Abstract
Obesity trends continue to rise in alarming proportions worldwide. Obstructive sleep apnea, an increasingly commonly recognized disorder, is characterized by recurrent episodes of upper airway closure during sleep, and obesity is proposed to be its strongest risk factor. Recognition strategies for OSA in obesity are overwhelmed by the sheer prevalence of obstructive sleep apnea, > 80% in those with a BMI > 40. Obesity has direct as well as indirect influences on upper airway mechanics and physiology. Obesity may also influence loop gain by exerting an influence on central chemosensory respiratory drive. Pattern of fat distribution rather than overall weight may have a modulatory effect on these influences. Obese patients also develop a syndrome of obesity-hypoventilation characterized by waketime hypercarbia, by mechanisms that are not entirely clear. Genetic mechanisms influencing obesity and OSA are bidirectional and likely exert mutually additive effects. Medical weight loss can be a treatment for OSA, but bariatric surgery has played an increasingly prominent role in the theraputic paradigm for OSA in the morbidly obese, with success rates of ∼85%.
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