Guest guest Posted September 29, 2001 Report Share Posted September 29, 2001 Rich, it is my understanding that 35% ,(only pharmacutical grade) h202 must be diluted with pharm. (glucose)down to 3% and dripped. This from my Dr......... Quote Link to comment Share on other sites More sharing options...
Guest guest Posted September 29, 2001 Report Share Posted September 29, 2001 Rich, This should go without saying...unless you're a doctor, don't attempt injecting H2O2 into your veins. The danger of killing yourself quickly and painfully is a little too great. A few people now and then have killed themselves with the accidental mis-use of natural therapies...and the pharmaceutical companies (and media) are quick to jump on that as a good excuse to further ban natural products. l) w/peace wes bennett wesbenn@... <A HREF= " http://www.wesbennett.com/ " >photography & graphics</A> > I would like to ask what is the safest maxim % of H2O2 > you can inject, also is it required to inject H2O2 > into a vain. Can you get the same results by inject in > to a muscle like a penicillin shot in the butt. > > Thank you > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted September 29, 2001 Report Share Posted September 29, 2001 The IV dose is .075%, not 3% as you stated. A dose of .150% is considered a overly strong dose. 3% H2O2 is designed for external use. jim alltogethernow@... wrote: > > Rich, it is my understanding that 35% ,(only pharmacutical grade) h202 > must be diluted with pharm. (glucose)down to 3% and dripped. This from > my Dr......... -- Light travels faster than sound. This is why some people seem bright until you hear them speak. --Lou Rubinacci jlambert@... http://www.entrance.to/madscience http://www.entrance.to/poetry Quote Link to comment Share on other sites More sharing options...
Guest guest Posted September 29, 2001 Report Share Posted September 29, 2001 Yep, my mistake. I am told by the healthcare assistant that the h202 is 3% BEFORE it is mixed into the glucose solution. (approx 1 liter) Quote Link to comment Share on other sites More sharing options...
Guest guest Posted September 29, 2001 Report Share Posted September 29, 2001 Yep, my mistake. I am told by the healthcare assistant that the h202 is 3% BEFORE it is mixed into the glucose solution. (approx 1 liter) Quote Link to comment Share on other sites More sharing options...
Guest guest Posted September 29, 2001 Report Share Posted September 29, 2001 <<Rich, it is my understanding that 35% ,(only pharmacutical grade) h202 must be diluted with pharm. (glucose)down to 3% and dripped. This from my Dr.........>> OUCH NO! HE'S 50 TIMES TOO HIGH!! From an authoratative article............. Hydrogen Peroxide is available currently in a 3% USP/NF grade and is ideal for intravenous use. It must be packed in an open vial however with a vented cap to allow the escape of oxygen pressure produced by the dismutation. Some physicians are concerned about sterilization because of the packaging but hydrogen peroxide is self sterilizing. Proper dilutions are simple. Add 1 mL of the 3% Hydrogen Peroxide USP/NF solution to each 100 mL carrier solution. A typical treatment plan would be to give 100 to 250 mL H202 of 0.03% concentration once or twice a week. After the initial schedule of 10 to 15 treatments, wait 30 to 60 days and evaluate the response. Within 1 hour after the intravenous infusion of 250 mL 0.15% H202 a 2% to 10% decrease was noted in the following blood constituents: Bun, Sodium, Potassium, Chloride, Uric acid, Calcium, Phosphorus, Total protein, Total bilirubin, Alkaline phosphatase, AST, ALT, GGTP, LDH, Iron and Globulin. Follow-up studies, 24 hours later, revealed all the above blood constituents had returned to normal pre-infusion levels. Here's the rest of this particular article.. _______________________ INTRAVENOUS HYDROGEN PEROXIDE THERAPY (Quick Overview) MECHANISMS Oliver (l) first reported the use of Intravenous Hydrogen Peroxide (H202), in 1920 in patients with Influenzal Pneumonia. An epidemic in Busrah in June and July of 1919, had a calculated death-rate over 80 percent. Oliver treated 25 critical patients with intravenous infusions of H202 and 13 fully recovered reducing the mortality to 48 percent. He was impressed with the rapid clinical response and postulated the effects were probably due to the oxidation of toxins more than the relief of hypoxia. Hydrogen peroxide used in surgical procedures had caused air embolisms, but he reasoned if the oxygen was released slowly, embolism should not occur. Venous oxygen embolism has been reported following the irrigation of anal fistulae (2), surgical wounds (3), and closed body cavities (4). Ulcerative colitis (5) has been produced in patients using H202 in enema solutions to break up fecal impactions. It has been shown, however, to destroy murine malaria parasites (7), and the bactericidal properties of H202 produced by neutrophils is well documented (8-10). Hydrogen peroxide appears to be involved in many intermediate biochemical pathways. Additionally, it appears to kill certain bacteria, parasites, yeast, protozoa, inhibit viruses, and oxidize immunocomplexes. T. Ramasarma (11), in his review on the " Generation of H202 in Biomembranes " , states: " H202 is a purposeful molecule in cellular metabolism and cannot be dismissed as a mere undesirable byproduct of oxygen species generation " . Hydrogen peroxide is generated in most biological membranes; cellular, mitochondrial, and nuclear. It is important for maintaining membrane integrity and regulating membrane transport through the alteration of Na-K ATPase activity. This was confirmed by Garner et al (12). Hydrogen peroxide fulfills the role of a secondary messenger in several hormonal pathways. As an example, H202 generation in the uterus is dependent on estrogen and is necessary for the production of progesterone. The iodination of thyroglobulin and thyroxine synthesis requires the presence of peroxidase, H202, and iodide (13). Thyroxine increases and hypothyroidism decreases hydrogen peroxide production in studies of liver mitochondria (14). Hydrogen peroxide has an insulin-mimic action and acts as a postbinding site on the plasma membrane to induce glucose transport (15). More recent studies of Helm (16) found the insulinomimetic action involves a common mechanism which links the generation of active oxygen species through the redox potential of the cell to the activation of a proteinase. It helps regulate metabolic control through protein modification which alters enzyme activities. Thermogenic control (11,14) appears to be exercised through the action of H202 on the mitochondria. At the mitochondrial level, H202 is generated by a number of substrates. Flavoproteins converge at ubiquinone which forms a link between H202 generation and the respiratory chain. Noradrenaline, thyroxine, and cold stimulate the system to generate heat. Heat increases the rate of H202 production and is dependent on alpha-adrenergic receptors which also control non-shivering thermogenesis. The balance of Ferric (3+) and Ferrous (2+) Iron in the body is critical to support lipid peroxidation of cellular membranes (27). It has been reported that a ratio of Fe(3+)/Fe(2+) of 1:1 to 8:1 is optimal to cause the formation of -OH radicals and lipid peroxidation. At ratios above or below these levels, lipid peroxidation does not occur. Physiological concentrations of either H202 or Ascorbic Acid may encourage lipid peroxidation and at these levels antioxidant protection is important. Increasing the concentration of H202, as occurs with therapeutic intravenous infusions, the Ferric/Ferrous ratio is maintained above 8:1 by keeping excess Ferrous (Fe2+) Iron oxidized to the Ferric (Fe3+) state. A principal mechanism of action of EDTA Chelation Therapy is reducing Free Radical damage and lipid peroxidation by complexing EDTA with Ferrous Iron (Fe3+:EDTA) which helps maintain the Ferric/Ferrous ratio above 8:1 (28) Weiss (8) reported H202 is an activator of neutrophils including aggregated immunoglobulin, activated complement components, immune complexes, or bacterial peptides. This would suggest the beneficial clinical effects observed with the use of ascorbic acid in inflammatory reactions, and its protective action against infections, is acting through the generation of H202. Also, there is no evidence H202 initiates or supports microsomal lipid peroxidation (51). The modification of (Na,K)-ATPase(12) by H202 also contributes to an increase in metabolic rate. Farr (40) reported whole blood specimens taken before, during, and after H202 infusions showed color changes consistent with oxyhemoglobin formation. Numerous blood profiles and CBC studies have been performed before and immediately after infusions of H202. Although early investigators reported no changes in blood elements and certain chemical constituents, except when injected into the carotid arteries, consistent changes have been reported. Within 1 hour after the intravenous infusion of 250 mL 0.15% H202 a 2% to 10% decrease was noted in the following blood constituents: Bun, Sodium, Potassium, Chloride, Uric acid, Calcium, Phosphorus, Total protein, Total bilirubin, Alkaline phosphatase, AST, ALT, GGTP, LDH, Iron and Globulin. Follow-up studies, 24 hours later, revealed all the above blood constituents had returned to normal pre-infusion levels. Some of the biological killing activity of H202 may be attributed to gamma interferon. Production of gamma interferon by human natural killer cells and monocytes, is stimulated by H202(58). Both exogenous and endogenous H202 appear to be in part responsible for immunoregulation. The rates of wound healing, stasis and vascular ulcers (18), peripheral occlusive disease (59,60), myocardial ischemia (33) and cerebral vascular disease (61) have all improved when treated with repeated intra-arterial infusions of H202 PHYSICAL PROPERTIES OF HYDROGEN PEROXIDE Hydrogen Peroxide was discovered in 1818 by the French Chemist Louis-Jacque Thenard. Hydrogen Peroxide, hydrogen dioxide (H202), is a colorless (blue in thick layers) odorless liquid; with a melting point -2 degree C: a boiling point 152 degrees C; decomposes 84 degrees C at 68 mm. pressure (68 degrees C at 26 mm.), soluble in water in all proportions; usually encountered as a dilute solution (3% H202) solution, that is, one volume of solution yields 10 volumes of oxygen), although available up to 35% strength. Its remarkable feature is its tendency to decompose readily into water and oxygen. Decomposition by light begins only in the near ultraviolet. Hydrogen peroxide solutions dismutate slowly, when undisturbed, at the rate of approximately 1% per month. The dismutation reaction is rapidly increased in the presence of particulate contaminates; i.e., dust, flakes of metal or glass or other particulate matter, at a rate which may be explosive. Cold retards dismutation and solution may be refrigerated or stored at temperatures below 0 degrees C. Hydrogen peroxide occurs only in traces in nature: mostly in rain and snow. It has not yet been detected in interstellar space. METABOLIC AND PHYSIOLOGICAL EFFECTS Numerous physiological effects are attributed to hydrogen peroxide and documented in the literature. Some of these effects may be broadly categorized as follows: 1. PULMONARY A. Increased oxygenation B. Alveolar debridement (31) 2. METABOLIC RATE A. Hormonal effect: Several hormonal effects have been reported to be regulated by the action of H202. Examples are: 1.Iodination of thyroglobin(13) 2. Production of thyronine (13) 3. Progestone production (107) 4. Inhibition of bioamines (108); dopamine, noradrenalin and serotonin 5. Prostaglandin synthesis (46,47,109) 6. Dopamine metabolism (110) 7. Regulates Reticulum Calcium Transport (111) 8. Oxidative stimulation: Hydrogen peroxide directly and indirectly stimulates oxidative enzyme systems. Micromolar amounts of infused H202 has been found to increase oxidative enzymatic activity to the maximum rate of reaction (40). 1. Increases GSH oxidation to GSSG which increases ATP production(112) 2. Activates Hexose Monophosphate Shunt(41) 3. Alters Na-K ATPase activity (12) 4. Regulates cellular (113) and mitochondrial (15) membrane transport 5. Regulates thermogenic control (11) 3. CARDIOVASCULAR RESPONSE A. Vasodilation 1. Dilation of peripheral vessels (31) 2. Dilation of coronary vessels (114) 3. Aortic strip relaxation response (115) 4. Cerebral arteriolar dilation (116,117) 5. Pulmonary arterial relaxation (118) B. Vasoconstriction 1. Essential Hypertension effect (31) 2. Peripheral vasoconstriction may occur in normal-tensive patients with concentrations at or below 0.0375% with no significant increase in mean pressures(123). C. Cardiac Responses (12-3) 1. Decreases Heart Rate 2. Decreases Vascular Resistance 3. Increases Stroke Volume 4. Increases Cardiac Output 5. Increases Cardiac Index 4. GLUCOSE UTILIZATION A. H202 mimics insulin (16) B. Increases glycogen production from glucose (119) C. Type II Diabetes Mellitus stabilized with H202 infusions (20) 5. GRANULOCYTE RESPONSE A. Depressed granulocytes after treatment then rebound measured after 24 hours (31) B. Secondary resistance to peroxide after exposure (109) C. Alteration of T4/T8 ratio with increase of T4 Helper cells (28) 6. IMMUNE RESPONSE A. Stimulates Monocytes (92) B. Stimulates T Helper cells (109) C. Stimulates Gamma Interferon production (58) D. Decreases B-cell activity (121) E. Responsible for immunoregulation (58) F. Regulates inflammatory response (122) INDICATIONS Intravenous Hydrogen Peroxide is used in the acute reactive conditions ; i.e., influenza, bronchitis, Herpes Zoster, asthmatic reactions, etc.) because of its direct killing effect on micro-organisms or its effect on vasospasm or bronchospasm. The long term effect, to regulate or modify the immune response through cellular activation or modification of immune dysfunction, such as EBV, Candida, CMV, Herpes, HIV, Diabetes Type II, COPD, vascular disease, arthritis, and etc., is an important therapeutic tool for every physician. The therapeutic use of intravenous H202 has been reported in the following diseases or conditions with varying results depending on the clinical investigator: l. Peripheral Vascular Disease 2. Cerebral Vascular Disease 3. Alzheimer 4. Cardiovascular Disease 5. Coronary Spasm (angina) 6. Cardioconversion 7. Arrhythmias 8. Chronic Obstructive Pulmonary Disease 9. Emphysema 10. Asthma 11. Influenza 12. Herpes Zoster 13. Herpes Simplex 14. Temporal Arteritis 15. Systemic Chronic Candidiasis 16. Chronic Recurrent Epstein Barr Infection 17. Diabetes Type II 18. HIV infections 19. Metastatic Carcinoma 20. Multiple Sclerosis 21. Rheumatoid Arthritis 22. Acute and Chronic viral infections 23. Chronic unresponsive bacterial infection 24. Parasitic infections 25. Parkinsonism 26. Migraine headaches 27. Cluster headaches 28. Vascular headaches 29. Chronic pain syndromes (multiple etiologies) 30. Environmental allergy reactors (Universal) Many in-vitro and some in-vivo studies have shown H202 to be bactericidal, fungicidal, parasiticidal, viricidal, and to lyse certain tumor cell types in cultures. The therapeutic benefit of H202 infusions in patients with any of the following infections and/or tumors may not be clinically documented. Therefore, no recommendation can be made until appropriate studies have been conducted. BACTERIA 1. Legionella pneumophila (62) 2. Treponema pallidum (63) 3. Escherichia coli (64) 4. Salmonella typhimurium (65) 5. Mycobacterium leprae (66) 6. Staphylococcus auerus (67) 7. Pseudomonas acruginosa (68) 8. Campylobacter jejuni (69) 9. Salmonella typhi (70) 10. Group B Streptococci (71) 11. Bacillus cereus (72) 12. Actinobacillus actinomycetem comitans (73) 13. Bacteroides (74) 14. Neisseria gonorrhoea (75) FUNGI 1. Histoplasma capsulatum (76) 2. Candida Albicans (77) 3. Coccidioides (78) 4. Paracoccidiodes (78) 5. Blastomyces (78) 6. Sporothrix (78) 7. Mucoraceae(78) 8. Aspergillus fumigatus (79) 9. Coccidioides immitis (80) PARASITES 1. Pneumocystis carinii (81) 2. Plasmodium yoelii (82) 3. Plasmodium berghei (82) 4. Toxoplasma gondii (83) 5. Nippostrongycus brasiliensis (84) 6. Naegleria fowleri (85) 7. Leishmania major (86) 8. Schistosoma mansoni (87) 9. Chlamydia psittaci (88) 10. Trichomonas vaginalis (89) 11. Tepanosoma cruzi (90) 12. Endameba histolytica (91) VIRUS 1. Human Immunodeficiency Virus (92) 2. Cytomegalovirus (67) 3. Lymphocytic choriomeningitis virus (93) 4. Tacaribe virus (93) TUMOR TYPE 1. Ehrlich carcinoma (94) 2. Neuroblastoma (95) CONTRAINDICATIONS PRECAUTIONS: Hydrogen Peroxide infusions are contraindicated in pregnancy, Chronic Granulomatous Disease (CGD), and any disorder of cell membrane stability (i.e. anemias). SIDE EFFECTS: The most frequent side effect reported (at concentrations above 0.0375%) is vasculitis, which may occur in the infused vein and/or its tributaries. This phenomenon is inconsistent, occurring repeatedly in some patients but rarely in others. According to Shingu, (97) epithelial and smooth muscle cells contain very little, if any, catalase and, therefore, may be sensitive to the effects of H202. There appears to be a critical concentration of H202 which is cytolytic, and will cause vasculitis if exceeded. It is, therefore, important to consider the concentration being infused and the size of the vessel. This reaction is less likely to occur if a larger vein in the antecubital area is used for infusion, and the rate of administration is reduced. Once the cytolytic concentration is exceeded, the cells swell up, become toxic and die. The exact mechanism by which H202 is cytotoxic are not defined, however, *NOTE* Recent studies have revealed the addition of 0.5 mg Manganese to the intravenous solution to be effective in controlling the endothelial damage caused by the H202 solution. It is reported that there may be no microscopic signs of cytotoxicity for 6 hours or longer after exposure of the cells to H202. Consequently, after you infuse a patient, the vasculitis may not be apparent until the following day. The application of heat may make the reaction more severe since heat speeds up the rate of most biochemical reactions, and this may be no exception. We recommend you use only the larger veins for infusion, and reduce the rate of infusion if you suspect the patient's blood flow rate is slower than usual. It has also been found useful to rotate between the veins and not use the same vein for two consecutive treatments. Rotate between veins and alternate treatments from one arm to the other. Some physicians report they have flushed the vessel post-infusion with additional heparin, or Decadron, but results have not been changed. All oral supplements and drugs should be withheld on the day of infusion. Taking antioxidants on the day of infusion would appear to be counterproductive and may aggravate the vasculitis. Intravenous H202 delays clotting by 20%, but reduces bleeding time approximately 50%. Caution should be exercised when giving H202 to patients taking anticoagulants since clinical data is not available at this time for comment. ALLERGIC PHENOMENON: Occasionally, a non-tender red streak will appear, tracing the route of the vessel above the point of infusion. This streak will often have a diffused fanned-out appearance radiating laterally from the central streak. No relationship has been identified between this superficial vascular phenomenon and the vasculitis previously described. This vascular phenomenon occurs randomly in patients and has been observed at a rate of about 1 in 50 infusions in concentrations greater than 0.0375%, but only 1 in 500 at concentrations at or below 0.0375%. Several hundred infusions have been given, and no other type of local or systemic allergic vascular reaction has been observed or reported. CHEST DISCOMFORT: Some physicians have reported occasional patient complaints of vague chest discomfort, sometimes associated with a feeling of shortness of breath. We received two reports that the chest discomfort was severe enough to discontinue the treatments. Bronchodilators should be withheld for at least a day before H202 is administered, if possible. INFUSION SITE PAIN: Pain at and above the infusion site is occasionally reported. The pain is described as a spastic ache and is most likely due to vasospasm. On rare occasions, the pain may extend from the point of infusion, at or below the antecubital area, up into the deltoid area. Reducing the rate of infusion, heat, and ice have all been ineffective in controlling the pain. We have found, when this occurs, the best thing to do is remove the needle and restart the infusion in another vein. We speculate the irritation to the vessel, at the point of penetration, causes a reflex vasospasm along the vessel. Changing the needle position or rotating its position in the same vein does little to relieve the discomfort. HERXHEIMER TYPE REACTION: Several physicians have reported an occasional Herxheimer-like reaction when treating patients with mucocutaneous candidiasis. Following infusions of H202 the patients were reported to have generalized migratory aching, nausea, headaches, chills, and fever. It has been reported to occur after one, two, and sometimes three treatments, but, thereafter, the patients report an improvement in their overall clinical status, and continue to improve with each succeeding treatment. No patients have been discontinued from treatments because of this reaction. It does not occur consistently nor is it predictable. TOXICITY Hydrogen peroxide is a product of intermediate metabolism, widely distributed throughout the body, and participates in a significant number of biochemical reactions. It is a principal electron receptor in the body in many RedOx reactions. A vast amount of knowledge exists about the chemistry of H202 in tissue slices, tissue cultures, bacteria, parasites, yeast, protozoa, blood cells, and isolated human, animal, and plant cells. Numerous examples of biochemical changes have been described in the literature, which are interpreted as toxic or damaging in the models studied. Clinically, however, no significant acute toxicity has been observed in several hundred patients, some receiving up to 40 to 50 infusions with concentrations up to 0.3 %. Also, no chronic or long term toxicity has been observed or documented up to two years post-multiple infusions. One patient received 3,600 mL of 0.15% of Hydrogen Peroxide intravenously in a period of 10 days without any side effect. This dosage is approximately 40 times greater than the currently recommended therapeutic dosage. Other studies suggest doses 500 times smaller than the currently recommended dose will have biological effect. This suggested intravenous infusions of Hydrogen Peroxide is extremely safe and has a very wide therapeutic range. Consequently, the majority of toxic reactions referred to in the literature, which occur with in-vitro studies under laboratory conditions, which could not exist in-vitro, have very little clinical application. Some of the in-vitro toxic effects are: A. Lipid Peroxidation (49,98) B. Single strand DNA breakage (99) C. Cytotoxic (concentrations above 10 mMol) (100) D. RBC hemolysis (26,101) E. Chromosomal Aberrations (102) F. Protein degradation (103) G. Glutathione Peroxidase depiction (104) H. Degredates Cytochrome C (105) I. Platelet Aggregation (106) FORMULAS INTRAVENOUS ADMINISTRATION OF H202 SOLUTION The PROPER DOSAGE is dependent upon the CONCENTRATION used, the VOLUME INFUSED, and the RATE OF INFUSION. The infusion mixture is prepared as follows: The preferred carrier is 5% Dextrose in Water or Normal Saline. Hydrogen Peroxide is available currently in a 3% USP/NF grade and is ideal for intravenous use. It must be packed in an open vial however with a vented cap to allow the escape of oxygen pressure produced by the dismutation. Some physicians are concerned about sterilization because of the packaging but hydrogen peroxide is self sterilizing. Proper dilutions are simple. Add 1 mL of the 3% Hydrogen Peroxide USP/NF solution to each 100 mL carrier solution. If you plan to give 250 mL treatment you add 2.5 mL of the peroxide in 250 mL of carrier, 5 mL to 500 mL carrier and etc. for the proper dilution. Select a medium to large vein close to the antecubital area for the infusion. Use a small winged needle and infuse slowly over a period of 1 to 1 1/2 hours. The rate of infusion and concentration are both important as explained below. THERAPEUTIC INFUSION SCHEDULES The dosage administered is dictated by the therapeutic and objective experience of the clinician. The physician should consider the clinical objective after the diagnosis has been properly established. A general rule: the more acute the pathology the greater the volume and concentration and the more frequent the infusions. The frequency may be maintained until the acute problem is considered stable, and then both dose and frequency reduced. As an example, a patient with acute influenza or Herpes Zoster may be placed on a schedule of 250 to 500 mL of H202 of 0.03% or less concentration, daily for 1 to 5 infusions or until clinical response is obvious. Occasionally, these patients may require a treatment once or twice a week for an additional 5 to 10 treatments, particularly in infections which have a tendency to become chronic such as Herpes or Hepatitis. A therapeutic regimen for a chronic, low grade infection or chronic illness would be to schedule smaller doses over a longer period of time. Examples of chronic illnesses in which long term therapy might be employed would include: Chronic candidias, chronic obstructive pulmonary disease, peripheral occlusive disease, chronic EBV, or Hepatitis, and etc. A typical treatment plan would be to give 100 to 250 mL H202 of 0.03% concentration once or twice a week. After the initial schedule of 10 to 15 treatments, wait 30 to 60 days and evaluate the response. Depending on the response, you may wish to give an additional series of 10 to 15 treatments and again wait and re-evaluate. An alternative is to keep the patient on bimonthly or monthly maintenance treatments for a year and then reevaluate annually. The following are examples of treatment schedules which have been employed in these selected cases. 1. ACUTE PULMONARY INFECTIONS INCLUDING INFLUENZA PNEUMONIA. Infusions of Hydrogen Peroxide have a rapid 'Alka-seltzer effect' in the lungs. If the patient has moist lungs and/or a productive cough, the treatment will usually cause coughing and mucous production to increase immediately. It may continue throughout the treatment but will subside soon after the treatment is completed. If the patient is quite ill and febrile, the initial treatment would be 250 to 500 mL of 0.03%. If the patient remains febrile the second day, give an additional 250 to 500 mL of 0.03%. Treat according to response, thereafter, every two to three days until the desired response is obtained. 2. CHRONIC LUNG DISEASE (COPD, BRONCHITIS, BRONCHIECTASIS, EMPHYSEMA) Chronic lung disease, which is moist and active, responds best to treatment. The response in dry emphysema or pulmonary fibrosis is less dramatic. Give 250 mL 0.03% weekly for 10 to 15 weeks. Frequently, the effects will be dramatic, with coughing and sputum production initially, and the patients reporting increased energy and ability to breathe within 24 hours. The effects of treatments are usually progressive improvement for 8 to 10 treatments, and then the effects plateau. Most patients will wish to continue on monthly maintenance treatments. 3. ALLERGIC REACTIONS, ASTHMA, ENVIRONMENTAL SENSITIVITY, ETC. The longer the patient has had their allergic reactive problem, the longer it will be before you will have a positive response. This general rule, however, does not always apply. Some patients respond rapidly, within 2 to 3 treatments. In these complex patients, schedule weekly treatments for 10 weeks, give the patient a 30 day rest, and repeat an additional 10 weekly treatments. You may give up to 40 to 50 treatments on this schedule, or until you feel maximum response has been obtained. Most patients will realize improvement after their first course of 10 treatments. Thereafter, patients show a gradual improvement with each successive group of 10 treatments. If the patient shows no improvement after 30 to 40 treatments, then no response is likely and therapy is discontinued. 4. ACUTE AND CHRONIC PAIN Angina, headaches, vasospasm, tumor pain, or neurological pain frequently show an immediate and dramatic response to one or two treatments. Chronic pain syndromes may require several (8-10) treatments but response is frequent. There is no good explanation why Hydrogen Peroxide should relieve pain, but, nevertheless, this has been a frequently reported clinical observation. Chronic, established pain of Post Herpetic Neuralgia may not respond to treatments, but the response in Acute Herpes Zoster is often dramatic. 5. EBV, CMV, HIV, HERPES, HEPATITIS ETC. Acute infections require frequent daily treatments, whereas, chronic infections require long term weekly treatments. Symptomatic response may occur after only 1 or 2 treatments, but antibody titers may not change until 10 to 30 weekly treatments have been given. 6. CEREBRAL VASCULAR, ALZHEIMER, TOXIC DEMENTIA, ETC. Perhaps the increased oxygenation can explain the sometimes rapid reversal of symptoms in these patients. Acuity, memory, recall, alertness, and other cerebral symptoms frequently improve quickly and the improvement appears to be long lasting. The results may also be related to changes in the bioamines in the brain because positive results are also seen in anxiety/depressive non-toxic young adults. Ten weekly treatments are usually given before the effectiveness of treatment is evaluated. 7. CARDIOVASCULAR AND PERIPHERAL VASCULAR DISEASE Using weekly treatments of smaller volume; i.e., 100 to 250 mL, can be very beneficial to these patients if your objective is to restore oxygenation to the tissue. If the objective is to push a gangrenous digit or extremity to the point of demarcation for surgical debridement, then 250 to 500 mL are given daily, for several days, until demarcation is completed. The following are actual case reports, from the initial studies (31) on the Intravenous Use of Hydrogen Peroxide. Higher concentrations were used in these studies than currently recommended. Same or similar cases have been repeated many times since, at the lower concentration of 0.03%, with equally good clinical results but WITHOUT vasculitis or other side effects. We, therefore, recommend you do not exceed the 0.03% concentrations. 1. Acute Herpes Zoster. 250 mL of 0.15% initially, then every two days for a total of 6 treatments. Comment: Resolved completely in less than 1 week with no residual. 2. Acute Influenza Syndrome. 250 mL of 0.15% initially, and 500 mL of 0.15% the second day. Afebrile after second day, but additional treatment the third day of 250 mL of 0.15%. Comment: Resolution of all symptoms after the second day with no residual. 3. Chronic Systemic Candidiasis: 250 mL of 0.15% once a week for 10 treatments, and then monthly followup for 10 months. Comment: Clinical response not observed until after the 4th treatment, then gradual improvement continued. Maintained on monthly treatments. 4. Severe COPD. Initial 250 mL of 0.15% which caused significant alveolar debridement and coughing up of copious amount of purulent material. Continued weekly infusions for 6 weeks, and by the end of the 6th treatment the patient no longer coughing. Pulmonary function improved and the patient returned to working full time. Comment: Maintained on treatment according to patients " feel the need " which re-occurs approximately every 4 to 6 weeks. 5. Acute Asthmatic Attack (12 yr old girl): Attack onset 24 hours prior to treatment Given 100 mL of 0.15% with complete resolution of the attack within 6 hours following the infusion. Comment: No followup treatment necessary. 6. Diabetes Mellitus Type II. 25 year history of diabetes taking 30 units NPH AM and PM. After 5 treatments of 250 mL of 0.15%, insulin reduced to 30 units AM and 15 units PM. Insulin reduced to 15 units AM only after 3 additional treatments because the patient was having symptoms of hypoglycemia. Discontinued all insulin after 10 treatments and given H202 on a monthly maintenance. Followup GTC appears more normal. Comment: Will maintain on schedule according to fasting blood sugars in future. 7. Chronic Post Herpetic Neuralgia: Post herpetic neuralgia persisting 1 year following a severe Herpes Zoster infection on right anterior and lateral chest wall. Given 250 mL of 0.075% weekly for 10 weeks. Neuralgic pain substantially reduced after 5th treatment and completely gone after 10th treatment. Comment: Will followup at 3 month intervals and as necessary. 8. Impending Cerebral Vascular Accident. 71 year old man with sudden onset two hours previously of confusion, paralysis, and weakness on left side of body, and drooling and unable to speak distinctively. Initial brood pressure 190/100, pulse normal. Given 250 mL of 0.03% H202 started immediately. All symptoms significantly improved within 30 minutes and completely resolved after 1 hour. Comment: Patient did not return for followup evaluation but was asymptomatic with blood pressure of 140/90 when he left the office. HYDROGEN PEROXIDE PROTOCOL REFERENCES 1. Oliver TH, Cantab BC, and DV: Influenzal Intravenous Injection of Hydrogen Peroxide. Lancet 1920; 1:432-433 2. Ramasarma T: Generation of H202 in Biomembranes. Biochemica et Biophysica ACTA 1982; 694: 69-93 3. Garner MH, Garner WH, Spector A: Kinetic ativity Change after H202 Modification of (Na,K)- ATPase. J Biolog Chem 1984; 259: 7712-7718 4. Wildberger E, Kohler H, Jenzer H, et al: Inactivation of Peroxidase and Glucose Oxidase by H202 and Iodide during In Vitro Thyroglobulin lodination. Mol Cell Endocrinol 1986; 46(2):149-154 5. Swaroop A and Ramasarma T: Heat Exposure and Hypothyroid Conditions Decrease Hydrogen Peroxide Production Generation in Liver Mitochrondia. J Biochem 1985; 226(2): 403-8 6. DH and Murray DK: Dexamethasone Inhibition of Hydrogen Peroxide-stimulated Glucose Transport. Endocrinology 1987; 120(l): 156-159 7. Jay BE, Finney JW, Balla GA, et a]: The Supersaturation of Biologic Fluids with Oxygen by the Decomposition of Hydrogen Peroxide. Texas Rpts Biol and Med 1964; 22: 106-109 8. Balla GA, Finney JW, Aronoff BL, et al: Use of Intra-arterial Hydrogen Peroxide to Promote Wound Healing. Am J Surg 1964; 108: 621-629 9. Zoschke DC and Staite ND: Suppression of Human Lymphocyte Proliforation by Activated Neutfophils or H202: Surviving Cells have an Altered T Helper/,r Suppressor Ratio and an Increased Resistance to Secondary Oxidant Exposure. Clin Immunol Immunopathol 1987; 42(2): 160-70 10. Finney JW, Balla GA, Race GJ, et al: Peripheral Blood Changes in Humans and Experimental Animals Following the Infusion of Hydrogen Peroxide into the Carotid Artery. Angio 1965; 16: 62-66 11. Mallams JT, Finney JW, and Balla GA: The Use of Hydrogen Peroxide As A Source of Oxygen in A Regional Intra-Arterial Infusion System. So M J 1962; 55: 230-232 12. Fuson RI, Kylstra JA, Hochstein P, et a]: Intravenous Hydrogen Peroxide Infusion as a Means of Extrapulmonary Oxygenation. Clin Res 1967; 15: 74 13. Minotti G and Aust SD: The Requirement for Iron(III) in the Initiation of Lipid Peroxidation by Iron(II) and Hydrogen Peroxide. J Biol Chem 1987: 262(3): 1098-104 14. Farr CH: The Therapeutic Use of Intravenous Hydrogen Peroxide (Monograph). Genesis Medical Center, Oklahoma City, OK 73139, Jan. 1987 15. Finney JW, Jay BE, Race GJ, et al: Removal of Cholesterol and Other Lipids from Experimental Animal and Human Atheromatous Arteries by Dilute Hydrogen Peroxide. Angiology 1966; 17: 223-228 16. 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 17. Urschel HE Jr: Cardiovascular Effects of Hydrogen Peroxide: Current Status. Dis of Chest 1967; 51: 180- 192 18. Finney JW, Urschel HC, Balla GA, et al: Protection of the Ischemic Heart with DMSO Alone or DMSO with Hydrogen Peroxide. Ann NY Acad Sci 1967; 151: 231-241 19. Urschel HC, Finney JW, Morale AR, et al: Cardiac Resuscitation with HydrogenPeroidde. Circ 1965; 31 (suppi 11): 11-210 20. Ackerman NB, Brinkley FB: Comparison of Effects on Tissue Oxygenation of Hyperbaric Oxygen and Intravascular Hydrogen Peroxide. Sur 1968; 63: 285-290 21. Germon PA, Faust DS, Brady, LW: Comparison of Arterial and Tissue Oxygen Measurements in Humans Receiving Regional Hydrogen Peroxide Infusions and Oxygen Inhalation. Radiology 1968; 91:669-672 22. Lorinez AL, y JJ, Livingstone MM: Studies on the Parenteral Administration of Hydrogen Peroxide. Anesthesiology 1948; 9: 162-174 23. Hothersall JD, Greenbaum AL, McLean P: The Functional Significance of the Pentose Phosphate Pathway in Synaptosomes: Protection Against PeroAdative Damage by Catecholamines and OAdants. J Neurochem 1982; 39: 1325-1332 24. Del Maestro RF, Thaw HH, Bjork J et a]: Free Radicals as Mediators of Tissue injury. Acta Physiol Scand 1980; 492(suppi): 43-57 25. Yamaja Setty BN, Jurck E, Ganley C et a]: Effects of Hydrogen Peroidde on Vascular Arachidonic Acid Metabolism. Prostag Leuko Med 1984; 14: 205-213 26. Polgar P, L: Stimulation of Prostaglandin Synthesis by Ascorbic Acid via Hydrogen Pcroxide Formation. Prostag 1980; 19: 693 27. Marshall PJ and Lands : In Vitro Formation of Activators for Prostaglandin Synthesis by Neutrophils and Macrophages from Humans and Guinea Pigs. J Lab Clin Med 1986; 108(6): 525-534 28. Tappel AL: Lipid Peroxidation Damage to Cell Component. Fed Proc 1973; 32: 1870 29. Shimada 0 and Yashuda H: Lipid Peroxidation and its Inhibition by Tinoridine. Biochem Biophys ACTA 1979; 572:531 30. Morehouse LA, Tien M, Bucher JR et a]: Effect of Hydrogen Pero)dde on the Initiation of Microsomal Lipid Pero)ddation. Biochem Pharm 1983; 32: 123-127 31. Dockrell HM and Playfair JH: Killing of Blood-Stage Murine Malaria Parasites by Hydrogen Peroxide. Infect Immun 1983;39: 456-459 33. Root R & Metcalf J, Oshino N, et al: H202 Release from Human Granulocytes during Phagocytosis. J Clin Invest 1975; 55: 945-955 34. Root RK and Metcalf JA: H202 Release from Human Granulocytes during Phagocytosis. J Clin Invest 1977; 60: 1266-1279 35. on JF and Schultz J: Studies on the Chlorinating Activity of Myeloperoxidase. J Biol Chem 1976; 251:1371-1374 36. Zgiiczynski JM, Selvaraj RJ, BB, et al: Chlorination by the MyelopcroAdase-H202-Cl antimicrobial system at Acid and Neutral pH. Proc Soc Exp Biol Med 1977; 154:418-422 37. Klebanoff SJ: Oxygen Metabolism and the toxic Properties of Phagocytcs. Ann Intern Med 1980;93:480-489 38. Slivka A, LoBuglio AF, Weiss SJ: A Potential Role for Hypochlorous Acid in Granulocyte- Mediated Tumor Cell Cytotoxicity. Blood 1980; 55: 347-350 39. EL: Mycloperoxidase, Hydrogen Peroxide, Chloride Antimicrobial System: Nitrogen-Clorine Derivatives of Bacteria [Components in Bacteria] Action against Eschericia coli. Infec Immun 1979; 23: 522-531 40. CF and Cohn ZA: Antitumor Effects of Hydrogen Peroxide in Vivo. J Exp Med 1981; 154:1539-1553 41. Munakata T, Semba U, Shibuya Y et al: Induction of Interferon-gamma Production by Human Natural Killer Cells Stimulated by Hydrogen Peroxide. J Immunol 1985; 134(4): 2449-2455 42. Lebcdev LV, Levin AO, Romank-ova MP, et al: Regional Oxygenation in the Treatment of Severe Destructive Forms of Obliterating Diseases of the Extremity Arteries. Vestn Khir 1984; 132: 85-88 43. Gusak V & Klioner LI, Belinski VE et al: Possibilities of Using Weak Solutions of Hydrogen Peroxide in the Treatment of Experimental Ischemia of the Lower Extremities. YJin Khir 1986;7: 31-33 45. Jepras RI and Fitzgeorge RB: The Effect of Oxygen-dependent Antimicrobial Systems on Strains of Legionella Pneumophila of Difference Virulence. J Hyg(Lond) 1986;97(l): 61-9 46. Steiner BM, Wong GH, Sutrave P, et al: Oxygen Toxicity in Treponema Pallidum: Deoxyribonucleic Acid Single-stranded Breakage Induced by Low Doses of Hydrogen Peroxide. Can J Microbiol 1984; 30(12): 1467-76 47. G, Sestili P, Pedrini MA, et al: The Effect of Temperature or Anoxia on Escherichia Coli ICIling Induced by Hydrogen Peroxide. Mutat Res 1987; 190(4): 23740 48. Norkus EP, Kuenzig W, Conney AH: Studies on the Mutagenic Activity of Ascorbic Acid in Vitro and in Vivo. Mutat Res 1983; 117(l):183-9 49. Klebanoff SJ and Shepard CC: Toxic Effect of the Peroxidase-hydrogen peroxide-halide Antimicrobial System on mycobacterium leprae. Infect Immun 1984; 44(2): 534-6 50. SA, Bia FJ, DI, et al: Pulmonary Macrophage Function During Experimental Cytomegalovirus Interstitial Pneumonia. Infect Immun 1985; 47(l): 211-6 51. Belotskii SM, Filiudova OB, Pashutin SB, et al: Chemiluminescence of Human Neutrophils as Affected by Opportunistic Microbes. Zh Mikrobiol Epidemiol Immunobiol 1986; Mar (3): 89-92 52. Moran AP and Upton ME: Effect of Medium Supplements, Illumination and Superoxide Dismutase on the Production of Coccoid Forms of Campylobacter Jejuni ATCC29428. J Appi Bacteriol 1987; 62(l): 43-51 53. Looney RJ and Steigbigel RT: Role of the Vi Antigen of Salmonella typhi in Resistance to Host Defense In Vitro. J Lab Clin Med 1986; 108(5): 506-16 54. CB and Weaver WM: Comparative Susceptibility of Group B Streptococci and Staphylococcus aurcus to Killing by Oxygen Metabolites. J Infect Dis 1985; 152(2): 323-9 55. Tenovuo J, Makinen & Sievers G: Antibacterial Effect of Lactoperoxidase and Myelopcroxidase Against Bacillus cereus.Antimicrob Agents Chemother 1985; 27(l): 96-101 56. Miyasaki K-T, ME, Genco RJ: Killing of Actinobacillus actinomycetemcomitans by the Human Neutrophil Mycloperoxidase-hydrogen peroxide-chloride System. Infect Immun 1986; 53(l): 161-5 57. Rotstein OD, Nasmith PE, Grinstein S: The Bacteroides By-product Succinic Acid Inhibits Neutrophil Respiratory Burst by Reducing Intracellular pH. Infect Immun 1987; 55(4):864-70 58. Archibald FS and Duong MN: Superoxide Dismutase and Oxygen Toxicity Defenses in the Genus Neisseria. Infect Immun 1986; 51(2): 631-41 59. DH: Studies on the Catalase of Histoplasma Capsulatum. Infect Inimun 1983; 39(3): 1161-6 60. Sasada M, Kubo A, Nishimura T, et al: Candidacidal Activity of Monocyte-derived Human Macrophages; Relationship between Candida Killing and Oxygen Radical Generation by Human Macrophages. J Leukocytc Biol 1987; 41(4): 289 61. Schaffner A, CE, Schaffner T, et al: In Vitro Susceptibility of Fungi to lulling by Neutrophil Granulocytes Discriminates Between Primary Pathogenicity and Opportunism. J Clin Invest 1986; 78(2): 511-24 62. Levitz SM and Diamond RD: Mechanisms of Resistance of Aspergillus fumigatus Conidia to Killing by Neutrophils In Vitro. J Infect Dis 1985; 152(l): 33-42 63. Gaigiani J N: Inhibition of Different Phases of Coccidiodides immitis by Human Neutrophils or Hydrogen Peroxide. J Infect Dis 1986: 153(2): 217-22 64. Pesanti EL: Pncumocystis Carinii: Oxygen Uptake, Antioxidant Enzymes, and Susceptibility to Oxygen-mediated Damage. Infect Immun 1984; 44(l): 7-11 65. Brinkmann V, Kaufmann SH, Simon MM, et al: Role of Macrophages in Malaria: 02 Metabolite Production and Phagocytosis by Spienic Macrophages During Lethal Plasmodium berghci and Self- limiting Plasmodium yoeiii Infection in Mice. Infect Inunun 1984; 44(3): 743-6 66. Murray HW: Cellular Resistance to Protozoal Infection. Annu Rev Med 1986; 37: 61-9 67. Paget TA, Fry M, Lloyd D: Effects of Inhibitors on the Oxygen kinetics of Nippostrongylus brasiliensis. Mol Biochem Parasitol 1987; 22(2-3): 125-33 68. Ferrante A, Hill NL, Abell TJ, et al: Role of Myeloperodase in the Killing of Naegieria fowleri by Lymphokine-altered Human Neutrophils. Infect Immun 1987; 55(5): 1047-50 69. Passwell JH, Shor R, Gazit E, et a]: The Effects of Con A-induced Lymphokines from the T-lymphocyte Subpopulations on Human Monocytc Leishmaniacial Capacity and H202 Production. Immun 1986; 59(2): 245-50 70. Kazura JW, de-Brito P, Rabbege J et al: Role of Granulocyte Oxygen Products in Damage of Schistosoma mansoni Eggs In Vitro. J Clin Invest 1985; 75(4): 1297-307 71. Rothermel CD, Rubin BY, Jaffe EA, et a]: Oxygen-independent Inhibition of Intracellular Chiamydia psittaci Growth by Human Monocytes and Intcrferon-gamma-activated Macrophages. J Immunol 1986; 137(2): 689-92 72. Owells RE: The Modes of Action of Some Anti-protozoal Drugs. Parasitology 1985; 90(pt4): 689-703 73. Wirth JJ, Kierszenbaum F, Sonnenfeld G et a]: Enhancing Effects of Ganima Interferon on Phagocytic CellAssociation with and Villing of Trypanosoma cruzi. Infect Immun 1985; 49(l): 61-6 74. Ghadirian E, Somcrficid SD, Kongshavn PA: Susceptibility of Entamoeba Histolytica to Oxidants. Infect Immun 1986; 51(l): 263-7 75. Murray HW, Scavuzzo D, s JI, et a]: In Vitro and In Vivo Activation of Human Mononuclear Phagocytes by Interferon-gamma. Studies with Normal and AIDS Monocytes. J Immunol 1987; 138(8): 2457-62 76. Podopiekina LE, Shutova NA, Fyodorov YuV: Influence of Several Chemical Reagents on Lymphocytic Choriomeningitis and Tacaribc Viruses. Virologie 1986; 37(l): 43-8 77. Doroshow JH: Role of Hydrogen Peroxide and Hydroxyl Radical Formation in the Filling of Ehrlich Tumor Cells by Anticancer Quinones. Proc Natl Acad Sci USA 1986; 83(12):4514-8 78. Zaizen Y, Nak-agawara A, Ikeda K- Patterns of Destruction of Mousc Neuroblastoma Cells by Extracellular Hydrogen Peroxide Formed by 6-hydroxydopamine and Ascorbate. J Cancer Res Clin Oncol 1986; 111(2): 93-7 79. Agrawal P and Harper MJ: Studies on Peroxidase-catalyzed Formation of Progesterone. Steroids 1982; 40(5): 569-79 80. Heikk-iia R and Cohen G: Inhibition of Biogenic Amine Uptake by Hydrogen Peroxide: A Mechanism for Toxic Effects of 6-Hydroxydopamine. Science 1971; 172: 1257-58 81. Grisham MB, VJ, Everse J: Neuromelanogenic and Cytotoxic Properties of Canine Brainstem Peroxidase. J Ncurochem 1987; 48(3): 876-82 82. Hess ML, Manson NH, Lower RR: Leukocyte-genreated Hydrogen Peroxide Depression of Cardiac Sarcoplasmic Reticulum Calcium Transport. Transplantation 1983; 36(l):117-9 83. Verhoeven AJ, Mommersteeg ME, Akkerman JW: Balanced Contribution of Glycolyte and Adenylate Pool in Supply of Metabolic Energy in Mitochrondia. 84. JA, Fischman AJ, Khaw BA, et al: Free Radical Mediated Membrane Depolarization in Renal and Cardiac Cells. Biochim Biophys Acta 1987; 899(l): 76-82 85. Rubanyi GM and Vanhoutte PM: Oxygen-derived Free Radicals, Endothelium and Responsiveness of Vascular Smooth Muscle. Am J Physiol 1986; 250(5 pt 2): H815-821 86. Silin PJ, Strulowitz JA, Wolin MS, et al: Absence of a Role for Superoxide Anion, Hydrogen Peroxide and Hydroxyl Radical in Endothelium-mediated Relaxation of Rabbit Aorta. Blood Vessels 1985; 22(2): 65-73 87. Wei EP, Christman CW, Kontos HA, et al: Effects of Oxygen Radicals on Cerebral Arterioles. Am J Physiol 1985; 248(2 pt 2): H157-62 Platelets. J Biol Chem 1985; 260(5): 2621-4 88. Kontos HA: Qxygen Radicals in Cerebral Vascular Injury. Circ Res 1985; 57(4): 508-16 89. Burke TM and Wolin MS: Hydrogen Peroxde Elicits Pulmonary Artery Relaxation and Guanylate Cyclase Activation. Am J Physiol 1987; 252(4 Pt 2): H721-32 90. Farr CH: Conference Presentation. First International Conference on Bio-Oxidativc Medicine. Dallas, Texas February 1989 91. Hofmann C, Crettaz M, Burns P, et al: Cellular Responses Elicited by Insulin Mimickers in Cells Lacking Detectable Plasma Membrane Insulin Receptors. J Cell Biochem 1985; 27(4): 401-14 92. Farr CH: Possible Therapeutic Value of Intravenous Hydrogen Peroxide. Plzen.lek Sborn., Suppl. 56, 1988: 171-173 93. Farber CM, Liebes LF, Kanganis DN, et al: Human B Lymphocytes Show Greater Susceptibility to H202 Toxicity than T Lymphocytes. J Immunol 1984; 132(5): 2543-6 94. Setty BN, Jurek E, Ganley C, et al: Effects of Hydrogen Peroidde on Vascular Arachidonic Acid Metabolism. Prostaglandins Leukotrienes Med 1984; 14(2): 205-13 Duncan --- Outgoing mail is certified Virus Free. Checked by AVG anti-virus system (http://www.grisoft.com). Version: 6.0.264 / Virus Database: 136 - Release Date: 7/2/01 Quote Link to comment Share on other sites More sharing options...
Guest guest Posted September 29, 2001 Report Share Posted September 29, 2001 <<Rich, it is my understanding that 35% ,(only pharmacutical grade) h202 must be diluted with pharm. (glucose)down to 3% and dripped. This from my Dr.........>> OUCH NO! HE'S 50 TIMES TOO HIGH!! From an authoratative article............. Hydrogen Peroxide is available currently in a 3% USP/NF grade and is ideal for intravenous use. It must be packed in an open vial however with a vented cap to allow the escape of oxygen pressure produced by the dismutation. Some physicians are concerned about sterilization because of the packaging but hydrogen peroxide is self sterilizing. Proper dilutions are simple. Add 1 mL of the 3% Hydrogen Peroxide USP/NF solution to each 100 mL carrier solution. A typical treatment plan would be to give 100 to 250 mL H202 of 0.03% concentration once or twice a week. After the initial schedule of 10 to 15 treatments, wait 30 to 60 days and evaluate the response. Within 1 hour after the intravenous infusion of 250 mL 0.15% H202 a 2% to 10% decrease was noted in the following blood constituents: Bun, Sodium, Potassium, Chloride, Uric acid, Calcium, Phosphorus, Total protein, Total bilirubin, Alkaline phosphatase, AST, ALT, GGTP, LDH, Iron and Globulin. Follow-up studies, 24 hours later, revealed all the above blood constituents had returned to normal pre-infusion levels. Here's the rest of this particular article.. _______________________ INTRAVENOUS HYDROGEN PEROXIDE THERAPY (Quick Overview) MECHANISMS Oliver (l) first reported the use of Intravenous Hydrogen Peroxide (H202), in 1920 in patients with Influenzal Pneumonia. An epidemic in Busrah in June and July of 1919, had a calculated death-rate over 80 percent. Oliver treated 25 critical patients with intravenous infusions of H202 and 13 fully recovered reducing the mortality to 48 percent. He was impressed with the rapid clinical response and postulated the effects were probably due to the oxidation of toxins more than the relief of hypoxia. Hydrogen peroxide used in surgical procedures had caused air embolisms, but he reasoned if the oxygen was released slowly, embolism should not occur. Venous oxygen embolism has been reported following the irrigation of anal fistulae (2), surgical wounds (3), and closed body cavities (4). Ulcerative colitis (5) has been produced in patients using H202 in enema solutions to break up fecal impactions. It has been shown, however, to destroy murine malaria parasites (7), and the bactericidal properties of H202 produced by neutrophils is well documented (8-10). Hydrogen peroxide appears to be involved in many intermediate biochemical pathways. Additionally, it appears to kill certain bacteria, parasites, yeast, protozoa, inhibit viruses, and oxidize immunocomplexes. T. Ramasarma (11), in his review on the " Generation of H202 in Biomembranes " , states: " H202 is a purposeful molecule in cellular metabolism and cannot be dismissed as a mere undesirable byproduct of oxygen species generation " . Hydrogen peroxide is generated in most biological membranes; cellular, mitochondrial, and nuclear. It is important for maintaining membrane integrity and regulating membrane transport through the alteration of Na-K ATPase activity. This was confirmed by Garner et al (12). Hydrogen peroxide fulfills the role of a secondary messenger in several hormonal pathways. As an example, H202 generation in the uterus is dependent on estrogen and is necessary for the production of progesterone. The iodination of thyroglobulin and thyroxine synthesis requires the presence of peroxidase, H202, and iodide (13). Thyroxine increases and hypothyroidism decreases hydrogen peroxide production in studies of liver mitochondria (14). Hydrogen peroxide has an insulin-mimic action and acts as a postbinding site on the plasma membrane to induce glucose transport (15). More recent studies of Helm (16) found the insulinomimetic action involves a common mechanism which links the generation of active oxygen species through the redox potential of the cell to the activation of a proteinase. It helps regulate metabolic control through protein modification which alters enzyme activities. Thermogenic control (11,14) appears to be exercised through the action of H202 on the mitochondria. At the mitochondrial level, H202 is generated by a number of substrates. Flavoproteins converge at ubiquinone which forms a link between H202 generation and the respiratory chain. Noradrenaline, thyroxine, and cold stimulate the system to generate heat. Heat increases the rate of H202 production and is dependent on alpha-adrenergic receptors which also control non-shivering thermogenesis. The balance of Ferric (3+) and Ferrous (2+) Iron in the body is critical to support lipid peroxidation of cellular membranes (27). It has been reported that a ratio of Fe(3+)/Fe(2+) of 1:1 to 8:1 is optimal to cause the formation of -OH radicals and lipid peroxidation. At ratios above or below these levels, lipid peroxidation does not occur. Physiological concentrations of either H202 or Ascorbic Acid may encourage lipid peroxidation and at these levels antioxidant protection is important. Increasing the concentration of H202, as occurs with therapeutic intravenous infusions, the Ferric/Ferrous ratio is maintained above 8:1 by keeping excess Ferrous (Fe2+) Iron oxidized to the Ferric (Fe3+) state. A principal mechanism of action of EDTA Chelation Therapy is reducing Free Radical damage and lipid peroxidation by complexing EDTA with Ferrous Iron (Fe3+:EDTA) which helps maintain the Ferric/Ferrous ratio above 8:1 (28) Weiss (8) reported H202 is an activator of neutrophils including aggregated immunoglobulin, activated complement components, immune complexes, or bacterial peptides. This would suggest the beneficial clinical effects observed with the use of ascorbic acid in inflammatory reactions, and its protective action against infections, is acting through the generation of H202. Also, there is no evidence H202 initiates or supports microsomal lipid peroxidation (51). The modification of (Na,K)-ATPase(12) by H202 also contributes to an increase in metabolic rate. Farr (40) reported whole blood specimens taken before, during, and after H202 infusions showed color changes consistent with oxyhemoglobin formation. Numerous blood profiles and CBC studies have been performed before and immediately after infusions of H202. Although early investigators reported no changes in blood elements and certain chemical constituents, except when injected into the carotid arteries, consistent changes have been reported. Within 1 hour after the intravenous infusion of 250 mL 0.15% H202 a 2% to 10% decrease was noted in the following blood constituents: Bun, Sodium, Potassium, Chloride, Uric acid, Calcium, Phosphorus, Total protein, Total bilirubin, Alkaline phosphatase, AST, ALT, GGTP, LDH, Iron and Globulin. Follow-up studies, 24 hours later, revealed all the above blood constituents had returned to normal pre-infusion levels. Some of the biological killing activity of H202 may be attributed to gamma interferon. Production of gamma interferon by human natural killer cells and monocytes, is stimulated by H202(58). Both exogenous and endogenous H202 appear to be in part responsible for immunoregulation. The rates of wound healing, stasis and vascular ulcers (18), peripheral occlusive disease (59,60), myocardial ischemia (33) and cerebral vascular disease (61) have all improved when treated with repeated intra-arterial infusions of H202 PHYSICAL PROPERTIES OF HYDROGEN PEROXIDE Hydrogen Peroxide was discovered in 1818 by the French Chemist Louis-Jacque Thenard. Hydrogen Peroxide, hydrogen dioxide (H202), is a colorless (blue in thick layers) odorless liquid; with a melting point -2 degree C: a boiling point 152 degrees C; decomposes 84 degrees C at 68 mm. pressure (68 degrees C at 26 mm.), soluble in water in all proportions; usually encountered as a dilute solution (3% H202) solution, that is, one volume of solution yields 10 volumes of oxygen), although available up to 35% strength. Its remarkable feature is its tendency to decompose readily into water and oxygen. Decomposition by light begins only in the near ultraviolet. Hydrogen peroxide solutions dismutate slowly, when undisturbed, at the rate of approximately 1% per month. The dismutation reaction is rapidly increased in the presence of particulate contaminates; i.e., dust, flakes of metal or glass or other particulate matter, at a rate which may be explosive. Cold retards dismutation and solution may be refrigerated or stored at temperatures below 0 degrees C. Hydrogen peroxide occurs only in traces in nature: mostly in rain and snow. It has not yet been detected in interstellar space. METABOLIC AND PHYSIOLOGICAL EFFECTS Numerous physiological effects are attributed to hydrogen peroxide and documented in the literature. Some of these effects may be broadly categorized as follows: 1. PULMONARY A. Increased oxygenation B. Alveolar debridement (31) 2. METABOLIC RATE A. Hormonal effect: Several hormonal effects have been reported to be regulated by the action of H202. Examples are: 1.Iodination of thyroglobin(13) 2. Production of thyronine (13) 3. Progestone production (107) 4. Inhibition of bioamines (108); dopamine, noradrenalin and serotonin 5. Prostaglandin synthesis (46,47,109) 6. Dopamine metabolism (110) 7. Regulates Reticulum Calcium Transport (111) 8. Oxidative stimulation: Hydrogen peroxide directly and indirectly stimulates oxidative enzyme systems. Micromolar amounts of infused H202 has been found to increase oxidative enzymatic activity to the maximum rate of reaction (40). 1. Increases GSH oxidation to GSSG which increases ATP production(112) 2. Activates Hexose Monophosphate Shunt(41) 3. Alters Na-K ATPase activity (12) 4. Regulates cellular (113) and mitochondrial (15) membrane transport 5. Regulates thermogenic control (11) 3. CARDIOVASCULAR RESPONSE A. Vasodilation 1. Dilation of peripheral vessels (31) 2. Dilation of coronary vessels (114) 3. Aortic strip relaxation response (115) 4. Cerebral arteriolar dilation (116,117) 5. Pulmonary arterial relaxation (118) B. Vasoconstriction 1. Essential Hypertension effect (31) 2. Peripheral vasoconstriction may occur in normal-tensive patients with concentrations at or below 0.0375% with no significant increase in mean pressures(123). C. Cardiac Responses (12-3) 1. Decreases Heart Rate 2. Decreases Vascular Resistance 3. Increases Stroke Volume 4. Increases Cardiac Output 5. Increases Cardiac Index 4. GLUCOSE UTILIZATION A. H202 mimics insulin (16) B. Increases glycogen production from glucose (119) C. Type II Diabetes Mellitus stabilized with H202 infusions (20) 5. GRANULOCYTE RESPONSE A. Depressed granulocytes after treatment then rebound measured after 24 hours (31) B. Secondary resistance to peroxide after exposure (109) C. Alteration of T4/T8 ratio with increase of T4 Helper cells (28) 6. IMMUNE RESPONSE A. Stimulates Monocytes (92) B. Stimulates T Helper cells (109) C. Stimulates Gamma Interferon production (58) D. Decreases B-cell activity (121) E. Responsible for immunoregulation (58) F. Regulates inflammatory response (122) INDICATIONS Intravenous Hydrogen Peroxide is used in the acute reactive conditions ; i.e., influenza, bronchitis, Herpes Zoster, asthmatic reactions, etc.) because of its direct killing effect on micro-organisms or its effect on vasospasm or bronchospasm. The long term effect, to regulate or modify the immune response through cellular activation or modification of immune dysfunction, such as EBV, Candida, CMV, Herpes, HIV, Diabetes Type II, COPD, vascular disease, arthritis, and etc., is an important therapeutic tool for every physician. The therapeutic use of intravenous H202 has been reported in the following diseases or conditions with varying results depending on the clinical investigator: l. Peripheral Vascular Disease 2. Cerebral Vascular Disease 3. Alzheimer 4. Cardiovascular Disease 5. Coronary Spasm (angina) 6. Cardioconversion 7. Arrhythmias 8. Chronic Obstructive Pulmonary Disease 9. Emphysema 10. Asthma 11. Influenza 12. Herpes Zoster 13. Herpes Simplex 14. Temporal Arteritis 15. Systemic Chronic Candidiasis 16. Chronic Recurrent Epstein Barr Infection 17. Diabetes Type II 18. HIV infections 19. Metastatic Carcinoma 20. Multiple Sclerosis 21. Rheumatoid Arthritis 22. Acute and Chronic viral infections 23. Chronic unresponsive bacterial infection 24. Parasitic infections 25. Parkinsonism 26. Migraine headaches 27. Cluster headaches 28. Vascular headaches 29. Chronic pain syndromes (multiple etiologies) 30. Environmental allergy reactors (Universal) Many in-vitro and some in-vivo studies have shown H202 to be bactericidal, fungicidal, parasiticidal, viricidal, and to lyse certain tumor cell types in cultures. The therapeutic benefit of H202 infusions in patients with any of the following infections and/or tumors may not be clinically documented. Therefore, no recommendation can be made until appropriate studies have been conducted. BACTERIA 1. Legionella pneumophila (62) 2. Treponema pallidum (63) 3. Escherichia coli (64) 4. Salmonella typhimurium (65) 5. Mycobacterium leprae (66) 6. Staphylococcus auerus (67) 7. Pseudomonas acruginosa (68) 8. Campylobacter jejuni (69) 9. Salmonella typhi (70) 10. Group B Streptococci (71) 11. Bacillus cereus (72) 12. Actinobacillus actinomycetem comitans (73) 13. Bacteroides (74) 14. Neisseria gonorrhoea (75) FUNGI 1. Histoplasma capsulatum (76) 2. Candida Albicans (77) 3. Coccidioides (78) 4. Paracoccidiodes (78) 5. Blastomyces (78) 6. Sporothrix (78) 7. Mucoraceae(78) 8. Aspergillus fumigatus (79) 9. Coccidioides immitis (80) PARASITES 1. Pneumocystis carinii (81) 2. Plasmodium yoelii (82) 3. Plasmodium berghei (82) 4. Toxoplasma gondii (83) 5. Nippostrongycus brasiliensis (84) 6. Naegleria fowleri (85) 7. Leishmania major (86) 8. Schistosoma mansoni (87) 9. Chlamydia psittaci (88) 10. Trichomonas vaginalis (89) 11. Tepanosoma cruzi (90) 12. Endameba histolytica (91) VIRUS 1. Human Immunodeficiency Virus (92) 2. Cytomegalovirus (67) 3. Lymphocytic choriomeningitis virus (93) 4. Tacaribe virus (93) TUMOR TYPE 1. Ehrlich carcinoma (94) 2. Neuroblastoma (95) CONTRAINDICATIONS PRECAUTIONS: Hydrogen Peroxide infusions are contraindicated in pregnancy, Chronic Granulomatous Disease (CGD), and any disorder of cell membrane stability (i.e. anemias). SIDE EFFECTS: The most frequent side effect reported (at concentrations above 0.0375%) is vasculitis, which may occur in the infused vein and/or its tributaries. This phenomenon is inconsistent, occurring repeatedly in some patients but rarely in others. According to Shingu, (97) epithelial and smooth muscle cells contain very little, if any, catalase and, therefore, may be sensitive to the effects of H202. There appears to be a critical concentration of H202 which is cytolytic, and will cause vasculitis if exceeded. It is, therefore, important to consider the concentration being infused and the size of the vessel. This reaction is less likely to occur if a larger vein in the antecubital area is used for infusion, and the rate of administration is reduced. Once the cytolytic concentration is exceeded, the cells swell up, become toxic and die. The exact mechanism by which H202 is cytotoxic are not defined, however, *NOTE* Recent studies have revealed the addition of 0.5 mg Manganese to the intravenous solution to be effective in controlling the endothelial damage caused by the H202 solution. It is reported that there may be no microscopic signs of cytotoxicity for 6 hours or longer after exposure of the cells to H202. Consequently, after you infuse a patient, the vasculitis may not be apparent until the following day. The application of heat may make the reaction more severe since heat speeds up the rate of most biochemical reactions, and this may be no exception. We recommend you use only the larger veins for infusion, and reduce the rate of infusion if you suspect the patient's blood flow rate is slower than usual. It has also been found useful to rotate between the veins and not use the same vein for two consecutive treatments. Rotate between veins and alternate treatments from one arm to the other. Some physicians report they have flushed the vessel post-infusion with additional heparin, or Decadron, but results have not been changed. All oral supplements and drugs should be withheld on the day of infusion. Taking antioxidants on the day of infusion would appear to be counterproductive and may aggravate the vasculitis. Intravenous H202 delays clotting by 20%, but reduces bleeding time approximately 50%. Caution should be exercised when giving H202 to patients taking anticoagulants since clinical data is not available at this time for comment. ALLERGIC PHENOMENON: Occasionally, a non-tender red streak will appear, tracing the route of the vessel above the point of infusion. This streak will often have a diffused fanned-out appearance radiating laterally from the central streak. No relationship has been identified between this superficial vascular phenomenon and the vasculitis previously described. This vascular phenomenon occurs randomly in patients and has been observed at a rate of about 1 in 50 infusions in concentrations greater than 0.0375%, but only 1 in 500 at concentrations at or below 0.0375%. Several hundred infusions have been given, and no other type of local or systemic allergic vascular reaction has been observed or reported. CHEST DISCOMFORT: Some physicians have reported occasional patient complaints of vague chest discomfort, sometimes associated with a feeling of shortness of breath. We received two reports that the chest discomfort was severe enough to discontinue the treatments. Bronchodilators should be withheld for at least a day before H202 is administered, if possible. INFUSION SITE PAIN: Pain at and above the infusion site is occasionally reported. The pain is described as a spastic ache and is most likely due to vasospasm. On rare occasions, the pain may extend from the point of infusion, at or below the antecubital area, up into the deltoid area. Reducing the rate of infusion, heat, and ice have all been ineffective in controlling the pain. We have found, when this occurs, the best thing to do is remove the needle and restart the infusion in another vein. We speculate the irritation to the vessel, at the point of penetration, causes a reflex vasospasm along the vessel. Changing the needle position or rotating its position in the same vein does little to relieve the discomfort. HERXHEIMER TYPE REACTION: Several physicians have reported an occasional Herxheimer-like reaction when treating patients with mucocutaneous candidiasis. Following infusions of H202 the patients were reported to have generalized migratory aching, nausea, headaches, chills, and fever. It has been reported to occur after one, two, and sometimes three treatments, but, thereafter, the patients report an improvement in their overall clinical status, and continue to improve with each succeeding treatment. No patients have been discontinued from treatments because of this reaction. It does not occur consistently nor is it predictable. TOXICITY Hydrogen peroxide is a product of intermediate metabolism, widely distributed throughout the body, and participates in a significant number of biochemical reactions. It is a principal electron receptor in the body in many RedOx reactions. A vast amount of knowledge exists about the chemistry of H202 in tissue slices, tissue cultures, bacteria, parasites, yeast, protozoa, blood cells, and isolated human, animal, and plant cells. Numerous examples of biochemical changes have been described in the literature, which are interpreted as toxic or damaging in the models studied. Clinically, however, no significant acute toxicity has been observed in several hundred patients, some receiving up to 40 to 50 infusions with concentrations up to 0.3 %. Also, no chronic or long term toxicity has been observed or documented up to two years post-multiple infusions. One patient received 3,600 mL of 0.15% of Hydrogen Peroxide intravenously in a period of 10 days without any side effect. This dosage is approximately 40 times greater than the currently recommended therapeutic dosage. Other studies suggest doses 500 times smaller than the currently recommended dose will have biological effect. This suggested intravenous infusions of Hydrogen Peroxide is extremely safe and has a very wide therapeutic range. Consequently, the majority of toxic reactions referred to in the literature, which occur with in-vitro studies under laboratory conditions, which could not exist in-vitro, have very little clinical application. Some of the in-vitro toxic effects are: A. Lipid Peroxidation (49,98) B. Single strand DNA breakage (99) C. Cytotoxic (concentrations above 10 mMol) (100) D. RBC hemolysis (26,101) E. Chromosomal Aberrations (102) F. Protein degradation (103) G. Glutathione Peroxidase depiction (104) H. Degredates Cytochrome C (105) I. Platelet Aggregation (106) FORMULAS INTRAVENOUS ADMINISTRATION OF H202 SOLUTION The PROPER DOSAGE is dependent upon the CONCENTRATION used, the VOLUME INFUSED, and the RATE OF INFUSION. The infusion mixture is prepared as follows: The preferred carrier is 5% Dextrose in Water or Normal Saline. Hydrogen Peroxide is available currently in a 3% USP/NF grade and is ideal for intravenous use. It must be packed in an open vial however with a vented cap to allow the escape of oxygen pressure produced by the dismutation. Some physicians are concerned about sterilization because of the packaging but hydrogen peroxide is self sterilizing. Proper dilutions are simple. Add 1 mL of the 3% Hydrogen Peroxide USP/NF solution to each 100 mL carrier solution. If you plan to give 250 mL treatment you add 2.5 mL of the peroxide in 250 mL of carrier, 5 mL to 500 mL carrier and etc. for the proper dilution. Select a medium to large vein close to the antecubital area for the infusion. Use a small winged needle and infuse slowly over a period of 1 to 1 1/2 hours. The rate of infusion and concentration are both important as explained below. THERAPEUTIC INFUSION SCHEDULES The dosage administered is dictated by the therapeutic and objective experience of the clinician. The physician should consider the clinical objective after the diagnosis has been properly established. A general rule: the more acute the pathology the greater the volume and concentration and the more frequent the infusions. The frequency may be maintained until the acute problem is considered stable, and then both dose and frequency reduced. As an example, a patient with acute influenza or Herpes Zoster may be placed on a schedule of 250 to 500 mL of H202 of 0.03% or less concentration, daily for 1 to 5 infusions or until clinical response is obvious. Occasionally, these patients may require a treatment once or twice a week for an additional 5 to 10 treatments, particularly in infections which have a tendency to become chronic such as Herpes or Hepatitis. A therapeutic regimen for a chronic, low grade infection or chronic illness would be to schedule smaller doses over a longer period of time. Examples of chronic illnesses in which long term therapy might be employed would include: Chronic candidias, chronic obstructive pulmonary disease, peripheral occlusive disease, chronic EBV, or Hepatitis, and etc. A typical treatment plan would be to give 100 to 250 mL H202 of 0.03% concentration once or twice a week. After the initial schedule of 10 to 15 treatments, wait 30 to 60 days and evaluate the response. Depending on the response, you may wish to give an additional series of 10 to 15 treatments and again wait and re-evaluate. An alternative is to keep the patient on bimonthly or monthly maintenance treatments for a year and then reevaluate annually. The following are examples of treatment schedules which have been employed in these selected cases. 1. ACUTE PULMONARY INFECTIONS INCLUDING INFLUENZA PNEUMONIA. Infusions of Hydrogen Peroxide have a rapid 'Alka-seltzer effect' in the lungs. If the patient has moist lungs and/or a productive cough, the treatment will usually cause coughing and mucous production to increase immediately. It may continue throughout the treatment but will subside soon after the treatment is completed. If the patient is quite ill and febrile, the initial treatment would be 250 to 500 mL of 0.03%. If the patient remains febrile the second day, give an additional 250 to 500 mL of 0.03%. Treat according to response, thereafter, every two to three days until the desired response is obtained. 2. CHRONIC LUNG DISEASE (COPD, BRONCHITIS, BRONCHIECTASIS, EMPHYSEMA) Chronic lung disease, which is moist and active, responds best to treatment. The response in dry emphysema or pulmonary fibrosis is less dramatic. Give 250 mL 0.03% weekly for 10 to 15 weeks. Frequently, the effects will be dramatic, with coughing and sputum production initially, and the patients reporting increased energy and ability to breathe within 24 hours. The effects of treatments are usually progressive improvement for 8 to 10 treatments, and then the effects plateau. Most patients will wish to continue on monthly maintenance treatments. 3. ALLERGIC REACTIONS, ASTHMA, ENVIRONMENTAL SENSITIVITY, ETC. The longer the patient has had their allergic reactive problem, the longer it will be before you will have a positive response. This general rule, however, does not always apply. Some patients respond rapidly, within 2 to 3 treatments. In these complex patients, schedule weekly treatments for 10 weeks, give the patient a 30 day rest, and repeat an additional 10 weekly treatments. You may give up to 40 to 50 treatments on this schedule, or until you feel maximum response has been obtained. Most patients will realize improvement after their first course of 10 treatments. Thereafter, patients show a gradual improvement with each successive group of 10 treatments. If the patient shows no improvement after 30 to 40 treatments, then no response is likely and therapy is discontinued. 4. ACUTE AND CHRONIC PAIN Angina, headaches, vasospasm, tumor pain, or neurological pain frequently show an immediate and dramatic response to one or two treatments. Chronic pain syndromes may require several (8-10) treatments but response is frequent. There is no good explanation why Hydrogen Peroxide should relieve pain, but, nevertheless, this has been a frequently reported clinical observation. Chronic, established pain of Post Herpetic Neuralgia may not respond to treatments, but the response in Acute Herpes Zoster is often dramatic. 5. EBV, CMV, HIV, HERPES, HEPATITIS ETC. Acute infections require frequent daily treatments, whereas, chronic infections require long term weekly treatments. Symptomatic response may occur after only 1 or 2 treatments, but antibody titers may not change until 10 to 30 weekly treatments have been given. 6. CEREBRAL VASCULAR, ALZHEIMER, TOXIC DEMENTIA, ETC. Perhaps the increased oxygenation can explain the sometimes rapid reversal of symptoms in these patients. Acuity, memory, recall, alertness, and other cerebral symptoms frequently improve quickly and the improvement appears to be long lasting. The results may also be related to changes in the bioamines in the brain because positive results are also seen in anxiety/depressive non-toxic young adults. Ten weekly treatments are usually given before the effectiveness of treatment is evaluated. 7. CARDIOVASCULAR AND PERIPHERAL VASCULAR DISEASE Using weekly treatments of smaller volume; i.e., 100 to 250 mL, can be very beneficial to these patients if your objective is to restore oxygenation to the tissue. If the objective is to push a gangrenous digit or extremity to the point of demarcation for surgical debridement, then 250 to 500 mL are given daily, for several days, until demarcation is completed. The following are actual case reports, from the initial studies (31) on the Intravenous Use of Hydrogen Peroxide. Higher concentrations were used in these studies than currently recommended. Same or similar cases have been repeated many times since, at the lower concentration of 0.03%, with equally good clinical results but WITHOUT vasculitis or other side effects. We, therefore, recommend you do not exceed the 0.03% concentrations. 1. Acute Herpes Zoster. 250 mL of 0.15% initially, then every two days for a total of 6 treatments. Comment: Resolved completely in less than 1 week with no residual. 2. Acute Influenza Syndrome. 250 mL of 0.15% initially, and 500 mL of 0.15% the second day. Afebrile after second day, but additional treatment the third day of 250 mL of 0.15%. Comment: Resolution of all symptoms after the second day with no residual. 3. Chronic Systemic Candidiasis: 250 mL of 0.15% once a week for 10 treatments, and then monthly followup for 10 months. Comment: Clinical response not observed until after the 4th treatment, then gradual improvement continued. Maintained on monthly treatments. 4. Severe COPD. Initial 250 mL of 0.15% which caused significant alveolar debridement and coughing up of copious amount of purulent material. Continued weekly infusions for 6 weeks, and by the end of the 6th treatment the patient no longer coughing. Pulmonary function improved and the patient returned to working full time. Comment: Maintained on treatment according to patients " feel the need " which re-occurs approximately every 4 to 6 weeks. 5. Acute Asthmatic Attack (12 yr old girl): Attack onset 24 hours prior to treatment Given 100 mL of 0.15% with complete resolution of the attack within 6 hours following the infusion. Comment: No followup treatment necessary. 6. Diabetes Mellitus Type II. 25 year history of diabetes taking 30 units NPH AM and PM. After 5 treatments of 250 mL of 0.15%, insulin reduced to 30 units AM and 15 units PM. Insulin reduced to 15 units AM only after 3 additional treatments because the patient was having symptoms of hypoglycemia. Discontinued all insulin after 10 treatments and given H202 on a monthly maintenance. Followup GTC appears more normal. Comment: Will maintain on schedule according to fasting blood sugars in future. 7. Chronic Post Herpetic Neuralgia: Post herpetic neuralgia persisting 1 year following a severe Herpes Zoster infection on right anterior and lateral chest wall. Given 250 mL of 0.075% weekly for 10 weeks. Neuralgic pain substantially reduced after 5th treatment and completely gone after 10th treatment. Comment: Will followup at 3 month intervals and as necessary. 8. Impending Cerebral Vascular Accident. 71 year old man with sudden onset two hours previously of confusion, paralysis, and weakness on left side of body, and drooling and unable to speak distinctively. Initial brood pressure 190/100, pulse normal. Given 250 mL of 0.03% H202 started immediately. All symptoms significantly improved within 30 minutes and completely resolved after 1 hour. Comment: Patient did not return for followup evaluation but was asymptomatic with blood pressure of 140/90 when he left the office. HYDROGEN PEROXIDE PROTOCOL REFERENCES 1. Oliver TH, Cantab BC, and DV: Influenzal Intravenous Injection of Hydrogen Peroxide. Lancet 1920; 1:432-433 2. Ramasarma T: Generation of H202 in Biomembranes. Biochemica et Biophysica ACTA 1982; 694: 69-93 3. Garner MH, Garner WH, Spector A: Kinetic ativity Change after H202 Modification of (Na,K)- ATPase. J Biolog Chem 1984; 259: 7712-7718 4. Wildberger E, Kohler H, Jenzer H, et al: Inactivation of Peroxidase and Glucose Oxidase by H202 and Iodide during In Vitro Thyroglobulin lodination. Mol Cell Endocrinol 1986; 46(2):149-154 5. Swaroop A and Ramasarma T: Heat Exposure and Hypothyroid Conditions Decrease Hydrogen Peroxide Production Generation in Liver Mitochrondia. J Biochem 1985; 226(2): 403-8 6. 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Mol Biochem Parasitol 1987; 22(2-3): 125-33 68. Ferrante A, Hill NL, Abell TJ, et al: Role of Myeloperodase in the Killing of Naegieria fowleri by Lymphokine-altered Human Neutrophils. Infect Immun 1987; 55(5): 1047-50 69. Passwell JH, Shor R, Gazit E, et a]: The Effects of Con A-induced Lymphokines from the T-lymphocyte Subpopulations on Human Monocytc Leishmaniacial Capacity and H202 Production. Immun 1986; 59(2): 245-50 70. Kazura JW, de-Brito P, Rabbege J et al: Role of Granulocyte Oxygen Products in Damage of Schistosoma mansoni Eggs In Vitro. J Clin Invest 1985; 75(4): 1297-307 71. Rothermel CD, Rubin BY, Jaffe EA, et a]: Oxygen-independent Inhibition of Intracellular Chiamydia psittaci Growth by Human Monocytes and Intcrferon-gamma-activated Macrophages. J Immunol 1986; 137(2): 689-92 72. Owells RE: The Modes of Action of Some Anti-protozoal Drugs. Parasitology 1985; 90(pt4): 689-703 73. Wirth JJ, Kierszenbaum F, Sonnenfeld G et a]: Enhancing Effects of Ganima Interferon on Phagocytic CellAssociation with and Villing of Trypanosoma cruzi. Infect Immun 1985; 49(l): 61-6 74. Ghadirian E, Somcrficid SD, Kongshavn PA: Susceptibility of Entamoeba Histolytica to Oxidants. Infect Immun 1986; 51(l): 263-7 75. Murray HW, Scavuzzo D, s JI, et a]: In Vitro and In Vivo Activation of Human Mononuclear Phagocytes by Interferon-gamma. Studies with Normal and AIDS Monocytes. J Immunol 1987; 138(8): 2457-62 76. Podopiekina LE, Shutova NA, Fyodorov YuV: Influence of Several Chemical Reagents on Lymphocytic Choriomeningitis and Tacaribc Viruses. Virologie 1986; 37(l): 43-8 77. Doroshow JH: Role of Hydrogen Peroxide and Hydroxyl Radical Formation in the Filling of Ehrlich Tumor Cells by Anticancer Quinones. Proc Natl Acad Sci USA 1986; 83(12):4514-8 78. Zaizen Y, Nak-agawara A, Ikeda K- Patterns of Destruction of Mousc Neuroblastoma Cells by Extracellular Hydrogen Peroxide Formed by 6-hydroxydopamine and Ascorbate. J Cancer Res Clin Oncol 1986; 111(2): 93-7 79. Agrawal P and Harper MJ: Studies on Peroxidase-catalyzed Formation of Progesterone. Steroids 1982; 40(5): 569-79 80. Heikk-iia R and Cohen G: Inhibition of Biogenic Amine Uptake by Hydrogen Peroxide: A Mechanism for Toxic Effects of 6-Hydroxydopamine. Science 1971; 172: 1257-58 81. Grisham MB, VJ, Everse J: Neuromelanogenic and Cytotoxic Properties of Canine Brainstem Peroxidase. J Ncurochem 1987; 48(3): 876-82 82. Hess ML, Manson NH, Lower RR: Leukocyte-genreated Hydrogen Peroxide Depression of Cardiac Sarcoplasmic Reticulum Calcium Transport. Transplantation 1983; 36(l):117-9 83. Verhoeven AJ, Mommersteeg ME, Akkerman JW: Balanced Contribution of Glycolyte and Adenylate Pool in Supply of Metabolic Energy in Mitochrondia. 84. JA, Fischman AJ, Khaw BA, et al: Free Radical Mediated Membrane Depolarization in Renal and Cardiac Cells. Biochim Biophys Acta 1987; 899(l): 76-82 85. Rubanyi GM and Vanhoutte PM: Oxygen-derived Free Radicals, Endothelium and Responsiveness of Vascular Smooth Muscle. Am J Physiol 1986; 250(5 pt 2): H815-821 86. Silin PJ, Strulowitz JA, Wolin MS, et al: Absence of a Role for Superoxide Anion, Hydrogen Peroxide and Hydroxyl Radical in Endothelium-mediated Relaxation of Rabbit Aorta. Blood Vessels 1985; 22(2): 65-73 87. Wei EP, Christman CW, Kontos HA, et al: Effects of Oxygen Radicals on Cerebral Arterioles. Am J Physiol 1985; 248(2 pt 2): H157-62 Platelets. J Biol Chem 1985; 260(5): 2621-4 88. Kontos HA: Qxygen Radicals in Cerebral Vascular Injury. Circ Res 1985; 57(4): 508-16 89. Burke TM and Wolin MS: Hydrogen Peroxde Elicits Pulmonary Artery Relaxation and Guanylate Cyclase Activation. Am J Physiol 1987; 252(4 Pt 2): H721-32 90. Farr CH: Conference Presentation. First International Conference on Bio-Oxidativc Medicine. Dallas, Texas February 1989 91. Hofmann C, Crettaz M, Burns P, et al: Cellular Responses Elicited by Insulin Mimickers in Cells Lacking Detectable Plasma Membrane Insulin Receptors. J Cell Biochem 1985; 27(4): 401-14 92. Farr CH: Possible Therapeutic Value of Intravenous Hydrogen Peroxide. Plzen.lek Sborn., Suppl. 56, 1988: 171-173 93. Farber CM, Liebes LF, Kanganis DN, et al: Human B Lymphocytes Show Greater Susceptibility to H202 Toxicity than T Lymphocytes. J Immunol 1984; 132(5): 2543-6 94. Setty BN, Jurek E, Ganley C, et al: Effects of Hydrogen Peroidde on Vascular Arachidonic Acid Metabolism. Prostaglandins Leukotrienes Med 1984; 14(2): 205-13 Duncan --- Outgoing mail is certified Virus Free. Checked by AVG anti-virus system (http://www.grisoft.com). Version: 6.0.264 / Virus Database: 136 - Release Date: 7/2/01 Quote Link to comment Share on other sites More sharing options...
Guest guest Posted September 29, 2001 Report Share Posted September 29, 2001 <<Rich, it is my understanding that 35% ,(only pharmacutical grade) h202 must be diluted with pharm. (glucose)down to 3% and dripped. This from my Dr.........>> OUCH NO! HE'S 50 TIMES TOO HIGH!! From an authoratative article............. Hydrogen Peroxide is available currently in a 3% USP/NF grade and is ideal for intravenous use. It must be packed in an open vial however with a vented cap to allow the escape of oxygen pressure produced by the dismutation. Some physicians are concerned about sterilization because of the packaging but hydrogen peroxide is self sterilizing. Proper dilutions are simple. Add 1 mL of the 3% Hydrogen Peroxide USP/NF solution to each 100 mL carrier solution. A typical treatment plan would be to give 100 to 250 mL H202 of 0.03% concentration once or twice a week. After the initial schedule of 10 to 15 treatments, wait 30 to 60 days and evaluate the response. Within 1 hour after the intravenous infusion of 250 mL 0.15% H202 a 2% to 10% decrease was noted in the following blood constituents: Bun, Sodium, Potassium, Chloride, Uric acid, Calcium, Phosphorus, Total protein, Total bilirubin, Alkaline phosphatase, AST, ALT, GGTP, LDH, Iron and Globulin. Follow-up studies, 24 hours later, revealed all the above blood constituents had returned to normal pre-infusion levels. Here's the rest of this particular article.. _______________________ INTRAVENOUS HYDROGEN PEROXIDE THERAPY (Quick Overview) MECHANISMS Oliver (l) first reported the use of Intravenous Hydrogen Peroxide (H202), in 1920 in patients with Influenzal Pneumonia. An epidemic in Busrah in June and July of 1919, had a calculated death-rate over 80 percent. Oliver treated 25 critical patients with intravenous infusions of H202 and 13 fully recovered reducing the mortality to 48 percent. He was impressed with the rapid clinical response and postulated the effects were probably due to the oxidation of toxins more than the relief of hypoxia. Hydrogen peroxide used in surgical procedures had caused air embolisms, but he reasoned if the oxygen was released slowly, embolism should not occur. Venous oxygen embolism has been reported following the irrigation of anal fistulae (2), surgical wounds (3), and closed body cavities (4). Ulcerative colitis (5) has been produced in patients using H202 in enema solutions to break up fecal impactions. It has been shown, however, to destroy murine malaria parasites (7), and the bactericidal properties of H202 produced by neutrophils is well documented (8-10). Hydrogen peroxide appears to be involved in many intermediate biochemical pathways. Additionally, it appears to kill certain bacteria, parasites, yeast, protozoa, inhibit viruses, and oxidize immunocomplexes. T. Ramasarma (11), in his review on the " Generation of H202 in Biomembranes " , states: " H202 is a purposeful molecule in cellular metabolism and cannot be dismissed as a mere undesirable byproduct of oxygen species generation " . Hydrogen peroxide is generated in most biological membranes; cellular, mitochondrial, and nuclear. It is important for maintaining membrane integrity and regulating membrane transport through the alteration of Na-K ATPase activity. This was confirmed by Garner et al (12). Hydrogen peroxide fulfills the role of a secondary messenger in several hormonal pathways. As an example, H202 generation in the uterus is dependent on estrogen and is necessary for the production of progesterone. The iodination of thyroglobulin and thyroxine synthesis requires the presence of peroxidase, H202, and iodide (13). Thyroxine increases and hypothyroidism decreases hydrogen peroxide production in studies of liver mitochondria (14). Hydrogen peroxide has an insulin-mimic action and acts as a postbinding site on the plasma membrane to induce glucose transport (15). More recent studies of Helm (16) found the insulinomimetic action involves a common mechanism which links the generation of active oxygen species through the redox potential of the cell to the activation of a proteinase. It helps regulate metabolic control through protein modification which alters enzyme activities. Thermogenic control (11,14) appears to be exercised through the action of H202 on the mitochondria. At the mitochondrial level, H202 is generated by a number of substrates. Flavoproteins converge at ubiquinone which forms a link between H202 generation and the respiratory chain. Noradrenaline, thyroxine, and cold stimulate the system to generate heat. Heat increases the rate of H202 production and is dependent on alpha-adrenergic receptors which also control non-shivering thermogenesis. The balance of Ferric (3+) and Ferrous (2+) Iron in the body is critical to support lipid peroxidation of cellular membranes (27). It has been reported that a ratio of Fe(3+)/Fe(2+) of 1:1 to 8:1 is optimal to cause the formation of -OH radicals and lipid peroxidation. At ratios above or below these levels, lipid peroxidation does not occur. Physiological concentrations of either H202 or Ascorbic Acid may encourage lipid peroxidation and at these levels antioxidant protection is important. Increasing the concentration of H202, as occurs with therapeutic intravenous infusions, the Ferric/Ferrous ratio is maintained above 8:1 by keeping excess Ferrous (Fe2+) Iron oxidized to the Ferric (Fe3+) state. A principal mechanism of action of EDTA Chelation Therapy is reducing Free Radical damage and lipid peroxidation by complexing EDTA with Ferrous Iron (Fe3+:EDTA) which helps maintain the Ferric/Ferrous ratio above 8:1 (28) Weiss (8) reported H202 is an activator of neutrophils including aggregated immunoglobulin, activated complement components, immune complexes, or bacterial peptides. This would suggest the beneficial clinical effects observed with the use of ascorbic acid in inflammatory reactions, and its protective action against infections, is acting through the generation of H202. Also, there is no evidence H202 initiates or supports microsomal lipid peroxidation (51). The modification of (Na,K)-ATPase(12) by H202 also contributes to an increase in metabolic rate. Farr (40) reported whole blood specimens taken before, during, and after H202 infusions showed color changes consistent with oxyhemoglobin formation. Numerous blood profiles and CBC studies have been performed before and immediately after infusions of H202. Although early investigators reported no changes in blood elements and certain chemical constituents, except when injected into the carotid arteries, consistent changes have been reported. Within 1 hour after the intravenous infusion of 250 mL 0.15% H202 a 2% to 10% decrease was noted in the following blood constituents: Bun, Sodium, Potassium, Chloride, Uric acid, Calcium, Phosphorus, Total protein, Total bilirubin, Alkaline phosphatase, AST, ALT, GGTP, LDH, Iron and Globulin. Follow-up studies, 24 hours later, revealed all the above blood constituents had returned to normal pre-infusion levels. Some of the biological killing activity of H202 may be attributed to gamma interferon. Production of gamma interferon by human natural killer cells and monocytes, is stimulated by H202(58). Both exogenous and endogenous H202 appear to be in part responsible for immunoregulation. The rates of wound healing, stasis and vascular ulcers (18), peripheral occlusive disease (59,60), myocardial ischemia (33) and cerebral vascular disease (61) have all improved when treated with repeated intra-arterial infusions of H202 PHYSICAL PROPERTIES OF HYDROGEN PEROXIDE Hydrogen Peroxide was discovered in 1818 by the French Chemist Louis-Jacque Thenard. Hydrogen Peroxide, hydrogen dioxide (H202), is a colorless (blue in thick layers) odorless liquid; with a melting point -2 degree C: a boiling point 152 degrees C; decomposes 84 degrees C at 68 mm. pressure (68 degrees C at 26 mm.), soluble in water in all proportions; usually encountered as a dilute solution (3% H202) solution, that is, one volume of solution yields 10 volumes of oxygen), although available up to 35% strength. Its remarkable feature is its tendency to decompose readily into water and oxygen. Decomposition by light begins only in the near ultraviolet. Hydrogen peroxide solutions dismutate slowly, when undisturbed, at the rate of approximately 1% per month. The dismutation reaction is rapidly increased in the presence of particulate contaminates; i.e., dust, flakes of metal or glass or other particulate matter, at a rate which may be explosive. Cold retards dismutation and solution may be refrigerated or stored at temperatures below 0 degrees C. Hydrogen peroxide occurs only in traces in nature: mostly in rain and snow. It has not yet been detected in interstellar space. METABOLIC AND PHYSIOLOGICAL EFFECTS Numerous physiological effects are attributed to hydrogen peroxide and documented in the literature. Some of these effects may be broadly categorized as follows: 1. PULMONARY A. Increased oxygenation B. Alveolar debridement (31) 2. METABOLIC RATE A. Hormonal effect: Several hormonal effects have been reported to be regulated by the action of H202. Examples are: 1.Iodination of thyroglobin(13) 2. Production of thyronine (13) 3. Progestone production (107) 4. Inhibition of bioamines (108); dopamine, noradrenalin and serotonin 5. Prostaglandin synthesis (46,47,109) 6. Dopamine metabolism (110) 7. Regulates Reticulum Calcium Transport (111) 8. Oxidative stimulation: Hydrogen peroxide directly and indirectly stimulates oxidative enzyme systems. Micromolar amounts of infused H202 has been found to increase oxidative enzymatic activity to the maximum rate of reaction (40). 1. Increases GSH oxidation to GSSG which increases ATP production(112) 2. Activates Hexose Monophosphate Shunt(41) 3. Alters Na-K ATPase activity (12) 4. Regulates cellular (113) and mitochondrial (15) membrane transport 5. Regulates thermogenic control (11) 3. CARDIOVASCULAR RESPONSE A. Vasodilation 1. Dilation of peripheral vessels (31) 2. Dilation of coronary vessels (114) 3. Aortic strip relaxation response (115) 4. Cerebral arteriolar dilation (116,117) 5. Pulmonary arterial relaxation (118) B. Vasoconstriction 1. Essential Hypertension effect (31) 2. Peripheral vasoconstriction may occur in normal-tensive patients with concentrations at or below 0.0375% with no significant increase in mean pressures(123). C. Cardiac Responses (12-3) 1. Decreases Heart Rate 2. Decreases Vascular Resistance 3. Increases Stroke Volume 4. Increases Cardiac Output 5. Increases Cardiac Index 4. GLUCOSE UTILIZATION A. H202 mimics insulin (16) B. Increases glycogen production from glucose (119) C. Type II Diabetes Mellitus stabilized with H202 infusions (20) 5. GRANULOCYTE RESPONSE A. Depressed granulocytes after treatment then rebound measured after 24 hours (31) B. Secondary resistance to peroxide after exposure (109) C. Alteration of T4/T8 ratio with increase of T4 Helper cells (28) 6. IMMUNE RESPONSE A. Stimulates Monocytes (92) B. Stimulates T Helper cells (109) C. Stimulates Gamma Interferon production (58) D. Decreases B-cell activity (121) E. Responsible for immunoregulation (58) F. Regulates inflammatory response (122) INDICATIONS Intravenous Hydrogen Peroxide is used in the acute reactive conditions ; i.e., influenza, bronchitis, Herpes Zoster, asthmatic reactions, etc.) because of its direct killing effect on micro-organisms or its effect on vasospasm or bronchospasm. The long term effect, to regulate or modify the immune response through cellular activation or modification of immune dysfunction, such as EBV, Candida, CMV, Herpes, HIV, Diabetes Type II, COPD, vascular disease, arthritis, and etc., is an important therapeutic tool for every physician. The therapeutic use of intravenous H202 has been reported in the following diseases or conditions with varying results depending on the clinical investigator: l. Peripheral Vascular Disease 2. Cerebral Vascular Disease 3. Alzheimer 4. Cardiovascular Disease 5. Coronary Spasm (angina) 6. Cardioconversion 7. Arrhythmias 8. Chronic Obstructive Pulmonary Disease 9. Emphysema 10. Asthma 11. Influenza 12. Herpes Zoster 13. Herpes Simplex 14. Temporal Arteritis 15. Systemic Chronic Candidiasis 16. Chronic Recurrent Epstein Barr Infection 17. Diabetes Type II 18. HIV infections 19. Metastatic Carcinoma 20. Multiple Sclerosis 21. Rheumatoid Arthritis 22. Acute and Chronic viral infections 23. Chronic unresponsive bacterial infection 24. Parasitic infections 25. Parkinsonism 26. Migraine headaches 27. Cluster headaches 28. Vascular headaches 29. Chronic pain syndromes (multiple etiologies) 30. Environmental allergy reactors (Universal) Many in-vitro and some in-vivo studies have shown H202 to be bactericidal, fungicidal, parasiticidal, viricidal, and to lyse certain tumor cell types in cultures. The therapeutic benefit of H202 infusions in patients with any of the following infections and/or tumors may not be clinically documented. Therefore, no recommendation can be made until appropriate studies have been conducted. BACTERIA 1. Legionella pneumophila (62) 2. Treponema pallidum (63) 3. Escherichia coli (64) 4. Salmonella typhimurium (65) 5. Mycobacterium leprae (66) 6. Staphylococcus auerus (67) 7. Pseudomonas acruginosa (68) 8. Campylobacter jejuni (69) 9. Salmonella typhi (70) 10. Group B Streptococci (71) 11. Bacillus cereus (72) 12. Actinobacillus actinomycetem comitans (73) 13. Bacteroides (74) 14. Neisseria gonorrhoea (75) FUNGI 1. Histoplasma capsulatum (76) 2. Candida Albicans (77) 3. Coccidioides (78) 4. Paracoccidiodes (78) 5. Blastomyces (78) 6. Sporothrix (78) 7. Mucoraceae(78) 8. Aspergillus fumigatus (79) 9. Coccidioides immitis (80) PARASITES 1. Pneumocystis carinii (81) 2. Plasmodium yoelii (82) 3. Plasmodium berghei (82) 4. Toxoplasma gondii (83) 5. Nippostrongycus brasiliensis (84) 6. Naegleria fowleri (85) 7. Leishmania major (86) 8. Schistosoma mansoni (87) 9. Chlamydia psittaci (88) 10. Trichomonas vaginalis (89) 11. Tepanosoma cruzi (90) 12. Endameba histolytica (91) VIRUS 1. Human Immunodeficiency Virus (92) 2. Cytomegalovirus (67) 3. Lymphocytic choriomeningitis virus (93) 4. Tacaribe virus (93) TUMOR TYPE 1. Ehrlich carcinoma (94) 2. Neuroblastoma (95) CONTRAINDICATIONS PRECAUTIONS: Hydrogen Peroxide infusions are contraindicated in pregnancy, Chronic Granulomatous Disease (CGD), and any disorder of cell membrane stability (i.e. anemias). SIDE EFFECTS: The most frequent side effect reported (at concentrations above 0.0375%) is vasculitis, which may occur in the infused vein and/or its tributaries. This phenomenon is inconsistent, occurring repeatedly in some patients but rarely in others. According to Shingu, (97) epithelial and smooth muscle cells contain very little, if any, catalase and, therefore, may be sensitive to the effects of H202. There appears to be a critical concentration of H202 which is cytolytic, and will cause vasculitis if exceeded. It is, therefore, important to consider the concentration being infused and the size of the vessel. This reaction is less likely to occur if a larger vein in the antecubital area is used for infusion, and the rate of administration is reduced. Once the cytolytic concentration is exceeded, the cells swell up, become toxic and die. The exact mechanism by which H202 is cytotoxic are not defined, however, *NOTE* Recent studies have revealed the addition of 0.5 mg Manganese to the intravenous solution to be effective in controlling the endothelial damage caused by the H202 solution. It is reported that there may be no microscopic signs of cytotoxicity for 6 hours or longer after exposure of the cells to H202. Consequently, after you infuse a patient, the vasculitis may not be apparent until the following day. The application of heat may make the reaction more severe since heat speeds up the rate of most biochemical reactions, and this may be no exception. We recommend you use only the larger veins for infusion, and reduce the rate of infusion if you suspect the patient's blood flow rate is slower than usual. It has also been found useful to rotate between the veins and not use the same vein for two consecutive treatments. Rotate between veins and alternate treatments from one arm to the other. Some physicians report they have flushed the vessel post-infusion with additional heparin, or Decadron, but results have not been changed. All oral supplements and drugs should be withheld on the day of infusion. Taking antioxidants on the day of infusion would appear to be counterproductive and may aggravate the vasculitis. Intravenous H202 delays clotting by 20%, but reduces bleeding time approximately 50%. Caution should be exercised when giving H202 to patients taking anticoagulants since clinical data is not available at this time for comment. ALLERGIC PHENOMENON: Occasionally, a non-tender red streak will appear, tracing the route of the vessel above the point of infusion. This streak will often have a diffused fanned-out appearance radiating laterally from the central streak. No relationship has been identified between this superficial vascular phenomenon and the vasculitis previously described. This vascular phenomenon occurs randomly in patients and has been observed at a rate of about 1 in 50 infusions in concentrations greater than 0.0375%, but only 1 in 500 at concentrations at or below 0.0375%. Several hundred infusions have been given, and no other type of local or systemic allergic vascular reaction has been observed or reported. CHEST DISCOMFORT: Some physicians have reported occasional patient complaints of vague chest discomfort, sometimes associated with a feeling of shortness of breath. We received two reports that the chest discomfort was severe enough to discontinue the treatments. Bronchodilators should be withheld for at least a day before H202 is administered, if possible. INFUSION SITE PAIN: Pain at and above the infusion site is occasionally reported. The pain is described as a spastic ache and is most likely due to vasospasm. On rare occasions, the pain may extend from the point of infusion, at or below the antecubital area, up into the deltoid area. Reducing the rate of infusion, heat, and ice have all been ineffective in controlling the pain. We have found, when this occurs, the best thing to do is remove the needle and restart the infusion in another vein. We speculate the irritation to the vessel, at the point of penetration, causes a reflex vasospasm along the vessel. Changing the needle position or rotating its position in the same vein does little to relieve the discomfort. HERXHEIMER TYPE REACTION: Several physicians have reported an occasional Herxheimer-like reaction when treating patients with mucocutaneous candidiasis. Following infusions of H202 the patients were reported to have generalized migratory aching, nausea, headaches, chills, and fever. It has been reported to occur after one, two, and sometimes three treatments, but, thereafter, the patients report an improvement in their overall clinical status, and continue to improve with each succeeding treatment. No patients have been discontinued from treatments because of this reaction. It does not occur consistently nor is it predictable. TOXICITY Hydrogen peroxide is a product of intermediate metabolism, widely distributed throughout the body, and participates in a significant number of biochemical reactions. It is a principal electron receptor in the body in many RedOx reactions. A vast amount of knowledge exists about the chemistry of H202 in tissue slices, tissue cultures, bacteria, parasites, yeast, protozoa, blood cells, and isolated human, animal, and plant cells. Numerous examples of biochemical changes have been described in the literature, which are interpreted as toxic or damaging in the models studied. Clinically, however, no significant acute toxicity has been observed in several hundred patients, some receiving up to 40 to 50 infusions with concentrations up to 0.3 %. Also, no chronic or long term toxicity has been observed or documented up to two years post-multiple infusions. One patient received 3,600 mL of 0.15% of Hydrogen Peroxide intravenously in a period of 10 days without any side effect. This dosage is approximately 40 times greater than the currently recommended therapeutic dosage. Other studies suggest doses 500 times smaller than the currently recommended dose will have biological effect. This suggested intravenous infusions of Hydrogen Peroxide is extremely safe and has a very wide therapeutic range. Consequently, the majority of toxic reactions referred to in the literature, which occur with in-vitro studies under laboratory conditions, which could not exist in-vitro, have very little clinical application. Some of the in-vitro toxic effects are: A. Lipid Peroxidation (49,98) B. Single strand DNA breakage (99) C. Cytotoxic (concentrations above 10 mMol) (100) D. RBC hemolysis (26,101) E. Chromosomal Aberrations (102) F. Protein degradation (103) G. Glutathione Peroxidase depiction (104) H. Degredates Cytochrome C (105) I. Platelet Aggregation (106) FORMULAS INTRAVENOUS ADMINISTRATION OF H202 SOLUTION The PROPER DOSAGE is dependent upon the CONCENTRATION used, the VOLUME INFUSED, and the RATE OF INFUSION. The infusion mixture is prepared as follows: The preferred carrier is 5% Dextrose in Water or Normal Saline. Hydrogen Peroxide is available currently in a 3% USP/NF grade and is ideal for intravenous use. It must be packed in an open vial however with a vented cap to allow the escape of oxygen pressure produced by the dismutation. Some physicians are concerned about sterilization because of the packaging but hydrogen peroxide is self sterilizing. Proper dilutions are simple. Add 1 mL of the 3% Hydrogen Peroxide USP/NF solution to each 100 mL carrier solution. If you plan to give 250 mL treatment you add 2.5 mL of the peroxide in 250 mL of carrier, 5 mL to 500 mL carrier and etc. for the proper dilution. Select a medium to large vein close to the antecubital area for the infusion. Use a small winged needle and infuse slowly over a period of 1 to 1 1/2 hours. The rate of infusion and concentration are both important as explained below. THERAPEUTIC INFUSION SCHEDULES The dosage administered is dictated by the therapeutic and objective experience of the clinician. The physician should consider the clinical objective after the diagnosis has been properly established. A general rule: the more acute the pathology the greater the volume and concentration and the more frequent the infusions. The frequency may be maintained until the acute problem is considered stable, and then both dose and frequency reduced. As an example, a patient with acute influenza or Herpes Zoster may be placed on a schedule of 250 to 500 mL of H202 of 0.03% or less concentration, daily for 1 to 5 infusions or until clinical response is obvious. Occasionally, these patients may require a treatment once or twice a week for an additional 5 to 10 treatments, particularly in infections which have a tendency to become chronic such as Herpes or Hepatitis. A therapeutic regimen for a chronic, low grade infection or chronic illness would be to schedule smaller doses over a longer period of time. Examples of chronic illnesses in which long term therapy might be employed would include: Chronic candidias, chronic obstructive pulmonary disease, peripheral occlusive disease, chronic EBV, or Hepatitis, and etc. A typical treatment plan would be to give 100 to 250 mL H202 of 0.03% concentration once or twice a week. After the initial schedule of 10 to 15 treatments, wait 30 to 60 days and evaluate the response. Depending on the response, you may wish to give an additional series of 10 to 15 treatments and again wait and re-evaluate. An alternative is to keep the patient on bimonthly or monthly maintenance treatments for a year and then reevaluate annually. The following are examples of treatment schedules which have been employed in these selected cases. 1. ACUTE PULMONARY INFECTIONS INCLUDING INFLUENZA PNEUMONIA. Infusions of Hydrogen Peroxide have a rapid 'Alka-seltzer effect' in the lungs. If the patient has moist lungs and/or a productive cough, the treatment will usually cause coughing and mucous production to increase immediately. It may continue throughout the treatment but will subside soon after the treatment is completed. If the patient is quite ill and febrile, the initial treatment would be 250 to 500 mL of 0.03%. If the patient remains febrile the second day, give an additional 250 to 500 mL of 0.03%. Treat according to response, thereafter, every two to three days until the desired response is obtained. 2. CHRONIC LUNG DISEASE (COPD, BRONCHITIS, BRONCHIECTASIS, EMPHYSEMA) Chronic lung disease, which is moist and active, responds best to treatment. The response in dry emphysema or pulmonary fibrosis is less dramatic. Give 250 mL 0.03% weekly for 10 to 15 weeks. Frequently, the effects will be dramatic, with coughing and sputum production initially, and the patients reporting increased energy and ability to breathe within 24 hours. The effects of treatments are usually progressive improvement for 8 to 10 treatments, and then the effects plateau. Most patients will wish to continue on monthly maintenance treatments. 3. ALLERGIC REACTIONS, ASTHMA, ENVIRONMENTAL SENSITIVITY, ETC. The longer the patient has had their allergic reactive problem, the longer it will be before you will have a positive response. This general rule, however, does not always apply. Some patients respond rapidly, within 2 to 3 treatments. In these complex patients, schedule weekly treatments for 10 weeks, give the patient a 30 day rest, and repeat an additional 10 weekly treatments. You may give up to 40 to 50 treatments on this schedule, or until you feel maximum response has been obtained. Most patients will realize improvement after their first course of 10 treatments. Thereafter, patients show a gradual improvement with each successive group of 10 treatments. If the patient shows no improvement after 30 to 40 treatments, then no response is likely and therapy is discontinued. 4. ACUTE AND CHRONIC PAIN Angina, headaches, vasospasm, tumor pain, or neurological pain frequently show an immediate and dramatic response to one or two treatments. Chronic pain syndromes may require several (8-10) treatments but response is frequent. There is no good explanation why Hydrogen Peroxide should relieve pain, but, nevertheless, this has been a frequently reported clinical observation. Chronic, established pain of Post Herpetic Neuralgia may not respond to treatments, but the response in Acute Herpes Zoster is often dramatic. 5. EBV, CMV, HIV, HERPES, HEPATITIS ETC. Acute infections require frequent daily treatments, whereas, chronic infections require long term weekly treatments. Symptomatic response may occur after only 1 or 2 treatments, but antibody titers may not change until 10 to 30 weekly treatments have been given. 6. CEREBRAL VASCULAR, ALZHEIMER, TOXIC DEMENTIA, ETC. Perhaps the increased oxygenation can explain the sometimes rapid reversal of symptoms in these patients. Acuity, memory, recall, alertness, and other cerebral symptoms frequently improve quickly and the improvement appears to be long lasting. The results may also be related to changes in the bioamines in the brain because positive results are also seen in anxiety/depressive non-toxic young adults. Ten weekly treatments are usually given before the effectiveness of treatment is evaluated. 7. CARDIOVASCULAR AND PERIPHERAL VASCULAR DISEASE Using weekly treatments of smaller volume; i.e., 100 to 250 mL, can be very beneficial to these patients if your objective is to restore oxygenation to the tissue. If the objective is to push a gangrenous digit or extremity to the point of demarcation for surgical debridement, then 250 to 500 mL are given daily, for several days, until demarcation is completed. The following are actual case reports, from the initial studies (31) on the Intravenous Use of Hydrogen Peroxide. Higher concentrations were used in these studies than currently recommended. Same or similar cases have been repeated many times since, at the lower concentration of 0.03%, with equally good clinical results but WITHOUT vasculitis or other side effects. We, therefore, recommend you do not exceed the 0.03% concentrations. 1. Acute Herpes Zoster. 250 mL of 0.15% initially, then every two days for a total of 6 treatments. Comment: Resolved completely in less than 1 week with no residual. 2. Acute Influenza Syndrome. 250 mL of 0.15% initially, and 500 mL of 0.15% the second day. Afebrile after second day, but additional treatment the third day of 250 mL of 0.15%. Comment: Resolution of all symptoms after the second day with no residual. 3. Chronic Systemic Candidiasis: 250 mL of 0.15% once a week for 10 treatments, and then monthly followup for 10 months. Comment: Clinical response not observed until after the 4th treatment, then gradual improvement continued. Maintained on monthly treatments. 4. Severe COPD. Initial 250 mL of 0.15% which caused significant alveolar debridement and coughing up of copious amount of purulent material. Continued weekly infusions for 6 weeks, and by the end of the 6th treatment the patient no longer coughing. Pulmonary function improved and the patient returned to working full time. Comment: Maintained on treatment according to patients " feel the need " which re-occurs approximately every 4 to 6 weeks. 5. Acute Asthmatic Attack (12 yr old girl): Attack onset 24 hours prior to treatment Given 100 mL of 0.15% with complete resolution of the attack within 6 hours following the infusion. Comment: No followup treatment necessary. 6. Diabetes Mellitus Type II. 25 year history of diabetes taking 30 units NPH AM and PM. After 5 treatments of 250 mL of 0.15%, insulin reduced to 30 units AM and 15 units PM. Insulin reduced to 15 units AM only after 3 additional treatments because the patient was having symptoms of hypoglycemia. Discontinued all insulin after 10 treatments and given H202 on a monthly maintenance. Followup GTC appears more normal. Comment: Will maintain on schedule according to fasting blood sugars in future. 7. Chronic Post Herpetic Neuralgia: Post herpetic neuralgia persisting 1 year following a severe Herpes Zoster infection on right anterior and lateral chest wall. Given 250 mL of 0.075% weekly for 10 weeks. Neuralgic pain substantially reduced after 5th treatment and completely gone after 10th treatment. Comment: Will followup at 3 month intervals and as necessary. 8. Impending Cerebral Vascular Accident. 71 year old man with sudden onset two hours previously of confusion, paralysis, and weakness on left side of body, and drooling and unable to speak distinctively. Initial brood pressure 190/100, pulse normal. Given 250 mL of 0.03% H202 started immediately. All symptoms significantly improved within 30 minutes and completely resolved after 1 hour. Comment: Patient did not return for followup evaluation but was asymptomatic with blood pressure of 140/90 when he left the office. HYDROGEN PEROXIDE PROTOCOL REFERENCES 1. Oliver TH, Cantab BC, and DV: Influenzal Intravenous Injection of Hydrogen Peroxide. Lancet 1920; 1:432-433 2. Ramasarma T: Generation of H202 in Biomembranes. Biochemica et Biophysica ACTA 1982; 694: 69-93 3. Garner MH, Garner WH, Spector A: Kinetic ativity Change after H202 Modification of (Na,K)- ATPase. J Biolog Chem 1984; 259: 7712-7718 4. Wildberger E, Kohler H, Jenzer H, et al: Inactivation of Peroxidase and Glucose Oxidase by H202 and Iodide during In Vitro Thyroglobulin lodination. Mol Cell Endocrinol 1986; 46(2):149-154 5. Swaroop A and Ramasarma T: Heat Exposure and Hypothyroid Conditions Decrease Hydrogen Peroxide Production Generation in Liver Mitochrondia. J Biochem 1985; 226(2): 403-8 6. 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First International Conference on Bio-Oxidativc Medicine. Dallas, Texas February 1989 91. Hofmann C, Crettaz M, Burns P, et al: Cellular Responses Elicited by Insulin Mimickers in Cells Lacking Detectable Plasma Membrane Insulin Receptors. J Cell Biochem 1985; 27(4): 401-14 92. Farr CH: Possible Therapeutic Value of Intravenous Hydrogen Peroxide. Plzen.lek Sborn., Suppl. 56, 1988: 171-173 93. Farber CM, Liebes LF, Kanganis DN, et al: Human B Lymphocytes Show Greater Susceptibility to H202 Toxicity than T Lymphocytes. J Immunol 1984; 132(5): 2543-6 94. Setty BN, Jurek E, Ganley C, et al: Effects of Hydrogen Peroidde on Vascular Arachidonic Acid Metabolism. Prostaglandins Leukotrienes Med 1984; 14(2): 205-13 Duncan --- Outgoing mail is certified Virus Free. Checked by AVG anti-virus system (http://www.grisoft.com). Version: 6.0.264 / Virus Database: 136 - Release Date: 7/2/01 Quote Link to comment Share on other sites More sharing options...
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