At the University of California, San Diego, researchers have uncovered an unexpected way that gut microbes might protect people with sleep apnea from heart disease—by modifying bile acids to disarm a dangerous receptor called FXR. The discovery, presented at ASM Microbe 2026, offers hope to millions of people worldwide who suffer from obstructive sleep apnea and its life-threatening cardiovascular complications.
Sleep apnea is a common disorder where breathing repeatedly stops and starts during sleep, starving the body of oxygen and allowing carbon dioxide to build up. Over time, this oxygen deprivation triggers a cascade of damage throughout the body, including the formation of fatty plaques in the arteries—a condition called atherosclerosis that can lead to heart attack or stroke. For years, researchers knew that low oxygen altered bile acids, the chemical messengers produced by the liver that help digest fats. But the question remained: what role did these altered bile acids actually play in disease progression?
Celeste Allaband, DVM, Ph.D., and her team decided to investigate whether blocking one of the key bile acid receptors—the farnesoid X receptor, or FXR—could protect against sleep apnea's cardiovascular damage. They compared two groups of genetically modified mice prone to heart disease: one group with the FXR receptor intact, and another with the FXR receptor removed. Both groups were exposed to either normal air or conditions that mimicked sleep apnea, while researchers tracked changes in their gut microbes and measured fatty plaque buildup in their arteries.
The results were striking. When the FXR receptor was knocked out, mice showed significantly fewer fatty plaques in their aorta and aortic arch—the major vessels that carry blood from the heart. Even more encouraging, the disruptions to the gut microbiome caused by sleep apnea-like conditions were minimized in these mice. "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," Allaband explained. "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."
What makes this discovery particularly exciting is that it points to a specific, targetable pathway: the conversation between gut microbes, bile acids, and the FXR receptor. This opens several doors for future treatment. Allaband's team is already planning to examine human datasets to see whether similar patterns hold true in people. They're also exploring whether supplementing specific bile acids identified in the study might prevent disease progression, or whether certain beneficial microbes could be given as probiotics to protect at-risk patients.
The work fundamentally changes how we think about sleep apnea's health impact. Rather than viewing the condition as simply a breathing problem, researchers now see it as something that triggers a disruption in the gut's microbial ecosystem—a disruption that can be intercepted and potentially reversed. With hundreds of millions of people worldwide affected by sleep apnea, transforming how we understand and treat its complications could have profound public health implications.