New Gut Link Found in Sleep Apnea Heart Damage

Researchers have identified a new biological target that could one day lead to treatments preventing the serious heart damage caused by sleep apnea, and the discovery points not to the airway, but to the gut.

The study, conducted at the University of California, San Diego, and presented at ASM Microbe 2026 on June 6, found that mice without a specific bile acid receptor developed significantly fewer fatty arterial plaques under sleep apnea-like conditions than mice with the receptor intact. The findings were published by the American Society for Microbiology.

This matters because sleep apnea, a disorder in which breathing repeatedly stops during sleep, depriving the body of oxygen, affects hundreds of millions of people worldwide and is strongly linked to cardiovascular disease, including atherosclerosis, the buildup of fatty plaques in arteries that leads to heart attacks and strokes.

Current treatments, primarily CPAP machines, target airflow. This study is among the first to show that the gut microbiome and the bile acids it modifies may be a viable alternative point of intervention.

How the Gut Is Connected to a Sleeping Heart

When sleep apnea repeatedly cuts oxygen supply during sleep, the body’s chemical environment shifts. Prior research had shown that this oxygen disruption alters bile acid compounds produced by the liver, stored in the gallbladder, and released into the intestines to aid fat digestion.

Crucially, bile acids are not confined to the digestive system. They enter the bloodstream and bind to receptors throughout the body, acting as chemical messengers that affect physiology well beyond the gut.

The UCSD team focused on the farnesoid X receptor (FXR), one of the primary receptors activated by microbially modified bile acids. Their earlier work had suggested bile acids were central to regulating sleep apnea’s cardiovascular impact.

Study first author Celeste Allaband, DVM, explained the research logic: “We were pretty sure from our previous studies that bile acids, especially microbially modified ones, were a key to regulating the disease, so we wanted to know what happens when one of the key receptors for them is missing. Does the disease go away?”

What the Experiment Found and What Comes Next

The study used two groups of mice: those genetically prone to heart disease and those prone to heart disease but without the FXR receptor. Both groups were exposed to either normal sleep conditions or sleep apnea-like conditions.

The researchers tracked gut microbiome changes through fecal samples during the study and measured arterial plaques at the end. Mice without FXR showed significantly fewer fatty plaques in the aorta and aortic arch, the main arteries under sleep apnea conditions, and their gut microbiome was less disrupted. Some plaques remained in the pulmonary artery, indicating FXR is not the complete answer.

Allaband described the findings’ significance directly: “Our study shows that the FXR host receptor, which can be activated or deactivated by bile acids, plays a central role in driving the buildup of fatty plaques in the arteries during sleep apnea-like conditions.

Strikingly, when this receptor was removed from the mice, the development of arterial plaques dropped significantly in some areas, and disruptions to the gut microbiome were minimized.”

The team is now pursuing several follow-up directions, including checking human datasets for comparable trends and testing whether specific bile acid supplements or probiotic microbes can prevent arterial damage.

Allaband said: “We also plan to take some of our key bile acids of interest and see if supplementation of these compounds alone can help prevent or reduce disease. We may also take some key microbes of interest and see if they can be given preventively as a probiotic.”

Human trials are not yet underway as the research remains in its animal-study phase, and any clinical application remains years away.