Jay Feldman  0:05  
Is vitamin A actually a poison? And how likely is it that you're dealing with vitamin A toxicity? We'll be answering these questions in today's episode of the energy balance podcast, a Podcast where we explore health and nutrition from the bioenergetic view, and teach you how to maximize your cellular energy to maximize your health. In today's episode, we'll be going over the research behind vitamin A toxicity and whether vitamin A is really a poison. We'll be discussing whether you need to be concerned about the use of Accutane. We'll also go over whether retinoic acid is really a chemotherapeutic agent and what this might mean. And we'll talk about whether grant General's claims about the toxicity of vitamin A are valid. This is our second episode discussing some of these claims. In the last one, we talked a bit more about vitamin A deficiency. So you can go ahead and take a look at that one as a starting place. As always to check out the show notes for today's episode, you can head over to Jay Feldman wellness.com/podcast relevant to the studies articles and anything else that we reference throughout today's episode. And with that, let's get started.

All right, so in the last episode, we were talking through kind of an overview of some of the vitamin A toxicity ideas. And then we dug into some studies discussing vitamin A deficiency and the claims made by Grant general and his book, poisoning for profits. And today, we're going to be continuing that series, second part of that series, and we'll be going over, in this case, more of the focus on vitamin A toxicity, again, mostly focusing on claims made by brand general and his book, poisoning for profits. And we'll be including some specific quotes and going over some of the studies that he cites. In particular, it is worth mentioning as a disclaimer. As we get started here, there's going to be some sort of provocative title and thumbnail on the episode. And for anyone listening who's coming from the vitamin A toxicity crowd, we will be challenging a lot of those beliefs, but our goal here is just to look at this objectively, evaluate the claims that are made and and help you to identify if this is something you should actually be considering as a possible health issue and what to do about it. So we have no goal here other than that. There's no you know, we talked about this in the last episode. We went into reading Grant's book, and, you know, his his blog and and listening to his interviews, looking to gain information, looking to consider this as a possibility, and, you know, figure out where on the spectrum this might be, in terms of how much it might affect our health, and whether we should be concerned about vitamin A toxicity or deficiency, and that's the extent of it. So so we don't have any other dog in this fight, and they're just trying to provide good quality, objective information for all of you. So if you are coming from that crowd, I highly recommend trying to kind of take a step back, take a deep breath and see if you can, you know, look through the different citations that we have, the the studies we discuss, and listen to what we're what we're suggesting, objectively and and it's worth mentioning as well. We're not discounting the experiences of anybody on a low vitamin A diet. You know, there's a lot of reasons why someone might have benefits on that diet. We'll talk a little bit about that in today's episode, and then we also will be, in some future episodes, discussing details of retinol and retinoids and their metabolism and their relationship with thyroid health and other hormones and metabolic health and nutrients and all the ins and outs there. We'll really be getting into that in these couple of episodes. Instead, we're just trying to dig into some of the real basic, fundamental foundational claims in the vitamin A toxicity world. And one other kind of intention that we we have had here in this series is just to also provide an example of looking at other people's thought processes and the kinds of theories that they're proposing and examining them as far as how logical they are and the support that's used, and whether and kind of to use it, almost as a as an example of why we should be really careful in evaluating anybody's claims, and shouldn't take anything that somebody says for, you know, on face value and and integrated, you know, instead, we want to integrate it into our view of physiology and try to really understand those claims to the extent that we can, so we can evaluate if they actually are solid arguments, and if we want to make changes based on what someone's suggesting. So ideally, it'll be a good practice in terms of kind of critical thinking and exploration of some possibly alternative ideas. So Mike, is there anything else you want to mention before we dig in here. No,

Mike  4:42  
I think you covered the vast majority of those points that that I would want to discuss to open the episode up.

Jay Feldman  4:49  
Okay, awesome. Well, with that, let's dig into some of Grant's claims in regard to hypervitaminosis A, which is basically vitamin A toxicity. And his general claim in his book is basically that vitamin A toxicity occurs at relatively low doses in in vivo studies. And so this is something that could be happening in anybody, and we need to be careful of it because of that. And so in this section, we'll be going over going through some of the quotes and studies in the subheading in his book titled vitamin A toxicity is proven in vivo. A couple other things to note before we dig into the research here. So just like in the last episode, we're going to be using beef liver equivalents for vitamin A dosing, just because it makes it a lot easier to conceptualize. You know, if we're talking about 1000s or even millions of IUs or micrograms of retinol. It's hard to conceptualize what that could mean, and so we'll be converting it to beef liver equivalents. The reason for that is because beef livers basically, by far, the most concentrated form of retinol that the average person, or average health oriented person, might consume, and it's way more than any other or the vast majority of other sources of retinol or other retinoids or carotenoids. So as an example, one ounce of beef liver is typically in terms of retinol, the equivalent of about 40 eggs, 71 cups of milk, six and a half carrots and around 2.8 sweet potatoes. And with the keratin sweet potatoes, that's using an equivalence between retinol and beta carotene based on an assumption of kind of absorption and conversion. But in any case, we're talking about very large amounts of these other foods, and we'll be talking about very large amounts of beef liver equivalents here when it comes to some of these studies. So it'll just help you recognize, really, one of the main points that we'll be getting at, which is that you're never going to accidentally consume these amounts of vitamin A or retinol. They're so massive, these amounts that we'll be talking about that it's, I mean, the likelihood that someone could accidentally induce vitamin A toxicity in the way that they're doing these studies is nearly impossible. It really is impossible. So that's it'll help with that kind of conceptualization. The other thing that's worth mentioning here is that Grant almost makes it sound as though the fact that hypervitaminosis a or vitamin A toxicity exists is support for the likelihood of this being an issue for a lot of people, and nobody that I know, of including us, disagrees with the fact that hypervitaminosis a exists. Basically, you can consume enough vitamin A to cause toxic effects. This is something that's been known for nearly 100 years. We'll be digging into some of the studies done throughout this time, but the fact that consuming or taking massive amounts of vitamin A is toxic doesn't mean that you need to avoid foods containing vitamin A. It doesn't mean that you're going to become vitamin A toxic just by consuming foods that are relatively high in retinol consumption, retinol amounts or concentrations. And it's also worth noting that this is the case for pretty much any vitamin or mineral or nutrient or intervention that you can think of. You can overdo it to the point where it becomes toxic and kills you, everything from even the most benign, something like water. If you drink too much of it, you'll, you'll die. You'll actually, you'll drown, and it's not even that much. You can have major issues from drinking the amount of water that you would typically drink in two days. If you drink that in an hour, you could die from that. So it's not, it's not like it even needs to be an insane doses. But of course, that doesn't mean that water is toxic. It doesn't mean that you drink, you know, drinking water is going to then cause seizures or brain swelling or a coma or death, just because very large doses in a short period of time will do so. So, you know, same thing can be said for sodium. Again, it's one of those things where if you consume too much in a short period of time, same thing can happen. It's also the same for other interventions. So whether we're talking exercise or sunlight, just because too much of these things can be really, really harmful. You know, if you were to sit out in the sun with your full all of your skin exposed, and it's, you know, you're at the equator, and you're on the sun all day, and you get severe, first, second, third degree burns. That doesn't mean that sunlight is toxic or harmful. It just means that too much is toxic or harmful. And so that, just like a conceptual, a concept to be familiar with when it comes to somebody making a claim like the idea that because there is vitamin A toxicity, vitamin A is toxic, vitamin A is a poison. And, of course, just two other quick examples, and then I'll let you go ahead. Mike, one would be stress hormones like cortisol or adrenaline. We obviously need them. If you don't have them, then that's a potentially lethal condition, but too much of them is also a lethal condition. Condition. If you administer too much epinephrine to someone, they'll die as well. So that doesn't mean inherently that adrenaline is or epinephrine is, is toxic. It's just that we have a certain need for it. And. Don't want to have too much or too little, and there's so many details to go into there. But just because too much is a problem, that does not mean that any amount is a problem. Same thing with thyroid hormones. If you were to give somebody huge quantities of t3 all at once, they can also die. That doesn't mean we don't want any t3 it doesn't mean t3 is toxic. It doesn't mean it doesn't have many beneficial effects. It doesn't mean that a lack of t3 is not going to cause various health issues. So those are just some things to to to mention when it comes to looking at studies on the toxicity of vitamin A.

Mike  10:35  
I think there's a couple points in there that that I want to touch on that, I think would be salient here. So the first one is even some of the substances that are promoted inside the low vitamin A camp, things like niacin, can be pretty toxic pretty quickly at certain dosages, for particularly for the liver, you start getting into gram dosages of the vitamin, which is relatively equivalent to what they're doing in these studies with hypervitaminosis A, where they're getting ridiculous doses of vitamin A and then, and then, the thing is, the researchers aren't saying, Look, vitamin A is toxic. Grant is saying, Look, vitamin A is toxic. And it the thing is, is like, yes, grant, it is toxic at these ridiculous dosages that we're seeing. So the second piece from there is the argument that's getting made is that vitamin A, since it is fat soluble, is cumulatively toxic. And the thing is, is that? Is that the case? Yes, but we also do understand the threshold for cumulative toxicity that comes out of the research, so it's pretty clear with like, what, where people can start to develop toxicity over a number of years, and the dosages look to be, excuse me, the dosage look to be greater than about 25,000 IU per day, at least, that's what's been set by some of the regulating bodies or some of the research. So we're seeing, we know that, yes, it can accumulate, but we also knowing that it can accumulate, have kind of set thresholds and targets to say, okay, at where? At what point do we start to concern? Have concerns about cumulative toxicity. And when we start to look at that, we start to say, Okay, it's probably somewhere greater than 10,000 IUs per day for number of years, and we're looking more like 25,000 to 40,000 IU per day over this extended period of time. Which leads me into the next into the next point. So there's been the title of the book is poisoning for profits. And there's this, this perspective that's generated that the regulating bodies in these different groups are actually just trying to poison people for vitamin with vitamin A, for some profit motive. And the thing is, when you look at the actual targets set like the RDA, the recommended dietary allowances. Basically, they're extremely low, like they're it's somewhere for for fully grown adults, somewhere between 900 micrograms of retinol activity equivalence. So basically, like, you know, if can that's being converting beta carotene into an equivalent dose retinol, because they're not the same. And then the tolerable upper intakes were set at 3000 micrograms per day. And so within that range, what they're basically saying is this is the amount that we need to prevent deficiency, which we already established in the last video, can indeed occur for humans. And then here's the level where we think that it's probably not like there's not really a massive benefit to going higher than that in most cases, and there could be some problems. And then even within that research, they start to say, Okay, well maybe it's about, you know, 25,000 or 40,000 IUs per day for a number of years or months to years. And then they there's also these points of the modifying factors. You know your liver function, are you drinking alcohol? Are you eating enough protein, and intake of certain things like vitamin D and things like this. So the it's not like there's this conspiracy to poison people with vitamin A, the doses that have been set are quite low. With accumulation information in mind. And then we also know that there's modifying factors. So I think it's a bit of a fallacious argument to try to set it up as two camps, and that people are trying are being poisoned with this for profits, especially to then cite the studies that grant sites here to show toxicity. Because, as we'll see in just a couple minutes. The dosage used in the toxicity studies are insane, and especially when you consider the lifespan of a rat, which we talked about in the previous in the in the previous video, is when you start to look at equivalent time frames in humans. It's ridiculously high dosages. Is for the equivalent of years, which is what is known already. So it's the grant is presenting this perspective, as if there's this, this this conspiracy to poison people with vitamin A, and it's like that's that's not really the case when you start to go through the research, when you start to look at what is excretion, what is metabolism, what is storage, what is utilization of the vitamin? And then also look at the studies that he's trying to use to cite for toxicity. So this is the, I think, that that we have to get rid of this idea that it's poisoning for profits, that people are just being poisoned by vitamin A. From these guidelines, we understand that there's a cumulative effect because it is fat soluble, but we the researchers, also know that. And so there's also been a an understanding that there's a there's a window where it's too much and not and where there's not enough. And then, besides that, like, as you pointed out, Jay every single substance, almost every single substance at certain dosages will create different problems. So it's a, it's a logical fallacy to go ahead and say, Oh, if this, this is toxic at this dose, then it just must be toxic so that that's the that's this, the component. So we establish that there is a requirement for it. It's not just like this thing that's present our food, that's purely a toxin, like we know that we have some need for it. We talked about that in the past video, and now what we're going to talk about here, the second points, which is Grant's major point, is that it accumulates to become toxic. It's like, at what threshold is that? And it's like, there's actually quite a bit of room before you start to get significant toxicity. And once you eliminate these two perspectives, the entire vitamin A toxicity thing from the low vitamin A camp kind of goes out the window and slows this poisoning for profits. Idea. It doesn't mean that vitamin A is not toxic at certain dosages, but it means this perspective that is being pushed based on the research and the information we have is just there. There's, there's no perspective here. Basically, there's this is this perspective is does not line up with reality, especially because we just in the past video, we destroyed the deficiency piece, and now we're going to destroy the the toxicity piece from this perspective,

Jay Feldman  17:20  
Definitely. And two real brief things I want to mention, and then we'll get into the study. So firstly, as you were highlighting from Grant's book, there's this idea put forth that, basically, the governing bodies are trying to poisoning you, trying to poison you. The pharmaceutical companies are trying to poison you. So you know, those limits that they set and the recommendations that they set those should be totally thrown out the window, as you're saying, Mike, they're actually pretty well supported. But also, if that's the case, then the studies cited by grant would need to suggest something vastly different from that, and as we'll get into, they don't. So that's the first thing. The second is that, as we get into some of these studies, and look at the different dosing that they're using, really, if anything, it will end up supporting how safe vitamin A is in absolutely insane doses relative to what anybody would normally eat. Looking at the levels in the blood and the liver, really, there's very little toxicity, until you get to even more insane doses. And well, as we kind of get into the numbers here, you'll see that it's probably really, really hard to create vitamin A toxicity unless you, even if you try, even if you try, it'd be really, really difficult unless, again, you're using a medication that's particularly highly dosed, like, you know, you're using it for cancer or something. But we'll, we'll get into that in a bit. So, yeah.

Mike  18:36  
Even then you basically, I think the biggest point here is because the concern I see, because I have clients asking me, they're like, Oh, should I should I stop? Like, should I not have liver? Should I not eat eggs? Should I not have butter because it has vitamin A? And in my answer is, pretty much you shouldn't stop eating those things, unless you specifically have a problem from eating those things, or you have a past where you took insane doses of vitamin A and then have have a like developed a cumulative toxicity from insane doses. But with that said, the way that you would do that, you would either have to be using some type of liver source in very high amounts, including cod liver oil or beef liver, or you would have to be taking vitamin A dosages in very high amounts as well, or you'd have to be using pharmaceutical retinal retinoid derivatives. So unless you're somebody who highly dosed vitamin A, and something to consider is that that's modifiable by other fat soluble vitamins, like vitamin D, the toxicity threshold adjusts. Unless you're somebody who's taking extremely high doses of vitamin A and, or liver and, or pharmaceuticals, the idea that you are vitamin A toxic is a bit tenuous, and so when I'm working with a client, I'm trying to gage what is their past history and use of some of these things, and then go and then basically run. From there. And then, with a lot of these animal studies, if you just stop the high dosages of some of these things, over time, the animals will recover from it. And then, even in the human case studies, where people have taken insanely high dosages and actually really damage their liver, they still recover after that, once they cease taking the vitamin A. So I think it's what is your context. In most normal circumstances, this is unlikely to be an issue. And then, if your context is reasonable, and reasonably fits this background where you took really high doses of vitamin A for a long time for whatever the particular reason is, and whatever the form is, then stop. And then the other thing is, make sure you're eating enough protein. I wouldn't drink a lot of alcohol. Maybe start to consume adequate amounts of zinc and vitamin D to kind of help offset whatever's going on. And then run from there. And then the liver function, these other components should improve over time from that. So it's, I think that's a very small case of people. And to the argument that we see here that everybody's just vitamin A toxic I don't think we're really going to see that, especially when we start talking about the the actual dosages that are needed to cause toxicity inside the animal studies.

Jay Feldman  21:18  
As you were saying there, there's a lot of things to consider in terms of things that could predispose us to vitamin A toxicity. We'll be digging into those more in our future episodes, discussing some of the details here and talking about how hypothyroidism or a lack of certain vitamins or minerals, as you were discussing, could predispose us to having, quote, vitamin A toxicity at a lower dose. But again, that's outside the scope of what we're going into here. We will kind of talk about that later on. In either case, still something that's not particularly likely to occur. Again, that doesn't mean you wouldn't you can't feel better on a low vitamin A diet. We you know, there's a lot of reasons why you could feel better. We'll talk about that as well. And the last point that you mentioned, that I do think is worth highlighting because it's pointed out in these studies, and it was in the in the previous studies on in the opposite way, which is basically that recovery from vitamin A toxicity is pretty quick in these studies. And this is intense, severe toxicity. So again, the idea that this is going to be something where once you're vitamin A toxic, it's going to take you many, many years until you're feeling any better is you know, these studies alone put that into question without digging into any further details. So with that, we're going to dig into two of the studies that grant sites for support for hypervitaminosis, a occurring in relatively low doses in vivo. And again, he only, there's really only two in vivo studies that he cites, so we're going to dig into each of those. But I do want to mention before you dig into the first one, that I'm assuming that if you're listening to this and you're interested in vitamin A toxicity, it's likely because you're dealing with lasting chronic health issues, and when it comes to determining the optimal diet for resolving these issues, there's a lot of conflicting information out there. So if you're looking to optimally support your metabolism, lose weight, improve your digestion, get amazing sleep, rebalance your hormones, boost your energy and recover from various other chronic health issues. And if you'd like to have clear action steps and strategies alongside personalized guidance from me. Then head over to Jay Feldman wellness.com/solution where you can find all of the information for the energy balance Solution Program. This program includes customized health coaching, a video library with videos on how to restore gut health, how to regulate blood sugar, how to lose weight without destroying your metabolism, how to get amazing restorative sleep, how to rebalance your hormones, and tons more. It also includes resources like sample meal plans and a supplement guide, as well as a private community. So again, head over to Jay Feldman wellness.com/solution, to check out all the details. All right, so digging into this first study here, Grant has a quote saying, I like the statement from their abstract. And he then quotes their abstract, which says rats were fed on massive doses of vitamin A for periods varying from 10 to 18 days. Grant then states, then in the experimental detail section of the report, they define exactly what massive means. It is one drop of halibut liver oil per rat per week. Therefore, for these rats, that's a whole three or four drops of hell halibut liver oil in their entire lifetime. That's all that was needed to induce serious disease and bone fractures. So in this quote from Grant, he's referencing a study titled the action, the Action of Vitamin K in Hypervitaminosis A from 1947 and as you said in that study, they use helbit liver oil. And helbit liver is extremely concentrated in vitamin A, far more so than beef liver and most other livers. It's one of the most concentrated, and each gram of helbit liver oil contains 40. 1000 IUs of retinol. This is a lot. We're talking about a very, very concentrated vitamin A dose. We're also talking about very small rats that weigh as little as 85 grams, so less than a quarter of a pound, and are pretty young as well. So it's not like, you know, when we think of a drop of some even a very concentrated vitamin A source. The idea that that could cause toxicity sounds a little crazy, but the concentration of the, in this case, supplement, needs to be noted as well as the size of these animals, right? A quarter of a pound, versus, let's say, an average human at 150 pounds. We're talking about a 600 times difference. So that's all worth considering. Now we'll get into some of the details here as well, but it's worth noting. The study was from quite a while back, and they never actually controlled for the exact dosing. They never actually measured the exact amount of vitamin A that was given, and they never stated that dose. They did state they used one drop of this oil. Typically, one drop is about 0.05 grams. So for a 40,000 IU per gram concentrated oil in the halibut liver oil, that would be about 2000 IUs, or 600 micrograms of retinol, this is still not a small amount. So for an 85 gram rat, which some of the rats that were used were 85 grams, I believe, and then others were 153 or maybe the 153 grams was later on in the study. In any case, those were kind of the two weights given for an 85 gram rat. This is a human equivalent dose of 1150 micrograms per kilogram, which for an average weight human, again, 70 kilograms, or 150 pounds. That's around 80,000 micrograms, or the equivalent of 27 ounces of beef liver. So this is still a massive dose of, you know,

Mike  26:49  
that's 27 ounces of beef liver in a per week, exactly.

Jay Feldman  26:53  
Yeah. So not something you're going to do accidentally, that's for sure. And then for the hundreds, 53 gram rat. So it's a little bigger getting the same dose, presumably, then it would end up being a lower dose of around 635 micrograms per kilogram for human equivalent dose, which comes out to about 44,500 micrograms per 70 kilogram humid and that's the equivalent of 15 ounces of beef lever per week. So these are still large doses. It's not like this is a small dose of retinol at all. But it also doesn't seem like they used that dose, because when you then look at the concentration of retinol in the liver, the and the total amount of retinol in the liver, when you're looking at the rats, the rat groups given this one drop versus the controls, the concentration was about 60 times the controls, and the total retinol amount was 55 times the controls. So pretty large amounts, and we'll be going through a study later that actually does provide the exact dosing used in a much more accurate and precise way than just a drop of some concentrated oil, and we see how much retinol ends up in the liver in those studies. And essentially, the dosing here does not at all correlate with those other studies. So, yeah, yeah. Basically, in these other studies, they like, if you were to compare the very similar amounts of retinol, and the actually, I think what it is, and we'll, we'll get into it later, is that in the in this other study, they use 70 times this presumed dose, so 70 times this 2000 IUs, and there is less retinol content in the liver in those other studies. So the dosing provided in this experiment doesn't seem accurate. It doesn't seem like we're getting full picture. They didn't even measure or provide the exact dosing given. So there's a lot of question marks here, and it doesn't at all fit with all of the other vitamin A toxicity data. Again, either way, it's worth pointing out. It's still a very large dose. But in the other studies that are using way higher doses, it it doesn't, it doesn't fit with those at all.

Mike  28:58  
Yeah, I think there's a couple. For me, when I went through that study, there's a couple key takeaways for it. And essentially one is that they don't really list out the methods very well, but it's from 1947 so the standardization, the standardized practice in terms of writing out methods in the sections for studies aren't the same as they are now. And so essentially, it says the only information we know is the rats get 40,000 IUs per gram, and they for of halibut liver oil, and they get one drop, and one drop is is not weighed, so we don't actually know how much of this vitamin they're getting. So you estimated it based on what a typical drop would be, and that gave you 2000 IUs per week. But when we actually look at the concentration of vitamin A or retinol inside the liver, it doesn't match up with the concentration that we see in other studies that give much higher dosages. So we actually, in fairness, to Grant's perspective, chose the lower dose here and. Even choosing a lower dose here out of trying to be as fair as possible from the perspective, it's still between one to two pounds of beef liver per week. And the other thing is, the one the two pound beef liver dosage per week is in young animals, which are more susceptible, which would be more susceptible to the toxicity vitamin A that's in a human equivalent dosages, that'd be the equivalent of one or two pounds of beef liver per week. So two pounds for a child and one pound for an adult, essentially, or one pound for like a like an adolescent middle like, not a fully grown or not a fully grown adult, but like an older and older human. And so basically, even with that, it's still a massive dose retinol, but based on the liver concentrations, and the reason we're looking at liver concentrations because vitamin A is mainly stored in the liver inside the body. So based on the liver concentrations that we that they did report in this study, where we're basically assuming is that the dose is actually probably closer to maybe 40,000 IUs per week, or something much higher than what we see at the 2000 which would make that human equivalent dose for the for liver, significantly higher than one and two pounds a week, like by by a multiple factor. So with this said the data, you could say, oh, well, here this is relatively lower dose for this study. But then when you look at the liver concentration, it's like, well, it depends on where you're estimating a dose, and we don't, we don't really know, we don't actually know the exact dose, but based on liver concentrations, it's much higher than was given. So this study is basically showing us again what we've already discussed, even if we take the lowest possible, considerable, reasonable dose, we're still looking at a very high amount of retinol per week, on the order of one to two pounds of liver per week for a human, which in most circumstances, that wouldn't be recommended, even in people who tend to favor vitamin A, you know, like Dr P, or people like Dr Chris masterjohn, there's not a recommendation to eat one to two pounds of beef liver per week. And by the standard governing bodies, that's definitely not a recommendation. And I think that invalidate just this alone, which, and we're starting with this study, because this is the lowest possible dose that alone invalidates this idea of poisoning for profits, right? Because this is the dosage here is insane. And what? When we get to the next dosages, it's like, it's not even a question, like it's not even going to be a question anymore when we start talking about what the equivalencies are. So this was probably the closest chance that Grant had to justify this toxicity, and it's not really great support, essentially like this, this study, we're using his study, and it's not supporting his point.

Jay Feldman  32:57  
Yeah, and and again, it's one thing if these same doses and the same liver retinol concentration and these same effects were seen in all the later studies, you know, in the past 70 plus years. And this was replicated, but it's not at all replicated. And as we'll talk about in that other stuff, one of the other studies we'll go through, they were using, instead of 2000 IU per week, they were using 161,000 IU per week, and they still only ended up with a liver content of 21 times what the controls were, whereas in this study it was 55 times. So the dosing here is not lining up. It is not replicated in future studies, even if, even if this was accurate, it would still be very large amounts of retinol, but what we actually find is it takes way more there. There's this study cannot be valid. It doesn't at all fit in with the other studies on vitamin A toxicity, of course, other than the fact that we just don't know the dosing. So you could say it's valid, but maybe they just dosed way more than they said they did. And there was, again, the methods weren't clear, as you were saying this was done very early on. So yeah, that's that's as far as this study can take us. When we look at other studies cited by Grant and some other studies that are worth looking at, we see that this, this doesn't hold up.

Mike  34:13  
When I went through it myself, my my assumption was they're telling me 40,000 IU per gram, because they're probably just giving the rats a gram, because they're not, they're not. They're saying, Oh, we give them, like, one drop per week. It's like that literally doesn't mean anything. Like, how, what? How many grams is a drop in this circumstance, again, in 1947 and it's not very clear. And then with the liver concentration, again, it's like, this is probably much higher than the estimated dose that we're running with, and then, if indeed it is, which it seems like it very likely is, then basically what we're looking at is it's in line with the rest of the studies that you need really high dosages of vitamin A to start to cause toxicity problems. So yeah, so for me, it's like this, yeah, we're seeing really high dosages still. Uh, even from the lowest dose to the highest dose that you could run with, there's, there's no way around the fact that it's a ridiculous amount of vitamin A that the vast majority of people are not consuming.

Jay Feldman  35:13  
Right, right? And in the next Grant, in the next study Grant sites, we're seeing these kinds of doses, the ones that are way, way higher, 70 times higher, in this case, than that first study. And again, this is cited by Grant, so I'm going to read this quote. And then Michael, let you go ahead. So grant then has a quote here, and he includes a quote from a study that we'll dig into, titled concerning the toxicity of vitamin A. He states very similarly, from an earlier study from 1937 we have and then he states that quote. And he says the rats were fed 0.5 CC daily, or a dosage of 20,000 units of vitamin A. The outstanding features of the disease produced in about 10 days were failure to grow, inflammatory changes in the eyes, with exothalamus, and changes in the bones resulting in spontaneous fractures. And he states this as if it's supporting his point, which in this case, he's talking about how the symptoms of vitamin A toxicity are similar to the symptoms of Vitamin A deficiency. So kind of operating on the assumption that these are actually symptoms of deficiency, and these rats are deficient, or sorry, that in the prior studies looking at deficiency, the rats were actually dealing with excess vitamin A, but we already talked about that pretty thoroughly in the last episode. But again, the dosing here, we're talking about 20,000 IU per day, not per week per day. And the rats here are even smaller. They're only 50 gram rats. So when we look at the human equivalent dose here, just of the one that he's quoting, of the aspect that he's quoting, and they actually did different doses in the study that we'll talk about. But just that one, that's a human equivalent dose of nearly 20,000 it's about 19,460 micrograms per kilogram for an average weight 70 kilogram human. That's 1,364,500 micrograms, or the equivalent of 454 ounces of beef liver. In this case, that so that would be 28.4 pounds of beef liver per day. That is the dose that's used in this study.

Mike  37:12  
It's really toxic. Man, you should stay away from that vitamin A stuff.

Jay Feldman  37:15  
Absolutely, absolutely.

Mike  37:20  
Yeah. I mean, basically this is just, it only goes downhill for the argument from here, because basically what we're just seeing is the doses get higher and higher and higher and to points where it becomes unreasonable to induce toxicity for humans like this. It probably it's physically impossible, I would say, to eat that much liver on a regular basis. So you would have to go out of your way to replicate this level of toxicity in a human by taking extremely concentrated, isolated forms of retinol or retinal palmitate or something like this. And it's just yeah, so if anything, this is a safety study, this is how much vitamin A you can get away with in a particular period of time, in 10 days, which, again, would be the equivalent of what was it is two weeks, was about a year for humans, so for six months and six months to create the toxicity in humans. And it's like nobody is doing this. This is not what people are shooting for. Nobody is saying this is a good idea. There's like, we're not, we're not having some vitamin A czar come on TV and say, Yeah, everybody needs to have 28 pounds of beef liver a day, and that that's the solution to all of our problems. Now, I'm, I'm like, partially straw Manning Grant's argument here to make, to make, to exemplify, like, how extreme the the situation is. But it's like, don't create like, to start to try to determine that there's toxicity for this thing at normal doses that people are having on a regular basis. You cannot use these studies as an example, and then to even highlight things like, for the previous one, oh, it's just one drop of this oil, this super concentrated oil, for a really small weight animal, for a time frame that's on the equivalency of months to years. In humans, it's like, no, it's that's actually, this is, this is like, a huge difference. It's like, oh, it's only in 10 days. It's like, okay, six months equivalency, almost maybe a little bit more. For humans, 10 months, 10 months, 10 months at a ridiculous dosage. So that's not this is not support for this argument. And the sad thing is, is these are the major pieces of information that he uses in his book to support the argument. The rest of the claims, as we talked about in the previous video, are largely unsupported by research. It's more just his personal hypothesis, which is fine, but then just categorize the book as fiction. Don't make it a non fiction research study with and don't supply and without really supporting your information. And then when you do support your information, you say, Oh, look how toxic, toxic it is. And then we when we adjust. Us to dose what humans would have. It's, it's basically, it's highly improbable, borderline impossible, that somebody is dosing at this level without trying to cause a problem for themselves,

Jay Feldman  40:13  
right? Right? One, here's, here's the kicker when it comes to the study. So he's citing a study titled Concerning the Toxicity of Vitamin A. And the quote that he uses is that the in the introduction of that study where they're discussing a different study. So they're discussing this other study where they use 20,000 IU of vitamin A per day, and they cause vitamin A toxicity in 10 days. He's stating it as if, like that is, that is what this study is supporting, but the study is actually refuting that study. So what they say? So what they're going through in this, this other study titled concerning the toxicity of vitamin A, is saying that this other study, which was done by Palazzo and Rodriguez, they're basically trying to replicate those findings and confirm that in 10 days, you can actually cause vitamin A toxicity with 20,000 IU per day, and what they find is that they use way higher doses, which we'll get to in a second. And they and what they find is not that, so they're they're actually refuting that that dose is toxic and that you need a far higher dose, at least if you're doing in that short of period of a period of time.

Mike  41:15  
Yeah. I mean, based again, like it's just going to ante up from here, that the dosages get higher and higher and higher on a consistent basis. And it's like, yeah, we see toxicity at these doses. But I think the takeaway for people listening is like, you would really have to try to get to this level, and you wouldn't be able to do it with most food sources, unless you're really drinking halibut liver oil or something like this on a regular basis. And even then, you would probably run into problems from other components in there, not necessarily even the vitamin A first, right? So this is it, would it? The big thing is, like, there's when we're when we're going through the vitamin A arguments, right? When you know clients are asking, or when people are reaching out and saying, just read the book. Just read the book. And then you read the book, and this is what's cited, and this is what's shown. It's like, this is a non argument for the for the perspective that there's this, this conspiracy to create toxicity, toxicity through vitamin A, and most people's problems are from vitamin A toxicity, and it happens at really low dosages. It's like it doesn't happen at low dosages, and then you can indeed get a deficiency, which we talked about in the previous in the previous video. And it's unlikely that most people's problems that they're dealing with are specifically from vitamin A toxicity. Even though it is possible for somebody to indeed become vitamin A toxic, it just the dosages required are quite high,

Jay Feldman  42:42  
right, right? So, yeah, let's, uh, let's go ahead and go through this, this study where they are looking at what doses it what dosages are actually legitimate for causing vitamin A toxicity. And this is the one titled concerning the toxicity of vitamin A. Again, they are refuting that earlier study by Collazo and Rodriguez, showing that 20,000 IU per day for 10 days is enough to cause toxicity. Mike, do you want to go ahead and start us off here?

Mike  43:09  
Sure. So basically, they replicate this study. They used a variety of different dosages. So and the rats, is important to note their weight, because we're going to change it into dosage per kilogram. So the rats were 50 grams, and then the dosages they gave them were 25,000 IU, 50,000 IU, and then 100,000 IU. Now when we convert this to an average weight, human, 70 kilo, human, 150 pounds, what we see is at the 25,000 IU per 50 gram rat, what we find that that eventually adjusts to for a human is about 35.5 pounds of beef liver per day. Then when we look at a 50,000 IU per 50 gram rat, what we see for a human that's the equivalent of about 71 pounds of beef liver per day. And then when we look at 100,000 IU per 50 gram rat, that's the equivalent for a human of about 142 pounds of beef liver per day. So the dosages required here to actually cause toxicity for these animals. And again, these, these, these researchers are trying to corroborate the previous study at the 20,000 IU per day, which was already the equivalent of 38 pounds or 28 pounds of beef liver for human per day. Are is insane, like we're between 35 pounds to 142 pounds of beef liver per day for humans. What? So it's just, I think that's like a mic drop, right? It's, it's who's eating this much beef liver? Not even liver King is eating this much beef liver on a you can't

Jay Feldman  44:55  
I'm mean you can't even eat that many calories in a day, right? No one's eating the equivalent of 35 pounds of beef liver.

Mike  44:59  
Or that much protein, or that much B vitamins or that much phosphorus. Like, there's multiple components in these dosages that would kill you, besides the vitamin A, before the vitamin A, in terms of beef liver equivalent. So again, you would have to try with pharma, with some type of pharmaceutical or supplemental vitamin A in a very concentrated form, at high dosages for long, much longer time frames than are given for these rats to replicate these results. So this is not an example of how toxic vitamin A is. This is more of an example of there is a high threshold before toxicity sets in, over for heat.

Jay Feldman  45:38  
In other words, how safe it is. Yes, and let's see what they find. Because, you know, you would think, all right, at a dose of 140 pounds of beef liver per day, these rats would definitely be getting vitamin A toxicity in 10 days. They would have to be dead, right? That's that would have to be the assumption. If you know such a small amount is toxic. Can you imagine having this much? But when we look at the results, that's not what happened. So in this first table, here is this series two, they're identifying some of the effects at these different doses. And what they basically found was that in group one, the 25,000 IU per day, they were totally normal in terms of their weight, and there was no identified issues. In group two, this is the 50,000 IU per day. There was fractures in two of the rats. All of them lived to 100 days. So they so even though they were having the equivalent of 71 pounds of beef over per day, they were totally fine for 100 days, which, keep in mind, multiplied that by 30 to get the equivalent in humans. So we're talking about 3000 days, which is about eight years. And then in the third group, which is the 100,000 IU per day, or the equivalent of 142 pounds of beef liver. Two of those rats, two out of the looks like eight that lived, and six had fractures and presumably died earlier. So that's our first result. And then in the second result, they looked at other rats. They set up the study slightly differently, but we're using similar doses, doses. Again, looking at 50,000 IU per day and 100,000 IU per day, looking at the amounts in the liver as well. And again, same thing for that 50,000 IU per day group, this is over 70 pounds of beef liver equivalent. All of the rats lived 100 days, and they were remarkably normal. And in the 100,000 IU per day group, three of the rats lived to 100 days, and two had fractures. Here we're looking at it looks like eight rats again, and I forgot to mention series one, where, again, the 100,000 IU group showed significant vitamin A toxicity effects. None of the rats lived 100 days, and they had fractures and hemorrhages. In the 50,000 IU group, one of the four rats died in 40 days. The rest lived all of the 100 days, and they all had fractures, so showing moderate signs of vitamin A toxicity. And then there wasn't any apparent evidence of toxicity in the 25,000 IU group, except for some decreases in weight. Now it's also worth mentioning, as you can see, they allude to this in the footnote here, that in the study, they evaluated the potency of the retinol and the oil they were using, and they estimated the biological activity to be about 1/3 less than the measured amount of retinol. But either way, and we're still talking about absolutely massive doses of retinol in all of the groups that were being studied. So contrary to this idea that you know, massive amounts of vitamin A are going to cause toxicity in a short period of time, this is a pretty good study in support of the safety of vitamin A, and they have a couple of quotes along those lines, and they state the term toxicity means poisonous. Many food materials such as sodium chloride or iodine can become deleterious in large quantities, but they are not called poisons. Neither should fish oils be called poisons because they are injurious when fed in enormous quantities. But some term is necessary to refer to this deleterious action in these experiments, and we have used toxicity with the understanding that in the usual doses, the various ingredients of such oils may be necessary in the diet. We may conclude from this experiment, which was repeated with the same result, that if vitamin A is toxic, it must be given in higher dosages than 100,000 IU daily to 50 gram rats, and that at least the greater part of the toxicity of the various fish liver oils must be due to some factor, some other factor than vitamin A. And that last part is a reference to those other studies, basically saying there's no way that even 20,000 IU per day for 10 days could have caused those effects. Again, we are not saying these are ideal doses of vitamin A. Nobody is talking about like No one is suggesting consuming these amounts of of beef liver or retinol equivalents and any other foods. Yeah, the but this is showing that you need massive, massive quantities to cause outright toxicity and death, and it's a far cry from what grant Grant's suggesting here.

Mike  49:55  
Yeah, I think that's the important point here. Is we're I want to make it clear we are. Not making the case that people should be taking massively high doses of vitamin A. All we are saying is that the dosages that were required to be caused the toxicity that grant is implying are ridiculously high in humans. That this, that's the important context. That's the frame to come out with this. It's not saying it's not it can't be toxic. It's also saying, You, what we're saying, you can have a deficiency. So where is optimal for your particular circumstance? We will talk about other specific contexts down, down the line in future video. But I think this is what we're trying to get at here. Is like, look this toxicity studies that grant is citing himself are ridiculously high for in their dosages, when you start looking at it in humans, and also the time frames are much longer when you start looking at equivalencies for lifespan. Yeah,

Jay Feldman  50:49  
all really solid points there. And so moving on to the next one. This is a study that that grant referenced in an episode of The rejuvenate podcast with Elwyn Robinson, and Elwyn was asking him, he was so Elwin was asking him. He was saying there are a large amount of studies that back up that vitamin A access is extremely dangerous. And was asking grant to share some of those studies. And grant shared this study titled hypervitaminosis a in the young pig. Mike, go ahead and start us off there. Yeah,

Mike  51:23  
so in the in the podcast is interesting, because Grant was talking about how terrible the effects of vitamin A were in these animals at really high dosages, or at the dosages in the study. And basically what they did is they took young pigs on an average weight of about eight kilograms, and they had them consume diets that contain 0, 1, 1,100 110,000 or 1,100,000 units of vitamin A per kilogram of diet, and then for all of the feed, or on average, for all of the feed consumption per pig, until you get to the 1,100,000 IU, vitamin A per kilogram of diet, most of the animals ate about a kilogram of food per day, so they were getting about the dosages that we saw one 111,000 or 110,000 IUs per day. But when they got to the 1,100,000 IUs per day. Because Are you possibly, because the dose was so high for vitamin A, it actually led to them eating a little bit less. So they ate roughly half a kilogram per day of food at the 1,100,000 IU per kilogram of food per day. Dose. Now what this winds up looking at and well, we're gonna take the two top dosages, the 110,000 and the 1,100,000 because the other dosages are not really that high. And basically what we're looking at for human, if we convert the 110,000 IU per kilogram of diet per day for human, that is the equivalent of about 78 ounces of beef liver per day, which is about 4.85 pounds of beef liver per day at the 110,000 dose. Now, when we get to the 1,100,000 dose, they didn't get that full dose per day, because, again, they only ate about half a kilo. So they got half of that dose. And basically what that would be would be the equivalent about 335 ounces of beef liver per day, or 21 pounds. And the interesting thing is, the only group of pigs in this study that developed significant or serious symptoms of vitamin A toxicity was the 1,100,000 IU per kilogram of diet per day dose, and and the 110,000 IU per kilogram per day diet dose didn't really have any significant obvious symptoms and were generally healthy so, or at least symptoms that would indicate toxicity. So this is even further evidence of this, the degree of safety that you have with vitamin A at high doses, again, that humans wouldn't really be consuming. We're not looking we're not no one was really be consuming almost five pounds of beef liver per day, or the equivalent of vitamin A in that intake, let alone 21 pounds. And even with that, the pigs were were relatively free of obvious symptoms for the for the duration of the study, at that the for the equivalency of five pounds of beef liver per day dose of vitamin A. So again, more evidence cited by Grant himself that is showing the relative safety of vitamin A, not necessarily the toxicity,

Jay Feldman  54:39  
right? And it's shared as though, look at how bad vitamin A is. Look at what it did to these pigs. They were, you know, dealing with all these really awful symptoms. They died in a few weeks. You know, this is so terrible. And it's, I mean, it's, it's, it's irresponsible to make it sound as though that has any. Anything to do with vitamin A that is consumed in a normal amount in a normal human. It's just Yes, yes, toxic doses, massive doses, of pretty much any nutrient, like they talked about in the last study. You do the same thing with iodine or sodium, you're going to cause issues at way lower doses relative to what is typically eaten. So it's, yeah, it's really awful. And so they they kind of state the results at the end of the study with a quote saying, toxicity appeared after 14 days, when three pigs fed the diet containing 1,100,000 IU of added vitamin A per kilogram died. No visible external men, infestations of vitamin A toxicity were evident before death. Post mortem examination revealed massive internal hemorrhages after 21 days, all remaining pigs on this diet, but none on the other diets, exhibited symptoms of hypervitaminosis, a similar to those previously described for other species, and there's a citation there, so again, no other symptoms or signs of excess vitamin A in those other groups, including the one that that was consuming nearly five pounds of beef liver per day. So, yeah, I mean, what more is there to say?

Mike  56:13  
Yeah, it's another mic drop. It's like you're looking at it. You're saying, okay, there actually is deficiency, which we've proved with other studies, and it's like the threshold for toxicity is pretty high. So it's like the entire argument, this entire low vitamin, a camp component, is just completely falling flat, like there's not really strong evidence cited by the originator of this stuff to validate his points. And that's the problem, is like, and the frustrating thing about it is that there's this perspective that, well, we know that there is vitamin A toxicity and and then even in videos that I made about it on my own YouTube channels, like I'm open to the idea that the threshold for toxicity is lower than than is stated by, you know, the current guidelines, but then when you look at these studies, it's like, Well, that just went out the window, that being open to that idea just completely went out the window. When you start really digging in the research in depth, and without even having to dig in the other research, just looking at the studies that grant cited here to you to support his point, it's like, you don't even have to look at some of the other research. We did it anyway, just because, out of curiosity, like I genuinely, genuinely wanted to know. Once I started looking more than I did, want to know more than I did. But when I for when I looked at these studies, it was like, wow, this is this is what all this is about. This is what the fanfare is about with this stuff. It's like, this is not well supported, and these studies are actually proving the opposite of his point. It's like, I don't even have to go outside of the studies that he used to counter the arguments, the two major arguments that are the foundational components. So it's like everything else inside the low vitamin A sphere is built upon this perspective, and the perspective doesn't even have foundational supports. So it's like, it's just a mic drop for these, for this, for these perspectives overall, for the vitamin A toxicity piece,

Jay Feldman  58:16  
yeah, yeah, absolutely. And this is, again, using the studies chosen by Grant that he's he's choosing to cite. So let's take a look at a different study. This is another one showing very large amounts of vitamin A being required in order to cause toxicity. And they also look at the retinal content in the liver and the concentration. And so this is that one that will compare with the original that first study that grant cited about the halibut liver oil, and will give us some some clear evidence that I mean obviously based on these other studies, that study is off certain things about it are not accurately reported, but most likely in the dose. And we see that here when we compare the effect, you know, the retinol concentrations in the liver. So this study is titled metabolism of retinol binding protein and vitamin A during hypervitaminosis a in the rat. And they did two different studies here. So in the first one, the rats were given a vitamin A deficient diet to start that was then supplemented with 1.2 micrograms of retinol per day, just to make sure they weren't actually deficient. But again, talking about the variation between diets, and going back to the original deficiency studies looking at lard versus butter, they take all those possible variables out here, all them are on the same diet with just different amounts of added vitamin A. The baseline diet is vitamin A deficient, and they add a little bit of vitamin A to prevent deficiency. And then once they reached a weight of 110 grams. They were split into three groups, so there's three groups, and they were each given different amounts of vitamin A per day in the form of retinal acetate. And they give the doses in milligrams per day, because this is a lot of micrograms. So the control diet gets, point one, four milligrams per day. That's 140 micrograms per day in a per per weight, which, or by weight which. Of course, they're. 410 gram rats, as we mentioned. And so the human equivalent dose for this control group ends up being 6300, micrograms of retinol per day, or two ounces of beef liver per day. So the control group here, the one that they're comparing vitamin A excess with, is getting a large amount of of vitamin A. They're getting the equivalent of two ounces of beef liver. And the next two groups, the second one is given 7.3 milligrams a day, so 7300 micrograms per day of retinol. The human equivalent dose here is 10,800 micrograms per kilogram, or 750,000 micrograms for an average weight human, getting us to 251, ounces of beef over per day. That's our first group, or our second group, and then the third group here is for 25 days, they're given 1800 micrograms of retinol per day, and then after that point, they're given 4100 sorry, 41,000 micrograms of retinol per day. So they're given a kind of moderately high dose for a bit, and then a very, very high dose. And again, remember, 25 days. This is not, we're not talking 25 days for a human. This is 25 days for a rat. So this is, you know, you're multiplying that by 30 we're talking over two years human equivalents here, just on, you know, on each of these doses. And so when you look at the 1800 micrograms per day, this is the equivalent of 27 ounces of beef liver per day. When you do the human equivalent, equivalents. And then for the 41,000 micrograms per day, or 41 milligrams per day, this is the equivalent of 620 ounces of beef liver. So the highest dose here that they're using is 620 ounces, equivalent of 620 ounces of beef liver per day, or nearly 39 pounds of beef liver. And then after day 50, the high vitamin A groups stopped receiving vitamin A, so that they were allowed to recover from the vitamin A toxicity. So we will look at how long that takes, and how well they recover when given these insane amounts of vitamin A, of retinal and then again, before we go into the results, I just want to touch on. So they did a second experiment as well within the study, where the rats were given the same vitamin, a deficient diet with the 140 micrograms of retinol per day, once they reached a weight of 300 grams, that are then split into two groups, one continued on as the control, getting the point, one four milligrams per day, and then the other group was given 34,000 micrograms per day of retinol. And this is the equivalent, based on their weight being higher at 300 grams, this is the equivalent of 429 ounces per day, or nearly 27 pounds of beef liver. Again, when you do the human equivalents. So just as the setup here talking about very, very large doses, and we can see how much it took to cause hypervitaminosity, how much it took to cause vitamin A toxicity, and also how quickly they recovered and what all the symptoms were. So looking at the results here, and we can take a look at this figure, which depicts it. So in the control group, of course, they grew fine and and then in group two, there was a slightly lower growth rate. It wasn't statistically significant, but a slightly slower growth rate, although they appeared totally healthy. Remember, this is the group that was getting the equivalent of 251 ounces of beef liver per day. Appeared healthy, slightly slower growth rate. Group three showed that their growth rate stopped, starting at day 25 when they went on to the massive quantity, the 41,000 micrograms per day, or the equivalent of 620 ounces or 39 pounds of beef liver with the human equivalent dose. So they were on that amount, and at that point they stopped growing, and they did experience signs of hypervitaminosis, a at that point, they had reduced food intake, depressed growth, alopecia, thickening of the skin, occasional bleeding from the nose, weakness or partial paralysis of their legs. They were also aggressive, so they had full on vitamin A toxicity symptoms during that 25 day period where they were eating the equivalent amount of retinol as 39 pounds of beef ever per day for an average weight human. So massive amounts. However, they didn't die. They were fine. And again, this was for 25 days, which is the equivalent of two years in human time. And then after they stopped supplementing them with that amount of vitamin A, and they recovered and grew totally fine. There was basically no issues other than fatty liver, which was still seen in groups two and three that were given these massive quantities, but they were basically able to live relatively normally, and they state this in a quote they say, varying degrees of vitamin A toxicity were observed. The rats fed a moderately excessive dose of vitamin A of 7.3 milligrams per day, grew somewhat less well than did the control rats, but appeared clinically healthy. Large excessive excesses of vitamin A, either 41 or 34 milligrams per day, however, produce severe manifestations of vitamin A toxicity and cessation of growth. Again, it's worth noting that these are not only massive quantities for extended periods of time that caused vitamin A toxicity, but the recovery was pretty immediate when they stopped the supplementation, which is so different from the narrative. That's being told in this circle, in this sphere. And then the last thing that's worth mentioning here that we alluded to prior was looking at the concentrations in the liver. So again, we're talking about extremely high doses here of of retinal and when they look at the amount of increase in the liver compared to the controls. There was a 21 basically a 21 times as much retinol in the liver compared to the control group. In that earlier study, we were talking about with the helbit liver oil, and they were supposedly only doing one drop a day of the 40,000 IU per gram, one drop per oil. Sorry, one drop per week. Thank you. In that study, the rats had 55 times as much retinol in their livers as the control group. So something is obviously not adding up here when they were given, supposedly a fraction of the dose, and yet, they had way more retinol in their livers when compared to what was looked at in this study.

Mike  1:05:56  
Yeah, I think the biggest takeaway from this, there's two for me. One, we have a study with really high dosages, where we see only a 21 times concentration of retinol in the liver compared to a control, which gives us some information to be able to put in context the 50 times concentration of retinol, or the 55 times concentration of retinol in the controls. And the halibut liver oil study that grants like, oh, look, they just took one drop of oil per week, and in the X number of weeks they got sick, it's like the dose is probably excessively high. And we could art, we could make the argument again, that is possibly 40,000 IU per week for very for low weight rats, which for human equivalent doses, is quite high and are possibly even higher than what what we are anticipating. But, and then the second piece here is that you have rats on dosages equivalent to what was it, almost 40 pounds of beef liver per day and vitamin A intake. And yeah, it really messed them up. It definitively messed them up. However, once they stop taking those dosages, they're able to recover. They're able to start to recover from those toxicity effects. And there are human case studies inside PubMed where you see people take really high dosages of vitamin A, and they do recover. Does it beat up on the liver? Yes, it does, because the liver is the main storage site of retinol, and you have certain types of cells, the stellate cells, that are going to store this vitamin A and as you take get really high doses, you start to go over capacity. You can start to cause problems. But the people do recover. People are able to recover from from the toxicity the liver takes a little bit more time, because there is a there is a it takes time to deplete the storage. But again, these are on extremely high dosages, and so I think that that's it's helpful to see, like, look, there is recovery potential here. It's not just this toxin that's just decimating these animals. And I don't want to open the full can of worms here, but the thing that we're seeing is like, I'm not I'm waiting to see all these autoimmune diseases in these rats. I'm just going to drop that here in these toxicity studies, because we're not seeing autoimmune diseases per se in these animals, which is one of Grant's arguments. We're just seeing the vitamin A toxicity stuff that they then recover from, even though they still have high stores of it, and once they stop taking those very high dosages. So I think that's also important to point out, and we're not, we're not really going to get into the autoimmune piece purely because there was no research cited to back that perspective up. There was just some interesting drawings within grants theory there. But we don't really, we're not really seeing those symptoms play out in the human toxicity studies, the case studies, or in these animals, these rat toxicity and these rat toxicity studies for vitamin A. Well, we are seeing vitamin A toxicity symptoms.

Jay Feldman  1:08:54  
Yeah. And not only were there no Was there no cited research for the autoimmune claims being made, but there wasn't even a cohesive argument being made for argument being made for it. Anyway, there's really nothing to even try to, like we were happy to try to look into it and then consider refuting it if there was anything to even look into in the first place. And there just wasn't. So anyway, when it comes to the vitamin A toxicity, the hypervitaminosis a, I think we can wrap that piece up here where, very obviously, the doses needed are are absolutely insane, staggering. Yeah, insane. And this doesn't mean that somebody can't have vitamin A toxicity, but the amounts that we would need to be talking about are pretty, pretty hard to get. It's not going to happen, probably by accident, unless you have some major other metabolic issues going on, which, again, we'll talk about the future. But the again, I think there's not much else to say on that regard, and we can move on and talk about the next piece that grant discusses, which is basically the. Toxicity, or potential toxicity, of retinoic acid, and his claims there. So let's dig into that. All right, so we're going to dig into some of the primary arguments made by Grant in regard to retinoic acid being toxic. And so this will be from the subheading in his book, which is titled retinoic acid as an acne drug, the toxicity stress test. And so what he basically does here is he talks about Accutane, which is a form of retinoic acid called 13 CIS retinoic acid, and he's suggesting that it's toxic, and because it's toxic, the assumption is that retinoic acid is therefore toxic as a whole. And this is really the primary argument he makes for the toxicity of retinoic acid, and it's all centered around Accutane and the effects of it, which, as we'll get at, are not particularly relevant to the question of whether, of whether retinoic acid is toxic for a number of reasons. For one, it has very little to do with any amount of I mean, the first off, it is just a single metabolite, or a single form of retinoic acid called 13, says retinoic acid, there are several others. And providing this one form of retinoic acid in extremely high doses is something that you can only recreate by taking massive amounts of this drug. It basically has nothing to do with anything that would happen from normal physiological effects of consuming retinol or beta carotene or anything, any other carotenoids you're going to have in your food. You're to say that this is equivalent to any effects of that is just. It just is, let's just say, not accurate, just just as is totally irrelevant. That being said, we're going to evaluate some of the claims he makes, even about the toxicity of Accutane, and then talk through some of the details in terms of Accutane as a chemotherapeutic agent as well used as chemotherapy. We'll be talking about that and some other aspects as far as retinoic acid goes. So as a starting place, you know, as a suggestion from that subheading, he's basically saying that, considering that retinoic acid is used as an acne drug and has certain toxicity, that is a suggestion that retinoic acid itself is toxic. First thing to note here is that Accutane, which is the acne drug he's referring to is 13 CIS retinoic acid, which does not have the same physiological effects as other forms of retinoic acid, like nine CIS retinoic acid or all trans retinoic acid, these are shown to have different physiological effects. So to say that because there are certain potential harms from 13 CIS retinoic acid does not mean that all forms of retinoic acid have those same effects, and that's one important thing to consider. But the next thing to consider is his evaluation of Accutane being toxic. And so he has a quote stating, or he says, just how toxic is Accutane. Well, over the full course of treatment for young adults, the total amount of the drug taken is about five or six grams. If that amount were taken in one shot, it could easily be a lethal dose. So a couple of points here, we'll talk about the kind of cumulative dosing for someone, and it could end up being in that five to six gram range over you know, when it's taken over, typically 16 to 20 weeks. So typically, the drug has taken over four to five months, at which point you would accumulate this, not accumulate you would have taken in a cumulative amount of five to six grams of retinoic of the 13 cyst retinoic acid. And that the fact that, let's say so, for one the there's no evidence cited for the fact that that could be lethal. I mean, you could say anything could be lethal and and you can get away with it because you're saying could and you're not actually saying anything. But if you actually look at the doses that are suggested for lethality in a single dose, if you look at the LD 50 for a rat, it's over 4000 milligrams per kilogram of Accutane. And if you convert that to a human equivalent dose for an average weight human that's the equivalent of 45 grams of Accutane. So not five or six grams, but 45 grams being required as the LD 50. I haven't seen any suggestion, suggestion of any other amount being toxic, but that's the amount that would supposedly kill 50% at least of rats in one given in a single dose. So for one that's many times higher, about nine times higher or eight ish, depending on five or six grams, it's quite a bit higher than the dosing he's talking about. But also, there are very few drugs, vitamins, minerals, substances where you could take the amount that you would be given, not only over four to five months, the amount that you would take in over four to five months, but in this case, if we're talking 45 grams, multiply that by again, eight or nine times. If you can take a substance that much, or you need to take that amount of a substance for it to kill you, that's actually a really good support for how safe. Is you can't, like, if you look at any vitamin or mineral for the most part. Or we talked about this earlier with water, with water with sodium, with iron. I mean, you could talk about with so many different things, selenium, certain B vitamins, if you were to take the amount that you would be I mean, and this is, this isn't a way higher dose than you would ever eat, right? We're talking about massive doses given in the drug. But if you were to take the total amount that you were going to have over 20 weeks and take it at once, there's a lot of situations where that could be toxic. That does not mean that the substance itself is a poison or is a toxic. That is or is toxic. It's terrible support for that concept. And so I'll kind of leave it there, unless you go ahead, Mike, but that's just a starting place here.

Mike  1:15:39  
I think the the overarching perspective that's really important for me when I think about this is that grant is trying to use Accutane as an example of vitamin A or retinoic acids toxicity. And then he's so first of all, like what you already pointed out, Jay, is that Accutane and retinoic acid, like the different these different structures, changes the effects of these compounds. And so to just try to try to conflate the things together to make your argument, doesn't make any sense. From the get go, you have to look at what the specific effects are of each different compound, because, as we already see, like retinol esters versus retinol versus retinoic acid versus different derivatives. From there, with different modifications to the structures, changes the effects massively. And we see this with many different areas. We see those many different substances, for example, just to put this in perspective for people, if you have regular bioidentical progesterone at structure may be semi similar to some of the synthetic progestins, but then what happens is, when you start adding and modifying the structure, you get different effects. And when you look at the research, what you see is bioidentical progesterone is at best neutral, if not possibly beneficial and protective or associated with protective benefit against breast cancer and things like this, whereas when you look at the synthetic progestins, it's like, oh, look, we have some toxicity here, and there's an increased risk of breast cancer with their usage. So to just say, like, Oh, this is, like, progesterone, and it's bad, so then progesterone is bad is that's not argumentation. That's just logical fallacy at the at its best. And so I don't think that, like with Grant's perspective here, like he's doing the same thing. And if this is from like, a logical perspective, this is not a logical argument. This is just him basically conflating a bunch of things together, which and then the it gets even worse, because then he started to say, oh, like, look, Accutane is toxic at this specific dosage. And it's like, he's not even correct there. He's not even right. You look at the LD 50 for rats, as you mentioned, Jay greater than 4000 milligrams per kilogram, and then you convert that to human dose, what's like 600 something milligrams per kilogram for a human, which gives you this 45 gram target. And grant is saying, Oh, look, five grams is five grams in one sitting. Could be lethal. It's like, well, actually we're seeing 45 grams. And then even beyond that, it's like the dosing for humans is not to take five grams in one sitting. There's not a single person saying those five grams of Accutane in one sitting, they're saying, Look, you have this schedule point, five to one milligram per kilogram over a period of 16 to 20 weeks. And then it's like, let's take this total amount of the 16 to 20 weeks and give it to somebody in one period of time and say, look, it killed them. It's like, I could do that for any single substance. I can do that for almost every substance that somebody's eating right now. I can look at whatever it's like as an example. And you have this set out in the argumentation here, Jay is, let's take water, take all the water that you're going to have over the next 16 to 20 weeks, and take it in one sitting and see if you live. It's like what? That's not just argument days. Yeah, that's not even an argument for why this is toxic, if anything, what you're seeing here is you could take a based on this dosing schedule, you could take the full 16 to 20 week course of Accutane in one sitting and still not approach the LD 50, which is the lethal dose for 50% of people at that dosage. And so it's like this is, again, it's the same thing with his toxicity arguments, and it's the same thing with deficiency arguments. He's actually supporting the opposite point with his with what he's saying and with the points that he's making. He doesn't even realize it. And again, you and I, neither of us are saying, like, Yeah, let's take a bunch of Accutane. Both of us agree it's not problem. It's like, a pretty problematic substance to use, and there's reasons why you wouldn't want to use it. And even, and this is the whole thing, is like poisoning for profits, the manufacturers and the doctors and prescribers are saying how toxic it is by saying, like, Look, you have to sign up to this database that says that you cannot, you have to be on birth control, and you cannot get pregnant while you take Accutane because of these problems. And they list out all the side effects of the drug. So it's like, they're telling you the risk beforehand, and then you are, you're making the decision around, do I take this drug or not? And it's like, if you look at the actual risk, like, yeah, probably not a good idea. There's problems with it. But we're also seeing like, here's this really toxic drug, and you could take really high dosage dosages of it, and it's. Giving you the toxicity that grant is saying, and then I'll leave this here so you can get into the next point, Jay, but it's like, would we ever see these levels under normal circumstances? Like, that's the next question, are we is it just when you take Accutane, or, like, will you get this under normal circumstances? Because you know, the toxicity is cumulative, right,

Jay Feldman  1:20:18  
right? And does. And the point you're getting at too is, does this have anything to do with the amount of retinoic acid you're ever going to be producing from retinol that you're consuming, or even if you were to consume retinoic acid in foods in the tiny amounts that it exists? Does that have anything to do with toxicity of Accutane? And the short answer is no. So when considering the dosing for acne, and then looking at the levels in the blood of 13 CIS retinoic acid and all trans retinoic acid, what you see is that the levels reach basically massive, massive amounts relative to what's ever normally seen in normal physiological states. So with Accutane, levels of 13 CIS retinoic acid in the blood are seen between 1005 1000 nanomoles per liter. Typical levels are one to five nanomol per liver per liter. So we're talking about 1000 times the normal amount in your blood. Again, there are very, very few things that you could add, like you could multiply by 1000 you could take 1000 times that amount that's normally in your blood, put it in your blood, and you could even be alive. Most things that are in your blood, you cannot add 1000 fold of them and put them in your blood and be okay. So this is actually, again, not saying that Accutane is a good idea or that it's a healthy thing, but it's actually support for how safe it is relative to things that are actually toxic or poisonous or even things that are totally benign. The point being this alone is not a at all good evidence for the toxicity of something. And when you look at all trans retinoic acid, which things like 13 CIS retinoic acid get converted into with the use of Accutane, you typically see levels of 50 to 100 Nanos per liter. And in a normal state, you're seeing levels of one to 10 animals per per liter. So at least, you know, on the low end, we're seeing 10 times the normal physiological levels, and on the high end, as much as 100 times. So this has, this is very, very far from anything that's ever happening physiologically. Which brings us to the next point, again, talking about dosing, talking about levels in the blood. Grant, and he said this in interviews. He says it in lots of different places. He talks about how, quote, retinoic acid is a chemotherapy drug. That's the that's the the general line. And he has that. He has a subheading titled Accutane as a chemotherapy drug, the extreme toxicity stress test. And he states the use of retinoic acid as an acne treatment originated from the use of it in chemotherapy. This is not just approximately the same drug? No, it is exactly the same drug, the same molecule, the same isomer of it, and even the same product named version of it, Accutane. So if the use of Accutane as an acne treatment is the medium stress test of retinoic acid toxicity on the human body, then being given the Accutane treatment in cancer cases is the extreme stress test. So again, the idea that looking at Accutane has anything to do with retinoic acids toxicity in the human body is absurd, at least in I mean, it's only relevant in so much as someone is using one of these drugs. It is completely irrelevant when it comes to somebody who is not using these drugs and is consuming even massive amounts of vitamin A you're never going to see these sorts of levels. And that is even more so the case when it comes to the use of it as a as a chemotherapy, chemotherapeutic agent. So yes, the same 13 cyst retinoic acid is used as a chemotherapeutic agent, and it's used in extremely high doses. And these doses, typically they're around five milligrams per kilogram per day. So again, massive doses, and this leads to concentrations, again, of 13 cysts retinoic acid that are over 1000 times normal levels. Again, this is if anything, support for its safety. The fact that you can get that, whether it's from Accutane for acne or Accutane for chemotherapy and not drop dead immediately, is if anything, support for the general safety of this compound. Again, not saying that this is a good idea, but just support for the fact that it is not particularly toxic or poisonous. And again, totally relevant to anything other than the situation where you are consuming massive doses of this medication.

Mike  1:24:18  
Yeah, and I think it's not particularly relevant to the idea that this is toxic in the normal amounts that you generally consume. So it's like, if you were to take the drug in high dosages or cancer, you will likely get a bunch of side effects, which you could argue are toxicity. But to talk about it and because the reason we're talking about it this way is because grant positions this in terms of the lethal dose, like, how much would be lethal? And it's like, we're not seeing lethal doses at these really high levels that are 1000s of times higher than what you would typically see with normal consumption patterns. And so it's like this again, like, I think grant needs to really understand the. Like, the specific context of what dosing is. So, like, trying to figure out, like, what does one glass of water do to you versus 1000 glasses of water? Like, really, trying to delineate, like, well, is water toxic because at 1000 glasses it causes problems. Is water toxic because at 500 glasses it causes problems? It's like, is that really going to be the barometer, or what you engage with things in terms of defining them as toxic? And if that is the case, like it's basically a non argument forever, because there's not really going to be any substance that you'd be like, Oh yeah, at these extremely high dosages and 1000 times what you would normally see it's this thing is toxic, so therefore it must be toxic. And then to like, I don't know if this is just, like, not understanding the level of argumentation, or if this is like, done on purpose, but it's like, it's a very, it's a very salesy tactic to be like, Oh, look, Accutane is a chemotherapy drug, so therefore it must be toxic. And like, kind of like, conflated in those types of things. It's like you can have a drug, like you can have an antibiotic, or a substance that helps you overcome infection that isn't necessarily toxic to your system, maybe it's helping you overcome infection by improving your own immune function. And so it's like the mechanism also becomes important to just say, oh, anything that's in this chemotherapy glass of drugs, or this chemo, like, it's determined as something that's helpful for cancer, or it can treat cancer in any type of way, is automatically toxic. Is like, that is also not a logical argument, and that's like a bit of a conflation. Is like, how exactly is this thing working? Is it working by reintroducing differentiation of a cell from an undifferentiated growth dominated state towards a cell that's moving to a differentiation state where it's incoherence of the organism, and it's doing that without creating toxicity. It's like, sure you could classify that as a chemotherapeutic agent, but it doesn't necessarily automatically mean it's toxic. And so he's not his arguments are imprecise. They're not logical, and there's tons of conflation going on. And so it's like, and then there's also not even sources for some of the stuff that he's saying. It's not like he's sourcing the toxicity doses in the LD 50s. Like, we are pulling this out from the research by ourselves to be like, okay, is he right? Is he like, clear on this? Is this correct? Is this the right value based on what the researchers are telling us? It's like, it's not even that. So it's like, where is this argument coming from? Is this individual coming from a perspective of, I think vitamin A is toxic, and therefore I'm going to try to create arguments to justify my perspective, or is he going into the research and saying, Hey, look at all these problems with vitamin A, and then, like, I think maybe it's toxic. And I think it's actually the former position. He took a position, and then is backwards, rationalizing his whole perspective, using non logical arguments. And then, like, and then adding spins to it. Like, oh, look at this cod liver dose. If I take one drop, I'm gonna in one drop in this time frame. It's super toxic. Like, vitamin A just be really toxins. Like, dude, what's the equivalency of a lifespan to a rat versus a human? And then how much is this dose on a per kilogram basis, and a human equivalent doses like, then you start to look at, like, okay, so this is like, what, like, 30 pounds of liver a day, equivalency for vitamin A. And it's the same thing here with with retinoic acid and Accutane. It's like, there's this molecule that's that has retinoic acid in the name, with some modifications to the structure. And if we give really high doses, it's toxic. See, retinoic acid is toxic. It's like, that's not how this works. It's like, what is the difference in how these molecules function? What is the dose where there is toxicity? What is the normal dose that we're having on a regular basis. And then let's determine, like, is it actually toxic? And basically, what we've done here and Jay, what you've laid out, is that there's not the toxicity at these normal dosages, and his arguments aren't even supporting that. They're supporting the opposite. It's like, Look, you have quite a bit of room before you really run into significant problems. And yeah, like, if you take this, this drug at high dosages to for like, really extreme context, you're definitely going to see some issues. But even then, it's not causing death, which is what, what Grant was initially implying,

Jay Feldman  1:29:11  
right, right? And as you were saying, too, there's a lot of things that will cause death, and much lower concentrations, much lower factors, right? If you took, if you take the amount of testosterone in your blood and multiply it by 1000 times. If you take the amount of triglycerides or free fatty acids or glucose in your blood and multiply it by 1000 times, or sodium, I mean, just pick, just pick something multiply by 1000 times and see what happens. That doesn't mean any of those things are toxic. So anyway, there's one less argument that grant makes that is worth touching on very briefly, because it's an argument that we see made in a lot of different contexts, where someone basically looks at a pathway, and they look at some part of that pathway or some end product, and they say, this thing is bad, so don't take the precursor, because it will automatically become that end product. And he does this with retinoic acid. Again, not that there's good support for the. Retinoic acid actually being toxic. But he then makes the argument that if you take any precursor, it will automatically become retinoic acid. And so he states, now there have been two very important points I wanted to make in this chapter. Firstly, that vitamin A will normally and naturally convert to retinoic acid. This is not a theory, and it is not speculation. It is completely proven in clinical research. Therefore, over time, we are all very slowly giving ourselves the retinoic acid treatment. For most adults, it is just going to ever so slowly, progressively get worse as we get older. So first off, just red flags when someone is saying that something is absolutely proven and they're they're really creating a they're using this like intensely persuasive type of language like this isn't a theory, it's not speculation. It's completely proven in the research. That should be a red flag, just in general, that's normally a claim that's being made that is way stronger than any of the substance that is behind it, and that's definitely the case in this situation. So to assume that any vitamin A will automatically convert to retinoic acid is a complete fallacy. It is completely ignoring all of the things that regulate the conversion from retinol to retinoic acid. Or if you want to look at the carotenoids and retinoic acid, there are multiple steps that have to be accomplished in order for that to be the case. And there's tons of different ways that those steps can be impeded, blocked, or that are generally just regulated. There's there's enzymatic regulation. There's factors like transport and availability of the different precursors, hormonal, you know, factors here that will affect the regulation here. And people make this argument with other things as well. So people will say, you know, there's this, this idea of the pregnenolone steel, where it's like, if you consume or use pregnenolone, it will automatically increase cortisol, or it'll automatically increase estrogen, despite the fact that pregnenolone actually reduces the conversion of precursors to cortisol or to estrogen. Same thing can happen with lots of other hormones. The same arguments are made. People often don't, but could make the same claim about GABA. You know, if you take GABA, it's automatically going to become glutamate, so don't take GABA. Or if you take glycine, it's automatically going to become oxalate, so don't take glycine. There's so many steps of regulation, so many metabolic factors, hormonal regulation, tons of things going on that need to be considered in this situation. And it's another argument that's been that was made quite a bit with vitamin D, right? If you're taking vitamin D, it's automatically going to become the 125 dihydroxy vitamin D. So there that is a fallacy in and of itself. And one of the most important things, and a very simple one to recognize in this case is that the production of retinoic acid is self limiting. It actually has its own negative feedback, where when you produce retinoic acid, it reduces its own production, basically, so that when you have enough of the end product, it slows its own production. And this happens in tons of different pathways. This isn't unique to retinoic acid. It's a really, really common phenomenon. And so there's a very clear depiction of it here from a study titled generation of retinaldehyde for retinoic acid biosynthesis. And they show it very clearly in this figure, the conversion from retinol to retinaldehyde and then to retinoic acid, and that retinoic acid has negative feedback on the conversion of retinol to retinaldehyde, which is done by different retinal dehydrogenase. So basically, as you have more retinoic acid, it reduces the conversion from retinol to retinaldehyde, and then it actually increases the conversion back from retinaldehyde to retinol by increasing these other enzymes, which are retinoid oxido reductive complexes, and those convert retinaldehyde back to retinol. So again, just mentioning that very briefly, it's something that, again, Grant claims as if this doesn't exist. It's proven that any retinol you take all will automatically be converted to retinoic acid. And so it's easy to create the toxic amounts that you would get from insane doses in something like Accutane. Yet, even even if you had massive doses of retinol, the production of retinoic acid is going to be self limiting, to a large extent, because of negative feedback loops like this and tons of other regulation that goes on between these different steps that is just really completely ignored.

Mike  1:34:17  
Yeah, I think it's it's interesting to just look at things in this extremely reductionistic pathway and say, look, look at see it. Can you convert down this direction? Instead of understanding like the end products have feedbacks, the intermediaries have feedbacks, and then the in the individual component itself affects those feedback loops, and you have multiple converging factors on the entire system where, basically, like the con the contextual state of the organism is shifting how things are being metabolized. So, like, if you take pregnant alone into the system, the pregnenolone can help to lower stress, select directly, which can help to lower its conversion to cortisol and any and then also, if the state is really bad, maybe it will increase cortisol. Some extent. But it's like, that's a big if, and it's considered, you have to, like, consider multiple factors with that and this, this goes to, like, what the big problem with all this vitamin A stuff is? Or even many of these, like, singular, reductionistic pathways in terms of trying to understand health, or, like, these different fads, is this idea that, like, Oh, it's just about vitamin A. Vitamin A just a toxin. It's everyone's problem. It's driving all these issues. It's like it is such a myopic perspective, especially when you start to consider all the other factors that are converging on health simultaneously. It's like, this is like, this can even this couldn't be right? Just like, as a heuristic, heuristic model as like, a general way to filter things. If there's like, this is just the one thing, and that's it. It's like, All right, that's probably, there's a probability that just this one thing is highly unlikely. It's most likely a combination of multiple factors. And sure, in some individuals, is vitamin A toxicity, a problem, that's definitely a possibility. That's definitely a possibility, but it would be dependent upon their individual context. And then, even with that said, like when we when you look with vitamin A toxicity, it's like, okay, they stop using vitamin A. And then there's multiple other components that can be converging. Maybe they have out, maybe they've been chronic alcoholics, maybe they have low protein intake, maybe they're vitamin D and E and K deficient, so it's exacerbating their vitamin A deficiency. Maybe they have a problem going on in the liver, like hepatitis or fatty liver, or something like this. So it's like, even with that model, there's multiple regulatory steps that have to be overcome, and there's multiple factors involved that can be problematic. So this Myo, this myopic perspective, is just and like this idea that just this, there's this pathway, and things are just going to move in this linear pathway, I think, is a lack of understanding, fundamentally, of how these things work. And I think it like thinking about things in that way exemplifies that this, the individual doesn't really understand how things, how things work, to some extent, or their level of understanding needs to be, needs to be like taken a next step further. This is not to say that I think that myself, No, like I myself, know all of these things, but I think it's safe to say that I know enough that I think it's unlikely that one component is going to just drive all of these problems and just move in this very reductionistic linear pathway, and that there's going to be multiple interlocking factors involved in the system. I think if you see, when you go through the Health Information enough, you're like, wow, this stuff is really integrated. And there's a lot of things to know and to just try to explain it to this one factor is like, I'll probably miss something if I come from that perspective.

Jay Feldman  1:37:36  
Yeah. And again, if you're going to make the assumption that this is a problem for most people, or even for a significant portion of people, there would there should be some really solid evidence behind the fact that this can happen easily, commonly. It doesn't take high doses. These things are very clearly problematic, and that's obviously not what we're seeing here, and that's why we just wanted to spend some time digging into the most fundamental claims that are that would need to be really well supported in order for this to be something that someone bases, not only a short term one month experiment of their health on, but we're talking about years and years because of the of this idea that in order to recover from the toxicity, you know, it's going to take, it's going to take years, and every little possible carotenoid that you're going to have exposed exposure to is going to put you back however many months. I mean, it's just, yeah, it's, I think we, we generally, I think we made it clear that the claims that we went through that are being made really don't hold any water and are very, very poorly supported, or just not supported at all. And in fact, the evidence is strongly against those claims that are being made. And these are some of the foundations of the vitamin A toxicity paradigm. Obviously, it's on everything, but most of it, I think, beyond this, is has, you know, is really not worth spending that much time going through. And we will be doing a follow up series digging into some of the details, not just necessarily from the vitamin A toxicity perspective, but just looking into the intro. Just looking into the intricacies of vitamin A and retinoid metabolism benefits and possible negatives of excesses and and negatives of deficiencies, and how much vitamin A we actually think somebody should be consuming, and what might predispose someone to vitamin A toxicity in that very rare case, and what to do about it, other than just avoiding vitamin A, not considering other factors. Again, still with the knowledge in mind that that's probably going to be a very, very rare case, but we'll talk about all those situations, and you know, in either regard, but we'll end the series there. And again, we'll, we'll have a follow up series digging into some of those other things that I mentioned, but we'll leave it there, Mike, where can listeners find more of your work?

Mike  1:39:42  
They can find me at my YouTube channel, Mike fave, and they can also find me at my website, mikefave.com

Jay Feldman  1:39:50  
Perfect. All right, if you did enjoy this episode in the series, please leave a like or comment if you're watching on YouTube and if you're listening elsewhere, please leave a review or five star rating. And all of those things really do a lot to help support the podcast, and are very much appreciated as always. To check out these show notes for today's episode, you can head over to Jay Feldman wellness.com/podcast we can take a look at the links to articles, studies or anything else that we've referenced throughout today's episode. And if you're dealing with any low energy symptoms, maybe you've been trying to resolve these with a low vitamin A diet. This could be issues like cravings and hunger, low energy or fatigue, chronic pain, weight gain, digestive symptoms, brain fog, poor sleep, hormonal imbalances, or various other chronic conditions like autoimmune issues, high blood pressure, insulin resistance, high cholesterol, or various others that head over to Jay Feldman wellness.com/energy, sign up for a free energy balance mini course. In this mini course, I'll walk you through how you can adjust your diet and lifestyle to maximize your cellular energy and resolve these low energy symptoms and conditions. So again, head over to Jay Feldman wellness.com/energy, to sign up for that free energy balance mini course. And with that, I'll see you on the next episode. You.