The underlying physiological processes responsible for the age-associated reduction in circulating levels and/or target tissue responsiveness to key endocrine signals, such as androgens, estrogens, and growth hormone. Understanding these mechanisms is prerequisite to developing effective endocrine support strategies. This decline impacts tissue repair and metabolic flexibility.
Origin
This area of study arises from the clinical observation of endocrinopathies common in older populations, synthesizing data from reproductive aging, somatopause, and adrenal fatigue models. It describes the multifactorial nature of endocrine system aging, moving beyond simple glandular exhaustion. The mechanisms reflect cumulative cellular insults over time.
Mechanism
Key mechanisms include reduced secretory capacity of endocrine glands, increased synthesis of hormone-binding globulins (e.g., SHBG, CBG) that sequester active hormones, and diminished receptor sensitivity at the cellular level. Furthermore, changes in upstream signaling from the hypothalamus and pituitary contribute significantly to overall systemic reduction. For instance, decreased amplitude of growth hormone pulses reflects somatopause progression.
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