Dr. Renata Trister DO
The Marshall Protocol is a medical treatment used by physicians worldwide to treat a variety of chronic inflammatory and autoimmune diseases including Chronic Fatigue Syndrome, Fibromyalgia, Crohn’s Disease, Sarcoidosis and Rheumatoid Arthritis. Dr. Marshall started his research after to being diagnosed with sarcoidosis. After reading studies that demonstrated Rickettsia DNA in sarcoid patients, and by noting that his disease was worsened by sunlight. He developed a hypothesis, and a treatment protocol to treat chronic inflammatory illnesses.
Sarcoidosis is a disease whose etiology is unknown, but is characterized by non-caseating granulomas. Granulomas are an immunologic response to infections, often fungal or mycobacterial. Sarcoidosis frequently causes dysregulation of vitamin D with increased levels in the blood, the vitamin D being made in the granulomas.
The Marshall Protocol is based on the hypothesis that “chronic diseases (termed T-helper [Th1] illnesses) are the result of infection by an intraphagocytic, metagenomic microbiota of chronic bacterial forms that are often referred to as the Th1 pathogens”. The term intraphagocytic refers to the fact that these bacteria have developed the ability to remain alive and proliferate undetected inside the cytoplasm of the cells they infect. These cells include macrophages (cells of the innate immunity), the very cells that the body uses to kill invading pathogens. Once inside these cells, they cause our own cells to release inflammatory cytokines (proteins that often generate pain and inflammation).
The term metagenomic indicates that there is a tremendous number of different species of these chronic bacterial forms. Finally, the term microbiota refers to the fact that these bacteria are also thought to sustain themselves by grouping into communities called biofilms. The bacteria inside a biofilm produce a protective matrix that allows them to more effectively evade the immune system and develop resistance to antibiotics.
Many of the Th1 pathogens are also postulated to be in a chronic state referred to as the L-form. Under certain conditions, L-form bacteria mutate from classical bacteria and lose their cell walls. Since L-form bacteria lack a cell wall, many antibiotics (that target bacterial cell walls) are not effective, furthermore these pathogens cannot be detected by standard laboratory tests.
The ability of the Th1 pathogens to proliferate in the body is directly related to the vitamin D receptor (VDR). Critically important to the body, the Vitamin D Receptor (VDR) controls the innate immune system – the body’s first line of defense against infection. It’s also responsible for turning on/off a wide array of genes and chemical pathways. One of the VDR’s myriad jobs is to control expression of several families of antimicrobial peptides (AMPs), proteins that kill bacteria, viruses and fungi by a variety of mechanisms including disrupting membranes, interfering with metabolism, and targeting components of the machinery inside the cell.
Although casually referred to as a vitamin by some members of the medical community, molecular biologists have long realized that the precursor form of vitamin D (25-D) is really a secosteroid. Elevated levels of 25-D can bind and inactivate the VDR, which subsequently shuts down the innate immune system.
Certain species of bacteria also produce substances that can bind and inactivate the VDR in a manner similar to 25-D. Consequently, people who are infected with the Th1 pathogens and consuming vitamin D are no longer able to produce the AMPs or turn on the innate immune response. This allows their bacteria to proliferate and spread.
When the innate immune system can no longer function, people have a very hard time keeping other pathogens under control. They often find that childhood viral infections reactivate, or that they acquire Candida (pathogenic yeast) and Mycoplasma as well.
Unlike its inactive counterpart, 25-D, that inactivates the VDR in healthy individuals, 1,25-D binds and activates the VDR. But in individuals who have 25-D and bacterial proteins blocking the VDR, 1,25-D is forced out of the receptor and into the surrounding environment. Causing 1,25-D to rise to an unnaturally high level.
The nuclear receptors affected by 1,25-D are receptors that regulate the body’s hormones – the glucocorticoid receptor, and the alpha and beta thyroid receptors, the adrenal receptors, and the progesterone receptors, among others.
This means that when 1,25-D is high, it competitively displaces cortisol, T3, and other metabolites from their target nuclear receptors, causing havoc on the body’s hormonal pathways. Thus, most people with chronic disease find they have difficulty tolerating stress, changes in temperature, and a variety of other hormone-related issues. Also, when levels of 1,25-D rise above 42 ng/ml, calcium begins to be leached from the bones, a process that results in osteoporosis and osteopenia.
When 1,25-D rises due to the processes described above, it also binds a receptor called the PXR. The PXR subsequently inhibits conversion of pre-vitamin D to 25-D, causing 25-D levels to drop. This means that low levels of 25-D – the form of vitamin D measured by most doctors – is not a sign of vitamin D deficiency. Instead, low levels of 25-D are a result of the disease process.
Patients on the Marshall Protocol take a medication called olmesartan (Benicar), which is able to bind and activate the VDR by pushing 25-D and bacterial proteins out of the receptor. Patients also lower levels of 25-D in the body by avoiding the kinds of vitamin D present in various foods. These measures renew the body’s ability to turn on the innate immune system and produce the anti microbial peptides. The immune system is then able to kill the Th1 pathogens and is once again able to manage viral and other co-infections.
At the same time, MP patients take pulsed, low-dose antibiotics. Antibiotics taken in this manner are much more effective against bacteria in biofilms and are able to greatly weaken the Th1 pathogens so that the patient’s own immune system is then able to destroy them. The antibiotics weaken the bacteria by blocking their ribosomes, which they need to produce proteins that help them survive and reproduce. It’s important to understand that when the Th1 pathogens die, there is a temporary change in a patient’s immunopathology.
Immunopathology refers to the changes in the immune system that result from bacterial death (another term sometimes used is the Jarisch-Herxheimer or “Herx” reaction). Dying bacteria release toxins into the bloodstream, stimulate the production of inflammatory cytokines, and generate temporary hormonal imbalances. This means that once patients begin the MP, each dose of antibiotic will cause them to feel bad for the period of time it takes their immune system to deal with the consequences of bacterial die-off.
Before starting the MP, many people may feel that they have improved through consuming vitamin D and taking steroids such as prednisone. In reality, these compounds further inactivate the VDR, preventing the immune system from effectively killing the Th1 pathogens. Since it is the death of these forms of bacteria that generates an increase in painful symptoms, people may experience short-term relief when using vitamin D or prednisone as their immune system shuts down and fewer bacteria are killed. However, in reality, this situation allows the bacteria to spread more easily.
Patients on the MP have dozens of different medical conditions. As evidenced by members’ reported progress on the marshallprotocol.com website, nearly all experience a powerful immunopathological reaction after taking a dose of antibiotics.
Many patients report great improvement, while some are approaching complete recovery.
Some of the diseases patients are currently using the MP to treat include (but are not limited to):
Chronic Fatigue Syndrome
Chronic Lyme disease
Multiple Chemical Sensitivity (MCS)
Apart from the symptoms or diagnosis indicating Th1 disease, the easiest way to find out if the Marshall Protocol may be applicable to your disease is to get a blood test and check the level of your D Metabolites. This test can detect the elevated level of 1,25-D often seen in patients with chronic disease, but must be done correctly in order to be of any value.
Patients can also use a therapeutic probe to determine whether the MP can be applied to their illness. A therapeutic probe refers to a trial period during which a person tests whether or not the taking the MP medications results in immunopathology or other symptom changes.