Red Meat Contributes to Cardiovascular Disease (CVD) Risk Due to Gut Bacteria
the Renal and Urology News take:
Bacteria in the gut metabolizes red meat in a way that greatly increases the risk of cardiovascular disease (CVD), a new study in Cell Metabolism has found.
In a previous study conducted by Stanley Hazen, MD, PhD, of the Cleveland Clinic, he and his fellow researchers found that consumption of red meat promoted atherosclerosis. This is due to gut bacteria converting L-carnitine, a nutrient found in red meat, into trimethylamine.
Dr. Hazen’s team has now found that gamma-butyrobetaine, another metabolite generated through the consumption of red meat, is produced to at an even greater extent due to gut bacteria and contributes to atherosclerosis. Gamma-butrobetaine acts as an intermediary metabolite by microbes at a rate 1000-times greater than the formation of trimethylamine.
These findings suggest new targets for preventing atherosclerosis through the inhibition of these gut microbial pathways or the use of probiotics in shifting gut bacterial composition.
“The present studies may help us to develop an intervention that allows one to ‘have their steak and eat it too’ with less concern for developing heart disease,” Dr. Hazen stated.
Bacteria in the gut metabolizes red meat in a way that greatly increases the risk of CVD.
New research provides details on how gut bacteria turn a nutrient found in red meat into metabolites that increase the risk of developing heart disease. Publishing in the November 4th issue of the journal Cell Metabolism, the findings may lead to new strategies for safeguarding individuals' cardiovascular health.
Previous research led by Dr. Stanley Hazen, of Lerner Research Institute and the Miller Family Heart and Vascular Institute at Cleveland Clinic, revealed a pathway by which red meat can promote atherosclerosis, or hardening of the arteries. Essentially, bacteria in the gut convert L-carnitine, a nutrient abundant in red meat, into a compound called trimethylamine, which in turn changes to a metabolite named trimethylamine-N-oxide (TMAO), which promotes atherosclerosis.
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