I’ve now reached the eight-year point on my ultra-low vitamin A diet experiment. Surprisingly, even after eight years I’m still seeing small incremental improvements in my overall health and well-being. But, much like with last year’s annual update I don’t have any major health improvements to report this year. So, on one hand, not much has changed for me. But, on the other hand, I do feel that I’ve turned a bit of a corner this year and my health is feeling really good. It’s hard to describe, but I’m just feeling more alive. Without a doubt my health is now the best it has been in decades. Contrary to what’s normal, as I’m getting older my health is still slowly improving. It’s also now clear to me that I was being adversely affected by vA toxicity since my mid 20s.
So, how long does it really take to fully recover from vA poisoning? Oh, it’s about say 3 to 5 to 10 years depending on your own personal situation.
One of the hallmarks of vA deficiency is xerophthalmia leading to poor vision, disintegration of the outer tissues of the eye and eventually blindness. Well, here I am eight years into a virtually 0 vA diet, and my daytime vision is now excellent. I’d rank my vision as being at least as good as it was in my 30s. I have no sign of xerophthalmia, nor any other related disease condition in the eye.
About seven or eight years ago I had reported the vascularization of the sclera that had developed in both eyes. Now, finally, after eight years, it has diminished. The vascularization is not completely gone, but it has very significantly improved.
One of the other hallmarks of vA deficiency is poor night vision or what’s been termed night blindness. I wrote about my experience with it in my 2022 Mid-Year update. After dropping the onions from my diet the condition has completely and totally resolved. My night vision is now once again excellent. If anyone wants to visit me here in Calgary we can go for a nice walk at night in the dark.
Body Weight and Strength
Last year I had reported that I felt I was still about 2-3 kg or 5 lbs overweight. Well, with no additional effort at all, I’ve lost 4 lbs this year. For the first time in my life I can see my abs.
I’ve been really busy with work, and some major home projects so I’ve not been able to exercise on a regular basis. I only exercise about once a week, if I’m lucky. Yet I’ve been able to at least maintain my strength in lifting weights. My single rep max on the bench press is 265 lbs. Although that’s nothing too exceptional for a 160 lb guy, that’s the heaviest I’ve lifted in my life. Now at age 62 I’m stronger than what I was at age 22.
Reversal of Colour Blindness
In a previous update I reported that some of the colours I was seeing were generally getting much brighter. It first started with yellows. Before I started on this experiment a yellow taxi cab, or a yellow traffic light, appeared to be a dull yellow to me. Now they are much brighter. They now appear almost a fluorescent yellow. Then, the same change slowly occurred with greens, and reds. What I didn’t appreciate was what I was really experiencing was the reversal of partial colour blindness.
About nine years ago I had a painter redo the trim around some interior doors in my house. When he painted the trim he told me that the colour match with the doors had turned out rather poorly and that he’d have to redo them. But, unlike him, I could not at all see the difference between the two colours. To me they were both the same off-white. So, I told him that since I can’t see the difference between them that he could just leave it as is. Well, now nine years later I can easily and clearly see the difference.
Could it be that my eyes are finally clearing the lifetime accumulation of lipofuscin in the retinal pigment epithelium?
Sparrow JR, Duncker T. Fundus Autofluorescence and RPE Lipofuscin in Age-Related Macular Degeneration. J Clin Med. 2014;3(4):1302-1321. doi:10.3390/jcm3041302
A few other people on my forum have also reported reversing their colour blindness. So, this is not just a one-off anomaly. I think this is a really interesting finding since millions of people have partial colour blindness.
Reversal of Varicose Veins
About 10 years ago I noticed that I was developing varicose veins down around my ankles. They didn’t bother me, and there was nothing I was going to be able to do about it, so I ignored it. Well, today, those same varicose veins have completely recovered. That’s another nice long-term win for the low vA diet.
As with last year’s update my dental health is excellent. My teeth and gums are feeling really strong and solid. My teeth are also smoother, cleaner, and I think whiter too. Somehow I still haven’t developed scurvy.
Before starting this experiment I had a lot of pain in my knees and general joint stiffness. The pain in the knees was moderate but chronic. Fortunately, It was also one of the first issues that I fully recovered from and it has never regressed. Anyways, 10 years ago kneeling down on a hard floor was just unthinkable. Now, I can kneel down on a concrete floor without pain.
An Urgent Need to Pee
Okay, this section is not directly related to my vitamin A elimination diet. Rather, it is about an inadvertent side-effect of it. Last year I started to develop an urgent need to pee. It’s a good thing I was working from home with ready access to the washroom. A few weeks before that condition showed up I had started drinking coffee again. I had no big reason for adding the coffee back into my diet, other than I liked the extra jump start it gave to my morning routine. I was at the same time still taking in quite a bit of salt with my 2-3 meals a day of my rice and beans soup. The combination of these two strong diuretics turned out to be too much for me. So, once again, I completely stopped the coffee and also cut way back on the salt. Now I have maybe a small pinch of salt per day. Anyways, within 4 days those two changes completely solved the problem of having an urgent need to pee.
My sleep quality remains excellent. I dream every night. But, the intensity of the dreaming changes a bit from month to month.
Blood Lettings and Other Miraculous Cures
I continue to make regular blood donations and I’m now on my 28th donation. I have a preference for making plasma rather than whole blood donations. That’s mostly because I can make plasma donations more often and it also better matches my goals. However, I do mix it up from time to time. Although, I do think that these blood/plasma donations are helpful I can’t say I notice any effect from them. Except, I do think they would offset any trace amounts of vA I may still take in from my diet. Of course, there is the public benefit of making blood donations. There’s been a large increase this year in the need for blood and plasma products here in Canada so I’m making my small contribution.
Okay, what about the other miraculous cures? Sorry, there are none that I know of. So, for now, I think time is one of the biggest factors in recovering from vA toxicity. Given enough time the body is hopefully able to heal itself. That in itself is a miraculous process.
Sorry, I have no labs to report this year
A few months ago my doctor’s office sent out a notice that they are overwhelmed and are triaging patients on a most urgent care needed basis. That news wasn’t a big surprise because the same phenomenon is being reported all across the country. For some mysterious, and completely inexplicable, reason there’s been a huge increase in all kinds of serious health issues, and in all age groups too. It includes depression, anxiety, heart attacks and strokes in young adults, partial paralysis, cancers, all kinds of new viral infections, and on and on.
Oh, gee, I wonder what it could be that caused it? Was there some new and nearly universal environmental factor introduced (forced on us) last year?
I mean, seriously, even a child could figure it out. Of course, the medical establishment will never admit it.
Anyways, given that situation and the trouble I had last year in getting basic labs, and being one of the unwashed (unvaccinated) folks, I felt it wasn’t even worth trying to get some more lab work done this year. The only numbers I can provide are for my blood pressure. Three years ago it was usually about 110/70. Now it’s down to 100/60 and my resting heart rate is consistently ~ 50 bpm. That’s another nice long-term win for the low vA diet.
The Black Swan Rule of Science
It’s time to invoke the “Black Swan Rule of Science” on the ancient vA theory. I think many people probably know the “There are no Black Swans” analogy. But, for those that have not heard about it, in a nutshell, it goes like this:
Let’s say the currently accepted, and long established, science states that all swans are white. Or, just that the experts say “Swans are white”, and therefore it’s a fact. Okay, fine. We can somewhat provisionally accept that statement. But, then one day someone travels to some far away land, and lo and behold they see a black swan and they take pictures of it. That’s it. At that moment the accepted and long established science stating that all swans are white is now trash. The point is that you don’t need to find 1,000 black (or pink etc) swans to demolish the prior science. You only needed one. You also don’t need big complicated studies, and you don’t need to dissect the black swans to prove it. No, it’s done, and just with that one case the previously established scientific fact is completely toast.
So too is it with the crusty 100 year old vitamin A theory. It is now toast, trash, and junk science. I’m a human and I’ve had virtually no vA in my diet for eight years. But, the well established science on vA claims that by year 4 or 5 with no vA people will get horribly sick, have their eyes and skin disintegrate etc., then they’ll go blind and likely die soon after. Well, nope, sorry, it hasn’t happened in eight years; and it won’t happen in the next eight years either. Of course, I’m not alone. There are quite a few people on muscle meat only carnivore diets (very-low vA) diets who are at or beyond the ten-year point and are in excellent health.
Retinol, retinoic acid etc, are not a “vitamin”. Rather clearly they are a poison, and nothing but a poison. If you don’t like that statement, too bad, it is now just a fact. If you can’t accept that fact then I think you should go for a long quiet walk and THINK about it. Just really, really think about it.
What’s next for me?
I’ve not been very active on the vitamin A topic this year. That’s not because I’ve lost interest in it. It’s mostly because I’ve been too busy with my day job and some big home projects. With those projects now wrapping up, I hope to get back into the vitamin A topic more this fall. One thing we’ve talked about before was to officially redo the 1925 Wolback and Howe study. It’s the cornerstone study supporting the vA theory. I would really like to pull that cornerstone study out and toss it into the scientific trash pile where it belongs. But, due to the pandemic and the related bizarre cult-like pseudo science atmosphere it has promoted I felt the time just wasn’t right for it. I felt regardless of the results, and how important they could potentially be for human health, it would just be ignored. So, this year I’ll get back on it and try to find a university to conduct this study.
I’ll definitely continue with my ultra-low vA diet for at least the next two years. I want to eventually get a vA lab test that reports 0.0 µmol/L, or whatever amount is below the detection limits of the test. Beyond that, I will very likely continue with my ultra-low vA diet for the rest of my life too. After all, this highly toxic vitamin imposter very nearly killed me. Therefore, I think it would be almost insane to reintroduce any foods in my diet with anything more than trace amounts of vA.
Thank you for your continued interest and participation in this investigation.
More than 100 million U.S. adults are now living with diabetes or prediabetes, according to a new report released today by the Centers for Disease Control and Prevention (CDC). The report finds that as of 2015, 30.3 million Americans – 9.4 percent of the U.S. population –have diabetes. Another 84.1 million have prediabetes, a condition that if not treated often leads to type 2 diabetes within five years.
Don’t you think there’s a major problem going on here?
That 100 million number should also look familiar. It’s the same as the number of Americans with fatty liver disease slowly creeping up on them. Clearly, something has gone drastically wrong with human health in North America, and worldwide. And, it’s forecasted to just get worse.
The prevalence of diabetes (type 2 diabetes and type 1 diabetes) will increase by 54% to more than 54.9 million Americans between 2015 and 2030; annual deaths attributed to diabetes will climb by 38% to 385,800; and total annual medical and societal costs related to diabetes will increase 53% to more than $622 billion by 2030
To help put that $622 billion dollar cost into perspective, that is almost twice as much as the total amount that all of America spends on gasoline annually. Yes, just the one disease of diabetes is hugely more costly, and of course profitable, than oil! But, that’s still only a fraction of the nearly four Trillion dollars Americans now spent annually on all health care costs. Of course, the human costs and long term suffering are much more devastating. The annual death rate due to diabetes is 2-3 times that of the current Covid-19 disaster. Naturally, we are not talking about just about North America. The diabetes pandemic now afflicts about 500 million worldwide.
If we don’t get this diabetes disease crisis under control it will surely destroy our economy. I do think we can bring this under control… but it’s not going to be easy. Continuing with the current band-aid type treatments is obviously not working. So, to have any chance at effectively turning this crisis around we need to first get to the correct root cause of it.
The last big breakthrough in diabetes research was back in 1921. Canadians Frederick Banting, Charles Best, and James Collip identified and isolated insulin and quickly went on to develop a process for extracting it from animal sourced pancreases. They licensed the patent for that process to the University of Toronto for the princely sum of $1. With that, insulin went into mass production, was priced at pennies per dose, and saved millions of lives. Today insulin is still the primary treatment for the disease. However, insulin is obviously just that; a treatment, and not a cure. And, today the giant pharmaceutical companies have worked their way around that pesky make it free-to-everyone patent and now sell synthetic insulin at what many consider to be extortionary prices.
The question that Banting and Best did not answer was why was the human pancreas failing in the first place? Maybe, like with most doctors today, they too were taught to believe that diabetes and all chronic diseases are just “bad luck”. Sadly, that ridiculous “bad luck” theory of disease causation is very widely accepted and has gone almost unchallenged even today. But, obviously “bad luck” does not cause organs to fail. It’s equally obvious is that the stupid “bad luck” theory is dead wrong because North Americans could not have gotten vastly more “unlucky” over the last several decades. There’s also no way that people living in the American Southeast are significantly more unlucky than those living in the Northwest.
Back in 1921 we did not have an epidemic of obesity and therefore obesity couldn’t be blamed for the cause of diabetes either. And, obesity most certainly can’t be blamed for Type I diabetes since the wasting the disease causes in children is the direct opposite of that. The presumption is that Type I diabetes is just another auto-immune disease, and auto-immune diseases are just more “bad luck”. We are supposed to believe that it’s the confused and rogue immune cells attacking their own host body. Well, if you’ve read my eBooks you’ll know what I think of the “auto-immune” disease theory. In a nutshell, it’s a bunch of rubbish. No, it’s not a confused or defective immune system. Rather, it’s that tissue cells have been poisoned. With their DNA/RNA being poisoned and damaged they then produce defectively structured proteins. To the immune system those defectively structured proteins appear to have come from a foreign source. The immune system then correctly attacks those cells.
To help better understand the root causes of diabetes we need to know that there’s a similar U-shape curve in the incidence rates that so many of the other chronic diseases follow. There’s a high incidence rate in young children, with a drop-off in rate during youth and teenage years, and then a slow progressive climb in rates with age in adults. Therefore, in adults it’s pretty clear that the disease is one of a slow accumulation.
Source: Rogers, M.A.M., Kim, C., Banerjee, T. et al. Fluctuations in the incidence of type 1 diabetes in the United States from 2001 to 2015: a longitudinal study. BMC Med 15, 199 (2017). https://doi.org/10.1186/s12916-017-0958-6
Now visually sync that chart up with the one I presented in my COVID-19 Vulnerability blog post showing the liver vitamin A concentrations by age. Note the huge spike in early childhood.
Obviously, there’s a lag time between the elevated liver vitamin A storage levels and the onset of the disease. Not at all unexpectedly, it does take some time to burn out the pancreas.
More importantly, we need to understand the exponential growth rates in the incidence rates of both Type I and Type II diabetes over just the last few decades. There is simply no way that this can be naturally happening in the human population. Something is clearly causing it to happen. We also can’t confuse something being really common for it being normal. Sure, diabetes is now very common, but in the historical context that is exceedingly abnormal.
Here’s a chart showing the diabetes prevalence rate here in Alberta.
And for across Canada the regional clustering looks like this:
Any disease that exhibits an exponential growth rate and a geographic clustering pattern like this is clearly a poisoning. It’s a slow poisoning from something that is obviously slowly accumulating and or picking away at cells in the body. It’s just that simple.
With the data presented above, if anyone tries to tell you that the root cause of diabetes is somehow rooted in genetics then simply ask them if they finished their grade 9 math.
Okay, now that we’ve agreed that diabetes is the result of a slow poisoning, let’s find out how likely it is that so-called vitamin A is responsible for it.
Type I Diabetes
As shown in the chart above, type I diabetes is most commonly occurring in children. It is considered to be an auto-immune disease where the defective immune system has wrongly killed off the pancreatic beta cells. With that, the pancreas is no longer able to produce adequate amounts of insulin. What “vitamin” do you know of that causes the rapid mitosis and apoptosis of stem cells?
Retinoic acid induces apoptosis by a non-classical mechanism of ERK1/2 activation Alfeu Zanotto-Filho, Martin Cammarota, Daniel P. Gelain, Ramatis B. Oliveira, Andres Delgado-Cañedo, Rodrigo J.S. Dalmolin, Matheus A.B. Pasquali, José Cláudio F. Moreira
Even though RA is involved in differentiation and apoptosis of normal and cancer cells, being sometimes used as adjuvant in chemotherapy, its mechanisms of action involve multiple overlapping pathways that still remain unclear. Recent studies point out that RA exerts rapid and non-genomic effects, which are independent of RAR/RXR-mediated gene transcription.
Yes, that’s the very functional definition of what the active form of “vitamin A” does to our stem cells. So much so, that it is regarded as the essential molecule that’s somehow needed to “differentiate” our stem cells. What does “differentiate” really mean? It means it causes stem cells that normally reside along a basement membrane to quickly mature into adult cells and separate off. This effect and process of vitamin A’s action is abundantly documented in many fields of medical science, and especially so with its use in dermatology and chemotherapy.
Type II Diabetes
Type II diabetes is characterized by the pancreas still able to produce insulin but for some unknown reason that insulin becomes less and less effective. The pancreas tries to compensate for this ineffectiveness by producing even more insulin. The condition is known as insulin resistance.
As with so many other metabolic diseases there’s a circular blame game going on. Many “experts” believe that obesity is the root cause of type II diabetes. But, of course, that can’t be correct because there are many type II diabetics who are lean. Other experts will claim that it’s the diabetes that’s causing the obesity. I think these guys are significantly more correct. But, not precisely correct. I think obesity is the body’s defensive response to a much more sinister and ongoing threatening condition that we need to be protected from. In other words, what if there’s some other driver that’s causing both obesity and diabetes at the same time? Likewise for the assumed to be diabetes caused comorbidities of kidney disease, cardiovascular disease, macular degeneration, dementia / Alzheimer’s, and, and you name it. Is there something else that could cause all of them to happen? Well, you bet there is. Vitamin A toxicity can, and is proven to, cause all these same comorbidities.
Except, what about this insulin resistance condition? What could be causing that? As I wrote about in a previous blog post, researchers are now identifying the association of elevated RBPs with insulin resistance.
“Until 2005, the sole known function for RBP4 was to mobilize retinol from tissue stores and deliver it to vitamin A-responsive cells where it can be converted to retinoic acid for use in regulating vitamin A dependent transcription and functions. In 2005, Kahn and colleagues reported that circulating RBP4 levels affect glucose clearance, with high RBP4 levels inducing insulin resistance (Yang et al., 2005; Graham et al., 2006). Specifically, Kahn and colleagues proposed that adipocyte-derived RBP4 is a signal that contributes to the pathogenesis of type 2 diabetes, linking obesity with type 2 diabetes, as well as other obesity-related metabolic diseases.”
So, retinol is definitely involved in insulin resistance. Next, we need to appreciate that all cellular receptors are actually proteins intrinsically made by the cell. We need to remember that vitamin A (the retinoic acid metabolite) has been shown to cause more than 500 different gene expressions. What are gene expressions? They are changes in the DNA structure that are detectable by variations in the different proteins that a cell manufactures. So, it’s very possible that the failing insulin receptor is just another protein that has been defectively produced as the result of retinoic acid induced gene expressions (a.k.a. DNA/RNA damage).
That outcome is not at all surprising because we now know that RA fractures and fragments DNA.
DNA fragmentation induced by all-trans retinoic acid and its steroidal analogue EA-4 in C2C12 mouse and HL-60 human leukemic cells in vitro Raghda S. Alakhrasa, Georgia Stephanoua, Nikos A. Demopoulosa*, Konstantinos Grintzalisa, Christos D. Georgioua and Sotirios S. Nikolaropoulosb
Abstract: We have recently shown that retinoic acid induces micronucleation mainly via chromosome breakage.
Do you think that that fracturing of your DNA might cause defectively produced insulin receptors and other proteins? I sure do.
How about conducting a Stress Test
As I mentioned in my eBooks, it is very common in engineering to stress test systems and components to their breaking point. Civil engineers do this everyday with concrete samples as a standard quality assurance practice. Jet engine manufacturers will spin new test engines to incredible speeds, and to the point that the engine explodes or otherwise self-destructs. These types of stress tests are very important as they not only tell us at what point a component will fail, it also helps set the safe operating ranges in real-world usage.
Somewhat likewise, if the theory that vitamin A toxicity is responsible for causing diabetes, then we should be able to conduct similar biological stress tests and see if diabetes can be directly induced by it. Thankfully, that stress test has already inadvertently been conducted for us.
The extreme stress test – Accutane
There have been many accounts of people who have developed type II diabetes shortly after taking accutane. It’s even documented as a known “side-effect”.
The effect of isotretinoin on insulin resistance and adipocytokine levels in acne vulgaris patients.
Soyuduru G, Ösoy Adışen E, Kadıoğlu Özer İ, Aksakal AB. Turk J Med Sci. 2019;49(1):238-244. Published 2019 Feb 11. doi:10.3906/sag-1806-44
Conclusions: All data suggests that five months of isotretinoin therapy in AV patients causes insulin resistance and the increase in insulin resistance is not dependent on age, BMI, BFM, and lipid levels of these patients.
Although this diabetes causing “side-effect” of accutane has been reported on for decades now, as usual it is downplayed and mostly ignored by the medical establishment. Here’s a great example:
Association Between Oral Isotretinoin Therapy and Unmasked Latent Immuno-Mediated Diabetes Ilaria Dicembrini, MD, Gianluca Bardini, MD, PHD and Carlo M. Rotella, MD
It is reasonable that latent autoimmune diabetes in adults (LADA) could be clinically revealed by drug-induced insulin resistance. In this case, the only remarkable change of lipid profile consisted in a reduction of HDL cholesterol during isotretinoin treatment; therefore, the previously reported physiopathological hypothesis (1–4) is not completely supported. However, this is the first report of an association between isotretinoin and an unmasking case of autoimmune diabetes.
Isn’t that a brilliant conclusion? Their ridiculous BS excuse is that the diabetes was already patiently sitting there just waiting to be “unmasked” by accutane use. They want you to believe that: No, no, wonderful accutane didn’t cause the disease, it just “unmasked” it. Who could buy such ridiculous nonsense and pharma propaganda? These are MD’s and PhD’s, no less, making such an idiotic claim. What about the many other disease conditions accutane has proven to cause? Were they then just “unmasked” too?
But, my point here is that we now know that many of us are getting small daily doses of “accutane” via our food sourced vitamin A intake. Thus, if a spiked dose of accutane is proven to cause diabetes, then obviously many low doses, but over a longer period of time, can have the same cumulative result. So, it’s just a matter of dose and time.
A lower range stress tests – Gestational diabetes.
“In the United States, about 1% to 2% of pregnant women have type 1 or type 2 diabetes and about 6% to 9% of pregnant women develop gestational diabetes.”
But, why and how does getting pregnant cause a woman to develop diabetes? That seems like a pretty high price to pay for having children. Something that women have been doing for millions of years now. Once again, there’s no way that nature could be that foolish for this to be normal.
Of course, the big assumption made by endocrinologistsis that gestational diabetes is caused by some vague hormonal imbalance. But, they in no way can explain why it only happens to some women. More importantly, it in no way explains why it’s become much more prevalent over the last few decades and the large regionally disparities in incidence rates.
However, retinyl ester levels doubled in the non-supplemented group immediately after the race (p < 0.001), whereas in the supplemented group similar high levels were observed not until 24 h post-racing (p < 0.001). The high levels of retinyl esters were paralleled to some extent by an increase in plasma triglyceride concentrations, which were significantly higher 24 h post-racing than immediately before (p < 0.001) and after exercise (p < 0.001) in both groups. The increase in retinyl ester concentrations might be indicative of their mobilization from liver and adipose tissue.
Thus, a sustained increased heart rate / blood flow stirs up more retinyl esters out of the liver and brings it into circulation.
A similar effect happens in women during pregnancy. Of course, it’s not just for 24 hours, rather it’s sustained for 7 or 8 months.
During pregnancy, the amount of blood pumped by the heart (cardiac output) increases by 30 to 50%. As cardiac output increases, the heart rate at rest speeds up from a normal prepregnancy rate of about 70 beats per minute to 80 or 90 beats per minute.
With that increased heart rate, more of the highly toxic retinyl esters are swept into circulation. Of course, the amount is probably proportional to the concentration already stored in their liver. Remember that retinol outside of the RBP can pass through cell membranes within about one millisecond. With that, there will definitely be a higher rate of conversion into retinoic acid. That prolonged elevated retinoic acid level would certainly explain the development of gestational diabetes. It would also explain other adverse accutane “side-effect” like conditions such as postpartum depression.
Quite interestingly, the same phenomenon has been observed in women recovering from breast cancer. Women who adopt a strenuous exercise regimen post cancer treatment have a much higher chance of their cancer recurring as opposed to women who only adopt a moderate exercise regimen. Likewise, emotional stress can have the same effect. This is why many people have reported that their first encounter with autoimmune diseases and cancer occurred shortly after a period of sustained emotional stress.
If this theory of vitamin A toxicity causing diabetes is correct then we might be able to confirm it with some intervention type studies using low vitamin A diets. There are indeed such studies. Let’s first consider Walter Kempner’s all rice and sugar diet. Kempner had his diabetic patients follow this diet for a period of up to 10 years and they had great results in reversing diabetes, obesity, and diabetic retinopathy.
Although some of his patients appear to have taken vitamin A supplements there’s no record of exactly what group those patients were in. Also, it’s very hard to know how much of it would have been absorbed on such an extremely low fat diet. Naturally, I think Kempner’s all rice and sugar diet is ridiculous and very dangerous. However, it completely contradicts the mainstream thinking on the role carbohydrates and sugar play in diabetes. None-the-less, it is very good evidence that we are on the right track here thinking that vitamin A toxicity is at the root cause of the disease.
Next, there’s another extreme diet from about the same era that had similar great results in reversing diabetes.
Blake Donaldson’s diet is the complete opposite of Kempner’s rice and sugar diet, yet it yields the same results with regards to reversing metabolic disease and diabetes. This “big fat steak” diet it’s now seeing a huge resurgence in popularity today. It’s called the “carnivore” diet. Why has the carnivore diet become so popular? Because it works! Like it or not, we have to look at the real-world results.
How can we explain these two diametrically opposed diets yielding effectively the same results in reversing diabetes? The common factor is that they are both inadvertently extremely low vitamin A diets. I think the carnivore diet is vastly superior to Kempner’s rice and sugar diet. But, in a way, when you combine these two dietary intervention studies they somewhat mutually exclude macro nutrients as being a major causative factor in diabetes. Therefore, that requires us to look deeper for mechanistic molecules. I say we go with putting the blame on the molecule who’s proven and very functional definition is one that destroys our stem cells. Yes, vitamin A is a stem cell killer.
Zinc – here it is yet again.
As with many enzymes, zinc is a key atom needed for the formation of insulin. Insulin is itself a protein based hormone.
The Structure of Insulin: Zinc is shown as the two magenta coloured spheres in the ribbon diagram on the right.
So, with background vitamin A toxicity putting a higher demand on the needed detoxification dehydrogenase enzymes, that could significantly reduce the availability of zinc needed for insulin production.
Could it be this simple?
For me at least, there’s no doubt that vitamin A toxicity is causing the diabetes and obesity epidemics. But, that’s just my own conclusion on it. With diabetes now being a major pandemic, it’s rather imperative that we find out. So, if you can, please help by tracking your A1C or blood glucose levels as you progress with this diet. You can then add more evidence (pro or con) to the case.
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.
I’ve had a number of people asking me to get a vitamin A test to see where my serum levels are now at. Of course, I was very curious about that too. It sounds simple enough, but it’s not. Here in Alberta, vitamin A testing is lumped in with vitamin D testing and our socialized medical system has stopped providing discretionary testing for these vitamins. Too many people were requesting the vitamin D test and it was costing the Province millions of dollars. Thus, it appears that they took the position that since “we know” that almost everyone is vitamin D deficient anyways, there’s no need to continue testing for it.
Since we can’t get enough vitamin D from food to meet our body’s needs, Alberta Health Services recommends that all healthy Albertans take a vitamin D supplement.
Here, they’ve provided the blanket recommendation that nearly everyone should just supplement with vitamin D. Yes; our medical experts think that we all should supplement with a vitamin that can also become toxic. Doesn’t that sound familiar? In the context of vitamin A, it’s:
Practical, reliable, field‑based techniques for assessing vitamin A status are increasingly in demand. Not so much to determine whether particular individuals need vitamin A – at 4¢ for 200,000 IU it will always easier, cheaper and safer to assume that they do – but as a way of identifying deficient populations that require community-based intervention.
Source: Vitamin-A Deficiency Health, Survival, and Vision Alfred Sommer and Keith P. West
Yes, it’s the same sordid story, just a different potentially toxic vitamin. Anyways, it took a bit of wrangling, but I was finally able to get the tests. The Results:
(Below low normal)0.1µmoI/L
With the following advisory warning: “Vitamin A levels less than 0.4 µmol/L correlate with severe deficiency. Supplementation is advised.”
Although it’s not the 0.0 µmoI/L value I was hoping for, it’s still extremely low. The average for men my age is more like 2.2 µmoI/L.
Therefore, my level is about twenty times lower than normal. Also, compare my serum level to the 1969 case study of the young man in Britain I’d referenced along with the Vitamin-A and epilepsy: A dietary contretemps study by Sharman IM, Stern G. After 5 ½ years of eating a vitamin A free diet he succeeded in getting his serum levels down to about ~0.2 µmoI/L. In that report, he was said to have had the lowest serum levels of vitamin‑A ever recorded in Great Britain. Now, with my levels down to 0.1 µmoI/L, I just may have beaten his long-standing record. I’ll continue with my diet to see if I can achieve the 0.0 µmoI/L within the next year. Getting to absolute zero is obviously hard to achieve. It just might be an asymptotic drawdown function. Or maybe the test is not designed to be accurate in this abnormally low range?
My vitamin D levels are at 72.0 nmol/L. Here in Alberta the – desired normal range is 80.0 – 200.0 nmol/L. I’m a bit on the low side, but not overly so. In US units that 72.0 nmol/L equates to 29 ng/ml. So, it’s still very close to being in the normal, or even in the optimal, range depending on whom you ask.
A few other people have suggested that my original health issues were due to a vitamin D deficiency. However, that assertion is completely nonsensical for a variety of reasons.
I had lots of vitamin D in my diet leading up to my disease conditions. Vitamin D did not prevent me from getting the diseases.
I then fully recovered from all my disease conditions by eliminating vitamin A, and not by adding vitamin D.
There’s been a massive amount of vitamin D supplementation going on here in Canada, and in other western countries too and there is no corresponding massive improvement in our rates of the chronic diseases. And forget about seeing massive improvements in disease rates, there’s been no improvement. Sure, vitamin D is probably helping people cope with the diseases, but it is not completely curing them either. So, clearly, a vitamin D deficiency is not at the root cause of the disease. Maybe vitamin D is acting much like many of the pharmaceutical drugs, and is just abating or blocking the symptoms?
Most importantly, the very concept of a vitamin deficiency is what has gotten us into this giant mess in the first place. I really have no research interest in vitamin D either. All I know is that vitamin D has been used as a rat poison for decades, and that is an absolute fact. Next, consider that rats are the de facto model used to test the toxicology of drugs and other chemicals. Yet, somehow, we are supposed to be so credulous and believe that vitamin D magically gets a free pass on it, and supplementing with it is somehow good for us? Sorry, I not buying it. I’m going with that real-world evidence and calling it for what it is. No one can argue that it’s not a toxic substance at high doses. Obviously, it is far less toxic than vitamin A. Since vitamin D binds to the same “cellular receptors” as does vitamin A then it’s possible that it just blunts the potential toxicity of vitamin A. It may be that vitamin D only appears to be so beneficial in bone growth and maintenance due to it obstructing the osteoporosis causing effects of vitamin A? I don’t know. I am not an expert on it. But, we should be careful with it. For now, I’ll stick with my single-minded focus on investigating vitamin A.
While doing the background investigation for my two earlier e-books, I often saw similarities between many of the aspects and characteristics of the chronic diseases and those of cancers. It was especially so for breast cancer. Thus, I’ve looked at the breast cancer topic a bit more. It has by no means been an exhaustive investigation. However, it has led me to two conclusions.
Breast Cancer is caused by a poisoning.
The primary causal toxin responsible for that poisoning is vitamin A.
I’ve tried to keep this e-book short. But, I think there is still ample amounts of evidence presented in it to sufficiently back up the above conclusions. As with my other e-books, this one is free. So, please download this e-book, and feel free to share it with anyone you want. All I ask for in return is that you comment on it as you see fit.
Another year has gone by, and now I owe my loyal followers an update. In a nutshell, here it is: I am still very much alive, doing quite well, and remain eczema free. So, that’s nice. Oh, and yes, I am continuing to live on my vitamin A elimination diet. That’s nice too.
But, I’ve not been sitting idle regarding the vitamin A topic either. In addition to my day job, and other life responsibilities, I’ve spent more time investigating the history and nuances of the vitamin A story. This investigation has now led me to make a rather profound discovery. That discovery is that vitamin A is not a vitamin, at all. Nope; in no way is retinol, nor it’s precursors, a vitamin. That grand theory and the esteemed vitamin label given to this toxic molecule is rooted in nothing more than botched science.
Of course, that’s not just my opinion, and no, I am not delusional. Rather, you’ll soon see that it is simply a fact. So, if you are like me, and have been wondering why the symptoms of so-called vitamin A deficiency are a perfect match for those of vitamin A toxicity, you’ll get the answer to that little 100-year-old mystery.
I’ve documented this investigation in a new eBook. Like with my prior eBook, this one is completely free too. There are no hooks or gotchas to it, nor advertising associated with it. There’s no monetary gain in any of this for me, or anyone else. However, there’s a gigantic amount of money being made in attempting to treat the endless autoimmune diseases. Thus, the title: Poisoning For Profits.
Please download the eBook and share it with as many people as you like. All I ask in return is for you to please comment on it as you see fit. Therefore, please feel completely free to contact me with any feedback and questions.
Like always, you most certainly should not just take my word, or anyone else’s word, on any of this. Rather fantastically, you get to conduct a very simple in-home experiment and prove the science of it. You’ll get to see the results of that experiment with your own eyes. In doing so, you’ll get to participate in one of the most important health science experiments ever conducted. Science just does not get to be any cooler than that.
About a year ago, I posted my initial theory that low dose chronic vitamin A poisoning was causing the epidemics of Alzheimer’s, Crohn’s/IBD, and eczema. That blog post was so long, and rambling, I doubt that many people even bothered to read it. Of course, there was a bit of a “just some wacko on the internet making absurd claims” sounding tone to it. After all, the entire gist of that theory was admittedly pretty crazy. Nonetheless, I was reasonably confident in making those assertions. Now, after a year of more investigation, I have no doubt whatsoever about it.
But, to have any credibility I needed to fully recover from my eczema condition before posting this update. It has taken a long time for me to make that complete recovery, and there have been a few setbacks along the way. The biggest challenge has been going through another cold, dry winter here in Alberta. Not only have I now fully recovered from my eczema, but I have also seen other significant improvements in my overall health too. More importantly, this extra time has allowed me to learn more, to put together more information, and to gain a much better understanding of the real mechanisms of these diseases. Lastly, I wanted to have gone on a near zero vitamin A diet for at least a year and a half too.
What I’ve learned is quite surprising, and will probably still be almost downright unbelievable for many people. Nevertheless, the truth is what the truth is. Therefore, this is mostly a good news story. It should be a majorly good news story for anyone afflicted with these diseases. It’s also a wee bit of a bad news story at the same time too. That’s because once you understand the mechanism of these diseases, you’ll see that it is going to take a long time to recover from them. The scope and magnitude of the devastation to the body’s cells and organs could be enormous, and it is simply going to take a long time to allow the body to recover and repair itself. Therefore, no magic pill is going to cure you. But, making a significant diet change probably will.
“If a sick person is fed, one feeds the disease.”
The first stage in recovering from these diseases is that you need to immediately stop poisoning yourself. The second stage is to give your body the time it needs to heal itself. Even though you won’t experience a full recovery right away, you should experience at least some improvement by the first three to four weeks, assuming you take this very seriously.
With that, let’s move on to other goods news aspects of the story. The good news is that these diseases are not at all what we’ve been told they are. They are not some incurable, remainder of life disease condition. The human body is not some weak, feeble machine that is prone to self-destruction like this. These diseases, the autoimmune diseases, of Crohn’s, colitis, Lupus, eczema, MS, psoriasis, asthma, arthritis, diabetes, celiac, Sjögrens, vitiligo, and others are indeed rooted in vitamin A poisoning. These are not some spontaneously occurring, or just random bad luck, diseases. That ridiculous concept is entirely wrong. They are completely not the result of a defective immune system either. They are auto-poisonings that cause the immune system to respond in the way it does. The only bad luck part here is that you probably live in a Western country that has fortified its national milk and dairy products with the very chemical that causes these diseases. Somehow, modern medicine has ignored what Hippocrates knew all too well some 2,500 years ago.
It is thus with regard to the disease called Sacred; it appears to me to be nowise more sacred than other diseases, but has a natural cause from which it originates like other affections. Men regard its nature and causes as divine from ignorance and wonder, because it is not at all like to other diseases. And this notion of its divinity is kept up by their inability to comprehend it, and the simplicity of the mode by which it is cured…
Hippocrates, On the Sacred Disease
There’s more good news here too. Many of the chronic thought to be brain diseases are also manifestations of chronic vitamin A poisoning. These include Autism, Alzheimer’s, ADHD, many cases of anxiety, chronic depression, and very likely schizophrenia too. Additionally, this same poisoning is the very root cause of many incidences of kidney disease, and non-alcoholic liver disease too. It is also a very significant factor causing obesity. It is most certainly also the very root cause of cataracts.
Now any reasonable person should assume that claiming that this long list of diseases as being caused by one common poisoning is completely absurd. I fully understand how absurd sounding these claims must be. On the other hand, it is not at all absurd sounding after you learn that this one chemical is indeed capable of poisoning every single cell in the human body. Additionally, whatever is causing these diseases, it has to be something amazingly ubiquitous in our environment. This is no ordinary poisoning either. This poisoning is a doozy, because it very slowly poisons the entire body, and thereby starts to destroy nearly every tissue in the body. Moreover, it coerces the ever powerful immune system into destroying the body too, the said to be “defective” auto-immune response.
The key to understanding all of this is the fact that all tissues associated with the chronic diseases, the thought to be diseases of aging, and the believed to be diseases of childhood, are all diseases of the stratified epithelial (and endothelial) tissues. Therefore, a gastroenterologist is dealing with the same tissue type (structure) as an ophthalmologist, and so is the dermatologist, the cardiologist, and the nephrologist, etc. The organ (the location of the disease, the gut, the eye, the skin or the kidneys, etc.) is irrelevant. The various named medical specialties are all attempting to treat the same tissue structure, it’s the stratified epithelium, with its all critical basal membrane. The subsequent downstream consequence of the body’s attempted defense of this endless destruction leads to bone loss, osteoporosis, and that directly leads to the long-term disruption in the balance of blood chemistry, resulting in chronic ischemic damage in the brain. Obesity is another defensive action taken by the body in trying to protect you from this self-destruction of the epithelium.
The takeaway here is that the chronic diseases of the inner ear, eyes, lungs, skin, GI tract, kidneys, pancreas (diabetes), liver, nose, throat, reproductive tissues, cardiovascular, myelin sheaths lining the nerves (MS), and all tissues with a cilia, such as of the ovaries, etc. are ALL epithelial diseases (it’s the slow and chronic apparent self-destruction of this TYPE of tissue). But, it is not some mysterious self-destruction going on, it is a slow poisoning. Surprisingly, there is only ONE food based poison known to medical science that can even possibly be causing it. There is a ton of medical research proving this fact, and it has been proven beyond any doubt. Therefore, this is not just a theory.
Paradoxically, it is also believed to be proven that a shortage of vitamin A causes the very same destruction of the stratified epithelial (and endothelial) tissues. Would it not be fascinating to find out why we have this striking paradox? I’ll publish a follow-up post on how the early researchers completely botched it. The studies proving the consequences of vitamin A deficiency showed nothing other than the incredible toxicity of vitamin A. These early researchers made some tragic mistakes, and the resulting consequence of those mistakes is the outrageous rates of chronic disease we now face in the developed countries.
Using the term “poisonings” might be somewhat dramatic sounding too. However, I have no intention of being dramatic sounding. I am just calling it for what it is. Once you consider the geographic and national clustering of these diseases, there’s no question that they are poisonings. Nonetheless, to be less dramatic sounding, let’s just use the term “abnormal underlying conditions”.
Secondly, once you understand that these diseases are not normal in the human body, then it is easy to consider that it is some abnormal underlying conditions causing them. When these underlying conditions persist, the diseases develop. The only difficult aspect in understanding that these diseases are indeed poisonings is the extended time frames involved. We are usually talking about decades of time. Basically speaking, a toxin is very slowly accumulating in the body at various locations. Yet, paradoxically, there is also a ton of complexity involved in the process. As that toxin is accumulating the body is also mounting its standard defense measures against it. However, over time the body’s defensive measures are worn down and eventually exhausted. Once that happens, the body crosses a tipping point into diseases. You will never recover from the diseases unless you change the underlying conditions that are causing them.
I am completely, and one hundred percent sure about the above statements. However, it does not matter one little bit about what I am sure of. What only matters here, is what the evidence says about it. And over the last year, I’ve been spending my spare time on collecting that evidence. I’ve been gathering that evidence and making the connections between it all. I am publishing this in a free eBook. The eBook is available using the links below. I’ve put this information into an eBook form because it is now just way too long to include in a blog post. The book is entirely free. There are no hooks or catches to it. There is no advertising, or any monetary gain in this book for me, or anyone else. The only cost to you is your time in reading it. This book is intended for the people who have these diseases, and for their families. Here’s the download link: Extinguishing the Fires of Hell.pdf
You can freely share this eBook with anyone, including your doctor, and I highly encourage you to do that. However, I don’t expect much of a positive reaction from doctors on this topic for several reasons. Firstly, it would take an incredibly brave doctor to follow this evidence to its logical conclusions. Secondly, most doctors have more or less had their hands tied. For many physicians, they cannot be recommending a diet change to treat diseases. Thirdly, medical science has been completely over analyzing these conditions and have therefore missed the most obvious aspect to them. That is the fact, that they are poisonings. Ironically, the key to understanding these diseases is not found by looking down through a microscope, but rather by looking at world maps. Moreover, in the near term, we are far more interested in knowing what is poisoning us, rather than knowing the exact microbiology of how it is poisoning us. Of course, the microbiology aspects of this poisoning are of huge scientific and academic interest. It will give us a much better understanding of how the body really works, and importantly the information needed to develop the right treatment and antidotes. Therefore, a good chunk of my investigation was focused on proving that these diseases are poisonings and exactly what poison is responsible for them.
The critical information you need to know is that the rates for these diseases in North America, and selected other industrialized countries, are a staggering 50 to 400 times higher than compared to the non-industrialized ones. When you stop and really think about it, there is only one plausible explanation as to why and how this has happened. Quite simply, it is because these diseases are poisonings. From that basic understanding, then the next question you need to ask is what known potential toxins in our common foods even have the capability of causing these diseases? The rather shocking answer to that question is that there is only one substance known to medical science that can do so. That chemical is vitamin A.
On the one hand, it is just that straightforward. Yet, on the other hand, it is a very tricky, and almost devious poisoning that slowly sneaks up on us. For most adults it usually takes decades. Sadly, kids are not so lucky because they are far more susceptible.
Naturally, I welcome any and all feedback. More than that, I invite anyone to try to challenge this finding. But, please do it publicly, here on this blog, or anywhere else. All I’ll ask is that you use your real name, and job title when doing so. I am just asking you to please go on public record as having refuted this theory. Obviously, you’ll need to have very solid scientifically supportable evidence backing your position. This investigation is about science and the facts. It is not about opinions, nor is it about quotes from so-called experts.
When I refer to evidence here, most people might be expecting complicated chemical equations, detailed and complex biological processes, glossy pictures, and downright virtual fingerprints. I think that kind of evidence is going to be pretty hard to come by in disease research, and it would be difficult to prove the case absolutely, and conclusively in chronic diseases other than in infections.
However, I am indeed providing much of that level of evidence here. I am providing pictures, biological processes, and references to massive amounts of data, and (inadvertent) large-scale clinical studies to make the case. But it is not to some extreme level of scientific sophistication, and rigor. Maybe a bit oddly, the answer to solving these diseases is not found so much in the minutia. Rather, the answer shows up and becomes entirely apparent when you take several steps back and look at all of the evidence collectively, and thereby see the bigger picture. There are some other surprising aspects of these diseases that have shown up in my investigation. Firstly, much of this information has been well known to medical science since about the 1940s. Secondly, you can literally see the large amounts of this toxin sitting in the skin, and you can see it with your own eyes. Thirdly, it is the very same, and the one chemical that is known to medical science that has been clinically proven, and proven millions of times over, to cause all of the symptoms of all the autoimmune diseases combined. Additionally, there is only one toxin (from foods) known to medical science that can possibly be causing osteoporosis. It is also the one chemical known to medical science that will cause the depletion of your tissue’s stem cells, and thereby cause the corresponding sclerosis of your epithelial tissues. It is the one chemical, therefore, capable of causing the pigment loss occurring in vitiligo. You can see this with your own eyes too. It is the one chemical that will cause the skin to shed and flake off as seen in eczema. It is the very same chemical that is scientifically proven to cause inflammation and the actual immune response we see in these diseases. Amazingly, it is the same chemical that has been proven to cause the head to toe destruction of the human body, and it has proven it millions of times over too. The points I’ve just made are a sampling of the details of the evidence you can dig into by reading the eBook.
Lastly, and rather incredibly, the very functional definition of vitamin A not only implicates it here but it also provides us with the unique virtual fingerprints on it. I could almost not even wish for more or stronger evidence. Everything I’ve found here is completely scientifically proven, and well-documented.
You’ll also see indisputable proof that these diseases are indeed poisonings. When you combine all of these facts, you should be left with no doubts. The bottom line here is that there is only one chemical known to medical science that can even possibly be causing these diseases. Very unfortunately, we’ve all been drinking it in our milk, eating it, and feeding it to our kids. The experts have seriously let us down and misled us. I believe that the vitamin A supplementation of our foods will go down in history as being one of the biggest scientific blunders of our time.
Don’t let the never-ending excuses thrown up by the naysayers and cynics distract you from pursuing the truth. The naysayers have not even begun to solve these diseases over the last fifty years, and they likely wouldn’t have solved a single one of them in the next fifty years either. Don’t let others with some financial interest try to talk you out of pursuing it either. Be strong, brave, and consider the evidence I am presenting on its own merits. This theory is not impossible. On the contrary, based upon the mountain of evidence here, it is highly probable. It is also not a difficult concept to understand either because this exact process is abundantly documented to be precisely what happens with this toxin in the human body. Additionally, and quite surprisingly, there is only one possible explanation as to why over 100,000,000 people in North America are now sick, and more are getting sick every single day.
To illustrate the point, imagine that you and your business partner have a company safe containing all your cash and valuables. There are only two people in the entire world that have a key to this safe: you and your partner. Your partner’s name is Joe Vital, and he is an unyielding type A personality. He has an immense influence on everyone he comes into contact with. With that, most people call him by his somewhat peculiar nickname “Vital A”. Then one day you open the safe, and everything is gone. You confront “Vital A”, and he’s sitting there red-faced, sweating, and has a plane ticket to South America in his pocket, and denying any part of it. His financial supporters are also steadfastly backing him and are waving their hands trying to distract your attention to elsewhere. So, just who do you think emptied the safe? You might not want to admit that your old friend has betrayed your trust, but you just now have to go with the evidence on it. There is only one possibility here. Of course, the cash and valuables in this analogy are your health; the calcium sucked out from your bones, and the all-important stem cells robbed from your skin, eyes, pancreas, kidneys, liver, other tissues, and even your brain.
Most importantly, regardless of what I say, or what anyone else has to say, the very final say, and evidence, on this is now up to you. You must now take action on it, and ultimately prove it one way or the other.
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