On the "Airway-Energy Remodeling" Hypothesis of Functionally Acquired COPD

The pathogenesis of traditional chronic obstructive pulmonary disease (COPD) has focused heavily on genetic susceptibility factors (such as SERPINA1 gene mutations causing α₁-antitrypsin deficiency, AATD) or exogenous chemical inhalation injury (such as smoking). This paper proposes a novel parallel pathogenesis that does not conflict with traditional theories: acquired functional COPD (acquired functional COPD). We hypothesize chronic physical and mental stress in certain groups (such as middle-aged man suffering from marital role overload, emotional betrayal, and economic pressure) triggers dysfunction of the hypothalamic-pituitary-adrenal axis (HPA axis) and autonomic nervous system functions, leading to physiological nasal cycle imbalance (manifested as a surge in unilateral nasal resistance and ventilation imbalance) and triggering nighttime upper airway collapse (severe snoring). To overcome the upper airway bottleneck, pathological negative pressure generated in the chest cavity causes the peripheral small airways to functionally close prematurely during exhalation, resulting in dynamic overinflation and gas trapping. This localized high intraluminal pressure (barotrauma) works synergistically with localized intermittent hypoxia, compressing alveolar capillary flow and triggering reactive oxygen species (ROS) bursts, ultimately mediating microscopic RNA oxidative damage and protein folding disorders in peripheral lung tissue.