Endotoxin in Jabs causes Pulmonary Hypertension
High Fatality rate with this progressive jab induced Heart damage might account for a significant part our current surge in Excess Deaths worldwide
I was prompted to start this article by a tweet from British lawyer Peter Todd, who pointed us toward a recent paper by Robert Sullivan and coworkers1 reporting 2 cases of Pulmonary Hypertension after Pfizer jabbing.
According to Mayo Clinic2 “There's no cure for pulmonary hypertension.”
Sullivan and coworkers reported:
Case #1 is a previously healthy 49-year-old male physician athlete, body mass index (BMI) 23, non-smoker. with a history of mild exercise-induced asthma treated with albuterol. The patient completed the primary series of Pfizer mRNA COVID-19 vaccine (BNT162b2), Dose 1 in December 2020 and Dose 2 in January 2021. Approximately three weeks after the second dose, the patient suddenly developed severe fatigue, flu-like symptoms, tachycardia, palpitations, orthostasis, right-sided chest pressure and dyspnea on exertion.
This case was reported to the Vaccine Adverse Event Reporting System (VAERS ID 1039123).
Case #2 is a previously healthy and active 56-year-old male, BMI 25, non-smoker, with a history of spontaneous deep venous thrombosis (DVT) on two occasions which were resolved with courses of anticoagulation without symptoms of pulmonary emboli.
The patient completed the primary series of Pfizer mRNA COVID-19 vaccine (BNT162b2) Dose 1 and Dose 2 in April 2021. Twelve days after the second dose, the patient experienced sudden onset fatigue, flu-like symptoms and dyspnea on exertion.
While the definition of pulmonary hypertension is precise, the gravity of the diagnosis is difficult to convey. Even “mild” pulmonary hypertension is considered incurable. It is usually progressive and, for many, a terminal diagnosis.
Pfizer reports of Hypertension
Looking at the Pfizer June 2022 report case numbers of Adverse Events we see the usual dispersal of signal by use of uncurated terms.
Pulmonary arterial pressure increased 24
Pulmonary arterial hypertension 30
Pulmonary hypertension 131
Pulmonary hypertensive crisis 2
Hypertension 14,859
Hypertensive crisis 1,659
Down Syndrome sufferers more prone to Pulmonary Hypertension link to Endotoxin
Down Syndrome sufferers are more prone to immune problems as illustrated in this figure from Huggard and coworkers.3
Note in this illustration the importance of Endotoxin induced Cytokines IL (Interleukin), VEGF (Vascular Endothelial Growth Factor), Epo (Erythropoietin), GM-CSF (Granulocyte-Macrophage Colony-Stimulating Factor).
Note they reported Endotoxin Hyperresponsiveness in CD11b neutrophils in Down Syndrome that can lead to deleterious inflammatory consequences.
Down Syndrome children had greater levels of both pro- (IL-2, IL-6) and anti-inflammatory cytokines (IL-10, IL-1ra), as well as other mediators (Epo, VEGF, GM-CSF) of
Cardiac Abnormalities linked to VEGF and EPO
Researchers in Mexico linked Heart problems, especially Pulmonary Hypertension in the newborn, to measured blood levels of HIF-1α (hypoxia-inducible factor-1 alpha), VEGF and EPO.4
Endotoxin and Pulmonary Hypertension
Once again the US government Comparative Toxicogenomics Database provides useful references to Pulmonary Hypertension with or without Thromboembolism.
Among the 6,484 chemicals linked to Pulmonary Hypertension we see Pfizer’s preferred Adjuvant Lipid A and various Endotoxins listed.
From there we can access numerous abstracts and links to full publications.5
Damås and coworkers identified elevated CD40 Ligand in patients suffering Pulmonary Arterial Hypertension.6
In vitro, recombinant sCD40L induced monocyte chemoattractant protein (MCP)-1 and interleukin-8 gene expression in endothelial cells, and plasma levels of these chemokines were raised in all PAH groups, significantly correlated to sCD40L and hemodynamic parameters.
Endotoxin is the top listed chemical for the related LINC01094 gene.7
Mechanisms involving Endotoxin
It has been shown8 that release of Endothelin-1 is triggered by Endotoxin Cytokines TNF-α and IFN-γ and that certain drugs might help by inhibiting the progression of the disease once initiated.
Research at Mitochondrial level links Pulmonary Hypertension to Manganese Superoxide Dismutase and Nitric Oxide pathways.9
November Update
A special feature article by Jenifer Block and 10in the British Medical Journal discusses failure of the VAERS system. The opening paragraphs are relevant here:
Three weeks after receiving a second dose of a covid vaccine, Robert Sullivan collapsed at home on his treadmill. An anaesthesiologist in Maryland, USA, he was a particularly fit 49 year old: the week before falling ill, he’d been happily skiing at altitude in Colorado.
Sullivan was given a diagnosis of sudden onset pulmonary hypertension, which is generally progressive, can be fatal, and in most cases can’t be cured. The condition is rare, especially in middle aged men. Sullivan decided to file a report in the Vaccine Adverse Event Reporting System (VAERS), which collects reports of symptoms, diagnoses, hospital admissions, and deaths after vaccination for the purpose of capturing post-market safety signals.
But the submission process was a glitchy race against the clock. “The format is cumbersome and it times you out,” he tells The BMJ. For his troubles, Sullivan received a confirmation by email and a temporary “e-report” number. He learnt from his doctor’s office that a VAERS representative had requested medical records. Then he didn’t hear back for a year.
Sullivan RD, Schults NV and Suzuki YJ. 2023. Case Report: Two Case Reports of Pulmonary Hypertension after mRNA COVID-19 Vaccination. https://www.mdpi.com/2079-9721/11/3/114
https://www.mayoclinic.org/diseases-conditions/pulmonary-hypertension/symptoms-causes/syc-20350697
Huggard D, et al. 2020. Immune Dysregulation in Children With Down Syndrome. https://www.frontiersin.org/articles/10.3389/fped.2020.00073/full
Lemus-Varela ML, et al. 2009. Expression of HIF-1α, VEGF and EPO in peripheral blood from patients with two cardiac abnormalities associated with hypoxia. https://www.sciencedirect.com/science/article/abs/pii/S0009912009004329
https://ctdbase.org/detail.go?acc=MESH%3AD006976&view=chem&sort=chemNmSort&page=78&type=disease&dir=asc
Damås JK, et al. 2004. Soluble CD40 Ligand in Pulmonary Arterial Hypertension. Possible Pathogenic Role of the Interaction Between Platelets and Endothelial Cells. https://www.ahajournals.org/doi/10.1161/01.CIR.0000139859.68513.FC
https://ctdbase.org/detail.go?type=gene&acc=100505702
Wort SJ, et al. 2002. Cyclooxygenase-2 Acts as an Endogenous Brake on Endothelin-1 Release by Human Pulmonary Artery Smooth Muscle Cells: Implications for Pulmonary Hypertension. https://molpharm.aspetjournals.org/content/62/5/1147
Fijalkowska I, et al. Hypoxia Inducible-Factor1α Regulates the Metabolic Shift of Pulmonary Hypertensive Endothelial Cells. https://ajp.amjpathol.org/article/S0002-9440(10)60427-0/fulltext
Jennifer Block. 2023. Is the US’s Vaccine Adverse Event Reporting System broken? https://www.bmj.com/content/383/bmj.p2582
I’ve clearly been sat at the back of the class not paying attention in your lectures. Pfizer’s preferred Lipid A Adjuvant - I thought this was a contaminant left over from the lack of cleaning up in Process 2. Is that correct or is it a planned product ingredient?
“we see the usual dispersal of signal by use of uncurated terms”
Is this a deliberate strategy by Pfizer et al?