Alcoholic liver disease (ALD) is one of the major causes of morbidity and mortality in the world (1, 2). It includes a broad range of progressive disease stages: fatty liver, liver fibrosis, liver cirrhosis, and hepatocellular carcinoma (3). Approximately 80–90 % of individuals with excessive alcohol consumption develop liver steatosis, of which 20–40 % progress into liver fibrosis without abstinence (2). Heavy alcohol consumption during pregnancy can alter the development of multiple organs in the fetus, including the brain, heart, and liver, leading to fetal alcohol spectrum disorders (FASD) (4). The reported hepatic abnormalities in subjects with FASD include hyperbilirubinemia, elevated levels of liver enzymes, and hepatomegaly, suggesting that excessive alcohol intake can lead to structural liver defects. Liver biopsy from a child with FASD has demonstrated parenchymal fat with portal and perisinusoidal fibrosis, which resembles the changes in adult human ALD (5). Animal studies have also demonstrated a wide range of liver defects under prenatal alcohol exposure (6, 7). Thus, both animal and human studies provide compelling evidence on alcohol-induced liver injury and dysfunction.
