Here’s an excerpt from a review article that I pulled from a hair loss forum…It describes how grey pubic hair (decreased pigmentation) is a direct result of androgen deficiency…
"N. Androgen and estrogen receptors
Sex steroid receptors belong to the superfamily of trans-acting transcriptional factors, similar to glucocorticoid receptor (GR) and mineralocorticoid receptor (MR) (36, 6Cool. They are widely distributed in all skin compartments, and their density and expression level vary depending on anatomic site and gender (3, 4, 12, 160, 161, 162, 163, 164, 165, 166, 167, 168, 169, 170, 171, 172, 173). The well recognized androgen effects on hair growth and sebaceous gland functions are related to expression of the corresponding androgen receptors (ARs) in epithelial cells of those adnexal structures and in specialized dermal papilla fibroblasts that regulate hair morphogenesis (161, 162, 163, 164, 165). ARs are also expressed in other adnexal structures, in epidermal keratinocytes and melanocytes, dermal fibroblasts, and resident and circulating cells of the skin immune system (3, 4, 12, 31, 160, 161, 162, 163, 164, 165, 169). Similar to ARs, estrogen receptors (ERs) are also expressed in the epidermal, adnexal, and dermal compartments of the skin (3, 4, 12, 166, 167, 168, 170, 171, 172, 173). ERs have been detected variably, depending on the sensitivity method and presence or absence of pathology, in epithelial cells of epidermis, hair follicle, sebaceous, eccrine and apocrine glands, in melanocytes, and in dermal fibroblasts. Thus, both estrogens and androgens regulate hair growth, sebaceous gland function, proliferation and differentiation of epithelial cells of the epidermis and adnexa, functional activity of dermal fibroblasts and fibrocytes, wound healing, and skin immune cells activity. There are also data showing that androgens and estrogens can modulate proliferation and melanogenesis in cultured melanocytes (169, 170, 171). Lastly, transgenic male mice overexpressing GH show overgrowth of the skin that is androgen dependent, e.g., it is not observed in females or in castrated males (97).
Clinical signs of androgen excess include acne, hirsutism, and androgenic alopecia (3, 36, 37, 163, 164). Acne results from follicular hyperkeratinization, increased sebum production, and from the release of lipases and proinflammatory mediators by Propionicum acnes. In these conditions, androgens [mainly dihydrotestosterone (DHT) and to a lesser degree testosterone] mediate the increased sebum production and follicular hyperkeratinization (3, 37, 163, 164). Hirsutism and androgenic alopecia are associated with increased production of DHT within the dermal papilla of androgen-responsive hair follicles of the face, chest, genital skin, and scalp (3, 12, 31, 37, 163). Conversely, in males with androgen deficiency, the skin remains thin and fine; sebaceous and apocrine glands and sexual hair follicles remain dormant; beard, axillary, and pubic hair do not develop and neither does androgenic alopecia; and there is also a general decrease in skin pigmentation (3, 37, 163). Increased estrogen levels, for example during pregnancy, can lead to hyperpigmentation of nipples, areolae, genital skin, and facial skin (3). The latter, known as melasma, is exacerbated by sun exposure (3). In addition, preexisting nevi and ephelides darken, and telangiectasia, spider angioma, and palmar erythema may develop (3, 37). "
