Roco Bama
Member
If igf-1lr3 is capable of raising igf level, do you think bb would be spending so much money on pharma hgh.Theres a scam/shill here somehow. Wait for it....
I never heard of research IGF-1 causing such a dramatic reading so fast .
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If igf-1lr3 is capable of raising igf level, do you think bb would be spending so much money on pharma hgh.Theres a scam/shill here somehow. Wait for it....
I never heard of research IGF-1 causing such a dramatic reading so fast .
Is that how we're gonna treat each other?Buy it from the same place I did.
Cut it out...the fucking mirror has dick to do with your arm looking abnormally large wise guy.Fucking guys killing me on a mirrored angle shot. Lol
At first I thought we knew each other and had discussed my monthly and yearly outbox for Serostim money. I posted a pic one time with my handle and the date on a piece of paper along with (23)6mg 126iu kits. I come across some decent deals out here. No doubt.If igf-1lr3 is capable of raising igf level, do you think bb would be spending so much money on pharma hgh.
Real LR3 can and will...If igf-1lr3 is capable of raising igf level, do you think bb would be spending so much money on pharma hgh.
Not really. From all the research I've done, the real lr3 in the early 2000s was also worthless. Igf lr3 is not a recombinant human igf-1 that is produced in our body, it contains 83 amino acids compared to 70. The recombinant human igf-1 of 70 amino acids is produced in us by ipsen under the trade name increlexReal LR3 can and will...
That's like saying your body can't absorb testosterone enanthate due to the enanthate ester, right? Well, obviously we know that isn't the case. It's simply IGF-1 comprising the complete human IGF-1 sequence with the substitution of an Arg (R) for the Glu(E) at position three, hence R3, and a 13 amino acid extension peptide at the N terminus.Not really. From all the research I've done, the real lr3 in the early 2000s was also worthless. Igf lr3 is not a recombinant human igf-1 that is produced in our body, it contains 83 amino acids compared to 70. The recombinant human igf-1 of 70 amino acids is produced in us by ipsen under the trade name increlex
You've said this before, I am VERY interested to learn more about what you're saying...Regardless of if it can or can't raise serum IGF levels, IGF-1 is NOT a potent muscle builder whatsoever.
AAS are the king of muscle builders but igf-1 induces muscle hyperplasia meaning it creates new cells. That's why some of us take hgh to take it to the next level after we reach genetic limit. Hgh is the only hormone available that can significantly raise serum igf-1 level. I have yet to hear someone that achieved success from igf lr3Regardless of if it can or can't raise serum IGF levels, IGF-1 is NOT a potent muscle builder whatsoever.
AAS are the king of muscle builders but igf-1 induces muscle hyperplasia meaning it creates new cells. That's why some of us take hgh to take it to the next level after we reach genetic limit. Hgh is the only hormone available that can significantly raise serum igf-1 level. I have yet to hear someone that achieved success from igf lr3

they said the same about AAS
You've said this before, I am VERY interested to learn more about what you're saying...
Regardless of it's abilities or not, I believe we are curious at this point about LR3's ability to raise bloodlevels if IGF-1. Your point is still very interesting to me, though.
they said the same about AAS
So every study is wrong bc some older studies used poor methodology/testing techniques and were misapplied? Strong logic.
AAS are the king of muscle builders but igf-1 induces muscle hyperplasia meaning it creates new cells. That's why some of us take hgh to take it to the next level after we reach genetic limit. Hgh is the only hormone available that can significantly raise serum igf-1 level. I have yet to hear someone that achieved success from igf lr3
According to Dave Palumbo, who I find to be VERY reputable, he says over 90% of the pros nowadays use it in arms and calves. Impossible to prove, of course.
That's like saying your body can't absorb testosterone enanthate due to the enanthate ester, right? Well, obviously we know that isn't the case. It's simply IGF-1 comprising the complete human IGF-1 sequence with the substitution of an Arg (R) for the Glu(E) at position three, hence R3, and a 13 amino acid extension peptide at the N terminus.
For what it's worth, per wikipedia:
"The consequences of these modifications are that IGF-1 LR3 retains the pharmacological activity of IGF-1 as an agonist of the IGF-1 receptor, has very low affinity for the insulin-like growth factor-binding proteins (IGFBPs), and has improved metabolic stability.[1][2] As a result, it is approximately three times more potent than IGF-1,[3] and possesses a significantly longer half-life of about 20–30 hours (relative to IGF-1's half-life of about 12–15 hours)."
Simplified, this appears to be similar to comparing testosterone base to testosterone (insert ester). Although the actual change is different in it's process, the result is an added "time release" effect, as opposed to standard IGF-1 which is cleared within 20 or so minutes.
As far as "pharma" LR3, I've heard of it almost countless times, yet never ONCE have I actually seen it.
Interesting! I was talking to @muscle96ss and we were discussing how the true advantage of GH may be hyperplasia, rather than hypertrophy.... Thoughts?From the research it seems to suggest that IGF-1 aids in muscular hypertorphy during the post-natal period by signaling downstream of the IGF-1 receptor. In adult non-growing muscle tissue, hypertorphy is refractory to elevated IGF-1.
"In conclusion, these data show that adult non-growing skeletal muscles are refractory to hypertrophy in response to the elevated IGF-1. By contrast, growing muscles respond by activating signalling downstream from the IGF-1 receptor (demonstrated by phosphorylation of Akt, p70S6K) to increase protein accretion by the myofibres. Thus, the IGF-1-mediated hypertrophy evident in adult transgenic muscles results from enhanced increase in muscle mass mainly during the postnatal growth phase. No differences were seen between hypertrophy mediated by the Class 2 or Class 1 IGF-1 Ea isoforms, indicating that these signal sequences do not influence the hypertrophic response or normal development of muscles.
The mechanism involved in IGF-1-mediated muscle hypertrophy in vivo is very complex and requires further investigation. A precise understanding of the responsiveness of adult muscle to IGF-1 is central to the considerable interest in potential therapeutic administration of skeletal muscle specific IGF-1 to increase postnatal muscle mass and especially to reduce muscle atrophy that occurs in many clinical situations."
A growth stimulus is needed for IGF-1 to induce skeletal muscle hypertrophy in vivo | Journal of Cell Science
