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.

Nevertheless, I’ve found that some people develop concerns about the treatment, many of which are not quite warranted. This piece is an attempt to address the most common misconceptions about the Marshall Protocol – misconceptions that I have heard people express on various message boards, over email, on this site, and elsewhere. Hopefully, armed with the following information, patients can approach the treatment with greater ease and confidence.

Note: Much of the information in this piece came from the Marshall Protocol study site, where it was collected by Meg Mangin RN and Belinda Fenter. A special thanks for their work.

1.If my blood pressure drops after starting the MP it’s because of Benicar.	2.If I feel bad after starting the MP I am suffering from side effects of Benicar.
3. Long-term antibiotic therapy is dangerous and I will develop antibiotic-resistant bacteria.	4.I’ve been told I’m allergic to one of the MP antibiotics, so I can’t do the treatment.
5.Dr. Marshall is not a medical doctor so his research can’t be trusted.	6. If my blood work (particularly that which pertains to kidney function) goes out of range after starting the MP, that’s a bad sign.
7.The MP needs to be described by a peer-reviewed double blind placebo-controlled trial before I can take it seriously.	8.If I do the MP, I will have to become a permanent cave dweller.
9.It’s okay if my doctor modifies the MP.	10.If my D ratio isn’t correct the MP won’t work for me.
11.Anyone who disagrees with Dr. Marshall is banned.	12.The MP does not take care of viral or fungal co-infections.
13.If people who reach a state of remission thanks to the MP don’t stop taking antibiotics and Benicar it’s because they can’t.	14.If I don’t do the Marshall Protocol, my illness might go away on its own.

Misconception #1:  If my blood pressure drops after starting the MP it’s because of Benicar.

Benicar acts as a blood pressure lowering medication only up to a dose of 40mg per day, or the amount contained in one pill. Beyond that, its effects on blood pressure are minimal. This means that taking Benicar more than once a day will not continue to lower blood pressure or deplete sodium.

Based on studies conducted by Sankyo, the pharmaceutical company that makes Benicar, you could take 10 or 20 doses of the medication in a day and still find that your blood pressure would not drop more than it did after the initial dose.

Furthermore, those people who take even one pill of Benicar a day are unlikely to find that their blood pressure drops very much since the drug is a very weak anti-hypertensive agent. Do you know anyone taking Benicar for blood pressure reasons? Probably not, since its effects are so minimal that doctors don’t use it very often.

In fact, a significant number of people in the test groups for the initial FDA Benicar trials exhibited an increase, rather than a decrease, in blood pressure. Dr. Marshall’s work has shown that this is because Benicar binds the nuclear receptors (receptors not involved in blood pressure) more strongly than the angiotensin receptors – the receptors the drug is intended to target which, in any case, have never been shown to directly control blood pressure.

Consequently, most MP patients see little change in their blood pressure while taking the dose of Benicar used by the MP, or four pills a day. Others note a drop in blood pressure, but the drop is almost always due to another reason - immunopathology, or the immune system’s response to bacterial death. The immune system secretes cytokines in response to L-form bacterial death, which along with toxins secreted by the bacteria as they die, cause a temporary rise in symptoms in the area in which bacteria are being killed.

Thus, as people progress through the MP, they find that all their disease symptoms return during the time their bodies are killing the bacteria responsible for causing the symptoms in the first place.

Because many people have experienced symptoms of low blood pressure prior to starting the MP, there is simply no doubt that these symptoms will return as immunopathology. The worse a person’s low blood pressure symptoms were before the MP, the more likely they are to find that after starting the treatment, their blood pressure will drop.

Since Benicar also binds receptors that allow it to palliate this inflammatory response to bacterial death, many patients who start the MP find that Benicar actually helps their blood pressure stabilize rather than drop.

For example, when Kas S. started the MP her blood pressure dropped due to immunopathology. But her doctor incorrectly thought Benicar might be to blame. “So one day, I took less Benicar,” states Kas “but I felt worse, and my blood pressure (BP) was even lower than it was on the correct MP dosage!” Today, after about a year on the MP, her blood pressure is still sometimes low, but during these occasions her symptoms are never affected. Furthermore, at her last doctor visit, while still on Benicar, her BP was 100/70. “If I feel bad during my working day, I take an extra 20 mg of Benicar and my BP actually goes UP, states Kas. “I feel heaps better.”

After 9 months on the MP, Claudia G. experienced a significant rise in immunopathology. In order to mitigate the reaction, she started taking a higher dose of Benicar. After that point, her blood work showed that her blood pressure started to stabilize. “Having increased my Benicar frequency to 6-hourly my blood pressure rose to a respectable 94/57,” states Claudia. “This is remarkable, as it had stabilized at 80/40 before that point.”

I once received a frantic email from a woman who had just started the MP and was concerned that Benicar had significantly lowered her blood pressure. “I am particularly worried,” she wrote, “because before starting the Marshall Protocol I already had extremely low blood pressure to begin with.”

I pointed her to information on the MP board, which explained that Benicar was not the culprit behind her low blood pressure. Since this woman said she had already suffered from low blood pressure before the MP, immunopathology that would “bring back” her symptoms of low blood pressure was inevitable. Patients on the MP have to “face” all of their diseases symptoms as they kill the bacteria making them ill, and unfortunately low blood pressure is one of them.

The fact that immunopathology, rather than Benicar, is to blame for most MP-related drops in blood pressure is supported by the fact that those people who struggle with very low blood pressure at the start of the treatment almost always find that after a year or so, their blood pressure begins to stabilize. After a doctor’s visit they are happy to learn that their blood pressure has returned to a normal range despite the fact that they are taking the exact same amount of Benicar as when they started the MP.

“Your BP will stabilize back towards ‘healthy normal’ as the MP progresses, and the disease is removed. The symptoms thought to be due to low blood pressure will resolve even if the low blood pressure persists,” states Marshall.

“Taking Benicar more than once a day will not continue to lower blood pressure or deplete sodium.”For example, Grace P. suffered from POTS (Postural Orthostatic Tachycardia Syndrome) before starting the MP. “When standing, or getting out of a chair within seconds my blood pressure would go from 120/90 to 80/40 and pulse 80 to 120. I would feel very faint, and my heart would pound” states Grace. But rather than exacerbate her blood pressure condition, Grace found that after taking Benicar along with the other MP medications, her POTS disappeared and rarely returns with immunopathology. “My resting heart rate was before MP 100 and now in the 80s and my BP now can be 90/70 or 120/80 but mostly I don’t feel the difference,” states Grace.

Other patients don’t have a blood pressure monitor but assume their blood pressure drops after starting the MP because they feel dizzy. Again, this dizziness is almost always the result of immunopathology. As described on the Marshall Protocol study site, “The endotoxins released when the MP antibiotics kill bacteria totally upset the body’s hormonal balances and the readjustment process can cause symptoms such as vertigo and dizziness. These symptoms indicate a temporary return of disease symptoms and not a lower blood pressure.”

Furthermore, if immunopathology induces low blood pressure after a patient starts the MP, there is not reason to be overly concerned. In 2004, the NIH issued new blood pressure guidelines for clinical practice. These guidelines state that only blood pressures below 120/80 are considered to be normal. In fact, people who are able to function while maintaining a low blood pressure have been shown to have lower rates of cardiovascular events than people with normal blood pressures.

The NIH has created no medical standards that define low blood pressure, or a range in which low blood pressure is considered dangerous. “Nor is there any proof that the values normally used to indicate low blood pressure in healthy patients have any relevance to patients with Th1 inflammatory disease,” states Marshall. “Marshall Protocol patients with extremely low blood pressure (85/55 or lower) have been able to continue taking Benicar.”

Note: When blood pressure is low, it can help to make sure one is adequately hydrated, so be sure to drink enough fluid. For some patients, additional salt can be helpful.

Misconception #2:  If I feel bad after starting the MP I am suffering from side effects of Benicar.

Benicar is one of the safest drugs on the market. It’s a fact. Nevertheless, some patients still worry that the drug could cause side effects.

These worries are unwarranted. Although they do so for many other drugs, the FDA has set no unsafe upper limit for Benicar. The FDA bases its safety data on ‘post-marketing experience’ - how many adverse events have been linked to the drug – and for Benicar, they are negligible. There has been no dose detected that results in an adverse event.

In fact, the FDA guidelines for Benicar, state that:

• The guidelines allow a dosage of “40 mg Q6hr” (the dose used by patients on the MP)
• Benicar dosing must be individualized.
• The overall frequency of adverse events is not dose-related.”

A recent study published in the Journal of of Pharmacology found Benicar to be safe and well tolerated at doses of up to 160 mg/day.^[1] Animal studies in mice, with Benicar doses up to 480 times the human dose of 40 mg per day (relative to body weight), showed that Benicar is not carcinogenic.

The label for Benicar states that the drug is well-tolerated. Adverse events were similar to those experienced by the placebo group – a group of patients who were not given the drug at all. Adverse events were generally “mild, transient and not related to dose.” The frequency of adverse events also had no relationship to the dose of Benicar.

In placebo-controlled trials, the only side effect that occurred in more than 1 percent of Benicar-treated patients vs. placebo-treated patients was dizziness (3 percent vs. 1 percent). The label does state that Benicar should not be used during pregnancy or breast-feeding, but since pregnant women are not allowed to do the Marshall Protocol, the warning is of little concern for those using the medicine to recover from Th1 disease.

“Adverse events were generally ‘mild, transient and not related to dose.’”According to the report, “In the dose-finding study, 792 patients were randomized to Benicar (2.5-80 mg) or placebo once daily… The results of the clinical studies in >3000 patients receiving Benicar showed that the frequency and profile of adverse events with Benicar were generally similar to those with placebo; the frequency of adverse events was not dose related. Benicar, with or without hydrochlorothiazide, was well tolerated over 2 years of treatment.”

In April 2007, the staff of Autoimmunity Research Foundation had a high-level meeting at the FDA in Maryland. One of the topics on the agenda was how we put an end to concerns physicians express about the safety of Benicar.

Those present included the head of the cardiovascular division at the FDA at the time when Benicar was officially approved. “He is expert on the drug’s behavior and is currently the medical director at the Food and Drug Administration division that evaluates drugs,” states Marshall.

“He made it clear that the hypotensive effect of Benicar is already in full effect at a low dose (less than 40 mg) and there is a graph in the package insert showing that beyond that beyond 40mg the dose really doesn’t affect BP any more. Second, he pointed out that the FDA has set no toxic level for Benicar, because its safety is not in question, and certainly not at the levels we are using.”

Furthermore, since the anti-inflammatory actions of Benicar actually protect organs, and reduce damage to the body from immunopathology. Any assessment of “safety” should take that into account.

As noted in The Townsend Letter for Doctors and Patients, examples of some of the documented protective effects of ARBs include the ability to:

• prevent migraines^[2]
• inhibit liver fibrosis and aid liver healing^[3]
• protect the kidneys in diabetic nephropathy^[4]
• reduce insulin resistance^[5]
• protect the heart from damage from inflammation in myocarditis^[6]
• protect the mitochondria from age-associated damage from oxidation^[7]

Here are more articles on the general safety of Benicar, which is called Olmesartan in countries besides the United States:

The most common reason that patients who begin the Marshall Protocol incorrectly assume that they are suffering from side effects of Benicar is that they mistakenly attribute the hormonal adjustments that accompany the onset of a Benicar blockade to side effects of the drug. These hormonal changes occur because in most patients with Th1 disease, the body has become accustomed to a higher than normal level of the hormone 1,25-D, which rises as part of the immune system’s reaction to bacteria.

But the Benicar blockade quickly and dramatically lowers 1,25-D - by as much as half in just two weeks. Since 1,25-D is a powerful hormone that affects nearly every cell in the body, and interacts with all the body’s major hormones, myriad other hormones are forced to adjust their levels according to the new lower level of 1,25-D. This often causes temporary neurological-type symptoms such as (but not limited to) fatigue, dizziness, headache, photosensitivity, irritability, sleep disturbances, brain fog, etc. As the body adjusts to this hormonal shift these symptoms dissipate, usually in a week or two.

The relationship between 1,25-D and the body’s other hormones can be observed in this chart created by Marshall.

Last, but not least, patients should not confuse the rise in symptoms that occurs due to immunopathology with side effects of Benicar. “The ability to accept and tolerate a certain level of immunopathology is a requisite of continuing with the Marshall Protocol and is not always predictable,” states the study site. “Usually symptoms wax and wane, but they can also be constant for varying periods of time. Immnopathology-generated symptoms often mimic a patient’s disease symptoms but they can also be surprisingly new, pointing to areas of previously undetected inflammation.”

Benicar is designed to reduce the impact on the tissues of the inflammatory substances released by the immune system as part of the immunopathological reaction. Also, taking the antibiotics as directed, in a controlled fashion, should minimize the risk of any permanent tissue damage.

“There is no guarantee that immunopathology won’t cause some permanent tissue damage, but we believe that you can control your therapy to avoid that,” state the MP board staff. “On the other hand, it is a given that not treating the underlying cause of your inflammation guarantees further permanent tissue damage and possibly even death.”

Note: Only plain Benicar, without hydochlorothiazide diuretic (HCT), should be used in the MP. Hydrochlorothiazide (HCT) is too hard on the kidneys and liver - organs where people with Th1 disease may have undetected problems. Also, hawthorne, lithium, and extra potassium supplements have the potential to negatively interact with Benicar. The label warns that in rare instances drugs that block the renin-angiontensin system have resulted in kidney failure in patients with severe congestive heart failure. However this problem has yet to be observed among patients taking Benicar.

Misconception # 3:  Long-term antibiotic therapy is dangerous and I will develop antibiotic-resistant bacteria.

For decades, doctors have prescribed minocycline for conditions such as acne at doses much higher than those used by the Marshall Protocol. In fact, minocycline was actually over-prescribed for teenage acne when it was released in 1968. Yet, in the 40 years since the drug’s release, no significant species have been shown to be resistant to it.

Recently, a multi-center double-blind placebo-controlled trial concluded that minocycline is safe and effective in patients with mild to moderate rheumatoid arthritis and supported its use (alone or as adjunctive therapy) in rheumatic diseases.^[8] Tetracyclines, of which minocycline is an example, have been also used effectively in urogenital, gastrointestinal, and lower respiratory tract infections.^[9] Minocycline is also one of the few antibiotics that remains active against the bacterial species Methicillin-resistant Staphylococcus aureus (MRSA), despite the fact that it has been prescribed for decades.

Of course, people starting the MP are already infected with bacteria that have developed without cell walls in order to resist the standard antibiotics. So people may start the MP with bacteria that are already resistant to minocycline. But when minocycline is taken in combination with the other phase 2/3 antibiotics, according to Marshall, the statistical chance that bacteria will evolve that cannot be killed when these antibiotics are used in tandem is so close to zero it is inconsequential. That is why using all combinations of each carefully chosen MP antibiotic is important in order to assure complete recovery.

“The MP is being used against antibiotic-resistant bacteria already in your immune system,” states Marshall. “The antibiotics have been chosen so as to minimize (essentially eliminate) the likelihood that any additional resistant strains will be formed (that is, any more strains in addition to the resistant strains you are fighting with the MP).”

“ The antibiotics have been chosen so as to minimize (essentially eliminate) the likelihood that any additional resistant strains will be formed.”The low doses at which phase two and three antibiotics are used also keep to an absolute minimum the chance of bacterial resistance. For example, the highest dose of minocycline used by the MP is only 100 mg every other day, and one of the phase 2/3 antibiotics is only taken every ten days. By way of comparison, when it’s prescribed for acne minocycline is taken 200-400mg daily. One of the phase 2/3 antibiotics is another case in point. On the MP, it is taken once every 10 days whereas for a number of other treatments, it is sometimes taken in doses twice as high and every day over the course of a week. Because they are taken at such low doses, the antibiotics seldom cause yeast infections.

According to the Physicians Protocol for Using Antibiotics in Rheumatic Disease, “Minocycline tends not to cause yeast infections. Some infectious disease experts even believe that it has a mild anti-yeast activity. Women can be on this medication for several years and not have any vaginal yeast infections.^[10]

Besides, L-form and other bacteria create substances that can bind and block the Vitamin D Receptor (VDR), a receptor that controls the production of many of the body’s antimicrobial peptides. The antimicrobial peptides are antibiotics naturally created by the body that kill bacteria by a variety of mechanisms including disrupting membranes, interfering with metabolism, and targeting components of the machinery inside the cell.

By killing L-form bacteria and restoring the activity of the VDR, the MP antibiotics allow these natural antibiotics to be produced in greater amounts – to the point where in later stages of the treatment, the antimicrobial peptides allow the body to kill bacteria even if the MP antibiotics are stopped.

If you or your doctor are still worried about long-term antibiotic use, you may want to consider the “side effects” of not doing a potentially curative treatment. The symptoms of multiple sclerosis are devastating disability and death. The symptoms of Chronic Fatigue Syndrome and fibromyalgia are minimally functional existence, loss of cognitive function, and unrelenting pain. The symptoms of rheumatoid arthritis are continual pain and encroaching disability and dysfunction. The symptoms of Alzheimer’s Disease are… well, you get the picture.

Misconception #4:  I’ve been told I’m allergic to one of the MP antibiotics, so I can’t do the treatment.

Most people who become symptomatic after taking a particular antibiotic used by the MP ultimately realize that they are not allergic to the antibiotic but are instead experiencing immunopathology.

When the MP antibiotics kill bacteria, it is inevitable that a patient will experience immunopathology (also called the Jarisch-Herxheimer Reaction), or, as described above, a temporary rise in symptoms caused by bacterial death. This means that after each antibiotic dose, a patient’s disease symptoms return for a period of time.

“ Once you understand the immunopathology resulting from killing these Th1 pathogens, all these so-called side-effects are shown up for what they are - immunopathology - and they disappear as you get rid of the pathogens.”Although Benicar plays a critical role in activating the immune system so that immunopathology can take place, before starting the MP, many people’s immune systems are still active enough to mount an immunopathological response. This means that even before the MP, a pill of minocycline can result in symptoms that doctors incorrectly label as an allergy reaction. In reality, these reactions are just a sign that the antibiotic is killing bacteria, as it will continue to do if the patient starts the MP.

“Immunopathology [in response to an antibiotic] is to be expected and should not be interpreted as a side effect, adverse reaction or intolerance,” states the Marshall Protocol study stie.

The paper “Observations of Jarisch-Herxheimer Reaction (JHR) in Sarcoidosis Patients” (which applies to all Th1 illnesses) states that the JHR reaction is sometimes mistaken for a “hypersensitivity reaction” or even the cause of a related, (probably pre-existing) disease such as lupus. Similarly, Pruritus, hives and rash induced by the JHR reaction can be misdiagnosed as an allergic (Th2) reaction to the antibiotic.

Indeed, most MP patients who were once told they had an “allergy” to antibiotics now acknowledge that they were just experiencing a normal immune system reaction.

“Once you understand the immunopathology resulting from killing these Th1 pathogens, all these so-called side-effects are shown up for what they are - immunopathology - and they disappear as you get rid of the pathogens,” states Marshall.

Because of its potent anti-inflammatory effects, Benicar goes a long way in helping patients manage immunopathology because of its ability to reduce inflammation and prevent further tissue injury. Consequently, those people who have reported previous “allergic” reactions to an MP antibiotic have, once on Benicar, generally have been able to tolerate it successfully as long as they use caution while ramping up the level of their antibiotics.

If it turns out that a person has a problem tolerating a particular MP antibiotic at one point in the protocol, for whatever reason, they can use another MP antibiotic in its place. Then later in the MP, when their bacterial load has dropped, they can generally tolerate the first antibiotic without a problem.

Misconception #5:  Dr. Marshall is not a medical doctor so his research can’t be trusted.

Several days ago, I attended a presentation by Dr. Leroy Hood , MD, PhD, president of the Institute for Systems Biology in Seattle, Washington. The first person to pioneer several cutting edge technologies for DNA analysis, Hood boasts a list of awards, achievements, and credentials that would impress anyone. Here is a man who has published in excess of 600 peer-reviewed papers, received 14 patents, and co-authored textbooks in biochemistry, immunology, molecular biology, and genetics. One of the many biotech companies he co-founded, Amgen, had a 2006 revenue in excess of 14 billion dollars. Smart guy.

Dr. Hood began his presentation “Systems Biology and Systems Medicine: Towards Predictive, Preventive, and Personalized and Participatory Medicine,” by describing how most currently active research teams study proteins and molecules in isolation, one at a time.

According to Hood, medical research has stagnated for wont of systems thinking, the kind of inquiry which is the hallmark of… engineers. To paraphrase one of the titles of his slides, Hood asked rhetorically, “What would an engineer’s approach be to medicine?” Dr. Hood told the audience “Biology is an information science. Systems thinking is a response to biological complexity.”

Throughout his presentation, Hood made the point, among others, that the pioneering researchers and doctors of tomorrow will have to be trained in engineering and computer science in order to understand the body’s “circuits” and feedback pathways.

“ According to Hood, medical research has stagnated for wont of systems thinking, the kind of inquiry which is the hallmark of… engineers.”According to his promotional website, “Dr. Hood has been driven by the conviction that the needs of frontier biology should drive the selection of technologies to be developed, and once a new technology has been developed, these technologies can revolutionize biology and medicine.” These technologies include a variety of molecular modeling programs.

To be sure, Dr. Marshall’s background in electrical engineering is somewhat unconventional, but that should not disqualify the man from researching medical phenomena. In fact, if you asked Dr. Leroy Hood and any number of other forward-thinking researchers, this background is very much an asset. He may even be exactly the type of researcher Hood envisions as a medical leader.

Marshall received his PhD in Electrical Engineering from the University of Western Australia in 1984 and also possesses an undergraduate and a masters (1978) degree in Electrical Engineering.

But rather than becoming an electrical engineer, Marshall successfully took his mastery of electronics and applied it to medicine and biotechnology. When Marshall moved to the University of Western Australia in 1978, he commenced his PhD thesis research while studying patients suffering from diabetes and infertility at the Charles Gairdner Hospital. This research allowed him to discover a novel way of using pulsatile LHRH for treating cryptorchidism, along with both male and female infertility.

In 1982, Marshall moved to California. He continued his PhD thesis research while becoming a “Visiting Scientist” in the Department of Surgery at the Hospital for Sick Children in Toronto, which at the time was a leader in pediatric diabetes research. This partnership led to his thesis “Modelling and simulation in diabetes care” and a paper on insulin infuser technologies. Shortly after, Marshall became interested in sarcoidosis and pursued a degree in biomedicine in order to further understand the disease.

Marshall has had plenty of experience in a medical setting in which he has worked successfully with researchers, doctors and patients. And his background in engineering has allowed him to pursue biological issues with a novel, systems approach.

Despite not having a medical degree, Marshall is still frequently invited to lecture on medical issues. Over the past two years he has given presentations to the FDA, the American Academy of Environmental Medicine, the Days of Molecular Medicine conference, and will be chairing a session about vitamin D and the VDR at the upcoming Conference on Autoimmunity in Portugal.

In 2007, Marshall was appointed Adjunct Professor in the School of Biological Sciences and Biotechnology at Murdoch University in Australia. He has also recently been cleared by a Continuing Medical Education committee as being competent to provide CME training for physicians.

The fact that Marshall has backed his findings with molecular modeling data is seen as a plus by those who understand the programs he uses. In a recent phone interview, Dr. Adam Godzik, Director of the Joint System for Molecular Modeling Institute at the University of California, San Diego, told me that molecular modeling can be quite accurate if the correct biological question is matched with the correct molecular modeling tool – an art at which Marshall has proven himself to be adept.

Of course, results obtained using molecular modeling software cannot be confirmed as 100% correct, but then again, as Godzik commented, experimental trials are never 100% accurate either. Godzik was quick to emphasize that molecular modeling and experimental medicine are overlapping fields – the best results are generally obtained when a clinical trial is preceded by molecular modeling research.

Let’s say a scientist wants to know which of 8,000 drugs will best bind a receptor in order to elicit a certain effect. By determining how the shape of each drug molecule fits with the receptor in question, molecular modeling software allows for the quick elimination of several thousands of the drug candidates, eventually leaving about 5 or so possibilities that can be further tested in a clinical setting. The above process saves countless hours of work and millions of dollars that would otherwise be spent on a multitude of clinical trials, most of them headed in the wrong direction.

When Marshall developed a disease model for sarcoidosis (a model that now holds true for nearly all inflammatory diseases) his decision to model how the drugs used by the MP interact with many of the body’s receptors was a logical move that allowed him to conserve accuracy while saving time – allowing him to put the MP treatment guidelines up on the web as quickly as possible under conditions where millions of lives are at stake.

Today, the Marshall Protocol study site serves as a trial in which hundreds or even thousands of patients with the aid of their physicians are testing Marshall’s model in a clinical setting. The drug interactions he predicted using modeling software have definitely held up in this clinical setting. The proof is in the pudding – patients are recovering from a wide array of previously incurable diseases.

Even absent a certain MD credential, Dr. Marshall’s experience in engineering and eclectic background may very well be the prototype of pioneering researchers to come. If we are to take Drs. Wood and Godzik at their word, we can expect to see many more researchers like Marshall in the future. In the meantime, just because medical schools have yet to integrate molecular modeling into their curriculum, and just because the average doctor is not used to making decisions based on molecular data, does not mean Dr. Marshall’s work should be not be viewed on par with that of any other knowledgeable research scientist.

On a personal note, as someone who has been repeatedly misdiagnosed and given treatments that have made me sicker by various board-certified physicians over the years— I genuinely welcomed Dr. Marshall’s somewhat novel perspective and experience set. I’m now convinced that a non-traditional perspective is exactly what was needed to rethink curative treatment options for inflammatory disease.

Misconception #6:  If my blood work (particularly that which pertains to kidney function) goes out of range after starting the MP, that’s a bad sign.

The result of any blood test must be considered in its clinical context. For patients on the Marshall Protocol, measurements that fall outside of established ranges are almost always a result of the chemical and immunological fluctuations that accompany immunopathology. This means after a patient starts the MP, changes in blood work are to be expected, and are actually a sign that the treatment is working to kill L-form bacteria.

For example, MP patients often find that percent lymphocytes drops. This is because some of the cytokines released by the immune system in response to bacteria cause down-regulation of lymphocytes, causing them to leave areas of high inflammatory action and migrate to the periphery. The down-regulation also reduces the number of lymphocytes being generated from stem cells.

“Lymphocytes are downstream bystanders,” states Marshall. “Their level of expression is dependent on the nuclear receptors, which is dependent on the bugs. As you get rid of the bugs everything else comes back to normal.”

“You can all expect your White Blood Cell (WBC) and differential, the balance of neutrophils, monocyctes, % lymphocytes, NK cells, and etc, to change a lot as the Th1 bacteria are killed. It is best not to get fixated on any expectation of ‘bad figures’ and ‘good figures.’ If Doc gets too concerned about the numbers then, IMO, you should back off your antibiotic dose and take the therapy a bit slower,” he continues. For more information see the thread “What do my lab tests mean? on the study site.

“C-Reactive Protein is an inflammatory marker which, if elevated [upon beginning the MP], returns to baseline along with Triglycerides, Alkaline Phosphatase and 1,25-D as the MP does its job,” states Marshall. These markers typically start to drop after about 6-12 months.
 SED rate (another measure of inflammation) will (hopefully) go way up in the early stages of the Marshall Protocol indicating that bacteria are being killed, and the body’s immune system is dealing with them. Later on (at 12 months or so) the SED rate will remain closer to normal, as fewer organisms are being killed. Eventually it returns to baseline.”

There is a tendency for doctors and patients to become particularly alarmed about fluctuations in markers of kidney or liver function after a patient has started the MP. However, for the vast majority of patients these test results are again an expected part of the healing process.

“ For the vast majority of patients these test results are again an expected part of the healing process.”Patients who start the MP are often unaware of the fact that their kidneys or liver are infected until blood work comes back out of range. This is due to the fact that inflammation in these organs tends to be “silent.” Before the MP, the kidneys are inflamed because they are infected with L-form bacteria. But the patient is largely unaware of the problem because their immune system, which has been weakened by L-form bacteria, doesn’t kill enough of the pathogens to cause a rise in bacterial byproducts that would be picked up on a blood test.

But once patients activate the innate immune system with Benicar, and begin rapidly killing L-form bacteria thanks to the MP antibiotics, the resulting immunopathology causes a rise in bacterial death, the effects of which are finally high enough to show up on lab tests.

“Because most kidney inflammation/disease is ’silent’, it is not uncommon for subclinical kidney inflammation to be exacerbated due to unavoidable immunopathology as part of the recovery process with the Marshall Protocol,” states the study site.

Thus, people on the MP should not be surprised to learn their kidneys are infected. Patients with Th1 disease have a high risk of kidney inflammation, and many doctors are unaware of the problem because they have no idea how sick their Th1 patients really are. Kidneys are also one of the organs that suffer significant fibrosis (collagen deposition and scarring) from the Th1 disease process.

“The kidneys of Th1 patients are almost always weak, some of them extremely weak. But none have ‘failed’, because weak kidneys start to reveal themselves as part of the healing process, and they are protected by the ARB (Benicar), and the reactivated innate immune system,” states Marshall.

So it is not unreasonable for the levels of BUN - a measure of the amount of nitrogen in the blood that comes from urea, a substance removed by the kidneys - to come back elevated, as bacterial endotoxins cause nitric oxide and subsequently more nitrogen to be generated in the inflamed tissues. Levels of creatinine - a breakdown product of phosphate that is filtered by the kidneys - may also become elevated after people start the MP. This is not unusual, as most short courses of antibiotics aimed at killing classical bacteria also cause spikes in BUN and creatinine. According to the study site, maintaining a level of creatinine 10-20% higher than normal indicates the kidneys are functioning adequately while the MP is inducing immunopathology to resolve kidney inflammation.

The important thing to keep in mind is that these markers fall back into range as the disease resolves and L-form bacteria are eradicated. Remaining on Benicar despite fluctuations in markers of kidney and liver function is a necessary part of the healing process.

In Journal of Nephrology Dialysis Transplantation, Biff Palmer of the Division of Nephrology at the University of Texas Southwestern, agrees that a rise in creatinine levels should not discourage doctors from keeping their patients on an ARB medication such as Benicar. “In the patient with an increase in serum creatinine concentration, decreasing the dose of [the ARB]… will cause the serum creatinine concentration to return to the original baseline,” states Palmer. “Unfortunately, such an approach is not optimal for the long-term preservation of renal function and should be discouraged.”^[11]

Researchers at Boston University in Massachusetts agree, stating that “High-dose ARB treatment in patients with chronic renal disease is not associated with any clinically significant long-term negative effects on serum creatinine or potassium and is thus an important therapeutic modality with which to achieve further reductions in urinary protein excretion.”^[12]

Instead, MP patients with kidney inflammation and their doctors should be extremely comforted by the fact that the patient is taking Benicar. This is due to the great number of studies, which have found that Benicar and other ARBs protect the kidneys from the effects of inflammation and cytokine damage.

The benefits of Benicar on patients with kidney inflammation include:

• decreased insulin resistance, fewer symptoms of the metabolic syndrome, and decreased inflammation in patients with chronic kidney disease.^[13]
• the ability to ameliorate renal injury and fibrosis in rats when taken at ultrahigh doses.^[14]
• decreased (intra)renal vascular resistance, increased renal perfusion, and significantly reduced oxidative stress in patients with type 2 diabetes.^[15]

…and the affects of ARBs in general on people with kidney inflammation include:

• improved patient prognosis in non-diabetic chronic kidney diseases with mild-to-moderate renal dysfunction.^[16]
• effectiveness in controlling UAE [urinary albumin excretion] in cases in which blood pressure is not well controlled, implying that ARBs have renoprotective actions independent of changes in blood pressure.
• Ability to actively control proteinuria and stabilize kidney function in children, providing an alternative to more toxic therapies, especially corticosteroids, in children with glomerular disorders such as those associated with obesity.^[17]
• The formation of a dosage-dependent, anti-inflammatory effect on the kidneys that is mediated by suppression of NF-kappaB activation and chemokine expression.^[18]
• Ability to retard the progression of advanced renal insufficiency.^[19]
• Effectively slow the progression of chronic allograft nephropathy (CAN)^[20]
• Ability to affect the local renin-angiontensin sytem (RAS) and thus improve renal injury and function in a rat model of potentially progressive glomerulosclerosis.^[21]

…among others.

Misconception #7:  The MP needs to be described by a peer-reviewed double blind placebo-controlled trial before I can take it seriously.

First, Dr. Marshall’s work has been peer-reviewed. His most recent paper, “Vitamin D discovery outpaces FDA decision making,” was by invitation and appeared February 1st in BioEssays – a prominent peer-reviewed journal. A total of four of his papers have been published in print journals and can be found in PubMed.

That said, peer review has a poor record for furthering medical knowledge, at least when it comes to game-changing and disruptive ideas. “The evidence against peer review keeps getting stronger,” says Richard Smith, former editor of the British Medical Journal, “while the evidence on the upside is weak.” Yet peer review is a sacred cow, largely because passing peer review confers great prestige - and often tenure.

Andrew Grove, the founder of Intel, is an outspoken critic of the way medical research is done. He has likened peer review to a “Middle Ages guild, where you have to sing a particular way to get grants, promotions and tenure.”

What provision is there for research that undercuts current dogma? For example, how would any researcher make a case in the medical literature that pathogens cause sarcoidosis? The answer is that publication would be prohibitively difficult– not because of weaknesses in methodology or shortcomings in data– but because the top posts for the defining journals in the field are occupied by pulmonogists who will never accept publication of a paper which points to pathogens as the cause of the disease. This doesn’t make the job of Trevor Marshall and research team impossible—just more difficult.

“The problem is that one does not publish in ‘a prestigious journal’ to help gain acceptance of the treatment protocol and the theory in general,” states Marshall. “It just doesn’t work that way. It works exactly the other way around, in fact. The way that the medical publishing process works is that one has to get general acceptance by the folk who will be chosen to peer review the paper before submitting it to a prestigious journal.”

One promising alternative to peer review is open peer review. Because he adopted the process of open peer review several years ago, all of Marshall’s work, including his presentations, has been reviewed at length by others in his field. “Our work has been peer-reviewed extensively, and been gone over with a fine-tooth-comb,” states Marshall. “Our Journal of Independent Medical Research (JOIMR) papers, for example, use open peer review, where the reviewers shed their anonymity to ensure the integrity of their reviews.” For example, take a look at the list of peer-reviewers at the end of this JOIMR paper.

Another common question among people familiar with the MP is “When will a standard randomized, double-blind, placebo-controlled study be done to ‘prove’ the efficacy of the Marshall Protocol?” While there is the promise of a cohort or case-control study at some point, there will probably never be a double-blind or placebo-controlled study.

The Marshall Protocol is unique because researchers conducting standard blinded study trials currently base their conclusions on data that reveals only a small (usually 5-20%) difference in statistical significance between those patients given treatment and those to receive a placebo. But the response rate of those patients taking part in the current phase II trial of the Marshall Protocol is essentially 100% - not to mention the fact that the treatment is also based on a very solid scientific model.

To date, the positive response of patients to the treatment is so definitive that to blind a separate study on the MP raises a ethical dilemma. For one, because the Marshall Protocol takes so many years to complete, it just isn’t ethical to give sick, suffering patients a placebo for multiple years—not when so many people die from these diseases every day.

This is supported by FDA guidance regulation ICH E-10, which states, “Where an available treatment is known to prevent serious harm, such as death or irreversible morbidity in the study population, it is generally inappropriate to use a placebo control.”

“For one, because the Marshall Protocol takes so many years to complete, it just isn’t ethical to give sick, suffering patients a placebo for multiple years—not when so many people die from these diseases every day.”This is not a novel argument. Paul Glasziou writes in his 2007 BMJ article “When are randomized trials unnecessary? Detecting signals from noise” that “Although randomised trials are widely accepted as the ideal way of obtaining unbiased estimates of treatment effects, some treatments have dramatic effects that are highly unlikely to reflect inadequately controlled biases.”^[22]

Glasziou goes on to invoke any number of historical examples, which illustrate cases, such as the MP, where the size of the treatment effect (signal) relative to the prognosis (noise) is so great as to make randomized trials completely unnecessary. These examples include insulin for diabetes, defibrillation for ventricular fibrillation, and blood transfusion for severe haemorrhagic shock.

Significantly, most major medical discoveries have not required double-blind placebo controlled trials in order to demonstrate their ability to impact disease. As MP patient advocate George Howell describes, “Alexander Fleming’s discovery of the bacteria killing power of penicillin was never put to a controlled double-blind study, nor a peer-review in some journal. It worked! It was used! It saved countless lives.” (Fleming did his work prior to the invention of double-blind studies, but never mind that!)

Another reason the placebos would be difficult or almost impossible to use, is that patients would know within days what group they were assigned. The relief and hormonal fluctuations brought on by the Benicar, the immunopathology caused by the antibiotics are undeniably strong and would undermine the blinding in short order.

Clearly, the MP will have to be tested in a manner that does not require a blinded study. “Please understand that we have spent the last three years working with NIH and FDA to define what a successful and rigorous trial will look like,” states Marshall. “When we conduct that trial it will be unlike anything that has ever gone before - because it will have an end-point of success - of ‘cure.’”

In order to start this process, Autoimmunity Research Foundation has achieved FDA designation for two of the MP antibiotics in sarcoidosis. But they need to spend another few years getting the same paperwork in place for CFS, RA, Lupus, Parkinsons, Diabetes, and, well, the list goes on and on. “In the meantime the alternative is to do what we have done, and what we are now doing. There is no other way,” states Marshall.

Indeed, under the circumstances, the staff of ARF have already initiated an alternate study design that is allowing them to successfully compile data. As mentioned above, this is the Marshall Protocol study site itself - an open based, phase II clinical study in which a large cohort of Marshall Protocol patients, with a variety of Th1 inflammatory diseases and supervised by their personal physicians, are reporting, via the Internet, dramatic improvement in their health. This is an unorthodox method of conducting a trial of a novel treatment protocol, but it has successfully allowed solid molecular science to be confirmed by a comprehensive proof-of-concept clinical trial.

Few would argue with Marshall’s choice to use this type of trial in the face of the urgency surrounding his discoveries. There are now thousands of people on the Marshall Protocol, most of whom are reporting improvement and recovery. Should Marshall have waited until he could conduct a more “standard” trial on the MP, these patients would have lost the opportunity to recover and some may have died—to say nothing of suffering that has been alleviated through the treatment. With the stakes this high, it is senseless to think that Marshall should sit on his discoveries until a standardized trial can be set up several years down the road.

Misconception #8:  If I do the MP, I will have to become a permanent cave dweller.

Light sensitivity is common among people who start the MP. But a patients’ ability to tolerate light is highly individualized and unique to their disease state.

The exact mechanisms behind why people on the MP become sensitive to light are largely unknown. One thing is certain – light sensitivity is not a side effect of the Marshall Protocol medications, except in the sense that some patients report that increasing their level of antibiotics, and thus their immunopathology, causes their light sensitivity to increase. This suggests that there may be a connection between bacterial load, more intense bacterial killing, and light sensitivity.

There is, however, no doubt about the fact that once L-form bacteria dysregulate a person’s vitamin D metabolism, light in the eyes, through mechanisms not yet fully understood, can generate symptoms in many other areas of the body. In patients with inflammatory disease, light in the eyes can also stimulate a portion of the brain called the amygdala that in turn generates an increase in neurological symptoms.

Similarly, exposure to sunlight and heat from the sun – which further dysregulates the body’s level of 1,25-D - can lead to neurological as well as physical reactions that are poorly understood.

Since in many cases light sensitivity does seem to correlate with bacterial load, patients who start the Marshall Protocol are required to buy special sunglasses that block a greater spectrum of the sun’s rays than normal sunglasses. When first starting the treatment, they are also highly encouraged to avoid sunlight by wearing thick dark clothing and closing the shades on windows that get direct light.

These precautions must be taken because MP patients often have no idea as to the extent of their infection until they see how strongly they react to the MP antibiotics. Immunopathology and bacterial load may turn out to be greater then expected, so a patient can never assume that they will not become sensitive to light and become symptomatic after light exposure.

Once immunopathology has begun, patients get a better idea of the nature of their bacterial load and their ability to tolerate light. Some (generally more ill) patients find that they can hardly tolerate the rise in symptoms generated by light exposure during the first phases of the treatment. and are forced to shut out all natural light, while using only a few low-watt bulbs inside the house.To protect their eyes from excess light, they block natural light and reduce artificial lighting to 30 lux, which is similar to the romantic mood lighting in a nice restaurant not a dark ‘cave’. These people learn to adapt their lifestyle, if needed, to accomplish necessary outdoor tasks and enjoy social outings after sunset.

Other patients find that they have trouble seeing when wearing their sunglasses and that when they take them off, or are exposed to moderate amounts of sunlight, they don’t feel a rise in symptoms. If this proves to be the case, the patient is not required to keep wearing the glasses.

Similarly, if a patient is willing to tolerate a rise in symptoms in order not to wear sunglasses, then they are not required to wear them. In most cases, this occurs when a person needs to continue working a job at which they simply cannot block light adequately. It is currently believed that exposure to sunlight, even though it raises the level of 1,25-D (and may raise the level of 25-D), does not cause a significant retardation of bacterial killing or inhibit overall long-term healing, as long as the patient’s level of 25-D is maintained below 20 ng/ml.

People who are forced to work in an environment where they must tolerate some symptoms of light exposure should be encouraged by the fact that patients have succeeded on the MP under these conditions. “There have been members on the MP who’ve had considerable sun exposure and still made progress,” states Meg Mangin of Autoimmunity Research Foundation. “Some have tolerated significant sun exposure symptoms, yet persisted.”

Thus, blocking light and wearing sunglasses is not something that is forced blindly on every person on the MP. Rather, patients block sunlight and light in their eyes due to necessity. They block light because they simply cannot tolerate the rise in symptoms that occurs if they are exposed to the sun or take off their glasses. Since patients are already dealing with symptoms of immunopathology, most are eager to block light in order to keep the total amount of symptoms they must deal with on a regular basis to a minimum.

“ Thus, blocking light and wearing sunglasses is not something that is forced blindly on every person on the MP.”Happily, while the majority of sunscreens are ineffective in blocking vitamin D production, sunscreens with zinc oxide, especially those with the highest percentage of the compound, have been shown to inhibit the production of both 25-D and 1,25-D. Their effect is still not strong enough to fully block sun flare symptoms (patients must still wear thick, dark clothing), but they can, in some cases, lower the severity of a light reaction.

Nevertheless, the goal of every MP patient is to reach a state where they will once again be able to tolerate a normal amount of light. As bacterial load decreases and dysregulated vitamin D metabolism is corrected, light sensitivity also subsides. Thus, as patients forge ahead and kill bacteria, they are gradually able to tolerate more and more light.

In order to take note of gains in light sensitivity, patients must often experiment by exposing themselves to a little more sun or light and assessing their reaction. “The only way to find out [if light sensitivity has decreased] is to try a few ‘baby-steps’ and see,” states Marshall. I usually say it takes 18-24 months to get back to any sort of ‘normal’ sensitivities though. But as you begin to feel better, you will venture out more. Through a process of trial and error you will discover how much sunlight exposure you can tolerate. It’s a very individual thing. I would, however, advise erring on the side of caution when experimenting with sunlight tolerance.”

Although it will take some people much longer than others, patients who stick with the MP and eliminate the bacteria causing their illness end up as completely normal people who can once again tolerate the same amount of light as a healthy person. “As you recover you will get to the point where you can’t see anything through those dark glasses any more,” states Marshall. “As one progresses through Phase 2, the risk of setback from occasional exposures becomes less and less. Eventually the risk disappears (although you will probably never want to sunbathe again). So relax, and start to enjoy life again.”

In other words, no, you will not have to wear those big glasses five years from now.

Misconception #9: It’s okay if my doctor modifies the MP.

It is important that patients who begin the Marshall Protocol take their antibiotics exactly as directed. Taking the antibiotics when not using Benicar, dosing the antibiotics at higher levels than directed, or not pulsing them, will significantly decrease or completely stop immunopathology from occurring. Patients may feel better temporarily, but they are no longer killing bacteria.

“Please understand that the Marshall Protocol may seem simple, but it has a lifetime of my own research behind it. Anything you change will likely get you into trouble,” says Marshall.

Marshall argues, “We have to remember that there are many species we are fighting against. Second, the immune system is so finely balanced between not killing them, and killing them, so that small changes to our lifestyle, or to our food, or caused by other drugs we are taking, might stop the immune system from killing the bacteria. If there is no killing the patient will generally feel better.”

The substitution of one MP antibiotic for another could lead to serious problems. For example, since the tetracyclines are all different at the molecular level, doxycycline is very different from minocycline (which is used by the MP).

Why does the MP use minocycline over doxycycline? One reason is that doxycycline doesn’t kill as wide a range of bacteria as minocycline. The other is that doxycycline has an effect on the brain beyond its anti-bacterial effects. “This is easy to verify,” states Marshall “if, when you are in phase 3, you try a couple of 200mg pulses of doxycycline. The feeling you get is nothing like the immunopathology you have endured for so long. And that feeling is addictive. There is a HUGE difference. I have seen people die on doxycycline, while they recover on minocycline and demeclocycline.”

Short-term (non MP) use of doxycycline (a month or so) will do no serious harm, but in the long term the species that are resistant to the antibiotic will continue to proliferate and exacerbate the chronic disease.

It is also extremely important that MP patients do not take alternative medications or supplements along with the MP medications.

“Once a patient starts Benicar, the body usually works well enough so that a person can get through the initial stages of the MP with a good balanced diet, and no specific supplementation, or, in the case of vitamins, supplementation at a fraction of the RDA levels,” states the study site

“ The reality is that the body works by setting up a delicate balance between the receptors and molecules that control numerous complex feedback pathways, many of which are intertwined.”Supplements can be over-the-counter (OTC) or prescription medications. Just because something is available OTC doesn’t make it safe or innocuous. The reality is that the body works by setting up a delicate balance between the receptors and molecules that control numerous complex feedback pathways, many of which are intertwined. Any substance, whether or not it is listed as a drug, can bind the receptors that control these feedback pathways. In the absence of research that tells us what receptors a supplement or drug affects, we have absolutely no idea what pathways it may be altering if it enters the body. It could bind a receptor that interferes with immune function, or dysregulate a pathway that regulates important hormones.

The study site concurs. “While a person may think that there is no problem with a particular supplement”, they simply can’t know that there is no problem with it.”

“Most of the body’s healing processes work better if they are left alone while you are on the MP. The concept that we should intervene in these diseases with supplements or therapies has not worked, and I deprecate it,” states Marshall. “I have seen this happen so often before…trying to Band-Aid the metabolite shifts (with supplements) will not help recovery, and will often make the disease worse. They are almost always counter-productive.

As Marshall describes on the MP study site, it’s important to understand that the body does not work by having specific “levels” of any particular substance. Instead, as described above it works by setting up a balance between all the various metabolites. So it is generally useless to try and force the body to have a particular level of any one metabolite when the body’s own homeostasis is working to lower it for some reason – a reason that is often associated with the disease process itself. All metabolites should come back into balance as the MP medicines kill off the pathogens making patients sick.

“Just because a particular metabolite is a certain level in ‘healthy’ individuals doesn’t mean to say that any good will be achieved by supplementation in sick folks,” states Marshall. Vitamin D is a prime example. Now that the low vitamin D levels often observed in patients with chronic disease have been shown to be a result rather than a cause of the disease process, giving a person with low vitamin D levels more of the substance only causes a rise in the immunosuppression that results when the secosteroid begins to block the VDR.

With regard to vitamin D, it has been found that even when supplements do not include vitamin D on the label, they may still contain the substance. This is because vitamin D is naturally found in some plant and animal products and the FDA does not require labeling of naturally occurring vitamin D found in foods, herbs, or supplements.

Herbal supplements are a problem because “natural” herbs, oils, etc., have an effect on the body because they contain chemicals. The problem is, nobody knows exactly what chemicals they contain, because there is no requirement to have them tested or quality-controlled, or even listed on the label. The FDA controls only pharmaceutical drugs. The truth is, very few herbs are “natural.” The natural products have been dried, crushed, compounded, and concentrated by a manufacturing process. These compounds have the potential to negatively affect the body’s feedback pathways in the same manner as drugs and supplements.

Take, for example, rosemary and sage, which have high levels of carnosic acid – a compound that binds and deactivates the VDR. Just tens of milligrams of the substance can negatively affect the immune system.

It’s okay to enjoy small amounts of carnosic acid in foods seasoned with rosemary and sage, but if the substance is part of an over the counter supplement, it could seriously affect progress on the MP.

It’s also important to understand that supplements that make people with Th1 disease feel good are rarely improving their health. If people with L-form bacteria feel better after taking a supplement it’s almost always because the substance is affecting a pathway that allows it to slow the activity of the immune system. By palliating the immune response, it temporarily decreases the inflammation generated in response to L-form bacteria, causing a feeling of “wellness.” Yet, as in the case of vitamin D, this situation in which the immune system is depressed simply allows L-form bacteria to spread with greater ease.

There are instances where it’s OK for MP patients to take supplements. If a supplement is providing a patient with needed palliative relief of intolerable symptoms, then they may continue its use. For example, if a patient has abdominal pain that is relieved by milk thistle, or if a supplement helps them to get much-needed sleep, then its use is permitted. Similarly, if a patient cannot get the RDA of a necessary nutrient, such as calcium, from diet alone, sometimes a supplement may be appropriate (of course this does not apply to vitamin D).

Since at this point no physician has been trained and certified to administer the MP, it is the patient’s responsibility to see that the prescribing doctor understands the effectiveness of the MP, and the dangers inherent in deviating from the guidelines.

“Under no circumstances should you assume your physician will understand the MP, no matter how many patients he/she may be caring for. The amount of time needed to understand the intricacies of the Th1 disease process is beyond the capabilities of most physicians to provide,” states Marshall.

Consequently, it is important that MP patients work closely with the moderators on the study site, in partnership with their physician, to navigate through the multiple paradigm shifts that are needed to induce recovery from chronic disease.

Patients should encourage their doctor to join the Private Section for Health Professionals where he/she can communicate with other medical professionals using the Marshall Protocol. If the doctor has any questions, he/she may contact Dr. Marshall via email or phone.

Patients must follow the MP as written and as counseled because safety is at stake. If a patient is committed to succeeding with the MP and his/her doctor insists on altering the treatment, then patients are strongly encouraged to find a doctor who has a better understanding of the MP or who is willing to learn.

Misconception #10:  If my D ratio isn’t correct the MP won’t work for me.

It is recommended, but not required, that patients who decide to start the MP test the levels of their D metabolites. This process consists of two tests – one for the active form of vitamin D called
1,25–D, and the other for 25– D, the precursor form of vitamin D obtained from supplements and high levels of sunlight. Armed with an understanding of the latest model of vitamin D metabolism, the MP moderators can infer some information about a patient’s disease state based on this data.

Dr. Marshall’s most recent research has revealed that low levels of 25-D are common in patients with Th1 disease because of the fact that high levels of 1,25-D inhibit the conversion of a substance called pre-vitamin D into 25-D. In essence, high levels of 1,25-D naturally downregulate levels of 25-D. So a low 25-D level is a good indicator of Th1 disease.

However, if a person has been supplementing with large amounts of vitamin D before the 25-D test, or has had excessive sun exposure, their 25-D level will almost certainly be artificially skewed upwards. This information is important because patients starting the MP must work to get their level of 25-D down into a range under 20 ng/ml so that the VDR, and subsequently the innate immune system, can function up to par.

Similarly, because rises as part of the inflammatory response, levels of 1,25-D above 30 pg/ml suggest systemic inflammation. If 1,25-D levels exceed the Merck maximum of 45 pg/ml, the patient is generally at risk of bone loss due to osteoclast (bone cell) stimulation by 1,25-D. Levels above 60 pg/ml indicate well-perfused inflammation, where the inflamed tissue is close to the bloodstream. Usually that indicates lung or heart involvement. Anybody with a 1,25-D over 80pg/ml is generally at greater risk for cardiac immunopathology.

So a low level of 25-D and a high level of 1,25-D is a good indication that a person is indeed suffering from Th1 disease. Yet, due to the number of variables that can affect the D test results, D levels that do not reflect Th1 inflammation should absolutely not rule out the possibility that a patient is suffering from D-mediated inflammatory disease.

It was previously thought that a low 25-D indicated a rapid conversion of the metabolite into 1,25-D. However with Marshall’s latest research showing that low 25-D levels are actually a result of the disease process, the D ratio (ratio of 25-D to 1,25-D) is no longer a sufficient indicator of vitamin D dysregulation, especially when 25-D levels rise above 15 ng/ml.

“Now that we know more about the molecular activity of vitamin D metabolism, the D ratio carries less significance,” states the Marshall Protocol study site. Also, since Benicar works to correct vitamin D dysregulation, the D ratio has no value after the MP has begun.

“ It’s extremely important that even if the D tests prove inconclusive, people considering the MP do what is referred to as a therapeutic probe.”One pitfall of the D tests is that the labs sometimes mishandle the 1,25-D sample. The sample is very sensitive and must be sent to the lab frozen where it must remain frozen until the time of the test. It helps to remind the technician at the drawing (satellite) lab to freeze the sample for shipping, but if a person shows symptoms of Th1 disease and their 1,25-D results come back with levels that don’t indicate Th1 inflammation, they should not discount the possibility that the sample wasn’t correctly frozen.

The MP site warns that 1,25-D results from Labcorp have proven unreliable even when the sample was shipped to them frozen. This may be due to a policy of allowing the frozen sample to thaw in the refrigerator before they run the test. This lab should be avoided if possible.

Also, you should know that several medicines are able to interfere with the levels of the vitamin D metabolites. If patients are taking these medications at the time of the test, they will receive incorrect results. For one, the antifungal medication Diflucan directly inhibits the enzyme CYP27B1, which is needed for the macrophages (white blood cells) to energetically convert 25-D to 1,25-D. Thus, patients taking this medication at the time of their D tests will obtain a false low level of 1,25-D. Use of immunosuppressants such as prednisone lowers 1,25-D by 25-40%.

One small 1982 study found that serum concentrations of 1,25-D fluctuate with the menstrual cycle. Levels of 1,25-D were shown to be dramatically higher near ovulation in women not on the pill, suggesting that 1,25D may be higher near ovulation and during the latter half of the menstrual cycle.

For all these reasons, it’s extremely important that even if the D tests prove inconclusive, people considering the MP do what is referred to as a therapeutic probe. A therapeutic probe is simply a way of saying that a patient should start the Marshall Protocol medications. If they are infected with L-form bacteria, Benicar will likely cause expected neurological-type adjustment symptoms and minocycline will almost always provoke an immunopathological response within the first month or two of treatment.

These reactions are proof positive that the patient is infected with L-form bacteria and thus should be given priority over the D tests to decide if a person should start the MP. This is particularly true if the person is displaying obvious symptoms of Th1 disease or has been diagnosed with one of the illnesses that the MP has been shown to successfully treat.

However, it is important to note that for patients who have been consuming high levels of vitamin D prior to the probe, their immune system (via the VDR) may be blocked from successfully killing their bacteria, even with the help of antibiotics, and the probe would fail. In this case, the level of 25-D should be checked, and if high, the protocol could be started– even in the absence of a response to minocycline– as long as the patient works to diligently remove vitamin D from his/her diet.

“Luckily, the time-honored therapeutic probe is an effective ‘acid-test’ in these Th1 diseases,” states Marshall. “The ultimate therapeutic probe is the Marshall Protocol itself - anything else will have both false positives and false negatives. If the patient starts the MP, and experiences immunopathology for themselves, then not only is it confirmation that the problem was/is occult bacteria, but also proof-positive to the patient that they are on the correct track. That is why we tend to suggest the MP even when the D data is uncertain. Your physician makes a risk-benefit analysis - evaluating the risk of the ARB and antibiotics (effectively zero to healthy individuals) with the degree of disability you are experiencing from your illness, and his/her expectation of whether the illness will get worse or better if left alone.”

Misconception #11:  Anyone who disagrees with Dr. Marshall is banned.

It’s true, a handful of people have been banned from the Marshall Protocol study site, but the banning of an individual is certainly not a common occurrence.

The relatively small number of people who have been banned from MarshallProtocol.com have failed to understand the purpose of the study site. The study site is not an “anything goes” discussion board, nor is it a site where members come to seek emotional support or engage in protracted debates. Rather, it has a single mission: to help guide patients who have educated themselves about the Marshall Protocol (by reading the information on the site) progress as successfully as possible on the treatment.

When asked about the Marshall Protocol in a phone interview, Belinda Fenter of Autoimmunity Research Foundation stated, “So, our website [the MP study site] was different from most that discuss disease. For the most part, other medical forums are places where free-for-all discussions take place, sites where people chime in about anything that comes to mind. Some boards serve as arenas where chronically ill people seek support and discuss the difficulties of coping with disease. We never wanted our website to follow either of these models. The aim was to create a study site that was focused on helping people understand the basics of disease and how to get better. We set a high bar for discussion topics - questions have to be directly related to disease or the treatment. Some people have a hard time adjusting to the fact that certain discussion topics are not appropriate. But we are intent on maintaining a level of accuracy and focusing on the science.”

“We encourage the exchange of information but posts which are merely speculative; challenge the authenticity of our scientific research; are skeptical or taunting in nature; are inaccurate, misleading or disrespectful of the moderators will not be tolerated and will be edited or deleted,” state the board staff.

“Keeping the information on the board accurate is critical.”Let’s say you have found that frog eye extract has helped your symptoms in the past. You come to the MP study site detailing the benefits of frog eye extract and repeatedly question the moderators on why frog eye extract is not a part of the Marshall Protocol. If you persist with these comments your posts will be deleted, and if you simply cannot drop the subject or you begin to insult the moderators and others on the board, you might be banned. Most patients on the MP site have a single focus and that is to get well.

The MP board staff are all volunteers who work long hours for no pay. With more and more people starting the MP every day, they only have the resources to deal with questions that pertain directly to the MP. This is particularly true because the moderators read every post on the board in order to ensure its accuracy. Keeping the information on the board accurate is critical. If a member accidentally writes something incorrect in his/her progress report or elsewhere on the site, other members could read the post and become confused. The incorrect advice might hinder fellow patients’ progress or even endanger their health.

Nevertheless, the moderators do try to discuss a range of scientific issues with members when they can find the time. To this end, Dr. Marshall has set up a forum called “Dr Marshall’s Perspective – a place to discuss the science underlying chronic disease.” The forum contains over 60 threads in which Dr. Marshall talks one-on-one with members, helping them understand the latest scientific breakthroughs (not just his own!). Members are also able to start their own topics where all kinds of studies are openly discussed, and people are free to comment about a range of topics. In this forum and elsewhere if you challenge Dr. Marshall politely and with respect, he will often try to address your concern and you will not get banned. If his response is a bit feisty, it’s only because it’s not easy to be a scientist who must constantly defend his discoveries to a medical community that is deeply embedded in the quagmire of incorrect consensus thinking.

Misconception #12:  The MP does not take care of viral or fungal co-infections.

Co-infections – such as Candida, Mycoplasma, Rickettsia, Mycobacteria, Bartonela, Babesia, HHV-6, the Eptein Barr virus, the Herpes virus - are commonly detected in people with Th1 disease. However, these pathogens are not driving the disease process. They simply “come along for the ride”, generating extra symptoms in people with inflammatory disease, because of the fact that people infected with L-form bacteria are, for the most part, severely immunocompromised.

The Th1 pathogens that underly the disease create ligands which are able to bind and block the Vitamin D Receptor – a fundamental receptor of the body that controls the activity of the innate immune system and the production of the antimicrobial peptides, proteins that kill bacteria, viruses, and fungae by a variety of mechanisms including disrupting membranes, interfering with metabolism, and targeting components of the machinery inside the cell. Thus, as more and more L-form bacteria accumulate, the body is left without tools to fight other pathogens that enter the body.

“The fact is, when the VDR is not functioning properly, and the innate immune system is overwhelmed by Th1 pathogens, then it cannot properly deal with co -infections which would otherwise be trivial for it to manage,” states the MP study site. “When the body is weakened by these Th1 diseases, co-infections are very common, as the immune system is ‘busy’ dealing with the pathogens which have parasitized the phagocytes (white blood cells) and can’t deal as effectively with the opportunistic infections.”

It’s analogous to “being seen at the scene of the crime but not actually committing it,” states Marshall. “The viruses, etc. are only co-infections, because the body’s immune system has been weakened by the Th1 pathogens, and is unable to fight the infection.”

But as people reach the later stages of the MP, they have killed off most of the bacteria that were previously creating VDR-blocking ligands. Because they have been avoiding vitamin D, 25-D is also no longer blocking the VDR. This means that their immune systems regain strength – vigor that allows their bodies to tackle co-infections that are unable to survive in the face of a functional immune system. The antimicrobial peptides (the body’s natural antibiotics) are produced again, making it even harder for co-infections to persist.

“Once the immune system is no longer under challenge, it will be able to cope with opportunistic infections,” states Marshall. “The MP is designed to allow your immune system to function and eventually kill all chronic infections, no matter what label has been put on any suspected infection. Once the Th1 bacterial pathogens are killed off, the immune system deals with the viruses it couldn’t clear while the bacteria were present. That’s why folks lose warts and other things as they recover on the MP.”

“Wait and see!” he continues. “A healing immune system is no longer ‘out of sync’ with the world, but copes normally with the various things life throws at it, instead of over-reacting.”

“ Once the immune system is no longer under challenge, it will be able to cope with opportunistic infections.”Mainstream medicine emphasizes the role of co-infections rather than the Th1 pathogens in chronic disease because while the pathogens that cause co-infections show up on laboratory tests, L-form bacteria do not. Thus, unaware of the tremendous amount of L-form and biofilm bacteria that their patients harbor, most doctors and researchers fail to understand the role these pathogens play in the disease process and incorrectly attribute all symptoms to co-infection instead.

“The issue is that the infections which can be easily detected in Th1 patients are co-infections, and not the cause of their illness,” states Marshall. “The Th1 pathogens hide so well that no antibodies are generated, and even molecular tools have difficulty detecting the traces of DNA from host-phagocyte apoptosis (bacterial death). The most dangerous and successful pathogens are the ones which are intra-cellular, and therefore do not show up on routine testing. These co-infections are not going to make you as ill as the Th1 pathogens.”

It helps to understand that viruses simply cannot cause Th1 disease because of the fact that their genomes generally don’t have a ribosome – or a protein that would allow them to translate their DNA. This means they are forced to rely on the host or upon bacteria to turn their DNA into proteins that can cause symptoms in the host.

“The viruses can’t create these proteins on their own so they just hang around as co-infections because the weakened immune system in Th1 patients can no longer kill them,” states Marshall. “The viruses are part of the pathogenesis, but only after the phagocytes have become parasitized by the bacteria that drive the primary disease process.”

“Everybody with a serious Th1 infection has HHV-6 and EBV (well, nearly everyone),” he continues. “The really nasty viral co-infections are things like active HIV and Hepatitis. There is usually no point in sweating the typical viral titers. They do not cause illness, despite what you read.”

Indeed, patients on the MP do find that co-infections resolve as they wear away at their L-form bacteria.

“I originally thought of myself as having a viral onset because I really began getting fatigued and started my downhill course after what seemed like a bad flu-like illness that was never identified,” states MP patient Joyce R. “I’m not sure what role the ‘virus’ played but I know that I have been responding well to the MP, just as predicted for a Th1 disease caused by bacteria blocking the VDR.”

Misconception #13:  If people who reach a state of remission thanks to the MP don’t stop taking antibiotics and Benicar it’s because they can’t.

Those new to the MP often express suspicion when hearing that many patients who have reached remission are still taking a combination of antibiotics and Benicar. Are MP patients deluding themselves by continuing to be on a treatment that is ultimately ineffective?

“If they stop the antibiotics will their symptoms come back?” skeptics ask. To that, the answer is no. People who reach the later stages of the MP have killed the vast majority of the bacteria that once caused their symptoms. They are dead – gone forever. Patients in remission who stay on the MP meds are well aware of the fact that if they stopped their antibiotics and Benicar they’d feel just fine.

Why then would a patient stay on the MP when their disease symptoms are gone?

People stay on the MP medications even after reaching a state of remission out of curiosity and a desire to be something of a pioneer - to discover what might happen if they are able to kill bacteria not necessarily associated with their old disease symptoms.

This is because even after a person on the MP is no longer symptomatic they may still have bacteria left to kill. The question is, “What role do these bacteria play in the body?” There is speculation that some persistent bacteria may be associated with the aging process, especially since diseases and symptoms of aging from cancer and cardiovascular disease to aches and pains– basically everything that makes getting older such a drag– are at their essence, inflammatory conditions. Because bacteria cause the immune system to mount a constant inflammatory response, the presence of L-form or other Th1 pathogens may very well be responsible for aging skin, wrinkles, and the wear and tear on organs.

People who haven’t completed the MP consider it inevitable that as they age, they will need to stock up on any number of medications including thyroid medications, cardiac meds, statins, NSAIDS, B/P meds, etc. But people who have reached the later stages of the MP see no reason why they cannot take their level of healing to a maximum – to a point where they will never need these medications and may experience great health during their elder years.

“ Why wouldn’t a patient want to explore what ‘better than ever’ means?”The desire to stretch the MP to its limits is compounded by the fact that for many people on the MP, it’s not enough to feel like one’s “old self.” Meg Mangin, an MP moderator who has chosen to stay on her MP meds despite reaching a state of health has commented that “she is determined to kill everyone of those little bugs” Why wouldn’t a patient want to explore what “better than ever” means?

What does it mean to be healthy? For most patients on the MP, “feeling healthy” before the treatment was not actually a real state of wellness. Essentially, since they were born or grew up with some of the symptoms of their disease, they assumed these symptoms to be part of a “normal” existence. How would they know otherwise? So as symptoms resolve, patients on the MP increasingly report reaching a state of health that they never knew was possible.

“Patients may continue to be surprised at the state of ‘normalcy’ they achieve. They eventually reach a higher level of functioning and reliable health than before treatment,” states the study site. “It is not just a simple ‘return to health’, it is a return to a state of good health we have never known, or certainly one that we can’t remember,” states Marshall. At this point few people consider stopping their antibiotics and Benicar. What if they can feel even better? How do you define better?

“I don’t know any of those who have reached the stage of ‘cure’ that feel otherwise,” states Marshall. “We have personally experienced that many of the so-called “diseases of the aging” are really bacterial diseases. And that is a very profound observation….”

The following is taken from my interview with Dr. Greg Blaney, another MPer to stay on his meds despite symptoms resolution.

“My own health has recovered to a point where I see signs of age reversal. My eyesight has improved, my hearing has improved, and my cognitive function is better than ever. After I exercise I feel invigorated – the way I used to feel when I was young, rather than drained. There is no doubt that the MP can have a significant effect on a patient’s longevity. Experts in the field of immunology are increasingly pointing to the fact that the aging of the immune system is a main factor influencing longevity. As people grow older, their immune systems are forced to deal with higher bacterial loads, which in turns means they have to manage a greater inflammatory response. The MP downregulates this inflammatory response, restoring the agility of the immune system, which significantly affects the aging process.

That means that I’m going to be greedy about staying on antibiotics until I’ve reaped every possible benefit of the MP. Come this Christmas I will have been on the MP for three years. All my symptoms are gone and I feel completely healthy. Except for one small issue. I still have occasional tinnitus. Some days it’s completely gone, but other days it’s still at about 20% of where it used to be. I’m staying on antibiotics until this issue is completely gone. I can see myself staying on antibiotics for at least another six months, maybe even a year. I have no concerns about staying on them for a longer period of time.

Some of the symptoms that I suffered from before the MP started when I was only 5-6 years old, so I had been sick for over 50 years. I have no intellectual concerns about spending 4-5 years on medications in order to reverse disease symptoms that had manifested over such a longer period of time, especially since I know how slowly L-form bacteria grow and how they can become dormant for periods of time. I also feel there are simply no adverse reactions or negative side effects that I need to worry about while taking the MP medications. It’s an extremely safe approach.”

That being said, people not interested in testing the boundaries of the MP can stop their antibiotics as soon as they feel that the symptoms of their disease have dissipated and they are no longer experiencing immunopathology. Obviously they can stop the meds before that if they want to – and settle for a state of lesser health.

“It is entirely an individual choice whether to go for total elimination of the pathogen, or stabilize at some lesser point and slow down the antibiotic dosing progression,” states Marshall.

Of course, once they have stopped the MP, people can once again pick up L-form bacteria. But they can eliminate the pathogens on a regular basis by doing “clean-ups” – or temporarily taking the MP meds at repeated intervals for a short periods of time. These clean ups could be done every year, or every five years etc - it’s up to the patient. One thing is for sure – if people who have completed the MP do regular clean-ups they will never again develop a load of L-form bacteria capable of causing a Th1 illness.

Furthermore, since people to complete the MP end up with innate immune systems that are in enviable shape, their bodies have the strength to naturally kill many of the L-form bacteria they may encounter. “The immune system seems to be able to do the cleanup job on its own, once folk have fully recovered. In my opinion, there is no harm in doing an annual cleanup though - but it no longer seems that it will be necessary to maintain good health,” states Marshall.

Misconception #14:  If I don’t do the Marshall Protocol, my illness might go away on its own.

The chronic inflammatory diseases treated by the MP never go away on their own. If you have been told that your illness has the possibility to go into “spontaneous remission,” then the person making such a claim fails to understand the actual definition of the word “cure.”

It’s not that patients with Th1 disease can’t and won’t go through periods where they might feel better. Unfortunately, these periods are usually a sign that the immune system has become severely compromised. Whether temporary “remission” is driven by immunosuppressive drugs, a high intake of vitamin D, excessive sun exposure, or simply the accumulation of a bacterial load that is so high that the VDR is almost completely shut down by bacterial ligands– these periods are times when L-form bacteria are alive and well, spreading, and surely infecting other tissues. This causes illnesses such as arthritis, heart disease, decreasing kidney function, diabetes, cancer and even diseases of aging to develop later in life. But because the immune system is no longer able to kill the pathogens, the inflammatory response to their death subsides, causing the patient to feel a sense of temporary relief that is often mistaken for “wellness.”

“ In reality, remission is accompanied by recurrence and relapses.”It comes as little surprise then, that members of the medical community who believe in spontaneous remission tend to base their information on studies that are notoriously poor at following subjects for long periods of time – periods of time that would allow researchers to take note of the declines that occur after bacteria have spread and any temporary periods of palliation have subsided. These studies would have to last for at least 5-10 years, with endpoints assessing systemic illness. Such studies would surely find that disease symptoms persist even in those people who had once experienced temporary periods of relief.

“There has somehow been a misconception that remission could last a lifetime,” states Marshall. “In reality, remission is accompanied by recurrence and relapses. Take, for example, sarcoidosis – which has the same basic pathogenesis as all other Th1 diseases. Researchers at Jefferson Medical Center in Philadelphia found a 74% relapse rate in sarcoidosis patients with treatment-induced remission, while only 60% of patients identified as having a favorable prognosis actually sustained remission over 130 months.^[23]

Many argue that the most accurate study of sarcoidosis to date is the 2003 NIH ACESSS study, which followed 215 sarcoidosis patients for two years - a period during which it is sometimes mistakenly thought that the disease can go into remission. The study found that measures of sarcoidosis severity remained unchanged over the two-year period, despite the fact that many patients were using corticosteroids and other drugs.

In fact, in the NIH ACCESS study there were no documented cases of spontaneous remission. Even in the positive-sounding “improved” category for clinical markers, the percentages described were at best “improved”, not “better” and certainly not “cured.” The study also concluded that most patients with persistent sarcoidosis at two years were “unlikely to have resolution of the illness” and that “end-stage pulmonary sarcoidosis usually develops over one or two decades.”

In simple terms, the study found that not one patient recovered over a two year period, and that any patient to remain ill with sarcoidosis for two years is likely to die from the disease over the following ten to twenty years.

It has also been argued that there is a gap between how patients themselves and members of the medical community perceive success and improvement, as well as their concept of cure. The medical community has a tendency to be satisfied by results that show a patient has stabilized thanks to a particular medication, without taking into account systemic effects of disease, such as fatigue and pain, which are often excluded as endpoints.

A 2005 Dow Jones Newswires article on gene therapy described patients who had undergone treatment as “basically cured” – even though three had developed leukemia and one died.

The above example is a misuse of the word “cure.” For one thing, an actual cure results from a treatment that allows all participants to become well, no side effects or long-term harm included. Did the above study check in with its subjects a decade down the road in order to access their health years later? Probably not. But if they did, the subjects were probably symptomatic again, as gene therapy has not yet been adopted as an effective way to treat disease.
The public often isn’t satisfied with the medical community’s perception of a “cure,” which is why so many patients have left mainstream medicine – searching for solutions among doctors that practice alternative medicine or even psychotherapists.

Unfortunately, for chronically ill patients, commercial culture and the media have combined to progressively define down what “better” means—so much so that assessing the significance of any new “breakthrough” becomes a tall order.

Television and the Internet abound with reports of products you can buy, supplements you can take to erase all the vestiges of illness. Promises, promises.

When I first fell ill with CFS I went to see a doctor, who was, and is, considered an expert on CFS. His website, which has since been changed, stated at the time that well over half (if memory serves, it was 79%) of his patients recovered.

At my first appointment I was prescribed a multitude of prescription drugs – drugs for ADD, seven sleeping medications, drugs for blood pressure, the adrenal glands, and on and on…. Then I was instructed to buy around 25 different supplements. Several months later I wrote an article in Fibromyalgia Aware magazine describing the utter horror expressed by my landlord when, while fixing the stove, he stumbled upon my drug cabinet and saw the amount of medication I was taking.

At my next appointment I asked my doctor – when do I get cured? When do I stop these meds? His answer was that I would need to take most of my medicines for the rest of my life in order to mask my symptoms. That was his definition of cure. At that point I realized that the cure I envisioned – the ability to run marathons, the ability to travel and to make plans without hesitation, the ability to pursue a challenging career – is not the “cure” offered by specialists like my former doctor.

The MP is different. It addresses the root cause of Th1 disease – the bacteria causing symptoms in the first place. And unless these bacteria are targeted and killed, Th1 diseases do not go away. If they went away on their own, why would there be hundreds of forums on the Internet where people with chronic disease discuss what it’s like to live a life full of relapses and pain? If they went away on their own, then why are “experts” like my former doctor still in business? If they went away on their own, then why would so many people who have tried myriad other treatments for their disease make a long-term commitment to the Marshall Protocol?

REFERENCES

1. Schwocho, L R, and H N Masonson. 2001. “Pharmacokinetics of CS-866, a new angiotensin II receptor blocker, in healthy subjects.” Journal of clinical pharmacology 41(5):515-27. [↩]
2. Tronvik, E., Stovner, L. J., Helde, G., Sand, T., & Bovim, G. (2003). ↩]