Brian (1s):
Coming up on the GET, LEAN Eat, Clean Podcast.
Jay (3s):
I think a lot of people listening are probably on board with the idea that the omega sixes are a problem because they're unstable. They lead oxidative damage. They do have some metabolites that are problematic and drive inflammation. The damaged omega sixes are implicated in, you know, plaque, in coronary artery disease and in pretty much every degenerative state you see these damaged fats and everything about the omega sixes. That's problematic. Also applies to the omega threes, but it's even worse for the omega threes because they have more double bonds, so they're even less stable, meaning that their susceptibility to damage is higher and the other metabolic problems or issues in the mitochondria are even more exaggerated with omega threes
Brian (41s):
This week, I interviewed pro metabolic health coach and podcast host of Energy Balance Podcast Jay Feldman We discussed Issues with Omega threes, Best Sources to Cook With advantages of eating meat versus chicken or pork. The True Cause of Weight Gain best carbs to add to your diet and much, much more. Really enjoyed my interview with Jay. I know you will too. Thanks so much for listening and enjoy the show. Alright, Welcome to the Get Lean Eat Clean podcast. My name is Brian Gryn and for the fifth time I've Jay Feldman on. Yeah, thanks for
Jay (1m 14s):
Having me again, Brian, happy to be here.
Brian (1m 16s):
Yeah, great to have you on. I've had you on by yourself some solos and then we've been on with Dr. Dom d Augustino a couple times, but always great to bring you back and anything new coming up with you down the pipeline? Nothing
Jay (1m 31s):
Too major. I mean always, you know, new podcasts in the queue and everything and some of the things we'll talk about today will be kind of previews of, of a few episodes coming out on insulin resistance. And I know we'll be talking about omega threes two. We just did a, a short series on that. So yeah, that's some of the main things right now. Yeah.
Brian (1m 48s):
And if you haven't already, check out his podcast Energy Balance Podcast. And that's with you and Mike Fave, right?
Jay (1m 55s):
Yeah.
Brian (1m 56s):
Excellent. And how did you meet Mike? I was, I was, I've always wondered that. Yeah,
Jay (2m 0s):
Yeah, Mike and I met in college kind of serendipitously and both had, you know, a keen interest in health and so, you know, we became friends and, and did a lot of research and and learning together. So
Brian (2m 13s):
Very cool. And yeah, I'm excited to have you on. I, I've, I, I listened to your podcast And, you know, some of the topics are, I don't wanna say controversial, but they're maybe against the mainstream, which you would normally hear from the mainstream. And you did a series on omega threes, so I thought it'd be cool to bring you on and we can sort of dive into that because I mean, you hear like r Dr. Rhonda Patrick and I've had Dr. Bill Harris on my podcast who has a company called Omega Quaint. And, you know, they do Omega-3 testing and And, you know, there's quite a bit of research done that he's been doing for 30 plus years. I would love to get him on with you. I don't know if that'll ever work, but I figured, you know, let's dive into omega threes a little bit 'cause it is sort of a mixed message out there and, and I wanted to, to just, you know, fill people in on that.
Brian (3m 3s):
So
Jay (3m 4s):
Yeah, and that series that we did was partially sparked by some disagreements that I've, you know, had on podcasts with people about omega threes and one of those was with Don de Gustino on, on your podcast not too long ago. you know, we ended up talking about omega threes and one of the things he pointed out was some of those Bill Harris studies on the Omega-3 content in the phospholipids or the red blood cells and associations with mortality. And so a lot of that series is kind of picking that apart and explaining why, just because that relationship is there doesn't mean we should be consuming more omega threes And, you know, digging into the number of confounding variables there. So
Brian (3m 43s):
Yeah, because I mean if you listen back to my interview with Dr. Bill Harris, he talks a lot about reduced inflammation. Would you say And what we'll get into a little bit more, I know you brought up, you're gonna bring up some studies and things like that, but are there obviously some benefits to consuming omega threes or did you find through your research that it really is just inconsequential?
Jay (4m 3s):
So what I would say is essentially they might be less harmful than other things, but I wouldn't say that there's really any benefit long-term or in a way that I would want to create a benefit. They can have a short term or create a short term reduction in inflammation, but I would say the way through which they do that comes at a cost and is not an ideal way to lower inflammation So, we could talk about that, but that, that I think is the only kind of benefit you can maybe point to or, you know, increases in, in certain antioxidant defense systems. But as maybe we'll get into, that's only because they're creating damage only because they're, they're causing oxidative stress and causing, you know, increasing oxidative damage.
Jay (4m 43s):
And so I would say most, mostly the benefits are not actually benefits. And, and when it comes to looking at omega threes in the membranes, interestingly, one of the things that that can signify is a lack of oxidative stress. So you have this chicken or the egg situation where is adding the omega threes helpful or is the fact that we see the omega threes actually a product of a lack of inflammation or a lack of oxidative stress? And I would say it's more of the latter. And that's because in states where we see increases in oxidative stress, the omega threes and the membranes get damaged and then get removed. So that's one of the confounding variables here where if you were to just look at the Omega-3 content in the membrane, that can just be a sign of a lack of overall infl inflammation and oxidative stress as opposed to something that's actually being driven by the omega threes or Omega-3 consumption.
Brian (5m 33s):
Got it, okay. Yeah, because like I was rec recently listening to Rhonda Patrick talk about like marine Omega-3 fatty acids and how they can may, might be able to lower cancer and cardiovascular disease risk. I'm curious to know, like obviously you can find a study for anything, right? And it's like a lot of times people don't, don't necessarily dive deep into studies, they'll just sort of read the outer layer and be like, oh, okay, that'll, that works for Omega. But like that's one thing I, I like listening to your podcast is you definitely dive into studies perhaps if you wanna share a few with with us, if you're watching on YouTube, share a screen and show us a few that sort of has led you down this path of, you know, your opinion regarding omega threes.
Jay (6m 15s):
Sure. And and to preface that, what I would say is a lot of, I think a lot of people listening are probably on board with the idea that the omega sixes are a problem because they're unstable, they lead oxidative damage, they do have some metabolites that are, that are problematic and drive inflammation. The damaged omega sixes are implicated in, you know, plaque in coronary artery disease and in pretty much every degenerative state you see these damaged fats and the everything about the omega sixes that's problematic also applies to the omega threes. But it's even worse for the omega threes because they have more double bonds. So they're even less stable, meaning that their susceptibility to damage is higher and their, the other metabolic problems or issues in the mitochondria are even more exaggerated with omega threes.
Jay (7m 1s):
And part of what we'll get to, and i, I think it'll, it'll be something that's in this study is actually what they find is replacing linoleic acid in the phospholipids with DHA is worse actually leads to worse outcomes because the omega threes are much more unsaturated in this case, DHA has, I wanna say maybe four more double bonds, it's about eight times as susceptible to damage versus linoleic acid. So that's one one kind of big picture thing to consider some other considerations before bringing up the study is just that we have on one hand this the susceptibility to damage, but we also have this incorporation into the structure of the mitochondria of all the cells and the phospholipids.
Jay (7m 42s):
And that's something we've kind of been touching on. you know, when we eat the omega threes, there will be some increased deposition in, in the actual cellular structure. Now there's a huge problem with that and that's encapsulated in what's called the membrane pacemaker theory of aging, which is essentially something that points out that when we have more polyunsaturated fats, more unsaturation in the membranes of the mitochondria specifically it leads to increased peroxidation, increased oxidative stress, it leads to much less efficient energy production because these fats are very unstable and therefore they're permeable to different ions kind of passing through in a way that we don't want. So just as you know, just to again to a minute detail, when it comes to how our mitochondria actually produce energy, it's, it essentially depends on creating a charge by moving protons which are positively charged to one side of, of the mitochondria.
Jay (8m 36s):
And then it kinda works like a battery it uses that charge to then produce a TP. And when we have more unsaturated fats in the membrane, we essentially have a leaky layer there that allows for those protons to leak back through. And so it leads to much less capacity for energy production for a TP production. In addition to that, there's other aspects of the cell that then essentially become leaky to ions like sodium and potassium, which then requires energy to bring those ions back to where they're supposed to be. you know, we wanna keep the sodium out and bring the potassium in and that requires a TP. And so those couple of things coupled with the increased oxidation or susceptibility to peroxidation has is so dramatically impactful that this membrane pacemaker theory of aging basically suggests that this is the number one determinant of lifespan among all species or between all species.
Jay (9m 29s):
So the main reason why we live longer than a rat or that a pigeon lives longer than a rat is due to the amount of unsaturated fats in these membranes. And this is then also corroborated when we look within a species, when we look among all the rats, the ones with the least unsaturation are gonna live the longest essentially. And also not only just the like lifespan but also health span and and degeneration and all of that is, is implicated here. So that's kind of the big picture or like kind of the preview that I think will be really helpful and when we pull up the study it'll be supporting that and also showing what happens when we add in omega threes as a, as a supplement. And when
Brian (10m 7s):
You touch on omega threes, are you talking about simply just the supplementation of it or are you, or are you also referring to just, you know, like having salmon and and things like that that are higher in in that? Yeah, yeah.
Jay (10m 19s):
So it doesn't make much of a difference, right? The, the Omega-3 content of our food is going to directly increase the omega threes that are available to be put into the phospholipids. And the difference, one thing that was, that's sometimes brought up is you know that different forms of omega threes are less or more susceptible to damage. And that's true when we're talking about something outside the body. But by the time it gets digested and then absorbed, those differences don't really matter anymore. And even with the omega threes in, in the quote most stable forms in something like cod liver oil, we find that even just digestion alone leads to peroxidation of the fats, even if it was perfectly stable and unoxidized before we consumed it.
Jay (11m 3s):
If we then consume it, it gets oxidized just in the di in the digestive tract, not even considering that then we absorb it then it's, you know, continually exposed to 98.6 degrees of body temperature. It's used in the mitochondria where there's lots of oxygen and free radicals flowing around. A lot of, you know, it's a very reactive environment And, you know, we, we can try to protect the omega threes that we're consuming by putting 'em in dark amber bottles and keeping 'em in the fridge. But we're putting them into a very reactive environment once we consume them. And so what, when we look at, you know, supplementation of omega threes with antioxidants looking at pharmaceutical grade fish oil and then the downstream effects and humans and athletes and and healthy humans, we see increased lipid peroxidation and the antioxidants or consuming omega or sorry, consuming vitamin E alongside it is not enough to fully combat this.
Jay (11m 53s):
and we still see elevated levels of lipid peroxidation. So the short of it is, is regardless of the source, this effect seems to happen.
Brian (12m 2s):
Interesting. And are there studies, I know you, you we're gonna pull up some in a second here. Are there studies done on humans for this or is most of the stuff that you found is done on the rats or animals or?
Jay (12m 13s):
There's a lot of studies showing that the consumption of omega threes in humans in different forms, very, you know, optimal forms, again pharmaceutical grade fish oil or cow liver oil, you know, with antioxidants in healthy humans still leads to elevated, considerably elevated lipid oxidation. What we don't have in humans is lifelong studies of humans fed higher or lower amounts of omega threes and then seeing the impact on different conditions or on lifespan or mortality or things like that. And that's because we just, it's not feasible to do that in studies, you know, that just doesn't exist. So when we're trying to look at that sort of effect, we have to look at animals and we want to consider that when we're looking at animals, sometimes there are differences in physiology that are important and mean that we can't extrapolate certain outcomes to humans.
Jay (13m 2s):
But that's not the case here. There's nothing here to suggest, at least that we know of that when we're looking at all these different animals, and this again applies regardless of which animal we're looking at, but also again in humans like we see all of the same mechanisms occur in humans. We just, there's no way to test this sort of outcome because we can only give humans omega threes for so many years and then look at some outcome and of course whatever outcome is gonna be affected not only by what they did those couple of years, but what happened the 50 years prior in their lifetime. So, so those sorts of studies just don't, like can't exist in humans yet.
Brian (13m 33s):
And maybe just for the audience to understand, 'cause I know you talk with terminology and sometimes people don't always understand everything you're saying but like lipid peroxidation maybe explain that and why that could be harmful.
Jay (13m 44s):
Yeah, so it's essentially
Brian (13m 47s):
The
Jay (13m 47s):
Lipids are just fats and oxidation is essentially just damage. We're talking about fats that are getting damaged. we can think about this if we put, you know some, if we put some fat in the pan and the pan is too hot and it starts to turn brown, we've got oxidation there, we've got damage to the fat. And that's essentially what we're concerned about happening internally in our digestive system, in our blood. But also especially in the mitochondria which are the powerhouses of the cell, it's where we produce energy. It's a very reactive situation. You can think of it like a nuclear reactor, like there's a lot going on in a very controlled manner, but if you put something that's really flammable or very vulnerable into that sort of reactive organelle, it's, it's dangerous.
Jay (14m 28s):
And that's essentially what we're seeing. So lipid peroxidation is the damage to a fat and we see a lot with the unsaturated fats, the polyunsaturated fats, whereas the monounsaturated and saturated fats are incredibly stable, hundreds of times more stable than the unsaturated fats.
Brian (14m 44s):
Yeah. And that's part of the reason why you talk about like cooking in perhaps like coconut oil or would you say butter? What would you say the best, best things to maybe cook in? 'cause that's where that can come into play out quite a bit, right?
Jay (14m 59s):
Yeah, I mean my general recommendations would be coconut oil, butter and beef tallow or you know, other tallow is probably the best sources. GH works as well. And, you know, somebody for whatever reason doesn't like those. Sometimes olive oil or avocado oil are okay but I prefer not to cook with those 'cause they still have about 10% of their fats as pufa, as polyunsaturated fats. But you know, if you're cooking at a super high temperature, we would want to use GH over butter. Right? Butter can burn at very high temperatures. So we want to consider something like that but as long as it's not burning those would be the fats I would favor.
Brian (15m 34s):
Okay, got it. Yeah, when you mentioned that it can turn brown, my wife makes these brown butter cookies and you have to, you have to actually have to burn the butter and it so it turns for, for the cookies and she doesn't make 'em a lot so I'm not eating but they're unbelievable. So, but yeah,
Jay (15m 52s):
And again like that's not the worst thing. We're much more concerned about that happening internally on a consistent basis. you know, I'm the, even then, even like the butter that's that's burning there, I'm pretty sure the burnt parts are more like some of the proteins getting damaged and some of the lactose in there. I'm sure there's some of the fat, but you know, GH is the exact same fat as the butter. So the only difference in stabilization there is just due to the, you know, purifying the butter or purifying the fat and separating it out from the protein and and sugar components. So I think those are the ones that are actually more getting damaged anyway.
Brian (16m 27s):
Okay. Did you wanna share your screen and and just touch on the study that, that you sent over? Yeah,
Jay (16m 33s):
Yeah, sure. So this is a study titled membrane fatty Acid unsaturation protection against oxidative Stress and Maximum lifespan Homeo Viscous Longevity adaptation and a lot of words there. But it's, it's, we're just gonna go through a few of the figures and, and kind of keep it simple, but there's a kind of broad quote here that I think is a good starting place where they state aging is a progressive and universal process originating endogenously that manifests during post mat maturation, life available comparative evidence supporting the mitochondrial free radical theory of aging consistently indicates that two basic molecular traits are associated with the rate of aging and thus with the maximum lifespan, the presence of low rates of mitochondrial oxygen, radical production and low degrees of fatty acid, unsaturation of cellular membranes and post mitotic tissues of long-lived homeo themic vertebrates in relation to those of short-lived ones.
Brian (17m 28s):
That's quite the sentence right there. Yeah,
Jay (17m 30s):
Yeah. But to, to simplify it 'cause it's, it's using a lot of like, you know, complex wording but it's, it's actually a pretty simple concept which is just that it's basically saying there are, there are two main drivers of aging and lifespan. One is how much reactive oxygen species are produced in the mitochondria and the other is the amount of unsaturation in the cellular membranes and the mitochondrial membranes And. what I would say is even then, and this has been I think more clearly identified is since the unsaturation of the membranes is such a large determining factor of the oxygen radical production, you could really just isolate it to just that as the main driver of, of aging and lifespan between species.
Jay (18m 14s):
Of course if you took the same species and they had the same saturation index and then one had a lot more oxidative stress and one had a lot less, the one with more would age faster and have more degeneration. So
Brian (18m 25s):
Right. So pretty much membrane, membrane fatty acid, unsaturated unsaturation is detrimental. Right. And and you're more prone to oxidative stress. Right, right, exactly. Yeah. And you're saying that consuming Omega-3, since they're so unstable, you're more prone to getting this unsaturation and being exposed to and being guess harmed from oxidative stress, is that correct?
Jay (18m 52s):
Right, right. And the omega threes are the unsaturation, right. When we consume those, they get inserted into the membranes and increase the unsaturation there and, and yeah and, and as I was saying, there's the oxidative stress component component and also the major differences or impacts on energy production where when we have more of these unsaturated fatty acids, it really reduces the efficiency of how well we produce energy and that's huge. It makes a really massive effect as well as the oxidation.
Brian (19m 18s):
Why do you think there's such a, you know like, like when we talked to Dr. Dino and he talked and he he he referred to those, have you looked at those studies that have shown the, to help that if you have a higher Omega-3 index that you, you know, your lifespan will increase, you know, like these anti-aging benefits regarding omega threes. Why is there such a discrepancy when you see, you know, that study compared to the other studies? Yeah,
Jay (19m 46s):
Yeah, so that's what I was kind of touching on in the beginning. There's, there's a number of confounding variables. Two of the most important. So one is the oxidative stress and inflammation component. If we're more inflamed in dealing with more oxidative stress, it damages the omega threes and then they get removed from the membranes. They get removed from the phospholipids. So if you look at two people and one has more omega threes in the phospholipids and one is less, that might have absolutely nothing to do with how many they consume. But rather the fact that the ones that have less have been under more inflammation and more oxidative stress and knowing that that's a driver of aging, it's a driver of degeneration. That alone can account for why it looks better. Like why the ones who have more omega threes live longer, it's not because they consume more omega threes, it's because they've been under less oxidative stress, less inflammation.
Jay (20m 32s):
So that's one confounding variable. Another huge one is omega six intake. So there's competition between omega sixes and omega threes in terms of the amount we consume and then how much gets incorporated into these phospholipids. And so we can consume very low amounts of omega threes and just change the omega six content of our diet and that will dramatically affect the Omega-3 content of the membranes or of the phospholipids. So there's an example in the messiah, which is a, you know, a native population that consumes extremely low omega threes, I wanna say it's like 0.15% of their diet and they also consume low amounts of omega sixes. It's not as low as it could be, but it's still very low, especially compared to the standard American diet.
Jay (21m 15s):
So I wanna say about 9% of their fat is from omega sixes. And what's
Brian (21m 21s):
Their diet, what's the Maasai diet like? Is that in that a lot of potatoes and things like that?
Jay (21m 25s):
No, they're, they're mostly relying on, on milk So. they do a lot of milk and some meat and, and some, some carbohydrates as well from, you know, like honey and things like that. But Okay. Largely milk based actually. And, and that might not be what their diet always was historically. They, I believe have been moved from there where they used to kind of live and some diet has changed over time. I, I might be conflating a little bit with the hanza who I know they d they are not as milk based, but I know that they were moved from their like ori you know, originally where they were. So anyway, it's, yeah, that's, that's a butchering of general messai diet, but at least largely milk based and, and meat as well.
Jay (22m 5s):
So
Brian (22m 5s):
That either way they, they are, they're very low in omega threes but also low in omega sixes.
Jay (22m 12s):
Right. And so what they find is that they have a relatively high amount of omega threes in their membrane and in their phospholipids of the red blood cells of their mitochondria just because their omega six intake is relatively low. So even though they still have a high omega six to Omega-3 ratio, their total amount of omega six consumption is very low, at least compared to, you know, western population. And that alone leads to a pretty large increase in the amount of omega threes in the, that are incorporated into the structure. So that leads to this other really clear confounding variable, which is that if we just eat less omega sixes, and this could be, you know, someone who's just on a low-fat diet, they're gonna eat less omega sixes or someone who's trying to avoid, you know, processed foods and fried foods that's gonna lower omega sixes.
Jay (22m 58s):
Those are probably some of the main sources in, in western diet. If you're just doing those things, you'll see higher amounts of omega threes in the membranes and in the phospholipids. Even if there's no increase or no what
Brian (23m 10s):
Someone said, what if, I'm sorry, what if someone said they want to eat, still eat their processed foods in their and their fried foods, but then they'll just supplement with omega threes and then, you know, that'll counteract that ratio And, you know,
Jay (23m 22s):
Well and it, and it might, but what it, but what we're more getting at is that when if, 'cause those original studies are just saying cure people with more omega threes in their, you know, in their red blood cells in the fossil lipids, here are people with less, the ones with more live longer So, we should then consume omega threes And. what I'm pointing out here is A, the ones who have more could just be doing that because they're generally healthier, they have less inflammation and less, less oxidative stress could be totally independent of diet. And then the other piece is they could just be eating much less omega sixes. They could still be consuming nearly no omega threes and they do these studies where they, where they take someone on a western diet and just lower their omega six intake and don't change the Omega-3 intake at all and they see the Omega-3 intake or the Omega-3 content of the cellular structure of these membranes with phospholipids increase.
Jay (24m 8s):
And so you can have that sort of population that I would say okay, they're definitely gonna be healthier, much less pufa, much less, less omega six and yet they didn't increase the omega threes at all. It had nothing to do with Omega-3 consumption. But you'll see that they're gonna live longer because they're generally healthier. So when you have confounding variables like that, I think it makes it really tough to say we have more omega people who have more omega threes in the structure of their cells live longer So, we should eat more omega threes. I think you could just as well say people who have more omega threes in their cellular structure live longer So, we should minimize oxidative stress and inflammation and we should reduce omega six intake as those could be more of drivers there than omega threes.
Brian (24m 46s):
Okay. So I, I see what you're saying. I see what you're saying. Yeah. 'cause I mean I I I don't know historically how much money is spent supplementation wise, but I would imagine that omega threes is probably one more the, the most money spent on, you know, as far as supplementation is concerned.
Jay (25m 5s):
Yeah, I think it's the third one of the studies that, that we cite in our Omega-3 series says that it's the third most, like third most purchased or like third most common supplement Yeah. In the US So yeah, it's, it's a huge industry for sure.
Brian (25m 20s):
And you would say obviously not necessary just focus on lowering your pofa con your pofa consumption which will lower your omega sixes. Yeah. Okay. Yeah. Main culprits, fried foods, that's probably the big one. Processed foods, you know, probably anything that, most things that have a label, there's probably some form of it.
Jay (25m 39s):
Yeah. And I think the, you know, a lot of people were told to cook with vegetable oils so that, you know, that that's another source I think in, in the healthy leaning population and people who are already trying to be healthy. The, the fried foods And, you know, cooking with vegetable oils is less common but in that case we can still have large sources of omega sixes from nuts and seeds and fatty chicken and fatty pork. The chicken and pork, it really depends on what they're consuming. So if they're consuming a lot of omega sixes, their fat will contain a lot of omega sixes. So that can be another large source for, for people. And I think those ones are talked about less relative to like the seed oils and yeah.
Jay (26m 20s):
And I would definitely consider those as well, especially if you've already cut out the seed oils, but we're still doing a lot of nuts and seeds, which are where those oils come from. Or we're eating a lot of fatty pork or fatty chicken that is not well raised or is raised eating a lot of those omega sixes. Those are huge sources of omega six and pofa overall.
Brian (26m 38s):
Yeah. Do you have not, I'm not saying that for this maybe on our next episode, but like as far as chicken is concerned, 'cause it's such a chicken is consumed so, so like it's so abundant especially in the states as, and it's quote unquote a healthy food, but obviously it can be very high in omega sixes and PUFAs. What, have you seen any studies or anything around how chicken can be, you know, might be, might not be healthy necessarily as, as people think?
Jay (27m 5s):
No, I haven't, I haven't really looked for it either.
Brian (27m 9s):
I'd be, yeah, I'd just be curious. Yeah, I mean we know that like chickens and and pigs, their digestive system is a lot different than, than the way like cattle are, right? They they, they, when they consume something it goes straight to their, their fat membrane, is that correct?
Jay (27m 24s):
Yeah, like us, right? Yeah. So cows have these massive digestive systems, they have four stomachs, essentially a ton of bacteria and they So they can convert unsaturated fats to saturated fats and they do. So even if cattle are fed all their fat is still gonna be almost all saturated and monounsaturated. But for us or chickens and pigs, if we consume pufa it's gonna really change the composition of our fat and everything and that's not good.
Brian (27m 49s):
Yeah, I'd just be curious to know like if you take, have someone that is a lean healthy individual versus someone who is overweight And, you know, let's just say obese, like what are their pofa levels And, what are the differences between the two of them? Yeah. Be we should come up with a pofa index, we should make a three index, we should come up with a pofa index. Yeah,
Jay (28m 10s):
Yeah, definitely. Right? Definitely. And like comparing that to, to the mono and, and saturated fats and I think they do do that with some of these fatty acid tests as well.
Brian (28m 19s):
So okay, we've hit on that. Let's get a little bit into, and you've talked about it with Mike on your podcast 'cause this is a big another sort of, I think maybe big con, big misconception is that weight gain is not caused by excess energy. you know, a lot of times people will just be like, well this individual's overweight because he's probably just been in an excess of calories over the last 20 years and it's just added up over time. Now there might be a little bit of truth behind that, right? I don't think it's a, a black and white thing, but I'm just curious to know your thoughts around that and, and I know you and Mike have talked about it.
Jay (28m 54s):
Yeah, so I have a couple of of issues with the notion that if we're gaining weight we're just eating too much and the solution is to eat less or to burn more by exercising more or maybe cold baths and things like that. So yeah, I think that that's really not good advice. I don't think it's actually getting at what is causing the issue. Even if you wanted to say it was calorie excess, the re there's physiological reasons why we would eat beyond what we would need and those are not solved by just saying eat less. 'cause then we're just hungry And, you know, forcing, forcing ourselves to lose weight using, you know, willpower and I don't think that A works well and BII think it comes at a cost and we'll kind of dig into that cost, but also I think it's totally ignoring what would lead to overeating in the first place.
Jay (29m 40s):
So that's part one. And then part two I think is the idea that excess calories equals weight gain I think is is just missing. It's just missing a lot. There's so many steps between those two things that I think it's really not, I just think it's entirely inaccurate for a number of reasons. So for one even, I mean to step back the idea that we could calculate to the calorie how much we burn in a day and how much we consume in a day is just, we're just kidding ourselves. If you want to go into a metabolic ward, sure you can identify exactly how many calories you might burn and that specific day with that specific activity, that specific amount of sleep you had the night before, that specific amount of light, all of those things in that particular instance.
Jay (30m 27s):
But most people aren't doing that. And all of those other factors I mentioned will affect what we expand and, and how many calories, you know, we're, we're running through so to speak. But then on the other side, the idea that we can actually accurately to the calorie estimate, not only our intake but how many calories get absorbed is just incredibly farfetched. So there are a number of studies looking at, you know, the the calorie count of certain foods and we look at the label and it says the number of calories and then they actually measure it and there's always several percentage points off at least if not like 30% sometimes. and we don't rec like we we, we pretend like that doesn't exist. Like these are exact measures and they're really not.
Jay (31m 9s):
There's one study think on almonds that was showing like a huge percentage difference. And it's not only with that and then you also have the factor of digestion and absorption. So not only does the composition of the food matter, how much fiber are we eating it with other foods, is it on an empty stomach? All of that will affect how much we absorb. But also our digestive state, how well are we breaking down the food? Is do we have a lot of bacteria that are also competing for the food? And all of those things affect how many calories actually get absorbed from what gets taken in. So to act as though, you know, we can measure that we ate an extra 50 calories every day And, you know, after a month that was 4,500 calories so now we've gained a pound and a half or, or you know, just under in terms of body fat is just not, it's just irrelevant.
Jay (31m 56s):
It's so far from what we could ever actually account for.
Brian (31m 60s):
Do you think there's any benefit, 'cause I've had, I mean you hear like a lot of individuals for example like Lane Norton is a big like calories and calories out guy. And do you think there's any benefit to tracking your calories at least initially?
Jay (32m 14s):
Yeah, so I'm not trying to say this is a worthless measure, let's throw it out at the moment. It's the best measure we have for getting a general idea of the potential energy in food. And that doesn't mean of course that 20 calories of protein equal 20 calories of fat or anything else. Like we can't equate things based on calories, but we can get a general idea of around how much we're eating and it makes more sense to use calories than weight, right? To say that we ate three pounds of food one day doesn't really help us 'cause we have to include water weight and there's also a difference in density of potential energy from fat versus carbs and things like that. So calories are the best estimate we have, but we just don't want to treat it as though it is a, a perfectly accurate measure or b, a perfectly applicable measure.
Jay (32m 58s):
But if we want to get an idea of our eating more now than we were before or less calories are gonna be our best option, you know, and same thing with estimating our, our expenditure. If we wanna get a general idea of how our metabolic rate is changing, calories are our best option for that.
Brian (33m 12s):
Yeah. What are other ways to understand our metabolic rate? I know a lot of times with, you know, rate Dr. Ray Pete talked about it was body temperature and things like that. What are other ways to understand our metabolic rate?
Jay (33m 26s):
Yeah, so body temperature and pulse rate are both good indicators of our metabolic status. If those are low, you know, if our, if our temperature instead of hitting 98.6 in the afternoon is getting to 97.6, that's a pretty clear sign of a low metabolic state, low low metabolism, low metabolic rate. And just to be clear, that doesn't necessarily mean we would see a difference in terms of our calorie expenditure, but rather where that calor, where those calories are coming from or how they're being expended so we can be under more stress and have a low basal metabolic rate but have higher stress hormones that are kind of making up the difference. But you know, those can be generally good measures and you can use how you feel as well. Do you have a lot of energy?
Jay (34m 6s):
Are your hands and feet cold? Do you feel cold? How, you know, do we have brain fog? Those kinds of things can give us an indication as well. we can look at blood work too if we wanted to, you know, get a thyroid lab, the panel tho those things can give us some information. But yeah, the also, again, speaking of estimations, looking at our calorie intake now versus before is another great way to do it. Are we eating 500 calories more and maintaining our weight? If so, that's a pretty good sign that we've increased our metabolic rate. And something I know you mentioned and your journey of bringing carbs in and, and eating a bit more and kind of reducing the time restricted eating and all of that is, you know, you're able to eat more now and maintain your body weight. So
Brian (34m 46s):
Yeah. Yeah, that was something I added in and was mainly doing about two meals a day. I added in a third meal, just felt like I couldn't get enough cons, wasn't consuming enough for my, you know, sort of activity level. And no, it's been good. I think initially I might've put on a little bit of weight, but then it sort of just like flattened out and got back to pretty much what I was before, which was a good sign. Yeah, so, so I think the, the point is that the calories and calories model is just too sim it's just too much of a simplified model to look at things, right? There could be so many other variables that could affect weight gain, whether it's, you know, maybe you're like, if, would you say if someone's not getting results and every day they eat chicken, would you say that that could be a variable that's affecting, you know, their, their weight loss journey?
Jay (35m 33s):
You you're saying because of the the pu of content?
Brian (35m 35s):
Yeah, yeah, yeah.
Jay (35m 36s):
And And, what I will say an important piece there is if you're eating chicken breast, there's very little fat in there and so there won't be much pufa. Okay. So that won't matter. But if you're eating a lot of chicken thighs or legs or you're making a broth and consuming all the fat with it, that would be a, a large source of pufa. Yeah. Okay.
Brian (35m 52s):
So calories don't equal energy. Perhaps dive a little bit into that. I know you've talked with Mike about that and a lot of times people think that that's just like a one-to-one relationship.
Jay (36m 2s):
Yeah. And so that's the biggest, you know, to me, elephant in the room that we didn't get to yet is there's all these issues with estimating calories in and calories out and all of that. But the biggest issue that I have with this calories and calories out equals change in weight or change in mass equation is that it's completely ignoring the fact that calories don't equate to energy. And this is, it is so universally like ingrained that people will say those as if they're the same things. People will say energy balance when they're just talking about calories and in and calories out, they'll talk about calories in as energy in. But there's a huge problem there, which is there are a lot of things that have to happen for us to go from a calorie quote unquote in a food into a TP, into energy.
Jay (36m 47s):
The food has to be taken in, has to be broken down through digestion and then has to be absorbed, then has to be taken to some issue tissue where it's going to be converted to energy. And then we have to actually go through that conversion process which requires, you know, in the case of carbohydrates, we have to go through glycolysis and then the kreb cycle and then the electron transport chain with fat. We go through beta oxidation and then kreb cycle and electron transport chain. And there's a lot of areas for those things to go wrong. And so in this paper that, you know, I'll share a quote from in a moment, what they basically point out is that in people who are gaining weight or who are obese or dealing with this kind of issue, they actually aren't converting the food that's coming in those calories, so to speak into energy very effectively.
Jay (37m 32s):
There's various blockages and they point out a certain enzyme in the kreb cycle, but there's a ton of other places that we can have blockages in terms of other enzymes in the electron eng enzymes in the TCA cycle and the kreb cycle enzymes in glycolysis in complex of the electron transport chain. There's all these places where there can be inhibition due to a nutrient deficiency due to oxidative stress, due to endotoxin, due to po. And those are gonna reduce how efficiently we can convert the fuel coming in into energy to convert the potential energy into actual usable energy in a TP. And when that happens, we then have excess fuel and that fuel then gets directed to be stored.
Jay (38m 12s):
That's another way of saying we have a low metabolism because we're not converting the fuel well to energy So. we have a lack of energy and at the same time we're converting excess amounts of the fuel or the substrate into body fat. And this is exactly what they describe in this study. And it's the exact opposite of what we're told, right? We're told that obesity, or if you're gaining weight, this is a state of excess energy and you have excess A TP and then there's a spillover because we don't need more a TP So, we just keep converting all the extra substrate to fat. But what's really happening is we have a lack of a TP and we're not able to effectively convert the fuel to energy to a TP. So then there's leftover fuel and it gets converted to fat So. we have low energy and fat gain at the exact same time.
Jay (38m 53s):
And. what that does is the low energy directly impacts our hunger signals. So in the liver and in the hypothalamus of the brain, these are basically our two sensors of our energy state and determinants of our hunger. And so if we have a lack of a TP in those places, we're then going to continue to have hunger signals, even though we're storing fuel as fat because we have a lack of energy and that energy is essential, that's how our bodies function. We need that a TP. So then you have the state where sure, then there's overeating, then there's even more fat storage, but the overeating isn't the problem. That's a product that's an effect of issues with energy production, of inhibition, of energy production. And so that's, I would say that is the, the clear like illustration of what's actually going on in someone who's gaining body fat and eating less and exercising more just makes that worse.
Jay (39m 41s):
It just leads to less energy. And over time actually makes it even worse in terms of converting that fuel into energy and then storing even more body fat. And we'll go through another study very briefly on that too.
Brian (39m 53s):
Yeah, let's, let's pull that up. That was well said. I mean, I think a lot of people think that, oh, well you're, you're overweight so you're just consuming too much. But there's, it's much more complicated than that right there, there, there that food is not converting into energy and a TP as efficiently as someone that is, you know, metabolically healthy.
Jay (40m 12s):
Yeah, yeah, exactly. Exactly. Yeah. So to share the quote that this is a paper titled Decreased Energy Levels can Cause and Sustain Obesity, and it's a great paper to, to look through, but just kind of in their, their summary, they state, we begin with the contradictory information that in obesity more calories are consumed than used up suggesting that obese people should have excess energy. On the other side, obese people experience fatigue and decreased physical endurance that indicates diminished energy supply in the body. The result of our work is a chain of metabolic events leading to obesity. The crucial event is the inhibition of the TCA cycle at the step of aconitase. It disturbs energy metabolism and results in a TP deficiency with simultaneous fat accumulation.
Jay (40m 55s):
Further steps in obesity development are the consequences of diminished energy supply. And this, this would be inhibition of beta oxidation, leptin resistance, increase in appetite and food intake and a decrease in physical activity. Thus our theory shows that obesity does not have to be caused by overeating and sedentary lifestyle, but may be the result of the obese change in metabolism, which is forcing people to overeat and save energy to sustain metabolic function functions of cells. This obese change is caused by environmental factors that activate chronic low grade inflammatory process in the body linking obesity with the environment of developed countries. So, they kind of laid out exactly what what we just described and they really focus on this inhibition of aase, a particular enzyme of the TCA cycle.
Jay (41m 42s):
But there's a number of different places that respiration, that mitochondrial energy production can be inhibited and they basically point out that that is the driver and then something like overeating is happening as a result of that. And this is, this is essentially the obesity state is a low energy state.
Brian (41m 60s):
Very interesting. Yeah, so, so overeating is the result of not being your body, not being able to metabolize that food in a correct manner. So that's, what would you say are reasons or some of the main reasons why sort of this process could be, I guess screwed up or, or not efficient and resulting in overeating?
Jay (42m 24s):
Yeah, and, and just to add in also So, they mentioned So, they mentioned that the overeating is a consequence, a consequence of low energy supply and they also mentioned that leptin resistance fits in there as well. And this is something that's so often focused on is that, you know, if we're obese, if we're overeating, it's an issue of leptin resistance. What they point out in this paper is that leptin resistance is just an effect of a lack of a TP because that the lack of a TP is more important. you know, if, if a cell, or let's say the whole liver has a lack of energy, but is getting the signal leptin saying stop eating that the lack of energy overrides that signal is so much more important to our physiology. So leptin resistance isn't actually kinda like insulin resistance isn't actually about, you know, excessive production of leptin and the cells just stop responding to it because they've gotten tired of responding.
Jay (43m 12s):
But rather it's because there's something more important going on, which is a lack of energy and that trumps the leptin signal. But yeah, so you're, you know, the question of what kinds of things cause this lack of energy, what kinds of things diminish the a TB supply? What kinds of things interfere with mitochondrial respiration? We touched on one of the biggest, which is the polyunsaturated fats. And so reducing those in favor of mono and saturated fats, I would say is key. That's probably universally, if we're just looking at the human population, right? Now, I think that's probably the biggest one. And second one, which is I would say probably the next biggest one would be the production of, of toxic byproducts from bacteria in the intestine.
Jay (43m 53s):
And so normally this is considered, or these toxic, these toxins are called endotoxin, which often refers to lipopolysaccharide, which is a component of bacterial cell walls and it's also just produced by the bacteria. But endotoxin can also be a broader term to incorporate or, or refer to other toxic things produced by bacteria or fungi. And these are implicated in obesity, in diabetes, in heart disease. We see this endotoxin component. And if we look at the effects of endotoxin on, or just specifically lip polysaccharide on mitochondrial respiration, we see inhibition along the electron transport chain And. what that means is that this main site for producing a TP, we're getting blocked by this liberal polysaccharide produced from the gut.
Jay (44m 40s):
If we're, if we have overgrowths of bacteria or we're not digesting our food well and it's excessively feeding bacteria, those kinds of things will lead to excess endotoxin, which will interfere with our ability to produce energy. And that also causes a cascade of oxidative stress and inflammation increases nitric oxide. And that's, those things are focused on, in this paper where they talk about how excess nitric oxide and reactive nitrogen species and inflammation and oxidative stress will inhibit enzymes like tase nitric oxide will also directly inhibit cytochrome c oxidase, which is complex for the electron transport chain. And when those things happen, you get this backup where we're not converting the field energy and we begin to shunt it toward fat storage.
Jay (45m 21s):
So those would be two of the biggest ones. We also have things like nutrient deficiencies, chronic stress, you know, heavy metals if we're exposed to large amounts of heavy metals or something like that. I mean, there's pretty much anything that affects us negatively does so through the effects on, on our capacity for energy production.
Brian (45m 40s):
Yeah, and I, you know, chronic stress is a, is a, is a big one I think for a lot of people by an individual come up to me and he's felt like he's been doing the right things, but he's not getting where he wants to go And, you know, then we started getting into stress and, and that was sort of like the big, that was sort of the big red flag I think is that excess stress. And I know you, I know, and then Dr. Ray, Pete talks talked a lot about, like, when you talk about stress, I think a lot of people talk think about like envi environmental factors and outside factors or just daily things that you're doing. But what, what other ways could people be causing stress on their bodies? Yeah, so
Jay (46m 19s):
There are all of the psychological factors. And, you know, a lack of sleep, which can increase our susceptibility to stress and affect our hormonal state stress from, from our jobs, you know, financial stress and time stress and, and all of those things. I mean that's without a doubt a huge component here and we don't want to ignore that. And that will contribute to all these things, like to this dysfunction, to this impairment in, in energy production. But we also wanna consider physiological stresses or stressors. And that'll be things like, for one, I mean the absence of carbs or calories, so low carb or lower calorie diets or even low fat, particularly low fat diets. All of those can cause a stress response because we don't have the fuel that we need and the areas that we need it.
Jay (47m 1s):
And essentially it's another way of causing low energy just due to a lack of fuel. And, and that'll create stress, which will then further impair our ability to convert fuel to energy. But we also have, I mean, various things that we could consume in our food like pollutants, And, you know, plasticizers and pesticides and things like that that'll contribute in a physiological way and also impair our capacity for energy production. We have excess exercise as basically causing a very similar effect to a low calorie diet. And that sort of excess chronic stress will, will create the same effect and we can do it a number of other ways, right? we can do it through a combination of cold baths and fasting and whatever else.
Jay (47m 42s):
And those are all intense stressors as well, causing the same physiologically stressful processes.
Brian (47m 48s):
Got it. Yeah. And so the, the, the main two things that are causing this sort of, I'd say lack of energy or lack of a TP is PUFAs and this endotoxin accumulation. Those are like the two big ones, would you say? Yeah.
Jay (48m 4s):
Yeah. And I think those are always the best starting places.
Brian (48m 7s):
Starting places. And the, and the last thing I wanted to touch on is you, and you mentioned it during our last interview, was that you said, and we can get into detail, so I just wanted to bring it up this time, is that fat burning is, is a, is a state for diabetics because you hear a lot of times people are like, well, you want to get into a fat burning state, but this might not necessarily be advantageous for people. And maybe explain to that what what you mean by that? Yeah,
Jay (48m 35s):
So there is this notion that insulin resistance and diabetes are characterized by a lack of fat burning. But what we, what we really find is that what's going on in terms of energy production is there's impairments in glucose oxidation. So the glucose is being converted through glycolysis to lactate and which doesn't produce a lot of energy and at the same time the mitochondrial burning fats. And so we're essentially in, and this, this by the way, happens anytime we're under stress, is we start to shift to that sort of metabolic state, the state of glycolysis alongside fat oxidation. We see it, you know, if you were to like induce any short-term stress, like going for a run or something like that, we also see it in, in any version of chronic stress.
Jay (49m 23s):
And we'll, you know, kind of provide some examples here. Not only of insulin resistance but also, you know, cardiovascular disease and fatty liver disease that the same metabolic state is seen. You also see it in cancer as well, And, you know, there's this focus in cancer on the fact that the cancer cells are using the glucose and converting it to lactate, which is true, again, that's a sign of a very deranged metabolism. It's not a a carbohydrate problem, it's a metabolism problem, but you also have cancer cells using fatty acids and of, and amino acids and things like that too. So I, I think it's been oversimplified much like the insulin resistant state, which again, I would characterize just like those other stress processes of a state of elevated fat oxidation, elevated fat release in, in lipolysis and very poor glucose oxidation.
Jay (50m 9s):
And so this idea that we need to fix our ability to burn fat and we need to become metabolically flexible is, I would say entirely misplaced on, like the focus is entirely misplaced. And instead we wanna focus on correcting our capacity for burning glucose efficiently as a fuel, as opposed to trying to burn more fat, which is actually already happening in these scenarios. And we can say, alright, in insulin resistance we're burning more fat and we're not burning glucose well, so let's avoid glucose. And you can do that and avoid the problem, you know, your glucose levels will come down, your insulin will come down. But we're not actually fixing the capacity for using the glucose, we're just kind of running on these backup pathways, which we were already running on. We were already using the fat as the fuel and we're just kind of avoiding the problem by taking out the glucose.
Jay (50m 52s):
Yeah. And did you wanna share any, anything regarding that? Okay, sure. Yeah. And there's, so again, this will be maybe a bit of a preview. We'll be going through insulin resistance in a few episodes, the Energy, Balance Podcast, and digging into all of it in, in a bit more detail. But here's kind of like some overview quotes in, in terms of some of these things that I've mentioned. So when it comes to insulin resistance, there's a paper title, insulin Growth Hormone and Sport. And they say that even under conditions of extreme ketoacidosis, there's no significant membrane barrier to glucose uptake. The block occurs lower down in the metabolic pathway where the excess of ketones competitively blocks the metabolites of glucose entering the kreb cycle.
Jay (51m 32s):
This is basically just talking about how insulin resistance is not a insulin signaling problem, which is a very related conversation, but a a little tangential, but then they state under these conditions, glucose is freely transported into the cell, but the pathway of metabolism is effectively blocked at the entry point to the kreb cycle by the excess of metabolites arising from fat and protein breakdown. As a result of this competitive block, at the entry point to the kreb cycle, intracellular glucose metabolites increase damning back throughout the glycolytic pathway leading to accumulation of free intracellular glucose and inhibiting initial glucose phosphorylation. And then they talk about, I'll just finish it out here, at least in the last sentence, where they say, thus, under conditions of ketoacidosis, glucose metabolism, but not glucose uptake is impaired as a direct consequence of the metabolism of fat.
Jay (52m 21s):
And they refer to the glucose fatty acid cycle, which is now known as the Randall Cycle. And again, we'll this is something that there's a lot more to unpack here, but just as far as a broad, big picture kind of idea, we're seeing in diabetes and insulin resistance, a situation where the glucose metabolism is impaired and fatty acid, as a result, fatty acid oxidation is favored, kind of like we were talking about earlier. If there's a lack of energy, we need to force the upregulation of of that and we'll do it through fat. and we see the exact same thing play out in, in fatty liver disease and in cardiovascular disease. And so I'll just share those quotes really quickly, where the first one, they state lipid oxidation products in the pathogenesis of non-alcoholic Sato hepatitis.
Jay (53m 6s):
This is in fatty liver disease, that's the title of the paper. And they state in non-alcoholic fatty liver disease, both lipid oxidation and the TCA cycle are enhanced, suggesting that hepatocytes try to counter excess lipid by increasing oxidation. The higher production of reducing equivalence by lipid oxidation causes an overflow of electrons throughout the mitochondrial respiratory chain, resulting in higher free radical degeneration. This may lead in turn to mitochondrial dysfunction with consequent progression of liver pathology. So they're essentially saying that fatty liver disease is the state of excess lipids, which also involves excess fatty acid oxidation. We also see excess lipolysis in this state, and that this is actually something that further drives the pathology by increasing reactive oxygen species production and increasing oxidative stress there and, and furthering it along.
Jay (53m 54s):
And we see the exact same thing in in cardiovascular disease. And so this is a paper titled Mitochondrial Fatty Acid Oxidation, alterations in heart failure, ischemic Heart Disease, and Diabetic Cardiomyopathy. And they state that in many forms of heart disease, including heart failure, ischemic heart disease, and diabetic cardiomyopathies changes in cardiac mitochondrial energy metabolism contribute to contractile dysfunction and to a decrease in cardiac efficiency. Specific metabolic changes include a relative increase in cardiac fatty acid oxidation rates, and in uncoupling of glycolysis from glucose oxidation in heart failure. Overall, mitochondrial oxidative metabolism can be impaired while an ischemic heart disease energy production is impaired due to a limited limitation of oxygen supply.
Jay (54m 36s):
In both of these conditions, residual mitochondrial fatty acid oxidation dominates over mitochondrial glucose oxidation in diabetes, the ratio of cardiac fatty acid oxidation to glucose oxidation also increases, although primarily due to an increase in fatty acid oxidation and an inhibition of glucose oxidation. And then this last part, which I think is still wor is, is worth mentioning. They then state recent evidence suggests that therapeutically regulating cardiac energy metabolism by reducing fatty acid oxidation and or increasing glucose oxidation can improve cardiac function of the ischemic heart, the failing heart, and in diabetic cardiomyopathies. Hmm. So what they're saying here is, is really notable.
Jay (55m 17s):
One, we see impaired glucose oxidation in the heart. In these situations we see reliance and excess reliance on fatty acid oxidation. And you also see this uncoupling of glycolysis from glucose oxidation. So we're running the glucose through glycolysis, we're producing lactate, but we're not going through the Creb cycle. We're not going to the electron transport chain. And then the other thing is, if you either increase glucose oxidation, you increase glucose burning, or you reduce fat burning, that actually improves cardiac function. It actually helps to reverse the state. So it's also saying that this is actually causative here is the increase in fat burning is actually part of the driving pathology here. And the lack of glucose burning is also driving the pathology here. So if somebody is suggesting, you know, you're insulin resistant or dealing with cardiovascular disease or fatty liver, you should be shifting away from the carbs because those, you know, you're not using them well, which isn't even said really.
Jay (56m 7s):
They just say carbs are the problem, so you should be using fat. Well, in doing so, you're actually driving that pathology further by a, avoiding the problem, which is problems with glucose oxidation, but also just inherently increasing fatty acid oxidation further in this case, you know, impairs cardiac function in the case of fatty liver drives further inflammation and oxidative stress driving the pathology and insulin resistance, same thing. So, so yeah, it's, it's the exact opposite of really what we should be doing. And something that I, I think is, is still pervasive and will continue to pervade for quite a while, that, you know, fat burning is the solution when really it's part of the problem.
Brian (56m 45s):
Interesting. Yeah. And, what would you say, so would you say that like having more of a, like a balanced diet is like ideal for most people as opposed to just cutting out a macronutrient? Yeah.
Jay (56m 57s):
Yeah. I think we have needs for both fat and carbs. I'm not saying go on a very low fat diet, I don't think we should ignore the cost of that or the cost of a low carb diet. So I, I would say we need both. The amount can vary. And if we're insulin resistance and overweight, we already have a lot of fat circulating So, we might not need as much, you know, maybe we only need to get 20 to 25% of our fat intake of our calorie intake from fats in a case like that. But as someone who's not in that case, you know, 30, 35, 40% of fat of calories from fat can be totally fine. And, you know, kind of on the carb side as well, you know, 40%, 50% depending on the, on the situation. And again, the, the, the, the thing that people commonly say is, you know, this makes sense if you're already insulin sensitive and you're active, but if you're not, if you're insulin resistant, that's when you need to reduce the carbs and you need to favor the fat.
Jay (57m 49s):
That's, we just described that actually contributes to the pathology. And again, a little sneak peek of some of those episodes that'll be on my podcast is that there's these studies where they increase carbohydrate intake in people who are insulin resistant or who have type two diabetes, and it helps to reverse the insulin resistance. It helps to increase insulin sensitivity because part of the driving pathology is the fat burning itself. It's not the only part. Right. We talked about endotoxin, we talked about pufa. There's a number of, there are a number of other factors. But, it is part of the thing driving it. And again, that doesn't mean we want zero fat, we never want to burn any fat But. it just means we don't want to be only burning fat, especially in the tissues that need to be burning carbs for optimal function.
Brian (58m 29s):
And, and if you're gonna have 20, 25% of your diet being fat, mainly the saturated fats obviously, right?
Jay (58m 36s):
Yeah. Saturated and monounsaturated. Yeah.
Brian (58m 38s):
And monounsaturated. So the things that you're cooking in, or obviously you're gonna get fats, the halt fats from eating, you know, meat and things like that. Yeah.
Jay (58m 47s):
Okay. Yeah. Meat, dairy, if we eat, digest the dairy, well, you know, it's always a, a caveat, you know, and, and there's certain, you know, we kind of mentioned nuts and seeds before. There's a couple that are very low in pufa, like macadamia nuts and coconut. So those are fine sources as well. So
Brian (59m 3s):
What about peanut butter and
Jay (59m 4s):
Cocoa? Like chocolate?
Brian (59m 5s):
What about peanut butter? Yeah,
Jay (59m 6s):
Peanut butter is, is,
Brian (59m 8s):
It's not even a nut, but Right. A legume peanuts on a legume. Right. But yeah, they're, are they high in pufa?
Jay (59m 14s):
Yeah, very high. There is one variety of high oleic peanuts that are actually very, very low in pufa. They're hard to find tiger nuts. Many products made with them. What's
Brian (59m 25s):
That? Tiger Nuts.
Jay (59m 26s):
I've never heard of tiger nuts or like, I, I don't know what their fat composition is, but yeah. Yeah, the vast majority of peanuts and, and peanut butters and al nut butters, you know, almond butter, walnuts, all that will be, will be very high in poof. But again, macadamia nut is an exception. Coconut's an exception. Hazelnuts are kind of, okay, they're not ideal, but not as bad as some of the others. So
Brian (59m 47s):
I just love peanut butter. I got away from it for a while, I've gotten back, but you know, it, it, it's like my one little vice. I, you know, I, you know, I guess we could have one vice here or there, right? Yeah.
Jay (59m 58s):
And I would maybe try to source one of the high oleic peanut butter options instead. So,
Brian (1h 0m 4s):
Okay. Do you have any vices, Jay? Not, not if you, if you were gonna cheat on,
Jay (1h 0m 9s):
I mean, so for me personally, when I was low carb, when I was fasting, when I was doing cyclical keto, I felt the need to cheat, right? I, I would, and it would, it would be, I mean, I would normally, in terms of commitment and willpower, like I was pretty strong, you know, like it was very rare, right? That, that, you know, I would ever really kind of make an exception. But over time, especially as I started getting into these ideas that carbs maybe weren't so bad, I started to allow myself to, to quote, cheat a little bit. And at that point, you know, and even prior to that, on low calorie diets, like at, you know, 'cause I would just try to eat less calories to get leaner, and I would definitely, you know, binge like really, really binge, you know, finish off a whole thing of brownies or, you know, sleeves of Oreos or, or
Brian (1h 0m 57s):
Chocolate,
Jay (1h 0m 58s):
Like bags of chocolate chips or something. Like, I could do that pretty easily. But when, when it was, you know, keto low carb, I would, you know, sometimes we would make, I, I mentioned, you know, Mike and I met in college, so around this time, you know, we would kind of give each other excuses to, to eat some of these things. So sometimes it started out with like pounds of, of berries, you know, frozen berries and just eating 'em outta the bag. But sometimes we would do, you know, coconut flour cookies or things like that.
Brian (1h 1m 22s):
This is when you were low carb, you're talking about?
Jay (1h 1m 24s):
Yeah, yeah.
Brian (1h 1m 25s):
That, that would be what you would splurge on. I mean now, now you're eating, what would you say, like when you people, we talk about carbs and getting 40 to 50% of your diet from that potentially, would you say mainly that's fruit, honey, and, and like maybe just like sweet potato or things like that?
Jay (1h 1m 42s):
Yeah. Well, and so that's what I was kind of going to get at is at the moment I don't, I don't really feel a need to diverge from what I eat, like I did at the time. Like I don't feel, I don't feel that, and if I do, it's, you know, it's like I'll have a couple bites of something, but the hunger signals are just like perfectly in line with what I'm eating. It's not like I could, I could never eat. Now what I did eat then, like I couldn't binge, like I eat more on a daily basis, but I couldn't binge like I did at that point. I mean, I would, you know, I don't know, like at some of those all you can eat steakhouses, you know, like Brazilian steakhouses, like I would eat till I was sick and I couldn't do that Now, like I just don't have the capacity for it. But because the hunger singles I think are much better regulated, whereas before, you know, it's like you can eat way past when you're full because the hunger singles are just chronic.
Jay (1h 2m 29s):
But you are asking about carb sources. So for me, you know, fruits, dried fruits, fruit juices, honey, maple syrup, those are primary sources. But I do a decent amount of starch as well. So,
Brian (1h 2m 42s):
Yeah. And I was just gonna, sorry to interrupt you, but starch is so like white, white potato, sweet potato. And when typically I'll have them, I'll cook them in coconut oil.
Jay (1h 2m 53s):
Yeah, yeah, that's perfect. And I'll do some plantains and white rice as well. Okay. Yeah. And those are, I think in people who struggle with weight gain, the starches are things I'd be more cautious about. But I know for me, especially with how my metabolism is currently, I need to have those that just due to food source availability and everything, it's just, it would be too hard to get enough without, without some starch sources.
Brian (1h 3m 17s):
Yeah. And I, what I will say, I know, you know, as far as satiety is concerned, I know white potato is fairly, it's fairly s satiating food, you know, which is good, I think a, a positive thing. I mean, I know it's not the end all, but Yeah, well,
Jay (1h 3m 31s):
I think when we're low carb, we lose sight of, of how many carbs are in things. and we think that you eat a bit of fruit and you've, like, you're on a high carb diet now, right. And I think people don't realize, like get, it's not easy when you're coming from low carb to eat 200 grams of carbs in a day. And that's still low, like low maybe digging in a moderate, but like, you know, low is really like 150 grams or lower in most cases. So we're just getting past that and it's like a lot of people struggle with it, and I don't think you would just wanna jump into 300 grams of carbs if you're eating 20, but I think people get surprised also, it's not easy to eat 200 grams of carbs from potatoes, like you're saying, or, you know, or fruits or
Brian (1h 4m 9s):
Blueberries, I mean, right. Like
Jay (1h 4m 11s):
Yeah. I mean there's impossible.
Brian (1h 4m 12s):
Yeah. Right.
Jay (1h 4m 13s):
Yeah. And, and it's funny how, you know, we think like we eat a banana, it's like we're now on a high carb diet and bananas are dense, right? They're dense as far as fruits go. But yeah, it takes a lot of carbs to, to fuel yourself. So,
Brian (1h 4m 27s):
Yeah. Well this was good, Jay, I think we hit on some, some good topics here. Omega threes, we got into weight gain and, and fat burning calories and calories out. Is there anything else you want to add before we sort of sum it up?
Jay (1h 4m 39s):
No, I mean, not too much. I think with each of those topics, those are things I've, I've dug into in more detail and articles on my website and podcast episodes. So I would refer people to those if they're hungry for more and they're kind of, you know, interest is peaked. I certainly don't subscribe to the idea that, you know, I shared one study, so now we should all be fully convinced and change everything we're doing. Like if you're eating omega threes and you've been listening to all these other people supporting their usage, it's okay to be skeptical. It's a good thing. I'm not expecting that you then walk away from this and And, you know, throw out everything, you know, throw all the, the omega threes and the garbage. But I would say hopefully it ped the ped your curiosity enough to dig in a little further and maybe we'll get to that point.
Jay (1h 5m 19s):
So that would be my suggestion. The other thing I'll mention as well is, you know, we were talking about fat sources and carb sources, And, you know, the concerns with fatty chicken and pork. And I have a food guide and energy balanced food guide that kind of lays that all out very nicely in a one page infographic. And so you can get an idea of which foods are optimal from that standpoint and the, you know, which foods are gonna be highest pufa. And it also has a separate scale. So, we talked about endotoxin and digestion, and it has an a separate scale to consider if we're dealing with some digestive issues. you know, we might wanna be more careful about certain foods than others, whereas if we don't have digestive issues, they might be totally fine. So I have two different scales on there.
Jay (1h 6m 0s):
One's like a general metabolic energy balance type scale, and the other's more digestion focused. So it, it can be really helpful resource for listeners. And if they'd like to for download that, they can head over to Jay Feldman wellness.com/guide.
Brian (1h 6m 16s):
Excellent. Yeah, and I'll definitely put that in the show notes and I'll include other studies that we cited today that, you know, if you weren't watching on YouTube, that if you want, you wanted to look up and, and read 'em yourself. 'cause like you said, this is not about necessarily like saying this is all the end all, but, you know, do your own research. And this is just, you know, this is one perspective and obviously you, you hear there's a lot out there. So I think everyone has to sort of do their own due diligence and, and come up with their own conclusions.
Jay (1h 6m 40s):
Definitely. I think it's so important to, to take that authority back and, and not subscribe to some, you know, figure or author authoritarian source that says something And, you know, anything that goes against that is now, you know, conflicting with like our, ourselves And, you know? Anyway, so yeah, I, I totally agree with that. And, and I think we want to take that authority back and And, you know, take learning and, and research back into our own hands as well. And so that's what I try to do with my podcasts and articles and resources, is give people those tools and And, you know, point them in, in directions to help make that process a bit easier.
Brian (1h 7m 18s):
All, right, Jay? Well, right, right On that note, my dogs are barking, so thanks for coming on again. I love it. Appreciate it. And Jay Feldman wellness.com. Have a great rest of the day and thanks for coming on.
Jay (1h 7m 30s):
Cool. And thanks for having me, Brian. I appreciate it.
Brian (1h 7m 31s):
Thanks for listening to the Get, Lean Eat Clean Podcast. I understand there are millions of other podcasts out there, and you've chosen to listen to mine, and I appreciate that. Check out the show notes at Brian Gryn dot com for everything that was mentioned in this episode. Feel, feel free to subscribe to the podcast and share it with a friend or family member that's looking to get their body back to what it once was. Thanks again, and have a great day.
