Alcohol as a Risk Factor for Cancer Burden: A Review

Alcohol is eliminated from the body by various metabolic mechanisms. The primary enzymes in such mechanism involved are alcohol dehydrogenase, aldehyde dehydrogenase, cytochrome P450 2E1, and catalase. Variations in the genes for these enzymes have been found to influence alcohol consumption. The consequences of alcohol metabolism include oxygen deficits (i.e., hypoxia) in the liver, resulting in the formation of harmful compounds (i.e., adducts) and highly reactive oxygen-containing molecules (i.e., reactive oxygen species) that can damage cell components. Approximately, worldwide 3.6 % of cancers derive from chronic alcohol drinking, including those of the upper aerodigestive tract, the liver, the colorectum and the breast. Although the mechanisms for alcohol-associated carcinogenesis are not completely understood, recent findings have focused on acetaldehyde, the first and most toxic ethanol metabolite, as a cancer-causing agent. Alcohol-related carcinogenesis may aggravate due to other factors such as smoking and being triggered by genetic susceptibility. Besides, the role of genetic polymorphisms of the alcohol-metabolizing enzymes could not be ruled out.