General Orange
Member
Were is the evidence Sir?Nope.
Estradiol can bind both alpha and beta, that's why it can regrow hair.
Follow along with the video below to see how to install our site as a web app on your home screen.
Note: This feature may not be available in some browsers.
Click Here if you want to upgrade your account
If you were able to post but cannot do so now, send an email to admin at raypeatforum dot com and include your username and we will fix that right up for you.
Were is the evidence Sir?Nope.
Estradiol can bind both alpha and beta, that's why it can regrow hair.
Were is the evidence Sir?
We know estrogens have a modulating role in hair growth cycle. So yes estradiol could grow hair, but it also can inhibit it for example via anandamide via cannabinoid receptors.Transgender & hair loss forums..
Namely, the endocannabinoid N-arachidonoylethanolamide (anandamide, AEA) as well as the exocannabinnoid delta (9) -tetrahydrocannabinol dose-dependently inhibited hair shaft elongation and the proliferation of hair matrix keratinocytes, and induced intraepithelial apoptosis and premature HF regression (catagen). These effects were inhibited by a selective antagonist of cannabinoid receptor-1 (CB1). In contrast to CB2, CB1 was expressed in a hair cycle-dependent manner in the human HF epithelium. Since we successfully identified the presence of endocannabinoids in human HF, our data strongly suggest that human HF exploit a CB1-mediated endocannabinoid signaling system for negatively regulating their own growth. Clinically, CB1 agonists may therefore help to manage unwanted hair growth, while CB1 antagonists might counteract hair loss. Finally, human HF organ culture offers an instructive, physiologically relevant new research tool for dissecting "nonclassical" effects of endocannabinoids and their receptor-mediated signaling in general.
Inhibition of human hair follicle growth... (PDF Download Available). Available from: https://www.researchgate.net/public..._follicle_growth_by_endo-_and_exocannabinoids [accessed May 23 2018].
I'm aware of that, Estrone synthesis is not dependent on testosterone in the skin, therefore a valid suspect in hair loss for women and men. See picture in OP, read linked document.Op you’re misunderstanding the fact that... ahem women aren’t men, that they have vastly different amounts of progesterone, estrone estradiol and estriol. That high testosterone is bad for them whereas it’s desirable for us. And so on.
Oh no? what is this......and estradiol isn’t indeed the hair villain....
We know estrogens have a modulating role in hair growth cycle. So yes estradiol could grow hair, but it also can inhibit it for example via anandamide via cannabinoid receptors.
If you cannot deliver evidence, what are you even doing here?
I want to see concrete evidence of claims please, not worthless bla bla bla.
-Well, yeah, but also with increased progesterone that helps with being a negative allosteric modulator against overactive Estradiol.less testosterone, more estrogen, is what constitutes the typical person losing hair though, like the guy with the giant gut, develop gyno, and has MPB, what are you saying, that only that specific type of estrogen will increase hair growth? it seems like a double edged sword right? how people taking diane35 or whatever will lose libido, or trans genders will lose testosterone, but develop hair, but regular men with the signs of MPB will also be increasing estrogen, but i dont know the difference between these two cases
Possibly... But also the follicle stay longer in the anagen or growth phase and less in the rest phase, which is also a difference between gender.Estrone elevations probably explain why the hair of pregnant women grows so long and thick.
Thank you for your input @benaoao , Any idea what is the mechanism behind excessive tissue DHT? how do you think we can reduce or rather prevent this tissue buildup of DHT? Would a DHT displacement on SHBG be something useful, like Beta sitosterols ? Massages ?The root issue is the same anyway, it’s a poor metabolism (too much stress, insufficient nutrition) leading to hypothyroidism and low enzyme activity. In men, this leads to low T, high tissue DHT. We certainly don’t care about estrone, and estradiol isn’t indeed the hair villain. A healthy thyroid has a healthy balance in DHT metabolites, one of them acting like an estrogen and being protective.
Thank you for your input @benaoao , Any idea what is the mechanism behind excessive tissue DHT? how do you think we can reduce or rather prevent this tissue buildup of DHT? Would a DHT displacement on SHBG be something useful, like Beta sitosterols ? Massages ?
Thank you for your input @benaoao , Any idea what is the mechanism behind excessive tissue DHT? how do you think we can reduce or rather prevent this tissue buildup of DHT? Would a DHT displacement on SHBG be something useful, like Beta sitosterols ? Massages ?
https://www.researchgate.net/figure...-the-production-of-more-potent_fig1_236201265
We see here the mechanism involved for getting DHT in the skin.
We see DHEA is chopped into A into T then the last step involved is 5AR > DHT.
Would 5AR be overactive and steal away our precious T ? Or 17bHSD be overactive?
Or something else be going on with Androstenedione?
Androstenedione comes in the skin tissue, see figure, and somehow does not go to hair growth receptors and is stuck there.
Lets assume some estrogen is needed for the hair growth receptor, like E1.
But somehow aromatase is not active enough to make E1.
In other words Androstenedione does not get synthesized into E1 via aromatase, so eventually catches 17bHSD > 5AR and becomes DHT.
DHT accumulates in hair follicle and shrinks it.
Now I must conclude something crazy: aromatase is not active enough, so Androstenedione is shunted into DHT.
I propose an inducer for aromatase would help in this situation.
Natural candidates are: quercetin and soy
Induction and inhibition of aromatase (CYP19) activity by natural and synthetic flavonoid compounds in H295R human adrenocortical carcinoma cells. - PubMed - NCBI
In theory topical application of these should reduce conversion of Androstenedione into DHT.
I grew new hair on my temples for free, wanna know how? Applied semen to the bald spots year ago. Only the hairs stay small, so something is inhibiting the growth cycles.There are people claiming this estrogen product helps regrow hair around the hairline. Tiny new hairs popping up within a few weeks. No sides reported so far.
https://au.iherb.com/pr/Life-Flo-He...N6GcWV2EUsq1Ji_BP4BoCWeQQAvD_BwE&gclsrc=aw.ds
- So females are better of with only Quercetin in their solution for hair growth.Recent in vitro studies have shown that 17β-estradiol inhibits female scalp hair shaft elongation (Nelson 2006), although stimulation occurs in hair follicles derived from frontotemporal male scalp (Conrad et al 2004; Conrad and Paus 2004). In addition, in female hair follicles the phytoestrogen, genistein inhibits hair shaft elongation to a similar extent as 17β-estradiol. Since genistein preferentially binds to ERβ, this opens the possibility that the inhibition of hair growth in response to 17β-estradiol may be mediated via ERβ rather than ERα (Nelson 2006). Therefore the development of selective estrogen receptor ligands may provide important clinical applications for the prevention and treatment of disorders of hair growth.
For instance, this year it was noted that balding males 18-35 years old were found to have increased adrenal production of DHEA, which was "significantly associated with increased clinical severity of male pattern androgenic alopecia.”[6] Moreover, the group had a mean thyroid stimulating hormone (TSH) level of 2.5 μIU/mL suggesting a higher functioning pituitary and enhanced cortisol secretion.[7] Another study performed this year also found increased levels of DHEA in those with premature baldness, in addition to higher levels of prolactin, and a lower sex hormone binding globulin (SHBG), which is a common feature of baldness.[8]
The Mysterious Conductor of the Hair Cycle ClockLevels of TGF-b1 are closely related to the progression of pattern baldness,[23] and alongside hypoxia, the accumulation and activation of mast cells,[24] and an increased concentration of prostaglandins reinforce the view that the defining feature of pattern baldness, a decreased anagen to telogen ratio, is the result of chronic scalp inflammation and an inability to repair.[25]
Using the synchronized hair growth mouse model (3, 4) we showed that topical trypsin treatment, immediately after depilation, induced cell death at the follicular papilla. This death signal, which is independent of the proteolytic activity of the protease, resulted in delaying hair growth and pigmentation (26). Here we show that the trypsin inhibitors STI and BBI also lead to delayed hair growth, as well as to reduced follicle dimensions and reduced pigment deposition within the hair shaft. Since we could not detect apoptotic cells in the papillae of soymilk, STI or BBI treated mice (not shown), we suggest that STI and BBI do not affect papillae cell death, but exert their effect on hair growth and size via a different mechanism.
Soymilk reduces hair growth and hair follicle dimensions in mouse model
M. Seiberg, J.-C. Liu, L. Babiarz, E. Sharlow and S. Shapiro