Mike Matthews: Simon, thank you for taking some time out of your busy day to talk with me and talk with the listeners.
Simon Hill: Thanks for having me, Mike. This one certainly has been a little while in the making. So grateful to be here with you guys. Yeah, I appreciate it.
Mike Matthews: So today’s discussion is going to be about health. And so you have written about, and you’ve spoken about 10 truths as you refer to them, or 10 biomarkers that you believe are the most critical predictors of longevity and.
That’s what I wanted to get you on the podcast to talk about. What are these 10 truths? What are these 10 biomarkers? And maybe we should start with just a simple definition of terms, what you mean by those things for people who are not even familiar maybe with what a biomarker is and why do they matter?
And, I don’t think we’ll have time to have an in depth discussion about all 10, but maybe you want to take the top three to five or so and get into more detail about why they matter and then also share with people the best way to track these things to measure and track them without having to go to great lengths in terms of inconvenience or inconvenience.
Thank you. Expense because we can’t all be, as you had mentioned offline, can’t all be Brian Johnson.
Simon Hill: So the 10 truths are, as you say, they are predictors of healthspan and longevity. And so the end of last year, I spent a lot of time, Mike, thinking about how do I take. All of the information that I’ve read and learned over the years and that I’ve received from working with individuals and also 300 plus episodes of information with scientists, academics, and put that into a framework that’s really accessible for people.
Like you, I’m sure you get, emails from people just saying, Mike, just tell me what to do. There’s so much information out there. So I went away and really thought long and hard about how can I create a framework that takes evidence based information. That we know is important when it comes to mitigating our risk of chronic diseases like cardiovascular disease, non alcoholic fatty liver disease, but also being healthy, fit and strong and vital in our day to day.
How can I put that into a meaningful framework that is accessible? And so step one was really thinking about, What matters in terms of the things that we can test, so if we’re going to be really objective about this, we want to be able to understand where our health is at today by testing certain things before intervening and then being able to retest.
So test, intervene, retest. That was really the framework and. In terms of thinking about what tests are actually meaningful, they needed to predict health span and longevity, but they also needed to be things that we can shift the needle on with some evidence based lifestyle intervention. My focus wasn’t on measuring things that we can’t actually improve through our lifestyle.
And essentially, we had a very long laundry list of different biomarkers and functional tests. And we narrowed this down to 10 different tests. That’s what led us to coming up with the sort of framework of the 10 truths. And these 10 biomarkers offer a sort of window into the health of your cardiovascular or cardiorespiratory system.
Musculoskeletal system, metabolic health, and psychological well being. So a window into kind of four key systems of the body. If you are living in a way, which is optimizing these 10 biomarkers slash functional tests, which we’ll get to, then the research should suggest you are going to be significantly reducing your risk of developing chronic disease.
That is, you are going to Live more years without disease, you’re compressing the number of years at the end of your life where you are affected by cardiovascular disease, heart attack or stroke, non alcoholic fatigue, liver disease, dementia, et cetera. If we start from the kind of top down, thinking about the 10 truths as a list, the, there’s 3 that kind of pertain or inform to the health of the cardiovascular system.
They are ApoB, blood pressure, and VO2max. For the musculoskeletal system, grip strength and bone mineral density, for metabolic health, HbA1c, fasting blood glucose, triglycerides, and waist to height ratio. And then for psychological well being, a scale called the flourishing scale. And what we were able to do is go through the literature and determine for your age, And for your gender, what is suboptimal?
What is normal and what is optimal for each of these 10 truths? And so before doing any type of lifestyle intervention, You can really see where your health is today, and we created a calculator where people can put their results in for each of the 10 truths, and then it will score them accordingly, depending if their result is suboptimal, normal, or optimal, and give them a kind of longevity score.
And where can people find that? Where is that calculator? So you can get that, you can go to theproof. com. This framework calculator, everything is freely available, zero cost. We believe that over time, as more and more research comes out, that calculator will be tweaked and it will only get better.
But it’s a really great starting point to give you a real an idea as to how you are faring in each of these four key systems of the body. And the reason that’s important is at an individual level where you focus Mike might look different to where a 50 year old woman focuses, perhaps for you, you score really well on grip strength and bone mineral density, but maybe not so good for APOB.
Whereas for someone else, APOB is great, but The grip strength is suboptimal. Now, the lifestyle interventions that are going to shift the needle most are going to be different for you to that person. So what we measure is the same for everyone, but how we intervene and what we focus on. More or focus less on is going to come down to our individual test results.
And that’s the kind of way that we created this framework just to draw attention to what matters and then give people the information so that they can tailor a lifestyle that’s going to benefit them most out of the individual level.
Mike Matthews: And my internet is struggling a little bit. So if you already said this, I apologize, but just want to interject that these things that, that.
That you are talking about are not only important for reducing the risk of disease and thereby improving longevity, which there’s a quantitative focus. I suppose you could say reducing risk of disease also has a qualitative component, but it also relates to very much your quality of life, not just how long you’re around for, but how well everything is going to work while you’re here.
Your functional age, so to speak, which refers to, again, how well are your various physiological systems working relative to norms. Your biological age could be 70, but because you’ve done a really good job taking care of yourself, your body, functionally speaking, is working at the functional age of, Maybe 60.
Simon Hill: Yeah. And I think that’s what we want people to focus most on. It’s not necessarily about extending life,
Mike Matthews: right? Because medicine has gotten quite good at that, but there’s a point where you have to wonder maybe doesn’t get as far as what am I living for? But if the quality of that time that you have gets, gets below a certain threshold, I’m sure that.
Those thoughts go through the mind of people who are experiencing those types of problems.
Simon Hill: Certainly, and I think it’s critical to think about where the average person’s health is at today, Mike. So latest data suggests only 7 percent of at least US adults would be considered metabolically healthy.
Mike Matthews: And can you
Simon Hill: explain what
Mike Matthews: that
Simon Hill: means exactly? Yeah, metabolically healthy typically that, that is synonymous with not meeting any of the criteria for metabolic syndrome, which would mean any of the following. Reduced HDL, elevated triglycerides, elevated HbA1c, elevated fasting blood glucose, or increased waist circumference.
Elevated blood pressure we can put into there. Less than 7 percent of people have all of those things I just reeled off, as what we would say are actually normal or healthy. 93 percent of the population have one or more of those that are not optimal. And there’s, a significant percentage of them Nearly one in two adults have cardiovascular disease.
30 percent of adults have non alcoholic fatty liver disease. About 10 or 12 percent have type 2 diabetes. 40 percent have pre diabetes. And then the rest of people that don’t have a diagnosis, Mike, they might think that they’re healthy. Particularly if they’re not doing the tests that we’re talking about here, but they’re well on the way towards a diagnosis.
Mike Matthews: Yeah, they’re just, things just haven’t gotten bad enough yet for them to be aware of what is actually going on.
Simon Hill: And if I was to go a level deeper, you asked, what does metabolically healthy mean. I’ve tried to really define this and also in conversation with various guests on my show that research this get really clear because metabolic health can be a very abstruse vague term that people use using differently the way that I would define it in a broad sense is that you are.
Able to efficiently convert chemical energy in food into mechanical energy, which requires really healthy mitochondria and skeletal muscle tissue. And then at the same time, you are storing fat where it should be. And what I mean by that is there are different compartments for body fat storage, subcutaneous, essentially under the skin, visceral, and ectopic, which are inside or between the organs.
The former, so subcutaneous fat, that is really or relatively benign. It’s not the kind of deleterious, harmful. fat. When we’re thinking about body fat that really wreaks havoc in terms of metabolic health, so throws out those things like triglycerides and HbA1c and fasting blood glucose, that is body fat that has spilled over and is now inside or between organs, visceral or ectopic fat.
And so people who are not metabolically healthy are Either well, a long way down the road with regards to storing fat in organs like the liver and the pancreas, or they’re at the early stages of that process, which is, dictated by how much body fat someone has and also their genes.
Mike Matthews: And are there any other factors that can weight someone’s fat distribution pattern toward visceral fat aside from just being too fat and maybe being genetically predisposed?
Simon Hill: Yeah, so there certainly is a genetic strong element, and I think we should underscore that. And that’s why you might see two people in front of you who are the same body fatness, but one of them is relatively metabolically healthier than the other.
And what you’ll find is that there is this kind of individual difference where one person can store more fat subcutaneously. And so that’s protecting them because it’s not spilling over into the visceral or ectopic fat depots. Whereas the next person, because of their genes, they are storing much less fat subcutaneously.
So at the same level of body fatness, they have a lot more fat building up in the liver and pancreas. Now outside of genes, yes. And this is an area of debate and ongoing research, but there are, for example, we know that post menopause, There are some significant changes in hormone status, particularly a big drop in estrogen and body fat distribution changes a lot during this time and women start to store much more fat around the abdomen and they’ll, often experience an increase in visceral fat that might be somewhat mediated by changes to hormone.
Status. Then there’s other research and this is a little hard to tease out looking at sleep deprivation. So if you take someone, Mike, who usually sleeps eight or nine hours a night and you force them to only sleep four hours a night and then you look at their food behavior and where they’re storing body fat in the weeks to come.
And you see an increase in calorie consumption, you see this kind of gravitation towards ultra processed hyper palatable foods in a sleep deprived state, and you see a shift in terms of where fat is stored. Some of that is mediated by the calorie surplus, but some of it seems to be independent of that.
So something’s happened happening during that sleep deprivation state that. Is changing the internal physiology environment in a way that leads to those excess calories being preferentially stored in between or inside organs and having more of a damaging effect on metabolic health. So there’s two.
potential examples outside of genetics that can influence body fat distribution.
Mike Matthews: And two, two comments on those things. One is with the hormonal shift that occurs in women as they get older and how that can change the fat distribution. That can be confusing. I’ve heard from many Women over the years who are confused because what they experience is that they are seeing now more fat accumulation around their midsection and that’s different than when they were younger when the excess fat or just body fat in general, if they were to notice expansion or even contraction, it would typically be lower down hips, thighs, but, and The confusion is also around their body composition in that their weight isn’t changing.
Now what they’re seeing in the mirror, they are less happy with, and they feel like they look fatter. And so just wanted to comment for any female listeners to understand that it’s, there’s a distribution pattern of the body fat that you have, and that can change, which can change the way that your body looks without changing your body composition.
You don’t necessarily have to gain body fat. more body fat and you are not necessarily gaining body fat even though it looks like you are in the mirror because you can see what’s happening with your stomach for example and you don’t see what’s happening on the back side of your body and so just wanted to quickly comment on that for female listeners who are experiencing that or who may experience that in the future just so they can.
Understands
Simon Hill: and there’s some speculation as to why body fat distribution changes for women from pre menopause to post menopause. Yeah, it could be hormonal driven, but from an evolutionary point of view if you look at women early in life they. Before menopause, they have a lower risk of cardiovascular disease compared to men.
And one of the hypotheses that may explain that is that before menopause, like you said, they tend to store fat more around hips, thighs, butt, which is the less kind of metabolically damaging place to store fat. Whereas men at the same age tend to store more fat viscerally for a given body fat level.
Yeah. Yeah. Or just midsection in general, right? And then the evolutionary kind of explanation for that might be that it’s not ideal for a woman to store a lot of fat around her abdomen if she needs the space for a growing baby. So it may have something to do with the, development of fetus being pregnant procreation, but It seems that change in fat distribution at least partly explains why once women get to, 50, 51 and into postmenopause, there is an increased risk of cardiovascular disease that’s observed at the same time as fat distribution changes.
Mike Matthews: Yeah, which, which for people listening you would expect as visceral fat accumulates, that’s basically what happens to everyone, right?
Simon Hill: Yeah. And this can be explained. So as the liver, particularly when the liver starts to build up with fat, you develop insulin resistance at the side of the liver and insulin It’s job at the liver is really to turn off glucose production because the liver produces glucose particularly when we’re in a fasted state to ensure the blood glucose doesn’t drop too low.
When we’re sleeping, for example, overnight and insulin’s role is to help turn that tap off if blood glucose is getting too high. When fat is building up in the liver, you get insulin resistance at the liver. So insulin’s not working as well. You can’t shut. down that glucose production as well.
So you get more glucose going into circulation. At the same time, you tend to get increased export of fat triglycerides out of the liver. And that gets packed, that has to get packaged up because fat, fat, unlike glucose is not water soluble. So glucose can just freely flow through blood.
Whereas fat has to be chaperoned by a protein. And that’s why we have lipoproteins. People have heard of LDL, low density lipoprotein. That’s essentially is just a way for us to take fats, triglycerides, which are an energy substrate and get them to tissues. We put them package them onto a protein.
And when you start to develop this fatty liver, you tend to get increased export of these fats into the blood on these lipoproteins. You get an elevation in low density lipoprotein. More broadly, what we would describe as ApoB, which I mentioned earlier, was one of the 10 truths and is probably the best single biomarker for predicting your risk of cardiovascular disease.
And this is why, we often like to put these things in buckets, non alcoholic fatty liver disease or type 2 diabetes and cardiovascular disease, but they’re all very much related. Really most people with poor metabolic health type 2 diabetes or non alcoholic fatty liver disease, they’re dying of cardiovascular disease eventually.
Mike Matthews: Yeah, I want to get to the cardiovascular biomarkers in particular. I think those are worth talking a bit more about. However, first I wanted to follow up with a question. The second thing I wanted to ask you was on this point of undersleeping and accumulating visceral fat, assuming there is a connection there, if you’re only sleeping four hours a night, you’re going to have many other problems.
That practically speaking, there probably aren’t many people out there who only sleep on average four hours per night. However, there are many people who sleep probably six, six and a half hours, which can be enough for maybe a small segment of people who are genetically lucky. But for most people that is it’s not under sleeping so severely that it would be considered.
a major deficiency, but it’s a, it’s an insufficiency. Would you expect that chronically under sleeping, just being chronically sleep insufficient would have maybe not as severe effects in terms of influencing visceral fat accumulation might have Effects nonetheless might again, just derange our physiology to a degree that actually matters in terms of visceral fat, not to mention many other elements of our physiology that suffer when we don’t get enough sleep.
But
Simon Hill: yeah, we’re having to. Extrapolate from a very short term study here to, what does this mean long term? And if the sleep deprivation isn’t, if the magnitude of kind of deprivation isn’t as great, but it’s something that’s happening for months and years, is it, is that having an effect?
And then is it compounding? I think we could hypothesize that you’re right. Certainly we have if we zoom out, we have data that shows, if you’re sleeping less than six to seven hours a night, you have increased total mortality. So premature death, same thing as if you’re sleeping more than nine hours a night.
So you, there’s this kind of sweet spot tends to be around seven to eight hours a night. And then either side of that, increased risk of cardiometabolic disease and premature death. Is that explained by changes to fat distribution? It could be, I don’t have a concrete answer on that, but it may well be, or at least poly explained by that.
Mike Matthews: One of the many reasons to get enough sleep.
Simon Hill: Yeah, and I think people there’s a few kind of very simple things to think about in your life that can help you get better sleep. And, I appreciate we’ve got a lot to get through. So I won’t go too deep here, but what is your eating window look like?
And when are you distributing your calories throughout the day? This is somewhat dependent on someone’s goals, but if sleep is an issue, I think there is an argument to be having more of your calories in the earlier and middle part of the day rather than late and then regular bedtime. Something we can easily overlook, but our circadian rhythms and our sleep quality, generally we do better if we’re going to bed at a similar time and waking up at a similar time each day, each night and day and thinking about light exposure at nighttime.
For many of us, we’re still staring at bright screens or we’re in rooms with bright lights on and you just have to appreciate that when you’re doing that. You might be sitting in Los Angeles and it’s 9 p. m, but your body thinks you’re in Australia in the middle of the day. Of course, when you just quickly run up to bed and jump in bed, it’s going to be difficult to get to sleep.
And some of that is explained by the way that light affects hormone production and you can get disruption of these circadian rhythms, which are really critical for both falling to sleep and then having good sleep quality throughout the night.
Mike Matthews: And something that I’ve seen that can be insidious, and I’ve experienced it myself to some degree, is we establish certain habits when we’re younger, and we get used to following that routine generally, and It doesn’t seem to negatively impact our sleep.
So that might include watching TV at night, being around bright lights in general, doing more active things at night, or at least in the maybe early evening period, and for a while, not. Having any sleep issues. And so there are no issues. And then though, at some point it changes and it’s typically as we get older and not realizing that our physiology has changed now and our habits are no longer sufficient for sleeping.
There, there can be this window of time when. Somebody is thinking it wasn’t that long ago and I wasn’t having any problems with sleeping and I wasn’t paying attention to any of these things. And so it must not be those things. Yeah. Like
Simon Hill: a lot of things in life, it’s easier to take our health for granted, particularly in our twenties.
And we feel invincible. And then, as time goes on, I didn’t
Mike Matthews: realize what I had when I could just sleep. Perfectly, basically always six and a half, seven hours, blackout, unconscious wake up before my alarm. Yeah. As time
Simon Hill: goes on we get away with far less and have to be much more
Mike Matthews: intentional.
Exactly. I want to now come back to the cardiovascular components of these truths, these biomarkers because they are some of the most important ones I would think on the list, because we need a healthy, a highly functional cardiovascular system to live a long life and to live a long good life to have.
Energy. Even starting, you mentioned mitochondrial health, starting there at a cellular level to have energy to do the things that we want to do, especially as we get older and we want to do things like play sports with grandkids and a lot of people listening. are probably doing a fair amount of resistance training.
A lot of people listening are also doing cardio, but a lot of people listening may not appreciate the importance. And that might be a consequence of age. A lot of people might be younger and they are more focused on Improving their body composition, they want to do it in a healthy way, but they haven’t begun to think about VO2 max, for example, and how important it is to maintain a high VO2 max, especially as we get older.
Can you talk a bit more about, again, these cardiovascular components of these 10 truths and what they are, why they matter, and how we can work to optimize them?
Simon Hill: And I missed at the beginning when I was explaining that the Tantras are these windows into these kind of four systems.
If we move psychological well being to the side for the moment, cardiovascular disease or cardiovascular respiratory system, really here I’m talking about How do we protect our arteries when I’m talking about metabolic health, I’m talking about how do we largely, how do we protect the liver and musculoskeletal skeletal system?
How do we protect the bones and muscle? So you’ve asked me here about cardiovascular disease. Really, if we want to avoid having a heart attack or a stroke or even experiencing conditions like vascular dementia, there’s a large vascular component to. Many forms of dementia, but certainly vascular dementia, then we need to protect our arteries.
And so the 3 of the 10 truths pertaining to the cardiovascular system that we’ve included, essentially, if you optimize these. Then you are going to be doing, you’re going to be doing as best as you can, you’re going to be reducing your risk of damaging your arteries day in, day out. And so these were ApoB, blood pressure, and VO2 max.
ApoB, if someone’s hearing this for the very first time, earlier I mentioned low density lipoprotein and that lipoproteins carry fats through circulation. Low density lipoprotein is one type of ApoB containing lipoprotein, but there are others, so there is IDL and VLDL. And just like low density lipoprotein, all of those are what we would describe as atherogenic.
In lay terms, what that means is they have the capacity to crash into the artery wall and get stuck or retained and then kickstart an inflammatory process in the artery wall, which leads to the accumulation of plaque and, after decades. a cardiovascular event like a heart attack or a stroke.
When we measure ApoB, we get the summation of LDL plus IDL plus VLDL. And while LDL Cholesterol generally tracks with ApoB. They don’t always. So it is now considered broadly that ApoB is a better predictor of cardiovascular disease risk of atherosclerosis, which is the building up of the plaque. So if someone can order that and measure it is going to be superior than ordering LDL cholesterol.
Mike Matthews: And can you talk a bit more on that point? Because although I don’t think it should be a matter of controversy, given the weight of the evidence it is. And that is the controversy over the claims around low density lipoproteins and cardiovascular disease. Of course, now, We have people on social media with big followings, a lot of influence saying there is no such relationship.
It’s completely fake. I would guess some of these people are saying it’s actually the opposite that you want to maximize your LDL levels because of course contrarian marketing works and helps you sell things to people who don’t know any better. But can you talk about that? Bit more about that for people listening who maybe are confused now because for so long they had heard what you just said, but now in the last few years, they’ve been hearing sometimes fairly credentialed people, well spoken people who seem like experts say that, Oh yeah that, that was old science.
Now we know. That the truth is otherwise that LDL, these smaller lipoproteins, they’re actually not a problem and the problem is something else. The problem is sugar or the problem is vegetables or whatever.
Simon Hill: Yeah usually Mike, a false dichotomy is created. The problem is sugar or the problem is insulin resistance.
And that’s a straw man argument because both elevated ApoB can be a problem at the same time as insulin resistance and eating a lot of refined sugars can be a problem. And so you can have a single biomarker that is causal and necessary for developing atherosclerosis like ApoB, and it is absolutely true, you can compound it and Basically, throw gasoline onto a fire by adding insulin resistance, a diet high in refined carbohydrates, high blood pressure, et cetera, but you’re just stacking risk factors on top of one another.
Of course, you would expect that person’s risk of cardiovascular disease to be greater. But what is ground zero in terms of atherosclerosis building up at the plaque? You have to have an increase in these ApoB containing lipoproteins in the first place. If ApoB is at what’s called physiologic levels, so 60 milligrams per deciliter or lower, particularly if it’s 40 milligrams per deciliter or lower, you do not see atherosclerosis.
It just doesn’t happen. Okay, so people need to appreciate that kind of first and foremost. And what is the body of literature that makes us so confident that ApoB increases risk of coronary heart disease? It’s not that we’re just looking at one type of study and it’s not that we’re looking at animal data.
It began in animals a hundred years ago, starting off in, in rabbits and then in mice and then in primates. But since then there’s been large observational research, cohorts with hundreds of thousands of people from all over the world. Where you see an association, elevated levels of ApoB, higher risk of coronary heart disease.
Okay, that’s just observational. Maybe there are other factors at play here. It’s not a controlled trial. We also have genetic data, basically nature’s randomized controlled trial. There are people at birth who have genetic mutations that give them either elevated ApoB or reduced ApoB to different levels.
And when you chart those out, their risk of coronary heart disease is determined by their level of ApoB reduction or increase, the magnitude of that. And it’s a linear relationship. Okay. What about randomized controlled trials? What about if we take people? that have heart disease and we put them on a drug that lowers ApoB.
We track them for 5, 6, 7 years. Now this isn’t as long as the genetic data. It’s not as long as the observational data because it’s a clinical trial. But what do we see in 5 We see reduced total mortality. We see reduced events. Is the risk reduction in those clinical trials as great as if someone wins the genetic lottery and has the same ApoB but achieved from birth?
As what the drug achieved? No. Why? Lifetime exposure matters, and that’s, in recent years, scientists have popularized this idea of cholesterol years, which is very similar to pack years when it comes to smoking. So you’re looking at what is your average cholesterol across your lifetime will determine your the kind of atherosclerosis burden, the amount of plaque that’s built up throughout their life.
Moral of the story, if you get ApoB down to a physiologic level, you will not be laying down plaque. In your day to day, when you go to bed at night, you’re not going to be laying down plaque. So I think it’s a sensible thing to optimize that. And in me saying that I’m not saying insulin resistance is not a problem.
I’m not saying refined sugars are not a problem. All of those can be a problem and contribute a contributory to poor health at the same time. One other pushback that often happens because Mike, and I’m not sure if you’ve heard this, people say it can’t be held healthy, lowering APRB or LDL.
cholesterol because cholesterol is very important for the synthesis of hormones. It’s very important for cell membrane fluidity. I’m not sure if you’ve ever heard people say that.
Mike Matthews: Yeah. And in connection with that, again, some people go as far as saying that therefore it’s a vital nutrient that you just want to get as much as you practically can
Simon Hill: of.
Yeah, so this is a misunderstanding of basic physiology. I’ll do my best to explain this. Firstly, all cells throughout the body and also astrocytes, neurons, have the capacity to produce all of the cholesterol that they need. All cells throughout the body have the capacity to produce all of the cholesterol they need.
They do not need dietary cholesterol or saturated fat to do that. Why is there cholesterol in lipoproteins, someone might ask. What’s cholesterol doing in circulation if it’s not being carried to cells? If cells don’t need it because they produce all the cholesterol that they need. It’s a great question.
It’s a question that I asked Dr. Thomas Dayspring on my show. I did seven hours with him on lipids. He’s a lipidologist and really cholesterol is only in these lipoproteins to create a spherical structure. So before I mention that fats. Can’t, they’re not water soluble, so they have to be carried by a protein.
Essentially, that protein is like the outer layer of a beach ball. And then inside is where the cholesterol and the triglycerides are. And it’s the cholesterol which gives that lipoprotein a spherical shape and allows you to pack triglycerides into it. So the lipoprotein, The purpose of it is to get these triglycerides and energy substrate to tissues, not to carry cholesterol to tissues.
So not only do we understand the physiology there, we also have studies looking at people who are put on severe lipid lowering drugs that get them down to 20 to 30 milligrams per deciliter. Do they produce an optimal amount of hormones? Yes, they do. What about people with genetically low LDL cholesterol?
So again, we’re talking about cholesterol in circulation. Are their cells still operating normally? Are they able to produce enough hormones? Yes. So this idea that low serum cholesterol impairs hormone production, I understand the kind of logical leap if someone’s not across the physiology, but when you look at the physiology and you look at clinical trials looking at subjects with low serum cholesterol, then it becomes clear that is more myth than science.
Mike Matthews: Can you address the related claim that by eating a significant amount of dietary fat, it’s usually saturated fat is what’s being pushed, that you can improve your hormonal profile? Because I’ve seen some people. They might grant you that and say, okay, fine, you don’t have to eat a lot of dietary fat and dietary cholesterol, but if you do, your hormones are going to be better.
Simon Hill: I would challenge someone to send us a study that shows independent of calories, you can improve hormone production by consuming saturated fat over say unsaturated fat. I do believe there are studies out there showing when you add fat to someone’s diet, you can improve hormone production. And in those studies, it seems that you’re taking someone from a kind of hypocaloric state to hyper, and we know that calories can certainly affect hormone status, hormone production, but I’m yet to see any evidence that suggests that saturated fat independent of calories is superior to any other macronutrient type for assisting the body with hormone production.
That said, also a low total fat diet. Can also I think be a problem for hormone production, but it would have to be very low. It have to be below 10 percent of total calories, which not many people are getting anywhere close to.
Mike Matthews: Yeah, it’s almost impossible. You have to be a dedicated bodybuilder really to even make that work.
And so coming back to April, then what are some practical things that people can do to. Reduce their or to maybe slow the accumulation of their cholesterol years, so to speak
Simon Hill: is that some of this is going to. To come down to individual genes, but let me just begin this kind of broadly at a population level.
Different types of fat affect the liver’s ability to clear ApoB containing lipoproteins from circulation. There is, what’s known as an LDL receptor on the liver. And that receptor, just imagine it as a gate, it’s a gate that can open or close. And when it’s open, the LDLs, the IDLs, and the VLDLs, which I mentioned are all ApoB containing lipoproteins that can cause atherosclerosis, they can get back into the liver.
So bringing ApoB down. in circulation. Saturated fats tend to down regulate the LDL receptor gene expression, which means when you’re eating a diet that’s higher in saturated fats, And we can double click on that if you want, because not all saturated fats are the same. But just broadly speaking, those saturated fats tend to close that gate a little bit, which means less of the ApoB containing lipoproteins can be cleared from circulation.
They build up, you have a higher ApoB when you perform this blood test. Whereas if you swap calories from saturated fats for unsaturated fats, particularly for polyunsaturated fats. You see a lowering in ApoB and polyunsaturated fats have the opposite effect on the LDL receptor. They up regulate gene expression.
They open the gate. So here I’m talking about, reducing foods in the diet, like butter, very fatty cuts of red and white meat, and instead eating either lean cuts of red or white meat. or better again, fatty fish, which is really rich in polyunsaturated fats tempeh, tofu, nuts and seeds, all rich in these polyunsaturated fats.
That kind of food substitution will generally result in a significant reduction in ApoB. And then from a cooking oil kind of perspective, swapping butter or ghee or coconut oil or palm oil out, for something like olive oil.
Mike Matthews: And you should probably also at least briefly touch on seed oils and how the weight of the evidence is basically the opposite of the general message that, that you find on social media.
Not that you have to intentionally add these to your diet if you, if your diet is rich in seed oils, of course, some people that’s just because their diet sucks and they eat a lot of highly refined, hyper palatable foods. It’s not because they are healthy. cooking their lean cuts of meat in canola oil or something.
So there’s this really critical point here where we need to make sure we’re not conflating seed oils with hyperpalatable ultra processed foods that can contain seed oils, but also contain a lot of artificial ingredients, refined sugars, high sodium, low protein, low water, et cetera. So when you independently look at seed oils, you’re right.
Simon Hill: We don’t see that they are inflammatory. They don’t seem to be in human studies. We don’t see that they’re obesogenic. In fact, we see that populations who consume more linoleic acid and have higher linoleic acid, which is an omega six. It’s the most abundant polyunsaturated fat found in seed oils.
Populations who have higher adipose tissue levels of linoleic acid and serum levels actually have lower risk of cardiometabolic disease and total mortality. So I think that the fear mongering is clearly not warranted. And I would argue personally, The majority of cardiometabolic disease burden is a result of, 50, 60 percent of total calories, maybe a little more being from ultra processed foods, which are hyper palatable, easy to over consume.
They’re driving the obesity epidemic. We’ve spoken about the problem with having excess body fat, particularly visceral fat already and how that influences cardiometabolic health, but I would throw it back to anyone who’s wants to blame seed oils. for chronic disease. I believe if you went out to the food environment and got all of those ultra processed, totally delicious, yummy foods and swap the seed oil out and just add butter in, I don’t think it makes a single difference to chronic disease incidents at all.
Mike Matthews: It may get worse with butter, which I want to follow up on the point that you had mentioned regarding certain saturated fats being different than others. And butter I know is one that as you mentioned if you are wanting to get down into the details of optimizing these different physiological systems, it’s not that you should never have butter, but.
You don’t want to be consuming large amounts of butter. Can you talk a bit more about that? And then also the difference between certain saturated fats and others?
Simon Hill: Yeah, I think I might walk back what I said before a little bit. I think you’re right. It’s if you swapped these seed oils in these ultra processed foods for butter, you’re right.
It might not make much difference or it could in fact worsen outcomes. So what’s the issue? With butter and why does butter associate with disease differently to other dairy fats like cheese and yogurt. Some of this has to do with the food matrix, particularly in this dairy conversation.
So it’s not just the amount of saturated fats or the type of saturated fats, it’s also the foods in which we consume them. which affect how they are digested, absorbed, and utilized, and therefore their impact on ApoB. And in dairy foods, there is what’s known as a milk fat globule. And that, when it’s intact, so in more kind of whole forms of dairy foods like yogurt and cheese, so less refined forms, that milk fat globule is intact.
And It actually affects the amount of fat that is absorbed when you eat those foods. And therefore, you see a much smaller increase in ApoB relative to a dairy food like butter, even for the same grams of saturated fat. Because in, in butter, because of that refining process, you break the milk fat globule and you liberate those saturated fats such that they now have a much more profound impact on blood lipids.
So that’s one of the kind of important things to keep in mind with butter. It is refined and in that process you make those saturated fats much worse from a cardiovascular disease risk point of view.
Mike Matthews: And what about ghee because that’s often presented as the less refined, more esoteric butter.
Simon Hill: Yeah. From the studies that I’ve seen, gay will still raise LDL cholesterol. The saturated fat profile is a little different to butter. I believe it’s not something that I’ve honestly deep dived. I’ve looked at coconut oil, which is a different saturated fat. profile to butter. So for the same grams of saturated fat, it still elevates LDL cholesterol, but not as much as butter does.
This kind of point on the type of saturated fat being also important here, just at a very high level, there are Short chain fatty acids, which are people may have heard when learning about the microbiome. Those are saturated fats. There’s medium chain fatty acids, which were popularized by the low carb keto community not so long ago.
And then there’s long chain fatty acids. And within each of these different types of saturated fat kind of families, there are Different types again, depending on the length of that chain, the most deleterious when it comes to ApoB are these long chain fatty acids, particularly myristic and palmitic and loric acid, those three.
which are predominantly found in tropical oils. So coconut and palm oil, butter, which we’ve mentioned, and then in fatty cuts of meat. So red meat and white meat. There is another long chain fatty acid called stearic acid. Which seems to be relatively neutral. Doesn’t seem to have that same effect on the LDL receptor.
It doesn’t seem to increase ApoB like these other saturated fats. And that is the predominant saturated fat that’s found in chocolate.
Mike Matthews: Yeah, thanks for clarifying that because it’s a dietary recommendation that I’ve made for a long time is to just be conscious of your butter and of your coconut oil, which I don’t know how popular that is now for a bit there.
It was pretty popular. A lot of people. I had heard from many people who were eating a lot of coconut oil because again, they thought that was a healthy thing to do. So they were trying to work it into various meals, maybe even replacing olive oil, for example, with coconut oil. Just wanted to make sure that the people listening got that information.
And before we wrap up. I wanted to also talk about VO2max, and if we have time, blood pressure as well, and maybe starting with VO2max, what is that, and why does it matter, and what can we do to improve it, and what can we do to maintain it, especially as we get older, because it is a lot easier, similar to you.
gaining muscle and to getting strong and retaining that muscle and retaining that strength. It’s a lot easier to do when we’re in somewhere, let’s say in the first half of our lives than it is in the second half. Not that you can’t, but if you are in the first half of your life and you have, The time and you have the inclination, you’re going to be happy if you start now on both of those things on your muscles and on your strength, as well as your VO two max, you’re going to be happy in the second half of your life.
If you start in the first half.
Simon Hill: So VA2max is, it’s an incredible predictor of total mortality, premature death. In fact, a couple of studies that have looked at this recently, it’s a better predictor than is having cardiovascular disease or having type 2 diabetes. And in some of these cohorts where they track people over 8 to 10 years and at the beginning look at their cardio respiratory fitness which is, pretty synonymous with VO2 max what is people who have, a high or elite VO2 max have a, 4 or 5 times less likely to die during that follow up period of 8 to 10 years.
And this really speaks to the health of their central cardiovascular system. Heart, large arteries, how efficiently they can pump oxygenated blood through the body and then be able to utilize that. The core definition is, the maximum amount of oxygen that you can pump through the body. In milliliters per kilogram per minute, and as I said, this is largely dependent on central cardiovascular health.
In terms of optimizing this in your life, the biggest kind of levers that you can pull are going to be your different Modalities of cardio vascular training, quote unquote, cardio, in particular, that high intensity, interval type training where you’re getting up to 90 percent of max heart rate, which is working extremely hard.
If you haven’t done that before, I think a lot of people underappreciate how hard that is. But you don’t have to be exercising at that intensity for a very long period to reap some pretty considerable rewards. Whereas if you’re wanting to improve your VO2 max by doing more moderate intensity cardiovascular training, then you need to go for much longer.
And as often as great debate, I’m not sure if you’ve covered this on your show about what’s better, high intensity interval training, moderate intensity, cardiovascular training and maybe if we’re thinking about bang for buck time invested hit is better, but it doesn’t necessarily suit everyone depends on their baseline.
Cardiorespiratory fitness, their balance, how likely are they to have falls? How confident are they? So this is going to look a little different for everyone. I think a good cardio program ideally includes both exercising at a moderate intensity for the majority of your minutes. you’re doing across a week, but then also supplementing that with some high intensity work.
And in doing the two of those, you’re targeting both, both the peripheral cardiovascular system also the skeletal muscle mitochondria that we spoke about earlier. And then you’re also hitting that kind of more central cardiovascular system and getting heart and large arteries to adapt in a way where you can now pump oxygen, oxygenated blood around the body more efficiently.
Mike Matthews: And how does strength training fit into this context? Because there are at least a few people listening who are probably pretty good about their strength training. They don’t do much cardio aside from walking. Maybe they get in there 10, 000 steps a day, but they don’t do it. Or they do very few cardio workouts properly. I think a
Simon Hill: good all round program is getting, 120 to 150 minutes a week of moderate intensity cardio that could be on a stationary bike. It could be rocking or hiking, there’s a lot of conversations around zone two and measuring your heart rate and all of these things.
It just depends on who you are and what your goals are. I think for the average person who’s just focusing on longevity, get out and do a 150 minutes of exercise cardio a week where you are breaking a sweat. You can probably still have a conversation, but you’re a little bit puffy. You can probably still breathe through your nose, but maybe for some people you can’t, but you’re not extremely exhausted.
You can do that type of cardio for a 45 minutes, relatively easy. So the intensity of that is going to be affected by your baseline cardio respiratory fitness for one person that might be a jog and for the other person that is a walk for the person who is relatively less fit. So 150 minutes of that per week. I usually recommend that on top of walking.
Mike Matthews: Regardless of the of what you’re doing for strength training, because there are many people who maybe would like to believe have heard and would like to believe that strength training, as long as you’re doing a few hours per week, that’s enough.
That’s enough for your cardiovascular health, especially if you lift the weights fast. That’s your cardio.
Simon Hill: I think it’s a different stimulus. You might look at your, you might have a whoop or you’re measuring your heart rate with something and you might look at your resistance training session and see that across the 60 minutes you’re in zone two for the majority of it, but it’s a different stimulus.
You have to appreciate that you’re lifting a weight and then you’re resting for two minutes. It’s different to continuous exercise over a 60 minute period. So I would treat them. a completely different stimulus. So stimulus is what’s going to cause the body to adapt. Your resistance training is primarily a stimulus that’s going to stimulate bone to grow stronger, lay down more bone, increase your bone mineral density, to be able to tolerate more force so you don’t experience a fracture where you’re less likely to.
And then it also stimulates tendon and muscle to adapt so that you can. Be stronger, under load. The cardio, that moderate intensity cardio that I’m talking about, I like to think of that as more of a a stimulus that targets the periphery, all of the smaller arteries that are going into muscle tissue, the muscle tissue and mitochondria itself.
So we are essentially. Creating a micro stress that causes that part of our body to update and grow more resilient to be at less risk of disease affecting those, that aspect of our physiology and then the high intensity. So let’s say you have 2 or 3 resistance training sessions a week. And you can split that up.
So you’re covering your whole body over the week. You have 150 minutes of this moderate cardio. I put that on top of walking because most people when they’re walking are in zone one or it’s not enough of a stimulus to get those systems. I was just talking about to adapt and then adding in some of that high intensity work, which really is, let’s call it, let’s call it 20 to 30 minutes of time invested once a week.
And that’s because you need to warm up and there’s rest periods, but that’s the time where you’re stimulating the kind of more central cardiovascular system, particularly the heart. And that all round program you’re providing three different stimuli that are, all leading to their own really important benefits in terms of your health span and frailty.
Mike Matthews: Makes sense. And let’s talk quickly about blood pressure before we wrap up as well. And why is that on the list? And how does it relate to, it’s going to relate to obviously some of the other things you’ve already talked about.
Simon Hill: Yeah. This is like a relatively unsexy biomarker and I’m not sure why, 55 percent of adults in the U S have hypertension.
You can get a a blood pressure cuff either for your arm or your wrist on Amazon for about 40 that are relatively accurate. I think it’s something that, that more people should be measuring routinely. For every 20 millimeters of mercury increase in your systolic blood pressure, you double your risk of cardiovascular disease.
And there’s quite a few mechanisms, high blood pressure probably makes our arteries more stiff. Supple and also damages the actual endothelial cells. That can make them more susceptible to those ApoB containing lipoproteins to penetrating and getting stuck. So earlier I mentioned that ApoB really matters, it’s ground zero, but you can stack risk factors.
Having high blood pressure is one of those. So if you have high ApoB and then you have uncontrolled high blood pressure you’re now creating, this perfect environment to be laying down plaque, which is, certainly what we see. The great news is, there are quite a few lifestyle kind of interventions, things that you can do that will greatly lower your blood pressure.
All of the exercise that we’ve just spoken about will do that. Acutely, exercise raises blood pressure, but chronically it lowers it, just to note that. And then the other kind of levers that you can pull are weight loss. So if someone is overweight every one kilogram above your ideal. Body weight adds about one millimeter of mercury to your systolic blood pressure.
So if you’re 10 kilograms above your ideal weight, that adds about 10 millimeters of mercury to your blood pressure. So weight loss can be something that, a lever that people can pull to lower their blood pressure. But independent of calories and body weight, the types of foods you’re eating also have a considerable effect.
And I’m not sure if you’ve heard of the DASH diet. But before.
Mike Matthews: Yep. I’ve recommended it to my father in law who has blood pressure issues. And I think he’s following it. I basically remind him every time I see him because his blood pressure is too high and I’m trying to be a good guy. Yeah.
Simon Hill: So this is a dietary patent.
Broadly it’s low saturated fat. It’s high fiber. It’s very plant rich. It is high potassium. It’s low sodium. It’s going to have an emphasis on, white meat and fatty fish, fruits, vegetables, legumes, whole grains, and low fat dairy.
Mike Matthews: It’s an all around great diet. If somebody is getting most of their calories from relatively unprocessed nutritious foods, that’s basically how they’re eating.
Of course, though, with the special emphasis on sodium, which means that maybe if you’re going to follow that diet, you’re not going to use as much salt as you might like to use, or you might get a potassium chloride instead or something, but
Simon Hill: exactly. Yeah. The potassium the low salt potassium chloride salts can be a great option for someone who is at higher risk of cardiovascular disease or has high blood pressure for sure.
Interestingly, like the biggest reduction in sodium for most people is sodium. removing ultra processed foods. So like 80 percent of the average person’s salt intake in Western countries, it’s not actually from the salt shaker. So like that is important, particularly if someone’s already done all of the whole food swaps and they still are wanting to lower their blood pressure more, but just by simply going to whole foods and trying to eat less of these ultra processed foods, most people will dramatically lower their sodium intake, which is amazing.
And potassium will generally go up, particularly if you’re eating a lot more fruits, vegetables, and also dairy. Dairy contains potassium, which might be one of the reasons why dairy foods tend to be associated with lower blood pressure. But potassium has the opposite effect to sodium on blood pressure.
Yeah, those are a couple of things that people can focus on if they want to lower their blood pressure through lifestyles, weight loss, and then thinking about the dietary pattern. That there can share me
Mike Matthews: and one other question regarding April B and VO two max people, some people may be thinking should I be measuring these things or should I just do the types of things that Simon’s talking about?
And and just hope that they are sufficient and working. And if you would recommend measuring, what are practical ways of doing that? Blood pressure is easy enough, like you said, you buy it on Amazon, it comes and you just strap it on, wait a minute, get your reading, you’re done.
Simon Hill: Yeah we’re glossing over a lot of this.
I will add that in the Living Proof Challenge PDF, which you can get at theproof. com, it goes over all the 10 truths, how to measure them, how to intervene on them in detail, again, that’s zero cost. But yeah, I think people should measure them. And I think so for a few reasons. One is it’s hard to optimize the things that you don’t measure.
So remember at the beginning, I said, you might focus on different lifestyle interventions than I. Mind, and that’s going to be based on our results. So it’s going to give you more specificity. Everyone’s time poor. We’re all time poor. We’re all busy. I want you to know where you as an individual should be focusing most.
What’s going to really make the biggest difference for your health span? That’s what measuring enables you to do most of these tests are very accessible in that they are free or very cheap or in the case where there is potentially a considerable cost and it’s inaccessible for some people like a VO two max kind of gold standard lab tests, which could be, depending where you live in the world between 100 and 300 well, you can actually perform what’s called a beep or shuttle test Have you ever, did you ever do those at school, between the two cones?
Mike Matthews: Maybe? It seems to ring a distant bell, but So long story short, there’s this test that many people listening at school probably did it, where you’re running between two cones and there’s a beep. You have to make it to the next cone before the beep. And then the time between the beeps is progressively getting shorter and shorter.
Simon Hill: That’s that you are running faster and faster. If you miss the cone, because the beep occurs before you get there, you have to make the next cone or you’re out. You cannot miss two cones in a row. When you miss two cones in a row, you end up with, something like level nine shuttle three, whatever it was that you were up to, because the recording is also along the way telling you what level and shuttle you’re up to.
There’s a few studies now that have looked at how well does this correlate to VO two max, and it actually correlates. Amazingly well, so you can and I have a table in that PDF. You can do the shuttle test on a basketball court. So you get level 9 shuttle 3 on the table. You just go to male or female and then your age and it will tell you what that equates to from a VO2 max point of view.
So now you’ve got your VO2 max as a kind of approximation with a high level of confidence. For nothing. So that’s what we’ve tried to do to make these things more accessible. But certainly, I think that there is huge benefit in testing as many of these things as you can. So you know where to focus.
And then the second reason is I think it’s it can be really inspiring and motivational for people. So a lot of the time we’re going through life and we have no idea what’s going on the inside. Remember before I said 7 percent of adults are metabolically healthy and there’s a huge percentage of people that don’t have a diagnosis but they’re not metabolically healthy?
Once they actually measure and they can see on paper, shit, I’m not doing so well here on this marker that’s important for cardiovascular disease, on this marker that’s important for metabolic health, they can be more motivated to buy into some of these new lifestyle habits that we’re hoping that they build.
Mike Matthews: And then see the improvements in Actual, let’s say it’s blood work versus hoping that things are getting better because something could be improving significantly that you’re not aware of. You still feel the same, but you are reaping considerable fruits. You’re just not aware of it. Consciously,
Simon Hill: and we’re still pulling together the data, but we’ve now had like over 20, 000 people go through the living proof challenge.
And so we have an enormous body of data where we have baseline results for the 10 truths and then post challenge results. And I can tell you, because this is a question I often get, like, how long does it take to. To change some of these things, it depends on the biomarker, like ApoB, you can change your ApoB in a couple of weeks with dietary change, really in days often, whereas something like bone mineral density or strength, I’m sure you could appreciate takes a little bit longer, but where we’re seeing.
People take four, five of these markers from suboptimal into normal or optimal over a 12 week period. Yeah, that’s fantastic.
Mike Matthews: And installing those habits that will serve people for the rest of their lives, because it’s really about building. A healthy lifestyle as opposed to doing some short term intervention, which is fine in some cases, but the biggest benefits special health and longevity, of course, are going to be in the things that we do consistently, whether good or bad.
Simon Hill: Yeah. So don’t let perfect be the enemy of good. We don’t want people to be perfect at this for 12 weeks and then just go back to their old lifestyle. Get it 70 to 80 percent right. Doesn’t mean you have to get it right every day or all the time, but do it for longer. Do it for decades. As you say, it’s going to be, have a much more significant impact on your health than any kind of two or four week type challenge.
Mike Matthews: And that of course is how fitness, how training works as well. You just want to be good enough. Most of the time. That’s enough. This was this was a great discussion. We got through mostly everything that, that I wanted to ask. And before we sign off here, why don’t we let people know, obviously they can they can find more material over at the proof.
com yeah, the proof.
Simon Hill: com and from there you can access the podcast, you can download the living proof challenge, you can find the YouTube channel, you can connect with me or the proof on social
Mike Matthews: media. Great. And that was my next question is where people can find you on social media, and that would be the proof on you’re on X as well as other networks.
Yeah. So it’s
Simon Hill: the proof on X. It is at Simon Hill on Instagram, and there’s also at the proof on Instagram where we just upload the podcast episodes that come out each week.
Mike Matthews: Awesome. This was a great discussion, Simon. I appreciate you taking the time again. Thank you. Thank you, Mike. Thanks for having me.
Appreciate it.
