Image by Jo Luijten from Pixabay
Recently, I wrote here on my paradigm shift regarding cholesterol. Briefly: cholesterol esters (or the typical lipid panel, including LDL, HDL, triglycerides, and total cholesterol) have no bearing upon heart disease, according to quite a few long-standing and huge studies—with one exception.
Lipoprotein(a) is the identical twin of LDL, except that it has an apolipoprotein(a) protein attached to its surface. But this apo(a) is quite significant: it sticks to any amino acids projecting from a damaged endothelium, initiating formation of a clot.
I first wrote about Lp(a) here, and again here regarding additional therapeutic approaches to lower it. But since it’s such a big player in development of cardiovascular disease, it deserves another look.
Statins Worse than Useless for Lp(a)
As I wrote here, while statins work to lower cholesterol esters (LDL, etc), it doesn’t really matter because LDL isn’t responsible for heart disease. On top of that, statins can cause diabetes, itself a major risk factor for heart disease.
It turns out, statins also increase Lp(a) levels, too.
Another great reason to get off of them.
CoQ10—because of Mitochondrial Support?
I wonder if statins tend to increase Lp(a) because they lower CoQ10 production, a cholesterol derivative.
It’s well-known that CoQ10 is an important nutrient for the heart, probably because the heart is one of the most metabolically active organs in the body. CoQ10 is the first stop in mitochondrial respiration, or the production of ATP, the body’s primary energy currency. Thus, any highly metabolically active tissue that has a high ATP demand will likewise have a high CoQ10 demand.
Does this have anything to do with why CoQ10 helps to lower Lp(a) levels? Perhaps—but it certainly does help.
Many studies that investigate CoQ10 for Lp(a) also investigate carnitine, another nutrient necessary (peripherally) for mitochondrial function, as carnitine helps to shuttle fatty acids inside of the mitochondria where they get broken down into ATP for energy. The two together are promising candidates.
Niacin for Lp(a): Beyond Flushing
Niacin (vitamin B3) has long been known to reduce Lp(a) levels, too. Regular niacin has the unpleasant side effect of flushing, but there are other versions that don’t—and oxidized NAD+ (a form of niacin) is one of the primary electron carriers for the mitochondria. (So it certainly seems like mitochondria are heavily implicated here.)
It’s also one of the darlings of the anti-aging world at the moment, as it helps to clean up oxidative stress like a champ—and oxidative damage can itself lead to endothelial damage and heart disease.
Other Antioxidants for Lp(a)?
In addition to CoQ10 and carnitine, this study demonstrated that to a lesser extent, resveratrol (the antioxidant in red wine, as well as red wine itself), and curcumin, the active constituent in turmeric, can help to lower Lp(a).
Finally, in addition to its other health benefits, coffee and tea (presumably their antioxidants) may also help to decrease Lp(a), too.
Lipoprotein(a) is a big player in heart disease, and it’s largely genetically determined. While some approaches mentioned in previous articles can be very helpful, including lysine and Vitamin C, estrogen therapy for women when appropriate, and a higher fat diet, mitochondrial support as well as antioxidant support may prove to be closer to root cause (though we’ll need more research to determine this), and have a synergistic effect.