Modern micro electrolytic oligodynamic* colloidal
silver (*active in small quantity) is naturally
microbicidal by virtue of disabling only the metabolic enzymes
of anaerobic unicellular micro-organisms, yet is uniquely harmless
to mammals. (1) The concentration necessary to sterilise
drinking water (or by extension, body fluids) contaminated with
pathogens is 40-200 gamma / .04-.2 ppm (1 ppm=1000 gamma) (2).
Soil depletion, food processing and water flocculation and or
filtration mitigate against receiving adequate amounts of this
protective element, which until recently, was supplemented by
food related silverware.
Following a lead by the US FDA
in banning all products containing colloidal silver (3)
associated with health information, the South African
Department of Health falsely misrepresents the facts
and claims that "all over-the-counter products containing
colloidal silver or silver salts are not recognised as safe and
effective" and that "indiscriminate use of colloidal
silver has resulted in cases of argyria, a permanent discoloration
of the skin and deep tissues" as well as "neurological
deficit, and renal and metal fume? damage". (4) It is noteworthy
that prestigious journals such as the Lancet, the British Medical
Journal and the Journal of the American Medical Association have
for decades attested to the safety and efficacy of traditionally
far more crude "grind method" colloidal silver,
commonly several thousand % more concentrated (5) yet
equally less effective than the micro electro-colloidal
silver used today. (1)
The lie behind this suppressive move against
the public’s access to this simple health protective substance
is revealed by the fact that there is not a single case
of argyria in modern medical history as a result of electro-colloidal
silver. All reference to this and other toxicities, on
careful checking, leads directly to the "abuse"
of orthodoxy sanctioned old medical silver products, usually not
even colloidal silver (and if so, by the grind method), and mostly
in the form of medicinal nose drops, capsules, pills, gum, pulverisers
etc, or in cases of severe toxicity, intravenous injections in
gram-plus quantities in animal experiments. (6) The lie is perpetuated
by the FDA and the likes of Messrs Fung, Bowen and Barrett, and
the world’s only contemporary argyria victim, Rosemary
Jacobs, who was poisoned more than forty years ago by
"silver nose drops of unknown composition". (5)
Fortunately, the Gaia protocol
colloidal silver..., incorporating the immuno-essential elements,
Cu, Zn & Mn, dynamically synergised with hydrogen peroxide,
is still legally accessible locally (7) via an inexpensive strategic
water purification and fortification treatment unit, resulting
from a far-sighted leading edge local development paralleling
advanced international water research and treatment trends. Both
silver and also hydrogen peroxide (especially in combination)
exhibit significant microbial inactivation at concentrations that
do not pose any health risk according to the EEC, WHO and US EPA.
(8) The EEC, WHO and Israel Ministry of Health have specifically
approved the use of colloidal silver as a drinking water disinfectant
at an MCL (Maximum Contaminant Level) of 80 ppb. (8) Switzerland,
Germany and Australia have given approval for the use of a commercial
formulation of colloidal silver and hydrogen peroxide as a drinking
water disinfectant. (8)
The US EPA has declared that silver
does not cause adverse health effects and has set a Maximum
Level at 100 ppb for all drinking water. (9) A new European
Union Drinking Water Standard in draft form has removed any upper
limit for silver in drinking water following the WHO’s Guidelines
for Drinking Water Quality which states that "it is not necessary
to recommend any health-based guidelines for silver as it is not
hazardous to human health". (9) One teaspoon (5ml)
of 1 ppm colloidal silver in a glass (250ml) of water equals 20
ppb. Since the guidelines relate to lifetime exposure for even
the most susceptible sub-groups, calculated at 2 litres a day,
one could safely consume 8 glasses each with 5 teaspoons (25 ml)
of 1 ppm of colloidal silver every day. The most commonly used
quantity is a mere teaspoon in a glass of water 3 or 4 times daily.
Clearly the FDA / MCC itself is
more hazardous to health!
References & Internet
- Thurman R et al, 1st International. Conference
on Gold and Silver in Medicine, Silver Institute.,Wash. 1989;
- Thomson N, Comprehensive Inorganic Chemistry,
Pergamon, NY, 1973;
- (FDA Talk Paper T99-39, Final Rule, Aug
- Letter, A Booysen, SA Dept of Health,
21 Oct, 1999, Status of Colloidal Silver, Ref. 5/2/13/13/1.C;
- (New England Journal of Medicine, May
- US EPA, Integrated Risk Information
System, Silver, 1998.
- Gaia Research Institute, P.O. Box 2147,
Knysna, 6570. Ph /fax (011-27) 044-5327765 <firstname.lastname@example.org>;
- Pedahzur, R et al, Water Science Technology,
Vol. No. 5-6, pp 123-129, 1995;
- Press Release,
The Silver Institute, March 25, 1997. "Silver Water Purification
Systems Offer Reliable Alternative to Chlorine".
WE ADVANCE THE COUNTER
IN DEFENSE OF IONIC COLLOIDAL SILVER
AS “DEBATED” ON
The Silver List
The silver-list is a moderated forum for discussion of colloidal
WE ALSO STATE AND FURTHER
ALSO IN DEFENCE OF IONIC COLLOIDAL SILVER
From: GAIA Research
(view other messages by this author)
Date: Sun, 21 Jan 2001 12:28:47
Dear Frank, Ivan and List members
Frank wrote in response to Ivan:
> Well lets see, exactly how does HCl
ionize Ag without forming AgCl?
> What am I missing?
> frank key
>An experiment testing the (zero) solubility
of silver in hydrochloric acid
>pH=2, same strength as found in the
stomach, is available.
ST: Are you not, to your
peril, ignoring the potential role of aqueous ammonia in this
equation, whereby I strongly suspect it plays a transmutational
role in the chemistry of the biological passage of silver into
the body (and I expect, its utility there, under the continued
influence of ammonia as well)?
I note that Frank's latest experiment
is once again conducted in vitro, with no attempt to approach
the complexity that exists in the real world, not even the temperature
is adjusted. The test medium is free of any organic material,
including bacteria and hence is sterile. Under these unnatural
conditions it would have been possible to attempt to measure the
medium for silver, but instead, a less sensitive measure of weight
is used. Is it not conceivable that the contaminants in the HCL
and or from dissolved gasses over the 26 hour period could have
replaced liberated silver atoms with other elements, making a
silver assay more definitive?
from my perspective, would be the possible role of ammonia, if
not in a limited experiment of this nature, then certainly in
the case of determining the possible bio-availability of AgCl,
which Frank maintains is insoluble and hence is not utilised in
Silver, Chloride & Ammonia
From: gaia research (view
other messages by this author)
Date: Wed, 21 Feb 2001
Dear Frank and List members.
Frank is conveniently ignoring the role
of aqueous ammonia when simplistically claiming that silver chloride
(AgCl) formed on contact of ionic colloidal silver with stomachic
hydrochloric acid is insoluble and hence inactive in the body,
indeed not assimilated at all. Frank has recently reiterated this
claim, stating: "Once silver chloride is formed, which is
instantly upon contact, then it is a compound, not dissociated
silver ions and chloride ions in solution. So the silver chloride
acts as a compound which is insoluble in the blood". I argue(d)
that ammonia plays a transmutational role in the chemistry of
the biological passage of silver into the body and its utility
Ammonia is a good solvent for AgCl (The
Merck Index; Hawley's Condensed Chemical Dictionary; Columbia
Electronic Encyclopedia)(Ongoing series undated).
By tying up silver ions and forcing extensive dissociation of
molecular silver chloride, ammonia pulls silver chloride into
aqueous solution (Encyclopedia Britannica). Solid AgCl can be
dissolved and separated from complexation by aqueous ammonia and
is quite soluble in concentrated solutions, until it dissolves
to the point at which the Ag ion is present even as a separate
species in solution (Zumdahl S,
Chemical Principles). AgCl is only a slightly soluble
salt, but ammonium salts are highly soluble
(Plambeck J, Introductory University Chemistry I, University of
Frank rejected this ammonia hypothesis
with the snide remark that: <"A human body containing
enough ammonia to dissolve silver is way past needing colloidal
silver">. I might legitimately state the converse, but
such a response is non-productive. Whilst Frank claims that silver
'ions' are ineffective in vitro, he also claims that "his"
silver 'particles' are effective. There has been much debate around
the definition of an ion, and my contribution is that "an
ion is an atomic or molecular 'PARTICLE' having a net electrical
charge" (Mc Naught A, Intnl
Union of Pure and Applied Chemistry Compendium of Chemical Terminology,
Blackwell Science, 1997). Perhaps Frank should rename
his "particle" to clarify exactly what it is.
Frank calculates the fate of silver, be
it ions or particles, only in the stomach and blood and then only
theoretically from a test tube extrapolation, yet the former is
the mere first step in its journey into bio-complexity. It appears
that Frank is intent on oversimplifying the biochemistry of silver
so as to maintain consistency with a preconceived commercial strategy
of one-upmanship over more conventional forms of electro-colloidal
silver. I find this rather disappointing for a professing professional
scientist. Frank's in vitro AgCl argument is so simplistic that
they have not progressed even to the level of a basic chemistry
set experiment, which at least might have demonstrated the ammonia
phenomenon. I restate my in vivo ammonia hypothesis in a little
more detail, since Frank has not scientifically or logically countered
Some time ago, I wrote: "In many
ways the alimentary canal is to us what the soil is to the plant.
Minerals (as 'particles' or ions) form chelates or complexes with
organic chemicals, such as organic acids, amino acids, proteins
and others. Complexing agents may also help to dissolve sparingly
soluble inorganic substances by complexing one or more of the
products of dissociation, thus shifting the chemical equilibrium
in favour of solution. Since naturally occurring complexing agents
are of biological origin, their formation by microbes can help
bring minerals into solution, and consequently into absorption."
Sadly, Frank refuses to consider ecology, physiology or biochemistry
in his stubbornly blinkered approach to this AgCl bioavailability
In a functional human body, ammonia plays
an important role in health. Ammonia is commonly found in rainwater,
in rivers at usually less than 6 ppm. Soil typically contains
about 1 to 5 ppm of ammonia and after fertiliser application,
more than 3000 ppm (obviously elevating water levels from run-off).
Food and water is absorbed into the bloodstream and is carried
throughout your body within minutes. You can taste ammonia in
water at levels of about 35 ppm. Lower levels than this occur
naturally in food and water. The FDA determined in 1973 that the
levels of ammonia and compounds normally found in food do not
pose a health risk; ammonia is necessary for normal functions.
Maximum allowable levels in processed foods are: 3.2% ammonium
bicarbonate; 2.0% ammonium carbonate; 0.6-0.8% ammonium hydroxide;
1.1% dibasic ammonium phosphate.
(Agency for Toxic Substances and Disease Registry, Public Health
Statement, December 1990)
Ammonia is my chief candidate as a viable
means to rendering silver bound as AgCl soluble once again in
the colon and also systemically once absorbed. I shall identify
some perceived weaknesses in Frank's argument. Frank presents
an over-simplified test-tube case and considers only total silver
chloride vs total ammonia in his rejection of my ammonia hypothesis.
This is also reflected in his recent very selective presentation
of "Normal Laboratory Values", in which the 'plasma'
value for ammonia (point 17- point 80 ppm) and the 'serum' value
for chloride are given. As previously stated, even common fasting
values are up to10mg/100ml in saliva, 4mg/100ml in gastric juice
and 0.3mg/100ml (3 ppm) in whole blood (Documenta Geigy Scientific
Tables), far higher, more realistic and meaningful figures than
Frank's, but this is by no means my main point.
Firstly, these values would have little
bearing on treating illness, since the values are for a healthy
population and so would apply only to prophylactic silver usage,
and even then only with very limited extrapolatory value, since
silver assimilated into the body, even though quickly rendered
relatively insoluble within the high internal chloride mille,
would become more available as the acidosis which precedes and
accompanies most illnesses and certainly most infectious conditions,
increases, rendering silver chloride soluble relative to the degree
of acidosis and consequential ammonia buffering response. The
purine nucleotide cycle moreover, although present in many types
of tissue, is normally particularly active in muscle and during
vigorous exercise, blood concentrations of ammonia can increase
five-fold (Salway J, Metabolism
at a Glance; Ament W, et al, Int J Sports Med, Jan, 18(1), 1997)
Frank underplays the normal concentrations
of and ignores the potential peak concentrations of ammonia in
the human body, especially during infectious illness and in particular
the importance of ammonia concentrations at certain sites in the
body, such as at the colonic lumen and the liver and kidneys.
Frank also ignores the significant chloride secretory inhibition
effect of ammonium at the epithelium of the colonic mucosa where
silver must be at its smallest molecular potential in order to
be assimilated. Perhaps a better comparison than the transitional
product ammonia with chloride, which widely interacts with other
elements and is critical in many normal bodily processes, would
be nitrogen, the ammonia substrate, which is twenty times more
abundant than chloride in the human body (Documenta Geigy, Scientific
Chronic metabolic acidosis enhances ammonium
re-adsorption due to increased NH4+ production. The mechanism
of ammonia secretion by diffusion furthermore confers ability
to this buffer system to replenish itself. Prolonged acidemia
causes increased uptake of glutamine into tubular epithelial cells
and subsequent metabolism into NH4+ and HCO3-. This flexibility
of the ammonia-ammonium buffer system to increase excretion of
NH4+ ten-fold from 30 mEq/day to well over 300mEq/day, is the
predominant means of acid excretion in chronic acidosis. (Guyton
A, Textbook of Medical Physiology; Rose B, Clinical Physiology
of Acid-Base and Electrolyte Disorders) Normal serum ammonium
concentrations are in the range of 20-40 mM but can increase in
illness until at about 400 mM it causes alkalosis and neurotoxicity
(King M, Medical Biochemistry,
Terre Haute Center for Medical Education, 1998).
Ammonia is readily, indeed reliably formed
in vivo via oxidative deamination and also by transmination in
the alimentary canal, primarily in the colon, by breakdown of
proteins (including blood from intestinal bleeding) to amino acids
and deamination by normal bacterial enzymes (Harrison's Principles
of Internal Medicine) and is actively absorbed, converted and
recycled via the ornithine (urea) cycle (Goodman & Gilman's:
The Pharmacological Basis of Therapeutics). Thus excretion of
ammonia counteracts blood acidosis and conserves alkaline reserve.
When living things die, including food products, host cells and
micro-organisms, their nitrogenous remains are “mineralized”,
ie converted into inorganic forms of nitrogen, mainly ammonia
(Lewis O, Institute of Biology
Studies in Biology, Series 166, 1986), which is formed
in quantity by putrefactive micro-organisms in the secum and colon
and is "absorbed" into the body
(Prosser C, Comparative Animal Physiology).
The colon, unlike most organs, is "normally"
exposed to high concentrations of ammonia, a weak base that exerts
profound and diverse biological effects on mammalian cells. The
colonic lumen normally contains up to 70 mM, actively inhibiting
chloride secretion in the colon, the transport event which hydrates
mucosal surfaces. (Prasad M, et
al, J Clin Invest, 96(5), 1995; Hrnjes B, et al, Gastroenterol
110, Suppl, 1996; Mayol J, et al, Am J Physiol 273 (Cell Physiol
42), 1997; Miyata R, et al, Inflamm Res, 48(5), 1999) Cell
membranes are generally highly permeable to small, lipophilic
molecules such as ammonia (Walter
F, et al, J Experiment Biol, 196(1), 1994).
Ammonia is an endogenous inhibitor of
intestinal chloride secretion and is equally effective mucosally
and serosally (O'Brien T, et al,
Digest Disease Week, 3355, 1998). Colon cells are
subjected to high concentrations of NH3 and NH4+. A sizeable portion
of this buffer is absorbed (Raminez
M, et al, Pflugers Arch (Eur J Physiol), 438(4), 1999).
Ammonia profoundly inhibits Cl secretion in human intestinal epithelia,
with half-maximal inhibition at 4-6 mM. The lumen of the lower
gastrointestinal tract is the setting for bacterial action on
ingested protein and the colon consequently experiences concentrations
of the protein degradation product ammonia that may reach 100
mM. (Hrnjez B, et al, Amer J Physiol,
Frank has also recently stated that: <"Silver
chloride forms very large molecules and larger yet particles which
are removed by the kidneys">. Now, a pertinent question
for Frank: IF ONLY SILVER IONS ARE COMPOUNDED WITH CHLORIDE TO
FORM INSOLUBLE AgCl, HOW THE HELL DOES THE SILVER CHLORIDE, WHICH
YOU STATE IS NOT ASSIMILATED INTO THE BODY, FORM LARGE PARTICLES
AND GET INTO THE KIDNEYS, LET ALONE HOW IS IT REMOVED FROM THE
KIDNEYS IF IT IS SO INSOLUBLE? I have reasonably shown that both
feats are possible only because of previously postulated complexations
and the action of ammonia. Since silver is NOT present in the
urine in measurable quantities, even after intravenous injection
(Casarett and Doull's Toxicology), it must be rendered soluble
by ammonia and reabsorbed into the body.
Distribution of Silver in Urine & Feces
From: gaia research (view other messages
by this author)
Date: Mon, 5 Mar 2001 08:24:32
Dear Roger, Frank and List members
Some time ago, we discussed Frank's silver
chloride hypothesis and later my counter ammonia hypothesis. Roger
threw a further wobble Frank's way when he reported measuring
high urinary silver levels following an intensive course of ionic
colloidal silver. Frank assumed that the major silver excretion
was unabsorbed silver chloride in the feces, but Roger actually
observed, first high urinary levels, followed by high fecal excretion,
putting a lid on that one of Frank's flights of fantasy.
Roger, I need to question the 6ppm, however,
since although it is antagonistic to Frank's silver chloride hypothesis
and complementary to my ammonia hypothesis, it does not correlate
well with the published records.
Roger wrote to Frank:
"The concentration of silver in my
urine reached 6 PPM in the first sample taken 5 days after stopping
ST: I don't doubt that the silver was
in the urine, but the 6ppm seems much higher than the "trace"
generally found in the literature, even in industrial and medical
settings. Bear in mind that besides certain circumstances possibly
influencing acidosis and ammonia buffering, it should also be
borne in mind that ammonia production increases progressively
in the bladder and in the sample flask over time and that this
could lead to increased solubility of trace Ag, in turn increasing
detectable Ag as per my ammonia hypothesis, thereby explaining
the relatively high urinary readings, even though silver is not
actively excreted in urine.
Frank wrote to Roger:
"This could also mean that ions made
it to the bloodstream where they combined with chloride and the
kidneys filtered out the silver chloride which is passed with
urine (as has been speculated by some, who shall remain nameless)".
ST: Earlier I asked Frank:
"IF ONLY SILVER IONS ARE COMPOUNDED WITH CHLORIDE TO FORM
INSOLUBLE AgCl, HOW THE HELL DOES THE SILVER CHLORIDE, WHICH YOU
STATE IS NOT ASSIMILATED INTO THE BODY, FORM LARGE PARTICLES AND
GET INTO THE KIDNEYS, LET ALONE HOW IS IT REMOVED FROM THE KIDNEYS
IF IT IS SO INSOLUBLE"?
I have received no reply to date. I note
that Frank wished to believe that: "If most of the silver
was found in the feces, that would be consistent with high ionic
silver forming silver chloride in the GI tract and not being absorbed".
One problem for Frank: The fecal silver came later than the urinary,
meaning that relatively high concentrations of silver completed
a systemic circuit. This is clearly contrary to your (Frank's)
silver chloride hypothesis. Again I beg an answer to the previous
I have reasonably shown that both feats
(urinary and secondary fecal presence) are possible only because
of previously postulated complexation and the action of ammonia.
Since silver is "not" present in the urine in 'relatively'
significant quantities, it must be rendered soluble by ammonia
and reabsorbed into the body. If the silver chloride hypothesis
does not hold, I believe it legitimately submits to the ammonia
Roger, the source which I referred to
previously as saying that: "Silver is NOT present in the
urine in "measurable" quantities, even after intravenous
injection", was from Casarett and Doull's Toxicology: The
Basic Science of Poisons, Fourth Edn, 1991, McGraw-Hill (Health
Professions Division), edited by Amdur, Doull and Klaasen. This
a classic text, regularly updated and what it specifically says
(direct quote) is that: "The major route of (of silver -
species unidentified) excretion is via the gastrointestinal tract.
Urinary excretion has NOT been "reported" to occur even
after intravenous injection".
My more accurately formulated position
therefore is that silver in urine has been detected in traces
only, ie barely measurable and always relative to total assimilated
and excreted silver. This is confirmed in another classic and
oft cited paper (DiVincenzo G,
et al, Int Arch Occup Environ Health, 56(3), 1985) (detailed
further on) which in the biological monitoring of workers exposed
to different species of silver, concluded that silver is eliminated
predominantly in the feces, since urinary concentrations did not
differ measurably from controls.
I submit the following additional details
in support of this contention:
Absorbed silver appears mostly associated
to blood cells and globulins and is cleared by the liver. Silver
that is not cleared may deposit in the liver, but also in other
organs. Fecal elimination was found to have two phases: During
the first phase the half-life was 1 day, which probably corresponds
with the initial fast clearance of unabsorbed silver in the feces.
In the second phase the half-life was 48-52 days, and has been
fairly conclusively identified with the liver clearance. (Jongerius
O and Jongeneelen F, Criteria document for metallic silver. CEC.
Occupational exposure limits; EUR 14314; 1992)
Silver is absorbed from the intestine
and partially excreted in the kidney.
Normal Reference Range:
Random Urine: 0-0.46 nmol/L; 24 Hour:
Method of Analysis: High Resolution ICP/MS,
London Health Sciences Centre.
Silver Urine Random.
Ranges for females from birth and up in
Normals: Low 0 High 3.4
Ranges for males from birth and up in
Normals: Low 0 High 3.4
In a biologic monitoring study of workers
exposed to different species of silver, atomic absorption spectroscopy
analysis revealed a mean silver concentration in the <blood>
of 1.10 ug/L, in <urine> at less than 0.005 ug/G, and in
feces at 15 ug/G. Comparatively, the concentrations in controls
were less than 0.5 ug/L in the >blood>, less than 0.005
ug/G in the <urine> and 1.5 ug/G in the <feces>.
(DiVincenzo G, et al, Int Arch Occup Environ Health, 56(3), 1985)
In a cross sectional study of precious
metal powder workers, 92% had raised <blood> silver concentrations
in the range of 0.5-62 ug/L with a mean 10 ug/L, whilst 96% had
raised <urinary> silver concentrations in the range of 0.5-52.0
ug/L with a mean of 11.3 ug/L (Rosenman
K, et al, Br I Ind Med, 44(4), 1987).
In atomic absorption spectrophotometric
monitoring of silver levels in silver sulfadiazine cream treated
burn patients, the concentrations of silver in subjects without
industrial or medical exposure was less than 2.3 ug/L in the <blood>
and 2 ug/Day in <urine>. In silver sulfadiazine (SSD.cream
treated patients, <plasma> concentrations reached a maximum
of 310 ug/L and in <urine>, a maximum of 400 ug/Day.
(Wan A, et al, J Clin Chem, 37(10 Pt 1), 1991)
Tentative reference values for the biologic
fluid content of therapeutic metals, proposed on the basis of
the most representative studies, suggest that the variability
in normal subjects range up to 10 ug/L in whole <blood>
and up to 1 ug/L in <urine> (a 10:1 ratio)
(Perrelli G and Piolatto G, Sci Total Environ, 120(12), 1992).
As can be seen from the above studies
and standard values, silver concentrations can vary quite considerably.
However, the highest urinary value in these studies still falls
far short of your 6ppm = 6 milligram/L <urinary> figure.
The Rosenman study showed a maximum <urinary> value of 52ug/L
= 0.052 milligram/L, which is still a hundred times (1000%) less
than your reading. I would advise that you check my comparisons
since conversions are definitely not my strong point.
If my figures are correct and you cannot
produce data to the contrary, then I suggest that you or someone
else with the means to do so, conduct appropriate tests to determine
accurate comparative concentrations in the blood, urine and feces
for ionic, mixed and pure particulate silver, since this remains
the only means of definitively proving or disproving Frank's silver
chloride hypothesis, already fairly well demolished by the considerable,
but patchy evidence already at hand. It is in the interest of
all who work with colloidal silver to help settle this matter
for once and for all.
Distribution of Silver in Urine & Feces
From: gaia research (view other messages
by this author)
Date: Wed, 14 Mar 2001
Dear Roger and List members
Since yours is apparently the only data
available for CS, and 6ppm figure is so high, I simply felt compelled
to check the figure and circumstances, especially since your observations
led you to conclude that: "Silver is excreted easily from
the body, primarily in the urine". I doubt very much whether
this is true generally for silver (species undefined), or even
specifically for colloidal or ionic silver. However, it is of
course possible that silver is secreted primarily in the urine
under certain circumstances.
You are not happy with my using other
exposures as comparatives, but in the absence of more appropriate
data, this is the only means we have of gathering a perspective
on your data, which comparative method is scientifically valid,
if not ideal. I did however consider the Rosenman study to represent
the highest urinary reading in the subsets previously provided,
stating that it "showed a maximum urinary value of 52ug/L
= 0.052 milligram/L, which is still a hundred times (1000%) less
than your reading". I could have calculated from the Wan
study which had a 400ug/Day maximum, but I did not feel confident
to extrapolate a 400ug/Day figure to 400ug/L, but I suppose, assuming
a passing of one litre a day, such an extrapolation is not unreasonable
for rough comparisons.
Some of the previous data was for burn
patients, where the application of silver to large surface areas
of weeping, blood vessel rich tissue, leads to relatively high
blood and urinary levels compared to other exposures, indicating
that ionic silver is appreciably assimilated into the bloodstream
and is subsequently excreted.
Having searched further, I have found
another such study indicating relatively high urinary levels.
It is interesting that these burn studies have used urinary analysis.
Fecal values are not presented, indicating, as per the following
Boosalis study, that there might be circumstances involved which
favour urinary excretion, leading researchers to conclude that:
"The 24-hour urinary excretion of silver appears to be a
very sensitive indicator of cutaneous absorption in these patients".
What factors are at play, both in your
study and these burn studies, compared to the studies of other
exposures? Could it simply be the most obvious common denominator,
namely ionic silver? Do you now see the potential value of comparative
studies, even if they are of quite different circumstances? Any
way you look at it, our man Frank's silver chloride hypothesis
is shot to pieces by the sheer weight of the evidence. It is in
fact we, not Frank, who are engaging in true science.
For the record, the confirmatory topical
silver burn study follows:
Although silver sulfadiazine has been
used extensively as an effective topical antimicrobial agent in
thermal injury patients, little is known about the cutaneous absorption
of the silver moiety in these patients. Therefore, we longitudinally
evaluated both serum silver concentration and 24-hour urinary
excretion of silver in 23 patients with second- and third-degree
thermal burns. Mean serum silver concentrations were modestly
elevated throughout the patients' hospital course. Urinary excretion
of silver was markedly elevated, especially in those patients
with more severe burns. Indeed, in patients who had burns covering
more than 60% of the total body surface area mean peak silver
excretion was 1100 micrograms/24 hr (normal, less than 1 micrograms/24
hr). Thus, silver ion is absorbed across the burn wound in thermal
injury patients treated with silver sulfadiazine. The 24-hour
urinary excretion of silver appears to be a very sensitive indicator
of cutaneous absorption in these patients.
(Boosalis M, et al, Serum and urinary silver levels in thermal
injury patients. Surgery, 101(1), 1987)
Please note the maximum figure of 1100ug/Day
highest in the most severely burnt patients. This is still five
times less than your maximum figure. I guess that I need not point
out that, as with our colloidal silver, the silver in question
entered the body as silver ions, as did presumably all of the
SSD studies provided and these are therefore quite appropriate
as comparatives. However, bearing in mind that the SSD ions did
not have the stomachic hydrochloric acid to deal with, your figure
of 6mg/L still remains incredible, and even though it would serve
to support my ammonia hypothesis all the more strongly, I would
still suggest that we could improve the science of colloidal silver
appreciably by replicating your experiment or even better, conducting
tests capable of determining accurate comparative concentrations
in the blood, urine and feces for ionic, mixed and pure particulate
silver. Furthermore, by delineating the circumstances leading
to the detection of such relatively high urinary values, this
phenomenon proves beyond a shadow of doubt, that ionic silver
is effectively assimilated into and circulated within the body.
Silver Chloride Ammonia Hypothesis Update
From: gaia research (view other messages
by this author)
Date: Mon, 19 Mar 2001 12:57:03
Dear List members:
Herewith an update on the abovementioned
Frank Key's "silver chloride hypothesis"
states that hydrochloric acid in the stomach renders insoluble
the ionic silver (largely produced by conventional CS generators).
The text for this item reads:
System: AgCl system
Stress Applied: added AgNO3
The addition of AgNO3 solution
caused the formation of a white precipitate indistinguishable
from the AgCl already in the tube.
addition of AgNO3 increased the concentration of silver ions in
solution. This increased the rate of the forward reaction. As
a result the equilibrium shifted to the right. In doing so more
AgCl precipitate is formed.
Frank implies that this proves that most
colloidal silver is useless, or useful only to the degree that
such colloids also contain traces of what he calls “particles
of silver”, which latter he estimates is usually less than
1% of such colloids and which he states nevertheless is entirely
responsible for the anecdotal efficacy of such colloids. He also
states that his process produces no ionic silver, but rather 100%
particulate silver, with the unstated, yet obvious implication
that his process is 99+% more effective.
Since this flies in the face of the practical
experience of all serious researchers as well as thousands (actually
millions) of casual users of conventional CS, I sought an explanation
and proposed a counter “ammonia hypothesis”. Frank’s
response to my critique of his hypothesis and to my counter proposal
has been to insult me rather than defend his position. I have
resorted to challenging that I shall assume that his inability
to defend means submission to the ammonia hypothesis. Still no
defence, just more insults.
I recently remarked that: “Frank’s
in vitro AgCl argument is so simplistic that it has not progressed
to the level of a basic chemistry set experiment, which at least
might have demonstrated the ammonia phenomenon”. The URL
(and the photo) provided above illustrates Frank’s hypothesis.
Clicking on the NH3 symbol on that page will show you my counter
argument to Frank’s hypothesis (the photo is reproduced
below), which he conveniently neglected to take account of and
still stubbornly refuses to acknowledge, resorting to insults
instead of scientific defence of his failed hypothesis.
The text for this section reads:
System: AgCl system
Stress Applied: added NH3
The addition of NH3 solution caused
the white precipitate of AgCl to disappear.
Explanation: The addition of NH3 decreased the concentration
of free silver ions in solution. This decreased the rate of the
forward reaction. As a result the equilibrium shifted to the left.
In doing so more AgCl precipitate dissolved (photo above).
For an additional verification of the
above experiment using pure silver chloride and the addition of
ammonia in colour from a chemistry textbook, see photo below.
The text reads ~ Aqueous ammonia is added to silver chloride (white).
The silver chloride, insoluble in water, dissolves to form Ag(NH3)2+(aq)
and Cl-(aq) (silver ammonia and chloride)
(Reference: Steven Zumdahl Ph.D [Professor
of Chemistry, University of Illinois] Chemical Principles, D.C.
Heath and Co, 1992, pg 315)
For the remainder, my in vivo ammonia
hypothesis data (also) remains unchallenged and hence I deem the
"silver chloride hypothesis" to submit to the "ammonia
hypothesis", both in vitro under certain conditions and invariably
in vivo. I add the following as further proof that silver ammonia
solutions are feasible in vitro and by extension, in vivo, and
also some facts as they relate to the production and concentration
of ammonia in the gut as well as systemically, in particular during
abnormal conditions of ill-health.
Consider for example, the Procedure for
Deactivation of Ammoniacal Silver Solutions:
Dilute the silver/ammonium solution with
15 parts of water for every one part of solution (15:1 water:
In another container, make a 5% hydrochloric
Slowly add the HCl solution to the silver/ammonium
solution until the pH reaches 2. Stir frequently.
When the pH reaches 2, silver chloride
should begin to precipitate out.
(Office of Research
Safety, Northwestern University)
Looking at this procedure to precipitate
out silver chloride, it is evident that a pH of approximately
2 is required before the process is begins in earnest. In reality,
the reverse of the above scenario actualy takes place in vivo
(in the alimentary canal). Silver combines with chloride to become
insoluble silver chloride. In the case of saline manufactured
colloids, the silver chloride formation simply starts weakly during
production, ie before contact with the HCl. However, as has been
seen, this process is dependent on the relative presence of sufficient
HCl and absence of ammonia. Sufficient HCl produces high acidity,
but usually this is short-lived, even in the stomach. Frank Key
would have us believe that this is the end of the line for ionic
silver. However, the ecology of the alimentary canal quickly changes
in favour of the reverse.
The pH of HCl in the stomach is between
1-3. When food enters the stomach, pH may rise to 4.0 due to the
buffering capacity of proteins (Winsemius, 1998). On duodenal
drainage, pH is already 5.5-7.5 (Normal
laboratory values - The Merk Manual). After food enters
the duodenum, bicarbonate ions are secreted to neutralize and
alkalinize the food mixture. The pH of the small intestine is
generally in the region of 8.0.
(David Winsemius, M.D., BA (physics), MPH)
Although kidney and muscle may liberate
ammonia, most is of gut origin with << portal vein concentrations
greatly exceeding systemic levels >> (Cordoba
J & Blei A, Am J Gastroenterol 92, 1997). Muscle
wasting may potentiate hyperammonemia. In liver disease, portal
blood ammonia is not converted efficiently to urea. Gut-derived
ammonia is produced by action of bacterial flora on dietary protein
and on epithelial and bacterial debris, as well as mucosal secretions
containing urea, amino acids, amines, peptides and purines. Protein
overload may lead to increased ammonia. (Summerskill
W & Wolpert E, Am J Clin Nutr 23, 1970: Dasani B, Am J Gastroenterol,
93(5), 1998; Wolf D, Encephalopathy, Hepatic from Medicine, Ob/Gyn,
Psychiatry, and Surgery/Gastroenterology, Topic update Aug 14,
2000. eMedicine.com, Inc. 2001)
Factors which contribute to increasing
blood levels of ammonia or produce hyperammonemia are the use
of sedatives, antidepressants, and antipsychotic agents, electrolyte
imbalances, gastrointestinal bleeding, excess dietary protein,
constipation, and hypokalemia-induced renal production, or renal
failure (Fessel J& Conn H,
Gastroenterol, 62, 1972; Vince A, et al, Clin Sci Molec Med, 51,1976;
Conn H, et al, Gastroenterol, 72, 1977; Vince A & Burridge
S, J Med Microbiol, 13, 1980; Weber F, et al, J Lab Clin Med,
110, 1987; Wolf D, Aug 2000, eMedicine.com). Diuretics increase
the movement of NH3 into cells (Kramer L, et al, Hepatology, 31(1),
Early studies of patients with liver disease
reported increased gastric urease activity associated with elevated
gastric and blood ammonia levels and the frequent colonization
of the upper small bowel with urea-splitting bacteria (Rappoport
W & Kern F, J Lab Clin Med, 61, 1963; Fleshler B & Gabuzda
G, Gut, 6, 1965; Lal D, et al, Gastroenterol 62, 1972).
<< Infection and drugs are also sources of ammonia>>,
and a late rise in its level after cure of Helicobacter pylori
infection could reflect progressive liver disease with less synthetic
function (Baertl J, et al, J Clin
Invest, 42, 1963). Ammonia levels increase as liver
function decreases (Rikkers L,
et al, Gastroenterol, 75, 1978). Increased levels
of ammonia may enter the systemic circulation because of portosystemic
shunting (Wolf D, Aug 2000, eMedicine.com).
Although ammonia synthesis is usually
attributed to fecal bacteria, the stomach, which possesses strong
activity when infected with Helicobacter pylori, is an alternative
site from whence urea readily diffuses from blood into the gastric
lumen where, in the presence of H. pylori, it is hydrolyzed to
ammonia, which is then rapidly absorbed and contributes to higher
circulating blood ammonia levels (Neithercut
W, et al, J Clin Pathol 46, 1993; Gubbins G, et al, Am J Gastroenterol,
88(11), 1993; Ito S, et al, Eur J Gastroenterol Hepatol 6, 1994;
Mokuolu A, et al, Am J Gastroenterol, 92, 1997; Dasani B, Am J
Gastroenterol, 93(5), 1998; Realdi G, et al, Digestive Diseases
and Sciences, 44(2). 1999). The presence of blood
in the upper gastrointestinal tract from gastrointestinal bleeding
results in increased ammonia and nitrogen absorption from gut.
Blood transfusions too, may result in mild hemolysis with resulting
elevated blood ammonia levels (Wolf
D, Aug 2000, eMedicine.com).
If the aforementioned in vitro phenomenon
are not convincing because these studies relate only directly
to ammonia, and not directly to silver chloride, consider a recent
Russian article dealing with <<< the management of patients
with purulent infection with intravenous infusions of silver chloride
ammonia solutions >>>
(Abrosimov I, et al, Khirurgiia (Mosk), 7, 1997).
(No Medline abstract is available, but the title informatively
<<< “THE MANAGEMENT OF
PATIENTS WITH PURULENT INFECTIONS WITH INTRAVENOUS INFUSIONS OF
"SILVER CHLORIDE AMMONIA SOLUTIONS"
So much for Frank Key's nonsense.
Admittedly we have not
reproduced a debate here, the reason being that the individual
proposing the silver chloride hypothesis refused to defend it
beyond those remarks repeated in the text. The original debate
may still exist on the net at the silverlist
THE AMMONIA HYPOTHESIS IN FULL (AS A PDF)
HYPOTHESIS AND OTHER RESEARCH)