Cadegiani et al.: Catecholamines (dopamine etc.) are key triggers of mRNA COVID-19 vaccine-induced myocarditis & sudden deaths (Pfizer & Moderna) (as well as via virus): hypothesis supported by

epidemiological, anatomopathological, molecular and physiological findings; supports our thesis (McCullough's & embraced by myself) that the 'DIED SUDDENLY' & 'DYING AT DAWN' is COVID VACCINE induced

Are catecholamines in a "hypercatecholaminergic" state the key trigger of SARS-CoV-2 mRNA vaccine-induced myocarditis and related crippling outcomes? Are there similar risks post COVID-19 infection? Is the adrenaline (catecholamine) rush when under stress or exercise conditions (or rising at dawn) what triggers the cardiac arrest and death in a ‘silent myocarditis’ vaccine-induced scarred heart?

Simply put, if you have ‘silent’ undiagnosed COVID vaccine caused myocarditis, and you engage in activity or some activity that drives increased adrenaline (catecholamines such as dopamine, epinephrine etc.), the evidence indicates that this adrenaline (catecholamines) can stress/strain the heart that is already damaged/scarred by myocarditis. And this can cause the heart to behave abnormally and can lead to death. Thus why we have written about dying rising at dawn and on the field when there is a rush of adrenaline.

SOURCE:

‘The rationale and data that supported the hypothesis were as follows: SARS-CoV-2 mRNA vaccine-induced myocarditis primarily affected young males, while the risk was not observed following COVID-19 infection; independent autopsies or biopsies of patients who presented post-SARS-CoV-2 mRNA vaccine myocarditis in different geographical regions enabled the conclusion that a primary hypercatecholaminergic state was the key trigger of these events;

SARS-CoV-2 mRNA was densely present, and SARS-CoV-2 spike protein was progressively produced in adrenal medulla chromaffin cells, which are responsible for catecholamine production; the dihydroxyphenylalanine decarboxylase enzyme that converts dopamine into noradrenaline was overexpressed in the presence of SARS-CoV-2 mRNA, leading to enhanced noradrenaline activity;

catecholamine responses were physiologically higher in young adults and males than in other populations;

catecholamine responses and resting catecholamine production were higher in male athletes than in non-athletes;

catecholamine responses to stress and its sensitivity were enhanced in the presence of androgens; and catecholamine expressions in young male athletes were already high at baseline, were higher following vaccination, and were higher than those in non-vaccinated athletes.

The epidemiological, autopsy, molecular, and physiological findings unanimously and strongly suggest that a hypercatecholaminergic state is the critical trigger of the rare cases of myocarditis due to components from SARS-CoV-2, potentially increasing sudden deaths among elite male athletes.’