The Role of Nutrition in Alcohol-associated Liver Disease

Abstract and Introduction

Abstract

Background: Malnutrition is a commonly encountered issue in patients with alcohol-associated liver disease. The role of nutritional supplementation in the management of alcohol-associated liver disease is integral to patient outcomes—it has been shown to decrease rates of hepatic encephalopathy, improve outcomes post-liver transplant, reduce 90-day hospital readmissions and lower mortality. Despite these benefits, many studies have shown nutritional support to be an underutilised tool in the care of patients with alcohol-associated liver disease.

Aims: To review the epidemiology, pathophysiology, recommendations for nutritional assessment and supplementation, as well as future directions for research of the relationship between nutrition and alcohol-associated liver disease.

Methods: A literature search was conducted via PubMed using MeSH terms to inform this narrative review.

Results: Decreased dietary intake, socioeconomic status, impaired absorption of nutrients and increased free radical species are implicated in the pathophysiology of malnutrition in alcohol-associated liver disease.

Conclusions: Malnutrition is common in alcohol-associated liver disease, and physicians should be aware of its association with poor clinical outcomes. Routine nutritional assessment, involvement of a dietician and nutritional supplementation are recommended to improve clinical outcomes in patients with alcohol-associated liver disease.

Introduction

As alcohol consumption increases globally, so too does the disease burden of alcohol-associated liver disease (ALD). ALD refers to a spectrum of disease states including asymptomatic steatosis, alcoholic hepatitis and cirrhosis.^[1] Progression across stages depends not only on alcohol consumption but additional risk factors such as genetic susceptibility, sex, presence of other concurrent liver disease and diet.^[1] ALD accounts for a substantial portion of the worldwide cirrhosis burden and is one of the leading indications for liver transplant. Patients with ALD are at increased risk for malnutrition, which has long been associated with poor clinical outcomes.^[2] This article will review the epidemiology, pathophysiology, nutritional assessment and supplementation recommendations for nutrition in the setting of ALD. A literature search was conducted via PubMed using MeSH terms to inform this narrative review.

Table 1. Mechanisms of malnutrition in ALD
Decreased dietary intake • Increased ingestion of 'empty' calories from alcohol • Anorexia	Results in fewer calories and nutrients available for utilisation
Impaired absorption and digestion of nutrients • Increased unconjugated bile acids and impaired bile acid metabolism • Exocrine pancreas insufficiency • Increased gut wall permeability • Portosystemic shunting • Early shift to gluconeogenesis in patients with cirrhosis while fasting	Results in decreased digestion and absorption of carbohydrates, proteins, and fats Results in impaired absorption of micronutrients due to downregulation of divalent cation transporters
Increased free radical species • Increased use of alternative metabolic pathways • Increased oxidative stress • Cytokines	Results in breakdown of skeletal muscle fibers and sarcopenia Leads to a systemic proinflammatory state that increases catabolism and resting energy expenditure
Socioeconomic status • Unbalanced diet with disproportionate amounts of processed foods and fructose • Food scarcity	Results in both macronutrient and micronutrient deficiencies

Table 2. Micronutrient deficiencies in ALD
Micronutrient	Prevalence	Symptoms	Assessment/supplementation strategies
Vitamin B12	25% of patients with alcohol use disorder	Peripheral neuropathy; macrocytic anaemia	Test on initial nutritional assessment and replete if deficient
Folate	80% of patients with alcohol use disorder	Macrocytic anaemia	Test on initial nutritional assessment and replete if deficient
Magnesium	Limited data	Weakness, decreased appetite, nausea, vomiting, cramping, seizure	The need for general supplementation is controversial. If noted to be low on initial assessment replete as appropriate
Thiamine	80% of patients with alcohol use disorder	Dry beriberi including Wernicke encephalopathy, Korsakoff's syndrome; wet beriberi	Prophylactic supplementation in those with alcohol use disorder
Vitamin A	Data are limited	Blindness; dry skin and eyes; hypogonadism	Do not recommend routine assessment or repletion unless patient exhibits a symptomatic deficiency
Vitamin D	86% of patients with cirrhosis	Bone demineralization; pain; fatigue; depression	Test on initial nutritional assessment and replete if deficient
Vitamin E	Data are limited	Muscle weakness; impaired reflexes; ataxia	Do not recommend routine assessment or repletion unless patient exhibits a symptomatic deficiency
Zinc	83% of patients with cirrhosis	Alopecia; hypogonadism; loss of appetite; dermatitis enteropathica (periorificial dermatitis); diarrhoea	Test on initial nutritional assessment if a symptomatic deficiency exists though may consider empiric supplementation regardless given existing data

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The Role of Nutrition in Alcohol-associated Liver Disease

Abstract and Introduction

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