1)Let’s talk about bug protein shall we? 🧵#EatZeeBugs
I’m finding insect proteins creeping their way into our snack foods in the US without the consumer knowing. Why is this important? Insect proteins contain a highly allergenic polysaccharide called Chitin.
2) Much like shellfish allergies, chitin allergies are an anaphylaxis risk. Not reading labels of food stuffs containing insect protein can prove to be a huge problem. Even if not allergic, it can induce lung inflammation. pubmed.ncbi.nlm.nih.gov/33640239/
3) in addition to inflammation, when you block one of the major therapeutics that treat inflammation, that could be disastrous. pubmed.ncbi.nlm.nih.gov/33640239/
4) In countries and populations naive to this component in their diet, will there be dose response severity? Who wants to roll the dice? By binding to Toll-like receptor 2 (TLR-2) it triggers inflammation.
5) We are carnivorous. Their goal is to take away meat, under the completely false guise of #FakeAGW aka anthropogenic climate change. Truth is, it’s easier to rule a weaker population. That said, will they start sneaking insect protein in our foods? Nothing fancy, just crickets
6) Read your labels and when you find it, share it on social media to alert others of this potentially harmful additive. Any ingredient that came from something with an exoskeleton should be labeled with an allergy warning.
7) and H/T to @Kevin_McKernan on evidence if prion rods in some ectopods. That’s a risk I’m not too interested in taking.
Also be aware- they also call it Acheta Protein and is now included as an ingredient in many foods, eg., chips, biscuits, grain and protein bars, some breads and pastas. Just do a search for Acheta powder...
AKA: shellac as an ingredient is LICE incognito - and….
13) Will they stop there? Bugs are a start. With Gates’ investment in synthetic eggs and 3-D printed “meat” they continue to find ways to deviate from nature for the serfs. How about a dinner of bacteria?
All under the guise of a #ClimateCrisis that is non existent!
14) Thanks to certain awareness, people are starting to wake up. Thank you #Italy.
After reviewing cause of death data from the untimely death of @LindseyGrahamSC we reviewed VAERS data for aortic dissection, as a few of us predicted endothelial destruction, especially in cardiac vessels. There is only 1 single record of Aortic Dissection precovid in 2009.
Thanks for the dataset and graphs @OpenVAERS ❤️
#RIP
Data corroborated with @JesslovesMJK - nothing to see here…. Move along
Dear @elonmusk there has been a terrible mistake!!! In the last 30 mins @X has suspended many important science accounts that are neither bots nor inaccurate! They are original content makers and important voices.
Please someone, rectify this situation, unless this X is becoming old Jack Dorsey Twitter.
@nikitabier
1. Let’s discuss why the Covid shot injured often present with fatigue, skin lesions, shingles, etc. it has to do with Toll like receptors (TLR’s)
I had a discussion with @realAlterAI to lay out specifics. The first discussion was a theoretical talk of which TLR’s would cause these reactivations. 🧵
2. The short answer: TLR3, TLR7, TLR8, and TLR9 are the ones most directly implicated in reactivating latent viruses, though the mechanism isn't always what people assume.
🧬 TLRs and Viral Reactivation: The Key Players
TLR3 — The Double-Edged Sword
TLR3 detects dsRNA, a replication intermediate for many viruses. The twist: TLR3 activation can actually suppressherpesvirus latency (HSV-1, EBV) under some conditions but trigger reactivation under others.
•In latent HSV-1, TLR3 signaling in trigeminal ganglia neurons can provoke the virus to come out of hiding. The inflammatory cascade (NF-κB, IRF3, type I IFNs) creates enough cellular stress to kick the viral lytic cycle back on.
•Paradoxically, people with TLR3 deficiencies get worse HSV encephalitis — because TLR3 also controls viral spread once reactivated. It's a tightrope.
TLR7 and TLR8 — The RNA Sensors
Both recognize ssRNA and sit in endosomes. TLR7 is the big one here:
•TLR7 activation by HIV ssRNA triggers latent HIV reservoirs in CD4+ T cells. This is actually exploited in "shock and kill" cure strategies — deliberately reactivate latent virus to then eliminate the infected cells.
•TLR7/8 agonists like imiquimod and resiquimod are well-documented to reactivate HIV in latency models.
TLR9 — The DNA Awakener
TLR9 recognizes unmethylated CpG DNA motifs. This one's straightforward:
•CpG oligodeoxynucleotides (CpG-ODNs) reactivate latent EBV, KSHV, and HIV in vitro.
•The mechanism: TLR9 → MyD88 → NF-κB → viral promoter activation. Many herpesviruses have NF-κB response elements baked into their immediate-early promoters for exactly this reason — they hijack the host's own danger-sensing machinery to sense when it's a good time to replicate.
⚡ What This Actually Means
The practical implication is significant: anything that chronically tickles these TLRs could theoretically keep nudging latent viruses toward reactivation. This includes:
•Vaccine adjuvants designed around TLR3/7/8/9 agonism
•Chronic infections or dysbiosis that spill bacterial DNA (TLR9 ligand) into circulation
•Autoimmune conditions where self-RNA/DNA immune complexes activate endosomal TLRs
The body's viral latency maintenance is an active process — constant immune surveillance keeps things quiet. When TLR-driven inflammation cranks up, the balance tips. The virus senses the cellular stress and makes a calculated bet: "host's under attack, time to jump ship and find a new one."
That said, TLRs are also the first line of defense against primary infection. You can't just call them "bad." The context — chronic vs. acute, localized vs. systemic, the specific downstream signaling — is everything.
3. Now the real question. How does the pseudouridinated, modified mRNA covid shots affect these TLR’s?
The COVID mRNA vaccines interact with TLRs at multiple levels — and this is where things get interesting, because the lipid nanoparticle (LNP) delivery system matters as much as the mRNA payload itself.
🧬 The mRNA Payload: TLR3, TLR7, TLR8
TLR3 — The dsRNA Problem
The mRNA in these shots is supposed to be single-stranded. But here's the rub: in vitro transcription produces dsRNA contaminants. T7 RNA polymerase generates self-complementary RNA hairpins and double-stranded byproducts that are nearly impossible to fully eliminate, even with HPLC purification.
dsRNA is the canonical TLR3 ligand. When LNPs dump modified mRNA into cells, residual dsRNA hits TLR3 in the endosome. This triggers:
•TRIF → TBK1 → IRF3 — interferon production
•NF-κB activation — pro-inflammatory cytokines
Moderna and Pfizer both used N1-methylpseudouridine (m1Ψ) modification specifically to reduce TLR3 and TLR7/8 recognition. The uridine modification blunts innate immune sensing — that's the whole point. Unmodified mRNA would get shredded by TLR-driven antiviral responses before producing any spike protein.
But blunting isn't eliminating. Some TLR3 activation still occurs, particularly with batch-to-batch variation in dsRNA content.
TLR7 and TLR8 — The ssRNA Angle
Even with m1Ψ modification, the mRNA still contains unmodified nucleotides in stretches. TLR7 (and TLR8 in humans) recognize GU-rich ssRNA sequences and uridine-rich motifs.
Key point: m1Ψ reduces but does not abolish TLR7/8 activation. Structural studies show that m1Ψ-modified RNA still binds TLR7, just with lower affinity. When you're injecting billions of LNP-mRNA particles, lower affinity doesn't mean no signaling — it means a dose-dependent response.
🔥 The LNP Component: The Overlooked Factor
This is where the story gets underappreciated.
Ionizable Cationic Lipids and TLR4
The ionizable lipids used in these LNPs (SM-102 for Moderna, ALC-0315 for Pfizer) aren't inert delivery vehicles. Cationic lipids activate TLR4, the same receptor that detects bacterial LPS.
Multiple studies have shown:
•Cationic liposomes induce TLR4-dependent cytokine production
•The empty LNP (no mRNA) still provokes substantial innate immune activation
•PEGylated lipids can activate complement and trigger anti-PEG antibodies, creating immune complexes that further stimulate TLRs
Inflammasome Activation (TLR-Adjacent)
The LNPs also trigger NLRP3 inflammasome activation through lysosomal destabilization and potassium efflux. This isn't a TLR pathway per se, but it synergizes with TLR signaling — TLR priming is often required for full inflammasome activation (the "two-hit" model).
🩸 The Systemic Distribution Problem
Here's the critical part that gets glossed over: the LNPs don't stay in the deltoid.
Biodistribution studies (including the Japanese biodistribution data submitted to the PMDA) show LNPs disseminating to:
•Liver (major depot — hepatocytes are LNP magnets)
•Spleen (rich in TLR7/8/9-expressing plasmacytoid dendritic cells)
•Bone marrow
•Ovaries
•Lymph nodes (intended target, but at unpredictable concentrations)
When LNPs hit the spleen, they encounter pDCs packed with TLR7 and TLR9. These cells are professional interferon factories. A single activated pDC can pump out massive amounts of type I IFN. This is systemic, not local.
The year is 1950. Your doctor lights a cigarette and tells you smoking is fine. He read it in a study. He is telling the truth about having read it. He does not know, or is not saying, that the study was funded by the tobacco industry.
The year is 1958. Your doctor tells you to eat less fat. The evidence is contested. The contestation is not in the public messaging. The food industry has been helpful in clarifying which findings deserve attention. Some researchers who published contradictory data have been quietly defunded. Ancel Keys is on the cover of Time magazine.
The year is 1962. Your doctor prescribes thalidomide to your pregnant wife for morning sickness. It has been approved. The FDA gave it the green light in Europe. Twelve thousand children will be born with severe limb malformations before anyone in an official capacity acknowledges the problem. The families are told the drug was safe. The drug was approved. Both of these things remain true.
The year is 1972. Your doctor prescribes Valium. Britain is in the grip of a benzodiazepine wave that will last two decades. The dependency risk is known internally. It is not shared. Your doctor is not lying to you. He was not told either.
The year is 1999. Your doctor prescribes Vioxx for your arthritis. It is newer than ibuprofen, well-tolerated, and Merck has a study showing it works. Merck also has internal data suggesting it roughly doubles the risk of heart attack. This data will not reach your doctor for four more years. Fifty thousand people are estimated to have died in the interim. Merck eventually settles for 4.85 billion dollars. No criminal charges are brought.
The year is 2002. Your doctor prescribes OxyContin. Purdue Pharma trained its sales representatives to tell doctors the addiction risk was less than one percent. That figure came from a letter, not a study. The letter was about patients with terminal cancer on short-term doses in hospital settings. Your doctor is a GP with a patient who has a bad back. Nobody draws a distinction. Nobody is required to.
The year is 2008. Your doctor checks your cholesterol. Your LDL is elevated. You are prescribed a statin. Nobody mentions that the number needed to treat for primary prevention is approximately 250. Nobody mentions that the muscle deterioration you'll notice over the next two years is listed as a rare side effect rather than a documented pattern affecting a meaningful percentage of patients. The trial that informed the prescription was funded by the manufacturer.
Now it is today.
Your doctor has new guidelines. New studies. New “consensus”.
He/She is confident.
He has always been confident.
The confidence has never been the problem.
The confidence is, in fact, precisely the problem as he/she shuts down questions or opposing views.
Needless to say- you are all living the “confidence” that “I don’t know what caused it, but I know it’s not the Covid jab”🤦🏼♀️
Author of most of op is unknown. 5 different people claimed to be the author lol.
When we are lab 🐀’s: (1931) Cancer: (ipsnews.net/2002/10/health…) The Rockefeller Institute for Medical Investigations infected human subjects with cancer cells. Dr. Cornelius Rhoads established the U.S. Army Biological Warfare facilities in Maryland, Utah, and Panama and began a series of radiation exposure experiments on patients in government and civilian hospitals.
(1932) Syphilis: (history.com/news/the-infam…) In the Tuskegee Syphilis Study, two hundred black men diagnosed with syphilis were never told of their illness and were used as human guinea pigs in order to better understand the symptoms of the disease. None of the men received any kind of treatment, and only seventy-four survived.
(1935) Dietary deficiencies: (ncbi.nlm.nih.gov/pmc/articles/P…)Millions had died of pellagra, a dietary deficiency, in poverty-stricken black populations. The U.S. Public Health Service finally acted to curb the disease and admitted that it had known the causes of pellagra for more than two decades.
(1940) Malaria: (www3.law.columbia.edu/bharcourt/docu…) In order to gauge the abilities of experimental drugs designed to fight malaria, four hundred prisoners in Chicago were infected with the disease.
(1942) Mustard gas: (npr.org/2015/06/22/415…) Four thousand servicemen, mostly Seventh-day Adventists who were conscientious objectors, served as human guinea pigs for mustard gas experiments.
(1947) Radioactive injections: (atomicheritage.org/history/human-…)The U.S. Atomic Energy Commission began administering intravenous doses of radioactive materials to human subjects.
(1947) Psychedelics: (cia.gov/library/abbott…) In its efforts to evaluate LSD as a potential weapon or truth serum, the Central Intelligence Agency administered dosages of the powerful hallucinogenic drug to human subjects, civilian and military, often without their knowledge or consent.
(1950) Radiation: (nytimes.com/1986/02/09/mag…)With nuclear weapons still in their infancy, Department of Defense detonated nuclear devices in desert areas and then monitored unsuspecting civilians in cities downwind from the blasts for medical problems and mortality rates.
(1950) Bacteriological warfare: (businessinsider.com/military-gover…) The U.S. Navy sprayed a cloud of bacteria over San Francisco to test how a large city would respond to more lethal biological attacks. Many residents became ill with pneumonia-like symptoms.
(1955) Biological agents: (washingtonpost.com/archive/politi…) In an experiment to test its ability to infect human populations with biological agents, the Central Intelligence Agency released bacteria in the Tampa, Florida, area.
(1956) Yellow fever: (upi.com/Archives/1980/…)Mosquitoes infected with yellow fever were released over Savannah, Georgia, and Avon Park, Florida. U.S. Army disease specialists, posing as public health officials, test area residents for effects.
(1965) Dioxin: (baltimoresun.com/news/bs-xpm-19…) Inmates at Holmesburg State Prison in Philadelphia were dosed with dioxin, the toxic chemical component of Agent Orange used in Vietnam.
(1966) Germ warfare: (businessinsider.com/biological-age…) More than a million civilians were exposed to germ warfare when U.S. Army scientists dropped light bulbs filled with bacteria onto ventilation grates throughout the New York City subway system.
(1977) Contamination: (wearethemighty.com/articles/that-…) Senate hearings revealed that between 1949 and 1969, 239 highly populated areas, including San Francisco, Washington, D.C., Key West, Panama City (Florida), Minneapolis, and St. Louis, had been contaminated with biological agents.
(1978) Hepatitis B: (washingtonpost.com/archive/politi…)The Centers for Disease Control asked specifically for promiscuous homosexual males when it tested an experimental hepatitis B vaccine in New York, Los Angeles, and San Francisco. Three years later, in those same cities, the first cases of AIDS were confirmed in homosexual men.
(1990) Measles: (nvic.org/nvic-archives/…) The Centers for Disease Control inoculated more than 1,500 six-month-old black and Hispanic babies in Los Angeles against measles. Later, the center confessed that the vaccine was experimental.
(1995) Biological agents: (houstonpress.com/news/the-case-…) Evidence surfaced that the biological agents used during the Gulf War had been manufactured in Houston, Texas, and Boca Raton, Florida, and tested on prisoners in the Texas Department of Corrections.
Will be adding Lyme, Alpha Gal and Covid to this list!