Re: Suggestions For Research Protocols And Precautions Lee Hesselink, MD

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> <http://www.bioredox.mysite.com/CLOXhtml/CLOXhome.htm> SUGGESTIONS

> FOR RESEARCH PROTOCOLS AND PRECAUTIONS

> IN THE ORAL ADMINISTRATION OF OXIDES OF CHLORINE Copyright 2008 by

> Lee Hesselink, MD Introduction And Disclaimers Since the

> publication of the experiences of Mr. Jim Humble, since the postings of

> numerous informative websites, since the postings of a plethora of

> blogs pertaining to the oral use of acidified sodium chlorite, and

> since the recent availability of solutions of sodium chlorite, numerous

> questions and concerns have arisen. The need for a biochemically and

> physiologically based commentary became apparent to this author. This

> is written to careful physicians for research purposes only. The writer

> offers this information for educational and safety minded purposes,

> exercising constitutionally protected freedom of speech and press. This

> is not to establish a doctor-patient relationship nor to provide

> medical advice. No promises nor guarantees nor labels of any kind are

> expressed or implied. The views, ideas, opinions, beliefs and

> suggestions expressed herein are subject to change without notice.

> Oxidants, Reductants And Antioxidants " Oxidants " are atoms or

> molecules which pull electrons off of or away from other atoms or

> molecules. Some atoms or molecules release electrons to oxidants. These

> are called " reductants " . Strong oxidants in high enough doses are

> generally toxic to living cells, because they react with too many

> oxidant sensitive molecules all at once. At lower doses certain

> oxidants may cause stress or damage if certain oxidant sensitive

> molecules are eliminated more rapidly than they are replaced. This is

> an important mechanism in various diseases which involve chronic

> inflammation, radiation or chemical poisoning. In efforts to minimize

> damage from oxidative stress, the so called " antioxidants " have been

> researched and made available. Antioxidants react with oxidants

> preferentially and thereby protect more precious cellular components.

> General Effects On RBCs At low dose exposures (in other words received

> in amounts well below the toxic threshold) oxidants can stimulate

> certain beneficial physiologic effects. In live red blood cells exposed

> to oxidants some of their glutathione (GSH) is converted to glutathione

> disulfide (GSSG). This is usually harmless as living red blood cells

> can rapidly replace the lost hydrogen atoms and replenish the

> glutathione (GSH). The restoration process produces

> 2,3-diphosphoglyerate (2,3-DPG) as a by-product. Increased 2,3-DPG

> causes a beneficial side-effect. It attaches to hemoglobin, the main

> oxygen (O2) carrying protein in red blood cells, and causes this to

> hold oxygen more loosely. As a result, blood flowing through the

> peripheral tissues releases more oxygen (O2). This enables the affected

> tissues to generate more energy. This explains why many patients

> treated with low doses of medicinal oxidants subjectively experience a

> boost in pep and energy. General Effects On WBCs White blood cells

> respond differently to oxidants. At suitably low doses living white

> blood cells are induced to produce " cytokines " . These are specialized

> protein messenger molecules, which diffuse throughout the body. When

> these cytokines contact other white blood cells of the immune system,

> such cells are stimulated to mount an enhanced attack against

> infection. This represents the usual or main benefit of oxidative

> medicine, to stimulate the immune system. If the oxidant dose is too

> high the effected white blood cells may be stunned because of oxidative

> stress and fail to produce cytokines. Therefore, protocols have been

> carefully developed to induce optimal immune stimulation without this

> contraproductive stunning effect. General Effects On Pathogens A

> third benefit of oxidative medicine is to use oxidants as

> disinfectants. These are traditionally applied externally. Examples are

> suitably calibrated solutions of iodine, hydrogen peroxide, sodium

> hypochlorite, ozone or chlorine dioxide. Many disease producing

> organisms are more sensitive to certain oxidants than are host cells.

> This is why at sites of infection activated white blood cells produce

> strong oxidants in vivo to directly kill pathogens. If a proposed

> medicinal oxidant can be safely tolerated internally, it becomes a

> candidate for internal use as an antimicrobial agent. This would mimic

> the natural immune function of using oxidants in vivo to destroy

> pathogens. However, this strategy will only succeed if the following

> conditions are met. 3 Conditions For Success

> 1. the pathogen must be sensitive to oxidation

> 2. a sufficiently high dose of oxidant must be delivered to the site

> of infection

> 3. the dose must be tolerable by the host

> Oxides Of Chlorine As Orally Applicable Disinfectants Sodium chlorite

> (NaClO2) and the more potent chlorine dioxide (ClO2) appear so far

> (anecdotally at least) to be good candidates for internal use. They

> both seem tolerable orally if appropriately dosed and suitably diluted

> in water prior to administration. Intermittent application in doses as

> high as 2 mg per kilogram per day have been safely administered. In

> many cases of malaria clinical success has been reported after as few

> as one or two treatments. Biochemical literature supports the view that

> Plasmodia are oxidant sensitive. Anecdotal reports of success in

> certain bacterial infections have also been noted. How this may work in

> the treatment of other infections remains to be carefully investigated

> and reported.

> Many have justifiably criticized the use of elemental chlorine (Cl2) as

> a food or water additive because of its tendency to react with

> hydrocarbons (C-H) to produce organic chlorides (C-Cl), which are toxic

> byproducts. Similarly elemental chlorine (Cl2) reacts with various

> amines (C-NH2) to produce chloramines (C-NH-Cl), which are also toxic.

> Chorine dioxide and sodium chlorite on the other hand fail to produce

> any significant quantities of these toxic byproducts.

>

> Optimal protocols for the oral administration of certain oxides of

> chlorine are discussed below. Comparative advantages and disadvantages

> of each protocol are discussed. It is the purpose of the author to

> minimize risk, while maximizing success, as these treatments are

> evaluated in the context of responsible and legal research. Special

> admonitions against acute overdosing and against long term overuse are

> included. Failure to heed appropriate warnings could cause unnecessary

> adverse reactions. This in turn could result in adversarial social or

> political or legal proceedings. This would wrongfully condemn

> potentially beneficial therapies. Then many people who need these

> therapies will suffer unjustly as access is idealogically or forceably

> blocked. Special precautions must also be heeded which are necessary to

> insure that the therapy is effective. If such issues are not

> consistently respected, then rampant clinical failures could also bring

> the therapy into disrepute.

> Sodium Chlorite Solutions The preparation of chlorine dioxide (ClO2)

> for oral use is now described. This procedure is low in cost and easy

> to provide. Sodium chlorite (NaClO2) not to be confused with sodium

> chloride (NaCl) is available from most manufacturers as " technical

> grade " . This is in essence actually 80% sodium chlorite and about 19%

> sodium chloride. The remaining 1% is sodium hydroxide (NaOH) and sodium

> chlorate (NaClO3). Chlorate (ClO3-) is left over from the manufacturing

> process and in this context can be considered a harmless excipient. A

> little hydroxide (OH-) is a necessary stabilizer to protect the

> chlorite (ClO2-) in water solution.

> Much of the sodium chlorite solution available over the internet lately

> is being sold as the so-called " MMS " . Mr. Jim Humble first recognized

> the effectiveness of oral sodium chlorite solution to treat malaria. He

> subsequently discovered enhanced effectiveness, if the sodium chlorite

> was acidified just prior to use. This process converts much of the

> chlorite into chlorine dioxide a more potent disinfectant. After

> careful experimentation with various concentrations, he came to prefer

> 28% technical grade sodium chlorite in water. The actual presence of

> sodium chlorite in such a preparation should therefore equal 80% times

> 28% or 22.4%. Therefore, every milliliter of this solution should

> provide 224 mg of actual sodium chlorite. He also preferred to dispense

> this solution using a dropper bottle. The particular droppers he

> favored dispensed 25 drops per ml. Therefore, using equipment modeled

> after his procedures delivers 224 mg / 25 = about 9 mg per drop. This

> would not present a problem if every dropper around the world were

> constructed exactly the same. " Drops " per se is a nonstandard means of

> communicating and metering dosages. The problem with " drops " is the

> high variability of drop sizes. Droppers are constructed which deliver

> drops as big as 15 per ml or as small as 30 per ml as any nurse or

> pharmacist could testify. Therefore to avoid misinterpretations and

> mistakes in dosing, all of the following protocol related information

> will be communicated in terms of internationally recognized units such

> as grams (g), milligrams (mg) and milliliters (ml) = cubic centimeters

> (CC). Those wishing to back-convert to " drops " must determine the exact

> drop size they are using. This is easy to do with a small graduated

> cylinder. Fill the dropper with fluid and then count the exact number

> of drops required to dispense exactly one cc of fluid into the

> graduated cylinder. Divide that into the known number of milligrams per

> cc of solution to calculate the actual milligrams per drop.

>

> The author favors the following procedures. It is relatively easy to

> weigh out 25 g of technical grade sodium chlorite and to dissolve this

> in 100 cc of water producing a 25% solution. Since technical grade is

> actually 80% sodium chlorite, the actual concentration of active

> ingredient is therefore 80% X 25% = 20%. This translates to a very

> convenient 200 mg per cc. Using a graduated pipette 1/2 cc dispenses

> exactly 100 mg. 0.2 cc dispenses 40 mg. 0.6 cc dispenses 120 mg. This

> technique is suitable for most adult dosages which range from 20 mg to

> 200 mg. If there is the need for smaller dosing such as in pediatrics,

> then 10% or 5% solutions of sodium chlorite can be prepared and

> appropriately labeled. 10% equals 100 mg per cc so 0.3 cc dispenses 30

> mg. 5% equals 50 mg per cc so 0.1 cc dispenses 5 mg. See the table

> below to correlate sodium chlorite concentrations with actual dispensed

> quantities.

> Sodium Chlorite (NaClO2) Concentrations: gross = percentage by weight of

> technical grade,

> prepared by weighing grams per 100cc water net = actual percentage of

> active ingredient mg/cc = milligrams per cubic centimeter using a

> graduated cylinder mg/.1cc = milligrams per 1/10th cubic centimeter

> using a graduated pipette mg/gtt = milligrams per drop using various

> droppers if # = drops per cc for that particular dropper type

> grossnetmg/ccmg/.1ccmg/gtt if 30mg/gtt if 25mg/gtt if 20mg/gtt if 15

> 28%22.4%22422.47.5911.214.9 25%20.0%200206.781013.3

> 12.5%10.0%100103.3456.7 6.25%5.0%5051.722.53.3 Dosing Of Sodium

> Chlorite Next is discussed the dosimetry of sodium chlorite (NaClO2).

> The weight of the patient should be determined in kilograms. If the

> weight is known in pounds, then that number must be divided by 2.2 to

> properly calculate the kilogram weight. For example, an adult weighing

> 187 lbs. also weighs 85 kg. A child weighing 8.8 lbs. also weighs 4 kg.

> The usual or appropriate dose so far seems to be about 1 mg per kg per

> day. Therefore the adult described above could take about 85 mg in one

> day. He/she might start at 20 mg for the first treatment. Later he/she

> could gradually work up at subsequent treatments to 170 mg maximum. The

> average 4kg child might take about 4 mg, starting at 1 mg or less, then

> working up to 8 mg maximum. Special care must be taken under all

> circumstances never to overdose using these oxidants. The lethal dose

> is estimated at about 100 mg per kg. Thus an adult could be killed

> taking 8 to 10 grams. This is about one hundred times (100x) the

> appropriate dose. An infant could be killed taking as little as 400 mg.

> One may consult the table below to avoid overdosing. Listed is the

> suggested dose per day in milligrams. Probable Dosages For Various

> Body Weights WeightWeightStartAverageMaximumLethal 9 lb4 kg1 mg4 mg8

> mg400 mg 13 lb6 kg1.5 mg6 mg12 mg600 mg 22 lb10 kg2.5 mg10 mg20 mg1 g

> 30 lb14 kg3.5 mg14 mg28 mg1.4 g 44 lb20 kg5 mg20 mg40 mg2 g 66 lb30

> kg7.5 mg30 mg60 mg3 g 100 lb45 kg11 mg45 mg90 mg4.5 g 154 lb70 kg17.5

> mg70 mg140 mg7 g 220+ lb100+ kg25 mg100 mg200 mg10 g Certain tests

> are reasonably expected to be useful to monitor toxicity. Elevated

> methemoglobin levels reflect overly oxidized blood. Elevated urea or

> creatinine levels reflect kidney damage. Whenever higher than usual

> doses are to be administered, special attention must be applied

> regarding kidney damage especially if the urine is acidic. Acid renders

> the oxides of chlorine more reactive. Alkalinity stabilizes oxides of

> chlorine. Urine pH should be measured if higher than average doses are

> going to be applied. If the urine is abnormally acidic (pH < 6),

> special measures should be taken to raise the urinary pH to protect

> the kidneys. Acidifying Sodium Chlorite Once the appropriate dose

> of sodium chlorite (NaClO2) is determined, this amount should be

> measured and dispensed into a test tube or cup. It may next be

> acidified by addition of an appropriately selected acid solution. The

> goal is to produce a pH of the reacting mix in the range of 2 to 3 pH

> units. This is optimal for the production of chlorine dioxide (ClO2)

> from chlorite (ClO2-). This can be accomplished using acetic acid,

> lactic acid, citric acid, tartaric acid or most other edible strong

> acids. Citric acid is preferred as it is available as a dry powder for

> easy packaging and delivery in dry plastic bags anywhere in the world.

> Citric acid is also relatively inexpensive and generally recognized as

> a safe food additive. Acetic acid and lactic acid are liquids which

> present special packaging and handling problems. Suitably diluted

> sulfuric acid, phosphoric acid or hydrochloric acid could be used but

> preparation from more concentrated source materials would be dangerous

> for those not experienced with chemical handling. Ascorbic acid must

> never be used as this is a reductant and would immediately destroy the

> oxidants in the preparation. Toxic acids must never be used.

> Citric acid solution is easy to prepare as a 10% solution, however, 5%

> to 20% could also be used. The important issue is the pH of the

> reacting mixture, which should be between 2 and 3 units. This can be

> checked using pH paper. It may seem that a large excess of citric acid

> solution would more assuredly accomplish the desired pH change. However,

> to get a decent yield of chlorine dioxide the volume of the reacting

> solution must be limited. Too large a reacting volume is actually

> contra- productive as this will diminish the rate of chlorine dioxide

> production. Upon mixing chlorite (ClO2-) with acid (H+) a small amount

> of chlorous acid (HClO2) is first produced. Chlorite (ClO2-) anions are

> stablized by their negative charge. They are repeled away from the very

> electrons they may want to oxidize. Chlorous acid (HClO2) however is

> neutral in charge and therefore more readily able to approach an

> electron and to abstract it. Therefore, if chlorous acid remains in

> close proximity to other chlorite anions it can successfully oxidize

> them. This explains exactly how chlorine dioxide (ClO2) is producible

> by acidifying a sodium chlorite solution. The following cascade of

> reactions occurs.

>

> ClO2- + H+ ---> HClO2

> HClO2 + ClO2- ---> ClO2 + [HOClO-]

> [HOClO-] + H+ ---> [HOClOH] ---> ClO + H2O

> ClO + ClO2- ---> ClO2 + ClO-

> ClO- + H+ ---> HClO

> HClO + ClO2- ---> ClO2 + [HClO-]

> [HClO-] + H+ ---> [HClOH] ---> Cl + H2O

> Cl + ClO2- ---> ClO2 + Cl-

>

> Adding these equations together describes the overall reaction as:

>

> 5 ClO2- + 4 H+ ---> 4 ClO2 + 2 H2O + Cl-

> Note that for these successively reduced species of chlorine compounds

> to be successful in oxidizing the chlorite anion, they must remain in

> close proximity. If these reactants are too widely dispersed by dilution

> the opportunities to react are severely limited. As a result production

> of chlorine dioxide slows markedly. Therefore one must add sufficient

> acid to start the reaction but not overly increase the reacting volume.

> It seems most practical to use 10% citric acid at a volume about equal

> to that of the sodium chlorite solution dispensed. Under most

> circumstances 3 minutes of reacting time is appropriate. Chlorine

> dioxide can be seen as a rapid color change to bright yellow. It smells

> exactly like elemental chlorine (Cl2). If for some reason a more rapid

> reacting time is desired, 20% citric acid can be used.

> The freshly prepared solution is now properly designated as " acidified

> sodium chlorite " . It contains unreacted sodium chlorite, freshly made

> chlorine dioxide, sodium chloride, citric acid and sodium citrate. This

> should be diluted about 100 fold before administrating to avoid burning

> the mouth and throat. One cup of water should be sufficient. The

> resultant drink is pale yellow and tastes like sour, salty, swimming

> pool water. This should be chased with more drinking water to minimize

> stomach irritation and nausea. This completes the treatment. To minimize

> stomach irritation the drink can be divided in half and administered in

> two separate sessions on the same day.

> Side Effects The usual direct side effects are a transient nausea,

> headache, sweating and drowsiness. The nausea is usually mild and lasts

> for under one hour. This usually readily remits upon drinking more

> water. It can be prevented or minimized by eating a starchy meal prior

> to treatment. Headache and drowsiness are highly individual in severity

> and duration.

> The most problematic side effects are not attributable to any direct

> irritating effect of the oxidants. Instead they are due to the rapid

> success of the oxidants in killing pathogens. As the disease causing

> organisms die off they disintegrate releasing antigens which in turn

> provoke an inflammatory response from the immune system. This is often

> observed in clinical practice using common antibiotics. The phenomenon

> and is conventionally designated the " Jarrisch-Herxheimer reaction " or

> " J-H reaction " . This is a necessary physiologic attack and clean-up

> process. The severity of symptoms depends on the number of dying

> pathogens, the antigenicity of the debris, the sensitivity of the

> immune system and the site of the infection. Possible symptoms are

> noted in the table below. J-H reactions usually last a few hours or

> rarely as long as a few days. Once the J-H reaction is completed, the

> patient begins to experience remission. The good news is that usually

> the more severe the J-H reaction, the more extensive the die-off, the

> more complete the remission and the longer the disease free interval.

> In such cases the need for frequent retreatments is minimized.

> Common Symptoms of J-H Reactions: feverchillsmalaise

> sweatingnauseapain tendernessheadachebody aches fatiguediarrhea With

> this in mind most patients prefer to accept the transient discomforts

> of the J-H reaction. However, such a level of courage and resolve may

> not always be necessary. If according to the clinical judgement of the

> treating physician or the tolerance of the individual patient an

> abortion of the J-H reaction is desired, four options are available.

> Options For Treating J-H Reactions

> 1. Firstly, any residual unreacted chlorine dioxide in the body can

> be rapidly quenched by taking a large dose of ascorbic acid (aka

> vitamin C). One to ten grams should suffice.

> 2. Since J-H reactions are primarily just manifestations of common

> inflammatory processes, any systemically active antiinflammatory drug

> can be taken. Examples would be: aspirin, acetaminophen, ibuprofen,

> naproxen, etodolac, celecoxib, et cetera.

> 3. Omega-3 oil supplements might also be found helpful.

> 4. Corticosteroids could also be used, if a superpotent

> antiinflammatory effect is deemed appropriate.

> Once the J-H reaction is aborted a suitable rest period may be

> determined.

> Afterwards retreatment at a lower dose may be applied. Mechanisms

> Behind Treatment Success Or Failure If the pathogen is especially

> sensitive to oxidation, retreatment should not be necessary.

> However, if one or more of the following variables contravenes,

> relative treatment failure may occur,

> and the treatment may need to be repeated. Confounding Factors

> 1. too little oxidant was administered;

> 2. the pathogen is fairly resistant to oxidants;

> 3. the pathogen converts to alternate forms such as spores, cysts or

> eggs;

> 4. the pathogen is sequestered in sites remote from oxidant

> penetration;

> 5. too many antioxidants or drugs were present at the time of

> treatment, which quenched the medicinal oxidants.

> Incompatibilities There are important substance-oxidant

> incompatibilities which must now be addressed. Various classes of

> substances must not be present in the stomach at the time of the

> acidified sodium chlorite treatment, if any beneficial results are to

> be expected. Of paramount importance is the avoidance of antioxidants

> together with the treatment. Antioxidants are usually thiol compounds

> or phenolic compounds, which can specifically eliminate chlorine

> dioxide. Chlorine dioxide is used in industry to specifically target

> and to destroy thiols and phenols, because they readily react together

> and destroy each other. Examples of chlorine dioxide quenching

> compounds are: N-acetyl-L-cysteine, glutathione, alpha-lipoic acid,

> ascorbic acid, polyphenols, tocopherols, bioflavonoids, anthocyanidins,

> benzaldehyde, cinnamaldehyde, juice concentrates and many herbal

> remedies. Most fruits especially grapes and berries are rich sources

> of polyphenolic antioxidants. Examples of herbs rich in antioxidant

> polyphenols are: chocolate, tea, coffee, turmeric, silymarin, licorice,

> ginkgo, olive. Sulfur rich foods also eliminate chlorine dioxide if

> present in the stomach at the time of treatment. Examples include:

> garlic, onion, leek, asparagus, beans, peas, egg, milk and even white

> potatoe (due to alpha-lipoic acid). Protein must also not be present in

> the stomach at the time of treatment. Proteins are made of amino acids

> which present an abundance of phenols, organic sulfides, thiols and

> secondary amines, which react with and eliminate chlorine dioxide on

> contact. L-tyrosine has a phenol group. L-methionine is a sulfide.

> L-cysteine is a thiol. L-tryptophan, L-proline and L-histidine have

> secondary amino groups. Certain B-complex vitamins are similarly

> reactive such as: thiamine, riboflavin, folate, pantothenate. Finally

> many drugs contain secondary amines, tertiary amines, thiols, sulfides

> or phenols. Under physician direction these may also need to be

> identified and withheld on the day of treatment or at least not taken

> at the time of treatment. While antioxidants and vitamin supplements

> are generally speaking healthy for preventive and longevity purposes,

> and while these are beneficial in the treatment of many chronic

> diseases, these are incompatible at the moment of the acidified sodium

> chlorite treatment. Therefore, fruit, fruit juices, fruit concentrates,

> wines, green drinks, herbs, protein, most vitamins and most drugs

> should not be taken at the time of treatment and certainly not mixed

> with the acidified sodium chlorite solution. If these principles are

> not respected, little if any oxidants will survive to kill pathogens

> and no benefit should be expected.

> If a person already ate some incompatible food such as protein or fruit

> prior to a scheduled treatment, then they must wait at least four hours

> for these items to pass through the stomach before taking the treatment.

> The next day after treatment the above described incompatible substances

> can be resumed. Protein could probably be eaten as soon as 3 hours

> after treatment.

>

> Anyone who claims success taking fruit juices with acidified sodium

> chlorite has succeeded in spite of this quenching problem. Higher and

> higher doses of oxidants would have to be administered to get past the

> antioxidants. If someone is already apparently tolerating especially

> high doses of oxides of chlorine, because these oxidants are being

> taken with antioxidants, then such a person is at risk of oxidant

> overdose if the concomittent antioxidants are suddenly stopped. The

> most appropriate action would be to hold the antioxidants and to back

> down to a much lower dose of the oxidants.

>

> Nutrient poor white starches on the other hand may be present in the

> stomach at the time of treatment. These may even be taken with or mixed

> with the diluted solution. These do not react readily with chlorine

> dioxide. Examples of allowable junky starchy foods are: white bread,

> casava, grits, white wheat pasta, white rice, saltines. Note that white

> potatoes are not included in this list because they are rich in

> alpha-lipoic acid a sulfur based antioxidant. Even though most sulfur

> compounds react with chlorine dioxide, oxidized sulfur compounds such

> as DMSO, MSM, taurine or sulfate are probably not reactive. Pending

> further knowledge it seems likely that carotenoids and polyunsaturated

> fatty acids do not quench chlorine dioxide.

> Incompatible Substances

> Classified According To Reactive Groups:

> * aldehydes

> * enediols

> * phenols & polyphenols

> * anilines

> * secondary or tertiary amines

> * thiols, sulfides, disulfides

> * transition metals in lower oxidation states

> Note: Most drugs contain one or more of the above reactive groups.

> A drug reference showing the structural formula must be consulted.

> When in doubt do not take most drugs with these oxidants.

>

> Incompatible Foods: all ascorbates

> all proteins, for example:

> wheat germ, nuts, peas, beans

> fish, poultry, meat, milk, eggs

> most antioxidants, for example:

> N-acetyl-L-cysteine, alpha-lipoic acid, SAME,

> glutathione, quercetin, BHT, BHA, tocopherol

> most B-complex vitamins, for example:

> thiamine, riboflavin, niacin, pantothenic acid, folic acid,

> para-aminobenzoic acid, cyanocobalamin, biotin, carnosine

> most fruit especially berries, apples, oranges, grapes,

> cherries, figs

> most herbs, for example:

> chocolate, green tea, coffee, turmeric,

> silymarin, licorice, ginkgo, olive, cinnamon

> Allium species:

> onion, leek, shallot, garlic, chive

> Brassica species:

> cabbage, kale, broccoli, cauliflower,

> turnip, mustard, wasabi

> Asparagus species

> Solanum tuberosum = white potato Choices Among Protocols Four oral

> protocols will now be described and the relative advantages and

> disadvantages discussed. 4 Oral Protocols 1) regular daily dosing of

> sodium chlorite

> 2) occassional dosing of sodium chlorite

> 3) regular daily dosing of acidified sodium chlorite

> 4) occassional dosing of acidified sodium chlorite Occassional can mean

> as often as every other day, once per week, or as rarely as once per

> month. In all protocols the starting dosage of sodium chlorite should

> be about 0.25 mg per kg per day or less and gradually increased to a

> maximum of 2 mg per kg per day as tolerated. Starting especially low is

> important in severely ill or debilitated patients who may have

> difficulty tolerating the oxidant primarily or who may experience an

> intolerable J-H reaction. In most cases of chronic infection protocols

> 2) and 4) are preferrable to 1) and 3) because the treatment free

> interval allows time to complete J-H reactions and to determine if

> there is a sufficient remission or a subsequent need for retreatment.

> If all signs and symptoms completely remit, then there is no good

> purpose to repeat the treatment. Unused precursor solutions may be

> saved in a cool dark place for future needs. In certain cases of

> chronic fatigue syndrome in which a chronic infectious illness is

> suspected but not identified, weekly dosing using protocol 2) or 4) may

> be appropriate initially. Treatment free intervals may be extended if

> warranted by long remissions. This minimizes any possible adverse

> effects of repeated oxidant exposure and only applies the oxidants when

> needed. In choosing between protocols 2) and 4), the advantage of 4) is

> the much greater potency of chlorine dioxide in killing pathogens as

> compared to sodium chlorite. The clinical success rates should be much

> higher, less frequent treatments should be required and longer

> remissions should be expected. On the other hand using the less potent

> sodium chlorite without acid activation should result in less nausea

> and less severity of J-H reactions. Another advantage of the

> intermittent protocols 2) and 4) is that beneficial nutrients,

> antioxidants and drugs may be continued between treatment days.

> Protocols 1) and 3) present the disadvantage of a constant conflict

> between the oxidants and beneficial nutrients, antioxidants and

> necessary drugs. Uninterrupted strong oxidant exposure over the long

> haul as in protocols 1) or 3) could dangerously deplete oxidant

> sensitive molecules of the host. This could contribute to chronic

> degenerative disease from oxidative stress. Continuous dosing of strong

> oxidants of any type would never allow effected cells to heal

> themselves through the normal physiologic process of antioxidant

> adaptation. If regular daily dosing is kept low enough to not defeat

> antioxidant adaptation and cellular restoration, then that dose would

> probably be too weak to kill any pathogens. Furthermore, chronic or

> repeated exposure of fetuses, infants or young children above EPA

> allowed limits of 0.8 mg/liter in public drinking water is thought by

> many to risk nervous system damage. The thyroid hormones T3 and T4 are

> phenols and therefore subject to destruction by chlorine dioxide.

> Therefore, it is preferable to avoid regular daily use of any oxides of

> chlorine except in special circumstances. For example, in severe life

> threatening acute infections such as pneumonias, bacteremias, cavitary

> abscesses or meningitides the risk of permitting the infection to

> progress may be far greater than any risks of oxidative stress or risks

> of thyroid hormone destruction. Possibilities With Cancer While it

> is too early to conject with any certainty, it is theoretically

> possible that protocol 1) may be the best option if oxides of chlorine

> are to be tested in the treatment of cancer. Repeated dosing using

> sodium chlorite should be better tolerated than acidified sodium

> chlorite, because alkaline or neutral chlorite is less reactive than

> chlorine dioxide towards most oxidant sensitive molecules of host

> cells. This should make plain sodium chlorite safer to continue

> repeating long term. In most cancer cases a selective advantage

> theoretically exists. Most tumors produce relatively high levels of

> carbonic acid and lactic acid. These acids in the tumor should activate

> the chlorite producing more potent oxidants as described by the

> chemical equations noted above. If these highly reactive oxidants are

> only produced in the tumors and nowhere else in the host, then highly

> acidic tumors could safely be destroyed.

> Unfortunately, tumors are not the only tissues known to produce or to

> concentrate acids. Isometric contraction of muscles is famous for

> rapidly producing large quantities of carbonic and lactic acid.

> Ischemic tissues anywhere in the body resulting from arterial

> obtruction or from localized swelling similarly suffer from acid

> build-up. Kidneys must at times concentrate acid for excretion. The

> parietal cells of the stomach actively produce hydrochloric acid for

> digestion. Therefore, if unusually high doses of sodium chlorite are

> needed, special attention and care must be applied to avoid damage to

> the muscles, ischemic tissues, kidneys and stomach. Risk of harm to the

> kidneys might be minimizable, if alkalinizing supplements are provided

> so that an acidic urine will not be produced. Incidently, most cancer

> patients, most allergic patients, and many chronically ill patients

> present initially with acidic urine and acidic saliva. A reversible

> inhibitor of hydrochloric acid production in the parietal cells should

> suffice to protect the stomach from side-effects including nausea.

> However, such inhibitor would need to be nonreactive with the oxides of

> chlorine. Unfortunately, every histamine-2 blocker, every azole-type

> proton pump inhibitor, and every anticholinergic in common use, that

> the author has checked structurally, contains functional groups

> probably reactive with chlorine dioxide.

> Conclusions Sodium chlorite proper or acidified sodium chlorite due to

> their unique chemical properties may sooner or later be proven to be

> powerful infection fighting remedies. Furthermore, these may find

> application in diseases for which no remedy currently exists and in

> diseases that have acquired resistance to current remedies. Research to

> support or refute these hypotheses is urgently needed. The author hopes

> this complilation of procedural instructions and admonitions is

> understandable and helpful. Physicians interested to legally

> investigate the oxides of chlorine in the treatment of difficult

> infections and possibly cancer are to be supported and commended.

> Please direct inquiries, reports and suggestions to Dr. Hesselink,

> bioredox1/at/gmail.com (/at/ is written here in place of the @ sign to

> thwart automated junk email programs.)

>

> Due to the potential of legal problems and liabilities, no guarantees,

> nor doctor-patient relationships, nor medical advice, nor labeling, nor

> medical obligations will be held forth or consented to.

> Back to home page.

> <http://www.bioredox.mysite.com/CLOXhtml/CLOXhome.htm>

>

[Guest guest]

Thanks for posting that - a very thorough and helpful article.

Carole in OzEideann & Fionn (Tristania GSDs)carole@...www.berigorafarm.com.au

[ ] Suggestions For Research Protocols And Precautions Lee Hesselink, MD

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