established a causal relationship between intake or plasma concentrations of lutein and/or zeaxanthin and risk for AMD.

Increasing evidence suggests that a number of common neurode-generative diseases, such as Alzheimer's, Parkinson's, and amyotrophic lateral sclerosis, may reflect adverse responses to oxidative stress. Small intervention trials with either vitamin C or vitamin E have reported symptomatic improvement in those already afflicted with the disease. However, these preliminary findings do not constitute adequate proof of the usefulness of these antioxidants in decreasing the development or delaying the onset of these diseases.

Although some evidence suggests that modifications observed in structural proteins in patients with diabetes mellitus may be attributable to either an oxidative stress or a stress due to reactive carbonyls, much of the research, with either single compounds or combinations of specific food components that may function as antioxidants, has been inconclusive. In addition, no clinical intervention trials have tested directly whether provision of antioxidants can defer the onset of the complications of diabetes.

Because the various forms of vitamin E are not interconvertible and because plasma concentrations of α-tocopherol are dependent upon the affinity of the hepatic α-tocopherol transfer protein for the various forms, it is recommended that relative biological potencies of the various forms of vitamin E be reevaluated. Until this is done, the actual concentrations of each of the various vitamin E forms in food and biological samples should be reported separately, wherever possible.

Five major types of information gaps were noted: (1) a dearth of studies designed specifically to estimate average requirements in apparently healthy humans; (2) a nearly complete lack of usable