If you don’t know your LP(a) statistics…you should do.
1 in 4 people has genetically high LP(a) and if you are one of them, your risk for heart disease has just increased dramatically.
This is a subject close to my heart (literally) as I discovered after my heart attack that I have very high genetic LP(a).
My LDL was low, triglycerides perfect, not overweight, non-smoker, and fit….but at 50 I had a near fatal heart-attack because my LP(a) is high, and I can’t get away with even normal levels of inflammation without paying the price.
Unbelievably, you can’t get a blood test from your GP in the UK to test for LP(a), but you can get a private blood test that will tell you your LP(a) levels. Here is one of them.
If you are told that you have “a family history” of heart disease…..or “your issue might be genetic” then check your LP(a).
High Lp(a) correlates with early atherosclerosis independently of other cardiac risk factors, including LDL. In patients with advanced cardiovascular disease, Lp(a) indicates a coagulant risk of plaque thrombosis.
Another challenge with LP(a) is that it is an independent risk factor, and it can be masked by low LDL numbers (people with low LDL can have high LP(a)) which effectively means that if you don’t test for it specifically, you might be blissfully ignorant of the massive heart problem awaiting you, whilst your doctor pats you on the back for having low LDL numbers (like I did before I spent two years researching the subject).
Todays research paper relates to LP(a).
Faghihnia N et al. “Changes in lipoprotein (a), oxidised phospholipids, and LDL sub-classes with a low-fat high-carbohydrate diet”. Published in the Journal of Lipid Research 2010 Nov;51:3324-3330
The study based at the University of California, looked at how a high-fat, low-carbohydrate diet (LFHC) and a low-carbohydrate, high-fat diet (LCHF) affected different types of cholesterol in 63 healthy subjects over a 4 week period.
The study sought to understand if 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. They sought to determine whether increases in plasma Lp(a) induced by a low-fat high-carbohydrate (LFHC) diet are related to changes in OxPL and LDL subclasses.
All subjects underwent a diet intervention involving 4 weeks of a high-fat low-carbohydrate (HFLC) diet and 4 weeks of an LFHC diet.
The HFLC diet was designed to provide 40% of energy from fat (13.0% saturated, 11.0% monounsaturated, 13.8% polyunsaturated, and 3.4% trans), 45% carbohydrate, and 15% protein.
The LFHC diet was designed to provide 20% of energy from fat (4.9% saturated, 9.9% monounsaturated, 5.1% polyunsaturated, and 2.4% trans), 65% carbohydrate, and 15% protein.
There were no differences in dietary cholesterol and the ratio of simple:complex carbohydrate was ∼50:50 between the diets. Nutrient composition was calculated using the Minnesota Nutrition Data System software, version 2.1, developed by the Nutrition Coordinating Center, University of Minnesota, Minneapolis, MN.
The trial showed that:
The LFHC diet increases levels of both Lp(a) and OxPL/apoB, and that this response involves a diet-induced increase in OxPL on Lp(a) particles.
The correlated changes in Lp(a) and OxPL/apoB were independent of changes in plasma triglycerides, total cholesterol, LDL cholesterol, HDL cholesterol, apoA-1, and apoB.
Diets low in total and saturated fat have been shown to increase plasma Lp(a) levels and there is evidence that this effect may be specific for saturated fat.
Niacin (Vitamin B3) has been shown to reduce the levels of Lp(a) in individuals with high levels of low-molecular weight Lp(a).
Links to the supporting article can be found here: