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Source: Forsyth LM, et al. Therapeutic effects of oral NADH on the symptoms of patients with chronic fatigue syndrome. Ann Allergy Asthma Immunol 1999; 82:185-191.
Chronic fatigue syndrome (cfs) is a disorder of unknown etiology, consisting of prolonged, debilitating fatigue, and a multitude of symptoms including neurocognitive dysfunction, flu-like symptoms, myalgia, weakness, arthralgia, low-grade fever, sore throat, headaches, sleep disturbances, and swelling and tenderness of the lymph nodes. No effective treatment for CFS is known.
The purpose of the study was to evaluate the efficacy of the reduced form of nicotinamide adenine dinucleotide (NADH) in a stabilized oral absorbable form. We conducted a randomized, double blind, placebo-controlled crossover study in patients with CFS. NADH is known to trigger energy production through ATP generation, which may form the basis of its potential effects.
Twenty-six eligible patients (17 female, mean age 39.6 years, mean duration of fatigue 7.2 years) who fulfilled the Center for Disease Control and Prevention (CDC) criteria for CFS completed the study. Medical history, physical examination, laboratory studies, and questionnaire were obtained at baseline, 4, 8, and 12 weeks. Subjects were randomly assigned to receive either 10 mg of NADH or placebo for a four-week period. Following a four-week washout period, subjects were crossed over to the alternate regimen for a final four-week period. An arbitrary symptom scoring system was externally validated with the use of a 50-item questionnaire.
No severe adverse effects were observed related to the study drug. Within this cohort of 26 patients, eight of 26 (31%) responded favorably to NADH in contrast to two of 26 patients (8%) to placebo. A 10% improvement in symptom score was considered a favorable response. Based upon these encouraging results we have decided to conduct an open-label study in a larger cohort of patients.
Collectively, the results of this pilot study indicate that NADH may be a valuable adjunctive therapy in the management of CFS.
CFS is a wearing, energy-zapping disease. Patients with it are very difficult to treat, and must accommodate to the chronicity of their illness; physicians who treat them search for new treatments regularly.
Immune abnormalities have been variably reported, as has metabolic dysfunction, including hypothesized depletion of cellular ATP. Also known as Coenzyme I, NADH catalyzes ATP production in mitochondria, and according to the authors, may catalyze a change in CFS symptoms. It does not have an accepted clinical use of which I am aware.
Sponsored in part by Birkmayer Laboratories, makers of the NADH preparation used in the study, and conducted by Georgetown and Birkmayer investigators, the study has a familiar investigator, Dr. Jorg Birkmayer of Austria, who has performed a number of other open-labeled studies of proprietary preparations of NADH in patients with Alzheimer’s, Parkinson’s, and depression. Thirty-five patients were initially enrolled; two dropped out because of nonadherence, and nine were excluded because they were receiving psychotropic medications. Three of 35 were found to be seropositive for hepatitis C virus, apparently previously undetected.
Limitations of the study include the drop-out rate, the short treatment period, the open design, and the absence of a control group.
NADH is an enzymatic cofactor which is a potential treatment in search of a disease. CFS would be a good one. It should be tested in a randomized, controlled trial. Its likelihood of harm appears to be small.