When it comes to falsifying the Germ Theory, I have always been acutely aware that as much as the Control Experiments run by The Virology Control Studies Project are incredibly necessary to prove the fraud of Isolation and hence all of the downstream methods of claimed evidence of “Viral” existence, it is not the easiest of things to understand entering into this subject. You have to have a good grasp of Laboratory techniques, be able to read and understand scientific jargon/lingo designed to confuse the Layman. More to the point even at the end of the Experimentation process that shows conclusively that Viruses do not exist, it still leaves the door open for pathogenic bacteria and parasites to cause claimed Contagious spread of diseases.

What the documentation of the Contagion studies through history demonstrates is that; it is irrelevant what is claimed on a Microbiological level to infect the fluid of sick people, if that fluid cannot produce the identical symptoms of disease when introduced through natural pathways, then the theory of Contagious spread of disease is falsified. It doesn’t matter whether something exists like Bacteria or Parasites, if you introduce them to healthy people and they do not get sick and you do this repeatedly, this is absolute proof they are not causing disease and hence all downstream preventions and drugs are unnecessary.

I consider the Contagion studies to be the ultimate proof of the topic that I write about, it was indeed the way that I found out about the fraud of Germ Theory and that information is the reason why I am sat here now. So I have always felt some sort of duty to document the complete list, leaving no stone unturned, to give the 360 picture of the fraud of Germ Theory according to their own authoritative sources of Peer Reviewed and Published literature.

Now, I wrote “my” version of this in the tone that I have become to be known as writing, with swear words, colloquialisms, memes and loose terminology. I have outlined why I do this on many occasions; firstly because I don’t want to be an authority source, I think it is unhelpful to divert your thinking to anyone else, or centralize around a figurehead as it is easy then for the State to stop - remove the figurehead. Secondly, this is just the way I think, I sit and type the thoughts that come to me, very little else “curates” my language so that you know or at least should be able to tell that I am trying to be as truthful as possible.

When it comes to my writing here on Substack, I cover a large area of Science, theoretical and experimental, from the political angle, to the absurd and illogical. Subscribers and readers have become used to the way that I express my feelings and the format of me… just banging my head against the keyboard… I feel truly blessed that you all have let me do that and engaged with what I have written and and have given me the flexibility to be free with what I write.

However, when it comes to this most crucial information, the information that is not mine, that is so deserving of exposure in raising awareness on this topic- I think it of utmost importance to remove my “character” as much as possible from it, to focus attention on the information presented. So when Unbekoming reached out to me and suggested that it would be great to work together to frame these Contagion studies in the aforementioned light I jumped at the chance.

The second thing that I had always felt when it comes to changing as many minds as possible on the topic- the task I have somewhat given myself, or fallen into, is the medium in which that takes place. I am acutely aware through experience that the digital panopticon run by the State and Big Pharma, limit my and by extension your reach of this information on Social Media. Despite there being data trackers claiming to show “views”, “readership” and “Restacks” if you have no idea of who that goes to or how that lands on the other side of the digital messaging service then you are relatively blind to its effects past just sheer numbers on a screen. By extension you get very little “real world” feedback other than the numbers on the screen. Although I have made friends, work colleagues and partners from doing what I do online, I think this is largely due to a shared interest to start off with, rather than necessarily the information I have showed them has changed minds.

The positives with the digital realm is that you can, in theory, reach a wider audience, but it is more of a scattergun approach. The negatives are is that it really doesn’t work as well with those closer to home. With family and friends it is more often than not an instant “invitation to ignore” a topic for debate when someone starts a conversation with “I read on Social Media”, or “someone who I follow on Twitter” indeed practically any mention of the Medium of “T’internet” is a Willy Wonka Golden ticket to “You are a Conspiracy Theorist” Town.

That is why I have always wanted to present this most crucial information, the gateway to understanding the entire Germ Theory Fraud in physical print. To have a book on the coffee table is a much more, dare I say it “respectable” source for proposing an “Ice Breaker” to friends and family, it is much easier to approach a subject, when the information is at hand right in front of you, where you can touch it and where you can feel it. Instead of saying “ hold on whilst I find the tweet”, you pass across the book and let them have a look.

Myself and shared this exact outlook and so I was overjoyed to work with them in Co-Authoring this book and publishing it in physical copy. We worked together to make the huge list of Contagion Studies easy to navigate. They are listed chronologically in the main catalog, but there is also an “Index of Diseases” at the front of the book that groups the studies by the specific disease each one tests — measles, polio, chickenpox, whooping cough, cholera, HIV, and so on — under three headings: “What medicine calls Viruses,” ” What medicine calls Bacteria,” and “What medicine calls Parasites.” Whenever someone comes to this material and asks “so what about chickenpox?” or “what about polio” — you can now open the book, look up the disease, and jump straight to the studies. That was the plan. With this in mind we have aimed this Printed physical copy to be THE introductory manual to understanding the fraud of Germ Theory.

has done a tireless job editing and formatting my original, grammatically error strewn, sweary informal verbiage into a much more palatable and pleasing on the eye and ear text. They have added their own viewpoints, huge amounts of additional referenced material and combined it with an equally important part “If not a Virus then how do we get sick/see patterns of disease”. This book we hope, should answer every single doubt and question on the topic of the Fraud of Germ theory in an easy to understand, inviting and comfortable way.

The two full-length case appendices developed for this edition — one on the connection between polio and the arsenic-DDT pesticide era, 1869 to 1960, and one on the 1918 flu covering both the chemical warfare of the First World War and the Rockefeller Institute’s meningitis vaccine trial at Camp Funston — give the reader the “what actually happened” answer for the two most-cited epidemics in the germ theory record: a documented pesticide poisoning sold as a virus, and a wartime combination of chemical exposure and mass military inoculation sold as a pandemic.

So we are delighted to announce that the book “No Contagion” is available to buy now from here: Buy the Book . Please click on the link or the image of the Book cover at the top, both take you through to the publishing website.

It has a very quick lead time of just 3-5 business days and ships to most countries worldwide.

Many thanks.

Jamie

1. This is a long article at over 125 pages that has taken years of research, more to this point is that whenever I have written longer articles like this with very deep research, Substack tend to Shadowban it, so having it free and open when it first goes out does me no help in just getting exposure (despite having 19k Subscribers).

2. I have quite a few paid for subscribers (thank you!) I am acutely aware that despite many big things going on behind the scenes there is not much you are seemingly seeing for your paid subscription, so early access can feel like it is a bit of a perk.

3. This will be going up as an Ebook on Shadowbanned Library for just a few dollars, if you really can’t wait you can buy the book over there. Here is a Discount code for all Substack subscribers, click there or on the image below or just use code “MULLIS” at the checkout.

I don’t really hate anyone, certainly not in my “real life” away from the Virology Control Studies Project. There are people whom I think are evil, the main characters involved with the machinations of 2020 are an obvious group of candidates, but ultimately what are you going to do about it? There comes a point where harboring hate for people, you will likely never meet, is just wasted energy. I am sure there is also some truth to them harnessing negative energy, at the very least, if you look at it through the eyes of a marketing exercise for the State and Big Pharma- “There is no such thing as bad publicity”. This is how controlled opposition and the beast system operate; they incentivize bad publicity by writing algorithms that benefit clickbait, ragebait, misinformation and cat videos. Anybody that wants to make a name for themselves has to essentially subsume an identity that is to be a purveyor of at least one of the seven deadly sins.

Given this, I tend not pay these fuckers much attention other than poking fun in their general direction, and like to focus on the “factual” underpinnings of their cult scam. However, when it comes to Kary Mullis, I hold a particularly dear part of my psyche dedicated to hating on this odious, self aggrandizing, sellout, fake, fraud, drug addled, arrogant, murderous, lying, shit stain. This was not a grudge that was developed overnight of course, I remain true to my statements above that I don’t tend to wear burdens that belong to other people, no, this was a long drawn out process of the realization of the actual damage done by this fraud, and in my opinion the summation of it would likely be far worse than all of the characters of 2020 put together. You see, what I feel viscerally about this particular character, this pretender, this Broadway villain twiddling his moustache was the fact that Kary was not cast as the Villain, far from it, he was painted as a Saint, a freedom warrior who stood up to the beast system, a brave dissident who was Martyred in 2019, waxed by the all powerful, so they could usher in 2020.

This is what really gets under my skin, as for the real fiat system of exchange I deal with in this life, as part of The Virology Control Studies Project is: Truth. Money is a means to an ends, it is good to have affirmation and the flexibility to carry out experiments with financial backing but ultimately this is just a stepping stone for the actual Fungible Token that is “The Truth” ( Or what seems like the truth to me- insert metaphysical wafflings). The reason why the story of Kary Mullis irks me so much is because it was one giant lie, the claim that he was a dissident against the beast system, the claim that his invention was not intended for “diagnosing disease”, the fact that his invention could be used for anything he claimed, likely the fact that he even invented PCR is a mountain of lies.

It is for that reason that when we take the current theatrics occurring with Anthony Fauci that I extra don’t care. His “no comments” are particularly puerile, of course, the orchestrated 2 minutes of hate are well justified. For when Josh Hawley asks basic questions such as; “what colour tie are you wearing?”, most honest people would at least break legalistic 5th pleading to show that you had a basic amount of humanity in return. But in this episode of The State-The Musical it is a carefully choreographed dance to entice you to froth at the mouth, to boo and hiss, to mock and jeer at the Abanazar villain. Quite simply they have elevated his caricature to Mainstream levels of “Bad Guy” by implying that he is dishonest in not answering basic questions. The “AntiVaxxers” who have called for his Guillotining since 2020 are vindicated and there has been a new vein of recruits, the Statist Conservative Overton Window Lickers can now murmur and grumble in this vague direction; “Poor Form”. It was as easy as that and we see that when we peel back the onion skin of deceit we can agree that everyone’s judge of character is largely determined by their perceived honesty.

That is why if you put these two characters, Mullis and Fauci, in a dock together and put them on trial for who is the biggest most murderous fucking dildo, out of the two of them, I am picking Mullis, hands down every day of the week. For as we have clarified above, when the discernable token for deciding the content of someone’s character is predicated on their honesty, at the very least Fauci has stuck to his guns and taken responsibility for his backing of political murder: He has always remained that he has championed and supported the use of AZT and Vaccines and Remdesivir and the entire arsenal of weapons used to murder people, under the guise of treating non existent pathogens. For in the war of truth you see that actually Fauci, dangerously deluded as he is, at least believes the fundamentals of the shit that he is peddling. He has taken responsibility for that direction of travel and will pay the price for it, his legacy will be blackened on Earth and in history and his soul, whatever happens will be judged based on the damage he has done, which is likely huge.

When we apply the same level of critique to Mr. Mullis however, this base level of honesty is simply not there, which ever angle you seek to discern his character from. He not only claimed to physically create a tool utilized in drugging, maiming and killing millions of people, he did so without the slightest of remorse for claiming this fraudulent piece of technology could do what it said. Even if you choose to believe the cockamamy controlled opposition narrative that he said it shouldn’t/couldn’t be used to “diagnose disease” (that I will prove in this article is weapons grade bullshit) at no point was he ever honest enough to question whether it worked at all. Whether you believe the crappy, hammy acting in the Punch and Judy play fight that he had with Fauci (which I prove in this article was also weapons grade bullshit) or not, his actions were that of to perpetuate the underlying narrative of Viral and DNA existence which wholesale supports drug intervention and vaccines to combat. So, I put it to you, the reader, that at the base level of discernment, Mullis has these glaring contradictions littered throughout his story, that should to anyone of intellectual honesty lead you to see Mullis not less than in the same light as Fauci.

For this is the real crux of the matter, the reason why this persons story irks me so much is that on the scale of global discernment as a true judge of character, Mullis’ name is currently pretty unblemished. From the State and Big Pharma he was heavily decorated in both Scientific accolades with the Nobel Prize, financially rewarded by the prize fund itself as well as heavy State and Pharma investment and he was equally rewarded by the opposition as he was logged into folklore with his terrible acting, playing roll of upstart dissident. So I have always felt a grave sense of injustice when I see his face and story being bandied about on the internet by the aforementioned Click/Rage baiters. His true character has always been protected by an industrial level, ne Big Pharma level of marketing hype and my reason for writing another article about Mr. Mullis is to point out the oddities of the way that his name is championed and whitewashed and ultimately my belief as to why.

As I say, I have already been compelled to write a fairly tame article on the “God of PCR”, picking apart his autobiography. Mentioned in there is that it was never really meant as a character assassination, however once it was released I came under deluge, an all out onslaught from many nameless faceless trolls on Twitter and Substack, ironically much alike when I share information about Vit D, or Ivermectin or indeed the fraud of Germ Theory. This is what inspired me to write a short Addendum at the end of that article as to a couple of the things he was noted for being contradictory to the truth. As time has gone on though, usually when I release articles that I have bothered to go into great detail with, in the most instance the trolls back down as they are directed toward the large pile of evidence. It is a much harder position to back. However after my first article, I would say the trolls have got worse, more frequent and more insistent on regurgitating the propaganda surrounding his name. I have come to the conclusion that I believe that the character of Kary Mullis is a carefully crafted Psychological Operation disseminated by the State and perpetuated in the same vein as things like Ivermectin that dresses up as being Anti-State but actually fulfills every goal and product that the State and Big Pharma wish.

It is for this reason that I want to systematically approach every talking point to do with his “story”, as I have done in every other article to serve as a reference to point to, to save me time on social media threads. But also to expose what I believe to be through pattern recognition a fake boosted persona to perpetuate the Cornerstone of the Big Pharma disease generation for profit treadmill; the Polymerase Chain Reaction .

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1. This is a very long article at 300 pages that has taken years of research, more to this point is that whenever I have written longer articles like this with very deep research, Substack tend to Shadowban it, so having it free and open when it first goes out does me no help in just getting exposure (despite having 18k Subscribers).

2. I have quite a few paid for subscribers (thank you!) I am acutely aware that despite many big things going on behind the scenes there is not much you are seemingly seeing for your paid subscription, so early access can feel like it is a bit of a perk.

3. This will be going up as an Ebook on Shadowbanned Library for just a few dollars, if you really can’t wait you can buy the book over there. Here is a Discount code for all Substack subscribers, click there or on the image below or just use code “FAIL” at the checkout.

   

When it comes to the question of “Viruses”, the field is littered with misdirection, fraudulent tests, bamboozling uncontrolled Laboratory techniques and a sheer icy cliff face of Group Think, Appeal to Authority Bandwagon Jumping Statist Drones. If you want to gather every piece of evidence known to man to debunk their shenanigans, I would think your schedule would look a lot like mine, as I type this at 2:30am on a Monday morning.

But fear not, even as a passive reader/sponge for knowledge, about the most important topic to us, our health (for what is life if you are not alive?), there is one piece of information that ends every single avenue of masturbatory procrastination in the arena of Germ Theory: The Contagion Study, or more correctly put- The Controlled Human Infection Model (CHIM).

For once again, if health is the most important topic to us, then the Germs in question must be proved to cause us ill health, as no amount of flashing lights, nasal dip sticks and somber news stories will mean a thing if truly Germs are an impotent passenger along for the ride of general imbalance.

This is where I started and had it not been for the political machinations of 2020 and a promise made to my children to make sure they never see that happen again in their lifetimes, I would have put down the bunch of mind numbing wank that encapsulates the Isolation protocol, Genomics and “Bio”Chemistry fraud and put my feet up in the knowledge that I am very comfortable that Germs are not the cause of disease and Contagion of Biological Pathogens is a myth. This is primarily due to the fact that this is what “The Science” says, not the titles, not the news reels, not the talking head social media gurus, but the actual logical conclusions of the results of potentially a couple of hundred thousand people experimented on.

So this is how I started; in the late Summer of 2020 I embarked upon the journey of sifting through every single Controlled Human Infection Model I could locate, my search really only in the sphere of “Viruses” as the in vogue, invisible flying goblin. It came in fits and starts, days and weeks with no returns and then hit a vein of gold as numerous papers were attached to historical truth seekers of their time. After a short while, certainly before Santa Claus would make his visit in 2020, I managed to collate enough data, that comprised of about 100 separate peer reviewed and published studies to satisfy my curious mind. What started out as mostly the lowly and humble Influenza or Rhinovirus challenges, by this time I had a real floral bouquet of invisible Top Trumps including “Smallpox, Measles, HIV, Herpes, Yellow Fever and of course the star of the show; Sars Cov 2”.

I documented these results on a Twitter thread under the woke auspices of Jack Dorsey and his ban happy minions. The thread gathered more than ten thousand retweets in the space of a week especially with the paper that showed zero transmission of Flu A conducted by the then UK Chief Medical Officer Jonathan Van Tam. I must have made some serious waves and pushed the right buttons as it was only a few more weeks before my account was permanently banned for “misinformation”, despite only posting the results to published, peer reviewed literature.

Looking back those were really the heydays of Social Media, at least they were boom and bust, if you managed to toe the line just enough for state approved narratives a lot of those people just retweeting basic news headlines with some emojis are sitting on top of 100k+ follower accounts now. But here we find ourselves under the new Emperor, Mr Musk Rat, pretender of Free Speech, where you are free to say some stuff (that is acceptable Overton Window chuff), but to not be shadow banned into oblivion it has to be the most statist, fearmongering, Horse Dewormer, rat Poison pushing Big Pharma Fellating, GoySoylent chuff the overlords are squirting out of the sausage factory.

I persevered however, as I think they do most of this stuff just so you give up- to make it seem like you are barking at a brick wall. The metrics may be correct that less people are seeing your work, but I have been somewhat invigorated by Substack with people reaching out to me in person and working together letting me know that it is not just bots and fake metrics in the digital panopticon of Twitter. I made new accounts and compiled the thread of failed contagion studies once more that still stands today, however in slight tatters as many people directly linked, their accounts no longer exist. But needless to say it picked up more than 1m views (despite now only having 85K of those views left- apparently people can unsee something in the world of Muskrat) and has changed a lot of minds and made a lot of impact. So here I am rekindling the most necessary information and putting it in one place where it should be safe, both here on Substack and as an Ebook on Shadow Banned Library.

But I really wanted to go further as I had enough material to make a sizable dent in the non existent “viral” scare story, but the returning plague that kept rearing its ugly head pertained to the rest of the germ theory of disease, namely Bacteria and Parasites. My position has never changed on the individual classification of claimed Microbiological “pathogens”: Viruses do not exist and Bacteria and Parasites do not cause disease. The first of these had been clearly dealt with in the thread, but especially the “Parasites cause Cancer, Covid, damage to structural timber, marital instability and road potholes (Only way to fix it is with Horse Dewormer) crew were forever frequenting to subjugate and misdirect. Of course in the rare handful of true contagion studies out there they take the raw fluids from sick people and introduce them to healthy people, this should be thought of a necessarily containing bacteria and parasites as they are ubiquitous to our “microbiome”.

I understand, however that this may be construed as tenuous, and you know how I like to be evidence based and all; so here is the full list of contagion studies, 258 to be precise, including massive amounts of direct challenges with many different strains of “viruses”, bacteria and parasites as well as huge amounts of mass testing data showing that Bacteria and Parasites claimed to be pathogenic are ubiquitous in our Microbiome. To truly understand the Contagion Hoax this is the one-stop shop for getting to know that the fluids of sick people cannot travel through the air, up someone else’s nose and make them sick. The fact is that even non natural modes of entry, when it is seemingly just biological material will also not make people sick with the diseases the respective pathogens are blamed on.

As you will see there is a mountain sized amount of chicanery that goes into these “experiments”. Extremely rarely will they just test natural modes of transmission by letting their air miasmas seep into healthy people. The roughly 4 or 5 times in history they have ever been totally honest in testing Germ Theory they failed 100% of the time, even with PCR tests. It is why they do not experiment in this fashion, largely because it is very obvious the entirety of Virology, Bacteriology, Parasitology and Immunology is a Fraud. So they drum up all sorts of concoctions to inject, cut and lance into people’s open wounds on top of setting such a ridiculously low bar for evidence of symptoms as well as keeping them mostly uncontrolled.

Of course they claim that transmission has been proven in these experiments, they even claim that they have made people sick in these experiments and some even have the audacity to claim they have proved Koch’s postulates when it comes to the pathogenicity of these critters. These claims will all be addressed once the evidence is laid out below and we can cross reference all of the different studies where they do happen to slip up and run placebo controls or when they do test more natural routes of claimed transmission. This is the only true way to evaluate the claims and has not been done by anyone, obviously not done by the establishment but also not done by a lot of people whom claim to be skeptical of the germ theory who have compiled some shortened versions of these lists.

The last part to this article will cover very briefly the only other rebuttal you will ever see of the failed Contagion Studies, that of ; “So if not a “Virus”/Bacteria/Parasite (Delete where applicable) then how do people get sick and why are there some sort of patterns of sickness. We can refer back to a few of these contagion studies that will reveal some of the patterns seen that will act as controls and also introduce another few variables to show that any observable patterns are totally attributable to the Terrain.

This is intended to be a one-stop manual for debunking the Germ Theory of disease, so without further delay:

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TRUTH BE TOLD EVENT ANNOUNCEMENT

Event Details: Thursday, September 17th, 2026. The livestream starts at 12pm EST / 11am CT / 10am MDT / 9am PST / 6am HST / 4pm UTC.

You will be able to access the livestream on September 17th here: https://shadowbannedlibrary.com/pages/truth-be-told

Virtual doors open 30 minutes before the event begins, so make some popcorn and come grab your virtual seat! We understand life can get hectic, so WE WILL SEND YOU A COUPLE OF EMAIL REMINDERS!

Below you will find an outline of each presenter and what they are bringing to the table:

PRESENTATIONS

The opening act will be Unbekoming, who will be providing an eye-opening presentation on The Unvaccinated—a topic that is of utmost importance in 2026. This presentation will hit you with a heavy dose of facts that are guaranteed to leave you flabbergasted.

Next up will be a new fan favorite, the incredible David Parker, who will be presenting The Nature of Reality. Have you ever wondered if there is a purpose to life and what happens to you when you die? Would you be surprised to learn that there is no such thing as a solid object? Have you considered what a ’Thought’ is made of? Is there any proof that there is an ‘out there’ out there’. The World that seems so solid and separate from you can be shown to be a trick of the senses. The apparent materiality of the World is no more real than a dream image. The consequences of this knowledge will require you to reassess everything you think you know about yourself and your World. After David’s presentation will be a 15-minute live question-and-answer period.

Now that you are geared up for truth, next to the virtual stage will be the groundbreaking, trailblazing Jamie Andrews, who, through the Virology Control Studies, used science to debunk science. Although Mr. Andrews is demolishing everything we thought we knew about viruses and bacteria, he has come to realize that this is not a war he can fight alone, so he will be teaching us all how we can run our own experiments! Jamie’s presentation, Decentralized Science Projects, will be epic! After Jamie’s presentation will be a 15-minute live question-and-answer period.

The next content creator taking the stage will be the woman with a massive target on her back, the social media influencer’s greatest nightmare, Medicine Girl. In her presentation, Emergency Medicine. For one hour, Medicine Girl will be blowing the lid off everything you thought you knew about emergency medicine. Her mission is simple: to arm you with the most cutting-edge, life-saving knowledge on the planet, no matter the cost. Here you will learn the jaw-dropping truth behind “standard” emergency advice, the #1 at-home emergency mistake, how to build a medicine cabinet that can handle real emergencies, live, no-BS demos of field-tested techniques you’ve never seen anywhere else, and more! After her presentation will be a 15-minute live question-and-answer period.

And lastly, to finish out the extravaganza, one of your favorite authors of all time, the one, the only, Agent131711. Agent will be providing you with a 60-plus-minute presentation that is so shocking that you can’t help but laugh at the absurdity of it all. What is the topic? Answer: The history that came before history, the pre-historic beasts, the Jurassic Park monsters: Dinosaurs. Here, Agent will methodically dismantle every aspect of The Dinosaur Hoax, and when this hour is over, you will never look at the museum the same way.

In between presenters, we will provide a 10-minute break, so if you need to refill your drink or grab some more snacks, you won’t miss anything.

This six-hour event will genuinely be one for the books! If you can’t make the livestream, no worries! The replay will be available shortly after the show has come to an end so you can watch any time that works for you at https://shadowbannedlibrary.com/pages/truth-be-told. Grab yourself a ticket today, support the content creators who are actually making a difference, and support the website that is giving people a consolidated place to access materials that are otherwise banned and shadowbanned from the internet. Every ticket purchased goes a long way in covering the costs of the war on truth. We thank you in advance. We look forward to putting on a show you will never forget, TRUTH BE TOLD!

Questions? Contact us! ShadowbannedLibrary@Proton.me

Click on the image below to book tickets with a $5 discount code:

There is a discount code for $5 off if you book through here: Code: JAMIE.

Direct link with coupon already filled in: https://shadowbannedlibrary.com/discount/JAMIE?redirect=%2Fproducts%2Ftruth-be-told-ticket

1. This is a very long article topping 140 pages that has taken months of research, more to this point is that whenever I have written longer articles like this with very deep research, Substack tend to Shadowban it, so having it free and open when it first goes out does me no help in just getting exposure (despite having 18k Subscribers).

2. I have quite a few paid for subscribers (thank you!) I am acutely aware that despite many big things going on behind the scenes there is not much you are seemingly seeing for your paid subscription, so early access can feel like it is a bit of a perk.

3. This will be going up as an Ebook on Shadowbanned Library for just a few dollars, if you really can’t wait you can buy the book over there. Here is a Discount code for all Substack subscribers, click there or on the image below or take an image of the QR code below that or just use code “HOAX” at the checkout.

4. The paid for price is set stupidly low at $35 for a years subscription, if you want to get early access then your donations are very much appreciated and are all put towards experimentally falsifying Virology.

The “Big C” has to be addressed at some point on the Virology Control Studies Project channel for the simple fact that it is the culmination of all of the hoaxes involved in Virology rolled into an endpoint Medical diagnostic of grave ill health. They have been attempting for years to tie in the fictious strands of Genetic code floating about in the air called “Viruses” with some Boogeyman “Genetic Mutation” of your cells called “Cancer”. I put “cancer” in quotation marks the same as I do “virus” at the start of anything I write to make it known that these are fraudulent terms given by the mainstream to describe the physical appearance of tissue to attribute a fake cause for disease in the whole (in some cases- apart from the asymptotic, lol).

“Cancer” is similar to a “virus” in that it does not exist as specified by the mainstream medical view of what they are. In the case of Viruses (assumed quotations from here on in) it is mislabeled cellular debris found in a cell culture from the breakdown of cell membranes and dispersion of hydrophobic membrane bound vesicles into surrounding culture medium. That breakdown can arise from imbalance at the tissue and cellular level due to the terrain of the whole being the tissue came from and/or starvation and stresses from the cell culture method. Similarly Cancer is a cellular imbalance mislabeled as a Genetic mutation that arises from a similar imbalance of the terrain of the whole. Both of these try to make the case that the disease signified (in most parts) by the cellular deformities are caused by genetics, they differ in the fact that where Viruses are a direct claimed Genetic tampering, Cancer may be “triggered” by lots of different things - Genetics, Viruses, Chemical Carcinogens, Ionizing Radiation, Heavy Metals/Metalloids and simply old age itself. At least when it comes to the formation of Cancer, for the moment they attribute it in the most part or at the very least give a sizeable amount of headroom to the notion of Terrain, environment and chemical toxicity causing Cancer. With Viruses this is pushed wholesale into the fictious story about the “arms race” of the Immune System Vs. the Foreign Invader.

Really when you lay out all of the information on a table they are the same hoax, with the same moving parts- Chemical/Environmental and Psychological stresses that cause premature disease and death blamed on a fake genetic cause that are “treated” with more Chemical stresses that cause more death and disease. Once you learn this fraudulent mechanism employed by the Allopathic death cult and their conveyor belt of death and disease you can learn how to A. Prevent and limit that initial imbalance, hence B. Not subject yourself to the Allopathic Conveyor belt C. Spot this mechanism employed in all areas of the Allopathic death cult past, present and future enabling you to protect yourself from A & B with all health decisions.

Once you fully realize the above information, you will understand that looking for a “cure” for Cancer is the wrong way of dealing with a case of imbalance. Certainly for cutting, burning and chemically poisoning ones self, which is the Allopathic way is never going to be beneficial to health. But more than that, to think you can take some sort of pill/chemical/ food stuff said to contain a chemical is also in my opinion not the way to make a change to a disease , that as we laid out above, is caused by environment, diet and lifestyle. The only way to deal with a disease caused by environment, diet and lifestyle is to… you guessed it… change your environment, diet and lifestyle. If you have been following along, the next bit should be an extension of logic in that these things, for the sake of balance, should be happening on a similar time frame as each other, a Ying to the Yang shall we put it: 3 decades of heavy drinking, smoking, processed food diets and pharma pill popping obviously cannot be undone by 3 months of cutting down on takeaways and quitting smoking whilst doing chemo (mustard gas).

So this article is a full scale falsification of the notion that Cancer/disease/ ill health can be caused by mutations of your (fake) genetics and that it can spread once you “have it” to different parts of your body like some sort of internal contagion called “metastasis”. This article started out as just focusing on the “metastasis” part in that Cancer cannot be contagious, of course, as contagion is a myth. But I think to appreciate the Metastasis Hoax we may as well include the entire Oncogenesis as a means of disease hoax in one longer format, so here we go:

CANCER PANDEMIC

As stated above, one of the main tasks set for the Virology department, certainly in the last 50 years is to culminate the Virus Hoax in a bought of deadly Cancer. The conveyor belt is easy to see: Create Fake Viral Scare> Vaccinate> Create Cancer and Fake Cancer Scare> Chemo> Die. It is a Cradle to Grave Business model of sickness for profit worth an estimated half a Trillion Dollar market cap. Not happy with this trajectory, just last year it was announced in a White House Presser by Trump and his bestest buddies Larry Ellison and Sam Altman that they were going to invest your money to the tune of another half a Trillion Dollars to build an AI Infrastructure which will “Cure Cancer”.

WASHINGTON — President Trump unveiled a $500 billion artificial intelligence infrastructure project Tuesday at the White House alongside reps from three tech and investment giants — with those business leaders asserting the initiative could cure cancer.

OpenAI, SoftBank and Oracle launched the project, called Stargate, to unleash the new technology with the help of large data centers based in Texas.

“These world-leading technology giants are announcing the formation of Stargate,” Trump said. “So put that name down in your books, because I think you’re going to hear a lot about it in the future — a new American company that will invest $500 billion at least in AI infrastructure in the United States.”

“We will see diseases get cured at an unprecedented rate. We will be amazed at how quickly we’re curing this cancer and that one — and heart disease,” added Altman, repeating that AI would “cure the diseases at a rapid, rapid rate.”

Oracle CEO Larry Ellison also expounded on the health benefits of the project.

“Little fragments of those [cancer] tumors float around in your blood. So you can do early cancer detection. If you can do it using AI, you can do early cancer detection with a blood test and using AI to look at the blood test,” Ellison said.

“Once we gene sequence that cancer tumor, you can then vaccinate the person —design a vaccine for every individual person that vaccinates them against that cancer. That mRNA vaccine, you can make that robotically, again using AI, in about 48 hours.”

He continued saying, “imagine early cancer detection, the development of a cancer vaccine for your particular cancer aimed at you and have it have that vaccine available in 48 hours. This is the promise of AI and the promise of the future.”

If we cycle back by a decade, the notion raised by Mr. Ellison that you could test for all Cancers and more from a single blood draw was by all means in motion put forward by a company called Theranos, whom unfortunately for them and CEO Elizabeth Holmes were a little too ahead of the curve:

**Theranos was a healthcare technology startup founded in 2003 by Elizabeth Holmes that claimed to revolutionize blood testing with a device called the Edison capable of running hundreds of tests from a few drops of blood. The company reached a peak valuation of $10 billion after raising approximately $700–945 million from investors, but its technology was never proven to work as advertised.

The collapse began in 2015 when Wall Street Journal reporter John Carreyrou published exposés revealing that Theranos was using traditional competitor machines for most tests and that its proprietary technology was flawed and inaccurate. This led to investigations by the FDA and CMS, which cited immediate jeopardy to patient health, causing major partners like Walgreens and Safeway to terminate their relationships with the company.

In 2018, the SEC charged Holmes and former president Ramesh “Sunny” Balwani with massive fraud, leading to the company’s dissolution. In January 2022, Holmes was convicted on four counts of wire fraud and conspiracy and sentenced to 11 years and three months in prison, while Balwani was convicted in July 2022 on ten counts of wire fraud and sentenced to 12 years and 11 months.

Unfortunately for Elizabeth if she had just waited 10 years and voted for the Orange Wotsit for a second term adjoining the first, she might not have ended up in the clink and may have just called her company Galleri (pronounced Gallery dontchaknow).

Blood tests on the horizon, and under federal regulatory view, may be about to transform cancer care — and survival.

The Food and Drug Administration has been evaluating a blood test called Galleri (pronounced like “gallery”) as a breakthrough device that can detect many different types of cancer in one test. FDA could approve it later this year, clearing the way for such testing to become broadly available.

If that happens, experts say such tools have the power to revolutionize cancer screening as it exists today — making it far easier, more comprehensive, and more accessible to a greater number of people.

Relatively few screening tests now

Currently, in the U.S. it’s common to screen for five cancers — breast, colon, cervical, prostate, and lung — each requiring its own scan, like a CT test, or exam, like a Pap smear. By comparison, the Galleri test can detect small amounts of DNA or other cancer markers for up to 50 cancers in a single vial of blood.

Galleri and another test called Cancerguard by Abbott are both multi-cancer early detection tests that already can be ordered in the U.S. under a special FDA designation. A more rigorous FDA approval process will be necessary for the tests to be covered by Medicare and other insurance.

Still, the stage is set for a new paradigm.

“It’s a real fundamental shift in how we think about cancer screening,” says Megan Hall, vice president of medical affairs for Grail, a research company founded to bring Galleri to market. “Instead of screening for individual cancers, we can now screen an individual for multiple cancers simultaneously.”

Catching more before Stage 4

A diagnosis will always require a follow-up exam, but the test offers solid guidance for doctors, Hall says.

“That cancer signal origin prediction is a really important feature of the technology because it directs your physician on where to go to look to confirm the presence or absence of that cancer,” she says.

Improvements in blood tests, meanwhile, dovetail with rapid developments in treatments for various cancers, making the disease ever more survivable or even curable.

Therefore, the ability to catch cancer at Stage 3 versus Stage 4 has never been more significant for survival, Hall says. “The treatment landscape has evolved so much over the past five to 10 years, that there are now a lot of treatments even for Stage 3 … and that’s a really big deal.”

Given this massive investment of your tax dollars into a previous piece of tech that landed the CEO of the bloodwork company in jail, this time it comes with Rubber Stamp approval from the State itself, so instead of pacing the yard and Tater Tots they have rolled out the Red Carpet for Celebrity Psy-op season. This in the UK mere weeks after Gelleri’s launch was Psuedo-controversial “former” BBC employer Jeremy Clarkson, who made a tear jerking announcement that he had “the Big C” at the end of his fun loving frolicking on his State subsidized farm.

He later went on to breathlessly claim on video that he was “really lucky” that he managed to “catch it early” with some bloodwork that was done, even though he “had no symptoms”…. All such a coincidence of course. He then took it up a Gear to appeal to the male bravado character that this fabulous new tech was so much better than getting a Doctor’s finger up your bum and encourage, well practically anyone with a Prostate to go and get “checked out”.

To anyone with even the slightest of discernment this was one hell of a transparent marketing push to get as many people on boarding themselves to the Allopathic death cult as possible.

Jeremy Clarkson has revealed he was diagnosed with an “aggressive” form of prostate cancer last summer and had an operation to remove 10% of his prostate, eight months after he underwent heart surgery for blocked coronary arteries.

In the final two episodes of the fifth series of his Prime Video documentary, Clarkson’s Farm, the 66-year-old presenter told his farm manager, Kaleb Cooper, and his land agent, Charlie Ireland: “I’ve got cancer.”

In the scenes, which were filmed last year and released on Tuesday night, the former Top Gear host added: “I had a medical, remember, back in May? I disappeared off the other week and I had a biopsy and it is cancer, and it’s aggressive.”

He said he “wasn’t thrilled” to receive the diagnosis but that it had been caught at a “really early stage”.

He said: “If I hadn’t have got myself checked out and they hadn’t caught the problem early, this could well have been my last harvest. It’s only because they did catch it early, there’s every hope that I’ll be harvesting this farm for many, many years to come.”

When Cooper asked him what type of cancer it was, he replied: “Where it is, is of no concern to anybody.”

But in later scenes, after undergoing a procedure, he revealed it was in his prostate. “The prostate, 10% of it’s dead,” he said. “The 10% where the cancer is.”

At the end of the series, he is filmed in a hospital bed. “So we started season five in a hospital bed and here we are at the end of season five, I’m back in a hospital bed,” he said, referring to the earlier heart operation. “Some of the treatment has gone awry, let’s say. I’ll probably be here for a little while.”

He told his viewers: “What I wanted to say was: if this is all successful, I’ll see you for season six. And if it isn’t, I won’t. Take care, everyone.”

On Tuesday evening he warned fans on social media he had some “sombre news” with regard to Clarkson’s Farm. “Ordinarily we try to keep the show bucolic and charming and cheerful. But the final two episodes which drop in the middle of the night tonight are none of those things, really – they’re a difficult watch.”

He sounded emotional as he added: “They’re really, really difficult.”

Following the episodes’ release, charity Prostate Cancer UK thanked Clarkson for sharing his diagnosis and treatment saying it would raise “vital awareness”.

Chiara De Biase, the charity’s fundraising and health strategy director, said: “Thankfully he found the disease at an early stage, but sadly this is still not the experience of many men across the UK.

“Over 10,000 dads, brothers, sons and friends are diagnosed too late for a cure every year, and today the responsibility to know if you’re at higher risk and to act on it rest entirely on men’s shoulders. This must change.

“Any men worried by Jeremy’s story should take our 30 second online risk checker or have a chat with their GP about a quick and simple blood test to check for any signs.”

Prostate cancer is one of the most common cancers in the UK, accounting for 28% of all new male cancer cases, according to Cancer Research UK.

Last June, Clarkson had urged men to go for prostate checkups, saying: “I’ve had too many friends go down with prostate cancer, and all it takes to get on top of the situation early is a moment or two of being a bit cross-eyed. You get the all-clear and the doc goes home happy. What’s not to like?”

There is no national NHS screening programme for prostate cancer, but men aged 50 or over – and those aged 45 or older who have a strong family history of prostate cancer or are of a Black or African-Caribbean ethnicity – can request a prostate-specific antigen (PSA) blood test from their GP.

ANALYSIS

We can see the exact trajectory of this thing, which is the identical roadmap of 2020, mass screening leads to Cancer Pandemic. This is obviously not going to be quick peaks as with this hoax they are going to slowly ramp this mother up until they fulfil their quote of everything with a pulse has Cancer. They have not deviated one iota away from the tools used in the Scamdemic, in that they are using PCR and Genomic sequencing as the front of house triage. As explained on this channel in depth, the PCR test is a group of reagents that act like a blank canvas, you can effectively achieve whatever result you wish in assay design by altering the intrinsic threshold that the fluorescent lights will go ping.

So we can update the flow chart as such: Create Fake Viral Scare>Fake PCR and Genetics test> Vaccinate> Create Cancer and Fake Cancer Scare>Fake PCR and Genetics test> Chemo> Die. With this model it is a bit like Quantitive Easing where Central Banks just print digital money and “inject” it into economy. Why not just put 6 zeros on the end of the number you just invented, it literally makes no difference, right?

CANCER IS NOT A GENETIC DISEASE

1. The first person to propose it: Theodor Boveri

The scientist most often credited with the original idea is Theodor Boveri.

In 1902–1914, Boveri studied sea urchin embryos under a microscope. He experimentally created embryos with abnormal numbers of chromosomes and observed that they developed abnormally. From this, he reasoned that chromosomes carry hereditary information and that cancers might arise when a cell acquires the wrong combination of chromosomes, causing uncontrolled growth.

What’s remarkable is that Boveri reached this conclusion before DNA was known to be the genetic material and decades before scientists could directly identify mutations. His proposal was largely theoretical, based on chromosome behavior and careful observation.

How the idea was confirmed

Boveri’s hypothesis wasn’t fully accepted until much later.

1. Chromosome abnormalities were found in cancer cells

During the mid-20th century, improved microscopy and cytogenetics revealed that many cancers consistently contain abnormal chromosomes. Scientists found specific chromosome changes associated with particular cancers.

One famous example was the discovery by Janet Rowley that a characteristic chromosome translocation occurs in chronic myelogenous leukemia, providing strong evidence that genetic alterations can drive cancer.

Boveri’s methods were ingenious for the time, because he had no molecular biology tools, no DNA sequencing, and no way to manipulate genes directly. He relied on experimental embryology and microscopy.

The key experiment: creating embryos with abnormal chromosome numbers

Boveri worked with the eggs of the sea urchin Sea urchin.

Normally:

1. One sperm fertilizes one egg.

2. The resulting embryo gets a normal set of chromosomes.

3. Development proceeds normally.

Boveri experimentally induced polyspermy—fertilization of a single egg by two sperm instead of one.

How he did it

He altered seawater conditions around freshly spawned sea-urchin eggs, increasing the frequency with which multiple sperm entered the same egg. (The exact procedures varied among experiments, but generally involved manipulating fertilization conditions rather than surgically altering chromosomes.)

The result was:

• Eggs receiving two sperm had three centrosomes instead of the normal two.

• During cell division, this often produced tripolar or multipolar spindles rather than the normal bipolar spindle.

• Chromosomes were distributed unevenly among daughter cells.

Under the microscope, Boveri could directly observe these abnormal divisions.

What he observed

Instead of every daughter cell receiving a complete chromosome set, some cells received:

• Too many chromosomes

• Too few chromosomes

• Different combinations of chromosomes

The embryos often developed abnormally or died.

This was important because many scientists at the time thought chromosomes were largely interchangeable. Boveri’s results suggested that individual chromosomes have distinct functions, because losing particular chromosomes caused specific developmental failures.

The logical leap to cancer

Boveri reasoned:

1. Abnormal chromosome combinations can produce cells with abnormal behavior.

2. A multipolar division occurring in a normal tissue could create a cell with a dangerous chromosome combination.

3. That cell might then proliferate uncontrollably.

4. Therefore, tumors could originate from chromosome abnormalities within a single cell lineage.

Today we’d describe this as a hypothesis that cancer arises from somatic genetic alterations.

An important caveat

Boveri did not directly create cancer in sea urchins.

His evidence was indirect:

• He demonstrated that chromosome abnormalities can fundamentally alter cell behavior and development.

• He observed chromosome abnormalities in many tumor cells reported by pathologists.

• He proposed that the same principle could explain malignant growth.

The direct demonstration that specific genetic changes cause cancer came much later, through:

• Cancer cytogenetics (e.g., specific chromosomal translocations in leukemia),

• Viral oncogene studies,

• Discovery of oncogenes and tumor suppressor genes.

So Boveri’s experiments were less “I induced cancer” and more “I showed that changing chromosome composition profoundly changes cell fate, and therefore cancer could be a chromosome disease.”

Q: A sperm triggers a rise in calcium in the ovum when it enters, correct? If two sperm enter one egg would there be chaotic calcium signaling and how might that affect the eggs development?

Yes—when a sperm enters the egg, it typically triggers a rise in intracellular calcium, usually as a series of oscillations rather than a single spike. In mammals this is driven mainly by the sperm-delivered factor PLCζ, which causes repeated release of calcium from the egg’s internal stores. These calcium oscillations are what “activate” the egg and start embryonic development.

If two sperm enter the same egg (a condition called polyspermy), the situation doesn’t usually produce a clean “double-strength” calcium signal. Instead, the normal regulatory sequence is disrupted.

Here’s what tends to happen:

• Each sperm can contribute activating signals, so you may get abnormally strong or irregular calcium oscillations.

• The egg is designed to respond to a tightly timed pattern of calcium spikes; multiple inputs can make the pattern less coordinated or prolonged.

• More importantly, the biggest problem is not calcium itself but chromosome balance: the egg now has extra sets of paternal chromosomes, which leads to severe genomic imbalance.

Even if calcium activation occurs, polyspermic embryos almost always fail because:

• The spindle cannot properly organize multiple haploid sets.

• Cell divisions become abnormal.

• Development arrests very early.

To prevent this, eggs have strong anti-polyspermy defenses:

• A fast block (brief membrane depolarization in some species)

• A slow block, where calcium-triggered cortical granules modify the egg’s outer layer to prevent further sperm entry

So while multiple sperm could in principle disturb calcium signaling, the dominant reason polyspermy is lethal is that it produces an unworkable chromosome set, not primarily because of calcium chaos.

ANALYSIS

Boveri more than half a century before they invented DNA, started to observe real, physical things, i.e Chromosomes. As explained in many other writings, Chromosomes are just physical structures that are the result of the separating of an Ionic solution. No much more than for instance seeing strings of melted cheese when you pull a hot Jalapeno Popper apart. The movement creates patterns of shear and elastic stresses in the gel phase in between solid and liquid. The different patterns (Chromosomes) are made if the consistency of the phase changes through altering the Ionic Concentration inside the membrane of the cell.

This was clearly acutely apparent to Boveri whom when trying his Sea Urchin Swinger’s Party made sure to use “Calcium Free Sea Water”. As with most of these “sciences” they start out making mostly real observations in completely inconsequential things and draw these strange all encompassing conclusions that are then double/tripled down on in the future, seemingly picked at random by people with Tests.

So what did actually learn from Boveri’s work? Well that if you take normal cells that you can observe reproducing and force more in that they do in nature, then the resultant cell is deformed. Why anyone felt the need to expand on this basic piece of logic is a bit baffling, considering that they already knew full well that altering the charge inside the Ovum but inducing Calcium release, if done to extremes arrests the development of the Ovum. They already had the mechanism of both reproduction and destruction; charge.

2. Alfred Knudson and the “Two-Hit Hypothesis”

Alfred G. Knudson proposed in 1971 that cancers like retinoblastoma require two genetic “hits” (mutations) before a normal cell becomes cancerous.

This became known as the two-hit hypothesis.

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📄 His key paper

Original paper (1971):
“Mutation and cancer: statistical study of retinoblastoma”

Link (PubMed record):
https://pmc.ncbi.nlm.nih.gov/articles/instance/389051/pdf/pnas00079-0129.pdf

This paper is one of the most famous in cancer genetics.

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🔬 What Knudson actually did (methods)

Importantly, Knudson did not use molecular lab experiments. His work was based on:

1. Epidemiological analysis

He studied cases of:

• Retinoblastoma

He compared:

• Early-onset cases (often bilateral tumors)

• Later-onset cases (usually unilateral tumors)

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2. Statistical modeling

He analyzed:

• Age of diagnosis distributions

• Frequency of single vs. multiple tumors

• Population incidence rates

He then asked:

Could the timing and pattern of disease be explained by mutation accumulation?

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3. Mathematical inference of mutation steps

He proposed two distinct mechanisms:

(A) Hereditary form

• Child inherits one defective allele (first “hit” already present)

• Only one additional somatic mutation is needed

• → earlier onset, often both eyes affected

(B) Sporadic form

• Both mutations must occur in the same retinal cell lineage

• → later onset, usually one eye

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4. Logical reconstruction of mutation timing

He modeled tumor formation as a multi-step stochastic process, where:

• Each “hit” is a rare mutation event

• Cancer risk increases with time as mutations accumulate

This was one of the first quantitative frameworks linking:

cancer = accumulation of genetic mutations in somatic cells

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🧬 Why this was revolutionary

Before Knudson:

• Cancer was often seen as “one catastrophic event”

After Knudson:

• Cancer became understood as a stepwise genetic process

His model directly supported later discoveries of:

• tumor suppressor genes (like RB1)

• somatic mutation accumulation

• multi-hit carcinogenesis

ABSTRACT Based upon observations on 48 cases of retinoblastoma and published reports, the hypothesis is developed that retinoblastoma is a cancer caused by two mutational events. In the dominantly inherited form, one mutation is inherited via the germinal cells and the second occurs in somatic cells. In the nonhereditary form, both mutations occur in somatic cells. The second mutation produces an average of three retinoblastomas per individual inheriting the first mutation. Using Poisson statistics, one can calculate that this number (three) can explain the occasional gene carrier who gets no tumor, those who develop only unilateral tumors, and those who develop bilateral tumors, as well as explaining instances of multiple tumors in one eye. This value for the mean number of tumors occurring in genetic carriers may be used to estimate the mutation rate for each mutation. The germinal and somatic rates for the first, and the somatic rate for the second, mutation, are approximately equal. The germinal mutation may arise in some instances from a delayed mutation.

PATIENT DATA The records of all retinoblastoma patients admitted to the M. D. Anderson Hospital, some 48 cases during the period 1944-1969, were reviewed. These cases are tabulated (Table 1) with respect to unilaterality or bilaterality, sex, age at diagnosis, and family history. Whenever possible, the number of tumors in each eye was estimated.

ANALYSIS

Ahem (clears throat), so this is one of the seminal papers showing that Cancer is caused by checks notes Genetics. Really we need look no further than the title being that it is a Statistical analysis, therefore is under the umbrella of Epidemiology and is hence absolutely and totally worthless in assessing causality. Epidemiology assumes causation and works off of this as a spring board, it is the literal definition of correlation ≠ causation.

It’s kind of alot worse than this given the absolute torture of the statistics. They have started with a cohort from a local hospital of just 48 kids spanning over the course of a quarter of a century. They take all these kids which have blemishes on their eyes, tell these toddlers they have cancer and then posthumously number crunch them to fit a predefined assumption. You have to assume that all records of family members are absolutely correct over this very long period and that everyone of the family members has been thoroughly clinically examined, neither of which should be assumed to be accurate as Knudson has compounded in his errors.

Anything that uses “Poisson Statistics” (French for- Fish, of which they attribute to pranking given that April Fools Day is Poisson D’Avril) to find a “rule of thumb” should be openly mocked as complete quackery.

3. Discovery of cancer genes

J. Michael Bishop and Harold Varmus are best known for showing that cancer-causing genes (“oncogenes”) are actually normal cellular genes that have been altered, not foreign viral genes. This was a major shift in cancer biology.

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🧠 What they discovered (core idea)

Before their work:

• Scientists thought oncogenes were only carried by cancer-causing viruses

After their work:

• Oncogenes are normal human genes (“proto-oncogenes”) that can become cancer-causing when mutated or misregulated

This helped establish cancer as a genetic disease of the cell itself, not something always introduced from outside.

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📄 Key papers

1. The famous SRC gene discovery (1976–1978 work leading to model)

A foundational paper:

• Stehelin et al., 1976 (Cell)
  “DNA related to the transforming gene(s) of avian sarcoma viruses is present in normal avian DNA”

Link:
https://pubmed.ncbi.nlm.nih.gov/181325/

This was one of the first demonstrations that viral oncogenes match normal cellular DNA.

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2. Classic Bishop & Varmus confirmation work

A key conceptual synthesis paper:

• “The discovery of cellular oncogenes” (review and synthesis of their work trajectory)

Link:
https://pubmed.ncbi.nlm.nih.gov/6347076/

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3. Related landmark work on src origin

• Bishop lab / Varmus lab studies showing viral src derives from cellular gene

Example foundational idea paper:
https://pubmed.ncbi.nlm.nih.gov/6267523/

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🔬 What methods did they use?

Their approach was very different from Knudson or Boveri. It was molecular virology + DNA hybridization, extremely cutting-edge for the 1970s.

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1. Tumor virus model system

They studied:

• Rous sarcoma virus

This virus causes cancer in chickens by transforming cells.

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2. DNA hybridization (key breakthrough technique)

They used nucleic acid hybridization:

• Viral RNA or DNA was used as a probe

• It was tested against DNA from normal chicken cells

What they found:

• Viral oncogene sequences (like src) had strong matches in normal genomes

👉 Meaning: the gene was already in normal cells.

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3. Restriction enzyme mapping (early molecular genetics)

They used:

• restriction enzymes to cut DNA

• gel electrophoresis to compare fragments

This allowed them to:

• map where viral genes aligned with cellular genes

• show structural similarity

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4. Molecular cloning (emerging at the time)

As techniques advanced:

• viral oncogenes were cloned

• compared directly to cellular DNA sequences

This confirmed:

• viral oncogenes are modified versions of normal genes

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5. Comparative evolutionary reasoning

They also used logic across species:

• If normal animals have homologous genes to viral oncogenes

• then those genes must be ancient cellular genes

This supported the “proto-oncogene” concept.

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🧬 What they proved conceptually

They established three key ideas:

1. Proto-oncogenes exist in normal cells

Normal genes like src, ras, myc

2. Cancer arises when these genes are altered

• mutation

• overexpression

• viral capture

3. Viruses “steal” cellular genes

Retroviruses can incorporate host genes and modify them

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🏆 Impact

Their work helped lead to:

• the concept of oncogenes

• the idea that cancer is fundamentally a genetic disease of somatic cells

• the 1989 Nobel Prize in Physiology or Medicine (Bishop & Varmus shared it)

DNA related to the transforming gene(s) of avian sarcoma viruses is present in normal avian DNA Infection of fibroblasts by avian sarcoma virus (ASV) leads to neoplastic transformation of the host cell. Genetic analyses have implicated specific viral genes in the transforming process¹⁻⁴, and recent results suggest that a single viral gene is responsible⁴. Normal chicken cells contain DNA homologous to part of the ASV genome⁵⁻⁸; moreover, embryonic fibroblasts from certain strains of chickens can produce low titres of infectious type C viruses either spontaneously⁹ or in response to various inducing agents¹⁰. None of the viruses obtained from normal chicken cells, however, can transform fibroblasts, and results with molecular hybridisation indicate that the nucleotide sequences responsible for transformation by ASV are not part of the genetic complement of the normal cell¹¹. We demonstrate here that the DNA of normal chicken cells.

“Here have a Nobel Prize for failing a Control and making some shit up”

ANALYSIS

We really don’t need to delve very far into this cacophony before we see them unload a 12 gauge shotgun straight into their toes. This more modern paper that came out ever so slightly before the invention of Sanger Sequencing piled even more assumptions onto the Everest amount of assumptions from their predecessors. How they thought that staining a gel with some dye and battery electrodes could infer anything is a constant source amusement especially given the absolute clanger that they introduce the paper with, i.e the fact that they find the same genes they are looking for in healthy animals, i.e they already failed their control.

Of course any intellectually honest people would have stopped there, packed up their bags and gone home, but not this lot. For a start it was pretty hilarious, but still unsurprising, that they were studying the “genetics” of fictitious “cancer” causing “viruses” in the first place. Add to this that they found this claimed “sarcoma Virus” in healthy birds, but strangely no mammals and you have the full picture for the crazy fairytale of Oncology and Virology. They invented the idea that this Cancer causing Virus was just standard part of a birds genetics and this means somehow that therefore genetics cause Cancer. It is such an art to be able to turn abject failure into somehow into a win, but Scientists especially Nobel Prize winning artists are masters at it seemingly.

MATH AIN’T MATHING

The Temporal Paradox

A fundamental challenge to SMT lies in its quantitative feasibility. Using a Poisson-Erlang waiting-time model, Olsen and Liisberg (2025) managed to out Fish their predecessors Fish when they tested whether empirically observed mutation rates and cell-division frequencies permit multi-hit carcinogenesis within biologically realistic timescales

Their analysis reveals a striking conclusion: even under optimistic assumptions, expected waiting times exceed progenitor-cell lifespans by several orders of magnitude.

The calculation is instructive. Each cell division introduces random copying errors at approximately 10⁻⁹–10⁻⁸ per base pair. Only a minute fraction of the genome—roughly 10³–10⁵ base pairs—can yield cancer-relevant driver effects when altered. SMT assumes that a single somatic cell lineage must sequentially accumulate five to seven independent driver mutations within a human lifetime

.

The limiting factor is lineage lifespan, not mutation frequency. Progenitor cells divide rapidly but exist too briefly (approximately six divisions before differentiation). Stem cells persist but divide infrequently (roughly 70 times per year). No lineage provides the temporal window required for stochastic multi-hit accumulation. This quantitative analysis renders sequential multi-hit carcinogenesis “statistically and biologically impossible.

Summary

The mutation paradox exposes a deep logical tension at the core of the Somatic Mutation Theory.

The very cells most consistent with SMT’s probabilistic requirements - stem and progenitor cells - already possess intrinsic proliferative ability and depend on contextual signals for regulation. Mutations cannot “add” proliferation to these cells; they can only erode the communication that normally restrains it, a process far more complex than SMT’s linear, gene-centric model allows. Empirical evidence that environmental normalization can restore malignant cells to order underscores the inadequacy of cell-autonomous explanations.

The next section broadens this analysis by situating carcinogenesis within the organism’s hierarchical organization, showing how proliferation, differentiation, and repair emerge from multi-scale communication rather than from isolated genetic events.

The Statistical and Conceptual Limits of the Somatic Mutation Theory

The Somatic Mutation Theory (SMT) provides a compelling narrative: a single somatic cell accumulates a sequence of random mutations that, over time, confer the hallmarks of malignancy.

Yet when the theory is evaluated against both quantitative constraints and biological organization, its explanatory power sharply declines. The preceding sections demonstrated that the probability of acquiring the necessary combination of driver mutations within a single lineage is vanishingly small, and that the cells most compatible with SMT’s requirements - stem and progenitor cells - already possess regulated proliferative capacity. Together, these observations reveal that SMT is limited not only by statistics, but also by logic: the model presumes both an improbable sequence of events and an implausible cellular context.

This mismatch between probability, lineage identity, and observed phenotype delineates the limits of a cell-autonomous view and motivates the shift toward a systems-regulatory framework.

The statistical boundary

The Poisson/Gamma waiting-time model clarifies the temporal horizon within which mutation-driven carcinogenesis could occur. Even under favorable assumptions - a mutation rate of 10^-8 per base pair per division, a large mutational target (10⁵ bp), and numerous parallel lineages - the expected waiting time for five to seven driver mutations remains on the order of months to years. Under realistic physiological conditions, it extends to centuries or millennia.

ANALYSIS

A pretty big whoopsie has occurred in modern times when looking at the Somatic Mutation Theory and using all of the Science Establishments own Fishy mathematics. In that the rate it would take for Cancer mutations to occur would be less like months and years and more like Centuries and Millenia. It’s a funny thing that happens when you go with their mountain of assumptions and just plug their own numbers into their own equations and find out that they were out by factors of 100, it’s as if they pulled these theories out of their backsides in the first place.

The “Unnamed Cell” Problem

The “Unnamed Cell” problem is a major problem of the Somatic Mutation Theory (SMT) of cancer, highlighting its vagueness from the fact that it was largely a figment of someone’s active imagination. Yes, control experiments have been conducted that challenge SMT’s predictions and would you have it, they fail, repeatedly.

The Somatic Mutation Theory (SMT) posits that cancer is a cell-autonomous disease, initiated by an accumulation of random mutations in a single cell’s DNA that cause it to proliferate uncontrollably. The “Unnamed Cell” points out that while SMT talks about a “normal cell” transforming, it fails to specify which kind of normal cell. Most cells in the human body, like neurons and muscle fibers, are terminally differentiated and cannot divide. Therefore, the cell that accumulates mutations must be one that retains the ability to proliferate—specifically, adult stem cells or progenitor cells . The problem is that SMT rarely makes this crucial distinction explicit. By leaving the “initiating cell” unnamed, the theory avoids the biological constraints that specifying a target cell would impose, such as the tissue’s specific control mechanisms. This vagueness allows SMT to appear universally applicable while sidestepping a key question: if a cell is already capable of regulated proliferation, what specific change makes it cancerous? It’s a reoccurring theme within Soyence that of a complete lack of Specificity.

THE FITNESS PARADOX

The “fitness paradox” in cancer biology describes a counterintuitive reality: mutations that we typically label as “cancer-causing” do not inherently make cells stronger or “fitter.” In fact, within a healthy tissue environment, these mutations often make cells less fit than their normal neighbors. A mutation’s value is not absolute; it is entirely dependent on the surrounding cellular ecosystem. This challenges the simple genetic view of cancer and is best understood through three interconnected principles.

1. Fitness is Context-Dependent, Not Inherent

The central idea is that the fitness of a cell is a property of its relationship with the environment. Normal cells have undergone millions of years of evolution to be exquisitely adapted to the healthy tissue environment. In this “lawn” of healthy cells, any random mutation is statistically more likely to disrupt this fine-tuning and reduce fitness

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• A Key Example: Take the PIK3CA mutation, a common oncogenic driver. In a healthy esophagus, a cell with this mutation can gain a slight competitive advantage and expand. However, this advantage is not fixed. Research has shown that the expansion of PIK3CA mutant clones is heavily influenced by the body’s metabolic environment.

• In conditions like type 1 diabetes or diet-induced obesity, the mutant cells’ competitive fitness is enhanced, allowing them to expand more rapidly.

• Conversely, the anti-diabetic drug metformin was able to reduce this mutant advantage. This clearly demonstrates that the “fitness” of an oncogenic mutation is malleable and responds to systemic changes like diet.

2. The “Decoy Peak” and Aging Tissue

This context-dependency explains why many cancer-associated mutations are found in healthy tissues without causing cancer. Evolutionary biologist James DeGregori and others have proposed an “Adaptive Oncogenesis” model to explain this.

• The Model: Healthy, young tissues are like a high, stable “fitness peak” that normal cells are optimized to occupy. Any mutation pushes a cell down this peak, decreasing its fitness

• Aging Changes the Landscape: As we age, the tissue environment degrades due to accumulated damage and changes in the microenvironment. This lowers the “fitness peak” for normal cells, creating a new landscape where certain mutations can now confer a relative advantage.

• The Decoy Peak: Some mutations, like those in NOTCH1, can place a cell on a lower, safer “decoy peak”

. These cells are more competitive in an aging tissue but have a low risk of progressing to cancer. They may even actively suppress tumor growth, which is why NOTCH1 mutations are common in healthy aging esophagus but rare in esophageal cancers. This suggests that clonal expansions in aging tissues are often a normal part of tissue dynamics and not, by themselves, a sign of impending cancer

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3. Implications: A Shift from “Targeting Mutants” to “Supporting Health”

The fitness paradox has profound implications for how we think about cancer treatment and prevention. The current focus is on developing drugs that directly kill cells with specific mutations. However, if a mutation is only dangerous in a damaged landscape, a more effective strategy might be to “fertilize the lawn” —improving the health of the tissue environment to restore the fitness advantage of normal cells

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This model elegantly explains Peto’s Paradox: If cancer were purely about random mutation accumulation, large, long-lived animals like whales should have astronomically higher cancer rates. They do not, because their tissues have evolved robust mechanisms to maintain a healthy landscape that suppresses the emergence of advantageous mutants.

The fitness paradox tells us that a mutation is only as dangerous as the environment allows it to be. This reframes cancer not as a genetic inevitability, but as a disease driven by the systemic and environmental context in which cells live.

Q: Are there any documented examples of wild Galapagos tortoises having cancer?

No. There are currently no clearly documented, published cases of a free-ranging wild Galápagos tortoise being diagnosed with cancer while living in the wild.

There are documented cases of cancer in Galápagos tortoises, including a mast cell tumor reported in a tortoise that had originally been captured in the wild but was living in a breeding center when the tumor was discovered and diagnosed.

So the concise answer is:

No documented published example of a wild, free-ranging Galápagos tortoise with cancer; documented cases are from tortoises in captivity or managed breeding programs.

ANALYSIS

It’s wonderful when not only you are comparing made up parameters with made up parameters within one small section of a major branch of science, but when you start to compare these things holistically is when the deep chasms of terrible logic reveal themselves. If these are in general “random mutations” then all old things are riddled with cancer. You’d basically only see a large tumor in a Tortoise Shell walking around the Galapagos Islands.

Funnily enough you never see “mutations” that are positive, they are always defects and by this very notion we can safely chuck the notion of “random mutations” in the bin, no matter what is the driving mechanism behind them. There is adequate natural growth and their is injury and deformity it’s as simple as that. So a two-fer in this tiny little section debunking Evolution and Genetic Mutations in one with some simple logic.

Control Experiments of the Unnamed Cell

The Bissell Experiment (and Similar Studies)

• This refers to a series of experiments where malignant cells were placed in a normal tissue microenvironment, causing them to revert to a normal, non-cancerous phenotype

• . This demonstrates that cancer is not an irreversible cell-autonomous state, as SMT would suggest, but is heavily influenced by signals from the surrounding tissue.

CANCEROUS cells can be forced to behave like normal cells by fine-tuning
their chemical communication with their environment, say researchers in the US.
They hope that this startling discovery could add a new dimension to breast
cancer research.

Mina Bissell and Valerie Weaver of the Lawrence Berkeley National Laboratory
in California and their colleagues made the discovery after looking at the way
breast cells group together. In normal breast tissue, around 8 cells cluster
into spherical groups, each surrounded by a fibrous protein mesh. But in
cancerous breast tissue, in which the cells divide uncontrollably, this mesh is
irregular and the cells clump together randomly.

The team made three-dimensional cultures of breast cells. They then added an
antibody to a receptor called beta-1 integrin, which allows cells to
“communicate” chemically with the extracellular matrix, the gel of proteins
between groups of cells. They found that the antibody linked up with tumour
cells in a more haphazard pattern than with normal cells, suggesting that the
beta-1 integrin molecules are not in the right places on the cell surfaces. The
tumour cells also had more receptors than usual.

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The researchers report in the current issue of the Journal of Cell
Biology that tumour cells soaked in an antibody that blocks beta-1 integrin
undergo a dramatic change, and become normal in appearance and behavior. “At
first I thought I had mixed the normal and tumour cell tubes up,” says
Weaver.

Repeats of the experiments confirmed that although the reverted cells still
harbour the genetic mutations that made them cancerous, they stop dividing
uncontrollably and regroup in normal clusters. Weaver suggests that this return
to the normal structure stops the cells dividing like tumours.

Until now, cancer research has been dominated by the study of genes that
trigger cancer when switched on, and those that protect against cancer. Ray
White of the University of Utah’s Huntsman Cancer Institute in Salt Lake City
foresees a change, however. “Bissell’s research opens up a third area of
regulation of cells through their interactions with their outside environment,”
he says.

Abstract.

In a recently developed human breast cancer model, treatment of tumor cells in a 3-dimensional culture with inhibitory b1-integrin antibody or its Fab fragments led to a striking morphological and functional reversion to a normal phenotype. A stimulatory b1-integrin antibody proved to be ineffective. The newly formed reverted acini re-assembled a basement membrane and re-established E-cadherin–catenin complexes, and re-organized their cytoskeletons. At the same time they downregulated cyclin D1, upregulated p21cip,waf-1, and stopped growing. Tumor cells treated with the same antibody and injected into nude mice had significantly reduced number and size of tumors in nude mice. The tissue distribution of other integrins was also normalized, suggesting the existence of intimate interactions between the different integrin pathways as well as adherens junctions. On the other hand, nonmalignant cells when treated with either a6 or b4 function altering antibodies continued to grow, and had disorganized colony morphologies resembling the untreated tumor colonies. This shows a significant role of the a6/b4 heterodimer in directing polarity and tissue structure. The observed phenotypes were reversible when the cells were disassociated and the antibodies removed. Our results illustrate that the extracellular matrix and its receptors dictate the phenotype of mammary epithelial cells, and thus in this model system the tissue phenotype is dominant over the cellular genotype.

ANALYSIS

There are again a couple of points to make with this one paper. Whatever they are using as an “antibody” titer is clearly supplemented with growth medium or somehow provides sustenance to the cell line as this has all of the hallmarks of the cell culture isolation fraud with happy/sad cells just based on their dietary modifications. It is hard to really pinpoint this as, unsurprisingly, there is no method for the making of the “Antibodies”. Whichever way you skin it they are adding something demonstrably non genetic that seems to undo what they claim is a disease caused by genetics. That’s a big problem, of course the story will be that it does genetic magic to undo the genetic terror, but they can make up whatever stories they like.

The compounding problem here is the fact that genetic mutations are meant to be permanent, yet here we have the proverbial Petri Dish Quasimodo that if you rub a little of the special tincture into his face, he is now Brad Pitt. This is pretty compelling evidence that Cancer (cell deformation) is just a state of balance. I will describe what is in my mind thusly. Take a balloon that represents the cell membrane. If you fill it with water, it will fill the balloon normally. If you filled it with Jam (strawberry preserve) it would sag and warp as the gel like consistency from the pectin clumps rather than provides equal hydrostatic pressure. If you put Mercury in the balloon it would burst under its own weight.

A SEA OF MUTANT CELLS

The absolute essence of Scientific falsification as we have become accustomed to by now is the humble but almighty Control. I wouldn’t have called my channel what it is, if I didn’t believe in what this simple logic gate does for revealing the truth about a subject. So really if we want to learn about the incidence of claimed “genetic mutation caused Cancer” we need to look at healthy tissue from healthy people and sequence it for genetic mutations. The key, paradigm-shifting finding from multiple control studies is that by middle to old age, a staggering proportion of cells in normal, cancer-free tissues harbor what would traditionally be called “cancer-driving” mutations.

Meta-Analysis of Normal Tissues: A landmark meta-analysis combined data from sequencing studies across multiple healthy tissues—including colon, endometrium, esophagus, skin, and blood . It revealed that in older age groups, over 50% of cells in these tissues had mutations in known cancer genes . The study calculated that an average older, cancer-free individual possesses at least 100 billion cells that carry at least one oncogenic mutation . This finding completely overturns the idea that these mutations are rare, early, and specific warning signs of cancer.

Abstract

BACKGROUND

To shed light on the earliest events in oncogenesis, there is growing interest in understanding the mutational landscapes of normal tissues across ages. In the last decade, next-generation sequencing of human tissues has revealed a surprising abundance of cells with what would be considered oncogenic mutations.

AIMS

We performed meta-analysis on previously published sequencing data on normal tissues to categorize mutations based on their presence in cancer and showcase the quantity of cells with cancer-associated mutations in cancer-free individuals.

METHODS AND RESULTS

We analyzed sequencing data from these studies of normal tissues to determine the prevalence of cells with mutations in three different categories across multiple age groups: 1) mutations in genes designated as drivers, 2) mutations that are in the Cancer Gene Census (CGC), and 3) mutations in the CGC that are considered pathogenic. As we age, the percentage of cells in all three levels increase significantly, reaching over 50% of cells having oncogenic mutations for multiple tissues in the older age groups. The clear enrichment for these mutations, particularly at older ages, likely indicates strong selection for the resulting phenotypes. Combined with an estimation of the number of cells in tissues, we calculate that most older, cancer-free individuals possess at least a 100 billion cells that harbor at least one oncogenic mutation, presumably emanating from a fitness advantage conferred by these mutations that promotes clonal expansion.

CONCLUSIONS

These studies of normal tissues have highlighted the specific drivers of clonal expansion and how frequently they appear in us. Their high prevalence throughout cancer-free individuals necessitates reconsideration of the oncogenicity of these mutations, which could shape methods of detection, prevention and treatment of cancer, as well as of the potential impact of these mutations on tissue function and our health.

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When investigating oncogenesis throughout the human body, it is important to consider a life history perspective – how natural selection has shaped our tissues to maximize survival and reproductive success and the limits of these selective pressures at older ages when we are less likely to reproduce.¹² In this light, we can better appreciate why some clonal expansions may be more tolerated than others and the age-dependence of this tolerance. Due in large part to the fact that our lifespan has increased significantly in recent centuries, age has become the biggest cancer risk factor and is a crucial component to investigating the transition from clonal evolution to oncogenesis.^1,13–15 Attention must also be paid to the fact that different turnover rates and mutation rates exist across epithelial tissues and the hematopoietic system, which when combined with very different microenvironment-driven selective pressures, leads to differing clonal evolution routes to cancer. Therefore, providing insight on the somatic mutational landscape and its potential to progress to cancer throughout the human body across age is critically important.

• Stroma-Dependent Carcinogenesis: In one study, normal mammary epithelial cells were transplanted next to stroma (connective tissue) that had been previously exposed to a carcinogen. These normal cells gave rise to tumors at a much higher rate than controls. This shows that the tissue environment (the stroma), not just mutations within the epithelial cells themselves, can be a primary driver of cancer.

Abstract

Understanding the early stages of carcinogenesis requires detailed insight into the abnormalities present in normal cells before cancer onset. In the past, it was difficult to analyze genomic abnormalities in small clones in normal tissues. However, recent technological advances in genomic analysis have shed light on the process of accumulation of somatic mutations in normal cells, which is driven by factors such as aging and environmental influences. Even in normal tissues, clones that have acquired driver mutations—either directly contributing to carcinogenesis or adapting to specific pathological or genetic backgrounds—are frequently selected, leading to clonal expansion. Normal cells undergo clonal evolution into cancer cells over several decades, with the initial acquisition of a driver mutation occurring in early life. This review presents recent findings concerning the accumulation of somatic mutations in normal cells, acquisition of driver mutations, and clonal evolution toward cancer.

Introduction

Most cancers originate from genetic abnormalities, specifically the accumulation of somatic mutations. These mutations accumulate in normal cells in all organs of healthy individuals and are driven by factors such as aging, environmental influences, and inflammation1 . This often leads to the expansion of clones with driver mutations, thereby increasing tumorigenesis risk, ultimately progressing to precancerous lesions and cancer. The genetic background also plays a role in somatic mutation accumulation and clonal evolution. Furthermore, clonal evolution progresses due to driver mutation acquisition, which may originate in the fetal state or at a young age. These findings provide an important foundation for understanding cancer development and is expected to contribute to the early detection and prevention of cancer in the future.

ANALYSIS

In the last 6 years since the Scamdemic there has bizarrely been a real flurry of Genetics testing for Cancer where they actually try and surveil widespread healthy populations. This seems like an incredibly dangerous position for them to take I would imagine we won’t see much more of this vein of questioning as the powers that be start to roll out the ubiquitous PCR for all Cancers. But here we are with the data (Before they try to cover it up or distract with more heaped pseudoscience) and considering this paper is from just 2022 it compounds as being a total Bombshell. They are admitting to not only more than half of all >Septuagenarians have “Cancer Mutations”, but in some cases they get very good signal in the bladder, endometrium and skin in the 30-50 yr old category. Essentially they have what they want with the fraudulent Genetic Diagnostic tests EVERYONE HAS CANCER!!

Now in this specific paper they try and coverup a lot of these earlier year signals (despite them being prevalent in more than 35% of all individuals) by claiming that this is just a by product of ageing. This is clearly discordant with two major points, the first being the topic of The Fitness Paradox as above, the second being that these were from healthy individuals i.e this should be yet another falsification of Genetics tests as this control study fails 50% of the time (seems to be a coin flip- which should be taken heavily into account if you are ever confronted with a Cancer Diagnosis).

The Cherry on top of the sprinkles on top of the cream occurs when we look at the even more recent (2025) paper that tests the younger population for the same type of Genetic Mutations. (Un)Surprisingly they have to fire up the Coping Coal fire as they start to receive signal even in the Fetus. Yes, that’s correct, they recon that literally EVERYONE HAS CANCER including the unborn. Instead of someone in these departments raising their hands as saying “it might just be that the tests are shit?” they all just settle on the total nature of Cancer being, just well….. a part of our Biology (but not Naked Mole Rats, Elephants, Bats, Whales and Tardigrades).

The Esophageal Paradox: The Protective Mutation

The NOTCH1 mutation presents a contradictory paradox in esophageal biology and is an obvious, in your face illustration of why cancer cannot be understood through genetics alone. The story begins with an unexpected observation: by middle age, they take a made up gene called NOTCH1 and claim it occupies the majority of the normal human esophagus, with some studies finding these mutations in over 80% of tissue samples. This prevalence is striking, as it makes NOTCH1 one of the most common mutations in healthy esophageal tissue. However, the paradox emerges when one looks at esophageal cancers, where NOTCH1 mutations are comparatively rare. This inverse relationship—common in healthy tissue but uncommon in tumors doubly compounds the obvious fraudulent claim of “genetic” driven Cancer.

Again in this flurry of modern “rebuttals” to the Genetics scam, this 2023 study published in Nature Genetics by Abby and colleagues set out to test this hypothesis directly:

Using a combination of human tissue sequencing and mouse models, they found that NOTCH1 mutations work by disabling the gene’s function. In the mouse esophagus, cells with a heterozygous Notch1 mutation had a competitive advantage over their normal neighbors, and this advantage was even stronger when the second copy of the gene was also lost. The mutant cells essentially colonized the tissue, but importantly, widespread loss of NOTCH1 had minimal effects on the epithelial structure and cell dynamics—the tissue remained healthy and organized. This demonstrates that a mutation can drive a cell to outcompete its neighbors without necessarily pushing it toward malignancy.

The most critical evidence came when the researchers induced tumors in these mice. They discovered that tumors in tissue lacking Notch1 were significantly smaller than those in normal tissue. This effect was so pronounced that it could be recapitulated by treating established tumors with an anti-NOTCH1 antibody, which also reduced tumor growth. Further analysis revealed that Notch1 null tumors showed reduced proliferation, indicating that while wild-type NOTCH1 actively favors tumor expansion, the loss of its function acts as a brake on cancer growth. This is a direct reversal of the typical “oncogene” narrative.

In conclusion, the NOTCH1 esophageal paradox shows that the same mutation can have entirely different effects depending on the context. In the normal, healthy tissue of an aging esophagus, a NOTCH1 mutation provides a fitness advantage that allows for clonal expansion without disrupting tissue architecture. But in the context of a developing tumor, the presence of this mutation is detrimental to cancer growth, as the wild-type NOTCH1 is required for the tumor to expand. This finding not only challenges the deterministic view of cancer genetics but also opens up exciting therapeutic possibilities, suggesting that blocking NOTCH1 could be a viable strategy for preventing or treating esophageal squamous cancer

NOTCH1 mutant clones occupy the majority of normal human esophagus by middle age but are comparatively rare in esophageal cancers, suggesting NOTCH1 mutations drive clonal expansion but impede carcinogenesis. Here we test this hypothesis. Sequencing NOTCH1 mutant clones in aging human esophagus reveals frequent biallelic mutations that block NOTCH1 signaling. In mouse esophagus, heterozygous Notch1 mutation confers a competitive advantage over wild-type cells, an effect enhanced by loss of the second allele. Widespread Notch1 loss alters transcription but has minimal effects on the epithelial structure and cell dynamics. In a carcinogenesis model, Notch1 mutations were less prevalent in tumors than normal epithelium. Deletion of Notch1 reduced tumor growth, an effect recapitulated by anti-NOTCH1 antibody treatment. Notch1 null tumors showed reduced proliferation. We conclude that Notch1 mutations in normal epithelium are beneficial as wild-type Notch1 favors tumor expansion. NOTCH1 blockade may have therapeutic potential in preventing esophageal squamous cancer.

ANALYSIS

Yet another modern set of studies reveals the Oncogene fraud and puts it front and center. A staggering control failure in the fact that they find this claimed mutation in up to 80% of healthy people (EVERYBODY HAS CANCER), the real stinger to this is the fact that this same measurement disappears in sick people with esophageal Cancer. I mean talk about a self own. But did we really think that they would stop kicking themselves when their limp and lifeless body was lying on the floor? No they really made sure of the humiliation ritual on this one, they found that this mutation actually prevented cancer when they experimentally induced it.

Typical of the Upside Down world in which Scientists occupy, they of course turned this multitude of total failure into a positive for them and now claim that this genetic mutation that does/doesn’t cause cancer can be used to prevent Cancer presumably by making sure that everyone has a Cancerous Genetic Mutation (EVERYONE HAS CANCER).

Foreign Body Carcogenesis

We are really starting to pile the mountain of evidence high and are probably not even half way through yet, but to put a stake in the heart of this hoax we are going to leave no stone unturned. In this classic experimental model, tumors can be induced simply by implanting a solid object, such as a plastic film or a filter with very small pores, under the skin of an animal. The critical finding is that the physical properties of the implant, not its chemical composition, determine its carcinogenic potential. For instance, a Millipore filter with a pore diameter of 0.025 μm (oncogenic) can induce sarcomas, while a filter of the exact same material but with a pore diameter of 0.45 μm (non-oncogenic) cannot . Similarly, large non-perforated polymer films are highly carcinogenic, whereas perforated or minced films of the same material are not.

This result is paradoxical under the SMT because the foreign body is not a chemical mutagen; it does not directly cause DNA mutations. If cancer were solely a genetic disease caused by DNA damage, the physical structure of the implant should not matter. However, under the Tissue Organization Field Theory ( TOFT) , which posits that cancer is a tissue-based disease, the explanation is straightforward. Carcinogens act by disrupting the normal interactions between cells and their surrounding environment, which is the equivalent of a “morphostatic field” . The implant’s physical presence creates a barrier that interrupts normal tissue architecture and cell-cell communication. The pore size is critical because it determines the type and extent of this disruption: a filter with tiny pores prevents the normal ingress of cells and signals, fostering a persistent state of chronic inflammation and tissue disorganization, while a filter with larger pores allows for normal tissue interaction and does not provoke the same pathological response . I mean it’s as if the establishment know that it is all about charge already.

Research by Moizhess and Vasiliev (1989) further supports the TOFT’s interpretation by showing that the process can be divided into stages, a concept that aligns with the theory’s view of cancer as a progressive breakdown of tissue organization. They demonstrated that a carcinogenic non-perforated film could act as an “initiator.” When this film was removed after 3.5 months and replaced with a non-carcinogenic perforated film, a high percentage of sarcomas still developed . This suggests that the initial disruption of the tissue field by the first film created a persistent, altered state in the stroma that could be “promoted” by a second, otherwise non-carcinogenic, implant. This two-stage process mirrors the principles of initiation and promotion in classic chemical carcinogenesis, but the initiating event is a physical disruption of tissue architecture, not a genetic mutation .

The experimental evidence strongly suggests that the stroma, the connective tissue framework of an organ, is a primary target of carcinogens in this model. The tumor formation is not a cell-autonomous event but an emergent property of the disrupted tissue field. Importantly, this perspective implies that the neoplastic phenotype is potentially reversible. If cancer is a problem of tissue organization, then restoring normal tissue architecture and cellular communication might “reprogram” neoplastic cells to behave normally again, a prediction that has been supported by other experiments within the TOFT framework.

Abstract

Implanted foreign bodies of certain shapes, especially large non-perforated polymer films, induce subcutaneous sarcomas in a high percentage of mice and rats; in contrast, implants of other shapes, e.g., perforated or minced films or Millipore filters with 0.45 μm pores, are non-carcinogenic or only weakly carcinogenic. Experiments described in this report have shown that when carcinogenic non-perforated film was removed at 3.5 months after implantation and one of the “non-carcinogenic” foreign bodies listed above was implanted into the same subcutaneous sites, a high percentage of sarcomas was induced. The same non-carcinogenic or weakly carcinogenic foreign bodies implanted in the mice after total body γ irradiation or after single injection of ethylnitrosourea induced subcutaneous sarcomas in significantly higher percentages of animals than the same foreign bodies implanted in control mice. Our data suggest that foreign bodies of “non-carcinogenic” or “weakly carcinogenic” shapes can act as efficient promoters of subcutaneous carcinogenesis initiated by other agents such as implanted “carcinogenic” foreign bodies, ionizing radiation or chemical carcinogen.

ANALYSIS

This one really is huge as it doesn’t involve any drugs, anything really to induce imbalance other than specific pore size of material that disrupt the terrain of cells. This is also a huge point of interesting in explaining the Metastasis Hoax in the fact that it is clearly just a tissue imbalance issue rather than some “spreading” contagious Cancer. The pore sizes affect the polarity and charge of the membranes of the cells and how they interact with each other. This is very clear when you look at how Cells become Confluent in Cell Culture. You want to create a monolayer where each cell can occupy its own niche and they form these distinct patterns, as soon as they as disrupted or overcrowded they begin to breakdown. This by the way is the problem with merely putting a different cell type from a sample into the cell culture and claiming apoptosis as an observable effect.

THE MOST DAMNING EXPERIMENTAL CONTROL

Oh, but please, do go on telling us all about those precious oncogenes and tumor suppressors. According to the high priests of the Somatic Mutation Theory, cancer is a genetic disease, written indelibly in the nucleus, a divine script that cannot be overwritten. So one might imagine their collective horror when Israel & Schaeffer (1987) had the audacity to take a malignant nucleus, plop it into normal cytoplasm, and watch the tumorigenic phenotype get extinguished. Just like that. Poof. No mutations fixed? No genetic destiny playing out? It’s almost as if the almighty nucleus isn’t the sole dictator of the cell’s fate—a thought that must send shivers down the spines of every grant reviewer still clinging to the genomic gospel. But surely, that was just a fluke, a minor embarrassment easily explained away.

Then came the 1988 follow-up, and this is where the SMT faithful really have to cover their eyes. Israel & Schaeffer took a perfectly “normal” nucleus—presumably unblemished by any of those sacred driver mutations—and dropped it into malignant cytoplasm. And what happened? Ninety-seven percent of the animals developed tumors. Let that sink in. A clean, genetically pristine nucleus, suddenly behaving like a thug because of the company it keeps. According to the SMT, this is impossible—or at least deeply inconvenient—so naturally, the preferred response is to dismiss it as an artifact, question the cell lines, or murmur something about “epigenetics” without admitting that the entire nuclear-centric edifice is starting to crack.

Of course, the defenders of genetic orthodoxy will insist that these experiments are old, messy, or irrelevant to human cancers. They’ll nitpick the word “extinguished” versus “suppressed,” as if quibbling over semantics can undo the fact that cytoplasm—yes, that goopy stuff they’ve been ignoring for decades—just overrode the nuclear genome with embarrassing ease. The SMT isn’t a theory anymore; it’s a coping mechanism. Because if a few bits of mitochondrial sludge can turn a healthy nucleus into a tumor factory, then maybe, just maybe, the billion-dollar mutation-hunting industry has been looking in the wrong place this whole time. But don’t worry—I’m sure the next whole-genome sequencing project will find that one elusive mutation that fixes everything. Any day now.

The one caveat to this theory ending control is the most notable people Championing this work such as Thomas Seyfried, use this abject failure of “Nuclear” SMT and try and turn it into to another whacked out theory on Mitochondrial disease attributed to the “Bio”Chemistry fraud. This guy is clearly controlled opposition and is desperately trying to claw these control failures back into an establishment win by prosing these hair-brained new reasons.

Using both normal and transformed rat liver epithelial cells to prepare cytoplasmic hybrids (cybridst we have found evidence to support the theory that the cytoplasm from a normal cell can suppress tumorigenicity. A unique aspect of this study is that all of the cells utilized, both normal and malignantly transformed, were derived from an original cloned cell. We found that fusing cytoplasts from normal cells to malignantly transformed whole cells resulted in cybrid clones which, when injected into newborn rat pups, isogenic with those from which the cell culture was initiated, yielded tumors in 51% of the animals injected compared to 92% of the animals injected with the tumorigenic parent. Those animals that did develop tumors from the cybrid cells survived longer than those injected with cells from the tumorigenic parent. Thus, the cybrid, formed of cytoplasm from both parents, was less tumorigenic than the malignantly transformed parent cell. When reconstituted cells were prepared by fusing cytoplasts from normal cells with karyoplasts from malignantly transformed cells, a situation in which essentially all of the cytoplasm of the reconstituted cell is derived from normal cells, the tumorigenic phenotype was extinguished.

SUMMARY

The relative roles of nucleus and cytoplasm in the induction and maintenance of the malignant state were studied. Cytoplasmic hybrid tcybrid) clones, derived from the fusion of cytoplasts from malignantly transformed cells to normal whole cells, produced tumors in 17% of the animals injected with them. Nuclear/cytoplasmic hybrid (reconstituted cell} clones, derived by fusion of cytoplasts from malignant cells with karyoplasts of normal cells, produced tumors in 97% of the animals injected. A unique aspect of this study is the fact that all of the cells utilized, both normal and malignantly transformed, were derived from an original cloned cell.

INTRODUCTION

In earlier studies by others, a variety of whole cell hybrids, cybrids (cytoplasm/whole cell hybrids) and reconstituted cells (nucleus/cytoplasm hybrids) were analyzed in order to understand the control mechanisms involved in the expression and maintenance of the carcinogenic state. Similar experiments from various laboratories yielded conflicting results. For example, studies of interspecific hybrids between normal and tumorigenic whole ceils, indicated dominance of the tumorigenic state ( 1,2,3 ~, wherea s, intraspecific hybrid studies suggested tumorigenic recessiveness (4,5,6), dominance (7) as well as recessiveness followed later by an appearance of a background of tumorigenic cells (8,9L In cybrid experiments, either recessiveness (10) or dominance of tumorigenesis t4,6,11,12) was seen. In reconstituted cells, the nucleus determined the progeny phenotype (13,14). These previous studies employed, as parental cells, cells from different species, cells from the same species but with diverse in vitro histories as well as revertant tumorigenic cells as the normal counterpart, nutagens commonly were employed to induce markers for the selection of fusion progeny thus generating possible additional alterations to the genotype. In addition, intrinsic cell/cell incompatibility, now recognized to play a role in the outcome of fusion experiments, was overlooked. Functional incompatibilities have been demonstrated between heterologous mitochondria, ribosomal subunits, cellular membranes and specific gene products t15-23). We developed a cloned, epithelial, rat liver-derived cell strain (24,25). Portions of the culture have been sequentially frozen so both early passage nontransformed (EP) and late passage transformed (LP) cells are retrievable for study. Since the normal and tumorigenic cells are parts of a cultural continuum, this system is uniquely suitable for a study of suppression or expression of the malignant phenotype unhindered by cytoplasmic incompatibilities. Recently (26), I Present address: Department of Veterinary Sciences, University of Wisconsin, Madison, Wisconsin 53706. 2 To whom requests for reprints shouM be addressed. we demonstrated that the cytoplasm of normal cells suppressed the malignant phenotype in cybrids and reconstituted cells. The cybrids exhibited partial suppression while, in the reconstituted cells, suppression was 100%. Here we present the data which, for the first time, provide unambiguous evidence indicating a role for cytoplasm in the expression of the malignant phenotype.

IT’S ALL CHARGE

Well, well, well, would you have it, yet another another inconvenient paper that the genomic fundamentalists will need to explain away. According to the sacred doctrine of the Somatic Mutation Theory, cancer is a genetic destiny, chiseled into the nuclear DNA by an accumulation of driver mutations that cannot be undone. So imagine the collective pearl-clutching when Maria Lobikin and Michael Levin decided to simply tweak the resting membrane voltage of a few frog cells and—lo and behold—induced a melanoma-like hyperpigmentation and invasive behavior without a single oncogene being activated or tumor suppressor being deleted. Just a little electrical nudge, and suddenly these cells are acting like metastatic troublemakers. It’s almost as if the nucleus isn’t the all-powerful dictator of cellular fate, but rather a middle manager taking orders from the cell membrane—a thought so heretical to the sequencing-obsessed establishment that it must be dismissed as “just a frog thing” before anyone gets any bright ideas about rethinking cancer origins.

The 2015 follow-up only made matters worse for the mutation-hunting crowd, because it traced this bioelectric mischief to serotonin signaling—yes, the very same neurotransmitter your grandmother recognizes as a mood chemical. Lobikin and her team showed that voltage changes could trigger an all-or-none conversion of melanocytes into a tumor-like state, and they pinned it to a serotonergic pathway downstream of the electrical signal. In plain English: a physical property of the cell membrane—something SMT proponents have historically treated as irrelevant background noise—was acting as an instructive signal for malignant behavior. No PCR test needed, no whole-genome sequencing required. Just a voltage dial and a serotonin bump, and suddenly the cell forgets its identity. It’s enough to make you wonder if the nuclear genome is less of a master blueprint and more of a passive employee following electrochemical memos from the cytoplasm and membrane.

Of course, the genetic orthodoxy will fire back with the usual defenses: these are frog embryos, not human patients, and “melanoma-like” isn’t the same as actual melanoma. And technically, they’re correct—it’s not a perfect one-to-one translation. But let’s not pretend that the SMT establishment hasn’t spent billions over decades hunting mutations that explain only a fraction of cancers, while targeted therapies keep failing as resistance inevitably emerges. Meanwhile, Levin’s lab is showing you can induce a metastatic phenotype with voltage tweaks, and Israel & Schaeffer showed you can suppress tumorigenicity by restoring normal cytoplasm. The evidence is piling up that the nucleus is reactive, not proactive. But please, by all means, keep throwing money at the next sequencing project. I’m sure this time, the magic mutation will appear and save us all. Any decade now.

Abstract

Cancer may result from localized failure of instructive cues that normally orchestrate cell behaviors toward the patterning needs of the organism. Steady-state gradients of transmembrane voltage (V(mem)) in non-neural cells are instructive, epigenetic signals that regulate pattern formation during embryogenesis and morphostatic repair. Here, we review molecular data on the role of bioelectric cues in cancer and present new findings in the Xenopus laevis model on how the microenvironment’s biophysical properties contribute to cancer in vivo. First, we investigated the melanoma-like phenotype arising from serotonergic signaling by ‘instructor’ cells-a cell population that is able to induce a metastatic phenotype in normal melanocytes. We show that when these instructor cells are depolarized, blood vessel patterning is disrupted in addition to the metastatic phenotype induced in melanocytes. Surprisingly, very few instructor cells need to be depolarized for the hyperpigmentation phenotype to occur; we present a model of antagonistic signaling by serotonin receptors that explains the unusual all-or-none nature of this effect. In addition to the body-wide depolarization-induced metastatic phenotype, we investigated the bioelectrical properties of tumor-like structures induced by canonical oncogenes and cancer-causing compounds. Exposure to carcinogen 4-nitroquinoline 1-oxide (4NQO) induces localized tumors, but has a broad (and variable) effect on the bioelectric properties of the whole body. Tumors induced by oncogenes show aberrantly high sodium content, representing a non-invasive diagnostic modality. Importantly, depolarized transmembrane potential is not only a marker of cancer but is functionally instructive: susceptibility to oncogene-induced tumorigenesis is significantly reduced by forced prior expression of hyperpolarizing ion channels. Importantly, the same effect can be achieved by pharmacological manipulation of endogenous chloride channels, suggesting a strategy for cancer suppression that does not require gene therapy. Together, these data extend our understanding of the recently demonstrated role of transmembrane potential in tumor formation and metastatic cell behavior. V(mem) is an important non-genetic biophysical aspect of the microenvironment that regulates the balance between normally patterned growth and carcinogenesis.

Abstract

Experimentally induced depolarization of resting membrane potential in “instructor cells” in Xenopus laevis embryos causes hyperpigmentation in an all-or-none fashion in some tadpoles due to excess proliferation and migration of melanocytes. We showed that this stochastic process involved serotonin signaling, adenosine 3’,5’-monophosphate (cAMP), and the transcription factors cAMP response element-binding protein (CREB), Sox10, and Slug. Transcriptional microarray analysis of embryos taken at stage 15 (early neurula) and stage 45 (free-swimming tadpole) revealed changes in the abundance of 45 and 517 transcripts, respectively, between control embryos and embryos exposed to the instructor cell-depolarizing agent ivermectin. Bioinformatic analysis revealed that the human homologs of some of the differentially regulated genes were associated with cancer, consistent with the induced arborization and invasive behavior of converted melanocytes. We identified a physiological circuit that uses serotonergic signaling between instructor cells, melanotrope cells of the pituitary, and melanocytes to control the proliferation, cell shape, and migration properties of the pigment cell pool. To understand the stochasticity and properties of this multiscale signaling system, we applied a computational machine-learning method that iteratively explored network models to reverse-engineer a stochastic dynamic model that recapitulated the frequency of the all-or-none hyperpigmentation phenotype produced in response to various pharmacological and molecular genetic manipulations. This computational approach may provide insight into stochastic cellular decision-making that occurs during normal development and pathological conditions, such as cancer.

FUTURE PREDICTIONS

This is the holistic view of the Genetics scam when it comes to lofty claims of predicting the future of inheritable traits, you have a fetus and they are going to give it a Polygenic Risk Score based on dodgy genetics tests for if it is predisposed to all sorts of diseases later in life:

1. The Oracle of the Lab Coat

Behold the latest and greatest crystal ball to emerge from the hallowed halls of genomics—because apparently, reading tea leaves wasn’t sufficiently opaque or expensive. Here we have a neat little number, distilled from the collective whisper of millions of genetic variants, each contributing a gravitational pull so infinitesimally tiny that it makes a butterfly’s sneeze look like a hurricane. And yet, with the unearned confidence of a startup CEO on a coffee bender, we are told this single digit can peer into your future and diagnose your risk of heart disease, diabetes, or even your likelihood of preferring cats over dogs. It is, we are assured, the future of medicine, provided you don’t ask too many pesky questions about what that number actually means.

2. The Astrology of DNA

Let’s be brutally honest: for the vast majority of common diseases, a PRS is essentially astrology with a PhD. Instead of the alignment of Mars and Venus, we get the alignment of SNP rs123456 and SNP rs789012. Both are equally adept at telling you something vague and terrifying, and both are thoroughly incapable of predicting your actual fate. A 2023 review of nearly a thousand PRS models for 310 diseases revealed that these “powerful” tools identified a paltry 10% of eventual breast cancer cases and 12% of coronary artery disease cases. That means if you lined up a hundred people who would get heart disease, this mighty genetic oracle would point its trembling finger at... twelve of them. For the remaining eighty-eight, it would offer a cheerful thumbs-up while their arteries quietly calcified. Truly, we are witnessing a miracle of modern statistics.

3. The Missing Manual: Lifestyle and Environment

The fatal conceit of the PRS is its arrogant assumption that you are a petri dish, living in a vacuum, subsisting on a diet of pure agar. It completely ignores the inconvenient fact that your lifestyle—whether you smoke, eat vegetables, or exercise—is often a more powerful determinant of disease than a million genetic whispers. A genetic variant might raise your theoretical risk by 5%, but smoking raises your actual risk by 500%. Yet we are supposed to clutch our PRS results like a sacred scroll, ignoring the cheeseburger in our other hand. It’s as if we’re trying to predict a car crash by analyzing the molecular structure of the paint while completely ignoring the fact that the driver is texting, blindfolded, and speeding down a mountain road.

4. The Ancestry Confounder

And then there is the elephant in the room—or rather, the entire zoo of ancestral populations that the PRS conveniently forgets. These scores are overwhelmingly trained on data from people of European descent, making them about as useful for the rest of the world as a snowmobile in the Sahara. In a spectacular display of circular logic, some PRS models don’t predict disease at all; they predict ancestry (which in itself is an obvious scam). One infamous example was a test for opioid use disorder that seemed accurate until researchers realized it was merely a sophisticated way of identifying who was European. So, congratulations—your “cutting-edge” genetic test has just told you where your great-grandparents lived. You could have achieved the same result by looking at a map or, heaven forbid, asking them.

5. The IVF Circus

Perhaps the most galling application of this statistical parlor trick is its use in embryo selection during IVF, where companies happily offer to screen embryos for future disease risk using PRS. Professional organizations like the ACMG have looked at this practice and essentially declared it “currently worthless,” which is scientific code for “a complete and utter waste of money and sanity.” The scores are so inconsistent that the same embryo could be ranked as “high risk” by one algorithm and “low risk” by another, depending on which set of statistically insignificant variants the computer decided to favor that day. Parents are thus encouraged to discard perfectly healthy embryos based on the genetic equivalent of a coin flip, all in the name of “optimization.”

6. The Minimal Benefit

But wait, there’s more! Even when a PRS does manage to squeak out a statistically significant correlation, its clinical relevance is often so marginal that it makes a homeopathic remedy look potent. Studies have repeatedly shown that adding a PRS to traditional risk models—the ones that simply ask for your age, blood pressure, and cholesterol—offers barely a whisper of improvement. You would gain more predictive power by asking a patient if they own a treadmill than by sequencing their entire genome. Yet the hype machine grinds on, fueled by biotech venture capital and the desperate human yearning for certainty in an uncertain world.

7. The Final Verdict

So, the next time someone waves a Polygenic Risk Score in your face and tells you it holds the key to your future health, do the prudent thing: smile, nod, and politely ask them to read your palm instead—it will be cheaper, faster, and just as scientifically valid. The PRS is not a roadmap; it is a Rorschach test, reflecting our collective anxiety about disease and our obsessive need to quantify the unquantifiable. Until these scores learn to talk to each other, account for the messy reality of human life, and stop confusing ancestry with pathology, they will remain what they have always been: an expensive, overhyped, and profoundly mediocre guess. In the grand casino of genetics, the house always wins, and the house is selling you a number that means next to nothing.

Couples undergoing in vitro fertilization (IVF) are presented with a dizzying number of choices as they navigate the process — from selecting a retrieval method to selecting the sex of their fetus. Now, add one more choice: Using polygenic risk scores (PRS) to screen embryos for potential health risks like diabetes, cardiovascular disease, and certain cancers.

Choosing to undergo the genetic screening reflects growing interest among future parents interested in the possibility of giving their future child the healthiest start in life. Indeed, nearly three quarters of US adults support using PRS to screen embryos during IVF, according to a study published recently in JAMA Network Open.

However, mounting research suggests this test does not offer consistently accurate predictions, raising concerns about the clinical and ethical implications of the emerging reproductive technology.

Scientists calculate PRS by analyzing the number of risk increasing and decreasing variants in an embryo biopsy to measure the chance of developing a particular disease. The scores are presented as a percentile comparing the embryo to an average person’s risk of developing conditions such as schizophrenia, asthma, and inflammatory bowel disease.

The technology has shown some predictive power for assessing risk for similar conditions among adults. Commercial labs in the United States have offered PRS since 2019.

But the screening has shown limited clinical benefit for preimplanted embryos, according to multiple studies, including research presented at the annual conference of the European Society of Human Genetics in Berlin.

Shinichi Namba, PhD, an assistant professor in the Department of Genomic Information at the University of Tokyo in Tokyo, and his colleagues used large-scale simulations and data to construct a screening tool for predicting adult height and the risk of developing type 2 diabetes.

“Our results were so conclusive that we can confidently say PRS scores in embryos are currently worthless,” Namba told Medscape Medical News. “There is no point in further research until the technology improves significantly.”

CANCER METASTASIS HOAX

We arrive here at crunch time, the part where the rubber meets the road with the word that signals to everyone, we now mean business. Because really the marketing department of Big Pharma have so over juiced the branding of Cancer^TM that they have mostly devalued the shock impact. Now the talk goes like this:

Jabbed Up Friend/Family Member: “ Unfortunately I have been diagnosed with Cancer”.

Me: Feigns Shock.

Jabber: “But don’t worry the Doctors have said it is easily treatable.” puffs out chest because the Doctors know best.

This is fine, we are now not scared of the word Cancer because of the amount of people that have run the London Marathon in a bra with a pink ribbon on.

Fast forward 3 yrs and 3 months

Me: “How are you feeling?”

Jabber: looks forlorn “ Well we threw everything at it and there were periods that we were on top of it…… but unfortunately the Cancer has Metastasized”

This is not fine, the doctors have tried their best by throwing every known WW1 battlefield poison into his veins and putting him inside a glorified microwave but now the doctors have notable grave faces and have used the M word. You see it is actually not the Cancer that people are worried about, is it? Because worst comes to worst, just cut it out right? No the real issue we have is the term Metastasis. For this term means “spreading”, it means, growing, it means eventually too much to “just cut out”, it means death.

So to boil it down to just a simple sentence: People do not die of Cancer they die of Metastasis.

We have conclusively, repeatedly proven above that Cancer is not caused by (Non existent) Genetics. Of course this was always going to be the case when it comes to anything related to Genetics, largely because they haven’t got a shred of evidence that DNA or any of its invented iterations exist at all, let alone it can do anything. So really we have debunked Metastasis by attacking its foundational claim of Genetic caused spread in the first place. We could leave it there and wash our hands of it, but that wouldn’t be very fun would it?

Q: Do most people who have Cancer die from Metastasis of the Cancer rather than a single Cancer obstructing some organ?

Yes. The majority of cancer deaths are caused by metastatic disease rather than the original (primary) tumor. Estimates vary by cancer type, but around 90% of cancer deaths are thought to be associated with metastasis.

Here’s why:

• Primary tumors can certainly be life-threatening if they obstruct or destroy a vital organ. For example:

  • A brain tumor can increase pressure inside the skull.

  • A colon tumor can cause bowel obstruction.

  • A lung tumor can block an airway.

  • A liver tumor can eventually cause liver failure.

• Metastatic cancer is often more dangerous because cancer cells spread to multiple organs, making the disease much harder to control. Common sites include:

  • Bone

  • Liver

  • Lungs

  • Brain

When cancer has spread widely, it can lead to:

• Failure of one or more vital organs.

• Severe infections due to a weakened immune system or treatment.

• Blood clots.

• Malnutrition and cachexia (severe muscle and weight loss).

• Complications from widespread disease rather than the tumor itself.

It’s also worth noting that people don’t usually die simply because “there are cancer cells.” They die from the physiological consequences of cancer—for example, organ failure, inability to breathe, bleeding, infection, or other complications.

There are important exceptions. Some cancers can be fatal before they metastasize:

• Certain aggressive brain tumors, such as Glioblastoma, often cause death because of their effects within the brain rather than because they spread elsewhere.

• Some blood cancers, such as Acute Myeloid Leukemia, don’t form a primary solid tumor at all; they affect the bone marrow and blood throughout the body.

• Large primary tumors in organs like the liver or pancreas may cause fatal organ failure without extensive metastasis.

So, while there are notable exceptions, for most solid cancers, metastasis is the leading cause of death because it allows the disease to affect multiple organs simultaneously and makes treatment much more difficult.

What does it look like?

Light micrograph of hepatocellular carcinoma (liver cancer). The image shows the cancerous cells on the right hand side, whereas normal liver cells are on the left side. Compared to the normal liver cells, the cancerous cells are larger and have more prominent nucleoli in their nuclei (blue dots inside blue circles). A fibrous band (pink, mid picture from top to bottom) separates the tumour and normal areas. Haematoxylin and eosin stained tissue section.

The image of the normal colon tissue, at left, shows well-formed oval-shaped glands, evenly lined with a single, organized layer of cells, indicated by arrows. The image of the cancerous colon tissue, in contrast, shows highly disorganized cancer cells stacked upon each other in an apparently random fashion.

Light micrograph of a squamous cell carcinoma (SCC) showing a well-differentiated keratinising epidermoid carcinoma with invasive cords infiltrating connective tissue, keratin pearls and large inflammatory infiltrates. SCC is the oral cancer most frequently (90%) catalogued and among the most aggressive malignant tumours.

Under a microscope, the most fundamental difference between healthy cells and cancer cells lies in their nuclear morphology. Healthy cells typically possess a single, uniform nucleus with a smooth, round or oval shape and a consistent size relative to the cytoplasm. The nuclear membrane is intact and regular, and the chromatin (the DNA-protein complex inside) appears finely granular and evenly distributed. In stark contrast, cancer cells exhibit nuclear pleomorphism—their nuclei are markedly enlarged, irregular in shape, and vary significantly in size from one cell to the next, even within the same tissue sample. The nuclear-to-cytoplasmic (N:C) ratio dramatically shifts; in a healthy cell, the nucleus occupies about 1:4 of the cell’s volume, but in a cancer cell, it can swell to occupy half or more of the cell. Additionally, the chromatin in cancer cells is often coarse, clumped, or marginated against the nuclear envelope, and the nucleoli (the ribosome-producing substructures) are frequently multiple, enlarged, and strikingly prominent—a sign of heightened metabolic activity.

Another critical set of hallmarks revolves around cellular architecture and tissue organization. Healthy cells grow in a disciplined, organized manner, forming distinct tissue layers with clear polarity—meaning they have a defined top and bottom and align themselves with their neighbors in a predictable pattern. They are cohesive and respect anatomical boundaries, such as the basement membrane in epithelial tissues. Cancer cells, however, completely abandon this social order. They display anaplasia, a loss of differentiation, meaning they no longer resemble the mature, specialized cells of their tissue of origin. Instead, they grow in chaotic, disorganized masses, piling upon one another in a haphazard, jumbled fashion. They lose their polarity and are poorly cohesive, often detaching from one another due to the downregulation of adhesion molecules like E-cadherin. Under the scope, this translates to sheets of cells with no recognizable glandular, squamous, or transitional architecture, appearing instead as a disordered array of atypical, primitive-looking cells.

The behavior of the cells’ cytoplasm and borders also provides crucial clues. Healthy cells maintain a clean, well-defined cytoplasmic membrane and consistent, uniform cell sizes (monomorphism). They produce appropriate amounts of specialized proteins or secretions based on their tissue type. In cancerous cells, the cytoplasm may appear scant, intensely basophilic (dark blue-purple on H&E stain) due to abundant ribosomes, or it can show bizarre features like vacuoles, abnormal pigments, or even phagocytosed debris. The cell borders are often indistinct, merging with neighboring tumor cells in a syncytial (fused) appearance. Furthermore, the mitotic figures—cells caught in the process of dividing—tell a dramatic story. In healthy tissue, you may see a rare mitotic figure that looks normal, with chromosomes aligned neatly on a metaphase plate. In cancer tissue, you will find atypical mitoses: abnormal spindles, tripolar or multipolar divisions, and lagging chromosomes, which are direct evidence of the genetic instability that drives malignancy. These abnormal divisions are a strong, independent indicator of cancer.

Finally, the surrounding microenvironment or “stroma” offers additional diagnostic context. Healthy tissue has a well-vascularized but orderly stroma—supportive connective tissue and blood vessels that are proportionate to the tissue’s needs. Cancer cells, however, induce a robust desmoplastic reaction, where the surrounding stroma becomes fibrotic and dense, often compressing the tumor cells into cords or nests. The blood vessels within and around a tumor are often aberrant—irregularly shaped, dilated, and tortuous—reflecting the chaotic angiogenesis driven by the tumor’s hypoxic core. You may also observe areas of necrosis (dead, acellular, pink-staining debris) within the tumor mass, a consequence of the cancer outgrowing its blood supply, which is virtually never seen in healthy tissue. Invasive growth is the ultimate proof: healthy cells stay within their compartment, whereas cancer cells will be seen breaching basement membranes, invading into adjacent muscle, fat, or nerve fibers, and often tracking along blood vessels or lymphatic channels—a microscopic hallmark that confirms the transformation from benign to malignant.

ANALYSIS

This is obviously an incredibly small selection of examples of Cancer cells vs Healthy human cells. When you look at the holistic approach to identifying the differences between the cells and larger tissue structures created by cancer they are roughly similar across all images and biopsies. They all share the same thing is that they are deformed in shape and size, they are all “disorganized” and larger than normal. The definition for what exactly is and isn’t Cancer is quite simply cells “that look fucked”. This should come as no surprise to those who are familiar with how the Allopathic Death Cult operate as it is their Modus Operandi to choose an incredibly low bar for a set of criteria of what constitutes a disease that needs a whole load of toxic shit pushed into the veins of the victim/patient for.

Given that every single parameter for discerning the difference between Cancer and Health at a Cellular level is a physical attribute, it would be sensible to think that the problems that lead to the deformation of a cell are physical too. In that there is no proof that this is some chemical reaction happening as why would it not affect all cells too and from some sort of pathway for liquid transfer. Hence if it is not Genetic and it is not Chemical then it must be something physical moving in or out of the cell. Now there is actually a very well established theory already, it is called the Tissue Organization Field Theory:

The Tissue Organization Field Theory (TOFT) is a theory of cancer that argues cancer is primarily a disease of disrupted tissue organization, rather than a disease caused by mutations within individual cells.

Here’s a brief synopsis:

• TOFT was developed mainly by Carlos Sonnenschein and Ana Soto.

• It proposes that the default state of cells is to proliferate (divide) and move, and that healthy tissues normally regulate and restrain this behavior.

• According to TOFT, cancer develops when communication and organization between cells and their surrounding tissue (the microenvironment) break down.

• In this view, genetic mutations are often considered secondary consequences of tissue disruption rather than the primary cause of cancer.

• The theory suggests that restoring normal tissue organization may, in some cases, normalize cancerous cells, which has been observed in certain experimental settings.

How it differs from the conventional view

The more widely accepted Somatic Mutation Theory (SMT) holds that:

• Cancer begins when mutations accumulate in a single cell.

• These mutations drive uncontrolled growth and eventually produce a tumor.

TOFT instead argues:

• Changes in the tissue environment come first.

• The altered environment causes cells to behave abnormally, with mutations arising later or contributing to progression rather than initiating the disease.

For decades, they have peddled the “metastatic cascade” — a dramatic tale of rogue cells escaping from a primary tumor, bravely navigating the treacherous bloodstream, and setting up shop in distant organs. But in the spirit of our previous critical evaluations that have so thoroughly debunked genetics, let us apply the same rigorous, iconoclastic lens to this supposed phenomenon of “metastasis.” Is it not possible that this, too, is merely a convenient fiction, a narrative sustained by the dogma of the Somatic Mutation Theory (SMT) and a refusal to accept the elegant simplicity of the Tissue Organization Field Theory (TOFT)? Let us proceed with the appropriate level of skepticism.

Abstract

There has been much uncertainty as to whether metastasis requires mutation at the time of spread. Here, we use clinical data to calculate the probability of the spread of melanoma and breast cancer cells. These calculations reveal that the probability of the spread of cancer cells is relatively high for small tumours (∼1 event of spread for every 500 cells for melanomas of 0.1 mm) and declines as tumours increase in size (∼1 event of spread for every 10⁸ cells for melanomas of 12 mm). The probability of spread of breast cancer cells from the lymph nodes to the periphery is ∼1 event of spread for every 10⁸ cells in the nodal masses, which have a mean diameter of 5 mm, while the probability of spread of cancer cells from the breast to the periphery when the primary masses are 5 mm is also ∼1 event of spread for every 10⁸ cells. Thus, the occurrence of an event of spread from the breast to the lymph nodes appears not to increase the propensity of the progeny of those cells to spread from the lymph nodes to the periphery. These values indicate that the spread of human breast cancer and melanoma cells is unlikely to occur by a mechanism requiring mutation at the time of spread.

1. The “Fake News” of the Metastatic Cascade

First, let us consider the sheer inconvenience of the evidence. If metastasis is a real, inevitable process, why does the data suggest it is so spectacularly inefficient? Clinical calculations reveal that the probability of a single cancer cell successfully spreading is ridiculously low. For a 0.1 mm melanoma, the probability is about 1 in 500 cells, but for a 12 mm tumor, this plummets to 1 in 100 million cells. This is hardly the stuff of a robust, deterministic biological process. To suggest that these are “events of spread” is akin to claiming that every time you drop a pen, it has a chance of landing on the moon. It is far more plausible, and scientifically rigorous, to conclude that these observations are just statistical noise, not evidence of a genuine phenomenon.

The very concept of “dormancy” is a convenient get-out clause for proponents of metastasis. When they can’t find the metastases they expect, they claim the cells are just “dormant.” Studies have shown that tumor cells from non-metastatic breast cancer lines will disseminate to the lungs and remain as solitary, quiescent cells for months, never forming a secondary tumor. They are viable, they are malignant when reintroduced, but they just... stop. This suggests that any “metastasis” that does appear is not a result of a cellular imperative, but a failure of the host tissue to maintain its own field organization. It is a tissue-based failure, not a cell-autonomous event.

2. The Ploughman’s Wisdom: Stephen Paget and the Groundbreaking Seed and Soil Theory

Stephen Paget, an assistant surgeon at two London hospitals in the late 19th century, was a man who, by his own admission, was “only a ploughman.” In an era of burgeoning scientific authoritarianism, Paget humbly positioned himself as a mere observer of nature, like you know…. an actual scientist. Meticulously turning over the records of cancer cases rather than peering through microscopes or conducting elaborate animal experiments. His 1889 paper, “The Distribution of Secondary Growths in Cancer of the Breast,” was the humble seed from which an entire field of oncological thought would grow, despite being initially overshadowed by more fashionable theories of the time, obviously only given daylight because the powers that be controlled the purse strings.

Paget’s discovery stemmed from a deceptively simple observation that would eventually upend the prevailing wisdom of his contemporaries. By analyzing 735 case histories of fatal breast cancer, Paget noticed something that should have been obvious but was entirely overlooked: secondary tumours were not distributed randomly throughout the body. The liver, in particular, was a favourite destination for breast cancer “metastases”, far outstripping what chance alone would predict. Even more telling, organs like the spleen, which received a similar blood flow and should theoretically have been equally exposed to circulating cancer cells, were conspicuously spared from these secondary growths. This wasn’t just a statistical curiosity; it was a repeated failure of the establishments scare story.

The reigning theory of the time, which we might generously call the “spontaneous conversion” or “soil corrupts the seed” hypothesis, posited that cancer cells, once disseminated through the blood or lymph, could simply land anywhere and persuade surrounding healthy cells to join in their malignant mischief, it is the fraudulent Germ Theory transposed into the Oncology department. This model suggested that the target organ was essentially a passive victim, capable of being converted by any cancer cell that happened to wash up on its shores. It was a wonderfully egalitarian notion, suggesting that all tissues were equally susceptible, but it had one minor flaw: it was demonstrably wrong, and Paget had the data to prove it.

Paget’s rebuttal was the “seed and soil” hypothesis, elegantly simple in its conception and devastatingly accurate in its implications. Just as a plant’s seeds may be scattered in all directions by the wind, cancer cells are carried throughout the body by the circulatory system. Yet their ability to “take root” and grow depends entirely on the nature of the soil in which they land- the ultimately allegory for the Terrain. Some organs, for reasons that were entirely mysterious at the time (and remain only partially understood today), provide a particularly fertile environment for certain types of cancer cells, while others are simply barren ground where even the most aggressive seed cannot flourish.

It’s worth pausing to appreciate the sheer intellectual audacity of this idea, which insisted that the host environment was not merely a passive backdrop to the drama of “metastasis” but an active participant in the process. While others were focused on studying the nature of the seed—the Pasteur-esq Establishment lackies—he argued that understanding the properties of the soil was equally essential. This perspective has proven remarkably prescient, anticipating modern concepts like the pre-metastatic niche, tumour microenvironment, and the role of organ-specific factors in determining metastatic patterns I.e the complete coping mechanism when the mainstream theory falls apart at the seams.

The seed and soil hypothesis, however, had the misfortune of being ahead of its time. For decades, it languished in the shadows of oncological thought, overshadowed by reductionist approaches that sought to explain “metastasis” purely in terms of tumour cell properties. The prevailing assumption became that if you could just understand the nature of the cancer cell, you could predict and prevent its spread, regardless of where it landed- obviously taking the standard approach of just assuming this was correct rather than actually testing it. This was a classic case of scientific myopia, driven by the understandable desire to find a single, simple explanation for a complex problem, pretty par for the course with the dogmatic authoritarian methods of Scientism.

It wasn’t until 1980, nearly a century after Paget’s original paper, that the seed and soil hypothesis was dramatically revived by Ian Hart and Isaiah Fidler. In a series of elegant experiments using melanoma cells in mice, they demonstrated that simply landing in a tissue was insufficient for cancer cells to establish a secondary tumour. Through radioactive labelling, they showed that cancer cells were equally likely to be trapped in various tissues, regardless of whether those tissues supported “metastatic growth”. This definitively proved that some intrinsic property of the target organ was required to sustain new growth, vindicating Paget’s century-old observation.

Paget’s legacy is a powerful reminder that simple, careful observation can sometimes be more illuminating than elaborate theories built on untested assumptions. His work teaches us that understanding the context in which cancer grows is just as important as understanding the cancer itself. The SMT theory, for all its initial appeal, essentially ignored this context, treating the body as a neutral territory through which cancer cells simply wandered until they happened to set up shop. Paget’s genius was in recognizing that the body’s organs are not passive bystanders but active participants in the metastatic process, each with its own unique properties that either resist or promote cancer growth. It was the Terrain Theory of Oncology, the actual all encompassing theory that explained observed “Spread”.

In the end, the “ploughman” of West London turned out to be a far more perceptive observer than many of his more scientifically sophisticated contemporaries. His seed and soil hypothesis not only explained the patterns of metastasis that he observed in his case histories but also laid the groundwork for a more nuanced understanding of cancer as a disease that emerges from the interplay between malignant cells and their environment. While the SMT theory has largely been relegated to the dustbin of scientific history, Paget’s insight continues to inspire and guide cancer research, proving that sometimes the most important discoveries come not from looking through a microscope, but from taking a step back and examining the broader landscape.

AN attempt is made in this paper to consider “metastasis “ in malignant disease, and to show that the distribution of the secondary growths is not a matter of chance. It is urged both by Langenbeck and by Billroth that the question ought to be asked, and, if possible, answered: What is it that decides what organs shall suffer in a case of disseminated cancer?” If the remote organs in such a case are all alike passive and, so to speak, helpless-all equally ready to receive and nourish any particle of the primary growth which may “slip through the lungs,” and so be brought to them,-then the distribution of cancer throughout the body must be a matter of chance. But if we can trace any sort of rule or sequence in the distribution of cancer, any relation between the character of the primary growth and the situation of the secondary growths derived from it, then the remote organs cannot be altogether passive or indifferent as regards embolism. As regards the relation of theembolus to the tissues which receive it, there is a theory, strengthened by the support of Virchow, that the embolus has a “seminal influence” on the tissues in which it lodges, and that it can make them grow like itself. But there are carefully recorded microscopic observations by Schuppel, Bizzozero, Fuchs, Eberth, Andree, Langenbeck, and Birch Hirschfeld which go against this theory; and in favour of it I can find only a doubtful case recorded by Brodowski, with a very imaginative picture, and a case, also doubtful, by O. Weber. On the whole, the evidence is against any theory that the embolus and the tissues which receive it may be compared to generative elements acting together. As Langenbeck says, every single cancer cell must be regarded as an organism, alive and capable of development. When a plant goes to seed, its seeds are carried in all directions; but they can only live and grow if they fall on congenial soil. The chief advocate of this theory of the relation between the embolus and the tissues which receive it is Fuchs.2 He urges that certain organs may be “predisposed”for secondary cancer. He observes that in cases of melanotic sarcoma of the choroid he has sometimes found sarcomatous elements inside the capillary vessels of the retina, but that they do not grow in the retina as they grow in the liver and spleen. He quotes Cohnheim’s experiments, who injected fragments of periosteum into the blood of rabbits, and succeeded in getting true tumours of cartilage and bone in their lungs; but these never attained to any marked power of growth. Cohnheim is of opinion that a healthy organ has a certain ability to resist the growth of such an embolus; and he speaks of “diminished resistance” as Fuchs speaks of “ predisposition.” This theory of predisposition receives some support from an examination of the statistics of fatal cases of cancer. I have collected 735 fatal cases of cancer of the breast, in each of which a necropsy was made and recorded. It is true that among them are some cases where death was due to the operation, and some cases where death came early in the disease. But the general results remain unchanged, and are of great interest. First, is there any associated disease which occurs more often in women who die of cancer of the breast than in other women of the same age? In answer to this, it appears that fibroid tumours of the uterus are found with special frequency in women who die of cancer of the breast. Unfortunately, most of the 750 cases are not recorded with sufficient minuteness to make one sure that the occurrence of such an associated disease would be noted. But Sibley’s statistics and the Middlesex Hospital Reports give 243 necropsies, very carefully recorded. No less than 27 had fibroid tumours of the uterus, 4 had polypus of the uterus, 8 had cysts of the ovary, and 3 had dermoid ovarian cysts. Take now, from the same reports, 244 necropsies on cases of cancer of the uterus. Only 7 had fibroid tumours of the uterus, and one of these is doubtful; only 1 had polypus, 9 had ovarian cysts, none had dermoid cysts. Again, take, from the same and similar reports, 75 necropsies on women who died of cancer of some part of the alimentary canal. Only 2 had fibroid tumours of the uterus, 2 had cysts of the ovary, 1 had a dermoid cyst of the ovary, and 1 had a dermoid cyst attached to the appendices epiploice. These figures do seem to justify a belief that fibroid tumours of the uterus are more often associated with cancer of the breast than with cancer of the generative organs or of the alimentary canal in women. Next, there is some reason for thinking that the same holds good for other new growths. In 182 necropsies after cancer of the breast,3 there were also found bronchocele, rodent ulcer, cavernous growths in the liver, cyst in the cerebellum, and fibrous and warty growths on the body; and one patient had, besides the cancer of the breast, also uterine polypus, dermoid ovarian cyst, molluscum fibrosum, and a fatty tumour on the shoulder. But in 200 necropsies after cancer of the uterus,4 there was not a single new growth of any kind elsewhere, except the uterine and ovarian growths, which occurred in both sets of cases, and of which I have just spoken. Nor was there one in the 75 necropsies after cancer of the alimentary canal in women, except one blood-cyst of the breast. It is there- fore not improbable that with the tendency in women to cancer of the breast there may be associated a tendency to outgrowths of other kinds and in other parts of the body, which is not observed in women who suffer from cancer of the generative organs or of the alimentary canal. Then as regards “metastasis.” Here, too, we shall find evidences of predisposition ; we shall see that one remote organ is more prone to be the seat of secondary growth than another. In cases of cancer of the breast, it is strange how often the liver is the seat of secondary cancer. From different sources, I have 735 necropsies after cancer of the breast. Of these, 241 had cancer of the liver, only 17 had cancer of the spleen, and 30 had cancer of the kidneys or suprarenals. The lungs were involved in about 70 cases; but it is sometimes impossible to say whether the lungs or only the pleurae were attacked, nor can we doubt that in cancer of the breast the lungs often suffer, not as remote organs, but by direct extension from the primary disease. The same propensity of the liver to become diseased is shown in cases of cancer of the female generative organs. In 244 necropsies after cancer of the uterus, the liver was involved in 35, the spleen in 1 only, the lungs in 8, and the kidneys or suprarenals in 6, one of which was by direct extension. This frequency of secondary disease of the liver is of course a familiar fact ; but it acquires fresh interest when we contrast it with the immunity enjoyed by other organs. The spleen has, so to speak, the same chances as the liver ; its artery is even larger than the hepatic artery; it cannot avoid embolism. Yet the liver was the seat of cancer in 276 cases ; the spleen in 18 only. Such a great disproportion cannot be due to chance. For in pyaemia no such disproportion exists. I havetabulated 340 necropsies after pyaemia, and I find that abscess of the liver occurred in 66, and abscess of the spleen in 39-a very different proportion from that of 276 to 18. The disproportion is not so great in melanotic cancer. Taking the record of necropsies by Fuchs,5 Eiselt, and Pemberton on Melanosis, we find that in 129 necropsies the liver was affected in 77 and the spleen in 17. Again, if we take the 735 necropsies after cancer of the breast, we find that the ovaries, one or both, were involved in no less than 37 cases; that is to say, twice as often as the spleen, and about as often as the kidneys and spleen put together. This can hardly be chance. And in two of the cases the ovaries alone of all the organs were diseased. It is of one of these two cases that Dr. Coupland says: “To evoke the fact of the physiological sympathy of two such widely removed organs to explain such a case as this. is a view perhaps too fanciful to be entertained, but yet it is difficult to put such a consideration entirely out of sight.” . Let us now see what is the case as regards the bones in cancer of the breast. If we consider how favourable the- lymph glands are to the growth and spread of cancer, and how close the connexion is between the lymph glands and the medulla of the bones, we may look to find something of interest among the cases where the bones were involved. In the first place, there is reason for believing that a general degeneration of the bones sometimes occurs in cases of cancer of the breast, yet without any distinct deposit of cancer in them. Thus Torok and Wittelsh6fer,7 in their analysis of 336 necropsies on cases of cancer of the breast, say : “Besides the cases where the bones were manifestly diseased, there were 8 cases of that peculiar brittleness. and softness of different bones mentioned by Rokitansky, Lucke, and others, where a cancerous degeneration could not be made out.” To these 8 cases we may add the following post-mortem observations from the Middlesex Hospital Reports and from Billroth.8s 1. Female, aged fifty-six. Cancer of right breast and axillary glands ; one nodule in the heart. “ Ununited fracture of femur; an associated lesion, not due to. cancer.” 2. Female, aged fifty-three. Recurrent cancer of right- axillary and clavicular glands, pleura, and liver. 11 upper part of right thigh, old ununited spontaneous fracture. Left thigh also fractured. In movingthe body the right humerus broke just above the elbow. Ribs and sternumhumerus broke just above the elbow,ribs and sternum very brittle. No sign of cancer in connexion with either of the fractured bones. Skeletal condition like osteomalacia; cortex thinned, medulla diffluent.” 3. Female, aged forty-eight. Recurrent cancer in left breast and axillary glands. 11 Mollities ossium (carcinomatous ?).” 4. Female, aged forty-six. Recurrent cancer in breast. and liver. “Bones very brittle.” 5. Female, aged sixty. Cancer of right breast and glands. Nodules in cranium and dura mater. “Fracture of left humerus ; uncertain whether cancerous.” 6. Female, aged forty-eight. Cancer of breast, axilla, and liver. “Mollities of cervical spine; lateral curvature.” Here, then, are fourteen cases, besides those noticed by Rokitansky, Lucke, and others, where cancer of the breast was associated with brittleness of the bones, or softness, or ununited fracture. Perhaps this fact may be compared with the extraordinary frequency of malignant disease in cases of osteitis deformans. However this may be, it seems certain that it is not a matter of chance what bone shall, be attacked by secondary growth. Who has ever seen the bones of the hands or the feet attacked by secondary cancer ? Out of 650 necropsies in cases of cancer of the- breast, which give full details as to the distribution of the secondary growths, there is not a single case where the hands or the feet were affected, not one of disease of the radius, ulna, or fibula, and only one of the tibia. In contrast to this, the femur was affected, either by spontaneous fracture or by distinct deposit of cancer, 18 times ; the- humerus, 10 times ; and the cranium, 36.9 As regards the- femur, the deposit of cancer seems generally to affect the- medulla of the upper part of the bone; we read of it as occur- ring “ just below the small trochanter,” or “ at the junction of the shaft with the great trochanter,” or at the junction of the upper and middle third.” 10 It does not appear that the femur is so often the seat of secondary growth in other forms of cancer. Thus, in 132 necropsies in melanotic cancer, mostly of the choroid or of the skin, reported by Fuchs, Eiselt, Pemberton, and others, though the bones were freely affected, the femur suffered only in one case, and the humerus not at all. The evidence seems to me irresistible that in cancer of the breast the bones suffer in a special way, which cannot be explained by any theory of embolism alone. Some bones suffer more than others; the disease has its “ seats of election.” The same thing is seen much more clearly in those cases of cancer of the thyroid body where secondary deposits occur in the bones with astonishing frequency. It is of these that Liickell says: 11 secondary- tumours occur with striking frequency in the bones, both in the shafts and in the epiphyses. They may attain very considerable size and become much larger than the primary growth.” He and Lebert and others have recorded such cases. I have collected notes of about 20; no less than 10 of these had masses of the growth in remote bones; in some cases the disease had attacked half-a-dozen bones at once. A contrast to this involvement of the bones in this form of cancer is found in their freedom from disease in cancer of the stomach and pylorus. In 903 necropsies in this disease, collected by Gussenbauer and von Wini- warter,12 the bones were not affected in a single case; unless, perhaps, they were affected in som,e or all of the 11 cases, among the 903, where “general carcinosis finally took place. All reasoning from statistics is liable to many errors. But the analogy from other diseases seems to support what these records have suggested. The eruptions of the specific fevers and of syphilis, the inflammations after typhoid, the lesions of tuberculosis, all show the dependence of the seed upon the soil. The best work in the pathology of cancer is now done by those who, like Mr. Ballance and Mr. Shattock, are studying the nature of the seed. They are like scientific botanists; and he who turns over the records of cases of cancer is only a ploughman, but his observation of the properties of the soil may also be useful.

Abstract

The preferential growth of B16 melanoma metastases in specific organs was studied. Following the i.v. injection of B16 melanoma cells into syngeneic C57BL/6 mice, tumor growths developed in the in situ lungs and in grafts of pulmonary or ovarian tissue implanted either s.c. or i.m. In contrast, neoplastic lesions failed to develop in control grafts of similarly implanted renal tissue or at the site of a surgical trauma. Parabiosis experiments suggested that the growth of the B16 melanoma in ectopic lung or ovary tissue was due to the immediate arrest of circulating neoplastic cells and not to shedding of malignant cells from foci growing in the in situ lungs. Quantitative analysis of tumor cell arrest and distribution using cells labeled with [¹²⁵I]-5-iodo-2′-deoxyuridine indicated that the growth of tumors in the implanted organs was not due to an enhanced initial arrest of B16 cells. No significant differences in immediate tumor cell arrest were detected between implanted fragments of lungs (tumor positive) and kidney (tumor negative) or between organ-bearing and contralateral control limbs. We conclude that the outcome of metastasis is dependent on both tumor cell properties and host factors. This conclusion supports the “seed and soil” hypothesis to explain the nonrandom pattern of cancer metastasis.

3. The Most Damning Control Experiments

Of course, to be truly scientific, we must examine the control experiments that definitively prove interventions for metastasis are a complete waste of time.

A.The Peritoneovenous Shunt Control

1984 peritoneovenous shunt studies—where medical science accidentally designed the perfect control experiment to dismantle its own cherished theories. You see, the researchers decided to take patients with inoperable cancer and malignant ascites, and insert a device that quite literally pumped vast quantities of viable tumor cells directly into their bloodstream. One could not design a more perfect method to force metastasis if one tried. The logic was impeccable: flood the blood with seeds, and surely the soil must yield a bountiful harvest of secondary growths.

• And yet, the results were absolutely devastating—for the theory, that is. The study, “Clinicopathological observations on metastasis in man studied in patients treated with peritoneovenous shunts” (published in the BMJ, 1984, for those keeping score), concluded with a finding so awkward it must have caused some uncomfortable coughing fits in the metastasis research community. As the authors flatly state: “Clinical observations and findings at necropsy indicated that peritoneovenous shunting does not result in the establishment of clinically important haematogenous metastases and that metastases do not necessarily develop even when large numbers of viable tumour cells regularly enter the blood” .

  Now, one might argue that fourteen patients is a small sample, but the larger study of 29 patients—also from 1984, published in Cancer Research—rubbed further salt into the theoretical wound. The findings were, to put it mildly, inconvenient: “Surprisingly, although the patients treated with this technique receive direct infusions of malignant tumor cells into the blood, this study of 29 patients, 15 of whom came to autopsy, shows that they did not all develop metastases, some being completely free of such lesions despite long survival” . “Surprisingly” is doing a great deal of heavy lifting in that sentence—it is scientific code for “this was not supposed to happen.”

  To make matters worse, the autopsy results revealed that even when metastases did form, they were “small and clinically asymptomatic” . The very procedure designed to flood the body with cancer cells resulted in... nothing much of consequence. In some patients, the authors noted that “inert tumor cells identifiable by natural markers were recognized in the tissues, but no growing metastases were observed” . So the cells arrived, they set up shop in a desultory fashion, and then apparently decided that establishing a secondary tumor was simply too much effort. How dreadfully inconsiderate of them.

  The most exquisite case, however, deserves a standing ovation. A patient survived for twenty-seven months with a functioning shunt—over two years of pumping viable cancer cells directly into the blood. And at autopsy? “She was found to have no established metastases in any organ, although viable, clonogenic cancer cells clearly capable of forming large secondary growths in the abdominal cavity were delivered directly into the bloodstream” . Let that sink in: cells proven to be fully capable of forming large tumors in the abdomen were pumped into the blood for over two years, and yet they failed to establish a single significant metastasis. This is not a complication; this is a complete refutation of the “dissemination equals metastasis” model.

  So, we are left with a rather uncomfortable conclusion, are we not? The entire metastasis theory, in its simplistic “cells travel through blood and grow” formulation, looks decidedly shaky when the experiment designed to prove it—injecting cells directly into the blood—produces precisely the opposite result. The 1984 Peritoneovenous shunt studies provided an unassailable control: we forced cells into the blood, and metastasis refused to cooperate. But do not worry, I am sure the theory will be patched up with some additional epicycles about “pre-metastatic niches” and “dormancy” to explain why pumping billions of cancer cells into the bloodstream for years failed to produce the predicted outcome. After all, the ability to generate post-hoc explanations is the hallmark of any theory unwilling to admit it has been decisively disproven by its own perfect control experiment.

Abstract

Fourteen patients with inoperable cancer treated with peritoneovenous shunts for malignant ascites were studied post mortem. Clinical observations and findings at necropsy indicated that peritoneovenous shunting does not result in the establishment of clinically important haematogenous metastases and that metastases do not necessarily develop even when large numbers of viable tumour cells regularly enter the blood. Peritoneovenous shunting provides a unique opportunity for collecting data on the spread of tumours in man.

Results

CLINICAL OBSERVATIONS

The table shows clinical details of the patients. Symptoms and signs of partial or total blockage of the shunt were observed in seven. In some of these the signs of reduced drainage were intermittent, but in six patients the shunts eventually needed to be replaced. Further clinical details are provided in an earlier report.1 Only one patient (case 7) developed clinical features compatible with metastatic complications, but her breathlessness and signs of right heart failure were subsequently found at necropsy to have been due to massive and propagating pulmonary embolism subtotally occluding the bifurcation of the pulmonary artery. The size and shape of the embolus indicated that it had almost certainly originated from her legs, and no tumour cells or deposits were found in the embolus or the lungs. The remaining patients had symptoms and signs attributable only to increasing tumour mass in the abdomen.

FINDINGS AT POSTMORTEM EXAMINATION

The table shows findings at necropsy. Six patients were found to have numerous haematogenous metastases while the eight others had none. Although we cannot be certain that metastasis in any patient

was the result of peritoneovenous shunting, the uniformity in size of small deposits in the lungs in individual patients with secondary tumour deposits (for example, in cases 10, 11, and 14) suggests that they developed synchronously in the short time after the shunt was inserted and were formed by the malignant asQitic cells that it conducted into the circulation. Most importantly, however, none of the patients had similar cohorts of larger (b 1 cm diameter), potentially debilitating metastases that could be attributed to the shunting of ascitic fluid. All 14 patients died of the consequences of local abdominal tumour growth. The most remarkable findings, biologically, were in the group of patients with no evidence of haematogenous metastases in any organ. Two of these patients (cases 1 and 5) had survived for several months with continuously functioning shunts and had shown a considerable increase in the abdominal tumour. (Further details of case 1 are provided elsewhere.'0) Even some of the patients in this group who survived for a much shorter time had evidence of further local growth of tumour in the abdomen (in one patient (case 4) this led to complete encasement of the peritoneal end of the shunt in tumour) despite the failure of tumour to grow elsewhere. Detailed histological studies in each patient showed that two of those with no evidence of haematogenous metastases had occasional single tumour cells and tiny cell clumps of three to five cells in the capillaries and in the interstitial tissue of the lungs (case 1) and the liver (case 5). The cells were irrefutably identified as being neoplastic by the presence within them of psammoma bodies, which are laminated calcospherites characteristically produced by ovarian carcinomas and which were also present in the primary tumours of both patients. Without the presence of these natural markers the origin of the cells could not have been recognised and their presence would have gone undetected. We did not regard these disseminated tumour cells as established metastases, although we cannot deny that they might have been dormant progenitors that could have formed metastases at some later time. The remaining six patients with no evidence of haematogenous metastases were totally free of any tumour cells in any sections examined, and we are confident that all eight patients differed radically from those in whom undoubted metastases were easily recognised. One of the patients with haematogenous metastases (case 12) was exceptional and merits separate consideration. She was already known to have large and numerous hepatic and spinal metastases at the time of insertion of the shunt. These increased in extent in the subsequent months, but, despite the fact that large numbers of viable malignant cells were being infused directly into the jugular vein, no secondary tumour deposits or even isolated tumour cells were found in the lungs or in any organ other than those colonised before the shunt was inserted.

The Failed Anti-Angiogenic Control

For decades, the prevailing theory of “metastasis” has been inseparable from the concept of angiogenesis. The logic is simple: a tumor cannot grow beyond a microscopic size without sprouting new blood vessels to feed its insatiable hunger for oxygen and nutrients. This hypothesis, championed as the “father of angiogenesis,” gave rise to a multi-billion-dollar industry of anti-angiogenic therapies designed to starve tumors by cutting off their blood supply. It was a beautiful theory that promised to choke cancer at its root. However, like many beautiful theories, it appears to have stumbled upon an inconvenient truth: reality. The failure of these drugs to curb the spread of cancer to lymph nodes suggests that the tumor cells, ever the clever tacticians, simply didn’t read the textbook.

The most glaring rebuttal to this dogma comes from the metastatic colonies that establish themselves in the lymph nodes. A study from the Massachusetts General Hospital Cancer Center delivered a damning verdict, finding that “the initiation and growth of node metastases did not involve the development of new blood vessels”. The theory demands sprouting angiogenesis, yet the evidence shows it’s absent. One can almost picture the metastatic cells smugly thriving in the lymph node, having bypassed the very process the drugs were designed to disrupt. This finding alone should have sent a tremor through the foundational beliefs of the field, suggesting that tumor cells are perfectly capable of highjacking the host’s pre-existing infrastructure rather than building their own- would you be surprised to find they didn’t change one iota?

If the first blow was theoretical, the second is a resounding clinical failure. If a tumor doesn’t need angiogenesis to grow, then choking off that non-existent blood supply should have no effect. And indeed, it doesn’t. The same MGH study confirmed this by comparing lymph node “metastases” from rectal cancer patients. They found that “comparing lymph node metastases...from patients who had been treated with the angiogenesis inhibitor bevacizumab with those from patients that received no antiangiogenesis therapy found no difference in blood vessel density within the metastatic nodes”. The drug, hailed as a revolutionary breakthrough, was effectively impotent against these lesions. This isn’t a case of a drug being outsmarted; it’s a case of the entire hypothesis of dependency on angiogenesis being fundamentally flawed.

Ultimately, this is not a failure of the drug; it is a failure of the theory. The story of metastasis cannot be reduced to a single variable. The data now clearly show that cancer cells are opportunistic, and will colonize, grow, and prosper in the lymph node without the need for new vessel formation. Dr. Timothy Padera, one of the researchers behind the MGH study, correctly concluded that “the primary implication of our findings is that, since lymph node metastases do not require the development of new blood vessels, antiangiogenic therapy will not inhibit lymphatic metastasis”. This is not a minor footnote; it is a fundamental crack in the pedestal upon which a generation of cancer therapies was built. It is time to stop force-fitting the evidence to the theory and admit that, in the complex world of “metastasis”, our assumptions about what tumors need to survive were simply, and critically, wrong. Once again, are they likely to change course? Are they fuck.

Abstract

There were high hopes for the new antiangiogenic medicament, bevacizumab, which could inhibit the creation of new blood vessels through binding to isoform A of vascular endothelial growth factor (VEGF). However, it is not only blood vessels that are responsible for tumor cell spread. During the process of tumor growth, lymphangiogenesis is mediated by other members of the VEGF family, specifically VEGF-C and VEGF-D, which act independent to bevacizumab. Therefore, based on the mechanism of bevacizumab action and the processes of angio- and lymphangiogenesis, we formed three hypotheses: (1) if the lymph nodes in primary ovarian cancers are metastatic, the outcome of bevacizumab treatment is worsened; (2) concerning the second-line treatment, bevacizumab will act in a weakened manner if recurrence occurs in lymph nodes as opposed to a local recurrence; (3) patients treated by bevacizumab are more likely to have recurrences in lymph nodes. These hypotheses raise the issue of the existing knowledge gap, which concerns the effect of bevacizumab on metastatic lymph nodes.

The “Metastasectomy is a Myth” Control

The ultimate control in any scientific experiment is the treatment itself. In oncology, the widespread practice of pulmonary metastasectomy—surgically removing lung metastases—rests on a foundation of belief they have never bothered to verify. The premise in a nutshell: without surgery, the 5-year survival rate for patients with lung metastases is less than 5%. It’s a number so confidently repeated that it has become a self-fulfilling prophecy, a mantra whispered in surgical suites and scrawled into textbooks. It justifies hundreds of thousands of invasive chest operations, each performed in the name of a cure that, until recently, had never been rigorously challenged. The theory was clean; the practice, unassailable. It was, in fact, a perfect theory, which should have been our first warning.

Enter the PulMiCC trial—the Pulmonary Metastasectomy in Colorectal Cancer randomized controlled trial—the only one of its kind to actually test this dogma- novel right? The results were so inconvenient that they threatened to upend an entire field of surgery. When they finally compared the survival of patients who had their lung metastases cut out to those who did not, the findings were nothing short of heretical. “The estimated survival in this study was 38% for metastasectomy patients and 29% in the well-matched controls”. The control patients—the ones who were supposed to be doomed, who were merely “monitored”—were walking around with a 29% survival rate at five years, basically shrugging off the disease. It turns out that the untreated patients were doing just fine, thank you very much, without any intervention to their chest. The data “confirms the lack of a significant survival difference (hazard ratio 0.93),” even showing that the control group had a longer median survival of 3.8 years compared to 3.5 years for the operated group. So much for the life-saving knife.

Of course, the true believers rushed to defend the faith. Big Pharma bits were rolled out to counter it arguing the trial was “underpowered” due to slow recruitment, a complaint that sounds reasonable until you inspect the logic. The trialists responded with a devastating piece of arithmetic: “It is generally believed that five-year survival without metastasectomy is zero. Even if it was 5%, the expected PulMiCC results would be 3/47 versus 18/46, P < 0·0002... Would that result be ignored on the basis of small numbers?” In other words, if the 5% myth were true, the trial would have been an overwhelming success with just its 93 patients. The fact that it wasn’t doesn’t mean the trial failed; it means the underlying assumption was catastrophically wrong. The only thing “underpowered” here is the imagination required to accept that our patients might not need the most aggressive surgery we can offer.

The real scandal, however, is why the medical establishment believed the myth in the first place. The answer is a textbook case of selection bias dressed up as evidence. The survival of patients who are selected for surgery is always good because they are younger, have fewer metastases, and better overall health. The PulMiCC authors pointed out that retrospective studies “relied on... a comparison was made with 57 patients who had been turned down for metastasectomy, precisely because they had much higher rates of the well-established negative prognostic features... a retrospective study so it was also already known that all 57 had died within five years”. Comparing the survival of healthy, oligometastatic patients who get surgery to the survival of sick patients who don’t is like comparing the life expectancy of marathon runners to hospital inpatients. The fact that we built a surgical specialty on such flawed reasoning is less a failure of science and more a triumph of surgical bravado over basic statistics. Why would you be surprised at massive data fraud and statistical manipulation?

This is the kind of evidence that should make us question the very foundations of oncological dogma. The PulMiCC trial’s authors summarized their findings with a conclusion that should be framed in every oncology boardroom: “Patients in the control group (who did not undergo lung metastasectomy) have better survival than is assumed”. They even noted that “there was no hint of a difference in survival” between the two groups. This is not a failure of the surgeons; it is a failure of a theory that equated aggressive intervention with life extension. The belief that metastasis is an automatic death sentence requiring immediate and radical local control has been exposed as a myth. The control arm lived. The dogma died. It’s a pity it took a randomized trial to prove what common sense might have suggested all along. But these people are paid to excise their commonsense when they get their PhDs.

Abstract Background: Lung metastasectomy in the treatment of advanced colorectal cancer has been widely adopted without good evidence of survival or palliative benefit. We aimed to test its effectiveness in a randomised controlled trial (RCT). Methods: Multidisciplinary teams in 13 hospitals recruited participants with potentially resectable lung metastases to a multicentre, two-arm RCT comparing active monitoring with or without metastasectomy. Other local or systemic treatments were decided by the local team. Randomisation was remote and stratified by site with minimisation for age, sex, primary cancer stage, interval since primary resection, prior liver involvement, the number of metastases, and carcinoembryonic antigen level. The central Trial Management Group were blind to patient allocation until completion of the analysis. Analysis was on intention to treat with a margin for non-inferiority of 10%. Results: Between December 2010 and December 2016, 65 participants were randomised. Characteristics were wellmatched in the two arms and similar to those in reported studies: age 35 to 86 years (interquartile range (IQR) 60 to 74); primary resection IQR 16 to 35 months previously; stage at resection T1, 2 or 3 in 3, 8 and 46; N1 or N2 in 31 and 26; unknown in 8. Lung metastases 1 to 5 (median 2); 16/65 had previous liver metastases; carcinoembryonic antigen normal in 55/65. There were no other interventions in the first 6 months, no crossovers from control to treatment, and no treatment-related deaths or major adverse events. The Hazard ratio for death within 5 years, comparing metastasectomy with control, was 0.82 (95%CI 0.43, 1.56). Conclusions: Because of poor and worsening recruitment, the study was stopped. The small number of participants in the trial (N = 65) precludes a conclusive answer to the research question given the large overlap in the confidence intervals in the proportions still alive at all time points. A widely held belief is that the 5-year absolute survival benefit with metastasectomy is about 35%: 40% after metastasectomy compared to < 5% in controls. The estimated survival in this study was 38% (23–62%) for metastasectomy patients and 29% (16–52%) in the well-matched controls. That is the new and important finding of this RCT.

4. Reasons Why Metastasis is Not a Thing

Based on the overwhelming evidence, here is a definitive list of reasons why metastasis does not occur:

1. It’s a Statistical Mirage: The probability of spread per cell declines as tumors grow. This is mathematically impossible if a genetic or inherent cellular program is involved. It’s clearly just a geometric constraint, not a biological event.

2. Dormancy is an Excuse: The fact that cells spread and then “sleep” for years is not evidence of a complex, multi-step process. It’s evidence that the tissue environment is so powerful it can simply turn off a cell’s malignant potential. This reinforces the TOFT view that cancer is a tissue-based disease, not a cellular one.

3. Metastases Don’t Metastasize: The data clearly shows that distant metastases do not metastasize in a clinically relevant magnitude. In a true cascade model, the first metastasis would seed the second, and so on. But the time intervals for the appearance of new metastases are far too short for this to be possible, and there is no histopathological evidence showing that a second-generation metastasis is more aggressive than the first. This is a fundamental flaw in the cascade model. Multiple metastases appear to arise from independent cells that disseminated from the primary, not from other metastases.

4. The “Seed and Soil” Theory is a Metaphor, Not a Mechanism: The “seed and soil” theory is a nice, poetic metaphor, but it provides no mechanistic explanation. Saying a cancer cell is a “seed” and an organ is “soil” is about as scientifically useful as saying a key fits a lock. It ignores the field dynamics and tissue organization that TOFT so eloquently describes.

5. We Can’t Even See It Happen: Despite modern technology, it has been impossible to clearly demonstrate the phenomena of intra- and extravasation of tumor cells in a patient. We have plenty of diagrams, but no definitive proof of the process in action. This suggests that the entire model is built on a series of unproven assumptions.

6. Treatments For It Don’t Work: If metastasis were a real biological process, we would have developed effective treatments for it. Instead, we have metastasectomy, which is based on a myth, and drugs that fail in systemic trials. This is the ultimate proof that the concept is flawed from the ground up.

4. Conclusion: A Resounding Victory for TOFT

The evidence is irrefutable. The data on metastasis is a collection of inconvenient truths that the establishment has tried to explain away with concepts like “inefficiency” and “dormancy.” The real story is that cancer is a tissue-based disease, and the concept of autonomous cells actively seeking out new homes is a relic of the discredited genetic paradigm. By finally accepting that metastasis does not occur as a cell-driven phenomenon, we can focus on the real issue: the disruption of the tissue organization field that allows for the appearance of a secondary tumor in the first place. It is time to stop chasing cancer cells and start fixing the tissues.

The Cancer-Alzheimer’s Paradox

L. Rebekah Feng’s recent commentary in npj Aging presents what is arguably one of the most inconvenient truths for modern oncology: a consistent epidemiological inverse correlation between cancer and Alzheimer’s disease that the Somatic Mutation Theory (SMT) struggles to explain without tying itself in knots. As Feng notes, “the risk of AD in patients with cancer is reduced by 25–35%,” while “the risk of cancer in patients with AD is halved” . This is not some minor statistical blip—this is a biological head-scratcher of epic proportions. After all, if cancer is simply a matter of accumulated genetic “hits” turning cells into proliferative renegades, why would the very same aging process that supposedly generates these mutations simultaneously protect against neurodegeneration? One might almost suspect that biology is trying to tell us something about our cherished theories.

The paper carefully documents that this inverse correlation appears uniquely tied to Alzheimer’s disease, as “similar associations are not observed with other age-related neurodegenerative diseases” . This specificity should give SMT proponents pause. If somatic mutations were the primary drivers of cancer, and if these mutations somehow conferred protection against neurodegeneration through some genetic mechanism, one would expect similar protective effects across neurodegenerative conditions sharing similar pathological features. Yet, as Feng points out, this pattern “was not observed for non-AD neurodegenerative pathologies, such as the presence of Lewy bodies, TDP43, or cerebrovascular pathologies” . The SMT framework, in its elegant reductionism, offers no compelling reason for this specificity—it simply waves its hands and mutters something about context-dependent effects.

What makes this paradox particularly delicious is that it challenges the very foundation upon which modern oncology has built its temple. As one critical re-evaluation of SMT puts it, the theory “portrays carcinogenesis as the cumulative outcome of random mutations occurring in somatic cells over the human lifespan” . Yet normal tissues routinely harbor “oncogenic” mutations without transforming, and “indolent and potentially premalignant lesions consistently contain driver mutations, yet rarely progress to cancer” . The uncomfortable truth, which Feng’s paper implicitly highlights, is that cancer and Alzheimer’s might represent opposite poles of a spectrum governed by tissue-level regulatory dynamics rather than simple genetic determinism—cancer representing excessive cellular survival and proliferation, Alzheimer’s representing excessive cellular death and degeneration .

The mechanistic explanations proposed in the paper are, frankly, far more interesting than anything SMT can offer. Feng describes how “APP and amyloid beta (Aβ) have been shown to act as tumor suppressors both in vitro and in vivo” and how “APOE4, the largest monogenic risk allele of late-onset AD, is associated with favorable outcomes in melanoma” . This is the kind of systems-level thinking that SMT, in its myopic focus on individual cell genomes, has historically dismissed as mere “background” noise. The theory treats “the tissue and organismal environment are viewed as secondary—shaping selection pressures but not fundamentally determining the malignant state” . Yet here we have evidence that proteins central to Alzheimer’s pathology appear to actively suppress tumorigenesis, suggesting that the tissue microenvironment and systemic regulation are not passive spectators but active participants in determining cellular fate.

Perhaps the most damning indictment of SMT’s explanatory power comes from the quantitative domain. A formal mathematical analysis of the theory’s premises reveals that “even under optimistic assumptions, expected waiting times exceed progenitor-cell lifespans by several orders of magnitude, rendering sequential multi-hit carcinogenesis statistically and biologically implausible” . The theory essentially requires that cells accumulate enough mutations to become cancerous within a timeframe that mathematical modeling suggests is virtually impossible. As Olsen and Liisberg note, SMT “does not so much explain the origin of cancer as presuppose it” . The cancer-Alzheimer’s paradox documented by Feng adds yet another layer to this critique: if somatic mutations were the primary drivers, the epidemiological patterns we observe would look very different indeed.

What Feng’s commentary ultimately accomplishes is to hold up a mirror to the field, reflecting back its theoretical blind spots and methodological dogmas. The inverse correlation between cancer and Alzheimer’s disease “has the potential to drive innovation and help to identify actionable targets for novel clinical interventions for both diseases” —but only if we’re willing to question our most deeply held assumptions. The SMT has served oncology well in many respects, guiding the discovery of oncogenes and tumor suppressors and enabling targeted therapies. However, as Feng’s paper makes abundantly clear, the theory’s explanatory reach has been dramatically oversold. Cancer is not merely a genetic disease, Alzheimer’s is not merely a neurodegenerative disease, and the relationship between them suggests that both are manifestations of fundamental disruptions in biological communication and regulation that transcend individual cells and their genomes.

CONCLUSION

To be able to fix a problem, you have to have a fairly good understanding of how it happened in the first place. If you don’t, then even if you do fix the problem it is more than likely to keep happening. This is true of anything in life whether it be a car, a friendship or indeed your own health. It should not take a genius to figure out that this has been the case with the Cancer industry since its inception, as no matter how many Billions of tax payers money and “charitable” donations are funneled into this hoax of Oncological Mutation, precisely nothing changes- a time honored tradition when it comes to the Medical Establishment. This is the superficial , entry level problem with this Marianas Trench of a chasm of fraud, death and disease, for it is not just Blind Pew innocently scrabbling around for the Buried Treasure of OncoGene Therapy. No this conniving pirate is deeply involved in the reason why many millions of people are all lost at sea.

A horrendous negative feedback loop has been set up in the Oncological department whereby the more they get involved, the worse it gets, largely because they are the people causing the thing they are claiming they are preventing. If you are thick skinned enough there are a vast number of clearly “unbiased” stories on unsuspecting victims of the Allopathic Death Cult. Mostly entitled “My Cancer Journey” or “I’ve got to tell you something”, the modern surge of podcasters and Youtubers documenting their health decline however grim is probably one of the most useful reminders of what not to do, Genuinely if you have normie friends and family this is a must watch as it only takes a bare minimum of “awake” commentary to figure out what is going on here.

From the hundreds of examples I have seen they all start off with our “hero” vlogger looking perfectly normal, sometimes pretty young in their 30s but certainly the best they look. They make an announcement that they have been diagnosed after presenting at a medical facility with low grade symptoms, usually fatigue or the like. Why at this point they just don’t give the Vlogging a rest for a bit and get some extra sleep we will not know, but really this is the Shroedinger’s Cat of foregone conclusions- if they had, we wouldn’t be watching them. They inevitably then proceed to subject themselves to the Medical Meatgrinder, cutting organs out, sticking themselves in giant microwaves and injecting themselves with Mustard Gas. All documented in 1080p in fortnightly spaced episodes the “hero” visibly declines, wastes away and usually start to display hideous growths and tumors and scars. They leave us with announcements that the Medical establishment “can’t do any more”.

As mentioned before, all it takes to put this into perspective is pointing out that with every single intervention that is a known poison/toxin or injurious surgery, the victim gets progressively worse. It is as simple as that, unfortunate people and their families have been convinced that to make themselves feel better from a position of feeling fine and being told they are going to get worse, they subject themselves to ever increasing strengths of poisons until the original predictions are fulfilled. It is the equivalent of the Milgram Experiment but the victim plays both the Questioner and Person sat in the electric chair and they are asked questions about how they feel and every time they answer negatively about an aspect of their own health they administer themselves a dose of “Electrotherapy”, with each incremental shock they have more negative to say about their health.

This is the sad reality of where millions find themselves today. One that desperately needs awareness so that innocent people will stop subjecting themselves to the slaughter. Let me reiterate, because I am seemingly stuck in my own perpetual negative feedback loop of explaining that NO DRUGS, POWDERS, PILLS will truly fix this. The Alternative, Controlled Opposition PharmaLite Cancer poisoning is doing a sterling job at cleaning up those that are skeptical of some of the mainstream poisons. The Big Pharma Reps in Sheep’s clothing will with one hand point at the death and destruction of Chemo, then in the other outsretched arm off you the same pharmaceutical poisons such as Ivermectin, Amygdalin, High Dose Vit D/C etc etc. They never address the root problem that likely in a vast majority of cases….. there is no problem. People have been convinced that they shouldn’t feel tired or ill and that tests mean everything. Just as a quick, beautiful example for you to understand; Bryan Johnson set out with a motto to “Live Forever” taking fistfuls of every “Bio”Chemical Supplement, “vitamin”, AltDrug an quackccine going. Instead of “Living Forever” he announced just a year later that his “Stomach was eating itself” with an “Aggressive Autoimmune” disease. That’s all you need to know.

So we find ourselves here; I have written a very long and comprehensive book on “What NOT to do”. We know that Cancer is NOT caused by your non existent genes, it does NOT spread and “metastasize” but rather an imbalance of tissue structure from repeated poisoning events causes first localized then generalized tissue imbalance and physical deformation leading to eventual apoptosis. We have seen this ratchet effect of systemic poisoning leading to worsening outcomes all repeatedly “verified” with fraudulent molecular tests, the takeaway being do NOT get tested in the first place. I truly believe that this line of reasoning is the greatest biggest step in improving your health and also “curing” cancer. The simple mentality change of “what can I take or ADD to make me better” rather than what can “I stop or do NOT do” to give my own body the chance to do what it does best which is find its way back to balance.

TRUTH BE TOLD EVENT ANNOUNCEMENT

Event Details: Thursday, September 17th, 2026. The livestream starts at 12pm EST / 11am CT / 10am MDT / 9am PST / 6am HST / 4pm UTC.

You will be able to access the livestream on September 17th here: https://shadowbannedlibrary.com/pages/truth-be-told

Virtual doors open 30 minutes before the event begins, so make some popcorn and come grab your virtual seat! We understand life can get hectic, so WE WILL SEND YOU A COUPLE OF EMAIL REMINDERS!

Below you will find an outline of each presenter and what they are bringing to the table:

PRESENTATIONS

The opening act will be Unbekoming, who will be providing an eye-opening presentation on The Unvaccinated—a topic that is of utmost importance in 2026. This presentation will hit you with a heavy dose of facts that are guaranteed to leave you flabbergasted.

Next up will be a new fan favorite, the incredible David Parker, who will be presenting The Nature of Reality. Have you ever wondered if there is a purpose to life and what happens to you when you die? Would you be surprised to learn that there is no such thing as a solid object? Have you considered what a ’Thought’ is made of? Is there any proof that there is an ‘out there’ out there’. The World that seems so solid and separate from you can be shown to be a trick of the senses. The apparent materiality of the World is no more real than a dream image. The consequences of this knowledge will require you to reassess everything you think you know about yourself and your World. After David’s presentation will be a 15-minute live question-and-answer period.

Now that you are geared up for truth, next to the virtual stage will be the groundbreaking, trailblazing Jamie Andrews, who, through the Virology Control Studies, used science to debunk science. Although Mr. Andrews is demolishing everything we thought we knew about viruses and bacteria, he has come to realize that this is not a war he can fight alone, so he will be teaching us all how we can run our own experiments! Jamie’s presentation, Decentralized Science Projects, will be epic! After Jamie’s presentation will be a 15-minute live question-and-answer period.

The next content creator taking the stage will be the woman with a massive target on her back, the social media influencer’s greatest nightmare, Medicine Girl. In her presentation, Emergency Medicine. For one hour, Medicine Girl will be blowing the lid off everything you thought you knew about emergency medicine. Her mission is simple: to arm you with the most cutting-edge, life-saving knowledge on the planet, no matter the cost. Here you will learn the jaw-dropping truth behind “standard” emergency advice, the #1 at-home emergency mistake, how to build a medicine cabinet that can handle real emergencies, live, no-BS demos of field-tested techniques you’ve never seen anywhere else, and more! After her presentation will be a 15-minute live question-and-answer period.

And lastly, to finish out the extravaganza, one of your favorite authors of all time, the one, the only, Agent131711. Agent will be providing you with a 60-plus-minute presentation that is so shocking that you can’t help but laugh at the absurdity of it all. What is the topic? Answer: The history that came before history, the pre-historic beasts, the Jurassic Park monsters: Dinosaurs. Here, Agent will methodically dismantle every aspect of The Dinosaur Hoax, and when this hour is over, you will never look at the museum the same way.

In between presenters, we will provide a 10-minute break, so if you need to refill your drink or grab some more snacks, you won’t miss anything.

This six-hour event will genuinely be one for the books! If you can’t make the livestream, no worries! The replay will be available shortly after the show has come to an end so you can watch any time that works for you at https://shadowbannedlibrary.com/pages/truth-be-told. Grab yourself a ticket today, support the content creators who are actually making a difference, and support the website that is giving people a consolidated place to access materials that are otherwise banned and shadowbanned from the internet. Every ticket purchased goes a long way in covering the costs of the war on truth. We thank you in advance. We look forward to putting on a show you will never forget, TRUTH BE TOLD!

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1. This is a very long article topping 130 pages that has taken months of research, more to this point is that whenever I have written longer articles like this with very deep research, Substack tend to Shadowban it, so having it free and open when it first goes out does me no help in just getting exposure (despite having 18k Subscribers).

2. I have quite a few paid for subscribers (thank you!) I am acutely aware that despite many big things going on behind the scenes there is not much you are seemingly seeing for your paid subscription, so early access can feel like it is a bit of a perk.

3. This is a trigger topic that I get a serious amount of hate mail for no matter what I write or how I phrase it. If you are interested in learning what I believe to be the honest truth according to my experience and research and you want to read it for free you will wait a week to do it. Hopefully this will put off the knee jerk reaction trolls.

4. This will be going up as an Ebook on Shadowbanned Library for just a few dollars, if you really can’t wait you can buy the book over there. Here is a Discount code for all Substack subscribers.

   

5. The paid for price is set stupidly low at $35 for a years subscription, if you want to get early access then your donations are very much appreciated and are all put towards experimentally falsifying Virology.

I have tried not to write this article for the 18 months that I have been on Substack but have finally buckled. Followers of me on Twitter will know all too well that I am very vocal about this subject and have drip fed information out, raising awareness of this pharmaceutical poison posing as some natural necessity. The problem is, that whenever I point out one area of this hoax is that my comments sections are filled with what I presume must be pharmaceutical bots repeating the same old tired rebuttals on loop. If I approach those in a different post, they switch back to the first. So it is out of necessity that I am putting it all down right from the history, the test to the poison itself. This is so I can link these bots to the complete argument and so not have to waste time merely typing it out as most of these posts I make on this subject is filled with hundreds of these people (here is a big red flag to it being a Big Pharma agenda that has clearly spent a lot of money marketing this poison).

Another reason for not wanting to write this article is because of the sheer amount of shit I get for it. When I did an impromptu video last Christmas, because the nefarious shills and Controlled opposition were seemingly simultaneously upping the ante on taking Vitamin D (Rat poison) to help with Non Existent “Viruses”, I got a tsunami of unsubscribes, paid cancellations and hate mail. Seemingly I am glutton for punishment, but really I would prefer people not follow me or even support me if they are going to poison themselves or recommend poisoning others. For what is the point in learning the truth about No Virus and hence cutting all Vaccines and Pharmaceuticals to do with them out of your life, if you are then just going to fall for an identical pharmaceutical hoax?

In that video I presented basically no evidence for the hoax of Vitamin D, despite knowing a mountain of it. In my opinion it should be obvious enough that once you learn the FACT that Vitamin D3 IS Rat Poison if I have done my job well enough on the Virology Control Studies project you should be discerning enough, or more importantly already been discerning enough that you need no more information to NOT eat rat poison. However I still do feel compelled to write the whole thing down + all of the research I have done into the foundations of the hoax, as I think when all of it is laid bare it will be impossible for anyone not making bank from selling this poison to disagree with.

I will put this into context and the reason why I have a bit of an extra axe to grind with this particular hoax is because unfortunately I fell for it and I have experience of its negative effects (As there are no positive effects). From the recommendations of some complete scumbag on YouTube doing affiliate marketing of this poison I started taking 5000IU a day, I took it for roughly 2 months.

One night I woke up in the early hours of the morning and my heart was racing, probably 120/130bpm and you could visibly see my chest pounding. I woke my wife up and suggested to her that she may have to ring for an ambulance as I was going to having a heart attack. Over the course of the next couple of hours I managed with some controlled breathing techniques to steady my heart rate a little so that I didn’t have to submit myself to the allopathic death machine. My wife asked me if I had taken anything and at that time it didn’t even dawn on me that Vit D was a drug, it is a natural supplement right! (Lol). Eventually I remembered I had been taking these and we Googled the side effects of “overdosing” (Of which according to the medical scumbags pushing this poison 5kIU a day is not) and the first and foremost symptom that came back was Heart Palpitations and Arrythmia.

So unfortunately I found out the hard way and I am here to tell you from experience and with heavy research of every angle of this hoax, that you don’t have to make the same mistakes:

A Rickety Start

Edward Mellanby (1919–1921)

Mellanby demonstrated that rickets was caused by a dietary deficiency and could be prevented or cured in dogs by feeding them cod liver oil.

This was a major breakthrough because it showed that rickets was a nutritional disease rather than an infectious one. However, Mellanby initially believed the anti-rickets factor in cod liver oil was vitamin A.

EXPERIMENTAL METHODS. Although it is well recognised that different breeds of dogs vary considerably in their susceptibility to rickets. no special type has been used in this work. In some ways this may be disadvantageous ; but, on the other hand, to be driven to associate rickets with a particular breed is in itself unsatisfactory and obviously leads the investigator into a blind alley if the ultimate object is.to extend the results to children. The experimental methods used to detect rickets have depended on (’1) X ray examination of the bones ; (2) calcium estimation of the bones after death ; (3) histological preparations of the bones. The calcium estimation of the bones has been made by Cahen and Hurtley’s modification of the oxalate method.

In the wild (or in free-ranging dogs and wolves), puppies older than about 8 weeks are generally not living on milk anymore as their primary food source. Instead, they transition to foods provided by adults.

Wolves

Gray Wolf pups typically:

• Begin tasting meat around 3–5 weeks.

• Receive regurgitated food from adults starting around 4–6 weeks.

• Eat increasing amounts of meat as they grow.

• Continue occasional nursing beyond 8 weeks, but milk becomes a decreasing part of the diet.

By 8–10 weeks, much of their nutrition comes from:

• regurgitated prey material

• partially consumed prey brought back to the den

• small amounts of prey they can eat themselves

Free-ranging dogs

Dog puppies often eat:

• scraps scavenged by adults

• regurgitated food

• discarded human food

• carrion

• insects and other opportunistic foods

Again, milk becomes progressively less important after about 6–8 weeks.

Q: There seems to be no xrays or images of the racitic puppies in Mellanbys experiment. Can you link to these xrays so we can see them. If you can’t find the link please say. short answer

Short answer: I could not find a public link to X-ray images of Mellanby’s rachitic puppies themselves. I found references stating that Mellanby used radiographs (roentgenograms) of the puppies’ long bones as evidence of rickets, but not the actual puppy X-ray plates online.

Q : Do you see many animals in the wild with rickets? can you show me pictures please

Short answer: yes, rickets does occur in wild animals, but it is uncommon and usually indirect (more often captivity or human-altered conditions than truly “natural wild”).

What we know

• In truly wild populations with normal diets and sun exposure, rickets is rare.

• It is more commonly seen in:

  • Captive wildlife (zoos, hand-reared chicks/cubs)

  • Domestic animals

  • Wild animals affected by human food sources or confinement

ANALYSIS

Mellanby, working for the Central Control Board of Liquor Traffic took on the problem of rickets that was so prevalent in the late 1800s to early 1900s. He studied puppies and gave them a diet that he claimed would reliably induce rickets that quite bizarrely all contained milk, which considering the puppies he took were 5-8 weeks old would still be nearly entirely milk fed from the mother. He claimed that when these puppies got rickets, from eating milk as well as oatmeal they could have their rickets reversed if given cod liver oil and some other fats. Again bizarrely in his own experiment, a thing that reversed the rickets in Diet 1 (Milk + Oatmeal + salt) was…. more milk.

We will never actually know if any of this actually happened, because the Xrays and histology showing he could induce rickets is absolutely nowhere to be seen. The entire experiment is on a purely “Trust me bro” basis. Needless to say that even if we accept that all of these diagnoses were correct it doesn’t really mean anything other than feeding oatmeal to a puppy is not going to help them in any way largely because dogs never had the foresight to harvest cereal crops in the wild.

The conclusions to this study, as is the rest of this decade of studies from his compatriots seem to balk the real world data of wild animals. It is extremely rare to see wild animals with rickets yet their diets would be extremely inconsistent through these vital growth periods where they claim basically they might get a little bit of regurgitated food or scraps from adults and some milk. Even in Mellanbys work did meat protein seemed to not stave off rickets, so unless his hypothesis is that wild dogs have a secret stash of Cod Liver Oil somewhere, he would have you believe that all wild dogs have bowed legs, especially Scottish Highland Terriers because of their lack of access to “wild sunlight”.

Elmer McCollum (1922)

Elmer McCollum took cod liver oil and destroyed its vitamin A activity. The oil still prevented rickets. This showed that the anti-rickets substance was not vitamin A but a different nutrient, which he named vitamin D.

This is why McCollum is often credited with the discovery of vitamin D itself.

Mellanby (2) was the first to associate the group of fats which, because of their content of fat-soluble A were frequently distinguished as “growth-promoting” fats with the prevention of rickets. His work focused attention upon the problem as to whether fat soluble A is itself a substance essential for the normal growth of bone. Mellanby (3) was so impressed with the power of butter fat to protect puppies against the abnormalities of bone growth that he stated: “These facts of agreement from the point of view of physiological reaction seem to me strong evidence that the substance in fats stimulating the calcification of bone is the same as Fat-soluble A, i.e. the factor which stimulates growth in rats.” He further says: “Rats as regards growth and puppies as regards rickets become more independent of the vitamin as they grow older. These facts are in favor of Fat-soluble A being also responsible for the anti-rachitic action of certain fats.”

We have found that cod liver oil treated with a stream of air bubbles at the temperature of boiling water for 12 to 20 hours no longer contains sufficient fat-soluble A to relieve rats from xerophthalmia when administered to the extent of 2 per cent of the diet. Cod liver oil which had been oxidized 4 hours, when fed as 2 per cent of the diet, cures xerophthalmia.

A few words of explanation are necessary regarding the column in Table I headed “Number of days in preparatory period.” In order to carry out the “line test” satisfactorily the animals are fed Diet 3143 until a pathological metaphysis has developed satisfactorily. This state we have come to recognize by certain peculiarities in the movements of the young rats which we use as the test animals. The gait is unsteady and the hind quarters waver from side to side. When they move off rapidly they hop, usually favoring one hind leg. We have found it safe to rely on young rats which exhibit this abnormality of movement to show the histological picture which is essential for the conduct of the test. We have examined histologically the bones of a large number of rats which have been kept on this diet, for varying periods, and have found considerable difference in the length of time required to prepare them for the test for the calcium-depositing vitamin. We have gained the impression that it takes their bones a decidedly longer time in summer than in winter to deviate from the normal histology in the manner desired. Certainly they do not all respond in a certain number of days so that it is not possible to state accurately when they will be ready.

ANALYSIS

Picking up from the presumably drunk work of Mellanby, McCollum having shown that Cod Liver Oil (It’s a theme) stopped baby rats from having slightly puffy eyes which he claimed was proof of Vitamin A (huge eye roll-pun intended). Elmer then echoed Mellanby’s earth shattering finding that milk products (butter) helps young animals grow. In Elmer’s paper he reiterates these findings but this time with baby rats, whilst keeping true to the scientific methodological rigor of Big-Head Ed he chooses to base his diagnosis of Rickets based on whether these newborn rats “wiggled” their hind quarters or seemed to hop off one foot more predominantly when moving quickly (This is highly technical work here peeps).

So Elmer claimed that this Cod Liver Oil contained something other than Vitamin A, because he managed to take the Vitamin A out… by bubbling oxygen through it and then it didn’t help rats puffy eyes so this took the magic vitamin out. I mean it probably isn’t worth unpacking every piece of conjecture wrapped up into this quackery but we will leave this section with the lie seeded by Elmer toward the end of this experimentation that seemingly showed that rats (animals in general) grew better in the summer than they did in the winter. This has to be arguably one of the most obvious lies ever uttered in science especially as it was presented with zero evidence to back it up (maybe a rat hip wiggle or two). But yes, Elmer reckons that we have half of the entire animal kingdom born in late Summer and Autumn whose growth has been permanently stunted because their weaning years fall in winter. This happens to be a massive double whammy because all of his experiments were conducted in the lab, with little to no natural light. This is a very important lie to highlight because this is the first movement toward exposing the hoax of “Sunlight’s effects on the skin = Vitamin D” and where it was seeded from.

Harry Steenbock

Harry Steenbock was an American biochemist and nutrition researcher at the University of Wisconsin–Madison who became one of the pioneers of vitamin research in the early twentieth century. Born in rural Wisconsin in 1886, he devoted his career to studying nutrition and deficiency diseases. In 1924, he demonstrated that exposing foods and related substances to ultraviolet light dramatically increased their ability to prevent rickets, helping establish the scientific basis for vitamin D and leading to the fortification of foods such as milk. His discovery played a major role in the decline of rickets worldwide, and the patents arising from his work were managed through the Wisconsin Alumni Research Foundation (WARF), which became a model for funding university research.

In attempting to use this method for determinations of vitamin A in butter a large series of experiments was run in which eight groups of rats, six animals to the group, were used (3). In each group two animals were exposed to ultra-violet light from a quartz mercury vapor arc, with the expectations that if there were a deficiency of the antirachitic vitamin in the ration, the two irradiated animals would, by their increased growth, reveal such to be the case. It merely remained, then, to find out at what level of butter fat irradiation no longer had any effect. This would be the level at which the butter furnished a sufficiency of the antirachitic vitamin. Contrary to what was expected, all the animals in each group, irradiated or not irradiated, irrespective of whether the butter was incorporated in the ration at an 8, 4, 2, 1, 0.5, 0.2, 0.1, or 0.0 per cent level, grew, on the average, equally well. This puzzled us because in dozens of other experiments, and in controls, irradiation had always been found to increase the amount of growth unless the animals gave signs of vitamin A deficiency as indicated by ophthalmia or infections of the respiratory tract. Then, of course, lack of vitamin A was the factor inhibiting growth.

Shortly after these results were obtained, there reached our hands an article by Hume and Smith (4) which appeared to have a bearing on this point. They irradiated glass jars with ultraviolet light and found that rats kept in such jars grew to a larger size than controls. Ozone, well known to be produced by the mercury lamp, was shown not to produce this effect nor did irradiated jars from which the air had been blown out after irradiation. They concluded that “it is the air and not some property impressed on the glass jars which is active.” They speak of ionization as being a probable factor.

A little later Goldblatt and Soames (5), studying what they erroneously speak of as fat-soluble A, found that, when the livers of rats in which growth had been induced by irradiation were fed to suitably prepared and rationed animals, growth previously inhibited was restored; with the livers of non-irradiated rats taken under the same circumstances and fed to similar animals this did not take place.

They were kept in our standard sized cages provided with false screen bottoms (6) in our rat room in which all the window curtains were drawn except those of northern exposure. This latter precaution was taken even though our experiments were started in early November and completed early in March, when solar radiation, especially such as finds its way through window glass, is virtually impotent.

At times, however, when we were obliged to use poor alfalfa hay in this ration we were forced to supplement the ration temporarily with a small amount of butter fat to keep up the rate of reproduction in our stock necessary to supply us with a sufficiency of experimental animals.

As a result of the poor demonstration of the effect of irradiation in the second trial, a third was carried out in which the ration was fortified with respect to its vitamin A content by the addition of 0.3 per cent of alfalfa (Chart III).

As growth in itself can hardly be taken as sufficient evidence of the existence of the antirachitic factor, we were led to make analyses of shaft bones, usually the femurs or humeri, for total ash content. These were dissected free from muscle and connective tissue and then cleaned by rubbing between folds of cheese-cloth. They were then dried for 2 days in a steam oven at 96^oC., extracted thoroughly with alcohol in a Soxhlet for 48 hours, then dried and ashed in an electric muffle furnace. In this series the femurs from two rats of the control group gave an average value of 47.2 per cent ash, four with direct radiation 56.6 per cent, and three on the irradiated ration 53.9

ANALYSIS

Where do we start with this absolute cacophony? This is about only half the “paper” by the way, but for time’s sake I have cut it short purely because the first half contained some of the most astounding stupidity, naivety , conjecture and woo woo I have read (In the last hour of reading about this subject- purely because it is all on this level).

He starts off by saying he proved his hypothesis wrong when irradiated rats grew the same as non irradiated rats. Ok, so a bit strange then that he has plowed on to some how try and tweak his experiment to show the opposite? He sings the praises once again of Milk products for the growth of young animals, thank you very much for this enlightening observation, Captain Obvious.

He then went in off the deep end of Woo woo claiming that rats kept in irradiated glass jars grew better than rats in non irradiated glass jars. This does come with a reference to a paper, which I can safely say without looking at it, is complete bollocks considering the state of this paper. Maybe they should try stirring some of the water given to the rats with one of Cowan’s magic crystal wands.

He then references others who feeds rats with irradiated and non irradiated Livers and presumably a fine chianti. Once again I am not particularly interested in reading the whole circus of clowns autobiographies, I am very confident this will be extremely low brow quackery.

Finally we get to the mainstage where in the first few lines he admits to basically keeping the rats in a bit of a black out by closing all but the dark side of the rooms (North facing) curtains. He uses a Mercury Vapor Arc Lamp which I am sure should probably ring some alarm bells, which also in the earlier Glass Jar Woo Woo study was noted that “Ionization was probably a factor” in a moment of clarity. Now the choice of lamp is probably the most crucial part to this in that this conjecture away from the natural can be applied to a good decades worth of experimentation. Why would you conclude that anything found with the use of a Mercury Lamp had anything to do with the sun? They are completely different things? Why not… I dunno…. use the sun?

Well even with his liquid metal mock-ups he even notes the second and confirmatory trial gave the opposite results to those he intended. Well that is now 2 to 1 against give his first admission, why didn’t he call it a day? Well we know why, because this is not science, and certainly not objective truth, it is a desperate manipulation of arbitrary and subjective data to try and fulfill a monied request from Big Pharma. This can be adequately seen from the complete horsehit methods used to “calculate” his “findings” (which mostly disagreed with his theory). Cremating baby rat femurs he found a 5% difference in the weight of the ash. What do you say really other than it is clear scientific fraud on display. One would also infer that if you keep baby rats in a cage, close all the curtains and feed them alfalfa hay, they probably aren’t going to be very fussed about living and growing, just a suggestion.

Adolf Windaus (1920s–1930s)

Adolf Windaus and his collaborators worked out the chemical nature of vitamin D and its relationship to sterols such as ergosterol and cholesterol derivatives. They isolated and characterized vitamin D compounds, laying the foundation for modern vitamin D chemistry.

How convincing was the evidence?

For the time, very convincing. Windaus’s strongest result was not “sunlight cures rickets”—that had already been shown by others—but that:

1. A purified sterol (ergosterol) could be isolated.

2. UV light transformed it into a potent anti-rachitic substance.

3. The non-irradiated sterol lacked that activity.

4. The irradiated product consistently prevented or cured rickets in biological assays.

the exact German papers are difficult to find freely online, but these are the key contemporary sources:

• Windaus & Hess (1927), cited in contemporary literature as:
  Nachrichten der Gesellschaft der Wissenschaften zu Göttingen, Mathematisch-Physikalische Klasse, 175 (1927). This is the paper often credited with demonstrating the activation of ergosterol by UV light.

One caveat: unlike many modern papers, the original 1927 Göttingen publication is not readily available as a free full-text PDF that I can verify. I can find reliable references to it, but I cannot currently find a working full-text scan of the original experimental paper itself.

ANALYSIS

Well unfortunately there isn’t much to analyze as his published paper doesn’t seem to be available online, and if and when they do deem it necessary it will be in German. So the entire Isolation and purification of Vitamin D at its foundation is on a purely “Trust Me Bro” basis. But yeah, take butter, separate off the fats and shine a mercury lamp at them and they help young animals grow, the same as they would do if you just gave them the milk that all of the by products came from.

VIT D Isolation method

• Obtain a sterol-rich source

  • Cholesterol: animal tissues, gallstones, brain tissue, egg yolk.

  • Ergosterol: yeast and fungal material.

• Extract the lipids

  • Grind the material.

  • Wash repeatedly with organic solvents such as ether, benzene, petroleum ether, chloroform, or alcohol.

  • This dissolves fats, oils, sterols, and other lipid-soluble substances.

• Saponify the extract

  • Heat with alcoholic potassium hydroxide (KOH).

  • Ordinary fats are converted into soap and glycerol.

  • Sterols remain in the “unsaponifiable fraction.”

• Separate the unsaponifiable fraction

  • Extract with an organic solvent.

  • Remove the aqueous soap layer.

  • Concentrate the solvent.

• Crystallize the sterol

  • Dissolve the residue in hot alcohol.

  • Cool slowly.

  • Sterol crystals form while many impurities remain dissolved.

• Repeated recrystallization

  • Dissolve and recrystallize multiple times.

  • Purity increases with each cycle.

• Characterize the product

  • Measure melting point.

  • Perform chemical derivatization (e.g., acetate or benzoate derivatives).

  • Compare properties with known sterols.

• Irradiate the purified sterol

  • Expose crystalline ergosterol solution or powder to UV light.

  • Test the irradiated material in rats fed a rickets-producing diet.

ANALYSIS

They take a basic fat (butter) or animal tissue (meat) i.e something that is obviously necessary for the growth of young animals, add toxic solvents to dissolve the lipids, heat with Potassium Hydroxide which they claims separates off the fat from the sterols and then irradiate those sterols to produce “Vitamin D”. This was the first way of making “Vitamin D” which despite the long list of toxic additives to do it such as Chloroform and Benzene, at least it comes from a natural food source, unlike todays synthesized Rat Pills.

Here we see our first foray into the “Bio”chemistry fraud, in that they take basic constituents parts of biological life such as a fat, which is largely defined by its hydrophobic properties (Very important), separate these things off once and call it all fat then put in Potassium Hydroxide and call the fat (because it has identical hydrophobic properties) something completely unique called a “sterol”.

Here we can see from the table of comparisons that the only things that separate Fats (claimed by unverifiable Mass Spec- Triglycerides) from Sterols is largely unverifiable, i.e can be “hormones” (another made-up classification), can be photochemically transformed (Unverifiable). Really the only difference is that it “can be made into soap” which is just a very slight mechanical property change. Really this thing a “Sterol” is just a fat/Potassium Hydroxide mix that has somewhat changed it’s physical properties from oily to waxy. It invokes the mental picture of the waxy build up of cholesterol in your arteries that form the hoax to push toxic Statins (probably another article FML).

SUNSHINE AND LEAD

Before we get totally wrapped up in the “Bio”Chemistry bollocks I want to finish off, once and for all this nonsense about a specific beneficial Vitamin coming from the sun that you can put in a pill. Of course the sun is beneficial, it is the bringer of life, it is an easily demonstrable necessity for the plant kingdom and hence must be extrapolated to the animal kingdom in the same light (apart from say the Naked Mole Rat which lives entirely underground its whole life- oops). Just as an interesting side note; plants do seem to grow just fine under fabricated UV light, not that this means you could fabricate light and put it in a pill form, no it is just energy/electricity/electromagnetism (wink wink, nudge nudge) that is used in the micro scale. However I do believe this fabrication is in part sucking the life out of our crops. I think it is the reason now why I find it almost impossible to smoke cannabis and the amount of psychosis that is prevalent from this stuff, I would put it down to the artificial light sources and chemicals used to bulk these plants (replace plants for people and UV lights for steroids and protein powders and you have my thoughts on Bodybuilders too).

Because this is the main thing that people say to me when they are trying to convince me that rat poison isn’t rat poison: “But Jamie, I live in a place where there is very little sun and I need the pills dude. Gimme the quick fix drugs maaan”. Firstly I am of Scottish ancestry, a country which is allergic to sunshine and it has had inhabitants like Mel Gibson since the dawn of mankind, quite happily. The same is to be said even further North into the Arctic circle in Scandinavia, where 99.99% of people ever to have lived there, have lived without the “help” of rat poison in pill format.

But let’s really put a stake through the calcified heart of this sunny hoax, by looking at where experiences rickets in the modern world:

Q: Where is Rickets seen in the Modern World?

Rickets is still seen in many parts of the modern world, including both developing and developed countries. It occurs when growing bones do not mineralize properly, most commonly because of vitamin D deficiency, though calcium deficiency and certain genetic disorders can also cause it.

Regions where rickets remains common

Africa

Rickets is reported in several countries across sub-Saharan Africa. In some areas, inadequate dietary calcium is a major factor, even where sunlight is abundant.

South Asia

Countries such as India, Pakistan, and Bangladesh continue to report cases, particularly among children with poor nutrition or limited sun exposure.

Middle East

Rickets is seen in parts of the Middle East despite strong sunlight. Factors can include indoor lifestyles, clothing that limits skin exposure to sunlight, and dietary deficiencies.

Why is rickets still seen today?

Modern lifestyles have reduced sunlight exposure through:

• More time spent indoors

• Greater sunscreen use

• Urban living with less outdoor activity

In addition, some populations have limited access to vitamin D–fortified foods or calcium-rich diets.

How common is it?

Rickets is much less common than it was in the early 20th century because of vitamin D supplementation and food fortification. However, pediatricians continue to diagnose new cases every year, especially in high-risk groups.

If you’re interested, I can also explain which countries currently have the highest reported rates of nutritional rickets and why those rates differ.

Q: Why is it that all of these places have effectively year round sunshine yet see rickets?

That’s an excellent question, and it highlights an important misconception: sunshine availability is not the same as vitamin D production.

Many regions where rickets occurs do have abundant sunlight, but several factors can prevent children from making enough vitamin D.

1. Limited skin exposure

In some sunny countries, children may spend much of their time indoors, especially in cities. Clothing can also cover most of the skin for cultural, religious, climatic, or practical reasons.

For example, a child living in a sunny city who is indoors for school, transport, and home life may receive surprisingly little direct sun exposure.

2. Darker skin requires more UV exposure

Melanin acts as a natural sunscreen. People with darker skin need longer exposure to ultraviolet B (UVB) light to produce the same amount of vitamin D as someone with lighter skin.

This does not mean darker skin causes deficiency by itself; it becomes a factor when combined with indoor lifestyles or other limitations on sun exposure.

3. Air pollution and urban environments

In some large cities, pollution can block a significant amount of UVB radiation before it reaches the ground. High-rise buildings and narrow streets can further reduce direct sunlight exposure.

4. Nutritional calcium deficiency

This is particularly important in parts of Africa and Asia.

A child may get adequate vitamin D from sunlight but still develop rickets if dietary calcium intake is very low. In several African countries, researchers have found calcium deficiency to be a major driver of rickets.

5. Infancy is a special case

Babies are often deliberately protected from direct sunlight. If:

• the mother is vitamin D deficient during pregnancy,

• the infant is exclusively breastfed,

• and vitamin D supplements are not given,

the infant can become deficient even in a very sunny climate.

6. Some cases are not nutritional

A minority of rickets cases are caused by inherited disorders affecting vitamin D metabolism or phosphate handling. These occur regardless of sunlight levels.

An interesting example

Countries around the Persian Gulf receive some of the world’s strongest sunlight, yet vitamin D deficiency has historically been common there. Researchers attribute this to a combination of:

• indoor, air-conditioned lifestyles,

• limited skin exposure,

• obesity (which can lower circulating vitamin D),

• and dietary factors.

One more subtle point

Humans evolved in sunny environments without rickets being widespread. Historically, children spent large amounts of time outdoors and diets often differed substantially from modern urban diets. The persistence of rickets today is therefore less about the amount of sunlight available and more about how modern lifestyles, nutrition, and health conditions interact with that sunlight.

ANALYSIS

So quite ironically the places in the modern world that still see rickets in the open population are some of the most consistently sunny places on planet Earth. It is absolutely hilarious the reasons why AI and presumably the Medical Authorities try to rationalize this out. They claim that cultural clothing blocks out more of the sun as well as darker skin tones which might be one of the most bizarre copes given that the entire reason for the darker skin tone is due to the amount of sun in their ancestral country. They then claim it in a lot of these African countries it is NOT the amount of sunshine people are receiving but indeed a deficiency in calcium, I mean at least they are forced into having to admit that the notion of a lack of sunlight in equatorial countries might not be a problem.

This is put to bed when if you ask AI independently about a calcium deficiency in Sub Saharan Africa it says that whatever nutritional deficit there may be from a lack of dairy/calcium intake after weaning would be balanced out by the increased levels of sunshine…. lol.

Q: Is there a claimed calcium deficiency?

If you’re asking why some people claim there is calcium deficiency in parts of sub-Saharan Africa despite widespread breastfeeding, the two issues are related but not contradictory.

Breastfeeding provides infants with calcium, but calcium deficiency can still occur for several reasons:

1. Maternal calcium intake may be low

Breast milk generally contains calcium even when the mother’s diet is not ideal, but mothers can draw on their own bone stores to maintain milk quality. In populations where diets are low in dairy products or other calcium-rich foods, women may themselves have low calcium intake.

2. Many traditional diets are low in calcium

In several regions, staple foods are cereals, roots, tubers, and grains. These can provide energy but relatively little calcium compared with diets containing substantial amounts of dairy, small fish eaten with bones, or calcium-rich leafy vegetables.

3. Bioavailability matters

Some staple foods contain compounds such as phytates and oxalates that reduce calcium absorption. So even when calcium is present in food, the body may not absorb it efficiently.

4. Deficiency claims are sometimes overstated

It’s important to distinguish between:

• Low dietary calcium intake (common in some populations), and

• Clinical calcium deficiency causing disease (less common).

Many studies report that average calcium intake is below recommended levels, but that does not automatically mean large numbers of people develop obvious calcium-deficiency diseases.

5. Vitamin D also plays a role

Calcium status depends not only on calcium intake but also on vitamin D, which helps the body absorb calcium. In most of sub-Saharan Africa, sunlight exposure is often sufficient for vitamin D production, which can partly compensate for lower calcium intakes.

6. Breastfeeding itself is not evidence of high calcium intake

Human populations have successfully breastfed infants for thousands of years under a wide range of dietary conditions. A mother’s ability to breastfeed does not necessarily indicate that she is consuming abundant calcium; her body prioritizes milk production.

A broader point

Sometimes discussions about calcium deficiency are influenced by comparisons with Western dietary recommendations, which are often based on populations consuming large amounts of dairy. Some researchers argue that calcium requirements may vary depending on diet, lifestyle, growth patterns, and adaptation, and there is ongoing scientific debate about the optimal intake level.

So the apparent paradox is:

• Breastfeeding rates are generally high.

• Calcium intake can still be relatively low in some populations.

• Low intake does not always translate directly into severe calcium-deficiency disease.

The next on the list of copes is that sunlight is blocked by pollution and people who live in Urban Environment are more likely to be inside more than in rural communities. Whilst these things are undeniably true this is surely the largest case of correlation ≠ causation as one would presumably include pollution as being a causative factor of disease as well as industry and modern building/transport/sewerage/drinking water chemical components raise in urban environments and follow suit with disease causing (which we are in the depths of the largest cover-up in human history as Big Pharma squirt Billions into trying to make people look at any other (non existent) cause instead).

So let’s look further into what was happening in the late 1800s to early 1900s when rickets was seen in Western Countries predominantly in Urban environments:

Q: In the 1900s was rickets mostly seen in urban or rural environments?

In the late 1800s and early 1900s, rickets was much more commonly associated with urban environments than rural ones. Historians and medical researchers often described it as a disease of industrial cities.

The main reasons were:

• Limited sunlight exposure in crowded cities, where children lived among tall buildings, narrow streets, and dense housing.

• Industrial air pollution (especially coal smoke), which blocked sunlight needed for vitamin D production.

• Indoor lifestyles and factory work, which kept many children out of the sun.

• Poor nutrition, particularly among working-class urban families.

Rural children generally had:

• More outdoor exposure to sunlight.

• Cleaner air.

• Often better access to fresh foods and dairy products.

Q: In the late 1800s and early 1900s were a lot of drinking water pipes in urban environments made of lead in Europe and the West?

Yes—lead pipes were widely used in many urban water systems in Europe and North America during the late 1800s and early 1900s, though the extent varied by city and country.

In that period, lead was considered a convenient material for drinking-water infrastructure for a few practical reasons:

• It was easy to bend and install, especially in dense urban street layouts.

• It was durable in certain soil conditions compared with early iron pipes.

• It was already well known and commonly used in plumbing (“plumbing” itself comes from plumbum, the Latin word for lead).

How widespread was it?

• Household service lines: Very common in many cities. Even where main distribution pipes were iron or masonry, the final connection into buildings was often lead.

• Urban networks: In some older European cities (including parts of the UK, France, Germany, and others), lead was used more extensively, though cast iron was increasingly dominant for mains by the mid-to-late 1800s.

• United States: Lead service lines were also widespread in many cities (e.g., New York, Chicago, Boston), especially into the early 20th century.

• Europe: Similar pattern—lead was common in service connections and plumbing fixtures, but large mains were often iron, stoneware, or later steel.

When did concerns start?

• By the late 1800s, doctors and engineers already suspected lead could be toxic, but the evidence was still being debated.

• In the early 1900s, growing medical and public health research increasingly linked lead exposure to neurological and developmental harm.

• However, widespread replacement didn’t happen quickly—many cities kept lead service lines for decades because replacement was expensive and disruptive.

Gradual phase-out

• Major reductions began mid-20th century, especially after stronger public health regulations.

• In many Western countries, lead service lines weren’t fully banned or systematically replaced until the late 20th or even 21st century in some places.

So in short: yes, lead water pipes—especially service lines into homes—were very common in urban Europe and North America in that era, and they remained in use long after the health risks were increasingly understood.

Q: Does Lead cause Osteoporosis and poor growth in children?

Yes. Lead exposure can contribute to poor growth in children, and there is evidence that it can negatively affect bone health, although its strongest and best-established effects are on the nervous system.

Poor growth in children

Research has found associations between childhood lead exposure and:

• Reduced height and weight gain

• Delayed physical development

• Impaired bone and tooth development

• Lower cognitive performance and behavioral problems

Children are particularly vulnerable because they absorb a higher proportion of ingested lead than adults and their bodies and brains are still developing.

Bones and osteoporosis

Lead has a complex relationship with bone:

• Lead is stored in bones, where it can remain for decades.

• It can interfere with calcium metabolism and normal bone remodeling.

• Long-term exposure has been associated with lower bone mineral density in some studies.

• In older adults, especially postmenopausal women, lead stored in bone can be released back into the bloodstream as bone is lost.

Whether lead directly causes osteoporosis in every case is less clear than its role in neurological harm. Osteoporosis has many causes (aging, hormonal changes, poor nutrition, inactivity, genetics, certain medications, etc.), but chronic lead exposure is considered a potential contributor to poorer bone health and increased fracture risk.

Historical context

One reason modern public health authorities became concerned about lead in water pipes, paint, gasoline, and industrial emissions is that even relatively low levels of exposure were found to affect children’s development. Today, organizations such as the World Health Organization and the Centers for Disease Control and Prevention state that there is effectively no known safe level of lead exposure for children.

Relative importance of effects

Among the health consequences of lead exposure, the evidence is strongest for:

1. Brain and nervous system damage

2. Learning and behavioral problems

3. Reduced growth and development

4. Anemia and kidney effects

ANALYSIS

As with all of the alternative scenarios that I propose, a trap that I want to avoid falling into is one the the medical establishment push of certain diseases being linked with a singular cause such as is the fictious world of Virology. With any of these diseases especially when they are historical, as finding truth documentation to determine a cause is terribly hard in cases that happened today, let alone over a Century ago. Narratives are bolstered and outliers are white washed, so finding out what the immediate environment around those who suffered with Rickets was really like, is probably now next to impossible. But we can get close enough by showing contributing factors that would likely add to the smorgasbord of dangerous persistent environmental toxins during the Industrial Revolution.

It is just an unfortunate fact that with the advent of household running water, a fantastic edition to human society afforded by Engineers (rather than Soyentists) there came a slight teething error in that they made most of their water networks out of toxic Lead pipework- oops. A fresh supply of neurotoxic, osteoporosis forming water to children, puppies and rats alike. The way that the Lead causes its damage is by replacing other “bio”metals such as calcium in deposits in the bones or brain and well- fucking shit up. Of course not every kid had Rickets during the industrial revolution so it is probably a combination of lead poisoning and malnutrition that leads to this stunted growth.

Vitamin D Tests

We are going to go head long into the fraud of “Bio”Chemistry here. unfortunately this tedious sophistry is necessary to point out if we are going to do a thorough tear down of the Vitamin D hoax. Luckily a lot of this will apply to every single vitamin as they measure all of these fraudulent “Bio”chemicals in identical fashion. They take a rough approximation of something in nature, brutalize it beyond all recognizability with a kitchen cupboards worth of noxious chemicals until it is as uniform a chemical product it can be, feed it into an expensive machine that effectively measures charge and then interpret the flashing lights and line graphs generated. This is the most accurate modern technique devised by the way. We aren’t really going to bother to much with the out of date Antibody tests as everybody agrees by now that those tests they used to claim were the height of scientific sophistication are now largely unreliable.

The first large issue when it comes to specifically Vitamin D is that when they made what they called Vitamin D by taking fat dissolved in alcohol and shining a UV lamp at it, when they gave it to rats and measured it, they couldn’t find it in the blood. lol. Instead of packing up and going home and admitting that maybe putting fat in a tanning bed hasn’t really got anything to do with an essential component of your blood, no they just chose another biomarker instead and claimed the Rat Pills had done important chemistry inside your body.

The discovery of 25-hydroxyvitamin D wasn’t the result of a test—it was the result of researchers trying to understand what happened to vitamin D after it entered the body.

The mystery

By the 1950s and 1960s, scientists knew that vitamin D prevented rickets, but they noticed something odd:

• Vitamin D itself disappeared from the bloodstream relatively quickly.

• Yet its biological effects lasted much longer.

• Blood contained compounds that looked similar to vitamin D but weren’t identical.

This suggested vitamin D was being chemically modified after entering the body.

Using radioactive vitamin D

A major breakthrough came when researchers synthesized vitamin D labeled with radioactive atoms (typically tritium, hydrogen-3).

They would:

1. Give radioactive vitamin D to animals or humans.

2. Draw blood and collect tissues.

3. Separate molecules using chromatography.

4. Detect radioactivity in the separated fractions.

Instead of finding only vitamin D, they found several radioactive compounds that had different chemical properties.

This showed the body was converting vitamin D into new molecules.

Finding the liver metabolite

Researchers discovered that one metabolite appeared consistently in blood and was more abundant than vitamin D itself.

By comparing its chemical behavior to known compounds, they determined that the molecule had gained an oxygen atom in the 25-position of the vitamin D structure.

First clue:

It was more polar than vitamin D

Vitamin D is very nonpolar (fat-soluble).

When researchers separated compounds using chromatography, they noticed one radioactive metabolite moved differently than vitamin D itself.

Because compounds with oxygen-containing groups (like alcohols) are generally more polar, the altered chromatographic behavior suggested the metabolite had acquired an oxygen atom.

A rough logic chain was:

• Vitamin D elutes at position A.

• Unknown metabolite elutes later/earlier depending on the system.

• Behavior matches a more polar molecule.

• Therefore the molecule likely gained oxygen.

This told them something was oxidized, but not where.

---

Second clue: Chemical derivatization reactions

Researchers exposed the metabolite to reagents known to react with alcohols.

If a molecule contains a hydroxyl group (-OH), it can undergo predictable reactions:

• Acetylation

• Silylation

• Oxidation

The metabolite reacted as if it contained an alcohol group.

Again, this indicated:

Vitamin D → vitamin D + hydroxyl group

But still not the position.

---

Third clue: Mass increased by exactly one oxygen

Using early mass spectrometry, scientists could determine molecular weight.

Vitamin D₃:

≈ 384 Da

25-hydroxyvitamin D₃:

≈ 400 Da

Difference:

16 Da

An oxygen atom weighs about 16 atomic mass units.

This strongly suggested:

The metabolite is vitamin D plus one oxygen.

Still, many possible positions existed.

That compound became known as 25-hydroxyvitamin D.

The liver was later shown to be the organ performing this conversion.

How they figured out the structure

They didn’t have today’s powerful instruments.

Instead they combined several methods:

• Chromatography (to separate molecules)

• Chemical reactions (to see how the molecule behaved)

• Mass spectrometry (in its earlier forms)

• Nuclear magnetic resonance (NMR)

• Comparison with synthetic standards made in laboratories

Scientists would propose a structure, synthesize it, and see whether it matched the unknown compound’s properties.

When everything matched, they knew they had identified the metabolite correctly.

Why test 25-hydroxyvitamin D instead of vitamin D?

Researchers then discovered that blood levels of vitamin D itself fluctuated rapidly depending on:

• Recent meals

• Supplement use

• Sun exposure

But 25-hydroxyvitamin D:

• Stayed in circulation much longer (weeks rather than hours)

• Reflected total body vitamin D stores

• Correlated better with deficiency and sufficiency

So by the late 1960s and early 1970s, scientists realized that measuring 25(OH)D would provide a much more useful clinical marker than measuring vitamin D itself.

Another surprise: 25(OH)D wasn’t the final active hormone

Scientists initially thought 25-hydroxyvitamin D was the active form.

Then researchers including Hector DeLuca and colleagues discovered that the kidney converts 25(OH)D into another molecule:

1,25-dihydroxyvitamin D (calcitriol)

This turned out to be the true hormonal form that acts on cells and regulates calcium metabolism.

So the sequence scientists uncovered was:

Vitamin D → 25-hydroxyvitamin D (liver) → 1,25-dihydroxyvitamin D (kidney)

That discovery transformed vitamin D from being viewed as a simple dietary vitamin into what is essentially a hormone system.

What’s fascinating is that 25-hydroxyvitamin D was discovered because scientists were tracing the fate of vitamin D molecules through the body. The test came afterward, once they realized this metabolite was the best indicator of vitamin D status.

Liquid Chromatography - Tandem Mass Spectrometry

This is a really long and complex way of saying “testing for charge”. You could have guessed it from a mile off right? As soon as we come to the end of the line for anything to do with “Bio”/Chemistry the machines *ALL* measure charge. In this particular instance it ionizes a pulverized spray after adjusting the pH to find the right charge for the sample you have previously assumed contains the thing you want to measure. One of the really funny things to note here is that the actual measurement of claimed Vitamin D in minute quantities by the way (nanograms per milliliter) is done on a predetermined scale that has markers for just a few different levels (10/20/50/100 ng/ml), the rest has to be a guestimate. Without wishing to bore the pants off of anyone this is also completely arbitrary where a curve is made out of assumed concentration and a “response ratio” ( a predefined calibration that ignores the actual test, Seriously!) So the point at where the rubber meets the road in this wormhole of conjecture, even then with the result it spits out, it is interpreted and manipulated.

LC-MS/MS (Liquid Chromatography–Tandem Mass Spectrometry) is the current gold-standard method for measuring vitamin D metabolites, especially 25-hydroxyvitamin D₂ [25(OH)D₂] and 25-hydroxyvitamin D₃ [25(OH)D₃].

Here’s a simplified but technically accurate walkthrough of what happens to a blood sample.

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Step 1: Draw the blood

A blood sample is collected, and the laboratory separates the serum or plasma.

The vitamin D metabolites are present at very low concentrations:

• Deficient person: ~10 ng/mL

• Sufficient person: ~30–50 ng/mL

• High supplementation: 100+ ng/mL

Most of the 25(OH)D is tightly bound to vitamin D–binding protein.

---

Step 2: Add an internal standard

Before any processing, the lab adds a known amount of a chemically identical compound.

For example:

• Deuterated 25(OH)D₃ (25(OH)D₃-d₆)

This molecule behaves almost exactly like natural vitamin D but is slightly heavier because some hydrogen atoms are replaced with deuterium.

This serves as a reference throughout the procedure.

If some vitamin D is lost during extraction, the internal standard is lost proportionally, allowing correction.

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Step 3: Release vitamin D from proteins

Vitamin D metabolites are bound to proteins.

The lab adds solvents such as:

• Acetonitrile

• Methanol

These solvents denature proteins and release the vitamin D metabolites into solution.

Proteins precipitate and are removed.

What’s left contains:

• 25(OH)D₂

• 25(OH)D₃

• Internal standard

• Other lipids and small molecules

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Step 4: Extract the vitamin D compounds

The lab concentrates the vitamin D metabolites.

Common approaches include:

Liquid-liquid extraction

A nonpolar solvent such as hexane is added.

Vitamin D prefers the organic solvent layer.

Many contaminants stay behind.

Solid-phase extraction

The sample passes through a cartridge.

Vitamin D sticks to the cartridge.

Impurities are washed away.

Vitamin D is then eluted.

At this stage the sample is much cleaner.

---

Step 5: Inject into the liquid chromatograph

Only a tiny amount is needed:

Typically 5–20 microliters.

The sample enters a high-pressure liquid chromatography system.

---

Step 6: Separation by liquid chromatography

This is the “LC” part.

The sample moves through a narrow column packed with microscopic particles.

Different molecules interact differently with:

• The column material

• The moving solvent

As a result they travel at different speeds.

Imagine a race:

MoleculeExit TimeCompound A3.2 minCompound B4.0 min25(OH)D₃5.1 min25(OH)D₂5.7 min

This separation is important because vitamin D metabolites are chemically similar.

Without chromatography, the mass spectrometer could confuse them.

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Step 7: Ionization

The separated compounds leave the column and enter the mass spectrometer.

The molecules must be converted into charged ions.

This is usually done using:

Atmospheric Pressure Chemical Ionization (APCI)

or

Electrospray Ionization (ESI)

The result:

25(OH)D₃ → charged ion

For example:

Molecule + H⁺ → [M+H]⁺

Now the instrument can manipulate it using electric fields.

---

Step 8: First mass filter (MS1)

The first mass analyzer selects ions of a specific mass-to-charge ratio (m/z).

For example:

• 25(OH)D₃ has one characteristic mass

• 25(OH)D₂ has another

• Internal standard has another

Only the ion of interest is allowed through.

Everything else is filtered out.

Think of this as selecting a single suspect from a crowd.

---

Step 9: Collision cell

The selected ion is accelerated into inert gas molecules.

Usually:

• Nitrogen

• Argon

The ion breaks into predictable fragments.

This is called collision-induced dissociation.

Example:

Parent ion → fragment A + fragment B + fragment C

Each vitamin D metabolite produces a characteristic fragmentation pattern.

---

Step 10: Second mass filter (MS2)

The second mass analyzer looks for a specific fragment.

This is why it’s called tandem mass spectrometry (MS/MS).

The instrument is essentially asking:

Did the parent ion have exactly the fragmentation pattern expected for 25(OH)D₃?

If yes, confidence becomes extremely high.

This greatly reduces false positives.

---

Step 11: Measure signal intensity

The detector counts ions.

More ions reaching the detector means:

More vitamin D was present in the original sample.

The instrument records a peak.

A typical chromatogram might show:

• Internal standard peak

• 25(OH)D₂ peak

• 25(OH)D₃ peak

The area under each peak is measured.

---

Step 12: Compare with calibration standards

The lab has previously analyzed standards with known concentrations.

Example:

StandardConcentrationA10 ng/mLB20 ng/mLC50 ng/mLD100 ng/mL

The machine builds a calibration curve.

The patient’s signal is compared against that curve.

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Step 13: Calculate the result

The software computes:

25(OH)D₂ concentration

25(OH)D₃ concentration

=

Total 25(OH)D

For example:

• 25(OH)D₂ = 8 ng/mL

• 25(OH)D₃ = 24 ng/mL

Total:

32 ng/mL

This is the number reported to the physician.

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Why LC-MS/MS is considered superior

Older immunoassays rely on antibodies recognizing vitamin D metabolites.

Antibodies can sometimes bind similar molecules and give biased results.

LC-MS/MS identifies compounds using two independent characteristics:

1. Retention time in chromatography

2. Mass/fragmentation pattern in MS/MS

It’s somewhat analogous to identifying a person by both:

• Their fingerprint

• Their DNA

instead of only one characteristic.

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Where LC-MS/MS can still struggle

Even LC-MS/MS is not perfect.

Potential issues include:

• Incomplete extraction

• Poor calibration

• Instrument drift

• Interference from rare vitamin D epimers

• Isobaric compounds (same mass, different structure)

• Sample degradation before analysis

However, when properly validated, LC-MS/MS typically achieves errors of only a few percent and is generally regarded as the most accurate routine clinical method available for measuring vitamin D status.

A useful way to think about it is that the chromatography answers “when did the molecule come out?” and the mass spectrometer answers “what molecule was it?”. Combining both gives a highly specific identification and quantification of vitamin D metabolites.

I’ve Got 99 Problems

Yes. There is actually a substantial literature showing that even LC–MS/MS, despite being considered the reference-class method for 25-hydroxyvitamin D [25(OH)D], is not immune to measurement problems, and there are several international standardization studies documenting significant differences among laboratories and countries.

1. Problems with LC–MS/MS measurement of vitamin D

LC–MS/MS is generally more accurate than immunoassays, but several technical issues can produce disagreement between labs:

A. C3-epimer interference

One of the best-known problems is the presence of 3-epi-25(OH)D3.

Some LC–MS/MS methods chromatographically separate the epimer; others do not. If the epimer is not separated, vitamin D concentrations can be overestimated. This is particularly important in infants but can also affect adults.

B. D2 vs D3 recovery differences

Labs differ in how well they measure:

• 25(OH)D2

• 25(OH)D3

• Total 25(OH)D

Studies have shown that samples containing high concentrations of D2 can produce significant assay-dependent bias. While this is a bigger problem for immunoassays, LC–MS/MS methods also differ depending on calibration and extraction procedures.

C. Calibration differences

Historically, different laboratories used different:

• calibrators

• extraction protocols

• internal standards

• chromatographic conditions

As a result, two LC–MS/MS laboratories could analyze the same sample and report meaningfully different vitamin D levels. This was one of the reasons the Vitamin D Standardization Program (VDSP) was created.

D. Matrix effects and extraction efficiency

Vitamin D metabolites are highly lipophilic and strongly protein-bound.

Differences in:

• protein precipitation

• liquid-liquid extraction

• solid-phase extraction

• ion suppression

can alter recovery and measured concentrations. These effects are well-recognized LC–MS/MS challenges.

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2. Are there studies showing inconsistency between laboratories?

Yes. This has been documented repeatedly.

Vitamin D Standardization Program (VDSP) Interlaboratory Comparison Study

One of the most important studies is:

“Baseline Assessment of 25-Hydroxyvitamin D Assay Performance: A VDSP Interlaboratory Comparison Study”.

Researchers distributed identical serum samples to laboratories around the world and compared results against reference measurement procedures.

Key finding:

• Large differences existed among laboratories before standardization.

• Some assays exhibited substantial bias relative to reference methods.

• Results varied enough to affect prevalence estimates of vitamin D deficiency in populations.

VDSP LC–MS/MS Intercomparison Study

Another major study specifically examined LC–MS/MS laboratories:

“Interlaboratory Comparison of 25-Hydroxyvitamin D Assays: VDSP Intercomparison Study 2 – Part 1 LC-MS/MS Assays.”

This study found that:

• Not all LC–MS/MS laboratories agreed.

• Differences in handling of 3-epi-25(OH)D3 contributed to discrepancies.

• Standardization improved agreement but did not eliminate all variation.

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3. Are there studies showing differences between countries?

Yes, and this became a major issue in nutritional epidemiology.

Before standardization efforts, countries appeared to have very different rates of vitamin D deficiency. Some of those differences were biological, but some were simply due to laboratory methodology.

The VDSP demonstrated that when measurements were recalibrated to common reference standards:

• national surveys often changed their estimated prevalence of deficiency,

• some countries moved substantially up or down in rankings,

• apparent international differences were reduced.

This was one of the strongest arguments for creating global vitamin D standardization programs.

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4. External quality-control programs found persistent variability

The best-known program is the Vitamin D External Quality Assessment Scheme (DEQAS).

DEQAS has repeatedly shown that:

• laboratories using the same general technology can report different results,

• bias can persist over years,

• standardization efforts improve but do not completely eliminate variability.

The existence of DEQAS itself is essentially an acknowledgment that vitamin D testing remains vulnerable to inter-laboratory variation.

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5. How large can the disagreement be?

Historically, differences of:

• ±10–20% between laboratories were not unusual,

• larger discrepancies occurred in some surveys and older datasets,

• deficiency classification could change depending on the laboratory.

For example, a true value near a clinical cutoff (e.g., 50 nmol/L or 20 ng/mL) might be reported above or below the threshold depending on assay bias. This has important consequences for both clinical practice and research.

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What many vitamin D researchers now consider the most important paper

If your interest is specifically “Can two good LC-MS/MS labs give different vitamin D results?”, the paper I’d start with is:

Interlaboratory Comparison of 25-Hydroxyvitamin D Assays: VDSP Intercomparison Study 2 – Part 1 LC-MS/MS Assays.

If your interest is “How much do vitamin D results differ across countries and surveys?”, start with:

Baseline Assessment of 25-Hydroxyvitamin D Assay Performance: A VDSP Interlaboratory Comparison Study.

Those two papers are probably the strongest evidence that:

1. LC–MS/MS is not perfectly standardized across laboratories, and

2. international vitamin D prevalence estimates can be significantly affected by laboratory methodology.

A particularly interesting follow-up question is whether the degree of laboratory variability is large enough to explain why some people report vitamin D levels changing from, say, 30 ng/mL to 50 ng/mL when they switch labs. There are studies on that specific issue as well.

Q: Are there times when people have started supplementing with vitamin d and it doesn’t affect their measured levels?

Yes. This is a well-documented phenomenon. While most people show an increase in serum 25-hydroxyvitamin D [25(OH)D] after supplementation, there is considerable variability, and some individuals show little or no apparent increase despite taking substantial doses.

The key question is whether the lack of change is due to:

1. True biological non-response, or

2. Measurement and testing issues.

The evidence suggests both can occur.

How common is a poor response?

Clinical trials consistently find large differences between individuals receiving the same dose.

For example, people taking 2,000 IU/day for several months may experience increases ranging from:

• almost no change,

• modest increases (5–10 ng/mL),

• large increases (20–40+ ng/mL).

Researchers often describe this as “inter-individual variability in vitamin D response.”

Reasons supplementation may not noticeably raise measured levels

1. Obesity

This is one of the strongest and most reproducible findings.

Vitamin D is fat-soluble and distributes into adipose tissue. People with obesity typically show a smaller rise in blood 25(OH)D for the same oral dose than lean individuals.

Many studies estimate they may require roughly 2–3 times higher doses to achieve the same serum concentration.

people with higher body fat often have lower measured vitamin D levels in their blood, not higher.

Here’s why:

Vitamin D is fat-soluble

Cholecalciferol dissolves in fat and can be stored in adipose (fat) tissue. When someone has more body fat, a larger proportion of vitamin D may be distributed into those fat stores rather than remaining in the bloodstream.

What blood tests show

The standard vitamin D blood test measures 25-hydroxyvitamin D. On average, people with obesity tend to have lower levels of this marker than people with lower body fat.

Does that mean they have less vitamin D overall?

Not necessarily. They may have substantial amounts stored in fat tissue, but less is circulating and available in the blood. The relationship is complex and still an area of research.

Practical consequence

Because of this effect, people with obesity sometimes require higher vitamin D supplementation doses to achieve the same blood levels as leaner individuals. Supplementation should be guided by a healthcare professional and blood testing when appropriate.

2. Malabsorption

Conditions that impair fat absorption can blunt response:

• celiac disease

• Crohn’s disease

• pancreatic insufficiency

• bariatric surgery

• some liver and biliary disorders

In these cases, a person may faithfully take supplements but absorb much less vitamin D.

3. Genetic variation

Variants in genes involved in:

• vitamin D binding protein (GC)

• vitamin D hydroxylation enzymes

• vitamin D transport

can influence how much serum 25(OH)D rises after supplementation.

This area remains active research, but genetics clearly contribute to response variability.

4. Baseline deficiency severity

People who start with extremely low levels sometimes show slower or less predictable early increases.

The relationship between dose and blood concentration is not perfectly linear.

5. Adherence problems

In clinical practice this is common:

• missed doses

• inconsistent timing

• incorrect dose strength

• supplement degradation

A patient may believe they are taking the intended amount while actual intake is lower.

6. Drug interactions

Certain medications accelerate vitamin D metabolism, including some:

• anticonvulsants

• glucocorticoids

• antiretrovirals

These can reduce the rise in serum levels.

7. Laboratory variation

As discussed previously, if the true increase is modest and close to assay variability, one test may not clearly detect the change.

For example:

• baseline: 24 ng/mL

• true follow-up: 29 ng/mL

A laboratory’s analytical variation might make those results appear unchanged or even slightly lower.

Are there studies where supplementation produced essentially no measurable increase?

Yes.

In supplementation trials, investigators frequently identify a subset of participants whose 25(OH)D concentrations rise very little despite receiving the same intervention as others.

However, complete absence of change is uncommon when:

• adherence is verified,

• absorption is normal,

• the dose is adequate,

• and follow-up is long enough.

In most cases, “non-responders” still show some increase; it’s just much smaller than expected.

An important distinction: blood level response vs biological response

There is also a fascinating literature showing that some people who exhibit similar increases in serum 25(OH)D show very different downstream biological responses.

For example, researchers have observed differences in:

• gene expression,

• immune markers,

• calcium regulation,

despite similar blood vitamin D levels.

So even serum 25(OH)D itself is not a perfect measure of vitamin D activity in the body.

What would make me suspicious?

If someone is taking:

• 4,000–10,000 IU/day,

• consistently for several months,

and their measured 25(OH)D remains essentially unchanged across repeated tests, I would consider:

1. laboratory-to-laboratory differences,

2. malabsorption,

3. obesity-related dose requirements,

4. medication effects,

5. supplement quality issues,

6. rare metabolic or genetic causes.

A complete lack of movement despite verified intake is unusual enough that many clinicians would want to investigate rather than assume the result reflects normal biology.

Abstract

An interlaboratory comparison study was conducted by the Vitamin D Standardization Program (VDSP) to assess the performance of liquid chromatography - tandem mass spectrometry (LC-MS/MS) assays used for the determination of serum total 25-hydroxyvitamin D (25(OH)D), which is the sum of 25-hydroxyvitamin D₂ (25(OH)D₂) and 25-hydroxyvitamin D₃ (25(OH)D₃). A set of 50 single-donor samples was assigned target values for concentrations of 25(OH)D₂, 25(OH)D₃, 3-epi-25-hydroxyvitamin D₃ (3-epi-25(OH)D₃), and 24R,25-dihydroxyvitamin D₃ (24R,25(OH)₂D₃) using isotope dilution liquid chromatography - tandem mass spectrometry (ID LC-MS/MS). VDSP Intercomparison Study 2 Part 1 includes results from 14 laboratories using 14 custom LC-MS/MS assays. Assay performance was evaluated using mean % bias compared to the assigned target values and using linear regression analysis of the test assay mean results and the target values. Only 53% of the LC-MS/MS assays met the VDSP criterion of mean % bias ≤ |±5%|. For the LC-MS/MS assays not meeting the ≤ |±5%| criterion, four assays had mean % bias of between 12 and 21%. Based on multivariable regression analysis using the concentrations of the four individual vitamin D metabolites in the 50 single-donor samples, the performance of several LC-MS/MS assays was found to be influenced by the presence of 3-epi-25(OH)D₃. The results of this interlaboratory study represent the most comprehensive comparison of LC-MS/MS assay performance for serum total 25(OH)D and document the significant impact of the lack of separation of 3-epi-25(OH)D₃ and 25(OH)D₃ on assay performance, particularly with regard to mean % bias.

Yes — and the actual DEQAS results are quite clear, and a bit more nuanced than the “everything agrees well” impression you sometimes get from summaries.

I’ll summarize the real findings from DEQAS LC–MS/MS and mixed-method comparisons using blinded human serum samples.

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📊 What DEQAS actually finds (real blinded serum, LC–MS/MS included)

1. Inter-laboratory variation is still real (even for LC–MS/MS)

Across DEQAS distributions:

• Overall inter-lab CV (coefficient of variation):

  • historically ~20–30% in early years

  • improved to roughly 10–15% in modern schemes

So even with LC–MS/MS:

labs do not fully converge on the same number for the same serum sample.

📌 Modern DEQAS summary:

• LC–MS/MS improves precision vs immunoassays

• but does not eliminate between-lab bias

ANALYSIS

Here we have it that on the face of it, even the most modern techniques where they are given smoothed and manipulated chemical titrations of samples and feed them to laboratories with near identical equipment, they are still returning variations of up to 30% difference between measurement, with 50% of those laboratories not meeting the NIST requirement for accuracy. Even when the game is rigged with all of the assumptions piled up, even with loaded die they can’t even reliably reproduce their own results. The real world is even more glib than this, that just sheer body fat seems to affect the difference of effects of the rat pills by up to 300%, this simple metric alone of body fat also greatly affects the vitamin D level measured in the blood as it is stored in fat. This is a deadly combo of storing vit d in fat, having lower measurements because of this AND seeing less biomarker change when you take the rat pills because once again it is storing in the fat, if you ever come to loose weight it could be deadly, and scientists haven’t actually studied this by the way. Ultimately as you will see in the second half (the most important half) of this article is that weight really does make a difference, literally a life or death difference as LD50 (the dose at which a poison is lethal) is measured by dosage per Kilogram of body weight.

VITAMIN D3 IS RAT POISON

Terad3 is a brand of rodenticide bait blocks containing 0.075% or 0.08% cholecalciferol (Vitamin D3) as its active ingredient, manufactured by Bell Laboratories, Inc. It is specifically formulated to control Norway rats, roof rats, and house mice in various settings, including agricultural, industrial, and residential facilities.

The product works by mobilizing calcium from the bone matrix into the plasma, causing hypercalcemia and subsequent death in rodents. Key features include its resistance to mold and moisture, a high melting point stable up to 200°F, and a reduced risk of secondary poisoning to non-target animals like birds and pets. Terad3 Ag Blox is also OMRI registered for use in organic production facilities.

Before we get into the nitty gritty of this I want to really pause and highlight what we are talking about here. The only active ingredient in some rat poisons are Vitamin D3, chemical name cholecalciferol. By weight the active ingredient is 0.08%, the rest being cereals and food that act as a bait to attract the rats to eat the poison. When I learned this fact my jaw hit the floor, not only because I had a very scary health episode at the hands of this poison, but even if I hadn’t I would have of course immediately stopped taking it. It defies any logic to take something that is a known poison that is used to kill biological animal life, there really should be no further questions.

The thing that is astounding to me given my lengthy experiences of calling this stuff out on social media is, the people that seem most upset by the facts, the vast majority are “Anti-Vaxxers”. People who would balk at being jabbed because it is poison. They have seen through this scam because they in a large part have been programmed to think that every cardiac episode since 2020 has been directly and solely caused by the Covid Jabs. The may well be correct in a few instances of very quick post jab deaths. But I believe it is not always that clear cut when people are going “suddenly” a few years afterwards. So I would proffer up the notion of entertaining the idea that there may be other drugs/poisons at play.

The funny thing to me is that these Anti-Vaxxers rightfully have seen through the “safe and effective” campaign for vaccines and the huge coverup of damages. However when it comes to Vitamin D, the establishment are incredibly forthcoming with the truth that YES this drug they want you to take does kill rats, infect it is so good at killing stuff, it is used worldwide for that exact purpose. Imagine if you will that they used the ingredients of vaccines, mixed them with some Cheerios and when animals ate them, it killed them, with such reliability vaccines were used world wide solely for this purpose. In what world would anyone not see the problem here, yet call it a “Vitamin” and all of a sudden we are “having a conversation about it”.

Well I am here to tell you, there is no conversation, you only need basic logic, indeed a basic sense of danger and distrust of Big Pharma (who make the rat poison). There is no need to be shown by Del Bigtree people dying of heart attacks and to be told it is Vitamin D that caused it (although it would raise awareness). No you have every available experiential data you need in the form of dead rats; you give them Vitamin D, they die, end of story.

But just to make sure it is all in one place, I am going to answer absolutely every dumbass question ,(non) point and bullshit attempted rebuttals made by the people who frequent the comments sections of anyone brave enough to highlight the Vitamin D hoax:

1. RATS AREN’T HUMANS THOUGH.

Q: Regardless of weight and size, does cholecalciferol have the same effects on humans as rats?

Yes, cholecalciferol (vitamin D3) has the same primary toxic effects in humans and rats (and most other mammals). The mechanism and resulting pathology are fundamentally the same, even if sensitivity (e.g., LD50 on a mg/kg basis) varies somewhat between species.

Shared Mechanism of Action

Cholecalciferol is metabolized in the liver to 25-hydroxycholecalciferol and then in the kidneys to the active form (1,25-dihydroxycholecalciferol/calcitriol). In overdose:

• It massively increases intestinal absorption of calcium and phosphorus.

• It mobilizes calcium from bones.

• It enhances renal reabsorption of calcium.

This leads to hypercalcemia (elevated blood calcium) and hyperphosphatemia, causing metastatic/soft tissue calcification (mineralization), especially in the kidneys, heart, blood vessels, and other organs. The end result is often acute kidney failure, cardiac issues, and death if untreated.

Effects in Rats (and Rodents Used as Rodenticide)

• Used in baits (e.g., 0.075% concentration) because toxic doses cause hypercalcemia → tissue mineralization → renal/heart failure.

• Clinical signs: anorexia, lethargy, weakness, polyuria/polydipsia, dehydration; death typically in 3–7+ days.

• Oral LD50 in rats/mice is around 30–44 mg/kg (varies by study/strain), with toxicity at lower doses (e.g., signs from ~0.1–0.5 mg/kg in related species).

  sciencedirect.com

Effects in Humans

• Identical core pathology: Excess cholecalciferol (from supplements, accidental ingestion, or megadoses) causes hypercalcemia and hyperphosphatemia, leading to the same mineralization, kidney damage/failure, and potential cardiac/neurological complications.

• Symptoms: nausea, vomiting, anorexia, constipation, polyuria/polydipsia, weakness, fatigue, confusion, bone pain, dehydration; severe cases involve kidney stones, nephrocalcinosis, arrhythmias, or coma.

  ncbi.nlm.nih.gov

• Human vitamin D supplements are toxic at high enough doses via the exact same mechanism as in rodenticide cases. Cases of severe toxicity and hypercalcemia from over-supplementation are well-documented.

  avs4pets.com

Key Similarities (Regardless of Body Weight/Size)

• The biochemical pathway (vitamin D receptor binding, calcium dysregulation) is conserved across mammals.

• Target organs (kidneys, heart, vessels) and outcomes (calcification, organ failure) match.

• No fundamental qualitative difference—it’s the same hypervitaminosis D syndrome.

Analysis

So the first lie to protect the rat poison hoax is easily disproven, that there is some sort of difference in the way the poison affects rats than it does to humans or indeed any other animal species. That is the thing with chemicals is they tend to just do damage to biological life, ultimately that is why you should bin all drugs/chemicals…

2. YOU’LL DIE IF YOU DRINK TOO MUCH WATER TOO!

Q: What is the LD50 of water in humans?

This is a bit of a trick question: water does not have a standardized LD50 in humans because LD50 (lethal dose for 50% of a population) is typically determined through animal studies, and it would be unethical to test in humans. However, we can estimate a lethal dose based on known cases of water intoxication (hyponatremia).

Estimated lethal oral dose of water in humans:
Approximately 90 mL per kg of body weight within a short period (e.g., a few hours).

So for a 70 kg (154 lb) adult:
~6.3 liters of water consumed in a very short time could be fatal.

Key points:

• This varies with age, kidney function, rate of consumption, and electrolyte status.

• For comparison, the LD50 of water in rats is roughly >90 mL/kg orally, but species differences matter.

• Death results from dilutional hyponatremia leading to cerebral edema.

Bottom line: No official human LD50 exists, but acute lethal water intake is around 6–7 liters for an average adult over 1–2 hours. Safe kidneys can excrete ~0.8–1.0 liters per hour maximum.

Q: How many people die a year from hyponatremia caused by drinking too much water. Can you give me an exact figure please.

There is no exact annual figure for deaths from hyponatremia caused specifically by drinking too much water.

Reliable sources (medical literature, CDC-related reports, and reviews) consistently describe such deaths as rare. No global, WHO, or comprehensive national database tracks a precise yearly total for this specific cause, as it is not a common or routinely categorized cause of death like heart disease or accidents. Cases are usually documented individually or in small clusters (e.g., military training, endurance sports, water-drinking contests, or psychiatric conditions like psychogenic polydipsia).

Key Context from Available Data

• Rarity emphasized across sources: Death from water intoxication (dilutional hyponatremia) is “rare,” “exceptionally rare” in healthy people under normal circumstances, and “quite rare” overall. Most people do not consume enough water fast enough for it to be fatal.

  healthline.com

• Documented examples (not annual totals):

  • Military: A few historical deaths (e.g., 3 in one referenced period); hundreds of non-fatal cases over years in US forces.

    en.wikipedia.org

  • Endurance sports/marathons: A handful of confirmed deaths over decades (e.g., several in marathons or high school athletes in specific years), with “more than a dozen” documented/suspected in some reviews.

    loyolamedicine.org

  • Other: Isolated cases from contests (e.g., 2007 radio show death), hazing, or medical/psychiatric situations.

    nbcchicago.com

• Broader hyponatremia deaths (e.g., hospital-related, postoperative, or from other fluid imbalances) are more common but not the same as pure over-drinking of water.

In summary, while real cases do occur and are preventable (by drinking to thirst and not forcing excessive intake), the annual worldwide number is very low—likely in the low dozens at most, based on scattered reports—but no verified exact figure exists. If you’re concerned about personal risk, stick to normal hydration guidelines and seek medical advice for symptoms like severe headaches, confusion, or seizures after heavy fluid intake.

Q : Is water considered a poison, based on the Hodges Sterner toxicology scale?

Under the Hodge–Sterner toxicity scale, whether something is considered toxic depends on its LD₅₀ (the dose that kills 50% of test animals), usually measured in mg/kg. The scale classifies substances with oral LD₅₀ values above 15,000 mg/kg as “relatively harmless” and 5,000–15,000 mg/kg as “practically non-toxic.”

For water, the reported oral LD₅₀ in rats is commonly cited around 90,000 mg/kg (90 g/kg), although values vary by study. That is far above the 15,000 mg/kg threshold. Therefore, on the Hodge–Sterner scale, water would be classified as:

Rating 6 — Relatively Harmless

ANALYSIS

So there is actually no official LD50 for water in humans, the exact dose “would” be too difficult to reliably calculate for 50% of the population to die, largely because it is a factor determined mostly about timing and sheer volume. It isn’t the liquid itself but the amount that your kidneys can handle at any one time and also how it dilutes sodium. This of course has nothing to do with the question at hand and is merely a distraction with a dim witted tautology. Of course everything in the world can and will kill you… it is a function of life itself, entropy that once you are living, you must die at some point, so naturally everything is deadly at some point given enough time, even one of the handful of things deemed essential for living.

There are really no year to year figures for how many people die of Hyponatremia, from water consumption, because it is claimed to happen so rarely. There are only a few documented cases in modern history and a couple of those, like Leah Betts sound to me like Psyops. They attempt to put a figure on it from claimed LD50 in rats which puts it at about 6-7 liters in a few hours. Given that we have the internet now.. it quickly becomes that these handful of rarities must have had some other underlying medical problem to give the idea that this might be the case. Here this guy (known for chugging many litres of sodas on Youtube) has a bit of a “detox” by chugging a gallon 4.5l of water in 50 seconds. If only he knew how close to death he came. lol.

Here is the link for people reading the Ebook

And here is 1.5 Gallons (6.8 Liters- a claimed lethal dose) in 2 mins and 3 seconds

3. THE DOSE MAKES THE POISON

Q: What is the LD50 of Cholecalciferol a good average across all sources.

Around 35–45 mg/kg (oral, rat) is a reasonable average LD50 for cholecalciferol (Vitamin D3), based on multiple reliable sources.

Key Values from Sources

• Many SDS and toxicity databases cite ~42 mg/kg (oral, rat) or closely related figures like 35–42.5 mg/kg.

  spectrumchemical.com +1

• AAT Bioquest lists 37 mg/kg (oral, rat).

  aatbio.com

• Merck Veterinary Manual references 88 mg/kg (LD50 in dogs/context) but notes toxic effects at much lower doses (e.g., clinical signs >0.5 mg/kg, lethality possible around 13 mg/kg or less in practice).

  merckvetmanual.com

• Other rodent studies (e.g., house rats, bandicoot rats) report values in the 30–35 mg/kg range, sometimes with slight sex differences (males often more sensitive).

  search.proquest.com +1

• Some older/EPA-linked studies show higher values (e.g., 350+ mg/kg in certain rat strains/conditions), likely due to formulation, vehicle, or strain differences.

  responsiblerodenticides.org

Important Context

• LD50 varies by species, route, sex, and study conditions — Rats and mice are relatively sensitive (often ~40 mg/kg oral), while dogs show toxicity at lower practical doses despite some reported LD50s around 88 mg/kg. Humans are far less sensitive to acute single doses but can experience toxicity from chronic high intake.

  vpisglobal.com

• Cholecalciferol is used as a rodenticide precisely because it causes hypercalcemia, leading to organ damage (kidneys, heart, etc.) at doses well below the formal LD50 in target and non-target species.

• This is for acute oral lethality in lab animals (typically rats). Real-world toxicity (morbidity/death) can occur at lower exposures, especially with repeated dosing or in sensitive animals.

Q: What category would that place it on the Sterner Hodges Toxicity Scale?

Highly Toxic (Class 2 / Toxicity Rating 2) on the Hodge and Sterner (or Sterner-Hodges) Toxicity Scale.

Quick Breakdown of the Scale (Oral LD50 in Rats, mg/kg)This is the classic Hodge and Sterner classification (often called Sterner-Hodges or similar variants):

• Your value of ~35–45 mg/kg clearly falls in the 1–50 mg/kg range → Highly Toxic.

• This aligns with its use as a rodenticide (it causes severe hypercalcemia and organ damage at doses well below the formal LD50 in many species).

Note: This is an older scale focused on acute lethality. Modern systems like GHS use different cutoffs (e.g., Category 2 for oral LD50 ≤50 mg/kg, which is also “highly toxic”). Always consider species/route differences and that real-world toxicity (especially repeated exposure) can occur at lower doses.

Q: What other substances are in this highly toxic category? Is Organic Arsenic in this catergory?

Highly Toxic (Hodge and Sterner Class 2: oral LD50 rat ≈1–50 mg/kg) includes many potent poisons, pesticides, and certain natural toxins.

Common Examples in This Category

Here are well-documented substances with oral LD50 values in rats (or closely related) falling in or near the 1–50 mg/kg range:

• Strychnine — ~2–16 mg/kg (rat, oral; often cited around 16 mg/kg but lower in some studies/sexes). A classic convulsant alkaloid.

• Nicotine — ~50 mg/kg (rat, oral; borderline but commonly grouped here; much lower in mice ~3 mg/kg).

• Aldicarb (a carbamate pesticide) — Extremely low, often <1–5 mg/kg range (highly toxic insecticide).

  en.wikipedia.org

• Arsenic trioxide (inorganic) — Variable but often in the low tens of mg/kg (e.g., ~15–50 mg/kg depending on study/vehicle).

• Other examples: Certain organophosphates, some rodenticides, aflatoxin B1 (~0.5 mg/kg), and various highly potent alkaloids or synthetic toxins.

Many highly/extremely toxic materials are organic (e.g., alkaloids, pesticides), though some inorganics qualify too.

ANALYSIS

So yes, I vaguely agree with you, dose does make the poison. It is the reason why Water is in the bottom category of Relatively Harmless having an assumed LD50 10x that needed to be in this category. It is also the reason why Vitamin D is in the Highly Toxic category of poisons deemed deadly to all living life in quantities of just 4ml or a teaspoons worth. This category is shared by some familiar faces with the likes of Strychnine, Arsenic, Organophosphates (such as Phosmet- From Mark Purdey’s quest to show it caused BSE) and Aldicarb a highly toxic insecticide. It’s a simple as that the doses that this stuff is in, is absolutely minute because of its sheer potency as a known highly toxic poison. Even as a disclaimer on the DCON website (another Rat Poison Brand using Vitamin D) it tells you that there is just 11 milligrams (11 thousands of a gram) in one block, this is considered a toxic dose to animals under 35lbs in other words that is a child of around 2-3 yrs old.

4. DOG CHOCOLATE

This is for those really desperate and hardened Pharma Pushers as it sneakily crafts in elements of copes 1, 2 & 3 and never really quite commits to an argument in any sort of detail in any of them. People whom use this one are usually the most dishonest and underhand of the lot as it wraps into one little ball a bundle of numerous logical fallacies into one large ball of conjecture and finishes it off with a healthy dollop of virtue signaling to boot. This is also seen with a few other claimed food stuffs that are seemingly fine for humans but claimed to be toxic for dogs, like grapes, onions, macadamia nuts and caffeine.

So let’s put the part to bed specifically relating to Rat Poison and then we can address a little bit (very quickly) the shaky science behind the notion of some human foods being poisonous to dogs:

Q : Is cholecalciferol poisonous to dogs? What is it’s LD50 ?

Yes. Cholecalciferol (vitamin D₃) can be highly poisonous to dogs when ingested in excessive amounts, especially in the concentrations used in rodenticides. It causes severe elevations of calcium and phosphorus in the blood, which can lead to kidney failure, heart damage, soft-tissue calcification, and death.

Regarding LD₅₀ (median lethal dose) in dogs:

• A commonly cited acute oral LD₅₀ is about 85–88 mg/kg for pure cholecalciferol (”technical material”) in dogs.

• However, veterinarians generally consider the LD₅₀ misleadingly high because dogs can develop life-threatening poisoning at much lower doses. Clinical toxicity has been reported at 0.1–0.5 mg/kg, and serious poisoning has occurred in the 0.5–3 mg/kg range.

• In one study, dogs given 10–20 mg/kg via a cholecalciferol rodenticide all died, despite those doses being far below the published LD₅₀.

To put that in perspective, for a 20 kg (44 lb) dog:

• LD₅₀ ≈ 1.7 grams of pure cholecalciferol.

• But clinically significant poisoning could begin around 2–10 mg total, and severe poisoning can occur with much less than the LD₅₀.

• Symptoms of cholecalciferol (Vitamin D3) poisoning in pets, such as from ingesting Terad3 rodenticide, result from severe hypercalcemia (high blood calcium) and hyperphosphatemia, leading to acute kidney failure and soft tissue mineralization.

  Timeline and Clinical Signs

  0–24 Hours (Early Stage) Clinical signs often appear within 12 to 36 hours after ingestion. Initial symptoms are non-specific and include:

  • Lethargy and weakness

  • Anorexia (loss of appetite)

  • Polydipsia (excessive thirst) and polyuria (increased urination)

  • Vomiting and diarrhea

  12–48 Hours (Progression) As calcium levels rise, gastrointestinal and systemic signs worsen:

  • Hematemesis (vomiting blood) or melena (black, tarry stool containing digested blood)

  • Hypersalivation (excessive drooling)

  • Elevated body temperature

  • Abdominal pain

  2–5 Days (Critical Stage) Without treatment, acute kidney failure develops, leading to severe complications:

  • Oliguria or anuria (decreased or no urine production)

  • Uremic halitosis (breath smelling of ammonia/urine)

  • Cardiac arrhythmias (irregular heartbeat) and bradycardia (slow heart rate)

  • Seizures, tremors, or depression

  • Death due to renal failure or cardiac arrest

  Species-Specific Observations

  • Dogs: Commonly exhibit depression, weakness, vomiting, bloody diarrhea, and cardiac irregularities.

  • Cats: Often show hypersalivation, halitosis, and are prone to pulmonary (lung) mineralization in addition to kidney damage.

Q: I just simply want an LD50 gross of amount of chocolate a dog would need to eat

A single “amount of chocolate” LD₅₀ is hard to give because different chocolates contain vastly different amounts of theobromine. Using a commonly cited theobromine LD₅₀ of ~300 mg/kg in dogs, you can estimate the chocolate amount needed to reach that dose.

For a 1 kg dog:

• Milk chocolate (~2 mg theobromine/g): about 150 g (5.3 oz).

• Dark chocolate (~10 mg/g): about 30 g (1.1 oz).

• Unsweetened baking chocolate (~20 mg/g): about 15 g (0.5 oz).

For a dog of weight W kg, multiply those amounts by W. For example, for a 20 kg dog:

• Milk chocolate: ~3 kg (6.6 lb)

• Dark chocolate: ~600 g (1.3 lb)

• Baking chocolate: ~300 g (10.6 oz)

These are rough LD₅₀-based estimates only. In practice, severe illness, seizures, dangerous heart rhythms, and even death can occur at substantially lower doses than the median lethal dose. Different sources report different theobromine concentrations and LD₅₀ values, so these numbers should be viewed as order-of-magnitude approximations rather than exact thresholds.

Q: Has there been an instance where a dog has died from eating a couple of grams of chocolate ever?

For a healthy, average-sized dog, a death from eating just a couple of grams of chocolate (for example, 2–5 g) would be extraordinarily unlikely.

Even very potent chocolate such as cocoa powder or unsweetened baking chocolate contains on the order of 20–30 mg of theobromine per gram. So 2–5 g would typically provide roughly 40–150 mg of theobromine total. For most dogs, that’s far below doses associated with severe poisoning.

There are a few caveats:

• Very tiny dogs or puppies (well under 1 kg) are more vulnerable because toxicity is based on body weight.

• Chocolate products can contain other toxic ingredients (e.g., xylitol in some baked goods or candies), which can be more dangerous than the chocolate itself.

• A dog with severe underlying heart disease or other medical problems could potentially be affected by smaller amounts than a healthy dog.

• Published case reports of fatal chocolate poisoning generally involve substantially larger exposures relative to body weight than “a couple of grams” of ordinary chocolate.

So while I can’t prove that no dog has ever died after eating a few grams of a chocolate-containing product under unusual circumstances, there are no well-known reports of a typical dog dying solely from ingesting a couple of grams of chocolate itself. The amounts associated with fatal chocolate poisoning are generally much larger.

Q: Given it takes 3kg of milk chocolate to kill a 20kg dog where would that put it on the sterner Hodges scale?

Using your rough example:

• A 20 kg dog

• LD₅₀ reached at about 3 kg of milk chocolate

An LD₅₀ of 150,000 mg/kg would therefore fall well beyond the highest category (”Relatively Harmless”) on the Hodge–Sterner scale.

This illustrates an important point: milk chocolate itself is not particularly toxic. The toxicity comes from the relatively small amount of theobromine it contains. If you classify the theobromine instead, using an LD₅₀ around 300 mg/kg, it falls into the “Moderately Toxic” category (50–500 mg/kg).

So depending on what you’re classifying:

• Milk chocolate as a food: roughly “relatively harmless” by Hodge–Sterner.

So the first of the vague insinuations that dogs can’t eat chocolates may somehow mean that humans can eat rat poison is shown to be certified lies. Of course Vit D is poisonous to dogs in fact, given that they have studied it with clinical trials with dogs (unfortunately) they found in one study that all the dogs died with a dosage of just 10/20mg/Kg .

They were 20kg dogs which is about the size of a Border Collie so also a fairly average sized dog. That equates to a lethal dose of just 1.7grams to reliably kill a 20kg dog. This is because, once again, Vitamin D is classified as Highly Toxic Poison, it only takes a tiny amount to kill and this is not the case for everything else listed as “inedible” for dogs. There has never been an instance ever of a dog dying from eating a few grams of chocolate, there has never been an instance of a dog eating a couple of grams of anything on the list of “inedible” human foods and dying. Therefore we can conclude the Muppets who claim “Dog Chocolate” as a rebuttal are talking certified strawman bullshit. In fact even by their own metrics (which they actually have very little evidence for) it takes 3000 times MORE in quantity to kill a 20kg dog in chocolate.

When we place “Dog Chocolate” on the Sterner Hodges Toxicity scale the globally accepted toxicological classification of poisons, it is firmly in the “Relatively Harmless” category the very lowest threshold that ironically also contains Water for humans even more ironically it is actually LESS toxic than claimed water for humans. Lol.

Q: Can you tell me how many dogs are claimed to die a year from chocolate poisoning and give me exact examples of a dog that has died from an exact amount of chocolate ingested please?

The short answer is that nobody really knows how many dogs die each year from chocolate poisoning.

There is no centralized worldwide reporting system, and many poisoning cases are treated by private veterinarians, poison-control hotlines, or not reported at all. What is known is that:

• Chocolate ingestion is one of the most common toxic exposures reported in dogs.

• Death appears to be rare relative to the number of exposures, especially when veterinary treatment is obtained.

• In a published study of 156 chocolate-ingestion cases, only 1 dog died (or was euthanized due to severity; the abstract reports 43/44 symptomatic dogs survived), giving a mortality rate under 3% among the symptomatic dogs treated at that hospital.

Documented fatal examples

Finding exact, well-documented fatal cases is surprisingly difficult because most veterinary reports focus on theobromine dose rather than “grams of chocolate.”

One historical case frequently cited in veterinary literature involved:

• An 8-month-old Airedale Terrier

• Weight: 12.3 kg

• Consumed approximately 250 g of chocolate

• Died about 6 hours later.

That works out to about 20 g of chocolate per kg body weight.

Another published series found symptomatic dogs had estimated theobromine exposures up to 332 mg/kg, which is above commonly cited lethal ranges, yet almost all survived with treatment. https://onlinelibrary.wiley.com/doi/10.1111/jsap.13329?utm_source=chatgpt.com

So very quickly we find that the mainstream are once again talking bollocks when it comes to this scaremongering. Out of a studied 156 ingestion cases only 44 of them had any symptoms at all and one would imagine, hyperactivity from the sugar rush would count as a symptom (which is all I think is happening here) . So less than a third show any change at at all.. There were ZERO deaths as the only death that occurred was at the hands of the vets when they euthanized the dog.

5. I’VE TAKEN IT FOR YEARS AND I FEEL FINE

This one is going to be dealt with very quickly as with the Hitchen’s Razor (what can be asserted without evidence can be dismissed without evidence). There are many many crack heads who claim the same thing, right up until the point that they do not feel fine any more.

SHOW ME THE BODIES

Unfortunately there isn’t a Billion Dollar Alternative health marketing budget to go around pointing at everyone that dies of a heart attack and saying that “It was the Vitamin D” that done did it… largely because the vast majority of those people make most of their bank off of selling Vitamin D and all the other quack poisons like Ivermectin and Methylene Blue and DMSO etc. When this alternative health market kicks into gear it can get some of these stories to be pushed into news articles and even influence the mainstream to start investigating at which point it is easier to find for researchers. I am not saying by any means that the devastation, death and disease caused by Vaccines is to be scoffed at or turned away, just that in a large proportion of these “Died Suddenly” cases, especially the ones a few years after vaccination, I doubt that the vaccines were the sole cause of death, rather it was a concoction of drugs, vaccines, diet and lifestyle, that combines together to what can be described as someone who is a “Vaxxer”.

That’s all well and good, but it makes my task here of finding the bodies specifically attributed as deaths to Vitamin D overdose a little more tricky. It doesn’t make it impossible, by any stretch of the imagination, for don’t forget that they have been convincing people to eat literal rat poison for a century now so:

🧭 FULL TIMELINE OF VITAMIN D TOXICITY OUTBREAKS (1920–2026)

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🟡 1920–1930: Discovery & early experimental overdosing

📌 Context

• Vitamin D identified as anti-rickets factor (early 1920s)

• Cod liver oil and irradiated ergosterol used therapeutically

💊 Doses

• Early crude preparations: highly variable

• Sometimes 10,000–100,000+ IU/day equivalent (unstandardized)

⚠️ Outcomes

• First descriptions of:

  • hypercalcemia

  • vomiting

  • kidney stress

• Toxicity initially confused with “impurities”

🧠 Key insight

• Toxicity recognized, but not well understood chemically

📚 Source context: early toxicity characterization literature and vitamin D history reviews

---

🔵 1930–1940: Mass fortification begins (first global exposure wave)

📌 Context

• Milk, bread, cereals, margarine fortified in US/UK/Europe

• Cod liver oil widely given to children

💊 Exposure level

• Typical intake:

  • 400 IU/day (target)

• BUT contamination/overfortification occurred:

  • thousands to >100,000 IU/day in some batches

⚠️ Outcomes

• First population-level infant hypercalcemia cases

• Symptoms:

  • vomiting

  • failure to thrive

  • dehydration

  • kidney calcification

💀 Mortality

• Some infant deaths reported in case series (limited documentation)

📚 Evidence:

• fortification-linked toxicity outbreaks described in medical reviews

---

🔴 1935–1945: “High-dose therapeutic era” (TB, arthritis, chronic disease)

📌 Context

Doctors used vitamin D as a pharmacologic agent

💊 Doses

• 200,000–300,000 IU/day

• Sometimes higher “shock dosing” regimens

⚠️ Outcomes

• Frequent hypercalcemia:

  • confusion

  • kidney injury

  • arrhythmia

• Reversible in most cases when stopped

💀 Mortality

• Rare, but severe illness common

• This is the first clear iatrogenic toxicity wave

📚 Source: endocrine and toxicology reviews

---

🟠 1940–1955: Infant fortification epidemic (largest historical outbreak)

🧨 This is the major event you asked about earlier

📌 Context

• Vitamin D added to:

  • milk

  • cereals

  • margarine

  • infant foods

• Combined with cod liver oil use

💊 Exposure levels

• Expected: ~400 IU/day

• Actual in some cases:

  • 1,500–1,725 IU/day (documented hypercalcemia cases)

  • suspected contamination: much higher in some batches

• Some infants received:

  • repeated high-dose prophylaxis (“stoss therapy” up to 600,000 IU)

⚠️ Outcomes

• Infant hypercalcemia syndrome:

  • failure to thrive

  • vomiting

  • dehydration

  • kidney calcification

  • vascular calcification

🧠 Key discovery (modern interpretation)

• Not all cases were overdose:

  • part genetic (CYP24A1 / Williams syndrome)

  • part true fortification excess

💀 Mortality

• Documented infant deaths in case series (small but real)

• Exact total unknown due to poor reporting systems

📉 Result

• Fortification restricted/banned in several European countries by 1950s

📚 Strong modern reviews:

---

🟣 1950–1960: Residual fortification contamination events

📌 Context

Even after regulation, errors occurred:

• dairy over-fortification

• inconsistent industrial mixing

💊 Exposure

• Sometimes hundreds of times label dose

• Example documented:

  • milk with extreme vitamin D excess

⚠️ Outcomes

• Small outbreaks:

  • infants hospitalized with hypercalcemia

  • rare severe complications

💀 Mortality

• Rare, mostly survivable with treatment

📚 NEJM analysis of contaminated milk events

---

🟢 1960–1990: Decline in outbreaks

📌 Context

• Fortification standardized

• serum testing improves

• vitamin D becomes better regulated

💊 Exposure

• mostly safe:

  • 400–800 IU/day typical supplementation

⚠️ Outcomes

• isolated overdoses only:

  • accidental high-dose supplement use

💀 Mortality

• extremely rare

---

🟡 1990–2010: Supplement era begins (sporadic toxicity cases)

📌 Context

• OTC vitamin D supplements widely available

• high-dose regimens (50,000 IU capsules) introduced medically

💊 Exposure

• accidental chronic overdosing:

  • 10,000–100,000 IU/day in some cases

⚠️ Outcomes

• case reports:

  • kidney failure

  • severe hypercalcemia

  • ICU admissions

💀 Mortality

• very rare, mostly survivable

---

🔴 2010–2026: Modern isolated severe overdoses

📌 Context

• supplement stacking (multiple products)

• compounding pharmacy errors

• misinformation-driven mega-dosing

💊 Exposure

• documented cases:

  • 100,000–200,000 IU/day for weeks–months

  • accidental multi-million IU errors

⚠️ Outcomes

• severe hypercalcemia:

  • renal failure

  • neurological symptoms

  • prolonged hospitalization

💀 Mortality

• extremely rare

• modern confirmed deaths are almost entirely isolated case reports

📌 Example modern fatal case:

• UK coroner-confirmed death from chronic supplementation (2023 case)

In the past, exogenous VDT was considered a rare adverse effect associated primarily with food fortification. From the1930s through the 1950s, public health officials in the United States and the United Kingdom recommended routine fortification of milk and other foods with vitamin D (4). That policy was implemented initially as an effective public health strategy to prevent nutritional rickets in children and then as an intervention to improve the general health of the population (4).

In the 1940s, massive doses of vitamin D (200,000–300,000 IU/day) were considered an effective treatment strategy for chronic illnesses as diverse as tuberculosis and rheumatoid arthritis. Because hypercalcemia was observed in some patients thus treated, individual doctors discontinued the massive doses and the symptoms of VDT disappeared after a few months (4, 12). However, those clinical observations alerted physicians to the possibility of VDT, and the practice of administering massive doses of vitamin D was later discontinued nationally. Those observations, however, did not influence fortification of foods and other products with vitamin D, which persisted through the 1950s (4). In the 1950s, several cases of infants with facial abnormalities, supravalvular aortic stenosis, mental retardation, and hypercalcemia were reported mainly in the United Kingdom. That was followed by additional reports of hypercalcemia in some infants in the United Kingdom as well as in other European countries (13).

An 80-year-old mystery linked to a wave of baby deaths in the 1930s and 1940s has finally been solved by researchers.

The fatal ingredient was found in household staples - milk, bread, cereal, margarine.

But it was put there to try and make children healthier. In the early 1900s, more than 80% of children were affected by the bone condition rickets, so food was fortified with vitamin D.

The fortification all but eradicated the disease. However, there were fatal side-effects as a result of the measure, as some babies could not metabolise vitamin D properly.

They had a condition which causes a build-up of calcium in the blood, leading to kidney damage and kidney stones, which can be fatal in babies.

Outbreaks of vitamin D intoxication in infants led to fortification bans in many European countries by the 1950s.

Research in 2011 revealed the condition, now known as infantile hypercalcaemia type 1 or HCINF1, is caused by a gene mutation.

But scientists were stumped to find about 10% of patients affected by HCINF1 do not have the genetic mutation.

We’re often told how dangerous vitamin deficiencies are for our health, which is why so many of us try to make up for what we’re lacking by taking supplements. But what you assume is boosting your wellbeing could be doing the exact opposite if you’re not careful. A new report out of the UK is highlighting the dangers of overdoing it with vitamins, after a man was killed by the vitamin D supplements he’d been taking for months.

When seven-year-old Roo suddenly became unwell last year - losing weight and guzzling water - his doctors and parents feared he might have a brain tumour.

But investigations found he had been accidentally poisoned with an overdose of vitamin D that had been prescribed for growing pains.

Roo’s bottle of vitamin D3 drops - which were about seven times more concentrated than they should have been - was from one of two bad batches distributed across the UK.

The dosage gave Roo an acute kidney injury and a leading expert has told BBC News the young child would have died if he had finished the prescribed course.

Case Description

In August 2020, a 3-month-old infant was referred to the pediatric emergency department for severe anorexia, vomiting, and weight loss. After an uncomplicated pregnancy (36 weeks and 5 days of amenorrhea), he was born at term, weighing 2.3 kg. Since, he had been exclusively breastfed and had not presented any medical problem.

At the time of admission, the infant weighted 4.5 kg. He had no fever, his heart rate was 109 beats per minute, his blood pressure was 107/85 mmHg, and his oxygen saturation was 99%. Blood pressure was later reassessed several times, and was found normal or at the upper limit of normal for the age. Clinical examination was unremarkable except a global hypotonia and the presence of moderate dark circles around the eyes. Natremia was 139 mmol/L, kalemia 4.4 mmol/L, alkaline reserve 21 mmol/L, hemoglobin 9.1 g/dL, leukocytes 11.11 G/L, platelets 471 G/L, and C-reactive protein (CRP) 13 mg/L with a negative procalcitonin. Blood gases analysis and liver function tests were within normal range. Natriuresis was <20 mmol/L for a kaliuresis of 33 mmol/L, suggestive of hypovolemia. Hemoculture, stool bacterial culture and virology, as well as lumbar puncture results were all negative. Lumbar puncture had been performed because the infant presented with global hypotonia and severe behavioral changes, in the absence of an obvious diagnosis.

Q: What is known about Vit D toxicity in the foetus?

Vitamin D toxicity in the fetus is rare but well-described, and it behaves differently from adult toxicity because the fetus is exposed through the mother’s calcium and vitamin D balance rather than direct dosing.

The key idea is:

⚠️ In pregnancy, vitamin D excess mainly harms the fetus indirectly by driving maternal hypercalcemia, which then disrupts fetal calcium regulation and development.

---

🧠 1. How the fetus is exposed

Vitamin D itself crosses the placenta, but the main problem is:

🔁 Maternal → fetal calcium transfer

If the mother develops:

• high 25(OH)D (vitamin D level)

• → high calcium (hypercalcemia)

Then:

• fetal calcium levels also rise

• fetal parathyroid system becomes suppressed

So the fetus is essentially “buffered” by maternal blood chemistry.

---

🧬 2. What fetal vitamin D toxicity actually causes

Most documented effects fall into three categories:

---

🟡 A. Suppressed fetal parathyroid function (most consistent finding)

Because calcium is high in utero:

• fetal parathyroid glands reduce activity

• fetal PTH becomes suppressed

After birth this can lead to:

• neonatal hypocalcemia

• muscle twitching / tetany

• seizures (rare but reported)

👉 This is often rebound physiology, not direct toxicity damage.

---

🔴 B. Fetal/neonatal hypercalcemia (in severe maternal overdose)

If maternal calcium is extremely high:

Possible fetal effects:

• hypercalcemia at birth

• lethargy

• poor feeding

• dehydration

• vomiting

• cardiac rhythm instability (rare)

---

🟠 C. Developmental and structural effects (less common, but reported in severe cases)

In very high or prolonged exposure:

• nephrocalcinosis (kidney calcium deposition)

• impaired kidney concentrating ability

• growth restriction (in severe maternal illness)

• possible vascular calcification (rare, mostly animal data or extreme cases)

---

📊 3. What dose levels are associated with fetal harm?

There is no single threshold, but reported risk tends to appear when:

Maternal exposure:

• chronic intake > 10,000–40,000 IU/day

• or massive bolus dosing (hundreds of thousands IU repeatedly)

• or accidental overdose (pharmaceutical error cases)

Maternal blood findings:

• 25(OH)D often >150–300 ng/mL

• elevated serum calcium

👉 Important nuance:
Many pregnancies with moderately high vitamin D levels do NOT show fetal harm, which is why toxicity is considered rare and dose-dependent.

---

🧪 4. What human case reports actually show

📌 Documented patterns in published cases:

Case types:

• accidental maternal overdose (supplements or injections)

• therapeutic “stoss” dosing in pregnancy (historical)

• fortified food excess (rare)

Outcomes:

• most infants survive

• common findings:

  • transient neonatal hypocalcemia

  • temporary feeding issues

• severe outcomes:

  • rare seizures from calcium imbalance

  • rare NICU admissions

  • extremely rare structural effects

📚 Reviews of vitamin D toxicity in pregnancy conclude:

• fetal death is not a typical outcome

• morbidity is usually metabolic and reversible once corrected

---

🧬 5. Why the fetus is somewhat protected

The placenta acts as a partial buffer:

Protective mechanisms:

• regulates calcium transfer

• limits extreme fetal exposure

• fetal kidneys are not directly exposed to maternal vitamin D spikes

So even when maternal levels are high:

fetal damage is usually biochemical, not catastrophic structural injury

---

⚖️ 6. Comparison: pregnancy vs adult toxicity

FeatureAdultsFetusMain issuehypercalcemiaaltered calcium regulationOrgan damagekidney, heartmostly biochemical disruptionDeath riskrare but possibleextremely rareLong-term effectskidney calcificationusually none if corrected

---

🧠 7. Important clinical paradox

Interestingly, modern obstetrics shows:

• low vitamin D in pregnancy is common

• and associated with:

  • low birth weight

  • preeclampsia risk (association, not always causal)

So clinicians aim for:

• sufficient, not high vitamin D levels

Typical recommended intake:

• ~600–2000 IU/day in pregnancy (varies by guideline)

---

💀 8. Has fetal death from vitamin D toxicity been clearly proven?

• Direct fetal death solely from vitamin D toxicity is extremely rare in the medical literature

• When fetal loss occurs in reported cases, it is usually:

  • combined with severe maternal hypercalcemia

  • or multiple metabolic complications

So the pattern is:

vitamin D toxicity → maternal illness → fetal metabolic disturbance
not
vitamin D toxicity → direct fetal organ destruction

---

🧾 Bottom line

Vitamin D toxicity in the fetus is:

• 🟡 primarily a calcium-regulation disorder, not a direct poison

• 🔴 usually secondary to maternal hypercalcemia

• 🟢 most cases are reversible after birth with treatment

• 💀 fetal death is very rare and typically indirect

ANALYSIS

When we lay these unfortunate victims out in front of us it is exceptionally clear that of the people that have been proved to have been directly killed and maimed by Rat Poison, the vast majority of them are babies, young children and the elderly. The most vulnerable in society, the smallest and the most fragile. The episode that they admit to with the most affect was hundreds to thousands of infant deaths across Europe because they were heavily fortifying dairy and infant milk powders with rat Poison, ironically to combat rickets ( Lead poisoning ). There is a huge amount of Peer Reviewed and Published science out there on the dangers of fortification and how in this instance it lead to thousands of innocents being murdered. The irony that AI describes this incident as an “outbreak” like it was some sort of Contagion of the Brain that lead to people putting Rat Poison in baby formula, which is doubly ironic as this is probably not far from the truth.

So they have learned this lesson right……. RIGHT!

Conclusions: Milk and infant-formula preparations rarely contain the amount of vitamin D stated on the label and may be either underfortified or overfortified. Since both underfortification and overfortification are hazardous, better monitoring of the fortification process is needed.

Yes unfortunately it is correct, every major supermarket brand of baby formula powdered milk fortifies with rat poison as does most kids yoghurt and dairy products.

FAUCI SAYS YOU SHOULD TAKE THE RAT POISON.

Dr. Anthony Fauci has publicly endorsed taking vitamin D supplements, particularly for individuals who are deficient.

• Endorsement Context: In a September 2020 Instagram Live interview, Fauci stated, “If you are deficient in vitamin D, that does have an impact on your susceptibility to infection. I would not mind recommending, and I do it myself, taking vitamin D supplements.”

• Dosage: Reports indicate that Dr. Fauci personally takes 6,000 IU of vitamin D every day.

• Additional Vitamins: He also mentioned that taking vitamin C (specifically a gram or two) is fine due to its antioxidant properties, but he advised against other “so-called immune-boosting” botanical supplements, calling them “fuggedaboutit.”

• Scientific Nuance: While Fauci highlighted the link between vitamin D deficiency and increased susceptibility to infection, experts note that while observational studies show a correlation between low vitamin D levels and severe outcomes, there is no randomized clinical trial proving that vitamin D therapy prevents or treats COVID-19 specifically.

Dr. Fauci Endorses Vitamin D

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Washington, September 15, 2020 | Timothy Svoboda (202-225-2476)

Tags: Health Care

Today, Congressman Glenn Grothman (WI-06) released the following statement after news that Dr. Anthony Fauci, Director of the National Institute of Allergy and Infectious Diseases, has made a public assertion that vitamins D and C can “lessen your susceptibility to infection” and recommended that people take vitamin D supplements as he does.

In April, Grothman sent a letter to Robert Redfield, Director of the Centers for Disease Control and Prevention (CDC), and Stephen Hahn, Commissioner of the Food and Drug Administration (FDA), asking if their agencies had evaluated the effects of vitamin D supplements in relationship with COVID-19.

In May, Grothman issued a press release addressing medical research studies out of Northwestern University and Trinity College in Dublin, Ireland asserting that vitamin D deficiency may play a role in increasing the severity of symptoms and overall mortality rate in COVID-19 patients. Since then, Grothman has encouraged people to take vitamin deficiencies seriously and has championed vitamin D supplements for those who need them.

In June, the assertion of Grothman’s press release was rated “True” by Politifact.

Grothman has repeatedly called on the CDC, even from the House floor, to further investigate the relationship between vitamin D and COVID-19, as well as other treatments, and explain the benefits of having a healthy immune system.

“It is imperative that we find treatment options for people suffering from COVID-19,” said Grothman. “Unfortunately, most media outlets have largely ignored possible treatments for COVID-19. The obfuscation of this research has been irresponsible and has no doubt cost lives.

“I am glad that Dr. Fauci has finally spoken up about the negative effects of having a vitamin D deficiency, something that I have been talking about since April, and the importance of keeping a healthy immune system to combat infections. As the country’s top epidemiologist, Dr. Fauci should use his platform to continue to promote the ways to obtain a healthy immune system and other things we can do every day to lessen the ill-effects of the novel coronavirus.

“I hope that I can count on my local media outlets to publicize this news that could save lives in Wisconsin and move us closer to a return to normalcy.”

ANALYSIS

So there you have it, from the Beagle Butcher himself; Dr Anthony Fauci, the Pol Pot of the NIH, his two favorite weapons of execution are Vaccines and Vitamin D. So there is no excuse if you are dyed in the wool MAGA/MAHA type that has seen through the Vaccine scam, to get out of this one you are going to have to do some Olympic Level gymnastics.

ANY POSITIVES?

No. There are no positives to knowingly ingesting Rat Poison. There are no positives to Micro dosing Rat Poison. There are no positives to loading up at the start of the Winter Months with Rat Poison. Once again, we shouldn’t really even have to look any further than the repeated classification of a substance being a Highly Toxic Poison and viscerally knowing it is incongruent with health.

In the interest of a fair trial we will look at the published literature and clinical outcomes of people who take rat poison vs people whom don’t:

For people who already get enough vitamin D, the list of proven benefits from taking extra vitamin D supplements is surprisingly short.

The strongest evidence is for:

• Preventing and treating vitamin D deficiency

• Preventing rickets in children

• Preventing osteomalacia (soft bones) in adults

• Helping maintain bone health when deficiency is corrected

Beyond that, the evidence is mixed or negative for many popular claims.

Benefits with reasonably good evidence

Bone health in deficient people

If someone is vitamin D deficient, supplements can:

• Improve calcium absorption.

• Reduce bone softening.

• Help maintain bone mineralization.

In older adults who are deficient, vitamin D (often combined with calcium) may modestly reduce fracture risk.

Muscle function in deficient people

Low vitamin D can cause muscle weakness. Correcting deficiency can improve:

• Muscle strength.

• Balance.

• Risk of falls in some older adults.

Benefits that remain uncertain or small

Researchers have investigated whether vitamin D supplements help with:

• Heart disease

• Stroke

• Cancer prevention

• Depression

• Cognitive decline

• Autoimmune diseases

• Type 2 diabetes prevention

• General immune enhancement

• Longevity

Large randomized trials generally have not found major benefits for the average person taking vitamin D supplements if they are not deficient.

For example, the large VITAL Trial found that vitamin D supplementation did not significantly reduce overall cancer incidence or major cardiovascular events in the general population.

Possible exceptions

Some evidence suggests vitamin D supplementation may have modest benefits in specific groups, such as:

• People with confirmed deficiency.

• Frail older adults.

• Individuals with osteoporosis.

• Certain people at risk of autoimmune disease (some studies have shown a small reduction in the incidence of autoimmune disorders, but the effect is not large enough to recommend high-dose supplementation for everyone).

Q: Is there evidence of people getting osteoporosis from vit d overdose?

Yes, there is some evidence that excessively high vitamin D levels or high-dose vitamin D supplementation can negatively affect bone density, but documented cases of osteoporosis caused solely by vitamin D overdose are relatively uncommon.

What the evidence shows:

• Several randomized trials found that very high doses of vitamin D (especially large intermittent doses or chronically high supplementation) were associated with decreases in bone mineral density (BMD) compared with more moderate dosing.

• A notable 3-year trial published in JAMA in 2019 compared daily vitamin D doses of 400 IU, 4,000 IU, and 10,000 IU in healthy adults. The higher-dose groups experienced greater reductions in BMD at certain skeletal sites than the 400 IU group.

• Case reports of severe vitamin D toxicity (typically involving extremely high blood vitamin D levels and hypercalcemia) have described bone pain and skeletal abnormalities, but these cases often involve multiple factors and do not always demonstrate classic osteoporosis as the primary diagnosis.

The proposed mechanisms include:

1. Excess vitamin D causing hypercalcemia.

2. Suppression of parathyroid hormone (PTH) below normal levels.

3. Altered bone remodeling that may favor bone loss under some circumstances.

That said:

• The strongest established harms of vitamin D toxicity are hypercalcemia, kidney stones, kidney damage, and soft-tissue calcification.

ANALYSIS

So here we have it, even the published literature thinks you are an idiot for taking the Rat Poison. It claims its only benefits are to top up the levels of Rat Poison, to prevent a disease caused by Lead in the drinking water and to prevent Osteoporosis, by taking Rat Poison, which…… causes Osteoporosis. It makes zero difference to any broadscale serious disease outcomes like cancer, heart disease, mental state (Depression) or indeed Life Span. So the only people that recommend taking rat poison, quite coincidentally are the people shilling it on Social Media.

CONCLUSION

If you have managed to read to here and are still gonna get up tomorrow and pop another Rat Pill all I can do it stand back and applaud at your dedication to poison yourself, there really is no help and nothing more I can say to convince you otherwise. The fundamentals are that there is no such thing as a chemical which is the sun’s effects on the skin, it is absolutely absurd to even entertain this notion, it is merely a lab value, a similarity of the vague properties of a sample. If you take a concoction of powdered chemicals and it makes the lights on a machine flash in the same way as when you stick the machine in someone’s nose or in a mushroom, that means only that the things you are testing have the same rough physical properties as measured by the machine certainly NOT that they are the same thing.
It's like developing a machine that measures how high something bounces, testing a lemon and a mobile phone and concluding because they repeatedly bounce the same height when dropped they must be the same thing.

If this has resonated with you and I have managed to make you see the wood for the trees specifically on this topic and have quit taking this shit then please do reach out and tell me, it brings me great joy. Thus far I count 14 people on Social Media that explicitly from my shouting and ranting and raving have quit the rodent rot. Think of it like this, even if you are unsure of the harms there are literally no positives to this and by quitting you will be, at the very least, saving your money and a small portion of your day having to remember to micro dose rat poison.

Please Subscribe and Follow Tim Truth here:

https://substack.com/@timtruth

I want to say a big thank you and shout out to Virology Control Studies Project Subscriber Matt Reese for sending me some of the information on this.

The previous article on the Ebola Hoax was very sizeable, being a 71 page book on its own, so for the sake of fatigue I thought I would split this up into a second part where we really flesh out the hypothesis made in the first. From the ground up, I can be very sure that any symptoms/deaths from hemorrhagic type fever, if they are confirmed to actually exist were not caused by a “contagious virus”. We have covered this part of the hoax in plenty of detail, with mountains of theoretical and experimental evidence all back up with Peer Reviewed and Published literature. But I wanted to take this one a little further by expanding upon the hypothesis I presented that if these violently quick hemorrhagic deaths were occurring they fitted an identical symptomology and speed of onset of disease more concurrent with Arsenic poisoning as well as potentially a few other Heavy Metals such as Lead, Cadmium, Cobalt and Mercury adding to the tapestry of disease (as well as what I believe to be a specificity problem within their testing too).

Another marginal reason for doing this, is that the wave of State paid actors employed to furiously shoot flak into the air as a smokescreen, simultaneously settled on a seemingly very obvious lie that Ebola patients were being tested for Arsenic poisoning.

Q: “Are Ebola cases in DR Congo being tested for Arsenic poisoning, short answer?”

Short answer: No, not as a standard or reported practice.

Ebola cases in the Democratic Republic of the Congo are investigated and tested using established public health protocols (viral PCR testing, epidemiological tracing, and sometimes testing for other common infectious causes). There is no credible evidence or official reporting that suspected Ebola cases are being routinely tested for arsenic poisoning.

If there were a poisoning concern, it would be handled separately on a case-by-case toxicology basis, not as part of Ebola diagnostics.

Of course this should be fairly self explanatory that once the medical authorities have been instructed that they are running the hoax simulation in their back yard, their immediate triage in a medical setting is to henceforth suspect anyone that complains of any ailment from sniffling noses to broken bones to bleeding out their eyes as being Ebola and so they are instantly going to reject any other cause for disease even if they share, or should I say especially if they share identical symptomology. Because here is the thing, Arsenic and Heavy Metal poisoning are very well known in Africa, especially in the mining communities, open cast mining releases all of these natural poisons into the air, soil and water as well as other poisons such as cyanide being used in the extraction process.

They are so acutely aware of this happening when the blinkers of infectious diseases are removed, that they have done country wide studies of Metalloid (Arsenic) and Heavy Metal poising in the environment as well as in people that both work and live in the mining areas. We are again going to focus in on one country to simplify the data and keep the amount of literature down, so we will stay in the area of DR Congo.

I’m listening to Heavy Metal

Abstract

In many countries, soil and water integrity is threatened by excessive accumulation of metal(loid) trace elements (MTEs), posing serious risks to human health. Despite increasing evidence of these impacts, contamination remains underrecognized in many regions due to limited data availability. This review compiles evidence on metal(loid) pollution across DRC, focusing on toxic elements such as arsenic (As), cadmium (Cd), cobalt (Co), copper (Cu), lead (Pb), mercury (Hg) and zinc (Zn), and their associated ecological impacts. Data were compiled from site-level studies and were analyzed using quantitative synthesis approaches to estimate pooled mean concentrations and identify regional differences. The findings indicate that Cu, Pb, and Cd occur at consistently high concentrations, frequently exceeding international reference values for agricultural soils. Spatial analyses reveal substantial heterogeneity, primarily driven by geological variability and inconsistencies in sampling methodologies. The Katanga Copperbelt provinces (Haut-Katanga and Lualaba) emerge as priority hotspots due to intensive mining activity, followed by Kinshasa, which also shows significant contamination levels. Nonetheless, a critical data gap remains in the eastern and northern mining zones, where soil quality and related agricultural risks are insufficiently characterized. These limitations, together with uneven spatial coverage and limited reporting of variance measures, restricts the robustness of comprehensive risk assessments. The review therefore underscores the urgent need for standardized monitoring frameworks, transparent data reporting, and region-specific policy interventions to enable evidence-based environmental management in mining-affected areas.

Mining activities are among the principal drivers of MTE contamination, as ore extraction, waste rock disposal, tailings storage, and acid mine drainage (AMD) mobilize toxic elements such as, Cd, Ni, Pb, Cu, Zn, and Hg, disrupting natural pedogeochemical balances (Dold, 2017; Fashola et al., 2016). Additional inputs arise from agricultural practices (e.g., fertilizers, sewage sludge, pesticides) and industrial and municipal sources, including fossil fuel combustion and inadequate waste management (Angon et al., 2024; Mohamed et al., 2025). While some metals (e.g., Co, Cu, Zn, Ni) are essential micronutrients, they become toxic at elevated concentrations, whereas Hg, Cd, As, and Pb are harmful even at trace levels (Jaishankar et al., 2014; Rai et al., 2019). These contaminants can bioaccumulate and biomagnify through food webs, posing serious ecological and human health risks (Bakshi et al., 2018; Angon et al., 2024; Sabir et al., 2022). Numerous studies conducted in agricultural, mining, and industrial landscapes have documented the widespread occurrence of soil contamination and its effects on higher trophic levels (Hou et al., 2025; Sabir et al., 2022; Haghighizadeh et al., 2024; Achouri et al., 2017). Worldwide, soil contamination affects over 20 million hectares and threatens more than one billion people via food chain exposure, with 14–17% of agricultural soils contaminated, particularly by Cd, Cu, and Co (Hou et al., 2025; Rodríguez-Eugenio et al., 2018; United Nations, 2015; Sanad et al., 2025). Consequently, sustainable remediation strategies, such as phytoremediation, are increasingly advocated to restore contaminated soils (Hou et al., 2020; Mohamed et al., 2025; Zhang et al., 2020; Reeves et al., 2017).

Fig. 5. Ecological risk indexes and classifications for toxic MTEs from mining sites.

Transfer from soils to plants and bioaccumulation of MTEs reported in RDC

Numerous studies in the Democratic Republic of Congo have documented the transfer of metallic trace elements (MTEs) from contaminated soils to food crops in both urban environments such as Kinshasa and mining regions including Lubumbashi and surrounding areas, raising serious concerns for food safety and public health (Kanyinda et al., 2025; Nsandji et al., 2023; Kalala et al., 2015; Mpundu et al., 2013; Langunu et al., 2023; Mputu et al., 2024; Mpundu et al., 2017; Kalonda et al., 2015; Katebe et al., 2018; Ngweme et al., 2021). Elevated concentrations of toxic metals, particularly Pb, Cd, Cu, Co, Zn, Cr, and As, have been reported in vegetables, fruits, and other food products, often exceeding FAO/WHO permissible limits and resulting in health risk indices above safety thresholds (Mputu et al., 2024; Ngweme et al., 2021). These contaminations originate from diverse sources including polluted soils, irrigation water, mining activities, traffic emissions, and agrochemical inputs (Nsandji et al., 2023; Kalala et al., 2015; Langunu et al., 2023; Katebe et al., 2018). Although several plant species exhibit metal tolerance or hyperaccumulation and show potential for phytoremediation (Reeves et al., 2017; Kanyinda et al., 2025), many edible crops such as amaranth, cassava, lettuce, spinach, and guava accumulate hazardous metal levels, highlighting the urgent need for improved soil management, remediation strategies, and environmental monitoring to protect food safety and public health (Kalala et al., 2015; Mpundu et al., 2013; Langunu et al., 2023; Katebe et al., 2018; Ngweme et al., 2021).

For consumers, chronic ingestion of contaminated crops elevates risks of cardiovascular, neurological, renal, reproductive, and carcinogenic effects linked to Cd, Pb, and As exposure (Angon et al., 2024; Rai et al., 2019; Alengebawy et al., 2021; Jomova et al., 2025). Without interventions such as pH adjustment, organic stabilization, phytoremediation, and land-use zoning to restrict cultivation in polluted areas, both agricultural sustainability and public health remain under serious threat. In this context, integrating Land Evaluation and Site Assessment (LESA) with Geographic Information Systems (GIS) can support effective land-use zoning by identifying soils suitable, marginal, or unsuitable for food production under contamination constraints (Akbari et al., 2022), an approach particularly relevant for managing the DRC’s widespread soil contamination crisis.

Therefore, the pervasive contamination of agricultural soils in the DRC represents both an ecological and public health crisis. To mitigate these risks, integrated management strategies, combining soil pH regulation, organic amendments, controlled crop selection, and regular environmental surveillance, should be prioritized. Establishing national frameworks for soil and food monitoring would not only safeguard public health but also enhance the long-term sustainability of the country’s agricultural systems.

Abstract

Introduction

Arsenic and cadmium exposures cause significant adverse effects. This study aims to determine the urinary arsenic and cadmium concentrations in men in order to analyze their profile in relation to sperm count test values.

Methods

We conducted an exposed-non-exposed analytical study of men exposed to arsenic and cadmium in a mining area in Upper Katanga, DRC and of non-exposed men living far from any mining area.

Results

Study results show that 48% of exposed subjects had semen pH below the threshold value of 7.2 versus 16% of non-exposed subjects. The risk of a lowering of pH below the standards was more than 4 times higher (OR=4.85[1.9-12.39]) among exposed men. The difference between the averages of the total number of spermatozoa was statistically significant to the advantage of non-exposed subjects. Abnormal number of spermatozoa was much higher in exposed subjects. It was recorded a more rapid spermatozoa mobility degradation in exposed subjects. In addition, 44% of exposed men had urinary arsenic concentration > 20 µg/L versus 8% of non-exposed subjects, the risk of excessive arsenic accumulation was nine times higher in exposed men than in non-exposed men (OR=9.04 [2.82-28.96]). Sixty percent of exposed men had urinary cadmium concentration ≥0.5µg/ml versus 38% of non-exposed subjects, with an Odd Ratio of 2.45 [1.1-5.47], reflecting a risk of excessive cadmium accumulation in exposed men. On the other hand, it was recorded that, among exposed men, high urinary arsenic and cadmium concentrations resulted in a proportional degradation of sperm count test values.

Conclusion

This study shows, on one hand, high urinary arsenic and cadmium concentrations and, on the other hand, more rapid and more severe alterations of sperm count test values in men living in mining area. This suggests a decline in male fertility which deserves to be further documented in future studies.

Abstract

Blood and/or urine levels of 27 heavy metals were determined by ICPMS in 41 patients with dilated cardiomyopathy (DCM) and 29 presumably healthy subjects from the Katanga Copperbelt (KC), in the Democratic Republic of Congo (DRC). After adjusting for age, gender, education level, and renal function, DCM probability was almost maximal for blood concentrations above 0.75 and 150 µg/dL for arsenic and copper, respectively. Urinary concentrations above 1 for chromium, 20 for copper, 600 for zinc, 30 for selenium, 2 for cadmium, 0.2 for antimony, 0.5 for thallium, and 0.05 for uranium, all in μg/g of creatinine, were also associated with increased DCM probability. Concurrent and multiple exposures to heavy metals, well beyond permissible levels, are associated with increased probability for DCM. Study findings warrant screening for metal toxicity in case of DCM and prompt public health measures to reduce exposures in the KC, DRC.

The blood arsenic concentration found in our subjects (0.39 µg/dL) far exceeds what has been reported in the general population of France (0.17 µg/dL) [47], Brazil (0.11 µg/dL) [50], Pakistan (0.21 µg/dL) [51], and China (0.23 µg/dL) [52]. Whether the association between DCM probability and higher blood levels of arsenic implies the later may contribute to the etiology of DCM is not known, but remains a possibility. Experimental studies in rodents, however, have demonstrated the toxic effect of arsenic on myocardial tissue through the inhibition of anti-oxidative stress defense enzymes [53,54]. Arsenic exposure has been associated with cardiopathologic effects, including ischemia, arrhythmia, and heart failure [55]. Possible mechanisms include increased oxidative stress, depletion of antioxidant status, DNA fragmentation, apoptosis by mitochondrial disruption, caspase activation, MAPK signaling and p53, functional changes in ion channels, and dyshomeostasis of trace elements [55]. It has also been revealed that arsenic can induce all kinds of diseases, including heart diseases through epigenetic modifications associated with hypermethylation of genes coding for ion channels and diverse proteins of oxidative stress and energy production [56,57].

Exposure to copper is associated with increased cardiovascular risk [58]. High copper concentrations had been associated with heart failure incidence [36,59,60,61,62,63] and bad outcomes such as re-hospitalizations and deaths over a one-year follow-up [64]. Copper is an important trace element in humans that is incorporated in several enzymes of vital functions. However, at high concentrations due to permanent exposure or in Wilson’s disease, for example, its free fraction increases in such manner that its infiltrates the myocardial tissue, induces cellular toxicity, and promotes harmful free radical formation [65,66,67,68]. Although the blood concentration of copper reported in this study was slightly higher than the upper limit of the reference value (143.7 vs. 140 µg/dL) [69], the urine concentration far exceeds levels reported as reference value [44,70] and in a very high-exposure environment [38]. This high urinary concentration, which, moreover, was strongly correlated with blood concentration (r = 0.73235, p < 0.000), was precisely such an indication of a strong recent exposure. It was also an indication of a permanent exposure to this metal, which, ironically, is the great wealth of the KC. Because of copper and cobalt, the KC has been invaded by many mining companies that are the main polluters in the region.

Abstract

Exposure to heavy metals can affect cell differentiation, neurocognitive development, and growth during early life, even in low doses. Little is known about heavy metal exposure and its relationship with nutrition outcomes in non-mining rural environments. We carried out a community-based cross-sectional study to describe the distribution of four heavy metal concentrations [arsenic (As), cadmium (Cd), lead (Pb), and mercury (Hg)] in the serum of a representative population of children aged 12 to 59 months old from the rural region of Popokabaka, Democratic Republic of Congo. The four metals were measured in 412 samples using inductively coupled plasma–mass spectrometry (ICP–MS). Limits of detection (LoD) and quantification (LoQ) were set. Percentiles were reported. Statistical and geospatial bivariate analyses were performed to identify relationships with other nutrition outcomes. Arsenic was quantified in 59.7%, while Cd, Hg, and Pb were quantified in less than 10%, all without toxicities. The arsenic level was negatively associated with the zinc level, while the Hg level was positively associated with the selenium level. This common detection of As in children of Popokabaka requires attention, and urgent drinking water exploration and intervention for the profit of the Popokabaka community should be considered.

Among the various HMs, arsenic (As), cadmium (Cd), lead (Pb), and mercury (Hg) are the most common and are considered harmful^9,10,11. Arsenic is widely distributed in natural waters, and groundwater is one of the primary routes of exposure to inorganic As¹⁵. Long-term exposure to inorganic As during infancy increases the risk of lower respiratory tract infection, gastrointestinal illnesses, and cancer^15,16. Lead, which has no physiological role in humans, is frequently found in household dust. More than 95% of the total Pb exposure ends up in the bones and teeth. Children are particularly vulnerable to lead because of its effects on growth and the developing nervous system¹⁷. Cadmium is mainly absorbed from the lungs, and tobacco smoke is one of the largest single sources of Cd exposure in humans¹⁸. It can accumulate in fatty tissues and human milk and be transferred through breast milk to children. Cadmium toxicity negatively affects reproduction, neurodevelopment, and hepatic, hematological, and immunological systems^10,18. Mercury is used in agriculture in fungicides or seed preservatives and pharmaceutical catalysts in organic syntheses. Higher levels of Hg are often found in seafood, and exposure to this element is also suspected to impair neurodevelopment in children¹² and cause dental, skin, pulmonary, and nephrotic damage¹⁹.

ANALYSIS

This is a small selection of what I could quickly find on Metalloid and Heavy Metal poisoning of people in the Democratic Republic of the Congo. This not only covers people whom work directly in the mines but indeed men, women and children in the general population. Probably the most damning evidence is when these extremely worrying levels of toxic elements are found in the urine and blood of Cardiomyopathy patients. They even go as far as to suggest causality, which to you and me shouldn’t be a surprise, but it is always good to have it confirmed by the establishments own sources. When you lay it all out on a table, that these elemental poisons are known to cause the exact palette of symptoms blamed on Ebola. They are highly prevalent in the food and water sources and found in people experiencing serious Cardio and Respiratory illness, we can see that it is an entirely plausible theory to suggest that, when and where you do have real death and disease that is being attributed to “Ebola”, it is actually far more likely it is metalloid/heavy metal poisoning instead (That and because viruses don’t exist).

But there is one slight issue with this theory, in the realms of the “negative” case for “Ebola” but the “Positive” case for areas of increased Metalloid/Heavy Metal contamination. I started this part 2 from a Ghanian report of Arsenic poisoning and its effects that Matt sent me (https://scitechjournals.com/articles/ecological-study-of-galamsey-activities-in-ghana-and-their-physiological-toxicity.pdf).

Please read it when you have the time as it is absolutely damning. Indeed this whole area of research is a literal gold mine of industrial harms perpetrated either directly or indirectly by the globalist operators in Africa. But the problem for me, personally with this particular article is that it doesn’t really match up with my theory in that Ghana has never had a claimed “ebola” outbreak. Now there is some wiggle room here in the fact that Ghana has seen a claimed “Marburg” outbreak in 2022 and Marburg is the identical hoax where the “Viruses” particles are identical, the symptoms are identical so we could “get away” with just continuing on oblivious. But I want to be a bit circumspect here and finish this hoax off with the final layer of the puzzle.

MONOCLONAL ANTI(Human)Bodies

Ebola-specific drugs (used once confirmed or strongly suspected in outbreak settings)

If Ebola is confirmed (or in some outbreak protocols when suspicion is very high), monoclonal antibody therapies are used:

• Inmazeb (atoltivimab/maftivimab/odesivimab)
  → A 3-antibody cocktail targeting the Ebola virus

• Ebanga (ansuvimab-zykl)
  → Single monoclonal antibody treatment

These are the main WHO-recommended treatments for Zaire ebolavirus disease.

4) Experimental/older treatments (less used now)

• ZMapp (older monoclonal antibody cocktail, largely replaced)

• Remdesivir (studied but not a standard Ebola therapy)

• Other antivirals have generally not shown strong benefit compared to antibody therapies

More than 11 years ago, six young men were left writhing in agony with their organs failing after agreeing to take part in a routine drugs trial in London.

The group were part of a team of eight who were each offered £2,000 for a three-day trial that would potentially help revolutionize cancer treatment.

The men, who had been selected to be aged between 19 and 34, had been told the worst symptoms would be a headache, nausea and, in rare cases, hives.

However, soon after receiving the drug, six were left vomiting and screaming in agony – with one having to have body parts amputated.

Now, a BBC documentary has revisited the dramatic events that left the human guinea pigs fighting for their lives in a private unit at Northwick Park Hospital in north-west London run by Parexel, a US company.

Throughout the Phase 1 trial, a number of the men suffered from swelling – with their heads inflating like balloons.

One of the victim’s family said he looked like ‘the Elephant Man’, which led to the TGN1412 legal proceedings’ nickname, ‘the Elephant Man drug trial’ – although the swelling was likely caused by the treatment for the reaction, which included administering large quantities of fluid and steroids.

The drug, which had been successfully tried out on monkeys, had never been tested on humans, making it a ‘first in man’ trial. It was later found that while macaques and humans are incredibly close from a DNA perspective, the cells that the drug targeted differ slightly between the species.

The incident quickly transformed into one of Britain’s most infamous medical emergencies.

Fortunately, doctors were able to save the lives of all of the young men – and a few weeks later, five of the men were able to leave hospital, however, the drug had attacked their tissue and left them with wasted muscles. One, David Oakley, said it had left him feeling like ‘an 80-year-old’.

Ryan Wilson, the sixth and youngest participant aged 21, spent the next four months being treated for heart, liver and kidney failure.

Sections of his feet were amputated and his fingertips also fell off.

It was later revealed that two of the participants were given a placebo and did not suffer the effects.

In the documentary, The Drugs Trial, which aired last night, doctors speak about the struggles they faced while attempting to bring the ‘mysterious’ situation under control.

Investigators also reveal that they were sent in and tasked with finding out what went wrong at the trial on March 13, 2006. They found that Parexel could not have known the ‘unpredictable’ biological reaction would occur, although the risk of cytokine storm – the effect that caused the reaction – was mentioned in Parexel’s own literature with the recommendation to treat with steroids.

Participant Raste Khan, who was 23 at the time and had been given a placebo, said: ‘Medical trials were like a get-rich-quick scheme. It was a no brainer.

‘It was all manic, everything was happening all at once. They were vomiting, they were screaming in pain, people were fainting, they couldn’t control their bowels… it was like a horror movie.’

In the documentary, it was revealed that families were told to say goodbye to their loved ones as they may be about to die.

Since the disaster, all six men have received undisclosed pay-outs from Parexel in private out-of-court settlements.

A report published by The Medicines & Healthcare Products Regulatory Agency in April 2006 had 22 recommendations to improve the safety of future Phase 1 trials, including that individuals given a ‘first in man’ drug in a trial should not receive the drug at the same time on the same day and high risk trials should take place in a hospital with access to intensive care.

The new recommendations have now been adopted across the whole of Europe.

Trial lead Dr Bradford, who had worked on 300 clinical trials before this one, said he has never worked on a trial of this nature again. ‘It was the last ‘first in man’ trial I did,’ he says. ‘I’d like to look them in the eye and say sorry.’

Trial participant David Oakley was found to have pre-cancer signifiers in his blood after the trial that may or may not have pre-dated the trial.

He married his fiancee months later but feared he could be left infertile. However, 10 years on, he has three children and no sign of cancer or other lasting effects. He now says: ‘I was unlucky. But it didn’t kill me, and that’s pretty good. Having my first child with the chance that we might not have been able to have kids, made it even more special.

‘Medical trials are very important to advance our knowledge of medicine. It’s only when you have a relative who’s sick and depends on drugs that have been through human trial that you understand how important it is that they are carried out.’

In 2013, TGN1412 was tested again in human trials in Russia under the new name, TABO8. The amount was 0.1% of the amount injected into the participants of the Parexel trial and it was infused 40 times more slowly.

The drug could still be used as a treatment for autoimmune disease in the future.

Q: Inmazeb (atoltivimab/maftivimab/odesivimab) have these got any bad known side effects?

Yes — Inmazeb (atoltivimab/maftivimab/odesivimab) does have known side effects, but most are tied more to infusion reactions and the severity of Ebola illness itself rather than “toxic drug effects” in the way some chemotherapy drugs behave.

Here’s the clean breakdown.

---

Most common side effects

In clinical studies, the most frequently reported effects (seen in ≥20% of patients) include:

• Fever (pyrexia)

• Chills / shivering

• Fast heart rate (tachycardia)

• Fast breathing (tachypnea)

• Vomiting

These often overlap with Ebola symptoms themselves, which makes interpretation tricky.

---

Infusion-related reactions (most clinically important risk)

Because it’s an IV monoclonal antibody, the main concern is infusion or hypersensitivity reactions, which can include:

• Sudden fever or chills during infusion

• Low blood pressure

• Shortness of breath

• Rash or itching

• Dizziness or fainting

• Rarely, severe or life-threatening allergic-type reactions

These are why patients are:

• monitored closely during infusion

• treated in high-acuity hospital settings

ANALYSIS

One of the treatments for Ebola is using that well known kidney melting drug Remdesivir, so we don’t really need to waste much time explaining the problem here. I really want to focus on the use of Monoclonal Antibodies as the “got to “ for confirmed Ebola patients. Looking at the “Elephant Men” drugs trial where they gave IV Monoclonal Antibodies that was supposed to “cure” Leukemia, i.e a blood cancer, these men in the trial very quickly started extreme bouts of vomiting, diarrhea, migraine, loss of consciousness and coma. This as they note was brought about by what they call a “Cytokine Storm” where the body floods itself with what the medical establishment believe is “immune cells” and eventually causes multiple organ failure .

The most stunning part to this story, and I really would recommend watching the BBC documentary on it if you want another example of Big Pharma and the Medical Industry’s ongoing genocide, is that this drug that almost killed the 6 men given it, was released back onto the market! They changed the made up acronym from TGN1412 to TAB08 and then used it at 0.1% concentration. Jaw-dropping really, but when you realize that the entire allopathic death cult is predicated on giving people little bits of poison until they either get better on their own despite the poison for the disease to come again soon or die from the poison.

Finally when we looked at the specific Monoclonal Antibodies used for Ebola, funnily enough they outright admit that the known side effects exactly match Ebola symptoms which makes “interpretation tricky”. Well yes indeed it would make it tricky if the drug you were giving people were causing the symptoms you are giving the drug for, that’s kind of where we are on this House-of-Horrors-Roundabout-Groundhog-Day-Purgatory we find ourselves burdened with when it comes to navigating the “health”care industries.

“EBOLA” Patient Dr. Ian Crozier

I want to leave you with the story from the mouth of a claimed “Ebola” survivor, Dr . Ian Crozier. Because this is going to be put into Ebook format that doesn’t have video embedded into it, I would urge you watch the full video here.

There are a couple of absolute zingers I want to point out to you from this testimony. Ian has very basic low grade symptoms of a fever, muscle aches and a headache, which could be interpreted as basically any disease in the entire smorgasbord of relabeling detoxing. The “emergency” situation was not brought about by symptoms at all, but would you know it was entirely started by a Positive PCR test (huge eye roll). Ian recounts this next phase in quite a bit of detail (because it is the last thing he remembers) that he was, in his own words, “clearheaded” and “fairly well”. However the moment he crossed the drawbridge into the Medical Dungeon was the moment it all seemed to go pear shaped (color me shocked I tell you). He developed severe gastrointestinal symptoms, vomiting and diarrhea, then a Cytokine Storm bringing about multiple organ failure.

Now, I mean called me cynical, but this man in his own words was “fairly well” and then displayed the identical symptoms of what can only be described as Monoclonal Antibody poisoning directly mirroring the poisoning of the “Elephant Men”. I hope you can see very clearly what is occurring here, well people with generic symptoms are being systematically maimed and killed with proven lethal chemical cocktails based on a PCR test and politics.

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This article is available as a downloadable EBook along with the rest of my work on ShadowBanned Library

This fake “virus” is an absolute firm favorite of the wibbles on the internet who have an enduring infatuation with the Germ Theory. If you don’t know the type by now, I will share my near daily experience of dealing with these bottom feeders for now more than half a decade (genuinely feels like only yesterday right? ).

The story goes a little like this: I put out a piece of peer reviewed science that completely contradicts the narrative of some part of the Germ Theory or Genetics. Germ Theory Enthusiast arrives on the scene at an inhumanely quick pace and either has a completely unprovable anecdote fitting the exact method that contradicts the science I presented OR jumps straight into death threat mode: “If germs aren’t real then why don’t you inject yourself with Ebola? Hahaha”. The Ebola part to that is where these agent provocateurs think they have been really smart, as people might agree to a bought of da “Flu” but nobody in their right mind would “risk” it with bleeding out the eyes with “Ebola”. It serves as the biggest scariest monster under the bed, the Top Trump on the list of Boogiemen to play when making their online threats.

Just to make this public for people whom have encountered this online, I will point out that this is a threat and is considered a serious crime in the US and EU. A person making a bet or encouraging people to inject themselves with what they believe will kill or seriously injure someone is a direct intent to encourage suicide or serious harm and carries a prison sentence of up to 10 years. So these trolls that think they are being funny or proving a point are actually committing a crime and will be reported for doing as such.

I don’t really need to explain myself, but I will anyway, the reasons why I won’t be partaking in any injections, of anything:

A. To prove or disprove Contagion you have to use a method that is a claimed natural pathway, there is no natural pathway that comes from a hypodermic needle being thrust intravenously.

B. These Contagion studies have been done for 200 years, experimenting with all of these claimed “viruses” and have never managed to make anyone sick with the claimed disease caused, all documented for anyone to read.

C. Injecting anything, even saline comes with its own set of hazards, and can actually induce cold and flu like symptoms as seen in many control groups in contagion studies and outlined experimentally below. The body is not used to having anything directly entering the bloodstream before it has been digested, broken down and filtered first. “Chemically” it is going from 0-100 almost instantaneously which is why it is the ultimate hit for drug abusers and usually ends fairly quickly once this stage of abuse is reached (The ultimate way to throw your body out of balance).

D. In the claimed “viral” isolates are plenty of noxious chemicals especially in the antibiotics area. Listed below are all of the ingredients in the cell culture, only 5/23 ingredients not being considered toxic to humans. Once again, injecting any of these things comes with potential harms.

• Water

• Sodium chloride (NaCl) — generally safe at culture concentrations

• Potassium chloride (KCl) — harmful in high doses

• Calcium chloride (CaCl₂) — irritant in concentrated form

• Magnesium sulfate (MgSO₄) — low toxicity

• Sodium bicarbonate (NaHCO₃) — low toxicity

• Sodium phosphate (NaH₂PO₄) — low toxicity

• Glucose (D-glucose) — safe nutrient

• Sodium pyruvate — low toxicity

• HEPES buffer — low toxicity, lab irritant possible

• Phenol red — possible endocrine activity in some studies; irritant in concentrated form

• L-glutamine — low toxicity

• Essential amino acids (lysine, leucine, valine, tryptophan, etc.) — generally safe nutrients

• Non-essential amino acids (serine, glycine, alanine, etc.) — generally safe

• Vitamins (thiamine, riboflavin, folic acid, niacinamide, choline, inositol, etc.) — generally safe at culture concentrations

• Trace iron/nitrates — irritant/toxic at high concentrations

• Fetal bovine serum (FBS) — biological material; contamination/allergy/infectious-agent risk possible

• Penicillin — allergy risk in humans

• Streptomycin — ototoxic/nephrotoxic at systemic doses

• Amphotericin B — significantly toxic systemically

• Gentamicin — nephrotoxic/ototoxic

• Trypsin-EDTA (used during passaging) — corrosive/irritant to tissue

• Antibiotic-antimycotic mixes — variable toxicity depending on components

E. Just viscerally I do not inject things into my body. Even if nobody had ever come to any harm from injection and you could somehow prove it, injecting stuff into ones body is for junkies, tramps, degenerates and people who believe in “Viruses” (Same thing alert). In the animal kingdom, injection through breaking the flesh is ONLY done by things looking to do harm, or seriously deter such as snakes, spiders, scorpions etc etc. They do this, as above, because their venom has the most possible chance of doing damage which is why such tiny creatures with such small amounts of poison can be so injurious to animals much bigger.

They distilled water, i.e made it completely sterile and with its injection produced fever and cold like symptoms in rabbits. But then somehow concluded that despite being distilled, still contained a pathogenic agent. Germ Theory Idiocy strikes once again.

EBOLA IS A HOAX

Sorry for that little detour, I think some of those things had to be put in an article at some point and was feeling a little zesty. Back to the millstone:

The first thing I want to point out is quite esoteric, it is not something that I really want to descend too far down the road with “evidence” based reasoning as largely it meanders down the wormhole of GeNEtICs and PrOtEOmIcs which in totality is a made up fairytale, so it would be extremely tedious. But one thing that is very apparent to me is that the claim is there are 1.67m distinct species of “virus” (Lol) and they range from being claimed to be endogenous to humans (I.e present at all times in our “genome”) right the way through to piss out your kidney and bleed out your ears in under 24 hrs with Ebola and everything in between.

The length of the claimed Viral Genomes which is all a “virus” is, a claimed string of 4 different nucleotides varies from around 1kb to 2.5mb whereby the length of the genome has absolutely nothing to do with its claimed pathogenicity. They claim that only small sections of these (genes) which code for “proteins” actually carry out the pathogenicity. This “pathogenicity” as we have seen ranges from nothing to dead in days, so really what they are claiming is that depending on what order you write 4 letters depends on whether you live or die…..

atcgtgtattatgcggcgatcgtacggtatg : That one is fine, that encodes for a “protein” that just does nothing.

ctactacggatgtttagaccaacgtcattcgc: That one encodes for a “protein” that liquifies your liver.

As I say I will spare you the magic roundabout that any investigation goes on in this area because all of the Science is based purely on a “trust me bro” basis. When it comes to pathogenicity they push everything into the realms of proteomics where it is just harmless or deadly, once again going down some rabbit hole of molecular chemistry with zero explanation or evidence about how or why it happens other than “it does happen” and we invented a story to fill in the gaps.

So my overarching point is the absurdity of claiming that the way 4 different claimed molecules are “ordered” is literally life or death, this should go to the same thinking as “genetic” and “Oncological” diseases and the general notion that the human body can and will attack itself. One of the most absurd lies in medical “science” that all of a sudden for no particular reason your insides just decide to kill themselves and take you with them. It is clear that this kind of thinking is just more of an insurance policy for industrial and medical harms.

The Numbers

Q: Are the vast majority of Ebola deaths in Africa? Can you give me a breakdown by country over time, please.

Yes — and very overwhelmingly so. Nearly all recorded deaths from Ebola virus disease have occurred in Africa.

Here’s a concise breakdown by major outbreaks and countries over time (rounded figures):

🕰️ 1976–1990s (first outbreaks)

• Democratic Republic of the Congo (then Zaire)

  • ~280 deaths (1976 outbreak)

• Sudan

  • ~150 deaths (1976 outbreak)

👉 Early outbreaks already concentrated in Central/East Africa

🕰️ 2000–2013 (sporadic outbreaks)

• Uganda

  • ~224 deaths (2000 outbreak)

• Republic of the Congo

  • ~200+ deaths across multiple outbreaks

• Gabon

  • ~150+ deaths

👉 Still entirely African, mostly Central Africa

🕰️ 2014–2016 (largest epidemic ever)

West Africa epidemic:

• Liberia

  • ~4,800 deaths

• Sierra Leone

  • ~4,000 deaths

• Guinea

  • ~2,500 deaths

Total: ~11,300 deaths

👉 This single epidemic accounts for most Ebola deaths in history

🕰️ 2018–2020 (DRC outbreak)

• Democratic Republic of the Congo

  • ~2,300 deaths

🕰️ 2020s (recent smaller outbreaks)

• DRC, Uganda, Guinea

  • Typically tens to hundreds of deaths per outbreak

🌍 Outside Africa (very rare)

• A few isolated cases in:

  • United States

  • Spain

• Deaths outside Africa: extremely few (single digits)

📊 Big picture

• Total Ebola deaths (all time): ~15,000+

• In Africa: >99.9%

• Outside Africa: negligible

🔑 Bottom line

👉 Ebola is almost entirely geographically confined to Africa, both in outbreaks and deaths, with the 2014–2016 West Africa epidemic dominating the global total.

The reason almost all deaths from Ebola virus disease occur in Africa isn’t one single factor—it’s a combination of ecology, exposure, and public health response.

🦇 1. Natural reservoir is in Africa

• Ebola is believed to be maintained in fruit bats (especially African species)

• These animals live in Central and West Africa, so spillover events start there

👉 No reservoir elsewhere → no sustained outbreaks elsewhere

Q: What other countries around the world have fruit bats?

Fruit bats (family Pteropodidae, often called flying foxes) are actually widespread across the tropics, not just Africa.

❌ Where they are NOT found

• Europe (native populations absent)

• Most of North America

• Most of South America

👉 These regions have bats, but not fruit bats (Pteropodidae)

🧠 Key takeaway

Fruit bats live across Africa, Asia, and Oceania, meaning:

• The presence of these animals alone does not explain Ebola outbreaks

• Other ecological and epidemiological factors matter too

Really we don’t need to go much further with our investigation here. In totality even the mainstream admit that it is the Terrain that makes the disease. Ebola is ONLY found in Africa, they claim it comes from a Fruit bat and people eating bushmeat, i.e eating bats (where have we seen that one before lol ). Yet Fruit bats are native to everywhere else in the entire world apart from Europe and the Americas. Once again, to point this out they claim that eating bat soup in Wuhan gives you a runny nose, but eating a bat in Uganda dissolves your kidneys. They strangely regard eating Fruit bat as a traditional delicacy in Samoa and Papua New Guinea. Just by sheer logic, if eating these things did make some tribes people (but not all obviously PMSL) piss out their kidneys and bleed out their eyes, one would have thought that they might have replaced the “Christmas bat” with something slightly less dangerous. So logic dictates that the “zoonotic” theory is bunkum obviously and everything points to this being a geographical problem specific to Africa.

EBOLA On My Mined

Q: All of the countries that have ever experienced an Ebola outbreak, are they all countries that have mining activities in them?

Countries with Ebola Outbreaks .

Ebola (various species like Zaire/EBOV, Sudan/SUDV, Bundibugyo/BDBV, and Taï Forest) has primarily affected Central and West Africa since 1976, with most cases in forested or rural areas linked to wildlife (e.g., fruit bats). Key countries with local/autochthonous outbreaks or transmission include:

en.wikipedia.org

• Democratic Republic of the Congo (DRC): Multiple outbreaks; heavily affected.

• Guinea, Liberia, Sierra Leone: Major 2014–2016 West Africa outbreak.

• Uganda: Several outbreaks.

• Gabon, Republic of the Congo: Multiple.

• South Sudan (formerly Sudan): Early outbreaks.

• Ivory Coast (Côte d’Ivoire): Taï Forest virus case.

• Others with smaller/local transmission: Nigeria, Mali, Senegal, South Africa.

Imported or limited cases (often single patients or short chains, no sustained outbreak) occurred in: Italy, Spain, UK, US, Philippines, Russia, and others.

mercycorps.org

Mining Activities in These CountriesVirtually all African countries with local Ebola transmission have active or historical mining (industrial, artisanal/small-scale). Africa is rich in minerals, and many Ebola-affected areas overlap with mining zones (e.g., gold, diamonds, iron ore).

en.wikipedia.org

• DRC: Major global producer of cobalt, copper, diamonds, gold; outbreaks have occurred in/near mining areas (e.g., gold mining villages).

  abcnews.com

• Guinea, Liberia, Sierra Leone: Significant iron ore, gold, diamonds, bauxite; mining was impacted but continued during the 2014–2016 outbreak.

  pmc.ncbi.nlm.nih.gov

• Gabon, Republic of the Congo: Oil, manganese, gold, timber-related extraction; historical gold-mining camp outbreaks.

  en.wikipedia.org

• Uganda: Gold, copper, and other minerals; artisanal mining present.

• South Sudan: Gold, copper, iron ore, limestone; artisanal gold mining is active and economically important.

  en.wikipedia.org

• Ivory Coast: Gold (major producer), diamonds, manganese, bauxite, nickel; growing formal and informal sector.

  en.wikipedia.org

• Mali, Nigeria, Senegal: Gold (Mali is a top African producer), plus other minerals.

Here we see that every single place that has experienced an “Ebola” outbreak is also an area of heavy mining and exploitation of raw earth materials. Africa has throughout the 19th and 20th Centuries been the playground of the Colonialists looking to exploit the locals for slave labor and the land for its natural resources, take back as plunder to the West. I want to chose the country in the news as the latest “Ebola” outbreak to focus in on just so we don’t spread ourselves too thinly and can deeply analyze it, being the Democratic Republic of the Congo ( sounds very official doesn’t it). We will see later on that the exploits of the colonizers has never really ceased, they just do it remotely now.

Rumble In The Jungle

The reign of Leopold II of Belgium in Central Africa (roughly 1885–1908) is widely regarded as one of the most brutal colonial regimes in history.

Leopold didn’t rule the Congo as a Belgian colony at first—he personally owned it as the Congo Free State, established after the Berlin Conference. He presented his rule as humanitarian and anti-slavery, but in reality it became a system of extreme exploitation.

The main goal was profit, especially from rubber and ivory. To maximize extraction, Leopold’s agents imposed strict quotas on Congolese villages. If people failed to meet them, they faced horrific punishments: beatings, hostage-taking, mutilation (most notoriously cutting off hands), and execution. These acts were often carried out by a colonial army called the Force Publique.

The human toll was staggering. While exact numbers are debated, historians estimate that millions of Congolese people died due to violence, forced labor, starvation, and disease during Leopold’s rule.

International outrage grew in the early 1900s, fueled by activists like E. D. Morel and Roger Casement, who exposed the abuses. Under mounting pressure, Leopold was forced in 1908 to hand control of the territory to the Belgian government, ending his personal rule.

In short: Leopold II’s Congo regime was built on forced labor, terror, and mass death—leaving a legacy that still shapes perceptions of colonialism today.

Smartphones, computers and electric vehicles may be emblems of the modern world, but, says Siddharth Kara, their rechargeable batteries are frequently powered by cobalt mined by workers laboring in slave-like conditions in the Democratic Republic of Congo.

Kara, a fellow at Harvard’s T.H. Chan School of Public Health and at the Kennedy School, has been researching modern-day slavery, human trafficking and child labor for two decades. He says that although the DRC has more cobalt reserves than the rest of the planet combined, there’s no such thing as a “clean” supply chain of cobalt from the country. In his new book, Cobalt Red, Kara writes that much of the DRC’s cobalt is being extracted by so-called “artisanal” miners — freelance workers who do extremely dangerous labor for the equivalent of just a few dollars a day.

“You have to imagine walking around some of these mining areas and dialing back our clock centuries,” Kara says. “People are working in subhuman, grinding, degrading conditions. They use pickaxes, shovels, stretches of rebar to hack and scrounge at the earth in trenches and pits and tunnels to gather cobalt and feed it up the formal supply chain.”

Kara says the mining industry has ravaged the landscape of the DRC. Millions of trees have been cut down, the air around mines is hazy with dust and grit, and the water has been contaminated with toxic effluents from the mining processing. What’s more, he says, “Cobalt is toxic to touch and breathe — and there are hundreds of thousands of poor Congolese people touching and breathing it day in and day out. Young mothers with babies strapped to their backs, all breathing in this toxic cobalt dust.”

National

In Idaho, America’s first, and only, cobalt mine in decades is opening

Cobalt is used in the manufacture of almost all lithium ion rechargeable batteries used in the world today. And while those outside of the DRC differentiate between cobalt extracted by the country’s high-tech industrial mining companies and that which was dug by artisanal miners, Kara says the two are fundamentally intertwined.

“There’s complete cross-contamination between industrial excavator-derived cobalt and cobalt dug by women and children with their bare hands,” he says. “Industrial mines, almost all of them, have artisanal miners working, digging in and around them, feeding cobalt into the formal supply chain.”

Sponsor Message

Kara acknowledges the important role cobalt plays in tech devices and in the transition to sustainable energy sources. Rather than renouncing cobalt entirely, he says people should focus on fixing the supply chain.

“We shouldn’t be transitioning to the use of electric vehicles at the cost of the people and environment of one of the most downtrodden and impoverished corners of the world,” he says. “The bottom of the supply chain, where almost all the world’s cobalt is coming from, is a horror show.”

Some 20,000 people work at Shabara artisanal mine in the DRC, in shifts of 5,000 at a time. The DRC produced approximately 74% of the world’s cobalt in 2021.

Junior Kannah/AFP via Getty Images

Interview Highlights

On how “artisanal” cobalt mines continue to operate in the DRC — despite being illegal

Technically, under the law, there should not be artisanal mining taking place in any industrial mine. And yet, lo and behold, at most of the industrial mines, there is some artisanal mining taking place. In some cases, predominantly artisanal mining is taking place. And the reason is, it’s a penny-wage way to boost production. I mean, imagine you’re in a part of the world where there are millions of people who barely get a dollar or two a day who are grindingly poor and will accept almost any labor arrangement just to survive. Well, you put them in a tight pit, cram them with 10,000 other people and pay them a couple of dollars, and they’ll produce thousands of tons of cobalt per year for almost no wages. And so that’s not legal, but it’s happening.

On why these conditions are on par with slavery

Imagine an entire population of people who cannot survive without scrounging in hazardous conditions for a dollar or two a day. There is no alternative there. The mines have taken over everything. Hundreds of thousands of people have been displaced because their villages were just bulldozed over to make place for large mining concessions. So you have people with no alternative, no other source of income, no livelihood. Now, add to that the menace in many cases of armed forces pressuring people to dig, parents having to make a painful decision, ‘Do I send my child to school or do we eat today?’ And if they choose the latter, that means bringing all their kids into these toxic pits to dig just to earn that extra fifty cents or a dollar a day, that could mean the difference between eating or not. So in the 21st century, this is modern-day slavery. It’s not chattel slavery from the 18th century where you can buy and trade people and own title over a person like property. But the level of degradation, the level of exploitation is on par with old-world slavery.

An artisanal miner holds a cobalt stone at the Shabara artisanal mine in the DRC.

Junior Kahhah/AFP via Getty Images

On the danger of collapse in artisanal mines

I spoke with many families whose children, husbands, spouses, had suffered horrific injuries. Oftentimes, digging in these larger open-air pits, there are pit wall collapses. Imagine a mountain of gravel and stone just avalanching down on people, crushing legs and arms, spines. I met people whose legs had been amputated, who had metal bars in where their legs used to be. And then the worst of all is what happens in tunnel digging. There are probably 10,000 to 15,000 tunnels that are dug by hand by artisanal miners. None of them have supports, ventilation shafts, rock bolts, anything like that. And these tunnels collapse all the time, burying alive everyone who is down there, including children. It's a demise that is almost impossibly horrific to imagine. And yet I met mothers pounding their chests in grief, talking about their children who had been buried alive in a tunnel collapse. And these stories never get out of the Congo. People just don't know what's happening down there.

Sponsor Message

On the trafficking of children to work in the mines

MacMillan

There's money to be made in every corner and every direction. And you've got these militias. Sometimes they're called commandos and they will abduct children, traffic children, recruit children from even other parts of the Congo. I met children who had come from hundreds of miles away and have been brought through militia networks down into the copper cobalt mines to dig. And as they dig and earn their dollar or two, that's what funds these militia groups. So children are the most heavily exploited of all the people down there. They're the most vulnerable and oftentimes trafficked and exploited in some cases in very violent circumstances.

On government corruption preventing change

Corruption is a big part of the problem. That's what allows so much of this abuse to persist. And the thing is, imagine the Congo. It's a war-torn, deeply impoverished nation that has been subjected to generations of pillage and ransacking going all the way back, now centuries, to the slave trade. And so when big foreign stakeholders come waving around large sums of money, it's not a long stretch of the imagination to see that there would be corruption. ...

World

Belgium returned a single tooth to the Congo this week. Here’s why

The first democratically elected president of the Congo [in 1960], Patrice Lumumba, made a pledge that the country's immense mineral riches and resources would be used for the benefit of the people who live there. And in short order, within six months, he had been deposed, assassinated, chopped to pieces, dissolved in acid and replaced with a bloody dictator, a corrupt dictator who would keep the minerals flowing in the right direction. So if you don't play ball with the power brokers at the top of the chain and with the Global North, Patrice Lumumba showed what's the outcome, what will happen. And I think that's also a part of this lesson that we need to understand historically, when we talk about things like corruption.

On how China came to own most of the industrial mines in the Congo

China cornered the global cobalt market before anyone knew what was happening. It goes back to the year 2009 under the previous president in the Congo,

The 33rd Element

You know how they like to leave their calling card with these hoaxes, well this one is really quite in your face. Outlined above is the appalling slavery of past and present that is quite obviously hazardous to human life, endangering the men, women and children forced either directly or indirectly ( because globalist corporations have mechanized the process elsewhere pushing more artisanal mining to occur to be able to keep up with the wealth disparity of inevitable inflation).

One thing that none of the news articles really seem to touch upon is the massive release of naturally occurring toxins, poisons and heavy metals released into the environment, waterways and air but also the vast amount of toxic chemicals that are used in the mining process itself. One of those that is very frequently occurring is Arsenic, which just so happens to be atomic number 33, the 33rd element in the periodic table (Huge Eye Roll). It is going to be the element we focus in on in this article, but for sake of clarity there are MANY MANY others involved and released in the mining activates including mercury, lead, manganese and cyanide.

🧱 1) Toxic elements released from the earth (naturally present in ores)

6

These are often locked in rock and become dangerous when mining exposes and processes them:

Heavy metals & metalloids

• Arsenic

• Lead

• Mercury

• Cadmium

• Chromium (especially toxic Cr(VI))

• Nickel

• Copper (toxic at high levels)

• Cobalt (can cause lung/heart issues)

• Manganese (neurological toxicity)

Radioactive elements (sometimes present)

• Uranium

• Thorium

What happens:

When exposed to air and water, these can form acid mine drainage and leach into rivers, soil, and drinking water.

⚗️ 2) Toxic chemicals used in gold mining

4

Main extraction chemicals

• Sodium cyanide

• Potassium cyanide
  👉 Used in cyanide leaching to dissolve gold

• Mercury
  👉 Used in artisanal mining to form gold amalgam (very dangerous)

Other associated chemicals

• Sulfuric acid

• Nitric acid

• Hydrochloric acid
  👉 Used in refining and ore treatment

• Lime (to control pH, but still reactive)

🔋 3) Toxic chemicals used in cobalt & copper mining

6

Cobalt is usually extracted alongside copper using hydrometallurgy:

Strong acids

• Sulfuric acid (the most common)

Solvent extraction chemicals

• Organic solvents (e.g., kerosene-based mixtures)

• Phosphoric acid derivatives (to separate metals)

Other reagents

• Ammonia

• Sodium hydroxide

• Hydrogen peroxide

These help dissolve, separate, and purify cobalt and copper.

☣️ 4) Toxic byproducts created during mining

Even if not directly added, mining generates dangerous substances:

Acid mine drainage

• Forms when sulfide minerals react with air + water

• Produces sulfuric acid + dissolved metals

Toxic gases

• Sulfur dioxide

• Hydrogen sulfide

Dust & particulates

• Silica dust (causes lung disease)

• Metal-laden dust (cobalt, uranium, etc.)

Putting 3 and 3 together.

As explained above, one of the elements regularly released in all of the different mining activities both artisanal and industrial is Arsenic. Not only direct poisoning but much worse it waterway and air contamination. Now we should all be very aware having heard of Arsenic as being used as one of the most prevalent poisons for thousands of years:

Arsenic has been used as a poison for thousands of years, and it’s one of the most infamous poisons in history.

🧪 Why arsenic was so widely used

Arsenic became a “classic” poison because:

• Colorless, tasteless, and odorless (in common forms like arsenic trioxide)

• Easy to mix into food or drink

• Causes symptoms (vomiting, diarrhea) that used to look like natural illness

• Widely available historically in medicines, pesticides, and pigments

🏛️ Historical use as poison

Ancient world

• Known in ancient Greece and Rome

• The Roman writer Pliny the Elder described arsenic compounds

• Poisoning was already associated with political intrigue

Renaissance & early modern Europe

• Became notorious among elites and nobility

• Sometimes called “inheritance powder” because it was used to eliminate rivals or family members

• Associated with famous poisoning cases (e.g., the Borgia family—though some stories are exaggerated)

18th–19th centuries

• Arsenic poisoning became extremely common

• Sold openly as rat poison and even used in cosmetics and medicines

• Earned the nickname “the king of poisons”.

So I mean call me a conspiracy theorist and stuff but I just thought I’d have a look at what the symptomology of Arsenic Poisoning was and compare it side by side with that of claimed “Ebola”, largely as outlined at the very start of this article that it just isn’t very plausible that some “viruses” do nothing then all of a sudden some just melt your face off. Just to really ram home the point I made a little infographic about it:

So interestingly enough, Arsenic poisoning happens to share absolutely identical symptomology with claimed “Ebola” (this gets better). I then made an infographic of the latest hotspots and cases of the 2026 “Outbreak” in DR Congo and laid it over a picture of known high Arsenic contamination levels in mining areas and waterway channels connected to them.

Would you know it that they neatly line up in these areas. Further to this it is well documented that many clusters of these come directly from mine workers themselves, as well as many other African countries that have supposedly experienced these “Outbreaks”.

Da “Virus”

We’ve kind of worked backwards in this article, usually we start with the smallest thing first (The non existent entity), work through its lack of contagion then finally onto the plausible substitutes for what is actually causing the blamed disease, if applicable. With Ebola, because of the so very obvious localized Terrain that this occurs in and with a culprit so bang on, I thought I would start with all of that evidence and leave the ridiculousness to the end. Really the Virological part to the “Ebola” hoax is so laughable it hurts, especially for the actual particle they claim it is.

First on the chopping board is claimed contagion. Obviously the “ethics” committee is in full flow on this one, because the gasping and shock horror sounds when you suggest that they provide you any evidence of human transmission that wasn’t don’t with Kary Mullis’ flashing fraud box. “No!” they proclaim “Why everyone would die! if we infected them with Ebola!!”. Again these torture junkies are salivating at the bit to kill lots of animals though aren’t they, so let’s have a look at when they gave what they consider to be purified “Kidney Melter” to a bunch of Rhesus Monkeys:

That’s right, shortly before Euthanizing them (once again the Ethics committee- the HR of the clinical trials world, weigh in on this one to cover up the failure) they logged the symptoms of these monkeys and the only thing they managed to track was a lack of biscuit consumption. I mean call me a skeptic but if you were trapped in a cage, held down and injected with shit and then saw all of your mates being taken away one by one, it might put you off your digestives a bit. But needless to say, not even a snifter of melted kidneys were seen in these symptom sets, as usual they kill the monkeys, dissect them and point at different color of the brutalized body parts they have brutalized with their dissection.

TEM

Mainstream Consensus:

From the Published, Peer Reviewed Journal of Virology images of claimed Ebola Virus in Vero Cells:

Source 2: Claimed Zaire Ebola on Research Gate

Source 3: Claimed Human Cell Expressing Ebola Protein with Ebola Virions visible

Source 4:

Control Culture TEMs:

Interpretation

Demonstrated in the clear images cross referenced that the particles that are being labelled as Ebola Virus are strands of Filopodia, the spacing where they intersect the 2d plain of the TEM slice some cross sectional, some longitudinal showing protrusions is identical in infected and uninfected. The American Society For MicroBiology even uses Vero cells to claim to show Ebola Virions, a cell that is well known to have plenty of Filopodia as shown in our uninfected culture TEM.

A Milky Culture

Thank you to Marvin Haberland and NEXT Level for pointing this ridiculously funny cell culture self own. In this paper it is about “Ebola” which is why I will include it here in this article, however it really isn’t anything specific rather than falsifying the Cell Culture Isolation Technique (Once again- as if it wasn’t already lying in tatters on the floor.

3.5. Breast Milk and Semen Induced Cytotoxicity Using In Vitro and In Vivo Isolation Methods

The matrix effect (cytotoxicity) of normal breast milk and semen was tested in MDM, Vero E6, and Huh-7 cells. Breast milk or semen, whether whole or clarified by centrifugation, were added to 90% confluent monolayers of each of the three cell types. A control flask with only media was incubated in parallel. Cell monolayers were photographed at days 0 (after 1-h incubation), 3, 7, and 10 post-exposure (not all images shown, Figure 5). Breast milk was cytotoxic on Vero E6 and MDM cells at volumes of 50 and 100 µL. However, breast milk visually appears less toxic in Huh-7 cells. Toxicity was initially identified (day 0 post-exposure) in the 100-µL treatment, and the cell monolayer recovered by day 10 post-exposure. Breast milk that was clarified by centrifugation was not toxic at the concentrations tested. Whole semen and semen clarified by centrifugation were both slightly cytotoxic in MDM cells but not Vero E6 or Huh-7 cells (Table 3). Images of cell monolayers at ten days following semen or breast milk exposure are displayed (Figure 5).

Figure 5. 10× images of MDM, Vero E6, and Huh-7 cells taken 10 days following exposure to select volumes of normal semen, breast milk, or cell culture media (control). Breast milk was toxic at 50 and 100 µL/T-25 flask on Vero E6 cells (no cells present after 10 days) and MDM cells, but toxicity was less on these cells than on Huh7 cells.

Additionally, two litters of suckling laboratory mice were injected IC with 10 µL of breast milk, semen, or cell culture media. No laboratory mice experienced fatality during the 10 days after injection (Table 3). Two animals exposed to semen did not recover from anesthesia and were not counted against the number of survivors.

To determine if matrix effect impacts virus isolation success, spiked semen and breast milk were inoculated onto VeroE6, Huh-7, or MDM cells as described above. Results were compared to media only preparations using the log binomial likelihood ratio statistic and compared to the chi-squared reference distribution with significance considered at the 0.05 level. Again, there was no statistical difference in isolation success for spiked media samples across cell types. VeroE6 and Huh-7 cells were both successful at isolating virus at the same dilutions (p = 0.96) and both demonstrated significantly better virus isolation success from spiked semen samples than MDM cells (p < 0.01). Virus was not isolated from any of the spiked breast milk samples even though the cell monolayers appeared healthy. Isolation success from spiked semen or media were not significantly different by across the cell types (Table 4).

Table 4. Virus isolation success from spiked breast milk and semen samples (n = 12).

4. Discussion

Potential semen- or breast milk-associated matrix toxicity was also assessed for these same methods. Huh-7 cells and brains of suckling BALB/c laboratory mice were the most resistant to breast milk-associated matrix toxicity. Interestingly, concentrations of breast milk that were shown to be toxic when unaltered were not toxic following clarification by centrifugation. This suggests the matrix cytotoxicity of breast milk is most likely related to components of the sample that were centrifuged out. Whole semen and semen clarified by centrifugation were both slightly cytotoxic in MDM cells but not Vero E6 or Huh-7 cells, suggesting the cytotoxicity is related to soluble matrix components that were not removed by the centrifugation process. Though the normal semen and breast milk used in this study were from individual healthy donors, it is unknown how much matrix toxicity would vary between donors or health status. Virus isolation was not successful from spiked breast milk and the mechanism of virus replication inhibition is unknown. The isolation attempts were made by two different users on two separate days in parallel with the isolation spiked semen or media control. If virus isolation from breast milk samples will be pursued in the future, altenative isolation methods will need to be identified. Additionally, although components of semen have been reported to increase EBOV infection in HeLa cells, in the present study virus isolation from spiked whole semen was as sensitive as the media matrix samples. The difference in results from these two studies may be explained by the use of whole semen instead of seminal plasma or components of semen as well as a differences in the in vitro effects of these matrices on the cell lines used

ANALYSIS

Why they decided to put breast milk into a cell culture is unclear, but I am very grateful they did as it sets up one of the most comedy falsifications in Virology. They note that in all cases uninfected breast milk put in as a sample to a Cell Culture produces CPE. This is again the same in most cases when they put uninfected semen in too (Don’t ask). Strangely after this they decided to spike in some “ebola” into the milk and cum and try and culture it. Even more strangely despite milk creating the CPE on its own, when combined with “Ebola” it then somehow undid the CPE.

What I believe is happening is that given these two fluids have a very different ionic balance for their very different roles, in the uninfected cultures they are not providing extra nutrients to the assumed reduced FBS (They don’t list a proper method- surprised, not). The cells go into starvation and produce the CPE. When they are coming to the “neutralizing matrix” with spike ins, they readily admit they compare them to the baseline they had (Which IS surprising, as benchmarking is a rarity in soyence). Potentially active semen would reduce the nutrients and cause extra CPE, the breast milk not and the addition of the spike in provided enough serum to keep the CPE observed the same. This invokes the John Enders “the samples both show CPE but look different” thing again.

They even carried out a control infection with the uninfected breast milk and semen and injected it into their newborn mice (Sick psychopaths). They proudly proclaim that the newborn mice survived the 10 day period they gave them to live claiming it was a “successful” control. Except when you read the fine print, 2 of the mice actually died, they just didn’t count them because apparently they died too soon SMH.

CONCLUSION

Whenever there are extreme claims of things happening within the reams of FakeVirusology it pleases me greatly. With the nothing burger ones like Sars Cov 2, Influenza etc the ground data so so easily obscured. With symptoms, even when claimed “symptomatic” they can be ridiculous things like a blocked nose (anosmia), coughing or a headache. Of course these things are just everyday occurrences, you can blame patterns of these things on practically anything and you would find some statistical significance. But here, right at the other end of the spectrum, is Ebola and Hantavirus, get some rat piss in your chicken curry on a cruise or get a dodgy bat burger whilst trekking through the Congolese rainforest and wham you are a goner. There is no leeway, no matter how much they kick and scream with these fake viruses.

It rules out the PCR/ Asymptomatic claim for even being too much of a clownmaxxing posture for the hoax perpetrators to pull off. Extraordinary claims require extraordinary evidence and so this wheelhouse of apocalyptic invisible bugs really does need some solid death stats when they are injecting animals with it. So when they are injecting it with syringes full of the stuff and instead of them pissing blood out their eyes they are measuring biscuit consumption we should be able to call hoax just on that one metric alone.

Really we should be able to call foul on the whole thing from, just the plain old illogical nature of the Germ Theory. If a contagious disease with a 40% death rate that causes you to piss the infected blood everywhere (like the MOVIE 28 days later) then humanity would have been wiped out many millennia ago, indeed there would be no life on earth, presumably apart from Ebola and the Rat Piss virus, just hanging out at a Club Med talking about the good old days when they had a host to infect.

For me personally the actual particle they claim is an “Ebola” virus is so funny. It is like they really went out of their way for the Hollywood props department to not choose the standard blob they find in the cell culture, no it is giving “Snakes on a Plane” vibes with this one, the serpent, the parasite feel to it. When I had a look at these cells under a Transmission electron microscope it was so comedically obvious, the filopodia, the hair like structures that a cell grows when stressed to become motile are being falsely labelled as “Ebola”. The fact that they always point to claimed Ebola right outside the cell exactly where these filopodia are usually located. The whole thing is absurd.

We saw how a long history of slavery by these demonic people forces innocent people to endanger their lives on a daily basis, how these mining activities, ironically for the Green Agenda are polluting the air, water and soil with incredibly toxic poisons and heavy metals that cause these exact extreme symptoms blamed on the non existent pathogen. Arsenic has the absolute identical profile for being the actual murder culprit whenever the extreme symptoms are seen. As with all these hoaxes I would still not want to say “All deaths blamed on Ebola are Arsenic Poisoning”, when it comes to health and hoaxes there are infinite variables at play. Firstly only 16k people have ever claimed died from Ebola in history, which is relatively miniscule especially in countries such as Uganda that have been home to many admitted Genocides.

So when analyzing these things, firstly has it happened at all? With only 16k in history we can be sure that the vast majority of those would not have the exact eye bleeding kidney melting hemorrhagic fever as described, if indeed they have died in anything other than by a Machete wielding Genocidal Maniac Politician and their henchmen. We then can move on and say, OK there are a few thousand dying in this hemorrhagic fashion but it might not all be because of Arsenic, the patterns might not match up. Well there is a raft of other natural earth poisons and heavy metals in these areas; mercury, lead, cyanide etc… it could always be a nice little cocktail. Any which way I hope you can see the very plausible nature of being able to explain violent symptomatic deaths like Hemorrhagic fever much much better with chemical/elemental poisoning.

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This article is available as a downloadable EBook along with the rest of my work on ShadowBanned Library

Thank you to Dr Lisa Hutchinson for pointing this out to me on a cold and miserable January day, it lifted my spirits.

This is one of those ones that as a common man, of just average intelligence I pride myself on being able to decipher complex issues based on a reliance of common sense and logic. Where more academically minded people are either indoctrinated or intentionally excising this part of their psyche, I always place it front and center as a kind of lock and key mechanism to discernment, call it the “bullshit test” if you will.

The only real 2 talking points of the celebrity “freedom” movement when is comes to PCR are massively tired now through their sheer repetition as well as their superficiality. They challenge nothing about the inherent mechanisms of this “Test” and assume nearly every moving part and reagent is as it should be, rigorously tested and benchmarked, and able to give good results if used correctly. These talking points are; PCR used at too many cycles is inaccurate and the fact that some establishment shill by the name of Kary Mullis once waffled on about some Buddhist notion of being interconnected and that his machine can “find anything in anybody”, which dim people interpret him as saying it can’t be used as a diagnostic (Despite him writing that it could in his patent, in the acceptance of his Nobel Prize and in a letter to the judge of a man accused of spreading “HIV” that Kary got jailed for 8 years).

When you lay everything out on the table this isn’t a very incisive rebuttal of THE machine that fakes pandemics, it’s almost as if most of these talking heads don’t actually want to show that the pandemic was a hoax and to keep the “Virus” lie alive. Of course any machine is inaccurate when you use it in the upper limits of its functionality this is about as crass a rebuttal as can come. Of course nefarious actors will claim they can use this piece of machinery to tell you whatever they want to be able to control you, “You have HIV, coz the machine went blip”… “You owe us $1540 in back payed Tax because the machine went blip”…. “You have been banned from all social media, because the machine went blip” so on and so forth.

So when I hear this piece of information, I literally burst out laughing. It was one of those pieces of information that flew out of the blocks ran straight at the lock and key mechanism on my mental discernment door and crack its head on the door frame, bent over and passed out. I instantly knew that there was no way that this was going to pass the “bullshit test” went put to scrutiny, yet it had been sitting there, quite comfortably bullshitting away under everyone’s nose:

A PCR CYCLE IS PHYSICALLY IMPOSSIBLE.

That is once again, as is becoming a bit of a habit written in a bit of a clickbait stylee. Of course a PCR cycle is physically possible, you just heat up the sample, then cool it down a bit and then heat it back up again. What I mean is that, and it would obviously be too long to put it in a subtitle, given the amount of time it is claimed and the strength and efficiency of the heating modules, it is physically impossible to heat up and cool down these samples in the allotted time they claim AKA A cycle is not a cycle as they claim AKA fraud.

Eppendorf Mastercycler X40 — Full Technical Specifications

General & Physical
Model: Mastercycler X40 (Touchscreen, order no. 6381000077)
Dimensions (W x D x H): 24.5 x 38.5 x 23 cm (9.7 x 15.2 x 9.1 in)
Weight: 7.25 kg (approx. 16 lbs)
Power supply: 100–240 V, 50–60 Hz
Power consumption: 500 W (max)
Noise level: 40.5 dB(A)

Thermal Performance
Block type: Aluminum, 96-well
Heating technology: Three Peltier elements
Temperature range: 4–99 °C
Max heating ramp rate: 3.3 °C/s
Max cooling ramp rate: 1.5 °C/s
Temperature accuracy: ±0.15 °C
Temperature uniformity (20–72 °C): ±0.2 °C
Temperature uniformity (72–95 °C): ±0.3 °C

Gradient Function
Gradient format: 12-column linear gradient
Gradient range: 1–30 °C
Gradient temperature range: 30–99 °C

Heated Lid
Type: SafeLid with sample protection
Temperature range: 37–110 °C

Compatible Consumables
0.1 and 0.2 mL tubes and strips
Full-skirted, semi-skirted, and unskirted 96-well plates

Memory & Interface
Max program storage: 5,000 programs
Display: 7-inch chemical-resistant glass touchscreen
Connectivity: Ethernet, USB (front), VisioNize ready (remote monitoring)

Key Operational Modes
Temperature control modes: Fast, Medium, Standard, Safe
Cycling capacity: 5,000 cycles of standard PCR
ACT certified for environmental impact

A PCR CYCLE RUNTIME

Standard PCR Run Time for 40 Cycles on Eppendorf Mastercycler X40

Total run time typically falls between 60 and 70 minutes for a standard protocol.

Standard Cycle Times (40 cycles)

Protocol per cycle (denature + anneal/extend) / Approx. total time:

• 15 sec denature + 60 sec anneal/extend = ~70 minutes

• 5 sec denature + 30 sec anneal/extend = ~43 minutes

• 5 sec denature + 20 sec anneal/extend = ~37 minutes

Ramping Speed Specifications (hardware limits)

Heating rate: 3.3 °C/second (max)
Cooling rate: 1.5 °C/second (max)

Quick Reference for Common Setups on the X40

Fast/short protocol (e.g., 5s denature, 20s anneal): ~37 minutes
Standard/typical protocol (e.g., 15s denature, 60s anneal): 60–70 minutes
Slow/long protocol (long hold times or Safe mode): ~2 hours or more

How to Decide PCR Cycle Times (Hold Times)

There are three steps: denaturation, annealing, and extension. Each has its own rules.

1. Denaturation (94–98°C)

This separates double-stranded DNA into single strands.

Factors that affect time:

• Template complexity: Genomic DNA (human, plant) needs 1–3 minutes for initial denaturation. Plasmids or simple templates need only 10–30 seconds.

• GC-rich templates: If DNA has high GC content (stronger bonds), increase denaturation time or temperature slightly.

• Cyclic denaturation: In later cycles, 5–15 seconds is usually sufficient because the amplicon is much shorter.

General rule: 10–30 seconds per cycle for standard templates. Longer for complex genomic DNA.

2. Annealing (50–68°C)

Primers bind to complementary sequences on the template.

Factors that affect time:

• Primer length and Tm: Annealing temperature is typically set 3–5°C below the primer’s melting temperature (Tm).

• Primer concentration: Higher primer concentration allows shorter annealing time (e.g., 10–15 seconds).

• GC content: GC-rich primers have higher Tm but do not need longer times.

General rule: 15–30 seconds is typical. Longer annealing times (1–2 minutes) are rarely needed and can increase non-specific binding.

3. Extension (72°C)

DNA polymerase synthesizes the new complementary strand.

Factors that affect time:

• Amplicon length: This is the single biggest factor. Standard Taq polymerase extends at ~1 kb per minute.

• Polymerase speed: Some engineered polymerases are faster (2–4 kb/min). Check the manufacturer’s datasheet.

• Complexity: For amplicons under 1 kb, 15–30 seconds is often sufficient.

General rule: 30–60 seconds per 1 kb of target length.

Quick Reference Table (Extension Times)

Amplicon length / Extension time (standard Taq) / Extension time (fast polymerase)

• Under 500 bp: 15–30 seconds / 5–10 seconds

• 500 bp to 1 kb: 30–60 seconds / 10–15 seconds

• 1 to 2 kb: 60–90 seconds / 15–30 seconds

• 2 to 4 kb: 90–120 seconds / 30–60 seconds

• Over 4 kb: 2–4 minutes / 60–120 seconds

Example: Choosing Times for a Typical Experiment

Scenario: Amplify a 750 bp fragment from human genomic DNA using standard Taq polymerase.

• Initial denaturation: 2 minutes at 95°C (human genomic DNA needs longer)

• Cyclic denaturation: 15 seconds at 95°C

• Annealing: 20 seconds at 60°C (primer Tm is 63°C; use 3°C below)

• Extension: 45 seconds at 72°C (750 bp = 45 seconds at 1 kb/min)

• Final extension: 5 minutes at 72°C (ensures all products are fully extended)

Total run time for 40 cycles on Mastercycler X40: Approximately 60–70 minutes using standard mode.

Key Takeaways

• Amplicon length drives extension time (1 minute per kb)

• Template complexity drives denaturation time

• Primer Tm drives annealing temperature (not really time)

• Polymerase speed can dramatically shorten extension times

Total Run Time Calculation for 40 Cycles on Mastercycler X40

Protocol used:

• Initial denaturation: 2 minutes at 95°C

• Per cycle (40 cycles): 15 seconds at 95°C + 20 seconds at 60°C + 45 seconds at 72°C

• Final extension: 5 minutes at 72°C

Step-by-Step Calculation:

Step 1: Initial denaturation
2 minutes = 120 seconds

Step 2: One cycle (hold times only)
15 + 20 + 45 = 80 seconds per cycle

Step 3: 40 cycles (hold times only)
80 seconds × 40 cycles = 3,200 seconds = 53 minutes 20 seconds

Step 4: Final extension
5 minutes = 300 seconds

Step 5: Total hold time
120 + 3,200 + 300 = 3,620 seconds = 60 minutes 20 seconds

Step 6: Adding ramp times (heating and cooling between temperatures)

Cooling from 95°C to 60°C (35°C drop): at 1.5°C/s = ~23 seconds

Heating from 60°C to 72°C (12°C rise): at 3.3°C/s = ~4 seconds

Total ramp time per cycle = ~27 seconds

Total ramp time for 40 cycles = 27 × 40 = 1,080 seconds = 18 minutes

Final Total Run Time:
Total hold time: 60 minutes 20 seconds
Total ramp time: 18 minutes
GRAND TOTAL: 78 minutes 20 seconds (approximately 1 hour 18 minutes)

ALUMINIUM HEATING BLOCK WEIGHT

Block Weight Estimate for Eppendorf Mastercycler X40

Total instrument weight: 7.25 kg (approx. 16 lbs)

Estimated aluminum block weight (alone): 1.1 – 1.5 kg (approx. 2.4 – 3.3 lbs)

The block accounts for roughly 15–20% of the total instrument weight.

Supporting data from other manufacturers (removable 96-well aluminum blocks):

• Gilson 96-well block: 0.91 kg

• LLG 96-well block: 0.70 kg

• Thermo Scientific 96-well block: 1.40 kg

Why the X40 block is likely heavier (1.1-1.5 kg range):

• The X40 block is not a simple passive block. It is an active thermoblock permanently integrated with three Peltier heating/cooling elements and temperature sensors.

• Removable blocks (0.7-1.4 kg) are passive and have no built-in electronics.

• The integrated design adds complexity and mass, placing the X40 block at the higher end of the weight range.

Comparison with other thermal cyclers:

• Mastercycler X40 total weight: 7.25 kg

• Mastercycler X50 total weight: 10.7 kg

• Typical competitor 96-well cyclers: 11-12 kg total

Important note: The 1.1-1.5 kg figure is for the aluminum block alone. It does NOT include the housing, electronics, Peltier elements, heated lid, or power supply. The remaining ~6 kg covers everything else in the instrument.

Eppendorf does not publish the block weight separately because it is a permanently integrated, non-user-replaceable component.

PELTIER MODULE POWER

Corrected Power Breakdown for Eppendorf Mastercycler X40

Total maximum power consumption (whole unit): 500 W

Estimated power draw by component:

• Three Peltier modules (heating/cooling): 300 – 400 W

• Heated lid (up to 110°C): 50 – 100 W

• Electronics, 7” touchscreen, fans, USB/Ethernet: 50 – 100 W

TOTAL: 500 W

Important notes:

• The Peltier modules are the dominant power consumer, using 60-80% of the total 500 W budget.

• The remaining 100-200 W is shared between the heated lid and the onboard electronics.

• These figures are estimates. Eppendorf does not publish the isolated wattage of individual components. Only the total unit power consumption (500 W) is specified in official documentation.

Reasoning for the corrected range:

• If lid + electronics draw 100 W (low end), Peltier modules draw 400 W.

• If lid + electronics draw 200 W (high end), Peltier modules draw 300 W.

Therefore, Peltier modules = 300 – 400 W.

Short answer: there isn’t a single time — it can range from a few seconds to over a minute depending on what you mean by “on its own.” But here’s the physically correct way to think about it:

Key point (important)

A Peltier module does not “heat itself up” efficiently in isolation — it moves heat from one side to the other.

So:

• One side gets hot

• The other side gets cold

• The temperature rise depends on load, heat sinking, and thermal mass

If you literally mean “bare module in air” (no load, no heatsink)

• Very low thermal mass (~20–40 g ceramic + semiconductors)

• Electrical input: ~100 W

Rough estimate:

• Heat capacity ≈ ~20–40 J/°C

• Energy for +35 °C ≈ ~700–1400 J

At 100 W:

• ~7–15 seconds (ideal)

• Realistically: ~10–30 seconds