Scientific Panel on Pathways to Health

International Seminar on Pathways to Health: How intermediary life conditions mediate or modify early life effects
Berkeley, CA (USA), 1-2 May 2012

 

Seminar organized by the
The IUSSP Scientific Panel on Pathways to Health
Berkeley Population Center and the Institute for the Study of Societal Issues

CALL FOR PAPERS

Deadline for abstract submission: 16 January 2012

Understanding the complex relationship between early life conditions and adult health and mortality is critical for the development of strategies for improving population health. Exposure to disease, nutritional deprivation, or adverse economic conditions early in life, possibly as early as in the fetal stage, have all been linked to decreased adult health or increased mortality. Evidence from natural experiments suggests that the association between these and other adverse early life conditions and later health may be causal. Often, however, the mechanism is unclear. In particular, it is not well known whether negative early life insults affect health directly through damage to cells and organs, indirectly through the ability to accumulate human capital, or through yet other pathways.

The IUSSP Seminar on Pathways to Health will explore the mechanism through which early life conditions influence adult and old-age health and mortality. Contributions may be empirical, methodological, or conceptual, and are invited from all disciplines, as long as they address the various ways in which early life insults and adversity can be mediated, modulated, or modified by intermediary life conditions and events.

Researchers interested in presenting their work at the seminar are invited to submit a 200-word abstract or paper by 16 January 2012 to Mikko Myrskylä (pathways@demogr.mpg.de), with copies to Tommy Bengtsson (Tommy.Bengtsson@ekh.lu.se) and Alain Gagnon (alain.gagnon.4@umontreal.ca). Authors will be notified by 1 February 2012 whether their paper has been accepted.

The seminar will be limited to a maximum of 15 contributed papers. Proceedings, an edited volume or a special journal issue will be produced after the meeting.

No travel funding will be available for this seminar. Participants must seek their own funding to cover their travel and accommodation costs. The meeting venue is at the Institute for the Study of Societal Issues at the Berkeley Campus. The participants may stay at a reduced rate at the Durant hotel which is located close to the meeting venue

Extended background information

IUSSP Seminar on Pathways to Health:
How intermediary life conditions mediate or modify early life effects”,
Berkeley, CA (USA) 1-2 May 2012

Understanding the complex relationship between early life conditions and adult health and mortality is critical for the development of strategies for improving population health. Exposure to disease, nutritional deprivation, or adverse economic conditions early in life, possibly as early as in the fetal stage, have all been linked to decreased adult health or increased mortality. Evidence from natural experiments suggests that the association between these and other adverse early life conditions and later health may be causal. Often, however, the mechanism is unclear. In particular, it is not well known whether negative early life insults affect health directly through damage to cells and organs, indirectly through the ability to accumulate human capital, or through yet other pathways. Further understanding of the mechanism through which early life conditions influence later health would have profound implications for public health policy.

The conceptual framework for understanding the link between early life conditions and later mortality were developed by Preston et al. (1998) and Ben-Shlomo and Kuh (2002). While Preston et al. (1998) discuss the difference between individual and population level associations, Ben-Shlomo and Kuh develop a framework for understanding the individual level associations. In their critical period model, exposures during specific development windows have irreversible health effects. Consistent with the critical period model, several studies suggest that inadequate nutrition in utero results in physiological and metabolic restrictions that increase the risk of cardiovascular mortality in later life (Barker 2006; Cameron and Demerath 2002). Prenatal nutritional deprivation has also been connected to higher prevalence of death due to infectious diseases in adolescence in a series of contemporary African studies (McDade et al. 2001; Moore et al. 1999; Moore et al. 1997).

Severe infection in infancy may also cause irreversible damage that increases mortality later in life. Two studies in England demonstrated that exposure to airborne infectious diseases at a young age are associated with cough, phlegm, and impaired ventilatory function later in life (Barker et al. 1991; Shaheen et al. 1994). In 18th-19th century Sweden, individuals born during years of smallpox and whooping cough epidemics had an increased risk of death after age 50 (Bengtsson and Lindstrom 2003). The effect was not indirect (via its influence on accumulation of wealth and obtained socio-economic status) but direct or, in other words, physiological scarring from severe infections at the start of life leads to higher mortality at older ages (Bengtsson and Brostrom 2009). These results are consistent with the hypothesis that reductions in the exposure to infectious diseases (and thus inflammation) made a major contribution to the historical decline in old-age mortality (Finch an Crimmins 2004; Crimmins and Finch 2006).

Further evidence suggesting that early life disease exposure may influence later life health comes from studies analyzing cohorts born during epidemics. Almond and Mazumder found that in utero exposure to the 1918 pandemic had a negative effect on self-reported health of adults over 50 (2005). Exposure in late stages of fetal development also led to low educational and job-market outcomes and higher cardiovascular disease prevalence (Almond 2006; Mazumder et al. 2009). Myrskylä et al (2010) found that in utero exposure to the 1918 Pandemic increased mortality risks from cardiovascular and respiratory diseases, positing a mechanism whereby resources are diverted to the maternal immune response at the detriment of fetal maturation. However, the same exposure decreased rather than increased the risk of death by cancer, indicating a potential trade-off in health outcomes for early life disease exposure (Myrskylä et al. 2010).

These studies show how much of the recent research has focused on identifying the causal association between early life, in particular in utero conditions and later life health. According to Ben-Shlomo and Kuh (2002), the aim of life course epidemiology goes beyond intrauterine and childhood circumstances to build and test theoretical models that postulate pathways linking later life health with exposures across the whole life course. Indeed, an alternative mechanism to the critical period model links socioeconomic disadvantage in early life, and throughout the lifecourse, to health at older ages through a process of ‘cumulative adversity’. In contrast to the critical period model, these models postulate that detrimental effects amass to influence health development throughout life, emphasizing the persistence of social and economic circumstances experienced in childhood. For instance, children from an impoverished background are more likely to be of low birth weight, to suffer from nutritional deprivation (quality or quantity), and to have fewer educational and occupational opportunities. They often consequently suffer higher mortality rates as adults (Frankel, Smith and Gunnell 1999; Smith et al. 1998). Recent studies have shown that socioeconomic inequalities in infancy and childhood are both directly and indirectly related to adult health and that being born in a recession increases mortality later in life, in particular for lower social classes (van den Berg, Lindeboom and Lopez 2009). Other detrimental childhood circumstances such as crowding or lack of tap water were also shown to significantly affect mortality later in life (Bobak et al. 2003).

A number of studies find that adjusting for midlife socioeconomic status and risk factors may attenuate the associations between early life conditions and later life health (Smith, Hart et al. 1998; Hayward and Gorman 2004; Elo, Martikainen and Myrskylä 2010). This suggests that intermediary life circumstances and events play an important role in the relationship between early life conditions and later life health. It also suggests that some individuals with difficult early life circumstances may improve their health by, for example, by upward social mobility. Yet, if many studies have showed that people experiencing poor conditions during childhood carry a high risk of mortality, independently of adult life transitions (Galobardes 2004; O'Rand and Hamil-Luker 2005), the pathways through which early life conditions may affect later life health and mortality have remained elusive. Further, selection processes and other complicating issues may often attenuate or blur the relationship between early life exposure and later life health and mortality (Gagnon and Mazan 2009; Myrskyla 2010; Preston, Hill and Drevenstedt 1998). It has been argued, for instance, that the effect of in utero nutritional deprivation and consequent fetal growth restriction has an adverse effect on adult health only if the post-natal and adult environment is nutritionally rich, that is, if there is a mismatch between early life programming and later life environment (Godfrey, Gluckman and Hanson 2010).

Early life effects are complex, and explicit statements of the temporal ordering of exposure variables and their multivariate relationships are needed (Ben-Shlomo and Kuh 2002; Bengtsson and Brostrom 2009; Bengtsson and Mineau 2009). The final aim is to translate the new knowledge produced by interdisciplinary work into interventions and policy advice designed to improve the long term health of individuals, social groups, and societies (Kuh et al. 2003). The IUSSP conference “Pathways to Health” aims to contribute to this process by pushing the frontier of our understanding of the mechanism linking early life conditions and later life health outcomes.

References

Almond, D. 2006. "Is the 1918 influenza pandemic over? Lont-term effects of in utero influenza exposure in the post-1949 U.S. Population." Journal of Political Economy 114(4):672-712.

Almond, D.and B. Mazumder. 2005. "The 1918 Influenza Pandemic and Subsequent Health Outcomes: An Analysis of SIPP Data." American Economic Review: Papers and Proceedings 95(2):258-262.

Barker, D.J. 2006. "Adult consequences of fetal growth restriction." Clin Obstet Gynecol 49(2):270-283.

Barker, D.J., K.M. Godfrey, et al. 1991. "Relation of birth weight and childhood respiratory infection to adult lung function and death from chronic obstructive airways disease." Bmj 303(6804):671-675.

Ben-Shlomo, Y.and D. Kuh. 2002. "A life course approach to chronic disease epidemiology: conceptual models, empirical challenges and interdisciplinary perspectives." Int J Epidemiol 31(2):285-293.

Bengtsson, T.and G. Brostrom. 2009. "Do conditions in early life affect old-age mortality directly and indirectly? Evidence from 19th-century rural Sweden." Soc Sci Med 68(9):1583-1590.

Bengtsson, T.and M. Lindstrom. 2003. "Airborne infectious diseases during infancy and mortality in later life in southern Sweden, 1766-1894." Int J Epidemiol 32(2):286-294.

Bengtsson, T.and G.R. Mineau. 2009. "Early-life effects on socio-economic performance and mortality in later life: A full life-course approach using contemporary and historical sources Introduction." Social Science & Medicine 68(9):1561-1564.

Bobak, M., M. Murphy, R. Rose, and M. Marmot. 2003. "Determinants of adult mortality in Russia: estimates from sibling data." Epidemiology 14(5):603-611.

Cameron, N.and E.W. Demerath. 2002. "Critical periods in human growth and their relationship to diseases of aging." Am J Phys Anthropol Suppl 35:159-184.

Elo, I.T., P. Martikainen, and M. Myrskylä. 2010. "Early Life Conditions and Cause-Specific Mortality in Finland. ." in University of Pennsylvania Population Aging Research Center Working Papers 10-04.

Frankel, S., G.D. Smith, and D. Gunnell. 1999. "Childhood socioeconomic position and adult cardiovascular mortality: the Boyd Orr Cohort." Am J Epidemiol 150(10):1081-1084.

Gagnon, A.and R. Mazan. 2009. "Does exposure to infectious diseases in infancy affect old-age mortality? Evidence from a pre-industrial population." Soc Sci Med 68(9):1609-1616.

Galobardes, B., Lynch, J.W., and Smith, G.D. 2004. "Childhood Socioeconomic Circumstances and Cause-specific Mortality in Adulthood: Systematic Review and Interpretation." Epidemiologic Reviews 26:7-21.

Godfrey, K.M., P.D. Gluckman, and M.A. Hanson. 2010. "Developmental origins of metabolic disease: life course and intergenerational perspectives." Trends Endocrinol Metab 21(4):199-205.

Hayward, M.D.and B.K. Gorman. 2004. "The long arm of childhood: the influence of early-life social conditions on men's mortality." Demography 41(1):87-107.

Kuh, D., Y. Ben-Shlomo, J. Lynch, J. Hallqvist, and C. Power. 2003. "Life course epidemiology." J Epidemiol Community Health 57(10):778-783.

Mazumder, B., D. Almond, K. Park, E.M. Crimmins, and C.E. Finch. 2009. "Lingering prenatal effects of the 1918 influenza pandemic on cardiovascular disease." J Dev Orig Health Dis 1(1):26-34.

McDade, T.W., M.A. Beck, C.W. Kuzawa, and L.S. Adair. 2001. "Prenatal undernutrition and postnatal growth are associated with adolescent thymic function." J Nutr 131(4):1225-1231.

Moore, S.E., T.J. Cole, A.C. Collinson, E.M. Poskitt, I.A. McGregor, and A.M. Prentice. 1999. "Prenatal or early postnatal events predict infectious deaths in young adulthood in rural Africa." IJE 28(6):1088-1095.

Moore, S.E., T.J. Cole, E.M. Poskitt, B.J. Sonko, R.G. Whitehead, I.A. McGregor, and A.M. Prentice. 1997. "Season of birth predicts mortality in rural Gambia." Nature 388(6641):434.

Myrskyla, M. 2010. "The relative effects of shocks in early- and later-life conditions on mortality." Popul Dev Rev 36(4):803-829.

Myrskylä, M., N. Mehta, and W. Chang. 2010. "Exposure to the 1918 Pandemic and Later Mortality by Cause: Evidence from the NHIS Data." Population Association of America Annual Meeting, April 15-17 2010.

O'Rand, A.M.and J. Hamil-Luker. 2005. "Processes of cumulative adversity: childhood disadvantage and increased risk of heart attack across the life course." J Gerontol B Psychol Sci Soc Sci 60 Spec No 2:117-124.

Preston, S.H., M.E. Hill, and G.L. Drevenstedt. 1998. "Childhood conditions that predict survival to advanced ages among African-Americans." Soc Sci Med 47(9):1231-1246.

Shaheen, S.O., D.J. Barker, A.W. Shiell, F.J. Crocker, G.A. Wield, and S.T. Holgate. 1994. "The relationship between pneumonia in early childhood and impaired lung function in late adult life." Am J Respir Crit Care Med 149(3 Pt 1):616-619.

Smith, G.D., C. Hart, D. Blane, and D. Hole. 1998. "Adverse socioeconomic conditions in childhood and cause specific adult mortality: prospective observational study." Bmj 316(7145):1631-1635.

van den Berg, G.J., M. Lindeboom, and M. Lopez. 2009. "Inequality in individual mortality and economic conditions earlier in life." Soc Sci Med 69(9):1360-1367.

 

 

 

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