High cholesterol may protect against infections and atherosclerosis

According to the modified ‘response to injury’ hypothesis of atherogenesis, there are at least two pathways leading to the inflammatory and proliferative lesions of the arterial intima. The first involves monocyte and platelet interaction induced by hypercholesterolaemia.
The second pathway involves direct stimulation of the endothelium by a number of factors, including smoking, the metabolic consequences of diabetes, hyperhomocysteinemia, iron overload, copper deficiency, oxidized cholesterol, and micro-organisms. There is much evidence to support roles for these factors, but the degree to which each of them participates remains uncertain.
However, the lack of exposure-response in the trials between changes in LDL-cholesterol and clinical and angiographic outcome, the inverse association between change of cholesterol and angiographic changes seen in the observational studies, the significant increase in complicated atherosclerotic lesions in the treatment group after cholesterol lowering by diet, and most of all, the fact that high cholesterol predicts longevity rather than mortality in old people, suggests that the role, if any, of high cholesterol must be trivial.
The most likely explanation for these findings is that rather than promoting atherosclerosis, high cholesterol may be protective, possibly through its beneficial influence on the immune system.

QJM: High cholesterol may protect against infections and atherosclerosis