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 hearts 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, 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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“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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