Elevated lipoprotein(a), usually written Lp(a), means having a high level of an inherited cholesterol-carrying particle in the blood, which raises the risk of heart attack, stroke and narrowing of a heart valve [1,4].
This page provides general information. It does not replace advice from a doctor or another qualified healthcare professional.
Cholesterol travels through the blood inside small parcels of fat and protein called lipoproteins. LDL, often called “bad cholesterol”, is one of them [7].
Lipoprotein(a), or Lp(a), is another. It is built around a particle much like LDL, with an extra protein called apolipoprotein(a) attached [5,7]. That protein is sticky and takes part in how blood clots, so Lp(a) holds on to artery walls more readily than LDL [5,6].
“Elevated lipoprotein(a)” means the level in your blood is high. It is a risk factor rather than an illness in the everyday sense. Over years it makes plaque, inflammation and clotting more likely, raising the chance of a heart attack, a stroke, poor circulation in the legs and stiffening of the aortic valve [1,4].
A routine cholesterol test can look reassuring while much of your LDL is carried by Lp(a) particles [7]. Lp(a) is separate from familial hypercholesterolemia, another inherited cause of high cholesterol, although one person can have both [3,4].
A raised level is common. The American Heart Association and the National Lipid Association both put it at roughly 1 in 5 people worldwide [3,4]. The National Heart, Lung, and Blood Institute gives 20 to 30 percent, using a threshold between 30 and 50 mg/dL [6], and the 2022 European Atherosclerosis Society statement estimates around 1.4 billion people [1].
These figures count people whose level would be high if measured, not people who have been diagnosed. Testing is rare: across six United States health centers, Lp(a) had been measured in only 0.3 percent of more than five million people [3]. Levels also differ between ancestral groups, so a single global percentage smooths over real variation.
Genes are instructions inside our cells, inherited from our parents. Your Lp(a) level is set almost entirely by a gene called LPA, which explains more than 90 percent of the difference between people [1,2]. Adult levels are reached by around age five and then stay broadly steady for life [1,7].
Levels differ between ancestral groups. In the UK Biobank study the middle value rose in sequence across Chinese, White, South Asian and Black participants, at 16, 19, 31 and 75 nmol/L [1]. People of African ancestry tend to have the highest levels [1,2]. The extra risk carried by any given level appears similar across groups, so specialists no longer set different thresholds by ethnicity [3].
Since the cause is inherited, close relatives often share a raised level, so testing parents, brothers, sisters and children is recommended [3,4]. Kidney problems, an underactive thyroid, pregnancy, menopause and inflammatory conditions can also raise a level [1,4,5].
A high Lp(a) level causes no symptoms of its own. Nothing hurts, nothing shows, and a person can feel completely well [4]. What appears later in life are the effects on the heart and blood vessels: chest pain on exertion, poor circulation in the legs, and breathlessness from a narrowed aortic valve [1,5].
When to seek urgent help. A raised level increases the risk of a heart attack and a stroke, and both are emergencies [4]. Anyone with sudden chest pain or pressure, sudden breathlessness, or sudden weakness, numbness or trouble speaking should call emergency services straight away. These events can arrive with no warning: Bob Harper, who has a high Lp(a) level, has said he had none of the usual warning symptoms before his cardiac arrest [11].
Lp(a) is measured with an ordinary blood test from a vein in the arm, and some laboratories ask you not to eat or drink beforehand [7]. It is not part of a routine cholesterol panel, so it has to be requested specifically, and it is often missed simply because nobody orders it [3,4].
The American Heart Association recommends every adult be tested at least once in their lifetime, and it matters most for anyone with early heart disease in themselves or their family, or familial hypercholesterolemia [4]. In the United Kingdom it is rarely measured in general practice and is usually arranged through a specialist lipid clinic after a referral [5].
One point genuinely confuses readers. Lp(a) is reported either by weight, in mg/dL, or by particle count, in nmol/L, and the same number means very different things in the two systems [5]. The National Lipid Association favors nmol/L and advises against converting between them with a fixed multiplier [3], while the European Atherosclerosis Society panel offers a working figure of 2.5 nmol/L to each mg/dL [2].
Thresholds differ too. The National Lipid Association treats under 75 nmol/L (30 mg/dL) as low risk and 125 nmol/L (50 mg/dL) or above as high, while HEART UK uses four bands running up to more than 400 nmol/L [3,5]. Lp(a) is read as a sliding scale, not a pass or fail line [3].
No medicine is approved anywhere specifically to lower Lp(a) [3]. Treatment means reducing every other risk to the heart and blood vessels, and for a few people filtering Lp(a) out of the blood.
Managing everything else. Diet, exercise and weight loss do not change an Lp(a) level, since it is set by genes [4,7]. They do lower overall risk, which is the point. The usual advice is to treat LDL cholesterol and blood pressure, control diabetes, avoid tobacco and stay active, more intensively and earlier when Lp(a) is high [1,3,4].
Medicines. Statins do not lower Lp(a), and on average raise it very slightly [3]. That is not a reason to avoid one: statins clearly reduce heart attacks and strokes by lowering LDL cholesterol [3]. PCSK9 inhibitors, a newer group of cholesterol-lowering injections, lower Lp(a) by around 20 to 30 percent as a side effect, although they are not licensed for that purpose [3,5,6].
Lipoprotein apheresis. For a few people with very high levels and heart disease that keeps progressing, blood can be filtered through a machine, much like kidney dialysis, to strip out Lp(a) and LDL cholesterol [1,3]. In the United Kingdom it is given every one to two weeks and can lower Lp(a) by up to 75 percent [5]. In the United States it carries the only specific approval related to Lp(a), limited to people who also have familial hypercholesterolemia, artery disease and high LDL cholesterol despite maximum medication [3]. Availability differs widely between countries, and there is no cure, since the gene itself cannot be changed [3].
For most people this means a long, ordinary life with closer attention to heart health than average. Once measured, the level usually does not need checking again, since it stays broadly stable [5]. Repeat testing is sometimes suggested after menopause, or for people who develop kidney or thyroid problems [3]. Children are tested selectively rather than routinely [3].
Finding out can be unsettling, particularly for someone who already eats well and exercises. A raised level does not mean an event is coming. It shifts the odds, and a great deal can be done about the rest of the picture [6].
Clinical trials are research studies that test whether a treatment works and is safe. Lp(a) is an active area of research, so studies do come up. Deciding whether to look into one is a personal choice, and it helps to take it in steps.
Be clear on what a study involves:
Every trial has rules about who can take part, called eligibility criteria. Some describe who can join, others who cannot. For a study in elevated lipoprotein(a), the criteria might include an Lp(a) level above a set figure in a stated unit, a particular age range, whether you have already had a heart attack or a stroke, your current LDL cholesterol level, which cholesterol medicines you take, and whether your kidney and thyroid function are stable.
trialport’s medifit helps people consider information related to possible medical suitability. It does not diagnose a condition, confirm eligibility or replace formal screening by the study team.
Explore elevated lipoprotein(a) clinical trials through trialport
A study can look like a good match on paper and still be hard in practice. Worth thinking through:
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Useful questions to put to a research team:
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The main effort is on medicines that stop the body making Lp(a) at all, working at the genetic level to instruct the liver to make less apolipoprotein(a) [3,5].
None is approved anywhere, and none should be assumed to work until those studies report [3,10].
Study status checked: 3 August 2026. Research moves, and what is being studied changes. For current information, start at app.trialport.com.
In the United States, the American Heart Association has the most approachable Lp(a) materials anywhere, including printable fact sheets and questions to take to an appointment [4]. The National Heart, Lung, and Blood Institute gives a short overview written for the public [6], and MedlinePlus explains the blood test itself [7].
In the United Kingdom, HEART UK is the cholesterol charity and the clearest source on testing within the National Health Service, including how to reach a specialist lipid clinic [5].
Coverage elsewhere is thin. There is no large international Lp(a) patient organization, and one United States charity devoted to Lp(a) closed in 2020. In Europe, Australia, New Zealand, Asia, Africa and South America the practical starting point is usually a national heart or cholesterol charity, or a hospital lipid clinic.
The fitness trainer and television presenter Bob Harper has spoken publicly about having a high Lp(a) level, which he learned about only after a cardiac arrest in 2017, and has encouraged people to find out their own number [11].
High Lp(a) is common and invisible, so many well-known people will have it without knowing or saying so. Public speculation about anyone’s heart condition is usually wrong, and this page names only people who have described their own situation in public.
Is high Lp(a) inherited?
Yes, almost entirely, so close relatives often share a raised level [1,3].
Can I lower it with diet and exercise?
Not meaningfully, though eating well and staying active still lower your overall risk of heart disease and stroke [4,7].
Do statins lower Lp(a)?
No, they raise it very slightly on average, which is not a reason to stop taking one [3].
My result is in nmol/L and my friend’s is in mg/dL. How do I compare them?
Carefully. The units are not interchangeable, and the National Lipid Association advises against converting between them with a fixed multiplier [3,5].
Is there a medicine for it yet?
Not one approved specifically to lower Lp(a), although several are in late-stage testing [3,10].
Does a high level mean I will have a heart attack?
No. It raises the odds rather than deciding the outcome, and people with high levels but otherwise good heart health fare better than people with lower levels and poor heart health [3,6].
Written by: trialport editorial team
Reviewed by: Keith Berelowitz, Founder and CEO, trialport
Reviewed on: 3 August 2026
Next review due: 3 August 2027
References last checked: 3 August 2026