The potential exists for zinc to influence numerous metabolic functions and to impact a range of diseases. In the present review we examine the reported relationships between zinc and plasma lipids, haemostasis and other factors postulated to play a role in atherogenesis. Ecological studies that investigated zinc intake or status, and incidence of coronary heart disease (CHD) reveal no consistent pattern. The conflicting observations may be explained by differences in the extent of CHD, site of atherosclerosis, or confounding factors. In most studies the diurnal variation in serum zinc concentrations, and the lifestyle factors that affect cholesterol metabolism were not explicitly considered. Results of randomised controlled trials show that low-density lipoprotein (LDL) oxidation and the concentrations of LDL-cholesterol (c), total cholesterol and triglycerides in plasma are unaffected by supplementation with up to 150 mg Zn/d. In contrast, plasma high-density lipoprotein (HDL)-c concentrations decline when zinc supplements provide a dose >50 mg/d. Limited data suggest that sustained hyperzincaemia predisposes individuals to thrombogenesis, whereas acute zinc depletion impairs platelet aggregation and prolongs bleeding time. In addition, Zinc supplements have been shown in some studies to decrease Cu/Zn-superoxide dismutase activity, primarily due to the antagonistic relationship between high zinc intakes and copper absorption. Besides the demonstrated adverse effect of zinc supplementation on plasma HDL-c concentrations in apparently healthy men, there is insufficient evidence to determine the role of zinc supplementation in influencing other risk factors for CHD such as antioxidant status and thrombogenesis.