|Poisoning For Profits||Source|
Contents ♦ click to select chapters
Poisoning for Profit goes on a deep dive investigating the very origin of the vitamin A theory. The author uncovers that the early scientific studies conducted in the 1920s used to establish so-called vitamin A being a “vitamin” were grossly flawed and therefore almost meaningless. Ironically, what these early studies did establish was the incredible, yet previously unknown and hidden, toxicity of so-called vitamin A. The author goes deeper and proposes that vitamin A is not actually a vitamin at all; rather it is a toxin, and only a toxin. However, vitamin A is a toxin that the human body is well prepared to deal with, but it can only handle it at a reasonable rate of consumption.
Tragically, based on the botched science from the 1920s the world has been led into a massive health disaster by having many of our common staple foods supplemented with an insidious toxin. The author explains and details the mechanism of how this so-called vitamin is likely responsible for many of the modern-day chronic diseases plaguing humanity. The primary diseases implicated are the autoimmune diseases, many soft-tissue cancers, IBD and other inflammatory diseases, infertility and the psychiatric diseases of epilepsy, schizophrenia, Alzhiemer’s / dementia.
Poisoning for Profit ends with a call to action for a grassroots and worldwide citizen driven research project to determine the truth about so-called vitamin A.
[editor's note] In P4P the author uncovers a diabolically evil project undertaken by the global elites to poison the entire human race. Although their primary objective was to drastically reduce human fertility, a “side-effect” of this project has also resulted in the massive chronic disease disaster most nations are struggling with. But, not to worry, the convenient “side-effect” has enabled the global pharmaceutical industry to become immensely wealthy and effectively take over most of the world’s governments.
You might find yourself thinking, “no way, not possible, they’d never get away with it”. But, they have gotten away with it for over 50 years now.
|Vitamin-A theory – the early years
The Experiment – the cornerstone of Science
The incredible toxicity of vitamin-A
The epithelial tissues - the foundation of the chronic diseases
The botched deficiency experiments
Real-world testing of the vitamin-A deficiency theory
Vitamin-A supplementation in SE Asia, and South America
Vitamin-A supplementation and Worldwide Infertility Rates
Vision as a chemical reaction
The greatest understanding in medicine - ever
Lutein / zeaxanthin - the hidden death trap
Vaccines and Vitamin-A – the perfect storm
Systemic scientific fraud
A Call to Action - We experiment
I am an engineer and geologist. I am 60 years old and live in Western Canada.
I have absolutely no medical experience. I am not offering or suggesting medical advice. I am not selling or promoting any product or services. My goal is to get a clear understanding of the root cause(s) of the autoimmune diseases.
If you have any questions or feedback, then please do not hesitate to contact me. The more people we have discussing this topic the faster it will get solved. Thank you.
Grant Genereux, P. Eng.
Poisoning for Profits
Edition 1.3.3, July 2017
The statements herein are not intended to diagnose, treat, cure or prevent disease. The information provided is for educational purposes only and is not meant to substitute for the advice provided by your doctor or other health care professional.
There are many references in this book to external sources, most with a URL link. At the time of writing, all links were valid. However, this is the internet, and things can and do change frequently. Therefore, if you find a broken link, just search for the source document by name.
I have two goals in publishing this e-book. The first is to challenge the determination of vitamin-A as being a vitamin. The second goal is to get to the true understanding of the root-cause of the autoimmune diseases.
This book is not about opinion or endless debates; it is about the facts. It is not intended to entertain you; it is to inform you and hopefully to call you into action. This e-book is also not about making money. You may freely share this e-book under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.
This book is a follow-on from my previous e-book publication, titled: Extinguishing the Fires of Hell. You can download it from a link contained on the page here: https://ggenereuxblog.wordpress.com/2016/04/22/ending-the-mystery-of-auto-immune/
In that earlier work, I built up what I thought was a pretty strong case for my theory that the autoimmune diseases, and some of the other major chronic diseases of our time, are indeed rooted in subclinical vitamin-A poisoning. I presented hundreds of different pieces of information and evidence to make that case. Every single bit of that evidence was backed up by references, and much of it was published in reputable peer-reviewed scientific studies. Although no single piece of evidence presented therein was conclusive, I felt that when it was all combined, that collectively it should have been very compelling. I was trying to piece together all the smaller and seemingly disparate pieces of evidence into a mosaic that would reveal the bigger picture. I felt that in doing that, the case implicating vitamin-A in the chronic diseases would be just so logical, and so overwhelmingly clear, that most people would see it.
However, for the most part, that was not the reaction I received. From the very few people who I could even get to read that e-book, the reaction was far less than supportive. A few other people were sitting on the fence about it, and gave it a qualified maybe. Even though there were a few people who did indeed “get it,” for most folks, it was a non-starter. They were just not even considering it to be a possibility. I could have blamed this reaction on say, they were just not open minded enough, or that they just did not try hard enough to see the connections, and / or that they were not curious enough to dig into the backup research and studies, etc. But, the reality is that if anyone’s to blame, it’s me. I think I fell into the trap of thinking that more, and more, and more evidence would make the case. The truth is that I probably presented too much information, and most people just don’t have the time to read, in depth, a 400-page book on some outsider’s wacko theory. Unless people have a horse in the race, so to speak, they are just not going to make the needed time investment, and do the investigative thinking, needed to “get it.” But, that’s only part of the reason they weren’t getting it. More importantly, I believe they were just not willing to consider such a theory, regardless of the evidence. This theory was both too simplistic, and too far in left field. To paraphrase a few people, the reaction I got was: “Oh, no way, the autoimmune diseases are just far more complicated, and it can’t be explained by such a simple theory.” Therefore, all the circumstantial evidence and logical arguments I presented just weren’t cutting it. Additionally, who was I to make such absurd assertions? I was not an expert at all, and I had no background whatsoever in the field of medical science. It was like, “nope, no way, this is a job for the experts,” and you are not one of them.
People needed some big official scientific study to directly make the case for them. I dislike making this statement, but, I felt they just weren’t willing to think this through for themselves. Rather, they were deferring the thinking to the so-called experts, and medical science. Sadly, I could see that for a few of these folks, logical thinking had been replaced by procedure, and following the “official” rules and processes. However, what they may have missed is that I wanted to follow the official process of science. I wanted them to help conduct a bigger experiment. I knew and clearly stated that my theory was just that, a theory. In science, a theory remains to be a theory until other people prove it to be true. Moreover, before a theory becomes accepted, it needs to be proven true by many others, and at least hundreds, if not thousands of times over too. Therefore, my intent in writing that first e-book was to at least make the case compelling enough to have people experiment with this theory on themselves. To me, it seemed to be at least a reasonable thing to consider, since it was just a diet-change experiment. After all, the alternatives are not looking too promising since there’s been no great progress made by official medical science in getting to the root causes of these diseases. But, not too surprisingly, there have only been a few people so far who have been willing to take on this experiment. I guess you’d have to be rather open-minded, and even a bit bold to make such a dramatic sounding diet change. Of course, the big concern for everyone is the risk of vitamin-A deficiency. Surely, the official processes of medical science didn’t get that wrong? After all, for over one hundred years now, official medical science has been telling us that we’ll all quickly go blind if we don’t get enough vitamin-A each and every day. We are also told that there are millions of kids in Southeast Asia sick or even dying every year from vitamin-A deficiency. So, in the face of these little facts, it probably seems somewhat risky to go on a zero vitamin-A diet. Therefore, the question most people probably ask themselves is something like this:
I am already suffering from autoimmune disease, am I really going to take on this silly experiment, with a very long shot chance of it doing any good, and risk the very real and dire consequences of vitamin-A deficiency? Am I willing to risk going blind too?
Naturally, that is exactly the question I had seriously asked myself too. Maybe oddly, the answer was easy for me. I thought that if I had a choice between going blind or having to deal with my skin burning off due to eczema for the rest of my days, I’d take the blindness. It was a decision I made in a heartbeat. Yep, I’d rather go blind than to live in continuous pain. However, I also knew that it was not necessarily an or condition. I could end up with both blindness and continued, unabated, eczema. However, based on my preliminary four hours of research, I was rather damn sure I was not going to go blind. I had determined I had a least a year’s supply of vitamin-A stored in my liver. I was also quite sure that eczema was none other than vitamin-A poisoning.
Therefore, I thought that I’d be able to at least improve my eczema condition well before any adverse symptoms showed up in my vision. I am a numbers type guy; I trust numbers. I am also a “science” type guy. I love and understand science. I also knew that science could and does occasionally get it wrong. That is just an absolute fact. I also knew that when science does get it wrong, it was the people who were interpreting the science who got it wrong. We all make mistakes. Therefore, it was only a bit surprising to me when my vision quickly became dramatically better on my vitamin-A elimination diet.
So now, after being on a vitamin-A-free diet for over three years by avoiding retinol and carotenoids (nearly zero molecules of any of these compounds), I no longer have eczema. Also, I am not typing this on a brail keyboard! Therefore, I know that the people in medical science did indeed absolutely get it wrong here.
Unlike numbers, I don’t trust people so easily, and especially so when there are large amounts of money in the equations. Human nature is almost as predictable as math and science in this regard; when there are large amounts of money to be made, there is usually large amounts of corruption too.
Therefore, the intent of this e-book is two-fold. One is to assure you that no, you are not going to go blind on a vitamin-A deplete diet. And two, to attempt to debunk the entire vitamin-A deficiency theory. Once you have that information, I hope you will apply it to your autoimmune disease.
If you’ve skipped the preface, and haven’t read my prior e-book then you will be missing some important context of what this book is all about. Please go back and read the preface before continuing here.
My early investigation into vitamin-A has been full of surprises. It was surprising to find that there are over fifty documented symptoms of vitamin-A toxicity, and there are over fifty named autoimmune diseases. That’s correct. Almost every significant symptom of vitamin-A toxicity has a correspondingly named autoimmune disease. Yet, there were a few paradoxes too. But, the one that I found most troubling and perplexing is that the symptoms of vitamin-A toxicity. That seemed so peculiar to me. It would be somewhat like seeing that the documented symptoms of dying from dehydration as being identical to those of dying from drowning. It was just so illogical. Something was just not adding up here with vitamin-A being both a deadly toxin and a critical vitamin at the same time, and with the same symptoms if you get too much, or too little of it. Someone, somewhere just had to have gotten their wires crossed on this one. Another perplexing question I struggled with was why had the human body built such a critical dependency upon a toxic molecule. This dependency was most certainly not impossible, it just seemed strange to me that after millions of years of being perfected by evolution (or by God’s creation if you prefer), that we’d have such a dicey dependency upon this one highly toxic molecule. It was hard to believe that nature (or God) could be this foolish.
Other areas of my investigation revealed many more apparent paradoxes and completely conflicting pieces of information. Additionally, in the various studies regarding vitamin-A, almost all the contradictions and paradoxes, are conveniently explained away, or glossed over, and done so with completely unsubstantiated rationalizations. Many of the so-called medical experts who blame illness on a vitamin A deficiency are either just making it up, blindly restating unsupportable prior theories as being fact, or just down right fabricating and obfuscating study results to fit a pre-established narrative. Sadly, it goes way beyond that. I could have never imagined that medical science was so rife with blatant scientific fraud.
Moreover, after carefully reading the very detailed descriptions by leading ophthalmologists of the progression of tissue destruction in the eye due to xerophthalmia (chronic dry eyes), it was an exact match for the description and progression of the tissue destruction I witnessed under a microscope with my own skin due to eczema. It was not just an approximate match, or a very close match, it was an absolutely perfect match. Yes, I knew all about those little cone shaped piercing blisters. The only difference is the named organ where the tissue destruction was taking place. However, somehow, more than one hundred years of modern medicine has failed to see the obvious; they are indeed one and the same condition. It is exactly, and precisely, the same condition occurring in two different organs. It was immediately clear to me that xerophthalmia and eczema are the same condition occurring in both the epithelial tissues of the eye and the epidermis.
Of course, the leading theory in ophthalmology (and that promoted by the World Health Organization) is that xerophthalmia is the direct result of vitamin-A deficiency. Although I am making an extrapolation here, xerophthalmia is effectively eczema of the eye. Thus, with the de-facto causation theory of xerophthalmia being that of vitamin-A deficiency, we should be able to conversely apply the same causation theory to eczema. Meaning, the leading theory in the causation of eczema should also be vitamin-A deficiency too. Therefore, just one of the great contradictions I want to highlight here is that there are now 30 million people in North America with eczema (with various degrees of severity), and there is simply no way they are vitamin-A deficient. There is simply no way even the tiniest fraction of them are vitamin-A deficient. So, how in the hell is it that vitamin-A deficiency can cause xerophthalmia in the eye due to vitamin-A deficiency, and for us to have exactly the same condition in the skin to occur in 30 million people who are clearly not vitamin-A deficient? However, once you factor into the equation that the tissue of the skin and the eye are both this beautifully structured stratified epithelial tissue, and the very well proven destruction too much vitamin-A will induce in this particular tissue structure, the mystery and contradictions disappear. What you are about to learn, is that the truth is that xerophthalmia is not caused by vitamin-A deficiency at all. Rather it is the exact opposite; vitamin-A toxicity causes it.
Of course, I’m only scratching the surface here regarding the obvious inconsistencies and contradictions in the vitamin-A story. The other primary, and obvious, contradiction, somehow also still being glossed over by modern medical science, is that if we are all so at risk of vitamin-A deficiency, and its horrible, if not deadly, consequences of going blind, how is it that we are here as a species at all? It is so gigantically illogical, this, by itself, should have quickly thrown the vitamin-A deficiency theory into the scientific trash can of nonsense. For example, some of the early experiments putting animals (dogs, rabbits, chickens, and most often rats) on vitamin-A deficient diets, and for them to quickly develop the systemic and catastrophic destruction of all their epithelial tissues should have raised serious questions as to the validity of the design of their experiments. In dogs, the epithelial destruction happened as quickly as in four weeks; in rats, it was around eight to ten weeks. Naturally, most of the animals died shortly after that. Therefore, how is that even possible for animals to be this critically susceptible to vitamin-A deficiency, and still be on the planet as a species? Having such a disastrously inherent design flaw resulting in the eyes, and many other organs, to quickly start self-destructing and to ultimately fail due to a vitamin-A deficiency in just eight weeks would immediately rule these animals, and us too for that matter, out of evolutionary existence. Having the eyes failing in just four to eight weeks, due to vitamin-A deficiency, would obviously be an end-of-life event. Without vision, any animal would quickly be eaten by predators, and if that did not kill them, they would not be able to find their own food. In other words, if this design flaw did exist in any species, then that species would have long ago become extinct. Therefore, the various experiments believed to have proven vitamin-A deficiency were so blatantly flawed that anyone’s grandmother could have told them that they had gotten it wrong. The experiments just do not pass the litmus test of common logic, and they most certainly cannot stand up against even the most trivial amounts of critical thinking.
In other words, these early scientists failed to ask the very most basic and fundamental questions. Biologically speaking, and in an evolutionary context, how is it possible for us to be here? One winter would have wiped out nearly all of these species, and us, from the planet. Seriously, can you imagine the skin and eyes disintegrating, burning off in mid-winter, weeping lymph fluid and so easily becoming infected, in just eight weeks, and yet these species have survived, and survived very well over tens of millions of winters? Talk about missing the obvious.
What I know from my early years growing up on the farm, is that rats can winter for at least nine months, living on nothing but grain, and do very, very well. Rats do extremely well for nine months, or more, without a single molecule of vitamin-A in their diets. They have perfect vision, and remain in great health. The bigger ones can grow to be about a third the size of a house cat. They have high energy levels, and vigorously and ferociously defend their territory. They reproduce, well like rats, too on their vitamin-A deficient winter diets. But, don’t take my word for it, just ask any prairie grain farmer if a rat can live all winter long on grain alone. Therefore, a simple grain farmer could have so easily debunked all the ridiculous vitamin-A deficiency theory from the esteemed academics in a matter of minutes. It appears that these academics had a complete disconnect from nature, reality, and sensible logical thinking too. With these very basic and obvious facts the entire premise of vitamin-A deficiency is nothing more than a complete myth. It is simply impossible, except for possibly in the most ridiculously long term and extreme periods of starvation. But, what you’ll soon learn is that animals, and humans, will die of starvation before they are truly vitamin-A deficient. In other words, both animals and humans will die first due to prolonged starvation before the eyes fail. Once again, from an evolutionary point of view, this is perfectly logical too. The body needs to maintain the eyes and vision to the very end of life.
So, where and how could these early researchers have gotten it so incredibly wrong? That’s the question we are going to investigate here. We are going to reopen the cold case of the very determination of vitamin-A being a vitamin at all. The surprising truth is that vitamin-A is not even a vitamin at all. No, it is a complete myth based upon bad science. So-called vitamin-A is simply far, far more of a toxin than being a vitamin. The sad truth is that it is a toxic molecule that has now killed tens of millions of people, and that’s just in the last few decades. Additionally, there are more than a 100 million people in North America who are now the walking wounded due to its insidious destruction of our epithelial tissues and associated organs. What you are also going to learn is that the names given to the chronic diseases simply hides the fact that most of them are really the same disease. They are the same diseases because they are all diseases of one tissue category; it’s the epithelial tissues. The names of the chronic diseases are obfuscations, and are pretty much meaningless labels. To make the point perfectly clear, consider the following: diabetes is a disease of the pancreatic epithelial tissues. Eczema is a disease of the skin, a stratified epithelial tissue of the epidermis. Heart disease and stroke are diseases of the epithelial tissues lining the blood vessels. Multiple sclerosis is a disease of the epithelial tissues making up the myelin sheaths wrapping nerves. IBD, Crohn’s, and colitis are diseases of the epithelial tissues making up the lower digestive tract. Cataracts is the disease of the epithelial tissues making the lens of the eye. Xerophthalmia (chronic dry eyes) is the diseases of the epithelial tissues of the tear ducts, and other glands within the eye. Asthma is a disease of the epithelial tissues of the lungs. The same applies to many of the other named chronic diseases. They can be more appropriately, and correctly, named as epithelial disease. However, we need to be a bit more precise; they are truly epithelial poisonings. There is only one potential poison in our foods that can be responsible for all of this, and it is vitamin-A!
Once again, the incredible irony here is that vitamin-A does not protect from xerophthalmia as claimed by the experts in ophthalmology and the World Health Organization; rather it causes xerophthalmia, and amazingly cataracts too. Almost unbelievably, these self-proclaimed experts, and proponents of vitamin-A supplementation, have got it completely, and perfectly, backwards. If any ophthalmologist happens to read this, the truth is that vitamin-A is causing the destruction of the vision in tens of millions of people around the world. You should be concerned about that. If you think I am wrong and are up for a large wager, I’m in.
Also, if you happen to be wondering why I’ve used an 11-point font in this e-book it is because I know that my intended audience, mostly people with autoimmune diseases, will need the larger font size.
What we are going to do in the next few chapters is to go on a deep dive into the evolution of the very discovery of vitamin-A. From there, we are going to carefully investigate the subsequent follow-on vitamin-A deficiency theory, and it’s supporting experiments. As we undergo that investigation you’ll see that we enter a bit of an alternative universe where things are often the inverse of reality, scientific “facts” are almost fabrications from vague, confusing, and totally conflicting experimental results. The evidence I am going to present in the subsequent chapters leads me to firmly believe that vitamin-A is not a vitamin at all. As I’ve stated above, it does not belong on the list. It is an imposter. I believe that it is simply nothing more than a poison. If I am correct about this, it will be a case where science has not only gotten it completely wrong; it has gotten it perfectly backwards too.
Of course, this is no harmless little scientific blunder. Rather it has been catastrophic for human health worldwide. By giving the prestigious vitamin designation to a highly toxic molecule and its subsequent supplementation into our major foods has resulted in the mass poisoning on an almost unbelievable scale. The resulting death toll is easily now in the tens of millions, and 100s of millions are now chronically diseased because of it (no drama intended, it’s just the facts).
The early part of the 20th century was the heyday of the discovery of vitamins. In the late 1890s, there was the evolution of the concept a vital, yet hidden, essential substances in our foods. In addition to the proteins, fats, and carbohydrates that were well known, researchers had concluded that there were other special components needed for human development, growth, and sustained health. Without these hidden substances, serious deficiency diseases would develop. Originally, these hidden substances were called “vital amines,” and thus the subsequent abbreviation to vitamins. The earliest classification of these vital components were divided into two categories, the fat-soluble A’s and the water-soluble B’s.
In the early 1900s investigators went on an exploratory expedition to isolate and determine what these special food components, or “factors,” were. Of course, with the discovery of these components came the potential for great academic recognition, prestige and possibly even the financial rewards in the form of Nobel prizes, and patents, etc. Therefore, these early researchers were highly motivated to make discoveries. The earliest, and the first fat-soluble vitamin, to be discovered and isolated was vitamin-A.
One of the first thought to be indicators of deficiency of the vitamin-A was the condition of night blindness. Now, it’s very important to understand what is meant by the term of night blindness. It is not actually being blind at night. It is the condition of the slow adaptation to darkening light conditions. To this day, it is still this slower adaptation to changing light conditions that is measured in determining the severity of vitamin-A deficiency. Therefore, night blindness is not a condition in the deterioration of the photoreception capability of the eyes.
Some of the early (circa 1900) well documented and most widely published examples of night blindness were in the Newfoundland fishermen. After being at sea during the day, with the eyes exposed to the glaring sunlight off the water, many of the men found it very difficult to adapt to the diminished light conditions as night fell. This night blindness condition was not only problematic but quite dangerous too as the fishing ships sailed back to the rocky shores. But, the night blindness condition was usually somewhat resolved by a good night’s sleep. Therefore, night blindness was not at all permanent damage to the eye.
Of course, the crafty and resourceful Newfoundland fishermen improvised effective workaround solutions to the problem. One solution was to wear a patch over one eye one day and then alternate the patch to the other eye the next day. Each day, as night fell, they would remove the patch, and they’d have reasonable night vision from the previously covered eye. Not surprisingly, this was a well-known technique used by pirates for decades before then too. However, for pirates, the motivation was not for the safe return of their ship to shore at night. No, for pirates, the quick adaption to low light condition was an essential life survival and battle skill. When they boarded, and raided other ships, and went below deck, they would be at a clear disadvantage to the well low-light adapted and sword wielding defenders.
In addition to wearing a patch on one eye, the Newfoundland fishing ships adopted a similar measure, where they would keep one crew member below deck all day long, and this designated crew member would then be brought up on deck upon nightfall to safely navigate the ship back to shore. But, the craftiness of the Newfoundlanders did not stop there. They also learned that if they dripped some cod liver oil into the eyes at night, it would accelerate their recovery to good vision by the next morning. There are many similar accounts in the writings from antiquity of using liver oil applied directly into the eyes to aid in the recovery from night blindness as well. There are of course accounts of consuming liver, or just the liver oil, curing night blindness too. But, the condition of night blindness was only one, and the far more minor one, of the conditions ascribed to the suspected vitamin-A deficiency. The other far more serious disease conditions were prolonged dryness of the eyes, the dryness then spreading over the cornea, subsequent scarring, lesions, and eventually significant degeneration of the eye. This spectrum of the disease conditions is termed: xerophthalmia.
As these more serious conditions progressed, the disintegrating tissues almost always became infected. If the condition were not remedied it would ultimately lead to complete, and irrecoverable, blindness. From these accounts, the early vitamin researchers logically concluded that there must be some special hidden factor in cod liver oil that was so beneficial to the eye in promoting the recovery from night blindness, dry eyes, and even quick healing of the lesions.
However, very early on there were clearly flaws showing up in the grand theory, but they were completely ignored or glossed over. One very important bit of information the early researchers failed to appreciate was the fact that Newfoundland fishermen also ate codfish nearly every single day. It was the staple protein, if not the primary food in the region’s diet for like 400 years. With that knowledge and two minutes of clear thinking, they should have probably concluded it was not even possible for it to be a deficiency condition at all. What was far more logical, and completely obvious even at the time, and what any self-respecting pirate could have attested to, was that it was the overexposure to sunlight that caused their night blindness. But, the problem for these researchers with that position is that you can’t make great discoveries, and there’s no money to be made, without finding a special deficiency. Therefore, to rationalize how the dripping of cod liver oil into the eye was getting the vitamin-A into the cells of the eye, they concocted this bizarre scenario of the liver oil running backwards in the (likely blocked) tear ducts, down through the nasal cavities, into the throat, down through the digestive tract, then into the blood, through the liver, released back into the serum, and then back up into the eye. Once into the eyes, the essential vitamin-A factor did its magic of repairing the condition of night blindness, and it did it in just eight hours. Damn, isn’t that brilliant! But, let’s not fault just the early researchers in this fabrication, because, the same accounts and illogical reasoning is parroted in modern scientific literature too.
One much earlier experiment, from around 1816, particularly stands out for me. A researcher named François Magendie put dogs on a starvation diet of just sugar water. Sure enough, within just four weeks, the dogs started to develop eye lesions. Damn! It was almost conclusive; it must be a vitamin-A deficiency (not B, not C, not D, nor proteins, nor fats, nor minerals, etc.). Of course, this is a completely unnatural diet for a dog. When in all of evolutionary history have dogs ever consumed sugar water? It is about as logical as using a diet of water and peach pits to prove vitamin-A deficiency. Even though these dog experiments were done way back in the early history, they too are still cited in contemporary, and current medical textbooks as evidence of vitamin-A deficiency. Of course, this ridiculous dog diet proved no such thing as vitamin-A deficiency. If nothing else, it simply proved the toxicity of sugar in the diet. Naturally, anyone with even a little experience with animals in the wild knows that animals don’t go blind in just four weeks even due to starvation. Once again, if that did happen, then the species would not even be here at all. Other species, such as the wolf, quite routinely do starve for much longer than four weeks, and their vision remains perfect. Of course, these very early experiments of sugar water diets are incredibly unscientific and are clearly almost senseless. Admittedly, they are only early starting points in the vitamin-A deficiency investigation. Yet, similar bizarre extrapolations continue to this very day to support the vitamin-A deficiency theory.
Before we move on, we need to understand some of the terms used to describe the various conditions and diseases of the eye. The more broadly used, and encompassing term, is “Xerophthalmia.” The simplest definition of Xerophthalmia is the condition of “abnormal dryness of the conjunctiva and cornea of the eye, with inflammation and ridge formation, typically associated with vitamin-A deficiency.”
Here’s a short glossary of some of the other related terms we’ll come across.
Bitot’s Spot - are the buildup of keratin located superficially in the conjunctiva of the eye. They are thought to be a key indicator in the diagnosis of vitamin-A deficiency.
Conjunctiva - the mucous membrane that covers the front of the eye and lines the inside of the eyelids.
Dermatitis - is a general term that describes an inflammation of the skin.
Keratomalacia – the softening and progressive disintegration of the cornea of the eye. Thought to be an indication of the more advanced stages of vitamin-A deficiency.
Night Blindness – impaired ability to adapt to low light conditions, or being temporarily blinded by bright lights at night. Thought to be a major clinical indicator of vitamin-A deficiency.
Ophthalmia – inflammation of the eye, especially conjunctivitis.
Retinol – the simple chemical name for what’s called pre-formed vitamin-A.
Ulcer – an open sore that has occurred without externally induced trauma.
Xerosis – generally means drying of the tissue, often used in the context of the condition of the eye.
|Table 1 Classification of Xerophthalmia conditions|
|Corneal ulceration (keratomalacia) < 1/3 corneal surface||X3A|
|Corneal ulceration (keratomalacia) = 1/3 corneal surface||X3B|
|Source: The WHO 1981|
The dry eye condition usually originates with the decreased production of mucus or tears. The mucus or tears are of course critical in keeping the eye lubricated, and it also helps protect against infections. However, as the dry eye condition worsens, and more tissue structures and surfaces become involved, it can develop into very serious eye disease. There is a spectrum of such conditions. Each one is uniquely named, ranked, and categorized according to severity. Somewhat confusingly, the entire spectrum is included under the umbrella term of Xerophthalmia. Maybe a bit oddly, even though Night Blindness is not a condition specifically of dry eyes, it too is included within the Xerophthalmia classification spectrum.
Now, it is very important to understand the conflation between the terms “xerophthalmia” and “vitamin-A deficiency.” The two terms are almost completely synonymous. The theory and belief, that vitamin-A deficiency causes all of the above conditions is so entrenched and ingrained in medical thinking; the two terms are nearly inseparable. So much so, that there’s an almost circular dependency between them, each term is used as an indicator of the presence of the other. Meaning, the presence of “xerophthalmia” is a measure of the “vitamin-A deficiency” in a population. And conversely, therefore, the degree of “vitamin-A deficiency” in a population is measured by the incidence rates of any of the “xerophthalmia” spectrum conditions. Okay, with that bit of terminology covered, we can move on here.
The next suspicious aspect in the evolution of the deficiency theory was that there were other early researchers who were showing that just having adequate amounts of dietary fats, and especially that of butter fat, could prevent and reverse the same “xerophthalmia” disease conditions of the eye.
Probably the most noted was the work of Dr. Masamichi Mori in Japan (not to be confused with S. Mori of Wisconsin who is another prominent early vitamin-A researcher). In 1904, Dr. Masamichi Mori provided a comprehensive account of the pathogenesis of the Hikan condition he observed in children in his clinic. The term Hikan is the Chinese name for these same diseases of the eye. There are some very important clues and information that Dr. Mori provides us in his report. Firstly, the disease condition occurred mostly in younger children, from ages 1 to 4½ years-old. Therefore, somehow younger children were more susceptible. Secondly, is that the condition was occurring more frequently in boys, at a ratio of about four boys to three girls. The next and the critically important observation made by Dr. M. Mori was that this disease was not at all limited to just the eyes. By Mori’s observation, and definition of the disease, it included five distinct symptoms (comorbidities if you prefer that term). These were: diarrhea, abdominal expansion, excessive appetite, night blindness, xerosis of the conjunctiva, and thinning of the hair.
In addition to these five specific symptoms, he also documented the children commonly having dry skin, and having significant sensitivity to sunlight too. One other very important little detail he documented was that the condition was more prevalent in the summer months. Therefore, clearly, the Hikan disease condition was much more than just an eye disease. Nonetheless, Mori very successfully treated the disease by just adding more fats to the diets of the children. He was quite certain that it was just the additional fats and not something special hidden within the fats, that was responsible for the recovery from the disease. But, to Mori’s American contemporaries, and modern day historians, their conclusion was that Mori had missed the mark with his hypothesis and that it was not just the additional fats that had ameliorated the disease.
However, what I hope to show you later, is that Mori was indeed correct. It was not some deficiency condition ailing these children at all. Rather it was a poisoning, and the additional butter fat in their diet was emulsifying and therefore protecting them from it.
Now, it is very important for us to remember Mori’s documented comorbidity pattern:
- more common in boys than girls
- the younger the child, the more susceptible they are
- abdominal expansion
- excessive appetite
- night blindness
- xerosis of the conjunctiva (dry eyes)
- thinning of the hair
- dry skin
- sensitivity to sunlight
The reason that it is important to remember this pattern is because we need to be able to recognize it again when presented in another context in a later chapter.
Next, in 1909, W. Stepp in Strassburg was conducting experiments on mice deprived of fats in their diets. He concluded that diets of just proteins, carbohydrates, and inorganic salts were not sufficient in sustaining life. However, as with M. Mori’s work, Stepp’s American counterparts made the determination that it must have been some hidden missing factor in the fats, and therefore it was a deficiency that caused the animals to become ill and die.
Naturally, there are other similar reported accounts from this era of fat deficiencies causing night blindness and xerophthalmia. Yet, these reports did not dissuade the vitamin-A deficiency theorists. The clincher study thought to have cracked the case in favor of the deficiency theorists is probably the work published by Bloch in around 1912. Bloch was a pediatrician working in Demark and was treating eight children with xerophthalmia. It is quite an interesting report because there are two distinct groups of children, those that get fat milk, and those that get fat free milk. Half of the children on the fat-free milk developed night blindness, and xerophthalmia. Of special note, like in M. Mori’s report, these children are very young, 1 and 2-years of age, and they also exhibited sensitivity to sunlight. Likewise, Bloch reported that the onset of the disease condition in the children occurred almost simultaneously in the months of May and June (when there’s more sunlight). Bloch treated the affected children with cod liver oil, and within just one week they had made remarkable recoveries. Once again, this recovery was attributed to the vitamin-A content in the cod liver oil, and therefore, it was concluded that it was the addition of vitamin-A that was the responsible curative agent, and not necessarily the oil itself.
So, with these studies, the researchers were zeroing in on the vitamin-A component so abundant in cod liver oil and to a lesser extent, in butter. Since it sure looked to be the case, they quickly assumed that it was responsible for accelerating the recovery and curing the children of the night blindness condition. Of course, they very logically assumed that conversely, a deficiency in vitamin-A would, therefore have, have caused the conditions to develop in the first place.
At the same time, the early American researchers quickly sped ahead and started conducting many more experiments on animals to prove their vitamin-A deficiency theory. By using vitamin-A deplete diets in their experiments, they quickly induced the xerophthalmia conditions, and many other severe conditions, in their lab animals. They claimed that the only significant missing nutrient from the animal’s diet was vitamin-A. Therefore, they felt that they had isolated it down to the disease being solely attributable to a vitamin-A deficiency. With that extrapolation, the blame, and root cause of night blindness, and the many assumed to be associated other diseases of the eye was pinned squarely upon a deficiency in vitamin-A.
From that presumptive observation, we all quickly fell into the cascading pit of failed and catastrophic so-called scientific investigation that led to the determination of vitamin-A being a vitamin. Looking at this evidence, and I suppose just due to our historical human conditioning, the thinking was that it just had to be a deficiency and not a toxicity condition causing the disease. In a strange way, this assumption of deficiency prevails even today. What I see today, is that almost everyone believes that when they get sick (and when clearly not due to infections), that they must be deficient in something.
Thus, by 1913 it was conclusive, the vitamin-A deficiency condition was proven as the cause of both night blindness and the more serious disease conditions of xerophthalmia and conjunctive xerosis. This conclusion then officially puts vitamin-A as the first vitamin on the list to be confirmed. The credit for the discovery of vitamin-A goes to the American researchers Elmer McCollum and Marguerite Davis. In 1913, it was simply called fat soluble A, and in 1920 it gets renamed to the more official and prestigious term “Vitamin-A.” However, McCollum’s legacy in this matter is not limited to just being given credit for the discovery of the vitamin. He also defines the official experimental lab diet that nearly all subsequent researchers use to replicate his results. With that bit of historical background, now here we are, over 100 years later, undertaking some forensic work to determine if they might have gotten it completely wrong.
Naturally, there have been far more rigorous, and scientifically conducted experiments in the 1920s, ’40s, and even the 1960s that are used to seal the deal, close the case, and put the question of vitamin-A deficiency to rest for once and all. However, there is a wickedly deceptive flaw exhibited in almost all these experiments. It’s hidden in the McCollum designed diet. In addition to the critical scientific flaw in their experiments, there other humanistic factors that prevent them from seeing that something is drastically wrong and completely illogical in their results.
The first major humanistic factor is their certainty about it. These early researchers are so certain that they’ve conclusively proven the case it makes them blind to what should have been obvious all along. The second major problem was that they failed to accept and appreciate that they were probably working with incomplete information.
We’ll investigate these follow-up experiments in a lot more detail in a subsequent chapter. For now, we just need to know the stated conclusions and interpretations made from them. Basically, and a bit simplified, it was that both animals and humans have the same almost razor thin tolerance for vitamin-A deficiency. Get too little of it, and you’ll go blind, or you’ll first go blind and then you’ll die; or get too much of it and you’ll die with your skin painfully burning off. Either way, it’s a dicey balancing act.
Yet, somehow these early researchers, and even researchers today, have completely ignored the fact that animal and human history is full of prolonged periods of complete starvation with no such “deficiency” lesions developing in the eye, and of course no blindness either. But, with fame and glory on the line, there’s not much time or effort allotted by these researchers to such logical thinking. Therefore, it was a vitamin-A deficiency, done deal, end of the story, let’s move on to filing patents, and making money. I’d like to say that these folks presented a lot of scientific arrogance in this endeavor. But, somehow, I don’t think that was the case. I think they were just too caught up in it, and therefore they failed to see that something was hugely amiss.
Either way, what you’ll soon find out, is that these so-called definitive experiments were completely botched, and almost as ridiculously flawed as this sick experiment with dogs on the sugar water diet. One source of the problems is that trying to design a viable, yet vitamin-A deplete, diet to experiment with is surprisingly rather tricky. The thing is, almost all foods on the planet have at least some vitamin-A in them. In other words, to come up with a completely vitamin-A deplete diet, you need to rule out so many other needed nutrients at the same time. But, that’s only the start of the problems introduced in these experiments. There was an unforeseen, and amazingly ironic, little unknown that secretly tipped the scales.
Before we dig deeper into the mysteries of vitamin-A deficiency, we need to back up a few steps and talk about how experiments fit into science and the basic rules of the scientific method. Even if you are familiar with this topic, please don’t skip this chapter, as it sets up some context needed for the subsequent chapters.
The “experiment” is one of the most critical cornerstones of science. The experiment is used to prove or disprove a theory. Before theories are tested with experiments, they are generally put forth as a hypothesis. As a hypothesis is being refined, and if it gains some strong supporting evidence it progresses to being called a theory. Only after hundreds of repeated experiments, yielding exactly, or very close to exactly the same results, and the experiments are conducted by many different scientists, and preferably from around the world, can a theory be regarded as a fact.
In addition to the “experiment,” the other cornerstones in science are what are called the pure sciences of mathematics, physics, and chemistry. Sometimes, they are referred to as the “exact” sciences. They are called this because they usually provide exact answers to questions and problems. Although they are referred to as being exact sciences, that does not in any way connote that they are complete sciences. It’s far from it, most scientists in these fields realize just how little they know. They are usually humble, and they know that they are never working with the complete picture. However, what they do know about, they are reasonably certain that it is correct. Even with that, there are sometimes complete upsets in the “exact” sciences. The current new discoveries being made in the world of quantum physics is a good example. How are these upsets proven? It is with the discovery of new information and then having it backed up by additional experiments.
There are other fields of science that are considered “inexact” sciences. A good example is geology. Geology is more appropriately called the science of concepts and related processes. These concepts are mostly “provable” via observations of the present processes in nature, and the extrapolation of them back through the millennia. Although geology is a wonderful science, it is far from exact, and it is often difficult to design experiments to conclusively prove geological scientific facts. Nonetheless, one of the most important lessons we can use from geological sciences is the concept of very slow processes applied over very long periods of time yielding dramatic results.
Further down the spectrum of the “exactness” scale of the sciences would be many of the medical sciences. Biological systems are amazingly complex and we only truly understand a very tiny fraction of what remains to be learned. Even further down the spectrum, would be the so-called sciences of mental health and psychology. Currently, these fields are anything but science. They are simply speculations, and guesses or hunches as to the real functioning of the human mind and the brain, at the very best.
When designing, and conducting experiments, there are a few golden rules that need to be followed. Firstly, the experiment must be completely repeatable. The results must be reliably measurable. When the experiments are repeated by others, they must yield exactly (within the margin of acceptable measurement error) the same results. If an experiment fails to meet these criteria, then it is deemed to be invalid. In other words, it probably proves nothing. If an experiment yields significantly varying results, then the experiment is not well designed. The scientist then needs to determine why the results are not consistent, and refine the experiment to narrow down, and eliminate, the source of the differences.
The second golden rule in experiments is to change only one variable at a time. If an experiment has two or more variables changing at one time, it can be very difficult to claim the outcome proves the effect of either one independently.
The third golden rule in experiments is to objectively observe, and see what you are looking at. There is no room for biases, or for manipulating the data to have it ultimately “prove” the result you are looking for. Manipulating the data, A.K.A. cooking the books, is called scientific fraud.
The final, and the most important, golden rule is that if the result of well designed, and valid experiments fails to support a theory, then the theory is very likely wrong. Although this can be frustrating, and disappointing, legitimate researchers must always accept the results as a fact. Just to repeat it: the critical point here is that if a well-designed and valid experiment fails to support a theory, even once, or even apparently just one time, then the theory is wrong.1
But sometimes even “failed” experiments can be hugely valuable. This is because when conducting an experiment to test a theory, and even though the experiment fails, it may reveal some other completely unexpected and intriguing results. Many major discoveries in science have indeed been made when conducting “failed” experiments that were in completely unrelated fields. Some notable examples are the discovery of microwaves from radar research inducing heat in food leading to the development of microwave ovens. Likewise, some of the major pharmaceutical drugs in use today were discovered by lab mistakes made in the textile, and fertilizer industries.
Therefore, to be a legitimate and successful scientist one needs to recognize that science is never complete, and you must always remain open-minded. What’s accepted as being the truth today could be overturned with new evidence tomorrow. You must always remain ever curious and be on the lookout for anomalies, even the tiny ones that appear completely insignificant to most other people. You must always have your eyes open and see what you are looking at. So often people fall into the trap of seeing only what others are telling them they are looking at.
So now, why did we need to review the background rules on conducting experiments? It’s for two primary reasons. Firstly, it is because we are going to analyze and review the early experiments used to “prove” the vitamin-A deficiency theory. Using these very basic rules you’ll be able to gauge the validity of those experiments, and that of the conclusion drawn from them.
The second reason for reviewing the ground rules for conducting experiments is because it will soon be your turn to be a scientist too. Don’t worry, you don’t need to have a background in science, or mathematics, etc., because anyone can conduct an experiment. I am going to ask you to conduct a trivial and fun little experiment with a few small animals such as gerbils, hamsters, or pet mice or rats. Although it will be a trivial, fun, and small experiment, when your results are combined with others who are conducting effectively the exact same experiment, it could be one of the most important experiments in human history. Also, don’t worry, no animals will be harmed. Of course, I’ve already conducted this small animal experiment, and I have my results. However, as I’ve stated above, the results from one person are not at all good enough. Therefore, I am asking you to be one of hopefully thousands of other people from around the world who do the same experiment and for you to contribute your results.
This is the fantastic thing about science. All the theoretical debates can’t hold a candle to the experiment. The experiment trumps the debate. The experiment is king! The experiment quietly cuts through even the loudest rhetoric, and regardless of who’s shouting it, and proves or disproves the theory. Obviously, this is not to say that critical and logical thinking isn’t just as important as the experiment. On the contrary, critical and logical thinking is extremely important. Thus, the experiment is in no way a replacement for critical and logical thinking; rather it complements it.
With that, by conducting a fun little experiment, and applying your own critical thinking, you’ll get to verify and see the results with your own eyes. Therefore, you don’t have to, and you never should just take someone’s word for it. Even though I’ve tried to back up every major statement and claim I make in this e-book with references, you most certainly should not just take my word for it either. At the very least, you should check and analyze those backup references. My interpretation of those referenced studies could be quite different than yours, and my conclusions might be entirely different too. Although I believe I am correct, I am still open minded too. I know I could be wrong. But, it does not matter if I think I am right or wrong, and it does not matter if you think I am right or wrong. What matters is that you help prove it one way or the other. What really matters here is that you conduct the experiment. You get to do it quietly with no outside influences, and therefore with no one’s thumb secretly tipping the scale so to speak.
Now, regarding the theory of vitamin-A deficiency, this is absolutely great because you get to participate in (potentially) overturning one of the most fundamental and longest held beliefs in modern medicine. I believe it also just happens to be the very root cause of most of the chronic diseases we are dealing with in the Western world too. Come on; you can’t resist being part of that, can you?
Even though we are investigating the theory of vitamin-A deficiency, we need to have a good understanding of the opposite side of that coin; that of vitamin-A toxicity. The primary reason we need this information is that we’ll have a much better understanding of the results from the vitamin-A deficiency experiments. That’s correct, knowing what to expect in the vitamin-A toxicity scenario will enable us to recognize what was really being demonstrated in the early vitamin-A deficiency experiments.
One of the most important aspects to fully understand and appreciate about vitamin-A toxicity is that it affects the entire body. It does not affect just one organ or show up in just one tissue type. No, the scope and breadth of the destruction it will cause is just staggering. It will slowly destroy everything from the hair on top of your head down to the nails on the ends of your toes. It will also slowly destroy every other organ and tissue in-between. Although vitamin-A toxicity will be most aggressively expressed by the destruction of the epithelial tissues, it will have profound and devastating cascading effects throughout the rest of the body too. Vitamin-A is very capable of destroying every cell in the human body. However, it’s most devastating effect is upon the body’s stem cells. Although most of the visible toxicity destruction takes place on the surface tissues, that of the skin, eyes, hair, and joints, that is just the beginning of its reach. It will slowly suck calcium out of the bones and teeth. It will distort the very shape of the spine and skull. It will be correspondingly destroying all the internal organs too. It will destroy the pancreas, the lungs, the kidneys, the digestive tract, the liver, the spleen, the thyroid, the lymph nodes, both the female and male reproductive organs, all mucus generating tissues, all villi structured tissues, the blood vessels, the heart valves, the eyes, the ear canals, and more. As the scope of the toxicity destruction progresses, it will seriously impair the functioning of the brain too. As the bones are slowly depleted of their calcium, that calcium reacts with the iron and oxygen in the blood. That exothermic reaction then not only causes intense inflammation, it drastically reduces and limits the blood’s ability to carry adequate amounts of oxygen. That limited oxygen supply then, in turn, can most certainly cause chronic fatigue, depression, psychoses, and even long-term brain damage.
Yes, all this destruction can be caused by getting too much of what modern medicine has termed, and wants you to continue to believe, is a “vitamin.” To me at least, that is one wicked sounding vitamin. Of course, with what I’ve just described, you should now be asking, if vitamin-A can be so toxic, why are we not all dead? Well, the two biggest variables here are just dose and time. Another big factor is that the human body is extremely well adapted to dealing with this toxin on a somewhat daily basis, but in reasonable amounts. Now, what’s happened is that our average daily consumption of this toxin has exceeded, and gone way past what’s historically been reasonable. Additionally, there’s a third important factor, and that is that retinol is a bit of an opportunistic toxin. If cells are protected with strong and integral fatty membranes, it is not going to easily get inside of them to where it can cause damage. So that, in a nutshell, is how and why we are now being slowly poisoned by it. Even though we are not all dead, at least half of us are now indeed mysteriously sick.
Naturally occurring forms of vitamin A include retinol, retinol esters, retinal and retinoic acid. The alcohol form, retinol, predominates in the circulation but it is too toxic for storage. Instead, the liver stores retinol as retinyl esters - principally palmitate.
Of course, there’s much more to this toxicity story. Another hugely important part of the story is that vitamin-A is a fat (lipid) soluble molecule. Therefore, it will naturally be absorbed (emulsified) by fats. This includes both dietary fats, and the body’s storage fats. For us, most of the storage of vitamin-A is in the fats within the liver, and to a lesser extent in the fats of the adipose tissues (the skin etc.) This storage ratio is not constant over time. As the liver becomes more and more saturated, more vitamin-A will remain in serum longer and slowly seep into and accumulate within the lipids of the adipose tissues.
Even with that, the vitamin-A stored within these fats is not yet toxic. In the early going, it is safely wrapped up, and therefore does not get rapidly exposed to cell membranes. Somewhat similarly, vitamin-A can be safely transported in serum within wrapper proteins. These wrappers are called the retinol binding proteins, the RBPs. When encased within the RBPs, no part of the vitamin-A molecule is exposed to the outside world. In this packaging, it is once again safe, harmless, and maybe even useful.
So, vitamin-A in reasonable amounts, given adequate amounts of dietary fats and proteins, is by itself not too terrible. However, there is a tipping point to where vitamin-A can, and does, easily convert into an extremely nasty, and highly toxic molecule (and the thought to be active form of the vitamin). This converted vitamin-A molecule is called retinoic acid. Retinoic acid is so incredibly toxic it is used as a chemotherapy drug. The reported functioning mechanism of the “drug” is that it quickly kills replicating cells.
However, it is critical to understand that every cell in the body will convert excess vitamin-A into retinoic acid. The overall rate of conversion is proportional to the number of cells that are exposed to the vitamin-A molecule. I believe it’s also proportional to the number of cells with damaged cell membranes. Therefore, to be safe, there should never be any excess vitamin-A in the body. What does excess vitamin-A mean? It means several things. One is that you never want to consume vitamin-A at a rate that exceeds your body’s safe storage rate. What’s your safe storage rate? It’s highly variable, and individualistic too, but it will depend mostly upon your current storage levels. The storage levels are dependent on not only our body’s lipid levels, but the composition of those lipids, and the current concentration of vitamin-A within those lipids. As we start to exceed the vitamin-A load carrying capacity of those lipids, we will move into the toxicity state. But, not only is the body well prepared to deal with vitamin-A, it is going to adapt in real-time in response to the potential threat. Our body is ultra-smart. It is going to force us to become fatter. Getting fatter is needed to protect us from the potential toxicity of having the vitamin-A molecule exposed to cell membranes. The body is also going to grow our liver larger, and larger, and larger too. But, as with most systems, there are limits. Once we approach these limits, more and more circulating vitamin-A will be exposed to cells, and the subsequent normal processes of converting vitamin-A to retinoic acid will take place.
It will start slowly, once cell at a time, and one molecule at a time. However, as more vitamin-A becomes exposed, the process will accelerate. Once again, the real big risk here is the conversion of vitamin-A to retinoic acid. Retinoic acid has about ten times the toxicity of vitamin-A (retinol). That is not to say that vitamin-A is not toxic. It is just not immediately toxic because it takes time to convert into retinoic acid. To better understand the relative toxicity between these two molecules, retinoic acid is by far the more toxic one. But, the conversion from vitamin-A (retinol) to retinoic acid is just a simple oxidation reaction. All that’s needed for the reaction to take place is a little activation energy and oxygen.
simply picks up the extra oxygen atom on the end of the side chain to become Retinoic Acid.
Vitamin A and the carotenoids are sensitive to oxidation, isomerization, and polymerization when dissolved in dilute solution under light and in the presence of oxygen, particularly at elevated temperatures.
Health, Survival, and Vision
Alfred Sommer and Keith P. West
With James A. Olson and A. Catherine Ross
Oxford University Press, 1996
See: page 223
Therefore, since the conversion of retinol into retinoic acid is so simple, we can think of vitamin-A as just being the devil in disguise. The true sinister identity of retinol is only revealed after it has metabolized into retinoic acid. The takeaway here, and what’s critically important to remember is:
Retinol is metabolized to retinoic acid in normal cells.
The natural metabolism of retinol into retinoic acid is very well known and widely documented. It is confirmed here in this excellent 2006 report titled: The acute and chronic toxic effects of vitamin-A.2
The A postprandial increase in serum retinol concentration may be blunted when vitamin-A is ingested with either food or ample dietary fat, whereas a significant amount of free (unesterified) retinol may circulate when vitamin-A is consumed without dietary fatty acids, which leads to excessive production of retinoic acid.
Source: The acute and chronic toxic effects of vitamin-A1–4, Kristina L Penniston and Sherry A Tanumihardjo
Therefore, depending upon a person’s particular storage situation and dietary intake scenarios there may be periods of time where excessive amounts of retinoic acid are produced. This has of course been directly confirmed in experimental studies.
Once again from the report on the acute and chronic toxic effects of vitamin-A.
An acute elevation of retinoids other than retinyl esters — eg, retinoic acid — occurs after the ingestion of a large amount of vitamin-A, possibly because the intestinal absorptive capacity is overwhelmed, which leads to the oxidation of retinol to retinoic acid by the intestinal enterocytes (30) and to the rapid formation of retinoic acid from retinol in certain cells (5). Whereas retinoic acid can be produced from excentric cleavage of beta-carotene in humans (31), it is generally considered a minor contributor to circulating concentrations, at least in normal, healthy persons.
Figure 1 The trapdoor Retinol consumption cycle
Therefore, the overload of vitamin-A consumption is a trap. The trapdoor loop looks like this:
Once you near your body’s storage capacity, and or the storage rate capacity for vitamin-A, all kinds of horrible things will start to happen. You’ve now fallen through an almost one-way trapdoor. There’s no known antidote, as far as I know of. So, with that, you’d think that the vitamin-A researchers, both the folks from the 1920s, ’30s, etc. and the modern day current so-called experts in the field would have realized the vital importance of getting it right. Given the dire consequences of getting it wrong, they should have been incredibly careful and gotten this whole vitamin-A dependency, and deficiency, theory exactly correct. It should have been verified, and re-verified at least a thousand times over, leaving absolutely no room for error. But, no, that did not happen.
So now, what’s the danger in getting into this elevated storage state? Well, it too is proportional, and highly variable. But, in small measure, or large, a dose of a chemotherapy drug can’t be a good thing to be dealing with on a repeated basis. When there is retinoic acid in serum, or in the intercellular fluids, there is sure to be cellular damage. Where’s this cellular damage going to happen most often? Well, once again it is going to be variable, and it depends, and it might be almost random. But, it is clearly going to most commonly show up in the eyes, and the adipose tissues, such as the skin.
The reason retinol and retinoic acid are so incredibly toxic is because being hydrophobic it easily slips through the cell’s fatty outer and nucleus membrane structures. From there the molecule’s cyclohexane group is a perfect fit into the cell’s RNA molecule.3
The perfect fit allows the retinoic acid to quickly substitute itself into the RNA sequence. Once that happens, the cell’s DNA processing mechanism is severely damaged. This damaged mechanism then breaks the cell’s ability to properly and precisely weave together intricate proteins. The cell either detects this DNA damage, or just errantly due to the broken machinery, then starts generating damage alerting proteins. This action is what is called retinoid-induced apoptosis (cellular suicide). But, the damaged cell simply can’t hold its breath and kill itself off. No, it needs some help. Therefore, the damage alerting proteins are truely pleas for that help being sent out to the immune system. The immune system responds, calls in the troops and kills the now damaged and defective cell. There’s a bit more to it, but this process is what modern medicine has mistakenly termed “auto-immunity.” This fabricated term is especially wickedly evil because “auto-immunity” is just the downstream consequence of subtly overdosing on a so-called vitamin.
What may surprise you is that these exact processes were observed and documented in the vitamin-A deficiency studies conducted back in the 1920s. However, since the term autoimmunity had not been coined until the 1960s, these early researchers referred to this unexplained phenomenon as the immune system’s foreign body response being activated when there was clearly no foreign body (bacteria or virus) present. These early researchers thought they were observing some mysterious immune response due to vitamin-A deficiency. But, they also clearly knew that the immune response was a follow-on reaction to the apparently already self-destructing tissue. These researchers were also quite certain that the immune response did not initiate the tissue damage. They were also very certain it was not due to infection. However, what they did not know, was that their experiments were not inducing vitamin-A deficiency at all.
Now, let’s get to know the vitamin-A and retinoic acid villains a little bit better. From the National Institute of Health:
Vitamin-A is a retinoid and a fat-soluble vitamin that is commonly found in eggs, milk and liver and in the form of provitamin-A in carotenoids in fresh fruits and vegetables particularly those with red, orange or yellow color. … and (cod liver oil)
Normal doses of vitamin-A are not associated with liver injury or liver test abnormalities, but higher doses (generally more than 40,000 IU daily, ~12,000 μg) can be toxic. Acute toxicity is caused by a single or a few repeated very high doses (generally >100 times the RDA arising within days to weeks with a typical symptom complex of severe headache, nausea, vertigo, blurred vision, muscle aches and lack of coordination, followed by skin desquamation and alopecia.
Chronic hypervitaminosis A usually arises 3 months to many years after starting moderately high levels of vitamin-A (generally 10 times the RDA) and is marked by dry skin, cheilosis, gingivitis, muscle and joint pains, fatigue, mental dullness, depression and liver test abnormalities.
Mechanism of Injury:
Vitamin-A in high doses is a direct toxin. Excess vitamin-A is stored in stellate cells in the liver and accumulation can lead to their activation and hypertrophy, excess collagen production, fibrosis and liver injury. The toxicity is dose-related and can be reproduced in animal models.
3 Image source: https://commons.wikimedia.org/wiki/File:Pre-mRNA-1ysv-tubes.png
There have been many experiments proving vitamin-A toxicity in animals. Here are a few that particularly stand out for me. Firstly, is “The action of vitamin K in hypervitaminosis A.”4 study from 1947. By S. E. WALKER, E. EYLENBURG AND T. MOORE. Dunn Nutritional Laboratory, University of Cambridge and Medical Research Council
Thus, by 1947 the toxicity of vitamin-A overdose had been very well established, and the authors of the above report are looking for potential antidotes to it. What they document is not only that do their lab animals quickly develop lesions and hemorrhages due to the excess vitamin-A they are fed, many of them suffer spontaneous bone fractures too. The vitamin-A toxicity action, and it occurs almost unbelievably quickly, depleted the calcium from the bones of the animals. So incredibly severe is this condition that the researchers report they were inadvertently breaking the bones just trying to handle the rats.
As already stated the most characteristic lesions in with hypervitaminosis A appear to be hemorrhages,
variable in intensity and distribution, and also spontaneous skeletal fractures, which occur mainly in young rats. Both these injuries were produced in various groups in the present experiments, and the apparent effect of age was confirmed. Thus, at autopsy the hemorrhages found in adolescent were more widespread and severe than those in young rats, but spontaneous fractures were absent.
I like this statement from their abstract: “rats were fed on massive doses of vitamin-A for periods varying from 10 to 18 days.” Then in the Experimental Details section of the report, they define exactly what “massive” means: it is “one drop of halibut-liver oil per rat per week.” Therefore, for these rats that’s a whole three or four drops of halibut-liver oil in their entire lifetime. That’s all that was needed to induce serious disease and bone fractures. Very similarly from an earlier study from 1937 we have:
The rats were fed 0.5 cc. daily, or a dosage of 20,000 units of vitamin A. The outstanding features of the disease produced in about 10 days were failure to grow, inflammatory changes in the eyes with exophthalmos and changes in the bones resulting in spontaneous fractures.
Quite amazingly, where we have a vitamin-A toxicity experiment producing the de facto primary vitamin-A deficiency condition of xerophthalmia! Astonishingly, it does so in just 10 days too.
An additional study I want to reference is:
The Effects of Vitamin-A and Citral on Epithelial Differentiation in vitro 1.
The Chick Tracheal Epithelium
by MARGARET B. AYDELOTTE
J. Embryol. exp. Morph., Vol. 11, Part 1, pp. 279-291, March 1963
Naturally, vitamin-A toxicity has also been proven many times in vitro (“in glass”). However, what makes this research so interesting is the effects of exposing various epithelial tissue types to high levels of vitamin-A in vitro.
Though vitamin-A deficiency appears to have relatively little effect on skin and other epithelia that are normally keratinized, these epithelia change with high concentrations of vitamin-A. When the vitamin was applied locally to the skin of rats (Sabella, Bern & Kahn, 1951) or administered orally in very large doses (Studer & Frey, 1949), the skin failed to keratinize normally, while the immature, non-keratinized cells proliferated rapidly and formed a thick epithelium.
The reason this report is important to us is that what we want to understand better is the effect vitamin-A has on the stem cells of these epithelial tissues. Firstly, I just want to highlight this report’s reference to earlier research done by Fell & Mellanby, in 1953; and Fell in 1957. Therefore, by 1953 the researchers were getting a pretty good understanding of the profound effect vitamin-A had on epithelial stem cells and the thought to be differentiation process.
High concentrations of vitamin-A also influenced epidermal differentiation in vitro: when embryonic chick skin grown by the organ culture method was treated with relatively high concentrations of vitamin-A, normal keratinization was inhibited and a mucus-secreting, sometimes ciliated epithelium, remarkably similar to that of the normal nasal mucosa, developed instead (Fell & Mellanby, 1953; Fell, 1957).
From these results it is clear that vitamin-A exerts considerable influence over epithelial differentiation: excess inhibits keratinization of epithelia and some-times induces mucous metaplasia, whereas deficiency in vivo inhibits mucus secretion and causes keratinization of many mucous membranes.
And then in the discussion section of the report, we have:
Although vitamin-A is essential for the normal maintenance of mucus secretory epithelia, and in high concentrations it can promote mucous metaplasia of some keratinizing epithelia, in the experiments just described high concentrations of vitamin-A actually inhibited synthesis and secretion of mucus by the chick tracheal epithelium. Previous experiments, however, show that the concentration of vitamin-A need not be abnormally high to inhibit mucus secretion by the tracheal epithelium; indeed, in young chicks, secretion is partly inhibited by the normal concentration of vitamin-A in the body (Aydelotte, unpublished).
Overall, this is an excellent study and report. But, as you dig into it you’ll see some rather confusing and apparently contradictory statements regarding similar effects induced by vitamin-A deficiency. However, once you understand what really happened in the vitamin-A deficiency experiments, you’ll understand why the author makes these statements. Additionally, when the author states that elevated vitamin-A levels: “induces mucous metaplasia” I believe what she was really witnessing was not mucus, rather it was leaking lymph fluids.
Figure 2 Killer-cell activity stimulated into action with retinoic acid
Source: The Retinoids:, Volume 2 By BAERT et al., page 383
Now, since this report documents the in vitro tissue response to elevated levels of vitamin-A we don’t get the benefit of seeing what the immune system’s follow-on responses and actions are to that tissue destruction. But, no worries, there are other reports that document it. At right is just one example.
There are many other research papers and hundreds of experiments reporting exactly the same effect. Unbound retinol, and retinoic acid absolutely do cause cells to initiate immune assisted apoptosis. Therefore, there can be no doubt that both retinol, and retinoic acids are toxins.
Next, let’s have a look at a partial list of documented side direct effects due to short and medium-term exposure to retinoic acid (as a medical treatment).
In my previous e-book, I wrote quite extensively about the use of retinoic acid being used to treat acne. I’ll summarize some of that information here. The most popular brand name used was Accutane. However, there are other brand names, and many generic versions of it too. The use of the drug is really a deal with the devil. It offers short-term gains in exchange for a potential lifetime of long-term pain and suffering. The government regulatory agencies are very well aware of the horror show this “drug” is inflicting upon our youth (tens of thousands of them), so they have put in some more restrictive guidelines, and produced some nice brochures. Of course, they have not pulled the drug off the market. Naturally, many doctors ignore these more restrictive guidelines and are still prescribing the “drug” for even mild cases of acne. The more common side effects are: (from the iPledge program page)
problems with the skin, pancreas liver, stomach, bones, muscles, hearing, vision, lipids, allergic reactions, blood sugar, or red and white blood cells. The most common, less serious adverse events include dry skin, chapped lips, dry eyes, and dry nose that may lead to nosebleeds.
Do you recognize these side effects? Yes, they are the symptoms of vitamin-A poisoning. But, wait, there are even more side effects, including fatigue, trouble sleeping, trouble concentrating. And, there are still even more serious side effects listed for this drug:
Psychosis (seeing or hearing things that are not real)
Suicide Some patients taking isotretinoin have had thoughts about hurting themselves or putting an end to their own lives (suicidal thoughts). Some people tried to end their own lives and some people have ended their own lives.
Patients on isotretinoin have been known to become depressed or to develop other serious mental health problems. Some people have had thoughts of hurting themselves or putting an end to their own lives. Some people tried to end their own lives and some have ended their own lives. There have been reports that people on isotretinoin were aggressive or violent.
That’s right, suicide is documented as just a side effect of taking this so-called acne medication. Are doctors really giving an extremely toxic and powerful chemotherapy drug to trusting teenagers for acne? You bet they are. And this wonder drug has been a huge seller.
One of the most shocking reported side effects of this wonder drug is reduced IQ, and even permanent brain damage. But, the medical establishment doesn’t seem to be too concerned about that little detail either, because they have more drugs to sell you for that new condition of reduced IQ.
The most immediate risk of using Accutane is that to the unborn child. Therefore, all women who could potentially become pregnant are asked to enter into the “iPLEDGE”5 program and contract, and are supposed to be closely monitored by their prescribing physician.
From the iPledge program Patient Introductory Brochure:6
There is an extremely high risk that severe birth defects will result if pregnancy occurs while taking isotretinoin in any amount, even for a short period of time.
What are the risks exactly?
Birth defects which have been documented following isotretinoin exposure include abnormalities of the face, eyes, ears, skull, central nervous system, cardiovascular system, and thymus and parathyroid glands. Cases of IQ scores less than 85 with or without other abnormalities have been reported. There is an increased risk of spontaneous abortion, and premature births have been reported.
Documented external abnormalities include: skull abnormality; ear abnormalities (including anotia, micropinna, small or absent external auditory canals); eye abnormalities (including microphthalmia); facial dysmorphia; cleft palate. Documented internal abnormalities include: CNS abnormalities (including cerebral abnormalities, cerebellar malformation, hydrocephalus, microcephaly, cranial nerve deficit); cardiovascular abnormalities; thymus gland abnormality; parathyroid hormone deficiency. In some cases death has occurred with certain of the abnormalities previously noted.
Wow! All that sounds awfully bad. So, what happens if a woman does become pregnant? Although it is not explicitly stated in the iPLEDGE brochure, other medical websites state it clearly: “Because the answer to a pregnancy [on isotretinoin] is a termination.”
Just how toxic is Accutane? Well over the full course of treatment for young adults the total amount of the drug taken is about 5 or 6 grams. If that amount were taken in one shot, it could easily be a lethal dose. What the drug makers want you to believe is that the functional mechanism of retinoic acid is in reducing the size of the sebaceous glands via some magical “sebosuppressive” effect.7 But, that’s not the truth. The real true mechanism is that it is poisoning and killing the stem cells that reside in the sebaceous glands, and elsewhere. If the process goes a little too far, it will destroy the functioning of the sebaceous glands altogether. Of course, if the stem cell kill-off was limited to just the sebaceous glands of the skin it might not be too horrible. But, it’s not. It kills stem cells all over the body.
Here’s just a partial list of the conditions most commonly being reported by people who have been adversely affected by Accutane, et al.
Arthritis, diabetes, migraines, pain disorders, intracranial hypertension, cheilitis, eczema, chronic dry eyes, glaucoma, acquired food sensitivities, acquired food allergies, acquired seasonal allergies, Inflammatory Bowel Disease, Colitis, Irritable Bowel Syndrome, Post-Chemotherapy Cognitive Impairment, Anhedonia, depression, anxiety, seizure disorders, Depersonalization Disorder, ADHD, Chronic Fatigue Syndrome, erectile dysfunction, reduced libido, reduced testosterone levels, hair loss, chronic dry skin, increased scarring of skin, weight loss, heat intolerance, raised liver enzymes, thyroid abnormalities, decreased ability to build muscle, and more.
In addition to the erectile dysfunction, reduced libido, reduced testosterone levels reported here, we’ll soon get a much better understanding why this wonder drug could have a devastating effect on longer term fertility too.
If you are wondering just exactly how does retinoic acid toxicity cause a disease such as diabetes, here it is in a nutshell. It causes the blockage and eventual disintegration of the ducts of the pancreas.
The use of retinoic acid as an acne treatment originated from the use of it in chemotherapy. This is not just approximately the same drug. No, it is exactly the same drug, the same molecule, the same isomer of it, and even the same product named version of it: Accutane. So, if the use of Accutane as an acne treatment is the medium stress test of retinoic acid toxicity on the human body, then being given the Accutane “treatment” in cancer cases is the extreme stress test. Here are some of the documented so-called side effects:
- Headache, fever, dry skin, dry mucous membranes (mouth, nose)
- Bone pain
- Nausea and vomiting
- Mouth sores
- Eyesight changes
- Back pain
- Pain in muscles and joints
- Allergic reaction
- Abdominal pain
- Poor appetite
- Numbness and tingling of hands and feet
- Loss of concentration, and sleep problems
- Hair loss (thinning)
- Dry eyes, sensitivity to light
- Decreased night vision, which may persist after treatment is stopped
- Swelling of the feet or ankles
- Low blood counts
- Anemia and/or bleeding
- Abnormal blood tests: increased triglyceride, cholesterol and/or blood sugar levels.
- Increases in blood tests measuring liver function. These return to normal once treatment is discontinued (see liver problems)
- Blood clots
- Pulmonary embolus or stroke
- Pancreatitis (inflammation of the pancreas)
- Skin desquamation (peeling and shedding)
- Problems with kidneys
- Inflammation of the liver
- Inflammation of the stomach
- Muscle problems
- Hearing loss, and ringing in the ears
- Problems with lipids
- Problems with blood sugars
- Inflamed, and peeling of the lips
- Dry nose and mouth, nosebleeds
- Thoughts of hurting oneself, or others
- Psychosis (seeing or hearing things that are not real)
- Bone density loss
- And even more …
Now that is definitely, and amazingly, the head to toe destruction of the human body. More importantly, we should all now recognize this list for what it really is. It is head to toe autoimmune diseases. How often has this “medication” been proven to cause all this destruction? Well, at least a million times over. That’s correct. Even though retinoic acid (Isotretinoin) is a really shitty, and highly ineffective chemotherapy drug,8 it has been widely used since the early 1960s. Of course, it is ridiculously ineffective. What the “drug” is doing is simply poisoning the entire body. What it is really doing is decimating the body’s stem cell population to such an extent, it appears to pause the cancer process. Naturally, for most of the few people that survive this medical torture treatment, their cancers just reappear after their stems cells start growing again. Where in the hell did this bizarre concept of attempting to poison sick people with cancer back into health even come from in the first place? You probably don’t want to know.
Even more astonishing is that there are studies that show that the use of retinoic acid in chemotherapy actually not only lowers one’s chances of survival when compared to placebo, it accelerates patients into even earlier death. Not surprisingly, it has been an enormously profitable “drug” too.
But, let’s not worry about those little poisoning for profit details for now. What we need to focus on is that retinoic acid has been used (and mostly unsuccessfully) millions of times over as a cancer treatment, and every single time it causes many of the above noted so-called side effects. And of course it has, because this is what they think they need the drug to do. Therefore, clearly, then these are not side effects. They are the direct response and results of a body-wide poisoning.
8 Mortality in the Randomized, Controlled Lung Intergroup Trial of Isotretinoin
The wonders of vitamin-A and retinoic acid have not been ignored by dermatologists either. Both vitamin-A and retinoic acid have been widely used in dermatology, and for over fifty years now too. These retinoids have been applied topically to the skin for its perceived skin thickening and thought to be rejuvenating properties.
To elicit a slow thickening effect, vitamin-A is used. To elicit a more rapid effect, retinoic acid has been used. The mechanism of the treatments is to induce more rapid cellular division of the stem cells of the skin. However, in both scenarios the treatment almost always eventually leads to inflamed skin and even thinner skin in the long run. Therefore, the skin thickening effect is always short lived. Additionally, in the longer term, most dermatology patients treated with the retinoids need to stop the “treatments” because the inflammation just becomes too severe, and other little complications such as skin lesions show up. That’s right, if the treatment is applied just a little too long, or at just a little too high of a concentration, the result is inflamed skin, and even hemorrhaging and lesions of the skin.
But, like the dermatologists prescribing Accutane for acne, the dermatologists here are glossing over the critically important little hidden consequences of forcing the more rapid stem cell division. That is, it is actually depleting the skin’s stem cell population at the same time. We’ll go into the reasons for why this is in a subsequent chapter.
Equally important, and what many of the dermatologists probably don’t understand, is that the stem cells are not just magically responding to the elevated levels of the retinoids. No, the stem cells are actually being poisoned. The body detects that they have been poisoned, and then tries to rapidly grow them off of the body. So, yes, the skin “thickens” for a while, but it’s temporary, and it’s definitely not a good thing. Ultimately, then the skin is left thinner and depleted of many of its important stem cells. Nice work guys.
Regarding the understanding of the real functioning of the retinoids, it appears that medical science catches on very slowly. It has taken over fifty years for dermatology to start to recognize and accept the fact that, in the long run, the retinoids are just not working out very well as skin conditioning treatments. Nonetheless, word does not travel fast. There are at least 700 everyday cosmetic products, such as creams or lotions, sunscreens, etc., that contain retinoids. Now, could this bad situation quickly get a whole lot worse? You bet it does. Just expose this retinoid loaded skin to sunlight, and you’ll vastly increase your chances of getting skin cancer. That’s more nice work guys.
Why and how does vitamin-A promote skin cancer? The condensed version of the story is that vitamin-A is an incredibly efficient light-absorbing molecule. This light absorbing property is probably one of the primary reasons it is present in nearly all plants. But, now with that same light absorbing molecule residing within the lipids and cells of our skin, it acts as little embedded microwave ovens when we go out into the sun. This embedded molecule then brings in a tremendous amount of solar radiation directly into our cells and quickly turns it into heat.
If you consume massive amounts of vitamin-A, over a short period of time, this results in what’s termed acute toxicity. People have been killed by doing it. There’s even a well-documented case of a man who was killed by overdosing just from drinking massive amounts of carrot juice. Other times, it’s from more inadvertent poisonings.
A newborn child, who mistakenly was given 0.09 mmol (25 mg) daily or 25 µmol per kilogram for 11 days died of apparent vitamin-A toxicity.
Health, Survival, and Vision
Alfred Sommer and Keith P. West
With James A. Olson and A. Catherine Ross
Oxford University Press, 1996
See: page 243
Of course, this extreme fatal vitamin-A poisoning scenario has been directly reproduced in animals.
Young monkeys, when given lethal doses by intramuscular injection, fall into a deep coma, often have convulsions and respiratory irregularities, and finally die of either respiratory failure or convulsions.
Source: Vitamin-A Deficiency; Health, Survival, and Vision, page 243
That’s right, if you get a bit too much of this so-called vitamin it can kill you. And, if it does not kill you, here’s a nice summary for the more common symptoms of its longer-term toxicity:
Signs and symptoms of Chronic Vitamin-A Toxicity:
Children: Alopecia, anorexia, bone pain and tenderness, bulging of fontanelles, craniotabes, fissuring at lip corners, hepatomegaly, hyperostosis, premature epiphyseal closure, photophobia, pruritis, pseudotumor cerebri, skin desquamation, skin erythema.
Adults: Alopecia, anemia, anorexia, ataxia, bone pain, bone abnormalities, brittle nails, cheilitis, conjunctivitis, diarrhea, diplopia, dryness of mucous membranes, dysuria, edema, elevated CSF pressure, epistaxis, exanthema, facial dermatitis, fatigue, fever, headache, hepatomegaly, hepatotoxicity, hyperostosis, insomnia, irritability, menstrual abnormalities, muscular stiffness and pain, nausea, negative nitrogen balance, nervous abnormalities, papilledema, petechiae, polydypsia, pruritis, pseudotumor cerebri, skin desquamation, skin erythema, skin rash, skin scaliness, splenomegaly, vomiting, weight loss.
Ellenhorn's Medical Toxicology: Diagnosis and Treatment of Human Poisoning. 2nd ed.
Baltimore, MD; Williams and Wilkins, 1997., p. 1021
And in the shorter timeframe, or if you are younger or smaller, it’s:
Early manifestations of hypervitaminosis A include fatigue, malaise, lethargy, irritability, psychiatric changes mimicking severe depression or schizophrenic disorder, anorexia, abdominal discomfort, nausea and vomiting, mild fever, and excessive sweating. Children may fail to gain weight normally, and adults may lose weight. Slow growth, premature epiphyseal closure, painful hyperostosis of the long bones, arthralgia, myalgia, hypercalcemia, and hypercalciuria have been reported. CNS signs and symptoms also include increased intracranial pressure, bulging fontanelles in infants, headache, papilledema, exophthalmos, vertigo, and visual disturbances. Dryness and cracking of the skin and lips, scaling, pruritus, brittle nails, alopecia, erythema, hyperpigmentation, and massive desquamation may also occur. Hypomenorrhea, hepatosplenomegaly, cirrhosis, jaundice, elevated serum AST (SGOT) and ALT (SGPT) concentrations, urinary complaints, anemia, leukopenia, leukocytosis, and thrombocytopenia have also been reported. Increased plasma concentrations of vitamin-A usually occur but do not necessarily correlate with the severity of toxicity.
Source: As above
Here’s Sommer’s shortened version of the list:
Approximately 50 signs of chronic toxicity have been reported, of which the most frequent are alopecia, ataxia, bone and muscle pain, cheiltis, conjunctivitis, headache, hepatotoxicity hyperlipemia, hyperotosis, membrane dryness, pruritus, pseudo tumor cerebri, various skin disorders and visual impairment.
Source: Vitamin-A Deficiency; Health, Survival, and Vision, page 243
Firstly, you’d think that seeing that there are over 50 signs of chronic toxicity it would have raised some serious doubts as to the claim that this is even a vitamin. But, it gets even better here. Aren’t those all the same symptoms of vitamin-A deficiency. I mean seriously, as Sommer and his co-authors were typing up this paragraph how could they have not possibly noticed that conjunctivitis, skin disorders, and visual impairment being the identical and primary symptoms to those encountered with so-called vitamin-A deficiency?
Also, in my prior e-book, I think I made a good case that the so-called “psychiatric changes mimicking severe depression or schizophrenic disorders,” are not at all just “mimicking” the severe depression or schizophrenic disorders. Rather, it’s the complete opposite. Those named conditions are being caused by vitamin-A toxicity. In other words, schizophrenia is simply caused by vitamin-A toxicity.
Vitamin-A toxicity is causing birth defects.
The teratogenic toxicity of vitamin-A is well known, and it’s very well-documented. It has been of course repeatedly proven in many animal experiments and widely recognized in humans. It was interesting for me to learn that out of the about 800 known toxins to humans only 20 of them are proven to be teratogenic. In other words, a toxin must be extremely hazardous to make it into this exclusive top 2.5% group of toxins. Amazingly, vitamin A is in that elite group, and of course retinoic acid is too and even on par with thalidomide. I’ve also devoted a considerable amount of space in my previous e-book to this topic of vitamin-A causing birth defects, so I’m not going to reiterate it all here. However, when combined with all the other information I’ve presented in this chapter, it’s rather damn clear that it is one hell of a toxic substance for us to be calling it a vitamin.
Are we sure this is Vitamin-A and not Poison-A?
With all the above, does it just not intuitively make you seriously question the claim that this is a vitamin at all? What’s your gut feel on it? What are your instincts telling you?
Now, there have been two very important points I wanted to make in this chapter. Firstly, that vitamin-A will normally, and naturally convert to retinoic acid. This is not a “theory,” and it is not speculation, it is completely proven in clinical research. Therefore, over time, we are all very slowly giving ourselves the retinoic acid “treatment.” For most adults, it is just going to ever so slowly progressively get worse as we get older.
The second, and more important, bit of information presented in this chapter is that you need to be very familiar with the description, scope, and magnitude of the tissue and organ destruction caused by retinoic acid. The reason you need this understanding is that I want you to be able to recognize these conditions again in the context of the early experiments conducted to prove the vitamin-A deficiency theory. What I am going to show you in a subsequent chapter is that the so-called vitamin-A deficiency experiments were nothing more than high dose retinoic acid experiments!
In my previous e-book, there’s a chapter on the autoimmunity flare-up process and how the stratified epithelium is the primary sites of destruction in response to vitamin-A toxicity, and especially so in the skin. If you have not yet had a chance to read that chapter, I believe that it is worth your time. I present a lengthy and logical explanation for the sequence of events involved. I explain how the inflamed and damaged cells lead to the supposed “auto-immune” response. I go over why the immune system is not at all defective in attacking the affected cells of the various epitheliums. Now, here in this chapter, we are going to add some more information and explanations as to why the epithelium is such an important tissue structure to fully understand and appreciate in the context of the chronic diseases.
I think one of the hardest aspects of my overall theory to accept is the claim that all the auto-immune diseases are fundamentally one and the same condition. I make the claim that the organ the named autoimmune disease most prominently presents in is a red herring, and is almost meaningless in regards to the etiology. Conversely, what’s extremely important is that the named disease presents itself in the epithelium of the organ. Therefore, the auto-immune diseases are all diseases of epithelium, and / or the consequences of the destruction of these epithelial tissues. Of course, there’s some very strong clinical evidence supporting this statement. Here’s just one example:
Much to our surprise, we found that immunologically, type I diabetes and multiple sclerosis are almost the same - in a test tube you can barely tell the two diseases apart," said Dr. Dosch, the study's principal investigator, a senior scientist in the HSC Research Institute, and a professor of Pediatrics and Immunology at the University of Toronto (U of T). "We found that the autoimmunity was not specific to the organ system affected by the disease. Previously it was thought that in MS autoimmunity would develop in the central nervous system, and in diabetes it would only be found in the pancreas. We found that both tissues are targeted in each disease.
ScienceDaily, 22 March 2001.
In both MS and in diabetes, the immune system is responding to the apparently misbehaving stem cells of the epithelial tissues. In the disease labeled Multiple Sclerosis, it just happens most aggressively in the epithelial tissues comprising the myelin sheaths wrapping nerves, and in the other disease labeled Diabetes, it just happens most aggressively in the epithelial tissues comprising ducts of the pancreas. However, the named organ is almost meaningless in understanding the real mechanism of the disease. The root mechanism of the disease is the destruction of the epithelial tissues within the organ. What so important about the epithelial tissues is that it is a fundamental tissue type that not only covers the exterior of the body, it also lines the cavities, gland ducts, blood vessels and organs throughout the body.
Now, if you’ve taken the time to read the reported details from the vitamin-A deficiency/toxicity experiments, regardless of the organ, what’s the primary tissue structure that’s always affected? It’s the various epithelial tissues. Therefore, it’s critically important to zoom-in and see that we are not looking at just organ destruction, rather it is the destruction of the epithelial structure within, or that makes up, the organ. From there, we then need to drill down just a little bit deeper to see that it’s the stem cells that are hosted along the basal membrane of that epithelial that are the primary source of the disease. This is because the stem cells are the primary target of vitamin-A toxicity. As the stem cells fall victim, the overall tissue slowly starts to degenerate, and ultimately disintegrates. Therefore, the disease quite literally progresses from the bottom up, or from the inside out. If this disease process happens in the epidermis, then you have eczema. If it happens in the pancreas, you have diabetes. If it happens in the lungs, you have asthma. If it happens in the reproductive tissues, then you have infertility. If it happens in the myelin sheaths surrounding the nerves, you have MS. If it happens in the eyes, you have xerophthalmia. If it happens in the nephrons of the kidneys, you have kidney disease. If it happens in the GI tract, you might have Crohn’s or colitis, and on and on. Well, you get the idea. Any organ or any epithelium can and will be affected by vitamin-A toxicity. This aspect of its toxicity is not just some “theory.” It has been absolutely and completely proven, and proven thousands of times over, in both animal experiments and with the so-called cancer treatments in humans.
Of course, in most people who experience vitamin-A toxicity (the so-called auto-immune diseases), it is usually not just one organ or tissue, that’s affected at one time. Often, it is two or three organs that are affected at the same time. But, naturally, that is just the beginning of the overall disease condition. As the various epithelial tissues of the organs begin to fail, the primary function of the organs obviously begins to fail too. From there we cascade down into the pit of disease and inflammation hell. Obviously, dealing with failing organs is damn horrific. However, the situation can, and very often does, get a whole lot worse. The disease condition will cascade throughout the body, severely affecting non-epithelial tissue such as the bones, the blood’s oxygen carrying capacity, and of course the brain too.
Naturally, with the self-destructing epithelium, in a range of organs, the tissue’s critical barrier function is also lost, leading to all kinds of chronic infections. Last, but not least, once the DNA damage stem cells are unnaturally forced off the basal membrane and into circulation, or possibly to the backside of the basal membrane, cancer is next on the agenda.
Figure 3 The basal keratinocytes driven onto the wrong path
Next, we now need to have a very good understanding of what the term “stem cell differentiation” means. Naturally, this is a man-made term applied to a process that stem cells undergo to maintain overall tissue structure. Within the epithelial tissues, all new cells originate from the stem cell population. The stem cells reside on, and along, a thin membrane at the base of the epithelial tissue. In the epithelial tissues, only stem cells are capable of dividing. Therefore, a healthy and properly functioning population of stem cells is critically important. For our discussion purposes here, we’ll primarily refer to the stratified epithelial tissue making up the skin.
I like to think of the basement membrane as a non-moving supply chain that continuously grows new cells to replenish the epidermis. Of course, the stem cells are very special cells in that when they divide they have a few choices as to what type of cell they want to grow up as. But, it is not a completely arbitrary choice either. That choice is tightly regulated and controlled. As cells are normally shed from the outer epidermis, hormonal messages are sent down to the stems cells to grow new replacement epidermis cells. But, a stem cell is a stem cell, not a more specialized one needed in the upper layers of the epidermis. Therefore, to accomplish the transformation feat of converting from stem cell to a more specialized one, the cell goes through differentiation. The differentiation process is not immediate. It is a slow process, and continually progresses until the cell eventually reaches the outside of the epidermis. As the cells migrate to the top of the epidermis, they continue the differentiation process and become more and more filled with keratin. Of course, this process goes on every day of our lives. If everything goes according to plan, as we shed and lose surface cells there’s always a slow-moving migration of new cells being grown up from the basement membrane to replenish them. If everything is kept in balance, we have nice smooth, moist, and beautiful skin to live in.
But, there’s just one little detail that I’ve glossed over. That is the resupply chain needs to be kept in equilibrium too. This means that the stem cells not only need to replenish the upper epidermis, but they also need to replenish themselves too. Clearly, if the differentiations were always in favor of epidermis cells, you’d quickly run out of source stem cells. Obviously, renewing the stem cells on the basal layer is just as important, and it needs to be renewed at almost precisely the same rate. Of course, this process must be closely regulated so that the skin does not become too thick, or too thin.
Figure 4 The stratified epithelial of the skin
Figure 5 The skin cell’s interlocking tight junctions
A common misconception that I’ve come across is that some people believe that when a stem cell divides, that the division of a stem cell produces one new stem cell and one new differentiating upper epidermis cell. This is not true. Once a stem cell has decided to differentiate it is committed to complete the process, and there’s no going back. Once it’s committed down one path, there’s no longer a choice. The decision was made in the RNA of the source stem cell. Therefore, both the prodigy will become what they have been programed for. So, either both the prodigy will become differentiating epidermis cells and cleave themselves from the basement membrane, or both will remain attached to the basement membrane and continue life as new stem cells.
For stem cells that have taken the differentiation decision, they start to make their slow migration out and will undergo several progressive transformations along the way. The first transformation takes place in the next layer up, termed the stratum spinosum, or the spiny layer. At this stage, the differentiating cells start growing spines. The spines serve a critical interlocking mechanism. The spines are proteins made up of cell adhesion molecules. You can think of the spines as the cells growing arms and hands so that they can grab and hold on to each other very tightly, yet elastically, and interlock. Gradually, as the cells migrate higher up, this interlocking mechanism will effectively and completely stitch all the cells together with what’s termed the tight junctions.
The cells with their completed tight junction matrix form a waterproof barrier that also prevents pathogens from getting back in.
Of course, what happened in the early vitamin-A deficiency experiments were that they induced profound, and the head to toe, destruction of all the epithelium based organs. Naturally, by failing to recognize that they were truly seeing a poisoning in action, they attributed this destruction to the deficiency. Needing to better understand the mechanism, subsequent follow-up experiments confirmed that vitamin-A had a direct and powerful influence on stem cell differentiation. The results of which only served to deepen and further solidify the belief in the vitamin-A deficiency theory. It was quickly assumed that without the retinoid influence, the stem cells had failed to differentiate properly, and this was the causal mechanism underlying the tissue’s degeneration and ultimate destruction. Therefore, retinoid influence on stem cell differentiation is one of the biggest factors in why vitamin-A is defined as a being “vitamin” in the first place.
The confirmation that vitamin-A influences stem cell differentiation was made as far back as the 1930s; so, it is not a new discovery. Therefore, the belief in the vitamin-A deficiency theory is very deeply ingrained in modern medical thinking. Of course, this knowledge of vitamin-A’s profound effect on stem cells keeps it at the very top of the list of the essential vitamins. For medical science, there’s no mistaking it.
Retinoids are ubiquitous signaling molecules that influence nearly every cell type, exert profound effects on development, and complement cancer chemotherapeutic regimens. All-trans retinoic acid (RA) and other active retinoids are generated from vitamin-A (retinol), but key aspects of the signaling pathways required to produce active retinoids remain unclear. Retinoids generated by one cell type can affect nearby cells, so retinoids also function in intercellular communication. RA induces differentiation primarily by binding to RARs, transcription factors that associate with RXRs and bind RAREs in the nucleus.
Journal of Cellular Physiology. 2011;226(2):322-330.
it’s just a goddamn poisoning!
From those observations, it was like “Yey, isn’t this great, aren’t we smart, we can influence stem cell differentiation.” Except, this is not smart science, it’s bad science and ridiculously flawed logic. Just because we can do something, does not mean that we should be doing it. But, not to miss out on a business opportunity, this new-found ability to artificially influence stem cell “differentiation” has led to vitamin-A being used in all kinds of medical treatments and applications. Moreover, it was obviously extrapolated that if a bunch of vitamin-A will significantly promote faster stem cell turnover, and differentiation, then just a little bit of it must be needed for the slower natural turnover rate too (man, I am so glad these people don’t build airplanes).
Although managing the differentiation ratio of stem cells is an important balancing act, the body (in both humans and animals) has been able to manage this process very well and has been doing it very successfully for tens of millions of years now without the retinoids. However, not only has modern medicine discovered that vitamin-A can be used to influence differentiation they’ve concluded that vitamin-A is needed for the differentiation decision. In a quantum leap of scientific arrogance and folly, they’ve concluded that vitamin-A is the secret molecule needed to control differentiation.
But, medical science has completely failed to see what they were looking at here. It wasn’t that they are magically influencing stem cell “differentiation” with added vitamin-A, it is that they are poisoning the stem cells with it. Once the cell is poisoned, the cell itself, and the body attempt to grow it off as fast as possible, often eliciting the help of the immune system along the way. Clearly then, just because we can influence stem cell differentiation with vitamin-A, does not mean we should be doing it at all. Moreover, it is a rather astonishing display of scientific arrogance to think that we are going to outsmart nature in this critical and fundamental process of managing our stem cells.
I believe that I’ve presented ample amounts of evidence to make this case against the sub-theory that vitamin-A is needed for stem cell differentiation. But, if I haven’t, nature and human history have. We now have overwhelming amounts of information and evidence that makes it glaringly obvious to see that the theory is a complete load of rubbish. This fact has been proven to be the case at least 1,000,000 times over in just the P.O.W.s of the Second World War alone. It is also proven in the evolutionary history in most of the animal species on the planet, and for like the last 100 million years now too. The stratified epithelium remains completely, and perfectly, intact in times of even prolonged multi-year starvation. This is plainly visible in both the skin, and the eyes, of humans, and in animals. Therefore, nope, the theory that vitamin-A is somehow needed to control stem cell differentiation is a complete myth and ridiculous nonsense.
Okay, if vitamin-A is not needed (at all) for normal stem cell differentiation, and we know that elevated levels of vitamin-A cause the stem cells to behave in bizarre and unnatural ways, so much so that the immune system decides to attack and kill them, what do you suppose vitamin-A really is? Well, maybe we should just listen to what the body itself is telling us it is. What the body is clearly telling us is that it’s simply a goddamn poisoning. Of course, this is no minor poisoning. It can have far-reaching and devastating downstream consequences. Next, I am now going to explain the processes and mechanisms of that poisoning in more detail.
As the differentiating stem cells migrate up into the epidermis, they need to flatten out and grow interlocking spines. The interlocking spines are needed for the cells to tightly, yet elastically bond with each other. The interlocking spines are built up from what’s termed cell-adhesion molecules. A huge number of cell adhesion molecules are needed to completely fill in the gaps between all the cells of the outer epidermis. These cell adhesion molecules then form a matrix that not only binds and holds the cells together; they form the tight junctions between the cells. Overall, this combined structure of cells and their matrix then provide the structural integrity of the tissue. If everything goes according to plan and stays on the correct schedule, we have a nice and critical barrier between the outside world and the inside of the body. The barrier function not only keeps the good things, such as water, blood and lymph fluid, in, it also keeps the bad guys out. Who are the bad guys? Oh, those are the little microorganisms that would love nothing more than to feed off our internal fluids and proteins.
Except, now with exposure to elevated retinol levels, things don’t go according to plan, nor stay on schedule. Firstly, due to the stem cell’s RNA and DNA being damaged by retinoic acid, the cell’s protein and molecule assembly machinery is broken or significantly compromised. Therefore, the cell can no longer produce the proper cell adhesion molecules. Thus, as the cell grows up through to the outer epidermis, it lacks the mechanism to bind with other cells. The critical intercellular matrix, the tight junctions, are not being properly formed and maintained.
Figure 6 The shed off outer layers of the epidermis – resulting in “mush”
Figure 7 The destroyed epidermis – leading to infections
Moreover, the migrating cells do not even have the time needed to build the required cell adhesion molecules. They are simply growing way too fast. This then leads to improperly forming replacement tissues, what’s termed metaplasia. In the early stages, the tissue appears to become a bit granular and almost crystalized. Next, it progresses to where the cells become less and less bonded together with each other, and the skin quickly starts to lose its overall structural integrity. Then it progresses to where the tight junctions are malformed, broken down, and ultimately non-existent. At this stage, you pretty much just have independent cells swimming in lymph fluid. This floating cell condition is what I’ve very scientifically and accurately described as a “mush”, and it is the same condition seen in the “melting” of the cornea of the eyes.
You might be wondering how I know this process so well? I’ve watched it happen, in real-time, under my microscope, on my fingers and on the backs of my hands too. I’ve spent probably at least a hundred hours looking down through my microscope watching this process taking place. Of course, with the lost tight junction matrix resulting in the cellular mush, the lymph fluid comes leaking out. Not only is it leaking out, the top layers of flattened out and keratin filled protective cells are now nonexistent too. Shown above (Figure 6) is a bit of a close-up photo with this condition on my fingers.
With the abnormally fast growth rate from the bottom up, more exterior surface cells will be forced to flake off. But, with the stratum spinosum, and granulosum layers being malformed, they fail to maintain adequate spines and adhesion molecules to bind with the outer surface layers. These outer layers then slough off, sometimes with entire regions of surface tissue cells being lost. Subsequently, the skin in these regions then simply leaks lymph fluid. This condition is definitely not to be confused with the cells now producing mucus. Nope, it’s not mucus, rather it’s the nice sticky new home for all kinds of bacteria and viruses to nestle into.
Although much of the discussion above has been regarding the stem cell damage in the skin, and eyes, the damage is in no way limited to just those organs. The damaging effects are going on in the pancreas to cause diabetes too.
Type 1 and type 2 diabetes are characterized by progressive β-cell failure. Apoptosis is probably the main form of β-cell death in both forms of the disease. It has been suggested that the mechanisms leading to nutrient- and cytokine-induced β-cell death in type 2 and type 1 diabetes, respectively, share the activation of a final common pathway involving interleukin (IL)-1β, nuclear factor (NF)-κB, and Fas.
Source: Diabetes - Mechanisms of Pancreatic β-Cell Death in Type 1 and Type 2 Diabetes - American Diabetes Association
Up next, chronic infections. There’s no getting around it. With the skin’s barrier function is lost, the body’s outer defenses to infection are nonexistent. Once this happens, then we essentially have a wide-open wound that won’t scab over, nor heal for months. Not only is it almost impossible to not get infections, but it is also incredibly difficult to heal from them too.
How do I know this? From firsthand experience, of course. And with both the left and right hands too. Topical antibiotics might be somewhat helpful, but they are almost completely pointless too. In my experience, the only way to beat the infection is to have the skin reform its structural integrity. However, this is incredibly difficult to achieve. Not only is it a failing pile of mush, inflamed and infected, the immune system starts attacking it too. It’s a total horror show of microbiology chaos. Of course, what I’ve just described is not limited to the body’s external skin, the epidermis. No sir, it can, and is going to happen to any epithelium that goes through this self-destruction process. Infections are just inevitable. In my experience, the only real cure for them is to stop fueling the process with morevitamin-A and let the tissue rebuild itself. Only then can the immune system finally accomplish its real job of clearing the infection. And no amount of vaccinations is going to magically protect you from the infections either. The very last thing you need is for your immune system to be chasing down more phantom infections. Naturally, the very best way to treat infections is not to get them at all. The very best way to not get infections is to have epithelium tissues that have strong and integral barrier functions.
Want infections? Just boost up your vitamin-A consumption.
In our animals, the first symptoms of a (thought-to-be) dietary deficiency, namely, failure to gain on the low fat soluble A diets, were often accompanied by certain well-defined symptoms — loss of appetite, snuffles and subsequently labored breathing. These conditions confronted us so often that we questioned whether they were the result of the dietary deficiency per se, or were due to an infection in an undernourished animal. It is perhaps significant that, in a colony of between 400 and 500 animals, those on the low fat-soluble A diets are the only ones that ever manifest such symptoms.
AMY L. DANIELS, Ph.D. AND MARGARET E. ARMSTRONG, M.D.
WITH THE COOPERATION OF MARY K. HUTTON, B.S.
IOWA CITY 1923
Naturally, the statement made above “those on the low fat-soluble A diets are the only ones that ever manifest such symptoms” probably appears very contradicting to what I’ve claimed. However, it is critically important to know that their “low fat-soluble A diets” used in these experiments were simply “high dose retinoic acid diets” in disguise.
Now if you’ve newly acquired an autoimmune disease, and are thinking of getting up to date on your vaccinations, be very careful. Your immune system is already hypervigilant, and adding the cytotoxic agents present in vaccines into the system could be like adding gasoline to a fire. Moreover, there’s very little a vaccination can do to help in this situation. Your immune system is going to have lots, and lots of time needed to build antibodies on its own to any new invaders. It also does not need to be tricked into building needless antibodies to food proteins that are now leaking into the serum from the gut.
What we need to remember, is that the epithelial structure is not present in just the epidermis. This is just a fundamental tissue structure making up much of the human body. Many other internal tissues are similar, but specialized, forms of epithelium. This include the ducts of the glands and organs. As proven in vitamin-A toxicity (and the botch deficiency) studies from the 1920s, ’40s etc. some of the most commonly affected, and the earliest affected epithelium tissues are the tear ducts, the ducts in the meibomian glands of the eye, the ducts of the pancreas, and the kidneys, and both the male and female reproductive organs.
Unlike the epidermis, the outer surface of the epithelium making up the ducts does not face the outside world. Rather, it faces the interior portal, or channel, of the duct itself. Therefore, as these interior epithelia become malformed, the rapidly growing off surface cells can’t just slough off to the outside world either. What happens is that they slough off and start plugging up the duct (tube if you prefer) too. Additionally, as the duct forming epithelium become inflamed, and swollen, the channel of the duct becomes more and more restricted, and may ultimately become completely blocked. If you’ve not read the reports from the 1920s, one other organ they reported being hugely filled with sloughing off epithelium cells, from its interior, is the bladder.
Most people are aware the autoimmune diseases go through periods of waxing and waning. But, hidden from sight, a more devastating situation is slowly and progressively developing. It’s the depletion of the stem cell populations. With excessive retinoids in circulation, and in the intercellular spaces, it is artificially influencing stem cell “differentiation” in one direction. The “differentiation” process is not just thrown off balance; it is vastly sped up too.
As the regular cells of the upper tissue layers are being destroyed, they are naturally emitting growth hormones to signal the stem cells to replicate faster. In the normal situation, the stem cells would be differentiating in a more controlled and rational manner. Normally, they’d need to differentiate at a ratio that maintains both the stem cell population, as well as resupply the upper tissue. But, by artificially influencing the “differentiation” decision in one direction they are far too often dividing to produce two upper tissue cells for every stem cell division. Therefore, the rapid cell division is producing and migrating an abnormal ratio of cells to the tissue’s outer surface, and depleting the basal layer of its source stem cells at the same time. Thus, over time we are slowly destroying the basal layer of the epithelium by using up our stem cells. Once we’ve sufficiently depleted the stem cell population, the tissue atrophies, and ultimately fails completely because it’s supply of new cells no longer exists.
In both the so-called deficiency, and toxicity studies from the 1920s, ’30s, etc. the researchers were aware of follow-on immune response to the cellular destruction. In a few of the 1922-1925 studies, they referred to this as witnessing the immune system’s foreign body response being activated. In one particular study, they were especially careful to make sure the animals did not develop infections. They kept the cages immaculately clean and hosted just one animal per cage. They were, of course, trying to isolate just one factor as causing the disease conditions. Therefore, they not only wanted to rule out infections as being the cause of disease but to also eliminate their effects on the progression and amplification of the diseases. Nonetheless, it was clear to them that the immune system was sometimes responding to the cellular destruction as though an infection were present.
Except, what they were really witnessing were early cases of induced autoimmunity. As the cytotoxin damages the cell’s RNA, the subsequent defectively constructed proteins start presenting on the cell’s surface membrane and are also being ejected off it. This strange new, and apparently foreign protein, then alerts the immune system to the cell’s malfunctioning behavior. To the immune system, the detection of strange new proteins and related cellular damage can only mean one thing; there’s pathogens present. But, unbeknownst to the immune system, it’s only a phantom pathogen. Its true identity is a cytotoxic molecule, and the artifacts produced by its damaging effects then masquerade as those of a pathogen.
I’ve detailed this process a lot more in my previous e-book. However, I just want to add a bit more to it here. Of course, the immune system then attacks the cell that’s emitting the strange proteins and hopefully kills it. If it involves just a few cells, it’s no big deal. However, as the process continues, the adaptive immune response starts to be activated. The macrophages start dragging off some of the broken cell fragments, with the damage association molecules stuck on it, into the lymph nodes. Within the lymph nodes, the immune’s beta cells use these fragments and their strange new proteins as templates to start building matching antibodies.
Other tissue cells that now present the same damage association molecules are then targeted for immediate attack. This targeting is the completely normal, expected, and required behavior by the immune system to effectively fight off pathogen infections. However, in this scenario, the damage association molecules are not generated in response to a pathogen’s damage, rather it is to a toxin’s damage. The lymph nodes will get so jamb packed with broken cell fragments they will become hugely swollen too.
Next, the killer T cells with their newly minted anti-body weaponry go on the hunt for the suspected pathogen. Of course, there is no pathogen to be found; it simply does not exist. Therefore, the immune system is never going to find it. Yet, mysteriously, more, and more of the damage association molecules keep on showing up. This is a strange new situation that effectively perplexes the immune system. The immune system can only respond more and more aggressively and keeps actively searching for the phantom pathogen. Since an apparently invading pathogen has been detected, the immune system is going to respond by sending more troops into the battlefield too. This response requires more, and more immune cells to be built. Additionally, the immune system is not interested in taking prisoners in this battle. No, whatever is going on, the immune system regards it as an existential threat that needs to be dealt with harshly and as quickly as possible. The immune system is smart, and it knows it does not necessarily need to find the actual pathogen, it may only need to find the cells that are harboring them. So, it now directly attacks any cell that’s foolish enough to present the same damage association molecules on the exterior of their cellular membrane. Of course, many other cells similarly affected by vitamin-A overload will be doing exactly that. You now have auto-immunity. However, things are not nice and tidy on this microbiology battlefield. As toxified cells are being damaged, killed off and otherwise breaking apart, fragments of those cells float away in the serum. Those fragments carry with them the new antibody targeted damage association molecules. If these fragments happen to stick on to other cells, the immune system is going to take no chances, and kill those completely innocent cells too. Let’s be very clear about this; the immune system is in no way defective in this battle. It is not confused or in some state of disorder. Rather, it is working perfectly and is heroically doing a very thorough job. The immune system is forever vigilant, and it is never going to give up the fight. Auto-immunity is auto-poisoning.
Now the process underlying autoimmunity that I have just described here should sound very familiar. What do we normally call DNA damaged, fast-replicating cells, and seemingly out of control collateral tissue growth and damage? Doesn’t that sound a lot like cancer? It’s similar enough that many people do refer to the autoimmune diseases as being non-lethal cancers. Not surprisingly, many people with autoimmune diseases do indeed have cancers at the same time too. However, the autoimmune diseases are not cancer. The crucial detail with autoimmunity is that the immune system is able to identify the damaged stem cells quick enough and efficiently to kill them off. The fight between the immune system and poisoned and misbehaving stem cells can go on for decades. The end stage is reached only when we’ve so completely depleted the stem cell population that the tissue structure fails, and thus the organ containing that tissue structure fails. Therefore, if we can maintain a healthy immune response, our autoimmune disease may just slowly kill us before we ever develop cancer.
However, there are scenarios where that’s not going to happen. As I’ve described before, once the DNA damaged stem cells (the entire cell, not fragments thereof) separate off from the basal membrane rather than properly migrating to the outer epidermis, they find their way into circulation. From there they may become attached to some other organ’s tissue, and start replicating within it. To the stem cell, it’s normal job is to diligently replicate on schedule. It’s perfectly normal behavior because when it’s natively hosted in the epithelial tissues, this is the source of all the new cells that are needed to maintain the tissue’s structure. However, now wrongly hosted elsewhere, we have a tumor developing. Exactly how many errant stem cells would be needed to start this tumor? Just one.
Naturally, if we have a healthy immune response, this errant cell may have been identified early and appropriately killed off. So, what do the experts prescribe us for treating our autoimmune diseases? Well, most commonly, it’s the steroids. The steroids function by blocking the immune system from detecting the damaged cells. This action is why it is now commonly accepted that the steroids significantly increase the risk of subsequently getting cancer.
Regardless of how and why a damaged stem cell fails to be detected by the immune system, there is an additional scenario we need to consider. With highly inflamed, and highly acidic environments, eventually, there is going to be damage to the basal membrane itself. Once there is a rupture of the basal membrane, stem cells, even completely normal, and non-damaged ones will travel to the underside of it. Next, these cells can get trapped on the wrong side of the basal membrane. Since there is nothing wrong with these stem cells, and they just reproduce on schedule, and perpetually. After all, their genetically programmed role in life is to perpetually resupply the epithelial tissue with new cells. But, by being trapped on the wrong side of the basal membrane, we now have cancer in the same hosting epithelial tissue.
There’s one more connection here between cancer and distressed epithelial tissue that I’d like to discuss, and that is vascularization. Vascularization is when new small blood vessels grow into tissue. Of course, these are not blood vessels that are normally present in healthy tissue. This phenomenon is readily observed on the face of many older people who have rosacea, and very commonly on the sides of the nose. It is also very commonly seen in people’s eyes as they become ill. Now, it is critical to understand that these new capillaries and micro-vascularization are not the expansion of existing ones. Rather, these are completely new vessels. The newly grown-in capillaries and micro vascularizations are the body’s response to the demands being made by the distressed tissue. The tissue is demanding more oxygen and nutrients and sends out special signals to entice more blood vessels to be grown in. This, in itself, is rather remarkable. Here, we can witness the amazing power of the body to not only adapt in real-time to a new demand, but it is also responding by altering its physical structure. Except, to be clear, having distressed tissues needing more blood vessels to be grown into them is not a good thing to have happen. It’s a huge red flag that a disease condition is present or developing. Of course, vascularization of the distressed tissue was induced in the so-called vitamin-A deficiency experiments, and it is almost always present in xerophthalmia too. What’s happening is as the outer layers of the epithelial tissue become dried out, and inflamed, they can no longer absorb adequate amounts of oxygen from the outside world. Distress messages are sent out, and the new blood vessels are then grown-in as alternative supply routes. Although that is absolutely remarkable, there is another disease condition that exhibits this same phenomenon, and that is cancer and of course cancer tumors. Many cancer tumors will have large and completely new blood vessels grown into them to supply them with their needed oxygen and nutrients.
A question that I keep thinking about is why is there such a high degree of variability in how the autoimmune diseases present themselves in different people. After all, if we are all being very slowly poisoned by the same toxin, then one might assume many people would present the toxicity in very similar ways. For example, why do some people first present with eczema, and others first present with MS (yes, I do know that many people present with both at the same time). What I was trying to come up with was a plausible explanation for why there are such big differences. However, on the larger scale, there are indeed recognizable patterns too. When we step back and look at the entire North American population, there are major patterns to the presentation clusters. Probably the top four most prevalent named autoimmune diseases are eczema, diabetes, asthma, and dry eyes. What’s rather astonishing, this is a very close-fit to the earliest presentation clustering seen in the rats of the early deficiency/toxicity studies done in the 1920s. What’s rather remarkable about this, is that unlike our highly variable human diets, this clustering was with all the animals on pretty much the same diet, and for the same duration. Therefore, I think it is clear, that the skin, lungs, pancreatic ducts, and the tear ducts of the eyes are the most susceptible to moderate toxicity levels. However, even with their animals on the same diet, there were variations too. Therefore, there is some apparent randomness going on.
In the human experience, there are a huge number of variables that are going to factor into who, when, and where (what tissue location) the disease conditions will first manifest themselves in. Most certainly, the studies by Mori and Bloch with fats in the diets provide us with what’s probably the most critical determining dietary factor, and that is the quantity and nature of consumed fats. On the one hand, sufficient fats are needed to emulsify and safely store retinoids. On the other hand, fats included in meals with high concentrations of plant-based sources could yield much higher absorption rates. Obviously, over the long run, fats from animal sources could be the most dangerous. The hidden vitamin-A in milk casein is right up there on the list too. Of course, then there’s the variability in one’s daily dose, animal source versus plant source (~1/20th absorbed), and the consumption of other carrier proteins such as gluten, etc.
Next, we need to keep in mind that these diseases usually develop very slowly over long periods of time. The disease has been in development well before there are any noticeable symptoms present. That’s because having just a few stem cells prematurely picked off every day is not going to manifest itself as a disease condition. It’s not until there’s been enough of a depletion of the stem cell population to cause the malformation of the tissue structure that symptoms arise. Likewise, even with the immune response selectively picking off a few misbehaving cells every day is only going to cause a very slight, and therefore not a noticeable increase in background inflammation.
From there, we need to ask the more important questions as to why does one adipose tissue collect higher concentrations of retinol than do others. Once again, I think variations in fats and the specific densities of the fats would play a significant role. The next highly variable, yet critical, factor is a person’s exposure to sunlight and drying weather conditions.
|Table 2: Mean concentration of triglycerides in males and females (mg/dL)|
|Percentile||5‐9 yrs||10‐14 yrs||15‐19 yrs||5‐9 yrs||10‐14 yrs||15‐19 yrs|
Source: Lipid and lipoprotein distributions in white children ages 6-19 yr.
The Lipid Research Clinics Program Prevalence Study.
Tamir I, Heiss G, Glueck CJ, Christensen B, Kwiterovich P, Rifkind BM.
One of the most important observations that threads its way through all this research is that boys are more susceptible than girls. I believe we can explain this phenomenon. It’s because young girls naturally have higher serum lipid levels than do young boys.
Therefore, with these higher lipid levels, girls are better able to emulsify the dietary retinoids that enter into serum, and thus allows it to be more readily and safely stored. So, in their younger years’ girls are more protected.
However, when we get to the teenage years the parameters going into the equation change a bit, and the ratio inverts. Additionally, it is well documented that zinc is an important mineral in protecting against retinoic-acid-induced cellular damage. Men naturally use up more zinc than do women, and over the long-term, they will have more quickly depleted their zinc levels. So now, it gets tricky. Over their lifetime, women due to their higher cholesterol levels will have accumulated more retinoids within their adipose tissues. Therefore, they will generally be more susceptible to the disease conditions, yet present the diseases more gradually. Whereas, in men, after they’ve reached a storage saturation point, they are less able to mount this subtle defense and will have a more acute response to high retinoid intakes. You can think of this response as being like the mechanism that causes pH levels to make the rapid, and non-linear, changes as seen in titration experiments.
In this chapter, we are going to review and analyze the experiments that are thought to have “proven” the grand vitamin-A deficiency theory. Therefore, this is one of the most important chapters in this e-book. Please don’t just skim over it.
Before we dive into the details of why and how these experiments were truly botched we need to cover off on some long-held beliefs and concepts around vitamin-A deficiency.
Today, most people, and even the experts in ophthalmology, generally believe that vitamin-A deficiency most predominantly affects the health of the eyes and vision. But, nothing could be further from the truth. What the early vitamin-A deficiency experiments proved was the absolutely devastating head to toe tissue destruction of the entire body. The scope and magnitude of the so-call deficiency that was proven in the early experiments is nothing short of astonishing. Here’s just a brief high-level summary (in no particular order):
That’s right. That long list is much closer to the real scope and magnitude of the disease conditions reported due to the so-called deficiency. Some additional comments are noteworthy here; younger rats are significantly more susceptible than older ones. Males are more susceptible than females. Hopefully, you are spotting the pattern here. Hopefully, you are also spotting the most common named human chronic diseases in this list too; such as eczema, asthma, diabetes, arthritis, lupus, kidney disease, MS, and Sjögren’s.
This observation about the astonishing scope of the supposed vitamin-A deficiency affecting far more than just the eyes, and affecting other organs far more seriously, is made in the introductory comments by Wolbach and Howe in their 1925 study:
TISSUE CHANGES FOLLOWING DEPRIVATION OF FATSOLUBLE A VITAMIN.
From the Department of Pathology, Harvard University Medical School, and the Forsyth Dental Infirmary, Boston.
Received for publication, September 4, 1925
A number of workers have assumed that the eye and its glands alone deserved study – organs which we have found to exhibit much less striking lesions than the respiratory and genitourinary tracts and certain glands. In light of the pathology described in this paper it is no longer tenable to characterize the condition of fat soluble A deficiency by names referring to the eye pathology; i.e., xerophthalmia–keratomalacia. Atrophy of many glands, arrest of growth, emaciation, and replacement of many different epithelia by stratified keratinizing epithelium actually characterize fat-soluble A avitaminosis. The specific pathology is the widespread keratinization.
The glaring problem here with this long list of disease conditions is, how could any reasonable thinking person believe that scope of destruction could even be possibly caused by a mere deficiency? The other major problem here is that all of this destruction happened in an amazingly short period of time.
If that long list of disease and tissue destruction did not cause them to pause and deeply, and very seriously question their deficiency concept, then the speed at which it happened surely should have. Most of the animals in their experiments had become extremely sick by the 8th week of being on a specially designed deficiency diet. By the 8th week, many of the animals were too weak, sick and diseased even to feed themselves. Bizarrely, the researchers resorted to force-feeding the animals for the remaining two weeks of their experiments. The scene in these laboratories must have been something like mini horror torture chambers.
Nonetheless, by the 10th week, nearly all the animals were either dead or very close to dying. That’s correct, in a mere 8 to 10 weeks on the deficiency diet all the animals were very seriously diseased or dead. Needing to force food down a rat’s throat should have been another major clue that there was something drastically wrong with it.
Each animal was fed and watched and after loss of smell occurred, the food was actually placed in its mouth until the ration was consumed. (page 575)
Maybe those lesions on the animal’s tongue (no doubt in the shape of the food pellet too) should have been another clue? Once again, seeing all this disease and destruction in response to a mere deficiency is so completely illogical. What any reasonable, and thinking, person would expect to see in response to a mere deficiency is a slow wasting and general tissue atrophy. After all, this is the response that’s always been witnessed in nature, and witnessed for over thousands of years too, due to prolonged and even complete starvation. Clearly then, there was something else drastically wrong with the artificial deficiency diet used in these lab experiments.
This takes us into the heart of the matter. What in the hell were they feeding these animals? It’s almost always the same diet used in these experiments. Basically, with only some slight variations, here’s the list of ingredients of the de-facto vitamin-A “deficiency” proving diet:
- Casein (“deactivated” milk protein)
- Starch (usually corn starch)
- Salt mixture
- Lard (rendered pig fat)
- Brewer's yeast (or vegemite yeast)
- Distilled water
To understand the rationale behind this diet, the researchers believed that it was deplete only in vitamin-A and that it was complete and sufficient in every other regard. The thinking was that the milk casein would provide adequate protein. The starch provided carbohydrates. The high concentration of salt mixture; well I’m not too sure what the purpose of that was. The lard provided ample fats, and the yeast provided the then known B vitamins. Therefore, even though not ideal, the diet should have been sufficient in sustaining the lab animals in somewhat reasonable health.
Hopefully to you, and any cardiologist you might ask, that’s not exactly a heart healthy diet to be on. Additionally, and as well as being acknowledged by subsequent researchers, this diet is not just deficient in vitamin-A. It is also deficient in vitamins D, B12, C, E, K, other usable fats, important minerals such as zinc, fiber and other essential proteins too. However, for our purposes here, we are not actually too concerned about these other deficiencies either. After all, most of these experiments were conducted on rats, and rats are pretty damn tough animals. Even the small lab ones should have been able to still survive for a quite a while on this diet.
As with regular milk pasteurization, the casein used in these experiments had to be sterilized too. After all, the researchers did not want to expose their animals to harmful bacteria such as salmonella, E. coli, and listeria that could easily be attached to the casein protein.
Somewhat overthinking the process, the researchers had the casein, starch, salt mixture, lard, and yeast combined into portion sized pellets. The pellets were then heat treated in an oven (presumably to further sterilize it). On the one hand, the pelletized food allowed the researchers to more easily monitor and control the amount rationed to each animal. However, on the other hand, it made it impossible for the rats to selectively pick only the ingredients they wanted. Tragically, I think that even the lowly, simple, rat would have soon figured out what not to eat from this meager menu.
Very tragically, essentially this same diet design is used by most follow-on researchers who repeat the experiments and confirm the vitamin-A deficiency results. This is not too surprising though, because this is kind of what you are supposed to do in repeating and confirming experiments. There is a bit of a flurry of others repeating these experiments in the early 1920s, some in the 1930s, ’40s, and even in 1960. They all use the same diet. There are a few tweaks made to it here and there, but it is effectively the same. The same diet yields the same results over and over. Similar experiments are repeated in guinea pigs, rabbits, and even monkeys. Almost all animals fed this diet became seriously diseased, and most died within just ten weeks.
So, there you have it. That’s the artificial diet that proved the vitamin-A deficiency theory. Although not ideal, to the casual observer it looks at least somewhat reasonably conclusive. However, we are not casual observers. We are inquisitive and critical thinkers. Some immediate questions show up here.
Firstly, why use such a complicated diet at all. This artificial diet is such a completely unnatural, and even bizarre, diet to try to feed rats on. When in evolutionary history have rats ever lived on casein, lard, and vegemite? Isn’t it a tad presumptuous to think that this human designed diet is going to be instantaneously adapted to by rats? Additionally, a high consumption of salt and fungus (yeast) is probably just not a great idea for a rat, or anyone else. Therefore, why not just use a simple vitamin-A deplete diet that would be more normal for rats in their natural habitats? What about oh say, nothing except just 100% brown rice, oats and a few peanuts?
But, by far, the most concerning question we need to raise is how could these researchers have been so completely disconnected from the norms in nature? As I was reading the various reports, I was thinking, are you kidding me? All that disease and destruction caused by a mere “deficiency?” I mean, to me at least, that is just so completely ridiculous. Additionally, all this lethal disease occurred in just 10 weeks (2.5 months) because of a “deficiency?” That too is so utterly illogical, because if these animals were so incredibly susceptible to this “deficiency” scenario, then they simply would not be on the planet as a species. It is absolutely impossible for animals to have this vulnerability. One winter would have killed them all off. Therefore, the more obvious questions these researchers should have been asking: when exactly did, these animals become this susceptible to this mystical vitamin-A “deficiency?” Just as importantly, why are these same disease conditions almost never seen in the animals while in nature?
Therefore, it should have been abundantly clear to every single one of the people involved in conducting the experiments that the animals were not responding to a deficiency at all. Nope, no way, not a chance of it. These sick experiments were simply poisoning the animals. The animals were responding to a toxicity and an incredibly powerful toxin at that.
Of course, there were at least a few critical thinkers among the early researchers who suspected something was not quite right. They conducted their own vitamin-A deplete experiments and by using diets of their own design. So, what happened in their experiments? Well, nothing happened.
In these other experiments, their animals did not succumb to the so call deficiency conditions at all. There are reports from Emmett, A. D., and Allen, F. P., in the Journal of Biol. Chem., 1920, and that of Stephenson, M., and Clark, A. B., in Biochem. Journal., 1920 where their animals showed no signs of vitamin-A deficiency.
These reports should have raised a major red flag. But, somehow, they did not. They were simply dismissed as being anomalies and disregarded. Now, if you recall from our golden rules regarding experiments, to any legitimate scientists this should have proven the vitamin-A deficiency theory as very likely being wrong. They now had other diet regiments still 100% completely deplete of vitamin-A, which were not producing the deficiency disease conditions.
the same disease conditions – flashing red lights!
Additionally, there was at least one study conducted using McCollum’s disease inducing “deficiency” diet but with abundant amounts of vitamin-A directly included in it. This study was conducted by S. Mori, of Wisconsin, in 1923.
Mori regards this form of ophthalmia as identical with that produced by deprivation of fat-soluble A.
From Mori, S., Am. J. Hyg., 1923, iii, 99.
In this study, he produced the same disease results. That’s correct, even with vitamin-A included in their diets, the animals still developed xerophthalmia and keratomalacia. This result was not just a red flag; it was full-size flashing red lights with sirens. Clearly, there was something hugely wrong with the “deficiency” theory.
This new information should have been the immediate show stopper. But, not to be dissuaded, the results of this experiment were discarded too, and with a completely unfounded rationalization. This action, of course, is also a clear violation of our golden rules for conducting experiments. You can’t just conveniently disregard results that you don’t like, or have some bias against. Now, once again, to any legitimate scientists, this should have proven the vitamin-A deficiency theory as being completely wrong. It should have made them immediately stop the presses, go back to the drawing board so to speak, and reexamine what was so wrong with McCollum’s disease inducing “deficiency” diet.
Naturally, what S. Mori did in adding vitamin-A back into the baseline diet is a standard practice in conducting experiments, and is more generally termed to be the control experiment. Of course, there are other researchers who do indeed investigate this control scenario of adding back the vitamin-A into McCollum’s disease inducing “deficiency” proving diet. The rational thinking is that if they add back only vitamin-A into the baseline diet, and if the diet then maintains the health of the animals, that would confirm that they’ve isolated it down to just this one “deficiency” factor causing the diseases.
On the surface of it, that sounds perfectly logical. However, it’s not quite that straightforward. This is where we need to remember another golden rule for conducting experiments, and that’s never to change more than one variable at a time. There are several vitamin-A “deficiency” studies from the 1920s that run this parallel control experiment, but they are primarily focused on reproducing the striking disease conditions induced in the eye. Therefore, the one I’d like to reference and discuss in this context is once again is the Wolbach and Howe study of 1925:
TISSUE CHANGES FOLLOWING DEPRIVATION OF FATSOLUBLE A VITAMIN.
From the Department of Pathology, Harvard University Medical School, and the Forsyth Dental Infirmary, Boston.
Received for publication, September 4, 1925
Source: Pharmaceutical Research Department,
F. Hoffmann-La Roche & Co., Limited Company,
Basle, Switzerland, 1989
What’s so important about Wolbach and Howe’s 1925 study, is that not only is it the premiere study that proved the enormous scope and devastation caused by the so-called deficiency, it is also the study referenced today as being the one to definitively close the case on the vitamin A deficiency theory.
Wolbach and Howe’s 1925 study is probably one of the most comprehensive vitamin-A deficiency studies done in this era. Not only does this study investigate the broader scope and magnitude of the vitamin-A “deficiency” induced disease conditions, it in parallel runs the needed control experiments. My perspective on this study is that it was well designed and well conducted. They conduct rigorous and thorough postmortem investigations of the extent of all the affected organs and tissues. Overall, their report is excellent, and I encourage you to read it in detail. The report completely supports and reconfirms the vitamin-A “deficiency” theory. Additionally, to prevent the complication, or conflation, of follow-on infections, they keep the animal cages meticulously clean and keep only one animal per cage. Actually, ruling out the involvement and contribution infections make in the overall disease picture is one of the key objectives of this particular study.
However, the authors of this study are also very dismissive of the other contemporary vitamin-A-deficient diet experiments that are not producing the disease conditions. From the report’s introduction, they state:
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.
They then go on to enumerate the other studies that have “resulted in wholly negative results” and attempt to rationalize them away with not much more than a single sentence. Although, this should alert us to the high probability that Wolbach and Howe had some biases. Even still, I don’t really think their apparent biases were a big factor since the results that they were looking at were indeed powerfully compelling. However, they do make a simple, and fundamental, scientific mistake. It’s a deceptively simple mistake. I believe they were led into making this mistake by the accounts of the very earliest researchers using butter and cod liver oil as sources of high concentrations of vitamin-A. As a means of adding vitamin-A back into the baseline diet, they substitute out the lard by replacing it with butter.
Control rats on the same diet, but with butter fat (prepared from fresh butter by melting and washing in hot water) in place of lard, grew normally and have been maintained in normal healthy condition for a year.
Not only was their control diet preventing the onset of the disease, but it was also promptly reversing it too.
The control diet was tested for its curative properties, and its administration was always followed by prompt amelioration and disappearance of the signs and symptoms of the deficient state.
Although this sounds like rather fantastically good news because it’s clear evidence that the disease condition was not only caused by diet but that a simple diet change could ameliorate it too. However, and somewhat counterintuitively, we can’t jump to their conclusion that the vitamin-A in the butter was solely responsible either. That’s because the substitution of the butter in place of the lard had not changed just one variable in their control experiment. Not at all. Rather, it had changed at least three variables at the same time. They’ve added vitamin-A, they’ve added vitamin D, and more importantly, they’ve changed the composition of the fat. In 1925, it was more or less assumed that a fat was a fat, and it was thought to just be a source of food energy. The butter fats most certainly could have much better emulsification properties than does lard in regard to the retinoids. Some important differences between butter and lard is that butter has about twice the concentration of cholesterol and saturated fats. Of course, modern medicine and nutritional science claims that higher levels of cholesterol and saturated fats are bad for us. But, please remember that we are now in a negative universe. What we’ve been told is the complete and total opposite of what’s true. In the context of a fat-soluble toxin, such as retinol, the higher density fats are hugely more protective.
But, there’s a hidden fourth variable they’ve changed with this simple butter substitution in place of the lard. It is something they could not have known about. It’s not what they’ve added into the diet; it’s what they’ve taken out of it.
You now have enough information to figure out the mystery here. What was really going on in these experiments? What substance(s) do you know of that can even possibly cause the scope of the disease and catastrophic tissue destruction exhibited in these animals? Additionally, what substance can cause all of that disease to happen so quickly? Of course, it also must be a substance that was inadvertently, and unknowingly, included in the animal’s diets of these experiments. I’ll bet you know its name.
Yes, it’s retinoic acid. The chemotherapy drug. The rats in these experiments were simply chemo’d to death. If true, where was the retinoic acid coming from? Well, there are two sources of it.
What is lard? Basically, it’s pig fat from the adipose tissue of the slaughtered animal (mostly the skin). Lard is produced via a process known as rendering. Rendering is exposing the remnants of the hog’s carcass to high heat or steam and separating off the fat. Although that might not sound too delicious, in the animal processing industry, nothing is wasted.
Here’s where I need to interject with some trivia. Of all the mammals on the planet, there are only about two that are known to collect retinol within the fats of their adipose tissues (the skin). It’s humans and domesticated (farmed) pigs. In most other mammals, there is no detectable retinol in their skin lipids. Of course, pigs are sent to feed lots for “finishing” where they are first deliberately fattened by feeding them heaps of corn. Yes, corn is excellent at fattening the animals, and it is also a very good source of the yellow carotenoid vitamin-A precursor, and it’s a reasonably good source of vitamin-A too. Naturally, us humans (in the domesticated Western world) are continuously at the feed lot eating tons of high vitamin-A content foods too. And, yes, just as with the hogs, we get fat too. With that juicy bit of trivia explained, let’s get back on track here.
Okay, so lard is rendered pig fats, and that fat would normally have significant levels of various forms of vitamin-A contained within it. But, after rendering, lard is reported to have virtually no vitamin-A, or maybe only trace amounts of it. So, what happens to the original quantity of it? Well, it mostly gets separated off into the yellow (yes, retinol is yellow), less market appealing lards. However, the separation process is not 100% perfectly efficient. More importantly, remember, retinol is easily converted into retinoic acid via oxidation. All that’s needed to create the oxidation reaction is heat and oxygen. Ample amounts of both are present in the “rendering” process used to produce lards. Therefore, the lard in these experiments contained retinoic acid. This is not just a theory of mine. We have hard evidence for it. We just need to skip ahead a few decades to another vitamin-A deficiency experiment done in 1953. This study is a fascinating account.
Studies in Vitamin-A
26. THE VITAMIN-A-REPLACING EFFECT OF LARD
In this experiment, the researchers have conclusively determined that there is some mysterious hidden factor in lard that is having the same effects on tissues as does vitamin-A. They conduct a rather extensive investigation trying to isolate this substance. They narrow it down to being in the yellowish constituents of the lard, but are never able to detect vitamin-A.
The lard used yielded 0-23% unsaponiflable material as a very pale yellow, low-melting solid which in concentrated solution fluoresced pale blue under ultraviolet illumination.
A solution of the unsaponifiable material in cyclohexane (8-6%, w/v) was yellow and gave a very pale-green color with the SbCl3 reagent. No absorption band could be detected in this green solution. The absorption curve of lard unsaponiflable material showed inflexions at 225 me. (El% 14-0), 250-300 mμ. (El% 270 mμ. 5-5), 315-365 mμ. (El% 330 mμ. 0-9), 445-460 mμ. (El% 450 mμ. 0-06) and 470-495 mμ. (El% 480 mμ. 0-04).
The unsaponifiable material was chromatographed on watered A1203 (Table 1), but neither preformed vitamin-A nor carotenoid precursors could be found in any fraction. (page 681)
Next, here’s where a bit of chemistry factors into the equation. A standard laboratory technique for detecting certain chemicals is the process of chromatography and fluorescence. When certain molecular structures are exposed to light of very specific wavelengths they will fluoresce (they glow). The color they fluoresce at is also very specific to the molecule. Therefore, the specific combination of the inbound induction wavelengths and the responding emission wavelengths can very reliably isolate specific molecules. Retinol’s absorption wavelength is at about 335 nm, and it’s emission wavelength is at 458 nm.
With this technique and associated equipment, the researchers in this experiment intensely search for retinol in their lard samples. To be clear, this is no trivial effort on their part, because they are almost certain it’s there. After all, they can directly see the influence something like vitamin-A is having on cells. However, the mystery chemical is not to be found. What they were not aware of in 1953 is that retinoic acid is the real heavy hitter in this dynamic duo of retinoids. What they are also not aware of is that retinoic acid does not fluoresce, not at all, not at any wavelength. With the oxidation process of converting retinol to retinoic acid, the molecule’s structure has changed, and that prevents it from fluorescing. Therefore, I believe that the vitamin-A effect they were seeing was that of retinoic acid.
The effects of vitamin-A deficiency on epithelial tissues are so definite that it is reasonable to expect some trace of the vitamin in those tissues which in avitaminosis exhibit the characteristic keratinizing metaplasia. In fact, however, Popper (1941, 1944) and his colleagues failed to discover any evidence for the presence of vitamin-A in the epidermis or epithelium of the mucous membranes, tissues which are considered to be the first sites of vitamin-A deficiency. The fluorescence technique used might well have revealed anything more than minute traces. (page 685)
Other researchers at the same time confirmed that lard does indeed also contain vitamin-A
According to Herb et al. (1953) lard contains 0-5-2 i.u. of vitamin A/g., which is of the same order as that we have found in the beef fat - mutton fat mixture.
By J. GILLMAN, K. BARBARA NORTON, D. E. A. RIVETT AND D. A. SUTTON
Joint Nutrition Unit of the S.A. Council for Scientific and Industrial Research and the University of the Witwatersrand, Johannesburg and
National Chemical Research Laboratory, South African Council for Scientific and Industrial Research, Pretoria (Received 22 August 1955)
Another significant source of vitamin-A in the earlier vitamin-A deficiency experiments would have been the milk protein, casein. Casein acts as a carrier molecule for retinol and highly bonds with it. It normally contains a relatively high concentration of vitamin-A.
See: Binding of vitamin-A by casein micelles in commercial skim milk.
Of course, the understanding of casein as a substantial source of vitamin-A is not at all a new discovery. McLaren acknowledges this fact in his 1963 textbook. In reference to an early paper by Powers Park in Simmons in 1923, he states:
For example, 1 of the 2 diets containing casein had three times more casein than the other this would be a good source of the vitamin, for special extraction methods were not in use at that time.
Source: MALNUTRITION and THE EYE, forward, page ix
However, if it was just retinol (not converted to retinoic acid) included in the casein, those tough little rats should have been able to tolerate that for a good long while, and much longer than just 8 to 10 weeks. Since retinol is normally found in casein, and these researchers knew that there was none remaining in the “deactivated” casein used in the rat diets, what happened to it? Well, they assumed that the deactivation process had destroyed it. But, no, it was not destroyed. They unknowingly provided the oxidation chemical reaction needed to convert that retinol into retinoic acid. As in the 1950s, back in the 1930s, the standard test for retinol was using fluorescence. At the specific induction wavelengths, retinol fluoresces a nice light blue color. It’s the key indicator that retinol is present. However, after conversion to retinoic acid, the molecule no longer fluoresces, at all. Therefore, they would have been quite certain that there was no retinol remaining in the casein used. But, in 1925, it appears they were not even aware of retinoic acid, nor its properties. Therefore, in their zeal for sterilizing the casein, they converted its included vitamin-A into its most toxic form. From Lowe and Morton’s 1953 report cited above, we have this description of the process they used to “deactivate” the casein used in their experiments.
Light white soluble casein (B.D.H. Ltd.) (400 g.) was boiled under reflux with abs. ethanol (2 1.) for 3 hr. It was then filtered at the pump and twice washed with 200 ml. portions of boiling ethanol. The casein was again refluxed with fresh ethanol (2 1.) for 3 hr., filtered and washed as before. It was then dried overnight at 110 C in an electric oven and on the next day ground to a fine powder and incorporated in the diet mixtures.
Next, we need to consider yet another earlier vitamin-A deficiency experiment done in 1927. They too were conducting control experiments to prove that by adding vitamin-A back into the base line diets it will prevent xerophthalmia and the other anticipated deficiency conditions.
The base diet they use is:
Group/.–(Diet -A-D.) This diet is deficient only in vitamins A and D, and consists of the following:
|Inactivated* technical casein (Merck)
Salt mixture, McCollum No. 185 (6)
Vegex (lVIarmite) (for vitamin B)
Decitrated lemon juice (for vitamin C)
* By heating and aeration (Goldblatt and Morltz (5)).
From the Department of Pathology, School of Medicine, Western Reserve University, Cleveland. 1927
The key detail here is that they use casein that had been “inactivated” by applying heat and aeration. Of course, using “inactivated casein” is a standard practice in nearly all the vitamin-A deficiency experiments. Here is another example from an even earlier study done in 1923.
The food of the animals on the vitamin-A low diets contained an adequate amount of the various food constituents—protein, carbohydrate, fat, inorganic salts and vitamin B (obtained from yeast). Since the casein which furnished the protein was extracted with hot alcohol for twenty-four hours and ether,
AMY L. DANIELS, Ph.D. AND MARGARET E. ARMSTRONG, M.D.
WITH THE COOPERATION OF MARY K. HUTTON, B.S.
IOWA CITY 1923
The China Study, or to use the more official name, the "China-Oxford-Cornell Study on Dietary, Lifestyle and Disease Mortality Characteristics in sixty-five Rural Chinese Counties”, was one of the most comprehensive epidemiology studies ever conducted. The study is summarized, and the results analyzed in the book of the same title, by T. Colin Campbell, Ph.D. of Cornell University. I highly recommend this book.9 The takeaway from the study is that much of the blame for the epidemics of our chronic diseases in North America is attributable to our high consumption of animal-based foods; such as meat, dairy, eggs, etc. But, if I could condense Campbell’s great book down to just a couple of sentences, here’s what I think his principal messages are:
- The disease rates in North America is absolutely off the charts in the context of the more normal worldwide rates.
- Our foods are causing our epidemics of chronic disease.
- The worst offenders are the animal sources of protein.
- Either you go vegan, or you are going to die young.
In addition to these messages, Campbell’s other prime conclusion is that the very worst (disease promoting) food from the animal sources is milk, and he pins the blame squarely on the casein protein within it. Naturally, much like in these early experiments, our zeal for sterilizing mass-produced foods, the mandatory pasteurization of the milk permitted in the national milk supply exposes the embedded retinol hidden within its casein protein to high heat. I wonder how much of its retinol gets converted into retinoic acid without us ever knowing it? Very unfortunately, Campbell goes off the rails a bit in his analysis. He mistakenly makes the extrapolation from milk casein being harmful to that of all animal proteins being harmful. That extrapolation is just plain wrong. And it’s quite tragic too because he was so close to getting it correct. Blaming an entire food group was a mistake, and he just needed to dig a little deeper. He would have seen that it’s not an entire food group that’s causing our chronic diseases. Rather, it’s a few select molecules sourced from many different foods (both plant and animal based) that’s causing them.
Like with the work done in the China study, more contemporary research is directly linking the consumption of cow’s milk, and specifically, the casein protein, with the subsequent development of both Multiple Sclerosis and diabetes.
A team of researchers led by Hospital for Sick Children (HSC) senior scientist Michael Dosch has determined that multiple sclerosis and type I (juvenile) diabetes mellitus are far more closely linked than previously thought, including the role cow milk protein plays as a risk factor in the development of both diseases for people who are genetically susceptible.
"Researchers Determine That MS And Diabetes Are Closely Linked Diseases."
ScienceDaily, 22 March 2001.
Of course, it’s not just that casein naturally contains vitamin A that makes it a big risk. Rather, it is that the vitamin A is wrapped up in the protein, and that enables it to bypass the body’s normal pathway for storage in the liver. The casein protein wrapper is allowing the retinol molecule to slip undetected beneath the body’s otherwise protective retinol radar, so to speak, and penetrate deeper into these other organ tissues.
The misunderstanding of casein containing vitamin-A back in the early 1920s is reflected in this comment from McLaren.
Elsewhere (McLaren, 1959) reference has been made to the belief, widely held at one time, that it had been demonstrated in the laboratory that diets containing protein of poor quality and deficient in vitamin-A cause xerophthalmia to develop more rapidly than those with good quality protein. Such a statement was made by no less and authority than Parsons (1932), without giving any source, and appears in the fourth edition of “The newer knowledge of nutrition” by McCollum and Simmonds (1929). The original source seems to be a paper by Powers, Park, and Simmons (1923) which describes the feeding of rats on 3 diets, all deficient in vitamin-A and containing protein of different qualities. It is evident that the diets were not equally deficient in vitamin-A. For example, 1 of the 2 diets containing casein had 3 times more casein than the other. This would be a good source of the vitamin for special extraction methods were not in use at that time.
Source: MALNUTRITION and THE EYE, page 110
In the early vitamin-A deficiency experiments, the result was usually the complete transformations of the various epitheliums, and almost always resulted in follow-on opportunistic infections, and following that, death. However, most of these studies from this era were just focused on reporting the striking degenerated epithelial tissues of the eye. The less publicized, yet critically important finding of the experiments was that the so-called deficiency was destroying almost all the epithelial tissues in the body, and almost regardless of what organ or gland it was contained in.
Likewise, and by a wide margin, in Wolbach and Howe’s 1925 study the common theme, and specific tissue most affected by the deficiency was the epithelial tissues. Therefore, this requires us to drill down into, and get a clear understanding of what’s happening with this specific tissue type. Let’s consider some the comments in Wolbach and Howe’s 1925 report regarding what’s happening to the various epithelial tissues.
Mucus is another substance which may be followed microscopically, and inasmuch as the commonest seats of the keratinizing changes are mucus-secreting epitheliums, we have tried to establish some association between the two.
AMY L. DANIELS, Ph.D. AND MARGARET E. ARMSTRONG, M.D.
WITH THE COOPERATION OF MARY K. HUTTON, B.S.
IOWA CITY 1923, page 762
What’s so important to understand here is that not only are the epithelial tissues the primary target of the disease condition, it is the way in which they are affected and respond. What’s observed is the rapid and accelerated mitosis of the basal stem cells.
Mitotic figures are numerous and growth may take the form of a thin layer of cells underlying the original epithelium or of a circumscribed clump.
With growth which is rapid, as attested to by the number of mitotic figures, the cells form an orderly stratified layer applied in normal fashion to the tunica propria; the superficial cells exhibit the sequences of normal keratinization as regards presence of keratohyaline globules and staining reactions. Throughout the duration of life, multiplication of the basal layer of cells continues at a rapid rate, and large numbers of keratinized cells are thrown off.
Source: As above, page 764
Seeing rapid and accelerated stem cell division should have been another major clue that they were not looking at a deficiency condition at all. Instinctively, we’d expect the normal response to a severe deficiency condition to be a slowing down, or even stalling, rather than a significant acceleration, in the rate of cellular division. Once again, it should have raised major alarms as to some other hidden force being present in these experiments. Even though it is completely obvious, we can now go through a simple elimination process to pin it down to one root cause. Currently, there are about two known food-based toxins that can provoke stem cells into a rapid replication as seen in these experiments. Additionally, here we have animals in these experiments restricted to an incredibly small number of unique food items. That does not leave us with many possibilities as to who the prime suspects are in causing the rapid stem cell replication. Actually there are only two possible suspects: retinol and / or retinoic acid.
Except, since these scientists had gone to great lengths to eliminate, and ensure, that all retinol was removed from the casein, and lard, that leaves us with one choice. It’s retinoic acid. And, of course, all the disease conditions induced in these animals is a perfect match for the same conditions induced in humans when being treated with retinoic acid. Therefore, I say we go with the highly logical maxim: if it swims like a duck, looks like a duck, waddles like a duck, and quacks like a duck, then it’s probably retinoic acid. Well, you get the point, it is retinoic acid.
Thus, it should be very clear that it was not so much the substitution of butter into the diet that had promptly ameliorated the disease conditions, rather it was the removal of the lard with its hidden retinoic acid. The researchers had simply removed one of the primary sources of the retinoic acid toxin from the diet. Therefore, while being fed lard, the rats were simply being poisoned to death. However, I have no doubt that the higher density fats and cholesterol of the butter helped significantly by emulsifying the retinoic acid hidden within the casein. The beneficial, and protective, aspects of these fats would have far outweighed any additional risk it’s own vitamin-A content may have presented. Regardless, the bottom line here is that these deficiency experiments were utterly botched. Not only did their so-called deficiency diets contain substantial amounts of vitamin-A, it is simply impossible for all of that disease to be the result of a mere deficiency. Seriously, anyone’s grandmother could figure that one out.
Oh; but wait a minute, maybe it was that the animals were deficient in retinoic acid too? Maybe, without retinol, the animal’s cells could not have normally been producing retinoic acid, and therefore they were deprived of its wonders. Well, by about 1959 scientists were getting a better understanding of retinoic acid, and were gleaning some insight into its magic powers to vastly speed up stem cell division. Also, around 1959, it had been determined that vitamin-A would be slowly metabolized to retinoic acid (vitamin-A acid). They also knew that retinoic acid could not convert back into retinal (termed retinene at the time).
In 1960, a research team at Harvard investigated this exact question I’ve just posed. They wanted to know what beneficial effect retinoic acid would have in a vitamin-A deplete diet. Basically, their hypothesis was that maybe animals don’t need vitamin-A so much, rather it is that they needed the downstream metabolite of it. In other words, maybe the animals in the early experiments were shortchanged by not getting enough retinoic acid?
In the Harvard team’s experiments, they still used a very similar (a nearly identical) “sick diet” as the deficiency researchers did 35 years earlier, (things don’t move fast in medical research). They just “supplemented” the diet design with retinoic acid too.
Normally the rat after about eight weeks on a vitamin-A-deficient diet become sick and rapidly dies, at about the same time as the retina is beginning to degenerate. By taking advantage of the fact that vitamin-A asset prevents general tissue degeneration and death, without being reduced in vivo to retinene or the vitamin, which are necessary for vision the Harvard workers (Dowling, 1960) have been able to follow the changes in the retina for as long as 10 months. Figure 14 shows the progressive changes in these animals.
After 2 months on the deficient diet supplemented with vitamin-A acid retina has begun to degenerate.
Source: MALNUTRITION and THE EYE, page 110
Sure enough, the Harvard team got very similar results as before. Although in their experiments some of their animals died less quickly. Nonetheless, their conclusion was, nope, not even retinoic acid could save the animals from the horrors of vitamin-A deficiency. They too were quickly producing xerophthalmia in the animals in just 8 to 10 weeks.
Next, let’s look at the real effects that retinoic acid treatment (when used as an acne drug) has on human vision, and the eye health. Here’s an excerpt from a recent medical textbook documenting the “mild” side-effects of isotretinoin (Accutane et al.). “Isotretinoin” is the more scientific chemical name for retinoic acid.
Mild, transient arthralgias and myalgias may occur with isotretinoin therapy, but these usually do not require discontinuation of therapy. There are also sporadic reports of arthritis responding to dose reduction and Achilles tendinitis.
Effects on vision and central nervous system. In addition to the xerophthalmia commonly experienced, and meibomian gland atrophy and corneal opacities reported with isotretinoin use, photophobia and decreased dark adaptation/night blindness can also occur. The loss of the dark adaptation maybe permanent.
Isotretinoin administration is known, rarely, to precipitate pseudo tumor cerebri, resulting in severe headaches. This side effect is reversible with discontinuation of isotretinoin in conjunction with the administration of a systemic corticosteroid.
Although a causal relationship has not been established, reports links suicidal depression to isotretinoin use even in individuals with no prior history of depression or suicide attempts. In general, nonetheless, that successful treatment of severe acne with systemic isotretinoin can have immensely positive impact on psychological outlook. There is no currently known pharmacological mechanism to account for the psychiatric symptomatology associated with isotretinoin in this issue remains controversial.
Anders Vahlquist, Madeleine Duvic
CRC Press, Jun 20, 2007 – Medical
See page 116
So, wow, would you look at that? Retinoic acid (isotretinoin) is known, and proven to cause xerophthalmia in humans. Also note the exact same condition develops in the meibomian glands in both the vitamin-A deficiency experiments and with isotretinoin usage (the meibomian glands are the sebaceous glands at the rim of the eyelids inside the tarsal plate, responsible for the supply of meibum. The meibum is the oily substance that prevents evaporation of the eye's tear film). So, there you have it, retinoic acid is documented to cause exactly the same conditions in the eye as does so-called vitamin-A deficiency.
Okay, I mean seriously, does anyone think for one second that a mere deficiency is going to have exactly the same catastrophic effects, and have it induced at about the same speed, as being treated with a powerful chemotherapy drug?
All of this should now explain the reason why we have the glaring paradox of vitamin-A deficiency being an exact match for vitamin-A toxicity. It is because they are exactly the same condition. The published symptoms of vitamin-A deficiency are really the symptoms of vitamin-A toxicity and or retinoic acid overdose.
If you want to get a sneak-peek at what really happens to rats after being on a diet completely, 100%, free of vitamin-A for more than ten weeks, here are two friends of mine who can show you.
In my prior e-book I detailed much of my personal experiences with, and significance of, using fluorescence to gauge the amount of vitamin-A in my skin. It is quite a fantastic tool because you can literally see the vitamin-A glowing in your own skin, and see it with your own eyes. The equipment needed is very low cost and can be used by anyone. The process is not invasive and yields immediate results. Of course, this is not a unique experience to just myself. It is well known about, and has been used as a diagnostic tool in the context of vitiligo. Vitiligo is the “autoimmune” disease that causes the loss of the pigment generating melanocytes from the skin and hair shafts.
An ultraviolet light can be used in the early phase of this disease for identification and to determine the effectiveness of treatment. Skin with vitiligo, when exposed to a blacklight, will glow blue. In contrast, healthy skin will have no reaction.
And then this:
Vitiligo is sometimes associated with autoimmune and inflammatory diseases such as Hashimoto's thyroiditis, scleroderma, rheumatoid arthritis, type 1 diabetes mellitus, psoriasis, Addison's disease, pernicious anemia, alopecia areata, systemic lupus erythematosus, and celiac disease.
Source: Same as above
That’s correct, they can literally test for and see the elevated levels of vitamin-A in the skin, and it correlates with all the above so-called autoimmune diseases. Obviously, it is not just the diseased skin that’s “reacting” with blue florescence, rather it is a molecule within the diseased skin that’s fluorescing. But, here’s the clincher detail. Many young people in Africa are now directly inducing the vitiligo condition in themselves to whiten their skin. They are doing this by taking isotretinoin (the same drug as Accutane and otherwise known as retinoic acid), or applying it topically. That’s correct, these people are directly inducing the vitiligo “autoimmune” disease in themselves using retinoic acid. It’s the result they very misguidedly think they want to achieve. Of course, what the toxic drug is really doing is killing off stem cells all over the body too, and not just the pigment producing melanocyte stem cells of the skin. The long-term result will be devastating for many of these people, and many undoubtedly will die early and painful deaths because of it too.
high dose retinoic acid
It is tremendously, and critically important to understand that these early experiments (1913-1927) are the same ones that definitively proved the existence of vitamin-A “deficiency.” That’s right, based upon these official experiments, the theory of vitamin-A “deficiency” was thought to be proven, reconfirmed and solidified. Vitamin-A was then crowned and given the center podium in the prestigious vitamin club. But, we now know better. The irony of the situation could not be greater. That’s because the so-called vitamin-A “deficiency” theory was proven by poisoning animals with the most toxic form of it. Therefore, retinol has never been proven to be a vitamin. Therefore, vitamin-A is not a vitamin at all. It has been an imposter foisted on us by bad science for over 100 years.
However, it is crucially important to understand that the disease conditions expressed in these early animal experiments formed the basis of how modern medicine now recognizes thought to be vitamin-A “deficiency.” When these same conditions now exhibit in people, it is often quickly diagnosed as vitamin-A deficiency. And, of course, why wouldn’t it be? Xerophthalmia is the primary example of this.
However, it goes way beyond that. For example, let’s consider Alzheimer’s disease. What’s now being reported,10 is that many patients with Alzheimer’s are also presenting the co-morbidity symptoms of so-called vitamin-A “deficiency” too. But, it’s not that the Alzheimer’s researchers are making the wrong determination. They are simply making the correct determination, but it’s based on the wrongly defined vitamin-A “deficiency” symptoms. It’s the very foundation of the definition of the vitamin A “deficiency” symptoms that’s wrong. Naturally, as I’ve claimed in my prior e-book, Alzheimer’s disease (the brain symptoms) and its presentation with all the co-morbidity symptoms of the thought to be vitamin-A “deficiency” are really the end result of long term vitamin-A poisoning.
You really need to appreciate the significance of what’s been presented in this chapter. These botched experiments no more proved that retinol was a vitamin than did they proved cyanide to be a vitamin. I believe that I’ve presented sufficient information to at least suspend retinol’s membership from the prestigious vitamin club. I have zero doubt that with time, it will not only be permanently kicked out of the club, but it will also be exposed for what it truly is. It’s a cytotoxin that has killed and diseased untold millions of people.
In the next chapter, we are going to step out of the artificial world of the laboratory and take the vitamin-A deficiency theory out into the light of day. We are going to test it in the real world. We’ll find out what really happens when people, and animals, are exposed to chronic and long-term vitamin-A deficiency.
In this chapter, we are going to conduct an in-depth and logical and physical examination for evidence of vitamin-A deficiency in the real world. Of course, it is going to be a bit problematic because we now have no proven or known symptoms of true vitamin-A deficiency to measure or identify it by. Nonetheless, we’ll do our best to make sense of what evidence there is.
Surely, if there is truly such a thing as a vitamin-A deficiency, and we are all so easily vulnerable to it, then we should be able to find numerous examples of it happening in people around the world. Of course, we are told this is hugely the case in South East Asia and Latin America where vitamin-A deficiency is reported to be endemic. However, once again, these reports are based on the field workers in these regions seeing the same documented symptoms induced with the botched science of the earlier animal experiments now showing up in people. Of course, when Western doctors working in Southeast Asia see kids with xerophthalmia, and / or night blindness they immediately attribute it to, and conclude, it’s vitamin-A deficiency. For most of these doctors, there are absolutely no doubts about it. And why would there be, since it’s literally the textbook defined definition of it? Sadly, for the diseased kids, it is exactly the opposite. Xerophthalmia and lesions on the eye are the symptoms of vitamin-A poisoning, and even that of retinoic acid poisoning (with sunlight and infections being significant contributing factors). So, is this truly vitamin-A deficiency they are seeing in these regions? The shockingly simple answer is, no, it is not. This is not my opinion; it is a fact.
The evidence for this is that the widespread so-called vitamin-A deficiency conditions in these regions are not reported in their long histories. If vitamin-A deficiency really existed on a wide scale in these countries, it would have been well documented and written about. Yet, there is no record of that that I could find. There are only a scant few references to blindness. Do you think people say 1,000, 500, 200, and 100 years ago would not have noticed great swaths of their populations going blind, and dying from all their skin mysteriously burning off? I’ve found no record of this at all. There are records of great plagues (infections), starvations, floods, and wars. But no records of widespread disease that sounds even remotely close to being attributable to vitamin-A deficiency. Can you imagine in the thousands of years of their documented histories, that there is no mention of the worst disease condition in their countries, one that burns the eyeballs out of children, being not written about?
Moreover, with the devastating effects that so-called vitamin-A deficiency has on both the male and female reproductive organs, how is it that India and China have built up to their billion person populations? How is it that these populations were doing just fine, and doing quite fine for the last 5,000 years too without vitamin-A supplementation? How is that the “endemic” regional vitamin-A deficiency has only shown up in the 20th century after we discovered the existence of vitamin-A, and had a product to sell them? However, this is just the starting point in revealing just how ridiculous the so-called vitamin-A deficiency theory is.
Now, here’s the kicker. We are told that vitamin-A deficiency is endemic to SouthEast Asia and that hundreds of thousands, if not millions, die every year from it. The key symptoms used to diagnose vitamin-A deficiency in SouthEast Asia are night blindness, and xerophthalmia (chronic dry eyes). In a later chapter, we’ll dig a whole lot deeper into the vitamin-A supplementation programs going on in SouthEast Asia, and South America. For now, let’s just consider the extremely conflicting large scale evidence being presented in North America using these same symptoms of night blindness and xerophthalmia as our measure.
Xerophthalmia: Dry eyes. Xerophthalmia can be associated with systemic diseases, such as Sjogren's syndrome, systemic lupus erythematosus, and rheumatoid arthritis; deficiency of vitamin-A; and use of some medications. It results from inadequate function of the lacrimal glands, which produce tears. When xerophthalmia is due to vitamin-A deficiency, the condition begins with night blindness and conjunctival xerosis (dryness of the eye membranes), progresses to corneal xerosis (dryness of the cornea), and in its late stages develops into keratomalacia (softening of the cornea). Treatment depends on the severity of the condition and ranges from artificial tears and ointments to plugging of the tear ducts. Also known as conjunctivitis arida.
So now, with xerophthalmia, and night-blindness being the de-facto disease conditions attributable almost uniquely to vitamin-A deficiency, and with North Americans being hugely dosed up on vitamin-A since at least the late 1970s, we should expect there to be incredibly few incidences of the diseases here. Not only is vitamin-A supplementation legislated into our staple food products such as dairy and margarine, but it is also commonly added to the flour, and breakfast cereals in the USA. We now eat huge amounts of high source fruits and vegetables year-round too. Even more importantly, on a per capita basis, we are one of the world's highest consumers of pre-formed vitamin-A from animal sources, such as meat, dairy, eggs, fish oils, and liver. Therefore, it is simply impossible for the average person in North America to be even remotely close to being vitamin-A deficient. Seriously, just based upon the historical diet of humans on the planet, the North American diet probably now has at least 100 to 1,000 times higher levels of vitamin-A consumption compared to that of just a few hundred years ago.
With that knowledge, we should expect the rates of xerophthalmia, and night-blindness in North America to be somewhere between micro-minuscule and completely non-existent. But, remember, we are in a negative universe here when dealing with vitamin-A science, and the funny thing is; it’s completely the opposite. It’s just a wee bit tricky. Because here in North America, the same condition is not generally called Xerophthalmia, rather it’s called “Dry Eye Disease.” You see, our doctors here can’t call it xerophthalmia because it does not fit with the narrative of vitamin-A deficiency. Xerophthalmia is just far too closely associated with vitamin-A deficiency, so much so that the incidence rates of xerophthalmia and Night-Blindness are used as a gauge of vitamin-A deficiency in populations. Therefore, physicians here need to call the conditions “Dry Eye Disease” or “Dry Eye Syndrome.” What’s the real difference between the medically defined disease of xerophthalmia and “Dry Eye Disease” or “Dry Eye Syndrome?” Not much at all, they are on the same spectrum, so it just comes down to someone’s opinion. Not surprisingly, even though there is “only” about 200,000 people officially diagnosed with full-blown xerophthalmia each year in North America, the other (but the same) conditions of “Dry Eye Disease” or “Dry Eye Syndrome” are incredibly common here.
Dry eyes are very common, and dry eye syndrome is a major reason for visits to the eye doctor. A recent online poll revealed that nearly half (48 percent) of Americans age 18 and older regularly experience dry eye symptoms.
Also see: Prevalence of Dry Eye Disease among US Men: Estimates from the Physicians’ Health Studies
Of course, there’s a huge disconnect and problem revealed with this information. That’s because it is simply impossible for almost anyone living in North America to be suffering from vitamin-A deficiency, let alone for 50% of the entire population being vitamin-A deficient. When compared to the rest of the world, we have huge amounts of vitamin-A in our diets, yet we have at least 4 million people with serious xerophthalmia, umm, oh, I mean “Dry Eye Disease,” and about 150 million people with intermittent “Dry Eye Disease.” How can that be possible?
Not surprisingly, the same sleight of hand shell game is applied to the terminology used to report the conditions of blocked meibomian glands. Remember, the blocked meibomian glands is one of the premiere and earliest conditions used in the determination of vitamin-A deficiency. However, since almost no one in North America can be vitamin-A-deficient, it can’t be associated with that, so here the condition is called Meibomian Gland Dysfunction11 and given the nice official-sounding acronym “MGD.”
But, if someone in North America is diagnosed with xerophthalmia, then the blame is often put on the person’s accompanying autoimmune disease. That’s right; we are told their mysterious autoimmune disease is magically causing their xerophthalmia syndrome too. There is this almost ridiculous circular blame game going on in an attempt to rationalize away the obvious. In no way is xerophthalmia a complication of these suggested other systemic diseases, such as Sjogren's, lupus, and arthritis. Obviously, the root cause of Sjogren's syndrome, lupus, and arthritis is the same of that of xerophthalmia. Rather, they are all the complications of vitamin-A poisoning! And, of course, xerophthalmia is xerophthalmia, regardless of what continent you happen to live on. Therefore, it is mathematically impossible for xerophthalmia to be caused by vitamin-A deficiency. The emperor wears no clothes.
Sadly, what we now know is that the same thing is causing both xerophthalmia and their comorbidity autoimmune diseases; it’s vitamin-A toxicity. Therefore, the xerophthalmia diagnosis by North American physicians is the perfect example of not seeing what should be blindingly obvious.
Now, if you happen to be still clinging to the notion that xerophthalmia in the developing countries has some connections with vitamin-A deficiency, then here’s a tidbit of information that should clear up any misunderstandings. Xerophthalmia is seasonal. That’s right; it is much more prevalent in the summer months. If xerophthalmia were a deficiency disease, then we’d expect the complete opposite. The summer months provide more fruits and vegetables and therefore provide more vitamin-A in the mostly plant based diets of the “endemic” regions. The summer also provides more green grass for grazing cows and goats, leading to more vitamin-A in their milk. So, why is there this very distinct increase in xerophthalmia during the summer months? The answer is hinted at by what M. Mori of Japan reported in 1904, and what Bloch reported in 1909. Both these physicians reported xerophthalmia showing up in the children in the months of more sunshine. They also both reported that the kids in their care were photophobic (avoided the sun). Vitamin-A is an incredibly efficient light-absorbing molecule. When a kid with elevated retinoid levels in the skin, and /or in the outer tissues of the eyes, gets a bit too much sun, boom, they very quickly pull a great deal of light energy into the tissue, causing it to heat up differentially, and that kick starts the destructive chain reactions. If a very young child in this condition of elevated retinoids makes the mistake of looking directly into the sun for more than just a few seconds, they are in even bigger trouble.
Next, we are going to consider what really happens when people are forced to endure long periods of chronic starvation, and diets completely void of vitamin-A. The prisoner of war camps during the second World War provides us with ample examples. Both the German and Japanese camps maintained hundreds of thousands of people under conditions of extreme starvation. For now, we are going to particularly focus on the Japanese run camps, because it is well documented that the only rations allotted to the men captive in these camps was one cup of rice per day. Additionally, with the fall of Singapore and Hong Kong at the very start of the Pacific war the Japanese had captured about 190,000 British and allied troops. These men (the ones that survived) were captive for the entire duration of the Pacific war, so that’s for about 3½ years. For the most part, they lived on nothing more than one cup of rice per day, and that’s if they were lucky. That’s it. Almost no protein, no fruits and vegetables, nothing else. In addition to the meager single rice ration, the men were forced into hard labor for twelve hours per day. That’s just the beginning of the gruesome conditions and horrors these men were subjected to. Many were brutally tortured, beaten, and exposed to all kinds of infections, had no medical care, were broiled in the sun, and lived in atrocious sanitation conditions. Not only were they exposed to extreme physical and nutritional stress, but they also had to endure extreme mental stress too. It was not just being captive, there was the constant threat of executions, sometimes by being beheaded.
Clearly, for most the men held in these camps they were not only extremely malnourished in all manner of essential proteins, fats, vitamins, and minerals, they had no vitamin-A whatsoever. This was undoubtedly the perfect conditions to induce widespread diseases and infections. Therefore, under these conditions and according to the VAD theory, every one of these men should have quickly gone blind and had all of their epithelial tissues, and therefore all of their internal organs and glands, completely and quickly destroyed. There should have been massive and widespread cases of xerophthalmia, and blindness reported. It should have been almost ubiquitous within the prisoner populations. Obviously, that was clearly not the case. Not only did that not happen, but it was also nearly the complete opposite. Upon liberation, many of these prisoners were examined by Western medical teams. What’s reported should have been, and to a certain extent was, downright astonishing. The eyes and vision in the men remained in exceptional health. The doctors made special notes of how perfect the eyes appeared in most of these men. The sclera was remarkably void of any vascularization (a condition that normally occurs with xerophthalmia), and was perfectly white. American doctors reported the same (very noticeable and surprising) findings in the men liberated from the German P.O.W. camps.
How can that be? These men were chronically starved for years, and many starved to the brink of death (and of course many did die). They probably did not consume even mere specks of vitamin-A for more than three years, and there were almost no signs of vitamin-A deficiency reported. These camps were huge, the Japanese camps each had something like 3,000 to 5,000 surviving men. The German-run camps had 10,000 to 30,000 prisoners each.
Seriously, you can (and must) see this for yourself. Just get online and look at the pictures of survivors from WWII P.O.W. camps, and even from the German death camps. You’ll see men starved down to being nothing more than mere skeletons. But, please look very carefully at the eyes, and look very carefully at the skin. There are no lesions in the eyes. There are no lesions on the skin even after living in conditions of horrid sanitation. In many pictures, the men are looking directly into the camera too. Figure 8a is just one example.
Do you see any lesions on their skin? Likewise, Figure 8b is another photo where the man is clearly looking directly at the camera.
Shown in Figure 8c is a photo of men, with Private Leo Ayres in the foreground, newly liberated from the Japanese camps who were reading the newspapers about the war having just ended. The point is that you need relatively good vision to read a newspaper.
Shown in Figure 9 is a bit of a zoomed-in view of the faces of men from a German concentration camp. You can clearly see the whites of their eyes (please see the original photo for a better view).
Figure 10 is a close-up photo of survivors from Dachau. Once again, please see the original photo for a better view of their eyes.
These young men are looking at the camera, and you can see the white sclera of the eyes. Even though their bodies have been horribly emaciated down to just living skeletons, remarkably they too have no lesions on their eyes and upper bodies. How can that be possible? According to the vitamin-A deficiency theory, they should be completely blind, and have all of their skin burning off from head to toe with bleeding and infected lesions. As should be all of their internal organs too. Once again, do you see any evidence of that here?
Additionally, this complete lack of vitamin-A deficiency symptoms is not just observable in the men that survived these horrors, its observable in the corpses of those who did not. You can find pictures from the Nazi death camps showing piles of corpses stacked up like cord wood. Clearly, almost all of these victims were horribly starved, and presumably many did die of starvation too. Look very closely; what is it that you don’t see in those photos? For most of them, there are no lesions on the skin.
Figure 11 The eyes of a starved Russian man from
the Dachau Camp
Now, of all the pictures that I looked at, one really stood out for me. Figure 11 is a picture of a young Russian man who’s been in the German Dachau camp for an extended period.
Although the caption on this photo states the person is a Russian woman, I believe it’s a young man’s face. Clearly, he’s been starved for a long while. His eyes are sunken back into the skull. But since this picture has been taken so close up to the man’s face we have a good view of the health of his eyes. Don’t those eyes look remarkably healthy to you? You can see that they’re moist and have no lesions. There’s no vascularization of the sclera. Just as importantly, his glistening eyes are mirroring the image from behind the photographer. You can see in his eyes the reflection of a structure in the background. The light is being reflected off the eyes because they are moist and protected with the tear film. Clearly, this young man’s meibomian glands are functioning just fine. Once again, please remember that the meibomian glands are one of the first to become blocked, and the most commonly affected glands, and as documented on the xerophthalmia spectrum to fail early due to vitamin-A deficiency. Likewise, there are no lesions on this young man’s face. On the contrary, his skin looks to be in remarkably good health too. How can that be?
McLaren summarizes some of these observations in his 1963 text.
During and immediately after the second world war, much greater attention was paid to the medical aspects of starvation and recovery therefrom. Generally speaking, disorders of the eye did not find a prominent place in these accounts.
When the resistance shown by the eyes of experimental animals to total inanition is recalled, this is what might be expected. In their monumental work on experimental human starvation, Keys and his colleagues noted no important deterioration in any sensory function after six months of semi-starvation. They do however state that the sclera and conjunctiva were unusually devoid of blood vessels, the whites of the eyes resembling unglazed porcelain and failing to redden even when soap solution was applied.
Source: MALNUTRITION and THE EYE, page 158
The makeup and structure of the eye is very similar across most species of mammals. The proteins of the eye are also not species specific. The primary nutrients found in, and making up the eye, are proteins, and the B and C vitamins. Of course, we’ve been bamboozled into thinking that only the human eye needs massive amounts of vitamin-A. That’s right, we are supposed to believe that after more than 100 million years of evolution on the planet we humans are the only species that need to supplement with vitamin A to prevent our eyes from self-disintegrating. That, in itself is just so absurd, that it’s almost laughable. Sadly, it’s not laughable because it is a big fat lie that’s at the root cause of our chronic diseases.
Of course, this big fat lie needs to be kept secret. If we were to learn that the human eye has the same structure, protein composition, and therefore the same nutrient needs as in most other mammals, we might question why it is that only humans need to supplement with vitamin-A. How is it that all animal species on the planet can endure prolonged periods of starvation and yet retain perfect eye health and humans don’t? According to the vitamin-A deficiency theory, we should see entire herds of animals on the great plains of Africa and in the Canadian Artic all dropping dead at about the eight-week mark into the dry seasons. All of them should have their eyes disintegrating, and their skin burning off, infected, and all their internal organs failing at about the same time too. Hopefully, you see just how ridiculously absurd that whole notion is. However, I needed to find a well-documented account of an animal kept in starvation conditions for a long period. This brings us to the wonderful and heart touching story of Judy the English pointer that loyally went to war with her owner. Judy was taken into captivity along with her owner, named Frank Williams, a young British navy man at the fall of Singapore in the spring of 1942. This account is documented in the book titled: Judy: The Unforgettable Story of the Dog Who Went to War and Became a True Hero, by author: Damien Lewis, published in 2014.12
Along with Frank, Judy spends the next 3½ years in a Japanese prisoner of war camp. She was even designated an official P.O.W. and given an identification number by the Japanese. Of course, being a dog, Judy was allotted no food and was only able to survive by men donating small portions of their own meager rice rations per day, the occasional piece of boot leather, and whatever she could scavenge. Therefore, Judy survived on not much more than one-third cup of rice per day. Much like the British POWs trapped in these Japanese camps the dog starved down to nothing more than mere skin and bones by the end of the war. So, that’s about 3½ years of chronic starvation. To appreciate just how horrid, and desperate the conditions in these camps became near the end of the war here are some highlights of the story. When the men became too sick and feeble even to walk they were left in their bunks to die. They were not allotted any rations, not even two grains of rice per day could be spared on them. For these men, their only potential source of food was just the flies that they might catch. For the other men in the camp who were still able to walk, they resorted to picking and eating maggots from the latrine as their source of food. The thing is, to catch flies and pick maggots you still need to have good vision.
At this late stage of the war, of course, Judy the dog was allotted absolutely nothing and was viewed as a potential meal to the then also starving Japanese soldiers. Therefore, this dog was not only chronically starved for a very long time; she starved to the near brink of death. Nonetheless, Judy had survived at least 180 weeks being almost completely void of any vitamin-A in her diet. That’s at least 20 times longer than what we should expect based on the vitamin-A deficiency theory and supporting experiments.
Yet, when reading about the very final days in this camp, there is no mention of xerophthalmia or eye disease developing in this dog, or the men. There is a passage in the book, as the men are digging what is presumably their own designated mass graves, they look up at the sky and identify high-flying American bombers on route to Japan. Once again, a person needs rather good vision to identify high flying planes. For Judy to make her final escape from the camp, she needed to perform a feat of remarkable mental and physical dexterity. She remained hidden back in the barracks as all the men lined up to be put on trucks. Frank had quickly trained her with a special hand signal just for this purpose. When signaled, she needed to come running and jump into a sack at the very last moment as the men boarded the trucks. You know what? She needed good vision to accomplish that little feat.
The lifelong bond formed between Frank and his dog is a rather incredible story. Damian Lewis has documented much of Judy and Frank’s experiences during their captivity, and some of it in the post-war period. There’s not one word of mention of Judy having developed any disease of the eye, skin lesions, or of any internal organs that had failed. How is that possible for this dog to have not developed xerophthalmia or any other symptom of vitamin-A deficiency? Of course, there’s only one explanation. Vitamin-A deficiency is a giant myth, if not a big fat steaming pile of lies with maggots crawling through it!
There have been several studies attempting to induce vitamin-A deficiency in humans (using volunteers), and it has never really been successful. Meaning, the volunteers just lost weight, and remained healthy, even after more than three years of being on near zero vitamin-A diets there were no signs of vitamin-A deficiency. Various strategies and menus were used in these experiments but for the most part what the researchers found out is that it is rather difficult to induce vitamin-A deficiency in humans. These studies were quietly ended. Nothing to see here, move along.
Probably the most famous of these experiments is the Sheffield experiment. Here’s McLaren’s summarization of it:
None of the 23 volunteers in the experiment carried out by the medical research Council and Sheffield, England who received a diet deficient in vitamin-A for periods ranging from 6½ to 25 months developed any change in the conjunctiva. In adults and older children, therefore in whom the deficiency progresses slowly conjunctival xerosis is not an early sign and for this reason plasma levels and the dark adaptation test, which may be readily carried out in these subjects, are of more value but have their own distinct limitations.
Source: MALNUTRITION and THE EYE, page 171
And then a bit later:
The results of the Sheffield experiment show that very exceptional circumstances are necessary before really marked evidence of vitamin-A deficiency occurs. Even in far Eastern prisoner of war camps where malnutrition deficiencies were rife, xerophthalmia was not usually encountered.
Source: MALNUTRITION and THE EYE, page 208
This brings us to another fascinating account from 1969 of thought-to-be vitamin-A deficiency deliberately self-induced in a person.
Proc Nutr Soc. 1973 Dec;32(3):105A-106A.
Vitamin-A and epilepsy: a dietary contretemps.
Sharman IM, Stern G.
This is an account of a young man who has had epilepsy from the age of twelve, and routinely (about once a month) experienced epileptic seizures. At age twenty, doing his own research on the destructive action vitamin-A has on cell membranes, he’s concluded that his epilepsy was likely caused by some form of subclinical vitamin-A poisoning damaging his nervous system. Based on this determination he goes on an extreme diet of zero vitamin-A and zero carotenoids too. He maintains this diet for more than five years. Remarkably, this strange diet does indeed cure his epilepsy. In this five-year period on his vitamin-A deplete diet he has had only one epileptic seizure, and that’s at the very start of it. But, after five years he is reported to have developed xerophthalmia and a strange gray skin condition. Although he’s been on his strange diet for five years and he’s reported to have the lowest serum levels of vitamin-A ever recorded in Great Britain, it’s between 4.1 µg/100ml and 7.8 µg/100ml. Therefore, somewhat amazingly, even after 5½ years of having no vitamin-A in his diet, some small amounts of it remains in his serum.
Also, remember that we now know that the documented symptoms of vitamin-A deficiency are really those a vitamin-A toxicity. Therefore, his eye and skin conditions could’ve been the result of a lack of fats in his diet. Also, he may have been missing out on other essential nutrients such as proteins, and the B and C vitamins, and zinc.
His doctors spend an extensive amount of effort trying to convince the young man to take vitamin-A supplements to treat his condition. They warn him that if he continues his foolish diet, he will eventually go blind. Even in the face of that threat, he decides to continue his diet. It’s not until his condition significantly worsens that he, very reluctantly, finally agrees to the treatment. He is treated with cod liver oil and his strange skin conditions, and his eyes quickly recover. His physicians, of course, attribute this quick recovery to the vitamin-A in the cod liver oil, and not the oil itself. After the young man has recovered, he immediately goes back to his strange diet of consuming no vitamin-A. I’ve not been able to find a long-term follow-up report of what happens to him after that.
Nonetheless, the material fact here is that he cured his epilepsy with a vitamin-A deplete diet. This fact did indeed spark at least some interest from a few folks in the medical community. After all, curing one’s epilepsy is no minor accomplishment. There is a small follow-up study conducted with eight other people with epilepsy, and they are all placed on vitamin-A deplete diets. There are two remarkable findings from this follow-up study. Firstly, all eight people recover from their epilepsy. That’s an astonishing 100% success rate. Is there any medical drug that has anywhere near a 100% success rate in treating a disease such as epilepsy? The second very noticeable observation made in this experiment is that all eight of these people quickly lose significant amounts of body fat. Therefore, I believe this is pretty clear evidence that vitamin-A consumption is causing the body to retain fat.
I’m not sure why, but the second study is quietly ended and scoffed off as being a case of dietary contretemps. Maybe, it’s because the medical professionals viewed the rapid drop in body fat is a negative response. Or maybe it was because Sharman was one of the most preeminent authorities on vitamin-A, and a big proponent of the grand vitamin-A deficiency theory that he just could not deal with the conflicting real-world evidence, and decided to sweep it under the rug so-to-speak. Moreover, of course, there’s no money to be made in curing people of epilepsy if they only need to make a simple diet change. One other noteworthy comment here is that in the original study it is clearly stated that this young man was on his vitamin-A deplete diet for 5½ years. However, when Wolf13 recounts this case in a follow-up summary report, he states that it’s only four years. I have no idea why Wolf dials back this timeframe number either. Maybe he too just couldn’t deal with the fact that a human can go for 5½ years with no vitamin-A? Yes, that 5½ year number certainly places a lot of doubt on the vitamin-A deficiency theory. The other highly suspicious thing about Wolf’s report is that he claims the vitamin A deficiency experiments can’t be repeated on humans because it would be “unethical”.
Next, we need to ask how vitamin-A toxicity can cause epilepsy? Well, we sure don’t have to look very far and long for evidence. From the so-called vitamin-A deficiency (really vitamin-A toxicity) studies we know that one of the observations was the peeling and disintegration of the myelin sheaths surrounding the nerves. Having this protective epithelial structure peeling off your nerves could definitely cause the epilepsy condition. Moreover, having nerves directly exposed to a molecule that can surprisingly produce an electric voltage could most definitely cause a weird nerve stimulus.
Naturally, this “dietary contretemps” story very much resonated with me. Because I too quickly concluded that my eczema was none other than vitamin-A poisoning. Secondarily, when I first went on my vitamin-A elimination diet, even though I was consuming at least 3,000 calories per day, and with lots of fat, I was dropping weight like crazy. Within about six months I went from being a pretty pudgy guy down to having a completely normal BMI. This ranking is also on the old normal BMI scale, and not the updated version of the scale that is currently being adjusted for the new normal of chunky people.
Not only was I dropping body fat, but somewhat remarkably my muscle strength was also strangely getting better at the same time. Now, after over three years of being on a vitamin-A deplete diet my BMI is still normal, but my muscle mass has gotten greater. I now have a body that looks like what a normal human male is supposed to look like. I most certainly did not drop this body fat because of some malnutrition. No, it was clearly that my body simply no longer had a need for it.
Okay, with all the above evidence, I think we can now see what really happens when people, and animals, are exposed to chronic and long-term vitamin-A deficiency. That’s right, nothing adverse happens. Ironically, they can even get healthier.
13 The Experimental Induction of Vitamin A Deficiency in Humans
George Wolf Department of Nutritional Sciences and Toxicology,
University of California, Berkeley, CA 94720-3104
In this chapter, we are going to analyze the on-going supplementation programs being undertaken in Southeast Asia and South America.
We are told that these large-scale programs are necessary to save the hundreds of thousands, if not millions, of kids who would otherwise surely go blind or die. However, once again, please remember that the vitamin-A world is in a negative universe. What you are about to learn, is that no, the supplementation programs are not saving kids. Rather, it’s the complete opposite. The supplementation programs are causing them to become diseased, go blind and even killing many of them. I believe it’s sterilizing their parents too.
Although we now know that the thought to be a vitamin-A deficiency (VAD) is, in reality, vitamin-A toxicity, we’ll gloss over that little fact here in our analysis of the supplementation programs. Since that’s a new bit of information, we’ll just go with the established VAD theory for much of this chapter.
Of course, in Western medicine, the concept of VAD has been so completely accepted, and so deeply entrenched in the medical thinking that no one even dares to question it. VAD and xerophthalmia are nearly synonymous in medical science. If a doctor now sees a person with a lesion on the eye or other related symptom, they’ll probably immediately suspect VAD. But, as I’ve stated before, the funny thing is; it depends on what continent the person lives on. If they live in Southeast Asia or in South America, then it is surely VAD. And who’s to blame these Western medical doctors for making this diagnosis. After all, it is based on the official science and definition of vitamin-A deficiency. That official definition has been parroted and documented in many medical textbooks by eminent Ph.D.’s on the topic.
However, if any proponent of these programs bothered to do even a few hours of research on the topic, they would quickly discover that it is nearly impossible for the people of these regions to be VAD. The thing is, nearly every food on the planet has some content of vitamin-A or vitamin-A precursor. Many of the green leafy vegetables have very high concentrations. Moreover, many spices are incredibly high in vitamin-A too. A mere pinch of parsley, chives, mint, paprika, oregano, thyme, and red pepper flakes, even once every other month would provide people with ample amounts of it. In many regions of South America sweet potatoes are popular, if not a staple food, and they have very high concentrations of vitamin-A too. The same goes for tomatoes, and bell peppers. Nearly all fruits and vegetables have at least some vitamin-A. As of course do eggs and most meats. Therefore, for the clear majority of the people in these regions, they can easily be getting ample amounts of vitamin-A in their regular diets. Of course, I am not the only person of this view:
A large number foods contain substantial amounts of either vitamin-A or carotenoids, and many these foods are widespread and inexpensive even for the very poor. Thus, in the logical sense, no reason exists for a vitamin-A deficiency to be a worldwide problem. But it is a worldwide problem.
James Allen Olson 1994
Of course, James Olson (a contributor to Sommer’s book) is absolutely correct. With vitamin A (or one or more of its precursors) being nearly ubiquitous, and found in almost every food on the planet, how could anyone be deficient in it. The only way for anyone to not get enough vitamin-A (assuming they need any of it at all) is for them to be eating nothing but rice or beans, three meals a day, seven days a week, and 365 days of the year. Oh, and they have been doing so for five or more years too. How many people do you know that fit into that dietary category? Of course, there’s another dietary scenario that would do it, and that’s one of complete starvation. But, obviously, to a kid facing complete starvation a shot of vitamin-A is not going to do very much for them. No, it is actually the very last thing they need. Remember that vitamin-A without protein and or fats is a direct cytotoxin, and that is not just a “theory,” it is a fact. So, nope, sorry, contrary to popular belief, poisoning a starving kid with vitamin-A is not going to help them.
However, that is just the start of it. In India, it is hugely customary to eat rice dishes that are loaded up on hot spices and various spicy sauces. The hot spices are not just for flavoring, rather it is a survival requirement to compensate for the lack of refrigeration. Without refrigeration, it is very common for most meats being included in the rice dishes to have acquired a heavy concentration of bacteria. Thus, the spices are added as a means of killing off much of that bacteria. One of the most common, and I think it is safe to claim, the primary spice used in India is chili peppers, and chili powders. At about 30,000 IUs of vitamin A per 100 grams, that’s no small factor in the national daily intake. Then consider that sweet potatoes are common there too. Given that, for many people in India they are obviously getting tons of vitamin A into their daily diets. In addition to that information, we have a very important food preparation rule handed down over the centuries through the long chain of knowledgeable mothers. That rule is that chilies must never be combined with milk. Chilies in a meal without milk or dairy is fine. Milk and or dairy in a meal without chilies is fine. But, the two must never be combined because “it will make you very sick”. Obviously, the casein protein within the milk is acting as the carrier molecule that then transfers too much of the vitamin A from the chili across the intestinal wall.
So, how is it that vitamin-A deficiency even exists, at all, in these regions? Well, I’m here to tell you that it does not exist. On the other side of the argument, the proponents of these programs will argue that it clearly does exist. Who’s correct? Well, let’s not get into some meaningless debate about it. Rather, let’s find out. You might very logically be thinking, some simple random blood tests to measure serum levels would clear up this question rather darn quickly. Yes, you’d think so. But, remember, we are living in the negative universe here when dealing with the so-called science of vitamin-A.
Of course, those blood tests are conducted, and wouldn’t you know it, people in these regions, and even the people with the symptoms of VAD have ample amounts of vitamin-A in their serum. And, yes, that’s by our Western standards, and they have completely normal amounts of it too. Even a bit more surprisingly, the people with higher serum levels of vitamin-A have even more symptoms of VAD. I bet you are thinking I must be making this up. But no, I am not. This information comes straight from one of the premier and definitive sources on the matter:
While serum retinal levels below 20 µg/dl or in (0.7 µmol /liter) are generally considered normal there are important caveats.
- Carefully monitored vitamin-A depletion of otherwise healthy adults demonstrates impaired dark adaptation at serum vitamin-A levels between 20 µg/dl - 30 µg/dl or higher.
- Non-xerophthalmic children with serum levels above 20 µg/dl have evidence of sub clinical functional disturbances like conjunctiva metaplasia which is directly associated with other health consequences.
- A significant proportion of children with clinical xerophthalmia have serum levels above 20 µg/dl, while an even larger proportion with seemingly normal eyes have levels below 20 µg/dl.
Alfred Sommer and Keith P. West; with James A. Olson and A. Catherine Ross
Oxford University Press, 1996 ISBN: 9780195088243
Now after more than fifty years of the field work on the ground, there are a few people who are starting to question the validity and benefit of the supplementation programs. The thing is, the programs are just not working out very well. This realization was becoming somewhat obvious to front line physicians even back in the 1960s, as McLaren noted in his 1963 book.
What on earth is nutritional science good for, if, even in the atomic age, it is not capable to contract one of the foulest consequences of bad nutrition? Do you realize, that since the days of Mori, 60 years ago, not in Japan, but in countries like Indonesia, not one step forward has been taken and spite of a mountain of thoughtful attention paid by doctors?
Source: MALNUTRITION and THE EYE, forward, page ix
Even though there are now more than one hundred countries that have implemented vitamin-A supplementation programs, and we are told millions of lives have been saved, it is estimated that, globally, 190 million children under five years of age are still affected by vitamin-A deficiency.14
After more than fifty years of massive supplementation programs in these regions, the problem of VAD appears only to have gotten worse. If I understand this correctly, the more vitamin-A they distribute, the more vitamin-A deficiency they’re reporting. Even more concerning, more and more evidence is surfacing that the programs are not only not helpful, but they also are, in actuality, harming kids, and sometimes doing far worse.
Michael Latham highlights many of these concerns in his excellent analysis: The Great Vitamin-A Fiasco15
The findings that high doses of vitamin-A, especially in well-nourished children, have adverse impacts on respiratory infections, should surely be grounds for serious concern.
Journal of the World Public Health Nutrition Association
Contrary to all the best intentions and the nice sounding political messages, the facts on the ground are simply revealing the true story. Despite all the claims from the so-called Western experts, the locals are starting to wise-up to the facts and see it for what it truly is. They have been seeing it with their own eyes for decades now too. The material facts, on the ground, are that the vitamin-A supplementation programs are not only not helpful, but they are also doing exactly the opposite and are harming many kids. That fact has just become so obvious now, that the programs are being rejected by local authorities in many regions of India. They might not know why the supplements are harmful, but they do know that something is very wrong about them.
Actually, the bigger and far more important predicament facing many children in these regions is chronic malnutrition and not having safe drinking water. What these children really need is a reliable meal with adequate proteins and fats and clean drinking water. Somehow, the Western medical experts blindly ignore this and believe they’re helping them out by giving them a large dose of vitamin-A every year. Not only is it completely delusional to think that this is helping these kids, but it is also just beyond idiotic. Who the hell do they think they’re kidding? The only people that could be fooled into believing this nonsense is themselves. But if this idiotic practice resulted in doing no harm to health then it would be somewhat okay. It would just be a big waste of money; not a big deal. However, not only is it harming many of these kids, causing many of them to get infections and chronic diseases, it’s even killing a quite a few of them too.
With the Western medical community so absolutely convinced of vitamin-A deficiency and its endemic nature in Southeast Asia they have been supplementing kids and adults in this region for decades and decades. Yes, it has been a huge humanitarian effort funded by tens of millions of dollars per year from Western taxpayers.
And for decades and decades, there’s been a repeated little glitch randomly showing up. This little glitch is in addition to the initiation of the infectious diseases, and the autoimmune diseases, the supplementation is causing. That glitch is that some kids simply die when given a dose of vitamin-A. That’s correct, giving a vitamin supplement to younger kids sometimes kills them. Yet, very paradoxically, the younger kids are the ones in the least need of the supplementation.
The apparent absence of a protective effect before four months may reflect special circumstances of the newborn breast-fed child who will have inherited considerable immunity from its mother and obtained an additional passive immunity and vitamin-A from breastmilk. Xerophthalmia is rare among they youngest children under two years of age so presumably is moderate to severe vitamin-A deficiency.
Health, Survival, and Vision, page 38
So, firstly, is it not interesting that there’s little evidence of vitamin-A deficiency in the newborn? It just doesn’t show up, that is until the western medical doctors get involved, and start supplementing them with it.
Less clear is the reason why the youngest children (one to three months) given a large dose of vitamin-A 100,000 IU may have suffered increased mortality. Very young infants probably metabolize vitamin-A differently than older children with more mature metabolic systems.
Health, Survival, and Vision, page 38
The nonsense and unsupported rationalizations really get going here. But, clearly, they know they’re killing children by supplementing them with what’s called a “vitamin.”
Even more surprising, the apparent (but not statistically significant) excess mortality is predominantly confined to the best nourished (i.e. lease wasted) children (Fig. 2 – 14) (West KP, Kats J., Sommer A. unpublished data). The following observations are consistent with preliminary reports from one mortality trial suggesting that an apparent increase in acute lower respiratory infections is most pronounced among better nourished children receiving high-dose vitamin-A. These unexpected findings await confirmation and a biological explanation.
Health, Survival, and Vision, page 38
This statement is a remarkable, if not astonishing, display of scientific arrogance. Who the hell are they to say that it’s not “statistically significant” to be killing children? I guess it’s not “statistically significant” when it’s not their kids that are being killed.
And if they are looking for a biological explanation, it is incredibly trivially easy to see it. The better-nourished children already have ample stores in their liver’s. Therefore, the rate at which they can absorb, and safely absorb, a large vitamin-A dose is less than other children. Since it cannot be stored quickly, and without adequate fats and proteins, it is toxic. Its toxicity causes the destruction of the epithelial tissue leading to infection and maybe even blindness. So, there, done; biologically explained! Just as astonishing is their refusal to see and come to terms with reality. The reality is that it’s the perfectly healthy infants who have the lowest vitamin A stores.
The mean liver stores of vitamin A in children (1 to 10 years of age) have been reported to range from 171 to 723 μg/g (Flores and de Araujo, 1984; Mitchell et al., 1973; Money, 1978; Raica et al., 1972; Underwood et al., 1970), whereas the mean liver vitamin A stores in apparently healthy infants is lower, ranging from 0 to 320 μg/g of liver (Flores and deAraujo, 1984; Huque, 1982; Olson et al., 1979; Raica et al., 1972;Schindler et al., 1988).
Standing Committee on the Scientific Evaluation of Dietary Reference Intakes, Food and Nutrition Board, Institute of Medicine. National Academy of Sciences.
Figure 12 Relative mortality rates with vitamin-A supplementation
I mean, seriously, isn’t it extraordinary that healthy infants have right down to 0 μg/g of vitamin-A in their liver stores? Isn’t it just as extraordinary that these researchers don’t bother to investigate this glaring paradox?
Next, we are going to do a bit of analysis of the data summary for relative mortality rates presented in Sommer’s figure 2-14 on page 39. A very close replica of the original is shown at right (equivalent to Sommer’s figure 2-14.):
The comment in the caption includes:
Indeed, better nourished vitamin-A recipients sometimes fared less well than for placebo recipients, especially children receiving 100,000 IU vitamin-A during the second through fourth months of life.
Health, Survival, and Vision, page 39
Please note that the chart shown above is not for relative morbidity ratios, it’s for relative mortality ratios. Thus, for Sommer et al., seeing children being killed by being given a single large dose of vitamin-A is simply termed as them having “fared less well.” It’s like, Oh, no big deal, better luck next time kid. Of course, the material fact here is that these well-intentioned do-gooders are indeed killing children. The self-appointed experts rationalize away this killing as being a necessary part of the program. It’s like; yes, some of the kids must die to save the many. It’s a sacrifice we, the experts, are willing to make (with other people’s lives. It’s an old argument; “Oh, it’s for the greater good.”
But, once again, who the hell are they to think that they can go around and just randomly kill children? Nonetheless, seeing kids being killed by a vitamin, and seeing it happen over and over for decades should’ve raised some serious questions and alarms. At the very least there should’ve been a major and intensive investigation as to why and how this was happening. Don’t you think there should have been an equally intensive investigation as to why younger children are more susceptible to being killed by a single dose of a vitamin? Wouldn’t you think these experts should have been incredibly curious and very motivated to get to the bottom of that little scientific mystery?
Another little scientific mystery presented in Sommer’s figure 2-14 is why has he used a log scale on the Relative Mortality axis? Why not use a simple linear scale? Of course, you’d normally use a logarithm scale when you need to straighten out an exponential curve, or compress down a very large range of numbers. But, that’s not at all the case here. Okay, so what does that ~ log 1.22 number in the larger children in the 1-3 Months 100,000 IU group really mean? The inverse log of it is = 10^1.22 = 16.6. Therefore the relative mortality rate is more like around 17 times higher than the baseline of those kids given a placebo. Hmm… so what do you make of that? That’s right, for kids in this age group given the vitamin-A dose they are 17 times more likely to die than compared to those kids who were not given the dose. I think I can see why he was obscuring that number in the log scale.
So how many kids are being killed each year by being “given the nice vitamin-A treatment?” Well, it’s hard to know for sure since it’s not exactly a number they’re proud enough of to be publishing. But, we have some good starting information to make a reasonable approximation of it.
The potential risk must be kept in perspective: in a Nepalese population studied, high-dose supplementation of children six months an older prevented over 150 deaths for each death to which it may have contributed among younger children.
Health, Survival, and Vision, page 38
What evidence do they have that they’ve really prevented any deaths with vitamin-A supplementation? Of course, based on the new information we have, we know it’s more than likely actually zero deaths that have been prevented with vitamin-A supplementation.
But, of course, that one death out of 150 so-called saved children, does not mean that they are killing one out of the 150 children supplemented. We need to run the numbers on the ratios to get a better indication just how many children this adds up to.
It now seems clear that improving the vitamin-A status of deficient children would not only prevent 5 million to 10 million cases of xerophthalmia and a half million children from being blind each year, but save a million or more lives annually as well. In the past two years, specialized agencies of the United Nations (WHO, UNICEF, FAO) have raised their level of concern and commitment. The UNICEF Governing Board, the world health assembly, the World Summit for Children, and International Conference of Nutrition have all called for the control or elimination of vitamin-A deficiency by the year 2000.
Health, Survival, and Vision, Preface page
Other modern estimates put the number of “saved” children at about two million per year. Nonetheless, we’ll just go with the lower number for our analysis. Okay, using their estimate of more than one million lives “saved” per year, let’s estimate how many kids they are killing.
So, in each decade that’s about 70,000 kids being killed with a “vitamin” dose. Now, if anybody else were responsible for the killing of seventy thousand children, it would be called mass murder, or at least mass homicide due to criminal negligence. Yes, it is homicide; as its definition is rather damn straight forward:
Definition of homicide:
- a person who kills another
- a killing of one human being by another
Firstly, if they are going to be randomly killing some kids to save the many, then they had better be 100% absolutely, rock solidly, correct in their so-called science about it.
Secondly, with all their intervention programs, and best wishes, and stated grand goals, here we are in 2017, and the problem has only gotten worse year by year. That’s right, no matter how much vitamin-A they distribute they just can’t seem to keep ahead of the problem. What the hell is it going to take for these people to stop the bus, wake-up, and see the obvious? The programs are not only not working; they are making the situation far worse. There are now more than 100 countries in the world where the vitamin-A supplementation programs are being run. In these countries, not only is there no end in sight for the vitamin-A deficiency problem, other plagues and epidemics are now becoming common. If we just take Vietnam as an example, they have an astonishing and completely new epidemic of autism. And maybe, with the new information revealed here that so-called vitamin-A is not a vitamin at all, they’ll finally understand exactly why. Yes, ironically, they are simply poisoning and killing kids with a toxin.
One of the other very commonly cited reasons and rationales for the supplementation programs is the belief that it helps fight infections. The primary evidence for this is that it is observed when a child encounters measles their vitamin-A serum levels are dramatically reduced. From that, it is rationalized that the body is somehow using the vitamin-A to fight the infection. But, even to the medical experts, it’s perfectly clear that having ample amounts of vitamin-A does not prevent anyone from getting the measles.
Interestingly, five cases of post-measles corneal melting were observed in Leipzig Germany, in a three-month period in 1955. The authors could not explain its genesis. Although the children were generally very ill. The authors ruled out vitamin-A deficiency by the absence of any significant clinical response to vitamin-A therapy.
Health, Survival, and Vision, page 206
But, what we now know is that one of the biggest contributing factors in getting infections is compromised skin integrity and that of other epithelial tissues. Therefore, the very best way to prevent infection is maintaining strong and perfectly structured and healthy skin. The very substance proven in all the early experiments to slowly destroy these tissues is the metabolite of vitamin-A. However, just as importantly, and completely obvious to anyone who has spent any time in these countries of Southeast Asia, the greatest risk of infection is due to the dearth of proper sanitation services. There are large numbers of people living in direct daily contact with open sewage. Of course, many people have their drinking water contaminated with it too. Therefore, for the folks at the WHO still thinking that they can prevent an infection by giving the kids and adults a shot of vitamin-A, it is complete lunacy. If they really want to prevent infection, they need to assist these towns and municipalities in building the proper sanitation services and modern sewage treatment facilities. What I would like to know is, how many sewage treatment plants has the WHO built in these regions? Today, in 2017, there’s still something like 600 million people in India alone that do not even have a flush toilet to use. The situation with the vitamin-A supplementation programs supposedly helping by preventing infections in this environment is simply beyond idiotic!
But, nonetheless, there is this well-observed correlation between getting the measles, and follow-on xerophthalmia, accompanied by a drop in vitamin-A serum levels. Yet in many other cases, xerophthalmia occurs with no precipitating measles,
Typically, xerophthalmia, in the absence of precipitating measles, has been observed in most areas of Africa in which measles associated blindness occurs in which it has been sought out. Estimates that one-fourth to one-half the cases of corneal involvement are associated with measles are consistent with observations in Indonesia and reports from El Salvador Vietnam, Japan and Jordan.
Health, Survival, and Vision, page 205
Even though this information may seem rather contradictory and rather confusing, it’s very easily explained. Kids with high serum levels of vitamin-A and not having adequate amounts of protective proteins and fats will experience higher levels of retinoic acid production. In the absence of widespread infection, their dietary fats and proteins are the biggest missing factors in controlling the conversion rate.
However, the equation quickly changes when getting a large-scale infection, such as the measles. Under attack by the virus, the cell membranes are damaged or otherwise compromised, and many cells activate their retinoid receptors. Or, and far more plausibly, the cell’s damaged membranes just more easily allow the circulating retinoids to pass through.
At the same time, as part of the overall immune response, the liver is releasing large amounts of stored vitamin-A into the serum. These combined factors then promote accelerated conversion rates, leading to even larger amounts of retinoic acid being produced and released back into the serum.
The xerophthalmia problem in the countries of the Middle East has not yet been fully investigated and documented. From recent personal observations it is evident that xerophthalmia only occurs mainly in association with measles and gastroenteritis in the summer months.
Source: MALNUTRITION and THE EYE, page 222
Not surprisingly, there is another common situation that causes a large number cells to activate their retinoid receptors at the same time, and that is when people are given vaccinations.
It is now well understood that the immune system uses pathogen-associated molecule molecular patterns (PAMPs) to activate pathogen-recognition receptors such as TLR, and also a host of other more recently discovered receptors: retinoic-acid inducible gene-based (RIG)-I like receptors, or RLRs, and cytosolic nucleotide oligomerization domain (NOD)-like receptors, or NLRs. These receptors bind various pathogen ligands … more.
By Stanley A. Plotkin, MD, Walter Orenstein, MD and Paul A. Offit, MD
Therefore, the more vaccinations a kid gets in one day, the greater the risk. Thus, the perfect storm scenario here is first jacking up the malnourished kids on copious quantities of vitamin-A and then giving them a bunch of vaccinations. Not too surprisingly, this is indeed the general practice when the WHO is distributing vaccines. It’s far more efficient, logistically speaking, to give kids their vitamin-A supplement and vaccines on the same day.
Yep, it’s almost perfect. We just need to expose these same kids to a highly infectious environment and lots of sunshine, and South East Asia has heaps of both of that. But, to really finish them off quickly, there are a few more hugely important and hidden variables, and they are completely unknown to the well-intentioned folks administering the vaccines. We’ll come back to this topic in a later chapter.
Regarding infections, there’s another commonly cited feature of vitamin-A magically “boosting” the immune system. But, once again the experts are failing, and completely failing, to see the obvious. Vitamin-A is not magically boosting the immune system at all. There are studies proving supplementing people of chronic diseases such as AIDS makes their situation far worse. And of course, it does. It’s because vitamin-A is damaging tissue cells. The body and immune system detect the damage to the tissue cells. The immune system then responds by building more immune cells. The body is simply responding to a toxin and its obvious threat by building the immune system bigger. In the case of AIDS, it backfires and makes the disease even worse, because having more circulating new immune cells gives the virus more opportunity to spread faster. Therefore, supplementing people in regions where there’s a high incidence rate of AIDS is going to be causing the disease to spread even faster, not just within the person, but within the community too.
In addition to this real-world evidence that vitamin-A does not help prevent or heal from infections, we have some rather interesting clinical evidence showing that it makes the immune response far less effective too.
"new evidence is emerging to show that vitamin A supplementation above and beyond normal levels may have negative health consequences. A new research report published in the July 2015 issue of the Journal of Leukocyte Biology may help to explain why too much vitamin A can be harmful. Too much vitamin A shuts down the body's trained immunity, opening the door to infections to which we would otherwise be immune. This study adds to the arguments that vitamin A supplementation should only be done with clear biological and clinical arguments. Furthermore, it also suggests that low vitamin A concentrations in certain situations may even be "normal."
Federation of American Societies for Experimental Biology
Not too surprisingly, in this bazaar world, in the negative universe of vitamin-A deficiency science, something very strange is going on. Remember, the very definition of vitamin-A being defined as a vitamin in the first place comes from the early experiments proving that the deficiency of it caused the dreadful melting lesions seen in advanced stage xerophthalmia. So much so, that the disease and the deficiency are used nearly completely synonymously in the medical textbooks.
Xerophthalmia’s Relationship to Vitamin-A Status
As the pathognomonic clinical sign of vitamin-A deficiency, the presence and severity of xerophthalmia has classically served as a surrogate for vitamin-A status in studies investigating the relationship between vitamin-A deficiency and factors which might interact.
Source: VITAMIN-A DEFICIENCY, Health, Survival, and Vision. Page 8
However, and of course, there is now just stunning and overwhelming evidence, and it’s being presented in the hundreds of millions of people who live in North America, that this can simply no longer be the case. Likewise, the amazing contradiction is that in Southeast Asia and South America, the reality on the ground is that most people there have completely normal, and adequate amounts of vitamin-A in serum. Yet, despite these glaring material facts, the experts believe that they continue to see the symptoms of vitamin-A deficiency. Rather than seeing and facing the facts, they need to rationalize away this apparent paradox. Naturally, they fabricate bizarre and ridiculous excuses. But, even that won’t cut it. So, with absolutely no scientific basis, they are adjusting and expanding the very definition of vitamin-A deficiency to fit the narrative.
It’s not serum levels; it’s now skin lipid levels
Here’s a quote from a WHO report indicating this shift and expansion, with a newer, and very vague definition of vitamin-A deficiency.
VAD is not simply defined. WHO defines it as tissue concentrations of vitamin-A low enough to have adverse health consequences even if there is no evidence of clinical xerophthalmia. In addition to the specific signs and symptoms of xerophthalmia and the risk of irreversible blindness, non-specific symptoms include increased morbidity and mortality, poor reproductive health, increased risk of anemia, and contributions to slowed growth and development. Because these non-specific adverse consequences may occur from other nutrient deficits as well, it is difficult to attribute non-ocular symptoms specifically to VAD in the absence of biochemical measurements reflective of vitamin-A status.
You would think that the so-called experts could at least get their story straight between themselves before they publish such nonsense.
Firstly, what’s with this ridiculous, and illogical, statement that “VAD is not simply defined?” Once again, the very reason vitamin-A is defined as a vitamin in the first place is because of the consequences of the deficiency of it. If there were no consequences of the deficiency of the said vitamin, then it would not be called a vitamin at all. Without the deficiency, that was “proven” to cause xerophthalmia, and the related diseases of the eyes, vitamin-A simply would not be on the list of vitamins. Of course, the consequences of the thought to be a deficiency of it are extremely well-defined. Therefore, their statement that “VAD is not simply defined,” is not only an oxymoron, but it's also pretty much just another blatant lie.
Obviously, the other huge crack in the grand theory is now being revealed. That is, how can it be that in people with more than adequate serum levels of vitamin-A be showing signs of vitamin-A deficiency? Clearly, and logically, that’s just impossible. Therefore, the definition of VAD needs to be conveniently expanded to fill in and mask this glaring contradiction. In the statement above, the WHO is pretty much just expanding the definition to simply having low tissue concentrations. Okay, so what does “low” mean? Does anyone know?
Well, they must have missed the memo on this one too. Somehow, and mysteriously, it’s only humans that seem to need to accumulate any vitamin-A in their adipose tissues. Why is that? Maybe, it’s because rather than us humans needing it, there’s a clear message that the body is sending us here. That message is that we are simply getting too much of it, and it is leaching into, and wrongly accumulating in these adipose lipids.
But, if this “low tissue levels” excuse doesn’t cut it, they throw in a few more excuses and distractions. Things like poor reproductive health, increased anemia, and slow growth. What the heck, why stop there? Why not just blame any adverse health condition on vitamin-A deficiency?
But, once again, doing only a few minutes of research debunks these additional notions. Firstly, regarding reproductive health. The lowest rates of birth defects are seen in women with the lowest serum levels of vitamin-A. That’s correct, odd as it may seem, women with an incredibly poor vitamin-A status give birth to anatomically perfect babies.
It has been suggested by Millen and Woollam (1958) that the teratogenic effects of hypervitaminosis A may be brought about by inducing a deficiency of vitamins of the