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1,25-D rises above its normal range it binds the alpha/beta
thyroid receptors, the glucocorticoid receptor (GCR) and the androgen receptor (AR),
displacing their native ligands and causing an array of hormonal imbalances
http://autoimmunityResearch.org/preprints/ProalAnnals2009Preprint.pdfResearchers have noted that the incidence of autoimmune diseases such as Hashimoto’s
thyroiditis is markedly higher in women than in men, but to date the reason for this
disparity has been unclear. The Vitamin D Nuclear Receptor (VDR) is expressed in the
human cycling endometrium. Because the VDR controls expression of the Cathelicidin
and beta Defensin antimicrobial peptides (AmPs), dysregulation of the receptor greatly
compromises the innate immune response. Increasing evidence indicates the presence of
a chronic, intraphagocytic metagenomic microbiota in patients with autoimmune disease
that may survive by dysregulating the VDR. VDR dysregulation in turn prevents the
breakdown of the active vitamin D metabolite 1,25-hydroxyvitamin D (1,25-D) by CYP24. In
silico data suggest that when 1,25-D rises above its normal range it binds the alpha/beta
thyroid receptors, the glucocorticoid receptor (GCR) and the androgen receptor (AR),
displacing their native ligands and causing an array of hormonal imbalances. If T3 is
displaced from alpha thyroid, thyroiditis may result. Since the VDR, GCR, and AR also
express multiple families of AmPs, expression of these natural antibiotics further wanes
in response to dysregulation by 1,25-D. The end result is a system-wide drop in AmP
expression that may allow pathogens to spread with greater ease. Because women have an
extra site of VDR expression in the endometrium, the drop in AmP expression associated
with nuclear receptor dysregulation may disproportionately affect them. This would cause
women to accumulate higher bacterial loads than their male counterparts, particularly
during early pregnancy when 1,25-D levels rise by 40%Anybody have experience with Marshall protocol ?
A significant number of patients diagnosed with sarcoidosis, post-treatment chronic Lyme syndrome, chronic fatigue syndrome, uveitis, Hashimoto’s thyroiditis, rheumatoid arthritis, fibromyalgia, diabetes, psoriasis, lupus (SLE), multiple sclerosis, and a number of other diagnoses are showing a promising response from being treated with the Marshall Protocol
Resources for physicians
Related articles: Science behind Pathogenesis, Science behind Protocol
The Marshall Protocol (MP) is the name given to a therapy devised by Professor Trevor Marshall, and is based on the pathogenesis he has elucidated for chronic disease.Marshall (and colleagues) observed that chronic inflammatory diseases, including many autoimmune diseases, are caused by a metagenomic microbiota: communities of bacterial pathogens, many of which persist intracellularly. A recent peer-reviewed paper describes this Pathogenesis in more detail.1
The Marshall Protocol, a medical treatment supported by Autoimmunity Research Foundation, has been available since 2002 and has applicability to a wide range of chronic inflammatory illnesses.
A significant number of patients diagnosed with sarcoidosis, post-treatment chronic Lyme syndrome, chronic fatigue syndrome, uveitis, Hashimoto’s thyroiditis, rheumatoid arthritis, fibromyalgia, diabetes, psoriasis, lupus (SLE), multiple sclerosis, and a number of other diagnoses are showing a promising response from being treated with the Protocol.
In determining whether a patient can be successfully treated with the MP, a specific chronic disease diagnosis is not as important as the clinical assessment by a knowledgeable health care provider, the results of a therapeutic probe, and outcome of the vitamin D metabolites blood test.2
According to the Marshall Pathogenesis, chronic inflammatory disease is characterized by dysregulation of the nuclear receptor pathways which control the innate immune response. The Vitamin D nuclear receptor (VDR) expresses many of the body’s antimicrobial peptides (along with TLR2). In addition to down-regulation of expression of the VDR itself by many common pathogens, antagonistic bacterial metabolites incrementally block ligands from activating it. Ingested vitamin D slows activity of the receptor in this same manner, preventing the body from killing the pathogens at the heart of the disease state. That is why avoidance of ingested vitamin D (in food and supplements) is essential for the innate immune system to function correctly while patients are on the MP.3 4
The MP uses four-times daily dosing of the ARB olmesartan medoxomil (Benicar, Olmecip, Olmetec) to re-activate the Vitamin D Nuclear Receptor, dislodging bacterial ligands in the process. Additionally, several pulsed, low-dose, bacteriostatic oral antibiotics are used to help the immune system recognize the pathogens in the metagenomic microbiota. Olmesartan also reduces inflammatory cytokine production by inhibiting the NF kappa-B transcription pathway. This inhibits, among other things, the release of TNF-alpha, helping to protect the organs from effects of excessive inflammation.
Patients on the MP ultimately will use up to five bacteriostatic antibiotics: minocycline, azithromycin (Zithromax), clindamycin, sulfamethoxazole-trimethoprim (Bactrim DS), and demeclocycline (Declomycin) to help their immune system weaken and attack components of the systemic microbiota.
Seriously ill patients may develop photosensitivity during the healing process, so avoidance of direct and indirect sunlight may be necessary. Patients may need to protect their eyes from bright lights to prevent further retinal damage and reduce neurological symptoms due to inter alia, the effect of ocular 1,25-D production on the brain. Some patients do not experience any significant photosensitivity during recovery, and those who do often find it more manageable after 12 to 18 months.
The VDR nuclear receptor is activated in healthy individuals by a vitamin D metabolite: 1,25-
dihydroxyvitamin-D. The body manufactures all the Vitamin D it needs from 7-dehydrocholesterol, and
the immune system works best in the total absence of exogenous steroid. When the operation of the
VDR is blocked by ingested Vitamin D, the immune system cannot kill the pathogens and one of the
resulting morbidities is chronic disease. That is why avoidance of ingested Vitamin D (in food and
supplements) is essential for the innate immune system to function correctly [4,5].
http://autoimmunityresearch.org/transcripts/AR-Albert-VitD.pdf
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