The Loss of Metabolic Control On Alcohol Drinking in Heavily Drinking Alcoholics
[Background:] Most physiological studies of alcoholism consider ethanol as a pharmacological agent rather than a nutrient. We conducted two studies to assess potent metabolic and endocrine factors of alcohol and nutrient intake regulation in alcoholic subjects and a possible role of a disruption of energy balance for the development of alcoholism. [Methods and results:] Study-1 consists of quantitative anamneses of eating and drinking habits among 97 alcoholics. The population was split around a median alcohol intake value of 12.5 kcal/kg/day. `Low alcohol´ drinking alcoholics had high BMI and Fat Mass (FM) and alcohol intake was compensated for by a decrease in non-alcoholic intake. `High alcohol´ drinking alcoholics had low BMI and FM and the total intake was largely above norms. In Study-2, 22 alcoholic inpatients submitted on day 2, 5 and 16 of abstinence to diet anamneses, calorymetry, and blood sampling for the measurement of biomarkers reflecting metabolism and satiety regulation were compared to 19 matched controls. We observed increased cortisol, leptin and PYY plasma levels and decreased plasma ghrelin, that might explain the observed decrease in non-alcoholic intake. However, both alcoholic and non-alcoholic intake correlated positively with basal metabolism and negatively with leptin and leptin/BMI. [Conclusion:] Below12.5 kcal/kg/day, alcohol intake is compensated for by a decrease in nutrient intake, probably due to changes in metabolic and satiety factors. Above 12.5 kcal/kg/day, alcohol accelerates metabolism and decreases fat mass and leptin levels, and the total intake largely exceeds norms. A dual model for regulation of energy intake in alcoholics is suggested.