zdiaa
Iron
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So far, GHK-cu has only been shown to impact IGF-1 in a couple of specific pathways which are isolated from hepatic IGF-1 secretion.
Specifically GHK-cu:
inhibits TGF-β1/Smad2/3 when it's pathologically elevated. When this is chronically overloaded, it can decrease mineralization and suppress osteoblast differentiation. Restoring to normal levels supports remodeling and osteoblast recruitment. This pathway has no impact on longitudinal growth, and by maintaining baseline levels locally, it can actually be supportive to bone remodeling in wolffs law. Additionally, by inhibiting Smad2/3 it converts downstream to Smad4, controlling RunX2 and ALPC gene transcription (upregulating drivers in osteoblast function)
downregulates TNF-α, IL-6, and NF-κB genes. These are pro inflammatory cytokines which are majorly catabolic, promoting bone wasting and suppressing IGF-1 receptor signaling. TLDR, these 3 genes are not conducive to anabolism and will only work against longitudinal growth and localized tissue healing.
GHK-cu's IGF-1 inhibition although at the gene level, is local and site specific undergoing fibrosis (lungs) and inflammation. Contrary to surface level research, it's mechanism of action in controlling IGF expression through these pathways could even be synergistic for bone development.
HGH works through the increase of hepatic IGF-1 secretion through activating the cell receptors within the liver (JAK2-STAT5 signaling cascade). This cascade of IGF-1 gene transcription through STAT5 elevates systemic IGF-1, allowing for accelerated tissue growth through increased receptor agonism. This pathway is responsible for approximately 80% of HGH's effectiveness in longitudinal growth and osteoblast differentiation
HGH also can directly drive growth by binding to growth hormone receptors in the growth plates activating IGF-1 production locally
GHK-cu is not known to impact STAT5, JAK2 or GHR nor IGF-1's cascading effects into PI3K/AKT and MAPK. If anything, GHK-cu could hypothetically enhance GH receptor sensitivity through indirectly lowering inflammation in pro-inflammatory genes.
TLDR: There is obviously no study using both GHK-cu and exogenous HGH to measure its impact on bone growth, however using evidence based reasoning GHK-cu would not impact bone growth outcomes and may even potentially enhance them. The claim that GHK-cu impacts IGF-1 in a way that would impact bone growth is not backed by current scientific literature
Specifically GHK-cu:
inhibits TGF-β1/Smad2/3 when it's pathologically elevated. When this is chronically overloaded, it can decrease mineralization and suppress osteoblast differentiation. Restoring to normal levels supports remodeling and osteoblast recruitment. This pathway has no impact on longitudinal growth, and by maintaining baseline levels locally, it can actually be supportive to bone remodeling in wolffs law. Additionally, by inhibiting Smad2/3 it converts downstream to Smad4, controlling RunX2 and ALPC gene transcription (upregulating drivers in osteoblast function)
downregulates TNF-α, IL-6, and NF-κB genes. These are pro inflammatory cytokines which are majorly catabolic, promoting bone wasting and suppressing IGF-1 receptor signaling. TLDR, these 3 genes are not conducive to anabolism and will only work against longitudinal growth and localized tissue healing.
GHK-cu's IGF-1 inhibition although at the gene level, is local and site specific undergoing fibrosis (lungs) and inflammation. Contrary to surface level research, it's mechanism of action in controlling IGF expression through these pathways could even be synergistic for bone development.
HGH works through the increase of hepatic IGF-1 secretion through activating the cell receptors within the liver (JAK2-STAT5 signaling cascade). This cascade of IGF-1 gene transcription through STAT5 elevates systemic IGF-1, allowing for accelerated tissue growth through increased receptor agonism. This pathway is responsible for approximately 80% of HGH's effectiveness in longitudinal growth and osteoblast differentiation
HGH also can directly drive growth by binding to growth hormone receptors in the growth plates activating IGF-1 production locally
GHK-cu is not known to impact STAT5, JAK2 or GHR nor IGF-1's cascading effects into PI3K/AKT and MAPK. If anything, GHK-cu could hypothetically enhance GH receptor sensitivity through indirectly lowering inflammation in pro-inflammatory genes.
TLDR: There is obviously no study using both GHK-cu and exogenous HGH to measure its impact on bone growth, however using evidence based reasoning GHK-cu would not impact bone growth outcomes and may even potentially enhance them. The claim that GHK-cu impacts IGF-1 in a way that would impact bone growth is not backed by current scientific literature
