Stress Axis Attenuation is the clinical strategy aimed at reducing the overall reactivity and output of the Hypothalamic-Pituitary-Adrenal (HPA) axis, particularly when it exhibits chronic hyperactivity that leads to pathological cortisol exposure. This attenuation seeks to restore a balanced, responsive stress system rather than suppressing all stress signaling. We aim for appropriate modulation of the body’s primary stress response.
Origin
This concept originates from psychoneuroendocrinology, recognizing the profound long-term detriment associated with chronic elevations of glucocorticoids like cortisol. Attenuation implies dampening the excessive signaling while preserving the necessary acute stress response capability. It addresses the cumulative impact of chronic environmental load on endocrine health.
Mechanism
Attenuation mechanisms focus on modulating the upstream drivers of the HPA axis, such as reducing neural input to the hypothalamus or improving glucocorticoid receptor sensitivity in target tissues. By enhancing receptor affinity, the cell requires less circulating cortisol to elicit the necessary response, effectively lowering the functional setpoint of the axis. This normalization supports better sleep architecture and mitigates systemic inflammation.
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