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Myositis facilitates preclinical accumulation of pathological prion protein in muscle
... Our findings provide new insights into the pathophysiology of PrPSc pointing out that myositis leads to enhanced prion colonization of muscle in subclinical prion disease.
Dr. Oz: Fibromyalgia is a diagnosis based on a grouping of symptoms including fatigue and muscle pain. While the pain and inflammation are very real, this conventional medical diagnosis itself doesn’t help us understand what causes the problem.
Subclinical (silent, systemic, low-grade) inflammation is a form of chronic inflammation (and chances are you’re suffering with it now)
Researchers now recognize that chronic inflammation may be present in a low grade, asymptomatic form for many years before its effects manifest as overt disease. This asymptomatic form of chronic inflammation is often referred to as subclinical inflammation (also silent inflammation, subacute inflammation, low grade inflammation, or systemic inflammation.) Subclinical inflammation can only be detected by laboratory tests or biochemical assays that assess levels of various markers of inflammation such as c-reactive protein, rheumatoid factor, anti-nuclear antibodies, cytokines, or other components, modulators or products of inflammation.
Subclinical inflammation is increasingly recognized as the cause of, or a substantial contributor to, a wide range of ailments, such as for example atherosclerosis, osteoarthritis, hypercholesterolemia, diabetes type 2, Alzheimer’s disease, some cancers, macular degeneration and a great many other ailments. Subclinical inflammation has been shown to increase disease risk, hasten disease onset and worsen disease prognosis. Subclinical inflammation is believed to increase the rate and severity with which signs and symptoms of aging appear.
Specifics vary from diet to diet, but in general anti-inflammatory diets suggest:
Eat plenty of fruits and vegetables.
Minimize saturated and trans fats.
Eat a good source of omega-3 fatty acids, such as fish or fish oil supplements and walnuts.
Watch your intake of refined carbohydrates such as pasta and white rice.
Eat plenty of whole grains such as brown rice and bulgur wheat.
Eat lean protein sources such as chicken; cut back on red meat and full-fat dairy foods.
Avoid refined foods and processed foods.
Spice it up. Ginger, curry, and other spices can have an anti-inflammatory effect.
10. Central Nervous System Inflammation and Prion Disease Pathogenesis
The study of inflammation in the prion diseases is relatively new. Indeed, for a number of years the accepted dogma was that the prion diseases lacked an inflammatory response in the brain (1–3). This persists in spite of a number of studies showing that the pathological hallmarks of the prion diseases (PrPSc deposition, astrocytosis, vacuolation, and neuronal loss) are associated with the presence of activated microglia (4–7). At the heart of this discrepancy is a simple matter of what is meant by inflammation. The innate inflammatory response is the tissue’s response to injury or infection, and, as so succinctly put by Metchnikoff in the late ninetenth century, “The essential and primary element in typical inflammation consists in a reaction of the phagocytes against a harmful agent” (8). Given that the microglia are the brain’s resident macrophages (i.e., phagocytic cells), we believe that the presence of activated microglia in prion-affected brains represents an inflammatory response (9–11).
Affiliation(s): (1) CNS Inflammation Group, School of Biological Sciences, University of Southampton, Southampton, UK
Book Title: Molecular Pathology of the Prions
Brain Inflammation Likely Key Initiator to Prion and Parkinson's Disease
…researchers of the Computational Biology group at the Luxembourg Centre for Systems Biomedicine showed that neuro-inflammation plays a crucial role in initiating prion disease.
Prion diseases represent a family of neurodegenerative disorders associated with the loss of brain cells and caused by proteins called prions (derived from ‘protein’ and ‘infection’). The diseases are found in both humans and animals, such as Creutzfeld-Jakob disease and mad cow disease respectively. Although mostly harmless, prions can transform into infectious agents, which accumulate in the brain and destroy the nervous tissue.
But how exactly does the accumulation of prions cause destruction of the brain? “Understanding the process by which prions destroy neurons is critical for finding a cure for prion disease”, says Isaac Crespo, first author of the publication. He and his colleagues tackled this question with a computational approach: They ran their own computer programmes on experimental data generated by other research groups, and identified a set of 16 proteins that seems to control the onset of the disease. Interestingly, almost all of these proteins have known functions in neuro-inflammation.
SFN is associated with a wide variety of diseases and disorders including diabetes, thyroid issues, sarcoidosis, vitamin B12 deficiency, HIV, neurotoxic medications (including chemotherapy and antiretroviral agents), celiac disease, Sjogren’s Syndrome, Lupus. With all these disorders, about 50% of SFN diagnoses are ‘idiopathic’; i.e., no discernible cause is found.
...doctors working for the insurance industry that have claimed fibro was a psychiatric disorder so that the insurance industry had to pay a lot less for treating these people.
On the Road to Dementia: Inflammation, Prions, Myositis and Fibromyalgia
Great thread - hope it helps a lot of folks. For those suffering, I also recommend exploring alternative treatments and healing if you are open to it. They saved my life.
After a life of 90 years of incredible health during most every phase of her life, the end was just wrong... and I feel guilty to this day still that I could do nothing.
I hope than none of you EVER have to travel this path.
In most cases doctors are doing blood test to DX fibro
reply to post by ANNED
For the OP:
Do you think there is a prion connection to Rheumatoid Arthritis (or any other form of autoimmune, inflammatory arthritis or spondyloarthropathy)? It has a reasonably high co-morbidity with Fibro, as many autoimmune diseases do, so I'm curious. I've rarely spoken to anyone with RA, that didn't also say they had FMS (or CFS on occasion).
2000: HLA-B27 misfolding: a solution to the spondyloarthropathy conundrum?
Compelling evidence indicates that HLA-B27 is directly involved in the etiopathogenesis of the spondyloarthropathies (SpAs). ...Recent work demonstrating that HLA-B27 misfolds offers a novel alternative hypothesis. Here, we review this new information on the folding and assembly of HLA-B27, and discuss consequences of misfolding that could be relevant to the pathogenesis of SpAs.
PRION 2009: HLA-B27 misfolding and spondyloarthropathies
...In this chapter we will review what has been learned about HLA-B27 misfolding in human cells and in the transgenic rat model of spondyloarthritis-like disease, considering it in the context of other protein misfolding disorders. ...
...Preliminary data indicating that HLA-B27 misfolding may be a stimulus for activating the IL-23/IL-17 axis, suggests a novel mechanism that may explain, at least in part, the role of HLA-B27 in colitis in transgenic rats. The striking convergence of the human genetic data and results from HLA-B27 transgenic rats provides a compelling argument that this axis needs to be further examined in SpA and AS.
A genetic disease does not have to manifest and the disease should be able to revert if the reason for the disease is eliminated. Many of these diseases are caused by eating food we should not be eating for our genetics.
A genetic disease does not have to manifest and the disease should be able to revert if the reason for the disease is eliminated.
I believe the "genetics" excuse is simply to try and convince people that there is nothing they can do to prevent the disease, so they should accept it as "normal" and ...