How does the oxidative process contribute to cardiovascular disease?
For many years there's been a hypothesis that one of the major problems generating cardiovascular disease is that some of our circulating lipoproteins—in particular, the so-called low-density or "bad" lipoprotein—can become oxidized, and that this oxidized low-density lipoprotein (LDL) is harmful. Therefore people began considering the possibility that if they could modify the extent of oxidation of low-density lipoprotein with antioxidants, they could modify either the onset or the course of coronary artery disease.
How does this new study question the value of vitamin E taken to lower risk of cardiovascular disease?
The main thrust of this article by Eidelman is when you look at large intervention trials—meaning that the investigators added vitamin E to the diet to see the effect on coronary heart disease—and you pool all of the data, as they did, there's simply no difference between the subjects that received vitamin E and the subjects that did not receive it. There is no difference in the cardiovascular events or cardiovascular deaths. So that would certainly make it look as if vitamin E has no effect.
But this is pooled data of seven different studies, and in a sense that's good, but in another sense, the studies were quite different, and you have to ask whether it's fair to pool all of this data and come out with a single answer. For example, some of the studies used synthetic alpha-tocopherol, whereas other studies used natural alpha-tocopherol, and there are differences in these compounds.