How much does finasteride increase Testosterone by?

[Mens Rea]

Indeed!

How's things by the way?

I fear fluridil is keeping me suppresed after all as I had about a week off as I ran out and my libido crept up significantly but has returned to it's new baseline again since back on the fluridil.

Shitter as I really need to keep my hair. Pointless having libido without it.

DHT made up of estrogen. WTF

It seems that alot of us are really reliant on CB-03-01 living up to the hype. It's basically the only thing that will be able to keep my hair.


I'm ok man. Getting by. Starting a very strict diet this week.

 

[Bryan]

A few days ago I read something that stated Estrogen and DHT remain at the same levels in a person regardless of how much Testosterone raises. If T goes up roughly 10% as a result of 5AR inhibition, it doesn't exactly make sense that estrogen would actually RISE by that amount, but that the ratios would just be out of whack.

Sure, it makes PERFECT sense, if the availability of testosterone is indeed the limiting factor in the production of estrogen. If there's plenty of aromatase around, why would it be so difficult to believe that a 10% rise in testosterone would also cause a 10% rise in estrogen? :dunno:

 

[Bryan]

This is what I was reading:

http://www.totalityofbeing.com/Frameles ... e_hair.htm

I'm not sure how factual all this is, but it is interesting if it is true. It says that DHT is made mostly out of estrogen.

That's preposterous. "Dr. Wong" doesn't know what the hell he's talking about! DHT is absolutely, positively NOT made out of estrogen! There are other things that guy says in that article that are incorrect, too, but the thing about DHT supposedly being made from estrogen is the most egregious. It's a real howler!! :laugh:

I'm not sure if that is true or not, but blocking 5AR would definitely result in increased estrogen if this were the case.

Did you mean to say that it would DECREASE estrogen?? (Blocking 5AR would decrease DHT, which would then decrease the production of estrogen, if what crazy "Dr. Wong" said were correct.)

 

[Wuffer]

Damnit, Dr Wong! You screwed us all again!

I admit I was skeptical of that article also.. Too bad I already bought all that crap from his webpage. Anyone want to buy ten cases of love tonic? It's good stuff! Dr. Wong's guarantee!

 

[Bryan]

Estrogen would raise only slighly as a direct consequence of the 15% increase in testostosterone. For the most part the increase in estrogen is a result of the lowered DHT. They counterbalance against each other. If you supplement DHT (proviron) estrogen will automatically be decreased. This is why it's the estrogen that tends to be the main issue with finasteride, really.

Are you saying that DHT acts as an aromatase inhibitor? I do _vaguely_ recall hearing about that myself somewhere, but I don't remember exactly where...

 

[Bryan]

Think about this feedback loop, Wuffer:

- DHT reduces by 65%.

- As a result, Testosterone increases (via less conversion to DHT)...

This is something I've talked about occasionally for years on hairloss sites: people always assume that testosterone increases while taking 5a-reductase inhibitors simply because less of it gets converted to DHT, so there's more of it "hanging around" the bloodstream as a result. However, I think the medical evidence rather strongly suggests that the real reason for that is that the body senses less androgenic stimulation while taking finasteride or dutasteride (DHT is a more potent androgen than testosterone), so the brain sends the chemical signals to the testes that tell them to start producing more testosterone.

 

[Bryan]

On the other hand, if someone took finasteride and had side effects (from the lack of DHT) then in an attempt to treat persistent problems took something like Nolvadex (anti-estrogen) then wouldn't the lack of estrogen in effect lower DHT again?

I don't see how lower estrogen would lower DHT "again"? Without finasteride, you would likely be increasing DHT by pushing down your E2 via the normal mechanisms....

Regardless of "Dr. Wong's" silly claim about DHT coming from estrogen, it's true that lower estrogen will increase both testosterone and DHT. That's what happened just a few years ago in that large study in which men were treated for BPH by giving them one of two different daily doses of an aromatase inhibitor drug, to lower their estrogen. Both their testosterone and DHT levels rose, and the effect was dose-dependent.

 

[Bryan]

It's in the prescribing information leaflet. Bottom of page 1, top of page 2.

No response to that Bryan?

Nope. I haven't seen that prescribing information leaflet before, so that's new to me! :shock:

None of the finasteride studies I've read have ever said anything that direct; in fact, they generally have said something like "No effect on estrogen was noted", even after sometimes mentioning small increases in testosterone! :dunno:

 

[Wuffer]

Yeah, i've seen studies state the same. A rise in estrogen is never noted in studies, and I would think I would have seen this a few times, and not just in this one. If you guys come across anything else that states that this might happen, I would like to see it too.

Possibly estrogen is the cause of problems in people that have sides. Maybe it raises for these guys, but not most others?

 

[Ende]

Estrogen would raise only slighly as a direct consequence of the 15% increase in testostosterone. For the most part the increase in estrogen is a result of the lowered DHT. They counterbalance against each other. If you supplement DHT (proviron) estrogen will automatically be decreased. This is why it's the estrogen that tends to be the main issue with finasteride, really.

Are you saying that DHT acts as an aromatase inhibitor? I do _vaguely_ recall hearing about that myself somewhere, but I don't remember exactly where...

I don't know if DHT interferes with aromatase enzymes, but DHT is the estrogen antagonist. That's what he's saying.

Do some research on medical use of Masteron, Proviron and Andractim.

 

[Mens Rea]

Estrogen would raise only slighly as a direct consequence of the 15% increase in testostosterone. For the most part the increase in estrogen is a result of the lowered DHT. They counterbalance against each other. If you supplement DHT (proviron) estrogen will automatically be decreased. This is why it's the estrogen that tends to be the main issue with finasteride, really.

Are you saying that DHT acts as an aromatase inhibitor? I do _vaguely_ recall hearing about that myself somewhere, but I don't remember exactly where...

Effectively, yes. Some bodybuilders even replace arimidex in their cycles with proviron.

 

[Bryan]

Estrogen would raise only slighly as a direct consequence of the 15% increase in testostosterone. For the most part the increase in estrogen is a result of the lowered DHT. They counterbalance against each other. If you supplement DHT (proviron) estrogen will automatically be decreased. This is why it's the estrogen that tends to be the main issue with finasteride, really.

Are you saying that DHT acts as an aromatase inhibitor? I do _vaguely_ recall hearing about that myself somewhere, but I don't remember exactly where...

I don't know if DHT interferes with aromatase enzymes, but DHT is the estrogen antagonist. That's what he's saying.

I'm still unclear what it is he's actually saying. I don't doubt that DHT and estrogen are "antagonists" in the sense of having opposite hormonal effects on certain tissues (hair follicles are an excellent example of that), but unless DHT also acts as an aromatase inhibitor, I wouldn't expect it to have any effect on the level of estrogen in the body, unless it can be shown that androgenic stimulation (like DHT) can influence the body's production of the aromatase enzyme. Hopefully he can clarify all this for us.

 

[Bryan]

[quote="Mens Rea":244qrp4r]Estrogen would raise only slighly as a direct consequence of the 15% increase in testostosterone. For the most part the increase in estrogen is a result of the lowered DHT. They counterbalance against each other. If you supplement DHT (proviron) estrogen will automatically be decreased. This is why it's the estrogen that tends to be the main issue with finasteride, really.

Are you saying that DHT acts as an aromatase inhibitor? I do _vaguely_ recall hearing about that myself somewhere, but I don't remember exactly where...

Effectively, yes. Some bodybuilders even replace arimidex in their cycles with proviron.[/quote:244qrp4r]

Your use of the word "effectively" bothers me! Does DHT act as an aromatase inhibitor or not? :dunno: Or does the activity of aromatase (and the estrogen it produces) stay the same, and those bodybuilders are simply using extra DHT to counter the hormonal effects of estrogen with a separate strong androgen? :dunno:

 

[Ende]

DHT has an effect on the estrogen level. All hormone levels decreases when the hormones express themselves. Take the breast tissue as an example; estrogen causes tissue to grow, DHT reverses the process. Both levels will decrease during the process; that's why ratios are important.

 

[Ende]

I don't think DHT works as an aromatase inhibitor, no.

 

[Bryan]

DHT has an effect on the estrogen level.

How do you know? As I said myself earlier, I keep thinking that I heard somewhere that DHT may be an aromatase inhibitor, but I can't remember for the life of me where it is that I saw that. I'm worrying now that I may be confusing that with something else!

All hormone levels decreases when the hormones express themselves.

I question the accuracy of such a broad claim, unless you're merely saying that when a hormone binds to a receptor, that specific molecule is gone for good. I'm not sure whether or not that's completely true.

Take the breast tissue as an example; estrogen causes tissue to grow, DHT reverses the process. Both levels will decrease during the process; that's why ratios are important.

I don't doubt that the growth of tissue can definitely be affected by some hormones; another perfect example of that would be androgens stimulating the growth of prostate tissue. The question here is whether levels of the hormones THEMSELVES can be directly affected by hormones. Several times I've mentioned the study by Happle and Hoffmann, which found that human scalp hair follicles were stimulated by testosterone to produce more 5a-reductase type 2, but NOT type 1. The correct answers to questions like these can depend on which specific tissue you're talking about, and which specific hormone.

I'm still wondering whether or not DHT acts as an aromatase inhibitor or suppresses the synthesis of aromatase, which would be the real issues here when we talk about levels of estrogen.

 

[Ende]

http://www.ncbi.nlm.nih.gov/pubmed/6354523

The reduction in the estrogen level could be caused by the suppression of the testosterone production, but when the estrogen level is reduced, more testosterone is likely to be produced afterwards. This changes the ratios.

 

[Ende]

All hormone levels decreases when the hormones express themselves.

I question the accuracy of such a broad claim, unless you're merely saying that when a hormone binds to a receptor, that specific molecule is gone for good. I'm not sure whether or not that's completely true.

Yes, that's what I believe.

 

[Bryan]

http://www.ncbi.nlm.nih.gov/pubmed/6354523

The reduction in the estrogen level could be caused by the suppression of the testosterone production, but when the estrogen level is reduced, more testosterone is likely to be produced afterwards. This changes the ratios.

Absolutely! When you mess with the brain's feedback loop (by giving aromatase inhibitors, for example), you can stimulate the production of testosterone. That's why giving "pure" antiandrogens systemically (like flutamide) can also greatly increase testosterone levels.

 

[Ende]

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.