Dietary restriction (DR) has been shown to prolong lifespan, as well as health span, in numerous animals and to have beneficial effects in humans. Suppression of mechanistic target of rapamycin (mTOR), a key nutrient sensor, is one of the mechanisms through which the beneficial effects of DR are mediated. Interestingly, mTOR signalling is dysregulated in cells in which LMNA, the gene encoding the nuclear lamina component lamin A, is mutated, but the underlying mechanisms are not fully understood. In this work, Daniel Bar and co-workers (Charar et al., 2021) investigate the role of lamin in health span using C. elegans, which has a single lamin gene, lmn-1, and show that lamin regulates multiple DR phenotypes. In DR animals, knockdown (KD) of lmn-1 results in an increase in animal size and fat content, which is counteracted by simultaneous deletion of RAPTOR, a subunit of the mTOR complex mTORC1. Furthermore, lmn-1 KD restores the nuclear localisation of the mTOR activator RAGC-1, a step that is necessary for mTOR signalling but prevented under DR. This suggests that an intact nuclear lamina is required to make transport into the nucleus less permissive under stresses such as DR. Taken together, these findings provide clear evidence that lamin acts on the mTOR pathway upstream of mTORC1 to regulate global metabolism. This work thus might have important implications for a better understanding of lamin biology and associated diseases.