Silver Bulletin e-News Magazine
Section 4: Disease News & Information
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Colloidal Silver Information
Q: Does
silver have a historical use other than as a medium of monetary
exchange?
Q: How
is silver able to kill one-celled micro-organisms?
Q: Are
colloidal silver and colloidal gold safe?
Q: Does
the common generic term “colloidal silver” have more
than one definition?
Q: What
is the USFDA’s definition of “colloidal silver”
and why are they concerned about it’s usage?
Q: Can
colloidal silver and colloidal gold be considered drugs or do
they interact with drugs?
Q: Can
colloidal silver or colloidal gold cause an allergic reaction?
Q: Can
colloidal silver cause Argyria?
Q: Can
colloidal silver cause flu like symptoms or diarrhea?
Q: Which
colloidal silver is most effective, ionic or non-ionic?
Q: How
important is silver particle size and is a high ppm colloidal
product required for effectiveness?
Q: Does
colloidal silver kill only “bad” bacteria, leaving
“good” flora unaffected?
Q: Are
colloidal silver products containing gelatins/proteins, salts,
or nitrates effective?
Q: Why
is there an EPA Reference Dose, (RfD) for silver if it has no
associated adverse effects ?
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More Information From the Centers of Disease Control
Cancer
Is Bacterial Infection
Carcinogenic?
by Kirstie Saltsman
Posted February 2, 2001 · Issue 95
from HMS BEAGLE
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Abstract
Can bacteria cause cancer? The author discusses the discovery of
a link between bacterial infection and cancer, the mechanisms by
which bacteria cause cancer, and the potential for treatment. Although
his work was later called into question, Johannes Fibiger, the winner
of the 1926 Nobel Prize in physiology, may not have been too far
off the mark. He was awarded the prize for his discovery that a
parasitic worm, Spiroptera carcinoma, causes gastric tumors in rats.
While dissecting rats infected with the tuberculosis bacterium,
he noticed that some had stomach growths, each of which contained
a parasitic worm. The growths later proved to be unrelated to the
parasite, and doubt was even cast upon his assertion that the growths
were malignant. Nevertheless, the idea that an infectious organism
could cause cancer turned out to be accurate and groundbreaking.
Infectious organisms cause about 15% of cancers. By the early 1970s,
nearly 30 mammalian oncoviruses had been discovered, and it is now
estimated that over 15 percent of cancers worldwide are caused by
infectious organisms. Although the idea that viruses can cause cancer
has been accepted for decades, the idea that bacteria can cause
cancer has begun to attract attention only recently. The most established
instance of this is the link between Helicobacter pylori infection
and gastric cancer, but bacterial infections have also been implicated
in other types, such as colon and gall bladder cancers.
The mechanisms by which bacteria cause cancer appear to be quite
different from those used by viruses. Viruses, by inserting their
genomes into host cell chromosomes, can alter expression patterns
of host cell genes and disrupt the intricately regulated process
of growth control. Human papillomavirus (HPV), for example, which
is associated with cervical cancer, induces cellular transformation
by inhibiting the host cell tumor suppressors p53 and Rb. In addition,
as in the case of human immunodeficiency virus (HIV), viral infection
can cause depletion of the immune system, leaving the host
less able to destroy cancerous or precancerous cells that arise
by spontaneous mutation. Kaposi's sarcoma and non-Hodgkin's lymphoma
are now considered AIDS-defining malignancies. Bacterial infections
can cause tumors via inflammation. In contrast, bacteria are thought
to cause cancer largely via an indirect mechanism. It seems that
it is the host's response to infection - inflammation - which damages
cells and predisposes them toward becoming cancerous. Phagocytes
drawn to the site of infection release reactive oxygen and nitrogen
species that can cause DNA mutations and damage cellular proteins
and lipids. In addition, loss of cells at the site of infection
stimulates cell proliferation in order to regenerate the tissue,
a process that leaves the site vulnerable to tumor formation. Proliferating
cells are one step closer to uncontrolled cell growth, and are also
susceptible to acquiring mutations due to errors in DNA replication.
Although inflammation and its molecular consequences are now known
to be major risk factors in developing gastric adenocarcinoma in
those infected with H. pylori, it was not until fairly recently
that a connection was made between the two. Although the association
between H. pylori and gastric cancer is among the better known examples
of a bacterial cause for cancer, Julie Parsonnet, associate professor
of medicine at the Stanford University School of Medicine's proposed
ERID (Emerging and Re-emerging Infectious Diseases) program, points
out that it is not the first such association to be made. She says
that "people have long recognized that chronic skin and bone infections
with bacteria can lead to aggressive skin cancers." Although it
had been suspected for some time that a widespread environmental
determinant was an etiologic factor in the development of gastric
cancer, it was not until 1991 that H. pylori, a gram-negative, rod-shaped
bacterium, was found to be involved. Over 50 percent of the world's
population is infected with H. pylori; however, in most cases, infection
has no serious clinical consequences. A complex interplay between
host and bacterial factors seems to determine the outcome of infection.
Among the bacterial factors is a group of genes - whose functions
are largely unknown - localized in a cassette called the cag pathogenicity
island. cag+ strains are more virulent than their cag-counterparts,
and there is a strong correlation between infection with cag+ strains
and the occurrence of both gastric cancer and duodenal ulcer disease.
However, those with H. pylori-induced ulcers are less likely than
the general population to contract gastric cancer, a finding that
underscores the importance of host factors in disease outcome.
Host genes influence susceptibility to bacterial tumorigenesis.
Because host factors are thought to influence susceptibility to
disease, a number of research teams are currently trying to pinpoint
disease-predisposing genetic determinants within the host. Among
those that are already known to influence the risk of gastric cancer
is the gene for interleukin-1-beta (IL-1-beta). Elevated levels
of this
cytokine promote inflammation and suppress gastric acid secretion,
which allows for more extensive bacterial colonization of the stomach.
In an attempt to identify other host genes that influence the risk
of gastric cancer, Karen Guillemin, a postdoctoral research fellow
in Stanley Falkow's lab at Stanford University, has devised a strategy
based on the use of human DNA microarrays and a tissue culture model
of infection. By comparing the host genes induced by the more virulent
cagA+ strain with those induced by a cagA- strain, she has distinguished
a subset that may be involved in disease. Some of these genes appear
to be involved in cell signaling or in remodeling the cell ultrastructure,
both of which may set a cell on a course toward malignancy. However,
others are likely to promote cancer indirectly by promoting the
growth of virulent strains. "Because infection with H. pylori is
a long-term, often lifetime condition, and because H. pylori populations
are known to undergo a lot of genetic changes and diversification,
similar to viruses, a complexity that I think will emerge is that
certain host genes will be found to promote particular gastric environmental
conditions that select for more or less virulent bacteria," says
Guillemin. Because only 1 percent of infected individuals have the
misfortune of contracting the disease, genetic determinants within
both host and bacteria are likely to affect the
outcome of infection. Vaccination against H. pylori may fight cancer
well. The finding that bacterial infections can cause cancer is
exciting because unlike a genetic predisposition or an environmental
factor, infections often can be treated or prevented. A recent study
published in the Journal of the National Cancer Institute has shown
regression of precancerous lesions upon treatment with antibiotics
among a high-risk population in southwestern Columbia. Other studies
are currently underway. However,
the use of antibiotics is unlikely to take hold as a widespread
preventive measure. The cost would preclude such a strategy, as
would the risk of inducing the emergence of antibiotic-resistant
strains. A more practical approach would be to induce protection
by vaccination, and trials in mouse models of infection have already
yielded promising results. Oral and intranasal vaccination has provided
mucosal immunity, and systemic vaccination has also been shown to
provide protection in the mouse model. It remains to be seen if
these promising results will be reflected in the human trials currently
being undertaken. In 1966, Peyton Rous was awarded the Nobel Prize
in medicine for his discovery that a virus (the Rous sarcoma virus)
could cause cancer. Now, a mere 35 years later, a significant proportion
of liver cancer is preventable thanks to a vaccine against hepatitis
B. In addition, vaccines against human papillomavirus are now being
tested in an effort to combat cervical cancer, and Epstein-Barr-virus-related
tumors in HIV patients are becoming less common thanks to immunotherapy.
Just as the discovery of the viral origin of certain cancers led
to useful therapies, it is probably not overly optimistic to expect
that the discovery of a link between bacterial infection and cancer
will soon lead to effective treatments and eventually curtail the
number of lives lost to this deadly disease. Kirstie Saltsman is
a freelance biomedical writer based in Baltimore. She received her
Ph.D. from Harvard in 1996 and did postdoctoral work at Stanford.
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Here is another
factor to consider regarding specifically Breast Cancer.
Almost 90% of Americans use deodorant. Most of it has an antiperspirant.
Most of that is Aluminum Chlorhydrate. This compound stops all pores
from allowing perspiration to exit the body at the arm pits. A large
amount of toxins are excreted here under normal circumstances. The
restriction of the sweat glands in this area is thought to contribute
to Breast Cancer and Lymphatic Cancer. It only makes sense. Though
studies continue, the evidence is mounting that this is true.
Our Advanced Colloidal Silver makes a perfect underarm deodorant
for those looking for ways to avoid Breast Cancer and Lymphatic
Cancer.
In our opinion, anyone who is sick with anything should undergo
a course of a month or so of colloidal silver to cleanse the body
of pathogens. It not only kills the pathogens, but takes the pressure
off of the immune system so it can do its job with less "drag" from
the stuff that colloidal silver so easily kills.
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