The dermatological and structural alterations observed in men corresponding to the age-related decline in androgen levels, specifically testosterone, a condition clinically termed andropause or late-onset hypogonadism. These changes manifest as a progressive thinning of the epidermis and dermis, diminished collagen density, and reduced elasticity. Clinically, this hormonal shift contributes to increased skin fragility, impaired wound healing capacity, and a reduction in sebaceous gland activity leading to dryness.
Origin
The term combines “andropause,” derived from the Greek andro (man) and pausis (cessation), and “skin changes,” referring to the resulting cutaneous modifications. This concept is rooted in endocrinology and gerontology, linking systemic hormonal shifts to specific organ system deterioration. It is a physiological descriptor within the continuum of male aging and hormonal regulation.
Mechanism
Reduced circulating testosterone diminishes its signaling through dermal androgen receptors, which are crucial for fibroblast activity and collagen synthesis. This decline in anabolic signaling leads to a net catabolic state within the dermal matrix, reducing the production of structural proteins like collagen and elastin. Furthermore, the decrease in androgen-dependent sebum production compromises the skin’s barrier function, contributing to xerosis and increased trans-epidermal water loss.
We use cookies to personalize content and marketing, and to analyze our traffic. This helps us maintain the quality of our free resources. manage your preferences below.
Detailed Cookie Preferences
This helps support our free resources through personalized marketing efforts and promotions.
Analytics cookies help us understand how visitors interact with our website, improving user experience and website performance.
Personalization cookies enable us to customize the content and features of our site based on your interactions, offering a more tailored experience.