There is some evidence that having a large amount of Lp(a) might be associated with heart disease. What is this Lp(a) thing you might ask? Well it is a protein that attaches onto ApoB which is an apoprotein found in LDL. It’s theorized that it can cause disease since it resembles plasminogen which is a precursor for plasmin that reduces fibrin clotting. Since LP(a) looks like plasminogen, it’s believed to increase the risk of heart disease by competing with plasminogen and therefore limiting conversion of plasminogen to plasmin. Additionally, LP(a) may also be the preferred carrier for oxidized phospholipids (OxPls) which may be associated with inflammation and the progression of arterial disease. Need more details? Here just watch this video instead:
One study decided to investigate how diet may play a role in Lp(a) and OxPls. They mention some previous studies that have found associations of Lp(a) and heart disease:
“Elevated plasma Lp(a) concentrations are associated with increased risk of cardiovascular disease (CVD) (13, 14), and there is increasingly strong data that they may be causal in the etiology of myocardial infarction.”
Alright so Lp(a) is bad, but what really shocked TheFatNurse was what elevated Lp(a). A large part of it is genetics and TheFatNurse recalls last year’s National Lipid Association panel stating that it was mostly genetic. However, there have been some recent studies suggesting there might be a dietary factor at play. Must be a high fat diet right?
“Low-fat diets have been shown to increase plasma concentrations of lipoprotein(a) [Lp(a)], a preferential lipoprotein carrier of oxidized phospholipids (OxPLs) in plasma, as well as small dense LDL particles.”
This is ironic since many people still advocate a low fat diet as pointed out:
“Low-fat diets are recommended to reduce risk of coronary heart disease, but LFHC diets have been shown to induce a more atherogenic lipoprotein profile in healthy individuals by increasing small dense LDL particles (Table 3), reducing HDL cholesterol, and increasing plasma triglyceride levels (Table 4) (27). LFHC diets result in increased concentrations of triglyceride-rich lipoproteins (TRLs) (46) and a reciprocal shift from medium-size LDL particles to very small LDL.”
Anyways, back to the original study that was trying to find associations between diet Lp(a), OxPls and LDL particles. What they discovered was an association between all these variables on subjects with a low fat high carb diet:
“These results demonstrate that induction of increased levels of Lp(a) by an LFHC diet is associated with increases in OxPLs and with changes in LDL subclass distribution that may reflect altered metabolism of Lp(a) particles.”
However, to be fair the difference in Lp(a) mg/dl was 2.17 +/- 4.5 (p value = <0.01). Is this increase enough to do serious cardiovascular risk? Certainly is worth exploring more and adds more interest for future studies between low fat and high fat diets.