Andropause pathophysiology describes the biological mechanisms and functional changes underlying the age-related decline in male reproductive and hormonal function, often termed late-onset hypogonadism. This process is characterized primarily by a gradual reduction in circulating testosterone levels, a phenomenon distinct from the rapid hormonal shift of menopause. The complex interplay of primary, secondary, and tertiary factors contributes to the diverse clinical symptoms observed in aging men. Understanding the pathophysiology is essential for accurate diagnosis and targeted endocrine intervention.
Origin
The term merges ‘Andropause,’ derived from the Greek andro- (man) and pausis (cessation), with ‘Pathophysiology,’ which combines pathos (suffering), physis (nature), and logia (study of). This etymology reflects the study of the disordered functional changes associated with the aging male’s hormonal environment. Clinically, it acknowledges that while not a complete cessation like menopause, the hormonal decline leads to a symptomatic state of diminished well-being.
Mechanism
The core mechanism involves a combination of hypothalamic-pituitary-gonadal axis dysfunction and intrinsic testicular aging. Luteinizing Hormone (LH) pulses may become less frequent or less robust, and Leydig cell responsiveness in the testes decreases over time. Furthermore, an age-associated increase in Sex Hormone-Binding Globulin (SHBG) often reduces the bioavailable free testosterone fraction. This cascade of events leads to a chronic state of relative androgen deficiency, impacting multiple organ systems including bone density, muscle mass, and neurocognitive function.
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