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
Podcast: Play in new window | Download
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).
Like what you’re reading? Get my free newsletter, recipes, eBooks, product recommendations, and more!
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.
Better supplementation. Fewer supplements.
Close the nutrient gap to feel and perform your best.
A daily stack of supplements designed to meet your most critical needs.
This topic has my concern – I am 59 white 5’3″ 123 lbs female – good health and active.
All my numbers are good – except.
LDL Pattern B, LDL peak 214.4, LIPO (a) 128 NMOL/L
LDL part size 1198, Sm 177, Med 189, Lg 11158
My Cholesterol 206, HDL 109, Trig 33, LDL 88
Cardio CRP 0.4 LP PLA2 109
Should I be worried? If so was Healthy options are there?
Vitaminc C lowered my Lp(a) and I understand Niacin will also lower it too, try both
If you are in the UK you may have seen tonights ‘Trust me Im a doctor’ TV doc’. Dr Mosely experimented with around 80 subjects testing virgin coconut oil v virgin olive oil v butter
Only the coconut oil reduced LDL and increased HDL. This seems in line with this study below although others perhaps refute this as the number of official bodies telling us not to eat it is long
Is this just another part of the big fat lie ?
The most compelling piece of evidence I have read surrounding heart disease of late is the work of Dr Kraft and his insulin assay analysis. If you are not familiar with it I would implore you to read up on it. You will realise that what we call the silent killer ie heart disease is not really silent at all, we just have not been listening hard enough. If anyone would like a summary I would be happy to cover it. I would also value Chris’s opinion too
I too, like Isabelle, have a high LPa and found the info most informative. Thank you! Fortunately, I had been taking most of what had been recommended and will ask my doctor about the other two. My question is…. what are your thoughts on Chelation Therapy in addition to the supplements?
My LPa is 156. I have heard that elevated LPa should not be a concern if LDL is low enough. Taking 10mg Crestor daily has lowered my LDL to 43. I am wondering if my LDL level is adequate for my elevated LPa? I would really appreciate any comments please.
Thank you very much.
i know there are studies that say getting LDL as low as possible is the goal then other studies saying LDL lower than 70s is too low, increasing infection rate, cancer rate and lowering immunity seems 70-90 is sweet spot. maybe cut back to every other day and also though statins do decrease LDL< they also can decrease large fluffy ldls and increase small ldls so a reading of say 90 of large particles is way better than a ready of 45 of small dense particles. best way to find out is get the NMR apo A and apo B test
I appreciated so much your helpful reply. I will get the NMR apo A and apo B test, then adjust after viewing the results.
I just found out my LPa is 258
I am taking fish oil, lipoprotein, methyl protect, and vitamin k but don’t know if it is working yet.
I also tried red yeast rice but wasnt able to tolerate due to severe muscle aches and I couldn’t take the flush from niacin either. I was also diagnosed with a fatty liver, and kidney stone former. I am heterozygous for mthfr and homozygous for MTR. And if that wasn’t bad enough I have food intolerances to Gluten, dairy, corn, oats, rice, chocolate and beef. If anyone out there has any advice I would greatly appreciate it. Thanks Michelle,
I have high LPa as well at 145 elevated LDL at 145 and have the mthrf and apoe 3/4 gene AND am celiac and dairy issues as well so i feel you pain Ive spent too much time obessessing over this so i have simplified my life and do the following and then just try to stay in the moment as long as i eat well, exercise everyday and take these supplements I will let me cholesterol be at the levels it may be happiest at Studies have shown that lpa levels are high in centarians! and athletes (bc micro muscle tears can trigger lpa to be released in higher levels as it is a “repair man”
in am after workout before breakfast
3 gram immediate release niacin, 2 capsules IP6, 3 grams lysine capsules, 3 capsules methy guard, 5 grams of vit d (critical for maintaining proper chol. levels) and 2 grams l glutamine and one capsule of microbiome L. reutri –the last two being for digestion. celiac/leaky gut issue. i eat whole foods, moderate carb fat protein and about 2 ounces of dark chocolate daily. maybe try adding a tbsp coconut oil its great for gut issues and though high in sat fat has been shown to be helpful in cholesterol and fat absorption/synthesis good luck!
michelle also i take a product called boulouke one capsule a day it reduces fibrin which is both higher with lpa and is also an inflammatory marker again in the am, after workout before breakfast with the other supplements re niacin i like the flush but you could try it again and add a baby aspirin half hour before hand and then take he niacin or take its after a meal instead of on empty stomach i feel niacin is vital in the regimen as it pretty much is proven and one of the only proven lpa reducers (in high doses usually at 3grams)
Thank you Amy,
I appreciate all your sincere feedback and tips. I am glad that you have found a protocol that works for you. Could I ask how much you were able too lower your LPa and Hdl?
I am a little overwhelmed as my LPa is almost 3x as high as yours and I am in the beginning stages of trying to Learn how to change it. I am 48 and approaching menapause and like you I try really hard to eat a healthy diet and exercise everyday. I also have been recently diagnosed with a non alcoholic fatty liver, and am a kidney stone former and have to be on a low oxolate diet and food intolerances is making my life extremely difficult and frustrating because I don’t know what to eat anymore either . I have been supplementing with folate methyl protect and liver support supplements and probiotics and have been able to lower my CRP and Gfr but I don’t feel like it is enough and am trying hard to find something that works for me but have not figured it out yet but I am fearful that my LPa is already way to high and that I will not be able to lower it.
Does anyone know if an LPa of 258 can be lowered ? I read that flax seeds can significantly lower LPa and have just started to incorporate them on a regular basis but I realize that this alone will not be enough.
Thank you Michelle,
Michelle, I have not yet gone back to measure I found I was becoming completly over focused on it creating a lot of anxiety . I feel if i am eating super clean (except for my 3 ox of chocolate daily) exercising and taking supplements that are shown to help I will trust my own body there have been studies that do show women are less affected by elevated Lpa as men What is your LDL as Lpa seems to be dangerous only in presence of high LDL with menopause on the brink I would suggest bio identical pro-est cream its usually presribed to a compounding pharmacy . i would do the niacin it is pretty benign if its immediate release why not try this for a few months then test and re evaluate
in am: methyl guard 3 capsules. 5000 of vit d3, 800 magnesium glycinate, 3000 vitamin c, 3000 lysine then at night 3000 g of niacin with a baby aspirin(which has been shown to reduce lpa) with niacin –titrate slowly first day -week 1000 at night, second week, 2000 at night, 3rd week 3000 at night then get tested after 3 months
BTW if you are not dairy intolerant, dairy fat has been shown not only to lower oxalate levels but also lower lpa (i would add a cup or grass fed whole milk or grass fed whole milk yogurt every day)
I am 45 years old very fit thin (actually a bit underweight as i have MAJOR gut issue–but thats another story) and have always had high LDL levels (high hdl around 90) and high LPA levels running btw 75-90 so I do agree the numbers can shift due to diet and exercise, at least a little bit.
my question is whether lpa in women like me is really a risk factor I have read initially lpa served a useful function protective of famine, disease and actually boosts immune system.its the poor sugar, refined fats and carbs eaten today coupled with LPa is what causes a problem. so if I am fit, working out every day eat 80% very healthy –combo of one vegan meal one — fermented dairy meal (breakfast) and one meat or fish based meal daily plus about 2-3 ounces (yes a lot!) dark chocolate each day,: if I eat healthy and exercise and have high Lpa ? my feeling is it is what it is and maybe i should leave it alone? one other question which contradicts what most studies claim as far as lpa and diet not being related I did read that stearic acid!! (in chocolate) raises lpa (but strangely lowers LDL) and that dairy fat lowers lpa (but again strangely raises LDL) so if I have BOTH high lpa and high ldl what the heck do i eat. plant fats raise lpa and animal fats raise ldl.. it is all contradictory and i need to make sure i eat what digests well (with my major gut issues) maintains my bodyweight and actually helps me gain weight and supports my athletic lifestyle -some days i feel like its like a science experiment –do i eat vegan? do i eat low carb/starch? do i eat high saturated fats? or plant fats?..again with gut issues, high ldl and high lpa all point to contradictory meal plans,
i think its easy to lower chol when you can diet and cut calories (carbs and fats especially) but I cant with my high metabolism, activity level and small frame and light bodyweight.. maybe everything in moderation? oh and i take 2 capsules boulouke every am and 3 grams niacin every am
Studies suggest Lp(a) may be more problematic when it is elevated in conjunction with LDL
Niacin works on both so you on the right track there. I found that my Lp(a) dropped (31 to 18) when I upped my Vit C intake. I take a supp’ in the morning along with a whole pink grapefruit and two Kiwi fruit on my porridge.
i have read about VIT c linus pauling theory my Lpa is 99 its crazy i’m just afraid that much Vit c may loosen bowels? how much do you take
and yes Niacin seems to be the only proven remedy though I have actually read an aspirin a day can help too?
i just wish there was more consistent information on food and its affect as I do believe it does affect lpa levels Im esp curious in reading the saturated fat lowers lpa and that plant fat , esp, stearic acid found in chocolate has always been touted as cholesterol neutral but then i have read that is actually raises it?
I take a bog standard 1000mg tab of Vit C
Ok I wonder how that works with the fact i tend to store iron bc of the mthfr defect and vit c increases iron absorption ? i do take methyl guard for increase b12 and folic acid to aid in methylation and IP6 to lower iron niacin i dont mind at 3 grams a day i like the flushing actually for now Ive just added the lysine part without the vit c and proline i take 3 g lysine Ill post when i see results
all this information makes me dizzy! What about the Dean Ornish diet, supposedly stops progression of heart disease and in a few cases actually reverses it. Very, very low fat diet. An opinion on that diet and his study would be much appreciated. Thanks.
Research has shown that low fat diet actually increases the LP(a) levels. (https://www.ncbi.nlm.nih.gov/pubmed/17556688) I did read a journal article that showed a high fat, low carb diet, basically ketogenic diet, had good results in lowering LP(a) but damned if I can find the research again.
There is this one (https://www.ncbi.nlm.nih.gov/pubmed/15930434/)but the one I read specifically showed benefits to high fat diet in lowering lp(a).
My LP(a) is in the very high risk category so have been supplementing with niacin, Vitamin C and trying the keto diet.
angela mine is in very high risk at 99 as well. yes, I have read that high carb low fat raises Lpa BUT lowers LDL but raises TRI’s and that high sat fat (especially high dairy fat!) lowers LPa but pf course raises LDL> so which is more important I guess for now, Ill focus on lowering LDL as LPa is a higher risk factor when coupled with high LDL. it is all confusing.. how much Niacin and Vit C do you take
I have high lp (a) and APOE 3/4 with normal fasting blood sugar but high diabetic after meal blood sugar. I had a heart attack 5 years ago and have 3 stents. I’m lucky I survived without major damage since i had 3 arteries clogged at 95 to 99%. Somehow the blood was able to find a way around during my heart attack. Might be because I was relatively young at 39 years old when this happened and built up collaterals due to exercising all my life. I was on a high fat low carb diet for 3 years to lose weight before the heart attack. I thought as long as I controlled blood sugar and loss weight i was healthy on low carb high fat. I didn’t realize at the time my body couldn’t process high fat because of the APOE 3/4. My APO(b) and LDL was extremely high on high fat low carb but my triglycerides were very low. I didn’t understand the risk of having high LDL and APO (b). I’m now on 10mg Atorvastatin, baby aspirin, plavix, coq10, fish oil, vitamin c, vitamin d3 5000, vitamin k2, magnesium. citrate, thorne B complex -#12 with Methyltetrahydrofolate. I try to stay lower carb and low fat most of the time now. Mainly vegetables, small amount of meat and rice. I try to stay away from processed foods.
I have a theory on the Ornish results. APOE 4/4 or 3/4 type people have a tendancy towards heart disease and are best suited to a low fat diet. Given that they only amount to about 26% of the population it statistically makes sense that the pop as a whole will do better on a high fat low carb diet even if 26% are suffering. Now Ornish treats patients or at least his study did, who already have heart disease. Could it be that given this, they may be predominantly type APOE 3/4. What if say 75% of his patients are 3/4?. They would then be responsive to his diet of low fat. I would be grateful if Chris or others could respond to this idea.
I am so curious too
I am APOE 3/4 very fit active but bc of celiac and other gut issues i am underweight and really struggle to maintain weight. I also Have SUPER high lpa and high LDL I am so confused as to how to eat to gain and maintain weight as I know both high fat AND high carb increase cholesterol esp in people like me who already overabsorb fat and cholesterol this stresses me out so much i feel like everyday Im trying to figure out what to eat and i spend way too much time worrying about it when I see all my family and friends eat anything they want and they all have low cholesterol
my lpa test came out 562 nmol……I feel as though I am a dead man….can anyone send me some words of hope???…lol….yes I’m laughing because the lpa is so high, you just through your hands in the air…
OK so mine is high at 99 but yes your is very high. I think Niacin is one of the first line therapys to try start with one gram for week one two grams week two and then three grams per day as maintenace and see if LPa lowers. If your LDL is ok i think LPa is less of a risk factor. what does your doctor say? also get your LDL particle size checked if its the good large ones, then the LPa will also be the largers less dangerous particles as well..
I am sorry to hear your LPa is that high. I just found out mine is very high at 258 and I feel the same way you do.
I was wondering if you have tried niacin aspirin therapy, fish oil, or statins or anything. I hope you are getting some help. I am taking fish oil, lipoprotein, methyl protect and vitamin k but don’t know if it working yet.
I also tried red yeast rice but wasnt able to tolerate it due to severe muscle aches or niacin because I have rosacea. Hope to hear from you take care Michelle
Vitamin C lowered mine fro 31 to 20
how much vit c a day i just added 1000mg once a day in the morning along with 3 grams lysine, boulouke, methyl b12, zinc, probiotics (l reuteri has been shown to favor cholesterol levels) 3 grams niacin and thinking of adding l carnitine, lots of studies have show l carnitine effective for lowering both LDL and lpa….your thoughts. i hesitate to go all out with the vit c (5-6 grams a day) like one lpa reducing protocol calls for b/c in such high doses antioxidants become pro oxidant. would love Chris to weight in on this
1000mg a day plus a pink grapefruit each morning and kiwi fruit on my porridge. 18 months ago I was away for 3 months and half way through ran out of Vit C tabs and did not bother to replenish. On my return I had one of my tests and Lp(a) was back at around 30 returning back down to the lower amount when I hit the vit C again. Niacin has also been shown to lower Lp(a) so you are right to try it. Basically test yourself then go on the regime and retest after say 3 months. Nothing is more motivating to keep things going than seeing the numbers.
I have seen evidence that if your Lp-LPA2 is low even with highest Lp(a) one would still have very low risk. I have high Lp(a) as well 250 nmol/L. BTW I think people are mixing up or not stating units in this discussion. Lp(a) can be measured in nmol/L and mg/dL.
Also I pushed my doctor to get a CT with calcium score which should further give me an idea of risk. Haven’t had the test yet though.
I’ve been following Dr. Ford Brewer on YouTube and he suggested using crestor/ rosuvastatin to lower inflammation. He also suggest using Enduracin a niacin product you can buy on Amazon to lower lp ‘a’. I started taking 1000mg of niacin and I can say that it lower my lp ‘a’ from 105mg/dl to 87mg/dl. Still high but any improvement is better than nothing. So I’m on both rosuvastatin and Enduracin to slow my heart disease.
My Lp(a) was 31 it is now 18. The reduction was achieved by increasing my Vitamin C intake which has also been backed up by research
what did you up vit c to?
do you take it once or multi times daily i know its water soluble so does not last long in system
Statins were mentioned not to do much (in terms of lowering mortality) for those with existing heart disease, is the same true for aspirin? I thought taking a low-dose aspirin is generally safe and possibly effective means of lowering cardio vascular risk.
In an interview with Rhonda Patrick, Peter Attia mentions that blood pressure and ApoB (which can be interpreted as the LDL particle count) trumps all other cholesterol/heart markers for predicting cardiovascular health. He didn’t mention it, but I imagine he would also favor ApoB/ApoA-I.
Cholesterol guru, Chris Masterjohn, however sees Total Cholesterol / HDL as the most useful metric, since ApoB/ApoA doesn’t capture the movement of cholesterol from HDL to LDL that occurs with increasing time of LDL spent in the blood.
Now we’ve added more with LDL’s Lp(A) in the mix, and even Lp-PLA2!
But the overall nutritional prescription seems to be the same, eat fish (for the Niacin/B3, Omega3s) and possibly supplement with liposomal vitamin-c, l-lysine, and l-proline, lumbrokinase, and vitamin-e.
Correction, Peter Attia thinks Lp(a)-P (particle count) is the useful measurement (I’m guessing that not the same as ApoB as I originally wrote)
There is a research article showing Lp(a) can be lowered in mice with Vit C and I have personally found that it works for me. I had it pinned at 21 and then for two months when I did not supplement it spiked up to 31 only to return downwards on supplementation. I have since adopted a morning grapefruit and it is now at 18
Just curious. Do you have the research article available? I’ve been doing the Vit. C and the amino acid approach. Will be retested in a few weeks to see if that has helped. Thanks!
Hi Jan, here is the link
Thank you Mark. I appreciate it.
Let me know your retest results please, would be interested
Yes, absolutely. I’m giving myself a couple more weeks to recoup from the holidays! lol
I didn’t have great results as I had hoped with the amino acid and Vitamin C protocol, but I must admit that I started out strong 3 x day, only to decrease it to 1 x day after a while. Was kind of a pain and unfortunately I didn’t receive the proper dosage. I’m still taking it until my supplies last. I wish that it had helped.
I find that dosing on Vit C supp’s can be a pain so I just take one modest 700mg one but what I do with habit is have a grapefruit each morning and 2 kiwi fruit on my porridge. The latter two are easy to adopt assuming you like grapefruit and Kiwi.
Thanks for the info and tips. For now, I’ll continue to take 1 g of Vitamin C in powdered form with 1/2 lemon juice and eat some fruit in the morning like an orange or berries so hopefully I am getting enough. Oh well. I don’t know what to think about this Lp(a).
i agree ..i have high normal LDL high HDL and super high lpa at 135 nmol. i take a protocol similiar to yours: i take 2 grams EPA eat fish 3 grams niacin immediate release, 1 grams vitamin-c, 3 grams l-lysine, two lumbrokinase, methyl b 12, magnesium, zinc and pycogenol and recently added k2 as it brings calcium to bones and out of arteries.
would love to hear Chris;s take on the high doses of vit c that the pauling theory calls for ( antioxidants becoming pro oxidat at high chronic levels ) and also his take on l carnitine (great for fat metabolism and lowers lpa) but what about the concern on l carnitine producing TMAO – is l carnitine lowering lpa at the expense of raising TMAO which has a negative effect on the CV system. wish there was one person who could decipher all of this Lpa stuff for us so much conflicting evidence bc up until recently most drs dont treat lpa as its “untreatable” with bob harper spreading the word, hopefully more drs will become educated in this area to help us
My Lpa is in the 400s . I was wondering when you inflammation is that high can your body feel as though you have flu like symptoms? I am doing all the right things to lower my Lpa .Is this normal when it is high or due to something else? I was 44 when I had a stent. Exercise 5 days a week, look like I’m the picture of health but feel terrible.
I just found out I have a high of 357 LIPOPROTEINS and had a stent when I was 44. I work out 5 days a week. I don’t know what to do to lower my level. What should I do?
Hi below are my lab results
LIPID PROFILE, BASIC, SERUM
Cholesterol Total 184.00 mg/dL <200.00
Triglycerides 77.00 mg/dL 50.00
LDL Cholesterol 125.60 mg/dL <100.00
VLDL Cholesterol 15.40 mg/dL <30.00
Non-HDL Cholesterol 141.00 mg/dL <130.00
GLUCOSE, FASTING (F), PLASMA
86.00 mg/dL 70.00 – 100.00
25.00 mg/dL 17.00 – 43.00
(Compensated Jaffe's reaction, IDMS traceable)
0.65 mg/dL 0.60 – 1.00
URIC ACID, SERUM
2.20 mg/dL 2.60 – 6.00
LIPOPROTEIN(a); Lp(a), SERUM @
85.60 mg/dL <30.00
My height 5 feet 4 inch
Age 25 Female(Indian)
Am I @ a high risk of heart attack
Plz reply me
Thanks in advance.
Thank you for the great article and information. I too have elevated Lp(a) and began the Vitamin C and Lysine, Proline, etc. protocol a couple of months ago after reading about it on line. Forgive me if this has already been addressed, but I was wondering if you have gotten any good results with your clients? Did it work? I’m just curious. I cannot tolerate the niacin flush and that affects homocysteine as well, which I am trying to bring down. Thank you.
I can confirm that my Lp(a) decreases when I stay on the VitC supp’s and rises on the odd occasion I have slipped from taking it. There is a Pubmed paper which also cites Vit c for lowering Lp(a) (not a Pauling/Rath one by the way). I have issued a couple of blog entries on this, here is one that is a summary of Dr William Davies interesting views