What it measures.
Lipoprotein(a) is a genetically determined particle similar to LDL but with an additional protein, apolipoprotein(a), attached. Elevated Lp(a) is found in approximately 20% of the population and significantly increases cardiovascular risk independent of other lipid markers.
Lp(a) measures a specific lipoprotein particle that consists of an LDL-like core with apolipoprotein(a) attached via a disulfide bond. Levels are 70-90% genetically determined and remain stable throughout life.
Why it matters.
Elevated Lp(a) increases risk of heart disease, stroke, and aortic stenosis by 2-4 fold. It's pro-thrombotic (promotes clotting) and pro-inflammatory. Unlike other lipid markers, Lp(a) is largely unaffected by diet, exercise, or statins—making it a hidden risk factor for many people.
Physiology.
Lp(a) particles carry both cholesterol (contributing to atherosclerosis) and a protein structurally similar to plasminogen (potentially interfering with clot breakdown). This dual mechanism makes Lp(a) particularly dangerous. The apolipoprotein(a) comes in different sizes based on genetic variants—smaller isoforms are associated with higher particle numbers and greater risk.
Testing & preparation.
How to prepare
- No special preparation required
- Fasting not necessary
- Can be measured at any time
- Note: different assays (nmol/L vs mg/dL) aren't directly convertible
When to test
Test once in adulthood—levels are genetically determined and stable. Test earlier if family history of premature heart disease, unexplained cardiovascular events, or familial hypercholesterolemia.
How often
Typically once in lifetime unless participating in clinical trials for Lp(a)-lowering therapies.
Interpretation.
High lipoprotein(a)
Common causes:
- Genetic variants in LPA gene (primary cause)
- Kidney disease can elevate levels slightly
- African ancestry associated with higher levels
- Menopause may increase levels modestly
Implications:
- 2-4x increased risk of cardiovascular events
- Increased risk of aortic stenosis
- Risk additive to other lipid abnormalities
- Family members should also be tested
- May explain 'unexplained' cardiovascular events
Low lipoprotein(a)
Common causes:
- Genetic variants leading to low production
- Some liver conditions
- Certain ethnic backgrounds have lower average levels
Implications:
- No Lp(a)-mediated cardiovascular risk
- Does not require monitoring or intervention
- Good prognostic indicator
Optimization.
Diet
- No dietary interventions significantly lower Lp(a)
Lifestyle
- Exercise and weight loss do not significantly lower Lp(a)
- Focus on controlling modifiable risk factors more aggressively
Supplements
- Niacin (1-2g daily) can lower Lp(a) 20-30% but outcomes benefit unproven
- L-carnitine may have modest effect
FAQs.
Should everyone test Lp(a)?
Most lipid experts now recommend testing Lp(a) once in every adult. It's especially important if you have family history of premature heart disease, personal history of cardiovascular events, familial hypercholesterolemia, or if standard lipid therapy isn't adequately controlling your risk.
Can I lower my Lp(a)?
Currently, no approved therapies significantly lower Lp(a). Lifestyle changes don't affect it. Niacin provides modest reduction but outcomes benefits are unproven. Promising new therapies targeting Lp(a) are in late-stage trials. For now, focus on aggressively controlling other risk factors like LDL.
My Lp(a) is high—what should I do?
First, test family members. Second, be more aggressive with LDL lowering (target LDL <50-70 mg/dL). Third, optimize all other modifiable risk factors (blood pressure, glucose, inflammation, smoking). Fourth, consider aspirin therapy if appropriate (discuss with your doctor). Finally, watch for emerging therapies.
Why are there different units for Lp(a)?
Lp(a) can be reported in mg/dL or nmol/L. Unfortunately, they can't be directly converted because apolipoprotein(a) varies in size. Approximately, 2.5 nmol/L ≈ 1 mg/dL, but this varies by individual. Use the same units for tracking over time.
Does Lp(a) change over time?
Lp(a) levels are mostly stable throughout life because they're genetically determined. Menopause, kidney disease, and certain conditions can cause modest changes, but a single measurement typically represents your lifetime level.