OSA is characterized by sleep fragmentation owing to repeated arousals and disruption of normal sleep architecture secondary to partial or complete closure of the upper airway during sleep (6,7). In nonobese subjects, OSA is typically described with the polysomnographic pattern of OSA and hypopnea and associated symp toms, particularly tiredness, fatigue an d /o r complaints of sleepiness. As many patients may be seen after years of evolution of undiagnosed sleep-disordered breathing, it is often difficult to identify the initial factor responsible for the OSA polysomnographic pattern. Was OSA present before the change in morphology, and did it play a role in the occurrence of the current morphology? Or was the noted abnormal breathing during sleep a consequence of change in the subject's morphol ogy? Often it is impossible to answer this question when patients are first seen, as they may clearly be overweight at entry. In fact it would be better not to use the term OSA in the presence of obese patients with polysomnographic patterns of sleepdisordered breathing. Also one should be careful in attributing specific complica tions such as cardiovascular (CV) or metabolic complications to OSA when obesity is present, as obesity per se can also lead to the same complications. Data analyses using specific statistical methods such as multiple regression analysis may help in a large cohort, but the cohort should include at least as many nonobese as obese individuals with OSA to provide valid responses. The major problem, as shown below, is that obesity per se, is a risk factor for OSA and sleep disruption.