|This is a diagram of a chylomicron or VLDL-c (high TG/C ratio) 'cos I couldn't find one for LDL-c!|
Cholesterol synthesised in the liver is exported in LDL particles. The more cholesterol that's synthesised, the more particles there need to be to carry it.
∴ LDL-P (particle number) ∝ LDL-C (total amount of cholesterol)
The particles are roughly spherical with a very thin wall (consisting of a phospholipid mono-layer, the yellow wiggly lines with a green end bit in the above diagram).
Volume of a sphere = 4/3 * π * r3, where r = half the diameter.
If there's a 10% reduction in LDL particle size, the volume reduces to 0.729, relative to the original size. Therefore, to carry the same amount of cholesterol requires 1/0.729 = 1.37 times more particles, which is a 37% increase in the number of LDL particles, relative to the original size.
∴ LDL-P (particle number) ∝ 1/LDLsize3
As it's LDL particle number that determines the infiltration of LDL cholesterol into the media of artery walls (see image below), it's advisable to keep cholesterol synthesis to a reasonable level by keeping fat intake to a reasonable level (i.e. not Nutritional Ketosis!) and keeping LDL particle size to a reasonable level by keeping added sugar (e.g. sucrose & fructose) intake and rapidly hydrolysed/overcooked starches (e.g. amylopectin & maltodextrin) intake to a reasonable level (i.e. a level that's oxidised by the body without having a chronic excess). An acute excess of carbohydrate can be stored as liver/muscle glycogen, provided that mean carbohydrate intake is less than mean carbohydrate oxidation.
|How COULD I write a post about LDL-P and forget to include THIS?|