Single marker guide · Lipoprotein(a), Lp(a)
Lipoprotein(a) is a cholesterol particle with a genetic extra that makes it stickier, more inflammatory and more likely to clot. Your level is set by your genes, fixed for life, and untouched by diet, exercise or statins. One in five people carries enough of it to meaningfully raise their risk of heart attack, stroke and aortic valve disease, and almost none of them know, because the NHS does not test it. You need to measure it once. Then you know.
Venous draw at 103 UK clinics or at home. UKAS-accredited laboratory. Report reviewed by a medical professional.
The short answer
Lipoprotein(a) is an ordinary ApoB-carrying LDL particle with an extra protein, apolipoprotein(a), bolted onto it. That extra protein does three things. It makes the particle stick to damaged artery walls more readily than plain LDL, so it builds plaque faster. It carries oxidised fats that drive inflammation inside the plaque. And it resembles the protein your body uses to dissolve clots, so it interferes with clot breakdown. The result is a particle that promotes atherosclerosis, plaque rupture and thrombosis at the same time, which is why a high Lp(a) independently raises the risk of heart attack, stroke and calcification of the aortic valve. ApoB blood test guide.
What makes it different from every other cardiovascular marker is that you cannot change it. Around 90% of your Lp(a) level is set by the LPA gene you inherited, it is established by early childhood, and it stays roughly constant for the rest of your life. Diet does not move it. Exercise does not move it. Statins do not lower it and may nudge it up. That is why one test is enough, and why the result matters so much: it tells you how hard you need to work on everything you can change.
Reference ranges
| Lp(a) result | Risk category (HEART UK) | What it means |
|---|---|---|
| Below 32 nmol/L | Minor | Where most people sit. Lp(a) is not contributing meaningfully to your cardiovascular risk. You can put this number away for life. |
| 32 to 90 nmol/L | Minor | Still low. A small contribution to risk that becomes relevant only if other risk factors are stacked on top. |
| 90 to 200 nmol/L | Moderate | Above the level European guidelines consider elevated (roughly 125 nmol/L). Your other cardiovascular targets, ApoB and LDL especially, should be set lower to compensate. |
| 200 to 400 nmol/L | High | A significant, lifelong contributor to risk. Worth a GP or lipid clinic conversation about aggressive management of everything modifiable, and about testing first-degree relatives. |
| Above 400 nmol/L | Very high | Roughly the top 5% of the population. Specialist lipid clinic referral is appropriate. Relatives should be tested. |
Categories follow the HEART UK consensus statement. Some laboratories report in mg/dL; the conversion is not exact but 50 mg/dL is roughly 125 nmol/L. Lp(a) rises modestly with kidney disease, menopause and hypothyroidism, and can read lower with liver disease; TrueVitals reports account for the markers tested alongside it.
Why it matters
Like ApoB, Lp(a) has no symptoms. What it has is a story that explains a great many otherwise puzzling heart attacks: the marathon runner at 48, the non-smoking vegetarian with a normal cholesterol, the family where every man has a cardiac event before 60. In each case the risk was sitting in a number nobody measured. Knowing it changes what you do with every other number.
People in the highest Lp(a) range have roughly two to three times the risk of a cardiac event of those in the lowest, independent of cholesterol, blood pressure and every other factor. The higher the level, the steeper the curve.
Because Lp(a) is not captured by a standard cholesterol test and is not lowered by a healthy lifestyle, it is the single most common hidden cause of cardiovascular events in people who did everything right. Testing it is how you find out whether you are one of them, while there is still time to compensate.
A high result means each of your children, siblings and parents has a 50% chance of carrying the same level. Cascade testing of relatives is standard advice, and it is one of the few blood results that changes what a whole family knows about itself.
Who should test
The European Society of Cardiology now recommends every adult measures Lp(a) at least once in their life. HEART UK singles out people with a family history of heart disease or stroke before 60, anyone with familial hypercholesterolaemia, anyone whose cholesterol has not responded as expected to statins, people with premature heart disease themselves, and those with aortic valve stenosis. Levels run higher on average in people of Black African and South Asian heritage, in whom cardiovascular risk is already elevated. And because Lp(a) rises after the menopause, women who have never been tested should consider it at that point. Health check at 50.Heart health blood test guide.
Read it in context
A high Lp(a) does not get treated directly, at least not yet. It gets managed by lowering every other risk factor further than you otherwise would. That makes the markers tested alongside it the ones that actually decide your risk.
The lever that moves. With a high Lp(a), preventive cardiologists set the ApoB target lower, often below 0.7 g/L, because every additional particle compounds the risk. ApoB is in every TrueVitals panel. ApoB guide.
Lp(a) carries the oxidised fats that inflame plaque, and inflammation is what makes plaque rupture. A high Lp(a) with a raised hs-CRP is the combination that most needs acting on. In every panel.
Insulin resistance multiplies cardiovascular risk from any source and it is the most reversible risk factor you have. With a high Lp(a), keeping metabolic health tight matters more, not less. Insulin and HOMA-IR are in Ultimate. Prediabetes guide.
Declining kidney function raises Lp(a) and raises cardiovascular risk independently. Cystatin C in the Ultimate panel measures kidney function more accurately than creatinine in people who are muscular or older.
An underactive thyroid raises Lp(a) and LDL together. If Lp(a) is high and TSH is raised, correcting the thyroid brings Lp(a) down partway, one of the few situations where it moves. Thyroid guide.
A second inherited-and-nutritional cardiovascular marker that compounds Lp(a) and, unlike it, responds to B vitamins. Included in the Signature panel alongside extended apolipoproteins.
Which test
Advanced
74 biomarkers · £269
ApoB, full lipids, hs-CRP, HbA1c, liver, kidney, thyroid and hormones. A strong cardiovascular baseline, but Lp(a) is not included at this tier.
View AdvancedIncludes Lp(a)
Ultimate
114 biomarkers · £349
Lp(a) with ApoB, full lipids, hs-CRP, fasting insulin, HOMA-IR, cystatin C, full thyroid and complete hormones. Everything needed to know your Lp(a) and to set the targets it demands.
View UltimateSignature
230 biomarkers · £799
Processed by Randox. Lp(a) with ApoA1, the ApoB:ApoA1 ratio, homocysteine and extended cardiovascular and metabolic syndrome markers, plus physical measurements. The deepest cardiovascular picture available privately in the UK.
View SignatureClinic draw £19 at 103 UK clinics. At-home phlebotomist £39 across 200+ areas. Fast from 10pm the night before. Pay monthly available.
Honest comparison
Because Lp(a) only needs measuring once, a standalone test is a perfectly rational buy for someone who already has a recent, comprehensive lipid and metabolic picture and simply wants the one missing number. Medichecks and others sell it for around £49. If your GP is willing, ask them to add it to your next NHS lipid profile; HEART UK's guidance supports testing in anyone with a family history, and some practices will do it.
For most people the standalone route is a false economy, because the value of an Lp(a) result is entirely in what you do with the markers around it. A high Lp(a) with no ApoB, insulin or CRP to read beside it tells you that you have a problem and nothing about how big it is or which lever to pull. Ultimate gives you the number and the plan in one draw. See how every UK provider compares.
After the result
Lp(a) is not a factor for you. Record it, tell your GP it has been measured, and manage cardiovascular risk on ordinary targets. There is no need to test it again.
Take your report to your GP and ask for Lp(a) to be recorded on your medical record. Set a lower ApoB target and work towards it with diet, exercise and, if your GP agrees, treatment. Blood pressure, smoking and insulin resistance all matter more now. Tell first-degree relatives it is worth testing.
Ask your GP about referral to a lipid clinic. Specialist treatment can lower Lp(a) partially (PCSK9 inhibitors reduce it by around a quarter) and the first drugs designed specifically to lower it are in late-stage trials. In the meantime, aggressive management of ApoB, blood pressure and blood sugar is the evidence-based route, and cascade testing of relatives is strongly advised.
This page is general information, not medical advice. Aspirin and other treatments are sometimes considered for high Lp(a); that is a decision for you and your clinician, not a blood test.
FAQs
Lipoprotein(a) is an LDL-like cholesterol particle with an additional protein, apolipoprotein(a), attached. The extra protein makes it more likely to build plaque, drive inflammation and promote clotting. Levels are around 90% genetically determined and stay stable through life.
HEART UK classes below 32 nmol/L as minor risk, 32 to 90 as minor, 90 to 200 as moderate, 200 to 400 as high and above 400 as very high. European guidelines treat roughly 125 nmol/L and above as elevated. About one in five people are above that threshold.
Not meaningfully with lifestyle, and statins do not lower it. PCSK9 inhibitor drugs reduce it by around 20 to 25%, lipoprotein apheresis removes it directly in severe cases, and antisense and siRNA drugs designed specifically to lower Lp(a) are in late-stage trials. The mainstay today is lowering every other risk factor further to compensate.
Not routinely. It is not part of the standard NHS lipid profile or NHS Health Check. Lipid clinics measure it, and HEART UK recommends testing in people with a family history of premature heart disease, familial hypercholesterolaemia or unexplained cardiovascular events. Some GPs will add it on request. What to ask your GP for.
Once is usually enough, because it does not change through life. Repeat testing is only worthwhile after a significant change such as menopause, starting a treatment that affects it, or developing kidney or thyroid disease.
Not for Lp(a) itself. TrueVitals panels also include glucose, insulin and triglycerides, so we ask you to fast from 10pm the night before your appointment and drink water as normal.
Ultimate (114 markers, £349) and Signature (230 markers, £799). Advanced includes ApoB and the full lipid profile but not Lp(a). If Lp(a) is the reason you are testing, Ultimate is the panel to choose.
Yes. A raised Lp(a) is inherited, and each first-degree relative has roughly a 50% chance of sharing it. HEART UK and European guidance both recommend cascade testing of parents, siblings and children so they can manage their own risk early.
114 or 230 biomarkers. Venous draw at 103 UK clinics or at home. A report that tells you what your results mean and what to do next.
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