A high intake of saturated fatty acids and cholesterol is associated with a high incidence of occlusive arterial lesions involving both atherosclerosis and thrombosis. The evidence is based on epidemiological, experimental, and clinical studies. Such dietary habits increase serum low density lipoprotein cholesterol, a main risk factor for atherosclerosis. The mechanisms by which dietary saturated fatty acids are connected to arterial thrombogenesis are only partly known. Experimental and epidemiological studies also indicate an association between dietary saturated fatty acids and venous thrombosis; however, the chain of evidence lacks documentation from prospective clinical studies. When unsaturated fatty acids of the (n-9), (n-6), or (n-3) families replace saturated fatty acids in the diet, risk factors related to atherosclerosis may be reduced and the development of atherosclerosis, inhibited. This potential is related both to the reduction of saturated fatty acids and, in varying degrees, to the individual unsaturated fatty acids. The very long-chain fatty acids of the (n-3) family and probably also linoleic acid of the (n-6) family have the potential to inhibit thrombogenesis. In this respect, the effect of the individual fatty acids seems even more important. To obtain an optimal dietary lipid composition for the prevention of atherosclerosis and thrombosis, it is important to appreciate the metabolic and structural effects of the individual fatty acids. The interaction between the various dietary fatty acids and their effects on lipid biosynthesis is still only partly known. The present nutritional recommendations include a low intake of saturated fatty acids and cholesterol and a balanced content of the unsaturated fatty acids and represent a well-documented approach to the prevention of both processes.