Cortisol Metabolism Control describes the deliberate clinical management of the entire lifecycle of the glucocorticoid cortisol, encompassing synthesis, transport, receptor binding, and ultimate inactivation within the liver and other tissues. Effective control prevents chronic exposure to high levels, which damages cellular signaling fidelity. We aim for appropriate diurnal flux rather than absolute suppression.
Origin
This concept arises directly from adrenal endocrinology and stress physiology, focusing specifically on the kinetics of the primary stress hormone. Control implies active intervention to modulate the half-life and clearance rates of circulating cortisol. It acknowledges the metabolic demands placed on the body by sustained HPA axis activation.
Mechanism
Control is exerted through modulating enzymatic activity, particularly the 11-beta-hydroxysteroid dehydrogenase (11β-HSD) enzymes that regulate local tissue sensitivity to cortisol. Furthermore, optimizing liver function supports efficient conjugation and excretion pathways for inactive cortisol metabolites. Supporting healthy sleep cycles directly supports the natural nocturnal decline of plasma cortisol concentration.
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