Lipoprotein (a) Lp(a)

Why is Lp(a) important for your Healthspan?

‍Lp(a) levels are an independent and often inherited risk factor for cardiovascular disease. Elevated Lp(a) can contribute to the formation of arterial plaque and increase the risk of blood clots, leading to a higher likelihood of heart attack, stroke, and aortic valve issues. Understanding one's Lp(a) level allows for a more complete assessment of cardiovascular risk, guiding more intensive management of other modifiable risk factors to support long-term heart health and overall vitality.

‍What is Lp(a)?

Lipoprotein(a), often abbreviated as Lp(a), is a type of lipoprotein particle found in the blood that is structurally similar to Low-Density Lipoprotein (LDL) cholesterol. However, Lp(a) has an additional protein attached to it called apolipoprotein(a) [apo(a)], which distinguishes it and gives it unique properties. While its exact physiological role is not fully understood, elevated levels of Lp(a) are strongly associated with an increased risk of developing atherosclerosis, the hardening and narrowing of arteries due to plaque buildup. Unlike most other cholesterol markers, Lp(a) levels are predominantly determined by genetics and tend to remain relatively stable throughout life, showing little change with typical diet or exercise interventions.

‍How do we take action?

If Lp(a) levels are found to be elevated, one should consult with a healthcare provider, especially if there is a personal or family history of early cardiovascular disease. Since Lp(a) levels are largely genetically determined and not significantly lowered by diet or exercise, the primary strategy involves optimizing all other cardiovascular risk factors. This includes managing LDL cholesterol, blood pressure, and blood sugar, while also adopting a healthy lifestyle with a balanced diet and regular physical activity. In some cases, specific medications might be discussed by a healthcare provider to reduce Lp(a) or further mitigate overall cardiovascular risk, supporting long-term Healthspan.

‍Additional Sources

1. Emerging Risk Factors Collaboration, Erqou, S., Kaptoge, S., Perry, P. L., Di Angelantonio, E., Thompson, A., White, I. R., Marcovina, S. M., Collins, R., Thompson, S. G., & Danesh, J. (2009). Lipoprotein(a) concentration and the risk of coronary heart disease, stroke, and nonvascular mortality. JAMA, 302(4), 412–423. https://doi.org/10.1001/jama.2009.1063

2. Malaguarnera, M., Vacante, M., Russo, C., Malaguarnera, G., Antic, T., Malaguarnera, L., Bella, R., Pennisi, G., Galvano, F., & Frigiola, A. (2013). Lipoprotein(a) in cardiovascular diseases. BioMed research international, 2013, 650989. https://doi.org/10.1155/2013/650989

3. Lim, T. S., Yun, J. S., Cha, S. A., Song, K. H., Yoo, K. D., Ahn, Y. B., Park, Y. M., & Ko, S. H. (2016). Elevated lipoprotein(a) levels predict cardiovascular disease in type 2 diabetes mellitus: a 10-year prospective cohort study. The Korean journal of internal medicine, 31(6), 1110–1119. https://doi.org/10.3904/kjim.2016.030

4. Nestel, P. J., Barnes, E. H., Tonkin, A. M., Simes, J., Fournier, M., White, H. D., Colquhoun, D. M., Blankenberg, S., & Sullivan, D. R. (2013). Plasma lipoprotein(a) concentration predicts future coronary and cardiovascular events in patients with stable coronary heart disease. Arteriosclerosis, thrombosis, and vascular biology, 33(12), 2902–2908. https://doi.org/10.1161/ATVBAHA.113.302479

5. Riches, K., & Porter, K. E. (2012). Lipoprotein(a): Cellular Effects and Molecular Mechanisms. Cholesterol, 2012, 923289. https://doi.org/10.1155/2012/923289

6. Bennet, A., Di Angelantonio, E., Erqou, S., Eiriksdottir, G., Sigurdsson, G., Woodward, M., Rumley, A., Lowe, G. D., Danesh, J., & Gudnason, V. (2008). Lipoprotein(a) levels and risk of future coronary heart disease: large-scale prospective data. Archives of internal medicine, 168(6), 598–608. https://doi.org/10.1001/archinte.168.6.598

7. Santangelo, G., Faggiano, A., Bernardi, N., Carugo, S., Giammanco, A., & Faggiano, P. (2022). Lipoprotein(a) and aortic valve stenosis: A casual or causal association? Nutrition, Metabolism and Cardiovascular Diseases, 32(2), 309–317. https://doi.org/https://doi.org/10.1016/j.numecd.2021.10.015

8. Tsimikas, S., Lau, H. K., Han, K. R., Shortal, B., Miller, E. R., Segev, A., Curtiss, L. K., Witztum, J. L., & Strauss, B. H. (2004). Percutaneous coronary intervention results in acute increases in oxidized phospholipids and lipoprotein(a): short-term and long-term immunologic responses to oxidized low-density lipoprotein. Circulation, 109(25), 3164–3170. https://doi.org/10.1161/01.CIR.0000130844.01174.55

9. Mora, S., Kamstrup, P. R., Rifai, N., Nordestgaard, B. G., Buring, J. E., & Ridker, P. M. (2010). Lipoprotein(a) and risk of type 2 diabetes. Clinical chemistry, 56(8), 1252–1260. https://doi.org/10.1373/clinchem.2010.146779

10. Ye, Z., Haycock, P. C., Gurdasani, D., Pomilla, C., Boekholdt, S. M., Tsimikas, S., Khaw, K. T., Wareham, N. J., Sandhu, M. S., & Forouhi, N. G. (2014). The association between circulating lipoprotein(a) and type 2 diabetes: is it causal?. Diabetes, 63(1), 332–342. https://doi.org/10.2337/db13-1144

11. Schmidt, K., Noureen, A., Kronenberg, F., & Utermann, G. (2016). Structure, function, and genetics of lipoprotein (a). Journal of lipid research, 57(8), 1339–1359. https://doi.org/10.1194/jlr.R067314

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