Nicotinamide adenine dinucleotide (NADH) is an important cofactor, or "assistant," that helps enzymes in the work they do throughout the body. NADH particularly plays a role in the production of energy. It also participates in the production of L-dopa, which the body turns into the important neurotransmitter dopamine.
Based on these basic biochemical facts, NADH has been evaluated as a treatment for jet lag, Alzheimer's disease, Parkinson's disease, chronic fatigue syndrome, depression, and as a sports supplement. However, only the first of these uses has any meaningful scientific evidence behind it, and even that is highly preliminary.
Healthy bodies make all the NADH they need, using vitamin B 3 (also known as niacin or nicotinamide) as a starting point. The highest concentration of NADH in animals is found in muscle tissues, which means that meat might be a good source—were it not that most of the NADH in meat is destroyed during processing, cooking, and digestion. In reality, we don't get much NADH from our food.
The typical dosage for supplemental NADH ranges from 5 to 50 mg daily, often taken sublingually (under the tongue). Products said to be "stabilized" are available.
Supplemental NADH has also been proposed as a treatment for Alzheimer's disease , chronic fatigue syndrome , depression , and Parkinson's disease . Additionally, it has additionally been tried as a sports performance enhancer . However, although a few studies have been performed to evaluate these potential uses, 2-7 none were designed in such a way as to produce scientifically meaningful results.
In a double-blind, placebo-controlled trial, 35 individuals taking an overnight flight across four time zones were given either 20 mg of NADH or placebo sublingually (under the tongue) on the morning of arrival. 8 Participants were twice given tests of wakefulness and mental function: first at 90 minutes and then at 5 hours after landing. Individuals given NADH scored significantly better on these tests than those given placebo.
The only other supporting evidence comes from an unpublished double-blind, placebo-controlled, crossover study funded by the makers of an NADH product. 9 In this study, 25 people were kept awake all night and their cognitive function was tested the following day. People given NADH performed significantly better on various measures of mental function than those given placebo. NADH did not, however, reduce daytime sleepiness or enhance mood.
These small but promising studies suggest a need for further research.
2. Birkmayer JG, Vrecko C, Volc D, et al. Nicotinamide adenine dinucleotide (NADH)—a new therapeutic approach to Parkinson's disease. Comparison of oral and parenteral application. Acta Neurol Scand Suppl . 1993;146:32-35.
3. Birkmayer JGD, Birkmayer W. The coenzyme nicotinamide adenine dinucleotide (NADH) as biological antidepressive agent: experience with 205 patients. New Trends Clin Neuropharmacology . 1991;5:19-25.
7. 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;103:1187-1193.
9. Moline ML, Rebeta JL, Flye BL, et al. Effectiveness of NADH in alleviating effects of sleep deprivation in healthy middle-aged adults. Abstract presented at: The First International Conference on Mechanisms of Action of Nutraceuticals; October 2001.
Last reviewed September 2014 by EBSCO CAM Review Board
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