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GH, IGF1 and should I combine them ? http://sciroxxonline.com/

sciroxx-lab

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I've been asked more then several times if IGF1 should be combined with GH, and why not to take it by itself or instead of GH usage ?
In a nutshell the ideal solution is using GH in combination with IGF1-lr3 and/or IGF1-DES

It's true that the IGF1 is the mediator for most of the anabolic effect of the GH, but we must consider 2 things -

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

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

Further more - many GH users are not aware to the fact that GH decreases insulin sensitivity. IGF1 increases insulin sensitivity, and negates this effect, which leads to optimal metabolic conditions. Some users use insulin in conjunction with GH but using IGF1 is much more effective in retaining optimum insulin sensitivity and much much safer

So the ideal solution is combining them both and by this keep optimal serum GH and IGF1 levels
 
I think using both together would be highly effective because of the exact reasons you stated, they essentially work together and compensate for what the other compound cant do so they work synergistically . Such as gh causing insensitivity to slin and igf increasing sensitivity they work together to cause a highly effective anabolism metabolic state. I think more people, myself included, would do both together but man tha'tll get expensive quick
 
Here is some scientific literature to support these claims -

ncbi.nlm.nih.gov/pubmed/8853443
===================================

GH may exert metabolic effects either directly or indirectly through increased production of IGF-I. GH administration increases circulating IGF-I levels via stimulation of hepatic synthesis and secretion of IGF-I; it may also enhance local IGF-I synthesis, which exerts paracrine or autocrine effects. Figure 2 summarizes the metabolic effects of GH and IGF-I. Administration of GH and IGF-I in adult humans has been demonstrated to enhance protein anabolism. Combined administration of GH and IGF-I was observed to be more anabolic than either IGF-I or GH alone. Evidence is presented that protein accretion results mainly from direct effects of GH on tissues; additional indirect effects via IGF-I production are also likely. Administration of GH has been reported to produce carbohydrate intolerance with elevated plasma insulin levels, resulting from insulin resistance. in contrast, insulin sensitivity increased during administration of IGF-I, which exerts hypoglycaemic effects even with concomitant suppression of insulin secretion. A major direct metabolic effect of GH is to increase fat mobilization and oxidation, and thereby to reduce total body fat; there is no evidence that IGF-I acts directly on adipose tissue in vivo. GH administration results in sodium retention via stimulation of Na-K-ATPase. It is suggested that part of the effects of GH on tubular function (e.g. phosphate reabsorption) are mediated via IGF-I. Energy expenditure may be increased by administration of either GH or relatively high doses of IGF-I. One of the reasons for this phenomenon is an increase in lean body mass; GH may increase energy expenditure additionally be enhancing the production of T3 and by increasing lipid oxidation
===================================
 

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