Ketogenic Diet Alters Gut Microbiome Leading to Reduced Levels of Proinflammatory T Cells
June 02, 2020 | Biotechnology
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The results of a small-scale study in human volunteers have shown how specifically low-carb, high-fat ketogenic diets (KDs)—which are widely publicized for their purported health and weight loss-promoting benefits—have a dramatic impact on the gut microbiome that differs to that of high-fat diets (HFDs). Additional studies in mice by the same University of California, San Francisco (UCSF)-led research team demonstrated that ketone bodies, which are a molecular byproduct that gives the ketogenic diet its name, directly change levels of certain types of gut bacteria, which led to reduced levels of intestinal pro-inflammatory immune cells. They suggest the results provide initial evidence for the potential benefits of ketone bodies as a therapy for autoimmune disorders affecting the gut.
“This is a really fascinating finding because it suggests that the effects of ketogenic diets on the microbiome are not just about the diet itself, but how the diet alters the body’s metabolism, which then has downstream effects on the microbiome,” said Peter Turnbaugh, PhD, a UCSF associate professor of microbiology and immunology, member of the UCSF Benioff Center for Microbiome Medicine, and a Chan Zuckerberg Biohub investigator. “For many people, maintaining a strict low-carbohydrate or ketogenic diet is extremely challenging, but if future studies find that there are health benefits from the microbial shifts caused by ketone bodies themselves, that could make for a much more palatable therapeutic approach.”
Turnbaugh and colleagues report on their studies in Cell, in a paper titled, “Ketogenic Diets Alter the Gut Microbiome Resulting in Decreased Intestinal Th17 Cells.”
A ketogenic diet involves dramatically reducing carbohydrate consumption in order to force the body to alter its metabolism to using fat molecules rather than carbohydrates as its prim... Want to read more? Find the entire article in the GEN Blog.
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