The Link Between Cholesterol and Heart Disease
Danish researchers said on Tuesday they have found the strongest evidence yet that an often ignored form of cholesterol can cause heart attacks.
They said people with higher levels of a little-understood form of cholesterol called lipoprotein (a), which varies up to a thousand fold from one person to another, were also more likely to have heart attacks.
If you’ve been reading my blog then you are already familiar with apo A and B particles because you’ve read about Robert Krause. So what is this “lipoprotein (a)?”:
Lipoprotein(a) (also called Lp(a)) is a lipoprotein subclass. Studies have identified Lp(a) as a putative risk factor for atherosclerotic diseases such as coronary heart disease and stroke.
Okay, no problem, but is this at all related to the apo B particles that Krause said were so bad?
High Lp(a) in blood is a risk factor for coronary heart disease (CHD), cerebrovascular disease (CVD), atherosclerosis, thrombosis, and stroke. Lp-a concentrations may be affected by disease states, but are only slightly affected by diet, exercise, and other environmental factors. Commonly prescribed lipid-reducing drugs have little or no effect on Lp(a) concentration. Niacin (nicotinic acid) and aspirin are two relatively safe, easily available and inexpensive drugs known to significantly reduce the levels of Lp(a) in some individuals with high Lp(a); they should be used under the supervision of a qualified physician.
So if diet doesn’t affect it or the usual suspects, then what can we learn from all of this? It seems the further our researchers get into things and ignore the obvious, the more worthless their work becomes to us. Most of the things they are interested in are things we can’t affect by what we eat or do. This fosters a sense of hopelessness concerning health matters and is not at all productive. Let’s see more of what the study provided:
To show the role of lipoprotein (a) role in heart attacks, the Danish team analyzed the genes of 45,000 men and women who gave blood samples for a large national survey starting in 1976, tested their lipoprotein (a) levels and then followed them until 2007.
People with the highest levels of this cholesterol had the most heart attacks, the study found. One certain genetic variation accounted for about a quarter of the cases of high lipoprotein (a).
“Liprotein (a) has been around for a long time as a risk factor but people hadn’t taken it too seriously because they didn’t think it caused heart attacks,” Nordestgaard said. “Now we show that, like LDL, it is causing heart attacks.”
This still appears to be an association to me. This only shows that people with high lipoprotein (a) have a higher risk of heart disease if there is some other factor present. Even the study author acknowledges:
One problem is that people have little control over the cholesterol, whose levels can vary up to a thousand-fold among individuals, Nordestgaard added.
This may be true with regard to lipoprotein (a) but we have plenty of control over the cholesterol that does matter.
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.
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.”
Two people can have identical LDL cholesterol levels and yet only one develops atherosclerosis and coronary heart disease and the other doesn’t. 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 packaged 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. Cardiologist Allan Snider 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 to 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!
If you want to see what happens to your cholesterol from eating an all-meat diet, read here!Share on Twitter