Lipoprotein(a) is heavily associated with cardiovascular risk—far more so than is elevated cholesterol. It’s very similar to LDL (the “bad” cholesterol), except that it has an apolipoprotein A attached to it. (LDL also has one apolipoprotein B protein attached to it, as does Lp(a).)
But unfortunately, we don’t know that much about Lp(a)—how it’s assembled, or how the body breaks it down. This is probably also why we don’t know all that much about how to lower it, once it’s high. We do know that, unlike with cholesterol levels, traditional diet and lifestyle recommendations have little impact on Lp(a) levels. We also know that high levels of Lp(a) are largely genetic.
But does that mean you’re just stuck with a higher cardiovascular risk if you lost that genetic lottery?
Lp(a) versus LDL
First, let’s discuss the concept behind cholesterol and cardiovascular disease, before we dig into Lp(a) specifically.
The walls of your blood vessels can get damaged just like your skin can. When damage occurs (from too much sugar or uncontrolled diabetes, from too many trans fats, from cigarette smoke, etc), you get a scab to protect the wound while your body repairs the damage. The scab is made up primarily of LDL.
So LDL is sort of like a band-aid. The more extensive the damage, the more cholesterol you need to form an adequate band-aid. It’s trying to help you—but, that’s why LDL makes up the majority of clots. (The underlying problem in a situation like this isn’t the cholesterol—it’s the damage that recruited the cholesterol in the first place.)
Now for Lp(a): once LDL et al show up to become part of a plaque, Lp(a) comes along for the ride. But it appears remain embedded in the arterial wall long after its job is complete. Since LDL and Lp(a) are largely the same except for the apolipoprotein a, the difference between the two seems to be due to the apo(a) protein’s tendency to “stick”: to the endothelial lining, to precursors for clot formation, and to other lipoproteins. It also seems to be inflammatory in and of itself, calling white blood cells to the site of injury for backup.
Presumably one of the functions of Lp(a) is to help with wound healing in other parts of the body, in which case all of these functions would be very helpful—but an abundance of Lp(a) trying to heal a damaged blood vessel might perpetuate the problem in that blood vessel, long after the original job is done.
Lipoprotein(a) and Cardiovascular Risk
Because of all these functions, excessive Lp(a) is considered a much greater risk factor for cardiovascular disease than are high cholesterol levels.
“High” Lp(a) is anything over 300 mg/L.
According to this large meta-analysis of 27 studies, those participants whose Lp(a) was in the top 33% were at a 70% greater risk of developing cardiovascular disease than those in the bottom 33%. The chances increase with additional risk factors, such as high LDL, low HDL, or risk factors for clotting such as Leiden Factor V, protein C deficiency, or antithrombin III deficiency.
What Causes High Lp(a)
As mentioned in the introduction, high Lp(a) is mostly genetic, and applies to some 20% of the population.
But Lp(a) can also temporarily increase in cases of renal disease. It also seems to increase temporarily after injury—which makes sense, if its physiologic function is to heal wounds.
How to Lower Lp(a)
While I’m not a fan of statins (at ALL), they are effective at lowering LDL (for whatever that’s worth). But they don’t have an effect on Lp(a) levels.
High doses of niacin do lower Lp(a) levels, but this can cause liver damage long-term. (Flushing is also common, and it’s not fun.)
For post-menopausal women, estrogen replacement therapy has been shown to be effective.
“Diet change” in general (at least a low fat diet) has no effect on Lp(a)—but high saturated fat diets actually lower Lp(a). Increasing monounsaturated fats and polyunsaturated fats is likewise effective—so the ketogenic diet might be the way to go!
This may also be why L-carnitine helps to lower Lp(a), as well: L-carnitine’s job is to help shuttle fatty acids inside the mitochondria, to get broken down into energy. When we know more about the mechanisms of action of Lp(a) and its relationship to fats, this will hopefully make more sense.
Bizarrely enough, alcohol intake seems to lower lipids in general, including Lp(a). (Though don’t overdo this, of course, or you’ll end up with other problems.)
And finally, this study demonstrates that a baby aspirin daily not only helps to mitigate clot formation, but also directly lowers Lp(a) levels.
If you have a strong personal or family history of cardiovascular disease, it’s worth asking your doctor to check your Lipoprotein(a) levels. If yours are high, consider increasing your (healthy) fat intake and adding in L-Carnitine at the very least. And you can certainly discuss some of the other interventions mentioned with your doctor, to determine whether they are right for you.