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After their genesis, cells and organisms are destined to grow old and die. Intriguingly, the past decades of gerontological research have taught us that the rate at which this process occurs is subject to modulation by evolutionarily-conserved biochemical pathways amenable to genetic or pharmacological manipulation. However, although conducive to the achievement of a longer lifespan, early perturbations in their activities are often inextricably linked to prohibitive developmental and reproductive costs. Clearly, intervening late in life would circumvent the problem altogether, but the post-reproductive capacity of gerontogenes to influence lifespan remains almost completely unexplored; in fact, given the rapidly faltering force of natural selection in the later phases of organismal life, it is not at all obvious that age-related pathways would even be responsive to this kind of therapeutic manipulation. A novel RNAi screen of 26 previously-described gerontogenes in aged (day 7) C. elegans adults uncovered several regulators of post-reproductive longevity, implying that the rate of ageing remains remarkably malleable until the very late stages of life. Strikingly, attenuation of insulin/IGF-1 signaling through daf-2 RNAi, previously reported to be ineffectual past the fifth day of nematode adulthood, was found capable of extending lifespan by ~25% even when initiated as late as the thirteenth day, with the neurons, the intestine, and the hypodermis emerging as the important tissues of daf-2 expression in this phenomenon. Importantly, the observed lifespan gains were, in certain cases, also accompanied by healthspan improvements, manifesting themselves as significant delays in the rate of locomotive and pharyngeal pumping decline. Nevertheless, the capacity for post-reproductive longevity modulation was not confined to genes of the insulin pathway, but extended to TOR pathway components, mitochondrial factors, epigenetic modifiers, and autophagy regulators. Surprisingly, pre-reproductive and post-reproductive knockdowns of the latter had converse effects on longevity, suggesting a gradual transmutation of autophagy from a cytoprotective quality-control system early in life into a pathogenic process that contributes to the toxic intracellular accumulation of malfunctioning proteins in late life. This work also features an investigation into the elusive mechanistic underpinnings of lifespan modulation through the tripartite MES/PRC-2 C. elegans complex, an H3K27 methyltransferase whose function is required for proper X chromosome repression and germline survival. In alignment with other experimental paradigms of sterility induction, abolishing the expression of any MES complex subunit via mutation or RNAi was found to improve longevity and healthspan by triggering lipophilic hormone signaling and DAF-16 nuclear translocation in the intestine. However, the existence of long-lived, fertile MES hypomorphic mutants also implied a germline-independent longevity-regulatory mechanism for the complex. Taken together, my findings constitute proof-of-concept that cost-free lifespan-extending interventions may indeed be possible, contributing to a short list of recent studies seeking to inspire a radical reevaluation of the manner in which we approach anti-ageing therapy implementation.