In a recent study published in The Journal of Clinical Nutrition, researchers investigated the relationship between ultra-processed food (UPF) consumption and hepatic well-being.
Study: Higher ultra-processed food intake is associated with adverse liver outcomes: a prospective cohort study of UK Biobank participants. Image Credit: Created with the assistance of DALL·E 3
The Importance of Liver Health
The liver is crucial to detoxification, metabolism, and immunity. Hepatic diseases, ranging from mild and reversible conditions such as non-alcoholic fatty liver disease (NAFLD) to potentially fatal ones such as liver cirrhosis and malignancies, pose considerable burdens on healthcare systems and are a health concern worldwide. Studies have positively associated UPF intake with diabetes and obesity; however, data on the impact of UPF on the liver are limited.
Study Objectives and Methodology
In the present prospective cohort study, researchers investigated whether increased UPF consumption could elevate the risk of liver diseases such as non-alcoholic fatty liver disease (NAFLD), hepatic cirrhosis or fibrosis, severe hepatic illness, and hepatic malignancy and alter serological biomarkers of hepatic health.
Sample and Data Collection
The study included 173,889 United Kingdom Biobank (UKB) participants aged between 40 and 69, recruited from 2006 to 2010. The individuals resided within 25 miles of 22,106 Scotland, Wales, and England centers, as identified through the National Health Service (NHS) registers. UPF consumption was evaluated using the NOVA classification and one-day diet recalls. Portion size, energy, and nutrient compositions for the food items were calculated using the 2002 UK McCance and Widdowson’s Composition of Foods, sixth edition guidelines.
Key Biomarkers Analyzed
Liver outcomes were identified using the International Classification of Diseases, tenth revision (ICD-10) codes documented in mortality registries, hospital files, and cancer registries. Serological biomarkers assessed included C-reactive protein (CRP), alkaline phosphatase (ALP), alanine transaminase (ALT), aspartate aminotransferase (AST), gamma-glutamyl transferase (GGT), high-density lipoprotein-cholesterol (HDL-C), low-density lipoprotein-cholesterol (LDL-C), triglycerides, glucose, glycated hemoglobin (HbA1c), platelet counts, total protein, total bilirubin, and albumin.
Cox proportional hazard modeling was performed to determine the hazard ratios (HRs) for the link between UPF consumption and hepatic health, adjusting for lifestyle factors (such as smoking status, alcohol intake, and physical activity), demographics [such as age, ethnicity, sex, body mass index (BMI), Townsend deprivation index], diabetes, total calorie intake, and aspirin usage.
Multivariate logistic regression modeling was performed to determine the associations between ultra-professed food intake and hepatic biomarkers. Sensitivity analyses were performed by excluding the cases reported in the initial two years of follow-up, assessing UPF consumption using different scales, using mean values from two or more dietary recalls, excluding individuals with missing physical exercise data, and excluding those with baseline fatty liver index values above 60.
Study Results and Sensitivity Analyses
In total, 210,964 individuals completed one or more dietary evaluations during follow-up. However, the team excluded 18,078 individuals reporting nutritional intake on untypical days, 14,674 individuals with prior cancer history, 1,079 individuals with liver cirrhosis at study initiation, and 417 individuals with extreme calorie intake (below 500 or above 5,000 kcal per day).
In addition, 409 participants lost to follow-up, or those diagnosed with hepatic diseases or malignancies before dietary evaluation, and 2,418 individuals with missing covariate data were excluded. As a result, 173,889 individuals were included in the primary analyses, and 137,173 individuals were included in the biomarker analyses, excluding 36,716 individuals with missing data. During the nine-year follow-up (median), 350 liver cirrhosis or fibrosis, 1,108 NAFLD, 550 severe hepatic illness, and 134 hepatic malignancy cases were reported.
Key Findings and Implications
Increased UPF consumption was linked to elevated risks of non-alcoholic fatty liver disease (HR for the fourth quartile (Q4) versus the first quartile (Q1), 1.4), liver cirrhosis or fibrosis (HR 1.2), and severe hepatic illness (HR 1.5), but did not increase that of hepatic malignancies (HR 1.0). Increased UPF consumption was significantly linked to elevated ALP, CRP, AST, GGT triglycerides, and reduced cholesterol.
UPF consumption based on absolute weight showed that the main contributors were drinks (25%), dairy products (15%), and bap and bread (15%). Individuals with increased UPF intake were younger, non-white, physically inactive, diabetic, and never or occasional alcohol consumers with an elevated BMI. Sensitivity analyses yielded similar results, indicating the robustness of the findings. By cirrhosis type, increased UPF consumption significantly enhanced the risk of compensated and decompensated cirrhosis, with HR for Q4 versus Q1 of 1.3 for both.
The Concluding Verdict
Based on the study findings, UPF consumption can elevate the risks of NAFLD, hepatic cirrhosis or fibrosis, severe hepatic illnesses, and alter serological biomarkers. Therefore, UPF intake must be reduced to enhance hepatic well-being. UPF could deteriorate hepatic health by increasing oxidative stress, inflammation, microbial dysbiosis, and insulin resistance due to its high content of saturated fat, energy density, salt, added sugars, salt, and additives, and low fiber and vitamin content.