October 10, 2017
October 12, 2017
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Our body has a defense system designed to protect this endothelium of the artery. In the event of injury, our body responds by sending in monocytes (a large phagocytic white blood cell within a simple oval nucleus and clear, grayish cytoplasm) in an attempt to eliminate the harmful oxidized LDL cholesterol. Here, the defense team of monocytes starts gobbling up the enemy in an attempt to minimize the irritation to the endothelium. If this inflammatory response is successful, the problem is over and the lining of the artery will be repaired. But this is not what usually happens. Let me explain this in simple theory. Think of a monocytes as a minivan. As it drives around, picking up people and letting them off in their proper places, it is limited to the number of people it can carry at any one time because it has only so many seats. On a good day the same is true for monocytes when we are healthy they zoom around, picking up native LDL cholesterol and dropping off other native LDL cholesterol. And just like minivan, monocytes can carry only so many native LDL cholesterol at a time. This is known as natural feedback mechanism.

When native LDL cholesterol becomes oxidized, the cholesterol particles are no longer harmless people, instead, they pose a threat to the body, and the monocytes pick them up via totally different method. Monocytes continue to gather the delinquent oxidized LDL cells, but they don’t let anyone out. This would be like a gang of unruly people clambering into the minivan through the door without its driver having any control whatsoever on the number of people getting in. if this were to happen, the van would be immobilized and breakdown. When the monocyte encounters bad cholesterol, it is in similar fix, because, there is no natural feedback mechanism, the monocyte gets crammed so full of oxidized LDL cholesterol (fat) that it becomes a foam cell. This is just like what you are visualizing in your mind, it is a cell that looks like a ball of fat. This foam cell then attaches itself to the lining of the artery and eventually forms the initial defect of hardening of the arteries, which is called a fatty streak.

The fatty streak is an inflammatory lesion, it is the initial step in this process called atherosclerosis. If the process would simply stop here, the body would at least have a chance to clear this defect. But this is not the case. As in any war, this process has some collateral damage. In other words the thin, vulnerable layer of cell lining of arteries is damaged even more by the very process that is supposed to heal it. This actually creates more inflammation, which attract more monocytes and in turn changes native LDL cholesterol to oxidized LDL. This leads to a chronic inflammatory response in the area around the lining of arteries.