Incretin-based therapies — particularly liraglutide and tirzepatide — demonstrate meaningful reductions in apnea-hypopnea index (AHI), sleep apnea-specific hypoxic burden, hsCRP, and systolic blood pressure in obese OSA patients. The SCALE Sleep Apnea trial established proof of concept for pharmacologic weight loss improving AHI, while SURMOUNT-OSA made AHI reduction its primary endpoint. Semaglutide contributes indirect cardiometabolic evidence but lacks dedicated OSA outcome trials. The dominant proposed mechanism is weight-loss-mediated anatomical unloading of the upper airway — plausible, but unconfirmed by serial imaging, Pcrit measurement, or physiological endotyping within incretin-treated cohorts.
This review arrives at a genuinely important clinical juncture. CPAP remains the gold standard for moderate-to-severe OSA but notoriously suffers from poor long-term adherence — a problem that pharmacologic weight reduction could partly circumvent by addressing root pathophysiology rather than masking it nightly. The incretin class has already reshaped obesity and type-2 diabetes care; their extension into OSA management represents a logical but not yet proven frontier. Critically, this narrative review — not a systematic meta-analysis — cannot quantify effect sizes or control for publication bias. Discordant vascular-imaging findings warn against assuming GLP-1-driven weight loss replicates PAP's cardiovascular protections. For clinicians, the current evidence supports incretin therapy as a meaningful adjunct in obese OSA patients, particularly those intolerant of PAP, but long-term cardiovascular event data remain absent. Incremental, not paradigm-shifting — yet.