The NADH Reaction
European Study Documents Effects Of NADH On Alzheimer Patients
by Jorg Birkmayer, M.D., Ph.D.
Professor of Medicine and Clinical Chemistry
This article has been sponsored by Menuco Corporation, a proprietary company.
President Ronald Reagan's recent public admission that he is in the early stages of Alzheimer's Disease has served as a powerful reminder that this terrible affliction can strike anybody, but especially those individuals in their twilight years. Alzheimer's has a tragic effect not only on its victims but on their families as well. Spouses and children of Alzheimer's patients can only watch helplessly as their loved ones slip slowly into the grips of this dreaded disease. The medical community, while it has spent a great deal of time and resources, has made little progress in discovering an effective treatment for Alzheimer's. Drugs such as Cognex have had little if any effect in improving the condition of Alzheimer's patients. Preliminary research conducted in Europe, however, on coenzyme Nicotinamide Adenine Dinucleotide (NADH), a substance that occurs in every living cell, has produced extremely encouraging results in both halting the progression of Alzheimer's and treating its symptoms. NADH, which is currently available as a food supplement in the United States, will be the subject of a series of studies at leading American medical institutions in 1995.
Background On Alzheimer's Disease
Alzheimer's Disease is caused by a steady loss of neurons, or nerve cells, that causes progressive dementia, resulting in a steady decline in mental and physical function. Symptoms of this disease include a gradual loss in memory, decline in the ability to perform routine tasks, disorientation in time and space, impairment of judgment and loss of communications skills. Alzheimer's strikes one in 12 Americans over the age of 65, and one in three over the age of 80, affecting between 2.5 million and 4 million Americans.
NADH was first discovered in 1934 by the renowned American medical researcher Dr. Nathan Kaplan. It plays the central role in the energy production of the cells; in other words, the more NADH a cell has available, the more energy it can produce. NADH is particularly abundant in meat, less so in vegetables and fruits, For the last two decades I have conducted research on coenzyme NADH. In the early 1980s, I studied the effects of NADH in treating patients suffering from Parkinson's Disease. In several clinical trials involving more than 2,000 individuals, NADH not only alleviated the impairment in motor skills caused by Parkinson's, but also effectively treated the corresponding cognitive dysfunction. The similarities between Parkinson's and Alzheimer's Disease, coupled with the success of NADH in treating cognitive dysfunction led me to test the effects of NADH in treating Alzheimer's patients.
NADH & Alzheimer's
NADH activity decreases in tangent with the human aging process. Researchers have measured that this decrease in NADH is magnified in Alzheimer's patients; cell activity related to NADH is 25% to 50% lower in Alzheimer's patients than similar age matched individuals. I believed that administration of NADH, by boosting Alzheimer's patients level of NADH, would alleviate the symptoms and halt the progression of the disease by playing a proactive approach in raising the body's levels of certain neurotransmitters, such as acetylcholine, noradrenaline and dopamine. The deficit in these key neurotransmitters has been identified as a key cause that produces many of the symptoms associated with Alzheimer's. By increasing cellular energy, it was my belief that NADH would prevent the premature death of brain cells, resulting in higher levels of acetylcholine, noradrenaline, dopamine, etc. which would reduce the effects and progression of Alzheimer's. A key to the research was to find a practical method to administer NADH as it is sensitive to light, temperature, oxygen, water and other reactive molecules. Following three years of extensive study, I and my research team produced a completely natural, patented tablet form of NADH that remains stable for a minimum of two years.
In an open label trial conducted in Austria, 17 Alzheimer's patients were treated with NADH for eight to twelve weeks. Each patient was given 10 mg of NADH in tablet form every morning, 30 minutes prior to their morning meal. (To get an equal amount of NADH from normal food, it would be necessary to consume approximately 4 pounds of steak). Prior to the start of the trial, the condition of these individuals ranged from mild symptoms of cognitive decline to moderately severe or severe dementia. Following just two weeks of treatment, a 240% increase in NADH Unbiquinone Reductase activity was observed. Along with this dramatic increase, noticeable improvements were noted in the patient's cognitive function and memory. All of the patients evaluated, including those with the most severe cases of dementia, experienced an improvement in cognitive function following NADH therapy. This improvement was paralleled by an increase in the production of dopamine and noradrenaline. By stimulating the biosynthesis of dopamine and noradrenaline, NADH treatment also increased the alertness and mental activity of the patients. The results of minimental state and global deterioration scale examinations (two effective tests for measuring changes in cognitive function) conducted before and after NADH treatment confirmed the patients' remarkable improvements. Based on the encouraging results of this Alzheimer's study, an FDA-approved study of NADH is being set up at a leading American medical institution, the purpose of which will be to further examine its efficacy in treating Alzheimer's.
As the principal catalyst of cellular energy, NADH has been tested as a general energy enhancer. Anecdotal evidence suggests that NADH is effective in boosting athletic performance in national class endurance athletes, in providing elderly individuals with greater levels of energy, and in acting as an effective antidepressant. Thus far, over 3,000 people have been treated with or taken NADH as a supplement. In not one of these cases has there been reported a negative side effect. Toxicology tests have indicated that NADH is safe in levels up to 500 mg per kg of body weight, over 7,000 times greater than the recommended level of 5 mg per day.
Predictions of panaceas have been made for hundreds of years. Nobody is claiming that NADH is a cure-all for every disease and illness known to humanity. However, as a principal catalyst of energy production, NADH could help treat or control the causes and symptoms of a number of afflictions whose victims lack the necessary energy to live normal lives. Based on the number of studies on NADH that will be conducted in the next year, a more complete understanding of the powers of NADH could soon be forthcoming.
Jorg Birkmayer, M.D., Ph.D.
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Jorg G.D. Birkmayer, M.D., Ph.D.
Professor of Medicine and Clinical Chemistry
Jorg G.D. Birkmayer, M.D., Ph.D., is a world leader in the field of medical research concentrating on Cancer Biology and Neurochemistry. His research in Neurochemistry has focused on possible treatments for Alzheimer's and Parkinson's Disease. Dr. Birkmayer is the Associate Professor of Medicine, Clinical Chemistry and Director of Laboratories in Neurochemistry at the University of Graz.
In addition to his academic work, Dr. Birkmayer is the Medical Director of Labor
Birkmayer, a laboratory for medical diagnostics in Vienna, and Director of Laboratories
for five private hospitals in Vienna since 1983. He previously taught Cell Biology and
Physiological Chemistry at the University of Munich. In 1988 he was appointed to the post
of Secretary General of the newly founded Birkmayer Institute for Parkinson Therapy. He
was Secretary General for 10 consecutive years of the International Conference on Human
Peer review journal articles that Dr. Birkmayer has had published includes:
"Nicotineamide Adenine Dinucleotide (NADH) - a New Therapeutic Approach to Parkinson's Disease Comparison of Oral and Parenteral Application," published in The Journal of Neural Transmission in 1993;
"Stimulation of Dopamine Biosynthesis in Cultured PC12 Phaeochromocytoma Cells by the Coenzyme Nicotineamide Adenine Dinucleotide (NADH)," in The Journal of Transmission in 1993;
"The Coenzyme NADH as a Biological Antidepressive Agent," New Trends in
Clinical Neuropharmacology 1991.
Dr. Birkmayer is a member of the following scientific organizations: New York Academy of Sciences, the International Academy of Tumor Marker Oncology, The United States Association for Clinical Scientists, The International Society for Preventative Oncology, and the Austrian Society for Clinical Chemistry and Laboratory Medicine.