Lp(a) is just regular LDL with an added lipoprotein-a molecule. The lipoprotein-a molecule comes in 3 genetically determined lengths with a short, medium, or long sticky section.
Lp(a) is made by the liver in response to cells signaling the presence of oxPhos in their cell walls. Lp(a) collects oxPhos from cell membranes, and is eliminated by the kidneys taking the collected oxPhos with it. (In contrast, regular LDL is eliminated primarily by the liver).
High Lp(a) is an indicator of too much poly-unsaturated fats in your cell membranes which is oxidizing easily. If you have the short version of lipoprotein-a your liver will have to make much more Lp(a) to handle a given oxPhos load. Reduce your oxPhos in your cell membranes and your liver will normally make less Lp(a).
Doctors misguidedly recommend high dietary poly-unsaturated fat in place of dietary saturated fat to reduce LDL and hence total cholesterol. High dietary poly-unsaturated fat results in the liver destroying a lot of oxLDL (containing oxPhos lipids) instead of releasing it. Then a lot more LDL oxidizes after being released.
Your body hates oxPhos and is not happy with high poly-unsaturated fat. The ratio of fats in heavy cream which evolution has likely optimized for young mammals is approximately 62% saturated, 29% mono-unsaturated, 2% poly-unsaturated omega 6, and 1% poly-unsaturated omega 3.
Macrophages consume oxLDL which leads to the formation of plaque (It's still an open question if LDL gets oxidized mostly after getting trapped in the artery wall, or if it gets trapped because its oxidized). I want my LDL as hard to oxidize as possible while still allowing for adequate membrane permeability.
High lp(a) is bad because the oxidation of lipids is bad. Many restaurants in the US are frying everything in poly-unsaturated oil. (Others are still using cheap trans-fats which are worse and not banned in the US until 2018). I personally will not eat anything fried in a restaurant.
Edited by RWhigham, 27 October 2016 - 07:08 AM.