Figure 6.

Model for sex-specific trade-offs and effects on cohort composition. (A) Model for sex-specific trade-offs. In female Drosophila, mating caused increased initial mortality rate and increased reproduction, consistent with an induced trade-off that causes lethality in the lowest-vitality individuals. The steroid hormone antagonist mifepristone/RU486 blocked the effects of mating, suggesting a role for steroid hormone signaling in the mating response. Increased concentration of yeast and sugar in the media also caused increased initial mortality rate and increased reproduction in female Drosophila, consistent with an induced trade-off. Finally, p53 mutation in female Drosophila and mTOR mutation in female mouse both decreased initial mortality rate, suggesting a normal role for these genes in diverting resources away from pathways important for health. In males, increased concentration of yeast and sugar in the media caused increased initial mortality rate, consistent with a diversion of resources away from pathways important for health. In contrast, p53 mutation in male Drosophila (and potentially mTOR mutation in male mouse) was associated with increased initial mortality rate, suggesting these genes normally regulate a diversion of resources towards health in the male. (B) Model for effect of trade-offs on cohort composition. Trade-offs between health and reproduction as shown in (A) preferentially cause lethality in the lowest-vitality individuals, thereby increasing initial mortality rate (parameter a). This leaves a cohort comprised of more robust individuals and therefore a slower age-dependent mortality rate acceleration (parameter b) (the S-M relationship). Similarly, during normal aging, the preferential loss of the lowest-vitality individuals can leave a cohort comprised of more robust individuals and a deceleration in mortality rates.