Covid long prevention
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Covid long prevention
Kea ideas- Iodine supports the immune system and has immune-modulatory effects.
- Iodine is well established as a broad-spectrum antimicrobial agent against bacterial, viral, fungal, and protozoan pathogens.
- Targeting and blocking ACE2 receptors at the surface of the cell prevent SARS-CoV from infecting this cell.
- There may be a U-shaped effect when taking HD D3 supplement. Note the supposition.
- Vitamin K as a support for the integrity of membranes and platelet aggregation. Vitamin K status was reduced in patients with COVID-19 and related to poor prognosis.
- Vitamin E is 100-fold more potent than usual anti-viral pro-drug advised.
- Targeting minimum 35 ng/ml vitamin D3 as prevention middle.
*) Excerpt 1: Respiratory Infections
Iodine is well established as a broad-spectrum antimicrobial agent against bacterial, viral, fungal, and protozoan pathogens and has been used as an antiseptic for the prevention of wound infections for several decades. A 2021 article in the Ear, Nose & Throat Journal published an in vitro study by Pelletier et al. establishing that nasal and oral povidone-iodine (PVP-1) solutions are effective in inactivating SARS-CoV-2 at various concentrations after a 60-second exposure. They concluded that the tested formulations could help reduce SARS-CoV-2 transmission if used for nasal, oral, or surface decontamination in confirmed or suspected cases of COVID-19 (3). (…)
3. https://www.zrtlab.com/blog/archive/curious-about-iodine-part-3-antioxidant-immune-support-anti-cancer/#B8
To be continued on my forum (in French, translator needed, but with English references). Read it later, to be coherent and to spare energy
*) Excerpt 2: Quitting smoking will be protective.
Exposing the cells to smoke increased ACE2 by 42% by smokers.
From a talk between Chris Masterjohn & Ray Peat. ACE receptors seen by Ray Peat (mail from Chris Masterjohn)
Excerpt, from CM mail:
Since ACE2 is the entryway for SARS-CoV-2, it is the overwhelming determinant of infection, after exposure. As discussed in the new paper, this is supported by several lines of evidence:
• Blocking ACE2 with specific antibodies prevents SARS-CoV from infecting a cell.
• Cells that do not express ACE2 cannot be infected. However, experimentally inserting ACE2 into these cells allows them to be infected.
The amount of ACE2 on the cell surface will determine the number of viruses that can get into cells, and thus the rate at which the infection progresses, especially before the immune system starts to get it under control. Since viral load is a major determinant of the illness, more ACE2 will generally mean a more severe disease.
https://www.biorxiv.org/content/10.1101/2020.03.28.013672v1 (new paper link)*) Excerpt 3: Losatran blocks the effects of ACE1 at its 'receptor'
ACE1 produces angiotensin, ACE2 inactivates the effects of ACE1 by breaking down angiotensin. The virus binds to the ACE2 and enters the cell through the Angiotensin 1 receptor. When the virus binds to the enzyme, it blocks ACE2's ability to deactivate angiotensin, so that ACE1 runs rampant producing angiotensin, and that matches with the effects we see in hospitalized patients.
Background (citing Chris Masterjohn).
ACE2 is an enzyme whose normal role in our physiology is to lower our blood pressure, and to prevent damage to tissues from fibrosis (laying down of scar tissue) and excess proliferation (cells reproducing at too high a rate, as occurs in tumors, for example).
SARS-CoV-2, the coronavirus that causes COVID-19, hijacks ACE2 on the cell surface in order to gain entry into the cell. All viruses must enter the cells of their host in order to hijack their protein-producing machinery, which they must do in order to replicate. No cell entry, no infection.
https://pubmed.ncbi.nlm.nih.gov/15165741/ (normal role link) (=> 2 x 50 mg Losartan).Excerpt 4: U-form effect of vitamin D supplement
RealNeat, PhDr, speaking: “Since the SARS-CoV-1 virus has a gateway via ACE-2 (it binds to this ACE-2 receptor), it may be inappropriate in some cases (when already contaminated, note’s editor) to try to substantially increase vitamin D3 intake at all costs. D3 stimulates the production of ACE-2.
However, we know that vitamin D deficiency impairs cellular resistance (microbial peptides). Therefore, there may be a U-shaped effect. Too little vitamin D weakens people (immunity decreases). Excessive supplementation (> 2,000 IU) could have a counterproductive effect”.
End of RealNeat intervention
Chris Masterjohn estimates that a reasonable upper limit, based on what is likely needed to maintain 30 ng/mL (75 nmol/L) for most people, would be 1700 IU per day of vitamin D3.Excerpt 4: Vitamin K as a support for the integrity of membranes and platelet aggregation
Coronavirus disease 2019 (COVID-19) is caused by severe acute respiratory syndrome, though most of the patients have mild symptoms.
Severe extrahepatic vitamin K insufficiency has been demonstrated in Covid-19 patients by a significant proportion of patients suffering from a poor status in vitamin K. Optimizing vitamin K status is thus potentially a modifiable risk factor in corona disease if we want to maintain / activate matrix Gla protein (MGP) which protects against pulmonary and vascular elastic fiber damage.
Vitamin K metabolism can be seen as the potential missing link between lung damage and thromboembolism in Coronavirus disease 2019.
Sources and References
*) Reduced Vitamin K Status as A Potentially Modifiable Prognostic Risk Factor in COVID-19
https://www.preprints.org/manuscript/202004.0457/v1
Vitamin K status was reduced in patients with COVID-19 and related to poor prognosis. Also, low vitamin K status seems to be associated with accelerated elastin degradation.
*) Dramatic Decrease of Vitamin K2 Subtype Menaquinone-7 in COVID-19 Patients
doi: 10.3390/antiox11071235 2022
The COVID-19 patients had significantly lower MK7 levels than non-COVID-19 pneumonia patients and healthy controls.
Conclusions: The present data identified significantly decreased vitamin K1, K2 (MK7), and increased MK4 levels in patients with COVID-19 compared to healthy controls. Vitamin K2 (MK7) was lowest in COVID-19 patients irrespective of potentially fatal courses, indicating consumption of this VK subtype by COVID-19 immanent effects, most probably inflammatory and oxidative stress factors.To be continued on this link: “English corner: Long Covid Prevention”
https://mirzoune-ciboulette.forumactif.org/t2100-english-corner-covid-long-prevention#30146
*) Can red light therapy improve lung function?
*) Vitamin E is 100-fold more potent than Remdesivir against SARS-CoV-2 / corona viruses.
*) Appropriate Levels of Vitamin D3 Reduce Virus Risk by Half and Optimize Recovery.
Vitamins A and D are needed for:- Antimicrobial peptides (AMPs). AMPs are small proteins that can disturb/disrupt microbial membranes, interfere with their metabolism, and damage cellular components.
- Lysozymes. Lysozymes are enzymes that damage bacterial cell walls by breaking down sugar bonds (bacterial LPS membranes).
- Iodine, the most effective halide for immune obliteration. When immune cells use phagocytosis against infections, they deplete the iodine contained in thyroid hormone.
*) Interaction between fat-soluble vitamins A D K
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Thank you LucH
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There is no 'covid virus', or any other virus for that matter. I thought we all understood this by now.
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To me (at this point) the people using this language are just talking/thinking at a high level of abstraction. It might be more problematic than them believing "viruses don't exist", but they really would have to believe that to be free of concern about it. And it still wouldn't absolve them of requirement to behave appropriately.
There definitely is an enzyme that's part of the RAAS and biotech wanted to plug it for some reason. Moving RAAS with stupid behaviour can definitely induce cold/flu like symptoms. I know that because I engaged in strategically stupid self experiments for science.
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Hmm. Are you involved in this Eduardo? Just curious.
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Simplified version of the description for immune failing: pathophysiology key-points. Hypothetical disease model. (from Eduardo).
Only a partial analysis, just to avoid losing energy because the link is not fundamentally targeting SARS-CoV pathology but well how to remain in the low-symptom category when suffering from a compromised health issue. Not very readable …
Key points- Biofilms are protective and are under control of some bacterial fila to avoid inappropriate expansion.
- If the microbiome has been compromised by a lack of protective species, pathogenic species could / are going to take the lead.
=> An ongoing slippery slope of microbiome dysbiosis is created by events which allow the surface area expansion of pathogenic biofilms. - These biofilms are degraded by helpful microorganisms, such as commensal various bacteria (Lactobacillus spp., Bifidobacterium spp., Bacillus spp. and other species), stomach acid, dietary intakes of biofilm degrading compounds and lifestyle choices.
- Low populations of bifidobacterium are routinely found in chronic disease.
- The protective microorganisms metabolize acetaldehyde into acetate, degrade biofilms and inhibit pathogenic species.
- Antibiotics have broadly deleterious effects on microbiome diversity and abundance.
- Acetaldehyde is well-known in chronic alcoholism for causing T-cell exhaustion, inhibiting glycolysis, decreasing NAD+/elevating NADH, inhibiting methylation, inhibiting collagen synthesis, dysregulating thiamine pyrophosphate metabolism and having a higher affinity for various aldehyde dehydrogenase (ALDH) isoenzymes required for eg. Neuro-transmitter degradation, histamine degradation and many other pathways.
Gliotoxin, other mycotoxins and endotoxins are also relevant to this cascade. - Immune system dysregulation caused by malnutrition, low NK cell counts, medications that alter Interferon signaling bias / cascade regulation, antibiotics, bio-toxins, IFN-alpha promoting antigen dominance (eg. SARS-CoV-2 spike protein / infection, influenza, reactivated herpesviruses, isocitrate lyase expressing microorganisms, lipopolysaccharides, medical interventions which provide antigens for immune imprinting), and chronic stress (as elevated cortisol, dysregulation of cytokines) can each provide a window of opportunity for unimpeded biofilm growth, increased endo/mycotoxin production and net acetaldehyde increase.
- Low grade inflammation: An inflammatory cascade is going to overcome and to create havoc.
- Description of the hormone chaos.
More details on this link from Eduardo (scroll till the bottom)
https://bornfree.life/2024/
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@ThinPicking no just posting info
