Nicotinamide Adenine Dinucleotide (NADH): Nootropic Benefits, Uses, Dosage, & Side Effects


nadh nootropic supplement cognitive benefits, mechanism of action, dosage, safety guidelines

NADH (nicotinamide adenine dinucleotide plus hydrogen) is the reduced, electron-carrying form of the coenzyme NAD+ that cells use to make ATP, and as an oral supplement it has been tested in small human trials at 5 to 30 mg a day.(1)(2)

Oral NADH is a different product from intravenous NAD+ given in infusion clinics and from the NAD+ precursors nicotinamide riboside (NR) and nicotinamide mononucleotide (NMN); results for one do not transfer to the others.

All six placebo-controlled chronic fatigue or jet lag trials of NADH had a link to a product maker: a Birkmayer-company author in two, and Vitae funding or tablets plus a Vitae-affiliated co-author in four. That link does not make the results wrong. Two studies with no stated maker link, an open-label dementia study of oral NADH and a placebo-controlled Parkinson’s study of injected NADH in 9 patients, found no significant effect.(3)(4)

What Is NADH?

NADH, the reduced form of NAD+, is a naturally occurring coenzyme found in all living cells that carries electrons from the breakdown of glucose, fats and amino acids to the mitochondria, where they are used to make ATP, the cell’s energy currency.

nadh chemical properties allow cellular energy production

Cells build NADH and NAD+ mainly from dietary nicotinamide, a form of vitamin B3 (niacin), and partly from the amino acid tryptophan,(5) so NADH is a coenzyme made from vitamin B3, not a vitamin itself. In redox (oxidation-reduction) reactions it gives up electrons to become NAD+, and NAD+ takes them back to become NADH. Meat and fish contain NADH, but the amounts and how much survives digestion are not established.

As a supplement, NADH is sold for energy, alertness and mental clarity; claims for mood and neuroprotection rest on small or uncontrolled trials and animal data.

What Does NADH Stand For?

NADH stands for nicotinamide adenine dinucleotide plus hydrogen: the H is the extra hydrogen, carried as a hydride ion (one proton, two electrons), that turns NAD+ into its reduced form. It is also called reduced nicotinamide adenine dinucleotide, coenzyme I in older texts, and nicotinamide adenine dinucleotide hydride in the 2008 exercise trial. NAHD is a common misspelling.

  • Identifiers: PubChem CID 439153, CAS 58-68-4, C21H29N7O14P2, 665.4 g/mol (NAD+: 664.4 g/mol); synonyms DPNH, beta-NADH, NADH2.(6)
  • Class: coenzyme, sold in the US as a “Dietary Supplement”; ENADA, the stabilized tablet in several trials, is a trademark of Birkmayer USA.(7)
  • Main target: complex I, the first enzyme of the mitochondrial respiratory chain.
  • Half-life and peak time after oral intake in humans: not established.

How Does NADH Function in the Body?

NADH works as an electron donor: enzymes that break down glucose and fats load electrons onto NAD+ to form NADH, and complex I in the mitochondria takes them back, passing them along a chain to oxygen to drive ATP production. NAD and its relatives also act beyond energy supply:(8)

  1. Oxidants: electron leaks from NADH in mitochondria are a main source of reactive oxygen species, while NADPH, the phosphorylated relative of NADH, supplies the antioxidant systems
  2. Ageing: NAD-dependent sirtuin enzymes take part in ageing
  3. Calcium signalling: cyclic ADP-ribose, made from NAD, helps regulate calcium inside cells

What is NADH Used For?

NADH is used for chronic fatigue, jet lag, mental energy, Parkinson’s disease, Alzheimer’s disease, depression and exercise performance, and the claimed benefits of nicotinamide adenine dinucleotide rest on 15 small human studies with mixed results. Two gave NADH only by injection and two by injection or mouth; 6 had no placebo group, and at least 7 of the other 9 had an author, funder or tablet supplier from a Birkmayer company or another supplement maker.

Use and studyDesign and sizeDaily doseDurationMain resultMaker or funder link
Chronic fatigue, 1999Randomized, double-blind, placebo-controlled crossover; 35 enrolled, 26 analysedOral ENADA, 10 mg4 weeks per treatment8 of 26 (31%) responded favorably to NADH, 2 of 26 (8%) to placebo; no severe adverse effects(9)Birkmayer Pharmaceuticals grant and co-run analysis; Birkmayer co-author
Chronic fatigue, 2004Randomized, no placebo, vs supplements plus psychological therapy; 31 randomized, 20 analysed (12 on NADH)Oral, 5 mg, raised to 10 mg if neededUp to 24 months; only patients on therapy at least 12 months analysedSymptom score fell from 3.8 to 2.2 (scale 1 to 4) in the first 3 months (p < 0.001), then similar in both groups; no adverse events(1)None stated
Chronic fatigue, 2010Randomized, double-blind, placebo-controlled; 86 enrolled, 77 completedOral, 20 mg2 monthsNo significant differences in most outcomes; anxiety fell 1.0 point on NADH (p < 0.05) and 0.2 on placebo(10)Funded by Laboratorios Vitae; Vitae-affiliated corresponding author
Chronic fatigue, 2015Randomized, double-blind, placebo-controlled; 73 womenOral, 20 mg NADH plus 200 mg CoQ108 weeksFatigue impact scale total fell more than on placebo (p < 0.05)(11)Supported by Vitae Natural Nutrition, which supplied the capsules; Vitae-affiliated co-author
Chronic fatigue, 2016Randomized, double-blind, placebo-controlled; 80 womenOral, 20 mg NADH plus 200 mg CoQ108 weeksMaximum heart rate in a cycle test fell from baseline (P = 0.022); fatigue fell versus placebo (P = 0.03); pain and sleep unchanged(12)Vitae supplied the tablets and supported the lead author; Vitae-affiliated co-author
ME/CFS, 2021Randomized, double-blind, placebo-controlled; 207 randomized (104/103), 144 analysed (72 per group)Oral, 20 mg NADH plus 200 mg CoQ108 weeks plus 4 weeks follow-upCognitive and total fatigue fell within the active group (p < 0.001, p = 0.022); fatigue domains moved in parallel in both groups(13)Vitae Health Innovation supplied the tablets, supported the lead author and employs one author
Jet lag, 2002Randomized, double-blind, placebo-controlled; 35 healthy adults (18/17)Sublingual ENADAlert, 20 mg onceMorning after an overnight flight across 3 time zonesBetter on 4 cognitive test measures (P ≤ .05) and less sleepy than placebo; no adverse effects(14)Product from Menuco Corp.; first author from Labor Birkmayer
Exercise, 2008Double-blind, placebo-controlled crossover; 8 menOral ENACHI, 30 mg4 weeks per treatmentNo difference in maximal oxygen uptake, anaerobic running time, reaction time, concentration or fatigue; counter-movement jump differed(2)Tablets donated by Birkmayer Laboratories; J. Birkmayer co-author
Alzheimer’s, 2004Randomized, double-blind, placebo-controlled; 26 patientsOral, 10 mg6 monthsHigher dementia rating scale total than placebo (p < 0.05); no difference in attention, memory or clinician-rated severity(15)Funding not stated in the abstract
Dementia, 2000Open-label; 25 enrolled, 19 completedOral ENADA, 10 mg3 monthsNo evidence of any cognitive effect on standard tests(3)None stated
Alzheimer-type dementia, 1996Open-label; 17 patientsOral, 10 mg8 to 12 weeksMini-Mental State score rose by a mean of 8.35 points(16)Birkmayer Institute
Parkinson’s, 1993Open-label; 885 patientsIntravenous (about half) or oral capsulesNot stated in the abstract19.3% very good and 58.8% moderate improvement, 21.8% no response; oral and intravenous comparable(17)Birkmayer Institute
Parkinson’s, 1996Open prospective; 15 patientsIntravenous, 10 mg7 daysRating scale improved (p = 0.025); plasma levodopa exposure rose (AUC p = 0.035)(18)Two co-authors from Mattern & Partner GmbH, whose NADH formulation work the paper cites; no funding statement
Parkinson’s, 1994Double-blind, placebo-controlled; 5 NADH, 4 placeboInjected, 25 mg (intravenous, then intramuscular)About 6 weeksSmall improvement in both groups, not statistically significant(4)Swedish research foundations
Depression, 1991Open-label; 205 patientsOral 5 mg, or 12.5 mg injected5 to 310 days93% showed a beneficial clinical effect(19)Birkmayer Institute

NADH for Chronic Fatigue Syndrome

NADH for chronic fatigue syndrome (CFS, also called ME/CFS) has been tested at 5 to 20 mg a day in 6 trials with mixed results: more responders on 10 mg in a crossover, no difference in most outcomes on 20 mg alone, improvement only in the first 3 months against standard care, and three later trials that combined 20 mg with 200 mg coenzyme Q10.

In the 1999 crossover, the gap between 8 and 2 responders out of 26 (23.1 percentage points) means about one extra responder for every 5 patients treated for 4 weeks; the authors’ P < .05 treated the two periods as independent samples, and 9 of 35 enrolled patients were left out because they took psychotropic drugs.(9)

The combination trials cannot separate NADH from coenzyme Q10. In 2015, the fatigue impact scale total (0 to 160) fell 7.5 points on the combination and 3.7 on placebo, and blood cells held more ATP (119.24 vs 67.45 nmol/mg protein).(11) In 2021, the authors wrote that the lack of differences between groups may have been due to the placebo effect; the placebo tablets contained phosphatidylserine and vitamin C.(13)

NADH for Jet Lag

NADH reduced jet-lag sleepiness and cognitive test deficits in one placebo-controlled trial of a single 20 mg sublingual dose after an overnight flight (table above). The trial was small, published in German and run with a Birkmayer-laboratory first author, so it supports a short-term effect after sleep loss, not a general alertness boost.

NADH for Parkinson’s Disease

NADH for Parkinson’s disease rests mostly on injected NADH in uncontrolled studies, and the one placebo-controlled trial, with 9 patients, found no significant benefit. Injected results do not describe oral supplements. The rationale is that NADH may activate tyrosine hydroxylase, the rate-limiting enzyme of dopamine synthesis, and so raise the body’s own levodopa production; in the 1996 infusion study, mean rating-scale scores fell from 59.3 to 50.0 points (about 16%; 11 patients improved, 3 worsened) with no control group.(18) A 1998 review concluded that recommendations for NADH in Parkinson’s disease were premature.(20)

NADH for Alzheimer’s Disease and Cognitive Decline

NADH’s placebo-controlled Alzheimer’s trial found better total dementia-scale scores but no difference in memory, and an open-label memory-clinic study found no cognitive effect at the same 10 mg dose. That study measured a mean Mini-Mental State change of 0.58 points (16.95 to 17.53), against the 8.35-point gain in the 1996 Birkmayer Institute series, and concluded that NADH is unlikely to achieve cognitive improvements to the extent reported earlier.(3)

NADH for Depression

NADH for depression rests on the 1991 open-label series from the Birkmayer Institute (table above) and on rat data: injected NADH reduced immobility in the forced swim test, a screen for antidepressant-like drugs, at 10 and 50 mg/kg and increased swimming at 5 to 100 mg/kg, a profile the authors compared with fluoxetine.(21) A mood effect in people is inferred, not measured.

NADH for Athletic Performance

NADH did not improve endurance, reaction time or concentration in the one exercise trial, in which 8 men took 30 mg a day for 4 weeks (table above). Jump height rose 5.8% over the NADH period from a slightly poorer start than in the placebo period, and the tablets supplied 18 mg of sodium bicarbonate a day, a buffer the authors discussed for anaerobic work.(2)

What Are the Nootropic Benefits of NADH?

NADH, like NAD+, is sold as a nootropic, but its nootropic benefits in healthy people rest on two small trials with different results: a benefit after an overnight flight and no change in rested men (table above). Claims of more brain energy, memory gains and neuroprotection come from NADH’s role in metabolism and from cell and rat studies.

nadh nootropic effects brain energy, memory and neuroprotection

Does NADH Increase Brain Energy?

NADH increases brain energy only in theory for people taking it by mouth: injected NADH reached the rat cortex, but brain NADH or ATP after oral NADH has not been measured in humans. In anaesthetised rats, 50 mg/kg injected into the abdomen raised cortical NADH by about 18% for roughly 30 minutes, 10 mg/kg had no effect, and oral NADH gave a smaller rise (relatively small bioavailability).(22)

Swallowed NADH is also unstable: at a stomach-like acidic pH it converted rapidly to an unknown compound,(5) and in rat intestine tissue about 5% crossed the gut wall when protected from acid.(23)

Can NADH Improve Memory and Learning?

NADH improved maze learning in old rats but not in young rats, and it did not improve memory scores in the human dementia trials. Rats aged 22 months injected for 10 days learned a water maze faster than untreated old rats, most clearly at 100 mg/kg, with no effect in 3-month-old rats.(24) A memory benefit in people is inferred, not shown.

What Are the Neuroprotective Effects of NADH?

Neuroprotective effects of NADH have not been shown in people; the evidence comes from cell and animal models, mostly using NAD+. In the author’s laboratory studies, NAD+ given through the nose was suggested to decrease ischemic (stroke-type) brain damage, and NAD+ was proposed as a therapy for some neurological diseases.(25) Because mitochondrial NADH also generates reactive oxygen species, a net antioxidant effect of supplemental NADH in the brain is not established.

Does NADH Help with Mental Clarity and Focus?

NADH helped attention and working memory after an overnight flight, but it did not improve concentration or reaction time in rested men (table above). A focus effect through dopamine would require NADH to raise dopamine synthesis in the human brain, which has not been measured.

How Is NADH Used as a Supplement?

NADH is sold as a dietary supplement in tablets, sublingual lozenges, capsules and powder, often labelled “stabilized” because it breaks down in acid, light, heat and moisture. Sublingual and liposomal forms are marketed as avoiding stomach acid, an inferred, unmeasured advantage. Injected NADH was used in the Parkinson’s and depression studies in the table and is not a supplement form.

nadh supplement user guide, dosage and side effects

NADH has no official dosage: oral trials used 5 to 30 mg a day, and the ENADA NADH 5 mg label directs 1 tablet daily in the morning on an empty stomach with water, 30 minutes before eating.(7) The label says to store it in a cool, dry place out of the reach of children.(7) No overdose data exist; after taking far more than the label amount, contact a doctor or poison control center.

  • Human study doses (oral): 5 to 30 mg a day (5 to 20 mg in chronic fatigue trials), measured from the morning after one dose to 24 months (table above).
  • Animal-to-human equivalent: the rat studies injected 5 to 100 mg/kg. By body surface area (rat dose x 6/37): 5 x 6/37 = 0.81 mg/kg, and 0.8108 x 70 = 56.8 mg, about 57 mg for a 70 kg adult; 100 x 6/37 = 16.2 mg/kg, and 16.216 x 70 = 1,135.1 mg, about 1,135 mg, or about 38 times the 30 mg top oral trial dose. These are estimated equivalents of injected doses, not tested doses.
  • Community reports: 5 to 20 mg a day, with more energy described within days to weeks (anecdotal, not studied).

Can NADH Be Taken with Other Supplements?

NADH has been tested in combination only with coenzyme Q10 (200 mg with 20 mg NADH, in the chronic fatigue trials above); other pairings rest on mechanism, and people on medicines should ask a pharmacist first.

  • Antioxidants (vitamin C, vitamin E) and B vitamins: synergy is inferred, not tested
  • Caffeine: caffeine adds its own alerting and sleep-disrupting effects; the pair is untested
  • L-Tyrosine: L-tyrosine is the dopamine precursor, so the pair is promoted for dopamine support (inferred); other options are under dopamine supplements

Is NADH Safe for Everyone & Does It Have Any Side Effects?

Oral NADH at 5 to 30 mg a day caused no serious adverse effects in trials that reported safety (benefits are in the table above), but the trials were small and lasted at most 24 months, so rare or long-term effects are unknown. In the largest placebo-controlled trial, 8 of 104 people on CoQ10 plus NADH (7.7%) and 11 of 103 on placebo (10.7%) dropped out for adverse effects, mainly stomach pain and dizziness.(13)

In a 26-week rat study, one 5 mg ENADA tablet a day caused no deaths, no blood-test or organ-weight differences and no visible organ toxicity, though treated females gained more weight; the authors’ 175 mg human equivalent is 35 times a 5 mg tablet, not the 175 times they wrote.(26)

Side effects reported in trials or by users:

  • Upset stomach or stomach pain, the most commonly reported
  • Dizziness, on both NADH and placebo in the largest placebo-controlled trial
  • Overstimulation, mild loss of appetite and heartburn, single cases in the 1999 trial(9)
  • Insomnia when taken late in the day, jitteriness and headaches (user reports)
  • Allergic reactions such as rash, hives or swelling, rare and needing urgent help

Are There Any Contraindications for NADH Use?

NADH has no formal contraindications from a regulator, but these groups should avoid it or ask a doctor first:

  • Pregnancy and breastfeeding: avoid unless a doctor advises it; the ENADA label says to consult a physician first(7)
  • Children: no pediatric safety data; not for under-18s without a doctor
  • Bipolar disorder or a history of mania: ask a doctor first, as users report overstimulation
  • Autoimmune, liver or kidney disease: no data; ask a doctor
  • Allergy to NADH, NAD or any product ingredient: avoid
  • Surgery: tell the surgical team about NADH beforehand

Does NADH Interact with Medications?

No drug interactions are documented for NADH, but interaction data are incomplete; one is plausible from published data, and the others are precautions inferred from the mechanism:

  • Levodopa and other Parkinson’s drugs: NADH infusions raised plasma levodopa exposure (table above); ask the prescriber first
  • Antidepressants, MAO inhibitors and stimulants: an added dopamine effect is inferred; ask a pharmacist or doctor
  • Anticoagulants, thyroid, blood-pressure and diabetes drugs: no known interaction; one CoQ10 plus NADH trial lowered maximum heart rate, so mention NADH to a doctor if taking heart-rate-lowering drugs
  • Sedatives and alcohol: a stimulating effect would oppose sedatives (inferred); alcohol’s effect is unknown

How Does NADH Compare to Other Nootropics?

NADH differs from most types of nootropics because its proposed action is metabolic, supplying electrons to mitochondria, rather than acting on nerve signalling, and it has few controlled cognitive trials (table above).

NADH vs NAD+, NR and NMN

NADH is the reduced and NAD+ the oxidized form of one coenzyme, while nicotinamide riboside (NR) and nicotinamide mononucleotide (NMN) are precursors cells turn into NAD+; NADH results do not apply to them.

  • Intravenous NAD+: 750 mg infused over 6 hours in 8 adults was rapidly and completely removed from the plasma for at least the first 2 hours; NAD+ Research Inc. co-funded the study.(27)
  • Nicotinamide riboside: 500 mg twice a day for 6 weeks raised NAD+ in blood immune cells by about 60% compared with placebo in middle-aged and older adults; ChromaDex, whose NR is sold as NIAGEN, provided the pills and partial funding.(28)
  • Oral NADH: in the 2015 chronic fatigue trial, blood cells on CoQ10 plus NADH held more NADH (247.3 vs 98.2 pmol per million cells) but less NAD+ (86.9 vs 189.4) than on placebo (both p < 0.001), so oral NADH has not been shown to raise NAD+.(11)

How Does NADH Stack Up Against Natural Nootropics?

Herbal nootropics act through blood flow, receptors or stress hormones rather than metabolism, and no head-to-head trials with NADH are established (more under best natural nootropics):

Is NADH More Effective Than Synthetic Nootropics?

NADH is not shown to be more effective than synthetic nootropics; no direct comparisons are established, and prescription stimulants act faster and more strongly, with more side effects:

  • Modafinil: prescription wakefulness drug; headache, insomnia and anxiety are side effects
  • Piracetam: racetam studied in cognitive impairment, not for energy
  • Adderall: prescription amphetamine for ADHD with addiction potential
  • Phenylpiracetam: stimulating racetam, more stimulating than NADH by user reports

Sources, Studies, and Scientific Research
  1. Santaella, María L et al. “Comparison of oral nicotinamide adenine dinucleotide (NADH) versus conventional therapy for chronic fatigue syndrome.” Puerto Rico health sciences journal vol. 23,2 (2004): 89-93. PMID: 15377055↩↩
  2. Mero, Antti et al. “Effects of nicotinamide adenine dinucleotide hydride on physical and mental performance.” Journal of sports sciences vol. 26,3 311-9. 1 Feb. 2008, doi:10.1080/02640410701474200↩↩↩
  3. Rainer, M et al. “No evidence for cognitive improvement from oral nicotinamide adenine dinucleotide (NADH) in dementia.” Journal of neural transmission vol. 107,12 (2000): 1475-81. doi:10.1007/s007020070011↩↩↩
  4. Dizdar, N et al. “Treatment of Parkinson’s disease with NADH.” Acta neurologica Scandinavica vol. 90,5 (1994): 345-7. doi:10.1111/j.1600-0404.1994.tb02735.x↩↩
  5. Kimura, Naoko et al. “Comparison of metabolic fates of nicotinamide, NAD+ and NADH administered orally and intraperitoneally; characterization of oral NADH.” Journal of nutritional science and vitaminology vol. 52,2 (2006): 142-8. doi:10.3177/jnsv.52.142↩↩
  6. National Center for Biotechnology Information. “PubChem Compound Summary for CID 439153, NADH.” PubChem, https://pubchem.ncbi.nlm.nih.gov/compound/439153↩
  7. NIH Office of Dietary Supplements. “ENADA NADH 5 mg, Source Naturals, label 273089.” Dietary Supplement Label Database, 22 Mar. 2023, https://dsld.od.nih.gov/label/273089↩↩↩↩
  8. Ying, Weihai. “NAD+/NADH and NADP+/NADPH in cellular functions and cell death: regulation and biological consequences.” Antioxidants & redox signaling vol. 10,2 (2008): 179-206. doi:10.1089/ars.2007.1672↩
  9. Forsyth, L M et al. “Therapeutic effects of oral NADH on the symptoms of patients with chronic fatigue syndrome.” Annals of allergy, asthma & immunology vol. 82,2 (1999): 185-91. doi:10.1016/S1081-1206(10)62595-1↩↩↩
  10. Alegre, J et al. “Nicotinamide adenine dinucleotide (NADH) in patients with chronic fatigue syndrome.” Revista clinica espanola vol. 210,6 (2010): 284-8. doi:10.1016/j.rce.2009.09.015↩
  11. Castro-Marrero, Jesús et al. “Does oral coenzyme Q10 plus NADH supplementation improve fatigue and biochemical parameters in chronic fatigue syndrome?.” Antioxidants & redox signaling vol. 22,8 679-85. 10 Mar. 2015, doi:10.1089/ars.2014.6181↩↩↩
  12. Castro-Marrero, Jesus et al. “Effect of coenzyme Q10 plus nicotinamide adenine dinucleotide supplementation on maximum heart rate after exercise testing in chronic fatigue syndrome – A randomized, controlled, double-blind trial.” Clinical nutrition vol. 35,4 (2016): 826-34. doi:10.1016/j.clnu.2015.07.010↩
  13. Castro-Marrero, Jesús et al. “Effect of Dietary Coenzyme Q10 Plus NADH Supplementation on Fatigue Perception and Health-Related Quality of Life in Individuals with Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: A Prospective, Randomized, Double-Blind, Placebo-Controlled Trial.” Nutrients vol. 13,8 2658. 30 Jul. 2021, doi:10.3390/nu13082658↩↩↩
  14. Birkmayer, G D et al. “Stabilized NADH (ENADA) improves jet lag-induced cognitive performance deficit.” Wiener medizinische Wochenschrift vol. 152,17-18 (2002): 450-4. doi:10.1046/j.1563-258x.2002.02072.x↩
  15. Demarin, V et al. “Treatment of Alzheimer’s disease with stabilized oral nicotinamide adenine dinucleotide: a randomized, double-blind study.” Drugs under experimental and clinical research vol. 30,1 (2004): 27-33. PMID: 15134388↩
  16. Birkmayer, J G. “Coenzyme nicotinamide adenine dinucleotide: new therapeutic approach for improving dementia of the Alzheimer type.” Annals of clinical and laboratory science vol. 26,1 (1996): 1-9. PMID: 8834355↩
  17. Birkmayer, J G et al. “Nicotinamide adenine dinucleotide (NADH)–a new therapeutic approach to Parkinson’s disease. Comparison of oral and parenteral application.” Acta neurologica Scandinavica. Supplementum vol. 146 (1993): 32-5. PMID: 8101414↩
  18. Kuhn, W et al. “Parenteral application of NADH in Parkinson’s disease: clinical improvement partially due to stimulation of endogenous levodopa biosynthesis.” Journal of neural transmission vol. 103,10 (1996): 1187-93. doi:10.1007/BF01271203↩↩
  19. Birkmayer, J G D, and W Birkmayer. “The Coenzyme Nicotinamide Adenine Dinucleotide (NADH) as Biological Antidepressive Agent: Experience with 205 Patients.” New Trends in Clinical Neuropharmacology vol. 5 (1991): 75-85.↩
  20. Swerdlow, R H. “Is NADH effective in the treatment of Parkinson’s disease?.” Drugs & aging vol. 13,4 (1998): 263-8. doi:10.2165/00002512-199813040-00002↩
  21. Rex, André et al. “Antidepressant-like effect of nicotinamide adenine dinucleotide in the forced swim test in rats.” Pharmacology, biochemistry, and behavior vol. 77,2 (2004): 303-7. doi:10.1016/j.pbb.2003.11.001↩
  22. Rex, André et al. “Bioavailability of reduced nicotinamide-adenine-dinucleotide (NADH) in the central nervous system of the anaesthetized rat measured by laser-induced fluorescence spectroscopy.” Pharmacology & toxicology vol. 90,4 (2002): 220-5. doi:10.1034/j.1600-0773.2002.900409.x↩
  23. Rex, Andre, and Heidrun Fink. “Pharmacokinetic aspects of reduced nicotinamide adenine dinucleotide (NADH) in rats.” Frontiers in bioscience vol. 13 3735-41. 1 May 2008, doi:10.2741/2962↩
  24. Rex, André et al. “Treatment with reduced nicotinamide adenine dinucleotide (NADH) improves water maze performance in old Wistar rats.” Behavioural brain research vol. 154,1 149-53. 23 Sep. 2004, doi:10.1016/j.bbr.2004.02.001↩
  25. Ying, Weihai. “NAD+ and NADH in neuronal death.” Journal of neuroimmune pharmacology vol. 2,3 (2007): 270-5. doi:10.1007/s11481-007-9063-5↩
  26. Birkmayer, J G D, and K Nadlinger. “Safety of stabilized, orally absorbable, reduced nicotinamide adenine dinucleotide (NADH): a 26-week oral tablet administration of ENADA/NADH for chronic toxicity study in rats.” Drugs under experimental and clinical research vol. 28,5 (2002): 185-92. PMID: 12635493↩
  27. Grant, Ross et al. “A Pilot Study Investigating Changes in the Human Plasma and Urine NAD+ Metabolome During a 6 Hour Intravenous Infusion of NAD.” Frontiers in aging neuroscience vol. 11 (2019): 257. doi:10.3389/fnagi.2019.00257↩
  28. Martens, Christopher R et al. “Chronic nicotinamide riboside supplementation is well-tolerated and elevates NAD+ in healthy middle-aged and older adults.” Nature communications vol. 9,1 1286. 29 Mar. 2018, doi:10.1038/s41467-018-03421-7↩

Jacob Kovacs is a cognitive neuroscientist and author at WholisticResearch, specializing in nootropics and neuroactive peptides. His expertise in neuroscience and psychopharmacology bridges cognitive science with drug development. Kovacs’ work focuses on enhancing cognitive functions and brain health through innovative, efficient neuroactive compounds that overcome traditional pharmacokinetic challenges. His contributions are pivotal in advancing the understanding and treatment of neurological diseases.