Tackling a Lifetime of Risk for OSA

Obesity continues to impose a heavy burden on individuals and healthcare systems globally [1], with patterns of inactivity and unhealthy eating often being established in childhood [2]. Similarly, obstructive sleep apnoea (OSA) is increasingly prevalent [3] and has a significant impact on patients' quality of life [4] and the broader economy, through the loss of productivity from daytime somnolence, increased healthcare utilisation due to associated conditions such as hypertension and diabetes, and costs arising from motor vehicle accidents among untreated patients [5]. While obesity has long been established as a major risk factor for the development of OSA, most studies have investigated the association in cross-section, with body mass index (BMI) being measured at a single time point. Few data exist that demonstrate the risk conferred by a trajectory of weight gain over several years during childhood and adolescence or during adulthood. Notably, the Bogalusa study demonstrated the association between the trajectory of obesity during childhood and the prevalence of OSA in middle life, independent of adult BMI [6]; however, the authors did not assess patterns of BMI change in adulthood and their potential influence on the risk of OSA. Similarly, Chan et al. found that increasing BMI from childhood through adolescence was associated with an increased risk of OSA by the age of 20 years [7]. The Wisconsin Sleep Cohort Study noted an increased risk of moderate-to-severe OSA at the age of 50 years among those who had gained weight in the preceding 4 years [8]. What has hitherto been lacking is evidence linking the trajectory of weight gain from childhood and adolescence through early adulthood and middle age with the risk of OSA in middle age. The study of Qian and colleagues, recently published in Respirology, aimed to close that gap [9]. They analysed longitudinally collected BMI data from the age of seven years to middle age (43 years old), in a large prospective cohort of 3609 participants enrolled in the Tasmanian Longitudinal Health Study and sought to establish associations between patterns of weight gain and the risk of OSA at the age of 53 years. They found that those who had initially been of average BMI but increased their BMI over the study period—the child average-increasing group—were at the highest risk of developing probable OSA (according to STOP-BANG criteria) and clinically significant OSA (as assessed by Type 4 sleep studies). This group had normal weight during childhood but increased their BMI in the transition between young adulthood and middle age (20–43 years old) by 10.2 kg/m2, representing an annual rise of 0.44 kg/m2. Unsurprisingly, participants who had persistently high BMI throughout childhood and adulthood into middle age (high trajectory group) were also at higher risk of OSA. However, the child high-decreasing group, that is, those who had high BMI in childhood but whose BMI had a decreasing trajectory into adulthood, were not at higher risk of OSA in middle age, even though this group was overweight on average by the age of 43 years. The prevalence of maternal asthma and maternal smoking was higher in both the child average-increasing and high trajectories, indicating potentially modifiable risk factors. The authors are to be congratulated on this elegant analysis of a large longitudinal cohort that sheds light on an important but understudied area: the influence of BMI changes in adulthood into middle age on OSA risk. They acknowledge the limitations of the study, most prominently the use of the STOP-BANG tool to define probable OSA when the score itself includes BMI as a component, although the authors state the conclusions remained unchanged when subjects with BMI > 35 kg/m2 were removed from the analysis. The study population was almost exclusively white Caucasian, so the generalizability of the results is limited. Finally, only a minority of participants had a diagnosis of clinically significant OSA confirmed, not by gold standard polysomnography, but by 3% oxygen desaturation criteria. Nonetheless, the important message that the study of Qian and colleagues conveys is that the development of OSA in a child who is overweight is not inevitable if subsequent weight loss occurs. Furthermore, while persistently high BMI is a clear risk factor for OSA in middle age, the greatest risk is conferred on those who gain substantial amounts of weight into adulthood. This study adds weight to the ongoing calls to increase investment in public health and education measures [5] to promote healthy eating and physical activity, targeting in particular weight gain in the transition between early adulthood and middle age. It provides a clear rationale for closer monitoring of BMI in the community setting and early intervention to prevent excessive weight gain during this crucial period, as well as timely diagnosis and effective treatment of emergent OSA. With the advent of proven pharmacological therapies to prevent weight gain [10], it may be that judicious prescription of these agents at an early stage may prevent the onset of many of the comorbid conditions associated with obesity, including OSA. The authors declare no conflicts of interest. This publication is linked to a related article. To view this article, visit https://doi.org/10.1111/resp.70002.