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Is my Lp(a) (Lipoprotein(a)) normal?

Free blood test checker · Standard + longevity-optimal ranges

nmol/L
OptimalBorderlineHigh

What is a normal Lp(a) level?

Lp(a) is a predominantly genetic lipoprotein particle — approximately 90% determined by the LPA gene — that is structurally similar to LDL but carries an additional apolipoprotein(a) chain. It is an independent risk enhancer for atherosclerotic cardiovascular disease (ASCVD) and aortic valve stenosis. Unlike LDL cholesterol, Lp(a) is largely unresponsive to statins, diet, or standard lifestyle changes. Levels remain stable throughout life. High-risk threshold is > 50 mg/dL (or > 125 nmol/L), which confers risk equivalent to heterozygous familial hypercholesterolemia. The European Atherosclerosis Society recommends measuring Lp(a) at least once in every adult.

RangeValues
Standard Reference0–75 nmol/L
Optimal0–30 nmol/L
Longevity Optimal< 50 mg/dL
High Risk> 125 nmol/L

What causes abnormal Lp(a) levels?

Lp(a) levels are >90% determined by genetics — specifically the LPA gene. Unlike LDL, diet, exercise, and most medications have minimal impact on Lp(a). Niacin can reduce Lp(a) by 20-30% but is not recommended due to side effects. PCSK9 inhibitors lower Lp(a) modestly (20-25%). Statins paradoxically increase Lp(a) slightly. Ethnicity matters: people of African descent tend to have higher Lp(a) levels than those of European descent.

When should you see a doctor?

See your doctor if Lp(a) is above 75 nmol/L (30 mg/dL), especially if you have a family history of premature heart disease or stroke. If above 125 nmol/L (50 mg/dL), discuss aggressive cardiovascular risk mitigation including lower LDL/ApoB targets and potential aspirin therapy. Every adult should be tested at least once.

Lp(a) and longevity

Lp(a) is arguably the most important cardiovascular biomarker that most people have never tested. Because it is genetically determined and stable over a lifetime, a single measurement provides permanent risk stratification. Elevated Lp(a) contributes to atherosclerosis through three distinct mechanisms: it carries atherogenic cholesterol into arterial walls like LDL, it promotes thrombosis by competitively inhibiting plasminogen activation (impairing clot breakdown), and it triggers arterial wall inflammation. Mendelian randomization studies confirm that lifelong elevated Lp(a) dramatically increases risk of myocardial infarction, stroke, and calcific aortic valve stenosis. Phase 3 trials of antisense oligonucleotide therapies (pelacarsen, olpasiran) show 80-90% Lp(a) reduction and may transform management within 2-3 years.

Where to get a Lp(a) test

Labcorp Lp(a) Test$69

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Related biomarkers

These biomarkers are often tested alongside Lp(a) for a more complete picture.

ApoB
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LDL
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Non-HDL
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Frequently asked questions

What is a normal Lp(a) level?
Optimal is below 30 nmol/L (12 mg/dL). Elevated is 30-75 nmol/L (12-30 mg/dL). High risk is above 75 nmol/L (30 mg/dL). Above 125 nmol/L (50 mg/dL) is very high risk. Approximately 20% of the global population has elevated Lp(a).
Can I lower my Lp(a)?
Currently, no approved drug specifically lowers Lp(a). Levels are >90% genetically determined by the LPA gene. Diet and exercise have minimal effect. However, Novartis (pelacarsen) and Amgen (olpasiran) have antisense oligonucleotide therapies in Phase 3 trials that reduce Lp(a) by 80-90%. Until these arrive, the strategy is aggressive reduction of other modifiable risk factors.
Why should I test Lp(a)?
The European Atherosclerosis Society recommends every adult get Lp(a) tested at least once in their lifetime. Since levels are genetically fixed, one test gives you a lifelong reading. Elevated Lp(a) explains many cases of premature heart attack in people with otherwise "normal" lipid panels.
How does Lp(a) differ from LDL?
Lp(a) is an LDL-like particle with an extra apolipoprotein(a) tail that makes it more atherogenic, more thrombogenic (it inhibits plasminogen and promotes clot formation), and more pro-inflammatory than regular LDL. Standard lipid panels do not measure Lp(a) — it must be specifically ordered.
Can you lower Lp(a) with diet or statins?
Lp(a) is approximately 90% genetically determined. Unlike LDL cholesterol, it does not meaningfully respond to statins, diet, or exercise. The FDA is reviewing novel antisense therapies (pelacarsen, olpasiran) that may reduce Lp(a) by 80-90%. PCSK9 inhibitors may modestly lower it by ~20-30%.

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Sources: Reference ranges based on AHA/ACC, ADA, and AACE clinical guidelines. Biological variation data from Ricos/Westgard database. Longevity-optimal ranges reflect targets used by preventive and functional medicine practitioners.

  • Lipoprotein(a) — European Atherosclerosis Society Consensus Statement

Last reviewed: April 2026. This tool provides general health information and is not a substitute for professional medical advice, diagnosis, or treatment. Always consult your healthcare provider about your specific results.

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