In the paper I’ll point out today, the authors provide evidence in support of the concept that it is specifically oxidized cholesterol that is the primary cause of atherosclerosis rather than the condition resulting from too much cholesterol in general. In atherosclerosis, fatty deposits form in blood vessel walls, weakening them and narrowing the vessels. This ultimately leads to fatal structural failure as stressed blood vessels rupture or are blocked. Atherosclerosis is arguably a condition that arises because the macrophages responsible for removing cholesterol from blood vessel walls become overwhelmed, inflammatory, and incapable of keeping up the work of maintenance and repair. They become foam cells and die, adding their contents and their remnants to grow an atherosclerotic plaque, and attracting more of their fellows to the same location to repeat the cycle.
Here it is argued that this foam cell fate is largely the consequence of oxidized cholesterol. The macrophages are reacting to oxidized cholesterol in ways that sabotage their efforts to remove local deposits of cholesterol. The approach to this condition adopted by the SENS rejuvenation research programs is to find ways to break down the oxidized cholesterol that our cells struggle to deal with. Removing