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NADHVisit The Healthy Living Bookshelf:
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. Which form of NADH is best? NADH appears to be a chemically unstable molecule that decomposes rapidly. For this reason, techniques have been developed to stabilize the NADH sold in tablet form. At the present time, it is not known which commercially available NADH products are most effective. 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. 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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