Many approaches to slowing aging in laboratory species target the same cellular maintenance processes activated by stress. One well-studied process is autophagy, which recycles damaged structures in the cell. Research shows that interventions like rapamycin and spermidine affect different parts of the regulatory system governing stress responses, ultimately slowing aging. The surge in endogenous spermidine is essential for rapamycin-induced autophagy and longevity. These findings underscore the importance of polyamine metabolism in aging processes and highlight the interconnected roles of various interventions in promoting longevity.