Obstructive Sleep Apnea in Psychiatric Practice: An Overlooked, Treatable Comorbidity

Abstract

Obstructive sleep apnea (OSA) is a sleep-related breathing disorder characterized by recurrent upper-airway obstruction during sleep, resulting in apnea or hypopnea, intermittent hypoxemia, sleep fragmentation, and fluctuations in intrathoracic pressure. OSA is highly prevalent in the general population; when mild disease is included, it is estimated to affect approximately 9%–38% of adults [1]. Common manifestations include habitual snoring, witnessed apneas, gasping or choking during sleep, nocturia, morning headache, dry mouth, excessive daytime sleepiness, fatigue, impaired concentration, and non-restorative sleep.

Untreated OSA is associated with hypertension, atrial fibrillation, stroke, coronary artery disease, metabolic abnormalities, obesity, accident risk, and cognitive impairment [2-4]. Intermittent hypoxia, sleep fragmentation, sympathetic activation, oxidative stress, and inflammatory responses have all been implicated in the cardiovascular and metabolic consequences of OSA. However, the extent to which these biological mechanisms contribute directly to the onset, persistence, or exacerbation of psychiatric symptoms remains insufficiently understood.

In this issue, Sommerhoff et al. report a timely systematic review and meta-analysis examining the prevalence of OSA in individuals with schizophrenia, bipolar disorder, and major depressive disorder [5]. Their review included 55 studies in the systematic review, of which 47 were included in the meta-analysis. The importance of this work lies not only in quantifying the frequency of OSA and elevated OSA risk in these populations, but also in highlighting a practical clinical message: sleep-disordered breathing should be routinely considered as part of comprehensive assessment in people with severe mental illness.

Importantly, these findings should not be interpreted as demonstrating that OSA causes psychiatric disorders, or conversely that psychiatric disorders cause OSA. Much of the available evidence derives from cross-sectional observational studies, and the temporal and causal relationships remain uncertain. The association between OSA and psychiatric disorders is likely to be influenced by multiple shared factors, including obesity, age, sex, smoking, alcohol use, diabetes, cardiovascular disease, lifestyle factors, and the effects of psychotropic medications.

Nevertheless, uncertainty regarding causality does not diminish the importance of detecting and treating OSA. Hypertension, atrial fibrillation, stroke, coronary artery disease, metabolic disorders, accident risk, and cognitive impairment—conditions associated with OSA—are already disproportionately common among people with severe mental illness. These physical health inequalities contribute substantially to the marked excess mortality observed in this population [6, 7]. Identifying a treatable sleep-related breathing disorder may therefore offer an important opportunity to improve sleep, daytime functioning, and cardiometabolic health.

A major challenge in psychiatric practice is symptom overlap and the resulting diagnostic blind spots. Fatigue, low energy, reduced concentration, psychomotor slowing, irritability, reduced motivation, memory difficulties, and sleep disturbance may readily be attributed to depression, schizophrenia, bipolar disorder, medication-related sedation, physical illness, or psychosocial stressors.

Monitoring sleep is essential in schizophrenia, bipolar disorder, and major depressive disorder, including for the prevention of relapse and recurrence. However, fragmented sleep, non-restorative sleep, daytime sleepiness, and cognitive complaints should not automatically be regarded as psychiatric symptoms alone. They may also signal the presence of OSA. In schizophrenia in particular, negative symptoms, cognitive impairment, social isolation, and treatment with sedating medications may obscure daytime sleepiness and reduced motivation related to sleep-disordered breathing.

Psychotropic medications may further complicate this clinical picture. Some antipsychotics and mood stabilizers are associated with weight gain and metabolic abnormalities, potentially increasing the risk of OSA indirectly [8, 9]. Sedating medications may also affect arousal responses, respiratory physiology, or patients' awareness of daytime sleepiness. However, the association between OSA and psychiatric illness cannot be reduced simply to medication exposure. Weight trajectory, physical comorbidities, lifestyle, illness stage, symptom severity, and treatment regimen should all be considered in the individual patient.

The relationship between OSA, obesity, and metabolic dysfunction is also complex and potentially bidirectional. Obesity is an important risk factor for OSA, whereas sleep fragmentation and impaired daytime functioning may adversely affect physical activity, eating behavior, and weight management. OSA can occur in patients without marked obesity, including younger adults. Body mass index (BMI) alone should therefore not be used to exclude OSA.

The prevalence estimates reported by Sommerhoff et al. also require careful clinical interpretation. Estimates of OSA prevalence may differ substantially according to the study population, recruitment setting, psychiatric diagnostic criteria, definition of OSA, and assessment method. Studies conducted in sleep clinics, psychiatric inpatient wards, community services, and specialist outpatient settings are likely to identify populations with differing levels of risk.

Questionnaire-based screening tools identify individuals at elevated risk; they do not establish an OSA diagnosis. Polysomnography (PSG) remains the reference standard for diagnostic assessment. However, home sleep apnea testing may be an accessible and practical alternative for selected adults with a high pre-test probability of uncomplicated moderate-to-severe OSA [10, 11]. The choice of assessment should be individualized, taking account of coexisting sleep disorders, medical comorbidities, cognitive difficulties, living circumstances, and the practical support needed to complete testing.

Such heterogeneity should not be used as a reason to dismiss the relevance of OSA in psychiatric populations. Rather, it emphasizes the need to interpret prevalence estimates within their clinical context and to conduct better standardized studies.

In routine psychiatric practice, the relevant question is not whether every person with schizophrenia, bipolar disorder, or major depressive disorder should undergo PSG. Universal PSG testing would neither be feasible nor necessary. A more useful question is whether psychiatric services routinely identify patients whose symptoms and risk profile warrant further evaluation. In many settings, the answer is still likely to be no.

A brief but sensitive OSA-focused assessment can be incorporated into routine psychiatric consultations. Clinicians should ask about habitual snoring, witnessed apneas, gasping or choking during sleep, nocturia, morning headaches, dry mouth on waking, non-restorative sleep, and unintended daytime dozing. Information from a partner, family member, caregiver, or—in inpatient settings—a roommate may be particularly valuable.

Assessment should also include BMI and, where possible, neck circumference, blood pressure, diabetes and cardiovascular disease, smoking and alcohol use, and treatment with sedative medications. The Epworth Sleepiness Scale (ESS) and STOP-Bang questionnaire can assist case-finding, but neither should be used as a substitute for diagnostic testing [12, 13]. Crucially, the absence of a strong subjective complaint of sleepiness should not exclude OSA. Some patients may normalize chronic fatigue, mask symptoms with caffeine or stimulant medication, or have difficulty recognizing and communicating their symptoms.

Clear referral pathways are essential. Where OSA is suspected, psychiatrists should be able to refer patients efficiently to primary care, sleep medicine, or respiratory services for appropriate assessment. Conversely, sleep clinicians should consider psychiatric symptoms, psychotropic medication use, cognitive impairment, social support, and the practical barriers that may affect diagnostic completion and treatment continuation. The most effective model is likely to be collaborative rather than sequential: sleep medicine and psychiatric care should not function as isolated systems.

Although effective treatment is available, implementation matters. Continuous positive airway pressure (CPAP) is the standard treatment for moderate-to-severe OSA and, in appropriately selected patients, improves respiratory outcomes, daytime sleepiness, and quality of life [14]. Other treatment options include weight management, positional therapy, oral appliances for suitable patients, treatment of nasal obstruction, and surgical approaches in selected circumstances [10, 15]. Management should be individualized according to OSA severity, anatomical factors, comorbidities, patient preferences, and living circumstances.

The assumption that people with severe mental illness cannot accept or manage CPAP should be challenged. Cognitive impairment, anxiety, sensory sensitivity, unstable housing, financial difficulties, stigma, and limited social support may affect treatment initiation and adherence. However, such barriers are not unique to psychiatric populations, nor are they necessarily insurmountable.

Early education, careful mask fitting, gradual acclimatization, behavioral support, involvement of family members or caregivers where appropriate, and close follow-up can make a substantial difference. Psychiatric teams are particularly well-placed to identify and address factors that may interfere with adherence.

Further research is needed to clarify the effects of OSA treatment on psychiatric outcomes. CPAP is not a first-line treatment for schizophrenia, bipolar disorder, or major depressive disorder itself. Nevertheless, treating OSA may reduce sleep fragmentation, fatigue, cognitive complaints, and the physiological burden that can amplify cardiometabolic risk. Even modest improvements may be clinically meaningful in a population with high rates of obesity, diabetes, cardiovascular disease, and premature mortality [6, 7].

Looking ahead, several research priorities remain. The work of Sommerhoff et al. demonstrates both the importance of this topic and the limitations of the current evidence base. Future studies should use standardized definitions and assessment methods for OSA, clearly distinguish screening-defined high risk from objectively confirmed OSA, and report findings separately by psychiatric diagnosis, age, sex, BMI, neck circumference, psychotropic medication use, duration and stage of illness, symptom severity, physical comorbidity, and treatment setting.

Prospective longitudinal studies are particularly needed to clarify temporal and causal relationships. Does OSA contribute to the onset or recurrence of depressive episodes? Does it influence mood instability in bipolar disorder, or cognitive and negative symptoms in schizophrenia? Can OSA treatment improve psychiatric symptoms, cognitive function, hospitalization rates, and cardiometabolic outcomes? What approaches most effectively support diagnostic completion and sustained CPAP use among people with severe mental illness?

Equity should also be central to this research agenda. The geographical distribution of the studies summarized by Sommerhoff et al. was uneven, with limited evidence from Africa and no evidence from Oceania. Future work should include more diverse populations and healthcare systems, especially in regions where access to sleep diagnostics and treatment remains limited.

In conclusion, OSA is common, clinically consequential, and treatable. In people with schizophrenia, bipolar disorder, and major depressive disorder, it may be overlooked because of symptom overlap, psychotropic medication effects, physical comorbidity, and fragmented models of care.

The systematic review and meta-analysis by Sommerhoff et al. should encourage psychiatric clinicians to look beyond insomnia and sleep duration and to ask a more fundamental question: “Is this patient breathing normally during sleep?”

Recognizing OSA will not resolve every psychiatric or medical problem. However, failing to recognize it may leave a treatable contributor to poor health and functional impairment unaddressed. Incorporating case-finding, appropriate referral, and collaboration between psychiatric and sleep services into routine mental healthcare is a practical and important step toward more comprehensive and equitable psychiatry care.

The author has nothing to report.

The author declares no conflicts of interest.

Data sharing not applicable to this article as no datasets were generated or analyzed for this editorial.