However, most women with FPHL have no other signs or symptoms of hyperandrogenism and have normal androgen levels, indicating that our understanding of the pathogenesis of the disorder remains incomplete. The age-related increase in FPHL and the highest rates in postmenopausal women may suggest a protective role of the estrogen. Supporting this theory, Sawaya and Price conducted a study in 12 young women and 12 young men (ages from 14 to 33) suffering from Androgenetic Alopecia or FPHL [
15]. Scalp biopsies were taken and androgens, expression of androgen receptor, type I and type II 5-reductase, and cytochrome p-450 aromatase enzyme genes were measured in hair follicles.
Both young women and young men had higher levels of type I and type II 5-reductase and androgen receptors in frontal hair follicles compared to occipital hair follicles explaining probably the patterned hair loss. However, the levels in women were approximately half the levels in men [
15].
The findings of this study suggest that the milder expression of FPHL may in part be the result of lower levels of 5-reductase and androgen receptors in frontal follicles of women compared to levels in men. Additionally, young women had much higher levels of cytochrome p-450 aromatase, enzyme capable of converting testosterone to estradiol, in frontal and occipital follicles than men. Those notable increased aromatase levels seem to play a protective role in the development of hair loss in women [
15]. Furthermore, supporting the androgen-dependent etiopathogenesis, low levels of sex hormone-binding protein (SHBG), glycoprotein that binds to androgens, inhibiting thereby their activities, have been linked to diffuse hair loss [
16]. Another part of FPHL and Androgenetic Alopecia pathogenesis is the gradual shortening of the growth phase of hair follicles. Over the successive hair cycles, the duration of anagen phase shortens from a normal duration of a few years to only weeks to months [
2].