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Oxygen
OXYGEN, OZONE, & HYDROGEN PEROXIDE
Majid Ali, M.D.
(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
References
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.
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