The role of nutritional therapy in alcoholic liver disease

Alcohol Research & Health, Winter, 2006 by Christopher M. Griffith, Steven Schenker

Alcoholic liver disease (ALD) evolves through various stages, and malnutrition correlates with the severity of ALD. Poor nutrition is caused both by the substitution of calories from alcohol for calories from food and by the malabsorption and maldigestion of various nutrients attributed to ALD. The only established therapy for ALD consists of abstinence from alcohol. Sufficient nutritional repletion coupled with appropriate supportive treatment modalities may be effective in reducing complications associated with ALD--particularly infection. Nutrition makes a significant positive contribution in the treatment of ALD, especially in selected malnourished patients. KEY WORDS: Ethanol metabolism; heavy alcohol use; alcoholic liver disease; alcoholic fatty liver; alcoholic hepatitis; fibrosis; alcoholic cirrhosis; gut; infection; anorexia; hepatic encephalopathy; nutrition; malnutrition; nutritional therapy; S-Adenosylmethionine (SAM); antioxidants; milk thistle; silymaryin; phosphatidylcholine; dietary fat; vitamins

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The study of malnutrition in patients with alcoholic liver disease (ALD) is based on several general concepts and observations. Researchers and clinicians previously believed that malnutrition was the primary cause of liver injury in ALD rather than the consequence of excessive alcohol consumption. This view was based on the prevalence of malnutrition in alcoholics and those with clinical evidence of liver (i.e., hepatic) dysfunction resulting from alcohol consumption (Mendenhall et al. 1984). It now is widely accepted that the quantity and duration of alcohol consumption are the principal agents in the development of alcoholic liver injury. This is based on animal and human data showing that ALD can develop in well-nourished individuals who consume large amounts of alcohol (Mezey 1991). However, a great deal of variability exists regarding the individual development of progressive alcoholic liver injury. Although more than 90 percent of people with excessive alcohol consumption will develop fatty liver (defined as greater than 5 percent fat in the liver), only up to 35 percent will develop inflammation of the liver caused by alcohol (i.e., alcoholic hepatitis) and only 20 percent will progress to scarring of the liver (i.e., cirrhosis) (McCullough and O'Connor 1998). Clearly, other risk factors, including genetic predisposition, obesity, concomitant viral hepatitis infection, and poor nutrition, may contribute variably to the development of ALD.

Indeed, in a large study of hospitalized patients with varying severity of ALD, malnutrition (especially the type caused by deficient protein and calories) was closely associated (although not necessarily causal) with the severity of liver injury (Mendenhall et al. 1984). All patients with clinical evidence of ALD (regardless of severity) exhibited some features of malnutrition. With regard to the possible value of nutritional therapy, it would seem logical that patients with more severe deficits would benefit more, although convincing proof of this, to our knowledge, is not available.

This article reviews the various forms of liver injury; the basis for and role of malnutrition in ALD, including the harmful effects of the products of alcohol metabolism; evidence for the benefits of nutrition; and special considerations for nutritional therapy in ALD.

DIVERSITY OF LIVER INJURY

Alcoholic liver injury is known to evolve through various stages. Patients exhibit a variety of clinical symptoms and signs in liver histology (as reviewed in Dasarathy and McCullough 2003). As previously mentioned, almost everyone with heavy alcohol consumption develops fatty liver. This often is a rather benign disorder and considered reversible upon cessation of alcohol intake. In some cases, continued drinking may result in the development of alcoholic hepatitis, which may--and often does--end in severe clinical disease. The severity of disease and liver dysfunction correlates with an increasing short-term mortality (as reviewed in Dasarathy and McCullough 2003). It is in this acutely diseased group that optimal nutritional therapy might have the most impact. Continued drinking in this group of patients may lead to the development of excess scar tissue in the liver (i.e., fibrosis) and the subsequent anatomical changes of cirrhosis. Cirrhosis is considered a late stage of the disease, clinically manifested by progressive liver dysfunction with associated yellowing of skin and whites of the eyes (i.e., jaundice)--caused by decreased liver clearance of bilirubin, fluid accumulation in the abdomen (i.e., ascites), and impaired brain function caused by the accumulation of ammonia in the brain tissues (i.e., encephalopathy) (as reviewed in Dasarathy and McCullough 2003).

These three disorders may occur separately or often in association with each other. In many instances, these stages of liver injury may be difficult to distinguish either clinically or by laboratory measures of liver dysfunction (as reviewed in Dasarathy and McCullough 2003). Prior studies regarding nutritional therapy in ALD often did not differentiate between these various types of liver disease, complicating researchers' abilities to assess the true benefit of nutritional therapy. This has been a problem in the assessment of such data in the past as well as for the present authors.