Dyslipidemia, more specifically, high-serum low-density lipoproteins and low-serum high-density lipoproteins, are known risk factors for cardiovascular disease. The current clinical treatment of dyslipidemia represents the outcome of a large body of fundamental basic science research on lipids, lipid metabolism, and the effects of different lipids on cellular components of the artery, inflammatory cells, and platelets. In general, lower density lipids activate intracellular pathways to increase local and systemic inflammation, monocyte adhesion, endothelial cell dysfunction and apoptosis, and smooth muscle cell proliferation, resulting in foam cell formation and genesis of atherosclerotic plaque. In contrast, higher density lipids prevent or attenuate atherosclerosis. This article is part 1 of a 2-part review, with part 1 focusing on lipid metabolism and the downstream effects of lipids on the development of atherosclerosis, and part 2 on the clinical treatment of dyslipidemia and the role of these drugs for patients with arterial disease exclusive of the coronary arteries.