IGF-1 LR3 was originally designed to test the effects of IGF-1 in cell cultures more accurately because IGF-1 was binding to locally secreted IGFBP’s.
These binding proteins are crucial for
- Transporting IGF-1 into the growth plate
- Transporting IGF-1 to muscle and bone
- Preserving IGF-1 half life
- locating the ternary IGF-1/IGFBP/ALS complex at the cell surface
Half life lies
The modifications of IGF-1 LR3 are not like a steroid esther and don't give it a long half life, it actually does the EXACT opposite.
By decreasing the binding affinity to these IGFBP’s the half life is only minutes long. The 20-30 hours is a LIE.
The only study that was done on "half-life" was in rats and noted that IGF-1 LR3 was undetectable after 4 hours (1). Which makes the half life anywhere from 20-30 minutes long.
Funnily enough, the IGF-1 variant IGF-1 DES which is supposed to have a short half life was still detectable. Which confirms the short half life of IGF-1 LR3.
Natural GH & IGF-1
Since IGF-1 LR3 is still able to bind to atleast some receptors, this means that it can also have negative feedback on natural GH levels. Since IGF-1 has a negative feedback loop on GH. Meaning that IGF-1 actually lowers the production of GH.
It does this by activating somatostatin neurons and deactivating GHRH neurons. Sadly, IGF-1 LR3 acts on these neurons, having the same effect as native IGF-1 which results in lower:
- Growth hormone
- natural IGF-1
- IGFBP's
Which was the result of a study (2) in pigs where IGF-1 LR3 lowered these levels.
This could also mean a reduction in height, since IGF-1 LR3 is crucial for getting IGF-1 to the growth plate.
Muscle building
LR3 is also useless for muscle building or bone. (3)
Since it doesnt have the ternary IGF-1/IGFBP/ALS complex which is like earlier mentioned crucial for carrying IGF-1 to muscle and bone.
The ternary complex is crucial for locating IGF-1 at the cell surface so that proteases like PAPP A2 can remove IGF-1 from the ternary complex and guide it toward the receptor.
Organ growth
Another study in fetal sheep showed that IGF-1 LR3 increased the size of their organs without increasing the size of muscle or bone. (3)
Which could mean IGF-1 LR3's chemical structure increases binding affinity to receptors in organ tissue rather than muscle and bone. Making it completely useless for hypertrophy in that regard.
What does it do?
The only true effect IGF-1 has is glucose modulation.
This is because IGF-1 LR3 provides a quick spike in available ligand which locates GLUT4 to the cell membrane via the mTOR/PI3K/AKT pathway and increases cellular glucose uptake in minutes.
Which is why the ONLY moment IGF-1 LR3 could be of any benefit is during your post workout meal.
All this while accelerating cancer growth. (4)
End
Now these studies are in animals and in-vitro, which means they rank pretty low on the scientific pyramid of evidence, but this is because there are simply NO human studies in IGF-1 LR3. So the studies I cited are the most important finding in my opinion.
And these studies alone, even though they are in animals and in-vitro, makes the risk-reward with the lack of human research a pretty easy decision to make.
That being said have a great day.
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