Reduction of Viral Load in AIDS Patients
with Intravenous Mild Silver Protein Three Case Reports
Ward Dean, MD, et. al.
Mild Silver Protein (MSP) has been used since the 19th century
as an anti-microbial agent, with a wide range of bactericidal,
fungicidal and virucidal properties. This paper reviews the
historical use of mild silver protein in medicine, and documents
the recent effectiveness of intravenous MSP to cause a dramatic
reduction in viralload of three patients with human
immunodeficiency virus (HIV+).
Silver (Ag) is atomic element number 47, with an atomic weight
of 108. It is one of the so-called heavy metals,
along with lead, mercury, cadmium and gold. Unlike its heavy
metal cousins, silver is surprisingly non-toxic to humans and
animals, and has a long history of successful medical and public
health use dating back 6000 years. Silver has been used to speed
wound healing, treat infections, purify water and preserve
beverages. The ancient Macedonians covered wounds with silver
plates to speed healing (1). N.R. Thompson (2) noted that
The germicidal properties of silver, although not recognized as
such, have been utilized since the times of the ancient
Mediterranean and Asiatic cultures, references being made to the
use of silver vessels to prevent spoilage of beverages, and
silver foil or plates in the surgical treatment of wounds and
The modern era of silver usage began in 1893 with C. Von Nageli
s report of the first systematic investigation into the lethal
effects of metals [especially silver] towards bacteria and lower
life forms. To primitive life forms, oligodynamic (solutions in
which the metal ion concentration is many orders of magnitude
below that which would be lethal to higher life forms) silver is
as toxic as the most powerful chemical disinfectants. Coupled
with its relative harmlessness to animal life, this gives it
as a disinfectant (2). Silver was one of the mainstays of
medical practice in Europe and America during the period from
1900 until the beginning of the modern antibiotic era, which
began in the 1940s with the introduction of sulfa drugs and
Various forms of silver were used to treat literally hundreds of
ailments, including pneumonia, tuberculosis and pleurisy (3),
gonorrhea and syphilis, (4) wounds, leg ulcers, pustular eczema,
impetigo and boils (4). It has been used in acute meningitis and
epidemic cerebro-spinal meningitis (3), Mediterranean fever,
erysipelas, cystitis, typhus, typhoid fever, and tonsillitis
(3), dacryocystitis, corneal ulcers, conjunctivitis and
blepharitis (5), and various forms of septicemia, including
puerperal fever, peritonitis and
post-abortion septicemia (3, 6). This list does not even begin
to exhaust the published medical uses for silver in Europe and
America, from 1900-1940.
In 1939, Hill and Pillsbury (7) listed 94 different proprietary
silver preparations in use at that time. With the development of
the antibiotic era, however, silver rapidly fell into
disuse and into the medical memory hole. By the late 1980s,
antibiotics were thought to have so succeeded in
controlling/eradicating most microbial diseases, that medical
researchers and pharmaceutical companies seriously slowed
research into new antibiotics, thinking that there was no longer
any need for newer and better antibiotics. Yet by the 1990s the
picture began to change again.
Some common and dangerous bacteria such as Staphylococcus aureus,
particularly the strains found in hospitals, are now known to be
resistant to all but vancomycin, and soon are expected to be
vancomycin-resistant too (8,9). In 1992 the Centers for Disease
Control(8) reported that 13,300 hospital patients died in the
U.S. of bacterial infections that resisted the administered
antibiotics. It is interesting to note that silver, both in
liquid solution and as an airborne-aerosol, has been known since
1887 to be extremely toxic to Anthrax spores (1,10-12).
Silver is unique among antimicrobial agents in its broad
spectrum of action. It has been claimed to kill some 650
different disease organisms (13). It effectively kills
micro-organisms of all major types: gram-positive and
gram-negative bacteria, spore-forming bacteria, fungus/yeasts,
viruses and protozoal parasites. Silver sulfadiazine (SS) is
used almost universally in hospitals to prevent serious burn
infections (11). It kills dozens of different bacteria,
(11,14,15), 95% of 72 strains of herpes virus (16), as well
as the malaria-causing Plasmodium berghei (17). Silver
sulfadiazine also kills various yeasts, including several
Aspergillus varieties, Mucor pusillus, Rhizopus nigricans and 50
different clinical isolates of Candida albicans (18). It is
widely reported in the medical literature that various forms of
silver, often at surprisingly low concentrations, routinely kill
bacteria that are known to be antibiotic resistant
Electrically-generated colloidal silver [Ag(e)] has been shown
to kill dozens of bacteria. This includes Providencia stuartii,
an organism already resistant in the 1970s to all antibiotics
except amikacin (19), as well as two strains of Enterobacter
cloacae that were isolated from burn patients and were
relatively resistant even to Silver sulfadiazine (20).
Electrically-generated colloidal silver has also proved adept at
killing various yeast/fungus species at very low silver
concentrations, including Candida albicans, C. parapsilosis, C.
tropicalis, C. pseudotropicalis, Torulopsis glabrata and
Aspergillus niger (20). This form of silver has been shown to
kill cysts of the common water-borne protozoal parasite
Entamoeba histolytica, and has also killed the protozoon
Paramecium when exposed to 2.2 ppm silver, as well as the
protozoa Varicella at 5.9 ppm silver (1). It was even somewhat
effective in killing Poliovirus in swimming pool water, at the
extremely low concentration of 0.015mg silver per liter of water
(15 parts per billion) (21). Pioneering silver researcher Dr.
Henry Margraf stated that silver is the best all round
germ-fighter we have (13).
Historically, silver has been used in 20th-Century medicine in a
wide variety of forms. It has been used as silver salts (e.g.
silver nitrate, silver phosphate, silver iodide) and Silver
compounds (e.g. silver sulfadiazine, silver arsphenamine,
zinc-silver allantoinate) (11). Many physicians using silver in
the first half of the 20th century preferred a colloidal form of
silver, either chemically or electrically produced (3,11).
Combining silver with protein (mild silver protein [MSP], and
strong silver protein [SSP]) results in an enhanced spectrum of
action. (13, 22) Thus, both modern science and early 1900's
medical practice support the therapeutic use of either colloidal
silver or mild silver protein (MSP)(11).
In 1994, William McFarland, a Louisiana-based businessman was
introduced to MSP by a physician friend. He began to use it
personally for minor viral infections, and
recommended it to friends for oral and topical use for a variety
of clinical conditions. As he became convinced of its efficacy
for both viral and bacterial infections, he speculated that it
might have positive effects in ameliorating serious,
difficult-to-treat infectious diseases, and that it might be
even more effective when administered
intravenously. He arranged for the first course of infusions to
be administered in Mexico, with subsequent infusions in New
Orleans. This paper reports on preliminary results of
intravenous MSP in three HIV+ patients.
Materials and Methods
In 1997, McFarland recruited three subjects with HIV to
participate in clinical trials with MSP. The initial protocol
involved progressively increasing amounts and concentrations
administered orally for 30-60 days, followed by a series of
intravenous infusions in concentrations ranging from 40 ppm to
1,500 ppm. Medical records for the three subjects were obtained,
to as great a degree as possible, from the personal physicians
of the subjects, and from the No AIDS Task Force at Charity
Hospital in New Orleans, LA.
MSP 40 and 1,500 ppm were provided by Discovery Experimental and
Development, Inc. MSP 400 was manufactured by Natrition, Inc.
Subjects were started on oral MSP 40 ppm and advanced to 400 ppm
at standard dosages consisting of several teaspoons daily in
divided doses for approximately one month prior to administering
it intravenously. Oral MSP 400 ppm was continued throughout the
The first phase of this small trial was conducted in Mexico. One
hundred twenty ml of MSP in concentrations of 40, 400, and 1,500
ppm respectively were given to each of 2 subjects [AP and RC],
one time each, in a carrier solution of 500 cc _ normal saline,
to which 10 cc of dimethyl sulphoxide (DMSO) was added. Each
given over two-three hours. The first three infusions were
administered in Mexico by VWL. Subsequent infusions were
administered in the U.S.
An adverse effect noted by all subjects to a greater or lesser
degree was a Jarisch-Herxheimer-like reaction, lasting from 2-8
hours. This reaction, which usually started from 1-4 hours after
the conclusion of an infusion, included nausea, vomiting, fever,
myalgias, and headache. The reaction appeared to decrease with
The patients were monitored twenty-four hours a day for 5-7 days
following each IV infusion, and once a week thereafter, via
office visits and almost daily telephone conversations.
AP was a white male, born in 1967. Records from Charity Hospital
reveal that he was diagnosed with HIV in February, 1993. At that
time, he weighed 137 pounds, and his only abnormal physical
finding was swollen inguinal lymph nodes. In April, 1995, AP was
treated for nausea, vomiting, diarrhea, and shingles. In August,
1996, he began to complain of anxiety, diarrhea, and weight
loss, for which he began to seek more regular medical treatment.
Intermittent courses of antibiotics had been prescribed for
diarrhea, acyclovir for shingles, and AZT. However, AP seldom
completed a course of any of these medications.
At the time he entered the experimental trial with MSP in
October 1997, AP was not receiving any medication at all. He
weighed 132 lbs, and was unable to walk without assistance due
to fatigue and weakness. His viral load was over 750,000 RNA
copies/ml'the maximum detectable limit of the instrument.
AP received his first IV infusion on 3 December, 1997. His
treatment chronology is outlined in Table I. After his only
infusion of 1500 ppm MSP on 7 December, AP suffered what was
interpreted at the time as a severe Herxheimer reaction.
However, the symptoms were more severe than usual, and the
weakness and severe myalgias persisted for days, instead of
hours. A complete blood count on 16 December revealed that AP's
hemoglobin had dropped to 8.9 g/dl, and his hematocrit to 26.9
(Table II). Nevertheless, by the fourth of January, AP reported
to the office demanding that he be given another infusion.
Because of the severity of his previous reaction, the dosage was
reduced again to MSP 40 ppm, which caused no adverse effects,
followed by an infusion the following day with MSP 400 ppm. By
January 8, AP's hemogram had rebounded to 11.1 g/dl, and his
hematocrit to 31.9 %.
Thirty five days after beginning MSP treatment, AP's viral load
was 39,000 RNA copies/ml. One month later, with no additional
infusions, the viral load was down to 400 RNA copies/ml (the
lowest detectable limit of the instrument) (Table I and Fig. 1).
AP continued to improve clinically, left New Orleans in February
of 1998, and was unfortunately lost to follow-up. Although he
apparently underwent extensive laboratory testing at Charity
Hospital's No AIDS Task Force, McFarland was unable to obtain
further documentation beyond that in Table 1.
RC was a Puerto Rican male, born in 1950. He did not smoke
cigarettes or marijuana, drank alcohol moderately, and ate a
healthy diet. His male roommate died of
AIDS/HIV at Charity Hospital in 1986 at the age of 30. RC's
medical history includes Hepatitis A and B. He had been a waiter
most of his adult life, and also worked as a carpenter with his
father on weekends, renovating houses.
In 1987, RC enrolled in Charity Hospital's No Aids Task Force
where he tested positive for HIV. No viral load or T cell count
data are obtainable. He had been under the impression that he
had only two years to live. For the next ten years, he kept
waiting to die. In the summer of 1997, he began to notice a
decrease in energy, and increased
requirement for sleep, causing him to discontinue his work as a
carpenter. He volunteered for the experimental MSP treatment
program in November, 1997.
RC received five IV infusions on the same dates and dosages as
AP (Table I)'the first three in Mexico, and the last two in the
U.S. He received a sixth infusion of MSP 400 ppm on 27 February
in the U.S. He continued on oral MSP 400 ppm until June of 1998,
when he discontinued participation in the program. Results of
in viral load are shown in Figure 2. Changes in his other
laboratory studies are shown in Table 3.
RC noted a dramatic restoration of his energy levels and
returned to his former occupation as a waiter, where he usually
worked up to two shifts a day from 12:00 noon until 12:00 or
1:00 in the morning. Because of his restored energy levels, RC
no longer felt a need to visit McFarland's office. Because he
would not return to the physician's office, McFarland went to
his place of employment with a physician friend every weekend in
March and April of 1998. RC promised to obtain additional
records from the State of Louisiana, but he unfortunately never
GH was a white male, born in 1948, who had been HIV+ since 1985.
He began taking oral MSP 400 ppm 1 tsp three times daily on 4
April 1998. His HIV-1 RNA (viral load) test on 9 June, 1998 was
13,752 RNA copies/ml. On 10 June, 1998 he was given one infusion
of MSP 400 ppm. He continued oral MSP through the end of July,
1998. On July 20, a second HIV-1 RNA test was performed, which
revealed a dramatic drop of viral load to 2,215 RNA copies/ml
The data in this study are admittedly fragmentary. There are
several reasons for this. McFarland, as stated previously, was a
businessman. He had no scientific or medical training other than
that which he obtained as an avid reader of medical and
health-related books, and what he gleaned from discussions with
his physician and scientist friends. However, he believed that
if he could demonstrate its safety and efficacy on a few
severely ill patients, the medical community would pick up the
baton and continue the studies of this innovative and relatively
inexpensive therapy under more controlled conditions.
To prove his case, he chose one of the most difficult-to-treat
conditions there is'AIDS. He set up a protocol based on
consultations with physicians in Mexico, Cuba, and the U.S., and
advertised for experimental subjects. The infusions in Mexico
were under the supervision of one of us (VW-L), and the
infusions in the U.S. were under the supervision of another
Patient information and laboratory data are derived largely from
patient records and laboratory reports held by the No-Aids Task
Force. Unfortunately, despite signed records release forms from
each subject, and intervention by attorneys, the administrators
of the No Aids Task Force were reluctant to cooperate.
Also, the subjects in the study were less than responsible, and
were not interested in continuing treatment beyond the point
that they felt well enough to return to their former destructive
lifestyles. Consequently, they were erratic in following through
with their treatments, and did not greatly assist with obtaining
All three subjects experienced a dramatic reversal in what had
been their rapidly-deteriorating clinical condition. This change
was so dramatic, in fact, that all felt well
enough to return to their former hedonistic lifestyles.
Unfortunately, they did not maintain the positive lifestyle
changes recommended by their physicians, and two of the subjects
(AP and GH) moved out of town. RC is actively employed, but
declines further treatment as he does not feel ill. The last
McFarland heard from AP and GH was that
they also did not feel ill, and saw no need to continue their
treatments. As far as we know, AP is still alive, and two (RC
and GH) are actively employed.
The only adverse effects noted during the course of any of the
subjects' treatment were the Herxheimer-like reactions from the
MSP 400 ppm infusions, and the severe pancytopenia experienced
by AP from the MSP 1500 ppm. Whether this reaction was a true
Herxheimer reaction, or an inflammatory/toxic effect of the
not been determined. However, any pathology appeared to be
self-limiting and rapidly reversible, as demonstrated by AP's
rapid rebound in hematological status following the 1,500 ppm
infusion, despite an intervening 400 ppm infusion (Table I and
As fragmentary and incomplete as these data and records are, we
believe the reductions in viral load in these subjects are so
dramatic that they deserve publication. The well documented
results are certainly no coincidence, and cannot be ignored.
First, IV MSP 400 ppm appears to be a safe, effective virucidal
agent in HIV-positive patients. Second, it is also clear that
high concentrations are probably toxic, as demonstrated by the
dramatic drop in APs hematological status following the 1500-ppm
infusion. Third, and most important, is the apparent ability of
MSP to dramatically reduce the viral load and cause clinical
reversals of rapidly deteriorating patients with HIV. Although
the optimum dosage and frequency of infusions has not been
determined, 1 or 2 infusions weekly appears to be a safe and
effective regimen. We believe the frequency should be adjusted
downward should severe Herxheimer-like reactions occur.
In future trials, we hope to see long-term follow-up, and to
observe how low and for how long the viral load can be reduced,
and to monitor changes in CD4-CD8 ratios. However, such changes
take more time than these patients were willing to give.
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