Archive for the ‘Inflammation’ Category

Alternative Treatments for Lyme Disease Symptoms Brings New Hope

http://  Approx. 3 Min

Alternative Treatments for Lyme Disease Symptoms Brings New Hope

Sept. 21, 2021

News Center Maine

The multi-step, laser therapy treatment targets the biofilm that surrounds the bacteria that causes Lyme disease.

Correction: 

The news segment falsely states that only 25% go on to suffer from lingering symptoms.  This article, reveals that they achieve that low number by only counting patients who are diagnosed and treated early.  There is a much larger patient group (30-40%) that due to being undiagnosed or misdiagnosed, that is diagnosed and treated much later (months to years).  When you simply add the two groups you discover that 60% of patients go on to suffer sometimes life-long symptoms. This is a big deal and needs to be corrected, but the CDC is constantly manipulating criteria and numbers for a pre-determined outcome that fits their accepted narrative.  And the accepted narrative for Lyme/MSIDS has always been and continues to be that it is hard to catch and easy to treat.

Some reasons these numbers matter:

  • using the faulty 25% downplays a real problem that is much larger in scope
  • research projects are typically done on issues involving the most people, so those suffering from persistent symptoms continue to be ignored in research
  • in order to qualify for entrance into research studies:
    • patients must test positive on the abysmally inaccurate 2-tiered CDC serology test that misses more than 70% of all cases and here 86%
    • patients must have the EM rash which is often missed or mischaracterized by physicians, can look different on patients, and which is often missing altogether in many
    • have a positive diagnosis which in a maddening never-ending loop is based on faulty testing 
Chronic Lyme patients are continually kicked to the curb due to faulty parameters that are regurgitated like a 3 year old reciting the alphabet with no understanding of it. 

I’ve posted on lasers before and we had a practitioner speak about them at support group. 

Please see:

Of course there are numerous types of lasers and the one presented in the news story is different then the class IV laser which I have had treatments with. Unlike the one presented in the news story, the class IV laser is very hot and must be moved continually or it would burn you.  The best way to describe the feeling is that it feels like your muscles have turned to butter.  I would compare it to a massage without the pain. It’s relaxing and quite effective against pain.  It does come with a price – when I had it done it was about $100 for about a 40 min. treatment.  I do highly recommend Raymond as he is not only trained with the laser but is a naturopath with great ideas. 

Until testing can distinguish between whether we are in active infectious state or just suffering from lingering symptoms that antimicrobials will not solve we are Guinea Pigs trying this and that for relief.

I’ve found the following things all help with pain:

Lastly, for me I had chronic headaches that felt like a horse kicked me in the head.  Seriously, I never knew that people could survive such unbelievable pain. Mostly at the brain stem (occipital area), the inflammation was so severe I eventually had a MRI to rule out Chiari.  I found that daily minocycline (a drug known to cross the blood/brain barrier) truly was one of the most effective things I used (I would put tinidazole in this category as well).  I do feel it’s important to layer treatment to mitigate any antibiotic resistance, so we always took 2-3 other antimicrobials simultaneously as well as pulsed diflucan to mitigate any yeast issues.

 

 

Category:

Inflammation, Lyme, Pain Management, Treatment

LDN Webinar

https://www.belmarpharmasolutions.com/resources/clinician-resources/clinician-library/the-ldn-book-volume-two/

**Please note this webinar occurred last year; however, they are making it available to all now.  Just go to the link, fill out info. and you will be directed to the Webinar that already took place.**

The LDN Book: Volume Two

October 12, 2020

By: Belmar Pharmacy

Belmar Pharmacy is presenting the launch of Author and Low Dose Naltrexone (LDN) Advocate, Linda Elsegood’s latest book, The LDN Book Volume 2.

Dr. Angela DeRosa, Belmar Pharma Solutions Medical Director and Tracy Crawford, Director of Customer Experience, speak with authors Linda Elsegood, Darin Ingels ND, FAAM, Olga Cortez MD, and Leonard Weinstock MD about their LDN expertise and their contributions to the book.

Also hear from, Samantha Lebsock, PharmD at Belmar Pharmacy – she will share her extensive knowledge of LDN from a compounding pharmacist perspective. 

This webinar is engaging for both practitioners and patients interested in learning more about LDN and how to get their hands on The LDN Book Volume 2 and all it has to offer.

Conversations contain some of the reasons practitioners prescribe LDN, including:

  • Autoimmune
  • Women’s Health
  • Lyme Disease
  • Thyroid
  • Chronic Skin Conditions
  • Gut Health

This webinar is intended for patients and prescribers. If you would like to watch the webinar, please fill out in the top link. You will be re-directed to the recording after the successful completion of the form.

For more on LDN:

Category:

Activism, Inflammation, Lyme, Supplements, Treatment

Vaccine-Induced Thrombocytopenia With Severe Headache – Why Lyme/MSIDS Patients Should Care

https://www.nejm.org/doi/full/10.1056/NEJMc2112974?

Vaccine-Induced Thrombocytopenia with Severe Headache

To the Editor:

Vaccine-induced immune thrombotic thrombocytopenia (VITT), a serious adverse event after vaccination with ChAdOx1 nCoV-19 (AstraZeneca) or Ad26.COV2.S (Johnson & Johnson–Janssen), is caused by platelet factor 4 (PF4)–dependent, platelet-activating antibodies.1-3 High-dose immune globulins and anticoagulation are the main treatments.4,5 In this report, we present evidence that vaccine-induced thrombocytopenia (VIT) without associated cerebral venous sinus thrombosis (CVST) or other thromboses and with severe headache as the heraldic symptom may precede VITT (“pre-VITT syndrome”).

Eleven patients presented with severe headache in the absence of CVST 5 to 18 days after ChAdOx1 nCoV-19 vaccination.

  • All the patients had thrombocytopenia (low platelets in the blood which can cause hemorrhaging)
  • high d-dimer levels (a test to detect blood clots – a high level indicates clot formation and breakdown in the body)
  • high levels of anti–PF4–heparin IgG antibodies
  • during follow-up, intracranial hemorrhage occurred in three patients (Patients 1, 2, and 3), with radiologic evidence of new CVST in Patients 2 and 3 (Figure 1, and Table S1 in the Supplementary Appendix, available with the full text of this letter at NEJM.org).
  • Only two patients (Patients 2 and 4) were initially admitted with conditions that met the criteria for VITT; both patients had pulmonary embolism, and additional splanchnic vein thrombosis was present in Patient 2.

In Patient 2, anticoagulation treatment had been initiated several days earlier for pulmonary embolism (without diagnosis of VITT) but was stopped after the onset of headache, shortly before CVST developed.

  • In two patients (Patients 1 and 3), peripheral thromboses were eventually identified during follow-up.

Thrombotic complications did not develop in seven of the patients (Patients 5 through 11); all but one of these patients received high-dose immune globulin, glucocorticoids, or therapeutic-dose anticoagulation within 5 days after headache onset. In contrast, in all four patients with subsequent thrombosis (Patients 1 through 4), therapeutic-dose anticoagulation either was not started until 6 to 9 days after headache onset or was stopped prematurely before the development of CVST.

Although the combination of thrombocytopenia and severe headache due to CVST has been recognized as the typical presentation of VITT,1,2 the experience with these 11 patients suggests that VIT with severe headache, elevated d-dimer levels, and strongly positive results on anti–PF4–heparin IgG enzyme-linked immunosorbent assay may precede VITT.

Our findings have immediate implications for clinical practice: in this pre-VITT syndrome, severe headache may not develop as a symptom secondary to CVST but instead may precede CVST by several days, potentially in association with microthrombosis in smaller cortical veins.

Consequently, patients who present with severe headache 5 to 20 days after adenovirus vector vaccination against coronavirus disease 2019 should undergo immediate testing for thrombocytopenia and d-dimer levels and, if available, testing for anti–PF4–heparin IgG antibodies.

When these antibodies are present at high titers, patients are at imminent risk for CVST, and it is likely that this condition can be prevented with immediate treatment, such as with intravenous immune globulin. The decision to initiate therapeutic-dose anticoagulation is a difficult one; the risk of emerging thrombosis, including CVST, has to be balanced against the risk of intracranial hemorrhage on an individual basis (e.g., with consideration of platelet count and fibrinogen levels).

Farid Salih, M.D.
Charité-Universitätsmedizin Berlin, Berlin, Germany

Linda Schönborn, M.D.
Universitätsmedizin Greifswald, Greifswald, Germany

Siegfried Kohler, M.D., Christiana Franke, M.D., Martin Möckel, M.D., Thomas Dörner, M.D., Hans C. Bauknecht, M.D., Christian Pille, M.D., Jan A. Graw, M.D.
Charité-Universitätsmedizin Berlin, Berlin, Germany

Angelika Alonso, M.D.
University Hospital of Mannheim, Mannheim, Germany

Johann Pelz, M.D.
University Hospital of Leipzig, Leipzig, Germany

Hauke Schneider, M.D., Antonios Bayas, M.D., Monika Christ, M.D.
University Hospital of Augsburg, Augsburg, Germany

Joji B. Kuramatsu, M.D.
University Hospital of Erlangen, Erlangen, Germany

Thomas Thiele, M.D., Andreas Greinacher, M.D.
Universitätsmedizin Greifswald, Greifswald, Germany

Matthias Endres, M.D.
Charité-Universitätsmedizin Berlin, Berlin, Germany

Supported by Deutsche Forschungsgemeinschaft project number 374031971–TRR 240 (to Prof. Greinacher) and EXC-2049–390688087 NeuroCure under the German Excellence Strategy (to Prof. Endres) and by the Domagk-Programm of the Universitätsmedizin Greifswald (to Dr. Schönborn).

Disclosure forms provided by the authors are available with the full text of this letter at NEJM.org.

This letter was published on September 15, 2021, at NEJM.org.

Profs. Greinacher and Endres contributed equally to this letter.

___________________

**Comment**

Both Thrombocytopenia and severe headaches are common with Lyme/MSIDS patients.

Therapy for thrombocytopenia requires treatment or removal of the underlying infection, in addition to maintenance of platelet counts and hemostatic function.

Hopefully it’s clear that a Lyme/MSIDS patient getting a COVID shot could be diagnosed with thrombocytopenia that either already exists or worsens after the injection.  Treating the underlying infection is imperative but won’t be considered by mainstream medicine.

For more:

Go here for the latest VAERS data and the mounting list of adverse reactions and deaths.

Category:

Heart Issues, Inflammation, research, vaccines

Cellular Blueprint of MS Lesions

https://www.nih.gov/news-events/news-releases/nih-scientists-build-cellular-blueprint-multiple-sclerosis-lesions

Friday, September 10, 2021

NIH scientists build a cellular blueprint of multiple sclerosis lesions

Study lays the groundwork for potential new therapies for progressive multiple sclerosis.
An MRI scan of a human brain with multiple sclerosis Mapping multiple sclerosis lesions. Researchers used single-cell RNA sequencing to map the cells found at the edges of chronic MS lesions.Reich lab, NIH/NINDS.

Chronic lesions with inflamed rims, or “smoldering” plaques, in the brains of people with multiple sclerosis (MS) have been linked to more aggressive and disabling forms of the disease. Using brain tissue from humans, researchers at the National Institutes of Health’s National Institute of Neurological Disorders and Stroke (NINDS) built a detailed cellular map of chronic MS lesions, identifying genes that play a critical role in lesion repair and revealing potential new therapeutic targets for progressive MS. The study was published in Nature.

“We identified a set of cells that appear to be driving some of the chronic inflammation seen in progressive MS,” said Daniel Reich, M.D., Ph.D., senior investigator at NINDS. “These results give us a way to test new therapies that might speed up the brain’s healing process and prevent brain damage that occurs over time.”

Chronic active lesions are characterized by a slow, expanding rim of immune cells called microglia. Microglia normally help protect the brain, but in MS and other neurodegenerative diseases, they can become overactive and secrete toxic molecules that damage nerve cells. Other cells found at the edge of the lesions, such as astrocytes and lymphocytes, may also contribute to ongoing tissue damage. Prior studies suggest that microglia are the main culprits behind lesion expansion, but the exact types of cells found near lesions and their biological mechanisms are elusive.

To better understand MS lesions, Dr. Reich and his colleagues used single-cell RNA sequencing, a powerful technique which enables researchers to catalog gene activity patterns in individual cells, to examine post-mortem brain tissue of five MS patients and three healthy controls. Samples were provided by the Netherlands Brain Bank, Netherlands Institute for Neuroscience, Amsterdam, the Netherlands, and the NINDS Neuroimmunology Clinic.

“Single-cell RNA sequencing technology allows us to do a much deeper dive into the types of cells present in MS lesions,” said Dr. Reich.

By analyzing the gene activity profiles of over 66,000 cells from human brain tissue, researchers created the first comprehensive map of cell types involved in chronic lesions, as well as their gene expression patterns and interactions.

Dr. Reich’s team found a great diversity of cell types in the tissue surrounding chronic active lesions compared to normal tissue, and a high proportion of immune cells and astrocytes at the active edges of those lesions. Microglia comprised 25% of all immune cells present at the lesion edges.

“Our dataset is very rich. The beauty of having such a detailed map is that now we have a better understanding of the entire network of cells involved in smoldering inflammation,” said Martina Absinta, M.D., Ph.D., a former post-doctoral fellow in Dr. Reich’s lab and current adjunct assistant professor at Johns Hopkins University, Baltimore, who led the study.

More detailed analyses revealed that the gene for complement component 1q (C1q), an important and evolutionarily ancient protein of the immune system, was expressed mainly by a subgroup of microglia responsible for driving inflammation, suggesting that it may contribute to lesion progression.

To determine the function of C1q, researchers knocked out the gene in the microglia of mouse models of MS and examined the brain tissue for signs of neuroinflammation. In mice lacking microglial C1q, they found significantly decreased tissue inflammation compared to control animals. Additionally, in another group of animals, blocking C1q reduced iron-containing microglia, revealing a potential new therapeutic avenue to treat chronic brain inflammation in MS and related neurodegenerative diseases.

According to the authors, it’s possible that targeting C1q in human microglia could halt MS lesions in their tracks.

In MS, the immune system attacks myelin, a protective layer that forms around nerve cells in the brain and spinal cord, leading to vision loss, muscle weakness, problems with balance and coordination, fatigue, numbness, and other debilitating symptoms. A subset of people develop progressive MS, resulting in extensive brain tissue damage and disability. Anti-inflammatory medications help patients manage their symptoms by dampening the responses of immune cells in the blood and lymph nodes. But treatments are not as effective for patients with chronic lesions who experience ongoing brain tissue inflammation.

“We have terrific therapies that block new inflammation but nothing to stop the inflammation that’s already there,” said Dr. Reich. “In order to make strides in developing new therapies for progressive MS, we’re going to need to pick apart the cellular and molecular mechanisms one by one.”

In 2019, Dr. Reich and his team reported that damaging, chronic active lesions may be a hallmark of progressive MS. The current study identifies microglia and C1q as promising targets for progressive MS and supports the use of chronically inflamed rim lesions as an MRI biomarker for disease progression.

There is no cure for MS, and no therapies that directly treat chronic active lesions. By gaining a deeper understanding of lesion features, this study may help pave the way toward early clinical trials to test new therapies for this aspect of the disease.

This study was supported in part by the Intramural Research Program at the NINDS.

NINDS is the nation’s leading funder of research on the brain and nervous system. The mission of NINDS is to seek fundamental knowledge about the brain and nervous system and to use that knowledge to reduce the burden of neurological disease.

About the National Institutes of Health (NIH): NIH, the nation’s medical research agency, includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. NIH is the primary federal agency conducting and supporting basic, clinical, and translational medical research, and is investigating the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit www.nih.gov.

NIH…Turning Discovery Into Health®

Article

Absinta et al. A lymphocyte-microglia-astrocyte axis in chronic active multiple sclerosis. Nature, September 8, 2021 DOI: 10.1038/s41586-021-03892-7(link is external)

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For more:

Category:

Inflammation, Lyme, research

Myocarditis After COVID-19 mRNA Shots But Just Mask Up & Shut Up

https://www.nejm.org/doi/full/10.1056/NEJMc2109975?

Myocarditis after Covid-19 mRNA Vaccination

This letter was published on August 18, 2021, at NEJM.org.

TO THE EDITOR:

The Centers for Disease Control and Prevention recently reported cases of myocarditis and pericarditis in the United States after coronavirus disease 2019 (Covid-19) messenger RNA (mRNA) vaccination.1 In recently published reports, diagnosis of myocarditis was made with the use of noninvasive imaging and routine laboratory testing.2-5 Here, we report two cases of histologically confirmed myocarditis after Covid-19 mRNA vaccination.

Figure 1. Histopathological Findings from Endomyocardial Biopsy and Autopsy.

Patient 1, a 45-year-old woman without a viral prodrome, presented with dyspnea and dizziness 10 days after BNT162b2 vaccination (first dose). A nasopharyngeal viral panel was negative for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), influenza A and B, enteroviruses, and adenovirus (Table S1 in the Supplementary Appendix, available with the full text of this letter at NEJM.org). A serum polymerase-chain-reaction (PCR) assay and serologic tests showed no evidence of active parvovirus, enterovirus, human immunodeficiency virus, or infection with SARS-CoV-2. At presentation, she had tachycardia; ST-segment depression detected on electrocardiography, which was most prominent in the lateral leads (Fig. S1); and a troponin I level of 6.14 ng per milliliter (reference range, 0 to 0.30). A transthoracic echocardiogram showed severe global left ventricular systolic dysfunction (ejection fraction, 15 to 20%) and normal left ventricular dimensions. Right heart catheterization revealed elevated right- and left-sided filling pressures and a cardiac index of 1.66 liters per minute per square meter of body-surface area as measured by the Fick method. Coronary angiography revealed no obstructive coronary artery disease. An endomyocardial biopsy specimen showed an inflammatory infiltrate predominantly composed of T-cells and macrophages, admixed with eosinophils, B cells, and plasma cells (Figure 1A and Figs. S2 through S4). She received inotropic support, intravenous diuretics, methylprednisolone (1 g daily for 3 days), and, eventually, guideline-directed medical therapy for heart failure (lisinopril, spironolactone, and metoprolol succinate). Seven days after presentation, her ejection fraction was 60%, and she was discharged home.

Patient 2, a 42-year-old man, presented with dyspnea and chest pain 2 weeks after mRNA-1273 vaccination (second dose). He did not report a viral prodrome, and a PCR test was negative for SARS-CoV-2 (Table S1). He had tachycardia and a fever, and his electrocardiogram showed diffuse ST-segment elevation (Fig. S1). A transthoracic echocardiogram showed global biventricular dysfunction (ejection fraction, 15%), normal ventricular dimensions, and left ventricular hypertrophy. Coronary angiography revealed no coronary artery disease. Cardiogenic shock developed in the patient, and he died 3 days after presentation. An autopsy revealed biventricular myocarditis (Figure 1B and Figs. S5 and S6). An inflammatory infiltrate admixed with macrophages, T-cells, eosinophils, and B cells was observed, a finding similar to that in Patient 1.

In these two adult cases of histologically confirmed, fulminant myocarditis that had developed within 2 weeks after Covid-19 vaccination, a direct causal relationship cannot be definitively established because we did not perform testing for viral genomes or autoantibodies in the tissue specimens. However, no other causes were identified by PCR assay or serologic examination.

Amanda K. Verma, M.D.
Kory J. Lavine, M.D., Ph.D.
Chieh-Yu Lin, M.D., Ph.D.
Washington University School of Medicine, St. Louis, MO

________________________

https://www.brighteon.com/b3d87a5a-faea-4341-bab6-0406b9d356f5  4 Min. Video Here

The HighWire with Del Bigtree
Published Aug. 16, 2021

‘MASK UP AND SHUT UP’

Entering the ridiculous, public health officials are now asking people not to talk to stop the Covid virus. Jefferey Jaxen dives into the science behind the latest Covid mitigation suggestion.

__________________

**Comment**

The video is revealing on many fronts:

  • Propaganda is alive and well.
  • The paper “Viral Load of SARS-CoV-2 in Respiratory Aerosols Emitted By COVID-19 Patients While Breathing, Talking, and Singing,” has numerous disclaimers in fine print, namely, that they couldn’t mechanically retrieve and isolate a viable virus from ambient air in the vicinity of patients.  Well, that’s inconvenient.
  • This study demonstrates perfectly the hypocrisy of our corrupt public health ‘authorities’ in that they demand perfectly done randomized, controlled trials on thousands of patients to approve COVID treatments, completely ignoring clinical results, but will accept and propagate poorly done science that pushes their continued fear narrative that lines their pockets. And even when there properly done RCTs they ignore them and then go on a smear campaign to malign them, and implement bandwagon to make the public believe their accepted narrative.
  • This duplicity has been going on in Lyme-land for over 40 years and continues today.  Hopefully people are waking up to it.

**Comment**

VAERS data released on 8/6/21 found 3,644 reported cases of Myocarditis or Pericarditis after COVID shots.

For more:

Category:

Heart Issues, Inflammation, research, Viruses