COLLOIDAL SILVER - Natural Antibiotic Alternative 
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 COLLOIDAL SILVER - Natural Antibiotic Alternative


    >Silver ions are the obvious mechanism for colloidal silver's
    >activity, but electron donation is another.

Huh?

    >Furthermore, metalic
    >silver is perfectly capable of staining tissue by itself (that's
    >what it is used for in electron microscopy).

Which says absolutely nothing about what happens in argyria.

    >There is no need for it
    >to be oxidized and covalently bound to sulfur residues to cause
    >staining.

"Need"?  And we're not talking about staining here.

    >I'm sure this happens to some extent, but the most common
    >kind of argyria reported in the old literature is from silversmiths
    >getting too much silver exposure (metal dust and tiny slivers) in
    >their fingers and hands.

What do YOU know about the literature?  Not very much, it seems.
Argyria also used to be seen after chronic systemic exposure to silver
salts in industry and after the chronic abuse of colloidal silver
preparations in attempts at self-medication.  It's not just a matter of
exposure to small particles of metallic silver.  This is not quite the
same as staining, since it's not an acute effect resulting from direct
contact.

    >Can you cite the author so that I might track down a reference to
    >silver oxidation in argyria?

Here are two references, and several more that you can look up:

Goodman and Gilman, _The Pharmacological Basis of Therapeutics_,
4th ed., 1970, p. 968-969.  Later edition of this textbook do not
go into as much detail, since even by 1970, the use of colloidal
silver as an antiseptic was all but obsolete.  One wonders if next
year's edition (they come out like clockwork every 5 years) will
be forced to address this topic again, with the irresponsible
promotion of "colloidal silver" by pyramid marketeers and gnuage
hucksters to ignorant sheep as an alternative to antibiotics.

                Minute amounts of silver are ingested daily, due to the
        wide use of this metal in eating utensils, and a portion is
        absorbed.  It has been demonstrated that silver gradually
        accumulates in the body and in the later decades of life
        reaches an appreciable concentration.  High concentrations of
        silver in the tissues, however, occurs only after the careless
        administration of silver-containing medicinals.  However,
        systemic effects do not follow absorption.  The absorbed silver
        is widely distributed in the body, especially in the
        subepithelial portions of the skin, and large amounts can
        impart to the skin a characteristic bluish pigmentation.  This
        pigmented condition is known as _argyria_.  The hue may range
        from gray to one suggesting marked cyanosis.  Part of the
        pigment may be silver sulfide, but is also partly metallic
        silver, which results from the reduction of silver in the
        tissues.  As in a photographic emulsion, the reduction is
        facilitated by light, and the pigmentation is accentuated by
        exposure to light.  Expecially those portions of the skin
        exposed to light may become discolored.  However, the first
        sign of argyria may be a slate-blue "silver line" in the
        gingival margins next to the teeth.  Argyria can be readily
        diagnosed and differentiated from other forms of pigmentation
        by direct illumination and dark-field examination of biopsied
        portions of skin.  The silver can be seen in the elastic fibers
        of the cutis, the connective tissue sheaths about the sebaceous
        glands and hair follicles, and the cutaneous vessels, muscles
        and nerves.  It is usually thought that the silver is deposited
        intra-cellularly.  However, Boersma and Baker (1948) claim
        that dark-field illumination causes extracellular deposits to
        appear as intracellular ones; they report silver to be
        deposited extra-cellularly, mainly in elastic fibers.

                The eye is particularly prone to manifest pigmentation from
        silver, the color ranging from a light bluish-gray to a brownish-
        black.  The ocular distribution of silver has been studied in only
        a few human cases; following {*filter*}administration in rats, the metal
        is found in highest concentration in certain portions of the
        choroid and ciliary body.  Only a few granules appear in the
        conjunctiva, cornea and sclera, and none is present in the lens,
        iris or retina.  The discoloration may appear after systemic or
        local administration and is often the first sign of argyria.  If
        silver compounds are being applied locally, ulceration of the
        cornea increases the possibility of pigmentation.  Clinical cases
        are on record in which pigmentation was observed within 10 days.

                Argyria can result either from industrial exposure to
        silver or to medication.  Despite the claims of some manufacturers
        that colloidal silver preparations are harmless and can be taken
        orally without impunity, many cases of argyria have resulted from
        their use.  Even the continuous application of silver compounds to
        the mucous membranes of the nose may result in swallowing of
        sufficient metal to cause cutaneous pigmentation.  The current [sic]
        use of silver nitrate in the treatment of burns may be expected to
        cause some cases of argyria.  Unfortunately, even if medication is
        immediately stopped upon its development, there is no guarantee
        that further pigmentation may not occur.

                The only injury sustained in argyria is a cosmetic one, but
        it remains for life.  The silver pigment is soluble in sodium thio-
        sulfate, but this agent is effective only in high concentrations.
        Successful treatment of argyria is rare, and requires the laborious
        intradermal injection of the entire involved area with 6% thio-
        sulfate solution and 1% potassium ferrocyanide solution.
        Dimercaprol has been sown to be ineffective; this is not
        unexpected, since the pigment is mostly free silver.

                The problem of argyria and the pharmacology of silver have
        been extensively reviewed by Hill and Pillsbury (1939).

In Casarett and Doull's _Toxicology_, 3rd. ed., (1986), chapter 19, "Toxic
Effects of Metals", p. 625, on silver:

                Industrial argyria, a chronic occupational disease, has two
        forms, local and generalized.  The local forms involves the
        formation of gray-blue patches on the skin, or may manifest itself
        in the conjunctiva of the eye.  In generalized argyria, the skin
        shows widespread pigmentation, often spreading from the face to
        most uncovered parts of the body.  In some cases, the skin may
        become black with a metallic luster.  The eyes may be affected to
        such a point that the lens and vision are disturbed.  The
        respiratory tract may also be affected in severe cases.

                Large {*filter*}doses of silver nitrate cause severe gastro-
        intestinal irritation due to its caustic action.  Lesions of the
        kidneys and lungs and the possibility of arteriosclerosis have been
        attributed to both industrial and medicinal exposures.  Large doses
        of colloidal silver administered intravenously to animals produced
        death due to pulmonary edema and congestion.  Hemolysis and
        resulting bone marrow hyperplasia have been reported.  Chronic
        bronchitis has also been reported to result from medicinal use of
        colloidal silver (Browning, 1969; Luckey, et. al., 1975.)

Boersma, D., and Baker, D.L., Sites of deposition of silver in argyria.
        _Archs Derm. Syph._, 1948, 57, 1009-1012.

Browning, E.: _Toxicity of Industrial Metals_, 2nd ed., Butterworths,
        London, 1969.

Granstein, R.D., and Sober, A.J.: Drug and heavy metal induced hyper-
        pigmentation.  In Marzulli, F.N., and Maibach, H.I. (eds.):
        _Dermatotoxicology_, 2nd ed.  Hemispheres Publishing Co.,
        Washington, D.C., 1983.

Hill, W. R., and Pillsbury, D. M., _Argyria: the Pharmacology of Silver_.
        The Willians & Wilkins Co., Baltimore, 1939.

Luckey, T.D., Venugopal, B., and Hutcheson, D.: _Heavy Metal Toxicity
        Safety and Hormonology_.  Academic Press, Inc., New York, 1975.

--
Steve Dyer



Fri, 06 Jun 1997 05:30:02 GMT
 COLLOIDAL SILVER - Natural Antibiotic Alternative


Quote:


>    >Silver ions are the obvious mechanism for colloidal silver's
>    >activity, but electron donation is another.

>Huh?

You know, electrons. They are subatomic particles that carry
one negative charge and surround individual atoms in "shells" and
"orbitals." Electron interactions characterize the field of
chemistry. Changes in electron configurations in single atoms
happen with excitation and oxidation-reduction (redox) reactions
(e.g., the conversion of metalic silver into silver ion, or vice
versa). Electrons also pool in metals when lots of atoms get
together. It can be thought of as an electron ocean which can
"accept" and "donate" additional electrons, becoming more or
less charged in the process.

Unlike individual atoms, the donation of electrons by metals does
not change their redox state. It is a distinctly different
phenomenon. As an analogy, it's like rubbing your feet on a carpet
and touching a doorknob. The spark that jumps from your finger to
the doorknob is a transfer of pooled electrons from your body
through the tip of your finger to the doorknob (or vice versa if
your feet-shuffling resulted in the depletion of electrons).

Although colloidal silver particles are exceedingly tiny by our
common everyday standards, they are composed of large clusters of
metalic silver atoms (I believe the figures range from hundreds of
atoms to hundreds of thousands of atoms). This is a substantial pool
of electrons on the subcellular scale.

Since the energy barrier to electron donation from a metalic
electron pool is small by comparison to the energy required to
oxidize a silver atom on the surface of the colloidal particle,
electron donation and acceptance is probably a much more common
phenomenon. Whether it is significant is the question.

Quote:
>    >Furthermore, metalic
>    >silver is perfectly capable of staining tissue by itself (that's
>    >what it is used for in electron microscopy).

>Which says absolutely nothing about what happens in argyria.

No? Isn't that the question I raised? I was advancing an alternative
possibility, that colloidal silver itself may be responsible for
staining (i.e., that ionic silver is *not* the *only* mechanism by
which staining can occur).

Argyria is characterized by bluish-gray staining of tissue. Why would
you state that staining by colloidal silver has "absolutely nothing"
to do with this discoloration? To state that something is impossible
requires proof. None of the several dozen papers (nor _Argyria_)
published between 1890 and 1934 that I've read provided proof that
colloidal silver does *not* stain tissues.

Given the fact that I had read all of this literature without such
proof, and the fact that Paul's uncited poster (you?) implied that
such proof existed, I wanted to track down whatever evidence might
exist about this issue. I still do.

Quote:
>    >There is no need for it
>    >to be oxidized and covalently bound to sulfur residues to cause
>    >staining.

>"Need"?  And we're not talking about staining here.

Need. Necessity. Requirement.

We're not talking staining here? I'm afraid you are being too brief
to be clear what you mean by this. *I* was certainly talking about
staining there. I was referring to silver sulfide (which is black,
and quite insoluble).

Quote:
>    >I'm sure this happens to some extent, but the most common
>    >kind of argyria reported in the old literature is from silversmiths
>    >getting too much silver exposure (metal dust and tiny slivers) in
>    >their fingers and hands.

>What do YOU know about the literature?  Not very much, it seems.
>Argyria also used to be seen after chronic systemic exposure to silver
>salts in industry and after the chronic abuse of colloidal silver
>preparations in attempts at self-medication.  It's not just a matter of
>exposure to small particles of metallic silver.  This is not quite the
>same as staining, since it's not an acute effect resulting from direct
>contact.

Oh. I get it. You are being snide again. Duh. No problem.

You are right about the industrial exposures which became rampant
with the expanding industrial use of silver salts during the early
part of this century, but argyria in silversmiths was common
before then. Given the type of occupational exposure for
silversmiths (grinding, filing, casting, soldering, buffing, etc),
metalic silver was the primary exposure (skin [especially the
fingers], eyes, mouth, nasal passages, and lungs).  Ionic silver
would largely have to have been produced by bio-oxidative reactions
in the tissues (ignoring the small amounts might have been produced
by etching with acid). The extreme localization of argyria in
silversmiths would suggest that this process, if it is *essential*
to argyria at all, would take place in deep tissues and that
oxidized silver, once produced, would quickly react with adjacent
molecules.

I don't know what you mean about "it's not just a matter of exposure
to small particles of metallic silver" and "this is not quite the
same as staining, since it's not an acute effect resulting from
direct contact." That such exposure is not acute, I agree. But
*chronic* exposure to metalic silver through slivers, and dust
through open cuts, was and is sufficient to generate argyria. Some
of these cases were sufficiently severe to prevent their continued
employment in the trade.  

Quote:
>    >Can you cite the author so that I might track down a reference to
>    >silver oxidation in argyria?

>Here are two references, and several more that you can look up:

Goodman and Gilman references the standard analysis of silver
sulfide and metalic silver as pigment, and go so far as to attribute
the metalic content of the pigment to "reduction of silver in the
tissues." It's not that I don't believe this happens (it obviously
does), it's whether or not it is the *only* mechanism. They cite the
photocatalyzed reduction of silver (like a "photographic emulsion")
as a mechanism, which explains the surface argyria on exposed skin,
but this does not seem sufficient to explain deep-tissue argyria in
internal organs that can accompany chronic excessive intake of
colloidal silver preparations.

Quote:
>In Casarett and Doull's _Toxicology_, 3rd. ed., (1986), chapter 19

Thanks, I hadn't read this source. They state "The respiratory tract
may also be affected in severe cases." but don't propose a mechanism
for the reduction. Thanks also for the Browning, Luckey, and
Granstein references. I'll definitely look them up.

Do you know if anybody has done EM studies of argyric tissue? If
the silver is in isolated atoms, or in sub-colloidal-sized clumps,
oxidation and subsequent reduction would seem the only reasonable
explanation. My search of Embase for the last 5 years found only
silver-staining studies.

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Cognitive Enhancement Research Institute        fax: 415-323-3864
PO Box 4029, Menlo Park, CA 94026 USA           alt: 415-321-6670
-----------------------------------------------------------------



Sat, 07 Jun 1997 04:33:53 GMT
 COLLOIDAL SILVER - Natural Antibiotic Alternative

   >>    >Furthermore, metalic
   >>    >silver is perfectly capable of staining tissue by itself (that's
   >>    >what it is used for in electron microscopy).
   >>
   >>Which says absolutely nothing about what happens in argyria.
   >
   >No? Isn't that the question I raised? I was advancing an alternative
   >possibility, that colloidal silver itself may be responsible for
   >staining (i.e., that ionic silver is *not* the *only* mechanism by
   >which staining can occur).
   >Argyria is characterized by bluish-gray staining of tissue. Why would
   >you state that staining by colloidal silver has "absolutely nothing"
   >to do with this discoloration? To state that something is impossible
   >requires proof. None of the several dozen papers (nor _Argyria_)
   >published between 1890 and 1934 that I've read provided proof that
   >colloidal silver does *not* stain tissues.

No, you're not understanding the point.  "Staining" is not the same as
argyria.  When you apply topical silver salts to skin, you'll produce
a superficial stain immediately.  Colloidal silver does not produce this,
because there aren't a lot of free silver ions in the preparation.

Argyria is a longer-term phenomenon; silver and silver sulfide
accumulate in the skin over time.  The metallic silver appears
when silver salts are reduced locally, and this is facilitated by
exposure to light (just like a photograph.)

   >We're not talking staining here? I'm afraid you are being too brief
   >to be clear what you mean by this. *I* was certainly talking about
   >staining there. I was referring to silver sulfide (which is black,
   >and quite insoluble).

I hope this clarifies this.

    >Goodman and Gilman references the standard analysis of silver
    >sulfide and metalic silver as pigment, and go so far as to attribute
    >the metalic content of the pigment to "reduction of silver in the
    >tissues." It's not that I don't believe this happens (it obviously
    >does), it's whether or not it is the *only* mechanism. They cite the
    >photocatalyzed reduction of silver (like a "photographic emulsion")
    >as a mechanism, which explains the surface argyria on exposed skin,
    >but this does not seem sufficient to explain deep-tissue argyria in
    >internal organs that can accompany chronic excessive intake of
    >colloidal silver preparations.

"Deep tissue argyria"?  I've only heard of argyria as a cosmetic issue,
as it affects the skin and eyes.  It's a superficial (but disfiguring)
phenomenon.

I don't see why you have a problem with colloidal silver causing this.
It's a source of silver ions, and therefore is like any silver preparation
in its propensity to cause argyria.

    >Do you know if anybody has done EM studies of argyric tissue? If
    >the silver is in isolated atoms, or in sub-colloidal-sized clumps,
    >oxidation and subsequent reduction would seem the only reasonable
    >explanation. My search of Embase for the last 5 years found only
    >silver-staining studies.

It's pretty much a dead topic, since this has been a clinical non-problem
for years.  It may have to be revisited.

In any case, the _ur_ text which my articles were addressing was the
claim that colloidal silver was both safe and effective.  There is absolutely
no reason to think that it's useful when applied or taken internally,
there is a documented history of self-medication with silver and
colloidal silver causing argyria, and anyone who knows how silver
is distributed in the body, knows that a claim that these "gnu age" colloidal
silver preparations are free from this side effect is blowing smoke.

--
Steve Dyer



Sat, 07 Jun 1997 06:56:42 GMT
 COLLOIDAL SILVER - Natural Antibiotic Alternative


Quote:

>No, you're not understanding the point.  "Staining" is not the same as
>argyria.  When you apply topical silver salts to skin, you'll produce
>a superficial stain immediately.  Colloidal silver does not produce this,
>because there aren't a lot of free silver ions in the preparation.

Steve, it's a circular argument stemming from your definition of
argyria as different from staining. But argyria is silver-mediated
staining of tissues, and staining with metalic silver does happen,
so can you exclude metalic-silver staining from argyria without
resorting to definition?

Quote:
>Argyria is a longer-term phenomenon; silver and silver sulfide
>accumulate in the skin over time.  The metallic silver appears
>when silver salts are reduced locally, and this is facilitated by
>exposure to light (just like a photograph.)

Yes. But this may only be a *piece* of the total process. I
understand photocatalyzed reduction, but it is practically limited
to surface tissues. Chemical mechanisms of reduction are necessary to
explain deep tissue argyria. I acknowledge that such chemical
mechanisms exist (e.g., the action of silver nitrate on deep tissues
is the same as surface tissues) and that "metabolic" mechanisms
exist, but I don't know if they are necessary or sufficient to
account for non-photocatalyzed argyria. None of the references I've
read address this issue. Do you know of any? Anybody else?

It is possible that photo-catalyzed reduction of silver is the
only mechanism and that silver migration from surface tissues
accounts for deep-tissue staining. I've seen no supporting data, but
it is possible.

Quote:
>I don't see why you have a problem with colloidal silver causing this.
>It's a source of silver ions, and therefore is like any silver preparation
>in its propensity to cause argyria.

I don't have a problem with colloidal silver causing argyria. I
never did. If you would read my postings more carefully, you would
know this. My questions, and my speculations, deal with alternative
mechanisms by which colloidal silver might cause argyria. The fact
that the oxidation/re-reduction process *is* driven by light does not
mean that it is *only* driven by light. And just because I question
that it is *only* driven by light, or speculate that oxidation and
re-reduction may not be the *only* mechanism of argyria, or that
oxidation to silver ions might not be the *only* therapeutic
mechanism for colloidal silver, doesn't mean that I deny these other
mechanisms. I don't. I'm merely asking questions that I can't yet
answer. I'm deeply appreciative of your assistance, and anybody else
who can offer data on these questions, but it is frustrating when
answers aren't to the questions asked.

Quote:
>    >Do you know if anybody has done EM studies of argyric tissue? If
>    >the silver is in isolated atoms, or in sub-colloidal-sized clumps,
>    >oxidation and subsequent reduction would seem the only reasonable
>    >explanation. My search of Embase for the last 5 years found only
>    >silver-staining studies.

>It's pretty much a dead topic, since this has been a clinical non-problem
>for years.  It may have to be revisited.

Yes. There has certainly been lots of new technology developed
over the last 60 years. If there is a need, it might get done.

When and if colloidal silver is ever proven and exploited in the
treatment of acute viral, bacterial and fungal diseases (especially
antibiotic and drug-resistant strains), orally or intravenously, as
a therapeutic alternative to antibiotics and antifingals, then we
will see some real analysis of it's mechanisms. We night even see
someone develop a biologically based assay of the colloidal silver
preparations, like Bruce Ames did with bacteriological assays of
mutagens and carcinogens.

If the biological activity of colloidal silver is directly related
to surface area, we might even be able to optimize the silver
preparations to have maximum short-term bactericidal and fungicidal
activity, with minimal silver content (and risk of argyria).

Any graduate students out there looking for a thesis project?

-----------------------------------------------------------------

Cognitive Enhancement Research Institute        fax: 415-323-3864
PO Box 4029, Menlo Park, CA 94026 USA           alt: 415-321-6670
-----------------------------------------------------------------



Sat, 07 Jun 1997 13:56:09 GMT
 
 [ 4 post ] 

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