LDL or Oxidized LDL to Predict Cardiovascular Risk?
by nutritionist on 24 December, 2019 in Prevention and Anti-aging 0
Decades of research into cardiovascular risk factors have provided substantial evidence of the causal role of lipoproteins containing Apolipoprotein B in the pathophysiology of cardiovascular disease, such as coronary heart disease, calcific aortic valve stenosis (CAVS), and stroke.
The only way a cholesterol particle may infiltrate the arterial wall is if an LDL lipoprotein puts it there, and that’s why LDL cholesterol is considered “the bad guy.” This accumulation leads to an oxidative process, with the consequent inflammation, which we now know is the origin of the disease. Our immune system reacts, sending out macrophages that engulf and digest oxidized cholesterol, thus increasing in size.

Dr. Alfonso Galán González – Neolife Medical Team

LDL oxidation is the first event that occurs in the formation of the foam cells of the plaque of atheroma, and the LDL in arterial lesions is highly oxidized.

Decades of research into cardiovascular risk factors have provided substantial evidence of the causal role of lipoproteins containing Apolipoprotein B in the pathophysiology of cardiovascular disease, such as coronary heart disease, calcific aortic valve stenosis (CAVS), and stroke.

This evidence currently supports the idea that lowering the number of particles containing Apo-B leads to beneficial effects at the cardiovascular level. Most of these lipoproteins are, of course, LDL.

For educational purposes, let’s briefly and simply review a number of concepts. Cholesterol is a vital compound for the body. Our cells are covered with a membrane made up mainly of fat and cholesterol. Cholesterol is essential for proper brain function, is the basis for synthesizing sex hormones and vitamin D, and is also a key compound for bile, which helps us digest fats. This cholesterol must be carried by the bloodstream from where it’s synthesized and absorbed to wherever it has to be used, and it does this while packaged in lipoproteins.

LDL (low-density lipoprotein) is responsible for bringing cholesterol to the cells, and HDL (high-density lipoprotein) collects excess cholesterol to return to the liver.

Atherosclerosis begins when cholesterol infiltrates the walls of an artery, its innermost layer, the endothelium, triggering a series of inflammatory processes that may lead to plaque buildup and potentially, over time, to the blockage of the artery.

The only way a cholesterol particle may infiltrate the arterial wall is if an LDL lipoprotein puts it there, and that’s why LDL cholesterol is considered “the bad guy.” This accumulation leads to an oxidative process, with the consequent inflammation, which we now know is the origin of the disease. Our immune system reacts, sending out macrophages that engulf and digest oxidized cholesterol, thus increasing in size.