Prions: One Of These Things Is Not Like The Others

A surprising development constitutes some unexpectedly good news.

Among the many terrible gain-of-function insertions to call SARS-CoV-2 home, the worst has long been - by some, anyhow - thought to be the inclusion of prionic domains in the spike protein, which would, hypothetically, set every one of us who suffered an infection, or received an mRNA hot shot, on a potentially decades-long, irreversible, and incurable path towards eventually fatal neurodegeneration and death. I have personally been concerned about it, and had been working on it, since March 18th, 2021, and made some good, albeit limited progress over time, with an unfortunate false start and a lot of difficulty along the way. While I wasn’t the first - I believe Dr. Kevin McCairn (not to be confused with Dr. McKernan, who recently sequenced SV40 DNA in the mRNA shots) rightly deserves that distinction, for his very early work on this - I was still pretty early, and it’s been a point of interest and investigation for me for quite some time. It has since been confirmed by NIH-affiliated scientists, and while there’s no planet on which ubiquitous exposure to a prion protein could be considered good news, there is in fact a saving grace which, in my opinion, makes this particular prion disease far less dangerous than initially thought.

Let’s dig into that.

Protein Folding

Every cell in our bodies, and a great number of the smaller components which are found both inside and outside of those cells, is made of proteins in various capacities. They are chains of amino acid molecules, organized and bound together in helices, sheets, turns, and coils, by the ribosomes which read the mRNA produced from our DNA. Not dissimilarly to a 3D printer, the ribosome uses the mRNA to determine the order in which amino acids are to be attached to the strand of protein being output; consider it a printer head, which is constantly changing material within the same stream of material. Every bond between the different amino acids exhibits different physical properties; these properties inform the strength, direction and orientation of their binding to the neighboring amino acids. Imagine a 3D printer outputting a stream of hot plastic; if not properly calibrated, that plastic will bend, loop, curve, and (only occasionally!) produce the straight line that you actually wanted from it.

Well, that wasn’t supposed to happen. Does look a lot like a protein, though! Source

Proteins are formed in the same way: upon being output, they fold into a practically limitless array of different conformations. This process is so complex, operating purely based on the various laws of physics which dictate the attraction and repulsion of atoms and molecules, that even in our modern era, it still takes massive computing resources to brute-force search through every possible permutation until the correct one is identified. This process, and also, separately, the computational work that goes into predicting it, is known as protein folding. Despite the infinite complexity of this process, our DNA has evolved, by trial and error, to (almost) always produce proteins in such a way as to create perfectly formed proteins.

Imagine trying to build a clockwork wristwatch, comprised of so many perfectly calibrated cogs, bars, springs and screws, one part at a time, with only the meandering, ostensibly random coils of a partially clogged 3D printer head to do it. That’s what our ribosomes are doing, all day every day.

Artist’s impression of ribosomal protein folding. Direct observations have also been made.

When It Goes Wrong

Of course, this process is, whilst nearly perfect, not entirely perfect. With such a complex system, occasional errors are to be expected. For this reason, we have a number of other proteins - that hopefully were formed correctly! - that stand guard and act as the quality control. Some, like the chaperones, which I covered in the article on cancer, will take a misfolded protein and attempt to re-fold it into its proper conformation. Others will simply destroy and recycle the base amino acid components of a misfolded protein. However, they are both imperfect and a double edged sword. Overactivity can result in the preservation of an extensively mutated cell’s proteins and permit a cancer cell to survive; and the evolution of protease-resistant misfolded proteins are a causative factor of numerous neurodegenerative diseases. They can’t, and don’t, do everything; some proteins can neither be reformed nor destroyed. Those proteins, rather than going off to live their lives as the cogs in the machine they were supposed to be, end up accumulating in piles of garbage, better known as plaques, both interfering with the proper functioning of various bodily systems and, by virtue of their absence, degrading the functionality of whichever system they were supposed to be part of. This is a major factor in Alzheimer’s disease, which I touched on in the very first article I ever published to Substack, among others.

However, these are still not prions.

When It Goes Really Wrong

A misfolded protein is bad enough; a misfolded protein will fail to perform its duty, and some will aggregate together to form a garbage heap, whether inside or outside of a cell, interfering in the ordinary operation of the microbiological machinery that keeps us ticking. However, it gets worse. Here, we come to prions.

A prion is a misfolded protein, just like the others. However, it is a misfolded protein which also causes other, properly folded proteins to become misfolded. Think of a prion protein like the pink-haired, trans-ally, elementary school math teacher; not only is it failing to teach the kids their math lesson, it’s dimming the lights and making the kids watch a video on how you too can become a eunuch, and expounding at length on how beautiful and normal that is. Not every protein is vulnerable. The teacher in this scenario is the prion seed. When a vulnerable, properly folded protein comes into contact with the prionic protein, the seed protein causes conformational changes to it, converting it into a similarly infectious shape. The best example of this is the eponymously named prion protein. In the proper, natural conformation, PrPC, it is an important cog in the brain’s machinery, thought to aid in cell signaling, protecting neurons, and facilitating synaptic plasticity. However, upon exposure to the misfolded form, PrPSC, the healthy PrPC changes its conformation, and becomes the prionic PrPSC form; having lost its original shape, it is no longer capable of performing its natural function, and instead begins adhering to a cell membrane, forming a disruptive plaque. Any healthy PrPC protein that is unfortunate enough to come into contact with the PrPSC protein will be converted into PrPSC. Eventually, the plaque reaches a critical mass, and instead of further aggregating into the plaque, they begin to instead form long fibrils, growing out from the plaque and dramatically increasing the surface area by which healthy proteins may be “infected.” At this stage, the plaques begin growing everywhere, significantly damaging and destroying brain tissue, and causing the symptomatic phase of such diseases as Creutzfeld-Jakob Disease, also known as CJD or mad cow disease, Kuru, and other similar ailments.

This process, at every stage, but especially the final fibrillization phase, is universally accepted to be incurable, and inevitably fatal, and usually in relatively short order upon presentation of symptoms. With the observation that the spike protein was exhibiting prion-like behavior, made so long ago and with extremely limited, but nonetheless convincing evidence, this was reasonably presumed to be the likely process that would be followed, and the inevitable outcome.

Healthy vs misfolded prion protein. Source

Now we know more, and amazingly, it’s actually much better news than I think anybody expected.

Spike-Prion Work Over The Years

Throughout the early work on this issue, there were many areas of uncertainty. Exactly which regions of the spike are supposed to be acting in this way? Which other proteins are they actually infecting and causing to become misfolded? How long should we expect the latent phase of the disease, wherein the prionic proteins are aggregating but not yet causing symptoms, to last, as opposed to the active, symptomatic and fatal phase? In my article, dated July of 2021, I proposed that the PrP may be affected, and speculated that a zombie apocalypse may eventuate. There are a number of other proteins known to exhibit amyloidogenic activity; tau, TDP-43, α-synuclein and PrP among them, all of which aggregate for different reasons, in different locations, and cause different issues.

I also took the step of soliciting and aggregating data on people who had developed symptoms of, obtained a diagnosis of, and/or died of Creutzfeld-Jakob-like symptoms, at various time intervals after their receipt of the spike-encoding mRNA vaccines, alongside early research work into potentially useful therapeutics. The results were very concerning, and helped to initiate broader research efforts by various individuals across the world. In sum, I collected data on approximately 60 cases. All of them demonstrated symptomatic onset between 7 to 30 days after the mRNA shots. There were questions about the brand of vaccine; they were heavily weighted towards Pfizer. There were also questions about whether it was simply background noise; while it is extremely rare, occurring in about 1 in a million people, there are many millions of people in the world, and while that dataset did not, very strictly speaking, exceed the background rate, it was definitely significant enough, alongside the temporal correlation to mRNA administration, to warrant a closer look.

My raw data on prion disease and death contemporaneous with vaccination, collected via self-reporting, in late 2021.

Unfortunately, the work was, temporarily, shelved, later in 2021. Unlike many these days, I do not approach a topic with a pre-determined answer, and then set out to massage the data to elicit a proof. Considering the heavy slant of the data towards the Pfizer shots, we found another, very plausible explanation: a footnote, at the bottom of an EU document relating to its approval, stated that due to their use of processed animal fats, primarily cows, to produce the lipid nanoparticles within which the mRNA is encased for administration, they acknowledged the possibility of prion protein contamination stemming from the processing of those animal tissues. It was also not yet established that approximately only 5% of the administered mRNA shots are actually active, with the remainder being partially or completely inactivated due to either storage concerns, or something perhaps more nefarious, and thus not actually capable of causing spike mRNA production.

In summary, the EU acknowledgement that a number of Pfizer batches may exhibit prion protein contamination, considered alongside the facts that the small number of cases linked to other brands certainly did not exceed the background rate, the yet-unknown even further diminishing of the disease rate due to the “hot shot” batch differentials, and the complete absence of any such reports connectable only to infection by the SARS-CoV-2 virus, it appeared that sufficiently strong evidence simply wasn’t there to firmly draw a connection between the spike and the observed prion diseases; the far more likely explanation was prion protein contamination of a very few Pfizer batches, and purely coincidental cases of people who happened to receive a vaccine of a different brand, the rate of which was well within the expected background rate.

Accordingly, I announced my findings, and, at least for a time, that was that; while this conclusion was tentatively agreed to be plausible by others who were also looking into it, not everybody was convinced, and fortunately, some theoretical research work went on.

Fast-forwarding 12 months to the beginning of this year, and those initial findings - specifically, the emergence of a new form of Creutzfeld-Jakob disease, noted to be affecting people shortly after having received mRNA vaccinations - have now been observed elsewhere, confirmed, and written up in a published study by Dr. Jean-Claude Perez et al. While unsettling, the samples are still just too small to firmly draw a conclusion, especially a wide-ranging one, such that every person who received a vaccine, or every person infected by SARS-CoV-2, should be looking forwards to an unfortunate, if long delayed, eventual expiration via prion-induced neurodegeneration. It certainly seemed that way to me; if the spike itself is the prion protein of concern, how could it not?

I will make note at this point that Omicron was a very strange emergence. First characterized in South Africa, it derived directly from the Alpha lineage. Before Omicron, there was Delta, and a long line of variants before it; the emergence of that virus, at that time, is something akin to an ancient zombie virus being discovered in the Siberian permafrosts. It just shouldn’t happen. Nevertheless, it did happen, and it came with a number of notable elements: particularly of relevance here is the absence of the inserted HIV residues (specifically, G142D/Δ143-145, within the 136-150 gp120 domain) which were among those on the spike expected to exhibit prionic activity. It sure seems like somebody took SARS-CoV-2, removed the very worst gain-of-function elements, improved the transmissibility whilst decreasing the virulence, and set it loose on the world to replace the escalatingly dangerous Delta variant.

If that is in fact what happened - of course there is no particular evidence of that, beyond a circumstantial look at the bigger picture, and how such a release might have factored into the geopolitical machinations taking place in the broad context of this pandemic - then we probably owe the responsible party some thanks. It is due to those modifications, specifically to the gp120 region, that every time somebody asks me whether it’s just the shots, or also exposure to the virus, that puts people at risk for prion disease, I will tell you that it is any of:

• People who received a hot shot (ie the 5% of the batches causing adverse events)

• People infected with any variant of SARS-CoV-2 prior to Omicron.

I count myself among the latter, having been infected early in March of 2020, and having reached a point of severe pneumonia, as well as some eye-opening neurological effects, before both discovering and then successfully using first ascorbic acid to hold it at bay, and then ivermectin to finally and fully cure it. However, the possibility of the presence of a slow-burning prion infection has been on my mind for years now.

So, that’s the (relatively) short version of the various types and locations of work that have been happening on the prion disease front over time. I could discuss the lab - but all I really have to say about that at this point is that I hope failure builds character. Since funding the development & readying of a non-invasive prion blood test, and the lab to provide it, as opposed to the invasive, dangerous, painful and standard spinal tap, I have had several false starts insofar as my desire to begin conducting broad, indiscriminate, population-level testing. Such testing and information would be able to tell us, once and for all, if we are in fact facing a latent, widespread prion pandemic. Alas, if it is to eventually be done, it doesn’t really seem at this point like I’m the one that is going to do it. It’s still there, gathering dust. Maybe one day it’ll be put to use.

The Good News

I did promise good news, didn’t I? It’s probably about time to get into that.

There is not, ordinarily, a whole lot of good news to be had concerning prion diseases. There have only been a very few, vanishingly rare cases in which a prion infection has been cured; whether by pure chance, or remission, or misdiagnosis, there have not been enough cases to say with any certainty. Let’s go back to the watch analogy; the entire watch body is made of steel, or aluminum, or whatever it is that they make watches out of these days; likewise, the components are made of the same parts. Take that watch, and start growing a little pile of metal within it; now you have a little pile of metal in the corner, not yet interfering with its operation, but ever so steadily growing. If you try to dissolve it, it’s going to destroy the rest of it; if you let it continue growing, it’s going to destroy the watch; and by the time anybody notices the gears aren’t turning properly, the cogs look more like blobs, and there’s really no salvaging it anymore. There is very little good news when it comes to prion diseases.

“But Adam,” they ask, “Surely they wouldn’t release a bioweapon without themselves having the cure, right? There must be one!” Considering how clearly premeditated this all is - and the fact that the people aiding and abetting this biowarfare have also themselves been, if not exposed to the real “vaccines,” at least infected with various strains of the virus - it’s a valid question, and one I have not, until now, been able to answer.

We still need a little more background before we get to that good news, though.

The Prion-Like Domains

The SARS-CoV-2 S protein has several prion-like domains. While initially it was thought that the addition of the HIV gp120 protein should have been primarily, or even solely responsible, we now have a firm identification of these domains. So, that’s great - but why is it good news?

Prionic proteins usually affect only other proteins that are just like them, although in some cases, such as Alzheimer’s disease, the downstream effects can, directly or indirectly, cause aggregation of other proteins. An outstanding question was, for some time - exactly which protein(s) can the spike actually turn into misfolded prion proteins? Is it tau? Perhaps TDP-43? PrPC?

Well, it binds to all of them.

Amyloidogenic spike binding resides. Click to expand. Nyström, S., & Hammarström, P. (2022). Amyloidogenesis of SARS-COV-2 spike protein. Journal of the American Chemical Society, 144(20), 8945–8950. https://doi.org/10.1021/jacs.2c03925

These residues on the spike bind to the many and varied amyloidogenic proteins, and those amyloid plaques begin to aggregate. Considering this action, in combination with the spike-mediated activation of platelets, heparin amyloidogenesis, and the trillions upon trillions of spikes delivered by one of those relatively rare, functional mRNA shots…

…and I think we just might have an answer as to where these come from:

Source (sorry)

There is no further evidence, that I’m aware of, yet, that there is any subsequent growth or actual prion seeding taking place; those proteins bind to the spike, and that’s the end of it. The more spikes, the more binding, but it doesn’t appear to be actually modifying any of them to turn them into prion seeds. So, what we essentially have here is, instead of a silently cascading apocalypse, buried deep inside parts of the brain that we will never reach, we likely, instead, have these long, stringy, vein-shaped agglomerations of the various amyloid proteins, binding together wherever they meet, and apparently at least somewhat resistant to being broken down by the body’s natural processes for dealing with such eventualities.

So, that’s the first part of the good news: unless something’s been missed - which I would be able to tell, if I had a lab, but nevertheless - it seems like the zombie apocalypse should be off. If there is no secondary activation of different prion proteins, then all this is going to do is cause circulatory issues, blood clots, heart attacks, strokes and pulmonary embolisms among those unfortunate and/or short-sighted enough to have taken the COVID vaccines. Note that this also applies equally to the adenovirus vectors, the subunit protein vaccines like Novavax, and generally anything that’s deploying large numbers of spike proteins. The more, the worse - but, if it hasn’t killed you yet, or done irreversible damage to one’s heart via myocarditis, or caused IgG4 immune tolerance of SARS-CoV-2, or pervasive damage to the circulatory system, or ….

Fine, it’s still pretty grim for the vaxxies. Long, long ways to go until they won’t be perennially worrying about whether bringing in some heavy groceries will be their last act on this fair Earth. However, that is not the only good news.

The Really Good News

Now, we should all be clear that proteins are, chemically speaking, simply chains of molecules. For one protein to cause some action or effect on another, it generally must fit into a well-matching receptor site, whether it is a purpose-made receptor, or in the case of the spike proteins, a region that (perhaps) coincidentally just happens to fit. When something gets in the way, whether it’s a neutralizing antibody or a chemical of some description, the protein loses its ability, at that site, to bind to other proteins and cause whatever effect it is going to cause.

It has been known for quite some time that, amongst its many, many, many and varied other modes of action, ivermectin binds directly to the spike protein itself. Specifically, within the receptor binding domain, at the L91 residue. This interaction is useful for preventing the interaction between the spike protein and the ACE2 receptor, as the ivermectin molecule physically places itself in the way; if the spike is a key to the receptor’s lock, then ivermectin would be a big chunk of debris attached to the top, preventing the key from ever entering the keyhole.

Guess what else it is, thusly, useful for?

Preventing the amyloidogenic aggregations to the spike protein!

The spike is not like a typical prion, which is why the wording has been “Prion-Like Domain.” It is like a prion protein, insofar as it has the capability to bind to other proteins - specifically, itself - to form plaques, and this mechanism may also be of relevance to the long, stringy, proteinaceous blood clots that have been occasionally reported. Just as with this recent, and alarming if true reporting of SV40 DNA being identified in the shots - I would like to see some reproducibility, a second or third or fourth test from another source that can independently corroborate it. Once is happenstance, twice is coincidence, and three times is a pattern; to my knowledge, we’re sitting at one report right now. There have also been reports of graphene nanobots, alien squids, and various other contaminants, which needless to say have not been credibly corroborated. The shots alone are quite bad enough without inventing fanciful and quite obviously false BS.

With that said, it is also, however, unlike a prion protein, in that there is no misfolding or conformational change either caused, or necessary, to facilitate this binding action. Instead of an infection-like change upon contact, and a newly recognizable conformation of the spike, this interaction is much more akin to a couple of Velcro pads on either protein: the key fits the lock, and if they interact, they bind together. That simplifies the problem: just keep them from interacting, and you’re not going to have any formation of proteinaceous aggregates taking place. This should, in theory, apply equally to both the virus and the vaccine.

Therapeutics

Considering the fact that the vast majority of us have likely been repeatedly exposed to the virus over time - not to even get into the poor fools taking booster after booster - there is likely some degree of aggregation having already taken place. This work is closely related to the ALS work I was pursuing; these same protein aggregates, albeit through very different methods, are also observed and are likely at least partially responsible for the signs and symptoms of the various well-known neurodegenerative diseases. A number of relevant investigational therapeutics are noted in the very first article I published on Substack, here; separately, an exploration of serrapeptase, a proteolytic enzyme which may also be of some use. Quercetin has been noted to be of particular use insofar as disaggregation. Consider a rope, made of many thin strands of fiber; if you take a pair of scissors to it, it’s going to be pretty slow going, but if you first separate those strands, you’ll get a whole lot further, a whole lot faster. Methylene blue is another candidate, as is resveratrol, found in red wine, which has a very broad range of useful actions. I have to imagine that at least a large part of the reason there has been so little progress on these neurodegenerative diseases is your run-of-the-mill pharma and charity corruption; if they actually solved the problem, there wouldn’t be any reason for them to fundraise anymore.

So, we have yet another application for ivermectin.

I’ve said it before, and I’ll say it again: the more you look at ivermectin, the more you will find. Ivermectin is, without a shadow of a doubt at this point, a true miracle drug: with so many applications, from antiviral, to cancer treatment, to anti-inflammatory, and of course in its originally recognized anti-parasitic application, there should be little wonder why the powers that be have done their best to diminish it as “horse paste.” Whether it may be of any utility insofar as disaggregating already assembled plaques is a question I cannot answer, but it should (pending some experimental validation, which is probably never going to come) prevent such aggregation from initiating or continuing.

Brain fog

It’s also worth noting that, regarding the various degrees brain fog that many have experienced post-covid, a very unscientific poll I conducted on Twitter regarding brain fog found 80% reporting that a single, low dose of ivermectin - typically 150mcg/kg - had significantly improved their condition, in apparently short order. That may or may not be related to this functionality, or it may be yet another undiscovered application - but it’s definitely worth a footnote. Even with as much as we know now, there’s still a lot to learn. It is certainly conceivable that there may be some degree of disaggregatory effect.

Wrapping up…

I certainly did not plan to be writing just one single article over a month.

I still have a few pieces I’ve promised that will be forthcoming - aging, and vascular health in light of covid, are at the top of that list, as well as the eventual followup on East Palestine. (Regarding East Palestine, there is now an article published to PubMed, saying pretty much exactly what I had said, albeit a couple of months too late to actually help anybody get out in time.) Generally speaking, though, $7 really isn’t going as far as it did even six months ago, thanks largely to Brandon and our spineless Congress printing themselves up never-ending trillions of dollars - and between the general Twitter shadowbanning, and the Substack shadowbanning on top of that, I have been having to spend less time writing and more time elsewhere to just be able to get by. If you would like to see more frequent, more informative, and - well, let’s be honest, better - writing, consider becoming a paid subscriber. Until Substack and Twitter resolve their differences - if ever - they have made it very difficult to continue putting as much time into it as once I was. For those of you who are, it is greatly appreciated, as is your patience with the rather dramatically reduced volume lately, and I hope you can stick with us. Hopefully this will be just a temporary setback. Also, the public metrics are apparently rather misleading: ~95% of y’all are free subscribers. We are not rich.

I’m also thinking about writing a criticism of Peter Hotez, his refusal to debate his conclusions and ostensibly sincerely held convictions, and the terrible impact this is going to have (and already has had) on the credibility and accuracy of the scientific method itself. We have, for some time, been told to just trust the science - which has, in practice, really meant trusting the scientists, like Fauci, like Andrew Hill, and like so many others whose conclusions are drawn not from an honest analysis of their work, but the imaginations and vested interests of whoever is lining their pockets. Moving forward from that era is starting to expose some of these people for what they really are; if we are to take their lead, then will we not simply be conducting science not by trial, error, and analysis, but by assertion and popular opinion? If I told you that everyone who took an mRNA vaccine was going to drop dead tomorrow, you might endorse that opinion, you might feel vindicated, and you might go tell others as much, and then they would do similarly. That might make me popular (until tomorrow, at least, unless I had a fawning media complex to clear it all up for me) - but would it be right?

Of course not. The lessons of Galileo are still as relevant today as ever. Science is supposed to be open; it is supposed to be questionable, falsifiable, and replicable; and now that this choice has been given to us, we should absolutely not stand for the kind of opaqueness that Hotez is telling us we should all just accept. If you have a position on something, and thousands or millions of people are taking your word for it and acting accordingly - especially if you have been telling them to take an experimental injection that has killed and maimed millions at this point - then you should be ready and willing to defend that position, and forsake it if you are proven wrong. I hold myself to that standard, and I expect nothing less of anyone else.

I have also been considering changing it up a little, and publishing short news updates on the health freedom movement, and the sprawling, many-faceted effort it has become over the years, in addition to these longer pieces. There’s been a lot of progress, on a lot of fronts, and more comes regularly as the world continues waking up. Let me know if you have any thoughts on that in the comments.

Thank you for reading, thank you for supporting us, and see you on Twitter!