Metabolic Consequences Sleep Loss refers to the cascade of adverse biochemical and physiological derangements that result from insufficient quantity or poor quality of sleep. These consequences include reduced insulin sensitivity, elevated evening cortisol levels, altered ghrelin and leptin signaling, and a propensity for increased systemic inflammation. Clinically, chronic sleep deprivation directly contributes to weight gain, impaired glucose tolerance, and increased risk for cardiometabolic disease.
Origin
This concept is a central tenet of sleep medicine and chronobiology, supported by extensive experimental and epidemiological evidence demonstrating sleep’s crucial role in metabolic regulation. The phrase highlights the direct, quantifiable damage that inadequate sleep inflicts on the body’s energy balance and hormonal milieu. It underscores the vital, restorative function of sleep for endocrine homeostasis.
Mechanism
Sleep loss acutely disrupts the hypothalamic-pituitary-adrenal (HPA) axis, leading to prolonged evening cortisol elevation, which drives gluconeogenesis and insulin resistance. Furthermore, the disruption alters the balance of appetite-regulating hormones: ghrelin, the hunger hormone, increases, while leptin, the satiety hormone, decreases, promoting overeating and weight gain. This combined hormonal and metabolic dysregulation creates a state of energy imbalance and systemic stress, accelerating the trajectory toward chronic disease.
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