The rush to mandate an HPV vaccine to prevent Cervical Cancer, may not even make sense as a preventive measure.
Is Human Papillomavirus the Real Cause of Cervical Cancer?
Memo on the mandating of HPV vaccine in NYS.
By Gary Krasner, CFIC
The pharmaceutical-supported mainstream media, and the Merck-supported Public
Broadcasting Service uncritically accept the claim that human papillomavirus is
the cause of cervical cancer in women, despite the
absence of supporting medical evidence. There's also no discussion of the one
pharmaceutical merchandise (i.e.: feminine hygiene products) that is the most
likely cause of this cancer.
Excerpts Supporting This Contention:
http://www.virusmyth.net/aids/data/pdlatvir3.htm
QUOTE
The following epidemiological and biochemical arguments cast doubt on these
HPV-cancer hypotheses:
1. Random allelic mutation of suppressor genes, as postulated by zur Hausen,
predicts a few cancers soon, and more long after infection. Since
cancers only appear 20-50 years after infection, cooperation between HPV and
mutations cannot be sufficient for carcinogenesis.
2. Further, the proposal of zur Hausen that inactivation of host suppressor
genes is necessary for viral transformation is not compatible with HPV
survival. Since HPV, like all small DNA viruses, needs all of its 8-kb DNA
for virus replication (13), suppression
of one or more HPV proteins by normal cellular
genes would effectively inhibit virus replication in all normal
cells.
Conversely, if viral transforming proteins were not suppressed by normal
cells, virus-replicating wart cells
should be tumorigenic because all viral genes are
highly expressed in virus replication (1, 13, 191).
3. The clonality of cervical cancers rules out the Howley hypothesis.
4. The lack of a consistent HPV DNA sequence and of consistent HPV gene
expression in HPV DNA-positive tumors is inconsistent with the zur Hausen
and Howley hypotheses and indicates that HPV is not necessary to
maintain cervical cancer.
5. The presence of HPV in no more than 67% of age-matched women with cervical
cancer (198) also indicates that HPV is not necessary for
cervical cancer.
6. The hypothesis also fails to explain the presence of clonal chromosome
abnormalities consistently seen in cervical cancer (16, 192-194)-except if
one makes the additional odd assumption that only cells with preexisting
chromosome abnormalities are transformed by HPV.
It follows that neither HPV nor HSV plays a direct role in cervical
carcinomagenesis. Moreover, the HPV-cancer hypothesis offers no
explanation for the absence of a reciprocal venereal male carcinoma.
Thus, detecting inactive and defective viral DNA from past infections in non-tumorigenic
cells with a commercial hybridization test (Vira/Pap, Digene Diagnostics,
Silver Spring, Maryland) or with the PCR (199) seems worthlessas a predictor of
rare carcinomas appearing decades later, in view of the "ubiquity" (191) of
these viruses in women and the total lack of evidence
that cervical cancer occurs in women with HPV more often than in those without.
This test, at $30-150, is currently recommended for the 7 million Pap smears
that appear "atypical" in the U.S. per year (Digene Diagnostics, personal
communication, 1991). By contrast only 13,000 cervical cancers areobserved
annually in both HPV-positive and -negative women in the U.S. (197). Indeed,
the test may be harmful, considering the anxiety a
positive result induces in believers of the virus-cancer hypothesis.
An alternative cervical carcinoma hypothesis suggests that rare spontaneous or
chemically induced chromosome abnormalities, which are consistently observed in
both HPV and HSV DNA-negative and -positive cervical cancers
(192-194), induce cervical cancer. For example, smoking has been
identified as a cervical cancer risk (204). The controlled study of age-matched
women described above suggests that 52% of the women
with cervical cancer were smokers compared to only
27% of those without (198). Indeed, carcinogens may be primary
inducers of abnormal cell proliferation rather than HPV or HSV. Since
proliferating cells would be more susceptible to infection than resting
cells, the viruses would be just indicators, rather than causes of abnormal
proliferation.
Activation of latent retroviruses like HTLV-I (Section III,A) (2), herpes viruses (12), and lambda phages (205) by chemical or radiation-induced cell damage and subsequent proliferation are classical examples of such indicators.
Indeed, Rous first demonstrated that the virus indicates hydrocarbon-induced
papillomas; it "... localized in these and urged them on ..." and
suggested that enhanced proliferation is a risk factor for
carcinogenesis (203).
According to this hypothesis, HPV or HSV DNAs in tumor cells reflect defective
and latent viral genomes accidentally integrated into normal or hyperplastic
cells, from which the tumor is derived. This hypothesis
readily reconciles the clonal chromosome abnormalities with the clonal
viral DNA insertions of the "viral" carcinomas. The inactive and defective
viral DNA in the carcinomas would be a fossil record of a prior infection that
was irrelevant to carcinogenesis.
UNQUOTE
and
http://www.virusmyth.net/aids/data/pdlecture.htm
QUOTE:
Most recently we are saying that cervical cancer in women is due to human
papillomavirus. Ten years ago, it was herpes virus, you remember. There was
just a study at Berkeley. It studied 400 female students on the Berkeley
campus. 250 were papillomavirus positive. In reality, 50% of all women
in this country have these papillomaviruses and men have them too, and the
incidence of cervical cancer is totally independent of it. The
percentage of women with cervical cancer with and without papillomavirus
reflects exactly the percentage of papillomavirus in
this country. No evidence whatever.
UNQUOTE
and
http://www.redflagsweekly.com/second_opinion/2002_nov25.html
QUOTE
Back in 1992, however, a question was raised about the dominant and
increasingly-entrenched theory that HPV causes
cervical cancer. It came from Peter Duesberg and Jody
Schwartz, molecular biologists at the University of California at Berkeley.
Among the various issues they raised about the
acceptance of HPV as the cause of cervical cancer was
their fundamental concern that there was a lack of
consistent HPV DNA sequences and consistent HPV gene expression in tumors that
were HPV-positive. They instead suggested that "rare spontaneous or chemically
induced chromosome abnormalities which are
consistently observed in both HPV and HSV
DNA-negative and positive cervical cancers induce
cervical cancer."
In short, Duesberg and Schwartz were pointing to the possibility that
"carcinogens may be primary inducers of abnormal cell proliferation rather
than HPV or HSV." And here's the key point: "Since proliferating cells
[cancer cells dividing wildly] would be more
susceptible to infection than resting cells, the viruses would just be
indicators rather than causes of abnormal
proliferation."
The concept they raised back in 1992 is still relevant today; only science has
gone on to assume that causation of cervical cancer has been well-established.
Even the National Cancer Institute( NCI) says that
"direct" causation has not been demonstrated; however, the NCI and just about
everyone else works with the principle that it has
been established. Lip service is paid to other
possible factors that may be involved in cervical cancer such as environmental
conditions, including smoking. Even dietary factors -particularly low levels of
Vitamin A and folate - have been suggested as associated with arisk for
cervical cancer.
UNQUOTE
and
http://www.aimoo.com/forum/postview.cfm?id=477113&CategoryID=184164&ThreadID=2
742501
Recently the alarm bells have been ringing about the risks of dying from
Cervical cancer. But HPV, the virus that is blamed for this disease is very
common and can be found in about 80% of both men and women. Most of us
have had, at one time or another, the HPV virus but most of us do not
suffer or die from Cervical cancer. In fact, only one percent of women do
develop cervical cancer with the year 2000 figures on
the mortality rates for cervical cancer being 3.3 women per 100,000 population
in the US and 4 women per 100,000 population in
Australia. In Australia there are about 740 cases of
cervical cancer each year and around 270 deaths from the disease. Mortality
rates generally increase with age with the highest
number of deaths occurring in the 75-79 age group.
Less than 6 per cent of cervical cancer deaths occur in women under 35 years
of age.
The US national cancer institute says that direct causation has not been proven
In a controlled study of age-matched women, 67% of those with
cervical cancer and 43% of those without were found to be HPV-positive.
These cancers are observed on average only 20-50
years after infection.
and finally,
This last tidbit of information about the prevalent use of feminine hygiene
products represents the most likely cause of cervical cancers in women.
The expression of any gene is determined by it's environment. The
long-term use of these chemicals alters the normal
bacterial environment in the uterus, which in turn induces pre-cancerous
lesions in the corresponding tissue cells.
Restoring the normal bacterial balance through the use of douches that don't
contain anti-septic ingredients or other chemicals will allow normal cells to
proliferate again, and force tumor cells into remission. For more information
about the nature of infectious disease and supposed sexually
transmitted diseases, email CFIC@nyct.net
and ask for Rational Bacteriology.pdf (a 2MB email
attachment). --Gary Krasner
http://209.85.165.104/search?q=cache:uJ3tLSdkv5EJ:www.hyde30years.nnaf.org/documents/aawefactsheet1.pdf+papillomavirus+%22feminine+hygiene%22&hl=en&ct=clnk&cd=7&gl=us
Feminine Hygiene Products
. Most doctors and the American College of Obstetricians and Gynecologist (ACOG)
suggest that women steer clear of douching.
. It is estimated that 20-40 percent of U.S. women ages 15-44 douche regularly.
Studies show that African American women douche at approximately twice the rate of Caucasian women. In an AAWE 2001 survey of 300 African American women, over half (52%) of respondents douched. 37% douched at least once per month, and 23% douched more than once per month.
Douching can break down the healthy bacteria or vaginal flora, which serves as the vagina's defense against infections.
Douching can spread existing vaginal infections to the uterus, fallopian tubes, and the ovaries.
Women who douche regularly have an increased risk of pelvic inflammatory disease (PID) and bacterial vaginosis or BV.
Douching can make the vagina more susceptible to STI's.
Douching may increase a women's risk of having an ectopic pregnancy.
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Background information on the vaccine itself (Gardasil):
http://www.vaccineinfo.net/immunization/vaccine/hpv/index.shtml
and
http://www.909shot.com/PressReleases/pr62706gardasil.htm
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