Enter PEG-Ec. Often mistakenly referred to as PEG-MGF the long lasting version of MGF has been produced by conjugation with Polyethylene Glycol. This safe and effective treatment protects the molecule and extends the life of the MGF to four hours. It is very selective to the IGF-1 receptors and has none of the disadvantages of IGF-1 LR3 which tends to migrate in a systemic fashion.
IGF-1 LR3 has the disadvantage of having a lower affinity for the IGF-1 receptor. The supposed advantage of IGF-1 LR3 is that it stays around for an extended period of up to ten hours. However that is in all likelyhood a disadvantage because regular use will trigger growth hormone-inhibiting hormone (GHIH) which causes negative feedback, and inhibits GH release. In addition it is understood that systemic IGF-1 LR3 may cause unwanted intestinal growth due to the large number of receptors located on the intestines.
IGF-1 naturally binds to IGF-1 receptors on the somatotrophs. Somatotrophs, are cells in the anterior pituitary, which secrete hormones when instructed. In this case GH. This eventually brings about an inhibition of GH release for a few hours through the release of the anti - GH hormone somotostain. It is a natural cycle with the creation of IGF-1 causing a subsequent release of somotostain, causing a falll of GH levels every few hours. As the effect wears off, more GH is released and the cycle starts again.
PEG-Ec when administered by intra-muscular injection is thought to act as IGF-1 but is not recognised as such by the body. If it inhibits GH at all, likely does so in for very limited time whereas synthetic IGF-1 LR3 (because it is around for up to ten hours) may produce prolonged inhibition of natural GH release.
What about IGF-1 receptor downregulation? This is not a concern with PEG-Ec.
What is "IGF-1 receptor downregulation"? Receptors don't live for long periods of time. They are constantly made, translocated to cell surfaces and then part breaks off and becomes a binding protein circulating in plasma and part gets internalized into the cell.
The important point is what happens when an IGF-1 ligand binds to an IGF-1 receptor. Chronic exposure could mean those intracellular events desensitize. This doesn't happen with natural IGF-1 or PEG-Ec (because it’s half life is not much greater than natural IGF-1).
In addition to PEG-Ec research has shown the the addtion of growth release peptides GRF(modified1-29) plus GHRP-6 (or GHRP-2) up to 3 times per day at a dose of 150mcg each time will increase GH levels, circulating IGF-1 levels and lean tissue development. The combination causes a systemic rise in growth hormone levels which aids in the development of muscle mass and has been shown to reduce body fat levels over time.
The half-life of PEG-Ec is around 3 to 4 hours. Dosage of PEG-Ec should be administered either half an hour before the work out into the muscles being targeted or as an alternative, just before bed into the muscles that were worked during exercise. Use a dose of 150mcg up to 200mcg into each muscle (split bi-laterally) being the muscles being targeted for research. ( eg both biceps)
If administering peptides in addition to PEG-Ec, the other peptides should be administed (GRF and GHRP-6 or 2) immediately prior sleep to produce a natural GH spike. This would appear to act synergistically with the use of PEG-Ec as it helps produce high levels of growth hormone and IGF-1 during periods of sleep.
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