How to minimize paradoxical acquired immune dysfunction from Spike protein
Fixing the reverse AIDS damage
This is a work in progress, and I am just publishing like this given how much damage and people asking for help I am getting. I did test these for months on hundreds of people, it usually solves most of their issues, except autoimmunity, this one I can’t solve…yet…
I will either update this sometimes and post something on Twitter, or work on a new one and just publish version 2.0.
I can’t explain this supplement yet, before going deep into research, and pathways, to actually prove my hypothesis in concerns to this and propose the use, so take it or leave.
If you or anyone has psychological issues like anxiety, depression, and others, they should just supplement Tryptophan. People, with fucked up guts, should do the same.
First, I wish I had more time to properly present the Reverse AIDS hypothesis, to properly make my case, but:
1) Everything is cascading faster than math could forecast, the castle of cards is going down too fast
2) People are getting really worried, and for a good reason, the number of diseases is skyrocketing, and you can quite tell “where” it is coming from.
So this isn’t going to be as extensive, as thorough as I could write, plus not that different from my Things Hidden Since the Splicing series (I, II, III here), this could be considered a spiritual Part IV of some sort. You NEED to read all the Reverse AIDS and virus posts linked there to understand the use of all of these.
Above anything else on this list, if you want to follow anything I write about, at the very least you NEED to take a daily multivitamin, otherwise everything else is useless. You don’t need an expensive one, just a decent one with as much of what you need as possible.
Just to prove a point, I will use this image. I removed the names, etc, because I don’t know how these doctors would feel about me exposing them. Not many people test or measure the markers we require, let alone publish their opinions and findings online.
The first thing you need is Melatonin, OR Turkey Tail Extract. Why ? From my perspective, from multiple pathways, the Spike is immuno-suppressing you, it lowers your CD8 levels, and the jab by orders of magnitude more than everything else.
Pharmacological advantages of melatonin in immunosenescence by improving activity of T lymphocytes
Taken together, we conclude that melatonin supplementation may enhance immunity in aged individuals by upregulating immunosenescence indices in association with T lymphocytes and may be an attractive pharmacological candidate for aged and immunocompromised individuals.
Melatonin: Buffering the Immune System (READ THIS ENTIRE ARTICLE)
The clinical relevance of the multiple functions of melatonin under different immune conditions, such as infection, autoimmunity, vaccination and immunosenescence, is also reviewed.
Conversely, melatonin significantly reduced the splenic CD19+ B-cell population in mice with experimental membranous nephropathy and diminished the overexpression of TNF-α, IL-1β and IFN-γ
Chronic administration of melatonin to antigen-primed mice increased the production of IL-10 and decreased the secretion of TNF-α, suggesting a Th2 response
Immune Modulation From Five Major Mushrooms: Application to Integrative Oncology
Any of the list that ups CD8, I usually tell people to just supplement with Turkey Tail Any of the list that ups CD8, I usually tell people to just supplement with Turkey Tail Extract… or… Melatonin, which I prefer.
The second is NAC. Which is pretty obvious why. I can NOT simplify enough, so if you want to do research, please feel free.
A decent portion of the vaccines, and virus, short, medium, and long-term side effects come from depriving you of essential nutrients. One of the most important ones is Glutathione, yes there are other ways to replenish it, but nothing comes closer to doing everything NAC does.
The short, and simplified, of it. By multiple pathways, by different means, the vaccine will drain your antioxidants, creating a lot of oxidative stress, and inflammation, that your body doesn’t have the necessary tools to “fight”. NAC will help with ferroptosis, and its nasty pathological effects, neurological issues, inflammation, chelating excess minerals (iron especially), lowering ROS, and better mitochondrial function.
Oxidative Stress and Treg and Th17 Dysfunction in Systemic Lupus Erythematosus
Oxidative stress can induce and aggravate SLE by linking environmental stimulation with immune imbalance. Oxidative stress contributed the Th17/Treg imbalance in SLE patients. Under the normal stage, Th17 cells and Treg cells stay in a dynamic immune balance, while oxidative stress was induced in SLE patients, which can further induce and expand the proinflammatory Th17 cells expansion and inhibit the anti-inflammatory Treg cell differentiation and aggravate autoimmune injuries.
In my opinion, every vaccinated individual should supplement NAC for a few weeks, at a very minimum. Add Glycine for better metallization of NAC and Selenium, it works together. The list is too big, just take the fucking thing. Here is my Twitter thread on NAC.
Next, and I referred to it a lot, and regardless of what you think, any vaccinated individual needs a lot, is Vitamin D. By the Reverse AIDS hypothesis, given all the different pathways, Vitamin D is one of the most important supplements, and I will make its case.
By merely skewing your immune response to one side, by multiple pathways, the vaccine will down-regulate some cytokines.
IL-10 is one of the most common culprits of being suppressed.
It’s not the first time I mention the paper below and you should read the entire thing.
CD8+ T-cell deficiency is a feature of many chronic autoimmune diseases, including multiple sclerosis, rheumatoid arthritis, systemic lupus erythematosus, Sjögren's syndrome, systemic sclerosis, dermatomyositis, primary biliary cirrhosis, primary sclerosing cholangitis, ulcerative colitis, Crohn's disease, psoriasis, vitiligo, bullous pemphigoid, alopecia areata, idiopathic dilated cardiomyopathy, type 1 diabetes mellitus, Graves' disease, Hashimoto's thyroiditis, myasthenia gravis, IgA nephropathy, membranous nephropathy, and pernicious anaemia. It also occurs in healthy blood relatives of patients with autoimmune diseases, suggesting it is genetically determined. Here it is proposed that this CD8+ T-cell deficiency underlies the development of chronic autoimmune diseases by impairing CD8+ T-cell control of Epstein-Barr virus (EBV) infection, with the result that EBV-infected autoreactive B cells accumulate in the target organ where they produce pathogenic autoantibodies and provide costimulatory survival signals to autoreactive T cells which would otherwise die in the target organ by activation-induced apoptosis. Autoimmunity is postulated to evolve in the following steps: (1) CD8+ T-cell deficiency, (2) primary EBV infection, (3) decreased CD8+ T-cell control of EBV, (4) increased EBV load and increased anti-EBV antibodies, (5) EBV infection in the target organ, (6) clonal expansion of EBV-infected autoreactive B cells in the target organ, (7) infiltration of autoreactive T cells into the target organ, and (8) development of ectopic lymphoid follicles in the target organ. It is also proposed that deprivation of sunlight and vitamin D at higher latitudes facilitates the development of autoimmune diseases by aggravating the CD8+ T-cell deficiency and thereby further impairing control of EBV. The hypothesis makes predictions which can be tested, including the prevention and successful treatment of chronic autoimmune diseases by controlling EBV infection.
Vitamin D Controls Tumor Growth and CD8+ T Cell Infiltration in Breast Cancer
Immune Modulatory Effects of Vitamin D on Viral Infections
Vitamin D Suppresses Th17 Cytokine Production by Inducing C/EBP Homologous Protein (CHOP) Expression*
Vitamin D has been shown to have immunomodulatory function, but the molecular basis for it has not been well understood. In this study, we found that vitamin D receptor expression was induced in a CD4+ effector T cell lineage, Th17 cells, which required the transcription factors, RORα, RORγt, and STAT3. Treatment of mice with an active ligand of vitamin D receptor (VDR), 1,25-dihydroxyvitamin D3 (1,25D3), ameliorated experimental autoimmune encephalomyelitis, accompanied with reduced IL-17 and IL-17F expression. In vitro, treatment of CD4+ T cells with the physiological doses of 1,25D3 preferentially inhibited cytokine production by Th17 cells, in a VDR-dependent manner, without affecting the expression of transcription factors or surface molecules. Moreover, at these concentrations, cytokine expression was suppressed only at protein but not at mRNA levels. Stimulation of Th17 cells with 1,25D3, in a concentration-dependent manner, induced the expression of C/EBP homologous protein (CHOP), a molecule involved in endoplasmic reticulum stress and translational inhibition. In addition, overexpression of CHOP in developing Th17 cells suppressed their cytokine production. Our results suggest a novel, post-transcriptional mechanism whereby Th17 cytokines are inhibited by VDR, which may underscore future therapeutic usage of vitamin D in treatment of autoimmune diseases.
So, the next one is… kinda…well. No way around. It is easier and cheaper for me to access the next one, but for all intents and purposes Berberine does almost the same thing, but I am not a Berberine expert lol. Here we fucking go.
[INFLUENCE OF THE METFORMIN THERAPY ON THE ACTIVITY OF ENDOTHELIAL-DEPENDENT MEDIATORS AMONG PATIENTS WITH ACUTE MYOCARDIAL INFARCTION AND CONCOMITANT TYPE 2 DIABETES MELLITUS]
It leads to the inhibition of the thrombocytes activation and differentiation of the monocytes to the macrophages able to product proatherogenic factors. It was established that metformin therapy among patients with acute myocardial infarction and diabetes mellitus type 2 leads to the faster decreasing of sCD40-ligand in comparison with insulin therapy, which can contribute to the improvemenet of the prognosis in this cohort.
At some point during our research, I had a little stupid game, when we found a new pathway, I would google whatever we found + metformin for the fun of it. You should do that too.
In some countries, Metformin is prescription only, while in others OTC. In the US it is prescription only, but in some states, you are allowed to import it for personal use, as long as it’s not quantity enough for you to distribute it. Inform yourself first, otherwise, use Berberine.
One nasty adverse effect of the vaccine and, to a lesser extent, the virus, is the clotting, and protein fuckery. Specially amyloid-based clots, which are way harder to deal with (it’s in one of my many virus posts).
In vitro and in vivo insulin amyloid degradation mediated by Serratiopeptidase
A transition of amyloidogenic protein by alternative folding pathway under certain conditions leads to the formation of protease resistant amyloid fibrils, having predominantly cross β structure. These amyloids are related to various neurodegenerative diseases and clearance of such amyloids may be a therapeutic approach for amyloid-related diseases. Insulin, that can form amyloids, is widely used as a model amyloidogenic protein for the study of various amyloid related diseases. In this study, insulin amyloids were formed in vitro and the potential of Serratiopeptidase (SP), a fibrinolytic-like serine protease, towards the dissociation of insulin amyloids was explored. The dissociation of the amyloids was demonstrated using in vitro and in vivo using zebrafish model. The amyloid dissociation property was compared with a standard amyloid dissociating enzyme nattokinase (NK). SP shows better amyloid dissociation ability than NK and therefore, SP can be considered as amyloid dissociating agent with potential as a drug candidate for different amyloid related disorders.
Serratiopeptidase: Insights into the therapeutic applications
Serratiopeptidase reduced the disease activity index and prevented colonic shortening, spleen enlargement, glutathione depletion, lipid peroxidation, and nitric oxide production as compared to the control group. Further, there was significant reduction in C-reactive protein level in serratiopeptidase treated mice as compared to control. Moreover, myeloperoxidase, an important enzyme marker of inflammation was reduced by serratiopeptidase treatment. These results confirm the anti-inflammatory potential of serratiopeptidase.
Fibrinolytic: Serratiopeptidase is known to dissolve blood clots and artherosclerotic plaques by breaking down fibrin and other dead or damaged tissue [2]. It can also remove deposits of fatty substances, cholesterol, and cellular waste inside the arteries. The fibrinolytic property of serratiopeptidase may also help with the problems of thick blood, risk of stroke, and thrombophlebitis
There is another use for Serratiopeptidase, but I will introduce the (insane) hypothesis later and the use for it.
Nattokinase: An Oral Antithrombotic Agent for the Prevention of Cardiovascular Disease
Nattokinase is considered to be a safe, powerful, low cost, and all-natural supplement for the treatment of heart and cardiovascular disease [5,6,7]. Animal [3,4,8] and human trials [9,10,11] have demonstrated that NK provides support to the circulatory system by thinning the blood and dissolving blood clots.
Both NK and lumbrokinase (derived from earthworms), unlike most proteins, are more resistant to the highly acidic gastric fluids in the stomach and can be absorbed in the later sections of the digestive tract.
Studies also indicate that NK can ameliorate other diseases such as hypertension [4], stroke [17], Alzheimer’s disease [18], and atherosclerosis [19].
Breaking the vicious loop between inflammation, oxidative stress and coagulation, a novel anti-thrombus insight of nattokinase by inhibiting LPS-induced inflammation and oxidative stress
Highlights
NK protects against LPS-induced AKI via inhibiting inflammation and oxidative stress.
NK inhibits LPS-induced TRL4 and NOX2 activation in macrophages.
NK inhibits inflammation and oxidative stress both in vitro and in vivo.
NK inhibits LPS-induced PAI-I levels, thereby blocking glomerular thrombus in mice.
NK may break the vicious loop between inflammation, oxidative stress and coagulation.
Nattokinase (NK) possesses many beneficial effects on cardiovascular system due to its strong thrombolytic and anticoagulant activities.
…thereby repressing the corresponding ROS production, MAPKs activation, and NF-κB translocation from the cytoplasm to the nucleus, where it mediates the expression of pro-inflammatory mediators, such as TNF-α, IL-6, NO, and PAI-1 in activated macrophage cells.
There are many videos from embalmers going around about the weird, and massive clots in vaccinated people that end up dying. I personally used Serratiopeptidase (serrapeptase), and by chance saw a comment of some lady with an autoimmune disease that basically recover a functional life by taking massive doses.
I took massive doses every other day for 2 months, and many of my followers did the same to varying degrees, and every single one had an increase in benefit and gain.
Fucoidan
Fucoidan is not strictly necessary, but it has amazing properties, it has extensive medical use, and history, and you can easily track down its effects in social media, or even reviews. It can get pretty expensive, especially the good quality ones, so use it only if you can afford it, otherwise, the rest of the stack and the supplement below will do, and do kinda the same.
Fisetin ameliorates oxidative stress, inflammation and apoptosis in diabetic cardiomyopathy
Highlights
Fisetin ameliorates hyperglycemia and dyslipidemia in diabetic rats.
Fisetin prevents hyperglycemia-induced cardiomyopathy in rats.
Fisetin attenuates oxidative stress, inflammation and apoptosis in the diabetic heart.
Fisetin protects against cardiac cell death through reduction of ROS production and caspases activity
Fisetin enhances viability of rat cardiomyocytes following hypoxia/starvation – reoxygenation. It inhibits apoptosis, decreases ROS generation and caspase activation and protects from DNA damage. Interestingly, fisetin also activates genes involved in cell proliferation. Fisetin is thus a highly promising candidate drug with clinical potential to protect from ischemic damage following MI and to overcome IRI.
New Perspectives for Fisetin
Fisetin enhances viability of rat cardiomyocytes following hypoxia/starvation – reoxygenation. It inhibits apoptosis, decreases ROS generation and caspase activation and protects from DNA damage. Interestingly, fisetin also activates genes involved in cell proliferation. Fisetin is thus a highly promising candidate drug with clinical potential to protect from ischemic damage following MI and to overcome IRI.
The anticancer activity of fisetin can be enhanced by some auxiliary substances. For example, fisetin significantly impairs carcinoma cell growth in the presence of ascorbic acid, which results in a 61% inhibition of cell growth, in 72 h
Other activities along this line include: enhancement of the long-term memory, antidepressant effects, inhibition of ischemic reperfusion injury and amelioration of behavioral deficits following a stroke
Immunomodulatory Effects of Flavonoids: Possible Induction of T CD4+ Regulatory Cells Through Suppression of mTOR Pathway Signaling Activity
Some properties of Fisetin include anti-cancer, anti-angiogenic, neuroprotective, neurotrophic, antioxidant, anti-inflammatory, anti-proliferative, and apoptotic effects (76). However, the powerful antioxidant property of Fisetin is due to the presence of phenolic hydroxyl group in the flavonoid structure (77). A few studies have examined the effects of Fisetin on the immune system. Song et al. assessed the immunosuppressive effects of Fisetin against T-cell activation in vitro and in vivo. Findings of this study showed that Fisetin significantly inhibited Th1 and Th2 cytokine production, cell cycle and the ratio of T CD4+/CD8+ cells in vitro. Furthermore, Fisetin suppressed mouse T lymphocytes through the suppression of nuclear factor kappa B activation and nuclear factor of activated T cells signaling in a dose-dependent manner. The in vivo finding showed that Fisetin also inhibited delayed-type hypersensitivity reactions in mice (76). One study on the effects of Fisetin on human mast cells (HMC-1) showed that Fisetin could down-regulate mast cell activation (73). In addition, two studies have reported that the anti-asthma properties of Fisetin are due to reduction of Th2 response as well as suppression of NF-κB (75, 78). In an experimental study using a mouse model of atopic dermatitis (AD), Kim et al. investigated the effects of Fisetin on AD-like clinical symptoms. They showed that Fisetin administration inhibited the infiltration of inflammatory cells including eosinophils, mast cells, and T CD4+ and T CD8+ cells. Furthermore, Fisetin was able to suppress the expression of cytokines and chemokines associated with dermal infiltrates in AD-like skin lesions. In a dose-dependent manner, Fisetin decreased the T CD4+ cell-induced production of interferon-gamma and interleukin-4, and in contrast, increased the anti-inflammatory cytokine such as interleukin-10 (79). Based on these findings, Fisetin is able to significantly affect immune system responses.
Fisetin is one of the strongest and best choices either for fighting a viral infection (SARS-CoV-2), antioxidant, and anti-inflammation, among many other uses. Given all its physiological properties it’s one of the most powerful additions to anyone's “stack’’, especially Long Covid, and given the papers above, jabbed. You should take Fisetin and high doses of C.
In fact, high doses of Vitamin C will solve a lot of this shit, but takes time, when used with other supplements, its turbos charge everything.
The NAD rabbit hole
This one might be a surprise for many, might not. Refer to my Things Hidden Since the Splicing for additional information.
Viral infection as an NAD+ battlefield
From their earliest replication intermediates, coronaviruses elicit an attack on cellular NAD+. Cellular NAD+ becomes a battlefield in which the innate immune system and the virus struggle for the upper hand. Based on preclinical work demonstrating transcriptional upregulation of NAD+-consuming enzymes and particular NAD+ biosynthesis pathways2, early clinical data indicate that NAD+ repletion might constitute an antiviral treatment approach3 that could be generally useful against infectious agents that activate the interferon system. The caveat—as with all approaches targeted to inflammation—is that inflammatory responses are themselves antiviral, although the severe cytokine storm associated with acute and chronic viral disease is considered a pathological overreaction.
Consistent with the view that viral infection leads to a bioenergetic crisis, blood from patients with severe COVID-19 contains lower levels of NAD+ metabolites and higher levels of AMP14. In addition, dysregulation of NAD+ metabolites and AMP in the blood of patients with severe COVID-19 correlates with high circulating levels of the inflammatory cytokines IL-6, IL-10, IL-8, M-CSF and IL-1α14. Notably, inflammatory cytokine gene expression is downstream of PRR engagement and associated with antiviral defenses. However, persistent high-level expression is a sign of severe disease.
Small clinical studies have shown that oral supplementation with the NAD+ precursor NR lowers circulation of inflammatory cytokines in healthy older adults
NAD+ regulates Treg cell fate and promotes allograft survival via a systemic IL-10 production that is CD4+ CD25+ Foxp3+ T cells independent
NAD+ protects against EAE by regulating CD4+ T-cell differentiation
CD4+ T cells are involved in the development of autoimmunity, including multiple sclerosis (MS). Here we show that nicotinamide adenine dinucleotide (NAD+) blocks experimental autoimmune encephalomyelitis (EAE), a mouse model of MS, by inducing immune homeostasis through CD4+IFNγ+IL-10+ T cells and reverses disease progression by restoring tissue integrity via remyelination and neuroregeneration. We show that NAD+ regulates CD4+ T-cell differentiation through tryptophan hydroxylase-1 (Tph1), independently of well-established transcription factors. In the presence of NAD+, the frequency of T-bet−/− CD4+IFNγ+ T cells was twofold higher than wild-type CD4+ T cells cultured in conventional T helper 1 polarizing conditions. Our findings unravel a new pathway orchestrating CD4+ T-cell differentiation and demonstrate that NAD+ may serve as a powerful therapeutic agent for the treatment of autoimmune and other diseases.
This one is more symptom based than a stay-in-the-stack. There is a hypothesis (it’s more of a theory, but let us just say it’s just a hypothesis) of nutrient storage and availability inside each person, after an accident, infection, or stress, genes are activated, and resources are used. This is paramount to understanding both viral infections, especially SARS ones, and the vaccine. Which isn’t a single "infection mimicking” event, but a literal cluster of antigen presentation of different pathogens.
I could spend literally days writing about the use of NAD+, and there are clinical trials using NAD+ supplements going on right now aimed at Long Covid. LC in my opinion is long-term, consistent, low-grade inflammation with low-grade immune dysfunction, among many other variables, the main drivers of said variables are the first two. And the paradoxical dysfunction many of the jabs develop is similar to LC but absurdly faster.
When we were researching the Reverse hypothesis I found many, many immuno-compromised and LC people on social media, who shared their tests, and values and talked about progression. The vast majority of them had to worsen of their symptoms, the answer should be obvious.
I personally take Niacin every day from 250 mg to 500 mg, and it has helped me with many symptoms of things besides post-SARS-CoV-2 infection. You can use the more expensive, and direct form of NAD+ booster, Nicotinamide Mononucleotide or Riboside. Or refer to my Things Hidden Part III.
One final note, there is one thing that every single jabbed, and in fact, every single person could do to help them recover from vaccine dysfunction, post-viral infection, or anything else.
Fasting.
That is what a ketogenic diet actually is, from a metabolic perspective, when you fast, your body turns on autophagy to eleven, and your bloodstream is flooded with endogenous ketones, especially BHB.
You should start small, with 1 day fast, and build up to a 3-day fast every 6 weeks, this will be extremely helpful.
Start exercising, and lifting weights when, if able to, start small, start slow. Fasting and exercise are a must, especially when you start recovering.
For actual damage, in relation to organ damage you need to read this one, I will add another peptide later, if you want to check it out before I do (might take a while) the name is TB-500.
Treat vaccine dysfunction, symptom-based if you are a doctor. You can make sense of symptoms and which supplement on this list will help with said symptom.
There are many other supplements you can use, plants, etc, but for now, these are the main ones, I might add more later.
If you can convince, or want to try to get tests out of pocket, a cytokine panel would be ideal, these are the main ones, and more helpful. (To me at least…)
IL-12
IFN-gamma
sCD40l
VIGF
TNF Alpha
IL-17 IL-23 (only on suspicion of some immune-related disease)
CD4, CD8 and CD4/CD8 ratio
And the main one is
TH1, TH2, TH17
For neurological symptoms, check this post, at the end of it I wrote the following.
For massive cognitive enhancements and healing, this is the best stack me and a friend came up with. The more “fucked up” your brain is the better its effect, for God knows why.
Morning - 150 mg of Thiamine (this one takes longer to see its sole benefits, stick to it)
Lunch - with your biggest meal
N Acetyl Cysteine 600 mg to 1200 mg
Piracetam 400 to 800 mg
Gingko Biloba - 40 mg+
NAC and Piracetam have a synergetic effect together, but there is something that truly pushes beyond what modern science thinks is possible with both, and I have seen this stack bring back people with mild levels of dementia to “I feel 40 something again” after weeks. The more fucked up your brain, the strong the effects.
When a said stack is taken with the following… drink, you turbocharge the effects of Piracetam, its effects on cell permeability, its antioxidants and neurocognitive enhancing properties, and by default, enhances NAC.
That something is a drink that contains phenylalanine, which has a side effect as being a mild calcium blocker, which does what I described earlier. Test it yourself, especially if jabbed or some neuro-cognitive issue.
Hope it helps people, subscribe if you want to.
I work with clients with all manner of health issues and for the greater majority gene treatment is in the mix but getting them to see the link is difficult. Their heads don’t quite compute. I have yet to work with an overtly damaged client although I might have 2 soon. Have seen plenty with Covid or Covid like illness. Work melatonin, NAC etc in to many programs. Will read through all the references, it’s the references that make this pure gold. All the articles of yours really stimulate the mind. I think at this point in basically an information war it’s important to thank those speaking out and sharing their research, these are weapons against the medical fascism we are fighting. Or the medical fascism that’s disguising the economic collapse whichever way you look at it.
I’ve only read the first section or so but I need to say thank you so much for this article, it’s a beast and a treasure trove of research.