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Dr. Mercola's Censored Library (Private Membership)

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Just steve's avatar
Just steve
Jan 15Edited

A healthy gut keeps junk from invading our bodies, allows a proper process so as to supply the necessary, needed nutrients to be delivered to and where they are needed and used. A Leaky Gut, a condition fueled by numerous offenders. Glyphosate comes to mind as it binds up critical minerals so our health building microbe communities can not process properly, lose the ability to maintain a proper population, or even die off in some cases. It is also considered an antibiotic. Leading to, the over use of antibiotics in livestock to get shared in our guts and causes indiscriminate loss of needed microbe populations. All kinds of meds providing the same, some could be considered as Direct Deposits bypassing the Gut altogether, but we won't mention any names being as there is a massive PR Campaign desperately hanging on to the old narrative Safe and Effective.

If fortunate enough to find actual good solid foods supporting the Gut so the in turn the Gut supports us, the difference in over all well being, health outcomes speaks for itself. Should we succeed in building healthy food production, proper diet, perhaps our country could return to the 5 to 7% of the population suffering Chronic Dis-Ease's of the fifties, instead of in the 70% + numbers of today. A possible massive increase in our Health Wealth, Social Wealth, Foundational Wealth Sources that make Material/Financial Wealth actually worth something.

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Guillermou's avatar
Guillermou
Jan 15

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, such as anti-inflammatory, immunoregulatory, anti-obesity, anti-diabetic, anti-cancer, cardiovascular protective, hepatoprotective, and neuroprotective activities.

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