Scalp Progesterone For Hair Loss Experiment

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It’s possible that some males’ sensitivity can be extremely low. Leading to more DHT in the scalp of some “non balding” men and a false idea that DHT is in fact protective. When it’s only a matter of being genetically blessed or not.
 

Luckytype

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One other thing i wanted to point out. From my understanding when women get androgenic alopecia their androgen levels spike but no where near the level of a mans normal AR levels. Means a women androgen sensitivity is much higher. While men even with androgenic alopecia probably have lower sensitivity compared to women in general.

Do you have a few studies that back this?

If this is indeed the case there should be other imbalances that lead to additional, similar behaviors, one example being those that follow steroid use which is not commonly the case
 
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One other thing i wanted to point out. From my understanding when women get androgenic alopecia their androgen levels spike but no where near the level of a mans normal AR levels. Means a women androgen sensitivity is much higher. While men even with androgenic alopecia probably have lower sensitivity compared to women in general.
First, androgenic alopecia does not exist for it is not caused by androgen sensituvuty. Peat says so.
second, therefore false and so further speculation based on that is false.
.
 
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It’s possible that some males’ sensitivity can be extremely low. Leading to more DHT in the scalp of some “non balding” men and a false idea that DHT is in fact protective. When it’s only a matter of being genetically blessed or not.
DHT in the scalp is a left over result from the disrupted pathway of androgens in scalp that convert to estrogens by lowered aromatase expression, so DHEA converts more via 5AR to DHT instead of the other way towards estradiol. Leaving too much estrone activity and without estradiol inhibits hair growth. I think aromatase expression could be upregulated by increasing DHEA applied topically. Therefore progesterone + DHEA should be applied to prevent follicle miniaturization.
 

brix

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Going back to the prolactin. Interestingly enough women who get pregnant their progesterone levels sky rocket where hair gets thicker. Then drop off after birth and they start losing hair fast back to baseline. Prolactin stays elevated after birth. I wonder..

Also anecdotal reports of peoples hair thickening up on bromocriptine. Dopamine agonist and anti prolactin

Doesn’t calcium lower prolactin as well??
 
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@General Orange if we perceive alopecia as miniaturization driven by a local inflammatory response to DHT-bound follicles then it may not be called androgenetic but the DHT remains causal, or rather a significant player in the process, assuming your immune system targets it. So that's the rationale behind the vitamin D suggestion I guess.

That's an interesting view you have on DHT in the scalp, and that would be consistent with my experience since I tend to be naturally low in estradiol on my blood tests, and that didn't benefit hair much. Note that if DHEA converts more to DHT instead of E2, the best solution is to go straight to the hormones you're interested in which is Estradiol and Estriol (ergo, the biEstro product which is recommended by few people out there), and indeed progesterone. I would never want more DHEA>DHT conversion.

However progesterone having an anti estrogen activity, I'm not sold on it.

@brix yes it does, it's suggested in one of the posts above: sodium calcium magnesium potassium zinc D3 K2... the usual suspects
 
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@General Orange if we perceive alopecia as miniaturization driven by a local inflammatory response to DHT-bound follicles then it may not be called androgenetic but the DHT remains causal, assuming your immune system targets it. So that's behind the vitamin D suggestion I guess.
Who said DHT cause inflammation? No, too much DHT and increase of androgen receptors in the hair, I my eyes is logical effect from inactivity of estrogens: not enough estrone + estradiol activity and probably reduced DHEAS sulfotransferase to DHEA, so the hair is not activated to grow and will shrink. Putting onions, sulfur and quercetin, on the scalp is shown to increase hair growth. Coz it activates DHEA and aromatase I guess.
 
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Modulator of scalp inflammation... that’s the auto immune theory. But it’s interesting to go more upstream in the sex hormone chain, as you do and as I always want to do. Not enough scalp estradiol is a very decent way to put it and sounds anti-Peat which is considered the ultimate sin around here at times.

I don’t think anyone can seriously claim estradiol and Estriol don’t have a positive impact on hair growth. DHEA could work by the way, it also activates both ER. However if you had defective enzymes properly converting DHEA to E2/Estriol, for whatever reason, what guarantee do you have that more DHEA will yield benefits? I’d go straight to the point, in this case the downstream hormones.

I don’t think anyone can claim DHT’s effect is a fable however. If it were, inhibiting 5ar (you know the drugs) or 17-20lyase (ketoconazole) would NEVER work. What is obvious indeed, is that regrowth is weak, and hair is brittle for many guys who only care about the Androgenetic aspect and are extremely scared of turning into a woman the moment they even think of topical estrogens+progesterone (the latter of which still bugs me).
 
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You can't control the metabolism of hormones /estrogens put on the scalp. The enzymes gonna strip them and they can enter the bloodstream. oops!
However if you had defective enzymes properly converting DHEA to E2/Estriol, for whatever reason, what guarantee do you have that more DHEA will yield benefits?

What you can better do is increase the master precursor DHEA and try to manipulate the expression of enzymes with phytoestrogens or drugs. But you have to do tests to check how the skin condition is too see what hormone is high / low or not. tricky.
The skin has is it's own HPA axis and steroid factory, earlier result from internal made changes are no guarantee for future positive result on the skin.
 
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If it were, inhibiting 5ar (you know the drugs) or 17-20lyase (ketoconazole) would NEVER work.
If you mean Fin and Dut, they are also progestins that's were the effect come from not the 5ARi. And Ketoconazol is also and more potent FAAH inhibitor, so it increases the uptake of Anandamide, another hair growth modulator, into cells, which functions are connected with estrogens.
 
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Stress-induced hair loss
The hair follicle apparatus expresses tachykinins, NKRs, and endopeptidases, and tachykinins have been implicated in stress- and autoimmune-evoked hair loss. Stress-induced premature induction of catagen and hair follicle apoptosis in mice requires expression of the NK1R and the presence of mast cells (15). ...

Mast cells

Mast cells are closely associated with SP-positive sensory nerves in many tissues, and there is a bidirectional communication between mast cells and primary sensory neurons, whereby sensory neuropeptides stimulate mast cells, and mast cell products control neuropeptide release. SP induces the release of TNF-α (78) and vascular endothelial growth factor (301) from mast cells, thereby contributing to inflammation, immunity, and angiogenesis.

Mast cell deficient and neurokinin-1 receptor knockout mice are protected from stress-induced hair growth inhibition. - PubMed - NCBI
Despite the lack of insight on distinct mediators in the skin orchestrating the pathophysiological response to stress, hair loss has often been reported to be caused by stress. Recently we revealed the existence of a "brain-hair follicle axis" by characterizing the neurokinin (NK) substance P (SP) as a central element in the stress-induced threat to the hair follicle, resulting in premature onset of catagen accompanied by mast cell activation in the skin.
...These results indicate that the cross-talk between SP and mast cell activation via NK-1R appears to be the most important pathway in the regulation of hair follicle cycling upon stress response.

...Observations of human skin biopsies and hair follicles in culture indicate that Substance P downregulates production of prolactin, which is important for hair growth (178):
Human scalp skin and hair follicles (HFs) are extra-pituitary sources of prolactin (PRL). However, the intracutaneous regulation of PRL remains poorly understood. Therefore we investigated whether well-recognized regulators of pituitary PRL expression, which also impact on human skin physiology and pathology, regulate expression of PRL and its receptor (PRLR) in situ.
...This study identifies substance P, TNFα and IFNγ as novel modulators of PRL and PRLR expression in human skin, and suggests that intracutaneous PRL expression is not under dopaminergic control. Given the importance of PRL in human hair growth regulation and its possible role in the pathogenesis of several common skin diseases, targeting intracutaneous PRL production via these newly identified regulatory pathways may point towards novel therapeutic options for inflammatory dermatoses.
Tumour necrosis factor alpha, interferon gamma and substance P are novel modulators of extrapituitary prolactin expression in human skin. - PubMed - NCBI

Substance P, NK1R, and neprilysin regulate the inflammatory response in a murine model of alopecia areata, an autoimmune disorder of the hair follicle associated with inflammatory cell influx around growing hair follicles (306).


Alopecia areata (AA) is an autoimmune disorder of the hair follicle characterized by inflammatory cell infiltrates around actively growing (anagen) hair follicles. Substance P (SP) plays a critical role in the cutaneous neuroimmune network and influences immune cell functions through the neurokinin-1 receptor (NK-1R). To better understand the role of SP as an immunomodulatory neuropeptide in AA, we studied its expression and effects on immune cells in a C3H/HeJ mouse model for AA.
..Additional SP supply to the skin of AA-affected mice leads to a significant increase of mast cell degranulation and to accelerated hair follicle regression (catagen), accompanied by an increase of CD8+ cells-expressing granzyme B. These data suggest that SP, NEP, and NK-1R serve as important regulators in the molecular signaling network modulating inflammatory response in autoimmune hair loss.
Substance P as an immunomodulatory neuropeptide in a mouse model for autoimmune hair loss (alopecia areata). - PubMed - NCBI
 
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Progesterone

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Indeed, magnesium oil overnight is great.

@Progesterone i think I like your nickname.

"Biology of Scalp Hair Growth", Clinics in Plastic Surgery -- Vol. 9, No. 2, 1982:

"Local Therapy {...} Progesterone was found to be a natural and significant 5aR inhibitor when tested in vitro, in the human skin microsome system, a rich source of 5aR, and in human scalp hair follicles. When a solution of progesterone in alcohol was applied to the pubic skin of normal males, it caused an average decrease of 75.2 per cent in 5aR activity after 24 hours of treatment.

"Moreover, while less DHT is made, more dihydroprogesterone (DHP; 5a-pregnane-3,20dione) is made. DHP competes with the residual DHT for the cytosol-nuclear binding protein for a further reduction in the amount of DHT interacting with genetic material.

"Progesterone works in reducing DHT production locally by competing for the active site of 5aR and would need to be present at the active site continuously because of the reversible kinetics. Treatment lapses result in the resumption of DHT production from testosterone.

"Since progesterone only partially inhibits DHT production and since DHP only partially inhibits binding of residual DHT, local progesterone at best can only ameliorate androgenetic alopecia and not arrest it.

"Because more than 70 per cent of topically applied progesterone is metabolized in the skin to weak, nonandrogenic by-products, it can be used in women at the rate of 1 ml of a 2 per cent solution BID, whereas higher doses result in menstrual irregularities."


I tend to think that hair loss is an imbalance between the Androgen receptor (overly expressed) and the Progesterone, Estrogen alpha and Estrogen beta receptors.

I’d say that the most critical pro growth are in that order PR ERb then ERa.

The 5ar reflexion above may make Finasteride a bad idea - good to inhibit DHT local expression, but Progesterone does just that and is pro growth.

@tankasnowgod thank you got making me rethink 5ar inhibitors, but not for the same reasons ;)

SERMs seem to increase progesterone expression.

I’m down to biEstro + RU58841 myself. RU stopped my GF’s hair loss like magic, according to her, but female pattern baldness isn’t that different from us - at least many of them suffer from increased Androgen to progesterone. Progesterone could be tried, she does have some signs of low Prog, unfortunately she’s dead scared of needles and blood testing in females is quite the challenge.

The last alternative I do feel like trying very soon is Nandrolone - I’m experienced with steroids and recovery from the craziest cycles, I don’t want kids for now, my GF is fine with me pinning weekly, nandrolone converts into the super weak DHN instead of DHT and is a progestin and a weak estrogen. No wonders old school bodybuilders had the most luscious hair.

Wait.. you're using the bio-estro cream? (estriol+estradiol)????

RU made me feel like ***t (constant full headache, tired, etc) Pretty sure it accelerated hair line loss as well.

Interesting info on Prog. I use Prog EOD, orally. 100mg of prog oil in a veggie capsule.

I think Prog holds my hairline, but doesn't do much for density/thickness. I'd like to run clomid once a week alongside the Prog EOD, but I am still a bit worried that clomid will hurt hairline (due to reading anecdotal reports)
 
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I used to think clomid once a week could be fine. Except that this report totally screwed up my intuition ha. Notwithstanding the potential beneficial role of SHBG, which clomid raises.

Clomiphene citrate elicits estrogen agonistic/antagonistic effects differentially via estrogen receptors alpha and beta. - PubMed - NCBI

However a guy on page 2 here observed solid hair growth on Clomid, just like me on SERMs. It could also be thanks to a better LH-induced conversion of cholesterol into downstream hormones. Who knows. DHEA and its metabolites are ERb activators.

This Paper Has Some Interesting Data About Estrogen In Androgenetic Alopecia

Hormone balance seems to be what they discuss and what I always come back to. I still see DHT and Progesterone affecting not only their own receptors but the whole balance in the scalp cells. So maybe 5ar inhibitors work thanks to being progestins, or maybe they work thanks to being progestins AND lowering DHT, obviously. Ketoconazole being a 17-20lyase inhibitor we get more 17-OHprogesterone when using it. So indirectly a progestin again?

The more I dig the more I see flaws with stuff like Rogaine, RU (but unsurprisingly works quite well in females who have the estrogens+progesterone). We want scalp ER agonism to balance out our AR signaling which is obviously stronger than in females. Years of stress and high estrogen exposure and lowered Testosterone may raise prolactin which increases the amount of AR and the sensitivity to DHT. Not good.

BiEstro seems to be very valid but sounds like a better idea if we use some AND reduce the Androgenetic factor. I don’t think anyone with a reasonable approach to the topic would go ahead and pop aromatase inhibitors / anti estrogens + use topical DHT for hair regrowth. Quite the opposite in fact. Ask steroid users. Who should just stick to nandrolone for a combined progestin + piss weak Androgen (DHN) + aromatizes to e2.

@General Orange PDE4 inhibitors could do what you’re posting. cAMP is where it’s at.

Cyclic Adenosine Monophosphate Signaling in Inflammatory Skin Disease

There’s also this study on the GR playing an important role for ER modulation. Drugs like Halotestin or Trenbolone may not be hair friendly, although the latter is a progestin and its metabolites are weak Androgens in vivo... most oral AAS and SARMs trash users’ health but that could be the low SHBG.

The modulation of aromatase and estrogen receptor alpha in cultured human dermal papilla cells by dexamethasone: a novel mechanism for selective acti... - PubMed - NCBI

These observations provide evidence for a glucocorticoid-dependent mechanism whereby the selective action of estradiol via ERbeta may be promoted.

Additionally, upregulation of aromatase combined with downregulation of ERalpha provides a basis for selective action of estradiol produced locally by autocrine or paracrine mechanisms.

Aromatase upregulation for hair growth. With an improved ERa/ERb ratio. Good luck with that. ;)
 

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