Alternative models for chronic disease

Autoimmune diseases are thought to arise from an overactive immune response of the body against substances and tissues normally present in the body. The autoimmune disease theory has yet to present a satisfactory reason, evolutionary or otherwise, why an immune system would attack human tissue.

Conversely, the Marshall Pathogenesis explains that so-called “autoantibodies” are merely antibodies generated in response to pathogenic bacterial cells that have been destroyed as a result of an active immune response.

At least forty different chronic diseases are suspected or accepted as being caused by an autoimmuneA condition or disease thought to arise from an overactive immune response of the body against substances and tissues normally present in the body response.

Co-infections – such as Candida, Mycoplasma, Rickettsia, Mycobacteria, Bartonella, Babesia, HHV-6, the Epstein Barr virus, the Herpes virus - are commonly detected in people with Th1 disease. However, these pathogens are not driving the disease process. They simply “come along for the ride”, generating extra symptoms in people with inflammatory disease, because of the fact that people infected with L-form bacteria are, for the most part, severely immunocompromised.

The Th1 pathogens that underly the disease create ligands which are able to bind and block the Vitamin D ReceptorA nuclear receptor located throughout the body that plays a key role in the innate immune response. – a fundamental receptor of the body that controls the activity of the innate immune system and the production of the antimicrobial peptidesBody’s naturally produced broad-spectrum antibacterials which target pathogens., proteins that kill bacteria, viruses, and fungae by a variety of mechanisms including disrupting membranes, interfering with metabolism, and targeting components of the machinery inside the cell. Thus, as more and more L-form bacteria accumulate, the body is left without tools to fight other pathogens that enter the body.

“The fact is, when the VDRThe Vitamin D Receptor. A nuclear receptor located throughout the body that plays a key role in the innate immune response. is not functioning properly, and the innate immune system is overwhelmed by Th1 pathogens, then it cannot properly deal with co -infections which would otherwise be trivial for it to manage,” states the MP study site. “When the body is weakened by these Th1 diseases, co-infections are very common, as the immune system is ‘busy’ dealing with the pathogens which have parasitized the phagocytes (white blood cells) and can’t deal as effectively with the opportunistic infections.”

It’s analogous to “being seen at the scene of the crime but not actually committing it,” states Marshall. “The viruses, etc. are only co-infections, because the body’s immune system has been weakened by the Th1 pathogens, and is unable to fight the infection.”

But as people reach the later stages of the MP, they have killed off most of the bacteria that were previously creating VDR-blocking ligands. Because they have been avoiding vitamin D, 25-DThe vitamin D metabolite widely (and erroneously) considered best indicator of vitamin D "deficiency." Inactivates the Vitamin D Nuclear Receptor. Produced by hydroxylation of vitamin D3 in the liver. is also no longer blocking the VDR. This means that their immune systems regain strength – vigor that allows their bodies to tackle co-infections that are unable to survive in the face of a functional immune system. The antimicrobial peptides (the body’s natural antibiotics) are produced again, making it even harder for co-infections to persist.

“Once the immune system is no longer under challenge, it will be able to cope with opportunistic infections,” states Marshall. “The MP is designed to allow your immune system to function and eventually kill all chronic infections, no matter what label has been put on any suspected infection. Once the Th1 bacterial pathogens are killed off, the immune system deals with the viruses it couldn’t clear while the bacteria were present. That’s why folks lose warts and other things as they recover on the MP.”

“Wait and see!” he continues. “A healing immune system is no longer ‘out of sync’ with the world, but copes normally with the various things life throws at it, instead of over-reacting.”

“ Once the immune system is no longer under challenge, it will be able to cope with opportunistic infections.”Mainstream medicine emphasizes the role of co-infections rather than the Th1 pathogens in chronic disease because while the pathogens that cause co-infections show up on laboratory tests, L-form bacteria do not. Thus, unaware of the tremendous amount of L-formDifficult-to-culture bacteria that lack a cell wall and are not detectable by traditional culturing processes. Sometimes referred to as cell wall deficient bacteria. and biofilmA structured community of microorganisms encapsulated within a self-developed protective matrix and living together. bacteria that their patients harbor, most doctors and researchers fail to understand the role these pathogens play in the disease process and incorrectly attribute all symptoms to co-infection instead.

“The issue is that the infections which can be easily detected in Th1 patients are co-infections, and not the cause of their illness,” states Marshall. “The Th1 pathogens hide so well that no antibodies are generated, and even molecular tools have difficulty detecting the traces of DNA from host-phagocyte apoptosis (bacterial death). The most dangerous and successful pathogens are the ones which are intra-cellular, and therefore do not show up on routine testing. These co-infections are not going to make you as ill as the Th1 pathogens.”

Many researchers have long argued that most chronic diseases are caused by humans' genetic predisposition for a condition. However, despite ambitious efforts, there is substantial evidence that chronic diseases are not caused by human genes.

According to the Marshall Pathogenesis, humans accumulate a plethora of pathogenic bacteria during their lifetimes, and it is the genetic mutations which result from active infection that play a major role in what is commonly thought of as “genetic susceptibility.”

The chronic inflammatory diseases treated by the Marshall Protocol (MP) never go away on their own. It’s not that patients with Th1 disease can’t and won’t go through periods where they might feel better. Unfortunately, these periods are usually a sign that the immune system has become severely compromised.

Whether temporary “remission” is driven by immunosuppressive drugs like corticosteroids, a high intake of vitamin D, excessive sun exposure, or simply the accumulation of a bacterial load that is so high that the VDR is almost completely shut down by bacterial ligands – these periods are times when the Th1 pathogens are alive and well, spreading, and surely infecting other tissues. This unchecked infection leads to illnesses that will only be discovered later in life such as arthritis, heart disease, decreasing kidney function, diabetes, cancer and even the diseases of aging. But during the “remission period,” when the immune system is not capable of killing the pathogens, there is no corresponding inflammatory response that would be occurring if the body was mounting a defense against the infection. This causes the patient to feel a sense of temporary relief during immune suppression that is often mistaken for “wellness.”