Published On: Sat, Apr 25th, 2020

No surprises as Covid-19’s exceptionality remains ignored and unreported; ACE2 crops up again

How incredible it is that British people have submitted to the UK Government resorting to issuing permissions, and have allowed it a right to do so all in the name of a disease that they know nothing about. Ask Joe Public to explain “Covid-19”, and one will no doubt become faced with a someone who talks in terms of “coronavirus” – a type of virus, not the name of a particular one. Joe Public will also ape the word “pandemic” in repetition of something that the BBC told them. However, Joe will not know the mechanics by which “coronavirus” can kill, and so how it can kill systematically. In fact, the exact nature of “Covid-19” is not just a mystery to Joe Public in his most average incarnation. Most of the opinion and expertise that one can find on the internet and in the forum of common digest does not appear to know what Covid-19 is, and indeed how very rare it appears to be.

At FBEL there has been an attempt to get to the bottom of the matter, most recently in the article called, A tale of two Covid-19s; potentially, the only real thing is the fight too far picked by UK Government. The reader is asked to be familiar with that piece because it contains certain data which has led to knowledge that will be presented here as if it is common, and not requiring sourcing or explanation.

From FBEL’s own tracking, it has been found that 95% of hospital deaths purportedly related to coronavirus involve a pre-existing illness [and, a Guardian article linked to in an update of that particular piece confirms the finding]. The latest data for the Intensive Care National Audit & Research Centre (ICNARC) informs that as of 23rd April, 2067 people died in critical care, purportedly of Covid-19. In the FBEL article cited above, it was conceded that these could represent the scale of “true” Covid-19, although the ICNARC death toll is somewhat larger than FBEL’s tracking would suggest it could be (by just over a thousand). We should note that NHS England presents in terms of “underlying conditions”, and has a long list of “illnesses” that would make a person at risk, for instance being seriously obese (a BMI of 40 and above) [and, as our exploration of the subject has found, this particular condition could lead to Covid-19 via ACE2 to SARS-COV binding – more of this, below]. On the other hand, ICNARC uses the term “very severe comorbidities”, and deals with BMI outside this categorisation, and so it’s quite clear that we are just dealing with a mismatch of definitions.

If we disqualify 177 patients reported by ICNARC who died with very severe comorbitities, we can work with its number of 1890, which we can think of as the number of patients dead from a “true” Covid-19. The point of showing this number is to demonstrate that it is still a long way short of the supposed national figure for numbers of dead by “Covid-19” in hospitals. It confirms that the number of Covid-19 deaths is tiny, whichever way anyone cares to look at it. And the reason, we might suppose, that this figure is so small is because of the specificity of the illness to a particular and uncommon permutation of factors.

The most recent ICNARC audit tells of out of 2667 patients who received advanced respiratory support, 1744 (or 65.4%) of them died. The upshot of this is that there is an extremely likely chance (verging on certainty) that 84% of all who died in critical care had been on a ventilator.

The reason for treading into this territory is because there has been a growing amount of discussion regarding treatment of “Covid-19” by ventilators, and how this appears to create the actual cause of death itself. In the article cited above, it was deduced that “Covid-19 could be a very specific illness, and the numbers presented by ICNARC could actually be precisely representative of that”. However, if a good deal of real Covid-19 is death by ventilator, or treatment of a mistaken case of infection by SARS-COV/SARS-COV-2, then that number of pure cases of Covid-19 must be even lower than we can already reckon it – or, in fact, the phenomenon might be intrinsically linked.

What apparently happens is that a Covid-19 patient on a ventilator can often develop an immune system overreaction, or indeed blunt-ended physical damage. Dealing with the latter first, there is a school of thought that appears to believe that while ventilation as the reaction is harmful, it is still Covid-19 that produces the problem. One can see the idea implied in the following extracts, which are from a Global Research article.

First of all, there is a quotation included into the writing from an authoritative piece:

….one of the most severe consequences of Covid-19 suggests another reason the ventilators aren’t more beneficial. In acute respiratory distress syndrome, which results from immune cells ravaging the lungs and kills many Covid-19 patients, the air sacs of the lungs become filled with a gummy yellow fluid. “That limits oxygen transfer from the lungs to the blood even when a machine pumps in oxygen,” Gillick said.

The writer of our lesson piece then offers an interpretation:

Can you see the problem? Virus victims develop a mucousy-yellow gunk in their lungs that prevents oxygen from transferring to the blood. Forcing more air into their lungs with a ventilator, doesn’t help that process, it just damages the lungs.

The interpretation attempts to be clearer than the quote: SARS-COV-2, it claims, causes the blockage, the reaction creates harm.

Now, the most useful part of this example piece is another quote it gives from its authoritative source:

Many (coronavirus) patients have blood oxygen levels so low they should be dead. But they’re not gasping for air, their hearts aren’t racing, and their brains show no signs of blinking off from lack of oxygen.†

From this we can see that the appearance of low oxygen levels will have triggered ventilation when it may not have been required. More significantly, we can ourselves ascertain from this something about the mechanics of Covid-19, and perceive that from a common sense point of view, if there is no actual lack of oxygen, the problem might not even be one of blocking at the lungs – which certainly does create a confusion of ideas. However, we will hold this thought, and instead appreciate that another school of thought thinks that it is the ventilation itself which causes an overreaction of the immune system (referred to in the following extract from a Science Daily article as “cytokine production”):

“This work suggests that there may be a ubiquitous inflammatory mechanism that cells have to respond to anything they perceive as a danger,” Ghadiali said. “At least in the lung, we now know the innate immunity pathway plays an important role, and this study showed that a mechanical force gets converted into cytokine production through this well-known pathway.”

In short, the lungs react to a ventilator as if it was an infection – and here is some vital information:

Scientists have known for more than a decade that mechanical ventilation causes inflammation in the lungs that lingers after an acute illness has been cleared, but they have had a hard time figuring out why the lungs respond in this way.

SARS-COV-2, then, is perhaps an entirely redundant factor in death by ventilator. Moreover, what is known as cytokine release syndrome (CRS) can have other causations, as was explored in the FBEL article, Covid-19 and pneumonic immune system overreaction. The short story is that medication for treatment is a likely suspect, and we must note that ventilation inevitably requires the application to a patient of a “workhorse medication”. Indeed, ventilation potentially can require quite a smorgasbord, as can be deduced from the following, which is taken from a piece concerned at the possibility of demand for the drugs outstripping supply:

John W. Devlin, PharmD, a professor of pharmacy at Northeastern University, in Boston,… said the shortages of sedatives, opioids and neuromuscular blocking agents are only likely to worsen as new COVID-19 cases surge across the country.

“In the Boston area, we are seeing an ever-increasing prevalence of COVID-19-associated acute respiratory distress syndrome (ARDS),” he said. “The complex ventilator settings and proning required to treat the severe hypoxemia found in these ARDS patients sometimes requires deep sedation to reduce oxygen consumption, high-dose opioids to reduce respiratory drive, and paralysis with neuromuscular blockers to reduce airway pressure and optimize ventilator compliance.”

Sedatives, opioids and drugs to induce paralysis: these are all in the mix. And then there is perhaps something else.

In the FBEL article, Pneumonia and Covid-19, and the veracity of the “one virus, one cause” paradigm, the following idea was posited:

….an overactive immune system – that will manifest as complicated illness – is caused by toxins that either suppress signalling, so the body doesn’t know when to stop reacting, or also generally interfere with how components for normal function chemically communicate.

This may have been very farsighted. The story of SARS-COV-2 is like the bad writing in a film of the sort that is all too prevalent these days where a Mary-Sue character can suddenly do all the things it used to take old, white males a life time to perfect. According to a report in the Daily Mail, scientists are claiming that it is possible for an ever-evolving coronavirus to now exploit interferon. Interferon is signalling protein connected with the immune system response to viral infection. The claim is that SARS-COV-2 affects this protein, which it well may do, but the actual problem comes, as we will discover, from the medical meddling.

The reader is asked to refer to the FBEL article, More on SARS-COV-ACE2 binding & “true” Covid-19 that discredits UK Government’s pretext for creating economic disaster, which provides an exploration into how interaction by SARS-COV-2 with something called ACE2 creates deficiency in the lungs.

Now look at this, from the same Daily Mail report:

The researchers’ data also revealed a correlation between the expression of the ACE2 gene with the activation of genes that are turned on by interferon — a protein which the body produces in reaction a viral infection.

When the researchers went on to conduct experiments in which they treated the cells of the human airway with interferon, they found that such turned on the ACE2 gene as well — the first time this connection has been established….

The team’s findings indicate that coronaviruses may have evolved to subvert part of their host’s natural defences, turning them to their advantage.

‘This isn’t the only example of that,’ Dr Ordovas-Montanes [of the Boston Children’s Hospital] noted.

‘There are other examples of coronaviruses and other viruses that actually target interferon-stimulated genes as ways of getting into cells. In a way, it’s the most reliable response of the host.’

Is this actually telling us that flooding with a signalling protein (“[which] turn[s] on specific genes that help cells to combat infection”) creates ACE2 prevalence, and therefore heightened opportunity for SARS-COV binding?

In the FBEL article cited above, it was argued that an imbalance of ACE2 is created by prescription drugs. Here, it would seem, is a tale told of similar artificial stimulation, and a connection between ACE2 and the immune system, and its over reaction, and this happening in relation to treatment of “airways”. It’s all very revealing.

Naturally, things are such (in whichever direction one might care to look) that the ever more noisy, raging, and “enbiggened” elephant in the room, which is ACE2 promoted artificially by medical treatment, is never discussed in relation to the cause of real Covid-19. Perhaps if it was, and there was due attention paid‡, there might even be a discovery of a connection with what appears to be a conundrum of working lungs but signs of low oxygen levels (or, the strange symptoms that have caused misapplication of ventilators and associated drugs).

And there is another point to make connected with the serious under reporting of real Covid-19, for which we must return to the same idea that was arrived at in the conclusion of the FBEL article that is the compliment of this one: if Covid-19 is so specific, and it clearly is, then there is no realistic way that it can be mistaken with anything else that could be called “Covid-19” [e.g. all that other death by underlying conditions]. That Joe Public, at every strata, does not know the difference is clearly due to a huge disinformation campaign, and this is evidence itself of a psychological manipulation of immense magnitude. If the public did know that less than a tiny, miniscule minority of people died of what looks to be artificially stimulated ACE2 assisted infection, then obviously it wouldn’t deign to be controlled in the way it has; it wouldn’t entertain the first thought of complying.



† Alternatively, we have also been hearing of cases in New York and Italy, as reported by John Rappoport, of

Extreme shortness of breath, life threatening, but without the usual indicators of respiratory failure or failure of the lungs to operate. The lungs can operate. The patients are apparently suffering from straight oxygen deprivation. Lack of oxygen. As if they were suddenly thrust into high altitude.

Several doctors are saying these patients must be given oxygen through breathing ventilators—but not at high pressure, because that could damage the lungs and even cause death. Instead, the increase in oxygen must be gently accomplished.

Rappoport goes on to speculate that 5G transmissions could “create a straight oxygen deprivation in the body—without structurally affecting the lungs themselves—creating the new condition”. The author is incredibly sceptical of such ideas, especially when there is clear evidence, which Rappaport ignores, of a particular sort of chemical treatment (and not just one) that is causing a condition in a host that makes it more susceptible to SARS-COV/SARS-COV-2.

Update, 26th April:

The reader might be seeing stuff like the following:

The results [of this study] showed the ORF8 and surface glycoprotein could bind to the porphyrin, respectively. At the same time, orf1ab, ORF10, and ORF3a proteins could coordinate attack the heme on the 1-beta chain of hemoglobin to dissociate the iron to form the porphyrin. The attack will cause less and less hemoglobin that can carry oxygen and carbon dioxide. The lung cells have extremely intense poisoning and inflammatory due to the inability to exchange carbon dioxide and oxygen frequently, which eventually results in ground-glass-like lung images.

The extract is taken from an article titled COVID-19: Attacks the 1-Beta Chain of Hemoglobin and Captures the Porphyrin to Inhibit Human Heme Metabolism. Clearly, the idea is to present Covid-19 as an attacker of the means by which the body can most efficiently use oxygen, and ultimately, if one is cynical, to promote the use of particular prescription drugs in the treatment of Covid-19.

On the other hand, as the following extract from a 2012 paper suggests, a problem with hemoglobin could have a much simpler explanation:

The ACE inhibitors (ACE-Is) and angiotensin II receptor blockers (ARBs) have been reported to reduce hemoglobin (Hb) levels in several patient groups at risk for secondary erythrocytosis, including patients with heart failure, hemodialysis, or chronic obstructive pulmonary disease, and after cardiac surgery or kidney transplant.

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Have Your Say
  1. Mara D says:

    You might be interested in David Crowe’s investigative journalism into SARS. His site can be found here:

    It is clear from his research that the vast majority of “SARS” deaths in 2003 were iatrogenic.

    • Mike Ellwood says:

      I strongly agree Mara. David Crowe has done an incredible amount of work over the years exposing the dubious nature of the orthodox paradigm regarding what are regarded as viral illnesses.

      Andrew Kaufman comes to similar conclusions regarding “SARS-CoV-2”.

      From a different perspective, I recommend people look at Andrew W Saul’s work (inspired by people like Linus Pauling and Abram Hoffer). Saul does not doubt viruses, but he says, with good evidence, that having good vitamin status (especially vitamin C and D, plus certain minerals, and good nutrition) can help people fight off any viral disease. With respiratory disease, the important thing is to prevent pneumonia developing, which large oral doses of vitamin C can help with.

      If pneumonia does develop, to the extent that hospitalisation is needed, then vitamin C should be given intravenously. Saul provides lots of evidence that this works.

      His website is
      His Youtube channel is Andrew W Saul’s Vitamin Channel.
      On Facebook he is The Megavitamin Man.

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