If you’re concerned with cardiovascular health, a special type of LDL particle, called Lipoprotein (a), should be top of mind. This special type of “genetic bad cholesterol” is elevated in millions of Americans and yet very few people are ever tested. In this episode of the podcast, we sit down with integrative cardiologist Dr. Joel Kahn to discuss current strategies for dealing with and lowering Lp(a). Dr. Kahn’s new book is called Lipoprotein (a): the Heart’s Silent Killer.
This Episode Covers:
- Bob Harper and Lp(a) [5:35];
- Lp(a), SNPs and genetic bad cholesterol [8:20];
- What is considered high Lp(a)? [13:00];
- What to do if you have high Lp(a)? [18:00];
- Plant sterols and high Lp(a) [28:30];
- COVID-19 and Lp(a) [34:00];
Dr Kahn: With the best of medicine, using standard approaches, we can reduce the risk of heart attack in somebody who has coronary artery disease 30%, 40%, 50%. These are huge numbers and very meaningful and powerful, but that leaves a big number that we have not impacted. That’s called the residual risk. Of that residual risk, we’ve come to recognize there’s a cholesterol particle, that we learned about in 1963, is different than LDL cholesterol, HDL cholesterol. And that’s called lipoprotein little a.
John: Welcome to “The Gene Food Podcast.” I’m your host, John O’Connor. Hey, everybody. Today, we have Dr. Joel Kahn coming back on the podcast to discuss a very important topic, which is called lipoprotein (a). It’s known to be a genetic form of “bad cholesterol.” You can see your risk for lipoprotein (a) by having a genetic panel done or by getting advanced blood work done. There’s a lot of people out there that have elevated lipoprotein (a), including some celebrities that have been vocal about their experience with lipoprotein (a), but most people are not being tested for it.
In Dr. Kahn’s new book “Lipoprotein (a), the Heart’s Silent Killer,” he gives an overview of the problem, as well as some of the solutions, the potential pharmaceutical agents that are out there on the horizon that can lower lipoprotein (a), some of the dietary strategies for lowering lipoprotein(a). You’ve seen Dr. Kahn everywhere. He’s been in “What the Health.” He’s been on “The Doctors.” He’s becoming a very well-known advocate for plant-based diets, but he’s also somebody who’s really on the cutting edge of laboratory testing and the science of preventative cardiology. So, we’re really lucky to have him on the podcast for a second time. Without further ado, here is an episode all about lipoprotein (a).
So we got Dr. Joel Kahn here. We’re gonna take a little bit of a coronavirus break and talk about his new book, all devoted to “Lipoprotein (a), the Heart’s Quiet Killer: A Diet and Lifestyle Guide.” And this is an important message. People out there, they don’t know that they have high Lp(a). They don’t even know what it is. Let’s tell them. Let’s get this on their radar.
Dr. Kahn: All right. And be sure before we say goodbye that let’s connect lipoprotein little a to coronavirus, because there’s at least a thin thread or two.
John: Yeah. Let’s connect it early on. Let’s do it. I love it.
Dr. Kahn: So, again, you got a real sophisticated audience. I’m a clinical cardiologist. My goal is to try and help patients and people have the lowest risk of heart attacks, bypass, and dropping dead. Still the number one risk to our health for men and women in the Western world. It’s a daunting and challenging concept. One wishes we would have attacked cardiovascular disease with the same ferocity we’re attacking controlling coronavirus. That’s no comment on the fact of whether what we’re doing is right or not. I hope it works. Of course, I’m very, you know, intensely involved in trying to control the virus spread with every measure everybody else is taking. But heart disease is still of great concern, and I have still, you know, patients showing up with advanced heart disease right in the midst of this, you know, pandemic.
There’s a concept though called residual risk, which is really critically important. You go to your doctor, and your doctor measures your blood sugar and your blood cholesterol, or maybe you send away to an advanced lab because you’re a bit more of an advanced biohacking type. Either way. You know your body weight. You know your BMI. You know your blood pressure. You know how many hours you sleep. You track all these things. With the best of medicine, using standard approaches, which can of course involve lifestyle, pharmaceutical drugs, and such, we can reduce the risk of heart attack in somebody who has coronary artery disease 30%, 40%, 50%. These are huge numbers and very meaningful and powerful.
But that leaves a big number that we have not impacted. That’s called the residual risk, that even the person that’s had a stent or bypass or heart attack and is on maximal everything, is still walking around on average with that kind of risk. Of that residual risk, we’ve come to recognize there’s a cholesterol particle, that we learned about in 1963, is different than LDL cholesterol, HDL cholesterol. And that’s called lipoprotein little a. In studies that look at what contributes to that other 50% or so that we’re not completely suppressing, the biggest factor seems to be this cholesterol molecule, which can be measured in every lab, in every hospital, in every LabCorp and Quest, and you can send away for it with a simple blood test. Part of it is the awkwardness of saying lipoprotein little a, it’s lower-case.
The problem is there’s also a capital A in the world of cholesterol measurements, called Apolipoprotein capital A. So, we’ve already lost half the people already, because they have to remember it’s a lowercase a, lipoprotein little a, or Lp(a), or I just call it the “sticky cholesterol.” But it’s a fascinating topic that in the next five years you’re gonna hear about all the time, because the pharmaceutical industry has taken their time, but is now focused on creating agents to hopefully help people, to promote to doctors and the medical world, as a solution for this residual risk. But you don’t have to wait till your friend Pfizer and Merck bring you something. We can talk about it now.
John: Right. I think a good way to get into this and kind of relate this story to people who are interested in the cardiovascular conversation, you’ve been on the forefront of bringing this out, Bob Harper. Bob Harper of “The Biggest Loser.” Everybody remembers “The Biggest Loser.” He’s ripped. He’s in great shape. He’s out there as a thought leader in the fitness space, but he has a heart attack. Why?
Dr. Kahn: Exactly. That was I believe February 2017, and it made headlines when it happened. And he didn’t just have a heart attack. He was in a gym running a treadmill in New York. He collapsed. He was in full cardiac arrest, and about 80% of those people will die. But he had the good fortune. He had a medical doctor right next to him on the treadmill, and he had a defibrillator in the gym right in front of him. And they were able to resolve the fatal arrhythmia, called ventricular fibrillation, but emergency stent, ventilator, and a prolonged recovery. But fortunately, he looks really good now.
But he announced on both social media and national TV about two months later, “I learned I inherited, along with about 1.8 billion people in the world, 25% of us, I inherited a very high level of a kind of cholesterol that sticks to the wall of my arteries, created plaque, created an acute myocardial infarction.” And it was reported in “The New York Times” and several very prominent articles. His role has faded a little bit. He still does some pharmaceutical ad work. But, yeah, that got the headline. I don’t think any other single event has brought that word lipoprotein little a into the public eye as much as Bob Harper. So we owe him a sense of gratitude for going public with it all.
John: And he probably had a normal lipid panel. I’m sure that he was getting blood work done at least on a regular basis, and not seeing the Lp(a), because it hides out…
Dr. Kahn: I don’t know for sure, you know, and I’m not…neither am I close friends with Bob Harper nor am I judging anything he did. The world’s a difficult place, but he was pretty fully plant-based, and then took a little dive into low-carb, keto, talking a little bit about Bulletproof Coffee for the couple of years before his heart attack. So, I don’t know what his panel looked like, but we do know that at least part of it was inheriting a complex cholesterol molecule. But if it were rare, there’s a lot of rare things in the world. We’re talking, you know, however many people right now are listening, one out of every four likely has the same inherited cholesterol that Bob Harper had. Not all will have heart attack, strokes, and valve problems. This is not a scare show, but it’s an educational conversation.
John: [inaudible 00:08:18] You could call it “genetic bad cholesterol.” I think it would be fair to say, right? I mean, you can see snips, like, we have snips in our fat scoring panel, even though there’s not always as much you can do with diet, that will show the Lp(a) region of the gene, there’s snips in Lp(a), and you can say, “Hey, like myself, I have a heterozygous snip for some of these Lp(a) genes, and I see it show up. I have moderately elevated…you know, usually moderately elevated Lp(a) in my blood work.”
Dr. Kahn: Exactly. You can do it via the 23andMe kind of approach and measure snips. You can actually measure the presence, if you inherited one of several gene sites. It’s called that Lp(a) intron. Part of it is, and maybe we’ll just go off for a minute without getting too boring here. It’s an interesting molecule. Lipoprotein little a, the sticky cholesterol, is an LDL particle, low density lipoprotein particle, with a protein coat around some amount of cholesterol, fatty acids, internal to the LDL particle. There’s a little bridge, a little, two sulfur bonds, and then there’s this weird extra piece. And the weird extra piece, when people draw pictures of it in textbooks, the LDL particle looks like a round tennis ball. The little bridge is just a tiny little stick. And this piece looks kind of like an arc, or almost like a cap on top of the LDL particle, and it’s called apolipoprotein little a. The thing about it is you can inherit very little of it, and your blood work will show a very low level, or undetectable amount of lipoprotein little a.
You can inherit a moderate amount, and you can inherit a lot. But you also can inherit it, this apoA, to be a very big, complex add-on or a smaller. The size varies tremendously. It’s called kringles, and it’s probably not worth going too deep on, because we have no way to measure it in routine practice. But there’s something unique about the apoA, the apolipoprotein little a, that’s part of this bigger molecule, lipoprotein little a, because it carries not only cholesterol on it, it carries some additional features called oxidized phospholipids, OxPL. And they exist in the blood. They’re not only found on lipoprotein little a. But they’re uniquely inflammatory and atherosclerotic particles. And if this molecule impacts on the wall of an artery or on the covering of heart valves, particularly the aortic valve, it can stick.
Lipoprotein little a has a particular affinity to stick to injured endothelium, injured artery lining, where there might be some collagen that’s disrupted, and some lysine and proline molecules are exposed. And it’s interesting. There’s a question, “Why does anybody have lipoprotein little a in the blood?” And sometimes we don’t know the answer. But there’s a theory that the ability of lipoprotein little a to stick to arteries that have injury and have exposed some collagen may form…and this is very, very simple, may form some kind of band-aid, temporary cover healing to the injured artery, presumably some advantage to avoid bleeding or other problem. But it dumps cholesterol, and it dumps oxidized phospholipids right into the endothelium, where they can be absorbed and get subintimal, and begin a plaque so that…
There’s even a little human data that it may reduce bleeding risk during delivery and pregnancy, but whatever advantage it has early in our life, possibly, and there’s only about four species on the planet that can even produce lipoprotein little a, which humans are one of the four, or we won’t be talking about this. There becomes a disadvantage later in life, because we live longer than living to reproductive years. Of course, we hope to. And there are the disadvantages, increased risk of atherosclerosis in the cerebral arteries, stroke, in the coronary arteries, heart attack, and in the aortic heart valve, causing aortic stenosis, so interesting thing.
And the idea here is, should people be aware if they, either by measuring snips, measuring genes, or just having a simple blood test, of your level of lipoprotein little a? Should you add it to your self-assessment, biohacking, risk assessment profile? And I would argue yes, and now the European Society of Cardiology has in 2019 finally come on board to say everybody should be tested once, earlier the better, so you can implement some sort of program if you find out you inherited it.
John: Right. So, interesting point. I believe the European Atherosclerosis Society, correct me if I’m wrong, have stated that anything that’s above 50 milligrams per deciliter is higher risk for Lp(a). What I just heard you say is fascinating, which is that the apoA tail varies in size, and you would assume that because the apoA tail varies in size, that that can throw off the weight-based measurement, which is the milligrams per deciliter weight-based measurement. Does that mean that we are better off, which I don’t believe hardly anybody is doing, by the way, testing for Lp(a) particle, as opposed to Lp(a) mass?
Dr. Kahn: Yeah. And I will admit, I’ve described it just as you’ve described it, that there’s…this is, again, unfortunately, there’s two ways to measure in simple blood work the level of lipoprotein little a. One is in milligrams per deciliter, as you said. It was the original one. Less than 30 was considered normal, 30 to 50 was intermediate, over 50 was of enough to perhaps drive a clinician to advise a patient that they’re higher risk, and implement some sort of plan. And then along came the other way to measure it, nanomoles per liter, nmol/L, nanomoles per liter, where it’s a slightly different range. Less than 75 is normal, 75 to 125 is intermediate, over 125 is considered high risk. The current trend is labs are converting over to the second, to the nanomoles per liter assay. It’s sometimes described as mass and weight and such, although when I’ve discussed this with Dr. Thomas Dayspring and all, that’s too simplistic. And I’m not sure we’re doing justice to [inaudible 00:14:49] by simplifying it to that degree. So, that’s just suffice it to say it’s very common when I am counseling with a patient, and they’re concerned, “My, God, my lipoprotein little a used to be 45 and now it’s 149. I mean, what happened?” It simply was the lab that they went to shifted the assay from milligrams per deciliter to nanomoles per liter. You can’t completely convert one to the other. But roughly, if you’re twice the upper limits of normal in one way, you’re gonna be roughly twice the upper limits of normal in the other. At least that’s been my general experience.
John: N equals one, I’ve had them done both ways, and I had them done like a couple weeks apart, like, I think it was Quest that did it in nanomoles per liter, and then I went to another lab that was milligrams per deciliter, and those two were concordant. Although I believe those are still two weight-based measurements, and I think there are…technically, I think you can get your total Lp(a) particle count. Do you know of any labs that would give you that?
Dr. Kahn: Not yet. The newest thing on the block, I’ve not ordered it, is, I think, you know, you’re aware of this, for the first time, a clinical lab has developed a way to measure oxidized phospholipids. Lots of research on elevated blood levels of oxidized phospholipids, which are carried by lipoprotein little a, but they’re also carried by other lipid particles, are a risk for heart attack, stroke, and other kind of vascular events. So, perhaps that’ll add a little bit of refinement to the whole discussion we’re having. But there’s only one lab that offers it, and I’ve not chosen to send any lab there, yet, any blood work.
John: Gotcha. And that was the doctors I believe, Tsimikas study, which I wanna give you the opportunity to tell the audience about. A lot of people who are listening to this podcast, they’ve already done internet research. They’ve come across stuff on, you know, some of the more keto-friendly Cholesterol Code type websites that love to publish a study that shows that because of the fact, as you mentioned, that oxidized phospholipids are this major problem for Lp(a), that eating a diet that was higher in saturated fat actually lowered Lp(a).
Dr. Kahn: Right. You know, there’s a study in 1997, and it’s an interesting first author because the name is Clevidence. It’s evidence with a CL. It’s this interesting last name. But if I was trying to practice evidence-based medicine, it would be a cool last name to have. I do try and practice evidence-based medicine. And they took 50 people, [inaudible 00:17:18] I don’t even think there were 50. But this is what’s important. They were healthy volunteers. And most of them did not have elevated lipoprotein little a. They were in the normal range. And they fed them four diets for a number of days, one high in oleic acid, about 40% of calories, one high in trans fats, which, that was 1997. We wouldn’t be feeding healthy volunteers trans fats. It’s largely been legislated out of the diet.
But one of the arms was a diet high in saturated fat, and there was a very small drop in lipoprotein little a in the saturated fat diet. There was either no change or actually an increase in the other diets. But it was a very small change, from a normal level. So, what is the clinical significance of that? To my knowledge…and Dr. Tsimikas from University of California, San Diego has done a follow-up study, too. But, you know, when you’re dealing with any listener you have, they go get their blood drawn because of this conversation, and they have a lipoprotein little a level of 250 nanomoles per liter, and in my clinic, that’s not a world record. And that’s not rare. They’re out there all over the place. I mean, that’s, you know, two to three times the high-risk upper limits of normal.
You know, there has not been a study looking at in that high a level plant-based diets versus keto diets versus Mediterranean diet. We are absent that kind of data. All the dietary studies have been done with people with nearly normal or completely normal levels, and it just begs the question how relevant is it. So, for a lot of other reasons, I wouldn’t recommend a high saturated fat ketogenic diet to somebody with a markedly elevated lipoprotein little a, because I’d worry about what it’s gonna do to their LDL particle numbers and particle sizes and viscosity of their blood, and if it’s gonna disrupt their microbiome and cause endotoxemia and all the other things that can happen. So it would seem self-defeating.
John: Right. That’s a great point. The people that are walking around with the Lp(a) of 4 milligrams per deciliter are likely not the people that are carrying the Lp(a) snips and are therefore not the people that are gonna have this break-off point of Lp(a) at 30 milligrams per deciliter, as you say, 100 milligrams per deciliter, 250 nanomoles per liter. So although I think…when our research team looked at it, they were like, “Yeah. It’s a very well-done study, but I don’t think it’s looking at the right people.” It’s not looking at the people who have, as you say, this residual risk for heart disease because of elevated Lp(a). So we’ve kind of set the table here. I think most people are listening, they’re thinking, “All right. We have this genetic type of bad cholesterol. Bob Harper had a heart attack. You know, this testing is gonna really be proliferating through the system as we go. What the hell can I do to lower this thing?”
Dr. Kahn: Right. So it would seem obvious that it’d be good to lower it. There are some genome-wide association studies, and for a moment, I’m blanking, I’ve actually done some of these genomic studies, but there’s another term for them, that do suggest if you have a inherited low lipoprotein (a) level for life versus an inherited medium or high level for life, there’s quite a bit difference in your, you know, lifetime risk of atherosclerotic events. You would imply by that that lower’s better. I think everybody would say that. What we don’t know for sure is lowering it better? I would assume it is, but we haven’t yet had the ability to have a really powerful agent that’s well-tolerated to test that hypothesis. I think we’d all anticipate.
So what the hell can you do? Number one, the current, kind of, recommendation, there’s a wonderful group called the Lipoprotein A Foundation with a website and very wonderful people, very dedicated, and passionate out of personal loss and personal tragedy to spread the word, they have a very well-respected advisory board for sure, of which Dr. Tsimikas is on it, would say, once you know you’re elevated, ignore the number. Don’t retest the number. This is right now. But do all the other things that are known to reduce risks, from diet, which I would promote would be largely or completely a whole food plant diet, fitness, sleep, management of blood sugar, blood pressure, stress, the whole lifestyle, and, if needed, pharmacological approach. And very often, use a statin, whatever statin of the day you like to use like atorvastatin (Lipitor), rosuvastatin (Crestor). Not because any of those are very likely to drop the lipoprotein (a) much, but they’ll deal with the non-residual risks, the part that we have reasonably good data for decades, we can reduce.
If you wanna push it to the extreme and you wanna implement an Ornish or an Esselstyn kind of diet, you’re on a pretty good foundation for lowering cardiovascular risk and event rates, but it hasn’t been tested in people with lipoprotein little a elevation. We’re just, again, transferring data and other sets to a recently recognized higher risk group. There are a few things out there. Coenzyme Q10 has a meta-analysis, it may lower lipoprotein (a) by 10 to 15%. It’s not a lot if your blood level’s high, but it’s a little bit. Ground flaxseed has a meta-analysis, lowers lipoprotein (a) a bit. Plant-based diets have one study, not very impressive, but it’s out there, may lower lipoprotein (a) a little bit more, 20%.
Women going through change of life who adopt hormone replacement therapy may lower their lipoprotein (a) quite considerably, and it’s not recommended they do it specifically for the lipoprotein little a, but if in their overall package of their menopausal assessment they wanna do it, they may experience a drop in their lipoprotein little a. I didn’t mention, there’s a prescription cholesterol drug I use a lot ezetimibe, or Zetia, that, cholesterol absorption inhibitor, doesn’t lower lipoprotein little a. I skipped by it, statins, which, you know, it’d be a home run if statins lowered LDL and LDL particle number and lipoprotein little a, but they don’t, with most of the literature. There’s a single long-term study that suggests, with, I think it was pravastatin, there may be a…If you go far enough out, a few years out, you can see lipoprotein (a) come down. But most of the statins don’t lower lipoprotein little a, and they sometimes cause it to go up, if you choose to retest the lab value. If you don’t choose to retest it, you won’t know that.
Fibrates, not very popular anymore, gemfibrozil, fenofibrate, don’t lower lipoprotein (a). So we’re going through this whole list. So we’re only left with a couple right now in 2020, niacin, as an over-the-counter prescription, vitamin B3, used to lower LDL cholesterol, raise HDL cholesterol, lower triglycerides. In some people, niacin will lower lipoprotein little a dramatically, and I have a lot of those people in my practice. Their lipoprotein little a went from 150 nanomoles per liter to 22 nanomoles per liter.
Dr. Kahn: Yeah. There are those that drop 80%. That’s also in the literature. Niacin isn’t the most popular drug in the world of cardiology right now. You need to watch for gout. You need to watch for ulcers. You need to watch blood sugar, liver enzymes. It’s been used for 50 years, but you can’t use it without at least a little concern. Of course, there’s the hot flushing, but that’s, for many people, not a big deal. And then there’s the injectable cholesterol drugs that were approved four to five years ago, PCSK9 inhibitors, Repatha, and Praluent, that are approved to lower LDL cholesterol either in people that can’t tolerate statins or that can tolerate statins, but they can’t reach the goal, very expensive drugs. But they happen to lower lipoprotein little a if it’s elevated in most of the people on it by 25% to 30%. It’s not everybody. I have one very frustrated gentleman I take care of in Pittsburgh that his lipoprotein little a went up on these injectable cholesterol drugs, although on average, that’s not what’s supposed to happen.
And then we’ve got, five years from now, the hope we’ll have a antibody. That’s in clinical trials now, although the clinical trial’s halted for the coronavirus situation because nobody can go to the clinical test centers. But there’s an antibody to lipoprotein little a that, in the first 200 patients, showed safety and could lower lipoprotein little a, again, by about 80%. This is a 7,000 patient randomized study looking at outcome, heart attacks, strokes, side-effects. So, you know, it’s never gonna be FDA-approved till the study has enrolled enough people. And it is only enrolling people obviously with elevated lipoprotein little a and some evidence of atherosclerosis, so, unlike these diet trials we were mentioning, which really don’t lead to much conclusion because they were largely tested in people with normal levels of lipoprotein little a. You know, these will be the real McCoy bullseye patients that need to get a therapy that they don’t have right now.
Just lastly, there is a therapy. I don’t know how much you know about it, John, or your listeners. But I’d say 25 years ago, some bright researchers adapted the dialysis that kidney patients were getting, end stage kidney patients, to create a cartridge that would capture LDL cholesterol in the cartridge, and for people with homozygous familial hyperlipidemia or severe heterozygous hyperlipidemia, it’s called lipoprotein apheresis. You sit in a chair with a needle in your arm for 2-3 hours every two weeks, and you may watch your LDL cholesterol go from 300 to 30, and over the next two weeks, it will creep back up. And you do this every couple weeks. That’s actually an FDA approved and insurance approved treatment that’s used quite rarely, but it’s used. It’s also insurance approved for elevated lipoprotein (a).
So in Germany, they’ve adopted this rather aggressively. They have some papers with more than 1,000 people with lipoprotein little a that are treated with apheresis, or ultra-filtration of their blood, through a specific cartridge that traps lipoprotein little a in the material, the cartridge. So when the plasma goes back into the patient, it has nearly or no lipoprotein little a. And again, for a couple of weeks, it’ll keep the blood level down. So, just to mention, for extreme cases with bad atherosclerosis, a few universities around the United States do offer this treatment.
John: Interesting. To harken back real quick to Zetia, if you have a patient who has elevated sitosterol, you know, they’re absorbing a lot of the fats in nuts and seeds, which I don’t know whether this, it’s a two-part question, whether the sitosterol tracks with the OxPL so that the more of the nuts and seeds you’re absorbing, more of those fats, the more of them oxidize. Zetia may not lower Lp(a), but could Zetia, by virtue of the fact that it’s blocking the absorption of these plant sterols that then oxidize and kind of make Lp(a) that much more atherogenic, could it be like a defensive shield against the atherogenicity of these Lp(a) particles, do you think?
Dr. Kahn: It could be. I mean, there’s a meta-analysis of six or eight studies, looking at lipoprotein little a levels in people put on ezetimibe, Zetia, and it’s pretty neutral. They don’t raise it like statins often do, but they don’t lower it. Nobody’s looked at OxPL levels. It may well do that. I think Zetia is a great add-on prescription in general because, you know, very small doses of a statin with the standard dose of Zetia will get you excellent cholesterol control without having to go to very high doses of a statin, and lower side effects and all. But its impact specifically on a shield because maybe you’re depleting oxidized phospholipid in your lipoprotein (a) particle is unknown to me.
I just wanna make sure I say this. One of the really unique things about lipoprotein little a isn’t just that it’s another cholesterol that promotes atherogenicity in the arteries. For reasons that aren’t completely understood, but it’s felt to be the oxidized phospholipid, that people with elevated lipoprotein little a are much more likely to develop scarring and calcification of the aortic valve. I’ve mentioned that. But there’s a fairly common condition called aortic stenosis, where doctor hears a murmur, or the patient’s short of breath or the patient’s starting to get chest discomfort or dizziness on exertion, and they hear a murmur, you do an ultrasound, and the aortic valve, the last valve in the heart that has to open to let blood eject, is terribly scarred and terribly calcified and isn’t opening well. And there used to be an open surgical procedure, aortic valve replacement, but many of them are now done through a innovative treatment through the leg called percutaneous or transcutaneous aortic valve replacement. Still a big procedure. Lipoprotein little a is felt to produce one out of every seven of these clinically advanced cases.
So, that was a couple hundred thousand people in the United States alone getting this kind of heart surgery. Maybe that number is a little lower than that on average in the United States. But one out of every seven was due to this particle that is never measured in people with aortic stenosis, although there are research studies that have done that. They’ve gone back, you know, “1,000 people that had this procedure, let’s look at their blood that we had in the blood bank.” And they find a very high frequency of elevated lipoprotein little a. But it’s not just a marker. It’s actually causative. It literally causes valve destruction, in some people.
There are people that have elevated lipoprotein little a live a long life, never develop a heart attack and never develop aortic valve problems. But physicians will be taught more and more, in a case of aortic stenosis, measure lipoprotein little a, and in a case of elevated lipoprotein little a, listen more carefully to the heart exam with a stethoscope or maybe order an ultrasound to directly look at the valve.
John: So what I hear you saying is… For somebody that’s looking for the top-level message, we’re gonna close out here on the immune system and COVID-19, which is an interesting angle. What I hear you saying is if you find out that you have elevated Lp(a), get very hawkish about your apoB number. Figure out the diet that works for you that gets your apoB number as low as possible, and go get a calcium score.
Dr. Kahn: Agree. And I’d just add and your high sensitivity C-reactive protein, giving a fair shake to, you know, the data that controlling inflammation through weight control and lifestyle and diet and perhaps supplements is, you know, pretty critical to the equation also. Some of your listeners may or may not know this. There’s a very cool website called astrocharm.org, which is a database from Dallas started about 15 years ago. Thousands of people were offered free calcium scores by CT imaging, but they also agreed to have a little bit of blood work at the beginning and be followed for 10 years. These were healthy people. Did you ever develop a heart attack, a stroke, need a bypass, and all the rest? So, if you know your calcium score, your standard cholesterol numbers, and your high sensitivity C-reactive protein, you can pop them all in and predict, “What does that mean for me over the next 10 years as my possible risk of heart attack and stroke?” It’s the best data out there. I bring that up only to elevate high sensitivity C-reactive protein to the level where it should be, on par with lipid numbers. That calculator doesn’t have lipoprotein little a because they didn’t acquire that data on everybody 15 years ago when the study began. But astrocharm.org, it’s available to anybody. I find it so useful in my practice.
So, just to wrap around Corona, Dr. Tsimikas has created a letter, that is available on social media, alerting people who are aware they have a significantly elevated lipoprotein little a that that does increase the risk of cardiovascular disease and thrombosis and inflammation, and therefore, in the era of a pandemic or the coronavirus, take special precautions, and perhaps alert your medical team that you inherited, you know, particularly a high level, because it’s still unclear in the literature if a high level of lipoprotein little a also promotes thrombosis, if it’s a prothrombotic inherited factor, where there’s a tremendous problem right now taking care of sick people in the ICU with COVID-19 and clotting everywhere, and having an elevated lipoprotein little a for certain people, that might be a component. Yeah. That’s totally at this point hypothesis.
John: I was really hoping that you were gonna say that Lp(a) was thought to be…
Dr. Kahn: Protective.
John: …very protective against COVID-19. If you get it, there’s some strange thing with the immune system where it’s gonna knock that stuff out, and [inaudible 00:34:42]
Dr. Kahn: There’s actually no data. So there’s no reason to be concerned. It’s a hypothesis of caution, but it doesn’t change what anybody should be doing anyways.
John: Yeah. I had my antibody test done earlier this morning in Wyoming in a driving snowstorm. So I’m gonna be doing a podcast and a blog about the results. There’s a physician here who’s doing 500 tests.
Dr. Kahn: If you were in your hometown of Detroit, you’d be in a driving snowstorm, too.
John: Yeah. Perfect. Yeah. Very much at home in that weather. This was a quick hitter, important information, genetic bad cholesterol. Dr. Kahn, you see him everywhere. He’s all over TV. He’s all over every single podcast. He’s America’s heart health doctor. He’s got his new book, “Lipoprotein (a), the Heart’s Silent Killer.” Killed it today. Great episode. [inaudible 00:35:27]
Dr. Kahn: Thank you so much. Stay healthy.
John: Stay healthy, my friend. We’ll talk soon.
Dr. Kahn: Okay. Peace. Out.
John: Bye. The “Gene Food Podcast” is our attempt to synthesize the latest developments in the fields of genetics, nutrition, and medicine, and offer you practical tips and stories you can use in your own unique health journey. If you enjoy this podcast, you can find more information online at mygenefood.com.