Androgen Decline refers to the progressive, age-related decrease in the production and circulating levels of androgens, primarily testosterone and dehydroepiandrosterone (DHEA), in both men and women. In men, this is commonly referred to as late-onset hypogonadism or andropause, characterized by a slow, steady reduction that often begins after age thirty. For women, the decline in ovarian and adrenal androgen production occurs during the perimenopausal and postmenopausal transitions. This hormonal shift can contribute to a spectrum of clinical symptoms, including reduced bone mineral density, diminished muscle mass, and changes in sexual function. Clinicians assess this state by measuring total and free androgen levels, often alongside gonadotropins, to confirm a biochemical deficiency.
Origin
The term androgen itself is derived from the Greek words andros, meaning man, and genes, meaning producing, reflecting the initial understanding of these hormones as male-specific. The recognition of a clinically significant, age-related decline in men gained prominence in the late 20th century, formalizing the concept of andropause. Subsequent research confirmed that androgens are critical for physiological function in women as well, leading to the broader clinical descriptor of androgen decline in the context of aging. This clinical understanding has evolved to view the decline as a natural, yet often symptomatic, component of the endocrine aging process.
Mechanism
The decline is driven by complex changes within the Hypothalamic-Pituitary-Gonadal (HPG) axis, the central regulatory loop for sex hormones. In the testes, the Leydig cells exhibit reduced responsiveness to Luteinizing Hormone (LH) stimulation, leading to a primary decrease in testosterone synthesis. Concurrently, there is often an increase in Sex Hormone-Binding Globulin (SHBG), which further reduces the bioavailable fraction of circulating androgens. This combination of decreased production and increased binding leads to a functional deficit at the cellular receptor level. The resulting lack of androgenic stimulation contributes to sarcopenia, mood changes, and other systemic effects observed in the aging population.
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