Apolipoprotein (apo) E polymorphism has emerged as a genetic trait that explains part of the normal variation in total and low density lipoprotein (LDL) cholesterol in men and women. Apo E polymorphism and its influence on serum cholesterol, triglycerides, very low density lipoprotein (VLDL), intermediate density lipoprotein, LDL and high density lipoprotein (HDL) cholesterol, lipoprotein (a) - Lp(a) and apos AI, B and E were studied in 113 healthy men (control group) and 202 male patients with extracoronary atherosclerosis. Both in controls and patients, weight showed an independent significant influence on serum triglycerides, VLDL and HDL cholesterol and apo AI. In healthy subjects but not in patients, alcohol consumption was significantly associated with serum cholesterol, serum triglycerides, LDL cholesterol and serum apo E. In patients, in contrast to controls, significant influence of smoking on serum triglycerides, and VLDL and HDL cholesterol was observed. Significant effects of apo E polymorphism was observed on total cholesterol and LDL cholesterol both in controls and patients. In patients, a higher impact of apo E*2 allele to lower total cholesterol (by 28 mg/dl) and LDL-cholesterol (by 17 mg/dl) than in controls (7 mg/dl in both cases) was found, whereas the effect of apo E*4 in increasing serum cholesterol (by 3 mg/dl) and LDL cholesterol (by 6 mg/dl) was lower than in controls (26 mg/dl in both cases). These findings could be explained by a different effect of apo E polymorphism on normal metabolism of triglyceride-rich particles in controls and on defective catabolism of the same in patients. No association was found between apo E polymorphism and Lp(a) levels in controls or patients, which suggests that Lp(a) catabolism, via the LDL receptor or others, is independent of apo E polymorphism. Finally, the influence of apo E polymorphism in controls and patients was lower than environmental variables such as weight, body mass index, smoking or alcohol consumption.