A Comparative Analysis of Aging Across Causes of Death

Although there is huge variation in how mortality changes with age across species, in humans, all-causes mortality increases at a relatively constant rate across populations and time. However, individuals die due to specific causes that include extrinsic and intrinsic sources. Here, we compared the rate at which mortality increases with age (i.e., the rate of aging) for the causes of death supposedly referring to extrinsic (infectious and parasitic diseases) and intrinsic sources (cardiovascular diseases and malignant neoplasm) in 12 human populations. Given that individuals are exposed to infectious agents across their entire lifespan, it is straightforward to expect a shallower rate of aging for infectious compared to cardiovascular diseases and malignant neoplasm. However, infectious and noninfectious diseases might target the same tissues/organs and tissue-specific repair mechanisms may strongly affect the disease severity. We, therefore, also compared the rate of aging for transmissible and nontransmissible diseases targeting the same tissues/organs. Contrary to the pattern observed when comparing infectious and noninfectious diseases overall, we found that diseases with shared target organs had similar rate of aging, whatever their etiology. We went a step further by assessing the changes in the distribution of cause-specific mortality across ages (i.e., lifespan equality), between 1955 and 2020, and by investigating whether they were accounted for by changes in early-life mortality, adult mortality or the rate of aging. This analysis showed that temporal changes in lifespan equality were essentially driven by changes in early-life mortality, with modest or almost no contribution from changes in adult mortality or the rate of aging. Overall, these results show that the rate at which mortality increases with age is relatively invariant for diseases targeting the same tissues/organs, suggesting that shared tolerance mechanisms, independently from the etiology of the disease, might be important drivers of age-dependent mortality schedules.