*2.7.1 Mechanism*

The mechanisms whereby chronic alcohol consumption has an effect on the development of CRC are diverse. Acetaldehyde (the first compound formed in ethanol metabolism) has mutagenic and carcinogenic activity. It is thought that it plays a critical role in CRC onset via toxic metabolites of ethanol oxidation that can be carcinogenic to colonocytes [35, 36]. Higher ethanol consumption can also induce oxidative stress through the increased production of reactive oxygen species which are genotoxic and carcinogenic [37]. Alcohol may also act as a solvent for cellular penetration of dietary or environmental (e.g., tobacco) carcinogens, affect hormone metabolism, and interfere with retinoid metabolism and with DNA repair mechanisms [38].
