October 23, 2021
THE SPIKE PROTEIN: NEUROTRANSMITTERS (INCLUDING SEROTONIN), HISTAMINE AND MONOAMINE OXIDASE ENZYME BINDING
We now have an explanation for the AGGRESSION, TREMORS and excess HISTAMINE seen post-COVID and post Spike Protein Therapies. We also have an explanation for the “Cocaine-like” effects of the Spike Protein via its indirect pathological upregulation of Serotonin and other neurotransmitters.
The Spike Protein of SARS-CoV-2 has been found to bind to Monoamine Oxidase (MAO) Enzymes. These are the proteins that metabolizes NE, DA and Serotonin. In other words it creates an artificial EXCESS of these neurotransmitters.
These enzymes also happen to be MITOCHONDRIAL enzymes.
First, the Spike Protein has been shown to have strong affinity for these enzymes. A very recent paper demonstrated that the docking and molecular dynamic simulations performed show that the affinity of the spike protein from the wild type (WT) and the South African B.1.351 (SA) variant towards the MAO enzymes is COMPARABLE to that for its ACE2 receptor.
So, this binding to these receptors interferes with their normal function. Let’s say you needed a certain bolt to hold the oil in an engine, in a production line. But ANOTHER company steals all those bolts from you. The production line keeps on moving. However, those bolts are not being added, the engine will clearly fail.
This is what is happening in SARS-CoV-2 with respect to certain neurotransmitters. They are actually becoming OVERABUNDANT as they are not being cleared out.
As a side note, I find it “amusing” that the accepted term for these enzymes is MAO.
So, what do the effects look like when these neurotransmitters are allowed to accumulate unchecked?
The immediate effects of the MAO inhibitors appear to be psychostimulant-like, as they substitute for the discriminative stimulus effects of cocaine. MAO inhibitors also increase serotonin. MAOA is an X-linked gene encoding MAOA, a mitochondrial enzyme that metabolizes monoamine neurotransmitters including NE, DA and Serotonin.
New studies suggest that increased extracellular serotonin in the ventral pallidum (VP) and orbitofrontal cortex (OFC) also may contribute to reward and may underlie cognitive deficits observed in users of the drug.
It can also explain the aggression being seen post COVID and post Spike Protein Therapies.
Monoamine oxidase-A is an enzyme that degrades neurotransmitters, such as serotonin, dopamine, and norepinephrine.
Evidence from preclinical and clinical studies support an association between monoamine oxidase-A brain levels and aggression.
Monoamine oxidase-A is a treatment target in certain mood disorders and neurodegenerative illnesses.
Monoamine oxidase-A levels have been shown to be lower in individuals with antisocial personality disorder.
Also, Serotonin Syndrome (excess Serotonin) is a factor in COVID-19. I reference two cases in the links that follow which resemble serotonin syndrome in COVID-19, but without identifiable inciting medications. There are many more in the literature.
Histamine is also a monoamine, which would not be degraded due to the downregulation of MAO. Monoamine Oxidase (MAO) is an enzyme that breaks down N-methylhistamine to N-methylimidazole acetic acid. SNPs in the gene that encodes for this enzyme can cause histamine levels to stay high rather than be degraded.
The other important findings is that MAO deficiency also causes cognitive impairment and kinetic tremors, at long last explaining the tremors in those post Spike Protein Therapies.
Once again. Please pause all Spike Protein Therapies until these pathologies can be addressed and assessed.
Histamine receptors and COVID-19
Relationship between COVID‐19 infection and neurodegeneration: Computational insight into interactions between the SARS‐CoV‐2 spike protein and the monoamine oxidase enzymes
Monoamine oxidase A deficiency
Disruption of Serotonin Contributes to Cocaine’s Effects
Effects of Monoamine Oxidase Inhibitors on Cocaine Discrimination in Rats
The Genetics Of Histamine Intolerance
Unprovoked serotonin syndrome-like presentation of SARS-CoV-2 infection: A small case series