The huge increases in the non-alcoholic variety of this disease (fittingly named non-alcoholic fatty liver disease) is a big contributor. The two diseases are

The huge increases in the non-alcoholic variety of this disease (fittingly named non-alcoholic fatty liver disease) is a big contributor. The two diseases are closely related, with very similar histologic and enzymatic features, and having one makes the liver more vulnerable to the other, likely in equal measure. The prevailing theories of pathogenesis of fatty liver disease (the "two-hit" or "multiple hit" hypotheses, or whatever) include fat accumulation in the liver as the first step toward liver disease. This first step can be achieved by heavy drinking or insulin resistance and obesity. Once that's in place, subsequent insults can take the liver down the path to alcoholic or non-alcoholic liver disease, or both. Edit: Good info here: https://www.emjreviews.com/hepatology/article/alcohol-or-not-a-review-comparing-initial-mechanisms-contributing-factors-and-liver-transplantation-outcomes-between-alcoholic-and-nonalcoholic-steatohepatitis/ https://www.emjreviews.com/hepatology/article/alcohol-or-not...