Lipoprotein(a): the cholesterol number you inherit

Lipoprotein(a), written Lp(a) and said "L-P-little-a", is an LDL-like particle with an extra protein, apolipoprotein(a), attached. Its level in the blood is set mainly by the LPA gene. It is reported in two ways: mg/dL, which measures the mass of the particle, and nmol/L, which counts particles. The two are not convertible by one fixed factor, because apolipoprotein(a) comes in different sizes from person to person. Compare like with like.

The guideline numbers

The EAS/EFLM consensus places 50 mg/dL at roughly the 80th percentile of the population it studied. A "normal" range printed on a lab report is often just the population distribution, and since Lp(a) is not something most people can change, there is no "optimal" claim worth chasing here. The useful question is simply which side of the thresholds you are on.

What raises and lowers it

• Genes, above all. Levels are largely fixed from early childhood. People of African ancestry tend to have higher levels on average.
• Kidney disease with protein loss can raise it.
• Lifestyle: diet, exercise and weight loss have little effect.
• Drugs: statins do not lower it and may nudge it up a little. PCSK9 inhibitors lower it modestly. Drugs designed specifically to lower Lp(a) are in trials. The 2022 EAS statement says those trials are needed to confirm that lowering it reduces events.

What it predicts

The 2022 EAS consensus describes a causal and continuous link between Lp(a) and cardiovascular events, and with narrowing of the aortic valve, and says high Lp(a) adds risk even when LDL is very low.

The genetic case was built largely in Copenhagen. In a 2009 JAMA paper, the Copenhagen City Heart Study followed 8,637 people for 16 years. Compared with Lp(a) below the 22nd percentile, the adjusted hazard ratio for heart attack was 1.6 between the 67th and 89th percentiles, 1.9 between the 90th and 95th, and 2.6 above the 95th. People who carried the gene variants that produce high Lp(a) had higher risk too, which is what points to cause rather than coincidence.

On GLP-1 drugs and weight loss

Lp(a) is not reported as a result in the pivotal semaglutide or tirzepatide trials, and because it is mostly genetic there is no reason to expect weight loss to change it much. If your Lp(a) is high, the practical consequence is that the things that do move, ApoB, LDL, blood pressure and glucose, matter more. That is the EAS advice: early, intensive management of other risk factors, matched to overall risk and the Lp(a) level.

How to test

• Once in adulthood. The EAS recommends at least one measurement for every adult. Repeat testing is rarely needed unless something changes, such as kidney disease.
• Fasting is not needed. The EAS/EFLM consensus found Lp(a) is unaffected by fasting.
• Family testing. A high result is a reason for first-degree relatives to be tested, and the EAS mentions cascade testing in familial hypercholesterolaemia and premature heart disease.
• Units. Note which unit your lab uses before comparing with anyone else's result.

Where it sits in Peptide AI

Lp(a) is not one of the markers Peptide AI groups and scores, partly because a once-in-a-lifetime test does not need a trend line. The lipid markers that do move, LDL, HDL, total cholesterol and triglycerides, sit in the metabolic panel. The longevity bloodwork guide covers how Lp(a) fits with them.

Tracking it in Peptide AI

The lipid markers that change over time are read from a lab PDF or manual entry, scored in the metabolic panel and plotted against your dose timeline. Log the draw date, whether you fasted, and anything unusual in the days before, such as illness, a hard session or a dose step, so the next result is compared like with like. Bloodwork tracking shows the series next to the dose log, weight and side effects, and the panels page lists every marker the app groups. More markers are in the bloodwork guides.