- Reaction score
- 1,027
He is now a She .Photo? What stage were you in when you started?
He is now a She .Photo? What stage were you in when you started?
If things don't start looking up, im adding 100mg/day medroxyprogesterone acetate.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.
how is your crown ??2 month
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 longerhow is your crown ??
What do you expect from medroxyprogesterone?If things don't start looking up, im adding 100mg/day medroxyprogesterone acetate.
Thank you for your reply! How long have you been on HRT?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.
Dunno, further nukeage of my gonads? If I'm not at castrate levels then why live?What do you expect from medroxyprogesterone?
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.Thank you for your reply! How long have you been on HRT?
I know this. Either way it will reduce the systemic donation of prolactin, resulting in lower levels in the follicles.Carbegoline does not target extra pituitary prolactin produced in the hair follicles so you will not have results from this.
do you eat dairy? my dad struggled with chronic psoriasis for years that completely cleared up when he stopped eating dairyBtw 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...
2 month
Let that hair growThe 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.
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.do you eat dairy? my dad struggled with chronic psoriasis for years that completely cleared up when he stopped eating dairy
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 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.
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.Wow, getting that NW0, I see. But for which price!?
I mean hiding a bald scalp is easier than female fat distribution and sunken chests and what not.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.
Firstly, these are not equivalent things in terms of negative impact on appearance.I mean hiding a bald scalp is easier than female fat distribution and sunken chests and what not.
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.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.
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.I know this. Either way it will reduce the systemic donation of prolactin, resulting in lower levels in the follicles.
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.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.