Introduction to the Marshall Pathogenesis

The Marshall Pathogenesis, upon which the Marshall Protocol is grounded, is a description for how bacteria interfere with the innate immune response. These pathogens survive and reproduce by disrupting the Vitamin D Nuclear Receptor, an evolutionarily consistent mechanism for survival, which leads to the development of chronic inflammatory diseases. Because these diseases are fundamentally bacterial in nature, the conditions are referred to as the “Th1 diseases.” The Marshall Pathogenesis is supported by an emerging array of evidence, including clinical evidence, evolutionary evidence, some in silico data, and environmental sampling studies.

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Microbes in the human body

According to a recent National Institutes of Health (NIH) estimate, 90% of cells in the human body are bacterial, fungal, or otherwise non-human.1) Although many have concluded that bacteria surely enjoy a commensal relationship with their human hosts, only a fraction of the human microbiotaThe bacterial community in the human body. Many species in the microbiota contribute to the development of chronic disease. has been characterized, much less identified. The sheer number of non-human genes represented by the human microbiota – there are millions in our “extended genome”2) compared to the nearly 23,000 in the human genome – implies we have just begun to fathom the full extent to which bacteria work to facilitate their own survival.

The NIH's ongoing initiative, the Human MicrobiomeThe bacterial community in the human body. Many species in the microbiota contribute to the development of chronic disease. Project, aspires to catalog the human microbiome, also referred to as the human metagenome. Emerging insights from environmental sampling studies have shown, for example, that in vitroA technique of performing a given procedure in a controlled environment outside of a living organism - usually a laboratory. based methods for culturing bacteria have drastically underrepresented the size and diversity of bacterial populations. One environmental sample of human hands found 100 times more species than had previously been detected using purely culture-based methods. Another study which also employed high throughput genomic sequencing discovered high numbers of hydrothermal vent eubacteria on prosthetic hip joints, a species once thought only to persist in the depths of the ocean.

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Th1 Spectrum Disorder

Main article: Th1 Spectrum Disorder

Th1 Spectrum DisorderThe overlap of different disease symptoms in different patients with similar diagnoses - caused by the fact that any one bacterial species can contribute to numerous disease states. refers to the group of chronic inflammatory diseases, which are hypothesized to be caused by the Th1 pathogensThe community of bacterial pathogens which cause chronic inflammatory disease - one which almost certainly includes multiple species and bacterial forms., a microbiota of bacteria which include 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., biofilm A structured community of microorganisms encapsulated within a self-developed protective matrix and living together., and intracellular bacterial forms. Although the exact species and forms of bacteria, as well as the location and extent of the infection, vary between one patient suffering from chronic disease and the next, the disease process is common: bacterial pathogens persist and reproduce by disabling the innate immune responseThe body's first line of defense against intracellular and other pathogens. According to the Marshall Pathogenesis the innate immune system becomes disabled as patients develop chronic disease..

Although patients who become infected with the Th1 pathogens are given a variety of diagnoses, there are often no clear cut distinctions between one disease and the next. Rather, symptoms frequently overlap creating a spectrum of illness in which diseases are more connected to one another than mutually exclusive disease states.

The evidence that chronic disease is ultimately a spectrum disorder with a common cause includes:

  • comorbidity of inflammatory diseases overlap observed between patients suffering distinctly defined diseases
  • the infrequency with which patients suffer from just a single disease or condition
  • failure of diagnostic compartmentalization: the frequent difficulty doctors have in clearly and definitively diagnosing a patient

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Role of vitamin D in chronic disease

Main article: Science behind vitamin D

A number of studies have suggested that patients with chronic inflammatory diseases are deficient in 25-hydroxyvitamin D (25-D) and that consuming greater quantities of vitamin D, which further elevates 25-D levels, alleviates disease symptoms.

Some years ago, molecular biology identified 25-D as a secosteroid. Secosteroids would typically be expected to depress inflammation, which is in line with the reports of short-term symptomatic improvement. The simplistic first-order mass-action model used to guide the early vitamin studies is now giving way to a more complex description of action.

When active, the Vitamin D nuclear receptor (VDR) affects transcription of at least 913 genes and impacts processes ranging from calcium metabolism to expression of key antimicrobial peptides. Additionally, recent research on the Human MicrobiomeThe bacterial community in the human body. Many species in the microbiota contribute to the development of chronic disease. shows that bacteria are far more pervasive than previously thought, dramatically increasing the possibility that the spectrum of chronic diseases is bacterial in origin.

Emerging molecular evidence suggests that symptomatic improvements among those administered vitamin D is the result of 25-D’s ability to temper bacterial-induced inflammation by slowing VDR activity. While this results in short-term palliation, persistent pathogens that influence disease progression proliferate over the long-term.

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Notes and comments

  • Legacy content


The human microbiome project.
Turnbaugh PJ, Ley RE, Hamady M, Fraser-Liggett CM, Knight R, Gordon JI
Nature449p804-10(2007 Oct 18)
Age-related inflammation: the contribution of different organs, tissues and systems. How to face it for therapeutic approaches.
Cevenini E, Caruso C, Candore G, Capri M, Nuzzo D, Duro G, Rizzo C, Colonna-Romano G, Lio D, Di Carlo D, Palmas MG, Scurti M, Pini E, Franceschi C, Vasto S
Curr Pharm Des16p609-18(2010)
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