I posted this excerpt in a different thread titled exploring the hormonal route.
I highly ask anyone following this thread to read the entire article and the relevant excerpts I summarized below:
According to this well known study:
https://academic.oup.com/edrv/article/27/6/677/2355194
The Hair Follicle Is An Estrogen Target And Source. I HIGHLY ADVISE EVERYONE ON THIS FORUM TO READ THAT PAPER BECAUSE IT WILL DEFINITELY BE WORTH YOUR WHILE.
I will try my very best to sum up the relevant excerpts:
Here you go. Brace yourselves as this post is going to be very long....
Taken from:
https://academic.oup.com/edrv/article/27/6/677/2355194
"For many decades, androgens have dominated endocrine research in hair growth control. Androgen metabolism and the androgen receptor currently are the key targets for systemic, pharmacological hair growth control in clinical medicine. However, it has long been known that estrogens also profoundly alter hair follicle growth and cycling by binding to locally expressed high-affinity estrogen receptors (ERs)."
"Besides altering the transcription of genes with estrogen-responsive elements, 17β-estradiol (E2) also modifies androgen metabolism within distinct subunits of the pilosebaceous unit (i.e., hair follicle and sebaceous gland). The latter displays prominent aromatase activity, the key enzyme for androgen conversion to E2, and is both an estrogen source and target."
"Estrogens are able to modify androgen metabolism within distinct subunits of the hair follicle (e.g., in the dermal papilla), diminishing the amount of 5α-dihydrotestosterone formed after incubation with testosterone."
"Also, many of the growth and transcription factors, cytokines, and hormones that are currently recognized to control hair growth (21, 34–36) are themselves modulated by estrogens."
"We still do not know exactly what cellular or molecular mechanisms control these vascular changes. Besides the two major recognized angiogenesis stimulators, vascular endothelial growth factor (VEGF) and hepatocyte growth factor (HGF) (65–67), processes of angiogenesis can generally be modulated by hormonal changes, including changes in estrogen levels (68). In fact, E2 reportedly even stimulates human hair follicle synthesis of VEGF."
"A multibillion dollar industry worldwide caters to the unmet needs in managing unwanted hair loss (alopecia, effluvium) and unwanted hair growth (hirsutism, hypertrichosis) (87), advertising allegedly hair growth-stimulating products or procedures such as vitamins, trace elements, exotic herbs, amino acids, etc., which typically have not been subjected to professionally designed and executed clinical trials (88). Although topical formulations containing either 17β- or 17α-estradiol have long been successfully employed for the treatment of androgenetic alopecia, where they appear to improve the telogen/anagen ratio of scalp hair follicles, this critique also applies here."
"Moreover, in different cell types, estrogen regulates the expression of EGF, IGF-I, and TGFα, suggesting that these growth factors are mediators of estrogen action (181). Thus, given the well-appreciated central role of IGF-I, EGF, and TGFα in hair follicle biology, the cross talk between peptide growth factors and ER signaling pathways may be highly relevant in hair growth control."
"ERs are more widely expressed, and importantly, ERβ is strongly expressed in the bulge region of the outer root sheath. This region contains stem cells for hair follicle keratinocytes that regenerate the follicle during the anagen phase. This suggests that these epithelial stem cells are targets for estrogen action."
"Estrogen target genes in the pilosebaceous unit."
"For human scalp hair, topical E2 has long been used in the management of telogen effluvium and androgenetic alopecia, especially in women (29, 58, 275). Although this remains to be unequivocally demonstrated in vivo, E2 has been proposed to decrease the telogen rate and to prolong the anagen phase in human scalp skin, justifying the use of topical E2 in the management of hair loss characterized premature catagen entry, such as androgenetic alopecia and telogen effluvium. This makes estrogen species-dependent as the opposite effects are shown in mice and rats."
"Although rodent hair follicles generally respond to E2 stimulation with an inhibition of hair shaft formation, this is not necessarily true for human scalp hair follicles, at least in males. Studying the isolated effects of E2 on human hair growth in vitro (in organ-cultured, microdissected human anagen hair bulbs), we recently showed that, in frontotemporal male hair follicles, E2 indeed slightly prolongs anagen and stimulates hair shaft elongation (11). Corresponding studies (279–281) have reported that E2 inhibits hair shaft elongation in vitro or that E2 does not influence the decay rate of organ-cultured human anagen hair follicles from occipital scalp skin (measured by morphology and autoradiographic 3H-thymidine incorporation) (279). These partially conflicting reports may become reconciled, once larger studies with organ-cultured human scalp hair follicles have been performed that systematically distinguish between male, female, frontotemporal, and occipital follicle populations, and that correlate hair shaft elongation with hair cycle effects. In addition, these in vitro studies need to be complemented by and compared with the results of clinical trials on the scalp hair growth effects of topical E2, documented by professional phototrichogram methodology."
"Estrogens act, either alone or together with androgens, directly at the level of the hair follicle in pubic skin to stimulate hair growth. However, in the absence of active androgen receptors, E2 cannot promote sexual hair growth, e.g., in patients with complete testicular feminization who do not grow pubic and axillary hair, despite signs of E2 effects in other tissues (33).
In human occipital scalp hair follicles, E2 may inhibit hair shaft elongation in both males and females in vitro (279, 280). However, we found sex-dependent differences of frontotemporal scalp hair shaft elongation after E2 treatment in vitro: in females the hair shaft elongation was inhibited, whereas E2 significantly stimulated hair shaft elongation in human frontotemporal anagen hair follicles from male patients in vitro (12, 281). This corresponded to a significantly up-regulated proliferation rate of the matrix keratinocytes in the male frontotemporal scalp hair follicles compared with female hair follicles (12)."
THIS ONE IS MY FAVORITE EXCERPT:
"Estrogens have been used for topical treatment of hair diseases for more than half a century (284) and constitute a firm staple of management strategies for female pattern androgenetic alopecia in central Europe (88)."
ANOTHER FAVORITE EXCERPT:
"Exciting new connections between the ER and other important factors critically involved in hair growth control were found in recent years. This is highlighted by the convergence of estrogen signaling with the Wnt signal transduction pathway (320, 321) (Fig. 6). The morphogenetic factors involved in this pathway have been the subject of studies centered on the hair follicle, including stem cell regulation, hair follicle induction, morphogenesis, and differentiation (323–326)."
Again. I highly urge all of you to read this study like your life depended on it.