Although LDL is thought to be the major cholesterol-carrying culprit causing heart disease, there is still scientific controversy over the form LDL must take to cause atherosclerosis. For nearly twenty years, atherosclerosis researchers have hypothesized that LDL must change once it’s in the artery wall in order to cause artery blockages. The dominant view has been that LDL must first be oxidized to a more inflammatory form in order to cause serious artery wall damage. Oxidation is the chemical reaction that causes metals to rust by changing the structure of the metals’ molecules. Similarly, oxidation may change the chemical structure of LDL molecules by breaking down large fat-containing molecular chains.
Although there are literally thousands of studies that have suggested a role for oxidized LDL in causing heart disease, the use of antioxidants, such as vitamin E, has not resulted in any convincing decline in atherosclerosis in humans. This isn’t proof that oxidation is unimportant, it’s just that we don’t know yet. The precise form LDL must take to set off atherosclerotic plaque formation remains a bit of a mystery, but the link between high LDL levels and coronary disease is firmly established.