Normal range: 0 – 75 nmol/L (lower is better)
Lp(a) is an LDL cholesterol particle wrapped in an extra protein that makes it roughly 6x more atherogenic than ordinary LDL, particle for particle. About 1 in 5 people have an elevated level, and above 100 mg/dL (214 nmol/L) the rate of cardiovascular events is 114% higher. Levels are 80-90% genetic and stable from age 5, so one test covers your lifetime. A standard cholesterol panel doesn't include it, which is why most people with high Lp(a) have never been told.
By Brandon Ballinger • Updated
On its own, Lp(a) costs about $40 but is usually measured in a panel alongside ApoB ($50), Vitamin D ($75), hs-CRP ($69), and ApoA1 ($50). You can test Lp(a) and 100 other biomarkers for $190 as part of an Empirical membership.
Lp(a) is typically billed under CPT 83695, which is the code to give your insurer when you check coverage. Empirical is FSA/HSA eligible, so you can pay with pre-tax dollars. Fast for 8-12 hours beforehand for the most accurate lipid and metabolic results, and expect results in days rather than weeks.
Lp(a) is the strongest inherited risk factor for heart disease, and about one in five people carry a high level. Most never find out, because a standard cholesterol panel doesn’t measure it. Your Lp(a) is set almost entirely by genetics, so a single test tells you your lifetime risk, and the 2026 AHA/ACC guidelines now recommend that every adult get it once.
This page covers what Lp(a) is, what counts as a high level, whether you can lower it, and how often to test.
| Measure | Value |
|---|---|
| Normal level | Below 75 nmol/L (about 30 mg/dL) |
| High risk | Above 125 nmol/L (about 50 mg/dL) |
| Very high | Above 200 nmol/L |
| How common | About 1 in 5 adults |
| Risk when high | 114% higher rate of cardiovascular events above 100 mg/dL (214 nmol/L) |
| Atherogenicity | Roughly 6x ordinary LDL, particle for particle |
| How often to test | Once in a lifetime for most people |
| What moves it | Almost nothing. It’s 80-90% genetic, and statins don’t lower it |
| Who should test | Every adult at least once, per the 2026 AHA/ACC guidelines |
| Cost | About $40 on its own, or $190 with 100+ biomarkers at Empirical |
Lp(a) is an LDL-like particle wrapped in an extra protein called apolipoprotein(a). That structure lets it do double damage: like LDL it drives plaque, and its tail promotes clotting and inflammation on top. Risk climbs with the level. People with Lp(a) at or above 100 mg/dL (about 214 nmol/L) had more than double the rate of major cardiovascular events compared with those in the normal range.
Cardiovascular event rates rise with Lp(a). At or above 100 mg/dL (214 nmol/L), risk was 114% higher than the reference group. Both mg/dL and nmol/L are shown because labs report either.
A normal Lp(a) is below 75 nmol/L, or roughly 30 mg/dL. Above 125 nmol/L (about 50 mg/dL) is high risk, and above 200 nmol/L is very high. Units matter here: nmol/L counts particles while mg/dL measures their mass, and the two don’t convert cleanly because particle size varies between people. The 2026 AHA/ACC guidelines prefer nmol/L for that reason, so check which unit your lab used before comparing to a threshold.
Lp(a) tends to rise with age (correlation with age, r = +0.10), but the change is small. Diet and exercise barely move it, which is why Lp(a) is treated as a fixed, once-in-a-lifetime number. The chart below shows the median by 5-year age bin and a linear trend line.
Median Lp(a) by 5-year age bin, with a linear trend line. The rise with age is modest.
For now, no lifestyle change or standard cholesterol drug meaningfully lowers Lp(a). Diet and exercise don’t move it, statins can nudge it slightly up, and PCSK9 inhibitors lower it by about a quarter. Several RNA-based drugs that cut Lp(a) by 80% or more are in late-stage trials, but none has yet proven it reduces heart attacks. A high Lp(a) isn’t a verdict, though. Because it’s only one part of your total risk, controlling everything else (ApoB, LDL, blood pressure, and smoking) sharply lowers your odds even when Lp(a) stays high.
Lp(a) is fixed, but LDL and ApoB, blood pressure, and smoking aren’t. Optimizing everything else cuts total risk even when Lp(a) stays high.
For more, see why a high Lp(a) isn’t a death sentence and Lp(a)-lowering medications. Talk to your clinician before starting or changing any medication.
Most people only need to test Lp(a) once, because a genetic level stays essentially constant for life. The 2026 AHA/ACC guidelines give this their strongest recommendation, and they add cascade testing: if yours is high, your first-degree relatives should be tested too. Testing appears to change outcomes, not just knowledge:
Patients with ASCVD who underwent testing for Lp(a) had lower mortality than those who did not get tested, likely due to more intensive lipid-lowering and antihypertensive treatment.
Retesting makes sense only in a few cases, such as kidney disease or starting an Lp(a)-lowering therapy. See the AHA’s Lp(a) testing recommendation and what to expect from the test.
Lp(a) is one piece of a particle-based risk picture. ApoB counts all your atherogenic particles and gives you a number you can actually lower, which matters most when Lp(a) is high. LDL cholesterol is the standard lipid measure, and hs-CRP adds the inflammation angle. For how these combine, see ApoB vs Lp(a) and adding Lp(a) and hs-CRP to PREVENT.
A normal Lp(a) is 0 – 75 nmol/L. Lower is better.
Lp(a) is almost entirely determined by genetics. If your parents have high Lp(a), you likely will too. Diet and exercise have minimal effect on levels. Kidney disease can raise Lp(a), and hypothyroidism may modestly increase it. Estrogen lowers Lp(a), which is why levels may rise after menopause.
Because Lp(a) is not very responsive to lifestyle changes, people with elevated levels should more aggressively control other modifiable risk factors like LDL, ApoB, blood pressure, and inflammation. Statins do not lower Lp(a) (and may slightly raise it), but PCSK9 inhibitors reduce it by about 20-30%. New targeted therapies specifically for Lp(a) are in late-stage clinical trials and may become available in the coming years. Niacin also lowers Lp(a) but is rarely used today due to side effects.
Lp(a) is most highly correlated with Apolipoprotein B and ALT. Here are the top biomarkers correlated with Lp(a), based on 500,000 tests done by Empirical Health.
The percentage shows how strongly two biomarkers move together. A higher number means the relationship is stronger. Green = rises and falls together. Orange = one rises as the other falls.
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Lp(a) is drawn at 2,200+ Quest and BioReference patient service centers across the US, so there's usually one within a short drive. Pick your state to see the metros we cover and every location in it.
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