Sleep is a conserved behavior across the evolutionary timescale. Almost all known animal species demonstrate sleep or sleep like states. Despite extensive study, the mechanistic aspects of sleep need are not very well characterized. Sleep appears to be needed to generate resources that are utilized during the active stage/wakefulness as well as clearance of waste products that accumulate during wakefulness. From a metabolic perspective, this means sleep is crucial for anabolic activities. Decrease in anabolism and build-up of harmful catabolic waste products is also a hallmark of aging processes. Through this lens, sleep and aging processes are remarkably parallel-for example behavioral studies demonstrate an interaction between sleep and aging. Changes in sleep behavior affect neurocognitive phenotypes important in aging such as learning and memory, although the underlying connections are largely unknown. Here we draw inspiration from the similar metabolic effects of sleep and aging and posit that large scale metabolic phenotyping, commonly known as metabolomics, can shed light to interleaving effects of sleep, aging and progression of diseases related to aging. In this review, data from recent sleep and aging literature using metabolomics as principal molecular phenotyping methods is collated and compared. The present data suggests that metabolic effects of aging and sleep also demonstrate similarities, particularly in lipid metabolism and amino acid metabolism. Some of these changes also overlap with metabolomic data available from clinical studies of Alzheimer's disease. Together, metabolomic technologies show promise in elucidating interleaving effects of sleep, aging and progression of aging disorders at a molecular level. process of aging is in part the result of progressive decline of physiological function at the molecular level. Key physiological processes impacted by aging include genomic instability, telomere attrition, epigenetic alteration, loss of proteastasis, nutrient sensing dysregulation, mitochondrial dysfunction, cellular senescence, stem cell exhaustion and altered intercellular communication [3].Along with molecular level changes, behavioral changes are also apparent with healthy aging. Memory impairment [4] and altered sleep wake activities are perhaps the most common signatures of aged individuals [4]. Both human population and rodent model studies have shown that aging individuals are unable to sustain sleep/wake state and generally