About Bacteriality.com
In 1934, a German scientist named Emmy Klieneberger-Nobel discovered that the bacteria in her Petri dish had changed form and lost their cell walls in the process. Seventy years later, biomedical researcher Trevor Marshall created a model describing how these bacteria, along with bacteria that live together inside protected communities called biofilms, might be able to cause chronic disease and dysregulate the immune system.
To date, there are over 50 known species of bacteria capable of transforming into the L-form, many of which have been implicated in a wide array of chronic diseases including sarcoidosis, Chronic Fatigue Syndrome, Lyme Disease, rheumatoid arthritis, Crohn’s disease and multiple sclerosis.
Similarly, in just a short period of time, researchers studying internal biofilms have already pegged them as the cause of numerous chronic infections and diseases, and the list of illnesses attributed to these bacterial colonies continues to grow rapidly. According to a recent public statement from the National Institutes of Health, more than 65% of all microbial infections are caused by biofilms.
Marshall has developed a treatment colleagues have named the Marshall Protocol. Patients on the treatment take pulsed, low-dose antibiotics and Benicar, a medication which activates the immune system. The goal is to kill L-form and biofilm bacteria that cannot be killed by standard antibiotic therapy. Hundreds of patients around the world with a variety of chronic diseases are using the treatment. Nearly all are reporting improvement and some claim complete resolution of symptoms.
Bacteriality.com delves into the fascinating and complex science underlying and related to Marshall’s work.
The present time is a watershed moment in medical research. Antiquated ideas like Koch’s postulates and the notion that many chronic diseases are “autoimmune” are quickly running their course. In their stead, some researchers are starting to make the connection between latent pathogens and disease, many of them casting their scientific gaze upon the Vitamin D Receptor (VDR), the fundamental receptor of the immune system.
Thanks to rapid advances in technology, scientists can now detect human pathogens that are unable to be cultured in a Petri dish. This has lead to the realization that the microorganisms living inside and on humans (the human microbiome) outnumber human cells by approximately a factor of ten. Some scientists estimate only that 1% of bacteria are able to be cultured without advanced technology. This means that approximately 99% of the pathogens capable of inhabiting the human body are just starting to be characterized and identified. The probability that many of these pathogens contribute to the development of inflammatory disease is extremely high.
Nevertheless, most of the research discussed on this site turns a lot of conventional medicine on its head, and the medical community, many of whose members are fixated on finding a purely genetic cause for all forms of disease, is painfully slow to warm to new insights. This is especially true in a world where powerful drug and supplement corporations stand to lose billions if chronically ill patients can now recover using a therapy that costs no more than a few dollars a day.
In 1982, Australian researchers Barry Marshall and Robin Warren discovered that ulcers, previously attributed to stress, are actually caused by H. pylori bacteria. When Marshall first put forth his research doctors walked out of his lectures, and he was shunned by many of his peers. Finally, Marshall actually swallowed H. pylori bacteria and developed an ulcer. It was only then, twenty years after his discovery, that the medical community and the public began to take him seriously.
Perhaps if we can understand and communicate Dr. Trevor Marshall’s research and that of other scientists investigating the human microbiome, it will not take decades for the medical community to embrace the notion that many inflammatory diseases are likely caused by a wide array of chronic bacteria.
For those who may be wondering, the image in the header is an illustration based on a video taken by British clinician Dr. Andy Wright. Dr. Wright used a Bradford Variable Projection High Resolution Microscope to view L-form bacteria in the blood.
I would like to thank Dr. Joyce Waterhouse for her help with the editing process.
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About Amy Proal
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 has Chronic Fatigue Syndrome and has been on the MP since April 2005. She is thrilled with her progress and looks foward to helping people better understand the treatment that is restoring her health.
Contact Amy at amy dot proal at gmail.com.
10 Responses for "About Bacteriality.com"
Well done Amy. Thanks for your insite and writing skills in producing such an understandable, valuable website. I will be sending my Dr you website address. I’m on the MP and follow your posts.
looks good Amy and Paul!
Wow - lots of great stuff there. Wonderful job.
Awesome, Amy. You sure put a lot of work into the articles and it paid off. Very good reading! Keep up the great work.
Love your new website layout. Good job at staying a step ahead of the expanding nature of your site!
Thanks Claire….Paul does a great job of staying on top of things and constantly updating features!
Nat Clin Pract Rheumatol. 2008 Jul 1. [Epub ahead of print] Links
Control of autoimmune diseases by the vitamin D endocrine system.Adorini L, Penna G.
L Adorini is Chief Scientific Officer at Intercept Pharmaceuticals, Corciano (Perugia).
1,25-Dihydroxyvitamin D(3) [1,25(OH)(2)D(3)], the biologically active form of vitamin D(3), is a secosteroid hormone essential for bone and mineral homeostasis. It regulates the growth and differentiation of multiple cell types, and displays immunoregulatory and anti-inflammatory properties. Cells involved in innate and adaptive immune responses-including macrophages, dendritic cells, T cells and B cells-express the vitamin D receptor (VDR), and can both produce and respond to 1,25(OH)(2)D(3). The net effect of the vitamin D system on the immune response is an enhancement of innate immunity coupled with multifaceted regulation of adaptive immunity. Epidemiological evidence indicates a significant association between vitamin D deficiency and an increased incidence of several autoimmune diseases, and clarification of the physiological role of endogenous VDR agonists in the regulation of autoimmune responses will guide the development of pharmacological VDR agonists for use in the clinic. The antiproliferative, prodifferentiative, antibacterial, immunomodulatory and anti-inflammatory properties of synthetic VDR agonists could be exploited to treat a variety of autoimmune diseases, from rheumatoid arthritis to systemic lupus erythematosus, and possibly also multiple sclerosis, type 1 diabetes, inflammatory bowel diseases, and autoimmune prostatitis.
Hi Bill,
Thanks for sharing an accurate description of the actions of 1,25-D. Of course, the vitamin D from supplements, food, and excessive sun exposure is converted into 25-D, not 1,25-D. 25-D is the secosteroid form of vitamin D that blocks the VDR. So it’s important to keep in mind that one cannot accelerate the activity of the VDR by consuming extra vitamin D or getting extra sun.
However, Adorini and team have failed to consider the alternate hypothesis when it comes to the low levels of 25-D they observe in autoimmune disease - levels they link to “deficiency.” Marshall’s molecular data (recently published in BioEssays), which is backed day in and day out by clinical data obtained from our phase II study, shows that a low 25-D is does not CAUSE autoimmune disease but is rather a RESULT of the disease process. As levels of 1,25-D rise in patients with inflammatory disease due to pathogen-induced blockage of the VDR, they naturally downregulate, through the Pregane Xenobiotic Receptor, a patient’s level of 25-D. So rather than serving as a sign of “deficiency”, low 25-D can actually be used as a marker to suggest that a person is infected with the chronic intracellular pathogens that cause autoimmune disease.
Adorini and team should be happy to know that Dr. Marshall has already identified an excellent VDR agonist. It’s the ARB Benicar, which activates the receptor to just the right level in order to maintain an effective innate immune response, but not an over-exuberant innate immune response. Benicar is the medication patients on the Marshall Protocol take four times a day in order to prime their innate immune systems to effectively kill the Th1 pathogens.
But it’s still good to hear that research teams are looking for even more potential VDR agonists.
Best,
Amy
How do we donate to you? Your studies should be supported.
LJ
Chicago
Dear LJ,
Sorry not to get back to you sooner. I have actually been having some discussions with the ARF board about donations. In any case, you can donate to ARF at the following site:
http://autoimmunityresearch.org/
Thank you very much for your generosity. I assure you your gift will be used as effectively as possible.
Best,
Amy
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