Edited by C. Owen Lovejoy, Kent State University, Kent, OH, and approved June 17, 2016 (received for review October 6, 2015)
Why has human life expectancy increased since 1850? A leading hypothesis proposes that limited exposure to childhood infections has reduced lifelong inflammation and enhanced survival, but tests of this hypothesis typically use all-cause mortality rates to estimate disease exposure. Meanwhile, links between early-life disease and reproduction have been neglected. We used data from preindustrial Finnish populations to show that early-life disease exposure was not associated with all-cause mortality, mortality from cardiovascular disease, stroke, and cancer, or reproductive success. Our study therefore does not support the prevailing contention that reduced exposure to early-life infections has increased life expectancy in modern populations.
A leading hypothesis proposes that increased human life span since 1850 has resulted from decreased exposure to childhood infections, which has reduced chronic inflammation and later-life mortality rates, particularly from cardiovascular disease, stroke, and cancer. Early-life cohort mortality rate often predicts later-life survival in humans, but such associations could arise from factors other than disease exposure. Additionally, the impact of early-life disease exposure on reproduction remains unknown, and thus previous work ignores a major component of fitness through which selection acts upon life-history strategy. We collected data from seven 18th- and 19th-century Finnish populations experiencing naturally varying mortality and fertility levels. We quantified early-life disease exposure as the detrended child mortality rate from infectious diseases during an individual’s first 5 y, controlling for important social factors. We found no support for an association between early-life disease exposure and all-cause mortality risk after age 15 or 50. We also found no link between early-life disease exposure and probability of death specifically from cardiovascular disease, stroke, or cancer. Independent of survival, there was no evidence to support associations between early-life disease exposure and any of several aspects of reproductive performance, including lifetime reproductive success and age at first birth, in either males or females. Our results do not support the prevailing assertion that exposure to infectious diseases in early life has long-lasting associations with later-life all-cause mortality risk or mortality putatively linked to chronic inflammation. Variation in adulthood conditions could therefore be the most likely source of recent increases in adult life span.
Author contributions: A.D.H., F.L.R., and V.L. designed research; A.D.H. performed research; V.L. collected the data; A.D.H. and F.L.R. analyzed data; and A.D.H. and V.L. wrote the paper.
The authors declare no conflict of interest.
This article is a PNAS Direct Submission.
Data deposition: The data have been deposited in the Dryad Data Repository (www.datadryad.org), dx.doi.org/10.5061/dryad.966qt.
This article contains supporting information online at www.pnas.org/lookup/suppl/doi:10.1073/pnas.1519820113/-/DCSupplemental.
