Can Mounjaro Reduce Sleep Apnea? What Two Clinical Trials Found

Obstructive sleep apnea and obesity are closely connected. Excess body weight, particularly fat deposited around the neck and upper airway, contributes directly to the airway collapse that characterises sleep apnea. CPAP therapy relieves the symptoms each night. It does not address the underlying cause.

Until recently there was limited high-quality evidence that weight loss medications could meaningfully reduce sleep apnea severity, not just body weight. Two phase 3 randomised controlled trials changed that picture.

What the SURMOUNT-OSA trials found

The SURMOUNT-OSA programme comprised two parallel phase 3 double-blind randomised controlled trials, published in June 2024 in the New England Journal of Medicine (Malhotra A et al., N Engl J Med, 2024;391(13):1193-1205).

Both trials enrolled adults with moderate-to-severe obstructive sleep apnea and obesity (mean BMI approximately 39). Trial 1 enrolled participants not receiving positive airway pressure (PAP) therapy at baseline. Trial 2 enrolled participants already on PAP therapy. Participants were randomised to the maximum tolerated dose of tirzepatide (10 mg or 15 mg) or placebo for 52 weeks.

The primary endpoint was change in the apnea-hypopnea index (AHI), the number of breathing pauses per hour of sleep. A higher AHI means more disrupted breathing.

Trial	Baseline AHI (mean)	Tirzepatide change	Placebo change	Difference (p-value)
Trial 1 (no PAP)	51.5 events/hr	-25.3 events/hr	-5.3 events/hr	-20.0 events/hr (p<0.001)
Trial 2 (on PAP)	49.5 events/hr	-29.3 events/hr	-5.5 events/hr	-23.8 events/hr (p<0.001)

An AHI of 51 events per hour is classified as severe obstructive sleep apnea. After 52 weeks of tirzepatide in Trial 1, the average AHI fell to approximately 26 events per hour, which corresponds to moderate severity. In Trial 2, the reduction was larger still. Both outcomes were statistically significant with a very low probability of being due to chance.

All prespecified secondary endpoints also improved significantly with tirzepatide: body weight, hypoxic burden (the amount of time spent with low blood oxygen), high-sensitivity C-reactive protein (a marker of inflammation), systolic blood pressure, and patient-reported sleep quality and daytime impairment.

Why an AHI reduction from severe to moderate matters

Sleep apnea severity is classified by AHI: fewer than 5 events per hour is normal, 5 to 14 is mild, 15 to 29 is moderate, and 30 or more is severe. Moving from severe to moderate does not mean the condition is resolved. It does mean fewer hypoxic episodes, lower cardiovascular load, and often meaningful improvements in sleep quality and daytime energy.

The cardiovascular significance is not trivial. Severe untreated sleep apnea is associated with increased risk of hypertension, atrial fibrillation, and adverse cardiac events. The reduction in hypoxic burden observed in SURMOUNT-OSA, alongside reductions in CRP and blood pressure, suggests the effect extends beyond the AHI number.

It is also worth noting that the trials ran for 52 weeks. They cannot tell us what happens over five or ten years, or whether the AHI reduction persists if tirzepatide is stopped. Weight regain after discontinuing GLP-1 therapy is well-documented, and the underlying mechanism of sleep apnea relief here is weight loss. If weight returns, it would be reasonable to expect some return of sleep apnea severity.

The mechanism: why weight loss helps sleep apnea

The upper airway is surrounded by soft tissue. In people with obesity, fat deposits around the pharynx and tongue can reduce the internal diameter of the airway and increase its tendency to collapse under the reduced pressure of inhalation during sleep. This is why obesity is the single most modifiable risk factor for obstructive sleep apnea, ahead of age and sex.

Weight loss reduces these fat deposits and improves the mechanical properties of the upper airway. It also reduces the inflammatory burden associated with excess adiposity, which may independently affect airway tone. The improvements in CRP and blood pressure seen in SURMOUNT-OSA are consistent with this systemic picture: tirzepatide appears to have addressed the obesity that was driving multiple downstream problems simultaneously.

What this means in an EU and Estonian context

In Europe, tirzepatide is marketed as Mounjaro and is approved for the treatment of type 2 diabetes and, more recently, for obesity in adults with a BMI of 30 or above (or 27 or above with weight-related comorbidities). It does not carry a specific EU marketing authorisation for sleep apnea as a distinct indication. That designation exists only in the United States under a separate brand.

This matters for how to frame the SURMOUNT-OSA data practically: if you have obesity and obstructive sleep apnea and you start Mounjaro for weight management, the evidence suggests your sleep apnea severity is also likely to improve. This is a consequence of treating the underlying condition, not a separate treatment for the airway problem itself.

Patients using CPAP who lose significant weight on tirzepatide may eventually find they need CPAP less, or at a different pressure setting. This should be evaluated with a physician and, where relevant, with a sleep specialist. Changing or removing CPAP without re-assessment carries risk.

Who this is most relevant for

If you have been diagnosed with moderate or severe obstructive sleep apnea and are currently managing it with CPAP, and if obesity is a contributing factor, then GLP-1 treatment may offer an additional therapeutic benefit beyond weight loss. This is particularly relevant if you find CPAP tolerable but have not yet achieved significant weight reduction through other means.

Sleep apnea is also frequently undiagnosed. Common presentations include snoring, observed pauses in breathing during sleep (often noticed by a partner), waking unrefreshed, morning headaches, and excessive daytime sleepiness. If these are present alongside obesity, assessment by a physician is warranted before starting any treatment programme.

Related reading: why visceral fat and liver fat matter during GLP-1 treatment, muscle preservation during weight loss, and planning a GLP-1 exit safely.

Frequently asked questions

Will Mounjaro cure my sleep apnea?

The SURMOUNT-OSA trials showed significant AHI reduction, but not elimination of sleep apnea in most participants. In Trial 1, the average AHI went from severe (51.5 events/hr) to moderate (approximately 26 events/hr) after 52 weeks. Whether an individual reaches the normal range depends on their baseline severity, how much weight they lose, and other anatomical factors. Some people with mild-to-moderate sleep apnea who lose significant weight may see their AHI normalise. Others will still need CPAP. This should be re-evaluated once weight loss is established.

Can I stop using CPAP if I start Mounjaro?

Not without clinical reassessment. CPAP removal or pressure adjustment based on weight loss should follow formal re-evaluation, ideally with a sleep study or home monitoring. Stopping CPAP prematurely based on subjective sleep improvement alone carries real risk of undetected residual apnea. If you are on Mounjaro and your weight has changed substantially, raise this with your prescribing physician.

I have not been diagnosed with sleep apnea, but I snore and feel tired. Should I be assessed?

Snoring, observed pauses in breathing, and unrefreshed sleep are the classic triad of obstructive sleep apnea. In the context of obesity, the likelihood of clinically significant OSA is high. Diagnosis requires a sleep study, which can now be done with home monitoring devices in many cases. An initial physician consultation is the right first step to determine whether this is relevant for you.

Sources

• Malhotra A et al., New England Journal of Medicine, 2024;391(13):1193-1205. SURMOUNT-OSA programme (two phase 3 RCTs, tirzepatide for obstructive sleep apnea and obesity). DOI: 10.1056/NEJMoa2404881