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Human Papilloma Virus may not be the Cause of Cervical Cancer


In June 2006, the FDA approved a new vaccine from Merck for the prevention of cervical cancer, which is thought to be caused by the Human Papilloma Virus. Under a new 'rapid approval' process, it took the FDA only 6 months to complete the evaluation of the vaccine and authorize it for the market.

"This vaccine is a significant advance in the protection of women's health in that it strikes at the infections that are the root cause of many cervical cancers," said Andrew C. von Eschenbach, MD, then Acting Commissioner of Food and Drugs, according to an FDA statement on the approval of this new vaccine.

Despite lingering doubts as to the exact genesis of cervical cancer, and despite a distinct lack of evidence that the vaccine will indeed be a useful preventive tool, Merck lobbied heavily to make the Human Papilloma Virus (HPV) vaccine mandatory for girls all over the United States. Texas governor Rick Perry's move to make the vaccine mandatory in his state drew heavy criticism, not to mention allegations that pharma money may have played a role in making this decision.

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? Gary Krasner thinks there may be other causes and that vaccinating every girl would be a waste, if not a danger because the real cause - antibacterial douches that tend to destroy the natural balance of flora in the vagina - tends to get covered up.

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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 worthless as 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 are observed 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 a risk 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 its 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

African American women and Reproductive Health

Feminine Hygiene Products

o Most doctors and the American College of Obstetricians and Gynecologists (ACOG) suggest that
women steer clear of douching.

o It is estimated that 20-40 percent of U.S. women ages 15-44 douche regularly.

o Studies show that African American women douche at approximately twice the rate of Caucasian women.

o 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.

o Douching can break down the healthy bacteria or vaginal flora, which serves as the vagina's
defense against infections.

o Douching can spread existing vaginal infections to the uterus, fallopian tubes, and the ovaries.

o Women who douche regularly have an increased risk of pelvic inflammatory disease (PID) and
bacterial vaginosis or BV.

o Douching can make the vagina more susceptible to STI's.

o Douching may increase a women´s risk of having an ectopic pregnancy.


Background information on the vaccine itself (Gardasil):



Gary Krasner, Director
Coalition For Informed Choice
188-34 87th Drive, suite 4B
Holliswood, NY 11423

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