Ultra-processed Food Is Associated With Features of Metabolic Syndrome and Non-alcoholic Fatty Liver Disease

Dana Ivancovsky-Wajcman; Naomi Fliss-Isakov; Muriel Webb; Itay Bentov; Oren Shibolet; Revital Kariv; Shira Zelber-Sagi

Disclosures

Liver International. 2021;44(11):2635-2645. 

In This Article

Abstract and Introduction

Abstract

Background & aims: High consumption of ultra-processed food (UPF) is associated with mortality and chronic morbidity but has not been studied concerning to non-alcoholic fatty liver disease (NAFLD). We aimed to test the association of UPF consumption with metabolic syndrome, NAFLD and related-liver damage.

Methods: A cross-sectional study among volunteers who underwent abdominal ultrasound (AUS), anthropometrics, blood pressure measurements, and fasting blood tests including FibroMax for non-invasive assessment of NASH and significant fibrosis. A food-frequency questionnaire was used to evaluate UPF consumption using the NOVA classification.

Results: A total of 789 subjects were included in the total sample (mean age 58.83 ± 6.58 years, 52.60% men), a reliable FibroMax test was obtained from 714 subjects, 305 subjects were diagnosed with NAFLD. High consumption of UPF was associated with higher odds for metabolic syndrome (OR = 1.88, 95% CI 1.31–2.71, P = .001) and its components; hypertension, hypertriglyceridemia, and low HDL, among the entire sample (OR = 1.53, 1.07–2.19, P = .026; OR = 1.51, 1.08–2.11, P = .017; OR = 1.55, 1.05–2.29, P = .028). In addition, it was associated with higher odds for NASH and hypertension (OR = 1.89, 1.07–3.38, P = .030; OR = 2.26, 1.20–4.26, P = .012 respectively) among subjects with NAFLD. Stratification by smoking status revealed an association between high UPF consumption and significant fibrosis among ever smokers in the entire sample and among subjects with NAFLD (OR = 1.89, 95% CI 1.03–3.45, P = .039; OR = 2.85, 1.14–7.14, P = .026 respectively).

Conclusions: High UPF consumption is associated with metabolic syndrome in the general population, and among those with NAFLD it is associated with NASH marker. Ever-smoking may act synergistically with UPF to amplify the risk for fibrosis.

Introduction

Ultra-processed foods (UPF) are often characterized by low nutritional quality, high energy density and the presence of additives, substances from packaging in contact with food, and compounds formed during production, processing and storage.[1,2] This food group includes industrial formulations, and usually contains many ingredients, typically five or more. Such ingredients often include sugar, oils, fats, salt, anti-oxidants, stabilizers and preservatives.

The consumption of ultra-processed products has increased dramatically worldwide. In Europe (among aged 35–74 years), highly processed foods contributed more than 60% of mean energy intake,[3] and 58% in the United States (among aged 1 year and older).[2] The average content of protein, fibre, vitamins A, C, D and E, zinc, potassium, phosphorus, magnesium and calcium in the diet decreases significantly across quintiles of the energy contribution of UPFs, while carbohydrate, added sugar, and saturated fat contents increase.[2] Ultra-processed foods contribute most of the added (free) sugars[4] in the western diet,[4] reaching 65% of the total dietary free sugars in the United Kingdom.[5] Several cross-sectional and prospective studies have shown an association between the dietary share of UPFs and the risk of various diet-related chronic diseases including; obesity, cardiovascular risk factors, type-2 diabetes, cardiovascular disease, cancer, gastrointestinal disorders, frailty and mortality.[1,6–11] In a work by our group, we have demonstrated an association of processed meat with non-alcoholic fatty liver disease (NAFLD) and insulin resistance (IR).[12] However, none of the studies have addressed a direct association of the entire UPF consumption with NAFLD and related markers for liver damage.

Smoking is another risk factor accelerating liver disease progression by itself and may act in synergism with the other risk factors.[13–16] Smoking has been demonstrated to be associated with the progression of fibrosis in NAFLD patients.[17,18]

Therefore, the aims of this study were to test the association between consumption of the group of foods classified as UPFs and NAFLD and related liver-damage markers and to elaborate on the association with metabolic syndrome and its components in a general population, as well as among NAFLD diagnosed subjects. We also aimed to test the potential modifying effect of smoking on the association of UPFs with liver fibrosis.

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