Exploring The Hormonal Route. Hair=life.

I'mme

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Lol, no. Your face will remain the same. Spironolactone has little to no effect on appearance of male individuals, mostly because it just lowers testosterone a little, and binds to androgen and estrogen receptors a little. It possibly can't effect formation of DHT much, and presumably has lower binding capacity than DHT. Moreover, androgens have many permanent effects on male bodies, mostly because of the coactivator function, which initiates a cascade of effects after binding to the androgen receptors even if it's just for once. Henceforth, the gene expression is permanently turned on, until you put something in there to stop the gene expression, like a dioxin, more preferably attached to androgen receptors. It can be made receptor specific by using testosterone-dioxin, but it is definitely not recommended to anyone. Another way to mess up the gene expression is to prevent the transcription of virilization genes via corepressor function of a compound that attaches to the very same receptors.
Lucky for you, Spironolactone is neither a dioxin nor possesses corepressor function. On contraire, Bicalutamide has corepressor function, so the probability of having those permanent effects reversed is slightly increased, though not well established, because it's dealing with gene expression only via partial hindrance to transcription.
Does this mean that Spironolactone will not cause fat redistribution either?
 

Ein

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Does this mean that Spironolactone will not cause fat redistribution either?
Fat distribution is not a permanent effect of androgens.
Permanent effects include bone development including facial bones like brow ridge, facial and body hair distribution and growth, face shape and features like nose and eyebrows, elongation and development of phallus, pubic hair, VOICE, etc.
Non permanent effects include fat distribution, libido, mood and aggression, sebum production, texture of stratum corneum, rate of melanogenesis, etc.
 

Ein

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Ein just remember that I was so afraid of science that I chose Business/commerce the very first time I got chance :) ie, in +1.
I will take 10+ minutes to understand this whole reply haha
Lol. Dude, I'm a computer science engineering student in an IIT. I have nothing to do with science of genetics and endocrinology. But after studying about all of this, I've realized that this is not a science which is very difficult to comprehend and understand tu its fullest. These are just some basic facts that have been extensively researched upon and all the citations are available. I just accept it and link it with each other and it all makes sense. That's why my father takes Bicalutamide on my word, despite so many warning from his dermatologist about it that it's a prostate cancer drug and all the bs.
 

I'mme

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Fat distribution is not a permanent effect of androgens.
Permanent effects include bone development including facial bones like brow ridge, facial and body hair distribution and growth, face shape and features like nose and eyebrows, elongation and development of phallus, pubic hair, VOICE, etc.
Non permanent effects include fat distribution, libido, mood and aggression, sebum production, texture of stratum corneum, rate of melanogenesis, etc.
What you're saying is permanent effects cannot be overturned/changed just with AA (and/or with estrogen). They would require surgery. But since libido, fab redistribution are non-performance effects they will get effected, right???

Which means me taking spironolactone is largely safe and is highly unlikely to cause noticeabe feminization?

Edit - cannot instead of can
 
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Ikarus

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You realise two type of men are most sought after - the ones who are tall, handsome, smecks of high T; and the ones who are pretty - espouse both masculine and feminine traits, look cute and sweet. Take Shawn Mendes of about 3-5 years ago.

Spironolactone can cause permanent Infertility? Gyno surgery is cheap and one of the least risky. (I plan to opt for Rhino some 6 months down the line, but may instead have to opt for gyno if I get it.)

I am more in the realm of those who have both masculine and feminine traits. I doubt spironolactone would cause permanent infertility, especially since it’s such a weak anti-androgen.
 

I'mme

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Lol. Dude, I'm a computer science engineering student in an IIT. I have nothing to do with science of genetics and endocrinology. But after studying about all of this, I've realized that this is not a science which is very difficult to comprehend and understand tu its fullest. These are just some basic facts that have been extensively researched upon and all the citations are available. I just accept it and link it with each other and it all makes sense. That's why my father takes Bicalutamide on my word, despite so many warning from his dermatologist about it that it's a prostate cancer drug and all the bs.
I was just about to ask you whether you're from IIT or not.. Lol. CSE man, you're going to have a great career. Best of luck!
 

Ikarus

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Does this mean that Spironolactone will not cause fat redistribution either?

Spironolactone doesn’t increase E enough for fat redistribution to occur. If you are young enough, it’s used as a puberty blocker, which prevents the significant effects of T such as voice deepening, facial hair, androgenic development..
 

Ikarus

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That's why my father takes Bicalutamide on my word, despite so many warning from his dermatologist about it that it's a prostate cancer drug and all the bs.

Taking advice from a dermatologist is the greatest mistake anyone could make. They just promote finasteride, and act as if it’s a medication sent from heaven. I never took advice from my dermatologist, and instead educated my dermatologist on why 5AR inhibitors aren’t as great as they say.
 

Ein

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What you're saying is permanent effects can be overturned/changed just with AA (and/or with estrogen). They would require surgery. But since libido, fab redistribution are non-performance effects they will get effected, right???
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.
 

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.
 
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