The incidence of myocarditis and pericarditis in unvaccinated Covid patients

Also quoting literally the first sentence of the abstract:

> The current report presents the case of a 76-year-old man with Parkinson’s disease (PD) who died three weeks after receiving his third COVID-19 vaccination.

If I had a nickel for every confounding variable implied by either "76-year-old" or "Parkinson's disease" (let alone both, let alone for a sample size of 1), the Powerball jackpot would look like pocket change.

> Do you believe they have all the data needed to make that a final conclusion?

There is no "final conclusion". There will always be more data. So far the data have rather strongly indicated greater benefit than harm, even among the reports asserting correlations between vaccines and adverse reactions, so it doesn't seem very surprising to see consensus on that among medical experts.

The consensus ain't always right, to be clear. Maybe the small minority of experts asserting more harm than good are onto something. The body of data supporting such assertions is far more lacking, so I wouldn't bet on it.

> Or are most of those medical professionals simply following certain leaders and descission makers?

It's usually the other way around: the "certain leaders and decisionmakers" in the pro-vaccination camp largely lead/decide based on how experts are informing them - and there's certainly no shortage of said experts.

It's a fair bit more varied in the anti-vaccination camp; some such leaders/decisionmakers do defer to experts (and it's simply a case of their pool of experts being in the anti-vaccination camp), but it seems like most instead assume they know better than the experts; they tend to be the sorts of folks who already reject scientific methodology for various reasons, and thus are not inclined to defer to experts informed by said methodology.

> That's not how it works.

That's exactly how it works.

> There is a clear casual relationship between certain COVID-19 vaccines and myocarditis.

No, there is not. Yet again: correlation does not equal causation. If you know of a study that actually asserts causation (and not just correlation), link it.

> For example, there has never been a study which proves that smoking causes lung cancer.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3749017/

Unlike either of the studies you linked, this one goes at great lengths to describe the myriad identified confounding variables (for which they can then be controlled) in the correlation between smoking and lung cancer, the exact mechanisms by which tobacco smoke causes lung cancer (and the exact carcinogens present in tobacco smoke), even the exact mutations in tumor-suppressing genes like p53. The studies linking mRNA vaccines to myocarditis don't come anywhere close to that level of examination.

Similar deal with this one: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9603183/

Consequently:

> But the correlation established through observational studies is so strong that causality is clear.

And that is very unlike the situation with vaccines and myocarditis, wherein the correlation is nowhere near as strong and for which the causality is nowhere near as clear. That vast difference is why - unlike either of the articles you cited - the myriad articles on the relationship between smoking and lung cancer are able to assert causation, and indeed do so.

Until that changes, it is deeply irresponsible to prematurely declare the relationship between vaccines and myocarditis to be in any way "causal". It's a "maybe" at best.

----

Speaking of smoking and its deleterious effects: https://pubmed.ncbi.nlm.nih.gov/20555426/

And gender variance in high school student tobacco use - including of smoking tobacco - does exist: https://www.cdc.gov/tobacco/data_statistics/fact_sheets/yout...

How many uncontrolled-for confounding variables do I need to pull up before you're willing to admit how utterly irresponsible it is to declare from on high that the link between mRNA vaccines and myocarditis in young males is "causal"?

I already had, and my point still stands. It makes no effort to control for said confounding variables. It's heavily reliant on family members' subjective evaluations of health deterioration (i.e. it makes no effort to differentiate between "the patient's health started to decline immediately after the second dose" v. "the patient's health had already started declining but family members only noticed it after the second dose"). Hell, it doesn't even specify whether the cardiac events actually happened after or before the first dose; it just says it was on the "same day", which would be a pretty quick onset of symptoms.

And that's just on the timeline of events. The autopsy itself only demonstrates the presence of spike proteins in the affected tissue; it does not demonstrate said presence to have caused the tissue to be affected, and it's just as likely that something else caused the inflammation (like, you know, the myriad health issues typical of elderly men) and kept the spike proteins around.

Glaringly, the immunohistochemical portion of the autopsy seems to focus solely on SARS-CoV-2, and from that combined with ANE not normally being associated with PD concludes that the ANE has some relation to the presence of SARS-CoV-2 spike proteins. Such an analysis entirely ignores that ANE's causes are already known to include many other viruses, not just SARS-CoV-2. Did he test for influenza A? Influenza B? Herpes virus 6? What about genetic factors?

Similar deal for myocarditis. Other viruses can cause it, like influenza (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7793451/). That the article is silent on that possibility is a rather glaring flaw in its analysis.

Variable after variable after variable after variable after variable, all entirely uncontrolled for, and I'm supposed to be convinced that this demonstrates a causal relationship?

> How do you “control”, when it’s a (high quality) report of a single autopsy?

By testing for and ruling out the myriad causes of myocarditis and ANE with already-established causal links, as I described above.

> The idea would be to encourage other autopsies which look for similar pathology.

And if those other autopsies fail to even so much as mention other more-well-known causes of myocarditis and ANE (let alone make any effort to rule out said causes), then they, too, will consequently fail to demonstrate causation.

> The foreign mRNA was supposed to stay at the injection site in the upper arm.

Okay, and it's good to know that it doesn't. That still doesn't do anything to establish a causal relationship between spike protein production and tissue damage.