Asthma is a heterogeneous chronic airway disorder affecting over 300 million people worldwide, characterized by airway inflammation, variable airflow limitation, and symptoms that often worsen at night [1]. Obstructive sleep apnea (OSA) is a sleep-related breathing disorder defined by recurrent upper-airway collapse during sleep, leading to intermittent hypoxia, sleep fragmentation, and excessive daytime sleepiness [2]. The “asthma–OSA overlap” has emerged as a clinically relevant phenotype, particularly among patients with severe or difficult-to-control asthma [3]. To move beyond mere descriptive epidemiology, this review establishes an original conceptual framework that bridges the gap between raw statistical correlation and definitive causation. By synthesizing epidemiologic associations, plausible mechanistic links, clinical consequences, and management strategies, we explicitly grade the current literature (preclinical vs. observational vs. interventional) to expose gaps in bidirectional evidence and prevent clinical over-extrapolation.

Observational studies and meta-analyses report an increased risk of OSA among people with asthma, with a prevalence ranging from 20% to > 60%, depending heavily on asthma severity, diagnostic criteria, and study setting [3–9] (Table 1). However, a critical methodological caveat must be raised: much of the existing large-scale data relies on screening questionnaires (e.g., STOP-Bang) [10] or retrospective international classification of diseases (ICD) administrative billing codes. These methods carry inherent selection and misclassification biases that inherently obscure causal directionality.

While longitudinal cohort data—such as the Wisconsin Sleep Cohort—demonstrate that asthma significantly predicts incident OSA over time [4], the reverse timeline (OSA driving incident asthma) remains epidemiologically less robust and relies heavily on unadjusted confounding factors like progressive weight gain [9]. Robust prospective cohorts utilizing baseline and serial gold-standard polysomnography (PSG) combined with standardized, objective asthma phenotyping are fundamentally required to transform these observed associations into confirmed chronological vectors [11, 12].

Shared modifiable risk factors and comorbidities linking asthma and OSA are summarised in Table 2, with the mechanistic bridges illustrated in Figure 1.

To address previous fragmentation in the literature, we propose a three-domain integrated model where mechanical, inflammatory/immunologic, and metabolic/neuroreflex pathways do not operate in isolation, but rather form an interlocking, self-amplifying pathological loop (Figure 2).

The asthma-OSA overlap syndrome produces a severe clinical burden, characterized by significantly poorer asthma control, higher rates of frequent asthma exacerbations, heightened nocturnal awakenings, worse health-related quality of life, and substantially elevated rates of emergency department visits and hospitalizations [41–44]. A critical challenge in daily clinical practice is the profound symptomatic overlap between the two disorders, which frequently leads to the underrecognition and underdiagnosis of OSA in asthmatic cohorts. Symptoms such as profound morning fatigue, unrefreshing sleep, daytime sleepiness, and impaired cognitive concentration are frequently misattributed by both clinicians and patients to poorly controlled asthma or the side effects of high-dose respiratory medications [45]. Conversely, frequent nocturnal asthma awakenings can mask underlying micro-arousals caused by repetitive upper airway collapses [46]. To systematically address this diagnostic blind spot, clinicians should maintain a highly vigilant, low threshold for comprehensive sleep evaluation. Validated screening tools, such as the STOP-Bang questionnaire [10], should be routinely integrated into the standard care workflow for any patient presenting with difficult-to-treat or severe asthma, particularly those with prominent nocturnal symptoms or persistent daytime impairment.

When managing the overlap phenotype, clinicians must carefully consider how standard asthma medications interact with underlying upper airway stability. Prolonged exposure to systemic corticosteroids and high-dose inhaled corticosteroids (ICS) is associated with an elevated risk and increased severity of OSA [47, 48]. The primary proposed mechanisms driving this risk include steroid-induced localized fat deposition in the pharyngeal tissues, localized myopathy of the upper airway dilator muscles, and altered pharyngeal sensory function [47]. However, a major confounding by indication exists: patients requiring high-dose steroids inherently possess more severe, poorly controlled asthma, which independently impairs sleep architecture and upper airway patency [49]. Biologic therapies targeting Type 2 (T2) high inflammation (e.g., anti-IgE, anti-IL5/R, anti-IL4/Rα) have transformed the management of severe asthma, significantly reducing exacerbation rates and systemic steroid requirements [50]. While these agents, such as dupilumab, frequently improve subjective sleep quality by eliminating nocturnal asthma symptoms [51], robust clinical evidence proving a direct, independent reduction in objective OSA severity parameters (such as AHI) remains limited [52].

Optimizing outcomes in the asthma-OSA overlap requires a coordinated, dual treatment approach that simultaneously targets the unique requirements of both underlying respiratory diseases while aggressively managing shared treatable traits (Table 3; Figure 3).

To transition the field from association to definitive precision medicine, the following five research priorities are established:

Mechanistically-informed prospective cohorts: Longitudinal studies tracking patients with severe asthma using baseline and serial objective PSG, coupled with deep molecular phenotyping and inflammatory biomarker panels (e.g., systemic and induced sputum cytokines) to chart the exact temporal and causal relationships governing the overlap phenotype over time.

The asthma-OSA overlap constitutes a clinically important, multifactorial phenotype with clear consequences for disease control, exacerbation risk, and health-care utilization [3, 59]. Current evidence supports a model in which mechanical (upper-airway collapse and intrathoracic pressure swings), inflammatory (intermittent hypoxia–driven systemic and airway inflammation), and metabolic/neuroreflex (obesity-related adipokine and insulin-resistance pathways) mechanisms interact to amplify both nocturnal respiratory instability and lower-airway disease activity. Furthermore, a recent study unveils shared genetic mechanisms associated with OSA and asthma risks, highlighting complex interactions between pathways governing immune response and inflammation [60]. However, the preponderance of cross-sectional and observational data, often derived from imperfect screening tools or administrative sources, precludes definitive causal inferences at the population level. Clinically, the overlap should be approached as a treatable, multidimensional syndrome. Routine, low-threshold screening for sleep-disordered breathing in patients with difficult-to-control or severe asthma is warranted (e.g., STOP-Bang, ESS), followed by objective diagnostic testing (PSG) when indicated. Management must be integrated and two-pronged: (1) targeted therapy for OSA (optimised CPAP or alternative device therapy, ENT management where appropriate) to remove the mechanical trigger of nocturnal bronchospasm and intermittent hypoxia; and (2) rigorous optimization of asthma care (inhaler technique and adherence, steroidsparing strategies including biologics where appropriate, and management of comorbidities). Parallel attention to shared, modifiable drivers—most notably obesity and GERD—should be standard practice, and metabolic interventions (including structured weight-loss programmes and GLP-1-based therapies) are promising adjuncts that require respiratory-focused randomized evaluation. Research priorities must shift from association mapping to mechanism-driven trials and longitudinal phenotyping. Highquality prospective cohorts that combine serial gold-standard sleep testing with deep molecular airway profiling, and adequately powered interventional RCTs (including CPAP vs. sham, bariatric/metabolic therapy trials, and mechanistic studies of biologics on objective sleep and airway endpoints) are essential to establish causality and to identify the subgroups most likely to benefit from specific interventions. Finally, integration of novel home-based sleep monitoring and digital phenotyping will be pivotal to scale screening and personalise care in real-world settings.

In sum, acknowledging and actively managing the asthma-OSA overlap offers a tangible opportunity to improve outcomes through coordinated, mechanism-aware care. Translating this promise into practice will require multidisciplinary clinical pathways, stratified interventional trials with objective respiratory endpoints, and routine incorporation of sleep assessment into severe asthma workflows.