Are fatty foods bad for us? | Masterclass

The fats that you eat could be the difference between a long healthy life and one where you battle chronic disease. But choosing healthy fats, thanks to marketing and low quality information online, is really harder than it needs to be. Here is a scenario that most of us are faced with each week. Picture this. You're standing in the grocery store, staring at rows of cooking oils.

Extra virgin olive oil, coconut oil, canola oil, avocado oil, ghee, and then only a short walk away butter and margarine in the refrigerated section. Which one or ones should you choose? If you've ever felt overwhelmed by this decision, you're not alone. By the end of this video, you'll navigate the grocery store like a nutrition expert, or at least that's my hope, making choices that could add years to your life and life to your years.

Number one on our list of five points we're covering today. There are four broad families of dietary fats or fatty acids. Saturated fats, trans fats, monounsaturated fats, and polyunsaturated fats. Fatty acids are chains of carbon atoms linked together by bonds. It's these bonds that determine whether a fat is saturated, monounsaturated, polyunsaturated, or trans, and also determines if the fat is solid

or liquid at room temperature. Saturated fatty acids like those that predominate in butter, ghee, coconut oil, palm oil, cacao, butter have single bonds between the carbon atoms. The absence of double bonds allows the fats to pack tightly at room temperature, forming a solid like butter. Whereas unsaturated fats like those that predominate in olive oil, canola oil, avocado oil, et cetera, have one or more double bonds between carbon atoms.

sometimes referred to as a kink in the carbon chain, preventing the fats from packing tightly together, which is why they're a liquid at room temperature. If a fatty acid has one double bond, it's a mono-unsaturated fat. If it has two or more double bonds, it's a polyunsaturated fat. A common point of confusion that I regularly encounter is that these oils, olive oil, avocado oil, et cetera, are free from saturated fats. That's why they're liquid. That's not true. These oils do have some saturated fats in them.

For example, about 12% of calories in olive oil are from saturated fats, but they're predominantly made up of unsaturated fats, which keeps them liquid at room temperature. But why do we call them saturated or unsaturated? Where does saturation, this idea of saturation, come into this? What I left out in the story so far, and this becomes important when we talk about trans fats, was that these carbon atoms not only form bonds between each other,

but also hydrogen atoms. When you only have a single bond between carbon atoms, as is the case with saturated fats, these carbon atoms have more capability to bond with hydrogen atoms. That's what saturation or unsaturation speaks to. How many hydrogen atoms each carbon is connected to? In a saturated fat, each carbon is connected to the maximum number of hydrogens possible, hence it's fully saturated with hydrogen.

Whereas for unsaturated fats, those double bonds mean less ability for carbon atoms to bind with hydrogen. The fat is no longer fully saturated with hydrogen atoms, so we call it unsaturated. The take-home point is that the naming convention, saturated or unsaturated, speaks to whether a fat is fully saturated with hydrogen atoms or not.

And this comes back to the presence of double bonds between carbon atoms. A quick and easy way to tell if a concentrated fat source is made up of mostly saturated or unsaturated fats is to see if it's liquid or solid at room temperature. If it's liquid, it's mostly unsaturated fats. If it's solid, it's mostly saturated fats. What about trans fats? While some trans fats occur naturally in foods such as butter, cheese, and meat,

Most of the trans fat consumption in the human diet over the past 100 years has come from hydrogenation. What is hydrogenation? The hydrogenation of edible oils to improve shelf life and or reduce the fluidity of oils is when you take an unsaturated fat, for example, a vegetable oil, and use a chemical process to partially or fully convert them to a saturated fat.

And this is done by breaking the double bonds, which allows for the carbon atoms to bond with more hydrogen, hence the name hydrogenation. All you need to know about this process for now is that partial hydrogenation produces trans fats, whereas full hydrogenation does not. Full hydrogenation removes all double bonds and produces saturated fats.

I'll repeat that, partial hydrogenation produces trans fats, whereas full hydrogenation does not. So when we're talking about trans fats, we are essentially referring to partially hydrogenated oils or PHOs. Okay, so we've gone over the fact that there are four different families of fats, and these are named based on their unique chemical structure, more specifically, the presence of double bonds, which affects whether they're liquid or solid at room temperature.

Some foods that are rich in saturated fats include butter, certain cuts of red and processed meat, chicken, full fat dairy foods, cocoa butter, as used in chocolate, and tropical oils like coconut and palm oil. Foods that contain trans fats include cookies,

cakes, pastries, vegetable shortening, pizza dough, cookie dough, et cetera. Foods rich in monounsaturated fats include olive oil, avocado oil, avocados, pistachios, pecans, macadamias, et cetera. Foods rich in polyunsaturated fats include walnuts, chia seeds, flax seeds, hemp seeds, soybean oil, sunflower oil, fatty fish, et cetera. Now we're up to number two on our list.

Some fats are considered essential, while others are considered nonessential. What's the difference here? Well, in short, essential fats are fatty acids that our body cannot synthesize. We need to consume these in our diet. Whereas nonessential fats are fatty acids, our body can synthesize or manufacture. Saturated, monounsaturated, and trans fats are nonessential fats. Strictly speaking, beyond the calories that they provide,

There is no requirement for these fats in our diet because we have the machinery required to make them. On the other hand, essential fatty acids that our body cannot make and thus we need in our diet to stay healthy are our polyunsaturated fats. There's two main classes of essential polyunsaturated fats, the omega-3 polyunsaturated fats and the omega-6 polyunsaturated fats.

We need both of these groups of polyunsaturated fats in our diet for good health. If we go one layer deeper, there are different types of omega-3s and omega-6s. On the omega-3 side, the essential fat that we need in our diet is ALA, which is short for alpha, linolenic acid. This is what we call a short chain omega-3. It's found in plant foods like flax, hemp, chia, walnuts, et cetera.

and is converted by our body to the longer chain omega-3s, DHA and EPA, which if you listen to this show regularly, you will be familiar with. These omega-3s, DHA and EPA, are thought to be particularly beneficial for heart and brain health. You might have noticed that I said ALA is essential. I didn't say DHA and EPA are essential. I have to say this is still heavily contested with some people believing if you give the body enough ALA

it will produce all the DHA and EPA needs. Whereas some believe this is a sub-optimal strategy and you can get better outcomes with a direct source of DHA and EPA from fish, fish oil or algae oil. Omega-3 fatty acids are the most important fat for the brain. True.

So far, to the best of our knowledge today, they are. And this comes from multiple different studies, studies that look at consumption of omega-3 fatty acids as food, and also omega-3 fatty acids as supplementation. Dean and I published a couple of papers

A couple of years ago, looking at multiple different papers that have come out that look at omega-3 supplementation in two populations. The majority of the studies were done in children and in elderly populations to see whether supplementation improved cognition, cognitive outcomes.

And they had different kind of neuropsychological testing. And points for children versus elderly. The data wasn't very clear. We don't have very clear outcomes, but there was a trend. There was a trend towards improved cognitive outcomes, both in children and elderly, when they had enough omega-3 fatty acids in their dietary patterns and when they supplemented if they needed it.

And when you look at the pathophysiology of, let's talk about the elderly population. As it happens, omega-3 fatty acids are necessary for maintaining the infrastructure of the neuron and the neuronal connections. As a matter of fact, 57% of our brain is made up of DHA.

And it needs to be replaced on a regular basis. Our reservoir goes down significantly when we don't get enough of it. People always think that we need to eat fat. You know, rain is made out of fat and we need to eat fat. And cholesterol. Yeah, and cholesterol. Yeah, it is made up of fat. You know, when you look at the dry weight of the brain, it's about 50% fat. But the kind of fat matters. We don't need saturated fats. As a matter of fact, our brain doesn't have the capacity to internalize saturated fats or cholesterol.

we do make enough cholesterol in the brain, in the neurons that would serve its purpose. But the one kind of fact that we need on a regular basis is the long chain fatty acids omega-3. And is there a kind of amount that you would recommend for people of different ages or what? I know that you supplement in your life. How do you approach that?

Again, the data is not clean. The data is flawed by two factors. We only saw signal later in life and in early life. It doesn't mean that in midlife, it's not beneficial. It's just that in midlife, our ability to detect delta, our ability to detect change, as far as cognition is concerned, is not good because there's an incredible and a cognitive reserve.

which means that our cognitive capacity is good enough that even if they're when there's vacillation, it's so minimal to not be able to be detected by the tools we have. That's a little complicated. But midlife, we probably are affected significantly by omega 3, but we don't have the tools to detect the change that wealth.

I want to put a pin on this comment because I think this is one of the concepts that is not really discussed in all of the different conversations about brain health and health in general. Just because we don't see a signal during midlife about something or if people feel fine, doesn't necessarily mean that we don't lay the foundation of disease during that period. Sorry, I just wanted to

Oh, it's beautiful. That's similar to cardiovascular disease. Correct. But even more so for heart, for the brain.

the brain infrastructure, 87 billion neurons, billions and trillions of connections. This is the infrastructure that you're creating after the age of 21. Before that, it's the cells, growth of cells. In fact, there's some programmed cell death around age five or so that you end up with less cells, but the connections are built thereafter. And much of the connections are related to your environment, how much you're challenged, a bunch of stuff.

but also the myelination continues all the way to early 20s. So now you have what they call brain capacity. But cognitive capacity, these are arbitrary terms that are created to describe certain things, cognitive capacity is the connectivity of the neurons. The infrastructure, imagine a building, a huge building that's held up by billions of pillars. And so if a few of them are knocked down, nobody sees any difference from outside.

Which means cognition hasn't necessarily changed in a way that would be observable. Yeah, observable. The building is functioning, nobody sees anything, but the pillars are being knocked down one at a time. And you're 20s. I want this to be emphasized because it's very difficult for us to emphasize brain health to younger people. We're writing a third book and a huge segment of it, actually more than a third, is around children and young adults and their brain capacity.

And those pillars are foundational. We're knocking them down or building them in our 20s. So everything you eat, your exercise, everything determines those pillars. So the pillars are knocked down, knocked down, knocked down. And then in your 60s, now there are enough pillars knocked down where you start seeing the wavering.

I think in that example, you mentioned building, so pillars in the building, right? And so if that building falling down is sort of synonymous with cognition impairment, right, being observable. Now you can take a peek into that building, you could do an inspection and notice, okay, some of these pillars have been knocked down. We might want to get on the front foot here before this sink falls down.

And maybe that's something we'll come back to because I know a lot of people will be interested in, okay, I'm 30, I'm 40. What can I measure? Are there biomarkers or tests or scans that I can do with my brain that will tell me, hey, you're on the road to Parkinson's or you're on the road to Alzheimer's dementia or Huntington's, whatever it may be.

I think it's the most critical topic that we should be speaking about, because it's in our 30s that it's not just that we're avoiding disease, but we're actually building capacity.

That's been our focus in the last few years. It's not just Alzheimer's, but younger people. How do you get the signals to the young people to show that, oh, look, you're losing some capacity here, or you're gaining capacity? That's something, because if you don't have those markers, people are not motivated. Motivation is a complex thing when your life is driven by other factors when you're younger. But that's when it starts, especially when it comes to your brain.

And it's foundational. So now when we looked at the data with omega-3, one of the factors, just one of many. We didn't see the, most of the papers came back negative because the population they had included were younger people. We didn't have the tools of detecting signal, but we know that it affects them as much of not more.

What we did see signal that I'm going to get to the dosage was later in life or even pre-dementia patients called MCI or mild cognitive impairment patients, which have a much higher perclevity for dementia. And these populations, you did see an effect.

Omega-3 did have an effect, DHA. And it was at higher doses. And the second flaw with a lot of studies were they never saw a signal because the doses were lower, dosage problem. And we were going to talk about other studies that would colline and other things where the dosage comes to us from many years ago accidentally, but nobody focused at those studies. They were looking at effect studies.

So in that population, the higher doses were the dose that saw signal, 1,000 milligrams, 1,500 milligrams. So it's not definitely not definitive as far as the dose. But we went on the higher dose as far as omega-3 is concerned. On the omega-6 side of the polyunsaturated fat fence, it is a very similar story. The essential omega-6 that we must get in our diet is linoleic acid or LA.

which is primarily found in vegetable slash seed oils like sunflower, safflower, soybean corn, and canola oils, and also nuts, seeds, tofu, tempeh, etc. Whereas it's possible to have insufficient intake of omega-3s, most people in Western countries consume more than enough omega-6s to meet daily requirements without thinking about it. Okay, now we're up to number three.

on our list. Now that we understand that different families are fat in our food, let's consider how they affect important biomarkers known to predict risk of disease and death. We're going to focus on four important risk factors, one by one. And I'm going to review the totality of evidence without deep diving into every single study. We'll look at LDL cholesterol or APOB, inflammation, liver fat, and insulin resistance. LDL cholesterol, or more specifically, APOB,

is causal in the development of atherosclerosis. This has been made clear by randomized controlled trials, Mendelian randomization studies, and long-term observational cohort studies. In plain language, when our LDL cholesterol or APOB is elevated,

two things that you can test on a blood test, we are at higher risk of developing plaque buildup in our arteries and having a cardiac event, a heart attack stroke, et cetera. In general, the predominant saturated fats in foods like butter, red meat, poultry, coconut oil, and palm oil, namely, palmitic acid, meristic acid, and loric acid, raised LDL cholesterol, and APOB.

We all know that too much of almost anything can become a problem, even water, you can over drink water. And so, saturated fat is no exception. When we look at what's been reported and distilled from the balance of evidence, for example, if we look at the largest meta-analysis of randomized control trials, the Cochrane from 2020, what they figured out at the end after compiling all the data,

is that the effect of saturated fat intake on cardiovascular disease is not a straight line. A lot of times people will imagine that something that might have detrimental effects at a certain dose might be just a linear effect. The more you eat the worse it is. That does not seem to be the case for saturated fat.

It's actually S-shaped. So in NerdSpeak, we call that a sigmoidal curve. And maybe you'll show the curve from the Cochrane on screen, or maybe if not, people can Google sigmoidal curve, and you'll see what it looks like. Basically, it's very simple. Initially, at low level, when you start when the intake of saturated fat gradually goes up, there's not much effect on risk. Then at a certain point, it shoots up kind of abruptly, and then it just stays high, risk-wise.

as the intake of saturated fat increases further. So low shoots up stays high. So right away you can see how this pattern, even though it's not that complicated, can generate a lot of confusion.

Because if you compare a population eating a high-ish intake of saturated fat to a population eating even higher, you're not gonna see much of a difference in risk. Conversely, low-ish to even lower, you're not gonna see much of a difference. It's only when you compare high to low or high-ish to low-ish that it crosses that critical threshold of effect and that jump in the curve, that's when you see the effect, right? So this is something we see all the time. It's a common source of confusion. People find a study

that reports no significant difference in risk with a change in saturated fat intake. And a lot of times the conclusion is, aha, saturated fat is harmless. All scientists are wrong. Here's the proof. Except you may be looking at the wrong range. So it's very important to bear this in mind and make sure that we're looking at the active range of the distribution.

By the same token. Yeah. I will put that graph. I think it's a great visual. I'll put that onto the YouTube video for those who are watching and then into the show notes just to kind of be a little specific here. So that threshold, if I'm correct, is about 8% to 10% of calories coming from saturated fat. Is that right? Yeah.

If I remember correctly, at 8%, it was still on the bottom. And then at the 9% point is where it first shoots up. I don't know how granular we can be, what the level of confidence is with that level of precision, but that's the ballpark. And in fact, if you look at most professional scientific organizations and most countries around the world, they recommend staying under 10% of calories from saturated fat.

Some people disagree and think it should be a little lower. The American Heart Association thinks it should be a little lower, but that's maybe for people at a higher risk who have high cholesterol or established heart disease at baseline. But yeah, that's the general range we're talking about.

Okay. So, but the general principle for people to understand here is that unless you're comparing two groups where one of the saturated fat intakes is below that threshold and one is above, so your contrast crosses that threshold, then you're unlikely to see a significant difference

with regards to risk of cardiovascular disease, but that in and of itself is not indicative of saturated fat being harmless. It's just the fact that you haven't appreciated the importance of this threshold. Yeah, we have to be careful with extrapolations always, right? So if you look to give you an example, if you look at a study where one population is eating or one

One group, one quartile or one quintile of that population is eating, let's say, 13% of their calories from saturated fat. And the other one is getting 18 or 19. I wouldn't expect much of a difference in risk. So yeah, the problem is extrapolating and saying, so this means saturated fat has no effect in any place of the distribution. It is OK to say this suggests that there's not much of an effect.

in this range, right? It's the overall extrapolation is that's where that's what trips us up. A lot of times these discussions on the internet tend to be artificially polarized and foods are either good or bad. And oftentimes both are oversimplifications. And so with saturated fat, we see exactly that with people hearing these messages and concluding that saturated fat is bad for us.

And I get people commenting on the videos and saying, so should I try to eat zero saturated fat in my diet? We should not. I don't know. I don't even know if that's possible. It's certainly not desirable because healthy, but the healthy dietary patterns contain some saturated fat. All healthy foods, I don't think there's an exception, but certainly the vast majority of healthy foods contain saturated fat.

fish contains saturated fat, olive oil, fruits and vegetables contain some saturated fat, even lettuce and kale contain some. It's just a very small amount. So it's not that saturated fat is bad, it's too much of it that causes a problem, just like everything else, cholesterol in the blood, glucose in the blood,

They are, they have physiological ranges and then they have ranges where you push it too high and you get problems. You run into problems, intake of saturated fat is not fundamentally different. So just that note of caution to not oversimplify because it then trips us up and it makes it harder to understand these kind of practical questions. There's a very beautiful graph in an open access 2023 paper.

published in the journal of atherosclerosis by Christensen et al., which you can access in the show notes, that clearly shows animal fats and tropical oils have much more of these particular saturated fats that negatively affect LDL cholesterol and APOB, than plant oils like olive oil and canola oil. Therefore, it's not surprising that when you swap calories from these foods, for calories from foods rich in monounsaturated fats, or better yet, polyunsaturated fats,

you typically see a significant reduction in LDL cholesterol and lipobate. You mentioned there that the doubling of the polyunsaturated fats has likely contributed to, I believe, the reduction in cardiovascular disease mortality. You can look at a curve. As the cardiovascular disease mortality has gone down, plant oil consumption has

gone up. But yet there are some people who are set on pointing the finger at vegetable oils and seed oils and, you know, canola oil, for example, and saying that these are actually harmful. They're inflammatory. They contribute to disease. And that typically is really directed at omega-6 limbic acid. And I'm sure that's something that you've seen. Why do you think that idea exists?

That's a good question. I've been asking her at college, where does idea come about that seed oils in Omega-6 are harmful? And I think the person really who was pushing that for quite a while was Artemis Somopoulos, whose work you may have come across. But actually, she really didn't do any work. I read her papers and there's no evidence, there's no research that she's done on this. The idea, I think, comes from the fact that we eat

Our main omega-6 and omega-3 fatty acids in the diet are 18 carbons long, and those fatty acids omega-6 and omega-3 are elongated and desaturated and become inflammatory or anti-inflammatory factors.

And the idea is that omega-6s compete against the elongation and desaturation of omega-3 fatty acids, and I believe there's evidence that omega-3 fatty acids have anti-inflammatory.

effects. And so there must be competition there and if omega-3s are good, omega-6s must be bad. I think that's the extent of the information or the hypothesis here. But this ignores the fact, several facts that omega-3 fatty acid levels are elongated to arachidonic acid and the body really wants that.

Because it's been staring me in the face for decades, but the amount of a rachidonic acid in the blood as a percent of fatty acids is about 20 times higher than the amount in our diet. So our body really wants to have a lot of rachidonic acid and regulates that very tightly. So these are not unregulated pathways. And rachidonic acid is really important.

It's a very major part of our central nervous system and involved in anti-inflammatory pathways that fight infections, for example. So these are tightly regulated pathways. They're not just allowed to compete directly with each other. But more importantly,

that polyunsaturate, it's omega-6, polyunsaturates have many other functions as well, that they down-regulate NF Kappa B, which is an inflammatory pathway, and they also are ligand for a P-par gamma, which is an insulin sensitizer as well. So it's pretty clear that replacing saturated fat with polyunsaturate fat reduces insulin resistance and diabetes risk.

Well, so I think there's a mistake just to look at the human biochemistry and biology is really complicated and to look just at one pathway and I said for an hypothetical reason make dietary recommendations. I think that's where it's coming from.

There are now dozens of studies that show that omega-6 fatty acids are not pro-inflammatory. In a number of the studies, they're actually anti-inflammatory. So we need both omega-6 and omega-3. They're both essential. And if we only had omega-6 piling on tetra, that wouldn't be a good situation. Either we need both of them.

The exact balance is not totally clear, but we have up to about 8% polyunsaturates, omega-6 in our diet. Taiwan is about, when I looked about the highest, about 15%. So we've looked, at some point, almost everything will start to become bad or too much, but we don't see that within our population.

Yeah, I think it's become a bit of a scapegoat, almost. I've seen some people point to ultra-processed foods and say, it's the limalake acid. That's the one thing that is obesogenic. But even if you look at the research on obesity, and I saw a really interesting paper in circulation, I'll put this on screen as well, that did a biochemical analysis, and they actually looked at limalake acid in serum and in adipose tissue. You've probably seen this. You might even be an author on this paper.

I'm not sure. But they saw an inverse relationship. So the higher the linoleic acid adipose tissue levels, the lower total mortality. Yeah. Men lower diabetes, lower cardiovascular risks. And we've also looked at weight gain too, that there was actually less weight gain with higher linoleic acid intake. But you're right. It's amazing how these myths develop and get propagated on the internet.

Here we're talking about the importance of the type of fat and if you're sort of downshifting on saturated fats including more polyunsaturated fats which from a food perspective would look like I guess less fatty cuts of meat and butter and more nuts and seeds and legumes and fatty fish.

Yeah, absolutely. Yeah. And I think that's really the right way to look at it is the whole food basis, because that's what we eat and that integrates all the other components that come along with these nutrients. And so from a mechanistic point of view, is the primary reason that's beneficial for the person that's making those changes, the effect on LDL cholesterol, or there are a variety of mechanisms that are at play when you swap saturated fats for polyunsaturated fats.

definitely a variety of mechanisms. The LDL cholesterol in itself would be important, but there are also these insulin sensitizing issues, anti-inflammatory issues and probably some other mechanisms that are not totally clear to us yet.

Are you of the view that a higher fat with a focus on healthy fats is better for cardiovascular health? Yeah, very, very much so. And I did my postdoctoral fellowship at University of Minnesota, which is quite a famous place for many reasons. But one is that there were a trio of scientists there back in the 50s and 60, Drs. Key Anderson and Grande.

who did a series of really studies that changed the way that people thought about fats. Because saturated fat, they very clearly showed race, serum cholesterol, but polyunsaturated fat, into a lesser extent, monounsaturated fat.

appeared to lower it, or at least was completely neutral. So the idea very clearly came that not all fats were equal, and that therefore a very low fat diet was probably not the way to go, even though that was the wisdom of the time really. Yeah, the keys equation was born from that research. Saturated fats down regulate LDL receptors on the liver.

Whereas unsaturated fats, particularly those polyunsaturated fats, upregulate LDL receptors. Downregulating means less receptors, and upregulating means more receptors. The more LDL receptors at the surface of the liver, the more LDL cholesterol, or APOB-containing lipoproteins, that are cleared from the blood, which causes blood levels of LDL cholesterol and APOB to come down.

allow me to underscore this one more time. Saturated Fats reduced the number of LDL receptors on the liver, whereas unsaturated fats increase them. A wonderful review on this topic was published in the Journal of Clinical Lipidology 2021 by lipid specialist Professor Kevin Mackey, who I hope to have on the show someday, titled Saturated Fats and cardiovascular health, current evidence and controversies. Here's a short clip from Dr. Mackey's conversation

with Dr. Jill Cavallo on his channel, Nutrition Made Simple. My conclusion is that the bulk of the evidence, which has limitations, supports the idea that we should be consuming more unsaturated fatty acids and try and replace saturated fatty acids with unsaturated fatty acids. Now, you might be thinking, but even though there's a great deal of evidence showing higher LDL cholesterol,

equals higher risk of cardiovascular disease. I've been saying studies showing that saturated fats themselves don't raise the risk of cardiovascular disease. I can see how someone could be genuinely confused here. It is true that there are some studies that don't show increased risk of cardiovascular disease with higher saturated fat intake. We'll come back to this soon when we get to health outcomes. But for now, I want to explain a few very important principles or points of consideration that you need to know

to make sense of what on face value may seem like contradictory findings. Firstly, the scientific principle compared to what. Whenever we are asking if a nutrient or food increases risk of a particular disease, we have to consider what someone is eating instead.

If we fail to consider this, it's very easy to get confused with what seems on the surface to be conflicting results. If I compare saturated fats to refined carbohydrates, for example, those found in many cakes and biscuits, that is a very different analysis to comparing saturated fats to unrefined carbohydrates, for example, those found in whole grains or polyunsaturated fats, for example, those found in fatty fish or nuts and seeds.

You mentioned earlier when we were talking about, where do you think omega-6 fats, vanilla acid, that it might not be a great idea if the substitution was something rich in saturated fats. And I presume that's your view because of the data that exists with regards to cardiovascular disease and that such a substitution would increase someone's risk of cardiovascular events.

But there is that idea out there that I mentioned at the start of this conversation that some people hold the view that a diet that's rich in linoleic acid will result in

an increased amount of polyunsaturated fats in the cell membranes, but also in lipoproteins, low density lipoproteins, specifically, these polyunsaturated fats are easily oxidized. And when they do oxidize, they can become injurious to the endothelium. They can penetrate the artery wall, damage it, and sort of kickstart the inflammatory process that leads to

atherosclerosis. Now, from my understanding, the substitution studies and the outcome data would refute that position. But it is a position that is held and I wonder what your views on that are. Yeah. So, I think this is, I mean, it's an interesting argument, the one about saturates versus linoleic. I believe

The data that show if you replace saturates or some saturates within LEC acid, you lower LDL cholesterol concentration.

It is true that you enrich LDL in, that you can enrich LDL in linoleic acid and that at least in a test tube, it becomes more prone to oxidation when that happens. I'm not sure that that happens actually in the human body. So it's more prone to oxidation, but I'm not sure that happens actually in vivo.

I think another element of this is that whenever you have polyunsaturated fatty acids around, typically you also have more antioxidants around. So for example, vegetable oils are richer in some antioxidants than animal fats, for example. And that's part of the protective mechanism. So again, I think the emphasis here has been on

increasing things, and what are the possible harmful effects of increasing? And I think an important question now, as I've already said, is actually what is the effect of decreasing some of these things and getting balances right? And you could argue that in all of these changes, there's like a risk and a benefit, and you've got to weigh them up. So if you believe the literature,

if you substitute little egg acid for saturates, you would increase LDL cholesterol by having more saturates. So you've got more there, but it's a little bit less prone to oxidation. So, you know, which of those things is more important? And I guess trials would say having less LDL cholesterol is an important

effect to achieve to promote cardiovascular health. Particularly in the context, it would seem of a diet that's really rich in antioxidants. I think the benefits, you might see a bigger overall benefit across the whole health space. If you had an adequate intake of antioxidants, yes. I think that would be an extension of the statement I just made.

Yeah, so having more polyunsaturates when you have an antioxidant poor diet, you know, I think that's not as good as if you've got an antioxidant adequate diet. Secondly, not all saturated fats are equal. As I just mentioned, coconut oil, palm oil, and other sources of animal fat tend to contain appreciable amounts of palmitic acid, meristic acid, and lauric acid. These are saturated fats that significantly raise LDL cholesterol and APOB.

But there are other saturated fats such as short chain fatty acids produced in the gut, medium chain saturated fatty acids or MCTs, and steric acid as found in chocolate that are all saturated fats that don't raise LDL cholesterol or APOB and seem to be beneficial or at worst neutral for cardiovascular health.

Just bearing in mind that saturated fat is one factor, but it's not as simple as looking at the saturated fat content of a food and immediately concluding that that determines the net effect by itself. So, for example, fish in olive oil contain a substantial amount of saturated fat. In fish, I don't remember exactly what percentage it is. In all of oil is about 14% of the calories are coming from saturated fat, but in both of those foods,

The overall net effect on health and the health outcomes are overwhelmingly positive, probably because they have a lot more unsaturated fats in there, so the net effect ends up being positive. Dark chocolate is another well-established exception to the rule, very high in saturated fat, but it's stearyic acid, which is an exception, saturated fatty acid that doesn't raise serum cholesterol and doesn't raise risk.

Dairy is an interesting beast because it depends on what you're comparing it to. In general, as you look at some of these analyses, comparing dairy fat to non-dairy animal fats, dairy tends to look a little better in terms of cardiovascular outcomes, but then dairy tends to be outperformed by poofus. Then even within dairy, there's a large heterogeneity because dairy is this super

You know, varied class. It's so weird to talk about dairy as if it were one food. And the third principle that we really need to consider. Isolated nutrients can have a very different effect on physiology compared to foods that contain that nutrient. In this case, we need to consider the foods that saturated fats are found in. Food is more than just fat. You know that. There are other dietary constituents. As a whole, we call this a food matrix.

It might be that a food contains saturated fats, but many other compounds that are health promoting, and thus has a positive net effect on health. For example, fatty fish. So when looking at studies, we have to be asking these types of questions. What type of saturated fats are we referring to? What foods are we talking about and compared to what? All very important things to consider when trying to answer this question are saturated fats good for cardiovascular health or not?

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What about trans fats? Just like saturated fats, trans fats also raise LDL cholesterol when consumed instead of calories from unsaturated fats. And trans fats also seem to raise LP to little A, a subtype of LDL that's extremely atherogenic, meaning that it's very good at causing plaque to accumulate in the artery wall. The next biomarker I want to explore with you is blood pressure. How do these different fats affect blood pressure?

In general, clinical guidelines recommend low saturated fat diets such as the Mediterranean or Dash diets for lowering blood pressure. Although, while these diets are low saturated fat, they're also low sodium and rich in blood pressure lowering compounds such as potassium and nitrates, which makes it a little difficult to know what's causing blood pressure to lower, consuming less saturated fats or consuming more of these other things.

When it comes to trials attempting to examine the independent effects of different types of fats on blood pressure, the data is inconsistent. And if there are effects, they're minor, especially in people with healthy blood pressure. There is some data and I stress some, certainly not unequivocal. That suggests EPA and DHA, these long chain omega-3 polyunsaturated fats, as found in fatty fish, fish oil,

and algae oil have a modest blood pressure lowering effect in the individuals with hypertension. That is blood pressure of 140 over 90 or higher. Is there an effect of polyunsaturated fats on blood pressure? So if someone has high blood pressure, could it be that increasing polyunsaturated fats could help lower their blood pressure? EPA and DHA do have a blood pressure lowering effect. It's very small.

So I think usually it's about two or three millimeters of mercury seems to be what comes out in individual trials and in meta-analyses. So this isn't, it's nothing like you would get with an anti-hypertensive drug, for example. But it's a small blood pressure lowering effect. And you could argue that someone who

uses omega-3 supplements or eats a good amount of oily fish right across their adult life course, gets multiple small benefits and together these lower their risk of developing cardiometabolic disease. So actually they might get a very small blood pressure lowering effect

right across adulthood, and they might start as having normal blood pressure, and this makes it less likely that they would get into the hypertensive state. It's a modest effect. They would have lower triglycerides,

they would have higher HDL, they would have lower inflammation and all the things we've talked about. And some of these would be small effects, but you know, these are multiple small effects that put people on a better trajectory. And again, if you look at epidemiology,

It's quite clear that there is a relationship between higher EPA and DHA intake, or higher blood levels of EPA and DHA, and long-term risk of particularly coronary heart disease, but calliometabolic disease in general. And I think the explanation for that is these multiple modest effects, which together sum to quite a big effect on the risk.

That same blood pressure lowering effect has not been shown for the Amiga 3 ALA, as found in walnuts, seeds, cheese seeds, etc. There is also a modest amount of evidence suggesting that low-fat dairy products are actually pretty good for lowering blood pressure, which is likely due to being rich in potassium. Interestingly, in recent years, clinical trials using whole food forms of dairy, as opposed to isolated forms of dairy like butter,

have not found a difference in blood pressure or cholesterol between three servings a day of full fat milk, cheese and yogurt, and the same number of serves per day from low fat milk, cheese and yogurt. One possible explanation for this is that these unprocessed full fat dairy foods contain a calcium, phosphorus, milk fat globule, which reduces the amount of fat that's absorbed in the intestine. Whereas in butter, a heavily refined dairy food, that milk fat globule is broken.

allowing more saturated fats to be absorbed. In general, focusing on fat to lower blood pressure appears to be somewhat of a red herring. There is far more robust data supporting the adoption of a plant-rich diet such as the dash diet and working towards your ideal body weight. Doing such can easily result in blood pressure going down by 15 to 20 points or more if you have elevated blood pressure. A great resource that might help

with visualizing this style of dietary pattern is the Danish dietary guidelines. I made this simple for you to download at theproof.com forward slash guidelines. Let's move on to inflammation. How do different dietary fats affect inflammation? A hallmark feature of conditions like atherosclerotic cardiovascular disease, non-alcoholic fatty liver disease, dementia, and even depression. There's this idea out there, mostly online, that the dietary guidelines are flawed.

Advising people to consume vegetable oils rich in omega-6 fats is a terrible idea, because while they may help lower cholesterol, they're inflammatory. I'm led to believe that many people have heard this, because one of the most common questions I got from my audience ahead of planning this episode was, are polyunsaturated fats inflammatory? With all of that noise, you would suspect that there was strong evidence supporting it, right? Perhaps some human clinical trials that have fed people omega-6

rich fat sources and observed an increase in markers of inflammation. That would be good evidence to support such a position. It just so happens there have been a bunch of human clinical trials

interested in getting to the bottom of this. Here's the conclusion from a 2012 meta-analysis of 15 human randomized controlled trials. And I quote, we conclude that virtually no evidence is available from randomized controlled intervention studies among healthy, non-infant human beings to show that the addition of linoleic acid to the diet increases the concentration of inflammatory markers.

We also have randomized controlled trials looking at liver fat accumulation and associated inflammation that consistently suggest, while saturated fats, if anything, tend to increase liver fat and inflammation, especially when in a calorie surplus, omega-6 rich polyunsaturated fat, rich oils, tend to reduce liver fat and do not increase inflammatory markers or oxidative stress.

There's also another interesting mechanism by which saturated fats may increase inflammation via the microbiome. Consumed in large amounts, saturated fats may increase lipopolysaccharide or LPS uptake in the gut, at least in the hours after eating a meal anyway. In lay terms, there's a current hypothesis with a growing body of evidence to support it,

both animal and human data, that saturated fats modify the microbiome in a way that results in more pro-inflammatory compounds, these lipopolysaccharides entering circulation. What this means is if you test someone looking for inflammatory markers in a fasted state, you might unknowingly miss that they're subject to a high inflammatory burden in the post-meal period, which may not be a great thing given most of us are in the post-meal state for many hours a day.

What about mono unsaturated rich oils like canola and olive oil? How do they fare against polyunsaturated fat rich oils? While health outcome data does not support their use over vegetable or seed oils, there is some clinical trial data looking at how these oils differentially affect inflammation that leads me to recommending olive or canola oil over other vegetable oils for regular cooking. Not that the other vegetable or seed oils are inflammatory, but just that olive and canola oil may have an edge when it comes to lowering inflammation.

perhaps due to their antioxidant content, especially in people with poor metabolic health. I'd like to see more studies directly comparing these oils in healthy adults. The other monounsaturated rich oil that's pretty commonly found in grocery stores is avocado oil.

But really, the take home point here is that when it comes to liver fat accumulation or inflammation, all of these oils are better than regularly cooking with butter, ghee, coconut oil, palm oil, etc. Personally at home, I tend to cook with olive or avocado oil. A couple quick caveats here. Firstly, please do not conflate this information.

with eating ultra processed foods that contain these oils, that's certainly not a good idea. Secondly, you don't want to be going out of your way to reheat cooking oils or cooking at a high temperature that produces smoke. Thirdly, and we'll revisit this at the end when we get practical, it is possible that higher omega-6 intake without a direct source of DHA and EPA omega-3s could increase inflammation. Not because omega-6s are inherently inflammatory.

but because a high intake could impair the body's ability to synthesize DHA and EPA omega-3s from ALA. And because DHA and EPA are thought to be anti-inflammatory, this might result in more information. The solution here, in my view, is to not fear omega-6 fats, but to make sure you get enough EPA and DHA from fatty fish, fish oil, and or algae oil. I recently had a really informative conversation

with a Dr. Philip Colder, PhD, a domain-specific expert on polyunsaturated fats, where we spoke about this very question, whether or not there's such a thing as having too many omega-6 fats in our diet.

we need to be conscious about not consuming too much omega-6s to the point that it starts to compete with the enzymes that are required to desaturate an elongate linoleic acid and alpha linolenic acid, or is it about placing more emphasis on a direct source of DHA and EPA in the diet?

Yeah, that's a great question. And I think it's both of those. So you ask, am I in a camp? So I think I probably have a foot in two camps, but I might have a bigger foot in one of those camps, I guess, if you look back. So I think we need, well, I think it's more helpful.

If we consume preformed EPA and DHA, I think that's really important. I've got no doubt about that. But most people don't do that. So if you look at what the recommendations are in any country, most people are not meeting the recommendations, probably because they're not eating enough fish.

which, you know, is a choice they make. So if you take not consuming preformed EPA and DHA and put that to one side, okay, that's important, but not everyone is doing that, then I think we rely on our metabolism. And that's where this relationship between linoleic and alpha-linolenic acid intakes is important. And to optimize our metabolism,

of alpha linoleic acid through that pathway, one thing we can do is keep an eye on our linoleic acid intake. Now, that can be a little bit tricky because lots of things that contain a lot of alpha, you know, a reasonable amount of alpha linoleic acid also contain a lot of linoleic acid.

although that's not universally true. So we need also to think about what are good sources of alpha-linolenic acid. So things like flax seed, chia seeds, stuff like that. I think we need to be thinking about and trying to cut back on the things which are really rich in linoleic acid and don't contain so much alpha-linolenic acid.

Some of the vegetable oils, like corn oil, sunflower oil, so on, don't contain much alpha-linolenic acid, but they contain a lot of little layer acid.

Right, and just to sort of emphasize something here, you're saying that dietary strategy emphasizing ALA rich foods that are somewhat not so rich in omega-6s, and then de-emphasizing some of these super omega-6 rich foods is a strategy that's more important for someone who is not consuming enough EPA and DHA in the form of bad-official supplement. Yeah, correct.

I think you got it in a nutshell there. I think that's dead right. So if you're not, at the moment for most people, if particularly fatty fish is not something that they're into,

They need to take this alternative approach, which is looking for sources of alpha-linolenic acid, particularly where linoleic acid content is not high. So helping their metabolism out, basically. There's definitely a lot of folks out there that

would be of the view will take a position at omega 6 fat. At least that a certain dose are inherently harmful, that they're pro-inflammatory, they cause oxidation, increased risk of atherosclerosis. All of these claims are out there.

It sounds like what you're saying here is that the main issue with omega-6 is competition for important enzymes. And if you have too many omega-6s in the diet, it might affect your ability to convert ALA into DHA and EPA, which again is most important if you don't have enough EPA and DHA in the diet. But I would like to step through omega-6s in a little bit more detail.

and sort of think about some of the claims that are out there and whether there is any validity to them. You just walked us through before the Amiga 3 pathway from ALA through to DHA and EPA. Perhaps you could do the same with the Amiga 6 pathway. Yeah, so it's an analogous pathway. So little like acid, which is essential, but it's probably, well, is consumed

in amounts which are way beyond what is necessary to overcome central fatty acid deficiency, that's for sure. So linoleic acid has 18 carbons, two double bonds in its chain, and it's converted through a pathway, the same pathway as alpha linoleic acid to EPA. Linoleic acid is converted to a rachidonic acid, which has 20 carbons and four double bonds.

Lilirac acid itself has biological activity, and arachidonic acid, its derivative, has high biological activity. And I think many of the arguments about possible problems, harms, if you like, from too much Lilirac acid, stem from its conversion to arachidonic acid.

Because arachidonic acid, the paint, you know, a simplistic picture, has activities which promote inflammation, promote thrombosis, that's blood clotting, promote some other things. So, you know, the view of arachidonic acid is that it has these adverse physiological impacts and its synthesis is driven by high intake of linoleic acid.

So that's where I think, you know, the balances between the omega-6 side and the omega-3 side are important. So sort of omega-3s have their own actions, but also that keeping the omega-6 actions in check, if you like. So the balance between them at different points along the pathway is really quite important.

In 2018, you wrote a paper with Jacqueline Inning's, I think, to about pronounce that correctly. Omega-6 fatty acids and inflammation. I think that was the paper that actually first put you on my radar.

And in this review, you were looking at different clinical interventions, including human studies, where humans were being fed to omega-6 as either linoleic acid or arachidonic acid, and looking at

inflammatory compounds. I was surprised in that study given that arachidonic acid is a precursor to some of these, I guess, pro-inflammatory compounds. I was surprised that these feeding trials when they fed humans, again, either linoleic acid or arachidonic acid, it didn't seem to significantly increase these inflammatory compounds. Did that surprise you?

in a way yes and but I think I'll deal with the little lack and a racodontic acid separately from one another maybe so if you if you give in a trial setting if you give people increased amount of a racodontic acid and that has usually been done through supplements you do increase

The concentrations of some compounds which are linked with inflammation I mean that that's been shown a few times I mean not many studies have been done with arachidonic acid in adults, but that has been shown So I think there is a link but an important subtlety here Simon is that Our cells already contain a lot of arachidonic acid because of a high omega-6 intake and

So it's already high, and if you give people a rachidonic acid as a supplement, the amount of rachidonic acid goes up only a very little bit. So you may not expect much of an impact. Now, I'm just going to go off slightly on a tangent here and then come back. So one of the things that EPA and DHA do is they decrease a rachidonic acid in cell membranes, and they do that

quite dramatically if you give high dose EPA and DHA again as a supplement. And that's believed to be one of the main mechanisms of the anti-inflammatory effects of omega-3s, okay, that's driving down the racodontic acid. So there's a gap in the literature in humans where

The studies with arachidonic acid have always given more arachidonic acid. So if I give more, will effects become even more extreme, I guess. But there aren't studies where you've actually tried to reduce the amount of arachidonic acid in the diet.

So going the other way, and you would have to do that through a dietary manipulation. And so that would be interesting. So does decreasing arachidonic acid have an effect, rather than, is there an effect of giving people even more? So the hypothesis there, Philip, being that

there could be a critical threshold. So you could be going from nothing to some arachidonic acid, which is currently baseline. And you've already crossed that threshold where you've cranked up inflammatory biomarkers. You've got it in one. You've got it in one. And so you're already, if you like, the system is already saturated. And the one effective way we know to counter that

is to drive a recordonic acid in cell membranes down with EPA and DHA. But my point is, no one has done the experiment to try to drive a recordonic acid down by decreasing a recordonic acid intake, except for one study that I'm aware of, which was done in people with arthritis, by a German researcher named Eric Adam.

I think published probably maybe in the late 1990s, I can't remember exactly when. So one of the main sources of a racodonic acid is meat. So what he did was he actually did an omega-3 study and he gave people with arthritis omega-3s against a normal dietary background and a dietary background where they decreased their meat intake. And he found that the omega-3s were actually more effective in people who decreased meat intake.

compared to if they keep their meat and take steady. So I think that helps with this argument that decreasing arachidonic acid could be a way forward. Your position, and correct me if I'm wrong here, is not so much that the Amiga 6s are inherently bad or toxic or inflammatory, but if we crank them up too much, it could affect that Amiga 3 pathway, which then affects their sort of

anti-inflammatory effects. Yeah, I think, I mean, I think that's one way to summarize it. Certainly, so in our research, we've looked a lot at relationships between arachidonic acid content of cells and the inflammatory response of those cells. And there is a relationship. In other words,

the higher the arachidonic acid content, the higher, let's call it the inflammatory potential of the cells. And therefore, I think ways of controlling arachidonic acid content are really important. And, you know, to me, the primary way of doing that is to increase intake of EPA and DHA. You know, that is the most effective

impact. And maybe that works better than lowering linoleic acid because of this threshold effect that we already talked about that you really have to lower linoleic acid a lot if you're going to decrease arachidonic acid. And I'm not sure anyone has ever shown that lowering linoleic acid will decrease arachidonic acid in anything other than a really controlled cell culture setting.

Whereas omega-3s, you know, you can take modest omega-3s and you decrease your racodontic acid levels. So increasing EPA and DHA will help decrease arachidonic levels. Do you think it would be a good idea to, for example, reduce certain animal foods in exchange for beans or is that just something that you just can't see people doing from an adherence point of view? Would it be effective?

Well, some people are doing that because people are moving away from making a choice to move away from animal.

animal-based foods towards more plant-based foods. So people are doing that and apparently in increasing numbers and so on. What I don't know is what the impact of that is on their arachidonic acid levels. I mean, that would be really interesting to look at Simon for sure. I do think that arachidonic acid intake has a relationship with arachidonic acid levels in cells and therefore strategies that decrease arachidonic acid intake

should decrease the amount in cells, although I would need to look for evidence of that. And that could be part of the health-promoting effects of a more plant-based diet. There's information, less tendency to thrombosis, stuff like that. In short, if you get a direct source of DHA and EPA in your diet, Dr. Colter doesn't believe a high intake of omega-6 fats,

from unprocessed foods and isolated vegetable oils is a problem. Everyone agrees it's a good idea to avoid hyper-palatable ultra-processed foods that contain omega-6 fats. But these foods like cookies, cakes, biscuits, et cetera, are far more than omega-6 fats. They're formulated to be easily over-consumed, energy dense, low protein, low water, low fiber, and usually high in added sugars. The last bio-micro I want to talk about is insulin resistance.

I've already mentioned to you that saturated fats, particularly when consumed in a diet supplying excessive calories, are really good at increasing liver fat. If you recall my conversation with Professor Roy Taylor, episode 287 of The Proof, one of my favorite conversations today, you'll remember that insulin resistance is largely a downstream consequence of storing fat in the wrong place. In muscle tissue and in between and within organs like the liver,

the pancreas. The twin-cidal hypothesis was my attempt to put together all the observations on how the body actually worked, how the body dealt with food and metabolism and what went wrong in type 2 diabetes.

So over the years, we'd learned firstly that muscle was very resistant to insulin and using MRI techniques, advanced MRI techniques, we could measure the glycogen in muscle. And in fact, use this to show that people who had normal insulin sensitivity in muscle

stored a lot of their food as muscle glycogen within the first five hours after eating. One third, really quite a lot. Whereas people who had low sensitivity to insulin in muscle, so-called insulin resistance, those people stored almost none.

And, from other work we knew that the only way that that glucose would be handled is not being stored properly.

The only way it could be handled would be for the body to turn it into fat. Now that sounds like magic, but that's exactly what the liver does. And so that excess glucose will be shunted into fat, and people will be more likely to build up fat in the liver. Now which shown, fat in the liver causes the liver not to respond to its leg.

Now, I put all this together, and the twin-cycle hypothesis runs like this.

Basically, a little too much food over a long period of time will cause fat to start building up in the liver. And when the liver starts getting resistant to insulin, it will start putting out too much glucose, because insulin usually dampens down the constant production of the liver, of glucose.

So, though we have Glucus rising a bit, but what happened next is that the pancreas kicks in and insulin levels rise a bit to just bring things under control. Now that's fine temporarily, but unfortunately insulin speeds up the process of turning Glucus into fat, and so we've got a vicious cycle that started running.

That will run on. And the glucose levels will gradually peg up. But it's not just the glucose that the liver butts out. The liver also puts out fat for the rest of the body. The liver really supplies you with the energy you need to live every day.

Overnight, it's the glucose coming out from the body that keeps your brain alive and the fat coming out from your liver that keeps the rest of the body alive. That's what they use to burn for energy, second by second. It's an astonishing process. But if there's too much fat in their liver, then that one liver cycle will have a knock-on effect because it will leave too much fat in the blood.

The liver puts out too much fat, it will be delivered to all tissues, now any excess fat would usually be stored under the skin, and metabolically that's safe, it doesn't cause any metabolic damage.

in the situation of excess and with a relatively full, subcutaneous under the skin compartment, then fat's going to build up elsewhere, and that's the problem. And it's when fat starts building up inside the pancreas that really the action starts, so we have a second vicious cycle in the pancreas. The fat stops the insulin-producing cells working properly,

Lo and behold, that means glucose levels are higher after every meal. And lo and behold, that means more glucose is going to be turned into fat. And so we have these twin vicious cycles interacting.

The importance of this twin-cidal diamond was that it explained type 2 diabetes as a simple chain of events, yes, interacting cycles, but a single cause. Now, that is simple. And what we see in populations is when they're overfed,

diabetes erupts. If the relatively starved, diabetes goes away. So all of a sudden, we had a handle on this, and it was a complete revelation and a move away from what all the experts were saying up to 2011. But type 2 diabetes was a complex heterogeneous disorder caused by multiple different factors. Well, that's nonsense.

Basically, you hit out your jeans. But, if you put on a bit too much weight, heavier than you could bear, then these twin vicious cycles will start turning. And, being a hypothesis, it could be tested and shown to be right along.

You said there that the twin cycle hypothesis provides an explanation for a single cause. What if someone is thinking, well, hang on, how can excessive calories explain this if not everyone who becomes overweight or obese ends up with type two diabetes?

That's a very good question. The first point to make is that there's a wide range of thresholds at which people will develop type 2 diabetes. So our most recent study, we've demonstrated that those slim people who get type 2 diabetes have got too much fat inside their organs. They simply don't show the fat. So does this matter of how much fat and this personal threshold for fat?

But there's a further point, which is really important. About 70% of people of white European ethnicity will never get diabetes, no matter how much they eat, how fat they become. And in fact, at the moment, 73% of people who have a body mass index over 40

do not have Type 2 diabetes, and show no signs of getting it in the near future. So we can see that it's only a proportion of people who are susceptible. And that is the stop-go of getting Type 2 diabetes. So there are really two stages. One is the eating too much, the other is the genetic factor. But why do I say that it's just one? Well, it's because

I'm talking to a group of individuals, they are one person each, and in my consultations with patients, I only have one person in front of me, and that person comes in, with their ready-made collection of genes, they are themselves. Now doctors have to practice the art of the possible. So I'm dealing with individuals. If a person presents to me with type 2 diabetes,

They have insulin-producing cells that are susceptible to fat. And that is the whole point. So this disease is simple to understand. Right, so it's not.

necessarily fat or being overweight or obesity, that is the single explanation, but it is fat getting inside these organs, the liver and the pancreas, specifically fat, I guess, where we could say it shouldn't be.

in individuals that are more susceptible to this. So certain individuals, as they're gaining weight, are more genetically predisposed to having fat stored within organs, whereas other individuals have a greater capacity, would that be the right terminology to store more fat subcutaneously and not inside these organs? Yes, that's absolutely right.

Okay, so let me throw back to you what I grasped from your explanation of the twin cycle hypothesis. So it all kind of begins with this positive calorie balance. So a very small calorie surplus over a long period of time coupled with muscle insulin resistance.

This results in an increase in blood glucose or that extra glucose. The body has to do something with it. Instead of forming glycogen and muscle tissue, you get an increase in de novo lipogenesis, which is the conversion of glucose to fat within the liver.

With the increase in liver fat, you get insulin resistance in the liver, insulin's job at the liver being to slow down or halt the flux of glucose from the liver into circulation. So with that, you get an increase in blood glucose.

The response from the pancreas there is to increase insulin. So insulin levels go up and insulin then increases or drives more fat production in the liver. Eventually the body has to do something with that excess fat being produced in the liver packages it up in lipoproteins.

these VLDL, very low density lipoproteins, which are an ApoB containing lipoprotein and are therefore atherogenic, and they go out into circulation. If the subcutaneous fat storage has been exceeded, that excess fat that is now in circulation and has to go somewhere, and eventually it can begin to build up in organs, particularly

the pancreas, which then can begin to affect the beta cells in the pancreas that produce insulin such that there is reduced insulin in response to ingesting a carbohydrate containing meal. And with that, you get increase in plasma glucose.

And the liver begins to convert more glucose into fat and so forth. The cycle kind of self perpetuates. Did I grasp all of that correctly? Yes. That's absolutely connected. Independent of energy, you mentioned before. And I spoke to Richard Johnson on my show about this and in preparation for that, I remember speaking to you a bunch of times and

You've also written about this quite extensively in one of your sigma blogs or statements that go through all of this research. We'll put that into the show notes actually. That's a fantastic read. But my understanding is that when you swap calories, even if we're at energy balance from saturated fat,

for polyunsaturated fats, we see a relative reduction in hepatic fat. Is that right? And perhaps you can kind of talk us through that body of literature and what the big takeaways are there.

Yeah, so we can even see that effect in the context of overfeeding. So if you compare saturated fat to sugar in the context of overfeeding, you can often see a greater increase

In hepatic fast in liver fast from from overfeeding saturated fast compared there's a really great paper leukin and colleagues 2018. And that overfed people by a thousand calories a day and one predominantly saturated fast in one group unsaturated fast in another and sugars in the other.

And the increase in liver fat was 55% in the saturated fat group, 33% in the sugar group, and 15% in the unsaturated fat group. So that's already giving us a signal that there's a bit of a hierarchy of effect here.

And so we've dealt with the sugar component, but what we could clearly see here was that there was an increase from overfeeding 1,000 calories a day of unsaturated fat, but clearly it was an effect that was attenuated relative to saturated fat in particular, and even relative to simple sugars.

And there is another study that is instructive in this regard because while the study of just mentioned didn't necessarily differentiate between sources of unsaturated fat, it was a broad, broad designation of unsaturated fat mix of poly and monounsaturated fat.

There was an intervention by Rosquist and colleagues looked at a comparison between saturated fashion enrichment, specifically kind of palmitate, and omega-6 linoleic acid enrichment. And this was deliberately designed to increase body weight by 3%. It was an overfeeding study. And what was fascinating was

After the seven weeks of the intervention, both groups had actually gained the same amount of absolute weight. So the intended aim of the intervention was effective in this regard. They gained 1.6 kilograms.

but liver fast increased 58% with the saturated fast and rich diet, whereas the increase was only about 5% on the Omega six polyunsaturated fast diet and body composition.

changed overall not just in relation to liver fat, there was greater lean mass increases with the polyunsaturated linoleic acid enrichment, and the ratio of lean to fat mass increase. Now that might, of course, beg the question from listeners, why, what potential mechanisms might be at play that relate to these differential effects,

they relate it appears based on current evidence to the degree of saturation of the fatty acids in the diet. Saturated fats have a number of potential mechanisms.

The first is, in terms of the overall contribution of where fatty acids come from in order to get to the liver, there are a number of pathways when we're talking about dietary intake. But the majority of fatty acids in triglycerides in the liver and in VLDL come from the systemic circulation of non-asterified or free fatty acids.

So this is important because one of the identified mechanisms of saturated fat is that it increases lipogenic pathways, the signaling for pathways that relate to lipolysis, the breakdown and release of stored fat into the systemic circulation. Saturated fatty acids stimulate lipogenic pathways.

The second is that saturated fats, in terms of from dietary intake, the primary vehicle is the transport of triglycerides through chylomicrons. And is chylomicron remnants? So these are leftover particles after triglycerides and chylomicrons have been broken down that arrive at the liver with a delivery of triglycerides. And there are also spillover fatty acids.

from that. Now there appears to be a degree of preferential oxidation of polyon saturation fats compared to saturation fats. So there is, and this has been demonstrated in a number of stable isotope studies as well,

So polyunsaturated fats appear to be preferentially oxidized compared to saturated fats, which are less prone to hydrolysis and oxidation. So there's a potentially greater delivery of dietary intake of saturated fatty acids to deliver. And then there's these compounds known as ceramides.

So ceramides, when measured in the plasma, these are compounds that are derived from saturated fasting acids.

that in fact increase insulin resistance because they inhibit the transport of glucose into cells. So it's one mechanism by which saturated fatty acids impair insulin sensitivity. But one study looked at a really, really interesting study, which looked at

the respect of contributions or impacts of saturated fat versus omega-6 polyunsaturated fats on plasma ceramide levels. And because these are derived from saturated fatty acids during polyunsaturated fat enrichment, all of these ceramides decreased across the boards.

But when saturated fat was enriched in the diet, total ceramide levels increased, and each specific class of ceramide increased. But what was interesting was this was a study that achieved saturated fat over feeding with enrichment with palmitate, which is a 16-carbon saturated fatty acid. And after adjusting for 16-carbon ceramides,

there was no longer any significant association between diet and liver fat. So the kind of effect of that adjustment would indicate to us that the increase in liver fat was directly associated with the increase in 16 carb and derived saturated fatty acid ceramide from the saturated fat overfeeding.

So there's a number of these pathways that appear to influence the differential metabolic fates of saturation compared to polyunsaturated fats, such that even in the context of overfeed heating, there is a somewhat protective effect of polyunsaturated fat enrichment and preferential effects on body composition.

versus the deleterious effects of saturated fat overfeeding. And fascinatingly, everything that I've just described there occurs or the evidence that we currently have demonstrates that this also occurs in the context of relative energy balance. So without an energy surplus, this appears to be the case and we have evidence from

Isocaloric studies, eukaloric studies of this effect of saturated fat. Although the direct comparisons with polyunsaturated fat, for the most part, are in the context of overfeeding.

But nevertheless, that seems to be that there is a differential effect of fat on the liver relative to the degree of saturation of the fatty acids such that overall polyons saturated fats exert a protective effect while saturated fats exert a negative effect. You said that polyonsaturated fats are preferentially oxidized.

And I think a number of people will hear that and they see oxidation as a negative thing and they'll talk about oxidized LDL is the preferential oxidation of polyunsaturated fats, anything to fear for any reason.

No, we're here, we're talking about, you know, kind of beta oxidation, we're talking about the utilization of fatty acids, we're not talking about oxidat of stress, so to speak. And so yeah, I understand that's a really important clarification, because unfortunately, that term has kind of been hijacked somewhat.

Particularly in the ongoing attempts to portray polyonsaturated fats and linoleic acid as uniquely deleterious for human health. We're talking here about the actual utilization of these fatty acids.

in a positive sense. And so a really good example of this is the fact that if you look at and you compare polyunsaturated fats to saturated fats,

you'll typically see lower levels of triglyceride with polyunsaturated fats. And that relates to the fact that it's primarily lower levels of chylomicron and VLDL triglycerides because there is this preferential expression of lipoprotein lipase, the enzyme that's responsible for breaking down the triglyceride that's stored in these lipoproteins and these chylomicrons.

liberating them as free fatty acids and then tissues like skeletal muscle utilizing those free fatty acids in the production of energy. And so those pathways are related to the utilization of fatty acids such that they're not either hanging around in the circulation or in this context being delivered to the liver and creating a burden that requires their storage in the liver.

So these are these are these effects that we're describing here are positive effects of polyunsaturated fats in the post-prandial period. Okay, so preferential oxidation of polyunsaturated fats, a positive thing. The second thing that I wanted to ask you was more about the robustness of this body of literature. I think certain people, Dr. Peter Itty comes to mind.

And I don't want to put words into his mouth, but generally speaking, I don't think he's convinced that there is a whole lot of benefit up for grabs for substituting the type of fats that you're consuming. And he seems to think that most, maybe not all, but most of how nutrition affects our health comes down to the total number of calories.

that we're consuming. And we've spoken here about the importance of energy balance and getting into a hypochloric state if we're trying to get liver fat down. How relatively speaking, how important is this substitution of saturated fat for polyunsaturated fat in the grand scheme of things if we're thinking about non-alcoholic fatty liver disease?

what's driving it and typical diets that people are consuming today.

Yeah, I think it just depends. I don't think there's a broad brush answer to that necessarily because if an individual is consuming a high level of saturated fat, then the evidence that we have clearly indicates that that would be something that should be modified and would be potentially contributing to increased liver fat levels, for example, even without necessarily much of an energy excess.

And this is similar to a lot of the claims that we typically see out of the fitness industry, related to calories and energy. And it just creates somewhat of a straw man for me. Does total energy intake matter? Is it overall the most deterministic factor? Yes.

That doesn't mean that dietary composition is not relevant. It's contextual and clearly in the research with specific regard to fatty liver and the available evidence from dietary interventions, many of them very well conducted. And with direct head-to-head comparisons of different levels,

of fatty acids, or indeed fat versus sugar, but at the same level of energy intake, clearly does indicate an effective diet composition that's relative to energy balance. So the idea that it's one or the other is just kind of an inappropriate dichotomizing. And I think when those kind of

statements arise that kind of, well, this doesn't matter because total energy, I think it fundamentally just misunderstands the nature of diet and nutrition as an exposure, because total energy, whatever that level of energy is, is comprised of a dietary composition.

They're not inseparable. They're part of an overall whole. So, of course, the given importance is going to depend on the specific context of an individual that we're talking about.

across a range of factors, their metabolic health, their dietary composition on average, et cetera, baseline, and all of these things. So yeah, I don't think they're necessarily indivisible. You're dividing one factor by the sum of its parts, essentially.

You mentioned the liver there, and that gets me thinking about insulin resistance. And I've seen a little bit of data out there looking at dietary substitution that happens to insulin resistance if you swap calories from saturated saturates for polyunsaturated fats. Is that something that you've researched or read from other groups? I mean, I'm not an expert on that, but obviously I've seen papers.

Observational, so epidemiological studies, usually in big populations where researchers have looked at either intake of fatty acids or blood status of fatty acids and risk of developing insulin resistance. Those studies suggest that both linoleic acid and EPA and DHA decrease risk of insulin resistance developing.

So that seems to be maybe it's a polyunsaturated fatty acid effect versus something else, which would normally be saturated. So I think the epidemiology says that those polyunsaturated fatty acids, both omega six and omega three, decrease risk of insulin resistance developing. With that in mind, it's probably no surprise to you.

that a meta-analysis of over 100 human trials, including more than 4,000 adults by Imamura and colleagues, found that replacing calories from saturated fat with polyunsaturated fat significantly improved insulin resistance and subsequently blood glucose control. When people ate less saturated fat and more polyunsaturated fats, their body was better at getting glucose out of circulation

and into cells to be used as a fuel source, whereas when people ate more saturated fat, they had more glucose hanging around in circulation, which we know over time can damage blood vessels and make them more susceptible to becoming blocked with plaque. As I was researching for this episode,

Yet another trial was published showing the same or similar results. Wait until you hear this one. In a new human randomized controlled trial, researchers put ghee, a form of butter, up against rapeseed oil, more commonly known as canola oil, ghee being a high saturated fat cooking oil and rapeseed oil being rich in unsaturated fats, both mono and polyunsaturated fats. The trial included 110 adults

average age in their early 40s who had already been regularly consuming ghee. The control group continued their ghee consumption, and the intervention group was told to swap all ghee with rapeseed oil for a 12-week period. The researchers were primarily interested in what happened to fat levels in the liver and liver enzymes. Both were significantly lower in the subjects consuming rapeseed oil. Secondarily, the researchers looked at glycemic control and blood lipids. No shock

Subjects consuming the rapeseed oil had significantly lower fasting blood glucose, significantly lower insulin, significantly lower insulin resistance, and significantly lower LDL cholesterol. Yeah, based on my read of the claims that are made online from people who are of the view that canola oil is, let's quote unquote, toxic or harmful or something that we should minimize exposure to. It usually comes back to

three or four things, and I think we've already hit on them. One is that it's a seed oil, and by default, it must be harmful, genetically modified, and then the processing, so the fact that there's deodorisation, the involvement of hexane, that it's heated. Would you agree that this is the basis of most of the

the claims that exist or have you seen people also pointing to specific forms of evidence to support the idea that canola oil is toxic? I think that's pretty accurate. I think it all sits on the idea of not being a natural thing, of it being an artificial food.

That, I think, is the basic idea. And it is very powerful in terms of messaging. And I wouldn't say that that's irrelevant either. And then I think most of these other concepts sit on it, the fact that it's refined, that there is an exane added, that is heated. The purification, all of this sits on this idea that it's an unnatural food that our ancestors didn't need it, that it's new evolutionarily

It all stems from this idea of what's natural and what's unnatural. Some people call it a naturalistic fallacy, but the original concern, I think, is that. And then with the linoleic acid, I think there's these concerns with inflammation as well. There is this link to the biochemical pathway of linoleic acid being converted to arachidonic acid and so on to

Proinflammatory compounds, liquid trianes, and prostaglandins, this kind of thing. So that's another concern is that perhaps eating foods or a diet high in linoleic acid might lead to an elevation of these compounds, which then would lead to inflammation in the body. Right. And canola oil enters that conversation because it

It contains more linoleic acid than, say, olive oil or butter, even though it has less than some of the other seed oils, it's still considered to contain, I guess, an appreciable amount. Or if someone's taking that position, that linoleic acid would increase inflammation, I assume that what they're saying is you could cook with better fats than can all oil that contain less linoleic acid. It's said differently.

What would you say, Jill, if someone said, look, I don't need any more information other than the fact that this is new. It's ultra processed. There may have been some selective breeding or GMO. It might be a GMO. There's heating and deodorization and the use of these solvents like hexane. That's enough for me to know that

This surely cannot be healthy. I don't need to be shown a meta-analysis or a bunch of meta-analyses or any studies. That's enough. At the level of individual choice, I don't think there's a problem there. If the person prefers or feels safer or feels more comfortable not consuming canola or not consuming any seed oils or any oils for that matter, some people prefer not eat any oils at all and just get their fats from whole forms of whole foods.

At a level of personal choice, I think that's completely fine. And it's not a problem nutritionally. You don't need canal oil in your diet. My concern is not that choice. My concern is basing firm beliefs on poor heuristics because sooner or later you're going to make decisions that are detrimental or potentially detrimental. And in fact, we see plenty associated with these ideas of seed oils. When people say, I avoid seed oils,

I don't see a problem. The problem is that the same influencers and the same logic then leads to making choices like, so instead of seed wells, I lather butter and lard on everything. So you get to things once you make one decision that's based on emotion or just these kind of these kind of one-liner first glance ideas that don't pan out scientifically in terms of the actual health effect of the foods.

you're going to be more prone to make all kinds of decisions in a chain on that logic. And so for example, swapping unsaturated fats for predominantly saturated fats, there's so much evidence stacked against that in the long run. We're talking about substantial amounts, right? If you have a little bit of butter and your lipids are good, whatever, but people being scared of unsaturated fats and eating a lot of butter and lard instead,

in a Western population is going to be a terrible decision. But if they prefer olive oil, if you'll say from olive oil or almonds or whatever, I don't see a problem. Another claim that's very common when it comes to seed oils is that they are inflammatory. I know you looked at inflammation. What did you find with regards to canola oil and whether this is pro-inflammatory or not?

Yeah, we found a number of trials as well, meta analyses that go over a couple of inflammatory markers. And so for example, the meta analysis of 42 trials reports CRP. And there was no significant difference also between canola oil and the comparators. We found also some of the trials with refined canola oil.

also report inflammatory markers, and there also no significant increase. And then the other thing that's worth mentioning is this temporality aspect, because maybe eating it for a couple of months doesn't raise inflammation, but eating it for years does. Certainly the little lake acid, the main thing that people worry about in regards to inflammation, the main component of seed oils,

there's long-term data on it. And if anything, people that eat more winnoleic acid have lower inflammatory markers. So again, I think there's lots of things that could be done and lots of trials that could be tried and lots of things that I would love to see permutations, but I don't see the support for the idea that it's inflammatory. And we have a whole video from like a year ago

going over inflammation and all of these seed oil systematically from flax, all the way to safflower, running the gamut of lainoleic acid content. And there is just an overwhelming balance of evidence against the idea that they're pro-inflammatory.

So that's the evidence that is out there that I've seen. If future evidence goes against that very well, I'm glad to change my mind, but I don't see the support.

What's the takeaway point here for someone, again, they're going to the grocery store and thinking about what they're going to cook their vegetables in or add to their recipe? Are they choosing corn oil, safflower oil, canola oil, olive oil, avocado oil, macadamia oil? How does someone navigate that?

So I would say you can't really go wrong with any of the ones that you mentioned. I would say the one, at least for blood lipids like LDL cholesterol, canola oils probably the best. It's also the highest in the omega-3 of the ones that you listed there. So that's a pretty bad rap though. I think a lot of people here canola.

and assume inflammatory, a baseogenic, increased risk of cardiovascular disease. Yeah, that's the challenge is it has this bad rap, even though the health outcome data is completely on the other side. And in fact, there's not a single study that's ever shown that it increases inflammation, not one. In fact, that goes for all seed oils. From what I've seen, I think many people form that view or convinced of that after hearing about how it's made.

Yeah, I agree and it's the whole, like, processing nature, industrial nature of it, I guess. I mean, but that goes for so many foods that we eat. That goes for olive oil as well, you know, in a lot of cases. And what I would say, though, is if someone is truly confused, if they're not convinced by what I'm saying here.

Go for a olive oil. You can't go wrong with that. And that's something that actually Tucker and I agreed on was that olive oil is a good option. So if you want some level of agreement there. This is a good thing for us to underline. There were some agreements. I think that both parties would agree that consuming ultra processed, highly palatable foods that contain seed oils, probably not a great idea.

YouTube may differ in why those foods are deleterious for health. He might isolate and say, look, out of all of those ingredients in that food matrix, the artificial ingredients, the additives, the other fats, the refined sugars, all of these things, the fact that there's no fiber, he might still say it's the seed oils. Whereas you would, and I'm sort of speaking for you, but I imagine you would say it's a combination of many factors.

Yeah. And more than anything, you nailed it with the hyper palatability. I think that's the number one factor which can be contributed to by the high fat content and the sodium content and all that stuff as well. But that's a little bit different to adding some kind of oil to your cooking on your vegetables or some olive oil on the salad. Yeah. That's not at all comparable. Okay. It's like actually an analogy I often use. It's like saying that water is deleterious to health because it's the main ingredient in Coca-Cola. Right. It's the package. It's not, it's not the water that's doing it.

The fact that on a calorie per calorie basis, saturated fats tend to increase insulin resistance compared to unsaturated fats is generally not something my keto friends want to hear. In fairness to them, this insulin resistance might not be such an issue if someone adheres to a very low carbohydrate diet for life in less than 40 to 50 grams of carbohydrates a day or so. But I do wonder how many people can really sustain this for life.

and as soon as you reintroduce carbohydrates and come back to a mixed diet, all of that excess saturated fat will make blood glucose control really difficult, especially if the person is no longer losing weight or worse yet is regaining weight after a short period of calorie restriction, which is often the case. This is one of the many reasons why I think a saturated fat rich keto or carnivore diet may be problematic in the medium to long term.

When we zoom out beyond a few months and beyond the anecdotes of highly motivated influences online, it seems to me that it's setting a lot of people up to fail. The highly motivated folks who stay lean and commit to low carbs for life, granted, they may do relatively well. But in my view, that's going to be a very small fraction of the people who start a ketogenic diet.

Number four on our list today, let's talk about health outcomes. How do different fats affect your risk of chronic disease and premature death? The stuff that we really care about. There's two main types of evidence that we need to consider here. Randomize controlled trials that have enough subjects and it carried out for long enough several years or more to detect differences in these health outcomes. For example, randomizing one group to eating butter and the other two vegetable oil.

and then following these subjects for many years. And then there are these long term observational studies where we can follow people for much longer, often decades long, and detect associations between the types of that people consume and their long term health, while at the same time controlling for other variables.

like exercise, smoking, drinking with statistics. So we can, to the best of our ability, see the independent effect that dietary fat has on their health. In reviewing this evidence, it becomes very clear that how a certain type of fat, saturated, monounsaturated or polyunsaturated, influences health very much depends on what you're comparing it to. Remember, this is a principle we spoke about before. The only exception to this is trans fats.

Trans fats are just consistently bad for heart disease risk across the board, no matter what you compare them to. Placing trans fats to the side, if you don't consider what we're comparing a given type of fat to, it's very easy to become confused here. For example, meta-analyses of these randomized controlled trials and also observational cohort studies clearly show that when you replace calories from saturated fat with the same number of calories from polyunsaturated fat,

monounsaturated fat, or even unrefined carbohydrates, especially from whole grains, you actually see a reduction in risk of cardiovascular events. However, if you've removed calories from saturated fat from the diet and replaced them with refined carbohydrates, it's a lateral move or may actually worsen cardiovascular disease risk. Hence why it's important to read beyond the abstract and look closely at what the comparator is.

When people are eating less saturated fat, what are they consuming instead? This is where a lot of people get tripped up. I regularly see people sharing reviews comparing saturated fat to carbohydrates as evidence that saturated fat is not a problem. The issue here is in these two or three reviews that are regularly cited, the researchers did not break carbohydrates down to unrefined and refined carbohydrates.

I'm sure you would agree with me that jelly beans aren't exactly the same thing as black beans, both sources of carbohydrates. Fortunately, in more recent years, research is placing more emphasis on getting clear on what type of carbohydrates people are consuming, refined or unrefined. An extra layer of nuance, if you will, is that the type of saturated fat matters.

Remember, not all saturated fats are equal. Dairy fat, for example, seems to have a different effect to the fat found in red and white meat. If you compare dairy fat to the fat in red or white meat, dairy actually looks quite positive when it comes to cardiovascular disease risk. But if you compare it to the fat found in vegetable oils or high quality carbohydrates from whole grains,

It doesn't look as good. Then there's the food matrix issue, and how refined a particular food is or not. It's not really that fair to lump butter and heavily refined food into the same group of foods as milk, yogurt, and cheese, for example. But in many studies, they often are. However, unlike butter, the effective milk, be it full fat or low fat, seems to be neutral with regards to cardiovascular disease risk.

and fermented dairy foods like yogurt and cheese are neutral or perhaps even beneficial for cardiovascular disease. Importantly, this is observed at total dairy intakes up to 200 grams per day, not more, so it's not an enormous amount. One review I read summarized this as a generous serving of yogurt a day and three serves of cheese a week.

You published a paper in 2016 with Chen Mu. Hopefully I pronounced that right. And it was on dairy fats. And that was, I found that paper to be particularly interesting. I'm interested in what were the major takeaways of that research and how your views have specifically maybe evolved when it comes to this food group dairy.

Yeah, well, Derry, I think the most interesting food group because it's very complicated and it's not like sugar, sweetened beverage, just everything is bad, no good. But Derry clearly has a lot of positive benefits, a lot of beneficial essential nutrients in it, but also some potential harmful effects as well, consumed in high amounts, especially all through life.

And actually our family has been a dairy family for generations and I grew up in a dairy research farm when I was young. So it's always been of interest. And basically, dairy looks like sort of in the middle of the spectrum between health food and unhealthy.

So if we look at total mortality, we see that, of course, the worst is processed red meat, then eggs and unprocessed red meat dairy.

in the middle, but if you really don't want to go to low risk, then healthy plant foods would be associated with the lowest mortality. So whether you say dairy's good or bad, again, it's the substitution that's so critical. If you're having some dairy foods replacing red meat or I sort of use the example of buying a sandwich, do you want bologna or cheese or peanut butter?

The best would be peanut butter and all of them on whole grain, of course. But for diabetes, it looks pretty, dairy is pretty neutral. For weight gain, there's some suggestion, some studies that there might be a little bit less weight gain. But when we looked at it in detail, it looked like most of that was coming, the benefit was coming from yogurt. And we adjusted for yogurt, we didn't see.

benefit for weight gain or type 2 diabetes.

What about the fat content? Is someone's trying to navigate this? So within the yogurt section of the grocery store or even milk, there's high fat versions and low fat versions. I think this is a really interesting thing to explore. There's a lot of research on what are the types of saturated fats that are in dairy. Are they behaving differently to saturated fats, say in meat? What would be important for people to understand here?

Yeah. Well, for yogurt, it looks like another dairy foods. It looks like it doesn't make a great deal of difference, whether it's high fat or low fat, for most of the outcomes we've looked at. But the worst, of course, is if it's low fat, and then you put back a lot of sugar in its place, that's not going to be the healthiest choice. And of course, if you look at the grocery store, shelves, a lot of these low fat dairy products are very high in added sugar.

But if we look just at dairy fat itself, it's definitely not an optimal fat. And I know there's been ideas that it's got some medium chain. Safe 15 pops up a lot.

That comes up. It turns out that's very non-specific. It's not specific to dairy. Doesn't your body make that as well? The body can make it a little bit, but it can also come from beef as well, and it can come from metabolized from other forms of other fatty acids as well. Unfortunately, it's not a very good indicator. I think I read one study where vegans had the highest C15 levels. Really? I had a super interesting.

Yeah, you can get it from non-dairy, definitely from non-dairy sources, but we did a paper specifically looking at dairy fat compared to other types of fat. Clearly, for total cardiovascular disease, total mortality, the plant oils were better than dairy fat. Fat from red meat looked a little worse than dairy fat, but that may be still other things in red meat that are contributing

to that. And there was one important study done by colleagues at LaValle University in Canada, actually funded by the dairy industry, to look at the question of was dairy fat from milk, or say the other way around, is dairy fat and cheese better than dairy fat from milk? And there's been a lot of talk about that over the years.

and they did a really well-designed study. As it turned out, there was a slightly less adverse effect on LDL cholesterol from dairy fat and cheese than from milk, but to their credit, they also had two other arms to the study. One was a high mono plant oil, and the other was a high polyunsaturated plant oil, and both of those had dramatically lower LDL cholesterol compared to either form of dairy fat.

And that's really exactly what compared to what? Yes. So if you're swapping out red meat for dairy, if that kind of made sense in a dietary swap, then that could be an improvement, slight improvement. But then going from dairy to some sort of plant fat would be an improvement again.

Right. Yeah. Or if you're thinking of these just as added fats, uh, also very important because we do add quite a bit, but maybe about 20% of our calories are added fats that cheese, I'm excited that butter is not going to be healthy compared to, uh, plant oils like olive oil or canola oil or soybean oil.

But it tends to have even worse effect on LDL right compared to cheese. My understanding was that was because of how refined it is that milk fat globule gets broken down. Is that why it would have a more deleterious effect? I'm not really sure there is, but I think those are small differences. And of course, it's hard to compare those directly because cheese has the protein and that's going to

other components and just the amount if you're using on a total gram basis, you get more saturated fat from butter than you would from cheese. Why yogurt and cheese are associated with lower risk of cardiovascular disease is actually really interesting to me. And it remains an open question. It could be the micronutrients that these foods provide. Vitamin K1, K2, calcium,

etc. or it could be that dairy contains a specific type of saturated fat known as penta, decanoic acid or C15 for short. There's some emerging data on this fat being associated with good long-term health outcomes. I'm going to dedicate a video to C15 shortly after I deep dive the literature so that I can give you a well-informed view.

The reason I find all of this interesting about dairy is that if we can better understand how dairy is affecting cardiovascular health, it may help us make better food choices should we choose not to consume dairy. Such information could help individuals be more precise when choosing replacement foods for dairy, and it could also inform new formulations for plant-based milks and yogis, et cetera. Most of the research looking at dietary fats and long-term health outcomes is focused on cardiovascular disease.

there is some data looking at other long-term health outcomes, perhaps the most robust being Wang et al's 2016 paper published in JAMA Internal Medicine that analyzed data from over 120,000 American men and women followed since the 1980s and found that replacing 5% of calories from saturated fat with 5% of calories from unsaturated fats significantly lowered the risk of dying, not only from cardiovascular disease,

but also from cancer, neurodegenerative disease, or death from any cause. In other words, the people eating less saturated fat and more unsaturated fats, especially these polyunsaturated fats, were living better for longer. Number five, the last item on our list today. Let's bring this all together. What does all of this information mean for your daily food choices, your dietary pattern and supplementation?

Starting very broad, I'd like to refer you back to the Danish dietary guidelines. That is a great template to start with that gives recommendations that are very much based on the information I've just walked you through. Getting a little more granular or specific. Let's pretend you're at the grocery store. Swap out butter, coconut oil and palm oil, and instead bring in olive or avocado or even canola oil for your cooking.

If you eat meat by the leanest red and white meat you can find, or even better, keep it to occasional rather than daily, and add in fatty fish, tofu, tempeh, beans, lentils, and or chickpeas instead. And remember, herbs and spices, they are your friend. The amount of times people say to me, am tofu is bland, how do you eat that? Well, yeah, just like chicken, you need a seasoning.

It's a vehicle for flavor. So it is on you to bring the flavor out. My go-tos in my own kitchen are smoked paprika, ground cumin and ground garlic. And then if I'm making a tofu scramble, I will work in a generous amount of turmeric too. My tofu scramble recipe, quick plug, is in my zero cost two week meal plan, which you can download at theproof.com. If you eat dairy, I would focus on fermented dairy, cheese and yogurt.

these are the forms of dairy that may even be beneficial for cardiovascular health. In fact, while we're here, when I'm asked by people what animal proteins I would recommend for someone who wants to eat an omnivorous diet, it is fatty fish and fermented dairy at the top of that list. The real problem with these sources of animal protein, fatty fish and dairy, is that they're unsustainable for the world to eat at mass. And if you eat too much of them, it comes at the cost of fiber,

and phytochemical rich sources of plant protein. So if you include them, try not to make them the star of the plate at every meal. If you don't do dairy, then I would go for an unsweetened plant based yogurt made from soy, cashews or almonds. I find the ones made from coconut to be very tasty, but also very high in saturated fat, which based on coconut oil trials is likely to raise your cholesterol. Although I haven't yet seen that,

in a specific study. As you can see, it is possible to optimize fats in your diet with various dietary patterns, omnivorous, pescatarian, vegetarian, or whole food plant-based. What I will say though, and this is where personalization comes in, is that if you measure some of the biomarkers that we spoke about, like ApoB, and you find it's elevated, you may want to consider trialing a period of four to eight weeks of a more plant-rich or plant-exclusive diet before retesting that market.

The extent to which someone will need to make changes to optimize a biomarker like Apo-B will differ from person to person depending on their genes. Generally speaking though, most people will need to eat considerably more plants and less animal foods to get their Apo-B level down to a safe level. A safe level being a level where we do not see arteries building up with plaque. For someone who's not at high risk of having a heart attack or a stroke, that Apo-B level

is 80 milligrams per deciliter or lower. If you're interested in making some of these dietary changes and getting your lab work done to know where your health is at baseline and after making changes, I strongly suggest downloading the Living Proof Challenge PDF at theproof.com. This is a zero cost science based program to help you navigate a pretty tricky Western environment and live better for longer.

We also discuss supplementation within the living proof challenge, which brings me to DHA and EPA and MEGA3s. If you caught my recent video dedicated to MEGA3s, you will know that based on my rate of the data, I do think it's a good idea to supplement with a DHA and EPA fish or algae oil if you're not regulating fatty fish like salmon, mackerel, sardines, anchovies, herring.

I personally use an algae oil and take about 1.5 grams of combined DHA and EPA per day. I recently measured my omega-3 index with omega quant, and it was 9.44%, which is considered ideal for cardiovascular disease risk. I used to supplement with much less, around 300 milligrams a day, and my omega-3 index was around 5%.

One to 1.5 grams of EPA and DHA per day is what I recommend if you're not eating fish and testing your omega-3 index with a company like Omega quant who I'm not affiliated with but have personally used and had a good experience with. There we go. I think we did it. The different types of fats in our diet, what makes a fat essential versus non-essential, how they affect biomarkers and health outcomes,

and what this means for your daily food and supplement choices. Was that helpful? Would you like more of these solo episodes? Let me know in the comments section on YouTube or labor review on the Apple podcast app. Either of those or both for extra brownie points really does help the show reach more people. And whether it's a good idea or not for my mental health, I do read all of the reviews and the comments in the hope that

I can use them to bring you more value each and every week. So if you do leave a review or comment, know that I will personally read it. Okay, bye for now.