Abstract

The coronavirus disease 2019 (COVID-19) lockdown dramatically changed people’s lifestyles. Diet, physical activity, and the PNPLA3 gene are known risk factors for non-alcoholic fatty liver disease (NAFLD). Aim: To evaluate changes in metabolic and hepatic disease in NAFLD patients after the COVID-19 lockdown. Three hundred and fifty seven NAFLD patients were enrolled, all previously instructed to follow a Mediterranean diet (MD). Anthropometric, metabolic, and laboratory data were collected before the COVID-19 lockdown in Italy and 6 months apart, along with ultrasound (US) steatosis grading and information about adherence to MD and physical activity (PA). In 188 patients, PNPLA3 genotyping was performed. After the lockdown, 48% of patients gained weight, while 16% had a worsened steatosis grade. Weight gain was associated with poor adherence to MD (p = 0.005), reduced PA (p = 0.03), and increased prevalence of PNPLA3 GG (p = 0.04). At multivariate analysis (corrected for age, sex, MD, PA, and PNPLA3 GG), only PNPLA3 remained independently associated with weight gain (p = 0.04), which was also associated with worsened glycemia (p = 0.002) and transaminases (p = 0.02). During lockdown, due to a dramatic change in lifestyles, half of our cohort of NAFLD patients gained weight, with a worsening of metabolic and hepatologic features. Interestingly, the PNPLA3 GG genotype nullified the effect of lifestyle and emerged as an independent risk factor for weight gain, opening new perspectives in NAFLD patient care.

Highlights

  • Nonalcoholic fatty liver disease (NAFLD) is defined by the presence of fat in more than 5% of hepatocytes in the absence of other causes of liver disease [1]

  • We demonstrated the negative impact of the COVID-19 lockdown on NAFLD because of worsening lifestyle habits, which play a key role in the therapy for these patients

  • We demonstrated for the first time that the COVID-19 lockdown had a dramatic negative impact in the NAFLD population, leading to weight gain and the worsening of steatosis, consequent to a deterioration of healthy lifestyle habits

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Summary

Introduction

Nonalcoholic fatty liver disease (NAFLD) is defined by the presence of fat in more than 5% of hepatocytes in the absence of other causes of liver disease [1]. Mostly type 2 diabetes (T2DM) and obesity [2,3], as well as genetic predisposition, especially polymorphism in the patatin-like phospholipase domaincontaining protein 3 (PNPLA3) gene [4,5,6,7], are risk factors for NAFLD onset and progression towards advanced liver disease. The most recommended diet regimen in patients with NAFLD is the Mediterranean diet (MD) [12,13,14,15,16], characterized by reduced daily intake of carbohydrates (30% of the whole daily caloric intake, preferably whole grain) and high fat consumption (35–45% of the total energy intake), mainly mono-unsaturated fatty acids (MUFAs) and poly-unsaturated fatty acids (PUFAs)—coming from olive oil, nuts, and fish —with a low intake of saturated fatty acids (

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