Ep. 107: Omega-3s DECREASE Lifespan and INCREASE Disease?

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In this episode we discuss:

  • Studies showing that omega-3 consumption decreases lifespan and increases disease processes 
  • The potentially harmful effects of omega-3 usage during pregnancy on offspring
  • The impact of omega-3s on inflammation, endotoxin, and mitochondrial respiration
  • The data in native cultures showing that omega-3 intake doesn’t improve cardiovascular disease or mortality
  • Extremely healthy populations that consume high-carb and high-saturated fat diets with almost no omega-3s

1:30 – studies showing that omega-3 consumption decreases lifespan and increases disease processes in animals

13:55 – studies on animals showing the harmful effects of omega-3 consumption during pregnancy on offspring 

 17:37 – studies showing that omega-3 consumption contributes to disease processes, increases inflammation, causes oxidative stress, increases endotoxin, and interferes with mitochondrial respiration 

28:19 – whether we should be concerned about saturated fats increasing endotoxin absorption 

29:33 – how omega-3 consumption leaves us more susceptible to damage when we’re under stress 

32:53 – whether we should be consuming fatty fish 

35:01 – the lack of benefit of omega-3 consumption in native populations consuming large amounts of fatty fish and seafood 

38:40 – low incidence of cardiovascular disease in native populations consuming very little omega-3s 

59:30 – concluding thoughts on whether we should consume omega-3s based on the data on omega-3s in RBCs and phospholipids and mortality 

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Jay Feldman  0:05  
Could omega threes actually decreased lifespan and increased disease. We'll be answering that question in today's episode, Episode 107 of the energy balanced podcast, a Podcast where we explore health and nutrition from the bioenergetic view, and teach you how to maximize your cellular energy to maximize your health. Today's episode is part three of our three part series, exploring the relationship between omega threes, mortality and lifespan. And in today's episode, we'll be going over the studies showing that omega three consumption decreases lifespan and increases disease processes. We'll also be going over the potentially harmful effects of Omega three usage during pregnancy on offspring, as well as the impact of omega threes on inflammation, endotoxin and mitochondrial respiration. We'll also be going over the data in native cultures showing that omega three intake does not improve cardiovascular disease, or mortality. And we'll be going over the extremely healthy populations that consume high carb and high saturated fat diets with almost no omega threes. To check out the studies and articles and anything else that we referenced throughout today's episode, head over to Jay Feldman wellness.com/podcast where you can find the show notes. And with that, let's get started.

Moving on to some research that I find exciting, which is looking at omega three consumption and supplementation in animals and the effects on lifespan and the effects on disease. So this is a situation where we can test very clearly what happens throughout the entire lifespan of an animal. With an intervention like this, we can't do this with humans, you can't have a human that, essentially from birth is given omega threes. And then you see what happens 80 years later with this huge cohort. But you can do this very easily in animals and you can see the effects on lifespan, you can see the effects on different disease processes. And we'll dig into the research showing it it's it's exciting stuff. Just

Mike  2:11  
to caveat before you start J there are there is a cohort of people that is currently taking omega threes from birth all the way until perhaps their entire lifespan currently, I just want to say between formula feeding and then supplemental omega threes for children in their milk. While they grew up, you know, the DHEA, fortified milk and whatnot that is currently happening despite the inconclusive nature of the research.

Jay Feldman  2:39  
That's true. And despite the you know, research, you know, the conflicting research research specifically on infants and infant outcomes and things like that. The other thing worth mentioning, too, I know you're saying this somewhat facetiously. Of course, there's not like a trial there. But we will be looking at populations that have very high omega three and taking this as not in the context of formula feeding and adding supplements to food but rather getting their omega threes directly from fully natural whole foods like fish and whales, blubber and things like that seals being the Inuits and Eskimos and we'll we'll come to that later. And it actually does also doesn't support that even consuming the Omega threes from the right sources in large amounts is a good idea. So but anyway, going back to this animal research, we'll go through a handful of studies here. The first one is titled dietary supplementation with low Vasa and krill oil shortens the lifespan of long lived F one mice and the LAHSA for reference is a pharmaceutical grade fish oil. So you know top quality here and then also krill oil as well which is sometimes suggested over fish oil because it has antioxidant capacity with the ESTA Xanthan. Yeah, exactly so so they state here they conclude that marine oil is rich in Omega three polyunsaturated fatty acids has been recommended as a preventative treatment for patients at risk for cardiovascular disease or diseases. These oils are also are the third most consumed dietary supplement in the USA. However evidence for their health benefits is equivocal. Individually Lavasa and krill oil non significantly shortened to meet median lifespan by 9.8 and 4.7% respectively. Lavasa increased the number of enlarge seminal vesicles 7.1 fold, Lavasa and krill oil significantly increased lung tumors 4.1 and 8.2 fold and hemorrhagic die thesis 3.9 and 3.1 fold taken together the results do not support the idea that the consumption of isolated omega three fatty acid rich oils will increase the lifespan or health of initially healthy individuals. So yeah, I don't know what what more to add we're seeing increased you know various diseases potentially reduced fertility or male fertility with those and large chemical vesicles. seminal vesicles are seeing a significantly well non significant but a large effect size was not significant but Large effects as as far as the short and medium lifespan of 9.8 and 4.7%. So, I mean, these are some pretty clear findings, and we'll go through some more clear ones suggesting that supplementing with pharmaceutical, pharmaceutical grade fish oil, or krill oil for a lifetime is probably not a great idea.

Mike  5:21  
Yeah, and you know, just some minor bleeding and cancer along the way. Nothing, nothing too serious. Nothing too serious. I'm making a making jokes about it. But I want to make this doesn't mean that people are going to necessarily get cancer and bleed out from fish oil. But just the basically what you're seeing is you're not if fish oil was so beneficiary not seeing the benefit with wall species of long lived Formula One driving mice. Right,

Jay Feldman  5:52  
right. Yeah, exactly. Do you want to go through the next one, Mike?

Mike  5:56  
Yep.

So the title of this one is long term intake of fish oil increases oxidative stress, and decreases lifespan in citizens accelerated mice. So just the caveat before we jump in are kind of like an explanation before we jump in the previous set of mice lived like generally lived a long time. And this set of mice has a proclivity to not live a long time they have it sent a sense, which is basically like, the cells move into a state of non replication and kind of like this, like limbo state, which is usually sorted associated with shorter lifespan. So these mice don't live as long. So we're gonna see the effects of fish oil, and these mice in the title already kind of gave it away. But

Jay Feldman  6:39  
what the Reese, it's our sorry, Mike, I think that it looks like they're more prone to like they experience cognitive decline, and Alzheimer's type affects younger. I don't know if they actually don't live as long. I think it's more just that they experienced

Mike  6:55  
the effects of the chronic diseases. Yeah, yeah.

Jay Feldman  6:59  
Yeah, it looks like it so they can study those sorts of things in a little bit more detail. I'm not 100% sure on that. It's, it doesn't matter too much. But

Mike  7:08  
yeah, either way, you have a set of mice that were their cells move into citizens quicker. So basically, like, but much less metabolically active cells that aren't replicating anymore. And it's usually the senesin cells are associated with chronic disease states, not a good thing. So the researchers start here, and they say the SAM eight mice. So these are the citizens accelerated mice. That's what I assume the SEM is stands for. Fed fish oil did not have a longer maximum lifespan and had a shorter average average lifespan than mice flit fed safflower oil. So there we go. Again, the safflower oil and the corn oil are outperforming. To examine the mechanism underlying these results, the effects on oxidative stress of long term ingestion of fish oil were examined. Sam P. Eight mice fed fish oil for 28 weeks showed strong oxidative stress that causes hyper oxidation of membrane phospholipids and a diminished antioxidant defense system due to a decrease in tocopherol compared with mice fed safflower oil. These findings suggests that the in that intake of fish oil increases oxidative stress, decreases cellular function and causes organ dysfunction and Sam Sam for Sam P eight mice, thereby promoting aging and shortening the lifespan of the mice. So I mean, the oxidative stress here is likely because the fish oil is has much more double bonds present in the fat. So we kind of already covered this specific piece, especially compared to the safflower oil, even though the safflower oil should tacking the increase more of the highly inflammatory mediators. But essentially, and these are mechanisms that we already covered previously. But the the increase oxidative or peroxidative stresses these fats inside the membrane phosphorus. So inside the actual structure, the cell membrane of the cells basically destroyed the antioxidant defense system depleted Vitamin E tocopherol. And then decrease the lifespan and the cellular function and increase organ dysfunction for these mice. So essentially, the way I kind of view this is if you build your house out of really crappy materials, then the cells or the house will not function very well. And they will have a much shorter lifespan, you're gonna have to get your roof repaired probably in five years instead of 30. And so basically, that's kind of what you're seeing with these rats and with the when you incorporate these highly unsaturated fats into the tissues. In the form of the for this was in the form of fish oil.

Jay Feldman  9:40  
Yeah, yeah, exactly. We're basically seeing the exact mechanisms played out that we were looking at earlier in those studies that were showing increases in pro oxidation being associated with shorter lifespan, increased oxidized ability index being associated with shorter lifespan across species. And they had then tested it they gave those rats fish oil, saw increased oxidative stress and said well probably is going to decrease lifespan. And here we see exactly that. And again, we're not comparing fish oil to olive oil to coconut oil to something that's very stable. We're comparing it to safflower oil, which are which is very high in Omega six is also very prone to poor oxidation, but just not quite as prone as fish oil. And you see hyper oxidation of membrane fossil lipids diminished antioxidant systems, as well as shorter average lifespan compared to safflower oil. So pretty clear demonstration here of exactly what we would anticipate to be the effects of fish oil.

Mike  10:32  
Yeah, and it follows the trends that we kind of already discussed with proxy digestibility index previously, where the more double bonds and more unsaturated the fats are, the more proximity of stress you induce. And then the more problems you essentially have, especially within the cell membranes in the cellular structure. The other thing I want to point out here, just slightly tangentially, but a lot of people Oh, well, there's all these studies that show that fish oil decreases oxidative stress. And what I want to mention here is that fish oil, at least from the mechanisms that I've gone through is decreasing oxidative stress by creating per oxidized fatty acid mediators, and then triggering hormetic pathways or basically triggering cell defense pathways to clean up the mess. And so the question becomes, okay, maybe inducing the a different antioxidant enzymes, glutathione, peroxidase, superoxide, dismutase, catalase, etc, perhaps that will decrease oxidative stress for a period of time. And, but it's in doing it because you already have the peroxidation from the beginning. And then the further problem is, is that sustainable long term? Can you run a marathon continuously? And what I mean by that is, can you put a stressor on the system on the body or on the cell over an extended period of time? And to get this? Suppose it out this suppose the outcome again, and this kind of goes into some of the hormetic arguments that we discussed previously. But I just wanted to put that in into perspective there, because it's the antioxidation you're seeing is not because the Omega threes are specifically antioxidants. It's because they're creating lipid peroxidase lipid peroxidation products that are triggering cell defense, which is a completely different mechanism than increasing your vitamin E or vitamin C content.

Jay Feldman  12:28  
Yeah, yeah. And we saw that earlier in one of those studies, I believe it was one on salmon. But yeah, and we've talked extensively about Hermes is, of course, I'll be linking back to those episodes. But yeah, to say that that's a good thing, I think is like to say that it's beneficial to, you know, increase antioxidant defenses by causing oxidative stress is not something we would agree with. And, you know, we go through all the reasoning for that in those in that series. So I'll definitely link back to that. So moving on to the next paper here. It's titled excess omega three fatty acid consumption by mothers during pregnancy and lactation causes shorter lifespan and abnormal ADRs in older adult offspring. So the first quote, here, they stayed the excess offspring. And this is excess, meaning excess fatty acid consumption. And then when they say control, it's normal amount of NES of omega threes, and a deficient is deficient in omega threes. So these are the three groups that they're comparing. So they stay the excess offspring, excess Omega three offspring had shorter lifespans compared to their control and deficient cohorts. And this is 506 days on average for the Xs 601. For the control and 585 are deficient, which is a difference between the access and control of 16%, I believe, about 15 16%. So a huge difference in lifespan between those two groups. When the study terminated on postnatal day 640, the excess offspring had a higher incidence of presbycusis, than the control of deficient groups a difference. So it's 33.3% for the excess, and the control is 4.3. And deficient was 4.5%. So we're talking about an eight times difference there about and the persistence of other sensory neurological abnormalities and lower body weights in old adulthood. So that is quite concerning to see the effects of excess amounts of omega threes in offs of offspring. So again, this is looking at what happens when the parent is fed the the mother is fed excess omega threes,

Mike  14:33  
so the prospect causes is age related hearing loss, just for anyone who's on doesn't know the term is a just a medical term. Yeah.

Jay Feldman  14:45  
Yeah. And seeing major major effects here. I mean, huge percentage differences in the lifespan and also in these sorts of disorders, neurological disorders and things.

Mike  14:55  
It's also interesting that the deficient didn't have such decrease compared to control. Like it was right, marginally less, at least on a percentage basis in comparison to the access versus a control.

Jay Feldman  15:09  
Right. Yeah. You're saying in in lifespan? Yes. Yes. Yeah. Yeah. So 601 days for control 585 For deficient, so a little bit less, although not sure if the difference. I don't think the difference between those two is significant, actually. Not 100%. Sure. And then looking at the excess was 506 days. So huge, huge difference there. Yeah. massive difference moving on to the next. What's that? Massive?

Mike  15:37  
It's a massive difference. Yeah,

Jay Feldman  15:39  
yes. So moving on to the next quote here, they state post hoc comparisons indicated that the excess offspring weighed significantly less than their control and deficient cohorts, whereas the control deficient offspring did not differ from each other. So again, now we're saying just at birth weight, or sorry, not birth weight, but the final weight of the offspring, so their general body weight is considerably lower when they have excess amounts of omega threes, which is a sign of major issues with development, that they conclude this aid in conclusion, omega three fatty acid over nutrition or imbalanced during pregnancy and lactation had adverse effects on lifespan and sensory neurological function in older adulthood. The adverse outcomes in the excess offspring were likely due to a nutritional toxicity during fetal and ordinary optimal development, that program to them for lifelong health disorders. The health implications implication is that consuming or administering large amounts of omega three fatty acids during pregnancy and lactation seems inadvisable and advisable because of adverse effects on the offspring. So I don't know if there's too much to that. I want to add they're so clear some what they said and incredibly concerned.

Mike  16:49  
Yeah, I mean, basically, I think the solution here, from my perspective, is that my children are gonna get high omega three formula.

Jay Feldman  16:59  
Exactly. Yeah, yeah. Sounds like a great idea.

Mike  17:04  
Yep. It's that in the Omega three enriched eggs throughout all of the all of their childhood.

Jay Feldman  17:13  
Yeah, yeah. And fish oil and salmon and all that. Yeah, for sure.

Mike  17:17  
Yeah. Fish oil, fish oil, gummies. And everything else? Fish oil?

Jay Feldman  17:25  
Definitely, yeah. So I do want to move on to two studies that are not looking at lifespan, changes in animals, but instead are looking at different disease processes and other effects that you can see in animals that are fed lifelong, high amounts of fish oil versus other fats. And I think this is some evidence that we've talked to her a bit earlier, but some very clear and important things to go through. Do you want to share this first one, Mike? Yeah,

Mike  17:50  
I think these come from the the fatty liver, some of the fatty liver studies we did Correct.

Jay Feldman  17:59  
Yeah, we definitely talked about both of these during the fatty liver episodes. Yeah. Okay. It's clear that omega threes are not the answer, but you may not know what the answer is. If you're looking to optimally support your metabolism, and lose weight, improve your digestion, get amazing sleep, rebalance your hormones, boost your energy and so much more. And that's one of the main goals of the energy balanced solution, a program that's designed to help you accomplish exactly those things with clear action steps and strategies, along with personalized guidance for me. So head over to Jay Feldman wellness.com/solution, where you can find all the information for the energy balanced solution program. This program includes customized health coaching a video library with videos on restoring gut health, losing weight without destroying your metabolism, how to boost your metabolism, how to get amazing restorative sleep, how to rebalance your hormones and tons more. It also includes resources like a sample meal plan and supplement guide, as well as a private community. So head over to Jay Feldman wellness.com/solution to check out all the details.

Mike  19:03  
The first study here is titled gene pathways associated with mitochondrial function, oxidative stress and telomere length are differentially expressed in the liver of rats fed lifelong on Virgin Olive sunflower or fish oils. What they start out here they say this study investigates the effect of lifelong intake of different fat sources rich in mono unsaturated so that's virgin olive oil, and six polyunsaturated so that sunflower oil are n three polyunsaturated fish oil, fatty acids in the age liver version, all olive oil led to the lowest oxidation and ultrastructure or ultra structural alterations. So that's kind of the structure of the liver of the cells, sunflower oil induced fibrosis ultrastructural alterations and high oxidation fish oil intensified oxidation oxidation associated with age, lowered electron transport chain activity and enhanced enhance the relative telomere length According to the results, virgin olive oil might be considered the dietary fat source that best preserves the liver during the aging process. The lipid profile was an analogue that was analyzed in the liver mitochondrial membranes since we have previously demonstrated that this is a good marker of dietary fat intervention at different tissue levels, including liver, brain, heart and skeletal muscle. The lipid profile resembled that of the original composition of oils using the diet with animals fed on Virgin Olive Oil showing the highest percent percentage on oleic acid, those fed on sunflower oil having the highest percentage of linoleic acid and animals fed on fish oil registering the highest percentage in Doxo hexanoic acid, so the linoleic acid is omega six and the doc the COSO. hexanoic acid is omega three. And then oleic acid is a mono unsaturated fatty acid. So olive oil is very high and the oleic acid sunflower oil is very high in linoleic acid. And in fish oils. Obviously, the fat that's very high into cosa, docosahexaenoic acid, otherwise known as DHA. And basically the the liver or the mitochondrial the liver mitochondrial membranes reflected the actual fatty acid composition. Within obviously we talked about there's a particular range, but you could tell which which mouse had which type of fat when looking at the liver mitochondrial membranes because of the change in percentage of these major fatty acids. And essentially, what you're seeing what is the the outcome of these changes, is the virgin olive oil. The rats fed virgin olive oil, they actually did pretty well, overall, they didn't really have a high amount of oxidative stress or oxidative damage. And the actual structure of the cells of the mitochondria of the liver were fine. Whereas the fish that had the sunflower oil, they had fibrosis. So fibrosis is usually damage to the cellular structure, and then a replacement with just flashing this tissue or basically inactive tissue tissue that doesn't really do anything, it's usually indicative of the damage. And then they had higher high levels of oxidation. And then they had the ultrastructural alterations as well. So the cellular structure was not really what it should be, it was a bit damaged. And in the fish oil had probably the worst oxidation, at least implied by what they're saying here. And then interestingly enough, is the electron transport chain activity, the actual flow of electrons in the mitochondria to produce ATP was decreased in the fish oil specifically, they note this here, which is very interesting overall, and but it also makes sense, with the mechanisms that we've discussed previously, we're incorporating fish oil into the membrane actually dissipates the proton gradient, and then leads to issues with production and ATP. So and it also makes the membranes very susceptible to oxidative stress, which you're also seeing here overall. So basically, I guess, if you want to think about this very simply, all while performing the performed the best safflower oil, or sunflower oil perform the second best. And then fish oil performed the worst of these three fatty acids. And basically what you're seeing is a mono unsaturated versus omega six, polyunsaturated versus at omega three polyunsaturated fatty acid.

Jay Feldman  23:20  
Yeah, yeah. And it's demonstrating very clearly a lot of the mechanisms that we had discussed earlier, increased oxidation and the extreme disruption in electron transport chain activity, there was also a major decrease in mitochondrial density in the official group. So definitely not outcomes that we're looking for in any intervention. And pretty clear to see here when you're looking at lifelong consumption of fish oil in these in these animals.

Mike  23:46  
Yeah, and again, it's not to say that this is exactly what happens in humans, because there's a diff, there's a degree of difference, although the cellular structures are indeed, relatively similar to some extent between humans and mice. But the overall picture here is, maybe you have this benefit of fish oil, in what not fish oil, you have this benefit of omega threes with the RBC phospholipids. And so you're thinking, Oh, I'm gonna go take fish oil. But when you start to see information like this, this is a huge pause, at least for me, because you're seeing such a stark, striking negative effect that's in line with some of the other cellular components. And then you're also you're seeing this in animals where you can actually test the effects across the lifespan, and we can't test the effects across the lifespan for humans. So we won't be able to see some of these things play out over the long term in humans, at least in studies. So yeah, this this gives that context for me.

Jay Feldman  24:49  
Right, and even though we didn't see it necessarily lifelong in humans, we did reference quite a few studies showing massive increases in lipid oxidation and oxidative stress issues. with mitochondrial respiration in humans, why an Omega three supplementation was was used as an intervention. So we're seeing the same thing series is not conflicting at all with what we were seeing as far as those effects. Yeah,

Mike  25:13  
so it doesn't conflict with the mechanisms. It doesn't conflict with those effects. You just can't really see the lifes the lifespan changes directly. It's kind of hard to read to parse those out specifically.

Jay Feldman  25:26  
Right? Yeah, definitely, definitely. And there's one more study I want to go through here, again, looking at some effects on the liver as a result of fish oil. And this was also one that we went over in that fatty liver disease series. And this is one of the Mangie papers, he's got a few good ones comparing the effects of different fats, and in terms of alcoholic fatty liver disease that are pretty shows a pretty dramatic effects in terms of protective effects with saturated fats, and extremely negative effects with unsaturated fats, especially fish oil. So this title is the title of this paper is dietary saturated fatty acids, reverse inflammation and fibrotic changes in rat liver, despite continued ethanol administration. And again, this is one of those nanjie papers. And the quote states, we investigated the potential of dietary saturated fatty acids to reverse alcoholic injury, alcoholic liver injury, despite continued administration of alcohol, so they're going to cause a alcoholic liver injury continue feeding ethanol or alcohol and that feed different fats. Rats in group wanted to were fed a fish oil ethanol diet for eight and six weeks respectively. So these ones started with fish oil and alcohol and then continued with it. Rats and groups three and four were fed fish oil on ethanol for six weeks before being switched title caloric diets containing ethanol with palm oil and group three or medium chain triglycerides group four for two weeks. So they were on the same initial diet then switched for just two weeks to palm oil or MCT. As with alcohol instead of fish oil. And then rats in group five were fed fish oil dextrose for eight weeks as kind of a control. The most severe inflammation and fibrosis were detected in groups wanted to as were the highest levels of endotoxin lipid peroxidation activation of NF Kappa Beta and M RNAs for Cox two and TNF alpha. These are the rats that were fed fish oil alcohol the entire time, by the way, just just referenced, they're using officially on alcohol diet to cause fatty liver issues and alcoholic liver injury. intentionally because that is the best like that creates even more dramatically and quicker, then they're switching it after so in groups wanted to that stayed on fish oil and alcohol, that the highest levels of endotoxin, lipid peroxidation. And all sorts of inflammatory mediators NF Kappa Beta TNF alpha, then we're looking at those other groups, the groups that were just switched for two weeks to the other fats. So it says after the rats were switched to palm oil or MCT, there was a market histological improvement with decreased levels of endotoxin and lipid peroxidation absence of NF Kappa Beta activation and reduced expression of TNF alpha and Cox

Mike  28:07  
two, but they were still drinking, they were still drinking out, they were still having

Jay Feldman  28:11  
alcohol. Yes, they were still being alcohol. And it just two weeks of having saturated fats in place of the fish oil, there are these major improvements. And they then conclude that a diet rich in saturated fatty acids effectively reverses alcohol induced necrosis, inflammation and fibrosis. Despite continued alcohol consumption, the therapeutic effects of saturated fatty acids may be explained at least in part by reducing endotoxemia lipid peroxidation, which in turn results in decreased activation of the inflammatory mediators NF Kappa Beta and reduced levels of TNF alpha and Cox two. So that I mean, there's so much meat to these, to these papers to these studies that Andy did. And he, you know, he's done a handful of different studies, you know, in different with different iterations of very similar protocol. But essentially, what you see is fish oils a great way to to enhance any sort of inflammation and oxidative stress. And we've seen, we've seen this at all the mechanistic data, we see it in the animal lifelong data. I mean, it's pretty clear, and it's very clear here and you see a very clear opposing effects from saturated fats. So yeah, I mean, I don't have too much to add here. I do think that one very, very small tangent that I don't want to get off on too much, but we talked about it before, especially in the fatty liver papers, is that there is some suggestion that saturated fats increase endotoxin absorption, and that that's a negative thing, but actually, in practice, they do carry endotoxin in from the intestines to the liver for detoxification. And so in doing so, they actually reduce endotoxemia lipid peroxidation as we saw here, so and they improve the response they reduce the inflammation cascade and oxidative stress cascade, so they should have a very protective effect and I would not at all be concerned about saturated fats, increasing endotoxin absorption or anything like that, which sometimes is was thrown around a bit. But do you have anything to add to this one, Mike? Yeah,

Mike  30:03  
I mean, so there's two major pieces, you already kind of you pretty much covered, the one that I wanted to talk about was that saturated fat caveat, because I get that one a lot. And if anybody's interested, you can go on PubMed. And you can find some studies where prior to inducing endotoxemia, or shock, if they feed the rats, a bunch of cream or something along those lines, that actually protects them from the sepsis, or the endotoxemia. I'll

Jay Feldman  30:29  
link to that study, because we we've referenced that a couple times. Yeah.

Mike  30:32  
And then the next piece I want to talk about here, we kind of covered this, this general idea previously, but inside fatty liver, there's this model, they call it, I think it's the two hit or the multiple hit model, I think that's the correct term for it. But essentially, when you when you load the liver up, or you and this is kind of like an analogy for other tissues, or an example, for other tissues, if you load these tissues up with tons of polyunsaturated fatty acids, and then you add a negative stimulus to those tissues, now you get a very negative outcome, because you have a whole bunch of very readily oxidizable fatty acids, that if you have a stress response, if you're exposed to epinephrine, if you're exposed to cortisol, and you have to ramp up fatty acid oxidation, you have increased RLS. And all your structure is incorporating all these, these different unsaturated fats or highly unsaturated fats will now you're likely to damage those fats inside the membrane. Or if you haven't exposure to endotoxin, or an immune stimulant, or alcohol or anything along those lines, it's basically you have a whole bunch of dynamite laying around and you liked the match. So that's the the moat the to hit, or the multiple hit model from fatty liver, the theory that they look to. And basically what they're talking about that is the conversion of just regular fatty liver to actually like a steatohepatitis, or an inflammatory response of liver. One of the things that determines that is on saturated fat content. But I think that's also an example for other tissues overall. And I think it's an important way or lens to kind of think about what happens when you fill your structure up with a bunch of unsaturated fatty acids. And then you're basically seeing this play out here inside the rat studies. And then the the endotoxin piece is, you know, another tangential piece, but also important or a saturated fat endotoxin piece.

Jay Feldman  32:24  
Yeah, yeah, all great points. And I did want to mention one other of the Nanji studies where one of them he, instead of continuing with alcohol administration, does, you know, takes off the alcohol and then has the different groups where they continue with just fish oil, versus the saturated fats. And in official group, despite not having alcohol, there was minimal improvement, they basically barely improved, despite the alcohol being removed and consuming the fish oil. Whereas when they took away the alcohol, and were fed saturated fats, there was major improvements, of course, even more so than there were here, where the alcohol administration was continued. So again, just shows such a major difference in the effects of these fats. And in the saturated fat groups without the ethanol and that other Nanji study, they were essentially they essentially came their liver healed basically to, you know, the normal. So yeah, I don't have anything else to add here. This was that was all the studies I wanted to mention, as far as the consumption of omega threes in animals and the effects on lifespan and disease. Do you have anything to add before we talk to a couple other points as far as context as far as omega threes go?

Mike  33:35  
I would just say if you're going to have a beer, just have some chocolate with it.

Jay Feldman  33:40  
Yeah, yeah, definitely. It's um, fructose to to help with the alcohol detoxification and everything. I'll link back to points where we talked about that. And, of course, in our fatty liver series, we talked about that quite a bit. Yep. So I did want to, I don't want to go through the studies looking at Fish consumption, specifically versus omega threes, and cardiovascular disease outcomes. There's, you know, just a whole other whole ton of other studies to go through. And again, it's pretty inconclusive, similar to what we had discussed earlier. And we mentioned in that Cochrane review how there was no effect from fish. There's, again, some conflicting reviews there and requires going through all the individual trials and all of that, but I would say largely, they're inconsistent and inconclusive in terms of showing any benefit to fish or fatty fish in terms of mortality or cardiovascular disease. So just worth mentioning here again, the most important point obviously, when it comes to fish consumption, we've got a handful of different variables, but we know with omega threes that omega threes will increase the Omega three content at the phosphor lipids. So if having a higher omega three content of phospholipids was the beneficial component with that was the beneficial thing from Omega three consumption, which is what is being suggested in those original association studies. If that was the case that fish oil would be enough it would be perfectly adequate it to have all of those benefits. And it's not we just went through all those studies looking at fish oil. So if that's the case that we know that it is nowhere near as simple as increasing Omega three content of phospholipids equals reduction in mortality or improved lifespan, especially when done via Omega three consumption. So that would be the the only small thing I wanted to mention there before talking about some real world examples of Omega three consumption or a lack of Omega three consumption. But do you have anything you want to add? First, as far as the consumption of fish goes? I know, we've already mentioned a few things in terms of how there could be other benefits to it. And, for example, there was a trial, which we'll go into where they found that the only benefit was of eating fish was actually due to a reduction in the consumption of like processed meats and things like that, which, again, healthy user bias is huge when it comes to fish consumption, as well. We've mentioned it before, too, in terms of those early trials.

Mike  35:54  
Yeah. Basically, if you're not seeing the benefit with the Omega three supplementation, I think that's probably like the clearest indicator overall. And in the fish, there's many other components there that I would argue there's probably tons of beneficial components to seafood and fish. And the Omega threes aren't really the major driver of that. It's just been how things have been explained. I mean, it's ad nauseam, right? Like every single blog, or every single website has like all the benefits of efficiency and mega threes. It's like thought it couldn't be the protein or the micronutrients or any of these other things. It's probably just these like these highly oxidizable fatty acids that help the fish deal with really cold water temperatures. But yeah, I think, yeah, there's no point of really going into that, as you said, just because we already the main point to Pete piece we're trying to look at as omega three specifically.

Jay Feldman  36:48  
Yeah, yeah. And omega three is in those phospholipids. And we know that omega three supplementation does accomplish that shift. So it does increase the Omega threes in the phospholipid. So yes, yeah. And we've talked about fish enough. But the last really important piece of context and evidence to look into is the amount of Omega three consumption in various native cultures. So we're not talking about Omega three supplementation, we're not talking about Omega three fortified Fishel, Omega three fortified formula feeding or anything like that. We're talking about a, quote, natural diet, and looking at that, and any benefit in terms or lack of benefit in terms of cardiovascular disease and mortality. And so I alluded to this earlier, which is the the first of these being the Eskimos and the Inuit. And what we basically see is that this is a population that has very high omega three consumption from fish and seafood. And yet they don't actually have a lower incidence of heart disease despite this. And there was for a while some thought that they did have very low incidence of heart disease. And it was kind of starting out a bit of a myth, and then it actually turned out not to be true. So this first study is just describing that, that they don't actually have any lower incidence of heart disease. And they the title of this paper is fishing for the origins of the Eskimos at heart disease story, facts or wishful thinking, and they stayed that during the 1970s to Danish investigators bang and dire Berg. On Being informed that the Greenland Eskimos had a low prevalence of coronary artery disease set out to study the diet of this population. thing a dyer Berg described to the Eskimo diet as consisting of large amounts of seal and whale blubber, ie fats of animal origin, suggested that this diet was a key factor in the alleged low incidence of coronary artery disease. This was the beginning of a pullet proliferation of studies that focused on the cardioprotective effects of the Eskimo diet. In view of data which accumulated on this topic. During the past 40 years, we conducted a review of published literature to examine whether mortality and morbidity due to coronary artery disease are indeed lower in Eskimo Inuit populations, compared with their Caucasian counterparts. Most studies found that the Greenland Eskimos and a Canadian and Alaskan Inuit have coronary artery disease as often as the non Eskimo populations, notably being in diabetic studies from the 1970s did not investigate the prevalence of coronary artery disease in this population. However, the reports are still routinely cited as evidence for the cardioprotective effects of the quote, Eskimo diet. So we've talked about this a lot how, you know, a line in a paper that might have no real basis is then cited in papers for years and years afterward. And you try to figure out where this idea is coming from. And you go back to the original paper, and it basically has nothing to do with it or isn't actually supported, or in this case, wasn't even looked at, at all. And it sounds like that's something that happened here with this, this myth or story that the Inuit and Eskimos have low incidence of heart disease. And so in this paper, where they actually looked into that, they, they found that the this was not actually the case. And just to finish up with this last quote here, they state we also reviewed studies that have assessed the prevalence of coronary artery, artery disease or other cardiovascular disease in the US Go Anywhere population populations in areas such as the Northwest Territories, and Nunavik, in Canada or in Alaska. The results of these investigations confirmed that the prevalence of coronary artery disease and Inuits is as high or higher compared to non Eskimo populations. In 2003, a thorough analysis of the incidence and availability and available mortality statistics among Inuit populations in Greenland, Canada and Alaska, by Eric Garner. Yeah, at all, also concluded that the totality of evidence from various northern areas makes a strong argument for for a high prevalence of cardiac cardiovascular disease in Eskimos. So, a lot of words, they're just describing that essentially, they were thought to have had much lower incidences of coronary artery disease and cardiovascular disease. And it turns out, they don't have any lower incidence. And in fact, it's probably a little bit higher than than the Caucasian counterparts.

Mike  40:57  
Yeah, I think there's a couple things to keep to discuss here. Overall, as I doubt when bang and dire Berg are going out and checking on what was going on with the Eskimos that they were doing and geographies and coronary artery calcium scans. Yeah. And I think there's a paper, there's multiple papers discussing this inside PubMed, the title, the specific titles, I don't know off the top of my head, but essentially, they they talk about, like, the way that they're determining the cardiovascular disease and whatnot is like, Isn't they weren't really seeing if they had coronary artery disease or not, they were just kind of like, trying to figure out if they actually had cardiovascular events. And it seemed, and some of the things that they were discussing was that they, they may or may not have had cardiovascular events. It's just that if they did have, then they wouldn't necessarily go get treatment for it. Because there's, you know, you're in the tundra, you're in the Arctic tundra. Now, the well, the

Jay Feldman  41:58  
other thing, too, is it sounds like they were just they were they had been operating on this myth that they already had low cardiovascular disease and didn't even kind of verify that they just were operating on that. And that's it. All right, well, what's their diet since that diet must be the key. But actually, the initial claims weren't true that there was low cardiovascular disease incidence.

Mike  42:17  
Yeah, in essentially there. There wasn't. There wasn't an there was a low cardiovascular disease incidents, but only because it wasn't like it couldn't be fully tracked. So of course, the incidence was low with time. You mean? Yeah, at the time, that was one of the big things is like, how are you really determining because even with the Kitab in populations, I think lung Lundeberg, or Thunderbird was the one who went to go look at the Kitab ins, I think that's the name. He couldn't fully I don't think he fully ascertain their cardiovascular disease risk, I think they did like EKGs and blood pressures and things like that, which doesn't, doesn't really show like, it doesn't really show if you have coronary artery disease or not, like you'd really have to go like looking specifically. And then as far as figuring out actual specific events, like that's another piece as well, like, heart attack strokes, etc. So they weren't, I don't think they actually, if I remember correctly, because I did go through this quite a while ago. They didn't. And I breezed through it again for this podcast, but they didn't actually like fully look to see these things, kind of as you're saying. They like did some minor testing for it, and then kind of asked around about the diet. So yeah, it's and then it got repeated over and over and over and over and over again. Oh, and then it was like, Oh, it must be the fish oil that they were eating this high, the high omega three consumption.

Jay Feldman  43:39  
Yeah, great points there and certainly important things to consider. And in this next paper looking at the Alaskan Inuit they do or the Alaskan Eskimos, they do try to draw a distinct correlation between the Omega three in the diet. So they're controlling for these things. So they look at just omega three consumption. And then they did do an ultrasound looking for atherosclerosis. And so we do have some data here, which is largely not concluding any benefit to omega threes. So this is a paper titled consumption of omega three fatty acids is not associated with a reduction in carotid atherosclerosis, the genetics of coronary artery disease in Alaska Natives study. So a population based sample of 1131 Alaskan Eskimos of age, at least 18 years old, underwent ultrasound assessment of carotid atherosclerosis, the meat consumption of total omega three fatty acids was 4.76 grams per day, and those without and 5.07 grams per day and those with plaque and models adjusting for relevant risk factors presence and extent of plaque were unrelated to intake of the 20 to 22 chain omega three fatty acids or total omega three fatty acids. So what they're finding here is that they actually did try to look specifically at this one marker of cardiovascular disease. Okay. Got plaque and the diet looking specifically at omega three consumption. And of course, that does help because the ones consuming more omega threes are likely having a much more traditional diet. And they found that there was no there it was unrelated to omega three fats and the presence and extent of plaque. And actually just looking at the numbers, there are higher omega three fatty acid consumption and those with plaque versus those without. Yeah.

Mike  45:27  
So in this specific study, basically, they did actually test it. And they basically not showing the benefit with the Omega three then on the cardiovascular disease here. So this actually clears up some of the other discrepancies I was talking about previously.

Jay Feldman  45:42  
Yeah, yeah. And of course, as you were pointing out, like, there's a lot of variables here, this is by no means like, take this study alone and make a major conclusion on it. This is just a piece of part of context in the constellation of all the others that we've brought up. So what you mentioned, as far as all those other things is certainly entirely relevant with all of this anytime we're looking at population data. And that's why this is not the primary mode of evidence that we would use to come to a conclusion, but it's helpful to, to look at. There's, you know, we've talked about the Messiah, we'll get to those, because that's, I think one of the clear examples here. But I wanted to talk about the hodza. Next, do you have anything you want to mention before that? No,

Mike  46:24  
no, that I think we covered that section pretty well.

Jay Feldman  46:28  
Okay, in general with some of these next one. So aside from the Maasai, which we have some clear data on in some of these other populations, the data is pretty unclear as far as diet and cardiovascular disease incidents, as you're kind of mentioning with testing and whatnot. So, you know, again, take all this with a grain of salt, but it's still worth mentioning. So when it comes to the hodza, how to have a diet that's extremely low in omega threes, yet, they don't presumably have any increased incidence of heart disease. So the men need a diet that's largely meat based and all of their meat is extremely low and polyunsaturated fats. Pretty much all the meat that they consume is from ruminant animals, and a couple others, like word hogs, which are extremely low in fat, and therefore very low in omega threes. And then they consume small amounts of smaller amounts of berries, tubers, fruits, and honey. And then the women of the hodza. Eat much more of the fruits of tubers, less meat, but also basically have no Omega three sources either. So presumably, and we don't have the exact data on the composition of their diet, as far as the fat, the fat composition. So we have the general amounts of how much of each thing they eat, but no data that I've could find as far as the specific amounts of each poofer that they consume, but presumably, would be extremely low in the Omega threes, I really have no source of Omega threes. And yet, again, they based on the data we have, there's no evidence of increased incidence of heart disease, but there's not a great, there's not great studies looking at it. So this white paper titled physical activity patterns and biomarkers of cardiovascular disease risk, and hunter gatherers, they state we found no evidence of risk factors for cardiovascular disease in this population. And this being the hodza. Low ie low prevalence of hypertension across the lifespan and optimal levels for biomarkers of cardiovascular health. So now, I don't remember who that's just the hub, HUD's are looking at a handful of different hunter gatherers. Of course, this is not using very extensive testing methods to find cardiovascular disease risk in an existence. But based on the data we have, it seems like despite an extremely low amount of Omega three consumption, there's not any evidence of increased cardiovascular issues.

Mike  48:43  
Yeah, yeah. I mean, I don't have too much specifically to add to the study there. It's, I think it's, it's another piece, that's pretty clear, you're seeing you have a relatively healthy population, at least, that doesn't have a high omega three intake and is not showing like tons of cardiovascular disease. And you can also see that to some extent with some of these other populations as well, like the Catalans or the Maasai. And again, there's there is there's always questions around like, how are we determining this, like cardiovascular disease prevalence, or coronary artery disease or anything along those lines or cardiovascular events, and it's obviously harder in these different populations, because they're, you know, it's, for some of them, it's not like, you can just go bring them to, you know, Mount Sinai Hospital and get the CAC scans done. It's your kind of like, out in a very rural area, and you're, you have access to like field equipment to some extent with this type of stuff. So it just interest there. It is seen within these groups that are at least it's understood to some extent that they don't obviously appear to have large amounts of chronic disease, like you would see within Western societies. And then it's also very interesting here to see for the for the hodza years Pacific They don't, as far as I understand, they don't live very close to the ocean. And the meat that we eat is all kind of inland meat. So it's not going to have a very high amount of Omega three content is what you're seeing here. And basically, they're they're basically, their diet is super low in the Omega three content and are doing okay. Which again, it's just one element of evidence that's going against this idea that you need to have a high omega three intake. And then there are mega six intake is also not massively high. No.

Jay Feldman  50:34  
Right. It's also it's going to be higher than the Omega threes, but but still very low. And yeah, go ahead.

Mike  50:41  
Well, my point is, that was some one of the things that we also theorized, because it's not like they're having their maybe they have some omega six, as you mentioned, from bayeaux biopsies, but it's not like they're frying that vejo Bob seeds in corn oil, you know, or frying their warthog in corn oil, or soybean oil or whatever the deal is.

Jay Feldman  51:02  
Yeah, yeah, exactly. Again, we don't have the clear data on this. But not only is there no suggestion that they would have increased cardiovascular disease incidence, but rather, it's I would say, it's much more likely that they have significantly reduced incidence compared to other populations. But yeah, it's just just something else to consider. So

Mike  51:20  
this is a slightly tangential point. But some people would argue that oh, well, they have a higher mortality, this higher mortality that and I see that like the same arguments kind of applied to well, people back in the day at higher mortality in these groups, and I don't know specifically about the hodza. But I do know, for some of the other groups that I've looked at, once you get past infant mortality, and once you get past a certain age in these groups, and it's usually a lot of mortality centered for like younger men, I think after like 30, or 40, they wind up actually living to like a relatively decent age because they don't die from accidents or, or things along those lines or die in childbirth or from like specific diseases. So the the a lot of the mortality data, I think, for these different groups, if somebody was to go and look at that, or they're going to try to make a counter argument about it isn't necessarily a chronic disease problem. It's more of like accidents, or attacks by animals or infant mortality, or like acute disease processes that are likely taking people's lives when they're like all across the lifespan, but probably when, particularly when they're younger, that would lower the actual average age, or increase the the total mortality and whatnot. But again, we're trying to figure out chronic disease situations here.

Jay Feldman  52:41  
Right, yeah, exactly, exactly. And there's quite a bit of evidence to that the all of the extension to lifespan that we have in Western society is not due to improvements in chronic health issues and actual reductions in aging and improvements in in, like, medical care for the long term. But rather, it's more improvements in our capacity to deal with acute issues and prevent infection, or deal with infection and things like that.

Mike  53:08  
Yeah, or even the changes in cardiovascular disease, and whatnot that they're starting that they started to see recently, as far as mortality and whatnot. It's just because interventions for cardiovascular disease problems, like acute heart attacks, and angina, and strokes, and all these different components have, like the treatment for that in the acute situations has actually gotten quite good. And so like when, you know, when a person has a heart attack, and they come to the hospital, is like an entire processes or stroke or anything like that entire process is set up to immediately address what's going on and help to rectify the problem as quickly as possible. And that does save I think that saves a lot of people's lives, particularly in the Western world. But it's again, it's not necessarily because people are, you know, living better overall, in terms of like trying to make the best decisions is that when they do have a problem, like it can be managed much more effectively. And those are very different situations and levels of prevention.

Jay Feldman  54:09  
Right? Yeah, yeah.

Yes. So there's, there's a couple other populations I want to look at. One is the Maasai, who he talks about earlier, we do have the clear data on their diet, and also on the red blood cell phospholipids. And we are seeing that huge discrepancy where they only consume, they consume a pretty low Omega three diet, only about 1% of their total diet of which 0.15% of their total diet is a long chain fats, long chain omega three fats. And despite that, they have much higher amounts of D fossil lipids. So we had that. In general though, what it was pointed to there is that they generally have a low Omega six diet, although it's still considerably higher than other populations that we'll talk about in a moment. And it's also considerably higher than their Omega three intake is just a little bit interesting. But anyway, so they have extremely low Omega three consumption. And yet, as As far as cardiovascular risk goes, they are rates of cardiovascular disease. They're in a pretty good spot. So this is a paper titled daily energy expenditure and cardiovascular risk in Maasai rural and urban by Bantu Tanzanians. And they state Several studies have revealed that the Maasai, pastoral, pastoral pastoralists in Tanzania have low rates of coronary heart disease despite diet high in saturated fat. So we do, it seems like there's quite a bit more data for for this population showing very low risk of coronary heart disease. Again, they're saying despite a diet high in saturated fat, you could add, you could say, despite a diet high in saturated fat, lower polyunsaturated fats at very low in omega three fats. Yeah,

Mike  55:43  
and I think the I mean, again, a little bit tangential. But I think the other side, I also changed from what their previous diets were in the past, because of the I think, like corn was something that had been introduced more recently, prior to the initial diet being largely centered around the pastoralist society. And then like some like Hunter gathering components for tubers, and, and fruits and different components along those lines, and that's in the in the last like, century or so, with the moving of lands and whatnot, within Africa, from the different Imperial stuff going on, actually looked at these for quite a while. Because there's a lot of these different population data that you look at for different countries has to be put in context of like the different time periods that you're looking at the information, because of the changes in diets and customs in response to different circumstances. Like even again, slightly tangential, but with the with the Japanese populations in longevity, you have this like the entire effect of World War Two on the food supply within Japan that you have to take into consideration where you're trying to understand what was the diet before? And then what was the diet after in these different areas that had high levels of longevity. And so the same thing applies. When you have a population like the Inuit or the Eskimo in Alaska, where are you looking at populations that are, you know, secluded in their particular area and eating a very normal traditional diet that, you know, that their culture has, you know, over an extended period of time? Or are they introduced to the food supply now that's coming from the west. And the same thing with the Maasai has their diet changed, compared to what it was previously as corn, a new introduction to the diet and higher amounts and than ever was previously because of changing of lands or introduction, this food into whatever. So those are also, I think, really important to consider over time with these different components. But it is also interesting to see over time, when they look at these things, that omega three intake isn't that high, but total poof is still low. And then the chronic diseases are also tend to be on the lower side. And also the, I think for some of these groups, depending on where they're situated, the they may be exposed to more types of either Parasitic Diseases, or general diseases, overall, infective processes that maybe other people wouldn't be exposed to, and they still aren't seeing like the same level of chronic disease overall, and some in some of the people who are reaching to older ages in these groups.

Jay Feldman  58:17  
Yeah, yeah, definitely. Definitely. There's a few other groups that I want to talk about that have extraordinarily low boof intakes. So this is the Tokelau and pukapuka Tokelau have a total polyunsaturated fat intake of 2% of their total calories. And the pukapuka are between two and 3%. So extremely, extremely low Hoover intakes, I mean, pretty sure it's as low as you can find as far as native cultures go. And, unfortunately, there's not rate data on their cardiovascular disease risk. But the data that we do have suggests that it's much lower than other populations. They're part of cardiovascular disease incidents. But again, there's not great data here. But there's also certainly not data that they are dealing with massive amounts of heart disease. And, you know, same caveat with these other populations. As you've mentioned, I still think it's worth like, I'll share a couple of quotes here talking about their supposedly lower risk in terms of cardiovascular issues. But a lot of the people who are just to interject with this, this an important comment, which is that a lot of people who are suggesting that we should be eating more omega threes are people who are considering considering that we should be eating ancestrally, we should be eating in a way that's evolutionarily consistent. And we should be looking at these native cultures, we should be looking at what we were eating X amount of time ago. And there are these native cultures that essentially ate no HuFa. And essentially, no omega threes. I mean, it's not literally not but it's very, very low, about as low as you could get from just eating and food. And yeah, and so yeah, maybe it's just, if that is the line of thinking that jives with you. Maybe these are some things to consider a little bit more heavily We've talked about our feelings on that. And areas where we think it's valuable and ways that we think it's really not valuable in previous episodes, especially those ones where we were talking about some comments from Rob wolf, the bioenergetic view of health, so I'll link to those but just a couple of quotes here on cardiovascular health in these populations. So this first study is titled, cholesterol, coconuts and diet on Polynesian a tolls a natural experiment, the pukapuka and Tokelau islands studies, the influence and they here's the quote, they state, the influence these traditional diets may have on development of atherosclerosis is an important question 12 lead ECGs have been taken in both groups, and the rate of sub normal Q waves was very low in both groups. The samples of adults on the two atolls are however too small for definitive studies of coronary heart disease, vascular disease, these populations are in the developing world where a coronary heart disease is uncommon or rare. So all the caveats we had before of course, this is not the clearest data that we would like here in the study. But it's the data that we have. And I'm just going to stick to share this last one before we have, we kind of finish up our comments here. This one is titled The Tokelau Island migrant study prevalence of various conditions before migration. And they were looking at effort pain, which is essentially is angina. And so they state effort, pain was reported in 2.2% of males and 3.6% of females. Criteria for coronary heart disease largely based on physicians assessment of angina yielded rates of 7.3% and 16.1%. In mayority, males and females, respectively, compared with 6.5% and 11.5%. In Europeans, these rates are so much higher than the Tokelau rates, that granted differences in diagnostic criteria criteria, the Tokelau rates can be regarded as relatively low. So again, not a great quality here, we're using different diagnostic criteria and trying to compare it. But the presumption based on the data we have is that their current coronary heart disease risk is likely or incidents is likely extremely low. But you know, and again, this would be despite an extremely low proven intake and a very low Omega three intake

Mike  1:02:16  
and have a very high saturated fat intake from coconuts. That too, yes, yeah, yeah, I've

seen the studies, it's, it's just frustrating because you can't like at this point, because a lot of these different areas have now been exposed to industrialization, and like some of these different products, you're actually starting to see the like, increase in disease processes in these different areas that are exposed to these foods. And so it's now it's like really hard to be at a point to get a group of people that's pristine, I would say, and like, test and see, okay, we know you eat this type of diet. And then this is your, this is your, you know, your angiography, or your coronary artery calcium score, like all these metrics that we can look at, and say, Okay, so like, there's a different picture going on here with these different components. And the reason why I think you would want to see this because they like would, it would support a lot of different ideas around the mechanisms and in humans, as opposed to in animal studies, it'd be like a more long term approach, right? Because you get to you get to see what's going on in the hearts of people who have ie in high saturated fat look, high saturated low PUFA or polyunsaturated fat diets for an extended period of time. And like they could be essentially like huge disproves to the whole cholesterol, heart disease hypothesis, saturated fat heart disease hypothesis, etc. And it also simultaneously disproved this massive benefits of polyunsaturated fats, omega threes, Omega sixes, whatever the deal is. So yeah, and that's why you know, looking at works of somebody like Weston A price like extremely groundbreaking work, it's just it's kind of frustrating because it you don't have the same level of diagnostics that you would really want to see to say, you know, okay, these these factors, we can say, like all these populations really didn't have heart disease, like a lot of the factors we're looking at are indirect. The it gives us a direction but it doesn't give us a clear enough point to make very strong arguments from which that's the, I guess, the biggest frustration and as soon as the end like you can't really do it anymore. It's sort of been nice to like yeah, do the scans back initially, but right now, you know, you had the 12 lead EKG, which is not super strong evidence is the hope it's a bit disappointing.

Jay Feldman  1:04:48  
Yeah, definitely. One other area that has actually been helpful, though, for is looking at carbon take, you know, the couple of populations that have extremely high carb intake yet are incredibly insulin sensitive and we can at least see that data clearly. But it will be nice of right? Yeah, that that too. And also the, you know, seeing the responses to glucose tolerance tests and things like that and having their lab work. So those things are nice, at least, to have. But yeah, it would be nice if if we could have more of the data as you were describing. But anyway, that's why this is a, you know, something to take with a grain, a grain of salt, to whatever extent but certainly does not provide evidence against any of the other things we presented today, or at least the things we're presenting from our view that we're really suggesting that, I'd say there's no benefit to the consumption of omega threes. And if anything, I would be quite concerned about their consumption. And I would argue that that would likely have some pretty negative effects. And I think we made that pretty clear with the data that we went through, in addition to and corroboration with the many mechanisms that we've cited outside of this data in previous episodes, as well. So I don't have too much else to add, I think we went through it quite a bit hash through the details hash for those studies. And so I think it's pretty clear. But was there anything you want to add? Mike?

Mike  1:06:08  
I think my the full takeaways, the initial question here was our omega three supplements or eating fish high in omega threes, like a benefit, because we add or worthwhile to pursue, because we have studies showing that omega three content of red blood cell phospholipids, are associated with lower risks of toll of mortality on multiple levels. And I think it's safe to say that perhaps that relationship does exist, it doesn't seem to be driven by omega 33 consumption, or high by omega three consumption in general. Even though Omega three consumption does modulate the Omega three content of red blood cell phospholipids. So there's other mechanisms to explore there as far as and we discussed some of those possible mechanisms, as far as what is specifically leading to these higher omega three red blood cell contents. And these the overall like, what is actually leading to that. The other thing is more studies without to be exploring, like, are these associate like re affirming these specific associations perhaps done by people who don't own companies that do this type of testing or involved in fish oil supplementation, you know, minimizing that that bias component? So maybe having like a kind of a third party do that type of study without having funding from it? Yeah,

Jay Feldman  1:07:40  
I think based on everything we went today, I went through today. And through these episodes, I certainly a as you came back to initially, which I think was great point. The question was based on this association data between omega threes and the fossil lipids, and mortality and lifespan, should we be consuming omega threes? Is that what does that data support that? And largely, I think we will conclude No, it does not based on those, based on that research, that that is not enough to conclude any of that because there are so many confounding variables, and because of all the evidence against it, all the evidence suggesting otherwise. So I think that's the most important takeaway here. As far as practical takeaways go. I'm going to link back to episodes where we've talked through general recommendations for from the bioenergetic view on the diet side, which in which we talked specifically about fat intake, including buffo omega threes, we talked about protein intake, talked about seafood and fish. I'll link back to that, as far as our discussions on that front. And, yeah, we'll leave it there. So all right, that's gonna do it for this series, exploring the relationship between omega threes mortality and lifespan. If you did enjoy it, 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 of those things really do a lot to help support the podcast and are very much appreciated. To check out the show notes for today's episode where you can take a look at the articles, studies and anything else that we referenced. Throughout today's episode, you can head over to Jay Feldman wellness.com/podcast. And when it comes to creating a healthy diet, there's a lot of conflicting information out there. And that's why I've created the energy balanced food guide to help you determine exactly what to eat to optimally support your metabolism and help you lose weight, improve your digestion, get amazing sleep, boost your energy and so much more. The energy balanced food guide is a one page infographic that organizes foods on a spectrum based on how effectively they support your metabolism. And it also has a separate scale that adjust the scale for you or the spectrum for you. In the case that you're dealing with various digestive symptoms. This food guide makes it extremely easy to get started with a bioenergetic approach to optimizing your health. So head over to Jay Feldman wellness.com/guide To download your free energy balanced food guide. And with that, I'll see you in the next episode.


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