What is a good Lp(a) level?
Updated October 31, 2026 · 14 sources · Written by the AumniVIDA team
UnitsShort answer
A good Lp(a) level is below 75 nmol/L (about 30 mg/dL), the low-risk cutoff used by the EAS and NLA. From 75 to 125 nmol/L (30 to 50 mg/dL) is a grey zone, and 125 nmol/L (50 mg/dL) or more is high. Because units convert only roughly, compare results in the same unit.
Lp(a) risk ranges and guideline cutoffs in nmol/L
- Low risk
- 0 to 75
- Grey zone
- 75 to 125
- High
- 125 to 250
- Very high
- 250 to 500
- 75 nmol/L: EAS, NLA low
- 105 nmol/L: ESC/EAS 2025
- 125 nmol/L: EAS, NLA, ACC/AHA high
- 200 nmol/L: HEART UK high
- 250 nmol/L: About 2x risk
- 430 nmol/L: ESC/EAS 2019
Key takeaways
What is a normal Lp(a) level?
Under the EAS and NLA cutoffs, below 75 nmol/L (30 mg/dL) is low risk. The median adult in UK Biobank had 19.6 nmol/L, and half of adults fell between 7.6 and 74.8 nmol/L.
Normal is tricky for Lp(a), because levels are skewed: most people are low and a long tail is very high. In 460,506 UK Biobank adults the median was 19.6 nmol/L, the middle half ran from 7.6 to 74.8 nmol/L, and 12.2% of people without heart disease were at 150 nmol/L or more [4].
Guidelines therefore define a good level by risk, not by population averages. The EAS calls below 30 mg/dL (75 nmol/L) the rule-out zone [1], and the NLA calls below 75 nmol/L low risk [2]. The ESC/EAS 2025 update says risk starts to rise slightly from 30 mg/dL (62 nmol/L) [5]. The lowest risk in Copenhagen was below 5 mg/dL [6].
What do the Lp(a) ranges mean by guideline?
Most guidelines call 125 nmol/L (50 mg/dL) or more high and below 75 nmol/L (30 mg/dL) low. The ESC/EAS 2025 update uses above 105 nmol/L, HEART UK grades risk from 32 to above 400 nmol/L, and Japan uses below 25 nmol/L as low.
Each group sets its lines differently, so the same result can be labeled low, intermediate or high [1][2][5][7][8][9][10]. Older thresholds follow the comparison by Kaur and colleagues [11]. The range chart shows the common bands with each guideline's cutoff.
| Guideline | Low | Intermediate | High | Very high |
|---|---|---|---|---|
| EAS consensus (2022) | Below 75 nmol/L (30 mg/dL) | 75 to 125 nmol/L (30 to 50 mg/dL) | Above 125 nmol/L (50 mg/dL) | Not defined |
| NLA focused update (2024) | Below 75 nmol/L (30 mg/dL) | 75 to 125 nmol/L (30 to 50 mg/dL) | 125 nmol/L (50 mg/dL) or more | Not defined |
| ESC/EAS focused update (2025) | Not defined | 62 to 105 nmol/L (30 to 50 mg/dL), slight rise | Above 105 nmol/L (50 mg/dL) | Not defined |
| HEART UK (2019) | Below 32 nmol/L | 32 to 90 nmol/L minor; 90 to 200 moderate | 200 to 400 nmol/L | Above 400 nmol/L |
| Canadian (2021) | Not defined | Not defined | 100 nmol/L (50 mg/dL) or more | Not defined |
| ACC/AHA (2026) | Not stated in the summary | Not stated in the summary | Above 125 nmol/L, about 1.4 times risk | Above 250 nmol/L, 2 times or more |
| ESC/EAS (2019) | Not defined | Not defined | Not defined | Above 430 nmol/L (180 mg/dL) |
| Japan consensus (2026) | Below 25 nmol/L | 25 to 125 nmol/L | 125 nmol/L or more | Not defined |
Lp(a) risk ranges and guideline cutoffs in nmol/L
- Low risk
- 0 to 75
- Grey zone
- 75 to 125
- High
- 125 to 250
- Very high
- 250 to 500
- 75 nmol/L: EAS, NLA low
- 105 nmol/L: ESC/EAS 2025
- 125 nmol/L: EAS, NLA, ACC/AHA high
- 200 nmol/L: HEART UK high
- 250 nmol/L: About 2x risk
- 430 nmol/L: ESC/EAS 2019
Why can't you convert Lp(a) mg/dL to nmol/L exactly?
Because mg/dL weighs Lp(a) and nmol/L counts particles, and each particle's weight depends on the size of its apo(a), which varies between people. A rough guide is 2 to 2.5 nmol/L per mg/dL, but no official conversion factor exists.
Apo(a) can carry a few or dozens of kringle repeats, so a single particle can be light or heavy. Two people with the same particle count, the number that drives risk, can have different mass results [3]. Many tests also bind large and small apo(a) unevenly [3].
The EAS declines to set a conversion factor because assays vary so much, and uses 2 to 2.5 nmol/L per mg/dL only as a rough guide [1]. You can see the looseness in the guidelines themselves: 50 mg/dL is written as 100 nmol/L by the Canadian guideline [11], 105 nmol/L by the ESC/EAS 2025 update [5] and 125 nmol/L by the EAS and NLA [1][2].
What to do with your own numbers:
- Compare results only in the same unit, ideally from the same lab.
- Prefer nmol/L when you have the choice [5].
- If you only have mg/dL, use the mg/dL cutoffs rather than converting.

Do normal Lp(a) levels differ by ancestry?
Yes. In UK Biobank, median Lp(a) was 16 nmol/L in Chinese, 19 in White, 31 in South Asian and 75 in Black participants, but each 50 nmol/L carried a similar added risk in every group.
The UK Biobank analysis found hazard ratios per 50 nmol/L of 1.11 in White, 1.10 in South Asian and 1.07 in Black participants [4]. The same cutoffs therefore apply across ancestries, though more people of African ancestry cross them. Japan's 2026 consensus notes that median levels there are lower than in Western populations and still sets high risk at 125 nmol/L [9]. How much the number of kringle repeats explains also varies by ancestry, from about 30% to 70% [1].
Does Lp(a) change with age or sex?
It rises through childhood and is then largely stable in adults. Women's levels can rise after menopause, which is why a second test is reasonable if a premenopausal result was borderline.
The EAS notes that levels can rise until adulthood, so a test in childhood may need repeating [1]. In adults, Lp(a) is highly consistent over years [12]. The ESC/EAS 2025 update says Lp(a) may increase after menopause and suggests a second test when an earlier result was borderline [5]. Postmenopausal hormone therapy is associated with about 25% lower Lp(a), but it is not used as an Lp(a) treatment [1].
Can Lp(a) be too low?
There is no known harm to the heart from very low Lp(a). The EAS notes that very low levels may be linked to a higher risk of type 2 diabetes, which needs more study.
In Copenhagen, people below 5 mg/dL had the lowest heart attack risk [6]. The EAS consensus flags a possible association between very low Lp(a) and diabetes as an open question [1]. As drugs that lower Lp(a) by over 90% enter outcome trials, their safety records will help answer it [13][14]. To track diabetes risk directly, see HbA1c and fasting insulin.
More about Lp(a)
- Lp(a): the full guideLp(a), or lipoprotein(a), is an LDL-like particle with an extra protein, apolipoprotein(a), attached.
- Lp(a) test: who should get one, cost and preparationAn Lp(a) test is a routine blood draw that needs no fasting, and most adults need it only once because genes set the level.
- What does a high Lp(a) mean?A high Lp(a), usually 125 nmol/L (50 mg/dL) or more, means you inherited a gene variant that raises your lifelong risk of heart attack, stroke and aortic valve stenosis.
- Can you lower Lp(a)?Not much, with today's tools.
Protocols that act on Lp(a)
Common questions
What is the optimal Lp(a) range?
Is 100 nmol/L Lp(a) high?
Is there an Lp(a) unit converter?
Any converter is only an estimate. The EAS uses 2 to 2.5 nmol/L per mg/dL as a rough guide and does not endorse a fixed factor [1].
Is there an Lp(a) levels chart by age?
Lp(a) does not need age-specific charts in adults, because it is set by genes and stays largely stable [12]. The same cutoffs apply at any adult age; see the range chart above.
Sources
- 1.Kronenberg F, Mora S, Stroes ESG, et al. Lipoprotein(a) in atherosclerotic cardiovascular disease and aortic stenosis: a European Atherosclerosis Society consensus statement. Eur Heart J, 2022. doi:10.1093/eurheartj/ehac361
- 2.Koschinsky ML, Bajaj A, Boffa MB, et al. A focused update to the 2019 NLA scientific statement on use of lipoprotein(a) in clinical practice. J Clin Lipidol, 2024. doi:10.1016/j.jacl.2024.03.001
- 3.Marcovina SM, Albers JJ. Lipoprotein (a) measurements for clinical application. J Lipid Res, 2016. doi:10.1194/jlr.R061648
- 4.Patel AP, Wang M, Pirruccello JP, et al. Lp(a) (Lipoprotein[a]) Concentrations and Incident Atherosclerotic Cardiovascular Disease: New Insights From a Large National Biobank. Arterioscler Thromb Vasc Biol, 2021. doi:10.1161/ATVBAHA.120.315291
- 5.Mach F, Koskinas KC, Roeters van Lennep JE, et al. 2025 Focused Update of the 2019 ESC/EAS Guidelines for the management of dyslipidaemias. Eur Heart J, 2025. doi:10.1093/eurheartj/ehaf190
- 6.Kamstrup PR, Benn M, Tybjaerg-Hansen A, Nordestgaard BG. Extreme lipoprotein(a) levels and risk of myocardial infarction in the general population: the Copenhagen City Heart Study. Circulation, 2008. doi:10.1161/CIRCULATIONAHA.107.715698
- 7.Cegla J, Neely RDG, France M, et al. HEART UK consensus statement on Lipoprotein(a): A call to action. Atherosclerosis, 2019. doi:10.1016/j.atherosclerosis.2019.10.011
- 8.Pearson GJ, Thanassoulis G, Anderson TJ, et al. 2021 Canadian Cardiovascular Society Guidelines for the Management of Dyslipidemia for the Prevention of Cardiovascular Disease in Adults. Can J Cardiol, 2021. doi:10.1016/j.cjca.2021.03.016
- 9.Yoshida M, Ogura M, Tada H, et al. Lipoprotein(a) in Japan: An Expert Consensus Statement. J Atheroscler Thromb, 2026. doi:10.5551/jat.66330
- 10.American College of Cardiology. Prioritizing Health | Lower Sooner: How the 2026 Dyslipidemia Guideline Changes Practice. ACC.org, 2026. Link
- 11.Kaur G, Abdelrahman K, Berman AN, et al. Lipoprotein(a): Emerging insights and therapeutics. Am J Prev Cardiol, 2024. doi:10.1016/j.ajpc.2024.100641
- 12.Emerging Risk Factors Collaboration, Erqou S, Kaptoge S, et al. Lipoprotein(a) concentration and the risk of coronary heart disease, stroke, and nonvascular mortality. JAMA, 2009. doi:10.1001/jama.2009.1063
- 13.Nissen SE, Ni W, Shen X, et al. Lepodisiran - A Long-Duration Small Interfering RNA Targeting Lipoprotein(a). N Engl J Med, 2025. doi:10.1056/NEJMoa2415818
- 14.O'Donoghue ML, Rosenson RS, Gencer B, et al. Small Interfering RNA to Reduce Lipoprotein(a) in Cardiovascular Disease. N Engl J Med, 2022. doi:10.1056/NEJMoa2211023