The Andropause Transition, often referred to clinically as Late-Onset Hypogonadism (LOH) or Age-Related Testosterone Deficiency, denotes the gradual, age-associated decline in circulating androgen levels, particularly testosterone, in aging men. This hormonal shift is a physiological process distinct from the abrupt cessation seen in female menopause, manifesting as a collection of non-specific symptoms including reduced libido, diminished energy, mood disturbances, and changes in body composition. Comprehensive clinical evaluation is necessary to distinguish this from other potential causes of hypogonadism.
Origin
The term is derived from the Greek words andros (man) and pausis (cessation), mirroring the structure of “menopause,” although the underlying endocrinology is fundamentally different. It gained clinical relevance as physicians recognized a pattern of symptoms in aging men correlating with decreased testicular androgen production. This biological process reflects the cumulative effect of aging on the hypothalamic-pituitary-gonadal (HPG) axis.
Mechanism
The primary mechanism involves a multifaceted failure within the HPG axis, encompassing reduced pulsatile secretion of Gonadotropin-Releasing Hormone (GnRH) from the hypothalamus and a decreased responsiveness of the testes to Luteinizing Hormone (LH). Leydig cell function in the testes diminishes with age, leading to a lower overall rate of testosterone biosynthesis. Concurrently, increased levels of Sex Hormone-Binding Globulin (SHBG) further reduce the bioavailability of free, active testosterone, exacerbating the clinical symptoms of androgen deficiency.
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