Covid19 Deaths and Ongoing Symptoms caused by Endotoxemia with or without Jabbing

Millions of people have died as the result of weaponization of Coronavirus. Not many focus on how they die, so let's trace the history from 2020 to current understanding.

In 2020 researchers in Thailand and USA¹ made a detailed preliminary investigation of Covid19 disease severity to look for comorbidities that might explain why the vast majority of people survived exposure to even the most virulent strains.

They concluded that the virus led to damage of the Lung, but mainly the Gut, leading to systemic Endotoxemia often resulting in Multiple Organ Failure (MOF) and Death.

Their Figure 6 caption reads:

Hypothetical pathogenesis of endotoxemia in COVID-19 pneumonia. At early stage, SARS-CoV-2 primarily infects type 2 pneumocytes in the lungs and causes pneumonia which can progress to ARDS and induces susceptibility of secondary bacterial infection by impairing the pulmonary immune response. The virus can enter the bloodstream causing viremia targeting organs with high ACE2 expression including the gut. SARS-CoV-2 infection of enterocytes causes inflammatory response of gastrointestinal tract which results in alteration of the intestinal microenvironment including epithelial hyperpermeability, attenuated local immune system, and dysbiosis of the microbiome. The perturbations of the intestinal microenvironment allow the pathogenic bacteria from the gut lumen to translocate to the bloodstream. Hence, we propose the sources of endotoxin to be majorly from the gut and minorly from the secondary bacterial infection of the lungs. COVID-19, the coronavirus disease 2019; SAR-CoV-2, severe acute respiratory syndrome coronavirus 2; ARDS, acute respiratory distress syndrome; ACE2, angiotensin converting enzyme 2; MOF, multiple organ failure

Subsequent research has confirmed their hypothesis and I have reviewed how a Covid19 jab in the arm opens the Gut to cause an inrush of toxic bacterial Endotoxin.²

In February 2021, after mass Covid19 jabbing had commenced, researchers in Karlsruhe Germany and Texas published³ a careful discussion of Covid19 induced Entotoxemia. They referenced many useful papers including the work of Kahn and coworkers⁴ that found

LPS (Endotoxin) stimulation caused a strong further enhancement of expression of all cytokines (especially of interleukin [IL]-1β) in COVID-19, but not in septic patients.

Krugilov and Scherer also referenced the work of Wyler and coworkers⁵ that showed the dangers of increased expression of microRNA 155 caused by Endotoxin. I have previously written that this is the cause of Endotoxin Induced Myocarditis and other organ damage.⁶

A paper submitted and published⁷ in May 2022 by researchers in Greece and Cyprus added to the understanding of Covid19 induced Endotoxemia. They found:

Enterocytes’ tight junctions (TJs) are disrupted, and the apoptotic death of intestinal epithelial cells is increased leading to increased gut permeability. In addition, mucosal CD4(+) and CD8(+) T cells, Th17 cells, neutrophils, dendritic cells and macrophages are activated, and T-regulatory cells are decreased, thus promoting an overactivated immune response, which further injures the intestinal epithelium.

Here is their Figure 2, extending the range of expected organ injury.

Researchers in Brazil submitted a paper⁸ in June 2022 that was not published until February 2023. They found increased expression of TLR-4 on CD14 + HLA-DR + monocytes in conjunction with higher NF-κB p65 phosphorylation in both CD14 + HLA-DR + and CD14 + HLA-DR low monocytes of severe COVID-19 patients. However the whole blood of severe COVID-19 patients presented lower production of IL-1β, IL-6, IL-10, CCL2, and TNF-α after Endotoxin stimulation at 1 and 10 ng/mL. They concluded that SARS-CoV-2 infection may induce Endotoxin Tolerance associated with the potential development of secondary infections.

Also in June 2022, Samsudin and coworkers in a wonderful collaboration between Singapore, Sweden, USA and Denmark submitted their exciting discovery (mentioned in my earlier articles) that the Spike Protein derived from the Coronavirus or Jabs, more effectively delivers Endotoxin to maximize cell damage throughout the body.⁹

Among their numerous elegant experiments they showed, using Deuterium exchange, that the supertoxic fragment of Endotoxin, Lipid A (see B in their Figure 2), Pfizer’s preferred adjuvant, binds to a number of identified sites within the Spike identified with atomic precision.

This discussion confirms the madness of jabbing every second day with Endotoxin LNP jabs as is happening in Canadian government funded clinical trials by Qu Biologics, a sister company of The Wellness Company.¹⁰

1. Phatadon Sirivongrangson, Win Kulvichit, Sunchai Payungporn, Trairak Pisitkun, Ariya Chindamporn, Sadudee Peerapornratana, Prapaporn Pisitkun, Suwalak Chitcharoen, Vorthon Sawaswong, Navaporn Worasilchai, Sarinya Kampunya, Opass Putcharoen, Thammasak Thawitsri, Nophol Leelayuwatanakul, Napplika Kongpolprom, Vorakamol Phoophiboon, Thitiwat Sriprasart, Rujipat Samransamruajkit, Somkanya Tungsanga, Kanitha Tiankanon, Nuttha Lumlertgul, Asada Leelahavanichkul, Tueboon Sriphojanart, Terapong Tantawichien, Usa Thisyakorn, Chintana Chirathaworn, Kearkiat Praditpornsilpa, Kriang Tungsanga, Somchai Eiam‑Ong, Visith Sitprija, John A. Kellum and Nattachai Srisawat. 2020. Endotoxemia and circulating bacteriome in severe COVID‑19 patients. https://icm-experimental.springeropen.com/articles/10.1186/s40635-020-00362-8

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3. Ilja L. Kruglikov and Philipp E. Scherer. 2021. Preexisting and inducible endotoxemia as crucial contributors to the severity of COVID- 19 outcomes. https://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1009306

4. Kahn R, Schmidt T, Golestani K, Mossberg A, Gullstrand B, Bengtsson AA, Kahn F. Mismatch between circulating cytokines and spontaneous cytokine production by leukocytes in hyperinflammatory COVID-19. J Leukoc Biol. 2020. https://doi.org/10.1002/JLB.5COVBCR0720-310RR

5. Wyler E, Mosbauer K, Franke V. Diag A, Gottula LT, Arsie R, et al. Bulk and single-cell gene expression profiling of SARS-CoV-2 infected human cell lines identifies molecular targets for therapeutic intervention. bioRxiv. 2020. https://doi.org/10.1101/2020.05.05.079194

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7. Stelios F. Assimakopoulos, Gerasimos Eleftheriotis, Maria Lagadinou, Vassilios Karamouzos, Periklis Dousdampanis, Georgios Siakallis and Markos Marangos. 2022. SARS CoV-2-Induced Viral Sepsis: The Role of Gut Barrier Dysfunction. https://www.mdpi.com/2076-2607/10/5/1050

8. Gilson P. Dorneles, Paula C. Teixeira, Alessandra Peres, Luiz Carlos Rodrigues Júnior, Simone Gonçalves da Fonseca, Marta Chagas Monteiro, Sarah Eller, Tiago F. Oliveira, Eliana M. Wendland, Pedro R. T. Romão. 2023. Endotoxin tolerance and low activation of TLR‑4/NF‑κB axis in monocytes of COVID‑19 patients. https://link.springer.com/article/10.1007/s00109-023-02283-x

9. Firdaus Samsudin, Palur Raghuvamsi, Ganna Petruk, Manoj Puthia, Jitka Petrlova, Paul MacAry, Ganesh S. Anand, Peter J. Bond and Artur Schmidtchen. 2022. SARS-CoV-2 spike protein as a bacterial lipopolysaccharide delivery system in an overzealous inflammatory cascade. https://academic.oup.com/jmcb/article/14/9/mjac058/6761401

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