The following HTML text is provided to enhance online
readability. Many aspects of typography translate only awkwardly to HTML.
Please use the page image
as the authoritative form to ensure accuracy.
relationships between specific dietary components and cancer risk are well established, it is not possible to quantify the contribution of diet to individual cancers (and thus to total cancer rates) more precisely. Nevertheless, these estimates help to emphasize the importance of diet in the etiology and prevention of cancer in the United States today.
Evidence Associating Dietary Factors with Cancer at Specific Sites
The discussion in this section is presented by specific cancer sites because the dietary associations are not the same for all cancer types. See Chapters 6 through 17 for more detailed review of evidence by dietary components.
Correlation analyses have shown direct associations between consumption of alcoholic beverages and esophageal cancer in Western countries (Breslow and Enstrom, 1974; Chilvers et al., 1979; Hinds et al., 1980; Kolonel et al., 1980; Lyon et al., 1980; Schoenberg et al., 1971). Case-control and cohort studies have also provided consistent evidence of an association between alcohol consumption and risk of esophageal cancer (Hakulinen et al., 1974; Potter et al., 1981; Williams and Horn, 1977). Alcohol consumption appears to act synergistically with cigarette smoking to increase the risk. Wynder and Bross (1961) found that increases in the use of alcohol and tobacco were associated with an increased risk of squamous cell carcinoma of the esophagus and that alcohol and tobacco exert a multiplicative effect. Similar effects have been observed in Paris (Schwartz et al., 1962), Puerto Rico (Martinez, 1969), Brittany (Tuyns et al., 1977), and Normandy (Tuyns, 1983). Alcohol also seems to have an independent effect on cancer risk in the absence of smoking (Keller, 1980).
In correlation studies conducted in different parts of the world, investigators have found positive associations between esophageal cancer and several dietary factors, including (1) low intakes of lentils, green vegetables, fresh fruits, animal protein, vitamins A and C, riboflavin, nicotinic acid, magnesium, calcium, zinc, and molybdenum; (2) high intakes of pickles, pickled vegetables, and moldy foods containing N-nitroso compounds; and (3) consumption of very hot foods and beverages (de Jong et al., 1974; Hormozdiari et al., 1975; Joint Iran-IARC Study Group, 1977; Thurnham et al., 1982; van Rensburg, 1981; Yang, 1980; Zaridze et al., 1985). Many of these findings have been supported by the results of case-control studies (Cook-Mozaffari, 1979; de Jong et al., 1974; Mettlin et al., 1981). The reported associations are consistent with the general hypothesis that certain nutrient deficiencies, such as found in many high-risk populations, including heavy alcohol drinkers, might increase the susceptibility of the esophageal epithelium to neoplastic transformation (van Rensburg, 1981). In the esophageal epithelium of humans, for example, riboflavin deficiency causes lesions that may be precursors of cancer (Foy and Mbaya, 1977), although an intervention trial with riboflavin (and zinc and retinol) in a high-risk Chinese population failed to show any effect of these nutrients (Muñoz et al., 1985).
In summary, esophageal cancer is associated with the use of tobacco and alcohol individually, but especially with their combined use. Studies suggest that consumption of certain types of preserved foods increases risk and that several vitamins and minerals are protective against esophageal cancer, but the reasons for these relationships are not yet clearly established.
A high incidence of stomach cancer is found in South America, Japan, and other parts of Asia, but not in North America or Western Europe where the rates are low and still decreasing (Stukonis, 1978; Waterhouse et al., 1976). In the United States, stomach cancer rates are now among the lowest in the world, whereas in 1930, this was the leading cause of cancer death for men and the second leading cause in women (Page and Asire, 1985). Gastric cancer incidence has recently begun to decrease in Japan, and a gradual decline in incidence over several generations has been noted among Japanese migrants to Hawaii (Kolonel et al., 1980). It seems most likely that these trends are related to changes in food consumption patterns, since several dietary factors have been implicated in gastric cancer risk.
Several correlation and case-control studies have shown positive associations between gastric cancer and the consumption of dried, salted fish, smoked fish, or pickled vegetables (e.g., Dungal, 1966; Haenszel et al., 1976; Hirayama, 1967; Joossens and Geboers, 1987; Risch et al., 1985). These foods contain high concentrations of salt,