Click for next page ( 131


The National Academies | 500 Fifth St. N.W. | Washington, D.C. 20001
Copyright © National Academy of Sciences. All rights reserved.
Terms of Use and Privacy Statement



Below are the first 10 and last 10 pages of uncorrected machine-read text (when available) of this chapter, followed by the top 30 algorithmically extracted key phrases from the chapter as a whole.
Intended to provide our own search engines and external engines with highly rich, chapter-representative searchable text on the opening pages of each chapter. Because it is UNCORRECTED material, please consider the following text as a useful but insufficient proxy for the authoritative book pages.

Do not use for reproduction, copying, pasting, or reading; exclusively for search engines.

OCR for page 130
~ Dietary Fiber Recently, attention has been directed toward the physiological significance of dietary fiber, which generally includes indigestible carbohydrates and carbohydrate-like components of food such as cellulose, lignin, hemicelluloses, pentosans, gums, and pectins. The principal characteristic of these indigestible substances is their provision of bulk in the diet. The major categories of foods that provide dietary fiber are vegetables, fruits, and whole grain cereals. Because of the complex composition of dietary fiber, the physio- logical functions and metabolic activity of its individual components have not been adequately studied. Most earlier analyses focused on the intake of so-called crude fiber. Therefore, they generally under- estimated the fiber content since crude fiber only determines cellulose and lignin. Consequently, early reports provided incomplete data on the amount and type of fiber consumed. During the past few decades, the consumption of dietary fiber has decreased in many parts of the Western world (National Academy of Sciences, 1980~. On the basis of observations concerning the rela- tionship of diet and the incidence of disease, Burkitt and Trowell (1975) hypothesized that many chronic diseases including cancer are associated with a low intake of dietary fiber. EPIDEMIOLOGICAL EVIDENCE The epidemiological data on fiber are related primarily to its possible role in protection against large bowel cancer. Several different mechanisms have been proposed for this protective effect: Fiber can dilute carcinogens present in the large bowel; it can de- crease transit time, thereby decreasing contact time between carcinogen and tissue; it can affect the production of putative carcinogens or procarcinogens in the stool such as the bile acids; or, by influencing the composition and metabolic activity of the fecal flora, it can alter the spectrum of fecal bile acids and their derivatives that are present in the stool. Most data on the fiber content of foods are incomplete, because they pertain only to crude fiber. Since any effect associated with dietary fiber may be restricted to selected components, epidemio- logical studies of dietary fiber will have limited value until detailed information on each of its constituents becomes available. Attempts to correlate the fiber content of diets with colorectal cancer risk have yielded mixed results. Malhotra (1977) suggested that the differences in colon cancer incidence among northern and southern 130 8-1

OCR for page 130
Dietary Fiber 131 populations in India might be explained by the high levels of roughage, cellulose, and vegetable fiber in the northern Indian diet and the very low levels in the southern Indian diet. There was a virtual absence of the disease in the Punjabis from the north. He also found that vegeta- ble fibers were abundant in the stools of Indians from the north, but completely absent in samples obtained from inhabitants of the southern regions. MacLennan et al. (1978) observed similar differences after comparing the diets of adult men from Copenhagen, Denmark (high risk group for colon cancer) and from Kuopio, Finland (low risk group). The Danes consumed less fiber and their stools weighed less than those of the Finns. These findings lend support to the hypothesis that dietary fiber plays a protective role in carcinogenesis. gingham et al. (1979) calcu- lated the average fiber intake by populations in different regions of Great Britain. They found no significant correlation between total fiber intake and corresponding mortality rates for colon and rectal cancers. However, the mean intakes of the pentosan fraction of total dietary fiber and of vegetables other than potatoes were inversely correlated with mortality from colon cancer. This finding suggested the importance of examining the specific components of fiber rather than crude or total fiber in studies of large bowel cancer. Other correlation analyses have not supported the hypothesis that fiber intake is inversely associated with the risk of colon cancer. Liu et al. (1979) examined mortality from colon cancer in 20 industralized countries between 1967 and 1973 and compared the rates to per capita food intake for these same areas from 1954 to 1965. Although fiber intake was inversely correlated with colon cancer mortality, this relationship was no longer significant in a partial correlation analysis controlling for cholesterol intake. The authors concluded that cholesterol, not fiber, was an important risk factor for colon cancer. In other studies, Drasar and Irving (1973) failed to find a correlation between colon cancer in- cidence in 37 countries and per capita intake of various fiber-containing foods, and Lyon and Sorenson (1978) found little difference in fiber intake between the population of Utah (low risk) and the population of the United States as a whole. In a number of case-control studies, investigators have attempted to examine the relationship between dietary fiber and risk of large bowel cancer, again with inconsistent results. Modan et al. (1975) assessed the frequency with which certain food items were consumed by colon and rectal cancer cases and both hospital and neighborhood controls. They a; ~h-fi her fnnd.c hv colon cancer cases was E controls, but there was ~ ., no such difference between rectal cancer cases and controls. Using a similar approach, Bjelke (1978) observed that the consumption of dietary fiber by colorectal cancer cases was lower than that of controls in parallel studies conducted in Minnesota and Norway. found that the consumption of .._~. ~ significantly lower than that of both groups 0 Dales et al. (1978) studied cases of colorectal cancer in U.S. blacks. Controls were selected from two hospitals and a multiphasic 8 - 2

OCR for page 130
132 DIET, NUTRITION, AND CANCER health check-up clinic. By assessing the frequency of consumption of selected food items, they found that the cases consumed fewer fiber- containing foods than did the controls, and that there was a consistent dose-response relationship. Significantly more cases than controls reported the consumption of a diet that was high in saturated fat but low in fiber. In a case-control study of diet and colorectal cancer in Canada, Jain et al. (1980) attempted to compute consumption of dietary fiber based on the actual fiber content of food rather than on a simple grouping of food items as other investigators had done. They found an elevated risk asso- ciated with increased consumption of calories, total fat, total protein, saturated fat, oleic acid, and cholesterol, but no association with the consumption of crude fiber, vitamin C, or linoleic acid. Unfortunately, data on the specific components of fiber were not available for their analysis. A direct association between fiber consumption and large bowel cancer was reported by Martinez et al. (1979), who conducted a case- control study in Puerto Rico. Based on frequency-of-consumption dietary histories, they found higher consumption of fiber and total residue in cases than in controls. They provided no explanation for this unusual finding, which, however, is consistent with the observation of Hill et al. (1979) that the highest socioeconomic group studied in Hong Kong had the highest incidence of colon cancer and a high intake of fiber and calories, whereas the middle and lowest socioeconomic groups had corre- spondingly lower incidence rates and intakes. Glober et al. (1974, 1977), compared bowel transit-times in men from three different populations: Japanese in Japan (low risk for colon cancer), Japanese in Hawaii (high risk for colon cancer), and Caucasians in Hawaii (also high risk for colon cancer). They found that bowel transit-times were similar in both Japanese populations, and were shorter than in the Caucasians. Mean stool weight, however, was similar in the two high-risk populations and was notably less than that for the Japanese in Japan. Thus, their data did not support the hypothesis that dietary fiber protects against colon cancer by decreasing transit time in the bowel, thereby decreasing the contact time between carcinogens and tissues. Dietary fiber can also affect the amount of bile acids excreted into the lumen of the intestine. However, since dietary fat influences bile acid excretion as well, the relative effects of both of these dietary components need further study. Studies of the composition of bile acids in the feces of humans are reviewed in Chapter 5. EXPERIMENTAL EVIDENCE A variety of chemical carcinogens cause colon cancer in rats. Among these are 1,2-dimethylhydrazine (DMH), azoxymethane (AOM), methyl- azoxymethanol (HAM) acetate, 3,2'-dimethyl-4-aminobiphenyl (DAB), and 8 - 3

OCR for page 130
Dietary Fiber 133 nitrosomethylurea (NMU). Colon cancer can be induced in these labora- tory animals by parenteral administration of DMH, AOM, HAM, and DAB; by feeding DMH; and by intrarectal instillation of NMU. Bran protects rats against DMH-induced colon cancer, regardless of whether the carcinogen is administered orally or subcutaneously (Barbolt and Abraham, 1978; Chen et al., 1978; Wilson et al., 1977~. However, it has no effect on the incidence or number of tumors in the duodenum or cecum. Cellulose has been found to protect rats against DMH-induced tumors (Freeman et al., 1978, 1980), but pectin does not (Freeman et al., 1980~. Cellulose does not appear to protect against tumors induced by AOM or NMU (Ward et al., 1973; Watanabe et al., 1978~. Fleiszer _ al. (1980) have studied the effects of different levels of fiber on DMH-induced colon cancer in rats. Four diets were used: very high fiber (28%) supplied as bran cereal; high fiber (15%) supplied as a special rat chow; low fiber (5%) supplied as standard rat chow; and a fiber-free, semipurified diet. Fewer cancers occurred in the rats fed the very high fiber and high fiber diets, than in those given the low fiber diet. Because the basal diet for the fiber-free group was con- siderably different, the response of these animals cannot be reasonably compared with those of the other animals. Although components of dietary fiber generally appear to exert a protective effect against DMH-induced carcinogenesis, Glauert et al. (1981) recently reported that dietary agar (a fiber-rich component of the diet) enhanced DMH-induced colon cancer in mice. The effects of dietary fiber have been compared in rats treated with AOM or NMU (Watanabe _ al., 1979~. The substances tested were alfalfa, pectin, and wheat bran fed as 15% of a diet that also contained 5% cell- ulose. When the carcinogen was given parenterally, pectin exerted a protective effect but alfalfa and bran were ineffective. When the car- cinogen was given by intrarectal instillation, alfalfa enhanced carcin- ogenesis, but pectin and bran were not protective. Alfalfa has a relatively strong ability to bind bile acids (Story and Kritchevsky, 1976~. Cassidy et al. (1981) demonstrated that substances with this binding capacity disrupt the topography of the colonic mucosa. The denuded epithelium would then be susceptible to the action of a locally administered carcinogen. Although some data suggest that some types of fiber (e.g., bran and cellulose) can protect rats from the action of certain chemical carcino- gens, the collated data from different experiments are difficult to com- pare or interpret, primarily because of the lack of uniform experimental protocols. The strains of rats, their diets, age, the carcinogens used, and routes of administration all differ. The animal model is useful to study the effects of fiber on carcinogenesis in the large bowel, but the lack of standardization must be borne in mind when assessing or comparing data. 8 - 4

OCR for page 130
134 DIET, NUTRITION, AND CANCER SUMMARY Epidemiological Evidence Both correlation and case-control studies have yielded results that either support or contradict the hypothesis that dietary fiber protects against colorectal cancer. In both types of studies, most analyses have been based on total fiber consumption estimated by grouping foods (such as fruits, vegetables, and cereals) according to their fiber content. However, in the only case-control study and the only correlation study in which the total fiber consumption was quantified rather than estimated from the fiber-rich foods in the diet, no association was found between total fiber consumption and the risk of colon cancer. Thus, the epidem- iological evidence suggesting an inverse relationship between total fiber intake and the occurrence of colon cancer is not yet compelling. In the only study in which the effects of individual components of fiber were assessed, there was an inverse correlation between the inci- dence of colon cancer and the consumption of the pentosan fraction of fiber (found in whole wheat products). Thus, it seems likely that further epidemiological study of fiber will be productive only if the relationship of cancer to specific components of fiber can be analyzed. Experimental Evidence A few laboratory studies have also shown that some types of high fiber ingredients (e.g., cellulose and bran) depress the tumorigenicity of certain chemical carcinogens. However, the data are inconsistent-- especially with respect to the type of fiber or specific chemical car- cinogen. Moreover, they are difficult to equate with the results of epidemiological studies because most laboratory experiments have examined specific fibers or their individual components, whereas most epidemio- logical studies have focused on fiber-containing foods whose exact compo- sition has not been determined. Further information is needed on the basic chemistry and biological effects of fiber and its components to pursue experimental studies that will produce meaningful results. CONCLUSION The committee found no conclusive evidence to indicate that dietary fiber (such as that present in fruits, vegetables, grains, and cereals) exerts a protective effect against colorectal cancer in humans. Both epidemiological and laboratory reports suggest that if there is such an effect, specific components of fiber, rather than total dietary fiber, are more likely to be responsible. 8 - 5

OCR for page 130
Dietary Fiber 135 REFERENCES Barbolt, T. A., and R. Abraham. 1978. The effect of bran on dimethyl- hydrazine-induced colon carcinogenesis in the rat. Proc. Soc. Exp. Biol. Med. 157:656-659. gingham, S., D. R. R. Williams, T. J. Cole, and W. P. T. James. 1979. Dietary fibre and regional large-bowel cancer mortality in Britain. Br. J. Cancer 40:456-463. Bjelke, E. 1978. Dietary factors and the epidemiology of cancer of the stomach and large bowel. Aktuel. Ernaehrungsmed. Klin. Prax. Suppl. 2:10-17. Burkitt, D. P., and H. C. Trowell. 1975. Refined Carbohydrate Foods and Disease. Some Implications of Dietary Fibre. Academic Press, London, New York, and San Francisco. 356 pp. Cassidy, M. M., F. G. Lightfoot, L. E. Grau, J. A. Story, D. Kritchevsky, and G. V. Vahouny. 1981. Effect of chronic intake of dietary fibers on the ultrastructural topography of rat jejunum and colon: A scanning electron microscopy study. Am. J. Clin. Nutr. 34:218-228. Chen, W.-F., A. S. Patchefsky, and H. S. Goldsmith. 1978. Colonic protection from dimethylhydrazine by a high fiber diet. Surg. Gynecol. Obstet. 147:503-506. Dales, L. G., G. D. Friedman, H. K. Ury, S. Grossman, and S. R. Williams. 1978. A case-control study of relationships of diet and other traits to colorectal cancer in American blacks. Am. J. Epidemiol. 109:132-144. Drasar, B. S., and D. Irving. 1973. Environmental factors and cancer of the colon and breast. Br. J. Cancer 27:167-172. Fleiszer, D. M., D. Murray, G. K. Richards, and R. A. Brown. 1980. Effects of diet on chemically induced bowel cancer. Can. J. Surg. 23:67-73. Freeman, H. J., G. A. Spiller, and Y. S. Kim. 1978. A double-blind study on the effect of purified cellulose dietary fiber on 1,2- dimethylhydrazine-induced rat colonic neoplasia. Cancer Res. 38:2912-2917. Freeman, H. J., G. A. Spiller, and Y. S. Kim. 1980. A double-blind study on the effects of differing purified cellulose and pectin 8 - 6

OCR for page 130
136 DIET, NUTRITION, AND CANCER fiber diets on 1,2-dimethylhydrazine-induced rat colonic neoplasia. Cancer Res. 40:2661-2665. Glauert, H. P., M. R. Bennink, and C. H. Sander. 1981. Enhancement of 1,2-dimethylhydrazine-induced colon carcinogenesis in mice by dietary agar. Food Cosmet. Toxicol. 19:281-286. Glober, G. A., K. L. Klein, J. O. Moore, and B. C. Abba. 1974. Bowel transit-times in two populations experiencing similar colon-cancer risks. Lancet 2:80-81. Glober, G. A., A. Nomura, S. Kamiyama, A. Shimada, and B. C. Abba. 1977. Bowel transit-time and stool weight in populations with different colon-cancer risks. Lancet 2:110-111. Hill, M., R. MacLennan, and K. Newcombe. 1979. Letter to the Editor: Diet and large-bowel cancer in three socioeconomic groups in Hong Kong. Lancet 1:436. 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. Liu, K., J. Stamler, D. Moss, D. Garside, V. Persky, and I. Soltero. 1979. Dietary cholesterol, fat, and fibre, and colon-cancer mortality. Lancet 2:782-785. Lyon, J. L., and A. W. Sorenson. 1978. Colon cancer in a low-risk population. AP1. J. Clin. Nutr. 31:S227-S230. MacLennan, R., O. M. Jensen, J. Mosbech, and 11. Vuori. 1978. Diet, transit time, stool weight, and colon cancer in two Scandinavian populations. Am. J. Clin. Nutr. 31:S239-S242. Malhotra, S. L. 1977. Dietary factors in a study of cancer colon from cancer registry, with special reference to the role of saliva, milk and fermented milk products and vegetable fibre. Med. Hypotheses 3:122-126. Martinez, I., R. Torres, Z. Fr~as, J. R. Colon, and M. Fernandez. 1979. Factors associated with adenocarcinomas of the large bowel in Puerto Rico. Pp. 45-52 in J. M. Birch, ed. Advances in Medical Oncology, Research and Education. Volume 3: Epidemiology. Pergamon Press, Oxford, New York, Toronto, Sydney, Paris, and Frankfurt. Modan, B., V. Barell, F. Lubin, M. Modan, R. A. Greenberg, and S. Graham. 1975. Low-fiber intake as an etiologic factor in cancer of the colon. J. Natl. Cancer Inst. 55:15-18. 8 - 7

OCR for page 130
Dietary Fiber 137 National Academy of Sciences. 1980. Recommended Dietary Allowances, 9th Edition. Committee on Dietary Allowances, Food and Nutrition Board, National Academy of Sciences, Washington, D.C. 187 pp. Story, J. A., and D. Kritchevsky. 1976. Comparison of the binding of various bile acids and bile salts in vitro by several types of fiber. J. Nutr. 106:1292-1294. Ward, J. M., R. S. Yamamoto, and J. H. Weisburger. 1973. Cellulose dietary bulk and azoxymethane-induced intestinal cancer. J. Natl. Cancer Inst. 51:713-715. Watanabe, K., B. S. Reddy, C. Q. Wang, and J. H. Weisburger. 1978. Effect of dietary undegraded carrageenin on colon carcinogenesis in F344 rats treated with azoxymethane or methylnitrosourea. Cancer Res. 38:4427-4430. Watanabe, K., B. S. Reddy, J. H. Weisburger, and D. Kritchevsky. 1979. Effect of dietary alfalfa, pectin, and wheat bran on azoxymethane- or methylnitrosourea-induced colon carcinogenesis in F344 rats. J. Natl. Cancer Inst. 63:141-145. Wilson, R. B., D. P. Hutcheson, and L. Wideman. 1977. Dimethyl- hydrazine-induced colon tumors in rats fed diets containing beef fat or corn oil with and without wheat bran. Am. J. Clin. Nutr. 30:176-181. 8 - 8