Is it possible to increase testosterone by lowering LH without shutting down endogenous production with exogenous sources?
I'm onto somethingNo, LH is necessary for T production/release. The only way it'd be possible to keep producing endogenous T with low LH is if you were also administering an LH analogue or somehow managed to dramatically increase LH receptor density/sensitivity.
New product?I'm onto something
Let's hear it!I'm onto something
I'm onto something
I mean, it already exists: forksolin. LH pulse won't change but the cAMP response in the testes will increase so T goes upNew product?
so far its lowering LH while increasing T with men in normal range...well its all preliminary blood that we couldn't stake a claim on but its an instant significant increase in 5 days and elevated up to 30 days. We are about to begin looking at increases in 24, 48, and 72 hours.I mean, it already exists: forksolin. LH pulse won't change but the cAMP response in the testes will increase so T goes up
Interesting… so decreasing LH production yet getting an increase in T? Something binding with LH binding sites in the testes stimulating T release?so far its lowering LH while increasing T with men in normal range...well its all preliminary blood that we couldn't stake a claim on but its an instant significant increase in 5 days and elevated up to 30 days. We are about to begin looking at increases in 24, 48, and 72 hours.
No change in SHGB initially so free test increased and estrogen did increase but not until the midway through testing, it will need a good AI or Anti-E...could effecting SGBH be causing this somehow downstream?
No change in SHGB initially so free test increased and estrogen did increase but not until the midway through testing, it will need a good AI or Anti-E...
Will the AI or Anti-E be included in the formula?
This is our theory as well currently..Another way is by causing the adrenal glands to release testosteone. By doing this you would decrease LH production because you are using an alternate route for testosterone excretion.
This is purely theoretical and I have never heard of anything being able to do either one of those proposed theories.
In males, this pathway is usually too minor to matter.This is our theory as well currently..
I agree with the first part (hence why I said the pathway doesn't really matter in males). You are quite wrong on the topic of NO though. For instance, nitrates act as an NO donor in regions of hypoxia. So when you exercise and induce skeletal muscle hypoxia, nitrates/trites in circulation will convert to NO. Furthermore, there are many other ways to systemically increase NO. You wouldn't drop dead from hypotension because NO has a 1-2 second halflife and is limited by endothelial contact and intracellular regulation of the cGMP pathway. For instance, the body can upregulate phosphodiesterase and remove the vasodilation if needed. This is why PDE5 inhibitors are relatively contraindicated with nitrates...because they remove the body's ability to regulate systemic increases in NO levels.I have mixed feeling about this route of testosterone elevation. Allow me to elaborate in the attempt to have an analytical conversation.A physiological increases of testosterone in healthy males does not equate to significant gains in the gym. To my knowledge, in order to truly reap the benefit of an increase of testosterone, one would have to increase levels to supraphysiological levels (this is why hormonal supplementation works so well and testboosters can't compare even if they do indeed raise physiological test levels).Keeping this in mind, to increase testosterone in a normal healthy male via an alternative route which may have the risk of decreasing HPTA activity, only to stay within a normal physiological level (even if it is the upper end) is inviting the risk of a SARM(primarily MK-2866 aka ostarine) or light pro hormone (like low to moderate dosing a 4-DHEA derivative) without the gain. The risk is proportionate to the level of HPTA suppression which in turn be proportionate to the level of adrenal secretion. The more the adrenal secretes, the less the Hypothalamus needs to signal the pituatary to release LH for the testes. This is why this pathway is significant in women and not so significant in men. Furthermore, to catalyze this release is a very tricky endeavor. You would have to create/find something that will selectively activate the cells in the zona reticularis responsible for producing androgens. And lets not forget the zona reticularis also produces DHT, DHEA and Androstenendione(Andro). If you increase DHEA or Andro you increase the risk of estrogen conversion. I would equate the difficulty of something like this to the proported benefits of NO boosters. NO boosters in reality do not work to increase NO. If they actually increased systemic NO like they said claimed, people would be dropping dead or passing out from systemic hypotension. Blood vessels around the body would dilate and a cascade of negative effects would ensue. NO is tightly regulated by the body under normal phsyiological conditions. And to my knowledge there is no known supplement with a true mechanism of action to selectively increase NO in certain areas only (skeletal muscle).Your thoughts USP? I understand my comments come off as negative criticism, but my desire is to engage in a biochemical and physiological discussion of the MOA of this new, unreleased product you are currently working on.
Nitric oxide in cells acts as a strong second messenger in the signaling cascade associated with endothelial vasodilation. Nitric Oxide in specific is a second messenger in this cascade, to my knowledge NO(nitric oxide) is not a donor, it is a second messenger. Nitric oxide once produced by NOS will freely cross the cell membrane barrier where it binds to guanylate cyclase(GC). GC will then synthesize the cGMP which initiates another cascade to relax smooth muscle.You are quite wrong on the topic of NO though. For instance, nitrates act as an NO donor in regions of hypoxia. So when you exercise and induce skeletal muscle hypoxia, nitrates/trites in circulation will convert to NO.
For instance, the body can upregulate phosphodiesterase and remove the vasodilation if needed. This is why PDE5 inhibitors are relatively contraindicated with nitrates...because they remove the body's ability to regulate systemic increases in NO levels.[/QUOTE]Furthermore, there are many other ways to systemically increase NO. You wouldn't drop dead from hypotension because NO has a 1-2 second halflife and is limited by endothelial contact and intracellular regulation of the cGMP pathway.
NERDS!
Zing... that's what popped into my mind as I read that.So this is pretty much just a promo thread for new USP product?
some one should give this dude a job.So tangent aside....still waiting for USP labs response to the test booster.
some one should give this dude a job.
University study planned and results should come end of summer and if all goes well product launches October or September...
We have in house evidence. Now we need published data to support the animal data.
In males, this pathway is usually too minor to matter.
how does this relate to my post about adrenal productionUnless you want a multi pathway product and genuinely create a product that is multi dimensional, for example:
1. SHGB
2.LH
3. AI
I'm responding to your post 21 in this thread. There must be confusion..how does this relate to my post about adrenal production
Curious how you come to the conclusion that only supraphysological levels of testosterone can benefit the end user? I don't think there has been any compound in the supplement industry proven to increase testosterone in normal healthy males. In one individual (just one which doesn't equate to all) the testosterone rose 250 points from 600...that's pretty significant and the decrease in LH was also insignificant. the LH decrease just maybe due to the timing of the blood draw. As you probably know to get an accurate LH reading it would require multiple blood draws over a period of time.I have mixed feeling about this route of testosterone elevation. Allow me to elaborate in the attempt to have an analytical conversation.
A physiological increases of testosterone in healthy males does not equate to significant gains in the gym. To my knowledge, in order to truly reap the benefit of an increase of testosterone, one would have to increase levels to supraphysiological levels (this is why hormonal supplementation works so well and testboosters can't compare even if they do indeed raise physiological test levels).
Keeping this in mind, to increase testosterone in a normal healthy male via an alternative route which may have the risk of decreasing HPTA activity, only to stay within a normal physiological level (even if it is the upper end) is inviting the risk of a SARM(primarily MK-2866 aka ostarine) or light pro hormone (like low to moderate dosing a 4-DHEA derivative) without the gain. The risk is proportionate to the level of HPTA suppression which in turn be proportionate to the level of adrenal secretion. The more the adrenal secretes, the less the Hypothalamus needs to signal the pituatary to release LH for the testes. This is why this pathway is significant in women and not so significant in men.
Furthermore, to catalyze this release is a very tricky endeavor. You would have to create/find something that will selectively activate the cells in the zona reticularis responsible for producing androgens. And lets not forget the zona reticularis also produces DHT, DHEA and Androstenendione(Andro). If you increase DHEA or Andro you increase the risk of estrogen conversion.
I would equate the difficulty of something like this to the proported benefits of NO boosters. NO boosters in reality do not work to increase NO. If they actually increased systemic NO like they said claimed, people would be dropping dead or passing out from systemic hypotension. Blood vessels around the body would dilate and a cascade of negative effects would ensue. NO is tightly regulated by the body under normal phsyiological conditions. And to my knowledge there is no known supplement with a true mechanism of action to selectively increase NO in certain areas only (skeletal muscle).
Your thoughts USP? I understand my comments come off as negative criticism, but my desire is to engage in a biochemical and physiological discussion of the MOA of this new, unreleased product you are currently working on.
Curious how you come to the conclusion that only supraphysological levels of testosterone can benefit the end user? I don't think there has been any compound in the supplement industry proven to increase testosterone in normal healthy males. In one individual (just one which doesn't equate to all) the testosterone rose 250 points from 600...that's pretty significant and the decrease in LH was also insignificant. the LH decrease just maybe due to the timing of the blood draw. As you probably know to get an accurate LH reading it would require multiple blood draws over a period of time.
The pathway referenced in post 21 is adrenal production of testoteroneI'm responding to your post 21 in this thread. There must be confusion..
My mistake. I didn't read Gohards post correctly. I now see the confusion.The pathway referenced in post 21 is adrenal production of testoterone