First, A Quick Refresher on BPC-157 Before we dive into injection sites, it's crucial to understand why BPC-157 is even in this conversation
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It highlights thiamines (B1) role in catalyzing enzymes such as Pyruvate Dehydrogenase and -Ketoglutarate Dehydrogenase, (e) riboflavins (B2) contribution to fumarate production, and niacins (B3) importance in the synthesis of -Ketoglutarate and succinate ( (d) Electron Transport Chain, emphasizing niacins (B3) role in redox reactions and riboflavins (B2) function as an electron-shuttling cofactor ( The pentose phosphate pathway, through the action of transketolase (TK), converts ribose-5-phosphate to glyceraldehyde-3-phosphate ( Given its numerous functions, low levels of thiamine can lead to reduced energy production due to impaired mitochondrial function, which damages neurons, and cells that have high energy demands, making them particularly vulnerable to potential damage or cell death ( In the CNS, thiamine deficiency can lead to Wernickes encephalopathy, characterized by nystagmus, ophthalmoplegia, mental status changes, and unsteady stance and gait, due to apoptotic cell death in sensitive brain areas, mainly areas with high metabolic requirement, causing symmetrically distributed lesions among structures such as the third and fourth ventricles, besides dorsomedial thalamus ( In the PNS, thiamine deficiency can result in polyneuritis and paralysis, as seen in dry beriberi, which affects the sensory system, causing pain, altered temperature sensitivity, numbness, reduced tendon reflexes, and leg atrophy ( Pan et al, in a in vivo study performed with transgenic mice, have shown that chronic treatment with benfotiamine, a thiamine derivate with better bioavailability, enhanced the spatial memory and reduced both amyloid plaque numbers and phosphorylated tau levels, suggesting that this thiamine derivative may be useful in clinical Alzheimers disease treatment, although others thiamine derivatives do not showed the same results ( Table 2 )
