Heart Disease Reversal & Low Fat Diets | Dr. Caldwell Esselstyn

And that green patch of ischemia was gone. And there's not much in olive oil that's healthy. And nuts are highly addicting. Once you start eating nuts, you don't stop. I have yet to see anybody who's fully compliant with the program, where the disease has progressed. How are you going to grow plaque when you're eating kale?

Dr. Caldwell Esselstyn is a physician, author, and Olympic gold medalist. He's the director of the Esselstyn heart disease program at the Cleveland Clinic, where patients with cardiovascular disease are advised to follow a plant-based, very low-fat diet. He has published over 150 scientific articles, and his book, "Prevent and Reverse Heart Disease," is a New York Times bestseller. I spoke to Dr. Esselstyn about heart disease reversal, low-fat diets, oil, animal protein, and a lot more. We had different views on a number of topics, so it was a really interesting conversation. We went over the evidence, and I really respect Dr. Esselstyn for being willing to come on and have an open conversation about the science. I'll come in at the very end to summarize everything and give you my takeaways. Here's our conversation. Enjoy.

When did you first start getting interested in nutrition? When was that shift? That's an unusual interest for a general surgeon, I grant you, but it was back in the late 1970s when I was chairman of our breast cancer task force that I began to become increasingly disillusioned with the fact that for no matter how many women I did in breast surgery, I was doing absolutely nothing for the next unsuspecting victim.

This led to a bit of global research, and it was quite striking to note that there were multiple cultures where breast cancer rates were 30 and 40 times less frequent than the United States, like Kenya. In rural Japan in the 1950s, breast cancer was very infrequently identified, but as soon as the Japanese women would migrate to the United States, by the second and third generation, they now had the same rate of breast cancer as their Caucasian counterparts. Now, in Japan, it was striking that in 1958, in the entire nation of Japan, how many autopsied proven deaths were there from cancer of the prostate? 18. The most mind-boggling public health figure I think I've ever heard. By 1978, 20 years later, they were up to 137, which still pales in comparison to the 28,000 who will die from prostate cancer in this country this year. As a matter of fact, my younger brother, at age 86, died from prostate cancer. But along about the same time in this journey, it was apparent to me that there were multiple cultures on the planet where cardiovascular disease was virtually non-existent, and it began to grow on me that perhaps there would be more bang for the buck if I could get people to eat to save their heart, because they would markedly diminish the likelihood of having the common Western cancers of breast, prostate, and colon, and so forth. Well, you just can't come back and make that as a pronouncement. You have to do the research to prove the point that you're making, and so that's how it all got started. So we actually started the program in 1985.

So you started advising more frequently and more intensely to your patients this dietary pattern. Can you summarize, kind of, your observations with your patients from that experience? Well, we've learned that the reason that my program succeeds where others fail, nobody else is as mean as I am. In other words, I wanted to take away absolutely everything that was going to injure them, whether it's not a drop of oil, no animal protein, no dairy, be very careful of sugary drinks, avoid sugary foods, cakes, pies, cookies, stevia, agave, excesses of maple syrup, molasses, and honey. Also, I did not want them to have peanuts, peanut butter, nut butters, cashew sauce, or avocado. And lastly, no coffee with caffeine. Decaf, yes, but no coffee with caffeine. And that sort of was the backbone of this original group, and I followed them for the 18 who stuck with us the whole time for up to 12 years, which probably made it one of the longest, if not the longest, study of it. I mean, for a 12-year study, nutrition is pretty unusual. Even after I left and I retired from surgery, it was just too hot to let go. Nobody else was interested. And it was tedious to talk to patients about nutrition. You have to really, the reason on our last paper in 2014, we were running about 89.3%, almost 90% compliance. And the reason for that, I think, is if you're going to get a patient to make a lifestyle change, you have to show them respect. The only way that I know to show patient respect is to give them our time. For instance, today, my present program is once about every six to eight weeks, usually limited to somewhere, it's virtual, limited to somewhere around 25 to 35 patients. It's a single day, five-hour course, five and a half hours. We feel that's more than any cardiologist has ever given for their patients. But in addition, every single one of those patients, since I'm old-fashioned, I insist upon talking with them, whether it's 35, 45 minutes, so I can get my arms around their story, and at the same time, provide them an opportunity to ask questions to me so that when they do come to the seminar after subsequent, maybe more than about two weeks, they already have a platform on which we can all move forward. It's so exciting about this. This isn't a rocket science. This is simply a food-borne illness, where people get all tied up in knots and cholesterol and family history and stress. It is the food.

So, in a nutshell, the progression of atherosclerosis. In some patients, we saw striking examples of disease reversal. The plaque is soft and made up of inflammation, fat, and cholesterol. The body can do a wonderful job when you completely commit. Often, patients when they're 60s and 70s may have a plaque that's been there for decades, and it may be made up of fibrosis and scar and calcification, less likely to go away. But still, interestingly enough, those patients seem to get full level of activity without restriction, which is very exciting. I can talk further about that if you want.

Yeah. We're going to go, hopefully, into detail on a lot of these topics, the different foods and everything. As I was going through the case series from the 90s, I didn't realize this, but it was a two-pronged intervention, right? It was the diet, and it was also a lipid-lowering treatment. Some of the patients did, but some of our most dramatic examples of reversal occurred before 1987, which is when statins came out. I haven't really made an issue with that because we've had such dramatic, some of our most profound examples of reversal occurred in patients who refused statins or couldn't take them. Okay. Interesting. I don't know of anybody who has a series of patients where they just give them statins and have disease progression and achieve disease reversal. Well, I've seen trials of lipid-lowering treatment where they achieve reversal. If the cholesterol is pushed low enough, there's an asteroid and these trials that are more recent. Yeah, that's been shown with lipid-lowering treatment, but it's impressive that you see that in some patients even without lipid-lowering treatment. I wonder if there's more than one way to get there as long as the risk factors are controlled. When you look at those nations throughout the world that have no heart disease, no statins. If you were to go to rural China 15 or 20 years ago, or the Papua Islands in New Guinea, the Tarahumara, Central Africa, I mean, none of that. Right. I wonder if also, so two things on that. One is whether there was capable diagnosis to really detect heart disease, or whether they were dying of other causes before they had a heart attack. Another question would be if indeed there was no cardiovascular disease there, because it's an ecological sort of association, ecological observation. Yeah, it could be the diet, but it could also be other lifestyle factors, right? It's hard to pinpoint from an ecological association. It's hard to pinpoint cause and effect because there are so many moving parts. But I completely agree, it's a very interesting observation that we then derive hypotheses from, and we design trials and cohort studies and case series like the one you did to sort of test that in another setting.

Yeah, it's going to be very hard to design a trial with whole, full plant-based nutrition and then without, because I mean, this isn't, I always say this, this is no longer an unknown. I mean, Ornish has published it out there. I've published it out there. We've seen what happens in wartime statistics. You see what, I mean, it's so profound. To me, it's a really black eye on the medical profession. Offered to their patients a tried and true method of eliminating this hideous, fatal disease often.

Yeah, so that was one of the questions I had. And I've had people ask me that, why hasn't there been, after all this time, as you said, Dr. Ornish and your work has been around for 30-plus years, very interesting, encouraging findings. Why hasn't someone taken that and run a randomized trial just with your diet, very low fat, plant exclusive or plant overwhelmingly plant, and seen if it reverses heart disease? It's surprising to me that that hasn't been done. Well, in a sense, there's never any nutrition in medical school that is worth, whether it's worth its weight. I mean, maybe in your freshman or sophomore year, you get a lecture on cholesterol, but not on the fact that it could have actually eliminated the leading killer of women and men in Western civilization. Now, there are other things that I've always resisted as a reason why people haven't jumped on it. Cardiology never gets any training in nutrition, even in their cardiology years. When we did it out of the American College of Cardiology, we did that survey, and the cardiologists themselves conceded that they get very little, it's negligible the amount of nutrition training they get. So when they are never trained, are never trained in the cure of the disease, or for that matter, they're never trained in the causation. There's no great surprise. And also, when you are doing, not everybody has sparks flying out of their eyes when they are asked to spend a half an hour talking with a patient day after day after day after day with nutrition and how to do it. Now, there's some of us who have that quirk about us that seem to enjoy that. Now, the other one I have avoided for the longest time, but I'm going to say it today. How much do you suppose you get paid for bypass surgery? How much do you suppose you get paid for stents or have a heaping drugs onto people compared to talking to somebody about Brussels sprouts and broccoli? I mean, there's a huge financial situation here that and almost every hospital worth its salt, the biggest bottom line figure on that hospital comes from their treatment of cardiovascular disease.

Yeah, yeah, I'm sure it's a factor. But yeah, I would love to see, in addition to all the trials that people are carrying out with Mediterranean diets and with DASH diets, it would be really interesting to see a trial where these different dietary approaches are compared side by side so we can have some more conclusive answers. I don't see how you can ask a patient to eat one of those diets when it's never been shown to arrest or reverse disease. I don't know how an IRB would ever quote it. When we've got data that shows it doesn't have to happen. So this is something that I was hoping to get your feedback on because I, in preparation for this, I went and tried to do a systematic search of any trials of nutrition that found regression or that claimed reversal or regression to any extent. And obviously, there's the Ornish trial, there's your work. And then I found trials that I had never heard about on social media. There's one in India. There is one in India. Yeah, the Mount Abu. No, no, that's the one. Yeah, right. So that was inspired by the Ornish trial, but I believe they didn't have a control group. So yeah, that's another one that sometimes is discussed on social media. But I found half a dozen randomized trials with control groups, a couple from the early 90s and then two more recent ones. So I'll just touch on some of these real quick and then I'd love to get your thoughts on them. The STARS trial from '92, conducted in the UK. They put their patients on a diet that was 27% of calories from fat, not vegan. They were getting about 200 milligrams of cholesterol a day. And they report net regression by angiography, so average reduction in plaque size. Then there's another trial from Germany around the same time. It was multi-pronged like the Ornish trial, but they used a 29% fat diet and they report regression in 39% of patients. Then there's another trial from Stanford. And then there are two trials that are more recent from the 2020s, actually one 2021, one 2022. Cordia prev used a Mediterranean diet and they didn't do angiography. They did an ultrasound of the carotid. They report in the intervention group, in the Mediterranean diet group, a reduction of IMT. So I'd love to hear your thoughts on the relevance of that. And then finally, the DISCO trial used the DASH diet, 30% of calories from fat, low-fat dairy allowed. And they found a significant reduction of soft plaque, of vulnerable plaque by CTA. So yeah, I had never heard of several of these and I thought it was interesting. Yeah, I would love to hear. Oh, again, what was the duration? Depends, somewhere about one year. Cordia prev was, I believe, six years. And DISCO, I don't remember, but they're usually one year to one year plus.

Yeah, that's, I've always felt that was a little bit timid. Because what you really want to know was, yeah, they may be on the angiograms, where all the angiograms, who did them, how were they done, and what were they compared to. But the real key is, of course, cardiac events. Yeah. And I, and it'd be interesting. I think it's a little bit, a little bit too quick to draw when you haven't had enough time to really look at whether there's been any cardiac events, because that's, I mean, a heart attack, stroke, and death would be something I'd be very interested in.

Yeah. No, I absolutely agree that the reversal of plaque is something that gets a lot of excitement. But at the end of the day, it's about, it's about events. And our first study was 12 years. Right. Yeah, I think, yeah. Yeah, in a random, I don't expect to see a randomized trial lasting 12 years. That's going to be unlikely. But yeah, that's an advantage of. Well, no, I would not be 12. Our second paper was only, what, four years. Yeah. Yeah. Yeah. Yeah. It would be interesting to see. I know, I know, Qartiyaprav reduced events. Some of these that were shorter either did not report or some did not find a reduction of events. So it would vary there. But yeah, I think it would be really interesting to kind of look. We didn't have events in our 2014 paper. Yes, there was one patient who had gone on vacation to China, absolutely began eating off the economy. He had hypertension, and of course, all the small, and he had a small cerebellar stroke. He did not follow the program. He is the one in the, he was somehow made it into the compliant group. That not compliance going on the economy. And so really, therefore, in that group, nobody had an event that was close to four years, 177 patients, which is usually about as much as most of the trials of, I would assume that the trials you were quoting had not too many more than that for Lou. It depends on the trial. Some are smaller. Some are about 100. Yeah, some are larger. But yeah, that's a good number of people. I think this is another difficulty, the compliance, which is, which is, of course, crucial. And in randomized trials, they usually are looking at the entire group that got assigned a diet, and not separating necessarily those that adhered better from those that didn't comply. So it's, it's hard to say. Yeah, it would just be really good to have data sets that are comparing these diets in parallel in the same conditions, same experimental design, that'd be great. But yeah, until we have those, I think we have all of these very interesting, very promising observations. And it's, I think the details are a bit more, a bit fuzzier, at least I find it hard to be completely sure, because the data sets are so different, different populations and different designs.

I wanted to get a little bit more into the angiography and the a little bit into the details. Let me just tell you one story. Yeah. This is about an N of one. Okay. This is one of the oldest patients I've treated. When they first came to me, he was 87. And he was somewhat frail. And he was he'd been told he had to have bypass surgery, or he would die. And he said, I want to try your plant-based approach. I said, fine. And he was very compliant. And he would call me about once a year to let me know how he was doing. Last year, when he called, he asked to see my wife. Because he wanted to ask and for about 50 recipes, because he was having a rather large party. Okay, well, what's the party about? And he said, Well, I'm celebrating my 100th birthday. That was the last year. This year, when we got a call from him, he said, I wanted to be sure to remind you that I'm now 101. Yeah. But so it works even in the elderly when they and this guy is compliant. Yeah. Yeah.

I mean, I see many reasons why that diet would move things in the right direction. Why would move all the risk factors. I have to tell you one more story, because it really blew my mind. This was a gentleman in September of 2023 began getting abdominal pain when he was eating. And it was worked up for diverticulitis. And that didn't seem to change much. Now that was September. So by early December, he tried to change his diet a little. He didn't know what direction he wanted to go in. 29th of December, he had a study with contrast, and they were able to find that he had a 75% blockage of his superior mesenteric artery. That was the 29th of December. The first week of January, he called me. I gave him a full bore, full bore, hardball plant-based nutrition. Third, by the third week in January, any pain with eating had disappeared. The next two weeks, early February the seventh, he got another study with contrast. The lesion in the superior mesenteric, which they described as atherosclerotic, was actually 100% gone, although there was a lot of turbulent flow. And it's that flow with his typical Western diet that probably accelerated a lesion there. But to me, it was the fastest that I ever had seen. Absolute rock-solid documentation, pre-treatment, and he hasn't stopped the treatment and during treatment, at least when his pain went away. So I just thought that, because most of the, I mean, I've had many other patients that seem to, on the basis of angiography, taken somewhere up close to two weeks. But, you know, they're markedly diminished, not all gone, but they start diminishing very early. And I think, why do you think it is that some of these patients with angina, within, on a PET scan, within two, four, six, eight, or 10 days, markedly diminished and sometimes their angina is gone. We haven't touched, in my opinion, we haven't touched in two or four, six, eight days, any of the major lesions, which are usually in the arteries that get all the publicity, the epicardial arteries, the right coronary, the LAD, and the circumflex, because they're riding on the surface of the heart, they get all the stents and they get bypasses. However, when I was doing a PET scan on this patient who was a downtown Cleveland stockbroker, on a PET scan, if it's orange or yellow, remember it's a good perfusion, but he had one little patch that was clearly where his symptoms were coming from that was ischemic. So I counseled him, and he came back three weeks later for another PET scan. And that green patch of ischemia was gone. And that just blew my mind. I said, wait a minute, we haven't, I mean, this is a little bit early in my training here, I guess, but we haven't removed that plaque in three weeks. What's going on here? So I talked to Rodriguez, who's chairman of the Cleveland Clinic cardiovascular pathology, who probably does 200 autopsies. I mean, who does 200 sections of hearts at autopsy and goes to see, obviously, per year. And I said, Rod, how often do you ever see plaque once the artery has dived into the intramuscular area? His answer? Never. Now I had the answer because what was why I have a beautiful slide that shows the three main arteries and then all the thousands to which they dive into, they were able to get a contraction of those. And you see this absolutely forest of thousands and thousands of intramuscular vessels, never had plaque. But what I'm sure is going on, why do they get rid of their pain? Because what happens is when I first see these patients, they are so beaten up and injured with their disease, they're hardly making any of the greatest phasodialyte, namely nitric oxide. That's way down. And in addition, the endothelial cells are now your enemy because they are now making two molecules that are vasoconstricted, endothelin and thromboxane. And as soon as you start feeding these people right and take away what's wrong, their dilator, their nitric oxide explodes, and they no longer are being pinched or vasoconstricted because you're no longer making endothelin and thromboxane. And it's so powerful to see those thousands upon thousands upon thousands of intramuscular vessels dilate, huge increase in flow. Posse's wall have flowed through the hollow biscus related to the fourth hour of the radius, tiny increase in huge diameter. I think that makes sense that vasodilation would explain a lot of the angina improvements. And I actually had a question about that with regards to the angiography pictures that sometimes are taken months apart or even years apart. If when it looks like the stenosis has improved or the lumen has increased, is it possible to distinguish between a case where the plaque has shrunk versus the artery having dilated but the plaque have been the same size? I don't know that I've ever addressed that and I think it's a good point. Okay. I mean, in both cases, it would be good news for the patient, but the implications would potentially be different. In one case, it would be an actual regression of the plaque. In another case, it would be dilation that would improve symptoms like angina. But I don't know if I would call that regression. I would call that a change in my... I should confess that although with our original study, because of the cardiologists who sent me to the patients and because of the patients themselves, a good number of those 18 had follow-up angiography. But along the way, I have heard of people who absolutely died getting an angiogram. It's not a benign procedure at all. And so I have thoroughly discouraged. I think it's very rare that I have any angiograms in the present groups. We follow them by largely by stress tests. In other words, especially if at the baseline, they've had a stress test, then if they get it repeated 10 or 12 months later, there is either marked improvement or it's back to normal. And there's nothing safer to me than a stress echo stress test. No contrast to enter the kidney. No radiation. That is as specific as an angiogram. But again, I have yet to see anybody who is fully compliant with the program where the disease has progressed. How are you going to grow plants when you're eating kale?

Here's a devil's advocate question that I've heard people pose. I see many reasons why this program and this diet would move risk factors in the right direction. Lipids and ApoB and blood pressure and body weight would all move in the right direction. But it's hard to distinguish if the effects are coming, for example, from the removal of ultra-processed foods and junk foods that normally would be in the diet of most Westerners or the weight loss, which could be achieved on a number of different diets, or if it's something specific to a low-fat plant-based diet. That is hard to distinguish. And that would have to come from a comparison to a diet where only one variable exists, right? Yeah, I agree. But yeah, not diminishing the value, especially for the patients that have clear improvements. It's just hard to know exactly what factor delivered the improvement. But yeah, I'm sure the patients who experience the improvements don't particularly care which lever was pulled.

Yeah, I had another question on the angiography. I've heard people ask about angulations. If the angle at which we're looking, since it's a two-dimensional picture, if the angle at which we're looking could be a confounder there and suggest a change in diameter. Sure, it could be. Yeah. Okay. Yeah, I think this is all stuff that would be interesting to see with more modern methods like Ultras. It had a trillion dollars and physicians who were committed to it. Right. Yeah, but in the meantime, we can labor along with things that have been shown to be pretty effective.

Yeah, we've touched already on this difference between plaque and actual risk, where it's the risk of events that ultimately matters. Something that I've heard you say in some of your interviews that I think is a very interesting, important realization for the public is that the largest segments of plaque are usually not where the heart attacks originate, right? Correct. They aren't the ones that rupture. Right, because I think this is a common misconception. People think that the plaque just grows, grows, grows until it blocks the artery.

Yeah, I think the best example of that would be one of the most frequent phone calls that I get. Dr. Esselstyn, I've been told I have to have bypass surgery. I don't want to have it. Will that be safe? I said, well, wait a minute. I said, that's the best advice of your decisions you've been seeing, but the decision is up to you. I can share with you information that is perhaps of another viewpoint, more conservative, but we have now so many patients, most of the ones that are beginning to get their bypass have had an angiogram that shows that one or two of their vessels has 100% blockage. You don't open that with diet. And the interesting thing is, we've done this often enough now. Some of them are recorded in that earlier paper, but so many are coming through now. I'm really almost confident enough to be able to say that almost anybody who has been scheduled to have an elective bypass, not an emergency, they don't have to have it. If they're willing to commit 100% to whole plant-based nutrition.

Yeah. In those cases of complete blockage, are those arteries growing with natural bypass? If you look at my website, there's one of the patients who's an antique dealer, Smithfield. I haven't looked at it in a while myself. Anyway, he had 100% blockage of his right coronary, 100% of his LAD and 70% of his circumflex. He had nasty angina, couldn't walk across the living room. His psychologist was pleading for him to have bypass. I said, well, you are pretty symptomatic, but I can tell you, here's how the program works. You can do with it what you want. He was one that had a hammer and tongs. I first encountered him in January, I think 2014. By April, he was out in the Rocky Mountains hiking. Still with those 100% blockages, obviously, but what happened is collateral develops obviously in some of those patients quite severely. Natural bypass, collateral arteries. Yeah, that's really quite profound. That's another example of why the large ones don't give a heart attack. They even got down to 100% blockage, and you can just see all of these streaming collaterals going past this blockage.

Along the same lines, while the size of the plaque absolutely matters, and it's an important measure, an important correlate, but the morphology of the plaque, the composition of the plaque is just as important, if not more. The morphology that informs how stable or how vulnerable the plaque is to rupture. Yeah, I think that's kind of interesting, but it's also interesting that we haven't seen the rupture. It seems that what happens when you start eating this way, you don't thin out the cap over the plaque. Strengthen the cap over the plaque, and no matter what the composition is inside it, if you have strengthened it, if you strengthen the cap over the plaque, it cannot rupture. If you cannot rupture your plaque, you've made yourself a heart attack proof.

You've seen that in imaging, or is that a possible explanation? No, that's the explanation. That's my explanation as to why we don't see heart attacks in our patients who are treated. That's what you think is going on there. What happens when they're eating this way, they no longer have available their metalloproteinases, stromelosynelastase, galaginase, myeloproxylase being made by the foam cell, because it's not a foam cell. So we extinguish, I think, the major enzymatic causation of ruptures. That could be tested with newer technology. They measure the thickness of the cap. I love you. Everything has to be measured. All that could be a variable. This could be a confounding thing. If you take that to the nth degree, there'll never be an end of it. There'll never be the perfect study. There'll always be something else confounding.

Yeah, you'll never have the perfect study, but I don't need perfect answers to decide what I do on a daily basis. I'm sure you don't eat meat, cheese, and bacon. I don't, but I'm not convinced scientifically that having a diet with some meat is necessarily a bad thing. But if you take somebody who comes to you with severe chest pain and angina improvement proven disease and say, here's some bacon, here's the cheese, here's the steak, go for it. No, I wouldn't say go for it. I would say address those risk factors aggressively. The ApoB, the body weight, the blood pressure, get everything really, really tight. But it is always the food. The food is a huge factor. I'm not disagreeing. My channel is called Nutrition Made Simple. Food is huge for me. I agree. You can have a low cholesterol, and if your hypertension was through the roof, you'd be in trouble. Yeah, yeah, I agree with that. I wouldn't want even one of those risk factors to be off the charts. Yeah, I agree. We want all of them to be optimized.

On this note, can we get a little bit more into root cause of heart disease, the endothelial injury, all these things? I know you talk about those. Yeah. Well, if a patient is going to take this message home, two things have to be done. One, you have to show them, as I mentioned before, you have to show them respect and give them your time. But I want them to understand in the simplest terms, now you won't be happy with my simplest terms, but I want them to be able to grasp the causation of their illness. Because if they understand the causation of the illness, because if they understand the causation of the illness, when they can say to themselves, it's what I did these previous 45 years, the way I ate was the cause of what went wrong. And here are the factors that it may go wrong. All right, here's we go. I need the patient, I understand I'm talking to you as a patient. I need you to understand that almost all experts in this disease would agree that where this disease has its inception, its onset, its beginning, is when we progressively injure the life jacket and the guardian of our blood vessels, which happens to be that delicate innermost lining called the endothelium. And the endothelium manufactures this truly magic molecule of gas called nitric oxide, which is responsible for the causation, salvation, and really a protection of all of our blood vessels because of the remarkable functions that nitric oxide possesses. For example, nitric oxide will keep all the cellular elements within our bloodstream flowing smoothly like Teflon rather than Velcro, keeps things from getting sticky. Number two, nitric oxide is the strongest blood vessel dilator in the body. When you climb stairs, the arteries to your heart, your legs, they widen, they dilate, that's nitric oxide. Number three, nitric oxide will protect the wall of the artery from becoming thick and stiff or inflamed and protect us from getting high blood pressure or hypertension. Number four, number four is the key. A safe and normal amount of nitric oxide will protect us all from ever developing blockages in the back. For example, you look at every person on the planet who has cardiovascular disease, has a disease because in the previous decades they have so sufficiently trashed, injured, compromised, and turned their endothelial system into an absolute train wreck that they no longer have enough nitric oxide to protect themselves from making blockages and plaque. However, the good news is this, this is not a malignancy, it's a benign foodborne illness, and once you can get patients to understand that never, ever, ever again are they to pass through their lips a single morsel that is going to further injure an already train wreck endothelium because then the endothelium will recover, make enough nitric oxide so we can halt disease progression and we often will see elements of disease reversal.

So what are the foods that every time they pass our lips we injure the endothelium? They are one, any drop of oil, olive oil, corn oil, soybean oil, safflower oil, sunflower oil, coconut oil, palm oil, oil in a cracker, oil in a chip, oil in a piece of bread, oil in a salad dressing. Do you do joke ever eat oil? All right, we got that out of the way. Next, we got to get rid of your animal protein, meat, fish, chicken, fowl, turkey, and eggs. How you doing on that? Okay. Also going to get rid of dairy, milk, cream, butter, cheese, ice cream, and yogurt. Okay. Also we want to be careful about sugary drinks, diet coke, Pepsi, and coke, and sugary foods, cakes, pies, cookies, stevia, agave, excesses of maple syrup, molasses, and honey. Also I don't like peanuts, peanut butter, nut butters, cashew sauce, or avocado. And finally coffee with caffeine. Decaf? Yes. Coffee with caffeine? No. Ingers endothelial cells.

Now, what are you going to eat? What are you going to eat? Oh, these marvelous whole grains for your cereal, bread, pasta, rolls, and bagels, 101 different types of legumes, lentils, and beans. All these marvelous red, yellow, green leafy vegetables, white potatoes, sweet potatoes, and some fruit. Now I should share with you that about a decade ago I made major change in the program. That change came about from an echo recognition of the fact that the endothelial production of nitric oxide is age dependent. So for example, you never heard of a boy or a girl at age eight having a heart attack, right? No, they have nitric oxide coming out of their ears. But by the time they're 50 and beautifully healthy, their endothelial production of nitric oxide is now 50% of what it was when you were 25. Now when you're 80, you've lost 70%. So the changes I made were two. One, a greater stimulation of the endothelial production of nitric oxide. And number two, we embraced the newer research that shows us that mankind has an alternate pathway for making additional nitric oxide. So here we go. I need you to chew six times a day a green leafy vegetable, approximately one-third of a cup. After it has first been steamed or boiled, five and a half to six minutes, so it's nice and tender. And then you must anoint it with several drops of a delightful balsamic or rice vinegar. Why? Because research has shown us that the acetic acid from those vinegars can restore the nitric oxide synthase enzyme contained within the endothelial cell and responsible for making nitric oxide. So you're going to chew this alongside your breakfast cereal. Again, it is a mid-morning snack. Again, with your lunch and sandwich, that's three. Mid-afternoon for dinner time, five. And I adore it when you have that evening snack of arugula or kale. Now, the second benefit, when you're chewing the green leafy vegetable, you are restoring the capacity of your bone marrow to make your capacity of your bone marrow to replace our senescent injured worn out endothelial cells. The third benefit, when you're chewing a green leafy vegetable, you are chewing a green nitrate. As you chew the green nitrate, it is going to mix with the facultative anaerobic bacteria that reside in the crypts and grooves of your tongue. Those bacteria will reduce the nitrate you've been chewing to a nitrite. When you swallow the nitrite, it is your own gastric acid, which is now going to reduce the nitrite to more nitric oxide, which can enter your nitric oxide pool. So think about it. What you're doing for minimal expense and no hideous side effects. All day long, dawn to dusk, morning to night, you are absolutely replacing the very molecule of nitric oxide, the deficiency of which gave you this disease in the first place. Now, there's a caveat to this. Toothpaste with fluoride, public drinking water with fluoride, and mouthwash will injure the beneficial bacteria in your mouth. And I do not like antacids because antacids will reduce your gastric acidity and you will be unable to reduce the nitrite to more nitric oxide. And I do not know, and I want to share with you the top six vegetables would be kale, Swiss chard, spinach, arugula, beet greens, and beets. If you want the whole list. Go for it. Swiss chard, kale, collards, collard greens, beet greens, mustard greens, carrot greens, cabbage, balsamic, broccoli, cauliflower, cilantro, parsley, spinach, arugula, and asparagus. The reason I go through that like that for you is you have to know how whole food plant-based nutrition can restore your memory. I don't think anybody doubts your memory capacity. I'm sorry to be so long, but that's what I just want to do is part and parcel what I do with the patient.

Yeah, we're going to touch on some of the food aspects because I have more questions about oil specifically and a couple of the others. Just want to touch real quick on something that has come out in the last decade or two that they figured out with regards to the idea that the endothelial injury or dysfunction is the cause of heart disease. They figured out that the endothelial cells can transport the lipoproteins physiologically. There's a physiological process they call it transcytosis where the lipoproteins are ferried across. Yeah, but I'm not going to get into transcytosis with patients. Oh, no. Yeah, yeah, yeah. I want to. Sure. But I try to get as close to the truth as I can without losing my patients. Sure, sure. No, I'm not suggesting that you go through that with every patient. My question is, because there is this mechanism where the lipoproteins that carry cholesterol can naturally and physiologically be carried across, injury to the endothelium is not needed for the plaque to start and progress. It could certainly make it worse, but it's not a necessary precondition. Just curious what your thoughts are on that.

No, I would agree if you look at the slide of Peter Libby from Harvard. Yeah. And, you know, it shows that once the process of oxidation has taken hold, then you get these cracks and fissures between endothelial cells so that an LVL molecule which is oxidized can then migrate successfully into the sub-endothelial space. And then once we have that oxidized small hard LDL particle in the sub-endothelial space, that then, my understanding, attracts the SWAT team. Namely, our macrophage will come through and behave like Pac-Man gobbling up, gobbling up, gobbling up all these small hard dense LDL cholesterol particles until it gets so full. We then change the name. It now becomes the foam cell. Defined the foam cell is the Darth Vader. And then once it starts manufacturing, there was metalloproteinase. And we're often running with thinning out of the cap over the plaque and black rupture and thrombosis. My understanding is that the oxidation takes place overwhelmingly inside the artery wall. So the lipoprotein is carried across. It doesn't need cracks. It crosses through this physiological process of transport. And then once it's inside the artery wall, outside of the lumen, then it oxidizes. But yeah, these are like nerdy mechanisms. Of course, I'm not suggesting that you should bore patients with all of this. I'm just curious because the idea of the endothelial. I'm not saying I'm boring them. I think they find it fascinating. But many of them, it's just beyond their pay grade. Sure, sure, sure. Yeah, I agree. It's not particularly actionable.

Yeah, so let's get into the specific foods. I wanted to clarify if these recommendations that you outlined, if you mean that for anyone or just people with established heart disease and high risk? Well, you know, this gets to be a fascinating question. Everybody on the planet who has heart disease at one time had no heart disease. Leave me on that. Of course. So the question you have to say to yourself, when I take a patient who's thoroughly ravaged with cardiovascular disease and I see that turn away and we're beginning to reverse, it's very hard in that setting to know why we shouldn't begin to be a little bit more, maybe more than a little bit more aggressive about their food. Let patients know that the reason that these nations, before they became westernized, had never had heart disease is not because they were taking statins or whatever they were doing or anything else. It was just the way they were eating. They right from day one ate a diet that would not injure them from the standpoint of catheterosclerosis. So how do you say to the son or no, let's say the wife of a patient who has got to make this change and the wife says, well, I'm not going to eat that way, but I'll have to make two meals, one for myself and one for my husband. That doesn't, you know, that doesn't work. So what you do to make your persuader is you say, sweetheart, we know that, although you don't want to admit it, you yourself right now at age 56, you're loaded with heart disease. He says, how do you know that? He said, well, there's a thing called autopsy studies. The first one of significant was our Korean GIs average age 20, 80% at autopsy of those dead, those who died in combat already had gross evidence of coronary artery disease. You could see without a microscope. That same study was then repeated 45 years later in 1999, looking at young women and men between the ages of 17 and 34 who had died of accidents, homicides and suicides. And now cardiovascular disease is ubiquitous. So unless you're not over 17, I have to look at you at age 56 and say, you've got disease. And that was confirmed by Lou Culler, our latest public health professor at Pittsburgh, who sadly died this past year, where he had a 10 year cardiovascular health study. So that everybody he said at 65 and 70 had cardiovascular disease. So you'd be a more general recommendation to avoid disease. Because obviously, I don't bring this up. I've insisted if I do it obliquely or gently. But what do you think about the fact that you know that this diet is killing people? And the data are there. And what can you do to somebody who has no heart disease, who's maybe 16 or 17, and they say, you don't want to die like my dad did?

Yeah, I think a diet that is heart healthy makes sense for the population at large, because it's the number one cause of death, especially people who have risk factors or family history. I'm less convinced of the specifics that it has to be zero oil or that it has to be zero animal protein. But I'm open to the data. I'm hoping that we can go through some of those specific questions. But I agree that in general, dietary recommendations to avoid heart disease in the first place are crucial for the Western world and actually for anyone right now, because it's the number one cause of death worldwide. And the Western diet is not getting us there. That's for sure. My dad had his first heart attack in 43. In 65, he became diabetic. Then he had cancer of the prostate, which was debated whether that killed him or whether it was another heart attack. My uncle had severe peripheral arterial disease, and he was a smoker as well. So with oil, there's a lot of questions on oil. But I just want to understand the recommendation to avoid all forms of oil in any form. What is mainly the pillar of pillars of data that led you to this conclusion? I wrote a paper called "Is Oil Healthy?" that was published in the International Journal of Disease Reversal and Prevention in 2019. Half of the paper was, I reviewed the animal studies that injure and dosage of the cells, and I reviewed the human studies that I found, and that showed that animals, that oil would injure endothelial cells. I decided with the appropriate references. I went through it. So the main argument, correct me if I'm wrong, has to do with FMD, with this assay of endothelial function, right? Oh, okay. At least the human data was about the flow-mediated dilation, right? Some of it, yeah. It's been about six years since I read the paper. Right. Yeah, I read it a couple of days ago. But so this is one of the main arguments that I've heard, this

The idea that after eating, for example, olive oil, flow-mediated dilation or flow-mediated dilation is inhibited post-sprandially, right? And this is one of the arguments that it then damages the endothelium, and so we should avoid oil. This is the gist of the argument. Well, there's a paper in there that very clearly showed how olive oil, palm oil, and injure endothelial cells. That was one of the major arguments. Yeah.

But I think the data would suggest that when I treat vegans for heart disease, one of the prime factors that they are eating to me is oil, which is giving them their disease, injuring their endothelium. And there was a large Spanish study that, Predamid. Yeah. Yeah, the Predamid study. And I remember there was a reporter from the New York Times after the paper came out that called me and said, Dr. Esselstyn, this seems to disagree with your philosophy. What do you think of it in the paper? And I said, well, I said I hadn't seen it. So she sent it to me. And I said, the title of the paper is, I forget that the title of the paper was somehow saying, the Mediterranean diet inhibits formation of heart disease. They had three groups, an oil group, a nut group, and then a low-fat group that was not low-fat at all. Yeah. And over the course of five years, in these 5,000, I think it was 5,000 patients, they found that in the oil group, I forget it was something like 85 to 86 major events, something like 93 in the nut group. And then of course in the low-fat group, which was not a low-fat group, it was like a hundred and something. So I said, no, I want to be sure because I talked around the phone and I said, they're claiming that the Mediterranean diet faults the progression of heart disease. But remember, every single patient who entered that study had to be checked and be sure that they did not have any heart disease. So in other words, they didn't have, they were documented as not having heart disease. And what I found is in all three groups, there had been scores of major cardiac events, heart attacks, stroke, and death. And I think you've got the title wrong. The title should be the creation of cardiovascular disease with the Mediterranean diet.

The events could be from black that is already there from before, but yeah, it's- But still, when you start with, when you start and you make the premise or declare that nobody has symptomatic or cardiovascular disease, they could identify and enter in a study. And then suddenly scores of patients in each category come down with major events. And that's why I object to the title. Yeah, I understand what you're saying. Yeah, I don't know if I would say that it's the diet they were on during the trial that's causing that, but it certainly seems to be a very partial effect. I agree. I know what you're saying. It's just a partial reduction and they're still having all these events that ideally we would want to avoid. Yeah, I agree with that. So whether that's because the compliance was not great or whether it's because of something else, yeah, it's hard to say, but it's an interesting point that you're making.

With the FMD data, I just wanted to bring up a couple of things that I found that I've never seen kind of discussed. I found that the effect on flow mediated dilation seems to depend on the type of fat. So with olive oil, they see this inhibition right after eating olive oil. But for example, with canola oil, no statistically significant effect on FMD, eating fish, no significant effect on FMD, eggs also. So basically, as I was going through this systematically, this postprandial effect seems to depend a lot on the type of fat. It doesn't seem to be a consistent effect of fat depressing FMD. That was one thing that I noticed. And then another thing that I thought was even more interesting was that it depends on the timing. So lots of things seem to affect FMD kind of acutely. After exercise, they see FMD be depressed, but then long-term exercise improves artery function. And with olive oil, the same pattern after a meal, we see FMD inhibited, but long-term in several trials, they see FMD improving on olive oil interventions. So it just seemed to me that the FMD argument was not very compelling based on the evidence that I've seen.

Well, isn't olive oil something like 17% saturated fat? Yeah, 14, I think. Yeah. These poor people who are vegans are thriving. And maybe not all brands of olive oil are the same. Sure. There's probably differences there. More than 14%. It's possible. But yeah. They don't, and there's not much in olive oil that's healthy. Well, I don't know about that. There's studies comparing with polyphenols and all these other components that suggest that those have beneficial effects. Also, the unsaturated fats, right? If the ratio of unsaturated to saturated is huge for unsaturated fats. So it has 14% saturated, but the rest is all unsaturated. It's all monos and polys, mostly monos. I have to go back to where my basic causation is. It does injure endothelial cells. I'm open to that, but yeah. It's in the paper. If you look at the references in that article, you'll find... I went through the references. There were three oils. So anyway, as long as I'm seeing an injury in my pet endothelium, that's where I come from. Yeah.

The other thing that kind of threw me off, I thought you had changed your mind on olive oil because of that review that came out in Jack in 2017. Whenever you are writing with a group, you make compromises. I felt so badly about this, but I was so outvoted or else they were going to throw me off the paper, which I probably should have done. Got it. Just to clarify, why... Yeah. People at home that might not know what I'm talking about, it's a review in Jack that recommends olive oil where you're an author, but yeah, that makes sense that there was a bit of some negotiation and ended up being a paper that recommends olive oil. That's a nice way of saying it. Yeah. A fight in the background. Yeah. No. The reason that I read that paper and I thought you had changed your mind is because honestly, the way it phrases the data on olive oil agrees with the data that I've seen. So one passage says, there is consistent evidence of beneficial effect on cardiovascular risk markers and morbidity and mortality. There's sufficient evidence to recommend its use. This matches the data that I've seen with olive oil in the outcomes. So that's why I was surprised to hear that you're still of the view that no oil period, but... Oh yeah. I'm still of that. I think the data are clear enough. Okay. I think we've clarified kind of our takes and the data that we've seen.

Other types of fat beyond oil. I know you've said no avocados, nuts, no nuts at all. Is that what you recommend? You said no peanut butter. If from my lips I say it's okay to have four or five walnuts, that is not what people would hear. Esselstyn now has said that you can have nuts. I have never said that and I'm not going to say it publicly. No, it's no nuts. See, what the bottom line is for me is that over the years, we finally have crystallized a program which is astonishingly effective and it is so powerful to embark on something that is devious from this that might threaten these various situations. I'm going to have to be wedded to a program that works, but very open-minded, hopefully. But I find it very hard for me to bring in something like olive oil when the paper after paper has shown me that it injures endothelial cells. As far as nuts go, there was a paper I think back in the 70s, Veselninovich or something like that. I remember that title. I don't know, but it was done with three different groups of rhesus monkeys. Sadly, one group got palm oil, peanut oil, inner oil, and I can't forget the other two, but they fed these oils to these rhesus monkeys for a year and then sadly they sacrificed them. And the group that had the peanut oil was just absolutely studded with disease far more than the others. I never hear anybody talking about that paper, but it was that plus the fact that nuts are really filled with saturated fat and nuts are highly addicting. And it's very rare that if you ever said nuts were okay that you'd find somebody who would have a tiny little handful of nuts. Once you start eating nuts, you don't stop.

The monkey paper, I believe you're referring to the Rudel paper. That may be Lawrence Rudel. Yeah. They had a group with saturated fat, one with mono and saturated fat, and one with poly and saturated fat. Both the saturated fat and the mono and saturated fat group had the same amount of plaque after five years, and the poly and saturated fat had less plaque. That was kind of the conclusion they titled it, compared with mono and saturated fat, poly and saturated fat protects African green monkeys from coronary artery atherosclerosis. So one thing there is they're pointing to differences in fat where poly and saturated seems to be protective at face value. But no, but wait a minute, but even though they weren't totally protected, they still had progression, right? They still had plaque, just less than the other two. That's not what I would call protection. Sure. I would call that just a slower rate of disease. Yeah, I think that's exactly what it was. It just kind of slowed them down. So I looked into that. They have another paper where they explain the diet that they use. There's a kink there. They use a diet with very high dietary cholesterol, which in monkeys causes plaque to appear, and then they change the types of fats on top of that. So they say it should be reiterated that the dietary cholesterol used in the monkeys is higher than the typical North American human, four times higher. This is needed to get total cholesterol into the 300 milligrams per deciliter range, a range permitting atherosclerosis evaluation in monkeys and representing high risk in humans. So I think this is how they create the plaque in the first place by giving these monkeys very high cholesterol.

What are your thoughts on people who have elevated cholesterol all their lives and no heart disease? Well, it's like with any risk factor, you're going to have individual variation, right? Some smokers never get lung cancer. So there's genetic factors that protect some people. Risk is always statistical. If we look at populations, some people just don't lay down plaque. They just have blessed genetics. I think that some people, of course, we've seen these people. And some of them with familial hypercholesterolemia going pretty high without disease. It's my feeling that if you have somebody who cannot lower their cholesterol, because we all have a different thermostat from a liver that makes cholesterol. And if you can take these patients and somehow, uh, when they are totally committed to whole food plant-based nutrition, their inflammatory indices are so incredibly low. They cannot set up a pathway for making atherosclerosis to really become fundamentally involved. I think that in other words, if somebody has a cholesterol of 200 or 220, that cholesterol is going to just be running through their bloodstream without creating injury, without inflammation. And I think our patients with heart disease, their inflammation is so low that one of the ways I know whether they're following or not is they have a nice low, low HDL. If their HDL is low, I know they're doing it correctly. The late Bill Connor went down to the Tarahumara Indians and found that their average HDL was 25, which would drive the average unknowing cardiologist absolutely apoplectic. I have to stress so much in our seminar with those people. You've got to know that if your HDL is falling when you do this, you are absolutely wonderful. I will congratulate you. It's not going to hurt you.

I completely agree that the HDL cholesterol is not a causal metric. Low HDL doesn't mean that people have higher risk. High HDL, you are getting more risk because the group from UCLA, when they looked at the APOA1 protein moiety of the HDL molecule, they found that when the HDL molecule was exposed to the Western diet and you injure that APOA1, you now have converted what ordinarily would have been a very powerful anti-inflammatory molecule of HDL to a pro-inflammatory molecule, joining with your LDL to injure you. That would be a change not necessarily in the HDL cholesterol level, but at the level of the function of the particle itself. The HDL particles do play important roles and that's still being figured out. There's a lot of mystery in that world. I think the distinction between HDL particle and HDL cholesterol level, which is what people a lot of times get hung up on the HDL cholesterol level and how do I get it up? How do I increase my HDL cholesterol? It's a wild goose chase a lot of the times.

Let's see, we touched on fat. Yeah, I think one thing that might be worth raising for a second, how do we reconcile all the outcome data on different types of fats? As I look at this, all the cohort studies, all the trials, what I consistently see is the focus on fat quality, not so much the fat quantity, but we consistently see higher risk for saturated and trans fats and lower risk for unsaturated fats, especially polyunsaturated fats, and this perfectly mirrors the effect of different fats on lipids like ApoB or cholesterol as well. How do we reconcile all those data with the idea that we should reduce all types of fat? I believe that's your recommendation. My patients, I don't specifically aim on that. It's just how it works out. What would be the source of the fat that they would want them to have? I usually ran into something that was going to injure them or hurt their vessels, so I ended up with the protein that they have without... What are the additional fats that you would be interested in having them have? Evidence-wise, I see benefits of all of these sources of mainly unsaturated fats, nuts, seeds, vegetable oils. Overwhelmingly, I see positive outcomes associated with those, so I include those in my diet. I just haven't seen convincing evidence that I should remove any drop of olive oil or nuts or seeds or things like that, or even fatty fish. Well, that's an honest difference of opinion. I'm terribly biased by my study.

Are you tonight in Portugal? I'm in Portugal. Yeah, I'm in Portugal. Yeah. How much... No, I think you said they have strokes over there. There's not so much the emphasis on coronary disease. There's a lot of myocardial infarction as well, but there's just more strokes. Isn't there a fair amount of oil in Portugal? Yeah, but there's also a fair amount of overweight people and smoking and whatever. It's hard to... I mean, I wouldn't pin it on oil. Congratulations on your persistence. What do you do besides read journals? My God, you're amazing. No, I mean, so basically my take is when we look at these cohort studies that compare the effect of whole form carbohydrate to, for example, polyunsaturated fat, we tend to see if anything lower cardiovascular risk on the polyunsaturated fats than on whole grain source carbohydrate. And that mirrors the data on lipids and ApoB. The polyunsaturated fats seem to be more powerful at lowering ApoB. Now, if we had a side-by-side comparison, an Esselstyn type diet, very low fat, quite exclusive compared to a diet that was also rich in plants, but had some oil and had some fatty fish and some nuts, but they were isocaloric. I don't know if one would come out on top. I honestly don't know. For me, it's a question mark. But yeah, it's interesting and fascinating to hear different views and explore this.

Yeah, on fish, kind of the same thing. As I look through the evidence, I mainly see good outcomes of fish. Associated with lower cardiovascular disease, depends on the type of fish, depends on the amount of fish, but fatty fish a couple of times a week. That's essentially the evidence that I've seen. I personally avoid fish, for example, for the environmental impact. Oh yeah, the fish are raised in a sewer. The pollutants and the contamination. Oh, it's brutal. Right. But we still see good outcomes of people eating fish. So something there is trumping the pollution, right? Isn't that the takeaway? I don't know. I personally avoid fish and seafood for the environmental impact that it has, but I have not seen evidence to convince me that having fish a couple of times a week is damaging. There's a slide I have of something like 16 studies, 22,000 people showing no benefit to fish oil, for cardiovascular disease. Okay, I'd love to look at that and see what... Any of the stocks that I have that have on that. Yeah. Yeah.

If we were to kind of wrap it up and conclude, I've heard you say heart disease is a toothless paper tiger. And they never exist. And if it doesn't exist, they'll never throw it. I love that. I think the contrast between how deadly heart disease is for humans and how much knowledge we have in terms of avoiding and even to some extent reversing, that contrast is so striking. And I think we can't overemphasize the importance of informing people on different ways to improve their cardiovascular health because we do have so much information on that with diet and other tools. Okay, quick summary of everything we talked about and my takeaways. Dr. Esselstyn's observations are really interesting and I wish they had gotten more follow-up over the years. I would love to see one of these large Mediterranean or DASH diet trials include a very low-fat Esselstyn style diet in parallel. I think we need more of these trials with multiple diets side by side. I'm not particularly surprised that his patients see improvements because this diet is going to push several risk factors in the right direction. It's going to help with weight loss, it's going to reduce cholesterol and ApoB and blood pressure. The weight loss is going to lower inflammation, it's going to lower fasting glucose and it's probably going to cause some vasodilation which is going to help a lot with angina. If I had to guess this is probably why he sees benefits in the patients who comply, not necessarily the lack of a drop of oil or a piece of fish or some dairy. I went through a lot of evidence systematically on flow mediated dilation, on this idea that oil injures the endothelium and I just don't find it convincing and the same for animal protein and endothelial injury and also the bulk of the scientific evidence supports some of those foods for heart health. We consistently see benefits of diets rich in fruits and vegetables, legumes, whole grains and we also see benefits of olive oil, fatty fish and fermented dairy like yogurt for example and in fact the Ornish trial included a small amount of eggs and dairy and Dr Esselstyn's case series, the first one from the 90s, also allowed some dairy and as we saw during the interview there are several randomized trials out there with other diets that are not vegan, that are not low fat, that also suggests some black reduction. Now of course people can choose to leave out oil or fish as a personal decision completely fine but to say that these foods are bad for the heart, that they cause heart attacks, that everybody needs to avoid them or even just people with heart disease, that requires a balance of evidence and I'm open to it in the future but right now I just don't see it. Another thing to bear in mind is these radical elimination diets for a general population are really really tough. People struggle to comply. Several trials have tried to do this, put people on low fat and low carb as low as they can go. We've looked at this before and it's only a very small number of people that are able to comply long term. Dr Esselstyn sees a remarkable compliance of 90% in his case series so that's very impressive but remember there's a lot of selection bias here. These are people who knock on his door, who already know who he is and what he promotes and they're excited about it or at least open to it and then on top of that you have all of his charisma, all of his commitment and excitement and the support system so he's able to get these spectacular compliance rates but we need other solutions even for the people who don't comply in his own program and then for a general population where the percentage is going to be much higher. So based on all the evidence we have, I think this is the key, healthy diet, fruits and vegetables, legumes, etc, low in ultra-processed foods, physical activity which most people in our society are not doing and then dialing in those key risk factors, not smoking, body weight, glucose, blood pressure, ApoB, as for a little bit of oil or a piece of fish here and there, I don't see the evidence to worry about it as long as those key risk factors are dialed in. If the balance of evidence changes my views will change. I also wouldn't call this reversal and these claims we sometimes hear on social media, it's the only diet ever shown to reverse heart disease. I think this is a wild overclaim. Reversal implies an actual reduction of plaque, a normalization of the artery and as we covered there are several open questions with angiography so there may or may not be an actual reduction of plaque in these patients.

After the interview I went over Dr. Esselstyn's case series again In adherent patients followed for 3.7 years, 81% improved, symptoms were either reduced or absent, 8% were stable and 10% got worse. In the non-adherent group no one improved, 38% were stable and 62% got worse. In the adherent group there were a couple strokes and heart attacks that coincided with medication changes so the authors reasoned they were probably unrelated to the nutritional intervention. Then there's a stroke that Dr. Esselstyn mentioned in the interview, the patient that went on vacation to China, and a couple interventions like bypass surgeries or stents. In the non-adherent there were two strokes and nine interventions. Bear in mind there were a lot more adherent people so one person having a stroke would be less than 1% of that population while two strokes in the non-adherent would be like 10% of that population. And finally five deaths in the adherent which they classified as non-cardiac and two deaths in the non-adherent which they classified as cardiac. So overall interesting observations would love to see an outcomes trial compare this diet to Mediterranean diet for example.

Before we wrap up a quick note on predimed which we touched on participants of predimed had no history of heart disease like heart attacks but they all had very high risk they all had to have either type 3 diabetes or at least three other major risk factors things like smoking, obesity, hypertension, etc. So those were the inclusion criteria all participants had to have those before entering the trial then they were split randomly onto their respective diets and by the end they saw lower risk of events like heart attacks on the participants on the Mediterranean diets 30% less. So as Dr. Esselstyn pointed out there were still plenty of events 70% of the events were not avoided. So the trial shows the superiority of the Mediterranean diet for cardiovascular health compared to the control diet that they used. It does not mean that the Mediterranean diet is a panacea that it makes you heart attack proof especially if you have several other major risk factors and possibly some black already there from prior exposure. So hopefully this gives you a bit more context. I loved having this conversation with Dr. Esselstyn. Should we do more of these? Let me know below. More conversations with doctors who have different ideas out there that might be unorthodox and we kind of go over the evidence. Tell me in the comments what you'd like to see on the channel. Thanks for watching. I'll see you next time.