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Although clinical magnesium deficiency is now recognized frequently in chronic alcoholics, its cause or causes are not clear. A poor dietary intake is undoubtedly important, but it is unlikely that magnesium deficiency results from dietary depletion alone, since it has been quite difficult to produce experimental dietary magnesium deficiency in man (2). Earlier workers have shown that the kidneys are reasonably efficient in conserving magnesium (2, 3). Thus, it is likely that some additional mechanism may be responsible for magnesium deficiency associated with chronic alcoholism. Recent studies have indicated that ethanol may induce increased urinary excretion of magnesium (4, 5). The purpose of the present study was to determine the effect of an acute ethanol load on urinary excretion of magnesium and other electrolytes, and to make preliminary observations on the mechanism responsible for an observed increase in urinary excretion of magnesium. METHODSFifteen studies were performed on nine normal and four alcoholic subj ects. Two of the alcoholic subj ects had significant hypomagnesemia at the time of study, while the other two had been repleted before study. One alcoholic subject was restudied several weeks later when he was readmitted to the hospital with acute alcoholic intoxication. All subjects were on a normal hospital diet and were fasted overnight before the experiments, which began at 8:00 a.m. Water-loading was achieved with 20 ml of water per kg of body weight and was maintained for the duration of the stu(ly by replacing the fluid vol- (7), and PAH by that of Smith and associates (8). Lactate was measured by the Marcus modification of Barker's and Summerson's procedure (9), and the method of Beutler and Yeh (10) was used for citrate. Total organic acids were determined by a modification of the method of Palmer (11). The methods for calculating correlation coefficient and probability are described by Snedecor (12). RESULTS

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