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Heart & Circulation

Lipoprotein (a) / Lp (a)

Lp(a) is an inherited kind of cholesterol you are mostly born with; a high level quietly raises your long-term risk of heart attack, stroke and a stiff heart valve. You are probably hoping for a simple "is my number OK?", and the honest answer is there is no single safe number. The good news: it barely changes through life, so one test usually tells you your lifelong level, and knowing it is the first step your GP uses to protect your heart.

Targeted Testing
CategoryHeart & Circulation
Reference rangeSee your report
Evidence○Targeted Testing
Last updated3 July 2026
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What is lipoprotein (a) / lp (a)?

Lipoprotein(a) — usually written Lp(a) and pronounced "L P little a" — is a type of lipoprotein very similar to LDL (low-density lipoprotein, the so-called "bad" cholesterol carrier) but with an extra protein attached called apolipoprotein(a). Like LDL, Lp(a) carries cholesterol through your bloodstream and can contribute to the build-up of plaque (fatty deposits) in artery walls over time. The most important thing to know about Lp(a) is that the amount in your blood is decided by the genes you inherit from your mother and father. This makes it quite different from LDL cholesterol, which responds to diet, exercise and medication. Lifestyle changes such as diet and exercise do not reduce Lp(a) levels, and most of the commonly used medications to lower LDL cholesterol — including statins — are ineffective at lowering Lp(a). That can sound discouraging, but knowing your Lp(a) is not a dead end: it tells your GP to pay closer attention to the heart-risk factors you can change, which is where the real difference is made.

Why is it tested?

Lp(a) is tested as part of cardiovascular risk assessment — to understand whether you carry a genetically elevated risk of heart disease and stroke (cardiovascular disease, or CVD) that other lipid tests might not capture. Higher levels of Lp(a) in the blood are a risk factor for the build-up of plaque in arteries, which raises the risk of heart attack and stroke. Elevated Lp(a) has also been linked to aortic valve stenosis (stiffening of the main valve out of the heart). Because Lp(a) is predominantly (more than 90 per cent) determined by genetics and barely shifts through a person's life, it is usually measured once. Repeated measurement does not generally improve risk prediction — and so a single test gives your GP a stable, lifelong data point to factor into your overall heart-risk picture.

Reference range (Australia)

No single 'normal' value — Lp(a) is a risk-based, largely inherited measure usually checked once in a lifetime; use the reference interval printed on your report nmol/L

Lp(a) is mostly fixed by your genes and stays fairly stable through life, so it is usually measured once rather than tracked over time. Risk rises continuously with the level rather than stepping up at a single cut-off. Internationally, the European Atherosclerosis Society (EAS) uses a level below 75 nmol/L to suggest lower risk and above 125 nmol/L to suggest higher risk — but these are international thresholds, not Australian-specific ones, and are in nmol/L (units differ from mg/dL on older reports). Always use the interval on your own report.

Reference intervals vary between laboratories. Always use the range printed on your own report.

What your result means

If your level is low

A lower Lp(a) is reassuring from a cardiovascular standpoint. It suggests this particular inherited risk factor is not contributing meaningfully to your heart risk. Your GP will still look at the rest of your lipid panel, blood pressure, family history and other factors — because cardiovascular risk depends on the full picture, not just Lp(a).

If your level is in range

You are probably hoping for a clear "OK" — and a result within range is genuinely reassuring for this marker. Because Lp(a) is a risk-based measure rather than a simple pass/fail, your GP will read it alongside your other heart-risk factors. A result in range means this inherited contributor is not flagging concern on the current measurement.

If your level is high

A higher Lp(a) is a risk factor for the build-up of plaque in the arteries, which raises the long-term risk of cardiovascular disease (CVD) — heart attack, stroke — and aortic valve stenosis. This is a recognised, causal relationship supported by genetic evidence. What this means in practice: because Lp(a) is largely inherited and does not respond meaningfully to the usual LDL-lowering approaches (diet, statins), the value of knowing your level is in informing the overall risk picture — not in chasing the number down. Your GP will use it to decide whether to be especially thorough about the other, modifiable risk factors: blood pressure, LDL cholesterol, smoking status, weight and physical activity. A high Lp(a) is not a verdict. It is a reason to be thoughtful about the whole picture with your GP.

What can affect your result

The overriding driver of Lp(a) is genetics. The amount of Lp(a) in your blood is decided by the genes you inherit, and it is predominantly (more than 90 per cent) determined by genetic variability at a specific gene locus called LPA. This means it is largely fixed from birth and does not respond to the lifestyle changes that shift LDL cholesterol. Lifestyle changes such as diet and exercise do not reduce Lp(a) levels. Most commonly used medications to lower LDL cholesterol — including statins — are also ineffective at lowering Lp(a). No routinely available medication has been shown to substantially lower Lp(a), though this is an active area of research. With some exceptions — such as kidney disease, liver disease, or acute infections — Lp(a) stays stable throughout a person's life. Repeated testing generally does not improve risk prediction.

When to act

If your Lp(a) is above the reference interval on your report, the most useful next step is a conversation with your GP about your overall cardiovascular risk — not a reason to panic. Because Lp(a) itself cannot be substantially lowered with available treatments, your GP may instead focus on the risk factors that can be changed, such as blood pressure, LDL cholesterol, smoking, physical activity and weight. A high Lp(a) can be a reason for your GP to be especially thorough about managing those modifiable factors. If your result is in range, that is a reassuring data point in your overall heart-health picture. Your GP will still consider the rest of your results and risk factors at your next visit. This page is general information and is not a substitute for advice from your GP.

Frequently asked questions

Lipoprotein(a) or Lp(a) is a type of lipoprotein very similar to LDL — it carries cholesterol through your bloodstream and can contribute to plaque build-up in the arteries. The key difference is what drives it: LDL responds to diet, exercise and medication, while the amount of Lp(a) in your blood is decided by the genes you inherit from your parents. That makes it a different kind of risk factor — one that is harder to influence but important to know about.

No. This is one of the most important things to understand about Lp(a). Lifestyle changes such as diet and exercise do not reduce Lp(a) levels, and most of the commonly used medications to lower LDL cholesterol — including statins — are also ineffective. Because Lp(a) is set by your genes, the strategy for a high result is to manage the other, modifiable heart-risk factors more carefully — blood pressure, LDL, smoking, physical activity — rather than trying to bring Lp(a) down directly.

Usually not. Lp(a) is predominantly (more than 90 per cent) determined by genetics, so it stays fairly stable through your life. With some exceptions — such as kidney disease, liver disease or acute infections — repeated measurement does not generally improve risk prediction. This means a single test usually gives your GP the information they need for your lifelong risk picture, which is why Lp(a) is often described as a "test once" marker. Newer research is starting to ask whether a repeat test could add value in specific situations, but that is not yet established or part of standard Australian practice, so a single test remains the accepted approach.

There is no single agreed cut-off. Internationally, the European Atherosclerosis Society (EAS) suggests pragmatic levels to help guide risk thinking: below 75 nmol/L to 'rule out' higher risk, and above 125 nmol/L to 'rule in' higher risk. These are international thresholds — not Australian-specific guidelines — and they are intended as a framework for your GP to use alongside the rest of your cardiovascular risk picture, not as a pass/fail verdict. The units also differ between labs (nmol/L versus mg/dL on older reports), so it is important to compare like with like.

Knowing your Lp(a) level gives your GP a fuller picture of your cardiovascular risk — one that other standard lipid tests do not capture. Higher levels of Lp(a) are a recognised risk factor for plaque build-up in the arteries, raising the risk of heart disease and stroke, and also for aortic valve stenosis (stiffening of the main valve out of the heart). Even if Lp(a) itself cannot be lowered easily, knowing it is elevated is a reason to be especially thorough about the risk factors that can be changed. That information can genuinely shape your GP's approach to your long-term heart health.

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