What is this lipoprotein(a) and what can we do about it?
Treating High Lp(a): A Risk Factor for Atherosclerosis
4.7/5 - (142 votes)
Below is an approximation of this video’s audio content. To see any graphs, charts, graphics, images, and quotes to which Dr. Greger may be referring, watch the above video.
What could explain severe coronary disease in someone considered to be at low cardiovascular disease risk with a healthy lifestyle? A young man ends up in the ER with a heart attack; ultimately found to have severe coronary artery disease, yet given his age, blood pressure, and cholesterol, his 10-year risk of a heart attack should only be like 2 percent. But what he did have was a high lipoprotein(a) level, also known as Lp(a), markedly high at 80, which may help explain it. You can see the same thing in women. A 27-year old with a heart attack with a high Lp(a). What is this Lp(a), and what can we do about it?
Lp(a) is an underestimated cardiovascular risk factor. It causes coronary artery disease, heart attacks, strokes, peripheral arterial disease, calcified aortic valve disease, and heart failure. And these can occur even in people without high cholesterol, because it is cholesterol. It’s basically an LDL cholesterol molecule linked to another protein, which, like LDL, transfers cholesterol into the lining of our arteries, contributing to the inflammation in atherosclerotic plaques. But it has yet to gain recognition by practicing physicians.
The main reason for the limited clinical use of Lp(a) is the traditional lack of effective and specific therapies to lower it. Lp(a) concentrations are approximately 90 percent genetically determined, so the conventional thinking has been that you’re just kind of born with higher or lower levels, and there’s not much you can do about it. Even if that were the case, you still might want to know about it, since if it was high, that would be all the more reason to make sure all the other risk factors that you do have more control over are absolutely as good as possible––like maybe help you quit smoking, and do everything you can do lower your LDL cholesterol as much as possible.
Lp(a) levels in the blood can vary a 1,000-fold between individuals (from less than 0.1 mg/dL to a hundred or more). Here’s the graph of odds of heart disease at different levels. Less than 20 is probably optimal, with greater than 30-50 considered elevated. Even when the more conservative threshold of greater than 50 is used, that describes about 10-30 percent of the global population, an estimated 1.4 billion people. So, if we’re like the 1 in 5 people with elevated levels, what can we do about it?
The way we know that Lp(a) causes atherosclerosis is that we can put it to the ultimate test. There’s something called apheresis, which is basically like a dialysis machine where they can take out your blood, wash out some of the Lp(a), and then give your blood back to you. And when you do that, you can reverse the progress of disease. Atherosclerosis continues to get worse in the control group, but better in the apheresis group. This is great for proving the role of Lp(a), but has limited clinical application, given the cost, accessibility, and the time commitment required for biweekly sessions of two to four hours each. It causes a big drop in blood levels, but they quickly creep back up, so you have to keep going in, costing more than $50,000 a year. There has to be a better way. We’ll explore the role diet can play, next.
Please consider volunteering to help out on the site.
- Cameron SJ, Block RC, Richeson JF. Severe coronary disease in an adult considered at low cardiovascular disease risk with a healthy lifestyle. J Clin Lipidol. 2013;7(5):526-30.
- Mobarek D, Karasik PA, Tomer M, Miller M. High Lp(a) associated with very premature coronary heart disease. J Clin Lipidol. 2019;13(3):402-404.
- Mellwig KP. Editorial Lp(a) - the underestimated cardiovascular risk factor. Clin Res Cardiol Suppl. 2017;12(Suppl 1):1.
- Enas EA, Varkey B, Dharmarajan TS, Pare G, Bahl VK. Lipoprotein(a): An independent, genetic, and causal factor for cardiovascular disease and acute myocardial infarction. Indian Heart J. 2019;71(2):99-112.
- Kotani K, Serban MC, Penson P, Lippi G, Banach M. Evidence-based assessment of lipoprotein(a) as a risk biomarker for cardiovascular diseases - Some answers and still many questions. Crit Rev Clin Lab Sci. 2016;53(6):370-8.
- Stulnig TM, Morozzi C, Reindl-schwaighofer R, Stefanutti C. Looking at Lp(a) and Related Cardiovascular Risk: from Scientific Evidence and Clinical Practice. Curr Atheroscler Rep. 2019;21(10):37.
- Von eckardstein A. Will you, nill you, I will treat you: the taming of lipoprotein(a). Eur Heart J. 2017;38(20):1570-1572.
- Kostner KM, Kostner GM, Wierzbicki AS. Is Lp(a) ready for prime time use in the clinic? A pros-and-cons debate. Atherosclerosis. 2018;274:16-22.
- Tada H, Takamura M, Kawashiri MA. Lipoprotein(a) as an Old and New Causal Risk Factor of Atherosclerotic Cardiovascular Disease. J Atheroscler Thromb. 2019;26(7):583-591.
- Hung MY, Tsimikas S. What is the ultimate test that lowering lipoprotein(a) is beneficial for cardiovascular disease and aortic stenosis?. Curr Opin Lipidol. 2014;25(6):423-30.
- Pokrovsky SN, Afanasieva OI, Ezhov MV. Lipoprotein(a) apheresis. Curr Opin Lipidol. 2016;27(4):351-8.
- Safarova MS, Ezhov MV, Afanasieva OI, et al. Effect of specific lipoprotein(a) apheresis on coronary atherosclerosis regression assessed by quantitative coronary angiography. Atheroscler Suppl. 2013;14(1):93-9.
- Pokrovsky SN, Afanasieva OI, Safarova MS, et al. Specific Lp(a) apheresis: A tool to prove lipoprotein(a) atherogenicity. Atheroscler Suppl. 2017;30:166-173.
- Man LC, Kelly E, Duffy D. Targeting lipoprotein (a): an evolving therapeutic landscape. Curr Atheroscler Rep. 2015;17(5):502.
- Tselmin S, Müller G, Schatz U, Julius U, Bornstein SR, Hohenstein B. Kinetics of Lipoprotein(a) in patients undergoing weekly lipoprotein apheresis for Lp(a) hyperlipoproteinemia. Atheroscler Suppl. 2017;30:209-216.
- Enas EA, Chacko V, Senthilkumar A, Puthumana N, Mohan V. Elevated lipoprotein(a)--a genetic risk factor for premature vascular disease in people with and without standard risk factors: a review. Dis Mon. 2006;52(1):5-50.
Video production by Glass Entertainment
Motion graphics by Avocado Video
Below is an approximation of this video’s audio content. To see any graphs, charts, graphics, images, and quotes to which Dr. Greger may be referring, watch the above video.
What could explain severe coronary disease in someone considered to be at low cardiovascular disease risk with a healthy lifestyle? A young man ends up in the ER with a heart attack; ultimately found to have severe coronary artery disease, yet given his age, blood pressure, and cholesterol, his 10-year risk of a heart attack should only be like 2 percent. But what he did have was a high lipoprotein(a) level, also known as Lp(a), markedly high at 80, which may help explain it. You can see the same thing in women. A 27-year old with a heart attack with a high Lp(a). What is this Lp(a), and what can we do about it?
Lp(a) is an underestimated cardiovascular risk factor. It causes coronary artery disease, heart attacks, strokes, peripheral arterial disease, calcified aortic valve disease, and heart failure. And these can occur even in people without high cholesterol, because it is cholesterol. It’s basically an LDL cholesterol molecule linked to another protein, which, like LDL, transfers cholesterol into the lining of our arteries, contributing to the inflammation in atherosclerotic plaques. But it has yet to gain recognition by practicing physicians.
The main reason for the limited clinical use of Lp(a) is the traditional lack of effective and specific therapies to lower it. Lp(a) concentrations are approximately 90 percent genetically determined, so the conventional thinking has been that you’re just kind of born with higher or lower levels, and there’s not much you can do about it. Even if that were the case, you still might want to know about it, since if it was high, that would be all the more reason to make sure all the other risk factors that you do have more control over are absolutely as good as possible––like maybe help you quit smoking, and do everything you can do lower your LDL cholesterol as much as possible.
Lp(a) levels in the blood can vary a 1,000-fold between individuals (from less than 0.1 mg/dL to a hundred or more). Here’s the graph of odds of heart disease at different levels. Less than 20 is probably optimal, with greater than 30-50 considered elevated. Even when the more conservative threshold of greater than 50 is used, that describes about 10-30 percent of the global population, an estimated 1.4 billion people. So, if we’re like the 1 in 5 people with elevated levels, what can we do about it?
The way we know that Lp(a) causes atherosclerosis is that we can put it to the ultimate test. There’s something called apheresis, which is basically like a dialysis machine where they can take out your blood, wash out some of the Lp(a), and then give your blood back to you. And when you do that, you can reverse the progress of disease. Atherosclerosis continues to get worse in the control group, but better in the apheresis group. This is great for proving the role of Lp(a), but has limited clinical application, given the cost, accessibility, and the time commitment required for biweekly sessions of two to four hours each. It causes a big drop in blood levels, but they quickly creep back up, so you have to keep going in, costing more than $50,000 a year. There has to be a better way. We’ll explore the role diet can play, next.
Please consider volunteering to help out on the site.
- Cameron SJ, Block RC, Richeson JF. Severe coronary disease in an adult considered at low cardiovascular disease risk with a healthy lifestyle. J Clin Lipidol. 2013;7(5):526-30.
- Mobarek D, Karasik PA, Tomer M, Miller M. High Lp(a) associated with very premature coronary heart disease. J Clin Lipidol. 2019;13(3):402-404.
- Mellwig KP. Editorial Lp(a) - the underestimated cardiovascular risk factor. Clin Res Cardiol Suppl. 2017;12(Suppl 1):1.
- Enas EA, Varkey B, Dharmarajan TS, Pare G, Bahl VK. Lipoprotein(a): An independent, genetic, and causal factor for cardiovascular disease and acute myocardial infarction. Indian Heart J. 2019;71(2):99-112.
- Kotani K, Serban MC, Penson P, Lippi G, Banach M. Evidence-based assessment of lipoprotein(a) as a risk biomarker for cardiovascular diseases - Some answers and still many questions. Crit Rev Clin Lab Sci. 2016;53(6):370-8.
- Stulnig TM, Morozzi C, Reindl-schwaighofer R, Stefanutti C. Looking at Lp(a) and Related Cardiovascular Risk: from Scientific Evidence and Clinical Practice. Curr Atheroscler Rep. 2019;21(10):37.
- Von eckardstein A. Will you, nill you, I will treat you: the taming of lipoprotein(a). Eur Heart J. 2017;38(20):1570-1572.
- Kostner KM, Kostner GM, Wierzbicki AS. Is Lp(a) ready for prime time use in the clinic? A pros-and-cons debate. Atherosclerosis. 2018;274:16-22.
- Tada H, Takamura M, Kawashiri MA. Lipoprotein(a) as an Old and New Causal Risk Factor of Atherosclerotic Cardiovascular Disease. J Atheroscler Thromb. 2019;26(7):583-591.
- Hung MY, Tsimikas S. What is the ultimate test that lowering lipoprotein(a) is beneficial for cardiovascular disease and aortic stenosis?. Curr Opin Lipidol. 2014;25(6):423-30.
- Pokrovsky SN, Afanasieva OI, Ezhov MV. Lipoprotein(a) apheresis. Curr Opin Lipidol. 2016;27(4):351-8.
- Safarova MS, Ezhov MV, Afanasieva OI, et al. Effect of specific lipoprotein(a) apheresis on coronary atherosclerosis regression assessed by quantitative coronary angiography. Atheroscler Suppl. 2013;14(1):93-9.
- Pokrovsky SN, Afanasieva OI, Safarova MS, et al. Specific Lp(a) apheresis: A tool to prove lipoprotein(a) atherogenicity. Atheroscler Suppl. 2017;30:166-173.
- Man LC, Kelly E, Duffy D. Targeting lipoprotein (a): an evolving therapeutic landscape. Curr Atheroscler Rep. 2015;17(5):502.
- Tselmin S, Müller G, Schatz U, Julius U, Bornstein SR, Hohenstein B. Kinetics of Lipoprotein(a) in patients undergoing weekly lipoprotein apheresis for Lp(a) hyperlipoproteinemia. Atheroscler Suppl. 2017;30:209-216.
- Enas EA, Chacko V, Senthilkumar A, Puthumana N, Mohan V. Elevated lipoprotein(a)--a genetic risk factor for premature vascular disease in people with and without standard risk factors: a review. Dis Mon. 2006;52(1):5-50.
Video production by Glass Entertainment
Motion graphics by Avocado Video
Republishing "Treating High Lp(a): A Risk Factor for Atherosclerosis"
Terms
You may republish this material online or in print under our Creative Commons licence. You must attribute the article to NutritionFacts.org with a link back to our website in your republication.
If any changes are made to the original text or video, you must indicate, reasonably, what has changed about the article or video.
You may not use our material for commercial purposes.
You may not apply legal terms or technological measures that restrict others from doing anything permitted here.
If you have any questions, please Contact Us
Title
Treating High Lp(a): A Risk Factor for Atherosclerosis
LicenseCreative Commons Attribution-NonCommercial 4.0 International (CC BY-NC 4.0)
Content URLDoctor's Note
I’ve been wanting to do videos about Lp(a), but there just wasn’t much we could do about it…until now! Okay, so how do we lower Lp(a) with diet? Stay tuned for the thrilling conclusion in my next video.
What can we do in general to minimize heart disease risk? My video How Not to Die from Heart Disease is a good starting point.
If you haven't yet, you can subscribe to our free newsletter. With your subscription, you'll also get notifications for just-released blogs and videos. Check out our information page about our translated resources.
Previous Video
Next Video
