Over the last few months I’ve learned of more people who have been strictly following a carnivore diet (exclusively muscle meats) for five or more years. Not at all surprisingly, they are doing very well. Combined with all the evidence I’ve included in my eBooks, and with my own 5+ years on a vitamin A free diet, it’s clear that the theory of vitamin A being an essential nutrient is patently wrong. According to the vitamin A theory these people, and myself, should have gone blind years ago, and had their skin and all their internal organs self-destruct and otherwise disintegrate. Not only has that not happened, it’s just the opposite. These people are thriving and healthier than many of their peers.

As I wrote about in my P4P eBook, the foundational studies used to establish the “it’s a vitamin” concept were pretty much just garbage science. I’m sorry, but poisoning a couple dozen rats to death does not prove the existence of a “vitamin”.

Although many people are now conceding this fact that it’s not a “vitamin” needed by adults, there are still people clinging to the claim that it’s essential for embryo development. I find that claim and position so strange because we know that too much vitamin A will cause horrible birth defects and often times spontaneous abortions. Yet, some people continue to believe that nature is so foolish to establish a critical dicey dependency on a highly toxic molecule to facilitate proper embryo development. This is their last bastion of hope in clinging to the claim that vitamin A is still somehow a “vitamin”.

It gets even more perplexing once you know that the so-called “active form” of vitamin A is 13-cis-retinoic acid (isotretinoin aka Accutane) and all-trans-retinoic acid (tretinoin). These thought to be “active forms” of vitamin A are as toxic to the human fetus as is thalidomide. The FDA has established “black box” warnings that a fetus exposed to “ANY” amounts of isotretinoin is at extreme risk for developing birth defects. Astonishingly, in the face of those facts the established “science” claims that a fetus somehow needs this exact same compound to properly develop. How do we square up these diametrically opposing statements? Of course, we can’t and clearly then there’s something seriously wrong with that claim.

Like with the early rat studies from the 1920s that supposedly conclusively established vitamin A to be a vitamin, we need to analyze the modern day studies that were used to prove the need for retinoic acid in fetal development. Here’s an overview of the premier studies that “unequivocally” established the critical dependency on retinoic acid during embryogenesis.

Symposium: Functional Metabolism of Vitamin A in Embryonic Development
Vitamin A and Embryonic Development: An Overview
Maija H. Zile
Department of Food Science and Human Nutrition, Michigan State University, East Lansing, MI 48824-1224
J. Nutr. 128: 455S–458S, 1998

I find it troubling that so much of medical “science” relies almost exclusively on “studies” such as this. The way I see it, these “studies” are a complete cop-out for genuine, critical and logical thinking. Depressingly, it only takes a few minutes of thinking to see the flaws in this one. It’s just more bad “science” layered upon many shaky assumptions. The parallels here with what happened with the Wolbach and Howe study back in 1925 are also rather remarkable.

TISSUE CHANGES FOLLOWING DEPRIVATION OF FAT SOLUBLE A VITAMIN.

BY S. BURT WOLBACH, M.D., AND PERCY R. HOWE, M.D.
From the Department of Pathology, Harvard University Medical School, and the Forsyth Dental Infirmary, Boston. Received for publication, September 4, 1925

The Wolbach and Howe study was conducted for about a 10-week duration. At the end of that duration, most of their test animals were either seriously diseased or had died. The fundamental conclusion from that study was that the animals had suffered their devastating tissue and organ disintegration as a consequence of a vitamin A deficiency.

One of the biggest issues with the Wolbach and Howe study is that although they acknowledged that other contemporary researchers were getting the completely opposite results, Wolbach and Howe simply made up excuses to ignore those inconvenient facts. But, the bigger issue is that they delusionally assumed that they were working with complete information.  Of course, they were not. They failed to appreciate that washing casein in alcohol and heat treating it at high temperatures could have toxified it. And, yes, somehow casein can become remarkably toxic.

Casein is a Carcinogen – Dr. T. Colin Campbell

Topic #1 – Casein is a Carcinogen. Really?

Many people have heard me say, “Casein [the main protein of cow’s milk] is the most relevant chemical carcinogen ever identified.” Guilty, as charged. Many times I’ve said this. For the sake of this discussion, let’s call it an hypothesis, that is, “Casein causes cancer”.

How can the most revered of all nutrients increase the most feared of all diseases? “Heresy”, the mob might shout.

But it’s true. In my laboratory research conducted over a quarter century, funded by taxpayer dollars with findings published in the very best journals, we studied this effect in many ways at a most fundamental, cellular and sub-cellular level as much research as for any other chemical deemed to be a carcinogen.

Campbell was not alone in this research and in his findings. There were similar studies conducted at the University of Illinois at Chicago that replicated these results. Very interestingly, although Campbell was mostly focused on liver cancer, the Chicago researchers found that casein was a very potent carcinogen in quickly initiating and promoting breast cancer in animals.

After Campbell, and the other researchers at the University of Illinois, had made this discovery about the rather incredible toxicity of casein there should have been some rather intensive follow-up research as to exactly why a milk protein could be so toxic. After all, since most mammals start out in life being breastfed, how could milk be such a potent cancer causing agent? On the surface of it, that doesn’t make any sense. However, when you get deeper inside of it and discover the vitamin A molecule contained within it, it becomes much more plausible. I have no doubt the standard casein based lab chow used in Campbell’s et al rat experiments was heat treated. Heat treating it is simply necessary to sterilize it from potential bacterial contaminants.

Except, with this revelation from Campbell et al about casein being a powerful carcinogen, why hasn’t anyone gone back in time and questioned the validity of the 1925 Wolbach and Howe study? After-all, they too used casein in their experiments. Couldn’t their animals have suffered from ‘the most relevant chemical carcinogen ever identified” rather than have suffered from a vitamin deficiency? Additionally, why has no one ever bothered to try to understand why the symptoms of the so-called vitamin A deficiency condition are a perfect match for those of its toxicity symptoms? Isn’t that odd?

I wrote about Dr. T. Colin Campbell’s China study in my P4P eBook. I really liked the China Study, and I still think that it’s a worthwhile read. Two very important conclusions Campbell makes in his book are:

1. Food is at the root cause of chronic disease (and particularly so for cancer).
2. The medical sector and medical science is driven by greed and is rife with corruption.

His third, and most important conclusion, is slightly correct, and mostly wrong. He concluded that it’s the milk protein, and therefore by erroneous extrapolation, that most animal sourced proteins are the culprit. However, it’s not the milk protein at all that’s the real culprit. Rather it’s the highly toxic oxidized retinol molecule that’s cased-in the casein that’s to blame. 

Aside: Quite remarkably, this information about the standard lab “rat chow” based diet that included sterilized casein being a potent carcinogen probably invalidates most of other animal based studies that have used this same feed. That’s likely thousands of studies in all aspects of medical research now being highly questionable, at best.

Let’s get back on track here with the more modern day studies that “unequivocally” proved the need for retinoic acid (RA) in embryogenesis. 

Vitamin A and Embryonic Development: An Overview
Maija H. Zile
Department of Food Science and Human Nutrition, Michigan State University, East Lansing, MI 48824-1224
J. Nutr. 128: 455S–458S, 1998

ABSTRACT:
Vitamin A is an essential micronutrient throughout the life cycle. Its active form, retinoic acid via retinoid receptors, is involved in signal transduction pathways regulating development. Both the lack and excess of vitamin A during embryonic development result in congenital malformations. Approaches to examine the function of vitamin A in embryonic development have included treatment with excess retinoids and the use of retinoid receptor knock-out mice, which have provided important insights into the complexity of the retinoid signaling system.

The entrenched current theory is that RA is a “metabolite” of vitamin A. What’s documented, and then simply blindly repeated hundreds of times over, is that RA is the downstream molecular product needed to “differentiate” our stem cells. However, even under a tiny amount of scrutiny that “theory” is nothing more than an assumption. One of the red flags that should pretty much jump off the page at us is that many of the horrible skeletal defects attributed to RA deficiencies are a perfect match for RA toxicity (or mere exposure to RA). They state:

The overlap of the teratological symptoms of vitamin A deficiency and excess indicates common targets and a critical role for A in the development of many organs. 

Doesn’t that sound familiar?  And then they make this statement.

It is important to keep in mind that the developing embryo is very sensitive to a lack as well as an excess of retinoids.

So, here we go again, having just a touch too much RA or too little RA and you get the same teratological results. Odd huh?

Of course designing an experiment to prove the effects of RA deficiency is rather difficult. They can’t just feed experimental animals a diet deficient in all sources of vitamin A because they “know” that the animals will quickly die, let alone allow them to breed through one or more reproductive cycles. So, what the researchers in this study have done is used genetically modified “knock-out” mice. The gene knock-out changes their DNA so that they will be unable to produce the retinoic acid receptors (RARs) needed to utilize RA.

Retinoic acid is now generally recognized as an important signaling molecule that as a ligand to its nuclear receptors, the RARs alters gene expression at the level of transcription (Gudas et al. 1994, Mangelsdorf et al. 1995, Pfahl and Chytil 1996, Roberts and Sporn 1984).

So, basically, their thinking is to disrupt the RA metabolism pathway so as to block the final critical step of having RA invoking those 500+ random gene expressions.

A recent approach to answering questions about the functions of vitamin A in development has been the use of transgenic mice with changes in retinoid receptor gene structure (Boylan et al. 1995, Chambon 1993, Giguere et al. 1996)

Normal vitamin A metabolism pathway

Knocking out the RARs and RXRs
Using their gene “knock-out” mice they’ve taken out the RARs, and RXRs.

The “disrupted” vitamin A metabolism pathway

Do you see the “disrupted” pathway? Actually, neither do I. 

But, sure enough, with that induced mutation they find exactly what they are looking for. Disrupting the RA metabolism pathway results in the development of horrible and catastrophic skeletal and organ defects. Of course, as predicted, their conclusion is that RA is essential for embryogenesis. 

Many of the abnormalities in these mutant mice resemble those observed in the fetuses from the vitamin A deficient animals reported earlier.

Obviously, there are some huge flaws with these experiments and in their logic. Firstly, what if that cellular process of dealing with RA is not one of “metabolism” but rather one of catabolism and detoxification? Of course, when a cancer patient is given the RA “treatment” their body is not metabolizing it, it is frantically detoxifying it. In the process, the result is the horrific widespread destruction the “medication” causes in almost all patients.

Differentiation syndrome (DS) is most current term; Occurs in Acute promyelocytic leukemia patients undergoing ATRA treatment (Tretinoin, Vesanoid).”

Differentiation Syndrome is a life-threatening complication of induction chemotherapy for patients with acute promyelocytic leukemia (APL). Manifestations of this syndrome include fever, hypoxemia, edema, and, in the past, has been referred to as “cytokine storm”.

Yet, somehow we are supposed to believe that the exact same chemotherapy drug is needed for proper embryogenesis. That should sound rather ludicrous to everyone.

Next, we need to consider what if the gene “expressions” are really manifestations of gene damage? But, most glaringly, what they haven’t proven at all is the condition of RA deficiency. No, there is still vitamin A and RA in the cell. They’ve only blocked its assumed to be one-and-only pathway. However, in no way have they limited the availability of RA to bind with and cause DNA damage. Obviously, even without the RARs, that RA molecule is still free to float around the cytoplasm and bind to the DNA/RNA. Therefore, what they’ve really done in this study is just proven that RA is very toxic to the embryo even when the retinoic acid receptors are not available. That outcome is not at all surprising because we now know that RA fractures and fragments DNA.  

DNA fragmentation induced by all-trans retinoic acid and its steroidal analogue EA-4 in C2C12 mouse and HL-60 human leukemic cells in vitro
Raghda S. Alakhrasa, Georgia Stephanoua, Nikos A. Demopoulosa*,
Konstantinos Grintzalisa, Christos D. Georgioua and Sotirios S. Nikolaropoulosb

Abstract:
We have recently shown that retinoic acid induces micronucleation mainly via chromosome breakage.

Next, what about the long-held assumption that the one-and-only pathway of RA metabolism is via the RARs? Well, it turns out to have been the wrong assumption.

Retinoic acid induces apoptosis by a non-classical mechanism of ERK1/2 activation Alfeu Zanotto-Filho, Martin Cammarota, Daniel P. Gelain, Ramatis B. Oliveira, Andres Delgado-Cañedo, Rodrigo J.S. Dalmolin, Matheus A.B. Pasquali, José Cláudio F. Moreira

Abstract:
Even though RA is involved in differentiation and apoptosis of normal and cancer cells, being sometimes used as adjuvant in chemotherapy, its mechanisms of action involve multiple overlapping pathways that still remain unclear. Recent studies point out that RA exerts rapid and non-genomic effects, which are independent of RAR/RXR-mediated gene transcription.

And they go on to state:

Classically, it has been described that the effects of RA are mediated by ligand-dependent activation of RA receptors (RAR) which act directly as transcription factors modulating gene expression by interacting with RA response elements (RARE) in DNA (Kastner et al., 1995). A number of RA target genes have been identified and many of them are associated with apoptosis and differentiation (Kastner et al., 1995; Pfahl, 2003). On the other hand, recent studies point out that RA modulates signaling pathways in a manner independent on retinoid nuclear receptor-mediated gene transactivation; this has been described as ‘‘non-classical” or ‘‘non-genomic” action of RA.

With that bit of new information, there’s now no legitimate evidence that RA is needed for embryogenesis. And of course there isn’t. How could anyone be so credulous to believe that a molecule as toxic as thalidomide to the developing fetus, and one that’s proven to fracture DNA,  cause cancer, cause 500+ other variations of DNA damage, and to induce rapid apoptosis is somehow needed for embryo development?

Moreover, it’s rather clear that the RARs are one of the last defense mechanisms against RA’s toxicity. 

Then, we need to ask the next obvious question. If the RARs are really part of the detoxification pathway, then what’s the result of that pathway being disrupted?  It’s cancer!

The disruption of RA signaling pathways is thought to underlie the etiology of a number of hematological and non-hematological malignancies, including leukemias, skin cancer, head/neck cancer, lung cancer, breast cancer, ovarian cancer, prostate cancer, renal cell carcinoma, pancreatic cancer, liver cancer, glioblastoma and neuroblastoma.

Retinoic acid receptors: From molecular mechanisms to cancer therapy

Alessandra di Masi, Loris Leboffe a, Elisabetta De Marinis b, Francesca Pagano, Laura Cicconi, Cécile Rochette-Egly, Francesco Lo-Coco , Paolo Ascenzi, Clara Nervib, 2014
http://dx.doi.org/10.1016/j.mam.2014.12.003

This finding is similar to the report I referenced in my Breast Cancer eBook where the researchers found that cancer tissues are depleted of the needed alcohol dehydrogenase enzyme. So, basically, it looks like when a cell can no longer defend itself from RA, it can become cancerous. Once again, that should not be a surprise to anyone because of the hallmarks of cancer are damaged DNA and rapid cell mitosis, and that’s exactly what RA does to cells. Hmm? What are the chances that the RARs and RXRs are in actuality the precursors proteins to the RBPs that we now know cells form around retinol and RA and then eject out of itself? 

Anyhow, it’s quite remarkable how the thinking process and conclusions in the Vitamin A and Embryonic Development study “unequivocally” proving that RA is needed for embryogenesis parallels that of the 1925 Wolbach and Howe study. Both teams find exactly what they are looking for and they both ignore huge amounts of evidence by other research and knowledge contradicting their conclusions. Most disturbingly, they just don’t seem to apply common sense to alert them to the fact there’s something drastically wrong with their conclusions. And, like with Wolbach and Howe back in 1925 these researchers are so sure of themselves that they completely ignore the contradictory findings from their contemporaries. I say that because ten years prior to them conducting these elaborate genetic knock-out studies, the HHS was quickly (in just 10-14 days) poisoning young mice to death with the very same molecule they are claiming to be essential for embryogenesis.

United States Patent 4,649,040

The United States of America as represented by the Department of Health and Human Services, Washington, D.C.
Mar. 10, 1987

Therefore, it’s all quite ridiculous and almost absurd. I mean seriously, with that information how could anyone continue to believe that a proven lethal and teratogenic poison is needed for embryogenesis?

Quite interestingly, both the studies by T. Colin Campbell in the 1990s, and that of Alessandra di Masi’s in 2014 both point to cancer causation, and even specifically to breast cancer causation.  Amazingly, Campbell was able turn on and off cancer progression just by turning up or down on the amount of casein being included in the animal diet. That’s a pretty good indication that cancer is being fueled by the ongoing supply of vitamin A.

Yet, as I wrote about in P4P, very disturbingly, when other researchers do find direct links with vitamin A and the retinoids causing cancer, they conceal it and cover it up. That isn’t science. I view it as criminal negligence, at best. It sure begs the question: how could so much of medical science be so screwed up? Is this deliberate scientific propaganda and manipulation to corral us into disease? Of course, there’s huge amounts of money being made everyday in cutting off the breasts of women. But, no one’s going to make a dime off of breast cancer if we reveal the true root cause of the disease, and can therefore prevent it. T. Colin Campbell was correct; corruption is not only endemic to modern medical science, it appears to be institutionalized in the medical establishment.

I wouldn’t be so snarky about it if this was some harmless mistake. But, it’s not. And, we are not just talking about melanomas and breast cancers either. The USA now has the highest rates of birth defects and spontaneous abortions in the world. We’re talking about nearly a million people in just the USA now living with birth defects. With the current CDC estimates that birth defects are occurring at a rate of 1 in every 33 infants born in the United States this represents an ongoing national disaster. Coincidentally, that 1/33 rate is about on par with the current rates of autism too. 

The human body is many thousands of times more advanced than the current state of medical science. This is clearly evidenced by the fact that the more health interventions and drugs pushed onto our populations the sicker we’ve become. And we’ve become vastly sicker, and on a massive scale too. That alone is conclusive proof that many of the so-called experts have no freaking clue what they are doing. The human body was and is perfect. We just need to learn how to stop chronically poisoning it. In order to do that we need to know when a bogus “vitamin” is in fact simply a poison.

Let’s consider just four basic facts.

1. The liver stores 80-90% of all vitamin A absorbed by the body.
2. The liver must, and does, get fatty in response to vitamin A consumed.
3. The rates and prevalence of NAFLD are so dramatically abnormal and geographically clustered, that it clearly tells us that the disease is a poisoning.
4. 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?

Big Pharma Banks on Fatty Liver Disease

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:

https://ggenereux.blog/discussion/topic/riboflavins-role-in-an-important-va-detox-pathway/?part=1

Thanks

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.

1. A restrictive diet alone is just too slow, and too unpredictable.
2. 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)
3. It looks like the people with a big VA supplementation history might be the ones more likely to encounter the detox cycle.
4. The majority of people have found themselves in this mess via VA supplementation or from accutane use.
5. Although most people do believe they are on the right track, their real results are still too few / slow.
6. 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.

What Next?

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.

The survey is available here:
https://forms.gle/rf8jPEk5ao3nNVtEA