Lipoprotein(a) is a small, dense, highly inflammatory lipoprotein and its level is strongly influenced by genetics. While Lp(a) is an independent risk factor for heart disease, there are interventions to consider before taking statins or baby aspirin.
The production of Lp(a) is controlled by a specific gene. So if you have a mutated version of that gene, then it can lead to higher Lp(a) levels. There are other genetic relationships, but Lp(a) is pretty strongly genetically determined. You could be doing everything right, frustratingly, and still have a relatively high Lp(a) level. The thing to understand is that Lp(a), in studies, has been associated with high risk of cardiovascular disease and heart attack, and it’s been validated as an independent risk factor for heart disease. That means your other risk factors can be normal, but if Lp(a) is high, your risk for heart disease will be higher than if Lp(a) wasn’t high.
In this episode, we cover:
2:34 What Chris ate for breakfast
4:43 What is lipoprotein(a)?
10:10 Four things to consider about Lp(a)
21:34 Other markers to keep an eye on
29:46 The Paleo Cure
Links we discuss
Steve Wright: Good morning, good afternoon, and good evening. You are listening to the Revolution Health Radio show. I’m your host, Steve Wright, co-author at SCDlifestyle.com. This episode of Revolution Health Radio is brought to you by 14Four.me. 14Four.me is your healthy lifestyle reset program. I don’t know if you’re like me, but you’re probably going home for the holidays. You might lose some sleep due to travel. You might indulge in some sweets because they taste great. You might fall off your exercise routine because you don’t have availability to do gyms, trainers, and things like that while you’re back home. What I want to let you know is that Chris Kresser has put together 14Four.me for all these types of scenarios, and just for everybody else who’s looking for a reset for their life. If you’re just not feeling the way you want to feel, if you’re still having some digestion issues, some sleep issues, some energy problems, 14Four.me will be your solution. It’s a step-by-step program that walks you through stress reduction, diet enhancement, movement, as well as…
Chris Kresser: Sleep.
Steve Wright: Sleep, as well as sleep. All four of those things are the key to having a great life.
Chris Kresser: Maybe you need some more sleep, Steve.
Steve Wright: I might need more sleep. Anyways, 14Four.me, check it out. That’s what this show is all about. Just kidding. With me is integrative medical practitioner, healthy skeptic, and New York Times bestselling author, Chris Kresser. Chris, take it away, man. I need to stop talking.
Chris Kresser: All right. We’ve got a great show today, a good question. I’m just hunkering down for the storm that’s coming in. We were warned to stock up on some water and do almost like earthquake prep, because there’s apparently a crazy storm coming that might knock out power and wreak some havoc around here.
Steve Wright: Really? Is it like an Arctic blast or what?
Chris Kresser: I don’t know. It’s supposed to be just a crazy, heavy rainstorm, like two to three inches of rain in a short period of time. We’ll see. Sometimes they warn about these things, and they never really materialize. It should be interesting.
Steve Wright: Hey, go with the Boy Scout motto. Better be safe than sorry.
What Chris ate for breakfast
Chris Kresser: That’s right. Yeah, let’s dive in. I know you’re going to ask me what I had for breakfast. That won’t take long because this is my breakfast right here: just coffee and cream this morning. Intermittent fast day. That’s it. Nothing too exciting.
Steve Wright: Well, you know what? When a storm’s a brewing, you have to simplify life, so I get it.
Chris Kresser: All right. This question is from Isabel. Let’s give it a listen.
Isabel: Hi, Chris. Thanks for your podcast. I am a female, 44 years old. I recently discovered that I had a SNIP that predicts high Lp(a) levels. So I measured my Lp(a) and it’s at 92 mg/dL. Otherwise, my LDL is 110 mg/dL; HDL is 75 mg/dL; and I have low triglycerides. My doctor wants me to take a statin and baby aspirin to lower my cardiovascular disease risk. I already know that there are some alternatives to baby aspirin from your podcast, but should I really go for the statin to reduce it between 40-70 mg/dL? What do you think? Thank you very much again for your podcast.
Chris Kresser: Thanks, Isabel, for your question. Please do keep the questions coming, people. As you have no doubt noted, that’s the new format for the show. I guess it’s not that new now. This is all listener-question driven, so please do keep sending us your questions. What’s the link, Steve?
Steve Wright: ChrisKresser.com/podcastquestion
Chris Kresser: So head over there and record your question. It helps us to make sure that the show is relevant to your interests and what you want to hear about.
What is lipoprotein(a)?
Anyhow, lipoprotein(a). We’re going to call it Lp(a), so I don’t have to say that throughout this whole episode, and that’s often what it’s referred to anyways. Lp(a) is an LDL. It consists of an LDL particle, which contains an apolipoprotein B molecule linked to another apolipoprotein molecule called apo(a). That’s quite a mouthful. Essentially, it’s a small, dense, highly inflammatory lipoprotein. That’s really kind of the takeaway and what you need to know about it. Lp(a) levels are strongly influenced by genetics. That’s probably the number one factor that influences their level, unlike some other lipoproteins like LDL and HDL, which are pretty heavily influenced by diet, exercise, and lifestyle. Lp(a) I think can be affected by those things, but not nearly to the extent that LDL, HDL, and total cholesterol are affected.
Steve Wright: Just for the listeners who haven’t gone back and reviewed High Cholesterol Action Plan or the rest of the podcast about this, HDL, LDL, and Lp(a) are all separate types of lipoproteins? Does Lp(a) stack underneath one of those?
Chris Kresser: Lp(a) is more related to LDL because it’s an LDL particle that contains apolipoprotein B linked to apo(a). So it’s a subclass of LDL but it’s a more atherogenic form of LDL. That means it’s a type of LDL that is linked to a higher risk of heart disease, much more so than LDL itself. The production of Lp(a) is controlled by a specific gene. So if you have a mutated version of that gene, then it can lead to higher Lp(a) levels. This is more common in African Americans and less common in Caucasians. There are other kind of genetic relationships, but what I’m trying to say here is that Lp(a) is pretty strongly genetically determined. So you could be doing everything right, frustratingly, and still have a relatively high Lp(a) level. The thing to understand is that Lp(a), in studies, has been associated with high risk of cardiovascular disease and heart attack, and it’s been validated as an independent risk factor for heart disease. That means your other risk factors can be normal, but if Lp(a) is high, your risk for heart disease will be higher than if Lp(a) wasn’t high. Now I’ll come back to that at the end, because calculating or figuring out your overall risk for heart disease is pretty complicated. You can never just do it based on one marker. But the point is that Lp(a) is an independent risk factor for heart disease. That’s because Lp(a) collects in the arterial wall. It’s thought to be involved in clotting. So it can increase the probability of endothelial damage because of that. And because it’s so small and dense, it kind of penetrates the fragile lining of the endothelium, which is the lining of the blood vessel. It’s thought to play a role in the rupture of plaque, which is the initiating event in a heart attack. It also is thought to carry a significant amount of oxidized fat. Oxidized LDL, as you know, if you’ve been following my work or listening to the show, oxidized fats are much more atherogenic than non-oxidized fats. So Lp(a) is not a good guy. It’s a bad guy overall.
Steve Wright: Well, it probably has some good functions, right, if we just wanted a certain level?
Chris Kresser: Yeah. It’s really interesting. Linus Pauling had a pretty interesting theory about Lp(a). It’s only really found in mammals that don’t synthesize vitamin C endogenously. Most animals make their own vitamin C, but primates like humans and monkeys, we don’t make our own vitamin C anymore. That’s why we have to get it through the diet. If we don’t get it, we get diseases like scurvy. The only animals that produce Lp(a) are the animals that don’t produce vitamin C. Vitamin C plays a role in collagen formation and clotting; so does Lp(a). Linus Pauling developed a hypothesis that Lp(a) acts as like a surrogate for vitamin C. Especially when vitamin C levels are low or there’s a deficiency of vitamin C, the liver will make more Lp(a) as a way of performing the functions that vitamin C would otherwise perform, like clotting and collagen formation, et cetera. So it does definitely play some potentially useful roles, as you pointed out, Steve, just like LDL and cholesterol does. But it’s one of those things where too much of a good thing ends up being a bad thing. There are a lot of things to consider when we talk about Lp(a). We’re going to go through those here. Then at the end, we’ll kind of summarize and talk about the overall picture.
Four things to consider about Lp(a)
The first thing is you have to get the right measurement of Lp(a). Isabel gave us her measurement in mg/dL. I think she said her level was 92 mg/dL. The problem with mg/dL as a measurement for Lp(a) is that it’s a weight-based measurement. Like other lipoproteins, you can have smaller, denser Lp(a) or you can have larger, more buoyant Lp(a). The larger, more buoyant Lp(a) will weigh more, but they don’t have the same—they’re not as harmful as the smaller, denser Lp(a). So in order to get a measurement of Lp(a) that’s not affected by weight, you need to measure it in nanomoles per liter (nmol/L). That’s thought to be a more accurate indicator of Lp(a)-mediated risk, is measuring it there. I’ve seen some people with a relatively high Lp(a) in terms of mg/dL, but a normal Lp(a) in terms of nmol/L. Those people would not be at increased risk. So that’s important to do, especially if you have a profile where you have large, buoyant LDL particles, because you’d be more likely to have higher mg/dL measure of Lp(a), but maybe not high in terms of nmol/L. That’s number one. Just so you know, the ranges for Lp(a) in nmol/L, ideal would be below 35 nmol/L, borderline would be 35-75 nmol/L, high would be 75-125 nmol/L, and very high would be over 125 nmol/L. So that’s number one.
Number two is Lp(a) is a risk factor, as I mentioned, and it is independent of other risk factors, but you really have to consider the overall picture when it comes to heart disease. It doesn’t occur in isolation. When we talk about heart disease, we’re talking about people, not just markers. A 44-year-old woman with no other risk factors and high Lp(a) is still likely at relatively low risk for heart disease over the next 10 to 20 years. Now that doesn’t mean you should ignore this and not do what you can to address it, but it does bring into question what the value of taking a statin drug for a 44-year-old woman is, because studies have shown that for women who don’t have pre-existing heart disease, statins do not extend life span. That would suggest that even if a statin did lower Lp(a) for a woman without heart disease, it wouldn’t necessarily prevent death from a heart attack or extend her life span in any way. So for me, that’s a big question mark then in terms of the value of taking a statin in that situation.
Third, and this is related to what I was just talking about, the evidence that lowering Lp(a) actually reduces heart disease risk is pretty weak. We know that high Lp(a) is associated with heart disease. But studies that have looked at lowering Lp(a) with medications have not found that heart disease risk necessarily goes down when you do that. What’s interesting is that’s actually true with HDL cholesterol as well, which is the good cholesterol. We know that high HDL levels are associated with better outcomes. But when you look at studies where they use drugs to increase HDL, the people don’t necessarily have a lower risk of heart disease as a result. That comes back to we have to look at the person and not just the markers. If you do some kind of drug intervention that just gooses the marker higher without addressing any of the other diet and lifestyle factors that led to that marker being low in the first place, then that’s not really a fix that’s going to work well over the long term. So there may be something similar with Lp(a), and we need more research to figure that out.
Steve Wright: Yeah. You’re tracking biomarkers that we haven’t confirmed actually do or don’t do things.
Chris Kresser: That’s right.
Steve Wright: The real event there is heart disease.
Chris Kresser: There are a lot of questions. We see that Lp(a) is higher in people who have heart attacks, but does that mean that Lp(a) is causing the heart attack? Or maybe Lp(a) is being produced at higher levels because there’s some underlying damage to the tissue that is causing both the heart attack and the Lp(a) to be high. This is why it’s so important to be careful with observational research and not only focus on markers, to look at the bigger, overall picture.
Number four is that despite—if you research online, you look into Lp(a), you’ll see claims that diet and lifestyle just absolutely have no impact on Lp(a) levels. But that’s not actually what I’ve seen in my work with patients, and I know from talking to other clinicians that they feel the same way. There is some anecdotal clinical evidence that Lp(a) responds to some natural treatment. I’ve seen when people add—if they’re not getting enough long-chain omega-3 fats like DHA and EPA, if they add those to their diet, I’ve seen Lp(a) levels go down. I’ve seen Lp(a) levels respond to a switch from a standard American or not very healthy diet, to a Paleo type of diet. If you think about it, Lp(a) is there to repair damage, and we’re following a lifestyle that’s causing endothelial damage. It makes sense that changing diet could potentially influence it. Then we have studies that have looked at some natural treatments and found that they’ve been effective to greater or lesser degrees. For example, a study in 1998 found that taking 2,000 mg of hexaniacinate, which is a time-release form of niacin, which is vitamin B3, for 96 weeks—so that’s a long time. You know, this was not an overnight effect.
Steve Wright: Almost two years.
Chris Kresser: It lowered Lp(a) by 39%. That’s a pretty significant decrease. That could definitely drop you from being in the high-risk category into being in the normal or slightly elevated category. That’s a big dose of niacin. As many people know, that high of a dose of niacin can cause flushing. So it’s probably a good idea to do that under some kind of medical supervision.
Steve Wright: Yeah. And if you haven’t flushed before, you’ll want somebody there.
Chris Kresser: You’ll not like it. Yeah, you will want somebody there. Another study found that 2 grams per day of L-carnitine amino acid lowered Lp(a) levels by about 20% after six months. Then finally, the clinical evidence has not really been that supportive of this, but as I said before, Linus Pauling hypothesized that Lp(a) might be a surrogate for vitamin C. He did some additional studies in animals that found that when vitamin C was low, Lp(a) levels were higher and there was higher risk for heart disease. So supplementing with vitamin C, along with L-lysine and L-proline, which also play a similar role, may lower Lp(a). I do want to point out that some of the studies that have been done used somewhat lower doses of vitamin C than he recommended. They used like 1 or 2 grams per day of vitamin C, whereas many people who recommend this treatment, including me, use more like 3 to 5 grams of vitamin C, along with 3 to 5 grams of both lysine and proline per day. I have some patients that I’ve used this and I think it’s safe. Vitamin C is nontoxic even at high doses, so there’s very little reason not to try this. I start patients with a lower dose, like 1 gram of lysine, proline, and vitamin C per day. Then I have them gradually build up to 3 to 5 grams per day of each; you know, with divided doses, not all at once. So that reduces the likelihood of any kind of adverse effect.
Steve Wright: With the vitamin C there that you’re using, is it a special kind, like liposomal?
Chris Kresser: Liposomal is better absorbed, but that can get pretty expensive at 5 grams per day. I think an ascorbic acid can work or a buffered form of vitamin C, if you have gut sensitivities to it. So depending on what you can afford and what makes sense, either one of those should work. If you add B3, you do carnitine, you do the lysine, proline, and vitamin C, and you put all those together, in most cases, we do see a decrease in Lp(a) over time. The fourth thing that I’ve seen some suggest but I haven’t done so much myself is lumbrokinase, which is an enzyme that assists in the breakdown of fibrin, which is a protein that’s involved in blood clotting, which Lp(a) plays a role in. So lumbrokinase, some other practitioners have used it with some success to lower Lp(a) levels. Delta- and gamma-tocotrienols, which is a different isomer of vitamin E. You know, most people, when they take vitamin E, they take alpha-tocopherol. Tocotrienols are another form of vitamin E. They have been shown to be effective in lowering LDL particle number, LDL, and total cholesterol. I don’t know if they lower Lp(a), but it’s probably worth a try because again, it’s safe. 200 mg of the tocotrienols are a safe and effective treatment for lowering LDL particle number. And since Lp(a) is a subfraction of LDL particles, it makes sense that that might work too.
As always, don’t consider this medical advice. Check with your doctor before doing any of this stuff. But all of the things that I’ve recommended, ranging from a Paleo, nutrient-dense, low-toxin diet, to increasing your intake of long-chain omega-3 fats, to the niacin, L-carnitine, lysine, proline, vitamin C, the lumbrokinase, and the tocotrienols are all safe interventions that—with the exception of niacin, which can cause flushing; it should be done under supervision—I would consider to be much safer than a statin drug, for example, which is often what’s prescribed in the case of high Lp(a).
Other markers to keep an eye on
Steve Wright: Are there some other markers, Chris, that people who are thinking about this should look at? Because on many other podcasts, we’ve talked about the fact that essentially, we’re looking at inflammation. You know, the arteries are getting damaged somehow.
Chris Kresser: Yeah.
Steve Wright: We’ve also linked this in other podcasts to leaky gut and other things. But as far as biomarkers go, if someone’s going to go back and retest their Lp(a) to get the nmol/L, should they ask for like hs-CRP or something else?
Chris Kresser: Yeah. CRP would be helpful; LDL particle number, the NMR LipoProfile that we’ve talked about before, where you’re measuring the actual number of lipoproteins instead of the amount of cholesterol that’s inside of the lipoproteins; doing, as you pointed out, Steve, a gut profile. You want to be looking for anything that could cause a chronic inflammatory response. So that could be SIBO, bacterial dysbiosis, fungal overgrowth, parasites, intestinal permeability. There are a lot of studies now that are linking the status of the gut microbiota with heart disease and that those are all likely mechanisms. Any kind of chronic viral or bacterial infection could potentially contribute to that. There are a lot of studies linking those things to increased risk of heart disease. An example is things like H. pylori, the bacterium that causes ulcers. So all the stuff that we generally talk about in terms of doing a thorough functional medicine type of workup are crucial. Then on the lipid front, you want to look at the NMR Lp-PLA2, which is different than lipoprotein(a). It’s a little confusing. That one is sometimes referred to as PLAC. That’s a specific marker for cardiovascular inflammation. It’s even more specific. You know, C-reactive protein (CRP) is a marker for systemic inflammation throughout the body, whereas PLAC—or Lp-PLA2; they’re the same thing—that’s more of a marker for inflammation within the cardiovascular system. So that can be helpful. Then doing something like a calcium score, which looks at the actual state of your arteries, if you have calcification in your arteries. That’s thought to be more predictive of future heart disease risk than any of the lipid markers. For example, if you have normal cholesterol Lp(a) and a high calcium score, you’re going to be at significant risk for a future heart attack. But if you have even high cholesterol or lipids and a normal calcium score, you’re probably not going to be at significantly increased risk of a heart attack.
As I’ve said a few times in this show, you have to look at all of these different variables to determine your overall risk profile. Remember not just to treat a particular marker, worry too much about one particular marker. Look at the whole, overall picture. Because we know that over 90% of people who have high cholesterol and go on to have a heart attack have another major risk factor, like high blood pressure, smoking cigarettes or something like that. So that tells us that high cholesterol alone and altered lipids alone are generally, in most cases, not enough to cause a heart attack.
Steve Wright: Chris, all that stuff sounds great. Just playing devil’s advocate here. But that’s just so much time, effort, money; all these resources to get all those tests done. What’s really wrong with a simple co-pay for statin and baby aspirin for the next 40 years?
Chris Kresser: Well, if you look at how many people take those, you might conclude that there isn’t much wrong with that and how often they’re prescribed. You know, as I’ve said before, there could be a time and a place for statins and baby aspirin. But I think the general principle of functional medicine is to address the underlying cause of a problem, because that leads to more lasting and effective healing, with fewer side effects, complications, and risks. My goal, as always, is to create the best—you know, I often tell my patients I use whatever works and causes the least amount of harm. So if I can accomplish preventing a disease or treating a disease by using dietary and lifestyle interventions to the same degree or a greater degree than the results that I would get with using a drug that has potentially serious and life-changing side effects, then I’m definitely going to choose the former. The patients that I tend to work with understand that and want that too. And if somebody doesn’t understand that and want that, there really is not much that I can do, Steve. If someone can’t be bothered to do those things, then they probably will end up taking a statin and taking baby aspirin, and there’s little that I can do about it.
Steve Wright: Yeah, I just wanted to throw that out there. Because there are side effects and there are negatives to taking those two, even though those seem so much simpler. You know, another way to look at this, another alternative to what Chris just said, would be that at 44, you’ve got a lot of life ahead of you. It doesn’t matter your age, but these are signals that something isn’t potentially quite right in your body. Maybe a statin and baby aspirin help avoid heart disease for a little while, but then maybe some other really serious health complication pops up in a few years. So I think there’s pivotal decisions, it seems like when I talk with people throughout their life, where they’re trying to get rid of a health issue. Sometimes they choose the simpler route because it seems so painful to go down the deeper route to fix things. Then everybody that I know, myself included, know people who are just “healthy,” and then they were gone the next day for a various number of reasons.
Chris Kresser: Yeah. And the thing about functional medicine, which I know we’ve discussed before, definitely is more expensive upfront. But I would argue that it’s far, far cheaper down the line. The principle is just different. The principle is you spend more money upfront to do the proper testing and investigation to figure out what the underlying cause of a problem is, and to address it then, which will save you enormous amounts of money, time, and grief later on. Because if you are able to prevent, for example, a heart attack, type 2 diabetes or an autoimmune disease by adjusting your diet, doing testing to identify SIBO and other gut issues, treating those, and doing other kinds of testing that we do in functional medicine—if you prevent a disease like type 2 diabetes, you’re going to save unbelievable amounts of money, time, and suffering from doing that. Unfortunately, I think it’s partly human nature and it’s partly our culture in the US that we don’t tend to think ahead like that. We’re mostly focused on what’s right in front of us. I think there are some evolutionary reasons for that. That’s how we survived in part. And while we do have some capacity to think further into the future, it’s much more difficult for humans generally to respond to the threat of something that could possibly happen later on, than it is for us to respond to something that is right there in front of our face. That’s the big challenge I think for everybody when it comes to preventative medicine. We need to be taking steps now to head off things that could potentially happen in the future. And it’s difficult sometimes, as you pointed out, Steve, for people to make that investment of time, money, and energy in the present for something that may or may not happen in the future. But that’s exactly what’s necessary if we want to stay healthy and prevent these diseases.
I hope that was helpful, Isabel and everybody else who is listening. Again, keep the questions coming in.
The Paleo Cure
I just want to make another announcement, because I think this show is coming out somewhere towards the end of December. There’s something else happening at the end of December, which is that my book, Your Personal Paleo Code, is being published in paperback. It’s being published with a different title. It’s called The Paleo Cure. Got a different cover and everything. It looks different.
Steve Wright: It looks pretty sexy.
Chris Kresser: I like the new cover a lot.
Steve Wright: Yeah.
Chris Kresser: And actually, I like the title too. It’s more a reflection of what we were trying to accomplish with the book in the first place. I just want to let everybody know that, first of all, so you’re not confused and think that I’m publishing a new book that I haven’t told you anything about. Number two, if you haven’t picked up the book yet while it was in hardcover, you have a chance to do that in softcover now. Obviously, it’ll be cheaper. It’s available on Amazon, Barnes & Noble, all the typical places that you would expect it to be.
Steve Wright: Did you make any updates or revisions?
Chris Kresser: No updates or revisions. I don’t really feel like the book needed that. It’s still all very current. My whole purpose in writing that book was to have one place where I had all, you know, my basic philosophy and approach on diet and lifestyle in one location. Because having a blog with tons of articles is great, but it’s not the most user-friendly way to find—you know, if I just want to tell somebody, “Hey, this is what you need to know about diet and lifestyle,” and then send them an email with like 1,500 links to posts, that’s not very useful. But one book is helpful. So that’s what it is. It’s a great resource. And especially after the holidays, if you’re looking to jump back on the wagon and you want something to help you do that, check it out, The Paleo Cure. If you search for that on Amazon, I think right now the hardcover will come up. But as soon as the book is published on December 30th, it will switch over.
Steve Wright: Congrats on pulling that off, Chris. I know it was a big project.
Chris Kresser: Thanks.
Steve Wright: Obviously, if a listener hasn’t picked up this book or you’re looking for a stocking stuffer, grab it. Put it in the stocking stuffer. Try to spread this message out there.
Chris Kresser: Thanks, everyone. Keep the questions coming. Have a very happy holiday.
Steve Wright: This podcast is created by you and for you, so keep your podcast questions coming, ChrisKresser.com/podcastquestion. So ChrisKresser.com/podcastquestion is where you can go to submit. In-between episodes, if you’re looking for new updates—like, Chris was actually just posting some fascinating new gut microbiome research on Facebook. If you missed that, it’s because you’re not following him. So go to Facebook.com/ChrisKresserLAc and Twitter.com/ChrisKresser. Happy holidays and thanks for listening.
Chris Kresser: Bye, everyone.
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