Weight Loss

Approximately 70% of patients with OSA are obese. The mechanism by which obesity increases the propensity for OSA is unclear, but likely involves fat deposition around the upper airway (23,24). These deposits compromise the size of the airway lumen and may put the upper airway dilating muscles at a mechanical disadvantage. Data from the Sleep Heart Health Study (25) confirms the relationship between weight gain and the development of OSA; almost 40% of patients who started the study without sleep apnea, and who gained 10 kg during the five-year follow-up period, developed moderate OSA as defined by a respiratory disturbance index of > 15. The beneficial effects of weight loss were not as striking as the deleterious effects of weight gain, particularly in women. Nevertheless, weight loss of 10 kg or more in men had approximately five times the odds of a 15 unit or greater reduction in respiratory disturbance index compared with weight stability, suggesting that all obese patients with sleep apnea should be counseled and encouraged to lose weight.

Unfortunately, treatment of obesity is notoriously difficult among those with OSA. In one series of 216 overweight patients with OSA, 11.1% were successfully treated by weight loss alone; however, after three years, only 3% had maintained this remission (26).

In obese patients, three types of therapy have been attempted to promote weight loss: diet and exercise, pharmacological therapy, and bariatric surgery.

Diet and exercise have had limited success in the treatment of obesity. The majority of those who enroll in a typical weight loss program will continue to be obese. No consensus has been reached regarding the optimal weight reduction diet in terms of the proportion of carbohydrates and fat (27). Kansanen et al. (28) showed that weight loss with a very low calorie diet is an effective treatment for OSA having favorable effects on oxygen desaturation index, blood pressure, and baroreflex sensitivity. Maintaining weight loss is another significant barrier to the success of this treatment with the majority of patients regaining weight after a period leading to a recurrence of OSA (26,29). Cognitive behavioral therapy appears to achieve satisfactory weight loss with improvement in OSA and may be of benefit in weight loss maintenance (30).

Weight-bearing exercise for more than 20 minutes five days a week can be helpful in promoting weight loss as well as improving overall health. Additionally, the effect of exercise on OSA extends beyond its effect on patient weight. Data from the Wisconsin Cohort Study indicate that a lack of exercise was associated with increased severity of sleep-disordered breathing independent of body habitus (31). Conversely, exercise training can improve sleep apnea without improving body mass index (BMI) (32)—whether this effect is a result of stabilized muscle tone or increased respiratory drive is unclear.

Pharmacological therapy for obesity is controversial, mainly due to side effects of medications and questionable efficacy. Aminorex (Menocil®), used historically in the 1960s, was associated with an increased risk of pulmonary hypertension. More recently, dexfenfluramine (Fen-Phen®) has shown an association with cardiac valvular abnormalities as well as pulmonary vascular changes (33,34). Newer agents have been successful in achieving weight loss while avoiding significant side-effects. Orlistat (Xenical®), a lipase inhibitor is effective in maintaining weight reduction after dieting (35) and in achieving weight reduction when used as part of a weight management program (36,37). Sibutramine (Meridia®), a serotonin reuptake inhibitor has also been successful in achieving weight loss, particularly when used in combination with lifestyle modification (38). Long-term follow-up data are lacking for these agents and there is no trial data indicating effects on sleep apnea parameters. One trial has been performed, which indicates that use of sibutramine was not associated with worsening of OSA as a direct pharmacological effect (39). It is likely that trial evidence will soon be available to clarify the role of these agents in the management of OSA.

Bariatric surgery encompasses a variety of operative techniques designed to promote weight reduction. Several randomized controlled trials (40-42) and many case series have demonstrated the efficacy of these surgical techniques in the treatment of obesity and its metabolic complications. Newer laparoscopic techniques appear to reduce operative morbidity while maintaining efficacy. No randomized trials report the effects of bariatric surgery in OSA patients but a comprehensive meta-analysis outlining the impact of bariatric surgery on weight loss and on four obesity comorbidities (including OSA) was published in 2004 (43). Comorbidity outcomes were separated according to total resolution or resolution/improvement of the condition. The percentage of patients in the total population (n = 1195) whose OSA resolved was 85.7% [95% confidence interval (CI), 79.2-92.2%]. The percentage of patients in the total population (n = 726) whose OSA resolved or improved was 83.6% (95% CI, 71.8-95.4%). Evidence for changes in OSA was predominantly available for gastric bypass patients. This was particularly so for the AHI, which decreased by 33.85 per hour (95% CI, 17.5-50.2 per hour). We currently would consider bariatric surgery for morbidly obese individuals (BMI > 40 kg/m2) who have failed conservative measures at weight loss.

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