Free Iron, as well as other transition metals, can catalyze free radical formation. For this reason iron is tightly bound to transport and storage proteins to prevent their involvement in free radical formation. It has been hypothesized that increased iron intake or iron stores may promote atherogenesis by increasing free radical formation and oxidative stress. While a coherent, plausible hypothesis as to how transition metals, such as iron, might accelerate the progression of atherosclerosis has been generated from basic research, iron status, measured as dietary iron intake, serum iron, serum ferritin, and transferrin saturation, has been inconsistently associated with cardiovascular disease in human epidemiologic research. In addition, limited data suggest that iron overload states do not appear to be strongly associated with increased risk of atherosclerotic disease. One real limitation of the existing data is the lack of a generally agreed upon and logistically feasible means of assessing iron status in free living humans. Further research, including basic research and large-scale epidemiologic studies, is needed to fully assess the association between iron status and the risk of CVD and other adverse outcomes. At present the currently available data do not support radical changes in dietary recommendations or screening to detect high normal levels nor do they support the need for large-scale randomized trials of dietary restriction or phlebotomy as a means of lowering iron stores.