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, substrate oxidation, and body composition in alcoholics during addiction and after several months of abstinence.

METHODS

A total of 32 alcoholics without liver cirrhosis and malabsorption were consecutively recruited. A total of 55 social drinkers, matched for gender and height, were studied as a control group. Anthropometry and bioimpedance analysis were performed to assess body composition, and indirect calorimetry was used to measure basal metabolic rate (BMR) and substrate oxidation. Total abstinence was then achieved in 15 subjects. At 1, 2, 3, and 6 months of abstinence, the metabolic variables and the energy intake were re-examined.

RESULTS

At enrollment (T0) alcoholics compared to controls showed a significant decrease in body mass index (22.2+/-2.71 vs 23.6+/-1.3 kg/m2; 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 nonprotein 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+/-0.02 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 alcoholics show values of body mass index (23.2+/-2.6 kg/ m2), fat mass (17.0+/-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 oxidation (0.11+/-0.04 g/min) comparable to those of controls; these values remained constant at 6 months.

CONCLUSION

Three months of abstinence from alcohol 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 chronic ethanol abuse.