Jay Feldman 0:04
Welcome to episode 91, of the energy balance podcast, where we teach you how to live without constant hunger and cravings, fatigue, brain fog, poor sleep and other low energy symptoms by maximizing your cellular energy. I'm Jay Feldman. I'm a health coach and independent health researcher, and joining me again today is my good friend Mike Fave. Mike and I have been studying health and nutrition together for a long time now, and Mike also draws on his experiences from working within the healthcare industry. Today's episode is a q&a episode where we will be answering questions related to caliber oil as well as the croissant diet. And in specific, we'll be discussing whether cod liver oil is an ideal source of vitamin A or retinol, and whether we should be concerned about the Omega three content in cod liver oil. And then, in terms of the croissant diet, we'll be discussing the idea that we want our fat cells to be insulin resistant, to lose fat, whether keeping insulin low is the key to fat loss and what hormones regulate fat loss. If you have any questions that you'd like us to answer on a future Q and A episode, you can send those into Jay. At Jay Feldman wellness.com that's j, A, y at Jay Feldman wellness.com if you're new to this podcast, then after listening through today's episode, and highly recommend you go back and listen to episodes one through seven, where we took some time to build a foundation of the bioenergetic view of health. To check out the show notes for today's episode, you can head over to Jay Feldman wellness.com/podcast where you can take a look at the studies and articles and anything else that we referenced throughout today's episode, and if you are dealing with any symptoms or chronic health issues related to the topics we'll be discussing today, maybe these are things that you've been trying to resolve using cod liver oil or omega threes. Maybe this is instead due to a weight related issue that you're trying to resolve with something like the croissant diet approach. Or if you're dealing with any other chronic health issues. Maybe this is chronic cravings and hunger, low energy or fatigue, chronic pain, digestive symptoms, bloating, brain fog, poor sleep, hormonal imbalances, or any other chronic health issues or low energy symptoms. Then head over to Jay Feldman wellness.com/energy, where you can sign up for a free energy balance mini course where I'll explain how these different symptoms and conditions are really caused by lack of energy, and I'll also walk you through the main things that you can do from a diet and lifestyle perspective to maximize your cellular energy and resolve these symptoms and conditions. So to sign up for that free energy balance mini course, head over to Jay Feldman wellness.com/energy, and with that, let's get started.

Right? Let's, uh, let's move on to cod liver oil. So we've gotten a lot of questions. We've, uh, yeah, we've gotten a lot of questions about toddler for oil since it's been something that's been circulating throughout the sphere, something that people are recommending as a vitamin A source. And yeah, so, you know, we've been asked a lot, what do we think about it? And along with that, too, I get a lot of people who I'm seeing on new calls and things like that, who are taking it, and me too, yeah, yeah. So with that in mind, let's discuss our thoughts. There's so in general, the main argument for it, from the people who are suggesting it is that it's a really good source of retinol, of the preformed vitamin A. And there are some other things in there as well. But you know, one is vitamin D. And a lot of people who are recommending this are not in favor of vitamin D supplementation, but they're saying, hey, it's, it's a small amount of vitamin D, and there's a lot of retinol, and the ratio is good, so it doesn't matter. And there's also a good amount of omega threes in there. One of the arguments, one of the counter arguments I've heard here, is that it's mostly monounsaturated fats. So like, don't worry about the Omega threes, which is, well, no, I mean, it's true, but there's still a huge amount of omega threes. Like, normally, when you're looking at any sort of, like, if there's a fat, like, very high poof of foods are, like, 20 to 30% poof normally, you know, when you're looking at nuts and seeds and seed oils and things that's a super high PUFA food. So they're majority MUFA. Normally they're majority monounsaturated fat, but there's still huge amounts of PUFA, which is a legitimate, like major concern, that really high poof of foods. So just because it's mostly monounsaturated fat doesn't mean that there's not enough polyunsaturated fat to be concerning. So I just wanted to kind of mention that. But you know, let's talk about the specifics here. I've got a breakdown of the composition of I'm using Rosita cauliflower oil, which is the one that's often recommended by, you know, from the people that we've heard recommending it. So in a teaspoon of Rosita cauliflower oil, you're getting 3900 IU vitamin A, three. 95 IU of vitamin D and 1.3 grams of omega three.

Mike 5:06
Which is, what, 25% Omega three because a teaspoon is about four grams Correct?

Jay Feldman 5:11
Yeah, I think it's about, yeah, right around 30 something percent omega threes. Yeah, the total fats like four and yeah, it's 1.3

Mike 5:18
So just, I want to clarify a point here. The Omega six oils usually run from depending some of them are high at like 50 60% but they usually run in that 20 to 30% range. But running in 20 to 30% fish oil is like or omega three fats is extremely high. You don't see that in anywhere except fish oil, essentially, usually the Omega three content is much, much lower. And even in the studies that they run, like there's problems with greater than, like, 1% of the diet in calorically as omega three fat. So just something to keep in mind, overall.

Jay Feldman 5:58
Yeah, this is the amount if you were getting a fish oil supplement, you'd normally be getting about one gram of omega threes. This is 1.3 grams. So this is, this is a fish oil supplement like that. You are getting the equivalent Omega three as a fish oil supplement with vitamin A and vitamin D, and, you know, 3900 IU, vitamin A, 395, vitamin D. So just to, yeah, I think that's kind of first piece is the composition. Let's make sure that I think a lot of people who might be taking this don't realize that. So just wanted to make that clear. And then, as a comparison, there are some really great retinol sources that don't have the Omega threes. So of course, we've got things like dairy and eggs, but beef liver is the one that's most commonly, yeah, recommended. And so the to get the equivalent 3900 IU of vitamin A in beef liver, you would need 0.82 ounces, tiny amount. And the other thing, of course, is vitamin A builds up. So if one time a week you're getting, you know, five ounces or so.

Mike 6:58
That's even too much. I don't even think you need to have five ounces a week. Sure, not that it's too much, not that it's too much, but like it, you don't even need to have that much to have adequate amounts of vitamin A from liver. Like, you don't even need to do five ounces a week. Like, it could be significantly, it could be half that you could do one ounce a week.

Jay Feldman 7:19
Yeah, I think most people, I normally recommend, you know, somewhere in the three to six ounce range, depending on body size, thyroid status, of course, because another concern here is excess vitamin A is an issue, and can be an issue for your hypothyroid and struggling metabolically. So there's some concerns with having too much vitamin A, for sure. But yeah, so anyway, if you wanted to get 3900 IU vitamin A every day from liver, you could have 5.6 ounces per week, and that would get you that same amount. So it's one meal of liver, maybe, if you split that between two. But we're not talking about a large amount. And of course, if you're having it every day, would be just point eight ounces. So a lot of people like to, you know, just have a little amount every day. And you could do that, and you can do that, and that would be the same amount of vitamin A. And with that vitamin A, for one you get 2.2 milligrams of copper, which is a lot of copper. And these people are normally suggesting that we get a lot of copper, so this is a great copper source, if that's what you're looking for. And you have 1.6 milligrams of omega threes. So that's point 00, 1% of the 1.3 grams that you would get in the Rosita omega threes.

Mike 8:29
The other thing to point out here, just while you're in this like talking about the nutrition. So one ounce of beef liver and chronometer shows four milligrams of copper and only 1.9 milligrams of iron, because, and the reason I bring up the iron is because they often discuss, I a lot of this, I think comes from that root cause protocol stuff. So whether you talk about iron being highly problematic, you could create a diet that has that incorporates one ounce of liver a day for the vitamin A, if that's something that you want to do, and still keep a low iron intake by just changing your other protein sources. So if your other protein sources were dairy or if your other protein sources were things like shrimp or scallops or cod or sole or flounder or chicken or turkey, you could easily have a low, low heme iron intake below the RDA, creating a diet like that. And then you could also minimize your iron intake by combining the foods that have iron with calcium. So it's like, I don't see calcium, and then other other foods that have tannins that can inhibit iron absorption. So you could easily do that, like, without having to take in large doses of omega threes.

Jay Feldman 9:40
Yeah. And we'll talk about in a second that those omega threes are a real problem, like very legitimate problem we've talked about in the past. And we'll at least kind of gloss over it and at least mention some of the reasons here. The other thing I wanted to mention is a lot of people are saying that they're taking the cauliflower oil and they're feeling like it's benefiting them. And I just wanted to point out that, sure, maybe the benefit is for. Um, vitamin A, but if you were already getting beef liver, then I don't know how you could argue that's from the vitamin A, because you're probably, you were probably getting more vitamin A from the beef liver. So it have to be some other difference either, that you're not getting something that was in the liver. Maybe you're you've been had, you've had excess copper issues, and so not getting as much copper from beef liver might be helping you. Then I don't think that's the best solution, then to get your Vitamin A from from cod liver oil. But just want to mention, like, there are other differences here that can account for those benefits, but it can't be the vitamin A if there's the same amount of in both. So the other possibilities also, though, are that either a or, I guess we're on B now, because I mentioned the copper, but either you're benefiting from the vitamin D in the caliphate for oil. And if you're someone who's in a place where, you know, you're not getting much sunlight, and you haven't for a while, and you're not taking any vitamin D already, perhaps you're actually getting some benefits from the, you know, basically 400 IU of vitamin D. And then also the Omega threes themselves. So we'll get into this with omega threes. But we've talked about it previously that omega threes in the short term are anti inflammatory and also immunosuppressive, and those things can be beneficial in terms of their short term effects, like in the same way that if you took glucocorticoids, if you took cortisone or something, it can clear up pretty much any issue, any inflammatory issue, which is virtually all of them, are kind of founded in an inflammatory base. So you can get a ton of benefits from that, but it's comes at a major cost long term. So I think that's something to consider, is that the benefits, like, if somebody's feeling better with the cauliflower oil, it might be because of the Omega threes, and that wouldn't be a good thing. That would be something that is, is going to create a problem long term. And so I would be really careful. And this is basically, again, a huge reason why we really aren't fans of getting vitamin A from Caliph oil or anything else from Caliph oil. If you want vitamin D, I don't think that's a good place to get it either, because of the huge issues that the Omega three create.

Mike 11:53
I do want to just point out here. So there's a study where they talk about fish oil. So the study title is fish oil tenuous, Omega three, Omega six, polyunsaturated fatty acid, induced dysbiosis and infectious colitis, but impairs lipopolysaturide, de phosphorylation, activity causing sepsis. So it's that fish oil study in rats that cause sepsis, and although it eliminated their colitis. So we've kind of, we've talked, we've mentioned this one before, the intake of fish oil inside that diet was so basically, they say, here I'm reading directly from the study. I don't know if you want me to share the quote Jay or we'll put it up. We'll just link the study. But the diet that they discuss here is they say, for omega six, proof of supplementation, we followed the guidelines set by the American Heart Association, recommending point five to 1.8 grams of long chain Omega three PUFAs per day to offset high omega six diets as EPA plus DHA, or 34% of fish oil by weight. Point five grams of EPA plus DHA is available in 1.5 grams of fish oil as 18 grams of omega six is present in 30 grams of corn oil. We added 1% fish oil with 19% corn oil, low Omega six. PUFA fed animals were also included in the study as a control, and they so they didn't get so essentially, they the in that study where they found the immunosuppressive effect in rats that were exposed to in a pathogen with from the so from the Omega threes. So the Omega threes are causing the immunosuppressive effect they gave rats the equivalent of point five to 1.8 grams of long chain omega three fatty acids. Just something to keep in mind, like, that's not a high dose. And we're talking about taking cod liver is a high dose, is basically what you're saying. Well, yes, that is a high dose. But what we're saying, what we're essentially saying here is you're taking 1.3 grams of fish oil from your cod liver supplement every single day. Now we're seeing in rats that at something at almost equivalent intake point five to 1.8 grams, they're showing an immunosuppressive effect. So if you're taking more than one teaspoon of cod liver oil a day, you're at like, 2.6 grams of, like, essentially a fish oil supplement. And we'll talk about those problems in a second, as you mentioned. But yeah, and then, well, there's other studies here. I'm not gonna, like, read those quotes or anything, but they also talk about giving rats, like, a low fish oil intake overall, and it causing problems. Yeah, as as for the mechanisms that we're about to discuss right?

Jay Feldman 14:27
Yeah and so, yeah, just real, to keep it real brief, because we've talked about this extensively, and I'll link back to the main PUFA episode, and also articles regarding why omega threes are a problem. But there are three main issues. One is that they're very easily damaged, which is through a process called lipid peroxidation. And they create these lipid peroxide byproducts, metabolites, and these basically cause huge amounts of oxidative damage. They're found in basically every single degenerative state. And I'll let you just mention Mike, I know you wrote, can do some studies. I'll let you get to those in a second. Or just at least acknowledge that in studies looking at Califor oil, you see this as a problem, and then the other two things that can happen don't depend on the Omega threes being damaged, so even if they're miraculously not damaged and not oxidized by the time that they're being used internally, right? Well, not not not by the time they're consumed. Let's say they're consumed, they go through the digestion, everything else you've got them, and they're not even damaged, which you'll talk about, the fact that that typically that doesn't happen. But let's say it did happen, there's still two major problems from the Omega threes. One is that they'll still be they still produce various metabolites, various eicosanoids that are what account for the, quote, anti inflammatory, but also immunosuppressive effect, much like cortisol, also a little bit similar to a estrogen and these, and again, I'll reference back to the studies, but these cause major issues. So that's that is one factor, and then the other, which is really the biggest one, is that even again, if they're not not damaged, on oxidized and they then get incorporated into the cellular structure, which is normally when they're looking at this in studies, they're looking at the membrane phospholipid composition and looking at how many omega threes are in there. When that happens, they cause major issues with energy production, where they essentially cause permeability in the in the membrane that impairs efficient energy production, so you can't produce ATP effectively, and along with that, then they're very susceptible to oxidation in that high, essentially, high oxygen environment, and they get damaged there, which causes a ton of issues and also blocks energy production. And this thing, this situation, I guess, another thing I should mention too, is they're also, they also lead to permeability to ions, so you're not able to keep the proper concentration of ions internally versus externally, which causes massive issues as well pH imbalance and on and on, which causes various dysfunction. And these things are so notable that looking at the Omega three content in and the proof of content overall, but really specifically omega threes, looking at the content of the Omega threes in the composition of the cells is the number one thing that accounts for differences in aging and lifespan, both within and across species. So if you're looking at an organism, the one that has the more omega threes incorporated into the structure of the cell is the one that's going to age faster and die sooner. And this is again, the same across species, so not just in humans, not just in rats, but across all species. And that's because of these dramatic effects in terms of energy production, susceptibility to damage and issues on from there. So yeah, this is a huge, huge factor, and why we don't recommend using fish oil supplements like cauliflower oil.

Mike 17:39
Yeah. So the first thing I want to point out from one of these studies, I'm going to read one little one little snippet here. It's one sentence. What they say here is, in vivo lipid peroxidation, assessed by urinary MALDI aldehyde excretion, was enhanced when diets containing greater than six greater than 1.8% fish oil were fed. So again, a very low amount of of the diet as fish oil increases lipid peroxidation. So that's the first thing.

Jay Feldman 18:07
Just two things to mention here. One, you're talking about a study looking at MDA, which is male dialdehyde, which is a lipid peroxide as a result of fish oil. And this is fish oil percentage, not omega three percentage. So the like one teaspoon of versita would be like four to five grams of fish oil with leading to 1.3 grams of Omega three. So they're talking about a 1.8% fish oil diet, which is not very much at all.

Mike 18:31
And the other thing is, those diets, in this study, the rats were fed a combination or different ratios of fish oil and beef tallow, and even when they were fed the beef tallow with the fish oil, like it's not protective of the of that of the peroxidation from the fish oil. So that's the first piece. So what we know is that now the other thing is, I have a study here that basically discusses that urinary excretion of Malda, Malon, Malin, dialdehyde is associated with lipid peroxidation strongly inside, inside the body, whether that's from having lipid peroxidation or from ingesting lipid peroxides. So we know that Malden, Malon dialdehyde excretion in the urinary and that's how they're measuring in these studies, is an indicator of lipid peroxidation. So we just need to clear up that association first. And malondialdehyde is a product of lipid peroxidation. It's one of the things that gets formed. So you have that. The second piece that I want to bring up really quick is, even if you were to have the most perfectly preserved omega threes that had nitrogen in the bottle as an amber bottle, and you kept it frozen for and it was like freshly produced and frozen whatever, like whatever it is, by the time it goes to your digestive tract, it is oxidized like that's not a question. The studies basically show, and it also depends on what you're eating. So if you if you have your fish oil with anything containing iron, it is going to get oxidized. The iron will oxidize it in your digestive tract. Even going through your digestive tract without the iron will oxidize the fish oil because it is that able to be peroxidized. So I don't care, like, how perfect your fish oil supplement is, the only way they've been able to minimize the oxidation overall is to in this is without even, I think, not through digestion, but just in general, has been to combine it with different antioxidants in the fish oil. So like, even sitting on the shelf, it goes rancid, and then they have to put it in triglyceride form and combine it with different antioxidants to protect it by itself, but I think even then, it'll still oxidize inside your digestive tract. Now the next problem is, once it's incorporated into your tissues, say it gets through your digestive tract, non oxidized, and then it gets incorporated into your tissues, like you still can have it oxidized in your own tissues. So there's a study here. What they were looking at was, let's see what they fed rats. This was actually specifically cod liver oil. And what they found was fasting, MDA excretion, let's see adrenocho tropic hormone and epinephrine administration increased urinary MALDI aldehyde further indicating that lipolysis either releases fatty acid peroxides from the tissues or increases the susceptibility of mobilized fatty acids to peroxidation. A decrease in fasting MDA description was observed, observed in rats previously fed a high level of antioxidants versus normal levels of vitamin E. Basically, what they're finding is that when you have these hormones, the stress hormones that are releasing free fatty acids for oxidation, the animals that were fed cod liver oil had higher amounts of the of the Malian dialdehyde from being released from the tissues. So even if you, even if you get it into your tissues, if you're going to release it to oxidize it, or even being present in the tissues, you can increase the Livid peroxidation, so that that's a huge problem overall. And then basically the last one is like the feeding the and the rat studies, feeding the the rats cod liver oil. And then even feeding humans cod liver oil increases, increases the MALDI aldehyde or lipid peroxides in the tissue. So just important things to consider here. And then there's even a human study here, basically showing the title studies mal dialdehyde excretion by subjects consuming cod liver oil versus a concentrate of n3 fatty n3 fatty acids. So the concentrate of n3 fatty acids, I think, was a pharmaceutical product that had been, had been what's it called, maintained in a particular form. I think it was a triglyceride form, and then combined with something called dodecall galley and vitamin E, which are antioxidants. And so the cod liver oil, by itself, increased the the urinary MALDI aldehyde, or malondialdehyde. So again, you're increasing it when you that's probably already in the cod liver oil, so you're going to have an increased amount of my of lipid peroxides. When it gets goes to your digestive tract, it'll probably be peroxidized. And then when it gets into your tissues, depending on what you have going on, it may oxidize in the tissues, or when it's released for oxidation, it's going to oxidize. So overall, you're having lipid peroxides galore with your cod liver oil supplementation. And overall, this just doesn't make sense when you can get adequate vitamin A from things like liver, eggs, dairy, et cetera, without having that the excess of the the pot the Omega six fatty acid, or omega three fatty acids.

Jay Feldman 23:26
Yeah, just for reference to kind of summarize the studies we were referencing these are, there are several studies here some were just looking at fish oil that you mentioned, but several studies here looking at colivr oil, showing that they directly cause lipid peroxidation just by their digestion, and then, if not, later on in the tissues. And this is pharmaceutical grade, high level cod liver oil, and they're comparing it to other things, and I'll cite these studies, but that's, that's the important piece here, is that you're seeing this direct effect of having cod liver oil, and you see it with fish oil as well. So, like, and that's, like, ubiquitous, like, there's so much research showing that in those cases, yeah.

Mike 24:04
And the other thing I want to point out is that the cod liver oil stuff, I think, as far as I understand, and anyone feel free to correct me if I'm wrong, is coming from the root cause, protocol camp type of thing, where vitamin A and is extremely helpful, and you want to have adequate amounts of copper, and you want to lower, you want to lower excess iron. Because, according, I think it's Morley Robbins is the one who's discussing this, the Vita, the iron is like, the number one problem is like, the cause of all of everything, essentially, to, I guess that perhaps that's a straw man, but the iron is a problematic. So the thing is, is you can, again, you can meet a vitamin A intake with adequate copper levels while minimizing your iron intake using liver or using these other foods without having to have the excess omega threes. So I think that's extremely important to keep in mind here I'm working. I'm trying to work from that perspective, because. Don't think that there's a justification for cod liver oil overall. And I think that a lot of people notice the benefits from the Omega threes, not because or from the cod liver oil, from the Omega threes, not because we recommend omega threes, but because they do have an immunosuppressive effect, and some of the mediators that they produce have an anti inflammatory effect, and that is known. And they're like, we're not even questioning that. That's just like people just describe that all the time. However, in the long run, this is highly problematic from a lipid peroxidation standpoint and from the immunosuppressive standpoint.

Jay Feldman 25:33
Yep, yep, absolutely All right, so we've gotten a few questions here related to a two part series we did discussing grand Marshall's croissant diet and a couple of the views that, or perspectives that that's based on. One is the Ross theory of obesity, or the reactive oxygen species theory of obesity, and the other is the CD one theory of obesity. So we had these two episodes discussing this. And there was, there were quite a few people who commented on there. You know, I'm assuming they're people who are in favor of his views and had questions. You could say some of them were, were nice, like questions, others were a little bit accusing, or, or I don't know. Anyway, I'm we'll discuss a couple of the questions and comments that people had regarding those episodes. So I'm just going to read a few of the different ones, and we'll kind of go through and address the points. So Matthew says, just to clarify, I really don't understand your objections. I thought Brad's main point to my understanding is that burning saturated fat is better than PUFA, which I don't think you clearly addressed. Do you think saturated fats are as bad as PUFAs? Do you agree with the AHA, that saturated fat consumption should be reduced to less than 7% of your daily calorie caloric intake. Also, you didn't really address the insulin resistance that happens in the fat cells, which seems to be a key component to reducing fat storage. Joe says, and this is he had two different comments at different points, so I kind of cut them together. So the first one part of it was saying that saturated fats and starch drive satiety. Is his other big argument. I think you misunderstand his theory. And in another comment, he said, This is a big point from Brad Marshall in SCD, one theory saturated fats. Saturated fat causes the adipose to reject insulin because of signaling reactive oxygen species, which allows for longer times between meals because energy isn't getting shunted to fat. ALA and La fail to produce the ROS required to suppress insulin signaling. However, PUFA does provide for pathological reactivation species and uncoupling. And then David asked, so how do we make our fat cells insulin resistant to lose weight on a bioenergetic diet? So a bit of a theme here, asking about this, the fat cells, the adipocytes, being insulin resistant, and it was something we did not actually address directly in our video discussing the Ross theory of obesity, because we think that it's a rather myopic reductionist point, and we'll discuss why in a second. But basically, I would say that this is not the goal that is going to result in fat loss, making the fat cells insulin insulin resistant. So we'll dig in on that. But there's a couple other things just to adjust real quickly from that first comment from Matthew.

Mike 28:11
So first off, we agree with the American Heart Association 100% just want to put that up there.

Jay Feldman 28:19
Yeah, just for reference, food pyramid is the way to go. So he said, I thought Brad's main point to my understanding is that burning fat, saturated fat is better than PUFA, which I don't think you clearly addressed. So we talked about this directly, that saturated fat creates more reactive oxygen species. Brad views this as a good thing, because it creates an insulin resistance that he says you need resistance that he says you need in the fat cells to create fat loss, and we and then PUFA creates less reactive oxygen species production when oxidized through the mitochondria, like through mitochondrial respiration. So that's why Brad doesn't like them. We provided a whole slew of reasons why we don't like PUFA and why they actually create more reactive oxygen species than do saturated fats, but not through controlled mitochondrial respiration. And that PUFA getting through controlled mitochondrial respiration is not the problem. That's not why we don't think, why we think that they're an issue. There's a ton of other reasons that are way more important and actually end up creating, as I was saying, more reactive oxygen species than if they are oxidized through a controlled way in the mitochondria. So we do. I mean, whether saturated fat is better, like burning saturated fat is better than PUFA, I would actually say not necessarily. PUFA are problematic because of all these other issues that they create. So that's kind of the first part there. And again, I don't know if, I don't know, I'm not sure if, like, the whole episode was listened to or what, but we, I think, very clearly, made it, like, made the point that we are not a fan of PUFA and we are a fan of saturated fat consumption, but for different reasons. So obviously, no, we don't think that you should be reducing saturated fat to less than 7% of your daily calorie intake. We were fine with a. Moderate fat diet that includes mostly saturated fat and having a moderate amount of carbohydrates, which is actually the same in terms of macronutrients, are very similar to what Brad suggests. And again, just to be clear here, I think Brad has some really great information. We agree on a lot of things. And you know, I really like his some of his articles and discussion, as far as changes in metabolic rate over time. I like the perspective that he's coming with in terms of actually digging into the physiology. He's actually acknowledging things that most people looking at, you know, who are in favor of saturated fats, are not talking about at all. Like this isn't an issue with Brad. And part of the reason why we're talking about is things because we think that there's value there, but we just disagree on interpretation and a few other things.

Mike 30:41
So nuance points we disagree on that lead to some different recommendations. But overall, I mean, he does have some great information, and I think his work is valuable for sure.

Jay Feldman 30:52
Yeah, yeah. And as we were saying, like we agree as far as fats go in terms of what you should do, but it just doesn't necessarily look the same in terms of the reasoning behind it, and that reasoning affects other things as well, such as where you might want to get your carbohydrates from, how much you might want to increase, and also whether you want to do other things to increase reactive oxygen species production and activate amp kinase, things like that that we definitely don't agree with that are kind of outside the realm of just saturated versus PUFA, saturated fat versus PUFA?

Mike 31:23
Yeah, I think that there's like, I think you covered it pretty directly. And I know we covered in the podcast the difference between the utilization of PUFA for energy and the difference between saturated fat and energy, as far as the ratios of FADH two and NAD and all that type of stuff, and ROS production. I think that overall, the again, as you discussed the we agree that there's problems with PUFA, but we think that there's other mechanisms related to to that, and it involves over peroxidation, incorporation and membranes, and then Adjustments and function of proton grading and whatnot, inside the mitochondria, et cetera. I think that the biggest discrepancy we have as far as the saturated fat piece, is like, and I'm gonna, I'll pose a question to you, is like, how do we know that if we have this large intake of saturated fat, and that's the vast majority of our calories, that we're just gonna get insulin resistance only inside the fat cells, and that's where I think we start to have the discrepancy with with the overall picture. It's like this. We're only generating ROS and and creating this, this, this situation inside the fat cells. And the other thing I want to pose to you there as well, or just bring up there as well, is that the stress response functions through the mechanism that Brad is describing by upregulating fatty acid oxidation, by ROS signaling inside the mitochondria, throughout all of the vast majority of the tissues in the body. So like, we're not necessarily promoting or trying to stimulate this response, whereas Brad is, and I think that's a major difference.

Jay Feldman 33:03
And another major kind of question here is, does our fat cells being insulin resistant actually mean that we're is that actually the state that we want to create for fat loss? Does that actually lead to fat loss? Is that the only way to create fat loss? What does that actually mean? And I think there's some misunderstanding, not necessarily from Brad. But, I mean, we definitely have disagreements here with Brad, but also, I think especially with some of these comments. You know, for example, on that second one from Joe, he was saying, like, as far as the insulin resistance piece, he says saturated fat causes the adipose to reject insulin because of signaling reactive oxygen species, which allows for longer time between meals because energy isn't getting shunted to fat. So there's, like, a conglomeration of a few different things there that are not really a aren't really accurate, and are important to like to discuss. And so I think that's kind of the next piece here, right? So you brought up the first point, Mike, which is that, how do we want to create systemic insulin resistance, or just insulin resistance, in the fat cells, and what is controlling those things? And then the second piece is, is, do we even want that in the fat cells? Is that how we lose body fat? And so the kind of general take from the the Chris Hunt diet perspective is that saturated fats are beneficial because they're creating a lot of reactive oxygen species, which is what stimulates further fat oxidation. So saturated fats cause fat burning, essentially, and create this insulin resistant state. And if we create this state in the fat cells, then our fat cells are just constantly going to be burning fat. They're not going to be storing any fat. So you're going to be losing fat. Simple, you know, like a simple problem, simple solution, right? And I think there's some major problems with that. And so I think maybe a good place to start is that insulin resistance and fat burning so they you. I think it's helpful to maybe think of it in turn into systems. So we've talked about this in terms of the Randall cycle, which is a major part here, which is basically that there are a bunch of mechanisms that go together when we're burning fat to allow us to burn fat, and then there's a bunch of mechanisms that go together when we're burning glucose to allow us to burn glucose. And so when we're in that fat burning state, there is certain inhibition of the glycolytic enzymes, and this production of the reactive oxygen species, a shift in NAD 10 ADH ratio to reduce the NAD 10 ADH ratio and create this insulin resistant state where the cell is not taking up glucose, what it is doing. And this is super important here, and I think is just completely ignored, is the cells don't need insulin to take up fat. They just need insulin to take up glucose. So they're still taking up fat in an insulin resistant state. Otherwise, if you had a diabetic person who is insulin resistant, they would never be able to get fat. But obviously they're generally excessively...

Mike 36:00
fatty acid oxidation, right? And the thing is, they can still burn glucose, but it's through glycolytic metabolism, right, right? And that's what you see, high amounts of lactate and diabetes.

Jay Feldman 36:12
Yeah, and all these degenerative states, you see high amounts of lactate, high amounts of lipid, peroxida, or, sorry, lipid oxidation, high amounts of fat burning, high amounts of lipolysis, high amounts of stress and insulin resistance that you see in fatty liver disease you see it in type two diabetes. That is what's going on here and so obviously, those are not states that result in lots of fat loss and health. So to take that to mean that in general, if we just create insulin resistance, we're okay and we're going to lose fat, I think, is missing this huge other piece, which is that, and I'll talk about like this in real application as well, but which is that the fat cells can still be taking up fat and still be gaining fat while they're insulin resistant, they just can't take up glucose, or aren't going to as easily take up glucose.

Mike 36:54
And the key feature of the stress response is the oxidation of fatty acids through these mechanisms where and it promotes the continue oxidation of fats by adjusting, it's the acetyl CoA and COA ratio, and then the NADH to FADH two ratio, and basically shutting down the connection, or pervaded dehydrogenase connection, of glycolysis to the Krebs cycle. So basically, so basically, all you're left with this continual beta oxidation. So it's literally a switch in that pathway to just continually move towards this fat oxidation. And I don't think that this is like the indiscriminate, like, discriminately, just the fat that this happens for. And I think that's a huge problem with the overall picture as well. Is like, are you just triggering this inside the fat cells, or are you triggering this, like, on a systemic level, like that? Yeah, I think that that's a big piece of the puzzle as well. So I'm not, I'm not a fan. I don't think either of us a fan is having, like, extremely higher or higher fat diets to try to promote fat oxidation, to lose weight. I think we would say that you want to have adequate amount adequate amounts of fat for differing functions, but you want to be having glucose oxidation because of the, because of these adjustments overall, because of because of the, essentially, the stress response is driven, drives this pathway overall, and there's problems. So just essentially running through fat oxidation chronically, on a larger scale.

Jay Feldman 38:23
Yeah, two things I want to mention here. One, for people who want to understand those mechanisms, or I know we're kind of glossing over like, what's going on in respiration, in terms of the fat versus carb oxidation. We discussed that in the first episode of discussing the Ross theory of obesity. So just go back and listen to that. I'll reference in the show notes. The other thing again, when we're looking at things systemically, and this is why we didn't focus on this as much, is because there are really important things going on systemically that I think are way made like way larger determinants of what's going to happen in terms of fat storage and fat loss. And as you're mentioning, Mike, so for one, carb intake is what is going to determine carb oxidation, or normally, just the food quotient that's coming in. So if we're taking in a lot of carbs, we're going to be burning a lot of carbs. If we're taking a lot of fat, we're going to burn a lot of fat. We're taking in, you know, equal amounts of each will mostly be burning equal amounts of each. And Brad isn't saying to go on a low carb diet, right? He's suggesting to have carbs and fats, which is what we suggest as well. So again, this is similar, but we think it works basically through different mechanisms, and it's important for when it comes to other recommendations, like sugar versus starch and on from there.

Mike 39:26
I think that he has a lower I think his his suggestions for carb versus bad intake are lower for carbs than we discussed. I think he's like in the 100, 150 gram range, if I remember correctly, with most of the things. I think most of the oxidation. I don't remember, because when we looked at it was a while ago, and I haven't looked at too much of his stuff recently, but I'm pretty sure he's like that 150 to 200 grams of the carbs somewhere there, and then a lot higher fat intake.

Jay Feldman 39:52
Maybe. Yeah, I don't I don't remember exactly what those numbers are, but either way, his idea here is that he's saying you need to have the carbs. For the brain, for the liver and things like that, to help with the hunger signals and prevent the stress and everything, which is something we definitely agree with. And then, as both of us say, you know, like we talked about this too, then you have fat intake that can be relegated to the areas that don't need as much to produce as much energy, like the muscles at rest, and potentially, like the fat stores as well, and so that's when fat oxidation, that's when we want fat oxidation is when we have low energy needs, because there are so many breaks that happen from oxidizing fat, the production of reactive oxygen species then leads directly to the stopping of energy production. And that's because the cell will get so damaged, and my mitochondria will get so damaged it can't continue that. Then you end up activating all these backup mechanisms, which then will drive it further and kind of like reset it, maybe throw uncoupling, maybe, you know, depending on the circumstances, and then we'll push things further. But that is a that is a limited pathway, like there are limits to being able to continually do that, and in a cell with low energy demands, that's not going to be forced so much, like in in a muscle at rest, you don't need, like, that's only going to happen when you're under the influence of stress hormones or, like, excess calcium, you know, coming into the cell and things like that. Like, you aren't needing to force the excessive Ross production and energy production through fat oxidation, unless there are higher energy demands there. That's why fat is not a good fuel for those areas, like the brain, but in these other areas, you're basically going to be relegated to low amounts of fat burning and low amounts of energy production, because that's all that's needed at the time, which is, again, it's fine when you're at rest, but the idea that you're just going to be like, burning high amounts of fats forever without a cost to these to the activation of these backup pathways, is not the reality, like, there's only so much NAD salvaging that you can do until you're depleting that. Like the activity of those pathways.

Mike 41:57
And a decrease in ATP production is a big problem as well. I think that's like a key function as well. When you have the excess ROS production and upregulation of uncoupling that comes at the cost of ATP production directly. So it's not and we talked about this in the hormesis series, where you don't like you want to have adequate ATP production, and then you can have uncoupling protein through the ROS you don't want to be having lack of ATP. You don't want to be having the excess ROS production from the shift with the ratios of NAD and FADH two and acetyl CoA and COA with fat driving and coupling, and then not having ATP production. Those are problematic. That's problematic. And it's like, is that hap like, are you just having that in the fat cells, or is that happening across like, multiple tissues in the body. And I so, yeah, so go ahead. I didn't mean to, like, completely cut you off, but I think that that's a key piece with what you're discussing as well.

Jay Feldman 42:49
Yeah, for sure. No, no, it's a great point. And so with that in mind, I think that it's like we're kind of getting at this point that just burning fat is not the solution here, and you see that in the real world as well, like when you're looking at so there's a great study I reference a lot, and it's not the only one, but there's, it's by Kevin Hall. He does this metabolic board study where it's a low carb versus a high carb diet, like low carb, high fat versus high carb, low fat, and the low carb, high fat diet has way more fat oxidation going on way lower insulin, and yet they lost the same amount of weight and less body fat. So if the only thing that determined how much body fat you lost was how much insulin you had circulating and and that was active, how insulin resistant you were and how much fat you were burning, then those people on the low carb, high fat diet would have lost tons more body fat and weight than the other group, but they didn't. They lost less body fat and the same amount of weight, which means that they lost fat free mass, which is a whole other issue, whole their problem. And I think it very clearly gets at the important piece here, which is that when you're burning more fat, it doesn't mean that you just lose fat all the time, like and I'm not saying that it's as simple as Brad saying that this is more of, like all of the low carb sphere. And just what we're all told, like, you need to burn more fat, and you can do it by cold thermogenesis or a low carb diet, or keto or fasting or whatever, and you know your zone two cardio and all that stuff, just the more fat burning, the better. Like that is not that doesn't mean fat loss. Like there are two sides to that equation. There's the fat coming into so first off, there's systemic fat burning. And then if you want to look at the fat stores, you have fat burning that's going on there in adipocytes. You have the lipolysis that's happening there, the fat release, and you have the fat that's being taken up there, the fat takes us, right? And then the production of fat within that fat cell, which, as you're saying, can happen either from fats coming in or from carbs, right? So we need to be looking at all those factors here. If you're just focusing on the fat burning, I think it's completely missing what's going on in fat loss. And again, if that was the case, if it was just as simple as burning more fat, then a low carb diet would lead to tons of fat loss immediately, or would so would fasting like you would be losing tons of. Of body fat. But that's not how it works, like there's so many other mechanisms that are going on here that we need to consider in terms of what's going on with the hormones that drive fat storage, not insulin, but things like glucagon, adrenaline and cortisol, as well as the activity of the thyroid hormones, the activity of the reproductive hormones. Those things all need to be considered and are going to be the main drivers of what, of whether you're actually going to be storing fat. And those depend on systemic energy availability. They depend on keeping the stress hormones low, on and on. And if you're on a lower carb diet, that's not going to be the case. You're going to be turning down the active thyroid hormones, you're going to be raising the stress hormones, you're going to be turning down the angiogenic hormones, and that is going to lead to a situation where you are driving fat production in adipocytes and fat uptake, even if they're insulin resistant, they'll be taking it up from fatty acids, you know, that are coming through from the chylomicrons, or just free fatty acids that are in the blood. They'll take those up as well. So, you know, in the LDL, you know, VLDL, LDL, those are going to drop off fat there as well. So, yeah, I think that's why, in that first episode, we focus so much on the systemic, like, what's going on metabolically and all that as being the thing that matters more, as opposed to just drilling in on what's going on at the adipocyte, because it's the adipocyte just completely ignoring what's actually going on in the larger context. Yeah. And I and I get like, I think we should have probably acknowledged this, like, talked a little bit about the whole insulin resistance at the fat cells then, because it would have cleared up maybe some some confusion and misunderstanding. But yeah, that's why we were focusing on that. And so from this alternative view, if, again, if we're reducing the things that drive the fat storage on the hormonal level, which are the things that represent low energy. Systemically, it doesn't lead to having, like a low carb diet. We need to have adequate carbohydrates. It's super, super important for doing that, among other things. It's not just as simple as having enough carbohydrates. We have to consider gut health, you know, endotoxin production, exposure to heavy metals, nutrient deficiencies, on and on and on. But yeah, the idea that we just need to be burning fat and we just need to create this physiological insulin resistance, either systemically or at the fat cells, is completely missing the point, and can and is not synonymous with fat loss.

Mike 47:14
And I also think the satiety like waxing the satiety mechanisms, isn't ideal either. I don't think we want to be like, eating a diet that allows us to just be super full on eating way less calories. I think that the mechanisms there involving that involve stress pathways. So I wouldn't be trying to, like, heavily ramp up the like these mechanisms to drastically lower my satiety by having large amounts of fat. But I don't think that that's a good idea in the long run, from not only from the stress hormone perspective there, but also from the like nutrient perspective. Like, if you're getting by on 1200 calories a day, like you like, there's a it's hard to meet all your nutrient requirements there. So I don't think it's a good idea to run that that approach either, and I think that that falls in line with the the these ideas that the problem that people are getting are gaining weight is like this, eat less, exercise more, or the Eat, eat food, not too much, mostly plants, like all those garbage ideas, or these other ideas, like, I think it's even ganye's idea that it's just like, Oh, we're just like, our brain is wired for these types of foods, and which is, like, sweet things and whatnot, and that's what makes us fat. And then I think nature wants us to be fat, yeah. So it's like this, this, in this original sin idea applied to our biology, that our, our our cravings and whatnot are making us fat. Instead of being like No, our cravings make sense. They go directly aligned with our hormonal profile. And what you're seeing in these situations is that the large food conglomerates in the food industry has essentially created products that are highly problematic but take advantage of the reward centers. Because I have to be 100% honest, I haven't seen somebody get fat eating a whole bunch of fruit. And I also haven't seen somebody get fat, you know, meeting their salt cravings, their sweet cravings, having eating chocolate. Like I haven't seen these things create obesity. What I've seen create obesity and things along those lines are a lot of processed food intake, a lot of vegetable oil, and take all of those types of things. So I don't think waxing satiety mechanisms is ideal overall, and it's not. I'm not. I don't when I'm working with somebody, I'm not shooting to make them extremely full so that they just don't want to eat anything, and by eating less overall, therefore they lose weight, especially in the context of trying to look at things from the from this hormonal perspective, if you're going to look at it from the hormonal and bioenergetic perspective, then discussing the satiety mechanisms and trying to just make people super full is, I think, tangential, and I wouldn't want to push that envelope. So I think that's another problem. And I'm not saying that Brad is necessarily waxing the satiety mechanism, but that was something directly discussed in one of the questions. So that is a piece to keep in mind. And I think part of the high fat mechanism is because it directly slows gastric emptying, so you're just like, you're super full. So again, I don't think that that's ideal. And then super high fat intakes, I don't think are ideal from a microbiome perspective as well, especially with limited intake from other plant foods and whatnot, which is again, a part of the SCD one or the part of that ROS SCD one perspective, the dial was like croissants and port wine or wine or whatever it was. I think that the plant foods, fruits and whatnot. Fruits and vegetables are extremely important for the microbiome, and that's a huge gaping hole in this perspective as well, especially when we talk about the things driving obesity. There's other theories that we've that we've discussed in this podcast with inhibition of like econotase, which is a paper that Jay and I had discussed, talking about, like the shunting of metabolism by inhibiting econotase through inflammatory mediators, like cytokines, like tumor necrosis factor alpha, il six, etc. So I think that that's like, there's multiple mechanisms here, and so that's why, you know, I think there's more to the picture. Just SCD one and then, like insulin resistant fat cells. I also think those, those are a bit like reductionistic perspectives,

Jay Feldman 51:24
Yeah, and again, just to clarify part of the reason why we're bringing up these discrepancies, even though there aren't such dramatic difference in terms of our recommendations. Because, again, Brett isn't saying low carb, of course, like croissants aren't, aren't carb free and and he acknowledges that we at least need some carbohydrates, but also, like some of the supplements he's looking to, the pathways that he's that he's talking about trying to activate that go along with the fat burning pathways are things that we pretty strongly disagree with for the reasons that we've discussed today, which is that just increasing fat burning shouldn't be the goal, and it leads you astray in this way. But also for other reasons that we've discussed in our hormesis series. So I'll refer back to that. I did want to mention a couple other things. So one, when it comes to like the processed foods you were mentioning, I would say that those are an issue largely because of the ingredients that are in there, the, you know, problems with PUFA, largely, maybe some, you know, the processed starch, like processed flowers and things like that. I don't think it's a problem with the reward centers and activity there, but rather like we that shouldn't be a problem when we're looking and I don't think we should be ignoring the things that regulate satiety. I just think the what really points to, the largest thing is ATP levels, is energy levels in the liver and the hypothalamus and so and that's not the only thing, but that is a major piece here, is is that? And so, of course, that's something that we talk about a lot, and something that is encompassed from the bioenergetic view. The other thing is, we've both acknowledged that low fat is a problem for satiety, like we've talked about this a lot, like someone on low fat tends to struggle a lot. They can't go long between meals on and on. And part of the reason for that is because when our fat, the free fatty acids in our blood drop too low, it triggers a stress response, just like when blood glucose drops too low. So we're not advocating for a low fat diet here. And so, you know, we're normally fine with up to, like a 40% fat. It's like total calories from fat that's like, normally at the high end of our limit. And so, you know, and then if you're at that point, you're kind of like a 40% fat, 40% carb, 20% protein. Percent protein. Again, this would be the highest amount of fat I would I would normally recommend that's like, maybe 45 you know, it depends on the context, but like, that's fine, and I think I don't, I don't want to put words in Brad's mouth, but I don't think he would necessarily have an issue with that macronutrient breakdown. The types of foods would probably be different. But again, it's also for very different reasons that I think is reasons that I think is highly important. As you were saying, we don't want to be driving satiety in terms of, like increasing protein intake, eating a lot of salads, like trying to eat as little as possible. And of course, Brett is not a fan of that either. He's talking about trying to raise your metabolic rate. Because our metabolic rates are way lower now than they used to be, in that that is a major problem. So just wanted to mention that I will say also, I think there's a place for bringing fat intake down to maybe as low as 20% and this is, you know, yeah, just for reference, for anyone listening like I think there's a place for that depending on what your fat needs are. If you have less muscle mass, that's going to be mean that you're going to have less need for fat. If you're less active, that's going to mean you have less need for fat. So I do think that in a lot of cases, it can be beneficial to drop fat down as low as 20% and in that case, you're probably bringing carbs up to, you know, 55% 60% 65% something like that. So I don't see an issue with that either. And normally 20% again, if your fat needs are low, it's still enough to prevent the stress responses from having too little fat coming in and still have the hormonal production and the digestive benefits and things like that.

Mike 54:45
Yeah, I agree.

Jay Feldman 54:47
All right, so before we wrap up this episode, I did want to make a clarification regarding the dosing that we were discussing with the study that Mike had referenced where fish oil supplementation caused. Immunosuppression, which then caused the state of sepsis in rats that had infection induced colitis. So in that study, Mike had included a quote discussing how they were using the equivalent of half a gram of 0.5 grams of omega threes from 1.5 gram of fish oil. That was the dosing that they're using, the equivalent dosing that they were using in their study. And I wanted to clarify that basically, cod liver oil is about five grams. A teaspoon is about five grams, and it's fish oil, and this results in about 1.3 grams of omega threes, considering it's nearly 30% omega threes. So it's basically the exact same as the 1.5 grams of fish oil used in that study, of course, minus some of the other minor differences, or differences between caldevoil oil and most other fish oil, but at least in terms of the total amount and then the amount of omega threes. It's the it's actually the same in terms of percentage, but about three times as much in terms of the actual omega threes. So just wanted to make that clarification there. If you did enjoy today's episode, 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 on iTunes. All those things really do a lot to help support the podcast, and are very much appreciated. If you have any questions that you'd like us to answer on a future Q and A episode, you can send those into Jay at Jay Feldman wellness.com that's j, A, y at Jay Feldman wellness.com or you can leave those in the comments if you're watching on YouTube, to check out these show notes for today's episode, where you can take a look at the studies and articles and anything else that we referenced throughout today's episode. You can head over to Jay Feldman wellness.com/podcast and if you are dealing with any symptoms or chronic health issues, maybe those are related to the topics we discussed today. Maybe you've been using caliber oil or fish oil to try to resolve them. Maybe you've been taking the croissant diet approach to try to resolve those issues, or for some weight loss. Or maybe you're dealing with other related or unrelated chronic health issues or low energy symptoms, things like chronic cravings and hunger, low energy or fatigue, chronic pain, digestive symptoms like bloating or intestinal inflammation, or maybe you're dealing with brain fog, poor sleep or insomnia, hormonal imbalances, or various other low energy issues or chronic health symptoms, chronic health conditions. Then head over to Jay Feldman wellness.com/energy where you can sign up for a free energy balance mini course, where I'll explain how these different symptoms and conditions are really caused by lack of energy, and I'll also walk you through the main things that you can do from a diet and lifestyle perspective to maximize your cellular energy and resolve these symptoms and conditions. So to sign up for that free energy balance, mini course. Head over. Jay Feldman, wellness.com/energy, and with that, I'll see you in the next episode.