1) AN UNEXPECTED, YET FASCINATING TURN
THE SPIKE PROTEIN, THROUGH HEPCIDIN MIMICRY, INDUCES IRON OVERLOAD AND MITOCHONDRIAL PROTON/ELECTRON LEAK: THE OBSERVED “RADIATION POISONING” IS THIS PROTON/ELECTRON LEAK: CACHEXIA, AGING, ENDOTHELIAL AND CARDIOVASCULAR COVID PATHOLOGIES
2) EXPLAINED
Hepcidin: The Dark Crystal
Hepcidin, a small polypeptide synthesized and secreted by the liver, is considered a master regulator of body iron homeostasis. The physiological function of hepcidin is to decrease circulating iron levels through down-regulation of FPN1 in
3) macrophages. The action of hepcidin is tissue-specific: in enterocytes, hepcidin does not change FPN1 levels but decreases DMT1 expression. Hepcidin-induced FPN1 degradation is transient reaching a maximal effect at 2–6 h, with FPN1 levels returning to control values at 24.
4) Hepcidin synthesis is stimulated by increased plasma iron levels and by inflammatory cytokines under conditions of infection by pathogens.
Recent studies show that hepcidin is also expressed in the central nervous system (CNS) and that its expression increases in response to
5) systemic administration of LPS (Wang et al. 2008). Hepcidin may provide a link between inflammation and iron accumulation in the CNS. Early studies showed increased activation of NF-κB and secretion of proinflammatory cytokines in microglia cultured with excess iron, and that
6) toxic concentrations of IFN-γ and TNF-α are lower in iron-loaded oligodendrocytes. These data suggest that iron accumulation enhances the toxic effects of inflammatory cytokines. Which are the sequence of events leading to neurodegeneration, inflammation, or iron accumulation
7) remains an open question. Stereotaxic injections of LPS in the striatum increase microglia activation, ferritin expression, and total nigral iron content in aged rats, an indication that inflammation drives iron accumulation. Nevertheless, cellular inflammation is not
8) necessarily dependent on iron deposition as demonstrated by microglia activation without iron accumulation in an animal model of multiple sclerosis. Recently, it was shown that TNF-α and TGF-β1 induce opposite changes in the expression of DMT1, FPN1, and ceruloplasmin in
9) astrocytes and microglia. TNF-α treatment results in increased iron retention by both astrocytes and microglia; in contrast, the anti-inflammatory, anti-apoptotic cytokine TGF-β1 causes iron retention in microglia but promotes iron efflux from astrocytes.
A secondary preamble:
10) TLRs
Several reports indicate that TLRs regulate mitochondrial activity. Activation of TLR3 results in reduction of mitochondrial oxygen consumption mediated by opening of the permeability transition pore. In co-cultures of cortical neurons with microglial cells, the TLR4
11) agonist LPS promotes decreased oxygen consumption and oxidative stress, with the subsequent nigral dopaminergic neuronal death in a rat model of inflammation. Although these studies strongly suggest a link between TLRs and mitochondria dysfunction, further studies should
12) clarify the molecular mechanisms involved and its relevance to particular neurodegenerative processes.
The absence of Hepcidin magnifies pathological effects
inhibition of mitochondrial complex I by endogenous and/or exogenous toxins or by inflammatory processes resulting
13) from trauma or other causes, engage a vicious cycle of increased oxidative stress and increased iron accumulation. In this scheme, inhibition of mitochondrial complex I by endogenous or exogenous toxins, or because of mutations in PD genes Parkin, Pink 1, alpha-synuclein,
14) DJ-1 or LRRK2, results in decreased electron transport chain activity and the ensuing ATP synthesis decrease and ROS increase.
However, ionizing radiation causes a transient increase in Reactive Oxygen Species (ROS), from the reduction of oxygen to form •O2− and H2O2, and
15) in RNS, derived from NO. Ward et al noted that low-dose, low-linear energy transfer (LET) radiation produces primary ionization events (electron tracks) and secondary reactive products that are INSIGNIFICANT COMPARED with those produced by ENDOGENOUS ROS (likely from
16) mitochondria — “mtROS”).
What must be emphasized here is the time frame and scale of the damage. It occurs in 0-3 minutes up to 12 hours, additionally, some can be chronic. Please see referenced table image.
Endothelial activation and inflammation is induced by this proton
17) leak. 1) The majority of mtROS are generated in the complexes I and III of electron transport chain (ETC); 2) Inducible proton leak and mtROS production are mutually regulated; 3) ATP synthase-uncoupled ETC activity and mtROS regulate both physiologica006C and pathological
18) endothelial cell activation and inflammation initiation; 4) Mitochondrial Ca2+ uniporter and exchanger proteins have an impact on proton leak and mtROS generation; 5) MtROS connect signaling pathways between conditional DAMP-regulated immunometabolism and histone
19) post-translational modifications (PTM) and gene expression. This explains the previously observed deleterious histone access.
So, why did I begin the thread referencing Radiation Poisoning? Because, in essence, it is the “espresso” of COVID. It is all VERY fast. This is why
20) studies MUST be done within minutes and hours of spike protein therapies. Also, continuously during COVID disease.
Transient generation of reactive oxygen or nitrogen (ROS/RNS), detected with dihydrodichlorofluoroscein by fluorescence microscopy, occurs within minutes of
21) exposing cells to ionizing radiation.
With regards to this radiation-like induced pathology: Metformin Protects against Radiation-Induced Acute Effects by Limiting Senescence of Bronchial-Epithelial Cells. And those with Down Syndrome are already predisposed to this
22) mitochondrial ATP deficiency.
All it takes is that sudden exposure, to open Pandora’s Box. I leave you with the words of Paul Simon:
"Fools", said I, "You do not know
Silence like a cancer grows.”
ncbi.nlm.nih.gov/labs/pmc/artic…
onlinelibrary.wiley.com/doi/10.1111/jn…
frontiersin.org/articles/10.33…

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More from @Parsifaler

15 Oct
1) UNDETECTABLE SPREAD?
THE SPIKE PROTEIN OF SARS-CoV-2: AN INTRACELLULAR MOONLIGHTING PROTEIN THAT DOES NOT REPLICATE BUT TRAVELS INCOGNITO VIA TROGOCYTOSIS, CELL TO CELL, WITH SIMILAR, THOUGH DELAYED, “VIRAL” EFFECT
Viruses replicate within cells to then burst forth from those ImageImage
2) cells to go on to infect other cells and repeat the process. This is how they “live.” However, viruses are also extremely good at delivering therapeutics. In fact, many vaccines are delivered on the backs of viruses. Think of some of the vaccines currently in use. Image
3) The Adenovirus, for example, is a very good virus for delivering a therapeutic.
So, let’s say we have a therapeutic that targets something within a cell. Let’s say it does something particularly nasty, like a piston preset on a modern pipe organ that turns on and off all the
Read 14 tweets
13 Oct
1) THE SPIKE PROTEIN: A PHARMACOLOGICAL “THERAPEUTIC” INTENDED TO INDUCE FATAL SYSTEMIC IRON DEPOSITION: DYSMETABOLIC HYPERFERRTINEMIA
First, please think about all we have read concerning COVID and its sequelae. Now please read this: Iron overload, irrespective of the underlying
2) etiology, has varying manifestations, depending on the organs affected by the excessive iron deposit. It may present as fatigue, skin color changes, abdominal pain, joint pain, irregular menstruation, infertility, impotence, irregular heart rhythm, heart failure, new-onset
3) diabetes or difficulty controlling established diabetes and elevation in liver enzymes.
And what of Hypoxia? Pathological? Certainly. Also, a possible adverse effect of a drug intended to induce fatal systemic iron deposition. While we have been scratching our heads trying to
Read 17 tweets
13 Oct
1) COVID AND TRANSFERRIN: UNITING IRON OVERLOAD, COAGULOPATHY, AGING, SENESCENCE, AND SHORTENED TELOMERES
A paper from May 2021 out of Wuhan noted that a previous study in Austria found that ferritin and transferrin were both associated with the risk for ICU admission in COVID-19
2) patients, and no significant relations were found in iron and other indices. This study indicated the relation between iron metabolism and the undesirable outcome of COVID-19, whereas the association with specific comorbidities warrants further investigation. In our study, we
3) found high serum iron level was associated with disease severity in COVID-19 patients.
Transferrin is a protein that binds iron and transports it throughout the body. It is the main iron carrier in the blood. Transferrin levels normally increase with iron deficiency. When iron
Read 12 tweets
12 Oct
1) LONG COVID AS A DISEASE OF (ACUTE?) IRON OVERLOAD
I will explore various aspects of Long COVID in the context of iron overload disease. We will now discuss iron overload and the weakness/exercise intolerance/weight loss/cachexia occurring in Long COVID.
Previously healthy mice
2) were injected with iron. The results are remarkably similar to what happens in Long COVID. If the body has too much iron, it upregulates Ferritin. Therefore, high ferritin in the ABSENCE of high serum iron may indicate that the muscles and organs are already overloaded.
Please
3) reference the graphic showing the ferritin levels of the mice injected with iron vs control.
How does this present clinically? Fatigue, exercise intolerance and muscle atrophy, which presents as weight loss. Please reference the graphic showing weight loss of the iron injected
Read 6 tweets
12 Oct
What if the spike protein, through its mimcry of Hepcidin and affinity for ACE2 receptors, caused such a massive efflux of iron into the bloodstream, that it mimicked an "iron injection?"

There is such a drug! Iron Dextran Injection.

What can happen?

Iron dextran injection may
cause severe or life-threatening reactions while you receive the medication. You will receive this medication in a medical facility and your doctor will watch you carefully during each dose of iron dextran injection. Tell your doctor if you experience any of the following
symptoms during or after your injection: shortness of breath; difficulty swallowing or breathing; wheezing; hoarseness; swelling of the face, throat, tongue, lips, or eyes; hives; itching; rash; fainting; lightheadedness; dizziness; bluish discoloration of the skin, lips,
Read 5 tweets
11 Oct
1) DELAYED SELF-POISONING (OR A QUICK DEATH VIA MACROPHAGE ACTIVATION SYNDROME)
THE SPIKE PROTEIN OF SARS-CoV-2 IS AN ENGINEERED BIOWEAPON DESIGNED TO CREATE MASSIVE, ALMOST CERTAINLY LETHAL (DELAYED, AS IS THE CASE WITH EXTREME IRON OVERLOAD) IRON EFFLUX FROM MACROPHAGES AND
2) RBCs. THE OBSERVED HYPOXIA IS PART OF THIS “PLAN.” THE BODY RELEASES YET MORE IRON UNDER HYPOXIC CONDITIONS: THE PARACRINE PARALLEL TO RADIATION POISONING.
A fascinating article appeared on ideas.ted.com in December of 2015. The chemist Rebecca Abergel realized the
3) way to cure people of radiation poisoning was to remove it from the body, as it spreads in a PARACRINE fashion.
At high doses, radiation blasts through tissues, ruptures DNA strands and alters the rhythms of cell division. Disrupted cells cause nausea, diarrhea and fever,
Read 11 tweets

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