My Fellow Superorganisms,

Those of you already familiar with the site may have noticed I’ve taken down quite a few pieces. Many of these were written about three years ago. I still stand by their general content, but want to make sure they are completely up to date before I put them back up. A second factor in their temporary removal is that, in retrospect, the tone of these pieces is stronger than the tone I would use today.

When I started this blog, I was writing as an advocate and, over time, I’ve evolved to think and write more like a scientist. I want to make sure that nothing that should be described as a hypothesis comes off in my previous writing as sounding like an established fact.

Just so readers know, the vast majority of the information and studies discussed on this site have now been repurposed as part of content for Autoimmunity Research Foundation’s Marshall Protocol Knowledge Base, which I would encourage you to have a look at.

Best,
Amy

A couple weeks ago, I had the pleasure of giving a presentation to a tri-chapter meeting of the Medical Library Association. The topic was why some patients with chronic disease are disaffected and how online social networks have met some of their needs. I try to offer a balanced perspective – both the good and bad of online social networks.

The live presentation was filmed but the room was a bit on the dark side. So, despite a laudable job filming by my colleague, Judy, I decided to put up a slideshow with voiceovers.

Not every culture reveres the sun as Americans do. In our recent trip to Chengdu, China with a stopover in Hong Kong, we saw hundreds of people, women especially, blocking light on a daily basis.

We’re not sure if these people are supplementing with vitamin D (there is certainly no vitamin D added to the food chain!) but they’re certainly not getting a lot of sun.

The Vitamin D Council insists that people must expose themselves to sunlight and eat vitamin D-fortified products, yet these people are going about their daily lives without any apparent ill effect.

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Men who have excessive faith in their theories or ideas are not only ill prepared for making discoveries; they also make very poor observations. Of necessity, they observe with a preconceived idea, and when they devise an experiment, they can see, in its results, only a confirmation of their theory. In this way they distort observation and often neglect very important facts because they do not further their aim….

Claude Bernard, An Introduction to the Study of Experimental Medicine

This article discusses our experience at the one-day Institute of Medicine workshop on vitamin D and calcium. Both of us had an opportunity to make comments before the committee. Here are Paul’s comments and slides and here are Amy’s comments and slides. Note that our 2009 paper in Autoimmunity Reviews discusses some of the science we allude to in further detail.

On the cab ride to the IOM committee meeting on whether to change the dietary reference intake (DRI) of vitamin D, Amy practiced her speech.

The cabbie had been silent for the whole ride, but broke character by talking to us. “So, let me ask you a question,” he said. “Do you take vitamin D?”

“Actually, no, we don’t,” Amy said. Amy explained briefly how our data suggests that the form derived from supplementation is immunosuppressive, meaning that while it may temporarily improve signs and symptoms of disease, we have found it may do so at the cost of long-term health.

We asked him if he took vitamin D. He said yes and explained that a few years back, he had a partially blocked artery. It scared him, so he searched the internet and found that high doses of vitamin D were being recommended for cardiovascular disease. He wasn’t clear about the evidence, but in his words, “I had to do something.”

Which brings us to this point in time. At least in the United States, rates of chronic disease are rising. One recent study predicted that if current trends continue, all Americans will be obese by 2040. Other studies have shown chronic disease is rising at rates faster than could otherwise be explained by an aging population and/or a general increase in population. One recent estimate says that by 2030, 171 million Americans will have a chronic disease. We have to do something, right?

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If I have seen further it is only by standing on the shoulders of giants a pile of driftwood.

Hello readers!  Suffice it to say I’ve been missing in action for several months.  For much of the time I’ve been traveling.  Some of you may know that I just got back from China where I gave a speech at the International Congress of Antibodies. That will be the subject of my next post when the video of my speech is ready. In the meantime, I finally have time to give you an update of what I was up to before I left for Beijing…just to keep things in chronological order.

Several months ago I travelled to Vancouver Island to stay with Paul’s brother and his wife. It was wonderful to be surrounded by nature again! We took hikes through 200 year old forests and climbed gnarled driftwood on the beach. It was the first time I’ve sat around a bonfire since getting sick. I even got to take a horseback riding lesson and stayed on the horse!

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Though the human genome was fully sequenced in 2001, the most promising work in genomics has just begun and not even in the study of human DNA. Human cells are outnumbered by bacterial cells by a factor of ten to one, and, as the rest of this site alludes to ad nauseam, there is strong reason to believe that bacteria are to blame for many of the chronic diseases from which humans suffer. Genetically speaking, we know relatively little about bacteria that persist in humans. The field is ripe for advances.

Colorful representations of sequenced genomes adorn the walls at JCVI.

You may wonder how a researcher can view and understand a particular bacterial genome. On their own, they cannot. Progress in genetics is a group effort, and requires partnering with one of the handful of heavyweight institutions in the world that have developed resources allowing for genome interpretation. Several such institutions exist in the US. The NIH has bacterial protein sequencing tools at its disposal. The Broad Institute at MIT as well as the Washington University Genome Sequencing Center have also developed tools that allow for genome sequencing.

Many would argue though that the Institution most on the bleeding edge when it comes to genome sequencing technology is the J. Craig Venter Institute, formerly known as TIGR. Headed by transformative iconoclast and entrepreneur J. Craig Venter, the Institute is a non-profit research center that was founded in 2006. It has facilities in Rockville, Maryland and La Jolla, California and employs over 400 people, including Nobel laureate Hamilton Smith.

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Note: Much of the information included in this piece was derived from two articles published in the May 28th edition of Nature News, a resource published by the medical journal Nature

Even those of us who live under rocks have heard of the Human Genome Project, a massive international scientific research project the aim of which was to understand the genetic makeup of the human species. Its primary goal was to determine the sequence of chemical base pairs which make up DNA and to identify the approximately 25,000 genes of the human genome from both a physical and functional standpoint.

The goal of the Human Genome Project was to understand the genetic makeup of the human species.

A working draft of the genome was released in 2000 and a complete one in 2003, with further analyses yet to be completed and published. Meanwhile, a parallel project was conducted by the private company Celera Genomics. Most of the sequencing was performed in universities and research centers from the United States, Canada and Great Britain.

Most researchers would agree that the Human Genome Project was launched in order to answer the long-standing question, “Who am I?” The goal was to identify and sequence every single human gene. By doing so, many researchers were certain they would uncover causes for most of the chronic diseases that plague humankind. At the project’s start, scientists were faced with a multitude of unknown sequences to decipher and understand. Surely such sequences would offer up answers to disease, and specific genes would be found that would correlate with specific illnesses. In a Gattaca-like environment, people would then be informed early in life that they had “the gene” for MS or “the gene” for breast cancer. Scientists would work fervently to identify and change the expression of such disease-causing genes, finally developing enough gene therapies to eradicate human disease. The above scenario has an abiding appeal, largely because the idea that our genes dictate our health is so temptingly simplistic.

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As humans, our environment consistently exposes us to a variety of dangers. Tornadoes, lightning, flooding and hurricanes can all hamper our survival. Not to mention the fact that most of us can encounter swerving cars or ill-intentioned people at any given moment.

Biofilms form when bacteria adhere to surfaces in aqueous environments and begin to excrete a slimy, glue-like substance that can anchor them to all kinds of material

Thousands of years ago, humans realized that they could better survive a dangerous world if they formed into communities, particularly communities consisting of people with different talents. They realized that a community is far more likely to survive through division of labor– one person makes food, another gathers resources, still another protects the community against invaders. Working together in this manner requires communication and cooperation.

Inhabitants of a community live in close proximity and create various forms of shelter in order to protect themselves from external threats. We build houses that protect our families and larger buildings that protect the entire community. Grouping together inside places of shelter is a logical way to enhance survival.

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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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Maybe vitamin D isn’t the answer after all.

Not only does the above statement ring true, it’s also the title of a recent post on “Dr. Len’s Cancer Blog” – a website written by Dr. Len Lichtenfeld, Deputy Chief Medical Officer for the national office of the American Cancer Society, in order to facilitate communication with the public on important issues related to cancer.

Dr. Lichtenfeld, as described by his website, is a frequent spokesperson on a variety of cancer-related subjects, and serves as a liaison for the Society with many professional and public organizations. He’s also a board certified medical oncologist and internist who was a practicing physician for nearly 20 years and serves on several national committees focused on physician payment, the quality of medical care, and the role of health information technology in healthcare delivery.

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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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What do Microsoft and medical research have in common?

Let’s start with the simple fact that they have both been wildly successful. Microsoft has 79,000 employees, global annual revenue in the year 2007 exceeding $51 billion, and has made more than 12,000 of its employees millionaires simply by increases in stock valuation. Additionally, Microsoft’s market share for the operating systems on desktop computers, by one 2003 estimate, is 90%. Not bad for a garage startup.

In the United States alone spending on medical research is at or near the $100 billion mark in the year 2007. That’s about $300 for every man, woman, and child and more than doubles what was spent just a decade ago. According to Dan Fox, president of the Milbank Memorial Fund, a philanthropic group that works on health policy issues, the data in a recent JAMA review makes it plain that “we are spending huge amounts of money, more than any other country, to develop new drugs and devices and other treatments.”

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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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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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