Lp(a): The Genetic Cardiovascular Threat
Lp(a) is an LDL-like particle with an additional apolipoprotein(a) protein attached via a disulfide bond. This structure makes Lp(a) both atherogenic (promotes plaque) and thrombogenic (promotes clotting). The apo(a) component structurally resembles plasminogen, a clot-dissolving protein, allowing Lp(a) to compete with plasminogen and impair fibrinolysis. This dual mechanism means elevated Lp(a) both accelerates plaque buildup and increases the likelihood that a plaque rupture leads to a complete arterial blockage.
90% Genetic
Lp(a) levels are primarily determined by the LPA gene. Diet, exercise, and most medications have minimal effect on levels.
Test Once, Know Forever
Because levels are genetically fixed, you typically only need to test Lp(a) once in your lifetime. The result informs your lifetime risk profile.
1 in 5 People Affected
Approximately 20% of the global population has clinically elevated Lp(a), but most have never been tested.
Optimal Lp(a) Benchmarks
Common Questions
Can I lower my Lp(a) naturally?
Unfortunately, Lp(a) levels are almost entirely genetic. Diet, exercise, and statins do not meaningfully lower Lp(a). New therapies targeting Lp(a) directly are in clinical trials.
If Lp(a) is high, what should I do?
Focus on aggressively managing all other risk factors: keep ApoB very low, maintain optimal blood pressure, avoid smoking, exercise regularly, and work with a cardiologist on a comprehensive prevention plan.
Do I need to test Lp(a) more than once?
Generally no. Since levels are genetically determined, a single test establishes your baseline. Retesting is only needed if you begin a therapy specifically targeting Lp(a).