Our response to Dr Pierre Kory
........on whether 'Spikeopathy' explains the 'novel' symptoms associated with COVID-19
A few weeks ago, we wrote an article titled “'Spikeopathy does not explain the 'novel' symptoms associated with COVID-19: An investigation into competing alternative explanations,” which was written in reaction to a WhatsApp conversation in a group containing a number of ‘frontline’ doctors includingand Dr Jackie Stone.
Dr Kory agreed to write a response to that article and has now done so here:
We strongly recommend that readers, read our first article, Kory’s response and then come back here and read this article.
Kory decided to also respond to many other points made in the WhatsApp conversation by three other prominent discussants – Sean Flanagan, Dr Mike Yeadon and Nick Hudson. This has muddied the waters somewhat, allowing Kory to change the frame for the conversation, dodge the specifics of our criticism, and instead address multiple points and arguments we did not indeed make (even though we might agree with them). Hence, much of Kory’s response is NOT the response to our article at all.
Additionally, in his response Kory summarised our main arguments and findings in his own words. He did invite us to comment on his article before publication, but we declined, thinking it best to allow him (and any of his unnamed co-authors) to comment in their own words, even if this risked him misrepresenting our arguments or evidence.
He summarised our arguments thus:
“Obviously, if you are interested in following the debate, the points raised and the points countered, it is mandatory you read the post above before proceeding with the below.
If you didn’t or don’t want to read it, I will instead summarize their main argument and findings. In no particular order, besides the post above, in the What’s App exchanges, these points were made by various members who have taken the position that “no novel pathogen existed.”
Clearly, rather than address evidence for/against there being a novel disease entity (covid19) which appeared around the world due to pandemic spread, with features exclusive to and explicable by the concept of spikeopathy, he instead addressed the argument that there was “no novel pathogen”. This was not the argument we made in our article. We are puzzled as to why the goal posts were shifted like this. It suggests he either didn’t bother to closely read our article or didn’t wish to address the questions we raised therein.
Likewise, his summary intentionally mis-framed our questions to his own readership. To date, his article has garnered 345 comments on his substack. In reviewing these comments, we were left with the impression that a vanishingly small number of readers even bothered to read our article and are perhaps not interested in the debate.
However, despite Kory moving the goalposts, we remain happy to play football.
Summary of our position
A summary of our position is that supposed unique symptoms of spikeopathy - such as CT-findings, ‘happy hypoxia’ and ‘dry-lung’ - can be readily explained by other diseases/pathogens. Furthermore, we argued that other symptoms reported by Kory that they associate with spikeopathy such as diarrhoea, loss of taste and smell and micro clotting or other ‘blood issues’ are not associated with covid-19 by other academic medical professionals. Hence none of these diagnostic features are specific to spikeopathy and thus they cannot be established as strongly or necessarily confirmatory of covid-19.
Note that the above is not a casual conclusion that can be glibly set aside. We conducted a thorough literature review and cited many academic studies that unambiguously contradict Kory’s ideas about spikeopathy and its supposed symptoms. Either all the other clinical studies are wrong, and Kory is right, or vice versa. Both cannot be true. And note that none of these studies were written by us – we simply presented the sum total of what is known to date.
It is well accepted that science progresses by a process of falsification and contradiction. In the old days at least, pointing out that the symptoms of a purportedly unique disease cannot be pinned down, are reported differently by different clinicians, and have massive overlap with other well established and known, unique diseases would be significant. After all, being able to define a phenomenon in a way that differentiates it from other phenomena, is a necessary first step in enabling other scientists to test hypotheses about the phenomena and replicate the mechanisms that generate it.
Scientists are also duty-bound to seek alternative causal explanations for the phenomena observed; otherwise, how do they know that A causes B (or vice versa), or that some other variable C causes B and not A at all? Hence, alternative explanations supported by strong prior evidence must be evaluated alongside competing novel explanations. Good medical practitioners should follow this proto-Bayesian process: determine what evidence supports which of the competing prior hypothetical explanations to conclude which, a posteriori, is the most credible in light of the evidence.
However, what we saw throughout the literature, and in Kory’s statements and papers, was a pre-formed belief that the only explanation for patient symptoms was spikeopathy, a categorisation based on a positive diagnosis of SARS-CoV-2, whether by test or clinical suspicion1. There is little to no evidence that other explanations were systematically considered and excluded by, Kory and others, such as bacterial pneumonia, which would affect the elderly, and lung injury caused by adulterated vapes, which would affect the young.
This omission seems particularly surprising given that what happened in New York City (Kory’s experience there being central to his beliefs) is so completely different2 from what happened elsewhere in the USA that to assume there is a single common cause in over simplistic and does not fit the data3.
We hypothesised that two or more sets of observed disease manifestations, with distinct groups of symptoms seen in some patients, were compatible with the symptoms reported in the literature and caused by one or more different pathogens entirely, where:
Many/most covid-19 cases would have been ‘ordinary’ influenza and bacterial pneumonia cases.
Some were not viruses or diseases at all but were potentially caused by toxicological events.
Each of these were misattributed to covid-19 either deliberately or through a process of human error.
In our view the first explanation is the most likely, for most cases, especially given there was a panic over covid-19 which would have created an overwhelming psychological pressure leading to confirmation bias.
Dissecting Dr Kory’s Response
Given the above, simply speaking, we believe Kory’s assertions cannot be corroborated. He was unable or unwilling to cite any scientific paper to substantiate his assertions, but to be fair, neither has most of the scientific medical community.
In our article we covered a lot of papers on CT findings which challenged the presumption that you could find uniquely diagnostic CT findings for Covid-19. Kory responded with these statements:
“Further, I would also then write “bacterial pneumonia is less favored given bilateral findings vs. unilateral, lack of consolidation on CT…..
There was a pervasive “bilateral organizing pneumonia” on CT scan (OP is an uncommon finding in general and “organizing” patterns are quite differentiating amongst diseases…
Often rapid progression to fibrosis on CT scans - this was novel to me, I had never seen such rapidly fibrosing lung findings on CT scans in ICU patients (again, not unique as there is a rare, rapidly fibrosing lung disease called AIP (acute interstitial pneumonia)”
Despite saying there are unique signs of covid-19 on CT, Kory contradicts himself a few paragraphs later when addressing our conclusion that radiologic findings cannot reliably differentiate between Covid-19, influenza like illnesses, and bacterial pneumonia, by responding:
“….despite the papers showing relatively equal incidences of various radiographic abnormalities overall - you are overlooking timing and stage of disease where radiography is a much better differentiator than those papers suggest)”
He offers no evidence of this pattern, and none of the papers on CT and covid-19 offer much, if any, either. Unfortunately, there is simply no substantiated evidence either that Kory cited or that we could find to support the belief that evidence of progression and timing of symptoms diagnostically discriminates for/against covid-19. If this is such a strong diagnostic criterion then we should expect him and others to have been very careful to document it, ‘in detail’, in scientific papers, and for other medical scientists to confirm the findings.
Kory repeatedly relies on his expertise in pattern recognition developed over many years:
“….might be better explained as “intuition”, it is almost an unconscious process when it occurs but I have been successfully relying on my pattern recognition skills to differentiate among causes of acute respiratory failure for 20 years.”
How this can be reliably applied to a supposedly novel pathogen with a wickedly complex set of signs and symptoms, we simply cannot imagine. Also, during the Spring ‘outbreak’ in NYC he had mere weeks to cut this Gordian knot.
Kory then goes on to list what he believes are the unique symptoms associated with this, leaving any reader overwhelmed by a cacophonous list of indisputable signs and symptoms of spikeopathy. Again, he makes no attempt to compare what he ‘sees’ with those symptoms reported by other physicians in the academic medical literature.
Kory favours homely personal anecdotes to support the claim that covid-19 can be reliably diagnosed, such as:
“like my oldest and best friend who simply got nauseous, started projectile vomiting, went to hospital and was eventually diagnosed with adult-onset multi-system inflammatory syndrome related to Covid (note he was Covid positive on admission). But know that he never had a preceding upper respiratory symptom however all the other findings were consistent with the new rarer syndrome of MISC-A.. So, atypical presentation, but his eventual A-MISC syndrome has criteria for diagnosis and he met all of them”
Note from the above we don’t not know whether the friend was tested for any other pathogen!
Again, he cannot resist another personal homily:
“One other troublingly unique aspect was that in the first wave in NY, doctors and nurses were dying on the front lines. One of the first to die was an absolute giant of my specialty, he died in Seattle right after their first influx of patients. I have NEVER lost a colleague to the same disease we were treating.. ever. And I knew of at least 3 who died in the first wave of Covid. And that’s just me.”
Kory reports healthcare workers were dying on the frontlines. We assume he means they experienced symptoms and complications of some kind and died within days or weeks, not that colleagues were falling down dead in hospitals. There were several media reports about doctors, nurses, other hospital staff, and EMTs being killed by Covid during the New York death event. That the nature and intensity of these stories was not replicated elsewhere or after spring 2020, as far as we know, is strongly suggestive that whatever is responsible for those deaths is not likely to be a flu-like illness.
Also, cases which are atypical of covid-19 are still typical of covid-19:
“I have also seen, on few occasions, other presentations that were atypical, i.e. more GI predominant than respiratory but the response to treatment was the same.”
Despite us pointing out that the myriad of covid-19 studies that did not report happy hypoxia, Kory simply ignores this and instead defaults to his unique expertise:
“Often presenting with “happy hypoxia” which is a clinical (i.e. observational) diagnosis not a defined mathematical one. In my career diagnosing and treating causes of acute respiratory failure/hypoxia, most patients with severe hypoxia evidence visibly obvious increased work of breathing”
Kory reports on ‘blood issues’:
“Lots of deep venous thromboses and pulmonary emboli on admission or soon after admission.”
We found little evidence of this reported in other papers; again, Kory’s report is based on personal evidence. (To his credit, he cites one of his own papers covering the symptoms from ten patients. However, his paper starts with the conclusion that covid-19 was the culprit, based on a positive PCR test result. Since no results from tests for other pathogens were reported so the paper is of little value in this debate).
Kory also refers to factors related to transmission, none of which appear in any of his papers or in any other academic papers. For example:
“illness beginning after a holiday party where a number of others also subsequently fell ill,…”
“obvious contagiousness as per history etc…”
“High transmissibility with clear evidence of aerosol spread - I have never seen a disease which spread so rapidly and widely, with numerous super-spreader events, well described in the media and the CDC.”
“The contagiousness within families and after group events despite social distancing and masks were consistent and reproducible (even my own household saw such spreads, multiple times)”
In our view, such statements are mere supposition and speculation. Surely, if we have a novel disease and risk-additive pathogen, these suspicions should be carefully documented and subject to scientific scrutiny. Instead, they are taken as givens. How would we know it wasn’t another respiratory ILI (influenza like illness)?
We are surprised that a clinician, whose expertise, and reputation is being challenged, would rely on personal experience of life at home to back up a theory of transmissibility4.
Note that Kory and other frontline physicians can diagnose covid-19, yet we are cautioned to be aware that there are different evolving levels of severity of covid-19:
“In terms of how deadly it was, this also gets complicated because the disease changed over the past few years.”
Despite this temporal change in what covid-19 symptoms are, Kory claims :
“the “pattern” of presentation of Covid was unique and easily discernible and distinct from other viral syndromes to a seasoned clinician.”
How can these contradictory statements be reconciled?
Kory tells us why it was not bacterial pneumonia:
“Why was it not bacterial pneumonia? Well, from the features above, bacterial pneumonias are not associated with OP, are generally unilateral (the vast majority of Covid was bilateral), most often consolidative rather than with ground glass.”
Again, he offers no evidential support for this claim, which is perhaps not surprising given we documented substantial evidence from many scientific papers that completely contradict his statement.
On bacterial pneumonia he says:
“….bacterial pneumonias are random, relatively rare events in most people’s lives, and instead mostly tend to affect the elderly”
We reject this assertion because it is well known that bacterial pneumonias are not random and are common in the elderly, the very cohort most affected by covid-19.
Likewise, Kory also rejects bacterial pneumonia because:
“Also, outside of TB, bacterial pneumonias do not exhibit human to human transmission so cannot explain all the transmission and dying unless someone was to argue that widespread immunosuppression developed making most of the population uniquely susceptible to bacterial pneumonia in their environment all of a sudden.”
How would he reliably know about transmission at the point of diagnosis? It can merely be presumptive. We, and others, have covered explanations for this in the form of community-acquired bacterial pneumonia, caused by antibiotics being withdrawn, and the elevated rate of ventilator-associated pneumonias in vented patients misdiagnosed as covid-195. We made no arguments about widespread spontaneous immunosuppression in our article.
Turning to the young and healthy he says:
“In the young and healthy, they are very rare events. I had too many young and healthy (relatively) on vents suddenly - why/how would a bacterial pneumonia suddenly do this unless it was a new superbug”
We did not argue that young healthy people were presenting with bacterial pneumonia. We argued that the young and healthy people whose symptoms best matched those that Kory thinks are uniquely diagnostic of covid-19 are consistent with those reported for younger people who have been injured by illicit vapes (containing fungicides and pesticides inter alia). Yet, despite this close match, Kory says this about vapes:
“Vaping can be ruled out by history-taking. The vast majority of patients were not vapers. Smokers and vapers make up less than 20% of the population. This syndrome spared no segment of the population, and I am unaware of data showing a massive increase in the sales of vapes at that time.”
This is a crude misrepresentation of our argument. We presented numerous papers supporting the possibility that vaping-associated lung injury (VALI) and covid-19 have coincident pathology, as reported by Kory himself.
By way of a conclusion, Kory says that there is new mystery virus whose transmission characteristics are unknown, and which is sometimes deadly in one place but sometimes not in others:
“….there are still things we don’t know about how and why the virus spread the way it did and why it behaved so deadly in some spots at certain times and not others. One possible clue might be this paper finding that all variants were created in a lab.”
And Kory wants us to believe that despite this almost unbounded level of complexity and variety he, and others, can reliably diagnose “it”.
In finishing his article Kory says:
“That’s all I got. I am not sure if I “squared the circle” in terms of making coherent sense of all the data and viewpoints and I think that is because there are still things we don’t know about how and why the virus spread the way it did and why it behaved so deadly in some spots at certain times and not others. One possible clue might be this paper finding that all? variants were created in a lab. Their concluding sentence: “The analysis showed that Omicron variants were formed by an entirely new mechanism that cannot be explained by previous biology and knowing how the SARS-CoV-2 variants were formed prompts a reconsideration of the SARS-CoV-2 pandemic.”
This suggests Kory had a strong prior presumptive belief that a novel deadly pathogen was circulating (a bioweapon?) and that a positive test for this pathogen confirmed this as a fact, and it was this sole explanation, to the exclusion of all others, that accounted for the symptoms experienced by patients in his care. We believe confirmation bias of this kind was not restricted to Kory and was shared throughout the medical profession.
Kory makes clear that diagnosis of complex diseases is notoriously difficult. We agree.
There are well established methods for performing diagnoses that provide a framework to minimise errors in diagnosis and to, conversely, maximise the likelihood that the diagnosis made is the correct one. These methods are routinely taught to doctors at all levels. One such method is called differential diagnosis, which involves a process of elimination.
The Cleveland clinic define differential diagnosis this way:
Your healthcare provider will compile a differential diagnosis, which is a list of conditions that share the same symptoms to help make a final diagnosis. The differential diagnosis will direct your healthcare provider to offer tests to rule out conditions and lead them to find the cause of your symptoms.
……they will begin a process to diagnose your condition. Since there are a lot of different conditions that often share similar symptoms, your provider will create a differential diagnosis, which is a list of possible conditions that could cause your symptoms. A differential diagnosis is not your official diagnosis, but a step before determining what could cause your symptoms.
The character called ‘House’ in the very popular TV medical drama of the same name applies this method:
House often clashes with his fellow physicians, including his own diagnostic team, because many of his hypotheses about patients' illnesses are based on subtle or controversial insights.
As a drama it is written to entertain but it is based on what a doctor actually (should) do.
Clearly a doctor should rule out the simplest or most common explanations before considering the most novel or complex. Hence, covid-19 should have been considered at the end of the diagnostic process, after already well understood conditions had been eliminated, and not at the start.
Despite being portrayed as a real-life Dr House, Kory’s response to us does not suggest he followed this method. He fails to refer to a list of possible alternative or competing diagnoses. Likewise, Kory does not show how these have been ‘whittled down’ using differential diagnosis. As a result, the competing conditions, that by necessity, must be considered during the process of arriving at a conclusive diagnosis are completely hidden from view: what we see is the conclusion only.
Unfortunately, this flaw is repeated in virtually all of the papers reporting symptoms of covid-19 and shows how vulnerable medicine is to epistemic capture.
To summarise, Kory’s response exhibits the following features:
A complete failure to address the contradictory evidence presented in the medical literature.
The doubling down and repetition of his opinions as if this is an argument in and of itself.
An insistence on a mysterious transmission mechanism as verification of spikeopathy.
An admission that covid varies in symptoms and severity by time and location, yet despite this it remains reliably diagnosable.
A quite causal and contradictory rejection of bacterial pneumonia as a cause of death, despite this being a leading cause of death in the elderly for time immemorial.
Misrepresentation of opposing views, quite carelessly in the case of vaping injury as a possible cause of some injuries and deaths attributed to covid-19.
A reliance on engaging homilies and stories of patients and people personally known to him as though this constitutes systematised scientific evidence.
Failure to transparently report the steps required by a differential diagnostic process.
Confirmation bias caused by a strong prior presumptive belief that a novel deadly pathogen was circulating and that a positive test for this pathogen confirmed this, and this was the only possible explanation for the symptoms experienced by patients in his care.
In conclusion we find nothing in Kory’s academic publications, articles, stories, testimonies, and other written comments to date that challenges our hypothesis that a novel deadly respiratory virus spreading from person to person is not responsible for what doctors observed in the spring of 2020.
Post publication addendum
This paper, by Fryman and Mayo in 2020 is a very nice illustration of the problem of associating observed symptoms with a positive covid test and neatly sums up how the actual cause of symptoms might be obscured by the test result or the intervention.
The case is summarised thus:
A 52-year-old man sought treatment for nonproductive cough, fever, and worsening shortness of breath. On admission, he was in respiratory distress with oxygen saturation at 73% on room air. The patient was admitted with coronavirus disease 2019 (COVID-19) pneumonia, which was confirmed by PCR antigen testing. Four days after admission, the patient required endotracheal intubation for progressive hypoxemic and hypercapneic respiratory failure.
On day 10 of medical ICU (MICU) care, the patient developed right anterior chest wall and neck subcutaneous emphysema with severe oxygen desaturation and hypotension requiring escalating doses of vasopressors. Concurrent with these events, the patient developed severe abdominal distention with a bladder pressure of 25 mm Hg.
The abdominal ultrasound findings are consistent with the presence of a large pneumoperitoneum (free air). The absence of gut sliding and the inability to visualize any underlying structures within the abdomen suggest that free air is interposed between the ultrasound probe and the peritoneal space. Given the patient’s shock state, elevation of plateau pressure, and intraabdominal hypertension, the MICU team established a diagnosis of abdominal compartment syndrome. This was managed by insertion of an ultrasound-guided catheter into the air-filled peritoneal space.
We asked an independent radiologist for their view of this case, and they said:
before 2020, this is a person that had ARDS and suffered a complication of too forceful/prolonged intubation.
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In his response Kory recounts a tale of a patient who had classic covid symptoms and who had a repeated negative covid test. He was adjudged to be a covid patient and treated as such.
Moreover, Kory admitted in the WhatsApp conversation that, as he had to accept that “it” was spreading in most places for months before the emergency was declared without causing unusual illness clusters or excess deaths, “something” must have suddenly changed in March 2020 to cause this new clinical syndrome, and he was unsure what it was. Yet now, apparently, he is.
The single citation he does provide in his response is to Claire Craig’s book “Expired”, but again this tells us something is spreading – there may be no doubt a respiratory virus is spreading at that time of year, but the question might be which ones, and does the particular one matter?