Three months of abstinence from alcohol normalizes energy expenditure and substrate oxidation in alcoholics: A longitudinal study

Objective: The aim of this study was to evaluate the energy expenditure, su bstrate oxidation, and body composition in alcoholics during addiction and after several months of abstinence. Methods: A total of 32 alcoholics witho ut liver cirrhosis and malabsorption were consecutively recruited. A total of 55 social drinkers, matched for gender and height, were studied as a con trol group. Anthropometry and bioimpedance analysis were performed to asses s body composition, and indirect calorimetry was used to measure basal meta bolic rate (BMR) and substrate oxidation. Total abstinence was then achieve d in 15 subjects. At 1, 2, 3, and 6 months of abstinence, the metabolic var iables and the energy intake were re-examined. Results: At enrollment (TO) alcoholics compared to controls showed a significant decrease in body mass index (22.2 +/- 2.71 vs 23.6 +/- 1.3 kg/m(2); p < 0.05), fat mass (14.1 +/- 4.5 vs 16.7 +/- 3.3 kg; p < 0.01), an increased BMR normalized by fat-free mass (34.5 +/- 3.7 vs 32.1 +/- 2.01 kcal/kg/day; p < 0.01), a lower nonpro tein respiratory quotient (npRQ: 0.76 +/- 0.03 vs 0.83 +/- 0.03; p < 0.001) , with a consequently higher lipid oxidation (0.08 +/- 0.02 vs 0.04 +/- 0.0 2 g/min; p < 0.01), and a lower carbohydrate oxidation (0.05 +/- 0.02 vs 0. 10 +/- 0.03 g/min; p < 0.01). Although at 1 and 2 months of abstinence the metabolic parameters had improved, only after 3 months of abstinence did al coholics show values of body mass index (23.2 +/- 2.6 kg/m(2)), fat mass (1 7.0 +/- 5.34 kg), BMR/fat-free mass (33.1 +/- 2.78 kcal/kg/day), npRQ (0.82 +/- 0.02), lipid oxidation (0.05 +/- 0.03 g/min) and carbohydrate oxidatio n (0.11 +/- 0.04 g/min) comparable to those of controls; these values remai ned constant at 6 months. Conclusion: Three months of abstinence from alcoh ol could represent the minimum time necessary to obtain a normalization of the metabolic variables considered and of the nutritional status for these patients, probably related to a regression of the functional alterations of the microsomal ethanol oxidizing system and of mitochondria secondary to c hronic ethanol abuse. (C) 1998 by Am. Coll. of Gastroenterology.