Lp(a) vs Cholesterol: Can Fish Oil Make a Difference?

You may have heard that “too much bad cholesterol can clog your arteries.” But there’s another type of blood fat that’s even more dangerous and often overlooked: Lipoprotein(a), or Lp(a) for short.

It’s determined by your genes—up to 80% genetic—which means no matter how clean you eat or how much you exercise, it’s very hard to bring it down. What’s worse, Lp(a) acts like a “fake cleaner”: not only does it pile up inside your blood vessels, it also blocks your body’s natural ability to clear out blood clots. The result? Plaques rupture more easily, vessels get blocked more suddenly, and heart attacks or strokes can strike earlier—and without warning.

People often ask: “If I take fish oil, will it help? Can EPA lower Lp(a)?”

This article will walk you through:

• What exactly is Lipoprotein(a)?
• Why EPA, even though it doesn’t directly lower Lp(a), still plays a key role by reducing inflammation, stabilising plaques, and preventing sudden rupture of your blood vessels;
• If your Lp(a) is already high, what steps can you take to truly protect your heart and brain?

Breaking it down in a way you can actually understand—especially when most doctors don’t explain it clearly.

1｜What Is Lipoprotein(a)? Why You Shouldn't Ignore It Even If It's Not on Your Test Report

Lipoprotein(a), abbreviated as Lp(a), is actually a special "mutated version of bad cholesterol."

Regular low-density lipoprotein (LDL) particles — what we commonly call “bad cholesterol” — are not cholesterol themselves, but rather “delivery packages” responsible for transporting cholesterol. Think of them as little floating balls in your blood that carry cholesterol from the liver to tissues and cells throughout the body.

You can imagine LDL particles as “delivery packages” filled with fats:

• Outer shell is a water-soluble phospholipid membrane, with a crucial delivery label called apolipoprotein B-100 (apoB-100). This label ensures that the cell recognizes the package is for it;
• Inside is packed with fat-soluble “cargo” like cholesterol esters and triglycerides — raw materials used for cell membrane synthesis, hormone production, and energy storage.

 

Only LDL packages with the correct “label” can be successfully “signed for” by cells and deliver cholesterol for use inside the cell.

So, what exactly is lipoprotein(a)?

You can think of Lp(a) as a regular LDL package with a “hidden attachment” secretly glued onto it.

Its “core” is still a standard LDL particle, but it has an extra tail made of a cysteine-rich protein called apolipoprotein(a), or apo(a) for short. This tail acts like a special kind of adhesive tape that alters the LDL’s original behavior, making it much more troublesome.

More specifically, this tail:
• Makes the package stick more easily to blood vessel walls, contributing to plaque buildup and atherosclerosis;
• Carries pro-inflammatory properties and antifibrinolytic effects, like a package containing fuel and fire retardants at the same time — increasing inflammation, promoting blockage, and making blood clots harder to dissolve.

The level of lipoprotein(a) is almost entirely genetically determined and remains stable throughout life. It is not significantly affected by diet or exercise and is slowly cleared by the liver. Since most routine health checkups do not include Lp(a) testing, individuals with a family history of heart attacks or strokes are advised to proactively request screening to understand their risk as early as possible.

2｜How Does Lipoprotein(a) Increase Thrombosis Risk? Why Is EPA Especially Important?

Many people think heart attacks and strokes are sudden events, but in fact, they are often the result of years of “chronic damage.” Lipoprotein(a) (Lp(a)) is one of the key hidden culprits that makes these damages fatal.

How Do Arterial Plaques Form Step by Step?

• Step 1: Elevated blood pressure, oxidative stress, or inflammation damages the endothelium of blood vessels, causing micro-tears.
• Step 2: LDL (bad cholesterol) particles sneak in and stick to the vessel walls.
• Step 3: The immune system mistakenly attacks the LDL, sending macrophages to engulf it. The result? Degenerated foam cells, which form "atherosclerotic plaques."
• Step 4: When plaques rupture, platelets and the coagulation system kick in to form a clot and seal the tear.

The Real Question—Can Your Clots Be Cleared Away?

Normally, your body has a built-in clot-clearing system that relies on the plasminogen → plasmin pathway, working like a cleanup crew to gradually dissolve clots.

But when Lp(a) levels are elevated, things take a dangerous turn—

• These “persistent” clots may travel to the brain, triggering a stroke;
• Or to the heart, causing a myocardial infarction (heart attack);
• They can even lead to pulmonary embolism or peripheral artery blockage, both potentially fatal events.

The Key Role of EPA: Not to “Lower Lp(a),” But to Reduce the Associated Risks

There is currently no proven drug that directly and significantly lowers Lp(a), but EPA (high-purity fish oil) has been shown to reduce Lp(a)-related threats through two critical pathways:

• Lower lipid precursors: Reduces VLDL and LDL production, helping to prevent plaque formation;
• Improve clot clearance: With anti-inflammatory and anti-aggregation properties, EPA promotes fibrinolysis, helping to clear micro-thrombi and counteract the “sticky clot” effect caused by Apo(a).

This is why more and more doctors are recommending: For those with a family history of stroke or heart attack—even if LDL is normal—it’s worth screening Lp(a) and considering long-term use of high-purity EPA fish oil as a protective measure.

In the upcoming articles, we’ll compare some of the most common high-EPA fish oils on the market—so you can choose wisely, take them correctly, and use them effectively.