ENERGY-EXPENDITURE, SUBSTRATE OXIDATION, AND BODY-COMPOSITION IN SUBJECTS WITH CHRONIC-ALCOHOLISM - NEW FINDINGS FROM METABOLIC ASSESSMENT

There is some controversy as to the effect of ethanol on body weight a nd alcohol energy contribution to body mass. The aim of this study was to evaluate the effect of alcohol addiction on resting energy expendi ture (REE) and body composition. Twelve patients with current alcoholi sm (A) without severe liver disease or lipid and carbohydrate malabsor ption were compared with a group of healthy social drinkers (B) matche d for sex, age, and height. Their caloric intake was computed on the b asis of a food diary. REE was measured with indirect calorimetry, and body composition was assessed by both anthropometry and bioimpedance. A significant decrease in fat mass in A compared with B was found (14. 8 +/- 5.39 vs. 19.0 +/- 3.50 kg; p < 0.05). No significant differences were observed in fat-free mass (FFM) or in total body water between t he two groups. A showed higher REE values normalized by FFM than B (35 .5 +/- 2.97 vs. 33.0 +/- 2.95 kcal/kg(FFM); p < 0.05). The nonprotein respiratory quotient was significantly lower in A than in B (0.76 +/- 0.03 vs. 0.86 +/- 0.03; p < 0.001), and A showed significantly higher lipid oxidation and lower carbohydrate oxidation than B (p < 0.05). Th e daily caloric intake provided only by food ingestion was found to be significantly higher in controls, but because the percentage of alcoh ol calories of total energy intake was 46.3 +/- 6.80 in alcoholics and 13.6 +/- 3.59 in controls (p < 0.0001), the total caloric intake, com puted as food intake plus alcohol intake, was higher in alcoholics tha n in control subjects. No statistical differences were found in urinar y nitrogen excretion and fecal loss between groups. Patients with alco holism showed an increased REE over predicted values and a preferentia l lipid oxidation with respect to controls; these findings could be re lated to induction of microsomal ethanol oxidizing system and to mitoc hondrial function adaptation secondary to chronic alcohol abuse. In ei ther case, the effects of such changes in energy metabolism may contri bute to alcohol associated hepatic injury.