Bacteria likely the missing link between TNF-alpha blocking medications and cancer
Author: Amy Proal13 Jun 2008
This week’s pharmaceutical fiasco? Federal regulators are investigating whether a group of best-selling arthritis drugs made by Abbott Laboratories, Schering-Plough Corp. and other companies heighten the risk of cancer in youngsters.
The drugs under review are called tumor necrosis factor blockers (TNF-alpha blockers) and include Enbrel, Humira, and Remicade. The current uproar over the medications began after the Food and Drug Administration received 30 reports of children and young adults developing cancer while taking the drugs over the last 10 years. Roughly half the cases were lymphomas, a type of immune system cancer. Others reported were leukemia, melanoma and cancers of various organs. The fact that a possible association between TNF-alpha blockers and some cancers has been recognized for years in adults has only heightened the FDA’s concern.
Since increased cancer risk marks just one of the many side effects associated with TNF-alpha blocking drugs, why are children and teenagers taking them in the first place? Sadly, TNF-alpha blockers are currently considered to be the most popular class of medications used to treat children with rheumatoid arthritis, Crohn’s disease, and other autoimmune conditions.
The link between TNF-alpha blockers and cancer has everything to do with the fact that inflammatory diseases such as rheumatoid arthritis and Crohn’s are actually caused by a chronic intraphagocytic microbiota of pathogens. The immune system constantly releases cytokines - proteins that cause pain and fatigue - in response to these pathogens, and TNF-alpha is one of the main cytokines released as part of the response. But since mainstream medicine still incorrectly considers arthritis, Crohn’s and other inflammatory diseases to be “autoimmune” in nature, most researchers have naturally concluded that TNF-alpha medications provide an optimal way in which to palliate what they incorrectly consider to be an over-active immune system response.
In reality, blocking the production of TNF-alpha requires slowing many components of innate immunity, meaning that the drugs are actually just another class of immunosuppressants. Armed with the understanding that “autoimmune diseases” are are actually caused by bacteria, it’s easy to see that while palliative over the short-term, TNF-alpha blocking drugs allow disease-causing pathogens to spread more easily over the long-run.
“Blocking TNF-alpha allows the bacteria to proliferate and produce lots of capnine-like stuff which blocks the Vitamin D Receptor [the receptor that controls innate immune function] and allows cancers to form and metastasize”, explains Marshall.
Consider the fact that cancers including lymphomas are also, almost certainly, the result of infection with a large microbiota of bacteria. It suddenly becomes clear that the increased rate of cancer seen among youngsters or adults taking TNF-alpha blocking drugs is not due to mysterious side effects of the medications, but rather the fact that any person taking a TNF-alpha blocking medication suffers from a decrease in immune function that allows cancer-causing bacteria to spread with greater ease.
In fact, the deleterious effects of TNF-alpha blockers on the innate immune response mean that the latest findings showing increased cancer rates among youngsters taking the drugs are far from the first reports of “side effects” associated with the class of medications. In 2005 Marcel Flendrie and colleagues, from Radboud University Nijmegen Medical Centre in the Netherlands, followed a population of 289 patients who had been undergoing treatment for rheumatoid arthritis with TNF-alpha blocking drugs for a period of one to ten years. The drugs the patients had been taking included two anti-TNF-alpha antibodies, infliximab and adalimumab, and the TNF-alpha receptors etanercept and lenercept.
The results of the study show that 25% of patients on the therapy suffered from a dermatological condition that led them to visit a skin specialist. In a control group of patients who were not undergoing TNF-alpha blocking therapy and had less severe disease only 13% visited a dermatologist during the same period of time.
The most frequent conditions that patients on therapy suffered from were: skin infections - 33 infections were recorded; eczema, which was diagnosed 20 times; and drug eruptions, which occurred mainly at the beginning of the treatment and were important enough for 7 patients to stop therapy. In addition, 12 patients were diagnosed with skin tumour and 9 with an ulcer. In total, 26% of the patients who developed a dermatological condition ceased their treatment due to the condition.
“Dermatological conditions are a significant and clinically important problem in rheumatoid arthritis patients on TNF-alpha blocking therapy” conclude the authors.
This is not to mention the fact that as noted on the CDC website, the FDA has determined that tuberculosis (TB) is a “potential adverse reaction” from treatment with TNF-alpha blockers. The association makes it abundantly clear that TNF-alpha blockers foster the spread of bacteria.
In fact, according to About.com, it turns out that patients taking TNF-alpha blockers are also at greater risk for developing MS and increasingly prone to develop congestive heart failure, as well as “autoimmune and lupus-like problems.” The drugs have been linked to blood problems like pancytopenia (a decrease in production of all blood cell types) and aplastic anemia (complete loss of production of red blood cells). Again, one must wonder: do TNF-alpha blockers mysteriously cause these other diseases, or do they simply facilitate the spread of the bacteria that drive their progression?
While it’s abundantly clear to those who understand the Marshall Pathogenesis - which implicates bacteria in inflammatory disease - that TNF-alpha blockers elicit “side effects” by nothing more than facilitating the spread of bacteria, the FDA is far from grasping this reality.
Instead, the government body plans to spend our tax dollars on several long-term studies to definitively assess the drugs’ potential to cause cancerous “side effects”, particularly in children. The agency has asked drug makers to provide all information about children who developed cancer while taking the medications, and regulators will report the findings of their review by November. The product of such time consuming and costly investigations will result in the following - a potential label on TNF-alpha medications saying the drugs may increase the risk of cancer. A true step forward for the medical community? Sadly not.
Meanwhile, the TNF-alpha blockers continue to generate large profits for the companies that make and market them. Considering that Abbott’s Humira was the company’s best-selling product last year with over $3 billion in sales, and Remicade also topped Schering-Plough’s portfolio with sales of $1.65 billion, there is little hope that such companies will be willing to embrace a true understanding of how their drugs foster the development of chronic disease.
Note: While Olmesartan reduces levels of TNF-alpha, it does so by blocking the generation of the substance in the first place rather than blocking its release after it has been produced. So Olmesartan is effective at palliating immunopathology, but does not cause the immunosuppression generated by TNF-alpha blockers.
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About Amy Proal
Amy Proal graduated from Georgetown University in 2005 with a degree in biology. While at Georgetown, she wrote her senior thesis on Chronic Fatigue Syndrome and the Marshall Protocol.
She has written for several publications and organizations including FibromyalgiaAWARE magazine, Immunesupport.com, Volta Voices magazine, and the National Policy Research Council.
Amy has Chronic Fatigue Syndrome and has been on the MP since April 2005. She is thrilled with her progress and looks foward to helping people better understand the treatment that is restoring her health.
Contact Amy at amy dot proal at gmail.com.
4 Responses for "Bacteria likely the missing link between TNF-alpha blocking medications and cancer"
Hi,
I really admire Dr. Marshall and I’m considering giving the MP a shot. However, allow me to play devil’s advocate for a moment. How can we be certain that the inherent anti-inflammatory properties of Benicar and the tetracyclic antibiotics aren’t responsible for putting people into remission? Why is blocking the release of TNF-alpha immunosuppressive, but blocking it’s generation (as you state to be the case with Benicar) not immunosuppressive?
I am concerned about this. I was on the tricyclic antidepressant amitriptyline for four years to help with chronic pain. While it did help with symptom control, my health really deteriorated while I was on it. I believe this is because amitriptyline, like many so-called “psychotropic” medications, has rather profound immunosuppressive properties. Like the medications mentioned in this article, it suppresses TNF-alpha release, albeit most certainly to a lesser degree. Nevertheless, I did develop a couple of internal cysts while on it and also had some skin issues.
Thanks,
Paul
Hi Paul,
I am glad you are researching the Marshall Protocol. I am extremely confident that Benicar and the antibiotics are not putting people into remission. That’s because during the vast majority of the time that MP patients are take the antibiotics and Benicar they feel worse, often much worse.
If Benicar works as an immunusuppressant, and the antibiotics work in the palliative manner - as they do when taken in high, multi-daily doses - then at atmosphere of relief would be created during the MP. The patient would feel better.
Instead, people on the MP face years of difficult immunopathology before reaching a state of remission. The anti-inflammatory properties of Benicar only help patients manage the bacterial die-off reaction to a certain degree. Instead, Benicar’s primary job is to serve as a VDR-agonist (a drug that strongly activates the Vitamin D Receptor). So it’s main action is stimulating the immune response and facilitating bacterial death.
Immunopathology is very difficult for MP patients. Antibiotics must be ramped over the course of years, often up to five or six years in cases of severe illness so that the patient can manage the die-off. Believe me, there is no palliation going on during the MP.
Furthermore, the MP antibiotics were specifically chosen via molecular modeling data from the Max Plank Institute in Germany so as to be administered at concentrations that essentially null the immunosuppressive effects they possess at high doses. For example, one of the phase II antibiotics is only taken every 10-14 days. That’s very low dosing with little possibility for immunosuppression. This article describes how the MP antibiotics were chosen in greater detail and would be a good read:
http://bacteriality.com/2007/10/11/antibiotics/
Finally, there is absolutely a difference between blocking a substance after it has already been created and blocking the creation of a substance in the first place. Once TNF-alpha has been created and released, blocking it’s actions unfortunately require blocking many other components of innate immunity. Hence the immunosuppression.
But Benicar has a subtle effect that causes less TNF-alpha to be created in the first place. If TNF-alpha is never produced, it never has to be blocked, and the innate immune response never has to be blocked. TNF-alpha is a potent inflammatory cytokine so having a little less of it around thanks to Benicar allows the patient to tolerate their immunopathology a little bit more easily, yet the strength of the rest of their immune response stays the same.
Hope this helps!
Best,
Amy
Hi Amy,
Thanks for the detailed response. It does help assuage some of the fears I have about being on medication again. Do you know if any patterns have emerged that might help predict how much immunopathology one might expect to face while on the MP. For instance, is length of illness or severity of debility more likely to impact one’s immunopathology?
Thanks,
Paul
Hi Paul,
Sorry for the delayed response. Yes, there are patterns that can predict the severity of immunopathology to a certain degree. The first thing to keep in mind is that bacterial load very often correlates with how long a person has been ill. Generally patients that have been sick for decades have accumulated larger bacterial loads, whereas those who start the MP closer to their time of diagnosis often have lower bacterial loads and thus deal with lower levels of IP.
Patients who have taken large amounts of immunosuppressive medications or steroid medications such as prednisone generally also have bacterial loads that have spread to a greater extent. So such patients usually experience stronger immunopathology. Of course, since dietary vitamin D is a secosteroid in its own right, anyone who has a long history of supplementing with vitamin D can generally also expect to have a higher bacterial load and thus stronger immunopathology when they begin the MP.
Many patient say that the level of their immunopathology doesn’t become too much worse than their disease symptoms in the first place, although there are definitely exceptions. To be more specific, I mean that most people find that if they can work before the MP they can generally still pull off working while on the treatment.
So there are a few clues that might allow you to predict what your immunopathology may be like. However, it’s often very hard for people to estimate bacterial load before the MP. Patients are often surprised that they get immunopathology in areas they didn’t even realize were infected.
So it’s really only after you start Benicar and minocycline that you will be able to get the most accurate impression of the immunopathology and light sensitivity that you will be dealing with.
So I hope you can start the MP soon!
Best,
Amy
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