Abstract
In this paper we develop a formal model to represent effects of early life conditions with delayed health impacts on old age mortality. The model captures several mechanisms through which early conditions influence adult health and mortality. The model is an extension of the standard frailty model in demographic analysis but has distinct and unique implications. We show that populations with Barker frailty experience adult mortality patterns equivalent to a class of time-varying and/or age dependent frailty. We demonstrate formally and via simulations that populations with Barker frailty could experience unchanging or increasing adult mortality even when background mortality has been declining for long periods of time. We also show that the rate of increase of adult mortality rates in populations with Barker frailty will change over time and will always be lower that the rate of increase of adult mortality in the background mortality pattern. We argue that Barker frailty should be pervasive in low-to-middle income populations, e.g. those that experienced a mortality decline fueled largely by post-1950 medical innovations that reduced the load and lethality of infectious and parasitic diseases.
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Notes
- 1.
Our model is a particular case of a more general representation that includes all the nuances associated with each of these three mechanisms.
- 2.
As we show later, the simpler functional form adopted here represents lower bounds of Barker effects in the sense that time trends in both adult mortality levels and age patterns are least affected by their presence.
- 3.
In a recent paper Vaupel and Missov (2014) proposes an equivalent age dependent effect of standard frailty but with no association to Barker’s conjecture. Coincidentally, we are using the same symbol, R, to express extra mortality in the special case when R(δ,y) \(= R(y) = R\) is constant.
- 4.
This simplified functional form for mortality decline avoids cumbersome algebra but leads to no loss of precision or generality.
- 5.
Below we explore the case when time dependency of Barker effects is linked not to mortality decline but to changes in the distribution f(δ).
- 6.
Expression (8.7) also holds with standard frailty. The difference between it and the standard frailty case is in the quantities that come into play: in the case of Barker frailty the value of \(\partial \ln (E_{y}(\delta,t))/\partial t\) depends on R (not just on δ) via the dependence of the integrated survival function on R (see Eq. (8.6)).
- 7.
This expression is also derived by Vaupel and Missov (2014) in the case of constant mortality.
- 8.
Note that, by construction, \(\frac{\partial \ln (\mu _{s}(y))} {\partial y} =\beta _{s}(y)\) is invariant over time. The implication of this expression seems to have gone unnoticed in the literature (but see Vaupel and Missov (2014) for an analogous expression and recent discussion). Even in the absence of Barker effects and with an age-invariant β s (y) at adult ages (as in a Gompertz baseline adult mortality pattern), the age-derivative of the average mortality pattern cannot be constant (across ages or across time when there is a mortality decline). The regime of frailty assumed here will always induce an age dependent slope smaller than the standard slope. This has important consequences for the study of old age mortality in that the standard interpretation of an empirical slope estimated after fitting, for example, a Gompertz function to a cohort’ s adult mortality rates is probably always incorrect. As suggested by (8.10), such estimate contains an age and time dependent downward bias. To avoid this bias one needs to estimate a Gompertz model controlling both for age and for the value of the (age and time varying) negative term in the expression. To our knowledge this has never been done in empirical studies. Elsewhere, we show that Barker effects and mortality decline will always induce a negative correlation between the levels of child mortality experienced by a cohort and the cohort’s adult mortality slope (Palloni and Beltrán-Sánchez 2015).
- 9.
An alternative way of interpreting Barker effects defined above is that they are tantamount to a shift of the standard mortality rates at older ages (y > Y 1), e.g. from μ s (y) to R μ s (y).
- 10.
By design, the random terms for frailty, δ, δ = ι + 1 where \(\iota \sim \ Gamma(1,\lambda )\). Thus, the frailty term we use has a minimum value of 1 and its mean is equal to 1 plus the conditional mean of the gamma random term.
- 11.
The simulated scenario is very easy to implement but it has an odd implication. Note that the mortality experience of the birth cohort born 50 years after the onset of secular mortality decline experiences a baseline life table with life expectancy at birth of roughly 60 years. Thus, the period life table corresponding to the year of their birth has a life expectancy at birth lower than 60 years. The sequence of baseline (period) life tables implied by the simulated birth cohorts includes a range of life expectancies at birth from 40 to less than 60 years. This range is only a small fraction of the observed improvements in period life expectancy of low to middle income countries after 1950.
- 12.
The idea that Y 1 should be random is consistent with theories of fetal origins according to which there are several chronic illnesses that could play a role and each of them has different time of onset after which Barker effects begin to be felt. Another interpretation is that Barker effects exert an impact on the rate of senescence itself and the slope of the mortality curve begins to accelerate by a random amount after a fixed age \(Y _{1}\).
- 13.
The study of the precise dynamics of Barker effects necessitates additional investigation.
References
Aalen, O. O. (1988). Heterogeneity in survival analysis. Statistics in Medicine, 7, 1121–1137.
Anson, J. (2002). Of entropies and inequalities: Summary measures of the age distribution of mortality. In G. Wunsch & M. Mouchart (Eds.), Life tables: Data, method and models (pp. 95–116). Dordrecht: Kluwer.
Barker, D. J. P. (1998). Mothers, babies, and health in later life (2nd ed.). Edinburgh/New York: Churchill Livingstone.
Barouki, R., Gluckman, P. D., Grandjean, P., Hanson, M., & Heindel, J. J. (2012). Developmental origins of non-communicable disease: implications for research and public health. Environmental Health, 11, 10–1186.
Beltrán-Sánchez, H., Crimmins, E. M., & Finch, C. E. (2012). Early cohort mortality predicts the rate of aging in the cohort: A historical analysis. Journal of Developmental Origins of Health and Disease, 3, 380–386.
Coale, A. J., & Demeny, P. (1983). Regional model life tables and stable populations (2nd ed.). Princeton: Princeton University Press.
Crimmins, E. M., & Finch, C. E. (2006). Infection, inflammation, height, and longevity. Proceedings of the National Academy of Sciences of the United States of America, 103, 498–503.
Danesh, J., Whincup, P., Walker, M., Lennon, L., Thomson, A., Appleby, P., Gallimore, J. R., & Pepys, M. B. (2000). Low grade inflammation and coronary heart disease: Prospective study and updated meta-analyses. BMJ, 321, 199–204.
Elo, I. T., & Preston, S. H. (1992). Effects of early-life conditions on adult mortality: A review. Population Index, 58, 186–212.
Finch, C. (2007). The biology of human longevity: Inflammation, nutrition, and aging in the evolution of life spans (1st ed.). Burlington: Academic.
Finch, C. E., & Crimmins, E. M. (2004). Inflammatory exposure and historical changes in human life-spans. Science, 305, 1736–1739.
Fong, I. W. (2000). Emerging relations between infectious diseases and coronary artery disease and atherosclerosis. Canadian Medical Association Journal, 163, 49–56.
Forsdahl, A. (1977). Are poor living conditions in childhood and adolescence an important risk factor for arteriosclerotic heart disease? British Journal of Preventive & Social Medicine, 31, 91–95.
Forsdahl, A. (1978). Living conditions in childhood and subsequent development of risk factors for arteriosclerotic heart disease. The cardiovascular survey in Finnmark 1974–75. Journal of Epidemiology and Community Health, 32, 34–37.
Gluckman, P. D., & Hanson, M. A. (2006). Developmental origins of health and disease. Cambridge/New York: Cambridge University Press.
Hougaard, P. (1986). Survival models for heterogeneous populations derived from stable distributions. Biometrika, 73, 387–396.
Kannisto, V. (1994). Development of oldest-old mortality, 1950–1990: Evidence from 28 developed countries (Monographs on population aging). Odense: Odense University Press.
Kuzawa, C. W., & Eisenberg, D. T. A. (2014). The long reach of history: Intergenerational and transgenerational pathways to plasticity in human longevity. In M. Weinstein & M. Lane (Eds.), Sociality, hierarchy, health: Comparative biodemography (pp. 65–94). Washington, DC: National Research Council Press. Book section 4.
Langley-Evans, S. C. (2004). Fetal nutrition and adult disease: Programming of chronic disease through fetal exposure to undernutrition (Frontiers in nutritional science). Wallingford/Oxfordshire/Cambridge: CABI Publication.
Manton, K. G., Stallard, E., & Vaupel, J. W. (1986). Alternative models for the heterogeneity of mortality risks among the aged. Journal of the American Statistical Association, 81, 635–44.
McDade, T. W., & Kuzawa, C. W. (2004). Fetal programming of immune function: The early origins of immunity in Filipino adolescents. In S. C. Langley-Evans (Ed.), Fetal nutrition and adult disease: Programming of chronic disease through fetal exposure to undernutrition (Frontiers in nutritional science, book section 13, pp. 311–332). Wallingford/Oxfordshire/Cambridge: CABI Publication.
McDade, T. W., Rutherford, J., Adair, L., & Kuzawa, C. W. (2010). Early origins of inflammation: Microbial exposures in infancy predict lower levels of C-reactive protein in adulthood. Proceedings of the Royal Society B: Biological Sciences, 277, 1129–1137.
Palloni, A., & Beltrán-Sánchez, H. (2015). Mortality regimes with Barker frailty and the warped dynamics of old age mortality. work-in-progress.
Palloni, A., & Souza, L. (2013). The fragility of the future and the tug of the past: Longevity in Latin America and the Caribbean. Demographic Research, 29, 543–578.
Steinsaltz, D. R., & Wachter, K. W. (2006). Understanding mortality rate deceleration and heterogeneity. Mathematical Population Studies, 13, 19–37.
Vaupel, J. W., & Missov, T. (2014). Unobserved population heterogeneity: A review of formal relationships. Demographic Research, 31, 659–686.
Vaupel, J. W., & Yashin, A. I. (1987). Repeated resuscitation – how lifesaving alters life-tables. Demography, 24, 123–135.
Vaupel, J. W., Manton, K. G., & Stallard, E. (1979). Impact of heterogeneity in individual frailty on the dynamics of mortality. Demography, 16, 439–454.
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Appendix: Main Definitions
Appendix: Main Definitions
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Palloni, A., Beltrán-Sánchez, H. (2016). Demographic Consequences of Barker Frailty. In: Schoen, R. (eds) Dynamic Demographic Analysis. The Springer Series on Demographic Methods and Population Analysis, vol 39. Springer, Cham. https://doi.org/10.1007/978-3-319-26603-9_8
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