NADH is the abbreviation for nicotinamide adenine dinucleotide, with the H indicating the reduced form that has an extra hydrogen atom. NADM functions as a coenzyme, meaning that it is a required cpfactor for a metabolic process. In the case of NADH, coenzyme functions include roles in energy generation and the production of neurotransmit-ters such as dopamine and norepinephrine. Thus, NADH supplements are generally promoted for increasing energy levels, reducing CFS, treating jet lag, and enhancing memory and cognitive function.
NADH supplements typically cost about $1 per 5-mg dose; therefore, an effective dose of the supplement may cost between $2 and $4 per day. Because of the nonexistence of any reliable treatment for chronic fatigue syndrome, the preliminary antifatigue benefits of NADH are promising. Nevertheless, the preliminary nature of these results also means that NADH may be most useful as an adjunct to more established antifatigue supplements such as cordyceps, rhodiola, and ginseng.
The precise cause of CFS is unknown (Calabrese et al., 1992). Symptoms include prolonged and debilitating fatigue, inability to concentrate, flu-like symptoms, muscle weakness, joint pain, headaches, and sleep disturbances (Chester, 1997; Komaroff and Buchwald, 1991). CFS affects about 500,000 Americans, but no effective treatment is known (Gantz and Holmes, 1989; Houde and Kampfe-Leacher, 1997). Researchers theorize that CFS stems from a lack of the chemical responsible for cellular energy, ATP (Klonoff, 1992). One theory is that both infections and stress deplete cellular ATP levels and lead to chronic fatigue, and that supplemental levels of NADH can stimulate ATP production and provide benefits to people suffering from fatigue and cognitive dysfunction (Colquhoun and Senn, 2000). Further benefits from NADH may stem from its role in stimulating the production of the neurotransmitters dopamine and norepinephrine (involved in brain function and memory) as well as from the stimulation of tyrosine hydroxylase, an enzyme involved in synthesizing neurotransmitters (Birkmayer el al., 2002).
Among the dozen or so clinical reports of NADU supplementation, however, only two arc randomized, double-blind, placebo-controlled trials (Birkmayer el al., 2002; Forsyth et a!., 1999). Of the many open-label studies of NADU administration to patients with Alzheimer disease, dementia, or Parkinson disease, most of the studies showing a positive effect come from the same clinic in Austria (Birkmayer et al., 2002), and the dosing regimens include oral as well as intravenous, parenteral, and intramuscular routes of administration. The positive benefits of NADU supplementation in these open-label studies have not been duplicated by other clinics or laboratories, and some open-label studies have shown no benefit of NADH supplements (10 rng/dayfor3 months) in cases of mild-to-moderate Alzheimer disease (Rainer et al., 2000).
In the two existing well-controlled studies of NADH supplementation, 10-20 mg of NADH showed some promising antifatigue effects. In one study (Forsyth et al., 1999), 10 mg/day of NADH for 4 weeks was effective in alleviating generalized symptoms of CFS in about one third of patients. In another study (Birkmayer el al., 2002), a 20-mg acute dose of a sublingual form of NADH improved cognitive function, mood, and sleepiness in subjects suffering from jet lag.
Some people report mild side effects such as nervousness and loss of appetite in the first few days of taking NADH. No serious side effects are documented, and animal studies have shown no problems associated with NADH supplementation (Birkmayer and Nadlinger, 2002). Commercial NADH supplements are generally available in 2.5-mg and 5-mg tablets, with suggested dosages ranging from 2.5-15 mg/day, depending on individual requirements (e.g., therapy or maintenance).