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Query: UMLS:C0699790 (colon cancer)
 28,837 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Bile acids and fatty acids may promote colon cancer by inducing colonic hyperproliferation. Dietary calcium inhibits the promoting effects of bile acids and fatty acids, possibly by precipitating these surfactants and lowering their cytolytic activity. Because bile acids and fatty acids are products of fat digestion, their effects may be dependent on the type of dietary fat. The effects of the type of dietary fat (energy percentage, 40) and of CaHPO4 supplementation (25 versus 225 mumol/g diet) on the luminal solubility of surfactants, cytolytic activity, epitheliolysis, and in vivo colonic proliferation were studied in rats using Western high-risk diets. The different types of commercially available fats were butter, saturated margarine, and polyunsaturated margarine. Supplemental calcium drastically increased fecal fatty acid excretion, the effect being dependent on the type of fat, and slightly stimulated fecal bile acid excretion. Soluble surfactant concentrations were drastically decreased by calcium supplementation with all three types of dietary fat. Consequently, cytolytic activity of fecal water was decreased by supplemental calcium. These luminal effects of calcium resulted in a lower intestinal epitheliolysis. The compensatory proliferation of the colonic epithelium was decreased by supplemental CaHPO4 for the butter and saturated margarine diets. Despite CaHPO4-dependent decreases in luminal effects and epitheliolysis, no significant decrease in proliferation on the polyunsaturated margarine diet was observed. Multiple regression analysis of soluble surfactants with cytolytic activity (R = 0.76), epitheliolysis (R = 0.74), and colonic proliferation (R = 0.84) showed highly significant associations. Cytolytic activity and epitheliolysis as well as epitheliolysis and proliferation were highly correlated (r = 0.97 and r = 0.88, respectively; n = 36) for control and CaHPO4-supplemented diets, suggesting cause-and-effect relationships. It is concluded that the antiproliferative effect of dietary calcium is mediated by the precipitation of luminal surfactants and is dependent on the type of dietary fat.
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PMID:The antiproliferative effect of dietary calcium on colonic epithelium is mediated by luminal surfactants and dependent on the type of dietary fat. 842 59

Calcium has been proposed to prevent colon cancer in subjects at risk for this tumour. This effect is supposed to be due at least in part to binding the bile acids to calcium, making them insoluble and harmless. To evaluate the effects of oral calcium supplementation on intestinal bile acids, 19 patients with adenomatous colonic polyps were supplemented with 35.5 mmol Ca2+ daily for 12 weeks. Duodenal bile, 24-h feces and 24-h urine were collected before and at the end of the 12-week period. In duodenal bile proportional concentration of cholic acid increased (38 +/- 4 vs. 51 +/- 3%, P < 0.001), whereas that of chenodeoxycholic acid decreased (35 +/- 3 vs. 25 +/- 2%, P < 0.01). Total fecal bile acid excretion increased (950 +/- 126 vs. 1218 +/- 137 mumol 24 h-1, P < 0.01), with proportional concentrations of the main primary and secondary bile acids remaining the same. Cytolytic activity of fecal water, measured by the degree of lysis of erythrocytes by the water, decreased (45 +/- 8 vs. 30 +/- 7%, P < 0.05). Total excretion of calcium increased as expected from the supplementary dose. It is concluded that calcium supplementation markedly affects intestinal bile acids and lytic activity of fecal water and that, in view of similar results during 1-week calcium supplementation in young healthy subjects, these effects remain constant over at least 3 months and occur both in healthy persons and in patients at increased risk for colon cancer.
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PMID:Effects of oral calcium supplementation on intestinal bile acids and cytolytic activity of fecal water in patients with adenomatous polyps of the colon. 844 75

Physical activity potentially encourages a healthy lifestyle and it could have a more direct preventive effect on certain forms of carcinogenesis (for instance, by speeding gastrointestinal transit, or by moderating sex hormone levels). However, there are also potential negative effects, particularly an excessive exposure to ultraviolet light in certain water sports. The many types of neoplasm and the equally varied sources of physical activity militate against finding any simple relationship between the risk of malignancy and the individual's physical activity history. Nevertheless, evidence that physical activity protects against certain forms of cancer can be deduced from studies of experimental animals, former athletes, people employed in active occupations, and those with an active recreational lifestyle. Many occupational surveys and a number of studies of recreational activity show an association between sedentary living and a risk of colon cancer, both in men and in women. Moreover, an application of Bradford Hill's criteria gives some support to the causal nature of the association. More limited data suggest that a history of active leisure is associated with a reduced risk of all-cause cancer and in women of breast and reproductive system cancers. The last observation must still be reconciled with an apparent increase in the risk of prostatic cancer in active men. Since moderate exercise elevates mood and helps to conserve lean tissue, it may finally be a helpful component of treatment after a neoplasm has been diagnosed.
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PMID:Exercise in the prevention and treatment of cancer. An update. 846 Feb 89

We have previously shown that thermolyzed sucrose in the diet promotes the growth of aberrant crypt foci (ACF) in the rat. HPLC analysis of the light caramel colored product showed that it contained 1% 5-hydroxymethyl-2-furaldehyde (HMF), confirmed by mass and NMR spectroscopy. To determine whether HMF was responsible for the promotion of ACF by thermolyzed sucrose, 45 F344 female rats were initiated with the colon carcinogen azoxymethane (AOM), and a week later were randomized to four groups receiving AIN-76 diets containing untreated sucrose, 20% thermolyzed sucrose, 20% butanol extracted thermolyzed sucrose (HMF free) or 1% HMF. Thermolyzed sucrose in the diet led to larger ACF as previously observed. Thermolyzed sucrose extracted to remove HMF, did not affect ACF size, but 1% HMF added to the diet led to a larger ACF both with relation to average size and number of ACF of larger sizes (P < 0.05). To determine whether HMF had initiating effects, 172 female F344 rats were given water, HMF (at doses to 300 mg/kg) or AOM (5 mg/kg) by gavage twice and the total number of ACF was scored 30 days later. The results demonstrated that HMF induces ACF in a dose-dependent manner (P < 0.02), though the effect was much weaker than that of AOM. We conclude that sugar heated under household cooking conditions may act as both an initiator and a promoter of colon cancer because of the presence of HMF.
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PMID:Initiation and promotion of colonic aberrant crypt foci in rats by 5-hydroxymethyl-2-furaldehyde in thermolyzed sucrose. 847 46

Luminal free fatty acids and bile acids may damage the colonic epithelium and stimulate proliferation, which may increase the risk of colon cancer. It has been suggested that only soluble calcium ions (Ca2+) precipitate fatty acids and bile acids, thus reducing their lytic activity. Consequently, precipitation of luminal Ca2+ by dietary phosphate should inhibit these effects. To evaluate the proposed antagonistic effects of dietary calcium and phosphate, we studied the intestinal interactions between calcium, phosphate, fatty acids, and bile acids in rats fed purified diets that differed only in the concentrations of calcium and phosphate. Increased dietary calcium drastically decreased the solubility of fatty acids in the ileum, colon, and faeces, as well as the solubility of bile acids in the colon and faeces. Although dietary calcium strongly increased the total faecal fatty acid concentration and hardly affected the total faecal bile acid concentration, the fatty acid and bile acid concentrations in faecal water were drastically decreased by dietary calcium. Consequently, the lytic activity of faecal water was decreased. Dietary phosphate did not interfere with these intestinal effects of calcium. These results indicate that dietary phosphate does not inhibit the protective effects of dietary calcium on luminal solubility and the lytic activity of fatty and bile acids.
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PMID:Effects of dietary calcium and phosphate on the intestinal interactions between calcium, phosphate, fatty acids, and bile acids. 847 85

Dietary casein cooked at 180 degrees C promotes the growth of aberrant crypt foci and colon cancer in rats initiated with azoxymethane. We speculated that promotion was due to a product that could be extracted by a solvent, such as 5-hydroxymethyl-2-furaldehyde (HMF), with tumor- promoting activity or the carcinogenic heterocyclic aromatic amines (HAA). This hypothesis was tested by extracting cooked casein with solvents and water. The extracts were then 1) assayed by high-performance liquid chromatography for HMF and HAA, 2) measured for mutagenicity on a frame-shift-sensitive strain of Salmonella typhimurium, and 3) fed for 100 days to azoxymethane-initiated rats to test the promoting effect on aberrant crypt foci. Data show that 1) no HMF or HAA was detected in cooked casein, 2) no mutagenicity was detected on strain TA98, with or without metabolic activation, and 3) promotion was not associated with the extracts but with the cooked casein residue. Therefore the promotion by cooked casein would not appear to be associated with a product that can be extracted by solvents.
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PMID:Lack of aberrant crypt promotion and of mutagenicity in extracts of cooked casein, a colon cancer-promoting food. 861 44

Use of calcium supplements has increased dramatically in recent years yet little is known about the effect of calcium supplementation on colon physiology. We supplemented 22 individuals with a history of resected adenocarcinoma of the colon, but currently free of cancer, with 2000 or 3000 mg calcium for 16 wk. The effects of supplementation on duodenal bile acids and important fecal characteristics including total fecal output, wet and dry weight, pH, bile acids (in solids and in fecal water), and concentrations and total excretion of calcium, magnesium, phosphates (organic and inorganic), unesterified fatty acids and total fat were determined. Calcium supplementation significantly decreased the proportion of water in the stool (P = 0.03), doubled fecal excretion of calcium (P = 0.006), and increased excretion of organic phosphate (P = 0.035) but not magnesium. Calcium supplementation significantly decreased the proportion of chenodeoxycholic acid in bile (P = 0.007) and decreased the ratio of lithocholate to deoxycholate in feces (P = 0.06). The concentration of primary bile acids in fecal water decreased after 16 wk Ca supplementation. Together with other reports of a "healthier" bile acid profile with respect to colon cancer when changes such as those observed in this study were achieved, these results suggest a protective effect of calcium supplementation against this disease.
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PMID:Calcium supplementation modifies the relative amounts of bile acids in bile and affects key aspects of human colon physiology. 861 39

Dietary calcium may reduce the risk of colon cancer, probably by precipitating cytotoxic surfactants, such as secondary bile acids, in the colonic lumen. We previously showed that milk mineral, an important source of calcium, decreases metabolic risk factors and colonic proliferation in rats. We now report the effects of the habitual intake of milk calcium on metabolic risk factors in healthy subjects. A double-blind, cross-over metabolic study was performed in 13 healthy males. Placebo milk products (calcium, 3 mM) were compared with regular milk products (calcium, 30 mm). In each 1-week period, the habitual diet was recorded, and urine and feces were collected for 1 and 3 days, respectively. Milk calcium significantly increased fecal pH and fecal excretion of phosphate (132%), total fat (139%), free fatty acids (195%), and bile acids (141%), indicating intestinal complexation. In fecal water, the concentrations of long-chain fatty acids, secondary bile acids (deoxycholic and lithocholic acid), neutral sterols, and phospholipids were about halved (P <0.05). Consistent with these changes in soluble hydrophobic surfactants, calcium decreased the cytotoxicity of fecal water from 68 +/- 9 to 28 +/- 12% (P < 0.005). Calcium in milk products precipitates luminal cytotoxic surfactants and thus inhibits colonic cytotoxicity. Therefore, habitual dietary calcium may contribute to a nutritional modulation of colon cancer risk.
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PMID:Calcium in milk products precipitates intestinal fatty acids and secondary bile acids and thus inhibits colonic cytotoxicity in humans. 876 20

This study measured fecal levels of short-chain fatty acids (SCFAs) relative to the severity of colitis in the cotton-top tamarin model of colitis and colon cancer. Severity of colitis was classified as mild, moderate, or severe by subjective scoring of colonic mucosal biopsies and quantification of inflammatory cell infiltrates in the lamina propria. SCFAs were determined by gas chromatography of SCFAs extracted from fresh feces. Tamarins with moderate or severe colitis had significantly reduced levels of fecal SCFAs. The percent dry matter of feces declined significantly in moderate and severe colitis, while total dry matter output per day increased, indicating that moderate and severe colitis in tamarins was associated with diarrhea and increased fecal water loss. In conclusion, this study found colitis in the tamarin model was associated with decreased fecal SCFA levels and progressive inflammation in a pattern similar to human colitis.
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PMID:Fecal short-chain fatty acids associated with inflammation in cotton-top tamarin model for idiopathic colitis. 876 89

The association between food groupings and adenocarcinoma of the colon was investigated in a population-based case-control study of men and women ages 30-62 years. Colon cancer cases (238 men and 186 women) diagnosed from 1985 to 1989 were identified from the Seattle-Puget Sound Surveillance, Epidemiology, and End Results Registry. Controls (224 men and 190 women) were selected using a random digit telephone dialing method. Dietary information was gathered using an 80-item food frequency questionnaire. Foods were grouped and analyzed by quartile of intake, with adjustment for age and total energy intake. Among women, a reduced risk of colon cancer was associated with a high intake of fruits and vegetables [adjusted odds ratio (OR) for highest versus lowest quartile, 0.48; 95% confidence interval (CI), 0.26-0.86; P for trend, P = 0.02]. Inverse associations were also observed for the consumption of total (hot and cold) cereals (OR, 0.47; 95% CI, 0.25-0.91; P = 0.05), dairy products (OR, 0.40; 95% CI, 0.21-0.79; P = 0.05), and water (OR for > 5 glasses/day versus < or = 2 glass/day, 0.55; 95% CI, 0.31-0.99; P = 0.004). Among men, colon cancer risk was inversely associated with the intake of breads and cereals (OR, 0.43; 95% CI, 0.22-0.82; P = 0.02) and hot cereal (OR for weekly versus never eating, 0.53; 95% CI, 0.32-0.87; P = 0.01). Water consumption was marginally associated with a decreased colon cancer risk among men as well (OR for > 4 glasses/day versus < or = 1 glass/day, 0.68; 95% CI, 0.38-1.22; P = 0.16). Total meat consumption was associated with an increased risk of distal colon cancer among men (OR, 2.20; 95% CI, 1.08-4.48; P = 0.01). These results were not confounded by body mass index or other measured health behaviors. Results of this research support previous findings which associate intake of fruits, vegetables, grains, and dairy products with reduced colon cancer risk, and meat intake with an increased colon cancer risk. This study also reports a new finding of a possible inverse association of water consumption (glasses of plain water per day) with colon cancer risk.
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PMID:Relationship of food groups and water intake to colon cancer risk. 926 83


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