In mice with clogged arteries, lowering cholesterol makes the immune cells inside the plaque stop multiplying, which is why the plaque gets smaller — not because fewer cells come in or leave.

Statins do not induce significant regression of established atherosclerotic plaque but reduce plaque progression and enhance plaque stability by lowering LDL cholesterol exposure to arterial walls.

Statins reduce intraplaque inflammation, thereby decreasing the likelihood of atherosclerotic plaque rupture and subsequent thrombotic events.

The cholesterol-lowering drug atorvastatin doesn’t get into the fatty plaques in arteries — so it must be working by lowering cholesterol in the blood, not by directly touching the immune cells inside the plaque.

When people took statins (cholesterol pills), cutting out saturated fat didn’t help them any more than just taking the pills alone — so the pills might be doing all the work, and diet changes don’t add extra benefit.

When people ate less animal fat, their bad cholesterol went down and their belly fat became less inflamed — and heart attacks dropped fast.