I’ve discussed this phenomenon before on this site but it’s well worth mentioning again. Traditionally measuring LDL, the so-called bad cholesterol, that has the capacity to block the arteries of our heart and quantifying HDL, the hero in this saga that does the opposite has been the blueprint we’ve utilized to assess our risk of having a heart attack. As it turns out only focusing on LDL, doesn’t inform us how many potentially dangerous atherogenic, heart vessel obstructing particles are looming large to cause a heart attack. For this we need to measure Apolipoprotein B, (ApoB) the primary structural component of LDL, that will enable us to quantify how many of these harmful particles we have. Likewise to assess how effective HDL can be we need to quantify another protein called Apolipoprotein A-1 (Apo A-1) to estimate it’s atherogenic reducing potential. An ideal ratio of these two proteins would be 2:1, the closer ApoA-1 is to being double the presence of ApoB the greater our chances of having healthy blood vessels with minimal LDL accumulation.
There is just one more item of vital information that will provide us with a total profile detailing LDL’s capacities. There are different LDL sizes that determine its lethality. Large LDL particles are relatively harmless whereas small, dense LDL is the principal protein initiating blood vessel occlusion. Ordering what is called LDL subfractions quantifies these disparate forms of LDL.
Once we have all these numbers we can take the appropriate action to reverse whatever predicament we find ourselves in.
