Cortisol Buffering Capacity describes the physiological ability of the body’s stress response system to effectively modulate and clear excess circulating cortisol, preventing prolonged tissue exposure to high glucocorticoid levels. This capacity reflects the resilience of the hypothalamic-pituitary-adrenal (HPA) axis and the efficiency of peripheral cortisol metabolism. A robust buffering capacity is essential for protecting tissues from the catabolic and inflammatory effects of chronic stress.
Origin
This term is a functional concept derived from clinical endocrinology and stress physiology, focusing on the dynamic regulation of the primary stress hormone, cortisol. It moves beyond simple cortisol level measurement to assess the system’s ability to maintain homeostasis under allostatic load. The capacity is fundamentally linked to the body’s adaptive reserves and metabolic health.
Mechanism
The buffering is mediated by multiple processes, including the efficiency of cortisol clearance by the liver and the action of the 11β-hydroxysteroid dehydrogenase (11β-HSD) enzymes. Specifically, 11β-HSD type 2 inactivates cortisol to cortisone in mineralocorticoid-sensitive tissues, protecting them from excess signaling. Furthermore, adequate binding capacity of Cortisol-Binding Globulin (CBG) and the feedback loops of the HPA axis contribute significantly to the overall systemic buffer against cortisol spikes.
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