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In white adipose tissue of obese, insulin-resistant and aged mammals, NNMT is dramatically upregulated and because it consumes both the universal methyl donor (SAM) and the NAD precursor (nicotinamide), its hyperactivity simultaneously depletes the cellular methylation reserve and the NAD-salvage pool [1,2]

The aim is to rapidly bring your body's B12 reserves back up to a healthy level, which is vital for stopping any further nerve damage and starting the repair process

Other findings include decreased insulin resistance by 69%, improvements in cognitive function, a decreased plasma concentration of inflammation biomarkers (IL-6, hsCRP, TNF), endothelial dysfunction (E-selectin, SICAM1, sVCAM1), and a decline in genomic damage