Cortisol suppression mechanisms are the physiological and pharmacological pathways that actively reduce the secretion and circulating concentration of the stress hormone cortisol. Physiologically, this is achieved through a negative feedback loop where high cortisol levels inhibit the release of ACTH and CRH from the pituitary and hypothalamus, respectively. Clinically, suppression tests are utilized to diagnose hypercortisolism, such as Cushing’s syndrome, by observing the response to exogenous glucocorticoids. These mechanisms are vital for preventing chronic stress-induced pathology.
Origin
The term combines “cortisol,” the stress steroid, with “suppression,” indicating a forced reduction, and “mechanisms,” referring to the underlying biological processes. The fundamental origin lies in the discovery of the Hypothalamic-Pituitary-Adrenal (HPA) axis and its intrinsic negative feedback regulation, a core principle of endocrinology. Understanding these mechanisms is vital for managing chronic stress and endocrine disorders.
Mechanism
The primary physiological mechanism involves cortisol binding to glucocorticoid receptors (GR) in the hypothalamus and anterior pituitary. This binding inhibits the transcription and release of CRH and ACTH, thereby reducing the signal for the adrenal glands to produce more cortisol. Pharmacological suppression, often via synthetic steroids like dexamethasone, leverages this negative feedback to assess the integrity and function of the HPA axis’s regulatory components. This self-regulatory process is essential for recovery.
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