COVID-19 Survivors Face Elevated Sleep Apnea Risk for Up to 4.5 Years Post-Infection
Quick Facts
What Does the New Study Show About COVID and Sleep Apnea?
A study reported in early 2026 analyzed a large dataset of electronic health records from Americans who had documented COVID-19 infections. Researchers compared the rate of new obstructive sleep apnea diagnoses in COVID survivors against matched control groups who had not been infected with SARS-CoV-2. This type of retrospective cohort analysis is consistent with methods used in prior post-COVID research, including large Veterans Affairs studies published in Nature Medicine.
The findings indicated that COVID-19 survivors had a substantially higher incidence of new OSA diagnoses that persisted for years following their initial infection. The elevated risk was observed across different age groups and demographics, though certain populations appeared to be more vulnerable. Women who had COVID-19 may show a particularly pronounced increase in OSA risk compared to men, a finding that aligns with emerging evidence that some post-COVID conditions disproportionately affect women.
These findings add to the growing understanding that SARS-CoV-2 can cause lasting changes to multiple organ systems, including the respiratory tract, cardiovascular system, and nervous system. Obstructive sleep apnea occurs when the upper airway repeatedly collapses during sleep, causing intermittent breathing cessation. The condition affects an estimated 936 million adults worldwide, according to a 2019 analysis in The Lancet Respiratory Medicine, and is associated with increased risks of hypertension, cardiovascular disease, stroke, type 2 diabetes, and cognitive decline.
Why Might COVID-19 Increase Sleep Apnea Risk?
Several biological mechanisms may explain the connection between COVID-19 and subsequent sleep apnea development. SARS-CoV-2 infects cells via the ACE2 receptor, which is abundantly expressed in the upper airway, including the nasal passages, pharynx, and larynx. Infection can cause direct tissue damage and persistent inflammation in these structures, potentially weakening the muscles and soft tissues that keep the airway open during sleep.
Additionally, SARS-CoV-2 is known to affect the nervous system, including the brainstem regions that control breathing patterns during sleep. Post-infectious neuroinflammation and microglial activation in these critical areas could impair the neural drive to the upper airway dilator muscles (particularly the genioglossus muscle), reducing their ability to maintain airway patency during the reduced muscle tone that naturally occurs in sleep. This mechanism is analogous to the central sleep apnea that has been observed following other viral encephalitides.
Post-COVID weight gain may also play a contributing role. Many COVID-19 survivors report reduced physical activity and metabolic changes during and after their illness, leading to weight gain — one of the strongest risk factors for OSA. Furthermore, COVID-19-related fatigue and deconditioning can reduce exercise capacity, creating a cycle of inactivity and weight gain that further increases OSA risk. The interaction between direct viral effects on airway physiology and these behavioral and metabolic changes likely explains the sustained elevation in risk observed over several years.
What Should COVID Survivors Watch For?
Given the elevated risk, healthcare providers and COVID-19 survivors should maintain heightened awareness for symptoms suggestive of obstructive sleep apnea. Key warning signs include loud, persistent snoring (particularly snoring that is interrupted by silent pauses followed by gasping or choking sounds), excessive daytime sleepiness despite apparently adequate sleep duration, unrefreshing sleep, morning headaches, difficulty concentrating, and irritability.
Bed partners often notice the most dramatic symptoms — witnessed apneas (breathing cessation episodes during sleep) are among the strongest indicators for OSA. However, many individuals with OSA sleep alone or may not be aware of their symptoms, which is why screening questionnaires such as the STOP-BANG questionnaire are valuable tools. The STOP-BANG assesses risk factors including snoring, tiredness, observed apneas, blood pressure, BMI, age, neck circumference, and gender.
If OSA is suspected, the gold standard diagnostic test is polysomnography (an overnight sleep study), though home sleep apnea testing is increasingly used for straightforward cases. Treatment with continuous positive airway pressure (CPAP) therapy remains the first-line treatment for moderate to severe OSA and has been shown to reduce cardiovascular risk, improve daytime functioning, and enhance quality of life. For those who cannot tolerate CPAP, alternatives include oral appliances (mandibular advancement devices), positional therapy, and in selected cases, surgical interventions such as hypoglossal nerve stimulation.
Frequently Asked Questions
No, but COVID-19 survivors who develop symptoms such as loud snoring, daytime sleepiness, witnessed breathing pauses during sleep, or morning headaches should discuss sleep apnea screening with their healthcare provider. The risk is elevated but not everyone will develop OSA.
Current research suggests the risk remains elevated for several years after infection. Whether the risk eventually normalizes beyond this timeframe is not yet known and will require longer-term follow-up studies.
References
- Benjafield AV, et al. Estimation of the global prevalence and burden of obstructive sleep apnoea: a systematic review and meta-analysis. Lancet Respiratory Medicine. 2019;7(8):687-698.
- Xie Y, Xu E, Bowe B, Al-Aly Z. Long-term cardiovascular outcomes of COVID-19. Nature Medicine. 2022;28(3):583-590.
- Cade BE, et al. Associations of variants in the hexokinase 1 and interleukin 18 receptor accessory protein genes with oximetry-defined hypoxemia during sleep. PLOS Genetics. 2019.
- American Academy of Sleep Medicine. Clinical practice guideline for diagnostic testing for adult obstructive sleep apnea. Journal of Clinical Sleep Medicine. 2017;13(3):479-504.