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

By Dr. Priyom Bose, Ph.D.Jan 23 2024

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

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

Background

NAFLD accounts for a wide range of liver ailments that include simple liver steatosis, liver fibrosis, non-alcoholic steatohepatitis (NASH), cirrhosis, and hepatocellular carcinoma (HCC). NAFLD has been characterized as an accumulation of lipids in 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 risk of obesity, cardiovascular events, diabetes, and hypertension. Around 30% of adult Americans have received an NAFLD diagnosis in recent years, making it a cause for public concern. The high consumption of fried foods, processed meat, refined grains, and fructose-rich foods enhances the risk of NAFLD. To date, there is no 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 preventing the progression of NAFLD. For instance, a higher intake of legumes, whole grains, probiotic dairy products, fruits, and vegetables reduces the risk 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 fruits and vegetables, whereas preformed vitamin A is found 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 produce retinol. Two key functions of retinoic acid (RA) are the enhancement of fat oxidation and triglyceride hydrolysis to reduce 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.

About the Study

The current cross-sectional study investigated the effect of dietary vitamin A, from varied sources on the risk of developing NAFLD. In 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 selected for this study based on the study criteria. The total dietary vitamin A intake was estimated in retinol activity equivalents (μg).

Study Findings

This study's participants were around 51 years old, and they consumed approximately 334 μg/1000 kcal/day of vitamin A from their diet. In 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.

The majority of participants with NAFLD were smokers, diabetic, obese, and hyperuricemic. In comparison 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 must be noted that provitamin A carotenoid consumption was inversely correlated with the risk of NAFLD. This association prevailed irrespective of age and gender. Furthermore, a linear negative dose&ndash response relationship was observed between provitamin A carotenoid consumption and the risk of developing NAFLD.

Several studies have contradicted the aforementioned findings of this study. These contradictions could be due to the lack of adjustment for potential confounders and inconsistencies in dietary patterns, study design, and ethnic background.

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

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

Conclusions

The current study demonstrated the association between dietary vitamin A consumption from various sources and the risk of developing NAFLD. Since no treatment for NAFLD is available currently, dietary intervention, i.e., consumption of provitamin A carotenoids, could be practiced to reduce NAFLD risk.