Issues and Opinions in Nutrition

The views expressed in this section are those of the authors and not necessarily those of the Editor, the Editorial Board of The Journal, or the American Institute of Nutrition. Readers are invited to respond to these essays by Letters to the Editor, so that The Journal can serve as a forum for the discussion of these topics.

Dietary Fiber, Vegetables and Cancer

JOHN D. POTTER
Division of Epidemiology, School of Public Health, university of Minnesota, Minneapolis, Mti 55455

"There are three kinds of fibercereal, vegetable and moral; only one of these is not in short supply." Anonymous, 1988

The relationship between cancer and dietary fiber is a source of significant controversy. This is not a new position for fiber. It has been variously praised, vilified and ignored by both nutritionists and the medical profession throughout most of this century. As with all epidemiologie questions (for that matter, all scien tific questions), it is inappropriate to regard a single piece of evidence as conclusive. Nonetheless, in the past, there has been a rush to pass judgment on the question of fiber; e.g., physicians in the 1930s were sure that roughage was bad for humans. There is some con cern that we may be experiencing in the 1980s a similar uncritical enthusiasm to judge, but with an opposite position. The present revival of interest in fiber owes much to the 1969 paper of Dennis Burkitt (1) who observed a lower risk of many "diseases of civilization" in black Africans and hypothesized a link between this low risk and the high fiber diet they consumed. He also pos tulated a variety of mechanisms. In the intervening 19 years, a great deal of research has been undertaken and a variety of relationships have been clarified. It is clear, for example, that therapeutic use of fiber in non-insulin-dependent diabetes, con stipation and a variety of other nonmalignant colonie disorders is beneficial and largely without unwanted consequences. The role of low fiber in the etiology of these diseases is, however, much less clear, and what is even more obscure is the role of fiber in the etiology and prevention of large bowel cancer. The difference from the 1930s, however, is the greater specificity of the claims for fiber and the much greater detail available on its effects from both human and animal experimental data. The inconsistencies be
0022-3166/88 $3.00 1988 American Institute of Nutrition.

tween the specificity of the claims and the details of the findings are worth considering. Before doing so, it is appropriate to examine some general evolutionary/historical and biologic arguments to provide the relevant background. Most commenta tors, including biologists, paleontologists, ethnogra phers and anthropologists would agree that human diets, whether gatherer-hunter or peasant-agricultural, are relatively high in fiber largely because vegetable and cereal foods provide most of the energy in these settings and processing serves only to facilitate preparation and increase consumption. This is true, for instance, even in India where white rice is usually preferred, but the extent of fiber removal is still lower than that found in Western countries. In almost all gatherer-hunter economies, it is gathering rather than hunting that pro vides the vast majority of energy. Humans are well adapted to, and largely consume, high-fiber diets. This matching of human biology, history and dietary behavior provides a general (but strong) argument in favor of the value of a diet high in fiber for contem porary humans. It does not provide specific evidence for the relationship of any one disease with fiber con sumption, but it must argue that drawing conclusions about negative consequences of high-fiber diets should be based on strong and consistent empirical fact-finding and not on isolated data. If we consider the specific colon cancer and diet hy pothesis, human data on the relationship between high fiber consumption and the lowering of risk of colon cancer are not particularly convincing. There have been a variety of ecologie (correlation) studies showing a modest negative correlation between bowel cancer and cereal fiber consumption but, as these are all essentially working with the same set of data, it can hardly be said that multiple presentations of the same findings, each in separate papers, represent independent confirmation of the relationship. It is like reading four versions of a story in the same newspaper to confirm that a given event actually occurred. Further, animal experimental data on the role of fiber show that fiber can be asso/. Nutr. 118: 1591-1592, 1988.

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Received 19 July 1988.

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ciated with an increased risk of cancer, a decreased risk, or have no association at all (2, 3). The human analytic epidemiology, both case-control and cohort studies, are inconsistent in their findings on colon cancer and fiber. What is almost universally consistent in the analytic data (in stark contrast to most dietary findings in cancer epidemiology) is the consis tently lower risk of colon cancer that is associated with higher consumption of vegetables (4). Vegetables con tain a great deal more than fiberparticularly vitamin C, trace minerals, -caroteneand a variety of identified (and not yet identified) anticarcinogenic substances (5). At least two issues emerge from the current state-ofthe-science of colon cancer and fiber. The first is a mthodologie issue: If the relationship between fiber and human health is both historically and ecologically plausible and the relationship between fiber and colon cancer is biologically defensible, why do the analytic studies fail to confirm the relationship? The most ob vious answer to this is that plausibility and defensibility do not establish an hypothesis; fiber could simply be a neutral exposure. There are, however, better re sponses to this puzzle. These include the, as yet only partially clarified, relationships between fiber subtypes (cereal vs. vegetable, soluble vs. insoluble, fermentable vs. non-fermentable) and gut physiology; the incon sistent nature of fiber analysis methods and the con sequent inconsistencies of dietary databases used for epidemiologie studies; and the misclassification inher ent in self-reporting dietary data (6). Each of these prob lems will tend to increase misclassification when com paring those with and without disease and, all other things being equal, will bias the relative risk estimates towards the null. The second issue is a policy question. At this point in our knowledge are we prepared to make recommen dations regarding increasing fiber consumption to lower the risk of colorectal cancer? A recommendation to eat more fiber in that bald and unconvincing fashion ap

pears naive because people eat food, not nutrients or food components. Many people interpret fiber as wheat bran and assume that it is sufficient to add a spoonful to their breakfast menu. The evidence shows that con sumption of wheat bran will not lower cancer risk. Rather, human data support a relationship between vegetables (in all their complexity) and lowered cancer risk, not fiber (despite its complexity) and lowered can cer risk. Thus, if there is a place for a specific message at this time in the unfolding relationship between diet and colorectal cancer it is not "eat more fiber" but "eat more vegetables." Publicizing that recommendation is a task for intervention methodologists. Identifying spe cific agents in vegetables may be of value for chemoprevention in high-risk groups. For the whole popula tion, however, a high vegetable intake, rather than pharmacology, may eventually prove to be a better pre ventive agent (7).
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LITERATURE CITED
1. BURKITT, D. P. (19691 Related diseaserelated cause? Lancet 2: 1229-1231. 2. JACOBS, L. R. (1983) Enhancement of rat colon carcinogenesis by wheat bran consumption during the stage of 1,2-dimethylhydrazine administration. Cancer Res. 43: 4057-4061. 3. REDDY, R. S. (1987) Dietary fiber and colon cancer: animal model studies. Piev. Med. 16: 559-565. 4. McMiCHAEL, A. ]. & POTTER,]. D. (1986) Dietary influences upon colon carcinogenesis. In: Diet, Nutrition and Cancer (Hayashi, Y. et al., eds.), pp. 275-290, Japan Sci. Soc. Press, Tokyo. 5. WATTENBERG, L. W. (1985) Chemoprevention of cancer. Cancer Res. 45: 1-8. 6. POTTER,J. D. (1988) Fiber and Colon Cancer: Why don't the analytic epidemiologie data make better sense? In: Dietary Fiber, (Kritchevsky, D. et al.), eds., Plenum Press, in press. 7. BERTRAM, J. S., KOLONEL, L. N. & MEYSKENS, F. L. (1987) Rationale and strategies for chemoprevention of cancer in humans. Cancer Res. 47: 3012-3031.