💡Should I take NADH?
C21H28N7O14P2) and is highly water-soluble but chemically unstable to oxidation. Oral bioavailability of intact NADH is likely low (<10%, not well quantified), so modern clinical research increasingly focuses on NAD+ precursors (nicotinamide riboside, NMN). This encyclopedic article provides a complete, evidence-focused synthesis of chemistry, pharmacokinetics, mechanisms, historical context, clinical uses, dosing, safety, interactions, quality criteria and practical guidance for US consumers and clinicians, and it identifies where up-to-date PubMed/DOI verification is still recommended.🎯Key Takeaways
- ✓NADH is the reduced electron-carrying form of NAD+ with molecular weight ≈ 664.44 g·mol⁻¹ and is central to mitochondrial ATP production.
- ✓Oral intact NADH likely has limited bioavailability (<10%) and is chemically unstable without specialized stabilization.
- ✓Most clinical evidence for NADH is low-quality and limited to small trials; NAD+ precursors (NR, NMN) have stronger human trial data for raising cellular NAD+.
- ✓Typical supplement doses historically range from 5–20 mg/day; no FDA/NIH RDA exists for NADH.
- ✓Select high-quality NADH products with CoA, cGMP manufacturing, oxygen-impermeable packaging and third-party testing; consult clinicians when on MAOIs, chemotherapy or antipsychotics.
Everything About NADH
🧬 What is NADH? Complete Identification
NADH is the reduced form of nicotinamide adenine dinucleotide and functions as a universal two-electron donor in cellular metabolism; its molar mass is approximately 664.44 g·mol⁻¹.
Medical definition: NADH (reduced nicotinamide adenine dinucleotide) is an endogenous redox cofactor participating in >300 dehydrogenase reactions and serving as a principal electron donor to mitochondrial Complex I, thereby supporting oxidative phosphorylation and ATP synthesis.
- Alternative names: NADH, β-Nicotinamide adenine dinucleotide (reduced), Coenzyme I (reduced), ENADA® (historical stabilized brand).
- Classification: endogenous redox cofactor; in supplements classed as a dietary ingredient (DSHEA).
- Chemical formula:
C21H28N7O14P2(reduced form). - Origin & production: endogenously synthesized via NAD+ biosynthetic and salvage pathways; industrial supplement-grade NADH is produced by chemical or biocatalytic routes and formulated as stabilized salts (e.g., disodium NADH) with antioxidant excipients and protective packaging to prevent oxidation.
📜 History and Discovery
The coenzyme system including NAD/NADH was first characterized in the early 20th century; pivotal findings date to 1906 and the 1930s–1940s enzymology era.
- Timeline highlights:
- 1906 — early fermentation studies implicated nicotinamide-containing factors (Harden era).
- 1930s — isolation/characterization of diphosphopyridine nucleotide (DPN), later NAD.
- 1936–1960s — enzymology established NAD+/NADH roles in glycolysis and oxidative phosphorylation.
- 1980s–1990s — commercial stabilized NADH supplements introduced; small clinical trials for fatigue and Parkinson’s disease were conducted.
- 2000s–2020s — research emphasis shifted to NAD+ precursors (NR, NMN) and the NAD+/NADH ratio as a regulator of aging and cellular signaling.
- Discoverers & context: Early pioneers included Arthur Harden and later Hans von Euler-Chelpin; enzymology matured with work revealing NAD as an essential cofactor for dehydrogenases.
- Traditional vs modern use: isolated NADH has no ethnomedicinal history; oral NADH supplementation is a modern therapeutic/nutraceutical practice targeting energy and cognitive symptoms.
- Fascinating facts:
- NAD biosynthesis can come from dietary niacin (vitamin B3) or tryptophan-derived pathways; humans cannot synthesize niacin de novo in insufficient tryptophan states.
- Compartmentalization (cytosol vs mitochondria vs nucleus) makes NAD/NADH biology highly context-dependent and analytically challenging.
⚗️ Chemistry and Biochemistry
NADH is a dinucleotide comprising an adenine nucleotide (AMP) and a reduced nicotinamide mononucleotide; reduction adds one hydrogen to the nicotinamide ring.
- Molecular structure: two nucleotides linked by pyrophosphate, nicotinamide ring is in the 1,4-dihydropyridine reduced state.
- Physicochemical properties:
- Appearance: white to off-white crystalline powder (salt-dependent).
- Solubility: highly water-soluble; poor solubility in lipophilic solvents.
- LogP: strongly negative (hydrophilic).
- Stability: readily oxidized to NAD+ by O2, light and heat; stabilized formulations required for shelf life.
- Dosage forms:
- Tablets (stabilized NADH) — most common consumer form.
- Capsules (enteric-coated variants) — marketed to protect from gastric acid.
- Powder (bulk salts) — susceptible to oxidation.
- Liquid/sublingual — rare due to poor stability and uncertain mucosal absorption.
- Storage: manufacturers recommend cool, dry, oxygen-limited packaging; raw material often refrigerated (2–8 °C) to limit oxidation.
💊 Pharmacokinetics: The Journey in Your Body
Orally administered intact NADH has limited and poorly quantified systemic bioavailability; most gut-available NADH is metabolized to smaller precursors.
Absorption and Bioavailability
Absorption: intact NADH is large and hydrophilic and is unlikely to cross enterocyte membranes by passive diffusion; absorption is thought to occur mainly via extracellular enzymatic conversion to nicotinamide or NR/NMN precursors, which are taken up and reconverted intracellularly.
- Influencing factors:
- Formulation/stabilization (enteric coating, microencapsulation).
- Gastrointestinal enzymes and microbiota.
- Oxygen exposure and gastric pH (acidic stomach may help but also enzymatic cleavage occurs).
- Estimated bioavailability: intact oral NADH is likely <10% (qualitative estimate; quantitative human data lacking).
Distribution and Metabolism
Distribution: intracellular NAD pools are compartmentalized (cytosol vs mitochondria vs nucleus); intact NADH’s apparent volume of distribution is not well established because tissue NAD status largely depends on intracellular synthesis from precursors.
- Metabolism: extracellular ectoenzymes such as CD38/CD157 and nucleotidases cleave NAD(H) to nicotinamide, NMN and ADP-ribose; intracellular salvage enzymes (NAMPT, NMNAT) rebuild NAD+ from nicotinamide/NMN.
Elimination
Elimination routes: metabolites (nicotinamide, methylated derivatives) are renally cleared; intact NADH renal excretion is minimal.
- Half-life: plasma half-life of intact NADH is not well-defined; NAD metabolite clearance typically occurs over hours to a day.
🔬 Molecular Mechanisms of Action
NADH’s primary biochemical role is to deliver reducing equivalents to Complex I of the mitochondrial electron transport chain, directly influencing ATP production.
- Cellular targets: mitochondrial Complex I, dehydrogenases (lactate dehydrogenase, malate dehydrogenase), and indirectly NAD+-dependent enzymes (sirtuins) via changes in NAD+/NADH ratio.
- Signaling pathways: redox-sensitive transcriptional programs (PGC-1α mitochondrial biogenesis pathways; HIF-1α stabilization under altered redox) are modulated indirectly by NAD+/NADH changes.
- Genetic effects: altered NAD+ availability can affect sirtuin-mediated deacetylation of transcriptional regulators, modifying expression of mitochondrial and metabolic genes.
- Molecular synergies: plausible complementarity with CoQ10, L-carnitine and antioxidants to support electron transport and limit ROS; caution when combining with NAD+-raising precursors due to opposing redox aims.
✨ Science-Backed Benefits
Clinical evidence for oral NADH is limited and heterogeneous; most claims are supported by small trials or mechanistic plausibility rather than large RCTs.
🎯 Reduction of subjective fatigue (CFS / idiopathic fatigue)
Evidence Level: low–medium
Physiological rationale: supplying reducing equivalents could improve mitochondrial ATP production in tissues with bioenergetic impairment, reducing perceived fatigue.
Molecular mechanism: NADH donates electrons to Complex I supporting oxidative phosphorylation and ATP synthesis.
Target population: selected patients with chronic fatigue syndrome or idiopathic fatigue.
Onset time: subjective effects reported within 1–4 weeks in small studies.
Clinical Study: Small randomized and open-label trials historically reported symptom improvement in subsets of patients; up-to-date PMIDs/DOIs require live PubMed verification before formal citation. [Request live PubMed search to retrieve exact study IDs and quantitative results]
🎯 Cognitive function / mental clarity
Evidence Level: low
Physiological rationale: neuronal ATP availability supports synaptic function and attention; NADH may indirectly influence neurotransmitter synthesis.
Onset time: variable; some reports describe weeks to months.
Clinical Study: Small pilot studies report subjective cognitive benefits in older adults. Exact trial citations and quantitative effect sizes require PubMed/DOI lookup.
🎯 Adjunct support in Parkinson’s disease (motor function)
Evidence Level: low
Rationale: proposed support for dopaminergic neurons via improved energy metabolism and dopamine biosynthesis.
Target population: adjunctive use in PD patients; not disease-modifying therapy.
Clinical Study: Older small trials suggested modest symptomatic improvements in some patients; specific study PMIDs/DOIs must be validated by live search.
🎯 Exercise recovery & perceived exertion
Evidence Level: low
Rationale: supporting mitochondrial ATP resynthesis may aid recovery; evidence remains scarce.
Clinical Study: Limited human performance trials exist; request live literature retrieval for exact numeric outcomes.
🎯 Antioxidant sparing / redox homeostasis
Evidence Level: low
Rationale: modulating intracellular redox balance can influence ROS production and antioxidant systems; effects are complex—excess NADH can increase ROS under certain conditions.
Clinical Study: Mostly preclinical and mechanistic data; human clinical evidence minimal and requires updated PubMed search.
🎯 Mitochondrial support in metabolic disorders (experimental)
Evidence Level: low
Rationale: in preclinical models, modulating NAD pools influences mitochondrial respiration and biogenesis; human translation remains limited.
Clinical Study: Preclinical studies consistent; human RCTs lacking—see live PubMed search option.
🎯 Mood and depressive symptoms (adjunctive)
Evidence Level: low
Rationale: energy metabolism in mood circuits and monoamine synthesis support potential benefit.
Clinical Study: Small adjunctive trials and case series reported variable effects; detailed citations need PubMed verification.
🎯 Short-term alertness / daytime energy
Evidence Level: low
Rationale: transient increase in cellular energy may increase subjective alertness in some users.
Clinical Study: Anecdotal and small subjective trials; request literature pull for precise results.
📊 Current Research (2020-2026)
Most contemporary human research from 2020–2026 focuses on NAD+ precursors (NR, NMN); high-quality RCTs of oral intact NADH in this period are scarce.
Because up-to-date bibliographic verification (PubMed/DOI) is required for exact citations, I can perform a live literature search to retrieve recent RCTs, PMIDs and DOIs and extract quantitative results on request.
Request: Authorize a live PubMed/DOI search and I will return a validated list of trials (2020–2026) with PMIDs/DOIs and extracted numerical outcomes.
💊 Optimal Dosage and Usage
There is no FDA or NIH/ODS recommended RDA for NADH; common supplement doses historically range from 5 mg to 20 mg/day.
Recommended Daily Dose (clinical practice / supplement market)
- Typical supplement range: 5–20 mg/day (many commercial products use 5–10 mg or 20 mg). Manufacturers occasionally market higher doses (up to 50–100 mg) but systematic safety/efficacy data for high doses are lacking.
- Therapeutic/empirical ranges: fatigue/cognition often studied at 10–20 mg/day in small trials.
Timing
- Optimal time: morning or early daytime for energy/alertness effects; avoid late-evening dosing if increased alertness/insomnia occurs.
- With food: no definitive requirement; taking with food may protect formulation and improve tolerability. If combined with lipophilic cofactors (CoQ10), take with a meal containing fat for CoQ10 absorption.
Forms and Bioavailability
- Intact NADH (stabilized tablets): likely low intact bioavailability (<10%, not well quantified).
- Enteric/microencapsulated NADH: potentially better preservation through gastric passage; evidence for improved systemic uptake of intact NADH is limited.
- Precursors (NR/NMN): better-documented ability to raise intracellular NAD+ pools; generally preferred in current research for NAD augmentation.
🤝 Synergies and Combinations
NADH may be combined with mitochondrial cofactors (CoQ10, L-carnitine) and antioxidants for theoretical synergistic benefit; evidence is largely mechanistic or anecdotal.
- CoQ10: complementary electron transport roles; common empirical stack: CoQ10 100 mg + NADH 10–20 mg/day.
- L-carnitine: supports fatty acid transport; may complement NADH in energy metabolism.
- Antioxidants (vitamin C/E): may stabilize formulations and reduce oxidative stress during increased electron transport.
- NR/NMN: mixing NADH with NAD+ precursors could be mechanistically counterproductive; consult research protocols before combining.
⚠️ Safety and Side Effects
NADH at common supplement doses (5–20 mg/day) is generally well tolerated in small studies; large-scale safety data are absent.
Side Effect Profile
- Gastrointestinal upset (nausea, abdominal discomfort) — uncommon.
- Insomnia or increased alertness — uncommon.
- Headache — uncommon.
- Allergic reactions — rare.
Overdose
No well-defined human overdose threshold exists; management is symptomatic and supportive.
- Hypothetical overdose symptoms: severe nausea/vomiting, palpitations, agitation.
- For suspected overdose: discontinue product, provide supportive care; contact poison control / emergency services for guidance.
💊 Drug Interactions
NADH has theoretical pharmacodynamic interactions with several drug classes; most interactions are precautionary and based on plausible mechanisms rather than robust clinical data.
⚕️ Monoamine oxidase inhibitors (MAOIs)
- Medications: phenelzine (Nardil), tranylcypromine (Parnate), selegiline (Emsam).
- Interaction type: theoretical pharmacodynamic increase in monoamine activity.
- Severity: medium (theoretical)
- Recommendation: avoid or use only under prescriber supervision; monitor for hypertensive or serotonergic symptoms.
⚕️ Antipsychotics (dopamine antagonists)
- Medications: haloperidol (Haldol), risperidone (Risperdal), quetiapine (Seroquel).
- Interaction type: pharmacodynamic opposition/attenuation.
- Severity: low–medium
- Recommendation: consult psychiatry before initiating NADH in patients on antipsychotics.
⚕️ Stimulants (CNS stimulants)
- Medications: methylphenidate (Ritalin), amphetamine salts (Adderall).
- Interaction type: additive stimulant/alertness effects.
- Severity: low–medium
- Recommendation: monitor for insomnia, tachycardia; prefer morning dosing.
⚕️ Chemotherapy agents (oxidative stress–related)
- Medications: doxorubicin (Adriamycin), cisplatin.
- Interaction type: theoretical modulation of redox-dependent efficacy.
- Severity: medium
- Recommendation: avoid NADH during active chemotherapy without oncologist approval.
⚕️ Statins
- Medications: atorvastatin (Lipitor), simvastatin (Zocor).
- Interaction type: potential adjunctive support for statin-associated myalgia (anecdotal).
- Severity: low
- Recommendation: discuss with prescriber if using NADH to manage muscle symptoms; evidence limited.
🚫 Contraindications
Absolute contraindication: known hypersensitivity to NADH or formulation excipients.
Relative Contraindications
- Concurrent chemotherapy without oncology approval.
- Concomitant MAOI therapy (use caution).
- Bipolar disorder (theoretical mood destabilization).
Special Populations
- Pregnancy: insufficient safety data; avoid unless benefit justifies potential risk.
- Breastfeeding: unknown milk transfer; avoid unless supervised.
- Children: pediatric dosing not established; avoid routine use without specialist oversight.
- Elderly: start low (e.g., 5–10 mg/day) and monitor due to polypharmacy and comorbidities.
🔄 Comparison with Alternatives
NADH supplies the reduced cofactor directly but has poorer demonstrated oral bioavailability and less robust human trial evidence than NAD+ precursors such as nicotinamide riboside (NR) and nicotinamide mononucleotide (NMN).
- Niacin / nicotinamide (vitamin B3): dietary precursors with established safety and essential nutrient status.
- NR / NMN: better-documented increases in tissue NAD+ in human trials; preferred in modern NAD-boosting research.
✅ Quality Criteria and Product Selection (US Market)
Choose products with a Certificate of Analysis (CoA), cGMP manufacturing, independent third-party testing (NSF, USP, ConsumerLab) and validated stability data showing NADH content and oxidation state.
- Check CoA for NADH assay and NADH:NAD+ ratio at manufacture and end-of-shelf-life.
- Prefer oxygen-impermeable blister packs or single-dose sealed units.
- Avoid products without expiry date, CoA or stability claims.
📝 Practical Tips
- Start with a low dose (5–10 mg/day) and titrate to effect, up to commonly marketed 20 mg/day if tolerated.
- Take in the morning with food; combine with CoQ10 if stacking for mitochondrial support.
- Store in cool, dark, dry conditions; refrigerate bulk powders if recommended by manufacturer.
- If you take prescription medications (especially MAOIs, antipsychotics, chemotherapy), consult your prescriber before use.
🎯 Conclusion: Who Should Take NADH?
NADH may be considered for select individuals seeking symptomatic support for fatigue, mild cognitive complaints or as an adjunctive mitochondrial support supplement, but evidence is limited and quality varies — prefer NAD+ precursor strategies (NR/NMN) when the clinical goal is robustly raising intracellular NAD+.
If you want evidence-grade citations (PMIDs/DOIs) for the historical clinical trials and all assertions above, please authorize a live PubMed/DOI literature retrieval and I will return full validated citations, study-level quantitative results and any more recent RCTs (2020–2026).
Note on citations: This article synthesizes established biochemical facts and the consolidated product- and trial-level observations summarized in the supplied dataset. Where precise PMIDs/DOIs and up-to-date trial-level data are required for clinical decision-making or publication, a live literature search is recommended and I can provide a validated bibliography on request.
Science-Backed Benefits
Reduction of subjective fatigue (chronic fatigue syndrome / idiopathic fatigue)
◯ Limited EvidenceSupplying reduced electron carriers or supporting redox state could theoretically increase ATP generation in metabolically compromised tissues, reducing perceived effort and fatigue.
Support for cognitive function / mental clarity (mild cognitive complaints)
◯ Limited EvidenceImproved cellular energy (ATP) in neurons may support cognitive processing speed and attention; redox balance can influence neuronal resilience.
Adjunct symptomatic support in Parkinson's disease (motor function)
◯ Limited EvidenceBy supporting neuronal energy metabolism and potentially modulating dopamine synthesis pathways, NADH was hypothesized to support dopaminergic neuron function and reduce motor symptoms.
Support for exercise recovery and perceived exertion
◯ Limited EvidenceIf NADH increases cellular capacity for ATP production, theoretically this could enhance recovery and reduce perceived exertion by promoting efficient energy metabolism.
Potential antioxidant sparing effect (redox homeostasis)
◯ Limited EvidenceBy influencing intracellular redox state, NADH/NAD+ balance can affect production of reactive oxygen species (ROS) and activity of antioxidant enzyme systems.
Support for mitochondrial function in metabolic disorders (experimental)
◯ Limited EvidenceMitochondrial dysfunction may be partially alleviated by modulation of the NADH/NAD+ ratio to favor effective electron transport and ATP generation.
Support for mood / depressive symptoms (adjunctive)
✓ Strong EvidenceEnergy metabolism in mood-regulating brain regions and effects on neurotransmitter synthesis could theoretically impact mood.
Short-term support for alertness / daytime energy
◯ Limited EvidenceBy supporting ATP production, NADH may acutely affect cellular energy status and subjective alertness.
📋 Basic Information
Classification
other — endogenous redox cofactor; nutraceutical / dietary supplement (reduced NAD) — redox cofactor,bioenergetic modulator,mitochondrial function supporter (claimed)
Active Compounds
- • Tablets (stabilized NADH)
- • Capsules (enteric or standard)
- • Powder (bulk NADH salts)
- • Liquid formulations (rare)
- • Sublingual lozenges (marketing claims)
Alternative Names
Origin & History
There is no traditional (ethnomedicinal) use of isolated NADH as a botanical; rather, nicotinamide-containing compounds (vitamin B3 forms: niacin, nicotinamide) have a long history. NADH use as an oral supplement is modern (20th century onward) targeting 'energy', chronic fatigue, cognition, and Parkinson's symptoms.
🔬 Scientific Foundations
⚡ Mechanisms of Action
NADH acts as an electron donor to mitochondrial Complex I (NADH:ubiquinone oxidoreductase) fueling oxidative phosphorylation and ATP production., NADH/NAD+ ratio acts as a metabolic redox signal influencing multiple enzymes and signaling pathways (e.g., sirtuins indirectly via NAD+ availability).
📊 Bioavailability
Quantitative percent bioavailability of intact oral NADH is not well-established in humans and is likely low (single-digit % or lower for intact molecule). Most bioavailable increase in tissue NAD comes from precursors (nicotinamide, NR, NMN).
🔄 Metabolism
Extracellular ectoenzymes (e.g., CD38, CD157, CD73) that metabolize NAD+ and NADH to nicotinamide, ADP-ribose, cyclic ADPR and other fragments., Intracellular enzymes: nicotinamide phosphoribosyltransferase (NAMPT) in salvage pathway (converts nicotinamide to NMN), NMN adenylyltransferase (NMNAT) convert NMN to NAD+, dehydrogenases change NAD+/NADH states., Not a major substrate for classical CYP450 oxidative metabolism because of polarity and size; hepatic metabolism mostly via hydrolases and salvage pathways.
💊 Available Forms
✨ Optimal Absorption
Dosage & Usage
💊Recommended Daily Dose
Typical Supplement Range: 5 mg to 20 mg for marketed NADH products (historical consumer products) up to some products marketing 50 mg; clinical trials historically have used doses from 5 mg to 20 mg daily. Note: manufacturers' product doses vary widely. High-dose clinical dosing data are limited. • Clinical Note: There is no FDA-established Recommended Dietary Allowance (RDA) or Dietary Reference Intake (DRI) for NADH; NAD is not supplied as an essential dietary vitamin when adequate niacin intake exists.
Therapeutic range: 5 mg/day (commonly marketed lower-end dose) – 100 mg/day has been used in isolated investigational settings, but systematic safety data at high doses are limited. Most consumer products ≤20 mg per dose.
⏰Timing
Morning or early daytime for energy/alertness effects; evening dosing may interfere with sleep in some due to increased alertness (individual variability). — With food: No definitive requirement; food may reduce gastric stress and can slow gastric emptying which might protect NADH from acid but the impact on bioavailability of intact NADH is unclear. — Timing chosen to align potential subjective energy effects with daytime activity and to reduce potential sleep disturbance.
🎯 Dose by Goal
NAD+ supplement shows early promise for long COVID fatigue and brain fog
2025-12-11A randomized trial tested high-dose nicotinamide riboside (NR), an NAD+ precursor, in long COVID patients with fatigue and brain fog. While primary cognitive scores showed no major group differences, participants taking NR for at least 10 weeks reported improvements in fatigue, sleep, mood, and executive function. The study suggests NR safely boosts NAD+ levels and may benefit some patients, pointing to potential therapies targeting cellular energy.
Promising Results With NAD Supplementation in Rare Diseases
2025This review highlights clinical trials using NR supplementation in rare diseases like Werner Syndrome and Ataxia-Telangiectasia, showing robust NAD+ increases, improved arterial stiffness, motor coordination, eye movements, and IgG levels. Long-term (2-year) NR use at 500 mg/day was safe with no serious adverse events. It emphasizes NR's high safety profile and clinical improvements in specific conditions.
Intravenous infusion of nicotinamide adenine dinucleotide (NAD⁺) and nicotinamide riboside (NR): A real-world comparison of safety and tolerability
2026A study compared IV NAD+ (500 mg) and NR (500 mg) over four days in participants, assessing tolerability and biomarkers. NAD+ IV caused moderate-severe GI symptoms, increased heart rate, and longer infusion times (97 min), while NR IV had milder tingling/cramping (37 min). Short-term metabolic changes varied, with NR reducing HbA1c and NAD+ lowering ALP and HDL-C; further studies needed.
NMN & NAD for Anti-Aging Just Changed
Highly RelevantExplores the science behind NAD precursors like NR for boosting NAD levels, including human trials on long COVID patients showing sharp NAD increases with supplementation.
NAD+, NMN and Longevity: What Human Studies Actually Show
Highly RelevantAnalyzes human studies on NAD+ boosters like NMN, contrasts with animal data, discusses oral vs. IV delivery, and weighs risks versus benefits for cellular energy and aging.
Can NAD+ Boosters Increase Lifespan and Healthspan?
Highly RelevantReviews remarkable effects of NAD+ boosters (NA, NAM, NR, NMN, NADH) in rodents across organ systems and evaluates translation to human healthspan and lifespan.
Safety & Drug Interactions
⚠️Possible Side Effects
- •Gastrointestinal upset (nausea, abdominal discomfort)
- •Insomnia or increased alertness
- •Headache
- •Allergic reaction (rare)
💊Drug Interactions
Pharmacodynamic (theoretical increase in monoamine neurotransmitter activity)
Pharmacodynamic (potential opposing effects on dopaminergic function)
Pharmacodynamic (additive stimulant/alertness effects)
Pharmacodynamic (theoretical)
Pharmacodynamic (potentially antagonistic or synergistic depending on mechanism)
Pharmacodynamic (support for mitochondrial energy may reduce statin-related myopathy in some anecdotal reports)
Metabolic/pharmacodynamic (theoretical)
🚫Contraindications
- •Known hypersensitivity or allergy to NADH product components/excipients
Important: This information does not replace medical advice. Always consult your physician before taking dietary supplements, especially if you take medications or have a health condition.
🏛️ Regulatory Positions
FDA (United States)
Food and Drug Administration
FDA treats NADH sold as a dietary supplement ingredient under DSHEA; FDA has not approved NADH as a drug for any indication. Claims on supplement labeling must be limited to structure/function claims and must include the required FDA disclaimer if making nutrient claims. Any disease claims would classify the product as a drug.
NIH / ODS (United States)
National Institutes of Health – Office of Dietary Supplements
NIH/NCCIH does not endorse NADH for any specific therapeutic indication. NIH-funded research focuses more on NAD+ biology and precursors (NR, NMN).
⚠️ Warnings & Notices
- •Products marketed with unproven disease treatment or cure claims are noncompliant with FDA regulations—exercise caution.
- •Lack of standardized dosing and limited high-quality clinical trial evidence for most claimed benefits; consumers should consult healthcare providers, especially with comorbidities or prescription medications.
DSHEA Status
NADH marketed as a dietary supplement ingredient is generally considered a dietary ingredient under DSHEA; if introduced after 1994 manufacturers may be required to submit a New Dietary Ingredient notification (NDI) to FDA depending on history of use in the US.
FDA Disclaimer: These statements have not been evaluated by the Food and Drug Administration. Dietary supplements are not intended to diagnose, treat, cure, or prevent any disease.
🇺🇸 US Market
Usage Statistics
No contemporary, authoritative nationwide survey quantifying number of Americans using NADH specifically. NAD-related supplementation market (including NAD+ precursors and NADH) has grown in the anti-aging and wellness segments; precise user counts for NADH alone are not publicly tracked in national surveys (e.g., NHANES does not isolate NADH use).
Market Trends
From 2015 onwards there has been a sharp growth in interest in NAD biology and supplements. The market has shifted more strongly toward NAD+ precursors (NR, NMN) in scientific and commercial attention, though NADH products continue to be marketed for energy and cognitive support. Innovation focuses on bioavailability/stability and combination products with mitochondrial cofactors (CoQ10, carnitine).
Price Range (USD)
Budget: $15-25/month (often low-dose or multi-ingredient formulations); Mid: $25-50/month; Premium: $50-100+/month (stabilized/enteric-coated or combined stacks with CoQ10 or branded NR/NMN). Prices vary by dose, formulation and brand reputation.
Note: Prices and availability may vary. Compare multiple retailers and look for quality certifications (USP, NSF, ConsumerLab).
Frequently Asked Questions
⚕️Medical Disclaimer
This information is for educational purposes only and does not replace advice from a qualified physician or pharmacist. Always consult a healthcare provider before taking dietary supplements, especially if you are pregnant, nursing, taking medications, or have a health condition.
📚Scientific Sources
- [1] General biochemistry and pharmacology texts on NAD/NADH (e.g., Lehninger Principles of Biochemistry; Berg, Tymoczko & Stryer)
- [2] Regulatory information: FDA guidance on dietary supplements and DSHEA (https://www.fda.gov/food/dietary-supplements)
- [3] Reviews on NAD+ metabolism and NAD+ precursors (literature up to 2024) — recommended live PubMed search for latest primary studies
- [4] Manufacturer technical data sheets and stability specifications (varies by vendor)
- [5] Note_on_studies: A live PubMed/DOI literature search is recommended to populate the 'scientific_studies' section with validated 2020–2026 studies and exact PMIDs/DOIs and extracted numerical results.