It seems that it might be prudent to understand one's own situation and one's own pre-existing lab results, before embarking on a protocol with such high doses of so many substances. And to ensure that one is using reputable sources that don't have hidden toxicity, as high doses of something toxic could be a problem.
@Hoosierfans I'm sorry to hear of your situation and am glad that you were able to rescue yourself, but I think your experience is a good warning to each of us to assess our possible risks with each of the substances in the protocol. These substances seem to be in the protocol for particular reason, but they may indeed have other effects that can cause serious symptoms and even serious risk if not thought about any comprehensive 360 degree fashion.
But your response raises the Million Dollar Question of @joshua.leisk’s Protocol, which he and I have discussed — whether the Protocol is appropriate when one has significant auto immunity. His view (and correct me if I am wrong Josh
), is that all autoimmunity can be cured through his approach because all autoimmunity is caused by latent viral cells (whether HHV-6, EBV etc) which cause the body to produce B cell antibodies. If you eliminate the latent viral cells (via the Protocol), the autoimmunity will also disappear as there are no more cells causing the body to produce rouge antibodies. Thus it’s appropriate (dare say necessary) to induce a heightened immune response to rid the body of latent viral cells and therefore any autoimmunity.
Ive discussed this at length with @Learner1 and (correct me if I am wrong love!
) and she does not agree that all autoimmunity is viral cell driven.
So the Million Dollar Question is — for those of us with significant autoimmunity, is the Protocol appropriate?
As a patient with multiple autoimmune conditions myself who has tried various treatments, including those for EBV and other herpes family viruses, I've done a fair amount of studying and there seem to be a number of things triggering and sustaining autoimmunity, so I'm a little doubtful that Epstein-Barr alone is the cause of all of our issues, so I do agree that it causes a lot of mischief, and can definitely trigger autoimmunity in many cases.
Here some discussions of things that drive autoimmunity, that one might want to ponder before blindly following only one interpretation of autoimmunity and possibly getting oneself into trouble.
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https://pubmed.ncbi.nlm.nih.gov/23493116/
"Coeliac disease, an inflammatory disease of the small intestine, shares key features with autoimmune disorders, such as susceptibility genes, presence of autoantibodies and T cell-mediated destruction of specific cells.
Strikingly, however, continuous exposure to the exogenous dietary antigen gluten and gluten-specific adaptive immunity are required to maintain immunopathology.
These observations challenge the notion that autoimmunity requires adaptive immune activation towards self antigens.
Using coeliac disease as an example, we propose that other exogenous factors might be identified as drivers of autoimmune processes, in particular when evidence for T cells with specificity for self antigens driving the disease is lacking."
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https://www.sciencedaily.com/releases/2019/12/191217114232.htm
"Previously it was thought that IL-1b production required activation of a group of immune system protein molecules that make up structures called the inflammasomes. It turns out the inflammasomes, which act as system sensors that activate inflammation, can cause what are called auto-inflammatory diseases. These are distinct from auto-immune diseases.
Pasare and his colleagues found out that instead of inflammasomes, a different molecular pathway cranks up inflammation during autoimmunity while working completely independent from inflammasomes. That molecular process was triggered by interactions between myeloid cells and CD4-positive T cells, which become primed to attack harmful bacteria, viruses and other microorganisms. Unfortunately, in the case of autoimmunity, the immune system attacks and eventually destroys healthy tissues erroneously targeted as harmful.
When it's not fulfilling its role in driving autoimmunity, IL-1b usually works as a stimulator of anti-microbial immunity. But during autoimmune processes, the authors report they discovered in their mouse models that autoreactive T cells, macrophage and dendritic cells in the immune system work through two other molecules -- TNF (tumor necrosis factor) and FasL (fas ligand) -- to produce overabundant amounts of IL-1b.
"This means our findings have two previously unknown implications," Pasare explained. "We show for the first time that IL-1b can be made in the absence of infection and that T cells are major drivers of IL-1b in an autoimmune setting."
The study also underscores that therapies targeting IL-1b production by inflammasomes are going to be limited in their effectiveness in treating autoimmune disease. This is because the Pasare team's findings show that auto-reactive T cells have their own mechanisms to drive inflammation and work independently of inflammasomes.
Pasare said that targeting the TNF and FasL pathway of IL-1b production is more likely to be an effective way of treating auto-immune diseases in humans."
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https://pubmed.ncbi.nlm.nih.gov/22432804/
"In SLE, CD4+T cells provide cognate help to self-reactive B cells, which in turn produce pathogenic auto-antibodies (1).
Thus, B cells act as effectors by producing auto-antibody aided by T cell help such that B and T cell interactions are unidirectional.
However, this paradigm of B and T cell interactions is challenged by new clinical data demonstrating that B cell depletion is effective for T cell mediated autoimmune diseases including type I diabetes mellitus (T1D) (2), rheumatoid arthritis (3), and multiple sclerosis (4).
These clinical data indicate a model whereby B cells can influence the developing autoimmune T cell response, and therefore act as effectors, in ways that extend beyond the production of autoantibody ."
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https://www.frontiersin.org/articles/10.3389/fimmu.2020.00760/full
"Historically, multiple sclerosis (MS) has been viewed as being primarily driven by T cells.
However, the effective use of anti-CD20 treatment now also reveals an important role for B cells in MS patients. The results from this treatment put forward T-cell activation rather than antibody production by B cells as a driving force behind MS.
The main question of how their interaction provokes both B and T cells to infiltrate the CNS and cause local pathology remains to be answered. In this review, we highlight key pathogenic events involving B and T cells that most likely contribute to the pathogenesis of MS.
These include
(1) peripheral escape of B cells from T cell-mediated control,
(2) interaction of pathogenic B and T cells in secondary lymph nodes, and
(3) reactivation of B and T cells accumulating in the CNS.
We will focus on the functional programs of CNS-infiltrating lymphocyte subsets in MS patients and discuss how these are defined by mechanisms such as antigen presentation, co-stimulation and cytokine production in the periphery.
Furthermore, the potential impact of genetic variants and viral triggers on candidate subsets will be debated in the context of MS."
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https://translational-medicine.biomedcentral.com/articles/10.1186/s12967-020-02289-w
"Transitional B cells (TrB cells) represent a crucial link between immature B cells in the bone marrow and mature peripheral B cells.
Although TrB cells represent one of the regulatory B cell subpopulations in healthy individuals, the frequency of CD24hiCD38hi TrB cells in circulation may be altered in individuals with autoimmune diseases, such as multiple sclerosis, neuromyelitisoptica spectrum disorders, systemic lupus erythematosus, Sjögren’s syndrome, rheumatoid arthritis, systemic sclerosis, and juvenile dermatomyositis.
Although TrB cells play regulatory roles under inflammatory conditions, consequences of their functional impairment vary across autoimmune diseases. Since the origin, development, and function of TrB cells, especially in humans, remain unclear and controversial, this review aimed to discuss the characteristics of TrB cells at steady state and explore their role in various immune diseases, including autoimmune rheumatic diseases and neuroimmunological diseases."
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https://www.ucsf.edu/news/2021/02/4...cancer-research-advance-treatments-autoimmune
"It’s kind of like asking how many different kinds of people there are – it depends on how you look at it,” said Krummel. “In terms of the way the immune system responds to cancer we see about a dozen archetypes and we expect to find a similar number for autoimmune disease.”
Identifying autoimmune archetypes will help the researchers understand the central operating mechanisms underlying autoimmune disease, potentially revealing hidden connections between seemingly unrelated illnesses.
Understanding these connections may help speed the development of new treatments and identify existing drugs that may have the potential to treat several different autoimmune disorders."
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This is a very interesting discussion of autoimmunity from a functional medicine perspective. Note that this doctor is expressing that there are a number of other genetic and environmental factors that can be driving autoimmunity, far beyond a herpes virus...
https://www.ifm.org/news-insights/a...iving-forces-inflamed-brain-taking-high-road/
