This dissertation focused on two central theories in experimental evolution; studying the death spiral and looking at trade-offs in adapted populations to a toxin in their environment. These results are summarized in Chapter 1. Chapter 2 focused on quantifying the efficacy of ingested dyes (using the ‘Smurf’ assay) to predict when an individual would die. This can be extremely useful for many research problems in aging. The death spiral is a short period prior to death that is marked by a dramatic decline in physiological health. The results show three key conclusions: that all blue dyes used had significant negative effects on mean longevity, only a small fraction of the flies showed the Smurf phenotype prior to death, and among the small fraction that did become Smurfs most (40-60%) become blue during their last 24 hours of life. The research in Chapters 3-5 focused on the phenotypic and genomic evolution of urea adapted populations. Insects are often exposed to many toxic substances in their environments. Urea and ammonia differ from most studies of resistance to toxic pesticides because of their wide-ranging effects on organismal and cellular physiology. The UX and UTB selection groups (adapted to high levels of urea in the larval stage of development), displayed slower larval feeding rates, slower larval growth rates, and lower starvation resistance compared to the other populations reared that had not adapted to urea. The UX and UTB selection regimes also showed higher viability, faster development time, and lower starvation resistance when reared on food supplemented with urea compared to controls. Chapter 4 of this dissertation studied genomic differentiation among populations subjected to different types of selection for tolerance to urea in their larval food. The RUX, reverse selected of the urea adapted populations still maintained measurable levels of adaptation to urea suggesting any reverse selection is slow. We saw parallel evolution occurring in the replicates of the same environmental populations, as well as genomic differentiation in the urea adapted lines, UX, UTB and RUX versus the control population of AUC. The starting conditions for the important gene regions might have been important and very different for the UX and UTB populations. These differences may account for why these populations share only 50% of the same significantly differentiated SNPS (single nucleotide polymorphisms). Chapter 5 sought to connect potential genes as the causative agents for specific phenotypes studied in Chapter 3. FLAM, the fused lasso additive model, is a statistical learning tool for determining which genes may affect differentiated phenotypes. The FLAM analysis provided us with 53 SNPS that had large effects on the four phenotypes studied – larval feeding rate, larval growth rate, development time and viability. Almost 500 genes were located to be potentially responsible for the 53 SNPS identified by FLAM.