Lipoprotein A, or Lp(a) for short (pronounced “LP little a”), is a unique lipoprotein and an established risk factor for cardiovascular disease. This particular cholesterol particle is coded in your DNA, so it is genetically linked.
Most doctors don’t check for Lp(a), but the TV actor Bob Harper made it mainstream news when he suffered a massive heart attack despite looking like he is in perfect health.
It has been established that high levels of Lp(a) can triple one’s risk of stroke and heart attack at an early age. A large Danish study looked at more than 9,000 participants over the course of 10 years and concluded that extremely elevated Lp(a) levels (>120 mg/dL) increased the risk of CAD by 3-4 times.
Interestingly, this inherited marker is pretty common with elevated levels affecting about 20-30% of the global population according to research. Furthermore, about 1 in 5 Americans have elevated Lp(a) and most don’t know it.
While doctors routinely test for HDL, LDL and total cholesterol, there are very few doctors who test for Lp(a) or even know what it is. However, this lipid is a significant cardiovascular risk factor and can cause more than just a little damage.
Lp(a) is a lipid particle that is rich in cholesterol and is similar to low-density lipoprotein (LDL), except that it promotes MORE inflammation and thrombosis.
It has one apoB-100 molecule along with cholesterol esters, triglycerides, phospholipids and cholesterol. What is unique to it is that Lp(a) has an apo(a) molecule attached to the apoB component (which distinguishes it from LDL). This bond is what determines many of Lp(a)’s effects on cells and its ability to potentiate atherosclerosis.
According to research, apo(a) has a chemical makeup of amino acids that are similar to plasminogen. Apo(a) can compete with plasminogen and inhibit fibrinolysis (which is the breakdown of blood clots). This is why it is such a significant risk factor for blood clots and other cardiovascular conditions due to its ability to prevent the breakdown of clots and to influence platelet aggregation.
The length of the apo(a) unit is what determines the mass of Lp(a) that will circulate in the blood.
The complete mechanisms for how Lp(a) causes atherogenesis and inflammation are still not entirely understood and more research in this realm is needed.
According to research, Lp(a) plays several key roles such as healing wounds, activating tissue repair, influencing structural changes of blood vessels and healing endothelial injuries. It clearly had several evolutionary advantages (such a preventing bleeding). Relatively new research also suggests that Lp(a) can play anti-cancer and anti-diabetic roles, as well.
There are essentially three different components of the Lp(a) molecule that contribute to atherosclerosis. The first part is the proinflammatory component, which is the apo(a) unit made up of oxidized phospholipids. The second aspect is the prothrombotic component, which is the apo(a) unit that mimics plasminogen, inhibits plasminogen activation, and prevents the breakdown of fibrous tissue/ blood clots. And the third part is the proatherogenic component, called the apoB unit, which does all the things that LDL does. Therefore, one of the main reasons Lp(a) is so detrimental is that it is a single particle that is proatherogenic, prothrombotic and proinflammatory.
Lp(a) promotes atherosclerosis and inflammation through multiple mechanisms. It can actually bind and transport proinflammatory molecules into the artery wall. Furthermore, Lp(a) is also susceptible to oxidative damage, which leads to additional production of inflammatory cells and atherogenic particles (like oxidized cholesterol).
While all other cholesterol markers are influenced by diet and lifestyle, Lp(a) is pretty much genetically determined.
While there are some evolutionary reasons for why individuals are predisposed to higher Lp(a) levels, there are also significant risks that can result.
Elevated Lp(a)levels are (most notably) associated with increased inflammation, atherosclerosis and clotting in artery walls, which are known risk factors for cardiovascular conditions.
In summary, some established risks of elevated Lp(a) levels include but are not limited to:
For the most part, Lp(a) is considered to be pre-determined by genetics. However, there are some established factors for high Lp(a). These include the following:
According to research, Lp(a) levels can be transiently increased with inflammatory processes or damage to tissues (such as during an acute heart attack).
There is research that has shown that individuals over the age of 75 years will show a mild increase in Lp(a) plasma levels.
Studies have shown that estrogen depletion in women is linked in increased Lp(a) levels.
Research has shown that Lp(a) concentrations can be affected by DHEA, the hormone produced by the adrenal glands.
A 2001 study showed that weight loss in individuals (who had high Lp(a) levels before treatment) was linked to a reduction in serum Lp(a) levels at the end of the weight reduction treatment.
New research has revealed that low total fat/ low saturated fat and high carbohydrate diets significantly increase Lp(a) levels. Furthermore, the low-fat diet was shown to increase the presence of very small LDL particles, a comorbid risk factor for high Lp(a).
Diverse conditions can elevate the levels of Lp(a). These include uncontrolled diabetes, familial hypercholesterolemia, severe hypothyroidism, nephrotic syndrome, chronic renal insufficiency, and obliterative thromboangiitis.
Studies have also shown that patients with anti-phospholipid syndrome (APS) have reduced fibrinolysis and increased levels of Lp(a).
Earlier research studies have also revealed elevated Lp(a) levels in autoimmune conditions like lupus and rheumatoid arthritis. Lp(a) is one of the mechanisms that links the increased incidence of cardiovascular conditions in autoimmune patients and why heart disease can be an “autoimmune” process.
It has been established that the gut microbiome has significant effects on lipid profiles and therefore could have an effect of Lp(a) expression (however, more research is needed for this area). There’s a delicate interplay of leaky gut syndrome, inflammation, oxidative stress, autoimmune conditions and Lp(a) in which more research is warranted.
While it can be tricky to lower Lp(a) it can be done. Furthermore, when it comes to lowering one’s risk associated with elevated Lp(a) levels is also best to lower other cardiac risk factors (see testing below).
It should be noted here that statins do not lower Lp(a) levels and in fact, they significantly raise them!
If you don’t know if you have high Lp(a) then the first thing to do is get tested! We recommend advanced cardiovascular testing to assess your Lp(a) level and your overall cardiac risk.
When it comes to assessing one’s risk of high Lp(a), all other biomarkers (like those found on our advanced cardiac panel) should also be taken into account such as apoA, apoB, apoA:B ratio, oxLDL and HS-CRP values, as well.
We offer free health coaching consults for those who are interested in learning more about this inherited cardiac marker and ways to best lower it.
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