Yet their statistical arguments are very convincing; it takes me back 40 years to when one of my friends from medical school, who like me became a rheumatologist, destroyed a number of clinical trial results on non-steroidal anti-inflammatory drugs by demonstrating how a large number of procedural errors invalidated them. These ranged from inadequate trial size through selection bias to the use of the wrong analytical process. Later on I walked out of a conference when the pharmacodynamics of a new drug were tested on 12 people; one subject had a prolonged excretion half-life but was excluded from the analysis as an outlier. I questioned how one could ignore nearly 9% of the sample, and did not get a satisfactory response.
Thus both the use of Bayesian analysis to debunk some of the vaccine trial results was both interesting and convincing. But a more fundamental issue raised by Fenton and Neil was how you should define someone who is vaccinated. To decide arbitrarily that someone was not vaccinated until 14 days after he had been always seemed to me to be bizarre, and the effect of this is, of course, to bias the numbers of subjects getting side-effects, or Covid-type symptoms, in the vaccines' favour.
From a clinical viewpoint the 14 day rule is quite simply wrong. The serious consequences of SARS-CoV-2, or its vaccine, both of which seem to relate to the effect of the spike protein on the immune system, will begin within hours. So what is now needed to set records straight is a complete re-analysis of all the trial and observational data using the baseline for 'date of vaccination' as the date it was actually given. Will such a re-evaluation happen? I doubt it. Even with all the growing evidence of side-effects and failures of principle (vaccines do not prevent transmission and have little to no effect on serious disease), repeat vaccination programmes have been set up. I was a good boy; believing what I was told I was 'done' three times. It didn't stop me getting the virus and on the third jab I got symptoms of myocardial dysfunction, though I have no concrete evidence to prove that I had myocarditis as our local health service is not geared up to check. But I am not having any more boosters.
So the vaccine experience has not proved successful. The evidence that they work well, or that they do not produce significant side-effects is either non-existent or flawed due to selection bias. In the context of NHS spending one has to question whether the vaccination programme is value for money.
Fenton and Neil have questioned also the entire basis of the pandemic and raised the question of whether SARS-CoV-2 is really the organism of concern. There I disagree. The evidence points overwhelmingly to a coronavirus variant; not least because of the extraordinary convulsions of those seeking to deny that they were involved in viral gain-of function research. Fenton and Neil have suggested that many of the seriously ill were actually suffering from bacterial pneumonia. Here I think they are wrong. Why invoke two organisms when one will do? Yes, Haemophilus influenzae may be cultured but it's a normal commensal organism so it would be surprising if it wasn't. Going back to 1892 reveals that a similar suggestion was made then, after one researcher, Richard Pfeiffer, found evidence of a bacillus, but during the 1918 Spanish flu pandemic it was not present more often than it was - and of course the identification of viruses then did not exist. CT scans cannot easily distinguish between pneumonia, alveolar haemorrhage or a combination of the two, so using scans as a marker for infective pneumonia is clinically inappropriate. One needs to have lung biopsies to prove the cause of the shadows, but for all sorts of good reasons these were never done. Neither, as I have said previously, were there any reasonable post-mortem studies because pathologists were ordered not to conduct autopsies.
I have long maintained that the serious consequences seen and attributed to SARS-CoV-2, or COVID-19, are due to a cytokine storm. If this is provoked by the spike protein then vaccines that cause the body to generate spike protein would similarly provoke trouble, which is exactly what we have seen. Why should the serious consequences of infection such as thrombosis, myocarditis etc. be reproduced by the introduction of spike protein alone (for most of the Covid vaccines are causing indigenous production of it) if it wasn't in the first place caused by the spike protein content of the virus? This observation alone undermines any anti-spikeopathy hypothesis. Bear in mind that the spike protein has been shown to have mutated and with new SARS-CoV-2 variants the risk of severe illness has diminished - but the vaccines are still using mRNA that causes production of the original spike. But, as I have repeatedly posted, cytokine storms can be provoked by all sorts of things - other infections, introduction of immunogenic proteins, genetic predisposition etc. (I still have to hear of anyone pontificating on Covid who has read the definitive cytokine storm textbook by Cron and Behrens. Furthermore I have yet to see a scientifically valid rebuttal of the cytokine storm theory of causation.) SARS-CoV-2, in my opinion, was simply better and quicker than some of the other known precipitants, but as the Northwick Park drug trial showed, a cytokine storm can arise within hours or even minutes.
The cytokine storm is a fairly acute phenomenon. The timescale of its development is rapid. The systemic effects parallel the lung damage. The more you look, the better it fits. But the more you look and read about it the more you begin to realise that the severe sepsis caused by bacterial infections is also a cytokine storm effect. There is now a huge literature on the subject. The damage one sees developing, with thromboses, myocardial dysfunction, renal impairment etc., leaves one starting to wonder whether every severe sepsis case, irrespective of the underlying causative organism, kills people not because of aggressive damage by rapidly proliferating bugs but by the overreaction of the body to their presence. If a myriad of infections produce the same common path end result, the actual organism itself may be irrelevant in management terms.
That is not to say that one should not treat an infection if you can. I would be the last person to withhold appropriate antibiotics from someone with a widespread bacterial infection and, having seen the devastating effects of joint infections in arthritis patients, antibiotics would be the first thing I would use. But the systemic sequelae will not respond to antibiotics and require specific immunosuppression. We knew this before Covid; Cron and Behrens specified the use of corticosteroids and specific interleukin antagonists (tocilizumab for Il-6, anakinra for Il-1). I have treated sepsis in multiple sclerosis with large steroid doses (and appropriate antibiotics, of course). I started doing so in the early 2000s and the effects were dramatic. The rationale is unquestionable and the evidence substantial. And yet, despite my repeated attempts to put the evidence before government and its SAGE committee, it was ignored. Then someone within the system came independently to the idea that steroids might work - and so a trial was set up to prove what was, in fact, already known. As a result the definitive treatments for the cytokine storm syndrome caused by SARS-CoV-2 were delayed by several months (November 2020 for steroids, early 2021 for tocilizumab) while I had urged their use in May 2020. I have speculated that the deaths in the intervening period that could have been avoided runs into thousands. In the U.K. alone. Panic drowned the voice of expert clinicians; the response (or lack of it, treatment-wise) was driven by the wrong experts.
Someone will no doubt argue that I should not be proposing the use of untested therapies while at the same time criticising the deployment of improperly tested vaccines. Yes, my recommendations were untested in COVID-19, but there was ample evidence for efficacy (and safety) in exactly equivalent settings, so that argument fails.
So while I would dispute Fenton and Neil's superinfection theory, and stick to the concept of the spike protein being the major precipitant of the hyperimmune response called COVID-19, it is not a unique response and occurs in lots of infections. Does it matter what exact bit of a bug sets it all off? Or even which bug? Should we therefore drop the designation of COVID-19 altogether, and start to discuss the real syndrome of which COVID-19 is but one manifestation? And rename that syndrome - think of a name that produces a neat acronym. I have come up with Triggered HyperImmune Sepsis Syndrome, or THISS. THISS might be the enduring legacy of Fighting Goliath but I invented it and claim my prize.
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