The disruption of normal physiological processes, particularly hormonal signaling and receptor binding, caused by excessive or inappropriately timed levels of the glucocorticoid hormone, cortisol. This interference can manifest as suppression of the hypothalamic-pituitary-gonadal (HPG) axis, leading to reduced production of sex hormones like testosterone and estrogen. Chronic stress, which elevates cortisol, is a common source of this endocrine interference. Clinically, recognizing this interference is essential for addressing symptoms that mimic primary hormonal deficiency and developing effective treatment plans.
Origin
The term is derived from the primary stress hormone “cortisol” and “interference,” meaning obstruction or hindrance. Cortisol’s widespread effects are due to its binding to glucocorticoid receptors found in nearly every cell type. The concept of its interference stems from the observation of cross-talk between the stress axis and other endocrine axes. High cortisol levels are known to directly inhibit GnRH release from the hypothalamus, providing a clear mechanism for its suppressive action.
Mechanism
Cortisol interference operates through several molecular pathways within the central nervous system. It directly inhibits the release of gonadotropin-releasing hormone (GnRH) from the hypothalamus and luteinizing hormone (LH) from the pituitary, thereby downregulating gonadal steroid production. Furthermore, cortisol can directly antagonize the action of other hormones, such as thyroid hormone, by altering receptor sensitivity or post-receptor signaling pathways. The net result is a state of functional hypogonadism or reduced metabolic efficiency, contributing to symptoms like fatigue and reduced libido.
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