Diet, endothelial permeability, and atherosclerosis

Cardiovascular disease remains the leading cause of death in the United States. Several lines of evidence suggest that part of the etiology of atherosclerosis involves damage to the vascular endothelium. This reduces its effectiveness as a selective permeability barrier to plasma components. Vascular endothelial cells normally are the only cells in the arterial wall exposed to high concentrations of lipoproteins which are rich in triglycerides and cholesterol. It has been suggested that excessive amounts of fatty acid anions, liberated during lipoprotein triglyceride hydrolysis, may cause localized endothelial injury. This may facilitate the penetration of cholesterol-rich remnant lipoproteins derived from chylomicrones or VLDL into the arterial wall, leading to lipid accumulation within the intima and ultimate plaque formation. To reduce endothelial injury and the accumulation of cholesterol in the arterial wall, dietary treatment should include both caloric balance and a decrease in total lipid intake.