Bacteriality — Exploring Chronic Disease

Four years ago, her eyesight and health were deteriorating. Then, after being diagnosed with sarcoidosis, this Belfast Ireland resident took action and started Autoimmunity Research Foundation’s Marshall Protocol. Today most of her symptoms are gone and she’s thrilled to have played a part in the treatment that’s revolutionizing medicine. Meet Julia Greer.

How were you diagnosed?

It would have been funny if it hadn’t been so serious.

For many months I’d had gradually worsening eye troubles - ripples of ‘light’, increasing floaters and cobwebs, a painful feeling of pressure, and sore tiredness. I had four courses of steroid drops that only gave temporary relief each time; then the uveitis would come back with a vengeance.

A baffled eye consultant passed me on to another one, and he in turn passed me on to a third. He was a tall, unsmiling Greek god, cold as marble. For weeks he carried out every test in his book, while I got steadily worse. I thought I was losing my sight.

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In 2003, this school teacher from Indiana was suffering from sarocoidosis, fibromyalgia, CFS, and myriad other symptoms. Today, thanks to Autoimmunity Research Foundation’s Marshall Protocol, she considers herself healthy and is traveling the world with her husband. Meet Carole Morgan.

What were you dealing with before starting the MP?

Before I found the MP, I was actually undergoing tests for cancer. I had originally visited the emergency room in December 2003 because my legs had become so swollen and painful that I could hardly walk. An abnormal chest x-ray revealed extremely swollen lymph nodes. My physician referred me to a pulmonologist who ordered more tests, including a CT scan for my bloated and painful stomach. He then referred me to an oncologist, feeling that I probably had cancer. More scans and tests were performed because they just weren’t sure what form of cancer I might be suffering from. First they thought it was lymphoma, then bone cancer, then finally lung cancer. While they were pondering a diagnosis, I started to do my own research on the Internet. Since the second possibility listed from the CT and PET scan reports was sarcoidosis (a disease that I had never before heard of), I started to research sarcoidosis on the web and found sarcinfo.com—a website created by Autoimmunity Research Foundation that was the predecessor to MarshallProtocol.com.

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Over the course of the past few decades, researchers have tested everything from seizure medications to Viagra on mice. Scientists have bred special strains or “lines” of rats specifically for experimentation, with names such as the albino Wistar rat, the Sprague Dawley rat, and the Lister black-hooded rat. Because they are quick to reach sexual maturity and are easily kept and bred in captivity, rodents have been praised as prime experimental subjects. But an increasing number of studies, including a wide body of molecular modeling research, have revealed substantial differences between the immune systems of rats and the immune systems of humans. These studies provide a novel line of reasoning on age-old questions - How many of our experiments are valid? Are men simply tall mice without tails? Can we really take the data derived from experiments on rats and apply it to human beings?

Mice have been used in labs for decades.

The answers to the above questions are important for anyone who hopes to fully understand chronic inflammatory disease. “Unraveling the intricacies of human [Vitamin] D metabolism is often made extremely difficult by the intermingling of murine [mouse] and human biologies in the literature,” says biomedical researcher Trevor Marshall PhD. Armed with an understanding of the differences between humans and mice, we can better determine the accuracy of the studies we are presented with, and detect the flaws in studies that do not support the correct model of chronic disease.

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Interview with Shirley J. (Saj) - Sarcoidosis

She used to alarm others with her wheezing and now she can run up the stairs of her house and not even think about her breathing. In fact, this Texan is literally singing about how good she feels thanks to Autoimmunity Research Foundation’s Marshall Protocol. Shirley J. will now take your questions.

When were you diagnosed with sarcoidosis? How did you feel?

I was diagnosed in 2004. It was very scary to be told I had a disease that other doctors believed has no cure. My doctors told me that few people die from sarcoidosis (which is incorrect), but right around that time football player Reggie White died from sarcoidosis. I was very alarmed.

I started researching sarcoidosis on the internet and found myself at a support site. Marshall Protocol nurse moderator Meg Mangin was also a member of the site. She emailed me an overview of the treatment and also warned me not to take prednisone because it is a steroid that suppresses the activity of the immune system and allows L-form bacteria to spread more easily. Then, Belinda Fenter, another MP moderator helped me find an MP doctor (we both live in Texas).

I started reading the information on Sarcinfo.com – a site created by Autoimmunity Research Foundation that was a predecessor to MarshallProtocol.com. As I started to read and understand the science behind the Marshall Protocol, I knew that Dr. Marshall was onto something. It makes so much sense that Th1 illnesses are not genetic but due to the spread of bacteria, and that pulsing the antibiotics gives the body the opportunity to fight these pathogens. I started the MP in January of 2005.

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Sam is a 32-year-old patient who is using the Marshall Protocol to treat CFS and depression (and doing extremely well). But Sam is certainly not the only person in his family suffering from Th1 disease – the name given to inflammatory illness caused by bacteria that reside undetected inside biofilms and the cells of the immune system. These bacteria, which are often in a cell-wall-deficient form (the L-form), are collectively referred to as the Th1 pathogens.

Sam’s mother suffers from fibromyalgia, accompanied by insomnia, fatigue, and irritable bowel disorder. His father recently had a stroke, and deals with substantial fatigue and depression. His older brother has debilitating back pain and is hard of hearing. His youngest sister suffers from alopecia, brain fog, depression, excessive fatigue, and mild attention deficit disorder. The youngest brother in the family has a severe case of bipolar disorder, as well as irritable bowel syndrome.

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Interview with Dr. Greg Blaney: MP physician

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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Interview with Robyn Russell - Lyme, myoclonus

She’s a Senior Principal Research Scientist and the Research Program Leader of Enzymology & Synthetic Biology for the Division of Entomology, Commonwealth Scientific and Industrial Research Organization, in Canberra, Australia. Despite her broad background in the biological sciences, and her PhD in immunology, she was unaware of the pathogens causing her son’s illness– that is until she learned about Autoimmunity Research Foundation’s Marshall Protocol. Dr. Robyn Russell will now take your questions….

When did Matt start to get sick? What happened?

Everything started in June 2004 when Matt was 12 years old. Matt started to have very painful headaches. It was in June that my husband and I first wrote one of Matt’s teachers a note saying that he wasn’t able to complete his homework because of his headache. We were concerned because a child his age should certainly not be suffering from debilitating headaches. We saw a doctor and he told us that Matt had a sinus infection. Over the next few months he was put on courses of high-dose antibiotics but the head symptoms would always return. Finally the doctor said, “I have no idea why Matt is not getting better.”

Robyn Russell and her son, Matt, who used the Marshall Protocol to recover from a variety of severe symptoms.

We were referred to an ear, nose and throat doctor but there was a three-month waiting list in order to see him. During the time we had to wait for the appointment Matt began to develop urinary tract infections as well, which is uncommon for a boy. We had a family vacation planned to Europe that was centered around a scientific conference that my husband and I were planning to attend. While on the trip, Matt continually woke up with a terrible headache. As the day wore on, we’d do everything in our power to distract him, saying “Look, the Louvre! The Mona Lisa!”, but Matt just wanted to go home and rest, and the distraction was a losing battle. During the trip Matt did find that swimming helped his headache.

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Is biomedical researcher Trevor Marshall PhD the only person implicating vitamin D in disease? No. A recent study by researchers at Duke University found that elderly men and women who consumed higher levels of calcium and, in particular, vitamin D are significantly more likely to have greater volumes of brain lesions, indicating regions of damage that can increase risk of cognitive impairment, dementia, depression and death. The team found that vitamin D intake, (mean 341 IU and maximum intake 1014 IU), was the only variable that retained a significant correlation with the brain lesions when analyzed by a multivariate analysis.

Payne found that subjects who consumed vitamin D were markedly more likely to have a higher total volume of brain lesions.

The research team was led by Dr. Martha E. Payne, an assistant professor in the department of psychiatry and behavioral sciences with the Neuropsychiatric Imaging Research Laboratory at Duke. Payne reported her findings at the 2007 Experimental Biology Conference in Washington D.C. Her presentation, which took place on May 1, is part of the scientific program of the American Society for Nutrition.

“This is one of the first studies to examine the relationship between diet and brain lesions,” said Payne. “Our finding of a relationship between brain lesions and consumption of both calcium and vitamin D raises the question about a possible downside to high intakes of these nutrients.”

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As we progress into the age of molecular medicine, unraveling the intricacies of the human immune system is an increasingly achievable goal. One can only marvel at the carefully regulated feedback pathways that, under a range of conditions, allow the immune system to maintain a natural state of homeostasis. What happens though when pathogens, medications, and supplements upset this delicate balance? Research that reveals how the immune system can be affected during an infant’s first weeks of life is shedding light on many of the factors driving the current epidemic of chronic disease.

The human immune system has two components – the innate immune system and the adaptive immune system. The innate immune system is the body’s first line of defense against invading pathogens. White blood cells of the innate immune system called phagocytes engulf and kill bacteria. The adaptive immune system is primarily made up of white blood cells called lymphocytes. Once lymphocytes encounter a pathogen, they create proteins called antibodies that allow the adaptive immune system to ‘remember’ the infectious agent and prevent it from causing disease at a later time.

A diagram from Rolf Zinkernagel’s paper showing how the group of newborn mice injected with CMV died when exposed to the virus at a later date

While the innate immune system is functioning at birth, it takes several weeks for an infant to develop a working adaptive immune system. Little is known about what happens when a baby encounters pathogens during this early period of life. However, a recent study by 1996 Nobel Laureate Rolf Zinkernagel and team at the Institute of Experimental Immunology in Switzerland illustrates how pathogens may affect infants during the period before their adaptive immune systems are up and running.

Zinkernagel and team injected a virus called Cytomegalovirus (CMV) into the brains of a group of mice that were only a few days old. Their adaptive immune systems had not yet developed and consequently they were not producing lymphocytes. The researchers found that the innate immune systems of the mice were able to eliminate CMV from most of the tissues except for those of the central nervous system. As a result, the virus persisted in the brains of the mice. Later in life, when the same mice were challenged by infection with a similar virus, they developed a condition resembling a type of autoimmune disease and died. The team referred to this concept as viral “deja-vu.”

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Interview with Belinda Fenter

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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Many people who are chronically ill are given antibiotics. But are these medications working in the correct manner to kill the pathogens responsible for their disease? New molecular modeling research strongly suggests that the stealth pathogens responsible for causing a wide array of chronic diseases can only be killed if carefully chosen antibiotics are taken in a very specific manner.

In what is emerging as a new understanding of chronic disease, researchers are increasingly implicating what are often referred to as the Th1 pathogens in a wide array of illnesses previously considered to be of unknown cause or “autoimmune” in nature. “It is our contention that several diseases that are usually regarded as ‘autoimmune’ or ‘idiopathic’, including rheumatoid arthritis, Crohn’s disease, ulcerative colitis, sarcoidosis and psoriasis, are caused by infection with related slow-growing bacteria,” states G.A.W. Rook in the journal Immunology Today.

The Th1 pathogens are hypothesized to be an intraphagocytic, metagenomic microbiota of bacteria, meaning that they are able to persist inside the cells of the immune system as well as group into colonies called biofilms. The bacteria inside a biofilm produce a protective matrix that allows them to more effectively evade the immune system and develop resistance to antibiotics administered in a standard manner. Essentially, high-dose antibiotics fail to eliminate all the cells that form a biofilm, leaving what are referred to as persister cells behind. The persister cells are eventually able to re-create the biofilm, allowing it to thrive again. There is a tremendous number of different species of these chronic pathogens.

Many of the bacteria that compose this microbiota are in what is referred to as the L-form. For over a century, scientists have realized that classical bacteria can transform into small forms that lack cell walls. These pathogens are known as L-form bacteria. Researchers have currently identified over 50 different species of bacteria capable of transforming into the L-form, and it is likely many other bacteria also have this ability. Brown et al have found evidence of L-form bacteria in the blood of more than 60% of healthy controls. In fact, the diseases generated by L-form bacteria are far more common than currently realized, and are often only noticed as subtle signs of aging, such as osteoporosis, obesity, fatigue and arthritis.

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Diet and Disease: Eating for health

“An apple a day keeps the doctor away.” Regardless of whether apples have proven to ward off disease, this statement reflects a long-held understanding of the fact that the foods and supplements we consume can impact our health. Recent research, which has demonstrated that a vast array of chronic diseases are bacterial in origin, now allows us to better understand the actions of the substances we ingest. By analyzing research that reveals how bacteria use and obtain vital nutrients, we can adapt our diets to ensure that we do not provide the pathogens we harbor with extra amounts of substances that foster their growth, including iron, folic acid, and carbohydrates. Furthermore, molecular modeling research now allows us to understand how various foods, including vitamin D, chlorogenic acid, carnosic acid, and soy, can alter the activity of the immune system. Together, this research reveals that eating large quantities of certain foods that make us feel good is not necessarily beneficial, and that a number of supplements may do more harm than good.

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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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Interview with Sue Andorn - Lyme, Babesia

By 2003 she had physically hit rock bottom and was completely unable to maintain her farm. Now, thanks to Autoimmunity Research Foundation’s Marshall Protocol, she has the energy she had in college. Sue Andorn will now take your questions.

1. How long have you been on the Marshall Protocol (MP)?

I started my 4th year on the Marshall Protocol in June 2007.

2. Tell me about your symptoms before you started the Marshall Protocol? How did you get sick?

When I was a child I was quite healthy. I walked four miles to get to school and had perfect attendance. My first sign of illness occurred in college when I got a polynidal cyst on my tailbone. It burst internally before it could be removed. I now know that it was probably filled with bacteria that subsequently drained throughout my body. I graduated from college with a degree in microbiology and proceeded to work at Sterling Drug Company, where our team began doing research on a measles vaccine. Because we were working with germs, I had to get an Asian Flu vaccine. Within minutes of receiving the injection I went into anaphalactic shock. Six months later I got extremely ill with the flu despite the vaccine. Knowing what I know now, it was a vaccine contaminated with L-form bacteria. I never really recovered. That was the start of a downhill slide that lasted 50 years.

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During the 1960s, a large number of studies began to point to the idea that estrogen therapy might ease the pangs of menopause. In a best selling book called Feminine Forever, a Brooklyn gynecologist named Robert Wilson argued that menopause was an illness rather than a natural state associated with aging. Soon, an increasing number of older women began to take supplemental estrogen in an effort to replace the hormones that their own bodies had stopped secreting. The treatment, known as hormone replacement therapy or HRT, became one of the most popular medical treatments in America.

The American Heart Association, the American College of Physicians, and the American College of Obstetricians and Gynecologists all agreed that a sufficient number of studies had been done to prove that HRT was unequivocally helpful in helping older women ward off heart disease and osteoporosis. By 2001, 15 million women were taking HRT, including 5 million elderly women.

Then, in 1998, a clinical trial concluded that estrogen therapy actually increases the likelihood that women with heart disease will suffer a second heart attack. It was followed by a trial in 2002 which concluded that HRT puts postmenopausal women at a greater risk for heart disease, stroke, blood clots, breast cancer and even dementia. Suddenly, It became painfully clear that HRT may offer a benefit to women who begin to use it early in life, but for those who start the treatment in their later years, it can be very dangerous.

Gary Taubes writes in The New York Times Magazine, “The question of how many women may have died prematurely or suffered strokes or breast cancer because they were taking a pill that their physicians had prescribed to protect them against heart disease lingers unanswered. A reasonable estimate would be tens of thousands.”

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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.

She has written for several publications and organizations including FibromyalgiaAWARE magazine, Immunesupport.com, Volta Voices magazine, and the National Policy Research Council.

Amy had Chronic Fatigue Syndrome. She looks forward to helping people better understand the treatment that restored her health.

Contact Amy at amy dot proal at gmail.com.

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