Fiber

The close relationship between bowel cancer and other non‐infective diseases of the bowel, such as benign tumor, divert ocular disease, and appendicitis, indicates that these conditions may have a common or related etiology. Their close association with the refined diet characteristic of economic development suggests that the removal of dietary fiber may be a causative factor. These diseases are all rare in every community examined which exists on a high residue diet, and common in every country where a low residue diet has been adopted. Dietary fiber has been shown to regulate the speed of transit, bulk, and consistency of stools, and together with other dietary factors is probably also responsible for the changes which have been demonstrated in the bacterial flora of feces. It seems likely that carcinogens produced by the action of an abnormal bacterial flora when held for a prolonged period in a concentrated form in contact with the bowel mucosa may account for the high incidence of these diseases in economically developed countries.

Dr Hugh Trowell, another strong advocate of dietary fibre, confirmed this in 1974, saying that 'a serious confusion of thought is produced by referring to the dietary fibre hypothesis as the bran hypothesis, for many Africans do not consume cereal or bran but remain almost free of constipation, irritable bowel syndrome and diverticular disease'.

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But it would be unfair to heap all the blame on the media. Commercial interests were quick to see the potential in the recommendation. AlthoughBurkitt's recommendations were based on vegetable fibre, bran has a far higher fibre content than vegetables and bran was a practically worthless by-product of the milling process which, until then, had been thrown away. Now, virtually overnight, it became a highly priced profit maker. Bran is quite inedible - there is no known enzyme in the human body that can digest it. Nevertheless, backed by Burkitt's fibre hypothesis, commercial interests could now promote it as a valuable food. The late John Yudkin, Professor Emeritus of Nutrition and Dietetics at London University, pointed out that 'perhaps one reason for the wide acceptance of the suggestion that fibre is an important, if not essential, dietary component is that it had the enthusiastic support of commercial interests.' He was writing in particular about the
high-bran products, All Bran and Branslim. 

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Sir,--As Dr N H Dyer says in his review of the Royal College of Physicians' report on dietary fibre, fashions change. Perhaps one reason for the wide acceptance of the suggestion that fibre is an important, if not essential, dietary component is that it had the enthuiastic support of commercial interests. A press release from the manufacturers of All-Bran says with dogmatic assurance, "A diet deficient in fibre makes people more prone to diseases like appendicitis, diverticular disease, cancer, and heart attacks." The makers of the product Branslim claim that the gram or so of bran it provides before each meal results in a feeling of satiety and so to a reduction in food intake. 
 

Now compare these claims with some conclusions in the report itself (my italics): "There is much evidence of an environmental factor at work in causing appendicitis, and possibly this is a lack of dietary fibre." "Patients with diverticular disease have probably eaten less dietary fiber than their diverticula-free compatriots." "There are reasonable grounds for the statement that, in genetically susceptible persons, large bowel cancer could be favorued by a fibre-depleted diet, but other explanations for the commonness of this cancer in Westernised countries are possible." "It is not yet possible to give specific recommendations to the general public about fibre's value in preventing heart attacks." "Although societies which exist on a fibre-rich diet have a low prevalence of obesity, this is not evidence that dietary fiber as such prevents obesity."

Neverless, it is a pity that the excellence of the report is marred by the  continual use of the inaccurate and misleading term "refined carbohydrate" in referring both to sugar and to white bread made from highly milled flour. It is inaccurate because white bread does not consist of pure starch but contains some 12% (dry weight) of protein, as well as significant amounts of vitamins and mineral elements. More important, the term "refined carbohydrate" is misleading because it implies that both sugar (sucrose) and white bread (or indeed starch) have the same effects on the body. But they have very different effects, and these differences are likely to be much more relevant to human disease than are the differences produced by wholemeal bread and white bread.
 

The major characteristic of Western diets is that, during the last 200-300 years, their total carbohydrate content has not changed much, but the nature of that carbohydrate has changed: the starch content has fallen considerably while the sugar content has risen to about the same extent. The association of "diseases of affluence" with changes in diet is at least as strong for this replacement of starch by sugar as they are for the diminution of dietary fibre.

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Dietary sucrose increases the concentration in the blood of cholesterol  and triglyceride, and of uric acid and insulin, it also reduces the concentration of high density lipoprotein cholesterol. It leads to a diminution of glucose tolerance. Aggregation and adhesiveness of the blood platelets are increases, as is their electrophoretic mobility in the presence of ADP.

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Dietary sucrose also results in several of the abnormalities seen in diabetics. In additon to diminished glucose tolerance and hypelipidaemia, it produces tissue insensitivity to insulin, retinopathy, and nephropathy. The most recent experiments show that the nephropathy is associated with changes in the glomerular basement membrane that are indistinguishable, in histology and in biochemistry, from the changes produced in experimental diabetes. It is tempting to see the production of the characteristics of both coronary heart disease and diabetes by dietary sugar as a clue to explaining the close clinical connection between the two diseases.

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It should be stressed that most of these changes occur in experiments with amounts of dietary sugar that are well within the range of the amounts habitually consumed by individuals in Western countries. All of this information is hidden when we use "refined carbohydrate" indiscriminately to mean sugar, or products of highly milled cereals, or both.

John Yudkin

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DIETARY FIBRE: FOOD OR FETISH? SIR,-Among the food components involved in the current campaign for "healthier eating" dietary fibre is unique since while we are being told to eat less fat, red meat, sugar, total calories, and salt, our fibre intake, as contributed by brown bread, breakfast cereals, vegetables, and fruit, should, we are told, be substantially increased. There is no novelty in this "fibrophilia". In the 1930s Arbuthnot Lanel promoted a "New Health" movement in which he urged, inter alia, that plenty of roughage should be included in the diet. Efficient defaecation and the passage of stools promptly after every substantial meal carried the hope that the incidence of intestinal disease would thereby be reduced. Thirty years later Burkitt suggested that the freedom of Africans from intestinal cancer might be related to their subsistence on coarse cereal foods, which promoted the frequent excretion of copious, loose stools. Lately, however, this theory has been questioned, with the suggestion that low cancer rates in East Africans may be due to high early death rates from other causes (so that many do not reach the age at which cancer incidence peaks in Europeans) and a growing scepticism in the United States that lack of fibre can cause cancer. Cancer apart, it seems beyond question that constipation has long been a nuisance and minor health hazard among developed populations. Memory, aided by the perusal of old advertisements, will summon up a parade of remedies mild or drastic, vegetable or mineral such as intestinal irritants, Epsom or Glauber’s salts, charcoal, liquid paraffin, enemas, and lavage. If a liberal intake of dietary fibre can make most of these treatments obsolete is that not ample justification for singling out this factor as being outstanding in its health-giving potential? Unfortunately things are not quite so simple. Praise for the virtues of fibre in the education of the general public should not be allowed to obscure the fact that fibre is by no means indispensable as a dietary component. No more material contribution is made by fibre to body building or energy production than could be made by an equal amount of finely chopped toilet paper. Moreover, there is always the danger of serious miscarriages in the chain of information coming down from expert committees to the unqualified people who organise press or television programmes or who draw attractive posters. Such a miscarriage must surely account for the title of the recent television series You are What you Eat. Presumably derived from the truism Der Mensch ist er isst, attributable to the philosopher Feuerbach (1804-72), this slogan was chanted repeatedly throughout the series, interspersed by dictory advice, gravely delivered by learned experts. But one impor- tant point seems to have been overlooked. In regard to dietary fibre, the food factor apparently to be prized above all others, "you" are certainly not what you eat, and the slogan so vigorously chanted should surely have been:

"Most of what you eat turns into you,

But dietary fibre just goes through."

Elsewhere on a television background poster depicted a strong man’s bulging biceps accompanied by the caption "fibre", thus suggesting that the muscle fibres of the human body are directly derived from an indigestible fraction of the diet. Intentionally or not there seems to have been an unhappy confusion between "brawn" and "bran". So is dietary fibre a food or just a fetish? Its value as a food is virtually zero. Whether or not it can justly be counted as a fetish ("something regarded with irrational reverence") requires deeper thought. A sensible balance may perhaps be reached by regarding fibre (roughage) as a bland natural agent that when consumed in moderate amounts facilitates the passage of food and solid waste products along the intestinal tract. In this limited role the fibre seems entirely praiseworthy. If through excessive, media-fanned enthusiasm, however, reasonable appreciation of the virtues of fibre should develop into a fetish, the ultimate effects could be unfortunate. For example, modern mothers of growing families, perhaps already obsessed with the virtues of slimming, could devote an excessive fraction of their limited household budget to the purchase of much advertised and expensive fibre-rich biscuits, breakfast foods, and out-of season greenery. With the balance tipped from nutrients to fibre, such pampered children could well lag behind in growth.

17 Chesterton Hall Crescent, Cambridge CB4 1AW

THOMAS MOORE

It had been shown in the mid-1980s that dietary fibre increased the risk of colon cancers. 

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A wealth of circumstantial evidence strongly suggests a positive relationship
between colonic cancer incidence and a high-fat, low-fibre diet
(Walker, 1976; IARC, Intestinal Microecology Group, 1977; Reddy et at.,
1978), high fecal pH (Thornton, 1981; Pietroiusti et at., 1983; Van Dokkum
et at., 1983), high fecal secondary bile acid levels (Reddy and Wynder, 1977;
Hill, 1981)- more specifically, high levels of lithocholic acid with respect to
deoxycholic acid (Owen et at., 1983)-and finally elevated ratios of strictly
anaerobic to facultatively anaerobic microorganisms within the gut (Legakis
et at., 1981). Clearly, then, with respect to colon cancer, elucidation of
factors influencing the intestinal milieu are paramount

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7. DIETARY FIBER, CELL PROLIFERATION, AND COLON CANCER

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Recent investigations have shown that consumption of a number of
different fibers, including wheat bran, pectin, guar, and cellulose, produces
colonic epithelial cell hyperplasia and associated changes in cell proliferation.
These growth-stimulating properties of certain fibers are of some theoretical
concern, since a hyperplastic response, due to nondietary perturbations, has
previously been associated with an increased incidence of experimentally
induced cancer, both in the colon and other tumor model systems. For
example, small bowel resection (Oscarson et al., 1979) and diversion of
pancreatic and biliary secretions to the large intestine (Williamson et al.,
1979) produce colonic mucosal hyperplasia and enhancement of experimental
colon carcinogenesis. Mice inoculated with the bacterium Citrobacter
freundii develop mucosal hyperplasia and increased expression of
chemical-induced focal atypia (Barthold and Beck, 1980). Feeding of bile
acids such as cholic acid also produces enhancement of colonic epithelial cell
proliferation and a greater frequency of colonic tumors (Cohen et al., 1980).
On the other hand, the feeding of ascorbic acid and butylated hydroxyanisole
decreases colonic epithelial cell proliferation (Deschner and Wattenberg,
1982; Deschner et al., 1983) and inhibits colon carcinogenesis (Wattenberg
and Sparnens, 1979; Reddy et al., 1982).

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These observations have led to the proposal that any dietary component
that stimulates intestinal cell proliferation, such as wheat bran, could enhance
colon tumor development. Evidence to support this comes from the recent
demonstration that colon carcinogenesis is enhanced in those rats fed wheat
bran during the period of 1,2-dimethylhydrazine (DMH) administration (Jacobs, 1983b). In a more recent followup study, it was found that dietary
wheat bran produced a stimulation of colonic crypt cell proliferative activity
(Fig. 7) that was most marked in the proximal colon and was greatest when
wheat bran was consumed during the stage of carcinogenic exposure (Jacobs,
1984). This suggests that wheat bran acts by modifying the stage of tumor
initiation. A possible mechanism of action is a greater susceptibility of
colonic cells to DNA damage, due to the stimulation of proliferative activity
and! or a reduction in the DNA repair mechanisms of the cell, occurring as a
result of the increased rate of cell turnover and hence a reduction in the time
available for effective DNA repair. Pectin, another fiber that stimulates
large-bowel cell proliferation, has in one report been found to increase
colonic tumor yield (Bauer et ai., 1979), and in another study (Freeman et
ai., 1980) to increase the number of small bowel tumors.