I’ve been a bit quiet for the last six months. But, I’ve not at all lost interest in the vitamin A research topic. It’s just that, like with millions of other families, we’ve been significantly impacted by the COVID-19 crisis. Fortunately though, no one in my family, nor myself, have been sick from COVID.
Redoing the 1925 Wolback and Howe study
In last year’s community survey, and in forum posts, I inquired about and wrote about interest in redoing the 1925 Wolback and Howe study. Towards that goal I had submitted a proposal to have this study replicated at an American University. However, due to the outbreak of the COVID pandemic, that proposal was cancelled.
This does not mean that we won’t be redoing this study at all. Rather, it just needs to be put on hold until after things get back to normal. I’m still very interested in having this study replicated. If you want to help me to get it re-organized please contact me directly.
Detox setback / diet failures / diet successes
The detox setback cycle is still being encountered by too many people. It’s often not short term and is causing people to abandon their low vA diets. In the past we’ve had several theories as to why people are encountering the setback cycle. We’ve suspected a vitamin B deficiency due to increased demands of higher carbs etc. on the B vitamins. We’ve suspected the lack of zinc and other resources needed to sustain the increased requirement for ADH and ALDH enzymes. We’ve suspected that a possible increase in protein intake is causing a surge of stored retinyl esters being released from the liver into bile, and with that the addition vA is being reabsorbed into circulation.
Probably all of the above suspected mechanisms are at play to some degree. Of course, it’s going to vary by individual. Whatever the reasons and mechanisms are, we’ve still not pinned it down enough to where people can reliably avoid getting into this detox state. I see this as a very serious problem, and one that we need to solve. But, it’s way beyond my capabilities to come up with a solution. We probably need some dedicated research on it.
Of course there’s a lot of good news with the low vA diet too. We are still seeing success stories. I hope there are many more successes as more people get into year 3+ with their low vA diets.
Over the last six months I’ve been looking more into how and why vA toxicity is likely causing both Type I and Type II diabetes. There’s actually a lot of research back over the last 30 years that supports this theory. So, diabetes will likely be my primary topic of interest next year. I’ve gotten a private email (not shared on my forum) from a parent about their child who has reversed Type I diabetes using a low vA diet. Although it is just one case, I see it as being really important. Firstly, it’s so important to know that the disease can be reversed, and is not always life-long. Secondly, if reversing the disease has happened once, it can most certainly happen again.
My personal health remains good. I’d say that I’m still seeing small improvements; such as the last few spots of dry/ damaged skin are improving. In August I’ll post a more comprehensive health assessment with my 7 year update.
I’ve also put up a video sharing my thoughts on the survey results.
For the following questions the instructions were:
For each of the following conditions, please state on a scale of 1 to 10 how severe this condition was BEFORE starting the diet, where 1 is “a minor annoyance,” 5 is “interferes with normal functioning”, and 10 is “severely debilitating.” Then mark how severe this condition is NOW using the same scale.
Therefore, seeing the bars in the charts shift over to the left hand side indicates that the condition is improving or becoming less severe.
I’ve now crossed the six-year mark on my vitamin A elimination diet. That’s a big milestone. I also turned 60 a few months ago. That’s also a big milestone. Except, it’s one that I’d rather not acknowledge as it now places me into the senior citizen category. However, I’ve not entered curmudgeondom just yet.
Like with last year’s update, my health has only slightly improved over this year. However, the accumulation of the annual small improvements is adding up. Subjectively, I’d say that my health is now the best it’s been in the last 10 years. So, as I am getting older I’m getting healthier. I think that’s a pretty neat trick, and especially so when you consider my diet of mostly just three basic foods.
So now, after six years of having virtually no vitamin A in my diet, and for the last three years being officially in a severe deficiency state, I have absolutely no signs of vitamin A deficiency. How can that be possible?
Oh, I know that there are people who’ll claim that it’s the trace amount of vitamin A I get from eating beef that has me still clingy to life. Except, that’s one of the reasons I mostly consume bison. It’s much lower in fat than beef. I buy my bison directly from a rancher here in Southern Alberta. Bison is also not sent to feedlots for finishing, unlike beef where the animals are fed grain and corn. The USDA database reports bison’s vitamin A concentration to be 0 IU / 100g.
Additionally, for the last two years I’ve been making regular blood donations.
I even recently doubled down on it by making plasma donations. Those donations should offset any tiny amount of vitamin A I might get from my food. So, what’s keeping my skin, teeth, bones, and eyes healthy? According to the vitamin A deficiency theory all these tissues should have developed metaplasia or even disintegrated or have become infected by now. But, most importantly, if vitamin A deficiency were a real thing, then I should see at least some early indication of it after six years of virtually no vitamin A in my diet. However, it’s completely the opposite. I have absolutely no sign of it, and I’m just getting healthier.
I had a complete eye exam done a few weeks ago. The results are that my eyes are in excellent health. There’s no sign, like none at all, of any eye disease; no glaucoma, no macular degeneration, no retinopathy. The pressure in the eye is at a low-normal (a good thing). Additionally, I now have no sign of cataracts. My vision is very good. It’s not quite perfect, but it’s still very good for a 60 year-old. The eye doc said that he could give me a prescription for reading glasses, except it would be so mild that there’s not much point in it. If it’s interesting to anyone, I’ve included a link here to the retinal scanning report he provided me. I think this result is very significant because the de facto disease defining conditions of vitamin A deficiency are poor night vision and progressive xerophthalmia. Yet, I have no sign of ANY eye disease, and my day and night vision is very-good to excellent too. Again, how is that possible?
I don’t know about you, but the science that I was taught is that if even a single experiment fails to support a theory, then the theory is wrong. So, it’s time to call it. The theory that so-called vitamin A is an essential “vitamin” needed for eye health, vision, cell differentiation, etc. is simply dead wrong!. Whether you like it or not, it is just a fact. It’s game over for so-called “vitamin” A. Of course, I do know that it will probably take another 5 – 10 years for that to become widely accepted.
I recently had my bi-annual dental checkup. As like for the past three years, everything was fine. No decay, no cavities, the x-rays showed good density in my teeth, and my previous gum recession has nearly completely resolved. After examining my teeth my dentist actually said to me “your teeth look fantastic.” That is the very last thing I ever expected to hear from my dentist regarding my teeth. Although my teeth do feel stronger, smoother and cleaner, I don’t think they look “fantastic”, but hey, I’ll take whatever compliment I can get about them.
This dental result is very important too because one other major sign of so-called vitamin A deficiency is the secession of enamel formation and the development of bleeding gums. Yet, after six years of nearly zero vitamin A intake, my teeth now are in the best shape that they’ve been in in a decade or more. So, what’s all the vitamin A consumption in North America really doing for people’s teeth? It’s clearly not helping. Check this out: CDC: Half of American Adults Have Periodontal Disease
My sleep has remained to be very good, and is always restful. I have no problem falling to sleep quickly. And, as I wrote about before, I continue to dream every night and often experience some rather intense dreaming. So, there’s definitely been some sleep benefit of my low vitamin A diet. I suspect the deeper sleep is mostly due to a drop in cortisol levels.
My weight has remained remarkably steady over the last 4 to 5 years, Most people would probably agree that losing weight is not the difficult part, rather it’s the keeping it off for the long term that’s really difficult. But, for me at least, keeping that weight off has been easy-peasy, like no problem at all.
My physical fitness has remained about the same as it was last year. But, I feel my muscle strength has gotten a bit better. I can now bench-press 225 lbs. Although that’s not particularly exceptional, it’s still not too shabby for a 160 lb senior citizen. My cycling endurance is still good, with long hill climbs being my measurement. I’m telling ya, it’s the rice.
I feel that my cognitive health and mental well-being continues to be very good. My learning ability and memory recall are good, I’m consistently quite calm, relaxed and almost nothing gets me stressed out. Even the occasional hate mail I get, with the childish name calling, doesn’t bother me one bit.
It’s been known for over a decade now that retinoic acid accumulates in the brain, as well in other tissues. It has also been known for decades now too that retinoic acid causes depression, anxiety, significant drops in IQ, and there are hundreds of suicides officially attributed to accutane use, etc. Therefore, it should be of no surprise that reducing the amount of RA nicely accumulating in our brains is going to result in our improved cognitive functioning. I mean, who would have thought it possible?
Updated labs for Cholesterol etc.
My GP would not authorize a requisition for getting updated labs done this year. Last year’s CRP level was <0.3, which is below the detection limit of the test. My HbA1C was 5.1, and my LDL was 1.04 mmol/L and he said that these values are exceptional for a 60 year old. So, his position was that since my current health is excellent, and combined with last year’s lab results, he could not justify the expenditure to our health system.
I really don’t want to personally spend the extra money on getting labs done privately, but am open to doing so if someone wants to help cover the cost.
Blood Glucose levels
I’ve tracked my blood glucose levels for a while now. It seems to hover around the 5.2 mmol/L (94 mg/dl) mark.
That’s a bit surprising considering that I’ve been eating rice three meals a day for the last six years. Maybe rice isn’t so bad for our blood glucose levels after all?
Better tolerance of Hot and Cold weather
One other odd observation I’ve made is that I now seem to be much more tolerant of hot and cold weather. Somehow, my skin and body temperature just adjusts very quickly to the outside temperature. I also almost never sweat in hot sunny conditions. Could this be because I have a lot less of a highly light absorbing molecule in my skin?
Faster wound healing
I’ve noticed that small cuts and bruises heal very fast now. How can that not be a good thing?
In summary, my health remains to be very good. I’ve not been afflicted by the horrible consequences of vitamin A deficiency. I know that I never will – because it does not exist.
But, what we do know, and we know it with certainty, is that vitamin A is a very toxic molecule. We know that the “active form” of vitamin A, retinoic acid, is an extremely toxic molecule. So much so that even back in 1987 the HHS termed it a direct “POISON.” Except, we should all now realize that it is not a vitamin, at all. What is it really? It’s the toxin that has poisoned a large percentage of the human population. It’s also very likely responsible for most of the mysterious chronic diseases slowly killing so many of us, and destroying the lives of our children.
Consider this nice progress report from the CDC on chronic disease:
6 IN 10 Adults in the US have a chronic disease 4 IN 10Adults in the US have two or more THE LEADING CAUSES OF DEATH AND DISABILITY and Leading Drivers of the Nation’s $3.5 Trillion in Annual Health Care Costs
Results: An estimated 43% of US children (32 million) currently have at least 1 of 20 chronic health conditions assessed, increasing to 54.1% when overweight, obesity, or being at risk for developmental delays are included; 19.2% (14.2 million) have conditions resulting in a special health care need, a 1.6 point increase since 2003.
We must do everything we can to turn this situation around.
What’s next for me?
I’ll continue with my diet for at least the next 4 or 5 years. I seriously doubt that I’ll ever again in my life consume any food that has more than negligible amounts of vitamin A or the carotenoids. But, my biggest motivation for sticking to this diet is not for health reasons, rather it’s to prove the scientific point.
I’ll also continue making the plasma donations for at least the next year. Of course, I don’t have some deep hatred for vitamin A. It would be silly to harbor hatred towards inanimate molecules. But, I will do whatever I can to keep expelling every last bit of this vile, poisonous, disgusting, reprehensible and scheming little yellow serial killer from my body.
In October I’ll put up another survey to gauge how people are doing with this experiment. Last year’s survey was put together rather hastily. That’s because that survey was kind of an emergency response trying to uncover why so many people were encountering the detox setback. Therefore, I’d like to do a much better job on his year’s survey. If you have any ideas or questions that you think are important to include in the survey, please let me know, or add a comment on the forum here.
More than 100 million U.S. adults are now living with diabetes or prediabetes, according to a new report released today by the Centers for Disease Control and Prevention (CDC). The report finds that as of 2015, 30.3 million Americans – 9.4 percent of the U.S. population –have diabetes. Another 84.1 million have prediabetes, a condition that if not treated often leads to type 2 diabetes within five years.
Don’t you think there’s a major problem going on here?
That 100 million number should also look familiar. It’s the same as the number of Americans with fatty liver disease slowly creeping up on them. Clearly, something has gone drastically wrong with human health in North America, and worldwide. And, it’s forecasted to just get worse.
The prevalence of diabetes (type 2 diabetes and type 1 diabetes) will increase by 54% to more than 54.9 million Americans between 2015 and 2030; annual deaths attributed to diabetes will climb by 38% to 385,800; and total annual medical and societal costs related to diabetes will increase 53% to more than $622 billion by 2030
To help put that $622 billion dollar cost into perspective, that is almost twice as much as the total amount that all of America spends on gasoline annually. Yes, just the one disease of diabetes is hugely more costly, and of course profitable, than oil! But, that’s still only a fraction of the nearly four Trillion dollars Americans now spent annually on all health care costs. Of course, the human costs and long term suffering are much more devastating. The annual death rate due to diabetes is 2-3 times that of the current Covid-19 disaster. Naturally, we are not talking about just about North America. The diabetes pandemic now afflicts about 500 million worldwide.
If we don’t get this diabetes disease crisis under control it will surely destroy our economy. I do think we can bring this under control… but it’s not going to be easy. Continuing with the current band-aid type treatments is obviously not working. So, to have any chance at effectively turning this crisis around we need to first get to the correct root cause of it.
The last big breakthrough in diabetes research was back in 1921. Canadians Frederick Banting, Charles Best, and James Collip identified and isolated insulin and quickly went on to develop a process for extracting it from animal sourced pancreases. They licensed the patent for that process to the University of Toronto for the princely sum of $1. With that, insulin went into mass production, was priced at pennies per dose, and saved millions of lives. Today insulin is still the primary treatment for the disease. However, insulin is obviously just that; a treatment, and not a cure. And, today the giant pharmaceutical companies have worked their way around that pesky make it free-to-everyone patent and now sell synthetic insulin at what many consider to be extortionary prices.
The question that Banting and Best did not answer was why was the human pancreas failing in the first place? Maybe, like with most doctors today, they too were taught to believe that diabetes and all chronic diseases are just “bad luck”. Sadly, that ridiculous “bad luck” theory of disease causation is very widely accepted and has gone almost unchallenged even today. But, obviously “bad luck” does not cause organs to fail. It’s equally obvious is that the stupid “bad luck” theory is dead wrong because North Americans could not have gotten vastly more “unlucky” over the last several decades. There’s also no way that people living in the American Southeast are significantly more unlucky than those living in the Northwest.
Back in 1921 we did not have an epidemic of obesity and therefore obesity couldn’t be blamed for the cause of diabetes either. And, obesity most certainly can’t be blamed for Type I diabetes since the wasting the disease causes in children is the direct opposite of that. The presumption is that Type I diabetes is just another auto-immune disease, and auto-immune diseases are just more “bad luck”. We are supposed to believe that it’s the confused and rogue immune cells attacking their own host body. Well, if you’ve read my eBooks you’ll know what I think of the “auto-immune” disease theory. In a nutshell, it’s a bunch of rubbish. No, it’s not a confused or defective immune system. Rather, it’s that tissue cells have been poisoned. With their DNA/RNA being poisoned and damaged they then produce defectively structured proteins. To the immune system those defectively structured proteins appear to have come from a foreign source. The immune system then correctly attacks those cells.
To help better understand the root causes of diabetes we need to know that there’s a similar U-shape curve in the incidence rates that so many of the other chronic diseases follow. There’s a high incidence rate in young children, with a drop-off in rate during youth and teenage years, and then a slow progressive climb in rates with age in adults. Therefore, in adults it’s pretty clear that the disease is one of a slow accumulation.
Source: Rogers, M.A.M., Kim, C., Banerjee, T. et al. Fluctuations in the incidence of type 1 diabetes in the United States from 2001 to 2015: a longitudinal study. BMC Med 15, 199 (2017). https://doi.org/10.1186/s12916-017-0958-6
Now visually sync that chart up with the one I presented in my COVID-19 Vulnerability blog post showing the liver vitamin A concentrations by age. Note the huge spike in early childhood.
Obviously, there’s a lag time between the elevated liver vitamin A storage levels and the onset of the disease. Not at all unexpectedly, it does take some time to burn out the pancreas.
More importantly, we need to understand the exponential growth rates in the incidence rates of both Type I and Type II diabetes over just the last few decades. There is simply no way that this can be naturally happening in the human population. Something is clearly causing it to happen. We also can’t confuse something being really common for it being normal. Sure, diabetes is now very common, but in the historical context that is exceedingly abnormal.
Here’s a chart showing the diabetes prevalence rate here in Alberta.
And for across Canada the regional clustering looks like this:
Any disease that exhibits an exponential growth rate and a geographic clustering pattern like this is clearly a poisoning. It’s a slow poisoning from something that is obviously slowly accumulating and or picking away at cells in the body. It’s just that simple.
With the data presented above, if anyone tries to tell you that the root cause of diabetes is somehow rooted in genetics then simply ask them if they finished their grade 9 math.
Okay, now that we’ve agreed that diabetes is the result of a slow poisoning, let’s find out how likely it is that so-called vitamin A is responsible for it.
Type I Diabetes
As shown in the chart above, type I diabetes is most commonly occurring in children. It is considered to be an auto-immune disease where the defective immune system has wrongly killed off the pancreatic beta cells. With that, the pancreas is no longer able to produce adequate amounts of insulin. What “vitamin” do you know of that causes the rapid mitosis and apoptosis of stem cells?
Retinoic acid induces apoptosis by a non-classical mechanism of ERK1/2 activation Alfeu Zanotto-Filho, Martin Cammarota, Daniel P. Gelain, Ramatis B. Oliveira, Andres Delgado-Cañedo, Rodrigo J.S. Dalmolin, Matheus A.B. Pasquali, José Cláudio F. Moreira
Even though RA is involved in differentiation and apoptosis of normal and cancer cells, being sometimes used as adjuvant in chemotherapy, its mechanisms of action involve multiple overlapping pathways that still remain unclear. Recent studies point out that RA exerts rapid and non-genomic effects, which are independent of RAR/RXR-mediated gene transcription.
Yes, that’s the very functional definition of what the active form of “vitamin A” does to our stem cells. So much so, that it is regarded as the essential molecule that’s somehow needed to “differentiate” our stem cells. What does “differentiate” really mean? It means it causes stem cells that normally reside along a basement membrane to quickly mature into adult cells and separate off. This effect and process of vitamin A’s action is abundantly documented in many fields of medical science, and especially so with its use in dermatology and chemotherapy.
Type II Diabetes
Type II diabetes is characterized by the pancreas still able to produce insulin but for some unknown reason that insulin becomes less and less effective. The pancreas tries to compensate for this ineffectiveness by producing even more insulin. The condition is known as insulin resistance.
As with so many other metabolic diseases there’s a circular blame game going on. Many “experts” believe that obesity is the root cause of type II diabetes. But, of course, that can’t be correct because there are many type II diabetics who are lean. Other experts will claim that it’s the diabetes that’s causing the obesity. I think these guys are significantly more correct. But, not precisely correct. I think obesity is the body’s defensive response to a much more sinister and ongoing threatening condition that we need to be protected from. In other words, what if there’s some other driver that’s causing both obesity and diabetes at the same time? Likewise for the assumed to be diabetes caused comorbidities of kidney disease, cardiovascular disease, macular degeneration, dementia / Alzheimer’s, and, and you name it. Is there something else that could cause all of them to happen? Well, you bet there is. Vitamin A toxicity can, and is proven to, cause all these same comorbidities.
Except, what about this insulin resistance condition? What could be causing that? As I wrote about in a previous blog post, researchers are now identifying the association of elevated RBPs with insulin resistance.
“Until 2005, the sole known function for RBP4 was to mobilize retinol from tissue stores and deliver it to vitamin A-responsive cells where it can be converted to retinoic acid for use in regulating vitamin A dependent transcription and functions. In 2005, Kahn and colleagues reported that circulating RBP4 levels affect glucose clearance, with high RBP4 levels inducing insulin resistance (Yang et al., 2005; Graham et al., 2006). Specifically, Kahn and colleagues proposed that adipocyte-derived RBP4 is a signal that contributes to the pathogenesis of type 2 diabetes, linking obesity with type 2 diabetes, as well as other obesity-related metabolic diseases.”
So, retinol is definitely involved in insulin resistance. Next, we need to appreciate that all cellular receptors are actually proteins intrinsically made by the cell. We need to remember that vitamin A (the retinoic acid metabolite) has been shown to cause more than 500 different gene expressions. What are gene expressions? They are changes in the DNA structure that are detectable by variations in the different proteins that a cell manufactures. So, it’s very possible that the failing insulin receptor is just another protein that has been defectively produced as the result of retinoic acid induced gene expressions (a.k.a. DNA/RNA damage).
That outcome is not at all surprising because we now know that RA fractures and fragments DNA.
DNA fragmentation induced by all-trans retinoic acid and its steroidal analogue EA-4 in C2C12 mouse and HL-60 human leukemic cells in vitro Raghda S. Alakhrasa, Georgia Stephanoua, Nikos A. Demopoulosa*, Konstantinos Grintzalisa, Christos D. Georgioua and Sotirios S. Nikolaropoulosb
Abstract: We have recently shown that retinoic acid induces micronucleation mainly via chromosome breakage.
Do you think that that fracturing of your DNA might cause defectively produced insulin receptors and other proteins? I sure do.
How about conducting a Stress Test
As I mentioned in my eBooks, it is very common in engineering to stress test systems and components to their breaking point. Civil engineers do this everyday with concrete samples as a standard quality assurance practice. Jet engine manufacturers will spin new test engines to incredible speeds, and to the point that the engine explodes or otherwise self-destructs. These types of stress tests are very important as they not only tell us at what point a component will fail, it also helps set the safe operating ranges in real-world usage.
Somewhat likewise, if the theory that vitamin A toxicity is responsible for causing diabetes, then we should be able to conduct similar biological stress tests and see if diabetes can be directly induced by it. Thankfully, that stress test has already inadvertently been conducted for us.
The extreme stress test – Accutane
There have been many accounts of people who have developed type II diabetes shortly after taking accutane. It’s even documented as a known “side-effect”.
The effect of isotretinoin on insulin resistance and adipocytokine levels in acne vulgaris patients.
Soyuduru G, Ösoy Adışen E, Kadıoğlu Özer İ, Aksakal AB. Turk J Med Sci. 2019;49(1):238-244. Published 2019 Feb 11. doi:10.3906/sag-1806-44
Conclusions: All data suggests that five months of isotretinoin therapy in AV patients causes insulin resistance and the increase in insulin resistance is not dependent on age, BMI, BFM, and lipid levels of these patients.
Although this diabetes causing “side-effect” of accutane has been reported on for decades now, as usual it is downplayed and mostly ignored by the medical establishment. Here’s a great example:
Association Between Oral Isotretinoin Therapy and Unmasked Latent Immuno-Mediated Diabetes Ilaria Dicembrini, MD, Gianluca Bardini, MD, PHD and Carlo M. Rotella, MD
It is reasonable that latent autoimmune diabetes in adults (LADA) could be clinically revealed by drug-induced insulin resistance. In this case, the only remarkable change of lipid profile consisted in a reduction of HDL cholesterol during isotretinoin treatment; therefore, the previously reported physiopathological hypothesis (1–4) is not completely supported. However, this is the first report of an association between isotretinoin and an unmasking case of autoimmune diabetes.
Isn’t that a brilliant conclusion? Their ridiculous BS excuse is that the diabetes was already patiently sitting there just waiting to be “unmasked” by accutane use. They want you to believe that: No, no, wonderful accutane didn’t cause the disease, it just “unmasked” it. Who could buy such ridiculous nonsense and pharma propaganda? These are MD’s and PhD’s, no less, making such an idiotic claim. What about the many other disease conditions accutane has proven to cause? Were they then just “unmasked” too?
But, my point here is that we now know that many of us are getting small daily doses of “accutane” via our food sourced vitamin A intake. Thus, if a spiked dose of accutane is proven to cause diabetes, then obviously many low doses, but over a longer period of time, can have the same cumulative result. So, it’s just a matter of dose and time.
A lower range stress tests – Gestational diabetes.
“In the United States, about 1% to 2% of pregnant women have type 1 or type 2 diabetes and about 6% to 9% of pregnant women develop gestational diabetes.”
But, why and how does getting pregnant cause a woman to develop diabetes? That seems like a pretty high price to pay for having children. Something that women have been doing for millions of years now. Once again, there’s no way that nature could be that foolish for this to be normal.
Of course, the big assumption made by endocrinologistsis that gestational diabetes is caused by some vague hormonal imbalance. But, they in no way can explain why it only happens to some women. More importantly, it in no way explains why it’s become much more prevalent over the last few decades and the large regionally disparities in incidence rates.
However, retinyl ester levels doubled in the non-supplemented group immediately after the race (p < 0.001), whereas in the supplemented group similar high levels were observed not until 24 h post-racing (p < 0.001). The high levels of retinyl esters were paralleled to some extent by an increase in plasma triglyceride concentrations, which were significantly higher 24 h post-racing than immediately before (p < 0.001) and after exercise (p < 0.001) in both groups. The increase in retinyl ester concentrations might be indicative of their mobilization from liver and adipose tissue.
Thus, a sustained increased heart rate / blood flow stirs up more retinyl esters out of the liver and brings it into circulation.
A similar effect happens in women during pregnancy. Of course, it’s not just for 24 hours, rather it’s sustained for 7 or 8 months.
During pregnancy, the amount of blood pumped by the heart (cardiac output) increases by 30 to 50%. As cardiac output increases, the heart rate at rest speeds up from a normal prepregnancy rate of about 70 beats per minute to 80 or 90 beats per minute.
With that increased heart rate, more of the highly toxic retinyl esters are swept into circulation. Of course, the amount is probably proportional to the concentration already stored in their liver. Remember that retinol outside of the RBP can pass through cell membranes within about one millisecond. With that, there will definitely be a higher rate of conversion into retinoic acid. That prolonged elevated retinoic acid level would certainly explain the development of gestational diabetes. It would also explain other adverse accutane “side-effect” like conditions such as postpartum depression.
Quite interestingly, the same phenomenon has been observed in women recovering from breast cancer. Women who adopt a strenuous exercise regimen post cancer treatment have a much higher chance of their cancer recurring as opposed to women who only adopt a moderate exercise regimen. Likewise, emotional stress can have the same effect. This is why many people have reported that their first encounter with autoimmune diseases and cancer occurred shortly after a period of sustained emotional stress.
If this theory of vitamin A toxicity causing diabetes is correct then we might be able to confirm it with some intervention type studies using low vitamin A diets. There are indeed such studies. Let’s first consider Walter Kempner’s all rice and sugar diet. Kempner had his diabetic patients follow this diet for a period of up to 10 years and they had great results in reversing diabetes, obesity, and diabetic retinopathy.
Although some of his patients appear to have taken vitamin A supplements there’s no record of exactly what group those patients were in. Also, it’s very hard to know how much of it would have been absorbed on such an extremely low fat diet. Naturally, I think Kempner’s all rice and sugar diet is ridiculous and very dangerous. However, it completely contradicts the mainstream thinking on the role carbohydrates and sugar play in diabetes. None-the-less, it is very good evidence that we are on the right track here thinking that vitamin A toxicity is at the root cause of the disease.
Next, there’s another extreme diet from about the same era that had similar great results in reversing diabetes.
Blake Donaldson’s diet is the complete opposite of Kempner’s rice and sugar diet, yet it yields the same results with regards to reversing metabolic disease and diabetes. This “big fat steak” diet it’s now seeing a huge resurgence in popularity today. It’s called the “carnivore” diet. Why has the carnivore diet become so popular? Because it works! Like it or not, we have to look at the real-world results.
How can we explain these two diametrically opposed diets yielding effectively the same results in reversing diabetes? The common factor is that they are both inadvertently extremely low vitamin A diets. I think the carnivore diet is vastly superior to Kempner’s rice and sugar diet. But, in a way, when you combine these two dietary intervention studies they somewhat mutually exclude macro nutrients as being a major causative factor in diabetes. Therefore, that requires us to look deeper for mechanistic molecules. I say we go with putting the blame on the molecule who’s proven and very functional definition is one that destroys our stem cells. Yes, vitamin A is a stem cell killer.
Zinc – here it is yet again.
As with many enzymes, zinc is a key atom needed for the formation of insulin. Insulin is itself a protein based hormone.
The Structure of Insulin: Zinc is shown as the two magenta coloured spheres in the ribbon diagram on the right.
So, with background vitamin A toxicity putting a higher demand on the needed detoxification dehydrogenase enzymes, that could significantly reduce the availability of zinc needed for insulin production.
Could it be this simple?
For me at least, there’s no doubt that vitamin A toxicity is causing the diabetes and obesity epidemics. But, that’s just my own conclusion on it. With diabetes now being a major pandemic, it’s rather imperative that we find out. So, if you can, please help by tracking your A1C or blood glucose levels as you progress with this diet. You can then add more evidence (pro or con) to the case.
“And, like with Wolbach and Howe back in 1925 these researchers are so sure of themselves that they completely ignore the contradictory findings from their contemporaries.”
I’ve been asked to provide supporting information to back up that statement. I’ll share that here in just a bit.
First, you might be wondering why we should care at all about some rat study from almost 100 years ago. However, I think it’s tremendously important. The 1925 Wolbach and Howe study was the one that supposedly definitively proved the essential need for vitamin A, and therefore, the one that solidified and confirmed the concept of it being a vitamin. If they got that wrong, and if we can therefore disqualify that study, then it should go a long way in disproving the entire “it’s a vitamin” claim.
I’m assuming that for most people knowing whether or not vitamin A is truly a vitamin does not matter too much. Vitamin or not, that verdict probably won’t change what they are doing. From a practical perspective, and in the short term, we just need to know that vitamin A is toxic once we’ve accumulated too much of it. We can apply that knowledge and hopefully still recover our health.
However, if we don’t go the extra mile and disprove this “it’s a vitamin” claim then the powers that be will just go on perpetually poisoning much of the human population with it. It will also continue to be very difficult to warn more people about the potential harms of over consuming vitamin A.
Okay, now let’s get back to the 1925 Wolbach and Howe study. One of the most fundamental requirements in scientific experiments is repeatability of results. If results are not repeatable (within some explainable margin of error), then the experiment proves nothing.
Here are some of the statements from the Wolbach and Howe study’s introduction effectively ignoring / dismissing the results of experiments from their contemporaries
Few pathological studies have been made, and the majority of these have resulted in wholly negative results and, therefore, erroneous conclusions as to the sequence of events and importance of infections.
Emmett and Alien in a comparison of changes due to vitamin A and B deficiency respectively in the rat report “no special outstanding pathological findings,” in the absence of fat-soluble A, in contrast to atrophies and hypertrophies found in B deficiency.
Stephenson and Clark failed to find a distinctive pathology in keratomalacia in rats.
Davis and Outhouse 4 studied only the kidneys, spleen, heart, lungs, pancreas, liver, and testes. As they report that the testes were normal in most of their cases, it is certain that either their diet was not deficient in fat-soluble (vitamin) A or that the duration of the experiments was too short.
Cramer, Drew, and Mottram ~ in a study of the effects of vitamin deficiency in rats upon the function of lymphocytes and lymphoid tissue found no pathology in fat-soluble A deficiency.
Wason found no lesions in any organ other than the eyes. She regarded the changes in the cornea as secondary to bacterial invasion.
Meyerstein ~ failed to find any characteristic pathology in either vitamin A or vitamin B deficiency in rats.
There’s yet another study from this era that I want to directly compare with Wolbach and Howe’s (W&H) study. It is:
THE NECESSITY OF CERTAIN LIPINS IN THE DIET DURING GROWTH.BY E. V. McCOLLUM AND MARGUERITE DAVIS.(From the Laboratory of Agricultural Chemistry of the University of Wisconsin.)(Received for publication, June 1, 1913.)
The reason I want to discuss this study is because they detail the diet used, and the outcomes. The diet used in this study was remarkably similar to the W & H study. However, McCollum’s 1913 study was only investigating the “growth” producing effects of some suspected fat soluble factor.
Here’s an example diet McCollum that fed his animals.
Here’s a chart for Rat # 104a (female)
Do you notice something? Up until period III, McCollum’s study diet is nearly identical to the one used by W&H. McCollum’s study diet is supposedly devoid of vitamin A too, yet his animals survive quite well to the 20 week mark, and beyond. Whereas, in the W&H study all of the animals were either dead or dying by the 8th-10th week. In the last two weeks of the W&H study the animals needed to be force fed their ration, and that finished them off. Except, here in McCollum’s study, not only have the animals survived at least 2X longer, there is no mention of sickness or disease, at all. In other words, his animals were probably very healthy, and obviously reproductive, at the 20 week mark. McCollum’s study presents similar results for male rats.
Then to investigate growth, in period III he adds in an egg extract, and the animals do gain weight. However, let’s not jump to the conclusion that it’s a good thing. What would you tell someone today who claims that gaining weight is the medical equivalent to growth? I think you’d tell them that they are confused. But, that’s a small technicality we are not too interested in right now (unless we wanted to consider this an inadvertent obesity causation study).
What’s critically important is that apparently the same diet regimen used by McCollum’s and W&H’s studies yielded completely opposite results. How can we explain that? When combined with the other studies mentioned above from this era , it is very clear that the animals in the W&H study did NOT succumb to a vitamin A deficiency. Therefore, with the diametrically opposing results between the McCollum’s and W&H’s studies, we have no experimental repeatability. Thus, we can’t legitimately derive any scientific conclusion from them. Therefore, the claim that vitamin A is a vitamin is completely unsupported, and is quite bogus.
However, there’s a subtle but very important difference in the diets used by McCollum and W&H. In W&H’s paper they state:
Distilled water, sufficient to make a dough, was added to the ingredients; small cakes were moulded, each containing five gm. of material, and dried in an oven.
For additional information about heat treating milk, and its correlation to early death in experimental animals please read about Wilhelm Stepp’s 1912 work in mice. Stepp kills his mice in just 3 weeks using heat treated milk. And, it looked to me that Stepp’s results (kill rate) correlated with the heating duration times in alcohol. https://academic.oup.com/jn/article/127/7/1255/4728852
Additionally, there is an even more fundamental problem with the McCollum and W&H studies. That problem is now revealed by the modern-day work of Collin Campbell et al with their work on the direct toxicity of casein on its own.
Therefore, with that huge red flag and confounding factor no rat study in history that’s used casein can be considered legitimate and valid. Clearly then, Wolbach and Howe’s 1925 study is complete junk science. Moreover, we have the previously ignored studies from Wolbach and Howe’s contemporaries actually proving that there is no dependency on vitamin A.
The W&H study is the foundational cornerstone of the grand vitamin A theory. Their conclusions were wrong, and they made the assumption that they had narrowed it down to this one molecule. Quite remarkably they made this assumption in 1925 even though the structure of the molecule had not been determined until 1931. Sadly, every vitamin A study since W&H’s has been layered upon that flawed foundational assumption. Very few follow-on researchers have had the courage to stick their heads above the parapet and call this out for what it is. But, there have been a few. Here’s a prophetic quote from Pitt:
… people seem curiously reluctant to recognize just how toxic is vitamin A. I have long asserted that considered as a chronic poison vitamin A is probably more harmful than cyanide, but I have usually been disbelieved …
I think that if modern day researchers stopped fabricating ridiculous follow-on theories and sub-theories to rationalize what they are seeing, and reevaluated their finding through the lens of vitamin A being a toxin, and nothing but a toxin, then all of it will make so much more sense.
The W&H study is garbage science, and needs to be tossed into the trash can. With that, so does the entire bogus claim of this toxic molecule being an “essential” vitamin.
Of course, vitamin or not, there’s no debate about the potential toxicity of so-called vitamin A. But, if we can finally correct the science on it then we might have a chance in stopping the global supplementation nonsense going on. Let’s consider this report:
WHO Library Cataloguing-in-Publication Data Report: WHO technical consultation on vitamin A in newborn health: mechanistic studies, Geneva, Switzerland, 1–3 December 2009. 1.Vitamin A – administration and dosage. 2.Vitamin A deficiency – prevention and control. 3.Infant, Newborn. 4.Infant nutrition. I.World Health Organization. ISBN 978 92 4 150316 7
High doses of retinyl ester are commonly provided to at-risk populations in areas where vitamin A deficiency is a problem. For women, 400 000 IU given as two doses of 200 000 IU at least 1 day apart and within 6 weeks postpartum are being recommended. Vitamin A supplementation programmes have been highly successful in addressing vitamin A deficiency but are not without risk. The doses administered are at toxic levels (200 000 IU retinyl ester is 85 times the recommended daily allowance (RDA) and 400 000 IU retinyl ester is 172 times the RDA). Acute toxicity may occur at dosages >100 times the adult RDA.
Do they warn these women and get their signed informed consent for the likely harm from that toxic dose? I highly, highly doubt it. Of course, they’ll claim that this deliberate poisoning of young women with known acute toxic doses is somehow necessary, ostensibly claiming that it’s to prevent vA deficiency.
But, what’s really going on here? Clearly, it might not be just bad science and there’s another possibility to consider. In the 1970’s the WHO and the global elites were absolutely obsessed with the runaway growth in the human population. It was viewed as the biggest threat to the planet. Then factor in that it’s been known since the 1960s that vitamin A is a reproductive toxin.
Check out the last entry in this table of lethal doses of some common substances:
Then in the 1970s the WHO’s vitamin A supplementation programmes were started up in about 100 countries, and vitamin A was added to the low fat dairy, etc., in North America and to sugar in South America, etc. Then, surprise, surprise, there’s been a massive drop in human fertility around the planet. And, by the early 2000s the WHO had gone mostly quiet about the risk about the global population. The WHO’s primary focus has now shifted to vaccines. Do you trust these guys? I hope not.
What’s emerged with the COVID-19 pandemic is a peculiar pattern of vulnerability. It’s being widely reported that older people are the most severely affected by the infection and are the demographic most likely to die from it. Whereas, children and teenagers often appear to sail right through the infection with only minor symptoms, or the just having symptoms equivalent to a cold or minor flu. Yet, at the lower end of the age spectrum, say in one and two-year-old’s, the severity of the diseases increases again.
Children of all ages are susceptible to COVID-19 and while their symptoms are generally less severe than those of adults, a small percentage — particularly preschoolers and infants — can become seriously ill, according to a new study.
An equally important observation is that many thousands of people have tested positive for having had COVID-19 and yet have remained completely symptom free. Therefore, it’s very critical to appreciate that just getting COVID-19 is not sufficient on its own to cause disease. Clearly, it’s COVID-19 and something else when combined that leads to the disease. What is that something else? We should all be very curious and striving to find out what it is.
In the context of COVID-19 infections, the general assumption is that older people just have weaker immune systems and are thus less able to fight off the virus. Except, it’s not just age that’s the primary factor. Rather it’s a person’s age combined with their pre-existing conditions, or comorbidities, that somehow makes them more vulnerable to having a severe response. Therefore, we can almost right away dismiss that assumption of a “weak” immune system being to blame because it is not at all just older people who succumb to the infection. Some younger people, even in their 30’s, are dying from the infection too. It’s just much more common to have a severe response in these younger people primarily when they have comorbidities. Therefore, the pre-existing comorbidities are the bigger risk factor. The cited highest risk comorbidities are diabetes, obesity, asthma, other autoimmune diseases, and cardiovascular diseases. If you’ve followed my blog for a while now, you’ll know that these are all diseases that I’ve been attributing to long term vitamin-A toxicity.
Let’s see if we can make some sense out of this. Could it be that there’s some mechanism whereby people with a higher level of vitamin-A storage could be more severely impacted by viral infections, and especially that of COVID-19? Firstly, let’s look at some interesting data regarding the liver storage concentration by age. For that, we’ll look at this 1973 study from Mitchell et al.
Source: G. Vaughn Mitchell, M. Young, C. R. Seward, Vitamin-A and carotene levels of a selected population in metropolitan Washington, D. C, The American Journal of Clinical Nutrition, Volume 26, Issue 9, September 1973, Pages 992–997, https://doi.org/10.1093/ajcn/26.9.992
Quite interestingly, here we have a similar U-shaped curve showing up in the data. Note that the horizontal red line at 286 μg/g is the documented toxic level for liver storage. Remarkably, this means that a large number of young children say from 1 to 5 years old are in the toxic range for liver storage. Then, as they get older their liver’s volume increases (roughly as a cubed function of its cross-sectional size) and they outpace the inbound dietary consumption rate. Then, as people get older their liver concentration slowly saturates to where they move into the toxic storage range once again, and through to the end of life. Let’s remember that this data is from back in 1973, just at the beginning of the foolish North American vitamin-A supplementation programs in dairy, breakfast cereals, etc.. Obviously, the liver saturation numbers will be far worse if sampled today. Just imagine the blue U-shaped curve being shifted up higher on the chart to where more people are over the red toxicity line. So, it’s no wonder why so many people are sick and diseased today. They are, by the very definition of the toxic level of vitamin-A storage, beyond that point. This also corresponds quite well with the fact that about one-third of the American population has NAFLD. That’s all bad enough, but could this somehow also make them more vulnerable to viral infections? Well, this has actually been well documented to be the case for a long time. But, for now, there’s one data point on the above chart that we need to focus in on.
What’s documented in the Mitchell study, and in others, is that very young infants have very low (and often even non-detectable) liver storage levels of vitamin-A.
The Amazing Infant Immune System
So, what do you suppose happens to very young infants exposed to the measles virus? Well, amazingly, often nothing adverse happens. That’s correct, they usually remain symptom and disease-free. Their immune system simply clears the virus. Additionally, most of them have probably acquired true life-long immunity from future infections of the measles virus.
Likewise, just what do you suppose happens to a very young infant exposed to the Dengue virus? Well, once again, often nothing adverse happens. Yes, those infants with their supposedly “weak” immune systems just clear the virus.
Next, just what do you suppose happens to a very young infant who is exposed to, and is subsequently infected by, the truly horrifying syphilis bacteria? Very often, they too remain symptom-free, and their “weak” immune systems clear the bacterial infection!
Even more astonishingly, what do you suppose happens to a very young infant who has a finger or toe severed? Amazingly it often grows back! Yes, these very young infants are amazing at surviving and dealing with very adverse events and pathogen attacks. Infants are starting in life with a great, if not perfect, immune system. Sadly, that all quickly changes once the so-called “medical experts” start administering their “health” intervention programs.
Yet, a great misconception persists in medical science in that very young infants are thought to have poorly developed immune systems. One of the primary reasons they make this assumption is because very young kids simply do not respond to vaccinations. Please consider this meta-analyses of the seroconversion rates by age:
Measles vaccination below 9 months of age: Systematic literature review and meta analyses of effects and safety
In a meta‐analyses of 20 papers, the proportion of infants who seroconverted (%SC) depended on the age at MCV1 vaccination. It increased from 50% (95% CI 29‐71%) at age 4 months to 67% (95% CI 51‐81%) at 5 months, 76% (95% CI 71‐82%) at 6 months, 72% (95% CI 56‐87%) at 7 months and 85% (69‐97%) at 8 months.
For the very youngest of children, there is only about a 50% seroconversion (meaning their immune response created detectable antibodies). The seroconversion rates then increase as they get older. Except, this phenomenon is not because their immune system is maturing. Rather, it’s because their serum levels of vitamin-A are creeping up with age too. We know this because the same effect has been studied in fully grown adults. In adults with abnormally low vitamin-A status, they too have a low seroconversion rate of ~50% when administered vaccines. Then, from other studies, we learn that when adults have their vitamin-A levels pre-boosted up before vaccination, then there is a higher “seroconversion” rate of around the more “normal” ~85% rates. Of course, most vaccinations are really low dose deliberate viral infections.
The known low “seroconversion” rate is why most childhood vaccines are delayed until two months of age. Some researchers claim that the extra vitamin-A has “enhanced” the immune response. But, we know that’s not exactly correct. What’s really happened is that the vitamin-A has enabled the virus to more rapidly replicate, and that then results in the “enhanced” immune response. But, do not for one second think that getting a higher seroconversion rate is a good thing to have happen. It’s the exact opposite. It’s clear evidence that higher background vitamin-A levels are resulting in the increased replication rates of the vaccine’s virus. And, vice versa, the run-away viral infection has increased the toxicity of their background vitamin-A levels too.
This is a super, critically, important point to understand. This is the underlying mechanism as to why kids in India and other countries of Southeast Asia can have such a devastating outcome from a measles infection. With high, or even moderate, vitamin-A serum levels, and a lack of sufficient dietary fats and proteins, the measles infection also increases the toxicity of their endogenous and circulating vitamin-A levels! It is also the underlying reason why some kids die when given their vaccines.
What’s going on here? As usual, it’s multifactorial, and there’s much more to the story. What we do know, and also very contrary to widely-held myths, is that vitamin-A actually subdues the immune system. What’s also been documented for like the last 50 years now is that vitamin-A weakens and otherwise damages cell membranes. It also damages the mitochondrial membranes. It’s trivial to see why too. Both the cholesterol molecule and the side-chains of the vitamin-A molecule are made up of isoprene groups. These isoprene groups are the base compound for natural rubber. So, if you’ve ever wondered why the cholesterol deposits surgeons pull out of arteries looks so much like rubber, it is because it is rubber. Ever wonder why the cholesterol deposits are yellow in color? It’s in good part because it has picked up and encapsulated the vitamin-A, and carotenoid molecules, within it.
Carotenoids are incorporated into very low density lipoproteins (VLDL) and exported from the liver into the blood. VLDL are converted to LDL by lipoprotein lipase on the surface of blood vessels. Plasma membrane-associated receptors of peripheral tissue cells bind apolipoprotein B100 on the surface of LDL, initiating receptor-mediated uptake of LDL and their lipid contents.
Source: Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc http://www.nap.edu/catalog/10026.html Page 94
Now, just as cholesterol with its isoprene groups nestles into the lipid bi-layer of the cellular membranes, so too does vitamin-A. This obviously weakens the integrity of the cell membrane.
Could the weakened cell membrane then make the cell more susceptible to viral infections? You bet it can. This has been documented in the context of HIV infections. Supplementing HIV patients with vitamin-A causes a more rapid replication of the virus, and results in worse outcomes. So, we have multiple pieces of real-world evidence that vitamin-A causes a faster replication rate of viruses. What about some laboratory-based evidence? Well, there is indeed, and even specifically for the coronaviruses.
Retinoic acid modification of cell culture used for reproduction of enteropathogenic viruses.
Abstract The 0.001-0.005% retinoic acid injection into the growth cultural medium of prime and continue cell cultures 12-24h before inoculation considerably raised the cell sensitivity to animal entero- and coronaviruses. The entero- and coronaviruses concentrations in cultural medium increased by 10(1.58) and 10(1.68)TCID 50/1.0 respectively. The optimized parameters of the cell culture processing for the enteropathogenic viruses reproduction improvement are proposed.
And a similar phenomenon is observed in the context of Zika infections. Cells being forced into “differentiation” via retinoic acid increased their infectivity to viruses.
Differentiation enhances Zika virus infection of neuronal brain cells
Here we investigated ZIKV infectivity in neuroblastoma SH-SY5Y cells, both undifferentiated and following differentiation with retinoic acid. We found that multiple ZIKV strains, representing both the prototype African and contemporary Asian epidemic lineages, were able to replicate in SH-SY5Y cells. Differentiation with resultant expression of mature neuron markers increased infectivity in these cells, and the extent of infectivity correlated with degree of differentiation.
So, we now have good evidence of vitamin-A (and specifically retinoic acid) promoting the replication of viruses. Of course, we all know that increased background storage levels of vitamin-A simply means more endogenously produced retinoic acid.
None of this is new information. As with most things related to vitamin-A science, it’s been well known about and reported on for a long time. Here’s a great paper from Anthony Mawson discussing the same comorbidity patterns in the context of the 2009 SARS-CoV infections. Back then it was also the people with the pre-existing conditions of heart disease, asthma, and autoimmune diseases who were at higher risks for severe disease and death.
Role of Fat-Soluble Vitamins A and D in the Pathogenesis of Influenza: A New Perspective
Anthony R. Mawson
Department of Health Policy and Management, School of Health Sciences, College of Public Service, Jackson State University, Received 4 April 2012; Accepted 3 May 2012 Academic Editors: M. C. W. Chan, N. Kawai, and Y. Lai
The Symptoms of Influenza A Infection Are Similar to Those of Hypervitaminosis A
As noted, the clinical spectrum of influenza A infection, including avian influenza H5N1, is not restricted to the lung and can range from mild influenza-like illness to severe pneumonia, acute respiratory distress syndrome (ARDS), acute lung injury (ALI), and multiorgan failure . Fever, rhinitis, myalgia, malaise, headache, cough, dyspnea, sore throat, and fatigue are the main presenting symptoms. Complications include pneumonia, bronchitis, or sinusitis, and rarely encephalitis, transverse myelitis, Reye syndrome, myocarditis, or pericarditis .
Mawson does a great job of explaining how and why this can be related to an overload of vitamin-A, and why a low vitamin D/A ratio is a very important factor. Oddly, this paper was not picked up by the major journals, say such as the BMJ, or Lancet. Why was there so little interest in this Mawson paper? Could it be that the medical establishment and the pharmaceutical industry have no genuine interest in understanding what’s really enabling and driving viral infections? Could it be that their primary, if not only interest, is their commercial interests? Of course, it is. These companies have multi-billion dollar vaccine divisions. Therefore, any non-vaccine solution to viral infections would be a serious and direct threat to that ongoing annual business model. Therefore, it is incredibly unlikely that we’ll ever see a non-vaccine based solution developed by the pharmaceutical industry. What if we all came to the understanding that the best way to protect ourselves from viral infections was simply to keep our vitamin-A consumption very low? That could devastate the industry. Therefore, that information cannot be allowed to be developed and confirmed. Therefore, the Mawson paper must be ignored.
The ACE2 Receptors
There’s been a lot of press lately about the important role that the ACE2 receptors play in COVID-19 infections. The virus’s glycoprotein binds to the cell membrane protein angiotensin-converting enzyme 2 (ACE2) and that’s how it gains entry into the human cell.
The novel coronavirus 2019 (2019-nCoV) uses the SARS-coronavirus receptor ACE2 and the cellular protease TMPRSS2 for entry into target cells
Here, we demonstrate that 2019-nCoV-SusestheSARS–coronavirusreceptor, ACE2, for entry and the cellularprotease TMPRSS2 for 2019-nCoV-S priming. A TMPRSS2 inhibitor blocked entry and might constitute a treatment option. Finally, we show that the serum form a convalescent SARS patient neutralized 2019–nCoV-S-driven entry.
Naturally, with the ACE2 receptor being the target site of virus entrance into the cell there’s been a ton of frantic research into looking into ways to block or down regulate the ACE2 receptors.
Correspondingly, there’s been a ton of interest and media attention given to a well-established anti-malaria drug named chloroquine. Here’s a study from back in 2005 discussing it.
Chloroquine is a potent inhibitor of SARS coronavirus infection and spread
Results We report, however, that chloroquine has strong antiviral effects on SARS-CoV infection of primate cells. These inhibitory effects are observed when the cells are treated with the drug either before or after exposure to the virus, suggesting both prophylactic and therapeutic advantage. In addition to the well-known functions of chloroquine such as elevations of endosomal pH, the drug appears to interfere with terminal glycosylation of the cellular receptor, angiotensin-converting enzyme 2.
Therefore, we can see that when the ACE2 receptors are upregulated, viral infection and replication rates increase. Conversely, when the ACE2 receptors are downregulated, viral infection and replication rates decrease.
Yet, something really strange happened with the medical establishment and the mainstream media regarding the potential use of chloroquine as a treatment. These people immediately started attacking it and doing everything they can to discredit it. Why would they do that? Could it be that chloroquine is cheap, off-patent, immediately available and most of all a potentially competitive alternative to the planned vaccine they have in the works?
Dr. Anthony Fauci almost jumps to the podium and claims that the evidence for its effectiveness is only anecdotal, and there is not enough evidence to support claims that chloroquine is effective in combatting COVID-19. But, that’s not quite true. There are existing clinical trials, and back in 2005, even its probable functional mechanism was understood too. Additionally, with very few other immediate options, why not quickly get going on finding out? Why so aggressively downplay it and try to dismiss it as an option? Who and what is he trying to protect?
Why are we no better prepared today for a viral pandemic than were we in 1918?
The last great viral pandemic to ravish the human population was the so-called Spanish Flu of 1918. So, now over 100 years later, we still don’t have any really effective treatments for viral infections. How can that be? After sucking trillions of dollars out of the worldwide economies the pharmaceutical industry has almost nothing meaningful and effective against viral infections. Sure, they have the horrible DNA, RNA chain terminator class of drugs that they claim to be “anti-viral” in action. But, not only are these drugs very expensive, they come with catastrophic “side-effects” that often decimate the overall health of the patient. They are not “medicines”, they are simply poisons that break the cell’s ability to build any proteins at all.
Fortunately, ER and intensive care teams are vastly more capable today in preventing people from dying from viral infections than compared to back in 1918.
What really matters most right now is finding remedies for people most severely affected by the virus. Contrary to the advice of many “experts”, taking vitamin-A is not one of them. The very last thing anyone one should be doing at this time is supplementing with so-called vitamin-A.
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.