When it comes to cardiovascular health, many of us will be familiar with names like LDL and HDL cholesterol and even perhaps triglycerides, for those with a stronger interest in this subject.
However, there is one important molecule that very few are talking about, including doctors when presenting you with your annual health check.
Lipoprotein(a), also abbreviated as Lp(a) (lp little a), is a lesser known lipoprotein that plays a significant role in cardiovascular health.
In this article I will be discussing it’s relevance to cardiovascular health, clinical reference ranges and if there are any natural strategies to manage elevated levels.
Lipoproteins are lipid carrying vehicles (primarily cholesterol and triglycerides) who’s primary job is to transport them around the body where they are needed.
The two most well-known lipoproteins are low density lipoproteins (LDL) and high density lipoproteins (HDL).
LDLs are generally regarded as the ‘bad’ type as they carry cholesterol to the peripheries and has a higher propensity to contribute towards atherosclerosis and therefore heart attacks and strokes whereas HDLs are considered more protective as they carry cholesterol away from the body back to the liver to be recycled.
Molecularly, Lp(a) is identical to an LDL particle but has a separate protein structure attached to it called apolipoprotein(a) which LDLs do not have. This in turn creates a supercharged ‘cousin’ of LDL and is significantly more atherogenic compared to LDL. Studies has suggested a direct causal relationship between Lp(a) and atherosclerotic cardiovascular disease (Lau & Giugliano, 2022). This is effectively the formation of fat in the arteries.
There are several reasons why Lp(a) are more atherogenic than your standard LDL;
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- Lp(a) interrupts the normal breakdown of fibrin, one of the main components involved in blood clotting (Farzan & Senthilkumaran, 2022).
- Lp(a) has a higher affinity to the vascular wall leading to higher incidences of depositing cholesterol into the sub-endothelial space, the layer beneath the lining of the blood vessels.
- Lp(a) has a stronger inflammatory effect resulting in increased damage to the blood vessel wall (Ugovsek & Sebestjen, 2022).
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While your LDL levels can be impacted through lifestyle measures (nutrition habits, movement levels, weight management etc), your Lp(a) levels on the other hand is a genetically pre-determined fate and typically not manoeuvrable via lifestyle changes.
The process of atherosclerosis and the narrowing of the artery walls that increases the risk of heart attacks and strokes is typically a process that spans across many decades. This process is sped up through a variety of poor lifestyle choices (excessive saturated fat intake, higher levels of body fat, smoking) which usually results in higher levels of LDL cholesterol.
On the other hand, the LPA gene that codes for Lp(a) is thought to be fully expressed by teenagerhood, therefore there have been incidences of premature and fatal cardiovascular diseases at earlier ages (Melita et al, 2022).
It is thought that about 20% of the population have a genetic predisposition which could lead to elevated levels of Lp(a) (Wilson et al, 2019). For this reason, we recommend adults get tested for their Lp(a) levels once to find out if they are at higher risk of atherosclerotic diseases.
If this is the case, then all the more important to stay on top of your cardiovascular friendly nutrition and lifestyle habits.
The clinical reference range for Lp(a) is <75nmol/L.
While elevated Lp(a) levels can certainly increase the risk of having a major adverse cardiac event (MACE), there’s no single blood test marker that can definitively indicate whether somebody will have one or not, as this area of health isn’t binary. It exists more like a spectrum where individuals will fall under a ‘higher risk’ category or low/moderate risk.
Your Lp(a) number will contribute towards the overall calculation which determines where you sit on this spectrum and probably has the biggest impact on those who are otherwise healthy.
In other words, if you have obesity, dyslipidemia (high triglycerides, high LDL, low HDL), metabolic diseases like insulin resistance, consume excessive amounts of saturated fats and smoke, your risk of MACE is probably already quite high and whilst having a high Lp(a) count will absolutely increase this risk further, it probably isn’t telling you something you already didn’t know.
Whereas, if you’re relatively healthy, haven’t got any major issues with your weight management but your body fat % has been creeping up year on year and your LDL levels are borderline high, then having a high Lp(a) count will change your overall picture in terms of risk. This means that you will need to really stay on top of the variables that you can control, such as your weight, triglyceride levels, exercise and diet to name a few.
Up to now, there have been very little in the form of concrete evidence to suggest that nutritional interventions can lower elevated levels of Lp(a) (Enkhmaa et al, 2020).
Therefore, for the 10-20% of the population who find themselves with elevated levels of Lp(a), the awareness of the other risk factors contributing towards cardiovascular disease must be heightened.
Smoking, excessive alcohol and saturated fat consumption are all risk factors. As are high stress levels, hypertension and a family history of CVD.
Finally, ensuring that the rest of your lipid panel is well managed through diet and exercise and that you’re looking after your blood glucose levels will vastly reduce your risk of having a cardiac event and support your longevity.
As they say, our genes load the gun but out nutrition and lifestyle choices pull the trigger.
- Duarte Lau F, Giugliano RP. Lipoprotein(a) and its Significance in Cardiovascular Disease: A Review. JAMA Cardiol. 2022 Jul 1;7(7):760-769. doi: 10.1001/jamacardio.2022.0987. Erratum in: JAMA Cardiol. 2022 Jul 1;7(7):776. PMID: 35583875.
- Enkhmaa B, Petersen KS, Kris-Etherton PM, Berglund L. Diet and Lp(a): Does Dietary Change Modify Residual Cardiovascular Risk Conferred by Lp(a)? Nutrients. 2020 Jul 7;12(7):2024. doi: 10.3390/nu12072024. PMID: 32646066; PMCID: PMC7400957.
- Farzam K, Senthilkumaran S. Lipoprotein A. [Updated 2022 Sep 2]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK570621/
- Melita H, Manolis AA, Manolis TA, Manolis AS. Lipoprotein(a) and Cardiovascular Disease: A Missing Link for Premature Atherosclerotic Heart Disease and/or Residual Risk. J Cardiovasc Pharmacol. 2022 Jan 1;79(1):e18-e35. doi: 10.1097/FJC.0000000000001160. PMID: 34694242.
- Ugovšek S, Šebeštjen M. Lipoprotein(a)-The Crossroads of Atherosclerosis, Atherothrombosis and Inflammation. Biomolecules. 2021 Dec 24;12(1):26. doi: 10.3390/biom12010026. PMID: 35053174; PMCID: PMC8773759.
- Wilson DP, Jacobson TA, Jones PH, Koschinsky ML, McNeal CJ, Nordestgaard BG, Orringer CE. Use of Lipoprotein(a) in clinical practice: A biomarker whose time has come. A scientific statement from the National Lipid Association. J Clin Lipidol. 2019 May-Jun;13(3):374-392. doi: 10.1016/j.jacl.2019.04.010. Epub 2019 May 17. Erratum in: J Clin Lipidol. 2022 Sep-Oct;16(5):e77-e95. PMID: 31147269.
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The above article was contributed by
Danny
Primary Author
