Hormonal aging refers to the progressive, often predictable decline and dysregulation in the production, secretion, and action of various hormones that occur with advancing chronological age. This process involves a reduction in the amplitude of pulsatile hormone release, altered feedback sensitivity within the neuroendocrine axes, and a decrease in receptor responsiveness in target tissues. The clinical manifestations include somatopause (GH/IGF-1 decline), andropause, menopause, and adrenopause, all contributing significantly to the overall aging phenotype and loss of homeostatic resilience. It is a core driver of many age-related health changes.
Origin
This concept is a central theme in geroscience and endocrinology, acknowledging that the endocrine system is a key driver and regulator of the aging process. The term frames aging not merely as a random decline but as a structured, albeit unfavorable, shift in endocrine set-points. Research in this area seeks to differentiate pathological decline from normal senescence.
Mechanism
The mechanism involves a complex cascade of events, including the age-related accumulation of cellular damage in endocrine glands, reduced enzymatic efficiency in hormone synthesis, and alterations in hypothalamic-pituitary signaling. For example, decreased pulsatile GnRH release contributes to the decline in sex steroids, while increased inflammatory signaling can dampen the sensitivity of peripheral receptors to circulating hormones. This systemic dysregulation compromises the body’s ability to maintain metabolic and reproductive function.
Molecular signatures of hormonal aging are proteomic shifts in tissues, revealing how endocrine decline orchestrates systemic aging at different rates.
Targeted lifestyle and clinical interventions can modulate neuroinflammation and support the systems that sustain cognitive function during hormonal aging.
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