In the past few decades, obesity has emerged as a significant individual and public health issue. Estimates of obesity rates in adults have doubled over the past 20 years in many countries,1 with this phenomenon occurring not only in Western nations and among adults, but increasingly in developing economies and among children. The health consequences of being overweight or obese are significant and worsen with increasing weight, reducing life expectancy2 and impairing health-related quality of life.3 The impact of excess weight on the respiratory system can be significant, especially when respiratory problems are already present. However, the contribution of excess weight to respiratory symptoms and poor response to therapy is often underestimated. Over the past 12 months, Respirology has published a series of articles on ‘Obesity and Respiratory disorders’ to address some of the issues associated with the coexistence of these two disorders.
Obesity impacts the respiratory system in numerous ways, reducing lung and chest wall compliance, altering breathing pattern and ventilation-perfusion relationships, worsening gas exchange and reducing lung volumes, most notably expiratory reserve volume.4 These reductions in expiratory reserve volume increase the risk of expiratory flow limitation and small airway closure, especially when lying supine. This not only increases the work of breathing but could also contribute to dyspnoea, a symptom commonly reported by obese individuals.5 In addition, ventilatory control may be altered by obesity and its metabolic consequences through the mediation of adipokines such as leptin, promoting hypoventilation and awake hypercapnia in some obese individuals.5,6
The two most common disorders influenced by obesity and managed routinely by respiratory physicians are obstructive sleep apnoea (OSA) and asthma. Obesity is the most frequent risk factor for OSA, although not all patients with OSA are overweight. The interaction between obesity and OSA is complex and the distribution of fat accumulation is important in understanding the mechanisms underlying closure of the upper airway during sleep. In his review, Isono7 uses the ‘collapsible tube in a rigid chamber’ model to illustrate the mechanisms whereby fat deposition can promote upper airway obstruction. Increasing the amount of soft tissue within the bony maxillomandibular enclosure or reducing the size of the enclosure itself creates an anatomical imbalance, narrowing the airway and increasing the likelihood of collapse. In those with a more central (abdominal) pattern of obesity, reduced lung volumes may promote pharyngeal collapse by reducing longitudinal traction forces on the upper airway. The impact of skeletal restriction on airway patency may be of more relevance in non-obese or overweight individuals, whereas reduced lung volumes may play a more important role in the development of OSA in those with more pronounced obesity.7
Considerable overlap exists between the occurrence of obesity and craniofacial factors, and a combination of these explains a large proportion of the variance in OSA severity. While the prevalence of OSA appears similar across various ethnicities, the interaction between obesity and craniofacial risk factors is influenced by ethnicity and described in detail by Sutherland et al.8 This balance has particular relevance to the Asia–Pacific region. Asian subjects tend to have more severe OSA at lower levels of obesity, suggesting that craniofacial factors, particularly skeletal restriction, may be more important for OSA risk in this population. However, the increasing levels of obesity in this region, along with the tendency for Asians to develop more abdominal or central fat, put this group at particular risk for developing the adverse health consequences and associated economic costs of more severe OSA.
The strong link between obesity and metabolic syndrome is well recognized, with more recent awareness of OSA as an important contributor to this disorder. While obesity is regarded as playing a key role in the development of OSA, Lam et al.9 highlights the possible bidirectionality of this relationship. Hypoxia and sleep disruption caused by repetitive upper airway obstruction could activate hormones that trigger pathways generating insulin resistance and abdominal fat accumulation, which in turn could worsen OSA. The review by Lam et al.9 further emphasizes the importance of treating not only coexistent OSA but also encourages appropriate lifestyle changes in order to best manage the metabolic syndrome.
Asthma in obese individuals is becoming increasingly prevalent and presents a significant clinical challenge. These individuals report a worse quality of life, utilize more health-care resources than non-obese asthmatics and have poorer control of asthma symptoms with medications.10 However, the mechanisms linking obesity and asthma remain unclear. As obesity is considered a low-grade inflammatory disorder, pro-inflammatory adipokines in the circulation could induce airway inflammation, although the effect of systemic inflammation on airway function in humans remains unclear. Alternatively, the mechanical effects of obesity favour breathing at lower lung volumes which could promote expiratory flow limitation, airway closure and dynamic hyperinflation.10 These changes could modify airway responsiveness and contribute to respiratory symptoms, and may require a different therapeutic approach compared with usual asthma management.
Obesity hypoventilation syndrome represents the extreme end of the spectrum with respect to respiratory complications from excess weight. The physical, health and social impairments of individuals with obesity hypoventilation syndrome are significantly greater than those experienced by people with obesity or OSA in isolation.6 Despite what could be considered very obvious clinical characteristics of this syndrome (i.e. morbid obesity, respiratory failure and cor pulmonale), individuals may go undiagnosed or misdiagnosed for some time despite frequent contact with primary care providers and repeated hospital admissions. The altered respiratory physiology related to morbid obesity reduces respiratory reserve and increases the likelihood of acute respiratory failure developing in the context of even minor insults such as infection or worsening cardiac function.11 Effective ventilator support is the cornerstone of managing respiratory failure (either acute or chronic) in obesity-related respiratory failure. While non-invasive ventilation is the preferred approach, severe acute respiratory failure may necessitate the use of invasive ventilation. Significant clinical and logistic challenges arise as the body mass index of the patient admitted to an intensive care unit increases. As pointed out in the review by Bahammam and Al-Jawder,11 obese individuals appear to be at greater risk of developing acute lung injury/acute respiratory distress syndrome. While the mechanisms underlying this relationship remain unclear, alterations in inflammatory biomarkers, endothelial dysfunction and oxidative stress that overlap these conditions likely play a role. In the longer term, control of sleep disordered breathing by adherence to positive airway pressure therapy is key to improving clinical outcomes including survival.6 However, inflammatory biomarkers are higher and endothelial dysfunction is more pronounced in obesity hypoventilation syndrome patients compared with those with eucapnic obesity, in keeping with the higher incidence of cardiovascular and metabolic disorders seen in obesity hypoventilation syndrome. Short-term interventional studies have failed to demonstrate significant modification of these inflammatory and atherogenic biomarkers with positive airway pressure therapy, highlighting that effective control of sleep disordered breathing is only one aspect of long-term management and not the complete solution.6
The best option for dealing with obesity epidemic and its impact on respiratory disorders is to prevent or limit the development of obesity in the first place. While many of the mechanisms linking obesity with respiratory abnormalities or aggravating pre-existing respiratory disease are yet to be fully uncovered, weight loss has been shown to be a potent strategy in achieving improvements in pulmonary function,4 dyspnoea, asthma control,10 severity of OSA12 and metabolic syndrome.9 However, most individuals find it difficult to lose weight and keep it off in the longer term. For the obese respiratory patient, this is an even greater challenge. Exertional dyspnoea is common, even in the absence of underlying respiratory disease. This can present a significant obstacle to effective management, not only through misdiagnosis and inappropriate therapy being instituted, but by promoting inactivity, deconditioning and further breathlessness. Obesity levels among participants attending pulmonary rehabilitation programmes are increasing, with these individuals demonstrating poorer functional capacity at baseline compared with normal weight participants.13 Despite this, significant improvements in functional activity and quality of life are achieved with pulmonary rehabilitation in this group.13 Weight limits on some training equipment and mobility issues related to musculoskeletal problems may necessitate modification of physical training programmes for some. Respiratory muscle endurance training and non-invasive ventilation show promise in the very dyspnoeic obese individual in whom usual physical training programmes are unsuitable.14 As the review by Dreher and Kabitz14 highlights, there are a lack of evidence-based recommendations for pulmonary rehabilitation programmes addressing obese clients and little data regarding the effectiveness of such programmes in achieving weight loss. Nevertheless, structured exercise and nutritional programmes need to be considered as a routine part of the management package of obese patients with respiratory disease.
Surgical approaches to weight reduction have been shown not only to produce larger increases in weight loss, but are more likely to sustain this weight loss in the longer term, conferring significant metabolic benefits, reducing sleep apnoea severity, improving symptoms and increasing the time spent physically active.15 In the final review of the series, Schachter12 outlines the various bariatric procedures available and describes the preoperative and postoperative respiratory care these individuals require. In particular, she discusses the management of OSA, emphasizing the need to evaluate residual disease in the follow-up period given that many individuals will still have moderate OSA despite significant weight loss.
Obesity has become the new challenge facing health-care systems around the globe. To meet this challenge, we need a better understanding of the pathways linking obesity and respiratory disorders in order to develop new approaches and novel therapies to tackle the problem. In particular, there is a need for weight loss strategies which are effective, practical and accessible to those limited by respiratory disease. I hope these reviews provide a timely reminder of the effect obesity can have on the respiratory system, the importance of considering excess weight as a cause of respiratory symptoms, as well as a highlighting obesity as a potentially modifiable factor in the management of the patient with respiratory disease.