Pathology Of Alcohol Abuse

Alcohol abuse affects all organs of the body (Lieber, 1992a). It atrophies many tissues, including the brain and the endocrine glands. Indeed, altered hepatic (liver) metabolism plays a key role in a variety of endocrinological imbalances (such as go-nadal dysfunctions and reproductive problems). Alcohol also exerts toxic effects on the bone marrow and alters hematological status (e.g., macrocytic anemias), and it scars the heart and other muscles. This article focuses mainly on the liver and gastrointestinal tract, since this is where alcohol penetrates into the body and has its most vicious effects; this focus will also allow exemplification of the insights and possible benefits that can be derived from the application of newly acquired knowledge in biochemistry, pathology, and molecular biology.

Liver disease, one of the most devastating complications of alcoholism, was formerly attributed exclusively to the malnutrition associated with ALCOHOLISM. Indeed, nutritional deficiencies are common in the alcoholic for various reasons, some socioeconomic, but also because alcohol is a unique compound. Alcohol is a drug, a psychoactive drug, but unlike other drugs, which have negligible energy value, alcohol has a high energy content— each gram of alcohol contributes 7.1 kilocalories, which means that a cocktail or a glass of wine will provide 100 to 150 kilocalories. Thus, alcoholic beverages are similar to food in energy terms, but, unlike food, they are virtually devoid of vitamins, proteins, and other nutrients; they act as a provider of empty calories.

As shown in Figure 1, because of its large energy load, alcohol decreases the appetite for food and displaces other nutrients in the diet, thereby promoting primary malnutrition (Lieber, 1991a). Nutrition is also impaired because alcohol affects the gastrointestinal tract. Alcohol-induced intestinal lesions, including pancreatitis, are associated with maldigestion and malabsorption, causing secondary malnutrition. Moreover, malnutrition itself will create functional impairment of the gut. Finally, alcohol (ethanol or its metabolite acetalde-hyde) also adversely affects nutritional status by altering the hepatic activation or degradation of essential nutrients.

Indeed, in experimental animals, malnutrition may produce a variety of liver alterations, including fatty liver and fibrosis; however, the extent to which malnutrition contributes to the development of liver disease in the alcoholic remains unclear. Furthermore, studies conducted in the past three decades have shown that either the initial liver lesion—the fatty liver—or the ultimate stage of cirrhosis can be produced by excess alcohol, even in the absence of dietary deficiencies (Lieber & De-Carli, 1991), because ethanol (via its metabolism and/or its metabolite acetaldehyde) exerts direct hepatotoxic effects. Thus, malnutrition plays a per-

Figure 1

Interaction of Direct Toxicity of Ethanol on Liver and Gut with Malnutrition Secondary to Dietary Deficiencies, Maldigestion and Malabsorption. SOURCE: Lieber, C. S. (1991a). Alcohol, liver, and nutrition. Journal of the American College of Nutrition, 10 602-632.

Figure 1

Interaction of Direct Toxicity of Ethanol on Liver and Gut with Malnutrition Secondary to Dietary Deficiencies, Maldigestion and Malabsorption. SOURCE: Lieber, C. S. (1991a). Alcohol, liver, and nutrition. Journal of the American College of Nutrition, 10 602-632.

missive, but not an obligatory, role in alcohol-related somatic pathology.

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