Tuesday, January 10, 2017

Brain cancer, the monkey virus, and the study fraught with errors

In my last blog, we reviewed extensively how the SV40 monkey virus acts as a destructive carcinogenic force at the cellular level.  During this blog, we are going to examine a case study as well as potential sources of the SV40 virus.  Where could we possibly be exposed to a monkey virus?

A young boy, by the name of Alexander (1), was diagnosed with brain cancer when he was only 2 years old.  First, he endured brain surgery.  After surgery, his parents flew to see Dr. Burzynski at The Burzynski Clinic in Texas only to be told that they could not use his treatments because they were not FDA approved.  Instead, they were forced to use chemotherapy prior to using the treatments from Dr. Burzynski.  Only after completing all the chemotherapy recommended by their oncologist, could they pursue Dr. Burzynski, the treatment that they preferred as a couple.

After only 3 treatments of chemotherapy, the cancer spread and the doctors found 30 new tumors in Alexander's little body.  Thus, Alexander did not survive long enough to take the treatments recommended by Dr. Burzynski.  The research surrounding the clinical effectiveness of chemotherapy in cases of medulloblastoma resounds as an abysmal failure. Firstly, the blood-brain barrier acts as a protective mechanism in the brain and blocks the absorption of cytotoxic chemotherapy agents (2).  In a peer-reviewed study, chemotherapy was compared to not using chemotherapy, and there was no evidence of effect in regards to chemotherapy agents in medulloblastomas compared to no treatment at all (3).  In fact, in one analysis of the effectiveness of chemotherapy on 22 types of cancers, the SEER report from 2004, found that brain cancer survival rate is only 4.9% five years after diagnosis (4).

Alexander's parents were devastated to lose their only son and searched endlessly for answers.  In their research, they discovered that some tumors develop in the body because of complications from viral infections.  In medulloblastoma tumors, the ingestion period for a viral contaminant would be about 7 months.  The only thing that Alexander had been exposed to 7-8 months prior to first signs of the brain tumor was his oral polio vaccine.  Surely this could not have been the source?

A quick search on the CDC website, one can find all the ingredients of a vaccination.  Here are the following ingredients within the polio vaccine:

2-phenoxyethanol, formaldehyde, neomycin, streptomycin, polymyxin B, monkey kidney cells, Eagle MEM modified medium, calf serum protein, Medium 199 (5)

One may wonder, monkey kidney cells in the polio vaccine?  Why?  Viruses need living cells to reproduce themselves.  Thus, in preparation of vaccinations, a variety of living tissue is used to multiple the virus.  Vaccinations use a variety of cell lines in which to grow the viruses including, but not limited to, egg, monkey kidney cells (as in the polio vaccine), and aborted fetal tissue.  When the polio vaccine was first developed, the main producers of this vaccine were focused on using rhesus monkey kidney cell lines for the growth of the virus.

Polio is contracted through the mouth, nose, or shed polio virus through feces (can be infected through changing a diaper or poor hygiene).  Most polio strains are absolutely harmless and the symptoms include a mild, cold-like illness with headaches, chills, and a low-grade fever.  However, in about 2% of the cases, a virulent strain of polio can travel from the gut to the central nervous system and attack the brain and spinal cord leading to paralysis.  In 1994, America became certified polio-free and yet, 5 shots are typically required for polio immunizations.

When the polio vaccine was first manufactured, rhesus monkey kidney cells were chosen primarily because of easy access to the kidneys.  The drawback of using monkey kidneys is that they tend to be full of pathogens, bacteria, viruses, and toxins.  There is a reason why offal from kidneys are not typically consumed.  Monkey kidneys specifically are loaded with dormant viruses. The reason that monkey kidneys tend to be contaminated with viruses is because of the main role of the organ in the body.  Kidneys help to metabolize Vitamin D in the body, manufacture erythropoietin, a chemical substance that stimulates red blood cell production, and act as a sewage plant for the body's circulating blood.  In fact, 425 gallons of blood are processed daily through the kidneys.  Everything contaminated in the blood is removed by the kidneys, including parasites, bacteria, unknown viruses, and microorganisms.

Bernice Eddy was a researcher when the polio vaccine was first released to the public.  She conducted a major experiment to determine potential side effects coming from the rhesus kidney cell extract.  She did this by freezing rhesus kidney cell cultures, grinding them up, and injecting them into newborn hamsters.  In the control group, she injected hamsters with feline and human tumor extracts.  None of the control group developed any abnormalities while 70% of the 154 hamsters exposed to the monkey kidney cells developed tumors.  Immediately, she alerted her boss to the findings of her study.  She also published her study and spoke in one conference regarding her results. Because of Eddy's research, other researchers began to conduct experiments to explore the potential carcinogenic effect of the rhesus kidney cells from the original polio vaccine.  Eventually, it was discovered that the carcinogenic affect was most likely coming from a virus that was named the SV40 virus.  In 1963, a basic population study was designed and enacted called The Fraumeni Study.  The results of this study concluded that the SV40 virus was cancerous to animals, but not to humans.

However, the study was fraught with errors and potential problems, including:
  • The study only followed children for 4 years after they had been inoculated by the polio vaccine.  Many cancers take more than 4 years to develop.  For example, cancer from asbestos exposure can take 20-40 years to develop. 
  • The study failed to detect small differences in cancer rates as caused by SV40
  • Only 3 types of cancer were surveyed:  brain, kidney, and connective tissue
  • Cancer was defined by cancer deaths, not diagnosis
  • During the 1960's, cancer was misdiagnosed many times
  • It was impossible to define who was exposed to SV40 and who was not
Even with the clear and apparent errors, this one study shoved the entire theory of the SV40 virus from the polio vaccine causing cancer under a rug for many years.  Many researchers continued to study the SV40 virus and how it could potentially link to human tumors.  In fact, there have been over 80 published studies connecting the SV40 virus to human tumors. 

In the case of Alexander, more than 30 years after the original release of the polio vaccine, his brain tumor was tested for the presence of SV40.  The testing did find SV40 within the brain tumor and found it to be cancer causing.  To find the potential source of the SV40 virus, both parents were tested for antibodies to the SV40 virus and neither matched as a potential source.  Further, the cord blood from pregnancy was also tested and found free of the SV40 virus.  The only other potential source was from the contaminated polio vaccine.

In 2000, Alexander's parents sued the Pharmaceutical company who produced the oral polio vaccine that their son received.  A leading SV40 researcher and expert, testified that the source of the SV40 was most likely from the oral polio vaccine that was given to Alexander when he was two years old. Despite all of the evidence, the court did not rule in favor of Alexander's parents.  The concern over SV40 exposure and the polio vaccine continues even today and for some researchers and SV40 experts, not enough has been done to ensure that the American public are protected against this cancer-causing monkey virus.  Justice has yet to be done.


1.  http://www.sv40foundation.org/alexander.html#_edn15
2.  https://www.ncbi.nlm.nih.gov/pubmed/82907
3.  https://www.ncbi.nlm.nih.gov/pubmed/25879092
4.  https://www.ncbi.nlm.nih.gov/pubmed/15630849
5.  https://www.cdc.gov/vaccines/pubs/pinkbook/downloads/appendices/B/excipient-table-2.pdf

Wednesday, January 4, 2017

How Modern Life creates cancer

In the fight to understand cancer, there are thousands of potential carcinogens to start to become familiar with in our modern world.  We are exposed to carcinogens every day of our lives.  However, in a healthy body, with a strong immune system, balanced gut flora, emotional intelligence/overcoming trauma, and a clean diet, our bodies have an amazing capacity to defend itself from daily carcinogenic exposures.

One of the potential carcinogens that I want to begin to review is the viral influence on the development of cancer in the body.  There are a handful of viruses that have been linked to cancer in research literature including, Hepatitis B and C, HPV, HTLV-1 (Human T-cell Lymphotropic virus type 1), and SV40.

Viruses have the potential of triggering a cascade of effects on the cellular level which in an immune-compromised, deficient, imbalanced host environment, can lead to the development of cancer. Viruses enter a cell and start replicating by overtaking the DNA of the cell, making literally thousands of copies of itself.  When the cell becomes so full of the virus, it may break open spilling all the contents and the viral copies into the body of the host.  A progression of viral invasion ensues with all the copies of the virus invading neighboring cells and the cycle continues.  This process will cause the person to become ill, but may not lend itself towards the development of a tumor.

Genetic factors play a role in the development of cancer.  Tumor suppressing genes must be mutated and oncogenes must be expressed for cancer to develop in the body.  One vital tumor suppressing gene is p53.  In fact, it has been estimated that 50-60% of all cancers involve damage, mutation, or inactivation of the p53 gene.  If p53 is not functioning properly, a cell with altered DNA may undergo mitosis instead of dying and the cell may start to reproduce wildly.  The p53 gene regulates mitosis, the process of cellular division.  During cellular division, if damage to the DNA is detected, mitosis is paused while the damage is fixed.  If the damage cannot be repaired, the cell undergoes apoptosis or programmed cell death.  If the damage is repaired, then the cell will reproduce a daughter cell before going through apoptosis.  Rbs is another important regulatory gene which is involved in protecting the cell from becoming oncogenic by acting as the final gatekeeper in cellular division.  If p53 does not express properly during the potential mitosis of a damaged cell, Rbs becomes the last line of defense to stop the damaged cell from dividing.

During cellular division, another control mechanism to dissuade the cell from becoming an immortal cancer cell is telomeres.  Telomeres were first discovered by Leonard Hayflick in the 1960s and the lifespan of the cell became known as the Hayflick limit.  Telomeres are microfibers at the end of chromosomes and shorten each time the cell divides.  When a cell divides, part of the telomere shortens and after many cellular divisions, the cell must go through apoptosis.  This protects the body and inhibits the cell from becoming immortal, one characteristic of a tumor cell.

For a virus to have a bigger impact than simply weakening or distracting the immune system and causing the person to be sick, fundamental changes in the genetic expression of the cell must be influenced by other carcinogenic factors.  The following environment must be created:  p53 must be inactivated, tumor oncogenes must be activated such as Notch-1 and Met, chromosomal damage must be induced, and telomerase must be stimulated.  Telomerase is an enzyme which allows telomeres to be lengthened every time the cell divides instead of becoming shortened, which leads to the immortality of the cancer cell.

One virus that I want to delve into today would be the impact of SV40 or Simian Virus 40.  SV40 was first discovered in a rhesus monkey kidney cell.  SV40 has been shown in molecular research to be a carcinogen that can act alone in initiating cancer in the body.  Most carcinogens need to act in tandem whereas SV40 is able to do the following in one fatal swoop:  1.  Blocks Rbs and p53 tumor suppressor genes  2.  Activates Notch-1 and Met oncogenes  3.  Alters/damages DNA  4.  Induces telomerase activity to allow immortality of the cells influenced by SV40.

Carbone is an Italian researcher that has extensively tested tumors for the presence of SV40, finding it in some cases.  He also discovered how a large T-antigen molecule within SV40 strangles p53 and other tumor suppressor genes in mesothelial cells.  Mesothelial cells contain very high amounts of p53, 4-5 times the amount within fibroblast cells.  Thus, the SV40 virus acts differently within fibroblast cells and does not lead to the development of cancer.  Within the p53-rich mesothelial cells, the large T-antigen binds with p53 and slows the pace of the SV40 replication which keeps the cell intact and the mesothelial cells can start dividing uncontrollably as all the other factors are triggered by SV40:  p53 and Rbs are switched off, oncogenes are turned on, DNA becomes damaged, and telomerase activity becomes stimulated.

There have been 25 new studies from 1997-2003 demonstrating SV40 in human pleural mesotheliomas (a rare lung cancer).  Further, there have been 80 published studies total connecting SV40 to human tumors, including brain, lymphoma, bone, lung, and non-Hodgkin's lymphoma.  Butel is a well-known researcher and did a meta-analysis of all the studies done on cancer and the SV40 virus and found the following odds ratio:  Lymphomas:  5, Brain:  4, Mesotheliomas (lung):  17, Bone:  25.  A meta-analysis of smoking and cancer demonstrated the odds ratio of 10 when all the studies where analyzed.

Exposure to viral carcinogens such as SV40 can take many years to express, depending upon the age of the person exposed.  For example, a child who is exposed to SV40 may develop a tumor within 7 months whereas an adult who is exposed may not develop a tumor for many years.  In my next blog, I will explore a case study of exposure to SV40 as well as potential sources of exposure to the SV40 virus.







Bookchin, Debbie & Schumacher, Jim. The Virus and The Vaccine.  2004.