This refers to the clinical strategy of deliberately reducing the magnitude and/or duration of the physiological response to stress mediated by the glucocorticoid hormone cortisol. While a healthy, transient cortisol response is vital for survival, chronic or excessive secretion can lead to detrimental catabolic effects, metabolic dysregulation, and cognitive impairment. Attenuation aims to normalize a hyper-responsive hypothalamic-pituitary-adrenal (HPA) axis, thereby promoting systemic resilience and preserving long-term health.
Origin
The term combines the endocrinological concept of the ‘cortisol response’—the body’s central stress cascade—with the clinical pharmacology term ‘attenuation,’ meaning to reduce the force, effect, or value of something. This approach acknowledges the allostatic load placed on the body by chronic stress and seeks to therapeutically modulate the stress-hormone feedback loop.
Mechanism
Attenuation is achieved by modulating the upstream release of corticotropin-releasing hormone (CRH) and adrenocorticotropic hormone (ACTH), or by directly influencing the adrenal gland’s output. Certain adaptogens or neurosteroids can interact with glucocorticoid receptors or mineralocorticoid receptors to buffer the cellular effects of excess cortisol. By calming the HPA axis, the body shifts away from a constant state of alarm, allowing for restorative processes, improved immune function, and normalized glucose metabolism.
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