• Please find below published journal articles proving that slightly elevating your body’s CO₂ content overcomes Sleep Apnea

• Our SAGE Rebreather employs a unique & patented delivery method for SAFELY delivering CO₂

• Our planned clinical research should prove this same outcome using a safe and clever device that can be put in your pocket

• We expect our approach to also mitigate most, if not all, Sleep Disordered Breathing (SDB)

• This page provides journal article support for our beliefs

• Note that elevating CO₂ levels has already been proven to OVERCOME Sleep Apnea since 1997, and soon should be able to be accomplished without the complications and discomfort of CPAP

• Please contact us with any questions you may have.

201906 | Department of Population Health Sciences, University of Wisconsin - Madison, Madison, WI 53726, USA, Jerome A. Dempsey | REVIEW ARTICLE

Full Abstract. Central sleep apnea is prevalent in patients with heart failure, healthy individuals at high altitudes, and chronic opiate users and in the initiation of “mixed” (that is, central plus obstructive apneas). This brief review focuses on (a) the causes of repetitive, cyclical central apneas as mediated primarily through enhanced sensitivities in the respiratory control system and (b) treatment of central sleep apnea through modification of key components of neurochemical control as opposed to the current universal use of positive airway pressure.

201604 | A Mulchrone, M Shokoueinejad and J Webster, Department of Biomedical Engineering, University of Wisconsin, Madison, WI 53706, USA | A Topical REVIEW

Full Abstract. Although almost completely unknown half a century ago, sleep disorders are gaining recognition as major issues to public health due to their growing prevalence and dire societal consequences. Despite being linked to several infamous catastrophic events such as Chernobyl, it is estimated that 90% of sufferers fail to get diagnosed and receive treatment, and a significant portion of the ones that do are often non-compliant due to the side effects of current treatments. This article presents a review of the current standard treatment for central sleep apnea, and investigates the advantages and possible consequences of using inspired carbon dioxide (CO2) as an alternative treatment option.

201304 | Ailiang Xie, Mihaela Teodorescu, David F. Pegelow, Mihai C. Teodorescu, Yuansheng Gong, Jessica E. Fedie, and Jerome A. Dempsey | J Appl Physiology (1985)

Full Abstract. To determine how the obstructive sleep apnea (OSA) patient's pathophysiological traits predict the success of the treatment aimed at stabilization or increase in respiratory motor outputs, we studied 26 newly diagnosed OSA patients [apnea-hypopnea index (AHI) 42 ± 5 events/h with 92% of apneas obstructive] who were treated with O2 supplementation, an isocapnic rebreathing system in which CO2 was added only during hyperpnea to prevent transient hypocapnia, and a continuous rebreathing system. We also measured each patient's controller gain below eupnea [change in minute volume/change in end-tidal PCO2 (ΔV̇ E/ ΔPETCO2)], CO2 reserve (eupnea-apnea threshold PETCO2), and plant gain (ΔPETCO2/ΔV̇ E), as well as passive upper airway closing pressure (Pcrit). With isocapnic rebreathing, 14/26 reduced their AHI to 31 ± 6% of control (P < 0.01) (responder); 12/26 did not show significant change (nonresponder). The responders vs. nonresponders had a greater controller gain (6.5 ± 1.7 vs. 2.1 ± 0.2 l·min−1·mmHg−1, P < 0.01) and a smaller CO2 reserve (1.9 ± 0.3 vs. 4.3 ± 0.4 mmHg, P < 0.01) with no differences in Pcrit (−0.1 ± 1.2 vs. 0.2 ± 0.9 cmH2O, P > 0.05). Hypercapnic rebreathing (+4.2 ± 1 mmHg PETCO2) reduced AHI to 15 ± 4% of control (P < 0.001) in 17/21 subjects with a wide range of CO2 reserve. Hyperoxia (SaO2 ∼95– 98%) reduced AHI to 36 ± 11% of control in 7/19 OSA patients tested. We concluded that stabilizing central respiratory motor output via prevention of transient hypocapnia prevents most OSA in selected patients with a high chemosensitivity and a collapsible upper airway, whereas increasing respiratory motor output via moderate hypercapnia eliminates OSA in most patients with a wider range of chemosensitivity and CO2 reserve. Reducing chemosensitivity via hyperoxia had a limited and unpredictable effect on OSA.

198500 | Jerome A. Dempsey, Ailiang Xie, David S. Patz, and David Wang | J App Physiol (1985)

Full Abstract. We review evidence in support of significant contributions to the pathogenesis of obstructive sleep apnea (OSA) from pathophysiological factors beyond the well-accepted importance of airway anatomy. Emphasis is placed on contributions from neurochemical control of central respiratory motor output through its effects on output stability, upper airway dilator muscle activation, and arousability. In turn, we consider the evidence demonstrating effective treatment of OSA via approaches that address each of these pathophysiologic risk factors. Finally, a case is made for combining treatments aimed at both anatomical and ventilatory control system deficiencies and for individualizing treatment to address a patient's own specific risk factors.

199400 | M. SAFWAN BADR, JAMES B. SKATRUD, AND JEROME A. DEMPSEY (With the Technical Assistance of James D. Lookabaugh and Heidi E. Bell) | J App Physiol (1994)

Full Abstract. We investigated the effect of chemoreceptor stimulation and inhibition on total pulmonary resistance (RL) during non-rapid-eye-movement (NREM) sleep in healthy subjects. Chemoreceptor stimulation was accomplished with brief isocapnic hypoxia (n = 8). Minute ventilation increased to 150% of room air control. RL at peak inspiratory flow decreased to 66% of room air control. Resistive pressure-inspiratory flow plots demonstrated lower resistive pressures for a given inspiratory flow. Chemoreceptor inhibition was accomplished by abruptly terminating brief hypocapnic hypoxia with 100% 0, (n = 7). Minute ventilation decreased to 63% of room air control. RL calculated at peak inspiratory or fixed flow did not change significantly, and pressure-flow plots at nadir ventilation showed no systematic change from room air control. We conclude that 1) hypoxic chemoreceptor stimulation is associated with decreased RL and enhancement of pressure-flow relationships, suggesting increased upper airway caliber; 2) upper airway patency is not compromised during periods of low ventilatory drive in normal subjects; and 3) upper airway dilating muscles and thoracic pump muscles are optionally coordinated with increased and decreased ventilatory drive.

• 1997 | Effects of Inhaled CO2 and Added Dead Space on Idiopathic Central Sleep Apnea

• 2008 | Long-Term Compliance with Continuous Positive Airway Pressure in Patients with Obstructive Sleep Apnea

• 2011 | The Effect of CPAP in Normalizing Daytime Sleepiness, Quality of Life, and Neurocognitive Function in Patients with Moderate to Severe OSA

• 2013 | Complex Sleep Apnea Syndrome REVIEW

• 2014 | Carbon Dioxide in Sleep Medicine— The Next Frontier for Measurement, Manipulation, and Research

• 2014 | Effect of Inhaled Carbon Dioxide on Laryngeal Abduction

• 2015 | Clinical Consequences and Economic Costs of Untreated Obstructive Sleep Apnea Syndrome

• 2016 | Prevalence of Central Sleep Apnea

• 2016 | Trends in CPAP Adherence Over Twenty Years of Data Collection— A Flattened Curve