Wednesday, May 26, 2021

The Biopolitics of Human Sacrifice: How Many Young People Will We Kill to Vaccinate Entire Population against Covid-19?


All vaccines have side effects. Expert authorities calculate cost-benefit ratios that include side effects. But what happens when the side effect is death and the population most at risk is valued less in our society than other segments?

This is not an idle question as the death count of young women under 40 killed by vaccines designed to prevent Covid-19 rises every day.


How many young people will die to save old people? This is a very important question that US news media will not address beyond repeating experts who assure us that the trade-off is acceptable. But acceptable for whom?

Today, I read that the country of Belgium is  halting the J&J vaccine for under 41-year olds after another young woman died after receiving that vaccine:

Belgium halts J&J COVID vaccine for under 41s after one dies

Belgium said on Wednesday it was suspending vaccinations with Johnson & Johnson's Janssen COVID-19 vaccine for people under the age of 41 following the death of a woman from severe side-effects after she was given the shot.G

"The Inter-ministerial conference has decided to temporarily administer Janssen's vaccine to the general population from the age of 41 years, pending a more detailed benefit-risk analysis by the EMA," said a statement issued by Belgium's federal health minister and sevenregionalcounterparts.

EMA is the European Union's European Medicines Agency. There was no immediate comment from EMA or J&J (JNJ.N).

The woman - who was under the age of 40 - died on May 21 after being admitted to hospital with severe thrombosis and platelet deficiency, the statement said.

Yesterday I read about a British woman who died in Cyprus after receiving the Astrazeneca vaccine:
British woman dies in Cyprus after AstraZeneca jab Issued on: 24/05/2021 - 14:07Modified: 24/05/2021 - 13:53

A 39-year-old British woman died in a Cypriot hospital after a blood clotting incident after receiving the AstraZeneca Covid-19 vaccine, the official Cyprus News Agency said Monday.

Charalambos Charilaou, spokesperson for the state health services, told CNA that the European Medicines Agency (EMA) would investigate the death.

The woman, treated at Nicosia General Hospital’s intensive care unit, received the first dose of the vaccine on May 6 in the resort town of Paphos on the western coast of the Mediterranean island.  The woman, who was not named, suffered symptoms days later. According to the Cyprus Mail newspaper, the woman suffered a brain haemorrhage and was in a coma before she died.
Update 5/28/2021 Yet another death of a young woman:

Campbell, Lucy (2021, May 27). Lisa Shaw death: BBC presenter had blood clots after AstraZeneca jab, family says. BBC

Update 6/21/2021 More Australians died of vaccine than virus:

John Bacon, Elinor Aspegren June 21, 2021More Aussies have died from AstraZeneca-related clots than COVID. USA TODAY
Since March, Belgium, Denmark and Iceland have placed limits on vaccines for younger (under 41 years old) people because of blood clots. 
If you read about these countries' decision to ban or limit vaccination for young people in the US media you will see dismissal of concerns, as found in this discussion by Newsweek of these countries' decisions:
But the questions really need to be asked:
  1. How likely is it that a woman in Europe or North America under 40 years old will die from Covid-19?
  2. How likely is it that a woman in Europe or North America under 40 will die from either the J&J or Astrazenca vaccine?
Covid-19 vaccine manufactures have been absolved or indemnified of liabilities from vaccine injuries in most countries, although India and Pfizer are at an "impasse" because India will not accept this indemnification - see Reuters here:
Removal of liability should prompt careful consideration of who is shouldering risk?
If women are more likely to die from these vaccines than the disease, then they are being asked to risk sacrificing their lives for older populations.
This question of odds needs to be systematically studied. However, the topic is being marginalized in the PUSH to get the entire population vaccinated using vaccines that have no legal liability and were not subject to long-term longitudinal studies.
Scientists who take up the question of whether we are unwittingly sacrificing lives in a flawed risk calculus are likely to be highly unpopular in their home institutions and professions and are not likely to be funded. Asking tough questions is not welcome when funding is at issue.
I am not anti-vaccine at all. However, requiring young women to risk sacrificing their lives to take a shot for a disease they are unlikely to die from and without any liability for vaccine manufacturers is human sacrifice. 
Moreover, there is now evidence of post-vaccine heart inflammation, especially afflicting young men
How many of those young men who experience heart inflammation will go on to have heart problems as a result of the vaccination or even die prematurely?
The "vaccine believers" in my life physically recoil when hearing of these adverse events and some have even expressed the desire to have news censored because such instances undermine confidence in the vaccines, which they see as integral to re-establishing normality. 
Such vaccine believers think that the statistical probability of adverse events from vaccines is less than from disease but yet the empirical question of whether someone under 40 is more likely to die of Covid-19 vaccines or virus has not been adequately considered in the US despite seeing bans on vaccination for young people with certain vaccines occurring in Europe.

The question of the intrinsic dangers of the spike protein in the absence of the rest of the vaccine must be addressed. The Salk Institute recently demonstrated that the topography of the spike protein can damage the vascular system in the absence of the rest of the virus. That is, the spike protein alone causes damage. See here:
People who had the virus seem to be more likely to have significant adverse side effects. Do people who were previously infected even need to be vaccinated?
There may be other types of vaccines or mechanisms for stopping transmission of an admittedly horrible disease that are equally effective and do not require that we make unwitting sacrifices of our young people.
If not, then the cost of our human sacrifices would need to be fully accounted for and agreed upon before inflicting it upon a critical segment of our population.


Merchant, H.A. CoViD vaccines and thrombotic events: EMA issued warning to patients and healthcare professionals. J of Pharm Policy and Pract 14, 32 (2021).

There are reports of antibodies present in CoViD-19 patients that activated platelets [4] and patients with thrombocytopenia following CoViD vaccination showed a favourable response to immune thrombocytopenia-directed therapies (corticosteroids and IVIG) [5].We proposed a likely mechanism on 15th March 2020 that the genetic CoViD-19 vaccines may directly infect platelets and megakaryocytes triggering mRNA translation and consequent spike protein synthesis intracellularly. This may potentially result in an autoimmune response against platelets and megakaryocytes resulting in reticuloendothelial phagocytosis and direct CD8+ T cell lysis [6]. The consequent thrombocytopaenia may lead to internal bleeding and spontaneous blood clots. On 19th March 2020, scientists from Oslo identified an antibody from vaccinated individuals which they suspect being responsible for attacking platelets and causing recent thrombotic events [7]. This discovery also supports our hypothesis [6] that CoViD genetic vaccines may have a direct role in spurring autoimmune response against platelets that may clinically manifest in thrombocytopenia, haemorrhage, and blood clots.

Pharmacovigilance can play a key role in early detection of potentially severe adverse events. The recent experience with Pandemrix raised fundamental questions on the regulatory approach to pharmacovigilance. It reminds us of the duty of the public health agencies to warn the public over possible harms of vaccines, the level of details that public should be made aware of, who should provide the information to public, and whether the provision of such information be proactive or passive [8]. The early signs of rare side effects during pharmacovigilance that may lead to severe adverse outcomes should never be dismissed just on the basis of prevalence statistics, but require thorough scientific investigations and clinical correlation to rule out a potential causal link. We, therefore, welcome EMA’s stance on issuing a caution to the public and physicians and support their decision of continued monitoring of thrombotic events more closely with necessary scientific investigations.

  "Vaccines and Rare Clotting Disorders: What's the Link?— Causal relation appears possible, but evidence still indicates it's extremely rare"
by Veronica Hackethal, MD, MSc, Enterprise & Investigative Writer, MedPage Today March 25, 2021

Whether these rare clotting events with low platelets in Europe and the ITP cases in the U.S. bear anything in common is anyone's guess right now.

One hypothesis is that the mRNA vaccines (Pfizer, Moderna) and those using adenoviruses (AstraZeneca, Johnson & Johnson) could induce synthesis of the COVID spike protein within platelets, which may then trigger autoimmune reactions against platelets, Hamid Merchant, PhD, of the University of Huddersfield in England, wrote in a letter to The BMJ.

"COVID genetic vaccines may have a direct role in spurring an autoimmune response against platelets that may clinically manifest in thrombocytopenia, hemorrhage, and blood clots. Clotting risks may be equally possible with all genetic COVID vaccines, and may not be limited only with the AstraZeneca/Oxford vaccine," he told MedPage Today.

Pruthi said ITP related to vaccination is probably a separate process involving a different autoantibody than the HIT reaction linked to the European CVST cases. ITP, when it causes clinical problems, usually results in bleeding because the autoantibody directly destroys platelets. In HIT reactions, the platelet factor 4 autoantibody activates platelets and promotes blood clots (see this MedPage Today story for further explanation of these distinct processes). The important point is that healthcare providers recognize the possibility that platelet factor 4 antibody could be involved in very rare cases of CVST with low platelets after vaccination for COVID-19.

Karron RA, Key NS, Sharfstein JM. Assessing a Rare and Serious Adverse Event Following Administration of the Ad26.COV2.S Vaccine. JAMA. Published online April 30, 2021. doi:10.1001/jama.2021.7637

This case series describes the first 12 reported cases of CVST with thrombocytopenia following Ad26.COV2.S vaccination in the US. In many respects, the clinical presentation and laboratory features were similar to those seen in Europe after ChAdOx1 nCoV-19 vaccine, another adenoviral vector COVID-19 vaccine.9-11

Similar to the initially described European cases of CVST with thrombocytopenia following ChAdOx1 nCoV-19 vaccination, the US cases of this condition also occurred primarily in women younger than 40 years and in patients without diagnosed thrombophilia.9,11 The European patients had a median platelet nadir count of 19 ×103/µL9,10 (US patients were also 19 ×103/µL), and several had non-CVST large-vessel thrombosis (30% of initially reported CVST cases following ChAdOx1 nCoV-19 vaccination9-11 vs 75% following Ad26.COV2.S vaccination).9-11 In the European cases of CVST with thrombocytopenia following ChAdOx1 nCoV-19 vaccination, 50% of patients died,9-11 compared with 25% of US patients who had CVST with thrombocytopenia.

Similar to the TTS cases (including CVST) described in Europe following receipt of ChAdOx1 nCoV-19 vaccine, the US cases of CVST with thrombocytopenia also had positive heparin-PF4 HIT antibody ELISA tests in the absence of prior exposure to heparin, as would be seen in autoimmune HIT.8 However, in the initial European CVST reports, 88% of patients tested with functional platelet HIT antibody tests had positive results9-11; in contrast, functional platelet HIT antibody test results were positive in only 1/9 (11%) of the US cases with results available. The heparin-PF4 ELISA detects presence of anti-PF4 antibodies; functional platelet HIT antibody assays determine the extent to which these antibodies activate platelets in the presence of heparin, leading to aggregation.20