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They are often discussed together because both are associated with recovery and tissue-support pathways
The vitamin is then transferred to TC2, which serves as the circulating plasma transporter, hereditary defects in the production of TC2 and its receptor may produce functional deficiencies in B 12 and infantile megaloblastic anemia, and abnormal B 12 related biochemistry, even in some cases with normal blood B 12 levels
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GHK-Cu blocks ferritin channels and the release of tissue-damaging free (oxidative) iron after injury, thus blocking iron-catalyzed lipid peroxidation that often occurs after injury and interleukin-1 damage to pancreatic islet cells
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