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Copyright 2008 by Thomas Lee Hesselink, MD
SUGGESTIONS FOR RESEARCH PROTOCOLS AND PRECAUTIONS|
IN THE ORAL ADMINISTRATION OF OXIDES OF CHLORINE
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.
Introduction And Disclaimers
"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.
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.
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.
Oxidants, Reductants And Antioxidants
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.
General Effects On Pathogens
|3 Conditions For Success
- the pathogen must be sensitive to oxidation
- a sufficiently high dose of oxidant must be delivered
to the site of infection
- the dose must be tolerable by the host
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.
Oxides Of Chlorine As Orally Applicable Disinfectants
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.
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.
Sodium Chlorite Solutions
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
|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|
|gross||net||mg/cc||mg/.1cc||mg/gtt if 30||mg/gtt if 25||mg/gtt if 20||mg/gtt if 15
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.
Dosing Of Sodium Chlorite
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.
Probable Dosages For Various Body Weights|
|9 lb||4 kg||1 mg||4 mg||8 mg||400 mg|
|13 lb||6 kg||1.5 mg||6 mg||12 mg||600 mg|
|22 lb||10 kg||2.5 mg||10 mg||20 mg||1 g|
|30 lb||14 kg||3.5 mg||14 mg||28 mg||1.4 g|
|44 lb||20 kg||5 mg||20 mg||40 mg||2 g|
|66 lb||30 kg||7.5 mg||30 mg||60 mg||3 g|
|100 lb||45 kg||11 mg||45 mg||90 mg||4.5 g|
|154 lb||70 kg||17.5 mg||70 mg||140 mg||7 g|
|220+ lb||100+ kg||25 mg||100 mg||200 mg||10 g|
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.
Acidifying Sodium Chlorite
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.
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.
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-
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.
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.
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.
|Common Symptoms of J-H Reactions:
Once the J-H
reaction is aborted a suitable rest period may be determined.
|Options For Treating J-H Reactions
- 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.
- 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.
- Omega-3 oil supplements might also be found helpful.
- Corticosteroids could also be used, if a superpotent
antiinflammatory effect is deemed appropriate.
Afterwards retreatment at a lower dose may be applied.
If the pathogen is especially sensitive to oxidation, retreatment
should not be necessary.
Mechanisms Behind Treatment Success Or Failure
However, if one or more of the following
variables contravenes, relative treatment failure may occur,
and the treatment may need to be repeated.
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.
- too little oxidant was administered;
- the pathogen is fairly resistant to oxidants;
- the pathogen converts to alternate forms such as
spores, cysts or eggs;
- the pathogen is sequestered in sites remote
from oxidant penetration;
- too many antioxidants or drugs were present at the time
of treatment, which quenched the medicinal oxidants.
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
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.
Classified According To Reactive Groups:
- phenols & polyphenols
- 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.
Four oral protocols will now be described and the relative
advantages and disadvantages discussed.
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,
most herbs, for example:
chocolate, green tea, coffee, turmeric,
silymarin, licorice, ginkgo, olive, cinnamon
onion, leek, shallot, garlic, chive
cabbage, kale, broccoli, cauliflower,
turnip, mustard, wasabi
Solanum tuberosum = white potato
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.
|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
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.
Possibilities With Cancer
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.
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,
(/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.
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