Athersoclerosis is characterized by the development of foam cells from mononuclear phagocytes, which progress to become fatty streaks and further into plaque in the arterial intima. It has long been associated with the development of cardiovascular disease (CVD) and coronary heart disease (CHD). Low-density lipoprotein (LDL), the plasma transport protein for cholesterol, are downregulated by the cellular concentration of cholesterol and therefore are unlikely to be the initiator of the development of foam cells, latty streaks, or atherosclerosis. It is clear that the development of loam cells is due to an altered state of metabolism and one of the most popular hypotheses for the development of foam cells from the mononuclear phagocytes is via an oxidative modification of the LDL molecule. This modification allows unregulated uptake of oxidized LDL (Ox-LDL) by the phagocyte scavenger receptor and through this process the development into the foam cell. There is much evidence in the literature to support this hypothesis. It is unlikely that the oxidative modification of the LDL is an initiator of foam cell development. Therelore it is unlikely that oxidation is the initiator for the development of atherosclerosis. Clearly there is a role for the oxidative process in the ongoing proliferation of atherosclerosis; however, the evidence to date does not support oxidation as essential to the initiation of the process of atherosclerotic development.