Nocturnal Cortisol Elevation describes a clinically significant deviation from the healthy cortisol diurnal variation, characterized by inappropriately high serum levels of the stress hormone cortisol during the late evening or the early sleep period. This aberrant pattern disrupts the necessary nocturnal nadir of the hypothalamic-pituitary-adrenal axis, leading directly to impaired sleep quality, increased arousal, and systemic metabolic dysregulation. It is often a sensitive clinical sign of chronic psychological or physiological stress or an underlying HPA axis hyperactivity disorder.
Origin
This term is a specific diagnostic descriptor within clinical endocrinology and functional medicine, used to precisely characterize a pathological or sub-clinical disruption of the normal circadian cortisol rhythm. It specifically focuses on the temporal error in the HPA axis output, distinguishing it from generalized hypercortisolism. The elevation is a key, sensitive indicator in the comprehensive assessment of adrenal function and various stress-related disorders.
Mechanism
The elevation mechanistically results from a dysregulated negative feedback loop within the HPA axis, frequently driven by chronic psychological or physiological stressors, which overrides the SCN’s inhibitory signal. The sustained, inappropriately high cortisol level antagonizes the action of melatonin and suppresses the entry into the deep, restorative sleep stages, leading to fragmented sleep architecture. Metabolically, this elevation promotes inappropriate nocturnal gluconeogenesis and systemic insulin resistance, significantly contributing to elevated morning fasting blood glucose levels and impaired metabolic health.
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