Why are we vaccinating children against COVID-19?

This article examines issues related to COVID-19 inoculations for children. The bulk of the official COVID-19-attributed deaths per capita occur in the elderly with high comorbidities, and the COVID-19 attributed deaths per capita are negligible in children. The bulk of the normalized post-inoculation deaths also occur in the elderly with high comorbidities, while the normalized post-inoculation deaths are small, but not negligible, in children. Clinical trials for these inoculations were very short-term (a few months), had samples not representative of the total population, and for adolescents/children, had poor predictive power because of their small size. Further, the clinical trials did not address changes in biomarkers that could serve as early warning indicators of elevated predisposition to serious diseases. Most importantly, the clinical trials did not address long-term effects that, if serious, would be borne by children/adolescents for potentially decades. A novel best-case scenario cost-benefit analysis showed very conservatively that there are five times the number of deaths attributable to each inoculation vs those attributable to COVID-19 in the most vulnerable 65+ demographic. The risk of death from COVID-19 decreases drastically as age decreases, and the longer-term effects of the inoculations on lower age groups will increase their risk-benefit ratio, perhaps substantially.

Introduction

Currently, we are in the fifteenth month of the WHO-declared global COVID-19 pandemic. Restrictions of different severity are still in effect throughout the world [1]. The global COVID-19 mass inoculation is in its eighth month. As of this writing in mid-June 2021, over 800,000,000 people globally have received at least one dose of the inoculation and roughly half that number have been fully inoculated [2]. In the USA, about 170,000,000 people have received at least one dose and roughly 80 % of that number have been fully inoculated [2].

Also, in the USA, nearly 600,000 deaths have been officially attributed to COVID-19. Almost 5,000 deaths following inoculation have been reported to VAERS by late May 2021; specifically, “Over 285 million doses of COVID-19 vaccines were administered in the United States from December 14, 2020, through May 24, 2021. During this time, VAERS received 4,863 reports of death (0.0017 %) among people who received a COVID-19 vaccine.” [3] (the Vaccine Adverse Events Reporting System (VAERS) is a passive surveillance system managed jointly by the CDC and FDA [3]. Historically, VAERS has been shown to report about 1% of actual vaccine/inoculation adverse events [4]. See Appendix 1 for a first-principles confirmation of that result). By mid-June, deaths following COVID-19 inoculations had reached the ˜6000 levels.

A vaccine is legally defined as any substance designed to be administered to a human being for the prevention of one or more diseases [5]. For example, a January 2000 patent application that defined vaccines as “compositions or mixtures that when introduced into the circulatory system of an animal will evoke a protective response to a pathogen.” was rejected by the U.S. Patent Office because “The immune response produced by a vaccine must be more than merely some immune response but must be protective. As noted in the previous Office Action, the art recognizes the term "vaccine" to be a compound which prevents infection” [6]. In the remainder of this article, we use the term ‘inoculated’ rather than vaccinated, because the injected material in the present COVID-19 inoculations prevents neither viral infection nor transmission. Since its main function in practice appears to be symptom suppression, it is operationally a “treatment”.

In the USA, inoculations were administered on a priority basis. Initially, first responders and frontline health workers, as well as the frailest elderly, had the highest priority. Then the campaign became more inclusive of lower age groups. Currently, approval has been granted for inoculation administration to the 12–17 years demographic, and the target for this demographic is to achieve the largest number of inoculations possible by the start of school in the Fall. The schedule for inoculation administration to the 5–11 years demographic has been accelerated to start somewhere in the second half of 2021, and there is the possibility that infants as young as six months may begin to get inoculated before the end of 2021 [7].

The remainder of this article will focus on the USA situation, and address mainly the pros and cons of inoculating children under eighteen. The article is structured as follows:

Section 1 (the present section) introduces the problem.

Section 2 (Background):

provides the background for the declared COVID-19 “pandemic” that led to the present inoculations;

describes the clinical trials that provided the justification for obtaining Emergency Use Authorization (EUA) from the FDA to administer the inoculations to the larger population;

shows why the clinical trials did not predict either the seriousness of adverse events that have occurred so far (as reported in VAERS) or the potential extent of the underlying pre-symptomatic damage that has occurred as a result of the inoculations.

Section 3 (Mass Inoculation) summarizes the adverse events that have occurred already (through reporting in VAERS) from the mass inoculation and will present biological evidence to support the potential occurrence of many more adverse effects from these inoculations in the mid-and long-term.

Section 4 (Discussion) addresses these effects further

Section 5 (Summary and Conclusions) presents the conclusions of this study.

There are four appendices to this paper.

Appendix A provides some idea of the level of under-reporting of post-inoculation adverse events to VAERS and presents estimations of the actual number of post-inoculation deaths based on extrapolating the VAERS results to real-world experiences.

Appendix B provides a detailed analysis of the major clinical trials that were used to justify EUA for the inoculants presently being administered in the USA.

Appendix C summarizes potential adverse effects shown to have resulted from past vaccines, all of which could potentially occur as a result of the present inoculations.

Appendix D presents a novel best-case scenario cost-benefit analysis of the COVID-19 inoculations that have been administered in the USA.

Background

Pandemic history

In December 2019, a viral outbreak was reported in Wuhan, China, and the responsible coronavirus was termed Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) [8,9]. The associated disease was called Coronavirus Disease 2019, or COVID-2019. The virus spread worldwide, and a global pandemic was declared by the WHO in March 2020 [10,11]. Restrictive measures of differing severity were implemented by countries globally, and included social distancing, quarantining, face masks, frequent hand sanitation, etc. [12,13]. In the USA, these measures were taken as well, differing from state-to-state [14]. At the same time, vaccine development was initiated to control COVID-19 [15]. In the USA, non-vaccine treatments were not encouraged at the Federal level, but different treatment regimens were pursued by some healthcare practitioners on an individual level [11,16,17].

By the end of May 2021, the official CDC death count attributed to COVID-19 was approaching 600,000, as stated previously. This number has been disputed for many reasons. First, before COVID-19 testing began, or in the absence of testing, after it was available, the diagnosis of COVID-19 (in the USA) could be made by the presumption of the healthcare practitioner that COVID-19 existed [4,18]. Second, after testing began, the main diagnostic used was the RT-PCR test. This test was done at very high amplification cycles, ranging up to 45 [[19], [20], [21]]. In this range, very high numbers of false positives are possible [22].

Third, most deaths attributed to COVID-19 were elderly with high comorbidities [1,22]. As we showed in a previous study [22], attribution of death to one of many possible comorbidities or especially toxic exposures in combinations [23] is highly arbitrary and can be viewed as a political decision more than a medical decision. For over 5 % of these deaths, COVID-19 was the only cause mentioned on the death certificate. For deaths with conditions or causes in addition to COVID-19, on average, there were 4.0 additional conditions or causes per death [24]. These deaths with comorbidities could equally have been ascribed to any of the comorbidities [22]. Thus, the actual number of COVID-19-based deaths in the USA may have been on the order of 35,000 or less, characteristic of a mild flu season.

Even the 35,000 deaths may be an overestimate. Comorbidities were based on the clinical definition of specific diseases, using threshold biomarker levels and relevant symptoms for the disease(s) of interest [25,26]. But many people have what are known as pre-clinical conditions. The biomarkers have not reached the threshold level for official disease diagnosis, but their abnormality reflects some degree of underlying dysfunction. The immune system response (including pre-clinical conditions) to the COVID-19 viral trigger should not be expected to be the same as the response of a healthy immune system [27]. If pre-clinical conditions had been taken into account and coupled with the false positives as well, the CDC estimate of 94 % misdiagnosis would be substantially higher.

Clinical trials

Clinical trials to gain FDA Emergency Use Authorization (EUA) approval

The unprecedented accelerated development of COVID-19 vaccines in the USA, dubbed Operation Warp Speed, resulted in a handful of substances available for clinical trials by mid-2020 [28]. These clinical trials were conducted to predict the safety and efficacy of the potential vaccines (which have turned out to be treatments/inoculations as stated previously), and thereby gain approval for inoculating the public at large [29]. An overview of the Pfizer clinical trials is presented in this section, and a more detailed description of the main clinical trials is shown in Appendix B.

Two types of inoculants have gained FDA EUA in the US: mRNA-based inoculants and viral vector-based inoculants, with the mRNA inoculants having the widest distribution so far. Comirnaty is the brand name of the mRNA-based inoculant developed by Pfizer/BioNTech, and Moderna COVID-19 Vaccine is the brand name of the mRNA-based inoculant developed by Moderna [30]. Both inoculants contain the genetic information needed for the production of the viral protein S (spike), which stimulates the development of a protective immune response against COVID-19 [31]. Janssen COVID-19 Vaccine is the brand name of the viral vector-based inoculant developed by Johnson and Johnson. Janssen COVID-19 vaccine uses an adenovirus to transport a gene from the coronavirus into human cells, which then produce the coronavirus spike protein. This spike protein primes the immune system to fight off potential coronavirus infection [32].

The results of these trials that allowed granting of EUA by the FDA can be found in the inserts to the inoculation materials. For example, the Pfizer inoculation trial results are contained in the fact sheet for healthcare providers administering vaccine (vaccination providers) [33].

There were two clinical trials conducted to gain FDA EUA for Pfizer: a smaller Phase 1/2 study, and a larger Phase 1/2/3 study. The age demographics for the larger clinical study are as follows (from the Pfizer insert): “Of the total number of Pfizer-BioNTech COVID-19 Vaccine recipients in Study 2 (N = 20,033), 21.4 % (n = 4,294) were 65 years of age and older and 4.3 % (n = 860) were 75 years of age and older.” Additionally: “In an analysis of Study 2, based on data up to the cutoff date of March 13, 2021, 2,260 adolescents (1,131 Pfizer-BioNTech COVID-19 Vaccine; 1,129 placebo) were 12 through 15 years of age. Of these, 1,308 (660 Pfizer-BioNTech COVID-19 Vaccine and 648 placebo) adolescents have been followed for at least 2 months after the second dose of Pfizer-BioNTech COVID-19 Vaccine. The safety evaluation in Study 2 is ongoing.”

The relevant demographics are presented in Table 7 on p.31 of the Pfizer insert. The age component of those demographics is shown below in Table 1.

Table 1

Demographics (population for the primary efficacy endpoint). The number of participants who received vaccine and placebo, stratified by age.

AGE GROUP	Pfizer-BioNTech COVID-19 Vaccine (N = 18,242) n (%)	Placebo (N = 18,379)n (%)
≥12 through 15 yearsb	46 (0.3 %)	42 (0.2 %)
≥16 through 17 years	66 (0.4 %)	68 (0.4 %)
≥16 through 64 years	14,216 (77.9 %)	14,299 (77.8 %)
≥65 through 74 years	3176 (17.4 %)	3226 (17.6 %)
≥75 years	804 (4.4 %)	812 (4.4 %)

Symbols: b: “100 participants 12 through 15 years of age with limited follow-up in the randomized population received at least one dose (49 in the vaccine group and 51 in the placebo group). Some of these participants were included in the efficacy evaluation depending on the population analyzed. They contributed to exposure information but with no confirmed COVID-19 cases, and did not affect efficacy conclusions.”, N: number of test subjects, n: number of controls.

There are very minor differences between most of the data in the above table and the preceding narrative shown, and they are probably due to different time horizons. The major difference is the number of adolescents used and appears to result from a much later reporting time.

Fig. 1 uses the official large CDC numbers (coupled with USA census data estimates from CDC Wonder) to show the COVID-19 deaths per capita as a function of age, circa early June 2021. Unfortunately, the most critical range, 85+, has the least resolution. It is obvious that most of the deaths occurred in the 55 to 100+ range, and the remaining individuals in the other ranges (especially under 35) have negligible risk of dying from the disease.

Fig. 1

COVID-19 Deaths per capita by age in the United States (as of Jun 5, 2021). Population-based on U.S. CDC WONDER Bridge-Race Population Estimate 2019. Data obtained from https://wonder.cdc.gov/bridged-race-v2019.html on 6/15/2021. Provisional COVID-19 deaths based on CDC data provided by the National Center for Health Statistics for the period 1/1/2020 – 6/5/2021. Data obtained from https://data.cdc.gov/NCHS/Provisional-COVID-19-Deaths-by-Sex-and-Age/9bhg-hcku on 6/10/2021.

The age distribution in Fig. 1 differs substantially from the age distribution in Table 1. Why is this important? When designing a trial for the efficacy and safety of a potential treatment, the focus should be on the target population who could benefit from that treatment. There is little rationale for including participants in a trial for whom the treatment would not be relevant or warranted.

For the COVID-19 Pfizer trials, based on the data from Fig. 1, the trial population should have been limited at most to the 45−100+ age segment, appropriately weighted toward the higher end where the deaths per capita are most frequent. That was almost the exact opposite of what was done in the Pfizer clinical trials. In Fig. 1, approximately 58 % of the deaths occurred in the age range 75+, whereas 4.4 % of the participants in the Pfizer clinical trial were 75 + . Thus, the age range most impacted by COVID-19 deaths was minimally represented in the Pfizer clinical trials, and the age range least impacted by COVID-19 deaths was maximally represented in the Pfizer clinical trials. This skewed sampling has major implications for predicting the expected numbers of deaths for the target population from the clinical trials.

Besides age, the other metric of importance in determining COVID-19 deaths is the presence of comorbidities. The more comorbidities, and the more severe the comorbidities, the greater the chances of death or severe adverse outcomes from COVID-19. It is not clear how well the number and severity of comorbidities in the clinical trial sample matched those reflected in Fig. 1, but the insert does mention the large number of conditions that excluded participation in the trials. In sum, the results from the clinical trials could not be expected to reflect the results that could occur (and have occurred) from mass inoculation of the public, given the unaffected nature of the bulk of the trial population from SARS-CoV-2 exposure.

The prior discussion on the clinical trials has focused on the efficacy and safety of the inoculants, and the relationship of the trial test population to the total target population. We have limited the focus so far to the safety and efficacy issues since these constituted the core of what was presented to the FDA for EUA approval. We have not focused on the trials from an early warning indicator perspective.

We will address summarily the science/early warning indicator issues associated with the Pfizer trials, and how the neglect of these issues has translated into disastrous consequences during the mass inoculation rollout. Standard practice for determining and understanding the impact of new technology (such as mRNA “vaccines”) on a system involves measuring the state and flux variables of the system before the new technology intervention, measuring the state and flux variables of the system after the new technology intervention, and identifying the types and magnitudes of changes in the state and flux variables attributable to the intervention. This would be in addition to evaluating performance metrics before and after the intervention.

In Pfizer’s proposed clinical trials for the mRNA “vaccine” (Study to Describe the Safety, Tolerability, Immunogenicity, and Efficacy of RNA Vaccine Candidates Against COVID-19 in Healthy Individuals - https://clinicaltrials.gov/ct2/show/NCT04368728), the focus was on determining 1) adverse events/symptoms, 2) SARS-CoV-2 serum neutralizing antibody levels, 3) SARS-CoV-2 anti-S1 binding antibody levels and anti-RBD binding antibody levels, and 4) effectiveness. These metrics are all related to safety at the symptom level and performance.

However, symptoms/diseases are typically end points of processes that can take months, years, or decades to surface. During that symptom/disease development period, many biomarker early warning indicators tend to exhibit increasing abnormalities that reflect an increasing predisposition to the eventual symptom/disease. Thus, serious symptoms/diseases that ordinarily take long periods to develop would be expected to be rare events if they occurred shortly following an inoculation. If the clinical trials that were performed by Pfizer and Moderna were designed to focus on efficacy and only adverse effects at the symptom level of description as an indicator of safety, the trial results would be limited to the identification of rare events, and the trial results would potentially under-estimate the actual pre-symptom level damage from the inoculations.

Credible safety science applied to this experiment would have required a much more expansive approach to determining effects on a wide variety of state and flux metrics that could serve as early warning indicators of potentially serious symptoms/disease, and might occur with much higher frequencies at this early stage than the rare serious symptoms. The only mention of these other metrics in the above proposal is in the Phase I trial description: “Percentage of Phase 1 participants with abnormal haematology and chemistry laboratory values”, to be generated seven days after dose 1 and dose 2.

A paper published in NEJM in December 2020 [34] summarized the Phase 1 results. The focus was on local and systemic adverse events and efficacy metrics (antibody responses). The only metrics other than these reported were transiently decreased lymphocyte counts.

We view this level of reporting as poor safety science for the following reasons. Before the clinical trials had started, many published articles were reporting serious effects associated with the presence of the SARS-CoV-2 virus such as hyperinflammation, hypercoagulation, hypoxia, etc. SARS-CoV-2 includes the S1 Subunit (spike protein), and it was not known how much of the damage was associated with the spike protein component of SARS-CoV-2. A credible high-quality safety science experiment would have required state measurements of specific biomarkers associated with each of these abnormal general biomarkers before and after the inoculations, such as d-dimers for evidence of enhanced coagulation/clotting; CRP for evidence of enhanced inflammation; troponins for evidence of cardiac damage; occludin and claudin for evidence of enhanced barrier permeability; blood oxygen levels for evidence of enhanced hypoxia; amyloid-beta and phosphorylated tau for evidence of increased predisposition to Alzheimer’s disease; Serum HMGB1, CXCL13, Dickkopf-1 for evidence of an increased disposition to autoimmune disease, etc. A credible high-quality safety science experiment would have required flux measurements of products resulting from the mRNA interactions, from the LNP shell interactions, from dormant viruses that might have been stimulated by the mRNA-generated spike protein, etc., emitted through the sweat glands, faeces, saliva, exhalation, etc.

Most importantly, these types of measurements would have shown changes in the host that did not reach the symptom level of expression but raised the general level of host abnormality that could predispose the host to a higher probability of serious symptoms and diseases at some point in the future. Instead, in the absence of high-quality safety science reflected in these experiments, all that could be determined were short-term adverse effects and deaths. This focus on symptoms masked the true costs of the mRNA intervention, which would probably include much larger numbers of people whose health could have been degraded by the intervention as evidenced by increased abnormal values of these biomarkers. For example, the trials and VAERS reported clots that resulted in serious symptoms and deaths but gave no indication of the enhanced predisposition to forming serious clots in the future with a higher base of micro-clots formed because of the mRNA intervention. The latter is particularly relevant to children, who have a long future that could be seriously affected by having an increased predisposition to multiple clot-based (and other) serious diseases resulting from these inoculations.

Mass inoculation

Adverse events reported for adults

This section describes the adverse effects that followed COVID-19 mass inoculation in the USA. The main source of adverse effects data used was VAERS. Because VAERS is used to estimate adverse event information by many other countries as well, a short overview of VAERS and its intrinsic problems is summarized in Appendix 1.

The period in the present study covered by the reported inoculations is mid-December 2020 to the end of May 2021. The population inoculated during this period is mainly adults. Child inoculations did not begin until mid-May. Because the different age groups were inoculated starting at different times based on priority, the elapsed times after inoculation will be different, and any adverse event comparisons across age groups will require some type of elapsed post-inoculation time normalization.

We examined VAERS-reported deaths by age group, normalized to:

the number of inoculations given

the period within seven days after inoculation.

This allows a credible comparison of very short-term adverse effects post-inoculation for all age groups. During this period, which is eight days post-inoculation (where day zero is the day of inoculation), ˜sixty percent of all post-inoculation deaths are reported in VAERS.

Fig. 2 below shows the results circa late May 2021 [3]. The age band ranges are different from those in Fig. 1 because the CDC provides inoculation after-effect age bands differently from COVID-19 death age bands. In general, the inoculation deaths by age per inoculant roughly parallel the COVID-19 deaths by age per capita (the curve structures are very similar), with one exception: the 0–17 demographic. In the normalized COVID-19 death graph (Fig. 1), the deaths per capita in the 0–17 demographic are negligible, while in the normalized inoculant death graphs (Fig. 2) the normalized deaths are small, but not negligible. The members of the 65+ demographic, where the bulk of deaths are occurring in Fig. 1, Fig. 2, have been receiving inoculations for ˜five months, whereas the members of the youngest demographic have been receiving inoculations only for a few weeks. More time needs to pass before more definitive conclusions can be drawn about the youngest demographic, and how its members are impacted adversely following the inoculations.

Fig. 2

Post-inoculation deaths per dose of inoculant. 7-day COVID-19 vaccine deaths per inoculation by age in the United States (as of 5/28/2021). Data shown includes the total number of all deaths up to 7 days after receiving the vaccine for both those administered 1 dose and the complete series of doses by age in the United States as of 5/28/2021 reported in VAERS (updated on 5/28/2021). COVID-19 Vaccinations (Inoculations) based on CDC data provided by ISSInfo up thru 5/28/2021. Data obtained from https://data.cdc.gov/Vaccinations/COVID-19-Vaccination-Demographics-in-the-United-St/km4m-vcsb on 6/10/2021. COVID-19 Vaccinations Deaths based on CDC WONDER VAERS Database as of 5/28/2021, obtained from https://wonder.cdc.gov/controller/datarequest/D8;jsessionid=4B5522C8D1DA68F1A364646B0DA5 on 6/9/2021.

The high death rates from both COVID-19 and the inoculations in the 65+ demographic should not be surprising. In both cases, the immune system is challenged, and in both cases, a dysfunctional immune system characteristic of many elderly people with multiple comorbidities cannot respond adequately to the challenge.

Specific short-term adverse events reported in VAERS

The most comprehensive single evaluation of VAERS-reported adverse events (mainly for adult recipients of the COVID-19 “vaccines”) we have seen is a non-peer-reviewed collection of possible side effects by Dr. Ray Sahelian [35]. We recommend reading this short data-rich summary of the broad types of events reported already, in the context that these events are very short-term. Dr. Sahelian identifies five mechanisms he believes are responsible for most of these events, with research potentially uncovering other mechanisms. These five mechanisms include:

“An overreacting inflammatory response is known as systemic inflammatory response syndrome (SIRS). This SIRS reaction, perhaps a cytokine storm, can range from very mild to very severe. It can begin the very first day of the shot or begin days or weeks later as a delayed reaction.”

“Interaction of the spike proteins with ACE2 receptors on cell membranes. Such cells are found widely in the body including the skin, lungs, blood vessels, heart, mouth, gastrointestinal tract, kidneys, and brain.”

“Interaction of spike proteins with platelets and/or endothelial cells that line the inside of blood vessels. This can lead to clotting or bleeding (low number of circulating platelets in the bloodstream). Some of the clots, even if tiny, cause certain neurological symptoms if the blood supply to nerves is compromised.”

“Immediate or delayed release of histamine from mast cells and basophils (mast cell activation syndrome, MCAS).”

5. “Swelling of lymph nodes in various areas of the body could interfere with blood flow, put pressure on nerves causing pain, or compromise their proper function.”

These reactions can be classified as Hyperinflammation, Hypercoagulation, Allergy, and Neurological, and can contribute to many symptoms and diseases, as VAERS is showing.

An excellent review of acute and potential long-term pathologies resulting from the COVID-19 inoculations [36] showed potential relationships to blood disorders, neurodegenerative diseases and autoimmune diseases. This review discussed the relevance of prion-protein-related amino acid sequences within the spike protein.

Potential mid- and long-term events and serious illnesses for adults and children from past vaccines

A detailed description of potential mid- and long-term events and serious illnesses for adults and children from past vaccines is presented in Appendix C. Most of these events and illnesses are not predictable, and most, if not all, would be possible for the COVID-19 inoculations in the mid- and long-term for adults and children.

Potential short-, mid-, and long-term risks of mass COVID-19 inoculation for children

Intrinsic inoculant toxicity

Children are unique relative to COVID-19. They have negligible risks of serious effects from the disease, as shown in Fig. 1. Given that the COVID-19 inoculants were only tested for a few months, and mid-or long-term adverse effects are unknown, any mid- or long-term adverse events that emerge could impact children adversely for decades.

We believe that mid-or long-term adverse effects are possible based on the recent emergence of evidence that would support the probability of mid-and long-term adverse effects from the COVID-19 inoculants, such as:

The spike protein itself can be a toxin/pathogenic protein:

S protein alone can damage vascular endothelial cells (ECs) by downregulating ACE2 and consequently inhibiting mitochondrial function [37].

it is concluded that ACE2 and endothelial damage is a central part of SARS-CoV2 pathology and may be induced by the spike protein alone [38].

the spike protein of SARS-CoV-1 (without the rest of the virus) reduces ACE2 expression, increases angiotensin II levels, exacerbates lung injury, and triggers cell signaling events that may promote pulmonary vascular remodeling and Pulmonary Arterial Hypertension (PAH) as well as possibly other cardiovascular complications [39].

the recombinant S protein alone elicits functional alterations in cardiac vascular pericytes (PCs) [40]. This was documented as:

increased migration

reduced ability to support EC network formation on Matrigel

secretion of pro-inflammatory molecules typically involved in the cytokine storm

production of pro-apoptotic factors responsible for EC death. Furthermore, the S protein stimulates the phosphorylation/activation of the extracellular signal-regulated kinase 1/2 (ERK1/2) through the CD147 receptor, but not ACE2, in cardiac PCs, the S protein may elicit vascular cell dysfunction, potentially amplifying, or perpetuating, the damage caused by the whole coronavirus [40].

“even in the absence of the angiotensin-converting enzyme 2 receptors, the S1 subunit from SARS-CoV-2 spike protein binding to neutral phospholipid membranes leads to their mechanical destabilization and permeabilization. A similar cytotoxic effect of the protein was seen in human lung epithelial cells.” [125].

The LNP layer encapsulating the mRNA of the inoculant is highly inflammatory in both intradermal and intranasal inoculation [41] and “Polyethylene glycol (PEG) is a cause of anaphylaxis to the Pfizer/BioNTech mRNA COVID-19 vaccine” [42]. “Humans are likely developing PEG antibodies because of exposure to everyday products containing PEG. Therefore, some of the immediate allergic responses observed with the first shot of mRNA-LNP vaccines might be related to pre-existing PEG antibodies. Since these vaccines often require a booster shot, anti-PEG antibody formation is expected after the first shot. Thus, the allergic events are likely to increase upon re-vaccination” [43].

There is also the possibility that the components of the LNP shell could induce the ASIA Syndrome (autoimmune/inflammatory syndrome induced by adjuvants), as shown by studies on post-inoculation thyroid hyperactivity [44] and post-inoculation subacute thyroiditis [45].

The spike protein has been found in the plasma of post-inoculation individuals, implying that it could circulate to, and impact adversely, any part of the body [46].

The spike protein of SARS-CoV-2 crosses the blood-brain barrier in mice [47], and “the SARS-CoV-2 spike proteins trigger a pro-inflammatory response on brain endothelial cells that may contribute to an altered state of BBB function” [48].

The spike proteins manufactured in vivo by the present COVID-19 inoculations could potentially "precipitate the onset of autoimmunity in susceptible subgroups, and potentially exacerbate autoimmunity in subjects that have pre-existing autoimmune diseases", based on the finding that anti-SARS-CoV-2 protein antibodies cross-reacted with 28 of 55 diverse human tissue antigens [49].

“The biodistribution of ChaAdOx1 [Astra Zeneca’s recombinant adenovirus vaccine candidate against SARS-CoV-2] in mice confirmed the delivery of vaccine into the brain tissues [50]. The vaccine may therefore spur the brain cells to produce CoViD spike proteins that may lead to an immune response against brain cells, or it may spark a spike protein-induced thrombosis. This may explain the peculiar incidences of the fatal cerebral venous sinus thrombosis (CVST) observed with viral vector-based CoViD-19 vaccines” [51,52].

A complementary perspective to explain adenovirus-based vaccine-induced thrombocytopenia is that “transcription of wildtype and codon-optimized Spike open reading frames enables alternative splice events that lead to C-terminal truncated, soluble Spike protein variants. These soluble Spike variants may initiate severe side effects when binding to ACE2-expressing endothelial cells in blood vessels.” [100].

A Pfizer Confidential study performed in Japan showed that "modRNA encoding luciferase formulated in LNP comparable to BNT162b2″ injected intramuscularly concentrated in many organs/tissues in addition to the injection site [53]. The main organs/sites identified were adrenal glands, liver, spleen, bone marrow, and ovaries. While damage to any of these organs/sites could be serious (if real for humans), adverse effects on the ovaries could be potentially catastrophic for women of childbearing or pre-childbearing age.

The main objective of credible biodistribution studies (of inoculants for eventual human use) is to identify the spatio-temporal distribution of the actual inoculant in humans; i.e., how much of the final desired product (in this case, expressed protein antigen/spike protein) is produced in different human tissues and organs as a function of time. That’s not what was reported in the Pfizer Confidential study.

Rats were used for the in vivo studies; the relationship of their biodistribution to that of humans is unclear. They were injected in different locations (hindpaw/intramuscular); the relationship to human injections in the deltoid muscle is unclear. They were injected with "modRNA encoding luciferase formulated in LNP comparable to BNT162b2″; it is unclear why they weren’t injected with BNT162b2, it is unclear why spike protein expression wasn’t evaluated rather than LNP concentration, and it is unclear how well the biodistribution from the actual inoculant used in the experiments compares to the biodistribution from BNT162b2.

They were injected once per rat. Given that a second injection would not be in the same exact location as the first, and that the circulatory system might have changed due to clotting effects from the first injection and other potential vascular complications, it is unclear how the biodistribution change with the second injection would compare with the first. If a booster injection is given to counter variants, it is unclear how its biodistribution would be altered as a consequence of the preceding two injections.

Clotting will occur with the highest probability where the blood flow is reduced (and more time is available for LNP-endothelial cell interaction). It is unclear whether the clotting process would show positive feedback behaviour where the initial inoculation constricts the flow in low-velocity regions even further by enhanced clotting, and subsequent inoculations further amplify this reduced flow-enhanced clotting cycle.

The rats were injected under pristine conditions; how that compares with humans, who have been, are being, and will continue to be exposed to multiple toxic substances in combination, is open to question. We know these combinations can act synergistically to adversely impact myriad organs and tissues throughout the body [23]. We don’t know how these toxic exposures in humans affect the permeability of the blood/tissue barriers, and especially the ability of the injected material to diffuse into the bloodstream (and also the ability of the manufactured spike proteins to diffuse from the bloodstream into the surrounding tissue).

Higher-level primates should have been used for these short-term experiments, to obtain a more realistic picture of the biodistribution of inoculant in human organs and tissues. In other words, these laboratory experiments may be just the tip of the iceberg of estimating the amount of inoculant that concentrates in critical organs and tissues of human beings.

The many studies referenced above indicate collectively that the mRNA-based COVID-19 inoculations (the most prolific inoculations used in the USA for COVID-19 so far) consist of (at least) two major toxins: the instructions for the spike protein (mRNA) and the mRNA-encapsulating synthetic fat LNP. The vaccine is injected into the deltoid muscle, at which time it contributes to inflammation at the injection site due in part to the LNP and potentially to anaphylaxis from the LNP PEG-2000 component. Some of the injected material stays at the injection site, where it combines with cells through endocytosis to express spike protein on the cell surface, stimulating the adaptive immune system to eventually produce antibodies to the spike protein [54].

The remainder of the injected material enters the lymphatic system and the bloodstream, and is distributed to tissues and organs throughout the body: e.g., “Drugs administered by the intramuscular (IM) route are deposited into vascular muscle tissue, which allows for rapid absorption into the circulation” [55]. The basis of this process is that the bulky muscles have good vascularity, and therefore the injected drug quickly reaches the systemic circulation and thereafter into the specific region of action, bypassing the first-pass metabolism [56]. The widespread distribution is greatly enhanced by the LNP PEG-2000 coating as follows: building from the success of PEGylating proteins to improve systemic circulation time and decrease immunogenicity [57]. PEG coatings on nanoparticles shield the surface from aggregation, opsonization, and phagocytosis, prolonging systemic circulation time. [57]. PEG coatings on nanoparticles have also been utilized for overcoming various biological barriers to efficient drug and gene delivery associated with other modes of administration. [57]

In the bloodstream, one possible outcome is that the LNPs coalesce with the endothelial cells on the inner lining of the blood vessels and transfer the mRNA to the cells through endocytosis. The endothelial cells would then express the spike protein on their surface. Platelets flowing by the spike protein express ACE2 receptors on their surface; therefore, one possible outcome would be activation of the platelets by the spike protein and initiation of clotting. Another possible outcome would be the modified endothelial cells being recognized by innate immune system cells as foreign. These immune killer cells would then destroy parts of the endothelium and weaken the blood-organ barriers. The LNPs would inflame the endothelium as well, both increasing barrier permeability and increasing the blood vessel diameter. This weakening of the blood-organ barriers would be superimposed on any inflammation due to the myriad toxic contributing factors operable [4]. The newly-formed cells with spike proteins would penetrate the blood-organ barriers and bind to tissue with expressed ACE2 receptors. Any LNPs that did not coalesce with the endothelial cells, but remained intact, could also pass through the permeable blood-organ barrier, and coalesce directly with the organ cells. This could lead to an attack by innate immune system cells, and be a precursor to autoimmunity [4].

In the preceding discussion of the Pfizer biodistribution studies, the issue of multiple inoculations on changes in biodistribution was raised. Similarly, the alteration of effects as described above by multiple inoculations must be considered. Each inoculation will have positive aspects and negative aspects. The positive aspects are the formation of antibodies in the muscle cells and lymphatic system. The negative aspects include, but are not limited to, the potential clotting effects and permeability increases for that fraction of the inoculant that enters the bloodstream. The first inoculant dose can be viewed as priming the immune system. The immune response will be relatively modest. The second inoculant dose can be expected to elicit a more vigorous immune response. This will enhance the desired antibody production in the muscle cells and lymphatic system, but may also enhance the immune response to both the blood vessel-lining endothelial cells displaying the spike protein and the platelets, causing more severe damage. If a booster(s) inoculation is also required, this may further enhance both the positive and negative immune responses resulting from the second inoculation. While the positive effects are reversible (antibody levels decrease with time), adverse effects may be cumulative and irreversible, and therefore injury and death rates may increase with every additional inoculation [58].

These effects can occur throughout the body in the short term, as we are seeing with the VAERS results. They can occur in the mid- and long-term as well, due to the time required for destructive processes to have full effect and the administration of further inoculations. For example, micro-clots resulting from the inoculation that were insufficient to cause observable symptoms could in effect raise the baseline for thrombotic disease [92]. Lifestyle activities that contribute to enhanced blood clotting would have less distance to travel to produce observable symptoms, and thus the serious effects of clotting would have been accelerated [59,60]. As an example: the risk of venous thrombosis is approximately 2- to 4-fold increased after air travel [61]. How much this rate would increase after the inoculations, where microthrombi have formed in some recipients, is unknown. These potential baseline-raising effects could impact the interpretation of the VAERS results, as we show at the end of Appendix 1.

Adverse inoculant effects on children

What are the potential mid- and long-term adverse health effects from the COVID-19 inoculation on children specifically, taking into account that they will be exposed not only to the spike protein component of the SARS-CoV-2 virus but also to the toxic LNP encapsulating-shell? This toxic combination will have bypassed many defensive safeguards (typically provided by the innate immune system) through direct injection [62]. As we have shown, the main reasons why we believe the spike protein could be harmful to children even though they don’t seem to get sick from exposure to SARS-CoV-2 are 1) the bypassing of the innate immune system by inoculation, 2) the larger volume of spike protein that enters the bloodstream, and 3) the additional toxic effects of the encapsulating LNP layer.

Potential mid-term adverse health effects

Examination of the myriad post-COVID-19 inoculation symptoms/biomarker changes for the 0–17 age demographic reported to VAERS circa mid-June 2021 provides some indication of very early damage [84]. Main regions/systems affected adversely (VAERS symptoms/biomarkers shown in parentheses) include:

Cardiovascular (blood creatine phosphokinase increased, cardiac imaging procedure abnormal, echocardiogram abnormal, electrocardiogram abnormal, heart rate increased, myocarditis, palpitations, pericarditis, tachycardia, troponin I increased, troponin increased, fibrin D-Dimer increased, platelet count decreased, blood pressure increased, bradycardia, brain natriuretic peptide increased, ejection fraction decreased, migraine)

Gastrointestinal (abdominal pain, diarrhoea, vomiting, alanine aminotransferase increased, aspartate aminotransferase increased.)

Neural (gait disturbance, mobility decreased, muscle spasms, muscle twitching, seizure, tremor, Bell’s Palsy, dyskinesia)

Immune (C-Reactive Protein increased, red blood cell sedimentation rate increased, white blood cell counts increased, inflammation, anaphylactic reaction, pruritis, rash, lymphadenopathy)

Endocrine (heavy menstrual bleeding, menstrual disorder)

In addition, there were large numbers of different vision and breathing problems reported.

All the major systems of the body are impacted, and many of the major organs as well. Given the lag times in entering data into VAERS and the fact that inoculations of children started fairly recently, we would expect the emphasis to be immediate symptomatic and biomarker reactions. More time is required for organ and system damage to develop and emerge. Cardiovascular problems dominate, as our model for spike protein/LNP circulation and damage predicts, and it is unknown how reversible such problems are. Many of the VAERS symptoms listed above were also found in COVID-19 adult patients [64].

Consider the example of Multisystem Inflammatory Syndrome in Children (MIS-C). It has emerged in VAERS with modest frequency so far, and it also occurred about a month after COVID-19 infection [65]. In both cases, the presence of the spike protein was a common feature. Many of its characteristic symptoms are those listed above from VAERS. MIS-C has similarities with known disease entities like Kawasaki Disease (KD), toxic shock syndrome (TSS) and macrophage activation syndrome (MAS)/secondary hemophagocytic lymphohistiocytosis (HLH) [66]. One presentation of MIS-C is in adolescents with a high disease burden as evidenced by more organ systems involved, almost universally including cardiac and gastrointestinal systems, and with a higher incidence of shock, lymphopenia, and elevated cardiac biomarkers indicating myocarditis [67]. Since the first reports of children developing MIS-C, it was evident that others presented with some of the classic symptoms of the well-recognized childhood illness KD [68]. Further, despite KD being ordinarily incredibly rare in adults, patients with MIS-A have also been reported with KD-like features. [68] Thus, an examination of the adverse effects from COVID-19 as evidenced through these diseases might shed some light on what can be expected further down the line from the inoculations.

The following section addresses Kawasaki disease (KD) and Multisystem Inflammatory Syndrome in Children (MIS-C) [65].

KD is an acute vasculitis and inflammation that predominantly affects the coronary arteries and can cause coronary artery aneurysms. Other KD manifestations include systemic inflammation of arteries, organs, and tissues, with consequent hepatitis and abdominal pain; lung interstitial pneumonitis, aseptic meningitis due to brain membrane inflammations; myocarditis, pericarditis, and valvulitis; urinary tract pyuria, pancreatitis; and lymph-node enlargement [69]. In general, although almost all children fully recover, some of them later develop coronary artery dilation or aneurysm [70]. Etiologically and pathologically, numerous studies indicate that KD is triggered by an abnormal autoimmune response caused by an infection [71]. The infection hypothesis is supported by epidemiology data showing that an infectious disease is involved at least as a starting point. Previously proposed infectious agents include Herpesviridae, retroviruses, Parvovirus B19, bocavirus, and bacterial infections such as staphylococci, streptococci, Bartonella, and Yersinia infections [72].

SARS-CoV-2 adds to these infectious agents by eliciting autoantibodies likely via molecular mimicry and cross-reactivity with autoantigens [72,73].

Then, the formation of antigen–antibody immune complexes can lead to KD symptoms via activation of the receptors of mast cells, neutrophils, and macrophages with consequent release of pro-inflammatory cytokines and increase of blood vessel permeability; activation of the complement system, stimulation of neutrophils and macrophages to secrete proteases and more proinflammatory cytokines [74], thus merging into the “cytokine storm” that characterizes MIS-C [75]. Indeed, features of KD are raised levels of Interleukin (IL)-6, IL-8, IL-15, and IL-17, with the cytokine level predicting coronary aneurysm formation in KD patients [76,77]

Potential long-term adverse health effects

In the long-term, SARS-CoV-2-induced KD vasculitis can lead to severe pathologies. Vasculitis has a predilection for coronary arteries with a high complication rate across the lifespan for those with medium to large coronary artery aneurysms [78]. The cytokine-induced inflammation produces endothelial dysfunction and damage to the vascular wall, leading to aneurysmal dilatation. Successively, vascular remodeling can also occur, but this does not imply resolution of the disease or reduction of risk for future complications. A rigorous follow-up to detect progressive stenosis, thrombosis and luminal occlusion that may lead to myocardial ischemia and infarction becomes mandatory [78]. Of equal importance, among other long-term outcomes, children with KD may have increased risks not only for ischemic heart disease, but also for autoimmune disorders, cancer as well as an increased all-cause mortality [71].

Additional questions regarding mass inoculation of children and adolescents include:

Do children, being asymptomatic carriers of SARS-CoV-2, transmit the virus?

Do recently vaccinated people, infected with SARS-CoV-2, transmit the virus?

There is evidence of children transmitting SARS-CoV-2 in community settings, but the existing literature is heterogeneous with regards to the relative rate at which they do so compared to adults [79].

Studies from South Korea and Thailand found a very limited number of secondary cases [80,81]. On the contrary, a large contact tracing study from India concluded that the highest probability of transmission was between case-contact pairs of similar age and that this pattern of enhanced transmission risk was highest among children 0–4 years of age as well as adults 65 years of age and older [80]

With regard to the second question, it was shown that household members of healthcare workers inoculated with a single dose of either Pfizer or Astra Zeneca COVID-19 inoculant were at significantly reduced risk of PCR-confirmed SARS-CoV-2 infection but at non-statistically significant reduced risk of hospitalization, compared to household members of uninoculated healthcare workers, fourteen days after inoculation [82]. This finding again underlines the association of severe disease to the characteristics of the infected person and not directly to the transmission, implying that the elderly should be inoculated and not the children.

Novel best-case scenario cost-benefit analysis of COVID-19 inoculations for most vulnerable

Traditional cost-benefit analyses are typically financial tools used to estimate the potential value of a proposed project. They involve generating cost streams over time, benefit streams over time, and then comparing the net present value of these two streams (including risk) to see whether the risk-adjusted discounted benefits outweigh the risk-adjusted discounted costs. Appendix D presents a detailed non-traditional best-case scenario pseudo-cost-benefit analysis of inoculating people in the 65+ demographic in the USA. In this incarnation of a cost-benefit analysis, the costs are the number of deaths resulting from the inoculations, and the benefits are the lives saved by the inoculations. The time range used was from December 2019 to end-of-May 2021. No discounting was done; an inoculation-based death occurring immediately post-inoculation was given the same importance/weighting as an inoculation-based death months after inoculation.

Why was this non-traditional approach selected for a cost-benefit analysis? In a traditional non-financial cost-benefit analysis relative to inoculations, the adverse events prevented by the inoculations would be compared with the adverse events resulting from the inoculations. Presently, in the USA, definitions, test criteria, and reporting incentives for COVID-19 and its inoculants have shifted over time, and we believe a standard approach could not be performed credibly. Appendix Da presents some of the problems with the COVID-19 diagnostic criteria on which the above statements are based.

In contrast to the pandemic buildup phase, where many who died with COVID-19 were assumed to have died from COVID-19 by the medical community and the CDC, the post-inoculation deaths reported in VAERS are assumed by the CDC to be mostly from causes other than the inoculations. We wanted to use a modified cost-benefit analysis that would have less dependence on arbitrary criteria and subjective judgments.

The approach selected can be viewed as a best-case scenario pseudo-cost-benefit analysis. We assume the inoculations prevent the deaths attributable to COVID-19 (these are the total deaths attributed to COVID-19 officially minus 1) the number of false positives resulting from the PCR tests run at very high amplification cycles and 2) the number of deaths that could have been attributed to one of the many comorbidities that were typical of those who succumbed, as shown in our results section) over the period December 2019 to end-of-May 2021, and relate that number to the deaths attributable to the inoculation (from January 2021 to end-of-May 2021) based on our computations in the results section. The results show that there are five times the number of deaths attributable to each inoculation vs those attributable to COVID-19 in the 65+ demographic. As age decreases, and the risk for COVID-19 decreases, the cost-benefit increases. Thus, if the best-case scenario looks for benefits from the inoculations, any realistic scenario will look . For children the chances of death from COVID-19 are negligible, but the chances of serious damage over their lifetime from the toxic inoculations are not negligible.

Discussion

Two issues arise from these results.

First, where is the data justifying inoculation for children, much less most people under forty? It's not found on Fig. 1, where the most vulnerable are almost exclusively the elderly with many comorbidities [83]. Yet, in the USA, Pfizer has been approved to inoculate children 12–17, and the goal is to accomplish this by the start of the school year in the Fall. As stated previously, there are plans to inoculate children as young as six months starting before the end of 2021.

What is the rush for a group at essentially zero risks? Given that the inoculations were tested only for a few months, only very short-term adverse effects could be obtained. It is questionable how well even these short-term effects obtained from the clinical trials reflect the short-term effects from the initial mass inoculation results reported in VAERS.

Fig. 1, Fig. 2 reflect only these very short-term results. A number of researchers have suggested the possibility of severe longer-term autoimmune, Antibody-Dependent Enhancement, neurological, and other potentially serious effects, with lag periods ranging from months to years. If such effects do turn out to be real, the children are the ones who will have to bear the brunt of the suffering. There appear to be no benefits for the children and young adults from the inoculations and only Costs!

The second issue is why the deaths shown on Fig. 2 were not predicted by the clinical trials. We examined the Pfizer trial results (based on a few months of testing) and did not see how (potentially) hundreds of thousands of deaths could have been predicted from the trials’ mortality results. Why this gap?

As we showed in the clinical trials section, 17.4 % of the Pfizer sample members were over 65, and 4.4 % were over 75. When the later phases of the trials started in late July 2020, the managers knew the COVID-19 age demographics affected from the July 2020 analog of Fig. 1. Rather than sampling from the age region most affected, they sampled mainly from the age region least affected! And even in the very limited sampling from the oldest groups, it is unclear whether they selected from those with the most serious comorbidities. Our impression is that the sickest were excluded from the trials, but were first in line for the inoculants.

It is becoming clear that the central ingredient of the injection, the recipe for the spike protein, will produce a product that can have three effects. Two of the three occur with the production of antibodies to the spike protein. These antibodies could allegedly offer protection against the virus (although with all the "breakthrough" cases reported, that is questionable), or could suppress serious symptoms to some extent. They could also cross-react with human tissue antigen, leading to potential autoimmune effects. The third occurs when the injected material enters the bloodstream and circulates widely, which is enabled by the highly vascular injection site and the use of the PEG-2000 coating.

This allows spike protein to be manufactured/expressed in endothelial cells at any location in the body, both activating platelets to cause clotting and causing vascular damage. It is difficult to believe this effect is unknown to the manufacturer, and in any case, has been demonstrated in myriad locations in the body using VAERS data. There appears to be modest benefit from the inoculations to the elderly population most at risk, no benefit to the younger population not at risk, and much potential for harm from the inoculations to both populations. It is unclear why this mass inoculation for all groups is being done, being allowed, and being promoted.

Overall conclusions

The people with myriad comorbidities in the age range where most deaths with COVID-19 occurred were in very poor health. Their deaths did not seem to increase all-cause mortality as shown in several studies. If they hadn't died with COVID-19, they probably would have died from the flu or many of the other comorbidities they had. We can't say for sure that many/most died from COVID-19 because of: 1) how the PCR tests were manipulated to give copious false positives and 2) how deaths were arbitrarily attributed to COVID-19 in the presence of myriad comorbidities.

The graphs presented in this paper indicate that the frail injection recipients receive minimal benefit from the inoculation. Their basic problem is a dysfunctional immune system, resulting in part or in whole from a lifetime of toxic exposures and toxic behaviors. They are susceptible to either the wild virus triggering the dysfunctional immune system into over-reacting or under-reacting, leading to poor outcomes or the injection doing the same.

This can be illustrated by the following analogy. A person stands in a bare metal enclosure. What happens when the person lights a match and drops it on the floor depends on what is on the floor. If the floor remains bare metal, the match burns for a few seconds until extinguished. If there is a sheet of paper on the floor under the match, the match and the paper will burn for a short time until both are extinguished. If, however, the floor is covered with ammonium nitrate and similar combustible/explosive materials, a major explosion will result! For COVID-19, the wild virus is the match. The combustible materials are the toxic exposures and toxic behaviors. If there are no biomarker ‘footprints’ from toxic exposures and toxic behaviors, nothing happens. If there are significant biomarker ‘footprints’ from toxic exposures and toxic behaviors, bad outcomes result.

Adequate safety testing of the COVID-19 inoculations would have provided a distribution of the outcomes to be expected from ‘lighting the match’. Since adequate testing was not performed, we have no idea how many combustible materials are on the floor, and what the expected outcomes will be from ‘lighting the match’.

The injection goes two steps further than the wild virus because 1) it contains the instructions for making the spike protein, which several experiments are showing can cause vascular and other forms of damage, and 2) it bypasses many front-line defenses of the innate immune system to enter the bloodstream directly in part. Unlike the virus example, the injection ensures there will always be some combustible materials on the floor, even if there are no other toxic exposures or behaviors. In other words, the spike protein and the surrounding LNP are toxins with the potential to cause myriad short-, mid-, and long-term adverse health effects even in the absence of other contributing factors! Where and when these effects occur will depend on the biodistribution of the injected material. Pfizer’s own biodistribution studies have shown the injected material can be found in myriad critical organs throughout the body, leading to the possibility of multi-organ failure. And these studies were from a single injection. Multiple injections and booster shots may have cumulative effects on organ distributions of inoculant!

The COVID-19 reported deaths are people who died with COVID-19, not necessarily from COVID-19. Likewise, the VAERS deaths are people who have died following inoculation, not necessarily from inoculation.

As stated before, CDC showed that 94 % of the reported deaths had multiple comorbidities, thereby reducing the CDC's numbers attributed strictly to COVID-19 to about 35,000 for all age groups. Given the number of high false positives from the high amplification cycle PCR tests, and the willingness of healthcare professionals to attribute death to COVID-19 in the absence of tests or sometimes even with negative PCR tests, this 35,000 number is probably highly inflated as well.

On the latter issue, both Virginia Stoner [85] and Jessica Rose [86] have shown independently that the deaths following inoculation are not coincidental and are strongly related to inoculation through strong clustering around the time of injection. Our independent analyses of the VAERS database reported in Appendix 1 confirmed these clustering findings.

Additionally, VAERS historically has under-reported adverse events by about two orders-of-magnitude, so COVID-19 inoculation deaths could be in the hundreds of thousands for the USA for the period mid-December 2020 to the end of May 2021, potentially swamping the real COVID-19 deaths. Finally, the VAERS deaths reported so far are for the very short term. We have no idea what the death numbers will be in the intermediate and long-term; the clinical trials did not test for those.

The clinical trials used a non-representative younger and healthier sample to get EUA for the injection. Following EUA, the mass inoculations were administered to the very sick (and first responders) initially, and many died quite rapidly. However, because the elderly who died following COVID-19 inoculation were very frail with multiple comorbidities, their deaths could easily be attributed to causes other than the injection (as should have been the case for COVID-19 deaths as well).

Now the objective is the inoculation of the total USA population. Since many of these potential serious adverse effects have built-in lag times of at least six months or more, we won't know what they are until most of the population has been inoculated, and corrective action may be too late.

All the authors contributed equally and approved the final version of the manuscript.

Author’s contribution

Kostoff RN contributed to this paper with conception, data analysis, and writing the manuscript; Calina D contributed to data analysis, writing the manuscript, and editing; Kanduc D participated in data analysis and writing the manuscript; Briggs MB participated in data analysis, results validation, and graphics development; Vlachoyiannopoulos P participated in writing the manuscript; Svistunov AA participated in editing and reviewing the manuscript; Tsatsakis A participated in editing and reviewing the manuscript; all the authors contributed equally and approved the final version of the manuscript.

Ethical approval

Not applicable.

Declaration of Competing Interest

The authors declare that they have no competing interests. Aristides Tsatsakis is the Editor-in-Chief for the journal but had no personal involvement in the reviewing process, or any influence in terms of adjudicating on the final decision, for this article.

Table A1

Expected deaths from non-COVID-19 causes for inoculees (Thousands).

Potential covid deaths/#non-covid expected	Mean time location/five months
	0	%REP	1/3	%REP	1/2	%REP	2/3	%REP	1	%REP
0	723	0.5	482	0.74	362	0.98	242	1.47	4.77	75
.5	1085	0.33	723	0.5	543	0.66	363	0.98	7.14	50
1	1446	0.25	964	0.37	724	0.49	484	0.74	9.51	37

˜BEST-CASE SCENARIO

Consider the ten days following inoculation (including day of inoculation). Approximately 2,000 deaths were reported in VAERS. Assume hypothetically that all these deaths were in the expected category; this can be viewed as a best-case scenario. In this ˜best-case scenario, where the concentration of deaths is the highest and is normalized to the expected number of non-COVID-19 inoculation deaths (excluding deaths due solely to COVID-19 inoculation), 2,000/47,270 % of actual deaths (inoculation-related or not), or 4.23%, are reported in VAERS. Thus, at best, VAERS is underreporting by a factor of ˜20.

Table A2

Actual COVID-19 inoculation-based deaths.

Actual COVID-19 inoculation-based deaths from vaers reporting
	Separate Groups		Overlapping Groups
Expected Deaths Reported	37	20	37	20
Range Of Days Inoculation Deaths	0−30	0−30	0−30	0−30
Total Reported Deaths Over Range	2901	2901	2901	2901
Total Expected Deaths Over Range	1147	620	1147	620
Inoculation-Based Deaths Reported	1754	2281	2901	2901
Expected Deaths Reported/Total Expected	.0077	.0041	.0077	.0041
Total Actual Inoculation-Based Deaths Using Expected Ratio (Above)	227792	556341	376753	707561

Table A3

Possible COVID-19 inoculation-based deaths.

Possible COVID-19 inoculation-based deaths from vaers reporting
	Separate Groups		Overlapping Groups
Expected Deaths Reported	10	15	10	15
Range Of Days Inoculation Deaths	0−30	0−30	0−30	0−30
Total Reported Deaths Over Range	2901	2901	2901	2901
Total Expected Deaths Over Range	310	465	310	465
Inoculation-Based Deaths Reported	2591	2436	2901	2901
Expected Deaths Reported/Total Expected	.0021	.0031	.0021	.0031
Total Actual Inoculation-Based Deaths Using Expected Ratio (Above)	1233810	785806	1381429	935806