Exploring The Hormonal Route. Hair=life.

Father_of_Shiseido

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Masculine traits are a result of two types of receptor binding to androgen molecules.
  1. In the first type, the receptors don't have any effect on the gene expression via any method and has more of a temporary androgen dependent effect, like
    • Muscle Development, because it's easier to store androgens which bind to proteins in muscles which just so happens to be a storage house of proteins like creatinine. (Estrogens are easily stored in fat cells, because why not. Their structure closely resemble lipids like their precursor cholesterol and can dissolve in lipid storing cells. And then there's aromatase storing too there).
    • Libido and male aggression, where androgens kind of have an effect that can trigger required neurotransmitters for this kind of effects. (Androgens aren't the only hormones that affect neurotransmitters to make people aggressive. We have things like cortisol, and adrenaline. An opposite effect is observed due to estrogens which bind to same receptors as androgens, progestogens which compete with cortisols for receptor binding sites, and norepinephrine that competes with adrenaline. Other hormones that affect neurotransmitters are melatonin, insulin, etc.)
    • Sebum and texture of stratum coreneum, which is temporarily affected by the messed up lipid barrier of the skin, because androgens don't like lipids. They like proteins and thus the skin becomes stiff and rough and dry, which the sebaceous glands try to improve by increased sebum production, but fail to do so.
    • Erections
    • Bone density (and not bone shape and size)
  2. In the second type, the receptors affect the gene expression inside the cells giving a more permanent and androgen independent effect, like
    • Facial hair and body hair
    • Bone shape and size (estrogens also have permanent effects here)
    • Shape of eyebrows and nose (estrogens also have permanent effects here)
    • Voice deepening
    • Size of penis
Gene expression:
When an individual is born, he/she is programmed with a set of bodily changes that'll be observed at a certain age or on exposure to certain substances. The information of these changes is stored in the genes. Now, these genes can only be expressed when they are first transcribed and then translated.
The above changes mentioned under gene expression happen after male puberty when respective receptors are exposed to androgen molecules.
Now, in order to stop the gene expression until puberty, the DNA molecule is folded in such a way that the transcription enzymes can't bind to the gene and form its respective RNA molecule. Exposure to androgen molecules makes the DNA unfold permanently in such a way that the gene is exposed to the transcription enzymes. These enzymes bind to the gene, transcribe it, form RNA, RNA translates in ribosome, proteins are formed and gene is expressed.
Since the unfolding is permanent, the masculinization is permanent.

That means Spironolactone or any anti-androgen can't change anything and surgery is necessary for a change, unless you can affect gene expression. Bicalutamide has corepressor function, and it prevents the transcription enzymes from binding to the DNA temporarily. Thus, RNA is not formed and gene expression is halted. Dioxin reverses the unfolding of DNA and folds it again permanently.

So, there is no way you're gonna see reversal of any of the masculine traits mentioned under the gene expression category.
As for the first category, it's not considered as feminizatiom at all. And particularly, Spironolactone is a very weak anti-androgen, so you'll see no change except sebum production, but that's not because of its anti-androgenic effects, I presume, because you'll still have rough and dry skin.
So, do you mean spironolactone wouldn't work for halting male pattern baldness?
 

I'mme

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Masculine traits are a result of two types of receptor binding to androgen molecules.
  1. In the first type, the receptors don't have any effect on the gene expression via any method and has more of a temporary androgen dependent effect, like
    • Muscle Development, because it's easier to store androgens which bind to proteins in muscles which just so happens to be a storage house of proteins like creatinine. (Estrogens are easily stored in fat cells, because why not. Their structure closely resemble lipids like their precursor cholesterol and can dissolve in lipid storing cells. And then there's aromatase storing too there).
    • Libido and male aggression, where androgens kind of have an effect that can trigger required neurotransmitters for this kind of effects. (Androgens aren't the only hormones that affect neurotransmitters to make people aggressive. We have things like cortisol, and adrenaline. An opposite effect is observed due to estrogens which bind to same receptors as androgens, progestogens which compete with cortisols for receptor binding sites, and norepinephrine that competes with adrenaline. Other hormones that affect neurotransmitters are melatonin, insulin, etc.)
    • Sebum and texture of stratum coreneum, which is temporarily affected by the messed up lipid barrier of the skin, because androgens don't like lipids. They like proteins and thus the skin becomes stiff and rough and dry, which the sebaceous glands try to improve by increased sebum production, but fail to do so.
    • Erections
    • Bone density (and not bone shape and size)
  2. In the second type, the receptors affect the gene expression inside the cells giving a more permanent and androgen independent effect, like
    • Facial hair and body hair
    • Bone shape and size (estrogens also have permanent effects here)
    • Shape of eyebrows and nose (estrogens also have permanent effects here)
    • Voice deepening
    • Size of penis
Gene expression:
When an individual is born, he/she is programmed with a set of bodily changes that'll be observed at a certain age or on exposure to certain substances. The information of these changes is stored in the genes. Now, these genes can only be expressed when they are first transcribed and then translated.
The above changes mentioned under gene expression happen after male puberty when respective receptors are exposed to androgen molecules.
Now, in order to stop the gene expression until puberty, the DNA molecule is folded in such a way that the transcription enzymes can't bind to the gene and form its respective RNA molecule. Exposure to androgen molecules makes the DNA unfold permanently in such a way that the gene is exposed to the transcription enzymes. These enzymes bind to the gene, transcribe it, form RNA, RNA translates in ribosome, proteins are formed and gene is expressed.
Since the unfolding is permanent, the masculinization is permanent.

That means Spironolactone or any anti-androgen can't change anything and surgery is necessary for a change, unless you can affect gene expression. Bicalutamide has corepressor function, and it prevents the transcription enzymes from binding to the DNA temporarily. Thus, RNA is not formed and gene expression is halted. Dioxin reverses the unfolding of DNA and folds it again permanently.

So, there is no way you're gonna see reversal of any of the masculine traits mentioned under the gene expression category.
As for the first category, it's not considered as feminizatiom at all. And particularly, Spironolactone is a very weak anti-androgen, so you'll see no change except sebum production, but that's not because of its anti-androgenic effects, I presume, because you'll still have rough and dry skin.
I would ponder on other points later - when I get time, but that spironolactone is a weak anti-androgen is simply a myth. If somebody take say 50mg then yes it is in most cases.
It works in three ways - blocks receptors just like Bicalutamide, reduces testosterone (in most cases), has estrogenic effects (which can be pretty potent at higher dosages. Note however that a higher dose may not works at all and/or may have opposite effect. Taker of this medicine has to know what s/he want with it and adjust accordingly).
 

Yar

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I hear a lot of times the spironolactone loses its effectiveness and they end up increasing the dosage over time.
spironolactone brings testosterone to values and not the maximum, that is, when taking estradiol, additional testosterone will be in the female norm.
 

Ein

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I would ponder on other points later - when I get time, but that spironolactone is a weak anti-androgen is simply a myth. If somebody take say 50mg then yes it is in most cases.
It works in three ways - blocks receptors just like Bicalutamide, reduces testosterone (in most cases), has estrogenic effects (which can be pretty potent at higher dosages. Note however that a higher dose may not works at all and/or may have opposite effect. Taker of this medicine has to know what s/he want with it and adjust accordingly).
Yes, about those three ways:
  1. The blockade of receptors is in no way comparable to that of bicalutamide. It is a steroidal selective androgen receptor antagonist. It works only by reducing the concentration of testosterone so that kinetics don't mess up with its binding. That's why it works only in people with female hormone ranges.
  2. The testosterone levels are lowered only when it is already very low and in female ranges, because it can't mess with HPG axis. Therefore, it works only with sufficient levels of estradiol, otherwise good bye to bone density and energy.
  3. Yes, it binds to estrogen receptors, but has no estrogenic effects in cells other than osteoblasts and hypothalamus.
Bicalutamide, on the other hand, makes all of the androgens useless and shifts the entire equilibrium to estrogenic support.
Spironolactone, can get easily replaced by androgens when used without estrogens to shift the equilibrium.
 

Ikarus

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Yes, about those three ways:
  1. The blockade of receptors is in no way comparable to that of bicalutamide. It is a steroidal selective androgen receptor antagonist. It works only by reducing the concentration of testosterone so that kinetics don't mess up with its binding. That's why it works only in people with female hormone ranges.
  2. The testosterone levels are lowered only when it is already very low and in female ranges, because it can't mess with HPG axis. Therefore, it works only with sufficient levels of estradiol, otherwise good bye to bone density and energy.
  3. Yes, it binds to estrogen receptors, but has no estrogenic effects in cells other than osteoblasts and hypothalamus.
Bicalutamide, on the other hand, makes all of the androgens useless and shifts the entire equilibrium to estrogenic support.
Spironolactone, can get easily replaced by androgens when used without estrogens to shift the equilibrium.

How much T does bicalutamide block? There appears to be so many different opinions on this...
 

Ein

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How much T does bicalutamide block? There appears to be so many different opinions on this...
It varies depending upon what area you're talking about.
50mg/day can block almost all of it (>93%) in the skin and hair. But the same blocks around 0% receptors on the gonads.
 

Ikarus

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It varies depending upon what area you're talking about.
50mg/day can block almost all of it (>93%) in the skin and hair. But the same blocks around 0% receptors on the gonads.

So, 50mg/day is enough for hair loss and acne? DHTcel explained that 50mg blocks 500 ng/dL of T, but other people say other things... It's quite confusing!
 

I'mme

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So, 50mg/day is enough for hair loss and acne? DHTcel explained that 50mg blocks 500 ng/dL of T, but other people say other things... It's quite confusing!
That only when increase in T is permanent. Moreover you don't want it to block T there in gonads as Ein said.
 

I'mme

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Yes, about those three ways:
  1. The blockade of receptors is in no way comparable to that of bicalutamide. It is a steroidal selective androgen receptor antagonist. It works only by reducing the concentration of testosterone so that kinetics don't mess up with its binding. That's why it works only in people with female hormone ranges.
  2. The testosterone levels are lowered only when it is already very low and in female ranges, because it can't mess with HPG axis. Therefore, it works only with sufficient levels of estradiol, otherwise good bye to bone density and energy.
  3. Yes, it binds to estrogen receptors, but has no estrogenic effects in cells other than osteoblasts and hypothalamus.
Bicalutamide, on the other hand, makes all of the androgens useless and shifts the entire equilibrium to estrogenic support.
Spironolactone, can get easily replaced by androgens when used without estrogens to shift the equilibrium.
Darling, what is this! Why are you comparing tmit to bicalutamide? I have always held that Bicalutamide is superior of all. In fact, new 2nd/3rd (don't remember) NSAA are more messy than bicalutamide. I was simply saying that Spironolactone effects are underestimated time and again. It sure has fuckin off-target effects, but for us males who want to remain males, it does the job. If ever I wunt have problem with feminization, I would simply opt for Bicalutamide.

Thanks anyway - you inspire me to do deep researches, but I'm pursuing CA which is one of the most crappiest designed course, takes lots of time, and return have not been good recently. Had I not opted for it, I could have spent my time doing sth else. But my fascination of money...!
 

I'mme

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So, 50mg/day is enough for hair loss and acne? DHTcel explained that 50mg blocks 500 ng/dL of T, but other people say other things... It's quite confusing!
DHTcel is doing what Itchymadsclap did: not giving treatments enough time and continously tinkering with them.
 
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