Exploring The Hormonal Route. Hair=life.

[Experimentality]

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]

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]

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.

 

[Experimentality]

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?

It never ceases to amaze me how complex hormones are. For example, take thyroid hormones. Adequate levels of T3 (most active form of thyroid) are necessary in order to have a normal hair cycle (i.e. no premature catagen). This balance is very delicate. Too high concentrations or too low concentrations induce massive catagen. So, it is not always better to saturate all cell surface receptors, because the induced transcription may be way too intense. For example, there may be proteins that are hair-protective in the correct amounts but highly damaging to the follicle in too high amounts (or too low). I am wondering if this is also the case with E2. The concentration is very hard to figure out, but I am doing well with 1mcg/mL. If anything I would sooner lower the concentration than increase it. I think 5mcg (total application amount) is very safe, and a commonly quoted 20% absorption (ethanolic vehicle) will only yield a 1mcg systemic absorption, which is totally acceptable. Good luck with it, and please report back!

Awesome that you sourced the AR degrader, it should be highly effective. Please be careful with it. Better start too low than too high.

I just use an ethanolic vehicle for Cyclosporine. I got it from the patent of RiverTown Therapeutics (now abandoned) here. They were using a concentration of 0.12%. There are also other formulations that used 1% concentrations where some results were observed. Eyedrops are using 0.05% which is effective for that purpose and FDA approved. Does not need a fancy vehicle as the extremely low percentage that is being absorbed probably is enough to induce effects. I am not sure about the concentration I am using (0.1%) and may increase in the future. However, I am very hesitant to do so as I am quite scared of systemic effects (and rightfully so).

 

[Solxama]

I don't think that it'll be possible as you are pretty much far gone. when did you start hrt? A month?

Like I said, NW0 is utopia. But NW2 is 100% possible, and NW1 is also pretty likely in the long run. At first I was trying not to be overtly exited, but my progress has been lightning fast. I'm down from NW4 to NW3 in the span of a month of HRT. My hair now looks like it used to at 20-21, so I've regained 4 years worth of hair in a month. HRT works very fast for me, and I couldn't be happier

Edit : Here is a recent pic of my crown, compare to my earlier pictures for reference.

 

[ReturnOfExtreme]

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.

Try oral minoxidil

 

[ReturnOfExtreme]

Like I said, NW0 is utopia. But NW2 is 100% possible, and NW1 is also pretty likely in the long run. At first I was trying not to be overtly exited, but my progress has been lightning fast. I'm down from NW4 to NW3 in the span of a month of HRT. My hair now looks like it used to at 20-21, so I've regained 4 years worth of hair in a month. HRT works very fast for me, and I couldn't be happier

Edit : Here is a recent pic of my crown, compare to my earlier pictures for reference.

View attachment 169779

Try oral minoxidil

 

[Solxama]

Try oral minoxidil

Only if my progress stops in a last resort situation. Body hair is one of my biggest dysphoria triggers and oral minoxidil makes you look like a werewolf. I got some topical on standby if my progress slows, but for now it seems Estradiol is doing it's job very well.

 

[ReturnOfExtreme]

Only if my progress stops in a last resort situation. Body hair is one of my biggest dysphoria triggers and oral minoxidil makes you look like a werewolf. I got some topical on standby if my progress slows, but for now it seems Estradiol is doing it's job very well.

Just take it sooner than later, you’ll end up regretting not making the decision earlier, even if it’s a lower dose like 2.5mg

 

[Solxama]

Just take it sooner than later, you’ll end up regretting not making the decision earlier, even if it’s a lower dose like 2.5mg

We'll see if it comes to that, I've seen people regain most of their hair without it. It might speed up the process, but I'm not shaving my whole body every second day if it can be avoided. If Estradiol is not enough then I'll take it.

Thanks for the suggestion, I do appreciate it, but dysphoria is a b**ch

Edit : This is a months progress with Estradiol only. Before HRT my crown was fully bald in a large chunk, now the bald spot is mostly gone.

 

[Norwoody]

Wait for real? I thought you guys were bestiees

Yeah I thought so too

 

[exwhyyou]

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)?

he was fighting it with various cremes and treatments for as long as i can remember... i had small bouts of it occasionally when i was younger but nothing serious, ive also been dairy free for 3 years and i cant recommend it enough

 

[Solxama]

Yeah I thought so too

Me too, and then she ruined it by crossing my personal boundaries.

 

[poopfeast420]

Love that name lol

 

[keepcoolmybabies]

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.

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.

Unless it's Diane 35, wherein it contains cpa and estrogen, why would cpa increase one's estrogen? I'd think, since it suppresses T production (and aromatase converts T to E), it would result in decreased E without any being taken exogenously

 

[MylovelyHair]

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.

Do you think after the regrowth you can maintain with dutasteride and minoxidil like noah?

 

[MylovelyHair]

Like I said, NW0 is utopia. But NW2 is 100% possible, and NW1 is also pretty likely in the long run. At first I was trying not to be overtly exited, but my progress has been lightning fast. I'm down from NW4 to NW3 in the span of a month of HRT. My hair now looks like it used to at 20-21, so I've regained 4 years worth of hair in a month. HRT works very fast for me, and I couldn't be happier

Edit : Here is a recent pic of my crown, compare to my earlier pictures for reference.

View attachment 169779

that is excellent, imagine hair density in a year!

 

[MylovelyHair]

We'll see if it comes to that, I've seen people regain most of their hair without it. It might speed up the process, but I'm not shaving my whole body every second day if it can be avoided. If Estradiol is not enough then I'll take it.

Thanks for the suggestion, I do appreciate it, but dysphoria is a b**ch

Edit : This is a months progress with Estradiol only. Before HRT my crown was fully bald in a large chunk, now the bald spot is mostly gone.

View attachment 169795 View attachment 169796

You gave me soo much hope with crown progress in just a month !! Cool things happen if you destroy androgens!

 

[Almas_NW0]

Do you think after the regrowth you can maintain with dutasteride and minoxidil like noah?

Noah does not support Dutasteride. When he stopped HRT, he started to go bald again. Now he needs a second course of HRT because his hair is of poor quality. Since he has long hanging hair, he is not as demanding on the quality of his hair as I am: in my case, I will not be able to style my hair up and have volume due to thinning

However, if you notice, recovery is faster than baldness. This is what led me to the idea of the possibility of HRT cycles. However, for many reasons, I am not sure that it will be possible to maintain ideal hair in this way, because progress on the temples is slow, and additional time on HRT is needed to improve the quality of the hair.

 

[MylovelyHair]

Noah does not support Dutasteride. When he stopped HRT, he started to go bald again. Now he needs a second course of HRT because his hair is of poor quality. Since he has long hanging hair, he is not as demanding on the quality of his hair as I am: in my case, I will not be able to style my hair up and have volume due to thinning

However, if you notice, recovery is faster than baldness. This is what led me to the idea of the possibility of HRT cycles. However, for many reasons, I am not sure that it will be possible to maintain ideal hair in this way, because progress on the temples is slow, and additional time on HRT is needed to improve the quality of the hair.

So it is impossible to reverse thinning with HRT and maintain with minoxidil and duta??