Dr. Sears has suggested that the size of LDL-C particles matters (Pattern A vs B).
Here is a link (Part V of a 10-part series) where-in the author dissects the entire Cholesterol concepts,
from beginning to end. In Part V - he discusses particle size.
(You can also use the link to work through the series starting with Part I.)
Here are some points he covered i Parts I through IV:
- Currently, most people in the United States (and the world for that matter) undergo a “standard” lipid panel, which only directly measures TC, TG, and HDL-C. LDL-C is measured or most often estimated.
- More advanced cholesterol measuring tests do exist to directly measure LDL-C (though none are standardized), along with the cholesterol content of other lipoproteins (e.g., VLDL, IDL) or lipoprotein subparticles.
- The most frequently used and guideline-recommended test that can count the number of LDL particles is either apolipoprotein B or LDL-P NMR, which is part of the NMR LipoProfile. NMR can also measure the size of LDL and other lipoprotein particles, which is valuable for predicting insulin resistance in drug naïve patients, before changes are noted in glucose or insulin levels.
- The progression from a completely normal artery to a “clogged” or atherosclerotic one follows a very clear path: an apoB containing particle gets past the endothelial layer into the subendothelial space, the particle and its cholesterol content is retained, immune cells arrive, an inflammatory response ensues “fixing” the apoB containing particles in place AND making more space for more of them.
- While inflammation plays a key role in this process, it’s the penetration of the endothelium and retention within the endothelium that drive the process.
- The most common apoB containing lipoprotein in this process is certainly the LDL particle. However, Lp(a) and apoB containing lipoproteins play a role also, especially in the insulin resistant person.
- If you want to stop atherosclerosis, you must lower the LDL particle number.
Basically in Part V he comes to the following conclusion:
(I have not gotten to Part VI and beyond, yet.)
At first glance it would seem that patients with smaller LDL particles are at greater risk for atherosclerosis than patients with large LDL particles, all things equal. Hence, this idea that Pattern A is “good” and Pattern “B” is bad has become quite popular.
To address this question, however, one must look at changes in cardiovascular events or direct markers of atherosclerosis (e.g., IMT) while holding LDL-P constant and then again holding the LDL size constant. Only when you do this can you see that the relationship between size and event vanishes. The only thing that matters is the number of LDL particles – large, small, or mixed.
“A particle is a particle is a particle.” If you don’t know the number, you don’t know the risk.