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I assumed he is german when I read it. On german forums ppl are all on tranny regimes. Yet they think they are still men even though some of them got actual milk shooting tits lmao.
How Different Types Of Estrogen Promote (and Hinder) Hair Growth
- Thread starter IdealForehead
- Start date
I assumed he is german when I read it. On german forums ppl are all on tranny regimes. Yet they think they are still men even though some of them got actual milk shooting tits lmao.
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What would be the benefit of switching to tablet in the context of what I posted regarding greater liver metabolism and higher cancer risk observed in studies from oral dosing?
No. See:
https://www.hairlosstalk.com/intera...gens-are-secondary.113256/page-4#post-1648846
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Lil warning about dexa, it increases dkk1 and while it also increases pge2 it sadly increases pgd2: https://www.ncbi.nlm.nih.gov/pubmed/28155238
That being said, I saw some really good result pics of ppl using SABA gel (dexa+tretinoin).
Maybe adding something that normalizes DKK1 (ascorbic acid) and deal with pgd2 (seti, ceti...) would utilize its full potential. Tretinoin deals also a bit with pgd2 respectively its enzyme ptgds. There is btw also a study for areata comparing minoxidil vs minoxidil + 0.05% dexa.
That being said, I saw some really good result pics of ppl using SABA gel (dexa+tretinoin).
Maybe adding something that normalizes DKK1 (ascorbic acid) and deal with pgd2 (seti, ceti...) would utilize its full potential. Tretinoin deals also a bit with pgd2 respectively its enzyme ptgds. There is btw also a study for areata comparing minoxidil vs minoxidil + 0.05% dexa.
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dat FERb tho giggity giggity
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well yes I know that
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Yeah I read that study. Doesn’t surprise me that dex seemed to randomly help people grow hair. There are quite a few things which upgregulate both pge2 and PGD2 annoyingly.
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As I am blasting estriol, I decided to look into the risks of gynecomastia and whether ER-beta is an issue for breast tissue.
Good news.
As per this article:
Estriol has both ER-beta and ER-alpha activity, so the ER-alpha activity can still pose a risk of gyno. But I think this can safely be said to be the lowest risk natural estrogen for gyencomastia, as it is weighted more strongly to ER-beta.
And it would suggest S-equol, as a highly selective ER-beta agonist, would not pose a risk of gynecomastia at all (except from the perspective of DHT sequestration and thus androgen deprivation).
This makes me feel a bit better about estriol. Inquiring with some suppliers on Alibaba about getting some powder now. Apparently they sell 2 grams for $82, which at 2 mg per day topically to the scalp should last years. Very cheap agent.
Good news.
As per this article:
The discovery of oestrogen receptor β (ERβ/ESR2) was a landmark discovery. We do not find evidence of expression in normal or cancerous human breast. This expression pattern aligns well with RNA-seq data.
This is good news for the principle of attempting to maximize ER-beta stimulation, as it means in theory a pure ER-beta agonist should have no risk of gynecomastia.
Estriol has both ER-beta and ER-alpha activity, so the ER-alpha activity can still pose a risk of gyno. But I think this can safely be said to be the lowest risk natural estrogen for gyencomastia, as it is weighted more strongly to ER-beta.
And it would suggest S-equol, as a highly selective ER-beta agonist, would not pose a risk of gynecomastia at all (except from the perspective of DHT sequestration and thus androgen deprivation).
This makes me feel a bit better about estriol. Inquiring with some suppliers on Alibaba about getting some powder now. Apparently they sell 2 grams for $82, which at 2 mg per day topically to the scalp should last years. Very cheap agent.
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Got a bit confused cause I searched for dexa and ended with saba gel. SABA is actually beta and not dexa + tretinoin. Still interesting though.
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I have been trying to determine proper transdermal estriol dosing. It is difficult even with the references I posted earlier.
I have been debating conversion between oral and transdermal dosing. If we know oral dosing must go through the liver first, thus being partially metabolized by the liver, shouldn't transdermal dosing be much stronger on a mg vs. mg level? Transdermal dosing avoids this initial liver metabolism and goes straight into the blood from the skin.
It appears this is truly the case, and to a possibly major extent.
I found this study:
The skin probably doesn't absorb nearly as well as the vaginal lining. But if vaginal: oral dosing can be established as ~1:16 to 1:24, then I bet skin: oral dosing is somewhere around 1:4 to 1:8 (being conservative), and thus a skin dose on par with a pregnancy peak would likely be around 1-2 mg.
2 pumps from the paraben free formulation of this estriol cream is 1.7 grams. The bottle says it has 50 mg estriol per oz (28.35 g). This means 2 pumps = 3 mg estriol. ie. This formulation has 1.5 mg estriol per pump.
Haha, No wonder I've been getting hammered so hard the past few days. I've been using an insane amount and going probably above pregnancy levels. Yesterday I did at least 4 pumps after work (6 mg estriol) which is probably the equivalent of 24 mg or more orally. No wonder I was so nauseous after.
I did 1 pump (1.5 mg) this morning and 2 pumps (3 mg) this evening. 1 pump is quite tolerable. 2 pumps gives me a 4-6 hour hot flash and at least moderate nausea.
This would suggest that with this formulation, the maximum one should use at one sitting is 1 pump (1.5 mg), and perhaps administer this amount 2-4 times a day for smooth dosing if tolerated.
Similarly it would suggest that for hair dosing, expecting similar absorption levels, we really don't want more than 1-2 mg at each application.
I have been debating conversion between oral and transdermal dosing. If we know oral dosing must go through the liver first, thus being partially metabolized by the liver, shouldn't transdermal dosing be much stronger on a mg vs. mg level? Transdermal dosing avoids this initial liver metabolism and goes straight into the blood from the skin.
It appears this is truly the case, and to a possibly major extent.
I found this study:
Estriol is thus readily absorbed by the vaginal route and peak levels of unconjugated E3 after insertion of 0.5 mg estriol seem to be comparable to those obtained after 8-12 mg estriol given orally.
Remember: 8 mg orally produces peak blood levels on par with pregnancy. So this study suggests 0.5 mg vaginally can produce equal or stronger peaks as pregnancy.
The skin probably doesn't absorb nearly as well as the vaginal lining. But if vaginal: oral dosing can be established as ~1:16 to 1:24, then I bet skin: oral dosing is somewhere around 1:4 to 1:8 (being conservative), and thus a skin dose on par with a pregnancy peak would likely be around 1-2 mg.
2 pumps from the paraben free formulation of this estriol cream is 1.7 grams. The bottle says it has 50 mg estriol per oz (28.35 g). This means 2 pumps = 3 mg estriol. ie. This formulation has 1.5 mg estriol per pump.
Haha, No wonder I've been getting hammered so hard the past few days. I've been using an insane amount and going probably above pregnancy levels. Yesterday I did at least 4 pumps after work (6 mg estriol) which is probably the equivalent of 24 mg or more orally. No wonder I was so nauseous after.
I did 1 pump (1.5 mg) this morning and 2 pumps (3 mg) this evening. 1 pump is quite tolerable. 2 pumps gives me a 4-6 hour hot flash and at least moderate nausea.
This would suggest that with this formulation, the maximum one should use at one sitting is 1 pump (1.5 mg), and perhaps administer this amount 2-4 times a day for smooth dosing if tolerated.
Similarly it would suggest that for hair dosing, expecting similar absorption levels, we really don't want more than 1-2 mg at each application.
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Further evidence on the subject of estriol and breast tissue (gyno or breast cancer risk):
We can see from Fig 2 that 17-beta estradiol (#1) and ethinyl estradiol (#2) are very highly stimulatory to breast tumors. However, estriol (#9) has almost zero affinity for breast tumors. From what I have read, not all tumors are created equal so there would be some variation.
But all this strongly suggests the risk of gynecomastia or other breast problems from topical estriol should be very, very low, even with systemic dosing levels.
(Oral estriol would not be advisable as that may increase cancer risk due to the liver metabolism issue as with all estrogens discussed above. All estrogens should ideally be delivered transdermally.)
Vaginal estriol has been shown to relieve local, vaginal and urinary symptoms without stimulating the breast tissue or endometrium. Estriol has a high relative binding affinity (RBA) for estrogen receptors in the bladder and vaginal tissue and a relatively low RBA for estrogen receptors in the uterus (myometrium) and breast tissue, figure 1, figure 2, (Bergink 84).
Because of the high RBA for the ER in the vaginal tissue and bladder, estriol will have a strong/beneficial effect in these tissues. Because of the low RBA for the ER in the myometrium and breast, estriol exerts only a weak effect in these tissues. Estriol is much less stimulatory to the breast and endometrial tissue than ‘strong’ estrogens like estradiol, which have much higher RBA in these tissues. Estriol acts as a selective estrogen receptor modulator, binding strongly to the ER in the bladder and vaginal tissue and weakly to the breast and endometrial tissue. Estriol also binds to the estrogen receptor in the breast tissue for a shorter period of time, 6 hours, thus causing less of an effect than the more stimulatory estradiol and estrone which bind to the ER for a longer period of time, 24 hours. Estriol acts as a weak estrogen in the breast, endometrium and liver while having full estrogenic responses in the vaginal and bladder epithelium (Kuhl 05).
As mentioned above, estriol has a low RBA (Relative Binding Affinity) for the ER in breast tissue and a rapid dissociation, 6h, from the Estrogen receptor (6h). Estriol does not increase breast density (Valdivia 00, Minaguchi 96, Takahashi 00). Major, large, peer reviewed trials have repeatedly shown that vaginal estriol does NOT increase the risk of breast cancer:
• Million Women’s Trial 03 RR 0.67
• Fournier 04 RR 0.7
• Fournier 07
• Rosenberg 06
• Lyntinen 02
• Bergvist 89
Vaginal estriol has also been safely used in breast cancer survivors (Dew 03). There was a decrease in 'recurrence of disease’ in vaginal estriol users (RR 0.57) vs. non-users and no adverse affect on mortality
Because of the high RBA for the ER in the vaginal tissue and bladder, estriol will have a strong/beneficial effect in these tissues. Because of the low RBA for the ER in the myometrium and breast, estriol exerts only a weak effect in these tissues. Estriol is much less stimulatory to the breast and endometrial tissue than ‘strong’ estrogens like estradiol, which have much higher RBA in these tissues. Estriol acts as a selective estrogen receptor modulator, binding strongly to the ER in the bladder and vaginal tissue and weakly to the breast and endometrial tissue. Estriol also binds to the estrogen receptor in the breast tissue for a shorter period of time, 6 hours, thus causing less of an effect than the more stimulatory estradiol and estrone which bind to the ER for a longer period of time, 24 hours. Estriol acts as a weak estrogen in the breast, endometrium and liver while having full estrogenic responses in the vaginal and bladder epithelium (Kuhl 05).
As mentioned above, estriol has a low RBA (Relative Binding Affinity) for the ER in breast tissue and a rapid dissociation, 6h, from the Estrogen receptor (6h). Estriol does not increase breast density (Valdivia 00, Minaguchi 96, Takahashi 00). Major, large, peer reviewed trials have repeatedly shown that vaginal estriol does NOT increase the risk of breast cancer:
• Million Women’s Trial 03 RR 0.67
• Fournier 04 RR 0.7
• Fournier 07
• Rosenberg 06
• Lyntinen 02
• Bergvist 89
We can see from Fig 2 that 17-beta estradiol (#1) and ethinyl estradiol (#2) are very highly stimulatory to breast tumors. However, estriol (#9) has almost zero affinity for breast tumors. From what I have read, not all tumors are created equal so there would be some variation.
But all this strongly suggests the risk of gynecomastia or other breast problems from topical estriol should be very, very low, even with systemic dosing levels.
(Oral estriol would not be advisable as that may increase cancer risk due to the liver metabolism issue as with all estrogens discussed above. All estrogens should ideally be delivered transdermally.)
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I’ve been using the estriol on my face and hairline for.. maybe a bit over a week now. Can’t say I notice anything great where my skin or hair is concerned. Actually I’ve been getting weird peeling skin on my nose for whatever reason.
Day 4 on progesterone/estradiol oral. Things were taking a turn yesterday when bleeding increasing along with some discomfort. Shed about 200 hairs.
This morning things are as i predicted they would be wel before starting this.
Pain is incredible. Bleeding is severe. Brushed my hair and about 10 strands comes out each time I run it through my hair. I’m not sure if I even want to count.
The hair on my body (well, scalp and body), has once again ceased growing.
Day 4 on progesterone/estradiol oral. Things were taking a turn yesterday when bleeding increasing along with some discomfort. Shed about 200 hairs.
This morning things are as i predicted they would be wel before starting this.
Pain is incredible. Bleeding is severe. Brushed my hair and about 10 strands comes out each time I run it through my hair. I’m not sure if I even want to count.
The hair on my body (well, scalp and body), has once again ceased growing.
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That's brutal, but doesn't it suggest to you that given that your hair responds so dramatically to estrogenic changes, that estrogens remain the most probable cause of your hair problems?
I'd be curious if you'd run down a brief listed chronology of year and issue for you:
ie.
20xx - went into menopuase
20xx - started noticing hair loss
20xx - went on Diane with __ outcome
20xx - went on minoxidil with __ outcome
20xx - went on spironolactone with __ outcome
20xx - went on dutasteride with __ outcome
etc.
etc. I think it would possibly be useful to review your full chronology in greater and more comprehensive detail.
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Well what’s bizarre is that I had been on the exact same pill in the past on and off throughout anorexia, for bone health and whatnot. My hair got a bit thinner because of the nutritional issues, but I never had a single issue in 7 years of randomly stopping and starting it until mid 2014. I think my body just had enough. That year was also a really stressful one for me and I’d lost a lot of weight. Looking back though. My hair definitely had begun to thin at the beginning of that year when I see photos. It just took me that long to notice. I just know that my hair was fine for years and years through all the sh*t I did to my body, then in late 2013 after years of not having a period, I got one, so I went on the pill because I had a boyfriend at the time. We broke up in Feb 2014, I stopped taking the pill, and by June I realised my hair was receding and thinning. It’s all been downhill from there.
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So then can we conclude that the time line for pre-existing factors leading up to your hairloss was:
1) Anorexia (2007-2014)
2) Diane 35 on/off (2007-2014)
3) Premature ovarian failure (~2010 onward)
4) Hair loss begins (2014) and progressively worsens since
(Please correct any wrong dates.)
The hair loss came on gradually, and has progressively worsened to full body progressive hair loss, which generally comes in cycles and waves.
If correct, this timeline would suggest one of three things to explain how your hair loss started:
- Anorexia itself did the damage to your hair follicles. In the same way as women who have been anorexic often have very poor looking skin for even years after, anorexia itself may have damaged the follicles and they are failing as a result of that damage now. I think this is unlikely though, since women with anorexia from what I understand should have stable hair after the anorexia resolves.
- The combination of ovarian failure and Diane 35 have given your hair years of unbalanced estrogenic signalling which is promoting catagen all over (my personal opinion).
- Your hair loss is unrelated to these issues, and is perhaps auto-immune given that you have a family history, but this is unlikely as the biopsies did not show any sign of auto-immune issues.
Am I missing something or does that make sense?
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I can tell you for sure that anorexia has nothing to do with it. I’ve known plenty of girls who had fabulous hair throughout and after anorexia. My sister was also anorexic and although had thinner hair when she lost like 20kg, it has grown back healthy over time through recovery.
Both of my sisters have been on Diane with no hair issues. I never had issues with it until 2014.
My family does have an incredibly long list of autoimmune diseases including hashimotos, coeliac disease, Addison’s, Chrones and a few others. That said, I have no detectable autoimmune issues. If anything, my immune system has been suppressed by chronically elevated levels of cortisol as is seen In hypogonadotrophic hypogonadism. Part of me wonders if the primary HPA/cortisol issues are a huge factor in why my case goes beyond menopausal or Androgenetic Alopecia hairloss.
I have read many studies which show that corticotropin releasing factors are inhibitory to normal hair growth cycling, and that immunosuppression caused by chronic hypercortisolism can inhibit t-cell and cytokine production, and there have been studies done which show that these are absolutely essential precursors to hair growth. (https://www.rdmag.com/article/2017/05/t-cells-could-be-triggers-hair-growth)
We need an immune response to growth hair, but not TOO much. We already know that I have eosinopenia, so it follows that my immune responses all ‘round are messed up. I’d also like to add that there is a distinct link between estrogen dominance and the prevalence of autommine diseases. My sisters all have very high estrogen levels and therefore suffer from very bad mentrual cycles, migraines, endometriosis etc. They all have one or multiple autommine conditions.
Low estrogen is associated with poor immune responses. So I have theories but I still don’t have answers. I’ll be very interested to see what growth factors + cytokines can do for me.
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I'm assuming you mean Europe.
You can buy estradiol pills from alldaychemist.com or inhousepharmacy.vu
inmyhead
Senior Member
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I appreciate your research, but isn't it strange that Luo sells every thing possible?
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He actually doesn't sell estriol. It was another Luo someone recommended to me and i got mixed up. Luo apparently is a common name over there.
So to clarify: Gang Luo (daro supplier) does not sell estriol. He does however do custom synthesis of any new or special compound you request. That's a big part of his company's business model.
Eg. I asked him to synthesize some pure procyanidin b2, because all the procyanidin b2 on Alibaba is extract from apples/grapes with loads of other polyphenols in the mix. I don't trust those not to react with my other more important topical agents. He said he could absolutely do it but the price was way too much to be justified.
Estriol is a common and cheap agent so it doesn't fit into that business model.
I'm still working on arranging an estriol powder supply.
Thanks for pointing out that post. I corrected it.
inmyhead
Senior Member
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Powder is a must? So a cream like this would suck? https://www.alldaychemist.com/evalon.html or https://www.biovea.com/eu/product_d...-CARE-with-Natural-Estriol-2-oz-60ml&PID=2438
i guess Biovea should be better. I would try minoxidil in the evening and estriol in the morning or smth