Creatine + Hairloss. New SA study

Yeah bro, the interesting thing about this study has nothing to do with hairloss. A slight increase in DHT close to the normal range will not affect anyone but the most sensitive.
What is interesting about this study is that it lends weight to the idea that creatine's mode of action is not just a cut and dry as providing more ATP replenishing creatine phosphate. It may also be directly linked to increasing androgen concentrations in the body.

Inja wrote:

No, this is where you are wrong and the reason this whole thing started.
Finasteride will still help in this case, because the molecule causing the problem is still DHT. So regardless of what the mechanism is that is causing the elevation of DHT in the body by blocking 5-AR you stop DHT production, and without a DHT factory I don't give a hoot how many receptors you have you will not get DHT related side effects.

I think we will just have to agree on that point.

I take it that’s a no on the agreeing to disagree??

AR not having an effect is buuuullshit-heavy squatting can increase test levels. How? By upregulation of the AR.
There will always be a dht factory, unless you're a eunoch. If you have more androgen receptors for given DHT production, you will have higher DHT.

And that wasn’t what was being said, the point was that finasteride MIGHT not be completely effective in negating androgenic effects if the increase in serum DHT is not from an increase in 5 alpha reductase, but in AR binding.


I never said not to take it. I said its effectiveness MIGHT be compromised-you could still experience DHT sides despite taking finasteride.

For a given level of test and reductase to DHT, if you increase the androgen receptors or upregulate them, you will have higher serum DHT. Just in the same way as taking spironolactone will lower serum DHT by competing at the receptor causing the given level of DHT not to be attached to the receptor.

By the same token, if you aren’t taking finasteride and then start taking finasteride with creatine supplementation, but the increase in serum DHT is caused by an increase in AR binding and not increased 5 alpha reductase, the finasteride will not be as effective as if the increase in DHT was because of an increase in testosterone or 5 alpha reductase functionality.

If the increase in DHT is caused by increased androgen binding, you will still reduce DHT levels by adding in the finasteride, but not by the factor that you would with the case of an increase in testosterone (or increased 5 alpha reductase of existing testosterone)

This leaves the possibility for androgen sides and still a risk of balding, despite taking the finasteride.



Agree??????????

Probably not, but this argument is getting old and way oversimplified anyway-it is never just a simple increase in one thing. In all likelihood there will be multiple changes in different hormones like SHBG, estradiol, 5 alpha reductase, testosterone and DHT AR binding etc that all have an impact.

I can cut the sexual tension with a knife, you boys get a room....

I must say I learnt a lot.... Please continue....

UltimateThug wrote:

I can cut the sexual tension with a knife, you boys get a room....

I must say I learnt a lot.... Please continue....

Must be all the DHT

Some karma to Inja for the discussion-agree or not, good discussion.

Bro look, I can see youjr a smart guy, and you make some decent points, but you are missing one key factor that is preventing you from understanding the full picture.
I will try to explain a little better.

It does not matter where the signal comes from for increasing production of DHT. It may come from upregulation of androgen receptor, or from some other place in the body. It does not matter, because this is just the beginning of the signalling pathway. If we use your example of the upregulated receptor then this upregulation would be the start of the signal. Another protein would pic up this upregulation and pass on the signal from protein to protein until the body gets the signal at the DHT factory that more DHT must be made.
However the DHT that must be made is made through 5-alpha reductase (5-AR). This happens either by increasing testosterone production so that DHT and estrogen are produced in higher quantities by Le Chateliers principle, or this may occur by altering expression / activity of 5-AR. In the latter case the effect of finasteride will be slightly reduced because you need more finasteride to inhibit more 5-AR but this effect would be very slight and not enough to effect DHT sides because of the affinity of finasteride for 5-AR.

So you see, whatever the route of the increase in DHT the pathway still has to go through 5-AR in order to make the DHT. By inhibiting this enzyme you prevent increasing DHT concentrations even in the presence of a signal to increase DHT (that might originate from the receptor), because it is not the receptor making the DHT.

You understand?

Alright, karma right back at ya then

Good discussion guys...now lets see how smart you really are?

Whats the recommended dosage for Finasteride ?? :laugh:

Inja wrote:

Bro look, I can see youjr a smart guy, and you make some decent points, but you are missing one key factor that is preventing you from understanding the full picture.
I will try to explain a little better.

It does not matter where the signal comes from for increasing production of DHT. It may come from upregulation of androgen receptor, or from some other place in the body. It does not matter, because this is just the beginning of the signalling pathway. If we use your example of the upregulated receptor then this upregulation would be the start of the signal. Another protein would pic up this upregulation and pass on the signal from protein to protein until the body gets the signal at the DHT factory that more DHT must be made.
However the DHT that must be made is made through 5-alpha reductase (5-AR). This happens either by increasing testosterone production so that DHT and estrogen are produced in higher quantities by Le Chateliers principle, or this may occur by altering expression / activity of 5-AR. In the latter case the effect of finasteride will be slightly reduced because you need more finasteride to inhibit more 5-AR but this effect would be very slight and not enough to effect DHT sides because of the affinity of finasteride for 5-AR.

So you see, whatever the route of the increase in DHT the pathway still has to go through 5-AR in order to make the DHT. By inhibiting this enzyme you prevent increasing DHT concentrations even in the presence of a signal to increase DHT (that might originate from the receptor), because it is not the receptor making the DHT.

You understand?

I hear what you're saying.
But then why does a drug like spiro affect serum levels of DHT? It's main action is through competition at the receptor, nothing to do with the manufacture of testosterone and its reduction to DHT. The body would be trying to produce a given level of testosterone and DHT reduction, it just wouldn't be effective because the androgen receptors are binding to the spiro and not the DHT/testosterone.

Hey where's my karma for finally getting you two to admit the love

UltimateThug wrote:

Hey where's my karma for finally getting you two to admit the love

There's some-it's a officially a threesome.
But I'm the top slice of the sandwich

Nice! Now i also understand a bit more.

Yohimbine - we know Inja probably gets paid by his boss to sit here and read discussions like these and to research the answers because its right up his alley and probably in the interest of the employer to let him do all this.

Whats your credentials? Sounds like the two of you might just sit around the corner from each other and probably in the building opposite BeeSting!!!

I think its good to have guys like Yohimbe and Inja on the forum, they can fight it out and let us know the outcome so we can carry on building the muscle.....

Well we all know Inja is a bit crazy, so maybe he got bored created another profile and argues with himself in threads on the forum.

Just joking. :laugh: But you still crazy man. :crazy Have some Karma

@jackrabbit1 - you understand better? Fuck my head hurts after all this. But you're also a bit of a smart guy if I'm not mistaken. Like an Engineer or something.

Yohimbe wrote:

I hear what you're saying.
But then why does a drug like spiro affect serum levels of DHT? It's main action is through competition at the receptor, nothing to do with the manufacture of testosterone and its reduction to DHT. The body would be trying to produce a given level of testosterone and DHT reduction, it just wouldn't be effective because the androgen receptors are binding to the spiro and not the DHT/testosterone.

Well there is not a lot on spironolactone affecting serum hormone levels except for that obscure 1986 Japanese paper you found, this is because the mechanism of spironolactone is not to affect hormone levels but rather to simply block the action of DHT at the receptor in the same way that tamoxifen blocks the action of estrogen in the breast receptors, even in the presence of high estrogen concentrations.

But if I was to pull an explaination off the top of my head I might go with something like this:
Once the spiro binds the receptor the receptor is internalised, although is does not act to trascribe DHT responsive genes in the nuceus, this nuclear-spiro complex is still picked up by the body. If the spiro is administered systemically and in high enough concentrations then high numbers of AR will be relocated to the nucleus without being bound to DHT. This is signal is picked up by the body that to many DHT-AR complexes are being formed because the body only picks up that the AR is bound to something. As a result it sends out the signals that DHT levels are to high and must be dropped. Eventually this signal reaches 5-alpha reductase which is told not to manufacture anymore DHT.

This is just off the top of my head but what I am trying to illustrate is that even though sprio acts by blocking the androgen receptor, this can only have an effect on serum DHT if the signal is finally routed to 5-alpha reductase.

milktuds wrote:

Well we all know Inja is a bit crazy, so maybe he got bored created another profile and argues with himself in threads on the forum.

:huh:

:haha

Inja wrote:

This is signal is picked up by the body that to many DHT-AR complexes are being formed because the body only picks up that the AR is bound to something. As a result it sends out the signals that DHT levels are to high and must be dropped. Eventually this signal reaches 5-alpha reductase which is told not to manufacture anymore DHT.

This is just off the top of my head but what I am trying to illustrate is that even though sprio acts by blocking the androgen receptor, this can only have an effect on serum DHT if the signal is finally routed to 5-alpha reductase.

Hmmm-the stubborness in me still isn't convinced that AR binding has no impact on DHT levels.

But you're argument does make sense.
I need to do some more research on AR binding and how it affects levels.

jackrabbit1 wrote:

Yohimbine - we know Inja probably gets paid by his boss to sit here and read discussions like these and to research the answers because its right up his alley and probably in the interest of the employer to let him do all this.

Whats your credentials? Sounds like the two of you might just sit around the corner from each other and probably in the building opposite BeeSting!!!

No credentials in this field-am in finance.
Just personal research and interest in AAS, with a few years of cycle experience.

Impressive....btw whats inja s credentials

Well y'all lost me at "5-alpha reductase"