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So would u want to start hgh in advance of igf-1 ?
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Not necessarily, but it's alsop an option, there are 2 basic notions -
1. GH and IGF1 has a synergistic effect and should be combined - 1+1=3 in this case ...
2. IGF1 has a great impact on the body, so like steroids, and unlike GH should be cycled
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Being igf & AAS both have a hard impact on the body I guess u shouldn't be cycling both at the same time?
I had no idea igflr3 was that hard on body.
Last edited by chadmack282; 05-22-2019 at 07:52 PM.
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1. IGF1 should be combined with steroids of course ! this is the most synergistic combo along with GH, and let me give here an example - a boy of 12 years old and a 16 years old adolescent have the same GHserum levels, it's the spike in testosterone which turns a boy into a man, so again we see a classic synergistic effect, here between the primal steroid testosterone and the GH/IGF
2. I explained that IGF1 has a great impact ion the body, I've never said it's harsh on the body, from many aspects it's actually healthy - it raises insulin sensitivity, and has a rejuvenate effect on almost any tissue. Hoevever for optimal effect it should be cycled
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Here is some scientific literature which reviews the synergistic effect between GH and IGF -
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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