The stress defence-cascade is mostly not biphasic as Cannon thought, the sympathicotonic stress response is preceded by a vagotonic phase called freeze response. Alteration of the carbon dioxide level plays an important role during defence-cascade as its changes interfere with stress hormones, e.g. with catecholamines, thus affecting the degree of arousal. In case of humans, learned behaviour dominates instead of instinctive, so the fight-or-flight often lags; the consequence can be persistent hypocapnia or hypercapnia. The hypoventilation or hyperventilation may continue even after a stressful situation, as tissular and renal compensation stabilizes and makes the pathological breathing patterns chronic. The organism tries to restore the original milieu intérieur (sec. Claude Bernard), but this cannot succeed without restoring pCO2. The regulation operates the preservation of intracellular and extracellular pH as a priority, while neurohumoral compensations change the ionic milieu in the body’s cells. Present hypothesis specifies the permanent lack or excess of carbon dioxide which can cause allostatic load by psychosomatic pathomechanism. Carbon dioxide is equivalent to stress hormones; its alterations become a means of somatization, resulting in ion-pattern changes in intracellular and extracellular spaces, consequently causing disintegration of the body’s function. (See also: network theory, ripple effect, metabolic remodeling.) Intracellular ion-pattern alterations emerge new genetic phenotypes to the surface. The variety of phenotypes explains the diversity of induced diseases. The theory appreciates the role of ions by considering the instantaneous ion pattern of the cytoplasm (all the ions together) as a decisive second messenger.
|Number of pages||11|
|Publication status||Published - Jun 1 2017|
ASJC Scopus subject areas
- Neuropsychology and Physiological Psychology
- Pharmacology, Toxicology and Pharmaceutics(all)
- Clinical Neurology