ABSTRACT
Excessive alcohol consumption is one of the strongest risk factors for upper digestive tract cancers.1 In addition, there is increasing evidence that heavy drinking may increase cancer risk also in other parts of the gastrointestinal tract. The exact mechanism of ethanol-associated cancers has remained obscure since ethanol itself is not a carcinogen.2 In contrast to alcohol, the first metabolite of ethanol oxidation, acetaldehyde, has multiple carcinogenic effects according to cell culture and animal studies.3 On the other hand, alcohol abuse has also been associated with several indirect tumor-promoting effects. These may include for instance malnourishment, increased exposure to other carcinogens, increased production of free radicals, and local effects of strong alcoholic beverages.4,5
After its oral intake, alcohol is at first absorbed to the portal blood from the stomach and upper part of the small intestine. Thereafter, it is rapidly transported by blood circulation to other organs including the digestive tract. Finally, ethanol is evenly distributed to the water phase of all organs. After the distribution phase, ethanol levels in saliva, tears, and urine, as well as in the contents of the terminal ileum and large intestine, are equal to those of the blood and the liver.6-8 Although the main organ for ethanol oxidation is the liver, there is increasing evidence that alcohol is not merely an innocent bystander in the digestive tract. Ethanol can be oxidized to acetaldehyde by many microbes representing normal gut flora, and also by salivary glands and mucous membranes. However, as compared to the liver, the detoxification of acetaldehyde by either microbes or mucous membranes is limited. This results after ingestion of alcoholic beverages in strikingly high local concentrations of carcinogenic acetaldehyde throughout the whole gastrointestinal tract.
