By : Robyn Chuter
As the experimental COVID-19 injection body count piles up, the need to develop effective therapies for the ever-growing laundry list of injuries is becoming increasingly urgent.
Yet people who have suffered such injuries face almost insurmountable barriers to receiving treatment within our existing “sick care” system:
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That’s the bad news. The good news is that outside the noxious echo chamber of the pharmaceutical-medical-industrial complex, the old-fashioned practice of patient-centred health care has been revived by the manufactured COVID crisis.
Independently-minded practitioners of both orthodox medicine and ‘alternative’ health care have realised that since they can no longer believe a word that comes out of the mouths of bought-and-paid-for public health officials and heads of regulatory and licensing bodies, nor a word printed in medical journals, they are going to have to revert to time-tested practices of caring for sick people:
N.B. None of the following constitutes medical advice, and you should always consult a knowledgeable practitioner to develop a treatment plan tailored to your personal situation.
How do COVID-19 injections cause harm?1. Microvascular thrombosesThe fact that, in a substantial proportion of people who receive them, COVID-19 injections cause microscopic blood clots in the tiny blood vessels that supply the brain, lungs, heart, kidneys, liver and other vital organs with blood, was first publicly discussed by Canadian doctor Charles Hoffe in July 2021.
Dr Hoffe used the d-dimer blood test to identify recently-formed blood clots in 62% of patients whom he tested within 4-7 days after they’d taken a COVID-19 injection.
Depending on the location/s where these microscopic clots form, individuals might experience persistent headache, confusion, stroke, personality changes and cognitive decline; pain, numbness or tingling in the extremities, progressing in more severe cases to the need for amputation; liver, kidney or heart failure; fatigue and reduced exercise tolerance; pulmonary arterial hypertension; miscarriage or stillbirth; or blurred vision or hearing loss.
The fact that 38% of Dr Hoffe’s recently-jabbed patients did not have elevated d-dimer levels speaks to individual differences in propensity to form clots, and some of these differences are subject to influence through lifestyle choices and therapeutic interventions.
Reducing the risk of microvascular thromboses:
1.11. Aspirin and related compoundsThe traditional mainstay of antithrombotic therapy, aspirin, is recommended in some protocols intended to prevent or reduce jab side effects (e.g. see here and here).
However, aspirin carries its own risks, and may not be suitable for everyone. Fortunately, there are many plant foods that are rich in salicylic acid – the principal metabolite of aspirin – and research has demonstrated that the range of blood levels of salicylic acid found in people taking low-dose aspirin overlaps with the range found in people on vegetarian diets.
Spices (especially cardamom, cumin, paprika and black cumin), herbs (especially rosemary, oregano and thyme), fruits (especially nectarines and berries) and tea all contain substantial amounts of salicylic acid and when consumed as part of daily meals, can help to maintain blood levels of this metabolite that may reduce clotting risk.
1.2. NattokinaseA potent blood-clot dissolving enzyme which has been used for the treatment of cardiovascular diseases, nattokinase is produced by the bacterium Bacillus subtilis during the fermentation of soybeans to produce the traditional Japanese food natto.
While natto is characterised as – ahem – an acquired taste, variously described as like old cheese, slime and snot, nattokinase is available in supplement form.
1.3. SerratiopeptidaseLike nattokinase, serratiopeptidase is a proteolytic (protein-degrading) enzyme. As well as helping to break down fibrin – a crucial protein involved in the formation of blood clots – serratiopeptidase also has anti-inflammatory, analgaesic (pain-relieving) and anti-oedemic effects which may be useful for some types of COVID-19 injection injuries.
Serratiopeptidase’s ability to break down dead or damaged tissue may also prove useful in clearing necrosis from areas affected by microthromboses.
Researchers have proposed using serratiopeptidase to treat COVID-19, and many of the mechanisms they identified – especially its anti-inflammatory, fibrin-degrading, antioxidant and mast cell-stabilising properties – are also relevant to injection injuries.
Originally derived from bacteria that inhabit the intestines of silkworms, it is now produced synthetically and marketed as serrapeptase.
1.4 QuercetinQuercetin, a flavonoid molecule found in many vegetables and fruits, especially berries, lovage, capers, coriander/cilantro, dill, apples, and onions, and also available as a supplement, prevents platelet aggregation which is a critical step in clot formation.
2. Damaging effects of spike proteinBoth the viral vector COVID-19 injections (AstraZeneca and Johnson & Johnson) and the mRNA injections (Moderna and Pfizer) insert instructions into your body’s cells for making the spike protein of SARS-CoV-2.
As mentioned in my previous post, Let’s talk about sin, baby (the original antigenic variety), spike protein is found in the bloodstream of people 1-2 days after receiving the Pfizer injection, at essentially the same levels as in people severely ill with COVID-19. Injection-induced spike protein is still detectable in 63% of injected people, one week after the first dose. Similar findings have been reported in people who received the Moderna injection.
Recall that the spike protein of SARS-CoV-2 is the part of the virus that enables it to sneak into our cells, by binding with ACE2 receptors on the cell membrane. Once inside, other parts of the virus’ genetic code hijack our cellular machinery, forcing our own cells to become virus factories which churn out new copies of the virus that eventually erupt out of the cell and seek other cells to infect.
Researchers at the Salk Institute conducted a series of experiments to find out if spike protein alone, without any other part of the virus that can actually replicate inside cells, could cause damage both in living animals, and in isolated human cells. And indeed it does.
The binding of SARS-CoV-2 spike protein to ACE2 results in damage to the mitochondria – the tiny ‘power plants’ inside cells that turn molecules derived from food into usable energy – resulting in impaired cell function and inflammation.
Many cell types express ACE2, including types of cells found in the lungs, heart, kidneys, intestine and the delicate lining of the blood vessels themselves (endothelial cells). Whilst circulating in the bloodstream, spike protein can and will be taken up by any of these cell types.
The cell type used in the Salk Institute studies was endothelial cells, and the researchers clearly demonstrated that the spike protein alone causes oxidative stress and inflammation (endothelitis).
And when endothelial cells become so damaged by this inflammation that they rupture, the spike protein inside them spills out and can enter the cells of the organ that the blood vessel was supplying, if they too express ACE2, and repeat the whole process of mitochondrial impairment, inflammation and cell rupture over again. In this way, injection-induced spike protein could work its way deeper and deeper into the body’s vital organs.
Furthermore, any cell which expresses the spike protein will be attacked by T cells, the immune system cells that defend against viral infections.
In most people who become infected with SARS-CoV-2, the infection – and therefore expression of spike protein by their own cells, and destruction of these cells by T lymphocytes – remains localised to the respiratory tract.
But COVID-19 injections are delivered into muscles, and from there enter the bloodstream and carry the instructions for making spike protein into cells throughout our bodies. That means that cells in many different organs begin displaying an abnormal, foreign protein, drawing T lymphocytes to attack and destroy them.
Do we see evidence of this spike protein-induced cell damage and T cell attack in people who have taken COVID-19 injections? Yes. Autopsies of people who died after receiving either viral vector or mRNA injections show
“1. inflammatory events in small blood vessels (endothelitis), characterized by an abundance of T-lymphocytes and sequestered, dead endothelial cells within the vessel lumen;
2. the extensive perivascular accumulation of T-lymphocytes;
3. a massive lymphocytic infiltration of surrounding non-lymphatic organs or tissue with T-lymphocytes.”
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Spike protein binders and neutralisers:In vitro (laboratory) studies have demonstrated the ability of a wide variety of substances to inhibit the ability of SARS-CoV-2 spike protein to bind to ACE2, thus preventing it from entering cells.
2.1 Prunella vulgarisThe herb Prunella vulgaris, a member of the mint family known variously as self-heal, heal-all, woundwort, heart-of-the-earth, carpenter’s herb, brownwort or blue curls, directly interrupts the binding of the spike protein to ACE2.
2.2 SuraminSuramin, an antiparasitic and antiviral compound which is on the World Health Organisation’s Model List of Essential Medicines, also directly interrupts the binding of the spike protein to ACE2. Suramin is not absorbed through the gastrointestinal tract and therefore must be administered via intravenous injection. Whilst suramin was originally synthesised from a distilled extract of pine needles, it is not at all clear – and in fact mechanistically unlikely – that pine needle tea has any binding effects on spike protein.
2.3 N-acetyl cysteine (NAC)The sulphur-containing compound NAC alters the 3-dimensional shape of the spike protein, preventing it from binding to ACE2. NAC also inhibits replication of SARS-CoV-2.
2.4 QuercetinA flavonoid compound found in many common plant foods and herbs, quercetin strongly binds to the SARS-CoV-2 spike protein, which prevents it from binding to ACE2. It also inhibits replication of SARS-CoV-2 and has anti-inflammatory and thrombin-inhibitory actions.
2.5 Artemisinin, thymol, carvacrol and emodinAll compounds found in many plants used in traditional Chinese and Western herbal medicine, artemisinin, thymol, carvacrol and emodin prevent the SARS-CoV-2 spike protein from binding to ACE2 on host cells at doses that are non-toxic and non-carcinogenic.
2.6 Neem bark extractAzadirachta indica (neem) bark extract binds to the spike protein, and also inhibits replication of SARS-CoV-2.
2.7 IvermectinA compound derived from the bacterium Streptomyces avermitilis, ivermectin docks with SARS-CoV-2 spike receptor binding domain preventing it from binding to ACE2. Ivermectin is also on WHO’s Model List of Essential Medicines and has broad-spectrum antiparasitic, anti-allergic, antimicrobial, antiviral, and anti-cancer effects.
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