“And, like with Wolbach and Howe back in 1925 these researchers are so sure of themselves that they completely ignore the contradictory findings from their contemporaries.”
I’ve been asked to provide supporting information to back up that statement. I’ll share that here in just a bit.
First, you might be wondering why we should care at all about some rat study from almost 100 years ago. However, I think it’s tremendously important. The 1925 Wolbach and Howe study was the one that supposedly definitively proved the essential need for vitamin A, and therefore, the one that solidified and confirmed the concept of it being a vitamin. If they got that wrong, and if we can therefore disqualify that study, then it should go a long way in disproving the entire “it’s a vitamin” claim.
I’m assuming that for most people knowing whether or not vitamin A is truly a vitamin does not matter too much. Vitamin or not, that verdict probably won’t change what they are doing. From a practical perspective, and in the short term, we just need to know that vitamin A is toxic once we’ve accumulated too much of it. We can apply that knowledge and hopefully still recover our health.
However, if we don’t go the extra mile and disprove this “it’s a vitamin” claim then the powers that be will just go on perpetually poisoning much of the human population with it. It will also continue to be very difficult to warn more people about the potential harms of over consuming vitamin A.
Okay, now let’s get back to the 1925 Wolbach and Howe study. One of the most fundamental requirements in scientific experiments is repeatability of results. If results are not repeatable (within some explainable margin of error), then the experiment proves nothing.
Here are some of the statements from the Wolbach and Howe study’s introduction effectively ignoring / dismissing the results of experiments from their contemporaries
Few pathological studies have been made, and the majority of these have resulted in wholly negative results and, therefore, erroneous conclusions as to the sequence of events and importance of infections.
Emmett and Alien in a comparison of changes due to vitamin A and B deficiency respectively in the rat report “no special outstanding pathological findings,” in the absence of fat-soluble A, in contrast to atrophies and hypertrophies found in B deficiency.
Stephenson and Clark failed to find a distinctive pathology in keratomalacia in rats.
Davis and Outhouse 4 studied only the kidneys, spleen, heart, lungs, pancreas, liver, and testes. As they report that the testes were normal in most of their cases, it is certain that either their diet was not deficient in fat-soluble (vitamin) A or that the duration of the experiments was too short.
Cramer, Drew, and Mottram ~ in a study of the effects of vitamin deficiency in rats upon the function of lymphocytes and lymphoid tissue found no pathology in fat-soluble A deficiency.
Wason found no lesions in any organ other than the eyes. She regarded the changes in the cornea as secondary to bacterial invasion.
Meyerstein ~ failed to find any characteristic pathology in either vitamin A or vitamin B deficiency in rats.
There’s yet another study from this era that I want to directly compare with Wolbach and Howe’s (W&H) study. It is:
THE NECESSITY OF CERTAIN LIPINS IN THE DIET DURING GROWTH.BY E. V. McCOLLUM AND MARGUERITE DAVIS.(From the Laboratory of Agricultural Chemistry of the University of Wisconsin.)(Received for publication, June 1, 1913.)
The reason I want to discuss this study is because they detail the diet used, and the outcomes. The diet used in this study was remarkably similar to the W & H study. However, McCollum’s 1913 study was only investigating the “growth” producing effects of some suspected fat soluble factor.
Here’s an example diet McCollum that fed his animals.
Here’s a chart for Rat # 104a (female)
Do you notice something? Up until period III, McCollum’s study diet is nearly identical to the one used by W&H. McCollum’s study diet is supposedly devoid of vitamin A too, yet his animals survive quite well to the 20 week mark, and beyond. Whereas, in the W&H study all of the animals were either dead or dying by the 8th-10th week. In the last two weeks of the W&H study the animals needed to be force fed their ration, and that finished them off. Except, here in McCollum’s study, not only have the animals survived at least 2X longer, there is no mention of sickness or disease, at all. In other words, his animals were probably very healthy, and obviously reproductive, at the 20 week mark. McCollum’s study presents similar results for male rats.
Then to investigate growth, in period III he adds in an egg extract, and the animals do gain weight. However, let’s not jump to the conclusion that it’s a good thing. What would you tell someone today who claims that gaining weight is the medical equivalent to growth? I think you’d tell them that they are confused. But, that’s a small technicality we are not too interested in right now (unless we wanted to consider this an inadvertent obesity causation study).
What’s critically important is that apparently the same diet regimen used by McCollum’s and W&H’s studies yielded completely opposite results. How can we explain that? When combined with the other studies mentioned above from this era , it is very clear that the animals in the W&H study did NOT succumb to a vitamin A deficiency. Therefore, with the diametrically opposing results between the McCollum’s and W&H’s studies, we have no experimental repeatability. Thus, we can’t legitimately derive any scientific conclusion from them. Therefore, the claim that vitamin A is a vitamin is completely unsupported, and is quite bogus.
However, there’s a subtle but very important difference in the diets used by McCollum and W&H. In W&H’s paper they state:
Distilled water, sufficient to make a dough, was added to the ingredients; small cakes were moulded, each containing five gm. of material, and dried in an oven.
For additional information about heat treating milk, and its correlation to early death in experimental animals please read about Wilhelm Stepp’s 1912 work in mice. Stepp kills his mice in just 3 weeks using heat treated milk. And, it looked to me that Stepp’s results (kill rate) correlated with the heating duration times in alcohol. https://academic.oup.com/jn/article/127/7/1255/4728852
Additionally, there is an even more fundamental problem with the McCollum and W&H studies. That problem is now revealed by the modern-day work of Collin Campbell et al with their work on the direct toxicity of casein on its own.
Therefore, with that huge red flag and confounding factor no rat study in history that’s used casein can be considered legitimate and valid. Clearly then, Wolbach and Howe’s 1925 study is complete junk science. Moreover, we have the previously ignored studies from Wolbach and Howe’s contemporaries actually proving that there is no dependency on vitamin A.
The W&H study is the foundational cornerstone of the grand vitamin A theory. Their conclusions were wrong, and they made the assumption that they had narrowed it down to this one molecule. Quite remarkably they made this assumption in 1925 even though the structure of the molecule had not been determined until 1931. Sadly, every vitamin A study since W&H’s has been layered upon that flawed foundational assumption. Very few follow-on researchers have had the courage to stick their heads above the parapet and call this out for what it is. But, there have been a few. Here’s a prophetic quote from Pitt:
… people seem curiously reluctant to recognize just how toxic is vitamin A. I have long asserted that considered as a chronic poison vitamin A is probably more harmful than cyanide, but I have usually been disbelieved …
I think that if modern day researchers stopped fabricating ridiculous follow-on theories and sub-theories to rationalize what they are seeing, and reevaluated their finding through the lens of vitamin A being a toxin, and nothing but a toxin, then all of it will make so much more sense.
The W&H study is garbage science, and needs to be tossed into the trash can. With that, so does the entire bogus claim of this toxic molecule being an “essential” vitamin.
Of course, vitamin or not, there’s no debate about the potential toxicity of so-called vitamin A. But, if we can finally correct the science on it then we might have a chance in stopping the global supplementation nonsense going on. Let’s consider this report:
WHO Library Cataloguing-in-Publication Data Report: WHO technical consultation on vitamin A in newborn health: mechanistic studies, Geneva, Switzerland, 1–3 December 2009. 1.Vitamin A – administration and dosage. 2.Vitamin A deficiency – prevention and control. 3.Infant, Newborn. 4.Infant nutrition. I.World Health Organization. ISBN 978 92 4 150316 7
High doses of retinyl ester are commonly provided to at-risk populations in areas where vitamin A deficiency is a problem. For women, 400 000 IU given as two doses of 200 000 IU at least 1 day apart and within 6 weeks postpartum are being recommended. Vitamin A supplementation programmes have been highly successful in addressing vitamin A deficiency but are not without risk. The doses administered are at toxic levels (200 000 IU retinyl ester is 85 times the recommended daily allowance (RDA) and 400 000 IU retinyl ester is 172 times the RDA). Acute toxicity may occur at dosages >100 times the adult RDA.
Do they warn these women and get their signed informed consent for the likely harm from that toxic dose? I highly, highly doubt it. Of course, they’ll claim that this deliberate poisoning of young women with known acute toxic doses is somehow necessary, ostensibly claiming that it’s to prevent vA deficiency.
But, what’s really going on here? Clearly, it might not be just bad science and there’s another possibility to consider. In the 1970’s the WHO and the global elites were absolutely obsessed with the runaway growth in the human population. It was viewed as the biggest threat to the planet. Then factor in that it’s been known since the 1960s that vitamin A is a reproductive toxin.
Check out the last entry in this table of lethal doses of some common substances:
Then in the 1970s the WHO’s vitamin A supplementation programmes were started up in about 100 countries, and vitamin A was added to the low fat dairy, etc., in North America and to sugar in South America, etc. Then, surprise, surprise, there’s been a massive drop in human fertility around the planet. And, by the early 2000s the WHO had gone mostly quiet about the risk about the global population. The WHO’s primary focus has now shifted to vaccines. Do you trust these guys? I hope not.
What’s emerged with the COVID-19 pandemic is a peculiar pattern of vulnerability. It’s being widely reported that older people are the most severely affected by the infection and are the demographic most likely to die from it. Whereas, children and teenagers often appear to sail right through the infection with only minor symptoms, or the just having symptoms equivalent to a cold or minor flu. Yet, at the lower end of the age spectrum, say in one and two-year-old’s, the severity of the diseases increases again.
Children of all ages are susceptible to COVID-19 and while their symptoms are generally less severe than those of adults, a small percentage — particularly preschoolers and infants — can become seriously ill, according to a new study.
An equally important observation is that many thousands of people have tested positive for having had COVID-19 and yet have remained completely symptom free. Therefore, it’s very critical to appreciate that just getting COVID-19 is not sufficient on its own to cause disease. Clearly, it’s COVID-19 and something else when combined that leads to the disease. What is that something else? We should all be very curious and striving to find out what it is.
In the context of COVID-19 infections, the general assumption is that older people just have weaker immune systems and are thus less able to fight off the virus. Except, it’s not just age that’s the primary factor. Rather it’s a person’s age combined with their pre-existing conditions, or comorbidities, that somehow makes them more vulnerable to having a severe response. Therefore, we can almost right away dismiss that assumption of a “weak” immune system being to blame because it is not at all just older people who succumb to the infection. Some younger people, even in their 30’s, are dying from the infection too. It’s just much more common to have a severe response in these younger people primarily when they have comorbidities. Therefore, the pre-existing comorbidities are the bigger risk factor. The cited highest risk comorbidities are diabetes, obesity, asthma, other autoimmune diseases, and cardiovascular diseases. If you’ve followed my blog for a while now, you’ll know that these are all diseases that I’ve been attributing to long term vitamin-A toxicity.
Let’s see if we can make some sense out of this. Could it be that there’s some mechanism whereby people with a higher level of vitamin-A storage could be more severely impacted by viral infections, and especially that of COVID-19? Firstly, let’s look at some interesting data regarding the liver storage concentration by age. For that, we’ll look at this 1973 study from Mitchell et al.
Source: G. Vaughn Mitchell, M. Young, C. R. Seward, Vitamin-A and carotene levels of a selected population in metropolitan Washington, D. C, The American Journal of Clinical Nutrition, Volume 26, Issue 9, September 1973, Pages 992–997, https://doi.org/10.1093/ajcn/26.9.992
Quite interestingly, here we have a similar U-shaped curve showing up in the data. Note that the horizontal red line at 286 μg/g is the documented toxic level for liver storage. Remarkably, this means that a large number of young children say from 1 to 5 years old are in the toxic range for liver storage. Then, as they get older their liver’s volume increases (roughly as a cubed function of its cross-sectional size) and they outpace the inbound dietary consumption rate. Then, as people get older their liver concentration slowly saturates to where they move into the toxic storage range once again, and through to the end of life. Let’s remember that this data is from back in 1973, just at the beginning of the foolish North American vitamin-A supplementation programs in dairy, breakfast cereals, etc.. Obviously, the liver saturation numbers will be far worse if sampled today. Just imagine the blue U-shaped curve being shifted up higher on the chart to where more people are over the red toxicity line. So, it’s no wonder why so many people are sick and diseased today. They are, by the very definition of the toxic level of vitamin-A storage, beyond that point. This also corresponds quite well with the fact that about one-third of the American population has NAFLD. That’s all bad enough, but could this somehow also make them more vulnerable to viral infections? Well, this has actually been well documented to be the case for a long time. But, for now, there’s one data point on the above chart that we need to focus in on.
What’s documented in the Mitchell study, and in others, is that very young infants have very low (and often even non-detectable) liver storage levels of vitamin-A.
The Amazing Infant Immune System
So, what do you suppose happens to very young infants exposed to the measles virus? Well, amazingly, often nothing adverse happens. That’s correct, they usually remain symptom and disease-free. Their immune system simply clears the virus. Additionally, most of them have probably acquired true life-long immunity from future infections of the measles virus.
Likewise, just what do you suppose happens to a very young infant exposed to the Dengue virus? Well, once again, often nothing adverse happens. Yes, those infants with their supposedly “weak” immune systems just clear the virus.
Next, just what do you suppose happens to a very young infant who is exposed to, and is subsequently infected by, the truly horrifying syphilis bacteria? Very often, they too remain symptom-free, and their “weak” immune systems clear the bacterial infection!
Even more astonishingly, what do you suppose happens to a very young infant who has a finger or toe severed? Amazingly it often grows back! Yes, these very young infants are amazing at surviving and dealing with very adverse events and pathogen attacks. Infants are starting in life with a great, if not perfect, immune system. Sadly, that all quickly changes once the so-called “medical experts” start administering their “health” intervention programs.
Yet, a great misconception persists in medical science in that very young infants are thought to have poorly developed immune systems. One of the primary reasons they make this assumption is because very young kids simply do not respond to vaccinations. Please consider this meta-analyses of the seroconversion rates by age:
Measles vaccination below 9 months of age: Systematic literature review and meta analyses of effects and safety
In a meta‐analyses of 20 papers, the proportion of infants who seroconverted (%SC) depended on the age at MCV1 vaccination. It increased from 50% (95% CI 29‐71%) at age 4 months to 67% (95% CI 51‐81%) at 5 months, 76% (95% CI 71‐82%) at 6 months, 72% (95% CI 56‐87%) at 7 months and 85% (69‐97%) at 8 months.
For the very youngest of children, there is only about a 50% seroconversion (meaning their immune response created detectable antibodies). The seroconversion rates then increase as they get older. Except, this phenomenon is not because their immune system is maturing. Rather, it’s because their serum levels of vitamin-A are creeping up with age too. We know this because the same effect has been studied in fully grown adults. In adults with abnormally low vitamin-A status, they too have a low seroconversion rate of ~50% when administered vaccines. Then, from other studies, we learn that when adults have their vitamin-A levels pre-boosted up before vaccination, then there is a higher “seroconversion” rate of around the more “normal” ~85% rates. Of course, most vaccinations are really low dose deliberate viral infections.
The known low “seroconversion” rate is why most childhood vaccines are delayed until two months of age. Some researchers claim that the extra vitamin-A has “enhanced” the immune response. But, we know that’s not exactly correct. What’s really happened is that the vitamin-A has enabled the virus to more rapidly replicate, and that then results in the “enhanced” immune response. But, do not for one second think that getting a higher seroconversion rate is a good thing to have happen. It’s the exact opposite. It’s clear evidence that higher background vitamin-A levels are resulting in the increased replication rates of the vaccine’s virus. And, vice versa, the run-away viral infection has increased the toxicity of their background vitamin-A levels too.
This is a super, critically, important point to understand. This is the underlying mechanism as to why kids in India and other countries of Southeast Asia can have such a devastating outcome from a measles infection. With high, or even moderate, vitamin-A serum levels, and a lack of sufficient dietary fats and proteins, the measles infection also increases the toxicity of their endogenous and circulating vitamin-A levels! It is also the underlying reason why some kids die when given their vaccines.
What’s going on here? As usual, it’s multifactorial, and there’s much more to the story. What we do know, and also very contrary to widely-held myths, is that vitamin-A actually subdues the immune system. What’s also been documented for like the last 50 years now is that vitamin-A weakens and otherwise damages cell membranes. It also damages the mitochondrial membranes. It’s trivial to see why too. Both the cholesterol molecule and the side-chains of the vitamin-A molecule are made up of isoprene groups. These isoprene groups are the base compound for natural rubber. So, if you’ve ever wondered why the cholesterol deposits surgeons pull out of arteries looks so much like rubber, it is because it is rubber. Ever wonder why the cholesterol deposits are yellow in color? It’s in good part because it has picked up and encapsulated the vitamin-A, and carotenoid molecules, within it.
Carotenoids are incorporated into very low density lipoproteins (VLDL) and exported from the liver into the blood. VLDL are converted to LDL by lipoprotein lipase on the surface of blood vessels. Plasma membrane-associated receptors of peripheral tissue cells bind apolipoprotein B100 on the surface of LDL, initiating receptor-mediated uptake of LDL and their lipid contents.
Source: Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc http://www.nap.edu/catalog/10026.html Page 94
Now, just as cholesterol with its isoprene groups nestles into the lipid bi-layer of the cellular membranes, so too does vitamin-A. This obviously weakens the integrity of the cell membrane.
Could the weakened cell membrane then make the cell more susceptible to viral infections? You bet it can. This has been documented in the context of HIV infections. Supplementing HIV patients with vitamin-A causes a more rapid replication of the virus, and results in worse outcomes. So, we have multiple pieces of real-world evidence that vitamin-A causes a faster replication rate of viruses. What about some laboratory-based evidence? Well, there is indeed, and even specifically for the coronaviruses.
Retinoic acid modification of cell culture used for reproduction of enteropathogenic viruses.
Abstract The 0.001-0.005% retinoic acid injection into the growth cultural medium of prime and continue cell cultures 12-24h before inoculation considerably raised the cell sensitivity to animal entero- and coronaviruses. The entero- and coronaviruses concentrations in cultural medium increased by 10(1.58) and 10(1.68)TCID 50/1.0 respectively. The optimized parameters of the cell culture processing for the enteropathogenic viruses reproduction improvement are proposed.
And a similar phenomenon is observed in the context of Zika infections. Cells being forced into “differentiation” via retinoic acid increased their infectivity to viruses.
Differentiation enhances Zika virus infection of neuronal brain cells
Here we investigated ZIKV infectivity in neuroblastoma SH-SY5Y cells, both undifferentiated and following differentiation with retinoic acid. We found that multiple ZIKV strains, representing both the prototype African and contemporary Asian epidemic lineages, were able to replicate in SH-SY5Y cells. Differentiation with resultant expression of mature neuron markers increased infectivity in these cells, and the extent of infectivity correlated with degree of differentiation.
So, we now have good evidence of vitamin-A (and specifically retinoic acid) promoting the replication of viruses. Of course, we all know that increased background storage levels of vitamin-A simply means more endogenously produced retinoic acid.
None of this is new information. As with most things related to vitamin-A science, it’s been well known about and reported on for a long time. Here’s a great paper from Anthony Mawson discussing the same comorbidity patterns in the context of the 2009 SARS-CoV infections. Back then it was also the people with the pre-existing conditions of heart disease, asthma, and autoimmune diseases who were at higher risks for severe disease and death.
Role of Fat-Soluble Vitamins A and D in the Pathogenesis of Influenza: A New Perspective
Anthony R. Mawson
Department of Health Policy and Management, School of Health Sciences, College of Public Service, Jackson State University, Received 4 April 2012; Accepted 3 May 2012 Academic Editors: M. C. W. Chan, N. Kawai, and Y. Lai
The Symptoms of Influenza A Infection Are Similar to Those of Hypervitaminosis A
As noted, the clinical spectrum of influenza A infection, including avian influenza H5N1, is not restricted to the lung and can range from mild influenza-like illness to severe pneumonia, acute respiratory distress syndrome (ARDS), acute lung injury (ALI), and multiorgan failure . Fever, rhinitis, myalgia, malaise, headache, cough, dyspnea, sore throat, and fatigue are the main presenting symptoms. Complications include pneumonia, bronchitis, or sinusitis, and rarely encephalitis, transverse myelitis, Reye syndrome, myocarditis, or pericarditis .
Mawson does a great job of explaining how and why this can be related to an overload of vitamin-A, and why a low vitamin D/A ratio is a very important factor. Oddly, this paper was not picked up by the major journals, say such as the BMJ, or Lancet. Why was there so little interest in this Mawson paper? Could it be that the medical establishment and the pharmaceutical industry have no genuine interest in understanding what’s really enabling and driving viral infections? Could it be that their primary, if not only interest, is their commercial interests? Of course, it is. These companies have multi-billion dollar vaccine divisions. Therefore, any non-vaccine solution to viral infections would be a serious and direct threat to that ongoing annual business model. Therefore, it is incredibly unlikely that we’ll ever see a non-vaccine based solution developed by the pharmaceutical industry. What if we all came to the understanding that the best way to protect ourselves from viral infections was simply to keep our vitamin-A consumption very low? That could devastate the industry. Therefore, that information cannot be allowed to be developed and confirmed. Therefore, the Mawson paper must be ignored.
The ACE2 Receptors
There’s been a lot of press lately about the important role that the ACE2 receptors play in COVID-19 infections. The virus’s glycoprotein binds to the cell membrane protein angiotensin-converting enzyme 2 (ACE2) and that’s how it gains entry into the human cell.
The novel coronavirus 2019 (2019-nCoV) uses the SARS-coronavirus receptor ACE2 and the cellular protease TMPRSS2 for entry into target cells
Here, we demonstrate that 2019-nCoV-SusestheSARS–coronavirusreceptor, ACE2, for entry and the cellularprotease TMPRSS2 for 2019-nCoV-S priming. A TMPRSS2 inhibitor blocked entry and might constitute a treatment option. Finally, we show that the serum form a convalescent SARS patient neutralized 2019–nCoV-S-driven entry.
Naturally, with the ACE2 receptor being the target site of virus entrance into the cell there’s been a ton of frantic research into looking into ways to block or down regulate the ACE2 receptors.
Correspondingly, there’s been a ton of interest and media attention given to a well-established anti-malaria drug named chloroquine. Here’s a study from back in 2005 discussing it.
Chloroquine is a potent inhibitor of SARS coronavirus infection and spread
Results We report, however, that chloroquine has strong antiviral effects on SARS-CoV infection of primate cells. These inhibitory effects are observed when the cells are treated with the drug either before or after exposure to the virus, suggesting both prophylactic and therapeutic advantage. In addition to the well-known functions of chloroquine such as elevations of endosomal pH, the drug appears to interfere with terminal glycosylation of the cellular receptor, angiotensin-converting enzyme 2.
Therefore, we can see that when the ACE2 receptors are upregulated, viral infection and replication rates increase. Conversely, when the ACE2 receptors are downregulated, viral infection and replication rates decrease.
Yet, something really strange happened with the medical establishment and the mainstream media regarding the potential use of chloroquine as a treatment. These people immediately started attacking it and doing everything they can to discredit it. Why would they do that? Could it be that chloroquine is cheap, off-patent, immediately available and most of all a potentially competitive alternative to the planned vaccine they have in the works?
Dr. Anthony Fauci almost jumps to the podium and claims that the evidence for its effectiveness is only anecdotal, and there is not enough evidence to support claims that chloroquine is effective in combatting COVID-19. But, that’s not quite true. There are existing clinical trials, and back in 2005, even its probable functional mechanism was understood too. Additionally, with very few other immediate options, why not quickly get going on finding out? Why so aggressively downplay it and try to dismiss it as an option? Who and what is he trying to protect?
Why are we no better prepared today for a viral pandemic than were we in 1918?
The last great viral pandemic to ravish the human population was the so-called Spanish Flu of 1918. So, now over 100 years later, we still don’t have any really effective treatments for viral infections. How can that be? After sucking trillions of dollars out of the worldwide economies the pharmaceutical industry has almost nothing meaningful and effective against viral infections. Sure, they have the horrible DNA, RNA chain terminator class of drugs that they claim to be “anti-viral” in action. But, not only are these drugs very expensive, they come with catastrophic “side-effects” that often decimate the overall health of the patient. They are not “medicines”, they are simply poisons that break the cell’s ability to build any proteins at all.
Fortunately, ER and intensive care teams are vastly more capable today in preventing people from dying from viral infections than compared to back in 1918.
What really matters most right now is finding remedies for people most severely affected by the virus. Contrary to the advice of many “experts”, taking vitamin-A is not one of them. The very last thing anyone one should be doing at this time is supplementing with so-called vitamin-A.
Over the last few months I’ve learned of more people who have been strictly following a carnivore diet (exclusively muscle meats) for five or more years. Not at all surprisingly, they are doing very well. Combined with all the evidence I’ve included in my eBooks, and with my own 5+ years on a vitamin A free diet, it’s clear that the theory of vitamin A being an essential nutrient is patently wrong. According to the vitamin A theory these people, and myself, should have gone blind years ago, and had their skin and all their internal organs self-destruct and otherwise disintegrate. Not only has that not happened, it’s just the opposite. These people are thriving and healthier than many of their peers.
As I wrote about in my P4P eBook, the foundational studies used to establish the “it’s a vitamin” concept were pretty much just garbage science. I’m sorry, but poisoning a couple dozen rats to death does not prove the existence of a “vitamin”.
Although many people are now conceding this fact that it’s not a “vitamin” needed by adults, there are still people clinging to the claim that it’s essential for embryo development. I find that claim and position so strange because we know that too much vitamin A will cause horrible birth defects and often times spontaneous abortions. Yet, some people continue to believe that nature is so foolish to establish a critical dicey dependency on a highly toxic molecule to facilitate proper embryo development. This is their last bastion of hope in clinging to the claim that vitamin A is still somehow a “vitamin”.
It gets even more perplexing once you know that the so-called “active form” of vitamin A is 13-cis-retinoic acid (isotretinoin aka Accutane) and all-trans-retinoic acid (tretinoin). These thought to be “active forms” of vitamin A are as toxic to the human fetus as is thalidomide. The FDA has established “black box” warnings that a fetus exposed to “ANY” amounts of isotretinoin is at extreme risk for developing birth defects. Astonishingly, in the face of those facts the established “science” claims that a fetus somehow needs this exact same compound to properly develop. How do we square up these diametrically opposing statements? Of course, we can’t and clearly then there’s something seriously wrong with that claim.
Like with the early rat studies from the 1920s that supposedly conclusively established vitamin A to be a vitamin, we need to analyze the modern day studies that were used to prove the need for retinoic acid in fetal development. Here’s an overview of the premier studies that “unequivocally” established the critical dependency on retinoic acid during embryogenesis.
Symposium: Functional Metabolism of Vitamin A in Embryonic Development Vitamin A and Embryonic Development: An Overview Maija H. Zile Department of Food Science and Human Nutrition, Michigan State University, East Lansing, MI 48824-1224 J. Nutr. 128: 455S–458S, 1998
I find it troubling that so much of medical “science” relies almost exclusively on “studies” such as this. The way I see it, these “studies” are a complete cop-out for genuine, critical and logical thinking. Depressingly, it only takes a few minutes of thinking to see the flaws in this one. It’s just more bad “science” layered upon many shaky assumptions. The parallels here with what happened with the Wolbach and Howe study back in 1925 are also rather remarkable.
TISSUE CHANGES FOLLOWING DEPRIVATION OF FAT SOLUBLE A VITAMIN.
BY S. BURT WOLBACH, M.D., AND PERCY R. HOWE, M.D. From the Department of Pathology, Harvard University Medical School, and the Forsyth Dental Infirmary, Boston. Received for publication, September 4, 1925
The Wolbach and Howe study was conducted for about a 10-week duration. At the end of that duration, most of their test animals were either seriously diseased or had died. The fundamental conclusion from that study was that the animals had suffered their devastating tissue and organ disintegration as a consequence of a vitamin A deficiency.
One of the biggest issues with the Wolbach and Howe study is that although they acknowledged that other contemporary researchers were getting the completely opposite results, Wolbach and Howe simply made up excuses to ignore those inconvenient facts. But, the bigger issue is that they delusionally assumed that they were working with complete information. Of course, they were not. They failed to appreciate that washing casein in alcohol and heat treating it at high temperatures could have toxified it. And, yes, somehow casein can become remarkably toxic.
Casein is a Carcinogen – Dr. T. Colin Campbell
Topic #1 – Casein is a Carcinogen. Really?
Many people have heard me say, “Casein [the main protein of cow’s milk] is the most relevant chemical carcinogen ever identified.” Guilty, as charged. Many times I’ve said this. For the sake of this discussion, let’s call it an hypothesis, that is, “Casein causes cancer”.
How can the most revered of all nutrients increase the most feared of all diseases? “Heresy”, the mob might shout.
But it’s true. In my laboratory research conducted over a quarter century, funded by taxpayer dollars with findings published in the very best journals, we studied this effect in many ways at a most fundamental, cellular and sub-cellular level as much research as for any other chemical deemed to be a carcinogen.
Campbell was not alone in this research and in his findings. There were similar studies conducted at the University of Illinois at Chicago that replicated these results. Very interestingly, although Campbell was mostly focused on liver cancer, the Chicago researchers found that casein was a very potent carcinogen in quickly initiating and promoting breast cancer in animals.
After Campbell, and the other researchers at the University of Illinois, had made this discovery about the rather incredible toxicity of casein there should have been some rather intensive follow-up research as to exactly why a milk protein could be so toxic. After all, since most mammals start out in life being breastfed, how could milk be such a potent cancer causing agent? On the surface of it, that doesn’t make any sense. However, when you get deeper inside of it and discover the vitamin A molecule contained within it, it becomes much more plausible. I have no doubt the standard casein based lab chow used in Campbell’s et al rat experiments was heat treated. Heat treating it is simply necessary to sterilize it from potential bacterial contaminants.
Except, with this revelation from Campbell et al about casein being a powerful carcinogen, why hasn’t anyone gone back in time and questioned the validity of the 1925 Wolbach and Howe study? After-all, they too used casein in their experiments. Couldn’t their animals have suffered from ‘the most relevant chemical carcinogen ever identified” rather than have suffered from a vitamin deficiency? Additionally, why has no one ever bothered to try to understand why the symptoms of the so-called vitamin A deficiency condition are a perfect match for those of its toxicity symptoms? Isn’t that odd?
I wrote about Dr. T. Colin Campbell’s China study in my P4P eBook. I really liked the China Study, and I still think that it’s a worthwhile read. Two very important conclusions Campbell makes in his book are:
Food is at the root cause of chronic disease (and particularly so for cancer).
The medical sector and medical science is driven by greed and is rife with corruption.
His third, and most important conclusion, is slightly correct, and mostly wrong. He concluded that it’s the milk protein, and therefore by erroneous extrapolation, that most animal sourced proteins are the culprit. However, it’s not the milk protein at all that’s the real culprit. Rather it’s the highly toxic oxidized retinol molecule that’s cased-in the casein that’s to blame.
Aside: Quite remarkably, this information about the standard lab “rat chow” based diet that included sterilized casein being a potent carcinogen probably invalidates most of other animal based studies that have used this same feed. That’s likely thousands of studies in all aspects of medical research now being highly questionable, at best.
Let’s get back on track here with the more modern day studies that “unequivocally” proved the need for retinoic acid (RA) in embryogenesis.
Vitamin A and Embryonic Development: An Overview Maija H. Zile Department of Food Science and Human Nutrition, Michigan State University, East Lansing, MI 48824-1224 J. Nutr. 128: 455S–458S, 1998
ABSTRACT: Vitamin A is an essential micronutrient throughout the life cycle. Its active form, retinoic acid via retinoid receptors, is involved in signal transduction pathways regulating development. Both the lack and excess of vitamin A during embryonic development result in congenital malformations. Approaches to examine the function of vitamin A in embryonic development have included treatment with excess retinoids and the use of retinoid receptor knock-out mice, which have provided important insights into the complexity of the retinoid signaling system.
The entrenched current theory is that RA is a “metabolite” of vitamin A. What’s documented, and then simply blindly repeated hundreds of times over, is that RA is the downstream molecular product needed to “differentiate” our stem cells. However, even under a tiny amount of scrutiny that “theory” is nothing more than an assumption. One of the red flags that should pretty much jump off the page at us is that many of the horrible skeletal defects attributed to RA deficiencies are a perfect match for RA toxicity (or mere exposure to RA). They state:
The overlap of the teratological symptoms of vitamin A deficiency and excess indicates common targets and a critical role for A in the development of many organs.
Doesn’t that sound familiar? And then they make this statement.
It is important to keep in mind that the developing embryo is very sensitive to a lack as well as an excess of retinoids.
So, here we go again, having just a touch too much RA or too little RA and you get the same teratological results. Odd huh?
Of course designing an experiment to prove the effects of RA deficiency is rather difficult. They can’t just feed experimental animals a diet deficient in all sources of vitamin A because they “know” that the animals will quickly die, let alone allow them to breed through one or more reproductive cycles. So, what the researchers in this study have done is used genetically modified “knock-out” mice. The gene knock-out changes their DNA so that they will be unable to produce the retinoic acid receptors (RARs) needed to utilize RA.
Retinoic acid is now generally recognized as an important signaling molecule that as a ligand to its nuclear receptors, the RARs alters gene expression at the level of transcription (Gudas et al. 1994, Mangelsdorf et al. 1995, Pfahl and Chytil 1996, Roberts and Sporn 1984).
So, basically, their thinking is to disrupt the RA metabolism pathway so as to block the final critical step of having RA invoking those 500+ random gene expressions.
A recent approach to answering questions about the functions of vitamin A in development has been the use of transgenic mice with changes in retinoid receptor gene structure (Boylan et al. 1995, Chambon 1993, Giguere et al. 1996)
Normal vitamin A metabolism pathway
Knocking out the RARs and RXRs Using their gene “knock-out” mice they’ve taken out the RARs, and RXRs.
The “disrupted” vitamin A metabolism pathway
Do you see the “disrupted” pathway? Actually, neither do I.
But, sure enough, with that induced mutation they find exactly what they are looking for. Disrupting the RA metabolism pathway results in the development of horrible and catastrophic skeletal and organ defects. Of course, as predicted, their conclusion is that RA is essential for embryogenesis.
Many of the abnormalities in these mutant mice resemble those observed in the fetuses from the vitamin A deficient animals reported earlier.
Obviously, there are some huge flaws with these experiments and in their logic. Firstly, what if that cellular process of dealing with RA is not one of “metabolism” but rather one of catabolism and detoxification? Of course, when a cancer patient is given the RA “treatment” their body is not metabolizing it, it is frantically detoxifying it. In the process, the result is the horrific widespread destruction the “medication” causes in almost all patients.
Differentiation syndrome (DS) is most current term; Occurs in Acute promyelocytic leukemia patients undergoing ATRA treatment (Tretinoin, Vesanoid).”
Differentiation Syndrome is a life-threatening complication of induction chemotherapy for patients with acute promyelocytic leukemia (APL). Manifestations of this syndrome include fever, hypoxemia, edema, and, in the past, has been referred to as “cytokine storm”.
Yet, somehow we are supposed to believe that the exact same chemotherapy drug is needed for proper embryogenesis. That should sound rather ludicrous to everyone.
Next, we need to consider what if the gene “expressions” are really manifestations of gene damage? But, most glaringly, what they haven’t proven at all is the condition of RA deficiency. No, there is still vitamin A and RA in the cell. They’ve only blocked its assumed to be one-and-only pathway. However, in no way have they limited the availability of RA to bind with and cause DNA damage. Obviously, even without the RARs, that RA molecule is still free to float around the cytoplasm and bind to the DNA/RNA. Therefore, what they’ve really done in this study is just proven that RA is very toxic to the embryo even when the retinoic acid receptors are not available. That outcome is not at all surprising because we now know that RA fractures and fragments DNA.
DNA fragmentation induced by all-trans retinoic acid and its steroidal analogue EA-4 in C2C12 mouse and HL-60 human leukemic cells in vitro Raghda S. Alakhrasa, Georgia Stephanoua, Nikos A. Demopoulosa*, Konstantinos Grintzalisa, Christos D. Georgioua and Sotirios S. Nikolaropoulosb
Abstract: We have recently shown that retinoic acid induces micronucleation mainly via chromosome breakage.
Next, what about the long-held assumption that the one-and-only pathway of RA metabolism is via the RARs? Well, it turns out to have been the wrong assumption.
Retinoic acid induces apoptosis by a non-classical mechanism of ERK1/2 activation Alfeu Zanotto-Filho, Martin Cammarota, Daniel P. Gelain, Ramatis B. Oliveira, Andres Delgado-Cañedo, Rodrigo J.S. Dalmolin, Matheus A.B. Pasquali, José Cláudio F. Moreira
Abstract: Even though RA is involved in differentiation and apoptosis of normal and cancer cells, being sometimes used as adjuvant in chemotherapy, its mechanisms of action involve multiple overlapping pathways that still remain unclear. Recent studies point out that RA exerts rapid and non-genomic effects, which are independent of RAR/RXR-mediated gene transcription.
And they go on to state:
Classically, it has been described that the effects of RA are mediated by ligand-dependent activation of RA receptors (RAR) which act directly as transcription factors modulating gene expression by interacting with RA response elements (RARE) in DNA (Kastner et al., 1995). A number of RA target genes have been identified and many of them are associated with apoptosis and differentiation (Kastner et al., 1995; Pfahl, 2003). On the other hand, recent studies point out that RA modulates signaling pathways in a manner independent on retinoid nuclear receptor-mediated gene transactivation; this has been described as ‘‘non-classical” or ‘‘non-genomic” action of RA.
With that bit of new information, there’s now no legitimate evidence that RA is needed for embryogenesis. And of course there isn’t. How could anyone be so credulous to believe that a molecule as toxic as thalidomide to the developing fetus, and one that’s proven to fracture DNA, cause cancer, cause 500+ other variations of DNA damage, and to induce rapid apoptosis is somehow needed for embryo development?
Moreover, it’s rather clear that the RARs are one of the last defense mechanisms against RA’s toxicity.
Then, we need to ask the next obvious question. If the RARs are really part of the detoxification pathway, then what’s the result of that pathway being disrupted? It’s cancer!
The disruption of RA signaling pathways is thought to underlie the etiology of a number of hematological and non-hematological malignancies, including leukemias, skin cancer, head/neck cancer, lung cancer, breast cancer, ovarian cancer, prostate cancer, renal cell carcinoma, pancreatic cancer, liver cancer, glioblastoma and neuroblastoma.
Retinoic acid receptors: From molecular mechanisms to cancer therapy
This finding is similar to the report I referenced in my Breast Cancer eBook where the researchers found that cancer tissues are depleted of the needed alcohol dehydrogenase enzyme. So, basically, it looks like when a cell can no longer defend itself from RA, it can become cancerous. Once again, that should not be a surprise to anyone because of the hallmarks of cancer are damaged DNA and rapid cell mitosis, and that’s exactly what RA does to cells. Hmm? What are the chances that the RARs and RXRs are in actuality the precursors proteins to the RBPs that we now know cells form around retinol and RA and then eject out of itself?
Anyhow, it’s quite remarkable how the thinking process and conclusions in the Vitamin A and Embryonic Development study “unequivocally” proving that RA is needed for embryogenesis parallels that of the 1925 Wolbach and Howe study. Both teams find exactly what they are looking for and they both ignore huge amounts of evidence by other research and knowledge contradicting their conclusions. Most disturbingly, they just don’t seem to apply common sense to alert them to the fact there’s something drastically wrong with their conclusions. And, like with Wolbach and Howe back in 1925 these researchers are so sure of themselves that they completely ignore the contradictory findings from their contemporaries. I say that because ten years prior to them conducting these elaborate genetic knock-out studies, the HHS was quickly (in just 10-14 days) poisoning young mice to death with the very same molecule they are claiming to be essential for embryogenesis.
United States Patent 4,649,040
The United States of America as represented by the Department of Health and Human Services, Washington, D.C. Mar. 10, 1987
Therefore, it’s all quite ridiculous and almost absurd. I mean seriously, with that information how could anyone continue to believe that a proven lethal and teratogenic poison is needed for embryogenesis?
Quite interestingly, both the studies by T. Colin Campbell in the 1990s, and that of Alessandra di Masi’s in 2014 both point to cancer causation, and even specifically to breast cancer causation. Amazingly, Campbell was able turn on and off cancer progression just by turning up or down on the amount of casein being included in the animal diet. That’s a pretty good indication that cancer is being fueled by the ongoing supply of vitamin A.
Yet, as I wrote about in P4P, very disturbingly, when other researchers do find direct links with vitamin A and the retinoids causing cancer, they conceal it and cover it up. That isn’t science. I view it as criminal negligence, at best. It sure begs the question: how could so much of medical science be so screwed up? Is this deliberate scientific propaganda and manipulation to corral us into disease? Of course, there’s huge amounts of money being made everyday in cutting off the breasts of women. But, no one’s going to make a dime off of breast cancer if we reveal the true root cause of the disease, and can therefore prevent it. T. Colin Campbell was correct; corruption is not only endemic to modern medical science, it appears to be institutionalized in the medical establishment.
I wouldn’t be so snarky about it if this was some harmless mistake. But, it’s not. And, we are not just talking about melanomas and breast cancers either. The USA now has the highest rates of birth defects and spontaneous abortions in the world. We’re talking about nearly a million people in just the USA now living with birth defects. With the current CDC estimates that birth defects are occurring at a rate of 1 in every 33 infants born in the United States this represents an ongoing national disaster. Coincidentally, that 1/33 rate is about on par with the current rates of autism too.
The human body is many thousands of times more advanced than the current state of medical science. This is clearly evidenced by the fact that the more health interventions and drugs pushed onto our populations the sicker we’ve become. And we’ve become vastly sicker, and on a massive scale too. That alone is conclusive proof that many of the so-called experts have no freaking clue what they are doing. The human body was and is perfect. We just need to learn how to stop chronically poisoning it. In order to do that we need to know when a bogus “vitamin” is in fact simply a poison.
The liver stores 80-90% of all vitamin A absorbed by the body.
The liver must, and does, get fatty in response to vitamin A consumed.
The rates and prevalence of NAFLD are so dramatically abnormal and geographically clustered, that it clearly tells us that the disease is a poisoning.
Vitamin A is yellow.
Bonus fact: excessive vitamin A is proven to cause cirrhosis in all kinds of tissues.
What am I missing here? Has no one ever before bothered to ask the obvious question: why has that NAFLDed liver turned YELLOW?
I mean seriously, even a sixth-grader could figure this out. So, why haven’t all the brilliant minds in medical research been able to see what they are looking at? Could it be that they are blinded by all the money they make?
With increasing rates of obesity and metabolic syndrome, nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH) have become increasingly common, such that they are now the most common cause of liver disease in Western countries. This has not gone unnoticed by those in the market of drug development. Where there is a disease to “treat” there is a buck to be made.
One of the goals of conducting our survey was to determine the prevalence of the detox setback condition people were encountering on a low vitamin A diet. Naturally, the primary goal was to see if we could spot any common factors that might be causing it.
As shown in the results, around 50% of people were reporting that their progress had stalled, and eventually, their overall health condition was slowly getting worse with time. But, others reported no such setback and stated they had made pretty good linear progress into better health. These mixed results were a bit of a paradox to me, and I didn’t understand why we saw such widely variable results. However, I felt it was important to highlight the failures, and not to overstate or focus on the successes.
I also wondered why people on the now popular carnivore diet are not reporting the detox setback trap many people here reported on their low vitamin A diet. Maybe, it was just not being reported by the carnivore folks. But, I think it is probably just not happening very often. I think it is a beneficial side-effect of eliminating carbs and not consuming other foods that contain aldehydes while on that diet.
Up until recently, most of my attention on recovering from vitamin A toxicity has been just on eliminating vitamin A from the diet. I was hoping that would be sufficient to enable most people to recover. With that, I didn’t focus too much on the body’s detoxification processes and mechanisms. So, I think we are now moving into the next phase of understanding that process and what’s needed to make it more predictable and successful.
The alcohol dehydrogenase enzymes
Back in October, when I posted the survey results, I had speculated that cauliflower was contributing to the detox setback trap. I still think this is indeed at least partially correct. That’s because several people have now reported back that after dropping cauliflower, they’ve experienced significant improvements. But, it’s not just food sources of methanol and formaldehyde that can overload and mess with the body’s alcohol dehydrogenase enzyme systems. It’s also some of the most common prescription drugs. These drugs include the Statins, the SSRIs, and even over the counter pain killers such as Tylenol. Almost any drug that is metabolized by the liver is going to either interfere with the production of or directly compete for your dehydrogenase enzymes.
The B vitamins of thiamine and riboflavin
I had also speculated that some people might be running into a vitamin B deficiency condition. This was supported by most people on our survey reporting that they were not eating brown rice, or only having it occasionally. But, I was too quick to dismiss this concern when I learned about the new carnivore diet. My thinking about it was that surely the carnivore diet folks would be running into the same vitamin B deficiency issues too then. Except, what I missed is that since the B vitamins of thiamine and riboflavin are needed to metabolize carbohydrates, then the carnivore diet folks won’t be as nearly susceptible to such a deficiency.
Whereas, if people here are eating a lot of white rice and have inadequate sources of the B vitamins (particularly thiamine and riboflavin), they could run into a deficiency situation quite quickly. There’s also some good evidence that vitamin A toxicity increases the demand for the B vitamins. The B vitamins are involved in the process of building the ADH and ALDH enzymes. Additionally, some of the B vitamin deficiency symptoms overlap and mimic those of vitamin A toxicity.
Now, with more feedback from people here, and based on the work from Dr. Garrett Smith, it is quite likely that some people here are running into a vitamin B deficiency. This scenario sure fits from a temporal perspective too. That’s because people here have reported hitting the detox setback in a matter of just a few weeks or a few months. In contrast, others have sailed right through on the low vitamin A diet for a year or more with no such setback.
Some good low vitamin A food sources of the B vitamins are black beans, brown rice, macadamia nuts, sunflower seeds, and coconut water. But, I know that many people are not able to tolerate beans; therefore, directly supplementing might be a better option for them.
I’m most certainly no expert on the B vitamins. Therefore, please use other sources of information, also consider looking into the work of Dr. Garrett Smith. Please contribute your thoughts and experiences on this topic here:
Thank you to everyone for taking the time to fill out and submit the survey. There were about 129 responses in total.
As somewhat expected, the results are kind of all over the place. That was expected because everyone is coming into this from different backgrounds, dietary histories, ages, etc. But, what’s unexpected, and rather clear is that too few people are making steady progress in regaining their health. Even before conducting this survey, quite a few people had reported that their early progress had stalled, or had even reversed as time went on. That’s a huge concern, and it’s the primary motivation that prompted this survey. The survey results confirmed those early sporadic reports. Many more people (~50%) are indeed hitting the “detox” setback and it’s far more common than I had previously thought.
At a very high level, here’s my preliminary assessment of the survey results.
A restrictive diet alone is just too slow, and too unpredictable.
We clearly need an antidote (I think the body has a built-in one, we just need to help activate it, see more on this topic below)
It looks like the people with a big VA supplementation history might be the ones more likely to encounter the detox cycle.
The majority of people have found themselves in this mess via VA supplementation or from accutane use.
Although most people do believe they are on the right track, their real results are still too few / slow.
Many more people have encountered the “detox” setback cycle than what I expected / was aware of. I see this as our biggest problem, and it needs immediate and serious attention.
But, it’s not all bad news, there’s still a lot of good news here too. Although it’s slow going, a lot of people are indeed recovering their health.
What does it all mean?
My private, and previously unstated, criteria for deeming the vitamin A toxicity theory to be considered valid, and on target is that we should see about a 95% success rate for people applying the elimination diet. To help frame the discussion, here are some illustrations (not real data). The following chart is what I think we should be seeing for most people. Of course, we should expect there to be some personal variabilities and small setback cycles too.
However, we are not seeing that trend, and almost not at all. It’s more like this for most people:
Currently, we are nowhere near the target 95% success rate. Maybe it’s still just too early. Realistically, we are probably closer to around a 5% – 10% rate in clear success. Nevertheless, from the survey, 67 of 130 people have still reported having made a significant improvement in their health. Quite remarkably, on the one hand that is still a far higher success rate in recovering from chronic disease than any pharmaceutical drug has proven to do. On the other hand, that particular comparison is such a pathetically low bar, it’s not very useful or meaningful to us.
Regardless of things generally moving in the right direction, something is clearly wrong here too. Either the base theory is wrong ( I don’t think so, but it’s possible), or we are missing some important confounding factors.
One of the early concerns I had about the strict elimination diet is that it removed so many other foods and nutrients, that it is easily possible that we are excluding something else from the diet that in the longer term is essential to our health. Say for example, some of the B vitamins, etc. So, it could really be a deficiency situation building up in resulting in people hitting the “detox” setback cycle. But. I somewhat dismissed this concern when I learned about the new “carnivore” diet being widely adopted. My thinking about it was surely the “carnivore” diet folks would be running into the same potential deficiency issues too then. And, if it’s happening, it is not being reported.
Additionally, over the last year or so, some people here were reporting that their serum VA levels were actually increasing as they progressed with the diet. This also fit with some accounts from published research papers. This makes sense too, because it’s what we should expect when about 70 million Americans adults have NAFLD, and the liver is probably starting to normalize in size and volume. This then better explained the “detox” setback cycle some people encountered. Therefore, it’s likely not a “detox”; rather, it’s really a “more tox” situation. So, my thinking was, OK, people just need to give it more time. Although my personal recovery did take a long time, my trend was generally pretty linear towards better health. I rationalized that I had been spared the big “detox” setback cycle because I had not been directly supplementing with VA, nor did I have a history of eating liver, etc. But, I too did have my share of smaller autoimmune flare ups and setback cycles along the way.
Very early on it became clear to me that we are not dealing with a simple toxicity situation either. Rather, it’s a very nasty and sinister one where the toxin binds to and messes with our RNA/DNA. So, for these DNA damaged cells we pretty much have to grow them off and out of our bodies. That’s just going to take a long time. Additionally, since it’s also a toxin that accumulates in our lipids, as we drop body fat, then more of it is going to be released into serum. Therefore, we are clearly in for a good long haul in detoxifying from this mess. But, that part of it does not quite fit with some of the real-world data reported in our survey. Some people have reported not losing weight, or have even gained weight, and have still slid down into the “detox” cycle.
Regardless of the reasons and mechanisms, I think having people slide backwards into poorer health is just not acceptable. Asking people to stick with it, and struggle through for months on end is not very acceptable either. Therefore, we need to get a clearer understanding of what’s really going on in the detox setback. Most importantly, we need to find an effective means of dealing with it. We need a reliable, safe, and most of all, a predictable recovery strategy. I think if the full recovery process takes say even four years, most people would still be okay with that, just as long as it’s progressive, and almost always in the right direction towards better health. The current non-predictability of it is almost a show-stopper for more people to take on this diet experiment.
One of the key statements I’ve repeated over the last few years is that we need an antidote. Diet alone is not cutting it, and being such a restrictive died it will never gain widespread acceptance. But, diet is the only tool we have in our collective toolkit right now. Therefore, I was seeing the diet-alone approach as just a starting point in this investigation. My thinking was that if we could use it to prove the case, then others would pitch in and help develop an effective antidote. Unfortunately, we are not at that point yet.
However, there are some other very important facts we need to remember. One is that humans have been dealing with vitamin A (in its various forms) for millions of years now. Yes, it is a toxin to humans, but plants love it, and it’s not going away. Therefore, we just have to learn to deal with it more safely. The supercritical and obvious conclusion is that the human body has already developed mechanisms to deal with, neutralize , and detoxify the retinoids. These biological processes are reasonably well understood by current medical science, and are actually quite well documented too. The key point to know here is that In addition to the physical elimination pathways, via the liver, skin, and the RBPs, the body has very likely already developed the needed antidotes to retinol and retinoic acid. I think these antidotes are primarily the alcohol and aldehyde dehydrogenase enzymes. These enzymes effectively slowly chop up the retinoid molecules.
So, why isn’t the alcohol and aldehyde dehydrogenase enzyme production keeping up with the new demand? One possibility is that they’ve been too overwhelmed or drained. Another possibility is that the needed manufacturing feedstock of nutritional elements is missing from our now very restrictive diets.
There’s yet another possibility, and that is that as people go very low on the consumption side of vitamin A, then the body’s perceived inbound threat is reduced, and the production of the dehydrogenase enzymes is slowed or even shutdown. Whereas, the backflow of retinyl esters from the liver is not quite the right molecule to trigger production of the dehydrogenase enzymes. This little sub-theory is actually supported by several people who have reported that keeping just some vitamin A content foods (like a single egg per day) in their diet prevents and quickly abates their “detox” setback cycle.
But, I want to be clear that I am NOT making the recommendation here that people start reintroducing VA foods back into their diets. That’s because other people have reported just the opposite effect. Clearly, it’s an individual thing, and people are going to need to experiment with it and find what works best for their own situations.
Next, there’s another really important possibility. Is there something else being included in our diets that would consume and preferentially compete for the same alcohol dehydrogenase enzymes?
Hmm, could it be the Cauliflower?
About 36 of the survey respondents reported including cauliflower in their diets. I suppose that I am probably responsible for starting that with the diet I document in my eBooks.
Although cauliflower has little to no vitamin A, one surprising thing to know about cauliflower is that it can have a pretty high content of formaldehyde (source). It’s not massively over the top, but it’s still relatively high. The thing is that the same alcohol and aldehyde dehydrogenase enzymes are needed to neutralize and detoxify that formaldehyde. Other foods to be on the lookout for in this regard are Asian pears, canned pears, and other canned fruits, and to a lesser extent even bananas. The other major culprit is the artificial sweetener Aspartame. Aspartame is a big problem because the breakdown pathway for it is that it first gets converted into formaldehyde. The resulting formaldehyde will therefore compete for our precious alcohol and aldehyde dehydrogenase enzymes.
Could it be that the cauliflower, and possibly these other foods, is sabotaging people’s recovery progress? I don’t know, but I’d sure like to find out. Therefore, for anyone currently including them in your diet, can you please try dropping them for a while and report any changes.
One more thing to be aware of is some of the pharmaceutical drugs are documented to interfere with the detoxification process of the retinoids too. The two that I am most aware of are the Statins and the SSRIs. But, we can assume that any pharmaceutical drug that is processed by the liver as being competitive for the liver’s detoxification resources. Obviously, consuming anything more than just minor amounts of alcohol is not going to help us either. So, any of these factors, combined with an environment where more retinyl esters are suddenly back flowing into circulation, could lead to the dehydrogenase enzymes being overwhelmed and exhausted.
Boosting our alcohol dehydrogenase enzyme production
Back in February when I posted my discussion on Statins and Cholesterol I made the suggestion that regular consumption of Apple Cider Vinegar would help ameliorate any calcium buildup in the arteries. And I still believe that it almost surely will do exactly that. But, what I did not know at the time was that ACV has some other major benefits. It helps boost bile production, and the source bacteria contains aldehyde dehydrogenase enzymes. ACV also helps boost our own production of the human version of enzymes. There are other foods that can help safely boost ADH and ALDH enzyme production. Dr. Garrett Smith is actively looking into this aspect of it.
Zinc – here it is again
It’s also important to know that zinc is a critical mineral needed for the formation of the dehydrogenase enzymes, just as it is for the RBPs. Therefore, if you are not eating red meat, you really should make sure that you are getting enough zinc from other sources. It looks like some of the B vitamins are also involved in the process of building the dehydrogenase enzymes.
The actual survey responses are summarized below.
The raw survey data are available here in an .xls format.
I’m conducting a survey of people’s experience with the diet. My goal with this survey is to see if we can find out what’s working, and what’s not. Most importantly I want to see if we can determine why some people encounter the detox setback cycle after being on the diet for several months. What I believe is happening in many cases is that as people take on a VA elimination diet their liver then releases the more toxic retinyl esters back into circulation. They therefore need more of the dehydrogenase enzymes to keep up with it. But, if their body can’t make the dehydrogenase enzymes fast enough, then they slide backwards into the “detox” phase.
Therefore, we now need to move into the second phase of the investigation and determine HOW people can safely and reliably detoxify from it. If we can accomplish that, then it will just be a matter of time for more people to recover.
I’ll post a summary of the results here by Oct 12th. I also will share the entire survey results (sans email addresses) for everyone to evaluate. So, please don’t include any personally identifiable information in the comments. If you want to submit a response, and don’t want to have it, or just your included comments, shared publically, then please contact me and I’ll remove it from the shared results. Thanks.
It’s now been five years on my low vitamin A diet. My health continues to be good. However, I’ve only seen small improvements over the last year. But at least they are improvements, and my health continues to move in the right direction.
My spine has continued to straighten out more, and I am therefore standing slightly taller.
My teeth are feeling stronger, smoother, and are just more solid. My gums are in excellent health too. My teeth also remain cleaner throughout the day.
My energy levels and physical stamina remain good and slightly improved over last year. Likewise, I’m finding that I need to eat less food per day, and yet I still maintain a good energy level throughout the day. My weight has remained constant.
I’m now quite regularly sleeping through the night. That’s a huge improvement compared to five years ago where I needed to get up at least every hour. Likewise for sun exposure. Five years ago, my maximum tolerance for bright sun exposure was about 10 seconds. Anything more than that, and my skin would start to burn. I can now take 30 minutes or more, and my skin once again tans.
One other very surprising improvement over that last year is the quality of my handwriting. It has become noticeably nicer, more fluid, and stylish.
My skin, fingernails remain to be nice and smooth and my hair remains to be very soft. I’ve not gone blind, and my organs have not disintegrated. Unfortunately, the amount of vascularization in my eyes has only slightly improved over the last year. The net is that I’ve not seen any big improvements in my health over the last year. So, I think I’ve probably reached more of a steady-state condition of being in pretty good health.
Small Diet Change Experiments
I’ve only tried two small diet changes over the last year. One is that I changed out the rice for white bread (made without dairy or eggs). I tested this change for about two months. It was a sourdough bread made with non-organic white flour, so it no doubt contained glyphosate. I had no negative reaction health-wise to the white bread. But I felt that it didn’t provide quite the same long-lasting energy that I was getting from rice. Also, as I commented before that a diet of white rice and beef alone could quickly turn into gut concrete. Well, it turns out that white sourdough bread and beef alone can turn into gut concrete with a compressive strength of about 25 MPa. The black beans helped a lot in mitigating that condition. Nonetheless, I feel that white bread is just not for me. So, I’m back to the white and (occasionally) brown rice.
The other diet experiment I tried was adding Brazil nuts. In theory, these nuts should have been safe; providing zinc, selenium, vitamin E, etc. But, after about two weeks, I felt I was starting to have a bad reaction to them. Of course, that bad reaction could have been a complete coincidence too. But, stopping them also seemed to coincide with resolving the negative reaction too. The negative reaction was mostly just the development of dry skin on my outer earlobes. Obviously, this one little personal experiment is not very meaningful. So, I’m just trying to be complete in reporting what happened with my health over the last year.
My blood test for vitamin A & D
I’ve gotten another blood test for my vitamin A and D levels. The results are as shown in the report below.
For some unexplained reason my first blood sample was rejected by the lab and I was asked to provide a second one.
I was seriously disappointed with that 0.1 μmol/l result. It’s the same value that I had a year ago. I find it a little hard to believe that after another year maintaining a nearly zero vitamin A intake diet that my serum level wouldn’t have moved lower. Unfortunately, because of where I live, I don’t have access to another lab to get a second opinion.
Although my vitamin A research is just a side-project, I remain fully committed to it. Therefore, I will continue with my vitamin A free diet for the foreseeable future. My current plan is to keep with it for at least five more years.
Other Progress Reports
This citizen-driven research project has gained a lot more interest over the last year. With that, more people are trying this diet change and are starting to send me progress reports.
Although, I’ve received some good early progress reports, for most other people it’s a long slow crawl in recovering their health. And, as I’ve written about before, some people go into a “detox” phase and then get worse. Therefore, I think the “detox” phase could be a “more-tox” phase. I’ve discussed this phenomenon with an academic researcher. We both suspect that it is due to more retinol esters getting released from the liver. It is quite possibly due to the liver starting to normalize its size and is part of the recovery process from a fatty liver condition. Likewise, it could be due to the adipose tissues normalizing in size too. Except, and a bit oddly, going into the “detox” phase is not happening to everyone. I’d say the number of people reporting going into the “detox” phase has been around 20%. It also does not appear to be age or gender-related.
Some other general themes and patterns are showing up in the progress reports. One is that younger people are indeed recovering faster. The second one is that people are reporting that they are overcoming their anxiety, becoming more social, more outgoing, and developing a positive outlook. Some people are stating that they’re thinking more clearly, and just generally being happier too. I think related to that is that quite a few people are telling me that the quality of their sleep has improved, and they are experiencing a significant increase in dreaming and dream recall. So, it appears that one of the early improvements of being on this diet is an improvement in cognitive function.
As I stated before, for most adults, it probably took decades to build up into this condition. Therefore, it is not unreasonable to expect that it will take a long time to recover from it. Diet alone is clearly not a quick fix. But, if we can be happier while trying to apply that fix, then I hope it’s not so bad.
Of course, for most people taking on this diet their goal is to improve their health. It would be great if more people can accomplish that. However, there is also the overarching goal of adding more evidence identifying the real culprit in what’s caused our chronic diseases to develop in the first place. So, I’m very grateful for all the people now participating in this investigation, and for everyone sharing information and their experiences. Thank you so much.
I also want to thank “Yi at LDT” for repeating the low vitamin A diet with his mice.
As I discussed in ETFOH, one common theme that cuts across all the autoimmune diseases, and even breast cancer too, is the comorbidity of eczema. At a more fundamental level, and what many others have reported on, is there’s another cross-cutting syndrome, and it’s that of insulin resistance. So much so, that many people feel that insulin resistance is at the root cause of many of the chronic diseases. The very definition of Type II diabetes is insulin resistance and metabolic disease. But, it goes well beyond that. Insulin resistance is hugely implicated in coronary artery disease, heart disease, and surprisingly even the brain diseases such as Alzheimer’s too. You’ve probably heard Alzheimer’s disease even being referred to as Type III diabetes. So, let’s see if we can make some sense out of all of this, and find some plausible common ground and the connections between them.
When I wrote about my theory of obesity causation back in October, I referenced this 2016 report documenting the adipose genesis effect of retinoic acid: Circulating Retinoic Acid Levels and the Development of Metabolic Syndrome.
Source: Yan Liu, Hongen Chen, Di Mu, Jiahua Fan, Jiayi Song, Yuan Zhong, Di Li, Min Xia; Circulating Retinoic Acid Levels and the Development of Metabolic Syndrome, The Journal of Clinical Endocrinology & Metabolism, Volume 101, Issue 4, 1 April 2016, Pages 1686–1692, https://doi.org/10.1210/jc.2015-4038
I was somewhat expecting people to call me out on my use of that study. One of the weird aspects to it was even though the authors documented the adipose genesis effect of retinoic acid; they also concluded that the elevated levels of retinoic acid were beneficial in reducing metabolic syndrome.
The serum RA level is inversely associated with the development of MetS independently of adiposity and insulin resistance.
So, even though one aspect of that study supported my sub-theory of obesity causation, it directly contradicted my overarching theory that retinoic acid was the real culprit in causing the modern chronic diseases. Of course, there is an absolute mountain of other studies and research proving the incredible toxicity of retinoic acid. To me, at least, something was not adding up here with their contrary findings. But, it is rather easy to see where they go wrong in their analysis.
Here’s the source of the problem stated in the Materials and Methods section of their report:
Determination of RA concentrations
Serum RA concentrations were measured using a commercially available ELISA kit according to the manufacturer’s instructions (catalog number MBS705877; MyBioSource). This assay has high sensitivity and excellent specificity for the detection of human retinoic acid.
Do you see it? They did not actually measure serum RA concentrations at all; rather they measured a biological proxy marker for it. Of course, there’s no such thing as “human retinoic acid” either. So, what are these ELISA kits? They are kits that test for and measure antibodies.
The enzyme-linked immunosorbent assay (ELISA) is a commonly used analyticalbiochemistryassay, first described by Engvall and Perlmann in 1972. The assay uses a solid-phase enzyme immunoassay (EIA) to detect the presence of aligand (commonly a protein) in a liquid sample using antibodies directed against the protein to be measured. Performing an ELISA involves at least one antibody with specificity for a particular antigen.
For example, you could use an ELISA test to detect and measure the antibody proteins to Measles. ELISAs are not usually used to measure and quantify specific compounds such as retinoic acid. Using gas chromatography and mass spectrometry is the more standard technique for identifying and quantifying the molecular makeup of compounds.
Of course, in the human body, most circulating retinoic acid (and retinol too) is bound up in wrapper RBPs. Therefore, what the authors meant to say was: “This assay has high sensitivity and excellent specificity for the detection of the human RBPs for retinoic acid.” So, yes, if the body is building the needed RBPs fast enough, then it will safely wrap up the otherwise highly toxic retinoic acid molecule. When wrapped up in the RBP, the retinoic acid will pose far less of a hazard and people are better protected from it. With this protective mechanism explained we can now understand their observations and paradoxical conclusion.
But, the use of the ELISA test is not some major error on the part of the report authors either. It’s probably a good surrogate test, and it appears to be a rather standard practice. Here’s another report where they’ve done the same, except it’s for retinol RBPs.
Retinol-Binding Protein 4 and Insulin Resistance in Lean, Obese, and Diabetic Subjects
By: Timothy E. Graham, M.D., Qin Yang, M.D., Ph.D., Matthias Blüher, M.D., Ann Hammarstedt, Ph.D., Theodore P. Ciaraldi, Ph.D., Robert R. Henry, M.D., Christopher J. Wason, B.S., Andreas Oberbach, Ph.D., Per-Anders Jansson, M.D., Ph.D., Ulf Smith, M.D., Ph.D., and Barbara B. Kahn, M.D.
Serum RBP4 was measured by an enzyme-linked immunosorbent assay (ELISA) (ALPCO Diagnostics) in groups 1 and 3 and by quantitative Western blotting with purified human RBP4 standards in group 2. Immunodetection was performed with a polyclonal antibody to human RBP4 (DakoCytomation).
In addition to the ELISA, they are also quantifying their measurements with the Western Blot test. But, like, with the ELISA, the Western Blot is another type of test for measuring antibodies. Next, let’s consider their results:
Serum RBP4 levels correlated with the magnitude of insulin resistance in subjects with obesity, impaired glucose tolerance, or type 2 diabetes and in nonobese, nondiabetic subjects with a strong family history of type 2 diabetes. Elevated serum RBP4 was associated with components of the metabolic syndrome, including increased body-mass index, waist-to-hip ratio, serum triglyceride levels, and systolic blood pressure and decreased high-density lipoprotein cholesterol levels. Exercise training was associated with a reduction in serum RBP4 levels only in subjects in whom insulin resistance improved. Adipocyte GLUT4 protein and serum RBP4 levels were inversely correlated.
This is an important finding as it is tying together serum RBP4 levels, insulin resistance, diabetes, metabolic syndrome, and more. Except, just for now, ask yourself why are they using antibody tests to measure RBP levels? Doesn’t something about that strike you as being a bit peculiar?
To be clear, these are not procedural anomalies. It appears to be a preferred measurement technique. Here’s another study where they use Western blotting to measure serum retinoic acid levels:
Valproic acid combined with 13-cis retinoic acid and 1,25-dihydroxyvitamin D3 in the treatment of patients with myelodysplastic syndromes
Timo Siitonen, Timo Timonen, Eeva Juvonen, Venla Terävä, Anu Kutila, Tuomo Honkanen, Maija Mikkola, Heikki Hallman, Marjut Kauppila, Pirkko Nyländen, Eira Poikonen, Auvo Rauhala, Marjatta Sinisalo, Merja Suominen, Eeva-Riitta Savolainen, Pirjo Koistinen
Of course, using mass spectrometry to measure RA acids levels is more problematic because the retinoid is entirely encapsulated within the RBP wrapper. Therefore, samples first needs to be dissolved in solvents to breakdown the protein shell and washout the embedded retinoids. From there, mass spectrometry can be employed. So, although the ELISA and Western Blot are measuring a biological proxy marker, they are probably more expedient tests and good enough for the purpose of their studies.
Okay, now we need to really think about this. If these laboratory tests used to measure serum levels of retinoic acid, and even that of retinol, are in actuality antibody tests, isn’t it pretty logical that the RBPs are indeed antibodies?
Except, for the last 50 years now, medical science has claimed that the RBPs are specialized transport proteins. The grand theory is that the liver first scrubs retinol out of serum and then sequesters it away into storage for later delivery. On an on-needed basis, the liver then releases the retinol wrapped up in the RBPs for transport. That’s a nice-sounding theory. But, there’s a huge flaw now showing up in the story. That flaw is because a large percentage of the RBPs are actually being built and released by the adipose tissues, and not just the liver. That’s correct, the origin of much of the RBPs is from the adipocytes.
RBP4 is an adipocyte-secreted molecule that is elevated in the serum before the development of frank diabetes and appears to identify insulin resistance and associated cardiovascular risk factors in subjects with varied clinical presentations. These findings provide a rationale for antidiabetic therapies aimed at lowering serum RBP4 levels.
Okay, it looks like the grand theory of the RBPs being transport proteins is starting to fall apart.
“Until 2005, the sole known function for RBP4 was to mobilize retinol from tissue stores and deliver it to vitamin A-responsive cells where it can be converted to retinoic acid for use in regulating vitamin A dependent transcription and functions. In 2005, Kahn and colleagues reported that circulating RBP4 levels affect glucose clearance, with high RBP4 levels inducing insulin resistance (Yang et al., 2005; Graham et al., 2006). Specifically, Kahn and colleagues proposed that adipocyte-derived RBP4 is a signal that contributes to the pathogenesis of type 2 diabetes, linking obesity with type 2 diabetes, as well as other obesity-related metabolic diseases.”
Very importantly, this then brings into question the entire premise of retinol’s “storage” in the liver. That’s because the thought to be delivery protein for it is being generated by, and secreted from the adipose tissues and not at all exclusively from the liver’s “storage” site!
Next, let’s think a bit about the cell’s response to viral infections. When a cell gets infected with a virus, it can very mistakenly start replicating and cloning more of the same virus. But, very often, it also wraps the newly made viruses up in a protein capsid. Some cells can then eject the entire capsid out of itself. Secondly, in response to viral infections the adaptive immune system will usually start to build antibodies to the virus. The goal and function of the antibody is to attach itself to specific binding sites of the viral protein. In doing so it effectively bulks up any free circulating viruses so that they become too large to pass through the cell membrane. If successful, the viral infection is brought under control. Except, now when a cell is contaminated by a toxin, it is by a non-protein based molecule. There are no protein binding sites (at all) to attach an antibody to it. Therefore, as with some viruses, the cell needs to wrap toxic molecules in a specialized hollow-core antibody (or capsid if you prefer). Unlike the currently recognized Y shaped antibodies, the RBPs are more barrel-shaped, That barrel-shape is needed to engulf the entire antigen. Shown below is a model of the RBP with its embedded retinol ligand.
Note the retinol molecule (ball and stick model) nestled inside of the far more complex wrapper (ribbon model) of the RBP. Remember that retinol is too toxic to be in serum alone. Here’s the spacefill model of the RBP showing that no part of the retinol molecule is exposed outside of the RBP itself.
Image created with the PDB ID and associated publication, NGL Viewer (AS Rose et al. (2018) NGL viewer: web-based molecular graphics for large complexes. Bioinformatics doi:10.1093/bioinformatics/bty419), and RCSB PDB.
Therefore, this molecular structure is an astonishing feat of chemical separation and isolation. Not only has the cell’s protein weaving machinery been able to detect and identify a single molecule, but it has also separated it out and wrapped it in a complex protein envelope. Remember too that nature is no fool, and it is not wasteful. This extreme measure of molecular assembly and folding dexterity has to be going on for a very good reason.
Why would the body resort to using such an elaborate and costly transport protein structure? Secondly, if this is truly a transport protein, then how does the receiving cell extract out the retinoid payload when no part of it is exposed to the outside world? And, how exactly does it do it in a toxic-safe manner? Why does the RBP only transport just one molecule at a time? And, once again, why are the adipose tissues generating and secreting the RBPs in the first place? Of course, no one knows the answers to these questions. At best, there are just some unsupported speculations tossed around about it.
“RBP is also bound to a carrier protein, transthyretin. The process by which RBP releases retinol for cellular availability is still unknown and not concisely determined.”
Additionally, if the RBPs are “transport” proteins, that are supposed to be so highly-regulated, then why do they accumulate with age?
The real clincher question is: if the liver is building RBPs to deliver retinol to the other tissues, then why are those receiving tissues then themselves wrapping up retinol in their own internally built RBPs and ejecting it? The current theory of the RBPs being “transport and delivery” proteins makes no logical sense.
Isn’t it just so much more logical that the RBPs are hollow-core antibodies? Isn’t it just more logical that as the body gets exposed to more of a toxic load outside of liver storage, the body builds more antibodies to combat and protect us from that now adipose accumulating toxin? Here’s another study indirectly indicating that’s the case:
Cellular retinol-, retinaldehyde- and retinoic acid-binding proteins were localized in rat retina during pre- and postnatal development by indirect immunofluorescence.
Source: Immunolocalization of cellular retinol-, retinaldehyde- and retinoic acid-binding proteins in rat retina during pre- and postnatal development De Leeuw, A.M., Gaur, V.P., Saari, J.C. et al. J Neurocytol (1990) 19: 253. https://doi.org/10.1007/BF01217303
What is immunofluorescence?
Immunofluorescence is a technique used for light microscopy with a fluorescence microscope and is used primarily on microbiological samples. This technique uses the specificity of antibodies to their antigen to target fluorescent dyes to specific biomolecule targets within a cell, and therefore allows visualization of the distribution of the target molecule through the sample.
Clearly, the RBPs are very antibody-like. But, since we now know they are not “transport” proteins, is it not highly likely they are indeed antibodies? They have just not yet been recognized as such. The next logical question is: if the RBPs are, in actuality, antibodies, then what does that tell us about retinol? It tells us that it is a toxin!
The famous amyloid plaques of Alzheimer’s disease
One of the key neuropathological hallmarks of Alzheimer’s disease is the accumulation of β-amyloid plaques in the brain. No one knows why they develop or what to do about them. What’s assumed is that they are just defective ribbon structured proteins that exhibit some weird and unexplained misfolding. But, doesn’t that sound a lot like the folded ribbon proteins of the RBPs? Here’s a description of the RBPs
Members of the lipocalin family, including the retinoid-binding proteins RBP, epididymal retinoic acid-binding protein and β lactoglobulin, share a very low sequence identity but display a highly conserved overall fold. They are composed of an eight stranded antiparallel β-sheet that is folded over itself to form a hydrogen-bonded β-barrel, which constitutes the ligand binding pocket (Figure 2). The N-termini of these proteins are folded around the back of the barrel, `capping’ that side of the pocket.
Next, we need to know and deeply appreciate that it’s not just the liver and adipose tissues that are excreting the RBPs. It’s also happening in the kidneys, lungs, heart, skeletal muscle, spleen, eyes, and testes too.
Functions of RBP
Retinol is secreted from its storage pools and circulates in blood bound to RBP. The main storage site for vitamin A and, correspondingly, the main site of synthesis of RBP, is the liver, although other tissues (including adipose tissue, kidney, lung, heart, skeletal muscle, spleen, eye and testis) express this protein.
Source: Retinoid-binding proteins : mediators of retinoid action Biochem. J. (2000) 348, 481±495 (Printed in Great Britain) 481 REVIEW ARTICLE Noa NOY1 Division of Nutritional Sciences, Cornell University, Ithaca, NY 14853, U.S.A
And then there’s this statement:
The mechanism by which retinol initiates secretion of RBP from cells is unknown, but appears to be conserved in yeast ectopically expressing RBP.
Source: As above
I think it is quite obvious that the cells of multiple tissue types are synthesizing their own RBPs as a protective measure in an attempt to rid themselves of a highly toxic molecule. Do you see where I’m going here? Yes, if the cells of the liver, adipose tissues, kidney, lung, heart, skeletal muscle, spleen, eye, and testis are all able to secrete RBPs, with the retinoid wrapped up inside of it, why shouldn’t we think that the nerve cells of the brain are not going to do the same? Just like the fact that the RBPs are unrecognized as antibodies, couldn’t the famous amyloid plaques of Alzheimer’s disease be unrecognized as RBPs generated by the brain too? Or maybe, since Alzheimer’s is such a new phenomenon in human existence, the amyloid plaques are an ongoing attempted synthesis of RBPs? Thinking that the cells of the nervous system can generate amyloids is not just speculation. As mentioned above, the RBPs are often bound in serum to transthyretin.
Transthyretin (formerly known as prealbumin) is a plasma protein involved in the transport of thyroxine and retinol and is secreted in great amounts by the choroid plexus epithelium.
Knowing that transthyretin is typically bound up with the RBPs it’s no surprise that so many people with diabetes, autoimmune diseases, and even dementia have the comorbidity of abnormal thyroid functions.
There are some rather remarkable similarities between the so-called defectively folded proteins of the amyloid plaques and that of the folded over proteins of RBPs. For example, here’s the CRYSTAL STRUCTURE OF THE PROTEASE INHIBITOR DOMAIN OF ALZHEIMER’S AMYLOID BETA-PROTEIN PRECURSOR
Image created with the PDB ID and associated publication, NGL Viewer (AS Rose et al. (2018) NGL viewer: web-based molecular graphics for large complexes. Bioinformatics doi:10.1093/bioinformatics/bty419), and RCSB PDB.
As with the RBPs, the Alzheimer’s disease defining proteins adopt a β‐sheet structure and sometimes form into amyloid plaques. Most importantly, when you consider that there has been an 800 times increase in the rate of Alzheimer’s disease since the early 1970s, it is completely, absolutely, undeniably, positively crystal clear that the disease is a poisoning. It’s then easy to appreciate that the cells of the brain are responding to that poisoning in very similar ways as do say the cells of the kidney, lungs, etc. However, once trapped inside the brain, there is no viable disposal pathway for these unusual proteins. The brain just slowly accumulates and clogs up with the amyloid plaques. Not only that, but all the energy and resources wasted in building the amyloid plaques has been taken away from the brain’s normal tissue maintenance and repair processes.
Very tragically, billions of taxpayer-funded dollars have now been spent by researchers going on a wild goose chase of blaming genetics for this disease. Of course, it is a colossal waste of money and time because it is completely obvious Alzheimer’s disease is not caused by genetics. Not only does it take thousands of years for a genetic shift to occur in the human population, the country with the highest genetic diversity on the planet now has the highest rate of Alzheimer’s disease in the world. And who cares about some supposed “genetic predisposition” to the disease because there’s absolutely nothing people are going to be able to do regarding their genetic makeup. So, investigating genetics is pretty much a meaningless distraction from the real culprit of the disease being environmentally caused. If people were not being slowly poisoned by some environmental factors, then their “genetic predisposition” would never be a problem.
Of course, it’s not just the brain that’s clogging up with amyloid plaques, it’s the heart and other organs too. Not at all surprisingly, that also directly correlates to the serum levels of the RBPs!
Identification of Transthyretin Cardiac Amyloidosis Using Serum Retinol-Binding Protein 4 and a Clinical Prediction Model
Findings In this case-control study that included 34 patients with transthyretin cardiac amyloidosis and 77 control participants, retinal-binding protein 4 was significantly associated with the disease independently of tested confounders. A prediction model composed of retinal-binding protein 4, transthyretin, and echocardiographic and electrocardiographic characteristics had excellent discrimination for transthyretin cardiac amyloidosis (deposition of amyloid).
Conversely, the vascularization of the brain in AD patients often shows the same type of damage as that presented in coronary artery and heart disease. The condition is called “vascular dementia.” Therefore, it’s very probable that the same root cause force behind that vascular damage is driving both diseases. Equally important is to know that almost no one dies directly from Alzheimer’s, rather they die with Alzheimer’s. Meaning, the real cause of death is one of their other conditions, such as kidney disease, heart disease, stroke, choking, pneumonia, etc.
Additionally, It’s well documented that persons with Type II diabetes are at a bigger risk (~200%) for developing Alzheimer’s disease. It is even claimed that the single biggest risk factor for developing Alzheimer’s disease is having Type II diabetes. Therefore, many people have made the erroneous assumption that the diabetes is somehow causing Alzheimer’s disease. But, that’s not quite true. Diabetes is not “causing” the Alzheimer’s. Rather, both diseases are simply joined at the hip, metaphorically speaking. And in both diseases we have the common themes of insulin resistance and the development of amyloid plaques. Obviously, diabetes is not “causing” the Alzheimer’s and Alzheimer’s is not “causing” the diabetes. Once again, something else is at the root cause of both diseases. As we’ve seen, elevated serum levels of the RBPs are a significant marker in both diseases too. It is also true for the development of amyloid plaques of the heart. So much so, that it is pretty much an undeniable fact that the RBPs are somehow involved. But, there is an even more direct connection between these two major diseases. As with heart disease, it’s the accumulation of misfolded proteins.
Protein misfolding and aggregation in Alzheimer’s disease and type 2 diabetes mellitus.
AD is characterized by the accumulation of amyloid-β (Aβ) in the brain, while T2DM is characterized by the deposition of islet amyloid polypeptide (IAPP, also known as amylin) within beta-cells of the pancreas.
It is becoming increasingly believed that islet amyloidosis is the progeny of many diseases, including T2DM. The production of islet amyloid polypeptide (IAPP) oligomers that results in amyloid deposition is considered as a major contributor in pathogenesis and progression of T2DM . This has been found present in 96% of T2DM patients and is recognised as a hallmark for diagnosis of this disease.
LINKAGE BETWEEN AD AND T2DM
AD and T2DM are both prevalent in the aged population. Whereas the cerebral accumulation of Aβ is a major pathological hallmark of AD , the deposition of a very different polypeptide, amylin, that likewise succumbs to β-sheet formation and self-aggregation occurs within the pancreas, especially in β-cells, in T2DM.
So now, just what do you suppose is responsible for causing the messed-up structure of the proteins generated by the pancreatic and other tissue stem cells? How about we seriously consider it to be a toxic molecule that has now been proven to cause about 500 different gene “expressions” in stem cells. Except, to most of us here it’s now clear these are, in actuality, sites of gene “damage” and not that of gene “expressions” at all. That gene damage then messes up the cell’s protein weaving machinery. Naturally, the follow-on consequence is going to be the defective structures of the manufactured proteins.
Somewhat like with the wild goose chase of genetics, there’s been a vast amount of research in trying to correct the misfolding proteins using pharmaceutical drugs. Of course, that effort has been futile. Additionally, most research is narrowly focused right down into trying to decipher what’s wrong with the protein structure, Oddy, it appears most people are only asking why the protein is misfolding, as if something has gone wrong with it post manufacturing. They they are not considering that it has been expressly manufactured that way due to RNA/DNA damage.
The RBPs tied-together with Insulin Resistance
GLUT4 – is the glucose transport protein used by cells to take-up insulin from serum. Obviously then if the GLUT4 proteins are not of sufficient quantity or quality, it then will cause the condition of Insulin Resistance. It’s not hard to imagine that if the cell’s energy and resources are tied up generating RBPs, that could be impairing their production and or functioning of the GLUT4 proteins. This scenario is indeed being demonstrated in clinical research. For example:.
Serum retinol binding protein 4 contributes to insulin resistance in obesity and type 2 diabetes.
This now brings us full circle to where I hope it shows how it’s all interconnected. The information presented here not only links the RBPs to Type II diabetes and the amyloid-β plaques; it seriously implicates it in causing coronary artery, heart disease, and of course Alzheimer’s too. Except, we need to be very careful here and not try to blame the RBPs. Rather it’s the overload of retinol that is the very root cause. It’s the overload of retinol that has forced production of the RBPs in the first place. There’s one more connection with insulin resistance that I’d like to discuss, and that is Mitochondrial Dysfunction. There are hundreds of research papers documenting that Mitochondrial Dysfunction and Diabetes are very closely coupled. But, as always, there’s more to the story, and that is the key role of the retinoids directly damaging the mitochondria.
Vitamin A and Retinoids as Mitochondrial Toxicants
Overall, such findings indicate a potential ability of vitamin A and its derivatives to negatively interact with biological membranes, an event that may lead to organelle stress, as, for instance, mitochondrial dysfunction, and to cell apoptosis or necrosis.
‘Vitamin A and its derivatives, the retinoids, disrupt mitochondrial function by a mechanism that is not completely understood. However, it accounts with impaired electron flux between the complexes of the METC, increased ROS production, and induction of oxidative and nitrosative stress to mitochondrial membranes. Additionally, vitamin A and retinoids alter the mitochondrial structure by causing swelling of the organelle. More investigations are needed to elucidate how vitamin A and retinoids affect mitochondria and whether there is a causative link between such event and the clinical manifestations observed both experimentally and in humans.’
Source: as above
Predictably, the thinking from some pharma funded researchers is the same. It’s viewed as an opportunity to try to develop a new drug that will block or intervene in the synthesis of the RBPs. Of course, it always comes down to needing a “drug” to “block” something. Using a non-drug based therapy is completely unthinkable to these folks. But, since we know with 100% certainty that Alzheimer’s is the result of a long term poisoning, the only “drug” that could even possibly work is one that acts as an antidote to whatever that poisoning is. Until then, almost all other drugs are just going to be useless, and most will cause even more harm. Now with the known connections between the elevated RBPs and the development of amyloid plaques, and having a better understanding of RBPs likely being an antibody response to a toxin, isn’t it very likely retinol is the responsible toxin?
Maybe it’s just me, but how about we just consume a lot less of the retinoids and let the body heal itself?
Are the RBPs antibodies? Please have a think about it and comment as you see fit.
Heart disease and stroke is the number one killer of North Americans. This disease accounts for over 600,000 deaths per year in the USA alone. And, like with the rest of the modern chronic disease epidemics we face, historically speaking, it is not a normal disease in the human population. Our extraordinary rate of heart disease is a relatively new phenomenon. It is considered to be just another disease of affluence and lifestyle. Obviously, we are somehow doing it to ourselves.
For decades now modern medicine has vilified cholesterol as being the primary culprit in causing heart disease and stroke. But, the exact mechanism behind why there’s a pandemic in increased cholesterol levels remains a mystery. For a long time now the elevated cholesterol levels have been very simplistically blamed on consuming too much saturated fat as part of the regular diet. However, things don’t move fast in medical research, and now finally after about 50 years that theory is losing its plausibility. If we are going to be realistic about it, with the massive real-world experience with the wide-scale adoption of low-fat diets, it has proven to be just dead-wrong. Yet, many folks in medical science still cling to the ridiculous notion that fat in the diet is the cause of high cholesterol. Not surprisingly, even with much of the population on long term low-fat diets the cholesterol levels for many people just remains way too high. And of course, the North American death rates due to heart disease and stroke are just as high as ever also. So, once again, the experts appear to have gotten it completely wrong. Regardless of what the experts claim, clearly, dietary fats are not the cause of high cholesterol.
Okay, but what about the very basic premise that high cholesterol is even the villain in causing coronary artery and heart disease in the first place? Surely, they can’t be wrong about that one too? After all, the arteries and the heart are being blocked up with plaque, and one of the main constituents of that plaque is cholesterol. I mean, just how much more evidence do they need to give us? Cholesterol is always found at the scene of the crime. Therefore, it must be guilty, right?
Well, not so fast. Here’s the little glitch in that theory. Only about 50% of people diagnosed with coronary artery disease (CAD) have elevated levels of serum cholesterol. Whereas, the other 50% of people with CAD have normal, or even low, serum levels. So, that’s a clear indication that there’s something vastly wrong with that “it’s the cholesterol causing heart disease” theory too.
Okay, what else do we know about the artery plugging plaque? Well, the two really interesting ones are that it is chocked full of dead macrophages and often calcium too. Next, we need to know that the walls of the arteries are an endothelium. The cells that make up the internal walls of the blood vessel are really just a specialized version of the epithelial cells. Then, the next critical detail to know is that the areas of the blood vessel walls where the plaque forms are almost always under distress from a non-healing lesion and chronic inflammation too. So much so, that many researchers now believe that the real root cause of the plaque formation is the inflammation. Their view is that the plaque is really the body’s internal band-aid trying to protect a chronic wound in the artery wall. Thus, in their view, the causal sequence goes like this:
Naturally, we need to look upstream and ask what can cause chronic lesions and inflammation in the blood vessel walls like that in the first place?
Long term exposure to retinoic acid would sure do it. Remember that retinoic acid indiscriminately attacks the basal membrane of the epitheliums anywhere in the body. Next, what about all those dead macrophages? Yes, retinoic acid, and even vitamin A, have been proven to cause that to happen too. What about the calcium? Yes, that too is very well documented to occur in high vitamin A conditions. That calcium has been drawn-out from the bones to bring the local pH levels back in line. Finally, what about the cholesterol itself? Yes, cholesterol is documented to be one of the chemical breakdown pathways for vitamin A.
See: Organic Chemistry Morrison and Boyd 3rd Edition Pages 278-280
With all of that, I think we have a perfect fit as to who the real culprit is in causing coronary heart disease. It’s not cholesterol itself. Instead, cholesterol is just one of the by-products of the breakdown of vitamin A. It’s also very likely that elevated cholesterol is just a defensive measure in response to the inflammation.
Either way, the real culprit in heart disease is whatever’s causing the lesions to occur. Obviously, cholesterol is not the root cause of the plaque at all. Therefore, elevated cholesterol is just another symptom of the chronic disease.
But, the medical establishment does not want you to think like that, or to think too deeply about it. The thing is that they have a magic drug to take care of that elevated cholesterol for you. It does not matter to them one little bit if cholesterol is the real culprit or not. It’s the drug they have, and it’s the drug they are going to aggressively try to sell you.
Of course, I’m referring to the now famous “statins.” This class of drugs is a huge blockbuster seller. With about 40 million people taking them daily, it’s been the biggest money maker in the history of the pharmaceuticals. Annual sales are in the hundreds of billions of dollars. And, the worldwide revenue generated in treating heart disease is approaching one trillion dollars. Therefore, there’s no compelling reason for anyone who is in the business to look any deeper into the cholesterol question. But, we will.
The statins have been on the market for about 30 years now. Like with so many other pharmaceuticals, the statins don’t actually cure disease or even prevent disease. They only mask or suppress the symptoms. For the industry, that’s the great thing about the statins. It’s precisely what the industry wants. They can get people hooked on them and have repeat and life-long customers.
Moreover, the statins actually do a pretty good job in suppressing the liver’s production of cholesterol. Therefore, for the average GP overseeing the treatment, it appears that they are even “working.” Okay, so almost everyone involved should be happy with that, right?
Well, that’s not the case at all for a lot of statin users. Many of them aren’t at all happy because they experience serious so–called “side-effects.” So much so, that a lot of patients can’t bear the suffering, and are forced to stop taking their statins after just one year. The other thing with the statins that most people shouldn’t be at all pleased about is that there’s almost no evidence that anyone is going to live one day longer by taking them.
The most commonly reported “side-effect” is that of muscle pain and weakness, and it’s often severe. So, right away the math just does not add up on it. If you are not going to live one day longer by being on a statin, but yet you could suffer in serious pain for every day that you are on them, and that’s potentially for the rest of your life too, why would anyone take them? Very sadly, it’s usually because their doctors have told them “You will die if you don’t take them.” Yes, it’s the same sordid story. They need to resort to scare tactics and fearmongering to keep selling their magic beans. Like with most pharmaceutical drugs, the real clinical trials for them start well after it has been approved and when it goes into widespread use. So, in a way, the patients are just human guinea pigs in these long-running experiments. The results of that long-term experiment with the statins are now showing up.
Of course, over the years, more and more evidence is leaking out that not only are the statins not preventing heart disease and stroke at all, but they are causing a massive amount of pain, suffering, and often accelerating people into other serious diseases and even early death. There are a bunch of very credible researchers now sounding the alarm, and asking serious questions about the statins. The industry, of course, is fighting back feverishly with propaganda, and marching out their own paid-off pundits to keep pushing the statin drugs as aggressively as ever. What exactly are the more serious long term complications of statin usage? In no particular order, they are significantly increased risks (often by about 50%) of:
Serious Liver damage
Dementia / Alzheimer’s disease
IBD / IBS
Debilitating muscle atrophy
Now, with all those severe and increased risks, and no proven benefit or even a decreased risk of having a first heart attack, who in their right mind would take a statin? How is the industry getting away with this nonsense? Of course, it’s with slick marketing, propaganda, fake science, rigged studies, aggressive media censorship, and with what I view as very deceitful manipulations. For example, seeing an increased risk of “Heart Failure” on the above list should have caught your attention. After all, aren’t the statins suppose to reduce the risk of Heart Attacks? Well, yes, they are. But, you see, technically speaking, catastrophic “heart failure,” due to the heart muscles being too weak to contract and pump blood, is not a “heart attack.” No, a “heart attack” is when a big slug of plaque peels off the artery wall and blocks it, or it gets lodged into the heart valve. Of course, to you and me, it’s just a bunch of weasel words to hide from the truth; there’s no material difference between dying from catastrophic “heart failure” or a “heart attack.”
The reason people on the statin so commonly experience debilitating muscle atrophy, muscle weakness, and sometimes catastrophic “heart failure” is because the drug does not just block the liver’s production of cholesterol. It also blocks the production of another critical enzyme called CoQ10, among other important processes. The CoQ10 enzyme is a key enzyme used by all cells, and especially so the muscle cells, to produce energy. So, the statins are just going to slowly drain the life force out of every cell in the human body. Remember too, that the liver is the body’s primary detoxification organ. Obviously “blocking” any aspect of its function is reckless if not just plain stupid. I don’t want to go more into that aspect of it here. But, please check out what other people are documenting on it. Here are a few good references.
Dr. Aseem Malhotra – Heart Stents, Cholesterol and Statin Smoking Guns?
Dr. Michael Eades – Statin drugs and diabetes
Dr. Maryanne Demasi – ‘Statin Wars: Have we been misled by the evidence?’
Some of the propaganda statements from industry pundits are so egregious, it’s just obscene. It’s as if they are saying, don’t worry about the vastly increased risk of dementia/ Alzheimer’s, my god man, you could have a heart attack. Don’t worry about the vastly increased risk for diabetes. We, the experts in medicine, have new synthetic insulin we can sell you for the rest of your life, and at 10x the old price too. And when your diabetes gets worse, and you lose the ability to circulate blood in your lower limbs, don’t worry, we can just simply cut off your legs. And ladies, don’t worry about the 50% increased risk of developing breast cancer; we, the experts in medicine, can just simply cut off your breasts. We are really good at that too. Don’t worry that you can become too fatigued and weak even to move. Just trust us, we are the experts. Above all else, don’t stop taking your statins, or “YOU COULD DIE.”
But, my purpose here is not to go bashing the statin drugs. Rather, it’s to highlight this list:
Serious Liver damage
Dementia / Alzheimer’s disease
IBD / IBS
Debilitating muscle atrophy
Do you recognize that list? It is, for the most part, the same list of the major diseases I’ve been attributing to chronic vitamin A poisoning. Here we now have substantial evidence showing that the statins are causing these same diseases. How can that be possible? Could they be caused by a deficiency in cholesterol? Well, no, because there are a lot of people with naturally low cholesterol levels, and we still have a massive epidemic in all of these diseases.
What about this little tiny detail of one of the breakdown pathways of vitamin A is to convert it into cholesterol? What if the statins are preventing this breakdown? On one hand that would sure lower the amount of cholesterol produced by the liver, as it indeed does. But, in doing so, what does that mean for serum vitamin A levels? They should be going up with statin use then too. Yes, they do.
Serum retinol levels throughout 2 years of cholesterol-lowering therapy.
In the entire population (N = 102), serum retinol was 3.46 +/- 0.08 mumol/L before therapy and 3.76 +/- 0.07 after 2 years of therapy (P < .001). Serum retinol increased in diet- and statin-treated groups, but not in fibrate- and resin-treated groups.
Quite remarkably, here we have a drug with massive market adoption, that is inadvertently increasing serum vitamin A levels. Almost all of the other reported so-called “side-effects” documented for the statins are a perfect match for those of vitamin A toxicity too. But, most amazingly, its use is now proving to result in significantly increased rates of above listed chronic diseases.
The silver lining in this dark cloud of the on-going statin fiasco is that it has inadvertently given us a tremendous amount of more strong evidence that chronic vitamin A toxicity is actually causing all of the above-listed diseases.
Additionally, there’s the other bit of very bad, and yet almost global, advice dished out by the medical experts regarding heart disease. They have pretty much vilified salt, and said that everyone should be on a low salt diet. The experts have correspondingly set ridiculously low guidelines for its intake. But, once again, it looks like that advice is entirely wrong. Here’s an excellent video presentation using historical references and data to show that higher intakes of salt actually reduce the rates of coronary and other chronic diseases.
But, there’s one other super important and connecting detail you need to know about salt and cholesterol. Much of the body’s cholesterol is excreted and disposed of by the liver via the bile salts. Therefore, you need adequate dietary salts to facilitate that critical process.
Now, if I didn’t know better, it’s almost as if much of the advice from the medical establishment is rigged to manipulate us into a chronic disease.
Anyhow, if the advice from the experts is so often wrong, what’s a person to do when they are concerned about high blood pressure, or heart disease and stroke? All I can do is share what’s happened in my case. After four years on my vitamin A elimination diet, my cholesterol levels have dropped in half. The various cholesterol ratios are like perfect too.
My blood pressure is excellent. And somewhat recently, my resting heart rate has fallen a bit more to now being usually around 50. That’s reported to be a standard heart rate for a well-trained athlete. But, I’m not a well-trained athlete and I’m now in my late fifties. Go figure?
Therefore, if I had a friend concerned with the long term risks of heart disease I would definitely encourage them to consider a low vitamin A diet. Lastly, there’s the concern for the potentially already built-up calcium deposits in the arteries. I think that a regular dose of apple cider or balsamic vinegar will quickly take care of that.
The human body was perfect and is perfect. We just have to be very careful in not poisoning it. Obviously, we should also never be taking any drug that “blocks” some critical function of it.
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