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: 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.
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. Thanks, Chris. It’s been a good one.
Chris Kresser: Thanks, Steve. Thanks, everyone. Talk to you next week.