Blood clots in COVID-19 patients: Simplifying the curious mystery

md_a

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Discussion & conclusion

Based on the literature and clinical observation of mysterious clots reported in the COVID-19 patients, expression of ACE2 in the endothelium of blood vessels, blood clotting pathways, interaction of the SARS-CoV-2 spike protein with host ACE2, the pathogenesis of SARS-CoV-2, and the role of ACE2 in RAS, we can hypothesize and end with the conclusion that the mysterious clots reported in the COVID-19 patients may be due to the binding of the spike protein of SARS-CoV-2 with the ACE2 receptor expressed in the endothelial cells of blood vessels which may cause, vasoconstriction and activation of the intrinsic pathway of coagulation and eventually results in the formation of blood clots.

 

tallglass13

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Thanks for this link and paper. It pretty much sums up what Ray Peat was saying a year ago, he basically said the exact same thing.
 

Perry Staltic

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They need to pay more attention to their own treatments rather than fixating so much on the virus. They hypothesize that the virus activates platelets which promote microthrombi, but it is known that biotrauma caused by mechanical ventilation (MV) can activate inflammatory pathways that promote de novo synthesis of adhesion molecules (precursors of microthrombi) in lungs and distal organs resulting in microthrombi, multiple organ failure and death.

Alveolar stretch imposed by MV did not only induce de novo synthesis of adhesion molecules in the lung but also in organs distal to the lung, like liver and kidney. No activation was observed in the brain. In addition, we demonstrated elevated cytokine and chemokine expression in pulmonary, hepatic and renal tissue after MV which was accompanied by enhanced recruitment of granulocytes to these organs. Our data implicate that MV causes endothelial activation and inflammation in mice without pre-existing pulmonary injury, both in the lung and distal organs.

 
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Lejeboca

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Discussion & conclusion

Based on the literature and clinical observation of mysterious clots reported in the COVID-19 patients, expression of ACE2 in the endothelium of blood vessels, blood clotting pathways, interaction of the SARS-CoV-2 spike protein with host ACE2, the pathogenesis of SARS-CoV-2, and the role of ACE2 in RAS, we can hypothesize and end with the conclusion that the mysterious clots reported in the COVID-19 patients may be due to the binding of the spike protein of SARS-CoV-2 with the ACE2 receptor expressed in the endothelial cells of blood vessels which may cause, vasoconstriction and activation of the intrinsic pathway of coagulation and eventually results in the formation of blood clots.

Thanks for the find.
Might this explain blood clots post injectus horribillis (astrazeneca) when the spike protein spikes and bind to ace2 receptor?
 

cedric

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How do surgical face masks affect functional MRI measurements? – Physics World
” Functional MRI measures the blood-oxygen-level-dependent (BOLD) response of the brain due to changes in blood flow during activation. The BOLD response is sensitive to the concentrations of oxygen and carbon dioxide (CO2) in the blood. Wearing a facial covering mixes the expired and inspired air streams. As you breathe out CO2, this mixing increases the amount of inspired CO2, resulting in mild hypercapnia (elevated blood CO2 levels). This hypercapnia increases cerebral blood flow and therefore elevates the measured BOLD signal, resulting in greater contrast in the fMRI compared with that seen in the absence of hypercapnia.
[…]
The resulting group activation maps from the sensory-motor task, which indicate the areas of the brain that are active during the task on-window, showed no significant differences between the mask-on and mask-off states. These results demonstrate that task-activation can be reliably detected while the participant wears a mask.

The baseline BOLD signal, which the team analysed using the nasal cannula air cycles, showed a significant difference between the mask-on and mask-off states. The results demonstrated that the face mask induced an average baseline signal shift of 30.0%, with the grey matter across the brain showing an evident deactivation (observed via an increase in signal without the air supply) in the group activation maps. The measured ETCO2 showed an average increase of 7.4%, confirming the predicted rise in inspired CO2 concentration with mask use.”
 

md_a

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Thanks for the find.
Might this explain blood clots post injectus horribillis (astrazeneca) when the spike protein spikes and bind to ace2 receptor?
Makowski, who recently published his hypothesis in the journal Viruses, believes the spike protein found on the surface of the virus might mimic proteins that regulate blood vessels and control the formation of blood clots, which could explain many of the non-respiratory complications of COVID-19.

The spike protein is an arm-like apparatus that the virus uses to attach to and enter healthy cells. At the tip of the spike protein rests a string of three amino acids called RGD. This structure is known for connecting cells to each other in the body.

..........

If not viral infection, what else could be causing injury to distant organs associated with COVID-19?

The most likely culprit that has been identified is the COVID-19 spike protein released from the outer shell of the virus into circulation. Research cited below has documented that the viral spike protein is able to initiate a cascade of events that triggers damage to distant organs in COVID-19 patients.

Worryingly, several studies have found that the spike proteins alone have the capacity to cause widespread injury throughout the body, without any evidence of virus.

What makes this finding so disturbing is that the COVID-19 mRNA vaccines manufactured by Moderna and Pfizer and currently being administered throughout the U.S. program our cells to manufacture this same coronavirus spike protein as a way to trigger our bodies to produce antibodies to the virus.

According to Whelan’s letter to the FDA, the “Pfizer/BioNTech vaccine is composed of an mRNA that produces a membrane-anchored full-length spike protein.”

A landmark study in Nature Neuroscience, published a few days after Whelan’s letter, found that the commercially obtained COVID-19 spike protein (S1) injected into mice readily crossed the blood-brain barrier, was found in all 11 brain regions examined and entered the parenchymal brain space (the functional tissue in the brain).
The researchers acknowledged that such widespread entry into the brain could explain the diverse neurological effects of S1 such as encephalitis, respiratory difficulties and anosmia (the loss of smell). The injected spike protein was also found in the lung, spleen, kidney and liver of the mice.

A second study published in December, 2020, in Neurobiology of Disease reported that the SARS-CoV-2 spike proteins showed a direct negative impact on endothelial cells and provide “plausible explanations” for the neurological consequences observed in patients with COVID-19.

The researchers demonstrated that the angiotensin-converting enzyme 2 (ACE2), a known binding target for the SARS-CoV-2 spike protein, is “ubiquitously expressed throughout various vessel calibers in the frontal cortex.”

In another investigation, researchers studying brain tissues from 13 fatal COVID-19 cases found pseudovirions (spike, envelope and membrane proteins without viral RNA) present in the endothelia of microvessels of all 13 brains. They concluded that ACE2+ endothelial damage is a central part of SARS-CoV-2 pathology and may be induced by the spike protein alone. Injection of the full-length S1 spike subunit in the tail vein of mice, as part of the same study, led to neurologic signs (increased thirst, stressed behavior).

An observed complication of SARS-CoV-2 infection in children is similar to the atypical Kawasaki disease shock syndrome characterized by multisystemic hyperinflammation, edema and vasculitis (MIS-C) that Whelan treats.

Research has found SARS-CoV-2 spike protein alone to be a potent inductor of endothelial dysfunction, suggesting that “manifestations of COVID-19 shock syndrome in children can be at least partially attributed to its action.”

Let’s now circle back to the concerns voiced by Whelan in his letter to the FDA:

“I am concerned about the possibility that the new vaccines aimed at creating immunity against the SARS-CoV-2 spike protein have the potential to cause microvascular injury to the brain, heart, liver and kidneys in a way that does not currently appear to be assessed in safety trials of these potential drugs.”

Whelan was referring to the fact that mRNA vaccines work by incorporating the genetic blueprint for the key spike protein on the virus surface into a formula that — when injected into humans — instructs our own cells to make the spike protein.

In theory, the body then will make antibodies against the spike protein to protect against SARS-CoV-2 infection.

The problem with this scenario, as we saw above, is that the spike protein alone — which the mRNA vaccines instruct the body to make — has been implicated as a key cause of injury and death in COVID-19 infections.

Based on the research conducted to date, it is very likely that some recipients of the spike protein mRNA vaccines will experience the same symptoms and injuries associated with the virus.

Again according to Whelan, “the potential to cause microvascular injury (inflammation and small blood clots called microthrombi) to the brain, heart, liver and kidney … were not assessed in the safety trials.”
 

Perry Staltic

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If not viral infection, what else could be causing injury to distant organs associated with COVID-19?

Read post #3. It's been known for decades.

 

md_a

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Perry Staltic

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These people are so pathetic. From the link above.

In a study of 18 COVID-19 patients with neurological symptoms who died in hospitals last April, Mukerji and colleagues found very low levels of viral RNA — the source of which is a mystery — in only five of the patient brains. Because the low RNA concentration “seems out of proportion to the profound deficits that people are experiencing,” Mukerji said, “I’d be extremely surprised [if] the majority of cases where people are having neurological symptoms are due to direct viral invasion.”

They can't make the obvious connection that the drugs used to comatize patients on ventilators for weeks and months can and frequently do cause severe neurological damage.


Nearly 80% of patients who stay in the ICU for a prolonged period—often heavily sedated and ventilated—experience cognitive problems a year or more later, according to a new study in NEJM.
 
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cedric

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Kounis syndrome after mRNA/PEG ?
"
Kounis syndrome is defined as acute coronary syndrome (symptoms such as chest pain relating to reduced blood flow to the heart) caused by an allergic reaction or a strong immune reaction to a drug or other substance.[1] It is a rare syndrome with authentic cases reported in 130 males and 45 females, as reviewed in 2017; however, the disorder is suspected of being commonly overlooked and therefore much more prevalent.[2] Mast cell activation and release of inflammatory cytokines as well as other inflammatory agents from the reaction leads to spasm of the arteries leading to the heart muscle or a plaque breaking free and blocking one or more of those arteries.[1][3]

The Kounis syndrome is distinguished from two other causes of coronary artery spasms and symptoms viz., the far more common, non-allergic syndrome, Prinzmetal's angina[4] and eosinophilic coronary periarteritis, an extremely rare disorder caused by extensive eosinophilic infiltration of the adventitia and periadventitia, i.e. the soft tissues, surrounding the coronary arteries.[5][6]

https://www.mdpi.com/2076-393X/9/3/221/pdf
 

StephanF

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In 2013, my mother had a bleeding ulcer, was hospitalized immediately and given a blood transfusion. She then had two massive strokes and died two days later.

Both, Thomas M. Riddick and Dr. T. C. McDaniel warned that blood transfusions can destabilize the blood’s Zeta Potential and can lead to strokes or heart attacks.

The Zeta Potential is an electrical measure on the stability of a colloidal suspension, such as blood. I posted in the past on this subject. I also posted a link to Riddick’s book, here it is again:


I also made a short introduction to the Zeta Potential that I handed out to physicians that treated my elder brother, who died from massive strokes from an 11-hour operation in 2018, where he also suffered a lung embolism, his heart set out and he went into a coma. Probably also from blood transfusions.

Riddick’s chapter on cardiovascular disease is presented on this website:


Zeta Aid, formulated by Dr. McDaniel, can be purchased here. I take it daily. It may possibly prevent the blood clotting during COVID-19 infection or from the vaccination:

 

charlie

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It may possibly prevent the blood clotting during COVID-19 infection or from the vaccination:
Do you think potassium bicarbonate can do this, or does it have to the be special mix of Dr. McDaniel's Zeta aid??
 

cedric

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Blood clots from masks?

Hypoxia Induces a Prothrombotic State Independently of the Physical Activity​

" Factor VIII and von Willebrand factor levels levels increased significantly in the active group, but not in the passive group. Plasma thrombin generation remained unchanged in both the active and passive group with increasing altitude and during 7 days of immobility in healthy subjects. However, by applying whole blood thrombin generation, we found an increased peak height and endogenous thrombin potential, and a decreased lagtime and time-to-peak with increasing levels of hypoxia in both groups. In conclusion, by applying whole blood thrombin generation we demonstrated that hypoxia causes a prothrombotic state. As thrombin generation in plasma did not increase, our results suggest that the cellular part of the blood is involved in the prothrombotic phenotype induced by hypoxia."
 

Tim Lundeen

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The spike protein on SARS-Cov-2 damages platelets and kills red blood cells, so that doesn't help. Vitamin C and thiamin are helpful.

I also made a short introduction to the Zeta Potential that I handed out to physicians that treated my elder brother, who died from massive strokes from an 11-hour operation in 2018, where he also suffered a lung embolism, his heart set out and he went into a coma. Probably also from blood transfusions.
Can you share that? :):

Also McDaniel has a book that is helpful,

Disease Reprieve: Living into the Golden Years​

Amazon product
 

cedric

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"
“Calling reported blood clots among hospitalized COVID-19 patients “a mystery,” an anxiety-raising report in Nature Magazine says blood clots arise in 20-30% of critically ill COVID-19 patients, blood thinners don’t reliably prevent these clots, and many hospitalized patients exhibit elevated levels of a protein fragment called D-dimer produced when clots dissolve, which is a “powerful predictor of mortality.”

Blood coagulation (clotting) in patients with COVID-19 is significantly deranged compared with healthy people, states a March 2020 report published in Clinical Chemistry & Laboratory Medicine. So modern medicine was aware of this problem over a year ago but it is only now gaining attention.
Hematologists have issued bulletins sounding the alarm over “severe abnormal blood clotting, leading to many micro-clots within the lungs” of COVID-19 patients. The alarm was issued when a report published in the British Journal of Haematology involving 83 patients, with 13 deaths, confirmed the problem.

A puzzling part of this problem is that blood platelet counts were normal. Increased fragments of clots (D-dimer) were observed only among patients admitted to the intensive care unit. Placing patients on heparin blood thinner prophylactically sometimes prevents the problem. But to add to the confusion, heparin did not significantly reduce D-dimer levels.

Antiplatelet and anticoagulant (blood thinning) drugs administered pre-admission to hospital do not seem to protect.

Another unnerving report published in E Clinical Medicine notes that 31% of COVID-19 patients in the intensive care unit have blood clots in their veins, but also 20% of non-hospitalized COVID-19 patients also were found to have venous clots.
By comparison, doctors observe arterial blood clots among patients with the flu are extremely rare. Blood clotting can occur among patients with the flu, but only in veins. For patients with COVID-19, blood clots can appear in either veins or arteries.

But maybe these cases of unexplained blood clotting that arise spontaneously are actually what is called pseudo-thrombotic microangiopathy, a recognized disorder that emanates from a vitamin B12 deficiency (often misdiagnosed as thrombotic thrombocytopenia purpura). Purpura refers to purplish bruises on the skin or in the mouth.[...]

Other Ways B12 Inhibits COVID-19

VITAMIN B12 IS NEEDED TO INHIBIT POLYMERASE, THE ENZYME THAT FACILITATES REPLICATION OF THE COVID-19 VIRUS, WHICH CAN REDUCE THE SEVERITY OF THE INFECTION.[...]

IT WAS WELL KNOWN, LONG BEFORE THE COVID-19 PANDEMIC, THAT A VITAMIN B12 DEFICIENCY MAY LEAD TO PSEUDO-THROMBOTIC MICROANGIOPATHY (CLOTS IN SMALL BLOOD VESSELS). CASES OF THROMBOSIS (CLOTTING) ARE RESOLVED WITH B12 SUPPLEMENTATION.

[...]
B12 Supplements

SURPRISINGLY, A RECENT REPORT INDICATES THAT METHYLCOBALAMIN B12CSUPPLEMENTS HAVE THE POTENTIAL TO REDUCE COVID-19-RELATED ORGAN DAMAGE AND SYMPTOMS.

ANOTHER REPORT REVEALS 500 MICROGRAMS OF B12 COMBINED WITH 1000 UNITS OF VITAMIN D AND 150 MILLIGRAMS OF MAGNESIUM REDUCED THE NEED FOR OXYGEN THERAPY IN THE INTENSIVE CARE UNIT.
[...]
ONE STUDY REVEALS 52.7% OF COVID-19 PATIENTS ARE MALNOURISHED. THIS IS A MASSIVE OVERSIGHT OF MODERN MEDICINE."
 

cedric

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Hypoxia-induced megaloblastosis in vitamin B12-deficient rats - PubMed
“Hypoxia-induced megaloblastosis in vitamin B12-deficient rats
Abstract
In rats, in contrast with human subjects who develop megaloblastic anaemia due to vitamin B12 deficiency, haematological abnormalities with anaemia were not observed under normoxic conditions even though plasma vitamin B12 concentration was reduced to <15 % of a normal concentration by depleting dietary vitamin B12.[…] In the vitamin B12-deficient rats in hypoxia, erythrocytes became abnormally enlarged, and haemoglobin concentration in peripheral blood was increased in proportion to the increase of mean corpuscular volume. […]In addition, in the vitamin B12-deficient rats, in contrast to the -sufficient rats, serum erythropoietin concentration was not normalized even after 6-week exposure to hypoxia. These results indicate that a megaloblastic anaemia-like symptom is induced when the vitamin B12-deficient rats are exposed to hypoxia."
 

cedric

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Multi-Vitamin B Supplementation Reverses Hypoxia-Induced Tau Hyperphosphorylation and Improves Memory Function in Adult Mice - PubMed
" . Supplementations of vitamin B6/B12/folate+choline could significantly ameliorate the hypoxia-induced memory deficits, observably decreased Hcy concentrations in serum, and markedly attenuated tau hyperphosphorylation at multiple AD-related sites through upregulating inhibitory Ser9-phosphorylated GSK-3β. Our finding give further insight into combined neuroprotective effects of vitamin B6, B12, folate, and choline on brain against hypoxia."

the diameter of capillaries is 4-5 mcm, macrocytes -8-9 mcm
How is Vitamin-B12 Related to Anemia?
" Macrocytic and Megaloblastic Anemia
When the body is deficient in vitamin B-12. it can produce red blood cells that are abnormally large, called macrocytes, which do not function properly. The main cause of macrocytic anemia is called megaloblastic anemia, which is due to reduction in DNA synthesis. When red blood cells are not functioning properly, the hemoglobin cannot bind to oxygen efficiently. Thus, many tissues around the body are not provided with enough oxygen to upkeep with their normal metabolism. This is called hypoxia and can lead to cell death. Deficiency in vitamin B-12 can also impair DNA synthesis, but the synthesis of RNA continues to happen without being converted into DNA. This causes lot of build-up of genetic material within the red blood cells, leading to abnormal size and lack of function."
 

cedric

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Severe Pernicious Anemia Predisposing to Hypoxic Hepatitis : ACG Case Reports Journal
Severe Pernicious Anemia Predisposing to Hypoxic Hepatitis
Abstract
Hypoxic hepatitis or ischemic hepatitis is most commonly encountered in critical care patients, most of whom have shock states secondary to cardiac or respiratory failure. We report a case of severe pernicious anemia predisposing to hypoxic hepatitis that had a good prognosis with simple treatment. Care should be taken in management of severe anemia, interpretation of serum vitamin B12 levels after blood transfusion, and the use of intravenous fluids.[…]

DISCUSSION
HH, shock liver, and ischemic hepatitis have been the terms used to describe the clinical syndrome characterized by rapid increase in liver transaminases in the setting of ischemia, shock, or hypoxia.1,2 Currently, diagnosis is based on 3 parameters: a state of reduced oxygen delivery to the liver, a significant and transient increase in serum transaminases, and last, the exclusion of other causes of liver injury like viral or medication or toxin induced hepatitis.3

HH is most commonly encountered in critical care patients with an incidence between 2% and 2.5%, and most of these patients present in shock states secondary to cardiac or respiratory failure.4–7 Our patient did not present with shock but with chronic severe anemia; indeed initial treatment with intravenous fluid might have been the precipitant of HH in our patient. A hemoglobin level of 1.8 g/dL could be compared with a shock state because there is an extremely low oxygen carrying capacity, and the infusion of 2 L of intravenous fluid before giving packed red blood cells might have worsened an already poor oxygen delivery state.
HH related to severe anemia was first described by Okras et al, which was followed by a study by Henrion suggesting that true shock is absent in up to half of the cases of HH.5,8 Apart from ischemia, several studies have also proposed the effect of free radical injury from reperfusion as a contributing factor in HH. This might also have been a contributing factor in the development of HH in our patient because giving intravenous fluids was the likely precipitant of HH.9,10 The typical pattern of AST and ALT elevation in HH is a peak within the first 24 hours, then levels drop down to half of the peak seen within 48 hours, then slowly return to baseline over the next 10–15 days. Lactate dehydrogenase (LDH) also elevates to a significantly higher level than that seen in viral hepatitis.1,5,11 The deranged liver function tests in the present case were consistent with this pattern and supports the diagnosis of HH. One feature worth mentioning is that the peak in LDH seen in this case can be attributed to 2 factors: the hemolysis caused by the B12 deficiency and the hypoxemia of the liver, both known to increase LDH levels. Given that the LDH levels were so drastically elevated, both factors likely contributed to this.

Prognosis of patients with HH is very poor. Mortality in hospitalized patients has been reported to be as high as 56%, the cause of death is not directly due to HH but is related to the underlying disease.1,2 Although there is no reported mortality of HH secondary to vitamin B12 deficiency anemia considering the rarity of this clinical entity, we postulate it maybe comparative considering the similarity in pathophysiology and the severity of the anemia that could very well be compared with any severely decompensated chronic condition or shock state.

The patient was transferred to the general medicine floors where she stayed for 6 additional days until her hemoglobin levels improved. Liver enzyme trend was consistent with the typical pattern of HH (Figure 2). She was discharged and seen in the clinic 3 weeks later, and her laboratory results showed methylmalonic acid level 152 nmol/L and vitamin B12 level was 675 pg/mL (Table 2)."
 
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