Last year in my Seven-Year Update post I mentioned that I was looking into the politically hot topic of viruses. When I first started to look into it I quickly came to the realization that the very basic science and fundamental understanding of viruses is almost completely wrong. It’s on par with so-called vitamin A science, and maybe even a lot worse.
Last year I said that I was going to write a more comprehensive investigation regarding viruses. But, as the censorship and squashing of any non-conventional information on the topic was cranked up to the maximum effort possible, I felt it wasn’t the right time for a lengthy blog post or maybe a new ebook on the topic. Unfortunately, that plays right into the hands of big pharma and their puppets in government under their control. Although I’m a complete no-body I think it’s important to choose the right time for picking such a battle. I decided that now’s not the time for it. Hopefully, the pandemic response by our governments and the medical establishment over the last two years has made it crystal clear to everyone just how incredibly corrupt the system is. What happened in Canada earlier this year is so disgusting to me I just can’t put it down into writing how I feel about it. So, for now, all I’m going to say about viruses is what’s below.
“Viruses” sure aren’t what we are being told they are. I think a key point we all need to fully appreciate is that viruses are not “alive”, and never ever become “alive”. Therefore, they are most certainly not parasites or pathogens. They don’t and can’t “evolve” or mutate. They consume no food, nor energy, nor resources. They can’t and don’t ever reproduce themselves. They have no locomotion, no organelles, no respiration, etc, etc. They have no life force, no will, no intent. And, contrary to a recent statement from a very prominent public health official they are not “clever”. They actually have the same intelligence as a rock. Therefore, they are not, and cannot be, out to get us. They are also not out to perpetuate their own “species”, because they are not a “species”, nor any life form. They are not living entities even by the wildest stretch of the imagination.
The key understanding is that all so-called viruses are manufactured by cells; and almost all of them in our bodies were made by our own cells. Therefore, viruses never “replicate” themselves, and they don’t hijack or trick the cell into doing it for them. They are simply proteins assembled by our own cells. However, some of these proteins can harm us. They are ones that contain defectively structured mRNA proteins. These are usually strands of bad RNA that the cell has decided is too defective to use. These defective garbage proteins (RNA molecules) are potentially so dangerous that they can’t be discarded without first putting them into a protective wrapper. Much like with the RBP that’s used to protect cells from vA’s toxicity. Thus, these protective wrappers are the famous protein capsids surrounding most “viruses.” But, given the right circumstances and conditions some of these proteins can start a chain-reaction, and we might get sick from it running out of control for too long.
There’s more to it of course. Since most harmful “viruses” are just defectively made messenger proteins we need to understand what causes the defective mRNA proteins in the first place. Well, since it is now established that retinoic acid can, and does, fracture DNA it should be one of the prime suspects. There’s no question there are other toxins and environmental hazards to blame sometimes too. But, the key takeaway here is that for the most part “viruses” don’t cause disease. Rather, it’s the direct opposite. Disease causes “viruses” to be created.
To use a more concrete example, let’s say someone gets diagnosed with hepatitis. Doctors using the now infamous PCR test will usually find a large number of “viruses” and claim the person has acquired a “viral infection” and that infection has caused the disease. But, no, that’s not it at all. The slowly developing liver disease with its corresponding massive number of damaged and dying cells is causing these cells and cell fragments to produce the “viruses.” Viruses are the artifacts of the diseased tissue.
Sometimes these proteins can be transferred between people and that can start a chain reaction in certain vulnerable people. However, we don’t ever really get “infected” with the “virus”. Rather we get contaminated by other people’s defective proteins.
I believe that if people are healthy, and have low vA levels then “viruses” pose almost no risk at all. Of course, there’s still much more to the story here. There’s also a fascinating understanding that there’s a hugely beneficial and critical role many so-called “viruses” play in our health and even our evolution. That understanding is that the vast majority of the billions of the “viruses” that are circulating in our bodies on any given day are actually extra-cellular message capsules. These message capsules are used to communicate with other cells and organs in the body. The cells of the body have formed a gigantic network of communication between themselves. The data packets used on this network are mRNA proteins encapsulated within “viruses” and exosomes. Darwin was correct (for those who have actually read his book). It’s not random mutations driving our evolution. Rather it’s our life experiences that’s programming the genetic code in our offspring. The driving mechanism of that programming is via “virus” encapsulated messages. So, when it comes to truly understanding viruses our current medical science is in the absolute stone age. I’ve only scratched the surface of it here.
But, obviously, big pharma needs to keep the myth of “scary and deadly viruses” alive to stoke endless fear and boost endless massive profits from their vaccines for them.
Bottom line, for the most part, “viruses” are a giant scam.
My Prison Food and Night blindness
I reported in last year’s annual update that I had once again encountered a period of reduced night vision. It was also accompanied by having quite dry eyes first thing in the mornings. Oh yes, I know that those are some of the key, if not the de facto, symptoms of vA deficiency. But, of course, I don’t believe vA deficiency even exists. I also think that it’s impossible to have a deficiency in a highly toxic molecule. Moreover, if these symptoms were due to a vA deficiency then they should have shown up and progressively gotten worse as time went on. Except, that did not happen. The periods of reduced night vision were sporadic and I had always recovered from it. My previous incidents of “night blindness” occurred in the winter months when the air here in Calgary, AB is very dry. However, oddly last year the condition was most notable in August. Coincidentally, last summer the city was covered in a lot of smoke from forest fires. It lasted for at least two months. So, at first, I rationalized that it was probably just the excessive smoke exposure that caused it to occur in the summer months this time. However, as the smoke finally cleared my dry eyes really didn’t get much better. So, what the heck was really going on?
Last year, as I am doing so this year, I was sticking pretty strictly to my diet of rice, bison/beef, and black beans. Although I usually cook one cup (measured dry) of rice per day I almost never consume it all in one day. Most days it is more like a half cup. So, a pretty standard practice for me is to put the remaining rice in a container and put it in the fridge. Then, the next day I’ll take the leftover cold rice, and either freshly cooked or cold leftover meat, and some cold black beans and dump it into a bowl. Then I’ll boil some water and add it to the bowl to make what I call my “soup”.
My wife hates that I call it “soup”. Whenever I call it that, she so lovingly tells me: “That’s not soup, it’s prison food!” Yes, it’s darn plain and boring. Except, I don’t think it’s really that bad either. It sure makes my meal planning and food shopping super simple. It’s also super easy and fast to put together. But, she’s right that it does lack flavor. So, as I also mentioned in last year’s update, I had gotten into the habit of spicing it up by adding some granulated dry onion powder to it. With that addition I think I could legitimately call it a soup. Sometimes my wife would dice up and fry onions and I added that to my soup rather than the onion powder.
Then, I got to thinking about it. If just cutting into an onion can quite quickly and quite strongly irritate the eyes then maybe, just maybe, it’s not such a good idea to be eating onions either. With that thought I completely stopped adding the onions / onion powder and went back to the “prison food” version of my soup. Quite amazingly, within four weeks my night vision completely recovered. Within four months my corresponding dry eyes also fully recovered. I’d rate my current night vision as being excellent.
I think this is an intriguing little sub-experiment in isolating it down to one probable cause. The only deviation / change in my diet last year was the addition of the onions and then following that change my night vision problems developed. Then when I made the one (and really only) change of stopping the consumption of onions the problem quickly resolved. So, yes, unlike viruses, I do think many plants are indeed out to get us. For me at least, onions are one of them. If you are eating onions and are also experiencing dry eyes and night vision problems you might want to try to replicate my findings.
That’s it for now. Overall, my health and well-being is currently very good. I’ll post a more comprehensive health update in August.
The conquest of scurvy and the discovery of vitamin C has been touted as one of the great accomplishments of medical science.
Here’s a dictionary definition:
Scurvy is a disease resulting from a deficiency of vitamin C, which is required for the synthesis of collagen in humans. The chemical name for vitamin C, ascorbic acid, is derived from the Latin name of scurvy, scorbutus, which also provides the adjective scorbutic. Scurvy often presents itself initially as symptoms of malaise and lethargy, followed by formation of spots on the skin, spongy gums, and bleeding from the mucous membranes. Spots are most abundant on the thighs and legs, and a person with the ailment looks pale, feels depressed, and is partially immobilized. As scurvy advances, there can be open, suppurating wounds, loss of teeth, jaundice, fever, neuropathy and death. Scurvy was at one time common among sailors, pirates and others aboard ships at sea longer than perishable fruits and vegetables could be stored and by soldiers similarly deprived of these foods for extended periods.
As defined, and as we’ve all been told and led to believe, scurvy is the result of a vitamin C deficiency. But is there any truth to it? Surprisingly, there’s not much. What you are about to learn is that there is actually incredibly weak evidence linking scurvy to vitamin C deficiency. You’ll learn that there’s very compelling evidence to show that scurvy is caused by a toxicity condition, and not a deficiency condition at all. You’ll soon realize that scurvy has also not been conquered; rather it has just been renamed and rebranded with other more modern disease labels.
To investigate the scurvy story, I read, and I’ll quote from, this book :
LIMEYS – The Conquest of SCURVY by David I. Harvie
David I. Harvie’s book is a good read and a good historical account of the scurvy story during the Age of Sail. His book very much supports the story that scurvy is a vitamin C deficiency disease. However, the last chapter of his book does list some modern day thinkers and other organizations that do refute the vitamin C theory.
Scurvy – the great disease of Sailors
One of the most important pieces of evidence we need to consider is that scurvy was by far most prevalent and common among sailors while aboard ships at sea. Almost all of the historical accounts of outbreaks of scurvy were of crews of various sailing expeditions. Although there are accounts of “land scurvy”, they represent a small fraction of recorded cases of the “outbreaks”.
Therefore, during the Age of Sail, scurvy was almost uniquely confined to inflicting sailors, and especially the crews of the British navy. So much so that the primary organization investigating the cause and treatments of scurvy was the Royal Navy. Since scurvy was widely accepted to be predominately a ship-side disease one of the strongest early theories regarding its cause was that it was the cold damp and stale air of the on-board living conditions. The cold, stale air theory persisted for 50 or more years. The Royal Navy developed better ventilation systems for their ships to try to prevent outbreaks of scurvy. However, the better ventilation systems yielded negligible results in combating the disease.
The second most important piece of evidence that we need to appreciate is that the “outbreaks” of scurvy usually started to occur after only 6 to 8 weeks at sea. Very oddly, the general public, and even sailors while on dry land, weren’t commonly getting the disease.
However, the worst effects of scurvy were seen at sea, and it is a sea disease that it is characterized.
LIMEYS – The Conquest of SCURVY – page 18
James Lind – and the first significant Clinical Study in medicine
What’s regarded as one of the first clinical studies in medicine is that by James Lind in 1747. Lind was investigating a possible treatment for scurvy. Lind was not investigating the causes of scurvy because he presumed he already knew the cause. Therefore, he was only looking for remedies.
As a result of his practical observations with the Channel Fleet, Lind himself was among those that were inclined to believe cold, moist sea air was the most important precondition.
LIMEYS – The Conquest of SCURVY – page 86
If you’ve read my eBooks and blog posts you’ll know that I’m not exactly a fan of clinical studies used in so-called medical research. Nor am I a fan of evidence based medicine (relying on big data sets). I have a lot of reasons for disliking clinical studies. The biggest reason is that by almost exclusively relying on statistical outcomes researchers are often not even attempting to use genuine critical thinking and problem solving skills.
Some other reasons I don’t like clinical studies is that they are so often fraudulent, or conducted so poorly that they are meaningless. Many studies are probably just deliberately misleading to promote the financial interests of their sponsors. Or, stated more concisely; many clinical studies are just rigged pharma industry propaganda.
Regardless of my personal views, the ultimate acid test for the usefulness of clinical studies is looking at the real world results they’ve yielded. With there now being millions of peer reviewed clinical studies published, are we, as a society, any better off health wise than we were 50 years ago? No, we are not. On the contrary, we are only vastly sicker, more diseased in every way imaginable, and are dying sooner.
Lind’s study is rather straightforward, and is documented in its entirety in just a few paragraphs. Lind’s study included 12 men and lasted for just 14 days aboard the ship named Salisbury while at sea.
Lind divided the 12 sick sailors into six pairs, and provided each 2-person arm of the study with a different supplement to their diet. These were: cider, vitriolic elixir (diluted sulfuric acid), vinegar, sea water, two oranges and a lemon, or a purgative mixture. Of course, we sure wouldn’t expect to see much benefit to come from the vitriolic elixir (diluted sulfuric acid), vinegar, sea water or purgative mixture. There was no control group in Lind’s study.
Lind claimed that one of the two men treated with the two oranges and a lemon had recovered and that the other man only somewhat recovered. Of course there was no long-term follow-up to determine if the treatment had only put the men into a temporary remission or not. So, the famous clinical study used to claim that vitamin C is a preventive and cure for scurvy is primarily based on merely one person (maybe two) having seen some temporary relief in their symptoms. What’s conveniently glossed over by modern day medical historians is that the basic diet used by the navy was not completely devoid of vitamin C. Raisins and black currants were a staple aboard ships in this era. Even Lind documents this in his own study write-up.
They lay together in one place, being a proper apartment for the sick in the fore-fold; and had one common diet to all, viz. Water-gruel sweetened with sugar in the morning; fresh mutton-broth often times for dinner; at other times puddings, boiled biscuits with sugar; and for supper, barley and raisins, rice and currants, sago and wine, or the like.
About 1 lb of raisins were allocated per man per week. Additionally, black currants actually contain quite a lot of vitamin C too. With one 80g serving of black currants providing almost 200% of the RDA for vitamin C. The navy diet also often included both potatoes and peas; another source of vitamin C.
There’s also some modern day speculation that Lind didn’t actually conduct this study, but rather that he might have just made it up.
Source: James Lind and Scurvy: The First Clinical Trial in History?
Wouldn’t it be ironically fitting if Lind’s study was indeed fraudulent? It would sure fit right in today with so many other fraudulent or rigged medical studies.
Nonetheless, there’s another major flaw in Lind’s study. Even though he knew that the scurvy was primarily caused by being aboard ships, he’s only looking for some therapeutic treatment to remedy it. In other words, he doesn’t appear to consider that there’s possibly an unknown toxic agent at play (other than cold, damp air) while being on board. So, his upfront bias is only allowing him to consider the disease to be that of a deficiency. Therefore, he adds supplements to the diet, rather than selectively eliminating items from it.
So uncompelling are Lind’s study results, even Lind himself does not really believe in the curative properties of oranges and lemons to prevent scurvy. So much so that he spent the next several decades of his career as a navy surgeon trying to have the air circulation aboard navy ships improved. Likewise, it took the British admiralty about another 100 years to fully adopt lemons and limes as a possible preventative measure against scurvy. But, a lot of other changes were made in the British Navy over those same 100 years too. There is one very important one we’ll discuss a bit later.
Just as importantly, even after the British Navy adopts the provisioning of lemons and limes as a somewhat standard practice, there are expeditions where it completely failed to prevent the outbreak of scurvy. Captain Cook regarded limes and lemons as being useless in combating scurvy.
I entirely agree with you that the dearness of the rob (the juice) of lemon and oranges will hinder them from being furnished in large quantities. But I do not think it is so necessary; for though they may assist in other things, I have no great opinion of them alone. Nor have I have a higher opinion of vinegar.
Captain Cook in a letter in 1776.
That’s correct. Lemons and limes didn’t at all reliably prevent scurvy, nor did it really very often cure scurvy either. The use of lemons and limes yielded very, very inconsistent results. So much so that even after conducting several large scale experiments with supplying them the Royal Navy never concluded that it actually worked. Isn’t that odd, huh? Clearly then, there’s something very wrong with the vitamin C deficiency theory.
There were other remedies attempted to prevent and treat scurvy. Just as there is today, there were charlatans and frauds pushing bogus pills and such.
In the face of two centuries of conflicting evidence and hearsay on remedies for scurvy, it may have been easy, if wholly inexcusable, for the Admiralty to rely on the kind of partisan lobbying that enabled a ‘society doctor’ as Joshua Ward to have his fraudulent pills authorised.
LIMEYS – The Conquest of SCURVY – page 147
Hmm… is this the early genesis of the pharmaceutical industry’s lobbying practice?
But, rather than pills, acidic and alcoholic beverages and fermented foods were the much more commonly attempted treatments.
Charles Bisset was another Edinburgh-trained surgeon who had served in the West Indies. In his treatise of 1755 he blamed salt provisions and heat, and recommended vegetables, wine, rum punch, spirits and in particular rice.
LIMEYS – The Conquest of SCURVY – page 86
Interestingly, one of the most common and standard therapies applied for scurvy was bloodletting.
Humans and Guinea Pigs
Another great claim of medical science is that of all the mammals on the planet, it’s only humans and guinea pigs that can’t endogenously synthesize their own vitamin C.
The claim is that after millions of years of evolution we humans have somehow lost the gene needed for it. We therefore need to get our vitamin C regularly from foods or from supplements. Doesn’t that sound a little suspect to you? I mean seriously, are we supposed to believe that the lowly rat can produce its own vitamin C, yet we humans, the species at the pinnacle of evolution, or of God’s creation, can’t? Maybe, just maybe, the “lost gene” theory is just more bad science? For myself, after about 5 years of virtually no vitamin C in my diet, I had this interesting statement show up on a 2019 lab test.
Odd huh? But, it does appear that I may have developed scurvy induced tumours.
Scurvy as a deficiency disease
Even under the slightest bit of scrutiny the theory of scurvy being a deficiency disease quickly falls apart. Once again, the biggest red flag going up here is that the disease commonly developed after being at sea for only 6 to 8 weeks. That just does not at all fit with the reality of life in Northern Europe in the 15th to 20th centuries. If scurvy were to develop in 6-8 weeks due to a vitamin C deficiency then at least half of the European and Russian populations would have died off each winter. Of course, that did not ever happen. Once again, therefore the vitamin C theory must be just simply wrong.
If we consider more modern day examples of prolonged starvation in large populations there is also a stark lack of scurvy being recorded. As I wrote about in my eBooks both the German and Japanese run POW camps from WWII provide clear evidence. Especially so in the Japanese-run POW camps where their prisoners were generally provided just one cup of white rice per day. There were all kinds of infectious diseases recorded in these camps, and many prisoners were brutally starved to death, yet there is almost no record of scurvy. How’s that possible? According to the vitamin C deficiency theory all of these prisoners should have died in six months or less from scurvy.
Somewhat likewise for the German-run POW camps – there’s little to no mention of scurvy. But, at least in the German-run POW camps potatoes were part of the food provided and would have been a source of some vitamin C. However, assuming the potatoes were boiled, they would have only provided a small fraction of the claimed to be daily requirement of vitamin C.
There are many other examples from around the world we can add to the evidence. Here are just a few that come to mind.
The Maasai of Africa whose traditional food is mostly Blood and Milk from cows. No source of vitamin C, yet, no scurvy.
The Inuit of Northern Canada where they live their entire lives without any source of vitamin C. Yet, no scurvy.
People following the muscle meat only carnivore diet for years. No source of vitamin C, yet, no scurvy.
My own experience. I’ve had virtually no vitamin C in my diet for the last 5 years, yet I have no sign of scurvy. On the contrary, my teeth and gums are now probably the healthiest they’ve been in the last 20 years.
So, what’s really going on here? The answer is the theory of scurvy being a vitamin C deficiency disease is obviously wrong. Okay, if scurvy is not a deficiency disease, then what is it? How about we consider it to be caused by an acute poisoning?
Scurvy as an acute poisoning
One of the major challenges for navies from the 18th through to the 20th centuries was the provisioning of ships with sufficient food stores to last them for potentially multi-year expeditions. It wasn’t so much the massive volume of food that was needed to be provisioned, rather it was trying to preserve and keep it from quickly spoiling while at sea. Canning using pasteurization hadn’t been invented until 1862 and didn’t come into widespread use until the late 1880’s. Steam powered refrigeration wasn’t adopted aboard ships until the early-mid 20th century. Therefore, some of the mainstays of the ship’s provisions were heavily salted beef and pork, oats, beer, very dry biscuits, and something called “portable soup”.
Quite remarkably, Portable Soup was a staple and standard provision for ships in the Royal Navy for almost 200 years. How long was Scurvy most prevalent in the Royal Navy? For about the same 200 years!
In 1757, the British began stocking their ships with a “portable soup.” The “portable soup” consisted of “all the offals of oxen killed in London for use of the Navy” with salt and vegetables added in. The soup, however, was dried so that it had the appearance of slabs of glue. Although the “portable soup” was unappetizing, it was perfect for the navy because it had a shelf life of years. In addition to the supplies stored at the beginning of each voyage, ships often traded for additional supplies in foreign ports and lands. In particular, rice, wince and other hard alcohols were particularly valuable when trading.
What are the “offals” of oxen? Well, they are simply quite awful.
Offal is a pretty broad term which not only includes the internal organs and entrails, but also includes the miscellaneous trimmings of an animal. It essentially includes everything except the muscle and bone.
Portable soup sounds rather disgusting to me. But, it couldn’t have been that bad because this “portable” soup was an absolute staple among British Navy and merchant ships for almost two centuries.
The portable soup may have also been used for dipping and softening the other navy staple food of rock-hard biscuits.
It was served with a pound of ship’s biscuit. Hard, ¼ pound disks of flour, baked 2 or 3 times until all moisture was completely gone. The men would soak these, usually breaking them into their stews, or letting them soak up the juices from their meat ration
To make it ‘portable,’ the soup was made as normal but then reduced using prolonged heating until it was gelatinous and dried. Let’s see here; taking the liver and kidneys with their high retinol and retinyl esters content and boiling it at high heat (enough to drive off the steam) for extended periods of time? What could possibly go wrong with that? How about the production of large amounts of retinoic acid?
Is Scurvy really retinoic acid poisoning?
Once again, one of the important points we really need to appreciate is that sailors usually developed scurvy within just 6 to 8 weeks after being at sea. But, based on worldwide and real world data we know that’s just way too fast for the disease to have developed from a deficiency condition. So, how about considering a stress test case with direct exposure to retinoic acid? Here’s just one such example: From:
Hi I have been on accutane for 2 weeks and have had really sore, red, sometimes bleeding gums for about a week now. Has anyone experienced this while on tane? This is my second course and I haven’t experienced it before, and never heard of it as a side effect so thought I would check if anyone else has had it or if I should go to the dentist to get it checked out! Thanks in advance.
Could the “portable soup” have been made to be any more toxic? Well, yes, it could of and probably was. The portable soup, as well as some other provisioned foods, were packaged in tin cans where the joints were sealed with a lead-based solder. So, we are probably talking about retinoic acid and lead poisoning combined. This theory is supported by the modern findings of lead poisoning in the human remains of the crew of the famous Franklin Expedition (nicely preserved in Canada’s frozen tundra for the last 170 years).
What about “land scurvy” ?
So far I’ve mostly discussed scurvy inflicting sailors while they were at sea. What about cases of land scurvy? There are indeed quite a few cases of scurvy reported for non-sailors. What then would have caused these cases? Well, we need to appreciate that “portable soup” was not exclusively used by the Royal Navy. It was also sold to the general public.
Mrs Elizabeth Dubois had been advertising the sale of her portable soup in the British newspapers since at least November 1746 when they appear to have first been available in this country.
But, of course portable soup couldn’t have resulted in all cases of land scurvy. We do know that eating organ meats was quite a common practice in England during this era too.
Okay, what about in North America? Well, there was another well established, semi-industrial scale, operation that we need to know about during this era. That was the harvesting of cod livers, and cod liver oils. Here’s a sketch and historical account of the practice from the early Canadian archives.
Drawn on the side of a map of America, this is the only existing image of a Newfoundland cod fishing station. From the days of Cabot and perhaps before, fleets of European fishermen sailed to the banks, and they soon discovered that they could stay longer and bring back more fish if they set up shore stations to split, salt and dry the catch. Some of these men may have overwintered. This would have been an early source for Americans to have gotten trade goods from the Europeans.
A View of a Stage & also of ye manner of Fishing for Curing & Drying Cod at NEW FOUND Land.
A. The Habit of the Fishermen (clothing, hooded coat, boots and apron)
B. The Line
C. The Manner of Fishing (casks were slung over the side of the ship and fishermen stood in them)
D. The Dressers of ye Fish
E. The Trough into which they throw ye Cod when Dressed
F. Salt Boxes
G. The Manner of Carrying ye Cod
H. The Cleansing ye Cod
I. A Press to extract ye Oyl from ye Cod Livers
K. Casks to receive ye water & Blood that comes from ye Livers
J. Another Cask to receive the Oyl
K. The manner of Drying ye Cod
Some fishermen collected the oil out of the fish they caught for cooking.
So, it looks like ye Oyl from ye Cod Livers was used for both North Atlantic trade and for local cooking. But, what happened to all ye Cod Livers they harvested?It was often put in barrels and left to ferment in the hot sun, and the resulting fermented mush later used as a spread on toast. Yum, huh?
It looks like the practice of canning and eating cod livers has been going on in Canada for about the last 400 years and continues to be so even today. Of course, this practice was not just limited to the Canadian east coast, it has also been going on in the Norwegian and Scandinavian countries for almost as long. Here’s an example of some current products available.
The Crusades, however, provide an example of one written account of scurvy during the 13th century. During Lent, when soldiers abstained from meat (except eel) and restricted their diets, a scurvy epidemic likely unfolded as “the barber surgeons were forced to cut away the dead flesh from the gums to enable the people to masticate their food.” However, it is noted that the Crusaders believed that the disease was caused by eating eel which supposedly ate the dead.
Well, I don’t know about eel eating the dead, but what I do know is that eel is very oily and is also very high in vitamin A too.
Modern outbreaks of scurvy
Even with the determination of vitamin C as the prevention and cure for scurvy there are still modern day outbreaks of the disease.
In Canada the years 1945-65 were marked by outbreaks of scurvy in bottle-fed infants given evaporated milk (then lacking in vitamin C).
Infantile scurvy emerged in the late 19th century because children were being fed pasteurized cow’s milk,
What do pasteurized cow’s milk and “portable soup” have in common? My bet is that it’s quite likely to be only retinoic acid.
Hooray – Scurvy is conquered and CURED!
Yes, we’ve all been led to believe that scurvy has been conquered and almost fully eradicated. But, is that really true? Well, very likely it’s not. Broadly speaking, scurvy manifested as two major disease conditions:
Swollen, bleeding gums, leading to loose teeth, and the teeth eventually falling out.
Ulcers and blisters on the lower limbs.
However, aren’t these same primary scurvy disease conditions still very common today? Oh yes, they are indeed:
Gingivitis and Gum Disease
Gum disease. A high percentage of older adults have gum disease. About 2 in 3 (68%) adults aged 65 years or older have gum disease.
How about we look at some nice modern day diabetic gum disease?
Common signs and symptoms of diabetic gum disease
Red and swollen gum that bleeds on brushing
Yellowish plaque deposits
Pus exuding from gums, tenderness or swelling in gums
Mobility of teeth
Consistent foul odour from mouth
Next up, here’s an early era drawing of the effects of scurvy on the lower limbs. Clearly there are some distinctly different manifestations of the disease. One of dark brown-black blisters, and then the other of inflamed and necrotic flesh.
But, aren’t these images not almost identical to diabetic ulcers so commonly reported today? Please judge for yourself.
“Diabetic dermopathy (skin spots) is the most common dermatosis associated with diabetes. Similar to necrobiosis lipoidica, it presents with reddish-brown patches on the shins, but they are usually much smaller (0.5 to 1.0 cm) in size and greater in number (five to 10, or more lesions). Skin spots gradually resolve to leave a brown, atrophic scar. They are thought to be caused by vascular disease, but there is no correlation with the extent or duration of diabetes.”
“ Leg rash is a common symptom in diabetes and can be caused by many reasons and can be prevented.”
So, no, “scurvy” has not been conquered. It has just been renamed, rebranded and hidden behind the modern day disease labels of Gingivitis, Gum Disease, and Diabetes.
Now with the massive supplementation with vitamin C in Western society today, why do we still have this massive incidence rate of “scurvy?” Quite clearly, “scurvy”, AKA diabetes, is not a vitamin C deficiency disease. Another way of stating it, “scurvy” is vastly accelerated diabetes. Either way, both “scurvy” and diabetes are the result of a poisoning.
Please have a think about it, and comment as you see fit.
From Wikipedia,: A Roman dodecahedron or Gallo-Roman dodecahedron is a small hollow object made of copper alloy which has been cast into a regular dodecahedral shape: twelve flat pentagonal faces, each face having a circular hole of varying diameter in the middle, the holes connecting to the hollow center. Roman dodecahedra date from the 2nd to 4th centuries AD and range from about 2-4 inches across.
The Roman dodecahedron remains a mystery, and no one really knows what they are.
A couple of years ago when I first learned of these objects I immediately had a pretty good idea as to what they really are. Now, with getting more and more bothered by what’s going on in the world of health related topics, I thought it’s time to take a departure from them here on this blog and discuss something else for once.
There are a number of prevailing theories as to what Roman dodecahedron were used for. One is that they were somehow a range finder device. Another one is that they were used for knitting gloves. But, I don’t think either is correct.
If someone has a really wild imagination, they might think these are 3-D bronze models of corona viruses as theorized by ancient Roman virologists. Although that would correctly put the ancient level of virology science on par with that of current modern-day virologists; no, that’s not it either.
One major clue we have is that some of the dodecahedrons have been found to have a wax residue in their central cavity.
So, what are they? I think they are simply little portable camp stoves used by soldiers while travelling and when stationed at their outposts. The camp stove would have been mostly fueled by a wax candle set up within the hollow core.
The dodecahedrons are actually a bit ingenious too. The shape allows the candle’s flame to be shielded from the wind. The various sized holes would have accommodated different sized candles with different heating capacities. The other holes around the perimeter provide lots of air flow to the burning candle.
The stand-off knobs around the perimeter allow a small pot or cup to be held above the candle’s flame and allow the heat to be more evenly distributed over the bottom surface of the pot. The dodecahedrons can simply be rotated and stood-up on the most appropriate size opening for the cooking task at hand. Say, using a smaller candle for just heating a cup of water and a larger one used for cooking a small meal. So, the dodecahedrons are miniature versions of modern day cooking ranges where we have a number of different and variable sized burners. But, the dodecahedrons are in a nice small portable package that would have been easily carried in a Roman soldier’s pack.
I happen to have a modern day version of a portable camp stove..
Of course, this unit is fueled by propane gas and not a candle.
Anyways, please have a think about it and share your thoughts as to what you think the Roman dodecahedron are.
I’ve now reached the seven-year point on my ultra-low vitamin A diet experiment. My overall health has remained good this year. As like with last year’s update, I’d say I’ve only seen some small incremental improvements this year. I feel that my skin texture in some areas has slightly improved, and that I have noticeably less gray hair on my chest. But I do still have two age spots on my face that seemed to have only faded a bit more in colour this past year. I think these two age spots are ever-so-slowly improving but I have no idea if they will ever fully recover. It could be that the skin has been permanently damaged in these areas.
Thus, as expected, this year I don’t have any big health improvements to report on. However, what’s surprising, even after seven years of following my extremely low vA diet, there is still some progress being made. It’s quite clear to me now that making a full and complete recovery from vA toxicity is a very long and slow process.
I’ve not changed my diet much over the last year. I’m still sticking to what I consider to be my primary “safe” foods. That’s rice, black beans, and beef / bison.
However, as I did last year, for a few months this year I swapped out the rice and replaced it with a simple white bread. The primary reason I made that change was out of the concern of getting too much arsenic from the rice. However, I did not have any lab work, or noticeable health reasons, to support that concern. I did email the rice producer of the brand that I use regularly asking them about the arsenic content of their product. They once again claimed that their products have no arsenic. Of course, I don’t really believe that, and they did not back up their claims with lab reports. Anyhow, after three months of eating the white bread, I decided to change back to mostly using white and brown rice again as a source of carbs. There’s no big reason that I changed back, other than I find the rice slightly easier to digest.
I’m still getting quite a lot of emails from people asking about my personal diet. I don’t think people should try to pattern their own diets based on what I do. I really think people need to find what works best for themselves. Moreover, I want to be clear that I’m not continuing to follow my extreme (and admittedly somewhat crazy) diet for health reasons. I’m sticking to it because I’m trying to prove a scientific point. Therefore, I don’t think other people need, or should try, to mimic my ultra-low vA consumption. Rather, I think that just being on a low vA diet is probably wiser, safer, and more sustainable.
Anyways, for those who are interested, my current diet is composed of:
White / Brown rice – usually white rice for 2-3 days, and then followed by a day with brown rice
Black Beans – organic canned
Beef / Bison – usually ground – about 75% of the time I go with Bison
Salt & occasionally some onion powder
My daily amounts are usually:
Rice ~ ¾ cup (measured dry)
Black Beans ~ 250- 350 ml ~ ¾ of a can
Beef / Bisson ~ 300 – 400 grams
I generally eat two meals per day and don’t snack much. But if I do snack it’s usually toasted white bread with honey.
I very rarely take supplements. However, I did try a thiamine supplement for several months this year. I had no detectable positive or negative response from taking it and have therefore stopped it.
Daily Calorie Consumption
I’ve been tracking my daily food consumption a bit more closely this year using a mobile app (MyNetDiary).
My daily food intake is usually about 1,500 calories. Some days it’s a bit more, some days it’s a bit less. Anyways, that’s probably about ½ of the daily calories that I was consuming before starting my low vA diet. Although 1,500 calories per day appears to be too low for an adult man, I find it perfectly adequate. Actually, I think that 1,500 calories per day is still a bit too much for me now.
As I have for the last 4-5 years, I’ve maintained a steady weight again this year. I’m holding at about 160-163 lbs (73 kgs). However, I do feel that I am still about 5 lbs (2kgs) overweight. For some reason, that last 5 lbs is just very stubborn and wants to hang around. But I’m not concerned enough about it to try harder to lose it either.
Some people might assume that the reduced need for calories is due to my older age. However, I don’t think so. That’s because I know a young man who’s also been on a low vitamin A diet for the last two years and he’s reported a very similar finding. His daily calorie intake is about 1/3 to ½ of what it was before he started with the diet.
I think the explanation for needing fewer calories can be at least partially explained by:
Overall metabolism is just running more efficiently.
A reduced rate of cellular turnover.
A significant reduction in background inflammation. I’ve read that about 25% of our daily calories is used just to fuel our immune system. Now with a low vA status, and my body no longer constantly auto-immuning in a futile struggle to fight off a phantom pathogen I need 20% or so fewer daily calories.
Whatever the mechanism is, I think this reduced need for daily calories is quite intriguing.
I get a weekly summary report from my food diary tracking app. Here are some noteworthy warnings I get each week.
Your average daily 115 mg of calcium does not reach 1000 mg recommended for you. Rich sources include dairy products (milk, yogurt, cheese), calcium-fortified soy milk and orange juice, sardines and salmon with bones. The calcium in dark green leafy vegetables is less bioavailable since it binds with plant acids.
Your average daily 4 IU of vitamin A does not reach 3000 IU recommended for you. Animal sources: liver, milk, cheese, and eggs. Plant sources (in the form of beta-carotene): orange colored fruits and vegetables (carrots, sweet potatoes, apricots, cantaloupe, and pumpkin) and dark green leafy vegetables (e.g. spinach and kale).
Your average daily 0 mg of vitamin C does not reach 90 mg recommended for you. Rich sources: most fruits and vegetables, but especially citrus, strawberries, cantaloupe, spinach, broccoli, and peppers.
Your average daily 115 mg of calcium does not reach 1000 mg recommended for you.
It looks like my daily calcium intake is about 1/10th of the RDA. I knew that I was low on calcium intake, but not that low. I just assumed that the beans and water I consume would somehow provide enough calcium.
But seeing this warning show up in the weekly report I was getting a bit concerned about what the long-term impact of following my diet for the last 7 years has had on my bones. Thus, I recently had a bone density scan (DEXA) performed. The scan results were surprisingly very good. My bone density is perfectly normal for my age, and I was told that I have absolutely nothing to worry about. I think this is another big win for a low vA diet. Apparently, that recommended 1000 mg / day is not needed if vA is not silently picking away at our bones. And, we probably don’t want a bunch of needless extra calcium in our diet that might otherwise contribute to clogging our arteries etc.
Although seeing that my current bone density was normal for my age was reassuring, I’m not exactly thrilled with that result either. I don’t feel that having just normal bone density for my age is ideal. I’d rather it be better than normal. Unfortunately, I have no reference data as to where I started from regarding bone density. I don’t know if it’s gotten better or if it’s gotten worse in the last 7 years. So, to be on the safe side I’ll probably start adding some mineral water to my diet this coming year. I’ll re-test my bone density again in 5 years.
Vitamin A warning:
Your average daily4 IU of vitamin A does not reach 3000 IU.
I’m not sure if that 4 IU the app is reporting is calculated as being sourced from the beans or from the beef / bison. Naturally, I wish it was closer to 0 IU /day, but I’m still okay with it. Oh, I know there will be a few naysayers who’ll claim that it’s those 4 IU that’s keeping me from going blind and not having all of my epithelial / endothelial tissues and their corresponding organs disintegrate. But that’s one of the reasons I make regular blood donations. I think the blood donations easily offset the trivial 4 IU I still might get from food.
Vitamin C warning:
Your average daily 0 mg of vitamin C does not reach 90 mg recommended for you.
I knew that my vitamin C intake was very low, but kind of like with calcium, I was assuming it would somehow be OK. Based on the early toxicity studies that I had read I was also pretty sure that scurvy was misdiagnosed vA toxicity. But there’s no question that 0 mg of vitamin C/day is awfully low.
Still, I’m not concerned enough about it, and I don’t plan to supplement with vitamin C.
Anyways, after ~5 years with a very low vitamin C intake I have no sign of scurvy. It’s the opposite. My teeth and gums are feeling really strong and solid; like never better. I think this is another win for a low vA diet. However, I do still think vitamin C is probably important in the early stages of taking on a low vA diet.
Here’s an interesting little ditty to consider:
A series of studies using guinea pigs with chronic latent vitamin C deficiency has provided clear evidence that bile acid synthesis is reduced in this condition.
Turley SD, West CE, Horton BJ. The role of ascorbic acid in the regulation of cholesterol metabolism and in thepathogenesis of artherosclerosis. Atherosclerosis. 1976 Jul-Aug;24(1-2):1-18. doi: 10.1016/0021-9150(76)90060-5. PMID: 942515.
Could it be that without adequate vitamin C we have a much harder time in clearing vitamin A via bile? I don’t know, but maybe that’s the real mechanism of action of how vitamin C appears to be able to prevent scurvy?
Sleep quality and Dreaming
One of the health changes that I had reported on in my first eBook was the return of dreaming at night. I was just trying to be complete and reported on it thinking it was probably just a weird personal little quirk. I now think this is an important finding as a number of other people are reporting the same effect. And thus, it’s not just a personal quirk.
I’ve attributed the return of nighttime dreaming to a likely drop in cortisol levels (but I have no personal lab tests to back up that theory). Regardless, for the last 5-6 years of my low vA diet I was getting a pretty good sleep. However, what’s surprised me is that it has kind of kicked into high gear this last year. The intensity and vividness of my dreams is often rather amazing.
Also, now when I go to bed I almost always fall asleep within just a few minutes of putting my head down on the pillow. I can also nap almost on demand, being tired or not, and almost at any time of the day. I’m kind of like a cat or dog in this regard where it appears these animals can nap anytime they want during the day.
The bigger change that I’ve noticed is that I now begin to dream in what seems to be only minutes after going to sleep. It also appears that I dream almost all night long. The same thing happens if I take even a one-hour long nap. I nearly immediately start dreaming. It’s quite remarkable. But like with so many other things on this diet, the intensity of the dreaming changes from month-to-month. Nevertheless, compared to where I started from seven years ago, my sleep quality has vastly improved. How can that not be a good thing? Clearly, vitamin A toxicity can profoundly and negatively affect our cognitive wellbeing.
I feel that my cardiovascular health is about the same as it was last year. The numbers are:
Historical the numbers looks like this:
My resting blood pressure is usually around 110/60 and my resting heart rate is about 50-55 BPM. My HbA1C has remained at 5.1% this year.
I was planning on getting more lab work done this year for this 7-year update report. I would have liked to have had a liver enzyme panel and a cortisol level test done. However, these are not discretionary labs that my GP would authorize. Last year I used an on-line lab service called LetsGetChecked.com. I was quite impressed with their service last year and was planning on using them again this year for these additional labs. Unfortunately, they have stopped providing their services in Canada.
Vision and Eye Health
I had another comprehensive eye exam performed a few weeks ago. The results were that my eye health and vision remain excellent. There’s no sign of any eye disease. There’s no glaucoma, no retinopathy, no cataract, no macular degeneration, etc. The pressure in the eye is again a low normal (no inflammation). My vision is also very good. It’s not quite perfect-perfect, but I still don’t need reading nor driving glasses. At the end of the exam, the eye doc said: “Whatever it is that you’re doing with your lifestyle and diet, keep doing it because your eyes are in great shape”. Naturally, I did not mention my low vA diet.
However, like what happened a few years ago, I did go through another period of poor night vision for several months this year.
I continue to make regular blood donations. I was having some quirky issues with the plasma donations (my blood was sometimes clogging up the machine), so I’ve gone back to just making regular whole blood donations.
Exercise and Fitness
I’ve been far less physically active this year than compared to last. The primary reason is my new work-from-home lifestyle does not require me to make the daily bike commute. The other reason is that all our gyms and other fitness facilities have been shut down for most of the year.
As with last year’s update, the takeaway from this year’s is that it’s clearly more evidence that so-called “vitamin A” is not a vitamin at all. I mean seriously, after seven years of having virtually no vA in my diet, and having no adverse effects, and my health has only gotten vastly better, how can anyone still legitimately claim it to be a “vitamin” needed by humans? I firmly believe that vitamin A is nothing more than a toxin and we are therefore hugely better off without it. I’ll continue with my ultra-low vA diet for at least the next three years.
Other thoughts – the current viral issue
I’ve spent a lot of time this year learning about so-called viruses. I say so-called, because I quickly concluded that they are not even really “viruses” at all. At least not in the sense of the accepted definition of that term. I see the science of virology as being as dodgy and on par with that of so-called vitamin A science. Vitamin A is not a “vitamin” and “viruses” are not really viruses. I’ll try to write more about this topic in the new year.
I’ve been a bit quiet for the last six months. But, I’ve not at all lost interest in the vitamin A research topic. It’s just that, like with millions of other families, we’ve been significantly impacted by the COVID-19 crisis. Fortunately though, no one in my family, nor myself, have been sick from COVID.
Redoing the 1925 Wolback and Howe study
In last year’s community survey, and in forum posts, I inquired about and wrote about interest in redoing the 1925 Wolback and Howe study. Towards that goal I had submitted a proposal to have this study replicated at an American University. However, due to the outbreak of the COVID pandemic, that proposal was cancelled.
This does not mean that we won’t be redoing this study at all. Rather, it just needs to be put on hold until after things get back to normal. I’m still very interested in having this study replicated. If you want to help me to get it re-organized please contact me directly.
Detox setback / diet failures / diet successes
The detox setback cycle is still being encountered by too many people. It’s often not short term and is causing people to abandon their low vA diets. In the past we’ve had several theories as to why people are encountering the setback cycle. We’ve suspected a vitamin B deficiency due to increased demands of higher carbs etc. on the B vitamins. We’ve suspected the lack of zinc and other resources needed to sustain the increased requirement for ADH and ALDH enzymes. We’ve suspected that a possible increase in protein intake is causing a surge of stored retinyl esters being released from the liver into bile, and with that the addition vA is being reabsorbed into circulation.
Probably all of the above suspected mechanisms are at play to some degree. Of course, it’s going to vary by individual. Whatever the reasons and mechanisms are, we’ve still not pinned it down enough to where people can reliably avoid getting into this detox state. I see this as a very serious problem, and one that we need to solve. But, it’s way beyond my capabilities to come up with a solution. We probably need some dedicated research on it.
Of course there’s a lot of good news with the low vA diet too. We are still seeing success stories. I hope there are many more successes as more people get into year 3+ with their low vA diets.
Over the last six months I’ve been looking more into how and why vA toxicity is likely causing both Type I and Type II diabetes. There’s actually a lot of research back over the last 30 years that supports this theory. So, diabetes will likely be my primary topic of interest next year. I’ve gotten a private email (not shared on my forum) from a parent about their child who has reversed Type I diabetes using a low vA diet. Although it is just one case, I see it as being really important. Firstly, it’s so important to know that the disease can be reversed, and is not always life-long. Secondly, if reversing the disease has happened once, it can most certainly happen again.
My personal health remains good. I’d say that I’m still seeing small improvements; such as the last few spots of dry/ damaged skin are improving. In August I’ll post a more comprehensive health assessment with my 7 year update.
I’ve also put up a video sharing my thoughts on the survey results.
For the following questions the instructions were:
For each of the following conditions, please state on a scale of 1 to 10 how severe this condition was BEFORE starting the diet, where 1 is “a minor annoyance,” 5 is “interferes with normal functioning”, and 10 is “severely debilitating.” Then mark how severe this condition is NOW using the same scale.
Therefore, seeing the bars in the charts shift over to the left hand side indicates that the condition is improving or becoming less severe.
I’ve now crossed the six-year mark on my vitamin A elimination diet. That’s a big milestone. I also turned 60 a few months ago. That’s also a big milestone. Except, it’s one that I’d rather not acknowledge as it now places me into the senior citizen category. However, I’ve not entered curmudgeondom just yet.
Like with last year’s update, my health has only slightly improved over this year. However, the accumulation of the annual small improvements is adding up. Subjectively, I’d say that my health is now the best it’s been in the last 10 years. So, as I am getting older I’m getting healthier. I think that’s a pretty neat trick, and especially so when you consider my diet of mostly just three basic foods.
So now, after six years of having virtually no vitamin A in my diet, and for the last three years being officially in a severe deficiency state, I have absolutely no signs of vitamin A deficiency. How can that be possible?
Oh, I know that there are people who’ll claim that it’s the trace amount of vitamin A I get from eating beef that has me still clingy to life. Except, that’s one of the reasons I mostly consume bison. It’s much lower in fat than beef. I buy my bison directly from a rancher here in Southern Alberta. Bison is also not sent to feedlots for finishing, unlike beef where the animals are fed grain and corn. The USDA database reports bison’s vitamin A concentration to be 0 IU / 100g.
Additionally, for the last two years I’ve been making regular blood donations.
I even recently doubled down on it by making plasma donations. Those donations should offset any tiny amount of vitamin A I might get from my food. So, what’s keeping my skin, teeth, bones, and eyes healthy? According to the vitamin A deficiency theory all these tissues should have developed metaplasia or even disintegrated or have become infected by now. But, most importantly, if vitamin A deficiency were a real thing, then I should see at least some early indication of it after six years of virtually no vitamin A in my diet. However, it’s completely the opposite. I have absolutely no sign of it, and I’m just getting healthier.
I had a complete eye exam done a few weeks ago. The results are that my eyes are in excellent health. There’s no sign, like none at all, of any eye disease; no glaucoma, no macular degeneration, no retinopathy. The pressure in the eye is at a low-normal (a good thing). Additionally, I now have no sign of cataracts. My vision is very good. It’s not quite perfect, but it’s still very good for a 60 year-old. The eye doc said that he could give me a prescription for reading glasses, except it would be so mild that there’s not much point in it. If it’s interesting to anyone, I’ve included a link here to the retinal scanning report he provided me. I think this result is very significant because the de facto disease defining conditions of vitamin A deficiency are poor night vision and progressive xerophthalmia. Yet, I have no sign of ANY eye disease, and my day and night vision is very-good to excellent too. Again, how is that possible?
I don’t know about you, but the science that I was taught is that if even a single experiment fails to support a theory, then the theory is wrong. So, it’s time to call it. The theory that so-called vitamin A is an essential “vitamin” needed for eye health, vision, cell differentiation, etc. is simply dead wrong!. Whether you like it or not, it is just a fact. It’s game over for so-called “vitamin” A. Of course, I do know that it will probably take another 5 – 10 years for that to become widely accepted.
I recently had my bi-annual dental checkup. As like for the past three years, everything was fine. No decay, no cavities, the x-rays showed good density in my teeth, and my previous gum recession has nearly completely resolved. After examining my teeth my dentist actually said to me “your teeth look fantastic.” That is the very last thing I ever expected to hear from my dentist regarding my teeth. Although my teeth do feel stronger, smoother and cleaner, I don’t think they look “fantastic”, but hey, I’ll take whatever compliment I can get about them.
This dental result is very important too because one other major sign of so-called vitamin A deficiency is the secession of enamel formation and the development of bleeding gums. Yet, after six years of nearly zero vitamin A intake, my teeth now are in the best shape that they’ve been in in a decade or more. So, what’s all the vitamin A consumption in North America really doing for people’s teeth? It’s clearly not helping. Check this out: CDC: Half of American Adults Have Periodontal Disease
My sleep has remained to be very good, and is always restful. I have no problem falling to sleep quickly. And, as I wrote about before, I continue to dream every night and often experience some rather intense dreaming. So, there’s definitely been some sleep benefit of my low vitamin A diet. I suspect the deeper sleep is mostly due to a drop in cortisol levels.
My weight has remained remarkably steady over the last 4 to 5 years, Most people would probably agree that losing weight is not the difficult part, rather it’s the keeping it off for the long term that’s really difficult. But, for me at least, keeping that weight off has been easy-peasy, like no problem at all.
My physical fitness has remained about the same as it was last year. But, I feel my muscle strength has gotten a bit better. I can now bench-press 225 lbs. Although that’s not particularly exceptional, it’s still not too shabby for a 160 lb senior citizen. My cycling endurance is still good, with long hill climbs being my measurement. I’m telling ya, it’s the rice.
I feel that my cognitive health and mental well-being continues to be very good. My learning ability and memory recall are good, I’m consistently quite calm, relaxed and almost nothing gets me stressed out. Even the occasional hate mail I get, with the childish name calling, doesn’t bother me one bit.
It’s been known for over a decade now that retinoic acid accumulates in the brain, as well in other tissues. It has also been known for decades now too that retinoic acid causes depression, anxiety, significant drops in IQ, and there are hundreds of suicides officially attributed to accutane use, etc. Therefore, it should be of no surprise that reducing the amount of RA nicely accumulating in our brains is going to result in our improved cognitive functioning. I mean, who would have thought it possible?
Updated labs for Cholesterol etc.
My GP would not authorize a requisition for getting updated labs done this year. Last year’s CRP level was <0.3, which is below the detection limit of the test. My HbA1C was 5.1, and my LDL was 1.04 mmol/L and he said that these values are exceptional for a 60 year old. So, his position was that since my current health is excellent, and combined with last year’s lab results, he could not justify the expenditure to our health system.
I really don’t want to personally spend the extra money on getting labs done privately, but am open to doing so if someone wants to help cover the cost.
Blood Glucose levels
I’ve tracked my blood glucose levels for a while now. It seems to hover around the 5.2 mmol/L (94 mg/dl) mark.
That’s a bit surprising considering that I’ve been eating rice three meals a day for the last six years. Maybe rice isn’t so bad for our blood glucose levels after all?
Better tolerance of Hot and Cold weather
One other odd observation I’ve made is that I now seem to be much more tolerant of hot and cold weather. Somehow, my skin and body temperature just adjusts very quickly to the outside temperature. I also almost never sweat in hot sunny conditions. Could this be because I have a lot less of a highly light absorbing molecule in my skin?
Faster wound healing
I’ve noticed that small cuts and bruises heal very fast now. How can that not be a good thing?
In summary, my health remains to be very good. I’ve not been afflicted by the horrible consequences of vitamin A deficiency. I know that I never will – because it does not exist.
But, what we do know, and we know it with certainty, is that vitamin A is a very toxic molecule. We know that the “active form” of vitamin A, retinoic acid, is an extremely toxic molecule. So much so that even back in 1987 the HHS termed it a direct “POISON.” Except, we should all now realize that it is not a vitamin, at all. What is it really? It’s the toxin that has poisoned a large percentage of the human population. It’s also very likely responsible for most of the mysterious chronic diseases slowly killing so many of us, and destroying the lives of our children.
Consider this nice progress report from the CDC on chronic disease:
6 IN 10 Adults in the US have a chronic disease 4 IN 10Adults in the US have two or more THE LEADING CAUSES OF DEATH AND DISABILITY and Leading Drivers of the Nation’s $3.5 Trillion in Annual Health Care Costs
Results: An estimated 43% of US children (32 million) currently have at least 1 of 20 chronic health conditions assessed, increasing to 54.1% when overweight, obesity, or being at risk for developmental delays are included; 19.2% (14.2 million) have conditions resulting in a special health care need, a 1.6 point increase since 2003.
We must do everything we can to turn this situation around.
What’s next for me?
I’ll continue with my diet for at least the next 4 or 5 years. I seriously doubt that I’ll ever again in my life consume any food that has more than negligible amounts of vitamin A or the carotenoids. But, my biggest motivation for sticking to this diet is not for health reasons, rather it’s to prove the scientific point.
I’ll also continue making the plasma donations for at least the next year. Of course, I don’t have some deep hatred for vitamin A. It would be silly to harbor hatred towards inanimate molecules. But, I will do whatever I can to keep expelling every last bit of this vile, poisonous, disgusting, reprehensible and scheming little yellow serial killer from my body.
In October I’ll put up another survey to gauge how people are doing with this experiment. Last year’s survey was put together rather hastily. That’s because that survey was kind of an emergency response trying to uncover why so many people were encountering the detox setback. Therefore, I’d like to do a much better job on his year’s survey. If you have any ideas or questions that you think are important to include in the survey, please let me know, or add a comment on the forum here.
More than 100 million U.S. adults are now living with diabetes or prediabetes, according to a new report released today by the Centers for Disease Control and Prevention (CDC). The report finds that as of 2015, 30.3 million Americans – 9.4 percent of the U.S. population –have diabetes. Another 84.1 million have prediabetes, a condition that if not treated often leads to type 2 diabetes within five years.
Don’t you think there’s a major problem going on here?
That 100 million number should also look familiar. It’s the same as the number of Americans with fatty liver disease slowly creeping up on them. Clearly, something has gone drastically wrong with human health in North America, and worldwide. And, it’s forecasted to just get worse.
The prevalence of diabetes (type 2 diabetes and type 1 diabetes) will increase by 54% to more than 54.9 million Americans between 2015 and 2030; annual deaths attributed to diabetes will climb by 38% to 385,800; and total annual medical and societal costs related to diabetes will increase 53% to more than $622 billion by 2030
To help put that $622 billion dollar cost into perspective, that is almost twice as much as the total amount that all of America spends on gasoline annually. Yes, just the one disease of diabetes is hugely more costly, and of course profitable, than oil! But, that’s still only a fraction of the nearly four Trillion dollars Americans now spent annually on all health care costs. Of course, the human costs and long term suffering are much more devastating. The annual death rate due to diabetes is 2-3 times that of the current Covid-19 disaster. Naturally, we are not talking about just about North America. The diabetes pandemic now afflicts about 500 million worldwide.
If we don’t get this diabetes disease crisis under control it will surely destroy our economy. I do think we can bring this under control… but it’s not going to be easy. Continuing with the current band-aid type treatments is obviously not working. So, to have any chance at effectively turning this crisis around we need to first get to the correct root cause of it.
The last big breakthrough in diabetes research was back in 1921. Canadians Frederick Banting, Charles Best, and James Collip identified and isolated insulin and quickly went on to develop a process for extracting it from animal sourced pancreases. They licensed the patent for that process to the University of Toronto for the princely sum of $1. With that, insulin went into mass production, was priced at pennies per dose, and saved millions of lives. Today insulin is still the primary treatment for the disease. However, insulin is obviously just that; a treatment, and not a cure. And, today the giant pharmaceutical companies have worked their way around that pesky make it free-to-everyone patent and now sell synthetic insulin at what many consider to be extortionary prices.
The question that Banting and Best did not answer was why was the human pancreas failing in the first place? Maybe, like with most doctors today, they too were taught to believe that diabetes and all chronic diseases are just “bad luck”. Sadly, that ridiculous “bad luck” theory of disease causation is very widely accepted and has gone almost unchallenged even today. But, obviously “bad luck” does not cause organs to fail. It’s equally obvious is that the stupid “bad luck” theory is dead wrong because North Americans could not have gotten vastly more “unlucky” over the last several decades. There’s also no way that people living in the American Southeast are significantly more unlucky than those living in the Northwest.
Back in 1921 we did not have an epidemic of obesity and therefore obesity couldn’t be blamed for the cause of diabetes either. And, obesity most certainly can’t be blamed for Type I diabetes since the wasting the disease causes in children is the direct opposite of that. The presumption is that Type I diabetes is just another auto-immune disease, and auto-immune diseases are just more “bad luck”. We are supposed to believe that it’s the confused and rogue immune cells attacking their own host body. Well, if you’ve read my eBooks you’ll know what I think of the “auto-immune” disease theory. In a nutshell, it’s a bunch of rubbish. No, it’s not a confused or defective immune system. Rather, it’s that tissue cells have been poisoned. With their DNA/RNA being poisoned and damaged they then produce defectively structured proteins. To the immune system those defectively structured proteins appear to have come from a foreign source. The immune system then correctly attacks those cells.
To help better understand the root causes of diabetes we need to know that there’s a similar U-shape curve in the incidence rates that so many of the other chronic diseases follow. There’s a high incidence rate in young children, with a drop-off in rate during youth and teenage years, and then a slow progressive climb in rates with age in adults. Therefore, in adults it’s pretty clear that the disease is one of a slow accumulation.
Source: Rogers, M.A.M., Kim, C., Banerjee, T. et al. Fluctuations in the incidence of type 1 diabetes in the United States from 2001 to 2015: a longitudinal study. BMC Med 15, 199 (2017). https://doi.org/10.1186/s12916-017-0958-6
Now visually sync that chart up with the one I presented in my COVID-19 Vulnerability blog post showing the liver vitamin A concentrations by age. Note the huge spike in early childhood.
Obviously, there’s a lag time between the elevated liver vitamin A storage levels and the onset of the disease. Not at all unexpectedly, it does take some time to burn out the pancreas.
More importantly, we need to understand the exponential growth rates in the incidence rates of both Type I and Type II diabetes over just the last few decades. There is simply no way that this can be naturally happening in the human population. Something is clearly causing it to happen. We also can’t confuse something being really common for it being normal. Sure, diabetes is now very common, but in the historical context that is exceedingly abnormal.
Here’s a chart showing the diabetes prevalence rate here in Alberta.
And for across Canada the regional clustering looks like this:
Any disease that exhibits an exponential growth rate and a geographic clustering pattern like this is clearly a poisoning. It’s a slow poisoning from something that is obviously slowly accumulating and or picking away at cells in the body. It’s just that simple.
With the data presented above, if anyone tries to tell you that the root cause of diabetes is somehow rooted in genetics then simply ask them if they finished their grade 9 math.
Okay, now that we’ve agreed that diabetes is the result of a slow poisoning, let’s find out how likely it is that so-called vitamin A is responsible for it.
Type I Diabetes
As shown in the chart above, type I diabetes is most commonly occurring in children. It is considered to be an auto-immune disease where the defective immune system has wrongly killed off the pancreatic beta cells. With that, the pancreas is no longer able to produce adequate amounts of insulin. What “vitamin” do you know of that causes the rapid mitosis and apoptosis of stem cells?
Retinoic acid induces apoptosis by a non-classical mechanism of ERK1/2 activation Alfeu Zanotto-Filho, Martin Cammarota, Daniel P. Gelain, Ramatis B. Oliveira, Andres Delgado-Cañedo, Rodrigo J.S. Dalmolin, Matheus A.B. Pasquali, José Cláudio F. Moreira
Even though RA is involved in differentiation and apoptosis of normal and cancer cells, being sometimes used as adjuvant in chemotherapy, its mechanisms of action involve multiple overlapping pathways that still remain unclear. Recent studies point out that RA exerts rapid and non-genomic effects, which are independent of RAR/RXR-mediated gene transcription.
Yes, that’s the very functional definition of what the active form of “vitamin A” does to our stem cells. So much so, that it is regarded as the essential molecule that’s somehow needed to “differentiate” our stem cells. What does “differentiate” really mean? It means it causes stem cells that normally reside along a basement membrane to quickly mature into adult cells and separate off. This effect and process of vitamin A’s action is abundantly documented in many fields of medical science, and especially so with its use in dermatology and chemotherapy.
Type II Diabetes
Type II diabetes is characterized by the pancreas still able to produce insulin but for some unknown reason that insulin becomes less and less effective. The pancreas tries to compensate for this ineffectiveness by producing even more insulin. The condition is known as insulin resistance.
As with so many other metabolic diseases there’s a circular blame game going on. Many “experts” believe that obesity is the root cause of type II diabetes. But, of course, that can’t be correct because there are many type II diabetics who are lean. Other experts will claim that it’s the diabetes that’s causing the obesity. I think these guys are significantly more correct. But, not precisely correct. I think obesity is the body’s defensive response to a much more sinister and ongoing threatening condition that we need to be protected from. In other words, what if there’s some other driver that’s causing both obesity and diabetes at the same time? Likewise for the assumed to be diabetes caused comorbidities of kidney disease, cardiovascular disease, macular degeneration, dementia / Alzheimer’s, and, and you name it. Is there something else that could cause all of them to happen? Well, you bet there is. Vitamin A toxicity can, and is proven to, cause all these same comorbidities.
Except, what about this insulin resistance condition? What could be causing that? As I wrote about in a previous blog post, researchers are now identifying the association of elevated RBPs with insulin resistance.
“Until 2005, the sole known function for RBP4 was to mobilize retinol from tissue stores and deliver it to vitamin A-responsive cells where it can be converted to retinoic acid for use in regulating vitamin A dependent transcription and functions. In 2005, Kahn and colleagues reported that circulating RBP4 levels affect glucose clearance, with high RBP4 levels inducing insulin resistance (Yang et al., 2005; Graham et al., 2006). Specifically, Kahn and colleagues proposed that adipocyte-derived RBP4 is a signal that contributes to the pathogenesis of type 2 diabetes, linking obesity with type 2 diabetes, as well as other obesity-related metabolic diseases.”
So, retinol is definitely involved in insulin resistance. Next, we need to appreciate that all cellular receptors are actually proteins intrinsically made by the cell. We need to remember that vitamin A (the retinoic acid metabolite) has been shown to cause more than 500 different gene expressions. What are gene expressions? They are changes in the DNA structure that are detectable by variations in the different proteins that a cell manufactures. So, it’s very possible that the failing insulin receptor is just another protein that has been defectively produced as the result of retinoic acid induced gene expressions (a.k.a. DNA/RNA damage).
That outcome is not at all surprising because we now know that RA fractures and fragments DNA.
DNA fragmentation induced by all-trans retinoic acid and its steroidal analogue EA-4 in C2C12 mouse and HL-60 human leukemic cells in vitro Raghda S. Alakhrasa, Georgia Stephanoua, Nikos A. Demopoulosa*, Konstantinos Grintzalisa, Christos D. Georgioua and Sotirios S. Nikolaropoulosb
Abstract: We have recently shown that retinoic acid induces micronucleation mainly via chromosome breakage.
Do you think that that fracturing of your DNA might cause defectively produced insulin receptors and other proteins? I sure do.
How about conducting a Stress Test
As I mentioned in my eBooks, it is very common in engineering to stress test systems and components to their breaking point. Civil engineers do this everyday with concrete samples as a standard quality assurance practice. Jet engine manufacturers will spin new test engines to incredible speeds, and to the point that the engine explodes or otherwise self-destructs. These types of stress tests are very important as they not only tell us at what point a component will fail, it also helps set the safe operating ranges in real-world usage.
Somewhat likewise, if the theory that vitamin A toxicity is responsible for causing diabetes, then we should be able to conduct similar biological stress tests and see if diabetes can be directly induced by it. Thankfully, that stress test has already inadvertently been conducted for us.
The extreme stress test – Accutane
There have been many accounts of people who have developed type II diabetes shortly after taking accutane. It’s even documented as a known “side-effect”.
The effect of isotretinoin on insulin resistance and adipocytokine levels in acne vulgaris patients.
Soyuduru G, Ösoy Adışen E, Kadıoğlu Özer İ, Aksakal AB. Turk J Med Sci. 2019;49(1):238-244. Published 2019 Feb 11. doi:10.3906/sag-1806-44
Conclusions: All data suggests that five months of isotretinoin therapy in AV patients causes insulin resistance and the increase in insulin resistance is not dependent on age, BMI, BFM, and lipid levels of these patients.
Although this diabetes causing “side-effect” of accutane has been reported on for decades now, as usual it is downplayed and mostly ignored by the medical establishment. Here’s a great example:
Association Between Oral Isotretinoin Therapy and Unmasked Latent Immuno-Mediated Diabetes Ilaria Dicembrini, MD, Gianluca Bardini, MD, PHD and Carlo M. Rotella, MD
It is reasonable that latent autoimmune diabetes in adults (LADA) could be clinically revealed by drug-induced insulin resistance. In this case, the only remarkable change of lipid profile consisted in a reduction of HDL cholesterol during isotretinoin treatment; therefore, the previously reported physiopathological hypothesis (1–4) is not completely supported. However, this is the first report of an association between isotretinoin and an unmasking case of autoimmune diabetes.
Isn’t that a brilliant conclusion? Their ridiculous BS excuse is that the diabetes was already patiently sitting there just waiting to be “unmasked” by accutane use. They want you to believe that: No, no, wonderful accutane didn’t cause the disease, it just “unmasked” it. Who could buy such ridiculous nonsense and pharma propaganda? These are MD’s and PhD’s, no less, making such an idiotic claim. What about the many other disease conditions accutane has proven to cause? Were they then just “unmasked” too?
But, my point here is that we now know that many of us are getting small daily doses of “accutane” via our food sourced vitamin A intake. Thus, if a spiked dose of accutane is proven to cause diabetes, then obviously many low doses, but over a longer period of time, can have the same cumulative result. So, it’s just a matter of dose and time.
A lower range stress tests – Gestational diabetes.
“In the United States, about 1% to 2% of pregnant women have type 1 or type 2 diabetes and about 6% to 9% of pregnant women develop gestational diabetes.”
But, why and how does getting pregnant cause a woman to develop diabetes? That seems like a pretty high price to pay for having children. Something that women have been doing for millions of years now. Once again, there’s no way that nature could be that foolish for this to be normal.
Of course, the big assumption made by endocrinologistsis that gestational diabetes is caused by some vague hormonal imbalance. But, they in no way can explain why it only happens to some women. More importantly, it in no way explains why it’s become much more prevalent over the last few decades and the large regionally disparities in incidence rates.
However, retinyl ester levels doubled in the non-supplemented group immediately after the race (p < 0.001), whereas in the supplemented group similar high levels were observed not until 24 h post-racing (p < 0.001). The high levels of retinyl esters were paralleled to some extent by an increase in plasma triglyceride concentrations, which were significantly higher 24 h post-racing than immediately before (p < 0.001) and after exercise (p < 0.001) in both groups. The increase in retinyl ester concentrations might be indicative of their mobilization from liver and adipose tissue.
Thus, a sustained increased heart rate / blood flow stirs up more retinyl esters out of the liver and brings it into circulation.
A similar effect happens in women during pregnancy. Of course, it’s not just for 24 hours, rather it’s sustained for 7 or 8 months.
During pregnancy, the amount of blood pumped by the heart (cardiac output) increases by 30 to 50%. As cardiac output increases, the heart rate at rest speeds up from a normal prepregnancy rate of about 70 beats per minute to 80 or 90 beats per minute.
With that increased heart rate, more of the highly toxic retinyl esters are swept into circulation. Of course, the amount is probably proportional to the concentration already stored in their liver. Remember that retinol outside of the RBP can pass through cell membranes within about one millisecond. With that, there will definitely be a higher rate of conversion into retinoic acid. That prolonged elevated retinoic acid level would certainly explain the development of gestational diabetes. It would also explain other adverse accutane “side-effect” like conditions such as postpartum depression.
Quite interestingly, the same phenomenon has been observed in women recovering from breast cancer. Women who adopt a strenuous exercise regimen post cancer treatment have a much higher chance of their cancer recurring as opposed to women who only adopt a moderate exercise regimen. Likewise, emotional stress can have the same effect. This is why many people have reported that their first encounter with autoimmune diseases and cancer occurred shortly after a period of sustained emotional stress.
If this theory of vitamin A toxicity causing diabetes is correct then we might be able to confirm it with some intervention type studies using low vitamin A diets. There are indeed such studies. Let’s first consider Walter Kempner’s all rice and sugar diet. Kempner had his diabetic patients follow this diet for a period of up to 10 years and they had great results in reversing diabetes, obesity, and diabetic retinopathy.
Although some of his patients appear to have taken vitamin A supplements there’s no record of exactly what group those patients were in. Also, it’s very hard to know how much of it would have been absorbed on such an extremely low fat diet. Naturally, I think Kempner’s all rice and sugar diet is ridiculous and very dangerous. However, it completely contradicts the mainstream thinking on the role carbohydrates and sugar play in diabetes. None-the-less, it is very good evidence that we are on the right track here thinking that vitamin A toxicity is at the root cause of the disease.
Next, there’s another extreme diet from about the same era that had similar great results in reversing diabetes.
Blake Donaldson’s diet is the complete opposite of Kempner’s rice and sugar diet, yet it yields the same results with regards to reversing metabolic disease and diabetes. This “big fat steak” diet it’s now seeing a huge resurgence in popularity today. It’s called the “carnivore” diet. Why has the carnivore diet become so popular? Because it works! Like it or not, we have to look at the real-world results.
How can we explain these two diametrically opposed diets yielding effectively the same results in reversing diabetes? The common factor is that they are both inadvertently extremely low vitamin A diets. I think the carnivore diet is vastly superior to Kempner’s rice and sugar diet. But, in a way, when you combine these two dietary intervention studies they somewhat mutually exclude macro nutrients as being a major causative factor in diabetes. Therefore, that requires us to look deeper for mechanistic molecules. I say we go with putting the blame on the molecule who’s proven and very functional definition is one that destroys our stem cells. Yes, vitamin A is a stem cell killer.
Zinc – here it is yet again.
As with many enzymes, zinc is a key atom needed for the formation of insulin. Insulin is itself a protein based hormone.
The Structure of Insulin: Zinc is shown as the two magenta coloured spheres in the ribbon diagram on the right.
So, with background vitamin A toxicity putting a higher demand on the needed detoxification dehydrogenase enzymes, that could significantly reduce the availability of zinc needed for insulin production.
Could it be this simple?
For me at least, there’s no doubt that vitamin A toxicity is causing the diabetes and obesity epidemics. But, that’s just my own conclusion on it. With diabetes now being a major pandemic, it’s rather imperative that we find out. So, if you can, please help by tracking your A1C or blood glucose levels as you progress with this diet. You can then add more evidence (pro or con) to the case.
“And, like with Wolbach and Howe back in 1925 these researchers are so sure of themselves that they completely ignore the contradictory findings from their contemporaries.”
I’ve been asked to provide supporting information to back up that statement. I’ll share that here in just a bit.
First, you might be wondering why we should care at all about some rat study from almost 100 years ago. However, I think it’s tremendously important. The 1925 Wolbach and Howe study was the one that supposedly definitively proved the essential need for vitamin A, and therefore, the one that solidified and confirmed the concept of it being a vitamin. If they got that wrong, and if we can therefore disqualify that study, then it should go a long way in disproving the entire “it’s a vitamin” claim.
I’m assuming that for most people knowing whether or not vitamin A is truly a vitamin does not matter too much. Vitamin or not, that verdict probably won’t change what they are doing. From a practical perspective, and in the short term, we just need to know that vitamin A is toxic once we’ve accumulated too much of it. We can apply that knowledge and hopefully still recover our health.
However, if we don’t go the extra mile and disprove this “it’s a vitamin” claim then the powers that be will just go on perpetually poisoning much of the human population with it. It will also continue to be very difficult to warn more people about the potential harms of over consuming vitamin A.
Okay, now let’s get back to the 1925 Wolbach and Howe study. One of the most fundamental requirements in scientific experiments is repeatability of results. If results are not repeatable (within some explainable margin of error), then the experiment proves nothing.
Here are some of the statements from the Wolbach and Howe study’s introduction effectively ignoring / dismissing the results of experiments from their contemporaries
Few pathological studies have been made, and the majority of these have resulted in wholly negative results and, therefore, erroneous conclusions as to the sequence of events and importance of infections.
Emmett and Alien in a comparison of changes due to vitamin A and B deficiency respectively in the rat report “no special outstanding pathological findings,” in the absence of fat-soluble A, in contrast to atrophies and hypertrophies found in B deficiency.
Stephenson and Clark failed to find a distinctive pathology in keratomalacia in rats.
Davis and Outhouse 4 studied only the kidneys, spleen, heart, lungs, pancreas, liver, and testes. As they report that the testes were normal in most of their cases, it is certain that either their diet was not deficient in fat-soluble (vitamin) A or that the duration of the experiments was too short.
Cramer, Drew, and Mottram ~ in a study of the effects of vitamin deficiency in rats upon the function of lymphocytes and lymphoid tissue found no pathology in fat-soluble A deficiency.
Wason found no lesions in any organ other than the eyes. She regarded the changes in the cornea as secondary to bacterial invasion.
Meyerstein ~ failed to find any characteristic pathology in either vitamin A or vitamin B deficiency in rats.
There’s yet another study from this era that I want to directly compare with Wolbach and Howe’s (W&H) study. It is:
THE NECESSITY OF CERTAIN LIPINS IN THE DIET DURING GROWTH.BY E. V. McCOLLUM AND MARGUERITE DAVIS.(From the Laboratory of Agricultural Chemistry of the University of Wisconsin.)(Received for publication, June 1, 1913.)
The reason I want to discuss this study is because they detail the diet used, and the outcomes. The diet used in this study was remarkably similar to the W & H study. However, McCollum’s 1913 study was only investigating the “growth” producing effects of some suspected fat soluble factor.
Here’s an example diet McCollum that fed his animals.
Here’s a chart for Rat # 104a (female)
Do you notice something? Up until period III, McCollum’s study diet is nearly identical to the one used by W&H. McCollum’s study diet is supposedly devoid of vitamin A too, yet his animals survive quite well to the 20 week mark, and beyond. Whereas, in the W&H study all of the animals were either dead or dying by the 8th-10th week. In the last two weeks of the W&H study the animals needed to be force fed their ration, and that finished them off. Except, here in McCollum’s study, not only have the animals survived at least 2X longer, there is no mention of sickness or disease, at all. In other words, his animals were probably very healthy, and obviously reproductive, at the 20 week mark. McCollum’s study presents similar results for male rats.
Then to investigate growth, in period III he adds in an egg extract, and the animals do gain weight. However, let’s not jump to the conclusion that it’s a good thing. What would you tell someone today who claims that gaining weight is the medical equivalent to growth? I think you’d tell them that they are confused. But, that’s a small technicality we are not too interested in right now (unless we wanted to consider this an inadvertent obesity causation study).
What’s critically important is that apparently the same diet regimen used by McCollum’s and W&H’s studies yielded completely opposite results. How can we explain that? When combined with the other studies mentioned above from this era , it is very clear that the animals in the W&H study did NOT succumb to a vitamin A deficiency. Therefore, with the diametrically opposing results between the McCollum’s and W&H’s studies, we have no experimental repeatability. Thus, we can’t legitimately derive any scientific conclusion from them. Therefore, the claim that vitamin A is a vitamin is completely unsupported, and is quite bogus.
However, there’s a subtle but very important difference in the diets used by McCollum and W&H. In W&H’s paper they state:
Distilled water, sufficient to make a dough, was added to the ingredients; small cakes were moulded, each containing five gm. of material, and dried in an oven.
For additional information about heat treating milk, and its correlation to early death in experimental animals please read about Wilhelm Stepp’s 1912 work in mice. Stepp kills his mice in just 3 weeks using heat treated milk. And, it looked to me that Stepp’s results (kill rate) correlated with the heating duration times in alcohol. https://academic.oup.com/jn/article/127/7/1255/4728852
Additionally, there is an even more fundamental problem with the McCollum and W&H studies. That problem is now revealed by the modern-day work of Collin Campbell et al with their work on the direct toxicity of casein on its own.
Therefore, with that huge red flag and confounding factor no rat study in history that’s used casein can be considered legitimate and valid. Clearly then, Wolbach and Howe’s 1925 study is complete junk science. Moreover, we have the previously ignored studies from Wolbach and Howe’s contemporaries actually proving that there is no dependency on vitamin A.
The W&H study is the foundational cornerstone of the grand vitamin A theory. Their conclusions were wrong, and they made the assumption that they had narrowed it down to this one molecule. Quite remarkably they made this assumption in 1925 even though the structure of the molecule had not been determined until 1931. Sadly, every vitamin A study since W&H’s has been layered upon that flawed foundational assumption. Very few follow-on researchers have had the courage to stick their heads above the parapet and call this out for what it is. But, there have been a few. Here’s a prophetic quote from Pitt:
… people seem curiously reluctant to recognize just how toxic is vitamin A. I have long asserted that considered as a chronic poison vitamin A is probably more harmful than cyanide, but I have usually been disbelieved …
I think that if modern day researchers stopped fabricating ridiculous follow-on theories and sub-theories to rationalize what they are seeing, and reevaluated their finding through the lens of vitamin A being a toxin, and nothing but a toxin, then all of it will make so much more sense.
The W&H study is garbage science, and needs to be tossed into the trash can. With that, so does the entire bogus claim of this toxic molecule being an “essential” vitamin.
Of course, vitamin or not, there’s no debate about the potential toxicity of so-called vitamin A. But, if we can finally correct the science on it then we might have a chance in stopping the global supplementation nonsense going on. Let’s consider this report:
WHO Library Cataloguing-in-Publication Data Report: WHO technical consultation on vitamin A in newborn health: mechanistic studies, Geneva, Switzerland, 1–3 December 2009. 1.Vitamin A – administration and dosage. 2.Vitamin A deficiency – prevention and control. 3.Infant, Newborn. 4.Infant nutrition. I.World Health Organization. ISBN 978 92 4 150316 7
High doses of retinyl ester are commonly provided to at-risk populations in areas where vitamin A deficiency is a problem. For women, 400 000 IU given as two doses of 200 000 IU at least 1 day apart and within 6 weeks postpartum are being recommended. Vitamin A supplementation programmes have been highly successful in addressing vitamin A deficiency but are not without risk. The doses administered are at toxic levels (200 000 IU retinyl ester is 85 times the recommended daily allowance (RDA) and 400 000 IU retinyl ester is 172 times the RDA). Acute toxicity may occur at dosages >100 times the adult RDA.
Do they warn these women and get their signed informed consent for the likely harm from that toxic dose? I highly, highly doubt it. Of course, they’ll claim that this deliberate poisoning of young women with known acute toxic doses is somehow necessary, ostensibly claiming that it’s to prevent vA deficiency.
But, what’s really going on here? Clearly, it might not be just bad science and there’s another possibility to consider. In the 1970’s the WHO and the global elites were absolutely obsessed with the runaway growth in the human population. It was viewed as the biggest threat to the planet. Then factor in that it’s been known since the 1960s that vitamin A is a reproductive toxin.
Check out the last entry in this table of lethal doses of some common substances:
Then in the 1970s the WHO’s vitamin A supplementation programmes were started up in about 100 countries, and vitamin A was added to the low fat dairy, etc., in North America and to sugar in South America, etc. Then, surprise, surprise, there’s been a massive drop in human fertility around the planet. And, by the early 2000s the WHO had gone mostly quiet about the risk about the global population. The WHO’s primary focus has now shifted to vaccines. Do you trust these guys? I hope not.
What’s emerged with the COVID-19 pandemic is a peculiar pattern of vulnerability. It’s being widely reported that older people are the most severely affected by the infection and are the demographic most likely to die from it. Whereas, children and teenagers often appear to sail right through the infection with only minor symptoms, or the just having symptoms equivalent to a cold or minor flu. Yet, at the lower end of the age spectrum, say in one and two-year-old’s, the severity of the diseases increases again.
Children of all ages are susceptible to COVID-19 and while their symptoms are generally less severe than those of adults, a small percentage — particularly preschoolers and infants — can become seriously ill, according to a new study.
An equally important observation is that many thousands of people have tested positive for having had COVID-19 and yet have remained completely symptom free. Therefore, it’s very critical to appreciate that just getting COVID-19 is not sufficient on its own to cause disease. Clearly, it’s COVID-19 and something else when combined that leads to the disease. What is that something else? We should all be very curious and striving to find out what it is.
In the context of COVID-19 infections, the general assumption is that older people just have weaker immune systems and are thus less able to fight off the virus. Except, it’s not just age that’s the primary factor. Rather it’s a person’s age combined with their pre-existing conditions, or comorbidities, that somehow makes them more vulnerable to having a severe response. Therefore, we can almost right away dismiss that assumption of a “weak” immune system being to blame because it is not at all just older people who succumb to the infection. Some younger people, even in their 30’s, are dying from the infection too. It’s just much more common to have a severe response in these younger people primarily when they have comorbidities. Therefore, the pre-existing comorbidities are the bigger risk factor. The cited highest risk comorbidities are diabetes, obesity, asthma, other autoimmune diseases, and cardiovascular diseases. If you’ve followed my blog for a while now, you’ll know that these are all diseases that I’ve been attributing to long term vitamin-A toxicity.
Let’s see if we can make some sense out of this. Could it be that there’s some mechanism whereby people with a higher level of vitamin-A storage could be more severely impacted by viral infections, and especially that of COVID-19? Firstly, let’s look at some interesting data regarding the liver storage concentration by age. For that, we’ll look at this 1973 study from Mitchell et al.
Source: G. Vaughn Mitchell, M. Young, C. R. Seward, Vitamin-A and carotene levels of a selected population in metropolitan Washington, D. C, The American Journal of Clinical Nutrition, Volume 26, Issue 9, September 1973, Pages 992–997, https://doi.org/10.1093/ajcn/26.9.992
Quite interestingly, here we have a similar U-shaped curve showing up in the data. Note that the horizontal red line at 286 μg/g is the documented toxic level for liver storage. Remarkably, this means that a large number of young children say from 1 to 5 years old are in the toxic range for liver storage. Then, as they get older their liver’s volume increases (roughly as a cubed function of its cross-sectional size) and they outpace the inbound dietary consumption rate. Then, as people get older their liver concentration slowly saturates to where they move into the toxic storage range once again, and through to the end of life. Let’s remember that this data is from back in 1973, just at the beginning of the foolish North American vitamin-A supplementation programs in dairy, breakfast cereals, etc.. Obviously, the liver saturation numbers will be far worse if sampled today. Just imagine the blue U-shaped curve being shifted up higher on the chart to where more people are over the red toxicity line. So, it’s no wonder why so many people are sick and diseased today. They are, by the very definition of the toxic level of vitamin-A storage, beyond that point. This also corresponds quite well with the fact that about one-third of the American population has NAFLD. That’s all bad enough, but could this somehow also make them more vulnerable to viral infections? Well, this has actually been well documented to be the case for a long time. But, for now, there’s one data point on the above chart that we need to focus in on.
What’s documented in the Mitchell study, and in others, is that very young infants have very low (and often even non-detectable) liver storage levels of vitamin-A.
The Amazing Infant Immune System
So, what do you suppose happens to very young infants exposed to the measles virus? Well, amazingly, often nothing adverse happens. That’s correct, they usually remain symptom and disease-free. Their immune system simply clears the virus. Additionally, most of them have probably acquired true life-long immunity from future infections of the measles virus.
Likewise, just what do you suppose happens to a very young infant exposed to the Dengue virus? Well, once again, often nothing adverse happens. Yes, those infants with their supposedly “weak” immune systems just clear the virus.
Next, just what do you suppose happens to a very young infant who is exposed to, and is subsequently infected by, the truly horrifying syphilis bacteria? Very often, they too remain symptom-free, and their “weak” immune systems clear the bacterial infection!
Even more astonishingly, what do you suppose happens to a very young infant who has a finger or toe severed? Amazingly it often grows back! Yes, these very young infants are amazing at surviving and dealing with very adverse events and pathogen attacks. Infants are starting in life with a great, if not perfect, immune system. Sadly, that all quickly changes once the so-called “medical experts” start administering their “health” intervention programs.
Yet, a great misconception persists in medical science in that very young infants are thought to have poorly developed immune systems. One of the primary reasons they make this assumption is because very young kids simply do not respond to vaccinations. Please consider this meta-analyses of the seroconversion rates by age:
Measles vaccination below 9 months of age: Systematic literature review and meta analyses of effects and safety
In a meta‐analyses of 20 papers, the proportion of infants who seroconverted (%SC) depended on the age at MCV1 vaccination. It increased from 50% (95% CI 29‐71%) at age 4 months to 67% (95% CI 51‐81%) at 5 months, 76% (95% CI 71‐82%) at 6 months, 72% (95% CI 56‐87%) at 7 months and 85% (69‐97%) at 8 months.
For the very youngest of children, there is only about a 50% seroconversion (meaning their immune response created detectable antibodies). The seroconversion rates then increase as they get older. Except, this phenomenon is not because their immune system is maturing. Rather, it’s because their serum levels of vitamin-A are creeping up with age too. We know this because the same effect has been studied in fully grown adults. In adults with abnormally low vitamin-A status, they too have a low seroconversion rate of ~50% when administered vaccines. Then, from other studies, we learn that when adults have their vitamin-A levels pre-boosted up before vaccination, then there is a higher “seroconversion” rate of around the more “normal” ~85% rates. Of course, most vaccinations are really low dose deliberate viral infections.
The known low “seroconversion” rate is why most childhood vaccines are delayed until two months of age. Some researchers claim that the extra vitamin-A has “enhanced” the immune response. But, we know that’s not exactly correct. What’s really happened is that the vitamin-A has enabled the virus to more rapidly replicate, and that then results in the “enhanced” immune response. But, do not for one second think that getting a higher seroconversion rate is a good thing to have happen. It’s the exact opposite. It’s clear evidence that higher background vitamin-A levels are resulting in the increased replication rates of the vaccine’s virus. And, vice versa, the run-away viral infection has increased the toxicity of their background vitamin-A levels too.
This is a super, critically, important point to understand. This is the underlying mechanism as to why kids in India and other countries of Southeast Asia can have such a devastating outcome from a measles infection. With high, or even moderate, vitamin-A serum levels, and a lack of sufficient dietary fats and proteins, the measles infection also increases the toxicity of their endogenous and circulating vitamin-A levels! It is also the underlying reason why some kids die when given their vaccines.
What’s going on here? As usual, it’s multifactorial, and there’s much more to the story. What we do know, and also very contrary to widely-held myths, is that vitamin-A actually subdues the immune system. What’s also been documented for like the last 50 years now is that vitamin-A weakens and otherwise damages cell membranes. It also damages the mitochondrial membranes. It’s trivial to see why too. Both the cholesterol molecule and the side-chains of the vitamin-A molecule are made up of isoprene groups. These isoprene groups are the base compound for natural rubber. So, if you’ve ever wondered why the cholesterol deposits surgeons pull out of arteries looks so much like rubber, it is because it is rubber. Ever wonder why the cholesterol deposits are yellow in color? It’s in good part because it has picked up and encapsulated the vitamin-A, and carotenoid molecules, within it.
Carotenoids are incorporated into very low density lipoproteins (VLDL) and exported from the liver into the blood. VLDL are converted to LDL by lipoprotein lipase on the surface of blood vessels. Plasma membrane-associated receptors of peripheral tissue cells bind apolipoprotein B100 on the surface of LDL, initiating receptor-mediated uptake of LDL and their lipid contents.
Source: Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc http://www.nap.edu/catalog/10026.html Page 94
Now, just as cholesterol with its isoprene groups nestles into the lipid bi-layer of the cellular membranes, so too does vitamin-A. This obviously weakens the integrity of the cell membrane.
Could the weakened cell membrane then make the cell more susceptible to viral infections? You bet it can. This has been documented in the context of HIV infections. Supplementing HIV patients with vitamin-A causes a more rapid replication of the virus, and results in worse outcomes. So, we have multiple pieces of real-world evidence that vitamin-A causes a faster replication rate of viruses. What about some laboratory-based evidence? Well, there is indeed, and even specifically for the coronaviruses.
Retinoic acid modification of cell culture used for reproduction of enteropathogenic viruses.
Abstract The 0.001-0.005% retinoic acid injection into the growth cultural medium of prime and continue cell cultures 12-24h before inoculation considerably raised the cell sensitivity to animal entero- and coronaviruses. The entero- and coronaviruses concentrations in cultural medium increased by 10(1.58) and 10(1.68)TCID 50/1.0 respectively. The optimized parameters of the cell culture processing for the enteropathogenic viruses reproduction improvement are proposed.
And a similar phenomenon is observed in the context of Zika infections. Cells being forced into “differentiation” via retinoic acid increased their infectivity to viruses.
Differentiation enhances Zika virus infection of neuronal brain cells
Here we investigated ZIKV infectivity in neuroblastoma SH-SY5Y cells, both undifferentiated and following differentiation with retinoic acid. We found that multiple ZIKV strains, representing both the prototype African and contemporary Asian epidemic lineages, were able to replicate in SH-SY5Y cells. Differentiation with resultant expression of mature neuron markers increased infectivity in these cells, and the extent of infectivity correlated with degree of differentiation.
So, we now have good evidence of vitamin-A (and specifically retinoic acid) promoting the replication of viruses. Of course, we all know that increased background storage levels of vitamin-A simply means more endogenously produced retinoic acid.
None of this is new information. As with most things related to vitamin-A science, it’s been well known about and reported on for a long time. Here’s a great paper from Anthony Mawson discussing the same comorbidity patterns in the context of the 2009 SARS-CoV infections. Back then it was also the people with the pre-existing conditions of heart disease, asthma, and autoimmune diseases who were at higher risks for severe disease and death.
Role of Fat-Soluble Vitamins A and D in the Pathogenesis of Influenza: A New Perspective
Anthony R. Mawson
Department of Health Policy and Management, School of Health Sciences, College of Public Service, Jackson State University, Received 4 April 2012; Accepted 3 May 2012 Academic Editors: M. C. W. Chan, N. Kawai, and Y. Lai
The Symptoms of Influenza A Infection Are Similar to Those of Hypervitaminosis A
As noted, the clinical spectrum of influenza A infection, including avian influenza H5N1, is not restricted to the lung and can range from mild influenza-like illness to severe pneumonia, acute respiratory distress syndrome (ARDS), acute lung injury (ALI), and multiorgan failure . Fever, rhinitis, myalgia, malaise, headache, cough, dyspnea, sore throat, and fatigue are the main presenting symptoms. Complications include pneumonia, bronchitis, or sinusitis, and rarely encephalitis, transverse myelitis, Reye syndrome, myocarditis, or pericarditis .
Mawson does a great job of explaining how and why this can be related to an overload of vitamin-A, and why a low vitamin D/A ratio is a very important factor. Oddly, this paper was not picked up by the major journals, say such as the BMJ, or Lancet. Why was there so little interest in this Mawson paper? Could it be that the medical establishment and the pharmaceutical industry have no genuine interest in understanding what’s really enabling and driving viral infections? Could it be that their primary, if not only interest, is their commercial interests? Of course, it is. These companies have multi-billion dollar vaccine divisions. Therefore, any non-vaccine solution to viral infections would be a serious and direct threat to that ongoing annual business model. Therefore, it is incredibly unlikely that we’ll ever see a non-vaccine based solution developed by the pharmaceutical industry. What if we all came to the understanding that the best way to protect ourselves from viral infections was simply to keep our vitamin-A consumption very low? That could devastate the industry. Therefore, that information cannot be allowed to be developed and confirmed. Therefore, the Mawson paper must be ignored.
The ACE2 Receptors
There’s been a lot of press lately about the important role that the ACE2 receptors play in COVID-19 infections. The virus’s glycoprotein binds to the cell membrane protein angiotensin-converting enzyme 2 (ACE2) and that’s how it gains entry into the human cell.
The novel coronavirus 2019 (2019-nCoV) uses the SARS-coronavirus receptor ACE2 and the cellular protease TMPRSS2 for entry into target cells
Here, we demonstrate that 2019-nCoV-SusestheSARS–coronavirusreceptor, ACE2, for entry and the cellularprotease TMPRSS2 for 2019-nCoV-S priming. A TMPRSS2 inhibitor blocked entry and might constitute a treatment option. Finally, we show that the serum form a convalescent SARS patient neutralized 2019–nCoV-S-driven entry.
Naturally, with the ACE2 receptor being the target site of virus entrance into the cell there’s been a ton of frantic research into looking into ways to block or down regulate the ACE2 receptors.
Correspondingly, there’s been a ton of interest and media attention given to a well-established anti-malaria drug named chloroquine. Here’s a study from back in 2005 discussing it.
Chloroquine is a potent inhibitor of SARS coronavirus infection and spread
Results We report, however, that chloroquine has strong antiviral effects on SARS-CoV infection of primate cells. These inhibitory effects are observed when the cells are treated with the drug either before or after exposure to the virus, suggesting both prophylactic and therapeutic advantage. In addition to the well-known functions of chloroquine such as elevations of endosomal pH, the drug appears to interfere with terminal glycosylation of the cellular receptor, angiotensin-converting enzyme 2.
Therefore, we can see that when the ACE2 receptors are upregulated, viral infection and replication rates increase. Conversely, when the ACE2 receptors are downregulated, viral infection and replication rates decrease.
Yet, something really strange happened with the medical establishment and the mainstream media regarding the potential use of chloroquine as a treatment. These people immediately started attacking it and doing everything they can to discredit it. Why would they do that? Could it be that chloroquine is cheap, off-patent, immediately available and most of all a potentially competitive alternative to the planned vaccine they have in the works?
Dr. Anthony Fauci almost jumps to the podium and claims that the evidence for its effectiveness is only anecdotal, and there is not enough evidence to support claims that chloroquine is effective in combatting COVID-19. But, that’s not quite true. There are existing clinical trials, and back in 2005, even its probable functional mechanism was understood too. Additionally, with very few other immediate options, why not quickly get going on finding out? Why so aggressively downplay it and try to dismiss it as an option? Who and what is he trying to protect?
Why are we no better prepared today for a viral pandemic than were we in 1918?
The last great viral pandemic to ravish the human population was the so-called Spanish Flu of 1918. So, now over 100 years later, we still don’t have any really effective treatments for viral infections. How can that be? After sucking trillions of dollars out of the worldwide economies the pharmaceutical industry has almost nothing meaningful and effective against viral infections. Sure, they have the horrible DNA, RNA chain terminator class of drugs that they claim to be “anti-viral” in action. But, not only are these drugs very expensive, they come with catastrophic “side-effects” that often decimate the overall health of the patient. They are not “medicines”, they are simply poisons that break the cell’s ability to build any proteins at all.
Fortunately, ER and intensive care teams are vastly more capable today in preventing people from dying from viral infections than compared to back in 1918.
What really matters most right now is finding remedies for people most severely affected by the virus. Contrary to the advice of many “experts”, taking vitamin-A is not one of them. The very last thing anyone one should be doing at this time is supplementing with so-called vitamin-A.