Early Social Origins of Premature Aging: How Do Childhood Exposures Shape Aging and Mortality?

TitleEarly Social Origins of Premature Aging: How Do Childhood Exposures Shape Aging and Mortality?
Publication TypeThesis
Year of Publication2018
AuthorsKemp, BR
Academic DepartmentSociology
Number of Pages169
UniversityPurdue University
Thesis Typephd
ISBN Number9780438332454
Keywords0351:Gerontology, 0626:Sociology, Aging and the life course, Childhood exposures, Cumulative inequality theory, Gerontology, Mortality, Social Sciences, Sociology, Telomere length

The early origins of health literature documents a distinct link between early life exposures and a range of pathologies in later life. However, it is still unclear if and which types of childhood events and experiences shape biological aging or increase mortality risk among older adults. The purpose of this dissertation is to examine (1) what types of early life exposures influence biological aging and mortality and for whom and (2) whether biological age acts as a marker of early life stress and a predictor of mortality. Drawing from cumulative inequality theory, this dissertation uses six waves of data (2004-2014) from the Health and Retirement Study, a panel survey of adults age 51 and over, to examine the effect of six domains of childhood exposures on biological age and mortality. This dissertation is divided into three empirical chapters. The first study investigates the influence of childhood exposures on biological age as measured by telomere length. Findings reveal that risky parental behaviors during childhood are associated with shorter telomeres, and thus older biological age, yet in somewhat different ways for men and women. In addition, the impact of childhood impairment and infectious diseases on biological age varies by race. Study two asks which childhood exposure domains increase all-cause or cardiovascular mortality risk. Findings suggest that the positive association between socioeconomic disadvantage and mortality risk likely operates through adult socioeconomic factors. As anticipated, childhood infectious diseases decreased the risk of all-cause mortality. However, unexpectedly, risky parental behavior also decreased the risk of all-cause mortality. Among cardiovascular mortality analyses, risky adolescent behaviors increased the risk and one impairment during childhood decreased the risk of cardiovascular mortality. The last empirical study uses the sample of adults with telomere data to examine the effects of childhood misfortune and telomere length on all-cause, cardiovascular, and cancer mortality. Socioeconomic disadvantage during childhood reduced the risk of all-cause mortality, yet no other childhood exposure or telomere length was related to all-cause, cardiovascular, or cancer mortality. The effect of telomere length on all-cause mortality risk did, however, vary by race where telomere length was positively associated with mortality for Black adults and negatively associated with mortality for White adults. Taken together, these studies demonstrate that early life exposures have long-lasting and latent effects on aging and mortality, yet in distinct ways. Several childhood exposure domains were associated with biological age and/or mortality, underscoring the importance of investigating multiple domains. Despite the negative implications of some types of childhood misfortune, children and adults are capable of adaptation and resilience. This dissertation identified childhood exposure domains that should be targeted in prevention efforts and revealed that some types of early life stressors may promote adaptive strategies.


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Citation Key10305