AOD is the lipolytic fragment of GH
So doing both you gets extra lipolysis and still the other benefits of GH
I only found this as a potential explanation why i reacted so anabolic on GHRP-2+CJC and did not (like a lot of peopel) on 4IU rHGH.
Its a different topic but i why not throw it in, maybe you find it interesting:
"I’ve mentioned this quite a few times already but, in an attempt to further drive this point home,
autocrine levels of IGF-1 appear to be far more important than endocrine levels of IGF-1 as it relates to muscle mass regulation. Further to this point, overexpression of autocrine IGF-1 within muscle causes fiber hypertrophy [374]. Overexpression of autocrine IGF-1 has also shown anti-catabolic effects, with animal models tending to demonstrate an overall resistance to the muscle atrophy normally observed with aging [375]. Localized IGF-1 also provides age-independent regenerative capacity in skeletal muscle cells [376].
There is also some compelling evidence that suggests endocrine IGF-1 acts directly as a negative feedback regulator on autocrine IGF-1 production. This negative feedback mechanism is PI3K/Akt pathway dependent [377-378]. In addition, elevated endocrine IGF-1 levels may also act indirectly to stifle autocrine IGF-1 production.
So, in other words, not only does endocrine IGF-1 have minor direct impacts on skeletal muscle mass regulation itself, but it also possibly suppresses the autocrine IGF-1 that has major impacts on hypertrophy.
Elevated levels of circulating IGF-1, and specifically elevated free IGF-1, act in a negative regulatory manner on GH ultimately resulting in a suppressed rate of downstream autocrine IGF-1 production [379]. It is not entirely clear, however, if IGF-1 negative regulation changes the half-life of IGF-1 mRNA or directly affects IGF-1 gene expression. Further to this, it has also been demonstrated that autocrine IGF-1 expression is downregulated in muscle cells following IGF-1 treatment [366]. Hepatic expression of IGF-1 mRNA has also been shown to be downregulated by acute IGF-1 exposure [127]. So ensuring we keep endocrine levels as suppressed as possible for a respective rHGH dose, while simultaneously elevating autocrine levels, is going to be a priority for the stack design.
GH is pulsatile by nature in all species. So it would stand to reason that many of the body’s built in processes are going to thereby be designed in a manner which will be optimized to exposure to GH in a similar manner. In accordance with this statement it has been shown that
only pulsatile GH administration, and not continuous infusion, has the ability to maximally stimulate IGF-1 mRNA expression in skeletal muscle [366,380-381]. Pulsatile delivery has also been shown to lead to increased overall postnatal growth potential, as compared to continuous delivery [89,382].
Pulsatile administration may also lead to comparable, or even decreased, serum endocrine IGF-1 levels [383] which is advantageous due to the potential negative regulatory capabilities it possesses on autocrine IGF-1 expression which were discussed earlier. Evidence also suggests that the peak itself, and not necessarily the number of peaks, may be of utmost importance to target tissues [384]. For maximal growth and hypertrophy potential the evidence tends to suggest that getting GH elevated, and then back to baseline multiple times per day, may be preferable as compared to keeping them elevated for longer periods of time.”
Full source:
The Most Effective Growth Hormone Protocol for Hypertrophy «
=> So maybe GHRP-2+ CJC simply raises autocrine IGF-1 levels through thats pulsative manner while rHGH primarly raises endocrine IGF-1 levels and therefore surpressing autocrine igf-1 levels, which probably "can ne overcome" with very high HGH dosages as used by probodybuilders.
This woukd also explain why many Probodybuilders swear on high HGH dosages even though HGH only raise IGF-1 to a certain level. HOWEVER in bloodwork the endocrine IGF-1 levels are messured and while more HGH may not lead to an increase in this level it probably increases the autocrine IGF-1 levels