Dr Rupy: Today we are going to be talking about cholesterol, heart health and cholesterol lowering dietary measures that you can use today to improve your risk of heart disease and lower the risk that you're ever going to have cardiovascular disease. We're going to specifically talk about what cholesterol is and why it's important. We're going to talk about how we measure cholesterol and what blood markers are associated with an increased risk of cardiovascular disease. The dietary patterns, ingredients and specific functional ingredients that may lower cholesterol and build you a healthier lifestyle around lowering heart disease. And to save you the hassle of listening throughout the episode and listening to the entire podcast episode, I'm going to start with a summary of all my suggestions, right? Start off, number one, replace meat with plant-based proteins. Number two, try a portfolio diet. I'm going to explain what the reasoning is behind all these suggestions as we go along and I'll talk to you a bit about what a portfolio diet is. Eat more plant fats, number three. And yes, I said more fat. And I'll talk to you specifically about why the type of fat is so important and it's not just as simple as monounsaturated fats versus saturated fats. Eat more fruit and vegetables, one of the reasons, I mean, something that kind of goes without saying, but it is amazing what it can do for cardiovascular risk. Eat legumes, number five, and specifically 100 grams per day, which is a specific dose, I know, but that's been shown in some large studies. Eat whole nuts and seeds, exactly 28 grams, you don't have to eat exactly 28 grams, but I'll tell you a little bit why and what that generally refers to. The specific functional fibres, number six, that I've come across in some studies, including beta glucans, psyllium and some others. And I'll end off with my hot take on specific supplements, garlic, red yeast rice and eggs, whether you should have them or whether you should not have them in your diet. All right, I'm not going to go into depth when it comes to the cholesterol processing in your body, how it's generated. There are some incredible podcasts and incredible sources of information that I'll link to in the show notes. Pods from Dr Peter Attia, for example, or Thomas Dayspring, there's Ronald Krauss, there's James O'Keefe, some incredible preventative cardiologists that have done wonderful resources and created wonderful pods that go into depth about cholesterol processing. That's not the place for this podcast today. And I just want to start off with cardiovascular disease actually encompassing a lot of different things. It's many different heart conditions including high blood pressure, coronary artery disease, atherosclerosis that can occur in multiple different sites of the body, including the abdomen, your peripheries, your brain. There are many risk factors for these conditions, but we are specifically going to be talking and hopefully succinctly going to be talking about cholesterol and what you need to know about cholesterol. I as a doctor wish I had over an hour to talk to all my patients about cholesterol and cholesterol lowering activities and specifically dietary measures that you can take today. So hopefully this is going to be a great resource for me, plus I'm getting asked by lots of colleagues and friends who are reaching an age whereby they're looking at cholesterol, they might have been told that they've got high cholesterol, they might have had a kid or are planning on starting a family and they want to be around for as long as possible and avoid the number one killer that we flicks us today, particularly in the in the Western world, but also gaining traction in different areas of the globe as well. So, we're going to start off with what is cholesterol? Cholesterol is a waxy fat-like substance that is found in all cells of the body. It is so important, not a lot of people realise this, but it is produced endogenously, that is to say in the body, by all nucleated cells. We produce enough cholesterol to sustain life. The reason why we do that is because it's so important that without cholesterol there is no life. It is the precursor to our hormones, oestrogen and testosterone for example, many other hormones. It has a major role in cell wall structure or cell integrity. It has a role in bile acids. Without cholesterol, there is no life. But there's also no reason to consume cholesterol endogenously, as we'll talk about in a little bit as well. When doctors and even scientists use the terms bad and good cholesterol, it's a misnomer, since there is only one type of cholesterol. There are not different types of cholesterol. But there are different cholesterol carriers. And the reason why you need cholesterol carriers is because cholesterol is insoluble in water. That is to say it can't freely travel around the body to different sites where it's required. You need carriers. And these carriers are called lipoproteins. The ones you've probably heard of are LDLC and HDLC. That stands for low density lipoproteins and high density lipoproteins. On a standard lipid panel, so whether you go to a doctor in the NHS in the UK or America, your family physician, on a standard lipid panel, you'll tend to get LDLC, HDLC, total cholesterol and triglycerides. Using those numbers, we can calculate a number of different ratios or estimations of other particles. And I do want to acknowledge at this point that there is controversy over the accuracy and the utility of a standard lipid panel. For example, LDLC, unless it's directly measured, which is very costly and it takes a while, tends to only be directly measured in specific laboratories or for research purposes. It's generally calculated using a formula. The most common formula that is used is one that was actually created back in 1972, something called the Friedewald equation, and it can be quite inaccurate at very high or very low levels of cholesterol and very high and low levels of triglyceride. There are newer equations that give some degree of extra accuracy, but there is controversy over the accuracy of all these estimations. Those new equations have flaws and I've linked to an article from the American College of Cardiology in the show notes on the doctorskitchen.com if you want to read more about them. But let's just appreciate the fact that LDL particle number is more accurate. And there is something becoming more popular and more accurate than that, which is called apolipoprotein B, or also known as ApoB. You're probably hearing this on podcasts that have been coming out over the last five, six years. ApoB, to put it very simply, is a phospholipid that encompasses and engulfs all these atherogenic particles. Atherogenic particles are those particles specifically that can enter the arterial wall and start the process of inflammation with their cholesterol that they're carrying that leads to the downstream effect of atherosclerosis and blocked arteries that leads to strokes and heart attacks. These atherogenic particles include chylomicrons, IDLs, VLDLs and LDLs. These are different types of lipoproteins and we don't need to know about them for the purpose of today's podcast. If you do want to know about them, there are many other podcasts that go into detail about what an IDL is, a VLDL, where they're produced, etc, etc. But for the purposes of this podcast, we're not going to go into too much depth about those. Think of ApoB as a tag for all these atherogenic particles or atherogenic lipoproteins. If you're interested in learning more about them, I'll link to them in the show notes. But let's just assume that the only panel that we are able to deal with today is a standard panel, i.e. one that has LDLC and total cholesterol. Most clinics in the NHS don't do more than that unless you're going specifically to a lipidology clinic whereby they have access to even more wonderful tests that use NMR technology and all the all the other stuff. As per European society guidelines, you can use LDLC to estimate your risk of cardiovascular disease. The information conferred by apoprotein, apolipoprotein B or ApoB as I'm going to say from now on, is similar to that of calculated LDLC. So we're going to use it as a proxy, but I do acknowledge that it is not as accurate as some of the newer markers that are less readily available. With that in mind, and I'll put I'll link to a table with all the sort of calculations between milligrams and decilitre per decilitre, which is what you tend to get in the states, and millimoles per litre, which is tend tends to be what we use in in Europe and the UK. There are differences between them, so I'm going to try and remind myself to use percentage reductions rather than actual amounts and where I do, I'll I'll give a a caveat and um uh a quick sort of um calculation. The aim of the game of trying to reduce your risk of cardiovascular disease is to try and reduce LDLC as much as possible because as we age, it goes up and there is clear consensus and evidence to suggest that not only is there a relationship between this increase in LDLC and higher risk of cardiovascular disease, but there's also specifically a causal relationship, i.e. LDLC or more accurately, ApoB containing lipoproteins are causally related to atherosclerosis. So it's not just correlation, it is causation as well. The reason why we know this is beyond mechanistic studies, beyond observational studies, there are also genetic studies, ones that are called Mendelian randomization or use a Mendelian randomization technique to decipher whether there is a causal relationship. Again, I'm not going to go into too much detail, but for the premise of this podcast, we just need to agree that high LDLC and high total cholesterol and high amounts of ApoB is causally related to cardiovascular disease. So the aim of the game is trying to try and reduce it. And so all the advice that I'm going to give you today is going to be related, is going to be uh within that context. Okay. A quick segue because I know at this point, if you're of another persuasion, one that is influenced by people who suggest that ApoB containing lipoproteins or LDLC for whatever matter are not related. The reason why and the quick explanation is the more particles you have that are atherogenic, the more chances you have of those atherogenic particles that are able to get into the arterial lining and lodge into arterial walls are going to carry which are carrying those cholesterol particles that are uh exposed to oxidization can start the inflammatory process of atherosclerosis. This isn't to say that cholesterol is bad. I I just want to make sure that's very, very clear. Cholesterol is inherently not bad. Like I said at the top of this pod, it's very important for a number of different processes. I just want to quickly explain why I'm of the opinion that ApoB containing lipoproteins or LDLC are causally related. There is mechanistic evidence, etc, etc. But the reason why is because if you're increasing the number of ApoB containing lipoproteins or LDLC in circulation, you're increasing the chances that these particles that are carrying cholesterol can lodge into the arterial wall at many different sites and start the inflammatory process of atherosclerosis where cholesterol that they carry can become oxidized. There are some people that say, well, as long as you don't have high amounts of systemic inflammation, it doesn't matter. I think that whatever happens as we age, the inflammatory process is always going to be an upward curve. So you want to lower the chances of you having that inflammatory process starting by lowering the number of particles in circulation. Remember, this isn't to say that cholesterol is inherently bad. Like I've said at the top of this pod, it is a very, very important molecule on our body, but the dose of cholesterol and where we find cholesterol and limiting the the chances of you putting that cholesterol in the wrong places is of utmost importance and that needs to be balanced. And the certain carriers of cholesterol, namely LDLC and ApoB, need to be reduced in circulation. That's why you see that the causal and the observational effect that we've said. The reason why most people have high cholesterol is because of a defect in something called the LDL receptor, which reduces the rate of LDL removal from circulation. That's the main reason why we see raised LDLC uh levels. There are some dietary things that I'll go into that can uh change that, but mostly gene defects are the reason uh for why we see high amounts of cholesterol in in the blood as well. There are some dietary factors, but just be in the knowledge that dietary factors can have somewhat of an effect, but in many cases people need to take um pharmaceuticals to lower cholesterol significantly if needed be. The point of this podcast is to give you dietary and lifestyle measures to mitigate the amount that you might need of those pharmaceuticals or try and avoid them all together as well if we can. So, the gene defect doesn't necessarily mean you've got something called FH, which is called which is standing for familial hypercholesterolemia. There are many different variations of high cholesterol that are signalled by uh caused by different gene defects. It doesn't necessarily mean that you've got FH, which is quite a significant condition. That's pretty much all I'm going to say about the biochemistry of cholesterol. We're going to talk about strategy now. So, people, I want to say this actually as a just a PS to what I've just mentioned. I want to get a fact clear from the start. There is a lot of confusion around this subject. People respond to dietary cholesterol differently. That's because of uh our variations in our genes that affect how much we absorb of cholesterol that we consume, how we process them in the intestine and throughout the rest of the body. There are genetic differences between us that impact how we absorb cholesterol from fats and from uh food. But in general, with a few exceptions for people with this genetic abnormality that increases the amount of cholesterol that they can absorb from food, the cholesterol we eat does not significantly raise the cholesterol we see in our blood. Essentially, the contribution of food to blood cholesterol is minimal. Dietary uh cholesterol is largely esterified, that means it's it's in a particular format that is not absorbable and it's largely excreted instead of absorbed. However, and this is where it gets complicated, so I'm going to be very mindful about the words I choose here. Cholesterol containing ingredients that are exclusively from animal-based products are not exclusively cholesterol. It's not when you eat an egg or you have a piece of steak that you're consuming pure cholesterol uh or nutrients for that matter in isolation. We eat these foods and they have a collection of different nutrients. They've got different types of fats, they've got proteins, they've got different molecules in, which is why this area is very, very complicated. To add more controversy, according to the European Society of Cardiology, trans fats and saturated fats have the greatest effect on LDLC levels, i.e. raising them. And the reason why they do that, many reasons why, but they down regulate the LDL receptors that take LDL out of circulation, thus increasing the amount of LDLC in circulation in the blood. The ingredients that tend to have more of these types of fat, trans fats and saturated fats in the composition are red meat, processed meat, pastries, fried snacks and cakes and that sort of thing, which is why they tend to get a bad wrap. But again, using the same thinking that I applied to cholesterol containing foods, you can't blame all saturated fat containing foods and all trans fats, even trans fats either, because there are many different types of fat that we find in ingredients. And even research on full fat dairy products that you would imagine are saturated fats purely, uh suggest that it can actually be protective. And that may actually be due to specific types of saturated fats that they consume, that they uh that they contain, things like stearic acid and palmitic acids, specific carbon chain lengths around carbon chain length 18. Um and even certain types of trans fats, conjugated linoleic acid, for example, uh that you find naturally in dairy products. So even when we isolate uh specific types of saturated fats, the way we talk about them seems to group them all into one category, but in in in when you actually look at them, there's variations of saturated fats, uh variations of specific types of polyunsaturated and monounsaturated fats, and also variations in the different types of ingredients that contain cholesterol as well. So, that might explain why some recent meta-analyses have found that dairy products have a neutral or maybe even a protective effect on cardiovascular disease. You're probably getting an idea as to why this is such a complicated uh topic as well. Again, I'll link to those meta-analyses in the show notes on the doctorskitchen.com. I'm a firm believer for this reason that we need to focus on ingredients rather than the specific uh blanket or blanket statements around uh saturated fat, carbs, protein, cholesterol. It is also the other thing to recognise is that it's a zero sum game when it comes to removing something. It's not like you just remove something and that's it, there's a big gaping hole. You tend to uh always replace it with something else. And with that in mind, we're going to dive into some of my suggestions for lowering cholesterol and thus your risk of cardiovascular disease. Let's start off with number one, plant protein. So published in the Journal of American Heart Association, there was a systematic review and meta-analysis of randomized control trials looking at replacing animal protein for plant proteins. So things like soy and pulses and nuts. And they suggested that one to two servings of plant protein in substitution for animal protein decreases LDLC and apoprotein, apolipoprotein B by around 4%, which is a meaningful amount. And in the authors in this particular study stated that it may have a clinically meaningful benefit in helping people to achieve lipid targets and reduce cardiovascular risk. Probably because of the positive distribution of the different types of fats that those uh two categories of ingredients contain. So where meats might contain a little bit more saturated fat, plants still contain some saturated fat, but in a lower amount compared to other polyunsaturated fats, and maybe the types of fats also differ there as well. They also contain fibre, which we're going to talk about a bit later, which can explain potentially that cholesterol lowering effect. This is not to say that you can never eat meat, but if you're being aggressive about trying to lower your cholesterol by any means necessary or trying to improve the efficacy of pharmaceuticals that you might already be on, we'll get onto that a little bit later, replacing your animal-based products with plant-based proteins is a strategy that I would advise and monitor with repeated blood tests over the time period that you're making that dietary change. We're going to talk a bit more about fibre and the constitution of those plant-based proteins as uh and provide some mechanistic reasons as to why we might be finding that as well. Okay, so point number one, replace meat for plant-based proteins. And if you can't replace all meat, then certainly inch towards replacing your animal-based products with plant-based proteins, being mindful of the protein amounts that you're replacing as well. I've done some pods on uh plant-based proteins and how to uh match those for meats and what it tends to come down to is making sure you've got a variety of different plant-based proteins in your diet and increasing the amount that you consume as well because plant-based proteins tend to have less protein per 100 grams and you also need to get a variety of them to make sure that you are protein replete because they have uh different ratios of amino acids and you tend to have to combine lots of different plant-based proteins to get the full nine essential amino acids. Number two, portfolio diet. So a portfolio diet is something that I wish I learned at uh about during medical school because a dietary portfolio is a plant-based dietary pattern that was um studied in the early 2000s and it has a portfolio of four cholesterol lowering foods and nutrients. These are specifically plant protein, viscous fibre, nuts and phytosterols. It's low in saturated fats, as it's largely plant-based, and those four components were 50 grams of plant-based protein. They were tends to be taken from soy or dietary pulses, for example, beans, chickpeas, legumes, that sort of thing. 20 grams of viscous soluble fibre from oats, barley, psyllium, eggplant, okra, certain fruits. We'll talk a bit about um soluble fibres and the reason why that might have a cholesterol lowering effect as well. 45 grams of nuts, things like tree nuts and peanuts, and two grams of phytosterols. I'll talk about where you get those two grams of phytosterols from as well. You can get them from many different types of foods. You can get them from uh vegetables and whole grains. It's hard to get two grams per day unless you're actually eating like me, for example, and you're getting loads of different types of phytosterols in your diet. So they initially in these studies included enriched spreads. They tend to get these margarines uh or different types of oils where they they bang in some phytosterols into them. In a controlled feeding study, two grams of phytosterols initially displaced cholesterol as as much as 25%. So these phytosterols are pretty powerful things. If we're looking at different types of ingredients, the highest uh phytosterol containing ingredients are pistachios, they have 271 milligrams per 100 gram serving. Uh you also got flax seed, 210 milligrams per 100 gram serving. There's also uh wheat germ, uh which has 197 milligrams per one half cup. I'm not too sure what the uh the conversion on that is. Early findings from these metabolically controlled randomized control trials, which are quite unusual to do and quite hard to do, is the reason why they're unusual, showed that LDLC was lowered by the portfolio diet similar to that of 20 milligrams of lovastatin, which is a type of statin medication that we use. And that those literal amounts were uh around 30%. So lowering your LDLC by 30%, which is pretty, pretty, pretty high. Um, 46 healthy hyperlipidemic adults were used in this particular study. So those are adults with high LDLC levels. They had a four-week intervention with three different arms. There was a control arm where they were put on a low saturated fat or low fat diet, essentially according to the current guidelines at the time. The statin group, which was on the low fat diet plus the lovastatin, the 20 milligram statin, uh pharmaceutical that they used, and the intervention arm which was the portfolio diet, which is the diet high in plant sterols and the soy protein and all the rest of it. Um, and that was shown to have the same lipid lowering effect as a statin, which is pretty, pretty awesome. Um, and in another systematic review and meta-analysis, again of metabolic controlled and other trials that didn't control exactly what they ate, they showed, so the real world studies, they showed that the portfolio diet significantly reduced LDLC by around 17% um among several other risk factors for cardiovascular disease including apoprotein, apolipoprotein B and C-reactive protein. So, pretty impressive results from these these other studies. The issue with these studies is that because they're relatively short, it's very hard to prove that just because a diet or any intervention for that matter lowers LDLC, that that actually converts into protection against death and cardiovascular disease. But in another study where they looked at the portfolio diet in action, it was the Women's Health Initiative study from 1993 to 2017. They looked at over 120,000 postmenopausal women, um who remember have high risk of cardiovascular disease as well. In this prospective cohort, higher adherence to the portfolio diet was associated with a reduction in incidence of cardiovascular and coronary events as well as heart failure. So, again, lots of flaws in how we collect this data and this nutrition information. We have to use things like food frequency questionnaires, but all these little pieces of information coupled together, you know, you've got randomized control trials, you have very rigorous metabolically controlled trials that are isocaloric, so you don't have the confounding issue of lowering your energy intake. Um, I think as a preventative measure, particularly if you have cardiovascular disease in your family, a portfolio diet is definitely something to try. I have looked at other um dietary patterns, Mediterranean diet, for example, DASH diets, um and they do report similar reductions in cholesterol, but I like the rigor of the portfolio diet. I think it's um uh something that is very attainable and certainly encompasses a lot of the things that I'm going to be talking to you about today. So number two, try a portfolio diet. Number three, plant fats. Now, dietary strategies that both lower LDLC and raise LDLC should have broad application when it comes to cardiovascular disease. We haven't really talked much that much about HDL and the role of that, but without going into too much depth, the higher your HDL, the better. That isn't a uh something that works when we pharmacologically try and raise HDL, but generally we want to see a higher HDL C number on your lipid panel. Your ratio of triglyceride to HDL is also something that can be calculated on a fasting lipid panel as well. You simply divide triglyceride, also known as TG, by HDL, and you want to have a ratio that's closest to one as possible. Anything higher than that, you have an elevated risk of uh heart attack and stroke. And one method of increasing your HDL cholesterol appears to be the use of monounsaturated fatty acids, which is key in something like the Mediterranean diet, for example, they have lots of nuts and olive oil and that and specifically if it replaces carbohydrates in the diet as well, uh or the proportion of carbohydrates, not completely. Um, this is where it appears to have a beneficial effect. Now, all the fat enthusiasts are going to come start coming my way now waving the high fat flags. I'm not saying that you should be eating a full uh a purely fat-based diet, but certainly increasing the amount of these specific types of fats seems like it could be beneficial. So much so that a fifth component to the portfolio diet was added in response to some of these studies, which now includes, when you go on a portfolio diet, as well as those four things that I mentioned earlier, they do include uh plant-based monounsaturated fatty acids in the form of olive oil, canola oil, high oleic acid, sunflower oils, or avocados around 45 grams per day. And they've used sterol containing margarines as well, but there are other ways to naturally include phytosterols uh and plant fats in the diet as well. Looking at uh the studies that um uh that they examined this in, published in the Canadian Medical Association Journal 2010, adding monounsaturated fatty acids to a dietary portfolio of cholesterol lowering foods in hypercholesterolemia, they substituted 13% of total calories as carbohydrates with monounsaturated fatty acids. So they removed around 15% of your carbs and added uh fats instead. Uh in 24 participants and over eight weeks, they provided all their meals. So this is a very well-controlled study. They gave all those different types of monounsaturated fatty acids. And in both the portfolio and the portfolio plus fat diet, they had a similar reduction in LDLC, but in the fat diet, they had a raise in their HDLC that they correlated with a better cardiovascular protective effect. So, the potential of these cholesterol lowering diets to reduce the risk of cardiovascular disease is pretty good. Um and definitely something that I would uh highly encourage people and other practitioners to think about as well whenever we're advising uh our patients. They also uh talked about replacing animal fats with other types of fats that are richer in polyunsaturated and monounsaturated fatty acids to reduce LDLC as well. Um the reason why is because these types of fats appear to upregulate the LDL receptor, which if you remember from the mechanism earlier on, is a way in which we can remove LDLC from circulation and thus lower cardiovascular risk. Just to call myself out there, like I don't uh like how these academic papers always have to refer to polyunsaturated fatty acids and monounsaturated fatty acids without really making it more practical for clinicians and scientists to converse with patients and the general public using the medium of ingredients because that's literally how we eat. In reality, you know, when you are having olive oil, you're not just having poofers and moofers, you're also having some saturated fats, you're also having vitamin E, you've got a whole plethora of different micronutrients contained within that ingredient. So, a better statement in my opinion is choose plant fats where possible and try and replace your carbohydrates with plant fats by around 10 to 15%. And remember, these are isocaloric substitutions. So without changing your energy consumption, that LDLC lowering effect appears to be preserved and the HDLC raising effect of plant fats. So, that's my third point. Try and eat more plant fats from good quality extra virgin olive oil. A side note on sunflower oils and corn oil and all that kind of stuff. I personally don't like the taste of them, um of the uh sunflower oils and corn oil. I think the extraction methods of these oils can also disrupt the quality of them as well. There is a a movement towards these high omega-6 oils being neutral or maybe even cardioprotective. I'm just always going to go with extra virgin olive oil from a flavour point of view. Uh but I think there is probably more nuance to that discussion that is currently being led on and for now, as a pragmatic approach, I'm always going to go for extra virgin olive oil or small amounts of um other types of oil as well, like avocado oil, although that is quite a lot more expensive. Fruit and veg, kind of goes without saying, like I said, but each 7 grams a day higher intake of total fibre is associated with a 9% lower risk of cardiovascular disease. A 10 grams of uh high fibre intake was associated with a 16% lower risk of stroke and a 6% lower risk of type two diabetes as well. According to the European Society of Cardiology, high fibre intake that we've talked about before might reduce your postprandial, so after eating glucose responses, so the blood sugar in your uh your sugar level in your blood. Um particularly after carbohydrate rich meals as well. And like I said, it kind of goes without saying increasing fruit and vegetables is clearly related to huge reductions in cardiovascular disease. There are so many different types of studies, it would be pretty futile for me to go through all of them. Um but one in particular from the Journal of Nutrition titled fruit and vegetable consumption and risk of coronary heart disease, a meta-analysis of cohort studies. They looked at nine eligible studies for inclusion in this meta-analysis around 90,000 men, 130,000 women and 5,000 coronary heart disease events. And the risk of cardiovascular disease was decreased by 4% for each additional portion of fruit and vegetables per day and 7% reduction for fruit intake as well, which might point towards the soluble fibre content or specific types of fibres that you find in fruit, namely like pectins and fructans, um which are very healthy. I know there's another movement that is kind of anti-fruit, but actually fruit is um fantastic when it comes to cardiovascular protective properties. The reasons why fruit and vegetables might be protective, well, you've got things like potassium, folate, vitamins, fibre, phenolic compounds, reducing antioxidant stress, improving those lipoprotein profiles, lowering blood pressure, increasing insulin sensitivity, improving clotting regulation, the list kind of goes on with increasing fruit and vegetables, but it's lovely to know that there is that increase uh improved cardiovascular protective effect for just every portion of fruit and vegetable or fruit per day. And I've said this before, but we need to be aiming for 10 portions of fruit and vegetables per day rather than the arbitrary five a day. And remember, a portion is 80 grams. I'm not too sure how to convert that into cups for the Americans, but 80 grams is what you want to be going for for every fruit and vegetable that you consume. Population studies, you know, have many limitations when it comes to food frequency questionnaires. So it's quite hard to ascertain the causality of these, but I think there is plenty of evidence to suggest the mechanism which makes it pretty plausible that increasing fruit and vegetable consumption is going to be related to um cardiovascular benefits. Again, limitations include the healthy user effect. If you're going to be consuming more fruit and vegetables, you're more likely to exercise more, go to the gym more, exercise in general. Um you're probably going to be more educated, you might have a higher income household. These are all things that are quite hard to tease out of these big, big studies. Um and you're probably going to be more prudent when it comes to uh the consumption of saturated fat rich foods or junk food or those sorts of things. So, with all that in mind, we'll use that as a a caveat, but still I think fruit and vegetable consumption and increasing that to 10 portions a day is a reasonable suggestion. And as nutrition is a zero sum game, you're generally going to be displacing meat and junk food when you increase fruit and vegetables and you put it on your plate. So point four, eat more fruits and vegetables if you want to lower your cholesterol. Let's turn our attention to some more specific ingredients in addition to the ones that we've already talked about within the portfolio diet, plant-based proteins, moofers, all that kind of stuff. Beans, legumes, and lentils. I know they're included in the portfolio diet, but they definitely deserve another mention. Big studies published in the American Journal of Clinical Nutrition entitled consumption of nuts and legumes and the risk of ischemic heart disease, stroke and diabetes, a systematic review and meta-analysis. They reviewed around 27 studies including over half a million subjects and showed that the consumption of 100 gram servings of legumes four times a week was associated with a 14% lower risk of ischemic heart disease. So again, the same limitations as the big studies that I just mentioned, but clearly getting more beans, lentils, chickpeas into your diet on a weekly basis, they said four, I would say daily, of at least 100 grams of cooked uh legumes would seem like it would be related to lower risk of ischemic heart disease. Why? Well, metabolically, they contain multiple different bioactive constituents that can improve cardiometabolic health, including fibre and folate and phytochemicals. They lower LDLC as published in the British Journal of Nutrition, a meta-analysis of 11 clinical trials showed that consumption of non-soy legumes lowered LDLC cholesterol by 7%, 6% and 17% respectively. They lower glucose spikes. They produce lower glycemic responses when you consume them compared to other carbohydrates. And also, they probably replace the amount of animal-based products that you are consuming as well that are tend to be higher in amounts uh higher in saturated fats uh and higher amounts of cholesterol if you are a hyper responder to cholesterol. At a chemical level, fibres have varying amounts of both insoluble and soluble fibres. That those two sort of big classifications of fibre tend to dominate uh the thinking whenever anyone talks about them. In reality, there are hundreds of different types of fibres, but let's just think about it quite um simply. More legumes tend to have more insoluble to soluble fibres as a ratio compared to fruits and grains, but they still do have some soluble fibres in them. And remember what those soluble fibre benefits are. So, in order for it to be uh a soluble fibre, it has to be resistant to hydrolysis by small intestine enzymes. So basically resistant to the breakdown of uh uh into smaller parts by the enzymes that you find further up in the digestive tract in the stomach, for example, but it's fermented into what's called short chain fatty acids lower down in the digestive tract in the large intestine. And these short chain fatty acids, we've talked about them before, things like acetate, propionate, butyrate. These short chain fatty acids lead to different uh and changes in the intestinal microbiota which contributes to the hypocholesterolemic effect. Um the reason why modulating the gut microbiota, and I just to uh explain again, the gut microbiota refers to all microbes that you find in the digestive tract, but largely concentrated in the large intestine. The reason why modulating this population has a beneficial and potentially therapeutic effect when it comes to reducing LDLC and and lower risks of things like ApoB as well, is because the the there is microbial conversion of cholesterol into something called coprostanol, which is a different type of sterol, which reduces the ultimate absorption of cholesterol into the bloodstream, which now which then gets packaged into LDLC. So overall, it can have an LDLC lowering effect. Microbes also trap cholesterol for removal via the digestive tract. They metabolize cholesterol into bile acids for excretion. So there are a number of reasons why improving the population of those microbes in your large intestine can have this hypo, i.e. low cholesterolemic effect in the body. Adding insoluble fibre also adds bulk to the diet, which absorbs and sequesters cholesterol, again, which removes its um uh which leads to excretion uh into the into the feces. So, again, it emphasizes the point that we don't need exogenous cholesterol to function. There is no need for us to consume excessive amounts of cholesterol. We produce enough. And with all those different above effects, you can explain why uh beans and legumes and all this kind of uh these kind of ingredients are so healthful from a cardiovascular standpoint. When you look at it from the the micro level, you can understand those LDLC benefits after just a few weeks. But again, the same question is, okay, well, it lowers LDLC, does that actually translate into a macro cardiovascular benefit? And yes, you see those macro benefits when you look at large observational studies of people who have high amounts of beans in the diet, it definitely correlates with a lower risk of cardiovascular disease. So, the take home here is adding dietary fibre can be used as a dietary strategy to lower LDLC, even complement statins as well. Um and hopefully even, you know, if somebody has to go on a statin, of which many people do, if you can go on a lower dose, you potentially lower the side effect profile, the tolerability of the drug, um and you potentially even lower LDLC before a drug is even required. So, my take home here, eat legumes, 100 grams a day is a minimum, there may be even more benefits beyond that as well. Next point, nuts, in particular, plant-based fats from nuts and extra virgin olive oil, but nuts in particular. So, these tend to have a higher ratio of monounsaturated fatty acids and polyunsaturated fatty acids. They also have saturated fats as well. Let's not forget all fats contain different amounts of all these different types and and various various subtypes of those types as well. But when you consume nuts, uh they lower postprandial, so after eating glucose spikes as well, they improve your insulin response. So again, that can have a beneficial cardiometabolic effect. I'll do another podcast purely on sugar, I think, and the potential of sugar to uh increase cholesterol, but we have mentioned it on a previous podcast recently as well. Nuts and plant-based uh fats are also rich sources of things like magnesium that can have anti-arrhythmic effects as well. And despite the um the consumption of nuts uh leading to more calories and more energy, which is always a bit of a concern, particularly when I talk to patients about having more nuts, they they always come back, particularly the older generation of, you know, well, I thought nuts were high in calories, so they're not good for me. And unfortunately, it's one of those sort of dietary dogmas that never fails to sort of um die. Um and whilst an overall balance of energy is important, when you get into the weeds of actually the quality of foods, that is what trumps everything else. So, you know, if you're eating whole nuts and whole seeds, you do not need to worry about the calorie density. And in fact, calorie dense nuts consumption has been associated with less adiposity, adiposity, fancy word for obesity, in observational studies as well, and does not contribute to weight gain in trials either. So the amount of energy that you're actually absorbing from these whole foods is probably going to be lower, um and it doesn't appear to have that obesogenic effect either. So, the benefits of nuts are, you even find the benefits of nuts that have been shown in the, you know, seminal PREDIMED trial. Uh it provides compelling evidence that nut consumption is cardioprotective, which is why they've added plant fats to the portfolio diet, which is why the Mediterranean diet is actually quite rich in fats from plant-based sources. And the question is, okay, well, how much? Um so, again, published in the American Journal of Clinical Nutrition, consumption of nuts and legumes and the risk of ischemic heart disease, they reviewed 27 studies including those half a million unique individuals I've already mentioned the study earlier above, and 28 grams specifically, I don't know why they put 28 grams specifically. Uh 28 gram serving of nuts was associated with 24% lower risk of ischemic heart disease, uh 22% lower risk of non-fatal ischemic heart disease and a lower risk of type two diabetes as well, just four times weekly. So, my suggestion is have a handful, it's about a handful, handful of nuts every single day can have an LDLC lowering effect, as shown in the portfolio diet and coupled with these big observational studies that show a cardioprotective effect, I think it's definitely something that's prudent to add. So, eat whole nuts and go for around 30 grams a day. Who knows, even more, I think could be beneficial as well, but there aren't massive studies to demonstrate that um either. Let's talk about oats. There's a lot of oat bashing going on these days. Uh and I think it comes down to the dose of oats that we consume rather than oats being a bad addition to one's diet. Um in this particular study that I'm going to talk about, they only use 70 grams of oats per serving, which is a relatively small amount. In fact, that's the amount that we tend to use whenever we do recipes on the app, the Doctor's Kitchen app that you can get from the App Store. Uh hopefully coming on Android soon. But in this uh short-term prospective open-labeled uh trial, uh which was randomized, um there were it was used in a subject of Asian uh uh patients as well, uh which are, you know, who who are more at risk of uh cardiovascular disease. Uh 80 patients, mildly hypercholesterolemic, so fancy word for high LDLC and total cholesterol. They randomized into two different groups. One had their normal diet and the other group had their diet with 70 grams of oats twice daily. That is uh equating to around 3 grams of beta glucan, which is a specific uh functional fibre that we'll talk about in a second. The group who had oats twice a day, so around 140 grams, but over the course of a day rather than one big setting, uh they found that there was an LDLC reduction of 10%. It's very small compared to the other things, but it's I think it's a it's a very small study, uh but it's a significant impact, but a very small study. And I think this is a good one to have for the Asian population in general. And the interesting thing about this study is that it wasn't necessarily in the form of oats, it was also in the form of upma, which is a thick porridge with seasoning and vegetables, and it's actually quite delicious as well. I tend to have oats with other things as well, things like nuts and seeds and full fat uh milk or coconut milk or whatever it might be. So, if you're having oats on its own, you don't really have much of a food matrix. If you're having it with other types of fats as well, I think it's going to have that beneficial impact and lower the uh potential risk of a high glucose spike. Some people don't do well with oats, and that's fine. I think we have to be respectful of that. But a lot of people would do great with oats. Um and certainly if it's replacing what tends to be a highly refined carbohydrate rich uh meal in the mornings. Um so and you can also have savory oats as well. And the way I eat it with hemp seeds, pumpkin seeds, uh other types of plant-based fats is probably a healthier way of consuming them too. Uh so my my recommendation is try oats, 70 grams twice a day or 80 grams, 75 grams in the morning, uh could be a good way to introduce beta glucans. Let's specifically talk about beta glucan because it's referred to as a functional fibre, which is a specific fibre that is extracted or isolated or synthesized and shows benefits to health. So other examples include fructans, gums, lignins, uh you've probably heard of polyols or psyllium. Um and prebiotics are a specific class of functional fibre that are unique in that they selectively stimulate the activity or growth of beneficial, I say that in in quotes, uh health promoting bacteria. In reality, I think all bacteria serve a purpose. It really just comes down to the dose of of that particular microbe. But these prebiotics are a specific class of functional fibre and they generally promote the growth of things like lactobacilli, bifidobacteria, uh and thereby improving the host's uh health. These particular fibre ingredients, like I mentioned before, should be resistant to the digestive enzymes that you find higher up in the tract and should not be absorbed in the higher in higher up in the tract and they should uh reach the area where they can be fermented by the gut uh microbiota into metabolites and things like short chain fatty acids as well. Psyllium husk is a type of uh functional fibre, a prebiotic. And in this uh recent meta-analysis of three, just three, I I I take that on board, three randomized control trials, they revealed that the addition of this uh what psyllium works uh as you might have heard from a previous podcast I did on glucose spikes by forming a uh a gel viscous uh uh substance. Uh and the reason why it slows uh it it prevents glucose spikes is because it slows the absorption of sugar, glucose into the bloodstream. Um and what they found from this dietary gel-forming viscous soluble fibre is that it doubled the efficacy of statins. So if you're trying to reduce the dose of a statin, uh then having some psyllium husk actually might uh be worth a shot as well. Again, I would do that with the uh with the advice of your practitioner. Uh we've already talked about the mechanism for why soluble fibres can improve LDLC and total cholesterol and all the rest of it. So I won't repeat it here, but it is definitely something that I would think about. Um psyllium husk is something that I might be taking myself. Specifically, there are different types of beta glucans. Uh one we already talked about in oats. You also find it in barley and actually in small studies published in the British Journal of Nutrition, uh they actually uh inject or they they they gave uh a small uh subject of a population of people, just 30 people with mildly elevated LDLC, um some breakfast uh beta glucan derived from barley. Uh and they they had them on a controlled uh diet for lunch and dinner. Um so in the breakfast in the breakfast they gave them this beta glucan and they found that uh the mechanism responsible for the LDLC lowering effect that they observed is probably because of uh these fibres stimulating the production of bile acids that then reduce the absorption of cholesterol and remove cholesterol through the digestive system. So, these are studies are all to say that I'm quite bullish on the idea of functional fibres and maybe there's even a product to be created whereby you have adequate amounts of all these different functional fibres in some sort of uh shake or um supplement or whatever it might be, uh to potentially reduce the dose required for statins or avoid them uh completely. Um which is uh which would be a fantastic thing. So, eat fibre and try functional fibres is definitely my uh take on for that. I'm going to do some hot takes on a few um on a few ingredients that I've definitely been asked about before. Garlic. Uh this is something I get asked about a lot as a GP. I think there's definitely rumors or old wives' tales about garlic. Uh for some reason, people take them in supplement form, in oil form. And uh there isn't great evidence for it. Uh I I the best that I found was a meta-analysis published in 2013. So there might be some newer ones that are more impressive. I'm not too sure. Uh but this one looked at 39 and this wasn't a very good study as well. So 39 trials uh involved 2,000 participants. Sounds really impressive, but when you dig into it, they included a range of different interventions in this meta-analysis. And the reason why you do a meta-analysis is because you want to pull lots of hopefully similarly and well-conducted studies into one big, big study to ascertain the overall effect of whatever intervention it is. In this case, it's garlic. But they used a range of interventions uh from garlic powder, garlic extract, garlic oil. I don't know why they did that. I don't know why they just didn't stick with one form. And then they also had a range of interventions from a dose perspective as well. So, some powders were 600 to 5,000 milligrams per day. Oil was 9 to 18 milligrams per day. Um raw garlic 4 to 10 grams a day. And if anyone knows a bit about garlic, you know, if you crush garlic and leave it for 10 minutes, you increase the uh amount of the phytochemical allicin in it. So, the method of extraction, the method of preparation is going to have a significant effect on the phytochemical profile of the ingredient that you're using. In this case, garlic. So, that that should have really been thought of, I think, in the analysis. And, you know, the good things are that in most of the trials, people had high cholesterol, they all came off lipid lowering medication at least four weeks before the intervention. But the the reductions in LDLC and total cholesterol were modest at best as per the author's um uh conclusion. So, I can't tell you whether garlic is good or bad. If you want to experiment with it, I would do an N of one experiment, i.e. you. Take garlic for at least uh eight weeks in whatever form you find. I can't I couldn't even tell you a a starting range to start off with with garlic because there's just there's so much heterogeneity in the interventions out there in these studies. Maybe that's why they had to use those poor quality studies because there weren't very good well well um conducted studies out there. Um and then monitor the effect on your LDLC or ApoB if you can afford to get an ApoB test uh after that eight weeks of whatever that intervention is and then figure it out, but otherwise, I would save your money for real foods. I I wouldn't really um advise garlic. Although garlic is fantastic, don't get me wrong, it's a prebiotic, it adds flavour to food and all the rest of it, but when it comes to supplemental form, I'm not bullish on that. However, I am bullish on red yeast rice extract, which is a cholesterol lowering nutraceutical. Now, I've definitely heard of red yeast rice, I've definitely seen it in like health food stores and places like that. Uh but I never really knew how interesting it was. And and this is my hot take on it. It's basically a statin. Um it's obtained in a natural way, so through the fermentation of rice. Um the red coloration is because of the fermentation process, so it it it pigments the um the the product. Uh but the effect of it is mainly due to a constituent uh a uh a chemical called monacolin K, uh which is a weak reversible inhibitor of three hydroxy three methyl glutaryl coenzyme A reductase. It basically works in the same way as a statin. Um published in the journal of atherosclerosis, so a good journal, they analyzed 20 randomized trials on over 6,000 patients and the LDLC lowering effect of this uh nutraceutical um compared to placebo was pretty pretty large. It reduced it by around 1 millimole per litre uh of LDLC, which is which is big. Um that corresponds to a cardiovascular risk reduction of 15 to 20%. So it is as efficacious as a statin. But the the benefits of this were that the incidence of kidney injury and liver abnormalities was less than 5%. Um it has a statin-like mechanism of action, like I've just described, but it seems to have lower side effects. So, the risk of myalgia, which is a common side effect with statins, which is basically uh muscle fatigue and soreness and it can be quite debilitating for a lot of people. In fact, I've taken people off statins and tried a different type of lipid lowering medication many times in the past because of this side effects. Uh so it could it could be an option for people who have that. I never really considered it myself uh uh recommending red yeast rice. Um it could be a therapeutic tool to support cholesterol lowering lifestyles as well, who and and obviously those who can't be treated with statins. Um and it appears there is a purified form of this as well. If you didn't want to take the the fermented product, monacolin K, 5 to 10 milligrams, that appears to be the sweet spot. Um the safety unfortunately of red yeast rice is scanty at best. Uh the reason why is because some commercial supplements are tainted with high levels of a toxin called citrinin. Uh so commercial products don't tend to have the same rigor of safety profiling as pharmaceuticals in that they can be um they they cannot have any of the constituents that they say on the label at all and they just don't have that uh independent verification process. So that is something that makes me a little bit worried about this particular nutraceutical, but, you know, if you can find a good form, the evidence suggests that it could be efficacious. So, you know, I it's one of those things that I was surprised to find positive studies on and it could be a something that people use, particularly if they're intolerant to statins for whatever reason or they have side effects as well. Okay, I'm going to close with eggs. Oh, the bane of my life. I'm asked about eggs all the time. Is it good for you? Is it bad for you? I really wish it was easy for me to say that eggs are fine, eat as many as you want, they're completely innocuous, cholesterol and eggs doesn't matter at all, or don't eat eggs, they're really bad for you, they're going to give you heart disease, there's clear evidence to suggest that. In reality, it's a bit of both and it's nuanced and it depends on your biology, your unique genetics and the rest of your lifestyle as well. So, first of all, let's talk about what eggs are. Eggs are a brilliant source of nutrients. They are full of protein, they contain micronutrients like lutein and zeaxanthin that are important for brain health and eye health. Uh not to mention B vitamins and choline, they have specific types of fatty acids that are fantastic for your brain, like omega-3, vitamin D, overall, if you look at the profile of eggs, it is a fantastic whole food that has been eaten for millennia. I eat them myself and I recommend other people eat them as well. The uncomfortable truth, however, is that consumption of more than two eggs per day is associated with and will raise your total cholesterol and LDLC as well. That is a fact. And unfortunately, that is an uncomfortable truth that even though I would love to have a cognitive bias, a cognitive dissonance away from it, when you look at the studies, it's quite hard to argue against that. But like any food that has saturated fat, like meat products, for example, or cholesterol, I always turn to Paracelsus. And that is to say, all things are poison and nothing is without poison, the dosage alone makes it so a thing is not a poison. That is to say, the poison is in the dose. The amount of eggs we consume coupled with the quality of the rest of our diet is an important factor in determining whether you choose to eat eggs or not. It is completely your choice. Plus, an individual's response to dietary cholesterol, just like we said at the top of this podcast, and saturated fat is highly variable, depending on your genetics, depending on your microbiota, you might be one of those people that who can eat three, four or five eggs and not have any impact on your LDLC or total cholesterol levels at all or ApoB levels at all. Very, very lucky if you are. It can have no impact on those levels. Or, on the other hand, you could be one of those very susceptible people who can have a sniff of those foods and have an impact on their ApoB levels and their LDLC levels as well, thus increasing your cardiovascular risk, as we've determined, LDLC raised levels will confer. Published in the in the Journal of Clinical Lipidology in 2015, dietary cholesterol has modest effects to increase total C and LDLC levels on average. So this is what people always say when they're trying to protect their precious cholesterol containing foods. However, in the same journal, they admit and they they say that there are hypo and hyper responders in the population. And unfortunately, at present, there is no widely available or inexpensive method for clinical use to predict who is likely to experience a change in atherogenic cholesterol or not. Basically, there's going to be an effect in some people, but there's no way for us to tell you whether you're going to be susceptible or not. You basically have to experiment yourself. There are also some people that say that no matter what their LDLC cholesterol level is, as I mentioned before, as long as my inflammation is low, it doesn't really matter what my LDLC level is. Or there are also people that will say, well, it raises my LDLC cholesterol level, but it also raises my HDLC cholesterol level. And it does in some studies actually demonstrate that. And so overall, that mitigates the effect of those atherogenic particles in circulation. Having a low carb diet with eggs improves your insulin sensitivity, so I don't need to worry about it. I think that's potentially dangerous and I prefer to play the numbers and actually reduce LDLC because it is causally related to the development of atherosclerosis. Everything is about trade-offs. So for the convenience of a nutrient dense food, how and delicious food, how willing are you to have a slight raise in your cholesterol levels? An average of an egg a day is unlikely to have a significant or clinically meaningful impact on your LDLC levels as per European society of cardiology guidelines and American uh lipid guidelines as well that I will reference on the podcast show notes. However, if you already have high cholesterol levels, ApoB, LDLC, total cholesterol, and you've optimized other areas of your diet, I think it would be a reasonable suggestion to remove eggs from your diet and monitor your bloods and see what impact that has. And if you are a hyper responder to to cholesterol and fats in your diet, particularly from saturated fats, again, it's something that I would consider removing from your diet as much as it pains me to say that. Um and it's hard to find a a nutrient dense food of the same magnitude as an egg that is convenient and in the whole form, but the facts are the facts, I'm afraid to say to myself. Probiotics are another one that get a lot of attention. Uh I've been asked about probiotics and the effect of uh cholesterol lowering effects. Um I think we've got a long way to go. The only things that I've come across are mouse studies, animal studies that aren't particularly useful because how something reacts in a mouse or an animal uh does not necessarily mean it's going to have any effect in humans actually. In a mouse study, a probiotic combination of VSL3, which is commercially available, it has lactobacilli, bifidobacteria and streptococcus and thermophilus and all these different strains. Uh that was found to improve lipid profiles in mice. In humans, again, very limited studies, a double blinded placebo controlled uh study involving just over 100 subjects with high cholesterol levels. The same uh uh group reported a decrease in the LDLC levels by around 9% uh after consuming the probiotic in the form of a yogurt. I think it's very, very early days for probiotics. I think I'm bullish on the mechanism of it having a cholesterol lowering effect because of what we know about fibre, the impact on modulating your microbiota and the hypocholesterolemic effect of that as well. But when it comes to cholesterol lowering effects of probiotics, the supplements don't tend to have great evidence for now. Not to say that you shouldn't have probiotics in your diet in the form of yogurts, kefirs, krauts, kimchis, uh but when it specifically comes to whether I can recommend this as a LDLC lowering ingredient, I can't really say that uh for now. So, you know, in conclusion, if I had a patient or you were my patient and I'm trying to lower your LDLC cholesterol levels, which is, you know, what I think would be a pragmatic thing to do uh given the the rates of cardiovascular disease and the causal effect of of cholesterol in in cardiovascular disease. What would I tell you to do? If you were a perfect patient and I was trying to aggressively and perfectly manage your diet, lifestyle alone and all the other stuff that we need to do as well, but just your diet, this is what I would do. I'd put you on a portfolio diet, which has those four cholesterol lowering foods plus plant fats. It would be supplemented with plant-based proteins. I would put you on an exclusively plant-based diet which had plant-based proteins ensuring that you were protein replete, which is something that can be quite hard to do exclusively in a whole food plant-based diet. I would add good quality fats from extra virgin olive oil uh and avocados as well as good quality uh extra virgin uh good quality nuts and seeds. I'd potentially even add supplements in the form of phytosterols that we discussed earlier, beta glucans, psyllium and flax as well. There is some evidence around spirulina having a hypocholesterolemic effect as well. So you could even get a green supplement with my prescription, my dietary prescription. And maybe if I could find a good source of red yeast rice, maybe that is something I would add as well, just because of the um the impact, the mechanism, the fact that it has statin like effects with potentially lower side effect profile. Um remember, all these things are great, you know, that that is a hypothetical situation where I am uniquely positioned to give you the prescription and you are 100% compliant with it. But it's not just about the knowledge of all these different foods. It's really about the implementation. It's something that I always go on about. The science is complex, as you've just heard. The solutions are simple, the implementation, that's the hard stuff. That's the really, really hard thing to do, which is why my focus is on doing the recipes for the app, doing the recipes in the cookbooks and making it easier and giving you practical tips like I've just gone through today to make it easier for you to implement on a daily basis. So, I really hope you found this useful. We're going to be doing an infographic on all these different tips uh in the newsletter. So make sure you sign up to the eat listen read newsletter, sign up for the app. The Android is definitely going to be coming soon. If you want to join the wait list, there is a wait list on the newsletter and on the website on the doctorskitchen.com. And if you want to look at the references of which there are going to be many for this podcast, make sure you check out the doctorskitchen.com as well. And I will see you here next time.
