Science to share with your doctor.
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 microbiota 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 Microbiome 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 vitro 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.
Horizontal gene transfer
Horizontal gene transfer (HGT), sometimes referred to as lateral gene transfer, is any process in which a bacterium inserts genetic material into the genomes of other pathogens or into the genome of its host. HGT represents a substantial blow to the validity of Koch’s postulates, which state that any given infectious disease is caused by a single discrete and well-defined pathogen.
“Increasingly, studies of genes and genomes are indicating that considerable horizontal gene transfer has occurred between bacteria.”
James Lake, Molecular Biology Institute at the University of California
In fact, due to increasing evidence suggesting the importance of the phenomenon in organisms that cause disease, molecular biologists such as Peter Gogarten at the University of Connecticut have described horizontal gene transfer as “a new paradigm for biology.”
Gorgarten insists that horizontal gene transfer is “more frequent than most biologists could even imagine a decade ago” and that this reality turns the idea that we can classify organisms in a simple “tree of life” on its head.
Instead Gogarten suggests that biologists use the metaphor of a mosaic to describe the different histories combined in individual genomes and use the metaphor of a net to visualize the rich exchange of DNA among microbes.
Comorbidity of inflammatory diseases
“One of the striking features of a variety of neuropsychiatric diseases (e.g., affective disorders) is their variance, with differences observed across individuals in terms of their susceptibility, in the combination of systems that are disturbed, and in the therapeutic and adverse responses to various medications…. The microbiome [may represent] a source of this observed variance.”
A. Gonzalez et al.1
When the Th1 pathogens compromise the immune response, they make it easier for other types of bacteria in other locations to infect the body as well. This phenomenon is known as comorbidity. Although a comorbid condition is traditionally understood to be unrelated to the underlying condition, the sheer number of common comorbidities points to a common pathology. Indeed, a 2012 Dutch analysis of patients showed that disease pairs occurred more frequently than would be expected if diseases had been independent.2
Epidemiological research may have its share of liabilities, but one contribution it has made is in demonstrating the strong connections between seemingly disparate diseases as evidenced by the number of patients who share diagnoses with two or more “unrelated” disease processes.
The following wheel shows how truly related chronic diseases are. Each “spoke” represents a published study which has demonstrated a significant statistical relationship between patients suffering from one disease and the next. As an example, diseases found to be co-morbid with Depression (highlighted) were found to be Inflammatory Bowel Disease (IBD), Multiple Chemical Sensitivity (MCS), Obesity, Psoriasis, Sarcoidosis, Vitiligo, Alopecia Areata, Anxiety, Asthma, Cancer, Cardiac Disease and Cardiovascular Disease.
Biofilms are densely packed communities of microbial cells that grow on living or inert surfaces and surround themselves with secreted polymers. Many bacterial species form biofilms, and their study has revealed them to be complex and diverse. The structural and physiological complexity of biofilms has led to the idea that they are coordinated and cooperative groups, analogous to multicellular organisms.1
Researchers have estimated that 60-80 percent of microbial infections in the body are caused by bacteria growing as a biofilm – as opposed to planktonic (free-floating) bacteria.
“There is a perception that single-celled organisms are asocial, but that is misguided. When bacteria are under stress—which is the story of their lives—they team up and form this collective called a biofilm. If you look at naturally occurring biofilms, they have very complicated architecture. They are like cities with channels for nutrients to go in and waste to go out.”
Andre Levchenko, PhD, Johns Hopkins University
Some external biofilm, namely chronic wounds and dental plaque, can be manually removed. Because of their inaccessibility and heightened resistance to certain antibiotic combinations and dosages, internal biofilm are more difficult to eradicate.
Biofilm bacteria are a part of what is known as the Th1 bacterial pathogens, which according to the Marshall Pathogenesis, collectively cause chronic disease.
The science behind Pathogenesis
The Marshall Pathogenesis, upon which the Marshall Protocol is grounded, is a description for how microbes, such as bacteria, fungi, and viruses, 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. The Marshall Pathogenesis is supported by an emerging array of evidence, including clinical evidence, evolutionary evidence, some in silico data, and environmental sampling studies.