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What you need to know about Lipoprotein (a) and cardiovascular health

When considering the prevention of – and support for – cardiovascular conditions, there are a large number of biomarkers that you would want to investigate, including standard normal lipid panels, inflammatory markers, and many others. You can find in-depth information about all of these in this webinar

But there is one biomarker that stands alone: Lipoprotein (a) (Lp(a)). This marker is an independent risk factor for cardiovascular disease, meaning it is associated with cardiovascular risk independently of other known risk factors such as age or lipid profile. More than a mere association, research suggests it is a causal factor for many cardiovascular (CV) conditions, including coronary artery disease, myocardial infarction (MI), stroke, peripheral arterial disease and heart failure. 

It is suggested that those born with an elevated Lp(a) have between 2 -4 times the risk of MI and other serious events and, as such, Lp(a) is a good marker for the assessment of risk in an otherwise healthy population with no known CV risks (even in the younger supposedly not at-risk population). The Lipoprotein (a) foundation estimates that as much as 20% of the population may have concerning circulating levels of Lp(a) in their blood.

Lp(a) concentrations are strongly genetically (chromosome 6) determined. They come in different sizes; with smaller size leading to greater concentrations. Size is dependent on how much of the apo(a) protein is wrapped around the core molecule.

What is it and why does it pose a threat?

  • It is a lipoprotein synthesised in the liver.
  • It consists of a cholesterol-rich LDL particle with one molecule of apolipoprotein B100 and one molecule of apolipoprotein A.
  • This molecule has a very wide range of concentrations that are 1000-fold between individuals, from 0.1 mg/dL to 300mg/dL!
  • Lp(a) has prothrombotic action. It both interferes with fibrinolytic activity via multiple mechanisms in vitro and nurtures atherosclerotic plaques with the deposition of Lp(a)-cholesterol. This means it promotes blood clotting and has a part to play in Atherosclerosis.
  • Individuals with high Lp(a) have a higher binding capacity for oxidised phospholipids and have more of these in their plasma and they have a higher risk for coronary artery disease.

Which clients would benefit from getting their levels tested?

  • People who have other known risk factors for cardiovascular disease (CVD).
  • People who have no known risk factors but have a family history of early heart disease.
  • People with familial hypercholesterolemia.
  • People who continue to battle with heart disease despite low levels of LDL cholesterol.

What can you do about it?

  • Whilst some pharmaceutical drugs have been successful in bringing Lp(a) concentrations down, these often act on other molecules relating to CV health, therefore it has been difficult to ascertain whether this reduction of Lp(a) corresponds to a reduced CVD risk. Further studies are required.
  • Lp(a) levels are strongly genetically controlled by the LPA gene locus and therefore are not easily influenced by age, diet or lifestyle. However, knowing someone’s levels can help identify a risk where there are otherwise no other obvious reasons for concern. Equally, it can help further quantify risk for someone who already has other known risk factors. In both of these cases, it can be a healthy motivation to address all other CV risk factors that respond well to lifestyle medicine to contain the risk as far as possible. For example, it would make sense to lower an individual’s inflammation baseline to not further contribute to atherosclerotic processes, as well as promote a healthy lipid profile, reduce oxidative stress and manage stress in general.
  • Crucially, other body systems can bear some influence on Lp(a) concentrations. It has been observed that the kidney has a role to play in Lp(a) catabolism. Therefore ensuring optimal kidney function may be of benefit. Furthermore, there is some controversy regarding the thyroid’s potential role in Lp(a) metabolism, as some studies point to its relevance, and others not. However, given the thyroid’s role in overall cholesterol metabolism, it stands to reason that supporting optimal thyroid function is relevant in managing other CV risk factors regardless, so this is another aspect that we as practitioners can support with.