Site Enhancement Theory using DES (1-3) IGF-1

I think a lot is being overlooked in the realm of igf-1 drugs and how to use them for hyperplasia (the growing of new muscle tissue). Why in the world would someone take peg-mgf and igf1-lr3 together to induce hyperplasia or for site-enhancement (injecting into a particular muscle to specifically make it grow lartger)? I say this because they are both long acting- mgf initiates the hyperplasia process (activation of satellite cells/proliferation) but inhibits the final phase (differentiation). Igf-1 causes differentiation, but inhibits proliferation. Take a long acting version of each and what the hell have you got? A cluster f#*^ where nothing productive is happening except a lot of insulin-like effects.

Plus, mgf is only produced, naturally, within the muscle cells themselves, never found systemically. So, when we inject it, we're basically "hoping" some of it will get into the intended muscle cells and still work as intended. Outside of the actual cells themselves it just acts like, and is recognized as igf-1! So, again, no matter how we approach injecting mgf, the results are iffy at best because even if some gets into the cells and starts the proliferation process on satellite cells, whatever is left over on the outside of the cells (on the igf-1 receptors) will be causing differentiation and inhibiting proliferation- all at the same time!!

Do these two processes (proliferation and differentiation) interfere with eachother? Of course they do. How else would they work in tandem in a natural environment. So, what do we do then? How do we get proliferation without accidentally causing differentiation by mistake?

Skip to the end in bold for the short answer to this.

I've mentioned this before. But, the more I think about it and it sinks in, the more I believe it makes sense. It's clear that mgf is most effective when produced within the muscle cells themselves. Mgf is produced during a workout- especially on the eccentric (lowering) portion of an exercise movement. This resulting production of mgf is one of the ways we grow and recover from hard training. It's basically a response to micro-trauma within the muscle.

There is only "so much" we can do to induce proliferation (activation of satellite cells) via injection with mgf or peg-mgf. And, having a longer-acting mgf like peg-mgf will not necessarilly lead to greater results when it comes to hypertrophy. All the successful studies on mgf were done with viral techniques where the muscles were programmed (by introduction of a virus) to produce mgf. This is where we see the 20% muscle weight gains etc. not by injection. Unfortunately, we gym rats don't have access (that I know of) to that kind of technology!

But, there are alternatives. Years back Pat Arnold talked about an alternative site-enhancement technique using a solution containing lambda carrageenan- a seaweed extract usually injected into meat products to provide a thicker, heavier product. Basically scientists injected a solution of various % of lambda carrageenan in a controlled way to produce specific muscle damage in leg muscles and tendons in mice. At some percentages the muscle damage was too great, at others it didn't produce a noticeable effect. But, at certain percentages the right amount of muscle damage was caused triggering a steady release of mgf in an effort to repair the damage. (You'll have to forgive me, but I can't seem to find the original study for the life of me! Hunt around on Google if you want. There are similar studies out there. The original was done in Japan and written in Japanese...)

I was able to get ahold of some lambda carrageenan powder and I did my own little experiment. To be honest, so many injections were needed and such a high volume of product that I got tired (not to mention sore!) of messing with it before I saw any real measurable results. But, years later when I gave syntherol (and oil based injectable site-enhancement product) a try, the constant dull-ache from the injections reminded my of my brief experiment with lambda carrageenan. See, there's nothing inherent in carrageenan itself that causes mgf expression. It's just an irritant- but, a controllable one. You can obviously get the same kind of inflamation from a shot of test prop or some other injectable like syntherol (or for that matter a well-made home brew, but that's another topic).

What stands out to me about the scientific study on mice is that even the lower doses of the carrageenan solution had some effect and elicited some mgf expression, but it wasn't enough to have substantial results. That tells me that mgf expression is somewhat determined by the amount of irritation caused. As long as there isn't too much to "come back from" where the muscle is seriously compromised, there should be enough mgf expression to both repair the damage and over-compensate by creating new tissue. It's my theory that this is a part of what makes syntherol site-enhancement techniques effective. The other parts are increased blood flow/nutrient uptake and stretching of the muscle fascia.

With everyone looking for the longest acting igf-1 drug available it appears the thinking is "whatever lasts the longest is most effective!" But, that's not true in this case. While drugs like peg-mgf and igf1-lr3 will give you the best insulin like effects (when compared to their shorter-acting counterparts) we don't necessarily want to affect our system for long periods of time with igf-1! For one thing it's dangerous. Many of the receptors are in the intestines and vital organs. If there is a cancer or growth present, igf-1 may/will cause that to grow at an increased rate. Plus, as it concerns site-enhancement/hyperplasia, igf-1's job is to cause "differentiation"- the part of the process that tells newly activated satellite cells to become muscle! If an igf-1 is constantly present in the system, then the actual activation of those satellite cells is inhibited!

What we want is to do is: 1) Induce proliferation (activation) of satellite cells and keep that going as long and as often as possible. 2) Induce differentiation to help form new muscle tissue briefly but often.

My basic theory is to add a schedule of using DES (1-3) igf-1 to a "normal" syntherol protocol. Using the syntherol, in conjunction with hard training and a good anabolic environment, will (in theory) cause mgf to be produced within the temporarily damaged muscle. 1/2 hr to 1 hr after said muscle is trained, a dose of DES (1-3) Igf-1 is injected into the specific muscle to induce differentiation. With the DES being out of your system within a half hour or so, this should allow the muscle to go back to producing more mgf and inducing more proliferation/activation of more satellite cells- do to continued irritation from injections of syntherol and subsequent training.

So, let's say you are injecting your bis and tris with syntherol. They are sore and swollen, but you are still doing your regular training. You can hit each on arm day, bis on back day, and tris on chest/shoulder day etc. with DES (1-3) IGF-1. However you work it, I think the theory makes some sense. Let me know what you think.