Alcohol-nutrition interaction: 1984 update.
Alcohol remains a prevailing cause of malnutrition resulting in a variety of deficiency states secondary to decreased intake of nutrients. In addition to various well described primary malnutrition syndromes, secondary malnutrition may result from the interaction of ethanol with nutrient digestion, absorption or utilization. Some of the latter alcohol-nutrient interactions have been recently defined and their pathogenesis is discussed in this review. Included are interactions with thiamine, folic acid, vitamin A and disorders secondary to amino acid imbalances. The rationale for various forms of therapy is reviewed, including the treatment aimed at correcting the "hypermetabolic state" in alcoholics ad the pitfalls of excess nutrient administration (particularly as it pertains to pyridoxine, vitamin A and amino acids). The desirability of recognizing early precirrhotic stages of alcoholic fibrosis is emphasized, in order to start therapy prior to the medical and/or social disintegration of the alcoholic.
D000437:Alcoholism / Q000150:complications* / Q000178:diet therapy / Q000378:metabolism; D000596:Amino Acids / Q000097:blood; D000818:Animals; D002796:Choline Deficiency / Q000209:etiology; D006801:Humans; D008099:Liver / Q000378:metabolism; D008108:Liver Diseases, Alcoholic / Q000378:metabolism; D008715:Methionine / Q000172:deficiency; D009748:Nutrition Disorders / Q000209:etiology*; D010101:Oxygen Consumption; D010215:Papio; D014364:Tryptophan / Q000097:blood; D014802:Vitamin A Deficiency / Q000209:etiology
D000596:Amino Acids; D014364:Tryptophan; D008715:Methionine