Sound Money Advocat. Following markets since 1989. GOLD/SILVERbug.
Hamburg, Germany
Joined February 2021
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Dirk Gerhardt aka SilverSit retweeted
Just launchedâŠ. It will only get better from here! epidemicoffraud.com/fauci-fiâŠ
Dirk Gerhardt aka SilverSit retweeted
$HL has never had a stronger balance sheet in its 135-year history. For the first time, the company can make and execute plans independently of the silver price.
I just watched the Q3 analyst call, and everything looks very strong. I just added a little more.
Every day I watch one earnings call. Today it was $HL, a company I personally own.
This slide refers to just one single mine within Heclaâs portfolio: Greens Creek.
Hecla presents itself as a primary silver producer, but Greens Creek specifically is a true multi-metal mine producing silver, gold, zinc and lead. Bookkeeping at this mine is done via the by-product credit model: all operating and sustaining costs are first absorbed by gold, zinc and lead.
In Q3 those by-products more than covered the full cost base of this one mine, which pushed the All-in Sustaining Costs per ounce of silver to â$2.55.
With silver trading around $58, the math is simple: the margin is well above $60 per ounce, and every additional dollar in the silver price now flows entirely into free cash flow.
With roughly 12 years of reserves at Greens Creek, this is not a short-term effect but a structurally embedded earnings engine.
Dirk Gerhardt aka SilverSit retweeted
SARS-CoV-2 Spike Protein Competes with ENaC for Plasmin Cleavage, Driving share.google/liTVANKxsZ9c8AKâŠ
Dirk Gerhardt aka SilverSit retweeted
COVID-19 Origins: A Comparative Audit of the Evidence
After an extensive examination of the scientific literature, intelligence assessments, and newly released documents, I've published an analysis of what the evidence canâand cannotâestablish about the origins of SARS-CoV-2.
The audit examines four possible pathways, separating documented observations from the inferences drawn from them. It also addresses a persistent problem: correlated evidence can be counted more than once, while missing evidence is often treated as proof of a preferred explanation.
The evidence is not equally strong for every hypothesis, but the available record does not justify precise numerical odds.
Science advances by asking what the evidence can bear, not by demanding more certainty than it provides.
Read the essay and examine the evidence:
davidlingenfelter.substack.câŠ
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.
xitter.gq/ydeigin/status/1694846âŠ
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 â 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 â out of 4 possible alanine codons â 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.
DEFUSEâs 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:
âN-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.â
The [77] paper cited in DEFUSE is a 2007 work by Han et al. titled âSpecific Asparagine-Linked Glycosylation Sites Are Critical for DC-SIGN- and L-SIGN-Mediated Severe Acute Respiratory Syndrome Coronavirus Entryâ. 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/articleâŠ
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/scienâŠ
Academic paper:
onlinelibrary.wiley.com/doi/âŠ
Dirk Gerhardt aka SilverSit retweeted
SV40 reveal: before, during, after lawsuit
Info Commissioner ordered disclosure of Health Canadaâs 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 Bodyâs Structural Scaffold Hold the Clue?
âĄïž A new hypothesis proposes that changes in the **extracellular matrix (ECM)âthe bodyâs structural support networkâ**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 rightâŠ. look at what actually happens (or doesnât) to uncover motives.
Perhaps nothing has been done about Covid and millions of children are still getting mRNA shots because MAHA doesnât want it to happen.
Dirk Gerhardt aka SilverSit retweeted
My origin story of how I went from a âtrust the scienceâ 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 didnât 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 werenât gasping for air. The doctors said their low sats meant they were about to crash. It went against everything Iâd been taught- treat the patient, not the numbers.
Visitors werenât 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- weâd wake them in a few days and theyâd 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 Iâd joked with and reassured hours or days earlier were gone. I kept thinking, âHow is this virus killing relatively young, healthy people this fast even with the best treatment we have?â
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 âonly the sickest get the drug.â
But that didnât 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 canât 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 âtrust the expertsâ to âwatch what happens to the patients and decide for yourself.â
If you were on the front lines and saw something different, say so. If you werenât, this is why a lot of us stopped automatically trusting the system and have dropped out of it.
Iâm the villain and the hero of my own story and itâs hard to reconcile with either.
Dirk Gerhardt aka SilverSit retweeted
đą 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.
đœI am sure this stems from the "12 symptoms psyop" from 2023.
đ€„ That distinction is completely false.
âïžâLC 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!
đ„The fallout isn't separate. It is the exact same chronic-viral fire impacting every major body system:
đ« Cardiovascular: Myocarditis, pericarditis, microvascular endotheliitis, arrhythmias, early heart attacks, and strokes.
đ« Respiratory: Pulmonary fibrosis, chronic dyspnea, microvascular gas-exchange defects, reactive airway disease, pulmonary nodules, nerve damage, asthma, COPD, and lung collapse.
đ§ Neurological & Cognitive: Neuroinflammation, small fiber neuropathy, autonomic failure, cognitive impairment, and neurodegenerative accelerationâincluding ALS, Alzheimerâs, Parkinsonâs, MS-like demyelination, intracranial pressure (pseudotumor cerebri), seizures, strokes, TIAs, and brain tumors.
đ©ž 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).
𧏠Oncological: Impaired immune surveillance, accelerated cancer progression, and oncogenesis across multiple organ systems.
đŠ 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 (Crohnâs/Ulcerative Colitis), polyps, and GI cancers.
đ« Renal & Urinary: Accelerated decline in kidney function, interstitial cystitis, and neurogenic bladder/spasms.
đ©ž Endocrine & Metabolic: New-onset Type 1 and Type 2 diabetes, thyroiditis, adrenal dysfunction, and systemic metabolic crash.
𩮠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).
đïž 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).
âïž 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 đ§ââïžđ©ș
đ€ Conflating primary autoimmunity with immune-complex pathology and antigen-driven targeting is one of the most destructive diagnostic failures in chronic-viral immunology.
đïžSiloing 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.
âŒïžTreating the outcome will not stop these from occuring.
âąïžIt is all the exact same chronic viral fallout.
#LongCovid #CovidFallout #Microvascular #MultiSystem #ChronicViral #ItsChronicYo
đ 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.
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/S1201âŠ
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 â ïžâïž
Ein Bild zeigt mehr als tausend Worte: Die schweren Folgen meiner GefĂ€ĂschĂ€digung
Heute hatte ich erneut eine kapillarmikroskopische Untersuchung. Das Bild zeigt das erschreckende Ergebnis meiner kleinsten BlutgefĂ€Ăe: massive, dauerhafte SchĂ€den.
Nach 5,5 Jahren wird hier noch einmal schonungslos sichtbar, womit ich tĂ€glich lebe â schwere Durchblutungsstörungen, Dauerfeuer an Schmerzen und zerstörte GefĂ€Ăstrukturen. Genau diese extremen GefĂ€ĂschĂ€den waren damals, rund sechs Wochen nach der Impfung, auch der Grund fĂŒr meine Darmamputation.
Das Foto macht unmissverstÀndlich deutlich, wie tiefgreifend diese Folgen bis heute in meinem Körper nachwirken.
Quelle zum linken gesunden Bild đ
share.google/jMEYgRaQBaOFj6yâŠ
An meine zukĂŒnftigen Mörder die an der Goldgrube 12 in Mainz sitzen.
Ihr seid Mörder â ïž und dafĂŒr bekommt ihr meine tiefste Verachtung
ImpfgeschĂ€digte durch Biontech Pfizer Charge EX8679 â at DĂŒsseldorf, Germany
Dirk Gerhardt aka SilverSit retweeted
Thatâs 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 âidiotypeâ 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.
âCollins 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.â The spike protein raises antibodies against both the spike protein and the ACE2 receptor. Given that SARS-CoV-2 spike RBD binds ÎČ-adrenergic receptors with high affinity, the spike protein probably elicits autoantibodies against ÎČ-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. âSegments of the SARS-CoV-2 S protein (residues 49â53, 226â230, 418â428, 529â536, 744â774, and 977â980) share structural and chemical similarities with some segments of the ACE2 receptor (residues 137â141, 335â345, 350â352, 463â471, and 545â573).â
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/4204âŠ
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 couldnât 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 lĂ€ngst 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 darĂŒber aufzuklĂ€ren. Und diese neuen Erkenntnisse entsetzen mich nicht wenig.
Dirk Gerhardt aka SilverSit retweeted
Cries for Help: Part Five xitter.gq/i/broadcasts/1pJkOXQeBâŠ
Dirk Gerhardt aka SilverSit retweeted
Waouh ! Great ! Beautiful... đ€đđ§đ«€đ°
Un vieux papier de 1998 qui montre dĂ©jĂ que le perlecan (un protĂ©oglycane Ă hĂ©parane sulfate) accĂ©lĂšre fortement la fibrillation de lâamylin / 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 gĂąteau, tu ajoutes aussi le rĂŽle potentiel de lâĂ©lastase des neutrophiles dans la libĂ©ration de fragments.
Je vais rajouter de mon cÎté un autre élément : RAGE.
pmc.ncbi.nlm.nih.gov/articleâŠ
pmc.ncbi.nlm.nih.gov/articleâŠ
RAGE sâinsĂšre assez naturellement lĂ -dedans. On sait depuis 2018 que RAGE lie prĂ©fĂ©rentiellement les intermĂ©diaires prĂ©-amyloĂŻdes de lâIAPP (pas les fibrilles matures) et que cette interaction mĂ©die une partie de la toxicitĂ© sur les cellules ÎČ (inflammation, apoptose, dysfonction).
Le perlecan et ses chaĂźnes dâhĂ©parane sulfate accĂ©lĂšrent la fibrillation de lâIAPP ; si Omicron (via une meilleure liaison HSPG / perlecan LG3) favorise la formation de ces intermĂ©diaires oligomĂ©riques toxiques, RAGE devient un amplificateur local.
Ensuite, le mode silencieux / immunotolĂ©rance. La Spike (et plus largement les complexes SpikeâprotĂ©ines endogĂšnes) peut activer RAGE et dâautres voies qui poussent vers la production dâIL-10, le recrutement de cellules myĂ©loĂŻdes suppressives (MDSC), et un basculement tolĂ©rogĂšne. Câest cohĂ©rent avec ce que je dĂ©cris depuis longtemps : la Spike nâest pas seulement pro-inflammatoire, elle a aussi un versant qui met le systĂšme immunitaire en sourdine, ce qui facilite sa propre persistance et celle dâĂ©ventuels dĂ©pĂŽts. Une meilleure interaction avec les HSPG pourrait aider la Spike (ou ses fragments) Ă rester plus longtemps dans certains microenvironnements, y compris le pancrĂ©as, tout en activant ce frein immunitaire.
DâoĂč le paradoxe Omicron : cliniquement moins sĂ©vĂšre en phase aiguĂ« (moins de tempĂȘte cytokinique massive), mais potentiellement plus efficace pour installer une interaction prolongĂ©e avec la matrice extracellulaire (HSPG/perlecan), favoriser des oligomĂšres dâIAPP, activer RAGE de façon plus chronique, et contribuer Ă un mode silencieux. Moins de bruit, plus de dĂ©pĂŽts progressifs et de dysfonction mĂ©tabolique Ă bas bruit. Câest exactement le genre de mĂ©canisme qui peut expliquer une hausse de diabĂšte ou de troubles mĂ©taboliques post-infection sans que lâĂ©pisode aigu ait Ă©tĂ© 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.
Iâll add another element from my side: RAGE.
pmc.ncbi.nlm.nih.gov/articleâŠ
pmc.ncbi.nlm.nih.gov/articleâŠ
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 ÎČ-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 Spikeâendogenous 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 Iâve been describing for a long time: Spike is not only pro-inflammatory;
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