I’m not sure whether I get your point correctly. So, let me try to shed some light on the pathogenesis of atherosclerotic lesions.

The initiating event is endothelial dysfunction (the endothelium being the cling-wrap type luminal lining of the arteries).

Once compromised, LDL particles can seep through into the subendothelial space where they accumulate. Oxidatively transformed LDL attract monocytes (a type of immune cell) that differentiate into macrophages and engulf the LDL intruder. These macrophages normally are cleared through a process of programmed cell death, apoptosis. Apoptotic cells are then removed by phagocytosis. As long as phagocytosis can clear the debris of dead cells, the formation of permanent atherosclerotic lesions can be prevented.

However, when the rate of apoptosis overwhelms the phagocytotic ability of the macrophages, the uncleared apoptotic cells undergo a secondary process, called necrosis. It is these necrotic cells which form the nucleus of atherosclerotic lesion, its necrotic core.

Once that core has established, remission of the atherosclerotic lesion becomes difficult if not impossible. Hence, its prevention is the best strategy to prevent atherosclerotic disease and their consequences. That strategy is to maintain endothelial function through sufficiently intense exercise and prudent diet. At that stage statins offer little to no additional benefit. That’s where I am anti-statin.

Once the atherosclerotic disease has developed to a diagnostically detectable extent, statins do make sense. But so does exercise and nutrition.