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. Author manuscript; available in PMC: 2017 Oct 26.
Published in final edited form as: Cell Syst. 2016 Oct 6;3(4):333–345.e4. doi: 10.1016/j.cels.2016.09.003

Figure 3. How does aging physiology differ between long- and short-lived individuals?

Figure 3

(A) “Starting Point” hypothesis: long-lived individuals start their adulthood healthier than short-lived individuals. (B) “Rate of Aging” hypothesis: long-lived individuals age more slowly than do short-lived individuals. (C) “Premature Death” hypothesis: short- and long-lived individuals are indistinguishable over the course of their lives. In this case, differences in lifespan arise from stochastic, inherently unpredictable causes of death or from factors outside our prognostic criteria. (D) Trends in the decline of prognosis over time, for each of the seven lifespan cohorts in Figure 2. These qualitatively match the “rate of aging” and “premature death” hypotheses from panels b and c. (E) We observe little quantitative relationship between lifespan and starting health (measured by an individual’s prognosis score at reproductive maturity). (F) In contrast, there is a strong negative correlation between lifespan and the rate of decline of physiological health. (G) Last, there is a moderate negative correlation between health at death and lifespan, suggesting stochasticity in death or unmeasured differences in functional health.