Oxygen, Ozone, & Hydrogen Peroxide
By Majid Ali, M.D.<email@example.com>
July 17, 2003
(Abridgement from The Journal of Integrative Medicine article: Oxidative Regression To Primordial Cellular Ecology (ORPEC))
The author's clinical experience has led him to conclude that oxygenative antioxidant therapies such as nasal oxygen and intravenous infusions of ozone-oxygen gas mixture and hydrogen peroxide are among the most beneficial therapies for reversing the ORPEC state.
Since oxygen, ozone and hydrogen peroxide act as oxidants in a laboratory setting, therapies employing those agents are generally deemed oxidative therapies.191-193 Until recently, the author accepted that view uncritically. However, it is clear from studies presented in this article that this is a gross error. In reality, such therapies in the context of the ORPEC state are powerful oxygenative and antioxidant therapies. The reason for that widespread misconception is the failure to clearly understand the complex biologic consequences of adding oxygen, ozone, and hydrogen peroxide to severely impaired enzymatic and cellular ecosystems in patients with accelerated oxidative injury.
A Burst of Thunderstorm, A Burst of Oxidants
An analogy of a burst of thunderstorm may be used to explain the possible mechanism action of ozone. The still air in a city on a hot, humid summer afternoon is thick with stagnant smog. The traffic on city streets is snarled. Tree leaves are dry and limp. Many persons are distressed by air pollution. Suddenly, dark clouds loom large and bring a heavy thunderstorm. Strong winds push out the polluted air. Tree leaves are bombarded by heavy rains. The healthy and robust leaves of trees withstand the storm well, while older and weakened leaves are severely damaged. Many withering leaves on tree brances are blown away. After the thunderstorm subsides, the air is clean and crisp. The trees looked washed, their leaves fresh and shiny. Bursts of intravenously injected ozone and hydrogen peroxide affect the blood elements the same way. The membranes of healthy erythrocytes withstand the oxidative stress of ozone and hydrogen peroxide well, recovering their normal morphology after initial membrane deformities. The senescent cells, by contrast, shrink and undergo lysis.
Below, some theoretical, clinical and experimental considerations are presented that shed light on the apparent paradox of agents that are oxidizing in their essential roles, and yet provide the basis for oxygenative antioxidant therapies.
Intermittent Nasal Oxygen
The oxygenative role of nasal oxygen is self-evident. Oxygen is also a powerful oxidizer, as discussed earlier in the section devoted to spontaneity of oxidation in nature. The ORPEC hypothesis provides a clear scientific basis for oxygen's ability to also serve the opposing antioxidant role. As discussed earlier, anoxia increases oxidative stress directly by facilitating the generation of toxic reactive species as well as indirectly by causing acidosis.
In this author's clinical experience, the use of intermittent nasal administration of oxygen (2.5 to 3.5 L/min given for periods of one hour two or three times a day) benefits most patients in the ORPEC state. It is also the opinion of the author that oxygen therapy is very underutilized in the care of patients in the ORPEC state, such as those with fibromyalgia, chronic fatigue state, severe autoimmune disorders, and spreading malignant tumors. Oxygen is readily and inexpensively available to all patients. Also available are inexpensive portable rental units that may be used in travel as well.
When used intermittently and in moderate doses as described here, this therapy has been found to be completely free of adverse effects. The author also has limited experience with oxygen therapy in patients with severe pulmonary emphysema and pulmonary interstitial fibrosis. Evidently, the use of oxygen in such patients must be monitored closely so that oxygen therapy does not cause further deterioration in the function of central sensors for oxygen and carbon dioxide.
Intravenous Ozone Therapy
Ozone is triatomic oxygen with a high electrovoltaic potential. Ozone gas infused intravenously at the Institute consists of a gaseous mixture with oxygen containing a very low concentration of ozone. It is prepared by passing pure oxygen through a high voltage field. The concentration of ozone generated depends on the rate of flow of oxygen as well as on the conditions of voltage and spacing of electrodes. The gaseous mixture used in our clinical practice is titrated to contain from 0.3 to 2.5% (30 to 50 ug O3/ml O2). Thus, intravenously administered "ozone" in reality represents 97 to 99.7% of pure oxygen.
Practitioners who have never administered ozone gas mixture intravenously often express concern about the possibility of air embolism caused by gas infusion. Such concern is totally unwarranted. Pure oxygen and ozone diffuse immediately into the blood and do not persist as gases. The author has tested for that on numerous occasions by injecting 2 ml of the ozone mixture into a large vein, then immediately drawing the blood back. Except on uncommon occasions, the blood drawn back from the vein is pink (ozone turns dark venous blood into pink blood) and free of any gas bubbles. One can safely presume that the process of dissolution of the gas mixture would be complete by the time it reaches the large veins in the thorax.
Another concern expressed by those unfamiliar with the clinical uses of ozone mixture is the toxicity of ozone as discussed by environmentalists. It must be recognized that those individuals are perturbed by the products of reaction of ozone with other ecopollutants such as oxides of nitrogen. Ozone is a highly reactive molecule. Indeed, ozone owes its many antiviral, antibacterial, and antifungal properties to this aspect of this specific aspect.
Microscopic Evidence for the Antioxidant Role of Intravenous Ozone Therapy
In the concentration used our in clinical practice, ozone causes temporary and reversible erythrocyte membrane damage as evidenced by clumping and red cell membrane deformity. The evidence for the oxidative nature of such erythrocyte membrane deformities has been previously demonstrated by the reversibility of such changes with antioxidants such as ascorbic acid, tocopherol, and taurine.56,57
How may the observed overall invivo antioxidant effects of ozone, a powerful invitro oxidant, be explained? Ozone has well established effects of improving tissue perfusion and cellular oxygenation.67 Just as the duality of oxygen allows it to be a molecular Dr. Jekyll and Mr. Hyde, reactive oxidant species also play dual roles. Not only do they inflict oxidative damage to enzymes, induce mutations, and damage cell membranes, they also serve many useful functions such as modulation of cellular redox dynamics, activation of gene transcription, signal transduction, and apoptosis.93-95 It seems that ozone evokes an upregulatory response from cell membrane-associated antioxidant enzyme systems just as all oxidants do from all biologic antioxidant systems. Though, direct quantitative data for those effects are not yet forthcoming. One may also, with good reason, speculate that ozone elicits similar responses from other matrix- and cell organelle-related antioxidant systems. There is yet an other important mechanism by which ozone protects patients with chronic illnesses from accelerated oxidative stress. Viruses, bacteria, fungi, PLFs and parasite inflict cellular injury by causing oxidative stress. Ozone also is a well established antiviral, antibacterial, and antifungal agent.58-63. Ozone through its powerful antimicrobial effects reduces the overall oxidative stress on persons with chronic viral, bacterial, fungal and PLF overgrowth syndromes. Thus, the ORPEC hypothesis carries strong explanatory power for the empirically observed biologic antioxidant effects of ozone.
Intravenous Hydrogen Peroxide Therapy for the ORPEC State
The biologic antioxidant effects of hydrogen peroxide, a potent oxidizer like ozone, are mediated by all the mechanisms cited for ozone in the preceding section. The clinical benefits of hydrogen peroxide infusions observed at the Institute in patients with fibromyalgia and chronic fatigue syndrome are the subject of a separate report.72
Reference from the complete article in The Journal of Integrative Medicine 1998;2:4-55
1. Ali M. Spontaneity of Oxidation in Nature and Aging. Monograph, Teaneck, New Jersey, 1983.
2. Ali M. The agony and death of cell. Syllabus of the Instruction Course of the American Academy of Environmental Medicine, Denver, Colorado, 1985.
3. Ali M. Molecular basis of cell membrane injury. In: Syllabus of the Instruction Course of the American Academy of Environmental Medicine. Denver, Colorado, 1990.
4. Ali M. Spontaneity of oxidation and chronic disease. In: Syllabus of the Instruction Course of the American Academy of Environmental Medicine, Denver, Colorado, 1992.
5. Ali M. Oxidative coagulopaty. In: Syllabus of the Capital University of Integrative Medicine, Washington, D.C., 1997.
6. Ali M. Spontaneity of oxidation in nature is the root cause of all illness. In: RDA: Rats, Drugs and Assumption. pp. 199-304. Life Span, Denville, New Jersey, 1995.
7. Ali M. Leaky cell membrane dysfunction. Monograph 1987. Teaneck, New Jersey.
8. Ali M. Oxidative plasma membrane injury and magnesium. Environmental Physician. Summer 1992. American Academy of Environmental Medicine, Denver, Colorado.
9. Ali M. Ascorbic acid reverses abnormal erythrocyte morphology in chronic fatigue syndrome. Am J Clin Pathol. 1990;94:515.
10. Ali M. Ascorbic acid prevents platelet aggregations by norepinephrine, collagen, ADP and ristocetin. Am J Clin Pathol. 1991;95:281.
11. Ali M. The basic equation of life. pp 225-236. In: The Butterfly and Life Span Nutrition. The Institute of Preventive Medicine Press, Denville, New Jersey. 1992.
12. Ali M. Spontaneity of oxidation and molecular basis of environmental illness. In: Syllabus of the 1991 Instruction Course of the American Academy of Environmental Medicine, Denver, Colorado, 1990.
13. Ali M. The Ghoraa and Limbic Exercise. The Institute of Preventive Medicine Press, Denville, New Jersey. 1993.
14. Ali M. What Do Lions Know About Stress? Life Span, Denville, New Jersey. 1996.
15. Ali M. The Cortical Monkey and Healing. The Institute of Preventive Medicine, Bloomfield, New Jersey. 1989.
16. Ali M. Healing, Miracles and the Bite of the Gray Dog. Life Span, Denville, New Jersey. 1997.
17. Ali M. Hypothesis: Chronic fatigue is a state of accelerated oxidative molecular injury. J Advancement in Medicine. 1993;6:83-96.
18. Ali M. The Canary and Chronic Fatigue. 1994. Life Span, Denville, New Jersey.
19. Ali M, Ali O. AA Oxidopathy: the core pathogenetic mechanisms of ischemic heart disease. J Integrative Medicine 1997;1:1-112.
20. Des Marais DJ, Strauss H, Summons RE et al. Carbon isotope evidence for the stepwise oxidation of the Proterozoic environment. Nature 1992;359:605-609.
21. Canfield DE, Teske A. Late proterozoic rise in atmospheric oxygen concentration inferred from phylogenetic and sulphur-isotope studies. Nature 1996;382;127-132.
22. Miller SM. The origins of life on earth. 1974. Prentice-Hall, Englewood Cliffs, New Jersey.
23. Margulis L. Biodicersity: Molecular biologica; domains, symbiosis and kingdon origins. Biosystems 1992;27:39-51.
24. Carpendale MT, Griffis J. Is there a role for medical ozone in the treatment of HIV and associated infections. Monograph. Bay Medical Research Foundation 1991.
25. Carpendale MT, Freeberg JK. Ozone inactivates HIV at non-cytotoxic concentrations. Antiviral Research 1991; 16:281-292.
26. Matassi R, D'Angelo F, Franching A, et al. Ozone therapy in Herpes Simplex and Herpes Zoster diseases. In: Laraus J. ed. Medical Applications of Ozone. International Ozone Association. 1985 pp 134-139. Norwalk, CT.
27. Botstein D, Chervitz SA, Cherry JM. Yeast as a model organism. Science 1997;277:1259-1260.
28. BLASTP analysis were done between all yeast ORF translations and all unique protein sequences in the human, mouse, rat, cow, and sheep sequences in GenBank as of 22 July 1997. We used the BLOSUM62 substitution mastrix and low-complexity filters seg and xnu. "Unknown function" means that the ORF had no entry in either the Gene_Product or Description fields within its SGD Locus page as of 30 July 1997. For all ORFs, 3783 (60.8%) have unknown function by this definition. BLASTP, version 2.0a, W. Gish, unpublished data; SF Altschul, W Gish, W Miller, EW Myers, DJ Lipman. J Mol Biol 1990;215:403.
29. Beale LS. Observations upon the nature of the red blood corpuscles. Trans Microsc Soc. London 1864:12:37.
30. Magath TB. Spirochetes in the blood. Am J Clin Pathol. 1953;23:691-693.
31. Mattman LH. Cell Wall Deficient Forms: Stealth Pathogens. CRC, Boca Raton, 1992.
32. Ali M, Ali O, Bradford R. et al Immunostaining of candida organisms in peripheral smears. (Abstract). 1995. American Academy of Otolaryngic Allergy, Spring Meeting, Palm Desert, CA.
33. Ali M and Ramanarayanan MP: A computerized micro-ELISA assay for allergen-specific IgE antibodies. Am J Clin Pathol 1984;81:591.
34. Ali M, Ramanarayanan MP, Nalebuff DJ, et al: Serum concentrations of allergen-specific IgG antibodies in inhalant allergy: Effect of specific Immunotherapy. Am J Clin Pathol. 1983;80:290.
35. Ali M. Altered States of Bowel Ecology. Monograph. Life Span, Denville, New Jersey 1983.
36. Lorian V, Waluschka A. Blood cultures showing aberrant forms of bacteria. Am J Clin Pathol 1972;57:406-409.
37. Lorian V, Atkinson B. Abnormal forms of bacteria produced by antibiotics. Am J Clin Pathol 1975;64:678-688.
38. Komber KR, Boon RJ, Sutherland R. Comparative effects of amoxycillin and ampicillin on the morphology of Eschercia coli in vivo and correlation with activity. Antimicrob Agents Chemother 1977;12:736-744.
39. Nakao M, Nishi T, Tsuchiya K. In vitro and in vivo morphologic response of Klebsiella pneumoniae to cefotiam and cefazolin. Antimicrob Agens Chemother 1981;19:901-910.
40. Davis KJ, Vogel P, Fritz DL, et al. Bacterial filamentation of Yersenia pestis by B-lactam antibiotics in experimentally infected mice. Arch Pathol Lab med 1997;121:865-8. -induced
41. Dwyer JJ, Burnett LE. Acid based status of the oyster Crassostrea virginica in response to air exposure and to infections by Perkinsus marinus. Biol Bulletin 1996;190:139-147.
42. Knoll AH, in Origins and Early Evolution of the Metazoa (eds Lipps, JH Signor, D.W.53-84. (Plenum, New York, 1992).
43. Holland HD. The Chemistry of the Atmosphere and Oceans (Wiley, New York, 1978).
44. Knoll AH. Breathing room for early animals. Nature 1996;382:111-112.
45. Mattman LH. Cell Wall Deficient Forms: Stealth Pathogens. CRC Press, Boca Raton, Florida, 1993.
46. Henning W. Phylogenetic Systematics. University of Illinois Press, Urbana, Il.) 1966.
47. Margulis L. Symbiosis in Cell Evolution. 1992 2nd edn. WH Freeman, New York
48. Gross M. Life on the Edge:Amazing Creatures Thriving in Extreme Environment. Plenum 1998. England.
49. Saccharomyces Genome Database (SGD) at http://genome-www.stanford.edu/Saccharomyces/;Yeast Genome from MIPS (Martinsried Institute for Protein Sequences) at http://speedy.mips.biochem.mpg.de/mips/ yeast/ www.proteome. com/YPDhome.html; A. Goffeau et al., Science 1996;274:546. The Saccharomyces Genome Database is suppported by an NIH research resources grant (HG 01315).
50. Kataoka T. Cell 1985;40:19-22.
51. Miller RV. Bacterial gene swpping in nature. Scientific American 1998;January; 67-71.
52. Ali M. Oxidant injury pokes holes in cell membranes. In: The Canary and Chronic Fatigue. pp 197-205. Life Span, 1995. Denville, New Jersey.
53. Ali M. Oxidative theory of cell membrane and plasma damage. In: RDA: Rats, Drugs and Assumption. Page 281-302. 1995 Life Span, Denville, New Jersey.
54. Ali M, Ali O. Leaky cell membrane dysfunction. In: AA oxidopathy: The core pathogenetic mechanism of ischemic heart disease. pp 72-74. J Integ Medicine 1997;1:6-112.
55. Ali M. Experience with intravenous nutrient therapy for allergic patients with chronic fatigue. Am Acad Otolaryngic Allergy Abstracts Summer 1992;p23.
56. Ali M. Intravenous Nutrient Protocols in Molecular Medicine. Institute of Preventive Medicine. 1989. Bloomfield, New Jersey.
57. Ali M. Leaky cell membrane dysfunction. Monograph 1987. Teaneck, New Jersey.
58. Yusuf, S. Calcium antagonists in coronary artery disease and hypertension-Time for reevaluation? Circulation 1995;92:1079-1082.
59. Furberg CD, Psaty BM, Meyer JV. Nifedipine: Dose-related increase in mortality in patients with coronary heart disease. Circulation;92:1326-1331.
60. Boden WE, Schelewaert R, Walters EG. Design of a placebo-controlled clinical trial of long-acting diltiazem and aspirin versus aspirin alone in patients receiving thrombolysis with a first acute myocardial infarction. Am J cardiol 1995;75:1120-1123.
61. Thadani U, Zellner S, Glasser S et al. Double-blind, dose-response, placebo-controlled multicenter study of nisoldipine: a new second-generation calcium channel blocker in angina pectoris. Circulation 1991;84:2398-2408.
62. Fisher A, Bogouslaviskt J. Further evolution toward effective therapy for acute ischemic stroke JAMA;279:1298-1303.
63. Woods, KL, Fletcher S. Long-term outcome after intravenous magnesium sulphate in suspected acute myocardial infaction: The second Leicester Intravenous Magnesium Intervention Trial (LIMIT-2). Lancet 1995;343:816-9.
64. Woods KL, Fletcher S, Roffe C, Haider Y. Intravenous magnesium sulphate in suspected acute myocardial infarction: Results of the second Leicester Intravenous Magnesium Intervention Trial (LIMIT-2). Lancet 1992;339:1553-8.
65. Ali M. Experience with intravenous nutrient therapy for allergic patients with chronic fatigue. Am Acad Otolaryngic Allergy Abstracts Summer 1992;p23.
66. Seelig MS, Elin RJ. Reexamination of magnesium infusions in myocardial infarction. Am J cardiol 1995;76:172-173.
67. Halstead BW. The Scientific Basis of Chelation Therapy. Golden Quill Publishers, Inc. Box 1278, Colton, Ca
68. Baldridge CW, Gerald RW. The extra respiration of phagocytosis. Am J Physiol 1933;103:235.
69. Berendes H, Bridges RA, Good RA. A fatal granulomatosis of childhood. The clinical study of a new syndrome. Minn Med 1957;40:309.
70. Cohen MS, Metcalf JA, Root RK. Regulation of oxygen metabolism in human granulocytes: Relationship between stimulus binding and oxidative response using plant lectins as probes. Blood 1980;55:1003.
71. Curnutte JT, Babior BM. Biological defense mechanisms. The effect of bacteria and serum on superoxide production by granulocytes. J Clin Invest 1974;53:1662.
72. Babior BM, Kipnes RS, Curnutte JT. Biological defense mechanisms. The production by leukocytes of superoxide, a potential bacterial agent. J Clin Invest 1973;52:741.
73. Ali M. Cell Membrane Stressors. Monograph 1987
74. Virchow R. Die Cellularpathologie in ihrer Bedeutung auf physiologische und pathologische Gewebslehre. Hirschwald, Berlin 1858
75. Bordue L. Recherches sur le tissu muqueux ou l'organ cellulaire. Paris 1767, 1 and 2.
76. Reichert CB. Vergleichende Beobachtungen uber das Bindegewebe und die verwandten Gebilde. Dorpat 1845, S.168.
77. Rokitansky C. v., Handbuch der pathologischen Anatomie. Wein 1846.
78. Pischinger A. Matrix and Matrix Regulation. 1975 Haug International, Brussels.
79. Bradford R. Henry A. Oxidology. 1997. Bradford Research Institute. San Diego
80. Keidel W. Lehrbuch der Klimatologie. G. Thieme Verlag. Stuttgart 1970.
81. Nimni ME. ed. Collagen 1-4. 1988 CRC, Boca raton, Florida.
82. Berg RA, Prockop DJ. Biochem. Biophys Res Commun 1973;52:115-120.
83. Holmgren SK, Taylor KM, Bretscher LE, et al. Code of collagen's stability deciphered. Nature 1998;392:666.
84. Shaw W. Role for certain yeast and bacteria byproducts discovered by organic acid testing in the etiology of a wide variety of human diseases. Bulletin of the Great 84.
85. Sell D, Monnier V. Structure elucidation of a senescence cross-link from human extracellular matrix. Implications of pentoses in the aging process. J Biol Chem 1989;264:21597-21602.Plains laboratory. Overland Park, KS 66204
86. Shaw W. Role for certain yeast and bacteria byproducts discovered by organic acid testing in the etiology of a wide variety of human diseases. Bulletin of The Great Plains Laboratory. Overland park, KS 66204 (913) 341-8949.
87. Gupta S. Aggarawal and Heads C. Dysregulated immune system in children with autism. Beneficial effects of intravenous immune globulin on autistic characteristics. Autism Develop Dis 1996;26:439-452.
88. Nagaraj RH et al. Suppression of pentosidine formation in galactosemic rat lens by an inhibitor of aldose reductase. Diabetes 1994;43:580-6.
89. Cuatrecases P, Tell GPE. Insulin-like activity of coconcanavalin A and wheat agerm agglutinin-direct interactions with insulin receptors. Proc Natl Acad Sci USA 1973;70:485-9.
90. Erickson RH, Kim YS. Interaction of purified brush-border membrane amniopeptidase N and dipeptidase IV with lectin-Sepharose derivatives. Biochim Biophys Acta 1983;743:37-42.
91. Pischinger A. Matrix and Matrix Regulation. Haug International. 1975, Brussels, pages 69-78
92. Klotz SA. A fibronectin receptor on Candida albicans mediates adherence of the fungus to extracellular matrix. J Infectious Dis 1991;163:604-6.
93. M. Kolarova. Host-tumor relationship XXXIV. Hyaluronidase activity and hyaluronidase inhibitor in the serum of patients with malignant tumors. Neoplasma 1977;24:285.
94. Savolainen ER. Enzymes of collagen biosynthesis in diseases of the liver and connective tissues. Changes in prolyl hydroxylase and galactosylhydroxylsyl glucosyltransferase in serum and tissues. Chem Absts 1979 91:1729Ilt.
95. Alitalo K, et al. Extracellular matrix proteins characterize human tumor cell lines. International Journal of Cancer 1981;27:755.
96 Harris DA. Bioenergetics at a glance. 1995. pp84-85. Blackwell Science.
97. De Stefano N, Argov Z, Matthews PM, Karpati G, Arnold DL. Impairment of muscle mitochondrial oxidative metabolism in McArdle's disease. Muscle & Nerve 1996;19(6):764-9.Harris
98. Sjostrand FS. Electron microscopy of mitochondria and cytoplasmic double membranes. Nature (London) 1953;171:30.
99. Lindane AW, Marzuki S, Ozawa T, et al. Mitochondrial DNA mutations as an important contributor to aging and degenerative diseases. Lancet 1985;1:642-5.
100. Babcock GT, Wickstrom M. Oxygen activation and the conservation of energy in cell respiration. Nature 1992;356:301-309.harris
101. Cui L, Schinazi RF, Gosselin G, et al. Effect of beta-enantriomeric and racemic nucleoside analogues on mitochondrial functions in HepG2 cells. Implication for predicting drug hepatotoxicity. Biochemical Pharmacology. 1996;52(10):1577-84.
102. Cui L, Yoon S, Schinazi RF, et al. Cellular and molecular events leading to mitochondrial toxicity of 1-(2-deoxy-2-fluoro-1-beta-D-arabinofuranosyl)-5-iodouracil in human liver cells. J Clin Invest 1995;95(2):555-63.
103. Hickman PF, Kemp GJ, Thompson CH, Salisbury AJ, Wade K, Harris AL, Radda GK. Bryostatin 1, a novel antineoplastic agent and protein kinase C activator, induces human myalgia and muscle metabolic defects: a 31P magnetic resonance spectroscopic study. British Journal of Cancer 1995;72(4):998-1003.
104. Altschuld RA, Jung DW, Phillips RM, et al. Evidence against norepinephrine-stimulated efflux of mitochondrial Mg2+ from intact cardiac myocytes. Am J Physiol. 1994;266:H1103-11.
105. McCully KK, Sisto SA, Natelson BH. Use of exercise for treatment of chronic fatigue syndrome. Sports Medicine 1996;21(1):35-48.
106. Eisenger J, Plantamura A, Ayavou T. Glycolysis Abnormalities in Fibromyalgia. J Amr Coll Nutr 1994;13(2):144-148.
107. Wysenbeck AJ, Shapira Y, Leibovici L. Primary fibromyalgia and the chroanic fatigue syndrome. Rheumatol Int 1991;10:227-229.
108. Plioplys AV, Plioplys S. Electron-microscopic investigation of muscle mitochondria in chronic fatigue syndrome. Neuropsychobiology. 1995;32(4):175-81.
109. Vecchiet L, Montanari G, Pizzigallo E, Iezzi S, deBigontina P, Dragani L, Vecchiet J, Giamberardino MA. Sensory characterization of somatic parietal tissues in humans with chronic fatigue syndrome. Neuroscience Letters 1996;208(2);117-20.
110. Cheney PR, Davidson M, Voyles CS, Wilson S. Bicycle Ergometry with gas analysis and neuroendoctrine responses to exercise in chronic fatigue syndrome. Albany, NY 1992.
111. Mengshoel AM, Forre O, Komnaes HB. Muscle strength and aerobic capacity in primary fibromyalgia. Clin Exp Rheumatol 1990;8:475-479.
112. Plioplys AV. High dose L-Carnitine improves the chronic fatigue syndrome in a prospective cross-over study. Neuropsychobiology 1997;35:16-23.
113. Is fibromyalgia caused by a glycolysis impairment. Nutr Rev 1994;52(7):248-250.
114. Kramer TR, Burri BJ. Modulated mitogenic proliferative responsiveness of lymphocytes in whole blood cultures after low carotene diet and mixed carotenoid supplementation in women. Am J Clin Nutr 1997;65:871-5.
115. Kuratsune H, Yamaguti K, Takahashi M, Misaki H, Tagawa S, Kitani T. Acycarnitine deficiency in chronic fatigue syndrome. Clin Inf Dis 1994; Volume 18, Suppl 1:562-67.
116. Rengisson A, Henriksson KG. The muscle in fibromyalgia - a review of Swedish studies. J Rheumatol 1989;16:144-149.
117. Schwartz, et al. SPECT imaging of the brain: Comparison of findings in patients with chronic fatigue syndrome, AIDS dementia complex and major unipolar depression. American Journal of Radiology. 1994 April;162.
118. Stevens SR. Using exercise testing to document functional disability in CFS. Journal of Chronic Fatigue Sundrome 1995;1 Numbers 3/4:127-129.
119. Trounce I, Byrne E, Marzuki S. Decline in skeletal muscle mitochondrial respiratory chain function: a possible factor in ageing. Lancet 1989;I(8639):637-638.
120. Wong R, Lepaschuk G, Zhu G, Walker D, Catelliger D, Burton D, Teo K, Collins-Nakaj R, Motague T. Low levels of cellular ATP following muscle exhaustion in vivo by phosphorus NMR in chronic fatigue syndrome. Chest 1992;102:1716-1722.
121. Ali M. Fibromyalgia: On The Moustache of a Mouse, (Work in progress). Life Span, Denville, New Jersey
122. Ali M. Oxidative coagulpathy and oxidative oxidopathy: Two core pathogenetic mechanisms of fibromyalgia. J Integrative Medicine. (in press).
123. Bradford coagulative and complement.
124. Rudel T, Bokoch G. Membrane and morphological changes in apoptotic cells regulated by caspase-mediated activation of PAK2. Science 1997;276:1571.
125. Xu DG, et al. Elevation of neuronal expression of NAIP reduced ischemic damage in the rat hippocampus. Nature Medicine 1997;3:997.
126. Vander Heiden MG, et al. Bci-xL regulates the membrane potential and volume homeostasis of mitochondria. Cell 1997;91:627.
127. Kothakota S, et al. Caspase-3-generated fragment of gelsolin: Effector of morphological change in apoptosis. Science 1997;278:294.
128. Research News. Death by Dozens of Cuts. Science 1995;280:32-34.
129. McGregor NR, Dunstan RH, Zerbes M, Butt HL, Roberts TK, Klineberg IJ. Preliminary determination of a molecular basis to chronic fatigue syndrome. Biochemical and Molecular Medicine 1996;1-9.
130. Freed DLJ. Dietary lectins and disease. In: Food Allergy and Intolerance. Eds: Brostoff J, Challacombe SJ. 1987 Bailliere Tindall, East Sussex, England.
131. Cuatrecases P, Tell GPE. Insulin-like activity of coconcanavalin A and wheat agerm agglutinin-direct interactions with insulin receptors. Proc Natl Acad Sci USA 1973;70:485-9.
132. Erickson RH, Kim YS. Interaction of purified brush-border membrane amniopeptidase N and dipeptidase IV with lectin-Sepharose derivatives. Biochim Biophys Acta 1983;743:37-42.
133. Freed DLJ. Non-Allergic Effects of Food. In Brostoff J, Challacombe SJ (eds.): Food Allergy and Intolerance. London, Bailliere Tindall 1987,375-400.
134. Ganguly P, Fossett NG. Evidence for multiple mechanisms of interaction between wheat gern agglutinin and human platelets. Biochim Biophys Acta 1980;627:256-261.
135. Hedo JA, Harrison LC, Roth J. Binding of insulin receptors to lictins: evidence for common carbohydrate determinants on several membrane receptors. Biochemistry 1981;20:3385-3393.
136. Hilgert I, Horejsi VA, Angelisova P, Kristofova H. Lentil lectin effectively induces allotransplantation tolerance in mice. Nature 1980;284:273-5.
137. Livingston JN, Purvis BJ. Effects of wheat germ agglutinin on insulin binding and insulin sensitivity of fat cells. Am J Physiol 1980;238:E267-75.
138. Nirmul G, Severin C, Taub RN. In vivo effects of con A. I. Immunosuppressive effects. Transplantation 1972;14:91-5.
139. Oppenheim JJ, Rostenstreich DL, eds: Mitogens in immunology. New York: Academic Press, 1976.
140. Shier WT. Concanavalin A as in inflammogen. In: Bittiger H, Schnebli HP, eds. Concavalin A as a tool. London: John Wiley and Sons. 1976;573-9.
141. Stillmark H. Uber rizin, ein giftiges ferment aus Samen von Ricinis communis L., und ainigen anderen Euphorbiaceen. Dorpat (Tartu), 1888. Inaugural dissertation.
142. Landsteiner K, Raubitschek H. Boebachtungen uber Hamolyse and hamagglutination. Zenbralbl Bakteriol 1907;45:660-7.
143. Boyd WC. Lectins. Ann NY Acad Sci 1970;169:168-90.
144. Renkonen KO. Studies on hemagglutinins present in seeds of some representatives of family of leguminoseae. Ann Med Exp Biol Fenniae 1948;26:66-72
145. Boyd WC, Shapleigh E. Diagnosis of subgroups of blood groups A and B by use of plant agglutinins (lectins). J Lab Clin Med 1954;44:235-7.
146. Hedo JA, Harrison LC, Roth J. Binding of insulin receptors to lictins: evidence for common carbohydrate determinants on several membrane receptors. Biochemistry 1981;20:3385-3393.
147. Hilgert I, Horejsi VA, Angelisova P, Kristofova H. Lentil lectin effectively induces allotransplantation tolerance in mice. Nature 1980;284:273-5.
148. Livingston JN, Purvis BJ. Effects of wheat germ agglutinin on insulin binding and insulin sensitivity of fat cells. Am J Physiol 1980;238:E267-75.
149. Nirmul G, Severin C, Taub RN. In vivo effects of con A. I. Immunosuppressive effects. Transplantation 1972;14:91-5.
150. Oppenheim JJ, Rostenstreich DL, eds: Mitogens in immunology. New York: Academic Press, 1976.
151. Edwards JE, Jr. Invasive candida infections: Evolution of a fungal pathogen. N Eng J Med 1991;324:1060-1062.
152. Ali M, Ali O, Bradford R. et al Immunostaining of candida organisms in peripheral smears. (Abstract). 1995. American Academy of Otolaryngic Allergy, Spring Meeting, Palm Desert, CA.
153. Ali M and Ramanarayanan MP: A computerized micro-ELISA assay for allergen-specific IgE antibodies. Am J Clin Pathol 1984;81:591.
154. Ali M, Ramanarayanan MP, Nalebuff DJ, et al: Serum concentrations of allergen-specific IgG antibodies in inhalant allergy: Effect of specific Immunotherapy. Am J Clin Pathol. 1983;80:290.
155. Ali M. The bloodstream: An Open Ecosystem. In RDA: Rats, Drugs and Assumption. Page 424-435. 1995 Life Span, Denville, New Jersey.
156. Ali M. Naked bacteria, naked yeast. In RDA: Rats, Drugs and Assumptions. Pages 455-457. 1995 Life Span, Denville, New Jersey.
157. Walsh TJ et al. Detection of circulating Candida enolase by immunoassay i patients with cancer and invasive candidiasis. N Eng J Med 1991;324:1026.
158. Roberts GD. Detetction of fungi in clinical specimens by phase-contrast microscopy. J Clin Micrbiol 1975;2:261-265.
159. Taschdjian CL, et al. Post Mortem Studies of Systemic Candidiasis I. Diagnostic Validity of Precipitin Reaction and Probable Origin of Sensitization to Dytoplasmic Candidal Antigens. Sabouraudia 1969;7:110.
160. Jarvis WR. and the National Nosocomial Infections Surveillance System. Centers for Disease Control. Nosocomial Fungal Infections. January 1980-April 1990. Presented at the Third International Conference on Nosocomial Infections. Atlanta July 31-August 3, 1990.
161. Mattman LH. L forms isolated from infections, in Microbial Protoplasts, Spheroplasts, and L Forms. Guze L.B., Ed., Williams & Wilkins, Baltimore, 1968, 472-483.
162. Mattman LH, Tunstall LH, Kispert WG. A survey of L variation in the salmonellae, Zentralbl, Bakteriol, Parasitekd, Infektionskr, Hyg. Abt. 1 Orig. 1969;210:65-74.
163. Mattman LH, Tunstall LH, Rossmoore HW. Induction and characteristics of staphylococcal L forms. Can J Microbiol 1961;7:705-713.
164. Almquist E. Studien uber das Verhalten einiger pathogenen mikroorganismen bei niedriger temperatur. Zbl. Bakt. I Abt Orig. 1908;48:175-186.
165. Almquist E. Variation and life cycles of pathogenic bacteria. J Infect Dis 1922;31:483-493.
166. Metchnikoff E. Untersuchungen uber die intracellular verdauung berwirbellosen thieren. Arb Zoologischem Inst Univ Wien 1883;5:141
167. Svoboda A. Regeneration of yeast protoplasts in agar gels. Exp Cell Res 1966;44:640-642.
168. Svoboda A, Necas O. Mechanisms of regeneration of yeast protoplasts. VI. An experimental blocking of regeneration of protoplasts. Folia Biol (Prague) 1968;14:390-397.
169. Mattman LH. Cell Wall Deficient Forms: Stealth Pathogens. CRC Press, Boca Raton, Florida, 1993.
170 Mattman LH. Cell Wall Deficient Forms: Stealth Pathogens. CRC Press, Boca Raton, Florida, 1993.
171. Prasad I, Bradley SG. Cell wall defective variant of Nocardia rubra. J Gen Microbiol 1972;70:571-572.
172. Emmons CW, Binford CH, Utz JP, Kwon-Chung KJ. Medical mycology. Lea and Febiger, Philadelphia. 3rd edition. 1976;192-196.
173. Rippon JW. Medical Mycology: The pathogenic fungi and the pathogenic actinomycetes. W. B. Saunders Co., Philadelphia. 1974;191-195.
174. Klotz SA. A fibronectin receptor on Candida albicansmediates adherence of the fungus to extracellular matrix. J Infectious Dis 1991;163:604-6
175. Louria DB, Stiff DP, Bennett B. Disseminated moniliasis in the adult. Medicine (Baltimore) 1962;41:307-337.
176. Lehrer RI. Measurement of candidiacidal activity of specific leukocyte types in mixed cell populations. I. Normal, myeloperoxidase-deficient, and chronic granulomatous disease neutrophils. Infect Immun 1970;130:241-245.
177. Lehrer RI, Cline MJ. Leukocyte candidacidal activity and resistance to systemic candidiasis in patients with cancer. Cancer (Phila) 1971;27:1211-1217.
178. Ali M. Oxidant injury damages energy enzymes. The Canary and Chronic Fatigue. 1994. Life Span, Denville, New Jersey.
179. Thompsen AM. The oxidizing capacity of the earth's atmosphere: probable past and future changes. Science 1992;256:1157-1165.
180. Tytgat J, Hess P. Evidence for cooperative interactions in potassium channel gating. Nature 1992;359:420-423.
181. Ism LL, De Jongh KS, Patton DE, et al. Primary structure and functional expression of the B1 subunit of the rat brain sodium channel. Science 1992;256:839-842.
182. Caliguiri M, Murray C, Buchwald D, et al. Phenotypic and functional deficiency of natural killer cells in patients with CFID. J Immunol 1987;139:3306-3313.
183. Targan S, Stebbing N. In vitro interactions of purified cloned human interferons on NK cells: enhanced activation. J Immunol 1982;120:934-935.
184. Suhadolanik RJ, Reichenbach NL, Sobol RW, et al. Biochemical defects in 2-5A synthetase/RNAase pathway associated with chronic fatigue syndrome with encephalopathy. In: The clinical and scientific basis of myalgic enceplalomyeltitis/chronic fatigue syndrome. Byron Hyde, ed. Ottawa, Canada. The Nightingale Research Foundation. (Chapter 67) 1992;613-7.
185. Linde A, Anderson B, Svenson SB, et al. Serum levels of lymphokines and soluble cellular receptors in primary Epstein-Barr virus infection and in patients with chronic fatigue syndrome. The J Inf Dis 1992;165-994-1000.
186. Buchwald D, Cheney PR, Peterson DL, et al. A chronic illness characterized by fatigue, neurologic and immunologic disorders, and active human herpesvirus-6. Ann Int Medicine 1992;116:103-131.
187. Teresaki P. In: Chronic fatigue syndrome. Goldstein J, ed. Chronic Fatigue Syndrome Institute, Beverly Hills, CA, 1990.
188. Gupta S, Vayuvegula B. A comprehensive immunological analysis in chronic fatigue syndrome. Scan. J Immunol 1991;33:319-327.
189. Handbook of Toxicology Vol 1. Spector WS. ed. W.B. Saunders, Philadelphia, 1956. Pages 184-5.
190. El-Ebiary M, Torres A, Fabregas N, at al. Significance of the isolation of Candida species from respiratory samples in critically ill, non-neutropenic patients: an immediate postmortem histologic study. Am J Respir Crit Care Med. 1997;156:583-590.
191. Aubourg P. L'Ozone medical: Production, posologie, modes d'applications cliniques. Bull Med, Paris 1938;52:745-749.
192. Payr E. Uber Ozone Behandlung in der Chirurgie. Munch Med Wschr 1936;82:220-291.
193. Hydrogen peroxide farr
194. Vosmaer A. Ozone: Its manufacture, properties and uses. Van Nostrand Publisher, New York 1916.
195. Roy D, Wong PKY, Englebrecht RS, Chian SK. Mechanism of enteroviral inactivation by ozone. Appl Environ Microbiol 1981;41:718-723.
196. Bolton DC, Tarkington BK, Zee YC, Osebold JW. An in vitro system for studying the effects of ozone on mammalian cell cultures and viruses. Environ Res 1982a;27:466-475.
197. Sleigh J, Linter SPK. Hazards of hydrogen peroxide. British Med J 1985;291:1706.
198. Shenep JL, Stokes DC, Hughes WT. Lack of antibacterial activity after intravenous hydrogen peroxide infusion in experimental escherichia coli sepses. Infect Immun 1985;48:607-610.
199. Dockrell HM, Playfair JH. Killing of blood-state murine malaria parasites by hydrogen peroxide. Infect Immun 1983;39:456-459.
200. Weiss SJ, Young J, LoBuglio A, et al. Role of hydrogen peroxide in neutrophil-mediated destruction of cultured endothelial cells. J Clin Invest 1981;68:714-721.
201. Root RK, Metcalf J, Oshino N, et al. H2O2 release from human granulocytes during phagocytosis. J Clin Invest 1977;60:1266-1279.
202. Farr CH. Possible therapeutic value of intravenous hydrogen peroxide. Second International Symposium; Chelating Agents in Pharmacology, toxicology and Therapeutics 1987; Charles University, Pilsen, Czechoslovak (In press).
203. Farr CH. Physiological and biochemical responses to intravenous hydrogen peroxide in man. J ACAM 1987; (In Press).
204. Ali M. Star Wars Medicine. In: The Cortical Monkey and Healing. pp 101-160. Institute of Preventive Medicine, Denville, New Jersey 1990. Bloomfield, New Jersey
205. Ali M. Enegetic- Molecular Medicine. In: RDA: Rats, Drugs and Assumptions. pp 1995. Life Span, Denville, New Jersey.
Comments always appreciated e-mail
Subscribe to our e-newsletter with our web updates e-mail us and say "subscribe"
Learn about the books of Majid Ali, M.D.
|All information posted on this web site is the opinion of the author and is provided for educational purposes only. It is not to be construed as medical advice. Only a licensed medical doctor can legally offer medical advice in the United States. Consult the healer of your choice for medical care and advice.|