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RHR: Does your diet affect your cholesterol level?


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Revolution Health Radio podcast, Chris Kresser

Today’s topic and today’s big question is, if dietary fat and cholesterol don’t raise cholesterol levels, why do total cholesterol levels drop after you stop eating those foods? That’s a really good question, and for all of the discussion about this topic, this is actually how I got started in blogging and writing. Way back in the Healthy Skeptic days, I started writing articles about the relationship between cholesterol and saturated fat and heart disease. It’s been a dominant theme of my work since then. There are lots of other people who are writing and speaking about this, and there’s still quite a bit of confusion out there, and it’s understandable because this can be a confusing subject.

In this episode, we cover:

12:22 Why you shouldn’t restrict dietary cholesterol
19:07 How saturated fat affects cholesterol levels
22:12 The relationship between saturated fat intake and heart disease

Full Text Transcript:

Steve Wright: Hey, everyone. Welcome to another episode of the Revolution Health Radio Show. This show is brought to you by ChrisKresser.com. I’m your host, Steve Wright from SCDlifestyle.com, and with me is integrative medical practitioner and New York Times bestseller, Chris Kresser. Chris, how are you doing?

Chris Kresser: I’m great. How are you doing, Steve?

Steve Wright: Well, I’m doing well; however, the apartment above me is being renovated apparently today.

Chris Kresser: Nice.

Steve Wright: So it might be a little sketch of a podcast today. We’ll see what happens.

Chris Kresser: All right. Well, if you need to duck out, just mute yourself and I’ll just ramble on as I often do!

Steve Wright: Perfect. Well, before we get rolling here, what was your breakfast?

Chris Kresser: Kind of the same old, same old this morning. I had some chorizo that came from Freestone Ranch, our local pig farmer, which was delicious, and some plantains fried in expeller-pressed coconut oil, and let’s see, some steamed kale with a little bit of olive oil on it, and some raw sauerkraut made from cabbage, beets, and carrots.

Steve Wright: Delicious as always.

Chris Kresser: Yeah.

Steve Wright: Rolling off of our Solving Leaky Gut launch here, I’ve been experimenting with smoothies for the first time in my life, trying to save time in the morning.

Chris Kresser: You would have fit right in at this conference I just spoke at, Revitalize at Miraval last weekend. There was a lot of talk about smoothies.

Steve Wright: Yeah, I’ve been resistant for many years here because everybody’s been banging the drum for smoothies for a long time, and typically if everyone’s headed one way, I try to look the other way, but right now it’s not too bad for this week.

Chris Kresser: Good. Well, we have a question from a reader today. Do you have that in front of you, Steve?

Steve Wright: I do, Chris, but I have a note here that I needed to remind you to give the listeners an update about where Revolution Health Radio is headed the rest of 2014.

Chris Kresser: Oh, right. Yeah, thanks for reminding me. Yeah, we’re making some changes to the show based on listener feedback, and what it’s going to look like from here on out is weekly episodes. At least, I’m going to do my best to do that. Of course, there may be times when I’m traveling or if I have another big project going on where we might fall out of that habit, but we’re aiming for weekly episodes now. They’re going to be shorter in general, probably more in the neighborhood of 20 to 30 minutes, unless we’re doing an interview. They’re going to be focused on a single topic. Instead of doing Q&A’s that have multiple topics within one episode, each episode will be focused on a single topic.

And we really want this to be listener driven and listener guided, so we’ve created a new way for you to ask questions, which I think will be fun. If you go to ChrisKresser.com/PodcastQuestion, you’ll see a button that says, “Record & submit an audio question,” so you can click that and then record your question, and then we’ll pick a question each week and we’ll play it back at the beginning of the episode, and then I’ll go on to answer that question and that will be the topic for that day’s show.

Of course, if you’ve been listening to this for a while, you know me and you probably know that I’ll also be just doing some episodes that may not be explicitly question driven but something really important that’s come up in the scientific literature or something that I’ve become aware of that I think you need to know about. Of course, we’ll still do that and still do some guest expert interviews as well. A little bit eclectic, but enough changes where I felt like it was a good idea to let you know what’s happening.

Another thing we’re going to be doing is posting the episodes as videos on my YouTube channel, which we started to do at one point but just fell out of the habit of doing, so we’re going to put those up on YouTube for all you YouTube watchers.

I think that’s about it.

Steve Wright: Are we going to have, like, a dress code policy going forward here, Chris?

Chris Kresser: I don’t think so! Yeah, we were thinking of actually doing video for the podcast. I realize what I said might not have been clear because some people just post, like, slides with the video or one slide and just have audio on YouTube, and we may do that. We may also actually do video and then record a split screen of Steve sitting in his pajamas in his apartment and me with my fancy audio gear, but we haven’t fully decided about that.

Steve Wright: Yeah, I think SpeakPipe is going to be awesome. This technology, it’s just amazing how fast everything’s changing. It’s going to take it to the next level.

Chris Kresser: Yeah, it’s pretty cool. So yeah, everybody, let us know what you think of the new format in the comments of this episode. You’ve noticed we’ve already been kind of shifting toward that format lately, so yeah, let us know what you think.

Steve Wright: Awesome, Chris. Well, before we get to today’s listener-generated question, I just want to let the listeners know that as of – I just checked – right now there are 105,083 people who have signed up for ChrisKresser.com to the membership site, and why that’s important other than those other 105,000 people is that those people are already going through Chris’ best tips and tricks for burning fat, for restoring gut health, working our your thyroid. There are lots of eBooks Chris has put together as well as guest expert interviews, other different menus and recipes and things that are hidden inside of Chris’ membership site that you won’t get if you’re just perusing the blog or listening to the podcast, so if you haven’t yet, I’d really encourage you to head over to ChrisKresser.com, sign up for his membership area, just put your name and email in there, and you’ll start getting the same access those other people have.

So, Chris, today’s topic and today’s big question is, if dietary fat and cholesterol don’t raise cholesterol levels, why do total cholesterol levels drop after you stop eating those foods?

Chris Kresser: That’s a really good question, and for all of the discussion about this topic, this is actually how I got started in blogging and writing. Way back in the Healthy Skeptic days, I started writing articles about the relationship between cholesterol and saturated fat and heart disease. It’s been a dominant theme of my work since then. There are lots of other people who are writing and speaking about this, and there’s still quite a bit of confusion out there, and it’s understandable because this can be a confusing subject.

There are actually two important questions in this question. One is, does diet affect cholesterol levels? That’s the explicit question. And the second question that’s kind of implied – or should be – is even if diet does affect cholesterol levels, do cholesterol levels determine your risk of heart disease? I think those are the two important questions that are on everyone’s mind regarding this topic, and as is often the case, I find myself inhabiting a kind of middle ground here. If we think of two extremes where one extreme is maybe we could call them the cholesterol believers, the dominant standard paradigm that holds that eating cholesterol and saturated fat raises cholesterol levels in your blood and high cholesterol increases your risk of heart disease, that’s the sort of standard paradigm, of course.

Steve Wright: Which is no longer TIME Magazine, thanks to the new butter article.

Chris Kresser: Yes, and we can talk about that, too. I’d like to, so remind me about that.

The other end of the spectrum would be the cholesterol skeptics, so these would be people who say saturated fat and cholesterol in your diet doesn’t have anything to do with cholesterol in your blood, and if even if it did, cholesterol in your blood has nothing to do with heart disease, so we should just not even really bother measuring it. Those are the two poles, and I think the truth is somewhere in the middle, at least what the research suggests. If I had to choose, I would say it’s probably closer to the cholesterol skeptics, but I’m certainly not ready to say that cholesterol levels have nothing to do with heart disease, nor am I ready to say that diet doesn’t affect cholesterol levels for 100% of people. The really important thing to remember about all of this is when we look at the scientific research, studies speak in terms of averages.

When you do a big study on whether saturated fat increases cholesterol levels in the blood, you’re inevitably going to have some people who experience no effect, you know, they eat more saturated fat and nothing happens to their blood cholesterol, you’ll have some people who experience a reduction in cholesterol, and you’ll have some people who experience an increase in cholesterol. But in the study, they’ll average those results out and they’ll come up with a conclusion, and they’ll say, on average – well, they don’t even say on average. They’ll say, in this study saturated fat intake did not affect blood cholesterol levels. Now, that doesn’t mean it didn’t affect them for anybody. It just means that when you pool all the results together, the average finding was that it didn’t affect cholesterol levels, and that’s absolutely crucial to understand when we discuss these issues, and I think it’s what causes a lot of confusion because averages like that are necessary when determining public policy and coming up with a general idea of how things affect us, but it’s not that useful in an individual clinical setting because we don’t treat averages in a clinic. We treat individuals, and you are not an average. You listening to this, you are an individual, you have your own individual responses to things, and that means the research can guide us and it can inform us, but it’s not the final say in terms of how you or I are going to react to something.

Steve Wright: As research continues to grow and the medicine field is changing, we’re starting to see studies coming out about genetic sensitivities to supplements. For instance, some people only need 1000 units of vitamin D3, where somebody might need 50,000 units to get to the same level, and we’ve talked on the show a number of times about how there’s who know how many variables that go into it, but it just speaks to the fact that studies help us, but they can really get confusing when you try to boil that all the way down to just helping yourself.

Chris Kresser: That’s a great example, Steve. I just saw a study come into my email inbox this morning that was talking about how genetic and epigenetic factors can affect your risk of mercury toxicity. This is a huge area of research. We’re going to be seeing a lot more about this in the future, how genetic and epigenetic, meaning gene expression, factors determine our risk for a whole bunch of different conditions and also determine our response to things like supplements, as Steve said in the case of vitamin D.

So we’re going to talk a little bit about studies that examine the relationship between cholesterol and saturated fat in the diet and blood cholesterol levels, but we always have to keep in mind this biochemical individuality that I just mentioned and the fact that these studies are just looking at averages.

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Why You Shouldn’t Restrict Dietary Cholesterol

Here’s what we know from the studies: On average, 70% of people are not affected by cholesterol in the diet. There have been very well controlled egg-feeding studies where they didn’t change anything else in the diet but they added two to four eggs per day to the diet and then measured people’s serum cholesterol levels, and in 70% of people, there was no discernible change at all. They ate four additional egg yolks a day, and their cholesterol didn’t go up and it didn’t go down. The other 30% were termed “hyper-responders,” and these people did experience an increase in serum cholesterol after eating four eggs a day, but they had an increase in both LDL, the so-called “bad cholesterol,” and HDL, the so-called “good cholesterol.” And the ratio between LDL and HDL is important and is a much more accurate indicator of heart disease risk than the total amount of either, so the researchers in these studies deemed that even in the 30% that are hyper-responders to dietary cholesterol, the increase that they saw in cholesterol levels was not clinically significant, which means it wasn’t likely to increase the risk of heart disease because although LDL did go up a little bit, HDL, the protective type of cholesterol, also went up.

That’s what we see in the studies on cholesterol, and in fact, the US is really the only significant industrialized nation that still has restrictions on dietary cholesterol. From what I understand, Canada, Australia, Japan, and the EU have all removed their restrictions of dietary cholesterol because the research no longer supports limiting it in your diet. I think the powers that be, the Big Food companies that have invested deeply in the low fat paradigm have really just – it’s going to take longer to change here because there are financial interests that are so deeply entrenched.

It’s weird to me, like, I’m so immersed in our nutrient-dense diet world that I think everybody knows about this, but I was at speaking at this conference last weekend. It was put on my MindBodyGreen. It was called Revitalize. MindBodyGreen, the audience for that website is, I would say, primarily vegetarian and vegan, and I was standing in the breakfast line. There was an omelet station where you could omelets made, and a couple people in front of me ordered an egg white omelet, and I was just blown away, you know?! It’s like, did you not get the memo?! That’s so 1995! It seems like everybody I know has heard that egg yolks are good for you and you don’t need to eat egg whites, and if you’re going to eat any part of the egg, it should be the yolk and not the white because that’s what contains all the nutrients, but obviously the memo has not gotten out completely because this is a conference with people who are ostensibly very interested in health and that was happening in 2014.

Steve Wright: Yeah. Well, I think we both actually live in communities where we’re in health bubbles as well.

Chris Kresser: Mm-hmm.

Steve Wright: But as I travel back to Michigan this summer to go visit friends and family, it’s always a shock just to leave our little health communities and go venture out in the world and be like, oh, right. It’s still a big deal to buy low fat Frito Lays or something.

Chris Kresser: Yeah.

Steve Wright: Being part of that.

Chris Kresser: Other things were nonfat lattes, soy milk lattes. Yeah, we’re in a bubble, and I sometimes forget, like, oh, yeah, everybody doesn’t know this.

Steve Wright: Did you try to scoop up their yolks? Like, no, no, no! Give me those!

Chris Kresser: No, I didn’t. You know, I’ve said this often on the show. I’m not the type of person generally that offers unsolicited advice. If they would have asked me, I would have answered, of course, but this was a situation where I found it pretty hard to hold my tongue! I want people to be healthy, and I want to help them, but at the same time, I’m respectful of people’s choices, and I don’t want to be that guy.

Steve Wright: Right. And you’ve been through the journey that we all reach at some point, which is that you recognize that unless someone’s asking for help, just because you see an opportunity, unless they’re asking, they actually don’t want any help.

Chris Kresser: That’s right. And I was one of the speakers at this event, and I was speaking about how paleo kind of saved my life and how transformative it’s been in my practice and just my own take on paleo as a starting place and not a destination, but I was speaking to a room that was probably 80% vegetarian and vegan! I really enjoyed it. It was one of the best conferences I’ve ever been. It was at Miraval, which is this beautiful eco-resort in Tucson. So I’m definitely not complaining about the group. I had a fantastic time and met some great people, but it was interesting because I’ve spoken a lot at paleo conferences and Ancestral Health conferences and Weston A. Price and things like that, where everyone’s kind of on board, and this was a different situation, but the talk was really well received. I had a few people come up to me and say, I’m a vegetarian right now, but I think I really need to try paleo based on your talk. It wasn’t my intention to convert people, but it looks like that might have happened at least in a couple of cases.

Steve Wright: I think we all share a lot in common with vegetarians and vegans, and we’ve talked about this before. They obviously, as you mentioned, are very well in tune with the environment, with their health, with food, and so – we probably should just stop there and get back to cholesterol!

Chris Kresser: Yeah, exactly. We should. But that was the dominant theme of the weekend. I was hanging out with Rich Roll, who is a vegan super-athlete, ultra-marathoner. The guy has done, like, five triathlons on five different Hawaiian Islands in seven days, so obviously it’s working for him! My thing is I’m interested in what works for the greatest number of people. We’ll come back to this. You’re right, we have to get back to the topic at hand, but it was an interesting diversion.

Steve Wright: Yes, of course.

How Saturated Fat Affects Cholesterol Levels

Chris Kresser: So the saturated fat studies. We talked about cholesterol in the diet. Now we’re going to talk about saturated fat. Most studies actually show that saturated fat, on average, does not affect blood cholesterol levels. There was a big study that recently came out about that. That’s surprising to a lot of people because a lot of people have seen in their own life that saturated fat does have an effect on their cholesterol level. In fact, I would say probably 20% of my patient population are people that have switched to paleo, to a higher saturated fat diet, and watched their cholesterol numbers go through the roof, so I guarantee you, it happens. It happens and it’s not rare. So with saturated fat, it’s a similar thing to cholesterol. There are hyper-responders. There are people who experience a significant shift in their blood cholesterol levels when they eat more saturated fat and experience a significant decrease in their cholesterol levels when they eat less saturated fat.

This gets back to the original question. The reason why some people do experience a drop in their cholesterol levels when they stop eating saturated fat is quite simply that saturated fat does affect blood cholesterol levels in some cases. I haven’t seen an exact percentage breakdown, like 70/30 with the dietary cholesterol, for saturated fat, but I would guess it’s probably around the same. And the next obvious question is, what’s the mechanism? Why do some people experience that increase in blood cholesterol when they eat saturated fat? And the answer is we don’t know for sure, but certainly there are genetic mutations or genetic differences that can affect that. Like, ApoE genotype can affect cholesterol levels and response to saturated fat. LDL receptor mutation, so each cell in the body has a receptor for the LDL particle, and there are some mutations in the genes that produce those receptors so that they don’t get produced adequately, and so the cells have fewer LDL receptors on them, which means that LDL just kind of is homeless in the blood and stays in the bloodstream for longer, so you can get high cholesterol and LDL levels for that reason.

The Relationship between Saturated Fat Intake and Heart Disease

Through experimentation, you can kind of figure out where you fall on this spectrum, but that leads us to the second main question that we’re going to talk about on the show, which is, OK, so let’s say you determine that you are one of these people for whom saturated fat affects your blood cholesterol levels, and you eat a lot of saturated fat, low carb paleo diet, and your total and LDL cholesterol go way up. Probably your HDL has gone up, too. Does that matter? That’s the real operative question here, and there are a lot of different ways to get at the answer to that question.

One is to look at the relationship between saturated fat intake and actual heart disease. What we’ve been talking about so far is the relationship between saturated fat and blood cholesterol levels, but looking at that is looking at an intermediary, right? The only reason people are concerned about cholesterol levels is because of the assumption that increased cholesterol increases your risk of heart disease, so why not just look directly at the relationship between saturated fat intake and heart disease and skip that intermediary marker, cholesterol? Of course, a lot of studies have looked at this, and there was just a large meta-analysis published, I think, in the Annals of Internal Medicine, I can’t remember, and it showed that there was no relationship between saturated fat and heart disease. And several other large studies have shown that, and some studies have any shown an inverse relationship between saturated fat intake and stroke, which means the more saturated fat people ate, the lower their risk of stroke. If we look at it from that perspective, it doesn’t seem like eating more saturated fat, even if it increases your cholesterol levels, would increase your increase of heart disease, but there are other ways to look at it, too, and they tell a little bit different of a story.

We know that LDL particle number is a better indicator of heart disease risk than total cholesterol or LDL cholesterol, which are only weakly correlated with heart disease risk. The difference between the two, if you haven’t been listening or reading for a while, is we can use an analogy. Imagine the bloodstream is like a highway. The cars on the highway are the lipoproteins. LDL stands for low-density lipoprotein. And then the cholesterol inside of the particle is like the passengers inside of the car, and the job of the lipoproteins, like LDL, is to transport cholesterol and other nutrients all around the body just like the cars transport passengers to wherever they’re going. For years, we have been focused on the amount of passengers in the cars or the amount of cholesterol in the LDL particles as the driving risk factor for heart disease, but now we know that it’s really the number of cars on the road or the number of LDL particles in the bloodstream that is the most dominant risk factor from a lipid perspective because, if you extend this analogy, if there are a lot of cars on the road, there’s a much bigger chance that one of them is going to veer off and crash into the side of the road. In this analogy the side of the road is the fragile lining of the artery, which is only one cell deep, and when an LDL particle penetrates the lining of the artery, it causes a tear, which then initiates the whole process of plaque formation, and then plaque forms, some of that plaque ruptures, it occludes the artery, and that’s a heart attack.

What the research suggests is that, all other things equal, if you have a higher LDL particle number, you are in theory at greater risk for heart disease. The concern is when people go on a really high fat diet and their LDL particle number shoots up – and I’ve seen this happen a lot – is that a problem? Is that a really big concern in terms of the risk for heart disease? So now we have two kind of different ways of looking at this that lead us to different outcomes or different ideas. We have the fact that there’s no connection between saturated fat and heart disease, but then we have this fact that mechanistic studies pretty clearly suggest that having a lot of LDL particles in your blood puts you at greater risk for heart disease.

So there’s a third thing that you need to be aware of, which is that 90% of people who have high cholesterol who go on to have a heart attack have another major risk factor, like high blood pressure or smoking cigarettes, so that means that high cholesterol alone 90% of the time is not sufficient to cause a heart attack.

If we take two hypothetical people and one person has high LDL particle number but they have no other significant risk factors, no significant family history of heart disease, like, their parents didn’t die of a heart attack before the age of 60, they have normal blood pressure, they’re sleeping well, they’re eating a good diet, they’re moving, and they’re healthy, but the only thing that’s wrong is they have this high LDL particle number, and you compare that with someone who has a high LDL particle number and who’s overweight, high blood pressure, smoking cigarettes, strong family history of heart disease, and several other risk factors, it probably goes without saying that the risk of those two people is going to be very different. The former will be at relatively low risk of heart disease, and the latter will be at relatively high risk for heart disease.

But let’s add a third person to this equation, which would be someone who not only is eating a good diet and taking care of themselves and all of those other things, but also has normal LDL particle number. To me, it also makes sense that that person is going to be at lower risk than even the person that had all of the great diet and lifestyle factors but the high LDL particle number. We don’t know that for certain, but based on what we currently understand about how heart disease happens, that makes sense to me.

You can see how this starts to get a little complex. It starts to really depend on biochemical individuality, and we start talking about shades of gray and degrees of risk rather than black and white, you’re at risk or you’re not at risk.

Steve Wright: Chris, a lot of people, I think, probably haven’t had an LDL-P test run, but they may have had the HDL, LDL, and total cholesterol panel typically run.

Chris Kresser: Mm-hmm.

Steve Wright: I know we’re in shades of gray here, but when we’re talking about hyper-responders and these numbers moving around, are there certain benchmarks of either one of those three values that would make you say, well, you know, family history of heart disease plus these numbers hitting a certain thing, you should be looking at an LDL-P right away to begin and then reflect on what Chris just covered on where your shades-of-gray risk comes in?

Chris Kresser: Yeah, great question. The ratio between total cholesterol and HDL – so you get that by dividing total cholesterol by HDL – should be less than 4, and there’s some research that actually indicates that’s just as accurate in terms of predicting heart disease risk as LDL particle number. Let’s say you have a total cholesterol of 220, but your HDL is 80. Your ratio there is going to actually be less than 3, and so that would suggest that your risk of heart disease isn’t higher even though your total cholesterol is technically above the limit that they suggest, which is 199, at 220.

That’s a cheap way to get a general idea without measuring your LDL particle number, but here’s the bottom line: Your risk for heart disease depends on a number of factors, one of which is the LDL particle number or total cholesterol-to-HDL ratio, but it also includes markers of inflammation because we know that the pathogenesis of heart disease is driven by inflammation, so things like C-reactive protein; Lp-PLA2, which is also called PLAC, that’s a specific marker for cardiovascular inflammation; lipoprotein(a); fibrinogen, which measures your tendency to clot; factor V Leiden, same thing. There’s a whole bunch of other markers, and then you can get things like a calcium score and a CIMT, carotid intima-media thickness test, which measures the flow of blood through the carotid artery. These other tests can also help determine whether you’re at risk for heart disease. If you have slightly high cholesterol and you have normal inflammatory markers, zero calcium scan, and the CIMT is clear, that’s a different clinical picture than having high cholesterol with high inflammatory markers and a high calcium score.

You really need to consider all of these different risk factors and, of course, your family history, your diet, your lifestyle, and your stress levels because it’s a whole life picture here. All of these factors are important. In fact, stress might be more important than all of them. There are some studies that suggest that stress is the single greatest risk factor for heart disease, and there was a study on African-American men who had already had a heart attack, and they taught them to meditate, and the group that did the meditation had a greater decrease in their risk for heart disease than the group that took statin drugs, so we know that stress management is crucial for reducing the risk of heart disease, and I just think it makes sense to consider this from a systems perspective, a functional medicine perspective.

There are also a lot of other things we can look at that directly can cause higher cholesterol levels. There are more underlying problems, like gut issues, adrenal problems, thyroid problems, and metabolic problems, so there’s a lot more to this than originally meets the eye, and if you want to learn more, there’s a free eBook on my website called The Diet-Heart Myth, and it has a lot of great information, and then there’s, of course, the High Cholesterol Action Plan if you really want to go into detail about this and learn more about the types of testing that I recommend and what to do if you find that you’re one of these people that does have high LDL particle number and higher inflammatory markers. I created that program because there was such a huge need for a path for people that are in this situation, and so I developed a kind of decision tree and algorithms to help you figure that all out, and that’s at HighCholesterolActionPlan.ChrisKresser.com if you want to check that out.

Steve Wright: Which are all amazing resources that I’ve definitely gone through. This has been a great primer, Chris, and I’m glad that you have those extra resources for those people who want to dive deeper. As we wrap up this show, I can’t help but leave a cliffhanger here with this idea that’s rolling around in my mind based on something you said earlier, which is that I had forgotten that the blood vessels, which arguably are kind of important for our health, are only one cell thick, and it brought me back to the gut lining, which is only one cell thick.

Chris Kresser: Mm-hmm.

Steve Wright: It’s quite fascinating that our bodies, these very sensitive membranes, these very sensitive systems that keep us all put together, are only relying on one cell. That’s really amazing.

Chris Kresser: Yeah, it’s amazing. We’re so resilient on one level and we’re so fragile at the same time. I’m going to be definitely talking about the relationship between the gut and cardiovascular disease, which is a fascinating topic that hasn’t really been explored that much, in my second book. We’re just getting ready to start shopping it around actually, and it’s going to be a book about – guess what? – the gut, particularly changing the paradigm so that people really understand that healing the gut is the key to overall health, even if they don’t have gut symptoms. I really want to shift the discussion in that direction.

Steve Wright: Awesome. I can’t wait for it, Chris. Well, this has been a great talk.

Chris Kresser: Yeah. I’ve enjoyed it!

Steve Wright: All right. Well, as Chris mentioned at the beginning of the show, let us know your feedback as we change the show over and start using the SpeakPipe application, which is ChrisKresser.com/PodcastQuestion. And if you want more information in between these shows, make sure you’re following Chris on Facebook, which is Facebook.com/ChrisKresserLAc, and then over at Twitter, which is Twitter.com/ChrisKresser.

Chris Kresser: Yeah, we’re also on Pinterest now and starting to do more over there, so all you Pinterest fans, come check me out. I think it’s Pinterest.com/ChrisKresser, but you can just search and find me. We’ll let you know on the next episode!

Steve Wright: All right. Thanks, Chris. It’s been a good one.

Chris Kresser: Thanks, Steve. Thanks, everyone. Talk to you next week.

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Join the conversation

  1. I don’t know about most people, but for myself, I just don’t have the time to wade through all this chit chat to get at the meat of the information. Personally, therefore, I think these podcasts are a colossal waste of time, and ditto for the transcripts. Who wants to wade through all this stuff? Is it all for “marketing”?

    Anyway, why not provide an abstract or summary or conclusion paragraph or two at the end or, preferably, the beginning of these?

    • I enjoy podcasts on various subjects, but alas, too many are simply long winded
      Editing would be greatly appreciated, for one thing
      Many could be broken down into separate podcasts, but the common podcast MO is to cram as much diverse information as possible into a pod
      20 minutes on one topic is my limit
      One “podder” I enjoy breaks up his pod with cooking and eating damn cookies! Why not a separate cookie cooking pod, I scream…But, alas, other podders break up an otherwise great pods with too much non sequitur stuff
      I get selling something to pay the freight, but come on, off with the non sequitur

  2. The assertion that LDL particle size is a good predictor of heart disease, particularly myocardial infarction, is far from settled science. As long as 2 years ago, Dr. Thomas Dayspring, one of the chief proponents of this idea, admitted in an interview with Jimmy Moore that he couldn’t explain how he could have sky-high LDL-P and a zero calcium blockage score.

    More recently, family physician Dr. Rakesh (Rocky) Patel wrote a blog post “Does LDL-P Matter?” (http://tinyurl.com/9vlsyfs), in which he described improvement in his carotid intima thickness despite a significant increase in LDL-C and LDL-P after switching to a carbohydrate-restricted diet. In correspondence, he’s said, “High LDL-P on a very low-carb ketogenic diet is an understudied issue. Unfortunately, all the trials in the literature involve the Standard American Diet. Really, I think that before we engage in any discussion regarding cholesterol, one has to establish if atherosclerosis is present in any form. So using testing like CT calcium scoring, carotid intimal thickness testing (CIMT), and genomic scoring (Corus CAD, Cardiodx) becomes imperative and certainly provides context to the lipids.” You can read the context for this comment and find links to additional blog posts from other experts on this topic at http://www.lowcarbdietitian.com/blog, the entry ”
    Plant-Based vs. Low-Carbohydrate Diets: Presenting the Evidence,” the section “What Do The Experts Say About Very High LDL-C and LDL-P?”

    If you watch Dr. Peter Atilla’s video “The Cholesterol Conundrum” (https://www.youtube.com/watch?v=fuj6nxCDBZ0&feature=youtu.be), at the 56:30 marke, he talks about a study showing that high Apo B particle numbers hardly raise risk in those with fasting insulin below 12. Over 12, particle number matters — a lot (which would explain Jimmy Moore’s situation).

    And according to yet another study (http://www.ncbi.nlm.nih.gov/pubmed/9714128), the ApoB/apoA1 ratio is a better predictor than either alone yet Dr. Dayspring doesn’t seem to address it. The best way to increase Apo A1 is to eat fat. Chylomicrons contain apo A1 and are actually better than HDL at reverse cholesterol transport.

    Frankly, the issue of how much cholesterol sub-types matter is in the early stages. It’s much too soon to make *any* assertions about cholesterol sub-types or particle number predicting CVD.

    • I believe that I said as much during the podcast. If we’re talking about lipid markers, I think LDL-P is more accurate a predictor than LDL-C. But I also mentioned that >90% of people with high cholesterol that go on to have heart attacks have another significant risk factor, like hypertension. Having a high LDL-P in the absence of any other risk factors may not put you at significant additional risk. I am constantly reminding my patients of this.

      • Chris,

        A few questions…

        – What should I eat for breakfast?
        – Is it okay if I chew gum?
        – Can I listen to Frank Sinatra on my iPod?
        – What color shirt should I wear?
        – Should I get a new job?

        Good grief. How do people function on their own?

        It wouldn’t hurt my feelings, if you closed the Comments on your blog. People are endlessly needy and will drain you dry.

        Thanks for your work.


      • What about oxidised LDL. I have high LDL and frightenly high ox LDL on a paleo diet. I have a client with the same. We are both post menopause – this seems to be something to do with it. I’m ApoE e3/3. But my LDL went up to 285 at its peak. I’ve made diet changes and it’s come back down to 200. Before menopause despite having Hashimotos, my LDL cholesterol 115.

  3. Good podcast Chris as usual.

    You mentioned that some countries like canada removed their limit on dietary cholesterol.
    Well it seems our very own dietitians did not get the memo.


    Here is what they say on their “fact sheet”

    “Cholesterol is not an essential nutrient. Your body can make what it needs. Therefore there is no recommended intake for this type of fat. You should consume as little dietary cholesterol as possible while still enjoying a nutritious diet. To help you make healthy choices the following guidelines are suggested:
    If you do not have heart disease, eat less than 300 milligrams (mg) of dietary cholesterol per day.
    If you have heart disease or are at risk for heart disease aim for less than 200 mg of dietary cholesterol per day.”

  4. There is an interesting inverse question. We know that low cholesterol levels are associated with shorter life, various diseases. What do you know about causation vs association in this? Are levels low because they are sick, do the low levels cause illness, or what?

  5. Thanks for a great podcast Chris. Especially like how you reference studies citing the “averages”, often leaving out the important details for that smaller percentage that may react oppositely.

    Heart disease is multi-factoral and one cannot simply look at cholesterol or NMR’s for that matter. Ive seen people who’ve had great NMR’s witl LDL-P under 1000, small-LDL’s under 100, high HDL, yet still have heart disease. But then you see they have high glucose. The same goes for inflammatory markers, some of these can still be normal in the presence of heart disease, so the entire big picture needs to be looked at.

  6. I want to know about particle size. LDL comes in large and small and from what I understand the smaller are the ones that are dangerous. In Europe they test this.

    • I am unable to get a paticle size test here in the UK, if anyone knows of where to get one please speak up. The next best thing is to test your Apo(b) reading which I believe correlates with particles size. I had mine tested with Blue Horizon

    • Yes, I got mine tested 12 years ago and had the good pattern i.e. plenty of the big fluffies and not so much of the little dense billiard balls that do the damage. It was called ‘Pattern A’. I got it done through a study I participated in for our local Lipid and Diabetes Research Group.

      The test was titled LDL Cholesterol Subclass Phenotype and the results were given as Average LDL Size (26.8 nm in my case) and Particle Size Distribution: Pattern A which was described as: Phenotype A is characterised by a predominance of large, buoyant LDL while Phenoype B is characterised by a predominance of small, dense LDL which is associated with increased risk of coronary heart disease.

    • Particle size is irrelevant. Search Chris’ website, and you’ll find a comment in an interview with Chris Masterjohn interview about the studies that initially indicated that LDL particle size was important. Later, these studies were re-analyzed and the importance of particle size disappeared.

    • LDL size loses significance after adjustment for LDL particle number. In other words, number is more important than size.

  7. You mention particle numbers but don’t address particle size. From what I have been reading the particle size of cholesterol is the important factor and when the cholesterol numbers go up after eating healthy fats usually the particle size is larger and not a cholesterol that is apt to be implanted in artery walls.

    • I quote Dr Peter Attia…..”A particle is a particle. Statistically speaking, someone with lots of large particles will have fewer, but once you know the particle number, size doesn’t predict risk.”

      • Rory, I am in no position to argue, but the LDL “pellet” size particle through the years would increasingly lodge in the wear and tear of the artery…The “fluffies” would float on through the blood stream…As a non pro here, I would think as these pellets built up, the artery would increasingly grow in both size (“rust”) and inflammation from other sources that could get snagged on the artery lining at these points, ultimately closing off the artery…Ergo, the amount of the “pellet” LDL would surely be a good number to know and work with, because of the potential inflammation

        • The takeaway is, having all large LDL particles but a high LDL-P count negates the benefits of having large particles. Yes, most large is better than small-LDL’s, but becomes somewhat of a moot point, if your LDL-P count is high.

          • What drives me crazy is experts come down on all sides of this issue…Frankly, I avoid Carbs, i.e., sugar as well as wheat products, because I lost 70 lbs and feel better without bread, crackers, cereals, and sweets…Also nice to have a healthy BMI

  8. LDL and HDL both consists of 5 “carriers”
    The culprit of LDL is the “pellet” size carrier of the 5 — This is what gets wedged into artery infections, etc damage
    Obviously, cholesterol will be found in this occlusion, but the cholesterol is healthy as long as it is flowing or soaking the brain
    What we want are the large, fluffy other carrier types of LDL and HDL

    I like your new format of shorter, to a specific point show

    • Another point in the insanely confusing world of Cholesterol is the Triglyceride/HDL Ratio (even to the professionals)

      In lieu of a “particle size evaluation,” this is a quickie test I can secretly conduct on myself, though I go with what my cardiologist recommends

      Even trying, the Worlds of Cholesterol and Fat is insane with even the professionals all over the freaking map — These worlds belong to the universe of the Kennedy Assassination Conspiracies: who is right when so many on paper are Officially knowledgeable?

  9. Hi Chris – thanks so much for article. You are right, confusion reigns in this area of health. Am I right in thinking that excess blood glucose is a major dietary culprit for inflammation which damages arterial walls (as per LDL) to which the body responds by increasing cholesterol to plug the hole. I’ve been taught to think if cholesterol as they guy on the white horse and excess blood glucose as the bad guy. Or is this too simplistic for most individuals?

  10. Great podcast. Kudos to Chris for acknowledging the ApoE4 connection. As a 4/4, I’m working on staying mildly keto-adapted to help protect my brain. My breakdown is 65% fat, 20% protein and 15% carb. My diet is decidedly Mediterranean, with lots of MUFAs. I’m also exercising daily and practicing mild CR. All biomarkers are great and LDL-P was 1089 at last count.

    I appreciate your questions, Kevin and your experience Elaine. I acknowledge the struggle all E4 carriers are experiencing with wildly contradictory advice from the medical community. Join us at http://www.apoe4.info as we try to hammer out a comprehensive prevention protocol. Chris, you’re welcome to join as well. We site you often 🙂

    • Thanks Julie. Yes, the suggestions for 4’s vary. I did a lot of cross referencing and testing , diets (from keto to AIP to all plant/no grain/legume which is what I’m thriving on now) on myself to gauge the best protocol. It’s like being blind. Found the FB group too. Thanks!

    • That’s because LDL size loses significance after adjustment for LDL particle number. In other words, number is more important than size.

      • Chris
        need your help here

        My wife dealt with many bouts of sinus infections and was given may doses of antibiotics. She then began having serious gut issues. She switched to a pure paleo eating meats, veggies, butter, coconut oil, etc. things got worse and she eventually was diagnosed with ulcerative colitis earlier this year. They wanted to start here on steroids but she decided to go with a GERD diet with bone broth, cooked carrots and broccoli coconut oils and other GERD foods. She has stopped all grains, sugar, hi carb foods. Trying to stick with It’s been 3-4 months and she has improved greatly. Also her achy hands and feet have stopped aching. Her allergies were gone too. She lost weight and overall the colitis symptoms (mucus and runny stools) and began having regular stools and everything seems to be working right. She has always had higher cholesterol thinking it’s due to FH. Like above the 200’s. she is 49 years old 5’2 120 lbs her BP is like 100/60 and pulse is usually in the 60’s. she is in great shape. She recently had here blood work done so we could see if she had the big fluffy partials. We got the results back and we were very shock.
        Here are the results
        Total 398
        LDL-C 290
        HDL-C 104
        TRI 58
        Non-HDL-C 294

        Apo B 198
        LDL-p 3150
        sdLDL-C 65
        SDldl-c 23
        Apo A-1 170
        HDL-P 48.4
        HDL2-C 50
        Apo B:Apo A-1 ratio 1:16
        Lp (a) 22

        Hs-CRP 0.4
        Lp-PLA 303

        All were optimal except
        Her free fatty acids were 1.40

        TSH 1.96
        T4 7.1
        T4 free 1.27
        T3 88

  11. Hi Chris,
    The tests you mentioned for hart disease risk, would that include heart failure (dilated cardiomyopathy)? It’s just that it runs in my family and I want to check for that risk of heart failure. Can you recommend tests to check for this?
    I recently had my CPR measured at 20+. I tend to have low blood pressure. 90/60 sometimes less. Other than that I look healthy-ish being naturally slim.

  12. Hi

    Where can one get a thorough battery of tests such as those outlined in the above discussion. I am talking about a clinic or doctor that will really drill down into your individual characteristics and assess your risk

  13. The NMR was mentioned above (the LDL-P test)–I just had one done, as well as a CMP, and have a question: when looking at cholesterol numbers (TC, HDL, LDL etc), which test is more accurate for determining these numbers? I asked Jimmy Moore, and got no answer, other than “welcome to the world of inexact science.”

    Should I be favoring the NMR over the CMP when it comes to cholesterol numbers? Which is most accurate? Don’t all the HD and IR risk calculations depend on accurate cholesterol numbers?

  14. I have low total cholesterol, at times under 110, never over 150. Since going low carb high fat, I feel better, but I also have a brother that is handicapped from a stroke (unknown etiology) at age 49. Far from being a hyper-responder, I’m not concerned about saturated fat, but I’m still a little freaked out that I am of the same nature as my brother. I like the Paleo approach, real foods, outdoors, sunshine, play, and avoiding a stressful lifestyle, and I’m hoping the rest (risk factors) falls into place. My parents are elderly, I don’t want them saddened by both of their sons having strokes.

  15. Thanks for addressing this topic, it is a very timely one for me. I have had high cholesterol, ranging from 280 to 310, after I began having adrenal fatigue (or HPAD) and a worsening of digestive issues, with SIBO for probably a few years. I suspect these issues could be underlying factors in the high cholesterol, but the numbers go over 300 when I eat more animal fat and coconut oil, which I’d hoped would help with inflammation and healing. I am wondering if I should focus on lowering cholesterol by eating less saturated fat, taking something like red yeast rice (this has helped before), or if it is more important to deal with the potential underlying problems of gut and adrenal health. Or both at the same time! It’s hard to know if the benefits of the animal fat and coconut oil outweigh the negatives.

    • Hi Melinda, a few questions come to mind:
      1) Are you exercising? Exercising can help reduce cholesterol.
      2) Are you taking supplements? Pantethine reduces high cholesterol better than many cholesterol-controlling drugs.
      3) Are you eating sugars/carbs along with the coconut oil and other saturated fat? If so, that could be part of our problem. Sugar + saturated fat=dangerous cholesterol levels.
      4) Are you taking CoQ10? You really, truly need it if you are taking red yeast rice, which is a very dangerous item to be adding to your diet. Like statin drugs, red yeast rice increases the need for CoQ10 and can cause damage if you’re not taking it.

      • hi Nils,

        1) I get light to moderate excercise, mainly walking. I would like to do more but am limited by fatigue.
        2) Didn’t know about pantethine, will have to look into it.
        3) Do you mean fat+sugars/carbs at the same meal? Then yes, in the form of fruits and tubers, about 60-95 g of carbs per day. I didn’t realize this was a problem. I don’t go lower on carbs due to adrenal issues and don’t go higher, at least for now, due to the SIBO. I’ve also read that it’s good to have some fat w/fruit.
        4) My red yeast rice suppl. does have coQ10 in it.

      • I also take curcumin, which I assumed was only for the inflammation part of things but after Googling saw that it reduces LDL too. I’d been slacking on that before my latest lab of 328, which they did not tell me to fast for (I thought I was just getting a vit.D test). Seems the increase could be due to a few things and I need to try to balance the variables better.

  16. Nothing new, still zero specific guidelines on how APOE 4/4 should adjust paleo diet. More saturated fat or less? How much more or less specifically in numbers? What macro-nutrient percentage breakdowns to shoot for? What foods to avoid (specifically because of APOE4/4), what foods to add? This the type of questions podcasts on cholesterol and heart healthy should start now, get those answered in first 10 minutes and then get 1000 deeper into APOE topic. Otherwise, it is just noise that is 5 years old.

    • I’m an APOE4 and was doing a paleo approach. I had terrible results lipid wise (blood sugar levels were great though) and also had some funky heart stuff going on sitosterol wise. I really took Gundry’s advice to heart and completely reversed my diet. Went plant based, my numbers evened out and my blood sugar stayed the same which was a concern of mine because I don’t want high triglyc or insulin levels (yup, eating more carbs obviously) and I stick to the ratios my heart lab suggested (under 15% fat for an APOE4). I personally am thriving and do believe that genetics (as well as gut bacteria) play a huge role in the equation.

      • Elaine, I agree that gut bacteria, gut motility, and gut lining integrity will play important roles here, though connections with conditions outside the gut have not been plain until the last year or two. Pieces of the jigsaw puzzle are starting to fall into place rapidly now, numerous very good minds working on this, lots already published and more to come, and I expect this topic will be a paradigm shift and sea change in integrative medicine even within the next 1-3 years.

    • Diet for APOE4’s (E4/4, E3/4) has gotten a lot of discussion on 23andme.com community boards, and on ww.apoe4.info. It’s a highly controversial topic at present, I suspect mostly because of individual differences and current status that could be surfaced via related testing to give a better integrative understanding of the person’s case. Estrogen levels at menopause and later seem to be a key factor to keep in view for E4 women. A person’s age can influence appropriate diet, and I think a lot can change between the mid-50s to mid-60s and beyond, at least it has seemed that way for me and others I know. There are a vast number of references on the two sites above for anyone serious about delving deep.

      • Yes Carol, my advice is to test , test , test protocols to see which one works for you as an individual.

    • This kind of response always cracks me up. It might be “5 years old” for you, but the average person on the street still thinks dietary cholesterol is harmful and should be avoided.

      There is no “formula” for APOE4 that applies to everyone with that mutation. I can tell you from doing a lot of genetic testing that all people with this mutation do not respond to saturated fat and dietary cholesterol in the same way. So as Elainie says, it’s still necessary to experiment to see what works for you—as I’ve always recommended.

      The same is true for many other single gene mutations, like MTHFR. I’ve had patients that are homozygous for C677T and are methylating normally according to functional testing, while others are heterozygous for A1298C (which isn’t supposed to cause problems) and they have low folate, glutathione, SAM, and other issues with methylation. Genes are only part of the picture.

  17. Thanks for addressing this! The minority of folks that do respond dramatically to dietary fat or cholesterol often get left out of the conversation.

  18. At one point in the interviewer, Chris brings up Rick Roll as an example of a vegan who seems to be getting good results eating a totally vegan diet. I did a web search for images of Rolls, and watched a video interview with him; he doesn’t look too healthy to me. He looks muscular, but also emaciated.

    A lot of vegans seem to have a kind of hyper energy, which again doesn’t look relaxed or healthy to me… like they can’t calm down or stay still. I’m not saying that’s true of all vegans, but it’s the impression I get, for example, from the vegans who have channels promoting veganism on Youtube… they are hyper, always excited, always “on,” and seem to talk and jabber in a way that frankly comes off as weird. People who eat paleo diets including healthy meats and fats tend to have a bit more meat on their bones, and seem more calm and down to earth.

    Just my two cents.