Also indexed as: Nicotinamide Adenine Dinucleotide
What does it do? NADH is the active coenzyme form of vitamin B3. It plays an essential role in the energy production
of every human cell. In the brain, increased NADH concentrations may result in improved
production of essential neurotransmitters.1
Large preliminary studies using oral or injected NADH to treat Parkinson’s disease, showed reductions in
physical disability and in the need for medication,2 3 but a small,
double-blind, short-term trial using injections of NADH found no significant
effects.4 A small, uncontrolled study showed that oral NADH improved mental
function in people with Alzheimer’s
disease.5 Preliminary research suggests that NADH may also help people with depression6 or chronic fatigue syndrome.7 These
promising results come from research conducted by the developer of the oral NADH supplement
and require independent confirmation.
Where is it found? NADH is found in the muscle tissue of fish and poultry and cattle, as well as in food products made
with yeast. However, it is not known whether the NADH from these sources can be efficiently
absorbed or utilized by the body. It is also available as a nutritional supplement.
NADH has been used in
connection with the following conditions (refer to the individual
health concern for complete information):
Who is likely to be deficient? NADH deficiency is known to
occur only in the presence of vitamin B3 deficiency,
which is rare in Western society except in some
alcoholics.
How much is usually taken? Researchers have used 10 mg per
day, taken with water only, on an empty stomach.
Are there any side effects or interactions? Clinical studies
of NADH using oral or intravenous administration have reported no side effects with up to one
year or more of use. Longer-term use has not been evaluated.
At the time of writing, there were no well-known drug interactions
with NADH.
References:
1. Kuhn W, Muller T, Winkel R, et al. Parenteral application of NADH in
Parkinson’s disease: clinical improvement partially due to stimulation of endogenous
levodopa biosynthesis. J Neural Transm 1996;103:1187–93.
2. Birkmayer W, Birkmayer JGD, Vrecko K, et al. The clinical benefit of
NADH as stimulator of endogenous L-Dopa biosynthesis in Parkinsonian patients. In: Streifler
MB, Korczyn AD, Melamed E, et al. (eds). Advances in Neurology, vol. 53 (Parkinsons
Disease: Anatomy, Pathology, and Therapy). New York: Raven Press, 1990, 545–9.
3. Birkmayer JG, Vrecko C, Volc D, Birkmayer W. Nicotinamide adenine
dinucleotide (NADH)— a new therapeutic approach to Parkinson’s disease. Comparison
of oral and parenteral application. Acta Neurol Scand Supp 1993;146:32–5.
4. Dizdar N, Kagedal B, Lindvall B. Treatment of Parkinson’s
disease with NADH. Acta Neurol Scand 1994;90:345–7.
5. Birkmayer JG. Coenzyme nicotinamide adenine dinucleotide: new
therapeutic approach for improving dementia of the Alzheimer type. Ann Clin Lab Sci
1996;26:1–9.
6. Birkmayer JGD, Birkmayer W. The coenzyme nicotinamide adenine
dinucleotide (NADH) as biological antidepressive agent: experience with 205 patients. New
Trends Clin Neuropharmacol 1991;5:19–25.
7. Forsyth LM, MacDowell-Carnciro AL, Birkmayer GD, et al. The use of
NADH as a new therapeutic approach in chronic fatigue syndrome. Presented at the annual
meeting of the American College of Allergy, Asthma & Immunology, 1998.
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The information presented in Healthnotes is for informational
purposes only. It is based on scientific studies (human, animal, or in vitro),
clinical experience, or traditional usage as cited in each article. The results reported may
not necessarily occur in all individuals. For many of the conditions discussed, treatment with
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before making any changes in prescribed medications. Information expires December 2003.
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