Written by Christopher Kelly
March 11, 2018
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Tommy: Hello and welcome to the Nourish Balance Thrive Podcast. My name is Tommy Wood and today I am joined by Ivor Cummins. Hello, Ivor.
Ivor: Hey, Tommy. Great to talk to you again.
Tommy: Thanks for coming and joining us. People who listen to the podcast will have heard you previously. They may have seen you on the Keto Summit, various places talking about cholesterol. You used to be the engineer that figured out cholesterol but then Dave Feldman joined you and is going even deeper into that. I'm actually interviewing him tomorrow.
You have been doing a bit of a tour recently, tour of podcasts, because of your book. I know you've had to tell your story a million times. So, you mentioned beforehand that if people really want to hear your background, if they didn't know much about you, they could go and listen to the Bret Scher Podcast, Boundless Health. So, go and listen to you on there to hear some of your background. Maybe you can just give us the highlights, the one sentence about you and then we can dive into a bit more of what you've been doing.
Ivor: Yeah, great. Briefly, around five years ago, I had a health issue in terms of poor blood test and I realized after talking to several doctors and not getting satisfactory answers that I'd have to research myself. Briefly, I'm a master technologist, a kind of a master problem solver in the corporate engineering sphere, have been for 25 years and that's kind of what I do.
I have a Biochemical Engineering degree, background in analysis. I just went to research this stuff on cholesterol and serum ferritin and then all of my other markers independently. In a short period, I had gotten all the answers I required. And then I went on to become obsessed with the whole field of longevity health. I got cholesterol sorted pretty quickly and then all the other biomarkers and then became fixated with cardiovascular disease and gave talks which went on YouTube.
Dr. Jeffrey Gerber, Denver's diet doctor, found me several years ago and we've had a collaboration ever since which has culminated in publishing a book together on the 26th of February coming in the US with Victory Belt called Eat Rich, Live Long.
Tommy: Congratulations for that. I'm very much looking forward to reading it. I know both you and Jeff pretty well and you've done some really great work over the years. Your original talks on cholesterol, I remember watching them and they're absolutely brilliant and we will link to some of those in case people haven't seen them.
But I wanted to ask you a little bit about your sort of evolution of your approach over time because when I first saw you talking about diet and health I think you were quite almost singularly focused, and you can certainly correct me if I'm wrong, but you're very focused on just carbohydrate intake and we've had some banter about that over the years between us.
Since then you've certainly started to integrate other things into your approach in terms of what it might take to both reverse metabolic disease and minimize cardiovascular disease risk and then also improve longevity now. So, could you tell us a little bit about your evolution of thought and how you've integrated more things into your overall approach?
Ivor: Yeah, great, Tommy. I did start out very carb-focused because that happened to be my primary problem at that time. I obsessed on that and researched it for around six months. And then I got into the whole insulin axis, insulin IGF-1 and the effect that carbohydrate can have on that. Yeah, I was very focused on lowering carb particularly dense acellular refined carbohydrate, very digestible, not so much the vegetables, obviously.
I did move on then. Interestingly, when you get deep into metabolic or insulin resistance syndrome you begin to find all the peripheral kind of issues and peripheral scientific papers. I started off maybe with a couple hundred papers I analyzed and I was hard core on carb and insulin and then I began to branch out and I discovered the importance of exposure to the sun in terms of systemic health.
I researched the whole vitamin D theory and around six or eight months after that I produced a vitamin D seminar which is, ironically actually, my most popular, I think 75,000 views, the whole vitamin D thing. But not just vitamin D but actually the benefits the sun can bring in terms of vascular health and nitric oxide release and blood pressure moderation. There's more to the sun than simply the vitamin D which is important in its own right.
Tommy: Absolutely.
Ivor: Yeah. I kind of added all that in. And then the minerals, I began to get into magnesium, potassium and various minerals and supplements that would be important. I guess, this whole health and longevity thing, it certainly is multifactorial. It's certainly not just carbohydrate, right? A lot of that work on magnesium, I never actually gave a lecture on magnesium specifically but I spent a lot of time going through the data. I think for anyone listening, James DiNicolantonio has a new paper out on magnesium and it's free to view.
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That's well worth looking at. He collates together an amazing amount of data around it. That's a one stop shop. The other things that came along afterwards were the importance of the adipose tissue. I had spent a lot of time on the liver as the seat of insulin resistance syndrome but with Gabor Erdosi of Hungary who runs the lower insulin group, I spent around four or five months last year intensively going through actually hundreds of paper which we shared between each other and realize that the adipose tissue health is perhaps the very root of many metabolic issues.
I gave a lecture on that at the Physicians for Ancestral Health in Miami last January. I'm kind of rambling around now but another important one which came from yourself and Dr. Gudmundur in Iceland, a lot of focus on is the whole gut health and the ways that that can actually drive metabolic distress in the body through the immune system response.
I dug into that quite a bit and it's very interesting. I didn't realize that there are actually human trials by administering lipopolysaccharides-
Tommy: Yeah, endotoxins.
Ivor: Endotoxins, exactly. That they have actually demonstrated a rise in insulin, insulin resistance and many downstream effects just through that intervention alone. I guess, I haven't got into it too deeply. I think you're the master of this one but the whole gut health and the microbiome is a very large area too that in itself can be causal.
Now, I will drop in a little caveat there though. I feel that the interventions to help with insulin and with blood glucose and all those other things as in low carb diet, moderate fructose, high fat healthy diet will also very likely help with many gut issues. So in a sense, it is good that the interventions you do may work through many different pathways, but it's still going to be pretty much the same interventions to optimize your health.
Tommy: Absolutely. I think they've shown multiple different ways that basically any way you can improve metabolic health will also improve the integrity of the gut and we don't really know as much as we like to about the actual bugs that are in there and which ones are good and which ones are bad and what to do about it but every time you fix somebody's metabolic health their gut seems to come along with it. You're absolutely right. I also briefly want to mention, there's another magnesium paper by a Canadian doctor called Stephen Genuis. It came out just a few months before James DiNicolantonio's paper. Between the two of them, there's a huge amount of data on magnesium and almost everybody should be making sure they're getting enough. Almost everybody is deficient somehow.
One thing that you didn't mention just now when you were talking about all the aspects of diet and the environment and health but which I know you've spoken about previously, and you've included it in some of your talks, is industrial seed oils and vegetable oils and their effect on health. Maybe you could tell us a little bit about what you've found there and maybe how they're causing some of the issues that they seem to be causing?
Ivor: Yeah, actually. I was just going straight from the top of my head there. Seed oils are personal hate of mine and many in this general movement, of course. I did push, we have hammered the seed oils from the first few chapters of the book at a high level and then we included an appendix going into much greater detail on that particular topic because it really needs to be teased out.
Basically, there's a huge amount of science indicating that refined seed oils, industrially processed, which were recommended by the American Heart Association, and still are for the last 50 years.
Tommy: Margarine.
Ivor: Yes, margarine. Interestingly, just as a side note, Unilever fired their head of margarine division a couple of years ago and they since divested and sold it to, I think, a Chinese corporation. The guys know the writings on the wall. Getting out. Yeah, the vegetable oil, we put in a whole series of studies.
One science of studies was, and it was interesting because this was never really tested in animal models even though we pushed vegetable oils based on associational data and weak RCTs for decades. In 2014 to 2016, there's a series of papers by a team that did very good mouse experiments. I know they're not perfect using mice but they were very well executed.
What they said in their paper was, look, we know that we take around 8% to 10% now of polyunsaturated vegetable oils and historically and ancestrally we had around 1% or so. So, wouldn't it be interesting to see what 1% seed oils do to mice versus 8% or 9% which is what we're eating now? What would happen?
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So, they used actually low fat diets, medium fat and high fat diets and in all cases they did the 1% and 8% omega six oils. In every case, they saw a major increase in liver fat and liver issues and negative biomarkers with the 8% in a marked contrast to the 1% seed oil. It was interesting that that's kind of the first time that someone really went in and did that properly after 50 years of pushing these things.
There's a series of animal experiments which hinted this. also, there is some really good experiments from the 1990s where they actually looked at alcohol induced damage on the liver and they had noted that countries in associational studies that had similar levels of alcohol intake but lower levels of polyunsaturated oil intake had less liver disease and less mortality from liver disease.
They hypothesized. They did a series of rat experiments and what they found is actually quite striking. When they gave a high saturated fat diet with very low polyunsaturates down at the 1% level, even though the rats were infused with very high levels of ethanol for basically their whole lives, it could not generate significant liver disease.
Stepwise, as they increased the polys and reduced the saturated fat, they went to moderate liver disease, very significant liver disease rise up to severe liver disease and necrosis. It was stepwise linear by increasing the polys. So, they concluded that polyunsaturated oils at reasonable levels are required for liver disease from alcohol, not just contributory but required.
That's another hint. I think if people want to go into more depth into seed oils and Cate Shanahan, Dr. Cate Shanahan at Deep Nutrition, she does a huge amount of work showing all of the reasons and the mechanisms in the body why these polyunsaturated oils, seed oils in excess can create an inflammatory cascade through many, many mechanisms and pathways.
The alcohol, the obesity, the liver damage and then there are the human trials that were pretty much suppressed. There were several well-executed human trials with high polyunsaturates replacing saturated fat like the Sydney heart study, the Minnesota. There was the Helsinki businessmen's trial, not too well known one, and one more I always forget. The Rose Corn Oil trial.
We have at least four trials of very solid significance where the high poly at higher cardiovascular death, all-cause mortality or both. These are very significant findings from randomized trials and they were largely suppressed. I think the problem with the evidence for polyunsaturates being a good thing is the associational evidence is riddled with healthy user bias as in the people of the decades who took the advice were the health focused people.
So then they gift the higher polys in the diet with an apparent benefit but it's false. The RCTs, there was a big meta-analysis done of all the RCTs on seed oils by Hooper in 2015. I met Professor Hooper last year and had a word with her about it. Basically, they concluded there was no improvement in mortality with polys, no improvement in cardiovascular mortality or stroke mortality or anything. There was only a slight decrease in current event rates.
The thing I'd say about seed oil is when looking at the health of the adipose, taking more polyunsaturates may give you a short term benefit in allowing you to expand your adipose tissue a little and give yourself a little buffer. But all these RCTs were only over two years. It's actually the ones that run longer that saw the excess cancer and other negative effects. I think the whole seed oil and polys being good for you is pretty much just one big scam.
Tommy: That's a nice way to summarize it. When we are talking about the health of the adipose tissue, there's certainly some mechanistic stuff about how polyunsaturates can increase in the short term adipose tissue, insulin sensitivity so you can stuff more fat into those cells in the short term but then you're pretty much playing a losing game in the long run, like you say. That's a good way to summarize it.
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Ivor: I might just add also just another quick last thing on seed oils. I know cancer is a very emotive topic and risk for cancer scares people but I've had to drop in that one of the big question around excess of PUFA or polyunsaturates is the question mark around increased cancer rates. Now, it's quite controversial. There are papers that are very good that went through mechanisms. I know there are data that would support this.
In rat experiments and in other experiments it was seen that the cancer increase risk from around 1% PUFA to around 3% PUFA rises in up to 4%. But after 4% PUFA in the diet, the cancer risk plateaus. So, if you have people taking 4% versus taking 12% or 18% there may not be much difference. And they observed that the modern population now is pretty much all taking more than 4% and they observed that if you look at associations of PUFA and cancer, you're not going to see anything.
Because the low PUFA are 4%, the higher 18%, there isn't really a difference. But if you had a large contingent of people taking 1% PUFA you may see a much lower rate of cancer. I think that's just another question around the PUFAs. Indeed the veteran administration RCT in the '60s saw that the cardiovascular improvements over several years were offset by an increase in cancer rates. I think it's still something to keep in mind.
Tommy: We are talking about focusing on a specific disease where I can say, "Well, the cardiovascular disease event rate went down a little bit." But if everybody's dying of cancer before they can get heart disease then that doesn't really leave you anywhere positive.
I also remember during my PhD when I was, obviously, looking at pediatrics stuff, there was a sort of talk on breast milk and breast milk composition. In the western world, breast milk composition, the fat in breast milk is almost 50% PUFAs from the diet just because that's what people are taking in. So, now, mainlining it into babies which, I mean, is terrifying.
Let's go, thought aside. Let's move on to just talk about the books. You mentioned the seed oil is part. You've given a lot to that particular topic. What else do you go through in the book and how do you then recommend people to implement changes such that they can improve their health and longevity?
Ivor: Right. Okay. I go through a kind of high level summary. We decided in the end, we wrangled about this, to do the structure to make it accessible. There's no point writing a book for an existing low carb community who are already very well versed. Our intention and my supporter, David Bobbett, the intention is to get the messages out to a broader population.
We made the first part of five chapters a fairly high level, very readable easy to absorb view on what went wrong on the past 50 years and why it was wrong, the advice we got, and then tilting around to what the correct advice is at a high level and what the optimum strategies are for health based on the science. That's kind of the first part to give you a run through from Ancel Keys right through to what we now know. That's to prepare the reader, if you will, to say, "Okay, I see now why it was wrong and I see now why there can be a much better way."
Part two then goes straight into what you do yourself starting with the chapter weight plus master class and going through -- Basically, we have 10 rules essentially which we develop over the next few chapters in part two. The ten things you do and it's somewhat the advice changes depends on whether you're insulin sensitive obese, insulin resistant obese or insulin sensitive slim or insulin resistant slim.
Because there's slightly different focus part of the 10 rules depending on what your current makeup is. We then go into, after explaining all of that and giving the plans, we give seven day and 14-day meal plans for the first week and the following couple of weeks just to really hold people's hand and make it easier because in the first week or so when you're changing your diet dramatically, the cliché of the keto flu, you may be low on minerals, you may need magnesium, potassium, sodium chloride.
We kind of bring people through meal plans to make it easier for the first few weeks. And then we have 50-plus recipes from a professional chef and they're all in glorious color. They're keto low carb recipes. They look really fantastic. That's the middle section. That's still very accessible and informative and easy to follow for people to actually make a difference to their health.
The last part, part three then goes into the science. It goes through insulin, fat, protein.
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We have a chapter on cancer as well to explain the mechanisms of cancer and where the primary risks likely lie. We go through a supplements chapter which goes through many supplements in some detail and then the best of the rest list to cover all the other ones we think are useful for various people. Part three is all the science. And then the appendices, I mentioned one of them on vegetable oils, they're even more detailed for the hard core people, at the back.
Tommy: That sounds great. But one thing that I put my ears up because I know it's probably something that people listening to this podcast will be interested in is your fat loss tips for the insulin sensitive because we have a lot of people who probably move pretty frequently, they may be pretty hard core athletes, some of them, but still might have some weight to lose. What are your tips for the insulin sensitive persons to lose any extra fat?
Ivor: Right. Well, that is a really tricky one. I know Jeff interviewed guys in Australia, Simon Saunders, and he actually had gone through this whole experience of being insulin resistant, getting rapid weight loss, some low carb, hitting a plateau and then realizing he was now insulin sensitive and it was extremely difficult to lose the further weight. There's still a lot to lose.
What we say for insulin sensitive obese, and unfortunately there's no simple easy way out, you have to focus more on the fasting behaviors which is one of our key rules. So, for insulin resistant people, probably not a hell of a lot of weight, they just cut the carb, moderate protein, high healthy fats, take the various supplements, blah, blah, blah, and you're going to get this really exciting weight loss.
This thing that people, when they go on low carb, they're amazed. It's amazing stories. But the fasting behaviors have to be emphasized, for insulin sensitive obese. And going ultra low carb and keto won't have the magic that it has for the other guys. So, what we recommend is to really implement the process of meal skipping. The beauty of it is you can't do it on the traditional food pyramid diet because you're going to be going crazy with hunger, right?
When you fat-adapt, you're on a very healthy optimized low carb diet, which we have defined very clearly, you can develop the habit of fasting and you will not suffer the hunger and the mental anguish that you would have otherwise. Really, that's one of the primary things. You need to replace the dietary fat that you're taking with body fat.
We give a lot of tips on how it feels, how to identify when you maybe do need to snack or have something to eat and we explained ghrelin. I have a phrase going back five years, love your ghrelin. All my friends actually kept joking with me about it, this phrase, love your ghrelin. But you have to love that slightly hallow feeling of hunger as you're burning your own body fat and not view it as you would have had it in the past life on a high carb diet where you know it's affecting your mental acuity, you're slumping.
You just feel this hallow feeling in your stomach and that's the sign of success. You know you're in a period where you're burning your body fat and your weight is going to be coming down and it does not have to impact your performance. In fact, you can feel good about it.
Tommy: That makes sense.
Ivor: Yeah. We call it, that scenario anyway of insulin sensitive overweight who can hit plateaus and basically go through it in enough detail that people at least understand what they're doing, know what they're doing and know why it's not working if it's not working.
Tommy: And what about the body composition aspect? Do you talk about lean mass, protein, strength training or anything like that to try and shift body composition in a certain way or you're mainly focusing on eating and when you're eating how much you're eating, that kind of side?
Ivor: Well, yeah, we go through protein as well and explain kind of lean body mass and how to calculate it but we don't go into too much detail because the book is intended as a practical guide for the large guidance and we found even on keto, if we go into like we cover keto diets, we cover the concepts, the basics, how to do them, the advantages, but again we don't get into real detail because there's so much in the book. It's more like a manual.
Jeff Gerber, for instance, Dr. Gerber, he's really excited at giving it to medical practitioners because you know that they are, perhaps the majority of them are not so well versed in nutrition and in insulin dynamics and all of these important things that don't take priority in the traditional medical education.
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So, we wanted a book that covers a lot, that covers the gamut of what's important. And as a result, we were limited with going into retail detail into sculpting your body and your lean body mass and all that. We have to draw the line somewhere.
Tommy: That makes sense. You very much said it that this is the first book to give to somebody that will get them the easy wins and then there's plenty more stuff that they could research and do but once you kind of got them on that train, you got them figuring out that this is maybe something that's going to give them a long term benefit then they're going to be more excited about learning more things as well.
Ivor: And become an enthusiast, exactly. Now, the protein chapter does go into the protein effect on satiety, on weight loss and how it can be used as a tool and also explains that you know how it does trigger insulin in its own right but also glucagon. It does explain how does an advantage in higher protein a potential downside.
We do go through the whole mTOR things. That's great topic at the moment. We're not highly supportive of the mTOR hypothesizing that excess of protein can be a major driver of disease. In fact, actually, Tommy, I'm not sure where you are on that one, the Ron Rosedale and the kind of latest mTOR fear regarding protein.
Tommy: Yes. So, this was actually -- This was going to be my next question. I have a very long question that I will still give you. Because of this whole field and Ron Rosedale, Valter Longo who is another big person in the longevity field, they're both down 0.3, 0.4 grams per pound of body weight per day of protein and, basically, to continually support autophagy and recycling of proteins.
I just don't think we know enough to really support that at all. They're worried about the IGF-1 axis. When you look at IGF-1 levels and mortality, there's a really nice U-shaped curve. If you're basically right in the middle of the population range for IGF-1, basically for your age, if you're basically at the mean, you have the best longevity.
People who have low IGF-1, they have fractures, sarcopenia. Those are the old people that are going to be falling and breaking hips and then dying of pneumonia in hospitals. I'm really worried about people focusing on protein as a problematic factor. Like you said, there's a huge amount of [0:27:23] [Indiscernible] IGF-1 and insulin. So, once you're removing large volumes of highly insulingenic carbohydrates then probably protein becomes less of a factor once you have some time restricted eating or some periods of fasting, you're probably getting some of those benefits. That's kind of where I've ended up and maybe you're in a similar place.
Ivor: Eerily similar, Tommy. Absolutely. The protein chapter we get into all of that and we explained it all. We do take some shots at Longo's study that produced the worldwide media coverage that eating eggs is as bad as smoking. Obviously, we ridiculed that. We also dissected the paper itself a little at a high level.
It's exactly as you say. I mean, I have papers literally all around the insulin IGF-1 axis and that's the way it has to be viewed. There's an insulin IGF axis. I mean, they even crosstalk with their various receptors. The two of them are intimately bound. We believe at a high level that if you manage your insulin or as per Gabor Erdosi, you focus on lower insulin then IGF is not going to have the same effect as it does in the associational studies you mentioned. Because we don't have people in there who are managing their insulin optimally.
The thing about protein, we'd be much more [0:28:42] [Indiscernible] on Protein Power, on his 0.6 gram nominal increase particularly combined with fasting to get the appetite suppressant benefits for certain people. And lower, we don't really see it. The answers are not in. Absolutely as you say, Tommy, but we don't see the lower than around 0.5 gram per pound. I don't the evidence is there and certainly not Longo's paper.
I mean, Longo's paper showed the linkages of IGF-1 and it showed higher mortality for people between, I think, it was 50 and 65, and lower mortality between 65 plus. On average, there was no effect. What really, really worried me about that paper was there was a massive higher rate of diabetes diagnosed in the high protein people. We know that doesn't make sense. But it does make sense that the high protein people were confounded with people who are eating in such a manner as to get diabetes. That's just one of five or six major worries I have about that particular well-known paper.
I think it's exactly as you say, 0.5 gram is the best shot per kilogram. Maybe if I had a cancer or a tumor, I might go on a very low protein diet targeted as a response to that, but as a healthy living low insulin person eating the right diet with fasting behaviors, the right types of exercise and having all your bloods in the right place, there's no way I'd be trying to drive my protein down. It wouldn't make sense.
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Tommy: Just to quickly ask, you said 0.5 per kilo, do you mean 0.5 per pound?
Ivor: Sorry. Yeah, absolutely, 0.4 to 0.6 per pound or roughly double that per kilo, yeah.
Tommy: Okay. Dr. Longo's work is really interesting and he's interesting because he's done some basic mouse studies, in vivo studies, which particularly when it comes to his fasting mimicking diet are actually pretty good and he's done a lot of work looking at populations, populations at the blue zones. But his epidemiology stuff, like you mentioned, that paper which showed better longevity in people who are over 65 with more protein but worse for people under 65, he actually does have a recommendation in his book to eat more protein if you're older than 65.
All of it is based on NHANES data. Anybody who does anything with nutritional epidemiology from NHANES data, they immediately go to the back of the class in my mind because that data is complete trash. Actually, I do have to include there's a paper that's often talked about in the low carb community where they use the NHANES data to say that the dietary guidelines cause obe sity. So, I have to throw that paper out too because I can't say one that I agree with and one that I don't agree with.
Anything to do with NHANES gets thrown out. But the interesting thing is that, obviously, Longo came from an area of Italy that's considered very similar to one of the blue zones and they eat a very low protein high carbohydrate low saturated fat diet and that's, obviously, were he kind of goes in terms of his dietary recommendations.
I have a question about where you think the kind of diet that you recommend fit versus the kind of diet that he recommends which, I think, would also help to manage insulin and some of these other factors although I do worry a bit about the protein recommendations. How do you kind of figure that stuff out? Is there a population on the planet that you see that eats the way that you recommend and then also lives a very long time?
Ivor: The population stuff is really hairy, to be quite honest. I mean, if you take the Kitavans, they had 70% maybe carbohydrate diet but it was all on processed ideal carbohydrate. Their omega three-omega six ratios were extraordinary. Their insulin was in their boots and it wasn't due to activity. There were studies in that. Their insulin was half that of an average Swede in the '70s and back then the Swedes were actually reasonably healthy and the Kitavans had half of the insulin and their glucose was on the floor.
So, they achieved that with lots of saturated fat but also a high on processed carbohydrate. But they had so many things going for them that are right like the sun exposure, the omega three-six ratio and they achieved really low insulin and low glucose and supreme health with a diet that you could say was high-ish carb with lots of saturated fat.
We kind of have the ten rules as we pick, eliminate sugar, eliminate the seed oils and eliminate processed food, bad processed food. We won't get into the definition but most people know. And then healthy low carb moderate protein high fat, fasting behaviors and then sun, stress, sleep as three crucial factors as well and then supplements and exercise preferably resistance.
So, if you take those ten plates and you pretty much do all of them, that's our belief has the best shot for longevity. Now, on the other hand, there is evidence that you can achieve insulin sensitivity and health with a very high carb, very, very low fat diet. And Peter Dobromylskij, I can never pronounce, who is on Hyperlipid went through some of the mechanisms and Denise Minger talked about it.
I would agree with that from the amount I've looked into it. If you find a precarious point of insulin sensitivity, eating a kind of a starvy, not so tasty diet of high, high carbohydrate and very, very low fat, if you take the fat from the dietary source, you can achieve an insulin sensitivity with a very high carb diet.
There are blue zones, I guess, who are doing that or the Chinese were doing that back at the turn of the century. It could be done. My question would be, why would you do it? I mean, why would you do it? Now, Longo, I know, is plant biased and there is that element and he has plant protein products and supplements. I think there's a lot of plant leanings there, right? And that's fine. So, that's the reason.
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If you're a vegetarian or a vegan, that's the reason to go for that precarious spot. But why would someone who doesn't have an ideological drive do that when you can have rich ancestral foods that are high fat and include animal products and make for a much more delicious way of living while still achieving insulin sensitivity and excellent health?
Tommy: I absolutely agree with you on all those points. A couple of things. Again, Longo's work has shown, he's seen dramatic benefits, again in clinical trials, and then for him to be able to recommend something to patients, so say his fasting mimicking diet which is being tested as part of chemotherapy and for metabolic health and autoimmune disease, and if those trials look good then you need -- People will want to recommend those in evidence-based manner. And then he has to have a product that's FDA approved that's used in studies.
I can kind of understand why he's created that product line that he has. However, I also think about my personal ancestors who are Scandinavian. This recently came up in another discussion I was having today which was that if you are plant based person in Norway or Iceland you would have starved pretty quickly before the advent of greenhouses and industrial freight, shipping.
But most of the people in my family lived well into their 90s, particularly the women, and they ate a diet that was mainly animal based and lots of saturated fats both from dairy and from -- So, actually, if you're eating lamb in Iceland there's a lot of monounsaturates in it, lots of omega threes and things too. It's not just saturated fat. It's very high fat animal based diet plus a few potatoes maybe and that's about it.
So, there's definitely multiple ways to skin this cat and it's always when people fall down on one side versus the other that I start to get worried and I think that's probably similar to you.
Ivor: Yeah, exactly. We have one paper at the start. We actually are quite fair minded. At the start of the -- Well, we don't want to take sides even though the book obviously takes a side because that's what we believe from the science. But we at the start of the insulin chapter pulled out one paper, very good paper, and it says that eight or nine out of ten of ancestral people were essentially on a lower carbohydrate diet like 30% or lower if you take the yearly average.
Certainly, the vast tracks of northern Europe, especially as you head further north, most of the year, those are all vegetation calories, essentially as you described. So, that's a given. But we also acknowledge that the Kitavans that I mentioned earlier achieved this excellent health on quite what you would call a high carbohydrate diet, maybe 60%, 70%. But again, I kind of went through why.
There are other routes. If you get enough of the livers switched to the right place you can handle the glucose. But it comes back to the question of why not follow an ancestral -- We're northern European descent, like you mentioned, why not follow an ancestral diet that all of the science is behind and it's even proven again and again to resolve to world's biggest disease, diabetes? Why not follow that rich ancestral diet that all the science support? I would say, well, the only reason not to is ideological reasons, I guess.
Tommy: Yeah. Like you mentioned, the livers, nine out of ten or eight out of ten of the livers that both sides of the argument, we recommended the same. It just comes down to where your food comes from. Maybe once you've done all the other stuff you could go one way or the other and do just as well. Based on your ideology, maybe if you descended from somebody who evolved much close to the equator then that might be something different too. So, taking that into account is important as well.
Ivor: It's a choice point.
Tommy: Yeah.
Ivor: That's exactly it. Yeah, I guess, that's essentially it.
Tommy: Okay, great. Now, I wanted to just change tracks a little bit. Let's talk about cardiovascular disease because that's obviously your other big passion like you mentioned. You've talked a lot about lipids and cardiovascular disease. You also talked about coronary calcium score. So, maybe we could just start by me asking about just the basic lipid panel, the kind of thing that everybody can get access to if they can't get access to more advanced lipids. Is there anything in there that's kind of useful for looking at that stuff? Or are you at a point where you throw all of that out and say, well, there's maybe not much that we can learn from this?
Ivor: Right. Well, basic lipid panel, I think it's very useful too and it's very low cost now and very available. Most people won't get the advance. I think it's great. But as the director of Framinghan, Castelli, the cardiologist, he was the data analysis kind of expert as well, he ran Framingham for many years and went through all the data. His point from the lipid panel, the basic one was unless LDL is higher than 7.8 millimole, that's around 300 milligrams, it has no value in itself in predicting people at risk.
[0:40:05]
That's something to keep in mind now. You could look at LDL and its value in combination with other things. But on its own -- That's from Castelli, and I agree totally. So, the LDL, you're not going to be looking up too much. But the triglyceride over HDL ratio is a very powerful proxy for insulin sensitivity. That's actually very useful. The total cholesterol over the HDL value, ideally it will be below 4.5, is similarly an excellent proxy for insulin sensitivity.
They are two really good measures without getting an insulin test done of your insulin sensitivity. They're really useful. Of course, are much, much more predictive of future health than LDL. Castelli himself, again from the same 1996 paper, said that those ratios are far more predictive than any individual value including LDL. We have it from the big guy from the 90s. It's interesting how no one or many doctors don't realize that. Many doctors in Ireland will prescribe and look at just the LDL. I'm not sure in America what percentage will still look at LDL.
Tommy: I think it's still a good number. They, obviously, have access to more advanced testing over here more readily but, I think, for most people that are still getting just the basic panel, when you look at most, studies that I've looked that just the basic lipids and, again, folks on all course of mortality, how long you're going to live, generally, particularly as you get older, the higher the cholesterol the longer you live. That's the same for LDL up to a certain point as well.
We've kind of shot ourselves in the foot a little bit by just focusing on that sort of associational stuff that doesn't really hold that much weight anymore. Do you have more to add to that?
Ivor: Well, just another quick thing. An excellent paper from 2009 which looked at coronary calcium and then we'll get to that in the moment. Coronary calcium blows away all risk factors in terms of predictive power because it sees the actual disease process in your body rather than an indirect risk factor. It's the king, if you will.
But interestingly, this guy wrote a book. He had 17, I think, or more cases where they had coronary calcifications for populations and people and their LDL and cholesterol readings. And there was essentially no real correlation between the LDL even for familial hypercholesterolemiacs, between the LDL and the degree of atheroscletoric arterial disease. That's just another thing. The LDL, many, many studies show, it's a very weak predictor. And even within familial hypercholesterolemiacs. So, most of them die in their 40s and 50s and have met heart attacks and some of them go on to live with the same essential condition very healthily. And guess what? There's no difference in LDL level or ApoB level between those two grossly different people.
Tommy: But there is a big difference in insulin sensitivity and HbA1c.
Ivor: Oh, yeah. The insulin sensitivity, insulin metrics, plotting factors and low HDL and all the old favorites show up strongly but not LDL. LDL fails at every significant turn. Plus the lipid panel, the ratio is the best thing you can get from it really. There is one other thing. If people look up cholesterolcode.com, Dave Feldman's work, he's been recently looking at remnant cholesterol and an excellent calculator for risk of heart disease in the future.
I forget the name of the -- You probably know it. It's a calculator where you put in your various standard cholesterol metrics and it calculates your risk but it's far more accurate than your usual use of cholesterol lipid values. A natural sclerotic index, I think, might be the name.
Tommy: So, is it the plasma atherogenic index? Is it that one? Because remember, that's just HDL and triglycerides, I think, but log-transformed and adjusted somehow.
Ivor: Actually, sorry it is. It's log-transformed. I think that was the enhancement that they did and triangulated it with many, many studies and it turns out to be more accurate than just the trig over HDL ratio but you can access it with just the basic factors, exactly. You will see many people going into that coming in at very low risk with very high LDL because it bypasses the meaningless one or near meaningless and it goes straight to what the real risk is. So, very useful.
Tommy: I did a podcast with Chris recently about cholesterol and we have some very different ranges from what your doctor might recommend as part of our blood chemistry calculator we put together and we actually calculated the plasma atherogenic index for people because for that exact reason.
Ivor: PAI, that's it.
Tommy: The PAI, yeah. But if people can get access to it and wants to know, see the disease in its process, we're talking about coronary calcium score, can you tell us a little bit about that, how it works and what it tells you?
[0:45:00]
Ivor: Yeah, for sure. So, this is the big one for me. Anyone that's middle aged, men above 45, women above 55 particularly, that's just in the guidelines, if you really want to know what your risk is, you got a quick calcium scan. We can look at all the blood markers you want and, in fairness, I'm obsessed with those -- If you know a lot of them and you can triangulate them all you can get a pretty good judgment on risk no doubt about it. You'd be wrong occasionally but you'll be a thousand times less wrong than the docs using LDL.
But still, at the end of the day, it's interpolation and all that. A calcium scan goes straight to the heart of the matter literally. Use the five-minute scan, high speed x-ray, radiation isn't much more than a mammogram. You hear that the radiation is a risk but that's trivial in my mind. It gets the amount of calcium that spills up in your coronary vessels. That predicts future heart events and all-cause mortality to an incredible degree.
If you take these blood measures and Framingham risk at all, if you're bad in them, you might be two or three times more likely to have an event or die. With coronary calcium, if you have calcification versus having none, you're around ten times more likely. And if you're very high, you can be up to 20 times more likely. In 2015, in the Imaging Journal, Cardiovascular Imaging, they showed that people with a zero score in middle age had a 1% approximately chance of future events or one to 1.7. If you're a very high score, it was 37% chance of a heart event.
In an engineering world where I come from, it's a no brainer. The scan beyond every production line and it would be the center piece of preventative technology basically.
Tommy: I was going to ask about people who already have some calcium. So, people might be coming to this late in the game. I've certainly recommended people get calcium scores and they already have some calcium there. I know that the stability of the plaque and how it evolves over time and how its score evolves over time is also very tightly linked to risks.
Maybe you could talk about that and then also how frequently maybe people should measure if they're worried that they have some already but they might be implementing things to try and change that or improve their risk and then how often should people be measuring to then track the evolution over time.
Ivor: Exactly. They're two really important points. So, I'll take the last one first maybe just to get that out of the way. If you get a calcium scan, if you have a zero score in middle age maybe seven or eight years time you can double check that you're still healthy. You've obviously been doing well or you've lower genetic susceptibility. Either way, you've done well. Keep doing well and check back later, seven or eight, nine years maybe.
But if you get a high score and you're a high risk person then you obviously want to check back sooner to make sure whatever things you do to stop that disease progressing and you better do something because you're a high risk going person you're heading for very likely events. You need to do something. What you do is what we talked about earlier in this conversation. You do the stuff you need to do and then maybe in around two years if you're fairly high score, you'll want to check back and make sure it hasn't gone up by more than 5% of 10% per year.
If the score per year is going up 10% or especially 15% or more per year, you've still got a major problem. Whereas my supporter David Bobbett he got a score of a thousand. He had a 75% chance of a heart event death in the following ten years, even though he had a 3% risk in Framingham. 75% was what he really had. But he has only been going up 5% per year against the usual 30% per year because he took action and he did a lot of what we're talking about.
That's the key really. High score, do the right thing, and then a couple of years verify that they haven't gone up by more than 5% of 10% a year. That's the test frequency. The first question, I'd have to check with you again. That was around the nuances within the score, or was it?
Tommy: It was mainly to do with speed of progression which you talked about, so keeping it below 10% or definitely below 15%, below 10% ideally, and then how frequently. So, you actually covered both of my questions even though you're only answering one of them. I did have another question which is a technical one just out of interest which is that as the density of your plaques increase, and maybe you can talk about the Agatston score and the density and volume scores, as the density increases, that generally is thought to become more stable disease.
So, what do you think about disease that you're not seeing because it's not calcified at all? Is that like an issue or is that just something that people are throwing out there because they're trying to throw shade on the coronary calcium score?
Ivor: Yeah. Okay, there's a lot of shade, Tommy. Radiation is one but certainly that's another one.
[0:50:03]
It doesn't see soft plaques. I did an interview last year with the world's top experts in imaging. He's a cardiologist professor in the west coast, Professor Matt Budoff. We went through that and many other questions. The reality is that calcification, when you develop soft plaque, it's possibly going to rapture. Soft plaque is dangerous and fibrous plaque. At some point you'll begin to recruit calcium to calcify and strengthen that plaque and stabilize.
It's true that the calcium scan doesn't see soft plaque but this is a numbers game. I mean, chance of death is a numbers game. If you have calcified plaque and how much you have, it's the tip of the iceberg and it indicates the iceberg of soft plaque beneath. So, if you have no calcium or low calcium or not progressing calcium, the soft plaque you have in a certain amount and is almost certainly safe or stable.
But if you have high calcium or rapidly increasing calcium, you've got an enormous burden of soft plaque invisible to the test but it's there. Like the iceberg, people in ships, when they see an iceberg coming, above the surface only, whatever it is, 7% or 8%. But they don't say, "Well, no, let's send divers down and see is there really an iceberg under the weather." Because they know. They bloody know.
That's the point. Calcification scan lets you see the iceberg. If you can't see calcium there's no real iceberg to worry about. You can still die of sudden cardiac death or arrhythmia or in rare cases of atherosclerotic rupture. It can happen. But calcium is overwhelmingly the best way to know whether or not it will happen.
The other thing, so that really annoys me, that shade because it's so stupid. I mean, it's like don't let perfect be the enemy of good. But in this case, they're happy with Framingham which is pretty rubbishy, weak. And they don't want something that's vastly better than all the risk factors put together because it's not 100% perfect.
Tommy: Yeah. That's hilarious.
Ivor: But there's reasons for that, political and financial reasons going back decades that's why they're against us. The other thing is density, yeah. There is a nuance. And Mike Eades usually brought this to my attention a couple of years ago and we have a YouTube clip from Breckenridge last year where we go through it. So, if your calcium is increasing more rapidly than you'd like, the Agatston score is a kind of a rolled up algorithm that adds together the volume, which is kind of like the amount of calcium spread around your coronary arteries, and the density which is the brightness on the screen or the concentration of calcium.
So, you've got volume and density. And the Agatston score that they give you is a combination of both. But there's a nuance. If your Agatston score rises a little faster than you'd like but it was density that was making it rise or contributing most to the algorithm, the higher number, then you could ironically be relatively safe. And if that Agatston score that they give you, the old overall score, was driving upwards mainly because of volume, increase in new plaque, then you could be very much more at risk.
There are papers on this and it is worth getting volume and density and saying which dominates, which is rising faster? If density is, you could be consolidating plaque. And as Mike says, he's seen many people going low carb do the right thing. He knows the risk have plummeted from the rampant disease but over the following few years in repeat tests their score keeps rising and they get a little concerned.
But he highlights that it's density driven or it's only 5% or 6%, 7% a year and they've gone from being very high risk to being essentially very safe. But the score does keep rising and it can be consolidation.
Tommy: Okay. That makes perfect sense. Great. I think that's everything that I wanted to ask you about. That's good timing as well. We've been talking for about an hour. So, maybe you can just tell us what your plans are with the book. Are you doing a tour? Where can people see you, find you online, all that kind of stuff?
Ivor: Well, online, just Google Fat Emperor and you'll get the YouTube and the website and blog and all that jazz. Twitter and Facebook, of course, if you want to have a scrap because of arguments. And Breckenridge, Low Carb Breckenridge in Colorado. Dr. Gerber's kind of event is on 1st of March, I think. I'll be over there. We'll have physical books, boxes of them. That will be the first event.
[0:55:01]
They don't let you do book tours anymore apparently. Apparently, that's going out of fashion. I think Keto Fest in the summer, I'll be making, I think, and Keto Con in Austin, Texas and Low Carb USA in July, I think in the west coast, in San Diego. And there's a London event in March with Gary Taubes speaking. I think it's ancestral doctors. I'm not sure.
Tommy: Is it Refined Health?
Ivor: Yes. That's Refined Health with Chris. Yes. I'm going to try and make that. Basically, I'm trying to target a lot of events rather than book tours. The last thing I'd say, maybe is the widowmaker, people Google and YouTube or search in YouTube for widow maker and put the words fat king in there as well, they'll readily get to a kind of a TV lens version of Widowmaker movie. I think it's a fantastic movie and anyone who wants to know about calcifications watch that and it's very available now on YouTube.
Tommy: All right, fantastic. We'll extract all the dates for all those things you mentioned and put them in the show notes so people can go and figure out where you're going to be if they want to see you in person. Well, thanks, Ivor. It's a huge pleasure as always and good luck with the book. I'm really excited. Like I said, I'm really excited to read it.
Ivor: Thanks a lot, Tommy. I really appreciate that. Yeah, good to talk to you.
Tommy: Cheers. Bye.
Ivor: Bye.
[0:56:28] End of Audio
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