The protective effects of both ADH variants appear to be applicable to all UADT sites, but are strongest for oesophageal cancer. Also, the protective effect is due to an interaction with alcohol exposure, because the variants have little or no protective effect in non-drinkers, and the protective effects are more apparent in heavier drinkers. Finally, Hashibe et al. [5] stated that neither gene variant seemed to be consistently associated with the amount of alcohol consumed in their studies, and that the effects of these variants are therefore likely to be due to modulating the carcinogenic effect of alcoholic beverages. It should be noted, however, that other studies have shown that ADH1B and ADH7 gene variants can affect alcohol consumption or the risk of alcoholism [6-8].
