We found that arrhythmic mutants lacking the critical circadian regulators period or timeless exhibit extended lifespan relative to controls. Circadian rhythm is known to affect a wide range of vertebrate physiologies, including many known to impact aging and lifespan. We set out to ask if loss of circadian regulation alters longevity. Unexpectedly, we found that male period and timeless mutants are long-lived relative to controls. Focusing on male per mutants, we found that they do not achieve longevity by mimicking diet restriction: to the contrary, per mutants eat more than controls and lack changes in metabolism and signaling pathways typically associated with diet restriction and longevity. While per mutants appear to age more slowly than controls, as judged by intestinal and muscle health, their extended longevity is also independent of microbiota and activity. Our results suggest instead that altered mitochondrial function leads to longevity in these mutants. We observed changes in per mutants' mitochondrial morphology and DNA copy number that correlate with extended longevity; genetic experiments suggest that their longevity is not due to mitophagy but due to mitohormesis. We are currently investigating specific, circadian-regulated changes in mitochondrial function that underlie per mutants' longevity phenotype.