Similar to oral ethanol consumption, endogenous ethanol production has been implicated in the development of non-alcohol-associated fatty liver disease, NAFLD (now known as metabolic dysfunction-associated steatotic liver disease, MASLD), and non-alcohol-associatedsteatohepatitis NASH (now metabolic dysfunction-associated steatohepatitis, MASH) (54, 58–63). One of the strongest evidence that MASLD can result from endogenous alcohol production by the gut microbiota comes from a preclinical study (54). In this study, the transfer of a high-alcohol-producing strain, Klebsiella penumoniae —isolated from an individual with ABS and MASLD—into germ-free mice, either through oral gavage or fecal transplant, induced MASLD. Importantly, selectively eliminating this strain prior to fecal transplantation prevented the development of MASLD in recipient mice (54). Furthermore, more than 60% of patients with steatotic liver disease in a Chinese cohort were carriers of this bacterial strain (54), suggesting that endogenous alcohol production may contribute to liver and other diseases more frequently than currently recognized. A recent study of individuals with and without MASL/MASH confirms and extends these findings. Fasting BAC measured in the portal veins of individuals with MASL/MASH were significantly higher than in individuals without
