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I see from the link provided that the paper is not freely accessible to the general public so I downloaded and included the full text for all you normal, general publical people if anyone wishes to read it...
(File Removed)
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More on topic, after a years gyming and creatine usage your test levels will rise as a result, but hairline shouldn't really thin...
How old are you?
What brand are you using?
Hmmm... If your hair is going like this you are probably just very genetically prone and I'm afraid you might have to just accept it.
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Yes for someone not using steroids finasteride will stuff up the libido, by eliminating DHT. However I think its pretty necessary for the rest of us that are on gear.
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Interesting..So is your theory that if you use Fin and your DHT levels aren't high then you at greater risk?
If that's the case, then maybe I'll try Fin but only if I can measure DHT levels.
Do you have numbers? TST and DHT levels ? You track it?
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If the testosterone levels didn't increase significantly but the DHT levels did, it means the androgen isn't totally coming from 5 alpha reductase of testosterone.
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Yohimbe wrote:
If the testosterone levels didn't increase significantly but the DHT levels did, it means the androgen isn't totally coming from 5 alpha reductase of testosterone.
:ohmy:
Well then if DiHydroTestosterone (DHT) is not being formed by the reduction of testosterone where exactly do you feel its coming from. Testosterone can be reduced in several ways but the considerable bulk is from the enzyme 5-alpha reductase which forms DHT.
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1)
How do you propose that creatine is able to increase one molecules (DHT) affinity for its target protein (androgen recptor) without altering the molecule?
1)
2)
How do you explain the measurable elevation of serum DHT with better recpetor binding? Even if DHT was magically binding better to the receptor (perhaps through some receptor conformational change however unlikely this magic scenario is) then why would this elevate serum DHT (produce more DHT molecules) and where would these molecule be increasingly produced if not from 5-AR?
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Inja wrote:
More on topic, after a years gyming and creatine usage your test levels will rise as a result, but hairline shouldn't really thin...
How old are you?
What brand are you using?
Hmmm... If your hair is going like this you are probably just very genetically prone and I'm afraid you might have to just accept it.
I'm 30, but never had issues with hair thinning or MBP before I started gym. I won't accept anything as unachievable. All you need is research and logic.
Rogaine Foam is the brand I use (import direct from the states because you cant get it here). They sell Regaine here (Minoxidil) but its not the foam version and is shit. Also Nizoral (chemical ketokonazole) shampoo also import. That regimen is the best.
I've researched it a fuckload. OK I lie you can use Propecia (chemical name finasteride) for even better results, but then you asking for major trouble. It can seriously fuck up your hormones permanently.
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Inja wrote:
1)
How do you propose that creatine is able to increase one molecules (DHT) affinity for its target protein (androgen recptor) without altering the molecule?
This is all pure speculation and no one knows based on one study, but there are many ways shown to increase androgen receptors or upregulate androgen receptors (L-Carnitine-L-Tartrate increases and up regulates androgen receptors, even eletrical shock treatment has shown it) so creatine doing the same is no more outrageous than it increasing 5 alpha reductase activity.
The fact testerone remains the same but dht increases shows it's not a simple factor increase as with injecting testosterone and consequent higer conversion to DHT. So finasteride might not do the trick, whereas increased testosterone levels, it will as it's following a proven mechanism
Inja wrote:1)
2)
How do you explain the measurable elevation of serum DHT with better recpetor binding? Even if DHT was magically binding better to the receptor (perhaps through some receptor conformational change however unlikely this magic scenario is) then why would this elevate serum DHT (produce more DHT molecules) and where would these molecule be increasingly produced if not from 5-AR?
Not saying DHT is not produced by 5 alpha reductase, saying increased androgen level may not be related to increased 5 alpha reductase activity, but from increased receptor actvity
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Regaine = shit..id like to differ with you buddy both the regaine sold commericially in SA and the stuff in the states sold as Rogaine has minoxidil as the active agent. So there is no way that the one can be categorized as being shit as the only differnce between the two is their topical application. Regarding nizoral, its only pushed on the other US websites as being great for hairloss as its so widely availabe there. Niz, Nizorelle and the kez shampoo all contain ketokonazole which will the same way nizoral does...but hey to each his own
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Yohimbe wrote:
Inja wrote:
1)
How do you propose that creatine is able to increase one molecules (DHT) affinity for its target protein (androgen recptor) without altering the molecule?
This is all pure speculation and no one knows based on one study, but there are many ways shown to increase androgen receptors or upregulate androgen receptors (L-Carnitine-L-Tartrate increases and up regulates androgen receptors, even eletrical shock treatment has shown it) so creatine doing the same is no more outrageous than it increasing 5 alpha reductase activity.
The fact testerone remains the same but dht increases shows it's not a simple factor increase as with injecting testosterone and consequent higer conversion to DHT. So finasteride might not do the trick, whereas increased testosterone levels, it will as it's following a proven mechanism
Inja wrote:1)
2)
How do you explain the measurable elevation of serum DHT with better recpetor binding? Even if DHT was magically binding better to the receptor (perhaps through some receptor conformational change however unlikely this magic scenario is) then why would this elevate serum DHT (produce more DHT molecules) and where would these molecule be increasingly produced if not from 5-AR?
Not saying DHT is not produced by 5 alpha reductase, saying increased androgen level may not be related to increased 5 alpha reductase activity, but from increased receptor actvity
No dude, you are still talking shit.
You are explaining one thing with something completely unrelated.
Increased androgen receptors allows for a low or normal level of serum DHT to still have the same or increased effect. But this does not account for actual increase in serum DHT. The DHT that is being shown in excess in the blood tests still has to come from somewhere, and this source is 5-AR. You keep going on about upregulating activity or expressionof the androgen receptor blah blah blah but this has nothing to do with increasing DHT levels. Which is what we are talking about here!
:rules
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No bro, you are still talking shit...
Spiro may bind the androgen receptors and this effect in the pituitary results in lowered test and DHT, but if we use the same scenario for increasing serum DHT (as you are suggesting with creatine) then the signal to produce more testosterone and DHT from the pituitary would still have to be played out via 5-AR. Because the DHT still needs to come from the 5-AR enzyme, regardless of where the signal for DHT originated from...
:fighting
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