Bacteriality — Exploring Chronic Disease

Category: horizontal gene transfer

Although it may not seem like a topic immediately related to the Marshall Protocol, I believe that it’s difficult to truly envision the new bacterial pathogenesis of inflammatory disease without taking horizontal gene transfer, or the ability of bacteria to swap DNA, into account. In other articles on this site, I’ve described how people with inflammatory disease gradually accumulate a “pea soup” of pathogens. I like the term because it hints at the fact that everybody’s bacterial load is unique and also brings to mind the image of something stirred or mixed. Everyone with Th1 disease acquires a large mix of different pathogens, but even the image of a great number of different but isolated pathogens does not do justice to the variety of different bacteria that each patient harbors. This is because, if bacteria can trade DNA, they are constantly trading genetic material which allows for the constant creation of new species, with new characteristics and new survival abilities. So the bacterial loads we harbor are probably much more complex than we envision and certainly more complex than what conventional medicine envisions. After all, conventional medicine is still trying to tie one pathogen to one disease, and that’s only if they even decide to factor bacteria into the picture at all.

In order to better understand horizontal gene transfer, I spoke with Dr. Peter Gogarten at the University of Connecticut and Dr. James Lake at UCLA, both of whom are leaders in the field of gene transfer. Both of them were extremely friendly and seemed excited to speak with me about the phenomenon. I asked them the same questions. Here is how they responded:

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My recent article Bacteria vs. genetic predisposition: the spread of Th1 disease in families discusses how the bacteria responsible for causing chronic disease can be passed from generation to generation. At the same time, the genetic mutations created by these pathogens are also passed from mother to child.

Just this month, researchers led by John H. Werren at the University of Rochester in New York elucidated yet another way that bacterial DNA is likely passed from person to person. This demonstrates just how easy it is for bacterial DNA to become incorporated into human DNA – a reality that is central to biomedical researcher Trevor Marshall’s model of chronic disease in which pathogens are constantly swapping genetic material with each other and their host.

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Do genetic defects cause the vast majority of chronic diseases? Not according to evolutionary biologist Paul Ewald, who teaches biology at University of Louisville. If chronic diseases were genetic in origin, he argues, “A disease-causing gene that reduces survival and reproduction would normally eliminate itself over a number of generations.” He contends that the thinking underlying today’s “Human Genome Mania” often violates the fundamental principle of biology, Darwin’s Theory of Natural Selection.

Paul Ewald

One example of this is schizophrenia; patients with this mental illness rarely reproduce. Ewald posits that if schizophrenia were a genetic illness, the genes that cause the disease would have gradually been eliminated from the population. And what about identical twins who share the exact same DNA? When one identical twin develops breast cancer the other twin has only a 10% – 20% chance of also developing the disease. Ewald argues that “for the common damaging chronic diseases, the evidence considered in light of evolutionary principles implicates infection” and that “adding infectious causation into the mix can best explain the documented epidemiological patterns, and does so in accordance with evolutionary principles.”

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In prehistoric times it was believed that illness was the result of punishment from the gods or the consequence of magic. During the Middle Ages, people attributed disease to toxic vapors or decaying earth.

However in 1867 a scientist named Robert Koch discovered that anthrax is able to cause disease and was able to successfully transfer the germ from cows to mice. Since that time, bacteria have been implicated in an ever greater range of diseases.

Over the past few decades, scientists such as Lida Mattman, Alan Cantwell and Trevor Marshall have provided great evidence for the hypothesis that chronic diseases ranging from arthritis to Alzheimers are the result of bacterial infection. Nevertheless, a great majority of the medical community still feel that these diseases are caused by toxins in the environment or are autoimmune in nature.

Koch’s Postulates

After working with anthrax, Koch developed a series of ground rules to determine whether a given organism can cause a given disease. These rules, known as “Koch’s Postulates” state that a scientist must find the same microbe in every person with a given disease. Furthermore, the specific microbe must be able to be grown on pure culture medium in the lab and when reintroduced into a healthy animal or person must produce the disease again.

Robert Koch in his laboratory
Robert Koch in his laboratory

Many researchers still believe that Koch’s rules are universal and correct despite the fact that a massive body of research has shown that the principles are outdated and can no longer be applied to a modern understanding of disease.

For example, in the early 19th century researchers realized that viruses invalidate Koch’s Postulate because they require another living cell in order to replicate. According to TD Brock at the American Society of Microbiology, attempts to rigidly apply Koch’s postulates to the diagnosis of viral diseases may have significantly impeded the early development of the field of virology.

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Understanding L-form Bacteria

In a 2006 the Centers for Disease Control and Prevention (CDC) released a paper stating, “Infectious agents have emerged as notable determinants, not just complications, of chronic diseases. To capitalize on these opportunities, clinicians, public health practitioners, and policymakers must recognize that many chronic diseases may indeed have infectious origins.”

According to the CDC, infectious agents likely determine more cancers, immune-mediated syndromes, neurodevelopmental disorders, and other chronic conditions than currently appreciated. In fact, they argue that the potential to avoid or minimize chronic disease by preventing or treating infections may yet be substantially underestimated. Those of us familiar with the Marshall Protocol know that they are absolutely correct.

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About Amy Proal

Amy and Zeus

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.

Amy has spoken at several international conferences and authored several peer-reviewed papers on the intersection of bacteria and chronic disease.

If you have questions about the MP, please visit CureMyTh1.org where volunteer patient advocates will answer your questions. Another good resource is the MP Knowledge Base, which is scheduled to be completed within the next year.

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