Colon cancer intake

An obvious factor for the inconsistent results of the effect of different intakes of dietary fiber on colorectal cancer is the variation in the analytical methodology used in different studies. There is also increasing evidence that total dietary complex carbohydrates may be as important as fiber. Analysis of stool weight from 20 populations in 12 countries showed that larger stools were correlated with a lower incidence of colon cancer. Intakes of starch and dietary fiber (rather than fiber alone) were the best dietary correlates with stool weight. A subsequent meta-analysis showed that greater consumption of starch (but not of NSPs) was associated with low risk of colorectal cancer in 12 populations. The examination also showed that fat and protein intakes correlated positively with risk. This meta-analysis is probably the first of its kind to... 

CUMMINGS J H (1992) Fecal weight, colon cancer and dietary fiber intake of non-starchy polysaccharide(dietary fiber). Gastroenterology, 103 1783-9. 

Slattery, M.L. et al., Carotenoids and colon cancer, Am. J. Clin. Nutr., 71, 575, 2000. Terry, P. et al., Dietary carotenoid intake and colorectal cancer risk, Nutr. Cancer, 42, 167, 2002. 

The risk of colon cancer appears to be inversely related to calcium and folate intake. Calciums protective effect may be related to a reduction in mucosal cell proliferation rates or through its binding to bile salts in the intestine, whereas dietary folate helps in maintaining normal bowel mucosa. Additional micronutrient deficiencies have been demonstrated through several studies to increase colorectal cancer risk and include selenium, vitamin C, vitamin D, vitamin E, and 3-carotene however, the benefit of dietary supplementation does not appear to be substantial.11... 

Figure 7- Correlation between colon cancer rate and the intake of cereals in 37 countries. (Adapted from Ref. 37.)...

First, there is no way to know whether, within each country, those groups of people who eat more meat exhibit greater rates of colon cancer than those who eat less or even no meat. Data concerning total or average meat consumption provide no clues about how that consumption is distributed among members of the population moreover, the distribution patterns in different countries are surely variable. The data are also uninformative on the question of duration of meat consumption - they do not reveal whether rates rise with increasing duration of meat intake. 

Perhaps meat consumption is related to some other factor and it is that other factor that is the real culprit. Do heavy meat eaters consume more alcohol than those who consume less Do heavy meat eaters consume less fiber Even if the latter were true, and we were to construct a figure relating fiber intake to colon cancer, and found that country rates went up as fiber intake declined, we would still fall short of demonstrating causal links between decreased fiber consumption and increased colon cancer rates. 

Relative risk of colon cancer according to the intake of animal fat. First quintile (1 on the graph) indicates the relative risk of twenty percent of the population (88,751 women) who consumed the least animal fat. Individuals in the fifth quintile (5 on the graph) consumed the most animal fat. 

Colorectal cancer Cancers of the colorectum are common in economically developed areas. Five studies have reported on tomato intake in relation to colorectal cancer risk. One study in the U.S. reported statistically significant inverse associations between tomato consumption and colon cancer risk for men and women. 

Wu, K, WilletWC.ChanJM.etal.Aprospectivestudyonsupple-mental vitamin E intake and risk of colon cancer in women and man, Cancer Epidemiol Biomarkers Prev 2002 11 1298-1304. 

Wynder and Shigematsu (15) were the first to suggest that nutritional factors in general and specifically differences in fat intake may be responsible for the international variation in colon cancer incidence. Subsequent descriptive epidemiologic studies have found a strong positive association between colon cancer mortality or incidence in different countries and per capita availability in national diets of total fat (4,16) and of animal fat, estimated from food balance sheets. Such international correlations may be supportive of a hypothesis, but they should be interpreted with caution because the dietary data were based not on actual intake information but on food disappearance data. 

A case-control study in Canada indicated an elevated risk for those with an increased intake of calories, total fat, and saturated fat (20,21). This study estimated levels of fat consumption by combining information from diet histories with information on the fat content of foods A recent case-control study in Utah Mormons indicated a positive association between dietary fat and colon cancer (10). 

The possible role of dietary fat on colon carcinogenesis has received support from studies in animal models. In several earlier studies on dietary fat and colon cancer, interpretation of results between high- and low-fat diets was complicated by the use of diets of varying caloric density and confounded by different intakes of other nutrients. However, recent studies in which the intake of all nutrients and total calories were controlled between the high-fat and low-fat groups, indicated that the amount of dietary fat is an important factor in colon carcinogenesis (27). 

Thus, the excretory pattern of fecal secondary bile acids observed in these studies correlated with colon tumor incidences in animal models. These studies also suggest that high dietary intake of certain types of fat may be necessary for the full expression of risk for colon cancer. 

The incidence of colon cancer is high in western populations except for Japan and low in most developing nations. The high incidence is associated with high dietary fat. Low fiber intake has also been associated with the high colon cancer incidence in some populations. 

Studies of the incidence of and mortality from colon cancer at the international level suggest an association of this neoplasm with total dietary fat (33,34). Lui et al (35), studying the disappearance rate of food and mortality from colon cancer between the years 1967-1973 in 20 industrialized countries, concluded that there was a direct correlation of this tumor type and the per capita intake of total fat, saturated and monounsaturated fat and cholesterol. Furthermore, fiber intake was inversely correlated with colon cancer in these studies. 

Berg and Howell (36) and Howell (37) reported a high correlation for meat intake and colon cancer, particularly beef. Enstrom, on the other hand (38) suggested that trends in per capita intake of beef... 

MacLennan et al (41) reviewed the diets of adult males from Kuopio, Finland and from Copenhagan, Denmark, the latter where the incidence of colon cancer is four times higher than Kuopio. Among other findings they noted that the estimated fat consumption was similar but fiber intake was higher in Kuopio men, associated with lower colon cancer rates. 

Selenium has been reported to have a positive, enhancing effect (42) or an inverse correlation between the intake of selenium and colon cancer (43,44). Birt et al (45) have reported inhibition of colon cancer in rats by dietary selenium. 

Polyunsaturated fat has also been found to be more effective than saturated fat in promoting the development of pancreatic tumors in rats (1 2). Similar results have been reported recently for colon cancer (22 ), although earlier experiments had indicated that saturated and polyunsaturated fats were about equally effective at high levels of intake (j l). It thus appears that there may be a general requirement for polyunsaturated fatty acids in promotion of carcinogenesis by dietary fat. 

International comparitive studies show a strong correlation between per capitut disappearance of fat and rates of colon cancer (Willett, 2001a Kushi and Giovannucci, 2002). Early animal studies suggested that dietary fat plays an important role in the initiation and promotion of colon tumorigenesis. However, later evidence showed that total energy intake, rather than fat intake, was more likely to influence tumor development (Howe et al., 1997). 

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