I have tried not to write this article for the 18 months that I have been on the focus of dismantling scientism but have finally buckled. People who are familiar with my discourses 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 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 friend up and suggested to him that he 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. ![[Pasted image 20260708212154.png]] > 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. ![[Pasted image 20260708212209.png]] ![[Pasted image 20260708212212.png]] 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. ![[Pasted image 20260708212640.png]] > 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. ![[Pasted image 20260708212746.png]] > 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 o==ur 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 96oC., 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). ![[Pasted image 20260708213125.png]] ## 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, 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: - Brain and nervous system damage - Learning and behavioral problems - Reduced growth and development - 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: - Give radioactive vitamin D to animals or humans. - Draw blood and collect tissues. - Separate molecules using chromatography. - 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. ![[Pasted image 20260709222115.png]] **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. --- ## 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. --- ## 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 --- ## 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. --- ## 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. --- ## 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. --- ## 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. --- ## 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. --- ## 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. --- ## 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. --- ## 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. --- ## 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. --- ## 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. ![[Pasted image 20260709222505.png]] ## **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_. --- ## 📊 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 ![[Pasted image 20260709222606.png]] > **==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. ![[Pasted image 20260709222656.png]] ### ==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. <iframe width="560" height="315" src="https://www.youtube.com/embed/D5FeSaf0ydc?si=3DaqdBa6eCoubldp" title="YouTube video player" frameborder="0" allow="accelerometer; autoplay; clipboard-write; encrypted-media; gyroscope; picture-in-picture; web-share" referrerpolicy="strict-origin-when-cross-origin" allowfullscreen></iframe> And here is 1.5 Gallons (6.8 Liters- a claimed lethal dose) in 2 mins and 3 seconds <iframe width="560" height="315" src="https://www.youtube.com/embed/sCRCXHFtpHY?si=EmhPnesZvwPaxAC3" title="YouTube video player" frameborder="0" allow="accelerometer; autoplay; clipboard-write; encrypted-media; gyroscope; picture-in-picture; web-share" referrerpolicy="strict-origin-when-cross-origin" allowfullscreen></iframe> ## 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): ![[Pasted image 20260709223300.png]] - 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. ![[Pasted image 20260709223359.png]] ## 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 ![[Pasted image 20260709223419.png]] 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** ![[Pasted image 20260709223652.png]] 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](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. ![[Pasted image 20260709223806.png]] ## 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) ## 🟡 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) ![[Pasted image 20260709223957.png]] 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](https://pmc.ncbi.nlm.nih.gov/articles/PMC6158375/?utm_source=chatgpt.com#B4)). 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](https://pmc.ncbi.nlm.nih.gov/articles/PMC6158375/?utm_source=chatgpt.com#B4)). 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](https://pmc.ncbi.nlm.nih.gov/articles/PMC6158375/?utm_source=chatgpt.com#B4), [12](https://pmc.ncbi.nlm.nih.gov/articles/PMC6158375/?utm_source=chatgpt.com#B12)). 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](https://pmc.ncbi.nlm.nih.gov/articles/PMC6158375/?utm_source=chatgpt.com#B4)). ==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](https://pmc.ncbi.nlm.nih.gov/articles/PMC6158375/?utm_source=chatgpt.com#B13)). ![[Pasted image 20260709224012.png]] **==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. ![[Pasted image 20260709224042.png]] We’re often told how dangerous [vitamin deficiencies](https://bestlifeonline.com/signs-of-vitamin-deficiency/) 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. ![[Pasted image 20260709224051.png]] 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. ![[Pasted image 20260709224110.png]] ## 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! ![[Pasted image 20260709224316.png]] ![[Pasted image 20260709224324.png]] ![[Pasted image 20260709224328.png]] ![[Pasted image 20260709224336.png]] ![[Pasted image 20260709224344.png]] **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** > [Share on Facebook](https://grothman.house.gov/news/documentsingle.aspx?DocumentID=1777#) [Share on X](https://grothman.house.gov/news/documentsingle.aspx?DocumentID=1777#) [Print this Page](https://grothman.house.gov/news/documentsingle.aspx?DocumentID=1777#) [Share by Email](mailto:?subject=I%27d%20like%20to%20share%20a%20link%20with%20you!&body=https://grothman.house.gov/news/documentsingle.aspx?DocumentID=1777) > > **Washington, September 15, 2020** | [Timothy Svoboda](mailto:[email protected]) (202-225-2476) > > **Tags:** _[Health Care](https://grothman.house.gov/news/documentquery.aspx?IssueID=14888)_ > > Today, Congressman Glenn Grothman (WI-06) released the following statement after [news](https://www.insider.com/fauci-takes-recommends-vitamin-d-and-c-supplements-immunity-boost-2020-9) 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](https://grothman.house.gov/UploadedFiles/Grothman_WI-06_COVID19_Letter_CDC_Reporting_Data_and_Treatment_Options.pdf) 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](https://grothman.house.gov/news/documentsingle.aspx?DocumentID=1575) addressing medical research studies out of [Northwestern University](https://news.northwestern.edu/stories/2020/05/vitamin-d-appears-to-play-role-in-covid-19-mortality-rates/) and [Trinity College](https://scitechdaily.com/vitamin-d-determines-severity-in-covid-19-researchers-urge-government-to-change-advice/) 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](https://www.politifact.com/factchecks/2020/jun/08/glenn-grothman/glenn-grothman-target-about-tie-between-vitamin-d-/). > > Grothman has repeatedly called on the CDC, even [from the House floor](https://twitter.com/RepGrothman/status/1299043153199222784), 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.