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Sleep Apnea, Sleep Deprivation and C-Reactive Protein
Virend K. Somers
Obstructive sleep apnea (OSA) is a highly prevalent disorder affecting between 15-20 million adult Americans. OSA has been linked closely to the development of cardiac and vascular diseases, including hypertension, heart failure, stroke and ischemic heart disease. Sleep deprivation has also been implicated as an independent contributor to future development of cardiovascular disease. It is thought that activation of systemic inflammatory mechanisms may be an important mediator of any etiologic link between sleep apnea, sleep deprivation and cardiovascular risk.
Hypoxemia is known to result in increases in CRP levels. Sleep deprivation has also been linked to increased CRP. Obstructive sleep apnea represents a condition of combined intermittent hypoxemia and chronic sleep deprivation. Indeed, several studies have reported that adults as well as children with obstructive sleep apnea have high levels of CRP.
Obstructive sleep apnea is also very closely associated with obesity. Obese individuals are at substantially greater risk for development of OSA. There is some evidence that OSA and sleep deprivation may also predispose to obesity. Patients with OSA have increased levels of leptin suggesting that OSA may be accompanied by resistance to the appetite suppressant effects of leptin. Emerging evidence also suggest a role for leptin in systemic inflammation. In normal subjects, increased levels of leptin are accompanied by high levels of CRP and leptin may act to increase heptocyte production of CRP. Recent data suggest that the heightened CRP may itself interact with leptin to attenuate appetite suppressant effects of leptin thus predisposing to weight gain. CRP may therefore contribute importantly not only to cardiovascular disease but also to weight gain in patients with OSA.
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