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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In 2005, for his TED talk, Dr. Aubrey de Grey was asked by an audience member who was seemingly puzzled by his long brown beard, “Since you talk about aging and try to defeat it, why do you make yourself appear like an old man?”

De Grey responded, “Because I am an old man. I am 158.”

Aubrey de Grey

It has been three years since then and at the ripe age of 161 (according to his Wikipedia bio, his birthday is in April), Aubrey de Grey presided over the latest of the Methuselah Foundation’s annual anti-aging symposiums. At the end of June 2008, a group of us with ties to Autoimmunity Research Foundation attended that meeting on the *very* sunny campus of UCLA. Our goal was to get researchers thinking about a bacterial explanation for diseases of the aging, and to get them to begin considering the Marshall Protocol as an anti-aging option.

Aubrey de Grey is always surrounded by people, be they prestigious presenters, researchers, conference organizers, or any of his small army of energized volunteers for which he plays field marshall.

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Feeling down? According to several new claims made by medical researchers, it seems you may be able to supplement with another hormone in the hopes of getting relief. Yes, yes, the phrase “supplement with a hormone” should, correctly, send chills down the spine of those familiar with the current “vitamin” D debacle. Nevertheless, let’s take a look at mainstream medicine’s latest take on what they’ve already labeled the “love drug.”

In general, oxytocin makes people more sociable and less phobic.

Produced naturally in the brain during social interactions, the hormone oxytocin promotes romantic feelings. It’s also the hormone that helps mothers bond with babies and, in general, makes people more sociable and less phobic. Oxytocin is released during orgasm and is also the key birthing hormone that enables the cervix to open and the contractions to work. In situations where labor has to be induced, it is often given to the mother intravenously to kick-start contractions.

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What if, rather than conferring a benefit to the digestive tract, probiotics worked by slowing the pace of bacterial die-off in organs near the gut, or even in other areas of the gut itself?

Many people go out of there way to buy probiotics, which can be purchased in myriad forms.

There’s been some discussion on the Marshall Protocol study site about how probiotics, or bacteria that are believed to beneficially improve bacterial composition in the gut, may be palliating symptoms but not improving overall health. This probably seems ludicrous to people who go out of their way to buy yogurt with “friendly” bacteria such as acidophilis, or people who dig into their savings to buy probiotics in numerous forms including little silver pearls.

And yet consider this hypothesis. Whereas it used to be believed that the adaptive immune system dictated the immune response in the gut, recent research has made it clear that the innate immune system – which is active inside the villi of the intestines and stomach – is actually largely responsible for keeping gut bacteria in check.

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At the 2008 Days of Molecular Modeling Conference in Sweden, biomedical researcher Trevor Marshall sat on the edge of his chair listening intently to a talk presented by Adriano Aguzzi of the University Hospital of Zurich. Aguzzi was discussing research that confirmed much of what Marshall had long suspected to be true about prions – small, potentially infectious molecules that are hypothesized to be made only of protein.

The protein structure of a prion.

Prions have been implicated as the cause of a number of diseases in a variety of mammals, including bovine spongiform encephalopathy (BSE, also known as “mad cow disease”) in cattle, and Creutzfeldt-Jakob disease (CJD) in humans. All thus-far hypothesized prion diseases affect the structure of the brain or other neural tissue, and all are considered untreatable or fatal by mainstream medicine.

Although prions have been studied to some extent in the lab for decades, very little research has delved into their actions when inside the human body (in vivo). Thus, many theories put forth about how prions might cause or contribute to neurological disease have been largely speculative.

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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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A few months ago I submitted an abstract to the committee planning the upcoming Days of Molecular Medicine Conference, which will be held this April in Karolinska Sweden. A week ago, I was quite happy to learn that my abstract was accepted and that I will be giving a poster presentation at the conference. The subject: “Cognitive dysfunction in women with Chronic Fatigue Syndrome: examining the role of the endometrium, the nuclear receptors, and the antimicrobial peptides.” So if all goes as planned, I’m headed to Sweden in about a month. I’m excited for many reasons, one of them being that before starting the Marshall Protocol I never thought I’d be able to board a plane again – the pressure changes and noise were too much for my head to tolerate. Yet, two 3/4 years later, here I am traveling half-way across the world, talking about many cognitive issues that were once a problem for me – a problem that has largely subsided.

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There’s a lot of information to absorb when learning about the Marshall Protocol. Not only do patients have to understand the treatment itself – how to dose their medications and manage their antibiotics – but they also have to grasp many of the fundamental scientific breakthroughs that underly the treatment.

During this time, it’s easy to become confused about some of the concepts that Dr. Marshall has put forth, or even just about how the medications work and affect the body. Happily, before starting the Marshall Protocol, patients can post questions at the website www.curemyTh1.org (Th1 refers to disease caused by L-form bacteria, hence the name Cure My Th1) where their questions are answered free of charge by patient advocates. They are also required to read a range of helpful information on the Marshall Protocol study site.

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