Male Reproductive Aging, clinically termed andropause or late-onset hypogonadism, describes the gradual, age-dependent decline in testicular function, leading to reduced testosterone production, impaired spermatogenesis, and alterations in the hypothalamic-pituitary-gonadal (HPG) axis feedback loop. This physiological process is characterized by a decrease in Leydig cell function and often an increase in Sex Hormone-Binding Globulin (SHBG). The net result is lower bioavailable testosterone and reduced fertility potential.
Origin
This is a clinical term derived from geriatric endocrinology and reproductive medicine, combining ‘male reproductive’ function with the biological process of ‘aging.’ The recognition of a distinct, age-related hormonal decline in men, separate from acute pathology, solidified the term’s clinical utility in the late 20th century. This phenomenon contrasts with the abrupt cessation seen in female menopause.
Mechanism
The primary mechanism involves Leydig cell senescence and cumulative oxidative stress within the testes, leading to reduced steroidogenic enzyme activity and lower testosterone synthesis. Concurrently, the pituitary gland may become less sensitive to negative feedback, and the hypothalamus may alter its GnRH pulsatility, collectively disrupting the precise HPG axis communication necessary for optimal gonadal function.
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