[USPlabsRep]

Is it possible to increase testosterone by lowering LH without shutting down endogenous production with exogenous sources?

[mr.cooper69]

No, 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.

[thehulk0316]

31 yrs old. I don't use or have ever used AAS and has been years since I used a Ph but my LH is lower than normal but my total and free test are very high. I don't have the exact numbers but my endocrinologist implied I was on TRT or using AAS as she stated my T levels were indicative of someone supplementing. Also, she is concerned about my Lh. I was taking Vit D, magnesium, zinc, fish oils, Vit C, probiotic and a bone health complex. Since I've dropped all of them but the fish oils and added red yeast rice and coq-10 for cholesterol issues.

[USPlabsRep]

No, 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.

I'm onto something

[money0351]

I'm onto something

New product?

[T-Bone]

I'm onto something

Spill the beans already.

[Bamski]

I'm onto something

Let's hear it!

[mr.cooper69]

I'm onto something

New product?

I mean, it already exists: forksolin. LH pulse won't change but the cAMP response in the testes will increase so T goes up

[USPlabsRep]

I mean, it already exists: forksolin. LH pulse won't change but the cAMP response in the testes will increase so T goes up

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.

[MonteRXS]

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.

Interesting… so decreasing LH production yet getting an increase in T? Something binding with LH binding sites in the testes stimulating T release?

[xR1pp3Rx]

could effecting SGBH be causing this somehow downstream?

[kisaj]

So is it bringing test subjects from low into normal range? I never saw the point in taking something that raises total test from normal to higher normal. It would be more significant to raise free test.

[USPlabsRep]

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...

[T-Bone]

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?

[USPlabsRep]

Will the AI or Anti-E be included in the formula?

working on that next plus a few cool additions..

[USPlabsRep]

cool data in yesterday

day 1 was baseline was normal on the lower side of 600
day 2 draw supplement dosed 2 hours before an increase of 80 points
day 7 draw supplement dosed 2 hours before an increase of over 200 points

there was a day three draw but the lab lost the results.

results are individual and by no means does this represent an entire population. Very promising emerging data.

[Punisher187]

Awesome news! Cannot wait til this is released!

[GoHardOrGoHme]

One way to lower LH and increase testosterone is to increase the sensitivity of LH signaling and testosterong production. So either you are upregulating a receptors on your leydig cells or you are increasing the leydig cells ability to release testosterone at a given LH level.

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.

[USPlabsRep]

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.

This is our theory as well currently..

[T-Bone]

Any updates on this as far as a beta release?

[mr.cooper69]

This is our theory as well currently..

In males, this pathway is usually too minor to matter.

[GoHardOrGoHme]

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.

[mw1]

So this is pretty much just a promo thread for new USP product?

[mr.cooper69]

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.

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.

[kisaj]

Science rules.