The search for the root cause of atherosclerosis was continued because every study clearly indicated that the dietary cholesterol-atherosclerosis theory didn’t fit the observations. For example, just as many people with normal cholesterol levels suffer heart attacks as those with higher levels.

Even more convincing was the evidence that a number of people with a hereditary condition called familial hypercholesterolemia — which is associated with cholesterol levels greater than 300 mg/dL — do not die of cardiovascular disease at a rate any higher than people without this dramatic elevation in blood cholesterol.

The defenders of the cholesterol-atherosclerosis theory then focused on LDL cholesterol as the real culprit — renaming it “bad cholesterol.” Yet even that idea ran into problems because research showed that many people with high LDL cholesterol levels still had a low incidence of heart attacks.

Not to be defeated, advocates of the theory subdivided LDL cholesterol into two types: a small dense form and a larger buoyant form. And now the small dense form became the “real” bad guy because the smaller LDL molecule was much more susceptible to being oxidized.

In fact, the large buoyant LDL molecule was shown to be just as protective as HDL cholesterol.

What they could not get away from was powerful scientific evidence that inflammation was the pathological cause of atherosclerosis — no matter what a person’s cholesterol level.