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Dht blocks estrogen. Increased testosterone levels increases estrogen.
Suffering From Severe Post Finasteride Syndrome- Help Please
- Thread starter saimee10
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Dht blocks estrogen. Increased testosterone levels increases estrogen.
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Testosterone also blocks estrogen at any local tissue, maybe not to the same extent as DHT, but it also excerts its androgenic properties just as fine. If 5ARIs gave you gyno, then it means you already were susceptible to it beforehand.
Your total androgen levels go down from finasteride. This makes it an anti-androgen.
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Wrong. Some of the leftover testosterone will turn into estrogen via aromatase.
I really don't know how you guys are still amazed or their statements and opinions? I mean, besides the fact that most of them are mentally ill insecure and frustrated 19 year olds that have no idea of what they are talking about and just think their smart or doctors or some kind of scientists just because they read studies online, without having any actual knowledge or experience of what they are reading, but also you have to keep in mind that these "guys" have their mind set already, they are taking drugs that destroy testosterone and encourage estrogen, what do you expect them to say, that testosterone is good? They have the prostate and balls the size of a peanut and it's not producing anymore those potent androgens, estrogen being dominant it took over their bodies, brains, the monthly cycle and the vagina is missing, but i'm sure they will take care of that one with time also...
For f*** sake they need an excuse/reason for their actions, take the guy who injected acid into his balls, what do you expect him to say, that he is mentally ill and that he made a mistake that he regrets? The deed is done, he/they must accept their new reality and that new reality does not have balls in it, or testosterone or any other thing, some of them have already done irreversible damage, their brains have auto adjusted and are trying to live by the new rules and they will never admit they were wrong or that they made a mistake, they are not normal and must not be treated as, in terms of what they are saying of course, as humans, we have the same rights, it's their bodies and from my point of view they could mutilate themselves until they feel happy about the results, it's not like it will impact somebody else excepts them...
But stop giving them attention, it only accentuates and encourages their mental illnesses, they feed with your attention, block them like i did, you will find the forum more informative and "enjoyable".
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Yes, i know that. But T will still block E at local tissues (let's not forget the remaining DHT that 5ARIs don't block). That's one of the reasons why transwomen need to lower their T to <50 ng/dl for E to have large effects. If we take 200 ng/dl T with 200 pg/ml E, the formal would be the dominating one.
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I mean, all it does is it makes you bald after puberty. The studies you quote that says "DHT is so important" are nullified by how millons of men take 5ARIs with no issues. I guess, for certain unfortunate individuals, DHT is important even in adulthood and beyond, but that's not what the majority agrees with. You can't be in a hairloss forum, and advocate DHT as a good hormone. That's not how it works.
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Blah blah blah, mental illness blah blah. You are so boring. I wish for you a perma ban next time. The mods gave you a third chance, and it looks like you are spoiling it already.
You are acting as if the increase in E is enough to turn you into a woman. That increase in E is what aids in regrowth.
Your DHT lessons, but your T increases. It creates an equal balance in most, preventing side effects, It’s barely an anti-androgen, you’re cancelling out one androgen to increase the other.
Come on man... finasteride reduces DHT with 70% and increases test with 15% (if you are lucky). DHT is 3 to 6 times as potent as test. If you take those numbers into account, do you really think that finasteride is not an anti-androgen?
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W
What, bald people should be banned from GourmetStyleWellness? You f*****g numpty.
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For some that increase in E is enough to cause side effects.
My bad. Edited it. Nope I am not forgetting that, I literally mentioned in my post that it only reduces DHT with 70%. I am also not saying that finasteride can castrate you, I am just pointing out the fact that finasteride is an anti-androgen.
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Damn, it's like you guys don't have google and you all call yourselves knowledgeable...
Pharmacology[edit]
Pharmacodynamics[edit]
Finasteride is a 5α-reductase inhibitor.[16][1] It is specifically a selective inhibitor of the type II and III isoforms of the enzyme.[1][47][48] By inhibiting these two isozymes of 5α-reductase, finasteride reduces the formation of the potent androgen dihydrotestosterone (DHT) from its precursor testosterone in certain tissues in the body such as the prostate gland, skin, and hair follicles.[1][49] As such, finasteride is a type of antiandrogen, or more specifically, an androgen synthesis inhibitor.[50][51] However, some authors do not define finasteride as an "antiandrogen," a term which can refer more specifically to antagonists of the androgen receptor.[52]
Finasteride results in a decrease of circulating DHT levels by about 65 to 70% with an oral dosage of 5 mg/day and of DHT levels in the prostate gland by up to 80 to 90% with an oral dosage of 1 or 5 mg/day.[47][53][54] In parallel, circulating levels of testosterone increase by approximately 10%, while local concentrations of testosterone in the prostate gland increase by about 7-fold and local testosterone levels in hair follicles increase by around 27 to 53%.[55][56] An oral dosage of finasteride of only 0.2 mg/day has been found to achieve near-maximal suppression of DHT levels (68.6% for 0.2 mg/day relative to 72.2% for 5 mg/day).[56][57] Finasteride does not completely suppress DHT production because it lacks significant inhibitory effects on the 5α-reductase type I isoenzyme, with more than 100-fold less inhibitory potency for type I as compared to type II (IC50 = 313 nM and 11 nM, respectively).[16][1] This is in contrast to inhibitors of all three isoenzymes of 5α-reductase like dutasteride, which can reduce DHT levels in the entire body by more than 99%.[47] In addition to inhibiting 5α-reductase, finasteride has also been found to competitively inhibit 5β-reductase (AKR1D1).[58] However, its affinity for the enzyme is substantially less than for 5α-reductase (an order of magnitude less than for 5α-reductase type I) and hence is unlikely to be of clinical significance.[58]
As of 2012, the tissues in which the different isozymes of 5α-reductase are expressed are not fully clear.[49] This is because different investigators have obtained varying results with different reagents, methods, and tissues examined.[49] However, the different isozymes of 5α-reductase appear to be widely expressed, with notable tissues including the prostate gland, seminal vesicles, testes, epididymides, skin, hair follicles, liver, kidneys, and brain, among others.[49]
By inhibiting 5α-reductase and thus preventing DHT production, finasteride reduces androgen signaling in tissues like the prostate gland and the scalp. In the prostate, this reduces prostate volume, which improves BPH and reduces risk of prostate cancer. Finasteride reduces prostate volume by 20 to 30% in men with benign prostatic hyperplasia.[59] Inhibition of 5α-reductase also reduces epididymal weight, and decreases motility and normal morphology of spermatozoa in the epididymis.[60]
Neurosteroids like 3α-androstanediol (derived from DHT) and allopregnanolone (derived from progesterone) activate the GABAA receptor in the brain; because finasteride prevents the formation of neurosteroids, it functions as a neurosteroidogenesis inhibitor and may contribute to a reduction of GABAA activity. Reduction of GABAA receptor activation by these neurosteroids has been implicated in depression, anxiety, and sexual dysfunction.[61][62][63]
So by definition, by inhibiting these two isozymes of 5a-reductase, finasteride reduces the formation of the POTENT ANDROGEN DIHYDROTESTOSTERONE. So even if however some authors do not define finasteride as an "antiandrogen" is still is from it's definition. It's like saying what it does, reducing one of the most potent androgens, but it's not considered an antiandrogen because Ikarus does not think it is or does not like how it sounds because Ikarus does not consider the most potent hormone in the male body, an androgen. Damn you guys, use that brain...
Pharmacology[edit]
Pharmacodynamics[edit]
Finasteride is a 5α-reductase inhibitor.[16][1] It is specifically a selective inhibitor of the type II and III isoforms of the enzyme.[1][47][48] By inhibiting these two isozymes of 5α-reductase, finasteride reduces the formation of the potent androgen dihydrotestosterone (DHT) from its precursor testosterone in certain tissues in the body such as the prostate gland, skin, and hair follicles.[1][49] As such, finasteride is a type of antiandrogen, or more specifically, an androgen synthesis inhibitor.[50][51] However, some authors do not define finasteride as an "antiandrogen," a term which can refer more specifically to antagonists of the androgen receptor.[52]
Finasteride results in a decrease of circulating DHT levels by about 65 to 70% with an oral dosage of 5 mg/day and of DHT levels in the prostate gland by up to 80 to 90% with an oral dosage of 1 or 5 mg/day.[47][53][54] In parallel, circulating levels of testosterone increase by approximately 10%, while local concentrations of testosterone in the prostate gland increase by about 7-fold and local testosterone levels in hair follicles increase by around 27 to 53%.[55][56] An oral dosage of finasteride of only 0.2 mg/day has been found to achieve near-maximal suppression of DHT levels (68.6% for 0.2 mg/day relative to 72.2% for 5 mg/day).[56][57] Finasteride does not completely suppress DHT production because it lacks significant inhibitory effects on the 5α-reductase type I isoenzyme, with more than 100-fold less inhibitory potency for type I as compared to type II (IC50 = 313 nM and 11 nM, respectively).[16][1] This is in contrast to inhibitors of all three isoenzymes of 5α-reductase like dutasteride, which can reduce DHT levels in the entire body by more than 99%.[47] In addition to inhibiting 5α-reductase, finasteride has also been found to competitively inhibit 5β-reductase (AKR1D1).[58] However, its affinity for the enzyme is substantially less than for 5α-reductase (an order of magnitude less than for 5α-reductase type I) and hence is unlikely to be of clinical significance.[58]
As of 2012, the tissues in which the different isozymes of 5α-reductase are expressed are not fully clear.[49] This is because different investigators have obtained varying results with different reagents, methods, and tissues examined.[49] However, the different isozymes of 5α-reductase appear to be widely expressed, with notable tissues including the prostate gland, seminal vesicles, testes, epididymides, skin, hair follicles, liver, kidneys, and brain, among others.[49]
By inhibiting 5α-reductase and thus preventing DHT production, finasteride reduces androgen signaling in tissues like the prostate gland and the scalp. In the prostate, this reduces prostate volume, which improves BPH and reduces risk of prostate cancer. Finasteride reduces prostate volume by 20 to 30% in men with benign prostatic hyperplasia.[59] Inhibition of 5α-reductase also reduces epididymal weight, and decreases motility and normal morphology of spermatozoa in the epididymis.[60]
Neurosteroids like 3α-androstanediol (derived from DHT) and allopregnanolone (derived from progesterone) activate the GABAA receptor in the brain; because finasteride prevents the formation of neurosteroids, it functions as a neurosteroidogenesis inhibitor and may contribute to a reduction of GABAA activity. Reduction of GABAA receptor activation by these neurosteroids has been implicated in depression, anxiety, and sexual dysfunction.[61][62][63]
So by definition, by inhibiting these two isozymes of 5a-reductase, finasteride reduces the formation of the POTENT ANDROGEN DIHYDROTESTOSTERONE. So even if however some authors do not define finasteride as an "antiandrogen" is still is from it's definition. It's like saying what it does, reducing one of the most potent androgens, but it's not considered an antiandrogen because Ikarus does not think it is or does not like how it sounds because Ikarus does not consider the most potent hormone in the male body, an androgen. Damn you guys, use that brain...
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The first post where you don't throw insults like a dog with rabbies. I gotta congratulate you on your success buddy.
DHT and the androgenic profiles of AAS are amazing for wellbeing. Ask anyone who’s taken something like tren - the self observed confidence is off the chart.
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Yeah, let's ask steroid abusers how they feel about steroids. And let's ask transwomen how they feel about E. It goes both ways.