Lp(a) — the cardiovascular risk you're likely born with
Paired condition: High cholesterol lab work
Quick answer
Lipoprotein(a), or Lp(a), is an LDL-like particle whose level is roughly 90% determined by your genes and stays fairly stable for life. A high Lp(a) independently raises the risk of heart attack, stroke, and aortic valve narrowing — and because it's inherited, one measurement usually tells your lifetime story. Statins don't meaningfully lower it, so a high Lp(a) is a reason to be more aggressive about every *other* modifiable risk factor, and to consider screening close relatives.
Reference ranges and interpretation
| Value / population | Classification | What it means |
|---|---|---|
| < 75 nmol/L (≈ < 30 mg/dL) | Lower risk | Below the commonly cited risk threshold. |
| 75 – 125 nmol/L (≈ 30 – 50 mg/dL) | Borderline / grey zone | Intermediate; interpret alongside overall risk. |
| > 125 nmol/L (≈ > 50 mg/dL) | High | Independent, graded increase in cardiovascular and aortic-stenosis risk. |
| One lifetime test (usually) | Testing note | Level is genetically set and stable, so it rarely needs repeating unless a therapy targets it. |
Report units vary: nmol/L (particle number, preferred) and mg/dL (mass) are not interchangeable, and there is no exact conversion. Use the same assay over time and read the lab's own reference range.
Why Lp(a) is different from your other cholesterol numbers
What a high Lp(a) means for risk
What to do when Lp(a) is high
- Control blood pressure, blood sugar, and smoking — every other risk factor matters more when Lp(a) is high
- Screen first-degree relatives — it's inherited, so a high result is family information
- Know your baseline aortic-valve status over time, since Lp(a) raises stenosis risk
Phi Longevity reads every marker on every lab you upload — together, against your history, against optimal ranges, and across time. The integrated picture tells you what a single number can't.
Start with my labs →Frequently asked questions
Do I need to fast before an Lp(a) test?
No. Lp(a) doesn't vary meaningfully with meals, so fasting isn't required. Because the level is genetically stable, timing matters far less than it does for triglycerides.
Can I lower my Lp(a) with diet or statins?
Not appreciably. Diet and exercise have little effect, and statins can even nudge it slightly upward. That's why a high Lp(a) shifts the focus to lowering LDL/ApoB and every other modifiable risk factor rather than chasing the Lp(a) number itself. Targeted Lp(a)-lowering drugs are in clinical trials but not yet approved for routine use.
Why are there two different units (nmol/L and mg/dL)?
nmol/L measures the number of Lp(a) particles and mg/dL measures their mass. Because particle size varies between people, there's no reliable conversion between the two. Modern assays report nmol/L, which is preferred. Compare results only when they use the same units and assay.
If my Lp(a) is normal, am I in the clear?
A low Lp(a) removes one inherited risk factor, but it doesn't cancel out LDL, blood pressure, smoking, or blood sugar. Lp(a) is one input to overall cardiovascular risk — a reassuring one when low, but read alongside the rest of your picture.
References
All citations verified against PubMed / publisher of record (see note below for this page's verification date).
- 1.Tsimikas S. (2017). A Test in Context: Lipoprotein(a) — Diagnosis, Prognosis, Controversies, and Emerging Therapies. Journal of the American College of Cardiology. 69(6):692-711. — Comprehensive clinical review of Lp(a) biology, measurement units, and interpretation.PubMed →DOI →
- 2.Kronenberg F, Mora S, Stroes ESG, et al. (2022). Lipoprotein(a) in atherosclerotic cardiovascular disease and aortic stenosis: a European Atherosclerosis Society consensus statement. European Heart Journal. 43(39):3925-3946. — Source for the once-in-a-lifetime testing recommendation and the risk-threshold framing.PubMed →DOI →
- 3.Nordestgaard BG, Chapman MJ, Ray K, et al. (2010). Lipoprotein(a) as a cardiovascular risk factor: current status. European Heart Journal. 31(23):2844-2853. — Foundational EAS statement establishing Lp(a) as an independent, causal cardiovascular risk factor.PubMed →DOI →
Reference ranges and units vary by lab and assay. This page is educational and not a substitute for individualized medical advice; cardiovascular risk and Lp(a) interpretation should be guided by a clinician.
By Steve Pinedo
Co-founder, Phi Longevity
Last updated: 2026-07-21
Steve Pinedo is the Co-founder of Phi Longevity, the AI application that turns a confusing stack of lab reports, wearable data, and clinical notes into a single, integrated picture of your health. He started Phi Longevity to make proactive health and wellness far easier to achieve. He realized how difficult it was for clients to manage their own care, records and coordination so he assembled a comprehensive M.D. led clinical team behind the platform, packaging the proactive-care experience that delivered measurable outcomes (lower triglycerides, reduced body fat, improved LDL, balanced hormones, relief from long-running autoimmune conditions) for any patient with a complicated lab to use now with an application. More about Phi Longevity →