Disordered eating may lead to diagnosable medical conditions such as anorexia and bulimia, to extreme weight loss or to obesity. While no animal model is able to mimic the entirety of any complex human disease or behaviour, Drosophila melanogaster can serve as an uncomplicated model to study the biological basis of abnormal eating patterns. The conserved insulin receptor pathway and its endpoint effector the foxo transcription factor are pivotal for survival during nutritional stress. The loss of foxo function results in a defective survival response to amino-acid starvation. Two modifiers of foxo activity, the Akt1 kinase and the Sir2 deacetylase, may adjust the activity of foxo to enhance survival. Novel Akt1 mutant lines exhibit a moderate decrease in lifespan and growth when aged upon standard media, yet they show a significant increase in survival on amino-acid deprived media. Replacement of Akt1 activity is sufficient to suppress these phenotypes. Combination of the novel Akt1 hypomorphs and the null foxo mutant reveal an epistatic relationship. Biometric analysis and longevity evaluation of these double mutants indicate a phenotype similar to the original foxo mutant signifying its necessity in the Akt1 phenotype. Unlike the Akt1 mutants, Sir2 mutant heterozygotes do not have altered growth when raised upon standard conditions. However, the Sir2 heterozygotes exhibit a greatly extended lifespan when reared on both a standard diet and when starved of amino-acids. These results indicate that the subtle manipulation of foxo, by either Akt1 or Sir2 mutants, can enhance survival during adverse nutrient conditions to model the survival of individuals undergoing nutrient deprivation. Ultimately, we believe that a Drosophila model of disordered eating could generate new avenues of potential therapies for related human conditions. Funded by an NSERC PGSD and a School of Graduate Studies Fellowship to JDS and an NSERC Discovery Grant to BES.