Exploring The Hormonal Route. Hair=life.

[Letsdoit]

Our persian brother got banned again, miss u bro!
#freedhtcel

We live in a society and if you break the rules you're out, he's out. Some people learn from their mistakes and deserves a second chance but he's doing the same sh*t over and over and over. Am I the only one here that thinks it's weird that he engages in conversation with multiple accounts mass liking and disliking post? Instead of petting his back why don't you question him, why do you feed his behavior?

 

[BRezende]

We live in a society and if you break the rules you're out, he's out. Some people learn from their mistakes and deserves a second chance but he's doing the same sh*t over and over and over. Am I the only one here that thinks it's weird that he engages in conversation with multiple accounts mass liking and disliking post? Instead of petting his back why don't you question him, why do you feed his behavior?

Look, im not feeding anything. The version he told me was different, but im not interest in this, because we are in a hair loss fórum, soo the only thing which matters for me here is informations about the disease we share, i dont give a f*** about likes and dislikes and you guys should do the same. DHTcel had a lot of information, thats why his presence is valueable for the discussion

 

[BRezende]

stop problematizing everything

 

[Father_of_Shiseido]

#freedhtcell

 

[Michael1986]

@MostoleTinker and @ikarus2 is DHTcel and he is mass disliking my posts because I dragged him on discord

We live in a society and if you break the rules you're out, he's out. Some people learn from their mistakes and deserves a second chance but he's doing the same sh*t over and over and over. Am I the only one here that thinks it's weird that he engages in conversation with multiple accounts mass liking and disliking post? Instead of petting his back why don't you question him, why do you feed his behavior?

You can't put an old head on young shoulders, unfortunately

 

[keepcoolmybabies]

It still remains unproven whether estrogen gives results by itself or because it blocks androgens more effectively. If we believe that androgens are a common cause in both men and women, then we can say estrogen doesn't cause regrowth because of increase in its levels because women have a lot of it) but because it reduces androgens. However, bridge and other folks here believe that estrogen directly promotes hair growth. We would never know unless there are studies on it.

Another point to note is that some people experience regrowth on finasteride so we can say it's blockage of androgens, but then finasteride also increases E.

Bottom line - you can't block/decrease you androgens without increasing E (possible w cypro though) and therefore we might never know for sure.

This is tricky as there's evidence for both high and low estrogen linked to loss or growth.

For instance, there are studies with eunuchs showing that while their hair loss stopped upon castration, they didn't get growth without supplementing estrogen. Moreover, women often get increased hair density while pregnant and their estradiol levels are sky high. But the caveat is so are their progesterone levels. So post partum hair loss might be due simply to a drop in E or because of a ratio imbalance between estrogen and progesterone. Not to mention, women are prone to experience FPHL once they hit menopause and their estrogen levels plummet (but again so do their progesterone levels).

On the other hand, higher estrogen can be linked to hair loss in the case of a "variation in the gene encoding aromatase, CYP19A1."

But it seems likely to help on most cases. However, it seems there's a delicate balance to hormone ratio and throwing it out of whack can possibly induce hair loss. I just want @bridgeburn to finally get his levels checked to see if there's a magic sweet spot he managed to hit to get the insane amount of regrowth he did. Do it for science!

 

[I'mme]

For instance, there are studies with eunuchs showing that while their hair loss stopped upon castration, they didn't get growth without supplementing estrogen.

Maybe because they're not taking anti-androgen and their adrenals were secreting more of androgen to compensate for the lack of it.

During pregnancy various processes occur, they also produce some p named substance/hormone which increase their height by a few cms.

If an increase in estrogen increases density, dermatologists around the world shouldn't be having any problems prescribing E to women. Also, many women on forums must have been using it, which also doesn't seem to be the case as they're trying techniques like inversion one lol

 

[bridgeburn]

"ERβ knockout mice display accelerated catagen development, along with an increase in the number of apoptotic hair follicle keratinocytes (28). This suggests that, contrary to previous working hypotheses (274), ERβ does indeed play a significant role in murine hair growth control: whereas the catagen-promoting properties of E2 are mediated via ERα, ERβ may mainly function as a silencer of ERα action in hair biology (28). Nevertheless, ERα is thought to serve as the predominant ER in the hair follicle of animals (31, 233, 254)."

"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). Orentreich observed in 1969 a decrease in daily effluvium during therapy with systemic estrogens (285), which were reported to increase the proliferation rate, slow down differentiation, and, thus, postpone telogen effluvium (286)."

"progesterone receptor, prolactin, and lactoferrin are examples of relevant target genes in the pilosebaceous unit with consensus EREs (263–265)."

"The number of genes that carry an ERE, whose transcription is known to be altered by E2 stimulation, is very large (294) (Table 3). Together with the fact that E2 modifies androgen metabolism and vice versa (250, 251) and the intriguing cross talk examples discussed above, this already renders the number of potential signaling cross talks and cross-modulation events that may impact how E2 can alter the growth of a given hair follicle in a defined gender and location daunting. This gets even more complicated if one enters additional recent findings into the equation. Suffice it here to list just two selected examples of this added level of complexity: possible cross talks between E2/ER and intrafollicularly generated hormones, such as melatonin (53) and prolactin (8, 9)."

 

[bridgeburn]

"Plucked human hair follicles demonstrate aromatase activity in culture (Schweikert et al., 1975), while a comparison of scalp biopsies from men and women with androgenetic alopecia revealed aromatase levels to be higher in hair follicles from occipital scalp when compared to those from the frontal scalp (Sawaya and Price, 1997)."

"Furthermore, the same study found that aromatase levels were approximately six times higher in the frontal hair follicles of women when compared to men."

 

[I'mme]

"ERβ knockout mice display accelerated catagen development, along with an increase in the number of apoptotic hair follicle keratinocytes (28). This suggests that, contrary to previous working hypotheses (274), ERβ does indeed play a significant role in murine hair growth control: whereas the catagen-promoting properties of E2 are mediated via ERα, ERβ may mainly function as a silencer of ERα action in hair biology (28). Nevertheless, ERα is thought to serve as the predominant ER in the hair follicle of animals (31, 233, 254)."

"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). Orentreich observed in 1969 a decrease in daily effluvium during therapy with systemic estrogens (285), which were reported to increase the proliferation rate, slow down differentiation, and, thus, postpone telogen effluvium (286)."

"progesterone receptor, prolactin, and lactoferrin are examples of relevant target genes in the pilosebaceous unit with consensus EREs (263–265)."

"The number of genes that carry an ERE, whose transcription is known to be altered by E2 stimulation, is very large (294) (Table 3). Together with the fact that E2 modifies androgen metabolism and vice versa (250, 251) and the intriguing cross talk examples discussed above, this already renders the number of potential signaling cross talks and cross-modulation events that may impact how E2 can alter the growth of a given hair follicle in a defined gender and location daunting. This gets even more complicated if one enters additional recent findings into the equation. Suffice it here to list just two selected examples of this added level of complexity: possible cross talks between E2/ER and intrafollicularly generated hormones, such as melatonin (53) and prolactin (8, 9)."

Umm.. maybe. When then some people like Anxiousandy, obsessive etc didn't respond to it?

 

[bridgeburn]

Umm.. maybe. When then some people like Anxiousandy, obsessive etc didn't respond to it?

Idk, some people don't respond to anything or hardly anything, even proven treatments

 

[I'mme]

To quote - "Among genetically predisposed individuals, androgenetic alopecia is characterized by an androgen-responsive hair loss. Pattern alopecia results in a decrease in hair follicle size accompanied by a decrease in the duration of anagen and an increase in the percentage of hair follicles in telogen with follicular miniaturization, which is the histological hallmark of androgenetic alopecia.'

To answer @keepcoolmybabies, bridge demolished androgens as well as increased the phase of anagen (oral minoxidil), so it's not wonder he saw such a tremendous regrowth.

 

[I'mme]

"In vitro, testosterone and estrogen inhibit hair growth, suggesting that scalp hair growth may be controlled by these sex hormones."

Haha.. I dunno what to say now.

 

[bridgeburn]

Whenever Estradiol is increased, so is SHBG. If that is increased too much it can also render estradiol less effective. Cause E also kills our androgens, Shbg binds preferentially in the following order: DHT > T > E2 > E1

we need a little bit of androgens in the blood or else SHBG which is increased by estradiol will bind to estradiol making the weaker estrone predominant.. but we certainly don't need those androgens on the receptors, just in the blood and not too much.. that's why I believe bicalutimide is perfect for this

(Estrone has greater affinty for ER alpha over Beta, during pregnancy Estriol is greatly increased which is very low any other time, estriol has preferiantial affinty toward ERbeta)

 

[bridgeburn]

"In vitro, testosterone and estrogen inhibit hair growth, suggesting that scalp hair growth may be controlled by these sex hormones."

Haha.. I dunno what to say now.

are they talking about mice?

(in vitro estrogen slows down human hair growth but keeps it in the growing phase longer, testosterone slows it down and puts in early telogen)

 

[I'mme]

That's what I've been saying time and again here mate - completely throwing T or DHT into oblivion is not the cure cause Androgenetic Alopecia isn't caused by increased levels of T or DHT directly, but because of increase AR sensitivity or Androgen Receptor density (note that increase in T also increases ARs so we definitely wouldn't want to increase T even though it may not be causing hair loss by itself).

 

[I'mme]

are they talking about mice?

(in vitro estrogen slows down human hair growth but keeps it in the growing phase longer, testosterone slows it down and puts in early telogen)

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5817427/

 

[bridgeburn]

Androgenetic Alopecia isn't caused by increased levels of T or DHT directly, but because of increase AR sensitivity or Androgen Receptor density (

It is caused by the local concetration in the follicles rather than the overall systematic amount.
that combined with sensitivity

"Balding scalp tissues also express higher DHT than non-balding hair-bearing scalp tissues from the same male [7] "

 

[Michael1986]

It is caused by the local concetration in the follicles rather than the overall systematic amount.
that combined with sensitivity

"Balding scalp tissues also express higher DHT than non-balding hair-bearing scalp tissues from the same male [7] "

Indeed. The male pattern baldness process is dependent upon the combined effect of androgen levels within the dermal papillae of the hair follicles and the sensitivity of these follicles to these androgens, the latter of which is determined by the number of androgen receptor sites in the dermal papillae (the more you have, the greater the sensitivity, and this is thought to increase with age).

 

[I'mme]

Indeed. The male pattern baldness process is dependent upon the combined effect of androgen levels within the dermal papillae of the hair follicles and the sensitivity of these follicles to these androgens, the latter of which is determined by the number of androgen receptor sites in the dermal papillae (the more you have, the greater the sensitivity, and this is thought to increase with age).

Exactly.. AR are dense in some people plus they are sensitive, causing them to bald frequently. @Ikarus for eg has very aggressive hair loss.

But as I said, lower T should also lower ARs - at least in theory.
Allso, no need to lower T if you can block or reduce ARs in the scalp.