The liver stores 80-90% of all vitamin A absorbed by the body.
The liver must, and does, get fatty in response to vitamin A consumed.
The rates and prevalence of NAFLD are so dramatically abnormal and geographically clustered, that it clearly tells us that the disease is a poisoning.
Vitamin A is yellow.
Bonus fact: excessive vitamin A is proven to cause cirrhosis in all kinds of tissues.
What am I missing here? Has no one ever before bothered to ask the obvious question: why has that NAFLDed liver turned YELLOW?
I mean seriously, even a sixth-grader could figure this out. So, why haven’t all the brilliant minds in medical research been able to see what they are looking at? Could it be that they are blinded by all the money they make?
With increasing rates of obesity and metabolic syndrome, nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH) have become increasingly common, such that they are now the most common cause of liver disease in Western countries. This has not gone unnoticed by those in the market of drug development. Where there is a disease to “treat” there is a buck to be made.
One of the goals of conducting our survey was to determine the prevalence of the detox setback condition people were encountering on a low vitamin A diet. Naturally, the primary goal was to see if we could spot any common factors that might be causing it.
As shown in the results, around 50% of people were reporting that their progress had stalled, and eventually, their overall health condition was slowly getting worse with time. But, others reported no such setback and stated they had made pretty good linear progress into better health. These mixed results were a bit of a paradox to me, and I didn’t understand why we saw such widely variable results. However, I felt it was important to highlight the failures, and not to overstate or focus on the successes.
I also wondered why people on the now popular carnivore diet are not reporting the detox setback trap many people here reported on their low vitamin A diet. Maybe, it was just not being reported by the carnivore folks. But, I think it is probably just not happening very often. I think it is a beneficial side-effect of eliminating carbs and not consuming other foods that contain aldehydes while on that diet.
Up until recently, most of my attention on recovering from vitamin A toxicity has been just on eliminating vitamin A from the diet. I was hoping that would be sufficient to enable most people to recover. With that, I didn’t focus too much on the body’s detoxification processes and mechanisms. So, I think we are now moving into the next phase of understanding that process and what’s needed to make it more predictable and successful.
The alcohol dehydrogenase enzymes
Back in October, when I posted the survey results, I had speculated that cauliflower was contributing to the detox setback trap. I still think this is indeed at least partially correct. That’s because several people have now reported back that after dropping cauliflower, they’ve experienced significant improvements. But, it’s not just food sources of methanol and formaldehyde that can overload and mess with the body’s alcohol dehydrogenase enzyme systems. It’s also some of the most common prescription drugs. These drugs include the Statins, the SSRIs, and even over the counter pain killers such as Tylenol. Almost any drug that is metabolized by the liver is going to either interfere with the production of or directly compete for your dehydrogenase enzymes.
The B vitamins of thiamine and riboflavin
I had also speculated that some people might be running into a vitamin B deficiency condition. This was supported by most people on our survey reporting that they were not eating brown rice, or only having it occasionally. But, I was too quick to dismiss this concern when I learned about the new carnivore diet. My thinking about it was that surely the carnivore diet folks would be running into the same vitamin B deficiency issues too then. Except, what I missed is that since the B vitamins of thiamine and riboflavin are needed to metabolize carbohydrates, then the carnivore diet folks won’t be as nearly susceptible to such a deficiency.
Whereas, if people here are eating a lot of white rice and have inadequate sources of the B vitamins (particularly thiamine and riboflavin), they could run into a deficiency situation quite quickly. There’s also some good evidence that vitamin A toxicity increases the demand for the B vitamins. The B vitamins are involved in the process of building the ADH and ALDH enzymes. Additionally, some of the B vitamin deficiency symptoms overlap and mimic those of vitamin A toxicity.
Now, with more feedback from people here, and based on the work from Dr. Garrett Smith, it is quite likely that some people here are running into a vitamin B deficiency. This scenario sure fits from a temporal perspective too. That’s because people here have reported hitting the detox setback in a matter of just a few weeks or a few months. In contrast, others have sailed right through on the low vitamin A diet for a year or more with no such setback.
Some good low vitamin A food sources of the B vitamins are black beans, brown rice, macadamia nuts, sunflower seeds, and coconut water. But, I know that many people are not able to tolerate beans; therefore, directly supplementing might be a better option for them.
I’m most certainly no expert on the B vitamins. Therefore, please use other sources of information, also consider looking into the work of Dr. Garrett Smith. Please contribute your thoughts and experiences on this topic here:
Thank you to everyone for taking the time to fill out and submit the survey. There were about 129 responses in total.
As somewhat expected, the results are kind of all over the place. That was expected because everyone is coming into this from different backgrounds, dietary histories, ages, etc. But, what’s unexpected, and rather clear is that too few people are making steady progress in regaining their health. Even before conducting this survey, quite a few people had reported that their early progress had stalled, or had even reversed as time went on. That’s a huge concern, and it’s the primary motivation that prompted this survey. The survey results confirmed those early sporadic reports. Many more people (~50%) are indeed hitting the “detox” setback and it’s far more common than I had previously thought.
At a very high level, here’s my preliminary assessment of the survey results.
A restrictive diet alone is just too slow, and too unpredictable.
We clearly need an antidote (I think the body has a built-in one, we just need to help activate it, see more on this topic below)
It looks like the people with a big VA supplementation history might be the ones more likely to encounter the detox cycle.
The majority of people have found themselves in this mess via VA supplementation or from accutane use.
Although most people do believe they are on the right track, their real results are still too few / slow.
Many more people have encountered the “detox” setback cycle than what I expected / was aware of. I see this as our biggest problem, and it needs immediate and serious attention.
But, it’s not all bad news, there’s still a lot of good news here too. Although it’s slow going, a lot of people are indeed recovering their health.
What does it all mean?
My private, and previously unstated, criteria for deeming the vitamin A toxicity theory to be considered valid, and on target is that we should see about a 95% success rate for people applying the elimination diet. To help frame the discussion, here are some illustrations (not real data). The following chart is what I think we should be seeing for most people. Of course, we should expect there to be some personal variabilities and small setback cycles too.
However, we are not seeing that trend, and almost not at all. It’s more like this for most people:
Currently, we are nowhere near the target 95% success rate. Maybe it’s still just too early. Realistically, we are probably closer to around a 5% – 10% rate in clear success. Nevertheless, from the survey, 67 of 130 people have still reported having made a significant improvement in their health. Quite remarkably, on the one hand that is still a far higher success rate in recovering from chronic disease than any pharmaceutical drug has proven to do. On the other hand, that particular comparison is such a pathetically low bar, it’s not very useful or meaningful to us.
Regardless of things generally moving in the right direction, something is clearly wrong here too. Either the base theory is wrong ( I don’t think so, but it’s possible), or we are missing some important confounding factors.
One of the early concerns I had about the strict elimination diet is that it removed so many other foods and nutrients, that it is easily possible that we are excluding something else from the diet that in the longer term is essential to our health. Say for example, some of the B vitamins, etc. So, it could really be a deficiency situation building up in resulting in people hitting the “detox” setback cycle. But. I somewhat dismissed this concern when I learned about the new “carnivore” diet being widely adopted. My thinking about it was surely the “carnivore” diet folks would be running into the same potential deficiency issues too then. And, if it’s happening, it is not being reported.
Additionally, over the last year or so, some people here were reporting that their serum VA levels were actually increasing as they progressed with the diet. This also fit with some accounts from published research papers. This makes sense too, because it’s what we should expect when about 70 million Americans adults have NAFLD, and the liver is probably starting to normalize in size and volume. This then better explained the “detox” setback cycle some people encountered. Therefore, it’s likely not a “detox”; rather, it’s really a “more tox” situation. So, my thinking was, OK, people just need to give it more time. Although my personal recovery did take a long time, my trend was generally pretty linear towards better health. I rationalized that I had been spared the big “detox” setback cycle because I had not been directly supplementing with VA, nor did I have a history of eating liver, etc. But, I too did have my share of smaller autoimmune flare ups and setback cycles along the way.
Very early on it became clear to me that we are not dealing with a simple toxicity situation either. Rather, it’s a very nasty and sinister one where the toxin binds to and messes with our RNA/DNA. So, for these DNA damaged cells we pretty much have to grow them off and out of our bodies. That’s just going to take a long time. Additionally, since it’s also a toxin that accumulates in our lipids, as we drop body fat, then more of it is going to be released into serum. Therefore, we are clearly in for a good long haul in detoxifying from this mess. But, that part of it does not quite fit with some of the real-world data reported in our survey. Some people have reported not losing weight, or have even gained weight, and have still slid down into the “detox” cycle.
Regardless of the reasons and mechanisms, I think having people slide backwards into poorer health is just not acceptable. Asking people to stick with it, and struggle through for months on end is not very acceptable either. Therefore, we need to get a clearer understanding of what’s really going on in the detox setback. Most importantly, we need to find an effective means of dealing with it. We need a reliable, safe, and most of all, a predictable recovery strategy. I think if the full recovery process takes say even four years, most people would still be okay with that, just as long as it’s progressive, and almost always in the right direction towards better health. The current non-predictability of it is almost a show-stopper for more people to take on this diet experiment.
One of the key statements I’ve repeated over the last few years is that we need an antidote. Diet alone is not cutting it, and being such a restrictive died it will never gain widespread acceptance. But, diet is the only tool we have in our collective toolkit right now. Therefore, I was seeing the diet-alone approach as just a starting point in this investigation. My thinking was that if we could use it to prove the case, then others would pitch in and help develop an effective antidote. Unfortunately, we are not at that point yet.
However, there are some other very important facts we need to remember. One is that humans have been dealing with vitamin A (in its various forms) for millions of years now. Yes, it is a toxin to humans, but plants love it, and it’s not going away. Therefore, we just have to learn to deal with it more safely. The supercritical and obvious conclusion is that the human body has already developed mechanisms to deal with, neutralize , and detoxify the retinoids. These biological processes are reasonably well understood by current medical science, and are actually quite well documented too. The key point to know here is that In addition to the physical elimination pathways, via the liver, skin, and the RBPs, the body has very likely already developed the needed antidotes to retinol and retinoic acid. I think these antidotes are primarily the alcohol and aldehyde dehydrogenase enzymes. These enzymes effectively slowly chop up the retinoid molecules.
So, why isn’t the alcohol and aldehyde dehydrogenase enzyme production keeping up with the new demand? One possibility is that they’ve been too overwhelmed or drained. Another possibility is that the needed manufacturing feedstock of nutritional elements is missing from our now very restrictive diets.
There’s yet another possibility, and that is that as people go very low on the consumption side of vitamin A, then the body’s perceived inbound threat is reduced, and the production of the dehydrogenase enzymes is slowed or even shutdown. Whereas, the backflow of retinyl esters from the liver is not quite the right molecule to trigger production of the dehydrogenase enzymes. This little sub-theory is actually supported by several people who have reported that keeping just some vitamin A content foods (like a single egg per day) in their diet prevents and quickly abates their “detox” setback cycle.
But, I want to be clear that I am NOT making the recommendation here that people start reintroducing VA foods back into their diets. That’s because other people have reported just the opposite effect. Clearly, it’s an individual thing, and people are going to need to experiment with it and find what works best for their own situations.
Next, there’s another really important possibility. Is there something else being included in our diets that would consume and preferentially compete for the same alcohol dehydrogenase enzymes?
Hmm, could it be the Cauliflower?
About 36 of the survey respondents reported including cauliflower in their diets. I suppose that I am probably responsible for starting that with the diet I document in my eBooks.
Although cauliflower has little to no vitamin A, one surprising thing to know about cauliflower is that it can have a pretty high content of formaldehyde (source). It’s not massively over the top, but it’s still relatively high. The thing is that the same alcohol and aldehyde dehydrogenase enzymes are needed to neutralize and detoxify that formaldehyde. Other foods to be on the lookout for in this regard are Asian pears, canned pears, and other canned fruits, and to a lesser extent even bananas. The other major culprit is the artificial sweetener Aspartame. Aspartame is a big problem because the breakdown pathway for it is that it first gets converted into formaldehyde. The resulting formaldehyde will therefore compete for our precious alcohol and aldehyde dehydrogenase enzymes.
Could it be that the cauliflower, and possibly these other foods, is sabotaging people’s recovery progress? I don’t know, but I’d sure like to find out. Therefore, for anyone currently including them in your diet, can you please try dropping them for a while and report any changes.
One more thing to be aware of is some of the pharmaceutical drugs are documented to interfere with the detoxification process of the retinoids too. The two that I am most aware of are the Statins and the SSRIs. But, we can assume that any pharmaceutical drug that is processed by the liver as being competitive for the liver’s detoxification resources. Obviously, consuming anything more than just minor amounts of alcohol is not going to help us either. So, any of these factors, combined with an environment where more retinyl esters are suddenly back flowing into circulation, could lead to the dehydrogenase enzymes being overwhelmed and exhausted.
Boosting our alcohol dehydrogenase enzyme production
Back in February when I posted my discussion on Statins and Cholesterol I made the suggestion that regular consumption of Apple Cider Vinegar would help ameliorate any calcium buildup in the arteries. And I still believe that it almost surely will do exactly that. But, what I did not know at the time was that ACV has some other major benefits. It helps boost bile production, and the source bacteria contains aldehyde dehydrogenase enzymes. ACV also helps boost our own production of the human version of enzymes. There are other foods that can help safely boost ADH and ALDH enzyme production. Dr. Garrett Smith is actively looking into this aspect of it.
Zinc – here it is again
It’s also important to know that zinc is a critical mineral needed for the formation of the dehydrogenase enzymes, just as it is for the RBPs. Therefore, if you are not eating red meat, you really should make sure that you are getting enough zinc from other sources. It looks like some of the B vitamins are also involved in the process of building the dehydrogenase enzymes.
The actual survey responses are summarized below.
The raw survey data are available here in an .xls format.
I’m conducting a survey of people’s experience with the diet. My goal with this survey is to see if we can find out what’s working, and what’s not. Most importantly I want to see if we can determine why some people encounter the detox setback cycle after being on the diet for several months. What I believe is happening in many cases is that as people take on a VA elimination diet their liver then releases the more toxic retinyl esters back into circulation. They therefore need more of the dehydrogenase enzymes to keep up with it. But, if their body can’t make the dehydrogenase enzymes fast enough, then they slide backwards into the “detox” phase.
Therefore, we now need to move into the second phase of the investigation and determine HOW people can safely and reliably detoxify from it. If we can accomplish that, then it will just be a matter of time for more people to recover.
I’ll post a summary of the results here by Oct 12th. I also will share the entire survey results (sans email addresses) for everyone to evaluate. So, please don’t include any personally identifiable information in the comments. If you want to submit a response, and don’t want to have it, or just your included comments, shared publically, then please contact me and I’ll remove it from the shared results. Thanks.
It’s now been five years on my low vitamin A diet. My health continues to be good. However, I’ve only seen small improvements over the last year. But at least they are improvements, and my health continues to move in the right direction.
My spine has continued to straighten out more, and I am therefore standing slightly taller.
My teeth are feeling stronger, smoother, and are just more solid. My gums are in excellent health too. My teeth also remain cleaner throughout the day.
My energy levels and physical stamina remain good and slightly improved over last year. Likewise, I’m finding that I need to eat less food per day, and yet I still maintain a good energy level throughout the day. My weight has remained constant.
I’m now quite regularly sleeping through the night. That’s a huge improvement compared to five years ago where I needed to get up at least every hour. Likewise for sun exposure. Five years ago, my maximum tolerance for bright sun exposure was about 10 seconds. Anything more than that, and my skin would start to burn. I can now take 30 minutes or more, and my skin once again tans.
One other very surprising improvement over that last year is the quality of my handwriting. It has become noticeably nicer, more fluid, and stylish.
My skin, fingernails remain to be nice and smooth and my hair remains to be very soft. I’ve not gone blind, and my organs have not disintegrated. Unfortunately, the amount of vascularization in my eyes has only slightly improved over the last year. The net is that I’ve not seen any big improvements in my health over the last year. So, I think I’ve probably reached more of a steady-state condition of being in pretty good health.
Small Diet Change Experiments
I’ve only tried two small diet changes over the last year. One is that I changed out the rice for white bread (made without dairy or eggs). I tested this change for about two months. It was a sourdough bread made with non-organic white flour, so it no doubt contained glyphosate. I had no negative reaction health-wise to the white bread. But I felt that it didn’t provide quite the same long-lasting energy that I was getting from rice. Also, as I commented before that a diet of white rice and beef alone could quickly turn into gut concrete. Well, it turns out that white sourdough bread and beef alone can turn into gut concrete with a compressive strength of about 25 MPa. The black beans helped a lot in mitigating that condition. Nonetheless, I feel that white bread is just not for me. So, I’m back to the white and (occasionally) brown rice.
The other diet experiment I tried was adding Brazil nuts. In theory, these nuts should have been safe; providing zinc, selenium, vitamin E, etc. But, after about two weeks, I felt I was starting to have a bad reaction to them. Of course, that bad reaction could have been a complete coincidence too. But, stopping them also seemed to coincide with resolving the negative reaction too. The negative reaction was mostly just the development of dry skin on my outer earlobes. Obviously, this one little personal experiment is not very meaningful. So, I’m just trying to be complete in reporting what happened with my health over the last year.
My blood test for vitamin A & D
I’ve gotten another blood test for my vitamin A and D levels. The results are as shown in the report below.
For some unexplained reason my first blood sample was rejected by the lab and I was asked to provide a second one.
I was seriously disappointed with that 0.1 μmol/l result. It’s the same value that I had a year ago. I find it a little hard to believe that after another year maintaining a nearly zero vitamin A intake diet that my serum level wouldn’t have moved lower. Unfortunately, because of where I live, I don’t have access to another lab to get a second opinion.
Although my vitamin A research is just a side-project, I remain fully committed to it. Therefore, I will continue with my vitamin A free diet for the foreseeable future. My current plan is to keep with it for at least five more years.
Other Progress Reports
This citizen-driven research project has gained a lot more interest over the last year. With that, more people are trying this diet change and are starting to send me progress reports.
Although, I’ve received some good early progress reports, for most other people it’s a long slow crawl in recovering their health. And, as I’ve written about before, some people go into a “detox” phase and then get worse. Therefore, I think the “detox” phase could be a “more-tox” phase. I’ve discussed this phenomenon with an academic researcher. We both suspect that it is due to more retinol esters getting released from the liver. It is quite possibly due to the liver starting to normalize its size and is part of the recovery process from a fatty liver condition. Likewise, it could be due to the adipose tissues normalizing in size too. Except, and a bit oddly, going into the “detox” phase is not happening to everyone. I’d say the number of people reporting going into the “detox” phase has been around 20%. It also does not appear to be age or gender-related.
Some other general themes and patterns are showing up in the progress reports. One is that younger people are indeed recovering faster. The second one is that people are reporting that they are overcoming their anxiety, becoming more social, more outgoing, and developing a positive outlook. Some people are stating that they’re thinking more clearly, and just generally being happier too. I think related to that is that quite a few people are telling me that the quality of their sleep has improved, and they are experiencing a significant increase in dreaming and dream recall. So, it appears that one of the early improvements of being on this diet is an improvement in cognitive function.
As I stated before, for most adults, it probably took decades to build up into this condition. Therefore, it is not unreasonable to expect that it will take a long time to recover from it. Diet alone is clearly not a quick fix. But, if we can be happier while trying to apply that fix, then I hope it’s not so bad.
Of course, for most people taking on this diet their goal is to improve their health. It would be great if more people can accomplish that. However, there is also the overarching goal of adding more evidence identifying the real culprit in what’s caused our chronic diseases to develop in the first place. So, I’m very grateful for all the people now participating in this investigation, and for everyone sharing information and their experiences. Thank you so much.
I also want to thank “Yi at LDT” for repeating the low vitamin A diet with his mice.
As I discussed in ETFOH, one common theme that cuts across all the autoimmune diseases, and even breast cancer too, is the comorbidity of eczema. At a more fundamental level, and what many others have reported on, is there’s another cross-cutting syndrome, and it’s that of insulin resistance. So much so, that many people feel that insulin resistance is at the root cause of many of the chronic diseases. The very definition of Type II diabetes is insulin resistance and metabolic disease. But, it goes well beyond that. Insulin resistance is hugely implicated in coronary artery disease, heart disease, and surprisingly even the brain diseases such as Alzheimer’s too. You’ve probably heard Alzheimer’s disease even being referred to as Type III diabetes. So, let’s see if we can make some sense out of all of this, and find some plausible common ground and the connections between them.
When I wrote about my theory of obesity causation back in October, I referenced this 2016 report documenting the adipose genesis effect of retinoic acid: Circulating Retinoic Acid Levels and the Development of Metabolic Syndrome.
Source: Yan Liu, Hongen Chen, Di Mu, Jiahua Fan, Jiayi Song, Yuan Zhong, Di Li, Min Xia; Circulating Retinoic Acid Levels and the Development of Metabolic Syndrome, The Journal of Clinical Endocrinology & Metabolism, Volume 101, Issue 4, 1 April 2016, Pages 1686–1692, https://doi.org/10.1210/jc.2015-4038
I was somewhat expecting people to call me out on my use of that study. One of the weird aspects to it was even though the authors documented the adipose genesis effect of retinoic acid; they also concluded that the elevated levels of retinoic acid were beneficial in reducing metabolic syndrome.
The serum RA level is inversely associated with the development of MetS independently of adiposity and insulin resistance.
So, even though one aspect of that study supported my sub-theory of obesity causation, it directly contradicted my overarching theory that retinoic acid was the real culprit in causing the modern chronic diseases. Of course, there is an absolute mountain of other studies and research proving the incredible toxicity of retinoic acid. To me, at least, something was not adding up here with their contrary findings. But, it is rather easy to see where they go wrong in their analysis.
Here’s the source of the problem stated in the Materials and Methods section of their report:
Determination of RA concentrations
Serum RA concentrations were measured using a commercially available ELISA kit according to the manufacturer’s instructions (catalog number MBS705877; MyBioSource). This assay has high sensitivity and excellent specificity for the detection of human retinoic acid.
Do you see it? They did not actually measure serum RA concentrations at all; rather they measured a biological proxy marker for it. Of course, there’s no such thing as “human retinoic acid” either. So, what are these ELISA kits? They are kits that test for and measure antibodies.
The enzyme-linked immunosorbent assay (ELISA) is a commonly used analyticalbiochemistryassay, first described by Engvall and Perlmann in 1972. The assay uses a solid-phase enzyme immunoassay (EIA) to detect the presence of aligand (commonly a protein) in a liquid sample using antibodies directed against the protein to be measured. Performing an ELISA involves at least one antibody with specificity for a particular antigen.
For example, you could use an ELISA test to detect and measure the antibody proteins to Measles. ELISAs are not usually used to measure and quantify specific compounds such as retinoic acid. Using gas chromatography and mass spectrometry is the more standard technique for identifying and quantifying the molecular makeup of compounds.
Of course, in the human body, most circulating retinoic acid (and retinol too) is bound up in wrapper RBPs. Therefore, what the authors meant to say was: “This assay has high sensitivity and excellent specificity for the detection of the human RBPs for retinoic acid.” So, yes, if the body is building the needed RBPs fast enough, then it will safely wrap up the otherwise highly toxic retinoic acid molecule. When wrapped up in the RBP, the retinoic acid will pose far less of a hazard and people are better protected from it. With this protective mechanism explained we can now understand their observations and paradoxical conclusion.
But, the use of the ELISA test is not some major error on the part of the report authors either. It’s probably a good surrogate test, and it appears to be a rather standard practice. Here’s another report where they’ve done the same, except it’s for retinol RBPs.
Retinol-Binding Protein 4 and Insulin Resistance in Lean, Obese, and Diabetic Subjects
By: Timothy E. Graham, M.D., Qin Yang, M.D., Ph.D., Matthias Blüher, M.D., Ann Hammarstedt, Ph.D., Theodore P. Ciaraldi, Ph.D., Robert R. Henry, M.D., Christopher J. Wason, B.S., Andreas Oberbach, Ph.D., Per-Anders Jansson, M.D., Ph.D., Ulf Smith, M.D., Ph.D., and Barbara B. Kahn, M.D.
Serum RBP4 was measured by an enzyme-linked immunosorbent assay (ELISA) (ALPCO Diagnostics) in groups 1 and 3 and by quantitative Western blotting with purified human RBP4 standards in group 2. Immunodetection was performed with a polyclonal antibody to human RBP4 (DakoCytomation).
In addition to the ELISA, they are also quantifying their measurements with the Western Blot test. But, like, with the ELISA, the Western Blot is another type of test for measuring antibodies. Next, let’s consider their results:
Serum RBP4 levels correlated with the magnitude of insulin resistance in subjects with obesity, impaired glucose tolerance, or type 2 diabetes and in nonobese, nondiabetic subjects with a strong family history of type 2 diabetes. Elevated serum RBP4 was associated with components of the metabolic syndrome, including increased body-mass index, waist-to-hip ratio, serum triglyceride levels, and systolic blood pressure and decreased high-density lipoprotein cholesterol levels. Exercise training was associated with a reduction in serum RBP4 levels only in subjects in whom insulin resistance improved. Adipocyte GLUT4 protein and serum RBP4 levels were inversely correlated.
This is an important finding as it is tying together serum RBP4 levels, insulin resistance, diabetes, metabolic syndrome, and more. Except, just for now, ask yourself why are they using antibody tests to measure RBP levels? Doesn’t something about that strike you as being a bit peculiar?
To be clear, these are not procedural anomalies. It appears to be a preferred measurement technique. Here’s another study where they use Western blotting to measure serum retinoic acid levels:
Valproic acid combined with 13-cis retinoic acid and 1,25-dihydroxyvitamin D3 in the treatment of patients with myelodysplastic syndromes
Timo Siitonen, Timo Timonen, Eeva Juvonen, Venla Terävä, Anu Kutila, Tuomo Honkanen, Maija Mikkola, Heikki Hallman, Marjut Kauppila, Pirkko Nyländen, Eira Poikonen, Auvo Rauhala, Marjatta Sinisalo, Merja Suominen, Eeva-Riitta Savolainen, Pirjo Koistinen
Of course, using mass spectrometry to measure RA acids levels is more problematic because the retinoid is entirely encapsulated within the RBP wrapper. Therefore, samples first needs to be dissolved in solvents to breakdown the protein shell and washout the embedded retinoids. From there, mass spectrometry can be employed. So, although the ELISA and Western Blot are measuring a biological proxy marker, they are probably more expedient tests and good enough for the purpose of their studies.
Okay, now we need to really think about this. If these laboratory tests used to measure serum levels of retinoic acid, and even that of retinol, are in actuality antibody tests, isn’t it pretty logical that the RBPs are indeed antibodies?
Except, for the last 50 years now, medical science has claimed that the RBPs are specialized transport proteins. The grand theory is that the liver first scrubs retinol out of serum and then sequesters it away into storage for later delivery. On an on-needed basis, the liver then releases the retinol wrapped up in the RBPs for transport. That’s a nice-sounding theory. But, there’s a huge flaw now showing up in the story. That flaw is because a large percentage of the RBPs are actually being built and released by the adipose tissues, and not just the liver. That’s correct, the origin of much of the RBPs is from the adipocytes.
RBP4 is an adipocyte-secreted molecule that is elevated in the serum before the development of frank diabetes and appears to identify insulin resistance and associated cardiovascular risk factors in subjects with varied clinical presentations. These findings provide a rationale for antidiabetic therapies aimed at lowering serum RBP4 levels.
Okay, it looks like the grand theory of the RBPs being transport proteins is starting to fall apart.
“Until 2005, the sole known function for RBP4 was to mobilize retinol from tissue stores and deliver it to vitamin A-responsive cells where it can be converted to retinoic acid for use in regulating vitamin A dependent transcription and functions. In 2005, Kahn and colleagues reported that circulating RBP4 levels affect glucose clearance, with high RBP4 levels inducing insulin resistance (Yang et al., 2005; Graham et al., 2006). Specifically, Kahn and colleagues proposed that adipocyte-derived RBP4 is a signal that contributes to the pathogenesis of type 2 diabetes, linking obesity with type 2 diabetes, as well as other obesity-related metabolic diseases.”
Very importantly, this then brings into question the entire premise of retinol’s “storage” in the liver. That’s because the thought to be delivery protein for it is being generated by, and secreted from the adipose tissues and not at all exclusively from the liver’s “storage” site!
Next, let’s think a bit about the cell’s response to viral infections. When a cell gets infected with a virus, it can very mistakenly start replicating and cloning more of the same virus. But, very often, it also wraps the newly made viruses up in a protein capsid. Some cells can then eject the entire capsid out of itself. Secondly, in response to viral infections the adaptive immune system will usually start to build antibodies to the virus. The goal and function of the antibody is to attach itself to specific binding sites of the viral protein. In doing so it effectively bulks up any free circulating viruses so that they become too large to pass through the cell membrane. If successful, the viral infection is brought under control. Except, now when a cell is contaminated by a toxin, it is by a non-protein based molecule. There are no protein binding sites (at all) to attach an antibody to it. Therefore, as with some viruses, the cell needs to wrap toxic molecules in a specialized hollow-core antibody (or capsid if you prefer). Unlike the currently recognized Y shaped antibodies, the RBPs are more barrel-shaped, That barrel-shape is needed to engulf the entire antigen. Shown below is a model of the RBP with its embedded retinol ligand.
Note the retinol molecule (ball and stick model) nestled inside of the far more complex wrapper (ribbon model) of the RBP. Remember that retinol is too toxic to be in serum alone. Here’s the spacefill model of the RBP showing that no part of the retinol molecule is exposed outside of the RBP itself.
Image created with the PDB ID and associated publication, NGL Viewer (AS Rose et al. (2018) NGL viewer: web-based molecular graphics for large complexes. Bioinformatics doi:10.1093/bioinformatics/bty419), and RCSB PDB.
Therefore, this molecular structure is an astonishing feat of chemical separation and isolation. Not only has the cell’s protein weaving machinery been able to detect and identify a single molecule, but it has also separated it out and wrapped it in a complex protein envelope. Remember too that nature is no fool, and it is not wasteful. This extreme measure of molecular assembly and folding dexterity has to be going on for a very good reason.
Why would the body resort to using such an elaborate and costly transport protein structure? Secondly, if this is truly a transport protein, then how does the receiving cell extract out the retinoid payload when no part of it is exposed to the outside world? And, how exactly does it do it in a toxic-safe manner? Why does the RBP only transport just one molecule at a time? And, once again, why are the adipose tissues generating and secreting the RBPs in the first place? Of course, no one knows the answers to these questions. At best, there are just some unsupported speculations tossed around about it.
“RBP is also bound to a carrier protein, transthyretin. The process by which RBP releases retinol for cellular availability is still unknown and not concisely determined.”
Additionally, if the RBPs are “transport” proteins, that are supposed to be so highly-regulated, then why do they accumulate with age?
The real clincher question is: if the liver is building RBPs to deliver retinol to the other tissues, then why are those receiving tissues then themselves wrapping up retinol in their own internally built RBPs and ejecting it? The current theory of the RBPs being “transport and delivery” proteins makes no logical sense.
Isn’t it just so much more logical that the RBPs are hollow-core antibodies? Isn’t it just more logical that as the body gets exposed to more of a toxic load outside of liver storage, the body builds more antibodies to combat and protect us from that now adipose accumulating toxin? Here’s another study indirectly indicating that’s the case:
Cellular retinol-, retinaldehyde- and retinoic acid-binding proteins were localized in rat retina during pre- and postnatal development by indirect immunofluorescence.
Source: Immunolocalization of cellular retinol-, retinaldehyde- and retinoic acid-binding proteins in rat retina during pre- and postnatal development De Leeuw, A.M., Gaur, V.P., Saari, J.C. et al. J Neurocytol (1990) 19: 253. https://doi.org/10.1007/BF01217303
What is immunofluorescence?
Immunofluorescence is a technique used for light microscopy with a fluorescence microscope and is used primarily on microbiological samples. This technique uses the specificity of antibodies to their antigen to target fluorescent dyes to specific biomolecule targets within a cell, and therefore allows visualization of the distribution of the target molecule through the sample.
Clearly, the RBPs are very antibody-like. But, since we now know they are not “transport” proteins, is it not highly likely they are indeed antibodies? They have just not yet been recognized as such. The next logical question is: if the RBPs are, in actuality, antibodies, then what does that tell us about retinol? It tells us that it is a toxin!
The famous amyloid plaques of Alzheimer’s disease
One of the key neuropathological hallmarks of Alzheimer’s disease is the accumulation of β-amyloid plaques in the brain. No one knows why they develop or what to do about them. What’s assumed is that they are just defective ribbon structured proteins that exhibit some weird and unexplained misfolding. But, doesn’t that sound a lot like the folded ribbon proteins of the RBPs? Here’s a description of the RBPs
Members of the lipocalin family, including the retinoid-binding proteins RBP, epididymal retinoic acid-binding protein and β lactoglobulin, share a very low sequence identity but display a highly conserved overall fold. They are composed of an eight stranded antiparallel β-sheet that is folded over itself to form a hydrogen-bonded β-barrel, which constitutes the ligand binding pocket (Figure 2). The N-termini of these proteins are folded around the back of the barrel, `capping’ that side of the pocket.
Next, we need to know and deeply appreciate that it’s not just the liver and adipose tissues that are excreting the RBPs. It’s also happening in the kidneys, lungs, heart, skeletal muscle, spleen, eyes, and testes too.
Functions of RBP
Retinol is secreted from its storage pools and circulates in blood bound to RBP. The main storage site for vitamin A and, correspondingly, the main site of synthesis of RBP, is the liver, although other tissues (including adipose tissue, kidney, lung, heart, skeletal muscle, spleen, eye and testis) express this protein.
Source: Retinoid-binding proteins : mediators of retinoid action Biochem. J. (2000) 348, 481±495 (Printed in Great Britain) 481 REVIEW ARTICLE Noa NOY1 Division of Nutritional Sciences, Cornell University, Ithaca, NY 14853, U.S.A
And then there’s this statement:
The mechanism by which retinol initiates secretion of RBP from cells is unknown, but appears to be conserved in yeast ectopically expressing RBP.
Source: As above
I think it is quite obvious that the cells of multiple tissue types are synthesizing their own RBPs as a protective measure in an attempt to rid themselves of a highly toxic molecule. Do you see where I’m going here? Yes, if the cells of the liver, adipose tissues, kidney, lung, heart, skeletal muscle, spleen, eye, and testis are all able to secrete RBPs, with the retinoid wrapped up inside of it, why shouldn’t we think that the nerve cells of the brain are not going to do the same? Just like the fact that the RBPs are unrecognized as antibodies, couldn’t the famous amyloid plaques of Alzheimer’s disease be unrecognized as RBPs generated by the brain too? Or maybe, since Alzheimer’s is such a new phenomenon in human existence, the amyloid plaques are an ongoing attempted synthesis of RBPs? Thinking that the cells of the nervous system can generate amyloids is not just speculation. As mentioned above, the RBPs are often bound in serum to transthyretin.
Transthyretin (formerly known as prealbumin) is a plasma protein involved in the transport of thyroxine and retinol and is secreted in great amounts by the choroid plexus epithelium.
Knowing that transthyretin is typically bound up with the RBPs it’s no surprise that so many people with diabetes, autoimmune diseases, and even dementia have the comorbidity of abnormal thyroid functions.
There are some rather remarkable similarities between the so-called defectively folded proteins of the amyloid plaques and that of the folded over proteins of RBPs. For example, here’s the CRYSTAL STRUCTURE OF THE PROTEASE INHIBITOR DOMAIN OF ALZHEIMER’S AMYLOID BETA-PROTEIN PRECURSOR
Image created with the PDB ID and associated publication, NGL Viewer (AS Rose et al. (2018) NGL viewer: web-based molecular graphics for large complexes. Bioinformatics doi:10.1093/bioinformatics/bty419), and RCSB PDB.
As with the RBPs, the Alzheimer’s disease defining proteins adopt a β‐sheet structure and sometimes form into amyloid plaques. Most importantly, when you consider that there has been an 800 times increase in the rate of Alzheimer’s disease since the early 1970s, it is completely, absolutely, undeniably, positively crystal clear that the disease is a poisoning. It’s then easy to appreciate that the cells of the brain are responding to that poisoning in very similar ways as do say the cells of the kidney, lungs, etc. However, once trapped inside the brain, there is no viable disposal pathway for these unusual proteins. The brain just slowly accumulates and clogs up with the amyloid plaques. Not only that, but all the energy and resources wasted in building the amyloid plaques has been taken away from the brain’s normal tissue maintenance and repair processes.
Very tragically, billions of taxpayer-funded dollars have now been spent by researchers going on a wild goose chase of blaming genetics for this disease. Of course, it is a colossal waste of money and time because it is completely obvious Alzheimer’s disease is not caused by genetics. Not only does it take thousands of years for a genetic shift to occur in the human population, the country with the highest genetic diversity on the planet now has the highest rate of Alzheimer’s disease in the world. And who cares about some supposed “genetic predisposition” to the disease because there’s absolutely nothing people are going to be able to do regarding their genetic makeup. So, investigating genetics is pretty much a meaningless distraction from the real culprit of the disease being environmentally caused. If people were not being slowly poisoned by some environmental factors, then their “genetic predisposition” would never be a problem.
Of course, it’s not just the brain that’s clogging up with amyloid plaques, it’s the heart and other organs too. Not at all surprisingly, that also directly correlates to the serum levels of the RBPs!
Identification of Transthyretin Cardiac Amyloidosis Using Serum Retinol-Binding Protein 4 and a Clinical Prediction Model
Findings In this case-control study that included 34 patients with transthyretin cardiac amyloidosis and 77 control participants, retinal-binding protein 4 was significantly associated with the disease independently of tested confounders. A prediction model composed of retinal-binding protein 4, transthyretin, and echocardiographic and electrocardiographic characteristics had excellent discrimination for transthyretin cardiac amyloidosis (deposition of amyloid).
Conversely, the vascularization of the brain in AD patients often shows the same type of damage as that presented in coronary artery and heart disease. The condition is called “vascular dementia.” Therefore, it’s very probable that the same root cause force behind that vascular damage is driving both diseases. Equally important is to know that almost no one dies directly from Alzheimer’s, rather they die with Alzheimer’s. Meaning, the real cause of death is one of their other conditions, such as kidney disease, heart disease, stroke, choking, pneumonia, etc.
Additionally, It’s well documented that persons with Type II diabetes are at a bigger risk (~200%) for developing Alzheimer’s disease. It is even claimed that the single biggest risk factor for developing Alzheimer’s disease is having Type II diabetes. Therefore, many people have made the erroneous assumption that the diabetes is somehow causing Alzheimer’s disease. But, that’s not quite true. Diabetes is not “causing” the Alzheimer’s. Rather, both diseases are simply joined at the hip, metaphorically speaking. And in both diseases we have the common themes of insulin resistance and the development of amyloid plaques. Obviously, diabetes is not “causing” the Alzheimer’s and Alzheimer’s is not “causing” the diabetes. Once again, something else is at the root cause of both diseases. As we’ve seen, elevated serum levels of the RBPs are a significant marker in both diseases too. It is also true for the development of amyloid plaques of the heart. So much so, that it is pretty much an undeniable fact that the RBPs are somehow involved. But, there is an even more direct connection between these two major diseases. As with heart disease, it’s the accumulation of misfolded proteins.
Protein misfolding and aggregation in Alzheimer’s disease and type 2 diabetes mellitus.
AD is characterized by the accumulation of amyloid-β (Aβ) in the brain, while T2DM is characterized by the deposition of islet amyloid polypeptide (IAPP, also known as amylin) within beta-cells of the pancreas.
It is becoming increasingly believed that islet amyloidosis is the progeny of many diseases, including T2DM. The production of islet amyloid polypeptide (IAPP) oligomers that results in amyloid deposition is considered as a major contributor in pathogenesis and progression of T2DM . This has been found present in 96% of T2DM patients and is recognised as a hallmark for diagnosis of this disease.
LINKAGE BETWEEN AD AND T2DM
AD and T2DM are both prevalent in the aged population. Whereas the cerebral accumulation of Aβ is a major pathological hallmark of AD , the deposition of a very different polypeptide, amylin, that likewise succumbs to β-sheet formation and self-aggregation occurs within the pancreas, especially in β-cells, in T2DM.
So now, just what do you suppose is responsible for causing the messed-up structure of the proteins generated by the pancreatic and other tissue stem cells? How about we seriously consider it to be a toxic molecule that has now been proven to cause about 500 different gene “expressions” in stem cells. Except, to most of us here it’s now clear these are, in actuality, sites of gene “damage” and not that of gene “expressions” at all. That gene damage then messes up the cell’s protein weaving machinery. Naturally, the follow-on consequence is going to be the defective structures of the manufactured proteins.
Somewhat like with the wild goose chase of genetics, there’s been a vast amount of research in trying to correct the misfolding proteins using pharmaceutical drugs. Of course, that effort has been futile. Additionally, most research is narrowly focused right down into trying to decipher what’s wrong with the protein structure, Oddy, it appears most people are only asking why the protein is misfolding, as if something has gone wrong with it post manufacturing. They they are not considering that it has been expressly manufactured that way due to RNA/DNA damage.
The RBPs tied-together with Insulin Resistance
GLUT4 – is the glucose transport protein used by cells to take-up insulin from serum. Obviously then if the GLUT4 proteins are not of sufficient quantity or quality, it then will cause the condition of Insulin Resistance. It’s not hard to imagine that if the cell’s energy and resources are tied up generating RBPs, that could be impairing their production and or functioning of the GLUT4 proteins. This scenario is indeed being demonstrated in clinical research. For example:.
Serum retinol binding protein 4 contributes to insulin resistance in obesity and type 2 diabetes.
This now brings us full circle to where I hope it shows how it’s all interconnected. The information presented here not only links the RBPs to Type II diabetes and the amyloid-β plaques; it seriously implicates it in causing coronary artery, heart disease, and of course Alzheimer’s too. Except, we need to be very careful here and not try to blame the RBPs. Rather it’s the overload of retinol that is the very root cause. It’s the overload of retinol that has forced production of the RBPs in the first place. There’s one more connection with insulin resistance that I’d like to discuss, and that is Mitochondrial Dysfunction. There are hundreds of research papers documenting that Mitochondrial Dysfunction and Diabetes are very closely coupled. But, as always, there’s more to the story, and that is the key role of the retinoids directly damaging the mitochondria.
Vitamin A and Retinoids as Mitochondrial Toxicants
Overall, such findings indicate a potential ability of vitamin A and its derivatives to negatively interact with biological membranes, an event that may lead to organelle stress, as, for instance, mitochondrial dysfunction, and to cell apoptosis or necrosis.
‘Vitamin A and its derivatives, the retinoids, disrupt mitochondrial function by a mechanism that is not completely understood. However, it accounts with impaired electron flux between the complexes of the METC, increased ROS production, and induction of oxidative and nitrosative stress to mitochondrial membranes. Additionally, vitamin A and retinoids alter the mitochondrial structure by causing swelling of the organelle. More investigations are needed to elucidate how vitamin A and retinoids affect mitochondria and whether there is a causative link between such event and the clinical manifestations observed both experimentally and in humans.’
Source: as above
Predictably, the thinking from some pharma funded researchers is the same. It’s viewed as an opportunity to try to develop a new drug that will block or intervene in the synthesis of the RBPs. Of course, it always comes down to needing a “drug” to “block” something. Using a non-drug based therapy is completely unthinkable to these folks. But, since we know with 100% certainty that Alzheimer’s is the result of a long term poisoning, the only “drug” that could even possibly work is one that acts as an antidote to whatever that poisoning is. Until then, almost all other drugs are just going to be useless, and most will cause even more harm. Now with the known connections between the elevated RBPs and the development of amyloid plaques, and having a better understanding of RBPs likely being an antibody response to a toxin, isn’t it very likely retinol is the responsible toxin?
Maybe it’s just me, but how about we just consume a lot less of the retinoids and let the body heal itself?
Are the RBPs antibodies? Please have a think about it and comment as you see fit.
Heart disease and stroke is the number one killer of North Americans. This disease accounts for over 600,000 deaths per year in the USA alone. And, like with the rest of the modern chronic disease epidemics we face, historically speaking, it is not a normal disease in the human population. Our extraordinary rate of heart disease is a relatively new phenomenon. It is considered to be just another disease of affluence and lifestyle. Obviously, we are somehow doing it to ourselves.
For decades now modern medicine has vilified cholesterol as being the primary culprit in causing heart disease and stroke. But, the exact mechanism behind why there’s a pandemic in increased cholesterol levels remains a mystery. For a long time now the elevated cholesterol levels have been very simplistically blamed on consuming too much saturated fat as part of the regular diet. However, things don’t move fast in medical research, and now finally after about 50 years that theory is losing its plausibility. If we are going to be realistic about it, with the massive real-world experience with the wide-scale adoption of low-fat diets, it has proven to be just dead-wrong. Yet, many folks in medical science still cling to the ridiculous notion that fat in the diet is the cause of high cholesterol. Not surprisingly, even with much of the population on long term low-fat diets the cholesterol levels for many people just remains way too high. And of course, the North American death rates due to heart disease and stroke are just as high as ever also. So, once again, the experts appear to have gotten it completely wrong. Regardless of what the experts claim, clearly, dietary fats are not the cause of high cholesterol.
Okay, but what about the very basic premise that high cholesterol is even the villain in causing coronary artery and heart disease in the first place? Surely, they can’t be wrong about that one too? After all, the arteries and the heart are being blocked up with plaque, and one of the main constituents of that plaque is cholesterol. I mean, just how much more evidence do they need to give us? Cholesterol is always found at the scene of the crime. Therefore, it must be guilty, right?
Well, not so fast. Here’s the little glitch in that theory. Only about 50% of people diagnosed with coronary artery disease (CAD) have elevated levels of serum cholesterol. Whereas, the other 50% of people with CAD have normal, or even low, serum levels. So, that’s a clear indication that there’s something vastly wrong with that “it’s the cholesterol causing heart disease” theory too.
Okay, what else do we know about the artery plugging plaque? Well, the two really interesting ones are that it is chocked full of dead macrophages and often calcium too. Next, we need to know that the walls of the arteries are an endothelium. The cells that make up the internal walls of the blood vessel are really just a specialized version of the epithelial cells. Then, the next critical detail to know is that the areas of the blood vessel walls where the plaque forms are almost always under distress from a non-healing lesion and chronic inflammation too. So much so, that many researchers now believe that the real root cause of the plaque formation is the inflammation. Their view is that the plaque is really the body’s internal band-aid trying to protect a chronic wound in the artery wall. Thus, in their view, the causal sequence goes like this:
Naturally, we need to look upstream and ask what can cause chronic lesions and inflammation in the blood vessel walls like that in the first place?
Long term exposure to retinoic acid would sure do it. Remember that retinoic acid indiscriminately attacks the basal membrane of the epitheliums anywhere in the body. Next, what about all those dead macrophages? Yes, retinoic acid, and even vitamin A, have been proven to cause that to happen too. What about the calcium? Yes, that too is very well documented to occur in high vitamin A conditions. That calcium has been drawn-out from the bones to bring the local pH levels back in line. Finally, what about the cholesterol itself? Yes, cholesterol is documented to be one of the chemical breakdown pathways for vitamin A.
See: Organic Chemistry Morrison and Boyd 3rd Edition Pages 278-280
With all of that, I think we have a perfect fit as to who the real culprit is in causing coronary heart disease. It’s not cholesterol itself. Instead, cholesterol is just one of the by-products of the breakdown of vitamin A. It’s also very likely that elevated cholesterol is just a defensive measure in response to the inflammation.
Either way, the real culprit in heart disease is whatever’s causing the lesions to occur. Obviously, cholesterol is not the root cause of the plaque at all. Therefore, elevated cholesterol is just another symptom of the chronic disease.
But, the medical establishment does not want you to think like that, or to think too deeply about it. The thing is that they have a magic drug to take care of that elevated cholesterol for you. It does not matter to them one little bit if cholesterol is the real culprit or not. It’s the drug they have, and it’s the drug they are going to aggressively try to sell you.
Of course, I’m referring to the now famous “statins.” This class of drugs is a huge blockbuster seller. With about 40 million people taking them daily, it’s been the biggest money maker in the history of the pharmaceuticals. Annual sales are in the hundreds of billions of dollars. And, the worldwide revenue generated in treating heart disease is approaching one trillion dollars. Therefore, there’s no compelling reason for anyone who is in the business to look any deeper into the cholesterol question. But, we will.
The statins have been on the market for about 30 years now. Like with so many other pharmaceuticals, the statins don’t actually cure disease or even prevent disease. They only mask or suppress the symptoms. For the industry, that’s the great thing about the statins. It’s precisely what the industry wants. They can get people hooked on them and have repeat and life-long customers.
Moreover, the statins actually do a pretty good job in suppressing the liver’s production of cholesterol. Therefore, for the average GP overseeing the treatment, it appears that they are even “working.” Okay, so almost everyone involved should be happy with that, right?
Well, that’s not the case at all for a lot of statin users. Many of them aren’t at all happy because they experience serious so–called “side-effects.” So much so, that a lot of patients can’t bear the suffering, and are forced to stop taking their statins after just one year. The other thing with the statins that most people shouldn’t be at all pleased about is that there’s almost no evidence that anyone is going to live one day longer by taking them.
The most commonly reported “side-effect” is that of muscle pain and weakness, and it’s often severe. So, right away the math just does not add up on it. If you are not going to live one day longer by being on a statin, but yet you could suffer in serious pain for every day that you are on them, and that’s potentially for the rest of your life too, why would anyone take them? Very sadly, it’s usually because their doctors have told them “You will die if you don’t take them.” Yes, it’s the same sordid story. They need to resort to scare tactics and fearmongering to keep selling their magic beans. Like with most pharmaceutical drugs, the real clinical trials for them start well after it has been approved and when it goes into widespread use. So, in a way, the patients are just human guinea pigs in these long-running experiments. The results of that long-term experiment with the statins are now showing up.
Of course, over the years, more and more evidence is leaking out that not only are the statins not preventing heart disease and stroke at all, but they are causing a massive amount of pain, suffering, and often accelerating people into other serious diseases and even early death. There are a bunch of very credible researchers now sounding the alarm, and asking serious questions about the statins. The industry, of course, is fighting back feverishly with propaganda, and marching out their own paid-off pundits to keep pushing the statin drugs as aggressively as ever. What exactly are the more serious long term complications of statin usage? In no particular order, they are significantly increased risks (often by about 50%) of:
Serious Liver damage
Dementia / Alzheimer’s disease
IBD / IBS
Debilitating muscle atrophy
Now, with all those severe and increased risks, and no proven benefit or even a decreased risk of having a first heart attack, who in their right mind would take a statin? How is the industry getting away with this nonsense? Of course, it’s with slick marketing, propaganda, fake science, rigged studies, aggressive media censorship, and with what I view as very deceitful manipulations. For example, seeing an increased risk of “Heart Failure” on the above list should have caught your attention. After all, aren’t the statins suppose to reduce the risk of Heart Attacks? Well, yes, they are. But, you see, technically speaking, catastrophic “heart failure,” due to the heart muscles being too weak to contract and pump blood, is not a “heart attack.” No, a “heart attack” is when a big slug of plaque peels off the artery wall and blocks it, or it gets lodged into the heart valve. Of course, to you and me, it’s just a bunch of weasel words to hide from the truth; there’s no material difference between dying from catastrophic “heart failure” or a “heart attack.”
The reason people on the statin so commonly experience debilitating muscle atrophy, muscle weakness, and sometimes catastrophic “heart failure” is because the drug does not just block the liver’s production of cholesterol. It also blocks the production of another critical enzyme called CoQ10, among other important processes. The CoQ10 enzyme is a key enzyme used by all cells, and especially so the muscle cells, to produce energy. So, the statins are just going to slowly drain the life force out of every cell in the human body. Remember too, that the liver is the body’s primary detoxification organ. Obviously “blocking” any aspect of its function is reckless if not just plain stupid. I don’t want to go more into that aspect of it here. But, please check out what other people are documenting on it. Here are a few good references.
Dr. Aseem Malhotra – Heart Stents, Cholesterol and Statin Smoking Guns?
Dr. Michael Eades – Statin drugs and diabetes
Dr. Maryanne Demasi – ‘Statin Wars: Have we been misled by the evidence?’
Some of the propaganda statements from industry pundits are so egregious, it’s just obscene. It’s as if they are saying, don’t worry about the vastly increased risk of dementia/ Alzheimer’s, my god man, you could have a heart attack. Don’t worry about the vastly increased risk for diabetes. We, the experts in medicine, have new synthetic insulin we can sell you for the rest of your life, and at 10x the old price too. And when your diabetes gets worse, and you lose the ability to circulate blood in your lower limbs, don’t worry, we can just simply cut off your legs. And ladies, don’t worry about the 50% increased risk of developing breast cancer; we, the experts in medicine, can just simply cut off your breasts. We are really good at that too. Don’t worry that you can become too fatigued and weak even to move. Just trust us, we are the experts. Above all else, don’t stop taking your statins, or “YOU COULD DIE.”
But, my purpose here is not to go bashing the statin drugs. Rather, it’s to highlight this list:
Serious Liver damage
Dementia / Alzheimer’s disease
IBD / IBS
Debilitating muscle atrophy
Do you recognize that list? It is, for the most part, the same list of the major diseases I’ve been attributing to chronic vitamin A poisoning. Here we now have substantial evidence showing that the statins are causing these same diseases. How can that be possible? Could they be caused by a deficiency in cholesterol? Well, no, because there are a lot of people with naturally low cholesterol levels, and we still have a massive epidemic in all of these diseases.
What about this little tiny detail of one of the breakdown pathways of vitamin A is to convert it into cholesterol? What if the statins are preventing this breakdown? On one hand that would sure lower the amount of cholesterol produced by the liver, as it indeed does. But, in doing so, what does that mean for serum vitamin A levels? They should be going up with statin use then too. Yes, they do.
Serum retinol levels throughout 2 years of cholesterol-lowering therapy.
In the entire population (N = 102), serum retinol was 3.46 +/- 0.08 mumol/L before therapy and 3.76 +/- 0.07 after 2 years of therapy (P < .001). Serum retinol increased in diet- and statin-treated groups, but not in fibrate- and resin-treated groups.
Quite remarkably, here we have a drug with massive market adoption, that is inadvertently increasing serum vitamin A levels. Almost all of the other reported so-called “side-effects” documented for the statins are a perfect match for those of vitamin A toxicity too. But, most amazingly, its use is now proving to result in significantly increased rates of above listed chronic diseases.
The silver lining in this dark cloud of the on-going statin fiasco is that it has inadvertently given us a tremendous amount of more strong evidence that chronic vitamin A toxicity is actually causing all of the above-listed diseases.
Additionally, there’s the other bit of very bad, and yet almost global, advice dished out by the medical experts regarding heart disease. They have pretty much vilified salt, and said that everyone should be on a low salt diet. The experts have correspondingly set ridiculously low guidelines for its intake. But, once again, it looks like that advice is entirely wrong. Here’s an excellent video presentation using historical references and data to show that higher intakes of salt actually reduce the rates of coronary and other chronic diseases.
But, there’s one other super important and connecting detail you need to know about salt and cholesterol. Much of the body’s cholesterol is excreted and disposed of by the liver via the bile salts. Therefore, you need adequate dietary salts to facilitate that critical process.
Now, if I didn’t know better, it’s almost as if much of the advice from the medical establishment is rigged to manipulate us into a chronic disease.
Anyhow, if the advice from the experts is so often wrong, what’s a person to do when they are concerned about high blood pressure, or heart disease and stroke? All I can do is share what’s happened in my case. After four years on my vitamin A elimination diet, my cholesterol levels have dropped in half. The various cholesterol ratios are like perfect too.
My blood pressure is excellent. And somewhat recently, my resting heart rate has fallen a bit more to now being usually around 50. That’s reported to be a standard heart rate for a well-trained athlete. But, I’m not a well-trained athlete and I’m now in my late fifties. Go figure?
Therefore, if I had a friend concerned with the long term risks of heart disease I would definitely encourage them to consider a low vitamin A diet. Lastly, there’s the concern for the potentially already built-up calcium deposits in the arteries. I think that a regular dose of apple cider or balsamic vinegar will quickly take care of that.
The human body was perfect and is perfect. We just have to be very careful in not poisoning it. Obviously, we should also never be taking any drug that “blocks” some critical function of it.
I am occasionally getting asked about the recovery time frame people might expect for themselves. Since everyone’s situation is unique, there are no easy and straightforward answers. All I can do is share what’s happened to me and from that information let people set their own expectations as to how long the road ahead might be. The only thing I can do is try to reassure people that I firmly believe it is at least on the right road.
Even with my own certainty about it, there are still a lot of unknowns. Firstly, there is a question of just how much tissue damage has occurred and how widespread it might be throughout the body. In the little bit I was able to determine about this, it looks like there can be 20% or more of tissue or organ atrophy/dysfunction before there are any real noticeable symptoms. Regarding the liver, the extent of the hidden damage can be much more significant. It can be somewhere around 80% damaged before people notice symptoms. In the context of blockage of coronary arteries, it might be as high as 50-80% before people notice it. Therefore, there could be a lot of damage that the body needs to repair and heal itself of. That’s just going to take a long time. Of course, there’s much more to the repair story. This type of damage is not as simple and as straight forward to recover from as recovering from say a wound or trauma-induced severe injury. This is not like a broken bone that usually heals in six weeks. What makes the chronic diseases so much more complicated is deeply-rooted in protein synthesis. After all, the disease itself is really the manifestation of defective protein synthesis. That’s what has caused the tissue to become damaged and malformed in the first place. Medical experts like to call this condition “metaplasia.” But, even though that’s a nice sophisticated sounding term, it does not mean that they understand even the first thing about the root cause of metaplasia.
Of course, I experienced this metaplasia often during my recovery period. It’s important to know that as time progressed, it became more and more localized, and then finally restricted to only a few small spots on my fingers. So, although I was making good and reasonably steady progress, it did take what seemed forever to fully redevelop well-formed, and regular and healthy skin again on my hands.
Okay, so let’s think about what’s really going on there. Why does it take so long to heal from the chronic diseases even after adopting a low vitamin A diet? The answer is partially found in this statement regarding the use of Isotretinoin, a.k.a. Accutane.
WARNING:Isotretinoin affects the entire body and can change not only the skin, but the entire body for the rest of a person’s life. This is why it is only approved for severe nodulocystic acne.
With a big warning label of: SERIOUS SIDE EFFECTS
The critical point here is that Accutane can, and often does, damage a person’s body permanently. Of course, since “Side effects are numerous and widespread, and affect almost all patients,” that damage is not a ridiculously so-called “side-effect” at all. Obviously, they are direct effects. And no, Accutane is not a “medicine” either, rather it’s a direct poison. And, no, doctors are not prescribing it for only “severe nodulocystic acne” either. Many are often prescribing it for mild acne too. It’s completely ridiculous to give this “drug” to any teenager, for any reason, ever.
But, for now, let’s just gloss over the fact that thousands of doctors are still routinely prescribing a drug for acne that has the well known “side-effect” direct-effect of permanently damaging a teenager’s body and often even inflicts brain damage on them too. What we are interested in understanding at this time is why and how does retinoic acid permanently damage the body. Why do so many people not fully recover from it after stopping its use, whereas, some others do?
The critical understanding needed to answer that question is found in the knowledge that the primary mechanism of retinoic acid’s magic action is that it causes “gene expressions.” Back in 1992, it was documented to be about 300 different gene expressions. The science has moved ahead a bit on it, and more modern literature now places the number at about 500 different gene expressions caused by retinoic acid (RA).
Next, we need to ask what are these gene expressions really? Of course, a major clue here is that RA is definitely documented as being a potentially deadly serious cytotoxin. And, since there are now more than 500 different gene expressions attributed to it, it should be self-evident. Has no one ever asked why are there so many different gene expressions? What’s the specific purpose of each one of them? It is also super critical to ask if RA is invoking these regulations of “gene expressions,” what molecule or enzyme is regulating that process? In other words, what governs and selects a particular one. For example, why does so-called gene expression #103 occur versus say gene expression #490? Of course, no one knows the answers to these questions. But, to any reasonably critical thinker, that number of 500 different gene expressions is the dead giveaway. They are not gene expressions at all. Rather clearly, they are merely random sites of where the RA molecule has bonded with the cell’s RNA and DNA and caused gene-damage. That’s right, they are indeed 500 different expressions of gene damage. Therefore, what we are really dealing with here are wide-spread RNA and DNA damage. So, for all the dermatologists who are still prescribing this wonder drug, that’s nice work guys, you are simply poisoning the RNA and DNA of your young patients.
Moving along here, and with that better understanding of the real mechanism of retinoic acid, we can ask what happens next? The short answer is metaplasia, inflammation and eventually so-called “autoimmunity” too. Of course, the body’s response is not always immediately noticeable. Retinoic acid picking off just a few cells at a time is not a big deal. In the development of the auto-immune diseases, it is usually a slow creeping process. It could take months, years, or even decades before someone has symptoms. But, we know that in the extreme case of Accutane use, it usually takes only about six months (depending on the dose and duration of the “treatment”).
There are at least two broad categories of the severity of the RNA and DNA damage going on. But, both manifest in defective protein synthesis. Cells are normally, and continuously, synthesizing proteins for cell repair, overall tissue maintenance, cellular replication, and for all kinds of other reasons. This is just a fundamental and necessary function of life. But, the supercritical detail we need to know here is that that the RNA and DNA is the cell’s protein weaving machinery. It’s very much like a super sophisticated biological loom that the cell uses to weave together all needed proteins. The generated proteins are beautifully and intricately structured molecules too.
The triple helix collagen protein molecule is an excellent example of one.
But, now with the retinoic acid molecule randomly stuck in the middle of the weaving machinery, the cell is going to be continually assembling defective proteins. Although defective, the cell is going to be diligently doing it over, and over, and for the rest of the cell’s life too. The cell is just doing the best it can manage. In one damage scenario, the generated proteins might be so severely malformed that it is just not usable at all.
In another scenario, the generated proteins may only be partially defective. Either way, the body is now trying to repair and maintain itself with faulty structured proteins. The tissue eventually develops metaplasia. And, that is the perverse and insidious mechanism as to how Accutane really “works.” It slowly wipes out the stem cells of the sebaceous glands of the skin, and many of them throughout the rest of the body too. So, that’s how it shrinks the sebaceous glands (and BTW often the testicles also, and sometimes it even results in the slow chemical castration of young men; that’s more real nice work guys).
And that’s how and why retinoic acid can permanently damage a person’s body for the rest of their life.
Therefore, even though we can adopt a low vitamin A diet, those DNA damaged cells still exist. How long they’ll last for depends on their host tissue and location. But, it could be going on for many years.
That’s probably not a very comforting thought. And, there’s even a bit more bad news here. Some of the defective proteins are going to be so malformed that they are going to appear to have come from a foreign species to the human body, or maybe even just foreign enough specifically to our own body. When that happens, the immune system is going to move in and attack the cells that are generating them, a.k.a. “auto-immunity.” I’ve already spent way too much time in ETFOH discussing this topic so I’ll just leave it at that.
With all of the above information, you can see why eliminating vitamin A from your diet is just the starting point in a recovery. It is not going to immediately, or even quickly, heal the body. All the existing RA damaged cells are still going to be perpetually assembling defective proteins. Thus, you could have on-going “metaplasia” in various tissues and organs for quite a long while.
But, I don’t want to paint too bleak of a picture here either. I have complete confidence in the human body and in its natural healing powers. I just want to set the expectation that it is going to take time to recover fully. In my personal experience, I was extremely sick too, and as about as sick as a person can be without dying, yet, I did recover from all of this mess. I made most of that recovery in about the first year. I was actually through the worst of it in about the first three or four months too. Of course, things rarely always work out in the first attempt. I foolishly thought that I should supplement with lutein and zeaxanthin. It didn’t hit me right away; instead it wasn’t until after six weeks into that supplementation I had realized my mistake. That little bit of carelessness was a huge setback, and it easily cost me at least another 6 months in more recovery time. I then more slowly made a complete recovery over the following three years. But, even just after the first year I was in pretty good shape and had nothing much to complain about. I expect younger people will recover faster.
Detox setbacks and symptoms
With that time expectation set, it would still be great if people just slowly yet progressively recover by adopting a vitamin A elimination diet. Although that is indeed sometimes happening, it is not happening for everyone. Some people have reported that they experienced an initial period of health improvement, and then they’ve moved into a phase where their condition and health gets far worse and even worse than before they started on the diet. Dr. Garrett Smith has called this a detox phase. I have a plausible hypothesis on why it’s happening. But, it’s just a hypothesis. So, please apply your own critical thinking to it.
I think what’s happening is that as the regular vitamin A serum levels start to decline, then just due to the mechanism of chemical equilibrium, more stored vitamin A is released from the liver. That’s just what we want to have happen right? Unfortunately, there’s a catch to it. There is a relative toxicity scale to the various forms of vitamin A. Obviously, retinol captured in the RBPs is not very toxic at all, next up is unwrapped retinol, and then it’s the retinyl esters, followed by retinoic acid. So, that storage form in the liver is actually quite toxic. And with it now being released faster than usual, people would experience its increased toxicity.
The following is from a 1981 report by Anthony R. Mawson and Gabriel I. Onor titled: Gout and Vitamin A Intoxication: Is There a Connection?
Retinyl esters react more randomly with the membranes of cells than the physiologically sequestered retinol bound in holo-RBP; hence, they are a major form of vitamin A toxicity.
Other sources back up and confirm this information.
Additionally, much of the liver’s retinyl esters are in the retinyl palmitate form, and that’s a more water-soluble molecule. Thus, that might explain why some people are experiencing foamy urine after being on a low vitamin A diet for a while.
Foamy Urine and leaking kidneys
Of course, it’s not normal to have protein leaking into the urine. It is a key marker for kidney disease. So, I don’t want to at all minimize these reports of foamy urine. It is definitely a serious concern. But this is not an ordinary situation for people to be in either. Therefore, let’s not jump to conclusions on it.
With that, and somewhat reluctantly, I now want to share my own account of being diagnosed with chronic kidney disease (CKD). It started way back in 2006 with a routine screening check for an insurance policy. The test had detected protein in my urine. Repeated tests by my GP over the following year revealed that my situation was worsening. A more comprehensive analysis showed that I was in trouble and I was referred to a specialist. A nephrologist. That was the first time I had even heard the term. Later I learned that the nephrons are the delicate structures in the kidneys that are responsible for filtering the blood and extracting water-soluble waste products into urine. Up until that time I had pretty much zero exposure to the medical sector, and I held doctors in high regard. Like most people, I felt these folks were the best of the best in science. Therefore, before seeing the specialist, I was not too concerned. After all, there’s been about a hundred years of advancement in modern medical science, so I thought that surely they’d be able to take care of me.
My appointment with the nephrologist didn’t go as expected, to say the least. Basically, I was sent to the nephrologist to have “the talk.” He was a nice young man, who appeared to be very knowledgeable.
He politely explained that actually, no, there was nothing he could do for me. He showed me the charts where they had plotted out my progressively increasing protein loss, with a nice regression curve fitted to it. He then told me that my condition had been detected early, and that I had about five years left, and that I should get my affairs in order. He told me to expect to be on dialysis in about the next two years. He went on to explain that dialysis is not a long term treatment, it just buys you some time. He also explained that things can get really ugly on dialysis and most patients just decide to stop it after two years, and they then die shortly after that. He went on and explained why I was not going to be a candidate for a transplant, and the odds of finding a donor were about the same as winning the lottery.
Very strangely, I was not too shocked by this information, and I wasn’t really upset by the news. I wasn’t being flippant about it either. I am just practical, and the news was what it was, and I would just have to deal with it. Yet, having two teenage boys, and knowing that I was not going to be around for them was really an unpleasant realization.
Next, here’s where the story gets really interesting, if not just wacky. Being the practical kind of guy that I am, and being very medically uninformed, I asked him, “What’s the big deal with losing protein anyways, why can’t I just eat an extra steak each week and make up for the loss?” He explained that the concern wasn’t that the protein was being lost, rather it was that the protein loss was a biomarker for the progressive breakdown and apparent self-destruction of the nephrons. He explained that medical science had suspected that additional protein in the diet might be stressing the kidneys, and it might actually be making the situation worse, or even accelerating the breakdown of the nephrons. He then went on and told me about a study he had just headed up to test this theory. It was a large study conducted between Canadian and UK researchers. They took 7,500 people with Chronic Kidney Disease and put them on a zero protein diet. He then said that it didn’t go very well, and I quote him: “we ended up killing most of them in three months.” Clearly, their “study” did not help these people at all; instead, it accelerated them into death.
I was stunned by what he had just told me. I could almost not believe what I had heard. I completely set aside my own grim diagnoses; it just didn’t matter to me after hearing that. I tried to remain calm, but my brain was racing ahead in trying to make sense of it. On the one hand, I thought good for him to be admitting this, but on the other hand, I had never met a self-confessed killer before, let alone a serial killer. I was really, and visibly, upset by this information. Maybe he thought the reality of my own diagnosis was starting to sink in, but that wasn’t at all the case. I was just getting angry about what he had told me.
Here’s the thing, I only have grade twelve biology, and maybe five undergraduate courses in chemistry, and a few in organic chemistry. But, what I do know is that there are about 50 trillion cells in the human body, and there are approximately 10 million cells that turn over every day. Every single one of those cells is built up by proteins. Protein is essential to their structure and functioning. Therefore, what they did was to take away the most basic building blocks of what these people really needed to maintain and potentially even heal their bodies.
How could modern medical doctors think that putting sick people on a zero protein diet was going to be viable? I mean, this is about as basic as it gets. I then thought about where do you get 7,500 study subjects from? Well, of course, it’s mostly from their GPs who refer them and enroll them in these studies. So, there would have been quite a few doctors involved in conducting and monitoring this study. How could all of these doctors have not raised serious concerns about their kidney patients being placed on a zero protein diet?
I then asked my nephrologist: “Why wouldn’t you have started with a 7 person, or even a 75 person, study just to be safe? Why start with such a large number of 7,500 people?” He went on and explained that I did not understand modern research, that it’s now all about “evidence-based medicine” and they needed to conduct these big studies to get a strong statistical significance in any finding. I retorted that even one dead person has a strong statistical significance to me.
I’ve subsequently learned that these “failed” studies are rarely published, even though they are usually taxpayer funded. They are quite often just swept under the rug and buried so to speak. However, I’ve never checked if this one was published or not.
I’m really not the type of person to jump to conclusions, but I had heard enough. I then asked him “Why do you even have a job?” What I really wanted to ask him was “Why aren’t you in jail?” I mean in any other field if you killed most of 7,500 people, you are going to be held accountable. I went on and asked, “If you can’t do anything for people, and you have no effective treatments, no cures, what’s the point of your job?” He explained that it was to plan and schedule people’s dialysis program. I stood up, thanked him for his time and told him to cross my name off his patient list, and that I would not be coming back. I told him I had no interest in his dialysis treatment, and that I would just let nature take its course with me. And that’s exactly what I did. Over the next few years, my health did get progressively worse. Even though my wife often asked me to go back, I never did.
To this day, I am still really bothered at how foolish their zero protein experiment was. I am shocked that this could have happened in Canada. It is something I might expect to have occurred in some third world banana republic. I can only hope that there were no children among the 7,500 people enrolled in that study. Still, I think it’s a shameful debacle. Even though I’ve subsequently learned that killing patients in studies like this is rather routine; there is no way I can accept it. There is something drastically wrong with medical science where this is allowed to go on. Killing people with gross incompetence is a crime. There is no way “doctors” should be getting a “pass” on it either. Not in the name of their pursuit of so-called “medical science,” or for any other reason.
By the end of 2013, my kidney function was severely declining. A few times I had blood in my urine, so I assumed that the end was near. Even with that, I wasn’t suffering too much. Ironically, learning about this nephrologist’s botched study was one of the best things to have happened to me. Because of that information, I had almost entirely checked out of the medical system. I had lost most of my trust in the system. And that was one of the best decisions that I have ever made.
But, the point of me relaying this story is not to go doctor bashing. Instead, it is to highlight just how little medical science truly knows about the human body. It’s also about how something so unbelievably basic can be overlooked or ignored by the experts. But, there’s a bunch of good news here too. Although having leaking protein from the kidneys is not normal, it is also not necessarily CKD either. It is just the body’s response to an extreme condition.
Most importantly CKD does not need to be chronic either, and that should be very good news for the now 30,000,000 people in the USA alone with progressive kidney disease. Additionally, being given a terminal diagnosis by the “experts” is not very meaningful either. Sure, in my case n=1, but I don’t give a hoot about their claim of needing large studies to prove some statistical significance. On the contrary, I think their reliance on some big “statistical significance” is a lazy cop-out for not using critical and logical thinking. In a way, it also rigs the system to where only big and well funded clinical organizations can do medical research. How convenient is that, huh? So, no, I’m not buying their nonsense, and n=1 can be hugely significant. All indications are that I’ve now made a full recovery from my CKD. I no longer have leaking protein.
If there’s going to be more of the retinyl esters back flowing from the liver into serum, is there something else people can do to mitigate the harm? Unfortunately, I don’t have any great answers. But, I’ve since learned more about vitamin C. What’s interesting about vitamin C is that it appears to be only moderately beneficial when people are healthy. Conversely, where vitamin C really shines is when taken when people are sick. It is also reported to be very protective in the context of vitamin A toxicity. So much so, that I think, scurvy might just be misdiagnosed vitamin A toxicity. The reason that vitamin C plays such a critical role is that it facilitates the formation of collagen and bone rebuilding. These are two of the first tissues affected by vitamin A toxicity. Although vitamin C is not at all a direct antidote for vitamin A toxicity, it appears to play a critical role in accelerating the body’s repair process from it. Even though I had mentioned the need for vitamin C in my eBooks, I think I seriously underestimated its importance. Here’s a rather now famous news report about its powerful potential.
Ironically, the doctors in this case appear to do everything they can to not treat this guy with vitamin C. And, rather than being thrilled about having cured his cancer with vitamin C, it’s almost as if they were afraid to have anyone find out about it.
Likewise, a similar beneficial effect applies to salt intake. What I did not fully appreciate earlier was the importance of salt in the proper development of bile. Salt is needed to bind with the retinoids, and probably with other toxins too. In doing so, they can be more safely released from the liver into the bile. Without an ample salt supply, this process is going to be severely hampered. Here’s a snippet from the 1925 vitamin A research report that reflects the benefit of salt in reducing the severity of vitamin A toxicity.
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
This mixture of inorganic salts was found by McCollum, Simmonds, and Becker to be adequate in the prevention and cure of a form of ophthalmia described by them, and which develops in rats supplied with fat-soluble A. It is interesting to note that Mori regards this form of ophthalmia as identical with that produced by deprivation of fat-soluble A, but his very brief description of the pathology does not support this conclusion.
Ironically, our more modern medical advice has for a long time now vilified salt. The “experts” have been warning people about consuming too much of it for fear of the risk it might have in thickening the blood and subsequently causing high blood pressure. But, they’ve entirely ignored salt’s very long history of its beneficial role in the human diet. Go figure?
At the risk of being overly repetitive, I just want to make sure that anyone who adopts a low vitamin A diet includes an ample amount of protein. An all-rice diet, or an all-potato diet, is definitely not going to cut it. It would also be very dangerous too. Personally, I believe that animal sources of protein are going to be better when adopting a low vitamin A diet. But, that’s just my opinion. As always, please apply your own good judgment on it.
I previously discussed the obesity causation topic a bit in the Weight Gain and Obesity chapter of ETFOH. However, I didn’t go too in-depth and didn’t sufficiently connect it causally with vitamin A. I’ll now try to more solidly establish that connection here.
When I first started on my vitamin A elimination diet one of the very unexpected side-effects was the effortless weight loss. My experience was not a one-off either. I had a (non-diseased) colleague report the same result. Even though we had vastly simplified our diets, it was still providing ample calories (3,000 or more) and all the required nutritional elements. Although n=2 in this study, for two men in their late fifties, to quickly drop around 30 pounds each, and without trying at all to do so, that result was quite intriguing. There was indeed something very unexpected going on here. It’s especially so considering that we’ve both effortlessly kept that weight off for three years now too.
So, with that experience, I had theorized that the body was simply getting rid of fat it no longer needed. More specifically, I had theorized that the body had originally stored the additional fat as a protective measure against excess circulating retinol. Basically, the adipose tissues were taking on some of the load from the liver and thereby scrubbing excess retinol out of circulation. After all, for the liver to take on more retinol storage, it absolutely must get fatter to accomplish that task.
But, at the same time, I was not very satisfied with that simplistic explanation for the adipose cells either. The problem with it was: why were these adipose cells that were taking on the extra retinol not themselves adversely affected by it too? Why don’t they become inflamed and invoke an auto-immune reaction as do the stem cells of the epithelium’s? Well, it took a while for me to see the obvious. Quite obviously, they are indeed being affected in almost the same way. The important distinction is that the adipose stem cells are much simpler in structure and don’t generate the complex cell adhesion proteins needed to tightly stitch themselves to each other. Since they don’t generate these proteins, then they don’t generate the immune-alerting defective and foreign‑species looking proteins. But, the way that the adipose stem cells do behave similarly to the epithelium stem cells in response to vitamin A toxicity is that they too are forced into a perverse state of abnormal rapid replication. At least that was my sub-theory on the causal mechanism.
Of course, many people will quickly conclude that it was the sugar reduction that was responsible for the fat loss my colleague and I experienced. However, that’s simply not true. I tested that possibility by consuming quite a lot of sugar, and the weight did not come back. I also used the following charts in ETFOH to demonstrate the sugar alone is not to blame for the original weight gain. Here’s a copy of that section for easy reference.
Let’s consider the obesity trends that are going on in the USA, Canada, the UK, and chocolate-loving Switzerland. This trend pattern is quite revealing.
Figure 1 Average Daily Sugar Consumption for Selected Countries
There are a few very important observations to make here. The first is to note that Switzerland’s average daily sugar consumption is higher than that of Canada’s, and has been consistently so for about the last five decades. The second observation is the significant and steady decline in consumption of sugar in the UK. Next, let’s look at the trend lines for obesity in these countries.
Figure 2 Average BMI for Selected Countries
Even though Switzerland has higher average daily sugar consumption than that of Canada, they have significantly less obesity. More striking is the slope of the trend lines. Canada’s trend is dramatically higher. Next, consider the contradiction in the sugar consumption between the UK, and Canada. Even though the consumption in the UK has steadily dropped significantly over this time, and Canada’s has steadily increased over this same time, the average BMI trend lines for these two countries are nearly identical. Therefore, this completely contradicts the theory that sugar consumption is causing obesity. Additionally, many other people who do eliminate sugar from their diets do not experience much weight loss, and if they do, they can’t seem to keep it off.
Then whenever I traveled to the USA, I noticed that there is a significantly higher rate of obesity, and even moderately overweight people there than compared to Canada. This is no small detail. Statistically, about 70% of all Americans over the age of 20 are now overweight or obese. (https://www.cdc.gov/nchs/fastats/obesity-overweight.htm).
But, you don’t have to look a statistical data; it is easy to see it almost everywhere you go. Just walk down a busy street, or go to a supermarket and scan the crowd. Just making a rough ballpark type guess, I’d put the USA at having about 30% more serious obesity than compared to Canada. How can that be possible? Both the USA and Canada have our dairy supply “supplemented” with vitamin A so that alone can’t account for the difference. But, it’s quite understandable when you learn that many of the breads, flours, and breakfast cereals in the USA are “supplemented” with vitamin A whereas in Canada they are typically not.
Some people might want to interject here and blame the differences in our national obesity rates just on lifestyle choices. But, that excuse does not cut it either because the lifestyle in the USA is very similar to that of Canadians too.
Then when I traveled in Mexico, the obesity epidemic there appeared to be even worse than that of the USA. There are a lot of poor people in Mexico who are clearly not living the high-life or sedentary lifestyles and are yet quite obese. What’s going on there? Doing just a trivial amount of investigation, this rate of obesity is completely and totally abnormal for the Mexican people too. Sure, there’s a lot more sugar being consumed in Mexico nowadays, but we know that sugar alone can’t be blamed. So then, what’s really going on? Well, when I learned that sugar in South America was being “supplemented” with vitamin A, it became rather clear. When I was in Mexico I went to a supermarket, picked up a pack of sugar, read the nutrition label, and sure enough pure table sugar was labeled to provide 10% RDA of vitamin A. That’s correct, some of their sugar is laced with vitamin A. Then when you see just how much soda is consumed in Mexico, and that vitamin A supplemented sugar is likely in their soda also, we have a prime suspect.
Next, let’s now get back to what’s happening in the USA and consider some supporting scientific evidence to make the case against vitamin A. Firstly, let’s look for some correlations.
Figure 3 Serum Retinol level and BMI in USA
Source: Serum retinol distributions in residents of the United States: third National Health and Nutrition Examination Survey, 1988–19941,2 Carol Ballew, Barbara A Bowman, Anne L Sowell, and Cathleen Gillespie
Isn’t that a remarkable correlation? As we get older, not only do our serum retinol levels creep up but so too does our BMI levels. Except, it’s not just the BMI levels that creep up with age, it’s also our incidence rates of the auto-immune diseases and cancers. Of course, as our obesity rates climb our life expectancy rates correspondingly decline. So, that drop off in BMI for the 80-90-year-olds shown in the chart is not because they are finally getting their weight under control. Rather, it’s because the more obese folks have died early and have thus statistically diluted the numbers.
Additionally, isn’t it peculiar that for young kids (when they have low vitamin A serum levels) they typically have tons of energy, nice thick hair, nice smooth skin, good vision, low cholesterol levels, and a normal BMI? Unfortunately, as we get older, we typically start to lose these indicators of good health. Next, let’s consider the vitamin A – BMI correlation in South Korea and see how it compares to that of the USA.
Figure 4 Serum Retinol level and BMI in the USA and South Korea
pISSN 1976-1457 eISSN 2005-6168 Vitamin A status of 20- to 59-year-old adults living in Seoul and the metropolitan area, Korea. Sungah Kim, Young-Nam Kim and Youn-Ok Cho
The average South Korean vitamin A serum levels of vitamin A are much lower than that of Americans of the same age. Correspondingly, so are their BMI levels. Maybe even more important is that the average BMI levels in South Korea are rather steady over a wide age range and only creep up slightly by age 60. So, it could be that serum levels above 1.5 µmol/L are dangerous, whereas those below are more safely manageable by the body’s regular defense mechanisms.
Of course, we all know that correlation alone does not determine causation. In the field of causation theory there is a fundamental premise that states that causation cannot be inferred without manipulation. What that means is that to claim a causal influence we need to prove that directly manipulating an input variable has a corresponding measured response (within some range of statistical significance).
Fortunately, we do indeed have that supporting evidence to claim a causal factor with the retinoids and obesity. Firstly, we have the somewhat inadvertent results from a study where dietary vitamin A (even in the form of beta-carotene) was increased resulting in obesity. I say inadvertent results, because neither the researchers, nor the subjects, were at all interested in, or even suspecting, to see a resulting change in body weight.
Source: Vitamin A and vitamin E in human blood 3 Levels in patients in psychiatric hospitals
BY 2. A. LEITNER 52 Welbeck Street, London, W I AND T. MOORE AND I. M. SHARMAN Dunn Nutritional Laboratory, University of Cambridge and Medical Research Council
This study is from 1951 -1962, the researches were working with patients in a UK psychiatric hospital, often including people with schizophrenia. What they noticed is that the serum levels of both vitamin A and the carotenoids in these patients was abnormally low. Somewhat surprising to me, the researchers did not appear to think that there may have been a possible connection between the patient’s mental health condition and their vitamin A status. Nonetheless, the researchers felt that it would just be in the best interests of the patient’s overall general health to bring their serum levels in line with what was deemed to be the more normal values as observed in the general public. With that, they added some higher concentration beta-carotene vegetables into the meal plan for the patients. The very surprising outcome of that diet manipulation was that many of the patients quite quickly became obese.
Our results have shown not only that mean values for carotenoids, and usually also for vitamin A, are low in mental patients, but that values approaching those for normal subjects may be induced by ensuring that large amounts of carotene are consumed, either in oily solution or in the form of vegetables.
Somewhat lower values were always found, for both carotenoids and vitamin A, in patients who had been resident in hospital for 2 years than in newly admitted patients. In certain groups of newly admitted patients the vitamin A levels were normal, but the carotenoid levels were always low.
Between the two stages of our work, begun in 1951 and in 1962, special attention has been given at Claybury Hospital to the provision of liberal supplies of vegetables. As in most other psychiatric hospitals, moreover, the use of tranquillizing drugs has improved the appetites of the patients, to such an extent that obesity has become a common problem. At the most these changes seemed to have caused only a slight increase in blood levels of carotenoids and vitamin A towards the normal range.
Yes, adding more vegetables, such as carrots to the diet (and the tranquilizing drugs) led to obesity. And then regarding the tranquilizing drugs being to blame for the improved appetites, they contradict themselves with the following rationalization statement:
A likely hypothesis is that the appetite of mental patients for vegetables is poor, and that these are not eaten in amounts typical of normal subjects unless special measures are taken. […] An alternative hypothesis, perhaps less probable, is that in mental patients the efficiency of the absorption and conversion of carotene is reduced. Increased quantities of carotene must therefore be given, above the requirements of normal subjects, in order to sustain levels of carotenoids and vitamin A equal to those in normal subjects.
Source: as above
Regardless, I like these types of inadvertent experiments because they are ideal double-blind studies. Neither the researchers nor the people in the studies realized or were even aware that the effect on obesity was being considered as an outcome. As a side note, many people with schizophrenia report a surge in weight gain just before their first encounter with the disease conditions. Also, very interestingly, the lower than normal level serum levels of vitamin A is observed in autism, IBD, depression, and Alzheimer’s disease too. Most surprisingly, it’s very significantly so in cystic fibrosis too. So, where is their serum retinol magically disappearing too? Could it be into retinoic acid? Isn’t it also interesting that the documented psychiatric side-effects of retinoic acid toxicity are a perfect match for the symptoms of schizophrenia, autism, and even Alzheimer’s? I digress. Let’s get back on track with investigating obesity causation.
Next, we have the opposite effect demonstrated in another study where the vitamin A input variable is manipulated in the other direction.
Proc Nutr Soc. 1973 Dec;32(3):105A-106A.
Vitamin-A and epilepsy: a dietary contretemps. Sharman IM, Stern G.
In this 1973 study researchers were considering the possible effect a low vitamin A diet may have had on epilepsy. Very surprisingly, and completely unexpectedly too, what they saw was a rapid loss in body fat. The study was terminated because they believed that the rapid drop in weight in their subjects was a sign of vitamin A deficiency.
And then in another experiment attempting to purposely induce vitamin A deficiency in volunteer adults we have:
From the sample menus he provided, one can estimate that on a typical day, a subject [person] would consume 80–160 IU of carotene. Thiamin was estimated to be adequate and ascorbic acid was given as a supplement. Energy density was kept high, to prevent weight loss due to lack of appetite and “for psychological reasons.” Indeed, for the first 3.5 mo, all subjects [persons] gained weight. After that time, for the following 2.5 mo, all 10 people simultaneously lost amazingly large amounts of weight, e.g., two persons lost 10 kg of their maximal weights (79 kg and 59 kg). The author interprets this weight loss to be a consequence of the exhaustion of the subjects’ vitamin A reserves, and compares it to the weight loss observable in vitamin A–deficient rats.
Source: The Experimental Induction of Vitamin A Deficiency in Humans George Wolf Department of Nutritional Sciences and Toxicology, University of California, Berkeley, CA 94720-3104
By combining the results of these three studies, we’ve satisfied one of the key requirements of making a causal association claim. Therefore, we have both a solid correlation and required manipulation experiments supporting our general theory. But, what about that specific sub-theory that retinol overload is driving adipose stem cells into an abnormal state of more rapid replication? Surely this has been investigated. After all, the retinoids and more specifically vitamin A, and retinoic acid are some of the most studied molecules in all of medical science. It has indeed been studied. Here’s a 2016 report documenting the adipose genesis effect of retinoic acid: Circulating Retinoic Acid Levels and the Development of Metabolic Syndrome
Adipogenesis is a differentiation process regulated by the complex interaction of some RXR heterodimeric partners (18). In 3T3-L1 adipocyte differentiation assays, retinoic acid effects vary as a function of the stage of adipogenesis and relative retinoic acid receptor, peroxisome proliferator-activated receptor-γ, and RXR expression (19). Inhibition of endogenous RA production by the inactivation of retinaldehyde dehydrogenase (the primary retinaldehyde metabolizing enzyme) increased energy dissipation and reduced abdominal fat accumulation, thus preventing and ameliorating diet-induced obesity (20). Although the role of RA in adipogenesis has been generally proven in vitro, little information on the relationship between serum RA level and MetS (as well as its components) is available for the Chinese population..
Source: Yan Liu, Hongen Chen, Di Mu, Jiahua Fan, Jiayi Song, Yuan Zhong, Di Li, Min Xia; Circulating Retinoic Acid Levels and the Development of Metabolic Syndrome, The Journal of Clinical Endocrinology & Metabolism, Volume 101, Issue 4, 1 April 2016, Pages 1686–1692, https://doi.org/10.1210/jc.2015-4038
Even though the documented adipose genesis is being induced by retinoic acid, we need to remember that retinoic acid is readily produced just by a somewhat high dietary intake of vitamin A.
Retinoic acid is present in both the fasting and postprandial circulations where it is bound to albumin. Immediately following consumption of a retinol-rich meal (~1 mg/kg body weight), mean plasma concentration of retinoic acid was observed to reach 254 nmol/L but was quickly restored to fasting concentrations of 14 nmol/L in 10 male volunteers (Arnhold et al., 1996).
Source: DRAFT SCIENTIFIC OPINION 1 Scientific Opinion on Dietary Reference Values for vitamin A1 2 EFSA Panel on Dietetic Products, Nutrition, and Allergies (NDA)2, 3 3 European Food Safety Authority (EFSA), Parma, Italy
The oxidization of retinol into retinoic acid will happen even more so once a person ages and starts approaching their liver’s maximum storage capacity. But, let’s not forget that in North America, much of our dairy is being directly supplemented with additional retinol too.
Vitamins A and/or D should be considered in the hazard analysis for plants fortifying milk products, as over-fortification could result in toxic levels (). The target level for vitamins A and D in milk manufactured in the US is 2000 IU/quart and 400 IU/quart, respectively. The US-FDA currently considers levels in excess of 6000 IU/quart vitamin A and 800 IU/quart vitamin D to be potential health concerns (Nichols, 1992). Vitamin fortification might be controlled under a CCP or a PP, depending on a firm’s hazard analysis. Preventing over-fortification is accomplished by careful monitoring of vitamin concentrate addition, proper measurement of pump feed rates, and determining whether the volume of concentrate used per product batch is in relative agreement with the theoretical value required to achieve the desired fortification level.
Therefore, the chances of surging one’s retinol intake are considerably higher with frequent milk and cheese consumption. And, yes, there has been a case in Canada where a dairy producer did not have the injection pumps set correctly, and some kids were subsequently killed by drinking the milk. Somewhat strangely, even though fortifying low-fat milk is a legislated requirement in Canada and the USA, it’s not in the UK. How can it be that all those people in the UK drinking low-fat dairy have managed to avoid vitamin A deficiency symptoms? Sorry, I digress again.
Pasteurized Milk Causes Scurvy
What about pasteurization? Could the heating of casein with its embedded retinol generate retinoic acid too? I think it probably does. Here’s why. Firstly, consider this report:
A 34% reduction in vitamin A is reported after pasteurization, and categorized as being “significant.”
Okay, so what happened to the missing retinol post pasteurization? Where did it disappear to? Of course, it didn’t just disappear. It was oxidized and otherwise broken down. Then consider this interesting little ditty? Pasteurized milk is reported to cause “scurvy” too.
Most people are familiar with scurvy, a disease that results from vitamin‑C deficiency. Fortunately, scurvy is rare in Western societies. (It is still seen in infants who are fed a diet of boiled or pasteurized milk). Osteoporosis can be caused by vitamin C deficiency and is seen in both infants and adults who have scurvy. Vitamin C is important in the production of a material called collagen. Collagen is perhaps best described as a fibrous tissue into which mineral is deposited in bone. Together with mineral, collagen gives bone its strength. While it is clear that vitamin C is necessary for bone health, vitamin C deficiency is rare. Vitamin C supplementation as a general preventative measure for osteoporosis does not appear to be warranted. […] Vitamin A is also popularly known today as beta-carotene. Beta-carotene is actually a precursor to vitamin A. Vitamin A is considered critical to normal growth of the skeleton, but excessive vitamin A poses real dangers. Vitamin intoxication causes weakness, fatigue, emotional disturbances, headache, aching in the muscles and bones. Unfortunately, vitamin A is also one of the vitamins often taken in excess in the United States because of recent reports suggesting its beta-carotene content may protect against cancer.
Source: The Osteoporosis Handbook Sydney Lou Bonnick Taylor Trade Publishing, Oct. 1, 2000 – Health & Fitness
How can it be possible that for infants drinking pasteurized or boiled milk instead of raw milk there’s an increased risk for scurvy? That does not appear to be logical because milk, pasteurized or not, contains only trace amounts of vitamin C at ~0 mg/100 g. But then consider the 1937 study, titled:
CONCERNING THE TOXICITY OF VITAMIN A
EDWABD B. VEDDEB AND CHABLES BOSENBEBG
Department of Experimental Medicine, George Washington University
Medical School (Received for publication December 17, 1937)
In this study, the researchers believed that they had induced “scurvy” in their animals just by having them on high vitamin A diets.
Since the rat is known to be capable of synthesizing vitamin C and is not susceptible to scurvy, it is difficult to explain this action of vitamin C. A possible explanation is that vitamin C destroys the toxic factor and that all the vitamin C synthesized by the rat is used up in this process, leaving it susceptible to scurvy. Scurvy of the rat has never been described, but the symptoms produced by fish liver oils are not unlike scurvy; they include failure to grow, hemorrhages, particularly from the eyes and nose but to some extent from other mucous membranes, and abnormal rarefaction and fragility of the bones.
In a few rats, the urine was collected and titrated with 2,6-dichlorophenol indophenol. After administration of jewfish liver oil equivalent to 100,000 units of vitamin A for about 3 weeks, the excretion of vitamin C decreased to the vanishing point, but reappeared in the urine in considerable amounts after the daily administration of 5 mg. of crystalline ascorbic acid. While this is suggestive, since the physiological action of vitamin C is quite unknown, the correct explanation of its remedial action for jewfish liver oil must await further experimentation.
So, even though rats can produce their own vitamin C, that wasn’t enough to protect them. Whereas the added vitamin C in these experiments was rather effective in protecting the animals from dying due to the toxicity effects of the vitamin A. Of course, there’s more to it. These researchers knew it was not just simply vitamin A alone causing the disease conditions. They make this very interesting and astute statement in their conclusion:
In addition to vitamin A, fish liver oils contain a toxic principle, at present not identified.
Since retinoic acid was discovered around 1960, these researchers back in 1937 would not have known about it as being the hidden additional toxic principle that was causing the “scurvy” in addition to all the other diseases and ultimate death in their animals.
Next, consider this little ditty from the same study:
When the unitage of vitamin D exceeded that of vitamin A, the combination was far more toxic than the same amount of vitamin A alone.
Of course, many people in North America have been consuming fish oils thinking that it is good for us. And then remember that those injection pumps at the dairy producers are pumping both vitamin A and D directly into our low-fat milk supply. Therefore, in North America, there is no shortage of possibilities for people to be getting too much retinol in their daily diet. Of course, it’s not just retinol, as reported above. It is also quite normal to have trace (nmol) amounts of retinoic acid in serum too. Those facts combined with the 2016 report documenting that retinoic acid induces adipose genesis, that eliminates the theoretical aspect of our sub-theory. Therefore, very slowly, over the years, vitamin A and daily spikes in its downstream metabolite of retinoic acid are just going to make us fatter and fatter.
So, with this final detail established, we now have solid supporting correlations, manipulation experiments, and a direct documented causal mechanism. That should leave you with so little doubt as to one of the major forces driving the obesity epidemic. That’s all rather bad news. But, the good news is that our intake of retinol is under our control, and obesity caused by it is quite readily reversible too. I am now getting direct reports from people who are dropping amazing amounts of weight after adopting a vitamin A-free diet. Here are just a few examples:
I have been losing a lot of weight – 50 pounds in the last 15 weeks – and expect to lose another 40 pounds in the months ahead.
In 6 months, I lost 80 Lbs and my Skin Cleared up.
After four months of being on a vitamin A elimination diet I’ve lost thirty pounds. It has just evaporated.
Even though I’m now consuming about 5,000 calories per day, I’m not gaining weight.
Nonetheless, I don’t want to put the entire blame for obesity on vitamin A either. Like with so many other aspects of the autoimmune diseases and the psychiatric disorders, there is no single cause. The root-causes and mechanisms are more complicated and multi-factored. For example, let’s consider the combined effects of retinoic acid and sugar. As that retinoic acid drives up the rate of adipose genesis, those new cells will in turn demand more energy. That then drives up the appetite and the craving for sugar or other sources of glucose. It’s all very subtlely and yet directly interconnected. I’m also quite sure that there are vitamin A free diets that could still induce the obesity effect if regularly over-consumed. But, at least you now know the identity of one of the most significant hidden factors. It’s a poison “vitamin” that’s making many of us fat and sick.
I’ve had a number of people asking me to get a vitamin A test to see where my serum levels are now at. Of course, I was very curious about that too. It sounds simple enough, but it’s not. Here in Alberta, vitamin A testing is lumped in with vitamin D testing and our socialized medical system has stopped providing discretionary testing for these vitamins. Too many people were requesting the vitamin D test and it was costing the Province millions of dollars. Thus, it appears that they took the position that since “we know” that almost everyone is vitamin D deficient anyways, there’s no need to continue testing for it.
Since we can’t get enough vitamin D from food to meet our body’s needs, Alberta Health Services recommends that all healthy Albertans take a vitamin D supplement.
Here, they’ve provided the blanket recommendation that nearly everyone should just supplement with vitamin D. Yes; our medical experts think that we all should supplement with a vitamin that can also become toxic. Doesn’t that sound familiar? In the context of vitamin A, it’s:
Practical, reliable, field‑based techniques for assessing vitamin A status are increasingly in demand. Not so much to determine whether particular individuals need vitamin A – at 4¢ for 200,000 IU it will always easier, cheaper and safer to assume that they do – but as a way of identifying deficient populations that require community-based intervention.
Source: Vitamin-A Deficiency Health, Survival, and Vision Alfred Sommer and Keith P. West
Yes, it’s the same sordid story, just a different potentially toxic vitamin. Anyways, it took a bit of wrangling, but I was finally able to get the tests. The Results:
(Below low normal)0.1µmoI/L
With the following advisory warning: “Vitamin A levels less than 0.4 µmol/L correlate with severe deficiency. Supplementation is advised.”
Although it’s not the 0.0 µmoI/L value I was hoping for, it’s still extremely low. The average for men my age is more like 2.2 µmoI/L.
Therefore, my level is about twenty times lower than normal. Also, compare my serum level to the 1969 case study of the young man in Britain I’d referenced along with the Vitamin-A and epilepsy: A dietary contretemps study by Sharman IM, Stern G. After 5 ½ years of eating a vitamin A free diet he succeeded in getting his serum levels down to about ~0.2 µmoI/L. In that report, he was said to have had the lowest serum levels of vitamin‑A ever recorded in Great Britain. Now, with my levels down to 0.1 µmoI/L, I just may have beaten his long-standing record. I’ll continue with my diet to see if I can achieve the 0.0 µmoI/L within the next year. Getting to absolute zero is obviously hard to achieve. It just might be an asymptotic drawdown function. Or maybe the test is not designed to be accurate in this abnormally low range?
My vitamin D levels are at 72.0 nmol/L. Here in Alberta the – desired normal range is 80.0 – 200.0 nmol/L. I’m a bit on the low side, but not overly so. In US units that 72.0 nmol/L equates to 29 ng/ml. So, it’s still very close to being in the normal, or even in the optimal, range depending on whom you ask.
A few other people have suggested that my original health issues were due to a vitamin D deficiency. However, that assertion is completely nonsensical for a variety of reasons.
I had lots of vitamin D in my diet leading up to my disease conditions. Vitamin D did not prevent me from getting the diseases.
I then fully recovered from all my disease conditions by eliminating vitamin A, and not by adding vitamin D.
There’s been a massive amount of vitamin D supplementation going on here in Canada, and in other western countries too and there is no corresponding massive improvement in our rates of the chronic diseases. And forget about seeing massive improvements in disease rates, there’s been no improvement. Sure, vitamin D is probably helping people cope with the diseases, but it is not completely curing them either. So, clearly, a vitamin D deficiency is not at the root cause of the disease. Maybe vitamin D is acting much like many of the pharmaceutical drugs, and is just abating or blocking the symptoms?
Most importantly, the very concept of a vitamin deficiency is what has gotten us into this giant mess in the first place. I really have no research interest in vitamin D either. All I know is that vitamin D has been used as a rat poison for decades, and that is an absolute fact. Next, consider that rats are the de facto model used to test the toxicology of drugs and other chemicals. Yet, somehow, we are supposed to be so credulous and believe that vitamin D magically gets a free pass on it, and supplementing with it is somehow good for us? Sorry, I not buying it. I’m going with that real-world evidence and calling it for what it is. No one can argue that it’s not a toxic substance at high doses. Obviously, it is far less toxic than vitamin A. Since vitamin D binds to the same “cellular receptors” as does vitamin A then it’s possible that it just blunts the potential toxicity of vitamin A. It may be that vitamin D only appears to be so beneficial in bone growth and maintenance due to it obstructing the osteoporosis causing effects of vitamin A? I don’t know. I am not an expert on it. But, we should be careful with it. For now, I’ll stick with my single-minded focus on investigating vitamin A.