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Dietary carotenoids may reduce risk of non-alcoholic fatty liver disease, study suggests

A recent Scientific Reports study investigated whether total dietary vitamin A influenced the danger of developing non-alcoholic fatty liver disease (NAFLD) amongst adults.

​​​​​​​Study: Association between dietary vitamin A intake from different sources and non-alcoholic fatty liver disease amongst adults. ​​​​​​​Image Credit: marilyn barbone / Shutterstock


NAFLD accounts for a big selection of liver ailments that include easy liver steatosis, liver fibrosis, non-alcoholic steatohepatitis (NASH), cirrhosis, and hepatocellular carcinoma (HCC). NAFLD has been characterised as an accumulation of lipids within the liver without having any link to excessive alcohol consumption or the prevalence of other liver diseases.

Several studies have shown that NAFLD increases the danger of obesity, cardiovascular events, diabetes, and hypertension. Around 30% of adult Americans have received an NAFLD diagnosis in recent times, making it a cause for public concern. The high consumption of fried foods, processed meat, refined grains, and fructose-rich foods enhances the danger of NAFLD. So far, there isn’t any effective drug that has received approval for the treatment of NAFLD. 

Antioxidants (e.g., vitamins A, C, and E) and dietary modifications have shown positive effects in stopping the progression of NAFLD. As an example, a better intake of legumes, whole grains, probiotic dairy products, fruits, and vegetables reduces the danger of NAFLD.

Vitamin A has dual properties, i.e., antioxidant and antifibrotic. This vitamin exists in major forms, namely, preformed vitamin A and provitamin A carotenoids. Retinol and retinyl esters belong to the category of preformed vitamin A, while β-carotene is an example of provitamin A carotenoids. Provitamin A carotenoids are mainly present in vegetables and fruit, whereas preformed vitamin A is present in animal products. 

Experimental studies have shown that carotenoids are absorbed via a passive diffusion process, and preformed vitamin A absorption occurs through carrier-dependent proteins. In liver cells, retinyl esters are hydrolyzed by retinyl ester hydrolase to provide retinol. Two key functions of retinoic acid (RA) are the enhancement of fat oxidation and triglyceride hydrolysis to scale back the progression of NAFLD. The antioxidant properties of carotenoids can alleviate hepatic dysfunction.

Although several studies have indicated the association between vitamin A and NAFLD, the effect of total dietary vitamin A intake on NAFLD risk is unclear.

Concerning the Study

The present cross-sectional study investigated the effect of dietary vitamin A, from varied sources on the danger of developing NAFLD. Within the US, the National Health and Nutrition Examination Survey (NHANES) was conducted by the National Center for Health Statistics (NCHS) of the Centers for Disease Control and Prevention (CDC). This survey provided demographic, dietary, health, and socio-economic information.

Out of 40,617 participants of the NHANES, 6,613 were chosen for this study based on the study criteria. The entire dietary vitamin A intake was estimated in retinol activity equivalents (μg).

Study Findings

This study’s participants were around 51 years old, they usually consumed roughly 334 μg/1000 kcal/day of vitamin A from their food plan. Within the study cohort, 36.7% of participants were diagnosed with NAFLD. Typically, older participants and individuals with lower education and household income were found to be more inclined to develop NAFLD.

Nearly all of participants with NAFLD were smokers, diabetic, obese, and hyperuricemic. As compared to non-NAFLD individuals, NAFLD patients were found to be linked with higher consumption of preformed vitamin A. Interestingly, after adjustment of potential confounders, no association between total dietary vitamin A intake and NAFLD risk was observed. 

It should be noted that provitamin A carotenoid consumption was inversely correlated with the danger of NAFLD. This association prevailed regardless of age and gender. Moreover, a linear negative dose&ndash response relationship was observed between provitamin A carotenoid consumption and the danger of developing NAFLD.

Several studies have contradicted the aforementioned findings of this study. These contradictions could possibly be as a result of the shortage of adjustment for potential confounders and inconsistencies in dietary patterns, study design, and ethnic background.

Previous studies have highlighted carotenoids’ capability to reverse inflammation, steatosis, and fibrosis progression in NASH. Mechanistically, carotenoids prevent the activation of macrophage or Kupffer cells and lower insulin resistance, which results in recovery from steatohepatitis.

Carotenoids and their metabolites have the capability to change adiponectin expression. Adiponectin can promote the downregulation of nuclear factor-kappa B (NFκB) and TNF-α, that are linked with increasing NAFLD risk.


The present study demonstrated the association between dietary vitamin A consumption from various sources and the danger of developing NAFLD. Since no treatment for NAFLD is on the market currently, dietary intervention, i.e., consumption of provitamin A carotenoids, could possibly be practiced to scale back NAFLD risk.

Journal reference:

  • Liu, C. et al. (2024) Association between dietary vitamin A intake from different sources and non-alcoholic fatty liver disease amongst adults. Scientific Reports. 14(1), pp. 1-9. DOI: 10.1038/s41598-024-52077-5,
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