Can obstructive sleep apnea (OSA) cause insomnia in adult patients, particularly those with a higher body mass index (BMI) or comorbid conditions such as hypertension or diabetes?

Does Obstructive Sleep Apnea Cause Insomnia?

Yes, obstructive sleep apnea can cause insomnia, and this comorbid condition (termed COMISA - comorbid insomnia and sleep apnea) is clinically significant, occurring in approximately 6.4% of OSA patients and associated with worse cardiovascular outcomes than OSA alone. 1

Recognition of OSA-Related Insomnia

The American Academy of Sleep Medicine explicitly recognizes that comorbid insomnia is a frequent problem in patients with OSA, and when OSA is suspected, a comprehensive sleep evaluation must address both OSA and other comorbid sleep complaints. 2 This is not coincidental—the pathophysiology of OSA directly contributes to insomnia symptoms through multiple mechanisms:

Clinical Presentation

A comprehensive sleep history in suspected OSA patients should specifically evaluate for sleep fragmentation and sleep maintenance insomnia as core symptoms, alongside snoring, witnessed apneas, gasping/choking episodes, excessive sleepiness, nocturia, morning headaches, and decreased concentration. 2

The insomnia in OSA patients manifests as:

• Difficulty maintaining sleep (sleep maintenance insomnia) due to repetitive arousals from apneic events 2
• Nocturnal awakenings with gasping or choking sensations 2
• Sleep fragmentation from respiratory effort-related arousals (RERAs) and cortical arousals associated with hypopneas 2

Cardiovascular and Metabolic Significance

The combination of OSA with insomnia (OSA+Insomnia) carries significantly worse cardiovascular risk than OSA alone, with essential hypertension occurring 1.83 times more frequently (OR=1.83,95% CI 1.27-2.65) in OSA+Insomnia versus OSA without insomnia. 1 Additionally, cerebrovascular disease risk may be substantially elevated (OR=6.58,95% CI 1.66-26.08), though this requires further validation. 1

The COMISA phenotype based on sleep breathing impairment index (COMISA-SBII) predicts incident diabetes (HR=1.82,95% CI 1.15-2.89) after adjusting for demographic characteristics, comorbidities, and behavioral risk factors, whereas COMISA defined by AHI alone does not show this association. 3 This suggests the insomnia component contributes independently to metabolic dysfunction beyond the apnea-hypopnea index.

Pathophysiologic Mechanisms

OSA causes insomnia through several interconnected pathways:

• Repetitive hypoxemia during apneic episodes triggers oxidative stress and autonomic dysregulation 4
• Autonomic nervous system dysregulation with surges in sympathetic activity and blood pressure fluctuations during arousal from apnea 4
• Intrathoracic pressure swings that alter cardiac loading conditions and fragment sleep architecture 4
• Systemic inflammation and endothelial dysfunction that promote both cardiovascular disease and sleep disruption 4

Clinical Implications for High-Risk Populations

Patients with higher BMI and comorbid conditions (hypertension, diabetes) have substantially elevated OSA prevalence, reaching 56-70% in obese individuals, with obesity being the strongest modifiable risk factor for OSA development. 5 In these populations:

• OSA prevalence in hypertensive patients approaches 60%, particularly in those with resistant hypertension 5
• Chronic intermittent hypoxia from OSA worsens insulin resistance, creating a vicious cycle with obesity and diabetes 5
• The metabolic syndrome components cluster with OSA, requiring assessment of fasting glucose, HbA1c, and lipid panels 5

Diagnostic Approach

Polysomnography remains the reference standard for diagnosing OSA, with diagnostic criteria requiring either:

• Obstructive RDI ≥5 events/hour with typical symptoms (unrefreshing sleep, daytime sleepiness, fatigue, insomnia, awakening with gasping/choking, loud snoring, or witnessed apneas), OR
• Obstructive RDI ≥15 events/hour even without symptoms 2

The RDI includes not only apneas and hypopneas (which comprise the AHI) but also respiratory effort-related arousals (RERAs), which are particularly relevant to insomnia symptoms as they cause sleep fragmentation without meeting criteria for apneas or hypopneas. 2

Treatment Considerations

CPAP therapy addresses both the OSA and associated insomnia symptoms by eliminating respiratory events and sleep fragmentation. 6 However, treatment adherence is critical:

• CPAP use of ≥4 hours per night reduces cardiovascular events from 11.02 to 7.90 events per 100 person-years 6
• Immediate intervention with mask adjustment or pressure modification prevents treatment failure when adherence problems emerge 6
• Weight loss improves OSA severity, hypertension, and insulin resistance in obese patients with COMISA 5

Common Pitfalls

Avoid attributing insomnia solely to psychiatric causes without screening for OSA, particularly in patients with obesity (BMI >30 kg/m²), neck circumference >17 inches (men) or >16 inches (women), hypertension, or diabetes. 2 The American Heart Association recommends screening for OSA in all hypertensive patients, as up to 60% of resistant hypertension has underlying OSA. 5

Do not rely on the absence of excessive daytime sleepiness to rule out OSA—insomnia symptoms may be the predominant complaint, and the COMISA phenotype may present differently than classic OSA. 1