Fructose intake is not associated to the risk of hepatic fibrosis in patients with Non-Alcoholic Fatty Liver Disease (NAFLD)

• Published in: Clinical nutrition (Edinburgh, Scotland) Vol. 40; no. 6; pp. 4275 - 4283
• Main Authors: Azevedo, Vittoria Zambon, Dall’Alba, Valesca
• Format: Journal Article
• Language: English
• Published: England Elsevier Ltd 01.06.2021
• Subjects: Adult; Aged; Cross-Sectional Studies; Diet - adverse effects; Diet - methods; Diet Surveys; Dietary fructose intake; Eating - physiology; Eating patterns; Female; Fructose - adverse effects; Humans; Liver - metabolism; Liver Cirrhosis - etiology; Male; Metabolic profile; Middle Aged; Non-alcoholic fatty liver disease; Non-alcoholic Fatty Liver Disease - etiology; Non-alcoholic Fatty Liver Disease - physiopathology; Nutritional assessment; Ultra-processed foods; Nutritional assessment; Dietary fructose intake; Metabolic profile; Ultra-processed foods; Non-alcoholic fatty liver disease; Eating patterns
• ISSN: 0261-5614; 1532-1983
• DOI: 10.1016/j.clnu.2021.01.022

Non-Alcoholic Fatty Liver Disease (NAFLD) has been linked to fructose intake (FI). The aim of this study was to evaluate whether the dietary FI from different food sources (added/industrial processing and natural/intrinsic to food) is associated with NAFLD and risk of hepatic fibrosis (HF). Cross-sectional study with 128 patients with NAFLD underwent clinical, functional, laboratory, nutritional and dietary intake by 3-day-diet-record evaluation. The proportions (in grams/milliliters) of foods and beverages in the diet for each subject was computed from the database NUTTAB and classified by their processing level according to the NOVA classification to identify the source of fructose. The mean age was 54.0 ± 11.9 years; 72.7% were women, and BMI 32.6 ± 5.4 kg/m2. Total fructose (TF) intake was 21.6 g, natural fructose (NF) 14.8 g and added fructose (AF) 6.8 g. TF, NF, and AF intakes not differ in patients with steatosis, steatohepatitis and cirrhosis (p-values 0.140; 0.101; 0.739, respectively), and not justify HF according NAFLD score, in view of the low correlation power found (r2 0.009; 0.040; 0.051) respectively for TF, NF and AF. Patients presented elevated cardiometabolic risk due to the prevalence of 78.0% intermediate/high risk of HF; 96.8% over waist-to-height ratio (WHtR), 79.7% of metabolic syndrome (MetS), 65.6% low hand grip strength (HGS), and 70.3% had sarcopenic obesity. Patients had low FI compared to the amounts presented in other occidental countries and studies. No association was found between FI and NAFLD or risk of HF. •Assessment of overall fructose intake in the usual diet of NAFLD patients.•Rating of the fructose origin according to the processing level of the food.•A low fructose intake from distinct origins was similar in the NAFLD stages.•A possible energy-mediated effect may be a NAFLD trigger rather than the fructose.