Fat and Fatty Acid Intake and Metabolic Effects in the Human Body

nants, to form foam cells. There is convincing evidence that foam cells can progress to form fibrous atherosclerotic plaques. There is a large body of scientific evidence, both in animal models and corroborated by human observational and intervention studies, showing that dietary fat intake is causally involved in atherogenesis and may also influence arterial thrombosis. With regard to the experimental feeding studies in animals, the evidence is convincing that elevations of plasma lipids caused by modification of dietary fat intake result in atherosclerosis. These animal studies indicate that fats high in saturated (SFA), monounsaturated (MUFA) and trans fatty acids (TFA) promote atherosclerosis [Brown et al., 2007], whereas diets containing oils high in polyunsaturated fatty acids (PUFA) inhibit atherosclerosis and low-fat diets do not promote atherosclerosis. This review focuses on the evidence from dietary intervention studies in man that dietary fat intake influences metabolic factors associated with risk of CVD.