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American Journal of Clinical Nutrition, Vol 20, 213-225, Copyright © 1967 by The American Society for Clinical Nutrition, Inc.
1 From the Research Institute of The Hospital for Sick Children, Toronto 2, Canada
The liver damage frequently encountered in patients with a history of prolonged and excessive consumption of alcohol has indicted it as a hepatotoxin in the view of some investigators. Others explain this association between the precipitation of cirrhosis and a high intake of calories from alcohol by invoking the induction of dietary imbalances and multiple deficiencies of essential food factors and vitamins by their dilution with empty alcohol-calories.
It has previously been shown that even advanced stages of cirrhosis induced in rats by dietary choline deficiency can be halted and reversed by treating the rats with completely adequate diets high in protein and all other known essential nutrients. If alcohol acted on the liver as a direct hepatotoxin, its continued consumption during treatment even with such completely adequate diets would be expected to retard the rate of improvement in hepatic structure and function. But in the experiments reported here, the addition of alcohol (36% of total caloric intake) to the nutritionally adequate super diets permitted regression of cirrhosis to the same degree as in comparably cirrhotic animals given the same diets without the added alcohol. This result provides evidence against the hypothesis that alcohol is cirrhogenic by virtue of a direct hepatotoxic action. By implication, it affords hope for achieving some recovery of liver function in even those alcoholics who cannot give up spirits, if only they can be induced to consume simultaneously high protein diets containing abundant vitamins and essential food factors.
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W. S. Hartroft, E. A. Porta, L. Feinman, and C. S. Lieber Fibrogenic Effect of Alcohol in Rat Liver: Role of Diet Science, January 26, 1973; 179(4071): 406 - 407. [PDF] |
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