Restoration of bone mass in male hypogonadal osteopenic subjects by androgens.

protective value are rather contradictory. Chronic alcohol consumption reduces the absolute level of the anti-atherogenic LpAI fraction of HDL while the LpAI:LpAII ratio improves the level.' Despite this observation, the risk-reducing effect of alcohol has been demonstrated in angiographically proven coronary artery disease.' It has also been suggested that alcohol has an important effect on thrombogenesis and the fibrinolytic system. In animal models, intravenous administration of alcohol (red wine) inhibits platelet aggregation and thrombogenesis in a mechanically stenosed coronary artery,' possibly through alterations in the prostacyclin-thromboxane system. Alcohol has a beneficial effect on the fibrinolytic system by causing a sharp but temporary increase in plasminogen activator inhibitor activity, plasminogen activator antigen levels and circulating tissue type plasminogen activator activity." This effect of alcohol probably explains its acute protective effect on myocardial infarction. Alcohol may also exert a protective effect through acetate (a metabolite of alcohol) mediated decrease in blood pressure and coronary vasodilation and by a reduction in psychological stress. The mechanism notwithstanding, alcohol has a definite protective effect against coronary artery disease. T~ study has reinforced previous observations on the protective effect of alcohol and quantified the amount required to prevent coronary artery disease. However, the limit of safe drinking is too narrow to be adhered to even when alcohol is consumed therapeutically. Can alcohol be recommended as a prevention for coronary artery disease? Possibly not! Chronic alcohol use and acute