Nicotinamide adenine dinucleotide (NAD) has become increasingly popular over the past several years. It’s a metabolite that’s very important in multiple metabolic functions, including DNA repair and energy production. For whatever reason, it’s concentration is known to decline during human aging by as much as 90%.

In aging mice, the intestines degenerate and colon function declines. The researchers in this monthly research highlight noted that this decline was also associated with a decline in NAD in the colon. They wondered whether restoring NAD to a level associated with a younger age would affect declining colon function.

These researchers reported that both colon motility and luminal dehydration was restored with nicotinamide mononucleotide (NMN) administration. NMN is a precursor to NAD and reliably increases serum NAD level. Restoration of colonic function with NMN is promising because NAD is involved in so many cellular processes, and it can also be easily restored in aging humans, whose NAD levels decline dramatically with age.

The researchers also found that they could recreate the age-related colon degeneration in young mice by reducing their NAD level by inhibition of its synthesis. This further supports the hypothesis that declining NAD concentration is a primary cause of age-related colon dysfunction in mice.

We hope that NAD restoration in older people can restore biological function in multiple tissues, and the results of this paper are consistent with that hope.

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