Alcohol-nutrient interactions in cancer etiology.

Abstract

The cancers for which there is the most compelling epidemiologic evidence of associations with both diet and alcohol are oral, pharyngeal, laryngeal, esophageal, and liver cancer. For lung, breast, stomach, and colorectal cancer, there is reasonably strong epidemiologic evidence of associations with diet, but only moderate or equivocal evidence of associations with alcohol. For pancreatic cancer there is suggestive evidence of associations with both exposures. It is probable that the quantitative relationship and the underlying biological mechanisms of the diet-alcohol interaction will not be the same for all cancers. Heavy alcohol consumption and generally poor nutrition, possibly a deficiency of several micronutrients and food groups, were the major risk factors for esophageal cancer in a case-control study of the unusually high rates for this cancer among Washington, DC black men. It is proposed that alcohol might increase risk of esophageal cancer, in part, by reducing nutrient intake. Two descriptive studies are presented that suggest that as the percent of caloric intake from alcohol increases, the daily consumption of protein, carbohydrate, fiber, and many micronutrients steadily and significantly decreases. Alcohol consumption and low fruit and vegetable intake, as well as snuff dipping and cigarette smoking, were shown to be risk factors for oral-pharyngeal cancer in a case-control study of the high rates of these cancers among North Carolina women. Since these women were not heavy drinkers, it is not likely that alcohol functioned by altering nutritional status. A number of mechanisms for the action of alcohol in cancer etiology are presented.