My newest book, 'Gut Cure: Stop the Rot, Restore Your Body From the Inside Out,' puts the spotlight on the modern epidemic of invisible gut dysfunction, and offers you a roadmap to true restoration.
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.
Butyrate functions as a "Histone Deacetylase (HDAC) inhibitor," meaning it can actually silence inflammatory genes at a cellular level. In my opinion, Mercola’s "Seed Oil Swap" is a vital bio-hack; replacing unstable fats with ghee or coconut oil doesn't just lower inflammation, it creates the oxygen-free environment necessary for butyrate-producing bacteria to thrive and heal your internal lining.
hello ! I’m so excited to see you’re on substack. My mom just informed me that you post on here. Can wait to read :) #spreadingthetruth
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.
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).--
Thoughts on GoodBelly? https://goodbelly.com
Butyrate functions as a "Histone Deacetylase (HDAC) inhibitor," meaning it can actually silence inflammatory genes at a cellular level. In my opinion, Mercola’s "Seed Oil Swap" is a vital bio-hack; replacing unstable fats with ghee or coconut oil doesn't just lower inflammation, it creates the oxygen-free environment necessary for butyrate-producing bacteria to thrive and heal your internal lining.