PubMed1981
Development of alcohol-related liver and other diseases appears to be modified by host and environmental factors that include diet and nutritional status, exposure to other drugs and toxins, and infection. The relative importance of alcohol toxicity and malnutrition in the induction of fatty liver and cirrhosis, the subject of this report, has been debated. Male rhesus (M mulatta) monkeys were fed purified liquid diets, adequate or marginally deficient in lipotropes (choline, methionine, and folate), containing ethanol to supply 40-50% of calories for 1.5-4.5 years. Controls, fed the diets with sucrose and fat isocalorically substituted for ethanol, grew well and were clinically normal. Ethanol-fed monkeys in both diet groups failed to gain weight and were slightly anemic, with mild derangements of serum electrolytes and small amounts of fat in their livers. None had fibrosis or cirrhosis until the severity of the lipotrope-deficiency was increased; then two of four deficient animals developed cirrhosis and one developed fibrosis. (The severe deficiency induced weight loss and fatty liver, but not fibrosis, in one of two controls.) We conclude that alcohol does not induce hepatic fibrosis or cirrhosis in rhesus monkeys fed a nutritionally complete diet, a result supported by studies in rats and another monkey, M radiata. Alcohol does induce cirrhosis when fed in combination with a lipotrope-deficient diet that is not, by itself, cirrhogenic.