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Low levels trigger a cascade that ultimately leads to cell injury and death, which accelerates aging
Most protocols plan for 4-8 weeks total rather than stopping immediately upon closure
The copper center's accessibility to redox cycling enables GHK-Cu to modulate oxidative stress responses in tissues experiencing inflammation or ischemic conditions
High blood sugar and obesity contribute to inflammation in fat tissue
The dependence of tyrosine hydroxylase on BH 4 necessitates the coupling to the action of dihydropteridine reductase (encoded by the QDPR gene: quinoid dihydropteridine reductase) as is the situation for tryptophan hydroxylase (see below) and phenylalanine hydroxylase
100,101 This is coupled with the upregulation of the cell cycle regulators P16, P21, and P53, leading to cell cycle arrest and diminished proliferative capacity
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