How Your Lipoprotein(a) Level Affects Your Risk of Heart Disease | RHR
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How Your Lipoprotein(a) Level Affects Your Risk of Heart Disease


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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.

Revolution Health Radio podcast, Chris Kresser

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 This episode of Revolution Health Radio is brought to you by 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 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, 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,, 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:

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, So 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 and Happy holidays and thanks for listening.

Chris Kresser: Bye, everyone.


Join the conversation

  1. I’m confused about the difference between mg/dL and nmol/L. I thought both are convertable just by calculation. Is there any difference in terms of methods in the lab? Can anyone clarify this?

    • yes, i also am confused.

      my (low carber) Lp(a) is 10 mg/dL

      good is supposed to be <29 mg/dL
      so 10 should be good.

      when converted with:
      get 0.36

      another conversion says just divide by 18
      (but this is not specific for Lp(a) (does that matter?))
      and this gives 0.55, still way different.

      these conversion results d not fit at all with the nmol/L range
      below 35 nmol/L as being good.

      where is the mistake?

  2. I’ve been trying to find research and a dr to treat elevated lipoprotein a levels in children. My son is 6. When he was 4 he fell on his head. Long story short they found a blood clot in his brain which they are not sure if it was from the fall or already existed. They checked for lipoprotein a levels and clotting disorders. His lipoprotein a levels remain at 227. And he also has MTHF mutation. No dr can give me any answers to what will happen with his levels being that high or even if that is a high level due to limited research on kids. I was hoping you would have some answers for me or any recommendation on who could help me get answers.

    • I was at the HeartUK conference in 2015 and a researcher gave a talk on Lp(a), I cannot remember her name but it could be a starting point for you.

    • Ok so I see he has the MTHRF as well that means the body is less effecient in clearing toxins and fat, cholesterol as well as heavy metals can build up I would do a heavy metal test,
      MTHFR is controlled by folic acid and METHYL b12 daily. his dr may prefer B12 shots if it is found he is deficient otherwise, sublinguals are best I buy thorne research Methyl Guard combines both folic acid and methyl b12 in the correct balance

  3. My son is 6 and has a slightly high bad cholesterol level and total cholesterol level. However is lipoprotein a is 227.5. We were advised to see a specialist but until then do u have any advice of us. And maybe tell him his rise of something happening now. (He had a clot in his brain already)

    • bouoluke is definitely worth a try it is an anti fibrin.anti clotting enzyme that also lowers LPa niacin is probably not an option for a year old at least immediate release. im sure your dr will mention Niaspan though’
      get him on one capsule of high quality salmon oil capsule a day and a capsule of pure curcurmin in meantime both safe

  4. Hi, I have pretty good markers now after radical diet changes. By the way I found that my Lp0a) spiked into the unhappy range when I came off my Vit C supp’ but went back into the normal when I restarted. Circumstances made this happen twice and on each occasion it went up but came back down. As a result I maintain my Vit C supp and add dietary boosts. It pretty easy if you adopt habits eg having a red grapefuit with your breakfast each day. My only marker that is out of synch is Lp-PLA2 which comes in at 210. It needs to be below 195 to be medium risk. I have had it tested 3 times and still I cannot put a reasonable dent in it. Any suggestions would be most welcome please

    • Excellent topic!
      If you don’t eat healthy and watch your body intake, you increase your chance for heart disease. 99% of Americans will have at least one heart procedure in the lifetime.

      This site written by cardiologists, provides excellent patient information on common heart procedures.

    • WOW amazing with re to LPa what is your Vit c dose a day?

      as far as Lp PLA add fish oil daily and a 500 mg curcurmin capsule a day keeping inflammation low is the key

      • I add Turmeric daily to my porrdige, turns it yellow but does not really effect the taste that much

  5. My lpa is 562 nmol…..yes I said “562”….I am on simvastatin and cholestrl numbers are now good…ldl about 85-95….overall 170 ish…..
    please comment…55 yrs old male….6 ft 175 lbs I do athletic things ….

    • LPa is a problem when coupled with LDL your LDL levels are beyond ideal maybe add 2 grams niacin each morning otherwise you seem in great health

  6. My husband’s age is 30. His total cholesterol level is 266.
    Ldl 195, hdl 35, lp(a)35, crp 5.75.
    He at times experiences chest n left arm pain. Also has a family history ( father died at the age of 42 due to heart attack)

    Stress test was normal 3 months back
    Plz reply what should be done for now to rule out heart problem
    N also what can be done to prevent heart attack..

    Plz reply

  7. Last year I changed my diet to a low carb, high fat one. My blood work has changed a lot, much of it for the better, but some I’m not sure.

    CrP still very low (0.3)
    HDL went from 75 to 114
    HDL2 (most protective) went from 11 to 52
    HDL3 (least protective but still good), went from 44 to 63
    VLDL (the smallest LDL) went from 20 to 17
    VLDL-3 (worst VLDL), stayed the same at 10 (normal is <10)
    Triglycerides went from 102 to 79
    LDL Density Pattern went from A/B "mixed" to A "good"
    lp(a) 14, up a bit (was 12, then 8), but still fairly low

    LDL went from 90 to 233
    apoB100-cal, which I believe is an approximation of LDL-P, went from 66 to 152
    LDL-R-C 76 to 197
    IDL cholesterol went from 7 to 23 (normal is <20)
    Remannt Lipo (IDL+VLDL3) went from 17 to 33 (normal is <30).

    I don't mind that my LDL went up, I think it was too low and wanted it to go up. But it went up more than I expected, and if LDL-R0C and/or APOB are representative of LDL-P, then it went up a lot too. Also the IDL went up a lot.

    I think that overall my result is improved, I just want to make sure this is the case. I was thinking of doing an oxidized cholesterol test, not sure what else might help clarify?

    I have family history of early heart disease and stroke, but much of my family has significantly higher lp(a) than I do.

  8. Well, I don’t know what to do to lower the number or size of my LDL-Ps. I am a 51 yr. old post-menopausal female (went into natural meno at 38). Using Estrace & compounded Testosterone creams. My Vitamin D is 97. My first blood test numbers were A1c of 5.8, LDL-P of 1660, LDL-C of 131, Triglycerides of 138, HDL of 69 and total cholesterol of 213. I got on the paleo bandwagon, picked up my cardio exercise, lost 20 lbs. and went in for more blood work. Now, my numbers are total cholesterol 206, HDL of 69, LDL-C of 119, Triglycerides of 71, A1c of 5.5 and LDL-P 1674 (the small dense kind). I have been taking Krill Oil, Vitamin C (1 gm/day), Alpha Lipoic Acid, Magnesium, Vitamin D3 and B-12. As you can see, my triglycerides are almost half of what they were and my A1c is down to an acceptable range. I don’t want to die of heart disease, but I don’t know what to do t lower the LDL-P count or size. I don’t want to take Niacin because of the weird flushing effect. I don’t want to take drugs. Why are all my other numbers good and this one bad? I don’t understand and at a loss of what to do. Doctor says to repeat blood work in 3 more months. It was 4 months between the first and second blood tests.

    • It’s great how well some of your numbers have responded. Do you know your CrP and/or LpPla2? Because inflammation is such a big part of this. Whenever I get worried about any of my numbers, I feel much better knowing that my inflammation is very low.

      As I understand it, a big reason why small particles are dangerous because they oxidize more easily. But just because you have them doesn’t mean they are oxidized. I believe the low carb diet will cause less oxidation. Oxidized cholesterol seems to be a good test to really show that, but it seems to be a hard test to find.

      BTW I used to take Niacin, and believe it or not you really get used to the flushing, you even start to look forward to it. But I had to stop taking it because it started making my ears hurt a lot.

      • Cindi, What was your lp(a) before you changed your diet and introduced supplements? Are you still on a high fat diet, low carb? Have you had any recent blood work? My Lp(a) was 136nmol/L after 5 months paleo, don’t know what it was before. I am not on any supplements but may start Vit C soon. Any thoughts now 1.5 years down the track from your last post of the factors that have helped your Lp(a) stay low?

      • I have my oxidised LDL test done in the Algarve in Portugal at one of any of the high street blood test clinics at a fraction of the cost in the UK

    • Stop the krill oil, switch to proper 18 carbon omegas-6 and -3 from plant sources. Your numbers will correct themselves and all traces of heart disease will resolve.

  9. Just curious if Lp(a) is something that is regularly tested in a blood panel? I was just looking over my blood work (I usually get 1-2 per year) and I can’t find it being tested. Since adopting a high fat diet (with the guidance of a nutritionist) to aid gut healing and severe eczema in my son (who is still being breastfed)… my serum total cholesterol is consistently high. Last time I checked a few months ago it was 286mg/dl (7.4 mmol/L). My HDL was 100.5 mg/dl (2.6mmol/L) and my LDL was 176 mg/dl(4.57 mmol/L). My triglycerides were very low at 19.3 mg/dl (.5 mmol/L). I, of course, was red flagged for my high total cholesterol and was then counseled to stop my high fat diet (which contains fats that are good quality, protein source “clean” and I eat very limited Carbohydrate foods). I would like more information on other people who have similar profiles as I do (blood wise). Perhaps I will have to review the suggested reading “High Cholesterol Action Plan”… anyone read it? Thanks for any insights in advance!

    • Hi Christine:

      My doctor would likely not order the Lp(a) blood test routinely, but when I request it he adds it to the form. Hopefully your doctor would do the same. By the way, your conversion from mmol/L to mg/dL for triglycerides is incorrect. The conversion factor should be 88.5, which means 0.5 mmol/L equals 44 mg/dL (not 19.3 mg/dL). Your other values for cholesterol are OK. The conversion factor for cholesterol is 38.6, so your numbers are basically correct. Some people think the factor of 38.6 applies to triglycerides as well, but it doesn’t. The factor you must use is 88.5 for triglycerides. And now for some personal opinions if you will allow me. With your low triglycerides and high HDL I would suspect you are on the right track with your low carbohydrate diet. Your high total cholesterol number is basically meaningless, especially because a good chunk of that value comes from your high HDL. Your LDL number seems high but could be meaningless too without knowing lipoprotein particle size and particle numbers. See if you can get your hsCRP tested. That’s a marker of inflammation. If it is normal, that would be good. Remember to exercise regularly (preferably every day). Your diet sounds good so keep doing what your doing.

    • you could have high LDL but they could be large fluffy which is a OK and looking at your trigs I would assume they are large fluffy which weigh more and thus would make for a higher mg level. low trigs usually correspond with larger ldl particles

      • The large fluffy is a bit of an exaggeration, yes large fluffy is less atherogenic but as Dr Greger put it, large fluffy is like being killed by knifing vs killed by a gun. Perhaps a clumsy analogy but what he is saying is the reduction in percentage risk is real but not as great as people would like to think. A better indicator which I think Kris has covered is particle count rather than particle size.

  10. I had a NMR LipoProfile done. It does not list Lp(a) but does list LDL-P of 2118 nmol/L. LDL-C of 173, HDL-C of 73, Triglycerides of 131. Total-C of 272 HDL-P (total) of 42.7 umol/l, Small LDL-P of 167 nmol/l, LDL size of 21.5 nm. TSH-T4-free-T3reverse all normal. CRP 1.00. I had to have my Naturopath order the panel for me. No CMD want’s to really talk about things they just want me to take statins. I’m female, 57. After reading this article I’m concerned with the particle number. Can you shed some light on what that actually means and how should I proceed with my investigation of my high numbers. Thanks, I’ve found your sight most helpful.

    • Chris has a great ebook on this site called “Diet Heart Myth” where he explains particle counts. He had an explanation which really sticks in your mind. To summarize:
      Lipoproteins are like cars that carry cholesterol and fats around your body, cholesterol and fats are like passengers in the cars. Scientists used to believe that the number of passengers in the car (concentration of cholesterol in the LDL particle) was the driving factor. More recent studies suggest it’s the number of cars on the road (LDL particles) that matters most. Why? The more cars there are on the road at one time, the more likely it is that some of them will crash into the fragile lining of the artery.

      Note that sometimes LDL cholesterol levels and LDL particle number track together, but other times they don’t. You can have one low and the other high.

  11. I read everything I can on lp(a), but your article had a lot of information I didn’t know. Thanks!

    My family has genetically high lp(a). One 40 year old healthy sister has lp(a) of 166nmol/L. My dad is similarly high and has CVD, as does most of his family. I am 50, my lp(a) used to be high but now it is low. I take many supplements so I don’t know which were responsible. We have also found that exercise helps keep it low. Another sister’s lp(a) always drops when she is training for a half marathon.

    One thing that puzzles me is that my lp(a) is low but I still have very high fibrin and barely bleed, and I thought lp(a) was the cause of the high fibrin. Do you have any comment about that? I have started taking nattokinase. Do you think lumbrokinase is better?

    • studies how lumrokinease is more effective on LPa than natto. I take bouolouke its is so $$ but health is worth it do you take Vit C and Niacin in your regime if so how much of each my LPa is 99 it ranges btw 75 and 99 and yes when im training for half mine drops a bit too so despite all the studies saying diet and exercise have no effect is hogwash your lpa dropped did you change your diet at all do you eat high carb low fat or high fatl ow carb or moderate in both

  12. Hi Chris,

    What are your thoughts on statins after you have already had a heart attack “caused” by cholesterol?

  13. Hi Chris,
    Love all of your articles and podcasts, they are really informative and easy to follow. I am a 41 year old who had a heart attack 10 years ago from a blocked LAD. I was put on a statin nd was told that it is different if you have had an “episode” than if you are preventing one. I only really jear about preventative medicine if yoi haven’t had a heart attack. What are your feelings on using a statin post episode?

    • I am not a doctor, and yes men who have had a heart attack are the only ones you have been shown in studies to benefit from statins. However, do you know what numbers you are trying to fix with your statins? Most people don’t, and IMO you shouldn’t be taking a drug if you don’t know specifically what it is supposed to be doing in your body, and if you aren’t measuring it to make sure it is doing that. If you aren’t measuring, then your statins are likely to be lowering your cholesterol way too much which causes a bunch of other problems like depression, poor brain function, and sexual/hormonal problems.

      Find a functional medicine doctor who tests the right things (most doctors don’t). Are you inflamed? (CrP and LpPla2) Is your cholesterol oxidized? Do you know the breakdown of it by particle size and count?

      • Statins have not been proven to benefit post heart attack patients. Most of the data to support this idea has been derived from meta analysis that incorporates dodgy trials done pre 2005. The significance of this year is that randomized control trials were tightened up after this date. If you examine data post 2005 the evidence changes. Check out the book at

    • Statins are of no use, period. They don’t follow human biochemistry. Use a balanced source of Omega-6 and Omega-3 (2.5 to 1 ratio) that are the 18 carbon, plant based sources, or eat a whole foods diet and you will reverse heart disease.

      • What is your evidence? Studies are very persuasive about their role in secondary prevention in cardiovascular disease. They increase the LDL receptor number on target cells allowing greater entry of LDL particles and out of the circulation. This is especially useful in people with the APOE4 status.

        • The studies funded by the companies themselves prove they don’t work. The NNT of statins is 80 to 140, that means they are 99% ineffective and with an NNH (number needed to harm) of 8, the risk benefit ratio clearly is against these medications. Besides which, cholesterol has no role in cardiovascular disease. The studies often quote Relative Risk Reduction (RRR). There is no denominator when this is done so absolute risk reduction (ARR) has to be calculated by the reader and if done you would realize the apparent benefit is minuscule.

    • who can argue with genetic expression its part of everyones constitution only people with the diabetes gene can develop type 1 diabetes, only people with celiac gene can develop celiac and genetic defects like MTHFR and APOE and LPa are real health issues I know first hand I eat incredibly clean exercise an hour plus every day and yet my LDL and LPa are sky high when I have friends that eat processed foods all day are sedentary and have LOW LDL and no LPa

      • Hi Amy,

        I also have high lp(a) and apoe 3/4. I had a heart attack at age 39 years old which happened 5 years ago. I was lucky to survive the heart attack without major damage. Probably because I was young, not overweight and had built up collateral blood vessels around my heart from lifetime of running and exercising. I’m currently on 10 mg of atorvastatin, baby aspirin, plavix, fish oil. I’m currently able to run 2 miles at 10 minute mile and bike 16 miles. From time to time I have chest pain from stress that does worry me. I had my doctor prescribe the new PCSK9 inhibitor to try to lower my high lp(a) which ranges from 88mg/dl to 130 mg/dl. The repatha -pcsk9 did lower my lp (a) but had side effects ( headaches, joint pain, abdominal pain). Had to stop taking it and go back on atorvastatin. The atorvastatin actually raises my lp(a) but lowers the LDL and inflammation. You should get the hs-CRP blood test to check for inflammation.

        • Albert. Interesting about the ok inhibitor as you are apoe 3/4 I suspect you have cholesterol absorption and clearance issues I suggest getting the Boston heart diagnostics cholesterol balance test it will give you more info on apo a and apo b levels but more importantly whether you overabsorb cholesterol – which would mean a staying does NOT work and you would be better off on Welchol a bike acid binder. But if you are a cholesterol over producer a statin is preferable.
          My crp is low and I take methyl guard to keep homocysteine low as well. My ldl and tris are good. My apo a is high and apo b is low. Calcium score zero but my LPa has gotten higher as I be eaten more plant based diet which cholesteroloversbsorbers can actually convert to ldl . I think I’m going to try scaling back on all fat. Actually up high quality carbs as I’m pretty carb tolerant and increasing lean protein. More
          Check out apoe diet book it may give you some ways to expand your current limited eating plan

          • I think the difference why I have heart disease with my high lp a is the 2 factors you don’t have. I have diabetic post meal blood sugars which is leading to possibly higher triglycerides levels and damaging blood vessels. In addition, you have low abo-b. My apo-b levels are in the 130 mg/do range if I don’t take lipitor. On 10mg of lipitor my apo-b goes down to 80 mg/dl.

            • Albert yea true. The blood sugar issue and apo b come into play for sure. With the statin working you are probably an overproducer But one reason you may want to ask dr re welchol is it not only lowers cholesterol but helps with blood sugar control statins do elevate LPa which welchol does not Its all so complex ESP with militiamen issues that call for opposing therapies

            • Albert yea true. The blood sugar issue and apo b come into play for sure. With the statin working you are probably an overproducer But one reason you may want to ask dr re welchol is it not only lowers cholesterol but helps with blood sugar control statins do elevate LPa which welchol does not Its all so complex ESP with multiple healthissues that call for opposing therapies

              • Hi Amy,

                Welchol sounds interesting but I read it could cause intestinal blockage. Unfortunately, I have IBS along with diverticulitis and narrowed colon due to strictures. I probably have to stick with statins combined with a PCSK9 inhibitor -repatha to control APO-B and lipoprotein a. I think the pcsk9 inhibitor and lipitor negatively effects blood sugar control. I feel like I can’t win. Lower cholesterol with these drugs but lose blood sugar control eventually.

                • I hear what you are saying I have IBS but D not C so welchol would help with that alternative is L Reuteri probiotic as it binds bile salts as well (like Welchol) but not the intestinal blockage issue and its shown to reduce ldl by using consistently, 12%. I feel for you having several issues that call for treatments, at time, that oppose each other. Tne PK drug sounds like a great option and as long as the statin isnt affecting your muscles and its helping LDL thats fantastic I know Niacin in addition to statin probably isnt an option bc it can have blood sugar effect. Maybe add Vit C/Lysine/Proline daily (Look up Linus Paluling/Rath LPa protocol) Its marketed under Heart Technology, it simple to incorporate daily (mix the powder into drink ) also I have read extensively that taking cholesterol meds at bedtime is optimal as cholesterol is synthezied over night good luck to you!

  14. I went to cardio doc 2 years ago and had stress test done. It was normal, they say, but I still have tightness in my chest and dull pain going under left arm. Total chol I’d OK,triglrcerides OK. Any suggestions?

    • Hi Rina:

      Have you had chest tightness and arm pain for two years? If so, does it seem to be getting worse? Does the pain increase when you exercise or when you are stressed? If it were me, I would be concerned. It has been two years since your last stress test, I would say it’s time to do it again. You might want to kill two birds with one stone and get a nuclear stress test, which might give a clearer idea of what’s happening in your heart. Keep in mind you can have up to 75% blocked arteries and a regular stress test can still come out looking “normal.” I would be curious to know what your triglyceride number is. Your doctor might tell you it’s good but the acceptable range is rather lenient, maybe too lenient.

  15. Wow, that was an education, Chris and Steve, and your commentary truly underscores the complexity of assessing the relevancy of various biomarkers to health.

    Fascinating to me is Apolipoprotein, particularly ApoE, which as you know, is a major component of a specific type of lipoprotein called very low-density lipoproteins (VLDLs) that do this (I’ll enumerate for your readers):

    – Combines with fats (lipids) in the body to form molecules called lipoproteins that “package” cholesterol and other fats and “carry” them through the bloodstream.

    – The VLDLs remove excess cholesterol from the blood and carry it to the liver for processing.

    Each of us have one of at least three slightly different versions (alleles) of the ApoE gene, which are called e2, e3, and e4, the most common being e3, found in more than half of the general population.

    From my reading (and writing) on the subject, I’ve learned that a person’s genetic ApoE largely determines how our bodies process dietary fat. There’s a very revealing chart called “Apo E Genotype – Metabolic Expression and Influence on Therapeutic Interventions” right here: (scroll down)

    The chart shows how various types of dietary fats and alcohol affect HDL and LDL density in people expressing ApoE2,3,4.

    Seems to me that if we got a blood test to determine our alleles, we could tailor our diets accordingly to help achieve optimal health.

    Any thoughts on this?


    P.S. Your ebooks are excellent – very educational and helpful.

    • Interesting chart, BUT I really wonder how useful it is when it just addresses fat as low vs high, without discussing the types of fat. Many past studies lumped all fats together, whether ones we know to be bad (trans fats and oxidized PUFA’s) or good (olive oil, coconut oil, other saturated fats). Now it is understood that it really is sugar that is really responsible for most of the things that have been attributed to fats.

      Many of the fat studies were poorly done in many respects (asking people to remember what they ate, mixing up correlation and causation, not considering sugar consumption, not separating out the various types of fat, and poor interpretation of study results.) Are these the studies that were used to come up with this chart?

      I just don’t have a lot of confidence in a chart like this because of all these factors.

      • Hi Cindi.

        I’m not an authority on ApoE, but have a few points to make in response to your comments.

        The chart does show the affect of fish oil on ApoE types, and like the other diet types (low and moderate fat), it has specific triglyceride, HDL and small particle LDL responses.

        Moreover, as the video under the chart states, people who conform their eating to their ApoE type become leaner and healthier.

        More grist for the mill.


      • at least for APOE 3/4 Ive read a lot about seem to thrive on low animal protein high carb, vegetarian type diet with little to no saturated fats and a small amount of PUFA’s and MUFA’s APOE 2, i think needs opposite, high animal protein and low carb

        APOE 3/4 overabsorb cholesterol and Fat and have trouble ridding body of it so apparently fat intake should be spread to once in a 24 hour window

    • wish it was that easy

      Im APOE 3/4 and a cholesterol and fat overabsorber I have LDL, no surprise, but SUPER high LPa the issue is complicated by that. APOE 3/4 High LDL diet is very high carb, very low fat very low animal protein…BUT diet to reduce LPa is low carb, high saturated fat go figure the diets completely contradict each other. maybe everything in moderation is best approach for all of us? i still have a part of me that feels some people have high cholesterol for a reason that they’re body needs it and it shouldnt be tampered with as long as the diet is clean overall 80%

  16. Thanks for answering my question. Very useful. In the meantime I went for an angiogram and my arteries look good, so that got me reassured a bit. So no statin and baby aspirin for now at least. I did not mention that I’m also a runner/sort of athlete and I really did not want to go the statin way because of muscle cramping with statins? Anyway, I’ll try your other recommendations in the meantime. I love your book and happy holidays from the other side of the Bay.


  17. This is a great podcast. I especially liked how you discussed how people don’t like to think of their future health – only putting out “fires” as they appear. My 40ish husband went in for a physical recently. We see a DO who is unconventional and quirky, but we like her because she is smart and thinks outside the box. She told him that everything looked good and specifically said that he probably wouldn’t have to worry about a heart event in the future because he has “fluffy” cholesterol. That was her layman’s term for my husband. He isn’t going to ask her to explain. Well, I think I know what she means now.

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