Patients with diabetic neuropathy may not notice minor injuries due to loss of feeling in their lower extremities. Since the Vitamin D Receptor is inactivated by bacterial ligands, a small cut or sore can become infected, and flare into a limb- or life-threatening condition in as little as three days. These wounds are so difficult to heal that most of medicine considers them a lost cause and treats them with amputation. Amputations are often considered to be the beginning of the end for patients with diabetes.

Dr. Randall Wolcott

70% of diabetics who undergo an amputation die within five years due to the stress placed on their heart from their altered circulatory system. During those five years they are likely to have more amputations and to rate their quality of life worse than cancer patients, according to some studies.

Nationally, an estimated 82,000 people with diabetes had lower-limb amputations in 2002, according to the Centers for Disease Control. But thanks to a doctor at the Southwest Regional Wound Care Center in Lubbock, Texas, who has teamed up with researchers from Montana State University’s Center for Biofilm Engineering, this situation is changing. After sending samples of the sludge on his patient’s wounds to the Center, Dr. Randall Wolcott was informed that his samples were largely composed of bacterial biofilms.

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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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Paul W. Ewald is an evolutionary biologist, specializing in the evolution of infectious disease. He received his Ph.D. from the University of Washington, in Zoology, with specialization in Ecology and Evolution. He is currently director of the program in Evolutionary Medicine at the Biology Department of the University of Louisville.

The first recipient of the George R. Burch Fellowship in Theoretic Medicine and Affiliated Sciences, Ewald’s publication of Evolution of Infectious Disease is widely acknowledged by doctors and scientists as a watershed in the emergence of the new discipline of evolutionary medicine. He has been featured in The Atlantic, Newsweek, Discover, and Forbes.

Professor Ewald is also the author of a groundbreaking book, Plague Time; How Stealth Infections Cause Cancers, Heart Disease and other Deadly Ailments.

How do the concepts of evolutionary biology support the idea that pathogens are to blame for most diseases?

When we consider the possible causes of disease, it’s important to make sure that at our starting point, we put all categories on the table. I believe the most useful way to do this is to think in terms of three main categories:

• inherited genes
• parasitic agents (this includes bacteria, viruses, fungi, protazoa spelling: protozoa)
• non-living environmental factors (too much or too little of a particular substance, radiation, exposure to a chemical etc.)

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Greg Blaney, MD, graduated from the University of Ottawa in 1974. Following internship at Edmonton General he joined a Community Health clinic in Ottawa. From 1987 to 1990 he was a teaching assistant in the College of Osteopathy of the CME program at Michigan State University, having trained in both conventional and manual medicine during the first two decades of his career. He went on to also gain competence in Acupuncture and Homotoxicology, was a medical advisor to the LaLeche league, the Childbirth Education Association, the RCMP and the Bank of Canada. He lectured in the University of Ottawa’s Residency program, and its Masters program in nutrition. Dr Blaney is currently using Autoimmunity Research Foundation’s Marshall Protocol to save the lives of hundreds of patients with a wide variety of chronic inflammatory diseases.

How did you become aware of the Marshall Protocol (MP)?

Before learning about the Marshall Protocol my work had evolved into a chronic pain practice, where I focused on osteopathy and trigger point injections. Despite the fact that some people seemed to benefit somewhat from these therapies, I always had a certain group of patients with chronic symptoms that simply did not respond to anything I tried. I had one patient who was actually aggravated by most of these therapies and displayed multiple symptoms in different areas of her body that did not respond to treatment. At the same time, I was also treating a woman who had been diagnosed with Lyme disease ten years before becoming my patient, however her symptoms had gone into temporary remission. Although she had been told by another doctor that she was “cured”, when she was in a car accident, all of her Lyme symptoms returned. After being tested, she was once again positive for Lyme.

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She’s a Marshall Protocol board moderator who has been with the treatment from the early days and has helped hundreds of patients down the road to recovery. Meet Belinda Fenter.

How did you first become involved with Dr. Marshall and the Marshall Protocol (MP)?

I actually met Dr. Marshall on the internet. At the time, I was undergoing testing for what was eventually diagnosed as sarcoidosis. I got online and started looking for information and treatment options. Dr. Marshall was posting online in a few forums. He seemed like the most knowledgeable person and he supported his ideas with scientific documentation. I had worked in a medical setting for several years and was researching sarcoidosis in the medical library. As far as I could tell, Dr. Marshall seemed to have the most comprehensive understanding of the disease and his views just seemed more plausible than any of the others.

I searched until I found Dr. Marshall’s email. I contacted him and we began collaborating. It wasn’t long before Dr. Marshall decided to start a new and unique website and asked me to join his efforts there. Dr. Marshall produced his model of disease pathogenesis, explaining that only undetected, persistent bacteria could provoke the granulomatous response (the formation of clumps of cells in the lungs) that is observed for no other obvious reason in sarcoidosis. Our work drew on the body of previous research by others, such as Alan Cantwell and Lida Mattman, who reported finding occult cell wall deficient bacteria in people with chronic diseases such as sarcoidosis.

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Dr. Alan Cantwell has investigated the phenomenon of cancer bacteria for over thirty years. A graduate of New York Medical College, Cantwell completed a residency program in dermatology at Long Beach Veteran’s Administration Hospital in Long Beach, CA and then practiced in the dermatology department of Kaiser-Permanente in Hollywood, California, from 1965 until his retirement in 1994. Dr. Cantwell is the author of more than thirty published papers on breast cancer, lymphoma, Kaposi’s sarcoma, Hodgkin’s Disease, lupus, scleroderma, AIDS, and other immunological diseases. These papers have appeared in many peer-reviewed journals, including Growth, International Journal of Dermatology, Journal of Dermatologic Surgery and Oncology, and the Archives of Dermatology. He has also written The Cancer Microbe and Four Women Against Cancer and several books on AIDS.

1. How did you become interested in looking for bacteria, first in diseases like scleroderma and later in cancer?

It all started when I was a second year resident in dermatology. I was in the medical library and I came across a paper in the Southern Medical Journal describing a group of people who had been given allergy injections and who subsequently developed deep skin infection with tuberculosis-like germs. It was thought the allergy injection bottles were contaminated with these bacteria.

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“Bacterial L-forms are among the most unusual creatures in nature. Once one has seen their strange habits and life style, one starts to work on L-forms with great enthusiasm because their existence in vivo and in vitro gives rise to more questions in classical microbiology, immunology and infectious diseases.

And just who is able to describe the process of culturing L-form bacteria so eloquently? She’s an Associate Professor at the Department of Pathogenic Bacteria Institute of Microbiology at the Bulgarian Academy of Sciences, who’s worked with L-form bacteria for the last 15 years. Meet Nadya Markova.

1. What led you to become interested in L-form bacteria?

I graduated as a medical doctor, but my interest in microbiology led me to the Bulgarian Academy of Sciences (where I defended my PhD thesis in the field of medical microbiology). Researchers already working there at the time had great experience in L-form research and had made many interesting observations about the bacteria, all of which sparked my interest. They were my teachers, who inspired me to continue their research in the same field.

2. How long have you been working with L-form bacteria? How many people do you currently work with and how to they contribute to the research environment?

I started thinking about how L-form bacteria change form in the beginning of the 90s, and my interest in them has risen ever since. Unfortunately, our research team is comprised of only 5 people. One of them must be mentioned, my teacher Professor Lilia Michailova. She is an excellent electron microscopist and, without her, our achievements wouldn’t have been possible. I’m really glad that she is still active and that we continue to work together.

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