The ability of ethosuximide, trimethadione, and 3,3-diethyl-2-pyrrolidinone to extend C elegans life span and delay age-related degenerative changes suggests they may have similar effects in other animals including human beings. While we have stressed the similarities between C elegans and vertebrates, it is apparent that there are also many differences. In this section we discuss existing evidence that these drugs delay vertebrate aging and experiments that could test this hypothesis. First, we consider the possibility that retrospective studies of patients treated with ethosuximide might be useful. Ethosuximide has been used to treat absence seizures for more than 40 years, and it is possible that the drug has delayed normal aging or the progression of age-related diseases in treated individuals. However, such effects would be difficult to detect retrospectively. First, detecting delays in age-related functional declines requires measurements of physiologic processes that are not routinely performed in such patients. Second, the analysis would require an appropriate control group, such as individuals with the same disease who were not treated with ethosuximide. Third, patients typically do not take ethosuximide during the part of their lives that is probably optimal for causing a life span extension. Absence seizures typically have onset in childhood and usually cease as patients grow older, allowing discontinuation of ethosuximide therapy in adulthood.11 However, our studies suggest that AEDs act during adulthood to increase C elegans life span. Exposure to trimethadione only during the developmental period before sexual maturity had no effect on life span, whereas exposure to trimethadione only during adulthood caused a significant extension of life span (Figure 1D). Overall, it seems that retrospective analysis in patients is unlikely to test the hypothesis.