Health Protocol for Mandatory Coronavirus Vaccination

[PlatonicSkeptic]

The article stated 3000 mg first thing in the morning, and 2000 mg every 2 hours thereafter until you reach bowel tolerance. So you can basically experiment and see how much you can handle before you start getting loose stools. I knew of someone who was able to handle more than double what I can and they are smaller and weigh less than I do. So I don't think size or weight plays a big role. Or at least not as big a role as what your overall health is like.

beware that these doses are used by bodybuilders in the pre contest week as diuretic, dehydration is possible.

 

[MK Scarlett]

The article stated 3000 mg first thing in the morning, and 2000 mg every 2 hours thereafter until you reach bowel tolerance. So you can basically experiment and see how much you can handle before you start getting loose stools. I knew of someone who was able to handle more than double what I can and they are smaller and weigh less than I do. So I don't think size or weight plays a big role. Or at least not as big a role as what your overall health is like.

Thank you Gaby and Keyhole for this thread and others for additional inputs; We are so in the need of works/shares like this one.

Regarding the previous, I'd like to share my own experiments on it. I weigh 52 kg (52 lbs.) and while I use to take around 4 to 6 g of Vit.C each day for usual back and neck pain, I increase this amount from time to time for reasons of greater pain than those usually encountered until around 10g a day.

Some months ago, I had a molar removed and that was planned in advance. I decided to increase the amount of Vit.C two days before to be able to reach at least 15g at the end of this very day. The day of the appointment at the dentist (around noon), I already had taken around 6g. I had took some Vit.C in my bag, so even before living the cabinet, I took another dose of 2g. During the trip between the dentist and my home (15 minute walk), I took another dose of 2g. I should mention that my dentist gave me a prescription for antibiotics and painkillers, although I told him I wouldn't take them. I never had done for antibiotics for long years, and very rarely for painkillers. Plus, I also thought it would be a good opportunity to see how many grams of Vit.C I could get up to.

As the effects of the local anesthetic diminished in the following hours, the pain became much more intense, much more severe, actually it was HUGE. I continued to take Vit.C on a rhythm of about 1g every 1/4 hour during the following hours, then every 1/2 hour, until I reach a total by going to bed pretty early of 33g. As I had planned to go around 15g for this very day, I had never thought about reaching that point! At no time did I feel any effects even at the digestive bowl. I told myself that Vit.C was being used by my body "under the stress of great pain" as quickly as I was taking it. The next day I took about 20g, then the next day about 15g, and gradually decreased until I returned to my usual dosage of 4/6g, which I reached about a week later after the dental operation.

Today, if needed, I can easily reach at any given time around 12/15g in 2/3 hours, without any side effects on the digestive bowl. I thought FWIW that I should share this here.

 

[Keyhole]

In the previous few posts, I discussed the relationship between mTOR signalling and mRNA translation into proteins via lipid nanoparticle delivery.

In devising a protocol designed to help protect against the potential detrimental effects of an LNP-mRNA vaccine, it is also important to consider the negative impact that the carrier molecules can have on the immune system. As mentioned previously:

For protecting against immune hyper-reactivity due solely to PEG, I am not sure about that just yet. Perhaps the basics would cover that, like Gaby mentioned (vitamin C etc).

Polyethylene glycol (PEG) and other lipids found in the LNP vaccine formulation have the capacity to aggravate/trigger systemic immune activation and lead to potential anaphylaxis and death in an acute fashion. Furthermore, the immune components which are stimulated by PEG may be involved in long-term autoimmune risk and neuroinflammation.

The basic mechanisms of immune activation seem to include:

1. Activation of the complement cascade (a specialized group of cells in the immune system) - notably C3 & C5
2. Stimulation of at least 8 different proinflammatory cytokines

Toxicity and immunogenicity concerns related to PEGylated-micelle carrier systems: a review


PEG has been known as a safe, inert, and non-immunogenic synthetic polymer. However, PEG-related immunological issues have received considerable attention [22–28]. Anti-PEG antibodies have been found in patients who were treated with PEGylated nonhuman enzymes [22–25]. Furthermore, circulating anti-PEG antibodies have been found in healthy subjects and are thought to be induced by PEG containing cosmetics and foods [26,28]. The use of PEGylation onto nanoparticles, such as liposomes, micelles, and nanoparticles, has faced PEG-related immunological issues owing to rapid blood clearance of PEGylated nanoparticles (PEG-NPs) upon repeated administration [29–31]. Despite the frequent use of PEGylation to improve half-lives of biopharmaceuticals and nanoparticle carrier systems, research has not elucidated PEG-related immunological issues. Furthermore, researchers have focused almost exclusively on rapid blood clearance of repeatedly administered nanoparticle carrier systems.

Complement activation cascade triggered by PEG–PL engineered nanomedicines and carbon nanotubes: The challenges ahead

Since their introduction, poly(ethylene glycol)–phospholipid (PEG–PL) conjugates have found many applications in design and engineering of nanosized delivery systems for controlled delivery of pharmaceuticals especially to non-macrophage targets. However, there are reports of idiosyncratic reactions to certain PEG–PL engineered nanomedicines in both experimental animals and man. These reactions are classified as pseudoallergy and may be associated with cardiopulmonary disturbance and other related symptoms of anaphylaxis. Recent studies suggest that complement activation may be a contributing, but not a rate limiting factor, in eliciting hypersensitivity reactions to such nanomedicines in sensitive individuals. This is rather surprising since PEGylated structures are generally assumed to suppress protein adsorption and blood opsonization events including complement. Here, we examine the molecular basis of complement activation by PEG–PL engineered nanomedicines and carbon nanotubes and discuss the challenges ahead.

Overcoming Nanoparticle-Mediated Complement Activation by Surface PEG Pairing

Many PEGylated nanoparticles activate the complement system, which is an integral component of innate immunity. This is of concern as uncontrolled complement activation is potentially detrimental and contributes to disease pathogenesis. Here, it is demonstrated that, in contrast to carboxyPEG2000-stabilized poly(lactic-co-glycolic acid) nanoparticles, surface camouflaging with appropriate combinations and proportions of carboxyPEG2000 and methoxyPEG550 can largely suppress nanoparticle-mediated complement activation through the lectin pathway. This is attributed to the ability of the short, rigid methoxyPEG550 chains to laterally compress carboxyPEG2000 molecules to become more stretched and assume an extended, random coil configuration. As supported by coarse-grained molecular dynamics simulations, these conformational attributes minimize statistical protein binding/intercalation, thereby affecting sequential dynamic processes in complement convertase assembly. Furthermore, PEG pairing has no additional effect on nanoparticle longevity in the blood and macrophage uptake. PEG pairing significantly overcomes nanoparticle-mediated complement activation without the need for surface functionalization with complement inhibitors.

Linkage between endosomal escape of LNP-mRNA and loading into EVs for transport to other cells​

Our results indicate that although the systemic delivery of both EVs and LNPs cause the expression of proinflammatory cytokines including IL-6, IP-10, RANTES, MCP-1, and KC in mice, the expression levels induced by EVs were not as much higher as LNPs did (Fig. 6). This indicates that EVs might be better tolerated by the recipient mice, since EVs contain fewer ionizable lipid molecules per mRNA nucleotides (1: 1 molar ratio) compared to LNPs (1: 3 molar ratio).

Since endo-EVs contained a three-fold lower level of ionizable lipids (which, despite being important compounds for LNP manufacturing, can be toxic) per mRNA than LNPs, we expected that endo-EVs should elicit a milder immune response than LNPs. The expression levels of eight different cytokines in the plasma of mice confirmed our expectation that endo-EVs induce less inflammatory cytokine responses than LNPs upon transferring an equal dose of hEPO mRNA to mice.

Higher levels of pro-inflammatory cytokine responses elicited by LNPs compared to endo-EVs could be related to several factors, e.g. (i) endo-EVs delivered 1/3 of the toxic synthetic ionizable lipids of LNPs, (ii) in contrast to LNPs, EVs are natural biological products, and might be better tolerated by the host, and (iii) the routes of cellular uptake differ between EVs and LNPs, which could behave differently to autophagic-lysosomal pathway. The advantage of using EVs for mRNA delivery would be that compared to synthetic products, EVs are biological products and might elicit a milder immune response in the host.

In the case of LNPs, cellular uptake is mediated by endocytosis, which could activate the cells’ autophagic-lysosomal pathway. Accumulating evidence indicates that endocytosis of nanoparticles generates autophagosomes, and their subsequent fusion with lysosomes leads to the digestion of their content45. Autophagosomal–lysosomal activation shapes the cellular immunity as a defence mechanism against foreign particles, by which innate immune effectors elicit inflammatory responses49,50,51. In the present study, the uptake of LNPs caused an increased cytokine release. The routes of EV uptake52,53,54 differ from those of LNPs and are not likely to elicit the autophagy–lysosomal pathway, as they release their content into the cytoplasm probably without undergoing lysosomal trapping. Additionally, because of their small size, EVs can escape from rapid phagocytosis, and steadily carry and deliver RNA in circulation, passing through the vascular endothelium to the target cells55.

Cytokine analysis in mouse plasma after mc3-EV and MC3-LNP delivery. Mice were intravenously injected with 100 μL of mc3-EVs or MC3-LNPs containing 1.5 µg of hEPO-mRNA (per mouse). The concentrations of eight pro-inflammatory cytokines including IL-6 (a), IP-10 (b), RANTES (c), MCP-1 (d), KC (e), IL1-β (f), TNF-α (g), and IFN-γ (h) were determined in mouse plasma after 5 and 24 h of mc3-EV, MC3-LNP or PBS injection. The levels of pro-inflammatory cytokines were significantly higher in mice receiving LNP injection than in those receiving EV injection

Moving forward, aside from mTOR inhibition and increased cell energy metabolism, a protocol should theoretically include high doses of molecules which have been shown to inhibit or prevent activation of the complement cascade and also exert a generalized anti-inflammatory effect to prevent immune hyper-reactivity.

• A key concept to understand is that immune hyper-reactivity, or the inability of the immune system to "switch off", is generally one of the mechanisms by which vaccine injury occurs. This immune dysregulation appears to be involved in exacerbated response to environmental toxins in general. When the immune system cannot switch off (and this involves the complement cascade), excessive tissue injury can occur.

Complement inhibitors to consider:

Unsurprisingly, many of the protective nutrients/molecules which we would already be using have been shown to modulate this system in a beneficial way.

Inhibition of the complement system by glutathione: molecular mechanisms and potential therapeutic implications

Glutathione (GSH), a component of the antioxidant defence system, plays a role in autoimmunity and the complement system is often responsible for tissue damage in autoimmune diseases. The aim of this study is to evaluate the effects of GSH on the complement system. The complement system was examined in the normal human sera (NHS) of 30 healthy subjects. Increasing quantities of GSH (1, 2, 10, 20 mg) were incubated in 1 ml of each NHS. The mixtures were evaluated for complement activities (THC, CPA and APA) and for the presence of cleavage fragments of activation of C3 and B. GSH was also incubated with human complement in the presence of classical and alternative pathway activators. The results showed an inhibitory effect of GSH on the complement system starting from a dosage of GSH≥1 mg/ml. Indeed, when NHS was incubated with GSH at such dosage, a significant reduction of the complement activities THC, CPA, and APA was observed (P<0.0001, P<0.005, P=NS, respectively), and no cleavage fragments of C3 or B were found. Further analysis demonstrated that the inhibition was exerted on C3-9 and to a lower extent on classical and alternative pathway C3-convertases. Our results indicate that GSH is capable of inhibiting the complement system. These findings are relevant for the design of interventions aimed at modulation of GSH metabolism to inhibit complement-mediated damage in autoimmune diseases.
Inhibition of the complement system by glutathione: molecular mechanisms and potential therapeutic implications - PubMed

Glutathione inhibits antibody and complement-mediated immunologic cell injury via multiple mechanisms​

Moreover, GSH potently prevented the antibody-mediated agglutination of red blood cells and aggregation of antibody-sensitized microspheres. Further analysis revealed that GSH inhibited antibody binding to antigens and promoted the conversion of the antibodies to its reduced forms. GSH also potently inhibited the formation and deposition of C5b-9 in MCs and suppressed both the classic and alternative complement activation pathway. Lastly, GSH attenuated P38 activation, an oxidative sensitive kinase that partially mediated the antibody- and complement-dependent MC lysis. Depletion of GSH via inhibiting gamma-glutamylcysteine synthetase or xCT transporter augmented P38 activation and sensitized MCs to the cell lysis. Collectively, our results indicate that GSH protects cells from immunological cell damage via mechanisms involving inhibition of antibody binding to the antigens, suppression of complement activation and augmentation of cellular defense mechanism. Our study provides novel mechanistic insights into the actions of GSH in the regulation of immune responses and suggests that GSH might be used to treat certain immune disorders.

Glutathione inhibits antibody and complement-mediated immunologic cell injury via multiple mechanisms

Rationale for the use of N‐acetylcysteine in both prevention and adjuvant therapy of COVID‐19​

Although the complement system is a key mediator of the innate immune response that protects against infectious agents, it also plays a critical role in promoting the inflammatory process that leads to tissue injury.21 In particular, complement may be involved in coronavirus pathogenesis, as inferred from the finding that C3 knockout mice infected with SARS‐CoV have less lung disease than wild‐type mice.22 Preliminary data provide evidence for activation of complement (sC5b‐9 and C5a) in patients with COVID‐19, with significantly higher plasma levels in the patients with severe disease than in those with moderate disease. Hence, complement activation has been suggested as a novel therapeutic target in COVID‐19.21 In this context, it is noteworthy that administration of NAC (2 × 600 mg/day for 8 weeks) in a placebo‐controlled study has been shown to reduce the plasma levels of inflammatory markers, including complement (C3), in peritoneal dialysis patients.23
https://faseb.onlinelibrary.wiley.com/doi/full/10.1096/fj.202001807

Worth noting is that NAC and glutathione also fulfill the role of inhibiting mTOR inside cells and activating AMPK. In fact, glutathione depletion is a key trigger for mTOR activation, and replenishing glutathione can prevent this activation:

Glutathione: A possible link to autophagy in systemic lupus erythematosus

Altered signal transduction; mTOR is activated by relative depletion of glutathione and supplementation of N-Acetyl Cysteine (NAC), a precursor of glutathione, replenishs intracellular glutathione and inhibits mTOR signaling and diminished oxidative stress mediated damage in SLE (Fernandez and Perl, 2010). Management of disease through supplement of NAC andrapamycin has been showing promising therapy in SLE patients. Recently, several lines of evidence from genetic, cell biology and lupus animal model studies suggests a pivotal role of autophagy in mediating the occurrence and development of SLE (Alessandri et al., 2012). Interestingly, autophagy is regulated by mTOR pathway and mTOR is activated by relative depletion of glutathione. Thus, redox signaling may provide a link between altered autophagy and depletion of glutathione and autophagy regulation by replenishment of intracellular glutathione may have a therapeutic intervention for the management of disease.

Glutathione supplementation suppresses muscle fatigue induced by prolonged exercise via improved aerobic metabolism​

PGC-1α is a central member of a family of transcriptional co-activators involved in aerobic metabolism. Activation of PGC-1α alters the metabolic phenotype through interactions with nuclear respiratory factor and peroxisome proliferator-activated receptor-α [8-10], which leads to increased mitochondrial biogenesis and activity. It has been reported that PGC-1α activation causes significant improvements in athletic performance [24,25], prevention and treatment of muscle weakness in the elderly, obesity, and other metabolic diseases such as mitochondrial myopathies and diabetes [10,11,26]. Here, we detected an increase in PGC-1α with 2 weeks of glutathione intake, along with an increase in mtDNA content, indicating the activation of mitochondrial biogenesis. Therefore, the observed elevation of PGC-1α by glutathione intake strongly suggests an acceleration in lipid metabolism. In addition, the increase of mitochondria content could also lead to a decrease of lactate generation by accelerating aerobic metabolism of glucose, which would prevent muscle acidosis during exercise even further.




The regulatory mechanism for glutathione-induced increases in PGC-1α is unclear. One explanation is the elevation of AMPK, which is an upstream factor of PGC-1α regulation [27,28]. Recently, it has been argued that oral intake of other antioxidants, including vitamin C and E, do not elevate PGC-1α in the skeletal muscle of mice and humans [29,30]; thus, this may be a specific action of glutathione as a signal factor, but not its antioxidant properties. We found that 2 weeks of glutathione supplementation did not affect plasma glutathione concentration in the basal state. However, glutathione is transported across the intestines with in its intact form [12], and its plasma concentration, along with the glutathione-derived dipeptides γ-glutamyl-cysteine and cysteinyl-glycine, is markedly elevated during the 60–120-min period after oral administration, as shown in our previous report [13]. Therefore, the transient elevation of glutathione or the derived dipeptides following supplementation over 2 weeks may indicate stimulation of specific signaling factors that lead to elevated AMPK and PGC-1α.

Glutathione supplementation suppresses muscle fatigue induced by prolonged exercise via improved aerobic metabolism

Another very interesting compound which fits the criterai for both mTOR inhibition and inhibition of the complement system is Rosmarinic Acid (from rosemary). Interestingly, this molecule is used within the alternative medicine community to reduce/combat the effects of EMF on the brain and nervous system.

Rosmarinic acid anti-inflammatory extraordinaire
Polyphenols are well known for their antioxidant properties and many of them also have anti-inflammatory effects too. Rosmarinic acid is a naturally occurring polyphenol and is no exception to this. No surprise then that the herb and its extract has been used in the traditional medicines of various cultures.

An open label trial assessed patients with osteoarthritis and rheumatoid arthritis given an extract containing rosmarinic acid over the course of four weeks (1). The researchers discovered that the hs-CRP (an index showing the presence of inflammation) had been decreased significantly in patients taking the supplement. There was also a decrease in the level of C-reactive protein, another biomarker for the presence of inflammation, in those patients who had elevated levels of CRP prior to the experiment. There were also no serious side effects observed.

Further evidence for the anti-inflammatory potential of rosmarinic acid was shown another study (2). It was shown that rosmarinic acid was able to disturb complement system activation by inhibiting C3b bonding and the dose was very low to do this. C3b is an essential part of the innate immune system and excessive levels of this can result in diseases such as atypical hemolytic uremic syndrome (aHUS), hemolytic disorders, and certain autoimmune disorders. Current standard of care is
treatment with the complement-inhibitory anti-C5 monoclonal antibody, eculizumab or similar. Rosmarinic acid presents a potential alternative approach to achieve similar reduction of C3b to manage these conditions.

Rosmarinic acid has also shown gastroprotective action against gastric ulcers, even more effective than commonly used Omeprazole (3). It is more effective because of its ability to inhibit neutrophil infiltration and it is able to reduce proinflammatory mediators, in particular TNF-a and IL-1 which are both involved in inflammatory responses and can lead to excessive inflammation when levels are too high. This could mean that rosmarinic acid could be a better solution to such conditions.

Here is the fulll article on the immune benefits of rosmarinic acid.

Rosmarinic acid is a potent inhibitor of the complement system:

The inhibitory effect of rosmarinic acid on complement involves the C5 convertase

Rosmarinic acid (RA), a naturally occurring extract from Melissa officinalis, inhibits several complement-dependent inflammatory processes and may have potential as a therapeutic agent for the control of complement activation in disease. Rosmarinic acid has been reported to have effects on both the classical pathway C3-covertase and on the cobra venom factor-induced, alternative pathway convertase. In order to define the mechanism of inhibition, the effect of RA on classical and alternative pathway lysis, C1q binding, the classical pathway convertase, the alternative pathway convertase, membrane attack pathway lysis and the generation of fragments of C3 and C5 during activation, was tested in vitro. The results showed that RA inhibited lysis by the classical pathway more than by the alternative pathway. This effect was dose-dependent with maximum inhibition of classical pathway lysis observed at 2.6 mmoles ff RA. There was little effect on C1q binding or on the classical and alternative pathway convertases. However, there was highly significant inhibition of lysis of pre-formed EA43b cells by dilutions of human or rabbit serum in the presence of RA (1 mM); this was accompanied by inhibition of C5a generation. We conclude that the inhibitory effect of RA involves the C5 convertase. Such inhibition could be advantageous to the host in disorders where the terminal attack sequence plays a role in pathogenesis.

The inhibitory effect of rosmarinic acid on complement involves the C5 convertase

Rosmarinic acid (RA), a naturally occurring extract from Melissa officinalis, inhibits several complement-dependent inflammatory processes and may hav…

www.sciencedirect.com

Rosmarinic acid: a new inhibitor of complement C3-convertase with anti-inflammatory activity​

Rosmarinic acid (RA) is a naturally occurring compound, isolated from Rosmarinus officinalis or Melissa officinalis which inhibits the in vitro immunohaemolysis of antibody-coated sheep erythrocytes by guinea pig serum. In further experiments this reduced immunohaemolysis was found to be due to inhibition of the C3-convertase of the classical complement pathway. The threshold concentration for inhibition of C3-convertase was 10(-6) mol/l. RA with an optimal inhibitory concentration between 5 and 10 mumol/l., resulting in about 70% inhibition of haemolysis. However, higher concentrations of RA were less effective at inhibiting C3-convertase. The inhibition may not be specific for C3-convertase, since another serine protease, elastase, was also weakly inhibited by RA in vitro. RA also exhibited inhibitory activity in three in vivo models in which complement activation plays a role. Thus, RA (0.316-3.16 mg/kg i.m.) reduced paw oedema induced by cobra venom factor (CVF) in the rat, and at 1-100 mg/kg p.o. inhibited passive cutaneous anaphylaxis in the rat. In addition, at 10 mg/kg i.m. RA impaired in vivo activation by heat-killed Corynebacterium parvum (i.p.) of mouse macrophages, as measured by the decreased capacity of the activated macrophages to undergo the oxidative burst. RA (0.1-10 mg/kg i.m.) did not inhibit t-butyl hydroperoxide-induced paw oedema in the rat, indicating selectivity for complement-dependent processes.

Rosmarinic acid inhibits mTOR:

Rosemary Extract Inhibits Proliferation, Survival, Akt, and mTOR Signaling in Triple-Negative Breast Cancer Cells​

Breast cancer is the most commonly diagnosed cancer in women. Triple-negative (TN) breast cancer lacks expression of estrogen receptor (ER), progesterone receptor (PR) as well as the expression and/or gene amplification of human epidermal growth factor receptor 2 (HER2). TN breast cancer is aggressive and does not respond to hormone therapy, therefore new treatments are urgently needed. Plant-derived chemicals have contributed to the establishment of chemotherapy agents. In previous studies, rosemary extract (RE) has been found to reduce cell proliferation and increase apoptosis in some cancer cell lines. However, there are very few studies examining the effects of RE in TN breast cancer. In the present study, we examined the effects of RE on TN MDA-MB-231 breast cancer cell proliferation, survival/apoptosis, Akt, and mTOR signaling. RE inhibited MDA-MB-231 cell proliferation and survival in a dose-dependent manner. Furthermore, RE inhibited the phosphorylation/activation of Akt and mTOR and enhanced the cleavage of PARP, a marker of apoptosis. Our findings indicate that RE has potent anticancer properties against TN breast cancer and modulates key signaling molecules involved in cell proliferation and survival.

Another useful paper here:

Rosmarinus officinalis L. (rosemary) as therapeutic and prophylactic agent​

To round up thus far, some key areas to focus on for devising a protocol:

• mTOR inhibition appears to be a useful strategy, potentially to reduce mRNA translation and to "protect" cells by boosting cell "clearout" and cleaning. This can be achieved through therapuetic ketosis, fasting, calorie restriction, intense cardiovascular exercise, cold therapy, and specific nutrients/supplements
  
  
  
• Certain areas of the immune system can become activated excessively with PEGylated molecules found in LNP vaccines : the complement system, and at least 8 pro-inflammatory chemicals (cytokines)
  
  
  
• Glutathione (and its precursor, NAC) can inhibit mTOR, activate AMPK, provide antioxidant powder to reduce excess oxidative stress, and inactivate/inhibit the complement system. For this reason, they may be useful in high doses for protection against PEG
  
  
  
• Rosmarinic acid inhibits mTOR, and also has been found to inhibit specific branches of the complement system - and therefore may be useful in protecting against PEG. This molecule also exerts systemic anti-inflammatory benefits and can reduce numerous pro-inflammatory cytokines.

 

[Jtucker]

Amazing work, Keyhole! Thank you so much!

 

[Keyhole]

Amazing work, Keyhole! Thank you so much!

Within the next day or two, I will put together a rough sketch up here of a basic protocol with dosing and products that others might add to

 

[Ant22]

There is a myth about iodine - the higher doses aren't more uncomfortable, the low doses are. People who start at 1000 mg (for example after chemo) react better than less contaminated people who start at 50-150mg. In case of vaccination, there is not better cure.

Biala 84, you have repeated this advice in multiple threads, as if it was perfectly safe for absolutely everyone to take high doses of iodine daily, and it was impossible for people to have any issues with that approach. This is not correct, have you by any chance read the entire Iodine thread on the forum? Or did you just read the the initial pages of it? Iodine mobilises heavy metals and other junk from the system, and a lifetime of toxicity exposure would mean all of that stuff hits the bloodstream at once. Advising everyone to take massive doses of iodine is NOT safe advice as we are all different.

I personally started off on very high doses of iodine, exactly the ones Brownstein recommends in his book, and I did not react well to such high doses at all. When I lowered the dose of only 8 drops I felt really well, detox symptoms stopped and I was able to experience improvement in my overall health. After around a year on 8 drops of 12% Lugol I started to experience detox symptoms again so I gradually lowered the dose to 4 drops. Again, I felt very well, detox symptoms disappeared and I continued to benefit from it.

Also, note that Brownstein recommended high doses of iodine for very serious illnesses, not for general toxicity. And it is the latter that most members fo this forum need iodine for.

 

[hlat]

beware that these doses are used by bodybuilders in the pre contest week as diuretic, dehydration is possible.

I disagree because these are relatively low doses. When I want to reach tolerance, I take 4000 mg to start and then another 2000 mg every 30-45 minutes. Spacing out to 2000mg every 2 hours is a very conservative approach.

 

[PlatonicSkeptic]

I disagree because these are relatively low doses. When I want to reach tolerance, I take 4000 mg to start and then another 2000 mg every 30-45 minutes. Spacing out to 2000mg every 2 hours is a very conservative approach.

no need to downvote my post, everyone's body chemistry is different, we assume that someone receiving a vaccine needs it and may not be in the best condition

 

[liam1310]

Thanks for the info guys. Nice to have as many tools in the box as possible. Best be prepared while also considering that the psychos will fail. Just a matter of time, hopefully sooner rather than later. I'll be in a position soon with the vaccine in work. Not sure how this will work out, im fasting, diets good, cold baths, sauna, iodine and supplements mentioned, all covered my end. I will avoid at all costs the vaccine, if it means leaving my job, so be it. Thanks again for the work keyhole and Gaby, its much appreciated and will no doubt help others.

 

[biala84]

ossible for people to have any issues with that approach. This is not correct, have you by any chance read the entire Iodine thread on the forum? Or did you just read the the initial pages of it? Iodine mobilises heavy metals and other junk from the system, and a lifetime of toxicity exposure would mean all of that stuff hits the bloodstream at once. Advising everyone to take massive doses of iodine is NOT safe advice as we are all different.
Biala 84, you have repeated this advice in multiple threads, as if it was perfectly safe for absolutely everyone to take high doses of iodine daily, and it was imp
I personally started off on very high doses of iodine, exactly the ones Brownstein recommends in his book, and I did not react well to such high doses at all. When I lowered the dose of only 8 drops I felt really well, detox symptoms stopped and I was able to experience improvement in my overall health. After around a year on 8 drops of 12% Lugol I started to experience detox symptoms again so I gradually lowered the dose to 4 drops. Again, I felt very well, detox symptoms disappeared and I continued to benefit from it.

Also, note that Brownstein recommended high doses of iodine for very serious illnesses, not for general toxicity. And it is the latter that most members fo this forum need iodine for.

I check high dozes on myself. I see You are not on Fb page where people reccomende one to another a higher dozes which mean 100 150 mg of iodine per day I would like to invite You and others meber if You are interested in using salt in general as a protection in these difficult times. Facebook Groups. To be truth i use double of this and small dozes only feed the bacteria and where is the cells protection? 50 mg of iodine cannot protect You from that. You see i use iodine first time 5 years ago and i start with high dozes. We are here on this forum to help one and another and because the wave is coming we have to clean our bodies and protect them from negative effects of radiation. There is another disinformation about iodine which Brownstein also supports and is small dozes. Why people think that doze 100-150 mg is high. For me is not, for me for example will be 500 mg as a high doze. !50 mg of iodine is moderate doze. To clean body from metals in case if You are taking iodine is not only iodine which can help. If You think that giving advice and sharing your knowledge is not correct than what is correct?

The negative effects of radiation. Biala 84, you have repeated this advice in multiple threads, as if it was perfectly safe for absolutely everyone to take high doses of iodine daily, and it was impossible for people to have any issues with that approach. This is not correct, have you by any chance read the entire Iodine thread on the forum? Or did you just read the the initial pages of it? Iodine mobilises heavy metals and other junk from the system, and a lifetime of toxicity exposure would mean all of that stuff hits the bloodstream at once. Advising everyone to take massive doses of iodine is NOT safe advice as we are all different.

I personally started off on very high doses of iodine, exactly the ones Brownstein recommends in his book, and I did not react well to such high doses at all. When I lowered the dose of only 8 drops I felt really well, detox symptoms stopped and I was able to experience improvement in my overall health. After around a year on 8 drops of 12% Lugol I started to experience detox symptoms again so I gradually lowered the dose to 4 drops. Again, I felt very well, detox symptoms disappeared and I continued to benefit from it.

Also, note that Brownstein recommended high doses of iodine for very serious illnesses, not for general toxicity. And it is the latter that most members fo this forum need iodine for.

--
Mod edit: Link removed

 

[Ant22]

I check high dozes on myself. I see You are not on Fb page where people reccomende one to another a higher dozes which mean 100 150 mg of iodine per day I would like to invite You and others meber if You are interested in using salt in general as a protection in these difficult times.

How does yours or FB group members' experience invalidate mine? It only goes to show that people are different and what works for some people doesn't work for others. Which is exactly the point I was trying to make in my above post.

And I use salt daily. I have since 2015. Trying to find holes in my protocol to prove that I didn't do it right is the approach vegans take when someone tells them veganism doesn't work for everyone.

 

[hlat]

no need to downvote my post, everyone's body chemistry is different, we assume that someone receiving a vaccine needs it and may not be in the best condition

That's exactly why they would need more vitamin C, so there's nothing to beware about taking vitamin C at 2000 mg every 2 hours and it has nothing to do with bodybuilders.

 

[NewEngland Seeker]

Thanks Gaby for starting this important and timely post. This is how we can be forewarned to be forearmed.

What I have learned is that nutritional supplements are passive energy forms and need to be actively enhanced to reach full potential. The best way to actively enhance is to employ the yin/yang principle to move the nutrients into the deeper tissues.

Exercise/rest: Endurance exercises will increase flow throughout the circulatory and lymphatic system. Taking supplements before exercising will help move the nutrients into the deeper tissues and into the lymphatics. The more you sweat, the more fluid flow and nutrient uptake/distribution will occur. Resting after the endurance exercise will increase the tissue and cellular uptake of the nutrients and oxygen. For intense response, an all-day walk followed by few days of increased rest/sleep is a great way to clear out a significant amount of toxins. It is also very regenerative.

Hot/cold: Saunas and hot baths are passive forms of increasing the internal heat of the body, while exercise is active and more effective. The increase heat (self-induced fever) increases the enzymatic activity which cleanses the body. When followed by cold will induce the shock affect which increases flow. This technique works best when done three times or until the cold no longer feels shocking.

Fasting/nourishing: The fast deplete the body of all excess nutrients which increases the cell’s need for nutrients, then followed by a nourishing cycle. If you feel very weak during the fast then your core nutritional needs are not being met or your core vitality is too low.

Another counter measure to the vaccine that comes to mind is an herbal poultice over the injection site. This could draw out the poisons back through the skin. Something as simple as a mustard/ginger pack, a castor oil pack or any herbal packs used for puncture wounds.

Digestive enzymes are the most surprising nutrients that I have found that helps with any nutritional protocol. Enzymes in general maximize the nutritional uptake of food and nutritional remedies. I have found that I need less nutrients if taking enzymes. They also enhance detoxification methods. I personally have found that Lysozyme Lysozyme - Wikipedia is extremely potent for the immune system. My go-to enzyme for any infection. I take lysozyme before exercising which I find enhances the cleansing affect of the sweating. It also attacks cancer cells which makes it my golden enzyme. For general information of digestive enzymes this website is a good primer. Digestive Enzymes Prevent Nutrient Deficiency & Support Gut Health

Gaby, I am so happy that you started this. This is a very positive approach and better than being afraid the vaccine. Fear will only increase its negative impact. Whereas, if we are fearless and confident of being totally unaffected by the vaccine then we're not going to be victims in this crazy scheme.

 

[Phill4]

I have a question, if it is delivered in a PEGylation, lipid nanoparticle membrane can BHT work to break down the membrane?

 

[biala84]

How does yours or FB group members' experience invalidate mine? It only goes to show that people are different and what works for some people doesn't work for others. Which is exactly the point I was trying to make in my above post.

And I use salt daily. I have since 2015. Trying to find holes in my protocol to prove that I didn't do it right is the approach vegans take when someone tells them veganism doesn't work for everyone.

Someon is sharing experience there is nothing to talk more :) Who want will take advice, who not won't :)
Ant22 do you remember what Cassiopaeans said in one session that we benefit only from high dozes of iodine :)
Have a nice day