Endocrine System Senescence refers to the gradual, age-related decline in the structural integrity and functional capacity of the body’s hormone-producing glands and their respective feedback loops. This process involves reduced hormone synthesis, altered receptor sensitivity, and less precise regulatory control. Common clinical manifestations include somatopause, andropause, and menopausal transition, all characterized by measurable shifts in circulating hormone concentrations. Understanding and mitigating this physiological slowdown is central to longevity medicine and hormonal optimization strategies.
Origin
The term is derived from the Greek word endon meaning within, krinein meaning to separate, and the Latin word senescere meaning to grow old. The recognition of age-related hormonal decline has been a focus of endocrinology for decades, moving from simple observation to molecular investigation. Research into the hypothalamic-pituitary axes has elucidated the complex changes in signaling that drive this systemic functional decrease. The clinical relevance is now paramount in addressing the multifaceted symptoms of aging.
Mechanism
Senescence is driven by several interconnected factors, including telomere shortening, increased oxidative stress within glandular tissues, and the accumulation of cellular damage. The hypothalamic-pituitary signaling often becomes less responsive, leading to blunted pulsatile release patterns, such as those observed with growth hormone. Furthermore, peripheral tissues may exhibit reduced receptor density or affinity, meaning that the remaining hormones are less effective at their target sites. This cumulative effect compromises metabolic function, bone density, and muscle mass maintenance.
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