We knew that Covid was fatal to some people. Then we started questioning if the vaccines we had produced were contributing to that toll. That is no longer a debatable question, it is fact. While we immerse ourselves in a mire of questions relating to motives, gain of function and more, we lose sight of the real question we should be asking. The only one that really matters from a human and scientific perspective.
WHY? What are the clinical reasons these vaccines cause death in some people?
Could the deaths arising from vaccination simply be ascribed to poor science, a flawed understanding of the associated mechanisms of action of ACE2 and the RAS pharma has targeted with vaccine produced protein? There has to be a pharmacological explanation for what we see unfolding around us in real-time. I think answering this question matters. Right now, it is the only question science should be focused on, especially as more treatments are developed and we expand mRNA-based Covid vaccines to healthy children.
Irrespective of the conclusions we arrive at, answering this question will save lives. It is perhaps the most urgent question of our generation based on the global scale of vaccine deployment. Saving lives continues to be the primary mission of medicine.
What follows is the result of many hours spent circling the forest to get the measure of the trees. I am not a virologist, but that, in some ways, may offer me a perspective that is distanced and more objective than the professionals who are overly invested in one school of thought or another. I have none of these biases; my motivation is to seek answers to this question – or raise other questions. This article is an effort to explore the potential answers.
Please note that much of the research quoted here predates the pandemic, for obvious reasons.
The discovery of ACE2, RAS and more
A little biology first before we launch into the meat of the article as I will use certain abbreviations repeatedly throughout the piece. Grasping these basics is key to following the argument that unfolds below.
What is the RAS system?
The renin–angiotensin system or RAS is a major regulator of blood pressure homeostasis – homeostasis refers to a state of balance among all the body systems needed for the body to survive and function correctly. We’ve known about RAS for more than a 100 years now, but understanding the intricacies of how it works has only really been possible in the last three decades, with the discovery of several novel components, including genes like ACE and ACE2.
The are five different forms of angiotensin and these are denoted by Roman numerals, angiotensin I through IV. These hormones, and the way they are activated, are what we refer to as the renin angiotensin system or RAS. The RAS is an incredibly intricate system that impacts our entire physiology and, like much of our biology, requires a delicate balance to function effectively. We understand the basic mechanisms underpinning the RAS, its component parts and some, but not all, of the systems many interactions and dependencies.
For instance, we have known for decades about the role angiotensin II (see below) plays in hypertension, but only recently discovered its influence on inflammation. Studies have shown that numerous tissues and organs contain their own locally generated angiotensin products. This local system has been shown to be responsive to various stimuli of physiological and pathophysiological importance and we continue to discover new associated systemic dependencies.
Angiotensinogen, a peptide hormone
The liver creates and releases a protein called angiotensinogen. This is then broken up by renin, an enzyme produced in the kidney, to form angiotensin I. This form of the hormone is not known to have any particular biological function in itself but, is an important precursor for angiotensin II. As it passes in the bloodstream through the lungs and kidneys, it is further metabolized to produce angiotensin II by the action of angiotensin-converting enzyme.
I will only mention the first two angiotensins in any detail for the purpose of this article.
Angiotensin I, a peptide hormone
Renin cleaves angiotensinogen, forming Ang I that in turn is converted to Ang II by ACE. Angiotensin I does not appear to serve much other function, aside from acting as a chemical precursor to Angiotensin II, which affects multiple systems in our bodies.
Angiotensin II, a peptide hormone
Angiotensin II is the main effector molecule of the RAS. It causes increases in blood pressure, influences renal (kidney) tubuli to retain sodium and water, and stimulates Aldosterone – Aldosterone is a steroid hormone secreted by adrenal glands. Its main role is to regulate salt and water in the body, thereby affecting blood pressure – but that isn’t the only role played by Angiotensin II in our bodies.
Besides being a potent vasoconstrictor, Angiotensin II also exerts proliferative, pro-inflammatory (causing inflammation) and pro-fibrotic activities. Importantly, numerous tissues and organs contain their own locally generated angiotensin products (angiotensin II, III, IV and Ang 1-7) These tissues and organs include, to name but a few, the brain, bone marrow, adipose, epididymis, carotid body, liver, and pancreas.
To summarize, Angiotensin II effects:
- Blood vessels – it increases blood pressure by causing constriction (narrowing) of the blood vessels
- Nerves: it increases the sensation of thirst, the desire for salt, encourages the release of other hormones that are involved in fluid retention.
- Adrenal glands: it stimulates production of the hormone aldosterone, resulting in the body retaining sodium and losing potassium from the kidneys
- The kidneys: it increases sodium retention and alters the way the kidneys filter blood. This increases water reabsorption in the kidney to increase blood volume and blood pressure.
The ACE Gene
This gene serves to convert Angiotensin I, produced in the liver by the protein angiotensinogen, to Angiotensin II, which is then, in turn, regulated by the ACE2 gene.
The ACE2 Gene
Angiotensin-converting enzyme 2 or ACE2 is probably a term you’ve heard repeatedly in the last three years, unless you walled yourself up in a cave when the pandemic broke. What is it exactly and what does it do. To start with, it is one of those novel components of the RAS, one we only discovered 2 decades ago and it serves a very important number of functions.
Scientists originally cloned ACE2 from a cDNA library prepared from the left ventricle of a failing human heart (Donoghue et al. 2000). It was found to share very similar properties (homology), greater than 40%, with angiotensin-converting enzyme (ACE) – homology is the scientific term for this in biology, things that share properties, like proteins. Not surprisingly, speculation abounded that the ACE2 gene played a key role in cardiac conditions. The relationship was later found to be indirect and complex.
ACE2 is known to be expressed in various human organs, and its organ- and cell-specific expression suggests that it may play a role in the regulation of cardiovascular and renal function, as well as fertility. There is lot we still don’t know about the full role of this gene.
ACE2 protein expression is present in heart, kidney, testis, lung (type I and type II alveolar epithelial cells), nasal, and oral mucosa and nasopharynx (basal layer of the non-keratinizing squamous epithelium), smooth muscle cells and endothelium of vessels from stomach, small intestine and colon, in smooth muscle cells of the muscularis mucosae and the muscularis propria, in enterocytes of all parts of the small intestine including the duodenum, jejunum, and ileum (but colon), skin (basal cell layer of the epidermis extending to the basal cell layer of hair follicles smooth muscle cells surrounding the sebaceous glands, cells of the eccrine glands), endothelial, and smooth muscle cell of the brain.
In short, ACE2 is present in all our organs.
Have you heard of the HCoV-NL63 coronavirus?
If you haven’t, you’re not alone. Despite blanket media coverage of the pandemic, this little beastie was notably absent from the news cycles. What is it exactly? This extract from a 2010 article published on the NIH website
“In Holland in 2004, another novel human coronavirus (HCoV-NL63) was isolated from a seven-month old infant suffering from respiratory symptoms. This virus has subsequently been identified in various countries, indicating a worldwide distribution. HCoV-NL63 has been shown to infect mainly children and the immunocommpromised, who presented with either mild upper respiratory symptoms (cough, fever and rhinorrhoea) or more serious lower respiratory tract involvement such as bronchiolitis and croup, which was observed mainly in younger children.”
What is of real interest is the statement following on this. Aetiological simply means ‘causing or contributing to the development of a disease or condition’.
In fact, HCoV-NL63 is the aetiological agent for up to 10% of all respiratory diseases.
It will come then as no surprise to learn how this coronavirus infects us. This article on PNAS, titled Human coronavirus NL63 employs the severe acute respiratory syndrome coronavirus receptor for cellular entry was published in 2005. It examines the pathways used by NL63 to infect us. An extract below, emphasis added by author.
‘An analysis of receptor engagement revealed that NL63-S binds angiotensin-converting enzyme (ACE) 2, the receptor for SARS-CoV, and HCoV-NL63 uses ACE2 as a receptor for infection of target cells. Potent neutralizing activity directed against NL63- but not 229E-S protein was detected in virtually all sera from patients 8 years of age or older, suggesting that HCoV-NL63 infection of humans is common and usually acquired during childhood. Here, we show that SARS-CoV shares its receptor ACE2 with HCoV-NL63.’
Perhaps, presciently, the paper summary closes with a warning.
Because the two viruses differ dramatically in their ability to induce disease, analysis of HCoV-NL63 might unravel pathogenicity factors in SARS-CoV. The frequent HCoV-NL63 infection of humans suggests that highly pathogenic variants have ample opportunity to evolve, underlining the need for vaccines against HCoVs.
I refer to these articles for a number of reasons. Primarily, it is to highlight the length of time we’ve known about the coronavirus’s proclivity for the ACE2 receptors, nearly for two decades, during the course of which, we failed to produce anything remotely amounting to counter measures, vaccine, anti-viral, or otherwise. Another extract from this article suggests
“The S proteins of CoVs, which provide virions with a corona-like appearance, mediate infection of target cells and play a central role in viral replication. The interaction of CoV S proteins with specific cellular receptors determines, to a large extent, which cells can be infected, and the entry process is an attractive target for antiviral therapy.”
While we understood the exact mechanisms that drive coronaviruses we lacked either the will or the medical technology to develop, over the course of two decades, agents that would prevent infection. Hindsight would suggest the former. Critically, we were also now aware of how altering the proteins expressed by the virus would impact its affects on our physiology, paving the way for expansive gain of function research over the last two decades.
Why focus on the RAS and ACE2 when considering vaccine related deaths?
Simply put, in a long list of potential culprits, ACE2 appears to be the most likely suspect, for a number of reasons, which I will gloss over below. We know that claims for vaccine related deaths tend to focus on two or three very specific conditions, affecting the circulatory system (blood vessels), the heart and the brain. Yes, other organs and systems are involved in the vaccine SAE’s, and, for possible reasons that we will explore below, that list coincides very closely with the organs and systems the coronavirus itself targets.
Logic dictates this overlap needs to be examined more seriously. How, potentially, could the vaccine be creating, in some instances, the same impact on our systems as the virus itself. The ACE2 receptors are targeted by the viral spike protein. The vaccine utilizes the same pathways to deliver its encoded messenger RNA which results in the production of the identical protein, one in an unlikely string of coincidences involving the ACE2 gene.
It is perhaps another coincidence that in 2022, Moderna announced an mRNA based treatment to address heart damage, a known consequence of both the virus and the vaccine. Pre-existing knowledge of issues surrounding treatments targeting ACE2 would have exposed another potential market and the development of a treatment, the same treatment launched less than two years after the release of the vaccine.
Scientists were well aware of the impact of ACE2 on cardiac related conditions prior to the pandemic, particularly those engaged in mRNA research.
Angiotensin II, ACE2 and inflammation
We know a lot about Angiotensins and the ACE genes, thanks in no small part to our understanding of their role in regulation of blood pressure and the pursuit of medicines to address hypertension. Known as ACE blockers (ramipril, lisinopril, enalapril) and angiotensin blockers (ARBs, e.g., losartan, valsartan, etc), these medicines have proven very effective for many patients. Below is research published in the Journal of Human Hypertension, in Nature’s online publication, looking at the role of Angiotensins in inflammation.
‘Angiotensin II (Ang II) increases adhesion molecules, cytokines and chemokines and exerts a proinflammatory effect on leucocytes, endothelial cells and vascular smooth muscle cells. Acting via the type 1 receptor, Ang II initiates an inflammatory cascade of reduced nicotinamide-adenine dinucleotide phosphate oxidase, reactive oxygen species (ROS) and nuclear factor-κB, which mediates transcription and gene expression and increases adhesion molecules and chemokines.‘
The paper, published in 2006, makes the following statement about the mechanism of action of Ang II blockers.
These anti-inflammatory and antioxidative effects, which are probably due in part to unopposed stimulation of the Ang II type 2 receptor, may be beneficial in acute coronary syndromes and may also contribute to the prevention of type II diabetes mellitus, as insulin resistance is mediated by inflammatory processes.
So there then, are two documented potential side effects of our bodies failing to correctly regulate the production of angiotensins. A process that is regulated exclusively by ACE2. Science is littered with more examples.
This 2010 paper looks at the binding of Ang II to its receptors (in particular AT1) mediating intracellular free radical generation that contributes to tissue damage by promoting mitochondrial dysfunction. Blocking Ang II signaling, the article points out, protects against neurodegenerative processes and promotes longevity in rodents.
On the topic of rodents, mice bred with inhibited ACE2 were exhaustively examined to establish a link between the down regulation of ACE2 and cardiac conditions. This 2008 study looked critically at the results obtained from earlier studies and attempted to isolate the exact mechanisms at play. Earlier findings had suggested;
“The dominant phenotype of these ACE2-deficient mice was a marked defect in cardiac contractility. This decrease in left ventricular systolic function, documented by echocardiography in anaesthetized mice, was more severe in older, male ACE2-deficient mice and was accompanied by reduced blood pressures. In 6-month-old male mice, left ventricular fractional shortening was reduced by as much as 40%. Additionally, cardiac structure was abnormal, with wall thinning and enlarged cardiac chambers. However, there was no indication of cardiac hypertrophy or fibrosis in the ACE2-deficient mice, and overall heart weights were very similar between ACE2 knockout and wild-type animals. (Donoghue et al. 2000; Tipnis et al. 2000)”
In summary, the paper reached the following conclusions;
ACE2 appears to have only modest effects on baseline cardiovascular functions and blood pressure control; these effects can be substantially modulated by genetic and, perhaps, environmental factors. In contrast, the activity of ACE2 may have more profound effects on susceptibility to pathological states, such as hypertension and cardiac hypertrophy. These actions require an active RAS, including capacity for generation of angiotensin II and activation of angiotensin II type 1 receptors.
SARS-COV2, the mRNA vaccines and the ACE2 gene
All the materials and research referenced in this section are post 2019.
To understand what is happening inside us when the coronavirus attacks, we need to unpack a few of the terms we’ve read about above.
Using the spike-like protein on its surface, the SARS-CoV-2 virus binds to ACE2 – like a key being inserted into a lock – prior to entry and infection of cells. ACE2 acts as a cellular doorway or receptor for the virus that causes COVID-19, allowing it to gain access to the cell. While this process is underway, the affected ACE2 molecule is effectively “out of the game”. It can no longer perform its primary goal of regulating and controlling Ang II.
ACE2, aside from residing in many of our organs, is also present in epithelial cells, which line certain tissues and create protective barriers. The exchange of oxygen and carbon dioxide between the lungs and blood vessels occurs across this epithelial lining in the lung. ACE2 is also present in epithelium in the nose, the mouth and the lungs. In the lungs, ACE2 is highly abundant in chambers within the lung called alveoli, where oxygen is absorbed and waste carbon dioxide is released.
The virus is introduced through the nasal passage and airways and heads directly to the lungs. By effectively “commandeering” ACE2 in these areas, the virus enables Ang II to wreak havoc in the absence of the ACE2 regulators. Remember, ACE2 converts Ang II to other molecules that counteract the effects of Ang II. As far as our lungs are concerned, left unchecked, ANG II can increase inflammation and the death of cells in the alveoli which are critical for bringing oxygen into the body.
Little wonder then that in some individuals, the disease is fatal.
Of course, we know now that ACE2 is present in many of our organs, and the damage isn’t simply limited to our lungs. Covid has shown its ability to exploit ACE2 throughout our systems, with heart, brain, digestive and other damage being inflicted. The kidneys, liver and digestive tract can also be injured. Blood vessels may also be a site for damage. Sadly, people with conditions like hypertension, coronary heart disease and diabetes tend to posses more ACE2, making them even more susceptible to the virus.
Central to the success of this biological hack on the part of the coronavirus is the protein that it manufactures and that allows it to lock on so effectively to the ACE2. It is, for all intense and purpose, the same protein that the mRNA vaccine induces our cells to produce.
Examining the SARS COV2 protein
What we know about the spike protein is now in the public domain and freely shared. For those who are interested in its exact structure, I’d recommend the following article titled Structural and functional properties of SARS-CoV-2 spike protein: potential antivirus drug development for COVID-19 published in Nature in August of 2020, which provides an excellent overview of the spike protein. An extract relating to the S Protein appears below.
With a size of 180–200 kDa, the S protein consists of an extracellular N-terminus, a transmembrane (TM) domain anchored in the viral membrane, and a short intracellular C-terminal segment [11]. S normally exists in a metastable, prefusion conformation; once the virus interacts with the host cell, extensive structural rearrangement of the S protein occurs, allowing the virus to fuse with the host cell membrane. The spikes are coated with polysaccharide molecules to camouflage them, evading surveillance of the host immune system during entry
Whilst this information on the S protein is made freely available to the scientific community you have to a little fishing to find the exact protein structures utilized by the mRNA vaccines. Both mRNA encodes the same S-2P protein which differ from the spike protein in the reference SARS-CoV-2 genome (NC_045512) by two amino acids, i.e., amino acids KV at sites 986 and 987 were replaced by PP to stabilize the resulting spike protein in the prefusion state to train the host immune system to recognize the virus before its entry into the host cell.
You can find the exact genetic sequencing of the initial vaccines released in 2020 here (World Health Organization Word document) for Pfizer and here for Moderna.
It is important to keep in mind that these proteins do not exist in the vaccines themselves, but rather that the encoded mRNA in the vaccine contains the instructions for creating the proteins within the body. These are extremely complex, cutting edge medicines that are only properly understood and programmed by a handful of scientists specializing in the field, most of whom find themselves in the employ of companies like Pfizer, BioNTech and Moderna.
Using the logic provided to account for the rapid development (less than a month) of a working model for replicating the required protein in vivo, I cannot resist pointing at the elephant in the room. Why was it this approach did not result in vaccines for both SARS and MERS? Did we only conveniently happen onto this in the same month the pandemic broke? If that convenient truth is to be believed, then it is reassuring to know we can now develop a vaccine in days for any novel virus we now discover. The next viral threat we face will no doubt settle this.
What is of real relevance here though is that the mRNA encoded protein was supposed to cling to the cell that produced it, thereby preventing it from circulating freely in the body. The spike protein is a recognized pathogenic protein with the potential to cause system wide damage, so it was seen as critical to bind the protein to the target cells.
In reality this didn’t happen. The released spike protein is shed into the medium and then eventually reaches the bloodstream causing systemic damage. ACE2 receptors are common in the heart and brain, and this is how the spike protein causes cardiovascular and cognitive problems. Here is one of many studies, confirming the wide spread presence of the vaccine released spike protein in the body. According to the research, published in Oxford Academic in May of 2021, they state;
Here we provide evidence that circulating SARS-CoV-2 proteins are present in the plasma of participants vaccinated with the mRNA-1273 vaccine. We report antigen and serological data of the mRNA-1273 vaccine in 13 healthcare workers at the Brigham and Women’s Hospital.
Why the mRNA vaccine’s don’t stay in your arm
If, like many laypeople and even scientific and medically trained individuals, you’ve been led into believing that the vaccine stays localized at the site of the injection and elicits the necessary cellular responses there, then you’re in for a rude awakening. It’s the lymphatic system that is the main pathway of delivery and to reach that, the vaccine travels. Everywhere, it turns out.
To work effectively, the mRNA vaccines need to reach dendritic cells, and not just any old dendritic cells. The ideal ones, that respond best to the instruction carried in the mRNA to manufacture the spike protein, are located in our lymph nodes. Your lymphatic system, consisting of nodes positioned all over your body (see image above) offers a direct gateway to your immune system. To ensure the mRNA Pfizer vaccine reached all these nodes, the developers utilized lipid nanoparticles to deliver the vaccine to every outpost of the body.
More from Özlem Türeci, the Chief Medical Officer of BioNTech, in a passage from The Vaccine, the book that Türeci and her husband, BioNTech CEO Ugur Sahin, wrote, where journalist Joe Miller explains why BioNTech’s platform specifically targets the lymph nodes;
What Ugur learnt was that the location to which a vaccine delivers its ‘wanted poster’ really mattered. The reason for this, the couple’s team in Mainz later realised, was that not all dendritic cells … were created equal. The ones that resided in lymph nodes – of which the spleen is the largest – were particularly adept at capturing mRNA and making sure the instructions it carried were acted upon. These kidney-bean shaped organs, found under our armpits, in our groins, and at several other outposts in the body, are the information hubs of the immune system. (p. 98)
The wide biodistribution of the mRNA that came to light after the vaccine rollout was never an anomaly, as claimed by some and supported by the CDC. Far rather, it was a necessary design feature of BioNTech’s mRNA technology, a feature that was not publicized for obvious reasons. This distribution also serves to explain the wide ranging adverse events experienced by some to the vaccines.
This revelation makes a complete mockery of the articles published far and wide across the internet in 2020 and beyond, suggesting in fact that the vaccines were localized to the injection site. Even sites like the Conversation, with the help of medical professionals, got it spectacularly wrong. Take this article, titled Why do we get shots in the arm? It’s all about the muscle, published in May of 2021. We are assured the vaccine stays put and the description of the vaccines mechanism of action shows how poorly mRNA technology was, and is, understood.
Muscles make an excellent vaccine administration site because muscle tissue contains important immune cells. These immune cells recognize the antigen, a tiny piece of a virus or bacteria introduced by the vaccine that stimulates an immune response. In the case of the COVID-19 vaccine, it is not introducing an antigen but rather administering the blueprint for producing antigens. The immune cells in the muscle tissue pick up these antigens and present them to the lymph nodes. Injecting the vaccine into muscle tissue keeps the vaccine localized, allowing immune cells to sound the alarm to other immune cells and get to work.
While completely correct in medical terms for the usual mechanism of action of traditional vaccines, this paragraph reflects the total lack of understanding relating to mRNA that is prevalent in the industry. These are new drugs, utilizing new technology and nano particles that are able to penetrate almost any barrier. It’s the stuff of science and fiction, morphed into medicine, and our lives and safety reside in the hands of a small number of individuals who actually understand this technology. History suggests this is not a safe place from which to practice medicine.
The CDC also uttered their own garbled version of so called vaccine-facts, on their advisory page, quoted below. These are the two opening bullet points on the page.
First, mRNA COVID-19 vaccines are given in the upper arm muscle or upper thigh, depending on the age of who is getting vaccinated.
After vaccination, the mRNA will enter the muscle cells. Once inside, they use the cells’ machinery to produce a harmless piece of what is called the spike protein…. After the protein piece is made, our cells break down the mRNA and remove it, leaving the body as waste.
This whole second paragraph is likely littered with inaccuracies, from start to finish. mRNA is detectable in some individuals a year after vaccination and the delivery method does not target the muscle, we simply cannot inject vaccines into people’s groins (lymph nodes), so the arm it is then. Should we believe the CDC, a group of scientists appointed because of their apparent expertise, has no idea of the mechanism of action of mRNA? More worryingly, is what else in this statement also inaccurate?
Particularly given recent acknowledgements that the mRNA vaccines don’t stop transmission of the virus (another blatant lie to coerce vaccination), we can now begin to question everything vaccine related that we have been fed over the past three years, with the onus on science to prove their statements, the most important of which is reflected in this one fundamental line of CDC vaccine propaganda;
“to produce a harmless piece of what is called the spike protein“
How harmless is this piece of protein? How harmless can a piece of any pathogenic protein be? The truth is, we really don’t know. We only have the assurances of the people who manufactured and profited from the vaccines, that this protein is in fact a harmless and perfectly safe way of generating an immune response against the SARS-COV2 virus. Emerging evidence suggests otherwise.
The American College of Cardiology published a paper in January of this year, titled Spike Protein Detected in Post–COVID-19 mRNA Vaccine Myocarditis. The researchers discovered the following.
Free full length spike protein (at a mean of ~34 pg/mL) was detected in the blood of adolescents and young adults who developed post-mRNA vaccine myocarditis. In this context ‘free’ refers to an antigen that is not attached or subject to any immune mediated response by the body. Elevated levels of free SARS-CoV-2 antigens were also detected in children suffering from Multisystem inflammatory syndrome (MIS) post vaccine.
“Thus, the spike antigen itself, which evades antibody recognition rather than invoking immune hyperactivation, may contribute to myocarditis in these individuals.”
More worrying, these free antigens were still evident weeks later, indicating the body was overwhelmed by the vaccine induced production of these proteins, allowing them to effectively travel freely throughout our systems, resulting in a host of adverse events.
The Crux
Here’s the kicker, and it’s the reason for the lengthy introduction and explanation regarding how the protein carried by the virus exploits our immune defenses and is so deadly. If, and it appears more and more likely with the passage of time, the SARS COV2 protein was manufactured in a laboratory precisely for the purposes of weaponizing the virus – something we have been studying since 2004 – then surely instructing the body to produce the identical protein, or even a portion thereof, would have the same or similar deadly consequences for our physiology?
It is a logical conclusion to draw and a concern that science must definitively address before we advance any further treatment. In the interim, while we consider and evaluate the real medical dangers associated with the Covid vaccines, it would behoove governments and scientists to proceed cautiously. They have been warned repeatedly and chosen to ignore the safety signals and adverse events surrounding the vaccines.
Considering a suspension of child vaccination programs appears sensible and practical, as there is no immediate risk to children from SARS COV2 and the risk of adverse reactions to the vaccines appears to offer a real and present danger to the public health of children across the globe.
We need more transparent, independent science, cautious science, directed at answering the questions raised above relating to the why. Why are vaccinated people dying, and why, given the evolution of the virus in less serious forms, do we still aggressively pursue vaccination campaigns for the very young?
