Cortisol reactivity profiles clinically describe the characteristic pattern and magnitude of an individual’s cortisol response to a standardized physiological or psychological stressor. These profiles quantify how quickly, intensely, and for how long the HPA axis is activated, and how efficiently it returns to baseline following the challenge. Understanding a patient’s specific profile is essential, as hypo- or hyper-reactivity can indicate different underlying states of HPA axis dysregulation and chronic stress adaptation. This personalized data informs targeted interventions to restore stress resilience.
Origin
This concept evolved from psychoneuroendocrinology, a field dedicated to studying the interplay between psychological processes, the nervous system, and the endocrine system. The term ‘reactivity’ emphasizes the dynamic, responsive nature of the HPA axis rather than just static hormone levels. Standardized stress tests, such as the Trier Social Stress Test, helped establish the methodology for clinically defining these individual profiles.
Mechanism
Upon perceiving a stressor, the hypothalamus rapidly initiates the release of CRH, leading to the pituitary release of ACTH, which stimulates cortisol secretion from the adrenal cortex. The magnitude and duration of the cortisol surge are determined by the sensitivity of the hypothalamic and pituitary receptors, the adrenal capacity, and the negative feedback efficiency of glucocorticoid receptors. A blunted or exaggerated response indicates a breakdown in this finely tuned neuroendocrine feedback loop.
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