Scalp Progesterone For Hair Loss Experiment

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What do you mean?

For hair we would WANT increased ER-beta...

Clomid, at least centrally is an antagonist of ER-beta, not agonist.

This tells you it increases ER-beta? Not sure where you got that we need to add an AI?
NO WAY we want higher E2 in body. ONLY scalp. how you gonna get E2 via clomid to scalp nicely? you tell m "hey clomiphene listen I like the T but please put E2 only in my hair oke? good boy" So we take AI to prevent E2 internally or a smart SERM phytoestrogen
 

Progesterone

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NO WAY we want higher E2 in body. ONLY scalp. how you gonna get E2 via clomid to scalp nicely? you tell m "hey clomiphene listen I like the T but please put E2 only in my hair oke? good boy" So we take AI to prevent E2 internally or a smart SERM phytoestrogen

Asking nicely would be one way to go about it.

How about using clomid and also using this, on hairline: https://www.amazon.com/Life-Flo-BiEstro-Care-Estrogen-Estradiol-Physician-Developed/dp/B003LYDBCG

a guy on a hairloss forum said he used this on his head and got RESULTS (better than fin, etc)
 
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minoxidil + dermapen on hairline and that stuff, could work better to activate stem cells become hair follicles and activate growth. but maybe you would need a mast cell inhibitor and anti inflammatory too and collagen repair. like Gotu kola cream
 

Progesterone

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minoxidil + dermapen on hairline and that stuff, could work better to activate stem cells become hair follicles and activate growth. but maybe you would need a mast cell inhibitor and anti inflammatory too and collagen repair. like Gotu kola cream

progesterone is also mast cell inhibitor

hmmmmmm
 

Progesterone

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... clomid rises estrogen, does it rise prolactin too?

Oh, sorry, didn't understand the question.

No it does not raise prolactin, I have looked into this. It doesn't raise cortisol either.

Raises T, E2, DHT, LH, FSH, SHBG.

Clomid is an estrogen agonist AND antagonist, btw (hence, SERM)

Many experts say not to worry about the increased E2 numbers on paper caused by clomid.
 

LCohen

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Oh, sorry, didn't understand the question.

No it does not raise prolactin, I have looked into this. It doesn't raise cortisol either.

Raises T, E2, DHT, LH, FSH, SHBG.

Clomid is an estrogen agonist AND antagonist, btw (hence, SERM)

Many experts say not to worry about the increased E2 numbers on paper caused by clomid.

E2 can stimulate prolactin itself. FYI.
 

Progesterone

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E2 can stimulate prolactin itself. FYI.

Yes, but the E2 raised by clomid, is very tricky..

Many say not to even worry about E2 numbers while on clomid because while that the serum number may be high, it also acts as an AI in many tissues so it's more of a false positive reading.

Many studies have been done on clomid and never once was Prolactin elevated over baseline.
 

Watson350

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In theory a massage can transmit mechanical stress to the hair follicle's dermal papilla cells and could help increase the thickness of hair.
I now feel crackling of what I assume are calcium deposits under scalp breaking apart after two months of apple cider vinegar and detumescence therapy. I have new baby hairs in my widow peaks and have started to notice a few a half inch behind hairline. I use infrared light once a week with and use a needle to act as microderm abrasion. k2, e, magnesium, calcium, taurine, b6, b12, etc.
 

Elephanto

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@Elephanto @General Orange can you all clue me in on the fibrosis side of hairloss more?
I feel like that may be a major cause and issue for me
:praying:
It has to do with an excess of collagen production that is promoted by Estrogen, Nitric Oxide and TGF-Beta (high in conditions of liver damage; which is promoted by Endotoxins, low ATP, Iron, low Zinc etc). I've mentionned excess keratinocytes proliferation several times before, which is similar and which is inhibited by IGFBP-3 and I believe it is one of the main ways it protects against hair loss (remember raising IGFBP-3 by a single standard deviation decreases balding risks by 38%). The kind of systemic approach I proposed in the "Root of Hair Loss" thread we have been posted on already includes tackling fibrosis, I've also added other TGF-Beta inhibitors in the Fibrosis thread. Agents that promote proper blood circulation and tissue oxygenation like CO2 and all the decalcifying agents also help preventing fibrosis.

Most factors that downregulate IGFBP-3 also increase Nitric Oxide. For reminder :
Here are things that both increase Nitric Oxide and decrease IGFBP3 : Arginine, Estrogen, Endotoxins, Iron, Vitamin D deficiency, Ammonia, lack of Magnesium,
lack of Vitamin A, lack of Zinc, Arachidonic Acid (PUFAs).
I also posted strategies that focus on each of these factors in the Root thread.
 
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Elephanto

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All samples presented with hyperplasia of the epidermis associated with local inflammation. The scar epidermis exhibited an increased expression of proliferating cell nuclear antigen, which revealed hyperproliferation of keratinocytes.
Altered proliferation and differentiation of human epidermis in cases of skin fibrosis after radiotherapy. - PubMed - NCBI

These results correlated with collagen and MMP-1 secretion and with cell proliferation, which were increased when keratinocytes were added [...] These observations strongly suggest that hypertrophic scar keratinocytes play a role in the development of pathological fibrosis by influencing the behaviour of dermal cells.
Epidermis promotes dermal fibrosis: role in the pathogenesis of hypertrophic scars. - PubMed - NCBI

We conclude that in vivo IGFBP-3 ensures epidermal homeostasis via downregulation of keratinocyte proliferation, and thus modulates the early stages of keratinocyte differentiation.
Insulin-like growth factor binding protein-3 (IGFBP-3) localizes to and modulates proliferative epidermal keratinocytes in vivo. - PubMed - NCBI
 
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