Alcohol and Nutrition

The nutritional status of alcoholics is often impaired. Some of the pathophysiological changes seen in alcoholics are direct consequences of malnutrition. However, in the 1960s, Charles Lieber demonstrated that many alcohol-induced pathologies, including alcoholic hepatitis, cirrhosis, and myopathy, are reproducible in animals fed a nutritionally adequate diet. Consequently, the concept that all alcohol-induced pathologies are due to nutritional deficiencies is outdated and incorrect.

Myopathy is a direct consequence of alcohol or acetaldehyde on muscle and is not necessarily associated with malnutrition. Assessment of nutritional status in chronic alcoholics using anthropometric measures (e.g., limb circumference and muscle mass) may be misleading in the presence of myopathy.

Acute or chronic ethanol administration impairs the absorption of several nutrients, including glucose, amino acids, biotin, folate, and ascorbic acid. There is no strong evidence that alcohol impairs absorption of magnesium, riboflavin, or pyridoxine, so these deficiencies are due to poor intakes. Hepa-togastrointestinal damage (e.g., villous injury, bacterial overgrowth of the intestine, pancreatic damage, or cholestasis) may impair the absorption of some nutrients such as the fat-soluble vitamins (A, D, E, and K). In contrast, iron stores may be adequate as absorption is increased.

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