Arthritis

Rheumatoid arthritis (RA) is a chronic and disabling autoimmuneA condition or disease thought to arise from an overactive immune response of the body against substances and tissues normally present in the body disorder. Growing evidence suggests RA is caused by infections.

Pain is a symptom of RA and can be exacerbated by immunopathologyA temporary increase in disease symptoms experienced by Marshall Protocol patients that results from the release of cytokines and endotoxins as disease-causing bacteria are killed.. Marshall ProtocolA curative medical treatment for chronic inflammatory disease. Based on the Marshall Pathogenesis. (MP) patients should always use 40mg of olmesartan (Benicar)Medication taken regularly by patients on the Marshall Protocol for its ability to activate the Vitamin D Receptor. every four hours before resorting to pain medications. There are also other strategies for managing pain.

When the usual strategies for managing immunopathology are not enough to control pain, may patients rely upon pain medications. Except for corticosteroidsA first-line treatment for a number of diseases. Corticosteroids work by slowing the innate immune response. This provides some patients with temporary symptom palliation but exacerbates the disease over the long-term by allowing chronic pathogens to proliferate., there is no pain medication contraindicated specifically because a patient is on the Marshall Protocol. Opioids are the preferred method of dealing with extreme pain in the MP cohort.

Managing Rheumatoid Arthritis with Dietary Interventions ¹⁾

Scher's and Abramson's 2011 review “The microbiome and rheumatoid arthritis” offers a variety of evidence pointing to a key role of microbes in RA.⁶⁾

An increasing number of studies are providing support for the view that “autoantibodies” can be generated in response to the persistent presence of a pathogenic microbiotaThe bacterial community which causes chronic diseases - one which almost certainly includes multiple species and bacterial forms.. While high titers of rheumatoid factor (RF) are associated with severe rheumatoid arthritis, they also appear in a number of other diseases including viral, bacterial, and parasitic infections.⁷⁾ Maturation of RF can be initiated by chronic infections.⁸⁾

During immune reconstitution inflammatory syndrome, HIV/AIDS patients experience the worsening or onset of systemic inflammatory clinical signs and symptoms following treatment with highly active antiretroviral therapy (HAART). This syndrome results when HAART allows for partial recovery of the immune response. This causes renewed and exuberant host immunological responses towards opportunistic infectious agents, agents that the host accumulated during prior periods of immunosuppression.⁹⁾

A number of well-known readily cultured pathogens have been conclusively linked to IRIS: the herpes viruses, cytomegalovirus, hepatitis B and C, M. tuberculosis, Mycobacterium avium complex and Cryptococcus neoformans.¹⁰⁾ However, many more microbes likely contribute to the reaction since AIDS clinicians do not yet have access to the metagenomic tools. Certainly, the existence of IRIS in culture-negative HAART patients suggests that more microbes may be present than the few that have already been isolated.¹¹⁾

Interestingly, patients experiencing IRIS often “develop” autoimmune conditions as a manifestation of immune restoration including rheumatoid arthritis,¹²⁾ This suggests that patients with RA accumulated microbes that are directly involved in the pathogenesis of this disease state.

• Gut-joint axis – One excellent example gut–joint axis hypothesis is represented by classic Whipple disease, in which the presence of a single bacterium in the small intestine, Tropheryma whipplei, is sufficient for the development of joint inflammationThe complex biological response of vascular tissues to harmful stimuli such as pathogens or damaged cells. It is a protective attempt by the organism to remove the injurious stimuli as well as initiate the healing process for the tissue. in predisposed individuals.¹³⁾ A 2008 comparison of the composition of intestinal microbiota of 101 patients with early rheumatoid arthritis with those diagnosed with fibromyalgia. In comparison to patients with fibromyalgia patients, RA patients had significantly less Bifidobacteria and bacteria of the Bacteroides-Porphyromonas-Prevotella group, Bacteroides fragilis subgroup, and Eubacterium rectale–Clostridium coccoides group.¹⁴⁾
• Presence of microbes in the synovium – Several reports have associated RA with bacterial overgrowth and deposition of resultant immune complexes in the synovial fluid.¹⁵⁾
• Periodontal disease comorbidity – Patients with RA often exhibit periodontal disease, which is associated with pathogens like Porphyromonas gingivalis. A 2010 study showed that P. gingivalis promotes early and later stages of apoptosis of primary human chondrocytes, which might contribute to the joint damage seen in the pathogenesis of RA.¹⁶⁾

Consistent with the Marshall PathogenesisA description for how chronic inflammatory diseases originate and develop., patients with RA tend to have higher than normal levels of 1,25-DPrimary biologically active vitamin D hormone. Activates the vitamin D nuclear receptor. Produced by hydroxylation of 25-D. Also known as 1,25-dihydroxycholecalciferol, 1,25-hydroxyvitamin D and calcitirol.. Mawer et al. found that 1,25-D levels were particularly elevated in the synovial fluid surrounding the joints of patients with rheumatoid arthritis (RA).¹⁷⁾ In this study, median serum levels of 1,25-D at baseline was not elevated in the RA patients — only 24 pg/ml. Thus, the extrarenal synthesis of 1,25-D was not obvious from the routine blood test for 1,25-D. There is no reason to think that the metabolism of other diseases is any different. Mice without functional Vitamin D ReceptorA nuclear receptor located throughout the body that plays a key role in the innate immune response. signaling develop arthritic symptoms.¹⁸⁾

1,25-dihydroxyvitamin D3 (1,25(OH)2D3), has potent anti-inflammatory effects on T-cells. However the efficacy of vitamin-D in an inflammatory setting is unclear. D 1,25

Evidence as to how human genes contribute to the development of RA has been weak. Genome-wide associations studies explain only 16% of disease variance.¹⁹⁾ Moreover, the prevalence of RA concordance in monozygotic twins in European studies is ≤15%,^{20) 21)} and it is unclear whether this level actually exceeds the risk of developing RA that exists in the general population.²²⁾

The following cases come from Autoimmunity Research FoundationNon-profit foundation dedicated to exploring a pathogenesis and therapy for chronic disease.'s peer-reviewed paper, “Immunostimulation in the era of the metagenome.”

B.G. is a 56-year old male who was first diagnosed with rheumatoid arthritis in June 2002. He also complained of fatigue and depression. In February 2004, B.G. was administered 200mg of minocycline every other day, 200mg of Celebrex daily, and Advil as needed. B.G. reported improvement in all major symptoms within weeks. In April 2005, Celebrex was lowered to 100mg every day. At this point, B.G. reported being “unaware” of rheumatoid arthritis symptoms. On a scale of 1-10, with 10 being the most severe, he rated his overall well-being as a 1. In September 2005, he was administered 40mg of olmesartanMedication taken regularly by patients on the Marshall Protocol for its ability to activate the Vitamin D Receptor. Also known by the trade name Benicar. four times daily. His symptom levels remained constant. After two weeks, 25mg of minocycline every other day was introduced. Within 48 hours, B.G. reported exquisite photosensitivityAbnormal sensitivity to sunlight and bright lights. Also referred to as "sun flare" or "light flare.", complaining that daylight “hurt his eyes” and “made him feel ill.” Over the course of several weeks, his symptoms increased greatly to the point where he rated his overall well-being as an 8.5. After five weeks, B.G. discontinued olmesartan and resumed 200mg of minocycline every other day. He reported immediate relief. In September 2005, B.G. resumed olmesartan four times daily and 25mg minocycline on alternate days. He experienced a spike in symptoms once more. Over a few months, immunopathology gradually decreased on this dose. At present, B.G. has been on the treatment for over 4 years. In September 2010, B.G. reported overall well-being at a 2.

Proal, et al., “Immunostimulation in the era of the metagenome”²³⁾

L.Z. is a 58-year old female diagnosed with rheumatoid arthritis in 1996. In the 5 years that followed, she was administered high-dose antibiotics along with frequent cortisone injections. Despite treatment, her disease progressed and she had joint damage in hands and feet. In 2001, L.Z. began 2,000-5,000 IU of vitamin D daily, DHEA, armour thyroid, hydrocortisone, and bioidentical hormone supplementation. In August 2004, L.Z.’s measured levels of antinuclear antibodies (ANA) were 1:160. Following the test, patient stopped vitamin D and was administered 40mg olmesartan 4 times daily. Over the course of several years, she was prescribed rotating combinations of certain subinhibitory antibiotics including minocycline, azithromycin, and clindamycin. This caused transient increases in symptoms of depression, gastrointestinal distress, and joint pain. In March 2005, ANA antibodies were measured at 1:320 while in August of the same year, this measure declined to 1:160. By August 2006, L.Z. was able to discontinue both Celebrex and all hormone therapy. One year later, L.Z. reported being able to hike with reduced joint pain. In November 2006 and in 8 subsequent tests, the patient tested negative for ANA antibodies (Figure 1). In December 2007, L.Z. discontinued all antibiotics but continues to take olmesartan.

Proal, et al., “Immunostimulation in the era of the metagenome”²⁴⁾

from DJ in California During the summer of 2013 I looked at 2,000 records of people using the Marshall Protocol.

I eliminated all records that had less than 20 messages, as these were usually inquiries into the treatment without actual participation. I eliminated all records from people who had been banned from the site. I eliminated all records from Health Professionals who did not actually have disease. I eliminated all records where I could not find a valid progress report. This left me with 864 meaningful records.

I tried my best to be unbiased as I was expecting to see about a 20% improvement in health of members, or in other words a 20-25% success rate. I was intending to compare this to the 10% success rate I found done on the use of prednisone to treat Sarcoidosis. That double blind report shows that 10% treated with prednisone achieve remission. (BTW remission in Sarcoidosis as far as I can find out is measured rather subjectively) The following information is what I found:

rheumatoid arthritis: 39 members; 27 success; 5 no success; 7 unsure

TOTALS: 864 members;573 report success; 119 report no success; and for 172 results are not clear.

SUCCESS RATES: Over all success rate 66.32% Over all unsuccessful 13.77% Over all unsure 19.91%

rheumatoid arthritis success 69.2%

All Other Th1 diseaseAny of the chronic inflammatory diseases caused by bacterial pathogens. success 59.8%

What we who are a part of this forum, who stuck with the protocol long enough, who endured the IP and were able to keep a doctor, report is that this has a better than 50% success rate.

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<div class=“patientinterviewboxl”> <div class=“patientinterviewimage”></html><html></div> <div class=“patientinterviewtext”> <div class=“patientinterviewname”></html>Roy P.<html></div></html>

sarcoidosis, rheumatoid arthritis

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<html> <div class=“patientinterviewboxr”> <div class=“patientinterviewimage”></html><html></div> <div class=“patientinterviewtext”> <div class=“patientinterviewname”></html>Ival Meyer<html></div></html>

rheumatoid arthritis, dyslexia

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Interviews of patients with other diseases are also available.

Do infections trigger juvenile idiopathic arthritis? ²⁵⁾

Gout is different from other forms of arthritis because it occurs when there are high levels of uric acid circulating in the blood, which can cause urate crystals to settle in the tissues of the joints.

Urate crystals may be present in the joint for a long time without causing symptoms. Infection, injury to the joint, surgery, drinking too much, or eating the wrong kinds of foods may suddenly bring on the symptoms, which include pain, tenderness, redness, warmth, and swelling of the joint. In many cases, the gout attack begins in the middle of the night. The pain is often so excruciating that the sufferer cannot bear weight on the joint or tolerate the pressure of bedcovers. The inflamed skin over the joint may be red, shiny, and dry, and the inflammation may be accompanied by a mild fever.

Eventually, stone-like deposits known as tophi may build up in the joints, ligaments, and tendons, leading to permanent joint deformity and decreased motion. medical-dictionary.thefreedictionary.com

I went on a ketogenic diet when I was getting intolerable gout flares and it seemed to help somewhat.

I drink about an extra 2.2 L (outside of meals) of water daily and I haven't had a major flare since doing so.

I recently heard that phytic acid is able to inhibit the enzyme xanthine oxidase that causes a build up of uric acid²⁶⁾. The supplement IP6 Gold is a good source of phytic acid but I have not tried it though. I am concerned that this supplement might be immunosuppressive as it works like Allopurinol which also blocks xanthine oxidase - we know that Allopurinol to be immunosuppressive. David

Herein, we report a positive relationship between serum UA and acute-phase reactants, such as high-sensitivity C-reactive protein, fibrinogen, ferritin, complement C3, and erythrocyte sedimentation rate, in a cohort of 2731 nondiabetic adults. The relationship remains significant after adjustment for several confounders, including age, sex, adiposity, anti-hypertensive treatments or diuretics use. To confirm the existence of a causal relationship, we examined the effect of UA on the expression of inflammatory biomarkers in human hepatoma HepG2 cells and characterized the signaling pathway by which UA acts. …….The effect of UA was completely blocked by the antioxidant N-acetylcysteine. ²⁷⁾