Nicotinamide adenine dinucleotide, or NAD+, is not a new discovery. The coenzyme was first isolated in the early 20th century, but the past two decades have seen a dramatic expansion in research interest, particularly in the context of aging and age-related disease.
The reason for this renewed attention comes down to its role in two major cellular processes. First, NAD+ is the primary substrate for sirtuins, a family of proteins (SIRT1 through SIRT7) that regulate gene expression, mitochondrial function, and stress responses. Second, it is a required substrate for poly-ADP-ribose polymerases, or PARPs, which play a central role in DNA repair. Both of these processes require NAD+ as a raw material, and both are increasingly implicated in the biology of aging.
Studies have shown that tissue NAD+ levels decline with age in humans and in animal models. A 2022 paper in Frontiers in Endocrinology reported measurable reductions in whole blood NAD+ concentrations correlated with age across a cohort of human subjects. Complementary work in mice has shown that restoring NAD+ levels through precursor supplementation can improve some markers of mitochondrial function and muscle endurance in older animals.
The research on NAD+ and sirtuins was significantly advanced by work from David Sinclair at Harvard and Shin-ichiro Imai at Washington University, whose 2013 and 2014 papers described age-related NAD+ decline and its relationship to vascular aging in mouse models. These findings have since been independently replicated and extended by multiple groups.
Cardiac research has also taken an interest in NAD+ biology. A 2021 review in Circulation discussed the evidence for NAD+ metabolism as a therapeutic target in heart failure, noting that mitochondrial dysfunction, which is a hallmark of cardiac aging, is closely tied to NAD+ availability.
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