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[DOI] [PubMed] [Google Scholar] 169.Sikiri P., Petek M., Rucman R., Seiwerth S., Grabarevi Z., Rotkvi I., Turkovi B., Jagi V., Mildner B., Duvnjak M., et al

GHK-Cu can directly scavenge harmful reactive oxygen species (ROS), thereby mitigating oxidative stress

BPC-157 demonstrates unique multi-system modulation across dopaminergic, serotonergic, glutamatergic, GABAergic, and nitric oxide systems simultaneously

Poor health outcomes in infants with vitamin B 12 deficiency include anemia, abnormal skin and hair development, convulsions, weak muscle tone, failure to thrive, mental developmental delay, and potentially abnormal movements.[4-8] Well-recognized at risk groups are exclusively breastfed infants of mothers with B 12 deficiency due to minimal or no dietary intake of animal products[9-21] or pernicious anemia caused by a maternal malabsorption of B 12 .[18,22] Infant vitamin B 12 status can be improved through maternal B 12 supplementation during pregnancy and lactation.[23-26] Deficient mothers who miss the opportunity to supplement during pregnancy should still be encouraged to supplement during early lactation since infant vitamin B 12 status correlates with milk vitamin B 12 levels in breastfed infants up to 6 months of age.[27-30] Although there are cases reported of exclusively breastfed infants with vitamin B 12 deficiency having biochemical and clinical improvement through adequate maternal supplementation alone,[9] direct supplementation of the infant is recommended when such treatments are available.[31-33] Drug Levels Methylcobalamin is the major form of vitamin B 12 in milk