How much does finasteride increase Testosterone by?

[wilderness20]

So can finasteride make a guys voice higher and cause him to develop breasts as estrogen levels are rising?

Also, finasteride causes Testosterone to raise 15%?

I did not have my free/total tes. level tested before I started finasteride a month ago because dr. said it wouldnt matter. I had them done in September though for an unrelated cause. Is this problematic? Why?

Please respond I would appreciate being awarded with your apt explanations.

 

[ice2613]

Wuffer, yeah I actually had my levels tested before jumping on finasteride and then a month after, I was only taking .65 mg eod and my dht levels dropped by around 33% and my total test doubled. My crown has improved but my diffuse thinning continues, which is y I'm looking for a topical anti androgen. I have the exact numbers somewhere on the forums if you want to see the exact info.

 

[Mens Rea]

Bryan: strictly speaking, DHT is definately not an Aromatase Inhibitor. Not as far as I know despite reading some people online seemingly claiming that DHT can be anti-aromatase.

It seems to be the case that bodybuilders successfully supplement DHT in their cycles (well, proviron or masteron) to reduce (or i should say, control given it is just stacked with testosterone) their estrogen levels and do so very succesfully.

That's what i meant when i said "effectively". I would enjoy reading a study on this very topic myself.

 

[Bryan]

That's right. The HPTA (to keep it very simple) manages a total amount of both testosterone and estrogen; if you reduce the amount of estrogen, it'll be able to produce more testosterone. That's why Andractim and Proviron have been used to treat men with andropause.

An anti-androgen manipulates the HPTA in the same way as a SERM, but since it controls a lot more testosterone than estrogen, an anti-androgen could increase the testosterone production drastically.

I'm not sure what it is you're implying by the sentence "The HPTA manages a total amount of both testosterone and estrogen; if you reduce the amount of estrogen, it'll be able to produce more testosterone." Simply put: testosterone, DHT, and estrogen are all players in the HPTA's feedback control of testosterone production. Artificially reducing the amount of any of those three substances will cause the brain to send the signals to the testes to make more testosterone.

 

[Bryan]

Bryan: strictly speaking, DHT is definately not an Aromatase Inhibitor. Not as far as I know despite reading some people online seemingly claiming that DHT can be anti-aromatase.

It seems to be the case that bodybuilders successfully supplement DHT in their cycles (well, proviron or masteron) to reduce (or i should say, control given it is just stacked with testosterone) their estrogen levels and do so very succesfully.

If DHT isn't an aromatase inhibitor, then supplementing it isn't going to "reduce" estrogen levels (except maybe just a bit by reducing the synthesis of testosterone slightly by way of the HPTA axis). I wish we would all make clear distinctions between reducing estrogen by inhibiting aromatase, and merely producing various hormonal effects by supplementing other hormones! :shock:

 

[Ende]

I'm not sure what it is you're implying by the sentence "The HPTA manages a total amount of both testosterone and estrogen; if you reduce the amount of estrogen, it'll be able to produce more testosterone." Simply put: testosterone, DHT, and estrogen are all players in the HPTA's feedback control of testosterone production. Artificially reducing the amount of any of those three substances will cause the brain to send the signals to the testes to make more testosterone.

Of course, I said to keep it very simple. Prolactin is another hormone which suppresses the testosterone production in large amounts. The amount of serum DHT is almost nothing compared to serum testosterone, and only steroid users will experience suppression because of DHT. Excessive estrogen on the other hand, is a common cause of secondary hypogonadism. The HPTA senses when the estrogen level raises, and it decreases the testosterone production accordingly. Why do you think Arimidex is a good treatment for andropause? It's because it suppresses the estrogen level, and thereby increases the testosterone level. It changes the ratios, and it stays this way long after treatment.

Steroids (DHT and some of its derivatives) changes ratios as well, by countering estrogenic effects on the body. That's why I'm occasionally using Andractim and Proviron, in addition to Primoteston Depot.

 

[Mens Rea]

Bryan: strictly speaking, DHT is definately not an Aromatase Inhibitor. Not as far as I know despite reading some people online seemingly claiming that DHT can be anti-aromatase.

It seems to be the case that bodybuilders successfully supplement DHT in their cycles (well, proviron or masteron) to reduce (or i should say, control given it is just stacked with testosterone) their estrogen levels and do so very succesfully.

If DHT isn't an aromatase inhibitor, then supplementing it isn't going to "reduce" estrogen levels (except maybe just a bit by reducing the synthesis of testosterone slightly by way of the HPTA axis). I wish we would all make clear distinctions between reducing estrogen by inhibiting aromatase, and merely producing various hormonal effects by supplementing other hormones! :shock:

I believe you are over-simplifying things.

In practice the HPTA feedback mechanism appears to work in the opposite manner to 5AR inhibition (i.e. increase in estrogen) with DHT supplementation. The percentages are higher than you guessed because you aren't looking at the full picture. Admittely, it's slightly above me too.

Not the best source in the world but it seems to make sense:

Anti-Estrogen Effects Of DHT

One important function of DHT in the body that does not get much discussion is its antagonism of estrogen. Some men that take Proscar learn this the hard way—by developing a case of gynecomastia. By reducing DHT's protection against estrogen in the body, these men have fallen victim to its most dreaded ramification-b**ch tits.

How does DHT protect against estrogen? There are at least three ways that this likely occurs. First of all, DHT directly inhibits estrogens activity on tissues. It either does this by acting as a competitive antagonist to the estrogen receptor or by decreasing estrogen-induced RNA transcription at a point subsequent to estrogen receptor binding.

Second of all, DHT and its metabolites have been shown to directly block the production of estrogens from androgens by inhibiting the activity of the aromatase enzyme. The studies done in breast tissue showed that DHT, androsterone, and 5alpha-androstandione are potent inhibitors of the formation of estrone from androstenedione. 5alpha-androstandione was shown to be the most potent, while androsterone was the least.

Lastly, DHT acts on the hypothalamus/pituitary to decrease the secretion of gonadotropins. By decreasing the secretion of gonadotropins you decrease the production of the raw materials for estrogen production testosterone and androstenedione (DHT itself cannot aromatize into estrogens). This property of DHT comes into particular utility when it is administered exogenously, and this is to be discussed in further detail in the next section.

http://www.bodybuilding.com/fun/reform8.htm

EDIT: Article also located here. Patrick Arnold

http://mesomorphosis.com/articles/arnold/dht.htm

 

[Bryan]

I believe you are over-simplifying things.

In practice the HPTA feedback mechanism appears to work in the opposite manner to 5AR inhibition (i.e. increase in estrogen) with DHT supplementation. The percentages are higher than you guessed because you aren't looking at the full picture. Admittely, it's slightly above me too.

I think that passage from bodybuilding.com EXACTLY supports what I've been saying in this thread! They state in plain English that suppressing the HPT axis by taking DHT (especially large amounts of it) will lower the production of testosterone, which is required to produce estrogen. As a result, estrogen levels would tend to go down a little.

Furthermore, they state in plain English that DHT does inhibit aromatase, which is contrary to what you said earlier! If that's correct, then estrogen will obviously go down even a bit more.

What they said about DHT possibly competing with estrogen at the estrogen receptor is something that has to do with the hormonal effects of these substances, of course; it doesn't have anything to do with actual levels of estrogens. Competing with estrogen at the estrogen receptor can be as beneficial as actually lowering levels of available estrogen.

 

[Mens Rea]

I think that passage from bodybuilding.com EXACTLY supports what I've been saying in this thread! They state in plain English that suppressing the HPT axis by taking DHT (especially large amounts of it) will lower the production of testosterone, which is required to produce estrogen. As a result, estrogen levels would tend to go down a little.

Furthermore, they state in plain English that DHT does inhibit aromatase, which is contrary to what you said earlier! If that's correct, then estrogen will obviously go down even a bit more.
.

Well im not sure if it's an anti-aromatase or not, but from what i've read, it would make sense if it is.

My point is that it doesn't require this negative feedback mechanism for DHT to begin suppressing actual levels of estrogen. That's my belief.

For instance - a non-suppressing amount of proviron would be 25-50mg ED. I guarantee that without compromising my testosterone levels, my E2 level would be lowered. I'll maybe showcase this on myself in future (I'm currently using arimdex but have proviron in the drawer).

What they said about DHT possibly competing with estrogen at the estrogen receptor is something that has to do with the hormonal effects of these substances, of course; it doesn't have anything to do with actual levels of estrogens. Competing with estrogen at the estrogen receptor can be as beneficial as actually lowering levels of available estrogen

As above.

I also note that SERM's such as clomid and tamoxifen don't actually vary the actual levels of estrogen (on paper), they just have weaker synthetic estrogens competiting for the receptors, too - much like what DHT would do, and also tricking the body into producing more testosterone. Despite this, i've seen it time and time again where the subjects actual estrogen levels have been notably lowered in their blood results despite higher levels of testosterone than previously. Strange, huh?

In practice there always seems to be more going on than the theory would suggest.

 

[Bryan]

Well im not sure if it's an anti-aromatase or not, but from what i've read, it would make sense if it is.

You're not sure whether or not you believe Patrick Arnold? :dunno:

My point is that it doesn't require this negative feedback mechanism for DHT to begin suppressing actual levels of estrogen. That's my belief.

How else would it do that, other than (1) inhibiting aromatase, or (2) suppressing the formation of androgens through the HPT axis? :dunno:

For instance - a non-suppressing amount of proviron would be 25-50mg ED. I guarantee that without compromising my testosterone levels, my E2 level would be lowered. I'll maybe showcase this on myself in future (I'm currently using arimdex but have proviron in the drawer).

Are you saying you've proved that on yourself with blood tests? How do you suppose that works?

I also note that SERM's such as clomid and tamoxifen don't actually vary the actual levels of estrogen (on paper), they just have weaker synthetic estrogens competiting for the receptors, too - much like what DHT would do, and also tricking the body into producing more testosterone. Despite this, i've seen it time and time again where the subjects actual estrogen levels have been notably lowered in their blood results despite higher levels of testosterone than previously. Strange, huh?

How do you suppose that works?

 

[Mens Rea]

You're not sure whether or not you believe Patrick Arnold? :dunno:

I haven't read it anywhere else which is a little strange. But i suppose it must be true given my observations.

How else would it do that, other than (1) inhibiting aromatase, or (2) suppressing the formation of androgens through the HPT axis? :dunno:

Maybe both?

I'm not really sure. Perhaps when DHT occupies the receptors over time less new estrogen is being made by the body. I don't know which category you would put that in?

Are you saying you've proved that on yourself with blood tests? How do you suppose that works?

Not on myself but i've seen it on other people various times when i was researching proviron and masteron.

How do you suppose that works?

Again, im not sure. Perhaps under a similar principle to what i've said above: when the receptors are being occupied (by the SERM weak synthetic estrogens) then there is more free estrogen circulating. Perhaps the HTPA regulates this with less additional production. Makes sense in my head

 

[Ende]

My point is that it doesn't require this negative feedback mechanism for DHT to begin suppressing actual levels of estrogen. That's my belief.

How else would it do that, other than (1) inhibiting aromatase, or (2) suppressing the formation of androgens through the HPT axis? :dunno:

Bryan, what do you think happens to the hormones when they bind to a receptor and express themselves?

 

[wilderness20]

Wow you homies are borderline nerdy hair loss experts. Might as well get your MD's. Too bad most dermatologists don't know 1/10 what the guys on here do.

 

[Mens Rea]

Wow you homies are borderline nerdy hair loss experts. Might as well get your MD's. Too bad most dermatologists don't know 1/10 what the guys on here do.

Bryan just loves to read.

Myself and Enden are learning this stuff by real life necessity thanks to finasteride side effects. uke:

 

[Oren19]

b"h

i'm asked a doctor, and he said the extra testosterone is convert to others hormons like estrogans

 

[Bryan]

Bryan, what do you think happens to the hormones when they bind to a receptor and express themselves?

I'm not sure about that.

 

[Ende]

Bryan, what do you think happens to the hormones when they bind to a receptor and express themselves?

I'm not sure about that.

I believe that's the end of them, and that the levels thereby decreases. If it didn't; steroids wouldn't be used regularly when treating certain conditions, like inflammatory diseases, diabetes, primary hypogonadism and hypothyroidism.

 

[abcdefg]

Who is Patrick Arnold is that the guy that has the big article on how dht is important and does a lot more then grow prostates and make our hair fallout type of thing? Is that guy a good person to believe what he said made sense to me if I am thinking of the right thing.

 

[dezertfox]

My T went up big time on finasteride but my estrogen stayed around the 20-25 mark which is low. T was over range at 1300 before it was 700 or so. Any reason why E wouldn't increase much but T would. LH went up too.

 

[badhabiz]

The amount of testosterone increase in response to finasteride is generally quoted as 10% by the studies, and sometimes not even that much happens. By the way, I've never even seen as increase in estrogen mentioned after finasteride intake, and I've read quite a few finasteride studies.

So, in your opinion, the side sexual effects that many people have experienced with oral finasteride come from inhibition of neurosteroids like allopregnanolone (and androstenediol) and not because of hormonal imbalance ?