The COVID 'vaccine' and the COVID 'infection' provoke increased blood clotting (thrombosis)? Is there evidence? Is there some treatment option to mitigate the effect of the vaccine clots?

by Paul Alexander

The real question then is, how do we prevent or manage the clots (often micro thrombi across the body/circulation) so that we can preserve life 'post' vaccine?

COVID is over, it is done! I am hoping you are realizing this, and OMICRON is really our stepping stone off this terrible COVID island. We have gained an ‘attenuated vaccine’ with OMICRON, a gift as Malone says. Vaccination will continue to drive variants (mass vaccination during a pandemic using a non-sterilizing sub-optimal vaccine with infectious pressure intersecting with mounting immune pressure) and side effects like dangerous blood clots. Vaccination MUST be stopped and NONE for our children!

Is there evidence of clotting (and/or bleeding)? Yes. An elevated D-dimer test result is almost a definitive confirmation of abnormal blood clotting taking place somewhere in the body. The clots can be microscopic (micro thrombi), at the finer capillary level, or even much larger, and even involving thrombosis of much large blood vessels. A post-vaccination syndrome which is called vaccine-induced prothrombotic immune thrombocytopenia (VIPIT) has emerged as a real blood-clotting concern in the COVID era. I present studies that document clotting and especially ones relating to vaccine as this is a cause for concern.

The proposed evidence for your review and reflection:

Biswas et al.: “High ACE2 expression in the endothelium of blood vessels facilitates the high-affinity binding of SARS-CoV-2 using spike protein, causing infection and internal injury inside the vascular wall of blood vessels. This viral associated injury may directly/indirectly initiate activation of coagulation and clotting cascades forming internal blood clots. However, the presence of these clots is undesirable as they are responsible for thrombosis and need to be treated with anti-thrombotic intervention.”

Magro et al.: “At least a subset of sustained, severe COVID-19 may define a type of catastrophic microvascular injury syndrome mediated by activation of complement pathways and an associated procoagulant state.”

Lazebnik:  A distinctive feature of the SARS-CoV-2 spike protein is its ability to efficiently fuse cells, thus producing syncytia found in COVID-19 patients. This commentary proposes how this ability enables spike to cause COVID-19 complications e.g. clotting as well as side effects of COVID-19 vaccines e.g. clotting, and suggests how these effects can be prevented.

Zhang et al: “Our findings uncovered a novel function of SARS-CoV-2 on platelet activation via binding of Spike to ACE2. SARS-CoV-2-induced platelet activation may participate in thrombus formation and inflammatory responses in COVID-19 patients.”

Iba et al: “Severe acute respiratory syndrome coronavirus 2/coronavirus disease 2019 frequently induces hypercoagulability with both microangiopathy and local thrombus formation, and a systemic coagulation defect that leads to large vessel thrombosis and major thromboembolic complications, including pulmonary embolism in critically ill hospitalized patients. D-dimers and fibrinogen levels should be monitored, and all hospitalized patients should undergo thromboembolism prophylaxis with an increase in therapeutic anticoagulation in certain clinical situations.”

Ng et al.: “It is also important to note that coronavirus disease 2019 (COVID-19) infection predisposes to an immuno-thrombogenic state, and a raised aPTT could also be due to the presence of a lupus anticoagulant. This has several clinical implications.”

Han et al: “The values of D-dimer, fibrin/fibrinogen degradation products (FDP), and fibrinogen (FIB) in all SARS-CoV-2 cases were substantially higher than those in healthy controls. Moreover, D-dimer and FDP values in patients with severe SARS-CoV-2 infection were higher than those in patients with milder forms. Compared with healthy controls, prothrombin time activity (PT-act) was lower in SARS-CoV-2 patients. Thrombin time in critical SARS-CoV-2 patients was also shorter than that in controls. Conclusions The coagulation function in patients with SARS-CoV-2 is significantly deranged compared with healthy people, but monitoring D-dimer and FDP values may be helpful for the early identification of severe cases.”

Tang et al.: “The present study shows that abnormal coagulation results, especially markedly elevated D-dimer and FDP are common in deaths with Novel coronavirus pneumonia.”

Zhang et al.: “D-dimer on admission greater than 2.0 µg/mL (fourfold increase) could effectively predict in-hospital mortality in patients with Covid-19, which indicated D-dimer could be an early and helpful marker to improve management of Covid-19 patients.”

Naymagon et al.: “Observational data suggest an acquired prothrombotic state may contribute to the pathophysiology of COVID-19. These data include elevated D-dimers observed among many COVID-19 patients.” 

Paliogiannis et al.: “Systematic review and meta-analysis showed that serum D-dimer concentrations in patients with severe COVID-19 are significantly higher when compared to those with non-severe forms.”

Rostami  et al.: “Studies have reported an increase in D-dimer and fibrinogen concentrations in the early stages of COVID-19 disease a 3 to 4-fold rise in D-dimer levels is linked to poor prognosis. In addition, underlying diseases such as diabetes, cancer, stroke, and pregnancy may trigger an increase in D-dimer levels in COVID-19 patients. Measuring the level of D-dimer and coagulation parameters from the early stage of the disease can also be useful in controlling and managing of COVID-19 disease.”

Favaloro: “In suspected VITT, there is a generally highly elevated level of D-dimer, thrombocytopenia, and PF4 antibodies can be identified by ELISA-based assays, but not by other immunological assays typically positive in HITT. In addition, in some functional platelet activation assays, standard doses of heparin have been identified to inhibit activation in suspected VITT, but they tend to augment activation in HITT.” 

Iba et al.: “Vaccine-induced immune thrombotic thrombocytopenia is an unexpected consequence of the coronavirus disease 2019 pandemic era. Vaccine-induced immune thrombotic thrombocytopenia is a serious complication of vaccination that is not feasible to anticipate or prevent. When the patient presents with sustained headache, neurologic symptoms/signs, abdominal pain, dyspnea, or limb pain/swelling beginning 5-30 days post vaccination, platelet count and d-dimer must be measured, and imaging for thrombosis performed. Confirmation of vaccine-induced immune thrombotic thrombocytopenia diagnosis should be ordered (platelet factor 4/polyanion enzyme-linked immunosorbent assay; platelet factor 4-enhanced platelet activation testing) as treatment is initiated (nonheparin anticoagulation, IV immunoglobulin).”

Scully et al.: “In the absence of previous prothrombotic medical conditions, 22 patients presented with acute thrombocytopenia and thrombosis, primarily cerebral venous thrombosis, and 1 patient presented with isolated thrombocytopenia and a hemorrhagic phenotype. All the patients had low or normal fibrinogen levels and elevated d-dimer levels at presentation.”

Thaler et al.: “Conclude that early initiation of VIPIT treatment results in a swift response without thrombotic complications.”

Perricone et al.: “The occurrence of adverse events and autoimmune phenomena has been described following vaccination, and ITP may represent one of this.”

Perry et al.: “Cerebral venous thrombosis is more severe in the context of VITT. Non-heparin anticoagulants and immunoglobulin treatment might improve outcomes of VITT-associated cerebral venous thrombosis.” 

Carli et al.: “Venous thromboembolic (VTE) complications have been consistently reported to be increased in SARS-CoV-2 infection, most probably as the results of a thrombophilic state secondary to inflammation and immune-thrombosis.”

Hadid et al.: “COVID-19 has become a pandemic in the United States and worldwide. COVID-19-induced coagulopathy (CIC) is commonly encountered at presentation manifested by considerable elevation of D-dimer and fibrin split products but with modest or no change in activated partial thromboplastin time and prothrombin time. CIC is a complex process that is distinctly different from conventional sepsis-induced coagulopathy. The cytokine storm induced by COVID-19 infection appears to be more severe in COVID-19, resulting in development of extensive micro- and macrovascular thrombosis and organ failure.”

Levi et al.: “Many patients with severe COVID-19 present with coagulation abnormalities that mimic other systemic coagulopathies associated with severe infections, such as disseminated intravascular coagulation (DIC) or thrombotic microangiopathy, but COVID-19 has distinct features.”

Reuben et al.: “The rising cases of severe adverse events following immunization (AEFI) with COVID-19 vaccines including thrombosis, thrombocytopenia, and in some instances, death have created serious global concerns and could enormously contribute to vaccine hesitancy.” 

Di Micco et al.: “Vaccines against Covid-19, in fact, exert a protective action for common people and reduce viral diffusion. Yet, vaccination of a large number of people raises the question of a well-known complication of several types of vaccines; this complication is immune thrombocytopenia, which is sometimes associated with thrombosis as well.”

Aleem et al.: “A new clinical syndrome characterized by thrombosis at atypical sites combined with thrombocytopenia was observed in multiple patients’ days after vaccination. This novel clinical syndrome demonstrated striking similarities to heparin-induced thrombocytopenia; however, in the absence of prior heparin exposure was named vaccine-induced immune thrombotic thrombocytopenia (VITT).” 

Cari et al.: “The immune reaction promoted by ChA vaccine may lead to not only thrombocytopenia and cerebral/splanchnic venous thrombosis but also other thrombotic and thromboembolic SAEs.”

Hippisley-Cox et al.: “Increased risks of haematological and vascular events that led to hospital admission or death were observed for short time intervals after first doses of the ChAdOx1 nCoV-19 and BNT162b2 mRNA vaccines.”

Levy suggests the following protocol with your doctor’s strong involvement to address the possible clotting (side effects) of the vaccine or infection:

  1. “For individuals who are post-vaccination or symptomatic with chronic COVID, vitamin C should be optimally dosed, and it should be kept at a high but lesser dose daily indefinitely.

    • Ideally, an initial intravenous administration of 25 to 75 grams of vitamin C should be given depending on body size. Although one infusion would likely resolve the symptoms and abnormal blood examination, several more infusions can be given if feasible over the next few days.

    • An option that would likely prove to be sufficient and would be much more readily available to larger numbers of patients would be one or more rounds of vitamin C given as a 7.5 gram IV push over roughly 10 minutes, avoiding the need for a complete intravenous infusion setup, a prolonged time in a clinic, and substantially greater expense (Riordan-Clinic-IVC-Push-Protocol, 10.16.14.pdf).

    • Additionally, or alternatively if IV is not available, 5 grams of liposome-encapsulated vitamin C (LivOn Labs) can be given daily for at least a week.

    • When none of the above three options are readily available, a comparable positive clinical impact will be seen with the proper supplementation of regular forms of oral vitamin C as sodium ascorbate or ascorbic acid. Either of these can be taken daily in three divided doses approaching bowel tolerance after the individual determines their own unique needs (additional information, see Levy, vitamin C Guide in References; Cathcart, 1981).

    • An excellent way to support any or all of the above measures for improving vitamin C levels in the body is now available and very beneficial clinically. A supplemental polyphenol that appears to help many to overcome the epigenetic defect preventing the internal synthesis of vitamin C in the liver can be taken once daily. This supplement also appears to provide the individual with the ability to produce and release even greater amounts of vitamin C directly into the blood in the face of infection and other sources of oxidative stress (

  2. Hydrogen peroxide (HP) nebulization (Levy, 2021, free eBook) is an antiviral and synergistic partner with vitamin C, and it is especially important in dealing with acute or chronic COVID, or with post-COVID vaccination issues. As noted above, the COVID virus can persist in the stool. In such cases, a chronic pathogen colonization (CPC) of COVID in the throat continually supplying virus that is swallowed into the gut is likely present as well, even when the patient seems to be clinically normal. This will commonly be the case when specific viral eradication measures were not taken during the clinical course of the COVID infection. HP nebulization will clear out this CPC, which will stop the continued seeding of the COVID virus in the gut and stool as well. Different nebulization approaches are discussed in the eBook.

  3. When available, ozonated saline and/or ozone autohemotherapy infusions are excellent. Conceivably, this approach alone might suffice to knock out the spike protein presence, but the vitamin C and HP nebulization approaches will also improve and maintain health in general. Ultraviolet blood irradiation and hyperbaric oxygen therapy will likely achieve the same therapeutic effect if available.

  4. Ivermectin, hydroxychloroquine, and chloroquine are especially important in preventing new binding of the spike protein to the ACE2 receptors that need to be bound in order for either the spike protein alone or for the entire virus to gain entry into the target cells (Lehrer and Rheinstein, 2020; Wang et al., 2020; Eweas et al., 2021). These agents also appear to have the ability to directly bind up any circulating spike protein before it binds any ACE2 receptors (Fantini et al., 2020; Sehailia and Chemat, 2020; Saha and Raihan, 2021). When the ACE2 receptors are already bound, the COVID virus cannot enter the cell (Pillay, 2020). These three agents also serve as ionophores that promote intracellular accumulation of zinc that is needed to kill/inactivate any intact virus particles that might still be present.

  5. Many other positive nutrients, vitamins, and minerals are supportive of defeating the spike protein, but they should not be used to the exclusion of the above, especially the combination of highly-dosed vitamin C and HP nebulization.”