Carotenoids and Nutrients Critical for NAFLD

Nonalcoholic fatty liver disease (NAFLD) is an increasingly common cause of chronic liver disease that can progress to nonalcoholic steatohepatitis (NASH).

Insulin resistance, oxidative stress, genetics and epigenetics, environmental exposures, cytokines, and hepatic microbiota combine to drive NAFLD. NASH patients have fatty infiltrates, fibrosis, and later cirrhosis, and even hepatocellular carcinoma.

Although NAFLD’s causes still aren’t clear, it seems like it’s related to metabolic syndrome.

Macrophages produce tumor necrosis factor-alpha and interleukin (IL)-1beta, which appear to induce insulin resistance and NASH. Lipopolysaccharides, interferon-gamma, IL-4, and IL-13 control the balance of M1 and M2 macrophage subtypes. Because M2 macrophages protect against M1 macrophages’ deleterious effects on NAFLD, macrophage subtypes appear to be new targets to treat NAFLD.

Existing NASH therapies (metformin, thiazolidinediones, and vitamin E) are only partially partial effective. Metformin doesn’t improve NASH pathophysiology as significantly as monotherapy, but pioglitazone improves steatosis and inflammation, and vitamin E improves all symptoms except fibrosis.

Physical activity, gradual weight loss, and dietary counseling decrease steatosis. Therefore, clinicians should encourage NAFLD patients to eat diets rich in fruits and vegetables.

Produce-rich diets provide bioactive components that have anti-inflammatory and antioxidative properties. Nutraceuticals that contain antioxidants and phenols (omega-3 fatty acids, anthocyanins, silymarin, and resveratrol) have been of great interest to researchers.

Carotenoids, such as astaxanthin, are of particular interest, although their efficacy is unclear. A Japanese team of researchers reported that carotenoids prevent and treat NASH in a recent article published in the journal Nutrients.

Dietary carotenoids collect in the liver for systemic distribution. The potent antioxidant carotenoid astaxanthin, found in a variety of edible marine species, has a potent negative effect on lipid peroxidation that’s 100 to 500 times greater than vitamin E’s effect.

Astaxanthin increases glutathione and superoxide dismutase, and it prevents steatosis, fibrosis, and insulin resistance in rodent models. Astaxanthin reduces steatosis, inflammation, and insulin resistance better than vitamin E. Astaxanthin promotes M2 activation directly and reverses hepatic fibrosis.

Carotenoids like astaxanthin act through multiple synergistic pathophysiology mechanisms to prevent and treat NAFLD.