NAD+

NAD+ (Nicotinamide adenine dinucleotide) is a small molecule studied for its effects on aging, recovery, and metabolic health. Essential cellular coenzyme for energy, DNA repair, and aging. Precursors (NMN/NR) or IV boost NAD+ levels. Cellular benefits proven, longevity unproven.

NAD+ (Nicotinamide Adenine Dinucleotide) is a critical coenzyme found in all living cells that plays essential roles in cellular metabolism, energy production, DNA repair, and aging processes. NAD+ levels naturally decline with age (up to 50% by middle age), contributing to mitochondrial dysfunction, reduced cellular repair capacity, and various age-related conditions. NAD+ serves as a crucial substrate for sirtuins (SIRT1-7) and poly(ADP-ribose) polymerase (PARP) enzymes that regulate cellular longevity, stress adaptation, and DNA repair mechanisms.

Overview

While NAD+ itself is poorly absorbed orally, precursor compounds including Nicotinamide Riboside (NR) and Nicotinamide Mononucleotide (NMN) effectively increase NAD+ levels via salvage pathways.

Clinical trials demonstrate NR/NMN supplementation (250-1000mg daily) safely elevates blood NAD+ levels, with observed improvements in mitochondrial function, insulin sensitivity, muscle performance, and cardiovascular markers.

However, experts emphasize there is no conclusive evidence that NAD+ supplementation extends human lifespan despite cellular benefits.

Common administration methods include oral supplementation (NR/NMN), IV infusions (500-1500mg, 2-4 hours), and subcutaneous injections (50-100mg weekly).

Side effects are generally mild and transient, including nausea, flushing, headache, and GI discomfort.

Potential concerns include unknown long-term safety profile, theoretical tumorigenesis risk (unproven in humans), and significant cost ($1000+ for IV sessions).

NAD+ restoration represents a promising but still investigational approach to cellular regenerative medicine, requiring more robust long-term human clinical trials to establish definitive therapeutic applications and longevity benefits.

Mechanism of action

Boosts cellular energy production and DNA repair. Activates longevity enzymes. Improves metabolism and mitochondrial health. Cellular benefits proven, human longevity unproven.

Reported effects

Effects reported in the literature and from preclinical models include:

• Oral nicotinamide, an NAD+ precursor, showed chemopreventive activity in high-risk patients with previous non-melanoma skin cancer by reducing new squamous cell carcinomas and actinic keratoses during active treatment. ^[3] Anecdotal
• Topical nicotinamide consistently improved wrinkles, texture irregularities, pigmentation, and skin barrier function in clinical studies. ^[3] Anecdotal
• Short-term intravenous NAD+ or NMN was associated with transient increases in circulating NAD+ levels in small uncontrolled human studies, though efficacy and long-term safety remain unestablished. ^[5] Anecdotal
• Human studies of NAD+ precursors in older adults showed potential but inconsistent benefits for mitochondrial efficiency, cellular stress responses, and cognitive performance. ^[2] Anecdotal
• Nicotinamide and NAD+ enhanced mitochondrial function and cognitive resilience in preclinical studies relevant to Alzheimer's disease. ^[1] Preclinical
• Nicotinamide protected retinal ganglion cells in preclinical glaucoma research by supporting NAD levels and cellular bioenergetics. ^[4] Preclinical

Evidence grades: FDA approvedApproved (non-US)Phase IIIPhase IIPhase IPreclinicalAnecdotal

Dosage and administration

Oral NMN

• Beginner: 250mg daily on empty stomach
• Intermediate: 500-600mg daily, split into 2 doses
• Advanced: 900-1200mg daily for intensive protocols

Oral NR

• Beginner: 100-300mg daily
• Standard: 500mg daily (most studied dose)
• Advanced: 1000-2000mg daily for therapeutic goals

IV Infusion

• Standard: 500-750mg per session over 2-4 hours
• Intensive: 1000-1500mg per session

Subcutaneous Injection

• Start: 50mg (0.5mL) once weekly for 4 weeks
• Maintenance: 100mg (1mL) 1-3x weekly

Timing

• Take oral forms morning/early afternoon (may affect sleep if taken late)

Frequency

• Oral daily, IV weekly to monthly, injections 1-3x weekly

Natty status

NAD+ is generally regarded as compatible with the natty designation, particularly when used for therapeutic healing purposes. Opinions vary across natural bodybuilding federations, and athletes who compete should consult the rulebook of their respective sanctioning body.^[6]

Research

The peptide has been the subject of 66 studies and reference works collected on this site. Additional bibliography is in § External links below.

Related compounds

Other peptides in this catalogue with overlapping mechanisms or status:

Frequently asked questions

What is NAD+?

Essential cellular coenzyme for energy, DNA repair, and aging. Precursors (NMN/NR) or IV boost NAD+ levels. Cellular benefits proven, longevity unproven.

What is NAD+ used for?

NAD+ (Nicotinamide adenine dinucleotide) is used for energy, healthy aging, and skin care. Small human studies found that its building blocks raise blood NAD+ levels, with mixed results for cell energy and thinking. A longer life is not proven.

How does NAD+ work?

A molecule every cell needs to make energy and to repair DNA. Levels fall with age. It is taken as capsules of its building blocks NMN or NR, as a drip into a vein, or as a shot under the skin.

Is NAD+ natty?

NAD+ is generally regarded as compatible with natural bodybuilding. Most sanctioning bodies do not prohibit its therapeutic use, though rules vary by federation.

Is NAD+ banned by WADA?

No. NAD+ is permitted under World Anti-Doping Agency (WADA) rules. Intravenous infusion above the volume limit of WADA method M2.2 is restricted whatever is infused, and the list is revised every year, so check the current edition before competing.

How is NAD+ administered?

NAD+ is typically administered via: oral supplementation, intravenous infusion, subcutaneous injection. Dosage and administration protocols vary; see the Dosage section for details.

References

1. ^ From DNA repair to neurodegeneration: PARP1 mechanisms and inhibitor strategies in Alzheimer's disease. Recent review
2. ^ Targeted Supplementation and Nutritional Strategies for Healthy Aging: A Review of Physiological and Molecular Benefits. Recent review
3. ^ a b Skin Cancer Prevention and Antiaging: Role of Nicotinamide. Recent review
4. ^ Prospects for Neuroprotective Therapies in Glaucoma: Drug Targets and Emerging Clinical Strategies. Recent review
5. ^ Narrative review of intravenous NAD(+) and NAD(+) precursors in wellness and translational medicine. Recent review
6. ^ a b World Anti-Doping Agency. (2026). Prohibited List 2026.

External links

• Wikipedia article
• Role of NAD+ in regenerative medicine
• Central role in aging prevention
• NMN safety and efficacy in healthy adults
• Chronic NR supplementation in older adults
• NR-SAFE high dose safety trial in Parkinson's
• NAD+ repletion improves mitochondrial function
• Insights into SIRT2 inhibition from machine learning-assisted multi-level screening of the NCI database.
• H(2)-dependent reduction of rubredoxin by FrhAGB hydrogenase in Thermococcus onnurineus NA1.
• Repurposing Syrosingopine for Cancer Therapy: Lactate Trapping and ISR Sensitization as Metabolic Vulnerabilities.
• Clinical and biochemical footprints of inherited cofactor disorders.
• Epigenetic Information Loss and Chronosenescence in Liver Aging: From Molecular Mechanisms to Therapeutic Interventions.
• Cofactor Engineering Strategy of Food-Grade Microorganisms: Redox Homeostasis Regulation and Functional Components Biofortification.
• From autophagy-lysosomal deficits to neurodegeneration in Niemann-Pick type C1 disease: implications for age-related neurodegenerative disorders.
• Nicotinamide N-methyltransferase in Inflammatory bowel disease: Multidimensional Regulation, Mechanistic Insights, and Therapeutic Potential.
• MicroRNA-SIRT1 crosstalk in liver diseases: molecular regulation of metabolism, inflammation, and cell survival.
• Nutritional Regulation of Ovarian Bioenergetics: Implications for Reproductive Aging and Female Infertility.
• The SIRT1/STAT3 axis as a central regulator of immune, inflammatory, and lipid metabolic dysregulation in rheumatoid arthritis: therapeutic implications.
• Mesenchymal Stromal Cell-Derived Extracellular Vesicles Mediate Mitochondrial Delivery in Injury: Mechanistic Insights, Evidentiary Tiers, and Translational Challenges.
• Nicotinamide N-methyltransferase as a stress-responsive metabolic-epigenetic regulator of tubular senescence in chronic kidney disease.
• Metabolic reprogramming of myeloid cells in cancer: from lactate-NAMPT axis to AI-guided therapeutics.
• Mitochondrial quality control in human ageing and longevity.
• The myofascial rheostat: hyaluronan molecular weight dynamics and purinergic signalling as a physiological feedback system.
• Acetylation as a dynamic regulatory interface between plant stress memory, cross-tolerance, and crop resilience design.
• Cell-Type-Specific Calibration of Mitochondrial Ubiquitination in Stem Cell Fate Decisions.
• Mitochondrial dysfunction and cellular senescence drive accelerated gestational aging in spontaneous preterm birth: a narrative review.
• SIRT5/7 desuccinylation in cancer: linking metabolism, immunity, and drug resistance.
• Network Destabilization in Aging: Mitochondrial Dysfunction, Nutrient Sensing, and Chronic Inflammation as Interconnected Drivers.
• The mitochondrial logic of inflammaging: how energy imbalance drives fibroblast SASP and tissue-specific aging.
• Factors Determining Sirtuin-1 Target Engagement.
• Navigating the Metabolic-Genomic Paradigm: Mitochondrial Reprogramming as a Driver of Cancer Plasticity.
• SIRT1 as a Key Regulator in Rheumatic Diseases: Integrating Molecular Insights with Traditional Chinese Medicine Approaches.
• Metabolic control of renal cell fate in kidney disease: nutrient rewiring, senescence and fibrosis.
• Decoding Context-Dependent Sirtuin Pharmacology in Cancer: Metabolic-Epigenetic Switches and Precision Therapeutic Targeting.
• Mechanistic intersections of empagliflozin and nebivolol in aging-associated redox and inflammatory pathways.
• Boron as a Context-Dependent System-Level Modulator: Mechanisms and Implications in Chronic Diseases.
• Metabolic therapeutic targets in Alzheimer's disease.
• Research progress on metabolic abnormalities in myocardial hypertrophy.
• Bidirectional regulation between mitochondrial metabolic reprogramming and epigenetic modifications in renal tubular epithelial cell injury of diabetic kidney disease.
• Deciphering the role of sirtuins in cancer immunoregulation through molecular cross-talk and docking-based interaction.
• NAD(+) supplementation and PARP inhibition following spinal cord injury in mice: Hurdles and considerations for therapeutic use.
• The organellar biology of aging: A mitochondrial vantage.
• Advances in sirtuin research in lung diseases (Review).
• Oxidative stress-driven epigenetic reprogramming of immune cells in COPD: from epitranscriptomic and metabolic crosstalk to treatable traits.
• [NAD kinases (NADKs) family proteins: Advances in metabolic regulation mechanisms and disease associations].
• Suppress, Stimulate, or Steer: Dioxygen Activation by Flavoenzymes and Their Oxygenation Strategies.
• Molecular mechanisms of traditional Chinese medicine in skin aging: a narrative review.
• Mitochondrial Proteostasis Links Diabetes and Sarcopenia: Cross-Scale Convergence from Experimental Models to Human Multi-Omics.
• Alcohol-induced dysregulation of tau and acetylation pathways in the pathogenesis of Alzheimer's disease.
• Molecular mechanisms of blood-brain barrier dysfunction caused by obesity: pathophysiological understandings and treatment targets.
• Mitochondrial homeostasis in musculoskeletal diseases: From pathogenic mechanisms to precision therapies.
• The Dimorphic Brain in Ischemic Stroke: How Sex and Age Shape Molecular Pathophysiology and Therapeutic Responsiveness.
• Cardiac fibrosis: mechanistic insights and translational advances.
• NAD(+)-sirtuin-mitochondrial quality control in lens epithelial cells: a candidate modulatory network in crystalline lens aging.
• Mitochondrial Modulation as a Therapeutic Entry Point in Neurodegeneration.
• Anti-phage defense systems in bacteria: molecular mechanisms and their role in shaping phage therapy strategies.
• Sensitizing Colorectal Cancer to PARP Inhibitors: Biomarkers, Mechanisms, and Combination Strategies.
• Therapeutic Timing at Mitochondrial Redox-Autophagy-Mitophagy Checkpoints in Age-Related Hearing Loss.
• From oxygen detoxification to peroxide supply: Microbial NADH oxidases in redox physiology and H₂O₂-coupled biocatalysis.
• NAD and NADPH in Neuronal Injury and Degeneration.
• Role of sirtuin 7 (SIRT7) in hepatic physiology and pathophysiology: mechanism, prospective and therapeutic potential.
• 500mg NAD+ — commercial
• NAD+ + Spray Kit — commercial
• Bacteriostatic Water Reconstitution Solution 10ml — commercial