NAD+, mitochondrial energy and cellular ageing research

NAD+: A Detailed Guide to Cellular Energy, Mitochondrial Function and Ageing Research

NAD+ has become one of the most closely studied molecules in metabolism, mitochondrial function and healthy-ageing research.

Often promoted as an “anti-ageing molecule” or “cellular energy booster,” NAD+ is biologically essential—but these simplified descriptions can exaggerate what supplementation or administration has been proven to achieve in humans.

Nicotinamide adenine dinucleotide, abbreviated to NAD+, is present in every living human cell. It helps cells convert nutrients into usable energy while supporting DNA repair, cellular signalling, stress responses and communication between the nucleus and mitochondria.

Scientists are investigating whether changes in NAD+ metabolism contribute to ageing and metabolic disease—and whether restoring NAD+ availability could produce meaningful health benefits.

This guide examines what NAD+ is, how it works, why NAD+ levels may change with age, the difference between NAD+, NADH, NMN and NR, and what research actually shows about NAD+ supplementation and intravenous NAD+.

What is NAD+?

NAD+ stands for nicotinamide adenine dinucleotide.

It is a naturally occurring coenzyme found in human cells. A coenzyme is a molecule that helps enzymes complete biological reactions.

NAD+ is not a peptide, hormone or conventional stimulant. It is a dinucleotide formed from two nucleotide components joined through their phosphate groups.

The molecule exists in two closely connected states:

  • NAD+, the oxidised form
  • NADH, the reduced form

NAD+ accepts electrons during metabolic reactions and becomes NADH. NADH can subsequently donate those electrons, returning to NAD+.

This continuous cycling between NAD+ and NADH is central to cellular metabolism.

What does NAD+ do in the body?

NAD+ has two broad biological roles.

First, it acts as a redox coenzyme, transferring electrons during the chemical reactions used to extract energy from carbohydrates, fats and amino acids.

Second, NAD+ acts as a substrate consumed by enzymes involved in cellular regulation, DNA repair, calcium signalling and stress responses.

NAD+ is therefore connected with:

  • Cellular energy production
  • Mitochondrial respiration
  • Glucose and fat metabolism
  • DNA-damage responses
  • Sirtuin activity
  • Circadian biology
  • Inflammatory signalling
  • Cellular stress adaptation
  • Calcium signalling
  • Immune-cell activity

These processes help explain why NAD+ metabolism is being studied across such a wide range of conditions.

However, the fact that NAD+ is involved in a biological process does not mean that administering additional NAD+ will necessarily improve that process.

NAD+ and cellular energy production

Cells obtain chemical energy by breaking down nutrients through linked metabolic pathways.

During glycolysis, the citric-acid cycle and fatty-acid oxidation, NAD+ accepts electrons and hydrogen, becoming NADH.

NADH then carries these electrons to the mitochondrial electron transport chain.

The electrons pass through a series of respiratory complexes within the inner mitochondrial membrane. Their movement contributes to a proton gradient, which powers ATP synthase—the molecular machinery responsible for producing ATP.

ATP, or adenosine triphosphate, supplies energy for:

  • Muscle contraction
  • Nerve signalling
  • Protein production
  • Membrane transport
  • Cellular repair
  • Immune function
  • Tissue maintenance

NAD+ does not directly “contain energy.” Instead, the NAD+/NADH cycle helps transfer the electrons required for ATP production.

NAD+ vs NADH: what is the difference?

NAD+ and NADH are two forms of the same redox pair.

Feature NAD+ NADH
State Oxidised Reduced
Primary role Accepts electrons Carries and donates electrons
Relationship Becomes NADH after accepting electrons Becomes NAD+ after donating electrons
Metabolic importance Supports oxidation of nutrients Supplies electrons to mitochondrial respiration

The balance between NAD+ and NADH can influence cellular metabolism.

A cell may contain NAD+, but if too much exists in the NADH state and cannot be efficiently reoxidised, important metabolic reactions can still be disrupted.

This is why NAD+ biology concerns more than simply increasing the total amount of the molecule. Researchers must also consider:

  • NAD+/NADH balance
  • Cellular location
  • Tissue type
  • Rates of NAD+ production
  • Rates of NAD+ consumption
  • Mitochondrial respiratory function

How does the body produce NAD+?

The body can make NAD+ through several interconnected pathways.

The de novo pathway

The de novo pathway begins with the amino acid tryptophan.

Tryptophan is converted through the kynurenine pathway into several intermediates, eventually contributing to NAD+ synthesis.

This is a biologically complex and comparatively inefficient route, and tryptophan has many functions beyond NAD+ production.

The Preiss–Handler pathway

Nicotinic acid, also known as niacin or vitamin B3, can be converted into NAD+ through the Preiss–Handler pathway.

Nicotinic acid is converted into nicotinic acid mononucleotide, followed by additional steps that eventually produce NAD+.

The salvage pathway

The salvage pathway recycles nicotinamide released when NAD+-consuming enzymes use NAD+.

Nicotinamide is converted into nicotinamide mononucleotide, or NMN, by the enzyme nicotinamide phosphoribosyltransferase—commonly abbreviated to NAMPT.

NMN is then converted into NAD+.

Because cells continually consume and recycle NAD+, the salvage pathway is an important method of maintaining NAD+ availability.

A related enzyme, nicotinamide N-methyltransferase (NNMT), methylates nicotinamide to form 1-methylnicotinamide, diverting some nicotinamide away from the salvage pathway. For this reason NNMT has become a research target in metabolic and NAD+ biology. 5-Amino-1MQ is a small-molecule NNMT inhibitor studied in this context in laboratory and animal research.

The nicotinamide riboside pathway

Nicotinamide riboside, or NR, can be converted into NMN by nicotinamide riboside kinases.

NMN can then be converted into NAD+.

This is why NR and NMN are referred to as NAD+ precursors: the body uses them as raw materials to synthesise NAD+.

NAD+ and mitochondrial function

Mitochondria require NAD+ and NADH to support oxidative metabolism.

NADH donates electrons to complex I of the mitochondrial electron transport chain. Efficient electron flow supports the proton gradient required for ATP production.

NAD+ metabolism is also connected with mitochondrial function through regulatory proteins such as sirtuins.

Mitochondrial sirtuins include:

  • SIRT3
  • SIRT4
  • SIRT5

These proteins influence aspects of metabolic-enzyme activity, oxidative stress, fatty-acid metabolism and mitochondrial adaptation.

Insufficient NAD+ availability could theoretically affect both energy-transfer reactions and NAD+-dependent mitochondrial signalling.

However, blood NAD+ measurements may not accurately represent NAD+ availability inside the mitochondria of a specific tissue. NAD+ metabolism is compartmentalised, meaning that concentrations and turnover can differ between the:

  • Cytoplasm
  • Nucleus
  • Mitochondria
  • Extracellular space
  • Different organs and tissues

This is one reason NAD+ research in humans is difficult to interpret.

NAD+ and sirtuins

Sirtuins are a family of enzymes that require NAD+ to function.

Humans have seven recognised sirtuins, known as SIRT1 through SIRT7. They operate in different cellular locations and influence different biological processes.

Sirtuin research has examined connections with:

  • Metabolic regulation
  • Mitochondrial biogenesis
  • Stress resistance
  • Inflammation
  • DNA maintenance
  • Circadian rhythms
  • Cellular ageing
  • Gene expression

When a sirtuin completes a reaction, it consumes NAD+ and produces nicotinamide and other metabolites.

This creates a relationship between NAD+ availability and sirtuin activity. If NAD+ availability changes, the activity of certain sirtuins may also change.

Much of the excitement surrounding NAD+ and longevity originated from animal research showing that altering NAD+ metabolism could influence sirtuin-associated pathways.

That does not establish that raising NAD+ in humans will reproduce every effect observed in laboratory models.

NAD+ and DNA repair

DNA is continuously exposed to damage from:

  • Normal metabolic activity
  • Reactive oxygen species
  • Ultraviolet radiation
  • Environmental exposures
  • Replication errors
  • Inflammatory processes

Poly(ADP-ribose) polymerases, commonly called PARPs, help detect and respond to certain forms of DNA damage.

PARPs consume NAD+ to create ADP-ribose chains that recruit and regulate DNA-repair machinery.

Moderate PARP activity supports normal DNA-damage responses. Extensive or persistent DNA damage can cause high PARP activity, which may consume substantial amounts of cellular NAD+.

This has led researchers to examine whether accumulated DNA damage contributes to changing NAD+ availability during ageing.

The relationship is complex because PARP activity is biologically necessary. Attempting to maximise NAD+ by indiscriminately suppressing DNA-repair pathways would not necessarily be beneficial.

NAD+, CD38 and inflammation

CD38 is a membrane-associated enzyme that consumes NAD+ and participates in calcium signalling, immune regulation and cellular communication.

Research suggests CD38 activity can increase with age in some tissues.

A 2020 animal study proposed that senescent cells encourage the accumulation of inflammatory CD38-positive immune cells, contributing to tissue NAD+ decline.

This model connects:

  • Cellular senescence
  • Chronic inflammation
  • Immune-cell activity
  • CD38
  • NAD+ consumption

CD38 has consequently become a research target in ageing and metabolic science.

Most mechanistic work in this area remains preclinical. Blocking CD38 could also affect immune and calcium-signalling functions, so the pathway cannot be reduced to “CD38 is bad.”

Does NAD+ decline with age?

It is frequently stated as fact that NAD+ levels fall substantially as everyone ages.

Animal research supports age-related changes in NAD+ metabolism across several tissues. Human evidence is more limited and inconsistent.

A major 2025 review concluded that a consistent age-related decline in human NAD+ has been demonstrated in only a limited number of studies. Results vary according to:

  • Tissue examined
  • Age range
  • Health status
  • Measurement method
  • Which NAD+ metabolite is measured
  • Sample handling
  • Time of collection
  • Diet and activity
  • Circadian timing

Blood measurements may not reflect NAD+ levels within skeletal muscle, liver, brain or mitochondrial compartments.

It is therefore more accurate to say that NAD+ metabolism may change with age and disease, but the scale, consistency and clinical significance of this change in humans remain under investigation.

Why might NAD+ metabolism change with age?

Several mechanisms have been proposed:

Reduced NAD+ synthesis

Activity of enzymes involved in the salvage pathway, particularly NAMPT, may change with age, inflammation or metabolic dysfunction.

Increased NAD+ consumption

Greater activity of NAD+-consuming enzymes such as CD38 and PARPs may increase NAD+ turnover.

DNA damage

Accumulated DNA damage can increase PARP activity and NAD+ use.

Chronic inflammation

Age-associated inflammatory signalling may influence CD38-positive immune cells and other parts of NAD+ metabolism.

Mitochondrial dysfunction

Impaired electron transport can alter the balance between NAD+ and NADH.

Circadian disruption

NAD+ synthesis and sirtuin activity interact with the circadian clock. Sleep disruption and altered daily rhythms may affect this relationship.

These mechanisms are interconnected and may vary between individuals and tissues.

NAD+ and ageing: what does the research show?

In animal studies, increasing NAD+ availability through precursors such as NMN and NR has influenced several age-associated processes.

Reported preclinical findings include changes in:

  • Insulin sensitivity
  • Mitochondrial function
  • Skeletal-muscle metabolism
  • Inflammatory signalling
  • Physical function
  • DNA-damage responses
  • Cardiovascular biology

Human trials have generally shown that certain NAD+ precursors can alter blood or tissue NAD+-related metabolites.

What remains less certain is whether these biochemical changes produce substantial, consistent clinical benefits.

A 2025 review of human NAD+ precursor research concluded that:

  • Human evidence for universal age-related NAD+ decline remains limited
  • NR and NMN can influence NAD+ metabolism
  • Effects differ between tissues and populations
  • Human clinical efficacy has generally been limited
  • Rodent findings cannot be directly extrapolated to people
  • Larger and longer clinical studies are required

There is currently no conclusive evidence that NAD+, NMN or NR supplementation extends human lifespan.

NAD+ vs NMN vs NR

NAD+, NMN and NR are related but are not the same molecule.

Compound Full name Biological position
NAD+ Nicotinamide adenine dinucleotide Active cellular coenzyme
NMN Nicotinamide mononucleotide Direct NAD+ precursor
NR Nicotinamide riboside Converted into NMN and then NAD+
NAM Nicotinamide Vitamin B3 form recycled through the salvage pathway
NA Nicotinic acid Vitamin B3 form used through the Preiss–Handler pathway

NAD+

NAD+ is the final coenzyme used in energy-transfer and enzyme reactions.

NMN

NMN is an intermediate used by cells to produce NAD+. Human trials show that oral NMN can alter NAD+-related metabolism, but clinical outcomes have varied.

NR

NR is converted into NMN before contributing to NAD+ synthesis. Several human studies have demonstrated that oral NR can increase NAD+-related metabolites in blood.

An increase in a blood biomarker is not equivalent to proven improvement in energy, ageing or disease outcomes.

What does human NMN research show?

A 2021 randomised, double-blind, placebo-controlled study investigated NMN in 25 postmenopausal women with prediabetes who were overweight or obese.

After ten weeks, NMN increased insulin-stimulated glucose disposal and aspects of skeletal-muscle insulin signalling compared with placebo.

However, the study was small and involved a specific population. It did not demonstrate:

  • Weight loss
  • Reversal of ageing
  • Increased lifespan
  • General effectiveness for healthy adults
  • Prevention of diabetes
  • Improved performance across populations

The findings are encouraging for further investigation but should not be generalised beyond the studied population.

Other NMN trials have reported acceptable short-term tolerability and changes in NAD+-related metabolites, but clinical benefits have not been consistent across all endpoints.

What does human NR research show?

Human studies have shown that oral nicotinamide riboside can increase circulating NAD+-related metabolites.

NR has been studied in areas including:

  • Healthy ageing
  • Obesity
  • Cardiovascular risk
  • Skeletal-muscle metabolism
  • Mitochondrial disorders
  • Inflammatory markers

Many studies have been relatively small and short. While biochemical changes are commonly reported, improvements in physical performance, insulin sensitivity, muscle function or other clinical outcomes have been mixed.

The evidence supports NR as an NAD+ precursor. It does not yet establish NR as a proven anti-ageing treatment.

Does oral NAD+ work?

Direct oral NAD+ presents biological questions involving digestion, stability, absorption and transport across cell membranes.

Large molecules may be broken down in the digestive tract or extracellular space before their components are absorbed. NAD+ may also be converted into smaller metabolites that subsequently contribute to NAD+ synthesis.

This means an oral product may influence NAD+ metabolism without intact NAD+ necessarily travelling directly from the digestive system into every target cell.

NR and NMN have received greater research attention as oral NAD+ precursors because they can enter NAD+ biosynthetic pathways.

Comparative evidence establishing which oral approach produces the most meaningful human health outcomes remains limited.

What is intravenous NAD+?

Intravenous NAD+, often called an NAD+ IV infusion, delivers NAD+ into the bloodstream through a vein.

Commercial clinics sometimes promote NAD+ IV therapy for:

  • Energy
  • Mental clarity
  • Recovery
  • Healthy ageing
  • Fatigue
  • Metabolic health
  • Addiction recovery
  • General wellbeing

These broad claims exceed the available clinical evidence.

A small 2019 pilot study examined the metabolic fate of intravenous NAD+ administered over six hours in 11 healthy male participants. The researchers measured NAD+ and related metabolites in plasma and urine.

During the initial phase of the infusion, plasma NAD+ did not rise substantially, suggesting rapid removal, metabolism or tissue interaction. Changes in metabolites were observed later.

The study provided useful pharmacokinetic information but did not test whether intravenous NAD+:

  • Improves energy
  • Reverses ageing
  • Treats fatigue
  • Improves cognition
  • Supports addiction recovery
  • Extends lifespan
  • Prevents disease

There remains a lack of large, blinded, randomised controlled trials evaluating commercial NAD+ infusion claims.

Is intravenous NAD+ better than NMN or NR?

There is currently insufficient comparative clinical evidence to conclude that intravenous NAD+ is superior to oral NMN or NR for longevity, energy or general health.

The routes are biologically different:

  • Intravenous NAD+ enters the circulation directly
  • Oral NMN enters precursor and metabolic pathways
  • Oral NR is converted through NR kinase and NMN-related pathways
  • Oral NAD+ may be broken down before absorption

Direct bloodstream delivery does not automatically prove greater cellular uptake or better health outcomes.

Questions remain about how extracellular NAD+ is metabolised, which tissues receive its metabolites, how long changes persist and whether biochemical effects translate into clinical benefits.

For a full route-by-route comparison of these approaches—including absorption, evidence and safety—see our guide to SubQ NAD+ vs IV NAD+ vs NMN capsules.

NAD+ injections and subcutaneous research

Evidence concerning subcutaneous or intramuscular NAD+ for general wellness is even more limited than evidence for intravenous infusion.

Safety and efficacy cannot be inferred solely from the fact that NAD+ occurs naturally in the body.

Route of administration matters. A substance that is normal inside cells may behave differently when placed into:

  • Subcutaneous tissue
  • Muscle
  • Blood
  • An unregulated preparation

Injectable products also introduce risks involving:

  • Sterility
  • Endotoxin contamination
  • Particulate matter
  • Incorrect concentration
  • pH and osmolality
  • Degradation
  • Storage conditions
  • Local tissue reactions
  • Infection

Research-labelled NAD+ should not be presented as an injectable medicine or supplied for self-administration.

NAD+ and exercise

Exercise influences mitochondrial adaptation, metabolic flexibility and NAD+-dependent signalling.

Changes in energy demand affect NAD+/NADH balance, AMPK activity and sirtuin-associated pathways.

Regular exercise may support the biological systems in which NAD+ participates through:

  • Mitochondrial biogenesis
  • Improved insulin sensitivity
  • Increased oxidative capacity
  • Better metabolic flexibility
  • Adaptation of skeletal muscle
  • Improved cardiovascular function

There is no convincing evidence that NAD+ supplementation can replace exercise.

The biological effect of exercise involves mechanical loading, cardiovascular adaptation, hormonal responses, muscle remodelling and nervous-system changes that cannot be reproduced by raising one metabolite.

NAD+, sleep and circadian rhythms

NAD+ metabolism interacts with the circadian clock.

NAMPT, an important salvage-pathway enzyme, is influenced by circadian transcription factors. NAD+ availability can then affect SIRT1, which interacts with proteins involved in circadian regulation.

This creates a feedback relationship between:

  • NAD+ synthesis
  • Sirtuin activity
  • Cellular metabolism
  • Sleep–wake timing
  • Circadian gene expression

Disrupted sleep may affect metabolic health through numerous pathways. Current evidence does not establish NAD+ supplementation as a treatment for insomnia or circadian-rhythm disorders.

NAD+ and brain research

The brain has high energy requirements, making mitochondrial and NAD+ metabolism important to neuronal function.

Preclinical research has investigated NAD+ pathways in:

  • Neuroinflammation
  • Axonal injury
  • Cognitive decline
  • Neurodegenerative disease
  • DNA-damage responses
  • Mitochondrial stress

Promising laboratory findings have not yet established NAD+ administration as an effective treatment for dementia, Parkinson’s disease or other neurological conditions.

Claims about improved focus or mental clarity are often based on personal reports rather than controlled clinical evidence.

NAD+ and metabolic health

NAD+ is integral to glucose oxidation, fatty-acid metabolism and mitochondrial respiration.

Altered NAD+ metabolism has been associated with:

  • Obesity
  • Insulin resistance
  • Type 2 diabetes
  • Fatty-liver disease
  • Metabolic syndrome

Human precursor studies have produced some encouraging signals, including the NMN insulin-sensitivity study in postmenopausal women with prediabetes.

Results remain population-specific and inconsistent. NAD+ boosters are not replacements for established medical treatment, nutrition, physical activity or other clinically appropriate interventions.

NAD+ and cancer: an important complexity

NAD+ is sometimes portrayed as universally protective because it supports DNA repair and normal cellular function.

Cancer biology makes this relationship more complicated.

Healthy cells require NAD+ for DNA maintenance and metabolic function. Cancer cells also require energy, DNA repair and metabolic substrates to survive and proliferate.

Depending on the context, researchers are examining both:

  • Strategies that increase NAD+ availability in healthy or ageing tissues
  • Strategies that disrupt NAD+ synthesis in certain cancer cells

This does not mean NAD+ supplementation causes cancer. It means there is insufficient evidence to assume that maximising NAD+ is beneficial in every biological situation.

People undergoing cancer treatment should discuss supplements or infusion therapies with their oncology team.

NAD+ safety and research limitations

NAD+ is essential to human biology, but “natural” does not automatically mean risk-free when concentrated or administered through an unfamiliar route.

Potential considerations include:

  • Limited long-term human evidence
  • Uncertain tissue-specific effects
  • Differences between NAD+ and its precursors
  • Product purity and stability
  • Unknown risks of unregulated injectable material
  • Interactions with medical conditions or treatment
  • Difficulty measuring intracellular NAD+ accurately
  • Theoretical concerns in some disease contexts

Short-term NR and NMN studies have generally reported acceptable tolerability, but this does not establish indefinite safety or clinical effectiveness.

Intravenous or injectable administration introduces additional medical and manufacturing risks.

Does NAD+ extend lifespan?

No study has demonstrated that NAD+, NMN or NR supplementation extends human lifespan.

Animal studies have shown that manipulating NAD+ pathways can affect metabolism, function and certain age-associated biological processes.

Human ageing is substantially more complex. Demonstrating lifespan extension would require long-duration trials, large populations and careful control of health and lifestyle factors.

More realistic near-term research questions include whether NAD+-targeted strategies can improve:

  • Specific metabolic endpoints
  • Physical function in defined populations
  • Symptoms of particular mitochondrial disorders
  • Tissue-specific NAD+ deficiency
  • Clinically meaningful healthspan measures

Until such outcomes are established, NAD+ should not be described as a proven longevity treatment.

NAD+ research: evidence versus marketing

Claim Current evidence
NAD+ is essential for cellular metabolism Strongly established
NAD+ participates in mitochondrial energy production Strongly established
NAD+ is required by sirtuins and PARPs Strongly established
NAD+ metabolism can change with age Supported, but human tissue evidence is inconsistent
NR and NMN can alter NAD+-related metabolites Supported by human studies
NMN may improve specific metabolic outcomes Early evidence in defined populations
NAD+ infusion increases energy and mental clarity Not established by robust controlled trials
NAD+ reverses biological ageing Not established
NAD+ extends human lifespan Not established
Injectable NAD+ is proven safe for self-administration Not established

Frequently asked questions about NAD+

What is NAD+?

NAD+ is nicotinamide adenine dinucleotide, an essential cellular coenzyme involved in energy metabolism, mitochondrial respiration, DNA repair and cellular signalling.

Is NAD+ a vitamin?

NAD+ is not itself a vitamin. The body can produce it using vitamin B3-related precursors such as nicotinamide and nicotinic acid.

Is NAD+ a peptide?

No. NAD+ is a dinucleotide coenzyme, not a peptide.

What is the difference between NAD+ and NADH?

NAD+ is the oxidised, electron-accepting form. NADH is the reduced, electron-carrying form. They continuously cycle during metabolism.

What is the difference between NAD+ and NMN?

NAD+ is the active cellular coenzyme. NMN is a precursor the body can convert into NAD+.

What is the difference between NAD+ and NR?

NR is a form of vitamin B3 that can be converted into NMN and subsequently NAD+.

Does NAD+ decline with age?

Some studies report age-related reductions in certain tissues, but human evidence is inconsistent. Changes vary by tissue, health status and measurement method.

Does NAD+ give you energy?

NAD+ participates in the reactions required for cellular energy production. This does not mean NAD+ supplementation has been proven to increase subjective energy in humans.

Does NAD+ help with weight loss?

There is no strong evidence that NAD+ administration is an effective standalone weight-loss treatment.

Does NAD+ slow ageing?

NAD+ pathways influence biological processes associated with ageing, particularly in animal research. No NAD+ intervention has been proven to slow human ageing or extend human lifespan.

Is NAD+ IV therapy clinically proven?

Human pharmacokinetic research exists, but robust clinical evidence supporting broad commercial claims about NAD+ IV therapy remains limited.

Can NAD+ be combined with MOTS-C or SS-31?

There is no established human clinical evidence confirming that combinations of NAD+, MOTS-C and SS-31 are safe or produce complementary benefits.

NAD+, MOTS-C and SS-31: how do they differ?

NAD+, MOTS-C and SS-31 all appear in discussions about mitochondria, but they represent different biological categories.

Compound Type Principal research role
NAD+ Dinucleotide coenzyme Electron transfer, metabolism and enzyme activity
MOTS-C Mitochondrial-derived peptide Metabolic signalling and stress adaptation
SS-31 Synthetic tetrapeptide Cardiolipin and inner mitochondrial membrane research

NAD+ supports metabolic reactions throughout the cell. MOTS-C is being studied as a signal encoded within mitochondrial DNA. SS-31 is designed to interact with cardiolipin in the inner mitochondrial membrane.

There is currently no validated “mitochondrial stack” combining these compounds.

For a closer look at how these two mitochondrial peptides are being studied, see our guide to MOTS-C and SS-31 mitochondrial peptide research.

NŪVO Research Perspective

NAD+ is not a newly discovered compound. Its fundamental role in oxidation and reduction reactions has been understood for more than a century.

What is new is the expanding understanding of NAD+ as more than an electron carrier.

NAD+ connects:

  • Nutrient metabolism
  • Mitochondrial respiration
  • DNA repair
  • Sirtuin activity
  • Immune regulation
  • Circadian biology
  • Cellular stress responses

This makes NAD+ an important research subject, but it also creates opportunities for marketing claims to move ahead of the evidence.

The strongest conclusion is not that NAD+ is a proven anti-ageing treatment. It is that NAD+ is an essential and highly regulated part of human biology whose therapeutic manipulation requires more precise, tissue-specific and clinically meaningful research. Browse the research catalogue — every compound is supplied for laboratory research only.

Research and medical disclaimer

This article is provided for general educational and scientific-information purposes only. It does not constitute medical advice, diagnosis, treatment instructions or a recommendation to administer NAD+ or any NAD+ precursor.

Research-labelled NAD+ is not a licensed medicine and must not be used for self-treatment or human administration. The safety, purity and clinical evidence associated with a regulated product cannot be assumed for unregulated or research-labelled material.

Anyone considering a supplement, infusion or treatment affecting NAD+ metabolism should consult an appropriately qualified healthcare professional.

Sources and further reading

  1. Covarrubias AJ, et al. NAD+ metabolism and its roles in cellular processes during ageing. Nature Reviews Molecular Cell Biology, 2021. View the review on PubMed
  2. Imai S and Guarente L. NAD+ and sirtuins in ageing and disease. Trends in Cell Biology, 2014. View the review on PubMed
  3. Vinten KT, et al. NAD+ precursor supplementation in human ageing: clinical evidence and challenges. Nature Metabolism, 2025. View the review on PubMed
  4. Yoshino M, et al. Nicotinamide mononucleotide increases muscle insulin sensitivity in prediabetic women. Science, 2021. View the clinical trial on PubMed
  5. Airhart SE, et al. An open-label study of the pharmacokinetics of nicotinamide riboside in healthy adults. PLOS ONE, 2017. View the study on PubMed
  6. Grant R, et al. A pilot study investigating changes in human plasma and urine NAD+ during a six-hour intravenous infusion. Frontiers in Aging Neuroscience, 2019. View the pilot study on PubMed
  7. Covarrubias AJ, et al. Senescent cells promote tissue NAD+ decline during ageing through CD38-positive macrophages. Nature Metabolism, 2020. View the research on PubMed
  8. Strømland Ø, et al. The balance between NAD+ biosynthesis and consumption in ageing. Mechanisms of Ageing and Development, 2021. View the review on PubMed
  9. Yoshino J, Baur JA and Imai S. NAD+ intermediates: the biology and therapeutic potential of NMN and NR. Cell Metabolism, 2018. View the article on PubMed
  10. Uchida H, et al. NAD+ metabolism as a target for anti-ageing research. 2025. View the review on PubMed
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