Genetic Factors & Family Risk
Why your genes determine how high your Lp(a) is
Your Lp(a) level is not a matter of lifestyle, diet, or luck — it is written in your DNA. Lipoprotein(a), or Lp(a), is a genetically determined blood marker passed on from your parents. It is controlled by one specific gene: the LPA gene. This means that some people naturally have much higher Lp(a) levels than others, regardless of how healthy they live. Because this risk is hereditary, it is wise to have not only yourself but also your family members tested.
What makes Lp(a) genetic?
The amount of Lp(a) your body produces is determined by the LPA gene located on chromosome 6. This gene contains the instructions for producing the protein apolipoprotein(a) — the unique component that distinguishes Lp(a) from regular LDL cholesterol. Some people carry a gene variant that causes their body to produce more apolipoprotein(a). As a result, the amount of Lp(a) in the blood increases — sometimes up to ten times higher than normal. Your Lp(a) level is therefore determined at birth and remains roughly the same throughout your life.
How elevated Lp(a) runs in families
The tendency to have high Lp(a) is dominantly genetic, meaning the increased risk can be passed down from just one parent, even if the other has normal levels. Each parent passes one copy of the LPA gene to their child. When one of these copies contains a variant that produces large amounts of apolipoprotein(a), the child’s Lp(a) level will typically be elevated. This explains why several members of the same family can develop heart or vascular problems at a young age, even when their standard cholesterol levels appear normal.
What you should know about heredity:
- A child’s Lp(a) level often closely resembles that of their parents.
- If one parent has an elevated Lp(a) level, there is a high chance that one or more children will as well.
- Lp(a) levels are not influenced by diet, stress, or physical activity.

Genetic variations and ethnic differences in Lp(a)
Not everyone has the same genetic predisposition for elevated Lp(a) levels. There are hundreds of variants of the LPA gene worldwide, resulting in significant differences between populations:
- People of African descent generally have the highest Lp(a) levels.
- People of European descent tend to have medium levels.
- People of Asian descent and some Northern European populations typically have lower levels on average.
These genetic differences explain why some individuals with otherwise perfect cholesterol values can still have an increased risk of heart and vascular disease.
Why genetic knowledge matters
Understanding that Lp(a) is genetically determined changes the way we look at heart disease. It’s not only about lifestyle or diet — it’s also about inborn risks that you can measure, understand, and manage. Your Lp(a) level reveals something unique about your genetic makeup. This knowledge allows you to take targeted action before symptoms develop.
If you know that your Lp(a) level is elevated, there are still effective ways to protect your heart:
- Take targeted preventive measures, such as lowering LDL cholesterol.
- Make heart-healthy lifestyle choices, including not smoking, regular exercise, and a balanced diet.
- Inform family members so they can be tested for the same genetic risk.
Because Lp(a) runs in families, knowing your value can provide important insights for your relatives as well.
It is wise for family members to get their Lp(a) level tested if:
- Heart or vascular disease occurs in the family before the age of 60.
- There is a history of aortic valve calcification or sudden heart problems.
- You personally have elevated Lp(a), even if your other cholesterol values are normal.
Genetic insight allows you to detect risks early, take proactive action, and protect the heart health of multiple generations.
Sources
Scientific sources and medical references. The information on this page about the genetic basis, inheritance, and biological mechanisms of lipoprotein(a) is based on the following scientific publications:
Clarke R, Peden JF, Hopewell JC, et al.
Genetic variants associated with Lp(a) lipoprotein level and coronary disease.
New England Journal of Medicine, 2009.
Landmark genetic study identifying variants in the LPA gene that determine Lp(a) levels and demonstrating a causal relationship between elevated Lp(a) and coronary heart disease.
https://pubmed.ncbi.nlm.nih.gov/20032323/
Burgess S, Ference BA, Staley JR, et al.
Association of LPA Variants With Risk of Coronary Disease and the Implications for Lipoprotein(a)-Lowering Therapies: A Mendelian Randomization Analysis.
JAMA Cardiology, 2018.
Mendelian randomization analysis providing strong causal evidence that genetically elevated Lp(a) increases coronary disease risk and supporting Lp(a) as a therapeutic target.
https://pubmed.ncbi.nlm.nih.gov/29926099/
Van der Valk FM, Bekkering S, Kroon J, et al.
Oxidized Phospholipids on Lipoprotein(a) Elicit Arterial Wall Inflammation and an Inflammatory Monocyte Response in Humans.
Circulation, 2016.
Mechanistic human study showing that oxidized phospholipids carried by Lp(a) directly promote vascular inflammation and immune activation, explaining its atherogenic properties.
https://pubmed.ncbi.nlm.nih.gov/27496857/
NL - Nederlands
EN - English
DE - Deutsch