Lipoprotein(a), molar (nmol/L)
A cholesterol-carrying particle like LDL with an extra protein attached, counted in nmol/L. Your level is mostly set by your genes and stays fairly steady.
AI-verified against cited sources. Awaiting expert reviewAlso called Lp(a), Lp-aLOINC 43583-4
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What it is
Lipoprotein(a), or Lp(a), is a particle in your blood that looks like LDL but has an extra protein, apolipoprotein(a), attached to it. Your genes set most of your Lp(a) level, and it usually reaches its adult level by about age 5. Diet and exercise change it very little. This version of the test counts Lp(a) particles in nanomoles per liter (nmol/L). Labs that report weight in mg/dL give a different kind of number, and the two cannot be converted exactly.
Why it matters
Higher Lp(a) is linked to a higher lifetime chance of heart attack, stroke and narrowing of the aortic valve. This link holds even when LDL cholesterol is low. Because the level is mostly inherited and rarely changes, several guidelines suggest checking it at least once in adulthood. A high result is a reason to look more closely at your other heart risk factors with your clinician. It is not a verdict on its own.
If it’s low
A low level is the usual finding and is generally not a concern. Some studies have linked very low levels to a higher chance of type 2 diabetes. Researchers are still studying this, and it does not usually call for any action.
Common causes
- Your genes. Most people have low levels, and variation in the LPA gene decides this
- Advanced liver disease, which can lower the amount your liver makes
- An overactive thyroid (hyperthyroidism)
- Severe acute illness such as sepsis or major burns, usually for a short time
What can help
- Nothing is usually needed for a low Lp(a)
- If you have other symptoms or conditions, ask your clinician whether the cause is worth checking
If it’s high
A result of 125 nmol/L or higher is considered high by several guidelines. Risk rises gradually as the level goes up. The 2026 US guideline links about 125 nmol/L to about 1.4 times the risk of heart and blood vessel disease, and about 250 nmol/L to about double. A high level raises risk but does not mean a heart attack or stroke will happen. Your overall risk also depends on your age, blood pressure, LDL cholesterol, smoking and family history.
Common causes
- Your genes. Variation in the LPA gene explains more than 90% of the differences between people
- Ancestry. Average levels differ between groups and tend to be higher in people of South Asian and African ancestry
- Kidney disease, especially nephrotic syndrome, which can raise levels 3 to 5 times
- An underactive thyroid (hypothyroidism)
- Pregnancy, when levels can roughly double
- Some inflammatory conditions and some HIV medicines
What can help
- Because Lp(a) is mostly genetic, lifestyle changes move it only a little. They still lower your overall heart risk
- Work on the risk factors you can change: blood pressure, LDL cholesterol, blood sugar, weight, activity and smoking
- Ask your clinician how your Lp(a) fits with your overall heart risk
- Ask whether close relatives should have their Lp(a) checked, since it runs in families
Usual ranges
What labs print as the reference range, by who was tested. Ranges differ a little between labs, so the range on your own report is the one your result is judged against.
For adults: up to 75 nmol/L. Source: Mayo Clinic Laboratories, Labcorp.
- 18+ (this one applies)up to 75 nmol/L
Sources: Mayo Clinic Laboratories, Labcorp
Labcorp Lp(a)-attributable risk categories (same cut-offs as EAS 2022 and 2018 AHA/ACC)
- Low Lp(a)-attributable riskbelow 75 nmol/L
- Intermediate Lp(a)-attributable risk75 to under 125 nmol/L
- High Lp(a)-attributable risk, rising with higher values125 and above nmol/L
If this applies to you
Lp(a) molar means a little more for some people. Open the one that fits you.
High cholesterol or heart risk
Lp(a) is mostly inherited. The 2026 U.S. guideline recommends measuring it at least once in all adults, counts a high level as a risk-enhancing factor, and prefers tests reported in nmol/L. It says one test is generally enough, unless something can shift the level, such as the menopause transition, pregnancy, or kidney, liver or thyroid disease.
Tracking for long-term health
Lp(a) is mostly inherited. The 2026 U.S. cholesterol guideline newly recommends measuring it at least once in all adults, and counts a high level as a factor that adds to heart risk. One test is generally enough unless something can shift the level, such as the menopause transition or kidney, liver or thyroid disease.
What can affect your result
- Genes: more than 90% of the differences between people
- Ancestry: in the UK Biobank, median levels were about 16 nmol/L in Chinese, 19 in White, 31 in South Asian and 75 in Black participants
- Assay design: antibody-based assays can over- or under-read depending on apo(a) size
- Kidney disease and nephrotic syndrome raise levels; advanced liver disease lowers them
- Thyroid status: an underactive thyroid raises levels and an overactive one lowers them
- Pregnancy can roughly double levels
- Women's levels are on average about 5 to 10% higher than men's
- Fasting and physical activity make little or no difference
- Many antibody-based assays read differently depending on the size of your apo(a) protein. Assays that are insensitive to apo(a) size and calibrated in nmol/L are preferred, but results from different labs may still not match. Use the same lab and assay when comparing over time.
- Labcorp notes that alcohol, aspirin, niacin and estrogen supplements may misrepresent true Lp(a); tell your clinician about them.
- Labs may reject grossly hemolyzed, lipemic or icteric samples (Labcorp).
- Kidney disease, thyroid disease, liver disease and pregnancy can shift levels (see factors affecting).
Mostly fixed by your genes. Lifestyle changes have little effect.
When to talk to a clinician
Talk with a clinician about a result of 125 nmol/L or higher, especially if you or close relatives have had a heart attack, stroke or aortic valve problems at a younger age. A level above about 430 nmol/L is linked to a lifetime heart risk similar to that of untreated inherited high cholesterol, so it is worth raising with your clinician soon.
Questions you could ask
- Which assay and units does my lab use for Lp(a), and can I compare this result with earlier ones?
- Do I need to recheck this, or is one result enough?
- How does my Lp(a) fit with my overall risk of heart disease?
- Should my other risk factors, such as LDL cholesterol or blood pressure, be reviewed more closely?
- Should my close relatives have their Lp(a) checked?
- Does my family history change how we should read this result?
Questions people ask
What do the 75 and 125 nmol/L cut-offs on my report mean?
Labs and guidelines use them as markers of how much extra heart risk Lp(a) may add. Below 75 nmol/L is considered low, 75 to below 125 is intermediate, and 125 or higher is considered high. Risk rises gradually, so these are not sharp lines. Your clinician can look at your Lp(a) together with your other risk factors.
My report shows mg/dL. Can I turn it into nmol/L?
Not exactly. mg/dL measures weight and nmol/L counts particles, and the size of the apo(a) protein varies between people and assays. Experts say 2 to 2.5 is only a rough guess for turning mg/dL into nmol/L, so please don't rely on it. Ask your lab, or compare results only in the same unit from the same lab.
Can diet or exercise lower my Lp(a)?
Very little. Your genes set most of your level, and lifestyle changes have a small effect at most. Healthy habits still lower your overall heart risk, and your clinician may focus on your LDL cholesterol, blood pressure and other factors.
Do I need to test Lp(a) more than once?
Often one test is enough, because the level is steady over time. Several guidelines suggest measuring it at least once in adulthood. Your clinician may repeat it if the first result was close to a cutoff, if the lab or assay changed, or if your health changes.
Show the science and sources
Is a change real?
Lp(a) molar naturally varies about 8.9% from test to test in the same healthy person. Between two results from the same lab, a rise of 30% or more, or a fall of 23% or more, is unlikely to be day-to-day noise or lab variation (95% reference change value). Source: The European Biological Variation Study (EuBIVAS): a summary report.
For clinicians and researchers
Lp(a) is an LDL-like particle whose apoB-100 is linked to apolipoprotein(a), encoded by LPA. Concentration ranges from under 0.2 to about 750 nmol/L, is more than 90% genetically determined, and is inversely related to apo(a) isoform size (the number of kringle IV repeats explains about 30-70% of the variation). Ideal assays use an antibody to a non-repetitive apo(a) epitope so each particle is counted once and results are in nmol/L. Most commercial assays use polyclonal antibodies that recognize repeated epitopes, which can read low in small isoforms and high in large ones; using calibrators that span isoform sizes partly corrects this, and the EAS asks labs to use isoform-insensitive assays traceable to official reference materials and to report in molar units where possible. Mayo (LIPA1) and Labcorp (120188) both use an immunoturbidimetric method. The EAS advises against a fixed nmol/L to mg/dL factor (2 to 2.5 mg/dL to nmol/L is only a best guess), and the 2026 ACC/AHA guideline treats the units as not directly interchangeable. Thresholds: EAS 2022 suggests a rule-out level below 75 nmol/L (30 mg/dL), a rule-in level of 125 nmol/L (50 mg/dL) or more, and a grey zone between; the 2018 AHA/ACC guideline names 125 nmol/L or 50 mg/dL a risk-enhancing factor; Labcorp reports below 75 as low, 75 to below 125 as intermediate and 125 or more as high Lp(a)-attributable risk. The 2026 ACC/AHA guideline recommends measurement at least once in adulthood and links about 125 nmol/L to about 1.4-fold, about 250 nmol/L to about 2-fold and about 430 nmol/L to about 4-fold relative ASCVD risk (as summarized in Life 2026). Above 430 nmol/L (180 mg/dL) lifetime ASCVD risk is similar to untreated heterozygous familial hypercholesterolemia. The relation is causal and continuous for ASCVD and aortic valve stenosis, and does not support Lp(a) as a venous thrombosis risk factor. Lp(a) carries cholesterol that is measured inside LDL-C; the EAS does not recommend routine correction of LDL-C except where familial hypercholesterolemia is suspected. Hormone therapy after menopause lowers Lp(a) by about 25%, and PCSK9 inhibitors lower it by 15-30% (EAS).
LOINC 43583-4 (primary). Specimen: serum-or-plasma.
Sources
- Lipoprotein(a), Serum (test LIPA1), Mayo Clinic Laboratories
- Lipoprotein(a) (test 120188), Labcorp
- Lipoprotein(a) in atherosclerotic cardiovascular disease and aortic stenosis: a European Atherosclerosis Society consensus statement, European Heart Journal (2022)
- 2018 AHA/ACC/AACVPR/AAPA/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA Guideline on the Management of Blood Cholesterol, Circulation (2018)
- 2026 ACC/AHA/AACVPR/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA Guideline on the Management of Dyslipidemia, American College of Cardiology / American Heart Association (2026)
- The 2026 ACC/AHA Dyslipidemia Guideline: A Critical and Transatlantic Perspective on Personalized Lipid Management, Life (MDPI) (2026)
- Prioritizing Health | Lower Sooner: How the 2026 Dyslipidemia Guideline Changes Practice, American College of Cardiology (2026)
- Lipoprotein (a) Blood Test, MedlinePlus (National Library of Medicine)
AI-verified against cited sources. Awaiting expert review. Last reviewed 2026-10-03. How we build and check these pages.