Sound Money Advocat. Following markets since 1989. GOLD/SILVERbug.
Hamburg, Germany
Joined February 2021
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Alles, was ich in 2 1/2 Jahren Recherchen herausgefunden habe, hier verlinkt. Mit über 2.000 Quellen.
facebook.com/100000447156810…
Das war es für mich fürs Erste.
PS: in der aufkommenden Erkenntniswelle ein Job, den ich auf keinen Fall haben möchte: des verlogenen Faktencheckers
Dirk Gerhardt aka SilverSit retweeted
3. Going Back to an Old Thread
I recently re-read a fascinating thread by @ydeigin from 2023 on the missing N370 glycan and the shared GCA codon.
teapawt.org/ydeigin/status/1694846…
It stuck with me. So, I decided to dig properly into the full glycan shield story of SARS-CoV-2.
1/
Besides the furin cleavage site (FCS), SARS2 has another unique feature mentioned in DEFUSE not yet seen in any natural SARS-like viruses – an ablated N-linked glycan at position N370. This glycan was ablated via a T372A amino acid mutation that came about via a double nucleotide mutation of the original ACT codon into GCA (the latter, incidentally, is the same codon as the one coding for alanine – out of 4 possible alanine codons – in the PRRA insertion which has created an FCS in SARS2).
Importantly, the T327A mutation greatly increases SARS2 infectivity in human lung cells but, just like an FCS, this kind of a mutation seems to have selective pressure AGAINST it in ancestral bat viruses.
DEFUSE’s interest in N-linked glycans stems from a very curious observation about SARS1 whose bat progenitor seems to have temporarily lost two of its N-linked glycans in civet SARS1 progenitors before re-acquiring them, and this led virologists to hypothesize that those glycans could be relevant for host switching. This is described in DEFUSE in a somewhat convoluted way:
“N-linked glycosylation: Some glycosylation events regulate SARS-CoV particle binding DC-SIGN/L-SIGN, alternative receptors for SARS-CoV entry into macrophages or monocytes [76,77]. Mutations that introduced two new N-linked glycosylation sites may have been involved in the emergence of human SARS-CoV from civet and raccoon dogs [77]. While the sites are absent from civet and raccoon dog strains and clade 2 SARSr-CoV, they are present in WIV1, WIV16 and SHC014, supporting a potential role for these sites in host jumping. To evaluate this, we will sequentially introduce clade 2 disrupting residues of SARS-CoV and SHC014 and evaluate virus growth in Vero cells, nonpermissive cells ectopically expressing DC-SIGN, and in human monocytes and macrophages anticipating reduced virus growth efficiency. We will introduce the clade I mutations that result in N-linked glycosylation in rs4237 RBD deletion repaired strains, evaluating virus growth efficiency in HAE, Vero cells, or nonpermissive cells +/- ectopic DC-SIGN expression [77]. In vivo, we will evaluate pathogenesis in transgenic hACE2 mice.”
The [77] paper cited in DEFUSE is a 2007 work by Han et al. titled “Specific Asparagine-Linked Glycosylation Sites Are Critical for DC-SIGN- and L-SIGN-Mediated Severe Acute Respiratory Syndrome Coronavirus Entry”. It looked at the 5 civet progenitor strains of SARS1 and showed that initially those strains did not have glycans around positions N227 and N699 but then eventually acquired them in civet progenitors and kept in human SARS1.
ncbi.nlm.nih.gov/pmc/article…
Dirk Gerhardt aka SilverSit retweeted
Here is a review of the safety issues regarding the mRNA products.
They are legion.
Press release:
ceres-science.com/post/scien…
Academic paper:
onlinelibrary.wiley.com/doi/…
Dirk Gerhardt aka SilverSit retweeted
SV40 reveal: before, during, after lawsuit
Info Commissioner ordered disclosure of Health Canada’s review into Pfizer shot DNA contamination, but HC only partially complied. An application in Federal Court forced HC to unredact the rest the day before their affidavit was due.
Dirk Gerhardt aka SilverSit retweeted
#LongCOVID & #Hypermobility: Could the Body’s Structural Scaffold Hold the Clue?
➡️ A new hypothesis proposes that changes in the **extracellular matrix (ECM)—the body’s structural support network—**may help connect LongCOVID with hypermobility disorders, mast-cell activation, small-fiber neuropathy and chronic fatigue. 1/
Dirk Gerhardt aka SilverSit retweeted
Security expert Gavin de Becker was right…. look at what actually happens (or doesn’t) to uncover motives.
Perhaps nothing has been done about Covid and millions of children are still getting mRNA shots because MAHA doesn’t want it to happen.
Dirk Gerhardt aka SilverSit retweeted
My origin story of how I went from a “trust the science” RN to telling people to use alternative & natural medicine whenever possible.
Before March 2020, I had never once seen a patient get intubated just because their oxygen number looked bad. We treated the person in front of us - if they were walking, talking, and not in distress, we didn’t sedate them and shove a tube down their throat to breathe for them.
Numbers were one piece of the picture, not the whole thing.
Then COVID hit and everything flipped overnight.
Suddenly we were intubating people who walked into the ER on their own, could hold a conversation, and weren’t gasping for air. The doctors said their low sats meant they were about to crash. It went against everything I’d been taught- treat the patient, not the numbers.
Visitors weren’t allowed, so we let them FaceTime their families right before we did it. I looked them in the eyes and told them it was temporary- we’d wake them in a few days and they’d be home in no time.
Right after the tube went in, we started Remdesivir.
For the first couple days it felt like we were doing something heroic.
Then the patients started dying. Multi-organ failure. The same people I’d joked with and reassured hours or days earlier were gone. I kept thinking, “How is this virus killing relatively young, healthy people this fast even with the best treatment we have?”
By day six I noticed something that made my stomach drop: the COVID patients who refused intubation, including elderly ones with a list of comorbidities, were doing fine. Not one of them died.
I started pointing it out to every doctor and nurse I worked with. They looked at me like I was crazy.
By day nine the picture got worse. Patients who refused the tube but still got Remdesivir were dying at roughly 50%. The explanation I kept hearing was “only the sickest get the drug.”
But that didn’t match what I was watching, what I was trained to see.
By day ten I was not so quietly telling every person I knew: if you end up in the hospital with COVID, do not consent to intubation or Remdesivir. Do not allow them to do that to your loved ones.
My ER kept doing both anyway. Even after the pattern was obvious to anyone who was actually in the rooms.
Later I found out hospitals were getting paid extra for COVID patients who were intubated, more if they got Remdesivir, and still more for every day spent in an ICU bed. Once you see the incentives, the refusal to change course stops looking like pure science.
I still can’t fully wrap my head around how fast the rules changed and how hard it was to get anyone to look at the actual results in front of us. I went from “trust the experts” to “watch what happens to the patients and decide for yourself.”
If you were on the front lines and saw something different, say so. If you weren’t, this is why a lot of us stopped automatically trusting the system and have dropped out of it.
I’m the villain and the hero of my own story and it’s hard to reconcile with either.
Dirk Gerhardt aka SilverSit retweeted
📢 Hey you guuuuuuuys!!!!!!
There is a silly misconception that "Long COVID" is just a narrow set of symptoms and somehow separate from all the other chronic-infection health crises popping up across society.
👽I am sure this stems from the "12 symptoms psyop" from 2023.
🤥 That distinction is completely false.
☂️☔LC is the entire umbrella of multi-system biological damage driven by a systemic, tissue-invasive, microvascular virus. It's not just the example of bedbound fatigued patients!
🔥The fallout isn't separate. It is the exact same chronic-viral fire impacting every major body system:
🫀 Cardiovascular: Myocarditis, pericarditis, microvascular endotheliitis, arrhythmias, early heart attacks, and strokes.
🫁 Respiratory: Pulmonary fibrosis, chronic dyspnea, microvascular gas-exchange defects, reactive airway disease, pulmonary nodules, nerve damage, asthma, COPD, and lung collapse.
🧠 Neurological & Cognitive: Neuroinflammation, small fiber neuropathy, autonomic failure, cognitive impairment, and neurodegenerative acceleration—including ALS, Alzheimer’s, Parkinson’s, MS-like demyelination, intracranial pressure (pseudotumor cerebri), seizures, strokes, TIAs, and brain tumors.
🩸 Hematologic & Vascular: Hypercoagulability, microclots, DIC, large vessel thromboembolism (PE, DVT), vasculitis, platelet hyperreactivity, micro-vessel swelling, and capillary loop ectasia.
⚡ Immunological & Mast Cell: Mast Cell Activation Syndrome (MCAS), autoantibody production, and viral/latent pathogen reactivation (EBV, CMV, Varicella, HHV-6, Hepatitis C).
🧬 Oncological: Impaired immune surveillance, accelerated cancer progression, and oncogenesis across multiple organ systems.
🦠 Gastrointestinal & Hepatic: Submucosal tissue damage, persistent gut viral reservoirs, severe dysbiosis, liver strain, Non-Specific Chronic Active Gastritis/Duodenitis/Ileitis, Eosinophilic Gastroenteritis (EGE), Eosinophilic Esophagitis (EoE), Leaky Gut (intestinal permeability), IBD mimics (Crohn’s/Ulcerative Colitis), polyps, and GI cancers.
🫘 Renal & Urinary: Accelerated decline in kidney function, interstitial cystitis, and neurogenic bladder/spasms.
🩸 Endocrine & Metabolic: New-onset Type 1 and Type 2 diabetes, thyroiditis, adrenal dysfunction, and systemic metabolic crash.
🦴 Musculoskeletal & Rheumatic: Severe myalgia, coat-hanger neck pain, tendon damage and spontaneous tears, diffuse fibrosis, Lupus and Connective Tissue Disease mimics, Rheumatoid and Reactive Arthritis, joint instability and dislocations (hEDS-like), costochondritis, Craniocervical Instability (CCI), and metabolic muscle collapse (ME/CFS).
👁️ Sensory & Integumentary: Tinnitus, sensorineural hearing loss, vestibular dysfunction, oscillopsia, retinal microvasculopathy, Keratoconjunctivitis Sicca (severe dry eye), parosmia, phantosmia, persistent anosmia, small fiber nerve pain, acral microvascular lesions ("COVID toes"), Livedo Reticularis and Livedo Racemosa, petechiae, purpura, capillary fragility, chronic urticaria, angioedema, dermatographism, and diffuse alopecia (telogen effluvium/alopecia areata).
⚕️ Reproductive & Hormonal: Menstrual cycle disruption, severe hormonal dysregulation, vascular Erectile Dysfunction (ED), Endometriosis exacerbation, Pelvic Congestion Syndrome mimics, Premature Ovarian Insufficiency (POI), Anovulation, Vulvodynia, Focal Vestibulodynia, Chronic Non-Bacterial Orchitis/Epididymitis, Primary Hypogonadism (testicular failure), Chronic Pelvic Pain Syndrome (CPPS), and Prostatitis mimics.
Nurses Thoughts of the Morning 🧑⚕️🩺
🤔 Conflating primary autoimmunity with immune-complex pathology and antigen-driven targeting is one of the most destructive diagnostic failures in chronic-viral immunology.
🗂️Siloing heart attacks, diabetes, cancer, arthritis, or kidney failure into isolated, unrelated diagnoses allows medicine and society to minimize what is actually happening. This is not going to get us proper tests and treatment for the pathology driving the onset of these outcomes.
‼️Treating the outcome will not stop these from occuring.
☢️It is all the exact same chronic viral fallout.
#LongCovid #CovidFallout #Microvascular #MultiSystem #ChronicViral #ItsChronicYo
🛑 Stop living in denial because you think this list is short. The trainwreck of this chronic virus is vastly bigger than people are willing to admit.
Universal 8
Das Omikron-Paradoxon:
Wenn Spike körpereigene Proteine zu Amyloid werden lässt
facebook.com/share/p/1SFSboS…
Danke an Joachim Gerlach, @Mitos_und_mehr und @AnneliseBocquet
Dirk Gerhardt aka SilverSit retweeted
University of Helsinki researchers studied 218 people and found elevated oral inflammatory proteins MMP-8, MMP-9, and TIMP-1 in Long COVID.
Findings suggest persistent inflammation and altered tissue breakdown, detectable through a simple mouth rinse.
ijidonline.com/article/S1201…
Dirk Gerhardt aka SilverSit retweeted
React19 has above 40.000 members by now. The old saying was for every one organized there are 50 to 100 who are not. Go figure @React19org
Dirk Gerhardt aka SilverSit retweeted
An meine Mörder ☠️❗️
Ein Bild zeigt mehr als tausend Worte: Die schweren Folgen meiner Gefäßschädigung
Heute hatte ich erneut eine kapillarmikroskopische Untersuchung. Das Bild zeigt das erschreckende Ergebnis meiner kleinsten Blutgefäße: massive, dauerhafte Schäden.
Nach 5,5 Jahren wird hier noch einmal schonungslos sichtbar, womit ich täglich lebe – schwere Durchblutungsstörungen, Dauerfeuer an Schmerzen und zerstörte Gefäßstrukturen. Genau diese extremen Gefäßschäden waren damals, rund sechs Wochen nach der Impfung, auch der Grund für meine Darmamputation.
Das Foto macht unmissverständlich deutlich, wie tiefgreifend diese Folgen bis heute in meinem Körper nachwirken.
Quelle zum linken gesunden Bild 👇
share.google/jMEYgRaQBaOFj6y…
An meine zukünftigen Mörder die an der Goldgrube 12 in Mainz sitzen.
Ihr seid Mörder ☠️ und dafür bekommt ihr meine tiefste Verachtung
Impfgeschädigte durch Biontech Pfizer Charge EX8679 – at Düsseldorf, Germany
Dirk Gerhardt aka SilverSit retweeted
That’s a possibility.
A virus triggers auto-antibodies by three mechanisms:
1) Anti-idiotype network
2) molecular mimicry (similar motifs)
3) tissue damage and release of self antigen
Autoantibodies against GPCR may be raised by anti-idiotype mechanism. The word “idiotype” refers to the antigen-binding part of an antibody. The viral spike protein elicits primary antibodies (Ab1), and if the level of Ab1 is too high, the body also produces secondary antibodies (Ab2) attacking the primary antibodies at the idiotype site. Ab1 is complementary to epitope on the spike protein, while Ab1 is also complementary to Ab2. Therefore, Ab2 may mimic the spike protein in shape, and Ab2 may behave like the spike protein to interact with human receptors.
“Collins et al. [108] showed that sequential SARS-CoV-2 mRNA vaccination of hACE2 transgenic mice can induce both anti-S and anti-ACE2 antibody responses, and the latter was gradually amplified with each boost.” The spike protein raises antibodies against both the spike protein and the ACE2 receptor. Given that SARS-CoV-2 spike RBD binds β-adrenergic receptors with high affinity, the spike protein probably elicits autoantibodies against β-adrenergic receptors by anti-idiotype mechanism.
In addition, some of the spike motifs mimic human proteins in the blood coagulation pathway, thus inducing production of pro-thrombotic autoantibodies. For example, TQLPP motif on spike mimics thrombopoietin and may induce thrombocytopenia. ELDKY motif on spike mimics protein kinase G1 (involved in platelet activation).
Spike RBD may share some degree of similarity with angiotensin II, since both function as ligands for ACE2 receptor. Antibody targeting spike RBD may cross-interact with angiotensin II, leading to undesired vascular pathology such as hypertension.
Some parts of spike protein mimic ACE2. “Segments of the SARS-CoV-2 S protein (residues 49–53, 226–230, 418–428, 529–536, 744–774, and 977–980) share structural and chemical similarities with some segments of the ACE2 receptor (residues 137–141, 335–345, 350–352, 463–471, and 545–573).”
ACE2 converts angiotensin II (DRVYIHPF) into angiotensin (1-7) (DRVYIHP). A G-protein-coupled receptor MAS1 binds angiotensin (1-7) to mediate vasodilation. Because the two receptors use very similar ligands, the ligand-binding sites on these receptors are also similar. Anti-ACE2 antibody may cross-react with MAS1.
Reference:
Bellavite P, Di Fede G, Mantovani M, Zanolin E. Autoimmune Features of Post-COVID-19 Vaccination Syndrome and Their Impacts on the Renin-Angiotensin System. Vaccines (Basel). 2026 Apr 16;14(4):354. doi: 10.3390/vaccines14040354. PMID: 42042830; PMCID: PMC13120093.
pubmed.ncbi.nlm.nih.gov/4204…
Dirk Gerhardt aka SilverSit retweeted
Last week @SenRonJohnson held a hearing on Capitol Hill that gave COVID hospital protocol survivors their first platform inside the US Senate. The HighWire streamed it live.
The testimonies documented what happened inside American hospitals when families tried to get ivermectin, hydroxychloroquine, or any alternative to remdesivir and ventilators: requests denied, families locked out, patients described as hostages who couldn’t receive water or food, doctors telling unvaccinated patients to their faces they were going to die, and a physician with 36 years of experience overhearing a hospitalist berating a patient begging for ivermectin.
One woman was told by doctors her lungs were permanently damaged and she would not survive outside their care. Her husband staged a six-hour standoff with hospital security to get her out. She fully recovered at home using treatments the hospital had refused her. A nurse who was inside these hospitals throughout COVID testified: behind closed doors, we knew we were committing these violations. Every doctor and nurse will tell you that. One of the witnesses testified on behalf of her son. Another on behalf of her husband. A third on behalf of a father whose final texts asked why no one was bringing him food.
Del connects this hearing to a pattern he has witnessed traveling the world: the same protocols, the same deaths, the same denial of alternatives happened in Italy, France, Poland, and across Europe, pointing to what he describes as an international coordination of medical response that prioritized a single pathway and systematically removed every alternative.
Dirk Gerhardt aka SilverSit retweeted
Das Problem ist: Wer will schon was vom "Omikron"-Paradoxon hören? Die "Ungeimpften" am Allerwenigsten. Die haben Covid längst hinter sich gelassen, ist ja nur das Problem der Gespikten und aus Sicht vieler haben die es nicht besser verdient. Dass sie selbst stark betroffen sind, verstehen sie nicht. Dass sie der gleichen kognitiven Dissonanz zum Opfer fallen wie die Gespikten, das wollen sie nicht wissen. Weil nicht sein kann, was nicht sein darf. Ich sehe im Moment wenig Chancen darüber aufzuklären. Und diese neuen Erkenntnisse entsetzen mich nicht wenig.
Dirk Gerhardt aka SilverSit retweeted
Cries for Help: Part Five teapawt.org/i/broadcasts/1pJkOXQeB…
Dirk Gerhardt aka SilverSit retweeted
Waouh ! Great ! Beautiful... 🤓😎🧐🫤😰
Un vieux papier de 1998 qui montre déjà que le perlecan (un protéoglycane à héparane sulfate) accélère fortement la fibrillation de l’amylin / IAPP.
Mon ami, tu relies ça à des données plus récentes : les variants Omicron ont une meilleure liaison aux HSPG / héparane sulfate, et le domaine LG3 du perlecan interagit de façon stable avec le RBD de la Spike (papier de 2024).
Et, cerise sur le gâteau, tu ajoutes aussi le rôle potentiel de l’élastase des neutrophiles dans la libération de fragments.
Je vais rajouter de mon côté un autre élément : RAGE.
pmc.ncbi.nlm.nih.gov/article…
pmc.ncbi.nlm.nih.gov/article…
RAGE s’insère assez naturellement là-dedans. On sait depuis 2018 que RAGE lie préférentiellement les intermédiaires pré-amyloïdes de l’IAPP (pas les fibrilles matures) et que cette interaction médie une partie de la toxicité sur les cellules β (inflammation, apoptose, dysfonction).
Le perlecan et ses chaînes d’héparane sulfate accélèrent la fibrillation de l’IAPP ; si Omicron (via une meilleure liaison HSPG / perlecan LG3) favorise la formation de ces intermédiaires oligomériques toxiques, RAGE devient un amplificateur local.
Ensuite, le mode silencieux / immunotolérance. La Spike (et plus largement les complexes Spike–protéines endogènes) peut activer RAGE et d’autres voies qui poussent vers la production d’IL-10, le recrutement de cellules myéloïdes suppressives (MDSC), et un basculement tolérogène. C’est cohérent avec ce que je décris depuis longtemps : la Spike n’est pas seulement pro-inflammatoire, elle a aussi un versant qui met le système immunitaire en sourdine, ce qui facilite sa propre persistance et celle d’éventuels dépôts. Une meilleure interaction avec les HSPG pourrait aider la Spike (ou ses fragments) à rester plus longtemps dans certains microenvironnements, y compris le pancréas, tout en activant ce frein immunitaire.
D’où le paradoxe Omicron : cliniquement moins sévère en phase aiguë (moins de tempête cytokinique massive), mais potentiellement plus efficace pour installer une interaction prolongée avec la matrice extracellulaire (HSPG/perlecan), favoriser des oligomères d’IAPP, activer RAGE de façon plus chronique, et contribuer à un mode silencieux. Moins de bruit, plus de dépôts progressifs et de dysfonction métabolique à bas bruit. C’est exactement le genre de mécanisme qui peut expliquer une hausse de diabète ou de troubles métaboliques post-infection sans que l’épisode aigu ait été dramatique.
English translation :
An old 1998 paper already showed that perlecan (a heparan sulfate proteoglycan) strongly accelerates the fibrillation of amylin/IAPP.
My friend, you link this to more recent data: Omicron variants have better binding to HSPGs/heparan sulfate, and the LG3 domain of perlecan interacts stably with the Spike RBD (2024 paper). And, as the cherry on top, you also add the potential role of neutrophil elastase in the release of fragments.
I’ll add another element from my side: RAGE.
pmc.ncbi.nlm.nih.gov/article…
pmc.ncbi.nlm.nih.gov/article…
RAGE fits quite naturally into this picture. We have known since 2018 that RAGE preferentially binds the pre-amyloid intermediates of IAPP (not the mature fibrils) and that this interaction mediates part of the toxicity on β-cells (inflammation, apoptosis, dysfunction).
Perlecan and its heparan sulfate chains accelerate IAPP fibrillation; if Omicron (via better HSPG/perlecan LG3 binding) favors the formation of these toxic oligomeric intermediates, then RAGE becomes a local amplifier.
Next, the silent mode / immune tolerance. Spike (and more broadly Spike–endogenous protein complexes) can activate RAGE and other pathways that push toward IL-10 production, recruitment of myeloid-derived suppressor cells (MDSCs), and a tolerogenic shift. This is consistent with what I’ve been describing for a long time: Spike is not only pro-inflammatory;
1/2
Dirk Gerhardt aka SilverSit retweeted
🧵1/2
Ich habe heute an Prof. Linden eine Mail geschrieben.
Betreff: Unautorisierte inhaltliche Eingriffe als Herausgeber im Kapitel "Chronisches Fatigue-Syndrom" (Köllner/Kupferschmitt) – Vertrauensbruch, fachliche Mängel und aktive Schädigung Betroffener
Sehr geehrter Prof. Dr. Linden,
mit Fassungslosigkeit habe ich die jüngsten Vorgänge um die Veröffentlichung des Kapitels zum Chronischen Fatigue-Syndrom im Verhaltenstherapiemanual – Erwachsene (Springer Nature) verfolgt. Als Herausgeber haben Sie eigenständig und ohne Autorisierung inhaltliche Änderungen an dem von Dr. Alexa Kupferschmitt und Prof. Volker Köllner verfassten Text vorgenommen. Diese wurden erst nach Drucklegung und Veröffentlichung der ersten Ausgabe bekannt – dokumentiert durch das Erratum des Verlags und das öffentliche LinkedIn-Statement von Herrn Prof. Köllner:
doi.org/10.1007/978-3-662-72…
linkedin.com/posts/volker-k%…
Laut Prof. Köllner wurden unter anderem Aussagen eingefügt, wonach Patientinnen und Patienten mit Post-COVID "nörglerisch-aggressiv" seien, man bei längerer Immobilität allein deshalb ein myalgisches Fatigue-Syndrom entwickle und ein Bezug zur hypochondrischen Störung hergestellt werde. Diese und weitere Passagen entsprechen ausdrücklich nicht der therapeutischen Haltung der Autor*innen und wurden ohne Rücksprache eingefügt.
Sollte dies so zutreffen, handelt es sich um einen hochgradigen Vertrauensbruch gegenüber den Autor*innen, dem Verlag und der wissenschaftlichen Öffentlichkeit. Es stellt sich die Frage, inwieweit Sie unter diesen Umständen noch als Herausgeber bei Springer Nature geeignet sind – oder generell geeignet, wissenschaftliche Fachliteratur zu verantworten, die in Ausbildung und Versorgung wirksam wird.
Die inhaltlichen und fachlichen Mängel des Kapitels gehen jedoch über diese unautorisierten Zusätze hinaus. Wie von der Patientenorganisation NichtGenesen und von Missing Doctors and Psychotherapists bereits detailliert beanstandet, enthält das Kapitel nosologische Fehler, evidenzhierarchische Fehlzuordnungen, psychopathologisierende Generalisierungen und Aussagen, die mit dem aktuellen Stand der Forschung zu PEM und ME/CFS in erheblichem Widerspruch stehen und patientensicherheitsrelevant sind:
Schreiben Missing Doctors and Psychotherapists: drive.google.com/file/d/1qHb…
Schreiben NichtGenesen: drive.google.com/file/d/1_9T…
Welches Bild von Betroffenen soll hier mit wessen Macht und zu welchem Zweck zwingend aufrechterhalten werden? Ein Bild, das sie als aggressiv, nörglerisch oder hypochondrisch zeichnet, Immobilität pathologisiert und biologische Krankheitsmechanismen relativiert? Ein Patient*innenbild, das den Zugang zu angemessener Versorgung erschwert und Fehlbehandlungen legitimiert?
Ich schreibe Ihnen auch aus eigener Betroffenheit. Mein Name ist Christina Koch. Ich bin 43 Jahre alt, ehemalige Lehrerin, und seit 2023 schwer erkrankt. Auslöser waren unter anderem eine COVID-Infektion, ein Kopfstoß und eine Vierfachimpfung innerhalb kurzer Zeit. Ich lebe nun mit ME, POTS, MCAS, Small-Fiber-Neuropathie, kraniozervikaler Instabilität und einem vorbestehenden Marfan-Syndrom. Ich habe Pflegegrad 3, bin zu etwa 90 Prozent haus- und bettgebunden und aktuell oft 23 Stunden am Tag bettlägerig. Mein Partner pflegt mich. Der Alltag ist auf das absolute Minimum reduziert; schon geringe Belastungen können PEM auslösen und den Zustand weiter verschlechtern. In den drei Jahren meiner Erkrankung hat sich an der katastrophalen Versorgungslage für Menschen mit diesen Erkrankungen faktisch nichts verbessert.
Solche Therapiemanuals sind nicht nur unwissenschaftlich und unter dubiosen Umständen veröffentlicht worden. Sie schaden Betroffenen aktiv, indem sie Stigmatisierung fortschreiben, Pacing und PEM-Sensitivität unterlaufen und Fehlbehandlungen begünstigen. Schlamperei und aktive Zuwiderhandlung gegen gängige wissenschaftliche Praxis – wie in diesem Fall – dürfen nicht zur gängigen Praxis werden.
Dirk Gerhardt aka SilverSit retweeted
@SitSilver @tommy_cleary @breakfast_dogs
Novel binding interaction: SARS-CoV-2 spike RBD interacts with β-adrenergic receptors and causes cardiac symptoms.
Besides eliciting autoantibodies, SARS-CoV-2 spike functions as cardiotoxin by itself. Long COVID patients who exhibit cardiac symptoms usually show higher level of spike S1 in circulation. Spike is experimentally proven to engage β1- and β2- adrenergic receptors (Kd=21.7 pM for β1 AR and Kd=90.4 nM for β2 AR). Of note, the spike protein binds β1-adrenergic receptor more tightly than to the canonical receptor ACE2. The spike protein functions as an agonist of β-adrenergic receptor by inducing over-production of messenger molecule cAMP.
As shown by docking model, spike RBD residues (N487, Q493) are involved in binding β1-adrenergic receptor, while spike RBD residues (Q493, Y473, and K417) are involved in binding β2-adrenergic receptor. The spike RBD engages β-adrenergic receptors by the ACE2 binding loop.
K417 is conserved for spikes of SARS-CoV-2, BANAL-20-52, RaTG13. PangolinCoV-MP789 has arginine at this spike position. The same position is occupied by valine for ZC45 and SARS-CoV-1.
Y473 is conserved for SARS-CoV-2, BANAL-20-52, RaTG13, and pangolinCoV-MP789. SARS-CoV-1 has phenylalanine at this position.
N487 is very well conserved for both SARS-CoV-2, BANAL-20-52, RaTG13, pangolinCoV-MP789, and SARS-CoV-1. This residue is probably natural.
Q493 is only specific for SARS-CoV-2, BANAL-20-52, and pangolinCoV-MP789.
SARS-CoV-1 spike protein probably cannot bind β-adrenergic receptors because the key interface residues are different from that of SARS-CoV-2.
Only the spike proteins of SARS-CoV-2, BANAL-20-52, and pangolinCoV-MP789 can interact with human β-adrenergic receptors.
Reference:
Deng X, Cui H, Liang H, Wang X, Yu H, Wang J, Wang W, Liu D, Zhang Y, Dong E, Tang Y, Xiao H. SARS-CoV-2 spike protein acts as a β-adrenergic receptor agonist: A potential mechanism for cardiac sequelae of long COVID. J Intern Med. 2024 Sep;296(3):291-297. doi: 10.1111/joim.20000. Epub 2024 Jul 29. PMID: 39073192.
pubmed.ncbi.nlm.nih.gov/3907…
