The inner half of an artery wall receives its nutrients by direct diffusion from blood in the lumen of an artery. According to one widely held theory of atherogenesis (fatty plaque formation), white blood cells called monocytes adhere to the surface of the intima in areas where microscopic damage has occurred (e.g., because of turbulent blood flow). These cells transform into macrophages and begin to ingest lipids from the bloodstream. Lipids and proteins from blood begin to accumulate in the intra- and extracellular spaces of the intima and as endothelial, smooth muscle, and macrophage cells begin to proliferate. As lipid deposits enlarge, they become visible as fatty streaks, which form as early as the first decade of life (Figure 3-10B). As fatty deposits grow and the arterial wall thickens, cells of the intima and media are forced farther away from their nutrient supplies and ultimately die and disintegrate, leaving behind a fat paste, or atheroma. In an effort to contain the damage fibroblasts form a fibrous connective tissue capsule around the atheroma. The encapsulated lesion, referred to as a fibrous (or fatty) plaque, appears as early as the second decade of life (Figure 3-10C).