Obstructive Sleep Apnea and the Metabolic Syndrome

Jamie C.M. Lam; Mary S.M. Ip


Expert Rev Resp Med. 2009;3(2):177-186. 

In This Article

OSA and Obesity

Obesity is an important risk factor for the development of OSA,[1,39,40] and it also plays a vital role in the pathogenesis of the core features of the metabolic syndrome.[16,18] Epidemiologic studies have reported a positive correlation between the severity of OSA and the degree of obesity in adults across various ethnic populations.[1] Waist-to-hip ratio, waist circumference and neck circumference have been reported to be better predictors of OSA severity than BMI in some studies,[1,39,40] and sleep apnea patients have a greater amount of visceral fat compared with obese controls matched for BMI, with a higher correlation between AHI and visceral fat than between AHI and BMI,[41] suggesting that central or abdominal obesity are more closely associated with OSA than general obesity. The detailed mechanisms by which adiposity and its distribution predispose to development of OSA are not clearly understood. Central or abdominal obesity impose a greater mechanical load on the upper- and lower-respiratory systems, while obesity-related inflammation may modulate upper-airway function, predisposing to pharyngeal collapse.[39]

In a longitudinal cohort study, a 10% weight loss was associated with a 26% decrease in AHI.[42] It has been speculated that OSA itself may modulate the secretion of hormones and other biological mediators with promotion of obesity or preferential abdominal fat accumulation, thus further engaging OSA and metabolic dysfunction in a vicious cycle.[26,39,43] but to date, there is no strong evidence to show that control of OSA per se affects fat accumulation or its distribution. One study reported a decrease in the visceral fat shown on CT scans, concomitant with a decrease in leptin levels with CPAP treatment of OSA,[44] although we were unable to detect any change in the abdominal or visceral fat shown on MRI scans after 3 months of CPAP treatment.[45] In a randomized interventional study, we noted that, in a small number of subjects, weight loss could result in complete resolution of OSA, especially that in the mild-to-moderate AHI range.[46] We also observed that the group on both CPAP and behavioral modification appeared to achieve better weight reduction compared with the group on the latter only, suggesting a contributory effect of CPAP treatment towards weight control.[46] However, the vast majority of clinical studies on CPAP treatment of OSA, admittedly in which weight change was not the outcome parameter of interest by design, did not observe any significant reduction in bodyweight at follow-up evaluation.

Weight reduction is best achieved by behavioral changes to reduce energy intake through dietary modifications and to enhance energy expenditure through physical activity.[47] For those with morbid obesity, bariatric surgery has been used and shown to improve the individual’s metabolic profile as well as their sleep-disordered breathing.[48] Reduction of adiposity will not only decrease the severity of OSA but also directly mitigate cardiometabolic derangements and disease outcomes. Hence, active measures targeted at weight control should be considered an integral part of OSA management.


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