Lp(a): the inherited risk number training will not change

The test measures how much Lp(a) is circulating in your blood, in grams per litre (g/l). At its core an Lp(a) particle is an LDL particle, complete with the single molecule of apolipoprotein B that every atherogenic particle carries. The difference is a second protein attached to it: apolipoprotein(a). That is exactly why Lp(a) is measured separately and cannot be inferred from your ordinary lipid panel. A tidy cholesterol profile tells you nothing about your Lp(a).

For anyone used to steering blood values, the key property is this: Lp(a) cannot be steered. The number of KIV-2 repeats in the LPA gene sets how large the apo(a) protein is and how much Lp(a) your liver releases. That predisposition is fixed from birth and explains more than 90 percent of the difference between people. Periodisation, carbohydrate restriction or ten kilos off change almost nothing about it. Where your triglycerides can turn around within weeks and your ferritin sinks within a block, Lp(a) stands still.

Finally, watch the unit. Your result is in g/l, a unit of mass; internationally you often see mg/dl (0.30 g/l is 30 mg/dl) or nmol/l. The latter counts particles rather than weight and is preferred internationally, precisely because the apo(a) protein is much larger in one person than in another. There is therefore no reliable fixed conversion factor between mg/dl and nmol/l. So do not line up results in different units as if they measured the same thing, and compare within the same laboratory where you can.

A sports panel is made almost entirely of things you can influence. Ferritin, glucose, triglycerides, LDL: every one of them responds to what you eat, how you train and how you recover. Lp(a) is the exception, and that makes it psychologically awkward. Anyone used to treating an out-of-range value as a project hits a wall here, because there is no protocol that brings this number down.

The right response is therefore a different one. A raised Lp(a) means that, with exactly the same LDL cholesterol and the same blood pressure as your training partner, you carry a higher lifetime risk of cardiovascular disease. Your risk begins from a higher starting point, and you did not choose that starting point. Which is exactly why everything that can be steered becomes more important.

In concrete terms, it is about the number of atherogenic particles grinding past your artery wall for years on end. You read that number from ApoB and non-HDL cholesterol, and not from your total cholesterol. Blood pressure, smoking, insulin sensitivity and visceral fat count too. With a raised Lp(a) there is simply less room in those values, and keeping them tight pays off more than it would for someone without this predisposition. How strict that needs to be is something your doctor decides with you.

Two things are commonly misunderstood here. First: a statin does not lower Lp(a) and in fact raises it slightly, so anyone hoping a cholesterol-lowering drug fixes this is hoping for the wrong drug. Second: medicines that specifically suppress Lp(a) production are in development. They lower the number steeply, but it has not yet been shown that doing so prevents heart attacks; those outcome trials are still running. Treat reports about them as promising and not yet as proven.

And then the sport itself. Endurance training improves your blood pressure, your insulin sensitivity and your triglycerides, and that remains entirely worth doing. Just not via Lp(a). Expect no effect there, and above all draw no conclusions about the quality of your training from the absence of one.

Measure once, then know. That is the entire testing frequency for Lp(a), and for anyone used to running a panel every quarter it takes some adjusting to. The value is genetically fixed and does not change with an offseason, a volume block or a competitive season, so a repeat measurement mostly produces noise. The 2022 European consensus accordingly advises measuring Lp(a) at least once in the life of every adult.

There is one moment when you should postpone the test: during or shortly after acute inflammation. Lp(a) behaves partly as an acute-phase protein, a protein that rises temporarily with inflammation, so an infection, surgery or a significant injury can lift the value for a while. A CRP in the same tube shows whether that is the case. A heavy training week or a competition is no reason to wait: those do not shift Lp(a) the way they shift CK or cortisol.

Two conditions can lift the value structurally: reduced kidney function or nephrotic syndrome, and an underactive thyroid. With an unexpectedly high result it is therefore worth looking at your TSH as well. You do not need to fast; a meal barely shifts Lp(a), so the test slots into an existing blood draw without trouble.

This is how you read the number. Below 0.30 g/l (30 mg/dl) this inherited factor plays no part in your case; the European consensus uses that limit to rule the risk out. Between 0.30 and 0.50 g/l you sit in the grey zone that same consensus names: it counts, but not on its own. From 0.50 g/l (50 mg/dl) the value is called raised; that is the cut-off of the Dutch GP standard, set at the 80th percentile, so roughly one in five people sits above it. From roughly 1.80 g/l the consensus speaks of markedly raised, with a lifetime risk on the order of inherited high cholesterol. One warning when reading your own report: the laboratory itself applies an upper limit of 0.30 g/l, so a value of 0.35 can be flagged high on the form while national guidance places it in the grey zone.

In nmol/l the European consensus works with 75 and 125 as the same two limits, but do not convert your g/l result to them yourself: the conversion differs from person to person with the size of the apo(a) protein. Finally, weigh your ancestry. The median Lp(a) is considerably higher in people of African descent than in people of European or South Asian descent, so the same result does not mean the same thing in everyone. Have your doctor place the value within your full risk profile.