Very Low Alcohol Consumption Is Associated with Lower Prevalence of Cirrhosis and Hepatocellular Carcinoma in Patients with Non-Alcoholic Fatty Liver Disease

Abstract

The role of moderate alcohol consumption in the evolution of NAFLD is still debated. The aim of this study is to evaluate the impact of current and lifelong alcohol consumption in patients with NAFLD. From 2015 to 2020, we enrolled 276 consecutive patients fulfilling criteria of NAFLD (alcohol consumption up to 140 g/week for women and 210 g/week for men). According to their current alcohol intake per week, patients were divided in: abstainers, very low consumers (C1: <70 g/week) and moderate consumers (C2). We created a new tool, called LACU (Lifetime Alcohol Consuming Unit) to estimate the alcohol exposure across lifetime: 1 LACU was defined as 7 alcohol units per week for 1 drinking year. Patients were divided into lifelong abstainers and consumers and the latter furtherly divided into quartiles: Q1-Q4. Stratification according to alcohol intake, both current and cumulative as estimated by LACU, showed that very low consumers (C1 and Q1-Q3) displayed lower frequency of cirrhosis and hepatocellular carcinoma compared to abstainers and moderate consumers (C2 and Q4). We can speculate that up to one glass of wine daily in the context of a Mediterranean diet may be a long-term useful approach in selected NAFLD patients.

Meta‐analysis: The impact of light‐to‐moderate alcohol consumption on progressive non‐alcoholic fatty liver disease

“…One cross‐sectional study used LACU, an indicator for lifetime alcoholic cumulative units defined as drinking years multiplied by median alcohol units in a week divided by 7, to assess the impact of moderate alcohol consumption on the development of cirrhosis. Patients in the lower three quartiles of moderate alcohol use had a lower risk of cirrhosis compared with lifelong abstainers (OR 0.42 (95% CI 0.19–0.95; p = 0.037)), an effect not observed for patients within the highest quartile (OR 1.35 (95% CI 0.54–3.36)) 39 …”

“…14,16,19,22,[24][25][26][27][28][29][30][31]33,[36][37][38]40,43 A total of 10 studies investigated both the effect of light and moderate alcohol consumption. 12,13,15,17,18,20,23,33,41 Of the 32 included studies, eight were performed in Europe (Italy, Finland, Sweden, United Kingdom, France and Spain), 17,26,28,29,33,38,39,43 nine in Asia (China, Japan, South Korea), 12,13,15,16,[20][21][22]37,42 10 in the United States, 23,25,27,[30][31][32]…”

Effects of COVID-19 Pandemic on Metabolic Status and Psychological Correlates of a Cohort of Italian NAFLD Outpatients

“…In particular, Mediterranean diet is based on a great reduction in the intake of highly processed food (such as sweets, sugars, sugary drinks, processed meat, ready and pre-cooked foods) in favour of complex carbohydrates (>40% of daily calories, mainly from whole grains, legumes and fibres), fats (35–45% of the total energy, mainly from mono and poly-unsaturated fatty acids) and proteins from vegetal and animal sources, with a preference for dairy products, eggs, fish and white meat. Adequate intakes of vitamins E, C and phenolic compounds, contained in nuts, seeds, vegetable oils, fruits, vegetables, coffee and tea, can protect the liver from NAFLD-related damage and the consumption of up to one glass of wine per day, as a part of a Mediterranean diet, may be considered in patients with non-advanced NAFLD [ 8 , 9 , 10 ]. Physical inactivity, which is common in patients with NAFLD, represents an independent risk factor for disease development and progression [ 11 ].…”

Liver Fat Quantification: When do We Need It?

“…The new proposal of MAFLD was set forward because the criterion for diagnosing NAFLD/NASH requires absence of any other chronic liver condition (e. g. viral hepatitis, immune-related cholestatic liver disease, etc) and absence of any over threshold intake of alcohol [1]. The terms NAFLD/NASH are correct to establish a diagnosis of liver disease purely caused by metabolic dysfunction, useful to better understand the natural history of the disease, especially in a scientific setting, but does not reflect the real-life situation, where many patients may actually suffer from metabolic liver disease on top of other liver conditions and the two conditions may or may not both contribute to the progression and complications of the liver disease with different and not well definable relevance [3]. For instance, the persistence of minimally elevated liver enzymes in slightly overweight patients after cure of HCV or after full dosage of ursodesoxycholic acid in Primary Biliary Cholangitis or Primary Sclerosing Cholangitis or after drastic reduction or the suspension of alcohol intake often raise the question whether an underlying MAFLD is present.…”

“…Allerdings spiegeln sie nicht die Lebenswirklichkeit wider, da viele Patienten zusätzlich zu anderen Lebererkrankungen auch an einer Stoffwechselerkrankung leiden können. Beide Erkrankungen können eine unterschiedliche und nicht genau definierbare Rolle spielen, was das Fortschreiten und die Komplikationen der Lebererkrankung anbelangt [3]. So stellt sich häufig die Frage, ob beispielsweise die Persistenz minimal erhöhter Leberenzyme bei leicht übergewichtigen Patienten durch eine zugrunde liegende MAFLD bedingt ist, wenn folgende Bedingungen zutreffen: nach Heilung einer HCV oder nach voller Dosierung von Ursodesoxycholsäure bei primär biliärer Cholangitis bzw.…”