The study investigates the genetic mechanisms underlying the life-extending effects of caloric restriction (CR) in *Caenorhabditis elegans*. CR has been shown to extend the lifespan of various animals, including mammals, and is thought to reduce oxidative stress and metabolic rates. In *C. elegans*, mutations in *eat* genes, which disrupt pharyngeal function and reduce food intake, significantly extend lifespan by up to 50%. The study found that *eat-2* mutants, which have severe feeding defects, live longer than those with milder defects, suggesting that the extent of the feeding defect correlates with lifespan extension. Additionally, *eat* mutants do not show extended lifespan when backcrossed to the wild type, indicating that the effect is due to reduced food intake. The study also examined the interaction between *eat* and *daf-16* genes, finding that *daf-16* does not suppress the long life of *eat-2* mutants, suggesting that these mechanisms operate through distinct pathways. Furthermore, *eat-2* and *clk-1* double mutants live longer than either single mutant, indicating that these genes may affect a common process. The findings suggest that CR and *clk-1* mutations may extend lifespan by reducing metabolic rates, potentially through decreased production of reactive oxygen species (ROS). The study highlights the importance of *eat* genes in mediating the effects of CR and provides insights into the genetic basis of lifespan regulation in *C. elegans*.The study investigates the genetic mechanisms underlying the life-extending effects of caloric restriction (CR) in *Caenorhabditis elegans*. CR has been shown to extend the lifespan of various animals, including mammals, and is thought to reduce oxidative stress and metabolic rates. In *C. elegans*, mutations in *eat* genes, which disrupt pharyngeal function and reduce food intake, significantly extend lifespan by up to 50%. The study found that *eat-2* mutants, which have severe feeding defects, live longer than those with milder defects, suggesting that the extent of the feeding defect correlates with lifespan extension. Additionally, *eat* mutants do not show extended lifespan when backcrossed to the wild type, indicating that the effect is due to reduced food intake. The study also examined the interaction between *eat* and *daf-16* genes, finding that *daf-16* does not suppress the long life of *eat-2* mutants, suggesting that these mechanisms operate through distinct pathways. Furthermore, *eat-2* and *clk-1* double mutants live longer than either single mutant, indicating that these genes may affect a common process. The findings suggest that CR and *clk-1* mutations may extend lifespan by reducing metabolic rates, potentially through decreased production of reactive oxygen species (ROS). The study highlights the importance of *eat* genes in mediating the effects of CR and provides insights into the genetic basis of lifespan regulation in *C. elegans*.