In order to prevent mitochondrial malfunction and sustain metabolic function/energy generation (ATP), NAD+ supplementation may counterbalance the age-related degradation of NAD+ and its precursor nicotinamide mononucleotide by NADases, particularly CD38.7 NAD+ replenishment, however, appears to support a number of other metabolic pathways via NAD+-dependent enzymes in research involving human and animal models (as well as samples and cell lines) (1,2,3)
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small sample size, lack of control group, lack of common diagnosis), it did demonstrate improved pain in 87.5% of patients who received injections containing BPC-157