Sleep Deprivation Consequences encompass the measurable physiological and cognitive impairments resulting from insufficient or poor-quality sleep, significantly impacting endocrine regulation and metabolic homeostasis. Acute deprivation rapidly elevates circulating catecholamines and impairs glucose tolerance, mimicking aspects of metabolic syndrome. Chronically, these consequences include blunted growth hormone secretion, dysregulated appetite hormones like ghrelin and leptin, and increased systemic inflammation.
Origin
This area of study originates from experimental sleep research, which systematically restricted sleep in human and animal models to quantify the resulting deficits in performance and physiological function. The clinical relevance grew as modern society exhibited widespread, subclinical sleep restriction, necessitating an understanding of its cumulative endocrine toll.
Mechanism
The primary mechanism involves the disruption of the HPA axis, leading to elevated nocturnal cortisol levels, which promotes insulin resistance in peripheral tissues. Furthermore, the suppression of restorative sleep stages directly inhibits the nocturnal pulses of Growth Hormone, impairing anabolic processes necessary for tissue repair. This endocrine disruption cascade contributes to increased sympathetic nervous system activity, elevating cardiovascular risk factors alongside metabolic dysfunction.
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