APPENDIX IV. OBESITY AND SLEEP APNEA

Obstructive sleep apnea is defined as an absence of breathing during sleep. Currently, it is recognized that sleep apnea is part of a continuum from health to disease (649, 650).  Apnea is currently defined as cessation of airflow for at least 10 seconds and is characterized as either central (if no respiratory effort occurs), obstructive (if continued effort is noted), or mixed (if both central and obstructive components are present) (651-653).  Apnea is associated with either a fall in oxyhemoglobin desaturation or an arousal from sleep.  Hypopneas, which are defined as partial reductions in airflow associated with falls in oxygen saturation or arousals from sleep, are also recorded. 

The sleep apnea syndrome has been clinically defined as recurrent apnea or hypopnea associated with clinical impairment usually manifested as increased daytime sleepiness or altered cardiopulmonary function. In general, the average number of episodes of apnea and hypopnea per hour are reported as an index (AHI) or as a respiratory disturbance index (RDI). Classically, an AHI of greater than five episodes per hour has been the definition of the presence of the sleep apnea syndrome (651, 652). Other commonly used cutoff points are an AHI of 10 or 15 episodes per hour or an overnight total of 30 apneic-hypopneic episodes (653).

There are several correlates of sleep apnea. It is well recognized that it is more prevalent in males, although the difference is less pronounced in population-based studies than in laboratory-based studies (20).  Some studies have suggested that the prevalence of sleep apnea in women increases after menopause. Snoring also correlates with sleep apnea, increasing up to late middle age and decreasing thereafter (20, 282, 654, 655). The other major correlate of sleep apnea is obesity (20, 653, 654, 656), in both men and women. In general, women have to be significantly more obese than men for the clinical syndrome to be apparent (657).  At present, no published epidemiologic studies have examined the relationship between race and sleep apnea. Given the high prevalence of obesity among specific populations and minorities, sleep apnea may be highly prevalent in these groups.

The major pathophysiologic consequences of severe sleep apnea include severe arterial hypoxemia, recurrent arousals from sleep, increased sympathetic tone, pulmonary and systemic hypertension, and cardiac arrhythmias (658).  These phenomena may result in acute hemodynamic and chronic structural change in the coronary arteries, possibly associated with relative myocardial ischemia, rupture of atheromatous plaques, and increased risk for thrombosis at the site of any unstable plaque (659).

Similar mechanisms acting in the cerebrovascular system may be involved in an increased risk of stroke.  Finally, the sympathetic tone may be associated with hypertension as well as increased platelet aggregability (660).

The primary goal for treatment of individuals with sleep apnea is to reduce the severity of the respiratory events that are associated with oxyhemoglobin desaturation and arousal from sleep.  There are only two cohort studies in clinic-based populations that demonstrate a significant reduction in cardiovascular mortality among sleep apnea patients who are treated progressively compared to those who are treated conservatively (661, 662).  However, both of these studies were retrospective and suffered from a significant bias of ascertainment.

The evidence that treatment of obesity ameliorates obstructive sleep apnea is reasonably well established. Although the studies are small, both surgical and medical approaches to weight loss have been associated with a consistent but variable reduction in the number of respiratory events, as well as improvement in oxygenation.  In general, surgical interventions, which have included a gastric bypass or jejunoileostomy, have been reserved for people who are severely obese (663-666).

While this approach to weight reduction was commonly used in patients with severe obstructive sleep apnea, it recently has been abandoned because of complications and side effects. However, the use of surgical gastric procedures has been successful in improving sleep apnea in a number of studies.

On the other hand, weight reduction has been associated with comparable reduction in the severity of sleep apnea, as well as improved evidence of renal function and hypertension (667-671).  Both medical and surgical studies have demonstrated that as little as 10-percent weight reduction is associated with a more than 50 percent reduction in the severity of sleep apnea. Moreover, more recent data suggest a possible "threshold" effect that is directly related to the collapsibility of the upper airway. Those individuals who demonstrate a minimally collapsible upper airway apparently achieve a greater effect for the same percentage of weight reduction (672).

Finally, there is evidence that standard treatments for sleep apnea do reduce specific cardiovascular risk factors. Specifically, the most commonly employed treatment, continuous positive airway pressure, has been shown to reduce waking arresting carbon dioxide and reduced heart rate, and pulmonary artery pressure decreased hematocrit and improved ventricular ejection fraction (673).

Other standard surgical approaches that have been employed to widen the upper airway have been shown to reduce the severity of the apnea, but there are no data examining the associated cardiovascular risk factors. No studies have specifically examined the effects of treatment of sleep apnea on obesity, but it generally has been noted that all nonweight loss treatments of sleep apnea have not been associated with any significant weight loss other than might be accrued from surgical interventions that temporarily reduce the ability to eat in the immediate postoperative period.