3 Comments
User's avatar
Guillermou's avatar

Increased dietary fiber intake has been associated with many beneficial effects, including improvements in obesity, insulin resistance, and cancer. Under normal conditions, carbohydrate fermentation maintains the stability of the gut microbiota; however, in chronic diseases, microbiota diversity decreases, and the metabolic pathway shifts from carbohydrate to protein fermentation, thus inhibiting butyrate production. Polysaccharides and proteins play a key role in regulating butyrate synthesis. As fermentable carbon sources, polysaccharides promote probiotic proliferation, reduce colonic pH, and inhibit anaerobic protein fermentation. However, excessive protein fermentation produces branched-chain fatty acids (BCFAs), ammonia, phenols, and other metabolites that inhibit butyrate production.

These effects may be due to the increased production of short-chain fatty acids, including propionate, acetate, and butyrate, during the fermentation of dietary fiber in the colon. In fact, oral and dietary butyrate supplementation alone has been shown to prevent obesity and insulin resistance induced by a high-fat diet. This review focuses on sources of short-chain fatty acids, with an emphasis on butyrate sources, the mechanisms of fiber and butyrate metabolism in the gut, their protective effects against colon cancer, and the peripheral effects of butyrate supplementation in peripheral tissues on the prevention and reversal of cancer, obesity, and insulin resistance. It should also be noted that bovine milk fat is a particularly rich source of butyrate, contributing approximately 4% by weight. Human breast milk has also been examined as a potential source of butyrate for newborns and as a modulator of the colonic microbiota. Recent pyrosequencing experiments have identified butyrogenic bacteria in human breast milk that may facilitate colonization of the neonatal colon.

Although numerous bacterial strains have been analyzed for their butyrate-producing capacity, Faecalibacterium prausnitzii and Eubacterium rectale/Roseburia have recently received the most attention, as they constitute 5% to 10% of the total bacteria in fecal samples collected from healthy adults. In addition to colon colonization by butyrogenic bacteria, it has been proposed that cross-feeding interactions between bifidobacterial strains and F. prausnitzii may ultimately enhance butyrate production. Butyrate is known to promote colonic epithelial growth but exerts a predominantly inhibitory effect on colorectal cancers.

Emerging evidence suggests that the paradoxical effects of butyrate can be explained by the Warburg effect observed in various types of cancer. Butyrate is not only responsible for the energy requirements of the colonic epithelium, but it also preserves these tissues by mitigating chronic inflammatory responses. Treatments with butyrate, or those that increase butyrate production, such as increased dietary fiber or bacterial colonization in the gut, have also been shown to prevent or attenuate obesity and insulin resistance. In addition to its preventive effects on body weight and adiposity, butyrate supplementation has also been associated with mitigating insulin resistance. Butyrate may regulate lipid metabolism in the liver and intestine, and several findings have demonstrated that it exerts beneficial effects on liver diseases. It is capable of downregulating the expression of nine key genes involved in the intestinal cholesterol biosynthesis pathway and, therefore, may inhibit hypercholesterolemia. Butyrate administration improves HFD-induced hepatic steatosis in mice by reducing intrahepatic lipid accumulation (triglyceride and phospholipid content) and liver weight. In-depth mechanistic research focused on the liver has shown that hepatic mitochondria are the primary target of butyrate's beneficial effect in reversing fat accumulation in diet-induced obesity. Islets are known to express the butyrate receptors GPR41 and 43, suggesting that butyrate may be involved in islet cell metabolism and function, as evidenced by the effects of butyrate pre-incubation on improving diabetes-induced islet histological alteration and functional damage. Butyrate is also capable of stimulating GLP-1 release from intestinal L cells. GLP-1 has the ability to reduce apoptosis and induce neogenesis and regeneration of pancreatic β cells, as well as induce insulin synthesis and secretion.

Isobutyrate is less readily absorbed and metabolized compared to butyrate, but it can act as an alternative energy source when butyrate levels are low or when butyrate oxidation is abnormal.

Butyrate also exerts dose-dependent effects on HCT-116 colorectal cancer cells, significantly reducing viability, cell proliferation, and confluence at certain concentrations. It induces apoptosis and cell cycle arrest by overexpressing pro-apoptotic genes and underexpressing anti-apoptotic and proliferative markers.

Acetate, propionate, and butyrate are the three main SCFAs, and their bioactivities have been extensively studied. SCFAs have many health benefits, including anti-inflammatory, immunoregulatory, anti-obesity, anti-diabetic, anti-cancer, cardiovascular, hepatoprotective, and neuroprotective activities.

https://www.mdpi.com/2072-6643/9/12/1348 (2017).---

https://www.mdpi.com/1420-3049/26/3/682/htm (2021).---

https://www.sciencedirect.com/science/article/abs/pii/S1043276020302526 (2021).--

https://lipidworld.biomedcentral.com/articles/10.1186/s12944-021-01491-z (2021).--

https://onlinelibrary.wiley.com/doi/full/10.1111/obr.13498 (2022).--

https://www.mdpi.com/2304-8158/11/18/2863 (2022).--

https://royalsocietypublishing.org/doi/full/10.1098/rsob.230014 (2023).--

https://www.frontiersin.org/journals/oncology/articles/10.3389/fonc.2023.1110235/full (2023).--

https://onlinelibrary.wiley.com/doi/abs/10.1002/mnfr.202400421 (2024).--

https://www.spandidos-publications.com/ijo/64/4/44 (2024).---

https://pmc.ncbi.nlm.nih.gov/articles/PMC12162265/ (2025).—

https://pmc.ncbi.nlm.nih.gov/articles/PMC11766496/ (2025).—

https://www.mdpi.com/2304-8158/14/21/3649 (2025).--

Lewis S. Coleman, MD's avatar

Dear Dr. Mercola,

I am forwarding this weblink to you because I believe you will find it interesting: https://substack.com/home/post/p-192289427

Be sure to watch the video interview of Dr. Yeadon, and then read the text in its entirety. I agree with his point that people shouldn’t be taking any drug on a daily basis. That invites long term effects and drug-drug interactions.

There’s massive confusion flying everywhere, and I have no doubt that Big Pharma is promoting it any way it can. The more confusion, the better, because it will defray and mulct attention on its criminal activities. They are using every trick in the book---and there’s no shortage of their dirty tricks----to defray attention from their role in causing the COVID contagion and its deadly fake immunizations. They are understandably trying to defray public attention from their pivotal role in COVID mass murder.

Note that the interview with Dr. Yeaden confers the impression that ivermectin will destroy fertility, but the text notes that there’s no evidence that supports that recommended doses of Ivermectin are dangerous. Yeaden was evidently looking at evidence based on gigantic overdoses. I’ve see the drug companies employ this dirty trick before. The most blatant example was when they tarred and feathered an excellent drug called Droperidol that provided anti-nausea and sedative effects in small doses, and didn’t synergize the respiratory depression of narcotics in the manner of other hypnotic agents. Droperidol was used almost universally to prevent postoperative nausea and vomiting, but its patent could no longer be maintained, and the drug companies wanted everyone to switch to odansetron, so that had the FDA declare a “black box warning” for droperidol that employed massive overdoses in animal studies to produce abnormal EKG patterns. Nowadays everybody is still using odansetron, and they still haven’t allowed the production of droperidol.

What I found in my anesthesia practice is that large doses of modern synthetic narcotics prevent harmful nociception which causes bowel ischemia that manifests as postoperative “bowel ileus” (the bowel literally quits working for a couple of days) and nausea. Small, inadequate narcotics dosage fails to control surgical nociception effectively and thereby gets blamed for causing it. I used generous narcotic dosage combined with hypercarbia that synergistically promoted bowel perfusion and oxygenation, and the results were excellent except when patients swallowed large quantities of blood during dental cases. You can’t do much to help that until the patient vomits the blood from his stomach.

Lewis S. Coleman, MD

Science Advisor, American Institute of Stress

www.stressmechanism.com

Just steve's avatar

Might be just me but the many kinds of probiotic products over the years made such a difference to improve one time gut issues. With more being realized, more research is showing those products are likely to be able to have even stronger results by firming up their foundation provided by the Butyrate, and the proper fiber to maintain it. This would allow the others to follow to fully express their full range of Health Building, Dis-Ease Prevention. Similar to applying Volcanic Ash to depleted soils allow the soils to feed the soil life to feed the plants in ways the plants can fully express their possible potential.

Being as the American diet is so loaded with Probiotic Gut Busters, Glyphosate, Plastics, Pest and other Ag Chemicals not only disrupting and destroying our guts, but also the Gut of the Soils. As those of us pursuing Biodynamic Regenerative Sustainable Methods progress, learn a larger range of practices, it is likely we can expand the range of life building microbes in our soils and foods. We are likely to see how fibers long lost in our being civilized to death can improve the range of microbes and how they keep in balance, if and when they are allowed to be.