Abstract
There is no doubt that spike-inducing Covid-19 vaccines are associated with a complex and diverse range of side effects, which have significant health consequences for those affected. The known causes, primarily the activation of the renin-angiotensin-aldosterone system, as well as other induced and manipulated spike effects, are not sufficient enough to provide a plausible explanation for unusual clusters or the occurrence of rare side effects. This study aimed to investigate various adverse drug reactions that have not been observed, or have only rarely been observed, when using conventional vaccines. The analysis focused on the most extensive ’reaction groups’ following vaccination with the spike-inducing vaccines Tozinameran and Elasomeran: nervous system disorders, psychiatric disorders, musculoskeletal disorders, and general disorders. The data were retrieved from the EudraVigilance Web Reports and were interpreted based on an analysis of original research papers and review articles published in scientific journals. Among the most common adverse reactions from the aforementioned reaction groups were headaches (248,567 reports associated with Tozinameran, 90,948 reports following Elasomeran), fatigue (211,056 and 77,531 respectively), myalgia (156,735 and 62,034 respectively), asthenia (53,968 and 15,303 respectively), muscular weakness (10,882 and 3,328 respectively), anxiety/ fear (8,009 and 2,054 respectively), memory impairment/amnesia (6,475 and 2,132 respectively), depression/depressive mood (5,395 and 1,517 respectively), brain fog (3,685 and 992 respectively) and muscle twitching (3,605 and 908 respectively).
Recent findings suggest that further pathophysiological spike effects, which can significantly impair the body’s ability to maintain homeostasis, must be taken into account as possible causes. This involves an impairment of the cholinergic nervous system, which normally acts as a counter-regulatory mechanism, thereby promoting or exacerbating the undesirable activation of the renin-angiotensin-aldosterone system. Impairment of the cholinergic nervous system is caused by neurotoxin-like structures in the spike glycoprotein, which can trigger the inhibition of nicotinic-cholinergic receptors. Consequently, this can result in exacerbated inflammatory processes throughout the body, including the central nervous system. It may also result in activation of the sympathetic nervous system, thrombogenesis, pathological neuropsychiatric and musculoskeletal reactions, and an imbalance in the autonomic nervous system. Taken together, these factors may help to explain why there has been an increase in the incidence of adverse inflammatory and immunological reactions, cardiovascular reactions, coagulopathies, and neuropsychiatric and musculoskeletal disorders. However, in concrete terms, it depends on the organ-specific expression of counteracting regulators, on opposing regulatory effects, dose-dependent effects and time-dependent effects within the regulatory systems, as well as on comorbidities, age, gender, drug interactions and genetic predispositions.
Therapeutic intervention should be aimed at restoring and stabilising homeostasis. There are two main options for achieving this. Angiotensin receptor blockers are the preferred choice for inhibiting the renin-angiotensin-aldosterone system activation, specifically for counteracting the effects of the main effector, Angiotensin II. To activate and restore impaired cholinergic functions, particularly the cholinergic anti-inflammatory pathway, acetylcholine analogues, acetylcholinesterase inhibitors (e.g. donepezil and rivastigmine), and vagus nerve stimulation may be considered.