ProHealth health Vitamin and Natural Supplement Store and Health
Home  |  Log In  |  My Account  |  View Cart  View Your ProHealth Vitamin and Supplement Shopping Cart
800-366-6056  |  Contact Us  |  Help

|
|
|
|

Trending News

New Option For Chronic Fatigue Syndrome

The Most Powerful Natural Antioxidant Discovered to Date - Hydroxytyrosol

Stop Bacteria With Nature's Antibiotics

Vitamin D Deficiency Linked to Neurological Diseases; Also Raises Risk of Asthma Attacks, and More

New Test Shows Promise in Identifying New Drugs to Treat Lyme Disease

Coenzyme Q10 Helps Veterans Battle Gulf War Illness Symptoms

Strengthen Cell Function with Energy-Boosting Niagen

Dietary Flavanols Reverse Age-Related Memory Decline

Vitamin D deficiency increases poor brain function after cardiac arrest by sevenfold

Study: Doubling saturated fat in the diet does not increase saturated fat in blood

 
Print Page
Email Article

Therapeutic effects of oral NADH on the symptoms of patients with chronic fatigue syndrome

  [ 229 votes ]   [ 1 Comment ]
By By: Linda M Forsyth, MD; Harry G Preuss, MD; • www.ProHealth.com • February 1, 1999


Reprinted from ANNALS OF ALLERGY, ASTHMA, AND IMMUNOLOGY, February, 1999, Volume 82, Number 2

Background: 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, headache, sleep disturbances, and swelling and tenderness of lymph nodes. No effective treatment for CFS is known.

Objective: The purpose of the study was to evaluate the efficacy of the reduced form of nicotinamide adenine dinucleotide (NADH) ie, ENADAâ the stabilized oral absorbable form, in a randomized, double-blind, placebo-controlled crossover study in patients with CFS. Nicotinamide adenine dinucleotide is known to trigger energy production through ATP generation which may form the basis of its potential effects.

Methods: Twenty-six eligible patients who fulfilled the Center for Disease Control and Prevention 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 4-week period. Following a 4-week washout period, subjects were crossed to the alternate regimen for a final 4-week period.

Results: No severe adverse effects were observed related to the study drug. Within this cohort of 26 patients, 8 of 26 (31%) responded favorably to NADH in contrast to 2 of 26 (8%) to placebo. Based upon these encouraging results we have decided to conduct an open-label study in a larger cohort of patients.

Conclusion. Collectively, the results of this pilot study indicate that NADH may be a valuable adjunctive therapy in the management of the chronic fatigue syndrome and suggest that further clinical trials be performed to establish its efficacy in this clinically perplexing disorder.

INTRODUCTION

Chronic fatigue syndrome (CFS) is a poorly understood disorder of unknown etiology, with a reported prevalence of up to 3/1000 population.

The commonly encountered features in patients with CFS are fatigue, impairments in concentration and short term memory, musculoskeletal pain and sleep disorders. The syndrome is characterized by profound, debilitating fatigue lasting at least 6 months often beginning abruptly after a viral infection and not meeting the criteria for other medical or psychiatric disorders, and is characteristically worse following levels of physical exertion that had been easily tolerated in the past and a combination of other prominent symptoms. The Centers for Disease Control and Prevention (CDC) in Atlanta, Georgia have defined criteria for the diagnosis of CFS. The CDC have established that unexplained, debilitating fatigue of at least 6 months duration must be present along with four or more of the following symptoms including neurocognitive dysfunction, myalgias, sore throats, headaches, post-exertional malaise, joint pain, sleep disturbances, or swelling and tenderness of lymph nodes. Chronic fatigue syndrome is therefore a clinically defined condition but there are no definitive laboratory parameters available for diagnosis made solely upon clinical symptomatology and exclusion of other diseases associated with fatigue. Symptoms can vary in intensity and frequency, and often a cyclic pattern is exhibited. Relapses or worsening of symptoms are common and duration of symptoms vary in individual cases. The disorder is more recognized in affluent cultures and is more prevalent in Caucasian females with an age predominant distribution between 30 to 50 years. The pathophysiology is unclear and there presently is no known consistently effective or generally accepted treatment for CFS.

Despite the dearth of knowledge concerning the cause of CFS, it is generally accepted that there may be a dysfunction of the neuro-crine-endocrinoiogic-immunologic (NEI) network in CFS and several theories have focused on each of the three limbs of the NEI network. One theory suggests that the syndrome results from a dysfunction of the immune system and several subtle immunologic abnormalities have been described in patients with CFS. These include low levels of specific immunoglobulins reported in 17% to 71% of cases, the presence of circulating immune complexes in over 50% of patients, and increased ratios of CD4/CD8 T-lymphocytes. Other abnormalities of the immune system included a decrease in natural killer (NK) cells which appear to play a major protective role in viral infection. A second theory emphasizes the role of neurally mediated hypotension (NHM). Studies utilizing a 3-stage tilt table test have shown an abnormal response in patients with CFS compared with controls and demonstrate an uncompensated NHM which is thought to be the cause of the fatigue. A third, but not mutually exclusive theory, is one that suggests metabolic dysfunction owing to stress, viral infection, allergic disease or a host of other factors. Patients with CFS have increased 2'-5' A synthetase and RNAse L activity. This in turn leads to a depletion of cellular ATP that may be the pivotal metabolic lesion responsible for severe fatigue, cognitive disturbances, and other manifestations of the syndrome. Since stress, allergy, and infections may either trigger or exacerbate the clinical course, control of these factors is critical in the management of patients with CFS. Nicotinamide adenine dinucleotide (NADH), the coenzyme, is known to trigger energy production through ATP generation. This knowledge has provided the rationale for the present study. It consists of the ability of the coenzyme to replenish depleted cellular stores of ATP, thus improving the fatigue and cognitive dysfunction characteristic of the disorder.

The purpose of the present study was to evaluate the efficacy of the reduced form of NADH administered orally to a group of patients with CFS in a double-blind, placebo-controlled crossover study.

MATERIALS AND METHODS

Entry Criteria
Patients fulfilling the CDC criteria for CFS were referred by a variety of physicians, self-referred or recruited from the Division of Allergy-Immunology of the Department of Pediatrics at Georgetown University Medical Center, Washington, DC. A standardized 50-question screening questionnaire was developed for use in all subjects to determine and consider patient eligibility and therapeutic outcome. Following initial assessment of the severity of fatigue and symptoms by a screening questionnaire, detailed telephone interviews were conducted by a physician with potential candidates. Before commencement of the study, approval was obtained from the Georgetown University Institutional Review Board and written informed consent was obtained from each subject prior to entry into the study. Subjects ranging from 20 to 70 years of age who met the CDC criteria for CFS were eligible for enrollment. Inclusionary criteria included at least 4 symptoms such as: mild fever or chills, sore throat, painful adenopathy (posterior or anterior cervical or axillary), generalized muscle weakness, myalgias, prolonged generalized fatigue after previously tolerated levels of physical activity, migratory arthralgias without swelling or redness, neuropsychologic complaints, sleep disturbances, and two physical signs, including low grade fever, non-exudative pharyngitis, palpable or tender anterior or posterior cervical lymph nodes. Subjects were allowed to continue taking currently used medications. Medications used 6 months prior the study and during the study were recorded as concomitant medications.

Exclusionary Criteria
Subjects with fatigue that could be explained by the presence of other evident medical or psychiatric illness, current psychotic and bipolar disorders, current substance or alcohol dependence, pre-existing and ongoing, depression at the time of onset of the chronic fatigue were excluded from the study. Patients with a history of established medical conditions that could be contributing to fatigue, such as, hepatitis untreated hypothyroidism, psychiatric illness, cancer, AIDS, severe anemia, multiple sclerosis, Lyme's disease and autoimmune diseases such as lupus were excluded. The use of antidepressants, lithium, neuroleptics, and monoamine inhibitors were generally considered exclusionary criteria.

Study Design
The study design [FDA approved (IND #49,635)] consisted of a randomized, double-blind, placebo-controlled crossover protocol. A thorough medical history, physical examination, laboratory studies, and completion of a questionnaire on the severity of fatigue and symptoms was performed at baseline, week 4, week 8 and week 12. Subjects were randomly assigned at week 0 to receive NADH or placebo for a 4-week period. At week 4, a 4-week wash-out period was begun in which no study drug was given. At week 8, a final 4-week period commenced in which subjects were crossed over to the alternate regimen. Subjects were monitored for toxicity throughout the study period with appropriate laboratory testing. The subjects were asked to report all symptoms that occurred during the treatment regimen, and all symptoms that did not occur at baseline were recorded as adverse experiences. Included in the physical assessment were the following: blood pressure, body weight and temperature, and hand dynamometry measurements as a test of strength and endurance. Peripheral venous blood and urine samples were also obtained from each participant for the measurement of hematologic, biochemical, and immunologic parameters.

Laboratory Assessment
Laboratory studies were performed at laboratories at Georgetown University Medical Center (Washington, DC) and at Birkmayer Laboratories (Vienna, Austria). The following laboratory studies were performed: a complete blood count with differential white blood cell count, erythrocyte sedimentation rate, a panel of 20 serum chemistry tests, urinalysis, serum quantitative immunoglobulin concentrations (IgG, IgM, IgA. and IgE), enumeration and quantitation of lymphocyte subsets (CD3, CD4, CD8, CD19, and CD161 56), and oxidoreductase enzyme assay. Baseline serologic titers of EBV, including early antigen (EA), nuclear antigen (NA) and IgG and IgM to EBV capsid antigen (anti VCA), screening thyroid function levels including T4 and thyroid stimulating hormone levels (TSH), serum antibody titers to human herpesvirus 6 (HHV-6), FUV, rheumatoid factor, and hepatitis B and C (HBS Ag, anti-HCV) were done. During the screening process, three cases of hepatitis C and one case of hypothyroidism were detected with laboratory blood studies. Data and statistical analysis were conducted by Birkmayer Pharmaceuticals (Vienna, Austria) and Georgetown University Medical Center (Washington, DC). The data were also submitted to an independent auditor to confirm and validate the findings.

Symptom Scoring System
The assessment of clinical well-being and severity of symptoms was assessed using a ± 50-item questionnaire that was developed by our staff, utilizing the currently accepted CDC criteria for CFS. Topics included fatigue, memory and concentration difficulties, muscle aches, muscle weakness, joint aches, lymphadenopathy, headaches, sore throat, sleep disturbance, mood changes, and other related symptoms. Each item in the questionnaire was assessed on a scale from I to 4 where I represented the minimum severity and 4 the maximum severity of symptoms (I = none of the time, 2 = some of the time, 3 = most of the time, and 4 = all of the time). Subjects also evaluated how they were feeling on the day of evaluation. A cumulative score was calculated with a range from 50 to 200, with 200 indicating the maximum and 50 the minimum score. Follow-up questionnaires were completed at monthly intervals upon each visit. An arbitrary symptom scoring system was developed according to the following formulation:



Statistical Assumptions and Analyses
External validation studies were conducted with normal healthy subjects and indicated a statistically significant difference when compared with parents with chronic fatigue syndrome. Average mean symptom scores for normals ranged from 0.01 to 0.13 in contrast to patients with chronic fatigue syndrome whose scores ranged from 10.9 to 55.8 (P < .001).

An analysis of reproducibility was determined when the questionnaire was given to the same subjects repeatedly. Treating the data as a repeated measures analysis (repeated measures on the same test subject), the null hypothesis is that ml = m2 = m3 = m4; that is, there is no difference in response among the four times (week 0, week 4, week 8, and week 12). The repeated measures analysis of variance gives a P < .001. Graphic analysis of residuals shows that the residuals are approximately distributed; that is, there is not a systematic variation among the four column means and it is appropriate to conclude that there is a difference in response among the weeks. Using a multiple comparison test to examine the differences between mean responses two at a time, there is no significant difference between week I versus week 2, week I versus week 3, or week 2 versus week 3. Week 0 is significantly different from all the others.

An individual was considered improved if s/he demonstrated at least a 10% improvement. The degree of improvement for the results to show a positive effect was an improvement by one point in 10 questions or by 2 points in 5 questions.

Analysis of Data
Data were analyzed using a test of difference betwee two proportions.



Drug Administration
Subjects were randomly assigned to either treatment or placebo groups and patient numbering occurred in the sequence of subject enrollment. Subjects were given 10 mg of NADH, ENADA®, the stabilized, oral able reduced NADH or the placebo equivalent (two 5-mg tablet formulation) at week 0. All study drugs were distributed in identically marked study, boxes, and the tablets both of identical appearance were contained in blister packs. Subjects were instructed to take the dosage two 5-mg tablets orally, once a day in the morning about 45 minutes before breakfast on an empty stomach with a glass of water. Subjects received the study drug for a 4-week period.

Compliance Monitoring
Participants also were strictly instructed to keep a diary and drug log throughout the study which was reviewed and monitored upon each visit. The study medication was counted and monitored at week 4 and week 12 and returned to the manufacturer for further evaluation and the patient compliance and adherence was evaluated at each visit.

RESULTS

Of the 35 subjects initially enrolled, 33 were able to complete the study and two dropped out due to non-compliance. Of the 35, 9 who were receiving psychotropic drugs were dropped from the study analysis leaving a total of 26 subjects available for analysis. Shown in Table I are the demographic characteristics of the study population.



Of the 26 evaluable subjects, 17 (65%) were females and 9 (35%) males. The subjects ranged from 26 to 57 years of age (mean 39.6 years) and had fatigue for a duration of I to 16 years (mean 7.2 years). Twenty-five patients were Caucasian and one patient was Afro-American. The presenting clinical symptoms in the study population are shown in Table 2. It can be seen that fatigue, neurocognitive difficulties, and sleep disturbances were present in, all patients. Postexertional malaise, headache, and muscle weakness likewise represented high frequency symptomatology and the remainder had decreasing frequency of myalgias, arthralgias, and lymphoadenopathy. Shown in Table 3 is a representative sample of questions from the questionnaire.

No detectable abnormalities were noted in the serum immunoglobulin concentrations or lymphocyte subset analysis in any of the subjects at baseline or after treatment and further immunologic testing was discontinued after the first group of patients. No correlation between immune function or clinical status nor treatment response could be established. No differences in oxidoreductase activity were observed before or after NADH treatments.



The results of the EBV serologic titers in the first group of 15 revealed that 9/15 (60%) subjects had EBV-EA >40. Results are shown in Table 4. There were 6/15 (40%) subjects who had HHV-6 titers = 1:160, suggesting current or recent infection. One of 26 subjects was anti-HCV positive. A history of allergies was reported in 21/26 (81%) subjects. All subjects tested were HIV negative and the rheumatoid factor (RF) was negative. Elevated levels of IgE were detected in 2/15 (13%) subjects. T4 and TSH levels were within normal limits for all subjects.

Clinical Outcomes
Although clinical and laboratory measurements were made as parameters of clinical outcome, the results showing efficacy came primarily from the subjective criteria of the questionnaire. The results of the outcomes were the symptom scoring system the results of which are shown in Table 5. Using the arbitrary scoring system, 8/26 (31%) subjects showed = 10% improvement while on the study drug in contrast to 2/26 (8%) who received placebo. Assuming that these improvements came from two independent samples of subjects, the success rate for the drug is 3 1 % and for the placebo 8% (P < .05).

Using a self-evaluated questionnaire, 9/26 (35%) subjects were able to correctly evaluate the treatment period they were on NADH. Further, 18 of 25 (72%) study patients thus far enrolled in a longer open label follow-up study reported significant improvement in clinical symptomatology and energy levels.

No severe adverse effects were observed related to the study drug. The related adverse events noted were single cases of being overly stimulated, mild loss of appetite, heartburn, increased incidence of gas and an odd taste and dryness reported on the first day of taking the drug. These events were mild enough that the subjects were able to continue taking the drug without problem. No interference was observed between NADH and other concomitant medications taken during the study investigational period.

Blood pressure and hand dynamometry were measured throughout the study with no significant difference noted. Patients with hypertension (I/ ,26), hypotension (2/26), and normotensives in our study did not show any decrease in blood pressure values following NADH administration. Laboratory testing also included the measurement of plasma neurotransmitter concentrations and the urinary concentrations of serotonin metabolites, ie, 5-hydroxyindole acetic acid (5- HIAA). The urinary concentrations of 5-HIAA were elevated prior to treatment in 50% of patients (P < .05). Following NADH treatment, these elevated 5-HLALA concentrations returned to the normal range. The urinary concentrations of the serotonin metabolite (5HIAA) were measured by high performance liquid chromatography. The interassay and intraassay precision ranged from 3.0% to 6.5% and from 2.5% to 5.8%, respectively using a method developed by Birkmayer Laboratories.

DISCUSSION

The results of the present study show a beneficial effect of NADH in the amelioration of the symptom score seen in patients compared with control subjects. Four times as many patients responded to NADH in contrast to placebo. This response was characterized by improvement in fatigue, decrease of symptoms, and improvement in quality of life.

In these preliminary studies, although we employed a dosage of 10 mg of NADH per day, it should be emphasized that different patients may have different needs. The reported feeling of one subject being overly stimulated, suggests that the dosage could be decreased. Other non-responding patients in contrast may require an increased dosage. In the present study modification of dosage was not made on the basis of weight. Although the duration of the study was 12 weeks, subjects received NADH for only 4 of the 12 weeks.



Perhaps a longer period of treatment might enhance the beneficial effects of NADH and could be reflected in a more beneficial and protracted response. This could be evaluated in a longer term open-label follow-up study which is currently being planned.

An additional important outcome of the study was the finding that 3 of the initial 35 screened subjects (3/35) were found to be seropositive for hepatitis C virus. This observation not only highlights the importance of this viral infection as a cause of fatigue, but also underscores the need for the clinician to consider this in the diagnostic approach of the patient who presents with fatigue. Our immunologic studies reveal no abnormalities of immune function before or after NADH administration. One should consider, however, that at the particular time of clinical evaluation and blood drawing there may not have been an exacerbation of the disease.

Although no significant changes were detected in blood pressure in the present study, other preliminary studies performed in our laboratories have suggested that NADH may cause a decrease in blood pressure in hypertensive rats (SHR). We, however, did not observe this effect in humans subjects who for the most part were normotensive. The lowering of blood pressure by NADH would have been an undesirable outcome particularly in hypotensive or NMH patients but our study showed no evidence that blood pressure was affected.

Stress, allergy, and infections appear to be critically involved in the pathogenesis or exacerbation of CFS. The involvement of the serotonergic and noradrenergic pathways appears to be disrupted in patients with CFS. Perturbations have been demonstrated in the metabolism of the 5-hydroxyindole acetic acid, 5-hydroxytrypamine, and prolactin. Measuring the urinary concentration of 5-HIAA may serve not only as a diagnostic aid for CFS but also be a predictive marker of physical and psychologic dysfunction occurring in patients with CFS.

The finding of a high incidence of allergies (21/26) was observed in our study group is significant since it is known that a worsening of the disease often can be attributed to untreated allergic disease. Allergists/immunologists therefore are perhaps the best suited physicians to diagnose and manage patients with CFS, since the pathogenesis involves immune dysfunction and the interplay of other environmental factors and the careful management of allergic disease can lead to a striking improvement, and therefore are uniquely poised to evaluate and manage patients with CFS. The use of NADH may thus be a valuable adjunctive therapy in the management of CF9 and the results of the present study suggest that further clinical trials be performed to establish its efficacy in this clinically perplexing disorder.

ACKNOWLEDGMENT

The authors would like to express their sincere. gratitude MaryLu Halperin, RN, MPH for her indefatigable efforts in monitoring the study.

REFERENCES

Straus SE. History of chronic fatigue syndrome. Rev Infect Dis 1991;13 (suppl 1):S2-7.
Lloyd AR, Hickie I, Boughton CR, et a]. Prevalence of chronic fatigue syndrome in an Australian population. Med J Aust 1990;153:522-528.
Bates DW, Schmitt W, Buchwaid D, et al. Prevalence of fatigue and chronic fatigue syndrome in primary care practice. Arch Intern Med 1993;153: 2759-2765.
Buchwald D, Umali P, Umaii D, et al. Chronic fatigue and the chronic fatigue syndrome: prevalence in a Pacific Northwest Health Care System. Ann Intern Med 1995;123:81-88.
Fukuda K, Straus SE, Hickie 1, et al. T'he chronic fatigue syndrome: a comprehensive approach to its definition and study. Ann Intern Med 1994;121: 953-959.
Komaroff AL, Buchwald DS. Chronic fatigue syndrome: an update. Annu Rev Med 1998;49:1-13.
Sharpe MC, Archard LC, Banatvala JE, et al. A report-chronic fatigue syndrome: guidelines for research. J R Soc Med 1991;84:118-121.
Holmes GP, Kaplan JE, Gantz NM, et al. Chronic fatigue syndrome: a working case definition. Ann Intem Med 1988;108:387-398.
Buchwaid D, Komaroff AL. Review laboratory findings for patients chronic fatigue syndrome. Rev Infect Dis 1991,13 (suppi):SI2-18.
Lloyd AR, Wakefield D, Boughton CR, Dwyer JM. Immunological abnormalities in the chronic fatigue syndrome. Med J Aus, 1989;151: 122-124.
Klimas NG, Fernando FR, Morgan R, Fletcher MA. Immunologic abnormalities in chronic fatigue syndrome. I Clin Microbiol 1990;28:1403-1410.
Mawle AC, Nisenbaum R, Dobbins JG, et al. Immune responses associated with chronic fatigue syndrome: a casecontrolled study. J Infect Dis 1997; 136-141.
Lloyd A, Hickie 1, Wakefield D, et al. A double-blind, ptacebo-controlled trial of intravenous immunoglobulin therapy in patients with chronic fatigue syndrome. Amer J Med 1990;89: 562-568.
Peterson PK, Shepard J, Macres M, et al. A controlled trial of intravenous G in chronic fatigue syndrome. Amer J Med 1990;89:554-560.
Lloyd A, Hickie 1, Hickie C, et al. Cell-mediated immunity in patients with chronic fatigue syndrome, healthy control subjects and patients with major depression. Clin Exp Immunol 1992;87:76-79.
Peakman M, Deale A, Field R, et al. Clinical improvements in chronic fatigue syndrome is not associated with lymphocyte subsets of function or activation. Clin In-Lmunopathol 1997;82: 83-91.
Bou-Holaigah 1, Rowe PC, Kan J, Calkins H. The relationship between neurally mediated hypotension and the chronic fatigue syndrome. JAMA 1995;274:961-967.
Sumaya CV. Serological and virologic epidemiology of Epstein-Barr virus: relevance to chronic fatigue syndrome. Rev Infect Dis 1991-,13 (suppi): S19-25.
Straus SE, Dale JK, Tobi M, et al. Acyclovir treatment of the chronic fatigue syndrome, lack of efficacy in a placebo-controlled trial. N Eng J Med 1988;319:1692-1698.
See DM, Tilles JG. Alpha interferon treatment of patients with chronic fatigue syndrome. In-Lmunol Invest 1996, 25:153-16-4.
Brook MG, Bannister BA, Weir WRC. Interferon-alpha therapy for patients with chronic fatigue syndrome (Letter]. J Infect Dis 1993; 168:791-792.
Bellanti JA, Forsyth LM, MacDowell AL, Preuss HG. Chronic fatigue syndrome (CFS): unraveling a new dilemma. J Am College Nutr 1998 (in press).
Sudadolnik RJ, Reichenbach NK, Hitzges P, et a]. Upregulation of the 2-5 A synthetase/RNase L antiviral pathway associated with chronic fatigue syndrome. Clin Infect Dis 1994.18 (suppl):S96-104.
Sudadolnik RJ, Peterson DI, O'Brien K, et al. Biochemical evidence for a novel low molecular weight 2- 5 A-Dependent Rnase L in chronic fatigue syndrome. J Interferon Res 1997;17: 377-385.
Straus SE, Dale JK, Wright R, Metcalfe DD. Allergy and the chronic fatigue syndrome. J Allergy Immunol 1998;81:791-795.
Birkmayer JGD, Vrecko C, Vole D, Birkmayer W. Nicotinamide adenine dinucleotide (NADH)-new therapeutic ,appmwh to Parkinson's disease, cornparison of oral and parenteral application. Acta Neurol Scand 1993;87 Suppl 146:32-35.
Birkmayer JGD. Coenzyme nicotinamide adenine dinucleotide, new therapeutic approach for improving dementia of the Alzheimer type. Ann Clin Lab Sci 1996;26:1-9.
Birkmayer JD, Birkmayer W. The coenzyme nicotinamide adenine dinucleotide (NADH) as biological antidepressive agent experience with 205 patients. New Trend in Clin Neuropharm 1991;5:75-86.
Bellanti JA, Forsyth LM, MacDowell-Carneiro AL, Birkmayer GD, Preuss HG. NADH and chronic fatigue svndrome (CFS): a new therapeutic approach [Abstract]. Ann Allergy Asthma Immunol 1998; 80:82.
Bushehri N, Jarrell ST, Lieberman S, et al. Oral reduced b-nicotinamide adenine dinucleotide (NADH) and lipid profile in hypertensive rats (SHR). J Geriatric Nephr Urol 1998; (in press).
Bakheit AMO, Behan PO, Dinan TG, et a]. Possible upregulation of hypodialamic 5-hydrotryptamine receptors in patients with postviral fatigue syndrome Br Med J 1992;304:1010-1012.
Forsyth LM, MacDowell-Cameiro Birkmayer GD, et al. The measurement of 5-HIAA concentrations as a predictive marker of efficacy of NADH in chronic fatigue syndmmw (manuscript in on) 1998.
[From the Departments of Pediatrics and Microbiology-Immunology and the International Center for Interdisciplinary Studies of immunology, the Department of Medicine, Division of Nephrology, Department of Family Medicine, Georgetown University School of Medicine, Washington, D.C. and Birkmayer Pharmaceuticals, Vienna, Austria. This work was supported by a grant from Birkmayer Pharmaceuticals. Received for publication August 1, 1998. Accepted for publication in revised form November 28, 1998.]

Request for reprints should be addressed to: Joseph A. Bellanti. MD - Georgetown University Medical Center 3800 Reservoir Rd. NW Kober-Cogan Bldg, Room 318 Washington. DC 20007



Please Discuss This Article:   Post a Comment 

Flower
Posted by: jerryy
May 15, 2012
Thanks for sharing this with all of us, Of course what a great site and informative posts. I will bookmark this site. keep doing your great job and always gain my support. Thank you for sharing this beautiful article…..
new york florist delivery
Reply Reply
 
Free Chronic Fatigue Syndrome and Fibromyalgia Newsletters
Subscribe to
Our FREE
Newsletter
Subscribe Now!
Receive up-to-date ME/CFS & Fibromyalgia treatment and research news
 Privacy Guaranteed  |  View Archives

Black Friday Sale

Featured Products

Coenzyme Q10 with Vitamin E by ProHealth (CoQ10) Coenzyme Q10 with Vitamin E by ProHealth (CoQ10)
Top Energy & Heart Support Nutrient
Pro Energy™ by ProHealth Pro Energy™ by ProHealth
Five Power-Packed Nutrients for Increased Energy
Energy NADH™ 12.5mg Energy NADH™ 12.5mg
Improve Energy & Cognitive Function
Mitochondria Ignite™ with NT Factor® Mitochondria Ignite™ with NT Factor®
Reduce Fatigue up to 45%

Natural Remedies

Fatigue & Fibro Fog: Could You Have a B-12 Deficiency? Fatigue & Fibro Fog: Could You Have a B-12 Deficiency?
Broad Spectrum Protection Against Brain Aging Broad Spectrum Protection Against Brain Aging
Research Links Green Tea to Weight Loss Research Links Green Tea to Weight Loss
Magnesium + Malic Acid: One-Two Punch for Pain & Fatigue Magnesium + Malic Acid: One-Two Punch for Pain & Fatigue
Are You Obtaining the Proper Enzymes? Are You Obtaining the Proper Enzymes?

FIBROMYALGIA RESOURCES
What is Fibromyalgia?
Fibromyalgia 101
Fibromyalgia Symptoms
Fibromyalgia Treatments
| CFS RESOURCES
What is CFS?
ME/CFS 101
ME/CFS Symptoms
ME/CFS Treatments
| FORUMS
Fibromyalgia
ME/CFS
ADVANCED MEDICAL LABS
WHOLESALE  |  AFFILIATES
GUARANTEE
CONTACT US
PRIVACY
RSS
SITE MAP
ProHealth on Facebook  ProHealth on Twitter  ProHealth on Pinterest  ProHealth on Google Plus
Credit Card Processing