I only have a problem with your statments ...
"There are primarily two theories as to how GH exerts its growth promoting effects. The first theory is called the Dual Effector theory (Green, 1985). The second theory is called the Somatomedin ("mediator of growth") Hypothesis (Daughaday, 1972). Both theories are fairly strait forward. Let's start with the Dual Effector theory.
The Dual Effector theory states that GH itself has anabolic effects directly on body tissues. This theory has been supported by studies looking at the effects of injecting GH directly into growth plates. Genetically altered strains of mice have also help to support this theory. When comparing mice that genetically over express GH and mice that over express insulin-like growth factor-1 (IGF-1), GH mice are larger. Those who support the dual effector theory site this evidence. Interestingly, when IGF-1 antiserum (it destroys IGF-1) is administered concomitantly with GH, all of the anabolic effects of GH are abolished. Clearly IGF-1 has got to be involved somewhere between the pituitary and the target tissue (i.e. muscle). The Somatomedin hypothesis clears things up somewhat.
The Somatomedin hypothesis states that GH exerts its growth promoting effects through IGF-1. More specifically, GH is first released from the pituitary and then travels to the liver and other peripheral tissues where it causes the synthesis and release of IGFs. IGFs work as endocrine growth factors, meaning that they travel in the blood to the target tissues after being released from cells that produced it, specifically the liver in this case. Many studies have been performed showing that animals that are GH deficient, systemic IGF-1 infusions lead to normal growth. Admittedly, the effects are similar to those observed after GH administration. In fact, additional studies have shown IGF-1 to be greatly inferior as an endocrine growth factor requiring almost 50 times the amount to exert that same effects of GH (Skottner, 1987). Recently rhIGF-1 has become widely more available and is currently approved form the treatment of HIV associated wasting. This increased availability allowed testing of this hypothesis in humans. Studies in human subjects with GH insensitivity (Laron syndrome) have consistently validated the somatomedin hypothesis (Rank, 1995; Savage, 1993). These results indicate that although IGF-1 might be the mediator of GH effects, it's not as simple as just getting the liver to release IGF-1.
So the main difference between these two theories is that the Dual effector theory states that GH doesn?t necessarily need IGF-1 to work, the Somatomedin hypothesis insists it does. In reality both theories are correct. It?s just that the Somatomedin hypothesis focuses on "circulating" IGF-1, the Dual Effector theory recognizes that although IGF-1 is still the active hormone, it doesn't have to come from the blood (liver), it can be produced on location by the very cells that use it.
In summary, by combining the Dual Effector theory and the Somatomedin hypothesis there are three main mechanisms by which GH makes things grow (Spagnoli,1996). First, the effects of GH on bone formation and organ growth are mediated by the endocrine action of IGF-1. As stated in the Somatomedin hypothesis, GH, released from the pituitary, causes increased production and release of IGF-1 into the general circulation. IGF-1 then travels to target tissues such as bones, organs, and muscle to cause anabolic effects.
Second, GH regulates the activity of IGF-1 by increasing the production of binding proteins (specifically IGFBP-3 and another important protein called the acid-labile subunit) that increase the half-life of IGF-1 from minutes to hours. Circulating proteases then act to break up the binding protein/hormone complex thereby releasing the IGF-1 in a controlled fashion over time. GH may even cause target tissues to produce IGFBP-3 increasing its effectiveness locally.
Third, GH may influence the activity of IGF-1 on an autocrine/paracrine level. Autocrine means that a hormone has an effect on the cell that produced it, paracrine means to have an effect on the "cell(s)" next to it as well. This is a completely localized effect, not dependent on the blood stream to carry things where you want them. Muscle growth from weight training is the result of IGF-1 being produced by the muscle cells themselves, not the liver. In fact, IGF-1 form the liver is genetically different from IGF-1 produced in your muscles. This information should explain why using IGF-1 systemically (from the blood stream) has been a hit and miss proposition." as so well stated by Bryan Haycock.
"Before I go on to my personal preferences on how to use IGF-1 and MGF, I think I should clearly state that I feel that the combination of those two (or even either one alone) is far superior to the use of hGH, for most purposes. In fact, lately I’ve been getting quite a bit of heat over my recommendations to use a combination of Lr3IGF-1 and MGF in lieu of hGH, and I think that at this point, it’s not too difficult to understand why I consider IGF-1 and MFG to be a very potent combination for muscular growth- far superior to hGH. IGF-1’s superiority to hGh is intuitive at some level, but has also been clearly elucidated clinically as well. In the following graphs taken from a rodent study comparing IGF-1 and hGH, a low dose as well as a high dose of IGF-1 was shown to be more anabolic than hGH. In comparison to hGH, IGF-1 produced an overall greater total protein content within the injected muscle as well as a greater final weight of the that muscle (called the "Tibialis Anterior" or TA) (9):
MESO-Rx (http://www.mesomorphosis.com)
So, in comparison (in this study), it seems to be the case that IGF-1 would be superior to hGH as an anabolic agent. In some clinical studies, that is not always the case, but in bodybuilders and athletes I’ve spoken to, greater results are often seen with IGF-1 over hGH - and it should be noted that they are often seen more quickly as well. And while an intact insulin and IGF-1 Receptor signaling system is necessary for hGH to produce an anabolic effect (10), an hGH receptor deficiency is not sufficient to stop IGF-1 from being anabolic. (11) This is another reason to believe that when you are using hGH, you’re really just hoping that it produces IGF-1, for an anabolic effect." by Anthony Roberts
If igf-1 is worthless ... there is just no way anyone can claim hgh is just so great. IMO, it is very hard to compare a 4 week cycle on an ED injection protocol or an EOD protocol for a few weeks longer depending on how much is injected (down regulation) to a months long hgh cycle, and anyone expecting major gains from igf-1 is fooling himself, that I can agree with ... results from igf-1 generally are something like 5-10 lbs of LBM/cycle, not impressive, but still valuable, for some only maybe 2 pounds, with increased vascularity, density, and fatloss.
Fair enough Mechano growth factor may have to be entered in the equation, but throwing igf-1 out the window ... is, IMO, a little extreme.