Stress Cortisol Impact refers to the widespread physiological and metabolic consequences resulting from chronic or dysregulated secretion of the glucocorticoid hormone, cortisol, in response to prolonged psychological or physical stress. While acute cortisol release is adaptive, sustained high levels negatively affect glucose metabolism, immune function, sleep architecture, and fat distribution. Clinically, mitigating this impact is essential for preventing adrenal fatigue, metabolic syndrome, and mood disorders.
Origin
This term is central to the field of neuroendocrinology, stemming from Hans Selye’s original work on the General Adaptation Syndrome and the subsequent characterization of the Hypothalamic-Pituitary-Adrenal (HPA) axis. The concept highlights the pervasive, detrimental effects of chronic HPA axis activation on systemic health. It connects psychological state directly to measurable endocrine function.
Mechanism
The impact is mediated by cortisol binding to intracellular glucocorticoid receptors in nearly every tissue, altering gene expression and cellular activity. Chronically elevated cortisol promotes gluconeogenesis in the liver, leading to hyperglycemia, and favors the deposition of visceral fat by increasing lipoprotein lipase activity. Furthermore, it suppresses immune responses and disrupts the normal diurnal rhythm of the HPA axis, leading to systemic dysregulation.
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