Endocrine system aging describes the complex, multifaceted process characterized by a progressive, measurable decline in the structural integrity and functional capacity of the endocrine glands and their central regulatory axes over an individual’s lifespan. This physiological decline is marked by altered hormone production rates, reduced sensitivity of target tissue receptors, and a compromise in the essential pulsatile secretion patterns of key regulatory hormones. Clinical manifestations include somatopause, adrenopause, and gonadal senescence, collectively contributing to the metabolic and functional changes associated with aging. Understanding this systemic degradation is fundamental to the clinical practice of longevity and preventative medicine.
Origin
The study of aging has always been central to physiology, but the specific focus on “endocrine system aging” gained significant clinical and research momentum in the latter half of the 20th century with the ability to precisely measure circulating hormone concentrations. This conceptual evolution recognized that aging is not merely a localized cellular process but a system-wide phenomenon heavily influenced by the neuroendocrine regulatory network. The term serves to differentiate between the inevitable, yet manageable, age-related changes and pathological endocrine disorders, providing a framework for targeted hormonal interventions.
Mechanism
The mechanism involves a combination of cellular senescence within glandular tissues, leading to reduced synthetic capacity and lower basal hormone secretion, as seen in the age-related decline of DHEA and growth hormone. Simultaneously, target tissues often exhibit reduced receptor density or impaired post-receptor signaling, resulting in functional hormone resistance, notably affecting insulin and thyroid hormone action. Furthermore, the central hypothalamic-pituitary unit demonstrates altered feedback sensitivity and reduced pulsatility, compromising the rhythmic, coordinated release essential for optimal physiological signaling. These interconnected failures lead to a less resilient homeostatic capacity and increased vulnerability to metabolic stress.
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