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NADH

NADH

Description

NADH (Nicotinamide Adenine Dinucleotide + Hydrogen) or Coenzyme 1, as its name implies, is derived from vitamin B3.

It is found in all living cells but is concentrated within the brain, heart and nervous system, where it is a key player in energy production.

Heart cells contain approximately 90 mcg of NADH per gram of tissue. Brain cells about half as much (50 mcg).


Method of Action

NADH is a cofactor for numerous enzymes, including those in the cell mitochondria where energy is produced.

One of these enzymes, Tyrosine Hydroxylase, converts the amino acid Tyrosine into dopamine. Hence NADH has been tried, with reported success, in the treatment of Parkinson's disease.

NADH also increases serotonin and noradrenaline production in the brain. One reason Parkinson's inflicts such a great burden is that dopamine is responsible for short-term memory, involuntary movements, emotional drive and spontaneous reactions. Serotonin has a calming influence, both on emotions and in directing the body to sleep. Noradrenaline is stimulating, which is good for alertness and concentration.

Therapeutic Approaches

NADH is the first and most energetic factor producing cell energy. Hence it is being tried for a range of conditions, including chronic fatigue and depression.

Some scientists are also hoping that boosting brain cell energy prophylactically, may prevent the onset of neurodegenerative diseases and even memory loss.

Consequently, NADH may have a large role to play in age-related brain diseases, including Alzheimer's and Parkinson's.

Generally, it may be useful for: chronic fatigue syndrome, depression and other degenerative diseases.

Even healthy people may experience increased concentration, energy and stamina.

Toxicity Factors

NADH is available over-the-counter as a nutritional supplement.

Sensitive patients, who take too high a dosage, report restlessness and insomnia. Once dosage is reduced, these symptoms disappear.

Clinical trials have not reported any negative side-effects. Toxicology tests indicate that NADH is safe at up to 500 mg per kg of body weight (almost 7,000 times greater than recommended levels).

Recommended levels tend to be in the range of 5 - 10 mg daily.

Abstracts

References

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Birkmayer W, Neumayr E. Die moderne medikamentose Behandlung des Parkinsonismus. Z Neurol 1972; 202:257.

Birkmayer W. Riederer P. Parkinson's disease, New York: Springer Verlag Wien, 1983.

Birkmayer W. Birkmayer JGD. Iron, a new aid in the treatment of Parkinson patients. J Neural Transm 1986; 67:287-292.

Birkmayer JGD, Birkmayer W. Improvement of disability and akinesia of patients with Parkinson's disease by intravenous iron substitution. Ann Clin Sci 1987; 17:32-35.

Birkmayer JGD, et al., Nicotinamide adenine dinucleotide (NADH) - a new therapeutic approach to Parkinson's disease. Comparison of oral and parenteral application. Acta Neurol. Scand. 1993 146S:32-35.

Kosel, S. et al., NADH dehydrogenase and CYP2D6 genotypes in Parkinson's disease. 2nd workshop Neurogenetics, Munich, Germany, October 19-21, 1995.

Nagatsu T., Levitt M, Udenfriend S. Tyrosine hydroxylase:The initial step in norepinephrine synthesis. J Biol Chem 1964; 239:2910-2917.

Nagatsu T., Namaguchi T, Kato T, et al. Biopterine in human brain and urine from controls and Parkinsonian patients: Application of a new radioimmunoassay. Clin Chim Acta 1981; 109:305.

Nagatsu T, Kato T, Numata Y, et al. Phenylethanolamine-N-methyl-transferase and other enzymes of catecholamine metabolism in human brain. Clin Chim Acta 1977:75:221-232.

Ott E, Birkmayer W, Birkmayer JGD. J Movement Dis 1988.

Rausch WD, Hirata Y, Nagatsu T, et al. Tyrosine hydroxylase activity in caudate nucleus from Parkinson's disease. Effects of iron and phosphorylating agents. J Neurochem 1988; 50:202-208.