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COVID Vaccine Side Effects: What Causes Them?
This lengthy excerpt from my COVID vaccine side effect guide is a review of the science that will be useful to anyone trying to understand the causes of these side effects.
I am done with my work on COVID vaccines, at least until I finish my Vitamins and Minerals 101 Book, so I am now making my scientific review on the likely causes of COVID vaccine side effects public.
This is an excerpt of pages 19-52 of my Healing From COVID Vaccine Side Effects guide (free to Masterpass members here) and contains 139 of the 221 references. It does not contain the protocol, but rather the scientific review used to judge the mechanisms most likely underlying the side effects. Since I am no longer working on this, I hope it proves useful to anyone doing further work on the topic. This was originally published on August 10, 2022.
The science described is not intended to be comprehensive. Rather, emphasis is placed on what is likely to provide insights into the mechanisms of side effects.
What Causes COVID Vaccine Side Effects?
Side effects to COVID vaccines could be driven by toxicity of the spike protein, toxicity of the delivery vehicles or minor ingredients, or dysfunctional immune responses to any of these.
One set of clues we can use to tease out these hypotheses is to consider the differences between the virus and the vaccines, and to similarly consider the differences between the different vaccine technologies. If side effects are shared across them all, they are most likely driven by what they share in common. If the side effects profiles differ among them, the differences in side effects may be explained by the differences in their components and in how they are distributed within the body.
Table of Contents
Components of the Natural Virus
Components of the Vaccines
Toxicity of the Vaccine Components
Immune Reactions to the Virus and the Vaccines
Comparing and Contrasting Adverse Effects of Vaccines vs Natural Infection
Comparing and Contrasting Adverse Effects of Different Vaccine Types
What is Driving Vaccine Side Effects?
Components of the Natural Virus
SARS-CoV-2, the virus that causes COVID-19 (hereafter called “COVID” and “the COVID virus”) is a coronavirus. Coronaviruses are named after the Latin word corona meaning “crown” because under electron microscopy the projections on their surface appear as a halo reminiscent of a solar corona, which is the outermost layer of a star’s atmosphere. The virus has a lipid envelope and a protein coat known as a nucleocapsid that it uses to transport the RNA contained in its core. The RNA codes for numerous proteins the virus needs to replicate with the help of human cellular machinery. Among these is the RNA for the spike protein, the most important protein we need to understand for the disease process of the virus, and the only protein we really need to understand when looking at the vaccines.
The spike protein is a spike-shaped protein that sticks out from the viral membrane and is responsible for its ability to bind to, fuse with, and enter human cells. It does this by binding to ACE2, a zinc-dependent enzyme on the surface of human cells.  The normal function of this enzyme is to convert angiotensin II to angiotensin(1-7). These are two compounds that regulate blood pressure and other aspects of physiology. ACE2 under normal circumstances is serving to keep our blood pressure from raising too much by making this conversion.
The spike protein sees ACE2 as a “receptor.”  It first binds to ACE2, and this associates it with the cell surface. Then, a human enzyme called “furin” splits the spike protein into two subunits, one called S1 and the other called S2. Furin is not the only enzyme that does this, but it is extremely ubiquitously expressed throughout human tissues, and because such a ubiquitous enzyme can make this cleavage, the virus can be expansively broad in the number of tissues it can infect. Thus, this cleavage site is named the “furin cleavage site” after the human enzyme. Once the furin cleavage has taken place, a second cleavage breaks the S2 subunit into S2’ (“S2 prime”) and the “fusion peptide.” The spike protein then undergoes a change from a “prefusion” state to a “postfusion” state that involves bending over backwards in a “jacknife” maneuver to stick the fusion peptide in the membrane and fuse the two membranes together. Then, the virus enters the cell.
Some, or perhaps much, of the free subunits can be shed into the circulation and go anywhere once this happens. This is most often discussed for the S1 subunit and is called “S1 shedding.”
Note that the significance for the virus of the prefusion-postfusion transition is that this is involved in entering the cell. However, vaccine manufacturers have an entirely different interest in this transition: during it, sugars move from the inside of the spike protein’s three-dimensional shape to the outside. This can block the immune system from recognizing it and make it less stimulatory to the immune system; that is, less “immunogenic.” To lock it into the most immunogenic shape, most vaccine spike proteins have been “prefusion stabilized.”
Components of the Vaccines
Spike Protein and Its mRNA and DNA
The mRNA (Moderna and Pfizer) and adenoviral vectored (Johnson and Johnson, hereafter “J&J,” and AstraZeneca) vaccines all code for the spike protein with only one or two modifications to the final protein, but substantial modifications to the underlying mRNA and DNA. In the case of mRNA, which is easily attacked by the immune system when outside cells and is normally degraded after a moderate amount of time within cells, the changes help the mRNA evade the immune system and last longer. The adenoviral vectored vaccines deliver DNA rather than mRNA. For both the mRNA and the DNA, the changes are made to make them be expressed into protein at a higher rate. [3–5]
The much more recently authorized Novavax vaccine uses direct injection of the spike protein into humans, rather than the DNA or mRNA that codes for the spike protein. Nevertheless, because the protein is manufactured by inserting its DNA into a virus that infects insect cells, the DNA used in production has been modified to be highly expressed in insect cells. 
The Pfizer, [7 ] Moderna,  and AstraZeneca  vaccines all retain the natural furin cleavage site, while the J&J and Novavax vaccines have had it removed. [6,9] The J&J and Novavax may be less likely to shed the subunits into circulation than the others because of this. However, other enzymes besides furin can split apart the spike protein. In fact, it was recently discovered that neutrophils can digest spike protein into 98 different peptide fragments, three of which are particularly toxic.  So it may be that some tissues but not others have high rates of subunit shedding and that neutrophils would be entirely capable of digesting it into further fragments. The subunits and the neutrophil-digested fragments could then travel anywhere throughout the body.
All but the Astrazeneca have been “prefusion stabilized.” [11,12] This is meant to make them more immunogenic. This should not impact spike protein toxicity. It would if the vaccine spikes were delivered as viruses. While the adenoviral vectored vaccines are technically delivered as viruses, they don’t have membranes that can fuse with human membranes, and they don’t carry spike protein on their surfaces. Thus, any restriction the prefusion stabilization imposes on the fusion peptide is irrelevant.
In terms of the actual biological activity of the spike protein, it should be nearly identical between the virus and the vaccines. This was a major goal of vaccine development, and was supported in the developmental research by showing that the vaccine spike proteins bind to ACE2 like the natural virus does. In fact, the vaccine spike proteins bind to ACE2 more strongly than the spike protein from the natural virus. [3,6,13–16]
In addition to these modifications to spike proteins or their coding nucleotides, the delivery systems of the vaccines employ different technologies, all of which are absent in the natural virus.
The Pfizer and Moderna vaccines are both mRNA vaccines that deliver mRNA using lipid nanoparticles. The exact structure of lipid nanoparticles  is debated within the literature and discussed using theoretical models. They likely are similar to the lipoproteins that carry cholesterol and fat-soluble vitamins in our blood, but several times smaller than an LDL particle and have their cargo arranged differently on the inside.
“Cargo” will be generally used here as the word for the contents being carried and transported by the particles. For the vaccines, the primary cargo is the mRNA.
Lipid nanoparticles are spherical. The outside is lined with phospholipids, which are water-soluble on the outside and fat-soluble on the inside. This allows fat-soluble things to be carried in the water-rich blood (this is why our lipoproteins have them), and allows material with an electric charge (such as mRNA) to stay inside the particle rather than dissolving in the blood.
Cholesterol stabilizes the membrane. Blended with the phospholipids are somewhat similar lipids bearing positive charges (cationic lipids), and others decorated with some variant of polyethylene glycol (PEGylated lipids). Water, sucrose, and various salts keep the pH and osmotic pressure optimized.
The mRNA is found inside the particle. Because it is negatively charged, it is stabilized by binding to the cationic lipids. The cationic and PEGylated lipids help the particles assemble during production. During delivery, it is thought that the PEG keeps the particle in circulation for longer while the cationic lipids help it get released inside cells by destabilizing the membranes of the vesicles that take them in.
Pfizer and Moderna both use lipid nanoparticles, but they use different buffers, variants of PEG, and cationic lipids.
A Pfizer document that was originally leaked was more recently released in a Freedom of Information Act (FOIA) request in a more detailed and formalized yet heavily redacted form.  In this paper, lipid nanoparticles with a radioactive tracer were injected intramuscularly into rats and the distribution of the tracer was monitored for 48 hours. The largest concentration of the tracer was found at the injection site, but it accumulated at high concentrations in the liver, adrenal glands, and ovaries, at somewhat lower concentrations in the bone marrow, and at non-zero concentrations in every single organ tested.
This study used a labeled form of cholesterol that is unable to leave cells and can be detected based on its radioactivity. If the cells take up the particles intact, then the label would tell us exactly which cells were first to take it up. However, as covered below, it is possible that specific components of the particles are exchanged with lipoproteins in the blood, or selectively harvested by some cells, all without the intact particle being taken up. It is also possible that specific components leave cells after being taken up. This study tells us nothing about these processes. Therefore, it does not have the last word on how the cargo is distributed.
In another Pfizer documented first leaked and then later FOIAed,  the nanoparticles were injected into mice using a so-called reporter gene, which expresses the protein luciferase. When activated, luciferase glows like a firefly, and researchers can determine where the luciferase wound up based on which part of the animal is glowing. This doesn’t tell us where the spike protein mRNA would go, because it is possible that the mRNA cargo has some influence on the distribution, but it gets closer than the rat study.
It doesn’t provide so much as a useful hint, however, at how long the spike mRNA lasts, because mRNAs for different genes are widely variable in their stability. This study did make it clear that the luciferase is found in the liver at 6 hours and disappears after 48 hours, but it didn’t clearly report whether the signal could be found in other organs. The graphics in the document are heavily redacted, and the images were clearly selected from among a much larger collection of pictures. For reasons I have described elsewhere, my impression is they are hiding pictures that show a signal in the ovaries.
There is no information available on how the specific cationic and PEGylated lipids in these two vaccines impact their distribution within the body under different physiological states. However, other research using these vehicles suggests that they exchange contents with lipoproteins in the blood,  that if they are injected systemically some 60% is taken up by the liver,  and that enzymes such as lipoprotein lipase (LPL) may be involved in harvesting their components.  This is in addition to their more well-accepted path of cell entry, in which they are taken up intact through processes known as endocytosis and macropinocytosis.
If, in fact, LPL plays a role in harvesting cargo from within these particles, it has enormous implications its biodistribution: 
It would mean that heart, skeletal muscle, and fat are major tissues that take up the cargo.
It would mean that LPL-expressing macrophages would actively bring the cargo into the lungs.
It would allow selective uptake in the brain, kidney, mammary gland, and likely other tissues.
In the fed state on a high-carbohydrate diet, less would be taken up by heart, skeletal muscle, and kidney, and more would be taken up by fat tissue and lactating mammary glands.
In the fasting state, after exercise, during stress, or on a ketogenic diet, much more would be taken up into the heart and skeletal muscle.
If fat tissue acts as a sink in some people, it could act as a release valve later on, potentially introducing a lot of variation in the duration of the contents between people.
The interaction with lipoproteins and enzymes can lead to selective transfer of specific components, not transfer of the entire particle. This emphasizes that there could be alternative patterns of distribution to those shown in the Pfizer rat study. It also underscores how widely variable the distribution could be in different people during different physiological states.
To my knowledge, biodistribution studies for the Moderna vaccine are only available in extremely summarized format in documents produced by regulatory agencies and cannot be analyzed in the same way the Pfizer studies were above.
Further, as discussed in the “Spike Protein mRNA and DNA” section, the spike protein can be cleaved from cell membranes and the cleavage products can be distributed throughout the body. This is not addressed at all in any of the biodistribution experiments.
Adenoviral vectors  are based on infectious viruses known as adenoviruses, which usually cause colds or flu-like illnesses. They are so named because they were originally isolated from adenoids (tonsils). They consist of double-stranded DNA inside a protein coat known as a nucleocapsid that takes a 20-faced shape known as an icosahedron. The AstraZeneca vaccine uses a vector derived from an adenovirus that infects chimpanzees, while the J&J vaccine uses one derived from an adenovirus that infects humans. Their surfaces are highly negatively charged, making them attracted to anything with a positive charge. This plays a role in a particular form of thrombosis (clotting disorder) they have been associated with, which will be discussed further later. Because they are derived from adenoviruses, antibodies to adenoviruses with which one has been previously infected can make them less effective.
There are a rather large collection of molecules on a cell surface that can act as receptors for adenoviruses or vectors derived from them,  making the potential uptake by different tissues hard to predict but certainly very broad.
In theory, these vectors are “replication incompetent” meaning they can’t reproduce like infection-causing viruses. However, certain cell lines used in labs allow them to replicate, so it may be that they replicate in humans in certain cells of certain tissues under certain conditions.  While these vaccines contain the DNA for the spike protein and that is the main protein expressed in the cells they enter, there is low-level expression of the other viral proteins in these cells.
To my knowledge, biodistribution studies for the adenoviral vectored vaccines are only available in extremely summarized format in documents produced by regulatory agencies and cannot be analyzed in the same way the Pfizer studies were above.
Further, as discussed in the “Spike Protein mRNA and DNA” section, the spike protein can be cleaved from cell membranes and the cleavage products can be distributed throughout the body. This is not addressed at all in any of the biodistribution experiments.
For the Novavax vaccine, a virus is engineered to express the spike protein and is used to infect insect cells. The spike protein is harvested from insect cells and then mixed with the other ingredients of the vaccine. As a result of the manufacturing process, each dose has traces of insect cell proteins (less than 1 microgram), lentil lectin (less than 25 nanograms), exceedingly trace amounts of DNA from the virus and insect cells, and various processing chemicals at low-microgram amounts. The main ingredient besides spike protein is the adjuvant, and these two are mixed together with phospholipids, cholesterol, buffers, and emulsifiers and then injected intramuscularly. 
The adjuvant is called Matrix-M, and is derived from a fraction of chemicals known as saponins, from the soapbark tree. This is an evergreen tree native to Chile. In mice, subcutaneous injection recruits cells of both the innate and adaptive immune systems to the site of injection, while very large doses cause inflammatory cytokines to increase in the blood. 
To my knowledge, no biodistribution studies are available in any form for this vaccine, not even summaries in the FDA documentation.
Is There Graphene Oxide in the Vaccines?
One independent analysis found graphene oxide in at least some batches of Pfizer, Moderna, and AstraZeneca, and found its possible presence in other batches of these as well as batches of the J&J vaccine.  The vaccine manufacturers deny the presence of graphene oxide in their products. Graphene oxide is used in biomedical research for potential “nanomedicine” treatments, as biosensors, and in a variety non-biological applications.  The paper identifying it in vaccines needs to be replicated before we can make it a major focus of our concern, but if there are ingredients observable in the vaccines that the manufacturers deny, this needs to be brought to light in an air-tight manner, confirmed by multiple independent parties.
Toxicity of the Vaccine Components
The Spike Protein and Its Subunits
The Spike Protein as a Pore-Forming Toxin
As I have covered in more detail elsewhere, the whole spike protein, and to a much greater extent its S1 and S2 subunits, appear to act as pore-forming toxins that disrupt cellular membranes and allow charged ions to cross them more freely. [31–33]
It is impossible to overstate the sheer breadth of cellular and organismal dysfunction this would be expected to create.
One of the consequences is that it allows calcium ions to enter cells more easily. Calcium ions in the general compartment of the cell, known as the cytosol, are normally kept at vanishingly low concentrations so that, when they enter at certain times, they can be used as an activation signal. For example:
Inflammatory chemicals like histamine and bradykinin act by causing calcium to enter endothelial cells – those that line the insides of blood vessels – and epithelial cells – those that line the other internal and external surfaces of the body and its organs. Thus, pore-forming toxins imitate inflammatory processes without the need for cytokines and immune cells. Nevertheless, by initiating the inflammatory process, the secretion of inflammatory cytokines and the recruitment of immune cells will inevitably follow.
Calcium entering endothelial cells in small amounts will cause nitric oxide to be made, and it will dilate the blood vessels and lead to healthy blood pressure. Larger amounts, however, lead to excessive vasodilation that can cause headaches or flushing of the skin.
In both endothelial and epithelial cells, larger amounts of calcium flowing in will lead to even greater amounts of nitric oxide being produced, and this will cause the barriers between the cells to open up. In many tissues, this causes edema, or swelling. In the lungs, such swelling is a hallmark of pneumonia. In the brain, this process opens up the blood-brain barrier. In the gut, it causes leaky gut. On the outside of the skin, it allows toxins and skin bacteria to get into the skin and generate local inflammation, and allows water to leave the skin, making it dry. When it happens to multiple organs at once, it causes multisystem inflammatory syndrome.
Calcium entering the end of a nerve cell causes neurotransmitter release.
Calcium entering a muscle cell causes the muscle to contract.
Calcium entering a platelet causes the clotting process to start.
Calcium entering the mitochondrion, the so-called “powerhouse of the cell,” acts as a danger signal that the mitochondrion uses to initiate a programmed cell suicide.
This is just the dysfunction we would expect from one single type of ion (calcium) crossing a membrane when it is not supposed to. We could add to this that if a pore-forming toxin messes with sodium and potassium transport along a nerve fiber, it could stop the transmission of a signal. But if it allows calcium to enter at the end of the fiber, it could start a signal that doesn’t belong.
If it allows hydrogen ions to cross the inner membrane of the mitochondrion, at low levels it would simply generate more heat; at high levels, it would crush the ability to make ATP – the general energy currency of the cell – leading to fatigue. Worse, since ATP is what is constantly used to power the pumping of ions across membranes, the loss of ATP would dramatically synergize with the pore-forming toxin effect, since cells would be less able to resist the inflow of ions by pumping them back across membranes.
In neurons, this would lead to imbalances of electrolytes needed to clear glutamate from synapses, and the resulting imbalance of glutamate and GABA could lead to seizures and demyelinating disorders.
We can take literally any physiological process, and at the center of it, we would be describing how, from start to finish, the ability of cell membranes to keep certain substances on one side and others on the other side is the central theme of how the process is orchestrated.
The spike protein experiments cited above show the following effects:
The pore-forming toxin role appears to start at concentrations at least as low as 0.1 nanomoles per liter of S1 or S2.
Recruitment of inflammatory cells is elicited at least as low as 10 nanomoles per liter of S1 or S2.
Mitochondrial impairment and fragmentation occur at least as low as 50 nanomoles per liter of S1.
Rampant cell death occurs within 24 hours when concentrations are between 1000 and 2000 nanomoles per liter of S1.
COVID-like illness, lung damage, and cytokine storm occur when 10 micrograms of S1 are blown into the lungs of mice.
The concentration of S1 in the plasma following Moderna injection is, on average, about 125 times lower than 0.1 nanomoles per liter, and, at maximum, 52 times lower.  However, the concentrations in cells have never been reported. If the subunits are slipping into cell membranes, cell membranes could act as a sink for the subunits, keeping circulating concentrations misleadingly low.
The best study to use for extrapolation to humans is the mouse study with 10 micrograms blown into the lungs. The mice received 400 micrograms per kilogram bodyweight. For a 70-kilogram standard reference man, this is the equivalent of 28 milligrams. For the average 197.9-pound male, we get 36 milligrams. For an average adult woman weighing 166.2 pounds, we get 30 milligrams. However, standard risk assessment methodology would divide the dose by 12 to adjust for surface area differences between mice and humans, by 10 to adjust for variation among humans, and by 10 again for this being a short-term study.  Dividing by 1200 would yield doses of 2.3-3 micrograms. Since the vaccine mRNA persists in humans for at least 37 days  I calculated elsewhere that a single shot of Moderna may yield 247-1,135 milligrams of total spike protein, and a single shot of Pfizer may generate 75-340 milligrams. If we use the Pfizer rat study showing 0.178% of the radiotracer in the lipid nanoparticles reached the lungs,  we could expect anywhere from 0.13-2.0 milligrams of spike protein to reach the lungs of humans. This is the equivalent of 130-2,000 micrograms and is in considerable excess of the 2.3-3.0 micrograms needed to warrant a safety concern.
Moreover, the quantity of spike protein that reaches the lungs after vaccination is completely unknown, as no true biodistribution studies exist, and LPL-expressing macrophages in the lungs could selectively harvest cargo from the nanoparticles at rates that exceed those implied by the tracer studies.
Biodistribution data for the other vaccines have not been made public. No data exist to my knowledge on how long the adenoviral vectored DNA persists in human cells, making it much harder to generate an estimate of the cumulative spike protein produced.
Novavax comes in two doses of 5 micrograms of spike protein each. While I am not aware of any data on its biodistribution, this exceeds the amount needed for safety concern if half it winds up in the lungs. While I doubt half of it winds up in the lungs, the lack of biodistribution data warrants more caution, not less.
The Spike Protein Causes Breakdown-Resistant, Amyloid-Type Clots
Initiating blood clots is a general feature of pore-forming toxins, although some of these toxins also destabilize clots once they are formed.  The spike protein, however, causes blood clots that are denser than normal clots, resistant to being broken down, and characterized by the branched fibrils.  These fibrils are made of fibrin, the main protein component of a blood clot. Fibrils are nano-sized fibers, and this branched fibril structure is known as amyloid. Neutrophils can break the spike protein into 98 fragments, three of which form amyloid fibrils on their own.  When mixed with blood, these fragments are particularly potent at making breakdown-resistant clots.
There are two issues here, one of amyloid clots, and the other of amyloid made from spike protein alone. We tackle the clots first.
Formation of amyloid clots can occur in a rare genetic disorder of clotting proteins. Beta-amyloid, a protein associated with Alzeihmer’s disease, can make fibrin clots take on an amyloid structure and cause breakdown-resistant clots to occur in the local blood supply of the brain. Such structures for fibrin clots have also been shown in female migraine-with-aura, diabetes, and stroke, and other causes include bacterial components (including, but not limited to lipopolysaccharide or LPS), oxidative stress, and high levels of free iron. [39–41]
Although these clots are difficult to break down, it probably just takes more enzymes and more time. One study of acute COVID and long-COVID patients found that the amyloid-containing, spike-induced, breakdown-resistant microclots in their blood could be dissolved with the enzyme trypsin after two treatments.  Spike-free blood had its clots broken down after a single trypsin treatment. Similarly, when an Alzheimer’s-related peptide is used to make amyloid clots, this increases the time it takes to completely dissolve the clots with enzymes by 35%.  So, more enzymes and more time, and the spike-containing clots do indeed get broken down, even if they are forming amyloid fibrils.
The lowest concentration used to show the amyloid clot formation is 1 nanogram per milliliter, [10,38] which is about ten times the concentration found in the blood after the Moderna vaccine.  The concentration needed for this might actually be vanishingly small. Other studies have used lipopolysaccharide (LPS), a component of bacterial cell walls, to do this, and found that it only takes one molecule of LPS to coordinate 100 million molecules of fibrin into amyloid form.  This is probably because blood clotting is normally an auto-catalytic process, where the formation of a clot begets extension of the clot. If it starts out misformed, it seems to continue misformed.
There are no studies in live animals we can use to determine what dose of spike protein is likely to cause this problems in humans, but it is likely to be exceedingly low, as supported by clotting being elevated two months out in 25.3% of recovered COVID patients. 
Can the Spike Protein Cause Systemic Amyloidosis?
One disturbing feature mentioned in the last section is the ability of three fragments of the spike protein created during its digestion by neutrophils to create amyloid fibrils all on their own.  These authors noted that all common coronaviruses that infect humans have sequences that predict amyloid formation. However, COVID vaccines are the first time we have ever injected these proteins into people, bypassing the normal mucosal barriers.
Typical amyloid proteins make fibrils on the order of 10-20 nanometers in diameter, whereas diabetes and other inflammatory diseases are usually accompanied by fibrin clots with fibril diameters closer to 40 nanometers.  The spike protein paper did not estimate the diameter,  but when I used a ruler and the scale in the legend of their abstract graphic to estimate it, I came up with a diameter in the 10-20 nanometer range. Thus, the amyloid formed from neutrophil-digested spike protein resembles typical amyloid proteins more than it resembles anomalous amyloid clots.
Could these spike-only amyloid fibrils deposit in tissues?
Many chronic diseases involve deposition of amyloid proteins in specific organs: Alzheimer’s in many parts of the brain; Parkinson’s in a specific part of the brain where dopamine is involved in controlling movements; or type 2 diabetes in the pancreas.  Amyloid fibrils overlap with prion diseases: prions are misfolded proteins that are autocatalytic, meaning they spread their own misfoldedness to other proteins in a domino effect. Prions often form amyloid fibrils. Amyloid proteins can also circulate systemically and deposit in many organs simultaneously. When amyloidosis becomes systemic,  it typically causes decreased clotting as a result of amyloid deposits in the liver that damage the production of clotting factors. This can lead to spontaneous bleeding, internal or external. It can cause high blood pressure when deposits are laid down in the kidneys. If the deposits impact the nervous system, blood pressure can go up or down, but the telltale sign is the change is caused by standing, and is therefore “postural” or “orthostatic.”
Other signs of systemic amyloidosis are shortness of breath or dry cough; swelling; disturbance in the rhythm of the heart; pain, tingling, or numbness, typically beginning in the feet or legs; autonomic dysfunction, leading to erectile dysfunction, dysregulated urination or defecation, or getting full without having eaten enough food; an enlarged tongue, difficulty swallowing, dry mouth, or cramping jaws; bruising without trauma; or joint problems, including carpal tunnel.
Many of these line up with reported vaccine side effects. Others are not commonly reported, and the decreased clotting usually found when amyloid deposits in the liver is at odds with the tendency for COVID and COVID vaccines to both cause thrombosis, and the likelihood that the liver is a major organ that takes up the lipid nanoparticles. Nevertheless, too little is known about how the spike protein, its subunits, its fragments, and its amyloid fibrils distribute throughout the body to rule it out. It may be that this happens in a certain subset of people.
The concentration of spike protein used to form amyloid fibrils is 0.1 milligrams per milliliter,  which is one million times higher than the concentration of S1 found circulating in the blood after the Moderna vaccine.  Therefore, this route of inquiry needs more research to substantiate it as a likely cause of vaccine side effects, but we should be on the lookout for any clues that arise.
Spike Protein: The Vaccine Vs. The Virus
In the “Components of the Vaccines” section, we covered why the biological activity of spike protein from the virus or from the vaccines should be more or less identical.
The difference is in how they are distributed.
In a respiratory illness, your first line of defense is the physical barriers of your epithelial tissues, which are designed to keep bad things out and get good things in. The second line of defense is your mucosal immune system. This responds locally to pathogens without needing assistance from the systemic immune system to get its job started. Some immunity preexists in the form of innate immune cells or non-inflammatory antibodies known as IgA that happen to be generally polyreactive (they respond to many things) or happen to be cross-reactive with the new illness (for example, antibodies from a cold that happen to also respond somewhat to COVID). On an as-needed basis, the mucosal immune system can develop more inflammatory responses, and can get assistance from the systemic immune system, which can launch a whole-body mobilization of resources.
Even when the systemic immune system has joined forces, it has as a major objective to not let the pathogen inside the body. If a pathogen is on the surface of the skin, eyes, nose, mouth, throat, lungs, or digestive tract, it technically is outside the body. Once it crosses the mucosa and mounts an invasion in the blood or the internal organs nourished by the blood, things have gotten much more serious.
So, when people get a natural infection, the spike protein is definitely present in their mucosa, but it is unlikely to penetrate that barrier except in severe cases.
By contrast, the vaccines are injected into the muscle of the shoulder. This completely bypasses the mucous membranes and places the spike protein firmly inside the body.
This general framework is supported by studies on the blood levels of spike protein or its mRNA in those with natural infection or vaccination.
In a small study of 64 hospitalized COVID patients, circulating viral proteins – in most patients, including the spike protein – were found in 79% of those who were admitted into the ICU but only 48% of those were hospitalized but never critical.  A broader study of 104 COVID patients included more categories of illness, but looked for viral RNA instead of viral proteins.  The RNA was found in the blood of 44% of those on a ventilator, 27% of those hospitalized, and 13% of those treated as outpatients. Taken together, these studies suggest that the virus and its proteins enter the blood primarily in severe disease, and only in a small minority of cases in mild disease. Presumably, in those who get infected but never officially diagnosed, this happens rarely.
In a small study of 13 patients who received the Moderna vaccine,12 of them (92.3%) had circulating spike protein in their blood.  The only patient who did not have any detectable spike protein in their blood had an extremely rapid induction of high levels of anti-spike antibodies upon vaccination. In all subjects, the spike protein was undetectable from 2 weeks after the first dose onward. Even the second dose did not make spike protein reappear in the blood.
The authors interpreted this as the spike protein being “cleared” by the antibodies. However, another study found that antibodies interfere with the detection of spike protein.  This means that the spike protein probably was never “cleared” from the blood. Rather, the rise in antibodies made it impossible to detect.
Similarly, the single subject who had no detectable spike protein in their blood probably did have spike protein in their blood: it just wasn’t detectable because their rapid rise in antibodies interfered with the lab assay.
While antibodies binding to the spike protein are likely to protect it from binding to other things, and therefore to protect it from causing harm, it doesn’t follow that because they have rendered it undetectable that they have also rendered it harmless. They may be transiently binding to it, grabbing it and letting it go in a back-and-forth manner. If they do this enough, they can jam up the lab assay, but in the “letting go” phase the spike protein can still do some harm. In fact, it could be constantly slipping from the blood into cell membranes, where it will no longer have any chance of being detected in blood, yet actively doing the most damage.
Thus, the difference between natural infection and vaccination for the spike protein is that in natural infection it is usually isolated by the mucosal barriers, though it commonly crosses those barriers in severe cases; with the vaccines, by contrast, systemic circulation is virtually guaranteed.
How Long Does the Vaccine Spike Protein Stay in the Body?
Both the spike protein and its mRNA have been found in the lymph nodes of the armpits of vaccinated individuals 60 days after vaccination.  The S2 subunit has been found circulating on membrane-bound vesicles that leave cells known as exosomes.  It peaks around day 14 or some time thereafter, and by four months it has declined from its peak but continues to persist. No studies have adequately shown a time point after vaccination when spike protein is no longer found.
One paper provided evidence that the mRNA from the Pfizer gene can be written into the genome.  I have some issues with this paper that have not been resolved, and I do not consider it the last word on the topic by any stretch. However, it is an important finding. There is also evidence for this with the natural virus. 
One criticism of this paper is that they did not show the DNA gets integrated into the chromosomes. While that would make the finding even more concerning, it doesn’t matter much to the overall point. DNA can exist as stable circular structures outside of the chromosomes and be expressed. This DNA can even be inherited by daughter cells as parent cells divide. [52–55]
If the mRNA can be written into the genome in certain cells, this is equally concerning for the adenoviral vector vaccines. Their DNA is meant to make mRNA. If the spike mRNA can be reverse transcribed, it shouldn’t matter how it got into the cell. Furthermore, the DNA itself has no self-destruct button. Why would it disappear after being stably expressed?
The only vaccine in our discussion that should be immune to this is the Novavax vaccine, since it uses two doses of 5 micrograms of spike protein with no intentionally included spike DNA or mRNA. However, there are minor traces of DNA and RNA in Novavax, so it is not inconceivable that this process could be relevant.
One criticism of the idea of spike persistence is that none of these papers have shown full-length spike protein on the surface of human cells lasting months. It may just be that the spike protein is no longer produced and bits and pieces of it are flying around. The jury is out on this, but bits and pieces are the worst part of the spike protein. As covered in the sections above, the subunits are more toxic than the whole protein, and the amyloidogenic fragments produced by neutrophils might be the worst.
The standard view is that, once a human cell is producing spike protein, it will endure only as long as needed to generate an immune response. Once that happens, T cells will recognize any cell presenting spike protein on its surface and destroy it. 
According to this view, lasting side effects would be far more likely to be driven by dysfunctional immune responses than persistent spike protein toxicity.
However, support for both of these phenomena can be found.
In a case of fulminant myocarditis emerging 24 days after the second dose of Pfizer, spike protein was found in biopsied heart muscle, alongside T cells and neutrophils.  This supports persistent spike protein toxicity.
In a fatal case of COVID-like ARDS caused by the Moderna vaccine, inflammatory cells were found but no spike protein was found in the patient’s lungs.  However, the spike protein produced elsewhere may have created systemic hyperinflammation, or the spike protein may have been in the lungs earlier on but been eliminated by the inflammatory response. Regardless, this is a case where the inflammation clearly created the fatal problem rather than spike protein toxicity.
In a case of hepatitis following Pfizer vaccination,  liver biopsy showed infiltration of vaccine-induced, anti-spike, killer T cells. Spike protein was not found in his liver, probably because it had been routed out by the T cells. The T cells had taken up permanent or semi-permanent residence and stayed there throughout the period of observation. He only stably improved after systemic immunosuppressive therapy. The anti-spike T cells stayed in his liver the entire time, but lost their “killer” phenotype under immunosuppressive therapy. Loss of the killer phenotype appeared to drive his clinical improvement. This supports the conventional model wherein T cells kill anything expressing a spike protein, and it is their hyperactivity hurting organ function by killing human cells.
My suspicion is that there are two major subtypes of post-COVID vaccine syndrome. In one subset, the antibody and T cell response is inadequate to clear the spike protein; these patients have spike protein toxicity as a dominant problem. In the second subset, antibody or T cell responses are hyperactive. They have cleared the spike protein, but they have created excessive tissue damage and generated an autoimmune response in the process.
Support for this general idea can be found in long-COVID patients. The most important study on persisting antigen to date in naturally infected patients was a series of irritable bowel disease (IBD) patients.  46 IBD patients who had previously tested positive for COVID came in for an endoscopy related to their IBD. The endoscopies were, on average, 7.3 months from their positive test. 59% of the patients were in remission as far as their IBD was concerned. Although viral RNA could not be found in their stool, it was found in biopsied gut tissue in 70% of the patients. In all of the patients whose gut tissue tested positive for viral RNA, the gut tissue also tested positive for viral proteins. However, in no cases could replicable virus be found. In other words, there is no chronic infection, but there is a lingering presence of bits and pieces of the viral proteins.
Strikingly, 46% of the patients reported long-COVID symptoms and all of them showed presence of persistent viral antigen. In trying to explain why the viral antigens persist in some but not others, they found that low levels of anti-nucleocapsid antibodies were associated with antigen persistence. They also noted that patients who used immunosuppressive drugs that block the inflammatory cytokine tumor necrosis alpha (TNF-alpha) had impaired T cell responses to the nucleocapsid protein.
Notably, these are naturally infected patients, so they have several differences with uninfected vaccinated patients: they have nucleocapsid antigen, which is not generated by the vaccines, but which has also been shown to be toxic in animal studies;  and the antigen is in their gut, which is “outside” the body on the “other” side of the mucosal barrier.
Still, it is striking that persistent long-COVID symptoms in these patients required a deficient immune response and the persistence of toxic protein.
It is also incredibly informative that there is a relatively immunodeficient phenotype that appears to be the primary driver of persistent viral proteins.
Presumably, in uninfected vaccinated patients, the persistence of spike protein in the body is determined by an inadequate antibody and T cell response to it, just like in these long-COVID patients.
One interesting finding buried in the tables of that paper and never discussed in the text is that vaccinated people were twice as likely as unvaccinated people to have persistent viral proteins in their gut. It may be that the vaccines mount a response so biased toward the spike protein that they leave the nucleocapsid behind, or it may be that there are immunosuppressive effects of the vaccines, which will be covered later.
PEG is widely used in cosmetics, many people have antibodies to it, and some people are allergic to it. PEG and cationic lipids are both inflammatory and serve as adjuvants in the mRNA vaccines. One study showed that the lipid nanoparticles on their own cause intense inflammation if injected into the skin of mice. If inhaled, a sufficiently high dose will kill 100% of mice.  At a lower dose that only killed 20% of the mice, the surviving mice appeared to fully recover in four to eight days. This suggests the problem is acute inflammation rather than lasting toxicity. The inflamed tissue featured a dramatic rise in neutrophils and eosinophils.
In the Pfizer rat study discussed above,  they injected the animals with enough lipid nanoparticles to yield the equivalent of 50 or 100 micrograms of vaccine mRNA. The high dose was used first, then when toxicity was observed, the protocol was altered and the lower dose was introduced. The high dose was only used in males. The low dose was used in both males and females.
At the high dose, all the animals stopped eating and lost weight within 24 hours. By 30 hours, three out of 21 animals were hunched over with their fur standing up straight, and remained like that until the experiment ended at 48 hours, at which point all the animals were killed to examine their tissues. One of them, however, was hypersensitive to noise stimulus and was killed at the 30-hour point to prevent further suffering. “Prominent lobular architecture” was found in his liver, but they do not elaborate on this.
At the low dose, all male rats were fine.
However, one out of 21 female rats was moving less and breathing irregularly at 30 hours, and at 48 hours was hunched over with her hair standing up straight.
There could be sex differences, but due to the difference in bodyweights between the male and female rats, this isn’t clear. The fact that only one out of 21 female rats showed symptoms suggests that her dose was very close to the lowest dose capable of causing those effects. Therefore, I believe we should simply pool the male and female data with the doses adjusted to bodyweight. The lowest dose where an adverse effect is observed is the 50 microgram female dose, while the highest dose where no adverse effects are observed is the 50 microgram male dose. Thus, the upper limit of safe dosing should be derived from the low male dose.
Standard risk assessment procedure calls for dividing the body weight-adjusted dose by 6 to account for surface area differences between rats and humans, by 10 to account for variation among humans, and by 10 to account for this being a short-term study.  The average body weight of the male rats was 244 grams. Dividing the dose by 600 and by bodyweight yields 0.341 micrograms per kilogram bodyweight. For the 70-kilogram “standard reference man,” the upper limit would be 23.9 micrograms. For the average 197.9-pound male, it would be 30.7 micrograms. For an average adult woman weighing 166.2 pounds, it would be 25.8 micrograms. Thus, the standard dose of Pfizer vaccine providing 30 micrograms of mRNA just barely falls within a reasonable upper limit for an average-weight adult male and exceeds that limit for leaner males and for women.
This is concerning because it doesn’t account for repeated dosing in even the two-dose “fully vaccinated” model let alone booster shots. The European Medicines Agency estimated that half of the lipid nanoparticles would be removed from the body in 1-2 months and 95% of them would be removed in 4-5 months.  Thus, the second dose in particular is raising the cumulative exposure to lipid nanoparticles very high, as it is adding a new dose when less than half of the first dose has been eliminated.
This raises an important question: what made the rats stop eating, in some cases hunched over with their fur standing up, made one male become hypersensitive to noise, and caused one female to breathe irregularly? If this was acute inflammation of the type that occurred in the mouse study, it may resolve within days rather than being related to the long-term cumulative dose. If, however, it was a classical cumulative dose-dependent toxicity, it may play a role in long-term vaccine side effects and imply a cumulative risk with successive booster shots.
Importantly, allergies to lipid nanoparticles would not be as strictly dose-dependent as toxicity, so these particles are likely to cause allergic reactions in a subset of people.
Adenoviral vectors are highly inflammatory adjuvants that carry a risk of adverse inflammatory reactions, but the risk that has been most well established is their promotion of thrombosis. This is because they are highly negatively charged, so they can bind to positively charged molecules and generate autoimmune antibodies to them. Specifically, they can bind to and create antibodies to platelet factor 4. This plays a role in “vaccine-induced immune thrombotic thrombocytopenia,”  which is discussed further in the “Comparing and Contrasting Adverse Effects of Different Vaccine Types” section.
The presence of graphene oxide has been alleged by one group  and denied by the manufacturers. Graphene oxide is not ready for medical applications and the means of protecting against its toxicity are poorly understood.  It can cause thrombosis as well as hemolysis of red blood cells. From the bloodstream, it preferentially accumulates in the liver, spleen, and especially the lungs. In the lungs, it causes pulmonary edema and fibrosis – typical of severe COVID pneumonia. Remarkably, it has even been shown to bind to platelet factor 4, the same problem identified for adenoviral vectors and thought to be the cause of vaccine-induced immune thrombotic thrombocytopenia.
Graphene oxide is mainly eliminated by macrophages, whose development is dependent on vitamin D. The vitamin D used in the protocol may be protective, if indeed this is a real risk.
Immune Reactions to the Virus and the Vaccines
A few differences in the immune response to the virus and to the various vaccines are worth noting.
Moderna is Most Immunogenic
When comparing the four major vaccines, the greatest antibody response is for Moderna; Pfizer is second; next is AstraZeneca; J&J has the least and most variable response, largely driven by low responses in older people. 
When comparing Moderna, Pfizer, and J&J, Moderna has the greatest antibody durability over time, J&J the least. Moderna stands out as having much better T cell durability than Pfizer or J&J. 
This is important because if antibodies bind to spike protein subunits, they are the best defense against their toxicity. If T cells eliminate infected cells, they are the best way to clear out the production of spike protein.
If we see hints that some side effects are worse with Pfizer than Moderna, this may represent a modestly well controlled inference that a more robust immune response helps control the side effects.
IL-6 vs IFN-Gamma
The inflammatory cytokine interleukin-6 (IL-6) is on average nearly doubled in moderate COVID patients and nearly quadrupled in critical patients.  Those with mild symptoms often do not have elevated IL-6, but those that do have a sustained rise throughout the first week of infection.  In severe cases that recover, IL-6 remains doubled for at least two months.  By contrast, IL-6 is not a dominant response to the Pfizer vaccine.  In one study it rose on average 50% in men and 100% in women, and in some individuals can quadruple.  However, that study did not show the time needed for it to return to baseline. In another study, the J&J vaccine nearly doubled IL-6, but it returned to baseline by the second day.  Overall, the IL-6 rise seems to be bigger on average in natural infection, and of much longer duration, when compared to the vaccines.
On the flip side, the vaccines provoke a much stronger increase in interferon-gamma (IFN-gamma). In response to the virus, IFN-gamma is on average increased by 11%,  whereas after the Pfizer vaccine it is increased 11.3-fold. 
One implication of this is that it may provide a convergence with the T cell suppression phenotype that drives severe COVID. This is produced by myeloid derived suppressor cells (MDSCs). In natural infection, IL-6 is a driver of MDSCs, but the sharp post-vaccination rise in IFN-gamma may represent an alternative route to activating them. 
Do MDSCs Rise After Vaccination?
In 56 healthy volunteers,  the Pfizer vaccine did not appear to induce a rise of MDSCs, according to the authors. However, the day after the second dose, myeloid cells rose 100-fold, largely monocytes. They characterized this monocytic population as cells that do not occur in natural infection and are most similar to those that increase in response to an H5N1 flu vaccine. They looked at two markers that can be used to identify MDSCs in COVID patients – HLA-DR and S100 – and determined that this vaccine-induced cell population neither occurs in natural COVID infection nor represents MDSCs.
However, they did observe an increase in STAT3 – a hallmark of MDSC activation – and the HLA-DR and S100 markers are not sufficient to determine whether cells are MDSCs.  The most important thing to do would be to evaluate the isolated cells for T cell suppression activity, and they did not do this. Thus, it is quite possible that this 100-fold increased population does represent MDSCs.
In addition, Extended Data Figure 6 from that study shows a population of cells that express the enzyme arginase 1 increasing up to 5-fold for three days after the second dose, and in some individuals more than 10-fold. One individual had these cells keep increasing through the end of the study on the third week after the second dose, at which point they had risen 15-fold. These cells have markers consistent with MDSCs, yet they are not discussed anywhere in the text of the paper. Although they did not evaluate these cells for T-cell suppressive activity, the arginase enzyme is a major mechanism of T cell suppression, because it is used to deplete the arginine that T cells need for growth. Regardless of how the cells are classified, they would be expected to suppress T cells by depleting arginine.
Therefore, it is very plausible that, in some people, the COVID vaccines are massively increasing MDSCs, leading to T cell suppression, and that this is a major mechanism by which spike protein would continue to be expressed in the body after months go by.
Do Autoantibodies Rise After Vaccination?
In a small study of 56 healthy volunteers,  two subjects developed autoantibodies to inflammatory cytokines after vaccination, but none had any that rose to clinical significance. Five of the subjects had existing autoantibodies that did not get any worse.
This suggests that autoimmunity is not the typical response to vaccination, whereas circulating spike protein is likely to be a nearly universal response to vaccination.
However, those suffering from post-vaccine side effects are likely to be enriched with autoimmune reactions. For example, in a React19 survey of those suffering from vaccine side effects, 21.8% had an existing autoimmune diagnosis before being vaccinated and 13.9% had a new autoimmune diagnosis arise.
In severe COVID infection, autoimmunity can become very broad. One individual had over 250 different autoantibodies develop.  The breadth of autoimmunity that can develop in such cases is not likely explained by “molecular mimicry,” where the body mistakes its own tissues for spike protein. It is much better explained by tissue damage. The immune system looks for signs of what is causing trouble so it can remove the problem. It looks for “danger-associated molecular patterns'' (DAMPs) and “pathogen-associated molecular patterns (PAMPs).” Tissue damage is a major sign that something nearby is harmful, and the immune system considers many of its signs to be DAMPs. The immune system will look for whatever is near the damage being caused and conclude that innocent bystanders are culprits and mount immune responses to them.
Spike protein toxicity and autoimmunity are therefore not opposing hypotheses. Spike protein toxicity will cause tissue damage, and this will often lead to autoimmunity.
With that said, there are cases where specific autoantibodies may be directed at spike protein-related targets. [76,77] One important class of these is anti-idiotype antibodies. If antibodies are mounted to the spike protein, and the spike protein fits very well into the ACE2 enzyme, then the spike protein-binding portion of the antibodies will have a very similar shape to the spike protein-binding site of ACE2. They have to, because their shape is what allows each of them to bind to the same part of the spike protein. If new antibodies are then mounted to those antibodies, they will likely also react to ACE2.
Essentially, this is like making a mold of a key, and then making a key from the mold. It’s probably going to open the same door.
This would lead to ACE2 inhibition and raise blood pressure. Something similar may happen with another protein that the spike protein can bind to, neuropilin-1, which may play a role in autoimmune neurological disorders.
Comparing and Contrasting Adverse Effects of Vaccines vs Natural Infection
Comparing and contrasting the adverse effects reported for vaccines versus natural infection will help us match differential signs and symptoms to what we expect to be the differential mechanisms. This will help us better narrow down the mechanisms behind the signs and symptoms, which will, in turn, help us better understand how to resolve them.
The purpose of this analysis is not a relative risk assessment. Therefore, I am not attempting to discover the true rates of any adverse effects. I assume that all of the data is seriously hampered by reporting bias, and hope that this bias is less impactful on the patterns that emerge among the signs and symptoms than it is on the actual rates of each sign or symptom.
All of my references to the US vaccine adverse events reporting system (VAERS) refer to data as it existed over the first weekend of August, 2022, and are documented in this spreadsheet.
Putting aside the acute fever that can accompany illness or vaccination, fatigue and headache are the most common symptoms reported to VAERS  and reported in studies of long-COVID. [79,80] One way to look for a difference in overall patterns would be to compare the adverse effects of the vaccines and of long-COVID by adjusting the rates of other effects to that of fatigue. In all cases – vaccines and long-COVID – the rate of fatigue is roughly twice the rate of dyspnea (trouble breathing), which is roughly twice the rate of having a cough. Surprisingly, even though COVID infects the lungs directly and would therefore be expected to cause lasting lung damage that the vaccines wouldn’t, these rates show the exact same pattern.
Since fatigue and dyspnea occur at roughly the same ratios, below I use either of them to normalize the other data, since some studies of long-COVID include one but not the other.
Some adverse effects are more often reported for long-COVID than for the vaccines. In long-COVID, smell and taste disorders are about as common as dyspnea, while in VAERS they are six times less common than dyspnea. Hair loss and attention deficit are extremely poorly characterized in long-COVID, but very limited evidence suggests they may occur at a similar rate as dyspnea.  In VAERS, hair loss is 44 times less commonly reported than dyspnea, and attention deficit is over 100,000 times less commonly reported. Studies that have looked at cognitive impairment alongside fatigue have suggested that in long-COVID cognitive impairment is 69% as common as fatigue,  while in VAERS any cognitive disorders are reported 76 times less commonly than fatigue.
On the flip side, some adverse effects are more often reported with the vaccines. Muscle pain is only 57% as commonly reported as dyspnea in long-COVID, but slightly more often reported than dyspnea for the vaccines. Diarrhea is only 23% as commonly reported as dyspnea in long-COVID, yet 48% as commonly reported in VAERS. Joint pain (arthralgia) is not well characterized in COVID,  but some studies suggest it occurs at 79% the rate of dyspnea,  whereas in VAERS it is reported at 91% the rate of dyspnea.
These suggest that muscle pain is 79% more commonly reported, diarrhea twice as commonly reported, and joint pain 15% more commonly reported in VAERS than we would expect if the mechanisms of post-vaccine side effects and long-COVID were similar.
The following differences, however, are much more dramatic:
Hypertension is not consistently reported as an effect of long-COVID,  but one study suggests it happens at a rate of only 4% of dyspnea.  Hypertension is reported at 36% the rate of dyspnea in VAERS. That is nine times more common than we would expect if the mechanisms of post-vaccine side effects and long-COVID were similar.
Myocarditis is 58 times less common than fatigue post-COVID with no mention of pericarditis,  while in VAERS myocarditis and pericarditis are only 7 times less common than fatigue. That makes them eight times more common than we would expect if the mechanisms of post-vaccine side effects and long-COVID were similar.
Long-COVID papers do not discuss menstrual changes. A prospective study showed that COVID infection does not alter menstrual cycles while the COVID vaccines nearly double the risk of an altered cycle.  In VAERS, among females, menstrual changes are reported nearly half as often as dyspnea, comprising 3% of reports among females, with over 28,000 cases listed.
New-onset neurological disorders or relapse of pre-existing disorders seems limited to sparse case reports with COVID,  in VAERS, by contrast, these disorders are reported at 60% the rate of dyspnea, comprising 3.7% of all reports, with over 51,000 cases listed.
In short, post-vaccine side effects overlap considerably with long-COVID, with striking parallels in the rates of respiratory issues, but they stand out in having a lower incidence of smell and taste disorders, a lower incidence of cognitive impairment, somewhat greater rates of muscle pain, joint pain, and diarrhea, a unique impact on menstrual cycles, and dramatically higher rates of hypertension, myocarditis and pericarditis, and neurological disorders.
The neurological disorders that are documented in published case reports to follow COVID vaccines with evidence of causation include multiple sclerosis,  generalized demyelination,  aneurysmal subarachnoid hemorrhage,  various neuropathies, [87,88] postural orthostatic tachycardia syndrome (POTS), [89,90] and various types of neuralgia [91–99] and myelitis. [100–109]
Since the commonality of the vaccines and the natural infection is the spike protein, while the differences are that the natural infection enters the respiratory tract and the vaccines enter the deltoid muscle, we must begin our analysis by asking whether we can easily explain this comparison and contrast through how the spike protein would be distributed. Specifically, spike protein should be limited to the mucous membranes in most COVID infections that are not severe, with it especially biased toward the respiratory tract. By contrast, the vaccine spike protein completely bypasses the mucosal barriers and can therefore more easily seep from muscle into systemic circulation, and may sometimes be accidentally injected directly into circulation through a vein. From there, it can reach a much broader distribution of tissues, such as the blood itself, the lungs, the gut, the heart, the ovaries, and the nervous system.
The Fatigue/Dyspnea/Cough Pattern
The fatigue:dyspnea:cough pattern in the 4:2:1 ratio is an interesting parallel between VAERS data and long-COVID studies, yet is not replicated in any of the vaccine trials, where fatigue is usually fairly common but dyspnea and cough are either rare or not recorded. [110–113]
One possibility is that the ratio in VAERS is a result of unrelated respiratory illnesses that just happen to follow vaccination.
However, my suspicion is that the lack of parallel to the vaccine trials must be systematic bias in the way adverse events are collected in those trials. When they are reported in these trials, they are reported as part of the “unsolicited adverse events” that are only tracked for 28 days after any injection, even if the trial continues for months, despite universally being used as part of the definition of COVID. We know from the FDA’s documentation that the two-month results of the Pfizer trial had 3,580 cases of “suspected COVID-19” based on symptoms, 95.3% of which tested negative on PCR.  Cough and shortness of breath are not discussed at all in the two-month report, or the later six-month report, except to say that they were used as part of the definition of COVID. [112,115] The J&J trial included a respiratory section in its 28-day adverse events but cough and dyspnea do not appear at all, despite being part of the COVID definition.  The 6-month results of the Moderna  and AstraZeneca  trials report cough and dyspnea in their 28-day adverse events at extremely low rates.
Even though the standard approach of these trials was to ask the participants to self-report COVID symptoms in order to get a PCR test, it seems that these very common COVID symptoms – cough and dyspnea – did not make it into the reports of unsolicited adverse events. So it seems that the self-reporting of suspected COVID may have sucked these symptoms into itself like a vacuum. If the PCR test was positive, they became COVID symptoms. If it was negative, they disappeared into the black hole of “suspected COVID” that, according to FDA documentation, represented 95.3% of all such symptoms at the 2-month mark of the Pfizer trial, but which never became part of any published trial paper.
For this reason, I am inclined to dismiss the lack of correspondence with the vaccine trials and to take the parallel between VAERS and long-COVID seriously.
One very simple explanation for this is that the amount of spike protein that reaches the lungs after vaccination is similar to the amount left over in long-COVID patients once the acute infection is over. As covered in the Toxicity of the Spike Protein and Its mRNA section, it is very reasonable to believe that the amount of spike protein reaching the lungs could have a risk of causing acute, severe COVID-like illness in some individuals, so it is quite possible that it commonly causes mild COVID-like illness. That could explain why long-COVID patients and vaccinated subjects both have such a strikingly similar fatigue/dyspnea/cough pattern.
The Lower Incidence of Disorders of Attention, Memory, Smell, and Taste
The vaccines seem to be less associated with attention, memory, smell, and taste disorders compared to natural infection. Since they are much more strongly associated with severe neurological disorders, we cannot explain this by suggesting the vaccine spike protein does not reach the nervous system while the natural spike protein does.
Notably, the vaccines also seem to be far less often associated with hair loss than natural infection.
However, this conflicts with a React19 survey, where 26.4% of subjects complained of hair loss and almost half reported memory loss. This may highlight that the community of people most motivated to find solutions to post-vaccine problems differ in certain respects from the much larger group of people from whom VAERS reports are being generated. Or, it may represent a bias in what medical professionals see as potentially related to the vaccines, or what the average person is likely to tell their doctor about. On the other hand, the React19 survey is consistent with VAERS in not showing reports of smell and taste disorders.
In my long-COVID protocol, I make the case that there is a cluster of patients with fatigue, dyspnea, and hair loss who are suffering from functional iron deficiency, and a cluster of patients with smell and taste disorders that are suffering from zinc deficiency. This is because interleukin-6 drives down plasma zinc  and leads to the storage of iron in ferritin,  making it unusable for biological needs. Deficiencies of iron and zinc appear to both drive ADHD in a subset of children and adolescents.  Deficiency of iron  but not zinc [120,121] drives cognitive decline, including dementia. Fatigue and dyspnea upon exertion are classic signs of iron deficiency,  and hair loss is also documented as a sign. [123,124]
It seems that the broader group of VAERS reports do not show the hair loss and cognitive decline pattern that long-COVID shows, while the React19 community is enriched with this pattern. This is suggestive of functional iron deficiency.
Although 7.68% of people in the React19 survey reported benefiting from zinc, the zinc deficiency pattern associated with smell and taste disorders that shows up in long-COVID patients does not appear to be common in this group. This is consistent with the VAERS data.
Hypertension did not arise as a signal from the vaccine trials. However, in one study,  about 5% of people receiving the Pfizer vaccine experienced a significant rise in blood pressure. This is consistent with the large signal from the VAERS data.
Blood pressure is a function of the volume of the blood and its viscosity, and the pressure that exerts on the vessel wall. The vessel wall can constrict, creating more pressure, or relax, creating less.
The rise in blood pressure is probably not related to the role of the spike protein as a pore-forming toxin. Minor changes to the permeability of cell membranes should increase nitric oxide signaling, which relaxes the smooth muscles that control blood vessels, causing them to dilate, lowering the blood pressure. Major disruption of the barriers of endothelial cells should cause blood to leak out of the vessels, lowering the blood pressure.  Granted, we cannot rule out disruptions to the neurological control of blood pressure or compensatory responses to the vascular leakage, but a rise in blood pressure would not be straightforwardly predicted from this mechanism.
In principle, thrombosis and clotting could raise blood pressure by increasing the viscosity of the blood, but this is not very straightforward either, because, outside of extremes, an increase in blood viscosity leads to a regulated relaxation of the blood vessels, causing blood pressure to return to normal. 
This mechanism would also make it hard to explain why hypertension is so much more commonly reported with the vaccines than with natural infection. D-dimer, a breakdown product of clots that can be used as an indicator of increased clotting, is elevated in 25.3% of COVID patients 2 months after infection.  This is more common than the rate of dyspnea in long-COVID. Why don’t we see commensurate increases in hypertension?
My hypothesis is that in a mild or moderate natural infection, most of the clotting is happening in the vasculature of the lung from spike protein subunits that are shed there, or neutrophils that metabolize them into tiny bits that create amyloid clots. It is mainly the breakdown of these clots in the pulmonary vasculature that is feeding D-dimer into the general circulation.
By contrast, with the vaccines, not only spike protein but the mRNA needed to produce it is entering the blood and seeding its continued production throughout the body. With whole S1 subunits in the general circulation, they can bind to ACE2, and thereby raise blood pressure. As noted earlier, the vaccine spike proteins are actually engineered in ways that make them react more strongly with ACE2 than natural spike protein.
I therefore favor spike protein binding to ACE2 and directly inhibiting it as the leading explanation.
Alternatively, anti-idiotype antibodies binding to ACE2 could explain this.
Myocarditis and Pericarditis
While the signal of myocarditis and pericarditis did not arise from the vaccine trials, their signals in the post-marketing surveillance data are so strong that the FDA now includes a myocarditis warning on the vaccine packaging. That the spike protein more easily makes it to the heart following vaccination is a simple explanation for this relationship, and is strongly supported by mouse experiments showing that intravenous vaccination dramatically increases the myocarditis and pericarditis response over intramuscular vaccination.  That is, whatever delivery route gets more spike protein into the bloodstream will deliver more of it to the heart, and thus cause more inflammation there. Natural infection delivers the least spike protein to the bloodstream; intravenous injection delivers the most. Typical intramuscular injection is in the middle.
The fact that spike protein has been found in biopsied heart tissue in a case of post-vaccination myocarditis supports its persistence in heart tissue as a cause of the myocarditis.  The fact that a similar pore-forming toxin from Streptococcus pneumoniae, pneumolysin, contributes to myocarditis in animals  supports the role for the spike protein as a pore-forming toxin in myocarditis.
Menstrual Cycle Changes
While menstrual changes did not arise as a signal from the vaccine trials, a prospective study has now shown that COVID vaccines double the risk of an altered cycle while natural infection has no impact on that risk.  The mechanisms are not clear, but the finding is reminiscent of the early concerns when leaked Pfizer documents showed that the lipid nanoparticles accumulate in the ovaries. This could imply the spike protein does the same. However, the prospective study showed that the J&J vaccine is just as likely to cause this issue as the mRNA vaccines, suggesting the delivery vehicle is not what drives the effect. Rather, this can be explained simply by the fact that the vaccine is injected into the muscle, bypassing the mucosal barriers, and delivering its cargo into the general circulation. Regardless of the vaccine type, intramuscular injection allows the cargo to reach the ovaries, or perhaps another location regulating the menstrual cycle, like the pituitary or the uterine lining.
Early on, the AstraZeneca trials saw several cases of transverse myelitis that they dismissed as unrelated to the vaccines,  and the mRNA vaccine trials showed more Bell’s palsy than placebo. [113,131] There are now over 51,000 neurological disorders reported in VAERS, and, as noted above, many case reports documenting multiple sclerosis,  generalized demyelination,  aneurysmal subarachnoid hemorrhage,  various neuropathies, [87,88] postural orthostatic tachycardia syndrome (POTS), [89,90] and various types of neuralgia [91–99] and myelitis. [100–109]
A recent NIH study found that some neurological patients respond to intravenous immunoglobulins and some to corticosteroids, and suggested that autoantibodies or T cells could be involved.  Unfortunately, they took biopsies but did not evaluate them for the presence of the spike protein. It is tempting to speculate that the patients who benefit most from immunoglobulins have trouble clearing the spike protein as their dominant problem, while those that benefit most from steroids have excessive inflammation as their dominant problem.
Regardless, the stronger association of neurological disorders with vaccines than with natural infection is supportive of the biodistribution hypothesis: more spike protein gets into the bloodstream with vaccines than with typical cases of natural infection, so more reaches the nervous system to cause toxicity or immune dysregulation.
Comparing and Contrasting Adverse Effects of Different Vaccine Types
Overall, the three major vaccines licensed in the US – Pfizer, Moderna, and J&J – have approximately the same rate of total events per person reported in VAERS if we assume people receive two or three doses of mRNA vaccines or one dose of J&J.
Permanent disabilities, deaths, tinnitus, allergies, and herpes-related reports have relatively little variation across vaccines that do not rise above the background noise. Specifically, these all have below-average coefficients of variation, which is a measure of how variable the data is within each category for each vaccine.
The most significant difference in the side effect profile of different vaccine types identified in the scientific literature is the association of the adenoviral vector vaccines – especially AstraZeneca – with a specific form of thrombosis. This is “cerebral venous sinus thrombosis” especially a subtype associated with low platelets that has been named “vaccine-induced immune thrombotic thrombocytopenia.”  Although this was initially associated mostly with AstraZeneca, the appearance of a case in the J&J trial is why the trial had been paused. 
Hypotheses to explain the disproportionate share found with AstraZeneca focus on the adenoviral vector. All of these cases show high levels of antibodies to platelet factor 4 (PF4). PF4 normally promotes blood clotting. Yet the antibodies to it can also promote blood clotting. Outside of this vaccine-induced subtype, this pattern is usually found in a subset of patients undergoing treatment with the anticoagulant heparin, where heparin binds to PF4, and the antibodies bind to the heparin-PF4 complex. PF4’s mechanism of action involves being very positively charged. Adenoviral vectors are very negatively charged, and are adjuvants that are designed to promote an inflammatory reaction that will immunize the host against its cargo. Since positive and negative charges attract each other, adenoviral vectors – used in both the AstraZeneca vaccine and the J&J vaccine – can bind to PF4 and immunize the body against it, resulting in anti-PF4 autoimmune antibodies. The AstraZeneca vector happens to have the most negatively charged surface, perhaps explaining why it is most strongly associated with this syndrome.
When looking in VAERS at this form of thrombosis – using “cerebral venous sinus thrombosis” and "thrombosis with thrombocytopenia syndrome" – the trend confirms an increased reporting with J&J. These only represent 4% of the total thrombosis reports, but the J&J has somewhere between 65% and 2.5 times as many reports per person as the Pfizer vaccine. The Pfizer vaccine has more than the Moderna, roughly in line with the total thrombosis reports described below.
Total thrombosis reports in VAERS have a weak trend implicating the J&J vaccine but a stronger trend favoring Moderna having the fewest reports. When considering all forms of thrombosis together, these constitute 3% of J&J reports, 2% for Pfizer, and 1% for Moderna. When normalizing to the number of doses administered, Moderna has the smallest share, Pfizer has twice as many, and J&J has six times as many. When adjusting for vaccinated people, however, the trend with J&J becomes ambiguous. If we assume each person got two mRNA shots, the J&J has 54% more reports than Pfizer. If we assume everyone with Pfizer got a booster, this makes the J&J look nearly identical to Pfizer. Most likely, the truth is somewhere in between. Moderna, however, has half as many thrombosis reports as Pfizer in any of these analyses.
This might easily be explained by the stronger antibody response to Moderna binding more spike protein and preventing it from causing clots.
In the UK Yellow Card system, the equivalent of the American VAERS, Bell’s palsy has been reported much more often with Pfizer than with AstraZeneca. Some authors argued this suggests it is driven by a mechanism specific to mRNA vaccines.  On the other hand, it was the AstraZeneca trial where transverse myelitis most clearly showed up.  In VAERS, where Bell’s palsy represents about 1% of total reports, it is about twice as commonly reported with Pfizer than Moderna, but Moderna and J&J are quite similar. When all neurological disorders are grouped together, the Pfizer/Moderna gap gets cut in half but the overall trend remains similar. This suggests that, if anything, there may be a Pfizer-specific mechanism rather than any relevance of mRNA versus adenoviral vector vaccines.
It is tempting to speculate that, on the one hand, the lipid nanoparticles are more effectively taken into the brain as a result of the brain expressing lipoprotein lipase (LPL), while, on the other hand, the greater antibody and T cell responses to Moderna cancel out this effect. Thus, Pfizer has the worst of both worlds, delivering more to the brain but not offering any extra protection.
In VAERS, the J&J vaccine seems to be disproportionately associated with menstrual problems. These account for 7% of the female reports, versus 3% for the mRNA vaccines. When adjusting for doses administered, even generously assuming everyone got three doses of the mRNA vaccines and only one dose of the J&J, the J&J still has 63% more reports about menstrual problems than the mRNA vaccines. The prospective study on menstrual changes found a stronger magnitude of change for the J&J vaccine than for the mRNA vaccines but it was not statistically significant.  Some explanations might be that adenoviruses are better delivered to the pituitary, the ovaries, or the endometrial lining than lipid nanoparticles, that there is some indirect influence of thrombosis, or that there is some autoimmune stimulation impacting menstrual cycles analogous to the anti-PF4 finding. This deserves further research.
Hypertension reports are quite evenly distributed among the vaccines. They are about 2.2% of total reports, with the J&J hitting the average almost perfectly, Pfizer falling a half percentage point above it, and Moderna a half percentage point below it. When adjusting for people vaccinated, assuming everyone either got two shots of mRNA vaccines or one shot of the J&J vaccine, the J&J comes in about average, Pfizer a little above it, Moderna a little below it. There’s a hint of fewer hypertension reports with Moderna, which does line up with Moderna having a lower risk of thrombosis, but the lack of any signal from J&J here makes thrombosis seem unrelated.
I believe this modestly strengthens the interpretation that hypertension is driven by ACE2 inhibition rather than by thrombosis.
The modest Moderna/Pfizer differential could be explained by the protective effects of Moderna’s greater immunogenicity.
For myocarditis and pericarditis, Pfizer seems to have the most and the J&J vaccine seems to have the least. As a percentage of each vaccine type’s share of reports, Pfizer is 2.2%, Moderna is 1.1%, and J&J is 0.4%. When adjusting for doses administered, Moderna and J&J group together with Pfizer having twice as many reports. When adjusting for people vaccinated, however, by counting each mRNA vaccine as two doses and each J&J vaccine as one, the original pattern reemerges. Accounting for many of the mRNA vaccines being booster doses makes J&J look even better. Overall, Moderna seems to have 2-3 times as many reports as J&J, and Pfizer twice as many as Moderna.
The heart is one of the three major organs that express LPL, along with skeletal muscle and adipose tissue. The myocarditis/pericarditis pattern may be explained by heart having much greater uptake of lipid nanoparticles, while the greater antibody and T cell response of Moderna mitigates this.
There is a strikingly similar pattern with Creutzfeldt-Jakob Disease, a prion disorder of the brain that sometimes involves amyloid plaques. On a per person basis, Moderna accounts for 2-3 times as many reports as J&J, and Pfizer accounts for 2.7 times as many as Moderna. With so few cases, not much should be read into this data. Nevertheless, it is consistent with LPL mediating greater uptake into the brain with a mitigating effect for Moderna’s greater immunogenicity.
This particular pattern is somewhat discrepant from the pattern for total neurological disorders, where Moderna is more in line with J&J. This might represent the heterogeneity of neurological disorders, where uptake into the brain rather than the peripheral nerves is not always relevant, or it might represent that the greater immunogenicity of Moderna is more protective for the majority of neurological disorders than it is for prion diseases.
Cognitive disorders are rare, only 0.17% of the reports. However, Moderna looks to have a disproportionate share. Normalized to doses administered, it is similar to J&J and both are 3.5 times that of Pfizer. However, when normalized to vaccinated people, Moderna has double to triple the share of J&J, and the 3.5-fold greater share than Pfizer remains throughout.
The ability of each vaccine to stimulate IL-6 has not been compared head-to-head, but Moderna’s greater antibody and T cell response might correlate with a greater cytokine response, in which case this would align with my hypothesis that cognitive impairment is largely driven by inflammation-induced decreases in iron and zinc status.
A Note on Novavax
Novavax was not included in the main analysis above, because it has been authorized more recently and the data is more sparse and less robust.
At the time of writing, there are only nine Novavax reports in VAERS. However, this may easily be explained by the fact that there have hardly been 7,000 doses distributed and it has only been authorized for two months. More time is needed to see what reports come in. In the FDA’s June 7 meeting when Novavax was authorized, the FDA reviewed data from several countries where the data was considered adequately administered. If we substitute this for VAERS data, the side effect rate per person seems to be half that of the other vaccines. Non-US data is less transparent than US data, and is mostly available in summary form. If we look at data from the European Union, making side-by-side comparisons of Novavax, J&J, AstraZeneca, Pfizer, and Moderna, considering the doses administered to date, Novavax stands out as having the least reports per dose, about four times fewer than Pfizer. However, if we look at Australia’s AusVaxSafety surveys for Pfizer, Moderna, AstraZeneca, and Novavax, Novavax has similar rates of total adverse effects per dose as the others, and this remains true if looking at effects that interfere with daily activities.
When the Novavax trial was published last year, there was only one death in each group.  However, in the briefing document of the FDA’s advisory board from June 7, 2022,  when Novavax was authorized, the followup had found twice as many deaths in the vaccine group (11) as the placebo group (5). Since there were almost twice as many people in the vaccine group as the placebo, this amounted to a 9% higher total mortality rate in the vaccine group, but which fails to reach statistical significance.
These data do not appear suitable for the type of analysis I performed above. Therefore, Novavax is not included in the comparison of side effect profiles across vaccines.
A Note on Cardiac Deaths in mRNA Vaccine Trials
In the Pfizer trial, there were nine cardiac deaths in the vaccine group and five in the placebo group. This represents an 80% increase, but it is not statistically significant. In the Moderna trial, there were seven cardiac deaths in the vaccine group and five in the placebo group.  This represents a 40% increase, but it is not statistically significant. The J&J trial unfortunately did not give a full accounting of the causes of death in the final 4-month followup.  However, there were no cardiac deaths in the vaccine group at two months even though there were three such deaths in the placebo group.  The AstraZeneca results are reported across different trials at 4-5 months. In the pooled results for the trials in South Africa, Brazil, and the UK, no cardiac deaths at all were reported.  In the pooled results for the US, Chile, and Peru, there was one cardiac death in the placebo group and none in the vaccine group. 
While these are not statistically robust comparisons, there seems to be a trend for excess cardiac death with the mRNA vaccines that is not emerging for the adenoviral vectored vaccines. The trend is strongest for Pfizer and more modest for Moderna. We may invoke Moderna’s greater immunogenicity to explain why it has a weaker trend than Pfizer, which implicates the spike protein since that is what the immune system primarily responds to. As to why this trend seems shared across these three vaccines but not the adenoviral vectored vaccines, my speculation is that the heart is a major expressor of LPL, so takes up more spike mRNA from Pfizer and Moderna.
Conclusions From the Adverse Effects Comparisons
These are the main conclusions I draw:
The spike protein is the major explanation for COVID vaccine side effects. Most adverse effects are shared across the vaccines. Where they differ from the effects of the virus can easily be explained by different tissue distributions.
Viral infection seems to cause a much higher rate of inflammation-induced deficiencies of iron and zinc, although this seems robust for zinc, while for iron, VAERS and React19 surveys conflict.
The vaccines cause a much higher rate of hypertension, heart inflammation, and neurological disorders and have a unique impact on menstrual cycles.
Compared across vaccines, adenoviral vectored vaccines definitely create an outsized risk of central venous thrombosis with thrombocytopenia, although the mRNA vaccines contribute to VAERS reports for these disorders as well.
While the toxicity of the lipid nanoparticles is very concerning for general health and may be driving side effects for some people, no adverse effect stands out as a unique effect of the mRNA vaccines. Greater uptake of these vaccines into the heart and brain via LPL can explain most of the differential rates between the vaccines.
Where Moderna has lower rates of reporting than Pfizer, it is usually best explained by a protective effect of the greater immune response. This, in particular, argues against a general hyperactivity of the immune response being the culprit. While autoimmune conditions may represent overactivity of the autoantibodies, a stronger immune response is generally a good thing when it comes to COVID vaccine side effects.
The exception seems to be for cognitive impairment, where Moderna is worse, perhaps due to greater inflammation-induced sequestration of iron.
What is Driving Vaccine Side Effects?
I believe spike protein toxicity is the most universal reaction to the vaccines. Whereas autoimmunity is not a typical response to them, circulating spike protein is the universal response.
The most likely mechanisms of spike protein toxicity are in acting as a pore-forming toxin, increasing the production of breakdown-resistant clots, and binding to ACE2 receptors to drive increases in hypertension.
Spike protein toxicity and autoimmunity are not mutually exclusive, but the causation starts with the spike protein. Spike protein toxicity will cause tissue damage, and tissue damage often causes autoimmunity.
Nevertheless, I believe that those suffering side effects can be broadly classed into those where the immune system is doing the bulk of the damage – as in the hepatitis patient with no spike protein in his liver but plenty of anti-spike T cells  – and those where the immune system running sluggish is driving the persistence of the spike protein and its enduring toxicity – as might have been the case in the fatal myocarditis victim whose heart tissue had spike protein found in it at the time of death. 
In support of this two-type model, a React19 survey found that corticosteroids – which have immunosuppressive properties – were the most polarizing medication, with many people reporting improvement but many people reporting getting worse.
The immunosuppressed type is most likely driven by vaccine-induced rises in MDSCs, as supported by the five-fold increase in arginase-expressing cells in the wake of Pfizer vaccination.
The autoimmune type is most likely driven by anti-idiotype antibodies to the spike protein that damage its targets, such as ACE2 and neuropilin-1, or by autoantibodies that rise in the wake of spike protein toxicity-induced tissue damage.
Nevertheless, there are at least some people for whom inflammation-induced sequestration of iron is the dominant theme. This is supported by the prevalence of hair loss and memory issues in the React19 survey, the outsized reporting of cognitive issues in VAERS for the more strongly immunogenic Moderna vaccine, and two case reports of young women in their 20s and 30s who developed dangerous autoimmune relapses after vaccination, with dramatically increased ferritin. [138,139]
I hope this proves valuable to people doing research on healing from COVID vaccine side effects.
My protocol can be accessed here:
References can be found below.
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