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#Nicotinamide is then methylated by the liver to form N1-methylnicotinamide, which can be excreted in the urine. This methylation process consumes a methyl group from [[S-adenosylmethionine (SAMe)]], the primary methyl donor in the body. | #Nicotinamide is then methylated by the liver to form N1-methylnicotinamide, which can be excreted in the urine. This methylation process consumes a methyl group from [[S-adenosylmethionine (SAMe)]], the primary methyl donor in the body. | ||
There could be a compensatory mechanisms that if methyl groups were being depleted at a concerning rate, the body would likely slow down the conversion of NMN to NAD+ or the methylation of nicotinamide. If not, there is a potential concern is that excessive NMN supplementation might lead a [[Methyl Donor Deficiency]] to a decrease in the body's available methyl groups, which play crucial roles in various biological processes including DNA methylation and neurotransmitter synthesis. | |||
For that reason, some individuals who take NMN also supplement with [[Trimethylglycine (TMG)]] | For that reason, some individuals who take NMN also supplement with [[Methyl Donors|methyl donors]] like [[Trimethylglycine (TMG)]] to ensure that they are not depleting their body's methyl groups. However, this is a precautionary measure and not necessarily based on concrete evidence. | ||
However, there | However, there is '''no clear evidence yet'''. While the pathway is known, the actual significance of NMN supplementation on global methyl group status is not well-established in humans. It's a theoretical concern, and it would require substantial NMN consumption to have a significant impact as well as the comsumption of methyl donors in the diet would be too low to replenish methyl groups. | ||
===Risks of NMN Supplementation=== | ===Risks of NMN Supplementation=== |