Type II comes later, when the immune system kicks in. Clotting is caused by the antibodies produced against platelet factor 4: https://www.nature.com/articles/s41586-021-03744-4 (the study is about vaccine induced clotting, but the real virus triggers the creation of these antibodies too). Additionally, the virus destroys ACE2, ACE to is also an enzyme that creates stuff that reduces oxidative stress, oxidative stress in the blood vessels raises the clotting factors. Silencing the immune reaction is done by the virus itself, it sends proteins into the nucleus that dampen the gene expression needed by the cell to produce stuff for self defence and to alert the immune system (ivermectin stops the virus from doing that).
Another theory about how the virus causes clotting is gaining traction. The theory is not substantiated by studies yet, but by a very successful treatment protocol in India based on the theory:
Blood clotting caused by inflammation of the inner cells of the blood vessels (caused by the oxidative stress and by the virus destroying the cells). Stop neutrophils (leukocytes) from moving to the sites of inflammation (after you have stopped the virus replication with ivermectin), and the patient will survive. Colchicine does the trick.
A safer and maybe more effective way is to give a 0.5 mg bolus of calcifediol, which will cause the inflammation to stand down. To cover yourself, you could test the calcifediol level, but if the patient is very sick, the calcifediol level is very likely to be in the deficient category.
Most doctors think that calcitriol is the go to, like Marik's Frontline Critical Care Alliance, but that's actually a mistake. There are several reasons, including the risk of hypercalcemia and hypercaluria, causing naive immune cells to specialize, likely using them up, because naive immune cells can't be replaced after 40 y.o. by the thymus, and turning off inflammation systemically when some locations may have an active infection or cancer.
Better to dose with calcifediol and let the immune system determine where to make calcitriol itself. Because the immune system can make calcitriol from calcifediol, just like the kidneys.
Calcitriol seems to be the way to go when the level is low and has to raise fast after an infection. Maybe the FLCCCs should make clear that calcifediol is sufficient for prevention.
From a data science, mathematician and computational economics standpoint, very little if any of the reporting on covid-19 since 2020 is meaningful or can be trusted.
The PCR tests in so far as the cycle thresholds being set to numbers above 28 amount to exploitation parameter setting in algorithms such as reinforcement learning that result in model over fitting. Therefore what you end up with are a lot of false positives and false negatives.
What makes the PCR testing even more problematic is the asymmetric testing that was happening once the vaccines started being rolled out, i.e. vaxxinated tested at thresholds of 28 while unvaccinated tested at a threshold of 45.
Therefore, not only do we not know if all the cases and deaths up until now have truly been covid or regular flu or cold. Compounding this is the decision to count everything as covid, so death with a positive covid test was counted as death from covid even if covid was clearly not the cause of death reported by the doctors.
The abnormal nature of contracts allegedly signed with the pharma companies in relation to the vaccines (such as IP protection and using military bases as collateral to fund vaccine purchases, etc) raises further questions around perverse incentives just as hospitals being paid per covid case and death reported.
The handling of the SARS-Cov2 outbreak has been beyond moronic from the get go and it continues to be as the various vultures circle. One could understand early on when no one knew what we were dealing with, but 18 months on and nothing has changed but things have become more entrenched. So while it would be welcome to see a stop to the mass vaccinations during an pandemic entailing a family of viruses known for their mutations, I am not convinced the insanity is going to end any time soon. Far too many financial and other interests (including pride and egos) at play it seems
Some of the papers referenced in the study have been questioned. Ackermann M, Verleden SE, Kuehnel M, Haverich A, Welte T, Laenger F, et al. Pulmonary vascular endothelialitis, thrombosis, and angiogenesis in Covid-19. N Engl J Med 2020;383:120–8, doi:http://dx.doi.org/10.1056/NEJMoa2015432. – was questioned by Felix Scholkmann, Ph.D.University Hospital Zurich, Zurich, Switzerland - https://www.nejm.org/doi/10.1056/NEJMc2022068.
Global spread of severe acute respiratory syndrome coronavirus 2 continues unabated. Binding of severe acute respiratory syndrome coronavirus 2's spike protein to host angiotensin-converting enzyme 2 triggers viral entry, but other proteins may participate, including the neuropilin-1 receptor (NRP-1). Because both spike protein and vascular endothelial growth factor-A (VEGF-A)—a pronociceptive and angiogenic factor, bind NRP-1, we tested whether spike could block VEGF-A/NRP-1 signaling. VEGF-A-triggered sensory neuron firing was blocked by spike protein and NRP-1 inhibitor EG00229. Pronociceptive behaviors of VEGF-A were similarly blocked through suppression of spontaneous spinal synaptic activity and reduction of electrogenic currents in sensory neurons. Remarkably, preventing VEGF-A/NRP-1 signaling was antiallodynic in a neuropathic pain model. A “silencing” of pain through subversion of VEGF-A/NRP-1 signaling may underlie increased disease transmission in asymptomatic individuals."
Here is your mechanism. Spike silences nociception by occupying NRP-1, and this occupation facilitates even more entry into cells.
Likewise, despite numerous available articles, prints, and reports on neuropilin-1 and SARS-CoV-2, I hear and see a great silence about this problem among both those who are greatly fearful of COVID-19 and those who are greatly fearful of governments' response to COVID-19. But there are many, many articles to find and read and understand. This is a problem.
Folks there is no Covid- we are dealing with a mass PCR Test fraud that does not Rule out BACTERIA- the old mans chart state he had Bacterial Pneumonia, CDC has renamed ordinary disease we have always died from as COVID to create a world wide market for vaccines. its shameful they actually call it PICS - Pnuemonia Influenza CoronaVirus and SEPSIS. corornavirus is COMMON COLD- Cytokine storm is SEPSIS. this is why Paul Mark MD from Eastern Virginia Medical was successfully treating supposed COVID patients in ICU and no deaths with IV high dose Vitamin C known as the MATH protocol bec he treated them all like SEPSIS. God help this scam on humanity and all those misdiagnosed and mistreated especially with deadly ventilators. and now deaths from the shots. www.vaccinedeaths.com
Dr David Martin and Esg Reiner Fuellmich explains the Patent and PCR test Fraud.
"The condition of silent hypoxia (or "happy hypoxia") describes some COVID-19 sufferers who present no outward symptoms at all"
I'm a fan of your writing, but this is a major error. Severe fatigue is a symptom of silent hypoxia. If you think about it a bit, it can be no other way.
Even in what you call "type 1" and others call "mild", you have issues with microclotting per the literature--just the severity of the microclotting is less than is the case if the disease progresses. The later stage immune response will magnify the impact of the microclotting.
Type II comes later, when the immune system kicks in. Clotting is caused by the antibodies produced against platelet factor 4: https://www.nature.com/articles/s41586-021-03744-4 (the study is about vaccine induced clotting, but the real virus triggers the creation of these antibodies too). Additionally, the virus destroys ACE2, ACE to is also an enzyme that creates stuff that reduces oxidative stress, oxidative stress in the blood vessels raises the clotting factors. Silencing the immune reaction is done by the virus itself, it sends proteins into the nucleus that dampen the gene expression needed by the cell to produce stuff for self defence and to alert the immune system (ivermectin stops the virus from doing that).
I will give it a read. Thank you for commenting. I am constantly learning more from so many people.
Another theory about how the virus causes clotting is gaining traction. The theory is not substantiated by studies yet, but by a very successful treatment protocol in India based on the theory:
Blood clotting caused by inflammation of the inner cells of the blood vessels (caused by the oxidative stress and by the virus destroying the cells). Stop neutrophils (leukocytes) from moving to the sites of inflammation (after you have stopped the virus replication with ivermectin), and the patient will survive. Colchicine does the trick.
https://odysee.com/@DrMobeenSyed:1/dr.-darrell-demello-discusses-covid-3:1
A safer and maybe more effective way is to give a 0.5 mg bolus of calcifediol, which will cause the inflammation to stand down. To cover yourself, you could test the calcifediol level, but if the patient is very sick, the calcifediol level is very likely to be in the deficient category.
Yes, while it's never too late (trial: vitamin D in hospital: https://www.sciencedirect.com/science/article/pii/S0960076020302764#bib0055) - better make sure you have a healthy level. The recommended daily allowance is way too low and your doctor can measure the level.
Yes, Castillo, et. al. did the pilot study.
Most doctors think that calcitriol is the go to, like Marik's Frontline Critical Care Alliance, but that's actually a mistake. There are several reasons, including the risk of hypercalcemia and hypercaluria, causing naive immune cells to specialize, likely using them up, because naive immune cells can't be replaced after 40 y.o. by the thymus, and turning off inflammation systemically when some locations may have an active infection or cancer.
Better to dose with calcifediol and let the immune system determine where to make calcitriol itself. Because the immune system can make calcitriol from calcifediol, just like the kidneys.
Calcitriol seems to be the way to go when the level is low and has to raise fast after an infection. Maybe the FLCCCs should make clear that calcifediol is sufficient for prevention.
From a data science, mathematician and computational economics standpoint, very little if any of the reporting on covid-19 since 2020 is meaningful or can be trusted.
The PCR tests in so far as the cycle thresholds being set to numbers above 28 amount to exploitation parameter setting in algorithms such as reinforcement learning that result in model over fitting. Therefore what you end up with are a lot of false positives and false negatives.
What makes the PCR testing even more problematic is the asymmetric testing that was happening once the vaccines started being rolled out, i.e. vaxxinated tested at thresholds of 28 while unvaccinated tested at a threshold of 45.
Therefore, not only do we not know if all the cases and deaths up until now have truly been covid or regular flu or cold. Compounding this is the decision to count everything as covid, so death with a positive covid test was counted as death from covid even if covid was clearly not the cause of death reported by the doctors.
The abnormal nature of contracts allegedly signed with the pharma companies in relation to the vaccines (such as IP protection and using military bases as collateral to fund vaccine purchases, etc) raises further questions around perverse incentives just as hospitals being paid per covid case and death reported.
The handling of the SARS-Cov2 outbreak has been beyond moronic from the get go and it continues to be as the various vultures circle. One could understand early on when no one knew what we were dealing with, but 18 months on and nothing has changed but things have become more entrenched. So while it would be welcome to see a stop to the mass vaccinations during an pandemic entailing a family of viruses known for their mutations, I am not convinced the insanity is going to end any time soon. Far too many financial and other interests (including pride and egos) at play it seems
"...18 months on and nothing has changed but things have become more entrenched."
Yes, deeper and deeper we go.
So we ramp up our critical thinking skills and separate the baby from the bathwater.
Trust, but verify. Blind trust is for weak minds.
Out of interest and some morr possible questions
Some of the papers referenced in the study have been questioned. Ackermann M, Verleden SE, Kuehnel M, Haverich A, Welte T, Laenger F, et al. Pulmonary vascular endothelialitis, thrombosis, and angiogenesis in Covid-19. N Engl J Med 2020;383:120–8, doi:http://dx.doi.org/10.1056/NEJMoa2015432. – was questioned by Felix Scholkmann, Ph.D.University Hospital Zurich, Zurich, Switzerland - https://www.nejm.org/doi/10.1056/NEJMc2022068.
See the paper Differentiating Coronavirus by Electron Microscopy- also stated Ackermann M et al - Unidentifiable structure Scholkmann et al. (29) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8007326/pdf/20-4337.pdf
The other issue is that PCR is being used as a diagnostic tool?
Then of course where was SARS-CoV ever identified and where has the aetiology of Covid nineteen been shown?
I notice zero toxicology testing was done?
"SARS-CoV-2 spike protein co-opts VEGF-A/neuropilin-1 receptor signaling to induce analgesia" https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7737878/
"Abstract
Global spread of severe acute respiratory syndrome coronavirus 2 continues unabated. Binding of severe acute respiratory syndrome coronavirus 2's spike protein to host angiotensin-converting enzyme 2 triggers viral entry, but other proteins may participate, including the neuropilin-1 receptor (NRP-1). Because both spike protein and vascular endothelial growth factor-A (VEGF-A)—a pronociceptive and angiogenic factor, bind NRP-1, we tested whether spike could block VEGF-A/NRP-1 signaling. VEGF-A-triggered sensory neuron firing was blocked by spike protein and NRP-1 inhibitor EG00229. Pronociceptive behaviors of VEGF-A were similarly blocked through suppression of spontaneous spinal synaptic activity and reduction of electrogenic currents in sensory neurons. Remarkably, preventing VEGF-A/NRP-1 signaling was antiallodynic in a neuropathic pain model. A “silencing” of pain through subversion of VEGF-A/NRP-1 signaling may underlie increased disease transmission in asymptomatic individuals."
Here is your mechanism. Spike silences nociception by occupying NRP-1, and this occupation facilitates even more entry into cells.
Likewise, despite numerous available articles, prints, and reports on neuropilin-1 and SARS-CoV-2, I hear and see a great silence about this problem among both those who are greatly fearful of COVID-19 and those who are greatly fearful of governments' response to COVID-19. But there are many, many articles to find and read and understand. This is a problem.
Folks there is no Covid- we are dealing with a mass PCR Test fraud that does not Rule out BACTERIA- the old mans chart state he had Bacterial Pneumonia, CDC has renamed ordinary disease we have always died from as COVID to create a world wide market for vaccines. its shameful they actually call it PICS - Pnuemonia Influenza CoronaVirus and SEPSIS. corornavirus is COMMON COLD- Cytokine storm is SEPSIS. this is why Paul Mark MD from Eastern Virginia Medical was successfully treating supposed COVID patients in ICU and no deaths with IV high dose Vitamin C known as the MATH protocol bec he treated them all like SEPSIS. God help this scam on humanity and all those misdiagnosed and mistreated especially with deadly ventilators. and now deaths from the shots. www.vaccinedeaths.com
Dr David Martin and Esg Reiner Fuellmich explains the Patent and PCR test Fraud.
here.
Explains No Delta Variant or any New Virus-
https://www.bitchute.com/video/et6pKCMRcS6G/
www.whatreallymakesyouill.com
I would have thought that the PCR testing only tests for the other genes of the virus and not that of the spike protein, or is that not the case?
I believe my article “The Pseudouridine Question” explains the mechanism behind why the symptoms are suppressed while the spike protein proliferates.
"The condition of silent hypoxia (or "happy hypoxia") describes some COVID-19 sufferers who present no outward symptoms at all"
I'm a fan of your writing, but this is a major error. Severe fatigue is a symptom of silent hypoxia. If you think about it a bit, it can be no other way.
Even in what you call "type 1" and others call "mild", you have issues with microclotting per the literature--just the severity of the microclotting is less than is the case if the disease progresses. The later stage immune response will magnify the impact of the microclotting.