Exploring The Hormonal Route. Hair=life.

Gynobro237

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The success of HRT lies in the following things:
Suppression of T to castration level
To complete the first step, you need to increase E above 200 pg / ml
Increasing E will stimulate growth
Take Bicalutamide and Finasteride as a safety net
If you have completed all these points and you are not getting better, I do not know how to help you.
If things don't start looking up, im adding 100mg/day medroxyprogesterone acetate.
 

Almas_NW0

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how is your crown ??
The situation is unusual. It is as thin as the parting. But what is more interesting - the hair along the parting and the crown is shorter than the rest, they do not grow longer
Hairdressers shift my parting over and over again and shorten it again, so I can't say how HRT affected them. In any case, the crown is usually easy to treat. And it will be restored before the temples.
 

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MylovelyHair

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The situation is unusual. It is as thin as the parting. But what is more interesting - the hair along the parting and the crown is shorter than the rest, they do not grow longer
Hairdressers shift my parting over and over again and shorten it again, so I can't say how HRT affected them. In any case, the crown is usually easy to treat. And it will be restored before the temples.
Thank you for your reply! How long have you been on HRT?
 
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Almas_NW0

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Thank you for your reply! How long have you been on HRT?
Exactly 3 months. This is a short time. This is enough to notice the first changes, but serious cosmetic effects take much longer. I think I will be Norwood 0 next spring. However, my hair may still be fine. To get high quality hair, I will probably have to use HRT for a very long time - 1 year. It is likely that I will have to use it all the time, because I will not get the perfect result, the return of adolescent hair quality within a year.

In general, time will tell. Most importantly, I answered that. I can do something about it. The rest is just a matter of time and what sacrifices I will have to make for my hair.
 

exwhyyou

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Btw I started developing psoriasis. I had it for a year on and in my both ears... but now it got even into my genital and a*** area. Its pretty devastating, I cried a lot. My mom has problems and my uncle has a serious case (whole skin on the body being literally DESTROYED).

Hairloss, skin disorders, digestive problems, hormones,... just got 18. I sometimes want to just leave this body for some time...
do you eat dairy? my dad struggled with chronic psoriasis for years that completely cleared up when he stopped eating dairy
 

Pls_NW-1

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The situation is unusual. It is as thin as the parting. But what is more interesting - the hair along the parting and the crown is shorter than the rest, they do not grow longer
Hairdressers shift my parting over and over again and shorten it again, so I can't say how HRT affected them. In any case, the crown is usually easy to treat. And it will be restored before the temples.
Let that hair grow
 

Pls_NW-1

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do you eat dairy? my dad struggled with chronic psoriasis for years that completely cleared up when he stopped eating dairy
Heeey, I looove milk, I usually drink soy milk, as my body can't tolerate lactose. Thats very cool to hear. I hear many people saying their psoriasis cleared up after changing diet, and yet that disease is chronical, auto-immune and inherited. Maybe... the DIET indeed is the trigger for the outbreak of it.

Btw, how serious was your dad's case? Do you have it?

And what do you think guys about crispr being used to cure psoriasis (all kinds of it)?
 

Experimentality

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I hooked up Cabergoline (a D2-dopamine receptor stimulator) to my regimen 38 days ago and so far I am not seeing any results. I will give this remedy 3 months.
It is a piece of the puzzle, obviously not a solution. Bayer showing interest with the PRL antibody is enough reason for me to underline the importance of prolactin in male pattern baldness. Plenty of research available as well. Maybe it would be better to block the PRL receptor locally by means of a topical (with the antibody). Not having any plans to do so, because the PRL antibody is outrageously expensive and I am very satisfied with my current regimen. If I were to add something to my topical in the future I would sooner look into mineralocorticoid antagonists (MR) like Finerenone.

I am primarily going to run Metergoline for anti-aging benefits (i.e. anti-serotonin) and not necessarily for hair. Any regrowth would be a nice bonus but not expecting it. Cabergoline does not have any of these cool effects (the serotonin antagonism), and could have some nasty side effects as well. Personally I would stay well clear of it.
 

Pls_NW-1

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I haven't paid anything yet. I can start paying off if I have to use HRT all the time. Then the consequences can be different. But whatever they are, they won't drive me to suicide, which baldness could do.
I mean hiding a bald scalp is easier than female fat distribution and sunken chests and what not.
 

Experimentality

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Carbegoline does not target extra pituitary prolactin produced in the hair follicles so you will not have results from this.

The spikes in prolactin are promoted by an upregulation of estrogen activity.
The reason why it doesn't affect negatively your hair is because ERa is the one that promotes prolactin and the predominant receptor in hair follicles is ERb, which silences the actions of ERa. So you should actually have less extra pituitary prolactin damaging your hair while at the same time getting the benefits of upregulated ERb. In fact this scenario is what I am trying to replicate without using exogenous estrogen or unwanted sise effects.

There is also the topic of inflammation and its relation with DHT/androgens, and how it could potentially signal the motility of PRL/ PRLR containing macrophages. But I will leave that for now.


Yes I am currently taking Cyproheptadine. I take it orally and I agree, it's very versatil.
Dutasteride works the same way: by oral administration it accumulates peripherally (i.e. in skin) and reduces scalp DHT as per many research papers (DHT is mainly a paracrine hormone). However, I am not sure how prolactin is produced within the follicle. Dopaminergic drugs reduce PRL by increasing dopamine, but I am not sure whether the scalp contains dopamine receptors.

Also good luck with the Cyproheptadine. Amazing compound.

I know this. Either way it will reduce the systemic donation of prolactin, resulting in lower levels in the follicles.
It do not think systemic concentrations (of a paracrine hormone) matter much when looking at a local problem. An individual can have low serum DHT but high scalp DHT, the same goes for PRL. The same does not hold for T, for example, because it is an endocrine hormone and is not produced locally in tissues (although tissue concentrations may still vary, and of course the testes are an exception). E2 is also a paracrine hormone, that is why I am always wondering whether the effects from oral E2 primarily come from its ability to suppress the gonads (or maybe even upregulation of aromatase, which increases local E2). I would guess high (or low) systemic concentrations of paracrine hormones have some effect, but ultimately it is the local concentrations that matter. Note that achieving a high systemic concentration of a paracrine hormone in absence of a high local concentration is only artificially possible through HRT.
 

MrOscar

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Thanks. Yes, I think these concentrations are in the ballpark where we want to be with such a topical regimen. 1mcg/mL (0.0001%) would give concentrations around 100nM (1000 times the EC50 value of 0.1nM, order of magnitude). I think 10mcg/mL (0.001%) is too much, since the concentration will then be closer to 1uM. Experimenting with WAY can probably give similiar results (since the scalp hardly has ER-alpha expression anyway), however I think it is redundant because E2 in such low quantities will not give systemic sides anyway, and it is way (no pun intended) more expensive and harder to source than plain E2. I am also still not sure if WAY is a full agonist of the ER-beta, which is a requirement to be effective. I have never seen evidence that this is the case, which makes me sceptical. For an AA, RU is absolutely inferior to Apalutamide or Darolutamide. I recently switched to Darolutamide (because the half-life is more favorable than Apalutamide) and it is really only needed at 0.1% (that may be overkill as well). Add in Finasteride or Dutasteride and the whole balding cascade has essentially been shut down. I really like how everything works in tandem:

-Finasteride/Dutasteride removes the most potent androgen (DHT), which increases the efficiacy of the AA.
-Darolutamide/Apalutamide blocks the AR, will cause AR upregulation.
-E2 directly counteracts AR upregulation.

I added Cyclosporine A (at 0.1%) because the extensive research I ran on it points at a reasonable safety profile at such topical concentrations. Cyclo addresses many problems of the balding cascade: in addition to stimulation the Wnt pathway by inhibiting sFRP-1, it also provides direct suppression of interleukins which are further down the chain (they are produced as a reaction of an androgen binding de AR in a "male pattern baldness-sensitive" follicle). So, it is both a growth stimulant through Wnt as well as a preventive agent through inhibiting IL's. Some people are running WAY-316606 instead, but that compound only inhibits sFRP-1 (and does nothing to counteract IL's).

I am still torn on Minoxidil (sulfate). It is very effective as a growth simulant, but it gives me horrible skin texture. Currently I am not using it and not really planning on using it again. If you can run it without any bothersome sides I would definitely include it in the topical formulation. Another bonus of the topical is that all drugs are FDA-approved: long term effects are all known and safety warnings have been published where applicable. I still recommend anyone who wishes to try this to research everything you are going to use extensively. FDA approved does not necessarily mean safe or without side effects.
I will test probably 5 mcg E2, whole scalp, that targets 200 nanoM at assumed 30 % dermal delivery. By assuming 20% systemic delivery it can't be a problem. The test is still based on in vitro effect on DP cells.
I have still a doubt about the target concentration, as under HRT with estradiol valerate 8 mg/day, E2 serum concentration is about 1 nanoM, that is approx 10 X the normal concentration for a male and compares to female pre-menopause serum concentration, so 200 nanoM could be still "topical E2 megadosing".
Hopefully, I'll run the test in combination with ARV-110 PROTAC AR degrader I have ordered, that should allow microdosing.

Cyclosporine is a relatively large molecule. What kind of vehicle are you using for it?
 

2TameDHT

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I've decided it will be best that I shave my head, not permanently, but to see how it grows back.
My hair was quite long when I started noticing my hairloss. As a result, it's hard to determine what the true damage is.
It has the added frustration of people close to me not taking me seriously when I tell them about it.
It also has damage from split ends and lack of consistent moisture recently (afro textured hair needs constant moisture and detangling).

My hair tended to grow back pretty quickly after haircuts, so it won't take long to see where I'm at in terms of coverage and miniaturization.

I'm thinking about adding dermarolling to my regimen, but I'm not sure what size to get.
I hear everything from 0.5 mm to 2.0 mm.

In terms of HRT, I've decided to start out with 6 mg daily, with a larger sized dose of Finasteride.
Many trans healthcare services prescribe Finasteride or Dutasteride as a substitute for AA's.

All in all, I'm still optimistic about my chances of success and cutting my hair seems like a chance to start fresh
and give it all the care it deserves, since I was pretty clueless about haircare when I started growing it out.
 
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