NADH (Reduced Nicotinamide Adenine Dinucleotide) · Evidence-First Fact Sheet

Quick Summary

Most consumers who walk into an NAD+ conversation in 2026 have heard of NMN. Many have heard of NR. A growing few have heard of NMNH, the newer reduced precursor that biotech press has started circling. Very few mention NADH — and almost none realise that NADH is the molecule that all of those precursors are trying, indirectly, to top up. NADH is the reduced form of nicotinamide adenine dinucleotide: the same nicotinamide-adenine backbone as NAD+, but carrying a hydride. That single hydride is what makes NADH the actual electron donor at the inside of every mitochondrion — the molecule that starts the chain reaction that produces the cell's ATP. The precursors (NMN, NR, the newer NMNH) are upstream feedstock. NADH is the working tool.

NADH is also, by some distance, the most clinically tested oral NAD-family compound in humans. Stabilised oral NADH has been sold under the US DSHEA framework for roughly 25 years. The first randomised trial appeared in 1999 — about a decade before the first controlled human NMN trial. This page reconstructs what 35 years of published human and mechanistic research actually says about NADH, where the evidence is strongest (fatigue, jet-lag cognition), where it is suggestive but underpowered (Parkinson disease, Alzheimer disease), and where claims have outrun the data. This sub-page is part of the NAD+ precursor cluster hub.

1. What NADH Is — And Why "Reduced" Changes the Story

1.1 The molecule

Nicotinamide adenine dinucleotide exists in cells in two interconvertible forms: NAD+ (oxidised) and NADH (reduced, carrying two electrons and one proton as a hydride on the nicotinamide ring). Together with their phosphorylated cousins NADP+/NADPH, these four molecules are the dominant electron-shuttling currency of central metabolism. The molecular formula of NADH is C21H29N7O14P2 (molecular weight 665.4 g/mol; PubChem CID 439153). Structurally, NADH is identical to NAD+ except for one extra hydride at the 4-position of the nicotinamide ring, which converts the aromatic pyridinium to a non-aromatic 1,4-dihydropyridine — the reason NADH absorbs light at 340 nm and NAD+ does not.

That one hydride is the difference between a passive cofactor pool (NAD+) and an energy-charged electron carrier (NADH). Inside mitochondria, NADH directly donates two electrons to Complex I (NADH:ubiquinone oxidoreductase), starting the proton-pumping cascade that drives ATP synthesis at Complex V. In other words, NADH is not a precursor to anything. It is the molecule that delivers electrons to oxidative phosphorylation.

1.2 Why precursors exist if NADH is already the active form

If NADH is the operative electron donor, why does the entire NAD+ supplement field focus on precursors (NMN, NR) that have to be enzymatically converted up several steps before reaching the dinucleotide pool? The textbook answer (Ying 2008 Antioxidant and Redox Signaling PMID 18020963) comes down to bioavailability and pool dynamics. Whole intact dinucleotides are large, polar, and unstable in the gut. Precursors such as nicotinamide riboside or nicotinamide mononucleotide are smaller and more stable, exploit dedicated salvage transporters and kinases (NRK1/NRK2, NAMPT), and reassemble into the dinucleotide pool inside the cell. NADH, by contrast, has to be pharmaceutically stabilised — the enteric-coated formulation pioneered by the Birkmayer group in Vienna is the canonical solution — and is absorbed largely intact, with some hydrolysis-then-resynthesis at the enterocyte and hepatocyte level.

The practical consequence is that oral NADH and oral NMN/NR are not interchangeable strategies even at equivalent nicotinamide-equivalent doses. They differ in absorption pathway, tissue distribution, and probably also in which sub-pools (cytoplasmic, mitochondrial, nuclear) they end up raising. The often-repeated assumption that "all roads lead to the same NAD+ pool" is not supported by the bioavailability literature, and it is the conceptual backbone of every comparison below.

1.3 The Birkmayer stabilisation and the Enada line

The commercial existence of oral NADH as a supplement is owed almost entirely to Walther Birkmayer (1910 to 1996), a Viennese neurologist who first administered NADH parenterally to Parkinson disease patients in the late 1980s (Birkmayer W, Birkmayer JG, Vrecko K. Advances in Neurology 1990 PMID 2239495). His collaboration with Vrecko and others through the 1990s produced the mechanistic groundwork (Vrecko et al. 1993 J Neural Transm PMID 8101444; 1997 Biochim Biophys Acta PMID 9247090), and the enteric-coated stabilised oral formulation they developed became Enada/ENADA — the dosage form used in essentially every subsequent human randomised trial cited below. Enada has been on the US dietary-supplement market under DSHEA since the late 1990s.

2. Chronic Fatigue Syndrome — The Strongest Human Evidence Cluster

2.1 Forsyth 1999 — the foundational randomised trial

The single most influential human trial of oral NADH was published in February 1999 by Forsyth, Preuss, MacDowell, and colleagues in Annals of Allergy, Asthma and Immunology (Forsyth 1999 PMID 10071523). The study was a randomised, double-blind, placebo-controlled crossover trial in 26 adults meeting CDC criteria for chronic fatigue syndrome (CFS / ME-CFS). Each participant received 10 mg/day stabilised oral NADH or matching placebo for four weeks, followed by four weeks of washout and crossover. The primary outcome was a composite CFS symptom severity score.

Forsyth and colleagues reported that 31 percent of subjects experienced a clinically meaningful improvement on NADH versus 8 percent on placebo during the active-treatment period, a difference that was statistically significant despite the small sample. No serious adverse events were recorded; minor side effects (loss of appetite, mild dyspepsia) occurred at low rates and did not differ from placebo. The historical weight of this trial is hard to overstate. It was, for nearly a decade, the only placebo-controlled trial of NADH in any indication, and it established CFS as the de facto first-line clinical claim for stabilised oral NADH. But honesty about its limits matters as much as honesty about its result: n=26 is small, and its effect size has never been independently replicated in a similarly powered NADH-monotherapy study.

2.2 Santaella 2004 and the open-label follow-ups

In 2004, Santaella and colleagues published an open-label study of NADH in Puerto Rican CFS patients (cited in subsequent reviews). The most extensive review of NADH in CFS is Alegre, Rosés, Javierre et al. 2010 in Revista Clínica Española (Alegre 2010 PMID 20447621). The review consolidates the small body of NADH-in-CFS literature — Forsyth 1999, the parallel open-label cohorts, and the early dose-finding work — and concludes that stabilised oral NADH at 10 mg/day is a reasonable, low-risk option in fatigue conditions, with the most robust signal being subjective energy and mental clarity rather than objective biomarkers.

2.3 The CoQ10 + NADH combination work

The most active recent line of NADH-in-CFS research has come from Castro-Marrero and colleagues at Vall d'Hebron (Barcelona). Their angle: reframe the question as a combined mitochondrial-support strategy. CoQ10 donates electrons further down the chain at Complex III via the ubiquinol/ubiquinone shuttle; NADH donates them at Complex I. The two should be complementary. Their 2015 paper in Antioxidants and Redox Signaling (Castro-Marrero 2015 PMID 25386668) reported that 8 weeks of 200 mg/day CoQ10 plus 20 mg/day NADH reduced perceived fatigue (Fatigue Impact Scale) and improved several biochemical markers — mitochondrial membrane potential, ATP synthesis, oxidative-stress markers — versus placebo in 80 CFS patients. The same group followed up in 2021 (Castro-Marrero 2021 Nutrients PMID 34444817) with a larger 8-week RCT in 207 patients on the same combination. They again reported improvements in fatigue perception and health-related quality of life with a clean safety profile.

The honest caveat is that these are combination trials: the marginal contribution of NADH versus CoQ10 alone cannot be parsed from this design. What the combined-strategy programme does establish is that NADH at 10 to 20 mg/day, in combination with CoQ10, is well tolerated over multi-month exposures in symptomatic CFS populations — an important safety signal at the upper end of typical supplement doses.

2.4 What the CFS evidence actually supports

A reasonable summary verdict for oral NADH in CFS / ME-CFS is Grade B: limited but consistent positive randomised evidence. The mechanism is highly plausible (mitochondrial Complex I substrate delivery in a condition with documented mitochondrial dysfunction). Direct NADH-monotherapy randomised trial: one positive small study (Forsyth 1999, n=26). Combination randomised trials (NADH + CoQ10): two positive trials totalling around n≈287, plus open-label confirmation. Safety: excellent across 25-plus years and more than 25 ClinicalTrials.gov entries. That is sufficient to support structure-function language under DSHEA in the United States, with the standard disclaimer, but it is not sufficient for a disease claim, and certainly not sufficient for marketing language that frames NADH as a "treatment" for CFS.

3. Parkinson, Alzheimer, and Cognition — Older, Less Robust

3.1 The Birkmayer Parkinson programme (1989 to 1997)

The clinical history of NADH begins in Parkinson disease, not in CFS. Walther Birkmayer — drawing on NADH's role as the electron-donating cofactor for tetrahydrobiopterin (BH4) regeneration, and therefore as a cofactor in tyrosine hydroxylase-mediated L-dopa biosynthesis — reasoned that supplying NADH might stimulate endogenous dopamine production in the parkinsonian brain. The first large clinical reports were open-label cohort studies in the late 1980s, summarised in Birkmayer 1990 Adv Neurol (PMID 2239495). Subsequent mechanistic work in PC12 phaeochromocytoma cells confirmed that NADH stimulates endogenous dopamine biosynthesis by enhancing BH4 recycling (Vrecko 1993 J Neural Transm Park Dis Dement Sect PMID 8101444; Vrecko 1997 Biochim Biophys Acta PMID 9247090). These papers established that NADH does what biochemistry predicts it should do in cellular dopaminergic systems.

What they did not deliver is a modern randomised placebo-controlled trial in Parkinson disease. The Birkmayer human data are open-label, observational, and from a single research group. Despite repeated calls for confirmatory phase III work over the following two decades, no such trial was ever published. The honest 2026 verdict is that NADH for Parkinson disease is mechanistically grounded but clinically unproven, and any "treats Parkinson" framing should be considered out of bounds.

3.2 Demarin 2004 — the Alzheimer randomised trial

A more rigorously controlled study in Alzheimer was published in 2004: Demarin V, Podobnik SS, Storga-Tomic D et al. Drugs under Experimental and Clinical Research (Demarin 2004 PMID 15134388). It was a randomised, double-blind, placebo-controlled trial of stabilised oral NADH (ENADA, 10 mg/day) over six months in 26 patients with probable Alzheimer disease. The NADH group showed significant preservation of cognitive function on the Mattis Dementia Rating Scale subscales — verbal fluency and visual-constructional ability — versus placebo, with no detectable difference on activities of daily living. The trial was small, single-centre, and has never been independently replicated. Demarin 2004 is best read as a positive signal in a small randomised trial in a difficult indication — comparable in evidentiary weight to Forsyth 1999 in CFS, and similarly in need of confirmation.

3.3 Jet-lag cognitive performance (Birkmayer 2002)

A more interesting cognitive context for the healthy reader is acute cognitive impairment after jet lag. Birkmayer GD, Kay GG, Vürre E. Wiener Medizinische Wochenschrift 2002 (Birkmayer 2002 PMID 12385067) reported a randomised, double-blind, placebo-controlled study of stabilised oral NADH (ENADA, 20 mg) versus placebo in 35 transatlantic air travellers, with cognitive performance measured before departure and after arrival using the CogScreen-AE battery (the FAA-developed cognitive performance test). The NADH group showed statistically significant preservation of cognitive performance across multiple sub-domains — reaction time, sustained attention, vigilance — versus placebo, with effect sizes that were clinically meaningful for occupational performance. The jet-lag application is interesting because it captures acute cognitive demand on a healthy population, rather than chronic supplementation in disease.

3.4 What the cognitive evidence supports

Combining Demarin 2004 (Alzheimer, randomised n=26, positive) and Birkmayer 2002 (jet lag, randomised n=35, positive) yields a Grade C+ to B− verdict for cognitive support under careful framing: healthy-adult acute cognitive support during jet lag and high-cognitive-demand windows at B−; mild cognitive decline / Alzheimer at C+ (one positive small randomised trial, no replication); Parkinson disease at C (mechanistic plus open-label only, no controlled trial).

4. Athletic Performance — Strong Mechanism, Weak Human Translation

4.1 The mechanistic case

The case for NADH supporting athletic performance is, on paper, almost overdetermined. Skeletal-muscle ATP turnover during high-intensity exercise depends critically on mitochondrial NADH-driven oxidative phosphorylation. The NAD+/NADH ratio drops during exhaustive exercise. Lactate production rises precisely because cytoplasmic NADH cannot be reoxidised fast enough at Complex I. Supplying additional NADH ought, by simple substrate-pool logic, to support ATP regeneration and delay fatigue. The mechanistic literature broadly supports that view. Nadlinger K, Westerthaler W, Storga-Tomic D et al. Biochim Biophys Acta 2002 (Nadlinger 2002 PMID 12399028) showed that extracellular NADH is metabolised by erythrocytes in a way that correlates with intracellular ATP levels, biochemical support for the idea that exogenously delivered NADH can influence cellular energy charge. Ying W. Antioxidant and Redox Signaling 2008 (Ying 2008 PMID 18020963) is the standard comprehensive review of NAD+/NADH and NADP+/NADPH in cellular function. Yuan X, Liu Y, Bijonowski BM et al. Communications Biology 2020 (Yuan 2020 PMID 33319867) extended the redox-rejuvenation concept to senescent human mesenchymal stem cells, showing that manipulating the NAD+/NADH ratio reconfigures cellular metabolism and reverses several markers of senescence in vitro.

4.2 Why the human randomised translation is thin

Despite that mechanistic depth, dedicated NADH-in-exercise randomised trials in healthy athletes are conspicuously sparse. A PubMed search done during the preparation of this brief (26 May 2026) returned no large placebo-controlled trial of stabilised oral NADH monotherapy on VO2max, time-to-exhaustion, or sport-specific performance endpoints. What is available consists of small open-label cohorts, mechanistic correlational studies in trained athletes, and inferential extrapolations from the CFS fatigue literature. The honest verdict is therefore Grade C for athletic performance: strong mechanism, plausible bench-to-side translation, but no controlled human efficacy trial of sufficient size to support a quantitative claim.

4.3 What can responsibly be said

Under FDA DSHEA structure-function-claim framing and EFSA's general supplement positioning (no authorised health claim for NADH itself — see section 7), the most that can responsibly be said about NADH and athletic performance is that NADH is the direct electron donor at Complex I of the mitochondrial electron transport chain, that mitochondrial NADH availability is a known limiter of sustained oxidative ATP output, that mechanistic studies support a relationship between NADH availability, intracellular ATP, and metabolic recovery, and that direct human randomised evidence for performance enhancement is limited and inconclusive.

5. Who Might Find NADH Useful — Goal and Lifestyle Integration

5.1 For the longevity stack reader

The longevity-stack reader is typically a 35 to 60-year-old adult who is already taking one or more NAD+ precursors (NMN, NR) or considering them, and who wants to understand where NADH fits in. The honest framing for this reader: NADH is the terminal reduced cofactor that the precursor strategies are ultimately trying to influence. Whether direct supplementation with stabilised oral NADH at 5 to 10 mg/day adds to, substitutes for, or is redundant with NMN/NR supplementation has not been tested in any controlled human trial. The most defensible position is that NADH and the precursors are mechanistically complementary rather than equivalent. Yuan 2020 (PMID 33319867) is the closest available evidence for the healthspan framing: manipulating the NAD+/NADH ratio in senescent human mesenchymal stem cells reconfigures their metabolism and reverses several markers of senescence — a cell-line finding, not a human outcome.

5.2 For the cognitive support reader

The cognitive-support reader includes knowledge workers facing sustained cognitive load, shift workers and frequent travellers (where the high-stress and jet-lag profiles overlap), and older adults concerned about age-related cognitive change. The most directly relevant evidence is Birkmayer 2002 (PMID 12385067) — randomised, jet-lag cognitive performance preservation, n=35, positive — and Demarin 2004 (PMID 15134388) — randomised, Alzheimer disease cognitive preservation, n=26, positive. DSHEA-compliant structure-function language ("supports cognitive performance during demanding cognitive tasks") is defensible; disease-claim language ("treats cognitive decline") is not.

5.3 For the athletic performance reader

The athletic-performance reader has the largest evidence-mechanism gap in the NADH literature. The honest framing: NADH supplementation has a strong mechanistic rationale for athletic performance. It is the direct electron donor at mitochondrial Complex I, and Complex I throughput is a primary determinant of sustained oxidative ATP production. However, dedicated human randomised trials in trained athletes are not available as of 2026. Athletes interested in NADH should treat it as a mechanistically reasonable but empirically unproven adjunct — not as a substitute for established performance support (creatine, beta-alanine, sodium bicarbonate, evidence-supported carbohydrate strategies).

5.4 For the heart health reader

NADH is not a primary cardiometabolic intervention. The mitochondrial substrate-pool framing of NADH is relevant to cardiomyocyte energetics, and the CoQ10+NADH combination trials in CFS (Castro-Marrero 2015 PMID 25386668; Castro-Marrero 2021 PMID 34444817) provide indirect context. CoQ10 has a substantial cardiovascular literature of its own. The honest framing here is mechanism plus indirect evidence, not direct cardiovascular outcome data.

5.5 For the senior 60+ reader

The senior 60+ context combines the longevity-stack, cognitive-support, and heart-health threads above. The single best-quality evidence for this reader is the Demarin 2004 Alzheimer randomised trial (PMID 15134388), together with the safety record of stabilised oral NADH across 25-plus years of commercial availability and more than 25 ClinicalTrials.gov entries with no significant adverse signal. The safety profile does support cautious use in older adults; the efficacy profile does not yet support claims beyond DSHEA structure-function language.

5.6 For the high-stress lifestyle reader

The high-stress reader is essentially the cognitive-support reader observed over longer time horizons — sustained cognitive load, sleep disruption, and the metabolic correlates of chronic stress. Birkmayer 2002 (jet lag, PMID 12385067) is the most directly relevant evidence; the Castro-Marrero CFS trials (PMID 25386668, 34444817) provide context for sustained-fatigue conditions. The responsible framing is acute and sub-acute support for cognitive performance under demand, not a chronic stress treatment.

5.7 For the athletic performance lifestyle reader

For the lifestyle athlete (training 4 to 6 times per week, recreational competition, healthy adult), the section 4 mechanistic framing applies. The Yuan 2020 PMID 33319867 redox-rejuvenation finding in stem cells is interesting context for recovery-and-repair claims but is not human evidence and should not be quoted as one.

6. NADH vs the Precursors and the Novel Reduced NMNH

6.1 NADH vs NMN/NR

The headline point: NADH and the precursors have never been compared head-to-head in a human trial. Each has its own evidence base, its own intended cellular impact, and its own commercial history.

6.2 NADH (classical reduced) vs NMNH (novel reduced)

A more recent class, NMNH (reduced nicotinamide mononucleotide), has emerged in the preclinical literature as a hypothetically more efficient precursor. NMNH human evidence is currently non-existent — zero registered or published human RCTs as of 2026-05-26 (see the NMNH page). For a consumer or formulator deciding between "classical reduced (NADH)" and "novel reduced (NMNH)", the evidence-driven 2026 answer is classical NADH — not because it is mechanistically superior, but because it has 25 years of human safety data and modest-but-real randomised efficacy signals, whereas NMNH has none.

6.3 The honest combined-strategy framing

A combined-strategy framing (NADH + NMN/NR, or NADH + CoQ10 as in the Castro-Marrero work) is mechanistically defensible but evidentially under-tested in non-CFS populations. Consumers asking "should I take NADH and NMN together?" should be told that no controlled trial has been published, that both compounds have acceptable safety profiles at typical supplement doses, and that the combined-strategy hypothesis is reasonable but speculative.

7. Regulatory Status — United States, European Union, Brazil

7.1 United States · FDA · DSHEA

NADH is a legal dietary-supplement ingredient under DSHEA. Stabilised oral NADH formulations (Enada and equivalent products) have been continuously available to US consumers since the late 1990s. Standard DSHEA structure-function claims are permitted with the FDA disclaimer "These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure, or prevent any disease." Disease-claim language (treatment of CFS, Alzheimer, Parkinson, or cognition) is not permitted regardless of evidence base.

7.2 European Union · EFSA

The EU Register of nutrition and health claims authorised under Regulation (EC) No 1924/2006 contains zero authorised health claims and zero non-authorised claims specifically for NADH (last reviewed against the internal regulatory record on 2026-04-21). NADH is sold in several EU member states as a dietary supplement under national rules, but no centralised EU health-claim authorisation exists. Marketing in EU member states must confine itself to general statements that do not invoke Article 13/14 health-claim language and must respect the Annex VIII restrictions on disease-prevention claims.

7.3 Brazil · ANVISA

ANVISA has no specific approval pathway for NADH as a dietary-supplement ingredient as of the most recent internal review. Commercial entry into the Brazilian market requires a case-by-case ANVISA submission and is not currently established. Brazilian readers should treat NADH content as scientific and educational background rather than as a product they can readily purchase locally under a regulated framework.

8. Safety, Dosing, and Quality Considerations

8.1 Safety profile across 25-plus years

The cumulative safety record of stabilised oral NADH across roughly 25 years of commercial availability and more than 25 ClinicalTrials.gov entries is excellent for a dietary-supplement category: no serious adverse events attributable to NADH have been reported in published randomised trials at doses up to 20 mg/day for up to 6 to 8 months; mild side effects (loss of appetite, mild dyspepsia, occasional headache) occur at low rates typically indistinguishable from placebo; no drug-supplement interactions of clinical concern have been published, though NADH should be discussed with the prescribing physician in patients taking L-dopa, because of a theoretical interaction via the dopamine biosynthesis pathway (Birkmayer 1990 PMID 2239495). The IL-6 modulation work (Nadlinger K, Birkmayer J, Gebauer F. Neuroimmunomodulation 2001 — Nadlinger 2001 PMID 11847482) suggests NADH may have mild immunomodulatory effects on peripheral cytokine production, which has been interpreted as part of the anti-fatigue mechanism in CFS but does not constitute a safety concern at supplement doses.

8.2 Typical doses across the literature

8.3 Quality considerations — formulation matters

Because oral NADH is unstable in the upper gastrointestinal tract, enteric-coated or otherwise pharmaceutically stabilised formulations are essential for absorption. The original Enada/ENADA formulation remains the canonical reference; products that do not specify their stabilisation strategy should be treated as bioavailability-unknown.

Related Goals and Lifestyles

Read the Evidence (deep dive long-form)

For deep-dive narrative on reduced NADH vs the (research-stage) NMNH redox-form and the broader 25-year NAD⁺-axis chronology, see the dedicated evidence articles:

• Reduced NADH vs NMNH — redox-form comparison · chemistry + history + 17 PubMed-verified citations · NADH ENADA clinical chronology + NMNH preclinical safety + Vinten 2026 first human pilot.
• 25 Years of NAD⁺ Clinical Evidence — full niacin → NMN/NR/NADH chronology · 30 PubMed-verified citations · Era 1-4 regulatory + RCT history + honest nulls.

Cross-reading these peer evidence articles alongside this NADH fact sheet builds the holistic NAD⁺-axis redox-form evidence picture.

References (14 PMIDs)

1. PMID 2239495 · Birkmayer W, Birkmayer JG, Vrecko K. 1990. NADH as stimulator of endogenous L-dopa biosynthesis in parkinsonian patients. Adv Neurol.
2. PMID 8101444 · Vrecko K, Birkmayer JG, Krainz J. 1993. NADH stimulation of dopamine biosynthesis in cultured PC12 phaeochromocytoma cells. J Neural Transm Park Dis Dement Sect.
3. PMID 9247090 · Vrecko K, Storga D, Birkmayer JG. 1997. NADH stimulates endogenous dopamine biosynthesis by enhancing the recycling of tetrahydrobiopterin. Biochim Biophys Acta.
4. PMID 10071523 · Forsyth LM, Preuss HG, MacDowell AL et al. 1999. Therapeutic effects of oral NADH on the symptoms of patients with chronic fatigue syndrome. Ann Allergy Asthma Immunol.
5. PMID 11847482 · Nadlinger K, Birkmayer J, Gebauer F. 2001. Influence of reduced nicotinamide adenine dinucleotide on the production of interleukin-6 by peripheral human blood leukocytes. Neuroimmunomodulation.
6. PMID 12385067 · Birkmayer GD, Kay GG, Vürre E. 2002. Stabilized NADH (ENADA) improves jet lag-induced cognitive performance deficit. Wien Med Wochenschr.
7. PMID 12399028 · Nadlinger K, Westerthaler W, Storga-Tomic D et al. 2002. Extracellular metabolisation of NADH by blood cells correlates with intracellular ATP levels. Biochim Biophys Acta.
8. PMID 15134388 · Demarin V, Podobnik SS, Storga-Tomic D et al. 2004. Treatment of Alzheimer disease with stabilised oral nicotinamide adenine dinucleotide. Drugs Exp Clin Res.
9. PMID 18020963 · Ying W. 2008. NAD+/NADH and NADP+/NADPH in cellular functions and cell death. Antioxid Redox Signal.
10. PMID 20447621 · Alegre J, Rosés JM, Javierre C et al. 2010. Nicotinamide adenine dinucleotide (NADH) in patients with chronic fatigue syndrome. Rev Clin Esp.
11. PMID 25386668 · Castro-Marrero J, Cordero MD, Segundo MJ et al. 2015. Does oral coenzyme Q10 plus NADH supplementation improve fatigue and biochemical parameters in chronic fatigue syndrome? Antioxid Redox Signal.
12. PMID 33319867 · Yuan X, Liu Y, Bijonowski BM et al. 2020. NAD(+)/NADH redox alterations reconfigure metabolism and rejuvenate senescent human mesenchymal stem cells in vitro. Commun Biol.
13. PMID 34444817 · Castro-Marrero J, Segundo MJ, Lacasa M et al. 2021. Effect of dietary coenzyme Q10 plus NADH supplementation on fatigue perception and health-related quality of life in individuals with ME/CFS. Nutrients.
14. T1-NADH internal evidence card · last regulatory review 2026-04-21.

Educational Disclaimer

This page is educational reference content and is not medical advice. It is not intended to diagnose, treat, cure, or prevent any disease, including chronic fatigue syndrome, Parkinson disease, Alzheimer disease, or any cognitive condition. Discuss any supplement use with a qualified healthcare provider, particularly if you are pregnant or breastfeeding, take L-dopa or other prescription medication, or have a diagnosed condition. Regulatory status varies by jurisdiction; this hub focuses on the United States (DSHEA), the European Union (EFSA), and Brazil (ANVISA).