The important role of high-serum cholesterol, especially a high level of low-density lipoprotein (LDL) cholesterol, as a risk factor for coronary artery disease is well established,60,61 and lowering of serum LDL levels reduces the risk for major coronary events.62-64 On the contrary, low levels of high-density lipoprotein (HDL) constitute an independent risk factor for cardiovascular diseases (CVD).65-67 Epide-miological studies have shown an inverse correlation between serum HDL concentration and CVD risk.68 HDL protects against cardiovascular disease,69 70 and recent studies have elucidated the molecular mechanisms for its action.7172 HDL has been proposed to decrease CVD by stimulating reverse cholesterol transport (RCT), a process by which HDL carries excess cholesterol from peripheral cells, including foam cells in the coronary artery, back to the liver for its removal from the body.73 Beyond reverse cholesterol transport, HDL was also shown to protect LDL from oxidation.72 HDL inhibits the oxidation of LDL by transition metal ions, but also prevents 12-lipoxygenase-mediated formation of lipid hydroperoxides. Inhibition of LDL oxidation by HDL is usually attributed to the high content of antioxidants in this lipoprotein, to the antioxidative properties of apolipoprotein A-I, and to the presence of several enzymes, such as paraoxonase 1 (PON1),74-76 which protect LDL from oxidation by degradation of oxidized bioactive products.
Several lines of evidence support the concept that raising HDL may provide substantial atheroprotective benefit. A rise in serum HDL by 1 mg/dL has been proposed to reduce the risk of CVD by 2 to 3%. Current approaches to increase HDL levels in plasma include dietary intervention.77-79 Several studies indicate that light to moderate alcohol consumption, including red wine, is associated with an increase in serum HDL levels,8081 along with a low prevalence of coronary heart disease.
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