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B12 deficiency is a known concern with long-term GLP-1 therapy, particularly because many researchers are simultaneously reducing their caloric intake

Research in rodent SCI models (clip compression, transection, contusion) demonstrates: Improved functional research applications (Basso-Beattie-Bresnahan locomotor rating scale scores) in BPC-157-treated animals compared to vehicle controls Reduced lesion volume at chronic timepoints, suggesting neuroprotection of spared tissue in the penumbra zone Enhanced axonal regrowth markers (GAP-43, growth-associated protein-43) in the injury zone Reduced glial scar (GFAP-positive astrocytic reactivity) at the lesion boundary a significant finding given that glial scar formation is the primary physical barrier to axonal regeneration The angiogenic mechanism of BPC-157 (VEGF stimulation, endothelial tube formation) is particularly relevant to SCI research: the spinal cord is highly vascular, and ischaemic secondary injury following disruption of spinal vasculature drives extensive secondary neurodegeneration

It was even assessed biomechanically

The cost of vitamin B12 injections varies depending on location, provider, and the treatment plan