Could non-alcoholic steatohepatitis be a disease of over-production of endogenous ethanol?

Fatty liver comes in two varieties – alcohol-related and non-alcohol related. Trouble is, it seems to be just one disease.

Some of the people who have this non-alcoholic disease are falsely claiming not to be drinkers or never to have been heavy drinkers. But what of the others who really do not drink?

Could there be sufficient endogenous ethanol production in non-drinkers whose nutrition is inadequate to produce this disease? In particular, people with a yeast overgrowth or a higher than normal yeast/bacteria ratio. With insufficient bacteria to convert the vast majority of endogenous ethanol into acetaldehyde, enough ethanol is metabolized through the liver that fatty liver disease might eventually develop in those with nutrient deficiencies, and/or comorbidities.

If no periodic yeast overgrowth is found in these people, could it be that the metabolism in liver of endogenously produced acetaldehyde is sufficient to generate this disease, given nutrient deficiencies (such as taurine or choline deficiencies in liver), and/or comorbidities?

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