LP(a) – The Genetic Heart Risk You May Never Have Heard Of
Most people who pay attention to their cardiovascular health can rattle off a few familiar numbers: LDL, HDL, triglycerides, blood pressure. But there’s another risk factor that flies almost entirely under the radar—and for some people, it quietly drives heart disease risk despite “normal” labs.
It’s called lipoprotein(a), or LP(a) (pronounced “LP little a”).
If you’ve never heard of it, you’re not alone. Even many people who’ve been tracking cholesterol for years have never had it measured. But for a meaningful percentage of the population, LP(a) is one of the most important—and least understood—drivers of cardiovascular risk.
In This Article”
The Danger of LP(a): What makes LP(a) more dangerous than standard LDL.
How LP(a) is Different: Why diet and exercise have little effect on your LP(a) levels.
Aortic Valve Disease: The underappreciated link between LP(a) and heart valve calcification.
The Blood Clot Risk: How this particle influences inflammation and blood clots.
Clinical Management: What to do if your LP(a) is elevated and how personalized management may be your best approach.
What is LP(a)?
LP(a) is a type of particle that circulates in the blood and carries cholesterol. Structurally, it looks similar to LDL, but with an important difference: it contains apolipoprotein B (ApoB)—the protein that allows cholesterol-carrying particles to enter the artery wall—plus an additional protein called apolipoprotein(a).
In prior Ikigai Insights posts, we’ve described ApoB-containing particles in detail, and this discussion assumes some familiarity with that framework.
Because LP(a) contains ApoB, it is included in what ApoB is measuring. ApoB reflects the total number of cholesterol-carrying particles that can penetrate artery walls and contribute to plaque. LP(a) is one specific, genetically determined subtype within that group.
What makes LP(a) different—and more dangerous—is the apolipoprotein(a) component. This added protein gives LP(a) properties that go beyond simply transporting cholesterol. It promotes inflammation, interferes with the body’s ability to break down clots, and accelerates calcification within blood vessels and heart valves.
Importantly, elevated LP(a) is not just linked to cardiovascular disease—it is considered a direct cause of both atherosclerotic cardiovascular disease (plaque buildup in arteries) and calcific aortic valve disease.
Why LP(a) is different from other lipid measurements
When we assess cardiovascular risk, we’re not actually measuring cholesterol itself—we’re measuring the particles that carry cholesterol through the bloodstream.
Many of these particles are influenced by lifestyle. Diet, exercise, weight loss, and sleep can meaningfully improve LDL-related particles, triglycerides, and insulin sensitivity.
LP(a) is different.
LP(a) levels are largely determined by genetics and tend to remain stable throughout life. For most people, lifestyle changes have little to no effect on LP(a).
That means:
You can be lean, active, and metabolically healthy
You can eat well and exercise consistently
Your LDL cholesterol can look “fine”
And LP(a) can still be high.
This is why LP(a) is often described as a hidden risk factor. Without measuring it, there’s no way to know it’s there.
Why LP(a) is especially concerning
Not all cholesterol-carrying particles carry the same level of risk.
LP(a) particles appear to cause more damage per particle than typical LDL particles. They are more likely to promote plaque buildup, inflammation, and calcification within arteries.
In practical terms:
ApoB tells us how many cholesterol-carrying particles you have
LP(a) tells us whether some of those particles are especially harmful
This helps explain why people with elevated LP(a) can experience heart attacks or strokes even when other risk factors appear well controlled.
LP(a) and valve disease
One of the most underappreciated effects of elevated LP(a) is its role in aortic valve disease.
LP(a) is a strong risk factor for calcification of the aortic valve—the valve that controls blood flow from the heart to the rest of the body. Over time, this calcification can cause aortic stenosis, a condition in which the valve becomes stiff and narrowed, making it harder for the heart to pump blood forward.
Unlike coronary artery disease, there are currently no medications that reliably slow this valve calcification once it begins. For many people, advanced valve disease eventually requires surgical or transcatheter valve replacement.
From a long-term health perspective, this matters. Valve disease can significantly limit exercise capacity, energy levels, and quality of life—even in people who otherwise feel healthy.
What about blood clots?
LP(a) also appears to increase the risk of clots forming within arteries, which can contribute to heart attacks and ischemic strokes (strokes caused by blocked blood flow).
This risk is thought to come from a combination of increased inflammation and reduced ability to dissolve clots once they form.
The relationship between LP(a) and clots in veins—such as deep vein thrombosis or pulmonary embolism—is less clear and appears limited to very high LP(a) levels. In contrast, the link between LP(a) and arterial events is well established.
How common is elevated LP(a)?
Elevated LP(a) is common.
Roughly one in four people worldwide has LP(a) levels high enough to meaningfully increase cardiovascular risk. Many don’t discover this until they undergo more advanced testing—or after a cardiovascular event.
Because LP(a) is inherited, it often runs in families. If one person has elevated LP(a), close relatives may as well.
Can LP(a) be lowered?
At present, there are no lifestyle interventions proven to meaningfully lower LP(a).
Common cholesterol-lowering medications have mixed effects:
Statins do not reliably lower LP(a)
PCSK9 inhibitors can reduce LP(a) modestly, while also lowering overall particle burden
Encouragingly, treatments designed specifically to lower LP(a) are in development. These newer therapies work at the genetic level to reduce LP(a) production and have shown large reductions in LP(a) levels in clinical trials. They are still being studied, and we are waiting for definitive evidence that lowering LP(a) reduces heart attacks and strokes—but the early data are promising.
For now, the focus is not on “fixing” LP(a) directly, but on managing the risk it creates.
What do we do if LP(a) is high?
If LP(a) is elevated, the goal is thoughtful prevention—not alarm.
That usually means:
Being more aggressive about lowering other cholesterol-carrying particles
Paying close attention to blood pressure and metabolic health
Using imaging to directly assess whether plaque is present
Personalizing prevention rather than relying on one-size-fits-all risk calculators
While some approaches rely on coronary calcium scoring, calcium alone can be misleading—especially in younger people or in those with soft, non-calcified plaque. This is why, at Ikigai, we often lean toward coronary CT angiography with advanced plaque analysis, which allows us to see both calcified and non-calcified disease. We’ve discussed this limitation of calcium scoring in prior Insights.
We use the best available science to guide these decisions, rather than following guidelines automatically. Guidelines are built for populations; our work is about caring for individuals.
Who should be tested?
Because LP(a) is genetically determined and stable over time, we measure it at least once in adulthood as part of a complete cardiovascular risk assessment.
If it’s normal, it usually doesn’t need to be rechecked. If it’s elevated, it becomes a permanent part of your cardiovascular risk profile—and an important input into how prevention is tailored over time.
The bottom line
LP(a) is one of the most underrecognized—and most consequential—drivers of heart and valve disease risk.
You can’t feel it. You can’t change it with lifestyle alone. And you won’t know it’s there unless you measure it.
But once you do, you can make more informed, personalized decisions to protect your healthspan over the long term.
Understanding risk is the first step toward managing it well.
Key Takeaways: The Reality of LP(a)
| Feature | The Facts |
|---|---|
| Origin | Almost entirely genetic; inherited from your parents. |
| Lifestyle Impact | Diet and exercise have minimal to no effect on levels. |
| Testing Frequency | Typically only needs to be measured once in a lifetime. |
| Primary Risks | Heart attack, stroke, and calcific aortic valve disease. |
| Management | Focus on aggressive control of other risk factors and advanced imaging. |
