Abstract
The concept that alcoholic liver disease (ALD) is as a toxic disease does not mirror the exact nature of the disease. ALD should be defined as an alcohol-associated lifestyle disease, the predisposition to which is largely governed by gene–environment interactions, much like other chronic diseases such as diabetes, atherosclerosis, and neurodegenerative diseases. The epidemiology and pathogenesis of ALD need to be re-addressed from this viewpoint. Specifically, the interactions between alcohol and secondary risk factors (high-fat diet, iron, tobacco, medications, female gender) and comorbidities (viral hepatitis, diabetes) are of urgent epidemiological importance. Molecular characterization of the interfaces of these interactions is essential for revelation or acquisition of new pathogenetic, preventive, and therapeutic insights.