Guest guest Posted June 28, 2004 Report Share Posted June 28, 2004 Aspirin: http://my.webmd.com/content/article/81/96946.htm >From: " Rodney " <perspect1111@...> >Reply- > >Subject: [ ] Vitamin D, Lithocholic Acid and Colon Cancer >Date: Sun, 27 Jun 2004 23:11:40 -0000 > >Hi folks: > >1. Quite an interesting article (but it is two years old now): > >http://www.cancer.org/docroot/NWS/content/NWS_1_1x_Vitamin_D_Protects_ >Against_Colon_Cancer.asp > >http://snipurl.com/7db2 > >2. I was trying to put together a list of things that protect >against colon cancer. Here it is. Would anyone like to add to it? > >Insoluble fibre. >Statins. >Vitamin E. >Calcium. >Coffee. >Copper. >Folic acid. >Exercise. >Avoid red meats. >Cruciferous vegetables. >CR. >Colonoscopies. > >Many of the above preventive measures are claimed to reduce cancer >probability by 50%. So if one does seven of them does that reduce >your chances to less than 1%? (0.5 ^ 7 x 100)% > >Rodney. > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted June 28, 2004 Report Share Posted June 28, 2004 Hi : Thank you. Also I forgot garlic as protective against colon cancer (Source: Iowa Women's Health Study) Rodney. > Aspirin: > > http://my.webmd.com/content/article/81/96946.htm > > > >From: " Rodney " <perspect1111@y...> > >Reply- > > > >Subject: [ ] Vitamin D, Lithocholic Acid and Colon Cancer > >Date: Sun, 27 Jun 2004 23:11:40 -0000 > > > >Hi folks: > > > >1. Quite an interesting article (but it is two years old now): > > > >http://www.cancer.org/docroot/NWS/content/NWS_1_1x_Vitamin_D_Protects _ > >Against_Colon_Cancer.asp > > > >http://snipurl.com/7db2 > > > >2. I was trying to put together a list of things that protect > >against colon cancer. Here it is. Would anyone like to add to it? > > > >Insoluble fibre. > >Statins. > >Vitamin E. > >Calcium. > >Coffee. > >Copper. > >Folic acid. > >Exercise. > >Avoid red meats. > >Cruciferous vegetables. > >CR. > >Colonoscopies. > > > >Many of the above preventive measures are claimed to reduce cancer > >probability by 50%. So if one does seven of them does that reduce > >your chances to less than 1%? (0.5 ^ 7 x 100)% > > > >Rodney. > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted June 28, 2004 Report Share Posted June 28, 2004 The only thing that will guarantee protection against colon cancer is a colonoscopy. Those other things are associations. If you check duke's database you will find thousands of anti cancer associations. Because of the way a cancer works, I find it hard to believe any food chemical will prevent any cancer, and I don't believe red meats cause cancer, even thought I seldom eat it. My perusal of prostate cancer docs (the only one I concern myself with), indicates to me inflammation is where it starts. So I use NSAIDS. Some herbs contain a natural NSAID, maybe even a natural source of chemo, but not in sufficient quantity. Cancers seem to feed on excess food so I think a minimizing of food slows its growth. That's another reason for CR, IMO. I'm not so sure the lowered temperature is conducive to slower cancer growth, however. Maybe someone has some ideas about that. In my case (HTN), I think even HTN meds will slow cancer growth because the fluid flow, and the nutrient flow that comes with it, is held down to normal levels. Regards. ----- Original Message ----- From: Rodney Sent: Sunday, June 27, 2004 6:11 PM Subject: [ ] Vitamin D, Lithocholic Acid and Colon Cancer Hi folks:1. Quite an interesting article (but it is two years old now):http://www.cancer.org/docroot/NWS/content/NWS_1_1x_Vitamin_D_Protects_Against_Colon_Cancer.asphttp://snipurl.com/7db22. I was trying to put together a list of things that protect against colon cancer. Here it is. Would anyone like to add to it?Insoluble fibre.Statins.Vitamin E.Calcium.Coffee.Copper.Folic acid.Exercise.Avoid red meats.Cruciferous vegetables.CR.Colonoscopies.Many of the above preventive measures are claimed to reduce cancer probability by 50%. So if one does seven of them does that reduce your chances to less than 1%? (0.5 ^ 7 x 100)%Rodney. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted June 28, 2004 Report Share Posted June 28, 2004 > Calcium. I would point out this is likely an effect of inorganic calcium that is unassimilated in the bowel, not organic. > Coffee. I think you should search up the negative effects of coffee on the bowel mucoidal lining. > Copper. > Folic acid. > Exercise. > Avoid red meats. > Cruciferous vegetables. > CR. > Colonoscopies. None of the above is as effective as bowel detoxification in terms of inducing peristalisis and vacuuming out fecal matter (with fiber-like blends of drawing substances) and healing up any polyphs and diverticulosis. Once every season is a good preventive measure. Logan Quote Link to comment Share on other sites More sharing options...
Guest guest Posted June 29, 2004 Report Share Posted June 29, 2004 I couldn't find the calcium study I had in mind. However, I believe the study concluded or theorized that the unabsorbed inorganic calcium from dietary supplementation acted as a protective effect in the colon. The coffee studies seem to be contradictory. I've ***emphasized*** in two references below. There are many substances that can act both as a " colon vacuum " and pathology inhibitor, not just the unique substance referenced below. As it says in the reference, this is an " emerging field " -- at least when it comes to published science! Rodney, here are other substances (with published science backing) to add to your list: Green Tea Selenium Resveratrol EPA and DHA Vitamins A Vitamins D Tocotrienols Modified Citrus Pectin Logan Effect of differently processed coffee on the gastric potential difference and intragastric pH in healthy volunteers. Ehrlich A, Basse H, Henkel-Ernst J, Hey B, Menthe J, Lucker PW. Medical Department Phase I, Institut fur Klinische Pharmakologie Bobenheim, Grunstadt, Germany. The gastric irritation potential of orally administered coffee (150 ml) was investigated in four healthy volunteers by continuous measurement of gastric potential difference (GPD) and intragastric pH. Furthermore, serum gastrin concentrations were measured up to 45 min after administration of the coffee. One of the coffees, untreated, had to be compared with a pretreated coffee. The evaluation of the target parameters Reiz-Index, AUB, Pdmax and ttot revealed a significant difference between untreated coffee and specially treated coffee: the improved coffee processing produced ***significantly less mucosal irritation***. Regarding the intragastric pH, no significant differences between the treatments were observed and no stimulation of gastric acid secretion following coffee was measurable. No consistent effect on serum gastrin concentration was seen: two of the four subjects had a steep increase in serum gastrin following administration with a clear difference between the differently processed coffees, whereas the other two subjects showed no change in serum gastrin. The results of this pilot study confirm the findings of former experiments on the reliability of continuous transmural GPD measurement when investigating the mucosal irritation potential of barrier breakers. Publication Types: Clinical Trial Randomized Controlled Trial PMID: 9604858 [PubMed - indexed for MEDLINE] The effect of unfiltered coffee on potential biomarkers for colonic cancer risk in healthy volunteers: a randomized trial. Grubben MJ, Van Den Braak CC, Broekhuizen R, De Jong R, Van Rijt L, De Ruijter E, s WH, Katan MB, Nagengast FM. Department of Gastroenterology and Hepatology, University Hospital Nijmegen, The Netherlands. m.grubben@... BACKGROUND: Epidemiologic studies suggest that coffee use might protect against colorectal cancer. Inconsistencies as to the effect of coffee use and colorectal cancer between epidemiologic studies might be related to the type of coffee brew. OBJECTIVE: We studied the effect of unfiltered coffee consumption on putative biomarkers for colonic cancer risk. DESIGN: A total of 64 healthy volunteers (31 men and 33 women), with a mean age of 43 +/- 11 years were randomly assigned to two groups in a crossover design, with two intervention periods of 2 weeks separated by a washout period of 8 weeks. Treatments were 1 L of cafetiere (French press) coffee daily or no coffee. At the end of each intervention period, fasting blood samples, colorectal biopsies and 48 h faeces were collected. RESULTS: No effect of coffee on colorectal cell proliferation, assayed by estimating the Proliferating Cell Nuclear Antigen labelling index, was seen. Additionally, no effects were seen on the concentrations of faecal soluble bile acids and colorectal mucosal glutathione S- transferase activity. However, unfiltered coffee significantly increased the glutathione content in the colorectal mucosa by 8% and in plasma by 15%. Other aminothiols in plasma also increased on coffee. CONCLUSION: ***Unfiltered coffee does not influence the colorectal mucosal proliferation rate***, but might increase the detoxification capacity and anti-mutagenic properties in the colorectal mucosa through an increase in glutathione concentration. Whether this effect indeed contributes to a lower colon cancer risk remains to be established. Publication Types: Clinical Trial Randomized Controlled Trial PMID: 10971235 [PubMed - indexed for MEDLINE] Inhibition of human cancer cell growth and metastasis in nude mice by oral intake of modified citrus pectin. Nangia-Makker P, Hogan V, Honjo Y, Baccarini S, Tait L, Bresalier R, Raz A. Wayne State University, School of Medicine, and Department of Pathology, Karmanos Cancer Institute, Detroit, MI, USA. BACKGROUND: The role of dietary components in cancer progression and metastasis is an emerging field of clinical importance. Many stages of cancer progression involve carbohydrate-mediated recognition processes. We therefore studied the effects of high pH- and temperature-modified citrus pectin (MCP), a nondigestible, water- soluble polysaccharide fiber derived from citrus fruit that specifically inhibits the carbohydrate-binding protein galectin-3, on tumor growth and metastasis in vivo and on galectin-3-mediated functions in vitro. METHODS: In vivo tumor growth, angiogenesis, and metastasis were studied in athymic mice that had been fed with MCP in their drinking water and then injected orthotopically with human breast carcinoma cells (MDA-MB-435) into the mammary fat pad region or with human colon carcinoma cells (LSLiM6) into the cecum. Galectin- 3-mediated functions during tumor angiogenesis in vitro were studied by assessing the effect of MCP on capillary tube formation by human umbilical vein endothelial cells (HUVECs) in Matrigel. The effects of MCP on galectin-3-induced HUVEC chemotaxis and on HUVEC binding to MDA-MB-435 cells in vitro were studied using Boyden chamber and labeling assays, respectively. The data were analyzed by two-sided Student's t test or Fisher's protected least-significant-difference test. RESULTS: Tumor growth, angiogenesis, and spontaneous metastasis in vivo were statistically significantly reduced in mice fed MCP. In vitro, MCP inhibited HUVEC morphogenesis (capillary tube formation) in a dose-dependent manner. In vitro, MCP inhibited the binding of galectin-3 to HUVECs: At concentrations of 0.1% and 0.25%, MCP inhibited the binding of galectin-3 (10 micro g/mL) to HUVECs by 72.1% (P =.038) and 95.8% (P =.025), respectively, and at a concentration of 0.25% it inhibited the binding of galectin-3 (1 micro g/mL) to HUVECs by 100% (P =.032). MCP blocked chemotaxis of HUVECs toward galectin-3 in a dose-dependent manner, reducing it by 68% at 0.005% (P<.001) and inhibiting it completely at 0.1% (P<.001). Finally, MCP also inhibited adhesion of MDA-MB-435 cells, which express galectin-3, to HUVECs in a dose-dependent manner. CONCLUSIONS: MCP, given orally, inhibits carbohydrate-mediated tumor growth, angiogenesis, and metastasis in vivo, presumably via its effects on galectin-3 function. These data stress the importance of dietary carbohydrate compounds as agents for the prevention and/or treatment of cancer. PMID: 12488479 [PubMed - indexed for MEDLINE] > And the scientific evidence for your statements is............????? > > Quote Link to comment Share on other sites More sharing options...
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