Exploring Links Between Smoking, Diet, and Oral Cancer Risk: What Should Be Message to Patients?

According to the American Cancer Society, smokers are six times more likely than nonsmokers to develop oral cavity and oropharyngeal cancers. The mechanisms of tobacco-associated carcinogenesis are quite well established, and investigators agree that carcinoma may form as a result of tobacco-induced damage to the DNA in the cells lining the oral cavity. Heavy alcohol use is another major risk factor for oral cancer in developed countries, and chronic smoking and excessive alcohol consumption comprise a particularly damaging combination.1

Especially for oral cancer, then, prevention of disease hinges on avoiding known carcinogens. Could there be an additional way to counterbalance the damage done by smoking? Investigators worldwide have, for the past two decades, explored the possible protective effect of diet against the development of cancer. Studies by epidemiologists in Italy have consistently found that diets rich in fresh fruits and vegetables appear to be related to lowered risk of several cancers, among them oral, colorectal, and other digestive tract cancers. Does this protective effect of foods containing micronutrients such as folates, antioxidants, and carotenoids extend to smokers? Should findings from studies of micronutrients modify the counseling messages otolaryngologists convey to their patients who smoke?

Studies of Links

Such studies as the 2006 meta-analysis in the American Journal of Clinical Nutrition, published by Pavia et al., have shown that consuming fresh fruits and vegetables is associated with a reduced risk of oral cancer.2 Carlo LaVecchia, MD, MSc, Director of the Laboratory of Epidemiology at Istituto di Recerche Farmacologiche Mario Negri in Milan, Italy, has investigated the link between diet and cancer risk for almost 20 years. He stated that “the relationship between diet and oral cancer is much stronger than that for breast or for colorectal cancer.” But, he said, “this is not strange. Any carcinogen or anticarcinogen that is contained in food will first make contact in the oral cavity, so it is easily understood.” And, more important, he asserted, even adjusting for the two major risk factors of tobacco and alcohol, the association between diet and risk of oral cancer is “strong and consistent.”

Erich M. Sturgis, MD, MPH, Associate Professor in the Departments of Head and Neck Surgery and Epidemiology at the University of Texas M.D. Anderson Cancer Center, believes it’s difficult to separately measure the contributions of diet and smoking when trying to ferret out cancer risk. One problem with case-control studies is that investigators often rely on participants’ self-reporting on diet questionnaires to reflect many years of nutritional exposure, he said. Whether some of the apparent effect of diet is indeed due to the confounding effects of tobacco and alcohol—because heavy drinkers and heavy smokers have a poorer diet—is subject to discussion. Another confounding factor is the genetic variation in metabolism of folates and other nutrients among members of the population, said Dr. Sturgis. For instance, a genetic propensity for folate metabolism that increases the levels in one person may mean that he or she could tolerate smoking-induced lower folate levels, and thus be at a lower-than-expected risk of developing oral cancer.