Abstract

Non-alcoholic fatty liver disease (NAFLD) is the most common cause of chronic liver disease worldwide, with a prevalence of 25–30%. Since its first description in 1980, NAFLD has been conceived as a different entity from alcohol-related fatty liver disease (ALD), despite that, both diseases have an overlap in the pathophysiology, share genetic–epigenetic factors, and frequently coexist. Both entities are characterized by a broad spectrum of histological features ranging from isolated steatosis to steatohepatitis and cirrhosis. Distinction between NAFLD and ALD is based on the amount of consumed alcohol, which has been arbitrarily established. In this context, a proposal of positive criteria for NAFLD diagnosis not considering exclusion of alcohol consumption as a prerequisite criterion for diagnosis had emerged, recognizing the possibility of a dual etiology of fatty liver in some individuals. The impact of moderate alcohol use on the severity of NAFLD is ill-defined. Some studies suggest protective effects in moderate doses, but current evidence shows that there is no safe threshold for alcohol consumption for NAFLD. In fact, given the synergistic effect between alcohol consumption, obesity, and metabolic dysfunction, it is likely that alcohol use serves as a significant risk factor for the progression of liver disease in NAFLD and metabolic syndrome. This also affects the incidence of hepatocellular carcinoma. In this review, we summarize the overlapping pathophysiology of NAFLD and ALD, the current data on alcohol consumption in patients with NAFLD, and the effects of metabolic dysfunction and overweight in ALD.

Highlights

  • Non-alcoholic fatty liver disease (NAFLD) and alcohol-related liver disease (ALD) are the most frequent causes of chronic liver disease worldwide [1, 2]

  • Mild wine consumption was associated with 50% reduced risk of elevated serum alanine aminotransferase (ALT) without effect in beer or liquor intake Mild (40–140 g per week) and moderate (140–280 g per week) alcohol intake reduced the risk of steatosis Alcohol consumption was associated with a reduced risk of steatosis

  • This reduction was independently of metabolic syndrome (MetS) and physical activity Fatty liver increased with obesity and decreased with alcohol intake The prevalence of steatosis was lower in drinkers than in non-drinkers’ men and women (p < 0.001 for both)

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Summary

Introduction

Non-alcoholic fatty liver disease (NAFLD) and alcohol-related liver disease (ALD) are the most frequent causes of chronic liver disease worldwide [1, 2]. Both entities have been increasing in the U.S and worldwide, contributing to the rising burden of cirrhosis and hepatocellular carcinoma (HCC) and surpassing the figures of viral hepatitis infection as chief etiologies of these conditions [3]. These temporal trend shifts in the contributions of NAFLD. NAFLD and ALD have a number of commonalities and may eventually coexist in the same individual In this context, it seems timely to review some basic and clinical concepts on these two intertwined conditions

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