Colon Cancer Abstracts
Colon Cancer Abstracts
Dietary fiber & Colon Cancer
Meat, Fat and Fiber
Wheat Bran and Rectal Cancer
The daily intake of total dietary fiber (TDF) was evaluated from data of the National Nutrition Survey (NNS) in Japan for 41 years since 1947. An interrelationship between the nutrient intake, including TDF, and the mortality from colon cancer in Japanese people was calculated.
TDF intake per capita decreased rapidly from 27 g in 1947 to 16 g in 1963, and subsequently decreased by a lesser rate to 15 g in 1987.
Fat intake increased rapidly from 18.0 g in 1950 to 56.6 g in 1987.
The age-adjusted mortality from colon cancer shows a significant positive correlation with both the intakes of animal protein and of total fat, and the fat energy ratio
The TDF intake was less than 17.9 g in 1965. At the same time, the mortality from colon cancer increased rapidly. A fat/TDF ratio above 3.0 resulted in a rapid increase in colon cancer mortality.
The cause of the increased mortality from colon cancer in Japan is positively related to the increased intake of fat and protein. In addition, the decrease in TDF intake has accelerated the mortality of colon cancer after a delay of 23-24 years.
Tsuji K et al., Time-lag effect of dietary fiber and fat intake ratio on Japanese colon cancer mortality. Biomed Environ Sci, 1996 Sep, 9:2-3, 223-8.
Meat, Fat and Fiber
In a review of over 88,000 women between 1980 and 1986, ages 30 to 59 years of age, without a history of cancer, inflammatory bowel disease or familial polyps, 150 incidences of colon cancer were found.
Animal fat was positively associated with colon cancer risk though vegetable fat was not. Those who ate a beef, pork or lamb dish daily had a 2.49 relative risk compared of developing colon cancer compared to those consuming these meats less than once per month.
Processed meats and liver were also associated, whereas fish and chicken without the skin were related to a decreased risk. The red meat to chicken and/or fish ratio was strongly associated with incidence of colon cancer.
A low intake of fiber from lack of fruits was an increased risk to colon cancer.
Data supports earlier evidence that animal fat increases the risk of colon cancer. The substitution of meats high in fat with fish and chicken without the skin is recommended.
"Relation of Meat, Fat and Fiber Intake to The Risk of Colon Cancer in a Prospective Study Among Women", Willett, Walter C. et al, NEJM. December 13, 1990;323(24): 1664-72.
Wheat Bran and Rectal Cancer
Wheat bran as a dietary supplement decreased the growth of rectal adenomatous polyps in patients with familial polyposis. There was a 22% overall reduction in observed rectal mucosal cell biopsy specimens.
Wheat bran fiber supplements can inhibit DNA synthesis and rectal mucosal cell proliferation of high risk patients.
"Effects of Dietary Wheat Fiber on Rectal Epithelial Cell Proliferation in Patients With Resection From Colorectal Cancer", Alberts, D.S., et al, The Journal of The National Cancer Institute, August 1, 1990;82(15):1280-1285.
Suggests there is more to the increased incidence of colon cancer in men than diet and physical activity. He suggests industrial-related environmental exposures from toxic substances are more closely correlated with the geographic and demographic variability of the disease and should be further investigated.
"Industrial Exposure and Colorectal Cancer", Lashner, Bret A., Journal of The National Cancer Institute, October 3, 1990;82 (19):1579.
Iron & Colon Cancer
Parenteral and oral iron's effect on rat carcinogenesis was evaluated and it was found parenteral iron augmented tumor yields while oral iron was found to augment tumor incidence. Phytic acid found in dietary fiber was found to reverse the augmenting effect of oral iron on tumor yield and incidence. Further evaluation implicates iron's effect on colorectal tumor induction during the promotional phase of carcinogenesis and not during the initiation phase. This study supports epidemiologic evidence that dietary iron may enhance the risk to colorectal cancer and dietary fiber may minimize colon cancer risk by the chelating of iron.
"The Effect of Iron on Experimental Colorectal Carcinogenesis", Nelson, R.L., et al, Anticancer Research, 1989;9:1477-1482.
Nutritional factors & Colon Cancer
Nutrition - risk factors
Hospital-based malnutrition is prevalent, especially among patients with gastrointestinal malignancy. Colorectal cancers produce malnutrition through impairment of gastrointestinal function and the liberation of cytokines. Malnourished patients who undergo operation have an increased likelihood of perioperative morbidity and mortality.
A nutritional assessment will identify such patients and provide a risk assessment profile. Preoperative parenteral nutrition is a major expense and delays surgical intervention.
Cumulative evidence suggests that a 7-10 day period of parenteral nutrition repletion in the severely malnourished patient will diminish the incidence of postoperative septic complications and mortality
The endpoint of therapy is poorly defined. The role of glutamine, arginine, omega-3 fatty acids, and growth hormone in the preoperative repletion process provide an exciting arena for future research.
Nutritional assessment and the role of preoperative parenteral nutrition in the colon cancer patient. Vitello-JM. Semin-Surg-Oncol. 1994 May-Jun; 10(3): 183-94.
Nutrition - risk factors
Reviewed epidemiologic evidence on the relation between nutrition and colorectal cancer.
Colon cancer varies approximately 20-fold internationally. Although there is clear evidence of genetic predisposition to colon cancer, much of this variation appears to be related to differences in dietary habits.
Vegetables are associated with lower risk, and that fiber alone does not account for this association.
Further, meat consumption is associated with increased risk but this, too, is not explained solely by its fat content. Mutagenic compounds, particularly heterocyclic amines, produced when protein is cooked, plausibly explain the meat association.
Several microconstituents of the diet may be associated with reduced risk--including folate and calcium--but phytochemicals of other sorts may be relevant.
The most consistent inverse association is with physical activity.
Alcohol is associated, though inconsistently, with increased risk.
Rectal cancer is less well studied but, at present, there are few data to suggest that the dietary risk factors are markedly different. Physical activity does not appear to be associated with a lower risk.
Colorectal adenomatous polyps also appear to share the spectrum of risk factors seen with colon cancer, although, for adenomas, tobacco smoking is also a clear and consistent risk factor.
Potter JD: Nutrition and colorectal cancer. Cancer Causes Control, 1996 Jan, 7:1, 127-46.
During the last 2 decades, substantial progress has been made in understanding the relationship between dietary constituents and the development of colon cancer in man. Unlike studies of cancer among smokers and nonsmokers, nutritional epidemiologic studies are confronted with the inherent difficulty of assessing reasonably precise exposures.
Some deficiencies in epidemiological studies of diet and cancer have been corrected; recent case-control studies demonstrated that high dietary fat is a risk factor for colon cancer development and that an overall increase in intake of foods high in fiber might decrease the risk for colon cancer.
The populations with high incidences of colon cancer are characterized by high consumption of dietary fat, which may be a risk factor in the absence of factors that are protective, such as whole-grain cereals and of other high fiber. Laboratory-animal model studies have shown that certain dietary lipids and fibers influence tumorigenesis in the colon.
Data of metabolic epidemiological and laboratory-animal model studies are sufficiently convincing with respect to the enhancement of colon cancer by type of fat and protection by certain dietary fibers.
Reddy BS: Nutritional factors and colon cancer. Crit Rev Food Sci Nutr, 1995 Jan, 35:3, 175-90.
Prostaglandins & Colon Cancer
Forty-four colorectal cancer patients were evaluated for prostaglandin E2 levels and found to have significantly higher levels in the local venous supply draining the cancer and in the peripheral blood when there was liver and lung metastasis. Also, cancerous tissue produced large amounts of PGE2. The authors suggest when you have increased local PGE2 levels in the blood, this may stimulate metastasis formation. Elevated levels of peripheral blood PG2 may be markers for metastases in colorectal cancer. Indomethacin has reduced PGE2 levels from the tumor, in the local tissue and blood supply in unpublished studies. Cyclo-oxygenase inhibitors along with chemotherapy, radiation and immunotherapy may help prevent metastatic recurrence in colorectal cancer.
"Relationship Between Blood Plasma Prostaglandin E2 and Liver and Lung Metastasis in Colorectal Cancer", Narisawa, Tomio, MD, et al, Diseases of the Colon and Rectum, October 1990;33(10):840-845.
Cholesterol & Colon Cancer
This was a 10 year case controlled study following serum cholesterol in 69 patients, 32 men and 37 women who eventually developed colon cancer. At the time of the diagnosis, these individuals had significantly lower serum cholesterol levels than their controls.
Ten years before the cancer diagnosis, 42% of these patients had lower cholesterol levels than their control counterparts while at the time of diagnosis, 77% had lower cholesterol. There was an average decline of 13% during the 10 years in the colon cancer group, whereas the control group had an average rise of 2% in their cholesterol levels during that 10 years.
Colorectal cancer patients share initial serum cholesterol levels similar to the general population, but 10 years prior to the cancer they start to have a decline in cholesterol levels while there is a rising level seen with age in the general population.
"Declining Serum Cholesterol Levels Prior to Diagnosis of Colon Cancer: A Time-Trend, Case-Controlled Study", Winawer, Sidney J., MD, et al, JAMA, April 18, 1990;263(15):2083-2085.
Cytotoxicity of Chemotherapeutic Agents
Cytotoxicity of Chemotherapeutic Agents in Colorectal Cancer
Five-fluorouracil (5FU) is the most effective treatment for advanced colorectal cancer, with a response rate of 20%. The antioxidants pyrrolidine-dithiocarbamate and vitamin E induced apoptosis in colorectal cancer cells. The antioxidants significantly enhanced the colorectal tumor growth inhibition by cytotoxic chemotherapy in vitro (5FU and doxorubicin) and in vivo (5FU). Chemotherapeutic agents used in conjunction with antioxidants may be a novel therapy for colorectal cancer.
Chinery, Rebecca, et al: Antioxidants Enhance the Cytotoxicity of Chemotherapeutic Agents in Colorectal Cancer: A p53-Independent Induction of p21WAF1/CIP1 via C/EBPb, Nature Medicine, November, 1997;3(11):1233-1241.
According to this study, rectal cancer is associated with duration of chlorinated surface water use, while chlorine exhibited no important increase colon cancer risk. Rectal cancer was also associated with several measures of lifetime trihalomethane exposure. The risk related to more than 40 years of exposure to chlorinated surface water was high for those with low fiber intake and low for those with high fiber intake. A similar risk differential was found with low and high levels of physical activity.
Hildesheim, Mariana E., et al: Drinking Water Source and Chlorination Byproducts. II. Risk of Colon and Rectal Cancers, Epidemiology, 1998;9:29-35.
Geraniol, a monoterpene found in essential oils of fruits and herbs, may inhibit the proliferation of human colon cancer cells, according to this study performed on cancerous Caco-2 cells. Inhibition of DNA synthesis occurred in 70% of cells subjected to geraniol, due to an inability to complete the S transition phase of the cell cycle. The enzymatic activity of ornithine decarboxylase, which is important to polyamine biosynthesis and essential to the unrestrained growth of cancer cells, was also found to be reduced 50% by geraniol.
Carnesecchi S, et al: Geraniol, a component of plant essential oils, inhibits growth and polyamine biosynthesis in human colon cancer cells, J Pharmacol Exp Ther 2001 Jul;298(1):197-200
Buckwheat protein may protect against 1,2-dimethylhydrazine (DMH)-induced colon tumors, according to this study conducted on male Sprague-Dawley rats. Growing rats were fed either casein or buckwheat protein for 124 days and were gavaged weekly with DMH during the first 8 weeks to induce tumor growth. While it did not appear to affect the incidence of colonic adenomas, buckwheat protein did reduce the incidence of colonic adenocarcinoma by 47%. Dietary buckwheat protein also caused reductions in cell proliferation and in expression of c-myc and c-fos proteins in the colonic epithelium.
Liu Z, Ishikawa W, Huang X, Tomotake H, Kayashita J, Watanabe H, Kato N: A buckwheat protein product suppresses 1,2-dimethylhydrazine-induced colon carcinogenesis in rats by reducing cell proliferation, J Nutr 2001 Jun;131(6):1850-3
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