An audio version of this post is available here.
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).
For more information, please see: https://rxisk.org/wp-content/uploads/2018/10/Citizen-petition-Sexual-side-effects-of-isotretinoin.pdf
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.