breast cancer patients and will facilitate the correlation of vascularity with molecular events.
References (/) FOUCMAN J: What is the evidence that tumors are angiogenesis dependent? J Natl Cancer Inst 82:4-6, 1990 (2) WEIDNER N, FOUCMAN J, POZZA F, ET AL: Tumor angiogenesis: A
new significant and independent prognostic indicator in early-stage breast carcinoma. J Natl Cancer Inst 84:1875-1887, 1992 (3) WEIDNEK N, SEMPLE JP, WELCH WR, ET AL: Tumor angiogenesis and
metastasis—correlation in invasive breast carcinoma. N Engl J Med 324:1-8, 1991 (4) TANDON AK, CLARK GM, CHAMNESS GC, ET AL: Cathepsin D and
prognosis in breast cancer. N Engl J Med 322:297-302, 1990
(5) MCGUIRE WL: Breast cancer prognostic factors: Evaluation guidelines. J Natl Cancer Inst 83:154-155, 1991 (6) PAGE DL: Prognosis and breast cancer: Recognition of lethal and favorable prognostic types. Am J Surg Pathol 15:334-349, 1991 (7) ELLEDOE RM, MCGUIRE WL, OSBORNE CKJ Prognostic factors in
breast cancer. Semin Oncol 19:244-253, 1992 (8) BOSARI S, LEE AK, DE1.FI I IS RA, ET AL: Microvessel quantitation
and prognosis in invasive breast carcinoma. Hum Pathol 23:755-761, 1992 (9) HARRIS AJ, HORAK E, AL EEX R, ET AL: Quantitative angiogenesis in
human breast cancer, correlation with lymph node metastases and assessment of vascular growth factors. Proc Am Assoc Cancer Res 33:75, 1992 (10) MACCHIARINI
P, FONTANNI
G, HARDIN
MJ, ET AL: Relation
of
neovascularisation to metastasis of non—small-cell lung cancer. Lancet 340:145-146, 1992
Fiber: Unanswered Questions
Unanswered Questions In 1991, the review by the Life Sciences Research Office (6) of the scientific evidence linking dietary fiber and cancer concluded that the findings to date were provocative but Vol. 84, No. 24, December 16, 1992
J. T. Dwyer, Department of Medicine, Tufts University Medical School, Boston, Mass.; New England Medical Center Hospitals, Boston; and U.S. Department of Agriculture Human Nutrition Research Center on Aging and School of Nutrition, Tufts University. L. M. Ausman, U.S. Department of Agriculture Human Nutrition Research Center on Aging and School of Nutrition, Tufts University. 'Correspondence to: Johanna Dwyer, D.Sc., Box 783 NEMCH, 750 Washington St., Boston, MA 02111.
EDITORIALS 1851
Downloaded from http://jnci.oxfordjournals.org/ at Rensselaer Polytechnic Institute on March 19, 2015
insufficient to be conclusive. The data are not conclusive because several important questions remain unanswered. Was fiber responsible for the beneficial effects, or was another component of the fiber-rich food, such as beta carotene or ascorbic acid, responsible? Epidemiological studies (7) of different populations compare intakes of fiberrich foods, and these foods may also contain plant constituents that have protective or inhibitory effect in the carcinogenic process. Johanna T. Dwyer,* Lynne M. Ausman Were the effects of fiber really present? Although most studies to date show decreased risk with increased fiber intake, results have not been entirely consistent. Now a new analysis—a useful contribution—sheds light Fiber was a foreign word to Grandma; she called it on these questions. In this issue of the Journal, Howe et al. roughage. No doubt her conviction arose from claims made (8) report on the combined analysis of 13 case-control by cereal manufacturers that bran and whole grains helped studies. The results of this analysis provide strong support the "bowels" to work properly. Although nutrition scientists for an association between increased dietary fiber intake and recognized the fecal bulking effects of fiber, they were decreased colorectal cancer risk. Instead of pooling estimates uncertain about the health importance of these observations of risk from published summary results (meta-analysis), (7). Scientific study of dietary fiber was inhibited by the these investigators pooled all the individual data records for heterogeneous nature of fiber in food. David Southgate and a common analysis, thereby minimizing effects due to other British investigators took the lead in analyzing foods variable procedures for coding and analyzing data. The large by using more sophisticated methods than the former sample size allows determination of whether specific effects Association of Official Analytical Chemists (now called of sex, site of cancer, age, and nutrient interactions also AOAC) technique for crude fiber, which destroyed many existed. Dietary fiber independently decreased risk of both classes of dietary fiber. But the health connection was left- and right-sided disease. In addition, vitamin C and beta missing, and fiber studies were few. In the early 1970s, carotene showed an inverse but weak association with Burkitt (2,3) proposed that dietary fiber deficiency was colorectal cancer risk after adjustment for fiber intake. Most linked to the development of colorectal cancer and other effects appeared to be associated with fruit and vegetable chronic diseases, an hypothesis that is still hotly debated. In consumption. the mid 1980s, the National Cancer Institute (4) published If fiber is protective, what type of fiber is most goals for the year 2000 and singled out two specific dietary effective? There is little doubt that soluble and insoluble steps toward achieving a decrease in cancer incidence: 1) increases in dietary fiber (to a total of 20-30 g/d) and 2) decreases in dietary fat (down to 30% or less of caloric intake). Only in 1990 did the Dietary Guidelines for Received October 30, 1992; accepted November 17, 1992. Americans (5) specify similar goals for reducing fat intake; Supported in part by contract 53-3K06-5-10 from the Agricultural recommendations on fiber remain qualitative. Research Service, U.S. Department of Agriculture.
Insufficient fiber consumption. Increased fat intake (either type or amount of fat) with resultant cholesterol and bile acid production causing increased risk. Insufficient calcium and vitamin D. Presence or production of mutagens, carcinogens, or promoters. Presence of other inhibitory qualities, such as phenolic compounds, sulfur-containing compounds, and flavones. High energy intake and/or low physical activity. Low intakes of beta carotene, ascorbic acid, and a-tocopherol (antioxidant nutrients). There are several, not necessarily mutually exclusive, mechanisms of action for dietary fiber and carcinogenesis. These include effects of high-fiber intake on the number of colorectal polyps or the degree of dysplasia in adenomatous polyps when they do form, as well as effects on microbial metabolism and resultant pH of the colon; adsorptive qualities of fiber; mucosal cytokinetics and enzymes; gut hormones, cytokines or peptides; enterohepatic circulation of steroid hormones or cholesterol; concentrations of soluble fecal fatty acids and secondary bile acids in the colon; and alterations in transit time through the colon (10). Could results be explained just as well by the common observation that high-fiber diets tend to be low in fat? Efforts to separate the putative effects of fiber from those of fat have not been entirely successful, and the present study does not help much in this regard. Human studies (77) continue to suggest that diets high in saturated fat are associated with colon carcinogenesis. It may be that the direct relationship with fat intake may be stronger than the inverse relationship with dietary fiber. It is also possible that diets high in fiber are low in substances that promote carcinogenesis, such as endogenous nitrosamines, tryptophan metabolites, or carcinogens produced in the cooking of meat. Furthermore, the protective effects observed for diets high in
1852
certain types of soy products (72,73) may be due in part to phytoestrogens rather than simply to fat and fiber. Finally, a new study (14) confirms earlier observations that excess weight and sedentary lifestyles may increase colon cancer risk. If fiber is active in reducing colorectal cancer risk and if there is a dose-response effect, what quantity of fiber intake is advisable? We still do not know with certainty the physical and chemical forms of fiber or the amounts that are likely to give optimal health effects. In their study, Howe et al. (8) used two models to examine the effects of dietary factors. In the first model, variables were separated into quintiles based on their distribution among all study subjects. In the second model, each dietary factor was represented by a continuous variable, and relative risks were expressed in scaled units corresponding to differences in the mean of the highest and lowest quintile of intake based on the control data obtained from three other North American studies. This method of analysis makes it possible to relate findings to usual dietary intakes. Is dietary fiber helpful in reducing risks of other chronic degenerative diseases? The association between high rates of coronary artery disease and high rates of colorectal and other cancers is well known on a population basis. Therefore, it is reasonable to ask if dietary fiber intakes alter intermediate indicators of coronary artery disease risk. Evidence continues to accumulate on the positive effects of dietary fiber, particularly soluble fiber, on reducing serum cholesterol levels and coronary artery disease risk (75). Additional positive effects of fiber on weight loss (75), laxation, diverticular disease, and glycemic response have also been suggested (16).
Study Issues We eagerly await the promised second report on this study from Howe et al. to address three additional and troublesome issues. First, how was differential response bias on dietary intake of cases and controls addressed? Did the dietary choices actually precede the cancer or vice versa? Present intakes cloud our views of past intakes. Second, how was the potential for publication bias addressed? It is odd that no unpublished work relevant to the issue was identified. Finally, one statement from the study by Howe et al. (8) is questionable: "The probability of 12 of 13 studies finding an inverse association by chance is only about .003." This statement is true if studies were chosen at random from a population of all studies that, on the average, showed no association, but studies that show effects are more likely to be published and therefore the probabilities may not apply to them. We trust that additional information on the effects of fat intake will be provided in the next report.
Conclusion The case is building for the role of high-fiber, low-fat diets in health promotion and in reduction of risk for colorectal cancer and atherosclerosis—two chronic degenerative dis-
Journal of the National Cancer Institute
Downloaded from http://jnci.oxfordjournals.org/ at Rensselaer Polytechnic Institute on March 19, 2015
fibers have different physicochemical effects. Also, whole foods high in fiber, high-fiber fractions of foods, concentrated fibers that have been altered in the course of their extraction and purification, and fiber-enriched foods all may have different physical characteristics and different biological effects (9). In experimental animals, only wheat bran appears to provide consistent protective effects against chemically induced colon tumors, and these effects are substantial when accompanied by caloric restriction. In epidemiologic studies, no consistent findings have yet emerged on the type of fiber that has the greatest association with protective effects. Furthermore, adjustments for levels of total dietary energy and levels of fat are often not made in studies, making interpretation difficult. A weak point in the study by Howe et al. (8) is that the definitions of fiber varied from study to study and, although assumptions were made to correct these differences, the errors may have still been considerable. How do these dietary fibers reduce risk? The following dietary factors have been implicated in colon cancer initiation or promotion:
eases. Given our present state of knowledge, the recommendations of several authoritative reports (77-27) make sense— to consume a diet higher in grains, fruits, and cereals and thus to increase dietary fiber and decrease fat. Debate continues about appropriate levels to be achieved. As for Grandma, she may have called it roughage, but maybe she was right.
(9) SPILLER GA, JENKINS DJA; Dietary fiber supplements, physiological and pharmacological aspects: A workshop report. In Proceedings of the Xlllth International Congress of Nutrition (Taylor TG, Jenkins NK, eds). London: John Ubbey, 1985, pp 184-185 (10) KLURFELD DM: Dietary fiber-mediated mechanisms in carcinogenesis. Cancer Res 52:2055s-2059s, 1992 ( / / ) GIOVANNUCCI E, STAMPFER MJ, COLDITZ G, ET AL: Relationship of
diet to risk of colorectal adenoma in men. J Natl Cancer Inst 84:9198, 1992 (12) HEILBRUN LK, NOMURA A, HANKIN JH, ET AL: Diet and colorectal
References
(4) NATIONAL CANCER INSTITUTE: Cancer control objectives for the
nation: 1985-2000. NCI Monogr 2:1-93, 1986
(16) COMMITTEE ON DIET AND HEALTH: Diet and Health: Implications for
Reducing Chronic Disease Risk. Washington, DC: National Academy Press, 1989 (17) US DEPARTMENT OF HEALTH AND HUMAN SERVICES: The Surgeon
General's Report on Nutrition and Health. DHHS (PHS) Publ No. 88-50210. Washington, DC: US Govt Print Off, 1988
(5) U.S. DEPARTMENT OF AGRICULTURE AND U.S. DEPARTMENT OF
(18) US DEPARTMENT OF AGRICULTURE, US DEPARTMENT OF HEALTH AND
HEALTH AND HUMAN SERVICES: Dietary Guidelines for Americans.
HUMAN SERVICES: Nutrition and Your Health: Dietary Guidelines for Americans, 3rd ed. Washington, DC: US Govt Print Off, 1990
Washington, DC: U.S. Govt Print Off, 1990 (6) KRITCHEVSKY D: Evaluation of Publicly Available Scientific Evidence Regarding Certain Nutrient-Disease Relationships: 5. Dietary Fiber and Cancer. FDA Contract No. 223-88-2124. Bethesda Md: Life Sciences Research Office, FASEB, 1991 (7) MORGAN MR, FENWICK GR: Natural foodborne toxicants. Lancet 336:1492-1495, 1990 (8) HOWE GR, BENTTO E, CASTELLETO R, ET AL: Dietary intake of fiber
and decreased risk of cancers of the colon and rectum: Evidence from the combined analysis of 13 case-control studies. J Natl Cancer Inst 84:1887-1896, 1992
(19) THE WORK
STUDY
GROUP
ON DIET,
NUTRITION
AND CANCER
(WEINHOUSE S, BAL DG, ADAMSON R, ET AL): American Cancer
Society guidelines on diet, nutrition, and cancer. CA Cancer J Clin 41:334-338, 1991 (20) NATIONAL
LIVESTOCK
AND MEAT
BOARD:
Meat
and
Colorectal
Cancer: A Current Review. Research Report No. 100-2. Chicago: 1992 (21) BAL DG, FOERSTER SB: Changing the American diet: Impact on cancer prevention policy recommendations and program implications for the American Cancer Society. Cancer 67:2671-2680, 1991
The Good News Is. . . A Healthy Diet May Reduce Cancer Risk Diet. Nutrition & Cancer Prevention: The Good News
The National Cancer Institute announces its new. free public education booklet on diet and cancer. It offers practical advice on healthy eating and identifies high-fiber and low-fat foods that may help to reduce the risk of cancer. Call 1-800-4-CANCER and order your copies of Diet, Nutrition and Cancer Prevention: The Good News.
Vol. 84, No. 24, December 16, 1992
EDITORIALS 1853
Downloaded from http://jnci.oxfordjournals.org/ at Rensselaer Polytechnic Institute on March 19, 2015
(1) LUSK G: The nature of the feces. In The Elements of the Science of Nutrition (Lusk G, ed), 4th ed. New York: Nutrition Foundation, Johnson Reprint Corp, 1976 (2) BURKITT DP: Some diseases characteristic of modern Western civilization. Br Med J 1:274-278, 1973 (3) BURKTTT DP: Epidemiology of cancer of the colon and rectum. Cancer 28:3-13, 1971
cancer with special reference to fiber intake. Int J Cancer 44:1-6, 1989 (13) LEE HP, GOURLEY L, DUFFY SW, ET AL: Colorectal cancer and diet in an Asian population—a case—control study among Singapore Chinese. Int J Cancer 43:1007-1016, 1989 (14) LEE IM, PAFFENBARGER RS JR: Quetelet's index and risk of colon cancer in college alumni. J Natl Cancer Inst 84:1326-1331, 1992 (75) LEEDS AR: Dietary fiber and obesity. In Obesity (Bjorntorp P, Brodoff BN, eds). Philadelphia: Lippincott Company, 1992, pp 677682
References (/) FOUCMAN J: What is the evidence that tumors are angiogenesis dependent? J Natl Cancer Inst 82:4-6, 1990 (2) WEIDNER N, FOUCMAN J, POZZA F, ET AL: Tumor angiogenesis: A
new significant and independent prognostic indicator in early-stage breast carcinoma. J Natl Cancer Inst 84:1875-1887, 1992 (3) WEIDNEK N, SEMPLE JP, WELCH WR, ET AL: Tumor angiogenesis and
metastasis—correlation in invasive breast carcinoma. N Engl J Med 324:1-8, 1991 (4) TANDON AK, CLARK GM, CHAMNESS GC, ET AL: Cathepsin D and
prognosis in breast cancer. N Engl J Med 322:297-302, 1990
(5) MCGUIRE WL: Breast cancer prognostic factors: Evaluation guidelines. J Natl Cancer Inst 83:154-155, 1991 (6) PAGE DL: Prognosis and breast cancer: Recognition of lethal and favorable prognostic types. Am J Surg Pathol 15:334-349, 1991 (7) ELLEDOE RM, MCGUIRE WL, OSBORNE CKJ Prognostic factors in
breast cancer. Semin Oncol 19:244-253, 1992 (8) BOSARI S, LEE AK, DE1.FI I IS RA, ET AL: Microvessel quantitation
and prognosis in invasive breast carcinoma. Hum Pathol 23:755-761, 1992 (9) HARRIS AJ, HORAK E, AL EEX R, ET AL: Quantitative angiogenesis in
human breast cancer, correlation with lymph node metastases and assessment of vascular growth factors. Proc Am Assoc Cancer Res 33:75, 1992 (10) MACCHIARINI
P, FONTANNI
G, HARDIN
MJ, ET AL: Relation
of
neovascularisation to metastasis of non—small-cell lung cancer. Lancet 340:145-146, 1992
Fiber: Unanswered Questions
Unanswered Questions In 1991, the review by the Life Sciences Research Office (6) of the scientific evidence linking dietary fiber and cancer concluded that the findings to date were provocative but Vol. 84, No. 24, December 16, 1992
J. T. Dwyer, Department of Medicine, Tufts University Medical School, Boston, Mass.; New England Medical Center Hospitals, Boston; and U.S. Department of Agriculture Human Nutrition Research Center on Aging and School of Nutrition, Tufts University. L. M. Ausman, U.S. Department of Agriculture Human Nutrition Research Center on Aging and School of Nutrition, Tufts University. 'Correspondence to: Johanna Dwyer, D.Sc., Box 783 NEMCH, 750 Washington St., Boston, MA 02111.
EDITORIALS 1851
Downloaded from http://jnci.oxfordjournals.org/ at Rensselaer Polytechnic Institute on March 19, 2015
insufficient to be conclusive. The data are not conclusive because several important questions remain unanswered. Was fiber responsible for the beneficial effects, or was another component of the fiber-rich food, such as beta carotene or ascorbic acid, responsible? Epidemiological studies (7) of different populations compare intakes of fiberrich foods, and these foods may also contain plant constituents that have protective or inhibitory effect in the carcinogenic process. Johanna T. Dwyer,* Lynne M. Ausman Were the effects of fiber really present? Although most studies to date show decreased risk with increased fiber intake, results have not been entirely consistent. Now a new analysis—a useful contribution—sheds light Fiber was a foreign word to Grandma; she called it on these questions. In this issue of the Journal, Howe et al. roughage. No doubt her conviction arose from claims made (8) report on the combined analysis of 13 case-control by cereal manufacturers that bran and whole grains helped studies. The results of this analysis provide strong support the "bowels" to work properly. Although nutrition scientists for an association between increased dietary fiber intake and recognized the fecal bulking effects of fiber, they were decreased colorectal cancer risk. Instead of pooling estimates uncertain about the health importance of these observations of risk from published summary results (meta-analysis), (7). Scientific study of dietary fiber was inhibited by the these investigators pooled all the individual data records for heterogeneous nature of fiber in food. David Southgate and a common analysis, thereby minimizing effects due to other British investigators took the lead in analyzing foods variable procedures for coding and analyzing data. The large by using more sophisticated methods than the former sample size allows determination of whether specific effects Association of Official Analytical Chemists (now called of sex, site of cancer, age, and nutrient interactions also AOAC) technique for crude fiber, which destroyed many existed. Dietary fiber independently decreased risk of both classes of dietary fiber. But the health connection was left- and right-sided disease. In addition, vitamin C and beta missing, and fiber studies were few. In the early 1970s, carotene showed an inverse but weak association with Burkitt (2,3) proposed that dietary fiber deficiency was colorectal cancer risk after adjustment for fiber intake. Most linked to the development of colorectal cancer and other effects appeared to be associated with fruit and vegetable chronic diseases, an hypothesis that is still hotly debated. In consumption. the mid 1980s, the National Cancer Institute (4) published If fiber is protective, what type of fiber is most goals for the year 2000 and singled out two specific dietary effective? There is little doubt that soluble and insoluble steps toward achieving a decrease in cancer incidence: 1) increases in dietary fiber (to a total of 20-30 g/d) and 2) decreases in dietary fat (down to 30% or less of caloric intake). Only in 1990 did the Dietary Guidelines for Received October 30, 1992; accepted November 17, 1992. Americans (5) specify similar goals for reducing fat intake; Supported in part by contract 53-3K06-5-10 from the Agricultural recommendations on fiber remain qualitative. Research Service, U.S. Department of Agriculture.
Insufficient fiber consumption. Increased fat intake (either type or amount of fat) with resultant cholesterol and bile acid production causing increased risk. Insufficient calcium and vitamin D. Presence or production of mutagens, carcinogens, or promoters. Presence of other inhibitory qualities, such as phenolic compounds, sulfur-containing compounds, and flavones. High energy intake and/or low physical activity. Low intakes of beta carotene, ascorbic acid, and a-tocopherol (antioxidant nutrients). There are several, not necessarily mutually exclusive, mechanisms of action for dietary fiber and carcinogenesis. These include effects of high-fiber intake on the number of colorectal polyps or the degree of dysplasia in adenomatous polyps when they do form, as well as effects on microbial metabolism and resultant pH of the colon; adsorptive qualities of fiber; mucosal cytokinetics and enzymes; gut hormones, cytokines or peptides; enterohepatic circulation of steroid hormones or cholesterol; concentrations of soluble fecal fatty acids and secondary bile acids in the colon; and alterations in transit time through the colon (10). Could results be explained just as well by the common observation that high-fiber diets tend to be low in fat? Efforts to separate the putative effects of fiber from those of fat have not been entirely successful, and the present study does not help much in this regard. Human studies (77) continue to suggest that diets high in saturated fat are associated with colon carcinogenesis. It may be that the direct relationship with fat intake may be stronger than the inverse relationship with dietary fiber. It is also possible that diets high in fiber are low in substances that promote carcinogenesis, such as endogenous nitrosamines, tryptophan metabolites, or carcinogens produced in the cooking of meat. Furthermore, the protective effects observed for diets high in
1852
certain types of soy products (72,73) may be due in part to phytoestrogens rather than simply to fat and fiber. Finally, a new study (14) confirms earlier observations that excess weight and sedentary lifestyles may increase colon cancer risk. If fiber is active in reducing colorectal cancer risk and if there is a dose-response effect, what quantity of fiber intake is advisable? We still do not know with certainty the physical and chemical forms of fiber or the amounts that are likely to give optimal health effects. In their study, Howe et al. (8) used two models to examine the effects of dietary factors. In the first model, variables were separated into quintiles based on their distribution among all study subjects. In the second model, each dietary factor was represented by a continuous variable, and relative risks were expressed in scaled units corresponding to differences in the mean of the highest and lowest quintile of intake based on the control data obtained from three other North American studies. This method of analysis makes it possible to relate findings to usual dietary intakes. Is dietary fiber helpful in reducing risks of other chronic degenerative diseases? The association between high rates of coronary artery disease and high rates of colorectal and other cancers is well known on a population basis. Therefore, it is reasonable to ask if dietary fiber intakes alter intermediate indicators of coronary artery disease risk. Evidence continues to accumulate on the positive effects of dietary fiber, particularly soluble fiber, on reducing serum cholesterol levels and coronary artery disease risk (75). Additional positive effects of fiber on weight loss (75), laxation, diverticular disease, and glycemic response have also been suggested (16).
Study Issues We eagerly await the promised second report on this study from Howe et al. to address three additional and troublesome issues. First, how was differential response bias on dietary intake of cases and controls addressed? Did the dietary choices actually precede the cancer or vice versa? Present intakes cloud our views of past intakes. Second, how was the potential for publication bias addressed? It is odd that no unpublished work relevant to the issue was identified. Finally, one statement from the study by Howe et al. (8) is questionable: "The probability of 12 of 13 studies finding an inverse association by chance is only about .003." This statement is true if studies were chosen at random from a population of all studies that, on the average, showed no association, but studies that show effects are more likely to be published and therefore the probabilities may not apply to them. We trust that additional information on the effects of fat intake will be provided in the next report.
Conclusion The case is building for the role of high-fiber, low-fat diets in health promotion and in reduction of risk for colorectal cancer and atherosclerosis—two chronic degenerative dis-
Journal of the National Cancer Institute
Downloaded from http://jnci.oxfordjournals.org/ at Rensselaer Polytechnic Institute on March 19, 2015
fibers have different physicochemical effects. Also, whole foods high in fiber, high-fiber fractions of foods, concentrated fibers that have been altered in the course of their extraction and purification, and fiber-enriched foods all may have different physical characteristics and different biological effects (9). In experimental animals, only wheat bran appears to provide consistent protective effects against chemically induced colon tumors, and these effects are substantial when accompanied by caloric restriction. In epidemiologic studies, no consistent findings have yet emerged on the type of fiber that has the greatest association with protective effects. Furthermore, adjustments for levels of total dietary energy and levels of fat are often not made in studies, making interpretation difficult. A weak point in the study by Howe et al. (8) is that the definitions of fiber varied from study to study and, although assumptions were made to correct these differences, the errors may have still been considerable. How do these dietary fibers reduce risk? The following dietary factors have been implicated in colon cancer initiation or promotion:
eases. Given our present state of knowledge, the recommendations of several authoritative reports (77-27) make sense— to consume a diet higher in grains, fruits, and cereals and thus to increase dietary fiber and decrease fat. Debate continues about appropriate levels to be achieved. As for Grandma, she may have called it roughage, but maybe she was right.
(9) SPILLER GA, JENKINS DJA; Dietary fiber supplements, physiological and pharmacological aspects: A workshop report. In Proceedings of the Xlllth International Congress of Nutrition (Taylor TG, Jenkins NK, eds). London: John Ubbey, 1985, pp 184-185 (10) KLURFELD DM: Dietary fiber-mediated mechanisms in carcinogenesis. Cancer Res 52:2055s-2059s, 1992 ( / / ) GIOVANNUCCI E, STAMPFER MJ, COLDITZ G, ET AL: Relationship of
diet to risk of colorectal adenoma in men. J Natl Cancer Inst 84:9198, 1992 (12) HEILBRUN LK, NOMURA A, HANKIN JH, ET AL: Diet and colorectal
References
(4) NATIONAL CANCER INSTITUTE: Cancer control objectives for the
nation: 1985-2000. NCI Monogr 2:1-93, 1986
(16) COMMITTEE ON DIET AND HEALTH: Diet and Health: Implications for
Reducing Chronic Disease Risk. Washington, DC: National Academy Press, 1989 (17) US DEPARTMENT OF HEALTH AND HUMAN SERVICES: The Surgeon
General's Report on Nutrition and Health. DHHS (PHS) Publ No. 88-50210. Washington, DC: US Govt Print Off, 1988
(5) U.S. DEPARTMENT OF AGRICULTURE AND U.S. DEPARTMENT OF
(18) US DEPARTMENT OF AGRICULTURE, US DEPARTMENT OF HEALTH AND
HEALTH AND HUMAN SERVICES: Dietary Guidelines for Americans.
HUMAN SERVICES: Nutrition and Your Health: Dietary Guidelines for Americans, 3rd ed. Washington, DC: US Govt Print Off, 1990
Washington, DC: U.S. Govt Print Off, 1990 (6) KRITCHEVSKY D: Evaluation of Publicly Available Scientific Evidence Regarding Certain Nutrient-Disease Relationships: 5. Dietary Fiber and Cancer. FDA Contract No. 223-88-2124. Bethesda Md: Life Sciences Research Office, FASEB, 1991 (7) MORGAN MR, FENWICK GR: Natural foodborne toxicants. Lancet 336:1492-1495, 1990 (8) HOWE GR, BENTTO E, CASTELLETO R, ET AL: Dietary intake of fiber
and decreased risk of cancers of the colon and rectum: Evidence from the combined analysis of 13 case-control studies. J Natl Cancer Inst 84:1887-1896, 1992
(19) THE WORK
STUDY
GROUP
ON DIET,
NUTRITION
AND CANCER
(WEINHOUSE S, BAL DG, ADAMSON R, ET AL): American Cancer
Society guidelines on diet, nutrition, and cancer. CA Cancer J Clin 41:334-338, 1991 (20) NATIONAL
LIVESTOCK
AND MEAT
BOARD:
Meat
and
Colorectal
Cancer: A Current Review. Research Report No. 100-2. Chicago: 1992 (21) BAL DG, FOERSTER SB: Changing the American diet: Impact on cancer prevention policy recommendations and program implications for the American Cancer Society. Cancer 67:2671-2680, 1991
The Good News Is. . . A Healthy Diet May Reduce Cancer Risk Diet. Nutrition & Cancer Prevention: The Good News
The National Cancer Institute announces its new. free public education booklet on diet and cancer. It offers practical advice on healthy eating and identifies high-fiber and low-fat foods that may help to reduce the risk of cancer. Call 1-800-4-CANCER and order your copies of Diet, Nutrition and Cancer Prevention: The Good News.
Vol. 84, No. 24, December 16, 1992
EDITORIALS 1853
Downloaded from http://jnci.oxfordjournals.org/ at Rensselaer Polytechnic Institute on March 19, 2015
(1) LUSK G: The nature of the feces. In The Elements of the Science of Nutrition (Lusk G, ed), 4th ed. New York: Nutrition Foundation, Johnson Reprint Corp, 1976 (2) BURKITT DP: Some diseases characteristic of modern Western civilization. Br Med J 1:274-278, 1973 (3) BURKTTT DP: Epidemiology of cancer of the colon and rectum. Cancer 28:3-13, 1971
cancer with special reference to fiber intake. Int J Cancer 44:1-6, 1989 (13) LEE HP, GOURLEY L, DUFFY SW, ET AL: Colorectal cancer and diet in an Asian population—a case—control study among Singapore Chinese. Int J Cancer 43:1007-1016, 1989 (14) LEE IM, PAFFENBARGER RS JR: Quetelet's index and risk of colon cancer in college alumni. J Natl Cancer Inst 84:1326-1331, 1992 (75) LEEDS AR: Dietary fiber and obesity. In Obesity (Bjorntorp P, Brodoff BN, eds). Philadelphia: Lippincott Company, 1992, pp 677682
