Pardon me,     Server error makes me post here ....
Colon cancer runs in my family & 1st cousin succumbed in his early 40s; USA colon cancer affects +/- 2% of men and +/-1.5% women aged 50 - 70, with higher rates among African-americans. Cancer pathology does not follow lineal constructs, so I will be generalizing (again); colon cancer can be hereditary non-polyposis, familial adenomatous polyposis (polyps), flat adenoma or sporadic colorectal cancer.

Dietary fiber provides the environment for intestinal bacteria to make butyrate for us; and butyrate is beneficial when it produces hydrogen sulfide (H2S). In the large intestine (colon) epithelial cells this butyrate H2S induces a proton "leak" in that cell's mitochondrial electron transfer chain (that cell uses & needs  less oxygen); this uncoupling slows that cell's cycle so that there is less cell division, and simultaneously depresses cytochrome c oxidase 1 & 2 enzymes which prevents that mitochondria from signalling for apoptosis (death). The boost in colonocyte (cellular) H2S also raises that cell's level of the anti-oxidant glutathione; and fosters other beneficial mitochondrial  processes by opening the mitochondrial membrane's K-ATP channel.

Dietary derived H2S comes from sulfurous protein (ie: amino acids methionine, taurine, cysteine & cystine) metabolized by intestinal bacteria;  and more significantly this type of  dietary induced load of H2S depresses the beta-oxidation of butyrate in colonocytes. When it comes to the sexes it is women who more readily produce H2S from sulfurous protein, yet men will produce a higher total amount of H2S; which may indicate why both sexes have similar colon cancer rates.

Sulphur rich cruciferous vegetables (broccoli, cauliflower, brussel sprouts, cabbage & kale) are not high in sulfurous proteins;  metabolism of their sulphur favors a bit more sulphur uptake into local colon tissue than bacterial H2S pathways. Think of the slow steady butyrate H2S output in colonocytes as a pre-treatment; this pre-conditioning is hormetic (hormesis is how a little bit of something potentially dangerous, like H2S, can be good for you that some might phrase as "what doesn't kill you makes you stronger").


Cancer of the colon unfortunately can side-step the preventative action of butyrate H2S when one of the enzymes (cystathine Beta-synthase) butyrate uses to generate H2S gets knocked out. How or why this happens in an individual is not dealt with here; the point is that a certain level of reliable H2S from butyrate will hold down the viabilty of colon cancer cells. Once the colon cancer cell has shifted  it's pheno-type from epithelial pheno-type to mesencymal pheno-type the same cellular protective effects of H2S (see 2nd paragraph above) will then unfortunately help that cancer cell avoid dying (apoptosis).

In a petri dish H2S will kill some colon cancer cell lines; this works because those cancers are not interfacing with the colon's bacterial dynamic. The "nooks and crannys" of the intestinal crypts have 2 distinct mucus (mucin) made up from long chain carbohydrates (oligo-saccharides); the sialo-mucin is more to the surface and usually deals with microbes, while the sulfo-mucins are in the lower depths of the crypts. We individuals have different antigens that affect the rate at which we degrade the sialo-mucin; furthermore, there is a drop in the number of sialo-mucins when the transformation of colo-rectal cancer occurs. It should be noted that the density of sialo-mucin and sulfo-mucin has differences all along the length of the colon and rectum, with nuances related to gender and can shift their ratios at a site.

There are specific colon bacteria which utilize the sulfate they get from sulfo-mucin; sulfate reducing bacteria use it for their own "respiration" and put out H2S. Yet "normally" sulfate reducing bacteria  are apparently not mostly using the sulfate we add to the colon from our food (this may be because certain  sulfur bacteria varieties, like "normal" desulfovibrio, have a cellular program to interact readily with an oligo-saccharide property of sulfo-mucin in order to take up that sulfate). When there is a shift to depleted sialo-mucin and extra ordinary sulfo-mucin the colon sulfur bacteria population varieties also alters; and certain sulfate reducing bacterial varieties become enriched at the expense of other bacteria.

At which time the colon levels of  bacterial produced H2S can rise and, just like high dietary spin off H2S; this then will depress butyrate's output of H2S  in colonocytes (where any incipient colon cancer's epithelial pheno-type needs to be held in limbo). The natural anti-cancer slow release of H2S from butyrate is then an altered state of high level of H2S in the colon;  with not enough sialo-mucin in the upper portions of colon crypts epithelial cells deeper in the crypt are more vulnerable .

Furthermore, with the shift toward excessive sulfate reducing bacteria (ex: desulfobacter, desulfobolbus and desulfotomaculum as opposed to  "normal" desulfovibrio) , there is the possibility that some cancer cell lines will use that bacterial supplied H2S to more readily morph into their mesenchymal pheno-type. This would be due to H2S impairing certain coloncyte cell line's DNA repair so that there is then damage to the original genome. For details see Mol Cancer Res 2006;4(1):9-14 "Evidence that H2S is a Genotoxic Agent"  complete text at http://
mcr.aacrjournals.org/content/4/1/9.full

To Greensleeves  (Server blocking where belongs),
You might enjoy this all sourdough rye study "Structural diff. btwn. Rye & wheat ...lower post-prandial insulin ..." in 2003 Am J Clin Nutri; 78(5):957-964 full text http://www.ajcn.org/content/78/5/957.full

And 2009 "Endosperm & whole grain rye breads ... beneficial blood glucose profile" in Nutrition Journal 2009, 8:42 full text http://www.biomedcentral.com/content/pdf/1475-2891-8-42.pdf