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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