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:
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.

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.

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.

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 and ask for Rational Bacteriology.pdf  (a 2MB email attachment).  --Gary  Krasner

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):