Hostname: page-component-586b7cd67f-vdxz6 Total loading time: 0 Render date: 2024-11-22T22:43:31.884Z Has data issue: false hasContentIssue false
  • English
  • Français

Early cohort mortality predicts the rate of aging in the cohort: a historical analysis

Published online by Cambridge University Press:  15 May 2012

H. Beltrán-Sánchez ,
E. M. Crimmins  and
C. E. Finch
H. Beltrán-Sánchez*
Affiliation:
Davis School of Gerontology and the Dornsife College, University of Southern California, Los Angeles, CA, USA Center for Population and Development Studies, Harvard University, Cambridge, MA, USA
E. M. Crimmins
Affiliation:
Davis School of Gerontology and the Dornsife College, University of Southern California, Los Angeles, CA, USA
C. E. Finch
Affiliation:
Davis School of Gerontology and the Dornsife College, University of Southern California, Los Angeles, CA, USA
*
*Address for correspondence: Dr H. Beltrán-Sánchez, Center for Population & Development Studies, Harvard University, 9 Bow Street, Cambridge, MA 02135, USA. (Emails [email protected], [email protected])
Get access Rights & Permissions [Opens in a new window]

Abstract

Early environmental influences on later-life health and mortality are well recognized in the doubling of life expectancy since 1800. To further define these relationships, we analyzed the associations between early-life mortality and both the estimated mortality level at age 40 and the exponential acceleration in mortality rates with age characterized by the Gompertz model. Using mortality data from 630 cohorts born throughout the 19th and early 20th century in nine European countries, we developed a multilevel model that accounts for cohort and period effects in later-life mortality. We show that early-life mortality, which is linked to exposure to infection and poor nutrition, predicts both the estimated cohort mortality level at age 40 and the subsequent Gompertz rate of mortality acceleration during aging. After controlling for effects of country and period, the model accounts for the majority of variance in the Gompertz parameters (about 90% of variation in the estimated level of mortality at age 40 and about 78% of variation in the Gompertz slope). The gains in cohort survival to older ages are entirely due to large declines in adult mortality level, because the rates of mortality acceleration at older ages became faster. These findings apply to cohorts born in both the 19th century and the early 20th century. This analysis defines new links in the developmental origins of adult health and disease in which effects of early-life circumstances, such as exposure to infections or poor nutrition, persist into mid-adulthood and remain evident in the cohort mortality rates from ages 40 to 90.

Keywords

cohort mortalitycohort survivalearly-life conditionsGompertz modellife course
Type
Original Article
Information
Journal of Developmental Origins of Health and Disease , Volume 3 , Issue 5 , October 2012 , pp. 380 - 386
Copyright
Copyright © Cambridge University Press and the International Society for Developmental Origins of Health and Disease 2012

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)

References

1. Kannisto, V. The Advancing Frontier of Survival: Life Tables for Old Age, 1996. Odense University Press: Odense.Google Scholar
2. Rau, R, Soroko, E, Jasilionis, D, Vaupel, JW. Continued reductions in mortality at advanced ages. Populat Dev Rev. 2008; 34, 747–768.CrossRefGoogle Scholar
3. Kermack, WO, McKendrick, AG, McKinlay, PL. Death rates in Great Britain and Sweden: some regularities and their significance. Lancet. 1934, 698–703.CrossRefGoogle Scholar
4. Barker, DJP. The origins of the developmental origins theory. J Intern Med. 2007; 261, 412–417.CrossRefGoogle ScholarPubMed
5. Barker, DJP. The developmental origins of well-being. Philos Trans: Biol Sci. 2004; 359, 1359–1366.CrossRefGoogle ScholarPubMed
6. Bengtsson, T, Broström, G. Do conditions in early life affect old-age mortality directly and indirectly? Evidence from 19th-century rural Sweden. Soc Sci Med. 2009; 68, 1583–1590.CrossRefGoogle ScholarPubMed
7. Bengtsson, T, Lindström, M. Childhood misery and disease in later life: the effects on mortality in old age of hazards experienced in early life, southern Sweden, 1760–1894. Populat Stud. 2000; 54, 263–277.CrossRefGoogle ScholarPubMed
8. Gluckman, PD, Hanson, MA. An adaptive perspective on the developmental origins paradigm. Am J Phys Anthropol. 2007; S44, 116.Google Scholar
9. Fogel, RW. The Escape from Hunger and Premature Death, 1700–2100: Europe, America, and the Third World, Vol. 38. 2004. Cambridge University Press: New York.CrossRefGoogle Scholar
10. Finch, CE, Crimmins, EM. Inflammatory exposure and historical changes in human life-spans. Science. 2004; 305, 1736–1739.CrossRefGoogle ScholarPubMed
11. Crimmins, EM, Finch, CE. Infection, inflammation, height, and longevity. Proc Natl Acad Sci U S A. 2006; 103, 498–503.CrossRefGoogle ScholarPubMed
12. Heuveline, P, Clark, SJ. Model schedules of mortality. In International Handbook of Adult Mortality (eds. Rogers RR, Crimmins EM), 2011; pp. 511–532. Springer: Dordrecht, The Netherlands.CrossRefGoogle Scholar
13. Gompertz, B. On the nature of the function expressive of the law of human mortality. Philos Trans R Soc London. 1825; 115, 513–585.Google Scholar
14. Strehler, BL, Mildvan, AS. General theory of mortality and aging. Science. 1960; 132, 14–21.CrossRefGoogle ScholarPubMed
15. Hawkes, K, Smith, KR, Robson, SL. Mortality and fertility rates in humans and chimpanzees: how within-species variation complicates cross-species comparisons. Am J Hum Biol. 2009; 21, 578–586.CrossRefGoogle ScholarPubMed
16. Zheng, H, Yang, Y, Land, KC. Heterogeneity in the Strehler–Mildvan general theory of mortality and aging. Demography. 2011; 48, 267–290.CrossRefGoogle ScholarPubMed
17. Yashin, AI, Begun, AS, Boiko, SI, Ukraintseva, SV, Oeppen, J. New age patterns of survival improvement in Sweden: do they characterize changes in individual aging? Mech Ageing Dev. 2002; 123, 637–647.CrossRefGoogle ScholarPubMed
18. Gavrilov, LA, Gavrilova, NS. The reliability theory of aging and longevity. J Theor Biol. 2001; 213, 527–545.CrossRefGoogle ScholarPubMed
19. University of California Berkeley (USA) and Max Planck Institute for Demographic Research (Germany). 2011. Retrieved June 30, 2011, from www.mortality.org.Google Scholar
20. Gurven, M, Kaplan, H. Longevity among hunter–gatherers: a cross-cultural examination. Populat Dev Rev. 2007; 33, 321–365.CrossRefGoogle Scholar
21. Barker, DJP, Osmond, C. Infant mortality, childhood nutrition, and ischaemic heart disease in England and Wales. Lancet. 1986; 327, 1077–1081.CrossRefGoogle Scholar
22. Finch, CE. The Biology of Human Longevity: Inflammation, Nutrition, and Aging in the Evolution of Life Spans, 2007. Academic Press: Burlington, MA.Google Scholar
23. van den Berg, GJ, Doblhammer, G, Christensen, K. Exogenous determinants of early-life conditions, and mortality later in life. Soc Sci Med. 2009; 68, 1591–1598.CrossRefGoogle ScholarPubMed
24. Mazumder, B, Almond, D, Park, K, Crimmins, EM, Finch, CE. Lingering prenatal effects of the 1918 influenza pandemic on cardiovascular disease. J Dev Orig Health Dis. 2010; 1, 26–34.CrossRefGoogle ScholarPubMed
25. Finch, CE, Pike, MC, Witten, M. Slow mortality rate accelerations during aging in some animals approximate that of humans. Science. 1990; 249, 902–905.CrossRefGoogle ScholarPubMed
26. Christensen, K, Doblhammer, G, Rau, R, Vaupel, JW. Ageing populations: the challenges ahead. Lancet. 2009; 374, 1196–1208.CrossRefGoogle ScholarPubMed
27. Yen, K, Mobbs, CV. Evidence for only two independent pathways for decreasing senescence in caenorhabditis elegans. Age. 2010; 32, 39–49.CrossRefGoogle ScholarPubMed
28. Finch, CE. Longevity, Senescence, and the Genome, 1990. University of Chicago Press: Chicago.Google Scholar
29. Flurkey, K, Papaconstantinou, J, Miller, RA, Harrison, DE. Lifespan extension and delayed immune and collagen aging in mutant mice with defects in growth hormone production. Proc Natl Acad Sci U S A. 2001; 98, 6736–6741.CrossRefGoogle ScholarPubMed
30. Schriner, SE, Linford, NJ, Martin, GM, et al. . Extension of murine life span by overexpression of catalase targeted to mitochondria. Science. 2005; 308, 1909–1911.CrossRefGoogle ScholarPubMed
Supplementary material: PDF

Beltran-Sanchez supplementary material

Appendix

Download Beltran-Sanchez supplementary material(PDF)
PDF 160.2 KB