Dr Rupy: Simon Hill has dedicated the last ten years of his life to a clean plant-based diet. He's a nutrition scientist and he's dedicated to simplifying health and nutrition information. But unfortunately, a recent heart screening shows he has early signs of heart disease. This episode is going to be unpacking how this has happened and what he's going to do about it. It's been a long time coming but I finally got a chance to sit across the desk with Simon Hill. And today we're going to talk about his personal experience with cardiovascular disease and what prompted him to have early screening for heart disease and what his results have shown, which is really quite surprising. Simon has early signs of heart disease and now he has a decision to make around whether he embarks on early drug treatment or delays treatment to watch how it evolves. He's thirty-nine. And many of us are going to find ourselves in a similar situation as we become more pragmatic about health screening, especially with the rise in popularity of full body scans. We have a discussion around fats, the types of fats in the diet and how one might choose to lower their cholesterol with diet and lifestyle. And we also go on a virtual trip to the supermarket with Simon to discuss the framework for how to choose fats and healthy ingredients to reduce our risk of heart disease. The things you also need to ask yourself about consuming fats which also include the dose and what you're eating it with. Before we start today's pod, I think it's prudent to define a few things because they crop up naturally in our conversation and I just want to make sure that everyone is up to speed. So atherosclerosis is the chronic progressive disease in which plaque builds up inside your arteries. These are the blood vessels that carry oxygen rich and nutrient rich blood around the body. Plaque is made up of things like cholesterol, fatty substances, calcium, cellular waste products and fibrin, which is a clotting material in the blood. And over time, this build up causes the arteries to narrow and harden and reduce blood flow, which can become prone to rupture and trigger a blood clot. Where it occurs, well, we typically think about atherosclerosis in the context of coronary heart disease, so that's in our in our hearts. But there's also arteries in your brain, the carotids, renal arteries, peripheral arteries in your legs and arms. So these can all become blocked and lead to downstream effects because of the lack of oxygen and the lack of nutrient supply. Cardiovascular disease on the other hand is an umbrella term that refers to a group of disorders involving the heart and blood vessels. So you've got coronary artery disease, which is narrowing or blockage of the coronary arteries, often caused by atherosclerosis, cerebrovascular disease, which is affecting blood flow to the brain that can cause strokes, peripheral artery disease, which is poor circulation to the limbs. But you've also got heart failure, arrhythmias, where you've got abnormal heart rhythms, congenital heart disease, hypertensive heart disease. And globally, cardiovascular disease is the leading cause of death worldwide. The relationship between the two is that atherosclerosis is the underlying cause of most cardiovascular diseases. We also talk about some funky new scans that are available. So you might have come across something called invasive coronary angiography. This is a catheter based intervention where we put a catheter into a large vessel in the leg and it enables you to visualise blocked arteries when we inject contrast and also intervene if we need to. So you can place a stent, you can use a balloon. It's really, really impressive and we've used this technology for for years. Clearly uses something different called a CCTA, a coronary computed tomography angiography. And what it does is it builds on this CT scan, which is something that we do already, using AI and interpretation of the plaque morphology. So you can look with great detail without doing the catheter based intervention at looking at the type of plaque that's there, the the whether it's soft, whether it's hard, whether it's calcified, and it gives you even more ability to interpret just how far gone the heart disease is. It doesn't allow you to intervene with a stent or anything like that, but it gives you a lot more detail than just a plain coronary computed tomography angiography. This is something that is available in the States and it's something that's becoming a lot more commonplace over there as well. Really, really impressive and this is what Simon had to determine his risk of heart disease and we get into as to why he had that done in the first place because of his family history. We talk about lipid lowering drugs, so these are drugs that reduce cholesterol in your bloodstream, things like statins and fibrates. And we also mentioned carotid arteries. These are the arteries in your neck and when these are blocked, they can lead to things like TIAs or strokes. A TIA is also colloquially known as a mini stroke. If you don't know Simon, Simon is a physio, nutrition scientist and he began his career in the physiology and anatomy related to optimal athletic performance. And then encouraged by his family history, he actually turned his attention to nutrition and nutrition's role in preventing disease and optimising health. He completed a masters in science in human nutrition at Deakin University and he has a really popular podcast that I was really privileged to be on called The Proof, which is widely available across all your pods. And he's also got a really cool company called 38 Terra with another friend of the podcast, Dr Will B, which is all about using natural ingredients to boost your microbes. I highly recommend you check that out as well. For now, this is my podcast with Simon Hill. I really, really hope you enjoy it.
Simon: Yes. So I decided to do an entire episode on my heart scan results. Which not everyone does, making those results public. So I'm I guess I am proud that I was able to do that and I think it's led to some pretty impactful conversations already. So my backstory is that when I was fifteen years old, I was with my dad and experienced him having a heart attack. And that whole long story there, but I'll make it quick. He survived and was taken to the nearest hospital by helicopter, actually, because we were quite a way away. And in the aftermath of that, I was kind of told by the cardiologist, this is a disease that runs in families, so you're going to want to keep an eye on this. And some years later, about a decade, I was at university.
Dr Rupy: How old was your dad, sorry?
Simon: My dad was forty-one.
Dr Rupy: Okay, so very, very young.
Simon: Yeah. And out of nowhere. He had, like you, not you had a different experience, but also heart related. He wasn't on any medications and had no diagnoses. It was from the outside a typical Australian dad, otherwise healthy. So certainly not something you expect. And you know, a decade or so later, I did my undergraduate degree in physiotherapy and then a masters in nutrition science and I was getting really interested in understanding how can we eat to live better for longer, particularly for me personally, how can I eat to lower my risk of cardiovascular disease so I don't have the same experience that my dad had. And you know, over time I learned that we have a lot more control and say in terms of how our health plays out than I had thought at the time. I had thought it was largely genetically determined, which is pretty disempowering as a fifteen year old. And so the evolution of that was picking up more and more information, feeling more empowered and then wanting to share that information publicly with many other people who are experiencing similar things in their families and wanting to be really proactive with their health and prevent disease before it kind of manifests as symptomatic. And so part of this process for me has been about making lifestyle changes and it's also about understanding what are the risk factors and things that we can monitor over time to ensure that we're doing our very best at reducing our risk of in my case, primarily cardiovascular disease. And so I'm thirty-nine now and my dad was forty-one when he had his event. So one of the things that I've been interested in is looking kind of underneath the hood, actually inside the arteries and the key arteries that are providing blood and oxygen to the heart and understanding how healthy they are, if I have soft plaque or hard plaque and the way of doing this is to use scans like CT angiogram and the coronary artery calcium scan, both of which I did. And
Dr Rupy: Just before we get to your investigations that we're going to go into, I just want to rewind ever so slightly and talk about how you landed on the dietary approach to prevent cardiovascular disease and what your diet actually has looked like.
Simon: Yes, so this was actually the motivation to go back and do a masters in nutrition science was that I was working as a physiotherapist and I had a mix of experience working with elite professional athletes, footballers in Australia with the AFL team Richmond and their feeder team Coburg, which you of course know given that you spent some time. And I mixed that with some private practice work in various suburbs and I realised that I myself was very confused about nutrition. And I was digesting the information that most people were at the time through the mainstream media, a little bit of social media, what people would say at dinner. And I realised that there are so many different conflicting ideas and there's a lot of conviction behind these ideas. And how can it be that you can have the same conviction for what appear to be very conflicting, contradictory ideas. There has to be some degree of certainty or truth within the literature that can show us what is a more evidence based direction or what is the evidence based direction to go down. And I realised I didn't have the skills to be able to read the literature to actually determine that, even though I had an undergraduate science degree. And so went back and learned about all the various types of nutrition science and what different studies tell us and what they don't tell us and how they kind of fit together to inform best practice guidelines. And to me, and there is no kind of truth with a capital T as such. Science is about reducing uncertainty. There's always open questions. But what did become clear to me is that there is a theme, a way of eating that consistently is associated with lower risk of cardiovascular disease, cardio metabolic diseases in general, and also a way of eating that shifts important risk factors that are established in a favourable direction. So we understand not only that people who are eating in a certain way are having less events, whether it's developing type two diabetes or having a heart attack, stroke or dementia, but we understand some of the mechanisms and the way in which those those dietary choices are affecting physiology. And while it's not one specific diet, there is a theme and those diets tend to be diets that are largely unprocessed. From a fat perspective, there's a bias towards unsaturated fats. From a protein perspective, a bias towards plant protein, and they're high in fibre, making them really healthy from a gut microbiome perspective. And you can kind of cut that up in a number of ways. It could be Mediterranean, it could be pescatarian, it could be plant based. It could be low carb, it could be high carb. And then learning that, I realised, well, my current diet's a long way off from that. So through my twenties and into my mid twenties, again, I'm in this environment of fitness and football. It was very much about maximising animal protein. And so with that, I was getting a lot of animal fats. I didn't have a very processed diet, which was a good, pretty good starting point. But my LDL cholesterol was sitting at almost one hundred and thirty milligrams per decilitre.
Dr Rupy: Okay, which we just converted.
Simon: Yeah, we did.
Dr Rupy: Which is, let me just bring the conversion up. It's above two point six millimoles per litre for LDL C. So it's definitely high.
Simon: It's high. Yeah. And
Dr Rupy: But in your twenties, you probably weren't even thinking about, I mean, a regular twenty year old who didn't have the experience that you had with your father, probably wouldn't even be checking their cholesterol, let alone worrying about a high one.
Simon: Yeah, and I understand why, because this disease kind of rarely rears its head in your twenties. It's bubbling away under the surface. And we know that it can begin as early as in the womb, depending on the mother's cholesterol. Certainly in infancy or in teenage years, it can begin with people who have sky high cholesterol, a genetic type of cholesterol called hypercholesterolemia. But it's not really, it's not causing an issue for most people until fifth decade or on where there's enough time for enough plaque to build up and it's affecting blood flow. But I had extra motivation because my dad had had a heart attack very early. And so I was in a slightly different position to most twenty year olds. I think often is the case in life, people are not compelled to make a change unless they themselves experience a health event or someone close to them. And up until that point, honestly, I just thought health was a given. I hadn't had a grandparent pass away and my parents were otherwise healthy. So I hadn't really seen, I hadn't seen health kind of almost disappear in a flash like that. And so I decided to look at all of that science and then see whether I could make some of these changes. And I was pretty, I was pretty worried about whether I'd be able to do it. I was eating tons of steak. Really? Tons of steak. I was the guy who every single time I'd organised dinner with my friends, it was the steakhouse. And I would have the biggest steak I could order with butter all over it. And honestly, I love steak and and I don't eat it today, but I can still say it tastes amazing.
Dr Rupy: That's a very brave of you to say that, you know, as a plant based.
Simon: It does. It it there's no denying that. So I understand why it's on people's plates and features largely in a lot of people's diets for sure. And I had all the concerns around, well, where am I going to get my protein and am I going to like these other foods that I've really have never eaten? And so it was a it was a real process and you know, I I took my time and made slow changes and didn't get there overnight making those changes. But yeah, fast track to now, that's been that was a decade, over a decade ago. And so I've been eating this way for a long time and I was interested in understanding what the current kind of state of health of my arteries looks like. And that would then help me help inform me as to whether I would just continue with my lifestyle as it is or whether I need to also consider medicine as another kind of preventative action here.
Dr Rupy: Yeah. And I guess from your experience doing your podcast and your books and the, you know, general interest you have in research has led you to even consider this at such an early age as well. And the fact that you've had conversations with lipidologists and other preventative cardiologists, probably was in part encouraging you to even do the test in the first place.
Simon: Yeah, and let me put my hand up and say that most people at thirty-nine don't need to do these tests. I'm in a unique position where I have a very strong family history of cardiovascular disease. So my dad's dad also had a heart attack in his forties. So genetics are not on my side when it comes to this disease. Also, does the scanning really inform the treatment a lot? For me, it does. Because I am already living a healthy lifestyle and I haven't had an event. If you were to scan me and see a significant amount of plaque, then there would be a strong case to say immediately get on medications, lipid lowering medications and get that down to a level where you're not seeing atherosclerosis or progression of atherosclerosis and perhaps see some regression. But you're not going to take someone like me who's otherwise healthy, healthy lifestyle, has never had an event and just say start medications.
Dr Rupy: Yeah, yeah. I think there's there's two kind of schools of thought here and we might have different opinions on the degree of investigations and how aggressive we should be with screening. During my experience in the NHS, there is a tendency to under investigate and we kick things down the road until quite late down in the disease state. And I think that needs to be course corrected. Over here in the States, we probably have the opposite problem, which is where we do a lot of investigations under this sort of like halo of what's what gets measured gets managed. Whereas actually, I think you really need to think about if you do come up with something, how are you going to manage it and almost have the treatment protocol in mind before you do the investigation. So I agree, I think in your case, it's probably warranted, but there is a burgeoning opinion that most of us in our, I mean, I'm in my forties now and I'm already thinking about doing cardiovascular screening. There is a burgeoning idea that we should actually be investigating earlier, which can motivate people, perhaps not to get on pharmacotherapy, but to really take consideration of the diet.
Simon: Yeah, and I agree with that. I think where I was coming was that it's access to this stuff is an issue for a lot of people from a pricing point of view. So I realise like I'm in a privileged position. And and so someone can still get pretty good treatment. For example, if someone went in to see their doctor and their cholesterol was at one hundred and thirty and they had a family history of cardiovascular disease and they were not prepared to make any lifestyle changes. That's different to me in terms of the medicine conversation because I was presenting as a thirty-nine year old now with an LDL cholesterol at like seventy-five typically. So it's already very low. And what I wanted to know was, am I going to get any extra benefit from really getting my LDL cholesterol down? And most cardiologists you walk in and ask that question, they're like, well, I don't know. I don't see patients like you. Right? You're an otherwise healthy guy coming in with no symptoms at all, strong genetic history, but you've made these massive lifestyle changes. I don't know what to do with you.
Dr Rupy: Yeah, yeah. You're in the real grey area there. And just for the listener, that that cholesterol that you mentioned there is like sub two for LDL C in millimoles per litre. So that's super low.
Simon: Yeah. So I've been able to achieve that with the dietary changes. So my question was this. Okay, I had, let's call it twenty-seven, twenty-eight years of high cholesterol because I really hadn't made the full shift in my diet until late twenties. At high at sort of one hundred and thirty, right? At a level where we do know that people are laying down plaque, usually pretty considerable rate of plaque progression. And we know from the PESA study, which was an amazing study that looked at a healthy population of people who did not have any risk factors for cardiovascular disease and was looking at the amount of plaque in their arteries. We know that at least fifty percent of people who have quote unquote normal LDL cholesterol, so what your doctor would say is normal. At least fifty percent of those people in their forties, so this is a cohort of people in their forties, have subclinical atherosclerosis. So then you look at someone like me who had, you know, better part of three decades, very high cholesterol, made some lifestyle shifts and had ten years of lower cholesterol. What's happening inside the artery? And that was the rationale to go and get the scans done. The cardiologist that I'd spoke, some of which have been on my show, and you alluded to it. I think I think maybe even now I've had the most extensive discussions on cardiovascular disease prevention with lipidologists out there. I think I might just be beating Peter Attia on that now. I've had like almost twenty hours between, you know, Thomas Dayspring and Dan Sofer and Lawrence Sperling and all these guys. But the decision making process was, well, let's have a look in there, see what we find, and then we can determine where you are at in terms of risk of an event. And even then, most risk calculators are like ten year risk. But for someone who's aged in their thirties, you really want like a thirty year risk calculation, right? So
Dr Rupy: And you alluded to this already, sorry, with your exposure to cholesterol, perhaps rewind for folks and explain why that exposure to high cholesterol is so important in the atherosclerosis process.
Simon: Yeah. It's it's cumulative. So the amount of plaque that you have laid down in your artery wall is a cumulative process. There is a cumulative burden of LDL cholesterol or more specifically atherogenic particles, which is just a fancy way of saying lipoproteins that can kind of crash into the artery wall and get stuck and build up, which includes LDL and most of them are LDL, which is why we've spoken about LDL cholesterol for so long. That's a whole other rabbit hole. I'm not sure whether we want to go into that. But it's a little bit similar to pack years for smoking. So your risk of developing lung cancer is like how many packs per day were you smoking for how many years and that determines your overall risk of developing lung cancer. It's a similar thing here. So I had this high burden over thirty years. I reduced that burden a little bit over the last decade. But you would expect that there probably was some damage done in the artery and that's what a CT angiogram in particular because it shows the soft plaque is is good at kind of elucidating in a specific way. So you can see not only whether you have soft plaque, but exactly how much and what arteries it's affecting.
Dr Rupy: Great. Okay. So we understand the exposure to cholesterol. We understand that it increases your probability of having this disease process. What did your results show?
Simon: Yeah, so I had some what you would describe as subclinical atherosclerosis. Subclinical meaning that you're not symptomatic. And many people walking around through society would have this. There would be people that have a lot of subclinical plaque and are completely unaware of it. The amount was very, very small. So total was like sixty-one millimetres cubed. Which is considered very, very minor, but as someone that wants to live to ninety or one hundred in good health, I want to make sure that's not progressing at a fast rate. So it's at this point, it's difficult to understand what that rate of progression looks like. Because it could be that since I made my dietary changes, and you know how I eat, it's very much in line with the way that you recommend. You would think based on the literature, based on like the types of fats I'm eating, the fact that I eat high fibre, I have a lot of these anti-inflammatory compounds, phytochemicals, you would think that my rate of progression has slowed down since my late twenties or early thirties. That would be the hypothesis and is in fact what most cardiologists I'm dealing with are saying. However, I'm also approaching this from an academic and kind of self-interest perspective. And I'm curious to understand how my current lifestyle, you know, maybe affecting that rate of plaque progression and comparing it to some of those other studies that we have that look at, okay, healthy people, people with diabetes, people on a ketogenic diet, and where do I land?
Dr Rupy: Speaking really honestly now, I'm going to push you on this. I know you're a man of science and I know that you are going to be led by the evidence based decision making. And whilst you say that you're really intrigued by the hypothesis and you're interested in the impact of your lifestyle, is there any degree of trepidation about starting lipid lowering therapy despite the advice from preventative cardiologists? I.e. the medications themselves?
Simon: I don't think so because I understand that there are some adverse effects that people experience that are real, but the risk of those is quite minor, at least in the short term from the studies that have looked at that. And there are so many options today with lipid lowering that I think I could navigate around that. So if a low dose statin wasn't working, there's bempedoic acid now, there's PCSK9 inhibitors, there's obviously ezetimibe. So there's different ways of getting your LDL cholesterol to goal that people didn't have available to them twenty, thirty, forty years ago. So I don't think I have any real trepidation towards it. I think I think that the evidence is really, really clear from multiple angles, whether it's observational, genetic, randomised controlled trials, that lower for longer is better, as you said, particularly for someone that, you know, I'm thirty-nine and clearly have a genetic predisposition here. So I do think that lipid lowering is going to be a part of my future and optimising so that I die with cardiovascular atherosclerosis, but not because of it. And that's what Thomas Dayspring always says and that most people are going to get to their fifties, sixties, seventies with some atherosclerosis. The question is, are you going to die because of it or with it? And so I think that's something that I will need to manage in the kind of second half of my life if I'm trying to optimise for for healthspan. But at the same time, given my interest in nutrition and healthy lifestyle, I have this interesting kind of understanding, you know, how much has the changes I've made, how much are they actually influencing this picture?
Dr Rupy: Yeah, yeah, yeah. And important side note, I'm assuming you've tested your LP little A and you're negative for that.
Simon: LP little A is like negligible, almost zero.
Dr Rupy: Okay. Yeah, yeah.
Simon: Fortunately.
Dr Rupy: It's really, really interesting this because I if I was in your situation, and this is not advice, I would probably be interested in a couple of things. A, trying to figure out what my rate of progression is. If not purely out of interest, purely out of speculation that my diet is actually halting or at least reducing the rate of progression of plaque. And the other thing that I'd like to think about are additions to my diet, whether that be supplemental or food to reduce my cholesterol even further. You mentioned it earlier, but if we get our LDL C down to really, really low levels, sub eighty or sub fifty, there is at least the idea or the theory that it would halt atherosclerosis in order to protect you in its entirety. Is that something that you would be aiming to do as well or
Simon: Yeah, and if I could get there with supplementation and lifestyle, that would be the ideal scenario. But I'm not sure that many of us can get below fifty milligrams per decilitre with just changes to nutrition. Like I can be completely honest, when I'm totally on top of my diet and you know, putting psyllium husk in my smoothie and making sure I'm not overdoing it on like coconut yoghurt and these these products that can contain a lot of saturated fat. My the lowest I've ever seen my LDL is like low seventies.
Dr Rupy: Which is very, very low.
Simon: And I do know that there are some people out there that can get lower, but genes play a role in how fatty acids, in particular, how fatty acids influence cholesterol levels and cholesterol clearance in the in the liver. So maybe I can get a little further, but I'm not sure I can get below fifty, which seems to be a threshold where you start to see kind of micro regression and some shrinkage of the plaque, which would be the goal for me. It's to to reduce events long term, I want to make sure the plaque is stable and I want to try and get it to regress a little bit. And so I think the the thought process at least from my end here is I'll I think I will be kept up at night if I don't know the rate of plaque progression. I'll always wonder.
Dr Rupy: You'll always wonder. Yeah, yeah, yeah. I'd be in a very similar situation actually. What what other additions are you adding to your lifestyle? So assuming you are going to make that decision, right, where you're going to retest but not take any lipid lowering therapy in the immediate term. You mentioned psyllium husk. Are there any other things that you're looking at?
Simon: I'm interested in in kind of I already supplement with coenzyme Q10. I am interested in and I'm going to do an episode on the research behind Kyolic garlic extract. Maybe niacin will be in that conversation, phytosterols will be part of that conversation. I already know there's no outcome evidence on phytosterols though. So we know they lower cholesterol, but whether they lower events is unclear. K2 will be part of that conversation. And there's a few other ones.
Dr Rupy: Yeah. Because there's the other idea that even if you were to get your cholesterol low with supplementation, let's say, because I've got a family member who similar story was having an ECG, standard ECG for a life insurance assessment and found some segments on the ECG that were suggestive of mild ischemia. This happens a lot when you do routine ECGs. I thought it was a nothing burger. Anyway, long story short, goes for an exercise ECG, still shows some issues, progresses to having a full suite of different investigations including a CT angio. Turns out there is a massive stenosis in his LAD, which is colloquially known as the widow maker. Has a stenting procedure. Prior to this,
Simon: No symptoms.
Dr Rupy: No symptoms. No chest pain, exercises, eats a healthy diet, does everything right, not an alcohol, no smoking, no real strong family history apart from having Indian genes, which is a risk factor for cardio metabolic disease. So I'm a lot more pragmatic when it comes to early investigation these days from not only that one of one experience, but also from my anecdotes during my GP days in the NHS as well and just seeing just how rampant it was. This individual doesn't like the idea of going on pharmaceuticals for whatever reason. So my suggestion is to put them on a suite of different supplements and just test or retest and reinvestigate aggressively their LDL C and apolipoprotein B levels to make sure it's at least going in the right direction. They were at relatively high levels. So if I was to convert that for an American audience, it would probably be about one hundred and twenty. And now we've got it sub eighty. And it's through a combination of things that you were saying, psyllium husk, flax, a relatively low calorie diet which is maintained in protein, garlic extract, not phytosterols, but red yeast rice because it's got monacolin K and I think it works in a very similar way to statins. Now, the cholesterol is really low, which his cardiologist is happy with, but there are some extra unintended benefits of statins as well on inflammation levels that might explain some of the outcome data that we have for cardiovascular patients. And so even though the numbers might look good, there is this sort of thing at the back of my head of it's like, okay, but the statins could be having an additive effect on more than just the cholesterol number.
Simon: And changing the plaque morphology. So statins can lead to a kind of conversion of soft plaque, which is often considered more vulnerable to calcified or harder, more stable plaque. And the other thing I would just add in that case study, and I think we all need to consider this is you were talking about the LAD artery in that in that case study. Usually what you pick up on a coronary artery scan is also representative of what's going on in the carotid arteries, which can lead to a stroke. So I want to emphasise that even though I'm entertaining this idea of not doing medical therapy for eight months from a purely academic interest, self-interest point of view, I do agree with lower, better for longer. And if I had a significant amount of plaque, I would be doing whatever I could to get regression, which is getting below fifty. And I would be thinking not just about my heart, I'd be thinking about the carotid arteries as well.
Dr Rupy: Yeah. It's a really important point and I think unfortunately this gets lost in the keto discussion. I know you had Nick on your podcast talking about this and I had Nick on mine and it was just before this paper came out. I haven't done a full deep dive into the paper. I've just heard the analysis from other folks, but needless to say, there is very strong plaque progression with astronomically high levels of cholesterol. And I think within this conversation, because people experience the benefits and I don't want to deny people actually having benefits and maybe even improving their symptoms with a ketogenic diet, which is very high fat, there is a trade off there that we all need to be reflective of. And I think the fact that you're being so open about your decision making is important because we are weighing up trade offs and I think sometimes people put their head in the sand without really wanting to dive into the trade offs that they are engaging in.
Simon: Yeah. And you know, energy balance matters a lot. And so for many people when they jump on a ketogenic diet, this can be one of the reasons why they gravitate towards and have success is that they lose a lot of weight. And that does lead to a lot of improvements of certain risk factors. Blood glucose control improves, blood pressure improves. Like these are significant risk factors. But often apoB and LDL cholesterol goes in an unfavourable direction. And so what I'd like to to add to this space is, I think you can have both. I think you can optimise all of these. It doesn't have to be an either or. I think there's a way to optimise both. And I even think that you can do it on a ketogenic diet. It just means thinking a little differently about the types of fats you're eating or more specifically the foods that you're eating that contain fats. And in doing so, you shift the balance as to what those types of fats look like and you get a more favourable blood lipid profile. And so I don't think this is an either or. It's not I have to ditch keto diet. It's not a, okay, I'm doing keto and therefore I have a high apoB, astronomical and I'm okay with that. I think you can have it all. Despite the dogmatism that kind of exists online.
Dr Rupy: Let's talk about fats because that's an interesting perspective around ketogenic diets and if you shift your fat type to one that is more favourable for cardiovascular disease, it's your view that it can not just mitigate against cardiovascular disease, but it can also be favourable. Is that my reading?
Simon: I think it's fair to say that you can you can have a favourable blood lipid profile on a well planned, thoughtful ketogenic diet. But that ketogenic diet is not necessarily going to look like the ketogenic diet that might first pop into everyone's head. It's going to be more of a imagine a Mediterranean diet where you have a bias for the foods that contain fat, fatty fish and olive oil, some dairy foods in there, particularly lower fat dairy, and having less calories coming from some of the carbohydrate rich foods in the in the Mediterranean diet, which might be your whole grains, for example. And that then becomes a ketogenic diet that is relatively low in saturated fats, is really rich in mono unsaturated and poly unsaturated fats, which we know are heart healthy. It's you know, high in fibre, it's anti-inflammatory and can still be low carb. So I think that's where this conversation around the ketogenic diet, particularly in light of this more recent study. And I know now the authors are kind of going back into it and are suggesting that clearly they're not happy with the clearly software.
Dr Rupy: Oh, really? Is that the explanation?
Simon: Well, it seems that the rate of they're acknowledging that the rate of plaque progression was high, but are now wanting to reanalyse it using a different software.
Dr Rupy: But they chose the software, right?
Simon: They chose the software and it is accepted as a validated, reliable software to kind of look inside someone's arteries and determine how much plaque they have and whether that plaque is soft or calcified. But nonetheless, we'll see how that kind of story pans out, but it does seem to me at face value they're trying to kind of bend the data to fit their hypothesis as opposed to kind of changing their views based on how the data presented. So we'll see how that unfolds. But I think there's enough research outside of all of that looking at particularly how do different fatty acids, whether it's saturated or mono unsaturated or poly unsaturated, how do they affect blood lipids and how do they affect blood glucose control and insulin sensitivity?
Dr Rupy: Yeah. Let's let's start with saturated fats actually, because I know we've alluded to the fact that saturated fats are unfavourable for cardiovascular disease. But within this sort of concept, and we can bring this back to food because I think that'll be really interesting for the listener because when we start talking about double bonds, single bonds, all that kind of stuff, people just glaze over. And actually, when you think about any type of fat, it's going to be a mixture of all these different types of fats. And when we say this is a saturated fat, what we're talking about is this is largely made up of saturated fats and certain types of saturated fats that are not great for your health. But it still does have some of the monos and some of the polys in, but it's just one that you want to avoid or at least moderate. So within the sort of picture of saturated fats given that caveat, what kind of foods are we talking about?
Simon: Yeah. And I might even go one step higher in that the we use broad brush strokes in guidelines for a reason. Keeps it simple. And the guidelines basically say to consume less than ten percent of total calories from saturated fat. And that's a very simple kind of overarching recommendation. But it does miss out on some of the details and you just alluded to some of them in that saturated fat is not one thing, there are many different types and they affect our physiology in different ways. And that is why you can't just look at a food and say it contains saturated fat, therefore it does this. And it's this context of like what type of saturated fat, what dose, compared to what. So if someone's not eating it, what are they eating instead? Are they eating French fries or are they eating legumes? In what food? So like the food matrix. In what dietary pattern is it surrounded with fibre? And for who? Whose genetics are we talking about? Right? And it's not until you kind of appreciate all those different layers of nuance that the conflicting ideas or discrepancies or studies that seem conflicting, it's not until that you realise they're not actually conflicting. They're fully explainable. Because it can feel like, oh, science is all over the place. Right? Which is a bit of a paralysing kind of place to find yourself in because you're like, no one's got it worked out.
Dr Rupy: For sure. Yeah, yeah, which is why there's a lot of backlash I think against dietary guidelines in general because of the oversimplification, but like you said, it's necessary.
Simon: It's necessary because if you led with what I'm about to go into. You know, most people would just wouldn't read it. And it would be so boring that, you know, it's not funny and then people just wouldn't make any changes. So the general heuristic of eating less saturated fat is a good one, although there is context and subtleties. So generally, this idea of eating less fatty cuts of meat, like red meat and even white meat that are fatty and less butter, these are great, great recommendations. Why? Because the saturated fats that are in those foods, we know in particular have a very significant effect on your blood cholesterol. They basically, I was thinking about this the other night, we talk a lot about like insulin resistance. I think we could talk about cholesterol resistance. Because these saturated fats that are in red meat and in chicken and in butter, they make the liver resistant to LDL cholesterol. Because the liver, one of the main jobs of the liver is to pull LDL, low density lipoproteins out of circulation back into the liver. And the type of fat we eat really affects how well it does that. When you're eating a lot of these saturated fats in those foods I mentioned, they down regulate the LDL receptor on the liver. They basically make the liver resistant to LDL cholesterol. And so what happens? LDL cholesterol, low density lipoproteins start to build up in the circulation. And we know that as the concentration goes up above those thresholds we were talking about earlier, that's when we start to see them going into the artery wall and getting retained and kind of kickstarting that cascade of inflammation and atherosclerosis. So when the guidelines say to eat less of those foods and more of foods that are rich in particularly polyunsaturated fats, because polyunsaturated fats do the opposite. They recruit more LDL receptors. They make the liver LDL, low density lipoprotein sensitive.
Dr Rupy: I love this analogy. This is great.
Simon: So when you're eating more fatty fish, and we spoke about this earlier when you were on my show, whether it's salmon or mackerel or anchovies or sardines, they contain a lot of polyunsaturated fats. Or you're eating more tofu or tempeh or nuts and seeds. And to a degree oils like olive oil and avocado oil, which are very mono unsaturated fat rich, it essentially is a signal to the liver, let's up regulate LDL receptors. And it then does a better job at clearing these LDLs out of circulation. So the best swap you can make from an LDL lowering point of view is swapping those particular foods, so fatty cuts of meat and butter for fatty fish, for tofu, for tempeh, for nuts and seeds. That's the that'll be the swap that has the greatest magnitude for LDL lowering. That got lost in the 1980 guidelines. Because it came out, the research was there and it became a low fat message. But what I'm saying is not a low fat message. It's a better fat message. So if you're cutting out red meat, white meat and butter, but instead of eating those foods I just listed, you decide to have more white flour, ultra processed foods high in refined sugars, what happens? Cardio metabolic disease probably increases based on the research. You know, it could be a lateral sideways move, but it's definitely not a superior. You're not you're not shifting risk factors in a favourable direction. Because while you might have some effect on lowering LDL, you're going to have these downstream negative effects on triglycerides and blood glucose control. So the shift that actually reduces your risk of having a heart attack most is swapping those saturated fats for polyunsaturated fats. And I've explained that at a very high kind of level because there are a myriad of other saturated fats. And the reason I left dairy out of there is because dairy kind of sits in the middle.
Dr Rupy: Yeah, it does, doesn't it?
Simon: And and butter is dairy, so butter is an exception in the refining process, it kind of liberates the saturated fats, frees them up of the food matrix. And so they have this more significant effect on LDL cholesterol and the receptors. Whereas fermented dairy or milk, their fats are within a milk fat globule and the way they're digested and affect LDL cholesterol is very different. So I think there is some potential LDL cholesterol lowering benefit moving from dairy to polyunsaturated fats, particularly from plant based foods, but it's much lower. And so I don't really think that's where the focus kind of should be for most people.
Dr Rupy: Yeah. So let's bring this back to your scenario and perhaps one of the listeners who might have a high cholesterol or may have even had an investigation that shows that they've got some plaque, right? They're going to the supermarket with you and you're primarily going to tell them what fats you're going to be consuming this week. And you can make this, you know, a little bit animal based as well as largely focused on plant based. So what kind of swaps are we making as we navigate the supermarket with you?
Simon: So start very, very simple. If if they're eating red and white meat, we're going for leaner cuts. Okay. But I am going to try and reduce the number of servings of those because they still contain more saturated fat even in the leaner version compared to some of the foods that we're going to swap them for. So number one is if we are eating red or white meat, we're getting leaner cuts. And we're going to try and reduce some of those serves and add fatty fish, more fatty fish, so two or three times a week if it's someone that's eating animal protein. And we're going to lean into some of these foods that people might not be eating, like tempeh, tofu and lentils. And I work with a lot of people that are eating mixed diets and often it's it's not a jump where they're, let's say their favourite dinner is a mince bolognese. It's not like overnight they're going to a lentil bolognese. So let's let's get the the beef bolognese that you're buying, buy the leanest type. And then let's take fifty percent of that and let's add in lentils. Mix it all up, you barely even know that it's in there, but you've really changed the overall profile of that meal from a fat and from a protein perspective and from fibre. We haven't even spoken about fibre. But fibre also has an effect on cholesterol. We can go into that if you want, but you know, that's just one example. We're going to add nuts and seeds into their diet and that can be toppings on meals like you talk about. It can be adding them into smoothies, it can be a small handful as a snack just to increase the amount of those mono and polyunsaturated fats that they're getting in their diet throughout the day, which are genuinely, and this is the point I want to get, they're not just better than saturated fat. They're inherently heart healthy. Key point. So we're finding ways to work those in either within meals, on top of or put it into a smoothie or just as a healthy snack themselves. And then when it comes to cooking oil, because that's another big one, we're going to either completely remove butter or just reduce it significantly and cook with something like olive oil. You know, another really simple swap that I think most people are pretty okay with.
Dr Rupy: Yeah, yeah. I think most people can agree that olive oil is a great ingredient to use across the board. You can cook with it, you can dress with it, you know, try and source the best quality you can find with high polyphenols. But I think within this, I mean, I had this conversation with Dr Kevin Mackie and I was trying to push him on saturated fat within meat. And even though red meat isn't the biggest contributor of saturated fat to the diet, it's usually mixed goods. So pizzas and cookies and basically ultra processed foods, it's still contributing some saturated fat. And if there is an opportunity to reduce it as much as possible for those lipid lowering and cardiovascular protective effects, it stands to reason that you'd want to at least go for the leaner cuts, if not moving transitioning completely to a plant based diet. But there's disagreement in that.
Simon: Well, I think this advice that I'm giving here is presuming that someone's already approaching their diet with a whole food perspective because I would agree like the first thing then if I was in the grocery store would be just moving away from the ultra processed foods because they do contain a lot of saturated fat as well. But I mean, there is research looking at, there's a study by Bergeron et al, it's only three or four years ago, even looking at lean cuts of meat compared to plant protein. And even if you match saturated fat in those foods, you still get a significant reduction in apoB from the plant based foods. And it could be that dietary cholesterol has a little bit of an effect, not as much as saturated fat, but does have a little bit of an effect on LDL cholesterol and apoB. And also, because none of this happens in a vacuum, as as someone is is reducing their meat consumption and increasing like tempeh or tofu or lentils, it's not just the change in the fat, they also get the added fibre, which is affecting cholesterol. So pragmatically, how would I approach this with someone? Well, you had a blood test. Where was your cholesterol at? Where do you want to get it to? Let's make some changes that you can adhere to, that are sustainable, that you enjoy. Because it doesn't matter if you do this for a week or two. Right? And then, you know, three, six months down the path, the track, retest. Did you get because the the magnitude of effect of those changes will be affected by your genes as well, how well you respond. Where did those changes leave you? Okay. Do you want to, are you in a position now to make further changes? And then that person might say, okay, well, now I'm actually going to remove some of that lean meat and consume tofu or tempeh. So I think there's an individualisation that's required. I agree with Kevin Mackie in that can red meat be part of a healthy diet? Yes. The volume tends the amount, the dose seems to matter. Right? So in in studies like Asian cultures where there's not a lot of red meat consumption overall and you compare high to low, high and low are both low in like a country like the US. So you're like comparing thirty grams a day to seventy and you see no effect. Then you come to an American cohort and you compare like one hundred and fifty to fifty and you do see an effect on cancer and cardiovascular disease. So the dose matters, but if you're down at like, you know, fifty grams a day kind of thing, I don't see any data that that convinces me that that is a problem. Particularly if someone's doing their blood work and their apoB and and blood glucose and all of this looks like it's in order, it's in range. So that's my pragmatic approach to that.
Dr Rupy: I agree. And I think, you know, within that, there is the degree of self-experimentation that you're alluding to by just doing your own blood work and titrating the amount of animal based products you want in your diet up or down depending on that. And I think there's like a safe zone around, you know, fifty grams a day, looking at those studies that you can start off with safely and then reduce as needed or maintain if you're happy with the state of your cholesterol. And then, as I mentioned earlier, the what's the dietary pattern that someone's consuming those foods within? Probably someone can get away with a little more red meat if they have a higher fibre intake and fruit and veg intake than someone who's just got red meat and ultra processed foods. Because the fibre is counteracting some of the effect of those saturated fats are having. And we know that that largely occurs during digestion where fibre is kind of binding up bile. And it clear bile is very rich in cholesterol. You know, it's pumped into the intestine through from the liver. And as you excrete it from your body, as fibre kind of binds it up and excretes it, the liver is left saying, hey, we didn't reabsorb much bile, we need more. And so what does it do? Well, it comes back to what we talked about earlier. It says, let's recruit more LDL receptors. All of a sudden the liver becomes insulin, sorry, the liver becomes LDL sensitive. So fibre, just like polyunsaturated fats, I'm finishing the story here, and mono unsaturated fats, make your liver low density lipoprotein LDL sensitive.
Dr Rupy: Yeah, yeah. I love that analogy, man. Honestly, I haven't thought about cholesterol resistance in that way. And I think, you know, if people lean on their understanding of insulin resistance, it makes total sense. Particularly when you look at those mechanisms. And I guess, there are two things that I want to touch on before we we sort of wrap up fats unless there's anything else that you wanted to to mention within the fat conversation.
Simon: I think we should definitely put a pin in why cholesterol is in lipoproteins and if low cholesterol is a problem.
Dr Rupy: Yes, absolutely. We'll definitely talk about that because I think you alluded to an earlier point that if people are artificially, and I say artificially in inverted brackets here, using pharmaceuticals to reduce cholesterol to very, very low levels that aren't generally humanly possible with diet and lifestyle despite pristine intentions, there is a worry that you are reducing endogenous cholesterol production within the cells, but you can go into that. Eggs. Yeah. Eggs. Do these factor into a heart healthy shopping basket for you or are these a no no?
Simon: What dose? Compared to what? And for who? And the for who on eggs is a big one. So I think largely at a dose that that most people might consume eggs, I think for most people, they're better than a lot of the alternatives. I'm not sure that they're better than the heartiest of hearty oatmeals or porridge. I think it's hard to beat that. But that's not the alternative for most people. And so it's true that eggs contain a lot of dietary cholesterol. They contain a little bit of saturated fat, particularly if you were to compare them to something like tofu, which could be an alternative. But the absorption of dietary cholesterol is complex and pretty inefficient. So about one in five people are cholesterol hyper absorbers. They absorb a lot of the cholesterol in their food. So from things like eggs and meat. And this has basically the simplest way of understanding this is when you consume something that contains cholesterol like eggs, it makes its way down through the stomach into the small intestine. And enterocytes, which are the cells in our small intestine, they have these kind of gates. There's a gate that allows cholesterol in, dietary cholesterol, and there's a gate that effluxes or pushes it out. I'm not going to go into the names because they're really long and escaping me. Okay, just there's a gate for in and there's a gate for out. And that's that then is in the space of the enterocyte and that's before it get this cholesterol gets pumped out in lipoproteins into the lymphatic system then into circulation. Depending on how your gates are functioning will dictate how much of that dietary cholesterol ends up going into the lymphatics in lipoproteins. Some people for that efflux transporter, they have a genetic mutation and so that gate is kind of shut. So they get the influx from the egg and they're not very good at pumping it out, which would be excreted if you could pump it out. And so what happens is the enterocyte ends up with a lot of dietary cholesterol to package into lipoproteins and push into the lymphatic system then into the blood. And it ends up being going down this this chain where VLDL, IDL and low density lipoproteins start to accumulate. So for that person, they're a hyper absorber. And we can there is a way to test to determine what you are and we can go into that.
Dr Rupy: Yeah, I was going to ask if there is a test.
Simon: You want to do that now?
Dr Rupy: Yeah, why not? Yeah.
Simon: Okay. So that's one in five people, so it's not a tiny number. And because this is a question I get all the time, like people get go to their doctor, get a high cholesterol and they're like, well, is it the eggs? And I'm like, it's not my first, it's not actually the first thing I'm looking at in your diet that I'm suspicious of. Really, it's the saturated fat foods we spoke about before, but for some people it is the eggs. And the way to test that is that those gates that I just mentioned, the influx and the efflux, they're they're a gate for any sterol, not just cholesterol, also phytosterols, plant sterols. So you can imagine if you just do a blood test and measure LDL cholesterol, you can't use that as a way of definitively saying, oh, you're absorbing too much dietary cholesterol. And the reason for that is the cholesterol that's in your blood is not just from what you've absorbed in your meal, the liver is also producing cholesterol. Right? So you can't tell where it's come from. Does that make sense? But our body doesn't make phytosterols. The only way that phytosterols get into circulation is through these gates. It influxes in the same gate and it should be pushed out, effluxed through the other gate. If you have a genetic mutation affecting that gate that effluxes, your phytosterols will be high. So you can do a blood test to test for sitosterol and campesterol. It's available in most countries. You can just search phytosterol lab test. And if those are really high, that's telling you that you have you're one of those one in five, twenty percent of the population that have a genetic mutation that leaves you as a cholesterol hyper absorber. You're the type of person that reducing eggs in your diet will make a big difference to your LDL cholesterol. For everyone else, reducing eggs might lower their LDL cholesterol by like ten percent, not a huge amount compared to saturated fats, which make much more of a difference.
Dr Rupy: That's epic. I thought you were going to say it was a genetic snip test that you could do online and then it would just tell you.
Simon: That would be nice.
Dr Rupy: Yeah, if there's some geneticists listening. But that's quite an elegant test to determine and it yeah, I love the way you talked about the gate and stuff. That's a really good analogy that's going to stick with people's heads. On the subject of cholesterol, let's talk about really lowering cholesterol to halt atherogenesis, like essentially the what you were talking about right at the start here. What are the complaints or worries that people might have with that given how important cholesterol is to health?
Simon: I think this is actually a really interesting and logical question or idea for someone to have because, you know, I mean, you know more than I do that cholesterol is important for the production of sex hormones. It's it plays an important role in the health of the cell and the cell membrane. And it's vital, right? The confusion is around what cholesterol is doing in our blood in the first place and where cholesterol comes from. So when cells are producing sex hormones, where is the cholesterol coming from that they're using for that process? Or the cholesterol that's in the cell membrane, where is that coming from? My understanding of this in my twenties, even in my early thirties, was that lipoproteins from the liver are packing in triglycerides and packing in cholesterol because these are not soluble in water, they're hydrophobic. Lipids are water fearing. So the human body had to invent a way to get them into the blood, different to glucose. Glucose is water soluble, just freely flows, perfect. Whereas we had to find a way to get particularly triglycerides, this energy source to use or to store, to transport it through the bloodstream. So we attach it to proteins, these apolipoproteins, which makes it water soluble. And my understanding was that the liver is pumping out these lipoproteins to get triglycerides to cells that need them for energy or to store energy, but also to get cholesterol to cells. That's not what's happening. The cholesterol that is in the lipoproteins really just serves a structural role where it allows that lipoprotein to be spherical. And in creating a sphere, you can pack in more triglycerides. So the lipoprotein transport system is all about getting triglycerides and phospholipids out to cells for energy. It's LDL cholesterol is not taking cholesterol out to cells. All cells produce all the cholesterol that they need. So that was my learning. And so when you lower, when we talk about lowering cholesterol, we're talking about lowering it in plasma, in the blood. All the cells throughout your body still have everything that they need to produce their own cholesterol that's required within that cell. Right? And many studies have shown that when you do artificially through medicine, like you said, lower LDL cholesterol down to really low levels, even like twenty milligrams per decilitre, which no one's saying that we need to go that low. But even then, people are still producing healthy amounts of sex hormones. So only in very, very extreme, you know, rare circumstances, the adrenals and the gonads, the testes, will require some excess cholesterol and they get it from HDL, not from low density lipoproteins. And that's a very, very rare. So we can kind of be reassured that if you lower your cholesterol through your diet or through medicine, we're talking about lowering it in the in the blood, which is a different compartment. All the cells through your body will still be producing the cholesterol that they need to make vitamin D for the cell membrane and all these different really important functions.
Dr Rupy: Absolutely. Yeah. So it's a really important distinction there. So when we're saying lipid lowering, we're not lowering cholesterol everywhere in the body and certainly not in the cells and we're not disrupting any cell's ability to produce their own cholesterol. It's purely in the plasma such that we reduce the probability of that cholesterol containing molecule bumping into an arterial wall where it can get lodged and then start the inflammatory process of atherosclerosis. So I think that's really well explained. It's a really good distinction to make actually because I think that's probably one of the fears around taking a lipid lowering therapy about the impact on their brain because they've heard like brain is, you know, largely cholesterol based, but you know, we get the brain cells make their own cholesterol and the fact that it's important for steroid hormones as well. So yeah, it's a really, really important distinction.
Simon: And these are these are genuinely questions I had myself.
Dr Rupy: Oh yeah, absolutely. That was one of my probably a big thing for me before I did my masters in nutrition was this misunderstanding of cholesterol. And I think most doctors, no judgment, we are not taught cholesterol metabolism well. And it goes way over our head. And I think the simple analogies you've just used here are really, really important and they're they're educational for not just the general population, but also for for people in in in medical positions as well.
Simon: I hope so. There's a there's a paper as well. I'll give you for the show notes by Peter Toth, who's really one of the leading experts in this space and can explain things much better than I can. So if there's if there is like doctors listening or students that are training and they want to deep dive, go into that paper for sure.
Dr Rupy: Absolutely. Yeah, yeah. Simon, I think we did it, man. This is this has been awesome. Like, thank you so much for sharing your story. I can't wait to, I mean, from a purely sort of voyeuristic perspective and seeing like what's going to happen in terms of your decision around your next investigations and whether you're going to take lipid lowering therapy or not. I just appreciate the fact that you're being super open about it because I think it's helping a lot of people navigate very similar decisions. So, yeah, and you're obviously your work and your podcast is phenomenal, mate.
Simon: Thank you, Rupy. Means a lot. It's a pleasure to be with you guys.
