Quote from: o_e_l_e_o on Today at 10:22:36 AM

If my data are cherry picked, then where are all the data showing that vaccines don't work?

SARS-CoV-2 has non-human reservoirs and is now endemic. It will never go away. Period. It cannot be eradicated by vaccination, and anyone telling you it can be straight-up eradicated like smallpox with a high level of vaccination is lying. The current agenda of boosters will lead, inevitably, to bi-yearly shots, because the vaccine antibodies are waning within 6 months.

https://www.medicalnewstoday.com/articles/waning-immunity-and-covid-19-vaccines-how-worried-should-we-be

https://www.realclearscience.com/articles/2021/08/23/lets_stop_pretending_about_the_covid-19_vaccines_791050.html

The rate of breakthrough cases is much, much higher than we are being told, because public health agencies are engaging in deliberately lax surveillance for them to make the vaccine appear more effective than it really is.

https://fee.org/articles/what-is-the-true-vaccine-breakthrough-rate-the-cdc-doesnt-want-you-to-know/

https://www.cbsnews.com/news/new-covid-19-cases-united-states-almost-all-among-people-unvaccinated/

There is a preprint paper indicating that current SARS-CoV-2 strains are about to completely escape antibodies produced by these vaccines, and that the antibodies may even become non-neutralizing and infection-enhancing:

https://www.biorxiv.org/content/10.1101/2021.08.22.457114v1

Shi Zhengli's own work indicates that betacoronaviruses such as SARS and MERS may have Dengue-like ADE:

https://journals.asm.org/doi/10.1128/JVI.02015-19

I tried raising the alarm on this back in February of 2020 and it went mostly ignored.

Vaccines failing due to inducing immune sensitization has a historical precedent in the recent past. Sanofi's Dengvaxia vaccine failed because it triggered enhanced disease.

https://jeffreydachmd.com/2021/08/director-of-cdc-rochelle-walensky-warns-of-ade-antibody-dependent-enhancement-from-israel-data/

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8427162/

Quote from: o_e_l_e_o on Today at 10:22:36 AM

The MATH+ protocol is written by a scan organization, provides no data to support their recommendations, and is headed by individuals with vested interests in the fake treatments they recommend. Looking at the treatments they and you are suggesting:

Vitamin C:

Quote from: https://www.covid19treatmentguidelines.nih.gov/therapies/supplements/vitamin-c/

There are no controlled trials that have definitively demonstrated a clinical benefit for vitamin C in critically ill patients with COVID-19, and the available observational data are inconclusive.

People with COVID-19 hyperinflammation are suffering from a form of sepsis.

https://www.healthleadersmedia.com/clinical-care/expert-severe-covid-19-illness-viral-sepsis

https://pubmed.ncbi.nlm.nih.gov/34590796/

It has previously been suggested that antioxidants are useful for treating sepsis, because sepsis involves the over-activity of pro-oxidant enzymes that the body uses to fight infection.

https://journals.lww.com/ccmjournal/Abstract/2007/09001/Antioxidant_supplementation_in_sepsis_and_systemic.25.aspx

It is entirely possible that COVID-19 hyperinflammation is, much like Keshan disease, a disease of low antioxidant capacity (redox equilibrium issues in the body due to chronic oxidative stress, i.e., endothelial dysfunction) that can be counteracted by raising levels of antioxidant substrates, such as selenium, glutathione, et cetera.

Many people who died of COVID-19 had issues pointing towards low antioxidant capacity. Low Vitamin D, low glutathione, low selenium, and so on.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7385774/

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7937041/

https://pubmed.ncbi.nlm.nih.gov/32463221/

This points to an inescapable conclusion; COVID-19 causes death by aggressive lipid peroxidation brought on by sepsis.

Though antioxidants seem like a logical counter to this (in South Korea, they tested the NADPH oxidase inhibitor APX-115 against the virus), there is no guarantee that they will have bioavailability to the affected cells. I'm not completely gung-ho about it; I understand that there are serious challenges involved here, and that what looks promising on paper may not always improve a patient's condition.

People are hunting for a magic bullet for COVID-19, but no such magic bullet exists. In my opinion, the best prophylaxis against COVID-19 is a balanced, micronutrient-rich diet, strenuous exercise, and maintaining a healthy BMI, because this induces physiological changes in the vasculature that make them more resilient (it raises nitric oxide levels and antioxidant capacity and reduces oxidative stress). This is reflected by evidence. COVID-19's severity is GREATLY enhanced with increasing body mass index.

https://www.sciencedirect.com/science/article/abs/pii/S1262363620300975?via%3Dihub

This isn't just a get-healthy-quick pill. It's a lifestyle change. It's also why I recommend against lockdowns, and perhaps for more aggressive distancing (as in 15+ feet) to compensate. A good, solid crosswind will blow any aerosols away, and UV from direct sunlight will degrade and destroy the virions. The greatest risk of transmission is mostly indoors, in tightly-packed rooms with stagnant air.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7673425/

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8305330/

People should be outdoors, they should be jogging and biking, and they should be maintaining a high activity level. Becoming sedentary makes COVID-19 infections way, way worse. It turns the blood vessels into a buffet table for the virus.

Quote from: o_e_l_e_o on Today at 10:22:36 AM

Fluvoxamine:
No evidence. Biggest ongoing trial to date (https://clinicaltrials.gov/ct2/show/study/NCT04668950) has just reported "No treatment effect" on early results.

That's disappointing, if true. I have been in contact with pharmacology experts who claimed anecdotal evidence for fluvoxamine improving patients' conditions, but there do have to be well-designed clinical trials to show whether or not it has any benefit. There are many plausible mechanisms by which fluvoxamine may improve a patient's condition.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8094534/

Quote from: o_e_l_e_o on Today at 10:22:36 AM

Budesonide does have some evidence, but it is inferior to IV dexamethasone which we have been using for all our inpatients for months.

Again, disappointing. Also, a little odd, given how promising it seemed before.

https://pubmed.ncbi.nlm.nih.gov/33844996/

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8310374/

Quote from: o_e_l_e_o on Today at 10:22:36 AM

The links in your original letter consider these drugs in the context of rodent peptic ulcers, among other things. Hardly applicable to humans with COVID.

Not necessarily true. Those papers describe a mechanism. While I would never argue that rodent gastric cells are the same thing as human airway or vascular epithelial or endothelial cells, there are many features that are homogenous between different eukaryotic cell lines, and an effect demonstrated in one type of cell might also be applicable to another. It's not conclusive proof of therapeutic effect, but it does point towards a fresh avenue of study.

The problem I have is that these drugs aren't really being studied as aggressively as they should be. There should be more trials of antioxidants, not just one or two here and there. They keep pushing antivirals that don't seem to work on hyperinflammatory COVID-19, when, at the very least, antioxidants have a plausible therapeutic mechanism. You'll never know if you never look.

I don't think any one drug will treat this on its own, but perhaps a cocktail of these may provide a marginal benefit. The trouble is that hyperinflammatory COVID-19 is a real son of a bitch.

Quote from: o_e_l_e_o on Today at 10:22:36 AM

There's some truth in this, but not to degree you state. If there was enough hypochlorous acid to destroy hemoglobin to such a degree, why do we not see a severe hyperchloremic acidosis?

See the following:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7757048/

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3222650/

This would be a logical result of neutrophilia and NETosis in COVID-19. Let's review the papers on that for a moment.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8376580/

https://www.sciencedirect.com/science/article/pii/S221249262030052X

Okay, so there are lots of NETs around. More than macrophages can reasonably be expected to clean up in a reasonable time frame. So, there is going to be a lot of extracellular myeloperoxidase lying around, making hypochlorous acid from hydrogen peroxide and chloride ions.

This would, necessarily, lead to the liberation of iron and tons of Fenton reagent lying around.

https://pubmed.ncbi.nlm.nih.gov/33974898/

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7836924/

Though metabolic and respiratory alkalosis are more common, some critically-ill COVID-19 patients who died did indeed have severe acidosis.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7236721/

https://pubmed.ncbi.nlm.nih.gov/33103442/

COVID-19 causes glucose and lipid-handling issues, as well.

https://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1009243

https://pubmed.ncbi.nlm.nih.gov/33043283/

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7570435/

The metabolic shifts are rather profound.

Quote from: o_e_l_e_o on Today at 10:22:36 AM

Why do we not see profound anemia due to hemoglobin destruction?

Decreased serum hemoglobin and increased serum ferritin have been found in COVID-19:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7753740/

https://casereports.bmj.com/content/13/12/e238118

https://link.springer.com/article/10.1007%2Fs10654-020-00678-5

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7267810/

Quote from: o_e_l_e_o on Today at 10:22:36 AM

Why does intubation and proning make the SpO₂ go from 70% to 95%? Why does it make the PaO₂ go from 60 mm Hg to 120 mm Hg?

Trying to claim that intubation and ventilation is actively killing people is just plain incorrect.

I said, in the letter, that it was a catch-22, because you need oxygen to live. Intubation does increase oxygenation, but also causes VILI-like damage and additional oxidative stress alongside that.

It's not just a blood problem. The blood-air barrier itself and gas exchange across it are also compromised due to the endothelial injury itself:

https://www.tandfonline.com/doi/abs/10.1080/21688370.2021.1937013?journalCode=ktib20

ARDS/Acute Lung Injury involves a great deal of neutrophilia in the pulmonary vasculature and oxidative damage to the tissues.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6801694/

Quote

Overproduction of oxidants and decrease in antioxidants lead to oxidation changes and cross-linking of proteins, lipids, DNA, and carbohydrates, deterioration of cell structures and their function, increased endothelial permeability and lung oedema formation, pulmonary epithelial dysfunction with impaired sodium ion transport and fluid reabsorption from the alveoli etc. [12]. In addition to intrinsically generated oxidants derived from phagocytic cells (recruited neutrophils and residential lung macrophages) and alveolar epithelial and endothelial cells [13], additional important source of oxidants is an inhalation of high oxygen concentrations used for mechanical ventilation of patients with severe ARDS [14].

Highly concentrated oxygen, like from mechanical ventilation, makes the oxidative stress of ARDS worse. In a virus like SARS-CoV-2 that suppresses antioxidant defenses of cells, this exacerbates the lipid peroxidation.

There are heaps of evidence that this is occurring.

https://www.nature.com/articles/s41420-020-00369-w

Quote

Ferroptosis can be classified into canonical and non-canonical types to date. Canonical ferroptosis is started with the failure of glutathione peroxidase (GPX4) defense, leading to excessive lipid peroxidation and cell death18. Inactivation of GPX4 and glutathione (GSH) depletion play a central role in the induction of canonical ferroptosis18,19. Iron (II) oxidizes lipids in the Fenton reaction (hydrogen peroxide, iron and lipid) is the hallmark feature of ferroptosis, thereby generating lipid ROS, causing cell membrane damage17,18,19. GPX4 eliminates lipid ROS by consuming GSH and protects cell membrane against lipid peroxidation and ferroptosis18. Moreover, cystine/glutamate transporter (xCT) is responsible for providing cystine to produce GSH for GPX4 to function normally. Iron is an important metal in cells. But there is no efficient mechanism for excreting iron in the human body and, as a result, iron homeostasis is vulnerable to stresses.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7357498/

Quote

Since the WHO declared COVID-19 a pandemic, a great effort has been made to understand this serious disease. Thousands of studies are being devoted to understanding its epidemiology, its molecular characteristics, its mechanisms, and the clinical evolution of this viral infection. However, little has been published on its pathogenesis and the host response mechanisms in the progress of the disease. Therefore, we propose a hypothesis based on strong scientific documentation, associating oxidative stress with changes found in patients with COVID-19, such as its participation in the amplification and perpetuation of the cytokine storm, coagulopathy, and cell hypoxia. Finally, we suggest a therapeutic strategy to reduce oxidative stress using antioxidants, NF-κB inhibitors, Nrf2 activators, and iron complexing agents. We believe that this hypothesis can guide new studies and therapeutic strategies on this topic.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8106525/

Quote

To determine NO-derived oxidants, we measured systemic levels of nitrotyrosine in the plasma from healthy controls and COVID-19 patients (Fig. 5). Nitrotyrosine levels were significantly higher among patients with COVID-19 compared to healthy controls (107.049 ± 7.907 nM vs 44.7606 ± 12.85 nM; P<0.0001; Fig. 5A). Analysis by race showed a significant increase in nitrotyrosine levels both in Caucasian COVID-19 patients (108.2 ± 13.62 nM vs 48.54 ± 16.92 nM; p = 0.01; Fig. 5B), and in African Americans COVID-19 patients (106.2 ± 10.01 nM vs 40.69 ± 22.01 nM; p = 0.006; Fig. 5C) compared to respective race matched controls.

Elevated serum nitrotyrosine = lots of peroxynitrite = lots of superoxide depleting nitric oxide = oxidative stress. It's a smoking gun.

Venting without protecting the cells from this lipid peroxidation will increase the inflammation and edema and make gas exchange across the capillaries even worse.

Treating sepsis is time-sensitive, because once lipid hydroperoxides are allowed to form, they recursively create inflammation and more lipid peroxidation in a positive feedback loop (PRRs pick up the signature of oxidatively-modified lipids, and the body starts forming autoantibodies against those lipids). Late treatments do nothing.

Early and proactive use of antioxidants, steroids, and non-invasive ventilation would likely render intubation pointless.

Quote from: o_e_l_e_o on Today at 10:22:36 AM

OK, so show me the randomized control trials which show ivermectin is an effective prophylactic. There is currently no evidence for this either:

Quote from: https://www.bmj.com/content/373/bmj.n949

Owing to very low certainty of evidence, the effect of ivermectin, compared with standard care, in reducing the risk of suspected, probable, or laboratory confirmed infection remains very uncertain; the certainty of evidence was rated down because of serious risk of bias and very serious imprecision.

I'm happy consider any treatment provided there is some evidence it works. You have failed to provide that evidence.

See for yourself who they enrolled for all the RCTs the media is citing as proof of the ineffectiveness of antivirals, like Oxford's completely botched RECOVERY study.

https://covexit.com/recovery-covid-19-research-blasted-for-toxic-dosage-towards-oxfordgate/

https://www.ox.ac.uk/news/2020-06-05-no-clinical-benefit-use-hydroxychloroquine-hospitalised-patients-covid-19

These studies virtually all enroll people who have COVID-19 hyperinflammation, have been symptomatic for around a week or more, and have been hospitalized. I have already explained why this is futile. The virus is gone. And I mean, it's gone. It's too late.

https://www.mdpi.com/1999-4915/13/6/963/htm

Quote

Figure 1. Course of COVID-19 and clinical benefits of antivirals. Following an incubation period of 3–6 days, SARS-CoV-2 infection generates a broad spectrum of clinical manifestations ranging from asymptomatic infection and mild illness to severe disease with high mortality. Viral load peaks around the day of symptom onset and rapidly declines thereafter. Accordingly, antiviral drugs like remdesivir (RDV) will only be effective early in infection when the number of new cells that become infected is still high. Antibody levels increase gradually and are commonly detectable after 7–14 days. Excessive immune responses, which may be curtailed by immunosuppressive agents like corticosteroids, lead to organ damage, intensive care admission, or death. Adopted from [19].

The same complaints are echoed by the COVID-19 Early Treatment Fund.

https://www.treatearly.org

Aggregations of early treatment studies do show a consistent benefit, not just for Ivermectin, but for early treatment in general.

https://ivmmeta.com

https://c19early.com

The problem is that doctors are sending patients home without treating them.

https://www.chicagotribune.com/coronavirus/ct-coronavirus-hospitals-sending-covid-patients-home-illinois-20201211-hsjihn5h2vc5famcappyjscrsy-story.html

https://www.houstonchronicle.com/news/investigations/article/Presumed-COVID-19-patients-often-sent-home-from-15385076.php

This widespread failure-to-treat is what is leading to unnecessary fatalities. Early outpatient treatment has not been tried on a large scale.

Quote from: o_e_l_e_o on Today at 10:22:36 AM

An article written by a computer scientist and a practitioner of "energy medicine", published in a fake journal which is not listed in PubMed, has no publisher, has literally zero impact factor, which is ran by a young Earth creationist and a lawyer who sues vaccine companies on behalf of "victims". And even then, they still state "there are no studies demonstrating definitively that this is happening". Roll Eyes

Come on. You seem smart enough to realize just how disingenuous and dishonest something like this is.

Very well, then. I shall go over my concerns in brief, citing my own letter (which, in turn, cites many other files).

https://mega.nz/file/HZNmyRKB#xF15FrsAEZkwBPi4tdUP5toBBqeRHDJJAHzZt6Hg_Qg

-The vaccine is not sterilizing and does not prevent transmission. The vaccinated are still contagious to others. This means that the virus no longer has any pressure to become less virulent; mutations that could be lethal to the unvaccinated may only cause a mild increase in illness in the vaccinated.

-Natural immunity from a prior infection results in antibodies to all of the virus's proteins, not just one.

-All of the current COVID-19 vaccines have undergone highly accelerated trial periods, not allowing any time for long-term side effects to appear.

-Messenger RNA vaccines, which deliver the active form of genes to cells to synthesize viral proteins and produce an antigen response that way, have never been tested in humans before. In Moderna's case, mRNA-1273 is actually their first-ever commercial product. Would you willingly put a company's first-ever product in your body?

-The production and validation of these vaccines involved fetal cell lines, which some may object to.

-The lipid nanoparticles from the mRNA vaccines have been shown to bioaccumulate all over the body, and do not stay in the shoulder.

-The PEGylated lipid nanoparticles in mRNA vaccines can occasionally trigger severe allergic reactions.

-Damaged mRNA can stall ribosomes by getting jammed in them, causing ribosome attrition and reduced protein synthesis.

-The method of making SARS-CoV-2 Spike inert, inserting prolines on the S1/S2 boundary to rigidly lock the trimers in the prefusion conformation, does not take into account any unexpected proteolysis or further processing of the Spike proteins by the body that may release the S1 subunits, allowing them to travel freely around the body and bind to things.

-SARS-CoV-2 Spike is, in itself, a pathogenic protein, capable of binding to ACE2, integrins, neuropilin-1, and bacterial LPS. It can induce autoantibody responses against healthy tissue, overactivate T-cells with a SAg region, penetrate the blood-brain barrier, and bind to heparin-binding proteins and induce amyloid aggregation and possible neurodegeneration, among many other unknown and possibly pathogenic effects.

-SARS-CoV-2 may have ADE, which means that a future strain may cause antibodies from vaccines based on the sequence of previous strains to become non-neutralizing, turning them into trojan horses that help virions infect leukocytes they would not have otherwise been able to infect.

-Messenger RNA that codes for Modified SARS-CoV-2 Spike may be integrated into the genome of cells by endogenous LINE-1 reverse transcription. There is a plausible mechanism whereby it can integrate itself into your DNA. That means that this is, in fact, potentially a gene delivery system.

Out of all of these, the most appalling thing is this:

https://pubmed.ncbi.nlm.nih.gov/33328624/

Quote

We show that intravenously injected radioiodinated S1 (I-S1) readily crossed the blood-brain barrier in male mice, was taken up by brain regions and entered the parenchymal brain space.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7988450/

Quote

The post-infection of COVID-19 includes a myriad of neurologic symptoms including neurodegeneration. Protein aggregation in brain can be considered as one of the important reasons behind the neurodegeneration. SARS-CoV-2 Spike S1 protein receptor binding domain (SARS-CoV-2 S1 RBD) binds to heparin and heparin binding proteins. Moreover, heparin binding accelerates the aggregation of the pathological amyloid proteins present in the brain. In this paper, we have shown that the SARS-CoV-2 S1 RBD binds to a number of aggregation-prone, heparin binding proteins including Aβ, α-synuclein, tau, prion, and TDP-43 RRM. These interactions suggests that the heparin-binding site on the S1 protein might assist the binding of amyloid proteins to the viral surface and thus could initiate aggregation of these proteins and finally leads to neurodegeneration in brain. The results will help us to prevent future outcomes of neurodegeneration by targeting this binding and aggregation process.

Not good. Huge red flag. As in, do not inject this shit into your body unless you've already written your will and were planning to check out in a few years anyway.

Quote from: ICENI_Spartacus on September 30, 2021, 09:42:53 PM

And the rest of your links go the same way as this one, and the same way as your original letter - off the deep end of conspiracy theories with absolutely no supporting evidence or facts.

You said there was no proof that mind-controlling nanoparticles existed. I showed you that not only do they exist, and not only did James Giordano give presentations about them before an entire class of stunned cadets at West Point, they are described explicitly in publicly-available materials.

Not only that, DARPA, DTRA, and vaccine researchers are intimately connected both to brain-computer interface research, and to GOF research at the Wuhan Institute of Virology.

The degrees of separation here are minuscule. When plotted out on a node graph, they would all cluster together. David Martin and M-CAM showed, beyond a shadow of a doubt, that GOF SARS strains and their features are basically patented products.

That's not a conspiracy theory. That is a RICO case the size of Mount Everest. It is also mass murder and treason.