Reading along this interesting thread I've encountered the notion that IGF1 is "stronger" then GH, or may replace it.
IGF1 by itself can't and should't replace GH, the GH has more all around systemic anabolic and metabolic effect
It's true that the IGF1 is the mediator for most of the anabolic effect of the GH, but we must consider 3 things -
1. GH triggers directly local (paracrine) growth factors release in any tissue and above all in muscle tissue, this phenomena can't be triggered by circulating IGF1
2. The GH has some direct metabolic effect by itself, both in releasing glucose and fatty acid into the circulation, and by this raising metabolism and releasing available energy for anabolic demands, The GH has also a direct effect on nitrogen balance not through the IGF1 path
3. The IGF1 itself has a direct suppressing effect on the endogenous GH release - so if u inject exogenous IGF you actually and directly suppress any GH present in the circulation and misses some of the distinct effects of the GH
So the ideal solution is combining them both and by this keep optimal serum GH and IGF1 levels
Based on scientific literature the ideal solution is simply combining GH and IGF1, they have a proven synergistic effect -
-
http://www.ncbi.nlm.nih.gov/pubmed/9129466
------------conclusions -
GH and IGF-I combined further enhanced fat oxidation while reducing protein catabolism. Serum insulin concentrations were significantly increased by GH but decreased by IGF-I. GH significantly decreased serum total triiodothyronine concentrations and IGF-I significantly decreased serum corticosterone concentrations.
- Effects of insulin-like growth factor-I and growth hormone in models of parenteral nutrition. - PubMed - NCBI
-----------results and conclusions
RESULTS:
Administration of IGF-I, but not GH, attenuates dexamethasone-induced protein catabolism and increases insulin sensitivity. Simultaneous treatment with GH and IGF-I additively increases the serum concentration of IGF-I, whole-body anabolism, and lipid oxidation. GH or IGF-I when given alone produces similar increases in the serum concentration of IGF-I. However, GH selectively increases skeletal muscle mass whereas IGF-I selectively attenuates the intestinal atrophy and abnormal intestinal ion transport induced by TPN. These tissue-selective anabolic effects of GH and IGF-I are associated with differential increases in protein synthesis in skeletal muscle and jejunum, respectively.
CONCLUSIONS:
Simultaneous treatment with GH and IGF-I may offer the greatest clinical efficacy because of improved nitrogen retention in association with enhanced lipid oxidation and stimulation of protein synthesis in multiple tissue types.