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1031 Editorial—Badr Obstructive sleep apnea (OSA) is a common disorder, characterized by recurrent episodes of apnea or hypopnea secondary to complete or partial upper airway obstruction, leading to significant adverse health consequences.1-4 The pathogenesis of obstructive sleep apnea is due to the interaction between anatomic upper airway susceptibility and sleep-related changes in upper airway function.5,6 The loss of the “wakefulness drive to breathe” results in decreased caliber of the pharyngeal lumen,7,8 increased upper airway resistance,9-11 and increased compliance of the upper airway wall.12 Extensive research has focused on the neuromuscular determinants of upper airway patency, especially the genioglossus muscle and the hypoglossal motoneurons13 and the effect of lung volume14 and tracheal traction15 on upper airway patency. However, available studies have not provided a satisfactory answer to a very simple question: what is the link between obesity and upper airway obstruction? In this issue of SLEEP, Brennick and colleagues provide a direct link between obesity and compromised upper airway lumen.16 The investigators examined the effects of obesity on upper airway structures in obese (OBZ) and lean (NBZ) Zucker rats, assessing tongue fat and volume using in-vivo magnetic resonance spectroscopy (MRS), MRI including Dixon imaging for tongue fat volume, ex-vivo biochemistry, and histology. The investigators found a large degree of fat infiltration in the tongue muscle in genetically obese Zucker rats, as compared to tongues of the nonobese Zucker rats. Interestingly, fat accumulated primarily in the tongue and not in other upper airway skeletal muscle. The volume of the OBZ tongue was not greater than the NBZ tongue. However, total fat volume measured by MR fat weighted Dixon image analysis was significantly greater in OBZ tongues. The susceptibility to fat deposition in the tongue may have significant implications for the pathogenesis of OSA. Excessive lingual fat deposits may increase collapsing tissue pressure and promote pharyngeal narrowing.17,18 The findings of Brennick et al.16 corroborate studies in humans that demonstrated greater fat deposits in sleep apnea antero-lateral to the upper airway in patients with OSA when compared to control participants.19 Similarly, mass loading in anesthetized rabbits, simulating excessive adipose tissue, was found to be associated EDITORIAL

Back to Basics Regarding Upper Airway Obstruction during Sleep—Size Matters