Nicotinamide mononucleotide (NMN) supplementation drives a 20% median lifespan extension in a premature aging mouse model and restores intestinal structural integrity in healthy, middle-aged mice.
Highlights
Published in Food & Function, Yu and colleagues from Wenzhou Medical University in China show that oral NMN extends the average (14%), median (20%), and maximum (10%) lifespans of mice that prematurely age. The researchers also found that NMN restored intestinal tight junction multiprotein complexes, crucial contributors to the intestinal barrier, in healthy, middle-aged mice not undergoing premature aging. Additionally, NMN revamped the abundance of beneficial intestinal bacteria, further highlighting its capabilities to restore gut health.
While other studies have already shown that NMN enhances gut health and improves the microbiome, this is the first to show lifespan extension in fast-aging mice (progeria mice). The findings of lifespan extension in genetically mutant mice that age prematurely may pave the way for future experiments testing whether NMN extends life in healthy, aged mice. Positive lifespan-extension findings using healthy mice would be one of the first steps to trigger research on whether NMN also extends human lifespan.
Since progeria mice’s lifespan only reaches about five months, compared to healthy mice that live up to 2.5 years, studying their lifespan is more time- and cost-effective. In other words, with their much shorter lifespans, studying NMN’s effects on progeria mice lifespan takes much less time, which requires less cost for laboratory work.
The observation that prematurely aged mice treated with NMN lived a 20% longer median lifespan bolsters the findings in another mouse model that NMN increases amyotrophic lateral sclerosis (ALS) mouse lifespan. In the case of the ALS model mice, median lifespans were only increased by about 3.5%.
In addition to NMN markedly increasing the median lifespan of progeria mice, it also extended the maximum mouse lifespan by about 10%. In contrast, NMN had no effect on maximum lifespan in ALS mice. With these findings in progeria mice, researchers could be more compelled to find whether NMN extends healthy mouse lifespan.
While another previous study showed that NMN increased gene activity for intestinal tight junction proteins (Claudin-1 proteins), Yu and colleagues went a step further by measuring protein levels. They showed that NMN increases levels of these tight junction proteins about fourfold compared to other middle-aged mice not given NMN. These findings corroborate other findings suggesting that NMN restores tight junctions, which are key to establishing a functional barrier between the gut and what enters circulation, in middle-aged mice. Since intestinal dysfunction may contribute to aging and a shorter lifespan, improving the intestinal barrier could be one of the ways that NMN extends life.
A healthy microbiome composition is crucial for avoiding digestive problems from age-related gut microbe imbalances — dysbiosis. In that regard, Yu and colleagues identified that NMN increases the abundance of a few beneficial gut bacteria, Bifidobacterium pseudolongum and Akkermansia muciniphila. As such, Bifidobacterium pseudolongum has been shown to possess anticancer properties. Furthermore, elevated Akkermansia muciniphila abundance has been associated with longer-lived individuals who reach 100 (centenarians). By increasing the abundance of these two species in the intestines, NMN may propel a healthier gut during aging.
As with NMN, nicotinamide riboside (NR) is a precursor of nicotinamide adenine dinucleotide (NAD+). NAD+ levels drop with age, and increasing its cellular concentrations with precursors like NMN or NR has been shown to alleviate age-related neurodegenerative, cardiovascular, and metabolic conditions. Interestingly, both NMN and NR have now been shown to extend progeria mouse lifespan. All the same, research has been conducted showing that NR does not extend healthy mouse lifespan.
Yu and colleagues’ findings that NMN extends the lifespan of progeria mice by ~20% offers a clue that it may do so in healthy mice. On the other hand, it could fail to extend healthy mouse lifespan just like NR.
Along those lines, Dr. Rich Miller, who is one of the architects of a consortium that tests potential lifespan-extending interventions in healthy mice (the Interventions Testing Program [ITP]), hints that his team may test NMN soon. In that regard, he says that he is collaborating with private NMN vendors to obtain enough of this supplement to test NMN’s effects on lifespan in healthy mice. If Dr. Miller and colleagues find that NMN does in fact extend healthy mouse lifespan, this would provide some evidence that NMN’s anti-aging effects are superior to NR’s.
Furthermore, if healthy mouse NMN experiments give positive lifespan extension findings, this could pave the way to further testing NMN’s potential in humans. In that regard, figuring out whether NMN boosts the number of healthy, disease-free years people live (healthspan) and lifespan would become paramount.
Such a scenario would come in the face of the FDA’s ban on selling NMN as a supplement. Along those lines, it is possible that positive effects on healthy mouse lifespan from NMN could also help sway the FDA to reverse its ban.
Model: Zmpste24−/− mice aged 5–7 weeks and male C57BL/6 mice aged 10 months
Dosage: Zmpste24−/− mice were fed 300 mg/kg of NMN by oral gavage on alternate days until natural death and C57BL/6 mice were fed 300 mg/kg on of NMN by oral gavage on alternate days for six months