Folate turnover in chronically alcoholic monkeys.

To study the pathogenesis of folate deficiency in chronic alcoholism, monkeys were fed nutritionally complete liquid diets containing 50% of energy as ethanol for 4 years. The initial excretion and subsequent turnover of a tracer dose of intramuscular 3H-folic acid was measured during a 25-day period prior to autopsy. Within the first 3 days, the excretion of tritium in the urine and feces was significantly greater in the ethanol-fed monkeys than in their pair-fed controls, and most of the folate recovered in the urine of the third day was unchanged 3H-folic acid. Analysis of total body tritium retention revealed a rapid phase of elimination (0 to 3 days), in which the half-time of elimination was shorter in the ethanol-fed group, and a slow phase (4 to 25 days) with similar half-times of elimination. At autopsy, the levels and total amounts of endogenous folates in the liver were decreased in the ethanol-fed monkeys, as was the recovery of tritium. These studies suggest that folate deficiency in chronic alcoholism is caused in part by increased urinary and fecal losses and resultant decreased hepatic incorporation of exogenous folate whereas long-term folate turnover is unchanged.