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17 The Relationship of Diet to Cancer at Specific Sites To present more clearly what is known about the relationship between diet and cancer at specific sites, the committee has reassembled the epidemiological literature and summarized it by site: esophagus, stomach, colon and rectum, liver, pancreas, gallbladder, lung, urinary bladder, kidneys, breast, endometrium, ovary, and prostate. Since most of these data have already been discussed in earlier chapters on specific dietary constituents, the information contained in the following pages has been greatly condensed. The organization of this chapter reflects the design of most epidemiological studies, which generally examine cancer at spe- cific sites. ESOPHAGEAL CANCER The incidence of esophageal cancer varies widely among different regions of the world. A belt of particularly high risk runs from the Middle East (notably the Caspian littoral of Iran) through central Asia to China. Other regions of high risk are the eastern and southern areas of Africa, and France has unusually high rates, especially in Normandy and Brittany. Correlational analyses have shown direct associations of alcohol drinking with incidence of and mortality from esophageal cancer in some parts of the world. These studies were based on both estimated per capita intakes and dietary interview data in special population groups in Western countries (Breslow and Enstrom, 1974; Hinds et al., 1980; Kolonel et al., 1980; Lyon et al., 1980a,b; Schoenberg et al., 1971~. Chilvers et al. (1979) found a consistent relationship between mortality from esophageal cancer and total ethanol intake in England and Wales. Other investigators reported high correlations of esopha- geal cancer mortality with death rates from cirrhosis and alcoholism (Lipworth and Rice, 1979; Tuyns et al., 1979~. The results from a number of case-control studies have confirmed the association with alcohol. Various investigators have demonstrated a dose-response relationship after controlling for cigarette smoking (Keller, 1980; Martinez, 1969; Pattern et al., 1981; Tuyns et al., 1979; Williams and Horn, 1977; Wynder and Brass, 1961; Wynder and Stellman, 1977~. Schmidt and Popham (1981) found a significantly in- creased risk for esophageal cancer in a retrospective cohort study of male alcoholics. Smoking and alcohol appear to act synergistically to increase the risk for esophageal cancer as they do for cancers of the oral cavity and larynx (Rothman and Keller, 1972; Tuyns et al., 1977~. 17-1 391

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392 DIET, NUTRITION, AND CANCER There has been no consistency in the type of alcoholic beverage most strongly associated with the risk of esophageal cancer. Some investi- gators found no specificity at all (Breslow and Enstrom, 1974; Williams and Horm, 1977~; some found a stronger association with hard liquor than with beer or wine (Pottern et al., 1981; Wynder and Bross, 1961~; and some reported a stronger association with beer (Hinds et al., 1980; Mettlin_ al., 1980~. Alcohol consumption cannot explain the pattern of esophageal cancer in Africa and Asia (Bradshaw and Schonland, 1974; Burrell, 1962; Collis _ al., 1971; Gatei et al., 1978; Higginson and Oettle, 1960; Joint Iran-International Agency for Research on Cancer Study Group, 1977; Yang, 1980~. Correlation studies have indicated that the intakes of pulses (e.g., lentils), green vegetables, fresh fruit, animal and fish protein, and the estimated intakes of vitamin A, vitamin C, and riboflavin, are lower in high risk regions of the Caspian littoral in Iran (Hormozdiari et al., 1975; Joint Iran-International Agency for Research on Cancer Study Group, 1977~. Similar studies in China have implicated low intakes of trace elements (particularly molybdenum), animal products, fat, fruits, vegetables, calcium, and riboflavin; high intakes of pickles, pickled vegetables, and moldy foods containing N-nitroso compounds (possibly produced by the fungal contaminants); and consumption of foods at very high temperatures (Coordinating Group for Research on Etiology of Esopha- geal Cancer in North China, 1975; Yang, 1980~. In Japan, Segi (1975) found a direct association between mortality from esophageal cancer and the intake of tea-cooked rice gruel. On the other hand, Stocks (1970) and Howell (1974) found no associations between international per capita food and beverage intakes and corresponding mortality rates for esophageal cancer. In view of the findings that nitrosamines and fungi contaminate some foods in China, it is notable that Marasas et al. (1979) found higher contamination levels of Fusarium mycotoxins in samples of corn (a dietary staple) from a high risk area for esophageal cancer in the African Repub- lic of Transkei, compared with levels in a low risk area. However, these mycotoxins, unlike aflatoxin, have not been shown to be carcinogenic. Furthermore, results of the studies in Iran indicated that there were no differences in aflatoxin (or nitrosamine) levels in foods in regions of high and low risk for esophageal cancer. A case-control study in Iran confirmed the inverse relationship be- tween esophageal cancer and consumption of fresh fruit and cooked vege- tables (Cook-Mozaffari, 1979; Cook-Mozaffari et al., 1979~. The authors concluded that the disease might be caused by opium use in combination with diets low in fresh fruit and vegetables. In a case-control study of white males in the United States, Mettlin et al. (1980) also found a statistically significant inverse relationship, including a dose-response gradient, between risk of esophageal cancer and frequency of consumption of fruits and vegetables. Similar inverse associations were found for indices of vitamin A and C intake, especially for vitamin C intake. In a case-control study among Chinese in Singapore, de Jong et al. (1974) 17-2

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The Relationship of Diet to Cancer at Specific Sites 393 found that a significant decrease in risk for esophageal cancer among males was associated with consumption of bread, potatoes, and bananas. They also found a direct association with consumption of very hot bever- ages. Ziegler et al. (1981) examined the role of nutrition in the etiol- ogy of esophageal cancer among blacks in the United States. They found that nutrition in general was poorer among cases than controls, but they identified no specific nutrient deficiency as responsible for the effect, which appeared to be independent of ethanol consumption. Warwick and Harington (1973) reported that large quantities of grain, especially wheat and maize, are commonly consumed in most areas with high risk for esophageal cancer. This observation was recently extended by van Rensburg (1981), who examined esophageal cancer in- cidence and relative frequencies with which dietary staples were con- sumed in several populations, primarily in Africa and Asia. The low- risk populations consumed millet, cassava, yams, or peanuts; the high-risk populations consumed primarily wheat or corn, which provide diets relatively deficient in zinc, magnesium, nicotinic acid, and possibly riboflavin. He suggested that such nutritional deficiencies, which may also occur in abusers of alcohol, might increase suscepti- bility of the esophageal epithelium to neoplastic transformation. Thus, it is possible that a common mechanism is involved in the causation of esophageal cancer throughout the world. In summary, a number of dietary factors appear to be associated with the risk of esophageal cancer. An increased risk in some parts of the world is associated with alcohol drinking, especially in combination with cigarette smoke, high intakes of pickles and moldy foods possibly contain- ing mycotoxins or N-nitroso compounds, trace mineral deficiencies, and consumption of very hot beverages. Frequent consumption of fresh fruits and vegetables appears to be associated with a lower risk for esophageal cancer. STOMACH CANCER There is a high incidence rate of stomach cancer in Japan, in other parts of Asia, and in South America; but in North America and Europe, the incidence is low and is decreasing (Stukonis, 1978; Waterhouse et al., 1976~. In Japan, gastric cancer has been associated with chronic gastri- tis (Imai et al., 1971) and with the consumption of spiced and pickled foods (Haenszel _ al., 1976~. Surveys have shown that there is substantial variation in inci- dence among different areas of Colombia (Cuello et al., 1976~. These variations have been correlated with different levels of nitrate in the diet and drinking water (Correct et al., 1976; Tannenbaum et al., 1979~. Broitman _ al. (1981) studied iron-deficient patients in Medellin, Colombia, who exhibited lesions that were precursors to gastric cancer. They found that hypochlorhydria and achlorhydria associated with iron 17-3

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394 DIET, NUTRITION, AND CANCER deficiency permitted bacterial colonization of the stomach. Reduction of dietary nitrate to nitrite, and subsequent endogenous synthesis of N-nitroso compounds from nitrite, could thus be mediated by the gastric flora. Ruddell et al. (1978) suggested a similar mechanism to explain the increased risk for gastric cancer in patients with pernicious anemia. An association between gastric cancer and high concentrations of nitrate in drinking water was suggested by Hill et al. (1973), who ob- served that mortality rates for stomach cancer were higher in Worksop, England, where the water supply contained higher concentrations of nitrate, than in nine control towns. However, Davies (1980) pointed out that Worksop was a coal-mining town, been associated with coal-mining regions ~ for coal mining and socioeconomic status abolished the excess mortality from stomach cancer in males in Worksop and reduced it markedly in females. ~ , ~ and that stomach cancer has in Great Britain. Adiustment In Chile, exposure of the general population to high concentrations of nitrate in drinking water or in food appeared to be associated with high rates of stomach cancer (Armijo and Coulsen, 1975; Zaldivar, 1977~. However, although nitrate levels were significantly higher in the urine of schoolchildren from two areas of central Chile with high mortality from stomach cancer than they were in the urine of schoolchildren from a northern, low risk area, levels of nitrate were also significantly higher in vegetables obtained from the low risk area (Armijo et al., 1981). Dungal (1966) observed that large quantities of smoked foods (e.g., mutton and trout) were consumed in high incidence areas of Iceland and that there was a lower incidence of stomach cancer in sailors than in farmers in Iceland. He noted that sailors often stock food obtained at foreign ports; thus, their diet contains a higher proportion of fresh food. Choi et al. (1971) showed that the mortality from gastric cancer among Icelanders in Manitoba was twice as high as that among people born in Manitoba. A dietary survey showed that the people born in Iceland had consumed high levels of smoked and pickled foods. Hakama and Saxen (1967) analyzed age- and sex-adjusted mortality rates for stomach cancer in 16 countries. They found a strong corre- lation (r = 0.75) with the per capita intake of cereals used for flour during 1934-1938. In the United States, counties with high mortality from stomach cancer tend to be concentrated in Minnesota, Wisconsin, and the upper peninsula of Michigan (Mason et al., 1975~. Kriebel and Jowett (1979) pointed out that although high rates in migrants from Northern Europe may explain part of this increased mortality, the rates are dispropor- tionately high. They suggested that native-born Americans have shared the increased risk of the migrants, possibly by adopting the "high-risk" diet of the foreign-born residents. 17-4

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The Relationship of Diet to Cancer at Specific Sites 395 Over several generations, there has been a gradual decline in the incidence of stomach cancer in Japanese migrants to the United States (Kolonel et al., 1980), suggesting that the risk factors for this cancer exert their effect early in life. Data from several countries indicate that there is a strong correla- tion between mortality from gastric cancer and cerebrovascular disease. Joossens and Geboers (1981) suggested that both diseases are related to salt intake. However, the use of salt to preserve food is often accom- panied by the use of nitrate for the same purpose (Weisburger et al., 1980~. Furthermore, Okamura and Matsuhisa (1965) found no correlation between the salt content of salted fish and the death rate from gastric cancer in Japan. In a number of case-control studies, investigators have attempted to define more specifically the role of diet and other factors in the etiology of gastric cancer. Acheson and Doll (1964) and Wynder et al. (1963) found no association with dietary factors. In another study, however, Meinsma (1964) observed that cases had eaten more bacon and less citrus fruits (and, thus, less ascorbic acid) than had the con- trols. Higginson (1966) found that cases had also consumed fried foods more frequently, especially bacon drippings and animal fats used for cooking. Hirayama (1967) reported that the daily consumption of milk was less frequent and the daily use of salted foods was more frequent among cases. Graham et al. (1972) observed that a low risk of gastric cancer was associated with the consumption of raw lettuce, tomatoes, carrots, coleslaw, and red cabbage and that there was a dose-response relationship for these food items. Haenszel et al. (1972) studied Japanese living in Hawaii. Migrants (Issei) continued to display an increased risk in Hawaii, but the Nisei offspring, who adhered to Western-style diets, did not. There were ele- vated risks for both Issei and Nisei users of pickled vegetables and dried/salted fish. Low risks were associated with the consumption of several Western vegetables, many of which are eaten raw. Using a simi- lar protocol, Haenszel et al. (1976) showed that farmers in Japan, representing the lower socioeconomic class, had the highest risk for gastric cancer. A lower risk was found for those whose diet included more frequent use of lettuce and celery. Modan et al. (1974) reported that starches were consumed more frequently by gastric cancer patients than by controls. B. jelke ( 19 78) f ound an inverse relationship between s tomach cancer and consumption of vegetables and vitamin C, especially in younger pa- tients and among women. He also reported preliminary findings from a prospective study, showing a reduced risk for those with a high consump- tion of vegetables in Norway, but not in Minnesota. The Norwegian study also suggested that frequent use of salted fish may be associated with a high risk of stomach cancer. In a large cohort study conducted in Japan, Hirayama (1977) reported that a protective effect against gastric cancer was associated with the 17-5

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396 DIET, NUTRITION, AND CANCER consumption of two glasses of milk daily and that there was an increased risk in cigarette smokers. Nonsmokers who ate green or yellow vegetables also had a lower risk of stomach cancer. Weisburger and Rainer! (1975) suggested that gastric cancer in humans may result from the in viva nitrosation in the stomach of as yet unknown substrates, with the production of alkylnitrosamides. They postulated that exposure to reducing agents such as ascorbic acid may interfere with the endogenous production of N-nitroso compounds by the reaction of dietary nitrite with amine s or amides (Weisburger et al., 1980~. Such a mechanism could explain the protective effect of green or yellow vegetables, raw lettuce, and other vitamin-C-containing vegetables. In summary, studies in migrants to the United States suggest that gastric cancer is related in part to dietary factors that exert their influence early in life. The factors increasing risk may include fre- quent consumption of smoked food (which in some parts of the world leads to increased exposure to polycyclic aromatic hydrocarbons) and frequent ingestion of salt-pickled foods or foods containing nitrate and nitrite (which may result in subsequent in viva production of nitrosa- mines) and other carcinogens produced in food by preservation treatments and cooking. Protective factors may include consumption of milk, raw green or yellow vegetables, especially lettuce, and other foods contain- ing vitamin C. COLON AND RECTAL CANCER Haenszel (1961) reported that the rates of colon and rectal cancer in migrants from Italy, Norway, Poland, and the Soviet Union more closely resembled those in the host country (the United States) than those in their country of origin, in contrast to the findings for stomach cancer. Haenszel and Dawson (1965) observed that mortality for cancer of the colon and rectum was higher in urban regions in the United States. Urban-born people who migrate to rural areas acquire the lower mortality of the rural areas; the reverse occurs for those who migrate from rural to urban areas. Mortality is higher in the North than in the South for long-term residents of these regions. De Jong _ al. (1972) found that in areas of high and intermediate risk there is a decreasing incidence from the ascending colon to the descending colon and a sharp increase at the sigmoid colon. Rectal cancer rates are generally higher than those for the sigmoid. In low incidence areas, there may be a low rate for sigmoid cancers. Berg and Howell (1974) reviewed international mortality from cancer of the bowel from 1952 to 1953 and from 1966 to 1967. The highest death rates were reported in Scotland, but these rates were falling, as were those for England and Wales. The rates for whites in the United States 17-6

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The Relationship of Diet to Cancer at Specific Sites 397 appeared to be stable, but those for the Federal Republic of Germany, Italy, and Japan were rising. The investigators interpreted differences between colon and rectal cancer rates as indicating that, although much of rectal cancer is caused by the same factors that cause colon cancer, there is a second set of factors that affect rectal cancers alone. Lee '1976) found that death rates from large bowel cancer in Japan have risen rapidly since World War II and that colon cancer has increased at a greater rate than rectal cancer. In Japan, each successive birth cohort had an increased rate of colon cancer, whereas those in the United States did not. Haenszel et al. (1975) investigated the incidence of large-bowel cancer in Call, Colombia in relation to place of residence, by census tract. They found that the upper socioeconomic classes were at higher risk. Lynch _ al. (1975) also reported a greater frequency of colon cancer in patients living in census tracts with higher average incomes. Similarly, Teppo et al. (1980) found a higher incidence of colon cancer in higher socioeconomic areas of Finland. Studies of the international incidence of and mortality from large bowel cancer in relation to dietary variables strongly support an association of colon cancer and, to a lesser extent, rectal cancer with total dietary fat (Armstrong and Doll, 1975; Wynder, 1975~. Irving and Drasar (1973) failed to find a correlation between cancer of the colon and the per capita intake of various fiber-containing foods. In studies of mortality rates for colon cancer, Berg and Howell (1974) and Howell (1975) reported that the highest correlations were found for per capita meat intake, and that the highest was for beef. However, Enstrom (1975) pointed out that the trends in per capita beef and fat intake in the United States do not correlate with trends in incidence of and mortality from colorectal cancer. Jansson_ al. (1978) correlated the selenium concentration in water samples from the eastern part of the United States with the incidence of colorectal cancer. They found a strong, direct relationship between the selenium content of water and colorectal cancer and observed that the mean mortality rate increased with increasing levels of selenium in the drinking water. Other studies, however, have shown an inverse correla- tion between the intake of selenium and colon cancer (Schrauzer et al., 1977a,b; also see the section on selenium in Chapter 10~. Lui _ al. (1979) evaluated food disappearance data for 1954-1965 and data on mortality from colon cancer for 1967-1973 from 20 industrialized countries. They found that the per capita intakes of total fat, satu- rated fat, monounsaturated fat, and cholesterol were directly correlated and that fiber intake was inversely correlated with mortality from colon cancer. The correlation of dietary cholesterol with colon cancer was highly significant and remained so when they controlled for fat or fiber. However, the correlations of fat or of fiber with colon cancer mortality were no longer significant when they controlled for cholesterol. 17-7

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398 DIET, NUTRITION, AND CANCER gingham et al. (1979) related the average intake of foods, nutrients, and dietary fiber in Great Britain to the regional pattern of death from colon and rectal cancer. They found that intakes of the pentosan frac- tion of total dietary fiber and of vegetables other than potatoes were inversely correlated with death rates for colon cancer. The possible importance of dietary cholesterol (and/or dietary fat) is supported by the correlations of mortality from colon cancer with mortality from coronary heart disease in different countries (Rose et al., 1974), correlations with large-bowel cancer among different social classes in Call, Colombia (Haenszel et al., 1975), and for cancer of the colon and rectum together and individually within 34 health-planning subdivisions in the Commonwealth of Massachusetts (Lipworth and Rice, 1979~. Stemmermann et al. (1979) noted the high rate of colon cancer among Japanese who migrated to Hawaii and observed that myocardial infarction, severe atherosclerosis, diverticulosis, and polyposis of the colon also occurred more frequently in this population, compared to Japanese living in Japan. In studies of cancer incidence in Seventh-Day Adventists, Phillips and colleagues reported that a lacto-ovovegetarian diet had a protec- tive effect against colon cancer (Phillips, 1975; Phillips et al., 1980a,b). The findings among Mormons in Utah (Lyon and Sorenson, 1978; Lyon et al., 1976, 1980a,b) and in California (Enstrom, 1980) confirmed that this group had a lower incidence of colon cancer than the U.S. average, but were less clear with respect to the impact of dietary fac- tors. In a preliminary dietary survey, Lyon and Sorenson (1978) found little difference in meat, fat, and fiber intake by the population of Utah and by the general U.S. population. Malhotra (1977) suggested that the virtual absence of colon cancer among Punjabis from northern India is due to their diet, which is rich in roughage, cellulose, vegetable fiber, and short-chain fatty acids contained in fermented milk products. MacLennan et _ . (1978) evaluated the diets consumed by adult men from Kuopio, Finland and compared them with the diets consumed by a similar sample from Copenhagen, Denmark, where the incidence of colon cancer is 4 times higher. They found that the high incidence group consumed more refined wheat breads, meats (especially pork), and beer, but less potatoes and milk than did the low incidence group in Finland. The estimated consumption of fat was similar, but the consumption of fiber was higher in the low incidence group. Reddy _ al. (1978) studied the dietary patterns and fecal constit- uents of a high risk group in New York and the low risk group in rural Kuopio. The average daily intake of dietary fat and protein was the same in the two groups, but a greater proportion of fat came from dairy products in Kuopio and from meat in New York. The daily stool output and fecal fiber excretion were also greater in Kuopio, where there was a high dietary intake of cereal products rich in fiber. 17-8

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The Relationship of Diet to Cancer at Specific Sites 399 These investigators found more mutagenic activity in the stools from New York subjects who were not Seventh-Day Adventists than in the stools obtained from subjects in Kuopio, who had a similar fat but a higher fiber intake (Ready et al., 1980~. However, they found no mu- tagenic activity in the stools from vegetarian Seventh-Day Adventist volunteers from New York, who had a lower average fat intake than the other two groups, but an intermediate level of fiber intake. A number of case-control studies have been conducted to examine the relationship between diet and cancer of the large bowel. Wynder and Shigematsu (1967) could not identify environmental factors that differed significantly between cases and controls. A study of Japanese patients with bowel cancer and hospital controls in Hawaii indicated that there was a higher risk for persons who regularly ate Western-style meals (Haenszel _ al., 1973~. Control for beef produced the largest downward displacement in estimated risks for other dietary variables. In Japan, a study conducted with similar methodology did not replicate these find- ings (Haenszel et al., 1980~; however, reduced risk was associated with consumption of cabbage. Modan _ al. (1975) found that fiber-containing foods were con- sumed less frequently by cases of colon cancer than by controls, but there were no differences for cases with rectal cancer. They also observed no differences in consumption of fat-containing foods by either cancer group or the controls. Parallel studies in Norway and Minnesota indicated that there was a slightly lower consumption of cereal products, milk, and coffee by colorectal cancer cases, compared to controls, and several vegetables were eaten less frequently by the cases (Bjelke, 1978~. The cases also had lower indices for consumption of vitamin A and crude fiber, both of which are associated with vegetable intake. In the United States, Phillips (1975) found that consumption of beef, lamb, and fish, and the heavy use of dairy products other than milk and other high-fat foods, were directly associated with the risk of colon cancer, and that there was a slight inverse association with the consumption of milk, vegeta- ble protein products, and green leafy vegetables. Dales _ al. (1979) reported that foods with at least 0.5% fiber content were consumed less frequently by colon cancer cases than by the controls, and that there was a consistent dose-response relation- ship. Cases tended to have eaten foods with at least 5% saturated fat more often than controls. Significantly more cases than controls re- ported a high saturated fat, low fiber food consumption pattern. Graham et al. (1978) reported that a decreased risk of colon cancer was associated with frequent ingestion of vegetables, especially cabbage, Brussels sprouts, and broccoli. Decreased risk of rectal cancer was associated only with frequent ingestion of raw vegetables and cabbage. 17-9

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400 DIET, NUTRITION, AND CANCER However, Martinez et al. (1979) reported that cases had consumed signif- icantly higher quantiELes of meats, cereals, total fats, total residue, and fiber. Jain _ al. (1980) observed that an increased risk of both colon and rectal cancer was associated with elevated consumption of calories, total fat, total protein, saturated fat, oleic acid, and cholesterol, but that there was no association with consumption of crude fiber, vitamin C, and linoleic acid. The highest risk was found for saturated fat consumption, and there was evidence of a dose-response relationship. The only cohort studies that have yet provided data on dietary vari- ables are the ongoing parallel studies in Norway and Minnesota (Bjelke, 1978~. These studies indicate that there is a reduced risk of colorectal cancer in the Minnesota subjects who have a high index of vegetable con- sumption. No such effect has been observed in Norway, but the number of cases in that country is small. Most information on the association between colon cancer and choles- terol levels has been derived from epidemiological studies and interven- tion trials to determine risk for cardiovascular disease. The findings have been conflicting, and it is not certain whether reported increases in risk of cancer (especially colon cancer) at low serum cholesterol levels reflect a causal association (Feinleib, 1981; Lilienfeld, 1981~. Rectal cancer has been associated with intake of beer in some stud- ies (Breslow and Enstrom 1974; Dean et al., 1979; Enstrom, 1977; Stocks, 1957), but not in all studies (Jensen, 1979; Schmidt and Popham, 1981~. McMichael _ al. (1979) suggested that there is a better correlation be- tween trends in mortality from rectal cancer and changes in beer intake than has been found for saturated fat. Wynder and Shigematsu (1967) showed that the proportion of beer drinkers among male colorectal cancer patients was significantly higher than in one control group, but not in a second control group. In a prospective study conducted by Bjelke (1973), there was a dose-response relationship between the risk of colorectal cancer and the frequency of beer and liquor consumption. The gradient was steeper for beer consump- tion. Conversely, case-control studies of intestinal cancer in Finland, Kansas, and Norway (Bjelke, 1971, 1973; Higginson, 1966; Pernu, 1960) indicated that there was no significant relationship with beer drinking. Vitale _ al. (1981) reported a correlation coefficient of 0.78 between alcohol consumed as beer and colon cancer in 20 countries. There were poor correlations for colon cancer and the intake of total ethanol, distilled spirits, or wine. In summary, three hypotheses appear to be supported by data of vari- ous strengths obtained from epidemiological studies of both colon and 17-10

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The Relationship of Diet to Cancer at Specific Sites 401 and rectal cancer: (1) a causal association with total, and perhaps satu- rated, fat; (2) a protective effect of dietary fiber; and (3) a protective effect of cruciferous vegetables. The diverse results concerning the im- portance of fat and fiber may be partly due to differences in the degrees of precision in the dietary methodology used in the various studies. The possible role of alcohol in the induction of rectal cancer requires fur- ther study. LIVER CANCER Primary liver cancer is relatively uncommon in the United States and most Western countries, but it is a major form of cancer in sub-Saharan Africa and Southeast Asia. Several different dietary agents have been reported as possible hepatic carcinogens, including alcohol, aflatoxin, safrole, pyrrolizidine alkaloids, and cycasin (Anthony, 1977~. Oettle (1965) suggested that the geographic distribution of liver cancer in Africa could be explained by differing levels of exposure to aflatoxin in the diet. In a number of studies, aflatoxin contamination of foodstuffs has been correlated with liver cancer incidence and mor- tality by geographic area or for different population groups in Africa (Alpert et al., 1971; Keen and Martin, 1971; Peers and Linsell, 1973; Peers _ al., 1976; van Rensburg et al., 1974~. Similar correlations_ _ have been found in Thailand,-China, and Taiwan, which also have high rates of liver cancer (Armstrong, 1980; Shank et al., 1972a,b; Tung and Ling, 1968; Wogan, 1975~. There is a strong correlation between the estimated levels of aflatoxin ingestion and liver cancer rates in these various studies, and no populations with documented high levels of afla- toxin ingestion have low rates of liver cancer (Linsell and Peers, 1977~. Numerous reports (e.g., Chien et al., 1981) have also documented a high correlation between primary liver cancer and exposure to hepatitis B viral infection, which has a worldwide distribution similar to that of aflatoxin. Many investigators believe that although primary liver cancer could be initiated by aflatoxin, there is a higher probability that liver cancer develops in individuals exposed to the hepatitis B virus. In Guam and Okinawa, which have high rates of liver cancer, the ingestion of cycasin (a toxic substance contained in cycad nuts) has been proposed as an etiologic factor. However, in a descriptive study conducted in the Miyako Islands of Okinawa, investigators found no correlation between mortality from hepatoma and the ingestion of cycad nuts (Hirono _ al., 1970~. Alcohol is the main dietary factor that has been suggested as an etiologic agent for liver cancer in Western, low-risk countries, al- though Armstrong and Doll (1975) reported a weak correlation between liver cancer incidence (but not mortality) and per capita intake of 17-11

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The Relationship of Diet to Cancer at Specific Sites 419 Howe, G. R., J. D. Burch, A. B. Miller, G. M. Cook, J. Esteve, B. Morrison, P. Gordon, L. W. Chambers, G. Fodor, and G. M. Winsor. 1980. Tobacco use, occupation, coffee, various nutrients, and bladder cancer. J. Natl. Cancer Inst. 64:701-713. Howell, M. A. 1974. Factor analysis of international cancer mortality data and per capita food consumption. Br. J. Cancer 29:328-336. Howell, M. A. 1975. Diet as an etiological factor in the development of cancers of the colon and rectum. J. Chronic Dis. 28:67-80. Imai, T., T. Kubo, and H. Watanabe. 1971. Chronic gastritis in Japanese with reference to high incidence of gastric carcinoma. J. Natl. Can- cer Inst. 47:179-195. Irving, D., and B. S. Drasar. 1973. Fibre and cancer of the colon. Br. J. Cancer 28:462-463. Ishii, K., K. Nakamura, H. Ozaki, N. Yamada, and T. Takeuchi. 1968. [In Japanese.] [Epidemiological problems of pancreas cancer.] Jpn. J. Clin. Med. 26:1839-1842. Jain, M., G. M. Cook, F. G. Davis, M. G. Grace, G. R. Howe, and A. B. Miller. 1980. A case-control study of diet and colo-rectal cancer. Int. J. Cancer 26:757-768. Jansson, B., M. M. Jacobs, and A. C. Griffin. 1978. Gastrointestinal cancer: Epidemiology and experimental studies. Adv. Exp. Med. Biol. 91:305-322. Jensen, O. M. 1979. Cancer morbidity and causes of death among Danish brewery workers. Int. J. Cancer 23:454-463. Jick, H., A. M. Walter, and K. J. Rothman. 1980. The epidemic of endo- metrial cancer: A commentary. Am. J. Public Health 70:264-267. Joint Iran-International Agency for Research on Cancer Study Group. 1977. Esophageal cancer studies in the Caspian littoral of Tran: Results of population studies--a prodrome. J. Natl. Cancer Inst. 59:1127-1138. Joossens, J. V., and J. Geboers. 1981. Nutrition and gastric cancer. Proc. Nutr. Soc. 40:37-46. Kato, H., J. Tillotson, M. Z. Nichaman, G. C. Rhoads, and H. B. Hamilton. 1973. Epidemiologic studies of coronary heart disease and stroke in Japanese men living in Japan, Hawaii and California: Serum lipids and diet. Am. J. Epidemiol. 97:372-385. 17-29

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