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SCURVY

18 Saturday Sep 2021

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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. 

Source: https://educalingo.com/en/dic-en/scurvy

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.

James Lind

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?

https://www.bbvaopenmind.com/en/science/leading-figures/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.

Other remedies

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”.

Portable Soup

What is “portable soup”? From Wikipedia:

Portable soup was a kind of dehydrated food used in the 18th and 19th centuries, originating from Great Britain. It was a precursor of meat extract and bouillon cubes, and of industrially dehydrated and instant food. It is also known as pocket soup or veal glue. 

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.”[307] The “portable soup” consisted of “all the offals of oxen killed in London for use of the Navy” with salt and vegetables added in.[308] The soup, however, was dried so that it had the appearance of slabs of glue.[309] Although the “portable soup” was unappetizing, it was perfect for the navy because it had a shelf life of years.[310] In addition to the supplies stored at the beginning of each voyage, ships often traded for additional supplies in foreign ports and lands.[311] In particular, rice, wince and other hard alcohols were particularly valuable when trading.[312]

Source: https://dash.harvard.edu/bitstream/handle/1/8852139/Mayberry.html?sequence=2

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.

Source: https://www.chefs-resources.com/types-of-meat/offal-varieties/

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

Source: https://www.warhistoryonline.com/history/how-royal-navy-fed-sailors.html

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:

Nikita Posted September 4, 2006

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.

Source: https://www.acne.org/forums/topic/114246-accutane-and-sore-gums/#comment-1332133

You can easily find many more such firsthand accounts of accutane rapidly inducing gum disease. For example:

https://www.google.com/search?q=receding+gums+accutane+site:www.reddit.com

The Franklin Expedition and Lead Poisoning

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.

Source: https://georgianera.wordpress.com/2014/11/20/portable-soup-as-supplied-by-mrs-dubois-to-the-royal-navy-in-1756/

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.

https://csphistorical.com/2016/01/24/salt-pork-ships-biscuit-and-burgoo-sea-provisions-for-common-sailors-and-pirates-part-1/

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.

https://www.amazon.com/s?k=canned+cod+liver

Sorry, I’m not offering any discount codes.

Next, we have another account of “land scurvy” from https://dash.harvard.edu/bitstream/handle/1/8852139/Mayberry.html?sequence=2&isAllowed=y

The Crusades, however, provide an example of one written account of scurvy during the 13th century.[133] 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.”[134] However, it is noted that the Crusaders believed that the disease was caused by eating eel which supposedly ate the dead.[135]

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).

https://www.thecanadianencyclopedia.ca/en/article/scurvy

And:

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: 

  1. Swollen, bleeding gums, leading to loose teeth, and the teeth eventually falling out.
  2. 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.

Source: Limeys and the Cure for Scurvy – JaneAusten.co.uk

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.”

Source: https://diabetestalk.net/diabetes/how-to-treat-diabetic-rash-on-legs

A 54-year-old man with type 2 diabetes mellitus 

Necrobiosis lipoidica is an unusual skin disorder that is strongly associated with diabetes mellitus.

Source: https://www.aafp.org/afp/2003/0101/p139.html

Diabetic Leg Ulcers:

Source: https://dermnetnz.org/topics/leg-ulcer

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.

Thanks

Diabetes – the pandemic of the 21st century

01 Saturday Aug 2020

Posted by in Autoimmune

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New CDC report: More than 100 million Americans have diabetes or prediabetes | CDC Online Newsroom

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.

https://pubmed.ncbi.nlm.nih.gov/19364826/

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

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5278808/

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. 

From: Fluctuations in the incidence of type 1 diabetes in the United States from 2001 to 2015: a longitudinal study

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.

Source: https://albertadiabeteslink.ca/professionals/alberta-statistics/

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

Abstract:

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. 

Source: https://pubmed.ncbi.nlm.nih.gov/30761880/

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.

Source: https://care.diabetesjournals.org/content/32/8/e99

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 endocrinologists is 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. 

Prevalence of Gestational Diabetes and Risk of Progression to Type 2 Diabetes: a Global Perspective

To propose a probable mechanism, let’s consider this interesting study on plasma retinol levels in sled dogs (shared by Dr. Garrett Smith).

Effect of Exercise on the Mobilization of Retinol and Retinyl Esters in Plasma of Sled Dogs

https://pubmed.ncbi.nlm.nih.gov/15189429/

From the abstract:

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. 

Intervention Studies

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. 

Walter Kempner’s Rice and Sugar diet of 1958

  • 100 consecutive patients
  • Over an 11 year period
  • ~ 100% carbs – yet great results – go figure??

Interestingly, Kempner would, on occasion, whip his patients to help compliance.

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 Strong Medicine – “big fat steak” diet – 1961

  • Steak 3 meals per day, 7 days per week
  • Over multi year period
  • ~ 100%  meat – yet good results – go figure??

No whipping required

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.

By Isaac Yonemoto. – Transferred from en.wikipedia to Commons. First upload to en.wp by Takometer, CC BY 2.5, https://commons.wikimedia.org/w/index.php?curid=1531881

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.