Academic journal article Demographic Research

Impact of Delayed Effects on Human Old-Age Mortality

Academic journal article Demographic Research

Impact of Delayed Effects on Human Old-Age Mortality

Article excerpt

(ProQuest: ... denotes formulae omitted.)


In the last decade or so, research guided by the Developmental Origins of Health and Disease (DOHaD) paradigm and related theories has grown rapidly (Bateson and Gluckman 2011; Gluckman and Hanson 2005, 2006; Rosenfeld 2008). While the original idea of delayed adult effects of early childhood conditions has been around for quite some time and in very disparate strands of the literature (Derrick 2006; Frost 1939; Kermack, McEndrick, and McKinlay 1934; Preston and van de Walle 1978), it was Barker's work on "fetal programming" that provided the initial impetus for the creation of what is now a very active field of empirical research (Barker 1998, 2012; Hales and Baker 2001; Lucas 1991). Ecological and epidemiological studies, natural experiments, as well as animal studies under controlled conditions, provide an array of evidence supporting DOHaD's key predictions. However, the implications of DOHaD for aggregate population patterns of human health, disability, and mortality have been neither rigorously formulated nor empirically tested. In this paper we contribute to fill this vacuum. First, we rely on a formal model of relations between early conditions and adult health and mortality conjectured by DOHaD to derive a handful of predictions. Second, we use a long time series of cohort mortality in countries of the Latin American and Caribbean (LAC) region, whose populations, we argue, are primed to manifest the impact of early conditions, to test two of the model predictions.

The plan of the paper is as follows: In Section 2 we briefly review mechanisms posed by DOHaD and related theories. Section 3 describes implications of delayed effects for human adult mortality patterns. Section 4 presents predictions and conditions of observability. Section 5 describes selected characteristics of our case study. Section 6 reviews the data and models. Section 7 discusses results and draws inferences. In the final section we summarize, highlight limitations, and identify future lines of research.

2.Background: Mechanisms for adult delayed effects

A diverse set of mechanisms could transform episodic or recurrent early exposures in utero, perinatally, and during infancy and early childhood into delayed impacts on adult illness, disability, and mortality. The mechanisms are associated with organ-specific embryo and fetal cell growth and differentiation (Bateson and Gluckman 2011; Gluckman and Hanson 2005, 2006), epigenetic changes (Gluckman, Buklijas, and Hanson 2016; Godfrey et al. 2007; Kuzawa and Eisenberg 2014; Meaney 2010), exposure to and contraction of early childhood diseases and sustained inflammation (Crimmins and Finch 2006; Elo and Preston 1992; Finch and Crimmins 2004; Fong 2000), and experiences with stressful conditions and environments (McEwen 1998; Meaney 2001, 2010). Furthermore, a large and influential body of empirical research documents the long-lasting impact of early nutritional status on adult health and mortality (Costa 2000; Fogel 2004; Scrimshaw 1997; Scrimshaw and SanGiovanni 1997). Finally, there is widespread empirical evidence demonstrating that more diffuse exposures, such as poverty and severe deprivation in infancy and early childhood, can also have lasting impacts (Bengtsson and Lindstrom 2012; Forsdahl 1987, 2002).

The mechanisms identified above are the focus of various strands of theories with unique histories and distinct disciplinary foundations. Different as they may be, however, they share an important trait as all invoke perturbations during critical periods of the development of a phenotype triggered by insults before conception, during embryonic and fetal life, perinatally, and across early stages of physical and cognitive growth. These early insults may then lead to disruptions in processes of organ growth, differentiation, and function; immune response; neurological development; metabolic regulation; and even the formation of adult preferences and behaviors. …

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