with vitamin D would improve cardiac structure, prevent plaque development, and lower blood pressure, among a host of other cardiovascular-related end points.3–8 The combination of these and possibly other factors have fueled the perfect storm, yet studies attempting to establish a causal relationship between vitamin D and cardiovascular disease are unlikely to be completed soon.9
See accompanying articles on pages 2633, 2639
Defining the level of circulating 25OHD below which replacement is necessary continues to …