The effect of zolpidem on sleep efficiency and obstructive sleep apnea severity in OSA patients: A systematic review and meta‑analysis

Abstract

Background:

Insomnia and obstructive sleep apnea (OSA) comorbidity is prevalent and leads to worse outcomes. While zolpidem may improve sleep in OSA, existing trials report inconsistent results on safety and efficacy. We aimed to perform a meta-analysis to systematically evaluate the effect of zolpidem in OSA patients.

Methods:

We systematically searched PubMed, Medline, Embase, Cochrane’s Library, Web of Science, and other online sources for related trials. Data were pooled using a random-effects model, and mean differences with 95% confidence intervals were calculated. The effects of zolpidem on sleep efficiency and severity of sleep apnea were analyzed.

Results:

5 controlled trials (4 randomized and 1 nonrandomized) were included. All studies claimed all participants were diagnosed with OSA. Treatment with zolpidem significantly improved total sleep time compared to placebo or no-drug (MD: 0.78, 95% confidence interval: 0.19–1.37, P = .009; I² = 38%). However, zolpidem did not alter OSA severity as shown by no systematic changes in the Apnea-Hypopnea Index (AHI). Total AHI, supine AHI, and AHI during non-rapid eye movement sleep or rapid eye movement sleep were unaltered on the drug night compared to the control group. Next-day sleepiness was measured in 4 studies, and the results showed no statistical difference, indicating that zolpidem was generally well tolerated with no major adverse events.

Conclusions:

Zolpidem can substantially increase sleep duration in OSA patients without worsening AHI or overnight hypoxemia, and appears well-tolerated without a next-day hangover. These findings are limited by the small number of studies, small sample sizes, and short-term nature of interventions. Further large-scale RCTs are warranted to confirm long-term safety and efficacy.

1. Introduction

Obstructive sleep apnea (OSA) is a sleep condition characterized by recurrent upper airway obstruction during sleep, resulting in periodic low oxygen levels and disrupted sleep. This condition is associated with a variety of negative health effects, such as heart diseases, metabolic disorders, and cognitive impairment.^[1-3] The incidence of OSA is increasing; nearly 1 billion adults aged 30 to 69 years worldwide have OSA, with approximately 425 million experiencing moderate-to-severe disease.^[4] Insomnia and OSA often coexist, a condition known as comorbid insomnia and sleep apnea (COMISA), which was formalized by Sweetman et al in 2017.^[5] Epidemiological studies indicate that approximately 30% to 50% of OSA patients have significant insomnia symptoms, and 30% to 40% of chronic insomnia patients meet the diagnostic criteria for OSA.^[6]

Insomnia and OSA often interact to amplify an overall greater illness severity. Many researchers suggest that the presence of insomnia symptoms reduces continuous positive airway ventilation (CPAP) acceptance, as a result leading to a worse outcome and higher management costs than the separate condition.^[7] On the contrary, the improvement of sleep quality in OSA patients has cardiovascular benefits. Thus, hypnotics are widely used, and they are vitally important for OSA patients. However, hypnotic use is not recommended due to concerns of worsening OSA via pharyngeal muscle relaxation, increased apnea duration, and hypoxemia. Nevertheless, human data are lacking. Increasing the arousal threshold with hypnotics may stabilize breathing and reduce OSA severity. However, studies conducted to date on the use of hypnotics in OSA patients have yielded mixed results. Some studies demonstrated that hypnotics, especially nonbenzodiazepine sedative-hypnotics (NBSH), can improve respiratory arousal thresholds and reduce the Apnea-Hypopnea Index (AHI).^[8,9] Nevertheless, some studies found that there was no systemic change in OSA severity.^[10,11]

Zolpidem is among the most commonly prescribed NBSHs for sleep complaints.^[12] Its potential mechanistic advantages in OSA are of particular interest. A physiological study has shown that zolpidem increases the threshold of respiratory arousal, and paradoxically, it also increases the reactivity of the congenital tongue muscle during airway stenosis; zolpidem increased median muscle responsiveness 3-fold during airway narrowing.^[13] While direct translation of these mechanistic findings from animal models to human clinical outcomes requires cautious interpretation, this unique dual action on both neural respiratory drive and muscle function suggests a theoretical benefit over other hypnotics that primarily exert sedative effects. However, the net effect of zolpidem on OSA severity – whether it improves, stabilizes, or worsens the condition – remains unclear due to contradictory results across existing controlled trials.

Therefore, to synthesize the current evidence, we aimed to perform an updated meta-analysis of controlled trials to evaluate the effects of zolpidem on both sleep efficiency (e.g., total sleep time) and OSA severity (e.g., AHI) in patients with OSA. We hypothesized that zolpidem would improve sleep efficiency without adversely affecting key metrics of OSA severity. This analysis was not preregistered in a public repository. To mitigate potential biases, we adhered strictly to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guideline,^[14] employed a comprehensive search strategy across multiple databases, and performed study selection, data extraction, and risk-of-bias assessment in duplicate.

2. Materials and methods

PubMed, Medline, Embase, the Cochrane Library (Cochrane Center Register of Controlled Trials), and the Web of Science were systematically searched for relevant controlled trials from their inception until March 11, 2024, which was the uniform search date applied to all databases. The search strategy was designed and executed by an experienced medical librarian. No language restrictions were applied during the search; however, only articles published in English were eligible for inclusion due to practical constraints in translation and resources. To identify unpublished and ongoing studies, we systematically searched gray literature sources including ClinicalTrials.gov, WHO International Clinical Trials Registry Platform, ProQuest Dissertations & Theses Global, and OpenGrey. We further performed manual backward citation tracking of the reference lists of all included studies and relevant review articles. The complete search strategy, including all specific terms, syntax, and filters used for each database, is provided in Supplementary Material 1, Supplemental Digital Content 1 to ensure full reproducibility. This study is a secondary analysis of a published literature-based systematic review and meta-analysis, and formal ethical approval from an ethics committee or institutional review board was not required. All original included trials completed ethical review and obtained informed consent from all enrolled participants before implementation, which was clearly stated in the original published articles. We did not collect individual private patient data, and all analyses were performed based on publicly available aggregated clinical data.

2.1. Inclusion criteria

• (1)Designed as controlled trials (both randomized and non-randomized) that evaluated the effect of zolpidem on AHI of OSA patients (diagnosed with OSA, defined by AHI ≥ 5 events/h).
• (2)Studies that compared patients administered zolpidem to a control group (placebo or no drug) and reported the subsequent AHI.
• (3)Sleep studies (polysomnography) conducted in-lab or at home to determine AHI.

2.2. Exclusion criteria

• (1)Studies that did not report AHI values quantitatively or qualitatively.
• (2)Studies where interventions involved hypnotics other than, or in addition to, zolpidem.
• (3)Studies conducted on pediatric populations or pregnant women.

Both parallel-group and crossover trials were eligible for inclusion. For crossover trials, we planned to extract data from the first period only to avoid potential carryover effects, if such data were available. If only combined data from both periods were reported, they were included and the potential for carryover was acknowledged as a limitation. Our search did not identify any multi-arm trials; had any been found, we would have combined all relevant experimental arms into a single group or compared them against a common control group as recommended by the Cochrane Handbook.

2.3. Literature screening and data extraction

Literature screening and data extraction were performed independently by 2 investigators using a pre-piloted, standardized form. Any discrepancies during either process were resolved through discussion or or, if necessary, by adjudication from a third reviewer. The extracted data included: first author, publication year, study design (noting whether parallel or crossover), sample size, patient baseline characteristics (age, sex, BMI, baseline AHI), intervention details (zolpidem dosage, control type), and all prespecified outcomes. For studies with missing or unclear data, we attempted to contact the corresponding authors via email to request the required information. Continuous outcomes were extracted as mean and standard deviation. If these were not reported, we calculated them from median, interquartile range, standard error, or 95% CIs using established conversion methods outlined in the Cochrane Handbook.^[15] The use of these transformations was necessary to include all relevant studies in the meta-analysis and ensure data uniformity; we acknowledge this as a potential source of uncertainty. Sensitivity analyses were planned to examine the impact of these converted data on the overall pooled estimates, but were not performed due to the limited number of studies (<10) ultimately included.

2.4. Quality assessment

The methodological quality of the included studies was assessed independently by 2 reviewers using the Cochrane Risk of Bias tool for controlled trials. The tool evaluates 7 domains: random sequence generation, allocation concealment, blinding of participants and personnel, blinding of outcome assessment, incomplete outcome data, selective reporting, and other sources of bias. Each domain was judged as having a “low,” “high,” or “unclear” risk of bias.

Disagreements in risk-of-bias assessments were resolved by consensus or by consultation with a third reviewer. Inter-rater agreement for risk-of-bias judgments was calculated using Cohen’s Kappa statistic (κ = 0.85, indicating strong agreement). The overall risk of bias for each study was considered when interpreting the results, and a sensitivity analysis was planned, which involved sequentially excluding studies with a high risk of bias to assess the robustness of the primary meta-analysis results.

2.5. Outcome measures

The primary outcome was the change in the AHI, which was selected as it is the standard, most widely reported metric for defining OSA severity and evaluating treatment efficacy in clinical trials. Secondary outcomes included:

• Sleep architecture: Measured by polysomnography-derived total sleep time, sleep onset latency, wake after sleep onset, and sleep efficiency. Actigraphy-derived measures were not included.

• Other respiratory parameters: arousal index, respiratory event duration, and nadir oxygen saturation during sleep.

2.6. Statistical analysis

For continuous outcomes, the mean difference with a 95% confidence interval (CI) was used for meta-analysis when outcomes were measured on the same scale (e.g., total sleep time in minutes). The Standardized mean difference was used for outcomes where different scales or measurements were anticipated across studies. Statistical heterogeneity among studies was assessed using the I-squared (I²) statistic and the chi-squared test. An I² value >50% was considered to represent substantial heterogeneity. Due to the anticipated clinical and methodological diversity among the included studies, a random-effects model (DerSimonian–Laird method) was used for all meta-analyses. All statistical analyses were performed using Review Manager (RevMan) software, version 5.4.1 (The Cochrane Collaboration, 2020), using the generic inverse-variance method for all pooled estimates.

3. Results

3.1. Database searching

The flowchart of the literature search is presented in Figure 1. A total of 544 studies were identified via an initial database search; 142 studies were excluded after duplicates were removed, and 376 studies were excluded after reading titles and abstracts because of their irrelevance. Of the remaining 26 studies that underwent full-text review, 21 were further excluded for the reasons listed in Figure 1. Finally, 5 controlled trials^[16-20] were included in the meta-analysis, with a total of 107 unique participants (cross-over trials adopted a self-control design; 1 parallel-group trial had 24 participants in the zolpidem group and 24 in the control group; Table 1).

Figure 1.

Preferred reporting items for systematic reviews and meta-analyses flowchart showing the search strategy.

Table 1.

Characteristics of the included studies.

Study	Country	Years	Type	Including criteria	Dose of zolpidem (mg)	Control drug	Intervention duration (d)	Washout time	Combination therapy	Group	Simple	Age (yr)	Female n (%)	BMI (kg/m2)
Ludovico Messineo	Australia	2021	RCT	AHI > 10	10	Placebo	1	1 wk	Ato-oxy	Zolpidem/control	12	55 ± 14	2 (16.7)	27 ± 5
Ludovico Messineo	Australia	2020	RCT	AHI > 10	10	Placebo	1	1 wk	None	Zolpidem/control	19	47 ± 12	2 (10.5)	29 ± 5
Jayne C Carberry	Australia	2019	CT	AHI > 10	10	No-drug	1	<5 mo	None	Zolpidem/control	12	48 ± 14	1 (8.3)	27 ± 5
David A Bradshaw	The United States	2006	RCT	AHI > 5	10	Placebo	14	None	None	Zolpidem control	24 24	40 ± 5 36 ± 5	0 (0) 0 (0)	32 ± 5 30 ± 5
Richard B Berry	The United States	2006	RCT	AHI > 30	10	Placebo	7	0 d	CPAP	Zolpidem/control	16	49 ± 12	2 (12.5)	36 ± 5

AHI = Apnea-Hypopnea Index, BMI = body mass index, CPAP = continuous positive airway pressure, CT = controlled trial, d = day, RCT = randomized controlled trial.

3.2. Description of the trials included in this study

The characteristics of the included studies and their participants are summarized in Table 1. Four of the 5 included trials adopted a crossover design, and 1 used a parallel-group design.^[19] In crossover studies, the data were analyzed using 2-tailed paired Student’s t tests or a Wilcoxon signed-rank test as appropriate. Four trials were randomized double-blind cross-over studies, and 1 was an open-labelpilot controlled trial.^[18] The mean age of participants ranged between 36 and 55 years. Data on body mass index (BMI) were all recorded. Trial populations were overweight or clinically obese, with mean BMIs ranging from 27 kg/m² to 36 kg/m². All participants had OSA confirmed by full polysomnography, and the severity of OSA was evidenced by AHI. Three studies enrolled OSA patients with AHI > 10 events/h, while 1 study recruited OSA patients with AHI > 5 events/h¹⁹ and the remaining study recruited participants with severe OSA (AHI > 30 events/h).^[20] All participants in 1 study were treated with CPAP, including during the study night.^[20] The dose of zolpidem in all studies was 10 mg. The intervention duration was 1 day in 3 studies, 7 days in 1 study (Berry 2006), and 14 days in 1 study (Bradshaw 2006).^[19] A total of 4 different studies on zolpidem were compared with placebo. All studies reported the effects of zolpidem on at least some measurements of sleep-disordered breathing (namely, AHI; arousal index; event duration; and oxygen saturation during sleep). In addition, 4 studies reported outcomes of symptoms on the sleepiness scale. The demographic characteristics, inclusion criteria, intervention details, and reported outcomes of each clinical trial participant are provided in Supplementary Material 2, Supplemental Digital Content 2.

3.3. Quality evaluation

The details of quality evaluation in each domain of Cochrane’s Risk of Bias Tool are listed in Figures 2 and 3. Overall, the quality of the included controlled trials was relatively high. Performance bias (blinding of participants and personnel) was judged as low risk in 4 studies and high risk in 1 open-label study. Detection bias (blinding of outcome assessment) was rated as low risk in 4 studies. All randomly assigned participants in the included studies completed the intervention, resulting in a low risk of attrition bias. However, all studies had small sample sizes (n < 30 per group), leading to a high risk of other biases.

Figure 2.

Risk of bias graph: review authors’ judgments about each risk of bias item presented as percentages across all included studies.

Figure 3.

Risk of bias summary: review authors’ judgments about each risk of bias item for each included study.

3.4. Effect of zolpidem on sleep efficiency and architecture

Meta-analysis of data from 4 studies showed that zolpidem increased total sleep time compared to placebo or no drug (MD: 0.78, 95% CI: 0.19–1.37, P = .009, I² = 38%; Fig. 4). Unfortunately, zolpidem did not result in a statistically significant benefit in improving percent supine, sleep onset latency, and wake after sleep onset. However, the reductions in sleep onset latency (MD: −1.07, 95% CI: −2.37 to 0.24, P = .11, I² = 86%; Fig. 4) and wake after sleep onset (MD: −1.04, 95% CI: −2.19 to 0.10, P = .07, I² = 75%; Fig. 4) on zolpidem, while suggestive of a trend, did not reach statistical significance. It should be noted that 1 study included in this meta-analysis,which could not be pooled for these specific outcomes, revealed that sleep latency was significantly shorter on zolpidem nights.^[20]

Figure 4.

Forest plot showing the effect of zolpidem on sleep efficiency and architecture with zolpidem group versus control group.

3.5. Effect of zolpidem on OSA severity

Zolpidem did not alter OSA severity, as shown by no systematic changes in AHI. Total AHI (MD: −0.53, 95% CI: −1.31 to 0.26, P = .19; I² = 80%), supine AHI (MD: −0.76, 95% CI: −2.13 to 0.62, P = .28; I² = 91%), and AHI during non-rapid eye movement (MD: −0.16, 95% CI: −0.71 to 0.39, P = .58; I² = 7%) and rapid eye movement (MD: −0.05, 95% CI: −0.55 to 0.45; P = .84; I² = 0%) sleep were unaltered on the drug night compared to placebo or no medications. Besides, arousal index (MD: −0.44, 95% CI: −1.23 to 0.36, P = .28; I² = 77%), respiratory event duration (MD: 0.08, 95% CI: −0.34 to 0.50, P = .71; I² = 0%), and nadir oxygen saturation during sleep (MD: −0.13, 95% CI: −0.44 to 0.18, P = .41; I² = 0%) were also not different between the zolpidem group and the control group (Fig. 5). However, the study published by Berry found that the arousal index was slightly but statistically lower on zolpidem nights (placebo: 19.0 ± 1.6 vs zolpidem: 16.5 ± 1.2 events/h; P < .05).^[20]

Figure 5.

Forest plot showing the effect of zolpidem on OSA severity with the zolpidem group versus the control group. OSA = obstructive sleep apnea.

3.6. Effects of zolpidem on next-day perceived sleepiness

Next-day sleepiness was assessed using the Karolinska Sleepiness Scale (KSS) in 3 studies and the Epworth Sleepiness Scale (ESS) in 1 study. Given the different rating scales, only quantitative data from the 3 KSS studies were pooled for analysis (Fig. 6), while the fourth study provided merely qualitative findings. No significant increase in next-day sleepiness was found in the zolpidem group relative to controls. Overall, zolpidem was well tolerated across all trials, with no severe adverse events or aggravated respiratory events reported. All participants completed the trials, and no one dropped out due to adverse reactions (Fig. 6).

Figure 6.

Forest plot showing the effect of zolpidem on next-day perceived sleepiness with the zolpidem group versus the control group.

4. Discussion

The increasing prevalence of OSA and its frequent comorbidity with insomnia (COMISA) presents a complex clinical challenge, as the conditions can interact to amplify overall severity and complicate treatment.^[21] Cognitive behavioral therapy is regarded as the first-line treatment for COMISA patients,^[22] and zolpidem is the most used adjunctive treatment. Therefore, it is necessary to comprehensively analyze the effectiveness and safety of zolpidem. This meta-analysis sought to evaluate the specific impact of zolpidem, a widely used non-benzodiazepine hypnotic, on OSA severity in patients with OSA, an area lacking synthesized evidence from controlled trials.

The primary finding – that zolpidem improves sleep initiation and maintenance without systematically exacerbating OSA severity – warrants a nuanced physiological interpretation. Zolpidem is consistently effective in reducing sleep latency and increasing total sleep time in insomnia patients,^[23,24] which is also equally valid in OSA patients, as the present study suggests. However, hypnotics reduce OSA severity in some studies,^[25,26] but not others.^[10,27] The absence of a significant net effect on the AHI likely results from zolpidem simultaneously exerting both potentially detrimental and beneficial effects on upper airway physiology. On 1 hand, its sedative properties may theoretically increase respiratory depression and upper airway collapsibility by reducing neuromuscular tone. On the other hand, zolpidem has been shown to increase the arousal threshold, which facilitated greater CO₂-mediated respiratory stimulation during sleep^[28] and improve pharyngeal muscle responsiveness, both of which should reduce OSA severity in people with impairment in these 2 phenotypic traits.^[13] In patients with a low arousal threshold (a key phenotypic trait in OSA), this can be beneficial by preventing premature awakenings from respiratory events, allowing for more time to restore ventilation and complete respiratory efforts, potentially leading to a stabilization of breathing and even a reduction in AHI. Conversely, in patients with a highly collapsible airway, the muscle-relaxant effects may predominate, potentially worsening AHI. The neutral overall effect observed in this analysis suggests that these opposing forces may cancel each other out at a population level, highlighting the critical role of inter-individual physiological heterogeneity (e.g., in airway collapsibility, loop gain, and arousal threshold) in determining response. One possible explanation for a lack of an additional benefit is that most OSA patients were already effectively controlled (AHI > 15 events/h), or in Berry’s study that included patients with severe OSA, AHI tended to be reduced in the zolpidem group.^[20] We have added a sentence to the discussion section to address this. We will note that the study by Berry et al was conducted on participants who were concurrently using CPAP, which likely mitigated the potential respiratory depressant effects of zolpidem. We will discuss that the inclusion of this study, which showed some unique findings (e.g., a lower arousal index), may influence the pooled estimates and should be considered when interpreting the overall results, particularly the safety profile in treated OSA patients. Of note, 1 study involving 10 healthy nonobese heavy snorers showed a small, yet statistically significant rise in AHI with the use of zolpidem when compared to the placebo.^[29] More experimental research into the polysomnographic effects of zolpidem is needed to answer these questions definitively.

The interpretation of AHI outcomes must also consider methodological factors. The included studies were predominantly small, short-term crossover trials (total n = 83), which increases the risk of a type II error (failing to detect a true change in AHI). Furthermore, the baseline severity of OSA varied. The trend toward AHI reduction noted in 1 study involving severe OSA patients might be explained by a higher prevalence of a low arousal phenotype in this group, making them more responsive to the threshold-elevating effects of zolpidem. The crossover design of most studies enhances statistical power for within-patient outcomes like sleep time but may introduce carryover effects that complicate the interpretation of respiratory outcomes. The positive effects on sleep efficiency and latency, while statistically significant, should be interpreted cautiously. The robust placebo effect well-documented in insomnia trials could account for a portion of this observed benefit, as the subjective experience of sleep onset can be influenced by expectation.

The main concern of zolpidem administration in OSA is its potential hangover effects.^[30] Regarding safety, the analysis found no significant increase in next-day sleepiness measured by KSS or ESS. However, this conclusion is constrained by the short-term nature of the trials (often single doses) and the lack of sensitive, objective measures of residual impairment, such as driving simulation or detailed cognitive testing. The finding of no significant “hangover” effects cannot be extrapolated to longer-term use or to safety-sensitive activities. Crucially, this analysis cannot address the long-term safety profile of zolpidem in OSA patients, including risks of tolerance, dependence, and complex sleep behaviors.

Our findings add a critical layer to the existing literature on hypnotics in OSA. While a previous meta-analysis concluded that NBSHs generally do not worsen AHI, our work specifically focuses on zolpidem within a COMISA population and integrates data on both efficacy (sleep parameters) and safety (daytime sleepiness), providing a more comprehensive risk-benefit assessment for this specific drug and patient group.

The clinical implications are multifaceted. For OSA patients struggling with insomnia despite standard care, a short-term, cautious trial of zolpidem may be considered to improve sleep continuity without expected worsening of OSA severity, potentially aiding overall recovery. However, it is not a treatment for OSA itself. A paramount concern is its use in patients on CPAP. While 1 might hypothesize that improved sleep could enhance CPAP adherence, the null finding on next-day sleepiness in a study by Bradshaw et al suggests that improved sleep with zolpidem may not automatically translate into reduced subjective sleepiness, a key motivator for CPAP use. Therefore, zolpidem should not be seen as an adjunct to improve CPAP compliance but rather as a targeted therapy for comorbid insomnia, with its use carefully weighed against behavioral strategies like cognitive behavioral therapy, which remains the first-line and guideline-recommended treatment for COMISA due to its durable efficacy and absence of pharmacological side effects.

This study has several important limitations. The most substantial is the very small pooled sample size (n = 83), which severely limits the statistical power to detect clinically meaningful changes in AHI and safety endpoints, increasing the risk of type II errors. The generalizability of findings is constrained by the lack of demographic diversity; participants were predominantly male, and geographic and ethnic representation was limited. Furthermore, the included trials may be subject to selection bias, as they likely enrolled healthier patients without significant comorbidities, which may not reflect real-world clinical populations. Due to the inclusion of only 5 studies, a formal assessment of publication bias was not feasible. Significant heterogeneity was observed in the measurement of sleepiness (using both KSS and ESS), making pooled interpretations less reliable. The duration of zolpidem exposure varied across trials, from single doses to 2 weeks, precluding any analysis of long-term effects. The short follow-up periods also mean that rare or delayed adverse events were unlikely to be captured. Finally, the inability to perform subgroup analyses, particularly by OSA severity or phenotypic traits, leaves key clinical questions about which patients might benefit or be harmed unanswered.

5. Conclusion

In conclusion, this meta-analysis suggests that short-term use of zolpidem can improve sleep efficiency in OSA patients without producing a systematic worsening of OSA severity or significant next-day sleepiness in controlled settings. However, these findings are tempered by a very small evidence base, short trial durations, and limited generalizability. Therefore, no firm clinical recommendations can be made. The neutral effect on AHI likely masks variable individual responses driven by underlying physiological phenotypes. Future research must prioritize larger, long-term RCTs that are powered to detect changes in respiratory and safety outcomes, incorporate objective measures of impairment, and strive to identify the phenotypic predictors of treatment response. Mechanistic studies are needed to clarify the dose-dependent effects of zolpidem on genioglossus muscle activity and arousal threshold. Until such data are available, zolpidem may be considered a second-line option for COMISA after cognitive behavioral therapy, used with extreme caution, for short durations, and with explicit monitoring, never as a substitute for primary OSA therapy.

Author contributions

Conceptualization: Bo Tan, Xiuping An, Xiuqin An.

Data curation: Bo Tan, Xiuqin An.

Formal analysis: Bo Tan, Xiuqin An.

Investigation: Xiuping An, Xiuqin An.

Methodology: Bo Tan, Xiuping An, Xiuqin An.

Software: Bo Tan, Xiuping An, Xiuqin An.

Supervision: Xiuping An, Xiuqin An.

Validation: Bo Tan, Xiuping An, Xiuqin An.

Writing – original draft: Bo Tan.

Writing – review & editing: Xiuqin An.