Written by
Louise W Lu, PhD, MPH, BMLS
Written/Reviewed by
Alexandra V Goldberg, Registered Dietitian
In our reader consultations, one of the most common questions I hear is:
“Is Lp(a) genetic? If it’s determined by my genes, does that mean I only need to test it once—and the result will be the same years later?”
In our last article, “Lp(a) vs Cholesterol: Can Fish Oil Make a Difference?”, we talked about Lp(a) as a special form of LDL cholesterol with an extra protein on its surface called apo(a). We also discussed how it differs from regular cholesterol, and the potential role of EPA fish oil.
This time, we’ll start from that very question and help you understand:
- Why high Lp(a) is often something you’re “born with”;
- How to test it, which units are used, and what levels count as high risk;
- What different cholesterol + Lp(a) combinations (high cholesterol + low Lp(a), low cholesterol + high Lp(a), or both high) mean for your health;
- And the practical steps you can take for each scenario.
Explaining Lp(a) testing and risk profiles in plain, clear language you can act on.
Jump to sections:
1｜Why High Lipoprotein(a) [Lp(a)] Is “Inborn”
Many blood lipid markers—such as total cholesterol, LDL (“bad cholesterol”), and triglycerides—can fluctuate depending on your diet, exercise habits, and changes in body weight.
But Lipoprotein(a) [Lp(a)] is different—it’s almost “set” from the moment you are born.
If you want to review the difference between regular low-density lipoprotein LDL (“bad cholesterol”) and Lipoprotein(a) [Lp(a)], go back to the previous article: “Is Lipoprotein(a) the Real Culprit Behind Heart Attacks? Can EPA Fish Oil Reverse the Risk?”
Studies have found that 80%–90% of your Lipoprotein(a) [Lp(a)] level is determined by a gene called LPA.
Two things to clarify first:
- Everyone has the LPA gene—it’s a normal part of human DNA, responsible for instructing the liver to produce Lipoprotein(a) [Lp(a)], which is essentially regular LDL with an extra protein called apo(a) attached.
- Why do some people have high levels and others low? The key lies in different “versions” of the LPA gene—some versions make the liver produce more, while others produce less.
What exactly is different between these “versions”?
The LPA gene contains a stretch of repetitive DNA known as Kringle IV type 2 repeats:
- More “pages” in the “instruction manual” → liver reads it more slowly → lower production frequency → lower Lp(a) levels;
- Fewer “pages” → liver reads it quickly and repeatedly executes → higher Lp(a) levels.
How are these versions inherited?
- They are inherited from your parents. If one parent carries the “high-production” version, the next generation has about a 50% chance of inheriting it (dominant inheritance).
- The probability is the same for males and females—sons and daughters are equally likely to inherit it.
When does it start to have an effect? Why does it often rise after puberty?
- The LPA gene is present from birth, but its “production speed” accelerates with hormonal changes during puberty;
- It usually reaches a stable “adult level” around age 20, and then changes very little throughout life.
Why is it often not detected in childhood?
- During childhood, Lp(a) often has not yet reached its final stable value;
- Routine pediatric check-ups usually don’t include Lp(a) testing, so many people only discover it during adult health exams or cardiovascular screenings.
Conclusion: A single Lipoprotein(a) [Lp(a)] test can essentially tell you whether you carry this “inborn cardiovascular risk card.” If your result is high, there’s no need to panic—but you should start protecting your cardiovascular health earlier and more consistently from now on.
2｜How to Test for Lipoprotein(a) [Lp(a)] and What Counts as High Risk?
Unlike total cholesterol, LDL, or HDL, Lipoprotein(a) [Lp(a)] will not automatically appear in the standard “lipid profile” test. Most health check-up reports don’t include it at all—you need to specifically request an “Lipoprotein(a) [Lp(a)] test.”
How is it tested?
- Same as a regular blood draw: fast → blood sample taken → sent to the lab → results will list “Lp(a)” or “Lipoprotein(a).”
- The result units are usually expressed as mg/dL or nmol/L (different labs may use different units, so be mindful when interpreting results).
What counts as high risk? (Based on commonly used international thresholds)
- Low risk: < 14 mg/dL (< 35 nmol/L)
- Moderate risk: 14–30 mg/dL (35–75 nmol/L)
- High risk: > 30 mg/dL (> 75 nmol/L)
- Very high risk: > 50 mg/dL (> 125 nmol/L) (especially important to monitor if there is a family history of early-onset heart attack or stroke)
Differences among ethnic groups
Genetic distribution affects the “baseline” Lp(a) level. Studies show that people of African descent generally have higher average Lp(a) levels than White or East Asian populations; South Asians (e.g., from India, Pakistan) are also more likely to have elevated Lp(a) and experience early cardiovascular events. Even at the same value, the actual risk may vary by ethnicity; however, once above the high-risk threshold, it should be managed seriously regardless of ethnicity.
How often should it be retested?
- Unlike LDL, Lipoprotein(a) [Lp(a)] is barely affected by diet or exercise, so one test can generally reflect your lifelong level.
- If your result is elevated, there is no need for annual retesting; reassessment is more valuable during major physiological or health events (such as pregnancy, menopause, or a cardiovascular event) or when starting a new medical intervention.
Who should consider testing Lp(a) early?
- Those with a family history of heart attack before age 55 or stroke before age 65;
- Those already with elevated LDL, arterial plaque, diabetes, or hypertension—other cardiovascular risk factors;
- Those whose genetic testing shows a high-risk variant of the LPA gene (final confirmation should always be based on blood testing).
Key takeaway: Add Lp(a) to your cardiovascular screening checklist; if your level exceeds the high-risk threshold, you should also manage other controllable risks (such as LDL, blood pressure, blood sugar, weight, smoking, and inflammation) at the same time.
3｜Risk and Management Strategies for Different Combinations of Cholesterol and Lipoprotein(a) [Lp(a)]
In health check-ups, many people only focus on total cholesterol and LDL (“bad cholesterol”), while overlooking Lipoprotein(a) [Lp(a)]. In reality, the combination of cholesterol level × Lp(a) level can more accurately determine your overall risk for atherosclerosis, heart attack, or stroke.
Why does the combination magnify the risk?
- High LDL: Like having “plenty of raw material”—cholesterol is more likely to deposit on artery walls.
- High Lp(a): Like “glue + a spark”—more likely to stick to vessel walls, trigger inflammation, and promote clot formation.
- When both are elevated: Raw material + glue together significantly speed up plaque buildup, increasing the risk of events.
| Combination | Risk Characteristics | Priority Management Strategy |
|---|---|---|
|
Normal LDL + Normal Lp(a) (Low-risk group) |
Lipid transport is relatively healthy; low risk of vascular inflammation and adhesion. |
|
|
High LDL + Normal Lp(a) (Moderate-risk group) |
The main issue is elevated LDL, which promotes cholesterol deposition, but without Lp(a)’s additional “glue effect.” |
|
|
Normal LDL + High Lp(a) (Hidden high-risk group) |
Lipid profile may “look good” on the surface, but high Lp(a) promotes inflammation and clot formation, and risk is often underestimated. |
|
|
High LDL + High Lp(a) (Very high-risk group) |
High cholesterol supply + strong adhesion/inflammation accelerate atherosclerosis progression and result in the highest clotting risk. |
|
Action Plan
- Step 1: Get an Lp(a) test to determine which group you belong to.
- Step 2: If LDL is high, the first priority is to bring LDL to target; if Lp(a) is high, focus on reducing inflammation, preventing clots, and managing total risk factors.
- Step 3: For very high-risk groups, long-term follow-up with cardiology/general practice is essential, combining medication and imaging assessments when necessary.
Note: Ethnicity and family history can alter the actual risk at the same numerical value; once above the high-risk threshold, you should work with your doctor to develop a personalized plan, rather than relying solely on whether your total cholesterol “looks good.”
