The Durk Pearson & Sandy Shaw®
Life Extension NewsTM
Volume 17 No. 6 • July 2014


How Dietary Fiber Helps Prevent Colorectal Cancer
The Butyrate Connection

A new paper1 identifies colorectal cancer as the third most diagnosed cancer in both men and women in the U.S. and also as the third most deadly cancer. In an analysis of potential mechanisms to explain the protective effects of dietary fiber against colorectal cancer, the author discusses the effects of short chain fatty acids,A especially butyrate, produced via fermentation of dietary fiber by gut bacteria.

In the gastrointestinal tract, low to moderate concentrations of butyrate released by gut microbes in the metabolism of dietary fiber acts as the preferred food source for normal colonocytes (colon cells), where it is metabolized (like other fatty acids) by beta oxidation in mitochondria. The author says that butyrate is selectively taken up by colonocytes and provides approximately 70% of their energy. Glucose is the preferred food for cancerous colon cells, however, as a result of their obtaining their energy via glycolysis (the Warburg Effect) while decreasing oxidative metabolism in mitochondria. At the high concentrations of butyrate found in the lower digestive tract, when there is too much butyrate for the colonocytes to metabolize, butyrate enters the cell nucleus where it acts as a histone deacetylase inhibitor, which inhibits cell division. For this reason, butyrate is often considered a candidate “tumor suppressor metabolite.”1 Because butyrate metabolism is decreased in colorectal cancer cells, it accumulates in the nucleus, and acts there as a histone deacetylase inhibitor, decreasing cell division.

Interestingly, the author notes that butyrate enemas “strongly ameliorate colonic inflammation associated with [ ] inflammatory bowel diseases (IBD) in both rodent models and human patients.”1 Now, there is an interesting suggestion—butyrate enemas! You can get a similar effect, however, by increasing your intake of fermentable dietary fibers such as the long chain inulin oligofructose (as is found in our hydrogen-producing formulation). Not quite as sexy as an enema, but a heck of a lot less messy. One of the major dietary changes in the human diet has been a reduction in the intake of fermentable fiber and the change in the gut microbiota that results from that. Your health has a lot to do with the proper feeding of the gut microbes that ferment dietary fiber, so don’t forget you aren’t eating for just one but for literally trillions!

Not discussed in this paper is the possibility that hydrogen produced in the gut by bacterial fermentation of certain types of dietary fiber could also be protecting against the development of colorectal cancer.3

Butyrate Binds to the Niacin Receptor

The paper mentions that butyrate binds to a receptor that niacin is known to bind to, GPR109A, a G protein coupled receptor that is highly expressed on the apical membrane of colonic epithelial cells.1 GPR109A is said to be silenced in human colorectal cancers, a mouse model of colorectal cancer, and colorectal cancer cell lines.1 It is also interesting to note, though not mentioned in the paper, that GPR109A is “the” niacin receptor.2

More on Butyrate


A. Tarini and Wolever. The fermentable fibre inulin increases postprandial serum short-chain fatty acids and reduces free fatty acids and ghrelin in healthy subjects. Appl Physiol Nutr Metab. 35:9-16 (2010).
1. Bultman. Molecular pathways: gene-environment interactions regulating dietary fiber induction of proliferation and apoptosis via butyrate for cancer prevention. Clin Cancer Res. 20(4):799-803 (2013).
2. Thangaraju et al. GPR109A is a G-protein-coupled receptor for the bacterial fermentation product butyrate and functions as a tumor suppressor in colon. Cancer Res. 69(7):2826-32 (2009).
3. Ohsawa et al. Hydrogen acts as a therapeutic antioxidant by selectively reducing cytotoxic oxygen radicals. Nat Med. 13(6):688-94 (2007).

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