Some serious unanswered question on igf-1 lr3

[flexshack]

i have been wondering about how using exogenous igf-1 lr3 will effect your natural production of igf-1 or even hgh in the future both near and far? obviously, the body will cease production when you are taking it exogeneously, right? but, does it start up again right away after you stop? does it come back but at much lower levels naturally? anyone have before and after igf-1 blood tests done to see if the exogeneous igf altered their production? thanks.

[einstein1905]

This is a really good question. IGF-1 does have a role in GH regulation, which is what'll be responsible for endogenous IGF-1 production. The active life of LR3 isn't clear. I've seen 12 hours or more. So, it's most likely that you will be inhibiting endogenous GH release during that period, at least in part. I lift in the AM and take my LR3 1x post w/o. So, I'll likely have normal GH release during the night. For those that lift in the afternoon/evening this probably won't be the case.
You also have to consider that the vast majority of GH's anabolic effects are directly mediated by IGF-1, which is what we're supplementing. The potency of LR3 compared to regular IGF-1 is incomparable. LR3 isn't susceptible to being bound by IGFBPs, so it's almost all bioavailable. Also, the mutation to arginine at position 3 makes LR3 have a much higher affinity for the IGF receptors.
What I'm getting at is that the LR3 you're injecting, even at low doses, will give you far greater potency than the IGF-1 that would be produced in response to 12 hours worth of GH release, even at night when GH release is highest. You're coming out ahead...by far.

i have been wondering about how using exogenous igf-1 lr3 will effect your natural production of igf-1 or even hgh in the future both near and far? obviously, the body will cease production when you are taking it exogeneously, right? but, does it start up again right away after you stop? does it come back but at much lower levels naturally? anyone have before and after igf-1 blood tests done to see if the exogeneous igf altered their production? thanks.

[flexshack]

This is a really good question. IGF-1 does have a role in GH regulation, which is what'll be responsible for endogenous IGF-1 production. The active life of LR3 isn't clear. I've seen 12 hours or more. So, it's most likely that you will be inhibiting endogenous GH release during that period, at least in part. I lift in the AM and take my LR3 1x post w/o. So, I'll likely have normal GH release during the night. For those that lift in the afternoon/evening this probably won't be the case.
You also have to consider that the vast majority of GH's anabolic effects are directly mediated by IGF-1, which is what we're supplementing. The potency of LR3 compared to regular IGF-1 is incomparable. LR3 isn't susceptible to being bound by IGFBPs, so it's almost all bioavailable. Also, the mutation to arginine at position 3 makes LR3 have a much higher affinity for the IGF receptors.
What I'm getting at is that the LR3 you're injecting, even at low doses, will give you far greater potency than the IGF-1 that would be produced in response to 12 hours worth of GH release, even at night when GH release is highest. You're coming out ahead...by far.

i understand that you come out ahead, but will the inhibition of endogenous gh be something to worry about upon cessation of exogenous igf-1? i mean, can the inhibition be permanent or at least permanently reduced or will production of endogenous gh come back to the way it was? sorry if my wording is confusing. if it is, i will try to explain better.

[einstein1905]

i understand that you come out ahead, but will the inhibition of endogenous gh be something to worry about upon cessation of exogenous igf-1? i mean, can the inhibition be permanent or at least permanently reduced or will production of endogenous gh come back to the way it was? sorry if my wording is confusing. if it is, i will try to explain better.

GH production/release is regulated by levels of somatomedins (IGF-1).
As levels of IGF-1 reach some threshhold level where negative regulation signals are less than positive regulation signals (where GHRH > somatostatin), another pulse of GH will be released, which will again cause increased production of IGF-1, which itself will either bind IGF receptors or become degraded until plasma levels again wane down to that threshhold level as mentioned above.

If you want an analogy, you can call this the HPLA (hypothalamus-pituitary-liver axis) akin to the HPTA when considering test and its endogenous regulation. The liver is responsible for the synthesis of the IGF-1 that will determine plasma IGF-1 levels (very similar to testosterone plasma levels being key to its own endogenous regulation). To make it simple, just assume that test itself is the only factor that regulates its own production....the high plasma test levels we build up during a cycle (high AAS level of any kind) take many days to fall down to that threshhold level that'll incite the hypothalamus to again begin the signaling for the production of endogenous test production. IGF-1 is just like test in this regard, with the exception that the IGF-1 levels will not "build up" due to very short half-life and it reaches the threshhold plasma levels that are low enough to cause the release of another pulse of GH in only a few hours or so (with LR3 making this time slightly longer).

To answer your actual question, there's no reason for me to believe that GH production would be altered at all upon the cessation of using IGF-1.

[flexshack]

GH production/release is regulated by levels of somatomedins (IGF-1).
As levels of IGF-1 reach some threshhold level where negative regulation signals are less than positive regulation signals (where GHRH > somatostatin), another pulse of GH will be released, which will again cause increased production of IGF-1, which itself will either bind IGF receptors or become degraded until plasma levels again wane down to that threshhold level as mentioned above.

If you want an analogy, you can call this the HPLA (hypothalamus-pituitary-liver axis) akin to the HPTA when considering test and its endogenous regulation. The liver is responsible for the synthesis of the IGF-1 that will determine plasma IGF-1 levels (very similar to testosterone plasma levels being key to its own endogenous regulation). To make it simple, just assume that test itself is the only factor that regulates its own production....the high plasma test levels we build up during a cycle (high AAS level of any kind) take many days to fall down to that threshhold level that'll incite the hypothalamus to again begin the signaling for the production of endogenous test production. IGF-1 is just like test in this regard, with the exception that the IGF-1 levels will not "build up" due to very short half-life and it reaches the threshhold plasma levels that are low enough to cause the release of another pulse of GH in only a few hours or so (with LR3 making this time slightly longer).

To answer your actual question, there's no reason for me to believe that GH production would be altered at all upon the cessation of using IGF-1.

i see, thanks. i had thought that maybe the body would become used to having so much exogenous igf-1 (therefore, not releasing any gh) that it would never return to producing its own gh upon cessation. i was thinking along the same lines as if someone were to go on an extremely long cycle of lets say deca and fina for 2 years straight. upon cessation of that cycle, i would think that one's natural test production would quite possibly never recover. so you don't think this theory is an issue when dealing with igf-1?

[einstein1905]

i see, thanks. i had thought that maybe the body would become used to having so much exogenous igf-1 (therefore, not releasing any gh) that it would never return to producing its own gh upon cessation. i was thinking along the same lines as if someone were to go on an extremely long cycle of lets say deca and fina for 2 years straight. upon cessation of that cycle, i would think that one's natural test production would quite possibly never recover. so you don't think this theory is an issue when dealing with igf-1?

Only if you had consistently elevated levels of IGF-1 for a long period of time (months? longer?), which never dropped low enough to allow for endogenous GH release would that even potentially be the case. Even then, I wouldn't say for sure that once IGF-1 levels dropped down again after being elevated for so long that GH production/release wouldn't return to normal.
It's not an issue at the dosages and dosing schedules most of us use (1x or 2x per day administrations for up to 4-5 weeks per cycle).

[flexshack]

Only if you had consistently elevated levels of IGF-1 for a long period of time (months? longer?), which never dropped low enough to allow for enogenous GH release would that even potentially be the case. Even then, I wouldn't say for sure that once IGF-1 levels dropped down again after being elevated for so long that GH production/release wouldn't return to normal.
It's not an issue at the dosages and dosing schedules most of us use (1x or 2x per day administrations for up to 4-5 weeks per cycle).

okay, excellent. thanks.