The fat molecules in the plaques that clog up our arteries and raise risk of heart attack and stroke may come from bacteria that live in our mouths and guts, not just from what we eat.
This was the main result of a study led by the University of Connecticut in Storrs that was published recently in the Journal of Lipid Research.
The researchers suggest that the finding may explain why gum disease is often linked to atherosclerosis – a
As the plaques build up, they harden and narrow the arteries, restricting the flow of oxygen-carrying blood to vital organs and tissues. This can lead to heart attack, stroke, other serious health problems, and even death.
The immune system also plays a role: immune cells can attach to the lining of blood vessels, feed on the fatty deposits, and multiply. This results in inflammation and thickening of the smooth muscle in the artery wall, which helps the formation of plaques and other growths known as atheromas.
Atherosclerosis can affect arteries that supply oxygen-rich blood to the heart, brain, kidneys, limbs, pelvis, and other parts of the body. This gives rise to various diseases, depending on which arteries are affected.
It was assumed that the fatty molecules, or lipids, that contribute to atherosclerosis came from eating foods high in fat and cholesterol, such as butter, eggs, meat, and fatty fish.
However, there is increasing evidence that this may not be the case – or at least not the whole story. There are groups of people who, despite eating foods rich in fat and cholesterol, do not develop heart disease.
For the new study, the team analyzed atheromas collected from patients being treated in hospital.
They found that the growths contained chemical signatures of lipids that could not have come from animals. Instead, they matched the signature of fat molecules made by bacteria belonging to the Bacteroidetes family.
Bacteroidetes make fats that are quite distinct in that the fatty acids that they contain have branched chains and an odd number of carbon atoms. Fatty acids in fats that come from animals do not typically have these features.
One of the researchers, Xudong Yao, associate professor of chemistry at the University of Connecticut, explains that if you compare the chemical makeup of human lipids with lipids produced by bacteria, they show subtle differences in weight.
“We used these weight differences and modern mass spectrometers to selectively measure the quantity of the bacterial lipids in human samples to link the lipids to atherosclerosis,” he notes.
“Establishment of such a link is a first step to mark the lipids as indicators for early disease diagnosis.”
Prof. Xudong Yao
The team suggests that perhaps the immune system triggers inflammation because when it encounters the fatty deposits in the artery walls, it recognizes that the lipids are not of human origin.
The researchers also found that there is an enzyme that breaks down the bacterial lipids into starting materials for making molecules that promote inflammation.
They suggest, therefore, that the presence of bacterial lipids has a “double whammy” effect on the arteries. First, the immune system spots them and sets off alarm signals, and secondly, the enzyme breaks them down into materials that assist inflammation.
The researchers also point out that it is not the bacteria themselves that are invading the blood vessels and causing problems.
Bacteroidetes, which colonize the mouth and gut, do not usually cause harm. Under certain conditions, they can give rise to gum disease; and, even then, they still do not invade the blood vessels. However, the lipids that they secrete can get through cell walls and into the bloodstream.
The team now plans to carry out a more detailed analysis of atheromas to find out exactly where the Bacteroidetes lipids accumulate.
If they discover that lipids from these specific bacteria are building up inside atheromas as opposed to the artery wall, then that would provide more convincing evidence that fat molecules from Bacteroidetes are linked to atheroma growth, and thus to heart disease.