BACKGROUND Obesity and obstructive sleep apnea tend to coexist and are associated with inflammation, insulin resistance, dyslipidemia, and high blood pressure, but their causal relation to these abnormalities is unclear. METHODS We randomly assigned 181 patients with obesity, moderate-to-severe obstructive sleep apnea, and serum levels of C-reactive protein (CRP) greater than 1.0 mg per liter to receive treatment with continuous positive airway pressure (CPAP), a weight-loss intervention, or CPAP plus a weight-loss intervention for 24 weeks. We assessed the incremental effect of the combined interventions over each one alone on the CRP level (the primary end point), insulin sensitivity, lipid levels, and blood pressure. RESULTS Among the 146 participants for whom there were follow-up data, those assigned to weight loss only and those assigned to the combined interventions had reductions in CRP levels, insulin resistance, and serum triglyceride levels. None of these changes were observed in the group receiving CPAP alone. Blood pressure was reduced in all three groups. No significant incremental effect on CRP levels was found for the combined interventions as compared with either weight loss or CPAP alone. Reductions in insulin resistance and serum triglyceride levels were greater in the combined-intervention group than in the group receiving CPAP only, but there were no significant differences in these values between the combined-intervention group and the weight-loss group. In per-protocol analyses, which included 90 participants who met prespecified criteria for adherence, the combined interventions resulted in a larger reduction in systolic blood pressure and mean arterial pressure than did either CPAP or weight loss alone. CONCLUSIONS In adults with obesity and obstructive sleep apnea, CPAP combined with a weight-loss intervention did not reduce CRP levels more than either intervention alone. In secondary analyses, weight loss provided an incremental reduction in insulin resistance and serum triglyceride levels when combined with CPAP. In addition, adherence to a regimen of weight loss and CPAP may result in incremental reductions in blood pressure as compared with either intervention alone.
Obesity and obstructive sleep apnea (OSA) tend to co-exist. Little is known about the effects of OSA, obesity, or their treatment on central aortic pressures and large artery stiffness. We randomized 139 adults with obesity (BMI>30 kg/m2) and moderate-to-severe-OSA to: 1) CPAP therapy (n=45); 2) weight loss (WL) therapy (n=48); or 3) combined CPAP and WL (n=46) for 24 weeks. We assessed the effect of these interventions on central pressures and carotid-femoral pulse wave velocity (CF-PWV; a measure of large artery stiffness), measured with arterial tonometry. Central systolic pressure was reduced significantly only in the combination arm (−7.4 mmHg, 95%CI: −12.5 to −2.4 mmHg; P=0.004), without significant reductions detected in either the weight loss-only (−2.3 mmHg; 95%CI: −7.5 to 3.0, P=0.39) or the CPAP-only (−3.1 mmHg; 95%CI:−8.3 to 2.0, P=0.23) arms. However, none of these interventions significantly changed central pulse pressure, pulse pressure amplification or the central augmentation index. The change in mean arterial pressure (P=0.008) and heart rate (P=0.027) induced by the interventions were significant predictors of the change in CF-PWV. However, after adjustment for mean arterial pressure and heart rate, no significant changes in CF-PWV were observed in any group. In obese subjects with OSA, combination therapy with WL and CPAP is effective in reducing central systolic pressure. However, this effect is largely mediated by changes in mean, rather than central pulse pressure. WL and CPAP, alone or in combination, did not reduce large artery stiffness in this population.
This study examined the association between depressive symptoms, as well as depressive symptom dimensions, and three candidate biological pathways linking them to Obstructive sleep apnea (OSA): (1) inflammation; (2) circulating leptin; and (3) intermittent hypoxemia. Participants included 181 obese adults with moderate-to-severe OSA enrolled in the Cardiovascular Consequences of Sleep Apnea (COSA) trial. Depressive symptoms were measured using the Beck Depression Inventory-II (BDI-II). We assessed inflammation using C-reactive protein levels (CRP), circulating leptin by radioimmunoassay using a double antibody/PEG assay, and intermittent hypoxemia by the percentage of sleep time each patient had below 90% oxyhemoglobin saturation. We found no significant associations between BDI-II total or cognitive scores and CRP, leptin, or percentage of sleep time below 90% oxyhemoglobin saturation after controlling for relevant confounding factors. Somatic symptoms, however, were positively associated with percentage of sleep time below 90% saturation (β = 0.202, P = 0.032), but not with CRP or circulating leptin in adjusted models. Another significant predictor of depressive symptoms included sleep efficiency (β = -0.230, P = 0.003; β = -0.173, P = 0.030 (β = -0.255, P = 0.001). In patients with moderate-to-severe OSA, intermittent hypoxia may play a role in somatic rather than cognitive or total depressive symptoms.
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