Nicotinamide Adenine Dinucleotide (NADH)


Originally discovered in 1905 in yeast, NADH is also known as the reduced form of coenzyme 1, a complementary enzyme utilized in the production and regulation of energy (oxidative phosphorylation). (1) A coenzyme is the active or working form of a vitamin. NADH is the reduced (electron-energy rich) coenzyme form of vitamin B3; while NAD is the oxidized (burned) coenzyme form of vitamin B3. NAD and NADH are converted into each other in numerous different metabolic activities. In some metabolic reactions, it is NAD which is the needed catalyst, with NADH a useful by-product; in other reactions the situation is reversed.

NAD and NADH also serve to activate various enzymes. NADH is the first of five enzyme complexes of the electron transport chain where much of the ATP bioenergy that runs every biological process of the body is formed.

NADH is necessary to oxidize all foodstuffs (fats, sugars, amino acids) into ATP bioenergy. As all living cells require energy to survive, NADH reacts with oxygen to form water and energy. One molecule of NADH yields three molecules of ATP (the stored form of energy), with the amount of NADH present dictating the amount of energy produced. The heart muscle cells contain 90mcg of NADH per gram of tissue, with brain and muscle tissue containing 50mcg per gram. Even red blood cells contain NADH with 4mcg per gram. The more NADH present in cells, theoretically, the more efficient they function in energy production.

NADH was never really considered as an oral dietary supplement due to its high reactivity and probable degradation in the blood. However, a stable, disodium salt oral form of NADH has been introduced and used clinically with reported effectiveness.

Dosage Info

Dosage Range

2.5-15mg once daily to once every other day. Take on an empty stomach, either one-half hour before meals or one hour after.

Most Common Dosage

Nutrition and Energy Enhancement: 2.5–5mg every other day to daily, depending upon individual requirements.

Therapeutic Support (Alzheimer’s, Parkinson’s, Chronic Fatigue): 10-15mg every other day to daily.

Dosage Forms


Adult RDI

None established

Adult ODA

None established

Active Forms

B-nicotinamide adenine dinucleotide; disodium salt form.


NAHD is readily absorbed from the intestinal tract.

Toxicities & Precautions


NADH is generally considered to be safe in recommended dosages.

Functions in the Body

Clinical Applications

Alzheimer's Disease

Seventeen patients suffering from dementia of the Alzheimer’s type in an open-label trial were treated with the disodium salt of NADH, 10mg daily. (2) Improvement in cognitive function was reported in all patients. Using NADH as a therapeutic choice in the management of dementia is based on the theory of the stimulation of the biosynthesis of endogenous neurotransmitters, in particular dopamine and norepinephrine. This should improve the mental performance of patients with cognitive dysfunction and/or dementia, as these neurotransmitters are reduced in certain areas of the brain in Alzheimer’s patients. (3)

The FDA approved a clinical trial at Georgetown University Medical Center to investigate the treatment of Alzheimer’s Disease with disodium NADH. Preliminary results from the study have indicated promising outcomes and warrant further research.


NADH was used in an open-label trial of 205 patients suffering from depression with various clinical symptoms. (4) NADH was given either orally (5mg daily) or by intramuscular or intravenous injection, with the duration of therapy lasting five to 310 days. Ninety-three percent of the patients exhibited beneficial clinical effects. Benefits were attributed to the positive effects that NADH has upon the synthesis of L-dopa, dopamine, norepinephrine, and other catecholamines.

Parkinson's Disease

Several studies have reported benefits in the use of NADH in Parkinson’s patients. (5) , (6) In an open-label trial of 415 patients with Parkinson’s Disease, NADH was given in its stable form as 5mg every other day for two weeks. Mobility, in particular walking, pushing, posture, and speech, as well as the ability to mimic another’s speech, showed improvement. (7) Research has reported that NADH stimulates endogenous L-dopa synthesis, the precursor of dopamine. (8)

Chronic Fatigue Syndrome

Characterized by a combination of flu-like symptoms including extreme fatigue, myalgia, impairment of short term memory, sleep disturbances, mild fever, and sore throat, Chronic Fatigue Syndrome affects millions of Americans, 70 percent of whom are women. Symptoms must persist for more than six months in order to comply with the definition of Chronic Fatigue Syndrome. A 12-week, double-blind, placebo controlled study reported very positive results using NADH in the management of Chronic Fatigue Syndrome. (9) Thirty-one percent of the patients who took the nutritional supplement reported improvement in symptoms, versus 8 percent in the placebo group. The dosage regimen of NADH was 10mg daily for four weeks on, four weeks off. The proposed mechanism of action of NADH in this disease is the replenishment of depleted cellular stores of ATP, thus improving the fatigue and cognitive dysfunction associated with Chronic Fatigue Syndrome.

Additionally, in a follow-up preliminary open-label study, 73 percent of the patients achieved marked improvement over time. Researchers identified no adverse effects from taking the disodium NADH product and no reportable drug interactions.

Jet Lag

In a double-blind study, subjects taking a "red-eye" flight spanning four time zones were tested with sublingual NADH or a placebo. The subjects who used the sublingual NADH tablets performed better on measurements of cognition and sleepiness compared to placebo controls and there were not any side effects. (10)

Symptoms and Causes of Deficiency

NADH is not an essential nutrient for humans and a deficiency condition has not been identified.

Dietary Sources

NADH occurs in many consumable foods, including red meats, poultry, fish, and products with yeast (such as breads).


  1. Alberts B, et al. Energy Conversion: Mitochondria and Chloroplasts. Molecular Biology of the Cell. 3rd Edition. Garland Publishing, Inc; 1994:653-720.
  2. View Abstract: Birkmayer JG. Coenzyme nicotinamide adenine dinucleotide: New therapeutic approach for improving dementia of the Alzheimer’s type. Ann Clin Lab Sci. 1996;26(1):1-9.
  3. View Abstract: Reinikainen KJ, et al. Neurotransmitter changes in Alzheimer’s disease: implications to diagnostics and therapy. Neurosci Res. 1990;27:576-86.
  4. Birkmayer JG, et al. The coenzyme nicotinamide adenine dinucelotide (NADH) as biological antidepressive agent experience with 205 patients. New Trends in Clinical Neuropharmacology. 1991;5:75-86.
  5. View Abstract: Birkmayer JG, et al. Stimulation of the endogenous L-Dopa biosynthesis – a new principle for the therapy of Parkinson’s Disease: The clinical effect of nicotinamide adenine dinucleotide (NADH) and nicotinamide dinucleotidephosphate (NADPH). Acta Neurol Scan. 1989;126:183-187.
  6. View Abstract: Birkmayer JG, et al. Nicotinamide adenine dinucleotide (NADH) – a new therapeutic approach to Parkinson’s Disease, Comparison of Oral and Parenteral Application. Acta Neurol. Scan. 1993;87(Suppl146):32-35.
  7. Birkmayer JG, et al. Nicotinamide adenine dinucleotide (NADH) as medication for Parkinson’s Disease. Experience with 415 patients. New trends in clinical neuropharmacology. 1990;4(1):7-24.
  8. Alberts B, et al. Energy Conversion: Mitochondria and Chloroplasts. Molecular Biology of the Cell. 3rd Edition. Garland Publishing, Inc; 1994:653-720.
  9. View Abstract: Forsyth LM, et al. Therapeutic effects of oral NADH on the symptoms of patients with chronic fatigue syndrome. Ann Allergy Asthma Immunol. Feb1999;82(2):185-91.
  10. Kay GG, Virre E, Clark J. Stabilized NADH as a countermeasure for jet lag. 48th International Congress of Aviation and Space Medicine. Rio de Janeiro. Sep2000.