Andropause, often clinically termed Late-Onset Hypogonadism or Age-Related Testosterone Deficiency, describes the gradual decline in bioavailable testosterone levels and the corresponding clinical symptoms experienced by some aging males. This physiological process is not an abrupt cessation like menopause but rather a slow, progressive reduction in gonadal function and subsequent endocrine signaling. Symptoms can include reduced libido, fatigue, decreased muscle mass, increased visceral adiposity, and subtle neurocognitive changes.
Origin
The term combines the Greek roots “andro,” meaning male, and “pausis,” meaning cessation or pause, paralleling the established term for the female transition, menopause. Although the phenomenon of age-related hormonal decline has long been observed, the formal clinical terminology gained traction as endocrinologists sought to define the syndrome associated with symptomatic testosterone deficiency in older men. This nomenclature reflects a clinical recognition of a distinct age-related endocrine syndrome.
Mechanism
The mechanism involves a complex interplay between primary testicular failure and secondary hypothalamic-pituitary axis dysfunction. The Leydig cells in the testes show reduced responsiveness to Luteinizing Hormone (LH), leading to diminished testosterone biosynthesis. Simultaneously, the hypothalamic-pituitary-gonadal axis exhibits altered pulsatility and sensitivity, contributing to the overall decline in circulating androgens. This reduced endocrine signaling perturbs the anabolic-catabolic balance and contributes to the clinical presentation of the syndrome.
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