129. Paul Saladino, MD: Why 'Heart-Healthy' Seed Oils Are Actually Poison

Speaker 1 You go to McDonald's, that is a metabolic toxin. You are actively poisoning yourself.

Speaker 1 If you have been eating McDonald's and lots of seed oils your whole life, if you stop today, it takes you potentially four plus years to fully recycle the membranes of all the cells in your body.

Speaker 2 I think that people don't realize all the places that they're hidden. I mean, they're everywhere.
Potato chips, nearly every dressing that you pull off of the shelf in breads.

Speaker 1 There are so many markers of inflammation that increase when you fill the body with these oxidation-prone oils.

Speaker 1 And yet, the mainstream perspective, Harvard, many apparently intelligent physicians in the community, longevity influencers are still holding fast to the claim that seed oils are benign for humans.

Speaker 1 And I would argue that the best trials with seed oils clearly show they're harmful. It's just that these trials have been suppressed.

Speaker 2 And you know what I find is that a lot of randomized clinical trials essentially end up proving what we know ancestrally from nature. It always takes us back to the basics.

Speaker 1 You can't go wrong eating simple whole foods. It's just unprocessed animal foods, unprocessed plant foods.
You'll be great.

Speaker 2 We take the narrative that these seed oils are bad for you. So I think we just need to put it into context.
Why are we attacking this plant? Why are we attacking the oil extraction method?

Speaker 1 The only thing that seed oils might have going for them is a...

Speaker 2 Hey guys, welcome back to the Ultimate Human Podcast. You know the drill.

Speaker 2 I'm your host, Gary Brecca, human biologist, where we go down the road of everything anti-aging, biohacking, longevity, and everything in between.

Speaker 2 One of my favorite house guests has paid me a visit again before Thanksgiving. And even though he didn't know it, I was like, let's go.
Like every time we meet in the kitchen,

Speaker 2 you know,

Speaker 2 we start running a podcast together. And I was like, dude, let's just go in the studio and rip this because this is really, really good content.
Welcome back to the show, Paul Saladino.

Speaker 1 It's always good to see you, man.

Speaker 2 Happy to do it. Yeah.
So Dr.

Speaker 2 Paul Saladino and I have formed an unbelievable friendship, you know, over the last few years, not just being in the same industry, but spending a lot of time in close proximity and really seeing that he practices what he preaches, that I practice what I preach.

Speaker 2 And,

Speaker 2 you know, every time we meet in the morning,

Speaker 2 I caught him this morning getting his sunlight and doing his stretches outside on the balcony in the sun. I was like, hey, I'm getting ready to go out there and do my breath work myself.

Speaker 2 And he comes back in, he goes, Let me show you my morning elixir. He starts breaking open these capsules of testicle and

Speaker 2 B vitamins and honey. And, you know, we've had raw colostrum over the last few days.
I feel amazing. And we just started

Speaker 2 going back and forth about a recent documentary that he published, which is phenomenal. I'm going to put the link in the show notes below.

Speaker 2 You've got to watch this documentary, which I think finally closes the chapter.

Speaker 2 on seed oils and the inflammatory nature of these oils and their implications in many of the chronic disease conditions that we are blaming on other natural compounds in the body like cholesterol.

Speaker 2 And that is not to say that we shouldn't keep an eye on cholesterol, but my point is that

Speaker 2 we have been blaming the firemen for the fire for too many years. And the notion that if we had less firemen, we'd have fewer fires is simply a fallacy.
And

Speaker 2 the large data is starting to prove that. So, Paul, I would love it if you would just give us a little background on the documentary, like what led to it,

Speaker 2 and give us an overview of what we're going to see in the documentary.

Speaker 2 And I specifically want to go down in detail the road of seed oils because just yesterday, one of the biggest gurus, longevity gurus in our space, we just talked about it. I won't name any names,

Speaker 1 posted that seed oils were safe. It's crazy.
So this is a mini documentary. It's only about 37 minutes long, and I did it in collaboration with Heart and Soil Supplements.

Speaker 1 So those testicle pills that I was emptying into your raw milk. They're actually pretty good.

Speaker 2 I mean, we put it in raw milk and then we added honey.

Speaker 1 Honey, yeah, yeah. You can't even taste them.
It was so good. Those are testicle pills from Heart and Soil Supplements.

Speaker 1 And Hardened Soil is just a company that I built to help people get organs and the capsules.

Speaker 1 But Hardened Soil has an amazing research team, and I collaborated with them to make this mini documentary on seed oils. It's called Fed a Lie, and it's a kind of an entry-level seed oil documentary.

Speaker 1 It's just to get people asking the questions. So I'm in the documentary.
Chris Kenobi's in the documentary. He's an MD, he's an ophthalmologist.

Speaker 1 And Nina Teischultz is in the documentary who wrote The Big Fat Surprise. The Big Fat Surprise.
Yep.

Speaker 1 Detailing a lot of the sort of corruption and confusion in the space around the history around saturated fat versus seed oil. You're not saying that there's corruption in our industry.

Speaker 1 In the food industry, imagine that. Perhaps a little bit of corruption.
We can talk about it.

Speaker 1 But what's so interesting when you think about this from the perspective of seed oils and the history is that we really have been, I believe, fed a lie regarding their benign nature or their health benefits.

Speaker 1 And as you suggested, it kind of all centers around this idea of cholesterol. So the only thing that seed oils might have going for them is that they lower APOB.

Speaker 1 They lower your cholesterol, quote unquote.

Speaker 1 And the mainstream medical paradigm, which I was trained in, perhaps propagandizing.

Speaker 2 He's a medical doctor, by the way. He is an MD.

Speaker 1 Yeah, is all about lowering cholesterol, often in a myopic view, right?

Speaker 1 So if you are an MD, you are basically trained to lower APOB and or LDL cholesterol no matter what, without much attention to other metrics that may have more weight on your cardiovascular risk or that are simply more relevant, like oxidized LDL, LP-little-A, LP-PLA2, which is lipoprotein-associated phospholipase A2.

Speaker 1 And this is where it starts to get interesting because I'll say this about seed oils. I think you could come to the conclusion that seed oils are benign for humans if you ignore all historical data,

Speaker 1 all evolutionary precedent, humans have never had this in our diets.

Speaker 1 You ignore all animal studies, which clearly show that seed oils increase rates of cancer, non-alcoholic steatohepatitis, which is liver injury. That's very bad in animals.

Speaker 1 They increase adiposity, they increase cardiovascular disease in animal models.

Speaker 1 You have to ignore all mechanistic studies, which clearly show that linoleic acid, this 18-carbon omega-6 fatty acid, is very susceptible to oxidation in the biological systems.

Speaker 1 And you also have to kind of cherry-pick the randomized controlled trials in humans and ignore the randomized controlled trials in humans that show that when you feed people seed oils versus olive oil or saturated fat, they have increased oxidized LDL, increased LP-little A, and increased LPP.

Speaker 2 Increased L P little A.

Speaker 1 Increased L P little A. 7 to 10%.

Speaker 2 Yeah. And that's usually a genetic, more of a genetic predisposition.
I actually, I actually have high L P little A. My cholesterol levels are great.

Speaker 2 And I'm very cautious about what I eat. So I take bergamot O, I take slow release niacin.
That's, that's helped. I've done TE, TPE total plasma exchange.

Speaker 1 That really helped. We can talk about L P little A because I want to share with you some data from my friend Dave Feldman about L P little A also.
Really? Yeah.

Speaker 2 I'm very interested in that because a lot of folks that are watching this, you know, that have

Speaker 1 little A.

Speaker 2 What's interesting, you know, before we get on this road is, and we talked about this before, is, you know, in the mortality space, when we were doing mortality research tables, when we were building these probabilistic models, it was very apparent

Speaker 2 to us that the people that were living

Speaker 2 the longest all had, and I'm just picking one, you know, isolated portion of cholesterol, but they all had elevated levels of LDL cholesterol at the time of their death.

Speaker 2 We would process a lot of death claims

Speaker 2 on folks folks that were, at the time that they passed, they were in nursing homes and they actually, we did have, you know, blood work on them.

Speaker 1 And I don't recall a time,

Speaker 2 there may have been, but I don't recall a time where we processed a death claim on a centenary and someone over the age of 100 that did not have clinically elevated levels of LDL cholesterol at the time of their death.

Speaker 2 And

Speaker 2 so we actually didn't use randomized clinical trials. We used big data.

Speaker 2 But I want to get back to the seed oils and I want to sort of walk people through this because I think inherently people think sunflower, good.

Speaker 2 Rapeseed, it's a plant, good.

Speaker 1 Well,

Speaker 1 yeah, yeah, yeah.

Speaker 2 You know, and I know the whole evolution of industrial, but I'm just saying for the general public, I see soybean oil.

Speaker 1 Soybeans are healthy.

Speaker 2 I mean,

Speaker 1 sunflower oil.

Speaker 2 Sunflowers are great. I eat sunflower seeds.

Speaker 2 And so

Speaker 2 then we take the narrative that these seed oils are bad for you. So I think we just need to put it into context.
You know, why are we attacking this plant?

Speaker 2 Why are are we attacking the oil extraction method?

Speaker 1 Right. So seed oils are often called vegetable oils.
And I think that's kind of a marketing claim, right? That's a euphemism. They're seed oils.

Speaker 1 They're called vegetable oils probably because we all associate vegetables with health, which is a separate conversation.

Speaker 1 But in order to get oil out of a plant seed, whether it's a rapeseed, which is the precursor of canola oil, or a soybean, or a peanut, or I mean,

Speaker 1 corn, right?

Speaker 1 Corn, canola, sunflower, safflower, grapeseed, rice bran, all of these are seed oils. You have to do refining, bleaching, and deodorization.

Speaker 1 And if anyone has ever seen a seed oil factory, it looks like an oil refinery because that's what it is. There's huge smokestacks with...

Speaker 1 you know, either water condensation vapor coming out or other pollutants coming out of the smokestacks. It's a huge process with grinding, with extraction, with degumming, with deodorization.

Speaker 1 We've talked about this extraction with

Speaker 1 hexane, contamination.

Speaker 2 So hydroxide. Right.

Speaker 1 Very often bleach. Yeah.
They're refined, bleached, and deodorized oils.

Speaker 1 And the heating process in seed oils, it starts with a grinding step, then they're heated to 200 degrees, then they're heated to like 300 degrees, and then they're heated to over 400, 500 degrees Fahrenheit.

Speaker 1 Remember, this is an omega-6 polyunsaturated fat-rich oil. Sometimes up to 55% of the oil is linoleic acid.

Speaker 1 And when you heat linoleic acid to 500 degrees Fahrenheit, you get massive amounts of lipid peroxides, which is essentially rusted oil or rancid oxidized oil.

Speaker 1 And it's just, this is the nature of the oil. This is organic chemistry.
You cannot avoid this. So people have looked at levels of lipid peroxides.

Speaker 1 These are oxidized oils and these are reactive products. When you put these into your body, they initiate a chain reaction.

Speaker 1 And that chain reaction can partially be quelled or stopped by things like vitamin E or vitamin C, depending on what whether you're in the lipid soluble or the water soluble fraction of your body, but it cannot entirely be abolished.

Speaker 1 Like you're, this uses up resources in your body. And the idea with seed oils is that when you eat polyunsaturated fats, whether it's from fish oil or from seed oils,

Speaker 1 we store these. And we talked about this last night in our previous four and a half years.
Essentially, yes.

Speaker 1 There is some interesting data about the kinetics of how we hold on to these oils. And it's not easy for us to get rid of them.

Speaker 1 So when you are eating french fries cooked in seed oils, which are even more oxidized because it's been a fryer oil that hasn't been changed for a week, you know, I've been to McDonald's, I've been to KFC.

Speaker 1 And I ask them, how often do you change the fryer oil? Both of them, about every, once a week. You know, you go to In and Out.
How often do you change the fryer oil? Once a week.

Speaker 1 Once a week, you're frying 16, 20 hours a day in this oil that's very susceptible to oxidation.

Speaker 1 And if you're getting french fries cooked in seed oils that have been fried in that for a week, you are getting massively increased levels of these lipid peroxides.

Speaker 1 Not to even mention the fact that increasing polyunsaturated fats in the human diet evolutionarily is inconsistent. And we store all of these.
It creates this oxidative stress burden in our bodies.

Speaker 1 It's just like having a bunch of dry wood stored at your cabin in the mountains in the middle of a lightning storm. This isn't a good idea.

Speaker 1 If you have a lot of dry wood in your body, the dry wood being the oxidation-susceptible linoleic acid, and you have lots of sparks, you're going to get lots of fires.

Speaker 1 And then you're going to overwhelm your body's resources and you can run into real problems. Now, people always say seed oils are inflammatory.

Speaker 1 And the counter argument is there's no evidence that seed oils are inflammatory because there are some studies which show that seed oils maybe don't increase canonical inflammatory markers like CRP.

Speaker 1 But I would argue that oxidized LDL, LP little A, and L P P L A 2 are clearly inflammatory markers. So this this is just, this is just semantics, I think.

Speaker 2 Yeah, cherry picking the

Speaker 2 specific marker of inflammation like C-reactive protein, you're like, it's not driving inflammation. Well, that's not the only marker of inflammation.

Speaker 1 There are so many markers of inflammation. And one of the things CRP does is bind to oxidized LDL, right? So CRP and oxidized LDL are intimately linked.

Speaker 1 And so to say that there's no inflammatory markers with seed oils is ludicrous. It's just closing your eyes and putting your hands in your ears and saying, la la la.

Speaker 1 You know, there's, I don't see any CRP.

Speaker 1 yeah you know just because esr doesn't go up erythrocyte sedimentation rate with seed oils there are so many markers of inflammation that increase right when you when you fill the body with these oxidation-prone oils and yet the mainstream perspective harvard mayo many

Speaker 1 apparently intelligent physicians in the community longevity influencers are still holding fast to the claim that seed oils are benign for humans. And so we just wanted it with Heart and Soil.

Speaker 1 I just wanted to make a documentary that got people talking about this and at a higher level asking questions about why we still think these are healthy, how anyone can even say that.

Speaker 1 Because when you look at the highest level of evidence, the randomized controlled trials with seed oils. And I have a whole thread on X that I did months ago about this.
And

Speaker 1 I just resurfaced the tweet this morning. I broke down all 11.
of the randomized controlled trials in humans with seed oils. Wow.
Because that's the highest level of evidence, right?

Speaker 1 I went through it earlier in this podcast. We talked about evolutionarily inconsistent.
We've never had seed oils in our diet.

Speaker 2 mechanistic studies how do we very bad how did we um how do we introduce seed oils because we've had polyunsaturated fatty acids but i mean

Speaker 1 in small amounts yeah right you know historically

Speaker 1 nuts basically small amounts of nuts but how many almonds can you eat you know almonds are a recent addition to the human diet they you know but sure there are some hunter-gatherers that have mongongo nuts like the khoisan but most of us historically throughout our evolution as humans had very small amounts of polyunsaturated fats in our diets and if you look at hunter-gatherers or indigenous cultures very small amounts, one, two percent of their calories from polyunsaturated fats.

Speaker 1 Now we are eating 40% or 10 to 15% of our calories, and then it increases even from there for us. So average Americans today eat five tablespoons of some combination of seed oils, five tablespoons.

Speaker 1 That's hundreds of calories.

Speaker 2 And I think that people don't realize all the places that they're hidden everywhere.

Speaker 2 Potato chips,

Speaker 2 in snack foods, in nearly every dressing that you pull

Speaker 2 on the shelf in breads. Breads have it.

Speaker 1 Like you said, dressings. Yeah.

Speaker 2 And even some of the good dressings. And

Speaker 2 it'll say, you know,

Speaker 2 what about expeller-pressed?

Speaker 1 So when you have an expeller-pressed oil, now, let's be honest, there's a very, very small fraction, probably less than a tenth of a percent of all seed oils are expeller-pressed. Right.

Speaker 1 You don't have the refining, the bleaching, and the deodorization. So that's a...

Speaker 1 less oxidized oil, but you still have a very fragile oil that has been stripped from the seed matrix and is going to be susceptible to oxidation.

Speaker 1 It's less oxidized, but I still think it's an evolutionarily inappropriate thing to consume as a human because you're still stuffing your cells with these oxidation-prone seed oils.

Speaker 1 And so, if we get back to the randomized controlled trials, of these 11 trials, right,

Speaker 1 the majority of them are flawed.

Speaker 1 Fundamentally flawed because they were done from the 1950s to the 1980s. And we didn't really have a good sense of trans fat in that time.

Speaker 1 Trans fat was really only banned from food in what, the late 1980s, early 1990s. So almost every single one of these trials has trans fats in the control group.

Speaker 1 And the control group in these randomized control trials is comparing saturated fat-rich diets in the control group to polyunsaturated fat-rich diets.

Speaker 1 So, what do you think happens in a randomized controlled trial if the control group eating saturated fat has significantly more trans fats than the experimental group eating polyunsaturated fats?

Speaker 1 That's a problem, right? And many of these trials are also multifactorial interventions.

Speaker 1 Things like, oh, in the control group, we're going to say eat your normal diet, which is perhaps animal fat-rich, but you're probably also eating margarine with trans fats because we didn't tell you to stop doing that.

Speaker 1 And the experimental group, we're going to say eat more seed oils, but also exercise more, eat more vegetables, and stop smoking.

Speaker 1 And these are the type of randomized controlled trials that form the quote bedrock of the fact checkers.

Speaker 1 When I get fact check on Instagram or meta, any meta platform for saying that seed oils are harmful for humans, they'll say, no, there's a randomized controlled trial here, or there's a meta-analysis here, or here's an AFP fact-check article where people have said seed oils are fine based on these foundationally, fundamentally flawed randomized control trials.

Speaker 1 And the randomized controlled trials that show seed oils to be harmful are suppressed.

Speaker 1 Sydney Diet Hart, Minnesota coronary experiment at the Rose Corn Oil Trial was one of the first trials done on seed oils in the late 1950s. And it was underpowered, but it clearly showed.

Speaker 1 that seed oils were very harmful for humans. A significantly higher amount of people in the seed oil group versus the saturated fat group had heart attacks.
And Wow.

Speaker 1 And the P-value was between 0.05 and 0.1. So there was less than a one in a thousand chance that this result showing seed oils are harmful happens by chance.
Less than one in a thousand.

Speaker 1 But because the p-value wasn't less than 0.05, people say it wasn't a significant finding. That should have been case closed for seed oils in the 1950s.

Speaker 2 Wow.

Speaker 1 But there were still 10 more randomized controlled trials that... many of which almost all

Speaker 1 funded by the food industry or which confuse the data, which are very complex trials.

Speaker 1 And there isn't a perfect trial done with seed seed oils, but I would argue that the best trials with seed oils clearly show they're harmful. It's just that these trials have been suppressed.

Speaker 1 And as you know, with a meta-analysis, a researcher like Darius Mazzafarian at Tufts, who gifted us with the food compass system, which tells us that fruit loops and Cheerios are healthier than ground beef and eggs, can write a meta-analysis on seed oils.

Speaker 1 And he's done this. And he can leave out things like Sydney Diet Heart.

Speaker 1 He can just choose which trials he wants to put in his meta-analysis and write in the abstract that seed oils are benign or trend toward cardiovascular benefit for humans. Wow.
This is ludicrous. Wow.

Speaker 1 This is ludicrous.

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Speaker 2 Well, we know that 74% of our nutritional research is actually funded by Big Pharma.

Speaker 2 Yeah, yeah, I think it's going to. And if you and I have anything to do about it, you know, it will.

Speaker 2 I mean, you know, I'm so excited to see the Make America Healthy movement taking off and having a shot at really affecting public policy because, you know, our public policy research research really should be independent.

Speaker 2 I mean, that should be taxpayer-funded, independent,

Speaker 2 third-party research, you know, with done through the public university system

Speaker 2 and completely independent. When you start to bring in private sector funding and you, you know, you privatize the profits from these and then you socialize the expense,

Speaker 2 then

Speaker 2 you're just creating a problem.

Speaker 2 And I don't think anybody would argue that our healthcare system is broken, you know, $4.5 trillion trillion dollars a year in healthcare, leading the world in morbid obesity, type 2 diabetes, infant mortality, maternal mortality.

Speaker 2 We're actually ranked 60th. When I started my podcast, we were ranked 58th.
We're now ranked 60th in the world.

Speaker 2 We actually were talking right before the camera started rolling about how there are, and it's hard to get your arms around this, but there are third world nations,

Speaker 2 third world countries that actually have longer life expectancies than us. Wow.
And

Speaker 2 by third world, you know, these are people that don't have consistent access to sanitation, to sanitary, clean drinking water. They might not have consistent access to sanitary sewage systems,

Speaker 2 removing

Speaker 2 the waste and sewage from close proximity to where they live.

Speaker 2 But they also don't have a lot of access to highly processed foods, seed oils.

Speaker 2 They're by... default eating whole foods.

Speaker 2 And it's astounding when you think someone living in a first world nation like the United States that spends $4.5 trillion a year on healthcare is actually not outliving somebody that is essentially living outside under a tin roof,

Speaker 2 you know, bathing in a stream where the cows bathe and defecate.

Speaker 2 It's pretty, it says a lot about the state of affairs of where we are.

Speaker 1 So what are, what is the,

Speaker 2 so you have this oxidized oil.

Speaker 2 And I think you could probably make the same argument for burned meat, you know, nitrates, a lot of, a lot of other things that can happen when, you know, if you overcook things or over-char things or,

Speaker 2 but, but you have this highly oxidized oil. It gets into the body.
And then what happens? I mean, I know we all know inflammation is bad, but what is it about the inflammation that is bad?

Speaker 2 What is it doing to the endothelial lining of the artery?

Speaker 2 Or how is it creating this contact surface that is attracting cholesterol, which I think a lot of people don't realize that cholesterol is called to the site of inflammation.

Speaker 2 It's usually called to repair a tissue. It doesn't just magically just jump out of the bloodstream and stick to the wall.

Speaker 2 I don't think it doesn't do that.

Speaker 1 No, no.

Speaker 2 Native LDL.

Speaker 1 Native LDL,

Speaker 1 you would have a hard time arguing, looking at the medical literature, that native LDL, that is unoxidized, unmodified LDL, is atherogenic, right?

Speaker 1 So something has to happen to our LDL to make it participate.

Speaker 2 Either to the LDL or to the endothelial wall or both.

Speaker 1 Probably the, I would argue the endothelial wall is the proximate event of atherosclerosis because

Speaker 1 we know that really uninjured endothelium, uninjured arteries don't really accumulate LDL.

Speaker 1 So you can think about this, and we may have talked about this on a previous podcast, but if we're talking about LDL or APOB containing lipoproteins, which is a slightly broader family than just LDL,

Speaker 1 we have I have the same amount of LDL circulating in my veins. You know, you have veins on your arm too.
You can see these are returning blood to my heart from my hands.

Speaker 1 Deeper in my arm, I have arteries that are pumping blood to my hands, and in between there are capillaries. So I have a continuous system of blood flow.

Speaker 1 The last time I checked my cholesterol, which was about a month ago, my LDL, I think, was 125 milligrams per deciliter. My ApoB is probably just over 100 or just below 100.

Speaker 2 So a lot of physicians would consider that high, above 90. Yeah.

Speaker 1 Yeah, somebody would consider it high. I have the same amount of LDL circulating to my hands, moving through the capillaries, and coming back in my veins.

Speaker 1 But in me and all humans, we do not see atherosclerosis occurring in native veins.

Speaker 1 So atherosclerosis doesn't occur in a vein at all. In humans, it's because it's lower pressure.
And when you have lower pressure in a vein, you don't denude the endothelium.

Speaker 1 You don't create proximate endothelial injury that is necessary to start atherosclerosis.

Speaker 1 If APO B containing lipoproteins, that is LDL plus its cousins, are atherogenic, why don't we get atherosclerosis in veins? They have the exact same endothelial lining on the inside.

Speaker 1 If you were in a little spaceship, like Rick Moranis and Honey Ice, or like, like, what is that, like in, you know, inner space or whatever?

Speaker 1 You know, if you're running through my body in the artery and the vein, if I put you inside a vein or I put you inside an artery and you're looking from the inside of the vessel to the wall, it looks the same.

Speaker 1 It looks the same. The inside of an artery and the inside of a vein are the same.
The endothelium is the same.

Speaker 2 Yeah, it's just on the outside of the endothelium, you'll have smooth muscle.

Speaker 1 Versus

Speaker 1 versus, yeah, versus more musculature or more musculature in the artery to help it contract.

Speaker 1 And you can actually take a vein and you can transplant it into the arterial circulation. So we do do this in coronary artery bypass grafting.

Speaker 1 You can take a vein usually from the leg or, you know, other places in the body and you can transplant it into the arterial circulation. So you can take a vein.

Speaker 1 and put it in the arterial circulation and it actually gets atherosclerosis very quickly because it is subjected to higher pressure and that denudes the endothelium.

Speaker 1 So when a vein is in the arterial circulation and it has that sort of proximate event, that arterial inner endothelial damage, it will accumulate atherosclerosis, but it doesn't happen in native circulation.

Speaker 1 And I would argue that is a very strong argument that Apo B is not causal because I have the same amount of ApoB in my veins.

Speaker 1 If it's so bad for my arteries and my veins, you know, if it's so bad for my endothelium, why isn't it damaging the endothelium in my veins? Because it needs a proximate event to have that happen.

Speaker 1 Now, circle back to humans today in 2024.

Speaker 1 There are many studies which suggest that 86 to 93% of us have at least one marker. of metabolic dysfunction, right? And these are the metabolic syndrome criteria.

Speaker 1 But I think if you look around our population today, which you were hinting at, it's pretty sad. Many of us are obese and many of us are on a continuum of insulin resistance.
Right.

Speaker 1 And when you start to develop insulin resistance, and I'll talk about how this is probably related to seed oils in a moment.

Speaker 1 When you develop insulin resistance, I think this is what's impairing your immune system. We know that diabetics, full-blown insulin resistance, have a lot of trouble regulating their immune system.

Speaker 1 They can get a cut on their toe and they can lose their foot, right? Because they have such poor immune function. So as you move along this continuum of insulin resistance, the immune system suffers.

Speaker 1 And this is shown over and over and over, that insulin resistance impairs immune function.

Speaker 1 So I believe what's going on here is that in a diabetic, in any human that is on this pathway of insulin resistance, which we know is related to our processed foods and our lifestyle, you have impairment of the immune system in the arterial wall.

Speaker 1 So when you cut your knee, say you're like surfing or you hit a reef or you're skateboarding or you're dancing or whatever, you're playing baseball and you skin your knee, your immune system goes there to repair the knee.

Speaker 1 Well, all of us are getting, quote, skinned knees on the inside of our arteries because all of us have higher pressure in our arteries.

Speaker 1 But diabetics, anyone on this insulin resistant spectrum or continuum is going to have trouble repairing the endothelial damage that happens from daily life.

Speaker 1 And that, I think, is what's going on for diabetics that is causing atherosclerosis. All of us get damage to the arteries.
Most of us can repair it.

Speaker 1 Just like we, you know, I was playing a pickleball in Phoenix recently. I was there to surf a wave pool and I ran into a wall, right? I was going off the court because I stink a pickleball.
And

Speaker 1 I ran into a cement wall that was there. And

Speaker 1 I had a little strawberry on my knee. I had a little skinny on my knee.
My immune system repairs it. Right.
But when you have insulin resistance, it doesn't get repaired in time.

Speaker 1 And I think that is where the atherosclerosis starts. Diabetics have continuous damage without functional, actual true repair on the inside of their arteries.

Speaker 1 And that, I think, is what's going on that no one's talking about. So the problem is not LDL.
We should pay attention to it. If you're diabetic, okay, pay attention to it.

Speaker 1 But the problem is not the LDL.

Speaker 1 The problem is the insulin resistance and the immune dysfunction that comes with it and the persistent damage to the endothelium, the persistent damage to arteries that comes with it, which leaves you susceptible.

Speaker 1 Going back to the wood analogy, we have LDL, and I'm mixing my metaphors here, but I think about LDL as wood. And wood doesn't cause a fire unless there's a spark, right?

Speaker 1 And you can build things out of wood. You can build a cabin out of wood.

Speaker 2 But when you have more sparks, hormones, cell walls, cell membranes, vitamin D3.

Speaker 1 It does all of these things.

Speaker 2 All kinds of things are made from class.

Speaker 1 Yes, sex hormones, cell membranes. We need LDL.
We need, LDL is the carrier.

Speaker 1 LDL is the carrier for all of these vital things in the human body. It doesn't initiate atherosclerosis, but if you have lots of sparks, that dry wood can light on fire, right?

Speaker 1 And again, I'm mixing my metaphors here. I talked about PUFA earlier as drywood, but let's talk about LDL as drywood here.

Speaker 1 So

Speaker 1 yeah, hopefully that's not confusing for people. But I get the idea that like wood doesn't spontaneously combust into a fire.
Right. Right.

Speaker 1 Wood is valuable. LDL is valuable in the human body.
It also has immune roles.

Speaker 1 So to say that Apo B is what we should be lowering without any attention to insulin sensitivity, oxidized LDL, LP little A, it's just ludicrous to me. There's so much more to the picture here.

Speaker 2 Yeah, we want to make it so simple that LDL high, cardiovascular risk high, LDL low, cardiovascular risk low. So all you have to do is hammer this down.
And you know,

Speaker 2 it is astounding to me that most of the time we're actually not talking about

Speaker 2 you know, the toxic soup that we're bathing our cellular biology.

Speaker 2 And we want to, we want to continue to bathe our cellular biology in this toxic soup and then and then come down on top of it with a chemical or a synthetic or pharmaceutical and and allow that to be the answer without actually changing the habitual pattern that it brought you there i mean a lot of times when people talk to me about really wanting to lose weight um i walk them through you know for not to sound harsh but what what why are you so fat right let's figure out why you're so heavy and then let's not do that um and in the process of doing that we're also going to put some components in place to make sure that you really, you know, you lose weight quickly and safely and everything else.

Speaker 2 But to reframe the way that we talk about the state of the condition that we're in, you know, if you've got metabolic syndrome, the answer isn't, okay, well, let's add insulin and metformin and, you know, beta blocker, calcium channel blocker, diuretic, blood thinner.

Speaker 2 It is not to take the.

Speaker 2 the results of this toxic soup and start to manage it with synthetics and and chemicals and pharmaceuticals, but it's to say, how did we get into this condition in the first place?

Speaker 2 And, you know, and I think, you know, as I became more and more aware of seed oils,

Speaker 2 I mean, I have to say, for the consumer, it's hard.

Speaker 1 I mean,

Speaker 2 it is difficult to walk down a grocery store aisle.

Speaker 2 And, you know, the deception, in my opinion, in food labeling too, you know, heart healthy is right on the seed oil bottle, by the way, brother.

Speaker 1 I was in Costco the other day filming, and the corn oil has a big big heart healthy label on it.

Speaker 2 It's got the little heart.

Speaker 1 How is this possible? It's like an emoji. Because it look, like this is, this is ludicrous.
So let's talk about, let's talk about how we get insulin resistant. And because this is interesting to me.

Speaker 1 So when you go to your doctor, and I want. the people that are listening to think about this and your doctor checks your cholesterol.

Speaker 1 How often does your doctor do any metric that approximates your insulin sensitivity? Right. They're not really telling you about a fasting insulin.

Speaker 1 I have to constantly talk to people and say, ask your doctor for a fasting insulin. It's a $30 test that your insurance should pay for, but maybe your insurance won't pay, but it's $30

Speaker 1 for the amount of information it gives you. And most.

Speaker 2 Glucose, hemoglamin A1C.

Speaker 1 All of those also, or ratios of triglycerides, right? But I think fasting insulin is such a good metric of insulin sensitivity. And no one is getting it.

Speaker 1 And you're interpreting lipids without any context of your insulin sensitivity.

Speaker 1 I think every lipid panel should be paired with insulin, fasting insulin, because your lipids matter in the context of your insulin sensitivity.

Speaker 1 And this goes back to Dave Feldman's research, which we will get to.

Speaker 1 But I think that what's happening here for people, and this is where it gets really interesting, and we don't have randomized controlled trials here.

Speaker 1 So we're approximating mechanistic data, but it's really interesting to say that. As we talked about earlier, when you eat polyunsaturated fats, they get stored in your body.

Speaker 1 We just are full of them.

Speaker 1 And you mentioned a number earlier that it's important to bring up again, which is the fact that looking at kinetic studies of how we accumulate fatty acids, most people estimate that if you have been eating McDonald's and lots of seed oils your whole life, it takes you potentially four plus years, if you stop today, to fully recycle the membranes of all the cells in your body, the fatty acid depots, like the fat tissue probably being the least quick to recycle.

Speaker 1 But it probably takes about four years to really fully change the composition of all the cell membranes and all the mitochondrial membranes. Wow.
That's a big deal, right?

Speaker 1 There are potentially ways to speed that up that we can talk about, but they're pretty intense. Yeah, I'd like to talk about those.
Yeah.

Speaker 1 So, but what's going on is we are stuffing our cell membranes and we are stuffing our mitochondrial membranes with polyunsaturated fatty acids our bodies change based on what we're eating this is the thing that like not all calories are created equally the last time we talked we talked about my my my frustration with the notion that you can just eat less calories and even eat bad food, that you can somehow out diet or out exercise a bad diet.

Speaker 1 And it's not true because if you are eating french fries, yes, you could lose weight eating french fries, but you are immediately stuffing all of your cell membranes, all of your mitochondrial membranes, all of the cells in your fatty acid deposit with more polyunsaturated fatty acids.

Speaker 1 We are in flux.

Speaker 1 And so, evolutionarily inappropriate diets of polyunsaturated fatty acids that are already oxidized and susceptible to further oxidation in the human body are causing major issues for people.

Speaker 1 And I think that there's mechanistic data that points to the actual problem here.

Speaker 1 There is evidence that as the membrane of your mitochondria becomes more highly polyunsaturated, you actually get proton leak.

Speaker 1 So, the mitochondria is is a quite a complex little organelle, right?

Speaker 1 Probably evidence of endosymbiosis, this primordial connection that we had with some sort of a bacteria hundreds of millions of years ago, where a

Speaker 1 you know, a nucleated organism actually engulfed a bacteria, and that bacteria started working for us. And now we have trillions of these mitochondria in our bodies, and this is the way that

Speaker 1 our this is the way that our bodies convert food energy into kinetic energy. It's through the mitochondria.
This is where beta oxidation and glycolysis happen

Speaker 1 or the downstream effects of the downstream biochemistry after glycolysis happen in the mitochondria. So this is where the Krebs cycle happens.

Speaker 1 And so in order to convert food energy, which is potential energy, to kinetic energy, actual usable ATP, which we use to repair DNA, to make hormones, to make cellular processes, to rebuild our bodies, to run our brains, everything in our body happens with kinetic energy, ATP that comes from food.

Speaker 1 But in between are our mitochondria. So potential energy in food, kinetic energy used to make a vital, fertile, happy, healthy human being.
In between is our mitochondria. Right.

Speaker 1 If you break the mitochondria, and you've spoken about this at length. If you break the mitochondria, you get stuck with potential energy.
And what does that look like? That looks like fat humans.

Speaker 1 Yeah. Yeah.
And so

Speaker 1 it's not just about insulin-resistant humans. Fat insulin-resistant humans.
It's not just about calories. It's about what are those calories doing to your cellular energy factories.

Speaker 1 If they are breaking your mitochondria, you are going to store more of those calories.

Speaker 1 So when you look at a label on Doritos and it says 200 calories per serving, that is baloney because you can't actually make that Dorito into 200 calories of kinetic energy because there are ingredients in that Dorito, all sorts of ingredients that are breaking your mitochondria.

Speaker 1 And so when you stuff your mitochondrial membranes, right, there's two mitochondrial membranes.

Speaker 1 The inner mitochondrial membrane is kind of the ground zero inside the mitochondria is where the Krebs cycle happens, in deep in there.

Speaker 1 As you are doing this electron transport chain, you are moving protons across those membranes to create a gradient.

Speaker 1 And then the protons moving down the gradient through the little ATP motor complex five of the mitochondrial electron transport chain that's what makes ATP but if those if those protons are leaking back across you're not making ATP and that happens when you stuff your mitochondria with polyunsaturated fatty acids at an evolutionarily inappropriate level so there's lots of mechanisms by which stuffing your cells full of polyunsaturated fats creates a lot of problems for humans at this formation of energy level and i think that's what's hard for people to wrap their head around because it's like this is mechanistic research and we don't have a study in humans to prove that because who would fund it?

Speaker 1 Right, right, right.

Speaker 1 It's so tricky. But I think that it's pretty clear that we are doing something very wrong as humans today.
It's not just that we are eating too many calories. We're eating slightly more calories.

Speaker 1 But, and I talk about this in the FedILI documentary, in the last 20 to 30 years in the United States, we have not increased calorie consumption at all. And obesity has gone from 30% to 42%.

Speaker 1 We're not eating more calories. We're just getting fatter.
What's going on? We're not converting the food energy to kinetic energy because we're breaking our mitochondria.

Speaker 1 And there are other things that I believe break mitochondria, but I think seed oils are a major factor. We've never had these in our diets at this level.

Speaker 1 And I think that the way out, which you want to talk about, is stopping eating so many polyunsaturated fats, particularly this omega-6 linoleum.

Speaker 2 And it makes so sense with the big data because, you know, you would think with... the parabolic rise in statins,

Speaker 2 you would have a parabolic reduction in cardiovascular disease. Still the number one killer worldwide.

Speaker 2 We don't see much of a reduction at all in cardiovascular disease despite the revolution of statins. So we are well capable of controlling cholesterol,

Speaker 2 but we're not capable of controlling the cardiovascular disease. So is it possible?

Speaker 2 This is just why I want to open people's minds because your primary care physician might staunchly disagree with this. Is it possible that

Speaker 2 we've been actually firing the magic bullet at the wrong target? Absolutely.

Speaker 2 I think that we have, you want to talk about a pandemic. I think we have a pandemic in this country of holding organs responsible for crimes they didn't commit.
We do this with the thyroid.

Speaker 2 We do this through the heart. We do this with the, you know, most people that have,

Speaker 2 you know, cardiovascular diagnoses of, let's say, hypertension, you know, essential hypertension or,

Speaker 2 you know, type two hypertension, whatever you want to call it.

Speaker 2 These. people that have essential hypertension, 85% of the time,

Speaker 2 their origin is idiopathic, meaning it's of unknown origin. And so when we don't know the origin, how do we know the organ to hold responsible?

Speaker 2 It always fascinates me when we say things like, well,

Speaker 2 you got high blood pressure. We don't know why, but we're going to medicate the heart.
Well, what did you find wrong with the heart? Nothing. So why are we medicating the heart? Well, because

Speaker 2 we don't have anything else to do. But if you don't know the

Speaker 2 origin, how do we... How do we go after the organ?

Speaker 1 Right.

Speaker 2 And so I think that, you know,

Speaker 2 I've been deep down the rabbit hole of this lately. And it's, I think the,

Speaker 2 you know, most of the answers to human physiology are a little more complex and a lot less linear than I think modern medicine likes to make them, right? We're an ecosystem.

Speaker 2 human beings thrive in communities. Our cells thrive in communities.
Very often what we do is we take cells out of the body. We study them in a petri dish.

Speaker 2 We look how they behave in a lab or in certain media,

Speaker 2 manipulated media. And then we assume that when we put that cell back into the human body, it's going to behave the same way.
And it doesn't because you have this giant community. right?

Speaker 2 And I think what you're talking about is the

Speaker 2 cause and effect, you know, like the downstream effect of highly processed foods, highly refined sugars,

Speaker 2 and then all of the direct insults, forget the hormone disruptors and everything that we're putting on our skin, but the fake food dyes, the pesticides, the herbicides, the insecticides, the preservatives.

Speaker 2 All of these things are entering this community in our cellular biology, and they are wreaking havoc on its capacity to communicate and exchange with its outside environment.

Speaker 2 It's clogging up our proton pumps, it's actually interrupting our cell walls and our cell membranes. And when you do this at such a microscopic level,

Speaker 2 because we're just a

Speaker 2 thriving community of these organisms, you get these macroscopic results. And then we oversimplify it by saying

Speaker 2 it's just one thing, right?

Speaker 2 And so

Speaker 2 anyway, I digress a little bit, but but so let's go back. We put these in,

Speaker 2 they're they're pro-inflammatory. And in

Speaker 2 your case, what you mean by pro-inflammatory is they can actually embed themselves into the cell membrane, which is a

Speaker 2 lipid bilayer, by the way, for the folks that are, you know, what's around your cells is something called a phospholipid bilayer, which is sort of

Speaker 2 a little ring of fat, if you will. And

Speaker 2 not all fat is created equal. And when these highly oxidized fats get into those cell membranes, they have a hard time getting out.

Speaker 2 And that cell membrane is super important because it's the gateway from the interior to the exterior. You know, all of the good stuff is out in the serum of your blood.
We got to bring it in.

Speaker 2 Sometimes there's waste, and by waste, I mean cellular waste that's got to get out. And if you interrupt these channels, now you have a metabolically unhealthy cell.

Speaker 2 And we know, for example, that all cancer is a metabolic shift in the in the cell, right?

Speaker 1 It's all connected.

Speaker 2 It's also connected.

Speaker 1 It's all connected.

Speaker 2 It's also connected. Guys, let me let you in on one of my favorite snack foods.
This is masa chips.

Speaker 2 If you actually look at the back of the ingredients here, you'll see things that you read and pronounce and understand. Non-GMO corn, organic beef, grass-fed tallow, and sea salt.

Speaker 1 That's it.

Speaker 2 Sea salt, beef tallow, and organic non-GMO corn. Those are the kinds of ingredients we should be using to fuel our body.
Those are whole foods in their natural state. I love these.

Speaker 2 They come in four or five flavors. These are great for your kids.
You can replace your Doritos and your other seed oil laden chips with these.

Speaker 2 They're not super high in sodium, but they do use a little Redmond sea salt. It's mineral rich.

Speaker 2 And you know how much I talk about minerals and the need for the body to actually have the 91 essential minerals. We can get these from natural salts.

Speaker 2 So imagine combining natural salts with organic grass-fed beef tallow and non-GMO corn. This is a perfect snack.
This is guilt-free eating. You can replace Doritos.

Speaker 2 You can actually make nachos with these, all guilt-free. Feed these to your kids.
I keep them on my shelf. Keep them around.
It'll become your favorite snack.

Speaker 2 Now let's get back to the Ultimate Human podcast.

Speaker 1 So linoleic acid, this 18-carbon polyunsaturated omega-6 fatty acid, is also the most abundant fatty acid in your LDL.

Speaker 1 So your LDL is a balloon that carries cholesterol and triglycerides. The most abundant fatty acid in there is linoleic acid.

Speaker 1 So even if that linoleic acid is not oxidized before it gets in the LDL, the population of the membrane of the LDL changes when you eat more seed oils.

Speaker 1 So, you make a membrane that is more susceptible to oxidation, and you make a membrane that is more difficult for your body to manage in terms of oxidative stress at the level of the LDL.

Speaker 1 So, your actual LDL particle is full of linoleic acid when you're eating french fries and cookies and cakes and crackers and dressings.

Speaker 1 And if you don't eat those things, your LDL remodels very quickly. So, let's talk about how to detox.

Speaker 2 Yeah, yeah, let's talk about that.

Speaker 1 This is really interesting to me because it connects,

Speaker 1 it starts to connect a lot of the dots. So,

Speaker 1 canonical thinking is four years. So, okay, that's a long time.
But if someone is listening to this and you are eating seed oils and you just stop today, right?

Speaker 1 Today is the day before Thanksgiving, 2024. If you stop eating seed oils today, we'll give you till the day after Thanksgiving.
Yeah, okay, we'll give them one more day.

Speaker 1 Don't tell them I'm eating one more Thanksgiving. All right, day after Thanksgiving.

Speaker 1 Black Friday. Black Friday.
Seed oil, black Friday. You're not eating seed oils and anything else for the rest of your, you know, next four years.

Speaker 1 you will almost essentially remodel all of your cells, all the fatty tissues, all of your mitochondria in four years.

Speaker 1 But there are ways to speed it up and there are things to do to protect your body against the oxidation of these seed oils. Let's talk about speeding it up.

Speaker 1 This is interesting and probably, I will say from the outset, maybe not super practical for most people.

Speaker 1 So there are studies in monkeys, sebus monkeys, and I saw this today, where they were able to speed up the remodeling from four years to 30 days. Wow.

Speaker 1 But they fed the monkeys a very, very low-fat diet. And when you feed a very low-fat diet as a human, you don't feel good, right? And I'm not really advocating for this.

Speaker 1 I'm just telling you, research shows this in monkeys. And then it reminded me of something called the rice diet.
You ever heard of Walter Kempner? This guy's fascinating.

Speaker 1 He died in the 90s, but in the 1950s and 1960s, he took diabetics and he gave them a diet of processed white sugar and rice. A 2,000 calorie, very low-fat diet of almost white rice and white sugar.

Speaker 1 And their diabetes got better. It reversed.
Wow.

Speaker 1 But in order to do this, he had to lock them in a hospital, right? And there's controversy because apparently he had to like whip them to get them. You cannot keep a human on this diet.

Speaker 1 I'm not advocating for humans being whipped in metabolic wars, but it's an interesting study that would never be repeated today, right? Right.

Speaker 1 So it's a very, it's an example of a very low-fat diet in humans. And the pictures in his studies are remarkable.
It's like a very rotund man, and he's real thin after six months. Really?

Speaker 1 And the diabetes completely reverses. And even when Walter reversed or liberalized their diet, the diabetes did not come back.

Speaker 1 So there are now multiple data points of very low-fat diets leading to resolution of metabolic dysfunction. And I think what's going on here is accelerated membrane remodeling, right?

Speaker 1 So I'm just saying there are ways to do this. It's not easy.

Speaker 1 If a human wanted to accelerate the remodeling of your membranes, you could potentially eat a lower fat diet for 30, 60, 90 days. Understanding that a low fat diet is not super sustainable for humans.

Speaker 1 Right. But the other thing you could do is eat a very low polyunsaturated fat diet.
You can look at the amount of linoleic acid in your diet and lower it, even after avoiding seed oils.

Speaker 1 Should you avoid olive oil? Olive oil can be 12 to 28% linoleic acid, right? Avocado oil can be 20% linoleic acid. So I think you could accelerate.

Speaker 1 the turnover of your membranes toward a lower linoleic acid membrane state by eating no olive oil, no avocado oil. Again, do it after Thanksgiving, right?

Speaker 1 And just lowering the amount of linoleic acid in your diet. Beef tallow, 1% to 2% linoleic acid.
Butter, 1% to 2% linoleic acid. Avocado oil, olive oil, 12% to 25%, right? Canola, 25% linoleic acid.

Speaker 1 Soybean oil, 50%,

Speaker 1 right? Cowboy. Corn oil, 45%.
Grapeseed oil, 55 to 60% linoleic acid.

Speaker 1 So if you focus on the low linoleic acid animal fats, the ones we've been told that are bad for us, you can accelerate the turnover of linoleic acid in your cell membranes.

Speaker 1 And butter especially, I believe, could be protective. And I'll tell you why.
This is the second piece of this equation.

Speaker 1 So lower fat oils or fats, animal fats that are much lower in linoleic acid, I believe this will accelerate the turnover of your membranes.

Speaker 1 There's a fatty acid we were talking about this last night called C15, pentadecanoic acid.

Speaker 2 Pentadecanoic acid.

Speaker 1 Pentadecanoic acid. Most of the fatty acids in your cells are odd-chain.

Speaker 1 Saturated fats, C12, C14, C16, C18, Lauric, Moristic, palmitic, and stearic acid. They're all odd-chain, they're all even-chain fatty acids, right?

Speaker 1 Odd-chain fatty acids, C15 and C17, are starting to be understood, or we're looking at research.

Speaker 1 And there's research that suggests that C15 levels in your cell membranes can be protective against oxidative stress in your membranes. So polyunsaturated fatty acid peroxidation, lipid peroxidation,

Speaker 1 induced cell death is called feroptosis. So apoptosis is programmed cell death, but ferrotosis is oxidative stress-induced cell death.

Speaker 1 And C15 levels in your cell membranes protect against ferrooptosis. Wow.
So the ideal level of C15 in the study that I think was published in 2024,

Speaker 1 I think it's by Ven Watson is the main author, was 0.4 to 0.64% of your cell membrane is C15. Where do you get C15 in your diet? Butter and raw, butter and dairy.

Speaker 1 Dairy fats and butter are good sources of C15. In fact, they track so much that you can look at someone's C15 levels and tell how much dairy fat they're eating.
Really?

Speaker 1 Again, dairy fat being something that's been vilified, but you and I had raw milk. And in fact,

Speaker 1 I have to tell the story. So we got raw milk from Southwest Ranches.
I love these guys here. I love these guys too.

Speaker 2 And they helped out to them.

Speaker 1 They gave us glass containers of raw milk. And this is raw milk from a cow.
And this raw milk is so good that you can see the cream on top of the raw milk in the fridge.

Speaker 1 I left to go out to dinner last night.

Speaker 2 And as soon as he left, I slowly poured the cream off the top of the corner.

Speaker 1 You stole the cream off my milk. I literally did.
He admitted to it. I did.

Speaker 2 When he he came back, he was like, damn, you dog. You took it.

Speaker 1 He took all the good cream. But this is such good raw milk.

Speaker 2 This is a price to stay at my house.

Speaker 1 I will willingly pay the tax. Thank you for having me at your house.
But you can see, and we'll post a, I'll post it on my stories or something. We can post a video together showing this.

Speaker 1 Because I want to show this because there's a lot of raw milk that I get that you can't see. This cream versus milk.

Speaker 1 But like that cream on top of the raw milk, what you did there, Gary, is you got a C15 infusion.

Speaker 1 By stealing the cream off of the raw milk, which I willingly give to you,

Speaker 1 happy Thanksgiving, you had C15. And that C15 changes the composition of your cell membranes.
And that looks to be protective against feroptosis, lipid peroxide-induced cell death.

Speaker 1 So what are we worried about? What are we worried about with polyunsaturated fats? We're worried about lipid peroxidation. We're worried about cellular damage.
Eat dairy fat.

Speaker 1 This means butter is healthy. Coils are garbage.
So doing more butter, and less or no seed oils could also be protective.

Speaker 1 So in summary, I think there are human and monkey or primate studies showing that low-fat diets can accelerate this.

Speaker 1 And I think if you really want to accelerate turnover of your cell membranes to detox from seed oils, you have to get low linoleic acid in your diet.

Speaker 1 Low linoleic acid, which probably means even avoiding, if you really want to optimize avoiding avocado oil, avoiding olive oil, and focusing on butter, especially with C15 or tallow.

Speaker 1 long term that would be i think that there's a case to be made for that in the research and look

Speaker 1 maybe in this administration we'll actually get some funding to do that study right Yeah. So this, this is the thing.

Speaker 1 I will freely say there is no randomized double-blind controlled trial to prove that, but I'm connecting the dots with the research that's out there. There are mechanistic studies.

Speaker 1 There are studies to suggest that this happens in both humans and in primates. And so I think it's very reasonable to do that.

Speaker 2 And you know what I find is that a lot of randomized clinical trials essentially end up proving what we know ancestrally from nature. You know, it always takes us back to the basics.

Speaker 2 It's interesting how it comes full circle. You know, we go deep down into into isolating the oils and

Speaker 2 their origin and whether or not they're processed or not. And it just basically gravitates us back towards the basic whole foods.
Simple things.

Speaker 2 How can you go wrong eating because nature designs it perfect?

Speaker 1 How can we go? You can't go wrong eating simple whole foods. It's just unprocessed animal foods, unprocessed plant foods, you'll be great.
Yeah.

Speaker 2 So we want to go down the road of supplementation, right? I mean, we have essential fatty acids, we have essential amino acids, you know, essential meaning they're necessary for life.

Speaker 2 I don't think many people are not getting these, but

Speaker 2 there's so many different fatty acid supplements, fish oil supplements, black seed oil supplements.

Speaker 2 I know plenty of people

Speaker 2 that do a shot of really good olive oil first thing in the morning, which I'm actually a fan of.

Speaker 2 I need enough of it that I don't have to do it, but I'm a fan of people that don't get enough doing that.

Speaker 1 So what are,

Speaker 2 you know, first of all,

Speaker 2 can you give a little explanation of the difference between an omega-3 fatty acid and an omega-6 fatty acid and why the ratio is important

Speaker 2 and where we get omega-3s and six.

Speaker 2 And, you know, if somebody's listening to this and they want to start taking a BPA or DHEA or needs to take a fatty acid supplement, you know, what do you recommend or do you recommend getting it from diet?

Speaker 1 So omega-3 is also polyunsaturated. And omega-3 versus omega-6 is just a nomenclature designation based upon where the first double bond is based from the the end of the molecule.

Speaker 1 So if you look at a fatty acid, it's a long chain of carbons with a carboxylic acid group on the end. And the first

Speaker 1 desaturation point, which is a double bond, if it's close to the end of the molecule, if it's three carbons from the end, we call it an omega-3.

Speaker 1 If it's six carbons from the end, we call it an omega-6.

Speaker 1 Omega-3s

Speaker 1 are in much smaller amounts in our diets than omega-6s.

Speaker 2 And need to be in higher amounts, yeah.

Speaker 1 Well, they probably should be in higher amounts for most of us, right?

Speaker 1 Many of us, you and I, get plenty of omega-3s and maybe don't need to increase, right? Right. Omega-3s occur naturally.

Speaker 1 And omega-3s we're talking about, ALA, which is alpha-linolenic acid, not linoleic, alpha-linolenic acid, DHA, docosahexanoic acid, EPA, I-cosa, or E-cosa hexa, or E-cosa pentanoic acid, and DPA, do-causea pentanoic acid.

Speaker 1 And there's a, there's a... sort of a biosynthesis pathway and the pathways parallel, right? So the there's the same exact series of enzymes.

Speaker 1 These are desaturases and elongases that turn ALA into DPA, and they also turn linoleic acid into arachidonic acid and other omega-6 downstream metabolites.

Speaker 1 And so D5D, D6D, these are shared enzymes between omega-3 and omega-6.

Speaker 1 And one of the things we know is that if you're eating a lot of omega-6, and I would argue that humans are eating evolutionarily inappropriately high amounts of omega-6, and probably for many, evolutionarily, inappropriately low amounts of omega-3,

Speaker 1 because processed foods don't have much omega-3, but they're full of omega-6. This is a problem because these parallels are path,

Speaker 1 these pathways are parallel.

Speaker 1 And when you eat too much omega-6, all the enzymatic activity of those shared enzymes goes toward the omega-6 pathway, and you can't really biotransform the omega-3s, right?

Speaker 1 You can get pre-formed omega-3s in your diet, but...

Speaker 1 you are not really going to be able to biotransform anything that you're, if you're getting ALA, alpha-inolenic acid, or any of the upstream omega-3 metabolites, and you want to turn them into DPA or downstream metabolites, you can't do that well if you're eating a lot of omega-6.

Speaker 1 So if you look at the amount of omega-3 that I eat, it's pretty small in my diet. Relatively speaking, I have egg yolks sometimes and I get my omega-3s from animal fats.

Speaker 1 There's omega-3s in that cream, on the milk, right? There's omega-3s in meat.

Speaker 1 I don't feel like I need to supplement with a fish oil because I'm eating unprocessed animal foods that are primarily fed grass. And my body can biotransform.
alpha-linolinic acid into EPA, DHA, DPA.

Speaker 1 I've done these checks and I have lots of EPA, DHA, and DPA in my body. And I don't take a fish oil supplement.
Good. Because I'm eating less omega-6.

Speaker 1 I have very low levels of omega-6, so my body can use those parallel elements.

Speaker 2 Where does the omega-6 come from?

Speaker 1 The omega-6 comes from seed oils, right? Primarily.

Speaker 1 Yeah, you can get a little bit of omega-6 if you're eating almonds. I don't think that's a problem for most people that you can digest almonds.
That's a separate conversation that we've had about.

Speaker 1 I don't think almonds are very digestible, but

Speaker 1 you're not getting a lot of omega-6 if you're eating unprocessed plant foods. You're just not.
But you're getting a lot of omega-6 from the seed oils. Now,

Speaker 1 asterisk: we are also getting evolutionarily inappropriate amounts of omega-6 from things like chicken and pork. Because

Speaker 1 going back to our previous point, humans, chickens, and pigs are all monogastric animals. We all store polyunsaturated fats.

Speaker 1 When you are eating a chicken and the chicken thigh is going to be fatty, or if you're eating a chicken thigh and that chicken is fed corn and soy, just like humans that are fed corn and soy oils, that chicken is accumulating linoleic acid in their fatty acid, in their tissues.

Speaker 1 So chickens historically, if you look at wild chickens, 4% linoleic acid in their fat. Chickens today, 20%.

Speaker 1 Wow. Same with pigs.
4% to 5% wild hogs, right? 4% to 5% linoleic acid in their tissues. Today, 20% linoleic acid in the tissues.

Speaker 1 So do I think that eating traditionally raised pork and chicken is the major contributor to linoleic? No. This is not the biggest.
It's mostly seed oils.

Speaker 1 But if somebody is really trying to be aware of evolutionarily appropriate, biologically appropriate consumption of linoleic acid. You have to start thinking about your bacon.
I'm sorry.

Speaker 1 And look, like you can do it, you know, raise your own pigs, let them root in the ground, let them eat bugs and worms and mice, because they do eat other animals, and let them eat roots.

Speaker 1 Don't feed them corn and soy, and your pigs will have much lower amounts of linoleic acid. There are more and more of these producers out there doing low LA pork.
Wow. Historically,

Speaker 1 we are eating.

Speaker 1 pork that is full of linoleic acid because of what they're fed.

Speaker 1 So most of it is coming from seed oils and it's coming from, and this also happens with our eggs, Gary, too, which is why it's important to eat chickens or eggs from chickens that are eating the right things, right?

Speaker 1 Right. So if chickens are eating better, there's less linoleic acid in their eggs.
But if chickens are eating corn and soy, they pour more linoleic acid into their eggs.

Speaker 1 And so there was recently an article that came out about this, you know, like the amount of linoleic acid in egg yolks is higher than it probably should be historically. Wow.

Speaker 1 So the quality of what your chickens is eating. And I don't want this, at this point, I'll pause and say, I don't want this to be overwhelming for people.
Right. Knowledge is power.

Speaker 1 Know better, do better. Right.
I'm just offering information that anyone listening to this can use wherever they are on their health journey. Right.

Speaker 1 If your first step is getting rid of seed oils, get rid of seed oils. Keep eating pork, keep eating chicken, keep eating your eggs.
Don't worry about that yet. That's step three.
That's step three.

Speaker 1 But I'm giving you all the steps, right? So that's where all of the linoleic acid is coming from in our diets. And it's kind of tough because when you think about it, we're getting it from all angles.

Speaker 1 If the chickens that you're eating are fed corn and soy and the pork you're eating is fed corn and soy and the eggs are coming from chickens that are fed corn and soy, and you're eating sweet oils, and then you're making and you're making sauces, you know, out of corn and soy.

Speaker 1 Yeah, yeah, then how is it any wonder? You know, like think about all of these inputs in our diets.

Speaker 1 And this, I'll go back to this phrase: evolutionarily inappropriate consumption of excess amounts of linoleic acid in our diet. And I think it's a real problem for humans.

Speaker 1 And again, it happens at every level. The good news here is that beef is a ruminant, right? Beef, so cows, bison, lamb, elk, deer, these animals do not bioaccumulate linoleic acid.

Speaker 1 They have the biochemical machinery to saturate polyunsaturated fatty acids. We do not.

Speaker 1 So if a cow is fed grains, it has essentially the same amount of linoleic acid in its fat as a cow that's fed grass.

Speaker 1 I think a cow is better when it's fed grass, but a grain-fed cow does not have the same magnification of linoleic acid in its tissue as a chicken because

Speaker 1 they're monogastric or a human, right? Not that we're eating humans, but like humans store this. So we have the same issue.

Speaker 1 There's evidence from, I guess, archaeology or anthropology that in our fatty tissues, humans historically had 2%, 3% linoleic acid. And now we're looking at 20-plus percent

Speaker 1 linoleic acid or fat. So we are the same as a chicken or a pig being stuffed.

Speaker 2 And what's the consequences of all of this linoleic acid? Is it because it's composition of the cell membrane?

Speaker 1 Back to the mitochondrial thing we talked about with the proton leak and, you know, potentially impairing at a cellular energy level, the hypothesis, which I think is supported by the literature, is that it's impairing the biotransformation of potential energy to kinetic energy.

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Speaker 2 You know what's interesting too is that I don't advocate really, really hardcore. dog dogmatic carnivore diets but for periods of time um i've used things like keto reset, carnivore reset.

Speaker 2 People's energy level goes through the roof. Now, I know that is a lot of it is eliminating the bad, right? I mean, that's probably 70% of it.
The other is the presence of the good.

Speaker 2 And I don't think that I've had a client that I've put on one of these reset programs, including Dana White, that went through it for 10 weeks,

Speaker 2 that didn't report like significant increases in energy, significant increases in mental clarity,

Speaker 2 significant reduction of gut-related issues, even if their gut-related issues were mild, and some were very severe.

Speaker 2 I mean, borderline, pathological diperticulitis, Crohn's, irritable bowel syndrome,

Speaker 2 you know,

Speaker 2 ulcerative colitis, you know, like really

Speaker 2 complicated

Speaker 2 concepts in the bowel.

Speaker 2 And

Speaker 2 you see reductions in almost as though it's healing that single-cell layer

Speaker 2 in the luminal wall of the intestine, too, because you actually do see inflammatory markers like C-reactive protein go down.

Speaker 2 And I see improvements in alkaline phosphatase. I see increases in EGFRs, these glomerular filtration rates, which is another sort of ancillary sign that inflammation is dropping.

Speaker 2 As you reduce inflammation, you can increase the filtration rate, lower the poison levels.

Speaker 2 So, you know,

Speaker 2 what's interesting is when

Speaker 2 you move people onto these transition

Speaker 2 diets, and the one that you just told me about is pretty aggressive, sugar and white rice.

Speaker 1 I'm not advocating for that one. That one really caught me off guard.
But it's low fat. It illustrates the point, right? Yeah, yeah, it's low fat.

Speaker 2 It illustrates the point.

Speaker 2 You actually see, it's like the tide raises and lowers all the ship.

Speaker 2 You see like increased, you know, the thyroid production of T4 starts to rise. C-reactive protein goes down, homocysteine levels drop, filtration rates increase in the kidneys.

Speaker 2 You see obviously hemoglobin A1C, three-month averages of blood sugar going down, fasting insulin reducing,

Speaker 2 overall insulin levels reducing, even alkaline phosphatase and liver enzyme levels, AST, GGT, you know,

Speaker 2 ALT,

Speaker 2 these sort of secondary markers of inflammation in the liver.

Speaker 2 You know,

Speaker 2 and

Speaker 2 not that all these levels collapse, but if you if you compare labs 10 weeks apart and all you did was really put them on something like a carnivore diet, or in some cases, a ketoreset,

Speaker 2 you see this systemic improvement in all of these levels. And, you know,

Speaker 2 that's probably a podcast for another time, you know, the gut being the gateway to the rest of the body. But

Speaker 2 I have seen those, you know,

Speaker 2 those results in patients too. And a lot of it is.
you know, probably eliminating these seed oils, but the positive effects are rather immediate.

Speaker 1 I mean, you know, I mean, you and I both, I mean, we talked about this on the first podcast that we did. I wrote a book about the carnivore diet.
Yeah.

Speaker 1 I think that something with more foods works better for me and a lot of people long term. But think about what happens if you just eat steak.

Speaker 1 You are just eating animal fat, which is very low in linoleic acid.

Speaker 1 You're essentially doing a gut reset because you're just eating meat, which is very highly digestible for most people, contrary to popular belief. And you're eating only animal fat.

Speaker 1 You're not eating olive oil or avocado oil. You're not eating anti-seed oils.
You're not eating any oils that are high in linoleic acid. A lot of things get better.

Speaker 1 I think that for a lot of people, it doesn't work long term. It gets a little too limiting.
Right. That's why I said temperature.
Yeah, yeah. But it can be really powerful.

Speaker 1 And I think that this is where I'm interested in this idea of an animal-based diet, kind of this in-between.

Speaker 1 And on some recent podcasts, I thought maybe animal-based is kind of like carnivore 2.0, right? You do, maybe you do carnivore as a reset, or you can just go right to animal-based.

Speaker 1 And animal-based, for people that don't know, it's just a term that I've used to help people understand the framework is like meat plus fruit. Right.

Speaker 1 So like, you know, I've got some squash in there on the table. Squash is a fruit.

Speaker 2 You're making orange juice in the rain. Making orange juice.

Speaker 1 Like, but the meat plus the fruit, and obviously you're getting the organs in there too, that works really well as well. And it's a little more sustainable.

Speaker 2 And you're not afraid of the, you know, the fructose, fructose in the blueberries. And it's, it's really the combination of having the glucose and the fructose together.

Speaker 2 I think the body's metabolizing those, not just the presence of fructose on its own.

Speaker 1 I think we talked about on the bottom. Because a lot of people attack blueberries.

Speaker 2 It's crazy.

Speaker 1 And I've even seen people attacking honey. Yeah.
and you and i we we geek out on honey because i brought you this honey from my house in costa rico

Speaker 1 mariola honey dude oh this is bum that you didn't bring it to me stingless bees i'm bringing it next time stingless bees those are my kind of bees they're amazing so i have a hive in my house mariola honey but there's been people attacking honey recently but if you look at the medical literature you can't attack honey yeah i mean honey improves insulin sensitivity sucrose not so much which is you know this pure molecule that's been extracted from the honey honey has over 300 bioactive compounds But honey improves metabolic function in humans and honey improves testosterone.

Speaker 1 And there's review papers written about honey for metabolic illness. It's wild.
And we get so myopic in medicine, kind of like with the LDL, we just focus on blood glucose. Right.

Speaker 1 Blood glucose is a symptom of underlying metabolic dysfunction. It's not the metabolic dysfunction.
Right. Eating honey does not cause insulin resistance.
Honey doesn't cause diabetes.

Speaker 1 If you have diabetes, honey is going to spike your blood sugar, but it didn't cause it.

Speaker 1 So if you have diabetes, yeah, don't eat as much honey as you or I, but small amounts of honey, probably beneficial and honey didn't cause the problem.

Speaker 1 We have to point, we have to point the weapons at the actual cause. Right.
If you point the weapon at the wrong cause, you're just putting your resources where they shouldn't be.

Speaker 1 And as we talked about, Apo B, wrong place to put your weapon, right? Insulin resistance. Glucose, fructose, wrong place to point your weapon.
Point your weapon at insulin resistance.

Speaker 1 The same thing with fruit. If you look at someone who's trying to make a case that fructose is harmful, invariably they will cite studies in animals who don't have the same biochemistry.

Speaker 1 They do much higher rates of de novolipogenesis when they are presented with fructose. Meaning, if you give fructose to a rat, it's making much more of that into body fat than we do as a human.

Speaker 1 We do 1%.

Speaker 1 You give a human, 1% of fructose goes to fat. via de novolipogenesis.
Most of it goes to glucose. It goes to, you know, glycogen.
It goes to lactate.

Speaker 1 Like glucose, I mean, fructose doesn't turn into fat in humans anywhere near like it does in animals.

Speaker 1 So you can't look at animal studies for fructose metabolism because it's completely different, right? It's completely different.

Speaker 1 And if you look at human studies with fructose, they are, as you suggest, invariably giving pure fructose.

Speaker 1 There's not a single fruit or honey or anything on the planet where you're getting pure fructose without glucose. Right.
And in the gut.

Speaker 1 It's all symporters. It's all transporters that need glucose and fructose to move across the gut lining.
Yeah. And so if you get free fructose in the gut, it gets stuck in the gut.

Speaker 1 Well, what happens if fructose gets stuck in the gut? It causes overgrowth of pathogenic bacteria. And then you get lipopolyphosa, you get lipopolysaccharide, you get endotoxin.

Speaker 1 So they've done these studies in animals where they'll give free fructose and they'll give something that blocks TLR 4 or 5, totalic receptor 4 or 5, which is what endotoxin triggers eventually.

Speaker 1 And the negative effects of fructose are essentially abolished. Wow.
So the negative effects of fructose at the level of the gut and humans is driven by endotoxin.

Speaker 1 And we don't get more endotoxin when we eat fruit.

Speaker 1 In fact, I think you could easily make a case that when you eat a blueberry or you're eating a persimmon or you're eating orange juice, endotoxin, which is lipopolysaccharide goes down.

Speaker 1 But the harmful effects of fructose in humans are isolated fructose feeding, leading to LPS. So it's just, it's again, it really mirrors a lot of the discussion around seed oil research or APOB.

Speaker 1 I think that the people, I think that people in the health space are well-intentioned and super intelligent, but I really hope we can all come together and consider all of the research in its entirety with candor with candor you know because i think that if you just if we're it's it's hard we need a lot of people to look at this because it's easy for one person and and i will raise my hand you know like i want to collaborate with people who think differently than me it's easy for one person just to see the research in less than its entirety and if you're only looking at the fructose research in humans that's isolated fructose feeding or you're only looking at the research with ldl in people that are insulin resistant or you're only looking at the seed oil research in the trials that are flawed because of their design right you're gonna come to the wrong conclusion Yeah.

Speaker 1 And that's the problem here.

Speaker 2 Yeah. I totally agree.
Well, what else is exciting you, man?

Speaker 2 What's new with Paul Saladino?

Speaker 1 Man, I think that all of this is super exciting for me.

Speaker 1 I mean,

Speaker 2 the ability to affect public policy research, we talk about this all the time. Is maybe to be

Speaker 1 Make America Healthy Again gets me pretty excited.

Speaker 1 I was pretty bummed to see RFK Jr. with the photo of the McDonald's on a plane.
You can bummed me up too. RFK, come on.

Speaker 1 But I believe his heart is good, and I'm really excited to see where it goes over the next four years. I mean,

Speaker 1 who Jay Bhattacharya, did you see this? Head of the NIH?

Speaker 1 Yeah, this researcher from Stanford was recently nominated for the head of the NIH. So Jay Bhattacharya was one of the guys kind of raising the alarm during COVID.

Speaker 2 Oh, yeah, yeah. No, no, I did just see, but he was pointing it.

Speaker 1 Yeah, he was nominated for the head of the NIH.

Speaker 1 RFK Jr., head of health and human services.

Speaker 1 I think Marty Macquarie is

Speaker 1 head of the FDA potentially, right?

Speaker 1 So it's going to be interesting to see where this goes. Yeah.

Speaker 1 Because I think that at the level of the Senate, you have a Republican-controlled Senate, but you have a lot of people in the Senate who have ties to big food.

Speaker 1 So I think that there's going to be an, hopefully, there's enough pressure.

Speaker 2 There's five lobbyists, according to Callie Means. I mean, five lobbyists for every member of Congress.

Speaker 1 This is crazy.

Speaker 2 It's mind-numbing.

Speaker 1 It's mind-blowing.

Speaker 2 Can you manage just five people whose 40-hour work week is is designed to do nothing but influence your decision? Decision-making. I mean, the amount of inbound that you must have to deal with, just

Speaker 2 five people assigned just to you for a single sector of what you're working on

Speaker 2 as a congressional service person. I mean, it's

Speaker 2 pretty intense. And I think there's a lot of light being shed on this now, the corruption in the food supply, the corruption in the nutritional research, you know,

Speaker 2 the conflicts of interest, you know, if not worse.

Speaker 1 At the USDA.

Speaker 1 So maybe somebody was, I mean, I wonder who's going to head the USDA, but Nina Teisholz, who's in this seed oil documentary, has pointed out 19 out of 20 members of the USDA Dietary Guidelines Committee 2020 to 2025 had ties to pharma and processed food industry.

Speaker 1 Things like ILSI, the International Life Sciences Institute, which is just a euphemistic title for a lobbying group for Pepsi and Kraft and General Mills.

Speaker 1 95% of them had ties.

Speaker 2 This is the USDA Dietary Guidelines Committee that makes policy for food and food stamps and school lunches yeah it's crazy it is it is really absolutely ludicrous the amount of corruption at those levels is sickening yeah and look the amount of damage that the corruption causes really what's sickening i mean you know um i think politicians have been taking you know money for favors for for for decades but You know, this is especially troublesome, you know, especially in the era where we have the highest rates of childhood cancer that we've ever had,

Speaker 2 highest rates of childhood obesity that we've ever had, the most skyrocketing rates of autism, Ashbergers, ADD, ADHD, OCD, manic depression, bipolar, and like these conditions that you just never heard of 30 or 40 years ago, 50 years ago, that are now so prevalent.

Speaker 2 You know, I remember RFK made a statement. It really hit home with me.
He said, when I graduated high school, and I graduated high school in 1988, so I'm really... dating myself there.

Speaker 2 You know, I just, I didn't know an autistic child. I didn't have any autistic friends.
I didn't know what that was. And I didn't know someone who knew someone who was.

Speaker 2 My 16-year-old knows 10 kids in her school. She could name 10 people that openly have autism or they're

Speaker 2 in

Speaker 2 programs that are related to

Speaker 2 autistic children or

Speaker 2 kids with other kinds of neuroinflammatory conditions.

Speaker 2 You think, wow, you know, that's super anecdotal, but in my mind, it went from zero to one, you know, to 10.

Speaker 1 And this is not increased screening. This is not, this is increased incidence, right? This is not that we're more aware of it.
No.

Speaker 1 When you were in high school, when I was in high school, there were not undiagnosed kids with, there was just no kids. Right, right.

Speaker 2 When someone has autism, this wasn't socially, you know.

Speaker 2 unpopular, you know, like like

Speaker 2 some of the sexual choices today. It wasn't wasn't that people were hiding it.
It was that they just didn't have

Speaker 2 to be.

Speaker 1 These are not something you can hide. Yeah.
This is increased incidence. This is humans getting less healthy in front of our eyes.
Yeah. You know, real time.

Speaker 2 To continue the corruption at that level with that kind of expense, it's crazy. You know, is astounding to me.

Speaker 1 And we talked about this earlier.

Speaker 1 The USDA recently came out and tweeted, we don't have enough data that ultra processed foods. And I saw that ultra-processed foods.
I was like, what is it on enough data?

Speaker 1 The USDA Dietary Guidelines Committee 2020 to 2025, thankfully they're out of here in like a year.

Speaker 2 Not even a couple months.

Speaker 1 Yeah, yeah. Okay.
So they

Speaker 1 tweeted, we don't have enough data. We need more data.
Who's going to fund it? That ultra-processed foods are behind the obesity crisis. Are you crazy?

Speaker 1 I mean, there's Kevin Hall did a study about this, and there's another study that was published that's essentially the exact same thing.

Speaker 1 You put people in a metabolic ward, you control everything they're eating for two weeks.

Speaker 1 When you give them the same amount of calories, but they can eat as much as they want in ultra-processed food or processed food, ultra-processed food or unprocessed food, they consistently eat more ultra-processed food.

Speaker 1 They gain two pounds a week. I think was the study.
Maybe, yeah, something like that. Two pounds pounds a week on ultra-processed food.

Speaker 2 Dr. Hyman talked about this.

Speaker 1 They're given the exact same calories. They try to match everything for sugar, salt, fat, macros.

Speaker 1 The ultra-processed food is just more addictive. It doesn't trigger satiety.

Speaker 2 It's more addictive and

Speaker 2 it's less, you know, it's nutrient-deprived, so it's less satiating, right? And if you look at the mechanisms for GLP-1,

Speaker 2 they have a lot to do with the nutrient density of food, releasing the GLP-1, giving us that satiation response.

Speaker 2 So if you don't release the GLP-1, if you don't create a satiation response, you're now just, you eat in the same volume and caloric intake

Speaker 2 and you're still hungry because your brain is like, I still need...

Speaker 2 beta-carotene and iron and you know i need a complex of b vitamins like i'm nutrient deficient so let's keep putting stuff in so i can just get the basics of of what i need i mean inherently we know that there's natural natural ozempic it's meat and you know plant foods like yeah try to overeat red rice yeah it's hard.

Speaker 1 Meat, try to overeat a steak, you know? Like, that's natural as Empic, man. Like, meat and a salad, meat and fruit.
It's hard to overeat that, which is why it's hard to hit it. It kind of kills me.

Speaker 2 You know, I think it's so, so crazy that we push down on the top of this pandemic of obesity rather than pushing up from the bottom. You know, I mean, again, it's the toxic soup.

Speaker 2 We're bathing our cellular biology and not just this magic, you know, obesity sort of. You know,

Speaker 2 I think classifying it as a disease makes people think it happened to them and not have

Speaker 1 in them.

Speaker 2 Yeah. Do you know what I mean?

Speaker 1 Like I caught this, like I caught the flu. Right.
Right. That happened.
That's genetic.

Speaker 2 You know, you got on the plane, you took a long flight, and then, you know, the next morning you woke up and you got a sore throat or, you know, you're sick.

Speaker 2 I mean, that, that, that, the influenza happened to you. Diabetes didn't happen to you, right? It happened within you.

Speaker 2 Um, and I think that if we can sort of shift the narrative a little bit, um, you know, get physical education back in the public school system.

Speaker 1 Um, put them in the sun.

Speaker 2 Stop, yeah, put them in the sun, put kids out of the street.

Speaker 1 They do let them go in recess.

Speaker 2 But I saw Tim Gray from the UK did a post the other day where he actually showed a study that

Speaker 2 prisoners,

Speaker 2 incarcerated prisoners, gets more sunlight on a daily basis than grade school children because they're actually required by law to be outside for an hour. They're given an hour outside every day.

Speaker 2 Whereas, you know, kids get in a covered, go from a covered house to a covered garage to a covered car to a covered school, staying there all day, and then go to a covered car to a covered garage, back to a covered house.

Speaker 2 And we just

Speaker 2 wonder why we're facing a lot of these crises. And eventually the research is just going to, again, it's going to bring us back to the basics,

Speaker 2 sunlight, grounding, you know, movement, exercise, whole foods. And, you know, the

Speaker 2 possibility of even cleaning up the

Speaker 2 public school food. You know, like

Speaker 2 when they made the announcement that, you know, the federal government was going to subsidize lunchables. for the public school system.
I was like, this isn't even food.

Speaker 1 What?

Speaker 1 So we're getting way off the going way down the rabbit hole, but

Speaker 1 it's all relevant. It's all connected.
We're not that far down the rabbit hole.

Speaker 1 And you've seen this clip of Fatima Stanford, who I think is a Harvard physician on 60 Minutes with Barbara Walters telling her that obesity is a genetic disease. I know.

Speaker 1 And I will paraphrase her, but I'm basically, this is pretty close to what she said. She said, even if you do diet and exercise right, 60 to 75% of people will become obese.
That is absolutely.

Speaker 1 That is absolutely not.

Speaker 2 Why didn't we have this in the 50s then? It's malarkey. We had genetics back then.
That's malararchy.

Speaker 1 Oh my gosh.

Speaker 1 And she's paid by Ozempic. She's on.
And going back to what we were saying earlier, Darius Mazafarian, who writes this meta-analysis on seed oils, paid by Bungie, seed oil manufacturer, right?

Speaker 1 So again, I'm not saying it's all like that. I think their researchers get it right, get it wrong, even if they're not funded by industry.

Speaker 1 Let's be honest about who's funded by industry and really talk about this. When,

Speaker 1 you know, when you're Tufts, you know, nutrition food compass guy is funded by seed oils. Yeah.
He's funded by ultra-processed food.

Speaker 1 And, you know, and then this, this woman at Harvard is on 60 Minutes saying it's a genetic disease.

Speaker 1 You're receiving funding from Ozempic. Come on.

Speaker 2 Yeah.

Speaker 2 What are we doing? Tell me what gene in the genome carries the fat gene. I mean, which gene gene gene gene gene gene.

Speaker 1 Where's the fat gene? Yeah. Yeah.
I don't know.

Speaker 2 I've spent the balance of my adult lifetime studying epigenetics, and I don't know about that gene.

Speaker 1 But it's genetic, so it's genetic.

Speaker 1 You can't avoid it.

Speaker 2 You know, we say it's genetic very often when it runs in families. And a lot of times that's another fallacy is that because things run in families, they're genetic.

Speaker 2 And that's absolutely patently false.

Speaker 2 I mean, there are certainly conditions that are genetically inherited, but significantly less than we've been led to believe. And one of them is definitely not obesity.

Speaker 1 I think you can be predisposed. Yes.
But the predisposition is not a predetermination.

Speaker 2 You can put somebody without the fat gene

Speaker 2 in the wrong environment. Right.
And they're going to be obese. Right.
I mean, obesity is in, you know, when I would go to Disney World or

Speaker 2 Universal Studios,

Speaker 2 you know, I always tell the story of, you know, I spoke at Access Hollywood one time and I was walking from

Speaker 2 the back of the park where they picked me up to the studio. And as we're cruising through the park, you know,

Speaker 2 I mean, you want to see what bad shape we're in as Middle America? Just go to Disney World and just take a look around. And I made a comment about the fanny packs that people were wearing.

Speaker 2 And I was like, what's with the fanny

Speaker 2 pandemic? And I was just making a joke because everybody I saw had a fanny pack on. And

Speaker 2 the security guard just very flippantly said, oh, that's because they can't put their hands in their pockets. And I was like, whoa, dude, you're right.

Speaker 2 They actually can't get their hands in their pockets. But, but my other point is that you could see the lineage.
You know,

Speaker 2 there was like obese grandma in the motorized wheelchair, very often with a two-liter of soda in the basket. Oh, yeah, yeah.
And then,

Speaker 2 you know, mom is, you know, kind of waddling not far behind. And then a rather obese 12, 13-year-old kid.

Speaker 2 And I don't think the grandmother passed the gene to the mother, passed it to the son. I think you look at the, you know, the epigenetic in the same way.

Speaker 1 They're all eating the same foods. They're all in the same environment.

Speaker 2 And then he's sitting on a, you know, a

Speaker 2 bench with a, you know, a funnel cake and a 64-ounce big goal. And I'm running the math in my head.
I'm like, 64 ounces of soda. Okay, so that's 29

Speaker 2 teaspoons of soda. Okay, so that's because it's five sodas.
Sugar, yeah.

Speaker 2 So like running the math. And a funnel cake is just white flour deep-fried in seed oil with 10x sugar.
Yeah, and he's just that's that's what's going in.

Speaker 2 I'm just like, you know, and of course, he's sniffling and wiping his face. And I just felt I felt bad, and I felt like how uninformed these people must be.

Speaker 2 Because, you know, if you, if you went to that mother, she loves her kid, you know, I consider it child abuse, but that, that also implies that they really are aware and know what they're doing.

Speaker 2 I think just the pendulums just swung that far. We're that far off of any semblance of even basic, you know, fundamental nutrition.

Speaker 1 So and I think that RFK Jr. put this in the right context.
This is poison. I think that you have foods that promote health in humans and then you have poison.

Speaker 2 Yeah, and you have non-foods and then you have poisons.

Speaker 1 I agree. I agree.
You have poisons. You got like, like,

Speaker 2 you know,

Speaker 1 serves you neutral. damage.
And these are metabolic poisons. Yeah.
Metabolic poisons that are legal. So cigarettes regulated, alcohol regulated, right?

Speaker 1 Raw milk is illegal in many places, but metabolic poisons are illegal. And that's what's not, I don't think we've really framed it in that perspective.

Speaker 1 That like, I would see this as you go to McDonald's, that is a metabolic toxin. You are actively poisoning yourself.
And look, we all do it. I've had alcohol in my life.
Alcohol is also a toxin.

Speaker 1 I've smoked one and a half cigarettes in my whole life. There's a whole story about that.

Speaker 1 But like, we all engage in some toxicity.

Speaker 1 It's part of being a human. Eat birthday cake with your kids.
But look, if you don't understand that that is a metabolic poison

Speaker 1 and your body will cross the threshold at which point your metasm, your metabolism, your mitochondria will become broken. We're missing the plot.
Yeah. I agree.
These are poisons. Yeah.
I agree.

Speaker 2 Paul, thank you so much, man.

Speaker 1 Yeah, brother. Five times love.

Speaker 2 And I'm sorry for stealing your cream.

Speaker 1 Yeah, we got more.

Speaker 2 It's been amazing having you on. You know, the last question that I always ask my guests, I asked you this last time.

Speaker 2 But what does it mean to you to be an ultimate human?

Speaker 1 And I probably will answer it in the same way.

Speaker 1 I don't remember exactly how I answered it.

Speaker 1 For me, it means being able to get up, put my barefoot, bare feet on the ground, put the sun in my eyes, hopefully go in the ocean and get some grounding, be in nature and spend time with people I care about in nature and have the health.

Speaker 1 and the vitality that is necessary to do that. Like being able, for me, the best part of my life is spending time with people I care about in nature.

Speaker 1 And I need health and I need vitality to do that, whether we're surfing, whether we're climbing mountains, whether we are snowboarding in the mountains, or whether we are in the ocean, you know, just in a river, like that is being the ultimate human.

Speaker 1 And like my vitality, my energy, my motivation, my strength comes from having a metabolism that works. And so

Speaker 1 I need to be healthy to be able to do those things and make the memories that I will treasure for my life. Yeah.

Speaker 2 Amen. Well, that's great, guys.
And as always,

Speaker 1 that's just science.