Historical Events

Nigro finds that fibre intake increases cancer in the large bowel.

Dietary studies of cancer of the large bowel in the animal model

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

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

7. DIETARY FIBER, CELL PROLIFERATION, AND COLON CANCER

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).

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.

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