NADH, a naturally-occurring coenzyme, shows promise in increasing cognitive function and energy levels.
Preliminary research on NADH, a coenzyme found in all living cells, shows that it may help treat some degenerative diseases and chronic fatigue syndrome.
Building on studies conducted by European researcher Dr. Georg Birkmayer, researchers at Georgetown University Medical Center began two double-blind human trials in 1996 testing Birkmayer’s patented form of NADH (nicotinamide adenine dinucleotide), marketed as Enada. The Georgetown trials focus on Alzheimer’s disease and chronic fatigue syndrome (cfs) and, so far, are encouraging, according to a Georgetown press release. Study results could be complete by late 1997 and 1998.
The trials have been approved by the U.S. Food and Drug Administration (FDA) through the Investigational New Drug process, which allows the FDA to stop trials of promising but unknown drugs if they appear to be dangerous to human health, according to Arthur Whitmore, an FDA spokesman. The process doesn’t indicate FDA approval of Enada’s use as a drug.
Georg Birkmayer, a medical doctor who has studied NADH since the mid-1980s, has published the results of many of his pilot studies on NADH. Birkmayer is director of the Birkmayer Institute for Parkinson Therapy in Vienna, Austria, and of the neurochemistry division at the University of Graz, Austria. He also is the secretary general of the International Academy of Tumor Marker Oncology and the European editor of the Journal of Tumor Marker Oncology.
During the early 1960s, Georg Birkmayer’s father, Waltham Birkmayer, researched L-dopa as a treatment for Parkinson’s disease. L-dopa is sold as the drug Sinemet, but it isn’t effective for all Parkinson’s patients after long-term use.
Because of that, the Birkmayers tested NADH on 470 Parkinson’s patients. According to their published research, the treatment improved symptoms for the study participants. The Birkmayers subsequently developed Enada, a stabilized, enteric-coated form of NADH that can be taken orally.
The Birkmayers then turned their attention to Alzheimer’s patients. Because levels of NADH are generally 25 to 50 percent lower in Alzheimer’s patients than in other individuals, Birkmayer reasoned that NADH, which helps increase cellular energy, might help prevent the premature death of brain cells. In one small, uncontrolled study, Birkmayer treated seventeen Alzheimer’s patients with NADH for eight to twelve weeks. Each patient was given 10 mg of NADH every morning thirty minutes before breakfast. Before the trial started, the participants’ condition ranged from mild symptoms of cognitive decline to moderately severe or severe dementia. After two weeks of treatment, all patients showed dramatic improvements in their cognitive function and memory, according to the study results. However, Birkmayer wrote that because the number of patients involved in the study was so low, no conclusion could yet be drawn.
Alan Gaby, M.D., professor of nutrition at Bastyr University and past president of the American Holistic Medical Association, has reviewed much of the research on NADH. Given the preliminary nature of the research and the lack of controlled studies, Gaby advises caution.
“The research is encouraging and something that definitely needs following up,” he says. “I know a few doctors who tried it and think their patients are doing better, but it has not been proven from a scientific standpoint.”
While the research continues, however, Gaby thinks it’s “worth a try,” given that NADH has shown no evidence of toxicity.
Birkmayer G.J., et al. ”Coenzyme nicotinamide adenine dinucleotide: new therapeutic approach for improving dementia of the Alzheimer type.” Annals of Clinical and Laboratory Science, 1996, page numbers unavailable.
———-. “Nicotinamide adenine dinucleotide (NADH)—a new therapeutic approach to Parkinson’s disease. Comparison of oral and parenteral application.” Acta Neurologica Scandinavica Supplementum 1993, 146:32-5.
Birkmayer, W., Birkmayer G.J., et al. “The coenzyme nicotinamide adenine dinucleotide improves the disabililty of Parkinsonian patients.” The Journal of Neural Transmission—Parkinson’s Disease & Dementia Section 1989, 1:4, 297.
Birkmayer G.J., Birkmayer W. “Stimulation of endogenous L-dopa biosynthesis—a new principle for the treatment of Parkinson’s disease. The clinical effect of nicotinamide adenine dinucleotide (NADH) and nicotinamide adenine dinucleotidephosphate (NADPH).” Acta Neurologica Scandinavica Supplementum 1989, 126:183-7
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