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Dietary restriction (DR), reduced food uptake without malnutrition, is the most universal intervention known to extend animal lifespan, from invertebrates to mammals [1]. However, despite impressive progress in identifying the key components of the DR pathway, many proximal effectors of DR induced longevity remain unknown to date [1]. One central obstacle in the search for such mechanisms is that DR causes a myriad of transcriptional and physiological changes that are either not - or only indirectly - related to its positive effects on lifespan. For example, DR often increases lifespan at the expense of fertility [1]. In turn, the inability to filter out non-longevity effects of DR might impede the development of therapeutic compounds that mimic DR without causing unwanted side effects. For instance, while manipulation of dietary methionine can uncouple the phenotypic association between DR induced longevity and decreased fertility [2-3], whether and how such pleiotropic effects of DR are functionally separable at the molecular level is currently not understood. In this May issue of AGING, Bauer and colleagues now make a major step towards identifying those downstream effectors of DR that specifically affect longevity [4].

Dietary restriction and other lifespan extending pathways converge at the activation of the downstream effector takeout