Stress Hormone Antagonism describes the therapeutic strategy aimed at mitigating the detrimental, long-term physiological effects induced by chronic elevation of catabolic stress hormones, principally cortisol, without necessarily eliminating the acute stress response itself. This involves blunting the downstream cellular impact of sustained glucocorticoid signaling, which often includes suppressing anabolic pathways and promoting insulin resistance. We seek to preserve anabolic potential despite ongoing psychological or physiological load.
Origin
Rooted in HPA axis research, this term denotes actively counteracting the effects of stress hormones once they are elevated, often through receptor modulation or the enhancement of counter-regulatory anabolic signals.
Mechanism
Antagonism can be achieved by enhancing the sensitivity of anabolic receptors to overcome cortisol-induced downregulation, or by promoting rapid cortisol clearance via optimized liver function and detoxification pathways. Furthermore, boosting endogenous anabolic signaling pathways, such as through IGF-1 or testosterone, provides a powerful physiological counterweight to the catabolic drive of chronic hypercortisolemia. This strategy aims to re-establish metabolic equilibrium favoring tissue maintenance.
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