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Interesting. But we can use an IGF test to get an idea how we are responding to gh? If we can't use an IGF test to see if IGF is legit, I guess our only other option would be to trust the suppliers at their word or send it off to a lab to get tested?
Here I copied his post, and I’ll put it here for reference.
I guess nothing really…. As long as you utilize a trusted sponsor I’d think they’d provide you with the appropriate product.
The only way to know would be to send it to get lab tested since apparently a blood test will show nothing. One reason I'm not into when we have access to gh and we can better verify it's real
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LR3 IGF-I vs. rhIGF-I similarities and differences are not the easiest to understand or communicate. But basically the two are equipotent in human skeletal muscle, but LR3 is the more potent anabolic agent used systemically (causing greater total-body growth). LR3 of all these growth factors has the greatest propensity to increase viscera (gut, organ) growth. LR3 is characterised by lacking any affinity for IGFBPs, that variously reduce and/or increase activity in different tissues. Since LR3 administration is unlikely to be detected as IGF-I due to the assays used to detect IGF-I in serum (and because its duration of activity is reduced by not binding to IGFBPs), it almost certainly will not be detected by serum IGF-I bloodwork as an increase to IGF-I; but might actually be detected as a reduction. Janoshik does indeed offer a test for LR3 IGF-I. The two have considerable differences in how they are to be stored and handled, and are both quite unstable.I think Janoshik or can test if it is real IGF-1 LR3/DES, imho that is the only way to know if it is the real deal. From my very limited understanding of the LR3 Version, I have heard some guys say that it just doesn't work in humans, it just gets into the bloodstream, flows around some time, until it eventually gets removed. The LR3 Modification seems to change the peptide too much, so that it doesn't dock to the igf receptors (I'm probably butchering the explanation, but it sounds plausible to me).
In the end, I don't think it is just that good of a compound, so few big Pro BBs are using it, they stick to aas+insulin+hgh; it just doesn't seem to work the way we thought it would.
Maybe @Type-IIx can chime in, and either rip me apart for being retarded or give some more context
Also, it is true that insulin is the more anabolic compound in muscle versus IGF-I and its analogues; it's available, cheap, and is therefore often just used rather than LR3/rh-IGF-I. The particular use case for LR3/rh-IGF-I is to stimulate muscle cell proliferation & differentiation without the myriad GH or insulin effects that those agents bring to the table. That can be advantageous or disadvantageous in different contexts.
It does not, that is indeed one of the advantages vs. slin.
Would def be curious if you have any opinion on combining LR3 with PEG-MGF, particularly wrt to all the different protocols bandied about.
I don't like PEGylated MGF or exogenous MGF (IGF-IEc in humans, -IEb in rodents). I believe that its exogenous administration will likely lay down noncontractile/collagen tissues rather than skeletal muscle. While autocrine MGF is a factor in the process of satellite cell activation (its mRNA expression being increased then as one mechanism of hypertrophy or muscle remodeling), it's part of a complex interplay of different factors in this. It is also a key factor in myogenesis (muscle repair, not hypertrophy). You see it overexpressed in aged muscle put on very high resistance training volumes in prior sedentary elderly subjects, aching to injury. To me this reflects its primary action as a myogenic factor (we don't try to destroy muscle and rebuild it by repair pathways, we try to stimulate hypertrophy; though some fuck this up massively with excessive training volumes). As anabolic as intracrine/paracrine MGF seems to be (especially as seen with IGF-IEb expression in rats), I'd advise rhGH and/or rhGH + LR3- or rh- IGF-I (combined), as IGF-I sequentially stimulates both myoblast proliferation & myogenic differentation by activating the ERK & PI3K/Akt pathways, respectively.
And if you are wondering the difference between the procollagenous activities of GH/IGF-I & MGF, it is that the former deposit collagen into the extracellular matrix (strengthening the muscle-bone attachment) & connective tissues, bone, tendon, ligament. Whereas the latter (exogenous MGF), like severe muscle damage, likely deposits collagen into the muscle fibers (i.e., necrosis).
Much appreciated, as always.
The hypoglycemic risk with LR3 IGF-I is very high, on par with slin. I wouldn't attempt it on a low carbohydrate diet. I think the benefits are worth the cost for a very advanced guy that is truly limited by the pool of available myofibers. If he has truly recruited and hypertrophied all of his muscle pool maximally, then its use makes sense to me. I think for most, the effects on gut/visceral growth, impracticalities with storage, handling, & shipping, et cetera make it a bit too exotic.
