Recent History
January 1, 1971
Epidemiology of cancer of the colon and rectum. 1971.
Lack of fiber in the diet was first postulated in 1971 as the cause of diseases such as diverticulosis, hemorrhoids and colorectal cancer
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.
January 1, 1986
Dietary studies of cancer of the large bowel in the animal model
Nigro finds that fibre intake increases cancer in the large bowel.
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.
January 1, 1990
Complex Carbohydrates in Food: The Report of the British Nutrition Foundation's Task Force (British Nutrition Foundation Task Force Reports Series)
The British Nutrition Foundation admitted that the hypotheses that IBS, diverticulosis and colo-rectal cancer are caused by a deficiency of fibre had not been substantiated, neither have those that fibre might protect against diabetes, obesity and CHD.
In 1990 The British Nutrition Foundation admitted that the hypotheses that IBS, diverticulosis and colo-rectal cancer are caused by a deficiency of fibre had not been substantiated, neither havethose that fibre might protect against diabetes, obesity and CHD.
The Seventh King's Fund Forum on Cancer of The Colon and Rectum agreed: 'TheForum commented that cereal fibre does not offer protection against cancer'.
Cancer of The Colon and Rectum: the Seventh King's Fund Forum. London: King's Fund Centre, 1990.
January 1, 1990
Jerimiah Stamler
NHLBI held yet another meeting on the problem of “significantly increased” death rates from cancer and other noncardiovascular causes for people with low cholesterol.
In 1990, the NHLBI held yet another meeting on the problem of “significantly increased” death rates from cancer and other noncardiovascular causes for people with low cholesterol. The lower the cholesterol, the worse it looked for cancer deaths, and damningly, it looked especially bad for healthy men who were actively trying to reduce their cholesterol through diet or drugs. But there was no follow-up to these meetings, and the results did not change the enthusiasm for the “prudent diet.” The effects of low cholesterol are still not well understood.
When I mentioned all this to Stamler, he didn’t remember any part of this cancer-cholesterol debate. In this way, he is a microcosm of a larger phenomenon that allowed the diet-heart hypothesis to move forward: inconvenient results were consistently ignored; here again, “selection bias” was at work.
