This is a highly valuable info, first time that I see in a scientific literature that the DES has 10 times higher affinity then the endogenous IGF1.
IGF1 has some very unique anti catabolic traits, that for instance GH by itself doesn't have, so the potential of the DEs-IGF1 is very dramatic for such purposes
Here are some examples for this -
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.
http://www.ncbi.nlm.nih.gov/pubmed/10571453
-----------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.