Researchers here report a correlation that suggests age-related changes in gut bacterial populations may contribute to the development of atherosclerosis. This is a condition in which damaged lipids in the bloodstream produce an inflammatory overreaction in blood vessel walls. The macrophages that arrive to help clear up damage are overcome and die, producing more inflammation and cellular debris. Over years this grows into fatty plaques that narrow and weaken blood vessels, eventually resulting in catastrophic structural failure or blockage. How might bacteria in the gut contribute to this process? The most plausible mechanisms involve secretion of compounds that encourage chronic inflammation or oxidative stress, changing cell behavior in ways that drives the creation of more of the damaged lipids that spur atherosclerosis. While a range of evidence supports such a role for the compounds mentioned below, this is an area of research in which much remains to be conclusively proven.
Researchers have shown a novel relationship between the intestinal microbiome and atherosclerosis, one of the major causes of heart attack and stroke. This was measured as the burden of plaque in the carotid arteries. In order to understand the role that bacteria in the gut may play in atherosclerosis, the researchers examined blood levels of metabolic products of the intestinal microbiome. They studied a total of 316 people from three distinct groups of patients - those with about as much plaque as predicted by traditional risk factors, those who seem to be protected from atherosclerosis because they have high levels of traditional risk factors but normal arteries, and those with unexplained atherosclerosis who don't have any traditional risk factors but still have high levels of plaque burden.
"What we found was that patients with unexplained atherosclerosis had significantly higher blood levels of these toxic metabolites that are produced by the intestinal bacteria." The researchers looked specifically at the metabolites TMAO, p-cresyl sulfate, p-cresyl glucuronide, and phenylacetylglutamine, and measured the build-up of plaque in the arteries using carotid ultrasound. The study noted that these differences could not be explained by diet or kidney function, pointing to a difference in the make-up of their intestinal bacteria. "There is growing consensus in the microbiome field that function trumps taxonomy. In other words, bacterial communities are not defined so much by who is there, as by what they are doing and what products they are making."