GHK is a tripeptide with the amino acid sequence glycyl-histidyl-lysine. It naturally occurs in human plasma, saliva, and urine. In plasma the level of GHK is about 200 ng/mL at age 20, but declines to 80 ng/mL by age 60. This decline in the GHK-level coincides with the noticeable decrease in regenerative capacity of an organism. Scientific research has revealed that GHK can assist in wound healing, infection control, hair growth, cancer, cognitive health, and facial cosmetic use.
GHK with and without copper affects a large number of genes related to an organism’s response to stress and injury (tissue remodeling, anti-oxidant, anti-inflammatory, anti-pain, anti-anxiety, blood vessel growth, nerve outgrowth, anti-cancer action). GHK sequence is included in the collagen molecule, and SPARC protein and GHK is naturally released after an injury due to protein breakdown.
Copper is a transitional metal that is vital for all eukaryotic organisms from microbes to humans. Since it can be converted from oxidized Cu(II) to reduced Cu(I) form, it functions as an essential cofactor in a multitude of biochemical reactions involving electron transfer. A dozen enzymes use changes in copper oxidation states to catalyze important biochemical reactions, including cellular respiration, antioxidant defense, detoxification, blood clotting, and the connective tissue formation. Copper is required for iron metabolism, oxygenation, neurotransmission, embryonic development and many other essential biological processes.
DNA damage is promptly repaired in young and healthy cells, however, as we age, DNA damage starts accumulating. Resetting activity of DNA repair genes can diminish deleterious effects of aging. GHK was primarily stimulatory for DNA repair genes (47 UP, 5 DOWN).
GHK Acts as an Antioxidant
Free radicals and toxic end products of lipid peroxidation are linked to atherosclerosis, cancer, cataracts, diabetes, nephropathy, Alzheimer’s disease and other severe pathological conditions of aging. GHK stimulates 14 antioxidant genes and suppresses two pro-oxidant genes.
The insulin family has been proposed as a negative controller of longevity; higher levels of insulin and insulin-like proteins reduce lifespan. GHK stimulates 3 genes in this system and suppresses 6 genes.
The insulin/IGF-1- like receptor pathway is a contributor to the biological aging process in many organisms. The gene expression data suggests that GHK suppresses this system as 6 of 9 of the affected insulin/IGF-1 genes are suppressed. Insulin/IGF-1-like signaling is conserved from worms to humans. In vitro experiments show that mutations that reduce insulin/IGF-1 signaling have been shown to decelerate the degenerative aging process and extend lifespan in many organisms, including mice and possibly humans. Reduced IGF-1 signaling is also thought to contribute to the “antiaging” effects of calorie restriction.
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