Exploring The Hormonal Route. Hair=life.

[Father_of_Shiseido]

[QUOTE = "Марки, должность: 1805722, участник: 104611"] Скорее всего, 1-2 мг не дадут вам сиськи. Если вы видите, что это начинается, просто перестаньте его принимать. [/ QUOTE]

A person cannot live without hormones. If they are not enough, you will feel sluggish and tired and you will not be able to do anything. Testosterone is the main hormone in men after the onset of puberty, it is also the cause of baldness in men that makes temples on the temples, testosterone continues this do throughout the life of a man. Before the onset of puberty, sex hormones are inhibited by melatonin. Therefore, the children's organism lives on melatonin. After the onset of puberty, testosterone is activated, temples appear more and more Ah. Male pattern baldness forms! You take finasteride, it starts to put pressure on testosterone, in response to this the body produces more testosterone, as you drop your testosterone. And estradiol is not enough in you. Therefore, you are bald and the top of the head becomes bald and all thinner !! I repeat once again your hair needs hormone estradiol !!!! Only from it your hair will grow !! testosterone hair does not grow and it falls out !!! Estradiol appearance of new hair and hair growth !!!

This was the way over my head.

 

[Frog]

I've been wading through this thread and wondering: should I try CPA or bicalutamide?

 

[Ikarus]

I've been wading through this thread and wondering: should I try CPA or bicalutamide?

In my opinion, it's a personal decision... When it comes to one being used alone, I would go for bicalutamide since that will provide sufficient results. CPA used on its own will halt hair loss, but the likelihood of regrowth is insignificant since it lowers E. On the other hand, since bicalutamide raises E sufficiently, you will halt hair loss and you will experience regrowth.

Personally, I believe bicalutamide is the better option due to its sustainability. It has a greater safety profile, in which you can assume that it can be used in the long-term. CPA has a questionable safety profile, considering with prolonged use it has the possibility to cause meningioma, prolactinoma and hepatic incidences.

 

[Yar]

[QUOTE = "Лягушка, пост: 1805833, участник: 96705"] Я пробую через эту ветку и задаю вопрос: я должен попробовать CPA или бикалютамид? [/ QUOTE]

I've been wading through this thread and wondering: should I try CPA or bicalutamide?

cpa + estradiol

 

[LastHope123]

When you drop testosterone with finasteride or any other antiandrogen, you need to take estradiol so that the body does not understand the difference! The body does not care what hormone you have. Testosterone baldness! Estradiol new hair and hair growth!

Finasteride and Dutasteride does not drop testosterone, only DHT. Testosterone does actually increase a few percents on these medications, but not significant. Only anti-androgens working directly at the AR receptor or inhibition of the 17β-HSD enzyme will either reduce the testosterone levels or inhibit their effects on the AR receptor. Estradiol will also reduce it since it works as an antigonadotropic at the hypothalamus in the brain, which reduces LH (for steroidogenesis) and FSH (for spermatogenesis) signals going to the testicles. This is why you cannot reduce testosterone levels this way without without running the risk of fertility problems - because without FSH, the leydig cells in the testicles will have limited ability to produce spermia. Without LH and FSH, the testicles will also reduce in volume and go dormant (and this may be irreversible when you come to a point) since they are no longer in production. GnRH antagonists will have the same effect in the brain - the difference is only that they have no estrogenic effect.

There are also talks about potential long lasting or even permanent damage at the hypothalamus in the brain when you start disrupting it with exogenous hormones affecting this mechanism. This is the infamous "reason" they talk of when steroid users talk about permanent hypogonadism because of anabolic/androgenic steroid abuse. The risk is supposedly higher if you are doing this early while your brain is still developing until about 25 years old.
I don't know if I believe in this since I think the research on it is limited.

Hormones are powerful stuff.

 

[Yar]

Finasteride and Dutasteride does not drop testosterone, only DHT. Testosterone does actually increase a few percents on these medications, but not significant. Only anti-androgens working directly at the AR receptor or inhibition of the 17β-HSD enzyme will either reduce the testosterone levels or inhibit their effects on the AR receptor. Estradiol will also reduce it since it works as an antigonadotropic at the hypothalamus in the brain, which reduces LH (for steroidogenesis) and FSH (for spermatogenesis) signals going to the testicles. This is why you cannot reduce testosterone levels this way without without running the risk of fertility problems - because without FSH, the leydig cells in the testicles will have limited ability to produce spermia. Without LH and FSH, the testicles will also reduce in volume and go dormant (and this may be irreversible when you come to a point) since they are no longer in production. GnRH antagonists will have the same effect in the brain.

There are also talks about potential long lasting or even permanent damage at the hypothalamus in the brain when you start disrupting it with exogenous hormones affecting this mechanism. This is the infamous "reason" they talk of when steroid users talk about permanent hypogonadism because of steroid abuse. The risk is supposedly higher if you are doing this early while your brain is still developing until about 25 years old.
I don't know if I believe in this since I think the research on it is limited.

Hormones are powerful stuff.

What I do not believe in dht! Baldness makes testosterone!

 

[LastHope123]

What I do not believe in dht! Baldness makes testosterone!

I don't know what you mean. Dutasteride/Finasteride only inhibits the conversion of testosterone to dihydrotestosterone and does not affect testosterone. Any androgen is bad for the hair follicles at the scalp, both testosterone and DHT. DHT is more androgenic and have more effect in the scalp and prostate compared to testosterone. Testosterone is more important for the gonads (testicles) and anabolism (muscle growth/repair). This is the reason why most males will not use medications or hormones that affects testosterone, but things that affect DHT. Reducing only DHT still have an effect. You can choose both and have even better effect, but you will most likely have more side effects in return. You choose yourself how much you want to sacrifice for your hair loss.

Technically, even if you annihilate both testosterone and dihydrotesterone, you still have androgens (albeit much weaker than test and dht) being produced in the adrenal cortex. Also, technically everyone is slowly going bald - even females. Cells in the body is limited of reproducing x amounts of times during a lifetime, so all cells at the scalp is slowly dying like the rest of your body. If there was a perfect solution, everyone would use the same regimen. And such a solution does not exist. It's like Dominos. If you remove a brick, the Domino path may be stopped after that point. If you disrupt or change a mechanism in your body, you are very likely do disrupt or change another process - because everything in your body is linked togheter in one way or another.

 

[Father_of_Shiseido]

I don't know you mean. Dutasteride/Finasteride only inhibits the conversion of testosterone to dihydrotestosterone and does not affect testosterone. Any androgen is bad for the hair follicles at the scalp, both testosterone and DHT. DHT is more androgenic and have more effect in the scalp and prostate compared to testosterone. Testosterone is more important for the gonads (testicles) and anabolism (muscle growth/repair). This is the reason why most males will not use medications or hormones that affects testosterone, but things that affect DHT. Reducing only DHT still have an effect. You can choose both and have even better effect, but you will most likely have more side effects in return. You choose yourself how much you want to sacrifice for your hair loss.

Technically, even if you annihilate both testosterone and dihydrotesterone, you still have androgens (albeit much weaker than test and dht) being produced in the adrenal cortex. Also, technically everyone is slowly going bald - even females. Cells in the body is limited of reproducing x amounts of times during a lifetime, so all cells at the scalp is slowly dying like the rest of your body. If there was a perfect solution, everyone would use the same regimen.

Is bicalutamide safer than spironolactone in terms of sexual dysfunction, sterility ?

 

[LEXUS]

Gyno is getting worse on spironolactone, especially my right side, wondering if cutting down to 100mg a day might be helpful with less sides. Didn't think gyno would bother me as much as it does...but it does lol. btw i have lost a stone since starting spironolactone.

Yes. I think I can do it soon.



Sorry. wrong. I did not write to you.

 

[LEXUS]

I'm a bit confused how spriro can be as effective whilst only limiting adrenal glands if, like you say, that only accounts for 30% of testosterone production. I take 100mg or spironolactone/day and my total testosterone has hovered around 10 ng/dl on subsequent blood tests. Considering typical average testerone levels are close to 600 ng/dl, I don't know how I can have 60 times lower testosterone, on average, if I'm only blocking 30% of adrenal production. Also, why would spironolactone also tank your sperm and potentially cause testicular atrophy over time if it doesn't affect testicular adrogens?

in the adrenal glands, other harmful androgens are also produced that cause baldness. antrostendion and androsterone. and many other hormones. CPA and SPIRONO still block receptors. maybe your eggs are small and the main testosterone is produced by the adrenal glands.

 

[LEXUS]

Can you give us multiple sources for your claim ?
Sorry but it didn't make sense at all. Lot of trans MTF take spironolactone and it lowers their testosterone, their balls produce less testosterone, not only the adrenal glands.

reduces but not much. not everyone needs to reduce testosterone to zero to get a result. on spironolactone it is written that it is an antagonist of adrenal hormones. I have already said that androsterone and androstenedione also cause baldness. On androkur it is written that it turns off the LH, thereby the eggs stop producing testosterone. spironolactone will never cause testicular atrophy. And in your case, I would advise taking avodart or finasteride. your testosterone is at zero. but DHT is very high. spirono and androkur drugs completely different actions. and bicalutam generally can eventually increase testosterone levels.

 

[LEXUS]

Makes sense.

How has been your progress? If possible, please upload before and after photos.

Yes. I think I can do it soon.

 

[itchymadscalp]

reduces but not much.

If you’re saying now spironolactone can reduce testosterone I agree with you. That’s not what you were saying and that why I disagreed.

 

[LastHope123]

Is bicalutamide safer than spironolactone in terms of sexual dysfunction, sterility ?

Bicalutamide is a selective silent androgen receptor agonists, meaning it actually act as a androgen. It binds to the androgen receptor and activates it, but it activates it much less than testosterone and dihydrotestosterone. So it binds to the androgen receptors and takes up the place were testosterone and DHT would attach, so you ultimately end up with less androgen signal transduction - but not zero. Since it is selective for the AR, it does not act as a estrogen or antiestrogen for example. So, since it only reduces AR signal transduction it will not affect testicle function through the brain pathway. It actually increases testosterone production which increases estrogen levels because of increased aromatization from testosterone (testosterone converts to estrogen through an enzyme - so more testosterone = more estrogen). Androgen receptors regulate how sensitive estrogen receptors are, so if you reduce androgen receptor activation you could potentially get side effects. So if you combine increased estrogen + inhibition of androgen signal transduction, the result is that you will most likely have a very high chance of getting gynecomastia - even if you do not take exogenous estrogen.

The problem with bicalutamide is that even though it does not reduce androgen levels, it still inhibits them from working properly. So you could still have some sort of sexual side effects. The good part is that your testicles will most likely not reduce that much in size and function - so I would guess you have a longer timeframe before you could have long lasting or permanent sexual side effects, if you have any at all. This is probably the reason why drugs such as bicalutamide is preferred in males with prostace cancer.

https://www.ncbi.nlm.nih.gov/pubmed/11260298

Spironolactone is a androgen receptor antagonist that blocks signal transduction. The result is similar to bicalutamide, just not quite the same mechanism. But it is also a weak steroidogenesis inhibitor. From what I've read, it inhibits the cholesterol cleavage enzyme so it inhibits steroidogenesis at the very start - so you could possibly get some sort of reduction in several types of steroids. It is classified as a anti-mineralocorticoid, perhaps it is through this mechanism (I'm not quite sure). It probably reduces testosterone and estrogen significantly because of this - also since it also inhibits steroid enzymes further down the steroid metabolic pathway. Probably not that much like cyproterone acetate, cause cyproterone acetate have from what I've read extra steroidogenesis inhibition on especially the steroids testosterone (+ DHT) and estrogens because it also have progestogenic effects that leads to antigonadotropic effects in the brain = less production of testosterone (= reduced estrogen levels) and sperm production in the testicles.

So in the end, I would say this is the best against sexual side effects (going from left to right):

Bicalutamide (or similar antiandrogens) > Spironolactone > Cyproterone acetate/GNrH antagonists.
You have to look for antiandrogens that are either selective androgen receptor antagonists or selective androgen receptor silent antagonists. The higher selectivity, the better - so cost and availability is probably your main concern.


But for side effects like gyno, the best is probably (going from left to right):

Spironolactone > Cyproterone acetate > Bicalutamide.

Maybe I'm wrong at some point or have not pointed out ALL the effects of these drugs (I would have to write pages), so take my words with a grain of salt. I have read some studies on the different side effect profiles of these different drugs, so I'm pretty sure (but not 100%).

 

[itchymadscalp]

women do not make sense to take CPA. there is no reason for a neutered man to take CPA. only spironolactone. testosterone in men without eggs is produced only in the adrenal glands.

Oh no. It was about castrated men taking CPA. Yeah I wanted you to source your claims. CPA acts also by binding to the androgen receptors, so it's not totally useless. If you were referring to the high risk of hyperprolactinemia because of CPA, OK. why not.

 

[itchymadscalp]

reduces but not much. not everyone needs to reduce testosterone to zero to get a result(1). on spironolactone it is written that it is an antagonist of adrenal hormones. I have already said that androsterone and androstenedione also cause baldness. On androkur it is written that it turns off the LH, thereby the eggs stop producing testosterone. spironolactone will never cause testicular atrophy. And in your case, I would advise taking avodart or finasteride. your testosterone is at zero. but DHT is very high (2). spirono and androkur drugs completely different actions. and bicalutam generally can eventually increase testosterone levels.

1 - I agree, never said otherwise.
2 - I took Dutasteride alongside Bicalutamide/Cyproterone/Lupron and it was useless.

I really don't get why you're saying all of this to me, I never asked you to explain - especially badly. I know what I'm dealing with, and I don't think you know a lot about endocrine system.

And don't forget, you're not a specialist, doctors, so don't tell people "you should take". Because you don't really know what they should take.
And what we are taking shouldn't be recommended ... especially when we don't really know the long term real issues.

 

[Ikarus]

What I do not believe in dht! Baldness makes testosterone!

Both contribute to hair loss...

 

[Father_of_Shiseido]

Bicalutamide is a selective silent androgen receptor agonists, meaning it actually act as a androgen. It binds to the androgen receptor and activates it, but it activates it much less than testosterone and dihydrotestosterone. So it binds to the androgen receptors and takes up the place were testosterone and DHT would attach, so you ultimately end up with less androgen signal transduction - but not zero. Since it is selective for the AR, it does not act as a estrogen or antiestrogen for example. So, since it only reduces AR signal transduction it will not affect testicle function through the brain pathway. It actually increases testosterone production which increases estrogen levels because of increased aromatization from testosterone (testosterone converts to estrogen through an enzyme - so more testosterone = more estrogen). Androgen receptors regulate how sensitive estrogen receptors are, so if you reduce androgen receptor activation you could potentially get side effects. So if you combine increased estrogen + inhibition of androgen signal transduction, the result is that you will most likely have a very high chance of getting gynecomastia - even if you do not take exogenous estrogen.

The problem with bicalutamide is that even though it does not reduce androgen levels, it still inhibits them from working properly. So you could still have some sort of sexual side effects. The good part is that your testicles will most likely not reduce that much in size and function - so I would guess you have a longer timeframe before you could have long lasting or permanent sexual side effects, if you have any at all. This is probably the reason why drugs such as bicalutamide is preferred in males with prostace cancer.

https://www.ncbi.nlm.nih.gov/pubmed/11260298

Spironolactone is a androgen receptor antagonist that blocks signal transduction. The result is similar to bicalutamide, just not quite the same mechanism. But it is also a weak steroidogenesis inhibitor. From what I've read, it inhibits the cholesterol cleavage enzyme so it inhibits steroidogenesis at the very start - so you could possibly get some sort of reduction in several types of steroids. It is classified as a anti-mineralocorticoid, perhaps it is through this mechanism (I'm not quite sure). It probably reduces testosterone and estrogen significantly because of this - also since it also inhibits steroid enzymes further down the steroid metabolic pathway. Probably not that much like cyproterone acetate, cause cyproterone acetate have from what I've read extra steroidogenesis inhibition on especially the steroids testosterone (+ DHT) and estrogens because it also have progestogenic effects that leads to antigonadotropic effects in the brain = less production of testosterone (= reduced estrogen levels) and sperm production in the testicles.

So in the end, I would say this is the best against sexual side effects (going from left to right):

Bicalutamide (or similar antiandrogens) > Spironolactone > Cyproterone acetate/GNrH antagonists.
You have to look for antiandrogens that are either selective androgen receptor antagonists or selective androgen receptor silent antagonists. The higher selectivity, the better - so cost and availability is probably your main concern.


But for side effects like gyno, the best is probably (going from left to right):

Spironolactone > Cyproterone acetate > Bicalutamide.

Maybe I'm wrong at some point or have not pointed out ALL the effects of these drugs (I would have to write pages), so take my words with a grain of salt. I have read some studies on the different side effect profiles of these different drugs, so I'm pretty sure (but not 100%).

Thank you! You made it very clear.

 

[bridgeburn]

Bicalutamide is a selective silent androgen receptor agonists, meaning it actually act as a androgen. It binds to the androgen receptor and activates it, but it activates it much less than testosterone and dihydrotestosterone.

Thats how cypro and spironolactone work, bica is not supposed to activate the receptor.
bica=NSAA
cypro and spironolactone= very weak partial agonists

 

[Yar]

[QUOTE = "LastHope123, сообщение: 1805895, участник: 141452"] Я не знаю, что вы имеете в виду. Дутастерид / финастерид только ингибирует превращение тестостерона в дигидротестостерон и не влияет на тестостерон. Любой андроген вреден для волосяных фолликулов на коже головы, как для тестостерона, так и для DHT. DHT является более андрогенным и оказывает большее влияние на состояние головы и простаты по сравнению с тестостероном. Тестостерон более важен для половых желез (яичек) и анаболизма (рост / восстановление мышц). Это связано с тем, что большинству людей не нужны лекарства или гормоны, которые влияют на тестостерон. Это имеет хоть какой-то эффект побочных эффектов. Вы сами выбираете, сколько хотите пожертвовать ради выпадения волос.

Технически, даже если вы аннигилируете как тестостероном, так и дигидротестероном, у вас все еще есть андрогены (хотя и слабее, чем тест и дхт), вырабатываемые в корейских надпочечниках. Кроме того, все женщины медленно лысеть. Клетки в теле ограничены, поэтому все клетки кожи головы медленно умирают. [/ QUOTE]

Both contribute to hair loss...

you need to figure out what are the distinctive symptoms of testosterone that he does and the distinctive signs of dht if there is one and what he does