Several common medication classes can cause or worsen sleep apnea by suppressing breathing drive, relaxing airway muscles, or changing body composition in ways that narrow the throat. Opioids and benzodiazepines carry the strongest and most consistent signals, but testosterone therapy, certain muscle relaxants, and long-term corticosteroids can also play a role. If you’re on any of these and experiencing new or worsening snoring, gasping during sleep, or daytime fatigue, the medication may be contributing.
Opioids: The Strongest Link
Opioid painkillers are the medication class most clearly tied to sleep apnea, particularly central sleep apnea, the type where the brain temporarily stops sending signals to breathe. Opioids act on receptors in a part of the brainstem that generates your breathing rhythm. This dulls the body’s normal response to rising carbon dioxide and falling oxygen levels, which are the two main signals that keep you breathing steadily during sleep.
Opioids also suppress reflexes in the upper airway, making the throat more likely to collapse and obstruct airflow. The effect is dose-dependent: patients taking daily doses above 200 morphine milligram equivalents (a standardized measure used to compare different opioid medications) show severe central sleep apnea and irregular, chaotic breathing patterns during sleep. But even moderate doses can shift the balance, especially in people who already have some degree of airway narrowing.
This applies to both short-acting opioids (like oxycodone or hydrocodone) and long-acting formulations (like methadone or extended-release morphine). The risk is highest during the first hours after a dose, when blood levels peak.
Benzodiazepines and Muscle Relaxants
Benzodiazepines, prescribed for anxiety, insomnia, and seizures, are the second most consistently implicated drug class. A large signal-detection study analyzing adverse drug reaction reports found that opioids, benzodiazepines, and muscle-relaxing agents all showed a significant association with the onset or worsening of sleep apnea.
The mechanism is somewhat different from opioids. Benzodiazepines primarily reduce the arousal response, meaning your brain is less likely to wake you up when your airway closes. They also relax muscles throughout the body, including those that help keep the throat open. The combination makes apnea events last longer and oxygen levels drop further, even if the total number of events doesn’t change dramatically.
Interestingly, Z-drugs (zolpidem, zopiclone, and similar non-benzodiazepine sleep aids) did not show the same association with sleep apnea in the same analysis. One study specifically tested zolpidem, zopiclone, and the benzodiazepine temazepam at standard doses and found that none of them changed the passive collapsibility of the upper airway during sleep. Zolpidem actually increased the tongue muscle’s responsiveness to airway narrowing, a potentially protective effect. This doesn’t mean Z-drugs are risk-free, but the evidence suggests they’re a meaningfully different category from traditional benzodiazepines when it comes to sleep-disordered breathing.
Testosterone Replacement Therapy
Testosterone replacement therapy (TRT) can worsen obstructive sleep apnea, particularly in the early weeks of treatment. In one study, testosterone administration worsened the oxygen desaturation index (a measure of how often blood oxygen drops during sleep) by about 10 additional events per hour at seven weeks, along with increased time spent in a state of low oxygen overnight. By 18 weeks, however, these effects had largely resolved compared to placebo.
Short-term, high-dose testosterone appears to carry the most risk. One trial found that treatment at doses producing high peak blood levels reduced total sleep time by about an hour per night and increased the duration of nighttime oxygen desaturation by roughly five minutes per night. The exact mechanism isn’t fully mapped, but testosterone is thought to affect breathing control during sleep and may alter upper airway anatomy through fluid shifts or tissue changes. Long-term therapy at lower, more physiologic doses may eventually improve symptoms, possibly by reducing obesity and related metabolic factors that contribute to apnea in the first place.
Corticosteroids and Airway Changes
Long-term corticosteroid use, whether systemic (prednisone, dexamethasone) or inhaled, can contribute to sleep apnea through several overlapping mechanisms. Corticosteroids promote fat deposition around the neck and pharynx, narrowing the space available for airflow. They can cause swelling (edema) in the walls of the upper airway, further reducing the opening. They may also weaken the muscles that actively hold the airway open during sleep, a condition sometimes called corticosteroid myopathy, reducing the force these muscles can generate.
Even inhaled corticosteroids, commonly prescribed for asthma and COPD, have been investigated as a potential risk factor. The local effects on the upper airway tissue, including swelling and changes in muscle function, may alter the pressure at which the airway collapses during sleep. This is especially relevant for people already on the borderline of obstruction due to anatomy or weight.
Antidepressants: A More Complex Picture
Antidepressants have a complicated relationship with sleep apnea. SSRIs like fluoxetine, paroxetine, citalopram, and sertraline all suppress REM sleep to varying degrees. Since obstructive sleep apnea is often worst during REM sleep (when muscle tone drops to its lowest), this suppression can theoretically reduce the number of apnea events in people whose breathing problems are concentrated in REM.
However, SSRIs also disrupt sleep quality in other ways. Fluoxetine increases time spent awake and in light sleep. Paroxetine increases the number of awakenings. These disruptions can worsen daytime fatigue and overlap with sleep apnea symptoms, making it harder to tell what’s causing what. In a study of 18 obstructive sleep apnea patients given paroxetine for six weeks, REM latency was prolonged but the actual amount of REM sleep didn’t change, likely because these patients already had very little REM sleep at baseline.
Older tricyclic antidepressants may have a modest protective effect. Imipramine reduced the apnea index and number of apnea events in a small study of sleep apnea patients after four months of treatment. But these medications carry their own sedating effects and side effects, so they’re not used as apnea treatments.
Anesthetics and Postoperative Risk
General anesthesia temporarily creates conditions that mimic and worsen sleep apnea. Anesthetic agents suppress airway reflexes, reduce muscle tone, and blunt the arousal response, all the same pathways that medications discussed above affect, but more acutely. For people with existing sleep apnea, the postoperative period carries heightened risk because residual anesthetic effects combine with opioid pain medications.
Current guidelines from the Society of Anesthesia and Sleep Medicine recommend using faster-acting anesthetic agents so that airway reflexes return more quickly after surgery. They specifically advise against combining sedatives, particularly benzodiazepines, and recommend opioid-sparing pain control strategies when possible. If you have sleep apnea and are scheduled for surgery, making sure your surgical team knows about your diagnosis is one of the most important things you can do.
Which Medications Are Safest
Not all drugs within a class carry the same risk. Z-drugs appear safer than benzodiazepines for people with sleep apnea who need help sleeping. Lower, physiologic doses of testosterone carry less risk than high-dose, short-term protocols. And among anesthetic approaches, regional techniques (nerve blocks, epidurals) carry less apnea risk than full general anesthesia.
The risk from any single medication also depends heavily on what else you’re taking. Combining an opioid with a benzodiazepine, for example, creates a synergistic effect on breathing suppression that’s far more dangerous than either drug alone. Body weight, baseline airway anatomy, and whether you already have untreated sleep apnea all change the equation as well. If you suspect a medication is affecting your sleep or breathing at night, a sleep study while on the medication can provide a clear answer.