Abstract Introduction The thesis is inspired by supporting evidence from evolution, physiology, and clinical studies. “Upper airway sleep health” is keeping the airway open enough to not disturb sleep too much. Losing this ability leads to obstructive sleep apnea (OSA). Methods Premise 1: What element drives upper airway functions during sleep? Premise 2: Is brainstem function the critical organ in the development of OSA? Results 1. The challenge starts with first breaths, and the cycle of breathing, sucking, and swallowing. As the interface between the environment and the lungs, its healthy functions adapt to posture, sleep state, growth and aging, and be resilient to stresses (allostasis), like an URI. Clinical examples of recovery are that ~50% of children with enlarged lymphoid tissue and disordered breathing resolve over time with “watchful waiting”; and, when weight loss in obesity addresses the mass and metabolic allostatic loading, sleep disordered breathing improves and may resolve. 2. In vertebrates, the brainstem is the breathing controller in a feedback system assessing successes of coordinated muscle activation informed by neural feedback. We propose that brainstem adaptability and resiliency are degraded in individuals progressively leading to OSA presentations. Allostatic features are common in pediatric and adult presentations, including gender, age, and craniofacial risks and co-morbidities like hypertension, cardiovascular disease, obesity and smoking; socioeconomic conditions producing psychologic factors; and genetic predispositions. After a latent phase, accumulated effects in those susceptible eventually leads to upper airway instability (allostatic overload) leading to OSA presentation, its individual phenotypes and endotypes. Conclusion Upper airway patency during sleep is resilient and when challenged by anatomic, neural, metabolic, and developmental factors, can generally adapt successfully. OSA in its various presentations has a latent phase in which chronic stressors produce a chronically unstable condition during sleep (allosteric overload), eventually expressed as clinical illness and the need for management. The task is to measure and detect predispositions to adult- and childhood-onset sleep disordered breathing early enough to initiate primary or secondary prevention to preserve heathy feedback control. Support (if any) Division of Pulmonary, Critical Care and Sleep Medicine, University Hospitals Cleveland OH
Strohl et al. (2026) studied this question.