Gut microbes associated with CV risk

You'll have to have your doctor explain this one to you and provide intervention protocols.

Gut microbes associated with CV risk

“Our largest environmental exposure is what we eat, and that is all perceived through the filter of our gut microbiome,” Stanley L. Hazen, MD, PhD, chair of the department of cellular and molecular medicine, section head of preventive cardiology and rehabilitation and director of the Center for Microbiome and Human Health at Cleveland Clinic, said in the presentation. “The gut microbiome is an active participant in many facets of cardiovascular disease and thrombosis.”

The initial discovery and structural identification of gut microbe-derived metabolites that are associated with CVD risk occurred nearly a decade ago with untargeted metabolomics, according to the presentation. Data from healthy patients were reviewed for the development of CVD over a period of time. Patients’ serum levels were analyzed for the chemical signatures that predicted future CVD risk, and of the metabolites that predicted risks, a third of them are linked to gut microbes, Hazen said.

A study published in Nature in 2011 found that three compounds linked to phosphatidylcholine metabolism, also termed lecithin, suggested a common pathway: choline, betaine and trimethylamine N-oxide (TMAO).

Diet and intestinal microbes are mechanically linked to atherosclerotic heart disease. A diet rich in phosphatidylcholine, a Western diet, also feeds the gut microbes. The microbes generate trimethylamine (TMA) as a waste product of dietary lecithin. After the TMA leaves the gut, it goes into the liver where it is converted to TMAO. In animal studies, TMAO accelerated heart disease development.

The clinical relevance of this was validated in a study published in Nature in 2011, which found that choline, betaine and TMAO dose-dependently track CV events. Beyond association, the study proved causation because a diet rich in choline led to TMAO generation and accelerated atherosclerosis, Hazen said.

“The relationship between plasma TMAO levels and incident CVD and mortality risks in subjects is a steeper curve than what you see with LDL cholesterol, triglycerides or C-reactive protein, for example,” Hazen said.

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