Below is a breakdown of major research-backed effects by physiological system, showcasing the molecule’s broad experimental utility:
Nicotinamide Adenine Dinucleotide (NAD⁺) is a crucial coenzyme found in all living cells, revered for its central role in cellular energy and longevity research. This molecule is a cornerstone in metabolism and is heavily studied for its potential in combating aging and supporting vital biological functions. NAD⁺ serves as a molecular “powerhouse” by participating in hundreds of enzymatic reactions that keep cells alive and healthy (Ref 9).
Cellular Energy & Metabolism
NAD⁺ is indispensable for energy production in cells. It serves as a central electron carrier in metabolism, accepting electrons during the breakdown of nutrients and then delivering them to the mitochondria to drive ATP synthesis. In fact, NAD⁺ is the major hydride acceptor in glycolysis and the TCA cycle, meaning that without NAD⁺, cells cannot efficiently convert carbohydrates, fats, and amino acids into usable energy. This coenzyme’s pivotal role in metabolism underpins its importance for all living cells, as energy (ATP) is the currency of life. High NAD⁺ availability has been linked to improved metabolic efficiency and resilience to metabolic stress in research settings (Ref 1).
DNA Repair & Genomic Stability
NAD⁺ is indispensable for energy production in cells. It serves as a central electron carrier in metabolism, accepting electrons during the breakdown of nutrients and then delivering them to the mitochondria to drive ATP synthesis. In fact, NAD⁺ is the major hydride acceptor in glycolysis and the TCA cycle, meaning that without NAD⁺, cells cannot efficiently convert carbohydrates, fats, and amino acids into usable energy. This coenzyme’s pivotal role in metabolism underpins its importance for all living cells, as energy (ATP) is the currency of life. High NAD⁺ availability has been linked to improved metabolic efficiency and resilience to metabolic stress in research settings (Covarrubias et al., 2021).
DNA Repair & Genomic Stability
NAD⁺ is a critical substrate for enzymes that repair DNA and protect the genome. Poly(ADP-ribose) polymerases (PARPs), key DNA-repair enzymes, consume NAD⁺ to mark DNA strand breaks and recruit repair machinery. Sufficient NAD⁺ thus powers the repair of DNA damage, maintaining genomic stability. Research indicates that when NAD⁺ levels are low, DNA repair processes are less effective – leading to accumulation of DNA damage and genomic instability over time. By supporting PARP activity and other repair pathways, NAD⁺ helps preserve the integrity of genetic information in cells. This function is crucial, as DNA damage and genomic instability are well-known contributors to aging and cancer development. In summary, ample NAD⁺ acts as a guardian of the genome, enabling continuous surveillance and mending of DNA lesions (Ref 9).
Mitochondrial Function & Autophagy
NAD⁺ has a profound impact on mitochondrial health and quality-control mechanisms like autophagy. Autophagy is the cell’s recycling system, whereby damaged cellular components (including mitochondria, via mitophagy) are degraded and removed. NAD⁺ levels regulate autophagy through NAD⁺-dependent enzymes such as the sirtuin family (for example SIRT1). High NAD⁺ activates SIRT1, which in turn promotes autophagy and the clearance of defective mitochondria. Studies have shown that a decline in NAD⁺ reduces autophagic flux and impairs mitophagy, causing cells to accumulate dysfunctional mitochondria and proteins. This can contribute to cellular dysfunction and has been implicated in various age-related diseases. By contrast, maintaining NAD⁺ levels supports effective autophagy, helping cells remove harmful debris and sustain efficient mitochondrial function. In research on model organisms, boosting NAD⁺ has been observed to restore mitophagy in conditions of metabolic or oxidative stress, thereby improving cell survival and function (Ref 3).
Aging & Longevity
NAD⁺ levels naturally decline with age in many tissues. This NAD⁺ depletion is thought to contribute to the physiological declines of aging, as it impairs critical NAD⁺-dependent processes like energy production and DNA repair. NAD⁺ insufficiency has been linked to virtually all hallmarks of aging, including genomic instability, mitochondrial dysfunction, stem cell exhaustion, and chronic inflammation. Numerous studies in animals show that restoring NAD⁺ can produce rejuvenating effects: enhanced metabolic function, improved cognitive and muscle function, reduced inflammation, and extended lifespan. For example, mice supplemented with NAD⁺ precursors exhibit improved insulin sensitivity, greater endurance, and fewer signs of age-related degeneration (Ref 2; Ref 11). Some age-related pathologies – from neurodegeneration to metabolic disorders – were slowed or even reversed when cellular NAD⁺ was replenished. These findings have led scientists to consider NAD⁺ restoration a potential strategy for promoting healthy aging and longevity. It is important to note that while these results are promising, NAD⁺ therapies are still under investigation; our NAD⁺ product is offered to enable further research in this domain (not for human use) (Ref 9).
Cognitive Function & Neuroprotection
NAD⁺ plays a vital role in the nervous system, where high energy demand and long-lived cells (neurons) make NAD⁺-dependent processes especially critical. In the brain, NAD⁺ fuels neuronal metabolism and also activates sirtuins (like SIRT1 and SIRT3) that protect neurons under stress. Research in rodents has demonstrated that enhancing NAD⁺ levels can improve cognitive performance and protect against neurodegenerative changes. For instance, studies showed that administering NAD⁺ precursors in mouse models of Alzheimer’s disease led to improved memory, increased neuron survival, and reduced buildup of toxic proteins. Similarly, NAD⁺ repletion helped preserve synaptic plasticity and boosted brain-cell health in aging animals. Conversely, NAD⁺ depletion contributes to increased neuronal vulnerability and cognitive dysfunction. Notably, excessive activation of NAD⁺-consuming enzymes (like PARP1 or CD38) during stress can deplete NAD⁺ in neurons, leading to cell death and memory impairment. These findings suggest that NAD⁺ is a critical regulator of brain health and a valuable target for cognitive research (Ref 12; Ref 13).
Immune Modulation & Inflammation
NAD⁺ influences the immune system and inflammatory responses through its involvement in a field known as immunometabolism. Immune cells require NAD⁺ for energy during activation and use NAD⁺-dependent pathways for regulation. For example, the enzyme CD38 — highly expressed in immune cells — breaks down NAD⁺ to produce secondary messengers that influence calcium signalling and immune responses (Ref 5). Adequate NAD⁺ supports immune balance and helps prevent over-activation. Low NAD⁺ levels are associated with “inflammaging” — a state of persistent low-grade inflammation that develops with age. Age-related increases in NAD⁺-consuming enzymes like CD38 and PARP contribute to this decline (Ref 9). In experimental settings, boosting NAD⁺ has been shown to reduce inflammatory cytokines and restore immune cell resilience, providing a new avenue of research for age-related immune decline (Ref 9).
Epigenetic Regulation & Cell Signaling
NAD⁺ is a key player in gene regulation, serving as a cofactor for sirtuins and other enzymes that modify DNA-associated proteins. Through SIRT1, SIRT3, and SIRT6, NAD⁺ regulates transcription factors, chromatin structure, and stress-responsive genes. It is also essential for maintaining circadian rhythms by modulating proteins like CLOCK and BMAL1. When NAD⁺ levels are optimal, these regulatory systems enhance antioxidant defence, mitochondrial function, and metabolic homeostasis. When NAD⁺ is low, chromatin becomes disorganised, and gene-expression patterns shift in ways that impair function and increase susceptibility to disease. In research models, NAD⁺ supplementation has been shown to stabilise gene-expression and promote cellular resilience to metabolic and oxidative stress (Ref 17).
