This is the first of a two part series on atherosclerosis and will explain:
What is atherosclerosis?
Atherosclerosis - commonly known as “ hardening of the arteries” refers to a disease process that causes damage to the arteries resulting in narrowing, blockage, occlusion and even rupture.
Atherosclerosis is the underlying cause of most cardiovascular disease (CVD) - including heart disease and stroke.
Atherosclerosis is both very common and very preventable.
Our view is that the key to prevention comes from really understanding how atherosclerosis develops. This involves getting past some common misconceptions that have resulted from an oversimplification of the disease through the two dominant conceptual models used to explain atherosclerosis:
The issue with each of these models is that they overlook some key facts and observations:
Before we go further here - let's back up and better understand the disease process:
To summarize, atherosclerosis is caused by an inflammatory response to oxidized lipoproteins within the artery wall. There are three main ingredients that trigger a lesion:
The developing process can be mitigated in its earliest phases by HDL-particles that take away the sub-endothelial cholesterol - even after it is taken up by the foam cells.
Evidence shows that the risk of atherosclerosis increases with increasing concentrations of LDL-particles in linear fashion - note this LDL-particle numbers, not LDL-cholesterol concentration. (while LDL-C and LDL-p are generally concordant, ie. they increase and decrease together, this is not always true - especially when insulin resistance is present). LDL-cholesterol is what is commonly reported on the standard lipid panel. A better test to understand your risk is the ApoB100 protein- which gives you the number of LDL-particles as each LDL-particle has one ApoB100
It must be stressed that LDL-P easily enter and exit the sub-endothelial space all the time - it is the oxidation of LDL-P that is key step in initiating atherosclerosis. Only oxidized LDP-P is taken up by macrophages and foam cells.
What triggers the oxidation of the LDP-P?
Damaged, inflamed or dysfunctional endothelial cells create the conditions for LDL-P oxidation.
Common causes of endothelial dysfunction are:
Another key point is that the process that leads to an atherosclerotic lesion is systemic - so just identifying and treating lesions that cause blockage (ie. plumbing model) does not sufficiently decrease risk as there may be other non-obstructive lesions that can rupture and cause acute occlusion.
So in essence, with atherosclerosis we have a reinforcing cycle of:
The take-home points to remember are:
At Wellness Garage - we can help you understand and take control of your health. Our comprehensive medical, fitness, nutritional and behavioral assessments give you baseline from which to measure your progress. Our coaching helps you improve your behaviors, one habit at a time.
For more information - please book a free consultation.
Dr. Brendan Byrne