Sahil Chopra, MD; Savit Raj Malhotra; Quynh Theresa Do, BS; Stacey Gunn, MD; Keilah Oberstein-Wright, NP-BC, MSN; Cali Bahrenfuss, CCSH, RPSGT; Robert Joseph Thomas, MD, MMSc
Sahil Chopra, MD, Principal Investigator; Savit Raj Malhotra, BS, Research Associate; Quynh Theresa Do, BS, Research Associate; Stacey Gunn, MD, Research Associate; Keilah Oberstein-Wright, NP-BC, Research Associate; Cali Bahrenfuss, CCSH, RPSGT, Research Associate; Empower Sleep, Irvine, CA, USA. Robert Joseph Thomas, MD, MMSc, Senior Researcher, Beth Israel Deaconess Medical Center, Division of Pulmonary, Critical Care & Sleep Medicine, Department of Medicine, Boston, Massachusetts, USA.
Corresponding author: Sahil Chopra, MD
E-mail: sahilchopramd@empowersleep.com
Keywords: Obstructive sleep apnea, positive airway pressure, sleep quality, longitudinal monitoring, systems physiology.
Introduction
Obstructive sleep apnea (OSA) is traditionally diagnosed and managed based on the frequency of breathing interruptions during sleep, typically quantified as the apnea–hypopnea index (AHI).1 While this event-based approach is useful for identifying airway obstruction, it does not fully capture sleep as a whole-body physiologic process. Sleep quality, oxygen delivery, autonomic balance, and recovery capacity reflect broader system-level health.
Patients using continuous positive airway pressure (CPAP) therapy may continue to experience disrupted sleep physiology despite apparent control of respiratory events.2 Underlying contributors to persistent sleep dysfunction may include cardiovascular disease, upper airway susceptibility, baseline autonomic dysregulation, and reduced physiologic adaptability.3-5 Common lifestyle and environmental stressors, such as irregular sleep schedules, alcohol use, late meals, psychological stress, and circadian misalignment, may further exacerbate nocturnal oxygen instability even when CPAP adherence appears adequate.6-8,10-12
Physiologic stress is a key mediator between treated OSA and downstream health outcomes. Sub-optimally treated OSA with CPAP may result in residual hypoxemic stress and autonomic arousals if the positive airway pressure is too low, or excessive sleep fragmentation if CPAP pressures are too high. Measures such as sleep quality indices (SQI) provide insight into impaired restorative sleep that may persist despite “normal” CPAP-reported AHI values. These unresolved physiologic stressors may contribute to long-term cardiovascular, metabolic, neurologic, and inflammatory risk, suggesting that event-based CPAP metrics alone may provide incomplete reassurance regarding overall sleep health.18-21
From a functional medicine perspective, sleep health and circadian rhythms are influenced by modifiable lifestyle factors, including sleep timing, duration, alcohol, caffeine use, physical activity, meal timing, and stress load.9-12,22 While CPAP remains the gold standard for correcting upper airway obstruction, its effectiveness is highly dependent on appropriate settings, physiologic response, and integration with broader lifestyle optimization.13-15 We highlight the importance of longitudinal, multidimensional sleep assessments to identify patients who may benefit from individualized therapeutic adjustments and targeted lifestyle interventions.
We examine sleep as an integrated physiologic system involving respiratory stability (the total volume of air in the lungs after a breath), oxygen delivery, autonomic regulation, and restorative capacity (the body’s ability to return to baseline following physiological stress). Our objective is to evaluate whether OSA patients using PAP therapy demonstrate meaningful differences in overall sleep health and quality when assessed using longitudinal sleep testing rather than CPAP-reported event counts alone.
Methods
From April 2023 to August 2025, our practice collected paired sleep data from CPAP devices and at-home physiologic sleep testing. This retrospective observational study analyzed de-identified clinical data collected during routine care.
Patients completed multi-night home sleep assessments using cardiopulmonary coupling (CPC) via a home sleep testing ring system (SleepImage Ring System), which provides nightly measures of respiratory stability, oxygenation, and sleep quality. SQI is a composite metric that considers stable sleep measured via high-frequency coupling as a percentage of total sleep time, sleep duration, and sleep fragmentation.16 SQI is further classified in our practice as Excellent (SQI of 50-100), Good (40-49), Mildly Reduced (30-39), Moderately Reduced (15-29), and Severely Reduced (0-14). Nights with complete physiologic data and ≥4 hours of usage for both devices were included.
Descriptive analyses focused on identifying patterns of residual physiologic burden, including reduced sleep quality during nights when CPAP-reported AHI suggested adequate OSA control. This multidimensional assessment reflects functional medicine principles by evaluating integrated physiologic function rather than relying solely on isolated event-based metrics. All research procedures were IRB-approved (Univo IRB, IRB Study Number: STU25090170, Study ID: 20250908UC174938).
Results and Discussion
465 patients (mean age 57.1 ± 14.8 years, 30.5% female, mean BMI 28.8 ± 6.0 kg/m2) contributed 24 939 nights of concurrent CPAP and CPC monitoring (median 22 nights per participant), with 22 338 nights showing CPAP AHI <5 events/hour while showing CPC AHI >5 events/hour. Clinically, AHI <5 events/hour indicates normal, non-disordered breathing during sleep, while AHI between 5-15 indicates mild OSA, 15-30 indicates moderate OSA, and 30+ indicates severe OSA.17 Of these 22 338 nights, 22 335 had corresponding SQI data. The median SQI of these nights was 29 (with a range of 11 to 97) (Figure 1).
Figure 1. SQI Range for All Nights Analyzed (n = 22 335)

Note: All nights analyzed relate to those with CPAP AHI <5 events/hour while showing >5 events/hour using CPC. Additionally, all analyzed nights have more than 4 hours of concurrent CPAP and sleep testing ring use (4 hours is the minimum for a home sleep study to be considered technically adequate, as per the American Academy of Sleep Medicine [guide]). The range of SQI spans from 11 to 97. The median SQI for these nights was 29, which would be classified as Moderately Reduced.
SQI revealed additional impairment in restorative capacity. Among nights classified as adequately treated by CPAP metrics, only 2699 (12.1%) nights showed that SQI was rated as Excellent; 2,868 (12.8%) nights showed SQI rated as Good; 5599 (25.1%) nights showed SQI rated as Mildly Reduced; 11 011 (49.3%) nights showed SQI rated as Moderately Reduced; and 158 (0.7%) nights showed SQI rated as Severely Reduced (Figure 2).
Figure 2. SQI Categories For All Nights Analyzed (n = 22 335)

Note: All nights analyzed relate to those with CPAP AHI <5 events/hour while showing >5 events/hour using CPC. Additionally, all nights analyzed have more than 4 hours of concurrent CPAP and sleep testing ring use (4 hours is the minimum for a home sleep study to be considered technically adequate, as per the American Academy of Sleep Medicine[guide]). The SQI categories reflect SQI scores as follows: Excellent (SQI = 50-100), Good (40-49), Mildly Reduced (30-39), Moderately Reduced (15-29), and Severely Reduced (0-14).
Table 1. Corresponding SQI For All Nights Analyzed (n = 22 335)
| SQI | n | Percent (%) |
| Optimal | 2699 | 12.1 |
| Good | 2868 | 12.8 |
| Mildly Reduced | 5599 | 25.1 |
| Moderately Reduced | 11 011 | 49.3 |
| Severely Reduced | 158 | 0.7 |
Collectively, these findings demonstrate that apparent CPAP success based on event counts frequently coexists with impaired sleep quality and ongoing physiologic stress that is not captured by traditional AHI-focused care models.
Without longitudinal follow-up sleep testing, ongoing physiologic stress may go unrecognized in patients on CPAP. This unresolved burden may contribute to adverse cardiovascular, metabolic, gastrointestinal, respiratory, and neurologic outcomes through sustained hypoxic exposure and impaired restorative sleep.18-21
Longitudinal SQI provides valuable insight into how physiologic stress can persist despite apparent disease control.22 These findings highlight the interconnected nature of sleep, oxygen delivery, autonomic regulation, and whole-body health. For patients who continue to experience symptoms or demonstrate physiologic disease burden despite CPAP adherence, additional testing may be necessary to determine whether therapy is truly optimized. This testing may include either at-home sleep testing or an in-lab polysomnography.
Conclusion
This analysis supports a personalized, systems-based approach to sleep care that moves beyond a binary “treated versus untreated” framework. Stratifying patients based on sleep quality allows clinicians to identify subgroups who may benefit from therapy adjustments, lifestyle-focused interventions, or adjunctive treatments. Circadian rhythm entrainment (i.e., timing of light and darkness), abstaining from alcohol, exercising regularly, modulating the vagus nerve to promote parasympathetic tone, and maintaining a nutrient-dense diet are all lifestyle changes that can help mitigate OSA symptoms. This approach aligns with functional medicine principles by addressing individual variability, underlying contributors, and the broader physiologic context in which OSA occurs.
Disclosure
All funding, supplies, and support for this research come from Empower Sleep. Dr. Chopra is a co-founder and owner of Empower Sleep. Dr. Thomas and the Beth Israel Deaconess Medical Center receive royalties for the technology described in the manuscript. Dr. Thomas is the co-inventor of the ECG/PPG spectrogram, patented and licensed by Beth Israel Deaconess Medical Center to MyCardio, LLC.
Funding
This study has received no external funding.
References
- Veasey SC, Rosen IM. Obstructive Sleep Apnea in Adults. Solomon CG, ed. New England Journal of Medicine. 2019;380(15):1442-1449. doi:10.1056/NEJMcp1816152
- Lal C, Weaver TE, Bae CJ, Strohl KP; Mechanisms and Clinical Management. Excessive Daytime Sleepiness in Obstructive Sleep Apnea. Ann Am Thorac Soc. 2021;18(5):757-768. doi:10.1513/AnnalsATS.202006-696FR
- Yeghiazarians Y, Jneid H, Tietjens JR, et al. Obstructive Sleep Apnea and Cardiovascular Disease: A Scientific Statement From the American Heart Association. Circulation. 2021;144(3):e56-e67. doi:10.1161/CIR.0000000000000988
- Tobushi T, Floras JS. Sleep Apnea, Autonomic Disturbances, and Blood Pressure Variability. Hypertension. 2024;81(9):1837-1844. doi:10.1161/HYPERTENSIONAHA.124.20433
- Finnsson E, Arnardóttir E, Cheng WJ, et al. Sleep apnea endotypes: from the physiological laboratory to scalable polysomnographic measures. Front Sleep. 2023;2:1188052. doi:10.3389/frsle.2023.1188052
- Wu S, Peng M, Zuo Y, et al. Social jetlag and obstructive sleep apnea severity: A retrospective study based on polysomnography. Sleep Medicine. 2025;134:106722-106722. doi:10.1016/j.sleep.2025.106722
- Simou E, Britton J, Leonardi-Bee J. Alcohol and the risk of sleep apnoea: a systematic review and meta-analysis. Sleep Med. 2018;42:38-46. doi:10.1016/j.sleep.2017.12.005
- Lopes T do VC, Borba ME, Lopes R do VC, et al. Eating Late Negatively Affects Sleep Pattern and Apnea Severity in Individuals With Sleep Apnea. Journal of Clinical Sleep Medicine. 2019;15(03):383-392. doi:10.5664/jcsm.7658
- Sejbuk M, Mirończuk-Chodakowska I, Witkowska AM. Sleep Quality: A Narrative Review on Nutrition, Stimulants, and Physical Activity as Important Factors. Nutrients. 2022;14(9):1912. doi:10.3390/nu14091912
- Meyer N, Harvey AG, Lockley SW, Dijk DJ. Circadian rhythms and disorders of the timing of sleep. Lancet (London, England). 2022;400(10357):S0140-6736(22)008777. doi:10.1016/S0140-6736(22)00877-7
- Kaleelullah RA, Nagarajan PP. Cultivating Lifestyle Transformations in Obstructive Sleep Apnea. Cureus. 2021;13(1):e12927. doi:10.7759/cureus.12927
- Foster RG. Sleep, circadian rhythms and health. Interface Focus. 2020;10(3):20190098. doi:10.1098/rsfs.2019.0098
- Gottlieb DJ, Punjabi NM. Diagnosis and Management of Obstructive Sleep Apnea: Review A. JAMA. 2020;323(14):1389-1400. doi:10.1001/jama.2020.3514
- Patil SP, Ayappa IA, Caples SM, Kimoff RJ, Patel SR, Harrod CG. Treatment of Adult Obstructive Sleep Apnea With Positive Airway Pressure: An American Academy of Sleep Medicine Systematic Review, Meta-Analysis, and GRADE Assessment. J Clin Sleep Med. 2019;15(2):301-334. doi:10.5664/jcsm.7638
- Lastra AC, Neborak JM, Mokhlesi B. Lastra AC, Neborak JM, Babak Mokhlesi. Diagnosis and Treatment of Obstructive Sleep Apnea. JAMA Intern Med. 2025;185(10):1280-1280. doi:10.1001/jamainternmed.2025.2318
- Yuanjie Z, Yunxiao W, Thomas RJ, Yufen T, Zhengli, Zhifei X. Cardiopulmonary coupling estimated sleep quality and memory in children with obstructive sleep-disordered breathing. Sleep Med. 2025;129:8-13. doi:10.1016/j.sleep.2025.01.024
- Slowik JM, Sankari A, Collen JF. National Library of Medicine National Center for Biotechnology Information StatPearls. Accessed February 27, 2026. https://www.ncbi.nlm.nih.gov/books/NBK459252/
- Azarbarzin A, Sands SA, Stone KL, et al. The hypoxic burden of sleep apnoea predicts cardiovascular disease-related mortality: the Osteoporotic Fractures in Men Study and the Sleep Heart Health Study. Eur Heart J. 2019;40(14):1149-1157. doi:10.1093/eurheartj/ehy624
- Punjabi NM, Beamer BA. Alterations in Glucose Disposal in Sleep-disordered Breathing. Am J Respir Crit Care Med. 2009;179(3):235-240. doi:10.1164/rccm.200809-1392OC
- Demeter P, Pap A. The relationship between gastroesophageal reflux disease and obstructive sleep apnea. J Gastroenterol. 2004;39(9):815-820. doi:10.1007/s00535-004-1416-8
- Engleman HM, Kingshott RN, Martin SE, Douglas NJ. Cognitive function in the sleep apnea/hypopnea syndrome (SAHS). Sleep. 2000;23(suppl 4):S102-S108.
- Norful AA, de Jacq K, Zhao J, et al. Exploring longitudinal physiologic stress measurement and sleep quality interventions to improve psychological well-being in nurses: a pilot study. Health Psychol Behav Med. 2025;13(1):2503376. doi:10.1080/21642850.2025.2503376

Leave a Reply