Aging research has long been focused on identifying mechanisms through which lifespan can be extended. However, there has been a recent trend away from simple lifespan extension and towards healthspan extension, that is, shrinking the extent of life in bad health, or “sickspan.”2 Caenorhabditis elegans has been an invaluable model in gerontologic research and through it some of the defining molecular mechanisms of lifespan extension have been discovered. However, there is a critical need to understand the mechanisms of healthspan extension as these would be most readily applicable as therapeutic targets for a globally aging population. This research project presents a combined lifespan/healthspan extension mechanism that may potentially represent a significant increase in both metrics. It is hypothesized that downregulation of both insulin/insulin-like signaling (IIS) through IIS receptor knockdown and electron transport chain function (ETC) through complex V knockdown leads to a six-fold increase in life- and healthspan.