Sleep Disorders and Sleep Deprivation: An Unmet Public

Sleep Disorders and Sleep Deprivation: An Unmet Public Health Problem
http://www.nap.edu/catalog/11617.html
72 SLEEP DISORDERS AND SLEEP DEPRIVATION
which may mediate the development of glucose intolerance, insulin resistance,
and, ultimately, type 2 diabetes. Because diabetes is also a risk factor
for cardiovascular disease, the interrelationships may partly explain why
OSA predisposes to cardiovascular disease (Punjabi and Beamer, 2005).
Obstructive Sleep Apnea May Contribute to Obesity
Up to 40 percent of people who are morbidly obese have OSA (Vgontzas
et al., 1994). This finding may reflect the role of obesity as a well-established
risk factor for the development of OSA. It may also reflect obesity
as a consequence of OSA, although the evidence is not yet conclusive
(Grunstein, 2005b). Patients with newly diagnosed OSA, compared with
controls matched for BMI and percent body fat, show recent weight gain
(Phillips et al., 1999). Data from the Wisconsin Sleep Cohort also show that
individuals with OSA have reduced levels of physical activity; OSA-related
sleepiness may contribute to changes in activity and energy expenditure,
and thus contribute to weight gain. OSA-related hormonal changes may
also contribute to obesity. In general, patients with OSA have higher levels
of leptin, the appetite-suppressing hormone (Phillips et al., 2000; Palmer et
al., 2004; Patel et al., 2004) than controls. However, their morning levels
are relatively lower than evening levels (Patel et al., 2004). Thus, either via
leptin resistance (where high levels of leptin are present, but tissues are
poorly responsive to leptin’s action) or because of disturbances in diurnal
variability in leptin, individuals with OSA may be predisposed to lower
effective levels of appetite suppressing hormones. Although CPAP reduces
leptin levels, it is not known whether such effects relate to differences in the
effectiveness of leptin’s actions (Chin et al., 2003). Furthermore, obesity
also affects the severity of OSA. Significant weight loss in adolescents who
underwent gastric bypass surgery (mean, 58 kg) was associated with a dramatic
reduction of OSA severity (Kalra et al., 2005).
Etiology and Risk Factors
In simplest terms, OSA is caused by narrowing or collapse of the airway
as a result of anatomical and physiological abnormalities in pharyngeal
structures. Apnea episodes cause hypoxemia (insufficient oxygen in the blood)
and hypercapnia (high concentration of blood carbon dioxide). The episodes
also increase the output of the sympathetic nervous system (Narkiewicz
and Somers, 2003), the effect of which is to restore pharyngeal muscle tone
and reopen the airway. Although increased sympathetic activity is beneficial
for restoring normal breathing and oxygen intake over the short term,
it has long-term deleterious effects on vascular tone and blood pressure,
among other effects (Caples et al., 2005). These early events—which are
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