Lab result explainedCholesterol and lipidsLast updated November 10, 2026

Lipoprotein(a) test: normal range, nmol/L to mg/dL, and what a high Lp(a) means

Lipoprotein(a) (Lp(a)) · Advanced lipid testing (ordered separately from the standard lipid panel) · reported in nmol/L (preferred) or mg/dL; no exact conversion, roughly 1 mg/dL ≈ 2–2.5 nmol/L

Lipoprotein(a), written Lp(a) and said "L-P-little-a", is a cholesterol-carrying particle in the blood that looks like LDL with an extra protein, apolipoprotein(a), wrapped around it. The amount you have is set almost entirely by the LPA gene you inherited, so it barely changes with diet, exercise or weight and stays roughly the same from childhood onward. A normal Lp(a) is below 30 mg/dL (about 75 nmol/L); 50 mg/dL (125 nmol/L) or more is high, and about 1 in 5 people worldwide is above that line.

A high Lp(a) matters because the particle does two harmful things: it deposits cholesterol in artery walls like LDL does, and its apolipoprotein(a) tail resembles plasminogen, the body's clot-dissolving protein, so it promotes clotting and inflammation. The result is a higher lifetime risk of heart attack, stroke, peripheral artery disease and, distinctively, narrowing of the aortic valve. People in the top 20 percent have roughly 1.5 to 2 times the heart-attack risk of people with low levels, and those above 180 mg/dL (430 nmol/L) have a risk comparable to familial hypercholesterolemia.

Because the level is genetic and stable, major guidelines now recommend measuring Lp(a) once in every adult's life, and particularly in anyone with early heart disease, a strong family history or a stubbornly high LDL. One result is usually enough. There is no diet or supplement that lowers Lp(a) meaningfully; what a high result changes is how aggressively the risks you can control, especially LDL cholesterol and blood pressure, are treated, and whether you might be a candidate for the Lp(a)-lowering drugs now in large trials.

Lp(a) at a glance

What it is: an LDL-like cholesterol particle with an extra apolipoprotein(a) protein; the level is about 90 percent inherited and stable over life.
Normal: below 30 mg/dL (below 75 nmol/L). Borderline: 30–50 mg/dL (75–125 nmol/L). High: 50 mg/dL (125 nmol/L) or more. Very high: above 180 mg/dL (430 nmol/L). Labs and assays differ; use the printed unit and cut-off.
nmol/L to mg/dL: there is no exact conversion because particle size varies, but dividing nmol/L by about 2.4 gives a rough mg/dL figure (125 nmol/L is roughly 50 mg/dL).
High Lp(a) raises the risk of heart attack, stroke, peripheral artery disease and aortic valve stenosis; the risk rises steadily with the level.
Diet, exercise and most cholesterol drugs do not lower it; niacin and PCSK9 inhibitors lower it 20–30 percent, and dedicated Lp(a) drugs are in late-stage trials. The main response to a high Lp(a) is tighter control of LDL, blood pressure, smoking and diabetes.
Low Lp(a) is common (about a quarter of people are under 5 mg/dL) and is not a cause for concern.

Have your whole report? Paste it into the free Lab Explainer

Every marker explained in plain language, in context with the others, with questions to bring to your appointment. No account needed.

What Lp(a) measures

Lp(a) is made in the liver by attaching apolipoprotein(a), a large protein coded by the LPA gene, to an ordinary LDL particle through a chemical bond to apolipoprotein B. The number of repeating segments (kringle IV type 2 repeats) in the apolipoprotein(a) gene varies from person to person: fewer repeats produce a smaller protein that the liver makes faster, so people with small apolipoprotein(a) have high Lp(a). This is why the level is so heritable (about 90 percent) and so stable: it is set by your genes within the first years of life and changes little thereafter.

The test measures Lp(a) in a blood sample by immunoassay. Results come in two units that do not convert exactly. Mass units (mg/dL) report the weight of the whole particle, including its cholesterol and protein, and are affected by the size of the apolipoprotein(a); molar units (nmol/L) count the number of particles and are the unit guidelines now prefer. A rough rule is that 1 mg/dL is about 2 to 2.5 nmol/L, so 30 mg/dL is roughly 75 nmol/L and 50 mg/dL roughly 125 nmol/L, but a result should be compared only with cut-offs in the same unit.

Fasting is not required. A few conditions move the level modestly: kidney disease, especially nephrotic syndrome, and hypothyroidism raise it; liver disease, hyperthyroidism and high-dose estrogen lower it; it rises slightly after menopause and during an acute illness, and statins raise it by around 10 percent. Because Lp(a) carries cholesterol, roughly 30 percent of its mass in mg/dL is counted within your LDL cholesterol result: someone with an Lp(a) of 100 mg/dL has about 30 mg/dL of their reported LDL that is actually Lp(a) cholesterol, which partly explains why some people's LDL responds poorly to statins.

Normal range for Lp(a)

Reference ranges vary between labs and by age, sex and pregnancy. Use the range printed on your own report.

Group	Typical range (nmol/L (preferred) or mg/dL; no exact conversion, roughly 1 mg/dL ≈ 2–2.5 nmol/L)	Notes
Desirable	Below 30 mg/dL (below 75 nmol/L)	About 70 to 75 percent of the population. Labs differ in assay and unit; use the printed cut-off.
Borderline	30–50 mg/dL (75–125 nmol/L)	Mild additional risk; matters most when other risk factors are present.
High	50 mg/dL or more (125 nmol/L or more)	Threshold used by the US National Lipid Association and the 2018 ACC/AHA guideline (risk-enhancing factor). About 20 percent of people.
Very high	Above 180 mg/dL (above 430 nmol/L)	Roughly the top 1 to 2 percent; the European Atherosclerosis Society regards lifetime risk here as similar to heterozygous familial hypercholesterolemia.
Risk relationship	Each 50 mg/dL (about 125 nmol/L) higher is associated with roughly 20 to 30 percent higher coronary risk	The relationship is continuous and causal in Mendelian randomisation studies; there is no level above which risk plateaus.
Aortic valve stenosis	Above 90 mg/dL (about 200 nmol/L)	Associated with about a 3-fold higher risk of aortic valve stenosis in the Copenhagen population studies.
People of African ancestry	Median about 2 to 3 times higher than in white or East Asian people	Guidelines still use the same cut-offs, since the risk per nmol/L is similar across ancestries.
Low	Below 5 mg/dL (below about 12 nmol/L)	About a quarter of people; not a concern. Weakly associated with a slightly higher risk of type 2 diabetes in observational studies.

High lipoprotein(a)

A high Lp(a) means you inherited a version of the LPA gene that produces a lot of this particle, and that your lifetime risk of atherosclerotic disease and aortic valve stenosis is higher than your standard lipid panel suggests. The risk is proportional to the level: at 50 to 100 mg/dL the extra risk is modest and comparable to another risk-enhancing factor such as a high CRP or a family history; at 100 to 180 mg/dL it is substantial; above 180 mg/dL (430 nmol/L) it approaches that of familial hypercholesterolemia, with roughly a 2-fold or greater risk of heart attack over a lifetime.

Lp(a) does not act alone. Its effect is multiplied by the risk factors you can change, so a person with high Lp(a) and a low LDL, normal blood pressure and no smoking history has a far lower absolute risk than someone with the same Lp(a) and uncontrolled risk factors. This is why a high result changes management even though no drug yet lowers Lp(a) to normal: guidelines use it to justify starting or intensifying statin therapy at a lower threshold, aiming for a lower LDL target, controlling blood pressure tightly and, in some cases, considering low-dose aspirin.

Because the level is inherited in a dominant pattern, a high Lp(a) also has implications for your family. Each first-degree relative has roughly a 50 percent chance of sharing it, and cascade testing of parents, siblings and children is recommended, especially where there is early heart disease in the family. A single measurement is usually sufficient, since the value changes little over time; a repeat is worthwhile only if the first was taken during an acute illness, pregnancy or a change in kidney or thyroid function, or if an Lp(a)-lowering treatment is started.

Common causes

Inherited LPA gene variants
The number of kringle IV type 2 repeats in the LPA gene explains most of the variation between people; fewer repeats mean a smaller apolipoprotein(a) that is produced faster and a higher blood level. Around 90 percent of your Lp(a) is explained by genetics, and the level is set by about age 5.
Ancestry
Median Lp(a) is about 2 to 3 times higher in people of African ancestry than in white or East Asian people, and intermediate in South Asian and Hispanic populations. The same cut-offs are used for everyone because the risk per particle is similar.
Chronic kidney disease and nephrotic syndrome
Reduced kidney clearance of apolipoprotein(a) fragments and, in nephrotic syndrome, increased liver production can double Lp(a). It falls after kidney transplantation.
Hypothyroidism
Low thyroid hormone raises Lp(a) by around 20 to 30 percent along with LDL; replacement therapy brings it back down. Hyperthyroidism lowers it.
Menopause and loss of estrogen
Lp(a) rises by around 10 to 20 percent after menopause; oral estrogen therapy lowers it by about 20 percent, although hormone therapy is not prescribed for this purpose.
Acute illness and inflammation
Lp(a) behaves as a mild acute-phase reactant and can rise transiently during infection, after surgery or a heart attack; a value drawn in hospital is confirmed when well.
Statin therapy
Statins raise Lp(a) by roughly 10 percent on average, probably by increasing apolipoprotein(a) production, while lowering LDL substantially; the net effect on risk is strongly favorable, so statins are still the first treatment for people with high Lp(a).
Pregnancy, growth hormone and some drugs
Lp(a) roughly doubles during pregnancy and returns to baseline afterwards. Growth hormone treatment and some antiretroviral drugs also raise it.

Symptoms that can go with it

None; a high Lp(a) causes no symptoms of its own, which is why it is only found by testing
Chest pain or pressure on exertion (angina) when coronary arteries have narrowed
A heart attack or stroke at a young age (under 55 in men, under 65 in women), often with a similar family history
Calf, thigh or buttock pain on walking that eases with rest, from peripheral artery disease
Breathlessness, chest tightness or fainting on exertion, with a heart murmur, from aortic valve stenosis
A family history of early heart disease that is not explained by LDL cholesterol, smoking or diabetes

Low lipoprotein(a)

A low Lp(a) is the most common and the most favorable result. Roughly a quarter of people have a level below 5 mg/dL, and anything under 30 mg/dL is considered desirable. It means you did not inherit a high-producing LPA variant and that this particular risk factor does not add to your cardiovascular risk. It does not lower your risk from other causes: LDL cholesterol, blood pressure, smoking, diabetes and family history still count in full.

The only observed downside of very low Lp(a) is a weak association with a slightly higher risk of type 2 diabetes in population studies, and with slightly lower levels in some cancers; the diabetes link is small and not a reason for concern or action. Lp(a) also falls in liver disease, hyperthyroidism and with estrogen or testosterone, but a low value is never investigated for its own sake.

Common causes

LPA gene variants with many kringle repeats
Large apolipoprotein(a) proteins are made slowly, so people who inherit long LPA alleles have low or undetectable Lp(a) throughout life. This is the normal state for a large share of the population.
Liver disease
Lp(a) is made only in the liver, so cirrhosis and advanced liver disease lower it along with other lipoproteins.
Hyperthyroidism
Excess thyroid hormone increases clearance of LDL-type particles and lowers Lp(a) by around 20 percent; it rises when thyroid function is corrected.
Estrogen, testosterone and some drugs
Oral estrogen (about 20 percent lower), testosterone, niacin (20 to 30 percent lower), PCSK9 inhibitors (about 25 percent lower) and lipoprotein apheresis all lower Lp(a). Aspirin lowers it slightly.

Symptoms that can go with it

None; a low Lp(a) does not cause symptoms
A low Lp(a) with symptoms of heart disease still needs the usual assessment; other risk factors remain fully relevant

Read it alongside

LDL cholesterol — the main modifiable partner; a high Lp(a) lowers the LDL level at which statin therapy is recommended and, because Lp(a) cholesterol is counted in LDL, explains some poor statin responses.
Apolipoprotein B — counts all atherogenic particles including Lp(a); a high ApoB with a high Lp(a) marks a particularly high particle burden.
Total cholesterol, HDL and triglycerides — the standard lipid panel; Lp(a) is reported separately and is not derived from it.
hs-CRP — another risk-enhancing factor; in some analyses the Lp(a) risk is largest when CRP is also raised.
A1C and fasting glucose — diabetes multiplies the absolute risk from any Lp(a) level.
TSH — hypothyroidism raises Lp(a) and LDL together; correct it before interpreting a borderline result.
Creatinine and urine albumin — kidney disease raises Lp(a); nephrotic-range protein loss can double it.
Coronary artery calcium score — often used to decide how aggressively to treat someone with a high Lp(a) and intermediate overall risk.

What usually happens next

One measurement is usually enough. Ask whether your result is in mg/dL or nmol/L and compare it with the cut-offs for that unit; do not convert between the two.
If Lp(a) is 50 mg/dL (125 nmol/L) or higher, expect a full cardiovascular risk assessment: lipid panel, ApoB, blood pressure, A1C, smoking status, family history, and often a coronary artery calcium score to refine risk.
The practical response is to lower the risk factors that can be changed: most people with high Lp(a) and any additional risk factor are offered a statin, with a lower LDL target (often under 70 mg/dL, under 55 in established disease), and tighter blood pressure control.
Tell first-degree relatives; cascade testing of parents, siblings and children is recommended because each has about a 50 percent chance of sharing a high level.
If you already have heart disease and a very high Lp(a), ask about PCSK9 inhibitors, lipoprotein apheresis (available in the US for Lp(a) over 60 mg/dL with LDL over 100 despite treatment) and whether you are eligible for a trial of the new Lp(a)-lowering drugs.
An echocardiogram is reasonable if you have a heart murmur or exertional breathlessness, since high Lp(a) is a specific risk factor for aortic valve stenosis.

Diet, lifestyle and natural levers with evidence

What can move Lp(a) once the cause is known. Nothing here replaces finding the cause.

Lower LDL cholesterol and blood pressure (the levers that change your risk)

Strong evidence

No diet or lifestyle change lowers Lp(a) itself by more than a few percent, but the absolute risk from a high Lp(a) is multiplied by LDL, blood pressure, smoking and diabetes, so these are where effort pays. In statin trials, people with high Lp(a) gained at least as much benefit per mmol/L of LDL lowering as everyone else, and in the UK Biobank a healthy lifestyle score roughly halved the absolute event rate in people with high Lp(a). Not smoking, 150 minutes of weekly activity and keeping LDL low are the proven response.

Do not switch to a very low-fat diet expecting Lp(a) to fall

Moderate evidence

Controlled feeding studies consistently show that replacing saturated fat with carbohydrate raises Lp(a) by around 10 to 15 percent, while diets higher in unsaturated fat lower it slightly. Weight loss, fiber, Mediterranean and plant-based diets change Lp(a) by less than 10 percent in either direction. Eat for LDL, blood pressure and glucose, which these patterns do improve, and accept that the Lp(a) number will barely move.

Niacin (vitamin B3) lowers Lp(a) but has not reduced events

Moderate evidence

Extended-release niacin at 1 to 2 g a day lowers Lp(a) by about 20 to 30 percent and more in people with the highest levels. However, in the AIM-HIGH (3,414 people) and HPS2-THRIVE (25,673 people) trials, adding niacin to a statin produced no reduction in heart attacks or strokes and increased side effects (flushing, raised glucose, infections, bleeding), so guidelines no longer recommend it for Lp(a). The number falls; the risk, as far as trials show, does not.

Niacin at these doses raises blood sugar and uric acid, can inflame the liver and interacts with statins; it is a prescription-level treatment to be used only under supervision.

L-carnitine

Preliminary evidence

A 2016 meta-analysis of 7 randomised trials (375 people) found oral L-carnitine, typically 2 g a day for 8 to 12 weeks, lowered Lp(a) by about 9 mg/dL compared with placebo, with a larger effect in people starting above 50 mg/dL. The trials were small and short and did not measure cardiovascular outcomes, so this is an interesting signal rather than a treatment.

L-carnitine is converted by gut bacteria to TMAO, which has been linked to higher cardiovascular risk in observational studies; the net effect is unknown. Discuss with your clinician before using it for this purpose.

Coenzyme Q10

Preliminary evidence

A 2016 meta-analysis of 7 randomised trials (409 people) found CoQ10 at 100 to 300 mg a day lowered Lp(a) by about 3.5 mg/dL, with the effect confined to people with baseline Lp(a) above 30 mg/dL. The reduction is small relative to the levels that matter clinically and no outcome data exist.

May reduce the effect of warfarin; check INR if you start or stop it.

Low-dose aspirin in carriers of high-risk LPA variants

Preliminary evidence

Aspirin lowers Lp(a) by only a few percent, but because Lp(a) promotes clotting, it has been studied as a targeted preventive. In the Women's Health Study and the ASPREE trial of older adults, carriers of the LPA rs3798220 variant (about 4 percent of people of European ancestry) who took aspirin had roughly half the rate of cardiovascular events compared with carriers on placebo, while non-carriers gained no benefit. This is a genetic subgroup finding and aspirin is not recommended for everyone with high Lp(a).

Daily aspirin increases the risk of stomach and brain bleeding; it is used for primary prevention only after an individual discussion of risk and benefit.

When to see a clinician promptly

Chest pain, pressure or tightness, especially on exertion or with breathlessness, sweating or pain spreading to the arm or jaw: possible heart attack, call emergency services (911 in the US).
Sudden weakness or numbness on one side, facial drooping, slurred speech or loss of vision, which are stroke symptoms and need emergency care whatever your Lp(a).
An Lp(a) of 50 mg/dL (125 nmol/L) or more, to review your full cardiovascular risk, LDL target and whether statin or other treatment is appropriate.
An Lp(a) above 180 mg/dL (430 nmol/L), which places you in a very high lifetime-risk group and warrants a lipid specialist referral and family testing.
Exertional breathlessness, chest tightness or fainting with a heart murmur, since high Lp(a) is a risk factor for aortic valve stenosis.
A heart attack, stroke or peripheral artery disease in a parent or sibling before 55 (men) or 65 (women), so that you and other relatives can be tested.

Frequently asked questions

What is a normal lipoprotein(a) level?

Below 30 mg/dL, or below 75 nmol/L, is considered desirable and is where about 70 to 75 percent of people sit. Between 30 and 50 mg/dL (75 to 125 nmol/L) is borderline. A level of 50 mg/dL (125 nmol/L) or higher is high and is used as a risk-enhancing factor in US and European guidelines; above 180 mg/dL (430 nmol/L) is very high. Labs use different assays and units, so compare your result with the cut-offs printed on the report.

How do I convert Lp(a) from nmol/L to mg/dL?

There is no exact conversion, because mg/dL weighs the whole particle while nmol/L counts particles, and particle size varies from person to person. As a rough guide, divide nmol/L by about 2.4 to estimate mg/dL (or multiply mg/dL by 2 to 2.5 to estimate nmol/L): 75 nmol/L is roughly 30 mg/dL, 125 nmol/L roughly 50 mg/dL and 430 nmol/L roughly 180 mg/dL. Guidelines prefer nmol/L and advise interpreting a result only against cut-offs in the same unit.

What causes high lipoprotein(a)?

Almost entirely your genes. The LPA gene variant you inherited determines about 90 percent of your level, which is set in early childhood and stays stable for life. It is higher on average in people of African ancestry. Kidney disease, nephrotic syndrome, hypothyroidism, menopause, pregnancy and acute illness raise it modestly, and statins raise it by around 10 percent. Diet, weight and exercise have almost no effect on it, in either direction.

How do I lower lipoprotein(a)?

Honestly, with current options, you mostly cannot. Diet and exercise move it by under 10 percent. Niacin lowers it 20 to 30 percent but did not reduce heart attacks in large trials. PCSK9 inhibitor injections lower it about 25 percent and do reduce events, and lipoprotein apheresis removes 60 to 70 percent per session for people with very high levels and established disease. Antisense and siRNA drugs that lower Lp(a) by 80 to 95 percent are in or completing large outcome trials. Meanwhile the proven strategy is to drive down LDL cholesterol, blood pressure and other risk factors.

Is a lipoprotein(a) of 100 dangerous?

An Lp(a) of 100 mg/dL (about 250 nmol/L) is high, roughly the top 10 percent of the population, and is associated with about 1.5 to 2 times the risk of heart attack and a higher risk of aortic valve stenosis compared with a low level. It is not an emergency and causes no symptoms; what it means is that your other risk factors should be treated more aggressively than the standard calculators suggest, usually with a statin and a lower LDL target, and that your close relatives should be tested.

Should I test my children for Lp(a)?

If you have a high Lp(a), each child has about a 50 percent chance of inheriting it, and the level is already established by around age 5. European guidance recommends cascade testing of first-degree relatives, and US lipid guidelines support testing children with a family history of early heart disease or very high Lp(a). Knowing early allows a lifetime of attention to the modifiable risk factors; no treatment is started in childhood for Lp(a) alone.

Do statins raise lipoprotein(a)?

Yes, modestly. Meta-analyses show statins raise Lp(a) by about 10 percent on average, and more in some people, probably by increasing apolipoprotein(a) production. This does not cancel the benefit: statins lower LDL by 30 to 50 percent and reduce heart attacks and strokes in people with high Lp(a) at least as much as in everyone else. A statin remains the first-line treatment for someone whose risk is raised by Lp(a). A rising Lp(a) after starting a statin is expected and is not a reason to stop.

Does lipoprotein(a) need to be tested more than once?

Usually not. Because the level is genetic and changes little over life, one measurement is enough for most adults. A repeat is reasonable if the first result was borderline, was taken during an acute illness, pregnancy, untreated thyroid disease or kidney disease, or if a treatment that affects Lp(a) (niacin, PCSK9 inhibitor, hormone therapy, apheresis) is started. Fasting is not needed.

References

Lipoprotein (a) blood test. MedlinePlus, US National Library of Medicine (2023)View source
Kronenberg F, Mora S, Stroes ESG, et al.. Lipoprotein(a) in atherosclerotic cardiovascular disease and aortic stenosis: a European Atherosclerosis Society consensus statement. European Heart Journal (2022)
Reyes-Soffer G, Ginsberg HN, Berglund L, et al.. Lipoprotein(a): a genetically determined, causal, and prevalent risk factor for atherosclerotic cardiovascular disease: a scientific statement from the American Heart Association. Arteriosclerosis, Thrombosis, and Vascular Biology (2022)
Wilson DP, Jacobson TA, Jones PH, et al.. Use of lipoprotein(a) in clinical practice: a biomarker whose time has come. A scientific statement from the National Lipid Association. Journal of Clinical Lipidology (2019)
Tsimikas S. A test in context: lipoprotein(a). Diagnosis, prognosis, controversies, and emerging therapies. Journal of the American College of Cardiology (2017)
Grundy SM, Stone NJ, Bailey AL, et al.. 2018 AHA/ACC/AACVPR/AAPA/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA guideline on the management of blood cholesterol. Circulation (2019)
Emerging Risk Factors Collaboration; Erqou S, Kaptoge S, Perry PL, et al.. Lipoprotein(a) concentration and the risk of coronary heart disease, stroke, and nonvascular mortality. JAMA (2009)
Kamstrup PR, Tybjaerg-Hansen A, Nordestgaard BG. Elevated lipoprotein(a) and risk of aortic valve stenosis in the general population. Journal of the American College of Cardiology (2014)
HPS2-THRIVE Collaborative Group. Effects of extended-release niacin with laropiprant in high-risk patients. New England Journal of Medicine (2014)
Serban MC, Sahebkar A, Mikhailidis DP, et al.. Impact of L-carnitine on plasma lipoprotein(a) concentrations: a systematic review and meta-analysis of randomized controlled trials. Scientific Reports (2016)
Sahebkar A, Simental-Mendia LE, Stefanutti C, Pirro M. Effect of coenzyme Q10 supplementation on plasma lipoprotein(a) concentrations: a systematic review and meta-analysis of randomized controlled trials. Pharmacological Research (2016)
Clarke R, Peden JF, Hopewell JC, et al.. Genetic variants associated with Lp(a) lipoprotein level and coronary disease. New England Journal of Medicine (2009)

Related markers

Related conditions

Evidence guides

Worried about your number?

Ask AskMN what your Lp(a) result could mean in the context of your other results, symptoms and medications. Free, unlimited, no account needed.

Ask about my Lp(a)

This page is educational and is not medical advice or a diagnosis. Lab results have to be interpreted together with your history, symptoms and other results by a clinician who knows you. Do not start or stop a supplement to change a lab value before the cause is known.