Tråd: Hydrogen Peroxide /Intravenous

Discovery and Natural Occurrence
Hydrogen peroxide was discovered in 1818 by the French chemist Louis-Jacques Thenard. He coined the term eau oxygenee, to express his belief that it was an oxygenated form of oxygen. It is not clear if he fully understood the enormous medical significance of his discovery. Hydrogen peroxide is colorless, heavier than water, and has a larger liquid range than water, the melting point ranging from -11C (70%) to -39C (70%). It is produced within the plant biomass and plays diverse and pivotal roles in the cellular communication and energetic systems in the plant kingdom. It is present in trace amounts both in rainwater and snow. Interestingly, it is found in higher concentrations in natural spring waters of many healing shrines, most notably in Lourdes in France, Fatima in Portugal, and St. Anne's in Quebec. In light of my observations of the clinical benefits of H2O2 therapies in a host of clinical entities, I am tempted to speculate that many of the putative benefits of the shrine waters accrue from the oxystatic roles of H2O2. It is also likely that the mineral compositions of such waters enhance their oxystatic benefits.

Hydrogen Peroxide: A Misunderstood Molecule
Hydrogen peroxide is a misunderstood molecule. It is a potent in vitro oxidant. And yet, it serves as an effective in vivo antioxidant in clinical states associated with chronic accelerated oxidative molecular stress.4,5 It is procoagulant under certain conditions and anticoagulant under others.6 It is proinflammatory in some roles and anti-inflammatory in others.7 It induces some genes and suppresses others.8,9 It is a critically important second messenger in many pathways. 10-14 It is procancer in some aspects and anti-cancer in others.

Hydrogen peroxide plays multiple Dr. Jekyll/Mr. Hyde roles in enzymatic dynamics of the body, inducing some and impairing the functions of others,15-19 including: (1) inactivation of xanthine oxidase by reactions that involve formation of hydroxyl radicals; (2) oxidation of the oxidation- sensitive thiol groups at the active site of glucose-3-phosphate dehydrogenase and so inhibits the enzyme, thus reducing ATP-dependent synthesis of many proteins; (3) inhibition of glyceraldehyde phosphate dehydrogenase (GAPDH), providing a mechanism by which hydrogen peroxide exerts a regulatory effect on endothelial pathophysiology; (4) regulation of activities of crucial energy enzymes, such as sodium-potassium ATPase18; activation of potent enzymatic antioxidant defenses, including glutathione peroxidase.19 Other important metabolic aspects of hydrogen peroxide include: (1) hexose monophosphate shunt20; (2) mitochondrial enzymatic pathways21; (3) enzymes of membrane transport systems22; (4) thyroglobulin iodinases23; (5) prostaglandin synthesis24; (6) bioamine metabolic pathways, including those of norepinephrine, dopamine, and serotonin25; and (7) progesterone and estrogenic synthetic pathways.26 By those and other roles, hydrogen peroxide activates a host of oxyenzymes—enzymes that are directly involved in oxygen homeostasis—and alters the expression of oxygenes in many ways.

The Beginning of H2O2 Therapeutics
In 1898, Cortelyou of Marietta, Georgia, reported successful results obtained in patients with disorders of the nose and throat.27 In the same year, I.N. Love reported his successful use of H2O2 for treating scarlet fever, diphtheria, pneumonia, and uterine cancer in the Journal of the American Medical Association.28 A clear record of what appears to be the first clinical use of intravenously administered hydrogen peroxide appeared in an article published in Lancet in 1920 by Oliver and Cantab.29 They were military physicians treating Indian Gurkha soldiers. During an influenza epidemic, they encountered 80% mortality among soldiers who developed pneumonia. In desperation—possibly emboldened by a lack of fear of serious censure if the treatment were to be fatal for some terminally ill Indian soldiers—they undertook intravenous infusions of hydrogen peroxide to treat pneumonia. They were fortunate. In their landmark paper, they reported more than 50% reduction in mortality — 13 of 25 treated soldiers survived! There were no cases with clinical or pathologic evidence of air embolism. It puzzles me why that report was not followed by widespread use of that treatment of pneumonia in Britain.

A pioneer of intravenous H2O2 therapy was Charles Farr. During the mid-1990s, he honored me by having me serve as his co-director of courses on bio-oxidative therapies. Farr made several important original clinical and experimental observations about intravenous hydrogen peroxide infusions. He documented short-term and long-term effects of that therapy on various aspects of the immune system. One of his astute observations concerned the dramatic changes—up to 100% increase from the pre-infusion levels—in oxygen consumption rate. He clearly established the fact that biologic effects of that therapy cannot be merely attributed to the miniscule amounts of oxygen liberated from the infused hydrogen peroxide.30

Mechanisms by Which H2O2 Improves Arterial, Venous, and Lymphatic Circulations
A large number of short-term and long-term observations have convinced us that H2O2 improves arterial, venous, and lymphatic circulation. Those effects are mediated by a host of mechanisms. Personal morphologic observations with phase-contrast microscopy have convinced me that the most important of those mechanisms is control of oxidative coagulopathy by myriad molecular mechanisms listed below. Microclots and microplaques in the circulating blood are readily detected by examination of freshly prepared and unstained smears of the peripheral circulating blood with high-resolution, phase-contrast microscopy.31-33 The arrest of oxidative lymphopathy occurs concurrently with control of oxidative coagulopathy, though a suitable lymph specimen for direct documentation of that phenomenon is generally not forthcoming.

The primary mechanism by which H2O2 exerts those circulatory effects is proteolytic dissolution of microclots and microplaques in the vascular channels. Less important effects of H2O2 include the following: (1) peripheral vasodilatation34; (2) coronary vasodilatation35; (3) cerebral arteriolar dilatation36; and (4) pulmonary vasodilatation37; and (5) peripheral vasodilatation.36

H2O2 and Phagocytosis
Antimicrobial properties of hydrogen peroxide were recognized soon after its discovery. It was to be expected that the seminal work of the Russian biologist, Elie Metchnikoff, concerning humoral immunity during the late nineteenth century would also bring hydrogen peroxide into sharper focus. That, indeed, happened. The classical concept of phagocytic microbial killing may be summarized as follows38-42: (1) The invading microbes are exposed to serum factors, opsonized, and engulfed within the phagocytic cells; (2) The engulfed microbes are encapsulated by a series of fusion processes culminating in the development of the mature phagosome41; (3) Phagosomes merge with early endosomes to increase the vesicle size; (4)Membrane-bound vacuolar ATPases and proteolytic enzymes necessary for particle and microbial degradation are acquired42; (5) Bactericidal molecular machinery of cytoplasmic granules is brought into action with the release of their granules; and (6) Actual demise of microbes is attributed to production of free radicals—superoxide, hydrogen peroxide, and others—during respiratory burst.43

H2O2, Matrix Regulation, and Microbial Killing
Recent studies have revealed that actual molecular dynamics of microbial killing are far more complex than simple destruction of mirobes by free radicals.44,45 Specifically, certain conditions of the granular matrix are essential for completing the process of microbial disintegration. The matrix within the granules is highly charged. Granular proteases are normally adsorbed to it in an inactive form. When the ionic strength in the vacuoles rises, the enzymes are activated and unleashed to serve their microbiocidal roles. Those enzymes function optimally at elevated pH levels which exist in the vacuoles under those conditions. The respiratory burst within the phagocytic vacuoles is accompanied by a surge in the intravacuolar pH—from 6 to nearly 8. A large influx of potassium ions through the vacuolar membrane occurs and offsets the anionic charge. That happens in spite of the release of predominantly acidic granular contents since protons are consumed in neutralizing the excess of basic superoxide ions and other radicals.46,47

Concurrently, osmotically potent degradation products are released from disintegrating microbes, rendering the vacuole markedly hypertonic and shrinking the viable bacteria by as much as 50%. Such microbial shrinking is prevented if protease inhibitors are introduced into the system. Undue expansion of the vacuoles is prevented by a dense network of membrane cytoskeletal proteins.

Neutrophilic myeloperoxidase, itself capable of destroying microbes, appears to protect proteases from oxidative damage, to which they are vulnerable, especially cathepsin G.48

The Role of Potassium Ions
The passage of electrons across the vacuolar membrane is electrogenic. Specifically, the superoxide-generating NADPH oxidase of human neutrophils is electrogenic and is associated with an H+ channel.49 There are important changes in H+ dynamics during phagocytosis. For example, protein C kinase activates an H+-(equivalent) conductance in the plasma membrane of human neutrophils. Activation of NADPH oxidase-related proton and electron currents occurs simultaneously in human neutrophils. Potassium ions play a central role in the microbial killing process. Oxidases generate a potential difference across the membrane. Potassium ions move to compensate for that difference and in doing so enable the pH to rise to a level necessary for optimal function of proteases. Potassium ions activate granule enzymes. When phagocytes are inactive (not engulfing and killing microbes), the granules contain a strongly anionic sulfated proteoglycan matrix that binds tightly to cationic proteases. In the bound form, proteases cannot digest microbes. There is evidence that hypertonic K+ driven into vacuoles by NADPH oxidase is responsible for unleashing (by solubilizing) those enzymes, since elevated pH on its own is unable to activate proteases. 50

Would one expect the other ionic channels to sit out the action of phagocytosis? Hardly, in view of Nature's preoccupation with complementarity and contrariety. Free calcium ions initiate, augment, or perpetuate an enormous variety of cellular processes. For example, calcium is involved with coupling of diverse stimuli to their respective specific responses,51,52 including: (1) light; (2) touch; (3) gravity; (4) cold shock; (5) hormones; (6) bacterial compounds; and (7) mycotoxins. Stimulus specificity appears to be encoded through a multitude of Ca2+ mobilization pathways. For example, vacuolar ligand-gated Ca2+ mobilization pathways may involve both Ca2+- and voltage- operated Ca2+ release channels in the same membrane, acting singly or coordinately. Directly or indirectly, such calcium-related responses are involved in nearly all crucial steps in phagocytosis. Not unexpectedly, many of the specific calcium responses depend on their spatio-temporal concentrations. To render the calcium-related cellular happenings yet more fascinating, some nuclear processes appear to be executed in response to an autonomously regulated nuclear calcium signal. It may be added parenthetically that chloride ions also play a role in phagocytic dynamics. Specifically, chloride efflux regulates adherence, spreading, and respiratory burst of neutrophils stimulated by tumor necrosis factor- (TNF) on biologic surfaces.53

In discussion of the structure and function of the matrix, little, if any, attention is given to the matrix within the cell as well as within cellular organelles. And yet, the matrix in those locations serves key redox metabolic and defense roles. The complexities in the phagocytic destruction of microbes should not be surprising because Nature, first and foremost, has to protect cells and vacuoles from the self-destructive impulses of their own enzymatic arsenals. An enormous number of phagocytic cells infiltrate the inflamed tissues invaded by microbes. Such cells deliver a huge load of autolytic enzymes fully capable of damaging autologous tissues. Thus, the 'packaging' of the enzymes provides the needed defense against self-inflicted injury triggered by free radical sparks. It may be added here that the matrix of phagocytic granules — seldom a point of focus — also plays a central role in destruction of microbes after phagocytosis.

I might point out here that matrix proteases perform the microbial killing rituals, but oxygen and the oxygen-driven oxidative phenomena provide the initial sparks.

Protocol for Hydrogen Peroxide Foot
Soaks and Baths
Hydrogen peroxide soaks can be used with different concentrations of and H2O2 and salt. The following is the standard protocol prescribed at the Institute protocol:

H2O2 Soaks Protocol
Water 20 parts
H2O2 3% 1 part
Salt One teaspoon
Time 20 minutes

The recommended choices of salt are as follow: (1) Epsom salt; (2) sea salt; and (3) common table salt.

Stronger solutions of H2O2, such as one part of H2O2 and 10 parts of water or 1 part of H2O2 and 15 parts of water may also be tried to test for variations in efficacy for individual persons.

For chronic conditions, I generally prescribe foot soaks on a four or five day a week basis. For subacute conditions, daily soaks are recommended. Uncommonly, I have prescribed such soaks on a twice daily basis.

There are several good brands of foot soak and foot massage units available on the market. The one made by Brookstone Company creates effective whirlpool conditions and includes a "nodule" for effective massaging of tender points on the feet or ankles.

References
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4. Farr CH. The Therapeutic Use of Intravenous Hydrogen Peroxide (Monograph). 1987. Oklahoma City, Genesis Medical Center.
5. Altman N. Oxygen Healing Therapies for Optimal Health & Vitality. 1995. Rochester, Vermont. Healing Arts Press.
6. Polgar P, Taylor L. Stimulation of prostaglandin synthesis by ascorbic acid via lydrogen peroxide formation. Prostag 1980;19:693.
7. Agrawal P, Harper MJ: Studies on peroxidase catalyzed formation of progesterone. Steroids 1982;40:569-572.
8. McFaul SJ. The mechanism of peroxidase-mediated cytotoxicity. Comparison of horseradish peroxidase and lactoperoxidase. Proc Soc Exp Biol Med 1986;182:244-249.
9. Yamaja Setty BN, Jurek E. Ganley C, et al. Effects of hydrogen peroxide on vascular arachidonic acid metabolism. Prostag Leuko Med 1984;14:205-213.
10. Ward JF, Blakey WF, Joner EL. Mammalian cells are not killed by DNA single-strand breaks caused by hydroxyl radicals from hydrogen peroxide endothelial cells against oxidant damage. Biochem Biophys Res Commun 1985;127-270-276.
11. Xu Y, Mayne L, Englander SW. Evidence for an unfolding and refolding pathway in cytochrome c. Nature Structural Biology. 1998;5:774-778.
12. Chen Y-R, Shrivastava A, Tan T-H. Down-regulation of the c-Jun N-terminal kinase (JNK) phosphatase M3/6 and activation of JNK by hydrogen peroxide and pyrrolidine dithiocarbamate. Oncogene. 2001;20,367-374.
13. 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;30:1467-76.
14. Boyington JC, Motyka SA, Schuck P, et al. Crystal structure of an NK cell immunoglobulin-like receptor in complex with its class I MHC ligand. Nature. 2000;405:537-543.
15. Gorren AC, Dekker H, Weaver R. Kinetic investigations of the reactions of cytochrome C oxidase with hydrogen peroxide. Biochem Biophys Acta 1986;852:81-92.
16. D 46 Yamaja Setty BN, Jurek E, Ganley C, et al. Effects of hydrogen peroxide on vascular arachidonic acid metabolism. Prostag Leuko Med 1984;14:205-213.
17. Polgar P, Taylor L. Stimulation of prostaglandin synthesis by ascorbic acid via hydrogen peroxide formation. Prostag 1980;19:693.
18. Del Maestro RF, Thaw HH, Bjork J, et al. Free radicals as mediators of tissue injury. Acta Physiol Scand 1980;492:43-57.
19. Babior BM, Kipnes RS, Curnutte JT. Biological defense mechanisms: the production by leukocytes of superoxide, a potential bactericidal agent. J Clin Invest 1973;52:741-744.
20. Hothersall JD, Greenbaum AL, McLean P. The functional significance of the pentose phosphate pathway in synaptosomes: Protection against peroxidative damage by catecholamines and oxidants. J Neurochem 1982;39:13252.
21. Eto K, Tsubamoto Y, Terauchi Y, et al. Role of NADH shuttle system in glucose-induced activation of mitochondrial metabolism and insulin secretion. Science. 1999;283:981-5. Also: DesMarias DJ. Science. 2000;289:1703.
22. Verhoeven AJ, Mommersteeg ME, Akkerman JW. Balanced contribution of glycolyte and adenylate pool in supply of metabolic energy.
23. Wildberger E, Kohler H, Jenzer H, et al. Inactivation of peroxidase and glucose oxidase by H202 and iodination. Mol Cell Endocrinol 1986;46:149-154.
24. Zoschke DC, Staite ND. Suppression og human lymphocyte proliferation by activate neutrophils or H202. Surviving cells have an altered T Helper/T Suppressor ratio and an increased resistance to secondary oxidant exposure. Clin Immunol Immunopathol 1987;42:160-170.
25. Heikkila R, Cohen G. Inhibition of biogenic amine uptake by hydrogen peroxide: A Mechanism for toxic effects of 6- hydroxydopamine. Science 1971;172:1257-1258.
26. Agrawal P, Harper MJ: Studies on peroxidase catalyzed formation of progesterone. Steroids 1982;40:569-572.
27. Douglas WC. Hydrogen Peroxide Medical Miracle. 1990. Atlanta. Second Opinion Publishing, Inc. (quoted in)
28. Love I. www.cancer.org/docroot/ETO/content /ETO_5_3X_hydrogen_peroxide_therapy.
29. Oliver TH, Cantab BC, Murphy DV. Influenza; pneumonia: the intravenous injection of hydrogen peroxide. Lancet 1920;1:432-433.
30. Farr CH. The Therapeutic Use of Intravenous Hydrogen Peroxide (Monograph). 1987. Oklahoma City, Genesis Medical Center.
31. Ali M: Ascorbic acid reverses abnormal erythrocyte morphology in chronic fatigue syndrome (abstract). Am J Clin Pathol , 94:515,1990.
32. Ali M, Ali O: AA oxidopathy: the core pathogenic mechanism of ischemic heart disease. J Integrative Medicine 1997;1:6-112.
33. Ali M, Ali O: AA oxidopathy: the core pathogenic mechanism of ischemic heart disease. J Integrative Medicine 1997;1:6-112.
34. Farr CH: The therapeutic use of intravenous hydrogen peroxide (Monograph). Genesis Medical Center, Oklahoma City, OK 73120, January 1987.
35. Rubanyi GM, Vanhoutte PM. Oxygen-derived free radicals, endothelium and responsiveness of vascular smooth muscle. Am J physiol 1986;2505 pt 2):H815-821.
36. Yamaja Setty BN, Jurek E. Ganley C, et al. Effects of hydrogen peroxide on vascular arachidonic acid metabolism. Prostag Leuko Med 1984;14:205-213.
37. Yamaja Setty BN, Jurek E, Ganley C., et al. Effects of hydrogen peroxide on vascular arachidonic acid metabolism. Prostag 1980;19"693.
38. Murray HW, Scavuzzo D, Jacobs JL, et al. In vitro and in vivo activation of human mononuclear phagocytes by interferon-gamma. Studies with normal and AIDS monocytes. J Immunol 1987;138:2457-2462.
39. Powell JH, Shor R, Gazit E, et al. The effects of Con A-induced Lymphokines from the T-lymphocyte subpopulation on human monocyte leishmaniacal capacity and H202 production. Immun 1986;59:245-250.
40. Levine A, Tenhaken R, Dixon R, et al. H202 from the oxidative burst orchestrates the plant hypersensitive response. Cell 1994;79:583- 593
41. Yahraus T, Chandra S, Legendre L, et al. Evidence for a mechanically induced oxidative burst. Plant Physiol 1995;109,1259-1266.
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45. 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 Leukocyte Biol 1987;41:289-294.
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48. Burdon RH, Alliangana D. Gill V. Endogenously generated active oxygen species and cellular glutathione levels in relation to BHK- 21 cell proliferation. Free Radical Res 1994;21:121-133.
49. Henderson LM, Chappel JB, Jones OT. The superoxide-generating NADPH oxidase of human neutrophils is electrogenic and associated with an H+ channel. Biochem. 1987;246:325-329.
50. Gutteridge JM, Wilkins S: Copper salt-dependant hydroxyl radical formation. Damage to proteins acting as antioxidants. Biochim biophys acta 1983;759:38-41.
51. Zgliczynski JM, Selvaraj RJ, Paul BB, et al. Chlorination by the myeloperoxidase-H202-C1 antimicrobial system at acid and neutral pH. Proc Soc Exp Biol Med 1977;154:
418-422.
52. TjelleT, Saigal B, Berg MF. Degradation of phagosomal components in late endocytic organelles. J Cell Sci1998;111:141-148.
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MATERIAL SAFETY DATA SHEET
http://msds.fmc.com/msds/100000010225-MSDS_US-E.pdf

verdt et lite besøk:
http://www.h2o2-4u.com/


Hydrogen Peroxide : Medical Miracle (Paperback, 1996) by William Campbell Douglas, MD; ISBN: 1885236077

Fy fløte, nå ble jeg stolt av min egen lille flaske med hydrogenperoksid! Weee!

Et ordentlig tryllestoff med andre ord

Informativ og interessant lesning med mange spennende linker - takker for flott innlegg Propell!

Nå har ikke jeg lest artikkelen enda, men i Samuel Fussell's bok "Muscle", bruker en av romkameratene hans en spiseskje hydrogenperoksid i uken for å unngå uren hud.
Er det noe i dette?

Opprinnelig skrevet av schakver

Er det ikke det jeg brukte til å bleike håret med ?

Dette er en vanlig kjemikalie å ha i husstanden ja..
I vårt tilfelle er det særs utynnet 3% løsning som nyttes oralt.

Opprinnelig skrevet av fowler

Nå har ikke jeg lest artikkelen enda, men i Samuel Fussell's bok "Muscle", bruker en av romkameratene hans en spiseskje hydrogenperoksid i uken for å unngå uren hud.
Er det noe i dette?

Det blir en indirekte relasjon mellom H2O2 og hudproblemer, siden det frigir oksygen i kroppen og chelaterer fremmed materiale.

Opprinnelig skrevet av Mr.Tynnfeit

Noen som så CSI igår...hehe...der to damer døde av hydrogenperoksid(mener ihvertfall å huske at det var det)
Men så er det vel en liten forskjell på å drikke en utynnet 3% løsning sammenlignet med å sette en 30% løsning rett i blodåra

Man trenger politi tillatelse for å kjøpe 30% løsning.
H202 blir i forsvaret brukt sammen med COOH som raktett akselrator, i f.eks. i forbindelse med utskytning av torpedoer. Det skal nevnes at man da snakker om løsning rundt >90%.

Når injesering er tilfelle, så vil H202 reagere med det første det treffer.
Uten å ha sett CSI episoden, så vil jeg anta at dødsårsak mtp hvite blodlegemer som reaktanter!?

I hvilken sammen heng skulle dem forresten injesere H2O2? gal drapsmann, eller helsefreaks(les: reversed age-prosess)?

Så også den CSI episoden i går, det var kvinnfolk som skulle ta en 3% løsning men som fikk 30% i stedet, husker ikke helt hva de sa skjedde i blodet, men den grafiske forklaringen var at de røde blodlegemene "eksploderte".

Personlig har jeg hatt en 3% løsning i drikkevannet mitt en uke, har ikke merket noen drastiske endringer, vet heller ikke helt hva jeg kan forvente meg da.
Gleder meg til å se referatet ditt fra det møtet du var på propellen.

Akkurat nå har jeg stor tro på H2O2, jeg bare vet ikke akkurat hva det er jeg tror på!

Potensialet er stort mener jeg.
Men først så må jeg se nærmere på H2O2s påvirkning av DNA.

Ax, husk at H2O2 ikke er sterkt basisk, derimot en svak svak syre!

Opprinnelig skrevet av propellen

Ax, husk at H2O2 ikke er sterkt basisk, derimot en svak svak syre!

Da må jeg stille meg bak et spørsmål dragon06 stilte i en annen tråd, hvordan kan noe som er surt bli basisk ved at man har noen dråper av det i en liter vann?
I pH boka står det svart på hvitt at man oppnår et mer basisk vann ved å tilsette pH dråper (herunder hydrogenperoksid eller kloroksid (ClO2). Også natriumkloritt (NaClO2) blir nevnt)).

Eller er det som sitronen, surt men basedannende i kroppen?

Opprinnelig skrevet av AxMataz

I pH boka står det svart på hvitt at man oppnår et mer basisk vann ved å tilsette pH dråper (herunder hydrogenperoksid eller kloroksid (ClO2). Også natriumkloritt (NaClO2) blir nevnt)).

Nei, du har forstått det litt feil.
Boka nevner H202,CLO2, NaClO2 og "ph-dråper".
Ikke at de førstnevnte kjemikaliene ER "pH-dråper".

Grunnen til at man nevne H2O2 i syre/base sammenheng, er dens antibakterielle effekt på kroppen, som videre kan relateres til syre/base forholdet.

Alle sykdomsfremkallende mikrober avgir elektroner når dem blir introdusert til et oksygenberiket miljø. Dette pga cellestrukturene til organismene.
Normalt når kroppen blir invadert av sykdomsfremkallende mikrober så angriper "spesialiserte" hvite blodlegmer, som forøvrig danner en essensiell del av immunsystemet, bakteriens overflate.
Under denne prosessen er mikrobene omgitt av H2O2, som er dannet inni hvite blodlegemer av vann og oksygen.
H2O2 reagerer videre med bakteriens cellestruktur og brytes ned til H20 og O.
Oksygen atomet som blir dannet oksiderer membranen til den sykdomsfremkallende cellen.

hmm. litt knotete forklaring dette. Men skjønner du relasjonen mellom H2O2 og f.eks. gjærsopp i kroppen?

Uansett, har lagt ut ny god artikkel om H2O2 på indreENERGI!

Opprinnelig skrevet av AxMataz

men den grafiske forklaringen var at de røde blodlegemene "eksploderte".

er nok hvite blodlemer som sprenges pga ubalansen som skapes ved for høyt H2O2 nivå.
(jfr. svar over)

Så pH dråper, H202, CLO2 og NaClO2 har helt forskjellige virkninger?
Kan man ikke evt bruke fler av gangen da?
Jeg vil gjerne at vannet jeg drikker skal virke basedannende på blodet samtidig som det tar knekken på mikroformene.

Det jeg har brukt er bare en 3% løsning kjøpt på apoteket.
Kjøp dråpeteller og ha ca 1 dråpe pr dl vann som skal drikkes, eksempelvis da 15 dråper 3% løsning i halvannen liter vann.

Hva er kilden til at du er interessert i dette?
Hvor mye er det anbefalt å ta og hvilket produkt?

Opprinnelig skrevet av perk

Jeg tror ikke 3% oppløsningen man kjøper på apoteket er noe særlig lurt å drikke

Hva baserer du den påstanden på?

Opprinnelig skrevet av AxMataz

Hva baserer du den påstanden på?

3% hydrogenperoksid brukes i klinikken til å bleke tenner. Tannkjøttet må da beskyttes med en gummiduk fordi det forårsaker brannskader, åpne sår og blemmer (Mind you, dette er når H2O2 står i flere timer i munnen).

Opprinnelig skrevet av vio

3% hydrogenperoksid brukes i klinikken til å bleke tenner. Tannkjøttet må da beskyttes med en gummiduk fordi det forårsaker brannskader, åpne sår og blemmer (Mind you, dette er når H2O2 står i flere timer i munnen).

Ja, det tror jeg på. Men her er det snakk om å blande det ut i vann, ca 1 dråpe pr dl vann.

Spørsmålet var egentlig hvorvidt en 3% løsning fra apoteket skiller seg ut til oralt bruk i forhold til en 3% løsning med tilnavnet "food grade".
Forskjellen såvidt meg bekjent er eventuelle tilsetningstoffer, i USA kan man finne alle disse som perk ramser opp, mens i norge får man kun phenacetin med på kjøpet om man kjøper 3% på apoteket.

Phenacetin er kort fortalt et smertestillende stoff som ble brukt før i tiden før paracet o.l. tok over.
Phenacetin har i dyreforsøk blitt påvist kreftfremkallende, hvilke doser vi snakker om da er meg 100% uvisst, men i følge denne siden: http://www.jtbaker.com/msds/englishhtml/h4070.htm indikeres det at det ikke er skadelige mengder det er snakk om her, spesielt om man tenker på hvor mye den tynnes ut i endelig løsning.


Jeg hadde en 3% løsning fra apoteket i drikkevannet mitt for endel år tilbake, da 1 dråpe pr dl vann, kjørte dette over en viss periode sammen med mange andre ernæringsmessige tiltak for å forbedre mitt eget helsebilde.
Resultatet av alt sammen var nærmest mirakuløst for min del, har utdypet dette i grøntvannposten min.

Hvorvidt phenacetinen kommer til å hjemsøke meg og fremkalle kreft i penis om 20 år vet jeg ikke, jeg har liten tro på at det var skadelig for meg.
Men dersom noen finner en food grade løsning her til lands så ser jeg jo fordelene det kan være ved å bruke denne i stedet.

De har fine produkter her: http://www.food-grade-hydrogen-perox.../1?shop_param=

Ser de selger en 35% løsning, mon tro om man får denne gjennom tollen?