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Inflammatory exposure and historical changes in human life-spans
Caleb E Finch1, Eileen M Crimmins
1Andrus Gerontology Center and Departments of Biological Sciencesand of Sociology, University of Southern California, Los Angeles, CA 90089, USA. cefinch@usc.edu
Science (New York, N.Y.)
|September 18, 2004
Summary
Reduced exposure to infectious diseases and inflammation across a lifetime, a cohort mechanism, has significantly lowered old-age mortality. Early-life mortality strongly predicts later-life outcomes, suggesting a persistent "cohort morbidity phenotype".
Area of Science:
- Demography
- Epidemiology
- Public Health
Background:
- Historical increases in life expectancy are often attributed to medical and public health advances.
- A cohort-based mechanism involving reduced lifetime inflammatory exposure has not been fully explored.
Purpose of the Study:
- To investigate the role of reduced lifetime exposure to infectious diseases and inflammation in the historical decline of old-age mortality.
- To examine the association between early-age mortality and subsequent mortality within birth cohorts.
Main Methods:
- Analysis of Swedish birth cohorts from 1751 onwards.
- Examination of mortality patterns across the lifespan within specific birth cohorts.
Main Results:
- Strong associations were found between early-age mortality and subsequent mortality in the same cohorts.
- This suggests a persistent inflammatory process, termed a "cohort morbidity phenotype," originating in early life.
Conclusions:
- Reduced lifetime exposure to inflammation, a cohort effect, is a significant contributor to declining old-age mortality.
- The "cohort morbidity phenotype" highlights the long-term impact of early-life inflammatory processes on later-life health outcomes.
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