What Exactly Is Cervical Cancer?
Cancer begins in cells, the building blocks of tissue which make up the organs. Normally, cells grow and divide to form new cells as the body needs them. When cells grow old, they die and are replaced with new cells. The problem comes in when abnormal cells “appear” and start multiplying. The abnormal multiplications form masses resulting in growth or tumors.
The National Cancer Institute estimates that Cervical cancer, in the lining of the cervix, will affect about 11,270 women in the U.S. each year. Cervical cancer occurs at an average age of 54. About 4,000 die. Worldwide, a half million get the disease and 225,000 die.
In the 1970s, herpes simplex virus (HSV) was touted as the cause of cervical cancer. This based on population studies that showed a correlation of the disease with HSV dna.
The blame shifted to human papillomavirus (HPV) in the 1980′s.
The HPV is a group of more than 100 viruses. About 30-40 of which are supposedly linked to cervical cancer.
Of these 30 or so, HPV-16 is said to be found in 50% of cervical cancers. HPV-18 supposedly accounts for 20%.
In 1992 molecular biologists of the University of California at Berkely, Peter Duesberg and Jody Schwartz, questioned the theory that HPV causes cervical cancer. They were concerned about the lack of consistent HPV DNA sequences and consistent HPV gene expression in tumors that were HPV-positive. They said quite possibly “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.”
Since 2003 even the FDA has been well aware that the human papillomavirus (HPV) does NOT cause cervical cancer. They acknowledged this fact in their statement March 31st 2003, “most infections by HPV are shortlived and not associated with cervical cancer. Most women who become infected with HPV are able to eradicate the virus and suffer no apparent long term consequences to their health.” Repeated transient HPV infections even when caused by high risk types of HPVs are characteristically not associated with an increased risk of developing squamous intraepithelial lesions, the precursor lesion of cervical cancer.
According to the New England Journal of Medicine, women face an increased risk of cervical cancer if their mothers took the world’s first synthetic female hormone during pregnancy. These women were known as ‘DES daughters’ because their mothers took diethylstilbestrol (DES) and labeled to have higher rates of infertility and miscarriages. DES has also been linked to a higher risk of developing a relatively uncommon type of cancer at an early age, known as clear-cell adenocarcinoma of the vagina and cervix.
Current guidelines from the American College of Obstetricians and Gynecologists suggest that most women should have annual Pap tests. The American Cancer Society guidelines suggest that screening less frequently than every year might be adequate for women who have had three negative annual tests. CDC backs this up by warning in a 2000 weekly report (MMWR), that women who get annual pap smears may receive no benefit over women who are tested less frequently. They even say it may in fact be causing harm since frequently tested women may also be at increased risk of unnecessary treatment and anxiety.
“Many times, especially for low-grade abnormalities, there’s a lot of false positives (results which appear positive, but are in fact negative), and women may be biopsied and receive other treatment because of the Pap test result,” Dr. Mona Saraiya from the CDC told Reuters Health. “These symptoms might have gone away if we’d left (the women) alone,” she added. “”There needs to be more research to show what actual harmful morbidity is associated with an abnormal Pap.”
The [CDC] researchers concluded that “Women who were screened annually rather than less frequently might have worse health outcomes if low-grade results of undetermined clinical importance lead to further testing and unnecessary patient morbidity and anxiety”. Thus the reason for recommending pap screenings once every three years only.
Dr. Nancy Lee is the Associate Director for Science, within the Division of Cancer Prevention and Control of the National Centers for Chronic Disease Prevention and Health Promotion, Centers for Disease Control and Prevention (CDC) in Atlanta, Georgia. She testified before the House Committee March 16, 1999 that the incidence rate for all U.S. women is about 8 per 100,000 and that cervical cancer rates have [already] been dropping for several years. The cervical cancer death rate declined 45 percent between the periods 1972-74 and 1992-94 and the overall incidence of the disease has decreased steadily from 14.2 per 100,000 in 1973 to 7.4 per 100,000 in 1995. According to the American Cancer Society, “Between 1955 and 1992 the number of cervical cancer death in the united states dropped by 74%”
Most young adults who have been sexually involved and exposed to HPV naturally clear the virus from their body, thus going on to live normal healthy lives. Deaths associated with cervical cancer are very low on the totem pole of leading cancer killers for women with lung cancer at 68,000 deaths annually, breast cancer at 42,000 deaths, colorectal cancer at 29,000 deaths, ovarian cancer at 14,000 deaths, skin cancer at 9,600 deaths, and uterine cancer at 6,500 cancer deaths. Pap smears potentially prevent nearly 100% deaths caused by cervical cancer.
One can only ask why Merck and CDC are pushing for a vaccine when the war against cervical canc already a success story.
The New England Journal of Medicine – June 22, 2000 – Vol. 342, No. 25
Testimony on Cervical Cancer by Nancy C. Lee, M.D. http://www.hhs.gov/asl/testify/t990316b.html
CDC Morbidity and Mortality Weekly Report 2000;49:1001-1003
http://vaers.hhs.gov VAERS (vaccine adverse events reporting system) 2006 database
Daily Press.com, Kimball Payne, Feb.11, 2007
JAMA Vol. 297 No. 8 February 28, 2007
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