kelvin_chia
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A couple of questions with elusive answers despite ploughing through pages after pages of post on IGF-1
1. How "fragile" is R3IGF-1? Not referring to the solvent here it is quite stable in BA (as pointed out by einstein1905). I am referring to the transportation process. As Author L. Rea puts it in his CME, "a loud noise, shaking a vial, and sudden heat changes can render it (IGF-1, he did not make specific reference to Long R3IGF-1) nothing more than a bunch of expensive amino acids". While I'm quite sure extreme heat will damage it, I'm not that sure if it can be damaged by just a loud noise. What's your opinion? Is this concern overblown? Or does it just affect IGF-1 and not R3IGF-1? Or is it just a bunch of BS?
2. Most vets advocated administering R3IGF-1 intramuscularly. I distinctively remember (from einstein1905's post again) that plasma levels were relatively unchanged after IM injection of IGF-1. If that was true, then would it be right to infer that systemic effects (distended gut, athritic symptoms etc) would not be experienced? Or is there some other mechanism beyond what can be monitored by plasma changes that would explain these systemic effects? For the record, I have never read any first hand posts on the occurence of systemic effects by IM users, but these effects have been theorized by many.
Any inputs is greatly appreciated. Thanks to all for your time and attention.
1. How "fragile" is R3IGF-1? Not referring to the solvent here it is quite stable in BA (as pointed out by einstein1905). I am referring to the transportation process. As Author L. Rea puts it in his CME, "a loud noise, shaking a vial, and sudden heat changes can render it (IGF-1, he did not make specific reference to Long R3IGF-1) nothing more than a bunch of expensive amino acids". While I'm quite sure extreme heat will damage it, I'm not that sure if it can be damaged by just a loud noise. What's your opinion? Is this concern overblown? Or does it just affect IGF-1 and not R3IGF-1? Or is it just a bunch of BS?
2. Most vets advocated administering R3IGF-1 intramuscularly. I distinctively remember (from einstein1905's post again) that plasma levels were relatively unchanged after IM injection of IGF-1. If that was true, then would it be right to infer that systemic effects (distended gut, athritic symptoms etc) would not be experienced? Or is there some other mechanism beyond what can be monitored by plasma changes that would explain these systemic effects? For the record, I have never read any first hand posts on the occurence of systemic effects by IM users, but these effects have been theorized by many.
Any inputs is greatly appreciated. Thanks to all for your time and attention.