Gary Taubes helps us to understand the implications between small, dense LDL and heart disease.  He describes the low-density lipoprotein (the “LDL”) as a balloon.  It has a single protein known as apo B for short, that serves as the structural foundation of the balloon and holds it together.  It hs an outer membrane that is composed of cholesterol and fats of yet another type called phospholipids.  Inside the balloon, inflating it, are triglycerides and more cholesterol.  The size of the LDL balloon itself can vary depending on the amount of triglycerides and cholesterol it contains.  Thus some people have mostly large, fluffy LDL with a lot of cholesterol and triglycerides inflating the balloon and some people have mostly smaller, denser LDL particles with less cholesterol and triglycerides. 

In the 1970s, investigators determined yet another way to quantify the concentration of these circulating lipoproteins by counting only the number of apo B proteins that provide the structural foundation to the LDL balloon.  Because there is only one  protein  per LDL particle, and because VLDL is also composed of identical apo B proteins, this technique measured the number of LDL and VLDL particles in a blood sample, rather than the cholesterol or triglycerides they contained.  As it turned out, the number of apo B proteins, and so the total number of LDL and VLDL particles combined, is also abnormally elevated in heart disease patients.   

To be fair, Krass says he only rediscovered this heterogeneity of LDL.  Waldo Fisher of the University of Florida and Verne Schumaker of UCLA discovered it independently a decade earlier but they did not pursue it any further.  Perhaps it violated the religion and they kept it quiet or perhaps they didn’t grasp the relevance of this information.  The public could sure benefit from knowing that carbohydrates elevate apo B particles in LDL and this is a direct heart disease risk unlike the many associations that dot the landscape of heart disease today.  It can’t all be about diet and exercise, can it? 

Back to our story, In 1980 (yes, twenty-eight years ago), Peter Kwiterovich, a lipid metabolism specialist from Johns Hopkins, together with Allan Snider man, a cardiologist from McGill University, collaborated with Krauss on the last of his three papers on the heterogeneity of LDL.  In 1983, they reported that the disproportionate elevation in the apo B protein in heart disease patients was due to a disproportionate elevation in the amount of the smallest and densest of the low-density lipoproteins.  This “disproportionate elevation” is caused by the overconsumption of carbohydrates, my friends.  As I say on my forum many times, “only the lucky ones get fat.” 

Obesity and heart disease are mere symptoms of metabolic syndrome which causes the chronic diseases of civilization as Tanchou called them.  Everyone doesn’t get fat, only 1 in 5.  However, 1 in 2 get cancer. 

Have I got your attention yet? 

This explains what Krauss set out to understand; how two people can have identical LDL cholesterol levels and yet only one develops atherosclerosis and coronary heart disease and the other doesn’t.   Yes, LDL is only seen as a marginal risk factor for heart disease.  The experts do advise us to lower LDL, but we do so at the cost of raising the apo B and lowering HDL which is protective of heart disease.  If we have low LDL cholesterol, but it’s packaged almost exclusively in small, dense LDL particles, that translates to a higher risk of heart disease.  If we have high LDL cholesterol, but its package4d in a smaller number of large, fluffy LDL particles, then our heart disease risk is significantly lower.  Small, dense LDL, simply because it is small and dense, appears to be more atherogenic; meaning, it is more likely to cause atherosclerosis.  Small, dense, LDL can squeeze through damaged areas of the artery wall to form incipient atherosclerotic plagues.  Sniderman described small, dense, LDL as the equivalent of “little bits of sand” that get in everywhere and stick more avidly.  The relative dearth of cholesterol in these particles may also cause structural changes in the protein that make it easier for it do adhere to the artery wall to begin with.  Small, dense LDL remains in the bloodstream longer than larger, fluffier LDL and it has more time and greater opportunity to do its damage.  It’s possible for LDL to be oxidized (read, rust) before it can play a role in atherosclerosis and the existing evidence suggests that small, dense, LDL oxidizes more easily than larger, fluffier, LDL. 

Therefore, when you get your cholesterol test and the doctor says you have high LDL and you need a statin, politely refuse and ask for the VAP test which will show particle size.  If you have the large and fluffy kind, then go on living your life and eating your low-carb or no-carb diet.  If you have low LDL, also ask politely for the VAP test and look at your particle size.  Don’t sit at home content because you have low LDL when you have a disproportionately high number of small, dense, LDL, the kind that leads to heart disease.  You always wondered how those world class athletes who are in impecable shape, fall dead from heart disease.  Well, now you know.  Too much reliance on the wrong fuel!

Tune in Friday when we conclude our series on Ronald Krauss and provide shocking details as to why you should consider carbohydrate restriction in your future! 

http://blog.zeroinginonhealth.com/?p=439