Lipoprotein(a) Above or Below the Normal Range: Causes in Athletes and What to Do
Lipoprotein(a), usually written Lp(a), is one of the few blood markers that training, diet and willpower barely touch. It is largely inherited, it is an independent risk factor for heart attack, stroke and aortic valve narrowing, and around one in five people in the UK carry raised levels without knowing it. For athletes the picture has an extra twist: some performance-enhancing drugs push Lp(a) down while damaging the rest of the lipid profile. Here is what the result means and what can sensibly be done.
What Lp(a) is and how it is measured
Lp(a) is an LDL-like particle with an extra protein, apolipoprotein(a), attached to its surface. Apolipoprotein(a) resembles plasminogen, a protein involved in breaking down blood clots, which is one theory for why Lp(a) promotes both atherosclerosis and thrombosis. The particle also carries oxidised phospholipids that fuel inflammation in the artery wall.
Laboratories report Lp(a) either in nmol/L (preferred, as it counts particles) or in mg/dL. The two units cannot be converted precisely because particle size varies between people. In the UK, HEART UK suggests a broad interpretation: below 32 nmol/L is considered minimal risk, 32–90 nmol/L minor, 90–200 nmol/L moderate, 200–400 nmol/L high and above 400 nmol/L very high.
Because levels are about 70–90% genetically determined and fairly stable over adult life, a single measurement is usually enough. The 2022 European Atherosclerosis Society consensus statement recommends that every adult has Lp(a) measured at least once.
Testing is not part of a routine NHS cholesterol check. It is usually requested by a GP or lipid clinic when there is a strong family history of early heart disease, familial hypercholesterolaemia or unexplained cardiovascular events.
Why Lp(a) can be high
The main cause is the LPA gene. Variants with fewer "kringle" repeats produce smaller apolipoprotein(a) isoforms, which are secreted more efficiently and give higher blood levels. Levels also differ between ethnic groups, being on average higher in people of African and South Asian ancestry.
Secondary factors can raise Lp(a) further, although usually less dramatically than genetics:
- chronic kidney disease and nephrotic syndrome;
- hypothyroidism;
- menopause, as oestrogen tends to lower Lp(a);
- acute inflammation, which can transiently increase the reading;
- some medicines, including statins in certain individuals, which may modestly raise Lp(a) while still lowering LDL and overall risk.
Training load does not meaningfully change Lp(a). An athlete with a high result has not "done something wrong"; it is simply part of their inherited risk profile, much like height or blood group.
This is why a fit, lean, non-smoking runner with excellent LDL can still have a raised Lp(a). Being athletic lowers many other risk factors, but it does not cancel this one.
Why Lp(a) can be low — and why that is not always good news
A low Lp(a) is generally favourable and needs no treatment. Many people have very low levels because of their genetic variant, and there is no recognised deficiency state for healthy adults.
In athletes, however, an unexpectedly low result sometimes has a pharmacological explanation. Anabolic-androgenic steroids and other androgens are known to reduce Lp(a), sometimes substantially. At the same time they sharply lower HDL cholesterol, raise LDL and increase blood pressure and haematocrit, so the net cardiovascular effect is clearly harmful.
Severe liver disease and malnutrition can also lower Lp(a), because the liver produces it. A low reading alongside abnormal liver enzymes deserves medical attention rather than reassurance.
In short, the context matters: a naturally low Lp(a) is good news, while a low Lp(a) produced by androgen use is a marker of exposure to a drug that carries its own serious cardiovascular risks.
What to do about a raised result
There is currently no licensed medicine in the UK specifically for lowering Lp(a). Several RNA-based drugs, such as pelacarsen and olpasiran, are in large outcome trials, but results are still awaited. In the meantime, the strategy is to lower overall risk as aggressively as is reasonable.
| Approach | Effect on Lp(a) | Effect on overall risk |
|---|---|---|
| Diet and exercise | Minimal | Important — improves BP, weight, glucose |
| Statins | Neutral or slight rise | Reduce LDL and events; often first line |
| Ezetimibe | Minimal | Further LDL lowering |
| PCSK9 inhibitors | Modest reduction (around 20–30%) | Large LDL reduction; specialist use |
| Lipoprotein apheresis | Large, temporary reduction | Reserved for selected very high-risk patients |
Niacin lowers Lp(a) but did not reduce cardiovascular events in major trials and is no longer recommended for this purpose. Supplements marketed for "cholesterol support" have no robust evidence of lowering Lp(a).
A raised Lp(a) is also a reason to tell close relatives, because they have a fifty-fifty chance of sharing the trait. Cascade testing of family members is encouraged by UK lipid specialists.
Practical steps for athletes
If your Lp(a) is high, the priority is to make every other modifiable risk factor as favourable as possible. That means keeping LDL cholesterol low, blood pressure in the healthy range, not smoking, and managing body weight and blood glucose. For many athletes these targets are already met, but they should be checked rather than assumed.
A sensible monitoring package includes a full lipid profile with non-HDL cholesterol, apolipoprotein B where available, blood pressure, HbA1c and kidney function. Some cardiologists also use a coronary artery calcium scan to refine risk in people with very high Lp(a).
Avoiding anabolic steroids and other androgens is especially important. Any apparent fall in Lp(a) on such drugs is outweighed by the drop in HDL, rise in LDL, thickening of the heart muscle and increased clotting tendency.
Finally, discuss symptoms seriously. Chest pain on exertion, unexplained breathlessness or palpitations in an athlete with a high Lp(a) warrant prompt medical assessment rather than "training through it".
Editorial team's conclusions
Lp(a) is a mainly inherited cardiovascular risk factor that ordinary lifestyle changes barely move. A high result calls for tighter control of everything else, family screening and, where appropriate, specialist input. A low result is usually welcome, but in athletes using androgens it can be misleading and sits alongside a worse overall lipid picture. One measurement in adulthood is a worthwhile investment for anyone serious about long-term heart health.
Related reading that may help you interpret your blood tests includes our guides to HDL and LDL cholesterol in athletes, how anabolic steroids affect the lipid profile, and what apolipoprotein B adds to a standard cholesterol test.
References
- 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;43(39):3925–3946.
- Mach F, Baigent C, Catapano AL, et al. 2019 ESC/EAS Guidelines for the management of dyslipidaemias: lipid modification to reduce cardiovascular risk. Eur Heart J. 2020;41(1):111–188.
- Cegla J, Neely RDG, France M, et al. HEART UK consensus statement on Lipoprotein(a): a call to action. Atherosclerosis. 2019;291:62–70.
- Tsimikas S, Karwatowska-Prokopczuk E, Gouni-Berthold I, et al. Lipoprotein(a) reduction in persons with cardiovascular disease. N Engl J Med. 2020;382(3):244–255.
- Hartgens F, Rietjens G, Keizer HA, et al. Effects of androgenic-anabolic steroids on apolipoproteins and lipoprotein (a). Br J Sports Med. 2004;38(3):253–259.
- Nordestgaard BG, Langsted A. Lipoprotein (a) as a cause of cardiovascular disease: insights from epidemiology, genetics, and biology. J Lipid Res. 2016;57(11):1953–1975.
