162018Mar

Atherosclerotic, Coronary Artery Disease and Inflammation

Free radicals are unstable molecules with an unpaired electron, thus an odd number of electrons.  Electrons are most stable in pairs.  So, the stable molecules are those with an even number of electrons.  Free radicals do their damage while “stealing” an electron (oxidizing) from stable molecules.  When the “attacked” molecule loses its electron, it becomes a free radical itself, beginning a chain reaction. Once the process is started, it can cascade, finally resulting in the disruption of molecules and cells.  Inflammation then increases to clean up the damaged molecules and cells.

Part of the reason atherosclerotic plaque gets started is that LDL becomes oxidized by free radicals.  When that occurs, the LDL becomes more sticky, adhering to and within the arterial wall.  Also micro insults to the arterial wall result from electron transfers in oxidation (as free radicals on the arterial lumen steal electrons from stable molecules) leading to the breaking apart of unstable molecules and triggering further inflammation to “clean it up”, resulting in a growing plaque in the lumen of the artery.

It is now well understood that atherosclerosis is a chronic inflammatory disease.  It is also understood that bringing inflammation down in the body is beneficial, as it is for most every single disease.  I challenge to name a disease where inflammation plays no role.

So, shouldn’t antioxidants be the panacea?  Our knowledge in nutritional medicine is growing exponentially. It is conceivable that antioxidants might not be the magic beneficial chemical in the food we eat after all.  So, to make sure, get your antioxidants from the food you eat: green tea, dark berries, salmon, green leafy veg to name a few potent sources.  Also, adding taking the RDA of vitamins C, E and D is currently a good approach.  Don’t forget to adjust hidden reasons for increased inflammation (free radical production) in your lifestyle as well.