Lipoprotein (a)

Lipoprotein(a), abbreviated as Lp(a), is a unique cholesterol-carrying particle in your blood that combines the harmful “LDL-like” properties of LDL cholesterol with an additional protein called apolipoprotein(a). A simple way to picture it is: Lp(a) is like an LDL particle with an extra protein “wrapper”, creating a structure that behaves differently from other blood lipids. This distinct structure is one reason Lp(a) is considered particularly relevant for cardiovascular risk.

Your Lp(a) level is primarily determined by genetics, driven by the LPA gene that controls how much Lp(a) your liver produces. Approximately 70–90% of your Lp(a) concentration is inherited and tends to stay relatively stable across your lifetime. This is very different from LDL-cholesterol or triglycerides, which can shift meaningfully with diet, exercise, and weight changes. Because Lp(a) is so genetically “set,” many guidelines recommend measuring it once in a lifetime to identify inherited cardiovascular risk.

The LPA gene has substantial natural variation, including many different sizes of the apolipoprotein(a) protein. In general, smaller apolipoprotein(a) sizes are associated with higher Lp(a) levels. If your Lp(a) is elevated, your close relatives (parents, siblings, children) are more likely to also have elevated Lp(a), which is why cascade testing (screening family members) is often recommended.

Elevated Lp(a) is recognised as a causal and independent risk factor for cardiovascular disease. “Independent” means it can increase risk even if your LDL-cholesterol, HDL-cholesterol, blood pressure, or other traditional markers look reassuring. It is also common: around 20–25% of the global population has Lp(a) above 50 mg/dL (or 125 nmol/L), which is associated with significantly increased long-term cardiovascular risk. Importantly, the relationship between Lp(a) and disease risk is continuous and log-linear — meaning risk generally rises as the level rises, with the steepest risk increases at very high concentrations.

Large population data show that individuals in the highest Lp(a) range (roughly the top 5%, e.g., >90 mg/dL or >190 nmol/L) have meaningfully higher risks across multiple outcomes, including heart attack and aortic valve stenosis, and increased risks for peripheral artery disease, heart failure, ischemic stroke, and cardiovascular mortality compared with people with low Lp(a). Another way this risk is described is that each ~50 nmol/L increase in Lp(a) is associated with about an 11% increase in cardiovascular disease risk, independent of other risk factors.

Lp(a) increases risk through multiple mechanisms, not just “cholesterol buildup.”

• Atherosclerosis (plaque buildup): The LDL-like portion of Lp(a) delivers cholesterol into artery walls, where it can become trapped and oxidized, accelerating plaque formation.

• Inflammation via oxidized phospholipids (OxPLs): Lp(a) is a preferential carrier of OxPLs — damaged fat molecules that promote inflammation, immune activation, calcium deposition in arteries and valves, and faster plaque progression.

• Clot-promoting effects: The apolipoprotein(a) component resembles plasminogen (involved in breaking down clots). This resemblance can interfere with clot breakdown, making clots more persistent at sites of plaque disruption — raising heart attack and stroke risk.

• Binding to fibrin and vessel-wall accumulation: Lp(a) can incorporate into injured vessel areas, contributing to progressive narrowing.

Beyond arteries, Lp(a) plays a specific causal role in calcific aortic valve stenosis (CAVS), where the aortic valve becomes stiff and narrowed due to inflammation and calcium deposition — processes strongly linked to the oxidized phospholipids carried by Lp(a). Risk related to Lp(a) often becomes more apparent with age (notably after ~50 years), consistent with cumulative lifetime exposure. Practically, this means elevated Lp(a) can increase long-term risk even when you feel perfectly well — so it’s most useful as a prevention-focused biomarker.

Genetics

Lp(a) is remarkably stable over life because it is overwhelmingly genetically determined. The LPA gene (and its structural variation, including kringle repeats) drives most differences between people. There are also differences in median Lp(a) levels between ancestry groups (with higher median levels in individuals of African ancestry), and Lp(a) levels are generally 5–10% higher in women than men.

Diet

Diet typically has minimal to modest effects on Lp(a) (unlike LDL and triglycerides). Some diet trials show that lowering saturated fat can change Lp(a) slightly — sometimes even increasing Lp(a) while lowering LDL, which highlights how differently Lp(a) behaves compared with standard cholesterol markers. Alcohol intake (particularly excessive intake, and in some studies red wine) may modestly raise Lp(a). Overall, dietary strategies are important primarily because they lower overall cardiovascular risk, even if Lp(a) itself barely moves.

Lifestyle

Exercise and physical activity show inconsistent and generally small effects on Lp(a) in studies (ranging from no change to modest reductions). Smoking is associated with modestly higher Lp(a). Even though lifestyle changes may not substantially lower Lp(a) directly, they are still essential—because with inherited Lp(a) risk, the strategy becomes to optimise every modifiable risk factor.

Hormonal and medical factors

Menopause can increase Lp(a), and hormone replacement therapy (HRT) in postmenopausal women has been shown to lower Lp(a) (with oral oestrogen generally having larger effects than transdermal preparations). Kidney disease can substantially elevate Lp(a). Inflammation can temporarily raise Lp(a) (including during acute illness/infection), and thyroid dysfunction, pregnancy, and diabetes may also modestly affect levels — so context matters when interpreting results.

• Optimal: < 75 nmol/L (≈ < 30 mg/dL)

• Borderline / intermediate: 75–124 nmol/L (≈ 30–49 mg/dL)

• High: ≥ 125 nmol/L (≈ ≥ 50 mg/dL)

• Very high: ≥ 200 nmol/L is often flagged as very high in clinical practice; some guidelines classify > 400 nmol/L as extremely high .

If your results are high

Your results are high, meaning your Lp(a) is elevated. Because Lp(a) is largely genetic and currently difficult to lower substantially, the focus is on improving all other modifiable cardiovascular risk factors with your healthcare provider.

Diet:

• Follow a Mediterranean-style or DASH-style pattern emphasising whole, minimally processed foods.

• Aim for 5–9 servings of vegetables daily (including 2–3 cups of leafy greens), 2–3 servings of whole fruit daily (especially berries/citrus/apples), whole grains (3–4 servings daily), and legumes at least 4–5 times weekly (½–1 cup per serve).

• Use extra virgin olive oil as your primary fat (2–3 tablespoons daily), include nuts (~¼ cup/1 ounce daily) and seeds (2 tablespoons daily), and consider ½–1 avocado daily.

• Eat fatty fish (~4 oz) 2–3 times weekly.

• Limit saturated fat from red meat, full-fat dairy, butter, and tropical oils (coconut/palm), keeping it below ~7% of calories (about 15–20 g/day), avoid trans fats, minimise refined carbohydrates and added sugars, and keep sodium <2,300 mg/day (ideally ~1,500 mg/day if you have hypertension).

• Keep alcohol moderate (≤1 drink/day for women, ≤2 for men) or consider avoiding it given potential modest effects on Lp(a) in some people.

Lifestyle:

• Aim for 150 minutes/week of moderate aerobic exercise (or 75 minutes/week vigorous) plus resistance training 2 days/week.

• If you smoke, prioritise smoking cessation as a key risk-reduction step.

• Support stress reduction (e.g., meditation 10–20 minutes daily, yoga 2–3×/week) and prioritise 7–9 hours of sleep nightly.

Supplements:

• No supplements have strong evidence for large Lp(a) reductions.

• Two supplements with the most supportive evidence for modest reductions in some studies include L-carnitine (2–4 g/day) and CoQ10 (100–300 mg/day), considered as adjuncts under medical supervision.

• Niacin can lower Lp(a) but is generally not recommended specifically for Lp(a) lowering due to side effects and lack of benefit in major trials when added to statin therapy.

Additional tests:

• Consider cascade testing for first-degree relatives

• since elevated Lp(a) is strongly inherited and family members may also be affected

1. Nordestgaard BG, Langsted A. Lipoprotein(a) and cardiovascular disease. Lancet (London, England). 2024;404(10459):1255-1264. doi:10.1016/S0140-6736(24)01308-4.

2. Reyes-Soffer G, Ginsberg HN, Berglund L, et al. Lipoprotein(a): A genetically determined, causal, and prevalent risk factor for atherosclerotic cardiovascular disease: A scientific statement from the American Heart Association. Arteriosclerosis, Thrombosis, and Vascular Biology. 2022;42(1):e48-e60. doi:10.1161/ATV.0000000000000147.

3. Enkhmaa B, Berglund L. Non-genetic influences on lipoprotein(a) concentrations. Atherosclerosis. 2022;349:53-62. doi:10.1016/j.atherosclerosis.2022.04.006.

4. Volgman AS, Koschinsky ML, Mehta A, Rosenson RS. Genetics and pathophysiological mechanisms of lipoprotein(a)-associated cardiovascular risk. Journal of the American Heart Association. 2024;13(12):e033654. doi:10.1161/JAHA.123.033654.

5. Wong ND, Fan W, Hu X, et al. Lipoprotein(a) and long-term cardiovascular risk in a multi-ethnic pooled prospective cohort. Journal of the American College of Cardiology. 2024;83(16):1511-1525. doi:10.1016/j.jacc.2024.02.031.

6. Lampsas S, Xenou M, Oikonomou E, et al. Lipoprotein(a) in atherosclerotic diseases: From pathophysiology to diagnosis and treatment. Molecules (Basel, Switzerland). 2023;28(3):969. doi:10.3390/molecules28030969.

7. Greco A, Finocchiaro S, Spagnolo M, et al. Lipoprotein(a) as a pharmacological target: Premises, promises, and prospects. Circulation. 2025;151(6):400-415. doi:10.1161/CIRCULATIONAHA.124.069210.

8. Di Fusco SA, Arca M, Scicchitano P, et al. Lipoprotein(a): A risk factor for atherosclerosis and an emerging therapeutic target. Heart (British Cardiac Society). 2022;109(1):18-25. doi:10.1136/heartjnl-2021-320708.

9. Atallah M, Nasrallah N, Harb T, Gerstenblith G, Leucker TM. The biology of lipoprotein(a): From genetics to molecular mechanisms. European Journal of Clinical Investigation. 2025;:e70133. doi:10.1111/eci.70133.

10. Santos HO, Kones R, Rumana U, et al. Lipoprotein(a): Current evidence for a physiologic role and the effects of nutraceutical strategies. Clinical Therapeutics. 2019;41(9):1780-1797. doi:10.1016/j.clinthera.2019.06.002.

11. Momtazi-Borojeni AA, Katsiki N, Pirro M, et al. Dietary natural products as emerging lipoprotein(a)-lowering agents. Journal of Cellular Physiology. 2019;234(8):12581-12594. doi:10.1002/jcp.28134.