Consequences of early events and conditions may be lifelong or long delayed. Such early onset illnesses as schizophrenia and epilepsy (West, 1991), the complications generated by rheumatoid fever (Barker, 1998; Elo and Preston, 1992), injuries due to violence, and impairments caused by substance abuse lead to proximate shifts in individuals’ health and mortality risks that endure for a lifetime. In contrast, impaired placental development, poor maternal nutrition, and extreme low birthweight may have effects not seen for a long time; all are suspected to be implicated in the late onset of coronary heart disease, non-insulin-dependent diabetes, lung disease, chronic bronchitis, and reduced immunocompetence (Barker, 1998; Chandra et al., 1989; Fall et al., 1998; Lucas, 1991, 1994; Lucas et al., 1999; Thurlbeck, 1992; Vagero and Leon, 1994). Similarly, early nutritional status may compromise later health status (Smith and Kuh, 1997).
The health effects of early events may not be immediately visible. For instance, there is early evidence of a link between early educational attainment and avoidance of cognitive decline late in life. This link could be due to synaptic connections in the brain, providing a cognitive reserve generated by education itself, or by higher levels of cognitive stimulation, or to the beneficial impact of higher self-esteem among the more educated (Hertzman et al., 2002; Manly and Mayeux, 2004). Similarly, the effects of stress may not be visible early in life. Although stress and resulting allostatic load have been investigated mainly in adults, it is possible that losses of plasticity of physiological response that increase the risk of chronic conditions could also be related to nonoptimal exposures to stress early in life (Hertzman et al., 2002).
Early health disadvantage may be compounded if individuals are put on pathways that, whatever their immediate affect on health, lead to poorer health later on. Research suggests that black children experience higher levels of poverty, more limited educational experiences, and more disruptive home lives—in segregated neighborhoods or with single mothers or unemployed parents. Such conditions constitute possible pathways to later health disadvantage.
Evidence regarding such pathways has accumulated slowly. The causative processes involved are complex, not readily amenable to representation in simple models, and often impossible to test without exceedingly rich information that spans the life of at least one cohort. Various dimensions of early environments can put one on a pathway, and only a few have been studied.
One important dimension is the socioeconomic status of the family of origin that may shape early life through numerous mediating mechanisms.