COVID has unleashed a pandemic of inappropriate use of the RCT/meta-analysis model as an instrument of hyper-scepticism to manufacture doubt as a tool of destructive mass propaganda. 🧵
Let's use the Cochrane model to assess the evidence for the earth being round. Here are some common proofs for the earth being round. All belong to the lowest level of evidence. How can you say we can safely traverse the oceans without falling off the edge of the earth?
To demand that the RCT/meta-analysis model be applied to non-pharmacological settings or in engineered safety systems where they've never been a Gold Standard, is to weaponize it as an instrument of manufacturing doubt. You could question whether the earth is round by this method
You could even use this model to cast doubt on anthropogenic climate change. Look at a climate change journal like @naturesustainab, and you won't see a single RCT being published to demonstrate climate change from rising CO2 levels. nature.com/natsustain/
This is the result of searching the Cochrane Library for “climate change” to see if mitigating rising CO2 levels would make a positive impact on health. The RCT/meta-analysis model is useless in tackling what will be a crucial determinant of health outcomes in the near future.
You can see why I call fetishisation of RCTs as a Gold Standard for all of science, “RCT idiocy”. The methods used in parts of the medical sciences aren't a universal scientific standard. You can't cast doubt on everything by decrying a lack of RCTs.
It's astounding that people take to Twitter to argue that lockdowns and respirators need RCTs, using social media as a medical communication apparatus without its safety/efficacy having been proven by an RCT, writing on devices never tested by RCT.
The problem is not whether science should be evidence-based but as in court what is admissible in the court of scientific arbitration as “evidence”. Through most of science, RCTs have a profoundly limited spectrum of applicability. #PhilosophyofScience
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I agree wholeheartedly with the criticism of the way the Conly Cochrane meta-analysis dismissive of masks has been conducted. But—sorry, team—I need to add some wee quibbles from a philosophy of science perspective. 🧵theconversation.com/yes-masks-redu…
The biggest shortcoming of RCTs of respirators is this: where direct mechanistic evidence retains predictive validity, this is the preferred form of scientific evidence. The invalidity of direct mechanistic modelling needs to be proven before falling back on RCTs.
Look at the key occupational PPE worn by this soldier: tactical respirator, helmet, body armour. None are tested by RCT. Some non-clinicians sitting in an office demand RCTs before the *same gear* can be issued to HCW before going into battle against COVID.
Who wins the award for my dumbest professorial reply of 2022? 🥁 Semmelweis used “non-pharmacological” (sic) principles with calculations based on applied physics and engineering to recommend handwashing with chlorinated lime—calcium hypochlorite Ca(OCl)2 aricjournal.biomedcentral.com/articles/10.11…
Yes, ladies and gentlemen, handwashing is a mechanically engineered protective intervention like seatbelts, bulletproof vests, helmets, parachutes, and respirators. Semmelweis was an engineer. You read that correctly! 🤡
If you really want to believe that the topical application of a corrosive chemical, 4% calcium hypochlorite, to the hands is a “non-pharmacological” mechanistic intervention based on applied physics and engineering, here is more info on caustic lime. en.wikipedia.org/wiki/Calcium_h…
1. Acute COVID led to maximal levels of P-selectin dependent platelet-neutrophil aggregation. There was reduced phosphatidylserine exposure and integrin αIIbβ3 activation. It means less primary aggregation and more leukocyte-mediated thromboinflammatory signalling. @JTHjournal
2. #Microclots are typically positive on staining for P-selectin (also known as CD62P). Selective activation of platelet P-selectin may be a feature of acute COVID. Whether the same feature is found in #longCOVID remains unconfirmed. #TeamClots
3. P-selectin binds to PSGL-1 (P-selectin glycoprotein ligand). It is found on leukocytes eg neutrophils, macrophages and T-cells. PSGL-1 is a mediator of immunothrombosis. In chronic viral infection, PSGL-1 promotes T-cell exhaustion. @fitterhappierAJcell.com/trends/immunol…
It's true that masks do not protect you from airborne illnesses. A mask, surgical or woven, scores a Fit Factor of ~5 of the 100 points needed for an N95 to pass a fit test. There is too much leakage to protect the wearer from airborne inhalation. Wear respirators, not masks.🧵
Does this mean wearing a surgical mask is useless? No, because there is a ~2/3 reduction in aerosol dispersion on exhalation—as seen in this RIKEN modelling. It might not protect the wearer, but it acts as source control. If everyone wears one, it serves a public health function
Studies by RIKEN have shown that even a mouthguard can act as modest source control by reducing aerosol dispersion. Again, there is too much inward aerosol leakage for it to protect the wearer.
Could PolyP be a key player in COVID contact-pathway thromboinflammation-driven microthrombi? Some thoughts from an emerging area of molecular wizardry. 🧵 #LongCOVID#TeamClots#PolyP
There is evidence in COVID of immunothrombosis being driven through the kallikrein-kinin-contact pathway—we'll just call it the “contact system”. It feeds into the renin-angiotensin system (SARS-CoV-2 binds to ACE2). @JTHjournalonlinelibrary.wiley.com/doi/10.1111/jt…
The still mysterious contact system, once mistaken for a haemostatic pathway, is now regarded as an immunothrombosis pathway. It may yet hold some secrets to how #longCOVID leads to #microclots. frontiersin.org/articles/10.33…
As a clinician, I've seen young patients die of sepsis from atypical organisms with lymphopoenia weeks after acute COVID. I've seen deaths from TB and endocarditis. I've treated multidermatomal shingles. I routinely look out for post-COVID lymphopoenia 🧵nature.com/articles/s4159…
Our mortality and morbidity meetings are full of cases of young patients dying of sepsis shortly after a COVID infection. Irrespective of what the underlying mechanism is, post-COVID immunosuppression is a phenomenon readily observable to the clinician.
If not my patients, then friends spontaneously ask me why they get unrelenting non-COVID viral infections and UTIs etc they have never previously had soon after a COVID infection. Like other COVID-cautious people who have never had COVID, I do not experience this.