Oxidized LDL and coronary heart disease
Part 1: Oxidized LDL
LDL has many vital roles in our bodies. Without sufficient LDL we would die. Where the problem with LDL lies is when fatty acids that are transported with LDL are attacked by oxygen and oxidised.[1] In 2004 a study was conducted with patients eating two different diets.[2] Both had reduced total fat and saturated fat intakes and increased polyunsaturated fat intakes.
Conventional wisdom says that these revised diets should be 'healthier'. In fact, what happened was that the levels of oxidised LDL in the bloodstream rose in both — by 27% and 19%. Another contributor to heart disease, lipoprotein (a), also rose by 7% and 9%.
Fatty acids come in a variety of lengths. As the chain length of a fatty acid increases, it acts more and more like an oil which will not mix with water or blood. Short and medium chain fatty acids will mix in blood; they exit the intestine bound to the protein, albumin, whereas long chain fatty acids with more than 12 carbon atoms do not mix and must be transported in lipoprotein carriers. LDL is used to transport these long-chain fatty acids.
LDL is only likely to be 'bad' if you eat a large proportion of 'healthy' polyunsaturated oils. This may be why, in a 10-year study of fats and the numbers of heart events, researchers found that only polyunsaturated fats significantly increased heart disease.[3]
There is also another anomaly: You may not be aware of it, but cholesterol levels are always measured in blood taken from a vein, yet nowhere in the medical literature is there a single case of cholesterol having caused obstruction of a vein: atherosclerosis only affects arteries. As blood moves far slower in veins than in arteries, wouldn't that make it be more inclined to leave cholesterol deposits — if the assumption that cholesterol was the cause were true?
The evidence is that it is while the cholesterol in LDL that is continually being maligned, it's the polyunsaturated fatty acids carried in LDL that are the real culprit.
That is why we are told to eat foods that contain antioxidants.
References
1. Cherubini A, et al. The VASA Study Group. High vitamin E plasma levels and low low-density lipoprotein oxidation are associated with the absence of atherosclerosis in octogenarians. J Am Geriatr Soc 2001; 49: 651-42. Silaste M-L, et al. Changes in Dietary Fat Intake Alter Plasma Levels of Oxidized Low-Density Lipoprotein and Lipoprotein(a). Arterioscler Thromb Vasc Biol. 2004; 24: 498-503.
3. McGee DL, et al. Ten year incidence of coronary heart disease in Honolulu Heart Programme — Relationship to nutrient intake. Am J Epidemiol 1984; 119: 667-676.
