In a 2006 the Centers for Disease Control and Prevention (CDC) released a paper stating, “Infectious agents have emerged as notable determinants, not just complications, of chronic diseases. To capitalize on these opportunities, clinicians, public health practitioners, and policymakers must recognize that many chronic diseases may indeed have infectious origins.”
According to the CDC, infectious agents likely determine more cancers, immune-mediated syndromes, neurodevelopmental disorders, and other chronic conditions than currently appreciated. In fact, they argue that the potential to avoid or minimize chronic disease by preventing or treating infections may yet be substantially underestimated. Those of us familiar with the Marshall Protocol know that they are absolutely correct.[1]
The same can be said for Dave Relman, PhD, assistant professor of medicine and of microbiology and immunology at Stanford University in California who argues, “The list of chronic inflammatory diseases with possible microbial etiologies is extensive; it includes sarcoidosis, various forms of inflammatory bowel disease, rheumatoid arthritis, systemic lupus erythematosus, Wegener granulomatosis, diabetes mellitus, primary biliary cirrhosis, tropical sprue, and Kawasaki disease….. the concept of pathogenic mechanism should be viewed broadly.”[2]
Fortunately, the stealth pathogens responsible for causing the vast majority of chronic diseases have already been identified.
Almost all of us have suffered from a bacterial infection. Sometimes the forms of bacteria causing our symptoms can be killed by antibiotics that work by targeting their cell walls.
However, part of the life cycles of many bacteria include phases where they transform into small forms that lose their cell walls. This means that they can no longer be killed by many commonly used antibiotics. These bacteria are called cell wall deficient (CWD) or L-form bacteria.
Multiple studies have also shown that when one of the Beta-lactam antibiotics (a class of antibiotics that includes penicillin) are applied to wild-type bacteria in a Petri dish, small colonies of L-form bacteria form on the edges of the plate. “Treatment with penicillin does not merely select for L-forms (which are penicillin resistant) but actually induces L-form growth,” states researcher Josep Casadesus in a paper about L-form bacteria published last month in the medical journal BioEssays.[3]
L-form bacteria are pleomorphic, a term that refers to their ability to change in size and shape. During much of their lifetimes they are tiny, about 0.01 microns in diameter, and can be found clustered together inside the cells of the immune system.
Since they are smaller than viruses or fungal particles, they cannot be seen with a normal optical microscope. The small, individual forms of L-form bacteria are often referred to as coccoid bodies. Coccoid bodies sometimes group together, assuming the appearance of a string of pearls
Occasionally L-form bacteria break out of the cells. In the lab they can grow into long, thin biofilm filaments that can reach 60-70 microns in length. The biofilm filaments are composed of L-form bacteria and a protective protein sheath. For reasons still unknown, L-forms can also grow into large “giant” bodies.
L-form bacteria replicate in various ways, including budding, filamentous growth and binary fission. Some species of L-forms such as Proteus can form large bodies that replicate by division. In other instances, granules bud from the body of the bacterium and give rise to small L-form colonies.
L-form bacteria also lack flagella, long slender appendages that allow some forms of bacteria to propel themselves forward by using a whip-like motion. Instead they glide to their destinations in a snail-like fashion.
Groups of L-form bacteria are often encased inside tubules. They are also separated from the environment inside the cell by a membrane or exoskeleton that keeps them from being digested by the cell.
Researchers have currently identified over 50 different species of bacteria capable of transforming into the L-form and it is likely that more species will be found in the coming years. “Probably most bacterial species can be converted into L-forms if treated with the antibiotics that inhibit cell wall synthesis,” states Casadesus.
Although scientists have known about L-form bacteria for over a century, many of them have not detected them in tissue and blood samples because they are very difficult to culture. However an increasing body of research has shown that these bacteria are responsible for causing a wide array of chronic diseases including rheumatoid arthritis, Chronic Fatigue Syndrome, Lyme disease, sarcoidosis, and Crohn’s disease.
Some of the species of L-form bacteria that have been implicated in chronic disease include Bacillus anthracis, Treponema pallidum, Mycobacterium tuberculosis, Helicobacter pylori, Rickettsia prowazekii, and Borrelia burgdorgeri.
Survival mechanisms
Classical forms of most bacterial species can be found in the bloodstream. However L-form bacteria have figured out how to successfully infect and live inside the very cells of the immune system whose job is to kill bacteria. Once inside these cells, they can no longer be detected by the immune system and are able to persist in the body over long periods of time. L-form bacteria can infect many types of cells but prefer to infect white blood cells called macrophages.
Several very recent studies have confirmed the fact that bacteria can live inside the cells of the immune system. In a paper published in the Jounal of Immunology by a team at the University of Michigan Medical School, Gabreil Nunez, senior author of the paper, stated “In our study, the presence of bacterial microbes inside the cell is what triggers the immune response.”
Similarly, a team of researchers at the Bacterienne Institute in France released a paper detailing how the bacteria E.coli is able to live inside the cells of the immune system. The researchers state that E.coli are “true invasive pathogens, able to invade intestinal epithelial cells and replicate intracellularly. Strains also survive and replicate within the macrophages.”
Infection with L-form bacteria
People are exposed to L-form bacteria in many places. Not all species cause disease.
Because they cannot be killed by pasteurization or chlorination, L-form bacteria can be found in milk, food, and water. They can be transmitted via sperm, intimate contact, and can be passed from mother to child during childbirth. Since they are too small to be filtered during the purification processes used in pharmaceutical manufacturing procedures, they can be transmitted through injectable medicines. They have even been cultured from dry soil.
Once macrophages and other cells have been infected with L-form bacteria, the bacteria circulate in the blood and tissues. In some cases they cluster together in clumps called granulomas. In other cases, they accumulate in regions such as the joints.
Once L-form bacteria have successfully invaded a cell, they begin to use the nutrients inside the cell to their own advantage, disturbing the cell’s delicate chemical balance. They are also able to take control of the host’s genetic material, which allows them to create proteins that enhance their ability to survive.
L-form bacteria cause inflammation and painful symptoms by taking control of a protein called Nuclear Factor Kappa B. They are able to activate proteins that increase the activity of Nuclear Factor Kappa B, which subsequently moves to the nucleus or center of the cell. Once there, it turns on a variety of genes that cause the release of inflammatory cytokines, proteins that generate pain and/or fatigue. These cytokines include interferon gamma and TNF alpha.
Thus, an inflammatory response is correlated with diseases caused by L-form bacteria. “An inflammatory immune response—one of the body’s primary means to protect against infection—defines multiple established infectious causes of chronic diseases, including some cancers,” argues Relman. “Inflammation also drives many chronic conditions that are still classified as (noninfectious) autoimmune or immune-mediated (e.g., systemic lupus erythematosus, rheumatoid arthritis, Crohn’s disease). Both [the innate and adaptive immune systems] play critical roles in the pathogenesis of these inflammatory syndromes. Therefore, inflammation is a clear potential link between infectious agents and chronic diseases.
The CDC concurs, stating, “The epidemiologic, clinical, and pathologic features of many chronic inflammatory diseases are consistent with a microbial cause.”
Detecting L-form bacteria
Once bacteria have transformed into the L-form they can no longer be detected by many standard laboratory procedures.
Regular forms of bacteria can be easily grown outside the body (grown in-vitro). However L-form bacteria have great difficulty surviving in a foreign environment. In order to grow them successfully in the lab, conditions must be similar to those in the human body (grown in-vivo). Consequently they can be cultured on a medium called blood agar at very specific temperatures and at a certain pH.
The concept that some bacteria cannot grow in-vitro is not new. Scientists have known for decades that neither (Syphilis Treponema pallidum ) nor leprosy (Mycobacterium leprae ) cannot be easily cultivated outside the body.
L-form bacteria take several measures to ensure they can survive for as long as possible inside a cell. They are able to infect all types of white blood cells, but prefer to infect macrophages, the type of white blood cell with the longest life span (about 45 days.)
Several studies have shown that once inside a macrophage, L-form bacteria are able to delay the process of apoptosis, or programmed cell death, allowing them to thrive inside the cell for a period of time even longer than 45 days.
Classical bacterial forms can be detected by a lab test called Polymerase Chain Reaction (PCR). PCR identifies and amplifies the proteins and DNA of bacteria that have been killed. However since L-form bacteria are able to persist inside the macrophages for such extended periods of time, few of them die and only tiny amounts of L-form bacterial proteins and genetic material reach the bloodstream at any given time; an amount so small that the PCR test cannot pick them up.
Even if a few small fragments from L-forms that have been killed are identified by PCR testing, the remains are often not from the bacterial species causing the most harm to the patient. This is because the most well adapted, persistent bacterial species are the ones who have developed the most effective survival mechanisms and are consequently least likely to die.
L-forms can also not be detected with antibody testing. Antibodies are Y-shaped proteins that are found in blood. They are used by the immune system to identify and neutralize foreign objects including bacteria.
However antibodies only form in response to bacteria that have died. Since L-form bacteria are able to persist for such long periods of time inside the cells, very few antibodies are created in response to their presence.
Gaining acceptance
Scientists such as Lida Mattman at Wayne State University have worked extensively with the L-form and figured out new ways to grow and view the pathogens. These techniques include a variety of special staining techniques.
British clinician Andy Wright and Danish researcher Marie Kroun have used a Dark Field Bradford Microscope to view L-forms in the bloodstream.
Nevertheless, many doctors and researchers still question whether the L-forms actually exist.
Mattman and other researchers have spent decades figuring out how to correctly culture the L-form. Applying their techniques correctly requires rigorous adherence to specific guidelines. Mattman has said that, over and over again, researchers misinterpreted just one of the steps required to correctly grow the bacteria. They then report to the medical community that no L-forms appear in their samples.
As Gerald Domingue, a (retired) professor at the Tulane University School of Medicine stated, “Unfortunately, in the area of L-form or cell wall-defective bacteriology, too often there have been conclusions (anecdotal) drawn without supporting scientific data. In my opinion, many of these studies have hampered progress in the field and especially the role of these cryptic organisms in bacterial persistence and expression of disease.”
“Features of a number of important but poorly explained human clinical syndromes strongly indicate a microbial etiology,” states Relman. “In these syndromes, the failure of cultivation-dependent microbial detection methods reveals our ignorance of microbial growth requirements.”[2]
There is also little incentive for scientists to study the L-form. Since the bacteria can be killed by simple low-dose antibiotic therapy, drug companies have little interest in investing money into related research. Researchers studying the L-form often find themselves with very little grant money but must still work long, tedious hours in the lab.
As Domingue states, “It is generally agreed among scientists that L-form bacteria are extraordinarily intriguing, interesting tools for biological study, yet the most neglected area of research has been on the role of these organisms in disease, particularly in host-pathogen interactions.”
Another problem rests with the fact that many researchers rely on a series of rules called “Koch’s Postulates” when interpreting research data. The postulates state that only one pathogen can cause a given disease. But research has shown each chronic disease is the result of infection with multiple species of L-forms.
This means that separate teams of researchers often detect different L-forms in patients with the same disease. For example both Borrelia burgdorferi and Rickettsia helvetica have been detected in patients with sarcoidosis. These findings make little sense to researchers still bent on adhering to Koch’s Postulates.
Hopefully as the medical community begins to better understand the role of the L-form in chronic disease, more and more researchers will take the time to learn how to correctly culture and interpret these forms of bacteria.
Most importantly, now that L-form bacteria can be effectively killed by the Marshall Protocol, the opportunity to curb chronic disease is groundbreaking. According to the CDC, chronic diseases represent the major health burden of established economies (>90 million people in the United States) and are a rapidly growing burden in developing economies.
“If a mere 5% of chronic disease is attributable to infectious agents, in the United States alone 4.5 million of the 90 million people living with chronic disease might benefit from strategies designed to prevent or appropriately treat selected infections. Worldwide, the impact could be far greater,” states the 2006 CDC report.
SOURCES
Bisset, K.A., & Bartlett, R. (1978). The isolation and characters of L-forms and reversions of Bacillus licheniformis var. Endoparasiticus (Benedek) associated with the erythrocytes of clinically normal persons. J Med Microbiol, 11(3), 335-349.
Domingue GJ, S., & Woody, H. (1997). Bacterial persistence and expression of disease. Clin. Microbiol. Rev., 10(2), 320-344.
Butler, H.M., & Blakey, J.L. (1975). A review of bacteria in L-phase and their possible clinical significance. The Medical journal of Australia, 2(12), 463-7.
Dienes, L. (1947). Further observations on the repro duction of bacilli from large bodies in Proteus cultures. Proc Soc Exp Biol Med, 66, 97-98.
Domingue, Sr , G., & Woody, H. (1997). Bacterial persistence and expression of disease. Clin Microbiol Rev, 10(2), 320-344.
Kagan, Y. (1968). Some aspects of investigations of the pathogenic potentialities of L-forms of bacteria. In Microbial Protoplasts, Spheroplasts and L-forms. Baltimore: Williams & Wilkins Co. (pp. 422-443).
Klieneberger-Nobel, E. (1951). Filterable forms of bacteria. Bacteriol Rev, 15(2), 77-103.
Klieneberger-Nobel, E. (1951). The L-cycle; a process of regeneration in bacteria. Journal of general microbiology, 5(3), 525-30.
Klieneberger-Nobel, E. (2005). The natural occurrence of pleuropneumonia-like organism in apparent symbiosis with Strrptobacillus moniliformis and other bacteria. The Journal of Pathology and Bacteriology, 40(1), 93-105.
Marshall, T., Fenter, B., & Marshall, F. Antibacterial Therapy Induces Remission in Sarcoidosis. Journal Of Independent Medical Research.
Mattman, L.H. (2000). Cell Wall Deficient Forms: Stealth Pathogens. CRC Press.
Onwuamaegbu, M., Belcher, R., & Soare, C. Cell Wall-deficient Bacteria as a Cause of Infections: a Review of the Clinical Significance. J Int Med Res, 33(1), 1-20.
Pfeiffer, R. (1895). Differential Diagnose der vibrionen de cholera asiatica mit hulfe der immun ieserung. Z Hyg Infekt Kr, 19, 75-77.
Pratt, B. (1966). Cell-wall deficiencies in L-forms of Staphylococcus aureus. J Gen Microbiol, 42, 115-122.
REFERENCES
- O’Connor SM, Taylor CE, Hughes JM. (2006). Emerging infectious determinants of chronic diseases. Emerging Infectious Diseases. [↩]
- Relman, D. A. (1998). Detection and Identification of Previously Unrecognized Microbial Pathogens. Emerging Infectious Diseases, 4(3). [↩] [↩]
- Casadesús, J. (2007). Bacterial L-forms require peptidoglycan synthesis for cell division. BioEssays : news and reviews in molecular, cellular and developmental biology, 29(12), 1189-91. [↩]
NEWS FLASH
Peer-Reviewed Papers
Essential Reading
Amy's Conference Presentations
Featured Articles
Patient Interviews
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.
Amy has spoken at several international conferences and authored several peer-reviewed papers on the intersection of bacteria and chronic disease.
If you have questions about the MP, please visit CureMyTh1.org where volunteer patient advocates will answer your questions. Another good resource is the MP Knowledge Base, which is scheduled to be completed within the next year.
46 Responses for "Understanding L-form Bacteria"
Amy, I like your website! You are succeeding in making the complex world of diseases caused by cell wall deficient organisms understandable and more available to the public. Your writing is clear and concise. Keep up the good work.
I tried to track down your senior thesis for my son, junior at Stanford, to read. Could you make that available to those who request it? He is struggling with a heavy burden of CWDs and chronic fatigue and does not yet fully grasp what is involved in becoming well again and is only a few weeks into the Marshall Protocol.
I also like your interview with Guss Wilkinson. The Q&A format worked very well. I wonder if Gus would consent to post pictures of him at the peak of illness, it would go nicely with the before and after answers to the questions you posed.
Dear Dr. Eckman,
Thanks for your comments about Bacteriality.
Unfortunately, I wasn’t able to delve too much into the Marshall Protocol while writing my senior year thesis. In fact, I’d written about 80% of my thesis before I learned about the MP, and I tried desperately to incorporate as much as I could about the MP prior to the due date. Still my understanding of the MP was fairly primitive at the time. There’s nothing in the thesis that I haven’t written on Bacteriality or can be easily found on the MP website.
It was really difficult for me to get by in college when I had CFS. It took me two years to finish my senior year of college– but, I didn’t have the MP, and I feel that since your son can take Benicar and dose his antibiotics as needed, he should find it easier to get through his coursework. At least I hope so.
My twin sister went to Stanford. Obviously, it’s an amazing school.
I look forward to writing more pieces and explaining other aspects of the MP. Hopefully, your son might find some of them to be helpful. Don’t forget that the moderators on the Board can answer a lot of his questions.
Amy
Dear Amy
Thank you for a great site.
So funny to learn you have a twin sister. I’m also a twin (brother). The Norwegian Sarcoidosis Organisastion says that twins are more likeliy to be affected by Sarcoidosis, but they cannot give sources for this. I wonder, since you have been studying this for such a long time, have you ever comed across papers concluding with this?
I have tried to search pubmed without luck.
Keep up the good work
BR
Martin
Is there a cure for Mercer bacteria, my sister was given this bacteria in hospital doing surgery. She has a open ulcer on her foot due to poor circulation and now she has bacteria and the and great pain from the ulcer to deal with. She has taking treatments in the hyperbaric chamber. She was told that the chamber would cure the bacteria and the ulcer but after ten treatments there is no change.
So my question goes back to what cures mercer.
Hi Margaret,
I just wrote you a little bit about mercer bacteria and the Marshall Protocol after your comment to the article “Bacteria implicated in obesity.”
Basically, I feel that the MP has great potential to treat MRSA infection and your friend should give it a try. You read about L-form bacteria in this article. Well, the staph bacteria that cause MRSA also have L-forms. So it is quite possible that the reason why MRSA infections tend not to go away is because the staph L-form is not being killed. The Marshall Protocol can probably target these staph L-forms, allowing your friend to finally beat the infection.
Read my other response for more info and be sure to post on http://www.curemyth1.org for more feedback on this topic.
Best,
Amy
amy pod i can not find the words to thank for this site it has educated me so much more and the imformation it is so much releif to know there is hope then just to be left in the dark has brought me much hope and peace i can handle anything as long as i know what the ups and downs are. and it has enlighten my DR to help much more i email him all the imformation
Hi Sherry,
I’m so glad to heart that the articles on Bacteriality have helped you better understand the Marshall Protocol. Thanks for writing and saying such nice things about the site. I hope you continue to make good progress and I hope your doctor continues to be interested in learning more about the MP.
Best,
Amy
Thank you so much for your response.
I would to know what is Marshall Protocol. I have been reading about it in your information. Is it a treatment.
Hi Margaret,
I’m happy to help! Yes, the Marshall Protocol is a medical treatment that is run by Autoimmunity Research Foundation – a California non-profit agency.
The treatment effectively kills L-form bacteria and other resistant biofilm bacteria that cannot be killed by standard antibiotic therapy. These bacteria are now believed to be responsible for causing a wide variety of disease including those considered to be “autoimmune” as well as CFS, fibromyalgia, MS etc.
The following is an article that gives an overview of the Marshall Protocol:
http://bacteriality.com/about-the-mp/
Here is an article that discusses the medicines used by the Marshall Protocol in greater depth:
http://bacteriality.com/2007/10/11/antibiotics/
In order to learn more about the Marshall Protocol you should also read as much information as possible on the Marshall Protocol study site. This forum is a good place to start:
“Essential information about the Marshall Protocol”
http://www.marshallprotocol.com/forum2/
After reading as much as you can about the Marshall Protocol, the best place to ask questions about the treatment is at a website called – http://www.curemyth1.org. (Th1 refers to diseases caused by L-form bacteria, hence the name Cure my Th1) The patient advocates on that site will address your concerns and answer your questions free of charge.
Good luck!
Amy
Dear Amy,
It is wonderful to find your site explaining the Marshall Protocol so easily. The MP site is also helpful, but is initially daunting to find one’s way around, and then one has to look all over and put together snippets to understand some of the basic scientific principles.
You have provided a wonderful resource making it much easier to quickly absorb some of this important information.
In one or two articles, you have answered many of my questions which remained following 1 1/4 of my daughter being on the Protocol. I knew from the first evening spent on the site (actually about 9 hours straight) as I realized how applicable the MP was to my daughter’s case and how it all made so much sense) but didn’t have that many days to spend putting together all of the details that I continued to have questions about. You have really helped make this quick and simple.
I just want you to know that some people are really benefitting from your efforts, and really appreciate all the volunteer work and effort that writing these articles and making up this site must have been.
Thank-you Amy!
Leslirae
Hi Leslirae,
Thank you so much for your kind comments about Bacteriality! I’m so glad to hear that the articles have helped you to better understand some of the key issues related to the MP. One of the reasons I started Bacteriality is that I know that out there, everyday, people are going through exactly what I went through before starting the MP – using treatments that do not target the root cause of Th1 disease and getting sicker and sicker. I wish I had learned about the MP before my illness got as bad as it did, and I hope this site may make that possible for some people. So it makes me so happy to heart that your daughter is on the MP and that hopefully the treatment will spare her from many years of relapses and pain.
Best,
Amy
Dear Amy:
Another vote of thanks for your excellent, well-organized website. You writing is top-notch. How exciting to be riding the wave of this new medical approach.
(I agree with a previous comment stating that the “official” website for the Marshall Protocol seems complicated and overwhelming — so many threads that are hard to follow.)
I have a question. In this article — “Understanding L-form bacteria” — there is reference to the innate immune system and the adaptive immune system.
Could you please give a brief explanation on the differences between these? I could probably research it on the internet, but it’s easier to ask you. And, there may be other readers of your site who have the same question.
Thanks very much.
Bethany
Hi Bethany,
Thanks for your kinds words about my site. It is very exciting to write about what I feel is groundbreaking research and to embrace alternate hypotheses (which often seem so logical!) on a number of issues.
I’m glad you asked about the two branches of the immune system as I agree that other readers probably have the same question.
The innate immune system is the body’s first line of defense against infection. By that, I mean it is the system that first recognizes pathogens when they enter the body. If the pathogen is identified as an invader or a pathogenic species that needs to be killed, the cells of the innate immune system go after it. These cells include monocytes, phagocytes, mast cells, leukocytes – all cells whose main job is to engulf and kill any invading pathogens as quickly as possible, and in a non-specific manner.
By non-specific, I mean that the cells of the innate immune system react to pathogens in a fairly generic manner, while cells of the adaptive immune system are highly specialized, systemic cells. If the there is a significant challenge to the innate immune system, it communicates with the adaptive immune system and activates the cells of that branch.
The cells of the adaptive immune system take the fight up another notch. They do this by creating factors that allow them to recognize and remember specific pathogens (to generate immunity), and to mount stronger attacks each time the pathogen is encountered. Hence the name adaptive immunity – the branch allows the body to adapt and be prepared for future challenges. The adaptive branch does this by creating antigens, or molecules that it can detect on the surface of invading cells that alert the body that the cells are invaders and not the body’s own cells. Cells called memory B and memory T cells are also created that help the body remember the nature of the pathogen that is challenging the body.
So the innate system is the branch that puts up a battle against pathogens that enter the body. If the battle becomes big enough, the adaptive branch is activated, which uses other cell types to create antigens that allow the body to better recognize the invader and also create a “memory” of the invading pathogen, so that if it enters the body again, the body will be much more prepared to fight and react to it immediately. This is why, for example, if you get the flu, you are not likely to get the same flu again a few weeks later.
In the case of the Marshall Protocol, the innate immune system is the branch that kills L-form bacteria. The body has not formed antigens or created any memory of L-form bacteria, as the pathogens are able to hide inside the immune cells and biofilms. So the battle against them is waged almost completely by the cells of the innate branch.
That is why it is so important that the Vitamin D Receptor, the receptor that controls the activity of the innate immune system, be active while a patient is on the MP. Benicar works by activating the Vitamin D Receptor, and the reduction of vitamin D in the diet also helps the receptor work more effectively.
Hope this helps!
Amy
Hi, Amy.
I have been reading a lot about the MP, as my wife is awaiting a confirmation
that she may be in the early stages of Sarcoidosis.
I’m just curious if you are aware of any study which demonstrates conclusively
that the MP does directly reduce the intra-cellular L-form bacteria count. By
this I mean taking various tissue samples from a host prior to commencement of
the MP and making up slides which show the intracellular CWD pathogens within
the cells of the tissue. Then doing similar samples after a period of time on
the MP and again checking for CWD pathogens. This could also be carried out
against controls. I guess this would, in the scientific community,
constitute irrefutable evidence that the MP does in fact reduce intracellular
CWD pathogens.
Regards
Michael Conte
Hi Michael,
You are not the first to suggest that such a study be done in order to confirm that the MP does indeed kill L-form bacteria. Autoimmunity Research Foundation (the non-profit that runs the MP) will probably carry out a study along the lines you have described at some point but there will be several differences when it happens. Some of the differences also explain why Autoimmunity Research Foundation (ARF) has not yet put the small amount of money it makes from donations towards such a study as of yet.
A study cannot be done where bacteria are cultured from the tissues. Many scientists to study the L-form have tried to pull off such studies and there work has not been taken seriously. Gerald Domingue and Lida Mattman among others have entire textbooks showing L-form bacteria cultured from the tissues of many of their patients. Their samples and pictures were dismissed by mainstream researchers who said that their samples were simply contaminated. Many doctors today still give that excuse when confronted with samples of L-form bacteria. They say, “Oh samples can be contaminated in the lab and we can’t take your study data seriously. ARF cannot risk such problems.
Also, growing L-form bacteria in the lab is incredibly difficult. L-form bacteria don’t grow when scientists use standard cultivation techniques. Researchers must go to long lengths to ensure that conditions mimic those of the human body and this can be very difficult. Lida Mattman, one of the top researchers to work with the L-form, stated again and again that other research teams would fail correctly follow just one of the careful procedures she had created for culturing L-forms. They would make just one tiny mistake and the pathogens would fail to grow. Since Dr. Marshall is not a microbiologist, another lab would carry out the process of culturing L-form bacteria from patients on the MP. If, for some reason, the lab made any mistake in the complicated procedures needed to culture the pathogens, they could very well come up with results saying that patients in the MP arn’t infected with L-form bacteria in the first place. That would be untrue, yet the medical community would take that data as real and it could severely hamper acceptance of the MP.
So, in order to perform a study that could confirm that MP patients have less bacteria as they start to recover, ARF will have to use some of the latest molecular tools. The only way that researchers can use these molecular techniques to detect all the L-form bacteria present in a given cell is to sequence entire cellular genomes. That means for each cell, all the DNA, not just part of the DNA must be sequenced which is an extremely lengthy task. At the moment there are only a few centers that have such technology available, one being the Human Genome Project which might be able to partner with ARF at some point but is not ready to do so today.
Because such expensive molecular techniques are the only way to conclusively prove to the medical community that patients on the MP are sick with bacteria in the first place and that they also kill these bacteria over the course of therapy, such a study will be very expensive. ARF will definitely have to partner with a university or organization to get the job done. Or it could get an amazing grant – none of which have happened yet because the treatment is so new and the concepts put forth so controversial.
In the meantime, I encourage people to donate to ARF so that it can continue to reach out to major universities and other scientific organizations so that they better understand the Marshall pathogenesis and see its merit. It is only a matter of time before this happens, but I cannot say when.
So at the moment there is, unfortunately, no such study that you can present to your wife’s doctor. You can, however, help her doctor fully understand the meaning of immunopathology.
Patients on the MP use a combination of Benicar and pulsed, low-dose antibiotics to elicit bacterial death which causes a rise in symptoms called immunopathology. Because patients note this increase in symptoms once they have started the MP meds, the presence of the immunopathological reaction is proof positive that the body is indeed killing bacteria – which in turn means that bacteria are undoubtedly driving the disease process in the first place.
A devil’s advocate would be hard-pressed to explain MP patients’ consistent immunopathology in any other way. After all, both Benicar and the antibiotics used by the MP have excellent safety profiles, so rises in symptoms can seldom, if ever, be attributed to the side effects of these medications.
Just as one might suspect, patients who increase their antibiotics find that their symptoms return with increased severity. Similarly, taking lower doses of antibiotics, which decreases the number of bacteria being killed, results in a reduction in symptoms.
Since each MP antibiotic targets different species of bacteria, patients can often switch from one antibiotic to the next in order to elicit different symptoms.
So it isn’t really necessary (although I agree it would be nice!) to test for bacteria in the tissues of MP patients, as the immunopathological reaction can be used to infer that a patient is indeed responding to the MP. I hope that ARF can do a study using the molecular techniques described above as soon as possible. Until that time though, I hope that the presence of immunopathology, along with the solid molecular data that forms the backbone of the MP, combined with a tremendous amount of data collected from the study site showing that patients are getting their lives back, can serve as enough of an impetus to have your wife’s doctor put her on the treatment.
Best,
Amy
Amy,
Thank you, for your prompt response.
I’ve read extensively the science behind the MP and concur that the study findings themselves are living evidence that Dr. Marshall’s theories about the pathogenesis behind chronic disease are correct and reproducible. However what is holding up the wider adoption of the MP and further research on the capability of the innate immune system to deal with chronic illness is the fact that it cannot be shown that the protocol directly kills off the pathogens which cause the symptoms of chronic disease.
Is it absolutely necessary to culture L-form bacteria, given acceptance in the general research community that this is not easy or sometimes possible without repeated efforts and also that it would be claimed by others that if successful, was as a result of contamination?
I’m suggesting that initially it would be far easier to demonstrate a lowering in the count of infective pathogens following time on the protocol through biopsy studies rather than to culture the pathogens. This is because it is far easier to deal with problems of contamination of biopsy samples by following strict preparation procedures and using controls.
I tend to agree that to sequence the complete genome of infected cells is complex and expensive and would no doubt raise more questions that it would answer.
Teresa, my wife, will commence on the program as soon as we find a Doctor. I’m certainly not waiting until the medical community catches up with the latest developments. Not when the MP has so much promise with only a few side effects. Particularly in her case, as she has been diagnosed very early and her pathogen load is small.
I’m reminded about Dr. Trevor Marshall’s name sake Dr. Barry Marshall, who had such a battle and was so derided about his theories that Stomach Ulcers were caused by a pathogen (Helicobacter Pylori). Dr. Barry Marshall then received the Nobel Prize for his work. I guess that their might by another Dr. Marshall on the honour roll in the near future.
Thanks
Michael Conte
Hi Michael,
I’m so glad your wife wife start the MP even when ARF has not yet done a study to look for bacteria in patients on the MP.
I do assure you that the study could not be effectively done using standard cultivation techniques. I’ve actually had several conversations with Gerald Domingue, a researcher who worked for years with the L-form at Tulane University, on the subject.
He is also confident that we could not get conclusive results if we tried to culture L-forms in the lab. The techniques are too difficult and the potential for error too great.
But he is a great believer that we should use molecular techniques to look for bacteria in patients on the MP. Last I heard he is actually working on a book that will describe how to effectively identify L-form bacteria using molecular techniques. So when that book comes out it may serve as an impetus for some university or foundation to partner with ARF and get the work done.
I agree that it’s important that patients start the MP as soon as possible. I’m so glad that your wife will start the treatment soon after her diagnosis. I’m sure her immunopathology will be much easier to handle and that she will progress through the treatment rapidly.
The Barry Marshall story is a testament to how slow the scientific community is to accept change – and he only had to prove that one species of bacteria was causing an ulcer. Acceptance of the MP will require several much larger paradigm shifts. But like you I look forward to the day when this research is embraced and Dr. Marshall is given full credit for his hard work.
Best,
Amy
Hello Amy,
My sister Lindsey Stice went to Stanford with your sister Sara. I am about to
get my 10 week old son vaccinated next month and I wanted to know if you had
any insight or articles relating to vaccinations.
Hi Jessica,
Good to hear from you! I’m sorry not to have written you back more quickly. I just got back yesterday in the afternoon from a week-long trip to Sweden for a medical conference. It was cool because our work was really well received.
I wish I could give you solid advice on what to do about vaccines. I asked the head of our foundation her opinion and she wrote the following:
“The issue of vaccinations is so controversial and weighted with emotion. We have no official policy other than to say we are confident CWD may ride along with those vaccines. IMO, immature immune systems may be too challenged by the multiple vaccinations advocated……single vaccines and delay as long as possible is a good compromise. It’s really a matter of risk (perceived or real) vs. benefit.”
To clarify what she is saying, it’s quite likely that the vaccines your son would get will be contaminated by the cell wall deficient bacteria (L-forms) that we find cause essentially every inflammatory disease. So vaccines are a way of introducing bacteria into your son. Read more about L-form bacteria here:
http://bacteriality.com/2007/08/15/l-forms/
However, if your son has a strong immune system (does he get sick a lot or does he seem resilient?) then his body may be able to naturally kill off the bacteria in any given vaccine. In that case, spacing out the vaccines as far apart as possible is a good idea. That way if there are any L-forms in the vaccine, your son’s immune system can have the time to kill them more gradually.
The problem is that if you don’t get your son vaccinated, he is at risk for other serious illnesses. You really don’t want him getting smallpox etc. The bacteria from those diseases could also turn into a chronic form sthat could contribute to a chronic disease later in life.
So, I guess if I were in your shoes I would try to do the vaccinations as far apart as possible. Then I would keep a good eye on your son. If he starts to suffer from any sort of chronic infections (for example asthma, strep throat, or really any type of pain or symptom that never really seems to go away), put him on the Marshall Protocol immediately. The Marshall Protocol is a treatment that will kill any of the bacteria that he would have acquired through the vaccines. If he starts it early it’s very easy to do and he should only have to spend a few months on antibiotics. So it’s hopefully a comfort to know that if you son does pick up L-form bacteria from a vaccine they can be killed off.
As you can tell this is a difficult and frustrating issue. The fact that the medical community is giving potentially contaminated vaccines to every child is a huge problem. That’s why our foundation is working so hard to get our research acknowledged!
Last, I would not stress the issue too much. L-form bacteria are present in our food, in our water, and exist naturally in the environment. Everyone picks up some of them as they grow older. If your son does show signs of chronic infection he can do a quick round of the Marshall Protocol and become totally healthy again.
Also, I should add that you should make sure that your son only consumes a reasonable amount of vitamin D, that which is found naturally in foods. That will allow his immune system to function more effectively and kill any L-forms he comes in contact with. So stay away from fortified milk, multivitamins with D, or anything else in which they have artificially added D to the product. You can read more about why extra vitamin D negatively effects immune function here:
http://bacteriality.com/2007/09/15/vitamind/
Hope this helps! Say hi to Lindsey for me!
Best,
Amy
Hello. I am shocked regarding vitamin D suppressing the immune system. I’ve been giving my husband 2,000 iu of D3 for the last 2 years. Lately he has had a squamous cell carcinoma appear on his leg.
It has been removed. He also now has an
inflamed foot (plantar fasciitis) is it possible the vitamin D then has encouraged this? Is 2 -3 years high D supplementation long enough to effect in this manner?
Rita
Hi Rita,
Unfortunately, yes, your husband’s carcinoma and and plantar fascitis could be directly related to his vitamin D consumption – or should I say secosteroid D consumption.
First off, I understand how confusing it is for a member of the public like yourself to make a decision about vitamin D at the moment. There are a group of scientists who refuse to consider the molecular modeling research which makes it clear that the “sunshine wonder drug” they tout is simply an immunosuppressive steroid. These “experts” are usually quoted by the media and I have read many articles where they do advocate high levels vitamin D supplementation. So I don’t blame yourself for following their advice when you didn’t yet realize that there is a different side to the vitamin D debate.
But now you are aware that there is a growing camp of researchers who view vitamin D in a completely different light. The diseases your husband is starting to show signs of are likely caused by chronic bacteria, and unfortunately vitamin D slows the immune system’s response to killing these bacteria. While this probably allows your husband to feel better in the short-term (less bacteria death causes less painful inflammation), his immune system is no longer working up to par. So any bacteria he harbors can spread with greater ease.
I truly urge you to stop giving your husband vitamin D. He may feel a bit worse when he stops taking the D because his immune system will once again start to more powerfully attack the bacteria making him ill. But an active immune system is a good thing and the situation will serve him best in the long-term.
Best,
Amy
Dear Amy,
Wonderful to see that you have raised awareness of and for treatment of L-form/mycoplasma diseases. More than fifty years ago mycoplasma were reported agents for rheumatoid arthritis. Today, mycoplasma are reported agents for Gulf War Illness, but drug companies don’t still don’t respond. Milton Wainwright’s “Extreme Pleiomorphism, a Forgotten Controversy” may explain why – deal with infectious agents at a primary molecular level and antibiotics will be history. Prof. Dirk Elston, wrote “bartonellosis spread by a louse will have different manifestations from bartonellosis spread by a biting fly”. Routine laboratory practices can obscure diagnoses, films need to be seen methanol fixed unstained, culture media should not contain bile salts that can emulsify lipid content forms, or substances that can induce microbes to produce L-forms that can evolve to cell wall-less forms that are seen as contaminants, not as atypical forms. I will be happy to send you electron and color microscope picutres and medium composition from our study “Microbes and sequestered substances…L-forms…,
Hi Faith,
It’s great to make contact with another researcher who is familiar with the techniques needed to culture L-form bacteria!
If you could send me a copy of your paper and the electron microscope pictures of the L-forms you have detected I would be thrilled. Why don’t you send them to my email address – amy.proal@gmail.com? That way I can (with your permission) put them up in a post on this site.
I look forward to seeing the photos!
Amy
I think you will find that Dr Wrights microscope is an optical microscope and not an electron one as shown by the picture.
Trevor,
You are correct. I have removed the incorrect caption and image. Thanks for pointing out my error.
Best,
Amy
My daughter has a chronic high SED rate and an abnornal ANA she has seen a Rheumatologist and all diseases have been ruled out. She is being “watched”. She also suffers from migraines, fatigue and joint pains. She had mulitple bouts of strep throat and Scalet Fever as a young child.We always completed her courses of antibiotics as prescribed. Her grand mother has heart disease which may be a result of untreated chronic strep in the 1930′s. And I, her mother, had Rheumatic Fever as a result of chronic treated strep.
It seems like L-foms of bacteria may be the cause of her current symtpoms.What should be ask of her doctor to make a diagnosis and what life style changes can we make to kill possible L bacteria ?
Dear Gerry,
I’m very sorry to hear about your daughter’s symptoms. Interestingly they sound very much like mine as I was getting sick. I too had scarlet fever, migranes etc. It took me years to get a diagnosis – I was finally told I had CFS. But in reality, the diagnosis changed nothing. I tried all the “standard” cures for CFS that did not treat the root cause of the illness and only made me worse in the long run.
Then I found the Marshall Protocol, which is the treatment described in greater detail on this site. It is now becoming increasingly clear that any illness that results in mysterious chronic symptoms of “unknown” cause are actually caused by different forms of chronic bacteria that the immune system is unable to kill. As they accumulate, they slow the immune system, allowing the patient to accumulate more and more bacteria which can eventually result in a system-wide infection and a large variety of symptoms that are often hard to classify into a specific diagnosis.
It sounds like your daughter falls into this category. I would say if you see enough doctors she would get diagnosis of CFS. But no matter what diagnosis she gets, the Marshall Protocol would still, in my opinion be her treatment option of choice since Lyme disease, lupus, arthritis, and myriad other inflammatory diseases are caused by different species of these same bacteria. The Marshall Protocol effectively targets the bacteria implicated in all these diseases.
What that means is that I think your daughter should start the Marshall Protocol (MP) as soon as possible. The treatment is run by a non-profit agency and there is no charge for any aspect of the MP. However you will have to find a doctor who is willing to prescribe her the necessary MP medications.
I recommend reading the following two articles about the MP that discuss the treatment in simple terms:
http://bacteriality.com/about-the-mp/
http://bacteriality.com/2007/10/11/antibiotics/
This video is very helpful. I describes the treatment and the science that forms its backbone.
http://bacteriality.com/2008/05/07/mpintro/
Here is a link to MP publications and presentations that you or your doctor may want to review:
http://mpkb.org/doku.php?id=home:publications:home
After you have gotten a better idea of what the treatment entails then you should post about your desire to start the MP at the following website:
http://www.curemyth1.org. (Th1 refers to bacteria, hence the name). The patient advocates on the site will help you get started and answer any questions you might have about the treatment. There is no charge for their advice. On the site, you can also request a list of MP doctors in your area.
The MP took me from bedridden with symptoms that sound very similar to your daughter’s to having a normal life again. I can’t describe what it’s like to feel well again. Young people usually progress very well on the treatment so your daughter is in a good place.
Best,
Amy
Hi Dr. Amy,
I am a veterinarian who is doing research on the origins of disease. This came about after my miraculous recovery from multiple ailments following my diagnosis of food intolerance, particularly celiac disease. I have chronicled my recovery and findings on my Website, http://www.dogtorj.com.
I’ve come to the conclusion that most of what we call “disease” are long-term symptoms arising from the “civil war” taking place in our body between its residents- our cells and those entities designed to help and protect those residents (e.g. viruses and bacteria) and the constant barrage of immune challenges that we throw at them (e.g. food lectins, carcinogens, chemicals/preservatives, trans fats, fluoride (an “antibiotic” and carcinogen), air pollution, etc. etc. These coupled with our horrific fast-food diets, lack of sleep/exercise/sunlight, and self-induced misery through alcohol/drug abuse and penchant for sugar has brought all of the plagues of Pandora’s Box on mankind.
And yet, we keep pointing the finger at microorganisms like viruses and bacteria, including L-forms and mollicutes, as the enemy. Granted, most don’t know or fully understand the true nature of viruses and bacteria- that they are crucial for our survival, being important instruments in our adaptation to this ever-changing environment in which we live. But shouldn’t intelligent people be asking why these guys are so ubiquitous and a relative few people are suffering from the “diseases” caused by these “culprits?
The fact is that viruses and L forms do what they do because they NEED to survive because they are crucial to OUR survival. Would you disagree that if we could snap our fingers and make all viruses and bacteria disappear from the planet that the entire ecosystem would collapse? Certainly, we know- and you have stated- that the vast majority of these bacteria are not pathogenic? What really distinguishes a pathogen from a saprophyte- or a helper?
When huge numbers of the population are infected with various “pathogenic” bacteria and yet remain asymptomatic, shouldn’t it give us pause as to why they become such culprits of disease in the “unfortunate” few? Are they just unfortunate or have they done something- or lived somewhere, in the case of pollution- that has brought this plague onto themselves. We know that the number one risk of developing Legionnaire’s Disease was/is cigarette smoking. Now there’s a surprise.
I believe down to my core that viruses and bacteria work in concert to help us all, especially when it comes to adaptation and survival. Bacteria form L-forms and viruses mutate because they NEED TO SURVIVE- they are critical to our survival and only become pathogens because we have forced them into doing so with the laundry list given above. Cancer is little more than a virus (and/or an intracellular bacteria) forcing that cell to duplicate out of control in a desperate attempt to protect itself- and the cell it was designed to protect- as well escape those noxious elements (we call them “carcinogens”) that have forced them into this final phase of adaptation.
Our immune system tried valiantly to deal with this during the preceding “autoimmune” phase, a term I no longer use because the thought of our immune system attacking itself for no reason is preposterous, especially in light of your research on L-forms. And we can’t say we weren’t warned by the broad array of symptoms we were given- the heartburn, IBS, allergies, hives, cough, migraines, seizures, fatigue/depression, etc, etc, etc.
Certainly, there are those who have become so afflicted and immune challenged that they need some pharmaceutical aid dealing with these helper-turned-“culprit” bacteria but to become dependent upon antibiotics for any significant length of time is both potentially dangerous and unnecessary. But if we stop the assault we are laying down on these misunderstood and reactionary residents, we can come off the drugs (like I did) and re-establish the status quo- and LONG before the two or three year mark in most cases, I believe.
People simply need to know that WE are the culprit, not these microorganisms at which we keep pointing our scientific finger. Why? Because these organisms- the viruses, bacteria, L-forms and mollicutes- are here to stay! It is we who are the transient visitors. And if we want to enjoy our stay, we’re going to have to learn how to treat ourselves- and those who reside within us- a whole lot better.
I do hope this helps,
John
John B. Symes, DVM
Dear John,
So based on your view of disease when you treat an animal with cancer do you get on its case for smoking?
Thanks for your feedback but I completely, wholeheartedly disagree with what you say. Clearly you have not read any of the other articles on this site?
This site describes a trial called the Marshall Protocol in which patients take a medication that activates the innate immune system and low, pulsed antibiotics to kill the bacteria that are increasingly being implicated in EVERY autoimmune disease. So people killing the bacteria in their bodies are recovering from a huge host of diseases that have never been reversed before.
Your explanations for chronic disease make no sense. Humans are made of 90% bacterial cells and only 10% human cells. That means there are trillions of bacteria in the body – in fact trillions in the gut alone. Do you really think it’s evolutionarily plausible that all these bacteria are just sitting around helping us? Such tremendous commensalism is not seen in any other ecosystem on earth. Or does it make more sense that the majority of bacteria have gradually evolved to take advantage of their human host? Certainly a great number of bacteria we have already characterized are extremely pathogenic. Eventually chronic bacteria cause the inflammation associated with the bulk of the world’s illnesses.
You “blame the patient” dogma has run its course. Have you ever met someone seriously ill with a chronic disease? To say that all their pain and diverse symptoms are simply their own fault and the result of some lifestyle experience is insane. People with chronic disease are dealing with a huge number of pathogens that make them ill and nothing but directly targeting these pathogens will make them better.
By the way, I never said the majority of bacteria in the body are commensal.
Best,
Amy
Amy, Nice site!
Taught me allot. I think a few things on this page need some clarification. I believe L-Form / CWD bacteria can be killed by chlorination and UV. Is this true?
So maybe pasteurization needs this???
That’s All.
-Justin
-Justin
Hi Justin,
Thanks for writing. Where did you read that L-form bacteria can be killed by UV and chlorination? Do you have a paper that states that? Just curious….
I Googled the topic and came up with some adds saying that exposing water to UV light apparently kill most microorganisms in the water. I’m not sure if L-forms have been studied in this context however or how accurate the claims are. Also, I’m not sure if there would be any dangers of exposing milk to UV rays. I hope it wouldn’t affect any of the important nutrients in milk, for example. The same concerns apply to chlorination.
Nevertheless, even though I can’t comment with authority on your suggestions, you are thinking smartly, IMO! We do need to think about processes that will better rid the food supply of many different forms of bacteria. L-form and other bacteria have shown to survive in water and milk, so better purification of these substances could likely improve population health.
Best,
Amy
Amy,
The UV C band specifically works by garbling DNA. That is why I think it will work for pasteurization. However I do not see oxidizing the milk or other foods with chlorine a probability.
Thanks for your quick reply!
-Justin
Amy,
Another thing!
I think this stuff goes as deep as mad cow disease, I have trouble believing in the Prion theroy as the L-form model works much better on the TSE diseases.
-Justin
Here a recent link about research on L-Form Bacteria:
http://www.nature.com/nature/journal/v457/n7231/abs/nature07742.html
It seems that the reproduction methods of L-Form bacteria may be very old, older then those of normal bacteria with cell wall.
Alex
Hi Alex,
Thanks for sharing. Let me correct you though by saying that there are more than two papers:
http://mpkb.org/doku.php/home:publications
The last five (!) are “in press.”
The other thing that stuck out at me is your comment about “independent studies.” You should look at Greg Blaney’s Porto presentation:
http://mpkb.org/doku.php/home:publications:blaney_congress_on_autoimmunity_2008
This talk is going to become a peer-reviewed paper in the next four or five months or so.
Best,
Paul
Hi Amy,
Wow! I sure didn’t expect such a negative and violent reaction to my post. You seemed to have missed my point entirely.
First of all, I have nothing but sympathy- and empathy- for the chronically ill patient, having been one myself. I have been a veterinarian for 30 years and dealt with my share of veterinary cases and seen many of my beloved pets and pet owners die of chronic illnesses. Although many of my clients have died “at their own hands” through smoking, drinking, drugs, horrific diets, past-paced lifestyles, lack of sleep, and poor choice of location (polluted cities), I would never go so far as to say it was “their fault”. Most people are simply unknowledgeable of the importance if these crucial elements or deceived into believing that they are doing all that they need to stay healthy.
As far as the role of bacteria is concerned, it seems that you’ve missed my point on that, too. Surely we agree that bacteria play a vital role in our everyday health, just as viruses do. But, they ARE capable of adapting to the challenges that WE throw at them. The main reason they are morphing into pathological entities is not because they have an innate desire to kill us but simply because they are defending themselves, adapting to those challenges in order to survive. You give reasons for bacteria to form L-forms and they are mainly responses to challenges that WE pose to them, right? How many of those potentially pathological bacteria (and viruses) lie dormant in the body for years and years before finally becoming a problem? What brought them out of hiding? What is the long-term solution for getting them back to their dormant state…antibiotics???
I agree that there are countless people out there that could benefit from specific and even long-term antibiotic therapy. Thanks in part to your article, I am using doxycycline to knock out some “idiopathic conditions” that most of my veterinary colleagues are still covering up with corticosteroids.
My main point was meant to be that if we focus on eliminating the reasons why these bacteria are morphing into pathogenic entities at the same time we use these antibiotics to rescue those in desperate need, we will not only enjoy better success rates but we should also be able to reduce the length of time these individuals are on antibiotics. That may sound elementary but when we understand that the very staples of our diets and environments are major contributing factors, then we see that we have our work cut out for us.
But if we choose to ignore these factors, then we had better be ready to fail in our attempts to control them with drugs alone. That is like taking an aspirin for a headache caused by a brain tumor.
I hope this clarifies matters,
John
Hi John,
I’m not sure “violent” is the word for Amy or her comment. I think “strident” would be more appropriate. In reference to Amy, I would also accept “firecracker.” Up until recently, I called Amy a “whippersnapper,” but that was only until I actually looked up the word. (It’s not flattering.)
In your response, you list a series of lifestyle factors that you claim have been implicated in chronic disease: “smoking, drinking, drugs, horrific diets, fast-paced lifestyles, lack of sleep, and poor choice of location (polluted cities).”
I’m not so sure. What about a fast-paced lifestyle allows bacteria to proliferate? Sick patients have tried for the longest time to manage, even micro-manage their lifestyle and they remain sick. When my Mom got pre-cancerous lesions, she was crestfallen. “How can I be sick when I’ve done everything right?” she asked.
I think Amy’s point is that if there’s anything which is unhealthy it is blaming these types of choices. If you need to, look at the studies. The best epidemiological evidence does not support the conclusion that these types of factors are largely responsible for bacterial proliferation and/or disease.
On Bacteriality, Amy does her best to stick with scientific evidence. For example, there is evidence that chronic pathogens grow when exposed to beta-Lactam antibiotics such as penicillin. Corticosteroids, which you mention avoiding (good!), are another drug which does not help patients sick with chronic disease.
Forgive me if I’m misinterpreting your words, but I think it’s wrong to assume bacteria are defending themselves. Bacteria are driven by a biological imperative, and that is to survive and pass on their genes. If it helped them survive, why wouldn’t they interfere with proper functioning of the body’s systems and in the process cause symptoms of chronic disease?
By the way, if you heard doxycycline was a good idea, I’m confident you did not hear it from Amy. It has been the experience of the Autoimmunity Research Foundation team that even though tetracyclines tend to have a strong track record, doxycycline leads to strange neurological symptoms that we think are unrelated to immunopathology.
Best,
Paul (not Amy)
p.s. “Dogtor J” is an awesome name.
Hello Amy,
Very interested in all the info on your site. I had glandular fever ( which had all the symptoms but was never actually diagnosed until recently when a doctor said my bloods say i have had GF ) when i was 17.
Soon after the Gf i was told i had Post Viral Sydrome or CFS.
I am now 35 and still dealing with a low stress tolerance which lead to a basic nervous breakdown 2 years ago,anxiety,aching muscles and extreme bouts of fatigue.
Although i have been able to live a pretty normal lifestyle for the past 15 years, everytime i increase my exercise in an effort to increase my health/wellbeing i am setback by fatigue.
Recently i had my annual blood tests done again in an effort to find a reason, only to be told they are all clear and anti depressants are my best shot! ( Just when i thought i was onto a good GP! )
I Have a great life, Wife ,bub on the way, great job, house, friends and family- i am NOT depressed !
The only time i become depressed is when my other symptoms arise,regularly!
Hence i am back on the net trying to self diagnose again. As you can imagine after nearly 20 years of this constant frustration i am extremely interested in the MP. I dont need further proof as i have tried everything else ive found/been suggested.The only problem i believe i mat have is finding a doctor to prescribe the meds.By the way i once again have said no to anti depressants as you may have gathered!
I think i also read somewhere on the site that it is getting very hard to get a place on the MP,is this correct?
Ps Thanks for the venting,feel bit better now,
Kind regards,
Sam
Hi Sam,
Amy is indisposed, so you’re stuck with me.
I don’t know if you got a chance to read my interview where I talk about my experience with some of the symptoms we share, namely being overly sensitive to negative life events and being intolerant to exercise. You’ll see in my interview that, unlike you, I was depressed.
On the other hand, your problem is that even though you aren’t depressed, you share a few of the characteristics of people who happen to be depressed. Amy is (or was) a good example of that.
One could argue that many diagnoses for patients with ill-defined chronic diseases are made out of cognitive convenience. It has been my observation that what a clinician thinks causes a disease is shaped by available treatment options for that disease.
Look at dentists. If you ask them if bacteria cause plaque or tooth decay, >99% will say absolutely. The fact that a DDS can employ a therapy against plaque (in this case, manually removing plaque with Inquisition-era instruments) clearly shapes their opinion about the etiology of the disease. That the intervention is at least temporarily effective also has something to do with it.
When it comes to lethargy or exercise intolerance, the mainstream treatment option, however unsuccessful it may be, is the anti-depressant. And you wouldn’t need anti-depressants if you weren’t depressed?
Best,
Paul
Hi Paul,
Thanks for the quick response!Yes i had read your interview,was actually the first item i came across in my search for treatments.
I did definetely relate to your story in particular as it is actually cycling i have been trying to get into for my exercise! I seem to be pretty good with the shorter rides but as soon as i stretch the distance a little i end up fatigue stricken once again. The annoying part is during the rides i feel really good and i can tell my fitness is increasing, but it can take days for me to recover due to the deep fatigue i seem to keep getting.Also i liked your plaque/depression analogy and completely agree that doctors only work with band aid medication for symptoms! Was curious to see whether you thought the MP was a good way for me to go ( or am i just asking the obvious after explaining my symptoms
Thanks again,
Sam
Hi Sam,
I feel strongly that the MP will help someone with your symptom presentation. If you’re interested, you can always get going by trying a therapeutic probe.
Best,
Paul
Hi Dr. Proal:
I suffer from SLE, my grandmother has Parkinson’s Disease, my cousins and aunt have been diagnosed with FM, so we share information as often as possible. One of my cousins has a neurologist who suggested she read up on the Marshall Protocol. I must admit, I have not read much, beyond this article, so you’ll have to bear with my ignorance.
It all made good sense till I came to the following:
“However antibodies only form in response to bacteria that have died. Since L-form bacteria are able to persist for such long periods of time inside the cells, very few antibodies are created in response to their presence.”
QUESTION:
If the above is true, why would the body develop an autoimmune response to the invasion? Or am I not understanding this correctly?
If you can help me understand a bit better, perhaps I would be able to more thoroughly discuss the Marshall Protocol with my practitioners. Thank you.
Hi Jennifer,
I’m glad you are looking into the science related to the MP. As for your question – we are presenting a model for “autoimmune” disease in which the inflammation seen in such diseases states in not due to the immune system attacking itself but is instead the result of the immune system continually attacking chronic bacteria.
This article describes how the current model of autoimmune disease that you are used to hearing about may be running its course and also gives you a better idea of research into “autoimmune” models that involve bacteria, such as ours:
http://mpkb.org/doku.php/home:pathogenesis:alternate_models:autoimmunity
However, antibodies are still produced in most people with autoimmune disease. We have hypothesized that once again these antibodies are not created in response to self (autoantibodies) but are instead a downstream result of antibodies being generated in response to cellular debri created by bacterial death. This speech, which I gave at the International Congress of the Antibody in China goes into the topic in further detail:
http://bacteriality.com/2009/06/11/ica/
This paper in Autoimmunity Reviews also discusses our research on autoimmune disease and antibodies:
http://AutoimmunityResearch.org/transcripts/AR-Proal-Metagenome.pdf
Hope this helps and I encourage you to continue reading more about the MP to get the full picture. If I had to start learning about the MP and the science related to the treatment I would begin by watching the following video:
http://bacteriality.com/2008/05/07/mpintro/
Take care,
Amy
PS I am not a doctor – I am a microbiology/molecular biology PhD graduate student.
After reading up on this Marshall Protocol this is something I might need for myself.
I was diagnosed with Eosinophilic Gastroenteritis in 2004 at NIH. My IgE fluxuates from a high of 790 to low of 200. My Vitamin D ratio of the two types is 3.6. My 1,25Dihydroxy Vitamin D is 99 for the past 2 years. My Urine Calcium is 400 on a scale of 0-300. My Eosinophil level absolute goes from 0.4 to 2.1 which is 37% when highest. I tested allergic to ALL foods and live on a pediatric formula.
Now I have little sarcoidosis bumps all over my trunk, ribs, back area. It went away with a trial of 20mg/day for 10 days.
Up to now I have found a far-infrared sauna has helped a lot but not completely.
I gave up Prednisone in 2005 due to it causing high blood sugar and affecting my vision. This was my first taking of prednisone in years and I know it only masks the problems.
I also have Adies Tonic Pupils – I always believed all these things were related but docs kept saying no and alluding that it is in my head.
I see that you are local, I am in Tysons Corner/McLean VA. Which doctor did you use locally that will do the Marshall Protocol?
The other question I had is where does the Marshall Protocol stand on Blood Transfusions? If UV is unknown to destroy these parasitic invaders, then years down the road there could be many problems developing? no?
Hi Amy,
You might be interested to know that the molecular basis of L-form bacteria has recently been published by Dr. Zhang’s group at Johns Hopkins in PLoS ONE. See link: http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0007316
This is first comprehensive genetic study that defines the molecular basis of L-form bacteria, which has been elusive for decades.
Hi Craig,
Sorry for the delay in responding. It sounds like you have several issues. I agree with your insights that your different conditions are connected in some way.
First of all, you may want to run your vitamin D results through the vitamin D metabolite calculator:
http://mpkb.org/doku.php/home:tests:vitdinterpretation
If your 1,25-D is in pg/ml, that is a very high level. I don’t know why you would want to use far infrared sauna to give your body even more 1,25-D. Given your symptom presentation and the level of your vitamin D metabolites, the only thing far infrared sauna is likely doing is suppressing your immune response… which might explain why you feel better. If you agree that microbes are causing your disease state, then you would also have to agree that suppressing your immune response would be the last thing you would want to do – no matter how much better it makes you feel.
http://mpkb.org/doku.php/home:othertreatments:saunas
If you read our post on the IOM workshop, you’ll see that even the pro-vitamin D crowd concedes that sarcies should not take vitamin D:
http://bacteriality.com/2009/08/10/iom/
I never was positive for antibodies, but I too had to live on a very limited diet. If you read my interview, you will see that that resolved on the MP.
http://bacteriality.com/2007/11/10/interview10/
Based on some of your other comments, here are some additional Knowledge Base articles that you might find useful:
http://mpkb.org/doku.php/home:pathogenesis:th1spectrum
http://mpkb.org/doku.php/home:starting
http://mpkb.org/doku.php/home:starting:physician:finding
http://mpkb.org/doku.php/home:patients
http://mpkb.org/doku.php/home:special:tissue_donation
By the way, Amy is actually not *that* local. She is currently based in New York.
Hope this helps.
Best,
Paul