Head and neck cancer (HNC) concerns more than 890,000 patients worldwide annually and is associated with the advanced stage at presentation and heavy outcomes. Alcohol drinking, together with tobacco smoking, and
human papillomavirus infection are the main recognized risk factors. The
tumorigenesis of HNC represents an intricate sequential process that implicates a gradual acquisition of genetic and epigenetics alterations targeting crucial pathways regulating cell growth, motility, and stromal interactions. Tumor microenvironment and
growth factors also play a major role in HNC. Alcohol toxicity is caused both directly by
ethanol and indirectly by its metabolic products, with the involvement of the oral microbiota and oxidative stress; alcohol might enhance the exposure of epithelial cells to
carcinogens, causing epigenetic modifications, DNA damage, and inaccurate DNA repair with the formation of
DNA adducts. Long-term markers of alcohol consumption, especially those detected in the hair, may provide crucial information on the real alcohol drinking of HNC patients. Strategies for prevention could include food supplements as
polyphenols, and alkylating drugs as
therapy that play a key role in HNC management. Indeed,
polyphenols throughout their
antioxidant and anti-inflammatory actions may counteract or limit the toxic effect of alcohol whereas
alkylating agents inhibiting
cancer cells' growth could reduce the carcinogenic damage induced by alcohol. Despite the established association between alcohol and HNC, a concerning pattern of alcohol consumption in survivors of HNC has been shown. It is of primary importance to increase the awareness of
cancer risks associated with alcohol consumption, both in oncologic patients and the general population, to provide advice for reducing HNC prevalence and complications.