Let me clarify. Papa's statements are not my own.
First off the argument made by many that IGF-1 LR3 is nothing more than a GDA is flawed. In order for IGF-1 LR3 to act that way it
must be binding to an IGF-1 receptor and mediating events.
Now that I think real hard on it ...a long time ago in this thread I probably DID say that IGF-1 LR3 only acted as a GDA.
I was wrong.
...and I think I have been very careful never to repeat the error, to research as much as possible and attempt to fully understand things.
IGF-1 LR3 is too small to stay in the extravascular space where it is injected and it will penetrate the vascular wall and travel systemically.
Some may bind to receptors where it is injected.
I have thought a lot about how I would try to make IGF-1 LR3 work if I used it by itself. Many have claimed that large doses gave them very noticeable local growth. But maybe one could split whatever dose is going to be used into 5 portions and pin in 5 areas in the worked muscle.
I have tried to interest a few research chem places into acquiring a small batch of IGF-1 prebound to IGFBP3 which when injected will immediately bind to ALS and end up being large enough to remain local...but in the end their suppliers couldn't come through.
But I am very open about people's experiences with IGF-1 LR3.
However when people want to combine IGF-1 LR3 with GH or GHRH+GHRPs I do have specific things to say about how they will interfere with one another.
I also fully understand and attempt to convey the importance of autocrine/paracrine IGF-1 & MGF and how testosterone & GH increase these growth factors.
Anyway I just wanted to clarify ...because Papa's statement made it sound like I was Razor Ripped (which is very, very, very anti-IGF-1 LR3) and that is simply not the case.