Ahmad Izuanuddin Ismail

"Obesity and obstructive sleep apnoea (OSA) are often approached as separate clinical problems: obesity as excess weight and OSA as upper-airway obstruction. This conventional framework, however, fails to capture the complex bidirectional relationship between adiposity, sleep-disordered breathing and cardiometabolic disease. Obesity is a chronic, relapsing disease characterised by dysfunctional adipose tissue, visceral and ectopic fat accumulation, inflammation, insulin resistance and altered neuroendocrine signalling. These processes can substantially influence respiratory mechanics, upper-airway collapsibility and ventilatory control, contributing to the development and progression of OSA. Conversely, untreated OSA produces recurrent intermittent hypoxia, sleep fragmentation and sympathetic activation, promoting oxidative stress, endothelial dysfunction, hypertension, insulin resistance and broader cardiometabolic consequences. The interaction between obesity and OSA therefore creates a self-reinforcing cycle that extends far beyond the airway. This presentation explores the pathophysiological continuum linking obesity, OSA and cardiometabolic disease, and considers its implications for public health. Traditional treatment strategies, including lifestyle intervention, positive airway pressure and metabolic/bariatric surgery, remain fundamental. However, emerging pharmacological therapies offer an opportunity to address upstream biological drivers of disease. In particular, GLP-1 receptor agonists and dual GIP/GLP-1 receptor agonists represent an important evolution in obesity management, with emerging evidence demonstrating improvements in OSA severity and cardiometabolic risk alongside substantial weight reduction. The future of sleep medicine may therefore lie beyond treating airway obstruction alone. A personalised, integrated approach—combining airway therapy, obesity treatment, lifestyle intervention and cardiometabolic risk reduction—offers an opportunity to treat the patient rather than simply the apnoea. Obesity is more than a weight issue, and OSA is more than an airway problem. "

"Obstructive sleep apnoea (OSA) affects an estimated one billion adults worldwide, most of whom are overweight or obese. Yet care remains largely mechanical: diagnose, prescribe positive airway pressure (PAP), advise weight loss, and judge success by device-reported AHI. Weight-loss advice is rarely structured or followed up, and PAP, while controlling AHI and symptoms, has not been shown to alter cardiometabolic trajectory. This presentation argues for a shift in the sleep physician's role. Weight loss is disease-modifying: a 20% BMI reduction is associated with an approximately 57% fall in AHI, acting chiefly on pharyngeal collapsibility, the dominant OSA endotype. In SURMOUNT-OSA, tirzepatide reduced AHI by 20–24 events/h versus placebo over 52 weeks, with or without PAP, alongside improvements in hypoxic burden, sleepiness, blood pressure, hsCRP and patient-reported outcomes. Mediation analyses show these cardiometabolic benefits are driven predominantly by weight loss, with AHI and hypoxic-burden reduction independently mediating selected outcomes. Meta-analytic and real-world data support a class effect. A practical model of care is then outlined: patient selection, clinical and financial consent, monitoring for gastrointestinal effects, lean-mass loss and weight regain, and multidisciplinary co-management with primary care, dietetics, exercise physiology and psychology. Incretin therapy is positioned as complementary to PAP, not a replacement. Finally, Asia-Pacific realities are addressed, including variable approval and reimbursement, out-of-pocket costs, and growing cosmetic and grey-market GLP-1 use, underscoring why sleep physicians must own the medical narrative."