Relatively new study, of which I can’t yet get the full text. However, its findings are truly striking. Namely, the humble vitamin B3 may treat the highly prevalent condition NAFLD/MAFLD. This condition, which is a precursor to the more serious NASH, cirrhosis and liver cancer, affects 35% of US adults and prevention/treatment options are desperately needed. The study below demonstrates that vitamin B3 (niacinamide anyone?) may stop the condition in its tracks and also reverse already established liver damage by suppressing a protein known as microRNA-93. That protein has recently been shown to drive NAFLD/MAFLD and chemicals suppressing that protein have been repeatedly shown to be beneficial for NAFLD/MAFLD. While I can’t get the full text of the study yet, other studies by the same authors as well as some Google previews of the current study suggest that the administered daily oral dose of vitamin B3 was the human equivalent of 15mg/kg, for 60 days. That means an adult human would need to take 1g-1.5g daily to match the design of the study. While the study did not mention other possible pathways, I would like to point out that vitamin B3 is a precursor to NAD+ and artificially lowering NAD+ (and thus ATP) levels by inhibiting its synthesis has been shown to reliably lead to NAFLD/MAFLD. Thus, it may very well be that the microRNA-93 is secondary to the energetic pathway, in regards to liver benefits.
http://dx.doi.org/10.1016/j.metabol.2025.156266
https://www.sciencedaily.com/releases/2025/09/250912195101.htm
“…Approximately 30% of the global population is affected by metabolic-associated fatty liver disease (MASLD), a condition that previously lacked targeted treatments. In a groundbreaking discovery, researchers have identified a genetic factor that exacerbates the disease, and remarkably, the FDA-approved drug that most effectively targets this factor is vitamin B3.”
“…MiR-93 is a specialized RNA molecule expressed in hepatocytes that functions to suppress the expression of specific target genes. The team observed abnormally elevated levels of miR-93 in both patients with fatty liver disease and animal models. Through molecular analysis, they demonstrated that miR-93 promotes lipid accumulation, inflammation, and fibrosis by inhibiting the expression of SIRT1, a gene involved in lipid metabolism within liver cells. In experiments utilizing gene editing techniques to eliminate miR-93 production in mice, researchers observed a marked reduction in hepatic fat accumulation, along with significant improvements in insulin sensitivity and liver function indicators. Conversely, mice with overexpressed miR-93 exhibited worsened hepatic metabolic function. Furthermore, screening 150 FDA-approved drugs revealed that niacin (vitamin B3) most effectively suppresses miR-93. Mice treated with niacin showed a significant decrease in hepatic miR-93 levels and a notable increase in SIRT1 activity. The activated SIRT1 restored disrupted lipid metabolism pathways, thereby normalizing liver lipid homeostasis. The research team explained, “This study precisely elucidates the molecular origin of MASLD and demonstrates the potential for repurposing an already approved vitamin compound to modulate this pathway, which has high translational clinical relevance.” They added, “Given that niacin is a well-established and safe medication used to treat hyperlipidemia, it holds promise as a candidate for combination therapies targeting miRNA pathways in MASLD.”
