The drug etanercept binds to TNF-alpha to block its action on the immune system.

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.

This week, in a study published in the New England Journal of Medicine, Dr. Thomas Platts-Mills of the University of Virginia and colleagues looked at reports of patients who experienced what they believe are severe allergic reactions to the cancer drug Erbitux. The drug, which is widely used — it had global sales of $1.1 billion in 2006 for use in treating colon, head and neck cancers — is a monoclonal antibody, a genetically engineered immune system compound designed to home in specifically on cancer cells.

The team tested 538 people, including 76 cancer patients who got Erbitux in Tennessee, Arkansas and North Carolina and healthy volunteers from Tennessee, California and Boston in order to gauge their reaction to the drug. Of the 76 cancer patients, 25 developed what were labelled “hypersensitivity reactions.”

Data revealed that the number of patients to develop a reaction to Erbitux varied depending on location. Platts- Mills and team found that as 22 percent of patients treated with Erbitux in Tennessee and North Carolina reported some kind of reaction, including anaphylaxis, which can rapidly lead to difficulty breathing, shock or fainting. Some of the reactions were described as life threatening. Even higher rates were reported from parts of Arkansas, Missouri and Virginia. But fewer than 1 percent of patients treated in the Northeast reported any reactions.

Unable to explain their results, the research team realized that ticks and other insects are more common in the states in which patients negatively react to Erbitux at higher rates. Although the team hypothesized that tick bites might generate antibodies that could cause an “allergic reaction” to Erbitux, a more likely explanation is that patients who get enough tick and other insect bites harbor greater numbers of the Th1 pathogens.

Contrary to mainstream thinking, ticks and other insects are able to transmit many more bacterial species then simply Borellia. Thus, people who get tick bites are more likely to accumulate a variety of Th1 pathogens – bacteria that proceed to create ligands that block the Vitamin D Receptor and subsequently the activity of the innate immune system.

Of the many people who are bitten by ticks on a daily basis, only a fraction of people report a bite that causes them to develop a rash and an array of debilitating symptoms usually labelled as Lyme disease. According to biomedical researcher Trevor Marshall, it is the state of the innate immune system that determines whether people who are frequently exposed to ticks develop such a reaction after a bite.

“Most people who are bitten by ticks don’t even realize it,” states Marshall. But a portion of the people bitten by a tick have already accumulated enough Th1 pathogens so that their innate immune systems are simply unable to deal with the new influx of pathogens from the bite. These are the people who develop a rash and become symptomatic after an insect bite – they are already immunocompromised, and their symptoms are an indication of the fact that their innate immune systems have lost the ability to deal with a new invading pathogen.”

Could this same phenomenon explain why those people who live in states with greater insect populations are more likely to develop a reaction to Erbitux? If a person accumulates enough L-form bacteria due to numerous insect bites, their innate immune system becomes increasingly impaired. If they proceed to develop cancer – a disease that also begins to destroy innate immune function – would those individuals with previously weakened innate immune systems find it much harder to handle the antibody introduced by Erbitux, leading to an immune reaction?

Sure, further research must be conducted to determine exactly how Erbitux might react with cancer causing bacteria in a way that causes immunocompromised people to develop such violent symptoms. But it seems logical that the state of the innate immune system is what determines whether or not a patient can tolerate the Erbitux antibody.

Will further research be done? Probably not in the near future, as mainstream researchers would be hard pressed to believe that such a great proportion of the population is infected with such high quantities of the Th1 pathogens, or that these bacteria affect the pathogenesis of cancer. Still, those of us who know how rampant the Th1 pathogens are can take a good look at this research and see that unfortunately, it confirms just how drastically their effects on the immune system impact all areas of medicine.