Sleep Apnea and Daytime Sleepiness and Fatigue
|Course Name||Sleep Apnea and Daytime Sleepiness and Fatigue|
Upon successful completion of this module, you will be able to:
- Define what is meant by the term “sleep apnea”.
- List the key elements of the pathophysiology of sleep apnea.
- Describe what is meant by the metabolic síndrome.
- List the effects of the metabolic syndrome on OSA.
- List the interactions between obesity, OSA, and hipertension.
Course InformationSLEEP APNEA is a common disorder associated with daytime sleepiness and fatigue, and significant morbidity and mortality due to accidents and cardiovascular events (1, 2). Male gender, advancing age, obesity, anatomical abnormalities (including small pharyngeal size due to fatty tissue of the neck), heredity, and instability of respiratory control during sleep, have been reported as risk factors for the development of sleep apnea. Two thirds of middle-aged apneic men suffer from obesity, particularly the android-central type, and one third have hypertension. Visceral obesity is associated with insulin resistance, and the so-called visceral fat or metabolic syndrome, i.e. dyslipidemia, dyscoagulation, hypertension, and diabetes mellitus type II, and their cardiovascular sequelae, mostly ischemic heart disease (3). Studies of the potential independent role of sleep apnea in the development of insulin resistance and/or vice versa have been inconsistent and inconclusive. Recent studies suggested that the effects of sleep apnea on insulin dynamics and effects could be accounted for completely by obesity (4, 5).
The pathophysiology of sleep apnea remains obscure, and most currently available treatments for this disorder are mechanical and associated with either variable response and/or poor compliance. Recently, we reported that the inflammatory cytokines tumor necrosis factor-? (TNF?) and interleukin-6 (IL-6), both of which produce sleepiness and fatigue, are elevated in sleep apnea and obesity and might play a role in the pathogenesis and pathological sequelae of both disorders (6). Like the adipostatic hormone leptin, these cytokines are released into the interstitial fluid of adipose tissue, and their circulating levels correlate positively with the body mass index (BMI) (7, 8, 9). TNF? correlates strongly with lipolysis, and this cytokine causes marked insulin resistance (7, 9, 10) and stimulates leptin secretion (11, 12, 13). Circulating concentrations of leptin are proportional not only to total body fat but also to the degree of insulin resistance (14). Chronic leptin administration has been associated with sympathetic system activation and elevation of blood pressure (15), suggesting that it might play a role in the pathogenesis of manifestations that frequently accompany sleep apnea, namely hypertension and its sequelae.
The purpose of this study was to evaluate whether the biochemical indexes of chronic inflammation, including the proinflammatory cytokines TNF? and IL-6, and the adipose-derived tissue hormone, leptin, are elevated in sleep apnea independently of obesity; whether sleep apnea is an independent variable in the development of insulin resistance; and whether among obese individuals it is visceral, rather than generalized, obesity that predisposes to the development of sleep apnea.