Obstructive Sleep Apnea Speeds Up Aging, But Treatment Reverses It

New research implicates obstructive sleep apnea (OSA) as a driver of accelerated aging, but the same research also shows that treating the sleep disorder can ameliorate the problem.

A study, published in the European Respiratory Journal, could have significant implications for scientists’ understanding of OSA, as well as its common comorbidities.

OSA has already been associated with a higher risk of several life-threatening conditions, including hypertension, stroke and diabetes. However, a team of researchers from the University of Missouri School of Medicine and Spain’s Miguel Servet University Hospital wondered whether OSA might be doing more than increasing the risk of particular conditions; they wanted to know if it was actually speeding up the body’s aging process.

Age acceleration is a term for when a person’s biology suggests they are further along in the aging process than their actual age would indicate. “Biological age” is an algorithm-based calculation determined by analyzing the DNA in a person’s blood sample. Those whose “biological” age exceeds their chronological age are considered to have epigenetic age acceleration. People with age acceleration have been shown to be at higher risk for a number of chronic conditions, and at a higher risk of mortality in general.

Rene Cortese

Rene Cortese, Ph.D., an assistant professor at the University of Missouri School of Medicine, told Managed Healthcare Executive®that he and his colleagues had already linked OSA with activation and propagation of oxidative stress and systemic inflammatory pathways. Since both of those factors have also been linked with age acceleration, the investigators suspected that patients with OSA would be more likely to have age acceleration.

The team recruited 16 adults with OSA as well as eight adult control subjects without OSA. The subjects were all non-smokers. Each of the 24 participants was given a blood test at baseline, followed by a second blood test one year later. In addition, patients with OSA were asked to use continuous positive airway pressure (CPAP) therapy following the baseline test.

As expected, the data showed that patients with OSA were at higher risk of epigenetic aging.

However, the follow-up analysis showed patients who adhered to the CPAP regimen (using it for at least 4 hours per night) were able to “decelerate” their epigenetic aging. Those who did not adhere to the treatment had no change in their aging trends.

Cortese said he was struck by the swiftness of the reversal. “Although it was within our expectations, the fact that deceleration of epigenetic age was so evident after one year of adherent CPAP treatment was very striking,” he said.

The study adds new layers to the complex interplay between aging, OSA and comorbid conditions. Cortese noted that biological aging is the natural deterioration of physiological processes, and brings with it increased risk of morbidity and mortality. OSA can affect virtually all organ systems, he said, and so it is possible that OSA therapy might also reverse the risk of specific related morbidities, in addition to throttling epigenetic age acceleration.

Though the study was conducted in adults, Cortese said it also opens up potentially meaningful questions about the impacts of pediatric OSA and the efficacy of current treatment protocols.

In children, OSA is considered a risk factor for cardiovascular morbidity and neurocognitive and behavioral dysfunction. The most important determinant of the sleep disorder is enlarged tonsils and adenoids, he said, because they result in a narrowing of the upper airway. For most patients, surgical removal of their tonsils and adenoids is the initial treatment option, yet Cortese said many children continue to have OSA symptoms even after surgery, albeit with milder symptoms. He said his study sheds light on the potential long-term implications of failing to fully address pediatric OSA.

“Our study opens a new research line in the effects of treatment in OSA-associated epigenetic age acceleration,” he said, “hence further research to determine the extent and mechanisms of epigenetic age acceleration in pediatric OSA and its associated morbidities is warranted.”