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Story at a glance:
- Long COVID refers to symptoms that persist for four or more weeks after an initial COVID-19 infection. Many are also reporting long COVID symptoms after getting the COVID-19 shot.
- Symptoms of long COVID include but are not limited to brain fog, memory problems, headaches, blurred vision, loss of smell, nerve pain, heart rate fluctuations, dramatic blood pressure swings and muscle weakness. The feeling of “internal electric shocks” are also reported.
- The primary difference between post-jab long COVID and long COVID symptoms after infection is that in people who get it from the infection, early treatment was withheld and the resulting infection severe. Post-jab long COVID, on the other hand, can occur either after very mild breakthrough infection or no breakthrough infection at all.
- Several different theories about the mechanisms behind long COVID are reviewed, as are treatment options.
- Swiss research has found the rate of subclinical myocarditis is hundreds of times more common than clinical myocarditis after mRNA injection and ALL mRNA shot recipients had elevated troponin levels, indicating they had some level of heart injury, even if they were asymptomatic.
However, while this condition has primarily been viewed as a side effect of the actual infection, many are reporting long COVID symptoms after getting the COVID-19 shot as well, regardless of brand.
As reported by Science magazine, “In rare cases, coronavirus vaccines may cause long COVID-like symptoms,” which can include (but are not limited to) brain fog, memory problems, headaches, blurred vision, loss of smell, nerve pain, heart rate fluctuations, dramatic blood pressure swings and muscle weakness. The feeling of “internal electric shocks” are also reported.
The primary difference between post-jab long COVID and long COVID symptoms after infection is that in people who get it from the infection, early treatment was withheld and the resulting infection severe.
Post-jab long COVID, on the other hand, can occur either after very mild breakthrough infection or no breakthrough infection at all.
Reluctance to publicly address post-jab long COVID
In January 2021, National Institutes of Health (NIH) researchers initiated testing and attempted treatment of patients suspected of having long COVID following their shot, but for unknown reasons the investigation petered out by the end of the year, leaving patients high and dry, without answers.
According to Science, NIH researchers did continue their work “behind the scenes,” and other researchers, worldwide, have also started studying the phenomenon. Still, there appears to be extreme reluctance to addressing post-jab long COVID symptoms publicly.
Dr. Avindra Nath, clinical director at the National Institute of Neurological Disorders and Stroke and the one leading the NIH’s investigation into long COVID, gives us a clue.
“Probing possible side effects presents a dilemma to researchers: They risk fomenting rejection of vaccines that are generally safe, effective, and crucial to saving lives,” Science writes.
“‘You have to be very careful’ before tying COVID-19 vaccines to complications, Nath cautions. ‘You can make the wrong conclusion … The implications are huge.’”
In other words, it’s all about protecting the vaccine industry, which has now merged with and become the experimental gene therapy industry.
Meanwhile, the human test subjects are left to suffer — many of whom don’t even realize that they ARE test subjects.
They bought the “safe and effective” and “rigorously tested” lies.
In Nath’s defense, he tried to publish a case series on about 30 of these patients but medical journals refused to publish it.
What’s causing long COVID?
As for the mechanisms behind long COVID, opinions vary. Research presented by Dr. Bruce Patterson at the International COVID Summit in Rome, in September 2021, suggests monocytes, shown to cause lung damage in patients with acute COVID-19, are also involved in long COVID.
In summary, the inflammatory cytokines that are supposed to trigger T cell activation fail to do so in some people, resulting in an inadequate antiviral response. Instead of T cells — which are needed to quell the infection — B cells and a particular subset of monocytes are elevated.
As described by HealthRising.org:
“When they used antibodies to look for evidence of coronavirus proteins in the monocytes … they found them — in spades. Seventy-three percent of the ‘non-classical’ monocytes in long-COVID patients carried the coronavirus proteins …
“These types of monocytes have often been thought to be anti-inflammatory, but recent studies show that they can, in some situations, produce pro-inflammatory cytokines. They’re mostly involved in ‘trash cleanup,’ and the antiviral response …
“The authors believe these monocytes were drawn to coronavirus-infected cells in the blood vessels, where they ingested them, and then put a coronavirus protein on their surface to alert the immune system.
“The problem in long COVID occurs when they are drawn to the blood vessels and injure them, or cause the blood vessels to inappropriately dilate.
“These nonclassical monocytes are the only monocytes to carry the CX3CR1 receptor, which when it binds to fractalkine, turns on an anti-apoptotic protein that allows the monocytes to survive longer than usual. It also causes the monocytes to revert from their anti-inflammatory state, and start pumping out pro-inflammatory cytokines.
“These are important steps as most monocytes die within a few days, and having very long-lived (up to at least 16 months) coronavirus protein-carrying monocytes is a crucial aspect of Patterson’s hypothesis …
“The monocyte binding also triggers the production of VEGF — which Patterson reports is elevated in almost all long haulers. VEGF then dilates the blood vessels causing, Patterson thinks, feelings of fullness in the head, migraines, and perhaps cognitive problems.”
The autoantibody theory
Another theory, put forth by Harald Prüss, a neurologist at the German Center for Neurodegenerative Diseases and the Charité University Hospital in Berlin, is that antibodies targeting the SARS-CoV-2 spike protein might be causing “collateral damage.”
“In 2020, while hunting for antibody therapies for COVID-19, [Prüss] and his colleagues discovered that of 18 antibodies they identified with potent effects against SARS-CoV-2, four also targeted healthy tissues in mice — a sign they could trigger autoimmune problems …
“Over the past year, research groups have detected unusually high levels of autoantibodies, which can attack the body’s own cells and tissues, in people after a SARS-CoV-2 infection.
“In Nature in May 2021, immunologists Aaron Ring and Akiko Iwasaki at Yale School of Medicine and their colleagues reported finding autoantibodies in acute COVID-19 patients that target the immune system and brain; they are now investigating how long the autoantibodies persist and whether they can damage tissues …
“In a paper Prüss and his colleagues are about to submit, they describe finding autoantibodies that attack mouse neurons and other brain cells in at least one-third of those patients.”
Researchers are also investigating whether post-jab long COVID might be due to autoantibodies against the angiotensin-converting enzyme 2 (ACE2) receptor, which is the target of the spike protein.
Since hormones can have slow and systemic actions, a dysfunctional or damaged endocrine system will generally be slow in its symptom onset and recovery, warned Dr. Flavio Cadegiani, a Brazilian endocrinologist.https://t.co/u5iJR3g7Gu
— Robert F. Kennedy Jr (@RobertKennedyJr) November 13, 2022
Other working theories
Other working theories include aberrant immune response caused by persistent activation of a particular subset of T cells, particularly in those whose long COVID symptoms include neurological complications.
Persistent microscopic blood clots is another theory being worked on by Resia Pretorius, a physiologist at Stellenbosch University in South Africa.
These clots then interfere with oxygen delivery, which can help explain symptoms such as brain fog.
Yet another theory is that the symptoms are caused by residual spike protein lodged in your tissues and organs — including your gut — which can take well over a year to clear after a serious infection.
As reported by Medical News Today:
“Researchers investigated the antigens of SARS-CoV-2 — the virus that causes COVID-19 — present in blood plasma samples collected from individuals with long COVID and typical COVID-19 infection.
“They found that one particular SARS-CoV-2 antigen — the spike protein — was present in the blood of a majority of long COVID patients, up to a year after they were first diagnosed with COVID-19. In patients with typical COVID-19 infection, however, the spike protein was not detected.
“This finding provides evidence for the hypothesis that SARS-CoV-2 can persist in the body through viral reservoirs, where it continues to release spike protein and trigger inflammation.”
In an effort to identify long COVID biomarkers, the researchers measured levels of three SARS-CoV-2 antigens: spike protein, the S1 subunit of the spike protein and the nucleocapsid (outer protein coat) of the virus.
All three antigens were found in the blood of 65% of the long COVID patients tested, but the spike protein was the most common and remained elevated the longest.
So, in short, a hallmark of long COVID is the long-term presence of spike protein, and spike protein is precisely what the COVID-19 jabs are instructing your cells to create.
Granted, the spike protein produced by your cells in response to the shot is genetically altered, so it’s not perfectly identical to the spike protein found on SARS-CoV-2 (which by the way also appears to be manmade), but regardless of their source, the spike protein appears to be a key pathogenic factor.
As such, it makes sense that many COVID-19 jab recipients are reporting long COVID-like symptoms, as their bodies are continually producing them.
mRNA shots injure hearts of ALL recipients
Contrary to initial claims, we know the mRNA in the COVID-19 shots travel throughout the body and accumulate in various organs. The cells in those organs then end up expressing the spike protein long-term.
Aside from the reproductive organs, your heart is a primary target, and recent Swiss research found the rate of subclinical myocarditis is hundreds of times more common than clinical myocarditis.
An estimated 1 in 27 women who got an mRNA COVID-19 shot had evidence of myocardial injury.
What’s more, they concluded that ALL recipients suffered some level of heart injury, even if they were asymptomatic.
In the video above, Dr. Vinay Prasad reviews this study and what it means to have subclinical myocarditis.
As reported by The Daily Skeptic:
“Crucially, the study found elevated troponin levels — indicating heart injury — across all vaccinated people …
“This indicates the vaccine is routinely injuring the heart (an organ which does not heal well) and that the known injuries are just the more severe instances of a far larger number occurring right across the board …
“These are not rare events, as is often claimed by medical authorities and in the media. They are alarmingly common.”
COVID jab deaths are being buried
All in all, evidence shows the COVID-19 jabs are an absolute health disaster, yet our health agencies are doing nothing to prevent it.
On the contrary, they’ve doubled and tripled down on their COVID-19 shot recommendations while simultaneously burying incriminating evidence.
In “How FDA and CDC Are Hiding COVID Jab Dangers” I detail how the U.S. Food and Drug Administration (FDA) and the Centers for Disease Control and Prevention (CDC) are refusing to release relevant data, have lied about trial findings, and even more egregiously, are now manipulating databases to artificially eliminate safety signals and hide excess jab-related deaths.
Originally published by Mercola.