Kirpich IA1, Feng W1, Barve SS1, McClain CJ1,2
1Department of Medicine and Alcohol Research Center, University of Louisville, Louisville, Kentucky, USA
2Robley Rex VAMC, Louisville, Kentucky, USA
Malnutrition, both protein energy malnutrition (PEM) and deﬁciencies in individual nutrients, is a frequent complication of alcoholic liver disease (ALD). Severity of malnutrition correlates with severity of ALD. Malnutrition also occurs in patients with cirrhosis due to etiologies other than alcohol, and thus is of global importance to liver disease. The mechanisms for this malnutrition are multifactorial. Alcoholics are frequently consuming 15 or more standard drinks per day and 2,000 or more calories per day which has limited nutritional value. Malnutrition frequently worsens in the hospital due to fasting for procedures and metabolic complications of liver disease, such as hepatic encephalopathy. Aggressive nutritional support is indicated in inpatients with ALD, especially those with severe alcoholic hepatitis (AH). Patients may need to be fed through an enteral feeding tube to achieve protein and calorie goals. Enteral nutritional support clearly improves nutrition status and may improve clinical outcome. Indeed, one multicenter study suggested that aggressive nutritional support in AH was as effective as steroids in reducing short term mortality, and better at reducing long term mortality. Moreover, late-night snacks for outpatient cirrhotics improve nutritional status and lean body mass. Micronutrient deficiencies are common. Zinc deficiency causes gut-barrier dysfunction and plays a critical role in oxidative stress and proinflammatory cytokine production in ALD. Zinc is a critical factor in multiple important zinc finger proteins. Magnesium deficiency is common in alcoholic cirrhotics and often leads to muscle cramps. Vitamin D metabolism is impaired in almost all patients with ALD and can lead to alterations in immune function and gut-barrier function. Altered intake/metabolism of macronutrients, such as dietary fat, is also frequently observed in ALD. Increased intake of linoleic acid plays a critical role in the development of experimental alcohol-related liver injury. Oxidation products of linoleic acid are highly toxic. Moreover, with an increase in omega-6 fatty acids, such as linoleic acid, there is usually an associated decrease in omega-3 fatty acids which are anti-inflammatory and which give rise to specialized pro-resolving mediators. Thus, with no FDA-approved therapy for ALD, careful nutritional intervention should be considered as frontline therapy.