The therapeutic objective of reducing the excessive or dysregulated output of cortisol from the adrenal cortex, often following chronic stress exposure that has hyperactivated the Hypothalamic-Pituitary-Adrenal (HPA) axis. Attenuation seeks to restore the natural diurnal rhythmicity of this critical stress hormone. This is crucial for mitigating catabolic effects on lean tissue and improving metabolic regulation.
Origin
This term directly addresses the clinical sequelae of chronic stress, where prolonged cortisol elevation leads to negative feedback resistance and tissue resistance to glucocorticoids. The concept of attenuation implies a gradual, controlled reduction in signaling intensity rather than abrupt cessation. It is central to managing adrenal fatigue paradigms.
Mechanism
Attenuation is achieved by supporting upstream neuroendocrine regulation, perhaps by modulating CRH signaling or improving pituitary sensitivity to negative feedback from circulating glucocorticoids. Furthermore, enhancing cellular resilience against oxidative damage caused by high cortisol helps protect adrenal tissue integrity. Balancing DHEA sulfate levels often complements this strategy for HPA axis normalization.
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