Transcription
The demonization of fat, the demonization of saturated fat, the demonization of cholesterol—all these things that we got wrong have just then been the bedrock of everything else that's gone wrong since. Fiber is literally many sugars of the indigestible kind. So, why would people be telling me to consume many sugars that I can't digest, let alone to the tune of 30 grams every single day? Why would that be happening?
If you look at what we need to get in the diet, and where do we find what we need to get, it just turns everything on its head because you say, okay, we need vitamins and minerals and essential fatty acids and complete protein. We find them in animal foods, particularly in red meat and oily fish and egg yolks and full-fat dairy. And that's actually all you need to eat. You don't actually need any plants, and you can get everything you need. They just came at it from completely the wrong point of view.
It is utterly mad that our governments are saying to us, have 350 to 400 grams of carbohydrate, but eat less sugar. It is all just sugar that the body then has to deal with. The idea that we're telling people to have more carbohydrate and less sugar is just another thing that is so misunderstood. It's just showing that whoever is telling you to do that is very, very ignorant when it comes to nutrition. "Zoë," when it comes to the current dietary guidelines, whether it be where you're at in the UK or here over in North America. What are we actually getting right, if anything?
It's definitely quicker to say what we're doing wrong, I think, which is just everything. What are we getting right? I just can't think of anything. And we got your guidelines, so you kind of kicked it all off. So, America started all of this nonsense, and then all the rest of the countries followed suit, including the UK, New Zealand, Canada, Australia, Europe. You kind of set the scene.
We just don't get much right. I guess they tend not to push processed food, which we could probably put a tick in the box. But in the UK, on our plate, we've got in the bottom left-hand corner, we've got a whole heap of processed food and junk. So, we don't even get that right. So, no, really, not very much at all, I'm afraid.
Okay, so our current situation not good. How does somebody begin to piece this together and find a diet that's right for them? I go back to first principles, and I think if the dietary guidelines had done this... They came with an agenda. So, when they were put together, I just slightly have to go back. I always have to explain this to people because it was such a penny-drop moment for me. If you picture a little pie in front of you and realize that protein tends to be a pretty constant 15% of any natural diet. And that actually holds for vegetarian diets as well as omnivore diets. You've then got two macronutrients that make up the rest, and that's fat and carbohydrate. When they introduced the dietary guidelines and they said, we're going to demonize fat. We think fat is really bad for you. You're going to have no more than 30% of your diet in the form of fat. It's inevitably telling us to have 55% of our diet in the form of carbohydrate. And they would happily have us have even less fat, even more carbohydrate. So, they've come at it from completely the wrong angle. They've come at it from fat is bad. And we can get into that because there was just no evidence for that. That was my "PhD" turf.
I come at it from a completely different angle, which is why do we eat? We eat because there are certain nutrients that we must get. If we don't get them, we can die. It's not just ill health we're looking at here. If there are some nutrients that we don't get, we can die. They're not called vital for nothing.
And if you look at what we need to get in the diet, and where do we find what we need to get? It just turns everything on its head because you say, we need vitamins and minerals and essential fatty acids and complete protein. And where do we find those things? We find them in animal foods, and we find them particularly in red meat and oily fish and egg yolks and full-fat dairy. And that's actually all you need to eat a selection of foods from the animal kingdom. You don't actually need any plants, and you can get everything you need. They just came at it from completely the wrong point of view.
Well, let's go deeper into this. You gave a general idea there of the healthy foods, but let's talk about the hierarchy, starting at the top and then working our way down. What's most nutrient-dense when we're piecing together our plates?
Yeah. So, it's within the animal food kingdom, and it's offal. It's livers, kidneys. Pretty much those two. The French eat everything. When people talk about the plant-based Mediterranean diet, it just makes me laugh. The French will just eat anything that moves, and they don't really mind if it's dead or not either. Snails, mussels, just chuck them down, frog legs, whatever, lightly fried.
It's offal, it's organ meats. And then within the hierarchy of animal foods, different animal foods provide different things. You can get everything you need from meat. So, the carnivores, like "Anthony Chaffee," "Ken Berry," "Shawn Baker," they're getting everything they need from meat. And I don't even think they're all eating nose-to-tail. It's actually mostly organ meat. But within the animal options it's the ones that I just touched on earlier. So red meat is more nutritious than white meat, oily fish is more nutritious than white fish. Both of them are good, but one is more nutritious than the other. The egg white, not so good. The egg yolk, very much so. And don't go for low-fat dairy because you're missing out on all the goodness in whole dairy not just the essential fats, but calcium, the bone nutrients, phosphorus, vitamin D, all the rest of it. There are reasons that all the nutrients that we need are in those animal foods. That's what we need to prioritize in our diet.
When you talked about the carnivores there, you mentioned them getting all they need from organ meats. I think you meant muscle meat though, correct?
Yes. So they—get all they need from meat, just basically meat. And I don't actually think they're eating the offal. I don't see those guys that often saying, oh, look, here's my meal of just liver. They really don't. You see "Shawn Baker" and he's got—four pounds of T-bone steak in front of him or whatever. So they are just getting what they need from, as you say, muscle meats even though organ meats are actually the most nutrient-dense foods of all.
So in your mind, when somebody is including plants, there's no additional benefit, it's more just for diversity of the diet?
Yeah, it can make some things a little bit easier. So, plants come from the ground, minerals are present in the ground, quality of topsoil is a separate issue but you do think of some plant foods as they're quite good for maybe magnesium or selenium. But there's still nothing in plants that you can't get from animal foods or that you couldn't get from just meat. So yes, I think they're good for variety. To me, just a piece of meat on the plate is just not enough. It would look a bit lonely, and I would miss the crunch that you get from plants. I like the taste of plants. Plants don't cause me any problems, so I think they're a useful addition to the diet. But there's nothing that we have to eat to get from plants that we couldn't get from animal foods.
All right, I'm sure we'll come back to plants, but I think it's important we set the scene right now and talk about how we got here. You mentioned the demonization of fat. Let's go back in history and talk about where that started and how we got to current day.
Great. I did a post on this actually over the summer, so it was called "The Origin of Our Beliefs on Fat." And they are beliefs, they're not facts, they're not evidence-based. So I traced it back to—the main person who features in this whole story is an American doctor called "Ancel Keys." A lot of people in this field will have heard of him. And he'd actually spent, he'd done a brilliant experiment. So he'd done the Minnesota Starvation Experiment, which was published in 1950. And he was studying people who didn't want to go to war, basically conscientious objectors. And he was studying the impact of caloric deficit, because that's what we thought was going to happen if America joined in the war and then you guys would start having rationing like we were going to have. So he was a prominent researcher, and then he turned his attention to heart disease in men, because heart disease in men was very much on the rise. And it was an interesting phenomenon, and he was a natural curious guy, so he started to have a look at this. And he first started to look at the work of the pathologists around the turn of the century in Russia, where they'd been cutting open people who'd died suddenly, most certainly from what we would now call a heart attack. And they were spotting that they had sort of blocked arteries and then fatty deposits around that area. So "Keys" started to—look at cholesterol and is cholesterol the problem? Well, "Keys" actually got to the point where he said, cholesterol in food is not a problem, it's not a problem with cholesterol in us. And we've kind of known that all along. Not many people know that, but he concluded that. So he said, I think it's fat. And started looking at population studies. Started trying to do some small-scale trials, but started trying to look at the association between dietary fat and what he was observing in men. And it really was just men.
And the really important study that I think kicked all of this off was in 1953, and he did a presentation which became known as the Symposium on Atherosclerosis and it was the Mount Sinai presentation, it was called. And he presented a graph and it had six countries on it, and it included England and Wales, Italy, the USA. And it really sort of anchored, one was up at the top right of the chart, one country was down at the bottom left. So he managed to get this really quite striking upwards graph showing that the higher the fat in the diet, the higher the death rate among men. And I think it was men aged 45 to 64 or so. And look, here's a really, really good association. Well, it's still just association. He hasn't done an intervention study. He didn't do a randomized controlled trial and give those guys loads of fat and those guys not so much fat, and see what happened. He didn't do any of that. It's just an association.
And then things didn't happen as quickly back then, with rapid responses on journal articles today, you'd have other researchers just going in so quickly saying, no, that's a load of nonsense, you've left stuff out. So it wasn't until 1957 that these two researchers called "Yerushalmy" and "Hilleboe" said, hang on a second, we've just had a look at the data that you used for that. And you took out six countries, but there were actually data for twenty countries. And when we put in the twenty countries and I've got this on a post on my site it's like a scatter diagram. You can't. You could draw a line left to bottom-right as much as you could from bottom-left to top-right. I mean, it's naughty. You just haven't used all the data. And he—was very scathing in his response, and it kind of gave us an insight into his character. He's a very arrogant man, by all accounts, very dismissive of other researchers at the time. It's kind of like, well, I'm right and you're wrong. And he basically said back to these guys, you cannot possibly think that fat hasn't got something to do with this. Serious, it was really condescending and really sort of gave us an insight. But anyway, they were all very polite then. Researchers are much less polite now.
So that kind of died away. And he'd already started on this study that your listeners will have heard of the Seven Countries Study. So that "Yerushalmy" and "Hilleboe" paper's published in 1957, 1956, he'd already started the Seven Countries Study across seven chosen countries with researchers that he'd worked with before. He knew them, he knew their views on fat, cholesterol, heart disease. Sixteen cohorts across those seven countries were studied, and that then wasn't published till 1970. And you mustn't confuse the Seven Countries Study with that six countries graph. There were some countries in that six countries graph that were part of the Seven Countries Study, but there were also ones that weren't. And they were just two entirely separate pieces of research, but one just gave him this idea in his head that fat is related to heart disease.
And a really interesting thing that not many people know is when he went into the Seven Countries Study, he clearly thought fat is associated with heart disease in men of particular age, middle-aged. And the conclusions of the Seven Countries Study did not say anything about total fat. So his three conclusions at the end, they were quite vague, and they had these words sort of tends to. So it was saturated fat tends to be related to cholesterol, cholesterol tends to be related to heart disease. Saturated fat and cholesterol and heart disease all kind of tend to be related to each other. And it just wasn't very strident in the claims nowhere near as strident as the claims that he was coming up with back in 1956. But that kind of sowed the idea that fat is bad.
Wind forward to about 1977, you've got Senator "McGovern" over in the US who was a failed presidential candidate, feeling a bit bruised, wanted to make his impact on the world, arguably has left more of an impact than whoever he lost to, who I can't even remember. Because he—basically laid the foundation for the dietary guidelines. So the "McGovern" Committee, 1977, he turned his attention from lack of nutrition—to what can we do for guidelines for all of Americans? I want to set the diet for America. No hubris there. And he came up with this low-fat diet. We're fearing fat—He personally had just been on a "Pritikin" type boot camp—So he was quite sort of enthusiastic about low-fat diets—at that time. And it was kind of, boom, everyone's going to go on this low-fat diet. And of course, the minute you take fat out of the diet, the only thing that can replace it is carbohydrate. And that's how—we got—the foundation of high-carb, low-fat—diets. And then what that low carb is, it just makes sense. It's going to be pasta, rice, potatoes, bread, and all the stuff that then ended up on the pyramid in the Dietary Guidelines for Americans in 1980.
So just to be 100% clear here, in your mind, fat there is no connection there to heart disease?
Well, I did my "PhD" on this, so I was fascinated by—obesity—and I was trying to understand why did obesity just take off in the last quarter of the last century like an airplane? And there's this brilliant "NHANES" chart where at 1976 to 1980, in America, it just takes off—like an airplane. So what happened there? Well, you changed your dietary guidelines. So I wanted to ask the question. Why did we change dietary guidelines, and should we have changed dietary guidelines? So my "PhD" basically used systematic review—and meta-analysis, which is the highest form of evidence that we can use in academia. And it said, if I pretended I was on the committee back in sort of 1976, 1980, 1983 in the UK, was the evidence there then? Would I have changed the dietary guidelines? Was it overwhelming that fat is an issue?
So first paper looked at randomized controlled trials. It went nuts. It was like the 64th most-cited paper—in 2015. It was bonkers in any discipline—because it basically said, no, there was no evidence, there was no difference in all-cause deaths. And when I say no difference, I mean no difference. 270 in this arm, 270 in that arm. Not even not statistically significant, literally no difference—No difference in heart deaths. Then I looked at the epidemiology, which included things like the Seven Countries Study, the Western Electric study, the London busmen, et cetera, et cetera. No evidence whatsoever. I then wound it forward and I said, okay, but that was back in 1980. I'm doing my "PhD" in 2016. There must be more evidence now. And that starts to then bring in things like the Women's Health Initiative, the Minnesota Coronary Survey—Again, no evidence whatsoever from randomized controlled trials, no evidence whatsoever from epidemiological studies. There is no evidence against dietary fat in terms of heart disease, heart deaths, all-cause mortality. There just isn't. And yet these guidelines still prevail.
Okay, well, we know heart disease—is a major problem right now. Number one killer, I believe, in the world. Let's talk about what you think the real cause of that is.
I happen to know someone—who is a friend as well as a person who was a colleague in a lawsuit I was involved in. And he's just an all-round fantastic guy. He'd be a family doctor, that's what you'd call him—over in North America. He's also done a lot in elderly care, and he's just had a lifelong fascination in heart disease. And—I bow to his knowledge. I think he's done an outstanding job with a book called "The Clot Thickens." And—he could list 250 things. It would be having a certain condition, pollution, smoking, stress, bad diet. There are so many different things, but he's managed to—get them into this sort of umbrella, sort of top-down of, okay, if you've got anything that's going to damage your arterial system, if you've got anything that's going to impair the repair of that arterial system because it will try to repair itself or if you've got anything that's causing clotting, that's your heart disease. And it is all-encompassing. We've simplistically got it down to—if you've got a high "LDL" cholesterol or high total cholesterol or something—that's what causes heart disease. That's wrong. It's not just simplistic, it's wrong. And it's ignoring about 250 other things that are almost certainly more important, if not equally important. There are definitely things in there that are way more important. And it's just like we just don't look at all of those anymore because this "LDL" cholesterol story—has just gone so nuts. "Malcolm Kendrick's" great, he's been on the show twice—I'm a big fan.
Excellent. Let's break down different lipoproteins, including "LDL." And then we can understand the story a little bit better.
Yeah, yeah. This is a really important one, actually, because so many doctors don't know this. And I try to encourage people, you've got to be bold when you have doctors talking about good and bad cholesterol. This is just so wrong. You have to correct them. We just must not let this terminology go unaddressed. So I always sort of hold up a bit of water and say, okay, that's water. We kind of liken that to blood. And if I drop some olive oil in there, it would not mix, it would just sit on the top. So if we imagined having fats in the bloodstream, olive oil in water, they just wouldn't mix. And you would have the situation where something could clog up in a narrower blood vessel vein rather than an artery kind of thing. And the body just wouldn't allow that to happen. So our incredible, brilliant body has designed this system called the lipoprotein system. And I think of it as a transporter system around the body. So I call them taxis. So the five main taxis that we need to know something about and these are in order of size. So if you actually, if we were able to sort of take them outside the body, the first one, the chylomicron, would be about the size of a football, and the end one would be about the size of a pea. And they sort of reduce down—The chylomicron is a lot bigger by a margin.
So the chylomicron, when we digest food and it goes through—our digestive system and then it goes out into our lymphatic drainage system. That's where the body—will use the chylomicron taxis—to package up any fats—that we need to take out of our food, that need to travel around the body to drop their cargo off at cells because the cells need those essential fat-soluble nutrients and all the rest of it. And that's the body taking the nutrients out around the body—You've then got something called very low density lipoprotein, which also gets shortened to triglycerides, which is a bit confusing, but kind of the liver is then making—"VLDL," very low density lipoproteins—And then those very low density lipoproteins—release some of their cargo and become—"IDLs," intermediate density lipoproteins. We don't hear so much about that one because you can't lower it or raise it or it's not good or bad or anything in their terminology. So they kind of just ignore that one—That one then drops off some cargo and become an "LDL," which we will have heard of. And doctors will call that—bad cholesterol. It's not even cholesterol, it's a taxi—carrying cholesterol. And then the final one that we've got is "HDL," which they call good—cholesterol. Again, it's not cholesterol, it's a taxi. And all of those taxis, all those five lipoproteins that I've mentioned, they all carry—cholesterol, triglycerides, phospholipids and protein, just in different proportions. So the "LDL" yeah, it does have more cholesterol than the other things—and the "VLDL" has more triglyceride than the other things, but they're all carrying—the same cargo—And the concept of density is just when you get down to the really small one, which is the "HDL," it's just more tightly packed because it's small, it's carrying similar things, but it's a smaller little taxi. So they're just more tightly packed—But it's not good and it's not bad.
And when people sort of say "LDL" or "HDL" and then they don't put that cholesterol on the end, again, you've got to pick them up on it and say, so you're talking about cholesterol now? Are you talking about carriers of cholesterol? And quite often they look at you quite baffled, as if, oh, I don't really know—I hadn't really thought about that. It's like, this is so important. Don't let people bamboozle you with technology, because that's how we end up—with a theory hypothesis that just doesn't withstand scrutiny if you don't really pin them down on. Are you talking about "LDL," that's the taxi, or are you talking about "LDL" cholesterol, that's a component part of the taxi. We're having a completely different conversation here. And when people start talking about small dents and large fluffy, you're now talking about taxis. Aside from the fact you're talking complete and utter nonsense, you're talking about taxis. So we're no longer having a debate about cholesterol and that's fine, but just stop demonizing cholesterol because you're now having a different conversation. So it's a very misunderstood area.
Let's go deeper into that small, dense versus large fluffy, you quickly went across that. There are people—saying, it's not "LDL" that's the problem. It's a small dense. So let's talk more about what that is and how you see it.
It's barking! It's barking! I can't remember the exact size of an "LDL," but you'd be able to look it up quite quickly. And it's measured in nanoparticles. I think "Malcolm" likened it to if you're in some massive stadium that you'd go and attend to watch some American football and it probably carries 80,000 people. An "LDL" in that kind of environment, might be a speck on a chair, kind of thing, just to try to get the scale of what we're talking about. So what they say about the small dense, large fluffy—apart from the fact they don't realize they're no longer having a debate about cholesterol, they're actually talking about lipoproteins and yet they don't make that clear. So that annoys me. There's this inference that if it's small apart from the fact it's infinitesimally small already if it's smaller than infinitesimally small, as opposed to slightly larger and fluffier than infinitesimally small, somehow it's going to be able to enter the endothelial wall. And you've just got to challenge that as a concept at the outset. That is what they are inferring. They're inferring that if it's small and dense, it's going to break through into the arterial wall and then it can do some damage. The body is not going to allow that to happen. We would not have "LDL" receptors on cells if "LDL" the taxis, remember could just bust their way into cells or—through the endothelial wall, we would not need "LDL" receptors. There is an "LDL" receptor on the cell, and as the "LDL" taxi goes by, the "LDL" receptor will grab it and say, thank you. I need you. I need your cargo. And then it'll dump off anything that it's not going to use. So this idea that you can just in any circumstance bust through the endothelial wall is just bonkers!
Now, when you can get through into the endothelial wall is when there's some damage, but that's got nothing to do with lipoproteins or cholesterol because you've got damage. So let's say you've got damage because you smoke, or because you have a high-sugar diet, or because you've got stress, or you're exposed to pollution, or all the other things. In "Malcolm's" great book, you've got damage to the endothelial wall. Now, the ultimate irony is that the thing that the body needs to go and repair that damage is "LDL." It needs the "LDL" taxi. And "LDL" receptors around that damage will try to take the "LDL" taxis to say, I've got some damage here. I need the lipids that you've got in your taxi to repair that damage. I need cholesterol, I need protein, I need triglycerides, I need phospholipids. I need that stuff. Send that over to me now. So the "LDL" is actually going to the scene of the damage. Now, if you've got a damaged endothelial wall, yeah, all bets are off. Plaque can break off, stuff can get in. You can get into a difficult situation. Your body is not working in the way that it should be working. But there is no way on earth that just because something is smaller than infinitesimally small, all other things being okay, some kind of "LDL" taxi can just bust its way through into your endothelial wall. So that's why I don't like the small dense, large fluffy stuff that goes on. And it goes on in our world as much as the "LDL" cholesterol heart hypothesis people's world as well. So it's kind of like the Six Graphs, Seven Countries, another one we need to clear up.
Now that we're deep into this hashing it out, let's bring in oxidized "LDL." This is another one you hear when "LDL" becomes problematic.
Again, you're talking about a taxi, you're not talking about cholesterol. So that's fine. But people will sort of say, oh, one of the reasons we need to take statins is oxidized "LDL," or whatever. It's like you're not talking about cholesterol anymore, you're talking about taxis. And if you're talking about oxidation that's the problem. Not the "LDL." The "LDL" taxi, the lipoprotein system, the way your body is designed, is all still in good order. Something is causing oxidation, and it's not only causing oxidation in one particular taxi, in one system in the body, which is called the lipoprotein system, it's going to be causing oxidation all over the place. So what is causing your oxidation? Are you consuming a high intake of seed oils? Are you cooking a lot with seed oils and actually inhaling all of those mutations as you go along? Are you exposed to pollution? Have you got environmental issues? Is your diet just not very good? We're back to all the things that actually are going to cause heart disease. They're also going to cause things like oxidation, inflammation, and general dysregulation within the body. So, don't blame the "LDL" taxi for the other things that we're going on. It's just going to be affected like any other part of the body is going to be.
You mentioned statins. Let's bring that in.
Okay. They're very effective at lowering cholesterol. They're very effective at lowering cholesterol, there is absolutely no doubt. And if you go on and put in—So, they're basically "HMG-CoA" reductase inhibitors. So, if you put in on a search engine the pathway by which cholesterol is made and the pathway by which statins block cholesterol, you come up with pretty much the same diagram. So, at the bit where you've got the sort of "HMG-CoA" reductase, that's where statins operate. And they basically impair that function in a pathway of the body. So immediately I'm thinking, I think my body's pretty well designed. I trust my body more than I trust the pharmaceutical industry. Immediately I'm thinking, I don't want to be blocking any pathway that my body has. I kind of assume it's got it for good reason. And actually, it does have it for good reason, because cholesterol is the absolute foundation of every single cell in our body. It is impossible to explain how important cholesterol is to the human body. If we didn't have cholesterol in our body, we would be a puddle on the floor. We'd be dead. We'd be no human, we'd be nothing.
Statins then operate at that part of the pathway. Now, one of the things in that pathway, at the bottom of that pathway is something called "CoQ10," which is also called the body's energy spark plug. So sometimes if people say to me, oh, I'm just feeling really wiped, really tired all the time, I might suggest to them, hey, why don't you just go and get a quality supplement, maybe try a bit of "CoQ10" and just see if you can get that sort of spark plug going again. When they first developed statins, they put "CoQ10" into the statin formula because they knew that they were blocking that pathway, and they knew that they were going to affect your energy spark plug. But then, for whatever reason my guess would be cost they just dropped it. So they block that pathway—They don't block it entirely, because if they did, the very first person who took the very first statin would have dropped dead. If you manage to stop the body instantly making cholesterol everywhere in every cell you become that puddle on the floor—instantly dead. And there's actually part of me that wishes that that had happened, because then we wouldn't have this whole—statin industry.
But we do have the statin industry—and—we have redefined what normal cholesterol is along the way. So when I try to research to see the normal distribution of cholesterol, and I try to go back about 30, 40 years before we started "statinating" as many people as we could, your normal cholesterol level. Do you deal in "mmol" or do you deal in "mg/dLs?"
I don't know, which one are you?
I'm in Canada—I'm the same as you. Okay. "Mmol." Brilliant, brilliant. So normal distribution the total cholesterol would go anywhere from 2 to 3 to 9 to 10. And in certain exceptional circumstances, you would have people over 10. But your main part of your normal distribution was anywhere between 2 to 3 to 9 to 10. So the actual norm was around 7 to 8. And that was the norm. But of course, they redefined the norm. And if you look at the history of people who were involved in redefining the norm, it was very heavily influenced by the pharmaceutical industry. So imagine you've got the norm at about 7 to 8, and then you just say—5 is now high. Well, you've just made 75% of people who were on the normal distribution, who still are on the normal distribution. You've now just made them in the high cholesterol category. It's just a stroke of a pen. In a stroke of a pen, you make 75% of the population eligible for statins.
And when you add in sort of things like risk assessments "Malcolm" and I have played with this. So everybody has what we call a statin-by-age. So if I play with the risk calculator in the UK and I put in—my blood pressure is really low, my cholesterol is actually really low. It's a shame, I'd like it to be higher. My "BMI" is really low. I'm female, I've got everything on my side. I'm not diabetic, etcetera. Put in all of that. And then I just change the age. And when I get to 67, they want me on statins. Doesn't matter that I'll still be in perfect health, none of those parameters will have changed. I should be on statins—and it can't be right that every one of us should be on a drug at a particular age, particularly because our cholesterol actually should go up as we get older, because we need more repair in all of our cells, everything else going on in the body.
So it's a massive industry, massive number of people—are on statins—Yes, they will lower your cholesterol. Do they actually have any impact on things that matter?
I'll take a breath in a minute see if you want to go there. And then we might want to get into side effects as well, because they are often also not talked about.
No, this is great. Take a drink of water and we'll continue.
Brilliant. I've actually just done a deep dive into statins. I've just published three notes. And what I really wanted to look at, because it's so seminal in the prescribing of statins, is there's a group in Oxford, in England, and they're called the "CTSU." I can't even remember what that stands for. It's something like Clinical Trial Service Unit or something. And then you've got the "CTT" group, which is the Cholesterol Treatment Trialists' Group. So it's a sort of—a unit, it's an actual physical unit that employs hundreds of people based at Oxford University. And then it's a research team based at Oxford, but they will also collaborate with people further afield. So sometimes you look at some of their papers and there are hundreds of names of collaborators on the papers. So they have done the seminal work. So they've basically done six systematic reviews and meta-analyses. And as I said earlier, that's the highest level of evidence. That's what I did with my "PhD." So what they've done is they've pulled together all the statin trials. So in my first note, I looked at what are all the statin trials? How many do we have? Which ones we're looking at statin versus a placebo? Which ones we're looking at higher-dose statin versus lower-dose statin? And there are 28 of them now in there. And—all but one had—the manufacturer of the statin what—Doctor "Michel de Lorgeril," who'd written a lot about—He did the Lyon Heart Study, written lots about the Mediterranean diet he looked at all of these. He said, there's only one where I wouldn't actually describe it as the pharmaceutical company is omnipresent. They're doing the stats, they're funding the trial, they're running the trial, their staff are involved in the trial, they are omnipresent, as he described it. And of course, the one that wasn't, that was actually independent, it didn't find anything. And actually most of the ones even funded by the statin manufacturers didn't actually find anything.
So you've got these core 14 trials, and they did a paper in 2005, and the first paper was, is there benefit prescribing statins? So to basically show that there's benefit, you've got to be getting into all-cause mortality because if you're into, oh, well, you had fewer heart attacks, but we gave them more cancer, or there was more suicide because cholesterol was so low and there is an association there—You've just got to look at all-cause mortality because somebody's either dead or they aren't. Did they have an angina attack or did they have indigestion? That's a whole different ball game. Did they die or did they not die? Now, the actual relative risk was very, very small, and they'd done a sort of modeling technique even to get that relative risk. So they didn't just look at how many deaths were there in the statin arm, how many deaths were there in the placebo arm when we pulled all of these together, they did it with a sort of modeling technique of per 1.0 "mmol" per litre reduction in "LDL" cholesterol, which is quite high, that's really quite big. As an intervention reduction in cholesterol, the placebo arm would not have achieved that at all. So kind of all your deaths are going into one sort of measure on the placebo side, and then maybe not all of your deaths are going in on the other side anyway. So they managed to get it off the line of no effect, despite only three of those trials individually made any claims for all-cause mortality. They were so compromised. I could go into some of those. Anyway, they start off with this baseline in 2005, and as I say, with all the caveats they won't allow any other research to access the data. They don't necessarily look at side effects and balance those out with this modeling technique, with the fact that pretty much all of the people they were looking at or 80% of them were male, 60% of them were not well. So we're not looking at healthy people, we're not looking at women. All of those caveats they managed to nudge it off the line of no effect when you look at the absolute risk, it's really like, do I care? It's like one in 100 or something; it's just not impressive.
So I then followed this through and I said, right, they used those core 14 again in 2008, and their research question was, okay, does it make a difference to people with diabetes? And I had not spotted this until I went into the deep dive. In the abstract of that paper, 2008—and I've just put this on open view. So go on my site, put in "CTT" statin papers, you can see the whole thing. In the abstract they say, so the reduction, the relative risk reduction was 0.91, brackets, and the confidence interval includes 1.01. So you've included the line of no effect. That is a non-significant finding, and it is not reported as a non-significant finding. So you didn't find anything for diabetes, so we can dismiss that one. So that's 2008.
2010, they say, let's look at more statin or less statin. Now, the bit in this note is just hilarious, because I was trying to separate out more versus less statin in all of those. They're now up to 26 trials. They've pooled more trials, but only five of them look at more versus less statin. So I go to "Grok" and I say, does it split it out anywhere? And "Grok" comes back and says, yeah, it does, and here's the result. And it's like 9% again and includes the number one. So it's a non-significant finding. And I'm like, where have you got that? And "Grok" says, oh, it's on this page. And I'm like, I'm looking at that page, I can't see it. And "Grok" is like, yeah, it's there. And then there's a table—and I'm like, I'm not seeing that. And then "Grok" says, show me your page 1676. So I do—"Grok" comes back, oh, my goodness, I'm so sorry, you're right. I'm looking at something that I've got in my data bank, which was an earlier version of the manuscript. So an earlier version of the published manuscript said, when you just look at those five trials, it doesn't count. I'm like, "Grok," don't apologize. I am so happy. This is an amazing find. Thank you.
Then I move on to 2012. 2012, they're trying to say, can we show that statins work in people at low risk of heart disease? And they muddy it with people who haven't had previous vascular disease. They're different things. Having had previous vascular disease is different to low risk of vascular disease, which they define as a risk below 10% over the next 10 years, five years, whatever, whatever. They didn't put that data in in the main paper. I found it in the supplemental. When you look at the data for low risk, it again does not achieve statistical significance. You can dismiss that one.
2015, they move on to women. Go to the supplemental again. There's no difference in deaths from vascular disease, no difference in deaths from non-vascular disease, no difference in any other deaths that they can't even define. And yet they claim there's a difference in all deaths overall for women. It's like, I'm not buying it.
And then the last one was one that I reported on at the time, that was 2019. They said in elderly people—there were big headlines across the UK. They did a big press conference. This Oxford Group, they said if all the over-75s were on statins, 8,000 lives could be saved. So I looked at, this is the main paper now. I looked at the over-75s. There's no statistical significance for deaths. Over-70s, the same. So 70 to 75, the same. I looked at primary prevention, which is what they were claiming. So in people who haven't had a heart attack yet, whether they're in the over-75s or whatever, no statistically significant difference. I don't know what to call this other than scientific fraud. I just don't know. I can call it naughty, I can call it disingenuous. There are hundreds of people working on this. This is not incompetence.
And this unit, there was a big hoo-ha that involved Doctor "Aseem Malhotra" and Doctor "John Abramson," and the "BMJ," and the editor of the "BMJ," Doctor "Fiona Godlee," at the time. And the Oxford Group had basically taken issue with a couple of papers that the "BMJ" had published by "Aseem" and "John Abramson." And "Rory Collins," who's the head of the whole sort of Oxford unit, had said to the "BMJ," you've got to retract those papers. It could cause untold harm. And "Fiona" held firm and said, I'm going to set up an independent panel, and we're going to look into this. And as part of that independent panel, they requested the pharmaceutical funding to the "CTSU" and the "CTT" paper group. And at that time this was back in 2014, I added it all up. They sort of like, oh, we got this from "Roche," and we got this from "Pfizer," and we got this from "Bristol Myers Squibb," and they were all millions and millions. And it added up to 268 million. That will be 400 to 500 million now. And those guys don't think that they have any conflicts in doing this work. And they won't allow people like me, Doctor "Malcolm Kendrick," Doctor "Maryanne Demasi," they won't allow us access to the raw data to actually look at the numbers for ourselves. So that was my recent deep dive, which as you can probably tell a lot of fun.
Given all that detail, it sounds like the answer is no. But can you think of a specific population, again, looking at the end result, deaths, that can benefit from a statin?
Yeah. And I asked that question—I can't remember which note it's in. I think it might be in note two. And there is some evidence that, in particularly males who have had a heart attack, there might be a benefit of a statin. But it then immediately comes with caveats. So what "Malcolm" does, which I think is brilliant, is say, we've got to stop talking about lives saved because we're not God, we can't save lives. All we can do is delay death. And that's what you're kind of looking for, aren't you? You're looking for cancer looks at it in terms of median likelihood of years of survival. And that's what you're interested in. I've just been diagnosed, how long have I got left, Doctor kind of thing. So this idea that statins are going to save lives or this intervention is going to save lives, it's a misnomer because we can't save lives. So by how long might we be able—to extend a life? And "Malcolm" does the research on a particular study that claimed a difference—for all-cause mortality, which was the "HPS." And I'm trying to remember what that stands for. It's a very famous study which the "CTSU" were involved in, by the way. So "Malcolm" did some research on that and—basically, you're going to extend it by days. And then there's another very famous study that was done by, I think it was a Dutch lead researcher. And again they said, so if you take statins for five years, we're not saving lives, but what's the kind of life extension that we're looking at? And it was something like 3 to 4.4 days or something like that. So take them for five years, you're going to buy yourself a few more days. Nobody knows that. If a doctor, I know Doctor "Aseem Malhotra" will present that kind of position—to his patients and say, okay yeah, you've had a heart attack. I'm now in the position where I'm saying to you, do you want to take a statin? Because there is some evidence that it's going to benefit you, but it's probably, on other evidence not influenced by the pharmaceutical industry, it's probably going to buy you a few days and then we need to factor in what else is going to happen within that five years. So if you go to this fabulous website called "thennt.com" that will work out for you what we call the number needed to treat and also the number needed to harm. So the number needed to
The flu jab will be, let's take the flu jab, because that's very topical at the moment. So we've got a Cochrane study, high gold standard study, before Cochrane went off the rails. And they said, what's the number needed to treat with the flu vaccine to avoid one case of flu in adults? And it's 71. So 71 people need to get vaccinated for one person to not get the flu. That's not great odds in my book.
And when they look at statins, so in secondary prevention you've had an incident it's going to be under 1 in 100. So I think from memory it's something like 1 in 80-something. So you've got a 1 in 80-something chance of avoiding an incident, which might be angina, it might be having a stent fitted, which is a procedure rather than an event, and it's a subjective procedure at that.
But then go and have a look at your numbers needed to harm. So the same group of people taking the statin for five years have got a 1 in 50 number needed to harm for type 2 diabetes, which is pretty serious, and a number needed to harm of 1 in 10 for muscle damage. And a lot of people stop taking statins because the side effects are so noticeable and so debilitating that they just say, do you know what? I don't even care if this is going to save my life. They don't know about the days saved. I don't even care. I can't even remember where I've left my keys. My brain has gone to mush, my sex drive is on the floor, my get-up-and-go has got up and gone. My muscles ache, my joints ache. Life is just miserable. I'm just coming off them. And most people who come off them, everything then will go back to normal within a couple of weeks. Mostly they don't leave lasting damage. So if you're feeling bad, then you could always come off them. That's not advice, obviously, that's a suggestion.
You made it clear when we got into statins that they do lower cholesterol. But we need to look at a bigger picture here... and determine whether that means anything or not. And earlier you brought up seed oils. And this is a food... that has been shown to bring down cholesterol as well. Let's bring them in and talk about the problems there. Nice connection.
Yeah, that's a really interesting one, actually, because this is where you get into the... That's a great, great parallel... because there's just this automatic view that if you lower cholesterol particularly "LDL" cholesterol it's going to do good... And there are actually some people out there who just think... you can't get it too low, like get it to zero or something, which is back into the territory of your body's just not going to function anymore. So seed oils and other things, other foods, plant foods, a lot of plant foods, things like porridge, but definitely seed oils contain things called plant sterols. And I think of those as kind of plant cholesterol. So we have our human cholesterol... Plant sterols is kind of plant cholesterol. And when we humans consume plant sterols, they compete in our body it's going on in the gut. They compete with our cholesterol to an extent and they win to an extent. So they do lower our total cholesterol levels. If we then went, if we took loads of plant sterols, went to a whole foods food shop and built up on those sort of shots that you can take... that advertise, we've got plant sterols. You can even buy plant sterol tablets, supplements... Start doing all of that kind of thing, your cholesterol will go down. And people just look at that and say, that's good in and of itself.
Well, I did a paper when I was doing my "PhD," so I started my "PhD" around 2012. I got it awarded early in 2016. Around 2014, my "PhD" supervisor was invited by "The Journal of Biological Sciences" to do an editorial. And he came to me and he said, you're kind of working in this field at the moment... Do you have anything that you think? It's only 850 words, so we haven't got much, but do you have anything? And I said, I do, actually, because I'm looking at this plant sterol thing because I'm trying to answer the question when I look at those randomized controlled trials like the Minnesota Coronary Survey or the low-fat diet, the London study, or the Rose Corn and Olive Oil Trial. When I'm looking at those, cholesterol is going down by more in those intervention groups, but it's making no difference to heart deaths and it's making no difference to all-cause deaths. So I've been looking into this and it's due to the impact of plant sterols. So I've then been going to the next stage which you should go to to say, but is that a good thing? Do we have any evidence out there for what happens when you consume plant sterols on end outcomes, things that actually count, like deaths or heart deaths or heart disease or even cancer? I touched on towards the end of this very short article, and the answer was no. The evidence is not good. You do not want to be lowering your plant sterols if you're concerned about your end outcomes. So it's just a beautiful evidence for the idea that lowering "LDL" cholesterol or lowering cholesterol in any form is not necessarily good per se... There's just this beautiful discrete part of nutritional evidence and heart disease evidence that just kind of blows that out of the water. And if you want to see that paper, put in my name, "Harcombe, Baker, 2014, Plant Sterols," and it will come back. It's on open view. It's 850 words... It's the paper that I've written that I've cited more times than any other paper because it's so powerful to be able to say this "ZOE" company I think it's trying to break into North America. It's huge over here, and there's this app and they're telling everyone to go plant-based, and plant sterols are great, and seed oils are great. And all these influencers, like I don't know, "Cate Shanahan" or whatever, saying that seed oils are bad they're so wrong. And all the rest of it, it's like, no, they're not wrong! I don't think it's the be-all and end-all, but they are not wrong that seed oils are bad for us.
Okay, so plant sterols, obviously they're in seed oils. When we zoom back to whole foods, plants, how many of them are in those? They're in a lot.
That's a good question. I should just go and check across the board because I like absolute nutritional principles. I like saturated fat is in every food that contains fat. I like absolutes like that.
They're in coconut oil, so stuff that's very high in saturated fat. But they're in there because it's a plant-based food. They're in porridge, they're in legumes.
I will get back to you on that one. I will go and see if I can find plants that don't... contain plant sterols. There will definitely be foods that contain more than others... And the reason that seed oils are so rich in plant sterols is because they're so concentrated as foods.
We don't naturally consume... rapeseed. If you go out and see rapeseed in the fields and it's that beautiful... yellow, we can't consume it in that form. So there's a massive processing that goes on to really concentrate it down into that... bottle of oil. So inevitably we're going to get a lot more plant sterols... in seed oils than we are in some other plant-based foods. But I'll put that on my homework list and get back to you.
Sounds good. But by the sounds of it, if we're eating a mixed diet, omnivore, we're going to be getting some of these. And the end goal isn't to get them right out of the diet.
Yeah, yeah. It's not that they're --- necessarily, as you say, harmful in natural foods. We don't need them because we don't need any plant food. So that's an absolute.
Would I worry if I was having a bowl of porridge... just because I fancied it on a cold winter's day? Would I worry that... it's got... plant sterols at the level that's going to kind of harm me in any way? No, I wouldn't worry about it at all. And it probably wouldn't be the primary reason why I would avoid seed oils. I would avoid seed oils just because they're highly processed, they're highly concentrated. I can't think of anything good about them. They've got no protein, let alone complete protein... They haven't got the essential fatty acids, certainly not in the form that I need them. They've got no minerals. They're very... high-calorie for not much... nutrition. So you're really not getting a big bang for your buck. So I would avoid them for that... reason... So now I don't think... there's something we have to avoid, but certainly don't go down to the "Whole Foods" and buy those things that say, get your plant sterols here.
And there's a brand called "Benecol" over here and don't have margarine with these plant sterols advertised. Instead of butter, you should be eating butter not fake plastic stuff that's gone through lots of iterations. You mentioned processing there in relation to the seed oils... Can you talk more to that?
I did look at this, actually. God, this is going to take me back a little bit, actually. So I looked in my obesity book and I was trying to... So I think I looked at... we had a product at the time that was actually called "I Can't Believe It's Not Butter." And I was comparing it to actual butter. So actual butter is really easy. You just get milk from a cow and you churn it and you end up with butter.
And you don't even have to add salt to it. So this thing. So they've got... highly unsaturated fats and they kind of.
They're gonna have to make this margarine sort of solid... in some way because then it does actually emulate butter. So we're not talking the seed oils here, we're talking the kind of margarine thing. So I'm just going to go for sort of the worst... of all the things in this processing group... So they want some sort of hard margarine at the end of it. So they're trying to make it more saturated. Now, if I can remember the structure of a saturated fat. So -- saturated fats are basically a line of hydrogens. Which way around is it? I'm sure it's hydrogens and they're carbon chain in the middle and they're holding hands with hydrogens. Or is it hydrogen? I think it's hydrogens in the middle and they're holding hands with carbons. Where you've got all the carbons holding hands with the hydrogens, we call that fully saturated. So all the places where you could have the carbon-hydrogen holding hands, we've got it. And it's therefore fully saturated and it's solid at room temperature, it's much more stable to cook with. When you start getting... one break in that chain, we call it a monounsaturated fat. There's only one... place where it's got that bond broken and it's therefore become a bit of an unsaturated fat. And then of course, we've got polyunsaturated fats where we've got more of those bonds... broken and then we've got more sort of instability. So what they try to do is.
Now I know which one it is. You've got the carbon chain and it's the hydrogen arms, because they try to fire hydrogens into this structure. So they put a ton of unsaturated oil into this massive, massive, massive, massive steel vat kind of thing. And then they're trying to fire hydrogens into it and they're kind of hoping... that those hydrogens will go into the places where the hydrogens are missing. But of course that doesn't... automatically happen, so you'll end up with more hydrogens on one side... and you've still got the sort of bonds missing on the other side. So you're kind of into a bit of trans fat territory... and they say now, oh, well, we don't do that anymore because that would be a trans fat. So we do... partial hydrogenation. It's like, well, I don't really know what you're doing there, but you're still trying to hydrogenate... this thing... in some way because you're trying to make it solid. And then you end up with this stinky, grey disgusting kind of gloopy mess. So then you're going to add... emulsifiers to try and make it a bit smoother. You're going to add some kind of colour because nobody's going to put grey margarine on their bread. You're going to add some kind of scent or something, at least, that eliminates the smell... You do all this stuff to it and then you put it in a... tub. And then they call it "I Can't Believe It's Not Butter." Well, I can believe it's not butter because it's so far from butter you don't even know where to start.
That's what they're doing when they're trying to make these, let's not eat saturated fat, let's make these healthier alternatives.
It was just a gift... to the fake food industry and it was an assault on human health... when they decided on all of this nonsense. But everything... stems from what we talked about earlier the demonization of fat, the demonization of saturated fat, the demonization of cholesterol. All these things that we got wrong have just then been the bedrock of everything else that's gone wrong since.
Okay, so we've made it clear seed oils are bad. There's... other oils that are kind of a side category there olive oil, avocado oil, coconut oil. How do you feel about those?
Okay, so they're still processed in some way... So the food that would naturally come in the form that nature... provides it is the coconut, is the avocado, is the olive. Why can't we just eat coconuts, avocados if you have to, and olives? Why do we have to? How many olives does it take to make olive oil? It's just massively processed. It's not an efficient use of the world's resources for one thing. It's still not giving you any complete protein, any essential fatty acids in the form that you need them, any minerals. It's still very calorific for very little nutrient return. So you've got all of that. The coconut oil, if you did want to stir-fry with something, it's more stable... because it's got more saturated fat in it. It's still got monounsaturated fat and polyunsaturated fat, but it's mostly... saturated fat. So it would be more stable, but it would overpower... let's say a stir-fry that you want to serve with some beef strips or something. Unless it's a Thai stir-fry.
So if I were doing a stir-fry at home, I would use olive oil. It's not as stable, so it's not as good, but it's better than the very unstable unsaturated rapeseed oil, sunflower oil, and all the rest of it. Avocado oil? That just seems massively inefficient to me. It's actually got a very similar profile to olive oil.
So it's mostly monounsaturated fat, but it still also has saturated fat and polyunsaturated fat.
But these things get just eulogized. Particularly olive oil, which has got a great... "PR" department. And it's -- the elixir of the... Mediterranean diet.
No, it's not. It's the sunshine. It's the rest of the stuff they eat. It's their lifestyle, it's their work-life balance.
There's really nothing special about olive oil, and it just has this fantastic reputation that it just doesn't deserve that much. The Mediterranean diet's come up a few times and people still believe... that is a superior diet for people seeking health and longevity. Can you talk more to that piece... and bust any myths there?
So there are two Mediterranean diets. There's the Mediterranean diet that is the actual Mediterranean. So I go to the Mediterranean at least once... every year and I've been doing it since my parents were kind enough to... take me on summer holidays. So we would go places like former Yugoslavia, which is now several different countries. We go to France, go to Malta, go to Spain, go to Portugal, go to Greece, go to Italy so all countries that are in or bordering the Mediterranean. And the real Mediterranean diet, I would best sum up as I mentioned it with France... earlier, if it moves, eat it. And they eat every animal under the sun. They eat horse, they eat rabbit, they eat quails, they eat frogs' legs, they eat snails, mussels... they just eat everything and they eat every part of the animal as well. And they tend to eat meat quite raw or rare. So you can have sort of steak tartare or something I forget what it is, but my hubby loves it. And it's basically raw... beef.
And they'll have raw beef and eggs and that kind of thing. So what they actually eat in the Mediterranean is really quite rich in animal foods. So your breakfast would probably be eggs of some kind, yogurt, never low-fat dairy. They don't even entertain the idea of... low-fat dairy. Yes, there would be some fruit, but it's not the five a day that we're told to eat. You might have some melon, you might have some berries.
Yes, they've got bread. So we'll move on now to the fictitious Mediterranean diet just to get the contrast. So the fictitious Mediterranean diet is plant-based, it's whole grains, it's legumes, it's loads of fruit, loads of vegetables, and it's just not. First of all, every grain that you find in the real Mediterranean is white. So French bread is that fantastic baguette it's white. Ciabatta in Italy it's white.
Risotto rice in Spain is white. Pasta in Italy is white. Everything... in the Mediterranean in grain terms is white. It is not whole grains. You might find whole grains now in a hotel, but only if Brits go there... because they've been asking for whole grains, so the hotel has got round to providing it. But the indigenous population has grown up on white grains. There's no whole grains. They might include legumes in dishes, but it might be something like a lamb tagine. And it would have some apricots in there and have some chickpeas in there, but it's not a whole dish based on lentils. They don't see that as the main protein part of their meal. Yes, they'll have some fruit, but as I've just said, it's not the massive fruit that we have. And they don't snack.
I'm talking about the traditional Mediterranean diet. Of course, the bad eating habits are creeping into the young people now, and they're eating almost American, British diet. So forget those. The real Mediterranean diet would have maybe melon as a starter, maybe berries as dessert.
You'd often have cheese with your evening meal instead of dessert. After you've had some substantial portion of meat, yes, you would have some vegetables, yes, you'd have some salad.
But they don't have grains in the kind of proportion that we have. So in France, for example, you're much more likely to have potatoes, and then it would be potatoes with cheese on top of them. So it would be -- Gratin dauphinois or whatever, which is another delivery mechanism for another animal food. If you have desserts in the Mediterranean, they're very much cream and cheesy kind of based rather than high in sugar. So it's not the sort of if they have the apple pie, it's mostly apples, and then there's a little bit of pastry. It's not that sweet. But more likely you'll get things like crème anglaise, crème brûlée.
What's the one that "Andy" likes? There's like a vanilla sort of mush kind of thing. But they're all cream-based. They're cream and egg-based and creamy and fatty rather than sugary and carby. And those are the two diets. So there's one that is actually eaten, and then there's one that academics have invented that nobody actually eats in the Mediterranean. It's a complete fiction of the academic world. And they want to try to convince you that that's how they eat in the Mediterranean, and then that's why they live longer. They don't. They live longer because of what I've said, sunshine, work-life balance. Family. Family and faith is so important in the Mediterranean, and that counts for so much in terms of having purpose in one's life, reason for getting up in the morning, reason for integrating with one's family, et cetera, et cetera. So Mediterranean diet, another very much misunderstood concept.
Let's zone in on fruit and talk about how our modern fruit has changed and where it becomes problematic.
Yeah, -- I contrast modern fruit in what I see, particularly in an American supermarket. So if I go over and do a conference in America, I must admit, I love going to your supermarkets because there's just so much I'm thinking, I want to eat all of this. It just looks amazing. You've got Medjool dates, and then I remember that they've actually got more sugar than toffee. And I love Red Delicious apples. And I look at them and they're all shiny and perfect and uniform, and every single one looks the same. And you wonder what on earth is on them that they're all shining like I could see my face in it. But that's not the fruit that I know. Having a garden that's got a lot of fruit and also living in the countryside where I can wander around on the walk in the autumn and actually pick some fruit. So there's a couple of things going on. One is real fruit that you will find in the real environment and what that is actually like. And then there's a sort of seasonal aspect to it, which is, when do we actually find that? So in the UK, and there will be parts of North America that are on our kind of latitude and have similar kind of access to fruit. You don't get any fruit in the year until about May. And then you start seeing maybe some wild strawberries, and they start coming in a little bit more in June. Then the raspberries pick up, June into July. Blackberries come along around sort of August into September. Apples start kicking in around August. They've got quite a good season. So you've got apples, pears... we've got a fig tree in our garden that really starts to do well around sort of August-September Apples will still be going on. We've still got a couple of cookers in the garden and we're now into December.
The eaters are mostly not there, but we've got some that we've stored with sort of newspaper in between them, so if one goes bad, it doesn't pollute all the others. So we can eat those really up until Christmas. And I've frozen a lot of blackberries that I picked in the autumn. We had a great year. So I'll be eating those into January and putting full-fat yogurt with them. But then that's it. There is then no fruit for the next five months of the year. And yet we have this way of living at the moment. And when they're telling us, we must have our five a day. It's a really important part of our healthy eating. Well, no, it's not. That's got no evidence base. That's just a fairy story. And it isn't natural to be eating pineapples on Christmas day or having access to avocados at all in the UK. It's not indigenous to our population. We shouldn't be having apples all year round, let alone dates and melon and all the stuff that I could get in the supermarket today, that is just not natural. And it's been shipped from all over the world. This is not a good use of our resources and it's not good for our body to be eating out of season.
Okay, so the fruit is sweeter. We have access all year round. We have access to fruits and vegetables that aren't even grown locally. You mentioned fairy tale. Another piece of the fairy tale here is that we need to eat these, you mentioned five a day to get our fiber. We did talk about this last time, but I want to go deep into fiber and bust that myth.
Okay, where do you want to go? Do you like fiber? I should ask you this. Do you rate fiber? Am I going into dodgy territory here or.
I'm... low carb, keto. I'm not someone that avoids fiber, but I don't go seeking it.
Okay, so... as you say, we went into it last time. What myths do we still have to bust on fiber?
Well, let's just give a 101. We're told we want to eat... diversity when it comes to plants... Get a lot of fiber. Get fiber from different plants. You mentioned "ZOE" before, not you, the other "ZOE." They're big on this. The "ZOE" app. So, talk about where we went wrong there. We're back to kind of the dietary guidelines. Where did we go wrong? Everywhere. We didn't get anything right. It's all wrong.
The fiber myth is -- one of those dragons that just won't slay. You're stabbing it and chopping its head off and chopping its legs off, and... it just keeps coming back for more and it's just.
Okay so, let's do carbohydrate 101, because that's going to get us into fiber... I think we need to do this because it also gets the point across that when we're talking about carbohydrate, we're talking about sugar, and people really need to land that point because there's this idea that carbohydrate is good and sugar is bad, and yet carbohydrate is just sugar. So carbohydrate 101, we have three, what we call monosaccharides. Mono meaning one, saccharide meaning sugar. So they're single sugars... and they are glucose, fructose, and galactose. Then we have three, what we call disaccharides two sugars... So we have sucrose, lactose, and maltose. And sucrose, that's the one that we're most familiar with. That's the table sugar, white packet of table sugar in the coffee shop. And sucrose is one molecule of fructose and one molecule of glucose.
Lactose, for interest, is glucose and galactose. Maltose is two units of glucose. All of them have got glucose in... So all of those disaccharides... are dumping glucose into the body. And of course, we know glucose goes into the bloodstream and we should only ever have... 4 grams of glucose in the bloodstream at any one time... The minute we put more than that in, the pancreas is called upon to attach itself to the glucose. Insulin attaches itself, takes it out of the bloodstream... because the body saw that the glucose was too high. We were in a crisis situation. So... you've seen immediately that all of those building blocks of two sugars... are putting glucose into the bloodstream and giving the body a crisis situation... where it has to start getting that glucose out of the bloodstream. So immediately you should be thinking, not just sugar, sugar, sugar, sugar. But... I'm chucking stuff into the body that the body is then going to have to deal with, because it sees it as a bad thing. Now we're getting close to fiber because we move on to... polysaccharides, many sugars, and these divide into two categories. So you've got many sugars of the digestible kind, which we know as glycogen in humans and starch in plants, and then we've got many sugars of the indigestible kind, and that is fiber. Fiber is literally many sugars of the indigestible kind. So the first thing that I want to say to people is why... would people be telling me to consume many sugars... that I can't digest. Let alone... to the tune of 30 grams of this many sugars that I can't digest every single day. Why would that be happening?
Okay, before we move deeper into fiber, you brought up an interesting point there where sugar in our world is always demonized, but carbohydrates... are often given a pass... or even promoted as being good when it comes to fruits and vegetables. Talk more about the fact that... if we go eat a big apple, there is so much sugar in that. That, yeah, it's not been refined to the point of sucrose or white sugar. But our body still has to deal with it.
It's the same. It's the same. I remember hearing a science program on a "BBC" radio program a while ago, and there was a guy in a lab, a doctor in a lab, a chemist and he was being asked about sugar in fruit. And the guy was like, oh, but it's fruit sugar, isn't it? It's kind of different to what we've just looked at with table sugar. And the guy scoffs. He literally --- goes, yeah, the body doesn't know. The body doesn't know the difference. And it just really sort of had an impact on me because it is just so true, the body doesn't know the difference. So you eat the tablespoon of white sugar, which is glucose and fructose in exactly equal amounts... You come over to the apple. So let's say we've got a big apple. One of those lovely Red Delicious apples, it's not exactly one molecule of glucose and one molecule of fructose it's very slightly different. So an apple would have more fructose and less glucose. A banana would have more glucose and less fructose. But where you've got those sort of equal amounts, the body is still saying, okay, that's glucose I've got to deal with, and that's fructose I've got to deal with. And to that extent, it's no different. The body has to see it in exactly the same way.
Talk more to the fructose piece, because whether it be in sugar or the fruit, this sugar reacts differently in the body.
Yeah. So the glucose is going into the bloodstream and the fructose is going to the liver. So when people say to me, oh, is glucose better than fructose? Or is fructose better than glucose? I say, okay, so do you want type 2 diabetes or non-alcoholic fatty liver disease? One's going to the liver, it's going to give you non-alcoholic fatty liver disease. The other's going into the bloodstream. Over time, too much of that too often, you're going to end up with type 2 diabetes. It is utterly mad that our governments are saying to us, have 350 to 400 grams of carbohydrate, but eat less sugar. I've just gone through 101 carbohydrate. There's no carbohydrate that I missed out. I didn't hide anything. There's no sort of separate sugar that I didn't cover or separate carbohydrate that I didn't cover that isn't just sugar or breaks down into just sugar. It is all just sugar that the body then has to deal with. So the idea that we're telling people to have more carbohydrate and less sugar is just another thing that is so misunderstood. It's just showing that whoever is telling you to do that is very, very ignorant when it comes to nutrition.
The other piece to this too, you mentioned an apple. We got into breaking that down and how it reacts in the body. There's also this layer of things like maple syrup, honey. You mentioned dates before... date sugar. Yeah. How do you look at those? And.
I don't get that. My first principle on what people should eat is real food. So the minute I see people saying, oh, you should be having this and this sweetener is great, and mix this with this, I'm just thinking, that's not a real food. If I walked into the natural environment, I would not find that growing on a tree. Something has happened, and therefore I'm suspicious about it immediately. And I don't think it's helpful. I think one of the reasons it's done is particularly these sites that have got loads of recipes. It's just a lot easier to create recipes when you're bringing in that kind of thing. So I've got a whole recipe book that somebody gave me at a conference. Virtually every recipe has this sweetener in that was developed by the people who put together the recipe book.
So I don't think it's natural, I don't think it's real food. I think it's a bit disingenuous because it's just sort of helping with, oh look, we can eat so much in the keto world. But you've brought in some fake stuff and that's really not going to help. And one of the really big things is that I think it perpetuates a taste for sweet things. And I just think that's going to be really unhelpful, because most of us who've ended up in the low-carb world, nutrition world, keto world, at some point maybe when we were at university we didn't eat as well as we do now. We were junior doctors or whatever. You're snacking on really bad food.
And we know how we felt when we were doing that. And the more we ate that sort of sweet, really bad food, the more we wanted that sweet, really bad food, because that's how it's been designed by the fake food industry. So when I was in that sort of situation, and when I first wrote a diet book back in 2004, I'm like do you know what? It's just easier to not eat that stuff than it is to try to eat it in moderation. It is not designed so you can have it in moderation. So don't have one chocolate from a chocolate box, because you're then going to want at least another handful, if not the whole box. Just don't start. It's just so much easier not to start. And when you stop eating sweet stuff, your taste buds change and it actually doesn't take that long. We're talking weeks, usually not even months. And then suddenly a cherry tomato blows the roof of your mouth off because it tastes so sweet. Milk tastes sweet because it's got lactose in it, which is glucose and galactose, it should taste sweet. It has milk sugars in it.
But it's this artificial sweetness that we've put into our diet, we've got used to. I just think the sooner we can get that out of our diet, the better.
There's so many different layers to this. We could even take it down another layer to things like stevia, monk fruit, which, again, in the health world are often considered great alternatives to things like sucrose or artificial sweeteners like aspartame.
Yeah, I think I looked at this one. So I might have an article on all the different types of sweeteners. If I haven't, then I should look at them. But I kind of just dismiss them all for the same reasons. Because they're artificial, because they're unnaturally sweet, because they're not going to help you get rid of a sweet tooth. Another thing that I haven't mentioned is actually some of the "ols," the mannitol, sorbitol, the ones that have got the "ol" at the end. They have warnings on the packet. So they may produce a laxative effect. And I won't name the chef or the company, but I was at a conference once where somebody... was demonstrating their produce and, oh, look how amazing this dessert is. And... people were hungry. Food wasn't provided at lunchtime, so... any stand that was offering some food, people would gravitate towards that stand. And it just looked lovely. It was like, okay, it looks like there's a bit of berry compote, and then it looks like there's some cream or some natural yogurt or something. And then it looks like there's some sort of granola on top of it. Just looks nice, we're gonna have some of that. And of course, some people went back and had more, and they had more, and they had more... And there weren't as many people at the conference the day after all of that, shall we say, as there were on the day that they were trying all of these things. Because there were so many people in the bathroom with stomach problems because this thing had given them gas and indigestion, diarrhea, really severe diarrhea. There were people sort of emerging the day after saying, oh, my goodness, I've literally lost a day of my life because of the laxative effect of some of these sweeteners. They're not great. They're not great. Don't go there. Eat real food.
Have you looked at allulose at all? This one seems to be gaining more momentum lately as... a mild "GLP-1" agonist.
Oh, crikey! It sounds like it's not something that's on your radar. No, I haven't looked at it. Again, I've put it on my homework list. I haven't looked at it yet.
Let's expand out to "GLP-1" agonists as a whole. What do you think about those?
They worry me. And they worry me for a lot of reasons... They worry me because they're new, we don't know enough about them yet. They've been on the market for a while for type 2 diabetes, but I think they're being taken at doses now that we haven't used for type 2 diabetes. Even though they've been used for type 2 diabetes for a few years, that's still quite early in the life of a drug that seems to be as powerful as this one. I know from a research interest in obesity for a long period of time that diet drugs tend to get withdrawn, and there are not many exceptions to that. So some of them get withdrawn very quickly because we observe very quickly that they're doing harm. Some of them take a little bit longer. So the one... that I was very interested in at the time was called "Reductil," sibutramine, and that was withdrawn around 2013, 2014, and it was discovered that it was causing heart attacks and cardiac incidents. And there were people who were as keen... on that drug then as are keen on "GLP-1s" now. So they were devastated... when it was taken off the market because it's like, I love it, it's helping, it's helping. It was a sort of appetite suppressant. It was working for them. But the regulators decided it was just too risky... to allow people to keep taking it. They didn't think the trade-off of, yeah, they're losing some weight, but they're getting heart disease, they didn't think that trade-off was acceptable. We've got deaths already... all over the place. We've got deaths in the numbers that would have taken any other diet drug up until now off the market already, and yet nothing is happening... I don't even know if they're being investigated. It's somewhere in the 80 to 100... in the UK.
Is there a panel looking into this? Why is it not off the market already? It baffles me at that level because it's the kind of thing that we should... be looking into... It's almost like they've taken such a hold so quickly already that there are too many obstacles to be able to look at them objectively or to take them off the market. And we've got conflicted researchers who are funded by "Novo Nordisk" is one of the big makers of these drugs funded by this same drug company... putting out papers saying, oh, it's not only obesity they're going to help with they're great for heart disease. And I did a Monday note looking at that, and it's like, no, that does not withstand scrutiny. This is a claim that we should not be running around making, but they're doubling down on it, and there are going to be more claims. They're going to say, oh, they're amazing for this condition or that condition, or they help depression, or they help with this. They're just going to build on this platform that they've got. This is going to make statins, which are approaching a trillion in terms of what they've earned the pharmaceutical industry, the "GLP-1" set of drugs is going to make the statins just look like child's play, quite frankly.
Yeah, I'm worried, I'm worried.
Okay, so the answer isn't the "GLP-1," but say a family member or friend came to you saying, "Zoë," I know you're into diet and nutrition. I'm stuck right now with my weight loss. I got a lot of extra fat on my body. How would you guide them?
Yeah, it's not to say I'm worried about the "GLP-1s." It's not a hard no. And I've got friends who are on them and I'm observing and I'm learning from their experiences. And a friend came to me and was dangerously obese to the point that it is impacting their health, maybe even type 2 diabetic... If you were going to go that route, I would say go as low a dose as possible for as short a period of time as possible and use that gift that you're going to be given because it is going to take your appetite away to do what I'm just about to say. Now, if you can do what I'm just about to say without taking the risk of the "GLP-1" because even at a low dose, for as short a period of time as possible, you could have an incident. There was a nurse in Scotland, I think it was first jab, second jab died.
You could in that game of Russian roulette, you could have a bad bullet in your gun, hoping that you wouldn't. If you need to go that route, then use it to do this. So my advice would be, you've got to eat real food. You've got to get away from this processed food, this idea that you'll be able to eat processed food in moderation or calorie count, which actually drives you down the processed food route because then you want to buy a particular thing because it says 52 calories on the packet. You can't estimate the calories in what I'm going to have for dinner tonight, which is steak and feta cheese and other cheese and yogurt and courgettes and whatever else "Andy's" up to down there at the moment. I could never estimate the calories in that. It would just be impossible. But I could eat a ready meal that tells me, that's 278, and then assume that that's true. So eat real food and then choose that real food for the nutrients it provides. Because then your body is going to start working with you. It's going to stop fighting you and saying, look, I'm still hungry.
That 278 calorie ready meal did nothing for me. That's not what I wanted. I wanted zinc and iron and "B12" and in fact all the B vitamins. And I wanted complete protein and I wanted essential fatty acids in the form that I want them. So please, will you just eat some red meat, some oily fish, some eggs, especially the yolks, and some full-fat dairy. And fine, if you want some green things and legumes and porridge every now and again, and nuts and seeds if you like them, and all the rest of it. But please, just give me what I need. So eat real food, choose that real food for the nutrients it provides and then don't graze. We need to be eating no more than three times a day. If you don't like breakfast, great, don't have it. Have brunch or lunch, whatever works for you, and then have another sort of substantial meal. But this idea that we can just be grazing all day long, snacking all day long we just can't. We can't we will walk into type 2 diabetes and obesity if we try to do that.
Talk more to the calorie piece and how this classical advice of eat less, move more is a trap.
It's a trap because your body will just work against you straight away. So the minute you try to eat less, the body will try to get you to eat more. It will also try to get you to do less. So it will work against you in the two ways that you don't want to happen. If you try to do more, it will try to get you to eat more to balance the do-more, or it will try to get you to do less. So there was a brilliant study that's actually done in Plymouth in England. It was called the Early Bird Study. And they studied school children and they managed to find school children from three different schools. And one was a group of poor kids and they didn't really have any playing fields or organized sport at school. The other was a kind of sort of middle of the road. They had some sport, but it wasn't too great. And then there was a real sort of top-end public school where you can do rugby and cricket and polo and all this kind of thing. And they monitored them with this equipment put on the kids and this is way before "Fitbits." And they monitored how much activity they did throughout the day and they did the same amount of activity. So the posh kids who did rugby at school went home and then sat and did their homework in the evening. And the guys who did a little bit of stuff maybe went home and maybe had an after-school club or went to "Boy Scouts" and did some activity at "Boy Scouts" and that was it. And the kids that had no sport at school and didn't really have a place to do homework and had 10 siblings or whatever, they were out playing on the street because Mum would be like just get out of the house, get away from under my feet. Go out, play. I don't want to see you until your dinner's ready. And they did the same amount of activity. So the body is going to compensate in some way. If you try to do more as well as eat less, the body is just going to fight you the whole way. It just is such a naive idea. They even put a number to it, which is just... another... myth. It's like five a day. I try to find out. So if you go to "Men's Health" magazine or something, they'll say if you cut back by 500 calories a day for a week, you will have a deficit of three and a half thousand calories and you will lose one pound of fat. And it's not just "Men's Health," it's in diet books, it's in... diet calculators. It's just another one of these nutritional myths. And I remember trying to find out where it came from and I ended up tracing it back to a book if I can remember the date, I think it was 1918. "Lulu Hunt Peters," and she talks about if you cut back by this number of calories, then you're going to lose this much weight. If somebody can find it earlier than that, great I'm all ears. I'd love to know... where this really, really, really kicked off. And of course, we've got the stuff by "Atwater," who was trying to measure the
actual calories and how many calories are in fat, and in protein and carbohydrates. So all of that was kind of going on around the turn of the century.
But this whole idea of if you cut back by... 500 calories, you're going to lose a pound. I unpack it in a presentation where I talk about calories and I think it was 2018. If you put my name in on the internet and put calories and kettles that's a bit of a curious word to put in, you'll find this presentation. And I unpack this whole sort of three-and-a-half-thousand calorie theory.
But this idea... that the body is just going to say, ah! You had three and a half thousand fewer calories I'm just going to give you a pound of fat. It's almost like, where do you want it? Do you want it off your waist? Do you want it off your bum? Do you want it off your bingo wings? There's almost this idea that the body is just going to give up that one pound of fat. It is not going to give up a pound of fat. The body is hardwired to do anything other than that. It does not want to lose fat. Fat is what has kept us alive ever since "Australopithecus Lucy" first walked upright.
So the body's going to say, how can I get you to eat more? How can I get you to do less? If you're determined, and you really are on this health kick, and you've got some willpower, and you really are trying to eat less, and you really are trying to do more, there's some things that I can do. I'm not going to give you that one pound of fat every week. I'm just not going to do it. You're going to be in a bad way really quickly. I'm going to turn off the heating system. You're going to get cold. You're going to grow... hair on your arms. I'm going to try to put some fur on you. I'm going to shut off your reproductive system. If you're females, your periods are just going to stop. You're not looking after yourself right now. You're in no fit state to have another baby, so that's just stopping. Lymphatic drainage system, I'm just not going to perform it as well as I could. Your face is actually going to get quite carby, quite puffy. Even though you're losing weight and you're eating as much, you're not going to be looking as good. What else can I do? I can not repair, I can not build bone density, I can not fight infection. You're going to get loads of colds. The Tour de France riders, their biggest single risk at the time of the Tour de France is getting a cold because they're down to body fat percentages of about 6% because every ounce on the bike counts. So they want their power-to-weight ratio to be perfect. Female riders long since never had periods, but the male riders are at the point, the slightest exposure to something -they're a mess. Your body is a mess. Your body is not going to give up fat. It's going to do everything other than that before it gives up the fat, and it's just going to make you really, really unhealthy. It's just a really bad idea all round.
I want to come back to fiber before we part ways. We quickly glazed over it and it's obvious you're not a fan, but I want to give some pushback in different areas and get your opinion where other people might say it's a necessity. First one being the microbiome. Okay, we don't need fiber, but what about our microbiome taking that fiber, processing it, making short-chain fatty acids that in turn benefit us? It still doesn't need fiber. So, what your microbiome needs is great parents, natural childbirth, breastfeeding, no antibiotics as a child, unless your life depends on it. Ideally, no antibiotics in your lifetime unless your life depends on it. - Don't eat processed food, because that's going to feed the bad guys. And then it's all about balance in the gut flora. If you remember that "Super Size Me" guy who just ate "McDonald's" for a month he managed to trash his whole health system in that time. So, don't eat the bad stuff. We haven't mentioned fiber or vegetables, and we've mentioned a lot of things. Then, do eat the good stuff and we still don't need fiber. So we can get that from blue cheese, from... natural live yogurt. - Kefir is a particularly fantastic thing to eat for your gut health. Fermented foods, pickled foods... and people go, ah, pickle that's a vegetable. Yeah, but... it's not that it's a vegetable, it's that it's pickled. It's that you're getting in the fermented aspect of the intake, and that's what makes for a great microbiome. So, there is still no need for fiber or vegetables which, remember, are things that you can't digest that are actually many sugars. So we don't need them.
The classic story, again, I said this before is to eat a diverse range of fruits and vegetables, get a whole bunch of fiber, and the goal there is to have a diverse microbiome. What do you think about that goal? Yeah. Because obviously you don't think fiber is what we need to get there... but do you think we even have the goal correct? That's a really interesting question, and it's another one on the homework list because it is an important one to look at. There is this assumption out there that the more diverse your gut bacteria, the better... But I don't know if that's the case. I don't know if it's not. - The more of the good guys that you've got, the better. I'm pretty sure having something like "Candida albicans," which I was writing about 21 years ago, way ahead of all this gut flora stuff. It's not good having that in there. It's certainly not good having that out of balance in there, not being kept in check... by the good guys like the "Lactobacillus" and "acidophilus" and all that kind of thing. That's definitely not good... But I know that the "ZOE" company over here, they've actually got a product in some of the posh supermarkets... where you can buy a sachet, which again, just doesn't feel that natural, but it's sort of here's your 30 plants for your diversity, for your microbiome. And I've started looking into this. So it is going to be a Monday note. And there's one paper that they've done... that they're relying on so heavily to say, 30 plants is marvelous and it's going to be great for your microbiome. And there you go, there's your 30 plants. I'll make it easy for you. You don't have to go out and buy all those 30 plants... I'll just put it in some sachet that you can buy for 15 bucks from "Waitrose," "Whole Foods" or whatever. -- And that's what they've come up with. --- It's an inference, it's an assumption. It's still a hypothesis in my view. I am not yet quite convinced that diversity is the most important thing. And I'm definitely not convinced that you have to have the plants to get that diversity.
Okay, sticking on fiber... Another... argument could be fiber helps me poop. "Metamucil." This is something that's sold to people, help keep them regular. Bring that in. So we're now talking about waste. And... there's no other area of life where I can think of that waste is actually a good thing. So when I have to get rid of my garbage... and the people come around to collect it each week the less I can produce, the better. - If I'm working in the kitchen or something, the less waste... I can produce, the better. -- The more I can use all the food I buy each week, all the ingredients, etc. When did waste ever become a good thing? And that's basically all it is. Remember, it's sugars that we can't digest... So it's got to come out of the other end somehow because we can't digest it. So what else is it going to do? The body's not able to strip it and... take out nutrients or whatever because we just can't digest it. So it's just got to pass through the system. So, yes, if you have a massive amount of fiber, you are going to have more to get rid of the next day. And if you're the kind of person that thinks, oh, I've had a big poop, I feel really good about that, okay, knock yourself out! You had to put more in to get more out. But you know what? It would have been so much better if you put less in and got less out, because you've just generally taxed your body less.
Now we went for a meal with friends. "Andy" and I don't eat much fiber... and we went for a meal with friends recently and it was delicious and it looked beautiful. They'd done a slab of beef on a bed of... mixed beans. So there were kidney beans and broad beans and other beans that I didn't even recognize. And sweet corn. It was like a whole tin of sweet corn in there. And there were -- raw red onion, there's some bits of avocado. - I can't even remember what else. It was just so much fiber and there was so much of it. And it was very tasty because it was in this sort of vinaigrette dressing, had the beef juices on it. It was really tasty. So we're like, we'll be polite here, we'll eat it. It was three days before we got over that. We were in so much discomfort. - It's just like, we've got to get rid of all of that because we got some nutrients from it. It wasn't all fiber. It's not like we ate "Fybogel." - But the fiber bit was the bit that we couldn't digest and they were all very fibrous ingredients and we were in trouble for a few days. It reminded me of a study that I often cite, 2012 study by "Ho et al." And it was about stopping fiber and the impact that that then has on chronic irritable bowel conditions. And these were really extreme. - There's 63 people with really debilitating constipation, diarrhea, stomach pain to the point that they couldn't function, they couldn't go to work and all the rest of it... And they took them off fiber for a few weeks and literally every complaint that they had cleared up. And then the end of the study was basically, do you want to go back to eating fiber? And anyone who goes back to eating fiber having got rid of all of that discomfort, they're mad because why would you do that? - I think if you've got any bowel problem whatsoever, it's not advice, but a suggestion. Try taking fiber out of your diet and just see if that helps, because I can't see that it won't. It's... not only not good for us, I think it's causing a lot of harm. And to me, this reminds me of the diversity piece, where I feel like a lot of people, the goal is to have those big poops every day. We gotta look at these goals and make sure we're actually aiming for the right thing because that's gonna determine the tactics in this case to jam in as much fiber as we can to have these big poops.
Yeah. And everything in nutrition, you look at ancestral guys and the "Weston A. Price Foundation" we've got roots in evolution. Why should we not eat less, do more because the body has only got to where we have. We're only here because we've managed to do the opposite. So if you look at big poop in that context, when we were tribes and when we lived in settlements, you couldn't go and do your big poop within the camp because that would be very unsociable. It would also be dangerous because you're attracting wild animals in with the smell and with the nutrients that they could get from your poop. So you're attracting those actually into the camp. So you've got to go outside the camp. Well, first of all, you're taking a risk if you're going outside the camp on your own because you can get picked off by a wild animal, but you're still giving signals around the camp, hey, wild animals. Humans over here with food. - And wolves, whatever animals would have been around at the time, you're putting the tribe at risk. So big waste is not good. If you've got some fixation on having a big poo every morning, I think you might want to go and talk to a psychotherapist or something, actually, because there's no nutritional benefit going on.
What do you think about this idea of, I want to take in fiber to gently scrape against and clean out my intestines? ---- I know someone who says this and it's someone I've got a lot of respect for, but I don't disrespect this particular arm of their general argument. - There's this sort of idea that fiber acts as some little sort of scrubby I think was the word used, little scrubby in the intestines. I'm pretty sure my intestines should not be having little scrubbies going on, and that's probably going to cause irritable bowel syndrome or cause some complications in some way. I just think the body's been really well designed. It'll keep "pH" perfect, it'll keep blood pressure perfect if we treat it with respect. It'll keep blood glucose perfect if we treat it with respect. -- It repairs things internally. Organs can repair themselves some of them. It's just the most incredible thing. If we needed little scrubbies in the intestine, I am really sure that the body would have them in some way. The fact that it doesn't tells me that we don't need them. Little scrubbies is another word for abrasion. I don't think we should be doing abrasive stuff internally. - We've got to respect the body and not block pathways and not do stuff that it's not designed to do. Just try to work with it rather than fighting it the whole time. Our poor bodies, all these things we're doing and causing it to have to react. Yeah, yeah, big time.! They're amazing to us, given what we do to them. The couch potato who's getting no exercise, maybe smoking, maybe drinking too much, maybe eating tons of processed food, carrying a body weight of three to four times what the body wanted to cope with. -- They're amazing that they're still functioning at any kind of level and that if the person then really tries to do the right thing to say, -enough is enough. I'm stopping smoking, I'm stopping drinking, I'm eating real food, I'm going to stop being sedentary, I'm going to lose that weight, I'm going to take back charge of my health. You see it, don't you, on some "Instagram" accounts or whatever, where they sort of shorten a year's program into a minute or something? And they take somebody who's just like, enough is enough. And you see them at the beginning, then you see them at the end and it's like, whoa, that's just incredible. That's incredible. The body didn't give up on that person in the kind of way that the person gave up on their own body. So we should respect it a lot -more.
All right, so you're not a fan of the scrubbies. By the sounds of it, you wouldn't be a fan of colonics. No, no. Talk about those. Well, you're taking out the good guys at the same as taking out the bad guys. And it takes a lot to get the good guys there. Go back to what I said, have great parents. Ideally, be born naturally, ideally be breastfed. - I do know there are complications, but this is all the ideal. Eat good food as a child, eat good food as an adult. Your microbiome should have been built up over your whole lifetime. And be a sort of powerhouse within your body. "Natasha Campbell-McBride," double "PhD," will call it your second brain in your body is your gut health. And then you go and trash it with a colonic. And for what? Because stuff comes out and maybe you feel lighter, maybe you get on the scale and you actually are lighter. It's bonkers! It's bonkers! Don't go doing that. That's really -- not what the body wants you to be doing. Don't go doing that kind of stuff. Stop it!
All right, we're going to end the fiber talk on this one last piece of pushback I could think of is being satiated by it. You hear this talk of eat fiber, you're going to feel full. Bring that in. Okay, so when we had that fiber meal recently, we felt full, but not in a good way. We felt bloated, we felt quite uncomfortable. - Normally I can wear the same clothes from morning till night, doesn't matter what I eat in my normal diet, no belt is going to get tight, no jeans are going to get uncomfortable. I'm not making myself bloat. My food is being handled in a normal kind of process. We shouldn't be bloated. And feeling fat after a meal and that kind of thing. We did feel full, but not in a good way.
Now, when you eat, bearing in mind that fiber is just a subset of carbohydrate, you might feel full when you've just had some carbohydrate, but it is so short-lived, not least because one of the things it's going to do is muck up your blood glucose level because you're at that four grams, that perfect four grams of glucose in your bloodstream. You eat an apple, let's say you've chucked in 20 grams of sugar into your body. Let's say 11 were fructose, nine were glucose. You've still put in two and a bit times the glucose that your body wanted in the bloodstream and the body then has to get it out. - Would your body then exactly get it right and get it right back to that perfect four-to-five-gram kind of level? No, maybe not. And particularly over time, it gets less good at that. So quite often people find that when they have a high-sugar carbohydrate, which that apple is, their blood glucose level will spike. If you wear a glucose monitor, not even as a diabetic, but just for interest, continuous glucose monitor, you'll see it spike and then the glucose level will go down. And observe it because quite often it will go down below where it was before you ate the apple. And then you've got the risk of the body saying, I'm getting a little bit towards that low blood glucose level now. I need to be getting some more glucose in. And if you've got your body used to fueling on carbohydrates, because remember it can fuel on carbohydrates or it can fuel on fat, and that's either dietary fat or body fat, or of course it can fuel on ketones. If you've got your body used to that, then it's just going to demand more carbohydrate. So you have a biscuit, you're not going to be full for very long. Have some porridge, you're not going to be full for very long. If you have porridge with full-fat milk, it will be the full-fat milk that will make you feel satiated. So what is going to make you feel satiated? Real food with fat and protein. So I say to people, sometimes if you want to do a test and you normally get a proper "Starbucks" or coffee or whatever on the way into work with proper milk, one day, try and ask for the skinny latte instead and just see how much sooner you get hungry because fat and protein makes you satiated. Carbohydrate is a very, very short-lived fake feeling of being full and not a very -- comfortable, healthy way of feeling full.
What are your thoughts on adding extra fat to a meal? Say taking some butter, putting it on the steak? So still within the paradigm you've been explaining today, but adding additional fat. I've seen it at a number of conferences. So you go to keto conferences and I've seen it happen. And there is only one circumstance in which it should happen, and that is that the person is following a ketogenic diet, they're fueling on fat. So by and large, their body is fueling on fat, straight ketones most of the time. They are very slim and very athletic, and therefore they need the extra fuel to fuel the sport. That's the only circumstance in which I would look over and see somebody adding butter to their steak and think, I can understand why they're doing that. And I've seen "Tim Noakes" do it. Professor "Tim Noakes." I've seen "Stephen Phinney" doing it, who's also a marathon runner. -- I've basically seen runners doing that. Where I've seen it, and it just horrifies me, is where I've been at a conference and we're all being served the same meal and I'm next to somebody with obesity and they're like making a point of, where's the butter? Any spare butter? Anyone got any butter going? And I'm kind of looking at them thinking, I am probably a third, a quarter maybe even of your size, and I'm not adding butter to my steak. Why would you do that? You are not a lean marathon runner. You have no need for that extra fuel. You have a lot of stored fat that your body would really happily use. In fact, it really wants to use it. And you have just stopped it using your body fat by adding dietary fat. And there was a period of time when people thought to go keto, it's about low-carb, high-fat. And they heard the high-fat more than they heard the low-carb. So they thought, I need to add fat to have this high-fat, low-carb diet. And that is just absolutely the wrong thing to do if you're trying to lose weight. If you want to lose weight, you go low-carb. Remember when we had that pie and we said, protein's about 15%. The minute you tell people not to eat more than 30% fat, the diet automatically becomes 55% carbohydrate. It works the other way around as well. So protein is about 15%. Something's going to happen to that in a second. 15%. You want to go on a low-carb diet. So let's say you want to go 10% carbohydrate... you're then looking at 75% fat... It is just going to happen naturally if you count the carbohydrate. Eat real food, choose that real food for the nutrients it provides. Your protein is going to go up a bit, but it's not going to go up much more than 20% because it's just really difficult to get your body above 20% protein intake. Unless you're doing really stupid things like protein shakes, fake food don't do it. Skinless chicken breasts not a real food. You need the skin on... white fish instead of oily fish, egg whites instead of egg yolks. Unless you're doing stupid things like that, your protein is going to be about 20%. It's going to go up a little bit, but you aim to get 10% and 70% is then going to form fat... So I've analyzed my own diet. I'm not keto, I'm not super low carb. But the minute you don't have porridge for breakfast, but you have Greek yogurt and whole milk in a large latte and maybe some eggs or maybe some cheese or whatever, you are in that fat-protein territory. You're in the low-carb because you chose not to eat the carb and the fat will just take up the slack. So if you're a... lean... marathon runner, okay. Any other circumstance, not okay.
Okay, so bottom line, if you have fat on your body you'd like to burn. Use it. Burn that versus the fat that you're going to add to your steak or whatnot. Yeah. Yeah, watch your fat intake. If you're trying to get your body to burn your body fat "Tim Noakes," "Steve Phinney" would love pork with the crackling on top, or rack of fatty lamb or something like that. Don't go for such high-fat things. The fat is going to come naturally, it's not for you to finish off the crackling. It's not for you to have the fattiest bit of the lamb. I'm not saying you need to go lean, because you do need those essential fats and fat nutrients in your diet. So you shouldn't fear fat, but you definitely shouldn't be seeking it out.
Okay, last question for today. Somebody who is eating in the realm of what we've been talking about any supplements they would want to consider on top of that to round things out? Yeah, the one, particularly for where I live and particularly for UK people, has got to be vitamin D, because it is so powerful. Is it a vitamin? Is it a hormone? I don't know. - I just know that it does seem to be unbelievably powerful for general health, for avoiding infections. There's evidence for cancer, there's evidence for heart disease. Yes, we can get it from the sun. Yes, we get it from animal foods in the form that the body wants it. - You'd have to eat a lot. I looked at it once. You'd have to eat a sort of 200-gram tin of sardines with the skin on, the bones in, to get all of those bone nutrients. So to get sort of 15 micrograms, I think it is, of vitamin D, to get your phosphorus, to get your calcium and so on. And there aren't many people doing that. And if you live in California and you go outside a lot with bare limbs, you're probably going to get a good dose from the sun. But for people where I live at the moment, where it's been dark for two hours already - in the winter, we just don't see the sun. And we don't even get daylight for more than about eight hours a day, and it's still not very good daylight. Even in the summer, we get a lot of rain, we get a lot of cloudy days. If you're not getting vitamin D from the sun, yes, supplement. And then if you take a vitamin D supplement, you should take "K2" with it because they work to make sure that the calcium impact of the vitamin D is going into your bones and sort of skeleton and not sort of hanging around in the arteries. -- Essential fatty acids, if you don't like oily fish, they're just so much richer. The "DHA," "EPA" is so much richer in oily fish than they are in meat. You can get more in grass-fed meat than you can from normal meat. But if you're not really going for much grass-fed meat or any oily fish, then omega. - Omega-3 supplements as well... but beyond that, not too much. Really, really, really try to get it from your food.
One final thing, we'll end on here as you're talking about different nutrients. You mentioned this quickly with vitamin D. There are different forms of some of the nutrients if we're talking plant versus animal. You mentioned "K2," that's one of them. And things like vitamin A versus beta-carotene. So, for people that are getting some of these through plants, just something to be aware of that usually, if not always, the animal form is preferred by the body. It's always, in my experience, I can't think of a circumstance when the body wants the plant version. So with vitamin A, as you've said, it wants retinol, it doesn't want carotene. "B12" is only found in animal foods. Vitamin D, it wants "D3," not "D2." - K, you can get "K2" from fermented foods, but the real value is in animal-based stuff like the natural yogurt, the blue cheese, the kefir and so on. The essential fatty acids it's the form in which they're found in animal foods. Protein it's complete protein, which is what you find in animal foods. It's not the incomplete protein, which is what you find in the plant foods. It's just such a clue to me that the body is trying to get us to eat animals. And that's as a person who was a vegetarian for about 20 years and lapsed into veganism for a very short period of time before I got ill, because my body was definitely trying to tell me, I need you to eat animals, because I can't convert carotene to retinol and I'm not getting "B12" at all. And you're not taking a supplement because you haven't studied nutrition yet. You're a student doing maths at Cambridge. You should know better than this but you don't. -- And it's animal food all the time. And I had a similar situation. We'll leave that for another day, but I can relate when it comes to eating only... plants. So, "Zoë," we're going to leave it there for today. Really enjoyed this. We're going to link up your website, your social media, everything in the show notes. Thank you. Thank you so much! And for my homework, I think I can thank you for that. Good luck there. Thank you. Now that you're done, you're going to want to stick around here and catch this other incredible episode. You don't want to miss it! I'll see you over there. I don't think that many doctors get this it's that energy delivery mechanisms are at the root of all pathological conditions. Almost without exception, they are vital in preventing and reversing dementia.