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Issues and Opinions in NutritionThe views expressed in this section are those of the authors and not necessarily those of the Editor, the Editorial Board ofT he Journal, or the American Institute of N utrition. R eaders are invited to respond to these essays by L etters to the E ditor, so thatThe Journal can serve as a forum for the discussion of these topics.

Dietary Fiber, Vegetables and CancerJOHN D. POTTERD ivis io n o f E pid em io lo gy , S ch oo l o f P ub lic H ea lth , u niv ers ity o f M in ne so ta , M in ne ap olis , M ti 5 54 55

"The re a re th re e k inds o f fib er ce re al,vegetable and mora l; only one o f these is notin short supply." A nonymous, 1988

The relationship between cancer and dietary fiber isa source of significant controversy. This is not a newposition fo r fiber. It h as been variously praised, vilifie dand ignored by both nutritionists and the medicalprofession throughout most of this century. As withall epidem iologie questions (for that m atter, all scientific questions), it is inappropriate to regard a singlepiece of evidence as conclusive. Nonetheless, in thepast, there has been a rush to pass judgment on thequestion of fiber; e.g., physicians in the 1930s w ere surethat roughage was bad for humans. There is some concern that we m ay be experiencing in the 1980s a sim ilaruncritical enthusiasm to judge, but with an oppositeposition.The present revival of interest in fiber owes much tothe 1969 paper of Dennis Burkitt (1) who observed alower risk of m any "diseases of civilization" in blackAfricans and hypothesized a link between this low riskand the high fiber diet they consumed. He also postulated a variety of m echanism s.In the intervening 19 years, a great deal of researchhas been undertaken and a variety of relationships havebeen clarified. It is clear, for exam ple, that therapeuticuse of fiber in non-insulin-dependent diabetes, constipation and a variety of other nonm alignant coloniedisorders is beneficial and largely without unwantedconsequences. The role of low fiber in the etiology ofthese diseases is, however, m uch less clear, and whatis even more obscure is the role of fiber in the etiologyand prevention of large bow el cancer.T he difference from the 1930s, how ever, is the greaterspecificity of the claim s for fiber and the m uch greaterdetail available on its effects from both human andanimal experimental data. The inconsistencies be

tween the specificity of the claims and the details ofthe findings are w orth considering.Before doing so, it is appropriate to exam ine someg en era l e vo lu tio na ry /h isto ric al a nd b io lo gic a rg um en tsto provide the relevant background. M ost com mentators, including biologists, paleontologists, ethnographers and anthropologists w ould agree that hum an diets,w hether gatherer-hunter or peasant-agricultural, arerelatively high in fiber largely because vegetable andcereal foods provide m ost of the energy in these settingsand processing serves only to facilitate preparation andincrease consum ption. This is true, for instance, evenin India where white rice is usually preferred, but theextent of fiber removal is still lower than that foundin W estern countries. In almost all gatherer-huntereconom ies, it is gathering rather than hunting that provides the vast majority of energy. Humans are welladapted to, and largely consum e, high-fiber diets.This m atching of hum an biology, history and dietarybehavior provides a general (but strong) argum ent infavor of the value of a diet high in fiber for contemporary humans. It does not provide specific evidencefor the relationship of any one disease with fiber consum ption, but it m ust argue that drawing conclusionsabout negative consequences of high-fiber diets shouldbe based on strong and c onsistent em piric al fact-findingand not on isolated data.If we consider the specific colon cancer and diet hypothesis, hum an data on the relationship between highfiber consumption and the lowering of risk of coloncancer are not particularly convincing. There have beena variety of ecologie (correlation) studies showing am odest negative correlation between bowel cancer andcereal fib er consum ption but, as these are all essentiallyworking with the same set of data, it can hardly be saidthat m ultiple presentations of the sam e findings, eachin se pa ra te p ap ers, re pre se nt in de pe nd en t c on firm atio nof the relationship. It is like reading four versions of astory in the same newspaper to confirm that a givenevent actually o ccurred. F urther, anim al experim en taldata on the role of fiber show that fiber can be asso-

0022-3166/88 $3.00 1988 American Institute of N utrition. R eceived 19 July 1988. /. N utr. 118: 1591-1592, 1988.1591

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1592 POTTERciated with an increased risk of cancer, a decreased risk,or have no association at all (2, 3).The human analytic epidemiology, both case-controland cohort studies, are inconsistent in their findingson colon cancer and f iber. What is almost universal lyconsistent in the analytic data ( in stark contrast to mostdietary f indings in cancer epidemiology) is the consistently lower risk of colon cancer that is associated withhigher consumption of vegetables (4) . Vegetables contain a great deal more than f iberparticularly vitaminC, trace minerals, -caroteneand a variety of identified(and not yet identified) anticarcinogenic substances (5).A t least two issues emerge f rom the current state-of -the-science of colon cancer and fiber. The first is amthodologie issue: I f the relationship between f iberand human health is both historical ly and ecological lyplausible and the relationship between f iber and coloncancer is biological ly defensible, why do the analyticstudies fail to confirm the relationship? The most obvious answer to this is that plausibility and defensi-bi li ty do not establ ish an hypothesis; f iber could simplybe a neutral exposure. There are, however, better responses to this puzzle. These include the, as yet onlypartially clarified, relationships between fiber subtypes(cereal vs. vegetable, soluble vs. insoluble, fermentablevs. non-fermentable) and gut physiology; the inconsistent nature of fiber analysis methods and the consequent inconsistencies of dietary databases used forepidemiologie studies; and the misclassification inherent in self- reporting dietary data (6) . Each of these problems wil l tend to increase misclassi fication when comparing those with and without disease and, all otherthings being equal , wil l bias the relative risk estimatestowards the nul l.T he second issue is a policy question. A t this pointin our knowledge are we prepared to make recommendations regarding increasing fiber consumption to lowerthe risk of colorectal cancer? A recommendation to eatmore fiber in that bald and unconvincing fashion ap

pears naive because people eat food, not nutrients orfood components. M any people interpret f iber as wheatbran and assume that it is suffici ent to add a spoonfulto their breakfast menu. The evidence shows that consumption of wheat bran will not lower cancer risk.Rather, human data support a relationship betweenvegetables ( in al l their complexity) and lowered cancerrisk, not f iber (despi te i ts complexi ty) and lowered cancer risk.Thus, if there is a place for a specific message at thistime in the unfolding relationship between diet andcolorectal cancer it is not "eat more fiber" but "eatmore vegetables." Publ icizing that recommendation isa task for intervention methodologists. Identi fying specific agents in vegetables may be of value for chemo-prevention in high- risk groups. For the whole population, however, a high vegetable intake, rather thanpharmacology, may eventual ly prove to be a better preventive agent (7) .

L ITERATURE CITED1. BURKITT,D. P. (19691 Related diseaserelated cause? Lancet2: 1229-1231.2. JACOBS,L . R. ( 1983) Enhancement of rat col on carci nogenesi sby wheat bran consumption during the stage of 1,2-dimethylhy-drazine administration. Cancer Res. 43: 4057-4061.3. REDDY ,R . S. (1987) D ietary f iber and colon cancer: animal modelstudies. Piev. Med. 16: 559-565.4. M cM iCHAEL , A. ]. & POT TER,]. D . (1986) D ietary influencesupon colon carcinogenesis. In: D iet, Nutri tion and Cancer (Ha-yashi , Y . et al ., eds.) , pp. 275-290, Japan Sci . Soc. Press, Tokyo.5 . WATTENBERG,. W. (1985) Chemoprevention of cancer. Cancer

Res. 45 : 1 -8.6. POT TER,J. D . (1988) Fiber and Colon Cancer: W hy don't theanalytic epidemiologie data make better sense? In: Dietary Fiber,(Kri tchevsky, D. et al .) , eds. , Plenum Press, in press.7. BERTRAM,.S ., KOLONEL,. N . & MEYSKENS,. L . (1987) Rationaleand strategies for chemoprevention of cancer in humans. Cancer

Re s. 4 7: 3 01 2- 30 31 .