The Weighty Issue of Obesity Management in Sleep Apnea

The interrelationships between OSA and obesity are complex in large part because of the multidirectional nature of not only the association between these two factors, but also their relationships with undesirable cardiovascular health outcomes. Indisputably, obesity serves as a risk factor for OSA not only because of its direct mechanical effects (ie, disadvantageously affecting upper airways critical closing pressure), but also potentially via pathophysiologic pathways involving a reduction in lung volume resulting in a loss of caudal traction of the upper airways and upper airways neuromodulatory effects of adipokines.¹

The importance of obesity in OSA from a population health level cannot be underestimated. Data from the Wisconsin Sleep Cohort suggest that more than one-half of cases of moderate to severe OSA are attributable to excess weight.² Although there is a widespread belief that by improving sleep quality and reducing fatigue OSA treatment can facilitate weight loss, data from randomized controlled trials have established that OSA therapy with CPAP does not produce weight loss and actually leads to modest weight gain.^3,4 Thus, to achieve weight loss in overweight or obese patients with OSA, adjunctive treatments specifically focused on weight are necessary.

A number of randomized trials have evaluated the impact of behavioral weight-loss interventions on OSA severity. However, there have been limitations in this literature, including such caveats as a focus on very low calorie diets that are extremely intensive and not readily available to most patients^5,6 or studying patient populations incidentally found to have OSA who are not necessarily representative of clinical OSA populations in terms of both severity of OSA-related symptoms and motivations to treat apnea.⁷ The study by Ng et al⁸ reported in this issue of CHEST (see page 1193) represents one of the first trials to evaluate a long-term lifestyle intervention in a population presenting for treatment of OSA.

The study recruited 104 Chinese participants with moderate to severe OSA to a trial designed to evaluate the impact of a 12-month lifestyle modification intervention compared with usual care. The focus of the intervention was to administer dietary education with a goal of a 10% to 20% reduction in daily caloric intake, although a physical activity recommendation was also made to engage in aerobic exercise for 30 min at least 2 to 3 days per week. In the intent-to-treat analysis, a significant reduction in BMI was observed at 1 year (−1.8 kg/m² in the intervention arm vs −0.6 kg/m² in the control arm), but the reduction in apnea-hypopnea index (AHI) was only marginally significant (−8.1 events/h in the intervention arm vs −2.9 events/h in the control arm).

The intervention was fairly aggressive, requiring weekly visits to a dietician for 4 months and then monthly for a year and, as might be expected, adherence to this protocol was suboptimal even though substantial attempts were made to fit the dietician visits into the participants’ schedules, including appointments after normal business hours. More than 20% of those randomized to the intervention arm made fewer than four of the scheduled 24 visits to the dietician. Given this, it is no surprise that the per-protocol analysis demonstrated much greater effects than the intent-to-treat analysis.

The improvement in OSA severity for the weight loss obtained in this study (mean 16.9% reduction in AHI for 5.8% reduction in BMI) is consistent with the 3:1 ratio reported in other studies using behavioral-dietary approaches, suggesting that the amount of weight loss is more important than the method of loss. By itself, these results suggest that behavioral weight loss is at best an adjunctive treatment of moderate to severe OSA and should not be used without more definitive treatments such as CPAP. Fortunately, the results from Ng et al⁸ suggest that adding behavioral weight loss to CPAP does not lower CPAP adherence.

Of course, the AHI is simply a surrogate marker and should not be considered the gold standard in assessing the efficacy of OSA treatments. Despite only modest improvements in AHI, Ng et al⁸ found clinically significant improvements in sleepiness (reduction in Epworth score of 2.5 points in the intervention vs 1.0 point in the control arm). Although a placebo effect cannot be excluded given the unblinded nature of the trial, these results suggest that weight loss may improve OSA-related symptoms through AHI-independent mechanisms. A growing body of evidence supports the notion that obesity may have apnea-independent effects on sleepiness.⁹ Similarly, weight loss has cardiovascular benefits above and beyond those obtained through its effects on OSA.¹⁰

The study by Ng et al⁸ now adds to the growing literature demonstrating modest benefits on AHI, but potentially larger benefits on downstream outcomes, in patients undergoing weight loss, whether it occurs through behavioral, pharmacologic, or surgical means. Despite these data, implementation of weight-loss treatments into everyday care has been limited at best. In part, this relates to a knowledge gap in physicians caring for OSA. Although sleep medicine fellowship programs emphasize core competencies in the use of such treatments as CPAP, oral appliances, and positional therapy, there is no required training in approaches to weight loss. Most physicians caring for patients with OSA have no training or experience in overseeing behavioral weight-loss programs, let alone prescribing weight-loss medications. Other barriers include access to ancillary staff such as nutritionists with expertise in weight loss and third-party payor coverage for weight-loss interventions. There is also a need for generalizable interventions. Surgical and pharmacologic interventions are often contraindicated in the sickest patients (eg, those with existing cardiovascular disease) who have the most to gain from weight loss. Very-low-calorie diets require close medical follow-up to ensure patient safety and are unappealing to most patients. Lifestyle interventions focused on a mild reduction in calories are a much more practical approach, but as evidenced by Ng et al,⁸ the intensity of the intervention can lead to a substantial reduction in adherence, which limits the practicality of application in routine care.

Recent guidelines identifying weight-loss counseling as a measure of OSA quality of care should energize providers to establish the infrastructure to incorporate weight-loss education and interventions into clinical care.¹¹ However, more research to identify effective yet feasible interventions is sorely needed. For example, incorporating weight-loss interventions into standard OSA care so that nutritionists/dieticians become integrated members of the sleep health-care team or equipping sleep technicians or respiratory therapists who are on the frontlines of optimizing CPAP adherence with the skill set to provide nutritional counseling may be potential solutions that would overcome many of the current barriers, although they would require a nontrivial investment in augmenting and/or retraining the sleep workforce.

There is little argument that losing weight is a good thing. How to effectively help patients achieve this goal in the real world remains a key challenge that physicians caring for patients with OSA need to focus on to optimize long-term health outcomes in these patients.