ghk cu receptor binding mechanism GHK-Cu Peptide PEPTIDES! ARE… Not as

PEPTIDES! ARE… Not as controversial as political party affiliation but not far off in the health and traditional medical space given the enormous explosion of GLPS which yes have randomized control trials

10.1016/j.maturitas.2013.01.019 Maturitas 244 RenekerJ

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Here’s how they work together: Folate’s role: Dietary folate converts to 5-MTHF (active folate) via the MTHFR enzyme 5-MTHF donates a methyl group to homocysteine This requires B12 as a cofactor for the enzyme methionine synthase The result: homocysteine converts to methionine B12’s role: B12 (as methylcobalamin) acts as a cofactor for methionine synthase It helps transfer the methyl group from 5-MTHF to homocysteine Without adequate B12, folate gets “trapped” and can’t donate its methyl group This is called the “methyl trap” What happens when one is deficient: Low B12 with adequate folate: Folate can’t function properly (methyl trap) Homocysteine rises despite good folate levels Methylation slows down Can mask B12 deficiency symptoms initially Low folate with adequate B12: Not enough methyl groups available for donation Homocysteine rises Methylation impaired DNA synthesis affected Both low: Severe methylation impairment Very high homocysteine Anemia (megaloblastic) Neurological damage risk Why MTHFR mutations affect this partnership: With MTHFR mutations: Your body can’t efficiently convert folate to 5-MTHF This creates a bottleneck in the methylation cycle Even with adequate B12, you don’t have enough active folate to work with it Result: elevated homocysteine, poor methylation The solution: Bypass the MTHFR bottleneck by taking pre-methylated folate (5-MTHF) that doesn’t require conversion