Gay Men, Pregnant Women and Foetuses - What do they have in common?

Let's look at CD4+ to CD8+ ratios, "Endotoxin Tolerance" and the role of the Brainstem and Vagal Nerves in mRNA Jab induced Harms - LongJab

I thank Walter M Chesnut¹ for bringing this journal article graphical abstract by Shin Jie Yong to my attention.²

I have shaved the top of the figure off for reasons which will become apparent.

The Figure by Shin Jie Yong was designed to help discuss Long Covid symptoms, however I want to show that all of the symptoms listed on the right hand side, which he points out can be related to the Brainstem, Spinal Cord and peripheral nerves can be explained by Endotoxin in the mRNA jabs (Red Arrow represents Endotoxin in my version).

Brain Damage

In an earlier article³ I showed that Endotoxin in the jabs creates Quinolinic Acid which acts as a Neurotoxin, Gliotoxin, Proinflammatory mediator, Pro-oxidant molecule and can alter the integrity and cohesion of the Blood–Brain Barrier.

I also showed that Endotoxin travels immediately directly into the Brain⁴, causing the common post-jab symptoms of Fatigue, Headache, Muscle Pain, Fever and Chills.

Gut Damage

The massive scale AusVaxSafety survey of millions of jabbed Australians found 1 in 9 people reported Gastrointestinal symptoms, including Diarrhoea, Vomiting, Nausea and Abdominal Pain after the second jab. This was considerably more than reports after their first dose. This indicates their bodies were made allergic to components.⁵

Altered Taste

I have discussed the common occurrence of Altered Taste, especially in people who have Nickel Allergy, in mRNA jabbees.⁶

Heart and Lung Damage

See my earlier articles describing how Heart Palpitations, Tachycardia and Myocarditis can be caused by Endotoxin via the iNOS and microRNA routes.⁷

Many jabbees report Chest Pain and this can be a warning sign of Heart and/or Lung Damage caused by the Endotoxin in the jabs. Victims need to get thorough testing to see whether they might have a Clot, or Inflammation.

Nerve Damage, MS and Gay Men

Walter Chesnut was most concerned about Demyelination, and he discovered that Fatal diseases like Multiple Sclerosis⁸ after the jabs can be seen among the numerous Autoimmune attacks on jabbees. I have reported that Dose of Endotoxin causing massive damage can be quite small because both Interleukin 6 (IL-6) and IL-1β (called the Apex Cytokine)⁹ are amplified by Positive Feedback Loops.¹⁰

The paper he cited reported 2 cases of Multiple Sclerosis (MS) with clinical and new radiological signs beginning in close temporal relation to spike (S) protein mRNA-based vaccinations. The authors studied both peripheral blood- and CerebroSpinal Fluid (CSF) derived CD4+ T cells and suggested CD4+ T cell clones might cross-recognize SARS-CoV-2 S protein-derived peptides and peptides derived from myelin proteins.

Of course I am following the probability that it is Endotoxin that is in those jabs causing the MS, rather than Spike.

I found a paper¹¹ and told Walter about it, where the authors studied HIV-negative men with Subclinical Endotoxemia linked to alterations in CD4/CD8 T cell ratio and plasma Cytokine levels. They summarized the results:

By comparing two samples of differing plasma LPS levels from each individual, we now show that subclinical levels of plasma LPS in vivo significantly alter T cell proliferative capacity, monocyte cytokine release, and HLA-DR expression, and induce TLR cross-tolerance by decreased phosphorylation of MAPK pathway components. Using this human in vivo model of subclinical endotoxemia, we furthermore show that plasma LPS leads to constitutive activation of STAT1 through autocrine cytokine signaling, suggesting that subclinical endotoxemia in healthy individuals might lead to significant changes in immune function that have thus far not been appreciated.

The range of Endotoxin circulating in the blood of the test subjects was 0 to an extraordinary high 125.3 EU/ml. Gay men are more at risk of E coli induced Endotoxemia. Presence of plasma endotoxin was associated with significantly decreased frequencies of CD4⁺Ki67⁺ and CD8⁺Ki67⁺ T cells

Evidence of Endotoxin Tolerance was presented “monocytes from LPS hi samples did not significantly increase cytokine production after LPS stimulation, whereas monocytes from the matching LPS lo samples (group 1) increased cytokine production (except for IL-8) by ∼8- to ∼150-fold”.

Palmer et al concluded:

elevated levels of subclinical LPS may induce an inflammatory state characterized by increased cytokine production and consequent STAT1 activation rather than a beneficial priming state, which might be promoted by lower levels of subclinical endotoxemia. This in turn has been postulated to contribute to reduced wound healing and multiple pathologies, including atherosclerosis, diabetes, and rheumatoid arthritis in populations with frequent elevated levels of plasma endotoxin

Chronic HIV-1 infection leads to higher response to Endotoxin compared to cells that were not pre-stimulated with TLR8 ligands or HIV-1.¹²

LongJab and loss of Endotoxin Tolerance

The consequences of repeated exposure to Endotoxin included chronic non-resolving inflammation expressed as diseases including Heart disease, Diabetes, reduced wound healing, Parkinson’s disease and Rheumatoid Arthritis.¹³ Morris et al. point out that, according to dogma, a second high dose of Endotoxin was thought to be characterized by less robust induction of pro-inflammatory cytokines and increased production of anti-inflammatory cytokines - known as Endotoxin Tolerance. However they point out that retreatment with a “very low” dose of endotoxin (picograms/milliliter), in contrast, has an opposite effect, potentiating or “priming” the pro-inflammatory response to subsequent endotoxin challenge, referred to as the Shwartzman-like reaction.¹⁴ Mice pretreated with super-low-dose LPS exhibit increased Mortality in response to challenge with a higher dose. This scheme by Morris et al demonstrates the complexity of Endotoxin poisoning.

Here LPS = Endotoxin; TLR4 = Toll-Like Receptor; MyD88 = Myeloid Differentiation primary response 88 protein; TRIF = Toll/IL-1R domain-containing adaptor protein inducing Interferon-β; IRAK = Interleukin-Receptor-Associated Kinase; GSK3 = Glycogen Synthase Kinase 3; JNK = c-Jun N-terminal Kinase; AKT = Protein kinase B (PKB); ERK = Extracellular signal-Regulated Kinase; IKK = IκB Kinase; NFκB Nuclear Factor κ of activated B cells

Conclusion

“Long Covid” for all jabbed infected people is likely to be in fact “LongJab”. The Endotoxin hitting the Mother transmits the inflammatory response to the Foetus.

We look forward to Pfizer publishing its detailed findings on the trial subjects who were HIV positive before and after recruitment.

1. An Urgent Update to the Global Demyelination Epidemic Hypothesis – Sudden Deaths/Long COVID explained?

2. Shin Jie Yong. 2021. Persistent Brainstem Dysfunction in Long-COVID: A Hypothesis. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7874499/

3. Parkinson's Disease after Pfizer jabs most likely due to Endotoxin in every vial

4. Fatigue, Headache, Muscle Pain, Fever and Chills after Pfizer Jabs match Endotoxin Effects

5. Diarrhoea and Vomiting brought to you by Pfizer

6. Endotoxins in Pfizer jabs mimic Nickel Allergy

7. Atrial Fibrillation is the most common type of Tachycardia, Anaphylaxis leading to Sudden Death caused by Endotoxin in mRNA Jabs

8. Sabatino JJ Jr, et al. 2022. Multiple sclerosis therapies differentially affect SARS-CoV-2 vaccine–induced antibody and T cell immunity and function. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8876469/

9. Teratogen Endotoxin in every vial of mRNA Jab

10. Autoimmune Diseases caused by Endotoxin in mRNA Jabs include Myocarditis, Pericarditis Lupus

11. Palmer CD, et al. 2016. Naturally Occurring Subclinical Endotoxemia in Humans Alters Adaptive and Innate Immune Functions through Reduced MAPK and Increased STAT1 Phosphorylation. https://journals.aai.org/jimmunol/article/196/2/668/108870/Naturally-Occurring-Subclinical-Endotoxemia-in

12. Mureith MW, et al. Exposure to HIV-1 encoded TLR8 ligands enhances monocytes response to microbial encoded TLR2/4 ligands. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2902699/

13. Morris MC, et al. 2014. Innate immune programing by endotoxin and its pathological consequences. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4285116/

14. https://en.wikipedia.org/wiki/Shwartzman_phenomenon